Veterinary Diagnostic Imaging - The Dog and Cat

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Veterinary Diagnostic Imaging: The Dog and Cat Copyright © 2003, Mosby, Inc. All rights reserved.

ISBN 0-323-01205-1

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permissions may be sought directly from Elsevier’s Health Sciences Rights Department in Philadelphia, PA, USA: phone: (+1) 215 238 7869, fax: (+1) 215 238 2239, e-mail: [email protected]. You may also complete your request on-line via the Elsevier Science homepage (http://www.elsevier.com), by selecting ‘Customer Support’ and then ‘Obtaining Permissions.’

NOTICE Veterinary Medicine is an ever-changing field. Standard safety precautions must be followed, but as new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current product information provided by the manufacturer of each drug to be administered to verify the recommended dose, the method and duration of administration, and contraindications. It is the responsibility of the licensed prescriber, relying on experience and knowledge of the patient, to determine dosages and the best treatment for each individual patient. Neither the publisher nor the author assumes any liability for any injury and/or damage to persons or property arising from this publication.

Library of Congress Cataloging-in-Publication Data Farrow, Charles S. Veterinary diagnostic imaging: the dog and cat / Charles S. Farrow. p.; cm. Includes bibliographical references and index. ISBN 0-323-01205-1 (alk. paper) 1. Dogs–Diseases–Diagnosis. 2. Cats–Diseases–Diagnosis. 3. Veterinary diagnostic imaging. I. Title. [DNLM: 1. Dog Diseases–radionuclide imaging. 2. Cat Diseases–radionuclide imaging. 3. Cat Diseases–ultrasonography. 4. Diagnostic Imaging–veterinary. 5. Dog Diseases– ultrasonography. SF 991 F246v 2003] SF991 .F38 2003 636.7¢08960754–dc21 2002041063 Acquisitions Editor: Liz Fathman Developmental Editor: Kristen Mandava Publishing Services Manager: Pat Joiner Project Manager: Rachel E. Dowell Senior Designer: Mark A. Oberkrom Interior Designer: Joan Wendt Cover Design: Studio Montage Printed in China Last digit is the print number: 9

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This book is dedicated to the heroic passengers and aircrew of United Airlines flight 93, who on September 11th, 2001, made their last stand in the sky. May God bless them.

About This Book

First and foremost this is a book about veterinary medical imaging. Although there are smatterings of medicine, surgery, and clinical pathology, you will need to read elsewhere for detailed accountings of such matters.

Content and Credit The backbone of this book has been constituted from the articles published in the American Journal of Veterinary Radiology & Ultrasound from 1963 to the present, nearly all of which are included among the references. In most instances I also included the name of the principal authors in the text (as well as in the chapter references) to properly credit the work and for the convenience of the reader. To provide a contemporary perspective beyond that of the “Journal,” I incorporated selected material from the publications of organizations such as the American Veterinary Medical Association, American Animal Hospital Association, and Journal of Small Animal Practice.

although we will soon have our own in-house MR imager. The majority of these examinations are of the brain and spinal cord, mostly tumors and disks. We rarely perform nuclear medicine, and as a consequence have only limited clinical material. Because radiation therapy is now a specialty in its own right, it has been omitted altogether.

“RDIs”: A Rational Substitute for Roentgen Signs In nearly three decades as a radiologist I have sought to devise a coherent, integrated method for teaching and learning radiographic fundamentals. To this end I have developed a series of radiographic disease indicators, or RDIs, for each radiology subspecialty. These diagnostic building blocks form the basis for radiologic diagnosis, much as words comprise the substance of a sentence. You will be introduced to an appropriate list of RDIs at the beginning of each section, and then see them applied in the subsequent chapters.

Organization

Figures and Captions

Given the anatomic foundation on which all forms of medical imaging are predicated, it is clear that any book on the subject must be organized on a similar basis. Accordingly, Veterinary Medical Imaging is divided into 7 sections: (1) Extremities; (2) Skull, Brain, Eye, and Ear; (3) Spine; (4) Hips and Pelvis; (5) Throat, Neck, and Thorax; (6) Heart; and (7) Abdomen. Each section is in turn divided into chapters—77 in all. To facilitate comprehension, as well as rapid reference, series of facts have been enumerated within individual sentences, presented as bulleted and numbered lists, or tabulated, depending on their number and complexity.

The medical images in a book such as this are in many respects like the actors in a play; they provide a means of expression for the playwright. To this end I tried to present the material in a more “intimate” fashion, incorporating wherever possible both orientation and closeup views, and in the case of the extremities, normal comparison views from the opposite limb. Instead of arrows to identify the salient points in an image, I employed electronic emphasis zones, hopefully making it even easier to appreciate the lesion, while obscuring none of its detail. As an aside, my students refer to this method of pointing out pathology, which I also use in the classroom, as the “electronic hot lamp.” Furthermore, I tried not only to portray a wide variety of disorders, but also to include an ample number of variants, especially of the more commonly encountered diseases such as osteochondritis of the

Imaging Emphasis The emphasis in this book is on radiology and ultrasound, just as in our hospital. Currently we perform MRI and CT examinations out of hours at local hospitals,

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elbow where lesions can range from the obvious, typically shown in most textbooks, and termed “classics,” to the obscure that often only experts can detect. Finally, with respect to captions, I tried to keep them as brief as possible so as not to try the patience of the reader. And to even further expedite the process, I bolded the diagnosis or key point, providing a “diagnosis-at-a-glance.”

Terminology The reader will perhaps note some peculiarities with respect to the anatomic nomenclature, especially in Section 1: The Extremities; these are deliberate and reflect my desire to simplify an increasingly complex (and at times unwieldy) anatomic lexicon. Please read and consider the following proposal, try it out, and be kind enough to let me know what you think—I am open to suggestions. Radiographic Views • Lateral radiographs of the limbs are described as lateral views, or lateral oblique views (as necessary). The term lateromedial is unnecessary since it is understood that the x-ray beam will penetrate the part in this manner. • Dorsopalmar, dorsoplantar, and craniocaudal radiographs will all be termed frontal views, or frontal

oblique views (as required). Changing terminology at the level of the radiocarpal and tibiotarsal joints is both cumbersome and confusing, especially to novices. Because images made from front to back are nearly indistinguishable from those made from back to front—very minor object-film and magnification considerations notwithstanding—there is no need for terms such as palmarodorsal and plantarodorsal. Extremital Anatomy • Shoulder or shoulder joint to replace humeral or scapulohumeral joint. • Elbow or elbow joint to replace cubital or humeroradial/humeroulnar joint. • Radiocarpal joint to replace antibrachiocarpal joint. • Forepaw to replace manus. • Hip or hip joint to replace coxofemoral or coxal joint. • Knee or knee joint to replace stifle or femorotibial joint. • Tibiotarsal joint to replace tarsocrural joint. • Hindpaw to replace pes. For those teaching radiology, to include those explaining medical images to owners, I recommend that whatever terminology is employed, it satisfy the following three criteria: simple, clear, and brief. Charles S. Farrow

Acknowledgment

Many talents are required to write, assemble, and publish a book such as this: author, medical photographer, editor, and compositor, to name only a few. But perhaps most important among this company, and often the most overlooked, is the project manager, the individual who brings everything together, solves problems, listens to excuses, keeps the project on track and on time—and all without hurting anyone’s feelings! Ours is the best, Rachel Dowell. Thanks for everything, Chuck Farrow

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S E C T I O N

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The Extremities

C h a p t e r

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Extremital Radiographic Disease Indicators

The following radiographic abnormalities are reliable indicators of extremital disease, or radiographic disease indicators (RDIs).

❚❚❚ PERIOSTEAL NEW BONE New Bone: The Term One of the common attributes of many different skeletal lesions is the presence of new bone, that is, bone that has developed as a direct or indirect result of an injury, infection, tumor, or some other local or systemic disease. Because the majority of new bone is produced by the periosteum (inner layer), it is often referred to as periosteal new bone or periosteal new bone formation. Most simply, it may be described as bone deposition. Regardless of the term used, the importance lies in what it represents: a response to an abnormal stimulus that is sometimes brief, often repeated, and occasionally sustained. In all cases, it is a stimulus that causes the bone to grow anew, in some instances repairing, and in others strengthening (or defending) it.

Other Related Terms Other terms also deserve mention because of their limitations, ambiguities, or deficiencies rather than for their virtues. Bone reaction: There may be two types: productive or destructive; thus the term bone reaction is ambiguous if not qualified. Sclerosis or sclerotic: Bone that appears excessively white radiographically; this term is often used to describe abnormal subchondral bone. This term is best replaced with increased bone density or opacity. Eburnation or eburnated: Smooth, polished, ivory-like bone surface; this term is often used to describe the articular surfaces of arthritic joints, and implies a complete loss of articular cartilage. This term appears better suited to the sense of touch than that of sight. Increased density: Bone that is radiographically lighter than normal and synonymous with increased opacity. Decreased density: Bone that is radiographically darker than normal and synonymous with decreased opacity. 1

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SECTION I ❚❚❚ The Extremities

Radiodense or radiodensity, radiolucent or radiolucency: The prefix radio- is redundant because it is understood that such observations pertain to a radiograph.

Origins of New Bone New bone may be created from existing bone on either the inner or outer osseous membranes: the endosteum and periosteum, beneath the joint cartilage; the subchondrium, along the joint margins; the periarticular region, on the surface of the epiphysis adjacent to the articular surface; the extraarticular region; and within muscle (myositis ossificans). Bone may also be produced by some primary bone tumors such as osteosarcoma, chondrosarcoma, and fibrosarcoma.

New Bone Stimuli Stress. As first elucidated by Wolf, bone is a highly adaptable and surprisingly labile tissue, which is amply demonstrated by the developing appendicular skeleton.1 For example, the distal ulnar growth plate of a young puppy may be fractured, and as a result, cease to grow. As the inevitable bony curvatures and dislocations develop, the affected long bone cortices begin to change or remodel through caudal and medial thickening and cranial and lateral thinning in the face of the changing force lines and weight distribution. Trabeculae become realigned, and subchondral plates become reinforced in an effort to cope with the new anatomic realities (Figure 1-1). Similar restructuring occurs after part of a bone has been surgically removed. For example, with a femoral head and neck ostectomy, the greater trochanter elongates, tapers, and aligns itself more closely with the

Figure 1-1 • Lateral and frontal views of a deformed midforelimb; the result of an earlier distal ulnar growth plate fracture, subsequent premature physeal closure, and secondary radial bowing.

femoral shaft. Concurrently the acetabulum atrophies and loses density as its mineral content is withdrawn in the absence of articular contact (Figure 1-2). Stress, in the form of weight bearing with related muscular contraction-relaxation, plays a dominant role in fracture healing, gradually incorporating calluses and eliminating angulations, so that in a majority of instances, even in the case of severely comminuted fractures, the damaged bone is largely restored (Figure 1-3). Injury. One needs only to observe a fracture callus to appreciate the potency of injury as a stimulus for new bone formation (Figure 1-4). After the initial repair is achieved, renewal of normal internal and external bone stress initiates, mediates, and maintains the process of bone restoration, often to the extent that the original injury defies recognition some months later. Ischemia, whether or not induced by injury, also stimulates osteogenesis, as exemplified by compartmental syndrome. Infection. Slowly developing, localized osteomyelitis usually allows the affected bone sufficient time to construct a bony perimeter around the lesion, which is termed an involucrum (Figure 1-5). Although substantive, such defensive bulwarks rarely achieve true “containment.” Some authors have termed this type of new bone reactive bone, a loosely mechanistic label that is redundant because all new bone reacts to one or more stimuli.

Figure 1-2 • Close-up frontal view of the proximal femoral stump in a cat 4 years after fracture and surgical removal. The elongated shapes of the greater and lesser trochanters reflect the structural adaptation of these muscular moorings to the removal of the femoral head and neck. The washed-out appearance of the acetabulum is the result of secondary demineralization caused by the removal of the opposing articular surface.

CHAPTER 1 ❚❚❚ Extremital Radiographic Disease Indicators

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A

Figure 1-3 • Full-length frontal view of a healed femoral fracture still encased in a lengthy callus months after the injury. In time, however, most calluses completely disappear by incorporating into the adjacent cortex, thereby restoring the bone to its former appearance.

B Figure 1-4 • A, A thick, smoothly surfaced callus surrounds the distal femur. The callus is the result of a badly comminuted fracture 3 months earlier. B, Lateral (left) and frontal (right) images of a badly displaced, untreated proximal humeral gunshot fracture that has healed end-to-side; like most such fracture calluses, the new bone deposition is asymmetric, reflecting a redistribution of mechanical forces on the limb.

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SECTION I ❚❚❚ The Extremities

Figure 1-5 • Close-up frontal views of the carpi of a dog quilled 6 weeks earlier show a spherical lucency in the bottom center of the right radial carpal bone (left), surrounded by a sclerotic ring (emphasis zone), indicating a localized osteomyelitis; the opposite normal carpus is provided for comparison.

Figure 1-7 • Lateral view of a tibial osteosarcoma shows cloudlike fronds of tumor bone extending outward from the diaphysis.

Soft tissue infections, if severe or chronic enough, cause bone to form beneath the periosteum, often termed periosteal new bone formation, or more simply, periosteal new bone (Figure 1-6). Rarely are bacteria actually residing and replicating in the bone in such instances; rather, the periosteum has been stimulated by the surrounding infection, often with associated thrombosis of portions of the periosteal blood supply.

Figure 1-6 • Frontal view of the distal antibrachium, carpus, and metacarpus show periosteal new bone formation on the outer surfaces of the distal radius, fifth metacarpal bone, and proximal part of the first digit. Moderate regional soft tissue swelling is the result of cellulitis stemming from bite wounds, prompting the described periostitis.

Malignant Bone Lesions. Some tumors are capable of producing bone, including osteosarcoma, chondrosarcoma, and fibrosarcomas (Figure 1-7). Appropriately, such tissue is termed tumor or cancer bone, to distinguish it from defensive bone produced by the host in the case of infection. Unfortunately and in contrast to most bone infections, tumors grow so rapidly that there is usually insufficient time to mount and sustain a defensive bony perimeter, so involucra and sequestra are rarely seen (Figure 1-8). Aging New Bone. In critically evaluating new bone, temporal considerations are often important. For example, is the estimated age of an observed bone deposit consistent with the time elapsed since the presumed injury? Or is an observed new bone deposit a relevant or incidental finding?

CHAPTER 1 ❚❚❚ Extremital Radiographic Disease Indicators

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Potential conclusions that may be reached from estimates of new bone age include: • Clinical relevancy • Historical compatibility • Lesion activity or inactivity

Morphologic Observations Configuration. The amount of observed new bone may be great or small, and its shape quite variable. It may be flat and closely applied to the outer cortical surface over a wide area, or it may project outwardly at a sharp angle from a narrow base, the latter situation termed an osteophyte. Margination. The surface of new bone deposits ranges from thick to thin, and from smooth to rough— features that are often reliable indicators of new bone maturity. Density. Like margination, new bone density can be used to estimate the maturity of new bone. In general, the denser the new bone, the older it is.

A

Estimating the Age of New Bone Deposits Immature New Bone. Immature new bone initially resembles fine strands of newly planted grass emerging from the cortical surface, or alternatively, the tips of the bristles of a paintbrush seen in profile. In a week or so, the new bone begins to assume a denser, rougher looking surface. Bone with this appearance has usually been produced within the past month or so (Figures 1-9 and 1-10). Developing New Bone. Developing new bone can assume a variety of appearances, ranging from even layering to interrupted, variably-sized bony mounds (Figures 1-11 and 1-12); at other times, a series of individual blocks of bone forms at right angles to the cortex, forming what is sometimes referred to as a palisade. New bone of this type is usually between 1 and 3 months old.

B Figure 1-8 • A, Close-up frontal view of a distal fibular osteosarcoma shows a mixed, productive destructive lesion. B, A month later the tumor has broken out of the fibula and is producing clouds of tumor bone in the adjacent soft tissues.

Mature New Bone. In its advanced stages of development, new bone more closely resembles the bone surface on which it resides. It usually appears smoothly surfaced and quite dense, often appearing more as a lump in the underlying bone, than a bony add-on. Such deposits are very difficult to precisely age because they may be as little as a few months old, or alternatively, years in duration (Figures 1-13 and 1-14). Unlike exterior bone deposits, interior (medullary or endosteal) bone deposits are difficult to evaluate because discrete margins are difficult or impossible to profile. Fortunately however, most such lesions are caused by panosteitis (Figure 1-15), a condition characteristically found in young German Shepherds being presented for lameness.

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SECTION I ❚❚❚ The Extremities

A

B

Figure 1-9 • Single lateral oblique views of right (A) and left (B) tarsi of a cat injured approximately 1 week prior show similar injuries bilaterally: badly displaced fractures of the distal tibial growth plate and distal fibular body. The left calcaneus has a detached apophysis. New bone deposition on the distal fibular fragments supports the fact that this is not an acute injury.

Figure 1-10 • Lateral view of the mid-forelimb of a cat containing an intravenous line shows recently formed periosteal new bone on the cranial surface of the radius (emphasis zone).

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Figure 1-11 • Lateral close-up of the proximal humerus shows recently formed metaphyseal new bone and a faint lucent band just below the growth plate, the characteristic features of metaphyseal osteopathy.

Figure 1-13 • Frontal close-up of the distal humerus shows a large, dense, smoothly surfaced bone deposit, the result of a previous fracture.

Caution: Growing long bones, especially early in their development, often exhibit roughened metaphyses, termed cutback zones (Figure 1-16). This is normal and usually persists for only a few weeks, depending on the time required to attain skeletal maturing.

❚❚❚ JOINT BODIES (INTRAARTICULAR BONE FRAGMENTS) As used in this context, “loose” usually refers to small bone fragments or joint bodies that appear separated from the normal osseous elements of the joint, although such bodies may be fixed in position by soft tissue. Caution: Care must be taken not to mistake normal sesamoids for loose joint bodies (Figure 1-17). Figure 1-12 • Close-up lateral view of the infected carpus of a dog shows a large chunk of new bone (intermediate duration) on the craniodistal aspect of the radius, in addition to smaller deposits on the carpal bones and proximal metacarpus. Numerous small areas of bone destruction are also present, especially in the distal radius and caudal carpus. Joint swelling is pronounced.

Loose intraarticular bodies are most often seen in the humeral, cubital, and genual joints of the dog. In the case of the dog’s shoulder, most joint bodies located in the caudal pouch are presumed to have originated from the caudal aspect of the humeral head, second-

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SECTION I ❚❚❚ The Extremities

Figure 1-14 • Lateral (A) and frontal (B) views of an old femoral fracture in a cat. A single wire band deeply imbedded in the callus is all that remains of the original implants.

A B

Figure 1-15 • Immature German Shepherd: lateral close-up of the elbow shows a patch of new bone in the interior of the proximal ulnar shaft (emphasis zone) typical of panosteitis.

Figure 1-16 • Close-up frontal view of the distal radius and ulna shows normally prominent metaphyseal cutback zones resembling periosteal new bone.

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Figure 1-18 • Close-up lateral view of a cat’s shoulder shows a large conforming joint body lying over the caudal aspect of the humeral head, presumed to be the result of an old injury. Figure 1-17 • Lateral close-up of the stifle of a dog that tore its cranial cruciate ligament 7 weeks earlier. The genual joint has developed a characteristic arthritic pattern consisting of osteophytes on the proximal trochlea, distal patella, and proximal tibia, in addition to being swollen. The small circular bone just proximal to the fibula is the popliteal sesamoid, which is not a joint body related to the dog’s damaged knee.

ary to osteochondritis. Humeral joint bodies in cats are more likely to be the result of a previous injury or immunoarthritis (Figure 1-18). Occasionally, osteochondritis occurs in unusual locations, suggesting trauma. Fortunately most such findings are present bilaterally, thereby decreasing the probability of injury compared with osteochondritis (Figure 1-19), whereas other findings are clearly incidental (Figure 1-20). Alternatively, these bony objects may represent synovial osteochondromatosis, a proliferative disease of undifferentiated synovial stem cells in which cartilage flaps or vascularized cartilage fragments are transformed into bone through the process of enchondral ossification (Figure 1-21).2 Bodies located cranial to the humeral tubercles are more problematic because they may be osteochondral fragments or regional dystrophic calcification (Figure 1-22). In the stifle, small, centrally located calcified bodies are most likely to have originated from avulsion of the cranial cruciate ligament (Figure 1-23, A, B). In older cats, loose joint bodies are most likely to be found in the cubital, antibrachial carpal, genual, and tarsocrural joints.3 The most probable cause of such bodies, especially if present bilaterally, is osteochondromatosis. Both dogs and cats may incur loose joint bodies as a result of articular or avulsion fractures, particularly when associated with dislocation.

❚❚❚ PERIARTICULAR OSTEOPHYTES Variably-sized triangular bone deposits on the articular margin of a joint are known as periarticular osteophytes and are generally considered to be the most characteristic feature of osteoarthritis (Figures 1-24 and 1-25).

❚❚❚ EXTRAARTICULAR OSTEOPHYTES Small bone deposits located adjacent to the articular margin are known as periarticular osteophytes. When present in a single joint, periarticular osteophytes are most likely to be the result of previous trauma (Figure 1-26), but when present bilaterally are more likely to be associated with osteochondritis or immunoarthritis (Figure 1-27).

❚❚❚ ENTHESIOPHYTES Enthesiophytes are often anatomically indiscernible from osteophytes, both possessing a roughly triangular appearance and bonelike density. Location distinguishes the osteophyte from the enthesiophyte because unlike osteophytes, enthesiophytes are formed within the origin or insertion of a tendon or ligament. Recall that osteophytes, the premier RDI of osteoarthritis, are characteristically found along the articular margin of one or more bones in a particular joint. Accordingly, they are termed periarticular osteo-

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SECTION I ❚❚❚ The Extremities

A

B

Figure 1-19 • Unusual osteochondritis: close-up frontal views (A, B) of the radiocarpal joints of a young Golden Retriever show multiple bone fragments alongside large irregular defects in the distal radius.

or around a joint, provided they are in the known location of a tendon or ligament because this is where they are formed. Clearly, declaring a periarticular bone deposit to be an enthesiophyte, rather than an osteophyte, is highly speculative business. Even if an enthesiophyte is identified with confidence, establishing its clinical importance can be quite difficult because many enthesiophytes are innocuous. For example, a painless enthesiophyte at the origin of the short radial ligament (frontal projection) is present in 14 percent of racing Greyhounds.4

❚❚❚ LOCALIZED BONE LOSS Aggressive Lesions Figure 1-20 • Close-up flexed lateral view of 8-month-old German Shepherd shows a small triangular bone fragment just above the center of the anconeal ridge. Because a similar fragment was also present in the opposite elbow, but more importantly that the dog was sound, final diagnosis was postponed pending future radiographic examination. Possible explanations for the described fragment can be found in the text.

phytes. Bone deposits that are similar in appearance and estimated to be in close proximity to the joint capsule are termed extraarticular osteophytes, and are the principal RDI of immunoarthritis. Enthesiophytes, unlike periarticular and extraarticular osteophytes, may be located anywhere within

Aggressive appearing bone lesions often prove to be cancerous. When located in the proximal or distal metaphysis, they are most probably primary bone tumors (Figure 1-28), whereas those found in the diaphysis are more likely metastases. Occasionally, aggressive appearing fungal infections occur in the shafts of long bones and resemble secondary bone tumors. Some advanced bone tumors so consume the bone that determining their origin is impossible (Figures 1-29 and 1-30). Although difficult to precisely define, the term aggressive is in wide clinical use. Most often, the term refers to a poorly marginated, primarily destructive lesion that often involves the marrow and an adjacent cortex. Accompanying plumes of calcification extendText continued on p. 15

CHAPTER 1 ❚❚❚ Extremital Radiographic Disease Indicators

A

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B

Figure 1-21 • Close-up frontal (A) and lateral (B) views of a cat’s elbow show numerous periarticular and extraarticular bone deposits, the result of synovial osteochondromatosis. As in most such cases, this was an incidental finding in an older cat.

Figure 1-22 • Close-up skyline view of the proximal tuberal groove shows focal bone deposits, which have been associated with tenosynovitis.

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SECTION I ❚❚❚ The Extremities

B

A

Figure 1-23 • Close-up recumbent (A) and standing lateral (B) views of the arthritic stifle of a dog that previously ruptured its cranial cruciate ligament. Note the dislocation (subluxation) apparent in the standing film but not in the conventional projection.

Figure 1-24 • Osteochondritis: close-up frontal view of an arthritic elbow in a middle-aged Labrador Retriever shows a characteristically beaked medial coronoid process.

Figure 1-25 • Long-standing instability caused by a third-degree cranial cruciate sprain 7 years earlier has resulted in severe osteoarthritis and a spectacular bone spur on the caudal aspect of the tibia.

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Figure 1-26 • Close-up frontal view of a severely arthritic stifle shows osteophytes in both the periarticular and extraarticular regions; the uneven joint width suggests instability and miniscal injury/degeneration.

A

B Figure 1-28 • A, Close-up ventrodorsal view of proximal femur in

Figure 1-27 • Frontal view of a dog’s carpus shows a large extraarticular osteophyte on the lateral aspect of the distal radius just below the physeal growth scar (emphasis zone), which is the result of chronic immunoarthritis.

an older dog shows a roughly spherical region of metaphyseal bone loss, surrounded laterally and distally by areas of new bone deposition and cortical disruption consistent with a moderately advanced primary bone tumor (fibrosarcoma). B, Close-up frontal view of the distal radius of a dog with an early primary bone tumor (osteosarcoma) shows new bone deposition on the exterior surface and mild destruction of the interior (emphasis zone).

B

A

C

Figure 1-29 • A, Ventrodorsal view of the pelvis and upper hind limbs of a dog with a secondary bone tumor in the midshaft of its right femur (emphasis zone). B, A full-length, close-up frontal view of the tumor reveals its predominantly destructive nature. C, A close-up lateral view shows a centrally located pathologic fracture (ragged dark line in the center of the emphasis zone).

A

B

Figure 1-30 • A, Close-up ventrodorsal view of pelvis, hips, and upper hind limbs of a dog with a primary bone tumor (osteosarcoma). B, Close-up view of the tumor, which shows the impossibility of determining exactly where it began.

CHAPTER 1 ❚❚❚ Extremital Radiographic Disease Indicators

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Figure 1-32 • Lateral oblique close-up view of the carpus shows the accessory carpal bone enveloped in a cloud of new bone, the result of a rare parosteal sarcoma.

Figure 1-31 • Close-up xerogram shows classic localized bone infection in the lateral aspect of the distal ulna, featuring a (1) sequestrum, (2) cloaca, (3) involucrum, and (4) new bone along the outer perimeter of the lesion.

ing outwardly into the surrounding muscle (tumor bone) further signal potential malignancy.

Nonaggressive Lesions Nonaggressive bone lesions, usually infections, are those that have a well-defined margin and are usually found in the diaphysis (Figure 1-31). Unfortunately, some malignant bone lesions initially appear this way, only later adopting the aggressive features of a malignancy.

❚❚❚ LOCALIZED BONE DEPOSITION Localized bone deposits, as already described, can form for a myriad of reasons, but are most often the result of a previous injury, infection, or tumor (Figure 1-32).

❚❚❚ METAPHYSEAL LYSIS Metaphyseal lysis is most commonly encountered after growth plate fractures (Figure 1-33, A-D). Metaphyseal osteopathy, which is also termed hypertrophic osteodystrophy (Figure 1-34), and some hematogenous infections (“puppy strangles”) may also produce lucent metaphyseal bands but are far less common.

❚❚❚ OSTEOPENIA Posttraumatic osteoporosis is a common sequela to many mid and distal long bone fractures and can be particularly pronounced in young dogs. Often mistakenly termed disuse osteoporosis, posttraumatic osteoporosis always develops distal to the fracture and/or dislocation (Figure 1-35, A, B), whereas disuse osteoporosis (a comparative rarity) involves the entire limb. Once the fracture forms a solid callus and the bone once again becomes rigid, bone density rapidly returns to normal. Chronic carpal and tarsal sprains, with or without fracture or fracture-dislocation, are also subject to mineral depletion caused by posttraumatic osteoporosis, which often leaves the bones faint and hollow looking (Figure 1-36).

❚❚❚ DISLOCATION (SUBLUXATION, LUXATION) Dislocations, which are also termed luxations or subluxations depending on the amount of articular displacement, are almost always accompanied by ligament injuries, such as injury to the collaterals in the elbow, the cruciates in the knee, and the teres in the hip. If untreated, dislocation may predispose to reinjury and eventually result in arthritis. Some dislocations relocate shortly after they occur, often defying radiographic diagnosis, unless stress or postural films are made. Occasionally, dogs may be born with dislocation of the elbow, which is nearly always bilateral, or suffer a traumatic dislocation as young puppies. In the

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SECTION I ❚❚❚ The Extremities

A

B

C

D

Figure 1-33 • Close-up frontal (A) and lateral (B) views of nondisplaced distal radial and ulnar growth plate fractures in a kitten show widened, irregular physes with a vague band of mineral depletion in the adjacent metaphyses. Views of the opposite carpus are provided for comparison (C, D).

CHAPTER 1 ❚❚❚ Extremital Radiographic Disease Indicators

Figure 1-34 • Radiolucent bands paralleling the growth plates of

17

A

the distal radius and ulna are the hallmark of metaphyseal osteopathy, as well as subacute growth plate fractures.

latter instance, and especially after a few months of remodeling, it can be very difficult to separate congenital from traumatic causes. Radiographically, most dislocations feature malalignment and varying degrees of articular overlap. As a result, the cartilage space may appear abnormally widened, narrowed, uneven, misshapen, or invisible. In some instances one or more small extraarticular bone fragments indicate the presence of avulsion fractures, potential clues as to which ligaments may have been injured (Figures 1-37 and 1-38).

❚❚❚ LIMB DEFORMITY (ANGULAR LIMB DEFORMITY) Most unilateral limb deformities in dogs result from injury, either to growth plates, in which case the deformity is of a secondary nature, or to the bones or joints directly. Figure 1-39 shows a severely bowed lower forelimb caused by a badly comminuted radial fracture (currently classified as a malunion). Bilateral limb curvatures, deficits, and deformities are more likely to be the result of congenital or developmental disorders.

❚❚❚ SOFT TISSUE SWELLING Soft tissue swelling, or more accurately (from a radiographic perspective) increased soft tissue area (and

B Figure 1-35 • Frontal (A) and lateral oblique (B) views of the carpus of a young kitten show the regional mineral depletion (posttraumatic osteoporosis) characteristic of a chronic carpal injury (sprain, fracture, and dislocation).

often density), is a nonspecific finding that is typically interpreted in the current clinical context: cellulitis, when present with puncture wounds (Figure 1-40), hemorrhage when associated with fracture, and so forth.

18

SECTION I ❚❚❚ The Extremities

Figure 1-36 • Severe posttraumatic osteoporosis of the tarsal bones of a cat (medial oblique projection).

A

B

Figure 1-37 • Lateral (A) and frontal (B) close-up views of a sprain, fracture, and dislocation of a cat’s elbow.

CHAPTER 1 ❚❚❚ Extremital Radiographic Disease Indicators

A

B

19

Figure 1-39 • Limb deformity.

Figure 1-38 • Frontal standing (A) and close-up (B) views of chronic sprain, fracture, and dislocation of a dog’s radiocarpal joint.

A

B

C

Figure 1-40 • Full-length lateral (A) and frontal (B) views of the mid-forelimb of a cat show uniform swelling, the result of numerous bite wounds. C, Lateral thigh region of a dog shows massive soft tissue swelling, which developed over a period of 4 months, the result of a leiomyosarcoma.

20

SECTION I ❚❚❚ The Extremities

References 1. Wolf J: The law of transformation of bone. Berlin, 1892, Hirshwald Verlag. 2. Edinger DT, Manley PA: J Small Anim Pract 39:397, 1998.

3. Hardie EM, Roe SC, Martin FR: Radiographic evidence of degenerative joint disease in geriatric cats: 100 cases (1994-1997), J Am Vet Med Assoc 220:628, 2002. 4. Guilliand MJ: Enthesiopathy of the short radial ligaments in racing greyhounds. J Small Anim Pract 39:227, 1998.

C h a p t e r

2

Extremital Injury

❚❚❚ MUSCLE BRUISES AND HEMATOMAS Bruise Varying degrees of bruising accompany most serious injuries in animals. Radiographically, bruising appears as a nonspecific soft tissue swelling that reflects deep or superficial hemorrhage and edema. Unlike a hematoma, which is often relatively localized and well marginated, bruising is diffuse and poorly delineated. Sonographically, an acute bruise often appears as a diffuse, ill-defined area of decreased echogenicity within the injured muscle. Within just a few days, however, the only remaining distinguishing feature may be a relative increase in overall muscle size compared with the opposite limb. Severe muscle swelling often results in spreading and distortion of the parallel white bands (striae) that characterize normal muscle.1

Hematoma Hematomas may be either intramuscular or intermuscular; the former is the more serious injury. Tearing of the muscle body in association with arterial rupture constitutes the optimal conditions for the formation of an intramuscular hematoma (Figure 2-1). Residual scarring or fatty infiltration can cause chronic pain and weakness with varying degrees of associated disability. Occasionally, a large, rapidly developing hematoma exerts enough pressure on the surrounding tissues to cause ischemia, anoxia, and, if the pressure is not relieved, eventual necrosis. This is termed a compartment or compartmental syndrome. Sonographically observed lesions compatible with hemorrhagic compartmentalization typically appear, depending mostly on duration, as discrete, oval, or circular anechoic; hypoechoic; or mixed echoic objects located in displaced, damaged, or otherwise abnormal muscle. In my experience, intramuscular hematomas often are located near a large, sonographically visible, artery (with or without a visible attachment to the hematoma).

In one reported case of compartmental syndrome, a large fluid-filled capsule containing a hematoma was removed from the thigh of a dog. Sonographically, the lesion was characterized by alternating light and dark rings radiating outwardly from a centrally located blood vessel.2 Hematomas also can form on the muscle exterior, either on the fascial sheath or in the large intermuscular septa. In these locations, especially higher in the leg, hematomas tend to migrate distally (especially with exercise) and in the process disperse over a wider area, making sonographic identification more difficult. On a positive note, however, the wider distribution of the migrating hematoma tends to relieve potentially dangerous pressure effects. Thus, an intermuscular hematoma is a decidedly less serious injury than a formed intramuscular hemorrhage and usually heals uneventfully. Sonographically, a hematoma can assume a variety of appearances. Initially, a hematoma usually appears anechoic and well demarcated (Figure 2-2). In the next few days, the hematoma gradually becomes more echoic and textured (Figure 2-3). Between 1 and 2 weeks later, most hematomas shrink and become hyperechoic. Afew disappear altogether. Although the sonographic progression of hematomas is predictable (dark to light), the rate at which these changes take place varies widely among individuals. Accordingly, hematomas can be difficult to age with any accuracy.3

Compartmental Syndrome (Compartment Syndrome) Compartmental syndrome is a term usually given to acute hemorrhage confined to a closed space or, more accurately, a potential space (typically, the space between a bone and adjacent fascia); as a result, it compresses surrounding nerves and blood vessels. People with this condition describe it as very painful and often associated with numbness in the distal part of the affected limb. As far as I can determine, this is a rare condition in pets or, alternatively, it is rarely recognized. 21

22

SECTION I ❚❚❚ The Extremities

Figure 2-2 • Sonogram shows relatively transparent appearance of a fresh intramuscular hematoma (24 hours old).

A

B Figure 2-1 • A, Sonogram shows a large intramuscular hematoma in the medial thigh region of a dog recently hit by a car. B, Close-up sonogram of medial thigh region shows two oval hematomas immediately to the right of the ruptured femoral artery (small black rectangle). A blood-filled muscle in the belly lies on the far lower right, depicted by widely spaced, parallel white lines.

Figure 2-3 • Progress sonogram of same lesion shown in Figure 2-2 (1 week later) shows increased echogenicity, the result of clotting and serum resorption, which are characteristics of a subacute hematoma.

Soft Tissue Gas Somewhat expanding the traditional definition of compartment syndrome, Williams and co-workers described a false aneurysm of a femoral artery that caused turgidity of the thigh region in a dog following repeated injuries sustained over 6 months.4 Sonographically, a cross-sectional view of the lesion and surrounding muscle resembled an intestinal intussusception: alternating light and dark concentric rings. Femoral arteriography showed contrast leakage confined to a small area around the distal aspect of the opacified femoral artery. During subsequent surgery, the leakage site proved to be a large, fluid-filled capsule, formed by the fascia of the semimembranosus and semitendinosus muscles, which communicated with the adjacent femoral artery through a 2-cm tear.

Soft tissue gas is usually the result of atmospheric contamination, made possible by one or more deep bite wounds or lacerations. The gas may accumulate in small pockets deep within the muscle (Figure 2-4) or as dark bands lying just beneath the skin or outlining deeper muscles and tendons (Figure 2-5, A). Alternatively, soft tissue gas may appear as a series of closely approximated but poorly defined pockets or bubbles located between a bone and nearby tendon, a pattern often found with bite wounds in the hock region (Figure 2-5, B, C).

Soft Tissue Calcification Soft tissue calcification occasionally is identified in extremital films of dogs and cats, nearly always incidentally. Presumably, most such deposits are dys-

CHAPTER 2 ❚❚❚ Extremital Injury

23

❚❚❚ STRAINS, TENDINITIS, AND BURSITIS Background

Figure 2-4 • Close-up frontal view of the stifle region of a dog shows multiple gas pockets deep in the severely swollen muscle medial to the genual joint (and superimposed on the distal femur), the result of multiple deep bite wounds sustained in a recent dogfight.

trophic, the result of a previous injury, although corroborating histories are often lacking. Extremital dystrophic calcification is most apt to be found near the apophyseal attachment of a tendon; for example, the proximal calcaneus (Figures 2-6, A, B and 2-7 A, B) and olecranon (Figure 2-8). Patterns vary, ranging from discrete calcific bands to amorphous foci, with the latter often displaying a linear arrangement. Tumoral calcinosis, a benign lesion typically appearing as a calcific cluster alongside the shoulder, elbow, stifle, or hock, has a highly distinctive appearance (Figure 2-9) that is not likely to be confused with other sources of soft tissue calcification. Rarely, a torn muscle will become partially ossified, a debilitating condition known as myositis ossificans.

High-density Foreign Bodies High-density extremital foreign bodies are usually readily apparent on radiographs: bullets, buckshot, air gun pellets (Figure 2-10), BBs, fishhooks, and needles, for example. Glass and gravel also are often visible, but they do not tend to penetrate as deeply and typically are found just beneath the skin or contaminating the surface of open road wounds.

In dogs (and less commonly in cats), complete tearing of a muscle belly, musculotendinous junction, muscle origin, or tendinous insertion is usually the result of a single trauma (as opposed to the overuse injuries so common in humans). Third-degree strain (large internal tears) and complete rupture also have been reported in a dog, occurring as a consequence of steroid-induced myopathy (triamcinolone).5 Avulsion fracture at the origin of the long digital extensor tendon has been described in dogs, both with and without a visible femoral fragment. Such injuries can occur without a history of known trauma, usually in large-breed puppies 5 to 8 months old. With subacute or chronic damage, the only indication of long digital extensor tendon injury may be a deeper and more lucent fossa. If a vascularized fragment of fossa is present, it may grow, becoming larger than the fossa from which it originated.6 Fitch and co-workers described a chronically detached long digital extensor tendon in a dog. Their report featured radiographic, computed tomographic (CT), and magnetic resonance images (MRIs) of the injury.7 Occasionally, following tearing, avulsion, or rupture, damaged muscle tissue changes to bone, a condition known as myositis ossificans.8 Little is known about this disease in dogs and cats, but in athletes such injuries can reduce performance substantially. Long and Nyland described the normal sonographic appearance of the canine shoulder, illustrating the utility of their findings with a number of case examples, including synovitis, bicipital bursitis, bicipital and supraspinous tendinitis, strained biceps, and dystrophic calcification.9

Imaging Findings Indirect mechanical stimulation, for example, that resulting from the prolonged licking of a skin wound (or a resultant lick granuloma), can cause fluid to accumulate in the tendon sheath (Figure 2-11). In my experience, there are no consistently reliable sonographic indicators of tendonitis in the dog.

❚❚❚ MAJOR TEARS, LACERATIONS, AND TRAUMA-RELATED INFECTIONS AND ABSCESSES Severe muscle tears (third-degree strains) often are associated with intramuscular bleeding (Figure 2-12), which can lead to compression-induced intramuscular or extramuscular ischemia. Hemorrhage resulting from deep muscle lacerations, although potentially

24

SECTION I ❚❚❚ The Extremities

B

A

C

Figure 2-5 • A, Full-length view of the crus of a dog recently cut by a barbed-wired fence shows large bands of gas beneath the skin and traces the gastrocnemius muscle and swollen Achilles tendon. B, Close-up view of distal half of mid-hindlimb shows bands of gas located between the tibial shaft and Achilles tendon. C, Opposite normal leg is provided for comparison.

CHAPTER 2 ❚❚❚ Extremital Injury

A

B

Figure 2-6 • Lateral close-up (A) and ultraclose (B) views of the proximal tarsus show the bony aftermath of a torn Achilles tendon: calcaneal remodeling, dystrophic calcification, and a thickened tendon.

A

B

Figure 2-7 • Close-up lateral (A) and frontal (B) views of the distal triceps field show soft tissue calcification consistent with an old injury.

25

26

SECTION I ❚❚❚ The Extremities

Figure 2-8 • Flexed lateral close-up of the elbow shows a band of calcification lying just beyond the edge of the medial epicondyle consistent with an old injury. Figure 2-10 • Lateral view of the soft tissue of the mid-hindlimb shows an air gun pellet just under the skin.

Figure 2-11 • Sonogram shows tendon sheath distended by fluid.

Figure 2-9 • Close-up frontal oblique view of tarsus shows a cluster of small and medium-sized calcifications lateral to the fourth tarsal bone characteristic of tumoral calcinosis.

debilitating, usually dissipates into the adjacent deep fascial planes and thus is not likely to cause intramuscular or extramuscular ischemia. Rupture or severe tearing of the Achilles tendon can be diagnosed physically, but lesser injuries or heavily scarred injuries usually require ultrasound, CT, or magnetography (Figure 2-13). Untreated deep puncture wounds, which typically close almost immediately, often become infected and may abscess (Figure 2-14, A, B). Ultrasound is required for diagnosis because radiographs, even using soft tissue technique, are unlikely to reveal more than nonspecific soft tissue swelling. Where sub-

CHAPTER 2 ❚❚❚ Extremital Injury

27

A Figure 2-12 • Sonogram shows freshly torn inner thigh muscle containing a large hematoma.

B Figure 2-14 • Long (A) and cross-sectional (B) views of a cylindrically shaped muscle abscess containing a foreign body (small, bright object).

denly and forcefully, the securing ligaments may stretch, tear, internally separate, or tear away from their bony moorings. Sprains are quantitatively described as first-, second-, and third-degree, depending on their severity; alternatively, they are characterized qualitatively as mild, moderate, or severe.

Carpal Sprains Figure 2-13 • Computed tomogram of the hock shows a ruptured Achilles tendon about 2 inches proximal to the calcaneus (as seen in the midsagittal plane).

stantial drainage is present or the abscess has been recently probed, one or more small gas pockets may be present.

❚❚❚ SPRAINS AND DISLOCATIONS Background Ligaments serve to set limits on normal joint movement. When these limits are exceeded, especially sud-

Overview. As one might expect, much has been published on the subject of carpal sprain in racing Greyhounds, including accounts of specific injuries, for example, the short radial collateral ligament.10 Severe carpal sprains may require surgical restoration of one or more torn ligaments. Where this is not possible, usually in chronic cases in which the damaged ligaments have become so badly frayed that reattachment is impossible, it may be necessary to immobilize the joint permanently by using a compression plate. This is sometimes erroneously termed fusing the joint; however, in most instances, the implants, not bony ankylosis, are preventing movement.11 Johnson documented the radiographic progress of grafted and nongrafted experimental carpal arthrode-

28

SECTION I ❚❚❚ The Extremities

A

B

Figure 2-15 • Lateral (A) and frontal (B) close-up views of a severely sprained carpus treated by prolonged casting and custom-built splintage. A year later, there is obvious swelling, especially of the radiocarpal joint, and some chronic appearing new bone on the face of the distal radius; however, the dog uses the leg normally.

sis in dogs and, predictably, the grafted carpi fused first.12 Nordberg and Johnson described the appearance of normal frozen canine carpi using a 1.5 T magnet and a human wrist coil. T2 gradient echoes provided the best combination of bone and ligament detail.13 Establishing the Degree of Carpal Injury. The severity of a carpal sprain injury is determined by using a combination of physical and radiographic abnormalities, listed in Table 2-1.14 Examples of Carpal Sprains and Diagnostic Tactics. Many carpal sprains can be successfully treated by prolonged external support, leaving only a cool, firm swelling as testament to the original injury (Figure 2-15, A, B). Intercarpal dislocation, especially if slight, can be difficult to detect without the aid of normal comparison films from the opposite carpus (Figure 2-16, A, B). Four views of a suspected carpal injury (frontal, lateral, and a pair of obliques) often make diagnosis easier, faster, and more accurate (Figure 2-17, A-D), especially when there are small, hard-to-see, minimally displaced fractures. A complete and accurate radiographic diagnosis of a serious carpal injury informs the prognosis, particularly with respect to potential long-term

consequences, such as osteoarthritis (Figure 2-18, A-C), disability (Figure 2-19, A, B), chronic pain, joint bodies (Figure 2-20, A, B), severe osteopenia (Figure 2-21, A-D), and traumatic capsulitis (Figure 2-22, A, B).

Elbow Sprains Most third-degree elbow sprains are associated with complete dislocation of the cubital joint (Figure 2-23, A-C). Somewhat surprisingly, O’Brian and co-workers showed that nonsurgical reduction, without collateral ligament repair, is as effective as open reduction with ligament repair, as long as the repair is done promptly. If not, posttraumatic osteoarthritis is likely to develop regardless of the method of reduction used.15 Arthriticfree healing of fracture–dislocations of the elbow (Figure 2-24) depends on both prompt surgical reduction and restoration (apposition and alignment) of disrupted articular surfaces.

Dislocated Shoulder Strictly speaking, there are no shoulder ligaments, although the humeral joint capsule functionally acts in such a capacity. Nonreduced scapulohumeral dislocations often lead to arthritis, joint bodies, pain, and severe forelimb disability (Figure 2-25, A-C).

CHAPTER 2 ❚❚❚ Extremital Injury

29

B

A

Figure 2-16 • A, Frontal close-up view of carpus shows swelling and proximal row displacement characteristic of an acute sprain–fracture–dislocation. B, Frontal view of the opposite carpus is included for comparison.

Table 2-1 • FACTORS THAT DETERMINE THE SEVERITY OF A CARPAL SPRAIN INJURY Abnormalities

Mild (First-degree) Sprain

Moderate (Second-degree) Sprain

Severe (Third-degree) Sprain

Physical

Minimal lameness Mild to moderate regional soft tissue swelling, which may be confined to the intracapsular location

Obvious lameness Obvious swelling Frank pain on palpation Pain readily elicited on minimal manipulation

Severe lameness often resulting in non–weight-bearing of the affected limb. Gross swelling that may extend well into the proximal metacarpus and the digits of the affected paw. Extreme pain on palpation and manipulation; frequently accompanied by crepitus or abnormal mobility

Radiographic

Minimal recognizable regional soft tissue swelling No bony lesions No apparent instability; stress films fail to identify spatial derangement

Prominent regional soft tissue swelling; usually both intracapsular and extracapsular in origin. Bony lesions rarely present. No apparent instability; stress radiographs may demonstrate spatial derangement

Gross regional soft tissue swelling. Bony lesions frequently present. Avulsion fractures are common and are often associated with subluxation. Instability often apparent and readily demonstrable with stress radiographs

Stifle Sprains The stifle is the most commonly sprained joint in the dog, followed by the carpus. In general, sprains heal slowly and are subject to reinjury, especially if normal activity is resumed prematurely. If during healing an injured ligament becomes elongated, it usually heals that way, causing the associated joint eventually to become arthritic, presumably because of intermittent incongruency related to instability. As to sprains to the genual joint, traditional belief has long held that there are two types of injury: one, the result of acute trauma; the other, the consequence

of chronic degeneration (presumably sustained over several years).16 This “either-or” explanation is probably an oversimplification, as recently suggested by Duval and co-workers.17 In the case of traumatic injury to the stifle, isolated cranial cruciate tears or avulsions are most common; however, multiple ligament injuries can occur, usually in young athletic dogs or as a result of being hit by a car. The cranial and caudal cruciate and lateral collateral ligament are most often sprained or ruptured.18 Isolated caudal cruciate injuries are exceptional.19 Occasionally, the bony mooring of the cranial cruciate detaches from the distal femur, leaving the ligament Text continued on p. 34

30

SECTION I ❚❚❚ The Extremities

B

A

C

D

Figure 2-17 • Four close-up views: frontal (A), lateral (B), medial oblique (C), and lateral oblique (D) of subacute carpal sprain–fracture– dislocations in a dog illustrate the diagnostic value of four views.

CHAPTER 2 ❚❚❚ Extremital Injury

B

A

C Figure 2-18 • A, Frontal view of an acute carpal sprain showing only mild to moderate swelling. The wavy, dark band traversing the distal ulnar metaphysis is edge enhancement or Mach band, caused by a congenital exostosis on the adjacent surface of the radius. Frontal (B) and lateral oblique (C) films made a year later show characteristic extraarticular new bone deposits on the cranial and medial surfaces of the distal radius and on various bones in the proximal carpal row.

31

32

SECTION I ❚❚❚ The Extremities

A

B

Figure 2-19 • Frontal (A) and lateral (B) views of a chronically unstable carpus sprained 7 years earlier. Although no films were made originally, the current arthritic pattern clearly suggests that the carpometacarpal joints were likely dislocated (and probably fractured as well).

B

A Figure 2-20 • When sprains are initially undiagnosed, untreated, or neglected, the only later indication of the injury may be one or two small bone fragments resembling normal sesamoids, and varying degrees of joint swelling, usually firm and cool (A, B).

CHAPTER 2 ❚❚❚ Extremital Injury

A

B

C

D

Figure 2-21 • Lateral (A) and frontal (B) views of the carpus and proximal metacarpus show chronic bone deposition over much of the face of the proximal metacarpus, causing it to appear abnormally white. Carpometacarpal swelling and severe regional osteopenia complete the picture. These changes are the result of a chronic sprain–fracture–dislocation. Also of note is the fact that another consultant diagnosed this as rheumatoid arthritis. C, D, The dog’s normal opposite carpus is provided for comparison.

33

34

SECTION I ❚❚❚ The Extremities

A A

B Figure 2-22 • Occasionally, particularly with severe capsular tearing

B

and excessive scarring, the capacity of the radiocarpal joint is reduced to the extent that there is insufficient synovial fluid to nourish the articular cartilage, a condition known as traumatic capsulitis. This volumetric difference can be appreciated best arthrographically by comparing the injured (A) with the uninjured joint (B).

stretched but intact. In such instances, it is often possible radiographically to identify a small intercondylar bone fragment and varying degrees of tibial dislocation.20 Partial cruciate tears (second-degree sprains) are less common than complete tears or avulsions (third-degree sprains), but when they do occur, they can potentially cause osteoarthritis, similar to that seen with more severe knee injuries. In my experience, the incidence of single and multiple ligament injuries in cats is much lower than in dogs. Some of the worst stifle trauma I have seen in cats has been the result of car accidents, mangling by large dogs, and various forms of entrapment.

Meniscal Injuries Medial meniscal injuries have been reported in nearly half of dogs with second- and third-degree cruciate

C Figure 2-23 • A, Dislocated elbow is readily seen in the closeup frontal view. B, It is somewhat harder to appreciate when viewed from the side. C, A comparable view of the opposite uninjured elbow is included for comparison.

CHAPTER 2 ❚❚❚ Extremital Injury

35

A

Figure 2-24 • Lateral view of the elbow region of a cat shows a displaced short oblique fracture of the proximal ulnar shaft and a dislocated radius. The beak-like bony projection ventral to the humeral condyle is the medial coronoid process, which may be mistaken for a fracture fragment.

sprains.21 In one elaborate classification, meniscal tears were divided into seven types according to location, orientation, and extent of the sprain:

B

Type 1: Folded caudal horn, which features an upward and forward folding of the caudal edge Type 2: Single longitudinal tear Type 3: Multiple longitudinal tears Type 4: Surface abrasions (termed by the authors as fibrillations) and a variety of partial-thickness tears Type 5: Axial-fringe tear Type 6: Bucket-handle tear Type 7: Transverse tear along inner margin

Imaging Findings Experimental Destabilization of the Canine Genual Joint. Experimental creation of osteoarthritis in the knees of dogs by severing the cranial cruciate ligament produces the following radiographic abnormalities (in order of appearance) 22: • Regional muscle atrophy • Joint swelling • Spurring on medial aspect of tibia, proximal aspect of patella, and lateral fabella • Spurring on the lateral aspect of the trochlear ridge, the caudal aspect of the tibia, and the distal aspect of the patella • Firm convex swelling centered over a medial collateral ligament

C Figure 2-25 • Ventrodorsal (A) and lateral (B) close-ups of a chronically dislocated shoulder in a cat show numerous spherical densities, most likely representing vitalized bone or cartilage fragments. C, See opposite shoulder for comparison.

36

SECTION I ❚❚❚ The Extremities

A A

B Figure 2-26 • A, Close-up lateral view of a stifle sprained 2 weeks earlier shows a partial dislocation, marked swelling, but as yet no osteoarthritis. B, The opposite genual joint is provided for comparison.

Using MRI (low-field strength imager), Baird and coworkers reported the development of a medium-sized, cyst-like lesion in the medial aspect of the proximal tibia within 3 months following cutting of the cranial cruciate ligament in healthy dogs.23 Naturally Occurring Cruciate Sprains in Dogs. Overall, the lateral view of the stifle is the most informative, especially in the detection of intraarticular swelling, which is often the only radiographic indication of an acute cruciate sprain (Figure 2-26, A, B). Partial dislocation occasionally is seen in recumbent images

B Figure 2-27 • Close-up lateral (A) and frontal (B) views of a young retriever’s stifle, sprained 2 months earlier, show marked joint swelling and early osteoarthritis.

but in most instances cannot be identified without the aid of postural (dog standing with a horizontally directed x-ray beam) or stress films. After 1 or 2 months, most seriously injured stifles begin to show signs of osteoarthritis in the form of triangular bone deposits located at the lower pole of the patella, on the proximal aspect of the femoral trochlea, along the outer surfaces of the femoral epiphysis, and on the ventral margins of the fabellae (Figure 2-27, A, B). In some dogs, the extensor fossa (as seen in lateral projection) begins to deepen, resembling a fracture bed (Figure 2-28, A). For most dogs,

CHAPTER 2 ❚❚❚ Extremital Injury

37

sesamoid in association with rupture of the cranial cruciate ligament, a radiographic abnormality also associated with avulsion of the popliteus muscle.25 In my experience, however, the standing lateral, even if the dog is only partially weightbearing, is still the most sensitive means of radiographically detecting dislocation of the stifle. Caution: Most standing projections differ from comparable recumbent views, and the standing knee is no exception (Figure 2-28, B).

A

B Figure 2-28 • A, Close-up lateral view of a stifle sprained 6 weeks earlier shows swelling and early osteoarthritis, but no dislocation. B, Close-up lateral view of the stifle of a healthy dog in standing position. Note the near-vertical position of the femur, the caudally sloped proximal tibia, and the cranially positioned articular contact point of the distal femoral epiphysis.

even those treated surgically, the resultant osteoarthritis is progressive, eventually leading to loss of articular cartilage and varying degrees of pain and disability. DeRoosten and van Bree devised a compression stress maneuver that can aid in the radiographic detection of cranial cruciate sprains.24 These same authors also reported the distal displacement of the popliteal

Intercondylar Stenosis. Montgomery and co-workers described a method of radiographing the intercondylar fossa, a postural projection they term the tunnel view (horizontally directed x-ray beam; dog in lateral recumbency). They contend that this projection is capable of detecting what they term “fossal stenosis,” a somewhat ambiguous term referring to the development of multiple inwardly projecting osteophytes following severe cruciate injuries, which may potentially encroach on the cruciate ligaments and limit joint extension. The authors contend that such information is important in planning reconstructive knee surgery. The amount of “stenosis” is described as a ratio (notch width index), calculated by dividing the width of the intercondyloid fossa by the width of the distal femur (epicondyle to epicondyle). The authors repeatedly cautioned that an accurate projection angle is critical because off-angle views result in false-positive diagnoses. The reported notch width index in normal Greyhounds was 0.25.26 The same group compared femoral fossa measurements made using CT with those obtained using conventional radiography. They concluded that CT images were more accurate in normal, arthritic, and unstable genual joints.27 Ultrasound. Reed and co-workers described the normal sonographic anatomy of the canine stifle.28 Regularly seen structures included (1) patellar tendon, (2) medial and lateral menisci, (3) cranial cruciate ligament, and (4) articular cartilage of the femoral condyle. The caudal cruciate ligament was seen in only two of four dogs; the collateral and meniscal ligaments could not be identified. The average weight of the dogs examined was 55 pounds. Kramer and co-workers described the sonographic appearance of both normal and abnormal canine stifles. Using a standardized examination protocol (patterned after one used by physician–sonologists), the authors claim to have diagnosed a wide variety of disorders, including the following: (1) tumors and nonneoplastic masses, (2) osteochondritis of the lateral femoral condyle, (3) ruptured cranial cruciate ligament, (4) meniscal injury, (5) nonspecific trauma, (6) degenerative joint disease, (7) patellar ligament sprain, and (8) patellar dislocation.29 Magnetic Resonance Imaging. Widmer and coworkers were among the first to discuss the appli-

38

SECTION I ❚❚❚ The Extremities

B A

C

D

Figure 2-29 • Close-up lateral (A) and frontal (B) views of a dog that tore its medial gastrocnemius muscle, resulting in dislocation of the associated fabella. Note how the degree of displacement varies with positioning. The opposite stifle is included for comparison (C, D).

cability of MRI to canine stifle injuries.30 Later, Widmer compared the relative sensitivities of radiography and magnetography in detecting the early signs of osteoarthritis in the stifles of healthy experimental dogs that had their cranial cruciate ligaments severed.31 Baird and co-workers also described the normal canine stifle using a lowfield MRI (0.064 T), including matched anatomic specimens.32 Magnetic Resonance Arthrography. Banfield and Morrison reported the use of magnetic resonance

arthrography in a small group of 11 military dogs suspected of having stifle injuries.33 Observed pathology included sprains and rupture of the cranial cruciate ligament, meniscal tears, medial collateral ligament injury, and synovitis. Optimal imaging planes are tabulated in Box 2-1. Fabella Injuries. Injuries to one or both fabellae are rare compared with cruciate sprains. Most are characterized by either displacement (Figure 2-29, A-D) or fragmentation and callus formation (Figure 2-30, A, B).

CHAPTER 2 ❚❚❚ Extremital Injury

A

39

B

Figure 2-30 • Close-up lateral (A) and frontal (B) views of the stifle show lateral fabella enveloped in bone, presumed to be the result of a former injury.

B o x

2 - 1

Optimal Imaging Planes for the Individual Elements of the Canine Stifle Stifle Structure

Optimal Imaging Plane

Articular cartilage

Sagittal (if 3DFSPGR sequence can be performed) Sagittal oblique (oriented along the cranial crutiate ligament) Dorsal plane

Cruciate ligaments Medial and lateral collateral Ligaments Patella and patella pendon

Sagittal

along the margins of the tarsocrural joint. Secondary lesions may develop in the proximal intertarsal joint, usually taking the form of one or more angular osteophytes along the leading edges of the talus and calcaneus. These findings are best seen in the lateral projection. Some sprains, especially those involving the tarsometatarsal joint, do little to change the radiographic appearance of the surrounding bones. In such cases, circumstantial evidence potentially may be obtained by performing stress radiography in the hope of showing dislocation. In some instances, it is also possible to show small corner fractures that are not evident in the initial nonstress images.

❚❚❚ SOFT TISSUE FOREIGN BODIES Tarsal Sprains Tarsal sprains range from the obvious, where there is an associated, displaced malleolar fracture, to the subtle, where there is little or no radiographic indication of the injury. Most serious tarsocrural sprains feature the combination of joint swelling, dislocation, and malleolar fracture. Mild to moderate sprains, however, although often very painful, typically result in tarsocrural swelling but no fracture or displacement. Not all severe tarsocrural sprains are diagnosed at the time of occurrence, but some are diagnosed later by their characteristic arthritic pattern (Figure 2-31, A, B), a pattern shared by osteochondritis of the talar ridge. Specifics include prominent periarticular lipping of the cranial and caudal aspects of the distal tibia, widening of the tarsocrural joint, and bone deposition

Currently, the most prevalent noninjurious foreign body in dogs is the microchip. Although most such chips appear to remain where they were initially placed, Burk and Eich reported the migration of a microchip from the soft tissues between the scapulae (where it was originally implanted) to the midcaudal aspect of the right brachium.34 Barrett described a variety of soft tissue foreign bodies in dogs, along with abnormal calcifications and gas pockets resulting from different causes.35 Shah and co-workers described the radiographic and sonographic appearances of a variety of foreign bodies (BB pellet, nail, steel wire, rock, gravel, glass, pencil lead, plastic, and wood) that were experimentally implanted in muscle.36 Table 2-2 indicates the imaging features of these objects.

40

SECTION I ❚❚❚ The Extremities

B

A

Figure 2-31 • Close-up frontal (A) and lateral (B) views of the tarsus of a dog badly sprained 1 year ago. Although treated immediately with casting, osteoarthritis developed within 3 months, primarily at the levels of the tarsocrural and proximal intertarsal joints.

Depending on clinical circumstances, in particular any operant diagnostic bias, an object located on the skin surface, such as small tumor, chunk of dirt or mud, or even an engorged tick, can be mistaken for an interior lesion, including a foreign body.37

❚❚❚ FRACTURES The following are the essential elements of fracture description: • Whether the fracture fragments are displaced or nondisplaced • The configuration of the fracture (fracture type) • Which bone or bones are broken • Where in a particular bone the fracture has occurred: shaft, metaphysis, growth plate (in skeletally immature animals), or epiphysis For example: There is a displaced, transverse fracture of the distal radial body. For another example: There is a nondisplaced, oblique fracture of the distal tibial metaphysis. Supplementary observations, such as the presence of fissures and joint or growth plate involvement, are

mentioned as necessary. Figures 2-32 to 2-34 further exemplify how fractures are described.

Fracture Types Apophyseal Fracture. An apophysis is an accessory growth center that requires intermittent traction to develop properly, in contrast to epiphyses, which require intermittent compression to thrive. Examples of apophyses are the greater and lesser trochanters of the femur, the tibial tuberosity, the proximal calcaneus, and the olecranon. Proximal displacement and associated growth plate widening characterize apophyseal fractures. Like many epiphyseal fractures, apophyseal fractures are often subtle, requiring opposite side comparison films to distinguish physeal variation from bona fide injury (Figure 2-35, A, B). Articular Fracture. An articular fracture enters one or more joints (Figure 2-36). Such injuries can lead to osteoarthritis if the affected articular surface is not restored. This is especially true if there is concurrent sprain, which further compromises joint congruency. In immature dogs and cats, articular fractures occur most often in the distal humerus and femur (Figures

CHAPTER 2 ❚❚❚ Extremital Injury

41

Table 2-2 • RADIOGRAPHIC AND SONOGRAPHIC FEATURES OF SOFT TISSUE FOREIGN BODIES IN DOGS Object Type

Object Size

Surface Echo Strength

BB Pellet

Nail

2 mm 5 mm 1 cm 2 mm 5 mm 1 cm 2 mm 5 mm 1 cm 2 cm

Strong Strong Strong Strong Strong Strong Strong Strong Strong Strong

Pencil lead 0.25 mm

2 mm 5 mm 1 cm

Pencil lead 1 mm Plastic

2 mm 5 mm 1 cm 2 mm 5 mm 1 cm 2 mm 5 mm 1 cm 2 mm 5 mm 1 cm 2 mm 5 mm 1 cm

Moderate Moderate Moderate to good Good Good Good Strong Strong Strong Strong Strong Strong Strong Strong Strong Moderate Moderate Strong

Glass

Gravel

Rock

Steel wire

Wood

Presence of Acoustic Shadow Comet-tail artifact Yes Yes Yes Yes Yes Yes Comet-tail artifact Poor Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes

2-37 to 2-39). Mature pets, on the other hand, are more likely to sustain articular fractures in the carpus and tarsus. Avulsion Fracture. Avulsion fractures occur near joints at the sites of ligament or tendon attachments and, as such, always should be considered potentially destabilizing (Figure 2-40). In most instances, the resultant fracture fragment is very small, which sometimes leads to the shortsighted dismissal of the injury as, “. . . just a chip” (Figure 2-41, A, B). If there is doubt about the integrity of a contiguous joint, stress radiography may resolve the question, but only if it is carried out in a pain-free manner. Avulsion fractures of the cranial cruciate ligament are usually quite small and in some instances nearly invisible. Occasionally, however, avulsion fractures of the tibia (with the attached cruciate ligament) are large enough that they can be surgically reduced.38 Normal sesamoids sometimes are mistaken for avulsion fractures or other kinds of joint disease. This type of diagnostic error can be avoided by knowing where the sesamoids are normally located (Table 2-3).

Presence of Reverberation Artifact

Presence of Radiographic Visibility

Yes Yes Yes No No No No No No Yes

Good Good Good Moderate Moderate Moderate Moderate Good Good Good

No No No

Invisible Invisible Invisible

No No No No No No No No No Yes Yes Yes No No No

Poor Moderate Moderate Invisible Invisible Invisible Moderate Good Good Good Good Good Invisible Invisible Invisible

Chisel Fracture. A chisel fracture typically is found in the cortex and may be of full or partial depth. Such fractures often involve bones that lie close to the skin surface, relatively unprotected by muscle. As the name chisel implies, these fractures usually are caused by sharp-edged objects that strike the bone obliquely, producing a bony “shaving” (Figure 2-42). Closed Fracture. A closed fracture is “closed” to potential outside microbial contamination by virtue of an intact surrounding skin. Other factors being equal, a closed fracture is much less likely to become infected than one that is open to the atmosphere. Comminuted Fracture. A comminuted fracture is composed of three or more fragments and often is associated with malalignment and disapposition (Figure 2-43). Compression Fracture. A compression fracture is one in which the bone is made to cave in on itself, making it appear smaller than normal. Compression fractures are most common in the thoracolumbar and lumbar spinal regions of dogs and cats (Figure 2-44). Text continued on p. 46

42

SECTION I ❚❚❚ The Extremities

A

B

C

Figure 2-32 • Long lateral (A) and frontal views (B) of a dog with a displaced, comminuted midshaft tibial fracture. Because of its distinctive triangular shape, the large central piece is known as a butterfly fragment (C).

CHAPTER 2 ❚❚❚ Extremital Injury

Figure 2-33 • Ventrodorsal view of the pelvis, hips, femurs,

43

A

and stifles in a cat recently hit by a car show a displaced, comminuted fracture of the right femur and a dislocated left genual joint.

Figure 2-34 • Close-up lateral view of a displaced comminuted fracture of the humeral shaft shows an arthritic elbow, most probably the result of osteochondritis of the coronoid process.

B Figure 2-35 • Close-up lateral (A) and frontal (B) views of an avulsion fracture of the tibial apophysis, a shearing-type fracture of the tibial epiphysis, and a displaced transverse proximal shaft fracture of the fibula. Intraarticular and extraarticular swelling are marked.

44

SECTION I ❚❚❚ The Extremities

A

Figure 2-36 • Close-up lateral view of the humeral joint shows a displaced articular fracture of the cranial aspect of the glenoid immediately caudal to the tubercle.

B

C Figure 2-38 • Frontal (A) and lateral (B) views of the elbow of a kitten show a displaced articular fracture of the medial half of the distal humeral epiphysis and associated medial epicondyle. A frontal view of the normal opposite elbow is provided for comparison (C).

Figure 2-37 • Frontal long-bone survey of a forelimb in an immature dog shows a displaced articular fracture of the distal humerus. The fracture travels diagonally through the medial side of the metaphysis, the central part of the growth plate, and the lateral aspect of the epiphysis into the elbow joint.

CHAPTER 2 ❚❚❚ Extremital Injury

A

45

B

Figure 2-39 • Lateral (A) and frontal (B) views of a displaced, comminuted articular fracture of the medial aspect of the femoral epiphysis (with secondary displacement of the medial fabella) in an immature dog.

Table 2-3 • LOCATIONS OF FORE AND HINDLIMB SESAMOID BONES IN THE DOG Body Area Forelimb

Sesamoid Bone

Location

Elbow

Within tendon of origin of supinator muscle on craniolateral aspect of proximal radius

Carpus

Within tendon of insertion of abductor pollicis longus muscle on medial aspect of the proximal metacarpus

Metacarpophalangeal joints

Single sesamoid within tendons of insertion of common digital extensor muscle and interosseous muscles on dorsal aspect of metacarpophalangeal joints Paired sesamoids within tendons of insertion of interosseous muscles on palmar aspect of the distal interphalangeal joints Single cartilaginous nodules on the dorsal aspect of the proximal interphalangeal joints and palmar aspect of the distal interphalangeal joints

Hindlimb

Stifle

Single sesamoid (patella) within insertion of the quadriceps femoris muscle in trochlear groove of the distal femur Paired sesamoids (fabellae) within medial and lateral tendons of origin of gastrocnemius muscle proximal to the caudal aspects of the medial and lateral femoral condyles Single sesamoid within tendon of origin of popliteus muscle distal to the lateral femoral condyle on the lateral aspect of the joint

Tarsometatarsal joints

Medial (intraarticular) and lateral sesamoid bones within the fibrocartilage plate on the plantar aspect of the tarsometatarsal joints

Metatarsophalangeal joints

Single sesamoid within tendons of insertion of common digital extensor muscle and interosseous muscles on dorsal aspect of metacarpophalangeal joints Paired sesamoids within tendons of insertion of interosseous muscles on palmar aspect of the distal interphalangeal joints Single cartilaginous nodules on the dorsal aspect of the proximal interphalangeal joints and palmar aspect of the distal interphalangeal joints

Modified from Mahoney PN, Lamb CR: Articular, periarticular and juxtaarticular calcified bodies in the dog and cat: a radiologic review. Vet Radiol Ultrasound 37:3, 1996.

46

SECTION I ❚❚❚ The Extremities

A Figure 2-40 • Close-up frontal view of the elbow of a dog recently hit by a car shows a subtotal, latch-type avulsion fracture of the medial epicondyle (emphasis zone).

Corner Fracture (Chip Fracture). A corner fracture is one in which a bone fragment breaks free from the outer articular margin of a joint. The resultant corner fragment is characterized by a right angle (Figure 2-45). Crush Fracture. Crush fractures are often seen in series, for example, two or more of the metacarpal or metatarsal bones. Most result from heavy objects being dropped on one of the lower limbs or by having one of the legs slammed in a door. Dogs occasionally get a paw caught in a steel trap, in which case the entire row of metacarpals or metatarsals are broken in the same place (Figure 2-46, A, B). Depression Fracture. A depression fracture occurs when a portion of a bony perimeter is driven into an adjacent cavity. Cranial and facial fractures are often of this type, with portions of the maxilla being driven into the nasal cavity or the frontal bone being displaced into the underlying sinus (Figure 2-47).

B Figure 2-41 • Close-up lateral (A) and frontal (B) views of the stifle of a dog that recently fell off a balcony show a swollen joint and a small avulsion fracture from the proximal part of the patella.

Diastatic Fracture. A diastatic fracture results when fibrous junctions, such as the sacroiliac joint or pubic symphysis, are torn apart (Figure 2-48). Expression Fracture. This relatively rare fracture type occurs when the fracturing force causes bone fragments to be displaced outwardly. Flat bones of the face, skull, scapula, and pelvis are most often involved. Fault-line Fracture. Radial carpal bone fractures are typically the result of injury and usually are associated with some degree of dislocation; however, Li and col-

Figure 2-42 • Close-up lateral view of the olecranon shows a chisel fracture caudally (emphasis zone).

CHAPTER 2 ❚❚❚ Extremital Injury

leagues reported radial carpal bone fractures in 15 dogs without known trauma. They speculated that these fractures occur along a pair of “fault lines,” potential points of structural weakness, located equidistant between the three ossification centers of the radial carpal bone.39 Greenstick Fracture. Greenstick injury occurs in immature long bones and is characterized by an indistinct or nearly invisible fracture line and the separation of only one cortex (Figure 2-49).

Growth Plate Fracture (Physeal Fracture, Epiphyseal Fracture). Growth plates come in a variety of sizes and shapes. Some, like that in the distal femur, are composed of a cluster of four individual cleats and sockets, roughly arranged in a square (Figure 2-50, A). By contrast, the growth plate in the distal radius is composed of a single large, billowy element (Figure 2-50, B), whereas that in the distal ulna is distinctly conical (Figure 2-50, C). Growth plate fractures must not be confused with accessory growth centers, which can be highly variable, especially in young puppies, where the growth plate is growing, changing in shape, assuming new positions, and fusing to adjacent bones (Figure 2-51, A-C). Structurally weaker than the flanking bone, the cartilaginous growth plate is susceptible to injury. Traditionally, growth-plate injuries have been radiographically described using a surgical classification developed by pediatric orthopedists (Salter and Harris); this classification focuses on prognosis relative to the specific type of fracture. In radiology, however, the focus is entirely anatomic (Box 2-2).

B o x

2 - 2

Salter-Harris Classification of Growth Plate Fractures Type I

Type II Type III

Type IV Type V

Figure 2-43 • Lateral view of a severely displaced, comminuted fracture in a dog.

Figure 2-44 • Lateral view of the thoracolumbar spinal region of a dog with a broken back shows shortening and distortion of L1, the characteristic features of a vertebral compression fracture.

47

A transversely oriented fracture, which results in entire growth plate and epiphysis being detached from adjacent metaphysis. Like type I, but also includes a small attached, triangle-shaped, metaphyseal fragment. A vertically oriented fracture that results in part of the growth plate and underlying epiphysis being detached from adjacent metaphysis. Like type III, but also includes a large metaphyseal fragment. An impaction type fracture in which the growth plate is crushed between the epiphysis and metaphysis. This injury may only be inferred from clinical signs since it is radiographically invisible.

48

SECTION I ❚❚❚ The Extremities

Numeric classification schemes, such as that by Salter and Harris, can be difficult to remember, both in their own right and also because they conflict with other medical schema. In an effort to overcome such problems, I devised a briefer, hopefully more intuitive method of growth-plate fracture description that focuses on the actual injury, in particular, the fractured epiphysis (Box 2-3). A crushed growth plate is not considered because it cannot be diagnosed radiographically.

B o x

2 - 3

Simplified, Nonnumeric Classification of Growth Plate Fractures

Figure 2-45 • Close-up lateral view of canine tarsus shows a displaced corner fracture of the fourth tarsal bone and sprain–fracture–dislocation of the tarsometatarsal joints.

Complete epiphyseal separation without metaphyseal fragment Complete epiphyseal separation with metaphyseal fragment Partial epiphyseal separation without metaphyseal fragment Partial epiphyseal separation with metaphyseal fragment

B

A Figure 2-46 • Lateral (A) and frontal (B) views of the front paw of a cat show displaced short oblique fractures of the second and third metacarpal bones in the context of severe soft tissue swelling related to the crushing nature of the injury.

CHAPTER 2 ❚❚❚ Extremital Injury

49

Figure 2-47 • Close-up ventrodorsal view of the facial region shows depression fracture of right zygoma (left) that has fused to the adjacent mandible, which was also broken, preventing the mouth from opening.

Figure 2-49 • Full-length frontal view of the radius and ulna of a dog shows a greenstick fracture in the medial aspect of the central radial body (left).

Distal Humeral Growth Plate Fracture. Untreated or unsuccessfully treated distal humeral growth plate fractures are likely to cause arthritis and varying degrees of limb deformity if not treated effectively.40 Figure 2-52, A-D shows examples of growth plate fractures. Gunshot Fracture. As the name indicates, gunshot fractures are caused by bullets, slugs, and, less often, buckshot. In the case of joints, it is important to determine whether there are any intraarticular fragments, which can cause harm beyond the obvious wounding capacity of such missiles. Figures 2-53 to 2-57 show various examples of gunshot injuries in dogs and cats. Hairline Fracture. A hairline fracture is one in which the fragments are only minimally displaced, such that the break is little wider than a hair (Figure 2-58, A, B). Figure 2-48 • Close-up ventrodorsal view of the pelvis and hips shows displaced right sacroiliac diastatic fracture, dislocated right hip, and displaced fractures of the left pubis and left central ischium.

Impacted or Impaction Fracture. In an impacted fracture, the bone fragments are driven into one another, with or without a visible radiolucent fracture line (Figure 2-59, A-C). Incomplete Fracture. An incomplete fracture is one that is typically transverse or oblique and is characterized by a partially visible fracture line but no overt fragment displacement (Figure 2-60).

50

SECTION I ❚❚❚ The Extremities

A

C

B

Figure 2-50 • A, Close-up view of opened distal femoral growth plate of a dog (caudal perspective) shows two of four cleat and socket pairs. B, Close-up view of distal radial growth plate of a dog (caudal perspective) shows a billowy type growth plate. C, Close-up view of distal ulnar growth plate (caudal perspective) shows conical type of growth plate.

A

B

C

Figure 2-51 • Close-up lateral views of the elbow of a puppy at 1 (A), 2 (B), and 3 (C) months of age.

CHAPTER 2 ❚❚❚ Extremital Injury

51

A Figure 2-52 • A, Lateral oblique views of right and left stifles of a 4-month-old Basset Hound puppy recently hit by a car; the distal femoral and proximal tibial growth plates are fractured bilaterally. Appearances vary as a result of differences in projection angles. Continued

52

SECTION I ❚❚❚ The Extremities

B

C

D Figure 2-52 • cont’d B, Close-up lateral view of the genual joint shows badly displaced distal femoral growth plate fracture (SH II [Salter-Harris], based on metaphyseal fragment attached to femoral epiphysis). C, Close-up, flexed ventrodorsal view of the coxal joints shows a displaced proximal femoral growth plate fracture. D, Close-up lateral and frontal views of the shoulder joint show displaced growth plate fractures of the humeral head and greater tubercle.

CHAPTER 2 ❚❚❚ Extremital Injury

53

Figure 2-53 • Flexed ventrodorsal view of the left hip of a dog recently shot with a high-powered rifle shows a shattered proximal femoral shaft seen against a backdrop of dozens of bone and lead fragments. A plume of gas can be seen extending from the wound site deeply into the thigh, attesting to the open nature of the wound.

A Insufficiency Fracture. Insufficiency fracture is another name for a pathologic fracture, an injury that occurs in diseased bone (Figure 2-61). Letter Fractures. Letter fractures are named for their resemblance to some of the letters of the alphabet; specifically, T, Y, and V. They typically occur in the distal humerus of immature animals and involve the growth plate. Even more importantly, these fractures extend into one or both elbow joints (Figure 2-62). Longitudinal Fracture. A longitudinal fracture is one that lies parallel to the long axis of the bone (Figure 2-63). Oblique Fracture. An oblique fracture slants across the long axis of the bone (Figure 2-64). Open Fracture. An open fracture is one that has broken through the skin and thus is presumed potentially infected; most contain gas (Figure 2-65, A, B). Pathologic Fracture. A pathologic fracture is one that occurs in diseased, structurally weakened bone; accordingly, these injuries are also known as insufficiency fractures. Whereas most pathologic fractures occur in cancerous bone, they also can take place at the site of a bone cyst, in bacterial or fungal osteomyelitis, or in bones that have undergone extensive mineral depletion as a result of nutritional secondary hyperparathyroidism.41-42 Spiral shaft and transverse metaphyseal configurations are the most common. Contrary to popular opinion, posttraumatic osteoporosis (less precisely termed osteopenia), which temporarily follows

B Figure 2-54 • Ventrodorsal (A) and lateral (B) close-up views of the scapula of a cat show flecks of lead along the medial surface proximally, the result of a glancing gunshot wound.

fracture repair, rarely leads to pathologic fracture (Figure 2-66, A, B). Segmental Fracture. Two or more complete separations in a single bone are termed a segmental or, less commonly, a multiple fracture (Figure 2-67). Sesamoid Fracture. Two-piece sesamoid fractures occur most often in the feet of sled and racing dogs. These injuries need to be differentiated from the fragmenting form of osteochondritis, especially in Rott-

54

SECTION I ❚❚❚ The Extremities

A A

B Figure 2-55 • Lateral (A) and frontal (B) close-ups of the distal humerus of a dog shattered by a gunshot. There is also a displaced fracture of the olecranon that enters the elbow joint, as do many of the humeral fractures.

B Figure 2-56 • Lateral (A) and frontal oblique (B) views of the

weilers, and benign congenital fragmentation, termed bipartite (two-piece) and tripartite (three-piece) sesamoids (Figure 2-68, A, B).43 Simple Fracture. A simple fracture comprises a single break, usually transverse or oblique, resulting in two fragments (Figure 2-69). Spiral Fracture. A spiral fracture is one that turns through the long axis of the bone, describing a full or partial spiral (Figure 2-70). Stress Fracture. Stress fractures (also referred to as march fractures, as in soldiers marching) are rare injuries in dogs, arising from repeated stresses on bone, usually

elbow region of a cat show a shattered distal humerus, the result of a gunshot.

in the context of overtraining or overwork. As with people, stress fractures are most likely to affect young dogs. Bilateral stress fractures have been reported in the distal ulna of a Great Dane puppy.44 Transverse Fracture. A transverse fracture is one that breaks across the shaft perpendicular to the long axis of a bone (Figure 2-71). Talar Neck Fractures. Talar neck fractures are more common in cats than in dogs.45 In most such cases, there

A

B

Figure 2-57 • Lateral (A) and frontal (B) close-up views of a malunion gunshot fracture of the distal femur. Note the intraarticular and extraarticular migratory patterns of the smaller lead fragments, which trace the trochlear and gastrocnemius contours in the lateral projection.

A

Figure 2-58 • A, Close-up lateral view of the elbow joint shows hairline fractures (emphasis zone) passing through the olecranon and anconeal process into the humeroulnar joint. B, Close-up lateral views of the midbodies of the radius and ulna show transverse and oblique hairline fractures, respectively (emphasis zone).

B

56

A

SECTION I ❚❚❚ The Extremities

B

C

Figure 2-59 • A, Close-up frontal view of the tarsus of a dog shows multiple impaction fractions located on the lateral aspect of the tarsocrural and proximal intertarsal joints. Close-up lateral (B) and frontal (C) views of the distal radius and ulna show a displaced biplanar impaction fracture of the radial epiphysis and a mildly displaced, oblique, greenstick fracture of the ulnar shaft.

CHAPTER 2 ❚❚❚ Extremital Injury

57

Figure 2-61 • Close-up lateral view of the distal radius and ulna shows insufficiency (pathologic) fractures of both the radial and ulnar epiphyses as a result of an osteosarcoma.

Figure 2-60 • Close-up view of an incomplete fracture in the cranial cortex of the radial body (emphasis zone).

Figure 2-62 • Close-up frontal view of the humerus in a puppy shows a displaced Y-fracture involving the metaphysis, growth plate, and epiphysis. Distally, the fracture enters the far corner of the humeroradial joint (left).

58

SECTION I ❚❚❚ The Extremities

Figure 2-63 • Close-up frontal view of a badly displaced longitudinal fracture of the lateral aspect of the calcaneal body. The fracture is also articular by virtue of its entering the proximal intertarsal joint.

are additional fractures and dislocations. At least four views of the tarsus—lateral, frontal, and a pair of frontal obliques—are necessary to determine the full extent of the injury.

Traumatic Amputation Cats seeking the warmth of an automobile engine compartment on a cold winter day may be caught unawares when the car is restarted, often resulting in serious injury, including amputation (Figure 2-72).

Fracture Classification Using Electronic Databases Fracture descriptions stored in computerized databases need to be as precise as possible to facilitate accurate retrieval. They also must be designed with computer input foremost in mind. Such electronic classification schemes typically use anatomic location and fracture complexity to create an alphanumeric code that can be entered and retrieved by standard computer databases. Although maintaining data input in such systems is time consuming and thus quite costly, electronic data-

Figure 2-64 • Lateral oblique view of the metatarsus shows multiple displaced short oblique fractures of the proximal metatarsal bodies.

bases are necessary in large facilities, such as group specialty practices and teaching hospitals. One such method, known as the Unger system, has been tested in a veterinary teaching hospital and is said to be effective.46

Fracture Repair Before discussing the radiographic evaluation of fracture healing, a few words (and examples) on the subject of fracture repair. First, the principles: 1. The closer the fracture fragments are approximated, and the less they move during callus formation, the more rapidly the fracture heals. 2. The better the blood supply, the better the healing.

CHAPTER 2 ❚❚❚ Extremital Injury

A

A

B Figure 2-66 • Lateral (A) and frontal (B) close-up views of a

B Figure 2-65 • A, Full-length frontal view of a badly comminuted humeral fracture in which many of the fragments are being traced by gas, indicating the open nature of the injury. B, Closeup frontal view of a stifle of a dog, recently bitten by another dog, shows numerous gas pockets and a chisel-type fracture lying just beyond the lateral margin of the medial condyle (emphasis zone).

displaced pathologic fracture through a suspected metastatic bone tumor located in the distal aspect of the body of the tibia (emphasis zones).

59

60

SECTION I ❚❚❚ The Extremities

A

Figure 2-67 • Close-up frontal view of a refractured radius/ulna in a dog shows a segmental fracture of the middle and distal aspects of the ulnar body and an oblique fracture of the distal radial body.

B Figure 2-68 • A, Close-up frontal view of the left paw of a dog with a comminuted sesamoid fracture, an uneven cartilage space, and a new bone deposit on the inside edge of the underlying first phalanx. These findings are consistent with a former third-degree sprain of the second metacarpophalangeal joint and sesamoid fracture–displacement. B, Close-up frontal view of the forepaw of a dog shows a fracture–dislocation of the seventh caudal metacarpal sesamoid.

CHAPTER 2 ❚❚❚ Extremital Injury

61

Figure 2-69 • Full-length view of dog’s femur shows displaced simple oblique fracture of the femoral midshaft.

Figure 2-71 • Lateral oblique view of the scapula shows a displaced transverse fracture through the midbody. Vertically oriented cracks (fissures) are present in both the proximal and distal fragments.

Figure 2-70 • Full-length frontal view of a dog’s tibia (and fibula) shows a minimally displaced, long uneven spiral fracture.

Figure 2-72 • Frontal view of a cat’s paw in which the distal half of the second digit was amputated by an automobile cooling fan at the level of the midproximal phalanx.

62

SECTION I ❚❚❚ The Extremities

A

B

Figure 2-73 • Close-up lateral views of displaced longitudinal midshaft radial and ulnar fractures before (A) and after (B) 1 month of casting. As expected in such cases, healing is slow, especially distally, where movement was maximal.

Splints and Casts. Splints and casts do a poor job of immobilizing displaced fractures. The result is that fractures repaired in this way take longer to heal and form large calluses than fractures treated by other means (Figures 2-73 to 2-75). Casts are inexpensive, however, and they preserve the uninjured regional blood supply. Pinning and Wiring. Pins and wire loops in the case of comminuted fractures or those requiring counter traction do a better job than casts and splints in approximating and immobilizing fracture fragments but usually allow varying degrees of axial rotation that prolong healing (Figure 2-76, A-C). External bars attached to pins inserted into the fracture fragments help reduce rotation, but they are heavy, awkward, and often uncomfortable. Fractures treated in this fashion are also often slow to heal, callous heavily, and often result in bone loss immediately surrounding one or more of the pins (Figures 2-77, A-D and 2-78, A-D). Some fractures are now being treated with large pins that contain holes through which transcortical screws can be placed to prevent fragment rotation. Based on the cases I have seen thus far, healing is generally pro-

tracted compared with plates or conventional pins or with pin and wire combinations. As most veterinarians are now aware, improperly applied circlage wires can retard, and in some instances even prevent, fracture healing. Generally speaking, overly thin wire loops and half loops are ineffective, and an excessive number of closely approximated loops can delay callus formation. External Bars. Transcortical pins, mounted on external bars, with or without circlage wires, often move back and fourth like small seesaws, creating small lucent bands between the pin surface and the adjacent bone, especially at exit points. Pin infections can create a similar appearance but usually are associated with lameness (Figures 2-78, A-D and 2-79, A, B). Plates and Screws. Among the various surgical devices designed to repair fractures, bone plates achieve the greatest degree of fragment rigidity; as such, the associated calluses are typically small and in some instances nonexistent. Because of greater stability, fractures that

CHAPTER 2 ❚❚❚ Extremital Injury

B

A

63

C

Figure 2-74 • Frontal and lateral views of mid-forelimb (A) show an incomplete fracture of the central radial diaphysis and a minimally displaced transverse fracture of the distal ulna. Following a month of casting (B, C) only a portion of the radial fracture line is visible, and the ulnar fracture has disappeared altogether.

are plated heal faster than those that are not plated. Additionally, severely comminuted femoral fractures that are treated with a bridging plate heal more rapidly than comparable fractures treated with a combination of fragment reconstruction and plating.47 Figure 2-80 shows a partially healed tibial fracture fixed with a plate and screws.

Fracture Healing Fracture Union. The restoration of a fractured bone depends most on vascularization (and revascularization) of the injury site. When a fracture is cast, pinned, or plated, the purpose is to prevent the bone fragments from moving, which facilitates revascularization, providing the optimal environment for callus development. The following of certain events occurring in and around the fracture site will in most instances lead to healing: hematoma formation, localized inflammation, callus development, bony consolidation, and bony remodeling.48

Radiographic Indications of Fracture Healing (Bony Union). Based on serial radiography, fracture healing is assessed using the following changes in the appearance of the fractured bone: • Fracture line or lines initially widen, then narrow, become faint, and finally disappear. • Fragment margins gradually smooth and become less distinct. • Fragments gradually draw closer together before disappearing altogether. • Callus gradually fills the gap between fragments, eventually uniting them. The bone first becomes a single entity and then is gradually restored to its original appearance (or at least a close proximity). The radiographic judgment of healing always must be rendered on an individual case-by-case basis, made in the context of: (1) the location and severity of the fracture, (2) the duration of injury, (3) the method of repair, and (4) the progress of the injury over time (as seen in sequential

64

SECTION I ❚❚❚ The Extremities

A

B

C

Figure 2-75 • Frontal close-up views of a displaced distal radial shaft fracture at admission (A), 3 weeks (B), and 6 weeks (C) after casting. The fracture is now strong enough to bear weight without further support.

A

B

C

Figure 2-76 • A, Close-up view of the elbow of a dog shows a dark, wedge-shaped band crossing the proximal ulna and entering the humeroulnar joint consistent with a displaced articular fracture. B, One month later, the fracture remains clearly visible. C, Two months later, the fracture line has become faint and is likely healed enough to allow removal of the implants.

CHAPTER 2 ❚❚❚ Extremital Injury

65

C A

D

B

Figure 2-77 • Lateral (A) and frontal oblique (B) views of a cat’s femur, seen against a backdrop of massive swelling, show a displaced long oblique fracture of the proximal femoral shaft. An immediate postoperative film (C) shows anatomic reduction, achieved with an intramedullary pin and circlage wires. Six weeks later, the fracture appears healed without evidence of an external callus, attesting to the degree of surgical rigidity obtained (D).

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SECTION I ❚❚❚ The Extremities

B A

C

D

Figure 2-78 • A, B, Paired nonstandard views of the pelvis, hips, and left femur of a cat recently hit by a car show a severely displaced, comminuted fracture of the left femur and an avulsion of the left ischium. C, D, Progress films made 7 weeks later reveal that the fracture has healed well enough to remove the pins and external support bar.

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67

A

Figure 2-80 • Close-up frontal view of a partially healed tibial fracture in a dog. This fracture was repaired with a bone plate.

B Figure 2-79 • A, Comminuted tibial fracture 2 months following repair shows a pair of radiolucent lines along the edges of the uppermost pin (emphasis zone). B, These lines flare at the exit points, the result of a mild pin tract infection and associated pin cycling.

postoperative radiographic examinations. Pertinent radiographic reports also should be reviewed before arriving at a final decision. This process is exemplified in Figure 2-81, A-H. Soft Tissue Viability and Fracture Healing. Arteriography and venography provide the greatest degree of vascular detail in damaged soft tissues and are the optimal means of assessing viability. Subtraction angiography provides an even better view of small vessels by removing potentially confusing background anatomy; however, angiography is time consuming, expensive, requires general anesthesia, involves vascular surgery, and most importantly may further injure an already compromised blood supply.

Although not as anatomically precise, Doppler ultrasound, in the form of a vascular pressure tracing, usually indicates whether blood flow is present, which in the case of a potentially devascularized fracture or freeze injury may be all that is needed. Doppler is safe, fast, inexpensive, and poses no danger to a tenuous blood supply. Doppler has been used to determine the likelihood of fracture healing.49 The Orthopedic Imperative. Without exception, all fracture reductions, regardless of the method of repair, must be radiographed immediately after completing the procedure. Fracture repairs also should be checked radiographically before the animal is discharged home in cases of unusually long postoperative hospitalization because not all implant dislocations can be detected by physical examination (Figure 2-82). Delayed Fracture Healing When Is Union Considered Delayed? There is no precise definition of delayed healing; it is not a

68

SECTION I ❚❚❚ The Extremities

A–D

E–H Figure 2-81 • Close-up lateral (A-D) and frontal (E-H) views of a fractured distal tibial growth plate in a puppy treated by casting and then checked 2 and 4 weeks later.

quantitative entity but rather a statement regarding the accuracy of an earlier prediction. For example, when an animal breaks its leg, the bone is cast, pinned, or plated, and a predication is made as to how long it will take to heal. If the fracture exceeds the predicted healing time, it is designated a delayed union. If it heals faster than predicted, the doctor is considered skilled, but no specific term is used to mark the event. The best way to monitor the progress of a healing fracture is to recheck it on a regular basis. My preference is to do so at monthly intervals beginning 30 days after the immediate postoperative radiographs are made, unless it appears that the fracture has become infected or that the implants have broken or become detached, in which case I recheck it immediately. Radiographic Indications of Delayed Union. The experienced veterinarian initially predicts healing time based on a number of variables, including the bone involved, severity of injury, method of repair, and skill and experience of the surgeon. Thereafter, estimated healing time is based on progress rechecks. Inexperienced veterinarians are almost entirely dependent on the opinions of colleagues and the relevant veterinary literature. Some veterinarians seem

reluctant to use the term delayed union, contending that it suggests incompetence; others avoid the issue entirely by making no predictions. To reiterate, by describing the healing of a fracture as delayed, all that one is saying is that the fracture is taking longer to heal than originally predicted. Possible reasons for delayed union include (1) instability; (2) devascularization; (3) comminution, disapposition, or malalignment; (4) misapplied or inappropriate surgical implants; (5) broken or dislocated implants; (6) infection; and (7) reoperation (surgical revision). Figure 2-83 shows an example of a delayed union related to implant dislocation. Nonhealing Fracture: Nonunion. A nonunion fracture is one that does not heal, although not everyone can agree on when this should be: 4 weeks, 8 weeks, or 16 weeks. Most of us appear inclined to delay as long as possible before uttering the dreaded “N” word. On a more practical note, reluctance to acknowledge the presence of a nonunion often needlessly delays corrective treatment. The problem has been at least partially remedied by Heppenstall, a physician–orthopedist, who proposed that any fracture that fails to show any radiographic improvement for at least 3 months should be considered a nonunion and treated as such. I strongly support this def-

CHAPTER 2 ❚❚❚ Extremital Injury

69

A A

B Figure 2-83 • A, Immediate postoperative ventrodorsal view of

B Figure 2-82 • A, Discharge ventrodorsal view of the pelvis of a dog recently operated on to improve the position of its left acetabulum, subluxated as a result of hip dysplasia, shows unsuspected implant dislocation (emphasis zone). B, Close-up view shows that the screws have pulled out of both the ilial and sacral fragments, eliminating surgical stability.

the pelvis shows plating of the right ilium and a tandem screw reduction of a left sacroiliac fracture–dislocation. B, A close-up of the right ilium made a month later shows that most of the bone screws have partially pulled out and that the plate has bent. Even though the caudal ilial fragment has become badly displaced, a callus has begun to form. Based on the described implant and fragment dislocations, a delayed union is inevitable.

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SECTION I ❚❚❚ The Extremities

Figure 2-84 • Lateral view of femur 4 months following fracture and attempted pin repair shows a hypertrophic nonunion (partially covered by marker).

inition of nonunion, as I have stated in previous publications. The classic clinical signs of a nonunion are (1) lameness, (2) palpable pain, and (3) fragment mobility. If these signs are noted, there is no need to wait 3 months for radiographic confirmation (Figures 2-81, A-H). Bear in mind that this is a working definition. The medullary blood supply of a suspected nonunion can be evaluated using osteomedullography, a form of angiography in which a bone biopsy needle is used to inject contrast solution into the distal part of fracture.50 If the contrast crosses the fragment gap moving distally to proximally, an intramedullary blood supply exists, along with the potential for a bony callus. Causes of Nonunion. The causes of nonunion are often the same as for delayed union except they are usually of greater magnitude and are more sustained. They include the following: • • • •

Inappropriate repair Incorrect repair Instability Devascularization

Figure 2-85 • Close-up lateral view of 1-month-old puppy, untreated radial and ulnar midshaft fractures shows complete malalignment of the radial fracture, with little or no bridging callus. In the context of pain, lameness, and palpable fragment motion, the fracture was judged to be a nonunion.

• Infection • Implant misapplication I have omitted the term implant failure (breakage, dislocation) from the preceding list because it is so unusual and replaced it with implant misapplication, which in my experience is far more common, especially in the case of inexperienced surgeons. Radiographic Indications of Nonunion. Radiographic signs suggesting nonunion usually include one or more of the following: • • • • •

Absence of a bridging callus Increased density and smoothness of fragment ends Fragment motion Pseudoarthrosis formation Smoothness and thickening of fragment margins

Figures 2-84 to 2-93 exemplify various types of nonunions. Abnormally Healed Fracture: Malunion. Malunion is another word that some veterinarians seem reluctant to use, at least in their medical records. In fact, there is nothing derogatory about the term; it merely indicates that the bone has yet to be re-

C

A

B

D

Figure 2-86 • Lateral (A) and flexed ventrodorsal (B) close-up views of a complete mid-calcaneal fracture 4 months after attempted repair show nonunion as indicated by the clear gap between bone fragments at the level of the distalmost wire. Three months later, following implant removal, the nonunion has been replaced by a malunion (C, D).

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SECTION I ❚❚❚ The Extremities

mities are based. Using the radius and ulna as examples, they described the complexity of synchronous growth and how even small disturbances in this collaborative skeletal development—in the form of a comparatively minor vascular injury to the distal ulnar physis—could later lead to striking physical and radiographic abnormalities.52 Carrig and Morgan used radiation to damage deliberately the distal ulnar growth plates of 10-week-old Beagle puppies to retard the longitudinal growth of the ulna and thus upset the dynamic balance between ulnar and radial development. They described the resultant limb deformity, catalogued the associated radiographic changes, euthanized the dogs, and studied their bones.53 A related publication using the same material focused on the radiologic and pathologic aspects of radiation-induced distal ulnar growth plate injury.54 In a later experiment, Carrig and colleagues showed that the distal ulnar growth plate could sustain a minor injury without perceptible limb deformity.55

Imaging Findings

Figure 2-87 • Frontal and lateral views of a failed radial repair (attempted 5 months earlier) show nonunions of both the distal radius and ulna. Posttraumatic osteoporosis is evident in all bones distal to the fracture sites.

stored to its preinjury form. More importantly, nonarticular malunion fractures rarely lead to pain, discomfort, or serious disability, nor do most cause arthritis. Figures 2-94 to 2-99 show a variety of malunions.

Regeneration Anderson and Muhlbauer described a case of a 6month-old Great Dane that appeared to partially regenerate a digit following fracture and successful repair.51

❚❚❚ LIMB DEFORMITY SECONDARY TO GROWTH-PLATE FRACTURE AND EARLY CLOSURE Background Riser and Shirer were among the first to set out the principles on which growth-plate–induced limb defor-

Injuries to the distal radial or ulnar growth plates typically cause the most serious limb deformities in dogs. Of equal or greater importance, however, are the related dislocations that develop in the elbow, which can eventually lead to osteoarthritis. Injuries to the distal radial physis can cause shortening, making it appear as if the radial head is pulling away from the humeroradial joint. Meanwhile, the ulna, which is attempting to grow normally, seems to be pushing the distal humerus proximally and, in the process, dislocating the humeroulnar joint. A damaged distal ulnar growth plate likewise causes shortening but with the reverse effects to the elbow joints: the radial appears to be pushing proximally, and the ulnar seems to be pulling distally. Injuries to the proximal radial growth physis resemble those to the distal growth plate but with less deformity and articular dislocation because the proximal radial physis contributes less to axial growth than the distal physis. Injuries to the proximal ulnar growth plate can lead to underdevelopment of the olecranon but usually little else. Recall that the olecranon is an apophysis, not an epiphysis, and as such it makes only a minor contribution to bone length. Figures 2-100 to 2-110 exemplify these and other types of growth-plate injuries.

❚❚❚ SUGGESTED READING For an overview of the sonographic appearance of extremital soft tissue injuries in pets, I recommend the following paper by Kramer and colleagues: “Sonography of the Musculoskeletal System in Dogs and Cats,” in Veterinary Radiology & Ultrasound 38:139, 1997. Text continued on p. 91

A

B

C

D

Figure 2-88 • Full-length lateral (A) and frontal (B) views of the radius and ulna of a dog that broke its leg 3 months earlier and was treated by casting. C, Close-up frontal view shows a nonpurposeful callus, one that develops around the fragment ends but fails to bridge the fracture gap. D, Nonunions such as this are often re-treated surgically by removing the bone ends, inserting a cancellous bone graft, and plating the fracture.

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SECTION I ❚❚❚ The Extremities

A

B

Figure 2-89 • Lateral (A) and frontal (B) close-up views of an ulnar nonunion operated on 6 months earlier. The cubital joint is arthritic because of an ununited anconeal process.

CHAPTER 2 ❚❚❚ Extremital Injury

75

C

A

B

D

Figure 2-90 • Lateral (A) and frontal (B) views before and after (C, D) pin removal of a femoral shaft fracture in a cat repaired with a large threaded intramedullary pin and a single wire loop. For the present at least, the circlage wire is inhibiting growth of the central portion of the callus, preventing it from bridging the fracture (nonunion).

76

SECTION I ❚❚❚ The Extremities

A

B

Figure 2-91 • A, Lateral view of the elbow of a middle-aged Irish Setter shows a nonunion fracture of the anconeal process, which was initially misdiagnosed as osteochondritis. B, Fortunately, the dog had been radiographed a year earlier for an unrelated problem, which provided a comparison view.

Figure 2-92 • Lateral view of a previously fractured distal femur shows a false joint (pseudoarthrosis), the result of a diaphyseal nonunion (hypertrophic type).

Figure 2-93 • Close-up frontal view of the stifle shows a nonunion fracture in the proximal half of the patella. Stress radiography conducted with the dog unconscious failed to show any fragment movement, indicating a rigid fibrous union.

CHAPTER 2 ❚❚❚ Extremital Injury

Figure 2-94 • Close-up lateral and full-length views of femoral malunion 2 years after surgery show abnormal angulations in both standard imaging planes, but as yet there is no osteoarthritis.

77

78

SECTION I ❚❚❚ The Extremities

B

A

C

D

Figure 2-95 • Close-up lateral (A) and frontal (B) views of an untreated femoral growth plate fracture in an immature dog about 3 weeks after the injury; films made a year later show severe malunion but no osteoarthritis (C, D).

CHAPTER 2 ❚❚❚ Extremital Injury

79

A Figure 2-96 • Lateral view of the tarsus of a cat shows a side-to-side malunion of the fifth metacarpal bone.

B

D

C Figure 2-97 • Full-length (A, C) and close-up (B, D) frontal and lateral views of a mid and lower forelimb show medial bowing at the level of the distal radius caused by a previous fracture.

80

SECTION I ❚❚❚ The Extremities

Figure 2-98 • Flexed lateral view of the elbow shows what at first glance appears to be osteochondritis of the coronoid but in reality is a healed articular fracture of the distal humerus with posttraumatic osteoarthritis.

A

A

B

C

D

B

Figure 2-99 • Lateral (A) and frontal (B) views show shortening, deformity, and outward distal rotation of the radius and ulna of a cat caused by an injury sustained as a kitten. Malunions are potentially most harmful when they occur before skeletal maturation because of their potentially deleterious effects on remaining bone and joint development.

Figure 2-100 • Postoperative films taken at 1 week (A, B) and 8 weeks (C, D) of a distal femoral growth plate fracture illustrating how some imperfectly reduced fractures of this type may self-correct over time, especially in the frontal plane.

CHAPTER 2 ❚❚❚ Extremital Injury

81

A

E D

C

B Figure 2-101 • Lateral (A) and frontal (B) views of the tibia and fibula in a cat recently struck by a car show badly displaced growth plate fractures at both ends of the tibia and distal end of the fibula. A frontal view of the uninjured opposite limb is included for comparison (C). Progress films made some months later (D, E) show shortening and deformity of the crus secondary to a combination of proximal and distal tibial malunions, and a distal fibular nonunion. The tarsocrural joint exemplifies posttraumatic osteoarthritis.

82

SECTION I ❚❚❚ The Extremities

B

A

C

D

Figure 2-102 • Close-up lateral (A), frontal (B), and frontal oblique (C) projections of the stifle of a cat show detachment and vertical splitting of the femoral epiphysis as a result of a growth plate fracture. Immediate postoperative images show near-anatomic reduction (D).

CHAPTER 2 ❚❚❚ Extremital Injury

E

F

G Figure 2-102 • cont’d Immediate postoperative images show near-anatomic reduction (E); later progress films show malunion and a small articular defect in the center of the lateral half of the femoral condyle (F, G).

83

84

SECTION I ❚❚❚ The Extremities

A

C

D

B Figure 2-103 • Full-length frontal (A), tarsocrural close-up (B), and lateral (C, D) views of the middle and distal portions of the hindlimb of an immature dog show multiple deformities (particularly of the genual joint and tibial tuberosity) caused by a previous injury. Normal opposite limb is provided for comparison.

CHAPTER 2 ❚❚❚ Extremital Injury

A

B

85

C

Figure 2-104 • Close-up lateral (A), frontal (B), medial oblique (C) views of a deformed tarsus of a cat, who, according to its owner, had been injured previously. Continued

86

D

SECTION I ❚❚❚ The Extremities

E

F

Figure 2-104 • cont‘d Lateral oblique (D) view of a deformed tarsus in a cat who, according to its owner, had been injured previously. Lateral and frontal views of the opposite tarsus are included for comparison (E, F)

CHAPTER 2 ❚❚❚ Extremital Injury

A

B

C

D

Figure 2-105 • Full-length lateral (A) and frontal (B) views of hindlimb in a 6-month-old Golden Retriever, deformed as a result of a previous proximal tibial growth plate fracture. The normal opposite limb is provided for comparison (C, D).

87

Figure 2-106 • Postural film (standing frontal view) of the tarsocrural joints of a dog thought to have sustained a distal tibial growth plate injury 6 weeks earlier. The combination of deviation, deformity, and swelling of the left tarsocrural joint (right) supports this diagnosis.

A

B

C

D

Figure 2-107 • Full-length and close-up lateral (A, B) and frontal views (C, D) of previously injured mid-forelimb show (1) upward dislocation of the articular portion of the proximal ulna, (2) downward dislocation of the articular portion of the proximal radius, (3) overall radial shortening, and (4) deformity or deviation (laterally) of the distal radius.

CHAPTER 2 ❚❚❚ Extremital Injury

E

89

F

Figure 2-107 • cont’d These findings are most likely the result of a distal radial growth plate fracture, secondary physeal closure, and reduced radial growth. Comparable views of the normal opposite limb are provided for comparison (E, F).

A

B

Figure 2-108 • A, Close-up lateral view of the distal radius and ulna of an immature dog injured 2 months earlier shows a large “sequestrum” in the center of a deformed and deviated radial metaphysis. B, The opposite limb is provided for comparison.

90

SECTION I ❚❚❚ The Extremities

B A

C

D

Figure 2-109 • A, Limb and joint deformities: ventrodorsal view of pelvis, hips, and upper hindlimbs of a young adult Borzoi injured as a puppy shows (1) left femoral deformity, (2) subluxation and arthritis of the left hip and stifle, and (3) lateral patella dislocation. Close-ups of the hips (B) and stifle (C, D) reveal further detail.

CHAPTER 2 ❚❚❚ Extremital Injury

Figure 2-110 • Limb deformity: Frontal view of the lower forelimbs (postural film made with dog standing and a horizontally directed x-ray beam) shows curvature of the distal radius and ulna and outward deviation of the paws (valgus deformity), the result of asymmetric physeal growth.

References 1. Fornage BD: Muscular trauma. In Fornage BD, ed: Musculoskeletal Ultrasound, New York, 1995, Churchill Livingstone. 2. Williams J, Bailey MQ, et al: Compartmental syndrome in a Labrador retriever. Vet Radiol Ultrasound 34:244, 1993. 3. Farrow CS: Musculoskeletal system. In Green RW, ed: Small Animal Ultrasound, Philadelphia, 1996, LippincottRaven. 4. Williams J, Bailey MQ, et al: Compartmental syndrome in a Labrador retriever. Vet Radiol Ultrasound 34:244, 1993. 5. Rewerts JM, Grooters AM, et al: Atraumatic rupture of the gastrocnemius muscle after corticosteroid administration in a dog. J Am Vet Med Assoc 210:655, 1997. 6. Salmeri KR: Radiographic diagnosis. Vet Rad 31:132, 1990. 7. Fitch RB, Wilson ER, et al: Radiographic, computed tomographic and magnetic resonance imaging evaluation of a chronic long digital extensor tendon avulsion in a dog. Vet Radiol Ultrasound 38:177, 1997. 8. Mahoney PN, Lamb CR: Articular, periarticular and juxtaarticular calcified bodies in the dog and cat: a radiologic review. Vet Radiol Ultrasound 37:3, 1996. 9. Long CD, Nyland TG: Ultrasonographic evaluation of the canine shoulder joint. Vet Radiol Ultrasound 40:372, 1999. 10. Guillard MJ, Mayo AK: Sprain of the short radial collateral ligament in a racing greyhound. J Small Anim Pract 41:169, 2000. 11. Denny HR, Barr RS: Partial carpal and pancarpal arthrodesis in the dog: a review of 50 cases. J Small Anim Pract 32:329, 1991. 12. Johnson KA: A radiographic study of the effects of autologous cancellous bone grafts on bone healing after carpal arthrodesis in the dog. Vet Rad 22:177, 1981. 13. Nordberg CC, Johnson KA: Magnetic resonance imaging of normal canine carpal ligaments. Vet Radiol Ultrasound 40:128, 1998. 14. Farrow CS: Carpal sprain injury in the dog. J Am Vet Rad Soc 18:38, 1977.

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15. O’Brian MG, Boudrieau RJ, Clark GN: Traumatic luxation of the cubital joint (elbow) in dogs: 44 cases (19781988). J Am Vet Med Assoc 201:1760, 1992. 16. Whitehair JG, Vasseur PB, Willits NH: Epidemiology of cranial cruciate ligament rupture in dogs. J Am Vet Med Assoc 203:1016, 1993. 17. Duval JM, Budsberg SC, et al: Breed, sex, and body weight as risk factors for rupture of the cranial crutiate ligament in young dogs. J Am Vet Med Assoc 215:811, 1999. 18. Bruce WJ: Multiple ligamentous injuries of the canine stifle joint: a study of 12 cases. J Small Anim Pract 39:333, 1998. 19. Soderstrom MJ, Rochat MC, Drost WT: Avulsion fracture of the caudal cruciate ligament. Vet Radiol Ultrasound 39:536, 1998. 20. Williams J, Fitch RB, Lemarie RJ: Partial avulsion of the origin of the cranial cruciate ligament in a 4-year-old dog. Vet Radiol Ultrasound 38:380, 1997. 21. Bennet D, May C: Meniscal damage associated with cruciate disease in the dog. J Small Anim Pract 32:111, 1999. 22. Lewis DD, Goring RL, et al: A comparison of diagnostic methods used in the evaluation of early degenerative joint disease in the dog. J Am Anim Hosp Assoc 23:305, 1987. 23. Baird DK, Hathcock JT, et al: Low-field magnetic resonance imaging of early subchondral cyst-like lesions in induced cranial cruciate ligament deficient dogs. Vet Radiol Ultrasound 39:167, 1998. 24. DeRooster H, vanBree H: Use of compression stress radiography for the detection of partial tears of the canine cranial cruciate ligament. J Small Anim Pract 40:573, 1999. 25. DeRooster H, vanBree H: Popliteal sesamoid displacement associated with cruciate rupture in a dog. J Small Anim Pract 40:316, 1999. 26. Montgomery RD, Fitch RB, et al: Radiographic imaging of the canine intercondyloid fossa. Vet Radiol Ultrasound 36:276, 1995. 27. Fitch RB, Hathcock JT, et al: Radiographic and computed tomographic evaluation of the canine intercondylar fossa in normal stifles and after notchplasty in stable and unstable stifles. Vet Radiol Ultrasound 37:266, 1996. 28. Reed AL, Payne JT, Constantinescu GM: Ultrasonographic anatomy of the normal canine stifle. Vet Radiol Ultrasound 36:315, 1995. 29. Kramer M, Stengel H, et al: Sonography of the canine stifle. Vet Radiol Ultrasound 40:282, 1999. 30. Widmer WR, Buckwalter KA, et al: Principles of magnetic resonance imaging and application to the stifle joint in dogs. J Am Vet Med Assoc 198:1914, 1991. 31. Widmer WR, Buckwalter KA, et al: Radiographic and magnetic resonance imaging of the stifle joint in experimental osteoarthritis of dogs. Vet Radiol Ultrasound 35:371, 1994. 32. Baird DK, Hathcock JT, et al: Low-field magnetic resonance imaging of the canine stifle joint: normal anatomy. Vet Radiol Ultrasound 39:87, 1998. 33. Banfield CM, Morrison WB: Magnetic resonance arthrography of the canine stifle joint: technique and applications in eleven military dogs. Vet Radiol Ultrasound 41:200, 2000. 34. Burk RL, Eich DW: Letter to the editor. J Am Vet Med Assoc 206:1838, 1995.

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35. Barrett RB: Radiography in trauma of the musculotendinous soft tissues of dogs and cats. J Am Vet Rad Soc 12:5, 1971. 36. Shah ZR, Crass JR, et al: Ultrasonic detection of foreign bodies in soft tissues using turkey muscle as a model. Vet Radiol Ultrasound 33:94, 1992. 37. Britt LG, Barbee DD, et al: Engorged ticks appearing as distinct radiographic opacities. Vet Radiol Ultrasound 41:145, 2000. 38. Huss B, Lattimer JC: What is your diagnosis? J Am Vet Med Assoc 204:1017, 1994. 39. Li A, Bennett D, et al: Radial carpal bone fractures in 15 dogs. J Small Anim Pract 41:74, 2000. 40. Cook JL, Jordan RC: What is your diagnosis? J Am Vet Med Assoc 210:329, 1997. 41. Boulay JP, Wallace LJ, Lipowitz AJ: Pathological fracture of long bones in the dog. J Am Anim Hosp Assoc 23:207, 1997. 42. Parker RB, Spencer CP, Shields RP: Radiographic diagnosis. Vet Rad 26:208, 1985. 43. Huss BT, Helmick KE: What is your diagnosis? J Am Vet Med Assoc 205:982, 1994. 44. Zontine WJ: Bilateral stress pattern in the distal ulna metaphyses of a Great Dane. J Am Vet Rad Soc 13:53, 1972. 45. McCartney WT, Carmichael S: Talar neck fractures in 5 cats. J Small Anim Pract 41:204, 2000. 46. Miller CW, Sumner-Smith G: Using the Unger System to classify 386 long bone fractures in dogs. J Small Anim Pract 39:390, 1998.

47. Johnson AJ, Smith CW, Schaeffer DJ: Fragment reconstruction and bone plate fixation versus bridging plate fixation for treating highly comminuted femoral fractures in dogs: 35 cases (1987-1997). J Am Vet Med Assoc 213:1157, 1998. 48. Marchiori DM: Trauma. In Marchiori DM, ed: Clinical Imaging, St. Louis, 1999, Mosby. 49. Anderson MA, Mann FA, Branson KR, et al: Use of an ultrasonic Doppler flow detector for determining tissue viability in a dog. J Am Vet Med Assoc 205:319, 1994. 50. Punto L, Puranen J, Mokka REM: Osteomedullography in tibial shaft fractures of the dog and pig. J Am Vet Rad Soc 18:102, 1977. 51. Anderson MA, Muhlbauer MC: Aberrant bone growth following phalangeal fracture. Vet Radiol Ultrasound 38:48, 1997. 52. Riser WH, Shirer JF: Normal and abnormal growth of the distal foreleg in large and giant dogs. J Am Vet Rad Soc 6:50, 1965. 53. Carrig CB, Morgan JP: Asynchronous growth of the canine radius and ulna—early radiographic changes following experimental retardation of longitudinal growth of the ulna. J Am Vet Rad Soc 16:121, 1975. 54. Carrig CB, Morgan JP, Pool RR: Effects of x-irradiation on the distal ulnar growth plate of the dog: gross radiographic changes. J Am Vet Rad Soc 16:211, 1975. 55. Carrig CB, Merkley DF, Mostosky UV: Asynchronous growth of the canine radius and ulna: effects of different amounts of ulnar growth retardation. J Am Vet Rad Soc 19:16, 1978.

C h a p t e r

3

Osteoarthritis

❚❚❚ THE LANGUAGE OF ARTHRITIS Osteoarthritis or Osteoarthrosis? The terms osteoarthrosis and osteoarthritis are synonymous. The suffixes osis and itis are for the most part cultural preferences, with the European medical community preferring osteoarthrosis, whereas North Americans generally favor osteoarthritis.

Generative or Degenerative Joint Disease A persuasive argument has been advanced in favor of the term generative joint disease over the currently favored expression, degenerative joint disease. Briefly, the line of reasoning supporting generative joint disease is that most of the radiographic signs of osteoarthritis, spurring (osteophytes), sclerosis, eburnation, and joint bodies, are additions to the joint—indications of a generative process, not a degenerative one. The only change that qualifies as degenerative is the gradual disappearance of the articular cartilage, as inferred by narrowing of the cartilage space. Moreover, angiographic studies on dogs with experimental and naturally occurring osteoarthritis consistently show localized and regional hyperemia, further attesting to the generative nature of osteoarthritis.1

Radiographic Appearance of Osteoarthritis First and foremost, osteoarthritis is characterized by periarticular osteophytes. As the disease progresses, the existing osteophytes enlarge, and new deposits form. Depending on which joint is affected, the cartilage space may narrow or even collapse. Although subchondral sclerosis is often mentioned as being a consistent and reliable indicator of osteoarthritis—presumably developing due to boneto-bone contact—I have found it to be inconsistently present. Another problem relates to the reliability of

this observation because periarticular osteophytes can mimic an increase in subchondral bone density (Figure 3-1, A, B).

MRI Appearance of Osteoarthritis Articular Cartilage. Baird and coworkers determined, based on experimentation with gelatin phantoms, that magnetic resonance imaging (MRI) can potentially be used to detect excessive hydration in articular cartilage, one of the pathologic precursors of osteoarthritis. Using a low-field strength magnet, T2, and inversion recovery with short inversion time provided the best images among the various sequences tried.2 Using experimental dogs whose cranial cruciate ligament had been cut, the authors were able to show a relative increase in signal intensity of the articular cartilage of the weight-bearing portion of the lateral femoral condyle and the caudal portion of the medial tibial condyle, presumably related to increased proteoglycan synthesis.

Synovitis: A Consequence of Osteoarthritis Osteoarthritis often leads to secondary synovitis, which if severe can cause extensive joint swelling. Cantwell described the use of arthrography to delineate the full extent of the resultant capsular distension.3

Categorizing Osteoarthritis Developmental Osteoarthritis. Hip dysplasia and osteochondritis are examples of common developmental diseases that cause osteoarthritis in part by decreasing or eliminating joint congruity (Figure 3-2, A, B). Posttraumatic Osteoarthritis. Dislocations, articular fractures, severe sprains, and arthroplasties are all capable of causing osteoarthritis, as shown in Figures 3-3, A, B, and 3-4. 93

94

SECTION I ❚❚❚ The Extremities

A A

B Figure 3-1 • Close-up lateral (A) and frontal (B) views of an

B Figure 3-2 • Two examples of developmental osteoarthritis in

arthritic stifle in a small dog, the result of an old injury, show a classic array of periarticular osteophytes.

the dog: hip dysplasia (A) and osteochondritis (B) of the coronoid process.

Specific Diseases Causing Osteoarthritis

replacement of the femoral head and neck was advocated (derotational osteotomy) but appeared to garner only limited interest.7 Another “corrective” surgery, acetabular relocation (triple pelvic osteotomy), often results in trading one problem for another. The hip is made more congruent, potentially decreasing the probability of osteoarthritis, but at the cost of narrowing the pelvic canal, which may then lead to chronic constipation. Additionally, the unstabilized ischial fragment often heals with a pronounced downward deflection, which can lead to an undesirable squatting posture.

Hip Dysplasia Background. Certain breeds of dogs are more susceptible to hip dysplasia than others, whereas others rarely develop it.4 Programs established to eradicate dysplasia in susceptible breeds have only been partially successful.5 As repeatedly shown in both people and animals with osteoarthritis, maintenance of body weight at or below the norm (for the individual) usually results in reduced pain and disability. My own observation is that daily nonforced exercise is even more beneficial.6 In the seemingly endless quest for a surgical solution to the problem of hip dysplasia, removal and

Imaging Findings Radiology. Morgan has drawn attention to a narrow, crescent-shaped ridge of bone located on the proximal

CHAPTER 3 ❚❚❚ Osteoarthritis

A

95

Figure 3-4 • Close-up lateral view of the stifle of a dog with a Steinmann pin protruding into the genual joint causing extensive dystrophic calcification. The tibia was fractured and subsequently pinned some months earlier. Also, note the focal bone loss at the base of the femoral trochlea, the result of repeated pin trauma, and the markedly swollen joint.

B arthritic stifle, the result of long-standing instability caused by a ruptured cranial cruciate, and second-degree sprain of the caudal cruciate ligament.

Figure 3-5 • Severe bilateral hip dysplasia with advanced osteoarthritis. Opinion differs as to whether the large cranial acetabular bone deposits are fractured osteophytes or merely atypical periarticular osteophytes.

aspect of the base of the femoral neck (as seen in the extended ventrodorsal projection). He terms this finding a “spur” and contends that it may be a very early indicator of canine hip dysplasia.8 However, most radiologic reports of osteoarthritis secondary to hip dysplasia have focused on new bone deposition, which initially develops at the edges of the joint capsule, and later, along the articular margins of the femoral head and acetabulum (Figure 3-5). As the hip becomes more arthritic, a large lip of new bone begins to form along the dorsal rim of the acetabulum; extending it laterally, in some cases by as much as 50 percent. This portion of the arthritic acetabulum is often mistakenly described as representing a line of

closely approximated osteophytes, or even more simplistically as subchondral sclerosis. In fact, this is a purposeful and predictable form of remodeling—an effort by the dysplastic acetabulum to accommodate the new dynamic of an excessively mobile femur. For its part, the contour of the femoral head begins to change from its normal spherical shape to a broader and shallower configuration. Concurrently, twin collars of new bone begin to form along the articular and capsular margins, which radiographically have often incorrectly been described as “filling in” or “thickening” of the femoral neck. Another misconception is that the bones of the coxal joint become incongruent. This is not the case. What

Figure 3-3 • Close-up frontal (A) and lateral (B) views of severely

96

SECTION I ❚❚❚ The Extremities

A

Figure 3-7 • Close-up lateral view of arthritic elbow (opposite side also affected, but not shown).

B Figure 3-6 • A, Defleshed elbow of a 2-year-old dog with osteochondritis (medial perspective) shows a myriad of bone deposits that characterize the arthritic pattern resulting from a detached medial coronoid process (emphasis zone). B, Closeup view of the articular surface of the detached medial coronoid process, photographed on the surface of a penny to enable the reader to better appreciate its actual size.

actually happens is that the area of congruency is reduced, with a commensurate loss of motion range. Ultrasound. Ultrasound as a means of early hip dysplasia detection in puppies is typically time-consuming, often ambiguous, and thus of little practical use.

Osteochondritis Osteochondritis, especially the fragmenting form (osteochondritis dissicans), causes opposing joint surfaces to become dissimilar, an incongruency that typically leads to osteoarthritis. If the affected part of the bone is weight bearing, for example, the medial coronoid process, the resultant osteoarthritis will be even greater due to partial dislocation and abnormal movement of the overlying bone (Figure 3-6). Detachment or relocation of the anconeal process also results in abnormal joint motion leading to severe osteoarthritis.

Figure 3-8 • Close-up frontal views of arthritic elbows of a dog afflicted by bilateral osteochondritis of the coronoid show the large bony beaks characteristic of the advanced form of the disease.

Figures 3-7 to 3-9 exemplify the characteristic arthritic pattern caused by osteochondritis of the elbow.

Avascular Necrosis, Legg-CalvéPerthes Disease Background. Lee was one of the first veterinary radiologists to graphically describe the radiographic disintegration of the femoral head in avascular necrosis (AVN).9 A unique, noninfectious form of bone necrosis, this disease initially causes core destruction, weakening the bone to the extent that portions of the perimeter fragment and collapse. The badly damaged femoral head then heals spontaneously, but not before becoming severely deformed. The resultant mismatch of the remodeled femoral head and normal acetabulum causes the hip to become gradually arthritic.

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97

A

Figure 3-10 • A ventrodorsal close-up view of the left hip of a dog with advanced Legg-Calvé-Perthes disease. In this final stage, the partially disintegrated femoral head has healed, but in a new shape that does not match the acetabulum (the cause of subsequent osteoarthritis).

Radiology (Human). Arlet and Ficat have proposed the following staging for human AVN, based on the following radiographic criteria10:

B Figure 3-9 • Close-up lateral (A) and frontal (B) views of a severely arthritic elbow caused by an ununited anconeal process in a 10-year-old Springer Spaniel mistakenly diagnosed as an osteosarcoma.

Imaging Findings Radiology (Veterinary). The first radiographic indication of AVN in dogs is a subtle widening of the hip joint—widening that often cannot be appreciated without an opposite side comparison. Next, the affected femoral head begins to take on a distinctive pockmarked appearance as the interior of the bone starts to become necrotic. As the damage becomes more extensive, so do the visible areas of bone loss. When there is sufficient trabecular destruction, the cortex begins to crack and then collapse. At this point, the femoral head may appear overtly fragmented. Healing is characterized by a reversal of the previously described events; however, the femoral head fails to regain its original spherical shape, instead, assuming a distinctive conical configuration. It is this deformity that provokes the structurally normal acetabulum to follow suit and become arthritic (Figure 3-10).

Stage 1: Normal radiographic appearance of the hip but abnormal bone scans; patient has pain and decreased range of motion. Stage 2: Radiographs show osteoporosis and multiple cystic or sclerotic lesions. Stage 3: Radiographs show marginal fissures, fragmentation, and collapse. Stage 4: Radiographs show overt disintegration of the femoral head. Stage 5: Severe deformation of the femoral head causes reciprocal acetabular remodeling and osteoarthritis of the hip. MRI. Little information appears in the veterinary literature on the magnetic resonance (MR) appearance on AVN in dogs, in part due to the fact that no satisfactory treatment currently exists. However, if core decompression (a treatment currently being tried in people with the disease) proves effective, MR could prove indispensable in the early identification of the AVN when decompressive surgery is believed to be most effective. In humans, AVN is characterized by variably sized and shaped areas of decreased signal intensity on T1weighted images. Intermediate-to-advanced lesions often appear as crescentic objects lying just beneath the articular surface of the femoral head.11 In an attempt to clinically stage the disease, Mitchell and co-workers devised the following classification (the lower the number, the better the prognosis).12

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SECTION I ❚❚❚ The Extremities

Class A: High-strength signal on short TR/TE images; medium strength signal on T2 (resembles fat). Class B: High-strength signal on both short and long TR/TE images (resembles blood). Class C: Low-strength signal on short TR/TE images (resembles fluid). Class D: Low-strength signal on all images (resembles fibrous tissue).

Intraarticular Calcification, Ossification, and Fragmentation (Table 3-1) Polyarthritis. Acute polyarthritis can sometimes be inferred radiographically because of bilateral swelling identified in the carpi, stifles, or hocks. In the case of the stifles, the observed swelling may be mistakenly attributed to cruciate trauma, especially if the animal is thought to have a unilateral lameness (Figure 3-11, A, B). Chronic polyostotic immunoarthritis often leads to multiple partial dislocations, especially in the carpal and tarsal joints. When the stifles are affected, these dislocations, combined with associated joint swelling, can be mistaken for a chronic cruciate injury resulting in posttraumatic osteoarthritis.13 So-called erosive polyarthritis (a term used almost exclusively by physician rheumatologists), which primarily affects the cubital, genual, and tarsocrural joints, has been described in a pair of 11-month-old Greyhounds. Radiographically, the elbows, stifles, and hocks were mildly swollen, whereas the distal radius and radial carpal bone appeared bilaterally osteopenic

with a narrowed cartilage space. Focal lesions in the articular cartilage (termed erosions by the authors) and synovial discoloration and plaque formation suggested immunoarthritis; however, the diagnosis could not be confirmed.14 Immunoarthritis (Immune-mediated Osteoarthritis) Background. Immunoarthritis is the simplest term for describing the various forms of immune-mediated polyarthritis found in dogs and cats. Laboratory testing is usually required to be more specific, for example, rheumatoid arthritis, rheumatoid-like arthritis, or systemic lupus. To describe arthritis as “deforming” or “nondeforming” does little to refine the diagnosis because deformity is more an indication of duration than of etiology. Imaging Findings. Among the radiographic features that potentially characterize immunoarthritis in dogs, multiple, variably shaped and sized areas of decreased bone density, especially in the carpal or tarsal bones, are the most reliable. In this latter regard a carpal fibrosarcoma has been reported, which radiographically appeared as numerous punctate lucencies resembling immunoarthritis. But unlike immune-mediated osteoarthritis, there were also large, poorly marginated lucencies with overlying soft tissue swelling in the distal radius and ulna.15 Animals that have had immunoarthritis for an extended period of time (months or years) are also likely to show varying degrees of osteopenia and joint laxity (Figure 3-12). Related postural abnormalities—

Table 3-1 • DIFFERENTIAL DIAGNOSIS FOR INTRAARTICULAR BONE OR BONELIKE DENSITIES Cause

Comment

Capsular dystrophic calcification Meniscal ossification

Capsular or pericapsular calcification suggests gout or pseudogout. Primary and secondary meniscal ossification/calcification have been reported but are extremely rare. Secondary meniscal calcification is believed to result from injury, including meniscal surgery. The cause of primary meniscal ossification is not known.20 Most often the result of serious knee injuries. Most common in the shoulder and hock. This disease is common in older cats, but rare in dogs. Usually very small, immobile fragments, positioned in the cranial aspect of the joint near the tibial tubercles. Rare, and when present, difficult to see.

Mineralized cartilage fragment Osteochondritis Osteochondromatosis Sprain-avulsion fracture of the caudal cruciate ligament Sprain-avulsion fracture of the cranial cruciate ligament Sprain-avulsion fracture of the medial or lateral collateral ligaments Strain-avulsion fracture of the long digital extensor tendon Torn medial or lateral meniscus

Typically best seen in frontal projection midway between the physeal growth scar and the joint cavity. Avulsion of the long extensor often produces a vary large fragment, which is readily identified in the lateral projection near an enlarged extensor fossa. Typically appears as a streaky form of mineralization in one of the miniscal fields, usually medially.

CHAPTER 3 ❚❚❚ Osteoarthritis

99

A

Figure 3-12 • Frontal view of the carpi of a dog with immunoarthritis shows characteristic swelling, focal areas of bone loss, and osteopenia in the surrounding bone.

B Figure 3-11 • A, Lateral close-up view of the genual joint of a dog referred for cruciate surgery (based on pain, swelling, and instability of the knee) shows severe swelling, but no dislocation or arthritis. B, Examination revealed similar signs in the opposite stifle, which was also radiographed, and found to have similar abnormalities. These findings are consistent with polyarthritis, probably of an autoimmune nature.

particularly evident in weight-bearing views—are typically most pronounced in the carpus (Figure 3-13), tarsus, and stifle, and in the case of the latter, may be mistaken for a ruptured cruciate ligament. Joint swelling and cartilage space narrowing are usually present in chronic cases but do little to distinguish immunoarthritis from other forms of osteoarthritis, except for the fact that they are found bilaterally. Some dogs with longstanding immunoarthritis have large extraarticular osteophytes, as well as numerous islands of periarticular bone. Joint surveys often reveal bilateral or quadrilateral limb involvement in such instances (Figure 3-14).

Figure 3-13 • Frontal, weight-bearing view of the carpi of a dog with immunoarthritis show bilateral: (1) valgus deformity, (2) joint swelling, (3) dislocation of numerous carpal bones, (4) cartilage space narrowing, and (4) focal areas of bone loss typical of immunoarthritis.

Postsurgical Osteoarthritis Most surgically repaired fractures in dogs and cats heal to the extent that the animal regains full and relatively pain-free use of the injured limb. When this does not happen, the surgery is deemed a failure or a partial success, depending on one’s level of optimism. Causes of failed orthopedic surgery include operatively

100

SECTION I ❚❚❚ The Extremities

A

B

C Figure 3-14 • Close-up frontal and lateral views of the elbows (A, B) and tarsi (C, D) of a dog initially diagnosed as having osteochondritis but later found to have immunoarthritis.

CHAPTER 3 ❚❚❚ Osteoarthritis

101

D Figure 3-14, cont’d For legend see opposite page.

Figure 3-15 • Lateral close-up view of the genual joint of a dog operated on for a cruciate injury 2 years earlier shows moderate osteoarthritis, especially of the femoropatella joint. Note the enlarged extensor fossa craniodistal aspect of femur, which some contend becomes larger with instability. The abnormally flattened femoral trochlea, which perfectly matches the deformed patella, is a true example of adaptive remodeling.

introduced infection; misapplied, dislocated, loosened or broken implants; malunion or non-union; and postoperative osteoarthritis (Figures 3-15 and 3-16). Reconstructive hip and knee surgery aimed at halting the progress of osteoarthritis has not always proven beneficial, in some instances creating problems more debilitating than those for which the animal was originally operated. Examples of such potentially hazardous procedures include the following: relocating the acetabulum of a dysplastic hip (acetabular reloca-

tion, triple pelvic osteotomy) and relocating the articular portion of the proximal tibial epiphysis (Figures 3-17 to 3-20).

Gout and Pseudogout False gout or pseudogout, also called calcium pyrophosphate dihydrate crystal deposition disease, has been reported in a 13-year-old dog with acute multiple limb lameness. Radiographs of the carpi

102

SECTION I ❚❚❚ The Extremities

A

B

C Figure 3-16 • A, Lateral close-up view of the elbow of a dog hit by a car shows a fracture–dislocation (Monteggia’s fracture). B, An immediate postoperative view shows near anatomic reduction. C, Three months later, after removal of all but one of the implants, the elbow appears severely arthritic.

CHAPTER 3 ❚❚❚ Osteoarthritis

A

103

B

Figure 3-17 • A, Ventrodorsal view of the pelvis and hips shows severe bilateral hip dysplasia with osteoarthritis on the right. B, After surgery to relocate the left acetabulum, the pelvic canal is severely narrowed, resulting in periodic constipation and a pronounced nonpainful mechanical lameness. Note the badly displaced left ischial tuberosity (emphasis zone, bottom right).

A

B

Figure 3-18 • Preoperative (A) and postoperative (B) ventrodorsal views of the pelvis and hips show bilateral acetabular relocations, which, although providing greater femoral head “coverage,” have severely narrowed the pelvic canal, causing chronic constipation.

104

SECTION I ❚❚❚ The Extremities

A

B

Figure 3-19 • A, Lateral close-up view of canine stifle operated on in an effort to restabilize the joint after acute cranial cruciate rupture. The joint is now painfully arthritic, and the stabilizing wire has predictably broken. B, In a second surgery, the cranial part of the proximal tibial epiphysis was relocated, but as seen in this lateral close-up, this only seems to have increased the degree of dislocation and amount of arthritis.

A B Figure 3-20 • A, Immediate postoperative film of a tibial relocation; B, subsequent progress check reveals a fracture proximally.

CHAPTER 3 ❚❚❚ Osteoarthritis

A

105

B

Figure 3-21 • Close-up lateral oblique view of proximal ulna (A) and rear view of distal humerus (B) show massive cavitation—the result of synovial storage disease. The shadow in the lateral oblique view, like a radiographic projection, shows the extent to which the articular contour has been altered.

showed faint mineralization on the perimeter of the antibrachial joints.16 Two other reports of false gout in dogs described capsular masses in the carpal and metacarpophalangeal joints.17,18

Storage Disease Doige and I have described a storagelike disease in a dog that featured marked subchondral cavitation of major limb joints caused by ingrowth of a hyperplastic synovium (Figures 3-21).19

References 1. Tirgari M: Blood pattern changes in primary and secondary osteoarthritis of the dog: an experimental study using intraosseous venography. J Am Vet Rad Soc 19:83, 1978. 2. Baird DK, Kinkaid SA, et al: Effect of hydration on signal intensity of gelatin phantoms using low-field magnetic resonance imaging: possible application in osteoarthritis. Vet Radiol & Ultrasound 40:27, 1999. 3. Cantwell DH: Radiographic diagnosis. Vet Rad 27:151, 1986. 4. Ackerman N: Hip dysplasia in the Afgan Hound. Vet Rad 23:88, 1982. 5. Leppanen M, Maki K, et al: Factors affecting hip dysplasia in German Shepherd dogs in Finland: efficacy of the current improvement program. J Small Anim Pract 41:19, 2000. 6. Impellzeri JA, Tetrick MA, Muir P: Effect of weight reduction on clinical signs of lameness in dogs with hip osteoarthritis. J Am Vet Med Assoc 216:1089, 2000.

7. Nunamaker DM, Biery DN, Newton CD: Femoral neck antiversion in the dog: its radiographic measurement. J Am Vet Rad Soc 14:45, 1973. 8. Morgan JP: Canine hip dysplasia. Vet Rad 28:2, 1987. 9. Lee R: Legg-Perthes disease in the dog: the histological and associated radiological changes. J Am Vet Rad Soc 15(1):24, 1974. 10. Arlet J, Ficat RP: Diagnostic de l’osteo-necrose femoro capitale primitive au stade. Rev Chir Orthop 54:637, 1965. 11. Murphy MD: The hip. In Haaga JR, ed: Computed Tomography & Magnetic Resonance Imaging of the Whole Body, ed 3, vol 2. St Louis, 1994, Mosby. 12. Mitchell DG, et al: Femoral head avascular necrosis: correlation with MR imaging, radiographic staging, radionuclide imaging, and clinical findings. Radiology 162:709, 1987. 13. Roberts R: Radiographs presented as part of the 1992 A.C.V.R. oral certification examination: musculoskeletal section. Vet Radiol & Ultrasound 34:185, 1993. 14. Woodard JC, Riser WH, et al: Erosive polyarthritis in two Greyhounds. J Am Vet Med Assoc 198:873, 1991. 15. Applewhite AA, Page RL: What is your diagnosis? J Am Vet Med Assoc 214:29, 1999. 16. DeHaan JJ, Anderson CB: Calcium crystal-associated arthropathy (pseudogout) in a dog. J Am Vet Med Assoc 200:943, 1992. 17. Gibson JP, Roenigk WJ: Pseudogout in a dog. J Am Vet Med Assoc 161:912, 1972. 18. Heimann M, Carpenter JL, Halverson PB: Calcium pyrophosphate deposition (chondrocalcinosis) in a dog. Vet Pathol 27:122, 1990. 19. Doige CE, Farrow CS, Gee BR: Astorage-like disease with skeletal involvement in a dog. Vet Rad 21:98, 1980.

C h a p t e r

3

Osteoarthritis

❚❚❚ THE LANGUAGE OF ARTHRITIS Osteoarthritis or Osteoarthrosis? The terms osteoarthrosis and osteoarthritis are synonymous. The suffixes osis and itis are for the most part cultural preferences, with the European medical community preferring osteoarthrosis, whereas North Americans generally favor osteoarthritis.

Generative or Degenerative Joint Disease A persuasive argument has been advanced in favor of the term generative joint disease over the currently favored expression, degenerative joint disease. Briefly, the line of reasoning supporting generative joint disease is that most of the radiographic signs of osteoarthritis, spurring (osteophytes), sclerosis, eburnation, and joint bodies, are additions to the joint—indications of a generative process, not a degenerative one. The only change that qualifies as degenerative is the gradual disappearance of the articular cartilage, as inferred by narrowing of the cartilage space. Moreover, angiographic studies on dogs with experimental and naturally occurring osteoarthritis consistently show localized and regional hyperemia, further attesting to the generative nature of osteoarthritis.1

Radiographic Appearance of Osteoarthritis First and foremost, osteoarthritis is characterized by periarticular osteophytes. As the disease progresses, the existing osteophytes enlarge, and new deposits form. Depending on which joint is affected, the cartilage space may narrow or even collapse. Although subchondral sclerosis is often mentioned as being a consistent and reliable indicator of osteoarthritis—presumably developing due to boneto-bone contact—I have found it to be inconsistently present. Another problem relates to the reliability of

this observation because periarticular osteophytes can mimic an increase in subchondral bone density (Figure 3-1, A, B).

MRI Appearance of Osteoarthritis Articular Cartilage. Baird and coworkers determined, based on experimentation with gelatin phantoms, that magnetic resonance imaging (MRI) can potentially be used to detect excessive hydration in articular cartilage, one of the pathologic precursors of osteoarthritis. Using a low-field strength magnet, T2, and inversion recovery with short inversion time provided the best images among the various sequences tried.2 Using experimental dogs whose cranial cruciate ligament had been cut, the authors were able to show a relative increase in signal intensity of the articular cartilage of the weight-bearing portion of the lateral femoral condyle and the caudal portion of the medial tibial condyle, presumably related to increased proteoglycan synthesis.

Synovitis: A Consequence of Osteoarthritis Osteoarthritis often leads to secondary synovitis, which if severe can cause extensive joint swelling. Cantwell described the use of arthrography to delineate the full extent of the resultant capsular distension.3

Categorizing Osteoarthritis Developmental Osteoarthritis. Hip dysplasia and osteochondritis are examples of common developmental diseases that cause osteoarthritis in part by decreasing or eliminating joint congruity (Figure 3-2, A, B). Posttraumatic Osteoarthritis. Dislocations, articular fractures, severe sprains, and arthroplasties are all capable of causing osteoarthritis, as shown in Figures 3-3, A, B, and 3-4. 93

94

SECTION I ❚❚❚ The Extremities

A A

B Figure 3-1 • Close-up lateral (A) and frontal (B) views of an

B Figure 3-2 • Two examples of developmental osteoarthritis in

arthritic stifle in a small dog, the result of an old injury, show a classic array of periarticular osteophytes.

the dog: hip dysplasia (A) and osteochondritis (B) of the coronoid process.

Specific Diseases Causing Osteoarthritis

replacement of the femoral head and neck was advocated (derotational osteotomy) but appeared to garner only limited interest.7 Another “corrective” surgery, acetabular relocation (triple pelvic osteotomy), often results in trading one problem for another. The hip is made more congruent, potentially decreasing the probability of osteoarthritis, but at the cost of narrowing the pelvic canal, which may then lead to chronic constipation. Additionally, the unstabilized ischial fragment often heals with a pronounced downward deflection, which can lead to an undesirable squatting posture.

Hip Dysplasia Background. Certain breeds of dogs are more susceptible to hip dysplasia than others, whereas others rarely develop it.4 Programs established to eradicate dysplasia in susceptible breeds have only been partially successful.5 As repeatedly shown in both people and animals with osteoarthritis, maintenance of body weight at or below the norm (for the individual) usually results in reduced pain and disability. My own observation is that daily nonforced exercise is even more beneficial.6 In the seemingly endless quest for a surgical solution to the problem of hip dysplasia, removal and

Imaging Findings Radiology. Morgan has drawn attention to a narrow, crescent-shaped ridge of bone located on the proximal

CHAPTER 3 ❚❚❚ Osteoarthritis

A

95

Figure 3-4 • Close-up lateral view of the stifle of a dog with a Steinmann pin protruding into the genual joint causing extensive dystrophic calcification. The tibia was fractured and subsequently pinned some months earlier. Also, note the focal bone loss at the base of the femoral trochlea, the result of repeated pin trauma, and the markedly swollen joint.

B arthritic stifle, the result of long-standing instability caused by a ruptured cranial cruciate, and second-degree sprain of the caudal cruciate ligament.

Figure 3-5 • Severe bilateral hip dysplasia with advanced osteoarthritis. Opinion differs as to whether the large cranial acetabular bone deposits are fractured osteophytes or merely atypical periarticular osteophytes.

aspect of the base of the femoral neck (as seen in the extended ventrodorsal projection). He terms this finding a “spur” and contends that it may be a very early indicator of canine hip dysplasia.8 However, most radiologic reports of osteoarthritis secondary to hip dysplasia have focused on new bone deposition, which initially develops at the edges of the joint capsule, and later, along the articular margins of the femoral head and acetabulum (Figure 3-5). As the hip becomes more arthritic, a large lip of new bone begins to form along the dorsal rim of the acetabulum; extending it laterally, in some cases by as much as 50 percent. This portion of the arthritic acetabulum is often mistakenly described as representing a line of

closely approximated osteophytes, or even more simplistically as subchondral sclerosis. In fact, this is a purposeful and predictable form of remodeling—an effort by the dysplastic acetabulum to accommodate the new dynamic of an excessively mobile femur. For its part, the contour of the femoral head begins to change from its normal spherical shape to a broader and shallower configuration. Concurrently, twin collars of new bone begin to form along the articular and capsular margins, which radiographically have often incorrectly been described as “filling in” or “thickening” of the femoral neck. Another misconception is that the bones of the coxal joint become incongruent. This is not the case. What

Figure 3-3 • Close-up frontal (A) and lateral (B) views of severely

96

SECTION I ❚❚❚ The Extremities

A

Figure 3-7 • Close-up lateral view of arthritic elbow (opposite side also affected, but not shown).

B Figure 3-6 • A, Defleshed elbow of a 2-year-old dog with osteochondritis (medial perspective) shows a myriad of bone deposits that characterize the arthritic pattern resulting from a detached medial coronoid process (emphasis zone). B, Closeup view of the articular surface of the detached medial coronoid process, photographed on the surface of a penny to enable the reader to better appreciate its actual size.

actually happens is that the area of congruency is reduced, with a commensurate loss of motion range. Ultrasound. Ultrasound as a means of early hip dysplasia detection in puppies is typically time-consuming, often ambiguous, and thus of little practical use.

Osteochondritis Osteochondritis, especially the fragmenting form (osteochondritis dissicans), causes opposing joint surfaces to become dissimilar, an incongruency that typically leads to osteoarthritis. If the affected part of the bone is weight bearing, for example, the medial coronoid process, the resultant osteoarthritis will be even greater due to partial dislocation and abnormal movement of the overlying bone (Figure 3-6). Detachment or relocation of the anconeal process also results in abnormal joint motion leading to severe osteoarthritis.

Figure 3-8 • Close-up frontal views of arthritic elbows of a dog afflicted by bilateral osteochondritis of the coronoid show the large bony beaks characteristic of the advanced form of the disease.

Figures 3-7 to 3-9 exemplify the characteristic arthritic pattern caused by osteochondritis of the elbow.

Avascular Necrosis, Legg-CalvéPerthes Disease Background. Lee was one of the first veterinary radiologists to graphically describe the radiographic disintegration of the femoral head in avascular necrosis (AVN).9 A unique, noninfectious form of bone necrosis, this disease initially causes core destruction, weakening the bone to the extent that portions of the perimeter fragment and collapse. The badly damaged femoral head then heals spontaneously, but not before becoming severely deformed. The resultant mismatch of the remodeled femoral head and normal acetabulum causes the hip to become gradually arthritic.

CHAPTER 3 ❚❚❚ Osteoarthritis

97

A

Figure 3-10 • A ventrodorsal close-up view of the left hip of a dog with advanced Legg-Calvé-Perthes disease. In this final stage, the partially disintegrated femoral head has healed, but in a new shape that does not match the acetabulum (the cause of subsequent osteoarthritis).

Radiology (Human). Arlet and Ficat have proposed the following staging for human AVN, based on the following radiographic criteria10:

B Figure 3-9 • Close-up lateral (A) and frontal (B) views of a severely arthritic elbow caused by an ununited anconeal process in a 10-year-old Springer Spaniel mistakenly diagnosed as an osteosarcoma.

Imaging Findings Radiology (Veterinary). The first radiographic indication of AVN in dogs is a subtle widening of the hip joint—widening that often cannot be appreciated without an opposite side comparison. Next, the affected femoral head begins to take on a distinctive pockmarked appearance as the interior of the bone starts to become necrotic. As the damage becomes more extensive, so do the visible areas of bone loss. When there is sufficient trabecular destruction, the cortex begins to crack and then collapse. At this point, the femoral head may appear overtly fragmented. Healing is characterized by a reversal of the previously described events; however, the femoral head fails to regain its original spherical shape, instead, assuming a distinctive conical configuration. It is this deformity that provokes the structurally normal acetabulum to follow suit and become arthritic (Figure 3-10).

Stage 1: Normal radiographic appearance of the hip but abnormal bone scans; patient has pain and decreased range of motion. Stage 2: Radiographs show osteoporosis and multiple cystic or sclerotic lesions. Stage 3: Radiographs show marginal fissures, fragmentation, and collapse. Stage 4: Radiographs show overt disintegration of the femoral head. Stage 5: Severe deformation of the femoral head causes reciprocal acetabular remodeling and osteoarthritis of the hip. MRI. Little information appears in the veterinary literature on the magnetic resonance (MR) appearance on AVN in dogs, in part due to the fact that no satisfactory treatment currently exists. However, if core decompression (a treatment currently being tried in people with the disease) proves effective, MR could prove indispensable in the early identification of the AVN when decompressive surgery is believed to be most effective. In humans, AVN is characterized by variably sized and shaped areas of decreased signal intensity on T1weighted images. Intermediate-to-advanced lesions often appear as crescentic objects lying just beneath the articular surface of the femoral head.11 In an attempt to clinically stage the disease, Mitchell and co-workers devised the following classification (the lower the number, the better the prognosis).12

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Class A: High-strength signal on short TR/TE images; medium strength signal on T2 (resembles fat). Class B: High-strength signal on both short and long TR/TE images (resembles blood). Class C: Low-strength signal on short TR/TE images (resembles fluid). Class D: Low-strength signal on all images (resembles fibrous tissue).

Intraarticular Calcification, Ossification, and Fragmentation (Table 3-1) Polyarthritis. Acute polyarthritis can sometimes be inferred radiographically because of bilateral swelling identified in the carpi, stifles, or hocks. In the case of the stifles, the observed swelling may be mistakenly attributed to cruciate trauma, especially if the animal is thought to have a unilateral lameness (Figure 3-11, A, B). Chronic polyostotic immunoarthritis often leads to multiple partial dislocations, especially in the carpal and tarsal joints. When the stifles are affected, these dislocations, combined with associated joint swelling, can be mistaken for a chronic cruciate injury resulting in posttraumatic osteoarthritis.13 So-called erosive polyarthritis (a term used almost exclusively by physician rheumatologists), which primarily affects the cubital, genual, and tarsocrural joints, has been described in a pair of 11-month-old Greyhounds. Radiographically, the elbows, stifles, and hocks were mildly swollen, whereas the distal radius and radial carpal bone appeared bilaterally osteopenic

with a narrowed cartilage space. Focal lesions in the articular cartilage (termed erosions by the authors) and synovial discoloration and plaque formation suggested immunoarthritis; however, the diagnosis could not be confirmed.14 Immunoarthritis (Immune-mediated Osteoarthritis) Background. Immunoarthritis is the simplest term for describing the various forms of immune-mediated polyarthritis found in dogs and cats. Laboratory testing is usually required to be more specific, for example, rheumatoid arthritis, rheumatoid-like arthritis, or systemic lupus. To describe arthritis as “deforming” or “nondeforming” does little to refine the diagnosis because deformity is more an indication of duration than of etiology. Imaging Findings. Among the radiographic features that potentially characterize immunoarthritis in dogs, multiple, variably shaped and sized areas of decreased bone density, especially in the carpal or tarsal bones, are the most reliable. In this latter regard a carpal fibrosarcoma has been reported, which radiographically appeared as numerous punctate lucencies resembling immunoarthritis. But unlike immune-mediated osteoarthritis, there were also large, poorly marginated lucencies with overlying soft tissue swelling in the distal radius and ulna.15 Animals that have had immunoarthritis for an extended period of time (months or years) are also likely to show varying degrees of osteopenia and joint laxity (Figure 3-12). Related postural abnormalities—

Table 3-1 • DIFFERENTIAL DIAGNOSIS FOR INTRAARTICULAR BONE OR BONELIKE DENSITIES Cause

Comment

Capsular dystrophic calcification Meniscal ossification

Capsular or pericapsular calcification suggests gout or pseudogout. Primary and secondary meniscal ossification/calcification have been reported but are extremely rare. Secondary meniscal calcification is believed to result from injury, including meniscal surgery. The cause of primary meniscal ossification is not known.20 Most often the result of serious knee injuries. Most common in the shoulder and hock. This disease is common in older cats, but rare in dogs. Usually very small, immobile fragments, positioned in the cranial aspect of the joint near the tibial tubercles. Rare, and when present, difficult to see.

Mineralized cartilage fragment Osteochondritis Osteochondromatosis Sprain-avulsion fracture of the caudal cruciate ligament Sprain-avulsion fracture of the cranial cruciate ligament Sprain-avulsion fracture of the medial or lateral collateral ligaments Strain-avulsion fracture of the long digital extensor tendon Torn medial or lateral meniscus

Typically best seen in frontal projection midway between the physeal growth scar and the joint cavity. Avulsion of the long extensor often produces a vary large fragment, which is readily identified in the lateral projection near an enlarged extensor fossa. Typically appears as a streaky form of mineralization in one of the miniscal fields, usually medially.

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A

Figure 3-12 • Frontal view of the carpi of a dog with immunoarthritis shows characteristic swelling, focal areas of bone loss, and osteopenia in the surrounding bone.

B Figure 3-11 • A, Lateral close-up view of the genual joint of a dog referred for cruciate surgery (based on pain, swelling, and instability of the knee) shows severe swelling, but no dislocation or arthritis. B, Examination revealed similar signs in the opposite stifle, which was also radiographed, and found to have similar abnormalities. These findings are consistent with polyarthritis, probably of an autoimmune nature.

particularly evident in weight-bearing views—are typically most pronounced in the carpus (Figure 3-13), tarsus, and stifle, and in the case of the latter, may be mistaken for a ruptured cruciate ligament. Joint swelling and cartilage space narrowing are usually present in chronic cases but do little to distinguish immunoarthritis from other forms of osteoarthritis, except for the fact that they are found bilaterally. Some dogs with longstanding immunoarthritis have large extraarticular osteophytes, as well as numerous islands of periarticular bone. Joint surveys often reveal bilateral or quadrilateral limb involvement in such instances (Figure 3-14).

Figure 3-13 • Frontal, weight-bearing view of the carpi of a dog with immunoarthritis show bilateral: (1) valgus deformity, (2) joint swelling, (3) dislocation of numerous carpal bones, (4) cartilage space narrowing, and (4) focal areas of bone loss typical of immunoarthritis.

Postsurgical Osteoarthritis Most surgically repaired fractures in dogs and cats heal to the extent that the animal regains full and relatively pain-free use of the injured limb. When this does not happen, the surgery is deemed a failure or a partial success, depending on one’s level of optimism. Causes of failed orthopedic surgery include operatively

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A

B

C Figure 3-14 • Close-up frontal and lateral views of the elbows (A, B) and tarsi (C, D) of a dog initially diagnosed as having osteochondritis but later found to have immunoarthritis.

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D Figure 3-14, cont’d For legend see opposite page.

Figure 3-15 • Lateral close-up view of the genual joint of a dog operated on for a cruciate injury 2 years earlier shows moderate osteoarthritis, especially of the femoropatella joint. Note the enlarged extensor fossa craniodistal aspect of femur, which some contend becomes larger with instability. The abnormally flattened femoral trochlea, which perfectly matches the deformed patella, is a true example of adaptive remodeling.

introduced infection; misapplied, dislocated, loosened or broken implants; malunion or non-union; and postoperative osteoarthritis (Figures 3-15 and 3-16). Reconstructive hip and knee surgery aimed at halting the progress of osteoarthritis has not always proven beneficial, in some instances creating problems more debilitating than those for which the animal was originally operated. Examples of such potentially hazardous procedures include the following: relocating the acetabulum of a dysplastic hip (acetabular reloca-

tion, triple pelvic osteotomy) and relocating the articular portion of the proximal tibial epiphysis (Figures 3-17 to 3-20).

Gout and Pseudogout False gout or pseudogout, also called calcium pyrophosphate dihydrate crystal deposition disease, has been reported in a 13-year-old dog with acute multiple limb lameness. Radiographs of the carpi

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A

B

C Figure 3-16 • A, Lateral close-up view of the elbow of a dog hit by a car shows a fracture–dislocation (Monteggia’s fracture). B, An immediate postoperative view shows near anatomic reduction. C, Three months later, after removal of all but one of the implants, the elbow appears severely arthritic.

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A

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B

Figure 3-17 • A, Ventrodorsal view of the pelvis and hips shows severe bilateral hip dysplasia with osteoarthritis on the right. B, After surgery to relocate the left acetabulum, the pelvic canal is severely narrowed, resulting in periodic constipation and a pronounced nonpainful mechanical lameness. Note the badly displaced left ischial tuberosity (emphasis zone, bottom right).

A

B

Figure 3-18 • Preoperative (A) and postoperative (B) ventrodorsal views of the pelvis and hips show bilateral acetabular relocations, which, although providing greater femoral head “coverage,” have severely narrowed the pelvic canal, causing chronic constipation.

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A

B

Figure 3-19 • A, Lateral close-up view of canine stifle operated on in an effort to restabilize the joint after acute cranial cruciate rupture. The joint is now painfully arthritic, and the stabilizing wire has predictably broken. B, In a second surgery, the cranial part of the proximal tibial epiphysis was relocated, but as seen in this lateral close-up, this only seems to have increased the degree of dislocation and amount of arthritis.

A B Figure 3-20 • A, Immediate postoperative film of a tibial relocation; B, subsequent progress check reveals a fracture proximally.

CHAPTER 3 ❚❚❚ Osteoarthritis

A

105

B

Figure 3-21 • Close-up lateral oblique view of proximal ulna (A) and rear view of distal humerus (B) show massive cavitation—the result of synovial storage disease. The shadow in the lateral oblique view, like a radiographic projection, shows the extent to which the articular contour has been altered.

showed faint mineralization on the perimeter of the antibrachial joints.16 Two other reports of false gout in dogs described capsular masses in the carpal and metacarpophalangeal joints.17,18

Storage Disease Doige and I have described a storagelike disease in a dog that featured marked subchondral cavitation of major limb joints caused by ingrowth of a hyperplastic synovium (Figures 3-21).19

References 1. Tirgari M: Blood pattern changes in primary and secondary osteoarthritis of the dog: an experimental study using intraosseous venography. J Am Vet Rad Soc 19:83, 1978. 2. Baird DK, Kinkaid SA, et al: Effect of hydration on signal intensity of gelatin phantoms using low-field magnetic resonance imaging: possible application in osteoarthritis. Vet Radiol & Ultrasound 40:27, 1999. 3. Cantwell DH: Radiographic diagnosis. Vet Rad 27:151, 1986. 4. Ackerman N: Hip dysplasia in the Afgan Hound. Vet Rad 23:88, 1982. 5. Leppanen M, Maki K, et al: Factors affecting hip dysplasia in German Shepherd dogs in Finland: efficacy of the current improvement program. J Small Anim Pract 41:19, 2000. 6. Impellzeri JA, Tetrick MA, Muir P: Effect of weight reduction on clinical signs of lameness in dogs with hip osteoarthritis. J Am Vet Med Assoc 216:1089, 2000.

7. Nunamaker DM, Biery DN, Newton CD: Femoral neck antiversion in the dog: its radiographic measurement. J Am Vet Rad Soc 14:45, 1973. 8. Morgan JP: Canine hip dysplasia. Vet Rad 28:2, 1987. 9. Lee R: Legg-Perthes disease in the dog: the histological and associated radiological changes. J Am Vet Rad Soc 15(1):24, 1974. 10. Arlet J, Ficat RP: Diagnostic de l’osteo-necrose femoro capitale primitive au stade. Rev Chir Orthop 54:637, 1965. 11. Murphy MD: The hip. In Haaga JR, ed: Computed Tomography & Magnetic Resonance Imaging of the Whole Body, ed 3, vol 2. St Louis, 1994, Mosby. 12. Mitchell DG, et al: Femoral head avascular necrosis: correlation with MR imaging, radiographic staging, radionuclide imaging, and clinical findings. Radiology 162:709, 1987. 13. Roberts R: Radiographs presented as part of the 1992 A.C.V.R. oral certification examination: musculoskeletal section. Vet Radiol & Ultrasound 34:185, 1993. 14. Woodard JC, Riser WH, et al: Erosive polyarthritis in two Greyhounds. J Am Vet Med Assoc 198:873, 1991. 15. Applewhite AA, Page RL: What is your diagnosis? J Am Vet Med Assoc 214:29, 1999. 16. DeHaan JJ, Anderson CB: Calcium crystal-associated arthropathy (pseudogout) in a dog. J Am Vet Med Assoc 200:943, 1992. 17. Gibson JP, Roenigk WJ: Pseudogout in a dog. J Am Vet Med Assoc 161:912, 1972. 18. Heimann M, Carpenter JL, Halverson PB: Calcium pyrophosphate deposition (chondrocalcinosis) in a dog. Vet Pathol 27:122, 1990. 19. Doige CE, Farrow CS, Gee BR: Astorage-like disease with skeletal involvement in a dog. Vet Rad 21:98, 1980.

C h a p t e r

4

Extremital Infection

❚❚❚ TERMINOLOGY Periostitis In the context of sepsis, periostitis refers to a primary or secondary surface infection, as indicated radiographically by the presence of periosteal new bone. Obviously, if there is an infection of the bone surface, it will necessarily come into contact with both the periosteum and the underlying cortical surface.

Osteitis Strictly speaking, osteitis involves the cortex of the bone but not the medulla. These infections are almost certain to involve the associated periosteum as well. Unchecked, osteitis may extend into the adjacent medullary cavity, erupt into a nearby joint or surrounding muscle, or kill and detach portions of the infected cortex—creating sequestra.

Osteomyelitis An infection that extends from the exterior to the interior surfaces of a bone is termed osteomyelitis. These infections are the result of one or more bacterial populations actively replicating within the substance of the bone.

Routes of Infection Local. Localized bone infections are usually the result of penetrating wounds, which carry to the bone surface, depositing one or more kinds of bacteria. In most cases, one bacterium outgrows the rest, eventually eradicating its competitors. Bite wounds are the most common form of localized bone infection. Somewhat surprisingly, there are relatively few true bone infections (bacteria replicating within the bone) caused by K-E pins, although there may be drainage and symmetric bone loss immediately surrounding one or more of the pins. 106

Less often, localized bone infections begin in the epiphyses or metaphyses of puppies, the result of a septicemia. In some instances, only a single lesion is present, whereas in others, two or more bones are affected. Because many of these lesions are intraarticular, they may cause a secondary septic arthritis. Regional. Regional infections are often initiated deep in the soft tissues, and like localized infections, are usually the result of penetrating wounds and deep lacerations. But unlike most localized infections, this form of sepsis rarely results in direct bacterial colonization of the bone. Rather, the nearby bone is stimulated by a combination of metabolic byproducts from the bacteria and the resultant host response. An exception to this is the surgical infection, which usually begins in the bones that are being manipulated. Disseminated. Disseminated infections may extend along either the exterior or interior surfaces of the bone, with the former being most common. Under the influence of gravity, most of these infections are inclined to spread gradually into the distal portion of the affected limb. If severe enough, some of these infections may resemble bone tumors, to include the development of an insufficiency fracture.

❚❚❚ METHODS AND SENSITIVITY OF IMAGING BONE INFECTIONS Radiology Most bone infections are associated with a known or suspected injury. They generally begin small and gradually enlarge if untreated. Drainage is common, but sequestration is rare compared with horses and cattle. Nonscreen film, owing to the greater detail it provides, will often reveal subtle lesions that are not apparent using screen film. Diagnostically, infections require differentiation from bone tumors, especially

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those unassociated with a known injury. This distinction can be more difficult than generally appreciated, especially in the case of small lesions. The speed at which a lesion enlarges and the rate at which bone is produced or destroyed are generally believed to be reliable means of distinguishing benign from malignant lesions. Tumor development outpaces that of infection; however, exceptions are regularly encountered.

Nuclear Imaging Bone scans are performed with either 99mTc-labeled polyphosphate or diphosphonate, compounds referred to as radiopharmaceuticals. Once injected into the body, these gamma-ray emitters congregate in the vasculature of bones, where they can be detected using a gamma camera and displayed as differences in gray scale: black representing hyperemia (typifying infection-inflammation), white indicative of avascularity, (in a sequestrum for example), and gray indicating a normal blood supply. In the case of osteomyelitis, bone scans are useful in determining the presence and extent of an infection at a known site, the existence of a sequestrum, and whether other bones are also infected.1 However, the entire radioactive tracer does not go to its intended destination; instead, it is divided between both the normal and abnormal soft tissues.2 Table 4-1 classifies soft tissue uptake as identified in delayed bone scans after administration of 99m Tc-labeled polyphosphate or diphosphonate.

Figure 4-1 • Frontal view of cat’s forepaw shows a cuff of new bone surrounding the proximal shaft of the fourth metacarpal bone, the result of osteomyelitis caused by a deep bite wound from another cat.

❚❚❚ RADIOGRAPHIC DISEASE INDICATORS OF BONE INFECTION

❚❚❚ SURGICAL INFECTIONS

The appearance of a bone infection is contingent on its duration; early on there is typically swelling of the overlying soft tissues but little perceptible change in the infected bone. However, as time passes, structural changes gradually become evident, largely in the form of surface new bone deposition and interior destruction. It is these three essential “ingredients”: bone loss, bone addition, and soft tissue swelling—often in different measures—that constitute the radiographic recipe for infection.

❚❚❚ NONSPECIFIC BACTERIAL BONE INFECTIONS Nonspecific bacterial bone infections are the most common form of osteomyelitis encountered in most veterinary clinics and hospitals. Of these, the majority occurs in cats, the result of bite wounds sustained in cat fights (Figures 4-1 to 4-3). Dogs also develop bone infections secondary to bite wounds but tend to develop these types of infections higher in their limbs.

The overall incidence of surgical infection in either private veterinary clinics or university teaching hospitals is unknown as far as I am aware. That said, I do encounter surgical osteomyelitis regularly (although infrequently) in both our own practice and in our referral material. A variety of surgical infections are exemplified in Figures 4-4 to 4-8.

❚❚❚ SOME SPECIFIC TYPES OF BONE INFECTIONS Hepatozoonosis Background. Systemic disease may lead to disseminated bone infection as exemplified by hepatozoonosis. In this tick-borne, protozoal infection, both long and flat bone may be affected. Associated signs of illness include fever, anorexia, lethargy, weight loss, myalgia, stiffness, lymphadenopathy, ocular discharge, and a waxing and waning course. Cases have also been reported from Oklahoma, Louisiana, Alabama, and Georgia.3

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Table 4-1 • TYPES OF RADIOPHARMACEUTICAL SOFT TISSUE UPTAKE Type of Soft Tissue Uptake

Examples

Physiologic Renal/bladder Mammary gland Uterus (during pregnancy) Normal calcification of cartilage Pathologic Heterotopic bone formation

Myositis ossificans Fibrodysplasia ossificans

Soft Tissue Calcification Metastatic Dystrophic

Idiopathic

Hyperparathyroidism Myocardial, pulmonary, vascular, or gastric mucosal calcification secondary to uremia Hypercalcemia (e.g., secondary to lymphosarcoma) Chronic inflammation Hyperadrenocorticism Parasitic calcification Primary tumor (not bony, e.g., chondrosarcoma, carcinoma) Primary soft tissue osteosarcoma Metastatic soft tissue osteosarcoma Calcified hematoma Infarct (e.g., myocardial) Fat necrosis Tumoral calcinosis Alveolar microlithiasis Nodular fat necrosis14

Urinary Tract Abnormalities Space-occupying renal lesions (e.g., cyst, infarct) Hydronephrosis, hydroureter Ruptured ureter or bladder Other Noncalcified Soft Tissue Lesions Dehydration Edema Various noncalcified soft tissue tumors (e.g., renal carcinoma) Therapeutically irradiated tissues Liver, spleen, or kidney uptake after chemotherapy Acute muscle injuries Myositis Muscle infarction or necrosis Strain, sprain Amyloidosis Artifacts Urine contamination Perivascular injection of radiopharmaceutical Lymph node uptake after perivascular injection Accidental intraarterial injection of radiopharmaceutical Thyroid, salivary, and gastric uptake due to free pertechnetate Diffuse whole body “activity” due to free pertechnetate Recent intravenous or intraarterial injection site (unrelated to radiopharmaceutical injection) Intramuscular injection site Diffuse liver or spleen uptake due to recent injection of sulfur colloid Modified from Lamb CR: Non-skeletal distribution of bone-seeking radiopharmaceuticals. Vet Rad 31:246, 1990.

A

B

Figure 4-2 • Lateral (A) and ultra close-up (B) views of the proximal radial diaphysis of a cat show a layer of recently formed new bone along the face of the radius, overlain by a large area of swollen soft tissue. In the context of multiple infected bite wounds, this finding indicates a secondary periostitis.

Figure 4-3 • Lateral view of the antibrachium of a cat shows an acute periosteal reaction extending the length of the radius (see emphasis zone for best view).

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B A

C

D

Figure 4-4 • A, Close-up lateral view of a freshly avulsed tibial tuberosity, in which associated hemorrhage has erased most of the normal facial planes. B, In the frontal view the displaced accessory growth center is seen superimposed on the lateral side of the proximal tibia growth plate. Postoperative films (C, D) reveal indications of infection including: (1) multiple areas of lysis in the tibial tuberosity, (2) new bone deposition unrelated to callus formation, and (3) localized extraarticular swelling.

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B

A

Figure 4-5 • A, Immediate postoperative frontal oblique view of badly fractured humerus. B, Three-week progress film shows abnormal lysis and nonpurposeful bone deposition indicative of infection, most likely surgical in origin.

Imaging Findings. Based for the most part on cases reported from Texas, Hepatozoon canis produces large, broad-based mounds of new bone on the exterior surfaces the pelvis, spine, femur, tibia, fibula, humerus, radius, and ulna.

Coccidioidomycosis Background. One in six dogs with pulmonary coccidioidomycosis subsequently develops osteomyelitis, usually in one or more limb bones. Most dogs with skeletal lesions appear lame. Imaging Findings. Characteristic bone lesions are mostly productive, in some instances, so productive that underlying cortical destruction is not recognizable. The presence of multiple, small spherical lucencies in the bone has been reported useful in differentiating coccidioidomycosis from tumors and other forms of osteomyelitis.4 In some instances (presumably chronic), the organism colonizes most of a long bone, causing it to assume a bizarre, bloated appearance, featuring a latticelike medulla5 (Figure 4-9).

Occasionally, mycotic osteomyelitis (particularly coccidioidomycosis and blastomycosis) closely resembles a primary bone tumor when initially diagnosed because it is in the metaphysis and features mixed production and destruction, in addition to cortical penetration (Figure 4-10, A). But when observed later, fungal bone infections often produce characteristic cortical bridges over the surface of the lesion, a feature rarely found in bone tumors (Figure 4-10, B).

Blastomycosis Background. Blastomycosis, like coccidioidomycosis, begins as a primary lung infection and may spread to other parts of the body, including the skeleton. In one report, two thirds of the dogs with the bony form of the disease had only a single lesion, whereas the minority had multiple bone infections—some as many as eight or nine. Imaging Findings. Roberts has reported that osteomyelitis caused by blastomycosis typically produces regional or locally destructive lesions in the ends of lung bones. Most are highly destructive and in some

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A

B

Figure 4-6 • A, Full-length lateral view of a dog’s femur fractured 6 days earlier. B, Six-week progress film after open surgical reduction shows severe, widespread bone destruction consistent with osteomyelitis.

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A

B D C Figure 4-7 • Lateral (A) and frontal (B) views of a displaced, short oblique, proximal femoral shaft fracture in an immature dog recently hit by a car. A 3-week progress film shows fragment and implant dislocation (C), whereas an 8-week close-up view (D) shows a nonunion, which appears infected based on the presence of a thick layer of new bone covering all visible bone surfaces.

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Figure 4-8 • Lateral sinogram shows contrast solution within the cubital joint, around the circlage wires, and at both ends of the pin, indicating infection.

A

B

Figure 4-9 • Close-up frontal (A) and lateral oblique (B) views of the proximal tibia/fibula show a mixed productive-destructive, partially expansile lesion involving the proximal thirds of the tibia and fibula. Also note the gradual, almost imperceptible change from abnormal to normal bone density. Although a long zone of transition is usually an indicator of malignancy, it wasn’t in this instance (coccidioidomycosis).

A

B

Figure 4-10 • A, Close-up lateral view of the proximal humeral metaphysis of a dog shows a large mixed productive-destructive lesion caudally. B, Similar projection made 1 month later shows cortical destruction and a distinctive cortical bridge, the result of coccidioidomycosis.

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A

Figure 4-12 • Close-up view of the distal half of the radius shows a mixed productive-destructive lesion occupying much of the distal shaft (but not the epiphysis or metaphysis) resembling a secondary bone tumor. Cortical bridging, however, suggests fungal infection, which turned out to be the case (blastomycosis).

B Figure 4-11 • Close-up (A) and ultra close (B) views of the proximal femur of a dog infected with blastomycosis show freshly deposited new bone (emphasis zone).

cases resemble primary bone tumors with respect to their aggressiveness. Flat bones such as the ischium are similarly affected, as are irregular bones like the talus and dorsal processes of the spine.6 Some reports of skeletal blastomycosis describe rather subtle changes, which in some ways resemble

previous injury: periarticular swelling, smoothsurfaced, extraarticular bone deposition, and faint bone loss.7 In contrast to the foregoing descriptions, many of the animals with skeletal blastomycosis imaged at our hospital initially show faint, somewhat ragged, layers of diaphyseal new bone without evidence of underlying cortical destruction (Figure 4-11, A, B). Some lesions are entirely diaphyseal and feature cortical bridging (Figure 4-12). Usually within 1 to 2 weeks, the appearance of the infected bone changes, showing multiple areas of cortical and medullary destruction, and a further build up of surface new bone (Figure 4-13).

Histoplasmosis Background. Typical of systemic fungal infections, the Histoplasma spores are initially inhaled, phagocytized

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Figure 4-13 • Dog shown in Figure 4-11, now worse. Progress film made only 8 days later shows a substantial increase in bone deposition, which is now accompanied by bone destruction.

by alveolar macrophages where they change into yeast, and then borne to other parts of the body (but rarely to the skeleton) by the blood and lymph. Imaging Findings. Aronson and co-workers have reported destructive, bilateral metaphyseal lesions in the radius and ulna of a cat with systemic histoplasmosis (as well as feline lymphosarcoma). The lesions resembled a severe case of metaphyseal osteopathy.8

Figure 4-14 • Close-up lateral view of the elbow and upper halves of the radius and ulna exhibits a uniformly moth-eaten appearance with fractures of both the anconeal and medial coronoid processes. Although the aggressive appearance of the lesions suggested cancer, this proved to be a fungal osteomyelitis.

Phialemonium obvatum Fungal osteomyelitis is often characterized as permeative in nature, creating deep corticomedullary lesions. However, there are exceptions. Phialemonium obvatum lesions have been shown to initially affect the exterior of the bone, causing smooth, broad-based, predominantly transparent lesions, closely resembling a severe subperiosteal hematoma.9

❚❚❚ CONSEQUENCES OF BONE INFECTIONS Pathologic Fracture The vast majority of pathologic limb fractures in dogs are caused by primary osteosarcomas (93 percent). Occasionally, bone infections become so destructive that the bone fractures. Because osteomyelitis is usually caused by the extension of soft tissue infection or open fracture reduction, when pathologic fractures occur, there appears to be little doubt about their cause. However, cancer is incorrectly assumed when the incit-

ing infection is blood-borne, an etiology that is rarely considered under such circumstances, particularly when there are obvious radiographic abnormalities in the fractured bone (Figure 4-14).10 Interlocking intramedullary pins (pins held in position by multiple screws) have been reported as an effective means of stabilizing a surgically infected femoral fracture.11

Chronicity Some bone infections, especially those caused by socalled super bugs that are often found in large hospitals, staunchly resist both medical and surgical treatment. Lingering infections of this sort, especially those whose progress has been somewhat impeded by ineffective treatment, often produce a distinctive form of new bone that resembles ocean coral (Figure 4-15). Unfortunately, coralization is not unique to chronic osteomyelitis. It has also been found in some slow-

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A

Figure 4-15 • Defleshed bone specimen (tibia, with attached surgical implants) taken from a dog with a chronic surgical osteomyelitis exhibiting marked coralization proximally.

growing primary and secondary bone tumors, as well as in fungal infections such as coccidioidomycosis. Figures 4-16 to 4-19 exemplify these types of infections.

❚❚❚ SEPTIC ARTHRITIS LEADING TO INTRAARTICULAR BONE INFECTIONS Bite wounds that puncture the joint capsule have the potential to infect the bones within, but because carpal and tarsal bones lack an inner layer of osteogenic periosteum, the development of characteristic radiographic indicators of bone infection is delayed, often for as much as 3 to 4 weeks. When signs do develop, they are usually first seen away from articular surfaces. Because of their avascular cartilage coverings, articular surfaces are capable of resisting bacterial encroachment longer than the adjacent unprotected bone. Porcupine quills imbedded in the carpus or other joints may break when being extracted, leaving intraarticular fragments behind that often cause an abscess. Occasional plant awns find their way into joints with similar consequences.

B Figure 4-16 • Frontal (A) and lateral (B) views of the proximal femur of a cat show signs consistent with either tumor or infection, which in this instance proved to be a malignancy.

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A

Figure 4-17 • Lateral view of the humerus shows full-length cloak of mature new bone indicative of chronic infection.

Intraarticular surgery, such as reconstruction of the genual joint, may also result in chronic septic arthritis and osteomyelitis (Figure 4-20).

❚❚❚ DIFFERENTIATING INFECTION FROM CANCER Generally, it is not difficult to distinguish osteomyelitis from bone cancer, especially in advanced stages. Subacute or chronic infection is usually more localized in nature and tends to be walled off (or at least relatively delimited) by surrounding new bone. Mature bone tumors, on the other hand, are more wide-ranging and usually quite destructive. Recent tumor growth and acute infection may share a number of characteristics such as subtle medullary bone loss, cortical bone formation, and soft tissue swelling. Occasionally, chronic osteomyelitis and longstanding bone tumors may resemble one another, with bone biopsy doing little or nothing to resolve the etiologic issue. Even the formation of sequestra, long

B Figure 4-18 • A, Close-up lateral stifle immediately before surgery for a third-degree sprain of the cranial cruciate ligament. B, Progress check of the same joint shows massive subchondral destruction as a result of a surgical infection.

believed to be the hallmark of chronic infection, can sometimes occur with bone cancer.12 Occasionally, a primary bone tumor may be mistaken for osteomyelitis, especially if it is atypically situated and grows slowly. For example, Rendano and co-workers described an osteosarcoma in the radial midshaft of a dog that initially resembled osteomyelitis, being characterized by a small area of localized bone loss surrounded by a thick cuff of mature-appearing new bone. It was not until 6

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Figure 4-19 • Close-up frontal (A) and lateral (B) views of the distal halves of the radius and ulna show multiple blocks of chronic appearing new bone arrayed along the edges of a coarsely thickened cortex. The distorted medulla contains numerous variably sized cavities interspersed among mounds of disorganized bone deposits. Chronic osteomyelitis.

Figure 4-20 • Close-up lateral view of the humeral midshaft shows a medium-sized defect in the cranial cortex associated with a pair of overgrown wire loops. A sterile abscess was found at surgery.

months later that the lesion began to reveal its true malignant nature as indicated by extensive cortical destruction.13 Some forms of osteoarthritis can also be mistaken for primary bone tumors. This is particularly true of long-standing osteochondritis of the elbow, in which associated new bone may extend well up into the humerus. The presence of a similar-appearing lesion in the opposite elbow is compatible with most forms of osteochondritis but inconsistent with a malignant bone tumor.

❚❚❚ ABSCESSES Bone abscesses are rare in animals, with most being sterile and often associated with surgical implants (see Figure 4-20). Many such lesions closely resemble localized bone loss caused by repetitive implant movement (RIM). Deep muscle abscesses may consist of a single cavity or multiple communicating cavities. Sinography is the optimal means of visualizing complex lesions, especially for surgical planning (Figures 4-21 and 4-22).

Figure 4-21 • Deep paraischial abscess: sinogram shows a mediumsized, rectangle-shaped abscess with multiple communicating cavities dorsally. The spherical lucency is the air-filled catheter cuff.

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Figure 4-22 • Sonogram of the lateral thigh region of a dog shows an abscess (oval-shaped area of decreased echogenicity in the far central field) resulting from a recent bite wound.

References 1. Gibson KL, van Ee RT, Watters J: Radiographic diagnosis. J Am Vet Med Assoc 28:231, 1987. 2. Lamb CR: Non-skeletal distribution of bone-seeking radiopharmaceuticals. Vet Rad 31:246, 1990.

3. Macintire DK, Vincent-Johnson N, et al: Hepatozoonosis in dogs: 22 cases (1989-1994). J Am Vet Med Assoc 210:916, 1997. 4. Millman TM, O’Brien TR, Suter PF, et al: Coccidioidomycosis in the dog: its radiographic diagnosis. J Am Vet Rad Soc 20:50, 1979. 5. Ackerman N, Owens J, Ticer J: Polyostotic Coccidioidomycosis in a dog. Vet Rad 22:83, 1981. 6. Roberts RE: Osteomyelitis associated with disseminated Blastomycosis in nine dogs. Vet Rad 20:124, 1979. 7. Widmer WR, Downing S: Radiographs presented as part of the 1995 ACVR oral certification examination, musculoskeletal section. Vet Radiol & Ultrasound 37:110, 1996. 8. Aronson E, Bendickson JC, et al: Desseminated Histoplasmosis with osseous lesions in a cat with feline lymphosarcoma. Vet Rad 27:50, 1986. 9. Smith AN, Spencer JA, et al: Disseminated infection with Phialemonium obovatum in a German Shepherd. J Am Vet Med Assoc 216:708, 2000. 10. Emmerson TD, Pead MJ: Pathological fracture of the femur secondary to hematogenous osteomyelitis in a Weimaraner. J Small Anim Pract 40:233, 1999. 11. Muir P, Johnson KA: Interlocking intramedullary nail stabilization of a femoral fracture in a dog with osteomyelitis. J Am Vet Med Assoc 209:1262, 1996. 12. Ackerman N, Halliwell WH, et al: Bone infection and sequestrum formation in a canine osteosarcoma. J Am Vet Rad Soc 16:3, 1975. 13. Rendano VT, Car B, Gilman M: Osteosarcoma in the middiaphysis of the radius in the dog. Vet Rad 28:127, 1987.

C h a p t e r

5

Extremital Bone Tumors

Metastatic bone tumors are relatively uncommon in dogs and cats compared with primary bone cancer— a frequency that is just the opposite in people. Soft tissue limb tumors are also comparatively rare. Radiology is, and in all likelihood will remain for the foreseeable future, the principal means of imaging bone tumors in pet animals. Obviously, there are far more sophisticated imaging methods available, such as computed tomography (CT), magnetic resonance imaging (MRI), and nuclear imaging, but these technologies are comparatively expensive, and as a consequence, tend to be used more sparingly. Although not employed routinely, ultrasound can be helpful in evaluating bone tumors, which have a juxtacortical soft tissue component. This is especially true of deeply situated tumors, such as those of the hip.1 Samii described using ultrasonography to assist in obtaining fine-needle aspirates of bone lesions in dogs and cats, primarily tumors.2

❚❚❚ BENIGN BONE TUMORS Background Excluding solitary and multiple hereditary exostoses (bone growths more accurately termed tumor-like lesions), benign bone tumors rarely occur in dogs and cats. Of these, the osteochondroma and enchondroma are most common.

Osteochondroma Osteochondroma in dogs is a benign, relatively rare tumor. Although it often closely resembles the lesions seen in multiple exostoses, it is an acquired, not a hereditary neoplasm. Radiographically, solitary osteochondromas are characterized by (1) expansion, (2) smooth margination, (3) lack of a discrete cortex in the region of primary tumor growth, and (4) interior trabeculation—often of a disorganized nature.3

Enchondroma Enchondroma is most often found in the feet of dogs, usually the metacarpals and metatarsals. These tumors typically expand the bone, thinning the cortex in the process. Although a pathologic fracture is certainly possible under such circumstances (as it is with any expansile lesion), I have yet to encounter one.

❚❚❚ MALIGNANT BONE TUMORS Primary Bone Tumors Background. Primary bone tumors almost always begin in the metaphyses of long bones. In the intermediate and advanced stages of their development, these tumors, for the most part osteosarcomas (estimated 85 percent of all canine primary bone tumors), begin by destroying a portion of the medulla and then attack the adjacent cortex. Once the cortex is breached, the tumor is then able to gain access to the surrounding soft tissues. Combined tumor and host bone often produce a dense calcific cloud surrounding the lesion, tending to underplay its severity. The more destructive the tumor becomes, the more likely the bone is to fracture. Occasionally, primary bone tumors originate in the shafts of long bones, rather than in the metaphyses, thus resembling secondary or metastatic bone tumors, or to a lesser extent, parosteal sarcomas.4 Most primary bone tumors occur in middle-aged and old dogs, but they occasionally develop in skeletally immature dogs.5 A majority of veterinarians believe that negative chest films of dogs with proven or suspected osteosarcoma do not eliminate the possibility of metastases. This belief stems from authoritative statements by experts that micrometastases (very small lung nodules, which are not detectable radiographically) almost always exist by the time a skeletal osteosarcoma is diagnosed, a viewpoint for which there is some support.6 121

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Table 5-1 • CLASSIFICATION OF PRIMARY BONE TUMORS Type of Bone Tumor

Classification

Cartilaginous Bone Tumors Benign

Malignant

Osteochondroma (hereditary exostosis: single and multiple) Chondroma (enchondroma) Parosteal chondroma (juxtacortical chondroma) Chondroblastoma Chondromyxoid fibroma Chondrosarcoma—primary or secondary

Osseous Bone Tumors Benign Malignant

Osteoma Osteoid osteoma Osteoblastoma Osteosarcoma Parosteal osteosarcoma (juxtacortical osteosarcoma) Periosteal osteosarcoma

Fibrous Bone Tumors Benign Malignant

Nonossifying fibroma Ossifying fibroma Fibrosarcoma Malignant fibrous histiocytoma

Fatty Bone Tumors Benign Malignant

Lipoma Liposarcoma

Modified from Juhl JH: Paul & Juhl’s essentials of roentgen interpretation, ed 4. Philadelphia, 1981, Haper & Row, p. 198.

Turrel and Pool reported on a small group of cats with primary bone tumors and concurrently reviewed the relevant literature.7 Juhl classified primary bone tumors as shown in Table 5-1.

Figure 5-1 • Close-up frontal view of a defleshed radius largely replaced by an osteosarcoma shows extensive coralization and large cortical breach—pathologic features shared with chronic osteomyelitis.

Osteosarcoma Background. Osteosarcoma is by far the most common type of primary bone tumor, typically developing in large and giant breed dogs at both ends of the age spectrum (1 to 2 years, and 7 years or older). The most common sites in the forelimb are the proximal humerus, distal radius, and distal ulna, and in the hindlimb, the distal femur and proximal tibia. Metastasis can be by either the blood or lymph systems, usually spreading first to the lung; although only about 10 percent of dogs show radiographic indications of pulmonary disease at the time the primary tumor is diagnosed. If the affected limb is amputated, and there is no chemotherapy, radiographically demonstrable pulmonary metastasis is likely to develop within 18 weeks. Occasionally, pulmonary metastasis causes hypertrophic pulmonary osteoarthropathy (HPOA), which is also known as hypertrophic osteopathy. The resultant metaphyseal inflammation typically produces severe quadrilateral lameness.8

Occasionally, osteosarcomas spread to unusual locations, as described by Daniel, who reported the scintigraphic detection of widespread subcutaneous metastases (from a distal radial osteosarcoma) that were not noted on either physical or radiographic evaluations conducted at the time of admission.9 Imaging Findings. Not all primary bone tumors look the same. Some are entirely destructive, others primarily productive. Most, however, exhibit some of both qualities, although usually not in equal measure. The following tendencies are shared by a majority of primary canine bone tumors, and thus are diagnostically useful: • • • •

Primarily destructive (“aggressiveness”) Appears to originate in the medulla Reduces and/or penetrates cortex Permeative (tumor penetrates the cortex and grows into surrounding soft tissue) • Exhibits coralization in advanced stages (Figure 5-1)

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B

A

Figure 5-2 • A, Close-up lateral view of the proximal humerus shows diffuse destruction characteristic of a primary bone tumor (osteosarcoma). B, Close-up lateral view of the proximal humerus shows a vague area of destruction in the greater tubercle. Broken strands of tumor bone can be seen extending deep into the adjacent muscle.

• Hard to distinguish precisely where tumor ends and normal bone begins (long zone of transition) • Rapid progression

A variety of primary bone tumors are exemplified in Figures 5-2 to 5-12.

Although most primary bone tumors begin in the central metaphysis, some do not, particularly in the proximal humerus where many osteosarcomas are eccentrically positioned (at least initially). In this respect, Carrig described an unusually well-circumscribed, half-moon–shaped osteosarcoma invading the lateral aspect of the proximal tibial metaphysis.10

Secondary (Metastatic) Bone Tumors

Chondrosarcoma Background. Although chondrosarcoma is the second most common skeletal tumor in dogs, it remains rare compared to osteosarcoma. Only one in four osteochondromas affect the limbs and even fewer involve long bones (14 percent). Chondrosarcomas show a clear preference for the flat bones: pelvis, scapulae, and ribs. Metastasis occurs about 20 percent of the time, initially to regional lymph nodes and then the lung.11 Imaging Findings. No single characteristic appearance exists. However, there is a tendency to large, billowy, centrally destructive lesions. Alternatively, the affected bone may simply disappear, seemingly amputated, leaving behind only a few small wispy densities.

Background. Secondary bone tumors exhibit a decided preference for the shafts (rather than the ends) of long bones, and in this way can often be distinguished from primary tumors. Unlike primary tumors, secondary bone tumors often develop in two or more bones simultaneously (polyostotic development), a trait that provides an additional distinguishing factor between primary and secondary bone cancers.12 The primary metastatic sites for canine osteosarcomas are the lung and skeleton. Less frequent sites of spreading include the liver, spleen, regional lymph nodes, kidney, heart, and amputation area. Bone scans are reported to be more sensitive than radiographic surveys in detecting skeletal metastasis.13 Walker and co-workers reported widespread skeletal metastasis from a plasma cell tumor, with ischial and femoral lesions appearing as small- to mediumsized lucencies. Atypically, one of the femoral lesions involved the distal metaphysis as well as the proximal diaphysis.14

Imaging Findings Fibrosarcoma. Fibrosarcomas are often intensely destructive, although like osteosarcomas and chondrosarcomas, they are capable of producing tumor bone in the surrounding soft tissues.

Radiology. Metastatic bone tumors share most of the radiographic features of primary bone tumors: centralized location, extensive medullary and cortical

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Figure 5-4 • Lateral view of the scapula shows a mixed productive-destructive lesion in the proximal blade (osteosarcoma) superimposed on the dorsal spinous processes.

destruction, and rapid progression. Occasionally, an undiagnosed secondary bone tumor will fracture, be conventionally repaired, and then be treated as a surgical infection as the tumor continues to grow. Figures 5-13 to 5-17 exemplify the radiographic features of a variety of secondary bone tumors.

A

Radionuclide Imaging. Radionuclide imaging is the best method of searching for skeletal metastases. Positive bone scans typically appear as variably shaped, dark areas, superimposed on a relatively light background. The dark areas clinically referred to as “hot spots” represent above average accumulations of an intravenously administered radiopharmaceutical (also termed areas of increased or intense uptake). Forrest and Thrall showed that radionuclide imaging is capable of detecting subclinical skeletal metastasis in dogs with osteosarcoma. Based on their findings, the authors advocate the use of nuclear medicine in such cases, claiming that it will potentially improve the effectiveness of treatment.15 Lamb and co-workers described the uptake of 99m Tc-MDP by regional lymph nodes during bone scans. They contend that if no perivascular loss of radiopharmaceutical has occurred, and if the identified lymph node drains a region containing a tumor, metastasis should be considered as a possible cause.16 B Figure 5-3 • Close-up lateral (A) and frontal (B) views of the shoulder joint show a subtle mixed lesion in the caudodistal aspect of the scapula, which turned out to be a chondrosarcoma. Caution: this part of the scapula, proximal to the infraglenoid tubercle and adjacent to the attachment of the teres minor, normally appears roughened and relatively decreased in density compared with the surrounding scapula.

Joint Tumors Synovial Sarcoma Background. Synovial sarcoma (also termed malignant synovioma) is the most commonly reported articular tumor in small animals. These tumors typically affect the larger joints in middle-aged and older dogs, only occasionally occurring in younger dogs. Thus acknowledged, it is important to realize that joint tumors, of this or any other cell type, are rarities, with many small animal veterinarians never having encountered one. Imaging Findings. Reported radiographic features are variable and include bone destruction-production and Text continued on p. 130

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A

B

C

D

125

Figure 5-5 • Close-up lateral (A) and frontal (B) views of the distal humerus show extensive bone destruction compatible with a primary bone tumor. The normal opposite elbow is included for comparison (C,D).

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A

B

Figure 5-6 • Lateral (A) and frontal (B) close-ups of distal tibia of a young adult Irish Wolfhound with an osteosarcoma.

A

B

Figure 5-7 • Close-up lateral oblique (A) and frontal (B) views of the distal aspect of the third metacarpal bone show a marked elevation of the periosteum in the lateral view and expansion in the frontal plane, the result of an osteosarcoma.

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B

Figure 5-8 • Lateral (A) and close-up lateral (B) views of the shoulder show destruction of a large part of the cranial aspect of the proximal humerus strongly suggesting a primary bone tumor (fibrosarcoma).

A

B Figure 5-9 • Ventrodorsal orientation view (A) of the pelvis and close-up view (B) of the right ischium show partial destruction strongly suggesting a bone tumor (chondrosarcoma).

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Figure 5-10 • Lateral close-up view of distal femur and stifle, previously fractured and surgically repaired, now appears infected. Biopsy showed osteosarcoma.

A Figure 5-11 • A, Close-up lateral view of the distal femur shows a relatively well-circumscribed area of metaphyseal bone destruction. Biopsy diagnosis was osteosarcoma, illustrating that not all primary bone tumors have long transition zones. B, The normal opposite distal femur is provided for comparison.

B

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B

Figure 5-12 • Lateral orientation (A) and close-up (B) views of cancerous ulna in a dog that is so destructive it appears at first glance that the distal part of the bone has been amputated.

Figure 5-13 • Close-up lateral view of the distal humeral shaft shows both interior and exterior bone deposition consistent with a secondary bone tumor (thyroid carcinoma).

Figure 5-14 • Close-up view of the stifle shows a mixed productive-destructive lesion centered on the distal femoral epiphysis, but also extending into the contiguous metaphysis. Faint areas of bone loss are also visible in the proximal tibial diaphysis. Biopsy showed metastatic fibrosarcoma in both sites.

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A

B

Figure 5-15 • Long lateral (A) and frontal (B) views of an undifferentiated metastatic sarcoma show near total envelopment of the tibia and fibula by the tumor, featuring a spectacular sunburst pattern.

joint swelling (Figure 5-18). Lameness is usually more pronounced than with posttraumatic osteoarthritis, but not as severe as with infection. Most synovial tumors develop slowly, and thus progress films should be spaced at longer intervals than in faster growing cancers such as osteosarcoma; (e.g., every 2 or 3 months rather than monthly). A recently reported case in the carpus of a cat was associated with new bone on the ulnar and accessory carpal bones and carpal swelling. In reviewing the literature, the author found only four other feline cases.17 The radiographic features of a primary synovial osteosarcoma18 and a synovial myxoma19 have been described in individual dogs, with the latter report also including sonographic and magnetographic images.

Metastatic Melanoma. A metastatic melanoma has been reported in the central tarsal bone of a dog, causing massive destruction. Metastatic melanoma has also been described in the elbow joint of a dog, destroying portions of the distal humerus and adjacent ulna.20

Other Tumors Parosteal Sarcoma Background. Parosteal sarcoma (also termed parosteal osteosarcoma and juxtacortical osteosarcoma) is a malignant bone-producing tumor of the periosteum. Parosteal sarcomas are uncommon malignancies that differ from other types of primary bone tumor by

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Figure 5-16 • Close-up of a proximal humerus shows a fresh pathologic fracture, as evidenced by a large but subtle area of bone loss and a patch of new bone. This was a metastatic carcinoma.

beginning on the exterior surface of the bone rather than in the interior. Typically, the underlying cortex is spared. However, there sometimes may be superficial involvement late in the course in the disease. Long bones, skull, and ribs are the usual sites of development, whereas spinal involvement is quite rare.21 Imaging Findings. The appearance of this uncommon tumor is quite variable, ranging from spectacular cortical cloaking, which all but obscures the underlying bone, to destructive-productive lesions involving much of the diaphysis. Occasionally, parosteal sarcomas may be eccentrically positioned at the end of the bone.22 Some parosteal osteosarcomas show seemingly normal bone surrounded by wispy strands of soft tissue calcification.23 Primary Hemangiosarcoma. Primary bone hemangiosarcomas are described as being rare. In one report of such a lesion, the authors asserted that arteriography was necessary for them to differentiate the described tumor from osteomyelitis. The included arteriograms showed extreme vascular distortion, said to be characteristic of malignancy.24

Figure 5-17 • Lateral view of the proximal two thirds of a barely recognizable humeral shaft shows massive bone destruction with a shaggy overlay of new bone, the result of multiple metastases (so-called skip metastases).

❚❚❚ CHARACTERIZATION AND DIFFERENTIATION OF DIGITAL TUMORS AND INFECTIONS The following facts regarding tumors and inflammation of the canine paw come from the work of Voges and co-workers25: • The incidence of tumors or inflammation is about the same in all feet. • The digits are more likely to be affected than either the metacarpus or the metatarsus. • As a generality, multiple lesions involving the toes are more apt to be inflammatory than neoplastic, but multiple tumors can occur. • Fore and hind paw tumors occur with about the same frequency as inflammatory lesions. • Tumors of the paw and toes are more likely to be malignant than benign.

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A

B

C

D Figure 5-18 • Close-up lateral (A) and frontal (B) views of the carpus of a dog with synovial sarcoma show destruction of the articular surface of the accessory carpal bone, swelling, and regional osteopenia. The normal opposite carpus is provided for comparison (C, D).

• Squamous cell carcinomas are the most common malignant tumor found in the feet of dogs. • Mast cell tumors and melanomas follow carcinomas in frequency of occurrence. • Soft tissue swelling is a feature of both tumors and inflammation, and thus does not distinguish one from the other. • Some tumors and tumorlike lesions are characteristically unassociated with bone involvement: mast cell tumor, hemangiopericytoma, plasmacytoma, fibrosarcoma, sebaceous gland adenocarci-

noma, histiocytoma, papilloma, and tumoral calcinosis. • The odds of a digital tumor or inflammation being associated with bone loss or addition (destruction or proliferation) are about even (52 percent). • There is a tendency for inflammatory lesions to be productive and cancers to be destructive. • Squamous cell carcinomas exhibit two distinct patterns: (1) distal phalangeal destruction, and (2) new bone deposition combined with overlying soft tissue swelling.

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Table 5-2 • BONE CYSTS Bone Cyst Type

Physical Features

Geographic Features

Etiology

Aneurysmal bone cyst

Large, lytic, expansive lesion, which can resemble a primary bone tumor

Located in the metaphysis or proximal part of the epiphysis of long bones

Theorized to develop secondary to a variety of vascular injuries induced by (1) trauma, (2) benign and malignant bone tumors, (3) tumorlike lesions such as fibrous dysplasia, and (4) unicameral or multicameral bone cysts34

Multicameral (complex, multilocular) bone cyst

Lytic, expansive (expansile) lesions, featuring internal compartmentalization May contain fluid and fibrous tissue Small, spherical, and often multiple Lytic, expansive (expansile) lesions that are often fluid-filled

Located in the metaphysis of long bones

Subchondral bone cyst Unicameral (simple, unilocular) bone cyst

Located within subchondral bone Located in the metaphysis, and less commonly, the shaft of long bones; in dogs, the distal radius is most commonly involved36

• Although it is not possible to predictably distinguish between benign and malignant lesions of the foot and toes, malignancy should be strongly considered in the face of a primarily destructive lesion.

❚❚❚ TUMORLIKE BONE LESIONS Bone Cysts Background. The cause (or causes) of bone cysts is uncertain. Many theorists focus on trauma, with subsequent hematoma formation within the developing metaphysis. Bone cysts are inconsistently classified according to a combination of etiologic, physical, and geographic features. Various types of bone cysts are described in the Table 5-2. Although most bone cysts are solitary findings, multiple bone cysts have been reported.26 Imaging Findings. Biery and co-workers provided an excellent pictorial account of solitary bone cysts in dogs.27 Solitary bone cysts are expansive, cystic lesions that are typically found in the metaphysis of long bones. Because they substantially thin the surrounding cortex, and thus greatly weaken the affected bone, cysts are susceptible to fracture—often the first and only indication of their presence. Shortly after fracture, repair begins, which may be mistaken for a malignant or infectious lesion. But with the passage of a few weeks’ time, most fractures heal spontaneously. Alternative explanations for these lesions include: (1) primary bone tumor, (2) enchondroma, (3) bone abscess, (4) fibrous dysplasia, and (5) nonossifying fibroma.

Theorized to form as a result of synovial invagination35

Multiple Exostosis in Cats (Feline Osteochondromatosis) In cats, multiple exostoses can appear malignant, featuring large, billowy, extraarticular lesions with irregular margins, and indistinct underlying cortex suggesting destruction. Unlike dogs, such lesions occur in skeletally mature individuals, and are theorized to be caused by feline leukemia virus (FeLV) infection of the periosteum—thus the resemblance to parosteal sarcoma. Multiple exostoses may occur in a wide variety of locations including long bones near joints, surface of the osseous bullae, hyoid bones, clavicle, spine, and ribs.28

Extraskeletal Chondroma Extraskeletal chondromas are rare in dogs and cats. Similar to parosteal sarcomas, these tumors develop outside the bone with most exhibiting the characteristic features of chondromas: a defined cortex and medulla (Figure 5-19).

Intraosseous Arteriovenous Fistulas Occasionally, puppies are born with skeletal arteriovenous fistulas (AV fistulas), which may locally or regionally cavitate and expand the affected bone. In one published report, the author described an external swelling on the cranial surface of the radius that vibrated synchronously with the heartbeat. Subsequently, angiography showed the swelling to be an AV fistula.29

Intraosseous Epidermoid Cyst Epidermoid cysts (epidermal cysts) are tumorlike lesions that are commonly found in the skin of dogs and occasionally in the skeleton. Although there are few reports of these cysts, what information that is

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A

A

B Figure 5-19 • Close-up lateral (A) and frontal (B) views of the carpus show a large extraskeletal chondroma resembling the patella, which exhibits a dense bony perimeter and a relatively lucent interior, radiographic features common to many chondromas.

B Figure 5-20 • Frontal (A) and lateral (B) close-up views of a

available indicates that most epidermal cysts are primarily lytic and may be mistaken for tumors like nailbed carcinoma.30

❚❚❚ SOFT TISSUE TUMORS THAT INVADE ADJACENT BONE Nailbed Carcinoma (Subungual Carcinoma) Squamous cell carcinoma and malignant melanoma are the most common cancers affecting the nailbed

severely swollen fourth digit show: (1) uneven bone deposition on the exterior surface of the middle phalanx, (2) expansive destruction of the third phalanx, and (3) dislocation of the distal interphalangeal joint. This was a squamous cell carcinoma.

of dogs, accounting for about 35 percent and 25 percent, respectively, of all tumors of the distal phalanx and nail. Dogs with nailbed cancer are most likely to be large (about 75 percent) and black (about 65 percent). Radiographically, extensive bone loss and relatively little new bone characterize these tumors. Skele-

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A

A

B Figure 5-21 • Lateral (A) and frontal (B) close-up views of a massively swollen tarsus in which the bones possess a distinctive moth-eaten appearance, characteristic of ingrowth from an adjacent soft tissue sarcoma.

B Figure 5-22 • A, Lateral close-up view of the distal half of a femur

tal metastasis may occur in the affected leg or in the other limbs, and usually has a combined productivedestructive appearance (Figure 5-20).31 Paronychia and osteomyelitis may also share some of these radiographic features, and thus deserve differential consideration.32

Soft Tissue Sarcoma In their advanced stages, soft tissue sarcomas, which extend into nearby bone, can be difficult to distinguish from primary bone tumors that grow into surround-

shows a gently arching periosteal elevation on the cranial aspect of the diaphysis proximally, and a shaggy periosteal reaction immediately below; soft tissue swelling is extensive. B, Frontal view of a proximal tibia shows a grapefruit-sized mass laterally and the ventral portion of a second mass on the lateral side of the femur. The lesion was an invasive lobulated soft tissue sarcoma.

ing muscle.33 However, in their early period of development, soft tissue tumors are more readily recognized because of their relatively large size and the subtle way they begin to erode the adjacent bony cortex. Figures 5-21 to 5-23 exemplify these tumors.

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Figure 5-23 • Close-up ventrodorsal view of the right hip shows a large, relatively organized bony mass overlying the proximal femur and paralleling the exterior surface of the adjacent ilium.

References 1. Kramer M, Gerwing M, et al: Sonography of the musculoskeletal system in dogs and cats. Vet Radiol & Ultrasound 38:139, 1997. 2. Samii VF, Nyland TG, et al: Ultrasound-guided fineneedle aspiration biopsy of bone lesions: a preliminary report. Vet Radiol & Ultrasound 40:82, 1999. 3. Ackerman N, Halliwell WH, et al: Solitary osteochondroma in a dog. J Am Vet Rad Soc 14(2):13, 1973. 4. Brodey RS, Riser WH: Liposarcoma of bone in a dog. J Am Vet Rad Soc 7:27, 1966. 5. Phillips L, Hager D, et al: Osteosarcoma with a pathologic fracture in a six-month-old dog. Vet Rad 27:18, 1986. 6. Spodnick GJ, Berg J, et al: Prognosis for dogs with appendicular osteosarcoma treated by amputation alone: 162 cases (1978-1988). J Am Vet Med Assoc 200:995, 1992. 7. Turrel JM, Pool RR: Primary bone tumors in the cat. Vet Rad 23:152, 1982. 8. Love NE, Millis D, et al: Radiographic diagnosis. Vet Rad 31:29, 1990. 9. Daniel BD, Avenell JS, et al: Scintigraphic detection of subcutaneous metastasis in a dog with appendicular osteosarcoma. Vet Radiol & Ultrasound 37:146, 1996. 10. Carrig C: Radiographs presented as part of the 1993 A.C.V.R. oral certification examination. Vet Radiol & Ultrasound 35:100, 1993. 11. Boudrieau RJ, Schelling SH, Pisanelli SH: Chondrosarcoma of the radius with distant metastasis in a dog. J Am Vet Med Assoc 205:580, 1994.

12. Anderson MA, Reed AR: What is your diagnosis? J Am Vet Med Assoc 204:211, 1994. 13. Forrest LJ, Thrall DE: Bone scintigraphy for metastasis detection in canine osteosarcoma. Vet Radiol & Ultrasound 35:124, 1994. 14. Walker M, Green R, et al: Radiographs presented as part of the 1994 A.C.V.R. oral certification exam: musculoskeletal section. Vet Radiol & Ultrasound 36:113, 1995. 15. Forrest LJ, Thrall DE: Bone scintigraphy for metastasis detection in canine osteosarcoma. Vet Radiol & Ultrasound 35:124, 1994. 16. Lamb CR, Schelling SH, Berg J: Lymph node uptake of 99m Tc-MDP during bone scintigraphy in dogs. Vet Rad 30:268, 1989. 17. Borenstein N, Fayolle P, Moissonnier P: What is your diagnosis? J Small Anim Pract 40:205, 1999. 18. Thamm DH, Maudlin EA, et al: Primary osteosarcoma of the synovium in a dog. J Am Anim Hosp Assoc 36:326, 2000. 19. Hayes AM, Dennis R et al: Synovial myxoma: MRI in the assessment of an unusual canine soft tissue tumor. J Small Anim Pract 40:489, 1999. 20. Alexander JW, Dueland R, Appel GO: Malignant melanoma with skeletal metastasis in a dog. J Am Vet Rad Soc 17:7, 1976. 21. Thomas WB, Daniel GB, McGavin MD: Parosteal osteosarcoma of the cervical vertebra in a dog. Vet Radiol & Ultrasound 38:120, 1997. 22. Burk RL, Ackerman N: Small Animal Radiology & Ultrasonography. Philadelphia, 1996, WB Saunders Co. 23. Huber DJ, Allen DG, et al: What is your diagnosis? J Am Vet Med Assoc 211:1509, 1997. 24. Barber DL, Thrall DE, et al: Primary osseous hemangiosarcoma in a dog. J Am Vet Rad Soc 14:17, 1973. 25. Voges AK, Neuworth L, et al: Radiographic changes associated with digital, metacarpal and metatarsal tumors, and pododermatitis in the dog. Vet Radiol & Ultrasound 37:327, 1996. 26. Huff RW, Brody RS: Multiple bone cysts in a dog—a case report. J Vet Rad Soc 5:40, 1964. 27. Biery DN, Goldschmidt MH, Riser W, Rhodes WH: Bone cysts in the dog. J Am Vet Rad Soc 17:202, 1976. 28. Magnussen KL: What is your diagnosis? J Am Vet Med Assoc 210:1734, 1997. 29. Tanabe S, Nakama S, et al: What is your diagnosis? J Am Vet Med Assoc 206:314, 1995. 30. Homer BL, Ackerman N, et al: Intraosseous epidermoid cysts in the distal phalanx of two dogs. Vet Radiol & Ultrasound 33:133, 1992. 31. Ackerman N, Spencer CP: Radiographic diagnosis. Vet Rad 26:10, 1985. 32. Barrand KR: What is your diagnosis? J Small Anim Pract 39:107, 1998. 33. Geiger T, McEntee M: What is your diagnosis? J Am Vet Med Assoc 214:1156, 1999. 34. Pernell RT, Dunstan RW, DeCamp CE: Aneurysmal bone cyst in a six-month-old dog. J Am Vet Med Assoc 201:1897, 1992. 35. Basher AW, Doige CE, Presnell KR: Subchondral bone cysts in a dog with osteochondrosis. J Am Anim Hosp Assoc 24:321, 1988. 36. Stickle R, Flo G, Render J: Benign bone cyst. Vet Radiol & Ultrasound 40:365, 1999.

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6

Extremital Soft Tissue Tumors

With the exception of fatty tumors, few soft tissue neoplasms possess any distinguishing radiographic features. A soft tissue tumor should be suspected when a slowly growing mass is present, particularly in an older dog or cat.

❚❚❚ LIPOMA Lipoma and its malignant counterpart, liposarcoma, are unique among soft tissue tumors in terms of their radiographic visibility. Because they are composed of fat, these tumors appear relatively dark and well marginated compared with their lighter muscular surroundings.1

❚❚❚ LIPOSARCOMA Large liposarcomas, like lipomas, also can be visible on plain films. In cats, liposarcomas have been associated with type C virus particles, feline sarcoma virus, and feline leukemia infections. Although no causative infectious agent has been identified in dogs, a potential association with skeletal-muscle foreign bodies has been suggested, similar to what has been reported in people.2

Figure 6-1 • Close-up lateral angiogram of a muscle tumor located caudal to the stifle joint in a dog. Note how the major blood vessels encircle the mass, generating characteristically undulant branches, which then penetrate deep into the interior.

resonance imaging, except for embolization or other therapeutic purposes (Figure 6-1).3

References

❚❚❚ IMAGING FINDINGS Radiography continues to be a valid departure point in the medical imaging of extremital tumors, particularly for detecting the involvement of nearby bone. Angiography, on the other hand, has been largely replaced by computed tomography and magnetic

1. DeHaan J, Ackerman N: What is your diagnosis? J Am Vet Med Assoc 203:371, 1993. 2. McCarthy PE, Hedlund CS, et al: Liposarcoma associated with a glass foreign body in a dog. J Am Vet Med Assoc 209:612, 1996. 3. Sutton D: Arteriography and therapeutic angiography. In Sutton D, ed: A Textbook of Radiology & Imaging. New York, 1993, Churchill Livingstone.

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Osteochondritis

❚❚❚ OVERVIEW Osteochondritis, especially of the elbows, appears to be increasing in incidence in North America. At our hospital, we believe this is due in large part to the immense popularity of Labrador and Golden Retrievers, breeds that have high incidences of osteochondritis. Based on the findings of several puppies in the same litter being affected and affected dogs producing affected puppies, we assume the disease is heritable, much like hip dysplasia. In our opinion, detachment or deformity of the coronoid process is not a separate disease but simply a form of osteochondritis and, accordingly, does not require special designation (fragmented coronoid process [FCP]). Neither do we use the modifier dissecans (dissected) unless we are able to image a discrete fragment, as is often possible with computed tomography (CT) or magnetic resonance imaging (MRI) but rarely with radiography.1 We believe the term elbow dysplasia is too vague and, from a pathophysiologic perspective, invites confusion with hip dysplasia. Likewise, the term elbow arthrosis, as proposed by Swenson and colleagues, seems equally ambiguous and does little to inform an already bloated taxonomy.2 The distinction between osteochondrosis and osteochondritis seems more cultural than clinical; thus somewhat arbitrarily, I have chosen to call the disease osteochondritis in this book, although I generally think of these terms as synonymous.

❚❚❚ COMMONLY AFFECTED BREEDS In our practice, Retrievers, both Golden and Labrador, are affected more than any other breeds. 138

❚❚❚ CHARACTERISTIC LESIONS ACCORDING TO SITE Elbow Medial Coronoid Process Historical Perspective. Ljunggren and Olsson are generally credited with discovering what they termed at the time “a new type of elbow dysplasia (ununited coronoid process) and osteochondritis dissecans.”3 Although the primary lesion was often radiographically invisible, the osteoarthritic aftermath was not subchondral sclerosis of the trochlear notch and periarticular bone deposits on the distal humerus, proximal ulna, and proximal radius. In 1984 Henry pointed out the benefits of frontal oblique and flexed lateral projections in detecting the typically elusive coronoid lesion.4 Later, Voorhout and Hazewinkel reviewed the radiographs and surgical findings of 14 young large-breed dogs with osteochondritis of one or both elbows.5 Armed with surgical hindsight, the authors were able to identify a variety of subtle coronoid lesions as well as more obvious defects and areas of reduced density in the subchondral portion of the medial humeral condyle. Like those before them, the authors attempted to develop a standard film series that would identify both early and late lesions. Their recommended protocol was as follows: (1) frontal, (2) frontal oblique, (3) lateral, and (4) extended lateral oblique views. Using this protocol, the authors drew the following conclusions: • A mature “osteochondral lesion” (author’s quotes to remind the reader that cartilage is radiographically invisible) of the coronoid process has a highly distinctive appearance. • Immature lesions, on the other hand, especially those that have not yet become overtly arthritic, are less striking but nevertheless distinctive in their own right.

CHAPTER 7 ❚❚❚ Osteochondritis

• Very early lesions (present in 6- to 12-month-old dogs) may or may not reveal signs indicative of osteochondritis. Berry then drew attention to the characteristic way in which the medial coronoid became blunted as seen in a partially (but not extremely) flexed view of the elbow, asserting that this finding strongly suggested a coronoid lesion.6 Shortcomings Associated With Sole Reliance on Hyperflexed Lateral View of Elbow. In 1995 attention was drawn to the dangers of relying solely on a flexed lateral view of the cubital joint, as is the practice of the Orthopedic Foundation for Animals (OFA), pointing out the following limitations inherent in such a practice.7 • The hyperflexed view makes accurate assessment of the humeroulnar and humeroradial joints difficult or impossible. Because these areas are usually first to become altered with either anconeal or coronoid process lesions, it seems likely that sole reliance on a hyperflexed view will delay radiographic detection. • The highly characteristic deformity of the medial coronoid process, indicative of osteochondrosis, is appreciable only in the craniocaudal view. Once again, sole reliance on a flexed lateral projection surely will impede diagnosis. • If the principal reason for the hyperflexed lateral projection is to evaluate the outer margin of the anconeal process with a minimum of superimposition by the medial epicondyle of the humerus, there must be awareness of the radiographic variation between the flexed and extended lateral views of the elbow. This is yet another limitation of having only one view. • The proximal border of the anconeal process varies among different dog breeds, in some instances resembling what has erroneously been termed an osteophyte, said to be indicative of “elbow dysplasia.”

139

Even in the face of growing concern that there were serious limitations to relying solely on a flexed lateral view to screen the elbows of dogs for osteochondritis, the OFA continued to insist that the flexed lateral projection “appeared to be sufficient” (to do the job). An article by Keller (an employee of the OFA) and coworkers, published in Veterinary Radiology & Ultrasound in 1997, purported to establish the validity of the flexed lateral view as a screening instrument for “elbow dysplasia” by demonstrating a positive radiographic– pathologic correlation in eight German Shepherds but continued to refer to an “abnormal periosteal reaction” on the proximal border of the anconeal process as being the radiographic basis for reliably identifying affected individuals.8 Imaging Findings Radiology Normal Anatomic and Radiographic Variation. The size, shape, and curvature of the anconeal process vary from one dog to the next and are unreliable disease indicators (Figure 7-1). Likewise, individual differences in the length and width of the medial coronoid process and the size of the cranial radial lip are inaccurate predictors of osteochondritis (Figure 7-2, A-D). Even the overall appearance of the proximal ulna can vary from extremely upright to moderately arched, with neither conformation providing any diagnostic clues. The variation of greatest concern is that which occurs along the lateral margin of the anconeal process, specifically the extent to which the lateral articular margin curls proximally, forming a lateral ridge (Figure 7-3). The larger the lateral ridge and the greater the angle of the anconeal process (as viewed frontally in Figure 7-4), the greater the likelihood it will be projected on or over the proximal edge of the anconeal process in a lateral radiograph, resembling a bone deposit (osteophyte), a finding that some consider to be nearly certain

Figure 7-1 • Defleshed proximal radius and ulna (lateral perspective) from four normal dogs show variation in size, shape, curvature, and position of the anconeal process.

140

SECTION I ❚❚❚ The Extremities

Figure 7-2 • Defleshed proximal radius and ulna (proximal perspective) from four normal dogs show variation in size, shape, curvature, and position of the coronoid process and cranial radial margin. Normal anatomic differences in the overall shape of proximal ulna also are regularly encountered but play little or no role in the diagnosis of osteochondritis.

evidence of “elbow dysplasia.” I term this normal variant a false ridge sign (Figure 7-5). It is also possible to produce false ridge sign when making a lateral radiograph by tipping the elbow, a common radiographic error (Figure 7-6). An even longer bony ridge exists on the medial side of the ulna, extending distally from the medial edge of the anconeal process to the tip of the medial coronoid process. Like the lateral ridge, the medial ridge varies in prominence from dog to dog (Figure 7-7). Larger medial ridges absorb more radiation than smaller ridges, resulting in increased density, which may be mistaken for so-called sclerosis and in the past supported a diagnosis of “elbow dysplasia.” Like bias, the flexed lateral view of the elbow can be either an ally or an adversary. It may reveal an abnormal anconeal process otherwise obscured by the medial epicondyle of the humerus in the nonflexed projection, or it may result in a false ridge sign, the result of oblique positioning (Figure 7-8).

Additionally, flexed lateral views of the elbow are often underexposed, making it difficult or impossible to evaluate the critical interior surfaces of the joint and the cartilage spaces (Figure 7-9). This is due in large part to the bulging of nearby muscles when the elbow is hyperflexed. This problem can be overcome by measuring the elbow in the flexed rather than in the extended position before setting the radiographic technique. Lesion Development and Progression. Osteochondritis of the coronoid process may result in deformity (Figure 7-10) or detachment (Figure 7-11) of the coronoid process. Thus, the term fragmented coronoid process is not always appropriate. As with osteochondritis of the anconeal process, most affected dogs develop severe osteoarthritis involving all the bones of the elbow. Although not affected with the frequency of the ulna, the humerus is usually secondarily involved irrespective of the primary site (Figure 7-12). Text continued on p. 145

CHAPTER 7 ❚❚❚ Osteochondritis

Figure 7-3 • Defleshed proximal ulna of a normal dog (lateral perspective) shows the distinctive curl on the lateral articular margin of the anconeal process, the lateral ridge (emphasis zone).

141

Figure 7-4 • Defleshed proximal ulna of a normal dog (frontal perspective) shows laterally to medially angled anconeal process (emphasis zone).

Figure 7-5 • Defleshed proximal ulna of a normal dog (lateral perspective) shows how tipping the ulna during radiography can create a false ridge sign by superimposing the lateral ridge on the proximal edge of the anconeal process.

142

SECTION I ❚❚❚ The Extremities

A

B

Figure 7-6 • A, Lateral view of a normal elbow shows a false ridge sign (faint bone density superimposed on the proximal border of the anconeal process, partially overlain by the medial epicondyle of the humerus), the result of nonstandard positioning (lateral oblique rather than true lateral). B, The frontal view is included for completeness.

Figure 7-7 • Defleshed elbow joints (minus the humerii) of four normal dogs shown in lateral perspective show variations in the medial ulnar ridge—the thin arch of bone connecting the anconeal and coronoid processes that marks the medial most aspect of articular surface of the ulna.

CHAPTER 7 ❚❚❚ Osteochondritis

143

A

B Figure 7-8 • A, Close-up flexed lateral view of a normal elbow in a young dog shows a false ridge sign (emphasis zone) caused by oblique positioning. B, A second lateral with improved positioning appears normal.

B

A Figure 7-9 • Close-up, flexed lateral views of the elbow of a healthy dog show a false ridge sign in the initial image, the result of inadvertent oblique positioning (A) and a normal anconeal process in a subsequent film (B). In both images, the upper slope of the anconeal process is clearly visible; however, in the more flexed of the two films (B), the joint spaces are underexposed (and thus invisible) because of greater part thickness resulting from a greater degree of flexion. In general, the more the elbow is flexed, the greater the obliquity and the more likely the possibility of a false ridge sign.

SECTION I ❚❚❚ The Extremities

144

A A

B

B Figure 7-10 • A, Defleshed bone specimens of the elbow of a dog with osteochondritis of the medial coronoid (lateral perspective, viewer’s left) and comparably sized normal dog (lateral perspective, viewer’s right). In the arthritic elbow, the anconeal process is normally positioned but is elongated and lacks a normal slope. Large, bony ridges extend distally from the proximal tubercles to the base of the lateral coronoid process. B, The medial perspective shows a badly deformed coronoid but no detached or ridge sign. Comparison of the shadows cast by the normal and abnormal elbows shows the characteristic disfigurement caused by this form of osteochondritis.

Figure 7-11 • A, Defleshed bone specimens of the elbow of a dog with osteochondritis of the medial coronoid process (medial perspective) shows (1) triangular coronoid fragment (emphasis zone), (2) radial saddle horn, (3) deformed anconeal process, and (4) a large medial ridge. B, A second view of the same specimen but with the coronoid fragment displaced is also shown. C, A lateral perspective shows a lengthy lateral ridge superimposed on the anconeal process (emphasis zone), producing a false ridge sign.

C

CHAPTER 7 ❚❚❚ Osteochondritis

145

I have yet to encounter any form of elbow surgery that either halts or slows the development of related osteoarthritis. Nor have I seen any dogs crippled by the disease, with the provisos that they exercise regularly and do not become grossly overweight (contrary to some published claims).

A

B Figure 7-12 • Lateral (A) and medial (B) perspectives of the distal humerus, with normal comparisons, show osteoarthritis that typically accompanies osteochondritis of either the coronoid or anconeal processes.

Not all coronoid lesions appear to develop at the same rate. For example, many retrievers show radiographic abnormalities in the second half of their first year; German shepherds, on the other hand, may show no abnormalities until they have finished growing. Chows may appear normal in all respects until they reach 4 to 5 years of age, at which time they begin to exhibit subtle lameness associated with deformity of the coronoid process and radial head. Follow-up examinations of mature dogs with osteochondritis of the coronoid or anconeal process (made 1 or more years apart) usually show progression but not always at a predictable rate (Figure 7-13).

Early Disease. Ridge signs usually are configured in one of three ways: shallow, medium, or deeply arched (Figures 7-14 to 7-17). Occasionally, ridges are blocked or irregular in appearance rather than smoothly arched. A fairly strong correlation exists between the overall size of the ridge and the extent of the related osteoarthritis elsewhere in the elbow. In some animals with osteochondritis resulting in secondary proximal migration of the anconeal process, osteophytes originating atop the olecranon merge with the lateral ridge, producing varying degrees of proximal ulnar disfiguration. The distal humerus also becomes secondarily disfigured as a result of osteoarthritis, particularly the lateral aspects of the condyle and epicondyles. As the arthritis progresses, the cranial aspect of the radial head also begins to change, developing a distinctive saddle horn cranially, presumably an adaptation designed to help retain an increasingly mobile humerus (Figure 7-18). In some instances of early or mild osteochondritis, there is no visible ridge sign; instead, there may be new bone deposits on the medial side of the distal humeral condyle and on the outer edge of the medial coronoid (Figure 7-19). This appearance is often seen in Chows and in other medium-sized breeds with delayed-onset osteochondritis of the elbows. Late Disease. As the elbow loosens because either the coronoid or the anconeal process has detached, deformed, or migrated, the resultant arthritis worsens, often taking the form of a large rhino-horn osteophyte emanating from the cranial edge of the medial condyle, as seen in the lateral view. The radial saddle horn, as mentioned previously, becomes larger, matching or surpassing the overlying humeral spike. The anconeal process becomes difficult or impossible to identify because more and more bone is deposited on the exterior surfaces of the elbow. In some instances, large cyst-like areas are present in the olecranon. In the frontal projection, distinctive osteophytes form on the medial epicondyle, medial coronoid process, and outer corner of the radial head, which, along with the new bone on the lateral humeral condyle, give the elbow a “lumpy-bumpy” appearance (Figures 7-20 and 7-21). False Disease. Occasionally, an old injury results in the formation of osteophytes, and plaques of new bone in and around the elbow can be mistaken for osteochondritis. Unlike osteochondritis, these deposits are usually away from the joint and typically are found unilaterally (as opposed to the characteristic bilateral

B A

D

C

E

F

Figure 7-13 • Close-up lateral (A), frontal (B), and frontal oblique views (C) of a mildly arthritic elbow in an 18-month-old Labrador Retriever caused by osteochondritis of the medial coronoid process (emphasis zones show subtle new bone deposits in characteristic locations). D to F, show the same elbow 1 year later, having worsened as indicated by increased arthritis (emphasis zones).

CHAPTER 7 ❚❚❚ Osteochondritis

147

A

Figure 7-14 • Close-up flexed lateral view of the elbow of a young dog with a ridge sign (shallow arch type) supporting osteochondritis of the coronoid.

B o x

7 - 1

Abnormalities Found in Computed Tomographic Examinations of a Series of Dogs with Elbowrelated Forelimb Lameness Ulna

Cracking of coronoid process Fragmentation of coronoid process

Radius

Humerus

B Flattening of medial aspect of humeral condyle Increased lucency of humeral condyle

Increased density of medial coronoid process Increased density of trochlear notch Irregularity of radial notch Lucency of radial notch Misshapen medial Proximal Increased density coronoid process osteophytes of humeral condyle Separation of coronoid process Ununited anconeal process

Figure 7-15 • A and B, Close-up flexed lateral views of the elbows of a dog show bilateral ridge signs (medium arch type).

involvement of osteochondritis). Figure 7-22 shows such an injury. Computed Tomography. Reichle and co-workers published their CT findings in a medium-sized group of dogs imaged because of elbow lameness.9 One of the most interesting aspects of this article is the variety of reported lesions. Although it seems probable that most of these less publicized abnormalities (lesions?) probably are related to osteochondritis (at least indirectly), it is also possible that they are not related and that we are encountering a new disease. More likely, however, is the explanation that CT simply provides better anatomic detail and less structural superimposition, allowing previously obscure changes to become apparent. The CT abnormalities found in the elbows of the described dogs are tabulated in Box 7-1. Additionally, the authors reported articular malalignment in all three components of the elbow joint: humeroulnar (53%), humeroradial (32%), and radioulnar (20%). It appeared that most of these subluxations were of a secondary nature. Figure 7-23 shows a CT image (including a three-dimensional reconstruction) of the elbow of a dog with osteochondritis of the medial coronoid process. Radiographs showing the characText continued on p. 152

148

SECTION I ❚❚❚ The Extremities

A

B

Figure 7-16 • Close-up natural and flexed lateral views of the elbow of a young retriever with coronoid osteochondritis. In the nonflexed view (A), a ridge sign is present but faint, whereas in the flexed view (B), the ridge sign (deep arch type) is clearly visible.

B

A Figure 7-17 • Close-up natural and flexed lateral views of the elbow of a young German Shepherd with coronoid osteochondritis. A, In the nonflexed view a ridge sign is partially visible; B, in the flexed view the ridge sign is more completely visualized.

CHAPTER 7 ❚❚❚ Osteochondritis

A

149

B Figure 7-18 • Close-up natural (A) and flexed lateral (B) views of the elbows of a young Golden Retriever fail to show a definite ridge sign; however, bone deposits on the humeral condyle and radial head circumstantially suggest coronoid disease.

A

B

Figure 7-19 • Close-up flexed lateral (A) and frontal (B) views of the elbow of a dog with very early osteochondritis of the coronoid process. Although there is no ridge sign, the radial head has developed a small lip, and there is abnormal roughening of the medial border of the distal humerus.

150

SECTION I ❚❚❚ The Extremities

B A

C

D

Figure 7-20 • Close-up lateral (A) and frontal (B) views of an arthritic elbow in a 5-year-old Labrador Retriever, the result of osteochondritis of the medial coronoid process. The cause of the oval lucency in the ulna was not determined, but since this finding was present bilaterally (C, D) and found unchanged in earlier films, it was not diagnostically pursued.

CHAPTER 7 ❚❚❚ Osteochondritis

B

A

C

D

Figure 7-21 • Close-up lateral (A, C) and frontal (B, D) views of the elbows of a 5-year-old Sharpei. Many abnormalities are present, including (1) abnormal proximal positioning and deformity of the anconeal process, (2) abnormal distal positioning and deformity of the medial coronoid process, and (3) partial dislocation of both the humeroulnar and humeroradial joints. Although there are bone deposits on the radial head and medial aspect of the distal radius indicative of osteoarthritis, they are not so pronounced as might be predicted given the described structural and spatial abnormalities. These findings are characteristic of a delayed form of osteochondritis.

151

152

SECTION I ❚❚❚ The Extremities

A

B

Figure 7-22 • A, Close-up flexed lateral view of a dog’s elbow shows no evidence of osteochondritis, but multiple bone deposits arrayed over the surface of the proximal radial shaft suggest a previous injury. B, The opposite elbow is provided for comparison.

teristic arthritic pattern of this disease also provide diagnostic comparison. Magnetic Resonance Imaging. Snaps and co-workers compared the relative merits of three different types of magnetography for imaging the canine elbow: spin echo (T1, T2), gradient echo, and fat saturation.10 Using the normal elbows of four large-breed dogs, each about 18 months of age, gradient-echo imaging (fast imaging with steady-state precession) provided the best images. Specifically, the fast-imaging gradient-echo images provided thin, highly detailed contiguous slices of both the anconeal and coronoid processes. Multiplanar capabilities resulted in comparatively brief scan times.

Anconeal Process Generally, the radiographic diagnosis of anconeal osteochondritis (also termed ununited anconeal process) is perceived as being straightforward, the diagnosis being based on a single finding: the physical separation of the anconeal process from the adjacent ulna. The resultant osteoarthritic pattern is similar to that resulting from osteochondritis of the coronoid. Reliance on a single disease indicator has its shortcomings, however. First, in older dogs that have had the disease for 2 or 3 years, secondary osteoarthritis may be so severe that it obscures the anconeal process, making close scrutiny impossible. Second, not all diseased anconeal processes are clearly separated from the ulna, or at least there may be some doubt concerning the matter.

A solution to this problem is to use a second, equally reliable disease indicator: the proximal displacement of the anconeal process. Although not widely appreciated, osteochondritis of the anconeal process may not result in a loose fragment (Figure 7-24); instead, the anconeal process remains attached to the ulna by nonosseous tissue but moves to a new location near the upper edge of the olecranon as the bone matures. Proximal displacement of the anconeal process also can be used in severely arthritic elbows to distinguish between osteochondritis of the coronoid and anconeal processes (Figure 7-25). Even though osteochondritis of the anconeal process secondarily deforms the coronoid process, it does not cause upward displacement of the anconeal process. Thus, if displacement is present, the disease probably began in the anconeus (Figure 7-26); if not, the problem is more apt to reside with the coronoid or, less likely, the distal humerus. Figures 7-27 to 7-29 exemplify the characteristic features of osteochondritis of the anconeal process.

Distal Humeral Epiphysis Fragmenting lesions of the distal humerus often cause an arthritic pattern that closely resembles osteochondritis of the coronoid or anconeal processes. Most such lesions originate from the articular surface of the distal humerus medially, just above the coronoid process (Figures 7-30 and 7-31). In some instances, it is difficult or impossible to differentiate a primary from a secondary lesion, the latter typically stemming from an underlying coronoid lesion.

CHAPTER 7 ❚❚❚ Osteochondritis

153

A B

C

D Figure 7-23 • A, Close-up cross-sectional view of a dog’s elbow at the level of the medial coronoid process (small bone fragment) shows complete detachment. B, A flexed lateral, three-dimensional computed tomographic reconstruction of the same elbow shows the coronoid fragment just below the medial epicondyle. Frontal (C) and lateral (D) radiographs of the same animal are provided for comparison.

154

SECTION I ❚❚❚ The Extremities

Figure 7-24 • Defleshed bone specimen of the elbow of a dog with osteochondritis of the anconeal process (proximal perspective) shows proximally displaced, detached anconeal process (white triangular object at top of joint).

A

Figure 7-25 • Defleshed bone specimen of the elbow of a dog with osteochondritis of the anconeal process (proximal perspective) shows proximally displaced but attached anconeal process.

B

Figure 7-26 • A, Close-up frontal view of the elbow shows a large coronoid “hook,” which may be seen with either coronoid or anconeal osteochondritis. B, However, the proximal displacement and detachment of the anconeal process seen in the lateral projection are unequivocal indicators of anconeal osteochondritis.

CHAPTER 7 ❚❚❚ Osteochondritis

A

155

B

Figure 7-27 • Close-up natural (A) and flexed lateral (B) views of the elbow of a dog with osteochondritis of the anconeal process; both images clearly show the characteristic lesion: separation and proximal dislocation of the anconeal process.

Figure 7-28 • Close-up flexed lateral view of the elbow of an immature German Shepherd with osteochondritis of the anconeal process shows: (1) proximal displacement of the anconeal process, (2) a large bony lip on the cranial aspect of the radial head, (3) widening of the humeroradial joint, and (4) malalignment of the articular surfaces of the radius and ulna. In addition (and a more likely explanation for the dog’s acute, painful forelimb lameness), there is panosteitis in the distal humerus as indicated by interior bone deposition.

Figure 7-29 • A most unusual case of an acute proximal olecranon fracture sustained by this dog after being struck by a car. The fracture enters the arthritic humeroulnar joint just below the base of the anconeal process, which shows the characteristic proximal displacement and deformity of osteochondritis. The opposite elbow featured a similar pattern but no fracture.

156

SECTION I ❚❚❚ The Extremities

A

B

C Figure 7-30 • Frontal (A), frontal oblique (B), and close-up frontal oblique (C) views of the elbow joint in a dog with humeral osteochondritis shows: (1) abnormal widening of the medial aspect of the humeroradial joint, (2) subtle flattening and decreased density of the articular surface of the humerus medially, (3) roughening of the medial margin of the humeral epiphysis, and (4) blunting of the medial coronoid process.

Much less frequently, the medial epicondyle is affected, usually bilaterally. A typical lesion consists of a long, relatively thick bone fragment lying just beyond the edge of what remains of the medial epicondyle (Figure 7-32). Moderate flexion of the elbow usually improves lesion visibility, provided the elbow is not rotated in the process, which could produce the opposite effect.

Shoulder Background. Osteochondritis of the proximal humerus often produces a highly characteristic

lesion requiring little or no differential diagnosis.11 Arthrography demonstrates a strong correlation between the size of a subchondral defect in the humeral head (as seen radiographically) and the amount of damage to the overlying articular cartilage. These observations correlate well with the presence and severity of pain and lameness experienced by most affected animals. Carrig and Morgan described the microvascular circulation of the normal canine humeral joint and determined that development of the medial aspect of the humeral head and its vasculature normally lags behind that of the lateral aspect. They hypothesize that this relative difference in intraepiphyseal maturation may

CHAPTER 7 ❚❚❚ Osteochondritis

A

157

B

Figure 7-31 • Close-up lateral (A) and frontal (B) views of an arthritic elbow in a young dog show a detached humeral fragment located just above the medial coronoid process consistent with osteochondritis. Progress films made a year later showed a classic coronoid hook and a portion of the humeral fragment.

Figure 7-32 • Close-up flexed lateral views of the right (left) and left (right) elbows of a dog show large, detached bone fragments from the margins of the medial epicondyles caused by osteochondritis.

render the medial side of the humeral head susceptible to injury, which in turn can lead to osteochondritis.12 Based on these findings, van Bree devised a radiographic measurement that he asserts will accurately predict the probable condition of the articular cartilage overlying an osteochondral defect and, by inference, the degree of probable associated morbidity. The measurements are made from a lateral projection of the humeral joint and include the lengths of the osteochondral defect and the humeral head. The length of the lesion then is expressed as a percentage of the sagittal diameter of the associated

humeral head. For dogs with clinical signs, the mean measured lesion percentage was 27.4, whereas dogs without clinical signs measured only 21.4%, a difference of about 20%.13 Imaging Findings Radiography and Radiology. Callahan and Ackerman described the diagnostic benefits of outward rotation when making a lateral projection of the shoulder joint to confirm osteochondritis of the humeral head.14 Not only can this supplementary view improve lesion

158

SECTION I ❚❚❚ The Extremities

detail, but it also may reveal otherwise undetectable bone flaps. A close-up conventional lateral view of the shoulder is provided for comparison with the following osteochondral lesions (Figure 7-33). The classic lesion is located along the caudal perimeter of the humeral head, as projected laterally, and consists of an elliptical defect and or closely approximated bone fragment. Lesions may range from a barely perceptible loss in bone density to a cavernous subchondral defect. In some instances, the entire subchondral margin may detach from the underlying bone (Figures 7-34 to 7-36). Following surgical removal of large marginal bone fragments and curettement of underlying subchondral defects, especially if they are long and deep, the femoral head often heals with a pronounced “scar” in the form of a marked flattening, plus or minus a ventral spur (Figure 7-37).

Figure 7-33 • Close-up lateral view of a normal shoulder joint.

A

B Figure 7-34 • A, Close-up lateral view of the right shoulder of a Newfoundland dog show a vague area of decreased density in the subchondral bone of the caudal aspect of the humeral head consistent with early mild osteochondritis. B, The opposite shoulder was similarly affected.

B

A Figure 7-35 • A, Close-up lateral view of the shoulder joint shows a concave defect in the caudal margin of the humeral head consistent with osteochondritis. B, Close-up lateral view of the shoulder joint shows a narrow but lengthy osteochondral fragment detached from the caudal third of the humeral head.

CHAPTER 7 ❚❚❚ Osteochondritis

159

A

B Figure 7-36 • A, Close-up lateral view of the shoulder joint of a dog with osteochondritis shows a large rectangular defect in the caudal third of the humeral head, littered with a number of small bone fragments. B, Close-up lateral view of the shoulder joint shows a large defect in the caudal part of the humeral head, the bottom of which contains a number of vague, nonstructured radiolucencies. The latter proved to be an elaborate network of necrotic channels that extended deeply into the underlying epiphysis, making the actual lesion approximately twice the size of that originally estimated from radiographs.

Arthrography. Story described the use of shoulder arthrography for both diagnostic and prognostic purposes (Figures 7-39 to 7-41).15 Van Bree and coworkers compared arthrographic with arthroscopic findings in 20 shoulder joints and concluded the following15:

Figure 7-37 • Close-up lateral view of the humeral joint shows a pronounced flattening of the caudal aspect of the humeral head consistent with healed osteochondritis (although there is no way to know the status of the overlying cartilage). Also note the decreased subchondral bone density in the cranial half of the humeral head.

Occasionally, gas is seen within the humeral joint appearing as bubbles or outlining one or both articular surfaces, an observation variably termed (1) the vacuum phenomenon (scientific) or (2) nature’s arthrogram (humorous). Although seen only occasionally, this is a normal finding, especially in the humeral joint (Figure 7-38).

• Arthroscopy confirmed the presence of 12 of 12 arthrographically identified cartilage flaps. • Only three of eight arthrographic studies showed a distinct crack in the articular cartilage of the humeral head, whereas arthroscopy revealed a fissure line in all eight shoulders. • Arthroscopy identified chondromalacia in two dogs; arthrography did not. • Arthroscopy identified a focal concave deformity in the articular cartilage in three dogs; arthrography did not. • Arthroscopy identified small joint mice in two dogs; arthrography did not. • Arthroscopy identified a kissing lesion in the glenoid, opposite a cartilage flap; arthrography did not. • Arthroscopy identified synovial inflammation; arthrography did not. The obvious conclusion from this study was that arthroscopy was capable of detecting smaller and subtler osteochondral and synovial lesions than was arthrography.16 The same investigators also determined that for shoulder arthrography, low osmolar, nonionic

160

SECTION I ❚❚❚ The Extremities

A

B

Figure 7-38 • A, Close-up lateral view of the humeral joint made during traction shows gas in the joint cavity indicating a vacuum effect; B, a comparable view of the opposite shoulder shows no intraarticular gas.

Figure 7-39 • Close-up lateral humeral arthrogram of a dog with osteochondritis shows disrupted articular cartilage over much of the caudal third of the humeral head. Additionally, contrast solution is faintly outlining a cartilage fragment.

Figure 7-40 • Close-up lateral humeral arthrogram of a dog with osteochondritis shows a short band of contrast dissecting beneath the articular cartilage of the caudal third of the humeral head.

contrast media are far superior to high osmolar, ionic agents.17 Osteochondritis also occasionally affects the greater tubercle, glenoid, and less often the supraglenoid and coracoid processes (Figure 7-42). As with most forms of osteochondritis, the lesions are usually present bilaterally. In some cases, associated lameness is minimal, although most lesions are uncovered in the course of a seeking a cause for an obvious abnormality.

Occasionally, dogs without known shoulder lameness have osteoarthritis in both humeral joints, which some attribute to previous osteochondritis. Although it is not my intention to generalize, especially based on a single individual, I have radiographed the shoulder region of a dog at 6 and later at 11 years of age for an unrelated problem. In the initial examination, the shoulder joints appeared normal, but in a subsequent examination performed 5 years later, both shoulders were arthritic (Figure 7-43).

CHAPTER 7 ❚❚❚ Osteochondritis

161

Figure 7-41 • Close-up lateral humeral arthrogram of a dog with osteochondritis shows intact articular cartilage above subchondral defect.

A

Tarsal Joint Disease Forms and Sites of Involvement. To date, there appear to be at least three forms of osteochondritis affecting the hocks of dogs: one involving the medial trochlear ridge of the talus; another, the medial malleolus of the tibia; and a third, the medial malleolus and the underlying talus. Alternatively, there may only be two primary forms of the disease, malleolar or talar, and any additional lesions, especially those on an adjacent joint surface, are of a purely secondary nature (a so-called kissing lesion). Talar Lesions. The most common type of tarsal osteochondritis in dogs occurs in the proximal aspect of the medial ridge of the talus, usually taking the form of a single small, semiattached bone fragment. In my experience, immature retrievers (often as young as 6 months of age) are most often affected, usually bilaterally. Clinically indicated by swelling and mild lameness, traction-stress radiography (under sedation) often is required to demonstrate the lesion. Unlike many other forms of osteoarthritis, the tarsocrural joints of dogs with advanced osteochondritis are often widened, especially medially. Figures 7-44 and 7-45 exemplify many of the radiographic disease indicators (RDIs) associated with osteochondritis of the canine tarsus. Figure 7-46 illustrates the strong resemblance between osteoarthritis caused by longstanding osteochondritis and that resulting from a severe tarsal sprain. Medial Malleolar Lesions. Newell and co-workers described the radiographic appearance of isolated osteochondral-like lesions of the medial malleolus

B Figure 7-42 • Close-up lateral views of the right (A) and left (B) shoulders of a dog show partial disintegration of the supraglenoid tubercles.

and combined malleolar–talar lesions in a small series of dogs in which all but one were Rottweilers.18 Radiographically, the isolated malleolar lesions often featured a detached bone fragment with variable degrees of associated lucency involving both the fragment and its bed. In the combined form of the disease, there was a fragment in the proximal part of the medial talar ridge in addition to the overlying

162

SECTION I ❚❚❚ The Extremities

A

A

B Figure 7-43 • A, Close-up lateral view of the humeral joint of a 6-year-dog, which at the time appeared normal. B, A second examination performed 5 years later showed severe osteoarthritis featuring large osteophytes extending from the caudal edges of the glenoid and humeral head (emphasis zone). The dog’s forelimb lameness was barely detectable and could not be definitely localized to the shoulder or any other bone or joint. The cause or causes of the arthritis were not determined, even after extensive diagnostic testing.

B Figure 7-44 • A, Close-up frontal view of the hock of a 5-month-

medial malleolus. Additionally, the tarsocrural joint was usually widened medially.

Stifle Osteochondritis of the stifle is uncommon in dogs, especially compared with the incidence of the disease in the elbow and shoulder. When it does occur, the lateral aspect of the femoral condyle is most often involved (Figures 7-47 and 7-48). As in other species, such as the horse, osteochondritic lesions range from distinct cysts to vague subchondral lucency. Marginal defects occur occasionally but only rarely in conjunction with fragments. Osteochondritis of the patella is rare, with diagnosis often being of a presumptive nature. Patella abnormalities asserted to be the result of osteochon-

old Golden Retriever shows joint swelling, which is characteristic of early osteochondritis involving the medial ridge of the talus. B, Opposite hock is provided for comparison.

dritis by one group of authors were (1) soft tissue swelling, (2) multiple small peripatellar fragments, and (3) marginal irregularity. A tangential projection (cranioproximal–craniodistal oblique) of the patella was necessary to establish the left lateral location of the lesion.19 I also have seen an 8-month-old dog with bilateral osteochondritis-like lesions of the tibial tuberosity, which resembled Osgood–Schlatter disease in humans. In addition to the tibial lesions, the animal also had bilateral osteoarthritis and subluxation of the stifles, presumed to be secondary to the tibial lesions (Figure 7-49).

CHAPTER 7 ❚❚❚ Osteochondritis

163

B

A

Figure 7-45 • A, Close-up frontal view of hock in a dog with osteochondritis shows: (1) marked widening of the medial aspect of the tarsocrural joint, (2) marginal irregularity of the apex of the medial talar ridge, and (3) regional subchondral demineralization. B, The opposite tarsocrural joint is included for comparison.

Table 7-1 • THE INTERNATIONAL ELBOW WORKING GROUP’S CLASSIFICATION AND GRADING SYSTEM OF “ELBOW DYSPLASIA” IN DOGS Grade

Grading Criteria

0

Normal. No signs of arthrosis or minimal increased radiographic density in the ulna, caudal to the trochlear notch and/or head of the radius. Mild arthrosis with one or more of the following findings: (a) Less than 2-mm-high osteophyte formation seen on the dorsal edge of the anconeal process (b) Minimal osteophyte formation (<2 mm in any direction) on the dorsal proximal ridge of the radius (c) Or the coronoid process (d) Or the lateral palmar part of the humeral trochlear (e) Obvious sclerosis in the area caudal to the distal end of the ulnar trochlear notch to the proximal radius Moderate arthrosis: One or more of the following findings: (a) Osteophyte 2- to 5-mm high on the anconeal process (b) Moderate osteophyte formation (2-5 mm in any direction on locations b, c, d [as described for grade 1]) Severe arthrosis: One or more of the following findings: (a) Osteophyte > 5-mm high on the anconeal process (b) Severe osteophyte formation (>5 mm in any direction on locations b, c, d [as described for grade 1])

1

2 3

Modified from International Elbow Working Group Protocol. Vet Radiol & Ultrasound 36:172, 1995.

❚❚❚ CLASSIFICATION SCHEMES The International Elbow Working Group (IEWG) proposed a classification for what they term elbow dysplasia. In the proposed scheme, dysplastic canine elbows are graded numerically 1 through 3, depending on which radiographic abnormalities are present. Judgment is rendered on the basis of a single flexed lateral projection of the cubital joint (elbow). The particulars of their evaluation system are shown in Table 7-1.20

Alternatively, Lang and colleagues proposed what they term the Elbow Dysplasia (ED) Score, asserting that it is more sensitive than the IEWG system (especially in large-breed dogs 1 to 2 years of age) because it screens for the presence of arthritis as well as for dislocation and the various forms of osteochondritis.21 Radiographic judgment is made on the basis of two projections: a flexed mediolateral and a 10-degree craniolateral–caudomedial oblique. The specifics of their method are shown in Tables 7-2 and 7-3.

164

SECTION I ❚❚❚ The Extremities

B

A

C

D

Figure 7-46 • Close-up lateral (A) and frontal (B) views of a dog’s hock that resemble osteochondritis but actually constitute an old sprain fracture that has caused instability and widening of the tarsocrural joint (especially well seen in lateral projection). An avulsion fracture of the medial malleolus is also evident in the frontal view. C and D, The opposite tarsocrural joint is provided for comparison.

CHAPTER 7 ❚❚❚ Osteochondritis

Figure 7-47 • Close-up frontal view of the stifle shows a centrally located dimple in the margin of the lateral femoral condyle associated with a diffuse loss of density in the surrounding bone, one of the variants of osteochondritis in the dog.

165

Figure 7-49 • Close-up lateral view of the stifle shows an enlarged, pockmarked tibial tuberosity, caudal inclination of the tibial articulation, caudal displacement of the femur, and a swollen joint. These abnormalities (present bilaterally) were hypothesized to be results of a congenital overgrowth of the tibial tuberosity.

Table 7-2 • THE ELBOW DYSPLASIA GRADING/SCORING SYSTEM Grade

Score

Normal Grade 1 Grade 2 Grade 3

0-1 point (criteria 3, 4) 1 point in criteria 1 + 2 or up to 4 points in total 5-8 points >8 points or 3 points in any of the criteria 5-7

Modified from Lang J, Busato A, Baumgartners D, et al: Comparison of two classification protocols in the evaluation of elbow dysplasia in the dog. J Small Anim Pract 39:169, 1998.

A Personal Perspective In my estimation, both the IEWG and ED scoring systems are too complex for routine clinical use. Additionally, by omitting a nonflexed projection of the elbow, valuable information concerning the width of the humeroulnar and humeroradial joints is not available for consideration, information that often is critical in deciding ambiguous cases. Accordingly, I propose the following simplified method of assessing the canine elbow:

Figure 7-48 • Arthrogram: Close-up frontal oblique view of the lateral femoral condyle in an immature dog with severe osteochondritis shows an absence of articular cartilage beneath multiple cystlike lesions.

• First, no grades or scores are given. Because the assessment is subjective, the descriptors should be qualitative. Stating that the disease is mild, moderate, or severe is sufficient. Numerical classification may sound scientific but usually serves to do little more than clutter already overtaxed memories.

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SECTION I ❚❚❚ The Extremities

Table 7-3 • CRITERIA FOR SCORING ELBOW DYSPLASIA GRADES Score

1

2

3

4

5

6

7

Osteophytes on anconeal process

Osteophytes on other locations

Density of trochlea notch, ulna head, and radius

Congruity of humerulnar joint, “step” radius/ulna

Medial coronoid process

Anconeal process

Medial aspect of the humerii

0 points 1 point 2 points 3 points Modified from Lang J, Busato A, Baumgartners D, et al: Comparison of two classification protocols in the evaluation of elbow dysplasia in the dog. J Small Anim Pract 39:169, 1998.

• Second, the term elbow dysplasia should be abandoned as imprecise and replaced with the term osteochondritis. • Third, where possible, the diagnosis of osteochondritis should be refined (for example, osteochondritis of the coronoid process) by using characteristic osteoarthritic patterns to determine the most probable disease site (coronoid process, anconeal process, humeral condyle). • Fourth, if the articular surfaces of the proximal radius and ulna are misaligned, and there are no other abnormalities, the diagnosis is radioulnar subluxation (mild, moderate, or severe), which may or may not eventually lead to osteoarthritis. Bear in mind, however, that osteochondritis of either the coronoid or anconeal processes produces characteristic dislocation of the humeroulnar joint. • Fifth, radiographic judgment should be based on at least three projections: (1) a nonflexed lateral view (neutral or natural limb position), (2) a flexed lateral projection, and (3) a standard frontal (craniocaudal) view. Additional oblique or penetrated views may be added where needed.

References 1. De Haan JJ, Goring RL, Beale BS: What is your diagnosis? J Am Vet Med Assoc 201:927, 1992. 2. Swenson L, Audell L, Hedhammar A: Prevalence and inheritance of and selection for elbow arthrosis in Bernese mountain dogs and rottweilers in Sweden and benefit:cost analysis of a screening and control program. J Am Vet Med Assoc 210:215, 1997. 3. Ljunggren G, Olsson S-E: Osteoarthrosis of the shoulder and elbow joints in dogs: a pathologic and radiologic study of necropsy material. J Am Vet Rad Soc 16:33, 1975. 4. Henry WB: Radiographic diagnosis and surgical management of fragmented medial coronoid process in dogs. J Am Vet Med Assoc 184:799, 1884. 5. Voorhout G, Hazewinkel HAW: Radiographic evaluation of the canine elbow joint with special reference to the medial humeral condyle and the medial coronoid process. Vet Rad 28:158, 1987.

6. Berry C: Evaluation of the canine elbow for fragmented medial coronoid process. Vet Radiol Ultrasound 33:273274, 1992. 7. Farrow CS: Radiographic assessment of the cubital joint for dysplasia: limitations of the hyperflexed lateral projection. Abstracts: 1995 Annual Meeting of the American College of Veterinary Radiology. Vet Radiol Ultrasound 36:351, 1995. 8. Keller GG, Kreeiger JM, et al: Correlation of radiographic, necropsy and histologic findings in 8 dogs with elbow dysplasia. Vet Radiol Ultrasound 38:272, 1997. 9. Reichle JK, Park RD, Bahr AM: Computed tomographic findings of dogs with cubital joint lameness. Vet Radiol Ultrasound 41:125, 2000. 10. Snaps FR, Saunders JH, et al: Comparison of spin echo, gradient echo and fat saturation magnetic resonance imaging for imaging the canine elbow. Vet Radiol Ultrasound 39:518, 1998. 11. Craig PH, Riser WH: Osteochondritis in the proximal humerus of the dog. J Am Vet Rad Soc 6:40, 1965. 12. Carrig CB, Morgan JP: Microcirculation of the humeral head in the immature dog. J Am Vet Rad Soc 15:28, 1974. 13. Bree H: Evaluation of subchrondral lesion size in osteochondrosis of the scapulohumeral joint in dogs. J Am Vet Med Assoc 204:1473, 1994. 14. Callahan TF, Ackerman N: The supinated mediolateral radiograph for detection of humeral osteochondrosis in the dog. Vet Rad 26:144, 1985. 15. Story EC: Prognostic value of arthrography in canine osteochondrosis. Vet Clin North Am 8:301, 1978. 16. Van Bree HV, Ryssen BV, Desmidt M: Osteochondrosis lesions of the canine shoulder: correlation of positive contrast arthrography and arthroscopy. Vet Radiol Ultrasound 33:342, 1992. 17. Van Bree H, Van Ryssen B: Positive contrast shoulder arthrography with iopromide and diatrizoate in dogs with osteochondritis. Vet Radiol Ultrasound 36:203, 1995. 18. Newell SM, Mahaffey MB, Aron DN: Fragmentation of the medial malleolus of dogs with and without tarsal osteochondrosis. Vet Radiol Ultrasound 35:5, 1994. 19. Brizzee-Buxton BL, Lewis DL, et al: What is your diagnosis? J Am Vet Med Assoc 205:1537, 1994. 20. International Elbow Working Group Protocol. Vet Radiol Ultrasound 36:172, 1995. 21. Lang J, Busato A, et al: Comparison of two classification protocols in the evaluation of elbow dysplasia in the dog. J Small Anim Pract 39:169, 1998.

C h a p t e r

8

Congenital and Developmental Bone Disease ❚❚❚ THE ROLE OF DIETARY CALCIUM IN THE DEVELOPMENT OF BONE DISEASE Voorhout and Hazewinkel determined that the development of secondary ossification centers and longitudinal radial growth are inversely related to calcium intake.1 They reached this conclusion by feeding high, normal, and below normal amounts of calcium to Great Dane puppies and then observing the radiographic effects on the radius and ulna over time. Their observations are tabulated in Box 8-1.

❚❚❚ PARTIAL ABSENCE OF DISTAL LIMB Carrig and co-workers, as part of a multiinstitution collaboration, described the various iterations of ectrodactyly, the partial absence of a paw.2 For those seeking more information on the subject, I suggest medical textbooks because comparatively little has been published about this condition in dogs and cats.

❚❚❚ PANOSTEITIS The cause or causes of panosteitis are unknown. The disease affects mostly immature German shepherds, 6 to 18 months of age, and causes varying degrees of bone pain and associated lameness. Because the disease affects different bones at different times, the pattern of lameness changes, a phenomenon often described as a shifting leg lameness. Most affected dogs recover in a few months irrespective of treatment (rest, steroids, antibiotics, reduction in dietary protein, supplementary bone meal, to name a few), but some do not recover. Occasionally, mature dogs develop the disease and, like young dogs, usually recover spontaneously.3

Patches of medullary new bone characterize panosteitis radiographically. These abnormal bone deposits are predictably located in the distal aspect of the humeral shaft, distal femoral shaft, proximal radius and ulna, and proximal tibia. Chronic lesions are often associated with a thin layer of periosteal new bone. Once the disease subsides, the described lesions gradually disappear over the next few months. Figures 81 to 8-3 illustrate the typical appearance of this disease.

❚❚❚ METAPHYSEAL OSTEOPATHY (HYPERTROPHIC OSTEODYSTROPHY) The cause or causes of metaphyseal osteopathy (MO) are not known. The incidence of this disease appears lower than in the past; however, I continue to see two or three cases a year characterized by the following clinical profile: skeletally immature dog; large to medium-sized breed; marked quadrilateral lameness; hot swollen “joints,” particularly the radiocarpal regions; and variable systemic signs of illness (fever, abnormal blood values). Radiographically, the lesions are symmetrically distributed throughout both forelimbs and hindlimbs, affecting the metaphyseal sides of the growth plates. Like most radiographically visible ailments, there is a spectrum of change, with most advanced lesions exhibiting the classic double growth plate sign as well as variable amounts of metaphyseal bony cuffing. In severe cases, the metaphyseal cuffs can become extremely large. Figures 8-4 and 8-5 show the salient radiographic features of MO. Riser and Shirer described two variations of what they preferred to call hypertrophic osteodystrophy (HOD). Large bony cuffs surrounding the metaphysis and adjacent diaphysis characterize the first form of the disease, which they refer to as type 1. The type 2 variant resembles type 1 with respect to abnormal bone deposition, 167

168

SECTION I ❚❚❚ The Extremities

B o x

8 - 1

Radiographic Observations in the Radius and Ulna of Great Dane Puppies Fed High, Low, and Normal Amounts of Calcium

Above Normal Dietary Calcium

• Retarded development of the ulnar styloid process • Retarded development of the humeral medial epicondyle • Retarded development of the olecranon apophysis • Retarded development of the anconeal process

Normal Dietary Calcium (Control)

Normal

Below Normal Dietary Calcium

• Faster than normal development of secondary ossification centers

but it also features a radiolucent band in the upper part of the metaphysis, which looks like a second growth plate.4 In radiographically screening for this disease, I recommend a long-bone survey consisting of a lateral view of one front and one hindlimb, centered on the elbow and stifle, respectively, using either two 7- by 17-inch films or a single (alternatively shielded) 14- by 17-inch film. In the face of characteristic lesions identified in lateral projection, frontal views are unnecessary to confirm the diagnosis. Further surveys usually are motivated by curiosity and rarely play any significant role in treatment planning or prognosis. Because the disease occasionally affects the mandible and distal ribs, these areas should be imaged as dictated by suggestive clinical signs or physical findings. Most dogs recover regardless of treatment, not surprisingly, given that MO is a disease of unknown cause. Eventually, the metaphyseal bone deposition subsides and the bones slowly resume their original shapes. Some affected puppies develop bilateral valgus deformities in their mid and distal forelimbs. Although corrective ostectomy or osteotomy has been performed in a few animals, I am not convinced that it is necessary because most of these animals recover fully without surgery.

❚❚❚ HYPERTROPHIC PULMONARY OSTEOARTHROPATHY Background Hypertrophic pulmonary osteoarthropathy (HPOA), also known as hypertrophic osteopathy, is a painful secondary bone disease of unknown cause. Usually (but not exclusively) triggered by a lung mass or lobar pneumonia, HPOA is characterized by a uniquely config-

A

B Figure 8-1 • Close-up flexed lateral views of the right (A) and left (B) elbows of a young Basset Hound show medullary opacification in the right humerus and left radius consistent with panosteitis.

ured bone deposition, which typically forms on the outside surfaces of the bones of the front or hind paws, and slowly progresses proximally. Occasionally, abdominal masses trigger the disease, but this is relatively rare. The cause (or causes) of HPOA is not known, but speculation continues to focus on a pair of possible explanations known as the humeral and neuronal theories, both of which attribute the characteristic new bone formation to peripheral hyperemia. Advocates of the humeral theory contend that HPOAdevelops as a result of peripheral vasodilatation secondary to the formation of arteriovenous shunts within the inciting lung lesion. Supporters of the neuronal theory also posit a peripheral hyperemia but instead ascribe it to a vagally mediated reflex initiated by the pulmonary mass.5

Imaging Findings The radiographic appearance of HPOA varies from relatively smooth, plaque-like bone deposit (Figure

CHAPTER 8 ❚❚❚ Congenital and Developmental Bone Disease

A

169

B

Figure 8-2 • Close-up lateral views of the proximal (A) and distal (B) aspects of the radius and ulna show medullary opacification consistent with panosteitis.

8-6) to coralization (Figure 8-7). Some animals exhibit a highly distinctive form of new bone deposition resembling a line of blocks stacked on the cortical surface.

❚❚❚ RETAINED CARTILAGE CORE (RETAINED HYPERTROPHIED ENCHONDRAL CARTILAGE IN THE ULNAR METAPHYSIS)

dislocate, eventually leading to osteoarthritis. In these respects, the retained cartilage core resembles premature closure of the distal ulnar growth plate following injury. Caution: Voorhout and co-workers showed that many normal Great Dane puppies have retained cartilage cores in their distal ulnar metaphyses between 15 and 21 weeks of age.6

Imaging Findings Background The so-called retained cartilage core has always been a rarity, but it is even more so now. Traditionally found in giant-breed dogs such as the Great Dane, and categorized as a metabolic bone disease (even though its cause was unknown), cartilage cores are now grouped with “pediatric” or developmental bone disorders. The retention of a core of hyaline cartilage within the distal ulnar metaphysis may adversely affect bone growth by retarding ulnar length, thus causing the radius to bow cranially and, more importantly, causing the humeroulnar joint to partially

Riser and Shirer published a brief but informative account of the radiographic features of this disease, which I have summarized as follows.7 • The disease is symmetric; that is, it affects both forelimbs: primarily the distal ulna and secondarily the radial shaft and elbow joint. • The lesion, located in the distal ulnar metaphysis and diaphysis, usually resembles the lateral profile of a cone, outlined by a radiodense band (Figure 8-8). Less often, the cartilage core appears solid and is shaped like a slim candle flame. Occasionally, the abnormal core appears to be composed of

170

SECTION I ❚❚❚ The Extremities

A

B

Figure 8-3 • Long (A) and close-up (B) views of the humerus of two dogs show medullary opacification consistent with panosteitis.

CHAPTER 8 ❚❚❚ Congenital and Developmental Bone Disease

171

B A

C

D Figure 8-4 • Close-up views of proximal (A) and distal (B) humerus, proximal and distal radius (B, C), and distal femur and proximal tibia (D). All show a dark band on the metaphyseal side of the growth plate, the hallmark of metaphyseal osteopathy.

172

SECTION I ❚❚❚ The Extremities

A

B

Figure 8-5 • Orientation (A) and close-up (B) views of the tibia of a dog with metaphyseal osteopathy show the characteristic bony blooms associated with chronicity.

CHAPTER 8 ❚❚❚ Congenital and Developmental Bone Disease

173

B

A

C Figure 8-6 • A, Close-up frontal view shows layers of new bone coating the profiled surfaces of the distal radial and ulnar bodies, the result of hypertrophic pulmonary osteoarthropathy secondary to a bronchogenic carcinoma (B, C).

high-density bone, outlined by a lucent band (or perhaps by a Mach band). • The radius may be bowed, depending on the influence (if any) of the cartilage core on ulnar growth. • The humeroulnar joint may be subluxated.

smaller by the time they reach 4 months of age. An abbreviated torso and short limbs, due to retarded axial and appendicular bone growth, also characterize affected puppies. This decreased stature, however, does not appear to be related to any disability.

Imaging Findings

❚❚❚ HYPOCHONDROPLASTIC DWARFISM Background Hypochondroplastic dwarfism, a heritable form of chondrodysplasia, has been reported in a number of dog breeds (Figure 8-9). Affected animals appear normal at birth but fail to keep pace with the growth of their littermates, usually appearing obviously

Sande and co-workers provided a detailed radiographic description of the skeletal abnormalities associated with dwarfism in Alaskan Malamutes from birth to maturity.8 These changes are shown chronologically in Table 8-1. Radiographic abnormalities associated with dwarfism have also been reported in Irish Setters, including shortening of long bones and variable degrees of forelimb curvature (bowing of the radius and ulna). Growth plates and flat bones appeared unaffected.9

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Table 8-1 • SKELETAL FORELIMB ABNORMALITIES IN ALASKAN MALAMUTE DWARFS Age

Radius

Ulna

Other Bones

7-10 days

Shorter than unaffected animals

Flattening of distal metaphysis (most consistent finding) Like the radius, the ulna is shorter than normal

Delayed ossification of accessory carpal bones

3 wk

Distal radial metaphysis is abnormally flattened and irregular, with a narrow, highdensity band situated along its margin Radius (and ulna) remains abnormally short

Distal ulnar metaphysis remains flattened and irregular instead of assuming its normal triangular shape

5 wk

Radial (and ulnar) length now noticeably shorter than normal

Distal ulna remains flattened or becomes concave Trabeculation appears haphazard rather than organized Ulnar body is the same length as that of the radius, where normally the ulnar shaft is decidedly longer Abnormal limb curvature is now physically and radiographically evident

Distal aspects of the ribs appear flared and concave

12 wk

Distal radial margin is concave and flared Dense band on the metaphyseal side of the growth plate has increased Difference in radial and ulnar length becomes more pronounced

Distal ulnar metaphysis is abnormally widened with course Trabeculation and a serrated margin Curvature increases, and is now accompanied by lateral deviation of the paw Width/length ratio of the ulna dramatically increases

The carpal bones appear immature

6 mo

Distal metaphysis remains wide and flat Gap between the radial and ulnar metaphyses continues to increase

Distal metaphysis increases in width and flares Overall length may be reduced by as much as a third (compared with normal) Trabeculae remain coarse and disorganized in appearance Curvature continues with adaptive thickening of the cortices along the lesser curvatures of the diaphysis Width of the ulna continues to be disproportionately wide compared with its length (approximately 1 : 10, compared with a normal ratio of 1 : 25)

11 mo

Radial (and ulnar) curvature persists Compensatory thickening of the caudal radius (and ulna) cortex remains

Distal ulnar metaphysis is now shaped normally as the associated growth plate closes Distance between radial and ulnar metaphyses is normal or near normal Disorganized trabeculation is present in the distal portions of both the radius and ulna, but metaphyseal trabeculation appears normal Increased width-to-length ratio persists

CHAPTER 8 ❚❚❚ Congenital and Developmental Bone Disease

Figure 8-7 • Defleshed distal radius and ulna of a dog with hypertrophic pulmonary osteoarthropathy shows bony coralization induced by a primary lung tumor.

175

Figure 8-9 • Radius and ulna from an Alaskan malamute puppy with hypochondroplastic dwarfism show the shortness and thickening characteristic of this disease.

❚❚❚ NUTRITIONAL SECONDARY HYPERPARATHYROIDISM Background

Figure 8-8 • Close-up frontal view of the distal radius and ulna show an inverted ‘V’ in the distal ulnar metaphysis (emphasis zone), signaling the presence of a retained cartilage core.

Nutritional secondary hyperparathyroidism is now a rarity among pet animals, although it is still regularly encountered in exotic animals, particularly pet iguanas. Hyperparathyroidism is caused by insufficient dietary calcium, a feature of all-meat diets, which are also low in phosphorus. The resultant mineral deficiencies are partially compensated for by (1) increased absorption of intestinal calcium, (2) decreased excretion of urinary calcium, and (3) resorption of skeletal calcium. Nevertheless, neither the body’s efforts to conserve calcium nor its aggressive removal of calcium from the bones can prevent an elevation in parathormone. The result is the further depletion of skeletal calcium, eventually causing a radiographically visible decrease in bone density (osteopenia).10

❚❚❚ SCOTTISH FOLD OSTEODYSTROPHY Scottish fold osteodystrophy is a heritable bone disease of kittens that initially is expressed as a short, thickened, rigid tail and later by thickened carpi and tarsi.

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Radiographically the metacarpal and metatarsal bones appear abnormally shortened, bowed, and have deformed, conical epiphyses. The vertebrae of the tail are abnormally short and disproportionately wide, with distinctively flared metaphyses and misshapen epiphyses.11

❚❚❚ SKELETAL AND OCULAR DYSPLASIA IN LABRADOR RETRIEVERS Carrig and co-workers described heritable, combined skeletal–ocular dysplasia in Labrador Retrievers.12 Skeletal abnormalities are confined to the limbs and include long-bone shortening and abnormal joint development, particularly of the cubital and coxal joints. The authors recommend using the abnormally shortened radius and ulna as a means of identifying affected pups. Associated ocular abnormalities, although not pathognomonic, include cataracts, vitreal strands, persistent hyaloid remnants, retinal folds, retinal dysplasia, peripapillary hyperreflectivity, and rhegmatogenous retinal detachment.

❚❚❚ CONGENITAL HYPOTHYROIDISM Saunders and Jezyk described the skeletal abnormalities associated with congenital hypothyroidism: (1) a short, broad skull; (2) shortened vertebral bodies, (3) epiphyseal dysgenesis, a condition in which epiphyseal centers may be irregularly formed or appear to be fragmented or stippled; (4) delayed epiphyseal appearance; and (5) delayed epiphyseal maturation.13

❚❚❚ DISSEMINATED IDIOPATHIC HYPEROSTOSIS Morgan and Stavenborn reported diffuse periarticular and extraarticular bone deposition in a 4-year-old Great Dane involving the spine, humeral, cubital, coxal, and genual joints.14 The authors termed the condition disseminated idiopathic skeletal hyperostosis, or “DISH,” noting that it resembled Forestier’s disease in people. Diagnostic criteria are extensive and include the following: • Flowing calcification and ossification along ventral and lateral aspects of three contiguous vertebral bodies leading to segmental bony ankylosis

• Relative preservation of the disc width within involved areas and absence of extensive radiographic changes of degenerative disc disease, such as endplate sclerosis, nuclear calcification, or localized spondylosis deformans • Periarticular osteophytes surrounding true vertebral joints • Formation of pseudoarthrosis between the bases of the dorsal spinous processes • Periarticular osteophytes and calcification or ossification of soft tissue attachments (enthesiophytes) in both axial and peripheral potions of the skeleton • Periarticular osteophytes, sclerosis, and ankylosis of sacroiliac joints • Bony ankylosis of the symphysis pubis

References 1. Voorhoot G, Hazewinkel HAW: A radiographic study on the development of the antebrachium in Great Dane pups on different calcium intakes. Vet Rad 28:152, 1987. 2. Carrig CB, Wortman JA, et al: Ectrodactyly (split-hand deformity) in the dog. Vet Rad 22:123, 1981. 3. Sebesstyen P: What is your diagnosis? J Am Vet Med Assoc 212:494, 1998. 4. Riser WH: Radiographic differential diagnosis of skeletal disease of young dogs. J Am Vet Rad Soc 5:15, 1964. 5. Wylie KB, Lewis DD, Pechman RD, et al: Hypertrophic osteopathy associated with Mycobacterium fortuitum pneumonia in a dog. J Am Vet Med Assoc 202:1986, 1993. 6. Voorhout G, Nap RC, Hazewinkel HAW: Aradiographic study on the development of the antibrachium in Great Dane pups, raised under standardized conditions. Vet Radiol Ultrasound 35:271, 1994. 7. Riser WH, Shirer JF: Normal and abnormal growth of the distal foreleg in large and giant dogs. J Am Vet Rad Soc 6:50, 1965. 8. Sande RD, Alexander JE, Padgett GA: Dwarfism in the Alaskan Malamute: its radiographic pathogenesis. J Am Vet Rad Soc 15:10, 1974. 9. Hanssen I, Falck G: Hypochondroplastic dwarfism in the Irish Setter. J Small Anim Pract 39:10, 1998. 10. Tomsa K, Glaus T: Nutritional secondary hyperparathyroidism in 6 cats. J Small Anim Pract 40:533, 1999. 11. Partington BP, Williams JF, Pechman RD: What is your diagnosis? J Am Vet Med Assoc 209:1235, 1996. 12. Carrig CB, Schmidt GM, et al: Growth of the radius and ulna in Labrador Retriever dogs with ocular and skeletal dysplasia. Vet Rad 31:165, 1990. 13. Saunders HM, Jezyk PK: The radiographic appearance of canine congenital hypothyroidism: skeletal changes with delayed treatment. Vet Rad 32:171, 1991. 14. Morgan JP, Stavenborn M: Disseminated idiopathic skeletal hyperostosis (DISH) in a dog. Vet Rad 32:65, 1991.

C h a p t e r

9

Miscellaneous Extremital Disorders ❚❚❚ DISLOCATION OF THE PATELLA (PATELLAR SUBLUXATION, PATELLAR LUXATION) Congenital Medial dislocation of the patella is most common in toy breeds. Typically, the major long bones of the knee, the femur, and the tibia appear S-shaped when viewed frontally. Arguments abound as to whether the displaced patella causes the change in bone shape or whether the deformed limb bones cause the dislocation of the patella. In general, small dogs dislocate their patellae medially (Figure 9-1, A), whereas large dogs do so laterally (Figure 9-1, B). Medium-sized dogs can go either way. An experimental study designed primarily to induce hip dysplasia in Greyhounds by administering estradiol coincidentally showed that the same drug also caused underdevelopment of the patellar groove and, subsequently, medial dislocation of the patella. This finding led the authors to challenge the then widely held belief that patellar luxation led to hypoplasia of the trochlear groove.1 In giant breeds (and some large breeds as well), congenital or developmental patellar dislocation is usually lateral (as mentioned previously). One theory to explain this difference between patellar dislocation in giant and toy breeds contends that lateral subluxation is induced by a preceding medial bowing of the hind limbs at the level of the stifles: a so-called genu valgum deformity. The authors hypothesize that this deformity is caused by a slowing of growth in the lateral aspects of the distal femoral and proximal tibial growth plates, which is prompted by a growth-related physeal ischemia.2

Traumatic Traumatic dislocation of the patella nearly always is associated with a sprain or sprain-avulsion fracture. The key to radiographic diagnosis is the position of the patella when the injured limb is viewed in the

neutral position. If the patella is displaced proximally, the distal patellar tendon is ruptured or the tibial tuberosity is avulsed. If the patella is displaced distally, the quadriceps is torn or the proximal patellar tendon is ruptured. If the patella is oriented horizontally, articular surface facing downward (when viewed in lateral projection), the proximal portion of the patella has torn free from the parapatellar fibrocartilages and femoropatellar ligaments and rotated backwards 90 degrees (rotary intraarticular dislocation).3

❚❚❚ MINERALIZATION OF THE SUPRASPINATUS TENDON Mineralization of soft tissue, particularly muscles and tendons, traditionally has been considered presumptive evidence of injury (dystrophic calcification). Precise radiographic localization is often impossible, however, to the extent that small chip fractures, detached osteochondral fragments, osteophytes, and vestigial sesamoid bones cannot always be distinguished from soft tissue mineralization. A case in point is the shoulder joint of large-breed dogs, where small, oval-shaped bony objects are regularly observed superimposed on or adjacent to the greater tubercle of the humerus and frequently are described as incidental findings (especially if present bilaterally in a sound dog). Flo and Middleton assert that abnormal bone densities in this location are potentially located within the supraspinatus tendon or on the surface of the underlying intertubercular groove. They advocate a skyline projection of the proximal humerus, which they contend optimizes the appearance of the lesion and differentiates supraspinatus from bicipital lesions.4 In a related article, Laitinen and Flo report that the mineralized tissue in the supraspinatus tendon, surgically removed from a series of dogs 5 years earlier, had re-formed, although all but one of the animals were 177

178

SECTION I ❚❚❚ The Extremities

A

A

B Figure 9-2 • Lateral (A) and tangential (B) views of the greater

B Figure 9-1 • A, Close-up frontal (viewer’s left) and lateral (viewer’s right) views of the stifle of a small dog show medial dislocation of the patella. B, Close-up lateral view of the stifle of a large-breed dog shows lateral dislocation of the patella.

now sound. These later findings cast further doubt on the merits of surgery compared with rest or medical treatment.5

❚❚❚ MINERALIZATION OF THE BICEPS BRACHII TENDON Muir and co-workers chronicle the case of a young Rottweiler in which they diagnosed mineralization of the biceps brachii tendon. Borrowing liberally from the literature on rotator cuff injuries in people, the authors term their finding calcifying tendinopathy and speculate that it was most likely the result of an earlier injury that had damaged the tendon’s blood supply, leading to metaplasia.6

❚❚❚ BICIPITAL TENOSYNOVITIS Barthez and Morgan reported using plain radiography and arthrography to diagnose bicipital tenosynovitis in the dog.7 The primary plain film radiographic

humeral tubercle show multiple bony densities on the lateral edge of the bicipital groove. Diagnosis is not clear-cut in this case, but tenosynovitis is a possibility.

disease indicator (RDI) for tenosynovitis is increased bone density in the intertubercular groove, as seen in lateral projection. Alternatively (and more frequently in my experience), the disease may appear as one or more discrete, fragment-like bone densities arrayed along the outer margin of the greater tubercle, as seen in lateral or frontal oblique projections (Figure 9-2, A, B). Arthrographic RDIs compatible with tenosynovitis include (1) diminished or incomplete filling capacity of the bicipital tendon sheath, (2) abnormal narrowing of the bicipital tendon sheath, and (3) marginal irregularity of the bicipital tendon sheath (Figure 9-3, A, B). Iohexol was used as a contrast medium at a concentration of 100 mg/ml and a dose of 0.4 ml/kg. The volume of contrast injected into an individual shoulder joint was determined by a combination of factors: (1) the completeness of bicipital tendon sheath filling (as observed fluoroscopically) and (2) increasing injection pressure.

❚❚❚ GASTROCNEMIUS AVULSION Both traumatic and atraumatic avulsion of the gastrocnemius muscle have been reported. In one especially unusual instance, bilateral atraumatic avulsion of the origin of the gastrocnemius muscle was

CHAPTER 9 ❚❚❚ Miscellaneous Extremital Disorders

179

A

Figure 9-4 • Close-up lateral radiograph of the proximal aspect of the calcaneus and distal part of the Achilles tendon shows marked swelling with islands of dystrophic calcification, the results of a third-degree strain.

B Figure 9-3 • A, Close-up tangential view of the greater humeral tubercle shows multiple bone-like densities on the proximolateral slope of the bicipital groove suggesting tenosynovitis. B, Closeup lateral arthrogram shows (1) synovial distension, (2) abnormal thinning, and (3) marginal irregularities of the bicipital tendon.

described. Associated radiographic abnormalities included (1) new bone on the caudal aspect of the distal femur, (2) bone spurs on the fabellae, and (3) displacement of a single fabella (inconsistent finding).8 Distal Achilles tears are more common, however, usually associated with calcaneal bone deposition, disfigurement, and dystrophic calcification (Figure 9-4).

❚❚❚ TUMORAL CALCINOSIS The term tumoral calcinosis refers to a comparatively rare, extensively mineralized soft tissue mass, which characteristically forms adjacent to the humeral, cubital, coxal, and genual joints of large breed dogs (Figure 9-5).9 Tumoral calcinosis also has been reported in the cervical musculature of German Shepherds, adjacent to the spine.10 Depending on the radiographic projection and the position of the mass relative to the adjacent vertebrae, tumoral calcinosis can be mistaken for a spinal tumor. It is difficult to distinguish tumoral calcinosis from other forms of soft tissue calcification, such as a calcified hematoma, other than on the basis of its preferred locations.

Figure 9-5 • Close-up frontal view of the elbow of a dog shows a calcified mass superimposed on the lateral aspect of the cubital joint (emphasis zone). The texture of the mass is distinctive, being composed of a number of closely approximated, roughly spherical bone-like densities, a feature strongly indicative (along with its periarticular location) of tumoral calcinosis.

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SECTION I ❚❚❚ The Extremities

❚❚❚ CALCANEAL DISLOCATION OF THE SUPERFICIAL DIGITAL FLEXOR TENDON

over the suspected lesion, constitutes strong presumptive evidence of an AV fistula.17

Imaging Findings The tendon of the superficial digital flexor muscle attaches to either side of the proximal part of the calcaneus. If one of these two insertions gives way, the tendon slips to the opposite side, where it is still attached, resulting in acute lameness and a characteristic eccentric swelling. Prevailing theory holds that dislocation of the Achilles is most likely the result of injury. Shetland Sheepdogs, especially if overweight, are thought to be at greatest risk, although there is no indication that this is a heritable trait.11

Plain films are useful in establishing the presence of bone involvement and also may be used to plot roughly the limits of the fistula (Figure 9-6). Whereas ultrasound can be used to identify the principal vascular components of an AV fistula, and to some extent the presence of accelerated venous blood flow, angiography is indispensable for accurate and effective presurgical planning (Figures 9-7 and 9-8).18

❚❚❚ BONE INFARCT

Lameness Secondary to Arterial Blockage by Heartworms

Bone infarction is a rarity in pet animals. Scattered reports by Riser and co-workers describe infarcts in the long bones of dogs caused by malignant bone tumors.12 Madewell and co-workers also reported finding long-bone infarcts in a dog with renal adenocarcinoma.13

Occasionally, heartworms obstruct a major peripheral artery, causing varying degrees of pain, lameness, and disability.19 In some instances, ischemic ulceration may develop on the paw surface.20 Again, angiography is required for diagnosis.

Radiation-induced Bone Lesions

❚❚❚ STRAINED ILIOPSOAS MUSCLE Breur and co-workers reported acute iliopsoas muscle strain in three dogs. They were able to diagnose the lesion by eliciting pain when the affected hip was simultaneously extended and internally rotated. Sonographically, the damaged muscle was described as hypoechoic and swollen.14 Seims and Breur published an account of a severe strain and subsequent contracture of the infraspinatus muscle of a Brittany Spaniel.15

❚❚❚ OSTEOPETROSIS SECONDARY TO MYELOPHTHISIC ANEMIA As described elsewhere in this section, osteopetrosis is most often a congenital disease, but occasionally it can be acquired, as exemplified by its development in a dog with severe myelophthisic anemia.16

❚❚❚ ARTERIOVENOUS FISTULA Background Most arteriovenous (AV) fistulas are caused by injuries, especially deeply penetrating wounds, such as gunshots. Other causes include severe bite wounds, lacerations, and amputations (both surgical and traumatic). Highly invasive tumors, necrotizing infections, and the inadvertent perivascular injection of thiobarbiturates and other highly injurious chemicals are also capable of creating direct AV communications. The presence of fremitus, a palpable vibration detectable

Morgan and Pool reported the appearance of bone lesions produced by experimental radium poisoning in dogs, some of which later became cancerous (malignant transformation).21 The precancerous lesions were, for the most part, destructive in appearance, initially appearing, in the words of the authors, as “linear cortical porosities.” Later, a futile attempt to restore the damaged cortex (a unique form of bone deposition) was observed; the authors termed it a neocortex. This resultant disturbance in the ability of the damaged bone to repair itself (as determined histologically) was termed radiation osteodystrophy. Eventually, the lesions began to assume the radiographic features of malignancy, such as poorly defined margins, long transition zones, and varying degrees of cortical disintegration.

❚❚❚ SKELETAL LEISHMANIASIS Background Turrel reported multiple bone lesions in a small group of dogs with visceral leishmaniasis, a protozoal disease transmitted by sand flies that is usually contracted in the Middle East and in countries bordering the Mediterranean Sea.22 The disease resembles Hepatozoon canis, which commonly affects the reticuloendothelial system (lymph nodes, spleen, liver, and bone marrow), kidneys, and skin.

Imaging Findings Lesions can develop nearly anywhere in the skeleton, including the shafts of long bones, bodies of irregular

CHAPTER 9 ❚❚❚ Miscellaneous Extremital Disorders

181

B

A

Figure 9-6 • Frontal (A) and lateral (B) close-ups of a hind paw show a large, full-length swelling over the lateral aspect that enlarged with exercise and shrank with rest. It later proved to be an arteriovenous fistula.

bones (e.g., carpus and tarsus), sesamoids (e.g., patella), flat bones (e.g., pelvis and scapula), and cranium. Longbone lesions resemble panosteitis, initially appearing as focal or regional areas of increased medullary density and later developing faint overlying periosteal cuffs. Lesions in other locations usually appear destructive. Joint swelling typically accompanies intraarticular lesions.22

❚❚❚ PERIPHERAL NERVE SHEATH TUMOR Platt and co-workers described a palpable malignant nerve sheath tumor (malignant schwannoma) in a dog. The tumor grew in the radial nerve adjacent to the proximal humeral body. The tumor imaged sonographically and with magnetic resonance caused chronic, progressive, unilateral forelimb lameness with associated

muscle atrophy. Electromyography showed denervation potentials in all muscles innervated by the radial nerve. T2 images revealed a medium-sized, welldefined hyperintense lobulated mass in the soft tissues of the proximal brachial region, which showed marked enhancement in T1, following administration of intravenous gadolinium.23

❚❚❚ NEUROMA Hudson and co-workers reported the sonographic identification of an 8-mm neuroma, which formed on the proximal stump of the tibial nerve following experimental transection 5 weeks earlier. The described neuroma appeared as a hypoechoic, tapered oval with a short blunted tail;24 however, the prospects of sonographically identifying naturally occurring neuromas appear remote.

182

SECTION I ❚❚❚ The Extremities

A

B

Figure 9-7 • Arteriovenous fistula: Lateral (A) and lateral close-up (B) arteriograms of a large posttraumatic arteriovenous fistula in the soft tissues of the mid lower forelimb of a dog show characteristic features, including (1) multiple large venous sinuses (patchy white areas), (2) an increased number of blood vessels, (3) vascular tortuosity, and (4) regional swelling (with a palpable vascular vibration).

❚❚❚ EXTREMITAL ISCHEMIA Goggin and co-workers reported the use of nuclear imaging to evaluate distal extremital perfusion in a variety of animals suffering from freeze injury, thromboembolism, vasculitis, electric shock, overly tight bandages, and devascularizing injuries. Limb scans were performed 5 and 10 minutes following injection of technetium-99 (99mTc)-MDP or 99mTc-DTPA. According to the authors, the results correlated closely with clinical outcome.25

❚❚❚ VILLONODULAR SYNOVITIS Background Villonodular synovitis occurs occasionally in horses (most often in the dorsal aspect of the fetlock) but

only rarely in dogs (carpus, stifle, hip). Most often, the lesion appears as a discrete mass and, as such, is amenable to surgical removal. At other times, the lesion is not so well defined, more closely resembling a diffuse synovial hypertrophy, which is not so readily extirpated. Some lesions are pigmented, but others are not, explaining use of the qualifier pigmented (as in pigmented villonodular synovitis). The precise cause of tumoral or diffuse villonodular synovitis is unknown; however, speculation continues to center on either repetitive injury or joint hemorrhage (hemarthrosis).

Imaging Findings Hanson described a case of villonodular synovitis in the carpus of an 8-year-old Shepherd cross.26 Radiographic abnormalities were confined to the craniome-

CHAPTER 9 ❚❚❚ Miscellaneous Extremital Disorders

A

183

B

Figure 9-8 • Close-up frontal views of proximal (A) and distal (B) radius and ulna of a dog with a proximal arteriovenous fistula caused by repeated surgeries to remove a suspected quill fragment. Close inspection of both images reveals many small intravascular filling defects, the result of blood clots caused by catheterization.

dial aspect of the distal radius and the underlying radiocarpal joint and included (1) multiple, vague areas of periarticular and extraarticular bone loss; (2) numerous small bone deposits; (3) decreased width of the cartilage space; and (4) eccentrically positioned joint swelling. As the author points out, these radiographic findings (or similar abnormalities) potentially may be shared by a wide variety of joint disorders, including posttraumatic osteoarthritis, immunoarthritis (immune-mediated osteoarthritis), infectious arthritis, parasitic osteoarthritis, tumors such as synovioma and synovial sarcoma, chronic hemarthrosis, amyloidosis, and osteochondromatosis.26 My preference in such cases is to begin with plain films to evaluate the nearby bone and joint

and then to follow with ultrasound (plus or minus an ultrasound-guided biopsy). Only rarely is singleor double-contrast arthrography necessary. In small dogs and cats, neither procedure tends to be informative.

❚❚❚ HINDQUARTER WEAKNESS AND PAIN DUE TO AORTOILIAC THROMBUS Drost and co-workers described the multimodality appearance of a caudal aortic–iliac thrombus in a dog with hindquarter weakness and pain.27 Radiographs showed calcification in the caudodorsal aspect of the abdomen thought to represent possible aortic calcifi-

184

SECTION I ❚❚❚ The Extremities

Figure 9-9 • Close-up lateral view of catheter fragment lodged in the cephalic vein of a dog (emphasis zone).

cation. Sonography showed narrowing and turbulent blood flow in the caudal aorta consistent with a thrombus, a diagnosis that was further supported by magnetic resonance angiography. Aortography revealed obstruction of the caudal aorta and the presence of sublumbar collaterals.

❚❚❚ INTRAVENOUS CATHETER FRAGMENTS Catheter fragments occasionally become lodged in receiving arteries or veins, leading to thrombosis and sometimes emboli. Small, superficially located catheter fragments are radiographically detectable if they contain a radiopaque marker; otherwise, they are invisible. In the latter instance, ultrasound can be used. Most catheter fragments lodge in the cephalic vein, simply because this is where most intravenous catheters are placed (Figure 9-9). Catheters do break off (or are cut off) elsewhere, for example, in the jugular vein. In some instances, these fragments eventually reach the heart or even the lung. Small fragments, lodged deep within the interior, can be extremely difficult to identify radiographically, even when they contain a safety marker. In human patients, radiologists, practicing one of the newer imaging subspecialties, interventional radiology, now often retrieve deep catheter fragments.

❚❚❚ DISLOCATED SURGICAL PINS Both the veterinary and medical radiographic literatures abound with descriptions of the unintended jour-

Figure 9-10 • Ventrodorsal view of the hips (right side slung) shows a dislocated intramedullary (IM) pin. The implant had been placed through the hip joint following dislocation to keep it in position while it healed but subsequently become dislodged, migrating deep inside the pelvic canal, doing considerable damage in the process.

neys of surgical implants, especially pins. Surprisingly, many of these stray implants seem to do little harm, but occasionally some do (Figure 9-10).

References 1. Gustafasson PO, Kasstrom H, Ljunggren G: Estradiol induced patellar luxation in the dog: an experimental study. J Am Vet Rad Soc 10:49, 1969. 2. Riser WH, Parkes LJ, et al: Genu valgum: a stifle deformity of giant dogs. J Am Vet Rad Soc 10:28, 1969. 3. Gee M, Lenehan TM, Tarvin GB: Rotary intra-articular dislocation of the patella in two dogs. J Am Vet Med Assoc 209:2082, 1996. 4. Flo GL, Middleton D: Mineralization of the supraspinatus tendon in dogs. J Am Vet Med Assoc 197:95, 1990. 5. Laitinen OM, Flo GL: Mineralization of the supraspinatus tendon in dogs: a long-term follow-up. J Am Anim Hosp Assoc 36:262, 2000. 6. Muir P, Goldsmid SE, et al: Calcifying tendinopathy of the biceps brachii in a dog. J Am Vet Med Assoc 201:1747, 1992. 7. Barthez PY, Morgan JP: Bicipital tenosynovitis in the dog—evaluation with positive contrast arthrography. Vet Radiol Ultrasound 34:325, 1993. 8. Robinson A: Atraumatic bilateral avulsion of the origins of the gastrocnemius muscle. J Small Anim Pract 40:498, 1999. 9. Mahoney PN, Lamb CR: Articular, periarticular and juxtaarticular calcified bodies in the dog and cat: a radiologic review. Vet Radiol Ultarsound 37:3, 1996. 10. Morgan PW, Cockshutt J: What is your diagnosis? J Am Vet Med Assoc 203:969, 1993. 11. Mauterer JV, Prata RG, et al: Displacement of the tendon of the superficial digital flexor muscle in dogs: 10 cases (1983-1991). J Am Vet Med Assoc 203:1162, 1993. 12. Riser WH, Brodey RS, Biery DN: Bone infarctions associated with malignant bone tumors in dogs. J Am Vet Med Assoc 160:411, 1972.

CHAPTER 9 ❚❚❚ Miscellaneous Extremital Disorders

13. Madewell BR, Wilson DW, et al: Leukemoid blood response and bone infarcts in a dog with renal tubular adenocarcinoma. J Am Vet Med Assoc 197:1623, 1990. 14. Breur GJ, Blevins WE: Traumatic injury of the iliopsoas muscle in three dogs. J Am Vet Med Assoc 210:1631, 1997. 15. Seims JJ, Breur GJ, et al: Use of two-dimensional realtime ultrasonography for diagnosing contracture and strain of the infraspinatus muscle in a dog. J Am Vet Med Assoc 212:77, 1998. 16. O’Brien SE, Riedesel EA, Miller ID: Osteopetrosis in an adult dog. J Am Anim Hosp Assoc 23:213, 1987. 17. Ackerman N, Ticer J: Phalangial arteriovenous fistula in a dog. Vet Rad 22:85, 1981. 18. Bouayard H, Feeney DA, et al: Peripheral acquired arteriovenous fistula: a report of four cases and literature review. J Am Anim Hosp Assoc 23:205, 1987. 19. Burt JK, Lipowitz AJ, Harris JH: Femoral artery occlusion by Dirofilaria immitis in a dog. J Am Vet Rad Soc 18:166, 1977.

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20. Berry CR: Answers for film reading session: 1995 A.C.V.R. annual meeting. Vet Radiol Ultrasound 36:449, 1995. 21. Morgan JP, Pool RR: Radium-236-induced bone lesions in beagles. Vet Rad 23:261, 1982. 22. Turrel JM, Pool RR: Bone lesions in four dogs with visceral leishmaniasis. Vet Rad 23:243, 1982. 23. Platt SR, Graham J, et al: Magnetic resonance imaging and ultrasonography in the diagnosis of a malignant peripheral nerve sheath tumor in a dog. Vet Radiol Ultrasound 40:367, 1999. 24. Hudson JA, Steiss JE, et al: Ultrasonography of peripheral nerves during Wallerian degeneration and regeneration following transection. Vet Radiol Ultrasound 37:302, 1996. 25. Goggins JM, Hoskinson JJ, et al: Scigraphic assessment of distal extremity perfusion in 17 patients. Vet Radiol Ultrasound 38:211, 1997. 26. Hansen JA: Canine carpal villonodular synovitis. Vet Radiol Ultrasound 39:15, 1998. 27. Drost WT, Bahr RJ, et al: Aortoiliac thrombus secondary to a mineralized arteriosclerotic lesion. Vet Radiol Ultrasound 40:262, 1999.

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Skeletal Deficiencies, Dysplasias, and Deformities ❚❚❚ DELAYED GROWTH PLATE CLOSURE IN CASTRATED AND SPAYED CATS Root and co-workers reported delayed growth plate closure in gonadectomized cats.1 Specifically, male kittens castrated at 7 weeks or 7 months had delayed distal radial closure compared with noncastrated animals. Females experienced similar delays, demonstrating the role of gonadal steroids in normal skeletal development.

❚❚❚ ECTRODACTYLY Background Ectrodactyly is the congenital absence of all, some, or parts of the digits. The malformation is also called splitpaw deformity, or lobster claw, and it can affect one or both front or hind limbs. Ectrodactyly may be associated with dislocation of the elbow, contracted tendons, limb curvature, and limb shortening.2 Importantly, most affected dogs limp to some degree, but few have pain, and most never develop arthritis. The merit of surgical treatment in affected cats and dogs appears dubious.

❚❚❚ RICKETS, SECONDARY TO CHOLESTASIS Extrahepatic biliary atresia leading to rickets was reported in a 17-week-old male Border Collie with painful lameness. A long-bone radiographic survey showed pronounced metaphyseal deformity (cupping), growth-plate widening, and poor bony mineralization, which were attributed to the dog’s inability to absorb fat-soluble vitamins, in particular, vitamin D.3 The precise cause of juvenile rickets is often unknown (Figures 10-1 and 10-2). In older dogs, advanced immunoarthritis bears some resemblance to rickets, but 186

it can be readily differentiated on the basis of related laboratory findings (Figure 10-3).

❚❚❚ CONGENITAL ELBOW DISLOCATION Congenital elbow dislocation (luxation or subluxation) is occasionally the cause of forelimb lameness in young dogs. This anomaly can assume a variety of forms, depending on the bones involved and their degree of displacement. A single cubital joint is most often involved, but occasionally both are affected. Displaced articular elements, particularly the radial head, characteristically appear small, dark, and misshapen, a consequence of their non–weight bearing.4 Typically, the proximal ulna appears abnormally arched when viewed from the side, a shape that reflects its abnormal alignment with the humerus (Figure 104, A). The latter is tipped medially as seen in the frontal plane, resulting in a pronounced varus deformity (Figure 10-4, B). The full extent of this malformation, including its effect on the carpus and foot, can be appreciated only by using stress radiography. In my experience, dogs with complete or near complete congenital dislocation of the radius do not become arthritic, although their bones undergo extensive remodeling, and they often have abnormal forelimb carriage and gait. Accommodative postural changes are usual in the opposite normal leg in cases of unilateral dislocation (Figure 10-5). Aside from revealing changes in size, shape, and volume of the involved joint cavities, arthrograms show what appears to be normal articular cartilage (Figure 10-6, A, B). On the other hand, mild or mild-to-moderate congenital subluxation of the elbow often leads to osteoarthritis (Figure 10-7), although there are exceptions (Figure 10-8). Once such deformities are discovered, rendering a sound, outcome-based prognosis is impossible because little other than anecdotal information is available on the subject.

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Figure 10-1 • Frontal postural view (standing) of the bilaterally deformed lower forelimbs in a puppy with rickets shows (1) medial bowing; (2) flared, scalloped, spiked metaphyses; and (3) increased physeal width.

Figure 10-2 • Lateral view of the forelimb of a young puppy with rickets shows characteristic enlargement and cupping of the distal radial and ulnar metaphyses.

Figure 10-3 • Close-up frontal view of the stifle joints of an old dog with chronic immunoarthritis shows severe subchondral bone destruction, which loosely resembles rickets in a puppy.

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A

B

Figure 10-4 • Congenital elbow dislocation: A, Close-up lateral view of the elbow shows (1) severely bowed proximal ulna; (2) shallow, elongated semilunar arch; and (3) subluxation of the humeroulnar joint. The proximal radius is clearly abnormal, but little more can be said with a frontal view. B, Close-up frontal view shows (1) lateral dislocation of a severely bowed radius with formation of a false joint, (2) compensatory centering and deformity of the proximal ulna, (3) compensatory remodeling of the distal humerus resulting in a downward medial angulation.

Figure 10-5 • Angular limb deformity: Frontal view of the lower forelimbs (postural film made with dog standing and a horizontally directed x-ray beam) shows valgus deformities at the level of the carpi and varus deformities at the elbows. This abnormal posture is due to a fracture dislocation of the left proximal radius (viewer’s top right), subsequent lateral bowing of the ulna, and postural compensation by the left limb.

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A

189

B

Figure 10-6 • Close-up lateral (A) and frontal (B) arthrograms in a young dog with a congenital dislocation of the elbow show how the soft tissues of the cubital joint can accommodate.

A

B Figure 10-7 • A, Close-up lateral view of a unilateral elbow dislocation in a small dog, presumed to have resulted from a congenitally deformed ulna (accounting for its deformity and downward displacement); B, a view of the opposite leg is provided for comparison.

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Figure 10-8 • Close-up lateral view of a nonpainful congenitally dislocated elbow in a small dog with no osteoarthritis.

❚❚❚ DIVIDED DISTAL RADIUS Although not as common as congenital deformities of the paw, additions, subtractions, and unnatural divisions of the middle and upper limb also occur. One such example is what I term miniatures (in lieu of more elaborate Latin descriptors), small replicas of bones or parts of bones. Displaced, longitudinally oriented articular fractures sometimes migrate proximally, giving rise to a miniature facsimile of the injured bone (Figure 10-9).

❚❚❚ INCOMPLETE OSSIFICATION OF THE HUMERAL CONDYLE Incomplete ossification of the humeral condyle is a developmental bone disease of spaniels in that the right and left halves of the humeral condyle are separated by a thin irregular gap. In the few published accounts of this rare disorder, the authors speculated that the described discontinuity structurally weakens the bone to the extent that it is predisposed to fracture. Alternatively, the underlying articular cartilage may give way beneath the subchondral crevice, resulting in the presence of interosseous joint fluid (with its attendant inflammatory properties). Radiographically, incomplete ossification of the humeral condyle is difficult to demonstrate because of the superimposition of the olecranon in both the frontal and frontal oblique projections. The lesion is invisible in lateral perspective. In one reported case involving a 10-year-old Cocker Spaniel, mature new bone deposition was noted on the lateral aspect of the distal shaft of the humerus; however, no mention was made of how this finding related to the primary articular lesion.5 Computed

Figure 10-9 • Close-up frontal view of the distal radius of a puppy with a lateral paw deflection shows a miniature “distal radius” emanating from the medial aspect of the metaphysis. Although the precise cause of this anomaly was not determined (congenital cause was the leading candidate), it did not appear to be traumatic because the opposite limb was similarly affected.

tomography is the superior method in revealing this type of lesion as demonstrated by Marcellin and co-workers.6

❚❚❚ OSTEOGENESIS IMPERFECTA Osteogenesis imperfecta is a heritable bone disease characterized by a loss of cortical and medullary bone density and the presence of numerous healed or healing fractures. In these respects, osteogenesis imperfecta resembles nutritional secondary hyperparathyroidism. Affected puppies appear stunted, often assume a crouched position when resting, have abnormal gaits, have pink teeth, and have marked muscle atrophy. Osteogenesis imperfecta is diagnosed by analyzing type 1 collagen from cultured skin fibroblasts.7

CHAPTER 10 ❚❚❚ Skeletal Deficiencies, Dysplasias, and Deformities

❚❚❚ ERYTHROCYTE PYRUVATE KINASE DEFICIENCY IN BASENJIS Severe chronic hemolytic anemia and osteopetrosis (osteosclerosis) clinically characterize pyruvate kinase deficiency in Basenjis. Radiographically, the marrow cavities, which normally look dark compared with the lighter cortices, instead appear completely opacified, making corticomedullary distinction difficult or impossible. Abdominal radiography often reveals hepatic and splenic enlargement; thoracic images may show cardiomegaly related to chronic anemia.8 The disease also was reported in three 2-month-old Dachshund puppies from the same litter. These puppies eventually were euthanized because they were unable to stand. Radiographically, their long bones and vertebrae appeared uniformly white. Microscopically, the medullae contained calcified cartilage, osteoid, and primitive bone, accounting for their abnormal opacity.9

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References 1. Root MV, Johnston SD, Olson PN: The effect of prepuberal and postpuberal gonadectomy on radial physeal closure in male and female cats. Vet Radiol Ultrasound 38:42, 1997. 2. Frey M, Williams J: What is your diagnosis? J Am Vet Med Assoc 206:619, 1995. 3. Extrahepatic biliary atresia in a border collie. J Small Anim Pract 41:27, 2000. 4. Farrow CS: Congenital elbow luxation. In Farrow CS, ed: Decision Making in Small Animal Radiology, Toronto, 1987, BC Decker. 5. Berry CR: Answers for film reading session: 1995 ACVR annual meeting. Vet Radiol Ultrasound 36:449, 1995. 6. Marcellin DJ, Roe SC, DeYoung DJ: What is your diagnosis? J Am Vet Med Assoc 209:727, 1996. 7. Campbell BG, Wootton JAM, et al: Clinical signs and diagnosis of osteogenesis imperfecta in three dogs. J Am Vet Med Assoc 211:183, 1997. 8. Giger U, Noble NA: Determination of erythrocyte pyruvate kinase deficiency in Basenjis with chronic hemolytic anemia. J Am Vet Med Assoc 198:1755, 1991. 9. Riser WH, Fankhauser R: Osteopetrosis in the dog: a report of three cases.

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The Skull, Brain, Eye, and Ear

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Radiographic Disease Indicators of the Skull The following are the principal radiographic disease indicators of skull disease in dogs and cats.

❚❚❚ NASAL MASS In older dogs and cats, nasal masses are nearly always malignant, although associated fluid often hides them from view.

❚❚❚ NASAL FLUID Nasal fluid may be the result of injury, infectious or noninfectious sinonasal disease, or cancer. In many instances, medium or large fluid volumes completely hide the conchae.

❚❚❚ DEVIATION AND DESTRUCTION OF THE VOMER Deviation or destruction of the vomer nearly always indicates cancer of the nasal cavity. Only rarely is infection associated with similar findings. Congenital defor-

mity or a serious facial injury conceivably could distort the vomer but in most cases would also distort the lateral facial bones and possibly the lower jaw.

❚❚❚ CONCHAL DISAPPEARANCE Inability to identify the conchae radiographically is usually due to one of two possible causes: (1) the conchae have been destroyed or (2) they are being hidden by fluid.

❚❚❚ LATERAL NASAL BONE DESTRUCTION Destruction of the lateral facial bones is nearly always the result of cancer and only occasionally the consequence of infection.

❚❚❚ INCREASED JAW DENSITY Widespread symmetric bone deposition in the lower jaw suggests metaphyseal osteopathy. New bone ori193

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ented about the temporomandibular joints, bullae, and vertical rami suggest mandibular osteopathy. Localized asymmetric sclerosis suggests possible callus, infection, or tumor, differentials that usually can be ranked and pursued according to clinical context (contextual diagnosis). It is particularly important to take radiographs of such lesions regularly where cancer is a contending diagnosis.

❚❚❚ DECREASED JAW DENSITY Marked loss of mandibular bone, to the extent that the teeth appear to be floating in space, usually heralds serious metabolic skeletal disease, such as renal osteodystrophy. When subtle osteopenia is observed, nutritional secondary hyperparathyroidism warrants consideration, especially if accompanied by extremital fracture. It is a good practice to perform long-bone surveys in such circumstances. Localized loss of jaw density is common with fractures, especially if they are not surgically reduced and immobilized. Focal, spherically shaped

areas of bone loss, particularly around tooth roots, are strong indicators of infection and abscess. Vaguely demarcated, marginal mandibular bone loss is often the earliest radiographic sign of squamous carcinoma.

❚❚❚ INCREASED CRANIAL DENSITY Increased cranial density usually is caused by new or old bone deposition. In the case of the latter, an old fracture is likely, especially if associated with deformity. A discrete object may be a benign or malignant bone tumor. Disorganized new bone may be the result of a recent injury, a response to localized infection, or the beginning of a tumor.

❚❚❚ DECREASED CRANIAL DENSITY A localized decrease in bone density often indicates the development of a tumor or, less frequently, an infection.

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Head Injury and Infection

❚❚❚ FACIAL INJURIES Facial depression fractures potentially can cause a variety of nasal cavity problems. Nasal or maxillary bone fragments can be driven into nearby turbinates or nasal passages, resulting in airflow obstruction. Because of the open nature of such fractures, infection is always a possibility, occasionally complicated by sequestration. With moderate or severe fragment displacement, there is usually accompanying devascularization, which encourages delayed healing and, in some instances, nonunion. Noninfectious sinusitis may develop after a serious sinus injury (Figure 12-1), although its precise cause often is not determined. Facial deformity, especially nonpainful asymmetry of the frontal sinuses, is often the result of an old injury.

❚❚❚ MANDIBULAR AND MAXILLARY INJURIES About 6% of all fractures in dogs and cats involve the mandible, usually the symphysis or body. Fractures of the vertical ramus and its bony extensions, the mandibular condyle and condyloid process, occur much less frequently. Although some of these injuries require surgery, many do not, for example, fractures of the condyloid process.1 Untreated hinge fractures— complete transverse breaks across the upper or lower jaws just behind the canine teeth—usually fail to heal and, depending on how they are treated, may have a higher incidence of postsurgical infection.

❚❚❚ TEMPOROMANDIBULAR JOINT INJURIES AND MOTION IMPAIRING DISORDERS Fractures or dislocations of the temporomandibular joint (TMJ), whether unilateral or bilateral, often are signaled by an inability to close the jaws fully or symmetrically (Figure 12-2). Ticer and Spencer published

a detailed description of the radiographic appearance of fractures and dislocations of the feline TMJ,2 and Schwarz and co-workers recently covered similar ground in a recent review article on the canine TMJ.3

❚❚❚ ANKYLOSIS AND IMPINGEMENT EXOSTOSIS Ankylosis or joint fusion may be of two types: primary ankylosis, in which the joint is actually fully or partially solidified and thus incapable of moving, and secondary ankylosis, in which the joint is structurally normal but unable to move (or move very little) because of an adjacent impinging callus. Such injuries are most common in cats that have been hit by cars4 and in dogs with severe depression fractures of the zygoma, which physically prevent opening of the mouth (Figures 12-3 and 12-4). The latter type of injury can require prolonged physiotherapy because the jaw muscles become severely atrophied under such conditions so that even after the zygoma is surgically removed, the tightened muscles still can prevent the mouth from opening. Occasionally, extraarticular callus, formed on or near the mandibular condyle, will behave like a fulcrum when the mouth is opened, causing complete or partial dislocation of the lower jaw, which in most cases is transient. In some instances, however, the jaw temporarily locks in the open position. Repeated dislocation can cause condylar remodeling, especially in a skeletally immature animal, which then can lead to chronic dislocation and the formation of a false joint.

❚❚❚ CONGENITAL TEMPOROMANDIBULAR DEFORMITY AND DISLOCATION Avariety of congenital condylar deformities, variously termed temporomandibular dysplasia, misplaced coronoid process, and jaw locking, have been reported in dogs, 195

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Figure 12-1 • Close-up lateral view of a healed depression fracture of the frontal sinus resulting in a shallow depression in its normally convex contour. The sinus is now abnormally clouded, the result of sinusitis, which was believed to have resulted from obstructed drainage.

Figure 12-2 • Mandibular fracture-dislocation: Close-up ventrodorsal oblique view of the temporomandibular joints shows bilateral dislocation; additionally, there are bilateral fractures of the condyloid processes and a comminuted fracture of the right vertical ramus (reader’s left).

Figure 12-3 • Frontal view of the face and jaw shows marked deformity of the right zygoma and mandible, the result of fractures. Currently, the dog can barely open its mouth because of secondary ankylosis.

most of which are associated with an inability to close the lower jaw fully and an absence of known injury.5–6 Radiographically, the key elements in these disorders are condylar displacement and deformity; however, it is usually impossible to know whether this is the result of (1) recent injury, (2) past injury, or (3) congenital disease. As a consequence, establishing dislocation does not necessarily establish cause. Flattening of the glenoid and hypoplasia of the retroglenoid process may accompany dysplasia but are also usually present in cases of trauma-induced dislocation of the TMJ, especially if the injury occurred before completion of skeletal development. With dislocation (subluxation), the articular surfaces of the glenoid and mandibular condyle overlap, producing a characteristic a thick white band (Figures 12-5 and 12-6). The best means of radiographically demonstrating a deformed or dislocated TMJ is with a traction–stress

maneuver. In this projection, the dog is positioned on its back, head flush against the table, with the closely collimated x-ray beam centered between the TMJ. The rostral aspect of the lower jaw is grasped by the canines and forcefully pulled forward, and the exposure made.7 There are few other projections of comparable value, although a conventional ventrodorsal projection can be somewhat useful, especially if made with a penetrated technique. Standard lateral and lateral oblique views usually contribute little to a diagnosis.

❚❚❚ CRANIAL INJURIES Subperiosteal Hematoma Background. Acute subperiosteal hematomas typically appear as nonspecific, localized soft tissue

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Figure 12-6 • The left temporomandibular joint is included for comparison.

Figure 12-4 • Ventrodorsal oblique view of the face and jaw shows marked deformity of the right zygoma and mandible, the result of fractures. Currently, the dog can barely open its mouth because of secondary ankylosis.

Imaging Findings. Radiographically, a cranial subperiosteal hematoma typically appears as a variably bordered, smoothly surfaced localized mound on the dorsal or dorsolateral aspect of the cranium. In some instances, the lesion may partially overlie the frontal sinuses. Its interior is usually semitransparent overall, but it may be partially calcified or ossified. Depending on the age of the lesion, interior fluid may be identified sonographically. In captive primates, especially adolescents, such lesions are common. Magnetic resonance imaging of such lesions clearly shows how the hematoma forms between the inner and outer layers of the frontal bone (the most common location), dramatically elevating the former.9

Cephalhematoma Following injury, young dogs or cats may develop an expansive bony swelling on the dorsal or dorsolateral aspect of the cranium, a common lesion in primate colonies.10

Cranial Fractures Figure 12-5 • Close-up lateral oblique views of the temporomandibular joints (TMJ) of a dog with a partially dislocated right TMJ.

swellings that gradually disappear over time. Some of these lesions, perhaps the most severe, leave a characteristic “fingerprint” that becomes discernable weeks or months later and can be used to infer the original injury. More importantly, awareness of this distinctive lesion can assist in helping to distinguish it from a bone tumor.8

Cranial fractures may result in protruding bone fragments (expression fracture) or intruding fragments (depression fracture), or they may be nondisplaced. Fractures in and around the basilar portion of the cranium are typically the most difficult to identify, often requiring multiple supplementary views (Figure 12-7).

Gunshot Wounds Gunshot wounds are usually fatal if the bullet (or bullet fragments) enters the brain (Figure 12-8). Nasal wounds may become secondarily infected because they are a form of open fracture, depending on the extent of the

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Figure 12-7 • Penetrated ventrodorsal view of the caudal basilar region of the skull shows a nondisplaced fracture through the lateral aspect of the left bulla (emphasis zone).

injury, and may lead to a chronic nasal discharge. Occasionally, lead fragments may lodge in one of the TMJs or the eyes or sever the facial nerve or nasolacrimal duct.

References 1. Salisbury SK, Cantwell HD: Conservative management of fractures of the mandibular condyloid process in three cats and one dog. J Am Vet Med Assoc 194:85, 1989. 2. Ticer JM, Spencer CP: Injury of the feline temporomandibular joint: radiographic signs. J Am Vet Rad Soc 19:146, 1978. 3. Schwarz T, et al: Imaging of the canine and feline temporomandibular joint: a review. Vet Radiol Ultrasound 43:85, 2002.

Figure 12-8 • A single high-powered bullet to the head killed this dog instantly as it lay on the front steps of a home. The fragment pattern supports a frontal entry wound.

4. Meomartino L, Fatone G: Temporomandibular ankylosis in the cat: a review of 7 cases. J Small Anim Pract 40:7, 1999. 5. Robins G, Grandage J: Temporomandibular joint dysplasia and open mouth jaw locking in the dog. J Am Vet Med Assoc 171:1072, 1977. 6. Widmer WR, Blevins WE: Radiographs presented as part of the 1995 ACVR oral certification examination: musculoskeletal section. Vet Radiol Ultrasound 37:108, 1996. 7. Farrow CS: Stress radiography. 8. Lutz SE, Williams J: What is your diagnosis? J Am Vet Med Assoc 206:1145, 1995. 9. Hill LR, Bernacky BJ, et al: What is your diagnosis? J Am Vet Med Assoc 216:1913, 2000. 10. Ardran GM, Kemp JR, et al: Cephalhematoma in squirrel monkeys. J Am Vet Rad Soc 18:70, 1977.

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Skull Tumors

Skull tumors vary in radiographic appearance according to both their cell type and location. For example, osteosarcomas of the cranial vault are typically productive with defined margins, whereas osteosarcomas in long bones are usually destructive and poorly marginated. Osteosarcomas of the face and jaw, on the other hand, typically feature creeping osteolysis, overt cortical destruction, and tumor bone extending into the surrounding soft tissue.1

❚❚❚ CRANIAL TUMORS Radiology and Computed Tomography Because of the pronounced curvature of the cranium, tangential views, made at right angles to suspicious surfaces, often produce a diagnostic image (Figure 13-1) where standard lateral and ventrodorsal projections of the same region fail to reveal any abnormalities (Figure 13-2). Some cranial osteosarcomas produce relatively little soft tissue swelling while extensively lysing underlying bone (Figures 13-3 and 13-4). Hathcock and Newton described the computed tomographic (CT) appearance of seven cranial and two facial bone tumors in dogs. These bones were optimally imaged using a bone window.2 The principal CT features of these tumors are shown in Box 13-1.

❚❚❚ FACIAL TUMORS

tinctive dished-out areas, reflecting areas of creeping substitution (Box 13-2).

❚❚❚ MANDIBULAR TUMORS Background Most mandibular tumors are actually squamous cell carcinomas (or other soft tissue tumors) of the gum or tongue, which become evident radiographically only once they invade the nearby jawbone. Primary bone tumors such as osteosarcoma, fibrosarcoma, and chondrosarcoma also may develop in the lower jaw but do so considerably less often (Figure 13-10). Thrall and co-workers reported the development of a mandibular osteosarcoma in a dog 77 months after orthovoltage radiotherapy for a fibromatous epulis (periodontal origin, acanthomatous type).3 To qualify as a radiation-induced bone tumor, a lesion must meet the following criteria (according to the authors): • Microscopic or radiographic evidence must exist that the original bone, whether normal or not, was nonmalignant. • The tumor must have developed within previously irradiated tissue. • The latent period between irradiation and tumor detection must be long. • The malignant nature of the tumor suspected to be radiation-induced must be proved.

Radiology and Computed Tomography

Imaging Findings

Radiographically, facial malignancies can be quite variable in appearance, ranging from intensely destructive (Figure 13-5) to moderately productive; alternatively, they may feature a combination of productive and destructive changes (Figures 13-6 to 138). Most, however, are primarily destructive (Figure 13-9). Tomographically, facial tumors often feature dis-

Most invasive gingival and glossal cancers cause local bony destruction; however, some do not. On the contrary, there are reports of invasive carcinomas causing intensely productive mandibular lesions resembling primary bone tumors.4 Mixed (destructive–productive) mandibular tumors occur as well (Figures 13-11 to 13-15). 199

Figure 13-1 • Osteosarcoma: A slightly oblique lateral view of the cranium of a dog shows a faint, smoothly surfaced mound of tumor bone, underlain by a ragged area of cortical destruction (emphasis zone).

Figure 13-2 • An earlier true lateral view of the same region predictably failed to show this eccentrically located bone tumor.

Figure 13-3 • Orientation view of the cranium of a dog shows a vaguely marginated area of uneven bone destruction (sometimes referred to as permeative), which in this instance is being caused by an osteosarcoma.

Figure 13-4 • Close-up view of the cranium of a dog shows a vaguely marginated area of uneven bone destruction (sometimes referred to as permeative), which in this instance is being caused by an osteosarcoma.

Figure 13-5 • Ventrodorsal open-mouth view of the skull of a cat with a highly destructive carcinoma that has destroyed much of the right side of the face (emphasis zone).

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Figure 13-6 • Lateral view of a cat with a squamous cell carcinoma of the rostral aspect of the right zygoma. Note how lesion visibility varies depending on projection, attesting to the fact that anatomically complex parts such as the skull often require customized imaging.

Figure 13-8 • Ventrodorsal open-mouth view of a cat with a squamous cell carcinoma of the rostral aspect of the right zygoma. Note how lesion visibility varies depending on projection, attesting to the fact that anatomically complex parts such as the skull often require customized imaging.

Figure 13-7 • Ventrodorsal view of a cat with a squamous cell carcinoma of the rostral aspect of the right zygoma. Note how lesion visibility varies depending on projection, attesting to the fact that anatomically complex parts such as the skull often require customized imaging.

Figure 13-9 • Intraoral projection of the upper jaw of a dog with a fibrosarcoma shows dissolution of much of the rostral aspect of the right maxilla and loss of most of the associated incisors.

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Figure 13-10 • Close-up lateral oblique view of the rostral mandible of a dog with an unusual osteosarcoma. The radiograph was deliberately underexposed to accentuate the frond-like cancer bone contained within the soft tissue bulk of the tumor.

Figure 13-11 • Ventrodorsal view of a dog with an unusually located squamous cell carcinoma on the medial side of its right mandible. The tumor features new bone production, combined with deep marginal bone loss (center middle of the close-up).

Figure 13-12 • Open-mouth view of a dog with an unusually

Figure 13-13 • Close-up open-mouth view of a dog with an

located squamous cell carcinoma on the medial side of its right mandible. The tumor features new bone production, combined with deep marginal bone loss (center middle of the close-up).

unusually located squamous cell carcinoma on the medial side of its right mandible. The tumor features new bone production combined with deep marginal bone loss (center middle of the close-up).

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Figure 13-14 • Squamous cell carcinoma. Lateral view of the facial region of a cat shows that the left zygoma has been destroyed and replaced with an amorphous calcified mass.

B o x

1 3 - 1

Computed Tomographic Features of Cranial Tumors in Dogs • Most tumors were located in or near the occipital region. • Tumors were characteristically large, protruding, spherical masses, which were sometimes lobulated. • Exterior tumor margins were for the most part smooth and of uniform thickness. • Interior tumor margins were relatively less well defined, often rough and irregular. • Tumor interiors typically appeared as granular bone densities arranged into multiple large, variably sized and shaped clumps. • Most tumors were associated with large defects in the cranium as a result of bone destruction.

References 1. Hardy WD, Brodey RS, Riser WH: Osteosarcoma of the canine skull. J Am Vet Rad Soc 8:5, 1967. 2. Hathcock JT, Newton JC: Computed tomographic characteristics of multilobular tumor of bone involving the cranium in 7 dogs and zygomatic arch in 2 dogs. Vet Radiol Ultrasound 41:214, 2000.

Figure 13-15 • The ventrodorsal view of the facial region of a cat shows that the left zygoma has been destroyed and replaced with an amorphous calcified mass.

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1 3 - 2

Computed Tomographic Features of Facial (Zygomatic) Tumors in Dogs • Most zygomatic tumors, like cranial tumors, appeared as large, well-defined convexities. • Unlike the described cranial tumors, tumors of the zygoma had a coarse, granular appearing interior.

3. Thrall DE, Goldschmidt MH, et al: Bone sarcoma following orthovoltage radiotherapy in two dogs. Vet Rad 24:169, 1983. 4. Madewell BR, Ackerman N, Sesline DH: Invasive carcinoma radiographically mimicking primary bone cancer in the mandibles of two cats. J Am Vet Rad Soc 17:213, 1976.

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Nasal Cavity Disease

Persistent nasal discharge characterizes most, but not all, chronic nasal disease, particularly malignant nasal tumors. Potential diagnoses and their probabilities have been reported and are tabulated later in this chapter.1 Although nasal passage tumors are diagnosed regularly, associated pulmonary metastasis is rare, making screening thoracic radiography a statistically debatable practice (Tables 14-1 and 14-2).2

❚❚❚ NASAL TUMOR (INTRANASAL TUMOR, NASAL CAVITY TUMOR) Background Nasal tumors usually occur in older dogs, particularly breeds with elongated faces (Figure 14-1). The most common cell types are squamous cell or adenocarcinoma, followed by osteosarcoma, fibrosarcoma, and chondrosarcoma.3 In cats, tumors of the nasal cavity account for about 3% of all neoplasms; like dogs, the most common cell types in cats are squamous cell and adenocarcinoma. Less common feline nasal tumors include fibrosarcoma, lymphohistiocytic sarcoma, chondrosarcoma, chondroma, and lymphoma.4

Imaging Findings Normal Radiology Nasal Cavity and Frontal Sinuses. The nasal conchae are visible in both the lateral and ventrodorsal views as somewhat vague, alternating light and dark gray lines. In the lateral projection, because of their natural curvature, the dorsal and ventral conchae give the impression of swirling objects (Figure 14-2). The openmouth view is the more valuable because of its lack of superimposition by the mandible; however, it must not be more than slightly oblique lest it falsely create the impression of unilateral disease (Figure 14-3). The same 204

restriction applies to the standard frontal sinus view, which although strictly speaking is not part of the nasal cavity, nevertheless is an integral part of most nasal series (Figure 14-4). Nasal Septum. In 1979, Harvey showed that the nasal septum of a normal dog was radiographically invisible, thereby overturning the long-held, prevailing belief of most of his contemporaries. According to Harvey, what was currently being called the nasal septum was actually the vomer bone. This discovery was extremely important because septal destruction was the principal, and thought by many to be the most reliable, diagnostic feature of nasal tumors.5 Cribriform Plate. Schwarz and co-workers described the radiographic appearance of the normal cribriform plate in canine cadavers, indicating that it may vary with both skull type and projection angle.6 Abnormal Radiology Fluid, Bone Destruction, and the Nasal Conchal Pattern. Destruction of one or more of the bony elements of the nasal cavity is believed by most authorities to be a strong and reliable indicator of malignancy and less often of mycotic or bacterial infection. Schmidt and Voorhout showed experimentally that surrounding fluid causes loss of the normal maxillary conchal pattern, which typically is characterized by a combination of fine and coarse, alternating light and dark parallel lines. When just the fine conchal striations disappear, leaving only the coarse trabeculation behind, bone destruction is probable. When extensive conchal destruction and fluid are combined, the nasal cavity becomes completely opacified.7 Although I have tried repeatedly to distinguish malignant from benign disease based on these criteria, I have generally been unsuccessful. In a conflicting report, however, Schwarz and colleagues found that nasal fluid appeared to have little or no effect on the normal turbinate pattern, support-

CHAPTER 14 ❚❚❚ Nasal Cavity Disease

205

ing the contention that despite the presence of diseaserelated nasal fluid or soft tissue, sizable defects in the nasal borders are still potentially detectable by radiographic means.8

Harvey and co-workers also reviewed canine nasal tumors, in addition to performing a metanalysis on previous radiographic reports on the subject. Their conclusions are discussed here, along with some examples (Figures 14-5 to 14-11; Box 14-1).9

Table 14-1 • POTENTIAL CAUSES OF CHRONIC

Differentiating Nasal Infection from Neoplasia. The presence or absence of lesion symmetry has been used to assess the relative probabilities of intranasal neoplasia and chronic rhinitis in cats.10 Predictors of nasal cancer include (1) unilateral involvement, (2) lysis of lateral bones, (3) turbinate destruction, and (4) loss of teeth. Alternatively, bilaterally symmetric nasal lesions suggest benignity in the form of chronic rhinitis. Russo and co-workers reported a significant lack of interobserver agreement in the interpretation of abnormal nasal radiographs in dogs. Additionally, they

NASAL DISEASE IN DOGS Diagnosis

Probability (%)

Comment

Aspergillosis Cancer

7 33

Extension of periodontal disease

10

Inflammatory rhinitis Nasal foreign body

24

Primary infection Adenocarcinoma is the most common cell type Usually secondary to apical abscess but also seen in conjunction with uncomplicated extractions and in cases where root fragments remain behind Probably underdiagnosed

Surgical injury, sequestrum, or bone fragments

?

7

Plant awns and miscellaneous plant fragments are the most common nasal foreign bodies seen in our hospital Intranasal bone fragments, presumably left over from an earlier rhinotomy, and identified with CT have been reported* The so-called nasal flush is likely more harmful than initially realized

Traumatic turbinate ? or vomer damage, diagnostic nasal irrigation

CT, Computed tomography. *Modified from Hawks DM, Daniel GB: Radiographic diagnosis. Vet Rad 32:307, 1991.

Figure 14-1 • Skulls of three dogs illustrating differences in facial length, from left to right: abbreviated, normal, and elongated.

Table 14-2 • DIFFERENTIAL RADIOGRAPHIC DIAGNOSIS OF NASAL CAVITY LESIONS IN DOGS RDI

Tumor

Trauma

Plant Awn

Infection

Sinusitis

Conchae fully or partially concealed by fluid

Often

Often

Often

Occasionally, depending on severity

Clouded frontal sinus or sinuses Destruction of one or more facial bones Exterior mass Fracture Missing teeth

Often

Occasionally

Occasionally, depending on duration of foreign body Rarely

Often

Occasionally

Occasionally

Often

Rarely

Occasionally

Never

Occasionally Very rarely Occasionally, depending on tumor type Often

Never Often Often

Never Never Never

Rarely Very rarely Rarely

Never Never Never

Occasionally

Occasionally

Occasionally

Rarely

Occasionally

N/A

N/A

N/A

N/A

Nasal septum invisible or partially destroyed Visible tumor bone

Modified from Morgan JP, Suter PF, et al: Tumors in the nasal cavity of the dog: a radiographic study. J Am Vet Rad Soc 13:18, 1972. RDI, Radiographic disease indicator; N/A, not applicable.

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further confirmed the ambiguity of the radiographic signs caused from nasal tumors and infections, which make diagnostic differentiation difficult.11 Like others before them, they sought to identify specific radiographic abnormalities that would strongly suggest either tumor or infection. Their findings are shown in Table 14-3. Evaluating Postoperative-Postradiation Nasal Radiographs. Progress studies of dogs that have had their nasal tumors partially removed (debulked) and then irradiated can be extremely difficult to evaluate. Even using earlier comparison films, it is often impos-

Table 14-3 • RADIOGRAPHIC DIFFERENTIATION

Figure 14-2 • Normal nasal cavity and frontal sinus. Lateral

OF NASAL INFECTION AND TUMOR

view of the nasal cavity of a healthy Labrador Retriever (“Sooner”). Tumor

Infection

Complete opacification, with concurrent loss or concealment of associated conchae Frontal sinus involvement: fluid, mass, or both Surrounding bone destruction, including the vomer

Focal or multifocal abnormalities

B o x

Localized lucency Localized densities Absence of frontal sinus involvement

1 4 - 1

Tendencies of Canine Nasal Tumors

Figure 14-3 • Open-mouth view of the nasal cavity of a healthy Labrador Retriever (“Sooner”).

• Dogs with nasal tumors show greater radiographic abnormalities of the nasal cavity and frontal sinuses than dogs with benign disease. • The combination of vomer bone destruction and an external mass strongly suggests cancer. Conversely, if both these features are lacking, tumor is highly unlikely. • Abnormal lucency of one or both sides of the nasal cavity suggests fungal infection, especially if the vomer appears normal. • About one third of the dogs with radiographically abnormal nasal cavities provide no indication as to the nature of their disease.

Figure 14-4 • Frontal sinus view of the nasal cavity of a healthy Labrador Retriever (“Sooner”).

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207

Figure 14-5 • Lateral view of the nasal cavity of a dog with a nasal adenocarcinoma, which features the following: (1) patchy areas of increased density; (2) reduced turbinate detail, especially on the left side; (3) abnormal thinning of the central vomer (implying destruction); and (4) clouding of the frontal sinuses (implying fluid). Typically, the ventrodorsal view is the more informative because of the lack of superimposition.

Figure 14-6 • Open-mouth view of the nasal cavity of a dog with a nasal adenocarcinoma, which features the following: (1) patchy areas of increased density; (2) reduced turbinate detail, especially on the left side; (3) abnormal thinning of the central vomer (implying destruction); and (4) clouding of the frontal sinuses (implying fluid). Typically, the ventrodorsal view is the more informative because of the lack of superimposition.

Figure 14-7 • Close-up intraoral view of the nasal cavity of a dog with a nasal tumor shows almost complete opacification of the right side.

Figure 14-8 • A skyline projection of the associated frontal sinus shows partial destruction of the right dorsolateral rim with tumor extruding through the defect.

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Figure 14-9 • Lateral view of the nasal cavity of a dog with a nasal osteosarcoma. The tumor has erupted from the right upper side of the face, opacifying much of the nasal cavity and disfiguring the face.

Figure 14-11 • Close-up intraoral view of a nasal adenocarcinoma in a dog shows extensive opacification of the left nasal cavity, combined with bowing, thinning, and partial destruction of the vomer.

Figure 14-10 • Intraoral view of the nasal cavity of a dog with a nasal osteosarcoma. The tumor has erupted from the right upper side of the face, opacifying much of the nasal cavity and disfiguring the face.

on a number of dogs with ambiguous radiographic findings, but generally we have found the technique unrewarding. Our few diagnostic successes have come when we have combined rhinography with postural radiography, specifically, supporting the head and neck of the unconscious dog on a large covered sponge, infusing a medium volume of high-viscosity diagnostic iodine solution into the nasal cavity, briefly letting the excess contrast drain away, and obtaining a lateral projection of the nasal cavity using a horizontal x-ray beam. One or two supplementary views then are made according to what was seen initially. Computed Tomography

sible to separate postoperative rhinitis from tumor regrowth or from radiation necrosis. All these diseases are inclined to cause intranasal fluid, and, as such, alterations in the conchae—assuming any remain—are difficult or impossible to appreciate (Figure 14-12).

Rhinography Goring and co-workers described the technique and clinical applications of positive-contrast rhinography in dogs.12,13 We also attempted contrast rhinography

Normal. Both Burk and George and Smallwood published articles illustrating the normal tomographic (computed) appearance of the nasal passages of the dog. The report by George and Smallwood went farther, including comparable xerograms and anatomic sections, additions that greatly enhance anatomic understanding of the CT scans.14,15 Losonsky and co-workers described the normal tomographic (computed) appearance of the nasal cavity and paranasal sinuses of the cat.16

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Table 14-4 • COMPARATIVE SENSITIVITIES OF COMPUTED TOMOGRAPHY AND RADIOGRAPHY IN THE DIAGNOSIS OF CANINE NASAL TUMORS AND MYCOTIC INFECTION Specificity Sensitivity

B o x

Radiography (%)

Computed Tomography (%)

76.5 54

98.8 100

1 4 - 3

Diagnostic Advantages of Computed Tomography Over Radiography in Identifying Nasal Disease

Figure 14-12 • Progress intraoral radiograph of a dog following removal of a nasal adenocarcinoma and radiation therapy. The tumor has regrown and displaced part of the vomer toward the right. No discrete conchae are apparent on the expanded left side, replaced in part by a smeared amorphous soft tissue density (tumor and fluid) and numerous variably sized lucent areas, believed to be caused by radiation necrosis.

B o x

1 4 - 2

Computed Tomographic Disease Indicators (CTDI’s) of Serious Nasal Cavity Disease in Dogs • Abnormal soft tissue located in the retrobulbar space • Areas of opacification containing patches of increased density • Destruction in one or both lateral maxillae • Destruction of the rostral portion of the dorsal maxilla • Ethmoidal destruction • Hyperostosis of the lateral maxilla • Nasal bone destruction

Indicators of Nasal Cancer. Burk was also one of the first to undertake a comprehensive review of a large number of computed tomograms made of dogs with nasal disease. This was done in an effort to establish reliable and predictive computed tomographic disease indicators (CTDIs).17 According to the author, seven CTDIs, or combinations of CTDIs, were regularly associated with serious nasal passage disease, especially tumors (Box 14-2).

• Abnormal opacification of the sphenoid sinus • Destruction of the cribriform plate, presphenoid bone, and horizontal portion of the palatine bone • Destruction of the frontal, nasal, maxillary, and vertical parts of the palatine bone • Destruction of the nasal septum or turbinates • Extranasal masses of the olfactory lobes of the brain, nasopharyngeal opening, nasopharynx, retrobulbar region, and oral cavity • Fluids, masses, or bone destruction in the frontal sinus

firmed nasal cavity cancer. CT proved more effective than radiology in identifying the following: (1) unilateral versus bilateral disease and (2) tumor spread to the cranial cavity, hard palate, and pterygopalatine fossa. They asserted that CT also may be superior to radiology for tumor staging, predicting possible treatment-related injury, and planning surgery and radiation therapy.18 Park and co-workers showed that CT is the superior method for evaluating nasal tumors in dogs and that it is far more sensitive than radiography in diagnosing the following pathology (Box 14-3). Schwarz also compared the relative specificities and sensitivities of radiography compared with CT in the diagnosis of canine nasal tumors and mycoses (Table 14-4).19 Equipped with three-dimensional reconstruction software, CT surpasses stereoradiography in its ability to convey a sense of anatomic depth, a feature that is indispensable for radiation therapy planning.20 Koblik and Berry reported the diagnostic advantage gained by dorsal-plane rather than transverse-plane imaging of the ethmoid region, particularly the cribriform plate of dogs with nasal tumors (squamous cell, transitional cell, and adenocarcinoma).21 In a followup project, the authors created cribriform lesions in previously healthy dogs and then compared images of these lesions using radiography, linear tomography, and CT.22

Plain Radiographs Versus Computed Tomography

Magnetic Resonance Imaging

Thrall and co-workers evaluated paired radiographic/tomographic examinations in dogs with con-

Moore and co-workers described the use of both magnetic resonance imaging (MRI) and CT in the diagno-

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adenocarcinoma, pointing out its value in presurgical or radiotherapy planning.24 Two case examples were included that showed tumor spread to the retrobulbar region in one instance and the intracranial area in another case.

❚❚❚ SINONASAL INFLAMMATORY DISEASE

Figure 14-13 • Transverse magnetic resonance images of portions the nasal cavity of a dog with chronic rhinitis and sinusitis show severe, predominantly right-sided mucosal thickening and frontal sinus fluid.

Diseases of the nasal cavity and frontal sinuses, also known as sinonasal inflammatory diseases, are best imaged by CT, even though MRI is more than capable of producing a diagnostic image (Figures 14-13 and 1414); sinonasal tumors are best seen with MRI. The latter is best performed with unenhanced routine sequences and postcontrast, fat-suppressed sequences.25 Sinusitis, in conjunction with bronchiectasis and situs inversus, has been reported in a dog; this condition is a rare combination of heritable disorders seen in humans, known as Kartagener syndrome.26

References

Figure 14-14 • Frontal sinus of a dog with chronic rhinitis and sinusitis shows severe, predominantly right-sided mucosal thickening and frontal sinus fluid.

sis of occult nasal tumors invading the rostral portion of the brain in four dogs. Although both types of imaging demonstrated the nasal and cerebral lesions, MRI provided superior anatomic detail. Even more importantly, MRI revealed peritumor edema and ventricular collapse, which were not appreciable in CT images made through comparable tissue planes.23 Voges and Ackerman used nuclear magnetic resonance imaging to assess the regional spread of nasal

1. Tasker S, Knottenbult, et al: Etiology and diagnosis of persistent nasal disease in the dog: a retrospective study of 42 cases. J Small Anim Pract 40:473, 1999. 2. MacEwen EG, Withrow SJ, et al: Nasal tumors in the dog: retrospective evaluation of diagnosis, prognosis and treatment. J Am Anim Heart Assoc 170:45, 1977. 3. Forrest LJ: The cranial and nasal cavities—canine and feline. In Thrall DE, ed: Textbook of Diagnostic Radiology. Philadelphia, 2002, WB Saunders. 4. Madewell BR, Priester WA, et al: Neoplasms of the nasal passages and paranasal sinuses in domesticated animals as reported by 13 veterinary colleges. Am J Vet Res 37:851, 1976. 5. Harvey CE: The nasal septum of the dog: is it visible radiographically? J Am Vet Rad Soc 20:88, 1979. 6. Schwarz T, Sullivan M, Hartung K: Radiographic anatomy of the cribriform plate. Vet Radiol Ultrasound 41:220, 2000. 7. Schmidt M, Voorhout G: Radiography of the canine nasal cavity: significance of the presence or absence of the trabecular pattern. Vet Radiol Ultrasound 33:83, 1992. 8. Schwarz T, Sullivan M, Hartung K: Radiographic detection of defects of the nasal boundaries. Vet Radiol Ultrasound 41:226, 2000. 9. Harvey CE, Biery DN, et al: Chronic nasal disease in the dog: its radiographic diagnosis. J Am Vet Rad Soc 20:91, 1979. 10. O’Brien RT, Evans SM, et al: Radiographic findings in cats with intranasal neoplasia or chronic rhinitis: 29 cases (1982–1988). J Am Vet Med Assoc 208:385, 1996. 11. Russo M, Lamb CR, Jakovljevic S: Accuracy of radiographic diagnosis of nasal lesions in fifty-five dogs. Vet Radiol Ultrasound 40:533, 1999. 12. Goring RL, Ticer JW, et al: Positive-contrast rhinography: a technique for radiographic evaluation of the nasal cavity, nasopharynx, and paranasal sinuses in the dog. Vet Rad 25:98, 1984.

CHAPTER 14 ❚❚❚ Nasal Cavity Disease

13. Goring RL, Ticer JW, et al: Contrast rhinography in the radiographic evaluation of disease affecting the nasal cavity, nasopharynx, and paranasal sinuses in the dog. Vet Rad 25:106, 1984. 14. Burk RL: Computed tomographic anatomy of the canine nasal passages. Vet Radiol Ultrasound 33:170, 1992. 15. George TF, Smallwood JE: Anatomic atlas for computed tomography in the mesaticephalic dog: head and neck. Vet Radiol Ultrasound 33:217, 1992. 16. Losonsky JM, Abbott LC, Kuriashin IV: Computed tomography of the normal feline nasal cavity and paranasal sinuses. Vet Radiol Ultrasound 38:251, 1997. 17. Burk RL: Computed tomographic imaging of nasal disease in 100 dogs. Vet Radiol Ultrasound 33:177, 1992. 18. Thrall DE, Robertson ID, et al: A comparison of radiographic and computed tomographic findings in 31 dogs with malignant nasal cavity tumors. Vet Rad 30:59, 1989. 19. Schwarz T: Comparison of sensitivity and specificity of conventional x-ray and computed tomography in nasal tumors and mycoses in dogs. Vet Radiol Ultrasound 36:428, 1995.

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20. Pechman RD: Stereoradiography of the dog and horse skull. J Am Vet Rad Soc 19:53, 1978. 21. Koblik PD, Berry CR: Dorsal plane computed tomographic imaging of the ethmoid region to evaluate chronic nasal disease in the dog. Vet Rad 31:92, 1990. 22. Berry CR, Koblik PD: Evaluation of survey radiography, linear tomography and computed tomography for detecting experimental lesions of the cribriform plate in dogs. Vet Rad 31:146, 1990. 23. Moore MP, Gavin PR, et al: MR, CT and clinical features from four dogs with nasal tumors involving the rostral cerebrum. Vet Rad 32:19, 1991. 24. Voges AK, Ackerman N: MR evaluation of intra and extracranial extension of nasal adenocarcinoma in a dog and cat. Vet Radiol Ultrasound 36:196, 1995. 25 Som PM, Curtin HD: Sinuses. In Stark DD, Bradley WG, eds: Magnetic Resonance Imaging, vol III, ed 3, St Louis, 1999, Mosby. 26. Stowater J: Kartagener’s syndrome in a dog. J Am Vet Rad Soc 17:174, 1976.

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Dental, Gum, and Tongue Diseases ❚❚❚ DENTAL DISEASE IN DOGS AND CATS Hamp (a dentist) and co-workers were among the first to provide a radiologic perspective on the problem of canine dental disease.1 From their extensive investigation of necropsy material, they reached the conclusions listed in Box 15-1. Zontine was one of the first North American veterinary radiologists to take more than a passing interest in dental radiography. First in Veterinary Clinics of North America and later in Veterinary Radiology, he described the imaging of a dog’s teeth, along with the appropriate anatomic descriptors.2,3 Subsequently, some veterinary radiologists and nonradiologists adopted purpose-built, human dental x-ray machines for use in dogs and cats. Most veterinarians, however, have continued to do their dental radiography with conventional x-ray machines, albeit with somewhat more sophisticated screen-film systems.4

❚❚❚ NORMAL TEETH The jaws of a puppy initially contain 28 temporary teeth, variably referred to as puppy, deciduous, milk, or baby teeth. Subsequently, these teeth are lost and are replaced by a permanent dentition (Figure 15-1) that includes 14 additional adult teeth, not preceded by temporaries. Thus, the final complement of permanent teeth in an adult dog is 42 (Figure 15-2).

❚❚❚ A SIMPLIFIED RADIOGRAPHIC APPROACH TO DENTAL DISEASE Veterinarians specializing in the dental diseases of pets by and large have adopted the terminology used in human dentistry. Adaptation of the existing human 212

dental lexicon has the advantage of a legacy literature, albeit a human one. The disadvantage of learning a new terminology, one that is unfamiliar to most pet owners, is that it would likely require some “translation.” For those desiring a simpler approach, as well as one with a radiographic emphasis, most dental disease can be conceptualized as consisting of two essential elements: the tooth and its socket. Obviously, the surrounding jawbone forms the backdrop for any dental assessment, particularly as concerns the focal bone destruction that often accompanies abscess. The following material illustrates the various types of structural changes that occur with a variety of dental diseases in dogs and cats. Tip: Placing both a right and a left marker along either side of the maxilla or mandible when making oblique dental projections, termed double-marking, provides additional assistance in identifying which side of the jaw contains the diseased tooth or teeth (Figure 15-3).

❚❚❚ PERIODONTITIS Like people, dogs and cats lose more teeth to periodontal disease than to any other cause; however, periodontitis must be well advanced before it can be appreciated radiographically. A better way to assess periodontal disease is to measure the depth of the natural pocket (sulcus) formed by the inside surface of the gum and the outer surface of the tooth. As periodontal disease worsens, the depth of the sulcus increases until the tooth loosens, becomes painful, and is eventually lost.

❚❚❚ DENTAL ABSCESS In my experience, the carnassial tooth of the dog (fourth premolar) becomes abscessed more often than any

CHAPTER 15 ❚❚❚ Dental, Gum, and Tongue Diseases

213

Figure 15-1 • Close-up right lateral oblique view of the maxilla of an older puppy shows a combination of temporary and permanent teeth, exemplified in the side-by-side adult and puppy canine teeth.

Figure 15-2 • Close-up right lateral view of the maxillary dentition of a young adult dog (excluding the incisors) shows the normal anatomy of healthy teeth and jaw.

B o x

1 5 - 1

Clinical Generalizations About Canine Dental Disease • Caries and root resorption were found less frequently than periapical destruction. • Missing teeth were common regardless of age. • Most dogs had dental calculus. • Periapical destruction was a common finding. • Periodontitis was the most common dental disease, becoming worse with advancing age. • Small dogs were more often affected with periodontitis than large dogs. • Within different breeds, periodontitis varied markedly. Figure 15-3 • Left lateral oblique view of the maxillary dentition of a normal dog featuring double marking.

other. Typically, these abscesses appear as relatively discrete circular areas of lucency surrounding the top of a single root, although occasionally multiple roots can be affected (Figures 15-4 and 15-5). In chronic disease, there also can be varying degrees of root destruction, in which case much or all the dental socket is destroyed and the adjacent jawbone is lysed (Figures 15-6 to 15-8).

Infected teeth usually do not involve the nasal cavity or frontal sinuses as they often do in horses, and only rarely are they associated with nasal discharge. Thus, when an infected tooth is detected in a nasal examination, it is in all likelihood an incidental finding (Figures 15-9 and 15-10).

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Figure 15-4 • Close-up lateral oblique view of an abscessed right maxillary carnassial tooth in a dog shows characteristic well-marginated, circular lucency surrounding the upper portion of the intact caudal root.

Figure 15-5 • A view of the normal left carnassial tooth is provided for comparison.

Figure 15-6 • Orientation view of the right maxillary carnassial tooth in a dog shows destruction of the dental socket and surrounding bone. The caudal tooth root is severely lysed, including the root canal. The visible rostral root contains a central teardrop-shaped cavity; the cranial cusp of the tooth is missing and shows evidence of associated decay (irregular marginal lucency).

Figure 15-7 • Close-up view of the right maxillary carnassial tooth in a dog shows destruction of the dental socket and surrounding bone. The caudal tooth root is severely lysed, including the root canal. The visible rostral root contains a central teardrop-shaped cavity; the cranial cusp of the tooth is missing and shows evidence of associated decay (irregular marginal lucency).

Figure 15-8 • The opposite healthy carnassial tooth is provided for comparison (left and right).

CHAPTER 15 ❚❚❚ Dental, Gum, and Tongue Diseases

Figure 15-9 • Open-mouth view of left maxillary carnassial tooth in a dog shows lateral alveolar expansion, the result of infection. Although it is not apparent, a small alveolar defect has allowed pus to leak into the adjacent soft tissues causing an abscess, which is suggested by adjacent swelling that is not present on the opposite side of the face.

215

Figure 15-11 • Intraoral view of a dog with combined cavitation and abscess of the left upper second and third incisors, teeth that were previously fractured. The associated canine tooth is absent.

❚❚❚ CAVITIES AND ROOT RESORPTION Cavities occur less often in dogs than in people, largely because of a combination of dental morphology and diet. Unlike humans, the benefits of canine dental hygiene, in particular brushing, are debatable. Except for the tops of broken teeth, cavities in dogs and cats are most likely to occur along the sides of teeth, often near the base. Basilar cavities are particularly common in older cats, giving rise to a variety of names, ranging from the straightforward to the pretentious: feline neck lesions, dental reabsorptive lesions, cervical line lesions, and odontoclastic reabsorptive lesions.5

❚❚❚ DENTAL FRACTURE AND DISLOCATION Figure 15-10 • Close-up view of left maxillary carnassial tooth in a dog shows lateral alveolar expansion, the result of infection. Although it is not apparent, a small alveolar defect has allowed pus to leak into the adjacent soft tissues causing an abscess, which is suggested by adjacent swelling that is not present on the opposite side of the face.

Dental fractures, particularly of the canine teeth, may or may not require treatment, depending largely on where they break off. When the nerve is exposed, a root canal is the only effective treatment, short of extraction. Left untreated, some such fractures may become infected (Figure 15-11). Occasionally, a canine tooth may be propelled upward into the rostral part of the nasal cavity and act as a foreign body.6

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Figure 15-12 • Close-up lateral oblique view of the first premolar of a dog with an infected retained root (emphasis zone) following a previous dental fracture.

Figure 15-13 • Close-up ventrodorsal openmouth view of the rostral maxilla shows extensive bone loss and dental displacement, primarily on the right side, the result of an undifferentiated dental tumor.

❚❚❚ RETAINED DENTAL ROOTS AND ROOT FRAGMENTS Occasionally, a root or root fragment is broken off during extraction of a diseased tooth. This is particularly a problem in older dogs and cats that have basilar reabsorption or ankylosis. In most instances, the remaining root is painful and must be removed. Atooth also may be sheared off just below the gum line as a result of injury, with the root remaining undetected until it eventually becomes diseased (Figure 15-12).

❚❚❚ DENTAL AND PERIODONTAL TUMORS In dogs, the oral cavity is the site of about 6% of all tumors, 60% of which originate in the dental or periodontal tissues.7 Occasionally, puppies develop dental

tumors, which are capable of radically deforming the nearby teeth and gums (Figure 15-13). In an adult dog, however, extreme dental displacement is more likely to be the result of a fibrosarcoma.

❚❚❚ GUM AND TONGUE As previously indicated, most mandibular and maxillary tumors are actually invasive soft tissue cancers such as squamous cell carcinomas. Most such tumors gradually erode away the margin of the adjacent bone, and others erase it completely. Some cause an uneven pattern of bone destruction that resembles a piece of lace. Solano and Penninck described the sonographic appearance of the normal tongue in dogs, cats, and horses. In addition, they also described a variety of tumors: squamous cell carcinoma, rhabdomyoma,

CHAPTER 15 ❚❚❚ Dental, Gum, and Tongue Diseases

melanoma, and adenocarcinoma, in addition to an abscessed foreign body.8 In my experience, most glossal tumors occur in older cats and are usually carcinomas. To date, medical imaging appears to be playing only a minor role in the diagnosis and treatment of such lesions, although I have used sonography to locate and remove abscessed porcupine quill fragments from the tongue of a large dog.

References 1. Hamp S-E, Olsson S-E, et al: A macroscopic and radiologic investigation of dental diseases of the dog. Vet Rad 25:86, 1984. 2. Zontine WJ: Dental radiographic technique and interpretation. Vet Clin North Am 4:741, 1974.

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3. Zontine WJ: Canine dental radiography: radiographic technic, development, and anatomy of the teeth. J Am Vet Rad Soc 16:75, 1975. 4. Roman FS, Llorens MP, et al: Dental radiography in the dog with a conventional x-ray devise. Vet Rad 31:235, 1990. 5. Lund EM, Bohacek LK, et al: Prevalence and risk factors for odontoclastic resorptive lesions in cats. J Am Vet Med Assoc 212:302, 1998. 6. Morris EL: Radiographic diagnosis. Vet Rad 30:119, 1989. 7. Theon AP, Rodriquez C, et al: Analysis of prognostic factors and patterns of failure in dogs with periodontal tumors treated with megavoltage irradiation. J Am Vet Med Assoc 210:785, 1997. 8. Solano M, Penninck DG: Ultrasonography of the canine and equine tongue: normal findings and case history reports. Vet Radiol Ultrasound 37:206, 1996.

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Brain Disease and Injury (Intracranial Lesions) ❚❚❚ METHODS OF IMAGING THE BRAIN: INTRODUCTION Radiography

on the basis of vascular displacement and deformity (Figure 16-3).3 The procedure was dangerous and often imprecise; as a result, it has become obsolete.

Other than in cases of head trauma where a fracture is suspected, plain radiography predictably does little to suggest, confirm, or exclude the presence of a brain lesion. Thus, there is little justification for plain radiography under most circumstances, even as an inexpensive preliminary screening technique. The task of imaging brain lesions is clearly now the purview of computed tomography (CT) and magnetic resonance imaging (MRI).

Ventriculography. Before the advent of ultrasound, CT, and MRI, hydrocephalus was diagnosed by ventriculography, a procedure in which a bone biopsy needle was first used to puncture the cranium, making way for a spinal needle that was then passed through the cerebral cortex into one of the underlying lateral ventricles. A diagnostic opaque then was injected to assess the size, shape, and patency of the ventricular system. The procedure was associated with a high incidence of seizures and protracted recovery periods.

Special Radiographic Procedures

Nuclear Medicine Imaging

Combined Linear Tomography and Cysternography. Voorhout described the use of linear tomography and cysternography to evaluate the pituitary gland in healthy dogs and how this imaging combination compared with CT.1 Although it may be perhaps of academic interest to some, this procedure is unlikely to garner any serious degree of acceptance, if only because most facilities have long since discarded their tomographic equipment.

Because of the far greater sensitivity of CT and MRI in localizing and characterizing brain disease, nuclear imaging is gradually fading from the diagnostic scene, with the exception of a few specialized indications, such as the evaluation of cerebral blood flow, cerebral metabolism, and cerebrospinal fluid (CSF) mechanics, investigative endeavors that are for the most part physiologically oriented.4 The occasional veterinary publication on the subject, however, does still appear.5

Venography. Cavernous sinus venography is currently used on a limited basis to investigate disorders of the cavernous venous sinus, in particular its influence on the eye (Figures 16-1 and 16-2). Among other things, cavernous sinus venography has been used to diagnose an adenocarcinoma of the olfactory lobe that was compressing the optic nerves and causing blindness2 and a retrobulbar arteriovenous fistula that caused a dog’s eye to protrude temporarily whenever the dog became excited.

Sonography

Cerebral Angiography. Before the advent of CT, and later MRI, cerebral arteriography (cerebral angiography) was the only means by which a medium-sized to large brain lesion could be imaged, albeit indirectly, 218

Ultrasound is a safe, effective, and rapid means of establishing the presence of moderate or severe hydrocephalus in puppies or kittens, but it is often useless once the cranial fontanels have closed. Sonography also can be used intraoperatively as a means to assess an exposed tumor or cyst.6 Hudson and colleagues reported the capabilities of color flow and spectral Doppler in evaluating the flow characteristics of selected cerebral vasculature (rostral cerebral, middle cerebral, and internal carotid arteries) in newborn puppies.7,8 Normal values (for the largest lateral ventricle featuring normal histology) appear in Table 16-1.

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Figure 16-1 • Lateral view of a normal cavernous sinus venogram in a dog.

Figure 16-3 • Normal ventrodorsal cerebral angiogram showing a focused digital subtraction of the circle of Willis.

Table 16-1 • MAXIMUM SONOGRAPHIC DIMENSIONS OF THE CANINE LATERAL VENTRICLE

Figure 16-2 • Ventrodorsal view of a normal cavernous sinus

Measured Structure(s)

Value (cm)

Lateral ventricular height Ventricle-hemisphere ratio Ventricle-mantle ratio

0.15 0.09 0.15

principle behind quantitative CT is that various kinds of brain lesions absorb iodinated contrast medium at different times following its intravenous administration (uptake, contrast enhancement); likewise, the contrast disappears from the abnormal part of the brain at different rates (washout). These differences in lesion uptake and washout then can be used to predict (but not always with great accuracy) the nature of specific lesions (Table 16-2).

venogram in a dog.

Magnetic Resonance Imaging Computed Tomography Computed tomography, like ultrasound, is a kind of cross-sectional imaging that is often used to detect intracranial lesions, primarily those affecting the brain. Fike and co-workers initially described the tomographic appearance of the normal dog brain in 1981,9 followed shortly thereafter by an illustrated essay on caudal fossa tumors.10 Fike and colleagues were also the first to describe the use of quantitative CT to discriminate between neoplastic and nonneoplastic brain lesions in dogs.11 The

Using examples of brain and spinal cord disease, Tryon and I have described, in the simplest terms possible, how MRI works. Thomson and co-workers also published an account of MRI, but as it specifically pertains to neurodiagnosis.12 Kraft and colleagues described the MRI of the normal canine brain,13 and Hudson and colleagues published a similar description on the cat.14 Karkkainen compared the quality of MRIs of the canine brain using high and low magnetic fields (1.0 and 0.1 T, respectively). The brain images obtained with the higher-field-strength imager were superior because of a better signal-to-noise ratio; however, both scanners

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Table 16-2 • COMPUTED TOMOGRAPHIC UPTAKE: WASHOUT INTERVALS AS A MEANS OF PREDICTING THE NATURE OF CANINE BRAIN LESIONS Lesion

Time of Maximum Contrast Enhancement (Contrast Uptake)

Washout Time (During a 15-min Observation Period)

Cystic encephalomalacia (secondary to tumor compression) Hyperthermia-induced lesions Mixed gliomas Nongliomal tumors

Continued to increase 5-15 min after administration

No washout

Radiation-induced brain damage

Continued to increase 5-15 min after administration

At time of administration (infusion) At time of administration (infusion)

No washout No washout Gradual disappearance (comparable to washout in normal brain) No washout

Table 16-3 • IMAGING STRATEGIES: CHOOSING BETWEEN COMPUTED TOMOGRAPHY (CT) AND MAGNETIC RESONANCE IMAGING (MRI) Perform CT

Perform MRI

Acute neurologic signs (48 hr or less) referable to the brain

Subacute neurologic signs (greater than 48 hr) referable to the brain Chronic neurologic signs referable to the brain Perform MR angiography when earlier CT suggests a primary vascular lesion MR exam suggests tumor; give intravenous contrast Give gadolinium for MR whenever there is clinical finding that suggests a specific neurologic localization

CT exam suggests tumor; give intravenous contrast In acute cases, do not give intravenous contrast unless abscess or tumor is considered probable

were able to produce diagnostic images.15 The signalto-noise ratio and examination time of low-fieldstrength imagers can be improved by using customized surface coils, as reported by Snellman and colleages.16

❚❚❚ NORMAL VENTRICULAR VARIATION De Haan and co-workers reported normal variation in the size of the lateral ventricles in Labrador Retrievers.17 Specifically, they reported that 5 of 62 normal dogs had symmetric ventricular enlargement, and 19 animals had ventricular asymmetry, which ranged from mild to severe in magnitude. In the absence of contrast enhancement, some caution needs to be exercised with regard to any diagnosis based entirely on increased ventricular size or asymmetry. Kii and co-workers made similar observations with regard to ventricular enlargement and asymmetry in Beagle-type dogs.18 The same researchers also characterized what I term the blooming of the lateral ventricles (expansion of the ventricular slits with CSF), which in the case of Beagle puppies, first becomes visible between 3 and 4 weeks of age (using MRI).19

❚❚❚ CHOOSING THE CORRECT STUDY As a general rule in brain imaging, CT is ideally performed early in the course of a neurologic illness, while MR

is more appropriate in subacute and chronic contexts.20 Specifics are described in Table 16-3.

❚❚❚ CRANIOCEREBRAL TRAUMA Injury Classifications Brain injuries can be divided into two types, depending on when the damage is done: primary and secondary. Primary injuries occur at the moment of impact as a direct result of the injuring force or forces. Secondary injuries are delayed, usually of a vascular nature, and often culminate in a mass effect. Brain injuries also may be classified according to where they occur relative to the point of impact. Injuries on the same side as the impact are referred to as coup or coup type, and those that develop on the opposite side of the head are termed contrecoup or contrecouptype injuries. Brain injuries also can be divided rather simply according to relative location. Interior parenchymal injuries are referred to as intraaxial trauma, and those affecting exterior structures such as the meninges or CSF are termed extraaxial (Box 16-1). In acute head trauma, a noncontrast-enhanced CT is preferable because it can be performed rapidly on most patients, even the critically injured. The major observation being sought is an extracerebral hematoma, an extremely serious condition, but one that can be reversed if operated on early. Intracerebral bruising also can be detected on CT but is not amenable to surgical

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A Simplified Method of Classifying Brain Injuries Extraaxial injury Epidural hematoma Subdural hematoma Subdural hygroma Subarachnoid hemorrhage Intraventricular hemorrhage Intraaxial injury Cerebral swelling Cerebral contusion and hematoma Diffuse axonal injury and brainstem injury Vascular injury

treatment and is associated with a less predictable outcome.

❚❚❚ SEIZURE If it is the patient’s first seizure, an intracranial tumor is a prime diagnostic consideration and accordingly must be diagnostically confirmed or denied. Contrastenhanced MRI or contrast-enhanced CT is the preferred initial examination. If the patient is in the immediate postictal state, or if residual neurologic deficit is present at the time of imaging, a noncontrast CT scan is a better initial choice. If the seizures are chronic, particularly if they are not helped by medication, a detailed MRI examination, especially of the temporal lobes, should be performed. In pediatric patients, contrast enhancement is generally not required because hydrocephalus is a more likely cause than tumor. Mellema and co-workers reported the disappearance of brain lesions theorized to have been caused by seizures. Specifically, similar lesions involving the piriform or temporal lobes of the brains of three dogs, identified with MRI and believed to be the result of seizures, inexplicably disappeared after 10 to 16 weeks of anticonvulsant medication.21

❚❚❚ FOCAL GRANULOMATOUS MENINGOENCEPHALITIS Lobetti and Pearson described the MRI appearance of focal granulomatous meningoencephalitis (GME) and pointed out the relative merits of MRI compared with CT (Box 16-2).22

❚❚❚ BRAIN TUMORS Brain tumors in dogs have a reported approximate incidence of 15 per 100,000. Such tumors typically develop in dogs that are 5 years of age and older and most often are heralded by seizures.23 Plain films are typi-

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Advantages of Magnetic Resonance Imaging Compared With Computed Tomography in Diagnosing Focal Granulomatous Meningoencephalitis in Dogs • Ability to differentiate extravascular blood from surrounding tissues • Able to image the caudal fossa of the brain without cranial artifacts, particularly from the petrous temporal bones • Better resolution (improved detail) • Multiplanar images

cally of no use in detecting brain tumors unless the tumor is large and heavily calcified.

Meningioma Background. Meningiomas are one of the most common brain tumors of older dogs. Typically slow growing and benign, these discrete masses usually develop in one of the following locations: (1) the convexities of the cerebral hemispheres, (2) the falx cerebri, and (3) the middle cranial fossa (on the ventral surface of the brain). These growths are highly pleomorphic, appearing as smoothly surfaced spheres or ovals, lobulated masses, or meningeal plaques. The bulkier versions of this tumor often cause pressure atrophy in nearby brain tissue; other forms may invade the interior cranium, causing localized bone deposition (radiographically termed hyperostosis). Some become partially mineralized. Imaging Findings Computed Tomography. Computed tomography provides superior imaging of cortical bone and soft tissue calcification; thus, CT will reveal meningeal mineralization, bony invasion, and hyperostosis, which are normally invisible to MRI. Magnetic Resonance Imaging. Because of its superior soft tissue imaging, MRI is optimally suited to the investigation of brain tumors and other intracranial lesions using either low- or high-field-strength magnets (0.064 and 1.5 T).24,25 In T1 images, most meningiomas appear light (hypointense) compared with surrounding white matter but variable to gray matter. In T2 images, meningiomas appear dark (hyperintense) compared with white matter and comparable or dark compared with cortex. When present, tumor calcification appears as multiple small, dark spots in both T1 and T2 pulse sequences. Because of their vascularity and extraneural origin, meningiomas readily absorb gadoliniumDTPA, improving the overall clarity of low-contrast (isointense) or low-volume lesions.

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Table 16-4 • MAGNETIC RESONANCE IMAGING (MRI) CHARACTERISTICS OF EIGHT MENINGIOMAS

Table 16-5 • MAGNETIC RESONANCE IMAGING (MRI) CHARACTERISTICS OF 11 GLIOMAS

MRI Feature

MRI Description

MRI Feature

MRI Description

Edema Hydrocephalus Lesion location Mass effect T1-weighted images

7 of 8: 5 mild, 2 moderate 2 of 8 6 forebrain, 2 brainstem 6 of 8: 5 mild, 1 moderate

Edema Hydrocephalus Lesion location Mass effect T1-weighted images

10 of 11: 2 mild, 8 moderate 4 of 11 9 forebrain, 2 cerebellum 9 of 11: 5 moderate, 4 severe

Border definition

5 poorly circumscribed, 3 well circumscribed Interior appearance 6 heterogeneous, 2 homogeneous Signal intensity 7 hypointense, 1 isointense Proton density-weighted images

Border definition

Border definition

7 poorly circumscribed, 1 well circumscribed 7 heterogeneous, 1 homogeneous Seven hypointense, 1 isointense

Border definition

5 well circumscribed, 3 poorly circumscribed 5 heterogeneous, 3 homogeneous 7 hyperintense, 1 mixed 7 marked, 1 mild

Border definition

Interior appearance Signal intensity T2-weighted images Border definition Interior appearance Signal intensity Contrast enhancement

Comparison of Meningiomas and Gliomas Thomas and co-workers also described the MRI features of meningiomas and gliomas in dogs.26 Detailed findings are tabulated below, but, in general, meningiomas are most likely to be extraaxial lesions that show marked enhancement with gadolinium-DTPA; gliomas are intraaxial masses with associated peripheral edema and variable degrees of contrast enhancement (Tables 16-4 and 16-5).

The Dural Tail Sign and Meningeal Enhancement Graham and co-workers conducted a retrospective review of a small series of dogs and cats with proven meningiomas and gliomas to determine the diagnostic specificity of the so-called dural tail or dural tail sign (also termed a meningeal tail).27 They concluded that although the detection rate differed markedly between participating radiologists (40% to 80%), the dural tail sign was a frequent finding in both canine and feline meningiomas and, as such, “may improve the confidence of the radiologist . . . in making this diagnosis.” Mellama and co-workers published their observations on meningeal enhancement seen in 15 dogs and 3 cats undergoing MRI for a variety of central nervous system disorders. They point out that although they have yet to discover any specific disease patterns, the presence of a dural tail sign, in combination with meningeal enhancement, strengthens the diagnostic possibility of a meningioma.28

5 poorly circumscribed, 6 well circumscribed Interior appearance 11 heterogeneous Signal intensity 10 hypointense, 1 mixed intensity Proton density-weighted images

Interior appearance Signal intensity T2-weighted images

Interior appearance Signal intensity Contrast enhancement

5 poorly circumscribed, 6 well circumscribed 10 heterogeneous, 1 homogeneous 11 hyperintense 5 well circumscribed, 5 poorly circumscribed 10 heterogeneous, 1 homogeneous 11 hyperintense 5 marked, 6 mild

Pituitary Adenoma (Pituitary Macroadenoma, Pituitary Microadenoma) Background. Canine hyperparathyroidism is pituitary dependent in 85% to 90% of affected dogs, with pituitary adenomas accounting for as many as 84% of these animals. Most of these tumors are small and grow slowly, but a few become large enough to cause hormonal and neurologic abnormalities. Imaging Findings Combined Cisternography and Linear Tomography. Voorhout and Rijberk described the use of combined cisternography and linear tomography to evaluate the size of the pituitary gland in dogs with pituitarydependent hyperadrenocorticism. Of the eight dogs imaged, one was normal, six had enlarged pituitaries, and one could not be evaluated because of the absence of contrast solution in the cistern around the pituitary gland. At necropsy, seven dogs had pituitary tumors. These authors concluded that the technique was capable of demonstrating pituitary enlargement and suprasellar expansion; however, it could not qualitatively or quantitatively assess the latter.29 Computed Tomography. Turrel and colleagues described the tomographic appearance of primary brain tumors in a series of dogs.30 Mattoon and Walker described the CT appearance of a dog with a pituitary macroadenoma appearing as a medium-sized, well-

CHAPTER 16 ❚❚❚ Brain Disease and Injury (Intracranial Lesions)

Figure 16-4 • Sagittal magnetic resonance image (T1) of a dog with a highly aggressive osteosarcoma that has destroyed a portion of the cranium and is compressing the underlying cerebrum.

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Figure 16-5 • Sagittal magnetic resonance image (T2) of a dog with a highly aggressive osteosarcoma that has destroyed a portion of the cranium and is compressing the underlying cerebrum.

marginated, suprasellar mass with focal mineralization. Contrast administration resulted in marked lesional enhancement.31 Magnetic Resonance Imaging. Graham and coworkers described the changing appearance of the normal pituitary gland over time using intravenous gadolinium, referring to the procedure as “dynamic” MRI.32 Enhancement initially was observed in the region of the pituitary stalk at between 52 and 65 seconds, followed by uniform enhancement seen at between 104 and 143 seconds. The described pattern was seen in all the dogs studied (Figures 16-4 to 16-9).

Cranial Nerve Sheath Tumors Background. Nerve sheath tumors are commonly classified as cranial, spinal, or peripheral, with most falling into the last category. Histologically, such growths are categorized as schwannomas, neurofibromas, or neurofibrosarcomas. In dogs, the most commonly affected cranial nerves are the vestibulocochlear, facial, and trigeminal; the last typically is associated with atrophy of the temporalis and masseter muscles. Although nerve sheath tumors often extend into surrounding soft tissue, and sometimes bone, they rarely metastasize. Imaging Findings Radiology. Watrous and co-workers described a malignant peripheral nerve sheath tumor that externally appeared as a large, fluctuant mass on the side of the head. Radiographs showed extensive destruction of

Figure 16-6 • Transverse magnetic resonance image of the brain of a dog with a pituitary adenoma.

portions of both the occipital and temporal bones, in addition to focal mineralization within the mass.33 Magnetic Resonance Imaging. Saunders and coworkers described the MRI features of an intracranial trigeminal nerve schwannoma in a dog that appeared in T1 as a strongly enhancing 8-mm mass in the right caudal fossa.34

Choroid Plexus Tumors Tumors of the canine choroid plexus, classified as either papillomas or carcinomas, typically develop in and

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Figure 16-7 • Transverse magnetic resonance image of the brain of a dog with a pituitary adenoma.

Figure 16-9 • Dorsal magnetic resonance image of the brain of a dog with a pituitary adenoma. All images are T1 weighted; all except Figure 16-6 are contrast enhanced.

❚❚❚ ENCEPHALITIS Computed Tomography

Figure 16-8 • Sagittal magnetic resonance image of the brain of a dog with a pituitary adenoma.

around the fourth ventricle, causing clinical signs referable to the cerebellopontine angle: head tilt, nystagmus, ataxia, and hemiparesis or tetraparesis. Typically reported MR features include (1) mass(es) in or around the fourth ventricle; (2) hypointensity on T1; (3) hyperintensity on T2 and proton density; (4) pronounced, homogeneous contrast enhancement; and (5) varying degrees of ventricular obstruction as evidenced by secondary hydrocephalus. In one reported choroid plexus carcinoma, multiple cystic lesions were identified on MRI that were hypointense on T1 and hyperintense on T2 and proton density but showed only minimal enhancement following contrast administration.35

Plummer and co-workers investigated the sensitivity of CT in the diagnosis of encephalitis. Specific types of encephalitis studied included (1) GME, (2) verminous encephalitis, (3) pug encephalitis, (4) fungal encephalitis, and (5) distemper. Dzyban and Tidwell reported a case of GME in a 2year-old Shih Tzu. Because the dog had an open fontanelle, it was possible to perform sonography in addition to CT.36 The sonographic study showed a 1-cm hyperechoic mass in the left frontal lobe with an associated right lateral shift of the falx and ventral displacement of the splenial sulcus (using a 10-MHz transducer). No hydrocephalus was seen. Differential diagnosis included tumor, granuloma, abscess, and hematoma. Examination by CT showed an abnormal brain featuring a mass compatible with what was seen with ultrasound, patchy areas of decreased density compatible with edema, and multiple foci of contrast enhancement. Accordingly, the differential diagnosis was narrowed to a diffuse inflammatory process or metastatic neoplasia. The dog was euthanized, and necropsy revealed GME. The authors concluded that although the great majority of dogs examined showed brain abnormalities compatible with encephalitis, they were not otherwise specific; nor did these abnormalities enable the interpreters to reliably differentiate inflammation from neoplasia (Box 16-3).37

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Computed Tomographic Abnormalities Potentially Associated With Encephalitis • Edema • Falcial deviation • Focal changes in parenchymal density (hyperdense or hypodense) • Focal contrast enhancement • Periventricular contrast enhancement • Ring-like pattern of contrast enhancement • Ventricular changes (enlarged, asymmetric)

Magnetic Resonance Imaging Lobetti and Pearson described two cases of canine GME diagnosed with MRI. In one case, the described mass exhibited abnormalities seen with both tumor and inflammation; in the other, no lesion was identified until contrast enhancement was used, which revealed localized staining within the cerebellum consistent with loss of blood–brain barrier integrity.38

❚❚❚ NECROTIZING MENINGOENCEPHALITIS (NECROTIZING ENCEPHALITIS) Computed Tomography Ducote and co-workers described the CT features of necrotizing meningoencephalitis in three Yorkshire Terriers, a disease that appears to show a decided bias toward small dog breeds such as Pugs, Maltese, and Yorkshire Terriers.39 The affected dogs showed similar clinical signs, including dullness, circling, ataxia, head tilt, facial paresis, anisocoria, and pain associated with manipulation of the head and neck. CT images revealed (1) numerous areas of decreased cerebral density, (2) asymmetric ventriculomegaly, (3) lack of contrast enhancement, and (4) absence of mass effect.

Magnetic Resonance Imaging Lotti and co-workers described the MRI appearance of necrotizing encephalitis in a Yorkshire Terrier showing clinical signs of right forebrain and brainstem disease.40 MRI revealed multiple lesions in the white matter of the cerebrum, diencephalons, and mesencephalon, which appeared hypointense in T1 and hyperintense in T2. No mass effects were noted, and there was only minimal enhancement following the administration of gadolinium.

❚❚❚ ASPERGILLOSIS Chronic aspergillosis, the form of the disease we encounter most often, is frequently characterized by

Figure 16-10 • Close-up intraoral view of the nasal cavity of a dog with chronic aspergillosis shows an absence of conchae and much of the vomer, replaced by patches of fluid and inflammatory tissue.

complete or partial destruction of the nasal conchae resulting in a nearly transparent nasal cavity other than any residual fluid or inflammatory tissue. Portions of the vomer also may be destroyed (Figure 16-10). Burk and colleagues reported a case of systemic aspergillosis in a cat, which produced lesions in the lungs and brain, the latter appearing on CT as hypointense nodules with irregularly marginated borders.41 Saunders and co-workers described the CT findings in 35 dogs with nasal aspergillosis.42 The following were their principal observations: 1. Moderate to severe conchal destruction, described by the authors as “cavitated-like turbinate lysis” accompanied by variable amounts of inflammatory tissue and fluid 2. Mucosal thickening involving the conchae, maxillary recess, and frontal sinus 3. New bone deposition that the authors described as “thickened reactive bony changes” The authors also cautioned against overreliance on CT attenuation numbers, which for the most part were found unreliable.

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❚❚❚ BLASTOMYCOSIS Saito and co-workers described a case of intracranial blastomycosis in which CT was diagnostically instrumental. Specifically, the authors reported the presence of marked perivascular contrast enhancement involving the lateral and third ventricle as well the mesencephalic aqueduct. These findings correlated closely with a histologic diagnosis of severe ependymitis. Intracranial screening was advocated for dogs with ocular or systemic blastomycosis.43

❚❚❚ ABSCESSATION (BRAIN ABSCESS) An abscess was described in the basal ganglia of an older German Shepherd in conjunction with a probable CSF infection and similar appearing abscess in a pterygoid muscle. On MRI, the brain lesion appeared as a ring enhancing mass; CSF in the nearby lateral ventricle was determined to be abnormal by using an inversion recovery sequence.44 Klopp and co-workers reported the MRI features of brainstem abscess in two cats.45 Both abscesses had a similar appearance: In T1 images, abscesses featured a hypointense center and thick relatively hyperintense parameter; T2 images showed a spherical, uniformly hyperintense mass. Following administration of

intravenous gadolinium, the outer band of the lesion showed marked enhancement. In one cat, it appeared that the abscess connected to the nearby bulla, suggesting a probable etiology. The authors also described the developmental aspects of brain abscess as described previously in people and experimental animals (Table 16-6).46

❚❚❚ HYDROCEPHALUS Background The incidence of debilitating hydrocephalus is relatively high in breeds such as the Chihuahua and Pekingese.47

Radiology Radiology is not a reliable means of establishing whether or not an animal is hydrocephalic, although in extreme cases it is sometimes possible to infer the disease based on (1) a disproportionately large cranium, (2) an abnormally rounded cranium, (3) thinner than usual cranial bones, (4) excessive fontanelle size, and (5) protracted closure time (Figures 16-11 and 16-12).

Sonography Hudson and co-workers described the sonographic appearance of hydrocephalus in the dog.48 The lateral

Table 16-6 • STAGING BRAIN ABSCESSES Developmental Stage of Brain Abscess

Stage Name and Time of Development

Stage 1

Early cerebritis: begins 1-3 days after infection

Stage 2

Late cerebritis: begins 4-9 days after infection

Stage 3

Capsule formation: occurs 10-13 days after infection

Stage 4

Mature abscess: occurs 14-19 days after infection

MRI, Magnetic resonance imaging; CSF, cerebrospinal fluid.

Pathology and Corresponding MRI The abscess is just beginning to form but as yet lacks a capsule. Central necrosis is under way, and peripheral vasogenic edema is forming T1: mild mass effect, with isointense to mildly hypointense peripheral region (compared with normal brain) representing vasogenic edema T2 and proton density: edema appears hyperintense compared with normal brain; necrotic center is isointense to hypointense compared with gray matter Abscess volume, peripheral edema, and central necrosis have all reached a maximum T1: edematous region now appears overtly hypointense (compared to adjacent brain) Necrotic center is hypointense (compared with white matter), and isointense to hyperintense (compared with CSF) As the capsule develops, the necrosis and edema begin to subside T1: Capsule appears hyperintense (compared with surrounding brain); abscess center is isointense to hyperintense (compared with CSF) and hypointense (compared with brain) T2 and proton density: Capsule appears hyperintense; abscess center is isointense to hypointense, sometimes featuring rings of alternating intensity Capsular formation is complete, central necrosis has decreased further, and gliosis has developed peripherally T1: Capsule is isointense to mildly hyperintense, but markedly enhances with gadolinium T2: Capsule is hypointense

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ventricles were considered enlarged if (1) ventricle height exceeded 0.35 cm, (2) ventricle/mantle ratio exceeded 0.25, or (3) ventricle/hemisphere ratio exceeded 0.19. Measurements were made at the level of (or caudal to) the interthalamic adhesion in the transverse plane. Some animals were discovered that, although neurologically normal, had ventricular enlargement. More importantly, there was poor correlation between ventricular size and clinical signs. Spaulding reported scanning the lateral ventricles in 28 dogs with open fontanelles, most of which were

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miniature and brachycephalic breeds. A strong positive correlation was demonstrated between the presence of an open fontanelle and ventricular enlargement, but no such relationship was established between fontanelle and ventricle size or between clinical signs and ventricle size.49

Magnetic Resonance Imaging Vullo and co-workers studied lateral ventricular volume in healthy adult Beagles using quantitative MRI and determined that there was a surprisingly high incidence of ventriculomegaly as well as individuals with ventricular asymmetry. In light of what appear to be normal anatomic variations, the authors caution that a diagnosis of hydrocephalus (versus normal variation) needs to be based on more than just the presence of ventriculomegaly.50 Vite and co-workers measured cerebral ventricular volume in English Bulldogs using quantitative MRI and found it proportionately greater than in Beagles. These data suggest both individual and breed variability.51

❚❚❚ BRAIN CYSTS Arachnoid Cysts

Figure 16-11 • Lateral view of the skull of a hydrocephalic puppy shows (1) enlargement and rounding of the cranium, (2) thinning of the cranial bones, and (3) abnormally widened fontanelles.

A congenital brain cyst located dorsal to the cerebellum and communicating with the right lateral ventricle was diagnosed in a 9-month-old Lhasa Apso using MRI. The dog also suffered from cerebellar atrophy and nonsuppurative meningoencephalitis.52 An arachnoid cyst located in the cerebellar pontine region of the brain and diagnosed with MRI also was reported in a cat.53 Vernau and co-workers described the CT and MRI appearances of intracranial, intraarachnoid cysts in six dogs, three of which were less than a year of age.54 Cysts appeared sharply defined in CT images, containing fluid that was comparable (isodense) to CSF. Intravenous contrast failed to enhance the cyst. MRI depicted arachnoid cysts as extra-axial, fluidcontaining lesions that failed to enhance.

Dermoid Cysts Target and co-workers reported the MRI features of medullary dermoid cyst causing secondary hydrocephalus in a 7-year-old Golden Retriever. The 2-cm cyst was predominantly hyperintense in both T1 and T2, with little edema and no enhancement with gadolinium. Enlargement of the lateral and third ventricles was attributed to obstruction by the cyst.

Epidermoid Cysts Figure 16-12 • Frontal view of the skull of a hydrocephalic puppy shows (1) enlargement and rounding of the cranium, (2) thinning of the cranial bones, and (3) abnormally widened fontanelles.

Platt and co-workers have described the MRI appearance of an intracranial epidermoid cyst in a 7-yearold Pitbull.55 On T2, the lesion appeared as a

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predominantly hyperintense, well-circumscribed, central cerebellar mass. On T1, however, the mass appeared different, being composed of two distinct layers: a foreground composed of a cluster of variably sized, interconnected, hypointense lobules and a hyperintense background. Following administration of gadolinium, T1 peripheral enhancement (rim sign) occurred.

❚❚❚ STROKE (CEREBRAL INFARCTION, CEREBROVASCULAR “ACCIDENT”) Imaging Findings Stroke in dogs is often diagnosed presumptively based on a history of an acute onset of central nervous signs, which may resolve over a period of days to weeks, depending on the severity and location of the lesion. Abnormalities include focal neurologic deficits, ataxia, paresis, paralysis, seizures, circling, behavioral changes, depression, and loss of consciousness. A stroke can be fatal.

Computed Tomography Tidwell and co-workers reported the CT appearance of an acute hemorrhagic cerebral infarct in a dog.56 Unenhanced, the lesion appeared as an ill-defined hyperdense area in the left frontal lobe, compatible with hemorrhage. Following contrast administration, the lesion developed a dense outer band attributed to edema and termed by the authors ring enhancement. Falcial displacement and nonuniform ventricular compression were also present. With respect to ring enhancement, Wolf and coworkers determined that, as in the case with humans with such lesions, this phenomenon is nonspecific, being associated with neoplastic and non-neoplastic diseases alike.57 The authors also point out the difference in the CT appearance of acute versus subacute intracerebral hemorrhage.

Acute Phase Fresh blood readily absorbs radiation, primarily because of its hemoglobin content, and therefore is visible on CT images of the brain as an area of increased density or, in the language of CT, an area of increased hyperdensity. A forming hematoma will dissect and compress brain tissue rather than simply diffusing within the parenchyma, creating a well-defined, homogeneous, hyperdense mass on unenhanced CT images. Hematomas are characteristically surrounded by edema (secondary to compressive ischemic necrosis), which appears as a subtle decrease in surrounding density. When contrast is given, there is no enhancement because there is no viable vasculature.

Hematomas of this type typically reach their maximum size in 4 to 5 days.

Subacute Phase Four to five days after the original injury, the damaged capillary beds surrounding the hematoma become reestablished, allowing administered contrast to reach the previously inaccessible tissues, which now appear as a discrete, hyperdense band, a CT observation termed ring enhancement.

Magnetic Imaging Resonance Thomas and co-workers described the MRI appearance of stroke in seven dogs (three hemorrhagic, four nonhemorrhagic).58 Nonhemorrhagic infarcts appeared wedge shaped, hypointense on T1, and hyperintense on T2. There was no enhancement with intravenous gadolinium. Hemorrhagic infarcts featured mixed signal intensity on both T1- and T2-weighted images and showed variable enhancement. A mature cerebral hematoma causing stroke-like signs in an old dog has been reported by the same authors.59 Based on circumstantial evidence, the authors speculated that the described bleeding was the result of a vascular malformation.

❚❚❚ NORMAL ANATOMIC VARIANTS Tentorium Cerebelli Osseum Drost and co-workers described a normal variation of the tentorium cerebelli osseum of the dog.60 Specifically, a “fatty element” within the tentorium cerebelli osseum, as identified with CT, was attributed to either an excessive amount of diploe or an atypical sinus formation.

❚❚❚ BRAIN BIOPSY Koblick and co-workers reported their experience using a sterotactic device to assist in the performance of CTguided brain biopsies in dogs.61 Using modified equipment originally designed for use in people, the authors performed 50 biopsies. All areas of the brain were accessible to biopsy, although some were associated with a lower success rate than others. In general, the more rostral the lesion, the greater the accuracy of needle placement, an occurrence that was attributed to the relative fit of the stereotactic device from front to back of the cranium. For a similar technical reason, small dogs were more difficult to biopsy than large dogs. Deeper lesions were more difficult to hit than shallow ones. In a follow-up communication, the authors described the histologic nature of the biopsied lesions, their loca-

CHAPTER 16 ❚❚❚ Brain Disease and Injury (Intracranial Lesions)

tions within the brain, CT or MRI appearance (or both), and procedure-related problems.62 In the 22 dogs where brain biopsies and surgical samples or necropsy findings were compared, there was a 91% correlation. Based on available data, it appears that stereotactic CTguided brain biopsy has an approximate fatality rate (direct and indirect) of 3%. Detailed morbidity information (including intermediate term follow-ups) has not been published.

❚❚❚ COMPUTED TOMOGRAPHIC EVALUATION OF THE POSTOPERATIVE BRAIN Bergman and co-workers reported the CT findings identified in two dogs immediately following removal of cerebral meningiomas.63 Subsequent CT assessments were made up to 9 months later on one dog and 6 weeks later in another.

References 1. Voorhout G: Cisternography combined with linear tomography for visualization of the pituitary gland in healthy dogs. Vet Rad 30:68, 1990. 2. Nasisse MP, Russell RG, Munger RJ: Radiographic diagnosis. Vet Rad 25:191, 1984. 3. Bailey MQ, Lowrie CT, Padgett GA: Radiographic diagnosis. Vet Rad 28:138, 1987. 4. Davies ER: Radionuclide scanning of the brain. In Sutton D, ed: A textbook of radiology and imaging, New York, 1993. 5. Dykes NL, Warnick LD, et al: Retrospective analysis of brain scintigraphy in 116 dogs and cats. Vet Radiol Ultrasound 35:59, 1994. 6. Hudson JA, Cartee RE, et al: Vet Rad 30:13, 1989. 7. Hudson JA, Buxton DF, et al: Color flow Doppler imaging and Doppler spectral analysis of the brain of neonatal dogs. Vet Radiol Ultrasound 38:313, 1997. 8. Hudson JA, Simpson ST, et al: Ultrasonographic examination of the normal canine neonatal brain. Vet Rad 32:50, 1991. 9. Fike JR, LeCouteur RA, et al: Anatomy of the canine brain using high resolution computed tomography. Vet Rad 22:236, 1981. 10. LeCouteur RA, Fike JR, et al: Computed tomography of brain tumors in the caudal fossa of the dog. Vet Rad 22:244, 1981. 11. Fike JR, Cann CE, et al: Differentiation of neoplastic from non-neoplastic lesions in dog brain using quantitative CT. Vet Rad 27:121, 1986. 12. Thompson CE, Kornegay JN, et al: Magnetic resonance imaging: a general overview of principles and examples in veterinary neurodiagnosis. Vet Radiol Ultrasound 34:2, 1993. 13. Kraft SL, Gavin PR, et al: Canine brain anatomy on magnetic resonance images. Vet Rad 30:147, 1989. 14. Hudson LC, Cauzinelle L, et al: Magnetic resonance imaging of the normal feline brain. Vet Radiol Ultrasound 36:267, 1995. 15. Karkkainen M: Low and high field-strength magnetic resonance imaging to evaluate the brain in one normal and two dogs with central nervous system disease. Vet Radiol Ultrasound 36:528, 1995.

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16. Snellman M, Benczik J, et al: Low-field magnetic resonance imaging of Beagle brain with a dedicated receiver coil. Vet Radiol Ultrasound 40:36, 1999. 17. De Haan CE, Kraft SL, et al: Normal variation in size of the lateral ventricles of the Labrador retriever dog as assessed by magnetic resonance imaging. Vet Radiol Ultrasound 35:83, 1994. 18. Kii S, Uzuka Y, et al: Magnetic resonance imaging of the lateral ventricles in Beagle-type dogs. Vet Radiol Ultrasound 38:430, 1997. 19. Kii S, Uzuka Y, et al: Developmental change of lateral ventricular volume and ratio in beagle-type dogs up to 7 months of age. Vet Radiol Ultrasound 39:185, 1998. 20. Seldenwurm DJ: Introduction to brain imaging and neuroanatomy atlas. In Brant WE, Helms CA, eds: Fundamentals of diagnostic radiology, Baltimore, 1994, Williams & Wilkins. 21. Mellema LM, Koblik PD, et al: Reversible magnetic resonance imaging abnormalities in dogs following seizures. Vet Radiol Ultrasound 40:588, 1999. 22. Lobetti RG, Pearson J: Magnetic resonance imaging in the diagnosis of focal granulomatous meningoencephalitis in two dogs. Vet Radiol Ultrasound 37:424, 1996. 23. Bagley RS, Gavin PR, et al: Clinical signs associated with brain tumors in dogs: 97 cases (1992–1997). J Am Vet Med Assoc 215:818, 1999. 24. Hathcock JT: Low field magnetic resonance imaging characteristics of cranial vault meningiomas in 13 dogs. Vet Radiol Ultrasound 37:257, 1996. 25. Kraft SL: Imaging diagnosis. Vet Rad 31:65, 1990. 26. Thomas WB, Wheeler SJ, et al: Magnetic resonance imaging features of primary brain tumors in dogs. Vet Radiol Ultrasound 37:20, 1996. 27. Graham JP, Newell SM, et al: The dural tail sign in the diagnosis of meningiomas. Vet Radiol Ultrasound 39:297, 1998. 28. Mellama LM, Samii VF, et al: Meningeal enhancement on magnetic resonance imaging in 15 dogs and 3 cats. Vet Radiol Ultrasound 43:10, 2002. 29. Voorhout G, Rijberk A: Cisternography combined with linear tomography for the visualization of pituitary lesions in dogs with pituitary-dependent hyperadrenocorticism. Vet Rad 31:74, 1990. 30. Turrel JM, Fike JR, et al: Computed tomographic characteristics of primary brain tumors in 50 dogs. J Am Vet Med Assoc 188:851, 1986. 31. Matoon JS, Walker MA: MRI case presented as part of the 1997 A.C.V.R. oral certification examination: computed tomography/magnetic resonance imaging elective. Vet Radiol Ultrasound 39:154, 1998. 32. Graham JP, Roberts GD, Newell SM: Dynamic magnetic resonance imaging of the normal canine pituitary gland. Vet Radiol Ultrasound 41:35, 2000. 33. Watrous BJ, Lipscomb TP, et al: Malignant peripheral nerve sheath tumor in a cat. Vet Radiol Ultrasound 40:638, 1999. 34. Saunders JH, Poncelet L, et al: Probable trigeminal nerve schwannoma in a dog. Vet Radiol Ultrasound 39: 539, 1998. 35. Lipsitz D, Levitski RE, Chauvet AE: Magnetic resonance imaging of a choroid plexus carcinoma and meningeal carcinomatosis in a dog. Vet Radiol Ultrasound 40:246, 1999. 36. Dzyban LA, Tidwell AS: Meningoencephalitis in a dog. Vet Radiol Ultrasound 37:428, 1996.

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37. Plummer SB, Wheeler SJ, et al: Computed tomography of primary inflammatory brain disorders in dogs and cats. Vet Radiol Ultrasound 33:307, 1992. 38. Lobetti RG, Pearson J: Magnetic resonance imaging in the diagnosis of focal granulomatous meningoencephalitis in two dogs. Vet Radiol Ultrasound 37:424, 1996. 39. Ducote JM, Johnson KE, et al: Computed tomography of necrotizing meningoencephalitis in 3 Yorkshire Terriers. Vet Radiol Ultrasound 40:617, 1999. 40. Lotti D, Capucchio MT, et al: Necrotizing encephalitis in a Yorkshire Terrier: clinical, imaging, and pathologic findings. Vet Radiol Ultrasound 40:622, 1999. 41. Burk RL, Joseph R, Baer K: Systemic aspergillosis in a cat. Vet Rad 31:26, 1990. 42. Saunders JH, et al: Computed tomographic findings in 35 dogs with nasal aspergillosis. Vet Radiol Ultrasound 43:5, 2002. 43. Saito M, Nicholas JH, et al: CT findings of intracranial blastomycosis in a dog. Vet Radiol Ultrasound 43:16, 2002. 44. Seiler G, Cizinauskas S, et al: Low-field magnetic resonance imaging of a pyocephalus and a suspected brain abscess in a German Shepherd dog. Vet Radiol Ultrasound 42:417, 2001. 45. Klopp LS, Hathcock JT, Sorjonen DC: Magnetic resonance imaging features of brain stem abscessation in two cats. Vet Radiol Ultrasound 41:300, 2000. 46. Klopp LS, Hathcock JT, Sorjonen DC: Magnetic resonance imaging features of brain stem abscessation in two cats. Vet Radiol Ultrasound 41:300, 2000. 47. Selby LA, Hayes HM, Becker SV: Epizootiologic features of canine hydrocephalus. Am J Vet Res 40:411, 1979. 48. Hudson JA, Simpson ST, et al: Ultrasonic diagnosis of canine hydrocephalus. Vet Rad 31:50, 1990. 49. Spaulding KA, Sharp NJH: Ultrasonographic imaging of the lateral cerebral ventricles in the dog. Vet Rad 31:59, 1990. 50. Vullo T, Korenman E, et al: Diagnosis of cerebral ventriculography in normal adult Beagles using quantitative MRI. Vet Radiol Ultrasound 38:277, 1997. 51. Vite CH, Insko EK, et al: Quantification of cerebral ventricular volume in English Bulldogs. Vet Radiol Ultrasound 38:437, 1997.

52. Koblik P: Magnetic resonance study presented as part of the 1994 A.C.V.R. oral certification examination. Vet Radiol Ultrasound 36:284, 1995. 53. Milner RJ, Engela J, Kerberger RM: Arachnoid cyst in cerebellar pontine area of a cat—diagnosis by magnetic resonance imaging. Vet Radiol Ultrasound 37:34, 1996. 54. Vernau KM, Kortz GD, et al: Magnetic resonance imaging and computed tomography characteristics of intracranial intra-arachnoid cysts in 6 dogs. Vet Radiol Ultrasound 38:171, 1997. 55. Platt SR, Graham J, et al: Canine intracranial epidermoid cyst. Vet Radiol Ultrasound 40:454, 1999. 56. Tidwell AS, Mahony OM, et al: Computed tomography of an acute hemorrhagic cerebral infarct in a dog. Vet Radiol Ultrasound 35:290, 1994. 57. Wolf M, Pedroia V, et al: Intracranial ring enhancing lesions in dogs: a correlative CT scanning and neuropathologic study. Vet Radiol Ultrasound 36:16, 1995. 58. Thomas WB, Sorjonen DC, et al: Magnetic resonance imaging of brain infarction in seven dogs. Vet Radiol Ultrasound 37:345, 1996. 59. Thomas WB, Adams WH, et al: Magnetic resonance imaging appearance of intracranial hemorrhage secondary to cerebral vascular malformation in a dog. Vet Radiol Ultrasound 38:371, 1997. 60. Drost WT, Berry CR, Fisher PE: Computed tomographic appearance of a normal variant of the canine tentorium cerebelli osseum. Vet Radiol Ultrasound 37:351, 1996. 61. Koblik PD, Lecouteur RA, et al: Modification and application of a Pelorus Mark III stereotactic system for CTguided brain biopsy in 50 dogs. Vet Radiol Ultrasound 40:424, 1999. 62. Koblik PD, Lecouteur RA, et al: CT-guided brain biopsy using a modified Pelorus Mark III stereotactic system: experience with 50 dogs. Vet Radiol Ultrasound 40:424, 1999. 63. Bergman RD, Jones J, et al: Post-operative computed tomography in two dogs with cerebral meningioma. Vet Radiol Ultrasound 41:425, 2000.

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The Ear

❚❚❚ INFLAMMATION AND INFECTION Inflammatory Stenosis of the Ear Canal The diameter of the ear canal can be evaluated radiographically, either by measuring the air cylinder on a plain radiograph (assuming one is present) or by performing aural canalography.1

Contrast Evaluation of the Invisible Eardrum Ordinarily, the eardrum, or tympanic membrane, is evaluated otoscopically. When otoscopic assessment proves difficult or impossible, typically because of past or present chronic ear infections, the eardrum can be appraised indirectly by filling the ear canal with diagnostic iodine solution. A subsequent ventrodorsal radiograph, or canalogram, will provide a cast of the aural cylinder, at the end of which lies the eardrum. The drum has a characteristically flattened appearance, constituting the furthermost wall of the opacified ear canal.2 Leakage of contrast into the associated bulla constitutes strong presumptive evidence of perforation or absence of the eardrum and, in the appropriate patient profile, otitis media.

Bulla Inflammatory Disease (Otitis Media, Middle Ear Disease) Imaging Findings Radiography. Radiography of the tympanic bullae is capable of detecting only diseases that substantially alter morphology: marked thickening or thinning or perforation of the bony perimeter (Figures 17-1 and 17-2). Perceived increases in chamber opacity are notoriously unreliable, most often the result of imprecise patient positioning or superimposition of the tongue (Figures 17-3 to 17-7).

The five standard bulla views are (1) lateral, (2) ventrodorsal, (3,4) right and left lateral obliques, and (5) open mouth (open-mouth rostrocaudal). Of these views, the last projection provides the least superimposition and therefore the clearest, least equivocal image. Hofer and co-workers devised a new closed-mouth, rostrocaudal oblique view of the bullae in cats that eliminates mandibular superimposition. They achieve this by angling the head backward by about 10 degrees (from the standard head-on position).3 Holt and Walker described the appearance of osteotomized bullae in dogs 5 to 7 years after surgery. Surprisingly, they discovered that, contrary to a previous report suggesting the inevitability of bulla obliteration following surgery, many of the operated bullae seemed to have regained their normal appearance. Of additional interest was the fact that surgical outcome did not necessarily coincide with full structural restoration because there was one dog with a normal appearing bulla that continued to have ear problems, whereas others with incomplete bullae seemed cured.4 Computed Tomography. Russo and co-workers published a pictorial essay on the computed tomographic (CT) anatomy of the normal canine ear.5 In it, they include numerous cross-sectional tomographic images of the relevant anatomy along with explanatory line drawings. Love and co-workers showed CT to be more sensitive than radiography in diagnosing otitis media in dogs; however, they contend that radiography should remain the first choice for screening, a recommendation with which I strongly disagree based on the extreme insensitivity of plain radiographs in revealing all but the most severe diseases.6 Caution: Barthez and co-workers confirmed that the wall of a fluid-filled tympanic bulla will falsely appear thickened when imaged with CT.7 This does not occur when the bulla is air filled.8,9 231

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Figure 17-1 • Open-mouth projection of bullae of a dog shows interior and exterior bone deposition and peripheral destruction of the right bulla compatible with chronic infection.

Figure 17-2 • Right lateral oblique projection of bullae of a dog shows interior and exterior bone deposition and peripheral destruction of the right bulla compatible with chronic infection.

Figure 17-3 • Close-up, right view of normal bullae in a dog.

CHAPTER 17 ❚❚❚ The Ear

233

Figure 17-4 • Close-up left lateral oblique view of normal bullae in a dog.

Figure 17-5 • Paired open-mouth views of normal bullae in a dog. Left, The first open-mouth view provides the clearest and most comparable view of the bullae with views in Figure 17-6 compromised by a combination of obliquity and superimposition by the tongue. Right, Close-up open mouth (correct and incorrect head positions). The oblique views were made at slightly different angles, making one bulla appear denser than the other, falsely suggesting fluid.

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SECTION II ❚❚❚ The Skull, Brain, Eye, and Ear

Figure 17-6 • Close-up open-mouth views of normal bullae with superimposition by the tongue, the former resembling disease.

Figure 17-7 • Close-up open-mouth views of normal bullae without superimposition by the tongue—the former resembling disease.

Magnetic Resonance Imaging. Dvir and co-workers described the magnetic resonance imaging (MRI) features of otitis media in a dog with vestibular signs.10 Abnormalities of the interior bullae consisted of epithelial thickening and a laminated mucosa. Soft tissue thickening also was observed in the surrounding soft tissues. Allgoewer and co-workers described the normal MRI appearance of the feline middle ear (Figure 17-8) and five cats with otitis media.11

❚❚❚ INFLAMMATORY POLYPS Background Feline nasopharyngeal polyps are benign growths that originate from the mucosa of the eustachian tube or middle ear. Polyps may grow into the tympanic bulla, nasopharynx, or ear canal. Polyps can produce a variety of clinical signs: ear infection, head tilt, nystagmus, vocalization change, dysphagia, rhinitis, and sneezing. Dogs with aural masses sometimes briefly paw at the affected ear immediately after barking.

Figure 17-8 • Close-up dorsal magnetic resonance image of normal ear canals and bullae of a cat.

CHAPTER 17 ❚❚❚ The Ear

235

metastasize. Carcinomas (squamous cell and undifferentiated) are most common and are optimally treated with a combination of surgical excision and radiation therapy.13

Arteriovenous Fistula An arteriovenous (AV) fistula was reported in the earflap of a young dog, which physically resembled an aural hematoma. But unlike a hematoma, a machinery murmur was present on auscultation. There was no indication of heart failure.14 Two-dimensional ultrasound can readily establish the existence of a peripheral AV fistula, and Doppler can be used to confirm related blood-flow abnormalities. Angiography is a necessity for accurate surgical planning. Figure 17-9 • Close-up left lateral oblique view of the right bulla of a cat with inflammatory polyps. The affected bulla is partially opaque, primarily because of chronic bone deposition, a consequence of the compressive effects of polyps.

Imaging Findings Radiology. In my experience, most inflammatory polyps, regardless of size, are radiographically invisible. Although thickening of the bulla can be associated with the compressive effects of polyps (Figure 17-9), it is more likely to be the result of a chronic ear infection. Occasionally, aural polyps may become so large that they “explode” the bulla, creating an appearance that some have termed aggressive, thus invoking the probability of malignancy. Computed Tomography. Seitz and co-workers showed CT capable of establishing the full extent of polyp development, in particular its extension into surrounding cavities.12

❚❚❚ OTOLITHS Rarely, multiple 1- to 2-mm stone-like objects form in the bulla. Known as otoliths, these objects may be incorporated in soft tissue or, alternatively, may be capable of moving freely about the interior of the bulla, coincident with changes in the animal’s head position. As I demonstrated previously, postural films can easily establish whether otoliths are free or fixed.

❚❚❚ AURAL TUMORS Background Malignant tumors of the ear in dogs and cats are uncommon and tend to be locally invasive but rarely

References 1. Eom K, Lee H, Yoon J: Canalographic evaluation of the external ear canal in dogs. Vet Radiol Ultrasound 41:231, 2000. 2. Eom K, Lee H, Yoon J: Canalographic evaluation of the external ear canal in dogs. Vet Radiol Ultrasound 41:231, 2000. 3. Hofer P, Bartholdi S, Kaser-Hotz, B: A new radiographic view of the feline tympanic bullae. Vet Radiol Ultrasound 36:14, 1995. 4. Holt DE, Walker L: Radiographic appearance of the middle ear after ventral bulla osteotomy in five dogs with otitis media. Vet Radiol Ultrasound 38:182, 1997. 5. Russo M, Covelli EM, et al: Computed tomographic anatomy of the canine inner and middle ear. Vet Radiol Ultrasound 43:22, 2002. 6. Love NE, Kramer RW, et al: Radiographic and computed tomographic evaluation of otitis media in the dog. Vet Radiol Ultrasound 36:375, 1995. 7. Matoon JS, Walker MA: MRI case presented as part of the 1997 ACVR oral certification examination: computed tomography/magnetic resonance imaging elective. Vet Radiol Ultrasound 39:154, 1998. 8. Barthez P, Koblik PD, et al: Apparent wall thickening in fluid filled versus air filled tympanic bulla in computed tomography. Vet Radiol Ultrasound 36:427, 1995. 9. Barthez P, Koblik PD, et al: Apparent wall thickening in fluid filled versus air filled tympanic bulla in computed tomography. Vet Radiol Ultrasound 37:95, 1996. 10. Dvir E, Kirberger RM, Terblanche AG: Magnetic resonance imaging of otitis media in a dog. Vet Radiol Ultrasound 41:46, 2000. 11. Allgoewer I, Lucus S, Schmitz SA: Magnetic resonance imaging of the normal and diseased feline middle ear. Vet Radiol Ultrasound 41:413, 2000. 12. Seitz SE, Losonsky JM, Marretta SM: Computed tomographic appearance of inflammatory polyps in three cats. Vet Radiol Ultrasound 37:99, 1996. 13. Londan CA, Dubilzeig RR, et al: Evaluation of dogs and cats with tumors of the ear canal: 145 cases (1978-1992). J Am Vet Med Assoc 208:1413, 1996. 14. Kealy JK, Lucey M, Rhodes WH: Arteriovenous fistula in the ear of a dog: a case report. 11:15, 1970.

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1 8

The Eye and Orbit

❚❚❚ SONOGRAPHY OF THE EYE: AN OVERVIEW Hager and co-workers compared the diagnostic merits of scanning directly on the corneal surface, through the eyelid, and with a standoff device. They concluded that the standoff device provided the best view of the anterior chamber and lens, whereas direct corneal contact resulted in superior imagery of the posterior chamber and retrobulbar tissues. Through-the-lid scanning produced unacceptable artifacts and was not recommended.1 These same authors described the use of sonographic imaging in various canine ocular disorders.2 Hamidzada and Osuobeni compared the relative accuracy of ocular measurements obtained using two different types of ultrasound: A-mode (measuring the amplitude of echo spikes on a sonographically generated tracing) and B-mode (measuring physical distance between two points on an echographic representation of the eye in which tissue brightness is a function of echo strength).3 Box 18-1 compares the differences between A- and B-mode, concluding that, in general, the deeper the thickness being measured, the greater the likelihood that A- and B-mode values will differ.

❚❚❚ MAGNETIC RESONANCE IMAGING OF THE EYE AND ORBIT: AN OVERVIEW Morgan and co-workers described the magnetic resonance imaging (MRI) appearance of the eye and orbit of the dog and cat.4 Box 18-2 contains generalizations based on their work. Morgan went on to describe the use of MRI in the diagnosis of both ocular and orbital disease, acclaiming its ability to characterize and localize with accuracy a wide variety of lesions,5 similar to what has been done with MRI in human ophthalmology.6 T1-weighted images provided the best overall anatomic detail, whereas proton-density imaging resulted in optimal 236

visualization of the optic nerve and improved margin definition in some retrobulbar masses.

❚❚❚ OCULAR DISEASE Ultrasound is often the only readily available and inexpensive means to see beyond an injured or infected segment of the eye; likewise, ultrasound is the ideal method to determine whether a detached retina accompanies a cataract, a finding that would obviate the benefits of surgery (Table 18-1).

Cataracts Background. Based on the work of van der Woerdt and co-workers, vitreal degeneration should be anticipated in about 25% of dogs with cataracts, with the incidence increasing as cataracts mature. Likewise, the incidence of retinal detachment (about 20% of cases) increases with cataract severity.7 Imaging Findings Sonography. Sonography is the most common and effective means of imaging and staging canine cataracts and any associated abnormalities. In a typical cataract evaluation, the assessments listed in Box 18-3 should be made. Lenticular degeneration begins as a thickening of the lens capsule accompanied by a corresponding increase in echogenicity, which may be uniform or irregular (Figures 18-1 to 18-3). Some cataracts have a slightly wrinkled appearance, whereas others are perfectly smooth. With increasing severity, termed maturity in the lexicon of ophthalmology, the interior of the cataract may take on a highly distinctive pattern resembling light being reflected off a convex metal surface, much as it might from the hubcap of an automobile (Figures 18-4 and 18-5). Because cataracts often prevent visualization of the posterior chamber and retina, and thus may conceal

CHAPTER 18 ❚❚❚ The Eye and Orbit

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Table 18-1 • A SONOGRAPHIC CHECKLIST FOR COMMON DISORDERS OF THE CANINE AND FELINE EYE Ocular Component

Trauma

Cornea, anterior chamber

Corneal edema, corneal defect, aqueous hemorrhage Dislocation (cranial or caudal)

Lens

Uveitis

Cataract

Tumor

Severity is determined by echogenicity, size and shape of lens

Iris, ciliary body

Edema, deformity (including tearing), hemorrhage

Anterior uveitis

Posterior chamber, vitreous chamber Optic nerve, retina, choroid, and sclera

Hemorrhage, foreign body Retinal detachment (partial or complete), tearing

Posterior uveitis Swelling of optic nerve?

Vitreal degeneration Fully or partially detached retina

Primary tumors: melanoma, ciliary body adenoma, and adenocarcinoma Metastatic lymphosarcoma Secondary vitreal hemorrhage Secondary retinal detachment

Taken in part from Gonzalez EM, et al: Review of ocular ultrasonography. Vet Radiol Ultrasound 42:485, 2001.

B o x

1 8 - 1

B o x

1 8 - 3

Accuracy of B-Mode Ocular Measurement

Sonographic Evaluation of Cataracts in Dogs

• • • •

• • • • •

B-mode overestimates corneal thickness B-mode overestimates anterior chamber depth B-mode underestimates lens thickness B-mode underestimates vitreous chamber depth • B-mode underestimates axial length

B o x

Presence or absence of lens dislocation Presence or absence of lens-induced uveitis Presence or absence of retinal detachment Presence or absence of vitreous degeneration Stage of cataract severity: immature, mature, or hypermature

1 8 - 2

T1, Proton Density, and T2 Images Produced Different Appearing Orbital Structures • T1 images provided the greatest contrast of the retrobulbar structures. • T1 images offered the best contrast thanks to a high signal to noise ratio. • The dorsal sagittal and oblique sagittal viewing planes were best for evaluating the entire optic nerve.

vitreal degeneration or a detached retina, ultrasound is often performed before surgery. Vitreal degeneration initially takes the form of a faint, uneven, often punctate solidification of the vitreous. As the condition worsens, discrete clumps and strands form, some becoming quite large (Figures 18-2 and 18-6). Retinal detachment may be partial or complete (Figure 18-7); if recent, it may be associated with hemorrhage. Computed Tomography and Magnetic Resonance Imaging. Although computed tomography (CT) and MRI remain in a relative state of diagnostic infancy as far as general veterinary medicine is concerned, the

Figure 18-1 • Close-up ocular sonogram of an early cataract in a dog indicated by two pairs of electronic cursors.

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Figure 18-2 • Close-up ocular sonogram of an early cataract in a dog shows (1) slight marginal wrinkling, (2) uneven capsular thickening and echogenicity, and (3) partial interior solidification.

Figure 18-4 • Close-up sonogram of a “mature” cataract in a dog featuring a “hubcap” sign.

Figure 18-3 • Close-up ocular sonogram of an early-tointermediate cataract in a dog shows capsular thickening and increased echogenicity, along with a plume-like pattern of vitreal degeneration.

use of CT is well established in the radiation and surgical treatment planning of orbital and periorbital masses. In many ophthalmology specialty practices, the use of CT and MRI is growing, as evidenced by a fledgling literature; for example, CT was used to precisely locate a dislodged lens in the vitreal body of a cat.8

Ocular Injury Corneal abrasion and bleeding into the anterior chamber (hyphema) are the most common types of eye

Figure 18-5 • Close-up sonogram of a “hypermature” cataract in a dog featuring a variant of the “hubcap” sign.

injuries in dogs. Acute and subacute corneal injuries usually cause corneal thickening as a result of edema; hemorrhage in the anterior chamber leads to varying degrees of echogenicity (Figures 18-8 and 18-9). Extremely forceful injuries also can cause dislocation of the lens and retinal detachment. Puncture wounds can result not only in chamber bleeding, collapse, and later infection, but they also

CHAPTER 18 ❚❚❚ The Eye and Orbit

Figure 18-6 • Close-up sonogram of a advanced cataract in a

239

Figure 18-8 • Close-up ocular sonogram of a dog with recent facial trauma shows a diffusely echogenic anterior chamber, the result of hemorrhage.

dog, accompanied by severe, structured vitreal degeneration.

Figure 18-7 • Close-up sonogram of a “mature” cataract in a dog associated with mild to moderate vitreal solidification and a complete retinal detachment (shallow V-shaped object located at the bottom center of the photograph).

Figure 18-9 • Close-up ocular sonogram of a dog with a recent eye injury shows an echogenic anterior chamber caused by hemorrhage.

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Figure 18-10 • Close-up ocular sonogram of a dog with a partially detached retina.

Figure 18-11 • Close-up ocular sonogram of a dog with a porcupine quill (thick diagonal band) lodged beneath a partially detached retina (left center of photograph).

can tear or dislodge one or more intraocular elements, depending on how deeply the globe is penetrated. Once intraocular fibrin begins to accumulate in quantity, and especially if it is accompanied by pus, sonographic orientation can be very difficult. In such instances, it is often prudent to perform a brief preliminary examination (5 or 10 minutes at most), study the initial images, consider the possibilities, check reference material as necessary, and then reexamine the eye. Hyphema. Hemorrhage in the anterior chamber of the eye, or hyphema, is usually a consequence of trauma. Depending on the extent of the bleeding, the chamber may become expanded, making it impossible to see beyond the clot, which in the latter instance necessitates the use of ultrasound to see farther (see Figures 18-8 and 18-9). Retinal Detachment. Retinal detachment may be partial or complete, which in the latter instance is characterized by a distinctive gull-wing appearance (Figure 18-7) and less often by a tulip-like configuration. Occasionally, a large strand or cylinder of inflammatory or degenerative tissue forms in the posterior chamber, resembling partial detachment (Figure 18-10).

Ocular Foreign Bodies Metallic ocular foreign bodies are radiographically detectable, provided at least two right-angle views are obtained; otherwise, ultrasound will be required to identify quill fragments, splinters, and the like (Figures 18-11 and 18-12).

Figure 18-12 • Close-up ocular sonogram of a dog with a porcupine quill piercing the back of the globe (brightly tipped thick line at bottom center of photograph).

Ocular Infection In my opinion, ocular infection—-with all its permutations—-is the most difficult type of eye disease to decipher sonographically. Even more challenging is the failed cataract surgery that becomes infected following surgery. In such cases, I prefer to image the opposite eye as a control, to include measurements, an indispensable aid when it comes to figuring out what is what in the infected eye.

Ocular Tumors A variety of ocular tumors have been reported, including primary melanoma, adenoma, and adenocarci-

CHAPTER 18 ❚❚❚ The Eye and Orbit

B o x

241

1 8 - 4

Potential Causes of Orbital Gas (Emphysema) • Orbital and periorbital fractures • Iatrogenic (attempted biopsy, aspiration, or drainage) • Bacterial cellulitis • Fungal cellulitis • Fibrosarcoma • Lymphosarcoma • Osteoma • Parosteal osteoma • Squamous cell carcinoma From Wolfer J, Grahn B: Diagnostic ophthalmology. Can Vet J 36:186, 1995.

Figure 18-13 • Lymphoma: Close-up ocular sonogram of a dog with a caudal segment tumor appearing as a medium-sized, stellate mass on the back surface of the eye.

noma. In the ciliary body, the last of these cell types may be associated with retinal detachment.9 By way of the unusual, a metastatic transmissible venereal tumor to the eye and brain has been reported.10 Metastatic lymphomas have a highly variable appearance (Figure 18-13).

Congenital Eye Disease Congenital eye disease is rare in dogs and cats. Borrofka and co-workers reported the sonographic appearance of persistent hyperplastic tunica vasculosa lentis, primary vitreous, and hyaloid artery in two dogs.11

❚❚❚ ORBITAL DISEASE AND PERIORBITAL DISEASE Imaging Findings Radiology. Radiology is capable of identifying orbital destruction, periorbital new bone deposition, and moderate to severe soft tissue swelling. Cranial sinus venography (also termed cavernous sinus venography and orbital venography) is capable of evaluating the veins of the orbit and the ventral cranial sinuses, especially with respect to identifying arteriovenous fistulas (Unpublished observations, 1979).12,13 The same special procedure has been used to identify metastatic pheochromocytoma in the retrobulbar region of a dog, one of which was associated with ophthalmoplegia.14,15 Pluhar and co-workers described an alternative method of performing cranial sinus venography in which a catheter is inserted into the external jugular vein and advanced to the level of the temporal sinus; then nonionic contrast solution is injected manually

(3-5 mL). Subtraction radiography, using survey films and venograms, is done to optimize vascular clarity, and the resultant images are interpreted. The authors contend that their method is superior to previously described methods because it opacifies both the dorsal and ventral sinus systems, whereas others only opacify one or the other. A detailed, labeled map of the relevant vasculature is included in the article.16 Ultrasound. Morgan reported using sonography to diagnose retrobulbar diseases in the dog and cat.17 Sonology is capable of identifying the eye and the soft tissues of the optic cone; however, orbital ultrasound is not routinely capable of discriminating benign from malignant lesions. Extraocular foreign bodies, such as foxtails, vary in their sonographic visibility, depending largely on their immediate background. Computed Tomography. Fike and co-workers initially described the tomographic anatomy of the normal canine orbit in a pictorial essay that appeared in Veterinary Radiology in early 1984.18 CT also has been used to diagnose aspergillosis in a cat.19 Magnetic Resonance Imaging. Magnetography (MRI) is diagnostically superior to radiology and ultrasound in the investigation of extraocular disease.20 It is very expensive, however, and as a result is currently used sparingly.

❚❚❚ ORBITAL EMPHYSEMA (Box 18-4) Orbital Tumors Background. In a recently reported retrospective study, Hendrix and Gelatt indicated that most orbital tumors are malignant, with osteosarcoma being the most common, followed by fibrosarcoma and nasal adenosarcoma.21 The average age of occurrence in dogs

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SECTION II ❚❚❚ The Skull, Brain, Eye, and Ear

is at about 8 years. Most animals have a history of slowly progressive and often painful exophthalmia. Differential diagnosis usually includes cellulitis and orbital abscess. An initial diagnosis of infection, based on rapid lesion development and improvement with antibiotics, may later prove incorrect because some cancers seem to develop suddenly and cause considerable local inflammation, resembling sepsis. Fineneedle biopsy proves diagnostic in about half of all cases, with a comparable percentage being euthanized or dying of their disease within 6 months. Imaging Findings Radiology. Plain radiographs may reveal destruction of orbital bone, an indication of serious and often fatal disease. On a probability basis, orbital lysis is more likely to indicate cancer than osteomyelitis, although both possibilities warrant diagnostic consideration. Ultrasound. Sonographically, orbital masses are quite variable and rarely provide clear evidence as to cell type. Most animals with an identified orbital tumor fail to show pulmonary metastases, although occasionally some do (radiographically).22 Tumors of the optic nerve may produce a focal concavity on the posterior surface of the eye that coincides with the insertion of the optic disc.23 Magnetic Resonance Imaging. Davidson and Kraft described an infiltrative retrobulbar lymphosarcoma diagnosed with nuclear magnetic resonance.24 Matoon and Walker reported the MRI appearance of a nasal adenocarcinoma that extended from the nasal cavity into the left periorbital region, through the cribriform plate, and into the rostral part of the brain.25 Morgan and colleagues described a retrobulbar meningioma that appeared as a well-circumscribed mass that could be differentiated from the optic nerve with some pulse sequences, but not with others, and could be seen extending caudally in the direction of the optic chiasm. The tumor was hyperintense to muscle in all pulse sequences.26

❚❚❚ EXOPHTHALMIA Exophthalmia and submandibular swelling have been reported in dogs as a result of sialadenosis: a bilateral, uniform, painless, and noninflammatory enlargement of the zygomatic or submandibular salivary glands.27 Exophthalmia also may be caused by pressure on the back of the eye from a mass, such as a tumor, abscess, or foreign body (with its attendant tissue reaction). Arteriovenous fistulas are capable of producing constant or intermittent exercise-induced exophthalmia. Tidwell and co-workers described a case of persistent exophthalmia diagnosed by using a combination of tomography, plain magnetic resonance, and magnetic resonance angiography.28

Figure 18-14 • Close-up orbital sonogram of a dog with a retrobulbar abscess (marked with electronic calipers).

❚❚❚ RETROBULBAR ABSCESS Background Retrobulbar abscesses most often result from penetrating foreign bodies, dental abscesses, or extension of a nasal or sinus infection. The bacteria cultured from such infections are typically normal nasal, oral, or skin flora.

Imaging Findings Retrobulbar abscesses, like retrobulbar tumors, exhibit variable echogenicity and morphology; thus, biopsy is required for definitive diagnosis.29 In general, however, abscesses develop more rapidly and are more painful (Figure 18-14).

❚❚❚ PERIORBITAL DISEASE Dacryocystitis Dacryocystitis, or inflammation of the tear sac, is usually caused by prolonged obstruction of the nasolacrimal duct. Secondary localized or regional dilation of the duct is a common sequela. Plain films are rarely of any use in such cases; however, dacryocystorhinography often can establish whether or not the nasolacrimal duct is patent and, if obstructed, whether or not there is secondary dilation.30

References 1. Hager DA, Dziezyc J, Millchamp NJ: Two-dimensional realtime ocular ultrasonography in the dog. Vet Rad 28:60, 1987. 2. Dziezye J, Hager DA, Millichamp NJ: Two-dimensional real-time ocular ultrasonography in the diagnosis of ocular lesions in dogs. J Am Anim Hosp Assoc 23:501, 1987.

CHAPTER 18 ❚❚❚ The Eye and Orbit

3. Hamidzada WA, Osuobeni EP: Agreement between Amode and B-mode ultrasonography in the measurement of ocular distances. Vet Radiol Ultrasound 40:502, 1999. 4. Morgan RV, Daniel GB, Donnell RL: Magnetic resonance imaging of the normal eye and orbit of the dog and cat. Vet Radiol Ultrasound 35:102, 1994. 5. Morgan RV, Ring RD, et al: Magnetic resonance imaging of ocular and orbital disease in 5 dogs and a cat. Vet Radiol Ultrasound 37:185, 1996. 6. De Potter P, Shields JA, Shields CL: MRI of the eye and orbit, Philadelphia, 1995, JB Lippincott. 7. Van der Woerdt A, Wilkie DA, Myer CW: Ultrasonic abnormalities in the eyes of dogs with cataracts: 147 cases (1986-1992). J Am Vet Med Assoc 203:838, 1993. 8. Abrams KL: Ultrasound/CT diagnosis. Vet Rad 31:186, 1990. 9. Hoskins BN, Koenig HA, Adaska J: What is your diagnosis? J Am Vet Med Assoc 203:1273, 1993. 10. Ferreira AJA, Jaggy A, et al: Brain and ocular metastases from a transmissible venereal tumor in a dog. J Small Anim Pract 41:165, 2000. 11. Boroffka SAEB, Verbruggen A-MJ, et al: Ultrasonographic diagnosis of persistent hyperplastic tunica vasculosa lentis/persistent hyperplastic primary vitreous in two dogs. Vet Radiol Ultrasound 39:440, 1998. 12. Oliver JE: Cranial sinus venography in the dog. J Am Vet Rad Soc 10:66, 1969. 13. Dixon RT, Carter JD: Canine orbital venography. J Am Vet Rad Soc 13:43, 1972. 14. Oliver JE, Fletcher OJ, et al: Pheochromocytoma to the retrobulbar region of the canine skull: demonstration by cavernous sinus venography. J Am Vet Rad Soc 11:17, 1971. 15. Griffiths IR, Lee R: Ophthalmoplegia in the dog and the use of cavernous sinus venography as an aid to diagnosis. J Am Vet Rad Soc 11:22, 1971. 16. Pluhar GE, Tucker RL, et al: Cerebral sinus venography in the dog: a new technique. Vet Radiol Ultrasound 38:112, 1997.

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17. Morgan RV: Ultrasonography of retrobulbar disease of the dog and cat. J Am Anim Hosp Assoc 25:393, 1989. 18. Fike JR, LeCouteur RA, Cann Christopher E: Anatomy of the canine orbital region. Vet Rad 25:32, 1984. 19. Hamilton HL, Whitly RD, McLaughlin SA: Exophthalmus secondary to aspergillosis in a cat. J Am Anim Hosp 36:343, 2000. 20. Dennis R: Use of magnetic resonance imaging for the investigation of orbital disease in small animals. J Small Anim Pract 41:145, 2000. 21. Hendrix DVH, Gelatt KN: Diagnosis, treatment and outcome of orbital neoplasia in dogs: a retrospective study of 44 cases. J Small Anim Pract 41:105, 2000. 22. Martin E, Perez J, et al: Retrobulbar anaplastic astrocytoma in a dog: clinicopathological and ultrasonic features. J Small Anim Pract 41:354, 2000. 23. Abrams K, Toal RL: What is your diagnosis? J Am Vet Med Assoc 196:951, 1990. 24. Davidson HJ, Kraft SL: Imaging diagnosis. Vet Radiol Ultrasound 35:282, 1994. 25. Matoon JS, Walker MA: MRI case presented as part of the 1997 A.C.V.R. oral certification examination: computed tomography/magnetic resonance imaging elective. Vet Radiol Ultrasound 39:154, 1998. 26. Morgan RV, Ring RD, et al: Magnetic resonance imaging of ocular and orbital disease in 5 dogs and a cat. Vet Radiol Ultrasound 37:185, 1996. 27. Boydell P, Pike R, et al: Sialadenosis in dogs. J Am Vet Med Assoc 216:872, 2000. 28. Tidwell AS, Ross LA, Kleine LJ: Computed tomography and magnetic resonance imaging of cavernous sinus enlargement in a dog with unilateral exophthalmus. Vet Radiol Ultrasound 38:363, 1997. 29. Homco LD: Retrobulbar abscesses. Vet Radiol Ultrasound 36:240, 1995. 30. Van de Woerdt, Wilkie DA, et al: Surgical treatment of dacryocystitis caused by cystic dilatation of the nasolacrimal system in three dogs. J Am Vet Med Assoc 211:445, 1997.

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Miscellaneous Diseases

❚❚❚ MANDIBULAR INFECTION Typically, mandibular infections are characterized by gradual new bone formation, followed by subtle marginal bone loss. In most cases, the new bone extends well to either side of the area of bone loss, prompting the adjacent soft tissues to become inflamed, swell, and sometimes drain. In deep infections, teeth may be lost, which in turn may lead to an insufficiency fracture. Mandibular infections, bacterial or mycotic, may closely resemble both primary and secondary mandibular tumors (Figures 19-1 to 19-6).

❚❚❚ CRANIOMANDIBULAR OSTEOPATHY Background Craniomandibular osteopathy is a unique disease of dogs that for the most part affects immature Scottish, West Highland White, and Cairn Terriers. Typically, large masses of new bone form along the caudal aspects of the ventral mandible and around the tympanic bullae, making chewing painful (and in some instances impossible). Occasionally, the long bones are also affected, taking the form of large bony cuffs on the distal diaphyses and metaphyses, resembling the reaction found in hypertrophic osteodystrophy. Affected dogs are typically feverish, head-sore, and appear ill. Once an animal matures, however, the abnormal bone deposition usually subsides, and the bones remodel, in some cases returning to normal.1 The cause (or causes) of primary craniomandibular osteopathy remains obscure; because of breed specificity, a genetic linkage seems likely. “Secondary” craniomandibular osteopathy has been reported in Irish Setter puppies with canine leukocyte adhesion deficiency 244

(CLAD), a rare blood disease that has also been associated with hypertrophic osteodystrophy and osteomyelitis.2

Imaging Findings Radiology Craniomandibular osteopathy typically results in one of two unique patterns of mandibular bone deposition. The first envelops the central and caudal thirds of the horizontal ramus, whereas the second affects the temporomandibular region as well as the mandible. The latter is the more serious variant because it can mechanically prevent the lower jaw from opening fully. Debate exists as to whether or not this disease causes dental pain. Computed Tomography. Hudson and co-workers described the computed tomographic (CT) appearance of craniomandibular osteopathy in a West Highland White Terrier, which they followed up from 41/2 to 161/2 months of age. The authors contend that CT provides optimal assessment of the critical tympanic bulla/ angular process region of the skull. As is usual in such accounts, no mention was made of imaging costs, which were assumed to be substantial.3

❚❚❚ CONGENITAL OROFACIAL DEFORMITY Orofacial anomalies are rare in dogs and cats. In most cases, they can be differentiated from a previous injury by the fact that an orofacial disorder typically involves both the maxilla and mandible (Figure 19-7), whereas injuries tend to affect one or the other. Additionally, the deformities attending a congenital disorder typically match one another, whereas those arising from trauma do not.

CHAPTER 19 ❚❚❚ Miscellaneous Diseases

Figure 19-1 • Orientation view of the ventral aspect of the lower jaw shows a ragged ridge of new bone resulting from bacterial infection.

Figure 19-2 • Close-up view of the ventral aspect of the lower jaw shows a ragged ridge of new bone resulting from bacterial infection.

Figure 19-3 • Mycotic osteomyelitis: Close-up lateral oblique view of the left mandible shows a thick, uneven layer of intermediate duration new bone (emphasis zone) caused by a blastomycotic infection.

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Figure 19-5 • Lateral oblique view of a chronically infected displaced mandibular fracture. The letter “O” marks a draining skin sinus.

Figure 19-4 • Lateral view of a chronically infected displaced mandibular fracture. The letter “O” marks a draining skin sinus.

Figure 19-6 • The normal opposite side is included for comparison (see Figure 19-5).

Figure 19-7 • Close-up open-mouth view made with soft tissue technique shows a congenital orofacial anomaly in an otherwise healthy dog.

CHAPTER 19 ❚❚❚ Miscellaneous Diseases

References 1. Riser WH, Parkes LJ, Shirer JF: Canine craniomandibular osteopathy. J Am Vet Rad Soc 8:23, 1967. 2. Trowald-Wigh G, Ekman S, et al: Clinical, radiological and pathological features of 12 Irish Setters with canine leukocyte adhesion deficiency (CLAD). J Small Anim Pract 41:211, 2000.

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3. Hudson JA, Montgomery RD, et al: Computed tomography of craniomandibular osteopathy in a dog. Vet Radiol Ultrasound 35:94, 1994.

S E C T I O N

I I I

The Spine

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Spinal Radiographic Disease Indicators ❚❚❚ DIAGNOSTIC IMPERATIVES: CAREFUL POSITIONING AND COMPARATIVE ASSESSMENT Nowhere else in the skeleton is meticulous positioning more important than in the spine. Specifically, if the spine is not positioned perpendicular to the x-ray collimator, it becomes difficult or impossible to assess comparatively the individual vertebral units and their associated intervertebral disks (Figures 20-1 and 20-2; Tables 20-1 and 20-2).

❚❚❚ DIMINISHED DISK SIZE (DIMINISHED DISK SPACE) Diminished disk size infers volume loss. In acute paralysis, this is usually due to disk rupture, also termed disk herniation or extrusion (Figure 20-3). When paresis and incoordination are present, however, the cause is more likely a bulging (protruding) disk. Accompanied by spondylosis, a narrowed disk probably has undergone some degree of related “degeneration”

(dehydration, calcification, nuclear solidification, scarring). Associated with endplate destruction, a reduced disk size usually means infection or discospondylitis (Figure 20-4), but it also may have resulted from a previous disk fenestration (Figure 20-5). Where broader bony disintegration is present, a spinal or paraspinal tumor becomes a strong possibility (Figure 20-6). Block vertebrae (also known as blocked vertebrae) often contain one or more narrow vestigial disks in addition to collation (Figure 20-7).

❚❚❚ NEW BONE DEPOSITION The most common cause of vertebral new bone deposition in dogs is spondylosis. Most authorities contend that spondylosis is innocuous, although this belief is in large measure anecdotal. Spondylosis can occur anywhere in the spine but is most common in the lumbosacral spinal unit. In its earliest stage of development, spondylosis is characterized by small, paired, beak-like bone deposits Text continued on p. 254

249

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Table 20-1 • NORMAL ANATOMIC VARIANTS THAT RESEMBLE SPINAL RADIOGRAPHIC DISEASE INDICATORS (RDIs) Anatomic Variant

False RDI

Gas in the intervertebral disk (disk space)

Intradisk gas may be mistaken for a by-product of bacterial infection. Actually, small amounts of gas can temporarily appear in the intervertebral disk (disk space) as a result of the vacuum phenomenon (nitrogen drawn into a joint from surrounding extracellular fluid, as a result of forceful distraction).* This finding is even more obvious on CT.†

Roughening or spicula of the caudal aspect of the dorsal spinal process of the axis (C2)

This is the attachment site of the nuchal ligament, and, as such, is necessarily quite irregular. Unaware of the anatomic variability of this part of C2, one is liable to misinterpret it as an old injury.

Variable overhang of dorsal spinous process of C2 above C1. Some small breeds have no overhang, whereas many larger breeds have nearly 100% overhang

Atlantoaxial sprain-dislocation

C2-3 spinal unit has a smaller disk (disk space) than adjacent spinal units, a normal anatomic difference

C2-3 ruptured disk

CT, Computed tomography. *Modified from Lamb CR: Letters. Vet Radiol Ultrasound 36:164, 1995. † Modified from Hathcock JT: Vacuum phenomenon of the canine spine: CT findings in 3 patients. Vet Radiol Ultrasound 35:285, 1994.

Table 20-2 • POSITIONAL VARIANTS THAT RESEMBLE SPINAL RADIOGRAPHIC DISEASE INDICATORS (RDIs) Positional Variant

False RDI

Variable space between occipital condyles and articular surface of C1, which is primarily related to degree of head flexion and beam centering

Atlantoaxial dislocation

One or two, large diagonally oriented bone densities overlying C1 (Figures 20-1 and 20-2), which represent the oblique transverse processes of C1

C1 fracture

C7 appears shorter in length than C6, a normal anatomic difference

C7 compression fracture

A series of spinal units (often T1 or lumbar) appear to have progressive narrowed disks, the result of radiographic decentering

Bulging or ruptured disks

The lumbosacral spinal unit contains a dorsally offset density resembling a calcified disk, the result of pelvic obliquity (Figure 20-3)

Calcified disk, and also by inference, cauda equina syndrome

Table 20-3 • CONTEXTUAL DIAGNOSIS OF ABNORMALLY SMALL INTERVERTEBRAL DISK (DISK SPACE) Context

Probable Diagnosis

Diminished disk size with acute paralysis

Ruptured intervertebral disk

Diminished disk size with mild pain or incoordination

Bulging intervertebral disk

Diminished disk size with chronic pain or neurologic deficit

Scarred intervertebral disk

Diminished disk size with spondylosis, but without pain or neurologic deficit

Noncompressive, nonirritating degenerative intervertebral disk

Diminished disk size with spondylosis, but without pain or neurologic deficit; history of prior back surgery

Preemptive surgical disk removal (disk fenestration)

Diminished disk size with spondylosis, but without pain or neurologic deficit; history of prior back surgery

Preemptive chemical disk removal (chemonucleolysis). Note: The radiographic changes associated with this procedure vary with method and spinal region. See the article by Atilola for details.*

Diminished disk size with spondylosis, but without pain or neurologic deficit; history of prior back surgery

Preemptive lasar disk removal

*Modified from Atilola MAO, Cockshutt JR, et al: Collagenase chemonucleolysis—a long term radiographic study in normal dogs. Vet Radiol Ultrasound 34:321, 1993.

CHAPTER 20 ❚❚❚ Spinal Radiographic Disease Indicators

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A

B Figure 20-1 • A, Close-up lateral oblique view of the proximal portion of the cervical spinal region is poorly suited to the task of evaluating the occipital condyles and C1-2 spinal unit. This view does provide an excellent view of the dens, however, which is otherwise obscured by the transverse processes of C1. Note: The vertebral endplates are separated from the vertebral bodies by growth plates, indicating skeletal immaturity. B, Close-up lateral oblique view of the proximal portion of the cervical spinal region of an immature dog shows multiple open growth plates unique to the C1-2 spinal unit.

Figure 20-2 • Close-up lateral (top) and lateral oblique (bottom) views of the lumbosacral spinal unit of a healthy dog illustrate how obliquity can simulate a calcified intervertebral disk and, by inference, cauda equina syndrome.

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Figure 20-3 • Close-up lateral view of the thoracolumbar spinal region of a dog with hind-limb paralysis shows a narrowed, partially calcified disk in the T12-13 spinal unit. The progressive narrowing present in the adjacent cranial spinal units is the result of nonparallel imaging, not further disease.

A

B Figure 20-4 • A, Close-up lateral view of the proximal cervical spinal region shows loss of the C3-4 disk and a portion of each associated endplate. B, An ultraclose view of C3-4 shows a mortise-like pattern of endplate destruction occasionally seen in cervical discospondylitis.

CHAPTER 20 ❚❚❚ Spinal Radiographic Disease Indicators

253

A

A

B Figure 20-5 • Close-up lateral (A) and ventrodorsal (B) views of a previously fenestrated T12-13 spinal unit show characteristic postoperative changes including partial disk loss, endplate sclerosis, and disfiguration. The new bone deposition on the ventral aspect of T13 is spondylosis; the new bone on the underside of T12 is the result of a minor surgical infection (spondylitis). Note the difference in the size, shape, and location of these abnormal bone deposits, features that can be used to distinguish between these two entities.

B Figure 20-6 • Close-up lateral (A) and ventrodorsal (B) views of the central cervical spine show collation of C4, C5, and C6, a congenital malformation termed block or blocked vertebrae.

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Figure 20-7 • Close-up lateral view of a severely spondylotic lumbosacral spinal unit in a dog shows characteristic features including (1) ventral bridging, (2) endplate sclerosis, and (3) decreased disk size.

A Figure 20-8 • Defleshed bone specimen (lateral perspective) of anticlinal region of the thoracic spine of a dog shows a mildly displaced fracture through a large, multiunit spondylotic bridge.

located on either side of the disk ventrally. Later, further bone deposition may occur along the lateral margins of the endplates, causing them to appear whiter than normal or sclerotic. In some instances, the spondylotic spurs become so large that they join each other, bridging the ventral aspect of the affected spinal unit (Figure 20-8). Irregular bone deposition on the underside of a vertebral body (as it appears in a lateral radiograph), especially when centrally located, suggests infection, also termed spondylitis, and less often, tumor (Figure 20-9).

❚❚❚ LOCALIZED BONE LOSS Ill-defined localized bone loss in the spine is unusual and usually is indicative of a tumor. Well-marginated foal bone loss is rare, as are the diseases that cause it (Figure 20-10). Occasionally, the lateral vertebral foramen of C1 is mistaken for a lesion.

B Figure 20-9 • Close-up (A) and ultraclose (B) lateral views of the proximal cervical spine of a dog show irregularly marginated bone deposition on the ventral aspect of C1 caused by infection (spondylitis).

CHAPTER 20 ❚❚❚ Spinal Radiographic Disease Indicators

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❚❚❚ DIFFUSE BONE LOSS Localized Diffuse bone loss involving a single vertebra is usually the result of a malignant bone tumor, although it is difficult or impossible to separate a primary from a metastatic lesion (Figure 20-11). Bone loss centered on an intervertebral disk unusually is caused by infection (discospondylitis). Loss of a dorsal spinal process or a portion of the lamina may be due to a tumor or a previous laminectomy. Bone loss extending over one or two spinal units is usually cancerous or, less often, the result of infection (Figure 20-12). A

Regional and Diffuse A generalized loss of spinal density in an older dog or cat is often age-related osteoporosis and to my knowledge is of no clinical consequence. In a young dog, however, a generalized decrease in spinal density may

B Figure 20-10 • Close-up lateral view of the midlumbar spinal

Figure 20-11 • Diffuse bone loss. Close-up lateral (A) and

region of a dog shows a circular lucency at the base of the dorsal spinal process of L3, a so-called target lesion, the result of multiple myeloma.

ventrodorsal (B) views of the C4-5 spinal unit show a near-complete absence of disk and a subtle loss in C4 bone density, the results of an osteosarcoma.

Figure 20-12 • Close-up lateral view of the cranial portion of a cat’s tail shows extensive destruction of the dorsal elements of three consecutive coccygeal spinal units caused by a fibrosarcoma.

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Figure 20-13 • Close-up view of caudal part of cervical spine shows a large block vertebra formed from C4, C5, and C6.

Table 20-4 • DIFFERENTIATING CONGENITAL BLOCKED VERTEBRAE FROM SPINAL DISEASE Disease

Comments

Congenital anomaly

Embryologically, individual vertebrae are formed by the coalition of many small elements. Occasionally, the components of 2 vertebrae join, forming a sort of super vertebra, which is predictably about twice the length of normal vertebrae. Often the associated intervertebral disk is absent, or only partially visible. Congenital fusion may also be partial, selectively involving the dorsal spines, facetal joints, or neural arches.

Discospondylitis

Healed discospondylitis may resemble blocked vertebrae. If the infection was severe or the involved endplates curetted surgically, the length of the vertebral unit in question is likely to be obviously shorter than that of 2 adjacent vertebrae.

Intervertebral disk fenestration

Although not as surgically popular as it once was, prophylactic disk fenestration with associated endplate trauma may produce a spinal unit that is indistinguishable from a congenital block vertebrae.

Laminectomy, hemilaminectomy

Laminectomy and hemilaminectomy sites can resemble blocked vertebrae, a misdiagnosis that is unlikely in the context of a complete surgical history.

Trauma

Although not very likely, old fractures or fracture-dislocations may resemble blocked vertebrae.

indicate a metabolic bone disorder, such as nutritional secondary hyperparathyroidism. Dogs that have become paralyzed in their hindquarters following a thoracolumbar or lumbar fracture or disk rupture gradually lose bone density from the caudal spine, pelvis, and hind limbs.

❚❚❚ ALTERED VERTEBRAL SHAPE

Table 20-5 • DIFFERENTIATING CONGENITAL HEMIVERTEBRAE FROM SPINAL DISEASE Disease

Comments

Congenital hemivertebrae

Although usually depicted as discrete triangles, hemivertebrae are quite variable in shape. They are most prevalent in the small, screwtailed breeds such as pugs or Boston Bull Terriers.

Infection

Severe vertebral infections sometimes deplete sufficient bone so as to resemble hemivertebrae; however, unlike hemivertebrae, they do not conform as well with the adjacent spinal units.

Trauma

Occasionally, healed vertebral compression fractures resemble hemivertebrae.

Blocked Vertebrae (Block Vertebrae) Individual vertebrae are formed embryologically from multiple smaller pieces. When more than the usual number of elements join together, the result is an elongated vertebra, which is also termed a block or blocked vertebra. Most block vertebrae are from 1.5 to 2 times the length of a normal vertebra. Occasionally, more than two vertebrae join, resulting in scoliosis or some other form of spinal curvature (Figure 20-13; Table 20-4).

Wedged Vertebrae (Hemivertebrae) Wedged vertebrae (also known as hemivertebrae) are created embryologically when individual vertebrae

CHAPTER 20 ❚❚❚ Spinal Radiographic Disease Indicators

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Table 20-6 • DIFFERENTIAL DIAGNOSIS OF ENDPLATE ABNORMALITIES Endplate Alteration

Comments

Displacement

Dorsal or ventral endplate displacement is invariably the result of spinal injury.

Fracture

Endplate fractures typically involve the upper or lower thirds of the bone, and are usually associated with mild to moderate displacement. The uninjured portion of the endplate remains fixed in position.

Distortion

Distorted endplates may result from a previous fracture (malunion), congenital anomaly, and occasionally, previous laminectomy.

Destruction

Infection (discospondylitis) is the most common cause of endplate destruction. Rarely, a portion of an intervertebral disk may become imbedded in the central third of the endplate.

Absence

Block vertebra may lack interior disks, or have only faint vestigial disks. The intervertebral disk may be destroyed by tumor or infection. Chronic spondylosis is often marked by an absence or marked diminishment of the disk. Although not as popular as it once was, disk fenestration results in the absence of an intervertebral disk, usually combined with endplate sclerosis and atypical spondylosis.

Sclerosis

Sclerosis, or increased endplate whitening

Production

Endplate new bone deposition may be seen in a variety of circumstances including injury, infection, tumor, and fenestration.

are formed from fewer than the normal number of somites. Hemivertebrae vary in shape from triangular to cube-like and in most instances have a rounded ventral aspect (as seen in a lateral radiographic projection). Occasionally, tumors, infections, and compression fractures can deform a normal vertebra so that it resembles a wedge vertebra. One way to differentiate these possibilities is to examine the adjacent vertebral bodies and disks, which typically will articulate more normally with a hemivertebra than with an acquired spinal deformity (Table 20-5).

❚❚❚ VERTEBRAL ENDPLATE ALTERATIONS Except for the first two cervical elements, immature dogs have a pair of discrete endplates at either end of each vertebra, separated by growth plates. Once the spine ceases to grow, the endplates are incorporated into the vertebral body, and the growth plates disappear. Potential alterations to the appearance of vertebral endplates in a dog include (1) displacement, (2) fracture, (3) distortion, (4), destruction, (5) absence, (6) sclerosis, and (7) production (Table 20-6).

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2 1

Congenital Spinal Malformations (Congenital Spinal Anomalies) Raffe and Knecht reviewed a series of dogs with cervical vertebral malformations.1 More than any other, however, Morgan has been responsible for pointing out the many radiographic variations of the dog’s spine, both congenital and acquired, and that most of these unusual- appearing vertebrae are of no clinical importance.2 The most common congenital spinal malformations in dogs are unilateral or bilateral sacralization of L7, lumbarization of T13, segmentation of the sacrum, hemivertebrae (brachycephalic breeds), and blocked vertebrae.

❚❚❚ BLOCKED VERTEBRAE (BLOCK VERTEBRAE) Bagley and colleagues, based on myelographic and surgical observations in four dogs, three of which were Dachshunds, theorized that blocked cervical vertebrae may predispose to adjacent disk hernia ion.4 My own observations in dogs that have undergone surgical fusion of cervical vertebrae, typically Dobermans with Wobblers syndrome, tend to support this hypothesis.

❚❚❚ HEMIVERTEBRA ❚❚❚ ATLANTOAXIAL DISLOCATION Some small-breed dogs are born with underdeveloped dens and without a dens ligament (Figure 21-1). As a consequence, the atlantoaxial spinal unit is vulnerable to dislocation, especially if abruptly jerked, for example, by a sharp yank on the animal’s leash (Figure 21-2). In instances where dislocation-relocation is suspected, or cervical images are equivocal, stress radiography (ventroflexion) may provide an answer. Caution: Spinal stress radiography should be performed only by an experienced operator while the animal is unconscious. Animals requiring surgery are likely to do better if they meet some or all of the following criteria: (1) its age is less than 2 years, (2) it has mild to moderate neurologic disability or pain, and (3) there is little or no delay in treatment following injury.3 I would also add that with or without surgery, dogs that have been healthy up to the time of injury do better than those who have had earlier neck disease. 258

Hemivertebrae can be found in any breed but occur most often in Pugs, Boston Bull Terriers, and Bulldogs. Most of the time, they cause no obvious abnormality (Figure 21-3), although they can be associated with spinal deformity, which includes marked dorsal, lateral, or combined curvature: kyphosis, scoliosis, and kyphoscoliosis (Figures 21-4 and 21-5). A butterfly vertebra is a type of hemivertebra that roughly resembles the silhouette of a butterfly viewed from above or, in the case of a radiograph, viewed in ventrodorsal/ dorsoventral projection. When disease develops, it is usually because of narrowing of the spinal canal related to severe deformity and, more importantly, hypoplasia and dysplasia (especially syringomyelia) of the associated portion of the spinal cord (Figure 21-6).5

❚❚❚ LUMBARIZATION Lumbarization is where either the last thoracic vertebra or cranial sacral element assume some of the physical characteristics of a lumbar vertebra, an anatomic blending referred to more generally as a transitional vertebra. Lumbarization may be of two types. In the

CHAPTER 21 ❚❚❚ Congenital Spinal Malformations (Congenital Spinal Anomalies)

259

A

A

B Figure 21-2 • Close-up lateral (A) and stress lateral, ventroflexion maneuver (B) views of a dog with a dislocated C1-2 spinal unit secondary to hypoplasia of the dens.

B Figure 21-1 • Close-up lateral (A) and ventrodorsal (B) views of the head and cervical spine of a dog show dislocation of the C12 spinal unit, the result of aplasia of the dens.

A

B Figure 21-3 • Hemivertebra. Close-up (A) and ultraclose (B) views of cranial portion of thoracic spine show a small, deformed T5 with normal spinal canal, dorsal spinous, process, and ribs. Note the deviation of the disk caudally.

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SECTION III ❚❚❚ The Spine

A

C B Figure 21-4 • Spinal deformity: Lateral (A) and close-up lateral (B) views of the thorax of a healthy dog show abnormal undulation of the thoracic spine. Although multiple hemivertebrae are present, they are difficult to see; however, hemivertebrae are strongly suggested by the close proximity of the rib heads (costal fanning). Scoliosis (convexity right) is apparent in the ventrodorsal view (C).

Figure 21-5 • Spinal deformity: Lateral view of the torso of a healthy dog with a severely recurved spine causing ventral tracheal displacement, a short vertical diaphragm, and a compensatory rearrangement the organs in the cranial portion of the abdomen.

CHAPTER 21 ❚❚❚ Congenital Spinal Malformations (Congenital Spinal Anomalies)

Figure 21-6 • Spinal deformity: Abnormal ventral curvature of the cranial portion of the thoracic spine of an ataxic dog shows narrowing of the spinal canal at the level of T6-7 caused by a hemivertebra. Additionally, the trachea and heart are being displaced ventrally, and the diaphragm is abnormally angled caudally.

Figure 21-7 • Lumbarization: Close-up ventrodorsal view of the first sacral segment, which is separated from the rest of the sacrum by a vestigial disk and contains an unattached left transverse process (emphasis zone).

Figure 21-8 • Sacralization: Close-up view of the seventh lumbar vertebra, which is canted upwardly, reminiscent of the sacrum.

261

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SECTION III ❚❚❚ The Spine

first type (cranial lumbarization), the 13th thoracic vertebra sheds one or both of its ribs resembling L1; alternatively, T13 may possess one or two undersized ribs (vestigial ribs). In the second type (caudal lumbarization), the sacrum is divided into two or three parts or segments, the first of which has one or two transverse processes. In cases where there is only a single transverse process, the opposite side may be attached to the adjacent ileum, which may in turn cause tilting of the pelvis (Figure 21-7), a situation that some contend is responsible for unilateral hip dysplasia. Caution: When performing a laminectomy, it is important to recognize the presence of such anomalous vertebrae to avoid an incorrect surgical exposure.6

❚❚❚ SACRALIZATION Sacralization can take a variety of different forms, as illustrated in Figure 21-8, some of which have been

incriminated in cauda equina syndrome and unilateral hip dysplasia.7

References 1. Raffe MR, Knecht CD: Cervical vertebral malformation— a review of 36 cases. J Am Anim Hosp Assoc 16:881, 1980. 2. Morgan JP: Congenital anomalies of the vertebral column of the dog: a study of the incidence and significance based on a radiographic and morphologic study. J Am Vet Rad Soc 9:21, 1968. 3. Beaver DB, Ellison GW, et al: Risk factors affecting the outcome of surgery for atlantoaxial subluxation in dogs: 46 cases (1978-1998). J Am Vet Med Assoc 216:1104, 2000. 4. Bagley RS, Cauzinille L, et al: Cervical vertebral fusion and concurrent intervertebral disc extrusion in four dogs. Vet Radiol Ultrasound 34:336, 1993. 5. Chauvet AE, Darien DL: What is your neurologic diagnosis? J Am Vet Med Assoc 208:1387, 1996. 6. Kwiatkowski TC, Greens KG, Meyer RA: What is your diagnosis? J Am Vet Med Assoc 209:2011, 1996. 7. Larsen JS: Lumbosacral transitional vertebrae in the dog. J Am Vet Rad Soc 18:76, 1977.

C h a p t e r

2 2

Developmental Spinal and Spinal Cord Disorders Causing Cord and Nerve Root Compression ❚❚❚ SPINAL ARACHNOID CYST Spinal arachnoid cysts result in a localized dilation of the dural sac that can compress the spinal cord or spinal nerves. Specifically, spinal arachnoid cysts are focal outpouchings of the arachnoid membrane that communicate with the subarachnoid cavity and thus contain cerebrospinal fluid (CSF). Spinal cysts are either intradural or extradural and usually are found in young dogs aged less than 18 months; occasionally, they are identified in older dogs or cats.1 Arachnoid cysts also may be intracranial. Arguments have been made for both congenital and developmental causes.2 Myelographically, intradural spinal cysts often cause a characteristic disfigurement in the contrastfilled dural sac, which has been described as teardropor drop-shaped.3-5 Scoliosis, in association with an arachnoid cyst, has been reported in a dog, and lordosis has been described as occurring in a cat.6,7 Galloway and co-workers compared various types of medical imaging used to diagnose spinal arachnoid cysts and concluded that for most cases myelography is sufficient.8 Comparatively speaking, computed tomography (CT) provided a more precise description of the lesion, including localization, lateralization, and degree of cord compression; magnetic resonance imaging (MRI) readily identified associated syringomyelia. Intraoperative sonography was capable of identifying the cyst wall, cavity size, and relationship to the adjacent spinal cord; in general, it provided a sense of spatial orientation before decompressive surgery was performed.

❚❚❚ DERMOID SINUS A dermoid sinus (also known as a dermoid, dermatoid, or inclusion cyst) is the term usually given to a small

hole on the surface of the skin, typically overlying the lumbosacral spinal region. The described opening is often wet and denuded of hair owing to the seepage of CSF through a narrow channel communicating with the dural sac. Alternatively, the channel may fall short of the dura and instead terminate in a cyst-like structure composed of skin and hair. The consequences of such communication are potentially serious and include myelitis and meningitis. Tshamala and Moens described less common forms of dermoid cysts along with a proposed classification.9 Although plain film findings occasionally have been reported in connection with dermoid sinuses, for example, “irregular thinning of the dorsal lamina of the sacrum” or “a soft tissue swelling dorsal to T3-4,” most spinal surveys are likely to appear normal.10,11 Myelography may reveal an abnormal dural profile dorsally, whereas sinography, using nonionic, dedicated aqueous contrast media in most instances will delineate the sinus tract and its intradural or extradural culmination.

❚❚❚ EPIDERMOID CYST The partial surgical removal of an intramedullary epidermoid cyst from the spinal cord of a dog was described in which myelographic diagnosis was instrumental. The cyst appeared as a focal cord swelling in combination with a dural filling defect. In the related discussion, the authors contend that intramedullary masses are potentially either neoplastic or cystic, whereas extradural and intradural extramedullary masses (meningiomas, nerve sheath tumors) are typically neoplastic.12 263

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SECTION III ❚❚❚ The Spine

❚❚❚ FACETAL, JUXTAARTICULAR, SYNOVIAL, AND GANGLION CYSTS Cysts originating from the margins (juxtaarticular region) of the facetal joints may grow large enough to compress the spinal cord or its nerve roots. Sometimes termed facet or facetal by virtue of their origin, these mass-like, potentially compressive objects may be filled with either mucinous or synovial fluid and are designated ganglion or synovial accordingly. On MRI, ganglia appear as typical cysts, featuring low signal intensity on T1-weighted images and high signal intensity on T2-weighted images. Rim and septal enhancement may be seen after gadolinium administration.13 Webb and co-workers reported a presumed case of multiple ganglion cysts in the lumbar spinal region of a 6-year-old dog in which they speculated that the lesions developed as a result of degenerative joint disease.14

❚❚❚ HYDROMYELIA Kirberger and colleagues reported three cases of canine hydromyelia, a congenital or acquired disease of the spinal cord in which a portion of the central canal becomes dilated.15 Hydromyelia is identified on the basis of opacification of a dilated central canal. The canal may appear uniformly dilated or may feature a distinctive saccular pattern of enlargement. Dilation of the fourth ventricle relates to the communicative nature of the disease and indicates hydrocephalus.

❚❚❚ SPINAL MENINGOCELE A spinal meningocele is a localized protrusion of the membranes of the spinal cord (meninges) through an overlying defect in the vertebral arch. A meningocele was reported in a Manx cat, which also had an intradural lipoma causing spinal cord tethering.16

❚❚❚ MENINGOMYELOCELE A meningomyelocele is a localized protrusion of the meninges and spinal cord through a defect in the vertebral arch.

❚❚❚ SYRINGOMYELIA Syringomyelia (also termed hydrosyringomyelia and syringohydromyelia) is a disease in which large fluidfilled, longitudinally oriented cavities (syrinx) form within the spinal cord. There are two types of lesions: communicating and noncommunicating. Communicating syringomyelia typically is found in the region of the atlantooccipital junction in associa-

tion with abnormal CSF flow and includes hydrocephalus.17,18 The cavitary cord lesions contain fluid closely resembling CSF. Syringomyelia also has been reported in association with occipital dysplasia.19 Noncommunicating syringomyelia is characterized by cavities filled with highly proteinaceous fluid and typically is found secondary to intramedullary injury (Figure 22-1).20

❚❚❚ SPINAL TUMORAL CALCINOSIS The cause of tumoral calcinosis (also termed calcinosis circumscripta) is not known. The term tumoral refers to the morphology of the lesion, not to its growth potential. Van Ham and co-workers reported on the CT appearance of compressive tumoral calcinosis in the C1-2 spinal unit of a dog.21

❚❚❚ VERTEBRAL ANGIOMATOSIS Vertebral angiomatosis is a type of benign vascular malformation reported in the thoracic spinal region of young cats. This condition causes pain and paralysis and may resemble a malignant bone tumor as seen radiographically and with CT.22

❚❚❚ CERVICAL SPONDYLOPATHY (WOBBLER SYNDROME, CERVICAL VERTEBRAL INSTABILITY, CAUDAL CERVICAL SPONDYLOMYELOPATHY) Background Wobbler syndrome afflicts great Danes and Doberman Pinchers more than any other breeds. The fundamental problem is excessive motion affecting one or more spinal units, usually in the caudal third of the cervical spine. This excessive motion eventually leads to irreversible cord damage, presumably due to the repetitive striking of the spinal cord by the wayward spinal elements. As far as I am aware, the precise cause or causes of wobbler syndrome is unknown. Some have blamed facet joint asymmetry or other types of vertebral incongruity, but this finding is commonly encountered in defleshed spinal specimens of middle-sized and large breed dogs. Others have suggested that dogs with relatively large, heavy heads somehow stretch their spinal ligaments, eventually causing excessive spinal motion and pinching of the cord. Many authorities believe that wobbler syndrome is heritable, a view that I strongly support. My own observations, based on radiographs of the cervical spines of nearly 150 nonclinical Dobermans in the standing lateral position, are that about one in four appear abnormal. Specifically, one or more

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265

A

B

C Figure 22-1 • Close-up lateral plain film (A) of the cervical region of a cat with cervical syringomyelia is unremarkable. Lateral (B) and ventrodorsal (C) myelograms show corresponding widening of the dural sac and spinal cord beginning at the thoracic inlet.

spinal units appear abnormally angled, usually C5-6 or C6-7. I have found such abnormalities in dogs ranging in age from 6 months to 12 years. To repeat, none of these dogs was reported to be abnormal by either their owners or by the veterinarians who initially examined them for unrelated problems. All dogs were radiographed solely on a survey basis. Accordingly, it seems appropriate to conclude that some Dobermans with the radiographic indicators of wobbler syndrome will be clinically normal and that both young and old may be so affected.

Imaging Findings Radiology. Lewis described a diagnostic strategy for the radiographic diagnosis of wobbler syndrome in Dobermans using conventional radiography. Like others before and since, the diagnostic emphasis is based on a combination of spatial and anatomic abnormalities.23 Figures 22-2 and 22-3 exemplify these disease features.

Figure 22-2 • Close-up standing lateral view of the C6-7 spinal unit (emphasis zone) of a Doberman with cervical spondylopathy. C4-5, C5-6, and C6-6 are all abnormally angled and characteristically deformed. Narrowing of the spinal canal is most pronounced over the C6-7 disk.

266

SECTION III ❚❚❚ The Spine

Postural and Stress Radiography. A lateral radiograph is the cornerstone of plain film diagnosis in dogs with cervical spondylopathy. Using the standing lateral view rather than the traditional recumbent projection further increases the diagnostic yield by eliminating confusing obliquity. Natural stress radiography is often possible in fully conscious dogs by using food to get the dog to bend its neck ventrally and then making the radiograph, a technique that I have described previously and termed the feeding stress maneuver (Figures 22-4 and 22-5). One of the most important findings in feeding stress radiography is how the C5-6 spinal unit consistently dislocates when the C6-7 unit contains a collapsed disk. A similar “compensatory” displacement often develops in Dobermans following spinal fusion.

artificial movements not normally made either by healthy dogs or by those with cervical spondylopathy. For example, when a dog lowers its head to eat or drink (as observed in standing lateral or feeding stress films), it flexes its neck at two points: at the base of the skull and at the base of the cervical spine. The intervening vertebrae remain relatively straight or at most gently curved, not exaggeratedly arched or extended, as in most stress films. Thus, many of the conclusions based on these views are likely to be invalid or, at the very least, oversimplifications.

Myelography. It has long been recognized that the dorsoventral myelographic projection is potentially more informative than the ventrodorsal view because the former view takes advantage of the natural trough effect created in the caudal cervical region when a dog is positioned on its sternum. Lamb published a detailed account of this anatomic advantage.24 Stress Myelography. Although it was incidental (they were actually reporting their preliminary experience with metrizamide), Lord and Olsson were instrumental in establishing stress radiography as an important part of the standard myelographic evaluation of suspected wobbler syndrome.25 My own view concerning myelographic stress radiography is that all the various stress maneuvers— traction, dorsal extension, and ventral flexion—are A

B Figure 22-4 • A, Standing lateral view of mid and caudal cervical Figure 22-3 • Close-up standing lateral view of the C6-7 spinal unit of a Doberman with cervical spondylopathy shows characteristic deformity, disk collapse, and spinal canal stenosis.

spine of a Doberman with cervical spondylopathy shows characteristic deformity and disk collapse of the C6-7 spinal unit. B, Feeding stress film shows abnormal dorsal angulation at C5-6 that was not evident in the earlier nonstress images.

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267

This is particularly true of the traction maneuver, which along with the nonstressed lateral, have been used by some authorities to support the idea of dynamic versus adynamic lesions. In point of fact, anyone who has performed myelographic stress radiography on dogs with cervical spondylopathy is aware that every compressive lesion can be made to change with manipulation of the head and neck, not just with traction. Accordingly, the terms dynamic and adynamic are superfluous and to some extent misleading. Some examples of stress myelography are shown in Figures 22-6 to 22-8. Spinal Cord/Spinal Canal Comparisons. The height of the spinal cord, compared with the height of the spinal canal at the same point, is termed the cord/canal ratio, measurements that can be obtained from a lateral myelogram. An increase in cord diameter or a decrease in canal diameter will cause this value to increase. Thus, it may be diagnostically useful to know what the normal values are for different breeds of dogs, especially in instances where abnormalities are suspected but are not immediately obvious or are of a questionable nature. Morgan and co-workers compared cord/canal ratios in the lumbosacral spinal regions of Dachshunds and German Shepherds,26 and Fourie and Kirberger published similar data on the cervical region of a variety of small- and large-breed dogs.27 In the latter study, it was determined, among other things, that small breeds have a larger cord/canal ratio than large breeds.

A

B Figure 22-5 • A, Standing lateral view of mid and caudal cervical spine of a Doberman with cervical spondylopathy shows characteristic deformity and disk collapse of the C6-7 spinal unit. B, Feeding stress film shows abnormal dorsal angulation at C5-6, which was not evident in earlier films.

Figure 22-6 • Close-up, flexed lateral myelogram of the central part of the cervical spine of a dog shows normal transient indentation of the ventral aspect of the dural sac.

Computed Tomography. Sharp and co-workers reported the CT appearance of caudal cervical spondylomyelopathy in Doberman Pinschers, classifying their observations into five categories based on cord appearance.28 Although the authors acknowledge that plain films and myelography continue to be the first choice in initial imaging of suspected wobbler syndrome, they assert that CT does a superior job in precisely locating the lesion and determining its compressive effect.

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Table 22-1 • NERVES OF THE CAUDA EQUINA

Nerve

Spinal Segment

Sensory Function

Motor Function

Coccygeal

Cg1 to Cg5

Tail

Tail

Pelvic

S1 to S3

Pelvic organs

Urinary bladder, rectum, erection of penis

Pudendal

S1 to S3

Perineum

Anal and bladder sphincters

Sciatic

L6 to S1

Hind limbs, excluding medial aspects)

Extension of hip, hock, and toes, flexion of the knee

Figure 22-7 • Close-up flexed lateral view (fulcrum-assisted) of a Doberman with cervical spondylopathy shows abnormal dorsal angulation of the C3-4 spinal unit, cord displacement, and compression. Facetal arthritis is also present.

Figure 22-8 • Close-up lateral view (traction) of the C6-7 spinal unit of a Doberman with cervical spondylopathy shows disk collapse, cord elevation, and thumbprinting of the overlying dural sac (emphasis zone). Subsequent magnetic resonance imaging showed that a ruptured intervertebral disk had caused the myelographic abnormalities.

❚❚❚ CAUDA EQUINA SYNDROME (LUMBOSACRAL STENOSIS, DEGENERATIVE LUMBOSACRAL STENOSIS) Background Ancient anatomists termed the caudal aspect of the spinal cord and its accompanying spinal nerves the cauda equina because of its loose resemblance to the tail of a horse, a name that persists to this day. The spinal nerves that make up the cauda equina are listed in Table 22-1. One or more of the abnormalities shown in Box 22-1 can cause compression of the lumbosacral spinal nerves, a condition also termed the cauda equina syn-

B o x

2 2 - 1

Causes of Cauda Equina Syndrome • Bulging intervertebral disk • Congenital malformation of one or more vertebrae with resultant narrowing or distortion of the associated portion of the spinal canal; hemivertebrae, blocked vertebrae, transitional vertebrae (sacralization of L7, lumbarization of S1), and spina bifida are all theoretically capable of causing compression of nervous tissue, but in reality most do not • Hypertrophy of one or more spinal ligaments • Impingement exostosis resulting from endplate damage caused by disk fenestration • Intraspinal scarring following disk surgery • Compressive mass effect caused by redundant, hyperplastic spinal ligaments involving the L7-S1 spinal unit • Ruptured intervertebral disk • Spinal canal deformity resulting from malunion fractures • Spinal canal encroachment by an arthritic facetal joint • Spinal canal encroachment by asymmetric or deformed facetal joints • Spinal unit instability caused by laminectomy or hemilaminectomy

drome, lumbosacral stenosis, or degenerative lumbosacral stenosis.29-31 Sacral Osteochondritis. Sacral osteochondritis–like lesions also have been proposed as possible causes of lumbosacral stenosis; however, conclusive proof of such an assertion is lacking. Consequently, this possible disorder appears to merit no more than theoretical consideration.32 Abnormal Lumbosacral Motion. Instability of the caudal lumbar portion of the spine (including the lumbosacral spinal unit) also has been proposed as a source of both direct and indirect caudal nerve root compression. Although this hypothesis is tenable, it is based largely on theoretical argument.33,34

CHAPTER 22 ❚❚❚ Developmental Spinal and Spinal Cord Disorders Causing Cord and Nerve Root Compression

Table 22-2 • RELATIVE SENSITIVITY OF PLAIN FILM DIAGNOSIS FOR VARIOUS FORMS OF LUMBOSACRAL STENOSIS Cause of Lumbosacral Stenosis

Potential for Nonmyelographic Radiographic Diagnosis

Bulging or rupture of intervertebral disk

Relatively high, unless associated with moderate or severe spondylosis in which case it will be difficult or impossible to accurately determine the disk size

Congenital stenosis of spinal canal

Low

Discospondylitis

Variable, depending on extent of disk involvement

Excessive lumbosacral motion

Low

Facetal joint encroachment

Low

Ligamentous mass effect

Low

Lumbosacral transitional vertebrae

Low

Spondylitis

Variable, depending on extent of bone involvement

Tumor

Variable, depending on extent of bone destruction

Vertebral fracture or dislocation

High

Vertebral osteochondritis (very rare)

Medium

Compression-induced Ganglial Ischemia. Jones and co-workers experimentally compressed the seventh lumbar nerve root in healthy dogs and then measured blood flow in the seventh lumbar spinal ganglion using Doppler ultrasound. Based on a demonstrated pressure-induced reduction in blood flow, the authors theorized that foraminal stenosis in the L7-S1 spinal unit may cause ischemia of the seventh lumbar ganglion.35

Imaging Findings Plain-film Diagnosis. The likelihood that lumbosacral stenosis can be diagnosed on plain films depends on the cause, as indicated in Table 22-2. Postural Radiography. Postural radiography is of no use in identifying dogs with lumbosacral stenosis. Stress Radiography. Both others and I have published our views on the use of plain film stress radiography to diagnose presumptively lumbosacral stenosis.36,37 In my opinion, none of these reports has shown clear evidence that this is consistently possible. My view is that stress radiography lacks both sensitivity and specificity as a means to identify abnormal motion in the lumbosacral spinal unit. Myelography, Epidurography, and Intraosseous Vertebral Venography. Hathcock and colleagues showed that myelography, epidurography, and osseous venography usually fail to reliably and consistently show

269

experimentally induced compression of the cauda equina.38 Lang described the use of stress radiography in the lumbosacral region of normal and abnormal dogs performed in conjunction with myelography.39 Based on data obtained from 22 normal dogs that underwent stress myelography of the lumbosacral spinal region, the author concluded the following: 1. The dural sac terminated in the sacrum in more than 80% of the dogs. 2. There were large individual differences in the appearance the caudal-most portion of the dural sac located within the sacrum. 3. The shape, length, position, and diameter of the dural sac at the level of the lumbosacral junction during stress radiography (flexion and extension maneuvers) were constant. Of the 26 dogs with proven lumbosacral compression, 21 were diagnosed using stress myelography: 7 using a flexion maneuver and 14 using an extension maneuver. Of the five dogs in which a myelographic diagnosis could not be made conclusively, two dogs had a dural sac that ended craniad to the lesion, two dogs had lesions that did not cause compression, and one dog had equivocal myelographic findings. Diskoepidurography. Barthez and co-workers described using combined diskography and epidurography (a procedure they term diskoepidurography) in diagnosing cauda equina compression in dogs.40 Using plain-film radiographic diagnostic indicators (i.e., spondylosis, sacral subluxation, decreased L7-S1 disk size [inferred collapse], stenosis of the L7-S1 spinal canal, and the presence of transitional vertebrae) in combination with diskoepidurography, the authors reported a diagnostic accuracy rate of 89%. Used alone, epidurography was 78% accurate, whereas diskography was only 67% accurate. As far as I am aware, no one has been able to replicate these results. Computed Tomography. Jones and co-workers described the CT appearance of the caudal lumbar and lumbosacral regions of the normal dog.41 The same group also compared CT findings in dogs diagnosed with lumbosacral stenosis with associated surgicalhistologic outcomes.42 Their CT/pathologic correlations are shown in Box 22-2. Feeney and co-workers, based on an extensive CT study of lumbosacral anatomy in healthy dogs, recommended that intravenous contrast enhancement be used in cases of suspected lumbosacral stenosis to aid in the differentiation of normal blood vessels located in the vertebral canal and adjacent to the intervertebral foramina from potential soft tissue lesions, such as a bulging disks, ligamentous hypertrophy, or fibrosis.43 Heeding this recommendation, Jones and coworkers studied the efficacy of contrast-enhanced CT in 12 dogs suspected of having cauda equina syndrome, comparing their preoperative imaging findings, as independently judged by three radiologists, with subsequent surgical observations.44 It was determined that, in general, contrast-enhanced soft tissues were most

270

SECTION III ❚❚❚ The Spine

B o x

2 2 - 2

Canine Lumbosacral Stenosis: CT-Pathologic Correlations • Unenhanced computed CT imaging of the lumbosacral spinal region is capable of detecting bone and soft tissue lesions • Similarities exist between dog and human CT lesions resulting from degenerative spinal disease and discospondylitis. • An increase in soft tissue density, without associated epidural fat, and with compatible clinical signs, supports spinal nerve compression (even in the presence of only minor degenerative changes) • The prevalence of spinal nerve compression secondary to epidural fibrosis has probably been underestimated. • Some dogs with cauda equina syndrome may have two or more physically separate lesions.

A

CT, Computed tomographic.

B likely to be responsible for the compression of nervous tissue or its vasculature and that such information, in the authors’ opinion, was critical to adequate surgical exposure in the event decompressive surgery was to be performed. Caution: Jones and Izana also described CT abnormalities found in the caudal lumbar and lumbosacral spinal units (L5-6, L6-7, L7-S1, S1-S2, S2-S3) of clinically normal dogs, many of which were older. The most common findings included stenosis, loss of epidural fat, and nerve tissue displacement. Less frequently encountered findings were spinal canal or intervertebral foraminal bone deposits, loss of foraminal fat, bulging disks (spinal canal or intervertebral foramen), facetal arthritis, free disk material in spinal canal, Schmorl’s nodes, dural ossification, transitional vertebrae, and sacroiliac osteophytes (arthritis?).45 Magnetic Resonance Imaging. Miyabayashi and coworkers evaluated the relative diagnostic merits of conventional and fast spin-echo MRI of the lumbar and lumbosacral spinal regions in healthy dogs. It was found that fast spin-echo (FSE) technique resulted in superior image quality that could be obtained in a shorter time. These improvements in image quality were made possible by (1) an increased number of excitations (NEX) and (2) increased matrix size, which combined to increase resolution and signal-to-noise ratio.46 Adams and co-workers described the MRI features of various types of lumbosacral stenosis in dogs.47 Identified spinal lesions included (1) intervertebral disk degeneration, (2) disk protrusion into either the spinal canal or intervertebral foramen, (3) articular process osteophytosis, (4) fractured articular process, (5) nerve root impingement by spondylotic bone, and (6) presumed postoperative scarring from previous back surgery. Figures 22-9 to 22-11 exemplify lumbosacral stenosis as diagnosed with magnetic resonance imaging (Tables 22-3 and 22-4).

C

D Figure 22-9 • Magnetic resonance (T1-weighted) image: Close-up lateral view (A) of the L7-S1 spinal unit shows a ruptured disk compressing the cauda equina. A T2-weighted image (B) reveals similar findings. T1 close-up views of ruptured C7-S1 (C) and normal C5-6 (D) are provided for comparison.

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271

B

A Figure 22-10 • Magnetic resonance (T1-weighted) image: A, Close-up lateral view of the L7-S1 spinal unit shows a ruptured disk compressing the cauda equina. B, A T2 image reveals similar findings.

A

B Figure 22-11 • Magnetic resonance (T1-weighted) image: A, Close-up lateral view of the L7-S1 spinal unit shows a ruptured disk compressing the cauda equina. B, A T2 image reveals similar findings.

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SECTION III ❚❚❚ The Spine

Table 22-3 • MAGNETIC RESONANCE IMAGING INDICATORS OF DISK DISEASE Disk-related Sources of Spinal Cord or Nerve Root Compression

Associated Magnetic Resonance Imaging Disease Indicators

Intervertebral disk degeneration without bulge or rupture

Reduced signal intensity from nucleus pulposus on T1, T2, and proton density images. This finding is attributed to disk dehydration and a reduction in total proteoglycan content.

Endplate marrow disease: 3 types

Type I: Vertebral endplate (and degenerated disk) shows decreased signal intensity on T1 and increased intensity on T2. No radiographic correlation. Type II: Increased signal intensity on T1 and isointensity on T2. No radiographic correlation. Type III: Decreased signal intensity on T1 and T2, correlating with endplate sclerosis found in plain films.

Bulging disk

Classically appears as a localized bulge in outer annular margin such that the affected part of the disk extends beyond the margins of the adjacent endplates. The outer annular fibers remain intact, portrayed as a discrete line of decreased signal intensity.

Ruptured disk

Classically appears as either a narrow-based, plume-like mass originating from the dorsal aspect of the intervertebral disk, or as an amorphous mass (sequestered disk fragment) that is physically unattached to either adjacent disk and often lies over the vertebral body. Both types of ruptured disk are assocted with varying amounts of dural sac displacement.

Secondary facetal joint arthritis

Secondary facetal disease has been attributed to dehydration and volume loss that occurs with disk degeneration, which in turn places the articular facets of the associated vertebrae in closer proximity leading to abnormal motion, and eventually osteoarthritis.

Dorsal longitudinal ligament integrity

Research done on humans has shown that MRI is poorly suited, and often incapable, of establishing the integrity of the dorsal longitudinal ligament (appearing as a continuous low signal intensity line dorsal to the abnormal disk).

Postoperative scarring

Ventral epidural scarring appears similar to the intervertebral disk (isointense) on T1 images, and increased in signal intensity on T2. Scar tissue tends to conform to the adjacent dura, to which it may become adherent. Lateral and dorsal scarring is similar in appearance, but not present as consistently.

Modified from Stark DD, Bradley WG, eds: Magnetic resonance imaging, ed 3, Philadelphia, 1999, Mosby.

CHAPTER 22 ❚❚❚ Developmental Spinal and Spinal Cord Disorders Causing Cord and Nerve Root Compression

273

Table 22-4 • MEDICAL IMAGING OF CAUDA EQUINA SYNDROME: ADVANTAGES, DISADVANTAGES, AND DIAGNOSTIC ACCURACY OF VARIOUS METHODS Medical Imaging Method

Advantages

Disadvantages

Diagnostic Accuracy

Computed tomography

Noninvasive, cross-sectional format, very good lumbosacral bone detail, soft tissue detail is better than with film, but inferior to MRI. Various types of image reformatting are available, including 3-D

Very expensive, increasing use but limited availability

High

Diskography

Few true advantages, most claims not substantiated by clinical experience

Invasive; can be technically difficult (depending on experience), requires fluoroscopy, added expense due to anesthesia and recovery room costs, images are sometimes nondiagnostic due to leakage of injected contrast solution. Generally, unreliable imagery

Low-to-medium, depending on the technical adequacy of study

Epidurography

Few to none

Invasive; procedure requires training and practice unless accustomed to doing epidurals, additional anesthesia costs. Some images are nondiagnostic. This procedure has all the attributes of a poor test: low sensitivity, low specificity, and low diagnostic accuracy

Low to medium, depending on the technical adequacy of study

MRI

Noninvasive, cross and long-sectional formats, excellent soft tissue definition: dural sac, CSF, spinal cord, nerve roots, intervertebral disk, spinal ligaments, epidural fat, but only mediocre bone detail.

Very expensive, increasing but still limited availability, protracted scanning time

High

Myelography

Enables interpreter to see the exterior but not the interior of the spinal cord

Invasive, cervical myelograms are Medium potentially dangerous if puncture is not done correctly; lumbar punctures can be technically difficult (or even impossible with obese animals); some images may be hard to interpret due to epidural leakage of contrast. Imagery sometimes unreliable

Osseous sinus venography

When contrast reaches the lumbosacral region in sufficient quantity, this procedure is capable of showing a medium to large extradural mass; the problem is getting it there

Invasive; can be technically difficult (depending on experience), requires fluoroscopy, added expense due to anesthesia and recovery room costs, images are sometimes nondiagnostic due to leakage of injected contrast solution, contrast often fails to reach desired area due to caval runoff. Generally, unreliable imagery

Low to medium, depending on the technical adequacy of study

Postural radiography

Noninvasive, requires specific training and practice, widely available, inexpensive, reliable imagery, capable of showing subluxation not visible in nonstress images

May require anesthesia, depending on the type and method of individual stress maneuver

Low but, unlike standard radiography, spatially variable lesions can be demonstrated

Standard radiography

Noninvasive, requires general training and practice, widely available, inexpensive, reliable imagery

No discrimination of soft tissues of interest (dural sac, CSF, spinal cord, nerve roots, intervertebral disk, spinal ligaments, epidural fat)

Low, what is diagnosed is typically inferential

Tomography (noncomputed)

None: even the best images appear blurry. It is no accident that linear tomography never became popular in veterinary medical imaging

Requires anesthesia, few hospitals have the necessary equipment to modify their existing x-ray machines, and even if they do, few radiographers and radiologists are practiced in the technique

Lower than with film, and with increased false-positive diagnosis

Modified from Ramirez O, Thrall DE: A review of imaging techniques for canine cauda equina syndrome. Vet Radiol Ultrasound 39:283, 1998. MRI, Magnetic resonance imaging; 3-D, three-dimensional; CSF, cerebrospinal fluid.

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References 1. Vignoli M, Rossi F, Sarli G: Spinal subarachnoid cyst in a cat. Vet Radiol Ultrasound 40:116, 1999. 2. Webb AA: Intradural spinal arachnoid cyst in a dog. Can Vet J 40:588, 1999. 3. Cambridge AJ, Bagley RS, et al: Arachnoid cyst in a dog. Vet Radiol Ultrasound 38:434, 1997. 4. Frykman OF: Spinal arachnoid cyst in 4 dogs: diagnosis, surgical treatment and follow-up results. J Small Anim Pract 40:544, 1999. 5. Vignoli M, Rossi F, Sarli G: Spinal subarachnoid cyst in a cat. Vet Radiol Ultrasound 40:116, 1999. 6. Bagley RS, Silver GM, et al: Scoliosis and associated cystic spinal cord lesion in a dog. J Am Vet Med Assoc 211:573, 1997. 7. Vignoli M, Rossi F, Sarli G: Spinal subarachnoid cyst in a cat. Vet Radiol Ultrasound 40:116, 1999. 8. Galloway AM, Curtis NC, et al: Correlative imaging findings in seven dogs and one cat with spinal arachnoid cysts. Vet Radiol Ultrasound 40:445, 1999. 9. Tshamala M, Moens Y: True dermoid cyst in a Rhodesian Ridgeback. J Small Anim Pract 41:352, 2000. 10. Pratt JNJ, Knottenbelt M, et al: Dermoid sinus at the lumbosacral junction in an English Springer Spanial. J Small Anim Pract 41:24, 2000. 11. Van Ee RT, Shull E: Radiographic diagnosis. Vet Rad 25:29, 1984. 12. Shamir MH, Lichovsky D, et al: Partial surgical removal of an intramedullary epidermoid cyst from the spinal cord of a dog. J Small Anim Pract 40:439, 1999. 13. Kransdorf MJ, Murphy MD: Juxtaarticular masses. In Stark DD, Bradley WG, eds: Magnetic resonace imaging, ed 3. St. Louis, 1999, Mosby. 14. Webb AA, Pharr JW, et al: MR imaging findings in a dog with lumbar ganglion cysts. Vet RadiolUltrasound42:9, 2001. 15. Kirberger RM, Jacobson LS, et al: Hydromyelia in the dog. Vet Radiol Ultrasound 38:30, 1997. 16. Plummer SB, Bunch SE, et al: Tethered spinal cord and an intradural lipoma associated with a meningocele in a Manx-type cat. J Am Vet Med Assoc 203:1159, 1993. 17. Taga A, Taura Y, et al: Magnetic resonance imaging of syringomyelia in 5 dogs. J Small Anim Pract 41:362, 2000. 18. Itoh T, Nishimura R, et al: Syringomyelia and hydrocephalus in a dog. J Am Vet Med Assoc 209:934, 1996. 19. Bagley RS, Harrington ML, et al: Occipital dysplasia and associated cranial spinal cord abnormalities in two dogs. Vet Radiol Ultrasound 37:359, 1996. 20. Rusbridge C, MacSweeny JE, et al: Syringohydromyelia in Cavalier King Charles Spaniels. J Am Anim Hosp Assoc 36:34, 2000. 21. Van Ham LM, van Bree HJ, et al: Use of computed tomography for assessment of spinal tumoral calcinosis in a dog. Vet Radiol Ultrasound 36:115, 1995. 22. Kloc PA, Scrivani VP, et al: Vertebral angiomatosis in a cat. Vet Radiol Ultrasound 42:42, 2001. 23. Lewis DG: Radiological assessment of the cervical spine of the Doberman with reference to cervical spondylomyelopathy. J Small Anim Pract 32:75, 1991. 24. Lamb CR: The dorsoventral cervical myelograms. Vet Radiol Ultrasound 36:201, 1995. 25. Lord PF, Olsson S-E: Myelography with metrizamide in the dog: a clinical study on its use for the demonstration of spinal cord lesions other than those caused by intervertebral disk protrusions. J Am Vet Rad Soc 17:42, 1976. 26. Morgan JP, Atilola M, Bailey CS: Vertebral canal and spinal cord measuration: a comparative study of its effect on lumbosacral myelography in the Dachshund and German Shepherd dog. J Am Vet Med Assoc 191:951, 1987.

27. Fourie SL, Kirberger RM: Relationship of cervical spinal cord diameter to vertebral dimensions: a radiographic study of normal dogs. Vet Radiol Ultrasound 40:137, 1999. 28. Sharp NJH, Cofone M, et al: Computed tomography in the evaluation of caudal cervical spondylomyelopathy of the Doberman Pinscher. Vet Radiol Ultrasound 36:100, 1995. 29. Watrous BJ: Cauda equina syndrome. In Farrow CS, ed: Decision making in small animal radiology. Toronto, 1987, BC Decker. 30. Watt PR: Degenerative lumbosacral stenosis in 18 dogs. J Small Anim Pract 32:125, 1991. 31. DeRisio L, Smith RW, et al: Predictors of outcome after dorsal decompressive laminectomy for degenerative lumbosacral stenosis in dogs: 69 cases (1987-1997). J Am Vet Med Assoc 219:624, 2001. 32. Lang J, Hansjurg H, Schwalder P: A sacral lesion resembling osteochondrosis in the German Shepherd dog. Vet Radiol Ultrasound 33:69, 1992. 33. Morgan JP, Bahr A, et al: J Am Vet Med Assoc 202:1877, 1993. 34. Morgan JP: Transitional lumbosacral anomaly in the dog: a radiographic study. J Small Anim Pract 40:167, 1999. 35. Jones JC, Hudson JA, et al: Effects of experimental nerve root compression on arterial blood flow velocity in the seventh lumbar spinal ganglion of the dog: measurement using intraoperative Doppler ultrasonography. Vet Radiol Ultrasound 37:133, 1966. 36. Wright JA: Spondylosis deformans of the lumbosacral joint in dogs. J Small Anim Pract 21:45, 1980. 37. Matoon JS, Koblik PD: Quantitative survey radiographic evaluation of the lumbosacral spine of normal dogs and dogs with degenerative lumbosacral stenosis. Vet Radiol Ultrasound 34:194, 1993. 38. Hathcock JT, Pechman RD, et al: Comparison of three radiographic contrast procedures in the evaluation of the canine lumbosacral spinal canal. Vet Rad 29:4, 1988. 39. Lang J: Flexion-extension myelography of the canine cauda equina. Vet Rad 29:242, 1988. 40. Barthez PY, Morgan JP, Lipsitz D: Discography and epidurography for evaluation of the lumbosacral junction in dogs with cauda equina syndrome. Vet Radiol Ultrasound 35:152, 1994. 41. Jones JC, Cartee RE, Bartels JE: Computed tomographic anatomy of the canine lumbosacral spine. Vet Radiol Ultrasound 36:91, 1995. 42. Jones JC, Sorjonen DC, et al: Comparison between computed tomographic and surgical findings in nine large-breed dogs with lumbosacral stenosis. Vet Radiol Ultrasound 37:247, 1996. 43. Feeney DF, Evers P, et al: Computed tomography of the normal canine lumbosacral spine: a morphologic study. Vet Radiol Ultrasound 37:399, 1996. 44. Jones JC, Squires PK, et al: Evaluation of canine lumbosacral stenosis using intravenous contrast-enhanced computed tomography. Vet Radiol Ultrasound 40:108, 1999. 45. Jones JC, Izana KD: Subclinical CT abnormalities in the lumbosacral spine of older large-breed dogs. Vet Radiol Ultrasound 41:19, 2000. 46. Miyabayashi T, Smith M, Tsuruno Y: Comparison of fast spin-echo and conventional spin-echo magnetic resonance imaging techniques in four normal dogs. Vet Radiol Ultrasound 41:308, 2000. 47. Adams WH, Daniel GB, et al: Magnetic resonance imaging of the caudal lumbar and lumbosacral spine in 13 dogs (1990-1993). Vet Radiol Ultrasound 36:3, 1995.

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Spinal Injury

❚❚❚ SPINAL FRACTURES AND DISLOCATIONS

with serious spinal injuries, this reserve becomes unavailable.4

Outcome assessment of dogs and cats treated medically or surgically for spinal injuries (fractures and dislocations) suggests that medical treatment is preferable or at least as effective as surgery under certain circumstances.1

Imaging Findings

❚❚❚ CERVICAL SPINAL FRACTURES Cervical vertebral fractures involve the C1-2 spinal unit (atlas and axis) in about 80% of cases. Seim theorized that this portion of the spine is especially susceptible to serious injury owing to the relative articular rigidity of this region compared with that of the caudal portion of the cervical region. These anatomic/functional differences, he believes, will lead to increased cranial stress, and thus increased vulnerability, when the neck is suddenly and forcefully hyperextended.2 It has been my experience that both fracture and fracture-dislocation are better tolerated in this portion of the spine than in others. This is due in part to the comparatively large diameter of the spinal canal compared with that of the cord, which affords greater opportunity for the cord to accommodate the compressive effects of extradural hemorrhage and edema. This hypothesis is supported by regularly published accounts of animals with partially displaced proximal cervical fractures that are showing only neck pain or paresis (as opposed to overt paralysis).3 Spinal fractures often are associated with gastric dilation, which develops as a result of pain and shock. The enlarged stomach may partially occlude the caudal vena cava, reducing venous return to the right side of the heart. Normally, in such circumstances, the intraosseous veins and venous sinuses of the spine provide the necessary collateral circulation, but

Radiology. In a lateral radiograph, fractures of the dens, unless badly displaced, often are concealed from view by the transverse processes of C1. A solution to this problem is to carefully rotate the head laterally, which in turn will cause C1 to be oblique, projecting the transverse processes above and below the dens rather than on top of it (Figure 23-1, A). Partially flexing the head while centering on the C1-2 spinal unit eliminates superimposition by the nuchal crest (Figure 231, B). Minimally displaced fractures of the dens are sometimes difficult to distinguish from normal growth plates in immature dogs. Occasionally, the dens is fractured, but not as a separate fragment. Instead, the dens is a part of a lager fragment incorporating much of the articular surface of C2. Such injuries are nearly always comminuted, dislocated, and often are accompanied by one or more C1 fractures (Figure 23-2). Not all neck fractures, even badly displaced ones, will produce paralysis and consequently may not be considered a likely source of neck pain. Relying entirely on lateral radiographs, usually because it is too painful for the dog to be on its back, may result in a significant lesion such as a fracture being overlooked (Figure 23-3). Myelography. Myelography is potentially dangerous when used to diagnose cord compression caused by a recent spinal fracture. Computed tomography (CT) and magnetography are far safer alternatives. The danger with an intrathecal contrast injection lies with the potential absorption of the diagnostic iodine solution by the spinal cord, which then may lead to direct neurotoxic effects and secondary swelling and malacia. The package insert contained with the contrast medium should be carefully scrutinized before con275

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Two paralyzed dogs also were examined using the same technique, one of which had a fracture-dislocation of the T7-8 spinal unit and the other a ruptured disk at T11-12. In both instances, sonography proved useful, and in the case of the disk rupture, indispensable, where additional, occult disk material was located with the aid of a second intraoperative ultrasound examination. In addition to identifying cord compression, spinal canal masses, and mass effects (free disk material), ultrasound also was able to detect a spinal pulse (rhythmic cord motion synchronous with the heartbeat), which the author suggested might be of prognostic value. The presence of spinal pulse suggests a relatively favorable prognosis; its absence suggests a relatively poor prognosis. There were insufficient sonographic observations in unhealthy dogs to predict pathology based on the echo texture of the spinal cord.5 Finn-Bodner and co-workers reported the sonographic appearance of normal and experimentally injured spinal cords in healthy dogs.6 Although the authors provided a detailed account of the surgical exposure of the spinal cord, they unfortunately failed to describe the nature or extent of the injuries other than to depict them as “a ventrally compressive model of spinal cord injury” based on a 1976 master’s thesis done at Auburn University.

A

Computed Tomography. Computed tomography is exceptionally well suited to evaluating spinal fractures, although it is not nearly as clear as magnetography in portraying related soft tissue damage. Magnetic Resonance Imaging

B Figure 23-1 • Lateral (A) and ventrodorsal (B) close-up views of cervical spinal region of a puppy show a subacute, displaced growth fracture of the odontoid process. In the lateral projection, the skull and C1 are deliberately oblique to spread the transverse processes of C1 so that the dens can be clearly visualized. The ventrodorsal view is far less informative.

Traumatic Cervical Dislocations. Kraus and coworkers reported a partial dislocation of the C5-6 spinal unit in which three-dimensional (3-D) reconstruction of a critical CT slice was instrumental in clarifying the true nature and extent of the injury. Specifically, the 3-D image was able to show that C6 had rotated in the axial plane, causing one of its articular facets to move beneath the corresponding C5 facet.7

Noncervical Spinal Fractures templating the risk of myelography performed under such circumstances. Based on personal experience, ionic media are potentially more dangerous than nonionic media, especially in the case of displaced or compression fractures. Associated dislocation is an additional risk factor. Caution: The owner of an injured dog or cat with an acute spinal fracture should be apprised of the additional risk related to myelography before the procedure is undertaken. Intraoperative Ultrasound. Nakayama reported the sonographic appearance of surgically exposed (ventral slot or hemilaminectomy) portions of the normal cervical and lumbar spinal cord regions in healthy dogs.

Thoracic spinal fractures are most often of the compressive type, in part owing to the lateral support provided by the ribs, and they usually appear shortened, sometimes overtly deformed (Figure 23-4). T13 fractures, on the other hand, are more likely to be comminuted than fractures occurring elsewhere in the thoracic spinal region because of a lack of rib support caudally (Figure 23-5). As mentioned previously, is best to delay myelography (assuming CT or magnetic resonance imaging is not available) for at least 48 hours to allow restoration of the blood-brain/blood-cord barriers. When the lateral cord displacement is observed by myelography in cases of spinal fracture, it is usually the result of extradural hemorrhage or a hematoma in the spinal canal.

CHAPTER 23 ❚❚❚ Spinal Injury

277

A

B

D

C Figure 23-2 • Lateral orientation view (A) of the cervical spine and close-up lateral view of the C1-2 spinal unit (B) show fractures of the dens and one of the transverse processes of C1. Ventrodorsal (C) and ventrodorsal close-up (D) views reveal comminution and angular displacement of the C2 fragment, subluxation, and a fracture of the right transverse process.

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B A

D

C Figure 23-3 • Lateral (A), lateral close-up (B), ventrodorsal (C), and ventrodorsal close-up (D) views of a dog with severe neck pain, suspected of having a bulging the C2-3 disk (based on a limited set of outside films, containing only lateral views). Radiographs instead revealed a fracture-dislocation of the C5-6 spinal unit and a displaced caudal endplate fracture of C4. Amazingly, the dog was mildly ataxic but otherwise outwardly normal.

CHAPTER 23 ❚❚❚ Spinal Injury

279

Figure 23-4 • Close-up lateral view of the thoracolumbar spinal region shows a displaced compression fracture of T-13, characterized by shortening (compared with the flanking vertebrae) and angular deformity. As a result, the diameter of the adjacent spinal canal is reduced by nearly half.

A

B Figure 23-5 • A, Close-up lateral view of the thoracolumbar spinal region shows shortening and angular deformity of T12, the result of a compression fracture, with only mild reduction in the diameter of the overlying spinal canal. B, A close-up lateral myelogram performed 48 hours after the injury shows the dorsal contrast band disappearing over the center of the T12-13 spinal unit, reappearing again above T11-12. C, A close-up ventrodorsal view shows right lateral displacement and partial loss of the left lateral contrast band (emphasis zone), the result of a hematoma in the spinal canal.

C

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A

B Figure 23-6 • Lateral (A) and close-up (B) views of the lumbar spinal region of a cat 24 hours following a presumed injury show a partially displaced caudal endplate fracture of L5, with only mild reduction in the diameter of the spinal canal. The increased width in the associated facetal joints is the result of facetal fractures and/or torn capsular tissues.

In my experience, vertebral endplate fractures are more common in cats (Figure 23-6) than in dogs, but they only occasionally lead to serious spinal dislocation (Figure 23-7) and related clinical signs. Most fractured endplates dislocate ventrally, with the attached disk and vertebra following suit. Biplanar endplate fractures (combined vertical and horizontal breaks) sometimes are mistaken for insufficiency fractures secondary to discospondylitis (Figure 23-8). Caudal lumbar fractures, especially those of C6 and C7, may or may not cause paralysis, depending on their severity and how far caudally the spinal cord extends. Even if the spinal cord is spared, however, the adjoining cauda equina is likely to be affected, resulting in bladder and bowel dysfunction as well as pain and hindquarter unsteadiness. Healed lumbar fractures can be mistaken for infections and tumors, especially if the animal’s past medical and surgical histories are unknown. Unlike osteomyelitis and neoplasia, however, most caudal lumbar malunions are associated with an obvious malalignment adjacent to the injury site (Figures 23-9 and 23-10). Some spinal fractures eventually scar (with or without surgery), causing varying degrees of pain and disability; others are aggravated by further injury

(Figure 23-11). In cats, caudal lumbar malunions sometimes are mistaken for congenital spinal malformations (Figure 23-12). Sacral and coccygeal fractures are most common in cats, usually as a result of being run over by a vehicle, and typically are signaled by a flaccid tail and anus.

❚❚❚ TRAUMATIC DISK RUPTURE When traumatic disk ruptures occur, they usually result in hind-limb paralysis. Diagnosis typically is made on the basis of a narrowed disk but can be difficult if there is an associated displaced spinal fracture obscuring the disk space. Neck and back pain often results in oblique projections, making it difficult to evaluate the intervertebral disks (Figure 23-13). Making a lateral image of the affected portion of the spine with the dog on its sternum and using a horizontal x-ray beam often can overcome the problems inherent in interpreting oblique images. If myelography is being considered, one must be mindful of the fact that the diagnostic iodine solution, even nonionic formulations, may be harmful to the spinal cord, especially if administered within the first 24 to 48 hours following injury.

CHAPTER 23 ❚❚❚ Spinal Injury

Figure 23-7 • Close-up lateral view of the caudal thoracic spinal region of a healthy cat shows an old remodeled fracturedislocation of the T10-11 spinal unit, which was detected incidentally in the course of an unrelated medical workup. Even with a 50% reduction in the diameter of the spinal canal, the cat showed no neurologic abnormalities in either the initial or subsequent physical examinations.

Figure 23-8 • Close-up lateral view of the caudal lumbar region shows an unusual fracturedislocation of the caudal endplate L6 in which the plate has been broken in two. Widened, displaced overlying facetal joints indicate additional probable fractures.

Figure 23-9 • Close-up lateral view of the caudal lumbar region (immediately after injury and 6 weeks later) shows severely displaced fractures of the caudal body of L6 and the cranial arch and facets of the sacrum. Healing is predictably slow in such fractures, especially when displaced.

281

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A

B Figure 23-10 • Close-up lateral views of an untreated displaced L7 fracture seen 1 (A) and 6 weeks (B) after the injury. Note that as time passes, the fracture line slowly disappears, the vertebra shortens, and a callus forms, but the spinal canal remains deformed.

CHAPTER 23 ❚❚❚ Spinal Injury

283

A

B Figure 23-11 • Aggravation of an old spinal injury: Close-up lateral (A) and ventrodorsal (B) myelograms of a dog with back pain after being caught beneath a bed. Four years ago, the dog sustained a fracture-dislocation of the L1-2 spinal unit, from which the dog presumably had recovered. Current films show thinning and uneven opacification of the dorsal contrast band that is most pronounced above L2. This myelographic appearance is likely the result of scarring related to the original injury. The calloused facetal joints are compatible with old fractures or fracture-dislocations. The spondylosis is less certain, but because there were no other affected areas, it too is probably injury related.

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Figure 23-12 • Close-up lateral view of the lumbosacral region of a cat shows an angular deformity of the L6-7 spinal unit, evidence of old fracture-dislocation, detected incidentally during an unrelated abdominal survey.

References

Figure 23-13 • Standing lateral view of the neck of a dog following suspected injury shows narrowing of the C6-7 disk, presumed and later confirmed to be a traumatic disk rupture. The narrowing of C3-4 is the result of obliquity caused by the animal’s position of protection (head and neck down and partially turned to the right).

❚❚❚ TRAUMATIC DURAL LACERATION Dural laceration, intraextradural hemorrhage, and cartilage fragments imbedded in the spinal cord, have been described in a Greyhound, injured just after the start of a race.8

1. Selcer RR, Bubb WJ, Walker TL: Management of vertebral column fractures in dogs and cats: 211 cases (1977-1985). J Am Vet Med Assoc 1998:1965, 1991. 2. Seim HB: Surgery of the cervical spine. In Fossum T, ed: Small animal surgery, St. Louis, 1996, Mosby. 3. McNicholas WT, Wilkens BE: What is your diagnosis? J Am Vet Med Assoc 215:1769, 1999. 4. Koper S, Mucha M: Visualization of the vertebral canal veins in the dog: a radiological method. J Am Vet Rad Soc 18:105, 1977. 5. Nakayama M: Intraoperative spinal ultrasonography in dogs: normal findings and case-history reports. Vet Radiol Ultrasound 34:264, 1993. 6. Finn-Bodner ST, Hudson JA, et al: Ultrasonic anatomy of the normal canine spinal cord and correlation with histopathology after induced spinal trauma. Vet Radiol Ultrasound 36:39, 1995. 7. Kraus MS, Mahaffey MB, et al: Diagnosis of C5-C6 spinal luxation using three-dimensional computed tomographic reconstruction. Vet Radiol Ultrasound 38:39, 1997. 8. Roush JK, Douglas JP, et al: Traumatic dural laceration in a racing greyhound. Vet Radiol Ultrasound 33:22, 1992.

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Disk Disease (Intervertebral Disk Disease, Degenerative Disk Disease, Extradural Degenerative Disease, Ventral Segment Disease) ❚❚❚ INTERVERTEBRAL DISK: RELEVANT ANATOMY The intervertebral disk, the principal “villain” in this piece, is composed of three parts: the (1) cartilaginous endplates, (2) annulus fibrosus, and (3) nucleus pulposus. Collectively these elements are termed the discovertebral complex. The collagenous annulus fibrosus forms a complete circle around the nucleus and serves to resist radial tension, which is induced by the horizontal loading of the disk through quadripedal posture. The annulus attaches cranially and caudally to the vertebral body at the site of the fused epiphyseal ring by Sharpey’s fibers and also attaches to the longitudinal ligaments dorsally and ventrally. The annulus is composed of different types of collagen: Type I collagen is prevalent in the outer annulus; type II collagen is present in the inner annulus and nucleus pulposus. Type I collagen occurs in parts of the body where tensile strength is needed, such as in tendons. Type II collagen occurs where compressive forces are high, as in the articular surfaces. The endplate is composed of hyaline cartilage and covers the cranial and caudal vertebral body surfaces. This plate has a key role as a mechanical and biochemical interface between the vertebral body and the nucleus pulposus.

❚❚❚ DIAGNOSTIC TERMINOLOGY There is no consistent terminology used to describe abnormal intervertebral disks, although the veterinary literature strongly suggests that individual authors in a variety of subject areas have clear-cut preferences for descriptors such as protrusion, extrusion, herniation,

and rupture. Some, however, appear content merely to describe an abnormal disk as degenerate, usually because of associated disk calcification, narrowing, or a combination of the two. Others (surprisingly, often not pathologists) seem to show a preference for a purely pathologic description, best exemplified by the terms type I and type II disk herniation (per the Hansen classification). Therefore, and in accordance with the principle of simplicity, I will use the following descriptors. Abnormal disks, such as those seen in medical images, are described on the basis of what is actually visible. From this information (and from the animal’s history and physical findings), necessary inferences will be made based on potential injury to the spinal cord. Where the disk is directly visible, as in magnetic resonance imaging (MRI), or indirectly seen, as in myelography, I propose the words bulging or ruptured be used. Although obviously not perfect, these choices do seem less ambiguous and confusing than the words protrusion and extrusion. Another advantage to such relatively simple terms is that most pet owners are already familiar with them, something that undoubtedly will improve doctor-client communications (or at least speed them up). For the sake of consistency, traumatic disk rupture is preferred over traumatic disk herniation. Because the intervertebral disk is composed of tissue, which is transparent to radiation, it is understandable that early radiologists chose instead to describe the disk space (particularly its width), and not the disk, when reporting their findings. It seems simpler, and certainly more direct, to describe the disk itself as either normal or narrowed. When the disk is unevenly narrowed (usually dorsally), it probably is better to say narrowed dorsally than to describe it as wedged. If wedged is preferred, it should be qualified, as in wedged dorsally. 285

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When describing a nonuniformly narrowed disk or disk space in the ventrodorsal projection, it seems prudent to be specific, as in right-sided or left-sided narrowing. Such information is often extremely important to the surgeon with respect to spinal cord exposure.

❚❚❚ LESION PREVALENCE Dogs Cervical Spinal Region. Dallman and co-workers reported the following radiographic prevalence data for the cervical spinal units of dogs with disk disease.1 I recommend that these figures be used as relative probabilities, not as absolute numbers. • • • • • •

C2-3: 29% C3-4: 24% C4-5: 21% C5-6: 15% C6-7: 9% C7-T1: 2%

These numbers reveal a clear trend: The closer a cervical disk is to the head, the greater its probability of becoming diseased. Thoracic Spinal Region. Thoracic disks rarely bulge or rupture. This “protected status” is theoretically attributed to a combination of physical and biomechanical properties found only in this region of the spine: the presence of an intercapital ligament, which provides additional physical reinforcement, and a normally lighter mechanical load (compared with other spinal regions). Thoracolumbar Spinal Region. Disk lesions, bulges, and ruptures occur most often in the thoracolumbar spinal region, a fact that is theoretically explained by the abrupt increased mechanical pressure on the disks in this location. Lumbar Spinal Region Lumbosacral Spinal Region: Cats. Cats so rarely rupture their intervertebral disks that it is impossible

to compile reliable prevalence figures.2 Multiple small disks suggesting degeneration, however, are often present in the spines of older cats being radiographed for nonneurologic disease (Figure 24-1).

❚❚❚ PLAIN RADIOGRAPHY (SURVEY RADIOGRAPHY) Relative Diagnostic Contributions of Plain Radiographs Versus Myelograms in Individual Animals Kirberger and co-workers reported the comparative advantages of radiography and myelography in the diagnosis of thoracolumbar disk disease in 36 Dachshunds.3 In the authors’ hands, plain films accurately localized the offending disk in 27 of 36 dogs, for a diagnostic success rate of 72%. Myelography, on the other hand, successfully identified the lesion in 35 of 36 dogs, a success rate of 97%. By way of counterpoint, my experience with the radiographic diagnosis of canine disk disease differs decidedly from that reported by Kirberger’s group, specifically with respect to plain films, which I reported to have a localization rate of 92%. Possible explanations for this disparity in plain film localization rates may be (1) reader experience (for example, at the time of this writing, I have been reading spinal surveys for nearly three decades) and (2) the development of a diagnostic dependency on myelograms that results when myelography is performed in every animal that is going to undergo surgery, irrespective of the conclusiveness of plain films. In this latter situation, I would argue strongly that in dogs that have become acutely paralyzed and have only a single plain film lesion, myelography is unnecessary unless the neurologic assessment disagrees with the radiographic diagnosis. Although myelography may be diagnostically indispensable in some instances, it clearly seems superfluous in others. Therefore, given the associated risks, costs, and additional anesthesia time of myelography, it is my recommendation that this special procedure should be used on an individual, case-by-case basis, rather than performed indiscriminately as part of a neurologic “work-up.”

Figure 24-1 • Narrowed disks in the thoracolumbar and proximal lumbar spinal regions of an asymptomatic cat (later confirmed at necropsy).

CHAPTER 24 ❚❚❚ Disk Disease

The Standing Spine Radiographing a dog in the standing lateral or sternal positions has the twin advantages of minimizing restraint and reducing or eliminating spinal obliquity. Where the costs of conventional spinal imaging (and associated anesthesia) are prohibitive, postural films such as these offer an inexpensive alternative (Figure 24-2). Diagnostic Strategy: The Three-Window Approach. While teaching neuroradiology over the past three decades, I developed a simplified method for analyzing the spine of dogs suspected of having a bulged or ruptured intervertebral disk. I call it the three-windows approach. It works as follows.

287

When a disk bulges, ruptures, or simply becomes dehydrated (disk degeneration as seen on MRI), it loses volume, causing the involved vertebrae to come closer together, a key point in radiographic analysis. This closer proximity results in the narrowing not only of the disk space but also of the intervertebral foramen and associated facetal joints. These are the three “windows,” openings not only in a physical sense but also “windows of diagnostic opportunity” (Figure 24-3). Continuing with the window metaphor, it is important to note that a particular lesion may not affect all spinal units to the same degree. In other words, some spaces may be only partially diminished, whereas others may not be affected at all. This variability is depicted in Figures 24-4 and 24-5. Free Disk Fragments: The Visible Disk Rupture. Calcified disks or, more usually, portions of calcified

Figure 24-3 • Close-up view of three front windows in a residential home illustrates the three-window approach to the plain-film diagnosis of disk disease involving assessment of (1) the disk, (2) intervertebral foramen, and (3) facetal joints.

A

B Figure 24-2 • Postural films: Full-length (A) and close-up (B) standing lateral views of a dog with unilateral forelimb pain show a small calcific density in the upper part of the C2-3 disk space, which eventually proved to be free, calcified disk material compressing a spinal nerve root.

Figure 24-4 • Close-up view of the midlumbar spinal region of a paralyzed dog shows (1) a slightly narrowed disk, (2) a triangular calcific cloud at the base of a narrowed intervertebral foramen, (3) narrowed facetal joints, and (4) a large, oval-shaped chunk of free calcified disk in the caudal aspect of the spinal canal just above the body of L2.

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Figure 24-5 • A, Close-up view

A

of L1-2 shows a thin calcific arch spanning an otherwise normalappearing intervertebral foramen, the result of free disk in the spinal canal causing hindlimb paralysis. B, Full-length lateral view of lumbar spinal region shows a free disk fragment in the intervertebral foramen of the L2-3 spinal unit.

B

disks, sometimes can be seen as clouds, plumes, or arch-like densities in the spinal canal, often superimposed on the intervertebral foramen. In some instances, free disk fragments (sequestered disks) appear as vague densities, without any particular shape. Figures 24-6 to 24-9 illustrate some of the potential appearances of free disk fragments in the spinal canal.

❚❚❚ MYELOGRAPHY Background and Beginnings Funkquest is generally credited with popularizing myelography in the dog, although the ionic contrast she used (Skiodan) usually caused seizures and occasional fatalities.4,5 Ticer and Brown were some of the first North American veterinary radiologists to promote vigorously the advantages of myelography in paralyzed dogs with normal-appearing spinal films.6 In his original paper, presented to the International Radiology Association in 1973, Ticer described the myelographic abnormalities in dogs with spinal cord compression caused by ruptured intervertebral disks (see specifics later herein). Comparable, in-depth publications on feline myelography are lacking, although there have been limited publications on the subject.7

Figure 24-6 • Close-up view of a partially calcified disk in the C5-6 spinal unit and a fully calcified disk in the adjacent C4-5 unit, both of which were intact and causing the dog no discomfort.

When to Perform Myelography The question of when and when not to perform myelography should always be a contextual one, jointly answered by all the involved parties, especially the radiologist or the person who is to perform the procedure.

Figure 24-7 • Close-up view of the L2-3 spinal unit shows a large spherical calcified disk fragment in the spinal canal that is graying the intervertebral foramen.

A

Figure 24-8 • Lateral (A) and ventrodorsal (B) views of the cervical spine show a distinctive plume of calcified disk that has erupted from the C4-5 disk and now lies free in the spinal canal.

B

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Sukhiani and co-workers have found that some dogs with back pain, but no neurologic deficits, may have substantial cord compression as determined myelographically. As a result of their findings and related surgical experience, the authors question the conservative, nonsurgical treatment traditionally provided for dogs with these signs. Further, they recommend that dogs with persistent or recurrent pain be evaluated myelographically and surgically decompressed if found to have a “mass lesion” (presumed bulging or ruptured disk or related scar). The authors claim “a generally favorable outcome” for the operated animals in this report, a conclusion that appears based largely on owner testimonials.8

Myelographic Risks Myelographic Contrast Media. The precise biochemical nature (or natures) of myelographic contrast media injury to the brain and spinal cord of dogs is not known, although theories abound. It is possible, however, to identify certain biochemical features of iodinated contrast designed for intrathecal use, which is potentially neurotoxic. Clearly, some of the early media, like Skiodan, were potentially quite dangerous, consistently causing postprocedural seizures that were often severe and protracted and occasionally death. Others, like Pantopaque

(oil-based), were less harmful initially but with time led to adhesive arachnoiditis. Not until the advent of metrizamide, and later iohexol and Omnipaque, did the risks of myelography become more acceptable. For a detailed account of the biochemical advantages associated with low osmolar contrast media, see the review by Dennis and Herrtage.9 Widmer and co-workers compared the neurotoxicity of iopamidol and metrizamide (as used in cervical myelography of dogs) and found the latter to be more harmful.10 Later, the same authors compared iopamidol with iohexol with regard to both toxicity and image quality.11 They found image quality comparable, with little or no difference in the incidence of adverse effects. Myelography, in which two or more contrast injections are made, especially if one is by cervical puncture, appears to be potentially more harmful (complications) than single-injection studies.12 Cervical punctures are far more dangerous than those performed in the caudal lumbar region. Procedural Risks. Little appears in the veterinary literature about the potential procedural risks associated with myelography, with most reports focusing on the dangers of the contrast medium.13-15 One important exception to this generality is the discovery by Tilmont and co-workers that a cisternal subarachnoid puncture may injure the spinal cord, even though the procedure

Figure 24-9 • A, Lateral view of the thoracolumbar spinal region shows an abnormal T13-L1 spinal unit featuring (1) faint opacification of the intervertebral foramen, (2) disk, and (3) facetal joint narrowing. B, A close-up lateral myelogram of the same region shows abrupt arching of the dural sac over T-13 and a complete absence of the dural opacification dorsally, compatible with a ruptured disk.

A

B

CHAPTER 24 ❚❚❚ Disk Disease

is carried out in accordance with a widely accepted protocol.16 Tillson and co-workers reported the accidental use of a nonmyelographic contrast agent containing diatrizoate meglumine and diatrizoate sodium in a dog with hindlimb paralysis. Although the dog suffered severe seizures and as a consequence had to be anesthetized repeatedly, it did eventually recover after being treated empirically.17 Because I have been able to find so little on the subject, I relate my own experience herein with myelography obtained over the past 30 years, during which I have performed more than 1200 myelograms. First, myelography, especially that involving a cisternal puncture, is a most serious matter, one that is potentially harmful and occasionally fatal. Needle wounds to the spinal cord, compressive intradural and extradural hematomas, and contrast overdose are all within the realm of possibility each time a cervical myelogram is undertaken, in addition to any toxic effects that the purpose-designed iodine solution might exert. Postmyelographic Removal of Contrast Media. Widmer and co-workers described the removal of metrizamide (actually, metrizamide in solution with cerebrospinal fluid [CSF]) by cervical puncture following myelography in normal dogs, which they referred to as “withdrawal myelograms.”18 As a result of removing what was estimated to be about 30% of the original dose of metrizamide, a significant decrease in the incidence of postmyelographic seizures occurred, prompting the authors to recommend “withdrawal myelography” even for the newer contrast media, such as iopamidol and iohexol. Using a similar technique in the early seventies, I found that it made little or no difference in postprocedural seizuring, but on average prolonged the examination time by as much as 20%. Myelographic Contraindications. The presence of blood in the CSF obtained following cisternal puncture, a so-called bloody tap, and whether or not contrast solution then can be safely injected is a somewhat contentious issue among radiologists. My preference, faced with this situation, is to remove the original needle

291

and puncture again with a new needle. If I again get a mixture of blood and CSF, I postpone the myelogram as a precaution against the development of a compressive intradural or extradural hematoma. Regarding the intermediate and long-term consequences of a contaminated cisternal puncture, Bartels and Braund were unable to find any histologic evidence to support the widely held notion that myelography, performed in the context of subarachnoid hemorrhage, potentially promotes arachnoid fibrosis.19 Postprocedural Cerebrospinal Fluid Analysis. Carakostas and co-workers analyzed CSF samples before and after metrizamide myelography and determined that CSF is affected in the ways listed in Table 24-1.20

Myelographic Techniques Epidural (Extradural) Injections. Inadvertent epidural (Figure 24-10) or, more usually, combined epidural/ intradural injections (Figure 24-11), occur regularly in practice. Combined injections, although visually confusing, can be figured out with experience. Weber and Berry described radiographic features that can be used to determine the location of myelographic contrast solution following lumbar injection (Table 24-2).

Table 24-1 • CHANGES IN CSF SAMPLES OBTAINED BY CISTERNAL PUNCTURE BEFORE AND AFTER MYELOGRAPHY CSF Constituent or Microscopic Observation Creatine phosphokinase Erythrocyte count Large mononuclear cells Neutrophils Pleocytosis Small mononuclear cells Total protein

Effect No change Increased No change Increased Decreased Increased

Cause Dural puncture Metrizamide Metrizamide Dural puncture Dural puncture

CSF, Cerebrospinal fluid.

Table 24-2 • DIFFERENTIATING SUBARACHNOID FROM EPIDURAL MYELOGRAMS Contrast Solution in the Subarachnoid Space (Lateral View)

Contrast Solution in the Epidural Space (Lateral View)

Appearance of caudal aspect of dural sac and associated spinal nerves

Tapered, smoothly blunted opacity ending midway over L7 or proximal sacrum (see Figure 24-16)

Contrast solution appears as a thick, uneven band that extends well into the sacral canal and lacks a discrete termination (see Figure 24-17)

Appearance of contrast bands

Discrete, relatively straight, parallel contrast bands; the ventral band is typically wider than the dorsal one

Regular, undulating, ventral contrast band that is convex over the intervertebral foramen and concave over the vertebral body

Distance between the inner surface of spinal canal and nearest contrast band

Small, fairly uniform gap

Absent

Location of contrast solution in spinal canal

Discrete dorsal and ventral contrast bands

Vague, variably located contrast

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Figure 24-10 • Close-up lateral view of a C5-6 test injection showing opacified cerebrospinal fluid within the dural sac.

Figure 24-11 • A, Lateral view of the caudal lumbar region shows an inadvertent epidurogram (contrast solution outside the dural sac) following a myelographic test injection in the L6-7 spinal unit. B, Close-up lateral view of a L6-7 myelographic test injection shows a mixture of dural and extradural contrast solution. The low image contrast is due to the dog being obese.

A

B

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293

A Fig. 24-12 • Extremely obese dog: Full-length view of lumbar spinal region of a medium-sized dog with 5 inches of back fat. Even using compression and a 3.5-inch spinal needle, it was impossible to puncture the lumbar dura, necessitating a surgical cutdown and an intraoperative myelogram. Decreased image contrast is the result of obesity.

Fat. The more fat over the spine, the greater the distance from the skin surface to the dural sac, where the contrast is to be injected (Figure 24-12). Longer target distances require longer spinal needles, which are more difficult to manipulate, being inclined to bend or be deflected as the operator attempts to pass them through the interarcuate foramen to the meninges below. In general, if there is more than four inches of lumbar fat, I recommend a surgical cut-down. Imaging Findings Survey Films. Premyelographic films are used to establish optimal radiographic technique and to survey the spine for any additional lesions. Protocols for spinal survey may be initially limited to lateral projections, followed by selected ventrodorsal views in the event that a lesion is discovered. Alternatively, full lateral and ventrodorsal imaging is performed, regardless of initial findings. Tip: If there are two or more potential lesions (disk narrowings), try a traction-stress lateral of the affected spinal region. Many recently ruptured disks will expand during traction, whereas older scarred disk will remain narrowed because of secondary scarring (Figure 24-13). Patient Positioning for Myelography. Dogs undergoing myelography usually are positioned on their side or sternum. Although most seem to prefer lateral recumbency, I am partial to the sternal position because it allows me to remain standing, where I am less likely to be accidentally bumped in a small room that is often crowded with assistants. It is also more comfortable to stand, especially when attempting a lumbar puncture on a very fat dog, which can be protracted. I recommend not using the suspended technique in which the dog is positioned on its sternum with its

B Figure 24-13 • “Dynamic” plain films: Close-up lateral (A) and lateral traction stress (B) views provide circumstantial evidence in support of a recent disk rupture. Specifically, if an initial plain film shows only a single narrowed disk and a subsequent traction stress image shows relative enlargement of that same disk, it is probably the site of cord compression.

hindquarters hanging over the end of the x-ray table. Advocates of this method claim that the resultant spinal traction opens the interarcuate foramina, making a caudal lumbar puncture easier, but typically neglect to mention the adverse effect on venous return, a potentially dangerous situation. Needle Placement. If necessary, correct positioning of the spinal needle can be verified with either a test film or fluoroscopically, if fluoroscopy is available. In my experience, a satisfactory lumbar puncture nearly always is accompanied by a tail or leg twitch. Once the spinal needle is positioned and the stylet is removed, CSF may or may not “well up” in the needle hub. A needle located in the central third of the spinal cord (Figure 24-14) may prevent all or some of the contrast solution from reaching the dural sac, instead entering the central canal or tracking dorsally along the surface and accumulating outside the spine. Inability to inject the contrast solution usually indicates that the needle has passed through the cord and into the disk below (Figure 24-15).

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Figure 24-14 • Needle position: A premyelographic test film shows the tip of a spinal needle positioned in or near the central canal of the spinal cord, an undesirable location for injection of the contrast solution.

it will be inadvertently bumped during radiography and the cord lacerated. Myelographic Signs of Disk Rupture (modified from Ticer and Brown6). • Narrowing of one or both subarachnoid spaces in lateral or lateral oblique projections. This was the most consistent sign associated with disk rupture and therefore was considered the most reliable. • Narrowing of right or left side of the subarachnoid space in ventrodorsal view. Narrowing of at least one portion of the subarachnoid space was consistently present in both standard views. • Spinal cord displacement (usually dorsally in a lateral radiograph, and to one side in the ventrodorsal projection. • Widening of the subarachnoid space caudal to the ruptured disk when contrast was administered by lumbar puncture and cranial to the lesion when administered in the occipital cistern. This phenomenon, also referred to as contrast backup, is best seen in lateral projection, and dissipates soon after it is initially observed. Figure 24-15 • Needle position: A premyelographic test film shows the tip of a spinal needle imbedded in the upper portion of an intervertebral disk. In this circumstance, a contrast injection is likely impossible; alternatively, if some contrast solution can be forced through the needle, it will accumulate outside the dural sac, where it will be of little or no use diagnostically.

Test Injection. It is advisable to inject a small volume of contrast solution before administering the full dose. If excessive epidural contrast is noted in the initial test film, the needle should be repositioned and another small amount of contrast given. Test injections are repeated until the desired appearance is obtained, at which time the remaining contrast is given. Although it is done, I recommend against leaving the spinal needle in position once the full dose of contrast solution has been administered. The longer the needle remains imbedded in the spinal cord, the greater the risk that

Examples of Myelographically Demonstrated Disk Lesions (Figures 24-16 to 24-19) Tip: When opacification of the subarachnoid space is faint, or where overlying viscera obscure a region of interest in the ventrodorsal view, compression radiography usually improves both the contrast and detail of the image. Caution: Scrivani and co-workers have challenged the validity of the so-called double line sign, sometimes seen during myelography, and said to represent an eccentrically positioned or lateralized extradural lesion (Figure 24-20). Instead, say the authors, either laterally or ventrally located extradural lesions may produce such double lines. Accordingly, the authors do not recommend reliance on the

CHAPTER 24 ❚❚❚ Disk Disease

295

B

A Figure 24-16 • Lateral view (A) of lumbar spinal region of a paralyzed dog shows dorsal displacement of the dural sac and spinal cord over much of the L2-3 spinal unit. A close-up (B) view shows a wispy arch of calcified disk material directly beneath the displaced dura.

Figure 24-17 • A, Lateral survey film of lumbar spinal region shows narrowed noncalcified disk at L5-6 and a calcified disk at L4-5. B, A close-up lateral myelogram shows a gradual ventral displacement of the dorsal aspect of the dural sac over the body of L4, the result of a dorsolateral disk fragment originating at L4-5.

A

B

doubleline sign to establish the position of an extradural lesion; rather, ventrodorsal or ventrodorsal oblique views should be used (assuming CT or MRI is not available).21 Stickle and co-workers have also discussed the fallibility of the double line sign, using computed tomography to further exemplify variation in the appearance of the ventral contrast band (“splitting”) caused by sagittal and parasagittal extradural lesions.22

Failure to Flow At times, cisternal contrast injections fail to flow much beyond the proximal or midthoracic thoracic spinal regions, with or without a demonstrable lesion (Figure 24-21). Gradual dissipation of the contrast medium

typically distinguishes failure to flow from the relatively abrupt stoppage of lesion-related contrast backup. Although there appears to have been ample informal speculation on the subject, the precise cause or causes of flow failure have not yet been determined. In an effort to encourage the movement of stalled intrathecal contrast media, numerous postural maneuvers have been developed, most of which are variations on the same basic theme: patient head up/rump down for varying periods following completion of the injection.23 These maneuvers seem based on the belief, seemingly justified in some cases, that the injected iodine solution is heavier (greater specific gravity) than CSF and, at least for a time, will remain concentrated in the cervical portion of the dural sac near where it

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A

B

C Figure 24-18 • Close-up lateral view (A) of the T12-13 spinal unit shows slight narrowing of the dorsal aspect of the disk, reduced foraminal area, and diminished facetal width. Close-up lateral (B) and ventrodorsal (C) myelograms of the suspected disk show encirclement and compression of the spinal cord beginning over the body of T13 and extending nearly the full length of T12, the result of a ruptured disk and associated hemorrhage.

Figure 24-19 • A, Full-length,

A

B

lateral view of lumbar spinal region of a paralyzed dog shows a narrowed L2-3 disk, foramen, and facetal joint compatible with a ruptured disk. B, Lateral myelogram of the same region shows lifting of the faintly opacified dural sac extending from the cranial aspect of L2 to the caudal aspect of L3, confirming the plain film diagnosis.

CHAPTER 24 ❚❚❚ Disk Disease

297

A

B

C

D Figure 24-20 • Double line sign: A, Full-length lateral view of cervical spinal region of a paralyzed dog shows narrowing of the C4-5 disk. B, Full-length lateral myelogram shows dorsal displacement of the opacified dural sac above the suspected disk (C4-5). C, A close-up lateral myelogram of the ruptured C4-5 disk shows a so-called double line sign ventrally, formerly thought to be a dependable indicator of an eccentrically positioned ventral disk fragment but later found to be inconsistent. D, A compression ventrodorsal myelogram (to displace the potentially confusing overlying endotracheal tube) shows the disk lying near the ventral midline, not to one side as suggested by the doubleline sign.

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Figure 24-21 • Failure to flow:

A

A, An attempted cervical myelogram failed as a result of the contrast solution not reaching the desired spinal level. B, Failure to flow in such cases typically is characterized by a gradual loss of contrast visibility.

B

has been injected. By elevating the patient’s head, the theory continues, the heavier-than-CSF contrast solution will avail itself of the newly created gravitational opportunity and will flow caudally (or so the story goes). Unfortunately, even when a dog is positioned vertically for 10 minutes or longer, the contrast does not always move, or it moves so slightly (as judged by the faintest of subarachnoid opacifications) that the procedure is considered a failure. In the case of known caudally located cord/dural compression, and faced with “failure to flow,” McKee and co-workers recommend the following simple twostep positioning procedure.24 1. Position the dog head up/rump down for 5-10 minutes, preferably with the head in traction. This can be done manually or with a tilt table. 2. Next, with the head and neck still elevated, use pads to elevate the caudal torso and pelvis. This creates a V-shaped body profile, which places the caudal cervical region at the lowest point on the table and theoretically concentrates the iodine solution where it is needed most, around the lesion.

Optimizing Myelographic Lesions With Postural Maneuvers Because diagnostic iodine solutions transiently pool in the dependent portion of the subarachnoid space during myelography, especially in the relatively voluminous cervical region, extradural lesions or, more precisely, their effect on the dural sac, often are more

apparent in one view than in another.25 This difference in visibility is related to the amount of iodine solution surrounding the lesion, so that in general the greater the amount of contrast surrounding a particular lesion, the greater its detectability. Thus the optimal standard myelographic protocol should include right and left lateral and ventrodorsal and dorsoventral views. Supplementary oblique and decubital projections can be added as needed. Computed Tomography. Computed tomography is capable of precisely locating a compressive disk lesion, which in a myelogram may appear only as a generalized cord swelling.26 CT myelography can also confirm a questionable localized cord displacement identified in an earlier myelogram.27 Olby and co-workers described the CT appearance of acute disk rupture in a small series of dogs, asserting that unenhanced CT is capable of quickly, precisely, and safely locating such lesions, especially when they are calcified.28 Further, they contend that recent lesions can be distinguished from older ones by the appearance of the herniated disk material, which in the case of chronic lesions, appears relatively more dense and homogeneous than recently herniated disks. Related extradural hemorrhage could also be identified with CT, usually occupying the lateroventral aspects of the epidural space, in keeping with the location of the paired spinal venous sinuses. In this latter regard, the authors suggest that what is often termed cord swelling, based on myelographic appearances, is in reality contiguous paraspinal hemor-

CHAPTER 24 ❚❚❚ Disk Disease

rhage. In another cautionary note, the authors theorized that a mineralized dorsal longitudinal ligament, seen in cross-section, could potentially mimic a small, rounded disk fragment located on the floor of the spinal canal. By way of limitation, and in addition to the relatively high cost of CT compared with myelography and its comparative lack of availability, tomographic examinations may be seriously compromised by a lack of contrast between the spinal cord and the offending disk. This problem is encountered in nearly a third of the described cases. Although the authors acknowledge that CT examinations do not survey as much of the cord as myelography, they contend that, based on probability (75% of disk lesions are found between T11 and L2) and a corroborating neurologic examination, CT is just as effective. Magnetic Resonance Imaging. MRI is the superior method of imaging disk disease, but unfortunately it is also the most expensive. MRI is capable of showing all aspects of disk lesions including: • the hydration state of the intervertebral disk • the discovery of whether or not the disk is merely bulging or has actually ruptured • the whereabouts of any free disk material (sequestered disk fragment) • the magnitude of cord compression and displacement • the presence of any related hemorrhage and edema MRI will also provide information on the other elements of the diskovertebral unit such as the vertebral endplates, and is very helpful in differentiating a fresh disk lesion from chronic postoperative scarring–-probably the most difficult of all disk-related MRI diagnoses. Other than its relatively high price point, the only other negative associated with MRI is its limited ability to image fine bone detail.

❚❚❚ CORD SWELLING Although seemingly of great prognostic importance, the length of observed cord swelling, as demonstrated myelographically, has proven an unreliable predictor of future recovery (or lack thereof).29

Subdural Contrast Injection The inadvertent injection of myelographic contrast solution into the dorsal aspect of the subdural space was radiographically identified in 58 of 654 myelograms (about 9%). The effect was to produce a high-density, linear band located dorsal to the opacified CSF (as seen in lateral projection). Using Indian ink injected into the subdural space of a cadaver, it was demonstrated that the denticulate ligaments restricted the ventral extension of the contrast medium.30

299

Scrivani and co-workers also reported subdural contrast injection in the proximal cervical region of a dog and two horses, characterizing the abnormal contrast accumulation as having smooth dorsal and undulating ventral margins.31 Lamb offered an alternative explanation for this unusual contrast pattern, contending that it is more likely “unmixed” contrast solution within the subarachnoid space.32

Central Canal Injection There appears to be no certain consequence to the injection of purpose-formulated, iodinated contrast media in the central canal of the spinal cord.33 Kirberger and colleagues hypothesized that rapid contrast injection (usually cranial to the L5-6 spinal unit) may result in “canalograms,” the author’s term for the presence of diagnostic iodine solution in the central canal; more importantly, it can lead to canal distension. Such inadvertent enlargement then may cause worsening of the dog’s condition, although precisely how this comes about is not known. The author also points out that a disease like hydromyelia is normally associated with dilation of the central canal.34

Myelographic Filling Defects Myelographic filling defects, as opposed to the typical cord displacement seen with bulging or herniated disks, most often are seen with medium and large intradural tumors, although any mass or mass effect is capable of creating such a finding.35 Although admittedly catchy, terms such as “golf tee,” used by some radiologists to describe the shape of a myelographic filling defect said to be indicative of an intraduralextramedullary tumor, are more often than not absent, even when such a lesion is present.

❚❚❚ EPIDUROGRAPHY, INTRAOSSEOUS VERTEBRAL VENOGRAPHY, AND DISKOGRAPHY Epidurography Although most original reports were optimistic36,37 (in retrospect, perhaps overly so), epidurography, in my opinion, never has lived up to expectations. Although an extradural contrast injection is potentially less harmful than an intradural one, lesion clarity is nowhere near as good. (This difference is now substantially less with the current crop of nonionic contrast media.) Worse, epidurograms consistently have had to contend with numerous variably positioned, variably sized filling defects caused by fat, some of which closely resemble abnormal disks. This is not to say, however, that the procedure is without merit; on the contrary, there are case reports illustrating its effectiveness.38

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Intraosseous Vertebral Venography (Transosseous Vertebral Venography) As was the case with epidurography, the initial clinical reports of spinal venography were highly optimistic. Also like epidurography, the diagnostic promise appears to have been unfulfilled.39-41 Venography has proven diagnostically insensitive as well as nonspecific and accordingly has largely been abandoned.

Diskography Wrigley and Reuter described cervical diskography in the dog,42 a technique that at first seemed promising but has never achieved a place in the diagnostic mainstream. The reasons for this lack of popularity likely emanate from three issues: (1) radiation exposure associated with the fluoroscopic guidance of the needle, (2) technical difficulties related to correct needle placement, (3) leakage of contrast medium following injection into or adjacent to the target disk, and (4) the fact that many subacute and chronic disks lack nuclear integrity and are thus not amenable to diskography. Furthermore, most veterinary clinics and hospitals lack fluoroscopy necessary for precise needle guidance.

that Schmorl’s nodes and fibrocartilaginous emboli may be related.44 Spinal Cord Compression. As previously mentioned, a ruptured disk (free or fixed) exerts pressure on the spinal cord as a function of its volume and distribution, with related hemorrhage often adding to the total mass effect. Cord edema magnifies this problem by increasing the size of the cord, causing a relative increase in the compressive effect of the ruptured disk. Nerve Root Compression and Traction-induced Stimulation. A dorsolateral disk rupture into the intervertebral opening may cause compression of the resident nerve root and associated limb pain, often referred to as a nerve root signature. If the discharged disk content is dense enough and extends beyond the lateral margins of the involved spinal unit, it may be possible to detect in a ventrodorsal radiograph.45

❚❚❚ MAGNETIC RESONANCE IMAGING The Preoperative Spine

❚❚❚ BULGING DISK A bulging but intact intervertebral disk is difficult to diagnose on plain films but often can be appreciated myelographically. When bulging disks are imaged with MR, they often reveal interior signal intensities compatible with dehydration, an indication of degenerative disease.

❚❚❚ RUPTURED DISK Disk Content in the Spinal Canal: Free or Connected? When a disk ruptures, the escaped content either may remain attached to the torn annulus or lie free (sequestered) in the spinal canal. The amount of pressure exerted on the spinal cord depends primarily on the amount and distribution of the resultant extradural mass effect.

Imbedded Disk Content (Intravertebral Disk Herniation) Rarely, an intervertebral disk will rupture and become imbedded in one or both adjacent endplates, creating a radiographically visible defect. In people, such lesions are called Schmorl’s nodes, typically appearing as well-outlined, hemispheric, or spherical defects in the vertebral endplate. Similar lesions have been described in dogs.43 Gaschen and colleagues suggested

Background. As already mentioned, the abnormal disk is classically considered to be an annular bulge or a herniation. An annular bulge is the result of degeneration with a grossly intact annulus, recognized as a general extension of the disk margin beyond the margin of the vertebral endplate. Imaging Findings. Karkkainen and co-workers described the MRI appearance of degenerative disk disease in the lumbar and lumbosacral regions of 14 dogs, 11 with lumbar pain and neurologic signs and 3 healthy animals.46 The authors obtained their results using low-field strength magnets (0.04 T and 0.02 T) and a human spinal surface coil. Normal disks appeared white, characterized by strong signal intensity in T2, and a somewhat less intense signal in T1 images, due to the large water content of the nucleus (nucleus pulposus). In T1 images, the disk perimeter (annulus fibrosus), cortical endplates, and adjacent ligaments appeared relatively dark, reflecting low signal intensity. Abnormal disks appeared black or dark gray, reflecting the reduced signal intensity brought about by dehydration.

The Postoperative Spine About 25% of human back surgeries, most performed to relieve pain, fail to provide any significant degree of improvement or relief. Characterized by pain and incapacitation, such patients are said to have failed back surgery syndrome. Possible explanations include (1) surgical inadequacy, (2) arachnoiditis, (3) epidural

CHAPTER 24 ❚❚❚ Disk Disease

scar formation, (4) stenosis, (5) further disk herniation, (6) mechanical instability, (7) nerve root injury, and (8) pseudomeningocele formation. In the immediate postoperative period, the laminectomy (hemilaminectomy) and diskectomy sites are usually obvious because of dorsal element removal and intervertebral narrowing. The site of bone and ligament resection appears heterogeneously isointense to muscle on T1-weighted images and hyperintense on T2. Mass effect on the thecal sac is unusual unless a postoperative hematoma develops. During the next few months, the immediate postoperative appearance gradually changes as scar tissue forms. The appearance of the so-called dorsal scar is highly variable, ranging from increased to decreased signal intensity on T2-weighted images. Changes from diskectomy are evident immediately after surgery. T1 images show increased signal intensity in soft tissue ventral to the thecal sac and an indistinct annular margin. The former (representing edema) may blend into the associated disk space, showing increased signal intensity in T2, resembling disk herniation and cord compression. These abnormalities gradually subside over the next 2 to 6 months, with the margins of the thecal sac eventually appearing normal. Sagittal T2 images of the diskospinal unit can define the operative site, seen as the characteristically bright signal of the nucleus pulposus extending dorsally into the area of the surgically disrupted annulus. The annular perforation heals within 2 to 6 months following surgery. Scar Formation versus Disk Herniation: Causes of Failed Back Surgery. Criteria for the evaluation of postoperative scarring versus further disk rupture in the postoperative period include: • Scar tissue enhances immediately after injection, regardless of the time since surgery. • Disk material does not enhance immediately after injection. • A smoothly marginated, polypoid ventral epidural mass is most likely to be a disk. • Scar is capable of exerting a mass effect and being contiguous with the disk space.47

References 1. Dallman MJ, Palettas P, Bojrab MJ: Characteristics of dogs admitted for treatment of cervical intervertebral disk disease: 105 cases (1972-1982). J Am Vet Med Assoc 200:2009, 1992. 2. Bagley RS, Tucker RL, et al: Intervertebral disc extrusion in a cat. Vet Radiol Ultrasound 36:380, 1995. 3. Kirberger RM, Roos CJ, Lubbe AM: The radiological diagnosis of thoracolumbar disk disease in the dachshund. Vet Radiol Ultrasound 33:255, 1992. 4. Funkquist B: Thoraco-lumbar myelography with water soluble contrast medium in dogs. I. Technique of myelography; side effects and complication. J Small Anim Pract 3:53-66, 1962.

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5. Funkquist B: Thoraco-lumbar myelography with water soluble contrast medium in dogs. II. Appearance of the myelogram in disc protrusion and its relation to functional disturbances and pathoanatomic changes in the epidural space. J Small Anim Pract 3:67-73, 1962. 6. Ticer JW, Brown G: Water-soluble myelography in canine intervertebral disk protrusion. J Am Vet Rad Soc 15:3, 1974. 7. Nykamp S, Scrivani P: Feline myelography. Vet Radiol Ultrasound 42:532, 2001. 8. Sukhani HR, Parent JM, et al: Intervertebral disk disease in dogs with signs of back pain alone: 25 cases (19861993). J Am Vet Med Assoc 209:1275, 1996. 9. Dennis R, Herrtage ME: Low osmolar contrast media. Vet Rad 30:2, 1989. 10. Widmer WR, Blevins WE, Cantwell D, et al: A comparison of iopamidol and metrizamide for cervical myelography in the dog. Vet Rad 29:108, 1988. 11. Widmer WR, Blevins WE, et al: Iohexol and iopamidol myelography in the dog: a clinical trial comparing adverse effects and myelographic quality. Vet Radiol Ultrasound 33:327, 1992. 12. Carroll GL, Keene BW, Forrest LJ: Asystole associated with iohexol myelography in a dog. Vet Radiol Ultrasound 38:284, 1997. 13. Funkquest B: Thoraco-lumbar myelography with water soluble contrast medium in dogs I. Technique of myelography: side-effects and complications. J Small Anim Pract 3:53, 1962. 14. Adams WM, Stowater JL: Complications of metrizamide myelography in the dog: a summary of 107 clinical case histories. Vet Rad 22:27,1981. 15. Carlisle CH, Pass MA, et al: Toxicity of the radiographic contrast media iopamidol, iohexol, and metrizamide to cell cultures. Vet Radiol Ultrasound 36:206, 1995. 16. Tilmant L, Ackerman N, Spencer CP: Mechanical aspects of subarachnoid space puncture in the dog. Vet Rad 25:227, 1984. 17. Tillson DM, Roush JK, et al: Inadvertent intrathecal administration of diatrizoate meglumine and diatrizoate sodium during myelography in a dog. Vet Radiol Ultrasound 35:89, 1994. 18. Widmer WR, Blevins WE, et al: Effects of postmyelographic removal of metrizamide in dogs. Vet Rad 31:2, 1990. 19. Bartels JE, Braund KG: Experimental arachnoid fibrosis produced by metrizamide in the dog. Vet Rad 21:78, 1980. 20. Carakostas MC, Gossett KA, et al: Effects of metrizamide myelography on cerebrospinal fluid analysis in the dog. Vet Rad 24:267, 1983. 21. Scrivani PV, Barthez PY, Leveille R: The fallibility of the myelographic “double line” sign. Vet Radiol Ultrasound 37:264, 1996. 22. Stickle R, Lowrie C, Oakley R: Another example of the myelographic “double line” sign. Vet Radiol Ultrasound 39:543, 1998. 23. McKee WM, Penderis J, Dennis R: Obstruction of contrast medium flow during cervical myelography. Vet Radiol Ultrasound 41:342, 2000. 24. McKee WM, Penderis J, Dennis R: Obstruction of contrast medium flow during cervical myelography. Vet Radiol Ultrasound 41:342, 2000. 25. Matteucci ML, Ramirez O, Thrall DE: Effect of right vs. left lateral recumbency on myelographic appearance of a lateralized extradural mass. Vet Radiol Ultrasound 40:351, 1999. 26. Fucci V: Radiographic diagnosis. Vet Rad 31:260, 1990.

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27. Widmer WR, Thrall DE: Canine and feline intervertebral disc disease, myelography, and spinal cord disease. In Thrall DE, Veterinary diagnostic radiology, ed 4. Philadelphia, WB Saunders, 2002. 28. Olby NJ, Munana KR, et al: The computed tomographic appearance of acute thoracolumbar intervertebral disc herniations in dogs. Vet Radiol Ultrasound 41:396, 2000. 29. Scott HW, McKee WM: Laminectomy for 34 dogs with thoracolumbar intervertebral disc disease and loss of deep pain perception. J Small Anim Pract 40:417, 1999. 30. Penders J, Sullivan M et al: Subdural injection of contrast medium as a complication of myelography. J Small Anim Pract 40:173, 1999. 31. Scrivani PV, Barthez PY, et al: Subdural injection of contrast medium during cervical myelography. Vet Radiol Ultrasound 38:267, 1997. 32. Lamb CR: Letters. Vet Radiol Ultrasound 38:479, 1997. 33. Kirberger RM, Wrigley RH: Myelography in the dog: review of patients with contrast medium in the central canal. Vet Radiol Ultrasound 43:253, 1993. 34. Kirberger RM, Jacobson LS, et al: Hydromyelia in the dog. Vet Radiol Ultrasound 38:30, 1997. 35. Sullivan SA, Coates J, Chambers J: What is your neurologic diagnosis? J Am Vet Med Assoc 207:304, 1995. 36. Kline AM, Steinberg SA, Pond MJ: Epidurograms in the dog: the uses and advantages of the diagnostic procedure. J Am Vet Rad Soc 8:39, 1967.

37. Feeney DA, Wise M: Epidurography in the normal dog: technic and radiographic findings. Vet Rad 22:35, 1981. 38. Douglas JP: Radiographic diagnosis. Vet Rad 23:20, 1982. 39. McNeel SV, Morgan JP: Intraosseous vertebral venography: a technic for examinations of the canine lumbosacral junction. J Am Vet Rad Soc 19:168, 1978. 40. Blevins WE: Transosseous vertebral venography: a diagnostic aid in lumbosacral disease. Vet Rad 21:50, 1980. 41. Koblik PD, Suter PF: Lumbosacral vertebral sinus venography via transjugular catheterization. Vet Rad 22:69, 1981. 42. Wrigley RH, Reuter RE: Canine cervical discography. Vet Rad 25:274, 1984. 43. Wise M, Faulkner R: Unusual disc herniation in a dog. Vet Rad 25:280, 1984. 44. Gaschen L, Lang J, Haeni H: Intravertebral disc herniation (Schmorl’s node) in five dogs. Vet Radiol Ultrasound 36:509, 1995. 45. Hart RC, Schulz KS, Walker MA: What is your diagnosis? J Am Vet Med Assoc 210:487, 1997. 46. Karkkainen M, Punto LU, et al: Magnetic resonance imaging of canine degenerative lumbar spine diseases. Vet Radiol Ultrasound 34:399, 1993. 47. Ross JS, Masaryk TJ, Modic MT: Lumbar spine. In Stark DD, Bradley WG, eds: Magnetic resonance imaging, St Louis, 1999, Mosby.

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Spondylosis, Facetal Arthritis, and Dural Ossification

❚❚❚ BACKGROUND The first detailed radiographic account of spondylosis (deforming spondylosis, spondylosis deformans) was by Morgan in 1967, a monograph that remains to this day the definitive reference on the subject.1 Briefer versions of the same work also appeared in Veterinary Radiology and the Journal of Small Animal Practice.2,3 Among other things, Morgan concluded that most dogs with spondylosis were unlikely to show clinical evidence of spinal or spinal cord disease. In other words, based on probability, spondylosis was most likely to be an incidental finding. Nearly two decades later, Morgan again addressed the subject of spondylosis, again concluding that it was almost always an irrelevant radiographic observation.4 In a more recent publication, Couteur and Grandy reiterated the benignity of spondylosis.5 There is, however, an exception to this generality: the lumbosacral spinal unit. Although the precise cause or causes of lumbosacral spondylosis are currently no more than medical speculation, some animals with this abnormality also have cauda equina compression. More importantly, most dogs with this disorder are neurologically and clinically normal. I am unaware of any published outcome studies relating either the magnitude or the extent of radiographically identified spondylosis to spinal cord disease. Nor am I aware of any published proof that links dorsolaterally developed spondylosis to radiculitis.

Imaging Findings Spondylosis has a highly characteristic appearance and develops predictably in certain portions of the spine, although not all areas of involvement are readily appreciable on radiographs. Spondylosis first becomes apparent as small triangular bone spurs located on the ventral aspect of the vertebral body, just behind one

or both endplates (Figures 25-1 and 25-2). It is quite common to see such bone deposits symmetrically arrayed on either side of the intervertebral disk when viewing the spine laterally. When spondylosis develops further, the small triangular spurs are replaced by much larger claw-like projections that may or may not be symmetric. In advanced cases, a false joint may develop, or transvertebral bridging may occur. When a ventrodorsal projection of the spine is viewed, it becomes apparent that spondylosis often involves more than just the ventral vertebral body. In fact, it is quite common for spondylotic bone to form off the lateral surfaces of the vertebral body adjacent to the endplates.

Diagnostic Strategy If for whatever reason spondylosis is believed to be causing spinal nerve root compression or irritation or is believed to be in some way related to cauda equina compression, then nuclear magnetic imaging is required to assess the suspected spinal unit. Computed tomography (CT) can be effectively used to assess the spinal canal itself, but it is inferior to magnetic resonance imaging (MRI) for evaluating its content. Radiography and myelography are not well suited to these purposes.

❚❚❚ FACETAL ARTHRITIS Facetal arthritis is a curious matter. Although it exhibits the prime radiographic feature of osteoarthritis (the periarticular osteophyte), facetal arthritis is often found in young, nonpainful dogs. Most are large breeds (Figure 25-3). In people, arthritic facet joints have been attributed to facetal instability secondary to the loss of volume that typically accompanies degenerative disk disease. 303

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A

Figure 25-1 • Close-up lateral view of an 8-year-old dog with severe thoracolumbar spondylosis.

B Figure 25-3 • Lateral orientation (A) and close-up (B) views of the lumbar spinal region of a 3-year-old dog with osteoarthritis of its facetal joints.

finding and unlikely to be the consequence or cause of spinal or spinal cord disease.6 Lamb and Guthrie described the identification of displaced, ossified dura in a plain cervical film made of a dog suspected of having a ruptured disk, a phenomenon they termed an automyelogram. The accuracy of the authors’ observation was confirmed in a subsequent myelogram.7

References Figure 25-2 • Close-up lateral view of a 5-year-old dog with severe midlumbar spondylosis.

❚❚❚ DURAL OSSIFICATION In the late 1960s, veterinary radiologists debated the importance of dural ossification, linear densities seen in the ventral aspect of the spinal canal, especially the cervical and lumbar regions. Some contended that it was the aftermath of a previous inflammation or infection (termed pachymeningitis), whereas others argued that it represented benign metaplasia. It was eventually determined that dural ossification was an incidental

1. Morgan JP: Spondylosis deformans in the dog. Acta Orthop Scand Suppl 7:96, 1967. 2. Morgan JP: Spondylosis deformans in the dog: its radiographic appearance. J Am Vet Rad Soc 8:17, 1967. 3. Morgan JP, Ljunggren G, Beadman R: Spondylosis deformans in the dog. J Small Anim Pract 8:57, 1966. 4. Morgan JP, Biery DN: Spondylosis deformans. In Newton CD, Nunamaker DM, eds: Textbook of small animal orthopedics. Philadelphia, 1985, WB Saunders. 5. Couteur RA, Grandy JL: Diseases of the spinal cord. In Ettinger SJ, Feldman EC, eds: Textbook of veterinary medicine. Philadelphia, 2000, WB Saunders. 6. Morgan JP: Spinal dural ossification in the dog: incidence and distribution based on a radiographic study. J Am Vet Rad Soc 10:43, 1969. 7. Lamb CR, Guthrie S: A rare example of an automyelogram. Vet Radiol Ultrasound 36:383, 1995.

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Spinal Infection (Vertebral Osteomyelitis, Vertebral Body Osteomyelitis) ❚❚❚ SPONDYLITIS Background Spondylitis occurs most commonly in young dogs and can affect any part of the spine.1 A single spinal unit or a series of consecutive units can be infected. Occasionally, the disease is widespread, affecting one or more vertebrae in all regions of the spine. Although we often see it listed as a differential diagnosis on consultation forms, it is a rare occurrence in our practice, seen only once or twice a year. Other veterinary colleges, however, particularly those located in warmer climes, see this disease with some regularity.

Imaging Findings In lateral perspective, spondylitis is characterized by bone deposition on the surface of the ventral half of the infected vertebrae and usually is accompanied by radiographically visible soft tissue swelling. In longstanding infections, there may be evidence of bone destruction and occasionally disk collapse. Diseases, old injuries, congenital spinal anomalies, or previous surgery can all resemble spondylitis radiographically. Some specific examples include: • • • • • • •

Diskectomy (disk fenestration) Congenital vertebral malformation Discospondylitis Healed spinal fracture Spinal tumor Spirocerca Spondylosis

Paraspinal Foreign Bodies Stick. Dogs occasionally impale themselves on wooden stakes, portions of which may remain behind

following removal. A draining tract often develops a few weeks later even though the initial wound appears to have healed. Dogs may also have a stick they are carrying or playing with puncture the pharynx and lodge deep in the neck, eventually abscessing. A parapharyngeal abscess in a dog caused by a wooden foreign body has been reported to cause hunched shoulders and rigidity of the head and neck, according to the author closely resembling discogenic pain.2 Plant Awn. Paraspinal foreign bodies, such as foxtails, characteristically produce diffuse back pain. The bacteria-laden plant awn is initially inhaled and then makes its way caudally through the lung and into the pleural space. Using a combination of its distinctive bellows action and the respiratory motion of its “host,” the foxtail then ascends the nearest diaphragmatic crus to its final destination in the sublumbar muscle ventral to the second and third lumbar vertebrae, where it inoculates the surrounding tissue with one or more anaerobic bacteria common to mucous membranes of the throat and lung. Radiographically, a subacute or more likely a chronic infection will reveal new bone on the ventral aspects of the affected portion of the spine (potentially one or more of the first four lumbar vertebrae) with associated muscular swelling. Sonographically, it is sometimes possible to locate a foxtail, especially if it lies in a pool of pus. Nuclear medicine and medical magnetography also can be used detect paraspinal foreign bodies.3 Quills. Porcupine quills occasionally work their way into the paraspinal muscles, causing abscess and referred back pain that closely resembles that caused by nerve root compression. However, most quills, like other foreign bodies, eventually reveal their true nature by forming a draining sinus. 305

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❚❚❚ DISCOSPONDYLITIS Background Discospondylitis (intradiskal osteomyelitis) is a form of spinal infection that is believed to begin in the intervertebral disk and subsequently spreads to the surfaces of the adjacent vertebral endplates. With time, the disk may collapse and occasionally will lead to subluxation and intermittent cord compression. Presumably, discospondylitis infections are blood borne, but why the intervertebral disk is selected for colonization is not known. Staphylococcus aureus is the most commonly isolated organism in dogs. Other less common isolates include Brucella canis and Escherichia coli. Uncommon isolates include Bacteroides capillosus, Streptococcus species, Corynebacterium species, Proteus species, Pasteurella species, Nocardia species, Actinomyces viscosus, Paecilomyces species, Aspergillus species, Mucor species, Mycobacterium species, Blastomyces species, and coccidioidomycosis. As for fungal organisms, it is organizationally useful to consider them in two groups: pathogenic and opportunistic, the latter typically gaining a foothold only when host resistance is compromised (Table 26-1).4 Infections may be postoperative, that is, following disk fenestration, vertebral fusion, or cord decompression. The lumbosacral disk also may be infected in conjunction with the administration of an epidural anesthetic5 or occasionally as a result of myelography (unpublished observations, 1973). Paralumbar foxtails, behaving as infectious vehicles, have been incriminated in discospondylitis. In the absence of potentially infective procedures, such as recent surgery, spinal injection, or wounds, most discospondylitis is presumed to be hematogenous, a hypothesis that is further supported by the presence of multiple, noncontiguous lesions.

Imaging Findings Radiology. Most reports of discospondylitis have been in dogs, although there have been occasional reports of this disease in cats.6-8 As with most radiologically identifiable diseases, discospondylitis is associated with a wide spectrum of bone and disk alterations, most of which are a function of disease duration and, to a lesser extent, virulence. The disease initially attacks the center of the spinal unit, the

Table 26-1 • PATHOGENIC VERSUS OPPORTUNISTIC FUNGI: A BRIEF FUNCTIONAL ORGANIZATION Pathogenic

Opportunistic

Blastomyces dermatitidis Coccidioides immitis Histoplasma capsulatum

Aspergillus fumigatus, A. terreus Paecilomyces species

intervertebral disk, and subsequently moves to the flanking endplates, which are physically connected to the disk. Because the disk is radiographically transparent (dark), the only early indication of disk infection may be a narrowing of the intervertebral space. Later, as the infection begins to gain a foothold in the adjacent vertebrae, a “counterattack” is mounted in the form of a defensive bony perimeter, which initially is centered on the endplates but later extends ventrally to the vertebral body, somewhat resembling spondylosis (Figures 26-1 and 26-2). Shamir and co-workers described the radiographic features of a dozen dogs during their recovery from discospondylitis.9 Not surprisingly, they determined that following antibiotic treatment, the dogs improved within 10 days of being treated, but their bone lesions continued to worsen. The authors considered lysis to be the primary radiographic indication of worsening (progression), whereas bone deposition (sclerosis) and vertebral ankylosis (bridging) were considered signs of improvement (recovery). Myelography. Davis and co-workers carried out a collaborative study and determined that the compressive effects of discospondylitis on the spinal cord are minimal as determined by myelography and epidurography and do not correlate with prognosis. They do, however, recommend stress myelography in cases where vertebral subluxation is seen on plain spinal films.10 Computed Tomography. Computed tomography of a dog with discospondylitis in the thoracolumbar spinal region has shown a combination of severe, irregular bone destruction involving the vertebral endplates and associated bone deposition, primarily on the ventral aspect of the affected spinal unit.11 Magnetic Resonance Imaging. Kraft and co-workers described the magnetic resonance imaging (MRI) appearance of discospondylitis in a dog.12 T1 images showed hypointensity of the lumbosacral spinal unit (to include the intervertebral disk) compared with the adjacent spinal units. Following the administration of contrast, the described areas of decreased signal intensity increased, especially the disk. Gonzalo-Orden and co-workers reported the MRI features of discospondylitis in a dog.13 T1 images showed decreased signal intensity in the infected intervertebral disk, flanking endplates, and underlying soft tissue. T2 images revealed increased signal intensity emanating from the same vertebral unit. The authors noted that these were the same MRI abnormalities seen in people with discospondylitis.

❚❚❚ VERTEBRAL PHYSITIS Background Physitis is a somewhat archaic and nonspecific term, originally used to describe growth plate infection in

CHAPTER 26 ❚❚❚ Spinal Infection (Vertebral Osteomyelitis, Vertebral Body Osteomyelitis)

A

B Figure 26-1 • Discospondylitis: Close-up lateral (A) and ventrodorsal (B) views of the lumbosacral spinal unit in a puppy show destruction of much of the lumbosacral disk; surrounding vertebrae are swollen with new bone deposition.

307

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B

A Figure 26-2 • Discospondylitis: Close-up lateral (A) and ventrodorsal (B) views of the lumbosacral spinal unit in an adult dog infected as a result of multiple attempts at epidural injection weeks earlier.

humans and physeal inflammation in horses. Like many medical terms, it has made its way in and out of the veterinary literature. Jimenez and O’Callaghan used the term physitis to describe what they termed a unique spinal lesion that resembles discospondylitis, but, unlike typical disk infections, the disease affects the caudal vertebral growth plate (physis) in skeletally immature dogs and the caudal vertebral metaphysis in mature animals. Because of this difference, the authors propose the name vertebral physitis. Furthermore, they assert that vertebral physitis is caused by fibrocartilaginous emboli, not by bacterial infection.14 Later, Siems and Jacovljevly used the same expression to describe the radiographic appearance of a destructive lesion in a vertebral growth plate of a dog, believed to have been caused by a Staphylococcus bacteremia.15

Imaging Findings Initially, vertebral physitis is characterized by caudal metaphyseal lysis, which in the case of skeletally immature dogs often is accompanied by physeal widening or ectasia. Later, the affected bone may fracture, resulting in shortening, fragmentation, and in severe cases dislocation of the spinal unit. Spondylotic-like new bone typically is initiated by the damaged vertebra, which in time will underrun the nearby disk and contiguous vertebral body, frequently leading to kyphosis.

❚❚❚ DEEP PARASPINAL ABSCESS Probably the most common paraspinal abscess seen in dogs is caused by nonabsorbable sutures left over from a spay, most of which drain from the flank. Before they are drained, these abscesses often cause nonspecific regional pain that can mimic a disk lesion. As previously mentioned, plant awns, quills, sticks, and

Figure 26-3 • Close-up lateral cervical sinogram shows a pair of soft tissue cavities, one above the other, joined by a thin vertically oriented channel, the result of a cervical abscess.

wooden splinters are all capable of causing such lesions (Figure 26-3).

References 1. LaCroix JA: Vertebral body osteomyelitis. J Am Vet Rad Soc 14:17, 1973. 2. Pratt JNJ, Munro EAC, Kirby BM: Osteomyelitis of the atlanto-occipital region as a sequela to a pharyngeal stick. J Small Anim Pract 40:446, 1999. 3. Frendin J, Funkquist B, et al: Diagnostic imaging of foreign body reactions in dogs with diffuse back pain. J Small Anim Pract 40:278, 1999.

CHAPTER 26 ❚❚❚ Spinal Infection (Vertebral Osteomyelitis, Vertebral Body Osteomyelitis)

4. Watt PR, Robbins GM, et al: Desseminated opportunistic fungal disease in dogs: 10 cases (1982-1990). J Am Vet Med Assoc 207:67, 1995. 5. Remedios A, Wagner R, et al: Epidural abscess and discospondylitis in a dog after administration of a lumbosacral epidural analgesic. Can Vet J 37:106, 1996. 6. Kornegay JN, Barber DL: Discospondylitis in dogs. J Am Vet Med Assoc 177:337, 1980. 7. Gilmore DG: Lumbosacral discospondylitis in 21 dogs. J Am Anim Hosp Assoc 23:57, 1987. 8. Watson E, Roberts RE: Discospondylitis in a cat. Vet Radiol Ultrasound 34:397, 1993. 9. Shamir MH, et al: Radiographic findings during recovery from discospondylitis. Vet Radiol Ultrasound 42:496, 2001. 10. Davis MJ, Dewey CW, et al: Contrast radiographic findings in canine bacterial discospondylitis: a multicenter, retrospective study of 27 cases. J Am Anim Hosp Assoc 36:81, 2000.

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11. Gonzalo-Orden JM, Altonaga JR, et al: Magnetic resonance, computed tomographic and radiologic findings in a dog with discospondylitis. Vet Radiol Ultrasound 41:142, 2000. 12. Kraft SL, Mussman JM, et al: Magnetic resonance imaging of presumptive lumbosacral discospondylitis in a dog. Vet Radiol Ultrasound 39:9, 1998. 13. Gonzalo-Orden JM, Altonaga JR, et al: Magnetic resonance, computed tomographic and radiologic findings in a dog with discospondylitis. Vet Radiol Ultrasound 41:142, 2000. 14. Jimenez MM, O’Callaghan MW: Vertebral physitis: a radiographic diagnosis to be separated from discospondylitis. Vet Radiol Ultrasound 36:188, 1995. 15. Siems JS, Jakovljeviy S: Discospondylitis in association with an intra-abdominal abscess in a dog. J Small Anim Pract 40:123, 1999.

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Spinal Tumors (Vertebral Tumors) and Tumorlike Lesions ❚❚❚ SPINAL TUMORS Background Spinal tumors can develop in a variety of locations, including (1) the spine, (2) spinal canal, (3) dural sac, and (4) spinal cord. Tumors also can originate outside the spine, termed paraspinal tumors, and then grow into the spinal canal and compress the cord. Generally, most spinal and paraspinal tumors, like bulging and ruptured disks, exert compression on the spinal cord, which typically produces progressive pain and disability. Spinal tumors may be primary, such as osteosarcoma, or secondary, such as thyroid carcinoma.1 In cats, lymphoma is the most common tumor of the spinal canal, followed by meningioma. Other reported tumor types include malignant nerve sheath tumor, meningeal sarcoma, chondrosarcoma, lipoma, and osteosarcoma. In general, cats with nonlymphoid tumors of the spinal canal have a better prognosis than do those with lymphoma.2 As he did earlier with lung patterns, Suter (and co-workers) brought the myelographic diagnosis of canine spinal tumors to the attention of veterinary radiologists. As with much of his previous work, Suter’s description of spinal tumors was marked by its highly organized and descriptive nature, and to this day it stands as one of the definitive articles on the subject.3 The following generalities are taken from this work: • Most spinal tumors (primary or secondary) are destructive (osteolytic). • Primary and metastatic spinal tumors occur with about the same frequency. • The thoracic and lumbar spinal regions are preferred sites for both primary and secondary tumors. • Unlike primary and secondary long-bone tumors, which do not normally cross joint spaces, spinal tumors often extend into adjacent vertebrae. 310

• Vertebral destruction (as determined radiographically) do not always correlate with the degree of neurologic disability demonstrated by the animal. Nearly a decade later, Morgan and co-workers repeated Suter’s work and reached similar conclusions.4

Imaging Findings Radiology. Regrettably, from the standpoint of radiographic diagnosis, most spinal tumors lack a characteristic appearance, although some do exhibit tendencies. A spinal osteosarcoma, for example, may appear productive, destructive, or reductive, or it may exhibit any combination of these appearances. Thus, spinal osteosarcomas lack any consistent appearance, although, as already mentioned, most are destructive. Spinal lymphosarcomas, on the other hand, often appear lytic as a result of bone destruction following lymphoblastic invasion. Severely destructive, structurally weakening spinal tumors are subject to fracture (pathologic fracture).5 Myelography. Although it is impossible to determine the cell type of a spinal tumor radiographically, by using myelography, most such lesions can be localized to the spine, spinal canal, or spinal cord (Table 27-1). The considerable variability of spinal and spinal cord tumors is exemplified in Figures 27-1 to 27-5. Computed Tomography. Compared with plain films and myelography, computed tomography (CT) is superior for visualizing spinal morphology. CT’s thin slice thickness eliminates much of the visual confusion created by the extensive anatomic overlap, which characterizes the spinal columns of dogs and cats. Subtle pathologies, such as small areas of bone deposition or bone destruction, become far more evident with CT than with plain films. Finally, the crosssectional nature of CT (as well as that of magnetic Text continued on p. 315

CHAPTER 27 ❚❚❚ Spinal Tumors (Vertebral Tumors) and Tumorlike Lesions

311

Table 27-1 • MYELOGRAPHIC LOCALIZATION OF SPINAL TUMORS Tumor Origin

RDIs (Plain Film)

RDIs (Myelographic)

Examples of Specific Tumors

Within one or more vertebrae as evidenced by bone destruction

Bone destruction Merits of myelography debatable Loss or partial loss of dorsal Blood-cord barrier may be inoperable, spinous process, or articular causing contrast to be potentially facet more toxic to the spinal cord Diminished vertebral dimensions Displacement of the dural sac and (possibly due to collapse of cord vertebral body) Narrowing or disappearance of one Obvious pathologic fracture or both sides of the opacified dural sac in the area of the lesion Relative and absolute widening of the opacified dural sac proximal to the lesion (contrast backup)

Primary bone tumors: osteosarcoma, osteochondroma, and fibrosarcoma Secondary bone tumors: metastatic carcinomas

Inside or mostly inside the spinal canal, but outside the dural sac (extradural)

No visible abnormality

Circumferential cord constriction

Osteosarcoma Lymphosarcoma Fibrosarcoma Plasmacytoma Ganglioblastoma

Inside the dural sac, but outside the spinal cord (intradural-extramedullary)

Usually no visible abnormality

Oval or spherical filling defects in the opacified dural sac

Malignant nerve sheath tumor

Inside the spinal cord (intramedullary)

Usually no visible abnormality

Localized cord enlargement, usually featuring tapered ends

Hemangiosarcoma

Modified from Northington JW: Metrizamide myelography in five dogs and two cats with suspected spinal cord neoplasms. Vet Rad 21:149, 1980. RDI, Radiographic diagnostic indicator.

A

B

C Figure 27-1 • A and B, Cord tumor: Close-up plain and myelographic lateral views of thoracolumbar spinal region show little or no appreciable difference in the appearance of T13 (arrowhead) compared with surrounding vertebrae. C, A ventrodorsal myelogram, however, reveals subtle but definite left-sided cord compression as evidenced by unilateral thinning and bowing of the opacified dural sac.

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A

B

C

Figure 27-2 • Lateral (A) compression ventrodorsal (B) and close-up ventrodorsal (C) views of a spinal tumor that has partially destroyed the arch and pedicle of T12.

D

E

F

G

Figure 27-2 • cont’d Myelography, including lateral (D), lateral close-up (E), ventrodorsal (F), and ventrodorsal close-up (G) views, shows that the tumor is compressing the cord laterally. The contrast injection was deliberately made at L2-3 by a nonradiologist, unable to perform a conventional lumbar puncture. Injection at this site is dangerous and should be avoided.

A

C

B Figure 27-3 • Spinal tumor: A, Close-up lateral view of the midthoracic spinal region shows what at first appears to be a hemivertebra. Unlike usual hemivertebrae, the caudal endplate appears normal in all respects, whereas much of the rest of the vertebral body is barely visible. The dorsal elements, however, appear normal. B, A close-up ventrodorsal view lacks contrast and detail, and thus is of little help. C, A close-up ventrodorsal oblique view clearly shows that the affected vertebra has collapsed, indicative of a pathologic fracture, in this instance due to a primary osteosarcoma.

CHAPTER 27 ❚❚❚ Spinal Tumors (Vertebral Tumors) and Tumorlike Lesions

315

Figure 27-4 • Close-up lateral view of the midlumbar spine in a cat shows new bone deposition over much of the bodies of L4-6, the result of a metastatic carcinoma.

Figure 27-5 • Cord tumor: Close-up lateral cervical myelogram shows localized cord swelling at the level of C-7 (emphasis zone), with uniform compression of the opacified dura sac and contrast backup cranially.

resonance imaging [MRI]) allows precise assessment of the spinal canal, which is not possible with radiography.6 As in the case of radiography, CT lacks the capability of distinguishing primary from secondary (metastatic) spinal tumors.7 Comparison of Imaging Methods for Identifying the Precise Location of Spinal Tumors. Drost and coworkers compared the relative abilities of radiography, myelography, and CT to identify the location of spinal cord tumors.8 With respect to vertebral tumors, in particular the identification of related bone loss or addition, CT proved best. On the other hand, myelography proved superior in establishing the location of spinal cord tumors: intradural/extramedullary or intramedullary. Magnetic Resonance Imaging. Kippenes and coworkers described the appearance of a small to medium-sized group of spinal tumors in dogs; the results are shown in Table 27-2.9

❚❚❚ SPECIFIC TUMOR TYPES Multiple Myeloma (Plasma Cell Tumor) Spinal multiple myeloma (plasmacytoma, plasma cell myeloma) has been described in both dogs and cats as

well as in other animal species and probably is best remembered radiographically for its so-called bullethole lesions.10 In my experience, such “bullet-hole” lesions are extremely rare, so much so that most veterinarians (including radiologists) have never seen one. The few plasma cell spinal tumors I have seen for the most part have been destructive, consistent with most published reports.11 Whatever their shape and location, however, not all plasma cell myelomas are lytic, as evidenced by a report that described multiple rib lesions resembling healed fractures (as well as a destructive dorsal spinous process lesion that looked like a bone tumor).12

Neurilemoma (Neurinoma, Schwannoma) Neurilemoma is a benign nerve sheath tumor that exhibits a strong preference for the cranial nerve roots, especially the fifth and the brachial plexus. Plain films are typically unrevealing, with diagnosis usually made myelographically (Figure 27-6) or with MRI.13

Hemangiosarcoma Spinal hemangiosarcomas may be either primary or secondary, with primaries accounting for about 5% of all skeletal tumors seen in dogs. Heman-

316

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A

B Figure 27-6 • A, Close-up lateral cervical myelogram shows a discrete, medium-sized filling defect above C6, caused by a nerve root tumor. B, A close-up ventrodorsal view shows characteristic cupping of the left lateral contrast band as it surrounds the mass (emphasis zone).

Table 27-2 • MAGNETIC RESONANCE IMAGING CHARACTERISTICS OF 21 CANINE SPINAL TUMORS

Tumor Location (No.)

Tumor Type (No.)

Extradural (11)

Fibrosarcoma (3)

Ganglioblastoma (1)

Lymphosarcoma (2) Osteosarcoma (3) Plasmacytoma (2)

Intradural/ extramedullary (9)

Malignant nerve sheath tumor (6) Meningioma (3)

Intramedullary

Hemangiosarcoma (1)

Tumor MR Signal Relative to the Spinal Cord (No.) T1 isointense T2 mixed hyperintense and isointense T1 mixed hypointense and isointense T2 slightly hyperintense T1 hyperintense T2 isointense T1 isointense T2 isointense T1 hyperintense; infiltrated bone marrow hypointense T2 isointense (1), hyperintense (2) T1 isointense T2 hyperintense T1 isointense T2 hypointense T1 isointense T2 hyperintense

Contrast Enhancement (No.) Moderate, heterogeneous

Marked, homogeneous

Moderate homogeneous Mild (1), moderate (1), heterogeneous Moderate, heterogeneous (1), mild, homogenous (1)

Moderate to marked, homogeneous Mild (1), marked (2), homogeneous Mild heterogeneous

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Figure 27-7 • Close-up lateral cervical myelogram shows a pronounced displacement of the spinal cord above C4, caused by an extradural soft tissue tumor.

giosarcomas can develop in any part of the spine but occur most frequently in the thoracic region. Typical of spinal tumors, hemangiosarcomas often are heralded by back pain and neurologic deficiency. Most hemangiosarcomas grow slowly but, because they gradually weaken the bone, can lead to pathologic fracture and acute paralysis, resembling a ruptured disk. Because of rapid hematogenous spread, spinal hemangiosarcomas carry a poor prognosis. Metastasis typically targets the liver and lung, often resulting in the death of the animal within 4 months of discovery of the disease. Radiographically, hemangiosarcomas tend to be destructive, causing the affected vertebrae to appear abnormally dark. In one report, a primary spinal hemangiosarcoma was described as having irregular ventral margins (as seen in lateral projection), an observation I have been unable to confirm14 (Figure 27-7). Following a pathologic compression fracture, a cancerous vertebra may resemble a hemivertebra.

Chondrosarcoma Chondrosarcoma is the second most common canine skeletal tumor, constituting about 10% of all bone tumors. Of these, about 10% affect the spine, frequently in large breeds. Chondrosarcomas grow slowly and only occasionally metastasize. They show a preference for the nasal turbinates and flat bones, such as the ribs, pelvis, scapula, maxilla, and mandible, although they can occur in long bones as well. Radiographically, chondrosarcomas are characterized by bone destruction and, like osteosarcomas, are capable of producing large amounts of tumor bone. Some of these tumors are quite expansive.15

Rhabdomyosarcoma Spinal rhabdomyosarcomas are quite rare. Moon and co-workers reported such a tumor in the thoracic spinal region of a 5-year-old cat. The tumor, which caused spinal cord compression, was characterized as sclerotic, reflecting vertebral necrosis and subsequent myelofibrosis and new bone deposition.16

Parosteal Osteosarcoma Thomas and co-workers described a parosteal osteosarcoma of the midcervical region of a dog, which appeared as a relatively benign new bone deposit on the ventral aspect of the body of C4 in plain films but in a subsequent myelogram showed severe compression of the overlying spinal cord.17

Meningioma Asperio and co-workers reported a meningioma in the caudal cervical region of a cat, diagnosed with MRI.18 The tumor was invisible in T1 and barely perceptible in T2; however, once enhanced with contrast, the lesion became clearly identifiable in T1.

Osteochondroma Osteochondromas are benign bone tumors that affect the limb bones, ribs, and spine, typically completing their growth before skeletal maturity. When only one such growth is present, which is rare, it is termed an osteochondroma or solitary osteochondroma; however, when multiple osteochondromas are present (a far more common hereditary condition), the disease then is called multiple cartilaginous exostoses. Occasionally, these lesions change composition, becoming osteochondromas, a process referred to as malignant transformation. When osteochondromas become cancerous, it is not always apparent radiographically.19 Although most spinal osteochondromas are of no clinical consequence, spinal cord compression has been reported.20 Radiographically, spinal and rib osteochondromas often have a distinctive billowy appearance, possessing a discrete, often undulant border and a smudged interior.

References 1. Bentley JF, Simpson ST, et al: Metastatic thyroid solidfollicular carcinoma in the cervical portion of the spine of a dog. J Am Vet Med Assoc 197:1498, 1990. 2. Levy MS, Mauldin G, et al: Nonlymphoid vertebral canal tumors in cats: 11 cases (1987-1995). J Am Vet Med Assoc 210:663, 1997.

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3. Suter PF, Morgan JP, et al: Myelography in the dog: diagnosis of tumors of the spinal cord and vertebrae. J Am Vet Rad Soc 12:29, 1971. 4. Morgan JP, Ackerman N, et al: Vertebral tumors in the dog: a clinical, radiologic, and pathologic study of 61 primary and secondary lesions. Vet Rad 21:197, 1980. 5. Suess RP, Martin RA, et al: Vertebral lymphosarcoma in a cat. J Am Vet Med Assoc 197:101, 1990. 6. Drost WT, Love N: Comparison of myelography and computed tomography for the evaluation of canine vertebral and spinal cord tumors. Vet Radiol Ultrasound 35:237, 1994. 7. Tassani-Prell M, Kessler M, Matis U: Vertebral tumors in dogs and cats: radiographic and computer tomographic evaluation of 12 cases. Vet Radiol Ultrasound 36:429, 1995. 8. Drost WT, Love NE, Berry CR: Comparison of radiography, myelography and computed tomography for the evaluation of canine vertebral and spinal cord tumors in sixteen dogs. Vet Radiol Ultrasound 37:28l. 1996. 9. Kippenes H, Gavin PR, et al: Magnetic resonance imaging features of tumors of the spine and spinal cord in dogs. Vet Radiol Ultrasound 40:627, 1999. 10. Bartels JE, Cawley AJ, et al: Multiple myeloma (plasmacytoma) in a dog. J Am Vet Rad Soc 13:36, 1972. 11. Berry CR: Answers for film reading session: 1995 A.C.V.R. annual meeting. Vet Radiol Ultrasound 36:449, 1995.

12. Jergens AE, Miles KG, Moore FM: Atypical lytic and proliferative skeletal lesions associated with plasma cell myeloma in a dog. Vet Rad 31:262, 1990. 13. Jans HE: Radiographic diagnosis. Vet Rad 28:174, 1987. 14. Parchman MB, Cramer FM: Primary vertebral hemangiosarcoma in a dog. J Am Vet Med Assoc 194:79, 1989. 15. Hamerslag KL, Evans SM, Dubielzig R: Coccygeal vertebral chondrosarcoma in a Saint Bernard dog: a case report. Vet Rad 21:194, 1980. 16. Moon ML, Saunders GK, Martin RA: Vertebral osteosclerosis in a cat secondary to rhabdomyosarcoma. Vet Rad 31:39, 1990. 17. Thomas WB, Daniel GB, McGavin MD: Parosteal osteosarcoma of the cervical vertebra in a dog. Vet Radiol Ultrasound 38:120, 1997. 18. Asperio RM, Marzola P, et al: Use of magnetic resonance imaging for diagnosis of a spinal tumor in a cat. Vet Radiol Ultrasound 40:267, 1999. 19. Green EM, Adams WM, Steinberg H: Malignant transformation of solitary spinal osteochondroma in two mature dogs. Vet Radiol Ultrasound 40:634, 1999. 20. Prata R, Stoll S, Zaki F: Spinal cord compression caused by osteocartilaginous exostoses of the spine in two dogs. J Am Vet Med Assoc 12:507, 1975.

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Miscellaneous Spinal Disease and Diagnostic Procedures ❚❚❚ HYPERVITAMINOSIS A I have included hypervitaminosis A in the section on tumors and tumorlike lesions of the cervical spinal region because of its resemblance to some of these diseases.1 Initially reported as a deforming cervical spondylosis, hypervitaminosis A eventually was recognized for what it is: a vitamin toxicity brought on by an overconsumption of raw liver or vitamin A supplement.2,3 Subsequent investigation showed the disease to be more extensive than first realized, affecting the limbs as well as the spine.4 In most cases, the structural abnormalities found in the skeleton of affected animals are months or years in the making. In the advanced stage of the disease, fusion of the vertebrae and the humeral and cubital joints often results in bizarre postures and gaits. Sternal and costal bone deposits superimposed on the lung in thoracic radiographs often create the erroneous impression of severe disease.

❚❚❚ MUCOPOLYSACCHARIDOSIS Mucopolysaccharidosis is a type of storage disease in which, because of an enzymatic deficiency, glycosaminoglycan fails to undergo normal degradation and instead is stored in various body tissues, including bone. The effects are particularly striking in the spine, where demineralization and epiphyseal deformities are pronounced. Additionally, there may be partial dislocation of the hips, underdevelopment of the hyoid bones and dens, and absence or hypoplasia of the frontal and sphenoid sinuses.5

❚❚❚ SPINAL CORD MALACIA In my experience, regional necrosis of the spinal cord (myelomalacia) usually is initiated by a ruptured disk and ultimately proves fatal. Myelomalacia also may

be caused by myelography, especially in the case of acute spinal fractures and traumatic disk ruptures. Sanders and co-workers described the magnetic resonance features of an unexplained focal myelomalacia in a cat. The lesion appeared hyperintense on T2, involving much of the cross-sectional area of the cord. The underlying disk was incriminated based on a combination of narrowing and hypointensity.6

❚❚❚ COLOR AND SPECTRAL DOPPLER OF SPINAL CORD VASCULATURE Hudson and co-workers described the use of Doppler ultrasound in the surgically accessed normal canine spinal cord.7 The described method proved capable of evaluating blood-flow velocity in small intraparenchymal spinal arteries. Although considerable variation was encountered in the course of obtaining data, the measurement techniques proved repeatable. Doppler traces showed high end-diastolic blood flow velocities, indicating low flow resistance.

❚❚❚ COMPUTED TOMOGRAPHIC SPINAL SURVEYS Kneissl and Schedlbauer described a simple method of doing spinal surveys using computed tomography (CT) in cats and small dogs.8 After being anesthetized, the animal is placed on a pillow, sternum downward. This maneuver will decrease the relative length of the animal, making it easier to fit into the bore of the gantry. The pillow and cat then are positioned at right angles to the long axis of the table, the laser positioning light is used to confirm spinal alignment, and the animal is advanced into the scanner. According to the authors, with the cat in this position, the entire thoracic and lumbar spinal regions can be seen in five to six 2mm–thick slices. 319

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References 1. Goldman AL: Hypervitaminosis A in a cat. J Am Vet Med Assoc 200:1970, 1992. 2. Seawright AA, English PB: Deforming cervical spondylosis in the cat. J Pathol Bacteriol 88:503, 1964. 3. Seawright AA, English PB, Gartner RJW: Hypervitaminosis A and deforming cervical spondylosis of the cat. J Comp Pathol 77:29, 1967. 4. Riser WH, Brodey RS, Shirer JF: Osteodystrophy in mature cats: a nutritional disease. J Am Vet Rad Soc 9:37, 1968.

5. Konde LJ, Thrall MA, et al: Radiographically visualized skeletal changes associated with mucopolysaccharidosis VI in cats. Vet Rad 28:223, 1987. 6. Sanders S, Bagley RS, et al: Focal spinal cord malacia in a cat. Vet Radiol Ultrasound 40:122, 1999. 7. Hudson JA, Finn-Bodner S, et al: Color Doppler imaging and Doppler spectral analysis in the spinal cord of normal dogs. Vet Radiol Ultrasound 36:542, 1995. 8. Kneissl S, Schedlbauer B: Sagittal computed tomography of the feline spine. Vet Radiol Ultrasound 38:282, 1997.

S E C T I O N

I V

The Hips and Pelvis

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Radiographic Disease Indicators: Pelvis and Hips ❚❚❚ PELVIC FRACTURES AND HIP DYSPLASIA Injury and hip dysplasia are the most common reasons for radiographing the pelvis and hips of dogs, whereas trauma is the prime motive for such examinations in cats. In the case of suspected injury, the pelvis and hips are analyzed for the following radiographic disease indicators (RDIs): • Asymmetry • Distortion • Discontinuity These RDIs can be recalled readily using the mnemonics “ADD” or “ADDing up the evidence (in support of pelvic fracture).” Pelvic fractures usually occur in groups of three or more, often in specific combinations. Thus, if one such frac-

ture is identified in a pelvic radiograph, the probability is high that others also exist. Multiple fractures of this sort are responsible for pelvic asymmetry, distortion, and discontinuity. With respect to the demonstration of pelvic bone discontinuity, standard radiographic projections may need to be supplemented with oblique views. The RDIs of hip dysplasia are as follows: • Dislocation • Deformity The paramount RDI of hip dysplasia is femoral dislocation. I prefer the term dislocation to the terms subluxation or luxation because it is more familiar to most people and thus requires little further explanation. Deformity of the coxal joint may be primary, related to abnormal growth and development, or it may be secondary to the formation of osteoarthritis.

321

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3 0

Pelvic Fractures

❚❚❚ FRACTURE PATTERNS AND THE CONCEPT OF THE WEIGHT-BEARING RING In analyzing the pelvis for fractures, the key radiographic feature is the appearance of the weightbearing ring formed by the sacrum, the right and left ileum, and the pubis. Substantial injury to two of these bones, plus the ischium, typically causes the ring to appear asymmetrical or distorted. The most common pelvic fracture pattern is (1) a sacral fracture-dislocation, (2) a pubic fracture, and (3) an ischial or ischial symphysis fracture. This combination of injuries will cause one half of the pelvis to shear away from the other, resulting in an asymmetric appearance. Rather than trying to memorize various fracture patterns, it is better to think strategically. For example, how is it possible for a particular part of the pelvis to be broken free from the rest? The tactical objective then becomes clear: find the two or three individual fractures or sacral or symphyseal separation. Caution: Inadvertently placing the pelvis in an oblique position during radiography produces varying degrees of geometric distortion that can mistakenly be attributed to fractures. Caution: Pelvic obliquity typically “opens” one sacroiliac joint while “closing” the other. Thus, comparison shows a difference that may mistakenly be diagnosed as a fracture-dislocation.

❚❚❚ ADVERSE OUTCOMES OF PELVIC FRACTURES Most pelvic fractures eventually heal and are undetectable other than by radiographic means. Uncorrected 322

dislocations and fractures of the hip usually lead to osteoarthritis and lameness. Femoral head and neck fractures treated by surgical removal have variable outcomes that range from complete recovery to crippling lameness (Figure 30-1). Narrowing of the pelvic canal secondary to one or more malunions can lead to intermittent or chronic constipation as well as dystocia in pregnant females (Figure 30-2). Acetabular relocation (triple pelvic osteotomy) has a spotty history and in my experience often creates more problems than it solves.

❚❚❚ ASSOCIATED INJURIES As with most fractures, especially those that are displaced, the surrounding muscles are bruised, punctured, or torn. Both intramuscular and extramuscular hematomas typically develop, causing varying degrees of vascular compression. Muscle power predictably is reduced or lost, but it usually is regained within a few weeks. Limb edema is initially marked but gradually subsides, especially with hydrotherapy. Spontaneous contractions are the rule during the first week or two postinjury and can be extremely painful. Disuse muscular atrophy and tendon tightening reduce joint motion, cause transient limb shortening, and typically produce a pronounced limp. Pelvic fractures often are associated with bruising of the urinary bladder causing bloody urine. It must be kept in mind, however, that caudal thoracic and cranial abdominal injuries may result in bruising of the kidneys, which also can produce blood in the urine. Urinary bladder rupture is less common but far more serious because it leads to chemical peritonitis. Occasionally, the uterus of a pregnant dog or cat ruptures, ejecting one or more fetuses into the peritoneal cavity. In some animals, severe compression fractures of the pelvis momentarily displace the rectum with such

CHAPTER 30 ❚❚❚ Pelvic Fractures

323

A

B

C Figure 30-1 • A, Close-up, flexed ventrodorsal view of the hips of a puppy with a fracture-dislocation of the right coxal joint and multiple fractures of the associated femoral body. B, Full-length, ventrodorsal view of the pelvis and hips immediately following surgery show that the proximal femur has been removed and the femoral shaft fracture plated. C, A follow-up film made when the dog was about a year old shows predictable atrophy and reduced density of the proximal part of the femoral remnant and filling in of the acetabulum. Note how the bone plate has moved proximally as the dog has grown.

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SECTION IV ❚❚❚ The Hips and Pelvis

A

C

B

D Figure 30-2 • Lateral (A) and ventrodorsal (B) views of the pelvis and hips of a chronically constipated dog believed to have a rectal tumor (based on palpation). Lateral (C) and ventrodorsal (D) barium marking studies show that the rectal narrowing is being caused by a nonunion fracture.

force that the caudal colon may be torn, leading to peritonitis. Pneumoperitoneum, abdominal fluid, or both may indicate a colonic or rectal tear, causing air and bacterial leakage. The absence of such radiographic findings, however, does not exclude this possibility.1

Reference 1. Cook JL, Philben JC: What is your diagnosis? J Am Vet Med Assoc 207:1033, 1995.

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3 1

Pelvic Infection, Tumor, and Miscellaneous Diseases Septic arthritis and osteomyelitis of the hip joint of a dog have been described. The case was unusual inasmuch as the dog had no history of previous infection or surgery. Following biopsy identification of a Staphylococcus intermedius infection, the femoral head and neck were removed, and the dog was treated successfully with antibiotics.1 Figure 31-1 shows how an unchecked septic arthritis can gradually destroy the hip.

only one hip at a time, it is often possible to detect subtle abnormalities by comparing the affected hip with the nonaffected hip.

❚❚❚ CAUTION: POTENTIAL MISDIAGNOSIS

• Increased width of the cartilage space • Multiple small, spherical areas of lucency in the femoral head • Irregular margination of the femoral head • Shrinkage of femoral head • Small nondisplaced or minimally displaced fractures in femoral head • Overt fragmentation of femoral head • Consolidation of fragmented femoral head • Reduction in angle of femoral neck (angle of inclination), eventually approaching 90 degrees • Shape of femoral head changes from spherical to square or tapered • Acetabulum becomes overtly arthritic • Bony cuff forms around femoral neck • Perimeter of acetabulum is gradually extended outward as a result of periarticular bone deposition • Further dislocation

Hornof and co-workers have cautioned that air, contained within an anal sac and superimposed on the medial aspect of either ischium, can mimic localized bone destruction.2 Such a finding would warrant consideration of disease with destructive potential, such as infection, tumor, bone cyst, and recent cancellous bone harvest site.

❚❚❚ AVASCULAR NECROSIS OF THE FEMORAL HEAD: LEGG–CALVÉ–PERTHES DISEASE Avascular necrosis (AVN) is a disease of young female small-breed dogs that can affect one or both femoral heads. AVN is unique in that it causes collapse of the femoral head, which then heals spontaneously but not before it becomes badly deformed. The deformed femoral head no longer matches the acetabulum, which eventually leads to osteoarthritis of the coxal joint. Radiographically, the degeneration of the femoral head, and subsequently the acetabulum, is marked by a highly predictable course, which is outlined subsequently here. Because the disease typically involves 325

❚❚❚ RADIOGRAPHIC DISEASE INDICATORS OF AVASCULAR NECROSIS (IN ORDER OF APPEARANCE)

The preceding abnormalities are exemplified in Figures 31-2 to 31-5.

❚❚❚ CONGENITAL EPIPHYSEAL DYSPLASIA Congenital epiphyseal dysplasia can cause joint pain in immature dogs, including the hips, which typically

326

SECTION IV ❚❚❚ The Hips and Pelvis

A

A

B

B Figure 31-2 • A, Close-up ventrodorsal view of the right hip of

C Figure 31-1 • Close-up ventrodorsal views (A–C) of the pelvis of an immature dog with a progressive infection of the right hip (viewer’s left) show (1) gradual widening of the coxal joint, eventually leading to dislocation; (2) loss of acetabular bone density; and (3) disintegration of the femoral head.

a dog affected by Legg-Calvé-Perthes disease shows (1) a widened cartilage space, (2) an irregularly contoured femoral head, (3) minimally displaced fractures, and (4) partial dislocation. B, The opposite normal hip is included for comparison.

CHAPTER 31 ❚❚❚ Pelvic Infection, Tumor, and Miscellaneous Diseases

327

Figure 31-3 • Close-up view of the right hip of a dog with Legg-Calvé-Perthes disease (emphasis zone) shows early signs of the disease: (1) a widened cartilage space and (2) a pock-marked femoral head.

Figure 31-4 • Close-up view of the left hip of a dog with Legg-Calvé-Perthes disease shows abnormalities found in the intermediate stages of the disease: (1) a widened cartilage space, (2) a deformed femoral head, (3) a decreased angle of inclination, and (4) multiple femoral head fractures.

Figure 31-5 • Close-up view of the hips of a dog with bilateral Legg-Calvé-Perthes disease. The badly deformed left hip (reader’s right), the first to become diseased, is currently in the healing stage but, because of its incongruity with the acetabulum, will soon lead to osteoarthritis. The opposite right hip, which later became affected, is still in the disintegration stage.

328

SECTION IV ❚❚❚ The Hips and Pelvis

A

C

B Figure 31-6 • Full-length ventrodorsal views of the coxal and genual joints of a Beagle with congenital epiphyseal dysplasia at 1 (A), 6 (B), and 12 (C) months of age.

disappears once the animal has finished growing (Figure 31-6). At 1 month of age, affected puppies show a femoral head that appears fragmented, loosely resembling aseptic necrosis or a comminuted fracture. Unlike these diseases, however, epiphyseal dysplasia affects all the long bones, not just the hips. As the puppy grows, the segmented femoral heads consolidate, eventually appearing solid. Although deformed, the hips (and other affected joints) do not become arthritic.

References 1. Levitt L, Fowler JD: Septic coxofemoral arthritis and osteomyelitis in a dog. Vet Radiol 29:129, 1988. 2. Davidson A, Hornof W, et al: What is your diagnosis? J Am Vet Med Assoc 203:1129, 1993.

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3 2

Fractures and Dislocation of the Hip Joint (Coxal Joint, Coxofemoral Joint) ❚❚❚ ACETABULAR FRACTURES Most acetabular fractures occur in the middle or caudal thirds of the joint and usually are only minimally displaced because of the collateral support afforded by the pubis. Therefore oblique projections often are required to demonstrate displacement clearly (Figures 32-1 to 32-3). Caution: Be careful not to mistake the acetabular growth plate of a skeletally immature dog for an acetabular fracture.

❚❚❚ PROXIMAL FEMORAL FRACTURES Classification of Femoral Fractures Fractures of the femur can be classified in a variety of ways, some simple, others complex. A classification of intermediate complexity, largely derived from human orthopedics, appears in the Textbook of Small Animal Orthopedics, edited by Newton and Nunamaker.1 In their scheme, the authors divide femoral fractures according to anatomic landmarks: (1) fractures occurring proximal to the greater trochanter, including the femoral head and neck; (2) fractures occurring just below the greater trochanter, or subtrochanteric; (3) shaft fractures; (4) fractures just above the femoral condyle, or supracondylar; and (5) intracondylar fractures.

❚❚❚ CAPITAL PHYSEAL FRACTURES Growth-plate fractures of the femoral head, also termed capital physeal fractures, are serious injuries. If untreated, these fractures typically lead to pain-related lameness, extreme muscular atrophy, and osteoarthritis. Even when reduced anatomically, related injury to the physeal blood supply eventually can undermine even the best of surgical efforts. 329

Blood Supply to the Proximal Femoral Growth Plate (Physis, Capital Physis) The proximal femoral growth plate lies within the coxal joint, surrounded by joint fluid and a synovial-lined capsule. The ascending epiphyseal arteries, which originate from the medial circumflex femoral and caudal gluteal arteries, provide its circulatory needs. This effective but fragile blood supply often is disrupted as a result of associated growth-plate injuries, potentially leading to avascular necrosis of the subphyseal bone of the femoral neck.

Evaluating Capital Physeal Repair Gibson and co-workers reported the results of surgical repair of proximal growth-plate fractures in 34 dogs. All the operated joints developed some degree of osteoarthritis, proximal femoral deformity, and resorptive bone loss. These authors concluded that such fractures using either pin or screw repairs would predictably lead to similar outcomes, especially if the injury occurred before the dog reached skeletal maturity.2 A variety of capital physeal fractures are shown in Figures 32-4 to 32-10.

❚❚❚ EPIPHYSIOLYSIS OF THE FEMORAL HEAD Periodically, accounts of femoral head growthplate fractures unassociated with trauma appear in the veterinary literature. Hard pressed to explain the cause of such “injuries,” some authors have asserted that the growth cartilage is defective, as described in humans with epiphysiolysis. Proof for such a contention is usually lacking, however, with most published accounts using disclaimers in their titles, such as “apparent,” “presumed,” or “resembling” epiphysiolysis.

330

SECTION IV ❚❚❚ The Hips and Pelvis

A

B Figure 32-1 • A, Close-up ventrodorsal view of the hips of a dog with a minimally displaced left acetabular fracture (reader’s right). B, Close-up view of the affected left coxal joint provides further detail of the injury.

Figure 32-2 • Close-up ventrodorsal view of the left hip of a dog with a displaced fracture of the ischial neck with cracks extending into the associated caudal acetabulum and ischial body.

Figure 32-3 • Close-up ventrodorsal view of the right hip of a dog with a displaced fracture involving the caudal acetabulum and ischial neck. Other fractures are present in the pubis and elsewhere.

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Figure 32-6 • Close-up ventrodorsal view of the hips of an immature dog shows a displaced right capital physeal fracture (reader’s left).

Figure 32-4 • Ventrodorsal view of pelvis and hips of an immature cat shows a displaced right capital physeal fracture in addition to fractures of the left acetabulum, pubis, and ischium.

Figure 32-7 • Close-up flexed ventrodorsal view of the hips of an immature dog shows a displaced left capital physeal fracture.

Figure 32-5 • Close-up ventrodorsal view of the pelvis and hips of an immature cat shows bilateral capital physeal fractures in addition to right sacroiliac and acetabular fractures.

Figure 32-8 • Close-up extended ventrodorsal view of the hip of a cat shows disappearance of most of the femoral neck consistent with an old devascularizing fracture of the capital physis.

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A

A

B Figure 32-10 • Ventrodorsal (A) and lateral (B) views of the pelvis and hips of a young cat that had a right capital physeal fracture stack pinned 6 months earlier. Although the pin tips were once within the femoral head, continued growth of the femoral neck and head eventually left the implants behind.

B

Given the foregoing account, and the tenuous data on which it is based, it is apparent that a diagnosis of epiphysiolysis is presumptive at best and should be seriously entertained only after more plausible explanations have been thoroughly investigated.

Figure 32-9 • A, Ventrodorsal view of the pelvis and hips of a mature cat with a chronic right capital physeal fracture sustained 3 months earlier. B, Healed fractures of the left pubis and ischium.

In 1997, Dupuis and co-workers published a report describing two young dogs that they asserted had bilateral epiphysiolysis. They based their claim on the abnormal radiographic appearance of the femoral neck(s), described as narrowed and decreased in density (resembling avascular necrosis). In subsequent images, one of the dogs was described as having a unilateral “slipped capital femoral epiphysis,” and yet ostectomies were required to remove both femoral heads in a subsequent surgery.3

❚❚❚ FEMORAL HEAD FRACTURES Primary fractures of the femoral head are rare, with most being comminuted (Figure 32-11). If left untreated (usually by surgical removal of the femoral head), the femoral fragments tend to disperse and often undergo further fragmentation (Figure 32-12). Congenital epiphyseal dysplasia can cause joint pain in immature dogs, including pain in the hips, which typically disappears once the animal has finished growing. At 1 month of age, affected puppies show a femoral head that appears fragmented, loosely resembling aseptic necrosis or a comminuted fracture. Unlike these diseases, however, epiphyseal dysplasia affects all the long bones, not just the hips. As the puppy grows,

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Figure 32-12 • Close-up ventrodorsal view of an untreated, chronic comminuted fracture-dislocation of the left hip shows a lytic, badly fragmented left femoral head adjacent to a deformed, arthritic acetabulum.

A the standard extended ventrodorsal projection usually demonstrates a femoral head that fails to move with femoral flexion, strong presumptive evidence of a fractured femoral neck.

❚❚❚ TROCHANTERIC FRACTURES Fractures of the greater trochanter usually are seen in conjunction with other hip injuries, such as fractured femoral growth plate or neck. Generally, the combination of femoral and trochanteric growth plate fractures is seen in skeletally immature dogs, but occasionally a trochanteric growth-plate fracture is found together with a femoral neck fracture.4 Many trochanteric fractures are more visible when the hips are flexed (Figure 32-14).

B Figure 32-11 • Ventrodorsal (A) and close-up (B) views of the pelvis and hips of a mature dog shows a dislocated hip with two large chunks of its femoral head remaining in the acetabulum.

the segmented femoral heads consolidate, eventually appearing solid. Although deformed, the hips (and other affected joints) do become not arthritic.

❚❚❚ FEMORAL NECK FRACTURES Femoral neck fractures are also uncommon. If untreated, these injuries, like proximal femoral growthplate fractures, usually lead to nonunion. In some instances, a clear gap between fragments is not visible (Figure 32-13). Adding a flexed ventrodorsal view to

❚❚❚ DISLOCATION AND FRACTUREDISLOCATION OF THE HIP Most dislocated hips are associated with avulsion of the round ligament at the point of its femoral attachment. This often produces a small subchondral defect, the result of an associated avulsion fracture. Typically, the fragment remains within the acetabulum and may or may not be visible, depending on the view. In some instances, bone is flaked off the dorsal acetabular rim, resulting in one or more small, illdefined densities lying along the outer margin of the joint (Figure 32-15). Occasionally, relatively large fragments detach from the interior joint margin, sometimes requiring an oblique projection to be fully appreciated (Figure 32-16). Isolated fracture dislocation of the hip is less common than multiple pelvic fractures without coxal

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Figure 32-13 • Close-up view of the hips of a dog that fractured its right femoral neck (reader’s left) 3 months earlier. The fracture is now a nonunion, with more than half of the original femoral neck having been reabsorbed, as determined by comparison with the normal opposite hip (emphasis zones).

Figure 32-14 • Flexed ventrodorsal view of the hips of an immature dog shows a displaced greater trochanteric fracture.

joint involvement, although occasionally such injuries occur together (Figure 32-17). Based on years of experience and hundreds of cases, dislocated or manually relocated hips rarely remain in place with bandaging alone. Most other techniques fare little better and often serve merely to postpone the inevitable femoral head ostectomy (Figures 32-18 and 32-19).

❚❚❚ POSTOPERATIVE ASSESSMENT OF FEMORAL OSTECTOMY MUSCLE FLAP Mann and co-workers devised a technique for measuring the thickness a muscle flap (created from the biceps femoris) placed over the femoral stump following surgical removal of the femoral head and neck. Using an extended ventrodorsal projection of the pelvis and hips, the shortest distance between the ostectomy site and adjacent acetabular rim was measured. It was hoped that these measurements could be used to

Figure 32-15 • Close-up view of the left hip of a cat shows a fracture-dislocation, the former being indicated by two curvilinear bone fragments lying along the lateral edge of the acetabulum and a small defect in the articular surface of the femoral head.

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Figure 32-16 • Close-up view of the dislocated left hip of a cat shows a large curvilinear bone fragment in the acetabulum and a spherical area of bone loss in the medial aspect of the femoral head.

Figure 32-17 • Full-length view of the pelvis and upper hindlimbs shows a dislocated right hip, multiple pelvic fractures, and a midshaft femoral fracture.

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A

B C Figure 32-18 • A, Close-up view of the dislocated left hip of a cat made shortly after the injury. B, Immediate postoperative film of the left hip shows a cluster of screws and washers used to hold the reduced femur in place. C, A 3-week progress film shows displacement of the greater trochanter and the screw and washer used to reduce it.

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Figure 32-19 • Close-up view of the hips of a dog with dislocation of the right hip as evidenced by the overlapping femoral head and acetabulum and a loss of most of the associated cartilage space. Following dislocation, the hip was manually reduced and bandaged. When rechecked in a week, the hip was again luxated.

predict future limb function, but unfortunately they did not.5

❚❚❚ PARACOXAL MASS IN DOBERMAN PINSCHERS Disabling paracostal masses containing a mixture of cartilage, bone, and fibrous tissue have been reported in Doberman Pinschers with von Willebrand disease.6,7 Radiographically, lesion visibility is dependent on the amount of calcification. If the lesion is large, a stress film using the mass as a fulcrum and the femoral shaft as a lever may partially dislocate the femoral head, providing presumptive evidence in support of the diagnosis.

References 1. Nunamaker DM: Fractures and dislocations of the hip joint. In Newton CD, Nunamaker DM, eds: Textbook of Small Animal Orthopedics. Philadelphia, 1985, Lippincott.

2. Gibson KL, van Ee RT, Pechman RD: Femoral capital physeal fractures in dogs: 34 cases (1979-1989). J Am Vet Med Assoc 198:886, 1991. 3. Dupuis J, Breton L, Drolet R: Bilateral epiphysiolysis of the femoral heads in two dogs. J Am Vet Med Assoc 210:1162, 1997. 4. Huss BT: What is your diagnosis? J Am Vet Med Assoc 205:1125, 1994. 5. Mann FA, Hathcock JT, Wagner-Mann C: Estimation of soft tissue interposition after femoral head and neck excision in dogs using ventrodorsal pelvic radiography. Vet Radiol Ultrasound 34:230, 1993. 6. Dueland RT, Wagner SD, Parker RB: von Willebrand heterotopic osteochondrofibrosis in Doberman Pinschers: five cases (1980-1987). J Am Vet Med Assoc 197:383, 1990. 7. Moser J, Meyers KM, Russon RH: Inheritance of von Willebrand factor deficiency in Doberman Pinschers. J Am Vet Med Assoc 209:1103, 1996.

C h a p t e r

3 3

Hip Dysplasia

❚❚❚ OVERVIEW

critics contending that it lacked both sensitivity and specificity.

Early Beginnings The late Gary Schnelle, former head of Boston’s famed Angel Memorial Animal Hospital, was one of the first North American veterinarians to publish the radiographic appearance of hip dysplasia in dogs. Schnelle was also one of the first to use stress radiography, sometimes termed wedge radiography, to assess the hips of dogs when dysplasia is suspected. In this technique, a large padded object was placed between the thighs of a dog to act as a fulcrum while its hindlimbs were extended and forced inwardly during radiographic examination. Later, speculation swirled concerning the cause of hip dysplasia, with one Swedish investigator stating, “Spontaneous hip dysplasia is probably caused by maternal estrogens which affect the fetus in utero” following experimental creation of the disease in immature Greyhounds using estradiol.1 In a concerted effort to understand better exactly what failed in the development of the dysplastic hip joint, Riser chronicled the radiographic development of both normal and abnormal hips, from birth to a year of age. Unfortunately, he used Greyhounds as his normals, a breed free of hip dysplasia, and as his abnormals, German Shepherds, a breed plagued by the disease. Nevertheless, the work had merit in that it afforded one the opportunity to see how the disease progressed, and it provided insight as to when one might first predict the existence of the hip dysplasia in an individual animal.2,3 Later, Bardens asserted that palpation could be used to detect what he termed “laxity” in the hips of young puppies, a finding that he contended was a reliable indicator of future hip dysplasia. This, claimed Bardens, eliminated the need for a 2-year wait while the hips matured sufficiently to allow conventional radiographic evaluation. Bardens’s method of predicting hip dysplasia eventually fell into disfavor, with its 338

More Recent Developments In the 1970s, I first began radiographing the hips of dogs without the use of any chemical or gas restraint. I later showed that it was impossible to differentiate radiographically between the hips of a conscious versus an unconscious dog, dispelling the belief that such differences routinely existed. In the 1980s, I began radiographing the hips of dogs in the standing position (my initial foray into postural radiography). This method of projecting the hips proved revealing in a variety of ways but, perhaps most importantly, showed that some dogs with normalappearing hips in standard recumbent radiographs actually were subluxating when imaged in the standing position. Also during this time, Smith, like Bardens and others before him, sought to predict hip dysplasia in young dogs by using stress radiography on unconscious dogs. Seemingly seeking to distance himself, his methodology, and his organization (PennHip) from Bardens, Smith criticized the palpation method used by Bardens as not being reproducible and thus, by inference, unscientific. Smith’s university-based research group later formed an alliance with Symbiotics, a commercial drug company that currently promotes his method on their corporate web site.

Role of Stress Radiography As mentioned earlier, stress radiography of the hips (in one form or another) has been used in dogs for more than half a century; I first assisted a veterinarian in this procedure in 1957. Fluckiger, promoting Smith’s technique, reviewed the role of stress radiography in the diagnosis of hip dysplasia, an article that merits perusal for those wanting more information on this subject.4

CHAPTER 33 ❚❚❚ Hip Dysplasia

Certification, Eradication, and the Orthopedic Foundation for Animals Any veterinary radiologist, whether university or privately based, can certify a dog’s hips. The Orthopedic Foundation for Animals (OFA) certification may be specifically required by the constitutions of some older breed clubs, written at a time when there were only a few qualified specialists, even in veterinary colleges. Although certification programs have reduced the incidence of hip dysplasia, they have not eradicated it. This is due in large part to the incomplete penetrance and variable expressivity of the disease. In other words, some dogs with radiographically normal hips are capable of transmitting the disease to their offspring. Initially, the OFA was established to provide expert radiographic interpretation of the hips of dogs being screened for hip dysplasia. Additionally, the organization tracked the incidence of the disease in individual breeds, periodically publishing their results. Over the course of time, the OFA has branched out and now certifies dogs as being free of a variety of ailments, including elbow dysplasia, patella dysplasia, and subaortic stenosis. In fact, the OFA will now interpret any radiographic examination for a fee.

❚❚❚ EARLY DETECTION OF HIP DYSPLASIA: A COMPARISON OF METHODS Adams and colleagues compared the abilities of palpation, ultrasound, conventional radiography, and stress radiography to detect canine hip dysplasia in its earliest stages.5 They contend that controlled stress radiography is the best method for evaluating the hips of immature dogs, a view that is not universally shared.

❚❚❚ WHEN TO CERTIFY The OFA requires that dogs be 2 years of age or older before having their hips submitted for certification, citing European studies indicating that 2-year-old dogs with normal hips probably will remain that way in the future. Canadian veterinary schools have certified large numbers of dogs at an even earlier age: The Ontario Veterinary College certifying all breeds at 18 months and the Western College of Veterinary Medicine certifying German Shepherds for the Royal Canadian Mounted Police (RCMP) at 1 year of age. The RCMP dogs are certified at this time to coincide with the beginning of their police training.

❚❚❚ MAKING AND MARKING PELVIC IMAGES FOR CERTIFICATION Rendano and Ryan collaborated with the OFA in describing a standardized method of making and

339

marking hip radiographs.6 My own research, later confirmed by Aronson, indicates that anesthesia has no effect on the radiographic appearance of the hips.7,8 Thus, we do nearly all of our hip assessments in undrugged, fully conscious dogs. We term our studies coxal joint evaluations rather than hip dysplasia examinations to reflect the primary objective of the assessment, which is to certify an animal’s hips as normal so that it can be bred with greater confidence. To term the study a dysplasia examination unnecessarily casts the procedure in a negative light and fails to reflect the fact that most dogs that we examine have normal hips.

❚❚❚ NORMAL BREED VARIATIONS Although it is true that some anatomic differences exist between the hips of different breeds of dogs, these differences are not great. Certainly, they are not so extensive that only an expert can determine which are dysplastic and which are not. In almost every instance, exclusive of breed, approximately one half or more of a normal femoral head is located within the acetabulum: the so-called 50% rule.

❚❚❚ RADIOGRAPHIC FEATURES Normal Canine Hip The principal difference between the best and worst hips is the depth of the femoral head in the acetabulum. Those that extend deepest into the acetabulum are judged the best (termed excellent conformation), whereas the others are relegated to lesser qualitative categories, such as good or fair. Transitional ratings (for example, fair to good) are assigned to animals that fall between the standard, fair, good, and excellent ratings. The individual coxal joints of some dogs may differ conformationally, for example, one being good and the other fair, or one being dysplastic and the other normal. Although some certifying organizations use the terms marginal or borderline to describe the hips of dogs submitted for evaluation, meaning the evaluator cannot make up his or her mind about whether the dog is normal, I would argue strongly against such a rating because it achieves little other than to frustrate owners and undermine expert credibility. Figures 33-1 to 33-5 exemplify the hips of some normal dogs.

Dysplastic Canine Hip The defining feature of hip dysplasia is an imperfect fit between the bones of the coxal joint, the femoral head, and the acetabulum. Like most diseases, hip dysplasia occurs in varying degrees, from mild to severe. Most but not all dysplastic hips eventually become arthritic. In my experience, a nonarthritic dysplastic

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A

B

Figure 33-1 • A, Close-up ventrodorsal view of normal hips in a 3-year-old Labrador Retriever. B, Close-up view of right coxal joint shows most of the femoral head within the acetabulum consistent with excellent conformation.

Figure 33-2 • Ventrodorsal view of normal hips in a 2-year-old German Shepherd. Close-up view of right coxal joint shows two thirds of the femoral head within the acetabulum consistent with good to excellent conformation.

CHAPTER 33 ❚❚❚ Hip Dysplasia

A

341

B

Figure 33-3 • A, Ventrodorsal view of normal hips in a 2-year-old German Shepherd. B, Close-up view of right coxal joint shows approximately half of the femoral head within the acetabulum consistent with good conformation.

Figure 33-4 • Close-up view of the hips of an 18-month-old German Shepherd shows fair conformation.

Figure 33-5 • Close-up ventrodorsal view of the hips of a 2-yearold Labrador Retriever shows good conformation on the left (viewer’s right) and fair conformation on the right (viewer’s left).

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A Figure 33-7 • Severe bilateral hip dysplasia with dislocation: Extended ventrodorsal view of the hips shows dislocation of the left hip and near dislocation of the right. The dog has yet to finish growing, and, like many immature animals with severe dysplasia, osteoarthritis is still minimal (although it should worsen with time).

❚❚❚ UNILATERAL HIP DYSPLASIA B Figure 33-6 • A, Close-up, extended ventrodorsal view of the hips of a 2-year-old German Shepherd shows severe dysplasia of the right coxal joint (viewer’s left), with resultant osteoarthritis. The left hip is normal with good conformation. B, Flexed ventrodorsal view of the hips of the same dog makes the dysplastic hip appear relatively better than it does in the extended view, the result of decreased dislocation.

hip usually is not painful, although it may change an animal’s gait or the manner it sits, rises, runs, and jumps. Atrophy of the hip and thigh muscles often develops, depending on how the action of the dysplastic hip is affected. Currently, the hips of most dogs are radiographically assessed using the extended ventrodorsal projection, although at one time it was popular to make both flexed and extended views (Figure 33-6). I do not find the lateral projection useful, although some radiologists attempt to justify it on the somewhat spurious basis of completeness. Figures 33-7 and 33-8 illustrate the appearance of dysplastic canine hips with and without osteoarthritis. Figure 33-9 shows how the volume of the dysplastic joint increases with dislocation. Lesser degrees of involvement are exemplified in the following section on unilateral hip dysplasia, where they are compared with the normal contralateral coxal joint.

In our practice, about 5% to 10% of the dysplastic dogs we examine have only one affected hip, a condition termed unilateral hip dysplasia (Figures 33-10 to 33-13). Some of these dogs also have an additional abnormality, a transitional vertebra (usually L7), which may or may not be associated with lateral malalignment of the pelvis. Larsen, in describing lumbosacral transitional vertebrae in dogs, contends that unilateral sacralization of L7 causes unilateral hip dysplasia, citing earlier work by Olson and Kangstrom (Figure 33-14).9,10 As far as I can determine, this is a case of “guilt by association,” which to date lacks convincing proof.

❚❚❚ STRESSING A SUSPICIOUS HIP As a radiologist, I have practiced stress radiography for nearly three decades on a great variety of joints, including the hip. Although I occasionally use fulcrumassisted distraction, I currently prefer what I term the push–pull maneuver. This technique involves pushing the suspect hip toward the head of the dog while simultaneously pulling on the opposite leg. The intent of this maneuver is to show that the femur, which is being pushed away from the operator, can be partially dislocated (Figure 33-15). Occasionally, a struggling dog can inadvertently achieve the same result (Figure 33-16).

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A

A

B

B Figure 33-9 • Arthrograms of the left coxal joint, made in both the flexed (A) and extended (B) positions, show how the femur is capable of moving in and out of the acetabulum, depending on limb position. To accommodate this greater range of motion, the ligament of the femoral head and the articular capsule stretch.

C Figure 33-8 • Severe bilateral hip dysplasia with associated osteoarthritis: Flexed ventrodorsal view (A) of the hips shows marked underdevelopment of the acetabula, which appears as shallow troughs rather than deeply concave cavities. In this position, one that optimizes the appearance of the hips, only the central third of the femoral head is in contact with the acetabulum. Close-up views of the right (B) and left (C) hips show severe osteoarthritis.

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Figure 33-11 • Close-up view of the hips of a 2-year-old Golden Retriever shows moderate to severe unilateral hip dysplasia without osteoarthritis (viewer’s right). Pelvic obliquity related to abnormally tight thigh muscles on the left exaggerates the degree of dislocation.

Figure 33-10 • Close-up view of the hips of an 18-month-old German Shepherd shows mild unilateral hip dysplasia (viewer’s right).

Figure 33-12 • Close-up view of the hips of a 4-year-old Labrador

Figure 33-13 • Close-up view of the hips of a 5-year-old Old

Retriever with moderate dysplasia of the right hip, accompanied by severe osteoarthritis.

English Sheepdog shows severe unilateral hip dysplasia and osteoarthritis. Note how the flattened femoral head matches the shallow acetabulum, mutually induced structural accommodations to chronic subluxation.

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A

345

B

Figure 33-14 • A, Full-length view of the pelvis and hips of a 2-year-old Labrador Retriever shows mild unilateral hip dysplasia with osteoarthritis (reader’s left). B, Close-up view of segmented, asymmetric sacrum shows rudimentary transverse process on the left, characteristic of congenital lumbarization. The relationship, if any, between congenital sacral deformity and unilateral hip dysplasia is the subject of considerable speculation but little fact.

A

B

Figure 33-15 • Close-up ventrodorsal views of the hips. Two films were made because the dog was thought to have spoiled the first by struggling. A, In the first film, where the dog was thought to have moved, the right hip is partially dislocated (viewer’s left). B, In the second image, the hip appears normal.

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A

B Figure 33-16 • A, Close-up ventrodorsal view of the hips of a 2-year-old Labrador Retriever shows suspicious appearing right hip (viewer’s left). B, Stress film using a push–pull maneuver confirms dislocation of the right coxal joint, compatible with dysplasia.

❚❚❚ DIFFERENTIATING THE DYSPLASTIC FROM THE PREVIOUSLY INJURED HIP When explaining a case of unilateral hip dysplasia to an owner, I am often asked whether the abnormal hip could be due to an old injury. In most instances, the answer is no, but there are occasional exceptions. Assuming there is no anecdotal evidence or proof of a previous hip injury, I usually approach the question as follows. If there are old pelvic fractures, especially evidence of a former acetabular injury, the possibility of trauma at least must be considered. If the hip in question is fully dislocated and lies along the lateral aspect of the ilial neck, the possibility of injury becomes even greater.

Effect of Femoral Shaft Fractures on the Hip Although there is often speculation to the contrary, femoral malunions that result in limb shortening almost never adversely affect the associated coxal joint (Figure 33-17). In the same regard, a limb amputation does not lead to arthritis in the remaining limb.

Traumatic Dislocation and the Dysplastic Hip I believe there is little doubt that the moderately or severely dysplastic hip is more susceptible to traumatic dislocation. Furthermore, I have examined dysplastic dogs with a history of acute, non–weight-bearing lameness that occurred while roughhousing with the owner and whose radiographs showed no evidence of a fracture or dislocation. Presumably, such injuries are the result of a momentary luxation of the hip and stretching or partial tearing of the round ligament, joint capsule, and attached muscles. Supporting this theory is that most such dogs fully recover in about a month unless the injury is aggravated, in which case recovery is usually protracted.

Figure 33-17 • Full-length view of the hips, femurs, and stifles in a immature dog with a slight limp, presumed to be mechanical and not due to pain, shows a side-to-side right femoral malunion. The relatively wide cartilage spaces in the coxal joints are normal for this age.

❚❚❚ EXPLAINING RESULTS TO OWNERS Before you begin your explanation, ask the owner whether he or she is familiar with the particulars of hip dysplasia. Many are, but some are not. The explanation needs to be tailored to to your perception of the owner’s ability to understand and then modified along the way. I strongly recommend that the examination be referred to as a hip or coxal joint evaluation, not as a hip dysplasia examination because the latter term is presumptuous. • Once you ascertain that the owner desires a detailed explanation, use normal and abnormal films to illustrate the radiographic differences between normal and dysplastic hips.

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A

B Figure 33-18 • Normal (A) and dysplastic (B) canine coxal joints (ventrodorsal perspective). The dotted line on the dysplastic acetabulum represents the original lateral margin prior to arthritic remodeling.

B

A Figure 33-19 • Normal (A) and dysplastic (B) canine proximal femurs (close-up ventrodorsal perspective).

• Be flexible with your terminology. Do not be afraid to use the terms thigh bone or ball and socket joint. The point is to make the owner understand about his or her dog’s hips—good or bad—not to give a lecture on radiographic anatomy. • If the owner needs to relay your message to someone else, help him or her keep it straight by providing simple sketches or a formal illustrated handout.

• Use a normal pelvis and femur to explain more clearly the anatomy of the hip joints and superimpose the bone specimens on their radiographic counterparts to improve comprehension. Using the coxal joint of a dysplastic dog makes your explanation even more meaningful (Figures 33-18 to 33-20). • Keep the matters of heritability and future breeding brief and focused. Avoid genetic jargon.

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A

B Figure 33-20 • Normal (A) and dysplastic (B) canine acetabula (close-up lateral perspective). The dotted line on the dysplastic acetabulum represents the original lateral margin prior to arthritic remodeling.

❚❚❚ PROGNOSIS FOR THE DYSPLASTIC HIP: MYTH AND REALITY To date, I have owned three dysplastic dogs, all given to me by breeders who, once they discovered the dogs were dysplastic, planned to have them euthanized (unless I took them). Two of the dogs were large male Golden Retrievers, and the other was a small female Springer Spaniel. I should add at this point that I knowingly accepted dysplastic dogs so that I might be able to advise the owners about such animals based on firsthand rather than secondhand knowledge. My experience has been as follows. The Springer Spaniel, “Mookie,” is now 13 years old and, except for her hips and a moderate hearing loss, is in good health. She exercises on and off leash with another dog about 30 minutes a day, 6 to 7 days a week. Following exercise, the dog climbs stairs more slowly, jumps more deliberately, and walks with a shortened stride. She appears fully recovered by the next day. If more than a few days pass without regular exercise, all the postexercise abnormalities become more pronounced and last longer, sometimes into the next day. Mookie’s hips have gradually become increasingly arthritic, as determined by periodic radiography. One of the Golden Retrievers, “Desi,” was diagnosed as being mildly dysplastic at 2 years of age. He died at age 7 years from disseminated hemangiosarcoma; but up to that time, his dysplasia had not worsened, and he developed only mild osteoarthritis in one hip. He never showed lameness even after lengthy runs. “Mason,” a large 90-pound Golden Retriever, was given to me 4 years ago when he was 15 months of age after he was diagnosed with mild to moderate unilateral hip dysplasia. He exercises daily without evidence of lameness. Progress radiographs have shown neither worsening of the dysplasia nor development of osteoarthritis.

In recounting my personal experience with three dysplastic dogs, it has not been my intent to make unsubstantiated generalizations but rather to point out that I do have some firsthand knowledge of the disease. Based on my considerable professional experience with hip dysplasia (including regularly speaking with the owners of these dogs), however, I have no hesitation in tendering the following observations: • Many, but not all, dysplastic dogs become worse with time. • Most, but not all, dysplastic dogs develop osteoarthritis. • The greater the degree of dislocation, the slower the initial development of osteoarthritis. • Related lameness is due to the subsequent development of osteoarthritis, not to the dysplasia per se. • Few dogs are crippled by hip dysplasia. • Regular, unforced exercise is the best treatment for hip dysplasia (as it is for many different types of chronic joint disease) and reduces secondary muscle atrophy. • Fit dysplastic dogs do better than those who are not fit. • Thin dysplastic dogs do better than overweight ones.

❚❚❚ SURGICAL TREATMENT OF HIP DYSPLASIA Femoral Head Relocation (Intertrochanteric Osteotomy) In 1974 Paatsama and Jussila described a new surgical treatment for hip dysplasia, advocating the 3 R’s: removal, redirection, and reattachment of the femoral head and neck. They claimed that by changing the direction of the proximal femur, and thus the coxofemoral contact surface, the joint would remodel, providing increased coverage of the femoral head. Presumably, this would slow the development of osteoarthritis.11

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B

A

Figure 33-21 • A, Severe bilateral hip dysplasia in a young Golden Retriever in which the right hip (viewer’s left) dislocates completely during weight bearing, as indicated by the extraarticular bone deposition on the cranial acetabulum. B, Following surgical relocation of the left acetabulum, the weight-bearing ring of the pelvis has become severely distorted, the pelvic canal has partially collapsed, and the left ischial tuberosity lies in the soft tissue lateral to the pelvis.

Acetabular Relocation (Triple Pelvic Osteotomy) Cutting the acetabulum free of the pelvis and then reattaching it can cause undesirable side effects, including chronic constipation or obstipation (as a result of narrowing of the pelvic canal) and a variety of postural and gait abnormalities related to the disfigurement of the caudal portion of the pelvis (Figures 33-21 and 33-22). I can offer the reader no persuasive evidence, largely because of a lack of long-term follow-up, that this surgery either consistently prevents or delays the development of osteoarthritis in a dysplastic hip. Continued modification of the surgery seems to bear this out.

The Artificial Hip The surgical installation of an artificial coxal joint (coxal arthroplasty, “total” hip replacement, “total” hip arthroplasty) usually is performed as a treatment for hip dysplasia. Surgical success is predicated on the proper placement and cementing of the implants. Surgical failure usually is related to implant loosening and subsequent dislocation, which may be septic or aseptic in nature. It is exceptionally rare for a canine hip prosthesis to fail structurally. According to one report, about 10% of artificial hip installations fail, a fact that most surgical reports euphemistically refer to as a complication requiring surgical revision. Causes of surgical failure include the following:

Figure 33-22 • Following left acetabular relocation, the left hemipelvis is now badly deformed, the left hip is subluxated, and the left obturator is nearly closed due to a left ischial malunion.

• • • • •

Dislocation of the prosthetic femoral head Femoral fracture (intraoperative) Improper preparation of prosthetic sites Incorrect placement of prostheses Insufficient or excessive amount of bone fixative

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SECTION IV ❚❚❚ The Hips and Pelvis

Immediate Postoperative Assessment: Implant Position and Cement Coverage • Acetabular component:Assessment is made according to the position of the associated marker wire. In the horizontal plane, the socket is described as retroverted, anteverted, or normoverted. In the transverse plane, it is characterized as open, closed, or ideal. • Femoral component: Assessment is based on the position of the femoral prosthesis within the femoral shaft. In the frontal view, the prosthetic stem is described as central, varus, or valgus. In the lateral view, the stem is characterized as central, cranial, or caudal. • Cement thickness and uniformity (coverage): Assessment is based on the thickness of the bone cement (termed the mantle). A thickness of 2 mm or greater is said to be adequate, whereas a thickness of less than 2 mm is termed inadequate. If the mantle contains defects (termed voids), the coverage is called inadequate. • Cement volume and location: Assessment is based on the amount and location of the cement. Cement that is more than double the norm (4 mm), highly uneven, spilling from drill holes or foramina, or far from its intended location is termed excessive.

A

Progress Examinations

B Figure 33-23 • Close-up preoperative (A) and postoperative (B) ventrodorsal views of a severely dysplastic dog that has had a prosthetic hip replacement. The cloudy density surrounding the operative site is bone cement, which is radiopaque.

• Loosening of the prosthetic acetabulum • Sciatic neurapraxia (failure of an intact nerve to conduct an impulse due to blunt trauma, compression, or ischemia • Thermal injury related to bone cement (methyl methacrylate) Artificial hips currently are evaluated using the radiographic criteria published by Konde and colleagues12 and later those of Massat and Vasseur.13 Preoperative and postoperative images of standard installation are shown in Figure 33-23.

• Development of a radiolucent band: Assessment is based on the development of a radiolucent band, which develops at the cement–bone interface. An even or nearly even dark band is described as complete; one that is obviously uneven is characterized as incomplete. Width of the band is recorded in the record. • Remodeling: Any change in the size, shape, or density of the associated bone is described.

Radiographic Indicators of Noninfectious Surgical Failure In my experience, most artificial hips loosen for technical reasons related to their installation rather than for some inadequacy related to the prosthesis or because the dog’s owner fails to comply with postoperative instructions. Reported radiographic indicators of aseptic loosening of the femoral implant after total hip replacements include the following:14 • Implant displacement, specifically, contact of the distal stem tip with the adjacent inner cortical surface • Lucent lines or bands between portions of the exterior surface of the prosthesis and adjacent bone cement • Localized new bone deposition on the proximal femoral shaft

CHAPTER 33 ❚❚❚ Hip Dysplasia

351

Figure 33-25 • Close-up flexed ventrodorsal view of the hips of Figure 33-24 • Close-up view of the hips of a 3-year-old dog

a dysplastic cat found incidentally while screening the pelvis for fractures after a car hit the cat.

whose artificial right hip has become dislocated.

Not all postoperative complications are as subtle as those just described, as illustrated by this case of complete dislocation (Figure 33-24). I also have observed a dislocated acetabular cup and a variety of proximal femoral shaft fractures. It is also my impression that an excess of bone glue (to the point that it spills widely into the surrounding muscle planes) often spells an unsatisfactory outcome.

Radiographic Indicators of Infectious Surgical Failure

the relationship between the acetabulum and femoral head appears normal, or there is only mild subluxation. The major abnormality takes the form of periarticular osteophytes, especially involving the cranial acetabulum. Some radiologists contend that this is primary osteoarthritis because it is usually seen in older cats, not hip dysplasia. I also have observed such changes in cats with confirmed immunoarthritis.

❚❚❚ SONOGRAPHIC EVALUATION OF PUPPY HIPS

Surgically infected artificial hips usually are associated with pain, disuse, swelling, and fever. Often the surgery has been technically difficult or for some other reason prolonged. Reoperation adds to the probability of sepsis. One or more of the following features typically characterize infected artificial hips:

Greshake and Ackerman described the sonographic appearance of normal hip joints in Springer Spaniel puppies from 1 day to 12 weeks of age, noting that a complete assessment was not possible after the puppies reached their eighth week.18 In my opinion, sonographic assessment of puppy hips is usually inconclusive, sometimes erroneous, and often technically difficult.

• Bone lysis • Increased distance between the acetabular marking ring and the femoral implant • Any change in the relative positions of the implants and bones observed between the immediate postoperative films and later progress examinations

Digital Versus Analog Hip Images

❚❚❚ HIP DYSPLASIA IN CATS Background Hip dysplasia has been reported in cats far less frequently than in dogs, reflecting both its rarity and, typically, its lack of clinical importance.15,16 The OFA has reported a hip dysplasia frequency of 6.6% in cats, based on a retrospective review of films obtained from 684 animals made over a 5-year period from 1991 to 1995.17

Imaging Findings The appearance of hip dysplasia differs markedly between dogs and cats (Figure 33-25). In many cats,

The OFA has determined that there is little or no difference in results when canine hips are interpreted from original films, displayed on a conventional view box, compared with scanned images (of the original films) displayed on a computer monitor.19

References 1. Gustafsson PO: Hip dysplasia in the greyhound: a study of estradiol induced skeletal changes. J Am Vet Rad Soc 9:47, 1968. 2. Riser WH: Growth and development of the normal canine pelvis, hip joints and femurs from birth to maturity: a radiographic study. J Am Vet Rad Soc 14:24, 1973. 3. Riser WH: The dysplastic hip joint: its radiographic and histologic development. J Am Vet Rad Soc 14:35, 1973. 4. Fluckiger M: Stress radiography for the detection of hip joint laxity in the dog. Vet Radiol Ultrasound 36:429, 1995. 5. Adams WM, Dueland RT, et al: Comparison of two palpation, four radiographic and three ultrasound methods for early detection of mild to moderate canine hip dysplasia. Vet Radiol Ultrasound 41:484, 2000.

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6. Rendano VT, Ryan G: Canine hip dysplasia evaluation. Vet Rad 26:170, 1985. 7. Farrow CS, Back RT: Radiographic evaluation of nonanesthetized and nonsedated dogs for hip dysplasia. J Am Vet Med Assoc 194:524, 1989. 8. Aronson E, Kraus KH, Smith J: The effect of anesthesia on the radiographic appearance of the coxofemoral joints. Vet Rad 32:2, 1991. 9. Larsen JS: Lumbosacral transitional vertebrae in the dog. J Am Vet Rad Soc 18:76, 1977. 10. Olson S-E, Kangstrom H: Etiology and pathogenesis of canine hip dysplasia: Proceedings Canine Hip Dysplasia Symposium and Workshop. J Am Vet Med Assoc 24, 1972. 11. Paatsama S, Jussila J: Healing process after intertrochanteric osteotomy in canine hip dysplasia: an experimental study. J Am Vet Rad Soc 15:61, 1974. 12. Konde LJ, Olmstead ML, Hohn RB: Radiographic evaluation of total hip replacement in the dog. Vet Rad 23:98, 1982.

13. Massat BJ, Vasseur PB: Clinical and radiographic results of total hip arthroplasty in dogs: 96 cases (1986-1992). J Am Vet Med Assoc 205:448, 1994. 14. Edwards MR, Egger EL, Schwartz PD: Aseptic loosening of the femoral implant after cemented total hip arthroplasty in dogs: 11 cases in 10 dogs (1991-1995). J Am Vet Med Assoc 211:580, 1997. 15. Patsikas MN, Papazoglow LG: Hip dysplasia in the cat: a report of 3 cases. J Small Anim Pract 39:290, 1998. 16. Hardie EM, Roe SC, Martin FR: Radiographic evidence of degenerative joint disease in geriatric cats: 100 cases (1994-1997). 220:628, 2002. 17. Keller GG, Reed AL, et al: Hip dysplasia: a feline population study. Vet Radiol Ultrasound 40:450, 1999. 18. Greshake RJ, Ackerman N: Ultrasound evaluation of the coxofemoral joints of the canine neonate. Vet Radiol Ultrasound 34:99, 1993. 19. Keller GG, Corley EA: Impact of video images on O.F.A. evaluation of hip status. Vet Radiol Ultrasound 35:19, 1994.

C h a p t e r

3 4

Hip Infections

❚❚❚ BACKGROUND Sepsis of the hip is rare in both dogs and cats, with most cases representing surgical infection. Coxal joint infections occasionally are caused (or presumed to have been caused) by a nonspecific bacteremia, usually in puppies or adolescent dogs, although a bilateral Staphylococcus aureus infection was reported in an 11year-old dog without any previous surgical history.1 Myer reported a case of septic arthritis in a 6-year-old German Shepherd that also had hip dysplasia, mentioning that this particular disease combination has been encountered previously at Ohio State.2 Some, but not all, dogs with septic arthritis of the hip (or hips) have a fever; most have a painful lameness. With bilateral infections, some dogs are unwilling to rise, resembling severe pelvic or hip injury or, in some instances, a spinal cord injury. As infections become worse, most dogs appear obviously ill.

❚❚❚ IMAGING FINDINGS In my experience, infection of the coxal joint is relatively easy to diagnosis radiographically in the advanced and intermediate stages, but it is difficult or impossible to detect in the early stages. The only disease I have seen that resembles coxal infection is the occasional case of long-standing hip dysplasia–osteoarthritis in which the femoral head and acetabulum have become extraordinarily osteopenic. Such cases usually can be differentiated from infection by their lack of systemic signs. Bacterial infections of the coxal joint usually first appear as immature bone deposition along the edge of the acetabulum. New bone may or may not form on the femoral neck but seldom develops on the femoral head because of the protective nature of its articular cartilage. The appearance of the cartilage space is highly 353

unpredictable, appearing widened, narrowed, or unchanged. As the infection progresses, the amount and maturity of the new bone increase, and lytic foci may begin to appear. Concurrently, the bones of the hip may undergo a generalized density loss, especially the femoral neck. The cartilage space may appear to widen, but this can be deceptive. In fact, the surfaces of the joint may be undergoing dissolution, or the round ligament or joint capsule may be becoming necrotic and no longer able to hold the femoral head in position. If the infection escapes the confines of the coxal joint and spreads into the periarticular tissues, abscess can occur, which is often discernible as a discrete soft tissue shadow, displacing adjacent muscles and their associated fascial planes. Periarticular abscesses can be readily identified sonographically and their content sampled for bacterial identification and chemical sensitivity. Diffuse cellulitis is predictably less well defined, but it is often suggested by a regional increase in periarticular density and loss of anatomic detail. Ultrasound will show the extent of any related regional hyperemia and associated edema. Computed tomography and magnetic resonance imaging can often detect a hip infection sooner and with a greater degree of certainty than plain radiography, although the latter is clearly a superior screening tool. Nuclear scintigraphy is best suited for cases in which structural changes are absent, but there is the potential for an alteration in the local circulation, admittedly a tenuous objective.

References 1. Harari J, Tucker RL, Alexander JE, et al: What is your diagnosis? J Am Vet Med Assoc 204:1159, 1994. 2. Myer CW: Radiographs presented as part of the 1992 A.C.V.R. oral certification examination: small animal section. Vet Radiol Ultrasound 34:87, 1993.

S E C T I O N

V

The Throat, Neck, and Thorax

C h a p t e r

3 5

Throat and Neck

❚❚❚ NORMAL PHARYNX

been my experience, however, that pharyngeal radiography performed for these reasons rarely proves diagnostic.

Background The pharynx can be thought of most simply as a cavity, an anatomic confluence of sorts, located immediately behind the oral and nasal passages. More specifically, the pharynx can be subdivided into three smaller chambers: the nasopharynx, oropharynx, and common pharynx. Breed variations can be pronounced, especially in brachycephalics such as English Bulldogs, where less regional contrast is present as a result of a greater amount of soft tissue (presumably, a disproportionately large soft palate). Long-nosed breeds, like Collies, have a more rectangular nasopharynx than medium-nosed dogs, such as Retrievers.1 It is extremely important to position the head and neck naturally when making a lateral radiograph of the throat because extension and flexion cause considerable variation in the normal anatomy.2 Possible reasons for radiographically examining the pharynx include (1) difficult or noisy breathing, (2) retching or gagging, (3) difficult eating, (4) excessive salivation, (5) coughing, (6) presumed sinus discharge, and (7) suspected proximal airway obstruction.3 It has

Imaging Findings Radiology. Perhaps the most difficult aspect of pharyngeal analysis is contending with normal variations, many of which resemble disease. These differences are for the most part the result of extension or flexion of the head and neck during radiography, which causes varying degrees of pharyngeal compression and distortion. Anatomic differences related to breathing, swallowing, and restraint further contribute to pharyngeal variability, as does the phase of respiration and oblique projection angles (Figures 35-1 to 35-3). Ultrasound. Bray and co-workers reported the sonographic appearance of the normal canine pharynx.4 My experience with this sort of examination—and I have performed many—is that it works well as a means to detect formed abscesses and medium-to-large sized foreign bodies. Small objects, however, like foxtails, wooden splinters, or quill fragments embedded in solid tissue, are surprisingly difficult to locate and, when 355

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SECTION V ❚❚❚ The Throat, Neck, and Thorax

A Figure 35-1 • Close-up lateral view of normal canine throat.

found, are often difficult to differentiate from small blood vessels and fascia. Ultrasound is a poor way to assess the exterior surfaces of the throat and trachea compared with radiography. Although ultrasound is capable of detecting motion—that of the epiglottis during swallowing, for example—the image is extremely crude compared with what one would see using a scope. As with many other skills, scanning competence requires regular practice. The time to become proficient in performing an ultrasound examination of the canine or feline pharynx, in particular becoming familiar with normal appearance and breed-related variations, is before actually encountering a pharyngeal disease.

❚❚❚ NORMAL LARYNX Imaging Findings Radiology. O’Brien and co-workers described the normal radiographic appearance of the dog’s larynx.5 It consists of three single cartilages—the epiglottis, thyroid, and cricoid—and one paired cartilage—the arytenoids. The latter contains two dorsal processes, the corniculate cranially and cuneiform caudally. I provided a similar description for the cat in an earlier textbook. Ultrasound. Bray and co-workers reported the sonographic appearance of the normal canine larynx.6 As already mentioned with respect to pharyngeal ultrasound, clinical applications are quite limited.

❚❚❚ SWALLOWING: A CINERADIOGRAPHIC PERSPECTIVE Watrous and Suter described the cineradiographic appearance of swallowing in normal dogs using three sequential phases: (1) oropharyngeal, (2) esophageal,

B Figure 35-2 • A, Lateral view of normal canine throat and neck shows fully open pharynx. B, When the head is raised the pharynx narrows and becomes more steeply angled. Also note how the soft palate elongates and contacts the epiglottis.

and (3) gastroesophageal. This classification scheme was previously reported for human patients.7 I have attempted to simplify the author’s account by eliminating some of the more esoteric jargon or, alternatively, including it as a parenthetical following a more commonplace description.

Normal Swallowing: A Triphasic Process 1. Oropharyngeal phase. This initial phase begins in the mouth and throat and is composed of four separate but coordinated steps: (1) grasping the food (prehension), (2) compacting the food (bolus formation), (3) constricting the pharynx to advance the compacted food (pharyngeal propulsion), and (4) opening the entrance to the esophagus to allow further passage of the bolus (cricopharyngeal relaxation). These steps occur rapidly and are marked by characteristic movements of the throat seen when a dog eats, closely resembling gulping in humans. 2. Esophageal phase. The intermediate phase of swallowing is composed of two types of peristalsis:

CHAPTER 35 ❚❚❚ Throat and Neck

357

A

C B Figure 35-3 • A, Close-up lateral view of normal canine throat in neutral position. B, When flexed ventrally the pharynx narrows, and the soft palate becomes blunted. C, When the head is raised the pharynx narrows, but not as much as when it is lowered. Predictably, the soft palate appears elongated and tapered.

primary and secondary. The first is initiated by the relaxation of the cricopharyngeal sphincter, followed by progressive, localized esophageal constriction, much like someone squeezes toothpaste on a brush. The second type of “peristaltic push” is generated within the esophagus by individual boluses that fail to transit initially. These steps are only vaguely visible when one watches a dog or cat eat. 3. Gastroesophageal phase. This is the final phase of swallowing in which the esophageal contents is propelled through the gastroesophageal junction into the stomach. This phase is not visible externally. In a later two-part publication, the same authors selectively damaged or destroyed the ability of a small number of healthy dogs to swallow normally, presumably as a result of a deficiency of naturally occur-

ring cases, creating what they termed phase-one oropharyngeal dysphagias.8,9

Timing the Openings and Closures of the Throat During Swallowing: Quantifying Pharyngeal Dynamics Using videofluoroscopy to record barium swallows in normal dogs, digitizing the resultant images, and then using purpose-designed software to analyze the sequences frame by frame, Pollard and co-workers were able to precisely time the various openings and closures of the throat as they relate to normal swallowing (Table 35-1).10 Once having established normal values, it then becomes a comparatively simple task to identify delays, accelerations, or asynchronous events in the swallowing sequence that are indicative

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SECTION V ❚❚❚ The Throat, Neck, and Thorax

Table 35-1 • NORMAL VALUES FOR THE DESCRIBED SWALLOWING EVENTS (TIMES MEASURED WITH THE POINT OF EPIGLOTTIC CLOSURE) Swallowing Event Maximal pharyngeal contraction Epiglottic opening Cranial esophageal sphincter opening Cranial esophageal sphincter closure

Liquid Barium (sec)

Barium-Coated Kibble (sec)

0.15

0.15

0.28 0.09

0.30 0.10

0.26

0.33

Table 35-2 • ABNORMAL VALUES FOR THE DESCRIBED SWALLOWING EVENTS (TIMES MEASURED WITH THE POINT OF EPIGLOTTIC CLOSURE): THREE DOGS WITH CRICOPHARYNGEAL ACHALASIA Swallowing Event Maximal pharyngeal contraction Epiglottic opening Cranial esophageal sphincter opening Cranial esophageal sphincter closure

Liquid Barium (sec)

Barium-Coated Kibble (sec)

0.16

0.18

0.32 0.31

0.41 0.37

0.44

0.60

of diseases such as cricopharyngeal achalasia (Table 35-2). Recorded and measured openings and closures related to swallowing were (1) maximum pharyngeal contraction, (2) epiglottic opening, (3) cranial esophageal sphincter opening, and (4) cranial esophageal sphincter closure.

❚❚❚ EXTERIOR FOREIGN BODY CAUSING PARTIAL STRANGULATION An elastic band placed around the neck of a kitten and then forgotten can slowly embed itself beneath the skin, where it soon becomes invisible. Acircumferential mass of scar tissue may then form, which, if extensive enough, can cause indirect tracheal compression. Radiographically, it may be possible to identify the point of obstruction based on localized tracheal stenosis and displacement, especially in the lateral projection.11 Similar constrictions have been reported in the lower limbs of pets, horses, and farm animals, usually involving elastic or wire bands. Abnormalities present in thoracic radiographs of animals with laryngeal or tracheal obstruction may include (1) underinflation on inspiration, (2) overinflation on expiration, and (3) variable combinations of pharyngeal and tracheal expansion or shrinkage (depending on respiratory phase).

❚❚❚ NATURE AND SONOGRAPHIC APPEARANCE OF CERVICAL MASSES Wiser and co-workers described the sonographic appearance of a variety of neck masses in dogs and cats.12 Benign lesions included reactive lymph nodes, hematoma, foreign body granuloma, pyogranulomatous lymphadenitis, arteriovenous fistula, and cellulitis. Malignant tumors consisted of thyroid carcinoma, lymphoma, metastatic leiomyosarcoma, and metastatic carotid body tumor.

❚❚❚ SPECIFIC PHARYNGEAL DISORDERS Traumatic Pharyngeal Perforation A variety of sharp and blunt objects can puncture the pharynx and become embedded in the surrounding tissue, causing development of abscess. Sticks are most common, followed by bones. Foreign body drainage may occur just behind the lower jaw or along the ventral half of the throat. Occasionally, fistulas develop, usually between the pharynx and esophagus, but only rarely involve the larynx. Chronic pharyngeal foreign bodies may lead to the formation of an arteriovenous fistula, especially when associated with one or more unsuccessful surgical explorations.

Pharyngeal Foreign Body A variety of nasopharyngeal foreign bodies have been reported in dogs and cats, including wood, plant awns, bone fragments, fishhooks, and quills13,14 (Figures 35-4 to 35-6). Sewing needles occasionally lodge in the pharynx, often penetrating deeply into surrounding tissue (Figure 35-7). When attached to a long thread, these objects can act as anchors, fixing the proximal part of the thread in the throat while the free-trailing portion acts as a potential lattice on which the intestine may “climb” and subsequently obstruct. Simpson and co-workers described a bizarre case of a dog attempting to swallow a small but live aquarium fish, which subsequently became lodged in its nasopharynx.15 In their account, the authors emphasize the advantages of using soft tissue technique (low kVp) and nonscreen film to obtain optimal image quality; they also stress that a ventrodorsal view is limited by extensive overlap from the skull base, hyoid bones, and proximal cervical spine.

❚❚❚ ABNORMAL LARYNX A variety of laryngeal and paralaryngeal injuries and diseases have been reported, including obstructing foreign bodies, hyoid fractures, laryngeal fractures, laryngeal dislocation, laryngeal perforation, epiglottitis, laryngitis, and tumor. Many of these lesions, because of their size, secondarily involve the pharynx

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359

A

Figure 35-6 • Close-up sonogram of a porcupine quill abscess in the neck of a dog. The quill fragment does not show.

B Figure 35-4 • A, Lateral sonogram of a dog with a stick in its throat (appearing here as a prominent curved white band), firmly lodged in the muscles just caudal to the pharynx, which it pierced earlier. B, Lateral sonogram or a portion of the cervical trachea shows its distinctive appearance, which often serves as a valuable anatomic landmark.

Figure 35-5 • Close-up sonogram of a claw-shaped dermoid cyst in the neck of a cat.

Figure 35-7 • Close-up lateral oblique view of a large sewing needle deeply imbedded in the throat of a cat.

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SECTION V ❚❚❚ The Throat, Neck, and Thorax

and, less often, the trachea. In such circumstances, it is difficult to determine the precise location (and thus the origin) of such lesions with either radiography or ultrasound.

❚❚❚ SPECIFIC LARYNGEAL DISORDERS Everted Laryngeal Saccules Rudorf and co-workers hypothesize that eversion of the lateral saccules (lateral ventricles) is the first step leading to laryngeal collapse, especially in brachycephalic dogs. They further contend that it is possible to identify everted laryngeal saccules using ultrasound, as indicated by a combination of abnormal findings, including (1) abnormally located air (presumably within the displaced saccules), (2) impaired movement of the arytenoid cartilages, and (3) arytenoid immobility. Sonography serves the further purpose of eliminating laryngeal mass or cyst from diagnostic consideration.16

Figure 35-8 • Close-up lateral view of the throat of a cat with a golf ball–sized paralaryngeal abscess.

Table 35-3 • RADIOGRAPHIC APPEARANCE OF CANINE AND FELINE LARYNGEAL AND TRACHEAL TUMORS

Laryngeal Cyst Epiglottic cysts are regularly diagnosed in horses, usually by endoscopy and less often by radiography.17,18 Similar lesions also occur in pets but with a much lower frequency. Cysts may develop on the vocal cords, sonographically appearing as small fluid-filled masses within the lumen of the larynx. Fluid content serves to differentiate cysts from solid masses such as lymphoma and potentially allows ultrasound-guided drainage.19

Species and Tumor Location

Common Tumor Types

Radiographic Appearance

Dog Larynx

Trachea

Epithelial cancers (e.g., rhabdomyoma, carcinoma, squamous cell carcinoma, mast cell tumor) Osteochondroma (sometimes calcified), epithelial cancers

Luminal mass

Luminal mass

Cat

Combined Laryngeal-PharyngealEsophageal Foreign Bodies Irregularly shaped mammalian bones, such as vertebrae or vertebral fragments and bird bones like the furcula (wishbone), can become caught in the throat, lodging partway between the pharynx and larynx, causing gagging and choking.20 Caution: Although it is presumed that laryngeal and tracheal foreign bodies will cause obvious signs of respiratory distress, occasionally this is untrue.

Laryngeal Polyps and Abscesses Laryngeal polyps are unusual in dogs; most are detected incidentally rather than as a result of illness. Radiographically, one might expect signs of cranial airway obstruction (dilated trachea and hyperinflated/hyperlucent lung), depending on the size and number of polyps. Like polyps, laryngeal abscesses are rare in both dogs and cats. In my experience, such lesions usually are found alongside the larynx and less frequently on the inner surface of the epiglottis. In the latter instance, interference with laryngeal closure often leads to choking on food or water and sometimes dyspnea (Figure 35-8).

Larynx Trachea

Lymphosarcoma, squamous cell carcinoma, adenocarcinoma Osteochondroma (sometimes calcified), epithelial cancers

Laryngeal thickening Luminal mass

Laryngeal Tumors Radiology. Carlisle and colleagues described the radiographic appearance of 13 canine and feline laryngeal and tracheal tumors from the files of two veterinary colleges. They reviewed the relevant English literature on the subject and their observations are presented in Table 35-3. Clinical signs seen in the described animals were deemed typical of cranial airway obstruction; surprisingly, however, only one animal exhibited pulmonary hyperinflation, an abnormality long believed (and often taught) to be a reliable radiographic indicator of “upper airway obstruction” in dogs and cats. Newell and co-workers described an unusual case of laryngeal cancer that, although it destroyed the basihyoid bone, failed to produce any signs of illness.21 Ultrasound. Rudorf and Brown described the normal sonographic appearance of the canine and feline larynx

CHAPTER 35 ❚❚❚ Throat and Neck

and the sonographic appearance of a small series of laryngeal tumors, primarily squamous cell carcinomas and lymphomas in cats.22

❚❚❚ SALIVARY GLAND DISEASE Normal Imaging Sonographic Appearance of Normal Salivary Gland. Wisner and co-workers described the normal sonographic appearance of the dog’s neck to include the mandibular salivary gland, which is found near the carotid bifurcation and typically appears as a dark oval structure surrounded by a distinct capsule. The gland has about the same echogenicity as the nearby digastricus muscle but is less echogenic than the thyroid.23 Sialography Background. Although earlier European publications described sialography, most radiologists were first made aware of the diagnostic possibilities of sialography thanks to the work of Harvey.24,25 Procedure. Sialography is the opacification and subsequent radiographic study of the salivary glands and their associated ducts. It is performed by injecting a small volume of dilute, nonionic diagnostic iodine solution into the appropriate salivary duct and then making biplanar radiographs of the gland in question. Cannulation of the various salivary ducts requires a small lachrymal cannula (preferably 25 or 27 gauge), a short extension set, a high-intensity light source, magnification, a means of keeping the animal’s mouth open, and an unconscious animal. Using the smallest possible volume of nonionic, low-viscosity iodine solution minimizes postprocedural glandular swelling and speeds injection time. How Much Contrast Solution to Use When Performing Sialography. As with diagnostic opacification of the urinary bladder or stomach, the volume of contrast used depends on what is being sought. In sialography, for example, is the salivary duct patent? Is it obstructed? Is there leakage? Is a mucocele present? In many cases, these are all possibilities, with some requiring a small volume of contrast to confirm, and others a large volume. The solution to this problem is to customize each examination, as opposed to using a standardized dosage based on body weight. Begin the study with a small test injection based on the estimated volume of the duct (given the size of the animal being examined). Once the patency and integrity of the salivary duct have been established, an additional aliquot can be administered to assess the interior duct system and associated glandular tissue. If a mucocele is detected, then more contrast can be injected if it is necessary to determine its volume precisely. Given the potential of multiple injects, the cannula and extension set should be left in place until the examination is complete, taking

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care not to irritate the delicate tissue of the duct and its opening. An anatomic review of the mandibular, sublingual, parotid, and zygomatic salivary tissues is a necessary prerequisite to successful sialography, even for experts, and especially useful for the less experienced. The relevant ductal anatomy is illustrated in most veterinary anatomy texts, as are the size and location of the associated salivary glands. I strongly advise practicing this procedure before attempting it on a clinical case to acquire both the necessary materials and experience to do a credible job when the time comes. Imaging Findings. As mentioned previously, most salivary gland diseases are inferred from facial swelling and subsequently confirmed with sialography or, less certainly, using ultrasound. Potential abnormalities include (1) ductal obstruction, (2) ductal leakage, (3) mucocele, (4) filling defects suggesting infection, and (5) deformity inferring postsurgical scarring or malignant tumor. Most of the salivary gland infections I have seen have been the result of secondary infections related to either repeated drainage or unsuccessful surgical treatment of mucoceles. Salivary Adenitis Secondary to Sialography. In my experience, sialography, performed with ionic contrast media, invariably causes some amount of glandular pain and swelling, depending on the volume and concentration of contrast solution injected. In some instances, the resultant glandular inflammation is so severe that a fever develops and dogs refuse to eat or drink for a day or two, presumably as a result of pain associated with opening the mouth and chewing. The adverse affects of sialography can be reduced or eliminated by using nonionic contrast media and especially by avoiding overfilling. In observing nonradiologists performing sialography, I have noted that most use an excessive volume of contrast and overfill the gland—a problem compounded by injecting the opposite salivary gland as a normal control. I also noted that those inexperienced in performing sialography often irritate the opening to the salivary duct as a result of repeated attempts at cannulation, which can result in papillary swelling and secondary obstruction. Cannulation is easiest performed with a high-intensity light and magnification, especially for the sublingual and maxillary glands. Additionally, by keeping the gums wet during the procedure, one can avoid atropine and its drying effect. Caution: When discussing sialography with owners, do not forget to mention the potential postprocedural soreness that may affect the animal’s eating and drinking for a few days but will gradually subside. Salivary Gland Necrosis. The following clinical features characterize salivary gland necrosis in dogs: • Hard, painful, swollen glands • Retching, regurgitation, and vomiting (variable)

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• Concurrent esophageal disease, including esophagitis, megaesophagus, and Spirocerca lupi infection • Salivary gland abnormalities that improve when concurrent esophageal disease is treated effectively The precise cause of salivary gland necrosis is not known; however, the temporal association between this disease and a concurrent esophageal disorder suggests the possibility of an efferent vagal reflex as postulated by Schroder and Berry.26 Like the triggering of symmetric long-bone lesions by some lung masses (hypertrophic pulmonary osteopathy), the authors hypothesize that a similar neuronal mechanism may explain salivary necrosis. In this instance, the efferent targets are the salivary glands instead of the limbs. A Salivary Mucocele Background. Salivary duct obstruction predictably leads to a buildup of saliva proximal to the blockage, which eventually extends into the gland if not relieved, causing it to enlarge and cavitate, forming a mucocele. Mucoceles that form alongside the base of the tongue as a result of sublingual or maxillary salivary gland/ duct obstruction are termed ranulas. Less commonly, obstruction of the sublingual salivary duct by a heartworm resulting in a salivary mucocele has been reported in a dog.27 Another rare source of cool, nonpainful swelling in dogs is the branchial cyst (a remnant of the fetal branchial arch system), which appears as a soft, fluctuant facial mass resembling a mucocele.28 Imaging Findings. Most mucoceles are best seen in lateral profile, where superimposition by the jaw and facial bones, customary in ventrodorsal and dorsoventral views, is avoided. A typical mucocele appears as a billowy, internally divided or folded opacified object located in the vicinity of the gland from which it originates (Figure 35-9). Bear in mind that there is nothing to distinguish a mucocele from any other type of facial mass. Ultrasound, on the other hand, usually can distinguish between fluid and solid interiors, although some necrotic tissues may resemble fluid.

❚❚❚ RETROPHARYNGEAL ADENOPATHY Swelling of the retropharyngeal lymph nodes, as with glandular enlargement elsewhere in the body, usually signals localized, regional, or systemic disease. Such swelling occurs commonly in response to a nearby infected wound, a cat bite abscess, for example, and usually disappears shortly after effective treatment. Similar swellings also may be of a more serious nature, such as in the case of malignant lymphoma. Occasionally, a single node may become enlarged without signs of infection or systemic illness. One such example was reported in a cat. A vascular web, termed

B Figure 35-9 • Close-up lateral (A) and ventrodorsal (B) views of an opacified mandibular salivary mucocele in a cat.

by the authors a plexiform vascularization, enveloped a swollen retropharyngeal lymph node.29 In this particular case, the mass was large enough that a radiograph of the throat showed ventral tracheal displacement (indirect evidence of a mass or mass effect), although I suspect this will prove an inconsistent finding.

❚❚❚ PARATHYROID MASSES Wisner and co-workers showed sonography to be an effective means of differentiating benign from malignant parathyroid masses Hyperplastic masses are usually smaller than 4 mm in any dimension, whereas neoplastic masses measure greater than 4 mm. Parathyroid adenomas were described as being round or oval

CHAPTER 35 ❚❚❚ Throat and Neck

and hypoechoic and typically measured between 5 and 7 mm in length.30 Wisner and co-workers also reported the sonographic appearance of parathyroid adenomas as well as parathyroid hyperplasia in dogs with persistent hypercalcemia. Scanned with a small parts transducer (10 MHz), adenomas appeared as medium-sized (5 mm or larger), well-defined, spherical hypoechoic masses located on the cranial pole of one thyroid lobe. Hyperplastic parathyroids were described as small (2 mm), well-marginated, hypoechoic structures. Both lesions appeared relatively dark compared with the nearby thyroid tissue.31 Swainson and colleagues reported a small parathyroid cyst located in the caudoventral aspect of the cranial mediastinum of a healthy 10-year-old cat. The mass was detected initially during screening thoracic radiographs, made as part of a “routine geriatric health check”; its cystic nature was subsequently revealed after surgical removal and histologic assessment.32

❚❚❚ THYROID MASSES AND HYPERTHYROIDISM Dogs Background. Between 1% and 2% of all canine tumors are of the thyroid glands, primarily adenocarcinoma and adenoma, with 85% of these being malignant. Older dogs, especially Beagles, Boxers, and Golden Retrievers, are more likely to develop these tumors than are other breeds. Clinical signs may or may not be present; if so, they are variable and include dysphagia, dyspnea, cough, weight loss, swollen throat, and facial edema. The prognosis for thyroid carcinoma is poor, with metastasis occurring early and far-reaching. Extensive local invasion and incorporation of the adjacent carotid artery or vagosympathetic truck can make surgical removal of the tumor difficult or impossible.33 Imaging Findings Plain Films. If the tumor is large, it may show as a distinct, ventrally convex mass beneath C2-4, causing pharyngeal compression and ventral displacement of the larynx and proximal trachea (Figure 35-10); small lesions are usually invisible. If an esophagram is made, it often reveals compression and displacement. Nuclear Medicine. Broome and Donner reported the detection of regional metastasis from a functional thyroid carcinoma in a dog using iodine-131 (131I), which was not detectable using technetium-99 pertechnetate (99mTcO4); accordingly, the authors recommended the use of 131I for imaging such malignancies.34

Cats Background. Hyperthyroidism is usually a disease of older cats (on average, older than 10 years), with no

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Figure 35-10 • Thyroid carcinoma: Lateral view of the throat and ventral jaw region shows massive soft tissue swelling, which has partially obstructed both the airway and the foodway.

apparent breed or sex predilection. Related clinical abnormalities include (1) weight loss, (2) enlarged or nodular thyroid gland, (3) heart murmur (in about 50 to 60%), and (4) a distinctive gaunt, large-eyed facial expression. The gastrointestinal, pulmonary, and musculoskeletal systems also may be affected, as can the animal’s behavior. Radiography often reveals a characteristic heart enlargement (triangular in ventrodorsal view and enlarged or bilobed in lateral projection) and abnormally high resting T4 level.35 Muscular weakness secondary to hypokalemia also has been reported in hyperthyroid cats but is an inconsistent finding.36 A medium-sized outcome study conducted by Slater and colleagues at Texas A&M following 131I treatment of 237 cats indicated the following: 1. Treatment was successful about 85% of the time. 2. Treatment failed about 5% of the time, but the cat became no worse as a result. 3. About 10% of the cats were cured of hyperthyroidism but as a result of treatment developed another disease, hypothyroidism, and as a result required thyroid supplements.37 Forrest and co-workers, investigating the efficacy of treating feline hyperparathyroidism based on the volume of hyperfunctioning thyroid tissue (volumetric analysis), concluded the following38: • Radioiodine treatment based entirely on the amount of hyperfunctioning thyroid tissue, as determined by pertechnetate scan, may be incorrect for cats with high thyroxine levels or large thyroids. • Oral radioiodine is not recommended as a means of treating hypothyroidism in cats. Adams and co-workers evaluated renal function in cats before and after 131I treatment for hyperthyroidism, identifying what the authors termed “a sig-

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nificant decline in renal function,” an important consideration when treating cats with chronic interstitial nephritis.39 Imaging Findings Plain Films. Radiology is unsuited to thyroid assessment, with the exception of large masses (usually tumors), which may be visualized against the backdrop of the air-filled trachea, or inferred by displacement or distortion of the latter. Ultrasound. Ultrasound can detect thyroid lesions in cats if a high-frequency scanner is used (termed a small parts scanner or transducer).40 Nuclear Imaging. Nuclear imaging, using either 99mTcO4 or isotopes of radioactive iodine (131I,132I), is capable of identifying functional thyroid adenomas and thyroid carcinomas in cats with hyperthyroidism.41,42 The diagnosis of feline hyperthyroidism is based on the increased radioisotopic uptake and symmetric enlargement in one or both lobes of the thyroid. Scintigraphy also can detect and display the spread of thyroid tumors to the thoracic cavity. Additionally, the percent thyroid 99mTcO4 uptake can be calculated to determine if it is increased: a form of quantitative thyroid imaging as well as compared with serum T3 and T4 concentrations.43 Using sodium pertechnetate for thyroid scans; it is also possible to detect pleural fluid, as previously reported in a cat with hyperthyroidism and occult heart failure.44 Pattricelli and co-workers reported detecting mammary gland uptake of sodium 99TcO4 in a cat being evaluated for thyroid surgery. Apparently, the cat had been previously treated with medroxyprogesterone acetate for unrelated problems and, as a result, developed gynecomastia, which accounted for the accumulation of pertechnetate (normally during thyroid scans, only the salivary glands, gastric mucosa, and choroid plexus trap pertechnetate).45

❚❚❚ PUNCTURED TRACHEA AND RUPTURED TRACHEA Background In dogs, the most common cause of peritracheal gas, deep and superficial emphysema, and pneumomediastinum, but almost never pneumothorax, are bites to the throat and neck. Occasionally, a small dog or cat is mauled by a much larger dog and has its trachea ripped completely free from the larynx or torn in two.46 Tracheal rupture also has been reported in cats undergoing general anesthesia, as a result of endotracheal tube overinflation.47,48

Imaging Findings The radiographic abnormalities associated with tracheal perforation are for the most part indirect

and may include (1) air on the exterior surface of the trachea, (2) deep fascial emphysema, (3) pneumomediastinum, (4) pneumoretroperitoneum, and (5) rarely pneumopericardium. In severe cases, subcutaneous air also may be present. With complete severance, localized or regional discontinuity may be evident, often combined with secondary pulmonary hyperinflation.49

❚❚❚ TRACHEAL STENOSIS A variety of diseases have been reported to cause (or potentially cause) tracheal stenosis in dogs and cats: (1) foreign bodies, (2) tumors, (3) granulomas, (4) parasites, (5) torsion, (6) collapse (congenital and acquired), (7) overinflation of an endotracheal tube cuff, (8) tracheostomy, (9) tracheal puncture or laceration, (10) postoperative scarring, (11) prosthetic and paraprosthetic-induced collapse, (12) acute extraluminal hemorrhage, and (13) inflammatory membranes and mucosal sloughs.50

❚❚❚ TRACHEAL DILATION Tracheal dilation is seen most often in puppies and older dogs and is usually of no consequence. Regional dilation may also occur in conjunction with pathologic narrowing or collapse. Typically in such situations the cervical region is dilated, and the thoracic portion is narrowed; conversely, the cervical trachea is collapsed, and the thoracic element dilated. Isolated dilation or ballooning of the cervical part of the trachea is seen occasionally in older dogs being screened for metastasis, animals that rarely show any indication of airway disease. Accordingly, I treat this finding as incidental.

❚❚❚ TRACHEITIS AND TRACHEOBRONCHITIS Although the trachea and bronchi can be come infected, there is almost never any radiographic indication of these diseases. Thus, it makes little sense to radiograph the trachea or lung of a dog or cat to confirm or deny a diagnosis of tracheitis, bronchitis, or tracheobronchitis. A more effective diagnostic approach would be to obtain a transtracheal aspirate and submit it for bacterial culture and antibiotic susceptibility. Angus and co-workers showed that nearly half of the samples obtained from dogs suspected of having caudal (“lower”) respiratory tract disease contained one or more species of aerobic bacteria, especially Escherichia coli. Based on their findings, the authors suggested that amikacin, ceftizoxime, enrofloxin, and gentamicin were all potentially effective as initial treatments for dogs in whom caudal respiratory disease is sus-

CHAPTER 35 ❚❚❚ Throat and Neck

pected before results of susceptibility tests become available.51

❚❚❚ THROAT AND NECK TUMORS Ruppert and co-workers reported a malignant nerve sheath tumor of the right vagosympathetic trunk, which appeared radiographically as a faintly calcified mass ventral to the body of C3. Sonographically, the tumor appeared as a well-defined, heterogeneous mass, featuring internal mineralization as indicated by numerous hyperechoic foci and acoustic shadowing. The dog’s clinical signs included (1) a right-sided Horner syndrome, (2) laryngeal hemiplegia, (3) coughing, (4) gagging, (5) dyspnea, and (6) vomiting. Alternative diagnoses focused on the calcified mass and

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included mineralized granuloma, abscess, and hematoma with secondary involvement of nearby nervous tissue.52 Apair of cervical tumors is illustrated in Figures 35-11 and 35-12.

❚❚❚ TRACHEAL FOREIGN BODY Most foreign bodies found in the throat and neck of dogs fall into one of four groups: (1) sticks and splinters that the dog was chewing, (2) bone fragments, (4) porcupine quills, and (4) plant awns. In the case of sticks and splinters, these usually get caught in the back of the throat, pierce the pharynx, and migrate variable distances along the deep or superficial planes of the neck, in some instances producing large, elaborate sinus tracts.53

A

C

B Figure 35-11 • A, Lateral view of the neck of a dog shows extreme ventral displacement of the larynx and proximal part of the trachea due to a subcervical sarcoma. Close-up ventrodorsal view (B) shows abnormal right lateral arching of the trachea, whereas an esophagram (C) shows ventral displacement and disfigurement, which are not appreciable in the noncontrast images.

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A

B Figure 35-12 • A, Lateral view of the throat and neck of a dog with a huge mass filling its cranial esophagus, outlined ventrally by the trachea and dorsally by a faint line of esophageal gas bubbles. B, A lateral esophagram clearly delineates the entire tumor (an undifferentiated sarcoma).

References 1. Simpson AM, Harkin KR, Hoskinson JJ: Nasopharyngeal foreign body in a dog. Vet Radiol Ultrasound 41:326, 2000. 2. Farrow CS: Radiology of the cat. St. Louis, 1994, Mosby. 3. Simpson AM, Harkin KR, Hoskinson JJ: Nasopharyngeal foreign body in a dog. Vet Radiol Ultrasound 41:326, 2000. 4. Bray JP, Lipscombe VJ, et al: Ultrasonographic examination of the pharynx and larynx of the normal dog. Vet Radiol Ultrasound 39:566, 1998. 5. O’Brien JA, Harvey CE, Tucker JA: The larynx of the dog: its normal radiographic anatomy. J Am Vet Rad Soc 10:38, 1969. 6. Bray JP, Lipscombe VJ, et al: Ultrasonographic examination of the pharynx and larynx of the normal dog. Vet Radiol Ultrasound 39:566, 1998. 7. Watrous BJ, Suter PF: Normal swallowing in the dog: a cineradiographic study. Vet Rad 20:99, 1979.

8. Suter PF, Watrous BJ: Oropharyngeal dysphagias in the dog: a cinefluorographic analysis of experimentally induced and spontaneously occurring swallowing disorders. I. Oral stage and pharyngeal stage dysphagias. Vet Rad 21:24, 1980. 9. Watrous BJ, Suter PF: Oropharyngeal dysphagias in the dog: a cinefluorographic analysis of experimentally induced and spontaneously occurring swallowing disorders. II. Cricopharyngeal stage and mixed oropharyngeal dysphagias. Vet Rad 24:11, 1983. 10. Pollard RE, Marks SL, et al: Quantitative videofluoroscopic evaluation of pharyngeal function in the dog. Vet Radiol Ultrasound 41:409, 2000. 11. Sadler VM, Wisner ER: What is your diagnosis? J Am Vet Med Assoc 216:1723, 2000. 12. Wisner ER, Nyland TG, Matoon JS: Ultrasonographic examination of cervical masses in the dog and cat. Vet Radiol Ultrasound 35:310, 1994. 13. Riley P: Nasopharyngeal grass foreign body in eight cats. J Am Vet Med Assoc 202:299, 1993.

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14. Tyler JW: Endoscopic retrieval of a large, nasopharyngeal foreign body. J Am Anim Hosp Assoc 33:513, 1997. 15. Simpson AM, Harkin KR, Hoskinson JJ: Nasopharyngeal foreign body in a dog. Vet Radiol Ultrasound 41:326, 2000. 16. Rudorf H, Lane J, Wotton P: Everted laryngeal saccules: ultrasonic findings in a young Lakeland Terrier. J Small Anim Pract 40:338, 1999. 17. Koch DB, Tate LP: Pharyngeal cysts in horses. J Am Vet Med Assoc 173:860, 1978. 18. Farrow CS: Larynx, pharynx, and proximal airway. In Thrall DE, ed: Textbook of veterinary diagnostic radiology, ed 3. Philadelphia, 1998, WB Saunders. 19. Rudorf H, Lane et al: Ultrasonic diagnosis of a laryngeal cyst in a cat. J Small Anim Pract 40:330, 1999. 20. Rendano VT, Zimmer JF, et al: Impaction of the pharynx, larynx, and esophagus by avian bones in the dog and cat. Vet Rad 29:213, 1988. 21. Newell SM, Mahaffey MB, et al: Laryngeal adenocarcinoma in a dog. Vet Radiol Ultrasound 35:217, 1994. 22. Rudorf H, Brown P: Ultrasonography of laryngeal masses in six cats and one dog. Vet Radiol Ultrasound 39:430, 1998. 23. Wisner ER, Matoon JS, et al: Normal ultrasonic anatomy of the canine neck. 32:185, 1991. 24. Harvey CE: Sialography in the dog. J Am Vet Rad Soc 10:18, 1969. 25. Harvey CE: Canine salivary mucocele. J Am Anim Hosp Assoc 5:155, 1969. 26. Schroder H, Berry WL: Salivary gland necrosis in dogs: a retrospective study of 19 cases. J Small Anim Pract 39:121, 1998. 27. Henry CJ: Salivary mucocele associated with dirofilariasis in a dog. J Am Vet Med Assoc 200:1965, 1992. 28. Clark DM, Kostolich, Mosier D: Branchial cyst in a dog. J Am Vet Med Assoc 194:67, 1989. 29. Welsh EM, Griffon D, Whitbread TJ: Plexiform vascularisation of the retropharyngeal lymph node in a cat. J Small Anim Pract 40:291, 1999. 30. Long CD, Goldstein RE, et al: Percutaneous ultrasoundguided chemical parathyroid ablation for treatment of primary hyperparathyroidism in dogs. J Am Vet Med Assoc 215:217, 1999. 31. Wisner ER, Nyland TG, et al: Ultrasonic evaluation of the parathyroid glands in hypercalcemic dogs. Vet Radiol Ultrasound 34:108, 1993. 32. Swainson SW, Nelson OL, et al: Mediastinal parathyroid cyst in a cat. Vet Radiol Ultrasound 41:41, 2000. 33. Cohn LA: Radiographic diagnosis. Vet Rad 29:234, 1988. 34. Broome MR, Donner GS: The insensitivity of technetium pertechnetate for detecting metastases of a functional thyroid carcinoma in a dog. Vet Radiol Ultrasound 34:118, 1993.

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35. Broussard JD, Peterson ME, Fox PR: Changes in clinical and laboratory findings in cats with hyperthyroidism from 1983 to 1993. J Am Vet Med Assoc 206:302, 1995. 36. Nemzek JA, Kruger JM, et al: Acute onset of hypokalemia and muscular weakness in four hyperthyroid cats. J Am Vet Med Assoc 205:65, 1994. 37. Slater MR, Komkov A, et al: Long-term follow-up of hyperthyroidism cats treated with iodine-131. Vet Radiol Ultrasound 35:204, 1994. 38. Forrest LJ, Baty CJ, et al: Feline hyperparathyroidism: efficacy of treatment using volumetric analysis for radioiodine dose calculation. Vet Radiol Ultrasound 37:141, 1996. 39. Adams WH, Daniel, et al: Changes in renal function in cats following treatment of hyperthyroidism using 131I. Vet Radiol Ultrasound 38:231, 1997. 40. Wisner ER, Theon AP, et al: Ultrasonic examination of the thyroid gland of hyperthyroid cats: comparison to 99m TcO4 scintigraphy. Vet Radiol Ultrasound 35:53, 1994. 41. Beck KA, Hornof WJ, Feldman EC: The normal feline thyroid. Vet Rad 26:35, 1985. 42. Peterson ME, Becker DV: Radionuclide thyroid imaging in 135 cats with hyperthyroidism. Vet Rad 25:23, 1984. 43. Mooney CT, Thoday KL, et al: Qualitative and quantitative thyroid imaging in feline hyperthyroidism using technetium-99m as pertechnetate. Vet Radiol Ultrasound 33:313, 1992. 44. Broome MR: The appearance of pleural effusion with sodium pertechnetate thyroid scintigraphy. Vet Radiol Ultrasound 34:363, 1993. 45. Patricelli AJ, Lappin MR, et al: Mammary gland uptake of sodium Tc-pertechnetate in a cat with a drug-induced gynecomastia. Vet Radiol & Ultrasound 40:87, 1999. 46. Cayler KB, Moore RW: What is your diagnosis? J Am Vet Med Assoc 205:561, 1994. 47. Hardie EM, Spodnick GJ, et al: Tracheal rupture in cats: 16 cases (1983–1998). J Am Vet Med Assoc 214:508, 1999. 48. Mitchell SL, McCarthy et al: Tracheal rupture associated with intubation in cats: 20 cases (1996-1998). J Am Vet Med Assoc 216:1592, 2000. 49. Barber DL, Rawlings CR: Radiographic diagnosis. Vet Rad 22:258, 1981. 50. Smith MM, Gourley, et al: Management of tracheal stenosis in a dog. J Am Vet Med Assoc 196:931, 1990. 51. Angus JC, Jang SS, Hirsh DC: Microbiological study of transtracheal aspirates from dogs with suspected lower respiratory tract disease: 264 cases (1989-1995). J Am Vet Med Assoc 210:55, 1997. 52. Ruppert C, Hartmann K, et al: Cervical neoplasia originating from the vagus nerve in a dog. J Small Anim Pract 41:119, 2000. 53. Duffy MH, Leveille R, Smeak DD: What is your diagnosis? J Am Vet Med Assoc 213:1557, 1998.

C h a p t e r

3 6

Thoracic Radiographic Disease Indicators Proficient diagnosis of canine and feline chest disease is predicated on recognizing individual thoracic radiographic disease indicators (RDIs) and interpreting their patterns. Of equal importance, however, is identifying normal anatomic and physiologic variants that can mimic thoracic disease, innocuous findings that are termed false RDIs.

❚❚❚ NORMAL ANATOMIC VARIANTS THAT RESEMBLE THORACIC RDIS A myriad of anatomic variants exist in the dog and cat, which under certain circumstances can lead to an incorrect radiographic diagnosis. Table 36-1 (including Figures 36-1 to 36-5) lists some common anatomic variants and the RDIs they resemble.1,2

❚❚❚ NORMAL PHYSIOLOGIC VARIANTS THAT RESEMBLE THORACIC RDIS Expiratory Films Expiratory films are extremely treacherous in that they can mimic various heart and lung diseases, the most serious of which are congestive heart failure (Figure 36-6) and pneumonia (Figure 36-7). Because of the decreased lung volume during expiration, the cardiacthoracic ratio increases, falsely making the heart appear enlarged. Because injured animals, especially those with chest trauma, often take shallow breaths, resulting in expiratory films, one should learn to interpret such images and to acknowledge diagnostic limitations as necessary.

Postural Atelectasis During general anesthesia, often within a few minutes of being anesthetized, the dependent half of the lung 368

partially collapses; concurrently, the upper half of the lung hyperinflates to compensate for the volume lost from the lower lobes. A cardiac shift and increased lung density are the consequences (Figures 36-8 and 36-9).

❚❚❚ POSITIONAL VARIANTS THAT RESEMBLE THORACIC RDIS Radiography Numerous position-related variations in thoracic films of dogs and cats can resemble heart and lung disease. With practice, these variants can be recognized and taken into consideration when the films are analyzed. The most common of these are compared in Table 36-2 (including Figures 36-10 to 36-14).

Computed Tomography Ahlberg and co-workers studied the effect of variable thoracic positioning on the tomographic (CT) appearance of the lungs.3 They determined that the dorsoventral (DV) position is best because it avoids vertical attenuation gradients, which can simulate or mask lung disease.

❚❚❚ TECHNICAL VARIANTS THAT RESEMBLE THORACIC RDIS Light films accentuate the pulmonary vasculature, the principal source of lung density. When combined with expiratory filming, this combination of technical faults can resemble a myriad of thoracic diseases (Figure 36-15, A and B). Dark films, on the other hand, create the impression of overinflation or, in a trauma setting, pneumothorax (Figure 36-15, C and D).

CHAPTER 36 ❚❚❚ Thoracic Radiographic Disease Indicators

369

A

Figure 36-2 • Diagnostic pitfall: Close-up lateral view of the ventral thorax of a dog shows a thick, gently curving diagonal band crossing the lower portion of the heart caused by skin folds.

B Figure 36-1 • Diagnostic pitfall: A, Lateral view of the thorax of a healthy but obese dog shows poor heart definition ventrally, mimicking pleural fluid. B, Dorsoventral view shows a widened cranial mediastinum resembling a mass but that is actually accumulated fat.

❚❚❚ THORACIC RADIOGRAPHIC DISEASE INDICATORS (THORACIC RDIS) Extrapleural Lesion (Extrapleural Swelling) The concept of an extrapleural space is, admittedly, somewhat abstract; but because it appears in the literature and does possess a measure of diagnostic utility, I have included it here. Meyer defined the extrapleural space as follows: “The potential space between the parietal pleura and the body wall or diaphragm, which communicates with the intermuscular fascia of the body via the thoracic inlet.”4 More simply, especially when considering the origin of a mass, I prefer to think of this region as the inner surface of the chest wall, which, admittedly, includes the parietal pleura. In my experience, lesions in this location are usually malignant, often originating in the adjacent muscle or rib, but only occasionally exhibit the characteristic broadly based convexity said to be the hallmark of such lesions.

Table 36-1 • NORMAL ANATOMIC VARIANTS (FALSE RDIs) THAT CAN MIMIC THORACIC RDIS Normal Variant

Mimicked RDI

Widened cranial mediastinum due to fat (Figure 36-1) Extracardiac fat, especially ventrally (Figure 36-1) Left caudal lateroventral aspect of the mediastinum (once mistakenly called the cardiophrenic ligament)1 Mammary gland nipple superimposed on lung2 Axillary skin folds (Figure 36-2)

Cranial mediastinal mass such as lymphoma or thymoma

Arching of the dorsal aspect of the caudal lung lobes of cats, as seen in lateral projection (Figure 36-3) Kinked trachea (Figure 36-4) Tissue defects or forelimb amputation (Figure 36-5)

Pleural fluid, pulmonary consolidation Pleural fluid between accessory and right caudal lung lobes, thickened pleura Pulmonary nodule Pleural fluid, lung margin (suggesting collapse especially when pneumothorax is suspected) Pleural fluid

Underlying cranial mediastinal mass Relatively hyperlucent right or left cranial lung field (depending on the side of involvement) resembling pneumothorax

RDI, Radiographic disease indicator.

Text continued on p. 376

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Table 36-2 • POSITIONAL VARIANTS (FALSE RDIs) THAT CAN MIMIC THORACIC RDIs Positional Variant

False RDI

Scapular overlay of one side of the cranial aspect of the thorax (usually associated with an oblique DV or VD projection) (Figure 36-10)

Pulmonary consolidation

One side of lung appears abnormally dense, the other abnormally lucent (always associated with an oblique or twisted DV or VD projection) (Figure 36-11)

In the context of trauma the lucent side of the chest resembles pneumothorax; the dense side of the thorax simulates pleural fluid or pulmonary hemorrhage

Forceful limb traction in cats during thoracic radiography may cause the thorax to assume a tapered appearance, which in turn increases the relative height and sternal contact of the heart (Figure 36-12)

Heart enlargement

Lateral thoracic obliquity projects the spine closer to the heart base, falsely increasing the vertical cardiac-thoracic ratio (Figure 36-13)

Heart enlargement

Flexion of one or both forelimbs during thoracic radiography results in varying amounts of elbow superimposition over the cranioventral portion of the chest (Figure 36-14, A)

Lung mass or consolidation; edema

When combined with expiration, forelimb superimposition can produce a particularly ominous appearance (Figure 36-14, B) RDI, Radiographic disease indicator; DV, dorsoventral; VD, ventrodorsal.

A

B Figure 36-3 • Lateral (A) and lateral close-up (B) views of the thorax of a cat show a gentle downward arching of the caudal lung lobes just beneath the spine—a normal anatomic variant caused by the adjacent muscle and fat. Occasionally, this normal finding is mistakenly attributed to pleural fluid.

A

B Figure 36-4 • Diagnostic pitfall: Close-up lateral views of the thorax centered over the cranial mediastinum. A, In the first film, the dog’s head and neck are arched backwards, causing a temporary kink in the trachea. B, In a following image, a more conventional extended position, the tracheal deformity has disappeared.

CHAPTER 36 ❚❚❚ Thoracic Radiographic Disease Indicators

A

371

B

Figure 36-5 • Diagnostic pitfall: Much of the density found normally in the cranial part of the thorax is attributable to the upper half of the front legs, as exemplified by these lateral (A) and ventrodorsal (B) images of a dog with an amputated left forelimb.

A

B Figure 36-6 • A, Diagnostic pitfall: Lateral thoracic radiograph of an older dog with asymptomatic mitral insufficiency made during full expiration. If the expiratory nature of this film was not recognized, and in the context of heart enlargement and a murmur, this dog might be misdiagnosed as heart failure. B, Second thoracic radiograph made immediately after the first, but during mid inspiration shows an enlarged heart but no signs of failure.

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B

A Figure 36-7 • A, Diagnostic pitfall: Initial lateral thoracic radiograph of a dog suspected of having pneumonia made on full expiration shows apparent consolidation caudal to the heart. B, Subsequent thoracic film shows that the suspected consolidation has disappeared.

B

A Figure 36-8 • Diagnostic pitfall: A, Close-up dorsoventral view of the thorax of a dog under general anesthesia shows increased density and a volume loss on the right side. The heart seems enlarged. B, Subsequent image made after the dog was bagged shows a clear lung and a normal heart.

CHAPTER 36 ❚❚❚ Thoracic Radiographic Disease Indicators

Figure 36-9 • Diagnostic pitfall: Close-up dorsoventral oblique view of the thorax shows the heart against the right side of the rib cage, the result of a predictable volume loss after prolonged right-sided recumbency while under gas anesthesia.

Figure 36-11 • Diagnostic pitfall: Ventrodorsal view of a dog recently hit by a car shows a relatively translucent left lung resembling pneumothorax. Actually, the left lung is normal, appearing overly dark because of the animal’s oblique position. Learn to recognize this common variant, and avoid unnecessary and painful retakes in trauma patients.

373

Figure 36-10 • Diagnostic pitfall: Dorsoventral view of thorax in which the scapulae overlie the cranial and middle lung lobes, innocent findings that can be mistaken for lung bruising, especially if such injuries are anticipated.

Figure 36-12 • Diagnostic pitfall: Lateral thoracic radiograph of a cat shows distinctive streamlined triangular appearance caused by forceful traction while being restrained. The overinflated appearance of the lung is an illusion and should not be mistaken for asthma.

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A

B Figure 36-13 • Diagnostic pitfall: Notice the differences in these lateral thoracic radiographs made of a healthy dog, minutes apart. One film (A) appears normal in all respects; the other (B) is too light, accentuating the normal blood vessels and bronchi, possibly prompting unwarranted concern about heart or airway disease. Oblique positioning makes the heart seem taller and rounder and often alters the appearance of the diaphragm. Superimposition of a forelimb mimics a lung or mediastinal mass.

B

A Figure 36-14 • Diagnostic pitfall: A, Lateral thoracic radiograph of an older dog undergoing a preanesthesia screen exemplifies how a light, decentered, expiratory film (in the context of heart enlargement resulting from asymptomatic endocardiosis) can closely resemble hilar edema and thus heart failure. B, The film was repeated, showing that the “edema” has disappeared.

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B

A

C

D

Figure 36-15 • Diagnostic pitfall: These films are all of the same dog, made minutes apart. A and B, The first set is flawed in two respects: the films are underexposed (too light) and were made during expiration. These faults combine to exaggerate the degree of heart enlargement and prominence of the lung vasculature, observations that might incorrectly lead to a diagnosis of heart failure. C and D, The second set of images, made with a darker technique and better inflation, more accurately portrays the thoracic anatomy in this individual and are less likely to lead to a misdiagnosis.

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Pleural Fluid

Imaging Findings

Background. Lord and co-workers were among the first to investigate the radiographic appearance and behavior of fluid in the pleural space of normal medium-sized dogs. They concluded the following5: • As little as 100 mL of saline was visible in both standard thoracic projections (lateral and ventrodorsal [VD]). • The mediastinum did not prevent the saline from freely moving from one side of the chest to the other. • In lateral projection, the fluid collected between the sternum and peripheral portion of the lung, causing lobar retraction, and giving the edge of the lung a distinctive scalloped appearance. • In the VD view, fluid accumulated between the diaphragm and caudodorsal aspect of the lung, causing blunting of the normally sharp costophrenic angles. • Also in the VD view, fluid collected between the middle and adjacent lung lobes, forming characteristic right- and left-sided pleural fissure lines. • In the erect VD projection (see the section on postural radiography for further details), as little as 50 mL of fluid was evident in the dependent portion of the chest between the lung and diaphragm. • The standing lateral view did not reveal small volumes of pleural fluid as well as did the erect position. • Decubitus films were capable of showing fluid volumes of as little as 100 mL. Causes of pleural fluid are listed in Table 36-3.

Radiology. The radiographic identification of pleural fluid depends most on its volume and, to a lesser extent, its location (Figures 36-16 and 36-17). In general, standard radiographic views (right and left lateral, DV, and VD) rarely show small volumes of pleural fluid; however, medium and large fluid volumes are usually visible, especially in high-quality images. Postural radiographs, particularly the decubitus view, are even more sensitive. Unless free pleural air is present, there will be no fluid levels in recumbent images, but there will be fluid zones in standing laterals (a progressive increase in thoracic density from spine to sternum related to dependent fluid, transitional atelectasis, and compensatory hyperinflation). Abnormalities associated with pleural fluid can include: • Increased density between the sternum and lung, often obscuring the ventral border of the heart • A generalized veiling of the lung—a subtle increase in lung density caused by widely distributed pleural fluid that results in decreased vascular detail but no visible bronchi (air bronchograms) • Lobar tracing (fluid outlining individual lung lobes) • Bandlike or narrow triangular densities situated between lung lobes • Clustering of partially collapsed lung lobes around the hilus as a result of flotational effect • Retraction of the outer lung margins from the sternum and rib cage Meyer, in her review of pleural fluid, has attempted to distinguish specific types of fluid on the basis of radiographic characteristics11 (Table 36-4).

Table 36-3 • CAUSES OF PLEURAL FLUID Cause

Comment

Accidental overhydration Chest trauma Diaphragmatic hernia

Not as common as generally believed Blood and occasionally chyle from a ruptured thoracic duct Blood from torn diaphragm; transudation from incarcerated liver or spleen; transudation from omentum Common in cats, occasionally seen in dogs

Heart failure Hypoproteinemia Mediastinal tumor Pericardiectomy Pleural mesothelioma Ruptured thoracic duct Thrombosis of the cranial or CVC

Warfarin poisoning CVC, Caudal vena cava.

Pleural effusion has been reported in approximately 1 of every 3 dogs after pericardiectomy, irrespective of cause6 Thrall and Goldschmidt reported 4 cases of canine pleuromesothelioma, all of which had pleural fluid7 Thrombosis of CVC is usually secondary to a variety of diseases including immune-mediated disease, endotoxic shock, protein-losing enteropathy, various kinds of cancer, and heart disease. Thrombocytopenia and central venous lines predispose. CVC thrombi may be identified with ultrasound. Most dogs with this condition die or are euthanized within 3 weeks of its discovery.8 A CVC thrombus has been reported in a dog with leishmaniasis, apparently having formed secondary to related glomerulonephritis (with nephritic syndrome) and hypercoagulability.9 Blood

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B A

C

D Figure 36-16 • Pyothorax: A, In the lateral view, fluid decreases the overall detail of the lung while increasing the density of the heart. The ventral half of the diaphragm—or more accurately, the pulmonary-hepatic interface because the diaphragm cannot actually be seen— has also been obscured by fluid. The seemingly tall heart is an illusion, created by fluid, flotational effect on the lungs, and the expiratory nature of the image. B, Ventrodorsal view shows pleural exudate concealing portions of the heart and lungs. The triangular shape of the heart suggests that one or middle lobes are partially consolidated, forming bilateral composite densities (cardiopulmonary silhouette sign). Left (C) and right (D) decubitus views, made with the dog on its side, and using a horizontally directed x-ray beam, show consolidation of the left middle lobe, which was later determined to be the source of the pleural infection.

Table 36-4 • RADIOGRAPHIC CHARACTERISTICS OF PLEURAL FLUID Fluid Type

Fluid Location

Chyle Exudate Hemorrhage

Bilateral Unilateral Either unilateral or bilateral Bilateral

Transudate

Fluid Mobility

Pleuritis(?)

Lobar Edges

Body Wall Involvement

Fixed Fixed Mobile

Yes Yes No

Rounded Rounded Variable

Yes No Yes

Mobile

No

Sharp

No

Modified from Meyer W: Radiography review: pleural effusion, J Am Vet Rad Soc 19:75, 1978.

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Figure 36-18 • Thoracic sonogram shows a triangular fluid

A

pocket in the ventral aspect of the pleural cavity just in front of the diaphragm and liver. The large, dark oval object is the gallbladder. Aspiration and analysis showed the fluid to be a transudate.

Figure 36-19 • Thoracic sonogram shows a ragged fluid pocket between partially atelectatic lung lobes. Aspiration and analysis showed that the fluid was chyle.

B Figure 36-17 • Lateral (A) and ventrodorsal (B) views of cat with chronic bacterial pleuritis. Like the cat in Figure 6-31, the principal source of the pleural infection is the left middle lung lobe, which is consolidated. The undulant appearance of the outer lung margins, especially on the right side, strongly suggests restricted inflation, typically caused by a pleural peal (a thick coating of fibrin on the visceral pleura).

Ultrasound. Ultrasound is more capable than radiography, even postural films, of identifying small amounts of pleural fluid. In most animals, scanning the underside of the chest while the animal lies on its side is most revealing (Figures 36-18 and 36-19). Standard and Postural Radiography Versus Sonography. Groves and Ticer showed that in the context

of pleural fluid, a VD projection of the thorax will reveal more of the heart, cranial aspect of the mediastinum, and cranial lung lobes than will a DV view. This improved clarity is due to the natural incline of the dorsal portion of the thorax, which allows the fluid to run caudally and away from the heart and lung when the dog is placed on its back.10 Among the most readily available methods of imaging small volumes of pleural fluid, ultrasound is usually the most sensitive, followed closely by postural radiography (Figure 36-20).

Pneumothorax (Free Pleural Air) Background. Free air in the pleural space, between the lung and interior surface of the thoracic cavity, is termed pneumothorax.Air located between the lung and diaphragm, exterior surface of the heart, or mediastinum also qualifies as a pneumothorax.12

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A

379

B

Figure 36-20 • Diagnostic pitfall: A, Ventrodorsal radiograph of a dyspneic cat shows heart enlargement and pleural fluid compatible with heart failure. B, An erect film made with a horizontal x-ray beam moves the fluid to the dependent part of the pleural space, revealing a cranial mediastinal mass and a normal heart.

Reported Causes of Pneumothorax. Reported causes of pneumothorax include the following:13 • Abscess (primary versus secondary lung abscesses; see text) • Endocarditis (secondary lung abscess with rupture); note that 75% of dogs with endocarditis have a positive blood culture • Fractured extrapulmonary bronchus • Heartworm • Improperly placed or dislocated chest drain • Lobectomy • Lung or mediastinal biopsy • Necrotizing bacterial pneumonia • Neoplasia (bronchoalveolar carcinoma) • Penetrating chest wound • Pulmonary granulomas • Ruptured bullae • Ruptured lung lobe • Thoracotomy • Torn pleural adhesion Imaging Findings Radiography. Like pleural fluid, the radiographic detection of pleural air is largely volume dependent; the more there is, the easier it is to see (Figures 36-21 and 36-22). Also, as with fluid, pleural air is best detected with postural films, such as the standing lateral or decubitus views (Figure 36-23). Caution: Skin folds can be mistaken for a pneumothorax.14

Aronson and Reed advise taking a DV rather than a VD view (in addition to a right or left lateral projection) when radiographing the chest for a suspected pneumothorax. Their reasons for this recommendation are twofold: first, the DV position is usually more comfortable for the animal; second, the DV view is more likely to reveal free pleural air than a VD view.15 Computed Tomography. Walker and co-workers described the CT appearance of experimentally induced, progressive pneumothorax in anesthetized bloodhounds. They related the diminishing lung volumes to heart rate, blood pressure, and arterial oxygen/carbon dioxide saturation.16 A word of caution: Experimental studies using normal dogs, in this instance to evaluate the radiographic appearance of pneumothorax, usually fail to fully, and in some instances accurately, depict naturally occurring disease. This is because the considerable influence of concurrent abnormalities such as pulmonary contusion, lung collapse, and chest wall bruising, injuries that strongly influence lung inflation (and thus the typical radiographic appearance of pneumothorax), have not been measured and cannot be reliably predicted. Thus the experimental context is overly simplified.

Pneumomediastinum (Free Mediastinal Air) An intrapulmonary rupture usually causes pneumomediastinum, with the escaped air subsequently dis-

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A

B

D

C Figure 36-21 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a dog in which a primary lung tumor was discovered accidentally during abdominal radiography. Following removal of the tumor, radiographs showed underinflation (pain-related), bilateral middle lobe atelectasis, a small-to-medium volume of pleural fluid, and a possible pneumothorax, which subsequently was confirmed with postural films. Right decubitus film shows hyperlucent region immediately cranial to diaphragm (C). Close-up of the same area (D) shows faint triangular density representing partially collapsed caudal lobe surrounded by free pleural air.

secting retrograde along the pulmonary veins into the mediastinum. Throat wounds are another common source of free mediastinal air. Iatrogenic causes of pneumomediastinum include “tracheal wash,” tracheostomy, dislodged chest drains, pharyngostomy tubes, and the like (Figure 36-24). Uncommon avenues of mediastinal air include bronchial leakage, avulsion or fracture, and dissection from distant wounds via communicating pathways such as the retroperitoneal space.

Cardiac Shift (Mediastinal Shift) Movement of the heart from its normal midline position toward either side of the chest is termed a cardiac

or mediastinal shift, a relocation that often provides important information about a diseased or traumatized lung lobe. Examples of cardiac shift are shown in Figures 36-25 to 36-27; causes of mediastinal shift are listed in Table 36-5.17

Pulmonary Consolidation Lung, or more precisely alveolar, consolidation occurs when the distal air spaces have their contents replaced by fluid or cells, typically producing visible bronchi, also termed an air-bronchogram sign (Figure 36-28). Although these consolidative substances have a similar radiographic appearance (varying shades of gray, depend-

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A

Figure 36-22 • Large-volume pneumothorax and compression atelectasis caused by multiple transthoracic fine-needle biopsies.

B Figure 36-24 • Lateral (A) and ventrodorsal (B) thoracic radiographs of an acutely dyspneic cat that was breathing normally 24 hours earlier, before the installation of a pharyngostomy tube. The films show mediastinal fluid and pneumomediastinum caused by dislodgement of the tube.

Figure 36-23 • Decubitus view of a 4-month-old Beagle puppy diagnosed in another hospital as having “spontaneous pneumothorax” shows collapsed, uppermost lung lobe blending with the adjacent heart shadow, surrounded by free pleural air.

ing on volume), they cannot be differentiated from one another: edema, blood, and pus all look the same. Their distribution within the lung, however, combined with a history, physical, and other radiographic abnormalities, often suggests probable cause, a process termed presumptive contextual diagnosis. For example, a fully vaccinated 3-month-old puppy with no history of injury stops eating, begins to cough, and develops a fever. Thoracic radiographs reveal a consolidated right middle lung lobe. Contextually, this is probably pneumonia (Figure 36-29). If a 12-year-old dog presented with similar signs but without fever and whose chest films showed symmetric consolidation and cardiovascular enlargement, the

Figure 36-25 • Ventrodorsal radiograph of a dog with chronic pneumonia causing adhesive alveolitis shows a severe right-sided volume loss commensurate with cardiac shift.

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A A

B B

Figure 36-26 • Tension pneumothorax in an injured kitten: A, In the lateral view, the completely collapsed caudal lobe appears as a distinctive, claw-like dorsal opacity; the heart seems to float in a nearly translucent thorax. B, The dorsoventral projection shows the heart pinned against the left side of the rib cage as a result of elevated pleural pressure.

Figure 36-27 • Lateral (A) and dorsoventral (B) thoracic radiographs of a dog with a herniated stomach as a result of being hit by a truck. Filled almost entirely with air and distended to the point that no reggae are visible, the displaced stomach, or more particularly its air content, resembles a tension pneumothorax, a potential misdiagnosis strengthened by a pronounced cardiac shift.

contextual diagnosis would be heart failure. Potential contents of consolidated lung include the following: • Water Hydrostatic pulmonary edema Heart failure Overhydration Increased capillary permeability Inflammatory edema Chemical pneumonitis Eosinophilic pneumonitis • Blood Traumatic contusion and laceration Hemorrhagic diathesis

• Pus Pneumonia • Cells Tumor • Protein Alveolar proteinosis (the lining of an alveolus with a thin layer of protein, which renders surfactant ineffective) • Inhalation Near drowning Fresh water Seawater

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Table 36-5 • CAUSES OF A CARDIAC (MEDIASTINAL) SHIFT Cause

Comment

Arterial thrombosis

Acute pulmonary arterial thrombosis may lead to a secondary volume loss, followed by a cardiac shift in the direction of the devascularized lobe. Heart passes through a large lateral tear in one side of the pericardium, usually the result of a severe deceleration injury. This is more a cardiac misdirection than a true mediastinal shift. Cats with allergic bronchitis (asthma) may transiently or permanently sustain widespread bronchial blockage (presumably from mucoid or mucopurulent plugging) leading to a volume loss and a cardiac shift. If the proximal part of a major bronchus becomes obstructed, it will cause the associated lung lobe to collapse. Predictably, a resultant cardiac shift will be in the direction of the atelectatic lobe. Chronic unilateral lung collapse may lead to some degree of cardiac shift to the effected side of the thorax. Large abdominal organs, displaced into the chest as a result of a ruptured diaphragm, particularly an air-filled stomach, often cause a marked cardiac shift away from the mass effect. Heart is fixed to chest wall.

Asymmetric pericardial hernia Bronchial obstruction (multiple medium and small diameter bronchi) Bronchial obstruction (single mainstem bronchus) Chronic pulmonary atelectasis Diaphragmatic hernia Pericardial adhesion to chest wall or collapsed lung lobe adhered to chest wall Pleuritis Pneumothorax Postinflammatory fibrotic lung mass Postural atelectasis

Primary lung tumor (mass effect) Secondary lung tumor Tension pneumothorax

Unilateral pleuritis may cause a cardiac shift toward the pleuritic lobe or lobes. As with postural atelectasis, a pneumothorax is usually associated with a volume loss in the damaged lobe or lobes, compensatory hyperinflation of the opposite side of the lung, and displacement (shift) of the heart in the direction of the injured lung. Chronically asthmatic cats occasionally develop fibrotic lung masses or lobes, possibly due to endogenous lipid pneumonia. The resultant underinflation (especially in the case of a caudal lobe) may lead to a cardiac shift in the direction of the mass. This is the most common cause of a mediastinal shift. Following prolonged lateral recumbency the lowermost lung becomes partially atelectatic, while the uppermost lung becomes hyperinflated. This causes the heart to shift toward the dependent portion of the lung due to the resultant volume loss and, to a lesser extent, because of the increased pressure from the opposite lung field. These effects are both accelerated and exacerbated by sedation, and especially by general anesthesia. Occasionally, a primary lung tumor becomes large enough to displace the heart to the opposite side of the chest. Some lung tumors may so reduce the air content of the diseased lobe that a cardiac shift results secondary to volume loss. If a lung lobe is badly damaged, it may leak enough air into the surrounding chest cavity to totally collapse the lung on the injured side, and displace the heart in the direction of the uninjured lung.17

Pulmonary Atelectasis

is consolidation, an extremely important diagnostic consideration given that both abnormalities can appear as abnormal lung opacities. Atelectasis can be broadly divided into interior and exterior types. Radiographically detectable interior atelectasis usually is caused by bronchial obstruction, resulting in partial or complete collapse of the associated lung lobe. Exterior atelectasis results from broadbased pressure such as that found with medium and large volumes of extrapleural air and fluid. For a detailed account of the pathophysiologic basis of lunglobe collapse featuring many excellent radiographic examples, see the article by Lord and Gomez.18

Most simply, pulmonary atelectasis may be thought of as some degree of lung collapse that can range from partial to complete. Like alveolar consolidation, atelectasis is associated with air loss. Unlike consolidation, however, there is no replacement of the lost air by edema, blood, pus, and so on. Accordingly, atelectasis is more likely to be associated with a cardiac shift than

Radiology. Pulmonary atelectasis can result from within or without the lung. Interior atelectasis can occur at the alveolar level as a result of pneumonia (Figure 36-30) or more proximally as a result of bronchial obstruction. Exterior atelectasis usually is caused by compression from an adjacent mass or by surrounding air or fluid (Figure 36-31).

Other (bucket of bleach, toilet filled with cleaner) Blood Esophageal or stomach contents Infected oropharyngeal material Ingested, vomited, and subsequently inhaled liquid poisons To remember the preceding list, use the mnemonic device: Why blue peacocks catch pretty insects. Water (W) Why • Blood (B) blue • Pus (P) peacocks • Cells (C) catch • Protein (P) pretty • Inhalation (I) insects.

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A Figure 36-28 • Bilateral inhalation pneumonia secondary to acquired megaesophagus: Dorsoventral view clearly shows the principal bronchi, structures that are normally only faintly seen. Because of surrounding lung consolidation, the bronchi are now outstanding. This form of heightened bronchial visibility, brought about by the marked contrast between the consolidated lung and adjacent bronchus, is termed the air-bronchogram effect, or simply an air bronchogram.

Solitary Lung Nodule Solitary lung nodules almost never cause discernible illness and, as a result, are almost always incidental findings. A variety of radiographic procedures have been used for the evaluation of animals with a single lung nodule (solitary pulmonary nodule). Currently, plain chest films and CT (where available) are of most clinical value. Once identified, diagnosed, but not removed, the purpose of radiographically monitoring a pulmonary nodule is (1) to see whether the nodule has changed, in particular, whether it has grown; and (2) to identify any new nodules.

B Figure 36-29 • Thoracic radiographs of a 3-month-old German

Multiple Lung Nodules Multiple pulmonary nodules may cause no clinical signs or, at most, an increase in breathing rate. In other instances, there is pronounced dyspnea but rarely any cough. Dogs with metastatic hemangiosarcoma may develop a secondary hemothorax. Differential Diagnosis of Multiple Lung Nodules • Bacterial abscesses • Cross-sectional projection of costochondral junctions (particularly well seen when calcified) • Cross-sectional projection of nipples (may or may not appear symmetrically paired in DV or VD views; will not appear in lateral projection)

Shepherd puppy with pneumonia show what appears to be an abnormally shaped heart in the lateral view (A), the result of extensive left-sided lung consolidation that is obvious in the opposite view (B).

• Cross-sectional projection of normal lung vessels, with the largest nodules arrayed about the hilus where the vasculature is largest • Cross-sectional view of secretion-filled bronchi in asthmatic cats • Cross-sectional view of secretion-filled bronchi in bronchiectatic dogs • Cross-sectional view of small skin tumor • Fluid-filled (edema, blood, exudate) alveolar sacs (the opposite appearance of an air alveologram);

A Figure 36-30 • Interior atelectasis of much of the right lung is responsible for a pronounced right cardiac shift, which is impossible to appreciate in the lateral view (A) but obvious in the ventrodorsal projection (B). In the same view, the diaphragm appears abruptly angled to the right, a common feature of volume loss.

B

A

B C Figure 36-31 • A and B, Exterior atelectasis caused by pleural fluid in a cat referred to our internal medicine service for heart failure. On viewing the outside images, medicine suspected a mass based on widening of the cranial mediastinum, a finding that disappeared once localized fluid was displaced from the area of interest with the aid of an erect postural film (C).

386

• • • •

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most commonly seen in early heart failure, just after interstitial phase of pulmonary edema formation) Fungal granulomas (calcification infers healed lesions) Inflammatory parasitic foci (occasionally calcified) Pulmonary metastasis (only rarely calcified) Pulmonary osteomas (also sometimes referred to as pulmonary ectopic bone formation)

Radiology. Diffuse pulmonary nodules (typically spherical objects, 0.5 cm in diameter or smaller) are usually indicative of metastatic lung cancer (Figure 36-32), although there are other explanations, as already detailed. In general, the greater the number of lesions, the more likely they are to be similar in size and shape; conversely, the fewer the number of lesions, the greater their diversity. Such lesions rarely become calcified.

A

Large Thoracic Masses Large single lung masses, especially when identified incidentally, are usually primary lung tumors (Figure 36-33). Other solitary lesions, such as plant awn abscesses, usually are associated with regional atelectasis or consolidation, pleural fluid, cough, and obvious illness. Cysts and discrete hematomas are rare. Mycotic pneumonia and pulmonary granulomatosis usually feature multiple masses. B

Cystic and Cavitary Lung Lesions Background. A forceful blow to the chest, pulmonary abscessation, certain chemicals (including stomach contents), and some parasites are examples of disorders that are capable of producing “holes in the lung” or, as they are also known, cavitary lung lesions. In the case of trauma, such lesions result from a sudden increase in intrapulmonary pressure, somewhat like a small explosion within the lung, which forces the ruptured alveolar walls outward in all directions, forming a thin-rimmed, hollow sphere or oval-shaped object. Within seconds, the resultant cavity fills with blood, which usually is reabsorbed in a day or two or, alternatively, drains through communicating bronchioles. In the latter instance, air may enter the cavity, which combines with the remaining blood, forming a fluid level. Cavitary lung lesions or abnormal lung spaces can occur anywhere in the lung.19 Those located just beneath the surface are termed blebs; those lying in the depths of the lung are called bullae. In my experience, injury-induced bullae (traumatic bullae) rarely rupture. On the other hand, infectious or parasitic bullae can and do burst, potentially causing a fatal pneumothorax. Efforts to determine the cause of cavitary lung lesions based on wall thickness and the appearance

Figure 36-32 • Lateral thoracic radiograph (A) and close-up (B) of a dog with pulmonary metastasis show considerable variability in the apparent size and shape of the individual tumors, much of which is due to the superimposition of multiple lesions, a phenomenon known as summation, which accounts for the poor correlation between radiologic and pathologic findings in such cases.

of inner and outer margins have met with only modest success (much of it unsubstantiated), especially in veterinary medicine.20 The composition of some differential lists on this subject appears to be strongly influenced by human literature on the subject21 (Table 36-6). Imaging Findings Radiology. The demonstration of cavitary lung lesions nearly always requires postural radiography, usually a standing lateral projection. In standard recumbent films, such lesions usually appear as solids rather than as spherical or oval-shaped objects containing a discrete fluid line or gas-fluid interface (Figures 36-34 and 36-35).

Dilated Esophagus (Megaesophagus) Localized and Regional Dilation. Persistent localized or regional esophageal dilation is often the result of

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387

B

A

Figure 36-33 • Primary lung tumor in a dog appears situated just above the carina, as seen in the lateral projection (A), but is actually located lateral to the right mainstem bronchus according to the ventrodorsal view (B, emphasis zone).

Table 36-6 • DIFFERENTIAL DIAGNOSIS OF CAVITARY LUNG LESIONS Cause Bacterial abscess Congenital lung cyst Foreign body Infarction Lipid pneumonia Mycetoma Parasitic development site Saccular bronchiectasis Traumatic bulla Tumor

Comment Very rare disease and a still rarer finding Occurs occasionally Very rare Contrary to some literature, this is an unusual feature in dogs and cats Most often seen in horses; usually aspergillosis in an immunocompromised animal Paragonimus A usual feature in a rare disease Most common cause of this lesion Relative rarity

obstruction, usually by a foreign body (Figure 36-36). A persistent aortic arch, typically seen in young regurgitating puppies, usually produces severe regional dilation extending from the throat to the heart base. Transient dilation usually represents a passing bolus of food or air. Small to medium volumes of air sometimes are observed in anesthetized dogs, but they disappear once they recover. Some tranquilizers and sedatives can have a similar effect. Dogs that strongly resist being radiographed also show esophageal air, but it is usually temporary.

Generalized Dilation. Persistent generalized esophageal enlargement implies a loss of muscular tone or, more simply, flaccidity. Depending on the degree of distension and the volume of content, an enlarged esophagus may or may not displace the underlying trachea and heart ventrally. The esophageal walls usually appear as fine, light-gray lines passing over the heart, gradually tapering as they enter the cranial abdomen (Figures 36-37 and 36-38). Aflaccid esophagus, as seen in sequential films, often fails to change shape when opacified with barium or diagnostic iodine. Typically, the esophageal interior appears medium to dark gray, reflecting its combined fluid and air densities. This content, and the oftenstriking associated fluid line, can be demonstrated clearly in a postural radiograph, such as a standing lateral (Figure 36-39).

Hilar and Cranial Sternal Adenopathy Hilar adenopathy is an inferential radiographic diagnosis made on the basis of lesion appearance and location. Specifically, hilar adenopathy is suggested when a medium- or large-sized mass effect is seen in a lateral thoracic radiograph over the heart base (Figure 36-40). Created by the enlargement of multiple, closely approximated paratracheal lymph nodes, the illusion is often that of a single, poorly defined mass (thus the expression, mass effect). The described nodal enlargement usually is seen in conjunction with varying degrees of ventral tracheal dis-

388

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A

B Figure 36-34 • A, Lateral thoracic radiograph of a dog with a cavitary lung lesion in the dorsal part of its right caudal lung lobe. B, Closeup view shows a thick, shaggy caudal wall (emphasis zone), an inconsistent finding in such lesions.

A

B Figure 36-35 • A, Lateral thoracic radiograph shows a large spherical mass (plant awn abscess) high in a caudal lung lobe. The associated lucency and densities are of an uncertain nature and may either be within the lesion or superimposed upon it. B, A postural film of a dog standing using a horizontally directed x-ray beam shows a distinct fluid level bisecting the mass, confirming its cavitary nature.

placement. Regional bronchi also may appear abnormal, ranging from apparently narrowed, to obscure, to invisible. Caution: Centrally located mediastinal masses and mass effects often appear to displace and deform adjacent bronchi, when in reality they are only partially masking the surrounding airways. Consequently, radiographically suspected airway obstruction secondary to hilar adenopathy should be confirmed bronchoscopically, especially if corticosteroid treatment is being considered for related cough.22 Like hilar adenopathy, enlargement of the cranial sternal lymph node (retrosternal lymph node in the parlance of human radiology) usually indicates lymphoma or some form of mycotic pneumonia (Figure 36-41).

Diaphragmatic Deformity Asymmetry of the diaphragm is normal, the right half of the diaphragm typically appearing “higher” than the left (closer to the heart in a DV or VD projection), but deformity is not normal. By deformity, I am referring to an obvious change in shape, for example, when one side of the diaphragm appears concave and the other convex. Another example would be where one side of the diaphragm is curved and the other flattened. These differences, of course, may be related, at least to some extent, to changes in the immediate surroundings, such as a full stomach or a deep breath; under such circumstances, diaphragmatic differences usually are not marked. Pronounced departures from normal usually signal genuine abnormality, such as a hernia, a pneumothorax, ascites, or occa-

A

B

Figure 36-36 • The esophagus is distended with air on either side of a large rectangular bone fragment. Characteristically, an esophageal foreign body is best seen in lateral view (A), where it is clear of spinal superimposition, a frequent limitation of dorsoventral or ventrodorsal projections (B).

A

B

C Figure 36-37 • A, Close-up view of the lateral esophageal field of a dog with megaesophagus, featuring characteristic ventral displacement of the heart and trachea. B, Ventral margin of the distended esophagus as it drapes over various objects in the adjacent mediastinum (emphasis zone). C, Ventrodorsal view in which the lateral borders of the esophagus appear as undulant white bands passing over the outer edges of the heart (emphasis zone).

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Figure 36-38 • Lateral view of the chest of a dog recently hit by a car shows a traumatic megaesophagus related to severe head injury.

Figure 36-40 • Close-up lateral view of the heart base of a dog shows severe hilar adenopathy.

Figure 36-39 • Close-up lateral view of a dog with a massive megaesophagus shows a thorax dominated by a fluid-filled, gas-capped esophagus resembling pleural fluid.

Figure 36-41 • Close-up lateral view of the cranial aspect of the

sionally diaphragmatic paralysis.23 Figures 36-42 and 36-43 illustrate examples of diaphragmatic deformity.

mediastinal masses, and (5) chylothorax secondary to lymphatic disease or heart failure. I, too, have had success using ultrasound-guided biopsy to diagnose a variety of thoracic diseases in pets, but only if they remain still during the procedure. When transthoracic ultrasound-guided biopsies are attempted using physical restraint, they are more likely to fail than to succeed, usually because the animal moves before a tissue sample can be obtained. Additionally, many animals bleed into the lung, mediastinum, and pleural space as a result of being injured by the biopsy needle; some develop pneumothorax. In my experience, inexperience with the technique of transthoracic ultrasound-guided fine-needle biopsy is the most common cause of harm to the animal. The key is time. Typically, the novice is too tentative, even

❚❚❚ ULTRASOUND-GUIDED THORACIC BIOPSY Reichle and Wisner advocate the use of ultrasoundguided biopsy to diagnose various chest diseases in dogs and cats.24 Their recommendation is supported by the fact that 91% of the animals on which they worked were correctly diagnosed using this technique. Among the described disease types were (1) tumors of the lung (including pleura) and mediastinum, (2) consolidative lung lesions, (3) lung-lobe torsion, (4)

sternum of a dog shows marked enlargement of the cranial sternal lymph node.

CHAPTER 36 ❚❚❚ Thoracic Radiographic Disease Indicators

391

Figure 36-42 • Close-up ventrodorsal view of the diaphragm of a dog flattened and displaced cranially as a result of a large volume of peritoneal fluid.

Figure 36-43 • Close-up ventrodorsal view of the diaphragm of a dog with diaphragmatic paresis and esophageal atony.

when closely supervised by an experienced person. This leads to prolongation of the procedure, which proportionately increases the probability of lung injury. CT also can be used to guide intrathoracic biopsies, but it first requires a strong working knowledge of the normal cross-sectional anatomy. To this end, Smallwood and George described the CT appearance of the Beagle thorax, including comparable xerograms and anatomic sections.25 Samii and co-workers authored a similar paper on cats.26

References 1. Burk RL: Radiographic definition of the phrenicopericardiac ligament. J Am Vet Rad Soc 17:216, 1976. 2. Kramer RW: The nodular pulmonary opacity—is it real? Vet Radiol Ultrasound 33:187, 1992. 3. Ahlberg N-E, Hoppe F, et al: A computed tomographic study of volume and x-ray attenuation of the lungs of Beagles in various body positions. Vet Rad 26:43, 1985.

4. Meyer W: Radiography review: the extrapleural space. J Am Vet Rad Soc 19:157, 1978. 5. Lord PF, Suter PF, et al: Pleural, extrapleural and pulmonary lesions in small animals: a radiographic approach to differential diagnosis. J Am Vet Rad Soc 13:4, 1972. 6. Kerstetter KK, Krahwinkel DJ, et al: Pericardiectomy in dogs: 22 cases (1978-1994). J Am Vet Med Assoc 222:118, 1995. 7. Thrall DE, Goldschmidt MH: Mesothelioma in the dog: six case reports. J Am Vet Rad Soc 19:197, 1978. 8. Palmer KG, King LG, Van Winkle TJ: Clinical manifestations and associated disease syndromes in dogs with cranial vena cava thrombosis: 17 cases (1989-1996). J Am Vet Med Assoc 213:220, 1986. 9. Font A, Closa JM: Ultrasonographic localization of a caudal vena cava thrombus in a dog with leishmaniasis. Vet Radiol Ultrasound 38:394, 1997. 10. Groves TF, Ticer JW: Pleural fluid movement. Vet Rad 24:99, 1983. 11. Meyer W: Radiography review: pleural effusion. J Am Vet Rad Soc 19:75, 1978. 12. Meyer W: Pneumothorax: a radiographic review. J Am Vet Rad Soc 19:12, 1978. 13. Forrester SD, Fossum TW, Miller MW: Pneumothorax in a dog with a pulmonary abscess and suspected infective endocarditis. J Am Vet Med Assoc 200:351, 1992. 14. Thrall DE: Misidentification of a skin fold as pneumothorax. Vet Radiol Ultrasound 34:242, 1993. 15. Aronson E, Reed AL: Pneumothorax: ventrodorsal or dorsoventral view—does it make a difference? Vet Radiol Ultrasound 36:109, 1995. 16. Walker M, Hartsfield S, et al: Computed tomography and blood gas analysis of anesthetized bloodhounds with induced pneumothorax. Vet Radiol Ultrasound 34:93, 1993. 17. Millman T: Unilateral tension pneumothorax in a dog. Vet Rad 22:17, 1981. 18. Lord PF, Gomez JA: Lung lobe collapse. Vet Rad 26:187, 1985. 19. Anderson GI: Pulmonary cavitary lesions in the dog: a review of seven cases. J Am Anim Hosp Assoc 23:89, 1987. 20. Silverman S, Poulos PW, Suter PF: Cavitary pulmonary lesions in animals. J Am Vet Rad Soc 17:134, 1976. 21. Lamb CR, Neiger R: Differential diagnosis of pulmonary cavitary lesions. Vet Radiol Ultrasound 41:340, 2000.

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22. Schulman RL, McKiernan BC, Schaeffer DJ: Use of corticosteroids for treating dogs with airway obstruction secondary to hilar lymphadenopathy caused by chronic histoplasmosis: 16 cases (1979-1997). J Am Vet Med Assoc 214:1345, 1999. 23. Barber DL: Radiographic diagnosis. Vet Rad 23:56, 1982. 24. Reichle JK, Wisner ER: Non-cardiac thoracic ultrasound in 75 feline and canine patients. Vet Radiol Ultrasound 41:154, 2000.

25. Smallwood JE, George TF: Anatomic atlas for computed tomography in the mesaticephalic dog: thorax and cranial abdomen. Vet Radiol Ultrasound 34:65, 1993. 26. Samii VF, Biller DS, Koblik PD: Normal cross-sectional anatomy of the feline thorax and abdomen: comparison of computed tomography and cadaver anatomy. Vet Radiol Ultrasound 39:504, 1998.

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3 7

Lung Patterns

❚❚❚ OVERVIEW In nearly three decades as a radiologist, I have concluded that pulmonary pattern recognition does not work; that is to say, pattern recognition in and of itself has made no difference in my ability to diagnose specific lung diseases other than to relegate them to a particular pattern group (or groups). Worse, this widely accepted but unproven method often leads to misdiagnosis. The greatest offenders are technically compromised thoracic radiographs (underexposed, expiratory, oblique), which often closely mimic one or more pulmonary disease patterns. These problems often are exacerbated in excessively thin or fat animals, which normally reveal increased and decreased lung details, respectively. In the following account, I first provide a brief historical background and then put forth a list of particulars in the case against pattern recognition. I conclude with a proposal as to how pattern recognition can be modified to improve its diagnostic accuracy.

❚❚❚ HISTORICAL PERSPECTIVE Pattern recognition is a diagnostic scheme developed and refined by physician radiologists (and later adapted by veterinarians)1,2 for the purpose of diagnosing the nature and causes of diffuse lung disease.3–6 Pattern recognition promised users diagnostic proficiency and efficiency in the form of substantially shorter differential lists (termed gamuts by some proponents). The method is used as follows. Diffuse abnormal lung densities are relegated to one of four subanatomic divisions of the lung: the (1) interstitial, (2) alveolar, (3) bronchial, or (4) vascular compartments. By determining which part of the lung is involved, supporters assert that the possible radiographic explanations would be fewer, thus improving diagnostic efficiency. Another claimed benefit for pattern recognition is that with more rapid radiographic diagnosis specific

treatment sometimes can be initiated before completion of cultures, thus improving the potential for a rapid, uncomplicated recovery. Later, Felson modified his original anatomically based pattern recognition scheme to incorporate the radiographic features of diffuse lung diseases that did not fit readily into the original categories. These hybrid categories included reticular, nodular, reticulonodular, linear, ground glass, acinar, and “destructive” patterns. Because pattern recognition was not always accurate, and because radiologists could not always agree on the appropriate pattern designation for a particular image, pattern recognition underwent further modification with the incorporation of selected elements from the International Labor Organization’s classification of occupational lung diseases. These consisted of additional subcategories relating to the diameter, thickness, and distribution (termed perfusion) of observed lung lesions. A more recent modification to pulmonary pattern recognition is what I term contextual diagnosis, whereby other presumed related thoracic and extrathoracic abnormalities also are factored into the diagnostic equation. For example, a diffuse alveolar pattern seen in association with cardiomegaly and increased pulmonary vasculature is likely congestive heart failure; on the other hand, a reticular interstitial pattern found in conjunction with an enlarged liver and spleen is most likely a lymphoma. Currently, contemporary human medical imaging texts mention pattern recognition almost exclusively in the context of diffuse industrial or agriculturally related lung disease, mostly interstitial.

❚❚❚ APPLICATION OF PATTERN RECOGNITION IN VETERINARY RADIOLOGY Most veterinary radiologists have embraced the previously described diagnostic methodology, largely 393

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intact. The only significant modification has been to add diseases that are specific to dogs and cats and to delete those that are specific to humans. The pattern approach to diffuse lung disease is as follows. Abnormal lung densities that have been identified on thoracic radiographs are relegated to one of four subanatomic regions of the lung: (1) interstitium (connective tissue scaffolding), (2) alveoli (and related terminal or respiratory bronchioles), (3) bronchi (radiographically visible), and (4) pulmonary vasculature (radiographically visible). Where the observer believes that there are two or more levels of concurrent involvement, the most affected region is chosen. If two regions are comparably involved, then the appropriate pattern types are combined or the more general term mixed pattern is used. Examples are interstitial pattern (single subanatomic compartment affected) and bronchointerstitial pattern (bronchial and interstitial compartments inseparably involved). Proponents of pattern recognition claim that by knowing which structural part of the lung is affected (as exemplified by a particular pattern or patterns), it becomes possible to devise a comparatively brief list of diagnostic possibilities, termed gamuts. It is further claimed that this technique is superior to etiologic- or morphologic-based methods because it requires no memorization, often derisively referred to as the Aunt Minnie approach. Although pattern recognition is taught to all North American veterinary students (in one form or another), there is no scientific evidence that it is superior to other methods of radiographic diagnosis. On the contrary, there is now evidence that pattern recognition is seriously flawed and may prove to be inferior to more traditional etiologic or morphologic recognition techniques.7 Recently published veterinary radiology texts differ with respect to the diagnostic value they accord pattern recognition.

Method Misuse Pattern recognition was developed for, and is intended for use with, diffuse lung disease only. Unlike their physician counterparts, most veterinarians commonly apply pattern recognition to localized or regional lung disease.

Method Unverified in Veterinary Medicine To date, no published reports have appeared in the veterinary literature showing consistent, predictable correlation between specific lung patterns and specific lung diseases. On the contrary, there is now evidence that many lung diseases can assume more than one pattern as they evolve. Worse yet, some may falsely appear to involve a specific portion of the lung, when in reality they involve another, thus leading to inaccurate diagnosis.

Inconsistent Terminology The absence of consensus in veterinary radiology as to what constitutes a lung nodule, as opposed to a lung mass, seriously hampers descriptive clarity. Expressions like “dirty lung,” “heavy interstitial pattern,” “destructive pattern,” “coarse lung markings,” and “diffuse pattern”8 only add to the semantic morass.

Disagreement Regarding Observed Pattern Types Often, even among specialists, disagreement exists as to the radiographic features of an abnormal lung. This disagreement results in a variety of often imprecise descriptions being applied to the same image, depending on who interprets the film.

Anatomic Variations Mistaken for Abnormal Patterns

❚❚❚ PROBLEMS WITH PATTERN RECOGNITION In my view, the problems associated with pattern recognition are as follows: • • • • •

Misuse of the method Lack of verification in veterinary medicine Inconsistent terminology Disagreement as to observed pattern types Anatomic variations being mistaken for abnormal patterns • Physiologic variations being mistaken for abnormal patterns • Technical variations being mistaken for abnormal lung patterns • Pattern recognition as a basis for final diagnosis

The lungs of normal obese dogs and cats often appear increased in density and decreased in detail, resembling an interstitial disease pattern. The lungs of thin dogs often show increased tracheobronchial detail, resembling a bronchial disease pattern.

Physiologic Variations Mistaken for Abnormal Patterns Films made during expiration typically show deceased vascular detail due to reduced lung volume and resultant vascular crowding and increased superimposition. Because these are the signs of interstitial lung disease, misdiagnosis under such circumstances is inevitable. Conversely, films made during full inspiration, especially in thin dogs, show comparatively few vessels arrayed against an overly dark background, signs often misinterpreted as a vascular pattern.

CHAPTER 37 ❚❚❚ Lung Patterns

Technical Variations Mistaken for Abnormal Lung Patterns Underexposed thoracic films are misinterpreted as having interstitial patterns because of their increased density. Likewise, patient motion unsharpness and resultant vascular blurring are also subject to the misdiagnosis. Some patterns are overrepresented, and others are superfluous. The great majority of abnormal chest films are categorized as having an interstitial, alveolar, or mixed pattern (inseparable interstitial and alveolar patterns). Using pattern recognition as it was intended, that is, for diffuse lung disease only, then the interstitial pattern is the runaway leader. The vascular pattern is used only occasionally, largely in dogs with hyperemic lungs resulting from congestive heart failure. It is used less frequently in animals with congenital intracardiac or extracardiac shunts, which, depending on the direction of blood flow (left to right, right to left), produce either overcirculated or undercirculated lung fields. The bronchial pattern is the least used because bronchial disease rarely alters the visible airways to the extent that it can be detected radiographically.

Pattern Recognition as a Basis for Final Diagnosis The radiographic identification of an abnormal lung pattern, for some, has served as a final medical diagnosis, most commonly “interstitial lung disease.” Although there are probably a few instances in which such a diagnosis is justifiable, its regular use more likely reflects a poor understanding of pattern recognition technique or a failure to follow through diagnostically.

❚❚❚ PROPOSED MODIFICATIONS TO PATTERN RECOGNITION If pattern recognition is to become a legitimate radiographic means of diagnosing lung disease in dogs and cats, certain changes must be made. • First and foremost, the method should only be used in cases of diffuse lung disease. • Students must be taught, and practitioners constantly alerted to, the ways in which anatomic and physiologic variations can mimic pulmonary disease patterns. Likewise, there must be ongoing quality assurance programs in all veterinary practices that employ radiology, and these programs must aim to eliminate technical film faults that may resemble abnormal lung patterns. • The alveolar lung pattern, which is rarely generalized, should be abandoned, or at least used sparingly. For example, in some cases of diffuse pulmonary edema, a designation of alveolar pattern

395

is justified, but for most cases of pneumonia, which is localized, it is not. • The terms consolidation and atelectasis are far more precise and thus have the advantage of being verifiable as well as being applicable to both localized and generalized disease. • The vascular and bronchial patterns are superfluous and should be discarded: there are few diseases in the former category (hyperemia and oligemia) and almost none (except bronchiectasis) in the latter. • The interstitial category should be retained, but with only two subcategories: structured and unstructured. Diseases that have one or more discrete, clearly defined, repeating shapes should be classified as structured; those that do not should be designated as unstructured. Using this approach, it should be far easier to correlate radiographic and pathologic findings and thus establish the reliability of the radiographic diagnosis.

❚❚❚ USING PATTERN RECOGNITION As already mentioned, I do not find pattern recognition, at least in its present form, very useful. Many of my colleagues do, however, and for this reason (and in the spirit of evenhandedness), I have included references from a series of excellent review articles on the subject, written for Veterinary Radiology by Wendy Meyer (formerly a radiologist at Ohio State University).9–11

❚❚❚ AGE-RELATED PULMONARY FIBROSIS (GERIATRIC FIBROSIS, “OLD DOG LUNG”: DOES IT REALLY EXIST?) As with lung patterns, a persuasive case for old dog lungs remains to be made. Based almost entirely on a single report by Rief and Rhodes, published in 1966, most veterinarians (including many radiologists) believe that the lungs of dogs become denser with age (often somewhat grandly termed geriatric fibrosis).12 Accordingly, when thoracic radiographs of older dogs are assessed, an unspecified amount of background density is often attributed to age (and presumed previous exposure to microbes and pollutants) rather than to current disease, technical film inadequacy, and so forth. Although the authors of the cited article attempted to show a radiologic–pathologic correlation to support their claims, the included radiographs were too small, featuring excessive contrast and poor detail. Thus, it was not possible to see the abnormalities described in the text. Nevertheless, teachers of veterinary radiology—radiologists and nonradiologists alike— embraced the idea of age-related lung change with little

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or no debate and proceeded to teach it to their students. To date, I have been unable to confirm that the lungs of dogs (or cats) predictably change in any way as a function of advancing age. In other words, and radiographically speaking, there is no such thing as geriatric fibrosis. In a similar vein, most lung diseases in dogs and cats leave no residual abnormality (scarring), at least none that can be detected radiographically.

References 1. Rief JS, Rhodes WH: Linear opacities in canine thoracic radiographs. Vet Radiol 9:57, 1968. 2. Suter PF, Chan KF: Disseminated pulmonary diseases in small animals: a radiographic approach to diagnosis. Vet Radiol 9:67, 1968. 3. Gould DM, Dalrymple GV: A radiologic analysis of disseminated lung disease. Am J Med Sci 238:622, 1959.

4. Felson B: Signs aiding the diagnosis of disseminated pulmonary alveolar disease. Rad News 4:2, 1966. 5. Felson B: Disseminated interstitial diseases of the lung. Ann Radiol 9:325, 1966. 6. Felson B: The roentgen diagnosis of disseminated pulmonary alveolar disease. Semin Radiol 2:3, 1967. 7. Farrow CS: Pattern recognition technique: has the promise been fulfilled? Vet Radiol Ultrasound 35:237, 1994. 8. Forrest LJ, Graybush CA: Radiographic patterns of pulmonary metastasis in 25 cats. Vet Radiol Ultrasound 39:4, 1998. 9. Meyer W: Radiography review: the alveolar pattern of pulmonary disease. J Am Vet Rad Soc 20:10, 1979. 10. Meyer W: Radiography review: the interstitial pattern of pulmonary disease. Vet Rad 21:18, 1980. 11. Meyer CW: Radiography review: the vascular and bronchial patterns of pulmonary disease. Vet Rad 21:156, 1980. 12. Rief JS, Rhodes WH: The lungs of aged dogs: a radiographic-morphologic correlation. Vet Radiol 7:5, 1966.

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3 8

Thoracic Trauma

Three important imaging principles should be kept in mind when thoracic trauma films are being analyzed:

also can originate from distant wound sites in the skin, throat, or airways.

1. The clinical and radiographic signs of serious lung injury are sometimes absent at the initial evaluation. 2. There is no consistent relationship between evidence of external chest wall injury (either clinical or radiologic signs) and the likelihood of serious underlying lung injury. 3. Radiographic examination generally underestimates the true extent of lung and chest wall injury.

Deep. Deep intramuscular gas usually originates from deep surface wounds or the lung. Gas found against the ribs suggests that it has originated from the lung subsequent to a pneumothorax (Figure 38-1).

❚❚❚ CHEST WALL INJURY Bruising Bruising of the chest wall can be quite painful, resulting in varying degrees of swelling, depending on the severity of the injury. Severe bruising usually erases individual facial planes. The presence of unilateral swelling can indicate the side on which the animal was struck or, alternatively, the side on which the animal landed after being thrown.

Extrathoracic Hematoma Extrathoracic hematomas are probably more common than generally realized, a contention supported by performing ultrasound on fresh thoracic wall injuries. Most dissipate in a few days, with the associated serum migrating to the dependent portion of the chest, where it is eventually reabsorbed. Crushing of the parathoracic muscles, tearing of the intercostals, and rib fractures—especially if displaced—cause the largest and most persistent hematomas.

Subcutaneous Gas Superficial. Gas located immediately below the skin is usually atmospheric in origin, resulting from overlying lacerations or punctures. Large volumes of air

Rib Fractures Traumatic. Given the high frequency with which posttraumatic thoracic screening is performed in dogs, rib fractures are a surprisingly infrequent finding. When present, they are usually unilateral, paired, or in small groups of three or four. Single fractures are unusual, and bilateral injuries are rare. Most such fractures are displaced (as opposed to cracked). Adjacent lung contusion, pneumothorax, and hemothorax usually complete the spectrum of injury. Badly displaced fractures are likely to cause deep, ragged lung lacerations, which in some instances will lead to a persistent pneumothorax (Figure 38-2). Resultant thoracic wall instability or flail chest typically develops when there are a series of fractures: three or more double rib fractures or five or more single breaks. The type of injury causes unique movement in the unstable portion of the ribcage. When air is drawn into the lung, all but the injured portion of the chest wall expands, and the flail segment contracts. As air moves out, the reverse happens; the flail segment expands, and the rest of the ribs contract. Accordingly, the movements of breathing are termed paradoxic. Pathologic. Pathologic rib fractures caused by hypophosphatemic oncogenic osteomalacia have been reported in an aged cat with nasal osteosarcoma (giant cell variant).1

❚❚❚ STERNAL FRACTURE Sternal fracture/dislocations occur occasionally in cats but only rarely in dogs. Undisplaced body frac397

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Figure 38-3 • Lateral close-up view of the ventral portion of the thorax in a cat shows a pair of sternal fracture/dislocations and multiple rib detachments (extremely painful injuries).

Figure 38-1 • Ventrodorsal radiograph of an injured cat shows both superficial and deeply situated gas accumulations beneath the skin of the thorax.

Figure 38-4 • Close-up lateral view of a displaced sternal fracture/dislocation (emphasis zone) in a cat.

❚❚❚ NORMAL STERNAL VARIANT OR OLD INJURY?

Figure 38-2 • Ventrodorsal radiograph of a cat shows multiple, displaced rib fractures on either side of the chest (left side, emphasis zone). An irregular band of gas is present deep in the left axilla.

tures are rare in dogs and cats. In most cases, sternal fracture/dislocations are associated with multiple ventral rib detachments (Figures 38-3 and 38-4). Because of the strong force required to cause such injuries, additional injury such as lung hemorrhage, or pneumothorax should be anticipated.

The most common sternal variant in dogs and cats is pectus excavatum, an upward deflection of the caudal aspect of the sternum, which is best seen in lateral projection.2 Although accounts of surgical correction exist in the veterinary literature, this is a benign, congenital deformity requiring differentiation only from trauma. Pectus carinatum, the congenital downward deflection of the caudal part of the sternum, is less common.

❚❚❚ STERNAL TUMORS, INFECTIONS, AND GAS Sternal tumors are rare, with osteosarcomas and chondrosarcomas likely the most common. Those I have seen have been both productive and destructive but for the most part remain confined to the sternebra of

CHAPTER 38 ❚❚❚ Thoracic Trauma

399

Interlobar hematomas often appear as medium-sized ellipses, usually between the middle and caudal lobes or between a caudal lobe and the diaphragm.

❚❚❚ LUNG INJURY Intrapulmonary Hemorrhage (Lung Contusion, Pulmonary Contusion)

Figure 38-5 • Substernal abscess: Lateral sinogram centered just beneath the midpoint of the sternum shows a medium-sized lobulated cavity, which was subsequently found to contain a porcupine quill.

origin. Davidson reported a sternal osteosarcoma, believed to have extended deeply into the cranial part of the thorax, resembling a large mediastinal mass.3 Occasionally, sternal or suprasternal abscesses develop, usually as a result of puncture wounds or buried quill fragments (Figure 38-5). Weber and co-workers described the presence of intersternal gas, terming it a vacuum phenomenon and attributing it to “degenerative instability and abnormal positioning stresses.”4

❚❚❚ PLEURAL HEMORRHAGE AND HEMATOMA Visible pleural hemorrhage secondary to blunt chest trauma may have many sources: lacerated lung lobe, ruptured intercostal blood vessels (especially when there are rib fractures), diaphragmatic tear, or mediastinal injury. Pulmonary contusions and pneumothorax sometimes accompany hemothorax. When pneumothorax and hemothorax occur concurrently, they are termed hemopneumothorax. Extrapleural hematomas occasionally are identified in the chests of traumatized dogs and cats, usually appearing as flattened, ovoid opacities superimposed on the ventral aspect of the heart as seen in lateral projection. Less often, such masses are seen as spherical opacities located just above the sternum, between the heart and diaphragm. Pleural hematomas usually can be distinguished from lung hematomas based on their respective locations in a lateral radiograph: pleural hematomas typically are situated ventrally in the vicinity of the heart, whereas lung hematomas are characteristically found in the dorsal aspects of the caudal lung lobes.

Blunt chest trauma often causes lung injury. In its mildest form, there is disruption of the alveolar/ capillary membrane with extravasation of blood and edema into the surrounding interstitium and terminal air spaces. Typically, lung contusions occur adjacent to solid structures, such as ribs, vertebrae, heart, and liver. In most instances, bleeding is short lived owing to the compressive effect of the surrounding lung. Only occasionally do progress thoracic films show worsening compared with initial images. On the contrary, clearing of the lung often begins to take place in the first 24 hours and is often complete within a week. With extensive lung contusion, especially in older animals or those with serious concurrent injuries, there may be respiratory failure secondary to a profound hypoxemia resulting from continuing perfusion through nonventilated lung (ventilation/perfusion mismatching). The principal radiologic sign of contusion is a pneumonia-like opacity in the lung caused by hemorrhagic edema. Air bronchograms may not be present if the associated bronchi contain blood rather than air. Contusive injury to the cranial lobes can be difficult to distinguish from scapular overlay, but this problem usually can be overcome by drawing the forelimbs back along the lateral chest wall while the dog lies on its back, a projection I term simply the pullback view (Figure 38-6).

Laceration, Collapse, and Creation of Posttraumatic Lung Spaces (Cavitary Lung Lesions, Traumatic Bullae) If a blow to the chest is forceful enough, one or more lung lobes may be ruptured. In such instances, the affected lobe (or lobes) loses volume, leaks air, and often bleeds both internally and externally. Adjacent uninjured lobes, particularly those on the opposite side of the chest, often hyperinflate to compensate for the resultant volume loss. As a result, the heart is often displaced toward the injured lobe or lobes, which is sometimes termed a mediastinal shift or, more precisely, a cardiac shift. Under these circumstances, especially when there is a medium-sized or large hemothorax, it becomes difficult to ascertain whether contusions are present. Lacerated lung lesions are variable in appearance and often are concealed by surrounding contusions. Although initially linear in shape, most lacerations (as identified in later progress films) appear as an oval opacity, a morphologic conversion resulting from the elastic recoil of the surrounding lung. If the initial lesion

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A

B

Figure 38-6 • A, Conventional ventrodorsal view of a recently injured dog shows questionable density in the right cranial lung field that may represent either contusion or superimposed soft tissue. B, A subsequent ventrodorsal film, made with the forelimbs drawn back along the chest wall, removes the scapulae from over the lung, revealing the underlying lung hemorrhage.

is stellate in nature, the resultant lung cavity is more likely to appear multilobular. Once created, the posttraumatic lung space may contain blood (hematoma), air (pneumatocele), or a combination of blood and air (hematopneumatocele). Such lesions also have been less precisely termed cavitary lung lesions or traumatic bulla (Figure 38-7). Disappearance of Posttraumatic Lung Spaces and the Restoration of Normal Lobar Volumes. Posttraumatic lung spaces usually resolve within a week of their creation, gradually losing volume and definition until they are no longer radiographically visible. Overall, the injured lung appears normal, with no evidence of volume loss or compensatory hyperinflation. If a cardiac shift was present, it too usually disappears by this time. I have yet to see such a lesion rupture, causing pneumothorax, although it is theoretically possible.

Extrapleural Air (Posttraumatic Pneumothorax) Posttraumatic pneumothorax results from the splitting open of one or more lung lobes after a forceful blow to the chest, most commonly delivered by an automobile. The injured lobe typically bleeds and becomes smaller (volume loss) in the process. The amount of escaped air depends on a number of factors, including the size and depth of the tear, the rapidity and effectiveness of clotting in the ruptured lobe, external wound compression by adjacent lung lobes, and the rate and depth of respiration. Examples of pneumothorax are shown in Figures 38-8 and 38-9, whereas Figure 38-10

illustrates a case of combined pneumothorax-pneumomedistinum. Strategies for Demonstrating Pneumothorax. In general, the smaller the volume of escaped air, the more difficult it is to detect radiographically. Air that is situated in the ventral portion of the pleural space is difficult to distinguish from underinflation, underexposure, fat, and nonstandard oblique radiographs. If there is a concomitant hemothorax so that one overlies the other, free pleural air becomes even more difficult to find. Occasionally, gas bubbles form in the pleural space when air and blood are mixed, but they are often hard to see and are short-lived.

Postural Radiography: Lateral Decubitus or Alternate-Side Radiography Small-volume pneumothoraces are best detected using postural radiography, specifically a decubitus view: the dog or cat is positioned on its right or left side, depending on which side a pneumothorax is suspected, and the x-ray beam is directed horizontally across the thorax. Under the influence of gravity, any free gas will rise to the highest point in the thorax, outlining the surface of the underlying lung. If safe, it is best to position the animal and then maintain it for at least a minute before making the exposure. This allows time for any free air to negotiate its way past the various anatomic obstacles in its path as it makes its way to the uppermost parts of the thorax. Conversely, any blood in the pleural space will move to the lowest point in the chest,

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401

B

Figure 38-7 • Ventrodorsal (A) and ventrodorsal close-up (B) views of a medium-sized cavitary lesion in the left caudal lung lobe of a cat recently hit by a car. Cavitary lesion.

A

B Figure 38-8 • Lateral (A) and lateral close-up (B) views of the thorax of a cat recently hit by a car show a medium volume of free pleural air located ventral to the cranial mediastinum and heart, and dorsal to the caudal lung lobes.

making the decubitus view an excellent choice for detecting small amounts of pleural fluid. In the event a movable x-ray tube head is not available, alternative-side radiography is the best alternative: the animal is radiographed from both the right and left sides and in the dorsoventral and ventrodorsal positions as well if this is not too painful for the animal (Figure 38-11). Using this approach, the objec-

tive is simply to provide a greater opportunity to identify any free pleural air. Status of Air Leak: Better, Worse, Unchanged? Identifying a pneumothorax is only the first part of a mandatory two-stage diagnostic process. The second step is to determine whether and when the leakage of air has stopped. If air continues to escape from a ruptured lobe,

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C

A

D

B

E

Figure 38-9 • Four standard projections and one postural view of the thorax of a dog with a large volume pneumothorax. The ventrodorsal (A) and dorsoventral (B) views are unrevealing—in part due to inadvertent overexposure. The right (C) and left (D) laterals are more informative, showing small and medium volumes of free pleural air, respectively. Only when the dog is positioned on its sternum (partially supported) and the x-ray beam directed horizontally is the full extent of the pneumothorax appreciable (E).

it may become necessary to aspirate or drain the air or, in cases of severe leakage, to perform a lobectomy. Rapid Continuous Leaks. Most ruptured lung lobes seal spontaneously, with the leaked air gradually being absorbed from the pleural space, usually within a week; however, some leaks persist. In such instances, it is important to monitor the situation to guard against the development of a tension pneumothorax. The interval

between progress films should be determined on a caseby-case basis, not by protocol. The more rapidly the air accumulates, the more often the chest should be filmed (Figure 38-12). Slow Continuous Leaks. Slow leaks often are characterized by a gradually increasing pneumothorax but only rarely by tension pneumonia. Occasionally, slow leaks are indicated by what is not seen. Let me explain.

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403

B

Figure 38-10 • Lateral (A) and ventrodorsal (B) views of a dog with a small pneumothorax, medium pneumomediastinum, patchy lung consolidation, and megaesophagus caused by a recent chest injury. The lateral projection is deceptive because the air-filled esophagus resembles a large pneumothorax, when in reality there is only a small amount of air just outside the lung on the right side (emphasis zone, VD). The pneumothorax was caused by a ruptured right caudal lobe, whereas the pneumomediastinum resulted from a small bronchial tear. The left lateral wall of the air-filled esophagus can be seen as a white line running diagonally over the left side of the heart in the ventrodorsal view.

B

A Figure 38-11 • Alternate-side radiography used to diagnose questionable lung injury: The right lateral view (A) suggests a pneumothorax; the left (B) confirms it. A barium marking study showed no evidence of a diaphragmatic hernia.

If in a series of thoracic films the amount of free pleural air remains constant, neither increasing nor decreasing, the implication is that the absorption is being matched by the leakage or, in other words, a steady state exists. Because the absorption of pleural air is dependent on both a normal systemic circulation and the integrity of the chest wall, injuries to either of these systems or regions will delay absorption. Chest Drains. When assessing thoracic drains (chest drains), it is important to determine their effectiveness

and whether they are causing problems. Because air rises, drains that are intended to alleviate a pneumothorax should be positioned so that their tips are located in the dorsal third of the pleural space, lateral to the midsagittal plane where occlusion is potentially greatest. Drains intended to remove fluid, on the other hand, should be positioned ventrally. The most serious problem related to thorax drainage, especially air, is having one or more drain holes outside the chest cavity. This usually is the result of the dog trying to remove its drain and in the process changing

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A

B

C Figure 38-12 • Progressive pneumothorax: A, Lateral thoracic radiograph of a dog made shortly after it was injured by a car shows: (1) moderate pneumothorax, (2) consolidation of or both caudal lobes, (3) varying amounts of atelectasis, and (4) pleural hemorrhage. B, An 8-hour progress film shows further dorsal consolidation, an anemic-appearing heart, and disappearance of the pleural fluid. The relative volume of pleural air is difficult to estimate due to the expiratory nature of the film, but it still appears to be substantial. C, A 24-hour recheck shows a large volume of pleural air consistent with a tension pneumothorax, resulting in extensive lung collapse.

its position. Occasionally, the exterior part of the drain is punctured or chewed off, a dangerous situation potentially leading to a tension pneumothorax. Experimental Pneumothorax. Kern and co-workers described the gradual dissipation of pleural air, which was placed experimentally into the chests of healthy dogs and monitored radiographically.5 They concluded that the most effective views for detecting free pleural air were (1) a standard left lateral and (2) a right lateral decubitus (horizontally directed x-ray beam with dog on its right side), exposed during expiration. The authors also determined that there was a direct correlation between the volume of air put into the chest and the time for it to be reabsorbed. For example, with

15 mL/kg, pneumothorax resolved by day 10, but with 45 mL/kg, the air took 2 weeks to disappear. In considering the predictive value of such numbers, it should be borne in mind that these are otherwise healthy animals, quite unlike the typical trauma case that often has a myriad of injuries in addition to a pneumothorax.

❚❚❚ THORACIC GUNSHOT WOUNDS The identification of a bullet, buckshot, or an airgun pellet in the chest may be causative or incidental. In general, causative gunshots are seen in conjunction with

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Figure 38-13 • Gunshot to the chest: Lateral (A) and dorsoventral (B) thoracic radiographs of a dog with shotgun wounds to the neck and chest. Both projections show cranial mediastinal widening, the result of localized hemorrhage, termed hemomediastinum. Oblique positioning is responsible for the false cardiac shift seen in the dorsoventral view.

other abnormalities: pneumothorax, hemothorax, hemomediastinum, pulmonary hemorrhage, and chest wall injury, usually in an obviously injured animal. Most are deep (Figure 38-13). Incidental wounds are usually relatively superficial, typically buckshot (Figure 38-14).

❚❚❚ MEDIASTINAL INJURY Background Pneumomediastinum usually develops following forceful chest injuries, which often cavitate the lung but almost never progress to a pneumothorax. Instead, the escaping air, which reaches the mediastinum by dissecting between the pulmonary vessels and axial pleura, disperses widely into the deep fascial planes of the neck and, if need be, into the vast spaces lying beneath the skin (subcutaneous emphysema). All but the most serious cases usually resolve spontaneously within a few days, and few exhibit related dyspnea. Less commonly, pneumomediastinum arises from tracheal or bronchial disruption (emergency room physicians refer to this as a tracheal or bronchial fracture). In such cases, the air leak may be massive and, of greater concern, difficult to contain. Attempting to establish the precise location of the leak is usually a frustra, time-consuming, and generally unrewarding experience, although bronchography (used in conjunction with bronchoscopy) has proven useful in

locating a presumed carinal stenosis in a cat 2 weeks after a car accident.6 Pneumomediastinum and pneumothorax also have been reported as a result of an anesthesia accident, the misconnection of a respiratory monitor to a Bain coaxial anesthesia system, in a cat undergoing portography.7 Although the authors presumed that the resultant pneumothorax was secondary to pneumomediastinum, such a conclusion is suspect. It appears more plausible that the pneumothorax resulted from an external lung tear, whereas the pneumomediastinum was caused by an internal parenchymal blowout. Spontaneous repair of a presumed tracheal rupture/separation was reported in a young cat with progressive dyspnea. Radiographically, the animal appeared to have a bulla-like structure in its cranial mediastinum joining the ends of the parted trachea.8 Occasionally, esophageal foreign bodies may perforate, causing gas or fluid to form in the mediastinal space. Solids in the mediastinum may be hard to distinguish from fluid, especially in the case of diaphragmatic hernia, in which blood and herniated abdominal viscera are often present together. An unsuspected pericardiodiaphragmatic hernia in a recently injured animal may be mistaken for caudal mediastinal hemorrhage or hemopericardium. Nearly all transtracheal irrigations/aspirations cause a pneumomediastinum, the volume usually being dependent on the experience of the operator: the faster the procedure, the less the needle moves; the smaller the opening in the trachea, the less the leakage.

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B

A

C Figure 38-14 • Lateral view (A) of a dog with metastatic lung cancer, in which close-ups of the cranioventral (B) and caudodorsal (C) lung fields show a lesion pattern composed of numerous small, similar sized, variably shaped objects (clusters of cancer cells). Note that the density of the caudodorsal portion of the diseased lung is greater than that of the cranioventral part. This is due to the relatively greater volume of the caudal lobes, and thus the larger number of metastases superimposed on one another, supplemented by the additive density of the regional pulmonary vasculature. The shotgun pellets are an incidental finding.

Mediastinal biopsies are dangerous and are best guided sonographically.

Imaging Findings Air or fluid in the mediastinum usually develops acutely, the result of a recent injury. Sources of air include the throat (pharynx and larynx), trachea, bronchi, or interior lung. Tearing or avulsion of major mediastinal veins can produce a large hemomediastinum, which usually is self-limiting. Most but not all major arterial injuries prove fatal. Mediastinal air may be readily seen or difficult to discern, depending on the amount. Classically, the errant air outlines the exterior surface of the trachea, increasing its radiographic visibility. Air also can accumulate in the esophageal adventitia, sometimes in thin, discontinuous bands and other times as small clusters of gas.

References 1. Berry CR: Answers for film reading session: 1995 A.C.V.R. annual meeting. Vet Radiol Ultrasound 36:449, 1995. 2. Smallwood JE, Beaver BV: Congenital chondrosternal depression (pectus excavatum) in the cat. J Am Vet Rad Soc 18:141, 1977. 3. Davidson M: Radiographic diagnosis. Vet Rad 26:35, 1981. 4. Weber WJ, Berry CR, Kramer RW: Vacuum phenomenon in twelve dogs. Vet Radiol Ultrasound 36:493, 1995. 5. Kern DA, Carrig CB, Martin RA: Radiographic evaluation of induced pneumothorax in the dog. Vet Radiol Ultrasound 35:411, 1994. 6. Berg J, Leveille CR, O’Callaghan MW: Treatment of posttraumatic carinal stenosis by balloon dilation during thoracotomy in a cat. J Am Vet Med Assoc 198:1025, 1991. 7. Evans AT: Anesthesia case of the month. J Am Vet Med Assoc 212:30, 1998. 8. Miles JE: What is your diagnosis? J Small Anim Pract 40:357, 1999.

C h a p t e r

3 9

Pneumonia

❚❚❚ BACKGROUND Pneumonia is both the simplest and most precise term available for describing lung inflammation. It can be further refined by using one or more modifiers, as described subsequently. The term pneumonitis, used by some to differentiate a chronic proliferative process from an acute exudative inflammation (pneumonia), lacks universal acceptance, therefore lessening its utility. The term pulmonary infiltrates is plainly archaic and no more useful than saying that a dog with hip dysplasia has “coxitis.”

❚❚❚ CLASSIFICATION Pneumonia has been classified in several ways: temporal, mechanistic, radiologic, and pathologic. Pneumonia also can be described in terms of its currency (active or inactive), its course (progressive or nonprogressive), and its magnitude (localized, regional, or diffuse).1

Temporal One means of describing pneumonia is to do so based on its clinical course, for example, acute or chronic pneumonia.Although these terms are relative and somewhat imprecise, they do convey a universally understood message and thus are clinically quite useful.

Acute Acute-onset pneumonia, as the name implies, is associated with sudden illness and onset of clinical signs. It is characterized by varying degrees and distribution of pulmonary consolidation, and, in many cases, vivid bronchograms.

right or left lateral cardiac shift (related to an associated pulmonary volume loss), increased pleural visibility (implying thickening or fluid coverage), and secondary bronchial dilation. Extension of infection into the pleural space, termed pleuropneumonia, usually causes excessive pleural fluid, which accumulates between individual lung lobes, spaces known as pleural fissures, forming what are termed fissure lines or interlobar fissures. Somewhat surprisingly, neither acute nor chronic pneumonia leaves any radiographically visible traces once the animal has fully recovered.

Mechanistic Another method of classifying pneumonia is according to its pathogenesis—inhalation or aspiration pneumonia, for example. Inhalation pneumonia often results from diseases that interfere with esophageal function, such as persistent right aortic arch or myasthenia gravis.2

Etiologic Classification by causative agent is popular among internists, for example, bacterial, viral, fungal, immunologic, parasitic, or lipid pneumonia. It is important to realize that many of the aforementioned types of pneumonia may share a similar radiographic appearance, depending on their duration and severity. It is also important to be aware that some pneumonic cats may appear to have nodular lung disease or, alternatively, bronchial disease. Secondary bronchial gland hyperplasia and medial arteriolar hypertrophy seen with a variety of feline lung diseases likely cause this deceptive appearance.

❚❚❚ IMAGING FINDINGS

Chronic

Radiology

Chronic pneumonia usually is associated with illdefined areas of consolidation, vague bronchograms,

Pneumonia usually results in varying degrees of pulmonary consolidation that causes the affected lobe or 407

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lobes to increase in density and thus become lighter in appearance. Normally invisible bronchi become apparent as dark branching bands, contrasted against the abnormally opaque lung (air bronchograms). Interstitial pneumonia, on the other hand, does not cause pulmonary consolidation, instead resulting in an increased interstitial density due to inflammation in the walls of the terminal air spaces. Less precisely, this is sometimes referred to as pneumonitis.

Ultrasound Where consolidation extends to the lung surface, it can be seen through the chest wall as an amorphous white to light gray echogenicity. The pleural surface varies in smoothness, depending on the amount of fibrin present, and often is covered by a thin layer of fluid. The deeper part of the pneumonic lobe also appears hyperechoic and often contains residual air, depicted by characteristic air artifact.

Computed Tomography The tomographic appearance of aspiration pneumonia in a dog was published in 1984, one of the earliest descriptions of this comparatively new imaging technique.3 Since that time, a number of additional case reports, case series, and textbook chapters on the subject have appeared.

❚❚❚ BACTERIAL PNEUMONIA Background Bacteria are the principal cause of pneumonia in dogs, although radiography can rarely distinguish one organism from another. Some bacteria are capable of causing localized necrosis, which subsequently can lead to a cavitary lung lesion. Other bacteria may secondarily infect the pleural space, resulting in pleuropneumonia. Bacterial infection also can follow on the heels of a viral pneumonia, although such combined infections are not detectable radiographically.

Imaging Findings In my experience, most lung infections in dogs and cats initially involve a single lung lobe, usually the right or left middle (Figures 39-1 and 39-2). Diffuse pneumonias are less common than localized or regional infections but generally are more serious (Figures 39-3 and 39-4). As mentioned, some bacterial pneumonias spread to the pleura, causing fluid to form in the pleural space (Figure 39-5). Others lead to abscess formation (Figure 39-6). Pneumonia does not visibly scar the lung, at least not so that it can be seen radiographically (Figure 39-7).

Figure 39-1 • Lateral thoracic radiograph of a dog with pneumonia shows two triangle-shaped consolidations: one located over the cranioventral aspect of the heart, and the other superimposed over the ventral aspect of the heart.

❚❚❚ ACTINOMYCOSIS Background Although they behave clinically like mycoses, Actinomyces are actually bacteria. There are three types of the disease in dogs: thoracic, abdominal, and cutaneous. The last of these is the most common. It is assumed that the thoracic form of the disease is initiated by the inhalation of the organism, which is believed to be a normal inhabitant of the oral cavity. There is speculation that trauma or other pathogens may predispose a dog to Actinomyces infection. Young dogs are affected more than older dogs are.

Imaging Findings Typical thoracic pathology centers on granuloma formation, with large mass-like lesions typically forming in the mediastinum and lung. Seen in the early developmental stages, the lung lesions more closely resemble consolidation than discrete masses. Occasionally, cavitation may occur. Large volumes of pleural fluid are also characteristic of the disease, sometimes associated with encapsulation.4

❚❚❚ PARASITIC PNEUMONIA Angiostrongylus vasorum Parasitic pneumonia, in particular, Angiostrongylus vasorum, may cause an immune-mediated thrombocytopenia, leading to mediastinal hemorrhage and simulating a mass. This parasite, which uses a slug as an intermediate host, has an interesting life cycle. Once

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A

B

C

Figure 39-2 • The rest of the story: The merits of alternate-side thoracic radiography are often exemplified by showing a pair of right (A) and left (B) lateral thoracic radiographs, and then pointing out that important information is present in one film, but not the other. However, in most cases it is possible to determine which half of the lung contains the lesion—in this instance, lobar consolidation—by searching the accompanying ventrodorsal or dorsoventral views (C).

into the intestine, the larvae travel to the mesenteric lymph nodes and liver and then to the right ventricle and pulmonary arteries, where they become mature strongylids. The adults deposit their eggs in the terminal pulmonary arterioles, where they hatch as firststage larvae. The larvae then migrate through the alveolar walls and into the terminal airways, where they are coughed up, swallowed, and excreted in the feces to seek out another slug and begin the cycle anew.5 Knowing the pulmonary migration pattern of the Angiostrongylus larvae should enable one to appreciate why the associated radiographic abnormalities are so subtle, often going unrecognized.

Filaroides hirthi Filaroides hirthi, also known as lungworm, is found in North America, Europe, and Asia. Entire Beagle

colonies can be infected, but fortunately individual pets only occasionally contract the disease. Although some infected dogs show no clinical signs, most cough or are dyspneic. Diagnosis is by fecal sampling and larval observation using the Baermann technique.6 In my experience, thoracic radiographs of dogs with lungworms are usually unrevealing; when abnormalities are present, they typically consist of a subtle increase in background lung density. Rendano and coworkers, however, reported a great variety of abnormal lung patterns in experimentally infected Beagle puppies, which they characterized as involving all subgross levels of the lung/peribronchial, interstitial, and alveolar tissues.7 Where frank consolidation is present in the thoracic films of a dog with proven lungworm, an additional cause, such as a secondary bacterial pneumonia,

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B

Figure 39-3 • Lateral (A) and ventrodorsal (B) thoracic views of a dog with pneumonia. This disease is unusual, being diffusely distributed, but through only one half of the lung (right).

B

A Figure 39-4 • Lateral (A) and ventrodorsal (B) views of a dog with severe pneumonia, for the most part involving most of the ventral half of the right lung. Looking closely at the ventrodorsal view, it becomes apparent that there is also left-sided disease, although it is mild by comparison.

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A

Figure 39-6 • Ventrodorsal view of a cat with a ruptured pleural abscess causing pneumothorax.

Toxoplasmosis gondii

B Figure 39-5 • A, Dorsoventral view of a dog with severe pleuropneumonia shows a medium volume of pleural fluid and atelectasis, primarily on the right side; B, a right lateral decubitus view shows partial consolidation of the right middle and caudal lobes. Although most of the pleural fluid has drained to the dependent left side of the chest, some fluid persists around the middle lobe.

should be sought because lungworm can cause immune suppression.

Paragonimiasis Pulmonary paragonimiasis is a fluke-borne parasitic lung disease of dogs and cats that is seen primarily in the central and southern parts of the United States. Cavitary lung lesions commonly form in dogs and may rupture, causing pneumothorax. Cats, however, are less likely to develop pneumatocysts.8

Toxoplasmosis, generally a subclinical disease of cats, may take a variety of forms when active: (1) generalized, (2) pulmonary, (3) abdominal, (4) hepatic, (5) pancreatic, (6) cardiac, (7) cutaneous, (8) neurologic, and (9) neonatal. Many affected cats have a concurrent multifocal iridocyclochoroiditis. Dyspnea, polypnea, and signs of abdominal discomfort were the most commonly reported clinical signs. Few cases can be confirmed antemortem. The disease can be transmitted to humans from contaminated vomitus, feces, urine, and exudates from skin ulcers. Thoracic radiographs of febrile cats with toxoplasmosis often show features characteristic of the disease: small, diffuse, poorly demarcated lung densities, pathologically correlated with pneumonic foci located within the interstitium and alveoli.9

Rocky Mountain Spotted Fever (Rickettsia rickettsii) Drost and co-workers infected healthy Beagles with Rickettsia rickettsii, an infection that produced a mild

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A

Figure 39-8 • Lateral view of the thorax of a dog with diffuse blastomycotic pneumonia (diffuse nodular form).

Pulmonary aspergillosis is a rare disease that occasionally affects young immunocompromised cats, often those already infected with panleukopenia. The disease typically appears as small, diffusely distributed lung nodules. Most cases are diagnosed at post mortem. The only dog I have seen with this disease had a solitary, medium-sized mycetoma in its right caudal lobe.

(the primary route of infection), lymph nodes, eyes, skin, and skeleton. The disease most often affects young, large-breed dogs living near major waterways of North America and in the central Atlantic United States. It has also been reported in New York state.11,12 Walker reported on the radiographic appearance of thoracic blastomycosis, describing it as characterized by a “diffuse miliary-to-nodular interstitial pattern.”13 A more recent report by Arceneaux indicates much greater lesion variability, ranging from solitary masses to structured and nonstructured lung patterns.14 Widmer and Downing reported a case of blastomycosis in a young Labrador Retriever whose lung contained a large number of vaguely outlined masses superimposed on one another to the extent that it was impossible to determine their actual size.15 My experience with blastomycosis is also that it can be quite variable, ranging in appearance from one or two small lung nodules to large lung masses. A classic blastomycotic lung featuring diffuse nodules is featured in Figures 39-8 to 39-10 that shows pulmonary mass variants; Figure 39-11 shows calcified hilar lymph nodes. I have yet to see a case of pulmonary blastomycosis in a cat, although a small number of cases have been reported. According to Alden and Mohan, feline thoracic blastomycosis may feature vague or distinct lung nodules, consolidation, atelectasis (as indicated by a cardiac shift), and pleural fluid.16

Blastomycosis

Coccidioidomycosis

Blastomycosis (Blastomyces dermatitidis) is a systemic fungal disease that shows preference for the lung

Coccidioidomycosis (Coccidioides immitis) is fungal disease seen primarily in the southwestern part of the

B Figure 39-7 • Close-up ventrodorsal views of the thorax of a dog before (A) and after (B) treatment for a right cranial lobar pneumonia.

increase in background lung density, which the authors referred to as an “unstructured interstitial disease pattern.”10

❚❚❚ FUNGAL PNEUMONIAS (MYCOTIC PNEUMONIAS) Aspergillosis

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A

B

C

D

E Figure 39-9 • Right lateral (A) and right lateral close-up (B) views of the thorax of a dog with blastomycotic pneumonia (regular mass form) show a small mass located over the caudal vena cava where it intersects the heart. Left lateral view (C) only faintly shows the lesion seen in A and B, but reveals another lesion over the caudoventral aspect of the heart (D). Ventrodorsal (E) and ventrodorsal close-up (F) views show that both lesions are located in the right caudal lung lobe.

F

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D B

C

E

Figure 39-10 • Right lateral (A) and right lateral close-up (B) views of the thorax of a dog with blastomycotic pneumonia (irregular mass form) show a vague crescent-shaped mass superimposed on the inner edge of the cranial heart margin below the aorta. Left lateral (C) and left lateral close-up (D) views also show the lesion, but with better definition, suggesting it is right-sided. The lesion is hidden by the heart In the ventrodorsal view (E).

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diffuse lung nodules. Sternal adenopathy also may be present.18

Histoplasmosis Young cats (less than 3 years old) are the most susceptible to pulmonary histoplasmosis. Burk and co-workers described the radiographic appearance of pulmonary histoplasmosis (Histoplasma capsulatum) in dogs, followed later by Wolf and Green’s description of the disease in cats.19,20 Like most fungal pneumonias, pulmonary histoplasmosis lacks a consistent disease pattern. Abnormalities range from a faint increase in lung density (termed by some an interstitial pattern) to widely disseminated nodules. Others exhibit large areas of lobar consolidation, which sometimes appear cavitated.

A

❚❚❚ FUNGAL-LIKE PNEUMONIAS: ACTINOMYCOSIS AND NOCARDIOSIS

B Figure 39-11 • Lateral (A) and lateral close-up (B) views of a dog with calcified hilar lymph nodes (emphasis zone in B). The adenopathy was thought to be the result of previous blastomycotic pneumonia.

Actinomyces and Nocardia organisms often are referred to as fungal-like diseases because of similarities in their development cycle and the lesions they produce. In my experience, most cases of thoracic Actinomycosis are associated with a large volume of pleural fluid that characteristically appears as a thick reddish brown fluid containing yellow granules. Nocardiosis, on the other hand, usually features hilar adenopathy and little or no pleural fluid. Either form of the disease may contain small diffuse structured or nonstructured lung densities. Suter made similar observations.18

❚❚❚ LIPID PNEUMONIA United States. The most common radiographic expression of pulmonary coccidioidomycosis in dogs is diffuse interstitial disease. Other, less common lung abnormalities include consolidation (Figure 39-12), cavitation, widely disseminated lung nodules, peribronchial cuffing, and hilar adenopathy. A variety of different lung patterns have been described, most of which involve two or more types of lung tissue, a socalled mixed pattern.17 The disease is extremely rare in cats.18

Cryptococcosis Canine thoracic Cryptococcus is rare, usually occurring in the context of widely disseminated disease. Potential radiographic disease indicators include multiple lung masses or nodules (granulomas) and hilar adenopathy. The radiographic appearance of feline thoracic Cryptococcus is highly variable, ranging from a vague increase in background lung density to

Background Dogs and cats sometimes are given mineral oil, vegetable oil, or butter to alleviate constipation or to facilitate the passage of hairballs. Owners attempting to administer such remedies may become overly forceful when animals resist, sometimes leading to accidental inhalation and, subsequently, lipid pneumonia. Oil-based dewormers also have caused pneumonia under similar circumstances, as has milk (or milk supplements) being given to orphaned pups or mature dogs that are not eating. Most simply, lipid pneumonia can be conceptualized as a type of pulmonary foreign body reaction, which occasionally becomes so severe that it cavitates the affected portion of the lung.21

Imaging Findings According to Hudson, there are few detailed radiographic accounts of canine or feline lipid pneumonia.18

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A

B

C

Figure 39-12 • Lateral (A), lateral close-up (B), and ventrodorsal (C) views of a dog with coccidioidomycosis show craniodorsal consolidation. A ventrodorsal view establishes that the lesion is in the right cranial lobe.

Available information suggests that mild lipid pneumonia is unlikely to do little more than subtly increase background lung density or, possibly, fail to change the lung at all. More severe disease has been reported to cause poorly circumscribed, multifocal, perihilar lung densities.

thin and have increased respiratory rates; some also have a soft cough. Most are hunting breeds, although not all hunt. In Canada’s prairie provinces, many such dogs initially are seen in the late fall or early winter, and most have been ill for at least a month.

Imaging Findings

❚❚❚ FOREIGN BODY PNEUMONIA AND ABSCESSATION Background Plant awns are the most common type of pulmonary foreign body. Presumably, most of these are inhaled, perhaps after first being swallowed. They then pass through the wall of a bronchus into the lung, where they embed and usually abscess. In my experience, the accessory and caudal lobes are most often affected. Dogs with plant-awn lung abscesses typically appear

Radiographically, most affected dogs have either isolated pulmonary consolidation or a combination of consolidation and pleural fluid (Figures 39-13 and 39-14). Ultrasound is usually needed to demonstrate the consolidated lobe if the volume of fluid is large and obscures the lung. Where sonography is unavailable, postural radiography can be used to relocate the fluid, allowing identification of the diseased lobe. Medium or full inflation often is required to demonstrate conclusively accessory lobe involvement, and the opacified lobe may blend imperceptibly with the heart in both standard projections.

Figure 39-13 • Ventrodorsal thoracic radiograph shows poorly marginated density over caudal vena cava, which eventually proved to be a wheat sheaf in the main bronchus of the right caudal lung lobe.

A

B

C

Figure 39-14 • Lateral (A), ventrodorsal (B), and ventrodorsal close-up (C) views of a dog with a plant-awn abscess appearing as lobar consolidation.

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References 1. Farrow CS: The thorax. In Farrow CS, ed: Radiology of the cat. St. Louis, 1994, Mosby. 2. King LG, Vite CH: Acute fulminating myasthenia gravis in five dogs. J Am Vet Med Assoc 212:830, 1998. 3. Punto LV, Nevalainen TO, et al: Computed tomography of aspiration pneumonia in a dog. Vet Rad 25:43, 1984. 4. Schmidt M, Wolvekamp P: Radiographic findings in ten dogs with thoracic actinomycosis. Vet Rad 32:301, 1991. 5. Gould SM, McInnes EL: Immune-mediated thrombocytopenia associated with Angiostrongylus vasorum infection in a dog. J Small Anim Pract 40:227, 1999. 6. Crawford P: What is your diagnosis? J Small Anim Pract 41:95, 2000. 7. Rendana VT, Georgi JR, et al: Filaroides hirthi lungworm infection in dogs: its radiographic appearance. J Am Vet Rad Soc 20:2, 1979. 8. Pechman RD: The radiographic features of pulmonary paragonimiasis in the dog and cat. J Am Vet Rad Soc 17:182, 1976. 9. Dubey JP, Carpenter JL: Histologically confirmed toxoplasmosis in cats: 100 cases (1952-1990). J Am Vet Med Assoc 203:1556, 1993. 10. Drost WT, Berry CR, et al: Thoracic radiographic findings in dogs infected with Rickettsia rickettsii. Vet Radiol Ultrasound 38:260, 1997. 11. Cote E, Barr SC, et al: Canine blastomycosis. J Am Vet Med Assoc 210:502, 1997.

12. Rudman DG, Coolman BR, et al: Evaluation of risk factors for blastomycosis in dogs: 857 cases (1980-1990). J Am Vet Med Assoc 201:1754, 1992. 13. Walker MA: Thoracic blastomycosis: a review of its radiographic manifestations in 40 dogs. Vet Rad 22:22, 1981. 14. Arceneaux KA, Taboada J, Hosgood G: Blastomycosis in dogs: 115 cases (1980-1995). J Am Vet Med Assoc 213:658, 1998. 15. Widmer WR, Downing S: Radiographs presented as part of the 1995 ACVR oral certification examination, musculoskeletal section. Vet Radiol Ultrasound 37:110, 1996. 16. Alden CL, Mohan R: Ocular blastomycosis in cats. J Am Vet Med Assoc 164:527-528, 1974. 17. Millman TM, O’Brien TR, et al: Coccidioidomycosis in a dog: its radiographic diagnosis. J Am Vet Rad Soc 20:50, 1979. 18. Suter PF: Lower airway and pulmonary parenchymal diseases. In Suter PF, ed: Thoracic radiology of the dog and cat. Davis, Calif, 1984, Stonegate Publishing. 19. Burk RL, Corley EA, Corwin LA: The radiographic appearance of pulmonary histoplasmosis in the dog and cat: a review of 37 case histories. J Am Vet Rad Soc 19:2, 1978. 20. Wolf AM, Green RW: The radiographic appearance of pulmonary histoplasmosis in the cat. Vet Rad 28:34, 1987. 21. Hudson JA, Montgomery RD, et al: Presumed mineral oil aspiration and cavitary lung lesions in a dog. Vet Radiol Ultrasound 35:277, 1994.

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Pleuritis

❚❚❚ BACKGROUND Most pleural infections in dogs are likely secondary in nature, having spread from the lung, where the initial infection began. These combined infections are most accurately thought of as pleuropneumonias. In severe cases, pus accumulates in the pleural space, a condition called pyothorax.

❚❚❚ IMAGING FINDINGS Radiology The radiographic visibility of pleural fluid depends on volume and location. Using standard positioning and

x-ray beam direction, medium and large volumes of pleural fluid usually can be identified easily as tapered gray bands located between lung lobes, potential spaces called pleural fissures. In dorsoventral or ventrodorsal views, larger fluid volumes often appear as thick gray bands located between the inner surface of the chest wall and the outer surface of the lung. The affected lung often is referred to as being retracted (from the chest wall). Small amounts of pleural fluid are best seen with postural films, such as decubitus, standing, or erect projections, in which the free pleural fluid, under the influence of gravity, is relocated to the lowest point in the thorax. The presence of pleural fluid neither confirms nor denies the presence of pleuritis; nevertheless, it does

A

B

Figure 40-1 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a cat with intestinal lymphosarcoma show unilateral pulmonary edema and a small volume of pleural fluid as indicated by short fluid-bands seen in the lateral projection.

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A

A

B Figure 40-3 • Pyothorax in a cat secondary to a ruptured pulmonary abscess: Lateral (A) and ventrodorsal (B) views show a large volume of pleural fluid that is collapsing much of the lung and partially obscuring the heart.

B Figure 40-2 • Cat with a large volume of pleural fluid and left middle lung lobe collapse as seen in conventional ventrodorsal (A) and postural (B, decubital) radiographs.

support it. On the other hand, thickened pleural surfaces are characteristic of the pleuritis. The presence of one or more partially or fully consolidated lung lobes, in combination with pleural fluid, strongly suggests pleuropneumonia. Bear in mind, however, that congestive heart failure produces similar radiographic findings. Thus, a diagnosis of pleuritis (or pleuropneumonia) must be made contextually. Figures 40-1 to 40-3 illustrate a variety of disorders featuring various amounts of pleural fluid.

Pleurography Although contrast pleurography is now rarely performed, being largely supplanted by ultrasound, the procedure did serve an instructional purpose, namely, to delineate the normal pleural outlines,

and thus define the individual lobes of the lung and the interlobar fissures, where fluid can potentially accumulate.1,2

Ultrasound Ultrasound is capable of detecting small amounts of pleural fluid as well as thickened or fibrin-covered pleura, provided the scanner is placed on the dependent surface of the thorax. Sonography also can be indispensable in obtaining small amounts of pleural fluid transthoracically.

References 1. Bhargava AK, Rudy RL, Diesem CD: Radiographic anatomy of the pleura in dogs as visualized by contrast pleurography. J Am Vet Rad Soc 10:61, 1969. 2. Bhargava AK, Burt JK, et al: Diagnosis of mediastinal and heart base tumors in dogs using contrast pleurography. J Am Vet Rad Soc 11:56, 1970.

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Chylothorax and Peripheral and Central Lymphangiography ❚❚❚ CHYLOTHORAX Background Except in the liver and spleen, blood does not come into direct contact with cells. Rather, exchange between the two takes place in the interstitial fluid. Some of the resultant capillary filtrate (to include plasma proteins) is returned to the venous system by the peripheral lymphatics, which eventually drain into either the thoracic duct or the right lymphatic duct, the central veins, and the heart.1 Functionally, the lymph system, in conjunction with the blood and vascular system, maintains the normal colloidal pressure of the blood plasma and interstitial fluid. A malfunction in the lymph system can lead to edema, and a loss of integrity can cause substantial leakage and an accumulation of chyle in the thoracic cavity (chylothorax) (Table 41-1). Although surgical ligation of the thoracic duct may prove curative, in some cases it fails, in part because of the inability of small collateral lymphatics to maintain, as well as contain, normal lymphatic flow in the face of abnormally high luminal pressure resulting from the ligation of the thoracic duct.2

❚❚❚ IMAGING FINDINGS As with all forms of pleural fluid, the pulmonary effect of chylothorax is mainly volume dependent. The greater the amount of fluid, the greater the amount of atelectasis, which in turn adds to the overall density of the thoracic contents and concurrently diminishes organ detail. Lobar distribution and configuration are often chaotic because of flotation effects. Chyle, like transudate, exudate, and blood, lacks a specific radiographic appearance; however, because of its composition and, to a lesser extent, its viscosity, it is sometimes possible to form inferences based on its effect on the lung. Specifically, animals with chylothorax often show a characteristic rounding of their lung lobes

that frequently persists after fluid removal. In this latter instance, the inability of the lung to fully inflate suggests pleural restriction, a frequent feature of chronic chylothorax.

❚❚❚ DIAGNOSTIC STRATEGY Many animals with large pleural fluid accumulations (to include chyle) and atelectasis are dyspneic, some, particularly cats, dangerously so. In such circumstances, I recommend that these animals be minimally restrained during radiography or sonography. One dorsoventral view is often adequate to estimate how much fluid is present and whether or not it should be removed before making any additional views. If ultrasound precedes radiography, it is best not to scan the animal while it is being restrained on its side or back. Better to allow the animal to sit or assume a prone position and then scan using available surfaces. I prefer to scan such cats while they recline in my lap or on my front thigh, where it is relatively simple to obtain an optimal scan angle. Possible harmful effects associated with transthoracic drainage of a chylothorax are indicated in the following list,5 and it is important to bear these potential complications in mind when reviewing subsequent films: • The lung surface may be lacerated or punctured, leading to pneumothorax, pulmonary hemorrhage, and occasionally a small volume hemothorax. • Circulatory insufficiency may occur as a result of a vagally mediated bradycardia. • So-called reexpansion lung edema may occur as a result of sudden and forceful shearing of the pulmonary capillaries as the lung reinflates following fluid removal. Once it has been established that a chylothorax is present and subsequently relieved, the question of source typically takes precedence. 421

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Table 41-1 • CAUSES OF CHYLOTHORAX Cause

Comment

Cardiomyopathy Certain types of pulmonary tumor Cranial mediastinal tumors

Cats in heart failure due to cardiomyopathy may have a chylous pleural transudate

Diaphragmatic hernia Heart failure Heartworm disease Long-term jugular catheterization Mycotic granuloma (blastomycosis) within cranial vena cava Trauma Venous thrombi

Some large cranial mediastinal tumors; for example, lymphosarcoma may cause secondary lymphatic obstruction, leading to a chylous transudate; other tumors may erode the thoracic duct, allowing chyle to leak into the pleural space Obstruction of cranial vena cava can have a similar effect Particularly those with right-sided failure3 Causes intrinsic obstruction of the cranial vena cava4

❚❚❚ PERIPHERAL AND CENTRAL LYMPHANGIOGRAPHY Background Quick and Jander described aqueous lymphangiography of the canine thoracic duct.6 Martin and colleagues reported a technique for direct lymphangiography of the thoracic duct in the cat.7 Central lymphangiography (cannulation of an abdominal lymphatic) is performed intraoperatively to evaluate the thoracic duct, both for leakage and for the presence of one or more collateral branches. Some advocate making lymphangiograms before and after surgery to avoid missing small collateral branches.8 Additionally, a postprocedural lymphangiogram will aid in the identification of freshly developed collaterals, which form once the thoracic duct has been ligated. Rigg and Riedesel described a method of temporarily occluding lymph flow to the thoracic duct by wrapping a snug (but not fully cinched) ligature around the aorta and closely approximated cisterna chyli. The advantage of this method over conventional dissection and ligation of the cisterna chyli is that it can be accomplished much faster and is less likely to damage the delicate lymphatics. It does not adversely affect aortic blood flow.9 Initially, lymphangiography was performed in unconscious dogs by cannulating a surgically exposed interdigital lymphatic, made visible by an earlier subcutaneous injection of patent blue dye. An oil-based organic iodine solution then was slowly injected, the skin closed, and films made immediately and 1 and 2 days later. Lymphatics and lymph nodes were visible in all films but were optimally seen in the later images. Injection into the hindpaw lymphatics will predictably show the following lymph nodes: superficial and deep popliteal, external and common iliac, and periaortic chain. Provided there is no obstruction and enough iodine solution is injected, the thoracic duct also can be shown. Lymph node opacification typically persists for 4 to 6 months.10

Great care must be taken not to cannulate a vein (instead of a lymphatic) by mistake because to do so, on injection, could lead to pulmonary oil embolism. Postprocedural adenopathy present in experimental dogs was attributed to infection, not to the contrast solution. Wisner and co-workers described the tomographic (computed) measurement of contrasted lymph nodes in miniature swine with the aim of improving the accuracy of cancer staging.11

References 1. Smith CR, Hamlin RL: Microcirculation and lymph. In Swenson MJ, ed: Duke’s Physiology of Domestic Animals, Ithaca, 1977, Cornell University Press. 2. Kerpsack SJ, Smeak DD, Birchard SJ: Progressive lymphangiectasis and recurrent chylothorax in a dog after thoracic duct ligation. J Am Vet Med Assoc 207:1059, 1995. 3. Fossum TW, Miller MW, Rogers KS, et al: Chylothorax associated with right-sided heart failure in five cats. J Am Vet Med Assoc 204:84, 1994. 4. Howard J, Arconaux KA: Blastomycosis granuloma involving the cranial vena cava associated with chylothorax and cranial vena caval syndrome in a dog. J Am Anim Hosp Assoc 36:159, 2000. 5. Fife WD, Cote E: What is your diagnosis? J Am Vet Med Assoc 216:1215, 2000. 6. Quick CB, Jander HP: Aqueous lymphangiography of the canine thoracic duct. J Am Vet Rad Soc 19:178, 1978. 7. Martin RA, Barber DL, et al: A technique for direct lymphangiography of the thoracic duct system in the cat. Vet Rad 29:116, 1988. 8. Birchard SJ, Smeak DD, Fossum TW: Results of thoracic duct ligation in dogs with chylothorax. J Am Vet Med Assoc 193:68, 1988. 9. Rigg DL, Riedesel EA: Circumaortic cysterna chyli ligation. Vet Rad 26:70, 1985. 10. Viamonte M: Lymphangio-adenopathy in dogs. J Am Vet Rad Soc 4:22, 1963. 11. Wisner ER, Siebert JA, Katzberg RW: Quantitative methods for indirect CT lymphangiography. Vet Radiol Ultrasound 39:110, 1998.

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Lung Tumor

❚❚❚ PRIMARY LUNG TUMOR Background One third of dogs with primary lung tumors have no discernible clinical signs; the remaining two thirds variably exhibit cough (58%), listlessness (12%), hemoptysis (9%), and dyspnea (6%). Occasionally, affected dogs develop pleural fluid or hypertrophic pulmonary osteoarthropathy. Diagnostically, radiographs have been most sensitive, identifying a large lung mass in all cases. On the other hand, fine needle biopsy was diagnostic in only a third of the dogs in which it was performed. Transtracheal wash was of no use. Median survival time after surgical removal of the tumor is about a year. As might be expected, dogs with well-differentiated, nonmetastasized, primary lung tumors unassociated with clinical signs survive longest.1 Compared with those in dogs, primary lung tumors in cats are rare, accounting for only 1 to 2% of all feline tumors. Adenocarcinoma is the most common, followed by bronchiolar-alveolar carcinoma and squamous cell carcinoma. Affected cats are usually older and exhibit dyspnea and malaise.

ary lung tumors that, for the most part, focuses on the size and number of lesions. Predictably, large size and small number characterize primary lung tumors, whereas small size and large number are the salient features of metastases.3 Exceptions to this diagnostic reasoning are pulmonary granulomatosis (most often found in Cocker Spaniels) and some types of mycotic pneumonia. Not all primary lung tumors are amenable to such simplified classification, however, as illustrated by this plasma cell tumor, which more closely resembles severe pneumonia than neoplasia (Figure 42-4). Caution: Large chest-wall masses superimposed on the lung have been mistaken for a variety of lesions, including primary lung tumors (Figure 42-5). Cats. Koblik reviewed the radiographs of a mediumsized group of cats with primary lung tumors and reached the conclusions found in Table 42-1.4 Additional features of primary lung tumors in cats included (1) calcification in about 15% of adenocarcinomas, (2) cavitation in about 25% of adenocarcinomas, (3) pleural fluid in about 50% of all tumor types, and (4) hilar adenopathy in about 37% of affected animals.

Imaging Findings Dogs. Primary lung tumors in dogs are often incidental radiographic discoveries (Figure 42-1). In some instances, centrally located primary lung tumors become so large that they resemble a second heart— an observation I have dubbed the double-heart sign (Figure 42-2). Affected animals sometimes have multiple lung masses, most of which are either bronchial or bronchoalveolar carcinomas. Most medium- to large-sized primary lung tumors can be readily identified because of their size, density, and welldemarcated borders (Figure 42-3).2 Suter and colleagues described a diagnostic strategy for discriminating between primary and second-

❚❚❚ PULMONARY METASTASIS (SECONDARY LUNG TUMOR) Lung Screening and Claimed Benefits for Alternate-side Radiography Miles and colleagues advocate routine lung screening for dogs diagnosed with cancer. Their argument is based on a retrospective analysis of thoracic examinations made in dogs diagnosed with nonpulmonary cancer. Using the criteria of single or multiple lung nodules, a presumptive diagnosis of pulmonary metastasis was made in 47 dogs, 27 of which eventually were confirmed as having lung cancer. Of these, most 423

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A Figure 42-1 • Primary lung tumor discovered accidentally during an abdominal examination.

Table 42-1 • RADIOGRAPHIC APPEARANCE OF PRIMARY LUNG TUMORS IN THE CAT Primary Lung Tumor Type

Radiographic Appearance

Adenocarcinoma

Three variants: Single, well-marginated mass Single intralobar consolidation Multiple, poorly marginated masses No consistent appearance

Bronchiole-alveolar cell carcinoma Squamous cell carcinoma

No consistent appearance

were highly malignant thyroid cancers, tumors with a high metastatic potential appearing radiographically as multiple lung nodules. Transitional cell carcinomas were the only other group of significant size (about a quarter of the total); they also appeared as diffuse lung nodules. The remaining metastases were a diverse group of epithelial and mesenchymal tumors with small metastatic potentials, in many cases featuring only one or two representatives. The authors further justified their position by asserting that, in addition to identifying pulmonary metastasis, thoracic screens can serve to establish the extent of the cancer or the presence of additional thoracic disease.5

❚❚❚ WHY LUNG LESIONS MAY SHOW BETTER IN ONE LATERAL VIEW THAN IN ANOTHER Briefly, alternate-side radiography enhances radiographic visibility by improving the contrast between the lesion and its background. This is accomplished by positioning the animal with the affected lung

B Figure 42-2 • Primary lung tumor is difficult to discern in lateral projection (A), but becomes more apparent in ventrodorsal view (B) as a large mass located on the left side of the heart (identified the overlying trachea). Based on probability, a large mass in the lung of a dog, which is about the size of its heart, is usually a primary lung tumor.

uppermost, thus ensuring maximum inflation, the primary source of background contrast. Conversely, when the affected lung is lowermost, it is subject to both mechanical and physiologic forces that promote atelectasis, thus relatively lightening the lung and diminishing the difference between a lesion and its background.6 The described postural-related differences in lung inflation are best exemplified in a normal unconscious dog in which postural atelectasis often becomes so severe that the downward half of the lung becomes nearly opaque while its uppermost half appears almost translucent.

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B

A

C

Figure 42-3 • Three different views of a large lung mass (primary lung tumor) where the lesion appears best in ventrodorsal view (A), and not the often highly touted right (B) and left (C) lateral projections.

A

B

Figure 42-4 • Atypical lung tumor: Lateral (A) and dorsoventral (B) views of a plasma cell tumor that resembles consolidation more than it does a mass.

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A Figure 42-6 • Lateral thoracic radiograph of a dog with pulmonary metastasis from a primary bone tumor (osteosarcoma).

Improving Lesion Clarity

B Figure 42-5 • Surface swelling projected on thoracic interior: Thoracic radiographs of a dog being screened for lung metastasis show a sharply edged opacity in the lateral view (A) and a poorly demarcated right-sided density in the ventrodorsal view (B), both resulting from a lipoma on the right lateroventral aspect of the chest wall.

Having expressed my opinion on the subject, I do not wish to leave the reader with the impression that the use of both right and left lateral views is without merit. On the contrary, there are times when alternate-side radiography is indispensable. For example, where a particular thoracic lesion (usually pulmonary in nature but not necessarily a tumor) appears vague in either a right or left lateral view, obtaining the opposite projection may improve lesion clarity and in particular better show its relationship to other nearby structures. Forest went so far as to recommend an opposite lateral view when pneumonia is suspected and the initial thoracic films are normal.9

Right or Left Lateral? Does a Second Lateral View of the Thorax Increase the Detection Rate of Pulmonary Metastasis? A third view of the thorax (typically a left lateral) is not necessary when routinely screening dogs with cancer for pulmonary metastases.7 Contrary to popular opinion, adding an additional thoracic projection does not increase diagnostic accuracy, nor is it likely to reveal solitary lung lesions, which are invisible in the two standard views. A third view does, however, add to the cost of the examination and to the irradiation of the animal and those who restrain it. Even provided with such objective information, however, some authors continue unabashedly to promote alternateside radiography, asserting that “right and left lateral views should always be included to maximize (diagnostic) sensitivity.”8

If only one lateral view is made, Lang and co-workers assert, the right lateral projection is more sensitive than the left in detecting pulmonary metastasis in the dog.10 Conversely, Tiemessen claims that a left lateral projection, combined with a dorsoventral view, is a reliable method for detecting thoracic metastasis of mammary gland tumors in female dogs.11

❚❚❚ TYPICAL APPEARANCES OF PULMONARY METASTASIS Metastatic osteosarcoma typically appears as multiple lung masses, ranging in size from small to large, tending to the latter. Some are discrete; others are not. Superimposition may exaggerate the size and shape of individual lesions—in some instances markedly, especially in lateral projections (Figure 42-6).

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427

A Figure 42-8 • Rapid breathing exhibited by many dogs and cats with severe pulmonary metastasis (undifferentiated sarcoma) often leads to expiratory images, causing individual lesions to become crowded together, resembling consolidation.

cular cross-section located behind a rib, can realistically mimic a lung nodule, resulting in misdiagnosis. Early in the development of metastatic lung cancer, when lesions are small and few, detection can be difficult, as exemplified in Figures 42-11 and 42-12. Where doubt exists, a second radiographic examination should be performed. The time of the follow-up examination should be based on the doubling time of the primary tumor. If the doubling time is not known, I somewhat arbitrarily reexamine in a month unless the animal’s condition worsens, in which case I redo the chest examination immediately. B

❚❚❚ IS THE LESION GROWING?

Figure 42-7 • Lateral (A) and ventrodorsal (B) radiographs of a dog with pulmonary metastasis from a mammary adenocarcinoma.

A typical metastatic carcinoma, on the other hand, usually appears as numerous small circular lesions. Once again, lesion superimposition often results in some lesions appearing much larger than they actually are (Figure 42-7). No matter what the cell type, the greater the number of lung lesions, especially if they are small and variable in size and density, the more difficult it is to appreciate the metastatic nature of the disease (Figure 42-8). In other words, it is a numbers problem; the more there are, the harder it is to see individual lesions clearly, even when photographically enlarged (Figure 42-9). In general, metastasis located behind a rib is more readily seen than one that is not (Figure 42-10); however, this same phenomenon, but involving a vas-

When judging the growth of previously identified suspected metastases or searching for new nodules, I prefer using paired, right, and left lateral projections. As mentioned previously, I strongly concur with the view that a right or left lateral view, combined with a dorsoventral or ventrodorsal projection, is adequate for metastasis screens.

❚❚❚ UNUSUAL RADIOGRAPHIC FEATURES OF PULMONARY METASTASIS Cavitation Occasionally, a pulmonary metastasis, such as squamous cell carcinoma, becomes cavitated, although in my experience lung cavitation is more a feature of infection than of tumor.12

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B

A

C

D Figure 42-9 • Lesion superimposition: The superimposition of multiple pulmonary nodules—as predictably occurs in many cases of pulmonary metastasis and some mycotic pneumonias—can exaggerate the size of individual lung lesions, especially in the lateral view (A). As the number of nodules per unit volume of lung increases, it becomes harder to accurately determine individual lesion size. Closeup lateral views of the cranioventral (B) and caudodorsal (C) lungfields illustrate the affect of superimposition. The ventrodorsal image (D), although still subject to the deceptive effects of superimposition, usually provides a better estimate of average lesion size, since each half of the lung can be viewed separately.

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429

A

Figure 42-11 • Close-up lateral thoracic radiograph of a dog with pulmonary metastasis shows a number of lesions, some of which are relatively obvious, like the one superimposed on the caudal aorta. The others are more difficult to identify. Try your luck!

B Figure 42-10 • Rib superimposition: Rib superimposition can be misleading; for example, when superimposed on uneven lung consolidation, overlying ribs can mimic pulmonary metastasis. But rib superimposition may also enhance vague or uncertain lesions, especially in the lateral projection as exemplified in this case of metastatic carcinoma (A, B).

Nonstructured or Poorly Structured Pulmonary Metastasis Some forms of pulmonary metastasis, such as lymphosarcoma, can resemble pulmonary edema by virtue of their symmetric, nonstructured appearance (Figure 42-13). Others may look like pneumonia (Figure 4214).

Spontaneous Regression Rarely, presumed or proven pulmonary metastases identified in an earlier radiographic examination disappear in progress studies. In cases in which the animal has received no specific therapy, this phenomenon is termed spontaneous regression (or by the owners, a miracle).13

mass, which then may spread to the regional lymph nodes, liver, and lung. Dogs with this form of cancer are reported to have a median survival time of 61 days.14

Mammary Carcinoma (Mammary Gland Adenocarcinoma) Mammary tumors account for 16% of all canine neoplasms, with approximately half being malignant or potentially malignant, typically spreading to the lung by way of the bloodstream. Radiographically, most metastatic mammary carcinomas appear as diffuse, fairly discrete pulmonary nodules. Adams and Dubeilzig, however, described a far more insidious form of the disease in which the tumor grows in the alveolar septa, resulting in little more than a vague increase in background lung density.15 Forrest and Graybush studied a group of cats with proven secondary lung tumors and found that 17 of 25 lacked definite radiographic evidence of metastasis, instead showing a variety of ill-defined lung densities, most of which were mammary adenocarcinomas.16

❚❚❚ SOME SPECIFIC TUMOR TYPES

Hemangiosarcoma

Malignant Fibrous Histiocytoma

Hammer and co-workers described the radiographic appearance of metastatic pulmonary hemangiosarcoma in the dog. Most commonly, metastatic pulmonary hemangiosarcoma appeared as small, poorly defined,

The giant cell variant of malignant fibrous histiocytoma most commonly begins as a subcutaneous

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B A

C

D

Figure 42-12 • Lateral thoracic radiograph (A) of a dog with pulmonary metastasis, including a close-up of the most cranially positioned lesions (B). Ventrodorsal view (C) shows a pair of lesions superimposed on the top right and bottom left surfaces of the heart. Ventrodorsal close-up view (D) shows increased lesion contrast provided by an underlying bronchus.

coalescing nodules. Less frequently, metastases took the form of full-fledged masses. In some instances, there was related lung hemorrhage, which appeared like any other form of consolidation. The authors proposed the following differential list for the ill-defined nodular form of metastatic pulmonary hemangiosarcoma, which included (1) lung edema, (2) lymphoma, (3) mycotic pneumonia, (4) pulmonary fibrosis, (5) “allergy” (my quotes), (6) toxicosis (specific type not specified), and (7) various types of metastatic carcinomas.17 My personal experience with metastatic hemangiosarcoma differs from that just described, insofar as the appearance of individual lesions is concerned. Specifically, the majority of lesions are small masses

(0.5 cm or greater in diameter) rather than nodules (<0.5 cm), and many of the lesions appear to have relatively lucent centers. The latter observation may be an illusion related to bronchial superimposition because the typical metastasis is no more than a thin-walled, blood-filled chamber.

Mast Cell Tumor Spann and co-workers reported a case of what eventually was diagnosed surgically as a metastatic mast cell tumor. The reason for the report, however, was to illustrate how computed tomography was able to confirm the existence of a lobar mass, something the authors contend was impossible using traditional

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A

A

B

B Figure 42-13 • Poorly structured symmetrical lymphosarcoma

Figure 42-14 • Full lateral (A) and cranioventral close-up

(A, B) more closely resembles pulmonary edema (for which it was initially mistaken) than lung cancer.

(B) views of the lung of a dog with unstructured pulmonary metastasis show a blotchy increase in lung density that partially obscures the lung vessels and bronchi.

methods of medical imaging (radiography and sonography).18

❚❚❚ BENIGN LUNG TUMOR

❚❚❚ PULMONARY LYMPHOSARCOMA Pulmonary lymphosarcoma almost never produces a clear-cut lesion; instead, it often results in a vague increase in pulmonary “linearity” (an increase in small lines with no particular orientation). As might be imagined, the detection of such “shadows” requires highquality films in addition to considerable film reading experience. If the hilar and sternal lymph nodes are also enlarged, the likelihood of lymphosarcoma is much greater.

In my experience, benign lung tumors are rare in both dogs and cats. Most of these initially were detected incidentally as solitary nodules on thoracic survey films. Although the benignity of some of these lesions was confirmed by biopsy, most were not. Instead, the nodule in question was monitored radiographically over a period of months or years; if no further growth occurred, the lesion was considered benign. The latter approach often was chosen for older dogs, in whom surgery or deep biopsy was judged to be dangerous and the owners were disinclined to have their animals operated on, regardless of the potential outcomes.

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References 1. McNiel EA, Ogilvie GK, et al: Evaluation of prognostic factors for dogs with primary lung tumors: 67 cases (1985-1992). J Am Vet Med Assoc 211:1422, 1997. 2. Miles KG: A review of primary lung tumors in the dog and cat. Vet Rad 29:122, 1988. 3. Suter PF, Carrig CB, et al: Radiographic recognition of primary and metastatic pulmonary neoplasms of dogs and cats. J Am Vet Rad Soc 15:3, 1974 4. Koblik PD: Radiographic appearance of primary lung tumors in cats. Vet Rad 27:66, 1986. 5. Miles KG, Lattimer JC, et al: A retrospective evaluation of the radiographic evidence of pulmonary metastatic disease on initial presentation in the dog. Vet Rad 31:79, 1990. 6. Spencer CP, Ackerman N, Burt JK: The canine lateral thoracic radiograph. Vet Rad 22:262, 1981. 7. Barthez PY, Hornof WJ, et al: Receiver operating characteristic curve analysis of the performance of various radiographic protocols when screening dogs for pulmonary metastasis. J Am Vet Med Assoc 204:237, 1994. 8. DeHaan C, Papageorges, Kraft SL: Radiographic diagnosis. Vet Rad 32:75, 1991. 9. Forest LJ: Advantages of the three view radiographic examination in instances other than metastases. Vet Radiol Ultrasound 33:340, 1992.

10. Lang JL, Wortman JA, et al: Sensitivity of radiographic detection of lung metastasis in the dog. Vet Rad 27:74, 1986. 11. Tiemessen I: Thoracic metastases of canine mammary gland tumors. Vet Rad 30:249, 1989. 12. Rief JS, Snider WR, et al: Cavitating pulmonary metastases in a dog. J Am Vet Rad Soc 10:12, 1969. 13. Stone EA, Mahaffy MB: Spontaneous regression of pulmonary metastases in a dog. Vet Rad 22:58, 1981. 14. Waters CB, Morrison WB, et al: Giant cell variant of malignant fibrous histiocytoma in dogs: 10 cases (1986-1993). J Am Vet Med Assoc 205:1420, 1994. 15. Adams WM, Dubeilzig R: Diffuse pulmonary alveolar septal metastases from mammary carcinoma in the dog. J Am Vet Rad Soc 19:161, 1978. 16. Forrest LJ, Graybush CA: Radiographic patterns of pulmonary metastasis in 25 cats. Vet Radiol Ultrasound 39:4, 1997. 17. Hammer AS, Bailey MQ, Sagartz JE: Retrospective assessment of thoracic radiographic findings in metastatic canine hemangiosarcoma. Vet Radiol Ultrasound 34:235, 1993. 18. Spann DR, Sellon RC, et al: Computed tomographic diagnosis: use of computed tomography to distinguish a pulmonary mass from alveolar disease. Vet Radiol Utrasound 39:532, 1998.

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Lung Edema (Pulmonary Edema)

❚❚❚ FIRST DECISION: CARDIAC OR NONCARDIAC? Cardiac Edema Cardiac edema, with rare exception, typically occurs in the context of cardiomegaly and pulmonary hyperemia. Cardiac edema is often unevenly distributed and almost never features the “bat-wing sign” that is commonly shown in human radiology textbooks. In my experience, about 5 percent of dogs in heart failure present with unilateral lung edema, a finding that can be confused with contusions or pneumonia. When increased lung density is not accompanied by heart and vascular enlargement, a diagnosis of heart failure

A

should be made with caution, and noncardiac possibilities should be seriously considered. Numerous examples of cardiac edema are found in the cardiology chapters.

Noncardiac Edema In my experience, many myths surround noncardiac pulmonary edema in dogs and cats. The greatest of these asserts that the edema usually is located in the dorsal portions of the caudal lobes. Although this may be true in some animals (Figure 43-1), it is not a consistent finding (Figures 43-2 and 43-3). Table 43-1 lists causes of noncardiac edema in dogs and cats.1,2

B

Figure 43-1 • Lateral (A) and ventrodorsal (B) views of the thorax of a dog that was recently electrocuted shows poorly outlined dorsal lobe consolidation. The seemingly straightened bronchi are an illusion; the result of inadvertent oblique positioning related the dog’s dyspnea.

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A

B

Figure 43-2 • Full ventrodorsal (A) and close-up views (B) of the lung of a dog suffering from severe heatstroke shows a vague, granular form of pulmonary edema surrounding a Y-shaped bronchogram (B, emphasis zone).

A

B Figure 43-3 • Lateral thoracic radiographs of a cat with acute, progressive pulmonary edema: on admission (A), and 24-hours later (B). As the amount of edema increases, the lung turns a lighter shade of gray, but more importantly, its tissue density increases, causing greater x-ray absorption. The result is a lung that now closely resembles its blood supply, making it difficult or impossible to distinguish between the two.

CHAPTER 43 ❚❚❚ Lung Edema (Pulmonary Edema)

Table 43-1 • CAUSES OF NONCARDIAC EDEMA IN DOGS AND CATS Disease

Comment

Cranial injury Electrocution

More specifically, brain injury Edema is usually located in the dorsal part of the lung, usually the caudal lobes

Heat stroke Hypoglycemia Laryngeal edema Laryngeal injury Laryngeal paralysis Laryngeal tumor Near drowning Pharyngeal edema Rapid reexpansion of collapsed lung Seizures Smoke inhalation Strangulation Thoracic injury

A form of pulmonary edema caused by anoxia of the brain A form of adult respiratory distress syndrome

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References 1. Drobatz KJ, Saunders M, et al: Noncardiac pulmonary edema in dogs and cats: 26 cases (1987-1993). J Am Vet Med Assoc 206:1732, 1995. 2. Stamply AR, Waldron DR: Reexpansion pulmonary edema after surgery to repair a diaphragmatic hernia in a cat. J Am Vet Med Assoc 202:1700, 1992.

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Miscellaneous Lung Diseases

❚❚❚ ALLERGIC BRONCHITIS (FELINE ASTHMA, ASTHMA) Allergic bronchitis, also known as feline asthma, is a disease about which much has been written but little proven, much like pattern recognition in dogs. Based on my experience with confirmed cases, I offer the following. About half of all cats suffering from asthma have normal thoracic radiographs when radiographed initially but may become abnormal in the future (Figure 44-1). Of the remaining population with the disease, half have hyperinflated lungs, to the extent that the first impression on viewing their radiographs is that the images have been overexposed. The remaining cats have abnormally dense lungs that feature a variety of abnormalities, including fine nodules, ring and line shadows, small areas of consolidation, and atelectasis. In some animals, the lung collapse is so severe that the heart lies against the chest wall.

❚❚❚ LUNG-LOBE TORSION Background Primary Torsion. Lung-lobe torsion, at least that diagnosed antemortem, is rare. In part, this is due to the highly variable appearance of lobar torsions and their concealment by associated pleural fluid. Middle lobes, particularly the right, most often develop torsion; cranial and caudal lobe torsions are rare. In my experience, there are no reliable radiographic or sonographic indicators of this disease. The few published reports that describe the radiographic appearance of lung torsion do not provide sufficient case numbers on which to base any reliable generalization.1 Thus there are no typical features, as recently asserted in the literature.2 In my experience, most dogs with an acutely torsed lobe are either dyspneic, shocky, or both, and their pleural fluid contains blood. 436

Secondary Torsions. Conversely, subtotal displacement and full lobar torsion, occurring secondary to a chronic pleural fluid buildup, are difficult to detect radiographically because, in such a context, all the lung lobes are displaced as a result of flotation forces. These animals rarely display any new clinical signs, probably because of the gradual nature of the displacement.

Imaging Findings Radiographic findings associated with lung lobe torsion may include some or all of the following: (1) large volume of pleural fluid, (2) invisibility of much of the lung, (3) pulmonary consolidation, (4) misdirected principal bronchus, (5) abbreviated principal bronchus, (6) absent principal bronchus, (7) nonspecific mass effect, and (8) cardiac shift (mediastinal shift). It should be noted at this point that lung lobes are always displaced to some extent when surrounded by medium to large volumes of pleural fluid. This is due to what I term the flotational effect, in which air-filled or partially air-filled lung lobes attempt to move to the highest point in the thoracic cavity while the associated pleural fluid attempts to do the opposite. The resultant visceral relocation often appears visually chaotic, especially in standard lateral projections. Radiographs made in these circumstances invariably show many of the abnormalities claimed by some to be indicative of torsion. Siems and co-workers reported an unusual case of lung-lobe torsion in a 6-month-old Bloodhound that had eaten warfarin a month earlier. Radiographs showed pleural fluid (with variable degrees of lobar displacement), pleural air, lung collapse, cavitation, compensatory hyperinflation, and increased density in the cranial mediastinum. Necropsy revealed hemothorax, hemomediastinum, and torsion of the right cranial and caudal lung lobes with associated alveolar rupture in the caudal lobe.3

CHAPTER 44 ❚❚❚ Miscellaneous Lung Diseases

437

A

C B Figure 44-1 • Ventrodorsal thoracic radiograph (A) of a dyspneic cat with a presumptive diagnosis of allergic bronchitis. Like many asthmatic cats, the lung appears normal. In a progress film made a year later (B), the lung density has increased and now features a fine nodular appearance (C).

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❚❚❚ SMOKE INHALATION Background I published my first experience treating dogs with smoke inhalation in 1975, followed by an additional report 2 years later.4,5 These initial communications were the basis for a series of chapters on this most fascinating subject, which appeared in Current Veterinary Therapy VI and VII, Decision Making in Small Animal Radiology, Emergency Radiology in Small Animal Practice, Feline Radiology, and Equine Respiratory Disorders. During the same period, I served as a consultant to the Society for the Prevention of Cruelty to Animals (SPCA) on kennel and barn fires. In addition to my own work, which presently focuses on the radiographic appearance of smoke inhalation in dairy cattle, Drobatz and co-workers at the University of Pennsylvania recently published timely updates on the subject.6,7 In both reports, the authors emphasize the fluctuating nature of smoke injury in pets and advocate dynamic prognosis (my expression for a dayto-day, continuously updated prognosis, made during the week immediately following smoke inhalation and burns). Smoke inhalation may or may not affect the lung so that it can be detected radiographically. Toxicity is variable, depending on what has burned, and thus the composition of the smoke: wood, plastic, paint, chemicals, and so forth. Associated bronchial injury (for the most part, burns) cannot be detected with conventional radiography, but these injuries can affect lung clearance in the event of infection.

Figure 44-2 • Smoke Inhalation: Ventrodorsal radiograph of a dog rescued from a house fire 24 hours earlier. Although the initial thoracic radiographs were normal, the follow-up films (shown here) revealed an edematous right lung. Delayed-onset pulmonary edema and/or pneumonia commonly occur after severe smoke inhalation.

deep or widespread skin burns may develop septicemia leading to pneumonia and, in some instances, adult respiratory distress syndrome (ARDS). Disseminated intravascular coagulopathy (DIC) is unusual.

Imaging Findings Lung abnormalities, as mentioned previously, are quite variable and often are not evident in films made during the first 24 hours after admission. In unconscious or sedated animals, varying degrees of postural atelectasis are frequently present and can be difficult to distinguish from lung edema. Barring infection, most dogs that have sustained serious smoke or heat injuries to the lung will have or will develop abnormalities in the first 72 hours after the fire. These abnormalities may be subtle, consisting of a slight increase in background lung density, or they may be overt, taking the form of multilobe consolidation. It is not unusual initially to observe unilateral lung involvement that may or may not later involve the opposite lung (Figure 44-2). Where progress of pulmonary edema secondary to smoke inhalation is being monitored, 24-hour progress films are justified, given the labile nature of excessive lung water. On the other hand, exudate formed as a result of chemical/particulate inflammation or bacterial infection is more slowly cleared from the terminal air spaces, warranting lengthier intervals between progress examinations. Where extensive bronchial burns are present, obstructive-like lung disease may develop. Dogs with

❚❚❚ NEAR-DROWNING Background Near-drowning is the survival, at least temporarily, after involuntary submersion in some sort of liquid medium, usually water. Resultant pathophysiologic alterations may arise as a consequence of asphyxia caused by reflex laryngospasm or, more commonly, as a result of aspiration of the drowning fluid.8 I have seen radiographs of animals nearly drowned in the ocean, rivers, lakes, farm dugouts, wells, and home swimming pools. One of the most common circumstances is where someone repeatedly throws a stick for his or her dog into a river, underestimating the strength of the current. Eventually, the dog tires and is carried down river, unable to reach the safety of shore. I also have had considerable experience with dogs that have gone through ice.

Imaging Findings As with smoke inhalation, the lung abnormalities of nearly drowned dogs and cats are extremely variable, ranging from a nonspecific increase in lung density

CHAPTER 44 ❚❚❚ Miscellaneous Lung Diseases

439

A

Figure 44-3 • Near-Drowning: Thoracic radiograph made shortly after dog was pulled unconscious from a river and subsequently resuscitated, shows mild consolidation in the central part of the right caudal lobe.

(Figure 44-3) to massive consolidation. Abnormal densities seen in initial films usually are inhaled water or, alternatively, vomit. Depending on the composition of the inhaled fluid, fresh or salt water, chlorine (in the case of swimming pools), algae (in the case of shallow, stagnant waters), bacteria (in the case of old wells used for dumping and containing rain water), secondary pneumonia may occur. In shallow, sandy-bottomed rivers with turbulent flow, animals can tumble along the bottom, inhaling sand in the process. As a result, these bronchi may be visible radiographically as the so-called sand bronchogram.

❚❚❚ NEAR-STRANGULATION Background Near-strangulation, depending on how long the brain has been deprived of oxygen, can produce symmetric lung edema, similar to what is found in congestive heart failure. Unlike heart failure, there is usually no heart enlargement; or if concurrent unrelated heart disease is present, there is no pulmonary hyperemia. Thus noncardiogenic edema caused by near-strangulation can be distinguished from heart failure.9

Imaging Findings As mentioned, near-strangulation (without a broken neck) may cause noncardiogenic edema, which in my experience has no single characteristic appearance. The

B Figure 44-4 • Strangulation: Lateral thoracic radiograph (A) made shortly after dog caught its head between a pair of fence posts shows what at first appears to be an expiratory radiograph but is actually caudal lobe consolidation—a deception revealed in the ventrodorsal view (B).

resultant edema, however, whether unilateral or bilateral, often predominates in the dorsal half of the lung, particularly in the caudal lung lobes. Another variation consists of complete consolidation of both caudal lobes, leading to a “swept-wing” appearance in the dorsoventral or ventrodorsal views (Figure 44-4). Patchy asymmetric consolidation occurs less often, usually in cats (Figure 44-5).

❚❚❚ WARFARIN POISONING Warfarin is an anticoagulant that is used in some animal rat poisons. Animals that eat warfarin-laced baits bleed internally, sometimes to death. An unsuspecting owner often brings a weak or recently collapsed dog that has consumed warfarin to the veterinarian (or an emergency clinic), where the possibility of poisoning may

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respiratory distress syndrome. Dogs that survive the acute period usually rapidly die of severe pulmonary fibrosis. Most dogs poisoned by paraquat die in a few days from adult respiratory syndrome, the result of fibrin lining the alveoli, which renders the surfactant inoperable, causing the distal air spaces to collapse, leading to suffocation. Radiographically, the acute paraquat lung is characterized by underinflation and widespread consolidation, the latter featuring greatly enhanced bronchial visibility as a result of air-bronchogram formation (Figure 44-8).

Idiopathic Pulmonary Fibrosis

Figure 44-5 • Strangulation: Ventrodorsal thoracic radiograph of a cat shortly after being caught by the neck in a garage door opener shows bilateral lung consolidation and underinflation.

or may not be considered, depending on the doctor’s familiarity with warfarin intoxication. In my experience, warfarin poisoning in dogs usually leads to lung hemorrhage, which may extend into the pleural space and mediastinum. Asymmetric consolidation appears to be the rule, a finding that may be misdiagnosed as pneumonia or, if the animal has been lost and then found, lung contusion. Widespread patch consolidation attributable to uneven lung bleeding may be mistaken for metastasis or mycotic pneumonia (Figure 44-6). A consolidated lung lobe, especially if combined with a large volume of pleural fluid, can be misinterpreted as lung-lobe torsion (Figure 44-7). Berry and co-workers described thoracic abnormalities caused by warfarin poisoning in dogs.10 These include (1) pleural hemorrhage, (2) mediastinal hemorrhage (in one third of these dogs there was associated tracheal narrowing), (3) cervical hemorrhage, (4) thoracic inlet hemorrhage, and (5) pulmonary hemorrhage. Thoracic radiographs returned to normal anywhere from 1 to 5 days after treatment with vitamin K1.

❚❚❚ PARAQUAT POISONING AND OTHER FORMS OF FIBROSING LUNG DISEASE Paraquat Poisoning Paraquat poisoning rarely occurs in dogs and is usually fatal. Early deaths are usually due to adult

As indicated by its name, the cause (or causes) of idiopathic pulmonary fibrosis (IPF) is unknown. Histologic findings are consistent with an active inflammatory disease that results in progressive pulmonary fibrosis. Corcoran and co-workers speculated that IPF is a form of immune-mediated pneumonia.11 For the most part, the disease affects middle-aged to older West Highland White Terriers that have a history of chronic, progressive illness, characterized by cough, dyspnea, inspiratory crackles (auscultatory), and decreased exercise capacity. Although thoracic radiographs were considered abnormal (increased interstitial lung density), little or no radiologic/pathologic correlation was found. I have yet to encounter this disease.

❚❚❚ ELECTRIC SHOCK Background The exact manner in which lung edema and hemorrhage occur as a result of nonlethal electrocution is not known; however, most authorities view it as a form of neurogenic pulmonary edema.

Imaging Findings Suter reported that nonlethal electrocution has a characteristic radiographic appearance, namely, consolidation of the middle portion of the caudal lung lobes.12 Others noted a high correlation between the presence of lung consolidation and gingival burns. I have been unable to confirm these generalities. Most dogs I have radiographed that have been observed by their owners to be biting an electrical cord (and become ill or incapacitated as a result) have not had caudal-lobe edema, although some have. Most, however, had some evidence of electrical burns in the mouth. Dogs that had not been observed biting into electrical cords, but rather had only been suspected of doing so by their owners or attending veterinarians, rarely had oral lesions. The edema pattern in this latter group was also highly variable, but many appeared normal (Figure 44-9).

CHAPTER 44 ❚❚❚ Miscellaneous Lung Diseases

441

A

C

B Figure 44-6 • Warfarin poisoning: Thoracic radiographs made of a dog recently poisoned by warfarin show lung, pleural, and mediastinal hemorrhage. These types of changes can be deceptive, especially if warfarin poisoning is not suspected. For example, the uneven cranial lobe hemorrhage seen in the full lateral (A) and cranioventral close-up (B) projections resembles metastasis, whereas the right caudal lobe bleeding seen in the ventrodorsal view looks more like pneumonia (C).

❚❚❚ DISSEMINATED INTRAVASCULAR COAGULATION Background Disseminated intravascular coagulation, or DIC as it is commonly termed, is a complex thrombohemorrhagic disorder that inconsistently (and thus unpredictably) develops subsequent to a number of different diseases, including septicemia, severe trauma, pancreatitis, various immune disturbances, shock, metastases, and myeloproliferative forms of cancer.13

Imaging Findings Suter reported DIC as having a nonspecific radiographic appearance that often is misdiagnosed as pulmonary edema or neoplasia. He hypothesized that the considerable variation observed in chest films of necropsy-proven cases was a reflection of the “phase and intensity” of the disease. The most common expression of DIC was described as a “barely perceptible increase in interstitial radiodensity.” A diffuse or mottled alveolar pattern, characterized as “acinar lesions,” was thought to be indicative of “severe pulmonary involvement.”

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A Figure 44-8 • Paraquat poisoning: Lateral radiograph of a dog poisoned by paraquat shows widespread consolidation, causing the trachea and bronchi to resemble a “tree in winter.” What appears to be a random expiratory film is actually atelectasis secondary to adult respiratory distress syndrome.

B Figure 44-7 • Warfarin poisoning: The cranial mediastinum (A) and most of the left side of the thorax (B) are obscured by pleural blood. The retracted lateral border of the left lung is faintly visible through the fluid.

Figure 44-9 • Electrocution: Ventrodorsal radiograph of a puppy that bit into a power cord shows right-sided lung edema. The angular opacity along the left side of the cranial mediastinum is the thymus.

CHAPTER 44 ❚❚❚ Miscellaneous Lung Diseases

Effectively treated animals showed rapid lung clearing.14 Like other medical imagists, I have been able to diagnose DIC with confidence only occasionally. Based on postmortem conformation and subsequent radiographic correlation, vague patchy, centralized consolidation has been the most common radiographic appearance, although it has been difficult to determine what part of the abnormal lung density is attributable to primary disease and what portion is the result of DIC.

443

❚❚❚ FELINE ENDOGENOUS LIPID PNEUMONIA Background Endogenous lipid pneumonia, as distinct from exogenous lipid pneumonia, results from pneumocyte injury, usually caused by obstructive lung disease, and, in particular, various forms of obstructive pulmonary neoplasia.

Imaging Findings

❚❚❚ ACUTE RESPIRATORY DISTRESS SYNDROME Background Acute respiratory distress syndrome (ARDS) describes a group of diseases that have as common features alveolar fibrin deposition (hyaline membranes), diffusion block, ineffective surfactant, atelectasis, and hypoxemia; the result is usually death. Similar pathologic findings also have been reported with severe chest injuries, resulting in the name traumatic respiratory distress syndrome. In 1978 we reported one of the first cases of respiratory distress syndrome in a dog, which was caused by paraquat poisoning.15 I later described similar disease mechanisms (along with their characteristic radiographic appearances) associated with near-drowning, smoke inhalation, and strangulation.16-18 In 1996 Parent and co-workers reported on a series of 19 proven cases of ARDS in dogs. Diseases believed to have initiated ARDS in these animals included (1) severe pneumonia, in some cases associated with mechanical ventilation; (2) inhalation of gastric fluids or a combination of gastric fluids and associated semisolids; (3) smoke inhalation; (4) oxygen toxicity associated with assisted ventilation; (5) DIC, near-strangulation, and organ torsion.19,20

Imaging Findings Like other progressive and often fatal lung diseases, ARDS results in a radiographic spectrum, the components of which are determined largely by the phase of the disease that the animal is in when radiographed. Ignoring any existing disease, little or no additional density should be expected as ARDS begins. As protein begins to enter the interstitium, a small increase in background lung density can be anticipated. Once fibrin begins to coat the inner surface of the alveoli, atelectasis begins, leading to a further increase in lung density and a commensurate loss in volume. As the collapse increases, the lung gradually becomes denser and the bronchi more visible.

Various nonspecific radiographic abnormalities reported in a small series of cats with endogenous lipid pneumonia included pleural fluid, “interstitial and bronchointerstitial lung patterns,” multifocal lung densities, pulmonary nodules, and hyperinflation. Only 2 of the 12 examined cats had normal thoracic films.21

❚❚❚ PULMONARY THROMBOSIS, PULMONARY EMBOLISM, AND PULMONARY THROMBOEMBOLISM Background A pulmonary thrombus is a discrete mass composed of platelets, fibrin, and a mixture of other blood cells, which originates on the inner surface of a pulmonary blood vessel (intima). Depending on its size, its location, and the availability of collateral circulation, it may result in the functional loss of some or the entire downstream portion of the lung. A pulmonary embolus is similar physically and functionally to a pulmonary thrombus, but it differs with respect to its nonpulmonary origins. Pulmonary thromboemboli occur in dogs more often than in cats, with the latter more susceptible to systemic emboli. Reported potential causes of pulmonary thromboembolism in dogs include the following: • DIC • Heart diseases, such as dilated cardiomyopathy and Dirofilaria • Renal glomerular disease • Pancreatitis • Malignant tumors • Bacterial and fungal infections • Hyperadrenocorticism • Immune-mediated hemolytic anemia Middle-aged to older dogs (mean, 9.8 years) with one or more of the aforementioned diseases (myopathy, cancer, infection, and others) are the prototypical victims, probably as a result of a combination of inciting, disease-related factors, including venous stasis, endothelial injury, and inappropriate coagulation. The presence of one or more indwelling catheters appears to increase risk greatly.

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Major clinical signs and laboratory findings are dyspnea, tachycardia, and arterial hypoxemia. Eighty percent of the dogs in one reported series had indwelling catheters installed within a month of their eventual deaths.22

Imaging Findings Until recently, little has been published describing the radiographic or sonographic appearance of pulmonary embolism in dogs and cats. Cats. Reported radiographic abnormalities in cats with pulmonary thromboembolism are equally varied and include the following:23 • Uneven diameter of some individual blood vessels • Variable number of visible vessels between right and left lung lobes • Normal to slightly enlarged central lung vessels, which disproportionately taper as they extend peripherally • Hyperlucent lung periphery • Poorly marginated areas of consolidation, usually located in the caudal lobes of the lung Sottiaux and Franck published such findings in an aged cat.24 A 14-year-old cat was diagnosed with pulmonary embolism 2 weeks after surgery to debride a dorsolumbar abscess. Additionally, the cat was found to have cor pulmonale. Radiographic abnormalities included (1) an abrupt termination of the right pulmonary artery, (2) right caudal lobe oligemia, and (3) right-sided pulmonary consolidation. Sonographic findings included (1) dilation of the right pulmonary artery, (2) right ventricular dilation, (3) decreased movement of the right ventricular wall, (4) right atrial dilation, and (5) tricuspid regurgitation. Doppler sonography showed elevated pulmonary arterial pressure (56 mm Hg). Interpretation of the described medical imaging was as follows: • The radiographic signs were indicative of circulatory disease, specifically, obstruction of the right pulmonary artery with resultant lobar oligemia. The consolidation was most likely the result of pulmonary edema. • The sonographic abnormalities supported pulmonary hypertension secondary to pulmonary embolism. • Specifically, the dilation of the right pulmonary artery (in the absence of a right to left shunt) is a sonographic indicator of pulmonary hypertension. • The diminished motion of the right ventricular wall (termed hypokinesis by cardiologists) is indicative of reduced contractility caused by impaired systolic function secondary to elevated pulmonary arterial pressure. • Right atrial dilation is attributed to tricuspid regurgitation, which is a complication of pressure overload.

Differentiation of Acute Versus Chronic Cor Pulmonale. Acute versus chronic cor pulmonale can be differentiated sonographically (on a probability basis) based on the thickness of the right ventricular wall. A thin right ventricular wall is most consistent with an acute cor pulmonale, whereas a thickened right ventricle supports chronicity. The thinking here is that adaptation, in the form of right ventricular hypertrophy, requires time. Simple dilation, on the other hand, can be nearly instantaneous. Dogs Radiography. Fluckiger and Gomez were the first to describe the radiographic findings in a series of dogs with pulmonary thromboembolism (PTE).25 They concluded that there were two major lung patterns: (1) regional oligemia (decreased blood supply), causing the affected lung to appear overly dark; and (2) regional consolidation, indicating either hemorrhage or infarction. Others made similar observations, including (1) mixed interstitial-alveolar lung patterns, (2) heart enlargement, (3) regional hyperlucency of the lung, and (4) pleural fluid. Although specific arterial abnormalities similar to those described in heartworm disease, such as pruning and prominence, have been mentioned occasionally in the literature on PTE, they are exceptional. Numerous reports have appeared in the literature describing arterial thrombosis in the lungs of dogs with heartworm disease, although many of these are unconfirmed, presumptive diagnoses.26 Nuclear Imaging. Koblik and co-workers performed perfusion and ventilation studies on the lungs of normal dogs, animals with experimentally created pulmonary emboli, and a single naturally occurring case. They concluded that technetium-99 (99mTc)-DTPAaerosol works well in evaluating pulmonary ventilation in dogs and when combined with 99mTc-MAA. In a later study, it was determined that nuclear ventilation-perfusion imaging (as described already) was diagnostically superior to either pulmonary angiography or digital subtraction angiography as a screening method for dogs in whom PTE was suspected.27 Positive diagnosis (for PTE) used ventilation/perfusion scans: abnormal perfusion, normal ventilation.28

❚❚❚ NEUROGENIC PULMONARY EDEMA Background Numerous pathologic pathways to account for neurogenic pulmonary edema have been proposed by medical authorities. These theoretical explanations in turn have been adopted or modified by veterinarians, including Suter, whose minimally edited scheme appears in Box 44-1.29

CHAPTER 44 ❚❚❚ Miscellaneous Lung Diseases

B o x

445

4 4 - 1

A Proposed Pathway for the Formation of Neurologic Pulmonary Edema • Hypothalamic injury, intracranial pressure increase • Massive central alpha-adrenergic discharge (overstimulation) • Generalized vasoconstriction of systemic circulation • High systemic and pulmonary vascular pressures • Redistribution of blood volume, increased venous return • Severe pulmonary capillary hypertension and increased pulmonary blood volume • Injury to pulmonary capillary endothelium • Increased vascular permeability leading to leakage and, eventually, pulmonary edema

Imaging Findings Theoretically, neurogenic pulmonary edema begins centrally and spreads peripherally, similar to the edema resulting from heart failure. Unlike cardiogenic edema, the heart and pulmonary vasculature are not enlarged. Where heart disease (endocarditis, for example) already exists before the onset of neurogenic pulmonary edema, differentiation between cardiogenic and noncardiogenic edema becomes more difficult.

Figure 44-10 • Ventrodorsal thoracic radiograph of a dog with allergic pneumonia (PIE syndrome) shows uneven consolidations, especially surrounding the heart.

❚❚❚ PULMONARY INFILTRATES WITH EOSINOPHILIA Background Pulmonary infiltrates with eosinophilia (PIE), or PIE syndrome, as the disease is also known, was first described in people with a variety of different allergic lung diseases that shared the common clinical characteristics of (1) partial lung consolidation and (2) peripheral eosinophilia. Thus the disease is termed a syndrome. Lord and co-workers gave the same name to a number of parasite-related lung diseases seen in dogs, which also featured pulmonary consolidation and elevated eosinophils.30

Imaging Findings Suter suggested that, as with humans, the type of immunologic lung disease (I–III) may be used to predict associated radiographic abnormalities (so-called type I–III immune reactions). To date, this hypothesis continues to await confirmation.29 In my experience, the most common appearance of PIE is either a diffuse pattern of patchy lung consolidation (Figure 44-10) or a generalized increase in central lung density.

❚❚❚ IDIOPATHIC PULMONARY OSSIFICATION Thrall and co-workers reported a case of idiopathic pulmonary ossification in a dog.31 Differential diagnosis

Figure 44-11 • Lateral thoracic radiograph of a dog being screened for pulmonary metastasis shows numerous fine nodules throughout the lung, a benign condition known as microlithiasis.

for pulmonary calcification includes (modified from Thrall31): • Adrenal tumor • Alveolar microlithiasis (Figure 44-11) • Calcification of pulmonary arteries secondary to systemic hypertension • Dystrophic pulmonary calcification • Idiopathic calcification • Idiopathic ossification

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• Metastatic pulmonary calcification • Some metastatic tumors such as osteosarcoma (rare)

❚❚❚ GENERALIZED PULMONARY CALCIFICATION SECONDARY TO CUSHING’S DISEASE Berry and co-workers described four cases of pulmonary mineralization secondary to Cushing’s syndrome. Radiographically, the appearance of the affected lung varied from a vague increase in background lung density to nearly imperceptible nodular densities interpreted as possibly calcific. Nuclear medicine studies using technetium methylene diphosphate revealed generalized pulmonary uptake in two dogs, but subsequent microaggregated albumin perfusion scans proved normal.32 A

❚❚❚ PULMONARY ARTERIAL AND PARENCHYMAL CALCIFICATION Lefbom and co-workers described a case of widespread arteriosclerosis in a cat, which appeared in both abdominal and thoracic radiographs and was believed to have been caused by systemic hypertension. Regional lung calcification was also present, although its cause was not determined.33

❚❚❚ CONGENITAL PULMONARY CYSTS Congenital lung cysts are rare; most are discovered incidentally or when a “spontaneous” pneumothorax occurs following rupture. Reported cyst sizes range from a few centimeters to nearly the size of an entire lung lobe. Postural films may reveal an air-fluid interface, especially following rupture.34

❚❚❚ RADIATION PNEUMONITIS Radiation pneumonitis, as implied in the name, refers to radiation-induced lung injury, an often unavoidable by-product of radiation therapy. The injury develops in two stages: an acute pneumonitis stage, following a variable latent period of 1 to 6 months, and a later developing fibrosis stage.

Stage 1: Acute Pneumonitis Phase of Pulmonary Radiation Injury In the acute pneumonitis stage, the alveolar epithelium and vascular endothelium are believed to be the primary sites of injury, leading to an exudation of fibrinladen fluid into the terminal air spaces, accumulation of mononuclear cells, and vascular congestion. This pathology is radiographically evident as a vague increase in background lung density.

B Figure 44-12 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a Cocker Spaniel with pulmonary granulomatosis show multiple lung masses resembling lung cancer.

Stage 2: Chronic Fibrosis Phase of Pulmonary Radiation Injury The chronic fibrosis phase of radiation-induced radiation injury develops unpredictably between 2 and 24 months after irradiation and permanently changes the lung. Interstitial fibrosis occurs as a result of fibrin buildup in the lung, which some theorists believe is due to an absence of fibrinolytic activity caused by earlier pneumocyte injury. This pathology is also radiographically detectable, appearing as a variable, nonstructured increase in background lung density.

CHAPTER 44 ❚❚❚ Miscellaneous Lung Diseases

447

granulomatosis, lymphomatoid granulomatosis, pulmonary eosinophilic granulomatosis, and eosinophilic granulomatosis.38-40 In my experience, Cocker Spaniels are affected more than any other breed of dog.

Imaging Findings Thoracic radiographs typically show 3 to 10 large, variably sized and shaped lung masses. In some animals, the bronchi are markedly dilated, resembling bronchiectasis. Figures 44-12 and 44-13 exemplify the radiographic features of this disease.

References Figure 44-13 • Lateral thoracic radiograph of a Cocker Spaniel with granulomatosis, which like the dog in Figure 44-12, resembles lung cancer. There is also dilation of the principal bronchi to the cranial lobes, an inconsistent feature of this disease.

❚❚❚ PULMONARY FOREIGN BODY Radlinsky and colleagues described a large wooden splinter embedded in the abscessed lung of a dog, which appeared sonographically as a shadowing, irregular linear echogenicity, surrounded by flocculent fluid. Comet tail artifacts also were detected within the presumed abscess and attributed to gas. At surgery, a large tract also was identified that had formed between the point of entry in the third intercostal space, the adjacent pleura, and the foreign body abscess.35

❚❚❚ PNEUMOCYSTIS CARINII PNEUMONIA Kirberger and colleagues reported Pneumocystis carinii in immunocompromised miniature Dachshunds. Radiographically, the observed lung abnormalities were described as ranging from “a mild interstitial and bronchial pattern, to an alveolar pattern.”36 Pneumocystis is normally a harmless lung parasite (most likely a protozoan) that becomes pathogenic only when its host becomes immunocompromised. In humans and horses, the earliest radiographic abnormality typically is found in the terminal air spaces, not surprising because this is where the organism resides.37

❚❚❚ PULMONARY GRANULOMATOSIS Background Pulmonary granulomatosis goes by several names, depending on the cellular composition and organization of the primary lesions: pulmonary lymphomatous

1. Brown NO, Zontine WJ: Lung lobe torsion in the cat. J Am Vet Rad Soc 17:219, 1976. 2. Brenner OJ, Ettinger SN, Stefanacci JD: What is your diagnosis? J Am Vet Med Assoc 216:1555, 2000. 3. Siems JJ, Jakovljevic S, Van Alstine W: Lung lobe torsion. Vet Radiol Ultrasound 39:418, 1998. 4. Farrow CS: Smoke inhalation in the dog: current concepts of pathophysiology and management. Vet Med & Small Anim Clin 40:4, 1975. 5. Farrow CS: Near-drowning in the dog. J Am Vet Rad Soc 18:6, 1977. 6. Drobatz KJ, Walker LM, Hendricks JC: Smoke inhalation in dogs: 27 cases (1988-1997). J Am Vet Med Assoc 215:1306, 1999. 7. Drobatz KJ, Walker LM, Hendricks JC: Smoke inhalation in cats: 22 cases (1986-1997). J Am Vet Med Assoc 215:1312, 1999. 8. Farrow CS: Near-drowning in the dog. J Am Vet Rad Soc 18:6, 1977. 9. Farrow CS: Strangulation. In Farrow CS, ed: Emergency radiology in small animal practice. Toronto, 1988, Decker. 10. Berry CR, Gallaway A, et al: Thoracic radiographic features of anticoagulant rodenticide toxicity in fourteen dogs. Vet Radiol Ultrasound 34:391, 1993. 11. Corcoran BM, Dukes-McEwan J, et al: Idiopathic pulmonary fibrosis in a Staffordshire bull terrier with hypothyroidism. J Small Anim Pract 40:185, 1999. 12. Suter PF: Lower airway and pulmonary parenchymal diseases. In Suter PF, ed: Thoracic radiology of the dog and cat. Stonegate Publishing, Davis, Calif, 1984. 13. Bateman SW, Mathews KA, et al: Diagnosis of disseminated intravascular coagulation in dogs admitted to an intensive care unit. J Am Vet Med Assoc 215:798, 1999. 14. Suter PF: Lower airway and pulmonary parenchymal diseases. In Suter PF, ed: Thoracic radiology of the dog and cat. Davis, Calif, 1984, Stonegate Publishing. 15. Gee BR, Farrow CS, White RJ: Paraquot toxicity resulting in respiratory distress syndrome in a dog. J Am Anim Hosp Assoc 14:256, 1978. 16. Farrow CS: Near-drowning. In Kirk RW, ed: Current veterinary therapy VIII. Philadelphia, 1983, WB Saunders. 17. Farrow CS: Inhalation injury. In Kirk RW, ed: Current veterinary therapy VIII. Philadelphia, 1983, WB Saunders. 18. Farrow CS: Strangulation. In Farrow CS, ed: Emergency radiology in small animal practice. Toronto, 1988, Decker. 19. Parent C, King LG, et al: Clinical and clinicopathologic findings in dogs with acute respiratory distress syndrome: 19 cases (1985-1993). J Am Vet Med Assoc 208:1419, 1996.

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20. Parent C, King LG, et al: Respiratory function and treatment in dogs with acute respiratory distress syndrome: 19 cases (1985-1993). J Am Vet Med Assoc 208:1428, 1996. 21. Jones DJ, Norris CR, et al: Endogenous lipid pneumonia in cats: 24 cases (1985–1998). J Am Vet Med Assoc 216:1437, 2000. 22. LaRue MJ, Murtaugh RJ: Pulmonary thromboembolism in dogs: 47 cases (1986-1987). J Am Vet Med Assoc 197:1386, 1990. 23. Norris CR, Griffey SM, Samii VF: Pulmonary thromboembolism in cats: 29 cases (1987–1997). J Am Vet Med Assoc 215:1650, 1999. 24. Sottiaux J, Franck M: Pulmonary embolism and cor pulmonale in a cat. J Small Anim Pract 40:88, 1999. 25. Fluckiger MA, Gomez JA: Radiographic findings in dogs with spontaneous pulmonary thrombosis or embolism. Vet Rad 25:124, 1984. 26. Burk RL: Radiographic diagnosis. Vet Rad 26:143, 1985. 27. Koblik PD, Hornof W, et al: A comparison of pulmonary angiography, digital subtraction angiography, and 99mTcDPTA/MAA ventilation-perfusion scintigraphy for detection of experimental pulmonary emboli in the dog. Vet Rad 30:159, 1989. 28. Cornielissen JMM, Wolvekamp WC, et al: Primary occlusive pulmonary vascular disease in a dog diagnosed by a lung perfusion scintigram. J Am Anim Hosp Assoc 21:293, 1985. 29. Suter PF: Lower airway and pulmonary parenchymal diseases. In Suter PF, ed: Thoracic radiology of the dog and cat. Davis, Calif, 1984, Stonegate Publishing.

30. Lord PF, Schaer M, Tilley LL Pulmonary infiltrates with eosinophilia in the dog. J Am Vet Rad Soc 16:115, 1975. 31. Thrall DE, Goldschmidt MH, et al: Generalized extensive idiopathic pulmonary ossification in a dog: a case report. Vet Rad 21:104, 1980. 32. Berry CR, Ackerman N, Monce K: Pulmonary mineralization in four dogs with Cushing’s syndrome. Vet Radiol Ultrasound 35:10, 1994. 33. Lefbom BK, Adams WH, Weddle DL: Mineralized arteriosclerosis in a cat. Vet Radiol Ultrasound 37:420, 1996. 34. Bjorling D: Radiographic diagnosis. Vet Rad 24:127, 1983. 35. Radlinsky MG, Homco LD, Blount WC: Radiolucent pulmonary foreign body. Vet Radiol Ultrasound 39:150, 1998. 36. Kirberger RM, Lobetti RG: Radiographic aspects of Pneumocystis carinii pneumonia in the miniature Dachshund. Vet Radiol Ultrasound 39:313, 1998. 37. Hyde I: Inflammatory diseases of the lung. In Sutton D, ed: A textbook of radiology imaging. Edinburgh, 1993, Churchill Livingstone. 38. Berry CR, Moore PF, et al: Pulmonary lymphomatoid granulomatosis in seven dogs (1976-1987). J Vet Intern Med 4:157, 1990. 39. Calvert CA, Mahaffey MB, et al: Pulmonary and disseminated eosinophilic granulomatosis in a dog. J Am Anim Hosp Assoc 24:311, 1988. 40. Postorino NC, Wheeler SL, et al: Asyndrome resembling lymphomatoid granulomatosis in a dog. J Vet Intern Med 3:15, 1989.

C h a p t e r

4 5

Airway Disease

❚❚❚ LARYNGEAL PARALYSIS Background Table 45-1 lists the causes of laryngeal paralysis.1

dyspneic. Dyspnea does not correlate well with radiographically observed tracheal narrowing, however. Measurement and comparison of tracheal diameter and thoracic inlet height fail to separate clearly normal from affected dogs. Normal Bulldogs appear to have smaller tracheas than most other breeds.4

Imaging Findings The radiographic diagnosis of laryngeal paralysis is based on indirect evidence and therefore is inferential. Radiographic abnormalities suggesting laryngeal obstruction, including laryngeal paralysis, are (1) increased pharyngeal area, (2) increased laryngeal area, (3) dilated trachea and principal bronchi, and (4) pulmonary hyperinflation. These findings are most convincing when identified in both inspiratory and expiratory radiographs, especially the latter.

❚❚❚ TRACHEITIS Bacterial and viral infections almost never result in radiographically identifiable changes and thus are unsuited for diagnosis by this means. A limited number of parasitic diseases, such as Cuterebra infection, also can cause tracheitis (cough and dyspnea) but, like their bacterial and viral counterparts, cannot be diagnosed radiographically.3

Imaging Findings Generally, I am skeptical about a diagnosis of tracheal hypoplasia in any breed, including Bulldogs. I have regularly seen small tracheas in dogs and cats undergoing unrelated radiographic evaluations, just as I often have encountered enlarged tracheas. Some dogs show a wide range of tracheal diameters in multiple chest films made over a 1- or 2-month span to monitor the progress of an unrelated disease such as pneumonia. These observations strongly suggest that at least some of the marked differences in tracheal diameter are of a secondary nature and, more importantly, are temporary. As an aside, I am equally doubtful about the supposed problems caused by small nares and large soft palates in brachycephalic breeds.

❚❚❚ TRACHEAL COLLAPSE Background

❚❚❚ TRACHEAL HYPOPLASIA Background Congenitally small trachea, or tracheal hypoplasia, has been reported to occur most commonly in Bulldogs and Boston Terriers. In the absence of cardiopulmonary disease, most dogs with small tracheas are clinically normal. Alternatively, dogs with a small trachea and congenital heart disease, megaesophagus, or cranial airway obstruction (“stenotic nares,” “elongated soft palate,” and everted laryngeal saccules) are usually

Tracheal collapse occurs most commonly in small dogs, in particular, toy and miniature breeds such as Yorkshire Terriers and Pomeranians. Affected animals are often obese and have histories of chronic coughing and intermittent periods of dyspnea. Occasionally, tracheal collapse is reported in medium or large breeds, such as the Boxer, Labrador, or Golden Retriever, but this is unusual.5,6 The precise cause of tracheal collapse is often uncertain, with diagnosis often based on circumstantial evidence. For example, if it can be demonstrated that a young dog without a history of respiratory disease has 449

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Table 45-1 • CAUSES OF LARYNGEAL PARALYSIS Cause

Comment

Atrophy of the intrinsic laryngeal muscles Hypothyroidism

Atrophy is neurogenic, but of unknown cause These dogs should also be checked for related cardiac disease, which predictably takes the form of impaired left ventricular function (decrease in shortening fraction and increase in left ventricular, end-systolic diameter)2

Nonspecific congenital disorders of the larynx Primary injury to the recurrent laryngeal nerve Regional or local myopathy Regional or local neuropathy Secondary injury to the recurrent laryngeal nerve

Intrathoracic or extrathoracic masses encroaching on the recurrent laryngeal nerve

tracheal collapse, by default, the animal is said probably to have congenital collapse. Alternatively, if a middle-aged or older dog collapses and has a history of proven or presumed chronic respiratory disease, its disease usually is presumed to be of a secondary nature. In either case, however, the trachea loses its normal rigidity, creating varying degrees of luminal obstruction. The trachea also may be collapsed or partially collapsed by an exterior mass or mass effect, such as a mediastinal tumor, abscess, cyst, hematoma, or dilated esophagus. The principal sign of collapse is cough (typically harsh and dry), either spontaneous or manually induced. Excitement or exercise often induces coughing in affected dogs. Luminal collapse is typically in the vertical plane and usually occurs intermittently during the course of the breathing cycle (as observed fluoroscopically). Areas of involvement may be quite localized, for example, the thoracic inlet or carina, but it also can involve the entire cervical or thoracic regions of the trachea.

Bronchoscopic Evaluation The bronchoscopic assessment of tracheal collapse is based on the estimated percentage of observed luminal collapse and as such is relatively imprecise. Grading is listed in Box 45-1.7

Imaging Findings Radiographs, which include the tracheal field (throat, neck, and thorax), may or may not show collapse because its occurrence is hard to predict. One way to try to overcome this problem is to make two lateral radiographs: one on inspiration, the other during expiration. In most toy breeds, the neck and chest will fit easily on a single film, although the neck may be somewhat overexposed. In medium-sized dogs, separate neck and chest films will be required. Dorsoventral or ventrodorsal projections are of little use and thus need not be included. Fusiform narrowing of the tracheal lumen, beginning just caudal to the larynx and extending into the cranial mediastinum, is most characteristic of this disease. The tracheal diameter is usually smallest at the thoracic inlet.

B o x

4 5 - 1

Bronchoscopic Grading of Trachial Collapse in the Dog Grade 1: 25% collapse (mild) Grade 2: 50% collapse (moderate) Grade 3: 75% collapse (severe) Grade 4: 100% collapse (total)

The esophagus can drape over much of the trachea at the thoracic inlet, mimicking collapse. This problem can be eliminated or partially overcome by administering barium to distinguish more clearly between the trachea and adjacent esophagus.8 Gentle compression using a thin wooden spoon usually provides further separation. Vascular superimposition at the heart base (especially during expiration) falsely makes the distal trachea and branching bronchi appear abnormally tapered, potentially leading to misdiagnosis. Fluoroscopy with videotaping is the most complete and accurate means of evaluating tracheal dynamics, but it can be difficult to restrain smaller dogs, a problem that can lead to excessive radiation exposure to assistants. Although the literature repeatedly mentions associated thoracic abnormalities such as obesity, air trapping, diminished vasculature, and abnormal lung density, I have been unable to locate any clear proof that such associations are any more than theoretical possibilities. Neither do I know that these are mere incidental findings. Therefore, and in the absence of confirmation either way, I suggest the issue be considered unresolved. At the risk of “preaching,” I remind the reader: An expert should be equally aware of what he or she does not know as of what he or she does know.

❚❚❚ ABNORMAL TRACHEAL DISTENSION (TRACHEAL DILATION, TRACHEAL BALLOONING) Some puppies and older dogs show abnormal tracheal distension in the cervical region. In most such cases,

CHAPTER 45 ❚❚❚ Airway Disease

the animals are being radiographed for another purpose and have no clinical signs referable to the trachea. For lack of something specific, I term this phenomenon ballooning and theorize that, in the case of puppies, it is due to increased tissue elasticity, in particular, greater malleability of the tracheal rings and associated connective tissue. In older dogs, I suspect the explanation may have something to do with age-related catabolism and possibly a reduction in tone of the trachealis muscle. Dogs with tracheal collapse, particularly collapse that has been attributed to chronic inflammation or infection, later may show tracheal ballooning in the same location. I am uncertain whether the ballooning is secondary to the collapse or whether it was always present but simply not identified. In either case, the ballooning is probably due to softening or malacia of the tracheal rings.

❚❚❚ TRACHEAL TUMORS Primary tracheal tumors are rare in dogs. Benign cell types include osteochondroma, enchondroma, extramedullary plasmacytoma, and undifferentiated mesenchymal tumors. Malignant cell types include chondroma, chondrosarcoma, osteosarcoma, leiomyoma, carcinoma, adenocarcinoma, and mast cell tumor.9,10 Radiographically, most tracheal tumors appear as oval intraluminal masses, whereas others are hemispherically shaped and are attached to the inner side of the tracheal wall.

❚❚❚ TRACHEAL POLYPS Ramirez and Hawkins reported an inflammatory polyp in the midsection of the thoracic trachea . The polyp appeared as an outstanding spherical opacity seen against the backdrop of the air-filled trachea.11

❚❚❚ TRACHEAL AND BRONCHIAL PARASITES Filaroides osleri This strongylus produces cyst-like dwellings in the mucosa of the trachea and main stem bronchi of young dogs. The eggs are released into the airways, coughed up, swallowed, and passed in the feces. Signs include chronic coughing, dyspnea, and exercise intolerance. In my experience, infection must be severe before any change in the affected airways becomes apparent. Described airway alterations include marginal irregularity and small luminal masses, especially in the carinal region. Bronchography potentially shows filling defects representing the locations of the adult worms.12

451

❚❚❚ DIFFERENTIAL DIAGNOSIS FOR A DISCRETE TRACHEAL MASS OR NODULE Differential diagnosis for a discrete tracheal mass or nodule includes the following: • • • • • • • • •

Benign tumor Encapsulated foreign body Inflammatory polyp Malignant tumor Nonencapsulated foreign body Noninflammatory polyp Old tracheotomy scar Parasitic granuloma Superimposed blood vessel (usually seen in lateral oblique view) • Superimposed lung nodule • Superimposed rib or old rib fracture (usually seen in lateral oblique view)

❚❚❚ BRONCHIAL FOREIGN BODY In my experience, low- and medium-density cranial lobe lesions, including foreign bodies, are easier to locate in lateral radiographs than in dorsoventral or ventrodorsal films. In searching a lateral thoracic radiograph for a cranial lobe foreign body, it is helpful to be able to distinguish the right from the left cranial lobe bronchus. According to Burk and Corwin, the right cranial lobe bronchus typically is situated dorsal to the left, as seen in a lateral chest film.13

❚❚❚ BRONCHOCUTANEOUS FISTULA Yamagishi and co-workers described the radiographic, sonographic, and computed tomographic (CT) appearance of a bronchocutaneous fistula in a dog.14 In my experience, most of these lesions have no characteristic appearance, and in fact most are radiographically and sonographically invisible. A better way to identify such lesions is to provoke a cough by injecting sterile saline into the skin sinus. If this crude test is positive (or equivocal), a small volume of a diagnostic iodine solution is injected into the sinus, and a pair of thoracic radiographs are taken to determine whether the contrast solution can be found in a bronchus. If it has, the physical relationship between the sinus and bronchus has been established.

❚❚❚ BRONCHITIS: THE INVISIBLE DISEASE Background Many veterinarians routinely make thoracic radiographs in an attempt to confirm a tentative diagnosis

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of bronchitis. If the image shows a reduction in expected bronchial clarity or an apparent increase in wall density or thickness, a diagnosis of bronchitis is made; if not, then it is denied. How reasonable are such conclusions? In my opinion, neither diagnosis is radiographically justifiable, nor has either been substantiated scientifically. Rather, it appears that the belief that bronchitis can be diagnosed radiographically is little more than a clinical myth, albeit a deeply entrenched one. In support of this contention, I first comment on the veterinary perspective and then on how physician radiologists view the issue.

The Veterinary Perspective Hawkins wrote in the Textbook of Veterinary Internal Medicine, “Thoracic radiology classically reveals a bronchial pattern. A concurrent, mild interstitial pattern is common. Patchy peripheral alveolar densities can occur owing to decreased clearance of mucus, secondary bronchopneumonia, or, in cases with eosinophilic inflammation, a more generalized hypersensitivity reaction. Sometimes air trapping can be appreciated radiographically as hyperinflated lungs with increased radiolucency of lung fields and flattening of the diaphragm.” He continues, “Radiographic changes are not always apparent in spite of marked clinical signs. Thoracic radiographs exposed during expiration or fluoroscopy can be useful in detecting collapse of larger airways.”15 Regrettably, no references are cited to corroborate the author’s statements, and thus we must assume that they represent opinion, presumably based on experience. Nelso and Couto divide bronchitis into two categories, allergic and chronic, an odd mix of etiologic and temporal considerations. On the radiographic diagnosis of allergic bronchitis, they write, “A bronchial pattern is generally present,” and then go on to say, “Increased reticular interstitial markings can also be present.”16 Here, also, the authors’ claims go unsubstantiated, again suggesting opinion. Bonagura and colleagues describe the radiographic appearance of bronchitis as follows: “The thoracic radiograph is abnormal in most cases. Typical findings include increased interstitial density with prominent peribronchial infiltrates.” Later, in the same paragraph, they reverse their position and caution, “It may be difficult to distinguish these findings from normal aging changes of the canine thorax (another unsubstantiated claim).”17 Once again, the authors provide no published corroboration. In the more recent veterinary literature, Lamb states, “The critical radiographic sign of a bronchial pattern is a change in the cross-sectional bronchus from a thin circle to a thick circle of the same diameter.” Lamb attributes the change to long-standing inflammation that is most often the result of chronic bronchitis or allergy, but, like the others, he fails to provide any supporting references.18 Perhaps more importantly, he makes no mention of how normal bronchial cross-sections regu-

larly appear thickened as a result of oblique positioning or differences in respiratory phase.

The Human Experience Physician radiologists are far more cautious than their veterinary counterparts when it comes to the radiographic diagnosis of chronic bronchitis. Juhl says of chronic bronchitis, “The roentgen diagnosis of chronic bronchitis, based on plain film study, is made infrequently and with great caution.”19 Klein and Fischbein begin their account of chronic bronchitis by reminding the reader that “chronic bronchitis is a clinical and not a radiographic diagnosis.” The authors continue, “Some patients will show peribronchial cuffing or tram tracks when thick-walled and mildly dilated bronchi are viewed end-on or in length . . . but that this radiographic appearance has no definite pathologic correlate.”20 Rubens states, “Approximately 50% of patients with chronic bronchitis have a normal chest X-ray. In patients with a plain film abnormality, the signs are due to emphysema, superimposed infection or possibly bronchiectasis.”21

A Personal Viewpoint In nearly three decades as a radiologist, I only occasionally have been able to make a diagnosis of bronchitis with even a modicum of confidence. By way of comparison, I often hear that my medical and surgical colleagues have diagnosed bronchitis during their ward rounds. Why this disparity? The problem, I believe, lies in the fact that the descriptions of chronic bronchitis, as they typically appear in most veterinary specialty texts, are based in part on dated veterinary literature; are often grossly oversimplified (especially with respect to the limitations inherent in radiographic imagery); and, perhaps most importantly, lack radiologic-pathologic correlation. With respect to my first point concerning the use of outdated references, I should point out that not all of the older literature is inaccurate. For example, Douglas and Williamson wrote, “The actual substance of the bronchial wall is not clearly defined in a normal chest radiograph and pathological changes are also difficult to recognize.” Bronchitis would (theoretically) result in a slight increase in the radiodensity of the bronchial tree, but this is seldom sufficiently marked to permit a diagnosis on radiologic grounds alone.”22 In summary, there are no reliable plain film findings in either acute or chronic bronchitis. Although it may be possible to diagnose the severest of cases, the probability of accurately identifying bronchitis in most pets is exceedingly small.23,24

Imaging Findings As mentioned previously, plain films are rarely of any use in diagnosing bronchitis in dogs and cats; however, Douglas reported successfully using bronchography to diagnose chronic bronchitis in dogs.25 He reports that

CHAPTER 45 ❚❚❚ Airway Disease

453

Figure 45-1 • Lateral radiograph of a dog with cylindrical bronchiectasis shows diffuse bronchial dilation, depicted by arched lucent bands, spheres, and ovals. Patches of dystrophic calcification are located dorsally.

in mild disease, the distal portions of the bronchi fail to fill, presumably due to abnormal luminal content. With more severe disease, the bronchi continue to fill improperly but also have become enlarged and distorted, progressing toward overt bronchiectasis. In my experience, bronchiectasis does not require special procedures to diagnose. Bronchitis, on the other hand, may require bronchography if high-resolution CT is not available. The most difficult aspect of bronchography is choosing how much contrast solution to administer so that it will reach the small bronchi but remain outside the alveoli. Diagnostic opaques in the terminal air spaces partially obscure smaller airways, are slow to empty, and potentially reduce ventilatory capacity.

❚❚❚ BRONCHIECTASIS

A

B Figure 45-2 • Asthmatic cat with diffuse saccular bronchiectasis and cranial lobe consolidation. The numerous spherical lung densities are actually fluid-filled bronchial saccules. The sternal deformity is congenital.

Background Bronchiectasis is the permanent dilation of bronchi, generally believed to result from chronic bronchial inflammation or infection. It is usually diffuse but occasionally may be confined to a single lung lobe. As with the human form of this disease, bronchial disfigurement may be of a cylindrical, varicose, or saccular nature, with the former being most common in dogs.26

Imaging Findings Radiographically, bronchiectasis is characterized by unchanging bronchial dilation, occasionally associated with localized ballooning, termed sacculation. Pneumonia, presumably related, is often a concurrent finding. Bronchography, with barium or diagnostic iodine solution (water or oil-based), greatly improves bronchial visibility but is usually unnecessary for diagnosis.27

Meyer and colleagues studied the effects of various bronchographic contrast agents on the lung and concluded that both barium and oil-based propyliodone are mildly toxic, with the effects of barium relatively less severe. Although both products are largely cleared from the lung by 3 days, residual contrast agent remains within pulmonary macrophages, small bronchioles, and peripheral lymphatics, causing mild interstitial fibrosis.28 Cantwell and Blevins reported diagnostic-quality bronchograms in normal dogs using aerosolized metrizamide powder with no harmful effects (as determined histologically).29 In my experience, true bronchiectasis is rare compared with compensatory (transient) bronchiectasis, which is commonly associated with a variety of consolidate lung diseases, including lung hemorrhage, lobar pneumonia, and congestive heart failure. I was unable to locate any

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A A

B Figure 45-4 • Only rarely can bronchitis be diagnosed using conventional radiography, even in the most chronic of cases; however, there are occasional exceptions, as exemplified by this chronically ill cat with numerous line and ring shadows throughout its lung.

B Figure 45-3 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a dog with chronic bronchiectasis show numerous severely dilated bronchi and secondary consolidation of the left cranial lung lobe.

information on prevalence, but two breeds come to mind before any others, the Malamute and the Airedale. Bronchiectasis is typically a diffuse disease in both dogs and cats (Figures 45-1 and 45-2) but occasionally may involve only one or two lobes (Figure 45-3). A milder, less destructive form of the bronchiectasis may develop in chronically asthmatic cats, which combined with preexisting disease often causes chronic hyperinflation and severe exertional dyspnea (Figure 45-4). Cocker Spaniels with eosinophilic granulomatosis also may have bronchiectasis, although I am uncertain whether it is primary or secondary to the associated lung lesions. Norris and Samii described bronchiectasis in cats, pointing out that it usually is found in aged men, and may or may not show clinical signs.30

❚❚❚ EMPHYSEMA Emphysema is a relatively rare disease in pets compared with humans. Much of what appears in the veterinary literature under the title of emphysema is actually compensatory hyperinflation, related to an existing lung disease. Additionally, few animals live long enough to develop full-blown chronic obstructive lung disease, and, as a consequence, there are few “pink puffers” and “blue bloaters.”

References 1. Schachter S, Norris CR: Laryngeal paralysis in cats: 16 cases (1990-1999). J Am Vet Med Assoc 216:1100, 2000. 2. Panciera DL: An echocardiographic and electrocardiographic study of cardiovascular function in hypothyroid dogs. J Am Vet Med Assoc 205:996, 1994. 3. Dvorak LD, Bay JD, et al: Successful treatment of intratracheal cuterebrosis in 2 cats. J Am Anim Hosp Assoc 36:304, 2000. 4. Coyne BE, Fingland RB: Hypoplasia of the trachea in dogs: 103 cases (1974-1990). J Am Vet Med Assoc 201:768, 1992.

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5. Radinsky MG, Fossum TW: Tracheal collapse in a young Boxer. J Am Anim Hosp Assoc 36:313, 2000. 6. Spodnick GL, Nwadike BS: Surgical management of extrathoracic tracheal collapse in two large-breed dogs. J Am Vet Med Assoc 211:1545, 1997. 7. Buback JL, Boothe HW, Hobson HP: Surgical treatment of tracheal collapse in dogs: 90 cases (1983-1993). J Am Vet Med Assoc 208:380, 1996. 8. O’Brien JA, Buchanan JW, Kelly DF: Tracheal collapse in the dog. J Am Vet Rad Soc 7:12, 1966. 9. Chaffin K, Cross AR, et al: Extramedullary plasmacytoma in the trachea of a dog. J Am Vet Med Assoc 212:1579, 1998. 10. Osuna DJ: Radiographic diagnosis. Vet Rad 26:27, 1985. 11. Ramirez O, Hawkins EC: Tracheal eosinophilic granuloma/polyp. Vet Radiol Ultrasound 39:422, 1998. 12. McDonald RK, Spaulding K: Radiographic diagnosis. Vet Rad 25:179, 1984. 13. Burk RL, Corwin LA: The right cranial lung lobe bronchus of the dog: its identification in a lateral chest radiograph. J Am Vet Rad Soc 19:210, 1978. 14. Yamagishi N, Yamada K, et al: Bronchocutaneous fistula in a dog. Vet Radiol Ultrasound 41:422, 2000. 15. Haskins CE: Diseases of the lower respiratory system. In Ettinger SJ, Feldman EC, eds: Textbook of veterinary internal medicine, St. Louis, 1995, Mosby. 16. Nelson RW, Couto CG: Disorders of the trachea and bronchi. In Nelson RW, Couto CG, eds: Essentials of small animal internal medicine, St. Louis, 1992, Mosby. 17. Bonagura JP, Hamlin RL, Gaber CE: Chronic respiratory disease in the dog. In Kirk RW, ed: Current veterinary therapy X, Philadelphia, 1989, WB Saunders. 18. Lamb RL: The canine lung. In Thrall DE, ed: Textbook of diagnostic radiology, Philadelphia, 1994, WB Saunders.

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19. Juhl JH: Airway disease. In Juhl JH, Crummy AB, eds: Essentials of radiologic imaging, Philadelphia, 1993, JB Lippincott. 20. Klein JS, Fischbein NJ: The lung. In Brant WE, Helms CA, eds: Fundamentals of diagnostic radiology, Baltimore, 1994, Williams & Wilkins. 21. Rubens MB: Chronic bronchitis and emphysema: pneumoconiosis. In Sutton D, ed: A textbook of radiology and imaging, Edinburgh, 1993, Churchill Livingstone. 22. Douglas SW, Williamson HD: The respiratory system. In Douglas SW, Williamson HD, eds: Veterinary radiological interpretation, Philadelphia, 1970, Lea & Febiger. 23. Farrow CS: Critical thinking: cough please! Can Vet J 36:244, 1995. 24. Mantis P, Lamb CR, Boswood A: Assessment of the accuracy of thoracic radiography in the diagnosis of canine chronic bronchitis. J Small Anim Pract 39:518, 1998. 25. Douglas SW: The interpretation of canine bronchograms. J Am Vet Rad Soc 15:18, 1974. 26. Meyer W, Burt JK: Bronchiectasis in the dog: its radiographic appearance. J Am Vet Rad Soc 14:3, 1973. 27. Hersman R, Kleine LJ, Gilmore CE: A clinical evaluation of propyliodone bronchography. J Am Vet Rad Soc 13:27, 1972. 28. Meyer W, Burt JK, Davis GW: A comparative study of propyliodone and barium bronchography in the dog. J Am Vet Rad Soc 15:44, 1974. 29. Cantwell HD, Blevins WF: Metrizamide insufflation bronchography: a new diagnostic approach. Vet Rad 22:184, 1981. 30. Norris CR, Samii VE: Clinical, radiographic, and pathologic features of bronchiectasis in cats: 12 cases (1987-1999). J Am Vet Med Assoc 216:530, 2000.

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Mediastinal Disease

❚❚❚ APPROACH TO MEDIASTINAL MASSES

❚❚❚ MEDIASTINAL MASS EFFECTS

For diagnostic convenience, the mediastinum or, more specifically, its anatomic content, can be divided into three areas or, as they are commonly termed, compartments: cranial, middle, and caudal.1 The cranial mediastinal compartment extends from the thoracic inlet to the heart and contains (1) the trachea; (2) the cranial third of the esophagus; (3) the thymus; (4) the brachiocephalic and left subclavian arteries, part of the cranial vena cava; (5) a variety of lymph nodes; and (5) various nerves. The middle mediastinal compartment runs the length of the heart and contains (1) the heart; (2) the proximal portions of the aorta and pulmonary artery; (3) the cranial and caudal venae cavae; (4) the distal part of the trachea, proximal portions of the principal bronchi (the carina), and the middle esophagus; and (5) tracheobronchial lymph nodes. The caudal mediastinal compartment contains (1) the caudal vena cava, (2) the central parts of the aorta and caudal vena cava, and (3) the caudal third of the distal third of the esophagus. Unfortunately, not all mediastinal masses are confined to a single compartment; for example, many thymomas and lymphomas become quite large, often involving both the cranial and middle segments. Obviously, these multicompartmental mediastinal lesions require expansion of the differential list.

Fat is the most common cause of cranial mediastinal widening as observed in dorsoventral or ventrodorsal thoracic radiographs of both dogs and cats. In general, mediastinal fat produces a more uniform widening of the cranial mediastinum than do masses such as lymphoma or thymoma (Figure 46-1).

❚❚❚ DIFFERENTIATION OF MEDIASTINAL AND PULMONARY MASSES

Hilar Adenopathy

It can be difficult to distinguish a mass located in the dorsomedial aspect of one of the cranial lung lobes from one located in the cranial mediastinum, especially if it is eccentric. Fortunately, most mediastinal masses are symmetric, reducing diagnostic uncertainty. 456

Fat

Thymic Hemorrhage In puppies, the thymus casts a distinctive triangular shadow along the left lateral border of the cranial mediastinum, as seen in ventrodorsal or dorsoventral projection, but gradually disappears as an animal matures (Figure 46-2). The converse also may be true, where an asymmetric cranial mediastinum mass mimics the thymus (Figure 46-3). Atelectatic and consolidated left cranial lung lobes can create a similar appearance. Severe mediastinal hemorrhage (with or without hematoma development) may cause secondary tracheal compression and obstruction (Figure 46-4).2 The most common cause of large-volume mediastinal bleeding is blunt chest trauma, followed by warfarin poisoning.3 Although unconfirmed, Mason and co-workers have reported a case of fatal mediastinal bleeding, which the authors hypothesize to have resulted from one or more ruptured intercostal arteries when the dog lunged violently while tied in the yard to a long chain.

Enlargement of the hilar lymph nodes, which may be pronounced in some types of lung cancer or mycotic pneumonia, can cause compression of the distal portion of the trachea or the mainstem bronchi. Radiographically, enlarged hilar nodes typically appear as a mass effect superimposed on the heart base, often causing some degree of bronchial displacement or distortion (Figure 46-5).

CHAPTER 46 ❚❚❚ Mediastinal Disease

457

A-C Figure 46-1 • Mediastinal fat: Ventrodorsal views of the thorax of three healthy dogs (A, B, C) show varying amounts of cranial mediastinal fat that can mimic a mediastinal mass to those unfamiliar with this normal variation.

Localized Esophageal Enlargement Depending on length, content, and the degree of distention, an esophageal foreign body can resemble a mediastinal mass (Figure 46-6). This is especially true of localized obstructions that do not contain bone or other high-density objects.

Sonography of Mediastinal Masses The ability to assess mediastinal masses sonographically depends on their size and particularly on their location. Large masses that extend ventrally to the sternum or to the chest wall in a cat are usually easy to access. Masses that abut the cranial margin of the heart are also relatively easy to identify (Figure 46-7). Small masses located fully within the mediastinum can be quite difficult to reach, however, because of interference from air in the surrounding lung. Sonographic strategies for imaging the mediastinum have been reported, as has a catalogue of cranial mediastinal lesions (mostly lymphosarcomas and thymomas).4,5

❚❚❚ CRANIAL AND MIDDLE MEDIASTINAL TUMORS Figure 46-2 • Close-up view of the cranial thorax of a puppy shows the thymus with its distinctive triangular shape, also referred to as a thymic sail.

Thymoma Background. Thymomas develop in the cranial part of the mediastinum from the epithelium of the thymus and cause varying degrees of vascular compression, depending on their size. This type of tumor also may grow into the cranial vena cava and right atrium.

458

SECTION V ❚❚❚ The Throat, Neck, and Thorax

A A

B Figure 46-3 • Lateral (A) and penetrated ventrodorsal

B

(B) thoracic radiographs of a dog with a large asymmetrical tumor in the cranial mediastinum. The triangular profile of the tumor resembles a puppy’s thymus, or an atelectatic lung lobe surrounded by free pleural air.

C Figure 46-4 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a dog with a severe bleeding disorder show cranial mediastinal hemorrhage compressing the trachea causing dyspnea. A stomach tube was passed and the dog reradiographed to assess esophageal patency and deflate the stomach (C).

CHAPTER 46 ❚❚❚ Mediastinal Disease

Affected individuals often present with a history of gradual swelling of the head, neck, and forelimbs. Canine thymomas are rare tumors that develop in the cranial mediastinum and are associated with esophageal dilation and myasthenia gravis in about 50% of cases. Fewer than 10% have other nonthymic tumors or hypercalcemia. Metastasis is reported to be rare. Imaging Findings. Radiographically, thymoma is characterized by a large mediastinal mass, which is equally likely to occupy either the entire cranial mediastinum or its cranioventral aspect. Only occasionally does this tumor form in the dorsolateral aspect of the mediastinum. As expected, tracheal and cardiac displacement usually can be found with larger masses. Pleural fluid occurs in about a third of all cases.6 Although a thymoma initially may appear as a comparatively discrete mass in the ventral part of the cranial

459

mediastinum, it rapidly outgrows this space and soon envelops the cranial part of the heart and its associated vasculature (Figure 46-8). Some thymomas so constrict the cranial vena cava and lesser veins that a regional chylous effusion forms, which may obscure many of the details of the mass. Cantwell demonstrated that cephalic venography is capable of showing partial obstruction of the cranial vena cava and diversion of blood flow to the thoracodorsal and lateral thoracic veins in a dog with a large thymoma.7 Sonographically, thymomas may reveal multiple fluid-filled areas within the mass, which represent necrosis. Sonographically guided biopsy often returns a diagnosis of nonneoplastic lymphocytes, which is not unusual for thymomas.8 Secondary Effects. The proximity of the cranial vena cava to most cranial mediastinal masses invites compression, occlusion, thrombosis—and, in the case of cancer, invasion. Suspected secondary caval involvement often can be confirmed sonographically or, alternatively, by using nonselective venography. Typically, obstruction of the cranial vena cava, which is also known as cranial vena caval syndrome, is signaled by (1) the full or partial cessation of flow beyond the point of caval blockage; (2) facial, neck, brisket, and forelimb edema; (3) distended jugulars; and (4) the presence of abnormal collateral circulation in the region of the heart (typically, as observed angiographically).9

❚❚❚ LYMPHOSARCOMA

Figure 46-5 • Hilar adenopathy: Lateral thoracic radiograph of a dog with lymphosarcoma shows a hilar mass effect representing a cluster of enlarged, deformed, cancerous lymph nodes.

Lymphosarcoma typically begins in the cranial-most part of the mediastinum, usually at the level of the first two or three intercostal spaces. In this stage of its development, the tumor is best seen in the dorsoventral or ventrodorsal views, where it appears as a circular mediastinal widening (Figure 46-9, A). A lateral projection is usually less revealing, with the mass often appear-

Figure 46-6 • Esophageal foreign body: Lateral esophagram shows localized distension cranial to the thoracic inlet containing a vague filling defect caused by a large piece of tendon eaten 2 days earlier.

460

SECTION V ❚❚❚ The Throat, Neck, and Thorax

B

A Figure 46-7 • Sonographic long (A) and cross (B) sections of a lymphoma in the cranial mediastinum of a dog.

A

B Figure 46-8 • Cranial mediastinal mass: Lateral (A) and ventrodorsal (B) views of the thorax of a cat with a large thymoma that is displacing the heart caudally and to the right, and the trachea dorsally.

ing as little more than a subtle bulge in the ventral mediastinum (Figure 46-9, B). As the tumor becomes larger, it widens, often extending laterally to the adjacent chest walls and caudally to the level of the aortic root (Figure 46-10, A). With further growth, the tumor often begins to displace the heart caudally, deforming the cardiac silhouette and producing an angular cardiac shift (Figure 46-10, B). Avariant on this theme is the large, conforming type of lymphosarcoma, which alters the size but not the shape of the precardiac mediastinum. In this type of lymphosarcoma, there is often an additional mass in the thoracic inlet (Figure 46-11).

In the most severe cases, often marked by edema of the face and neck secondary to vascular occlusion, the tumor can become so large that it extends alongside the heart, displacing it caudolaterally in the process. In the lateral projection, the portion of the tumor superimposed on the heart may resemble pulmonary consolidation. At this stage in their development, mediastinal lymphosarcomas often are accompanied by visible hilar adenopathy. Starrak and co-workers determined that the presence of cranial mediastinal lymph node enlargement in dogs with lymphosarcoma indicates a poor prognosis.10 Some lymphosarcomas become so large

CHAPTER 46 ❚❚❚ Mediastinal Disease

461

A A

B

B Figure 46-9 • Lateral (A) and ventrodorsal (B) thoracic

Figure 46-10 • Progressive lymphosarcoma: A, Initial thoracic

radiographs of a dog with a golf ball–sized cranial mediastinal tumor, barely visible at the level of the second intercostal space.

film shows a large cranial mediastinal mass with secondary inhalation pneumonia, especially in the left caudal lobe. B, Progress film indicates that tumor has enlarged, and the pneumonia has become more extensive.

that they may extend well into the middle mediastinum, mimicking a primary lung tumor (Figure 46-12).

Mountain dogs and less often in Rottweilers and Golden Retrievers. Other breeds also have been reported but not with the frequency of these breeds. The term histiocytic refers to macrophages, the cells that make up these tumors. Like eosinophilic and lymphoid granulomatosis, histiocytosis often produces multiple, often large masses in the lungs. Associated mediastinal growths also may become extremely large, causing a tracheal shift and marked displacement of one or both cranial lobe bronchi (Figure 46-13).

❚❚❚ HISTIOCYTOSIS (MALIGNANT HISTIOCYTOSIS, HISTIOCYTIC SARCOMA) Histiocytic sarcomas of the cranial mediastinum, lung, and hilus have been described in related Bernese

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SECTION V ❚❚❚ The Throat, Neck, and Thorax

A

Figure 46-11 • Ventrodorsal view of a conforming type of lymphosarcoma shows a widened but otherwise normal precardiac mediastinum. However, on closer inspection, there is a large, asymmetrical mass near the thoracic inlet.

Sternal and hilar adenopathy are also frequently present. Abdominal lesions are also common, occurring in the liver, spleen, and lymph nodes (mesenteric, sublumbar, and sacral). Less frequently, the disease attacks the skeleton, where it typically causes osteolytic lesions. Extradural histiocytomas causing spine cord compression have been reported.11 Regrettably, the disease is nearly always fatal, although short-term remission following combined chemotherapy has been reported.12

❚❚❚ VASCULAR MEDIASTINAL TUMORS Vascular tumors, such as hemangiosarcomas and hemangiopericytomas, can become quite large, often producing large volumes of mediastinal or pleural fluid. As with any large mass in the cranial mediastinum, facial and brisket edema is common. Sonographically, it is often possible to visualize such tumors as they encase the large vessels of the cranial mediastinum.

❚❚❚ MEDIASTINAL CYSTS Occasionally, cysts form in the cranial mediastinum (and neck) of dogs and cats but normally are not associated with illness or disability. Most cysts result from a maldevelopment of the pharyngeal pouch network before birth and accordingly are termed branchial cysts.

B Figure 46-12 • Thoracic lymphoma: Lateral (A) and ventrodorsal (B) views show near complete opacification of the cranial thorax in combination with caudolateral displacement of the heart consistent with a large, asymmetrical cranial–middle mediastinal mass. The curved object superimposed on the heart in the lateral projection is the caudal aspect of the mass as it comes around the heart.

Detection is nearly always incidental, occurring when the thorax is radiographed for some other reason. Mediastinal cysts are rarely identified that are unrelated to embryologic error or some primary disease.13

❚❚❚ MEDIASTINAL INFECTION Mediastinitis Background. Mediastinal infections are nearly always the result of esophageal perforation secondary to a

CHAPTER 46 ❚❚❚ Mediastinal Disease

463

Sonographically, the coexistence of mediastinal and pleural fluid should arouse suspicion as to the source of the pleural disease because mediastinal fluid rarely develops secondary to pleuritis.

❚❚❚ MEDIASTINAL ABSCESS Background Mediastinal abscesses are usually the result of esophageal perforation by a foreign body. The resultant breaches are most likely to occur where there is the least amount of space around the esophagus and, accordingly, a minimal capacity for compensatory distension required to accommodate a foreign body. The thoracic inlet, heart base, and diaphragmatic opening are the most common points of foreign body entrapment. Amediastinal abscess also may develop as the result of a pharyngeal perforation—by a stick or bone fragment, for example, with local infection spreading to the mediastinum via the deep fascial planes of the neck. Occasionally, foxtails may work their way into the mediastinum using the same route.

A

Imaging Findings Thoracic radiography usually shows a medium- or large-sized mediastinal mass but does little to reveal the cause. On the other hand, ultrasound not only will identify the presence of a mass, but it is also capable of characterizing its interior. In the case of cysts or abscesses, sonography can be used to facilitate sampling and drainage (where indicated).14

❚❚❚ MEDIASTINAL AIR (PNEUMOMEDIASTINUM) B Figure 46-13 • Histiocytosis: Lateral (A) and dorsoventral (B) views of an extremely large, multilobulated mass that has grown into both the cranial and middle portions of the mediastinum, compressing and displacing the left cranial–middle lung lobe in the process.

trapped foreign body and many prove fatal. Less often, traumatic pharyngeal perforation leads to mediastinitis. Imaging Findings. Radiographically, mediastinitis is characterized by fluid that first accumulates in the mediastinum, causing an increase in density and a commensurate loss of mediastinal contrast and detail. Pleuritis usually develops in animals that survive the septic shock that frequently attends acute bacterial mediastinitis. The large volume of pleural fluid that typically results usually hides any mediastinal fluid that is also present. Thus, in chronic cases, the actual cause of the animal’s illness may go undiscovered until the animal dies and goes to necropsy.

The most common cause of pneumomediastinum in dogs is diagnostic transtracheal aspiration, or so-called tracheal wash. In general the longer the procedure takes, as practiced by a novice veterinary student, for example, the greater the volume of air that escapes from the tracheal puncture site and migrates through the neck into the cranial mediastinum. Deep throat and neck wounds can puncture the cranial airways and lead to pneumomediastinum, as can a leaking tracheostomy devise. Laryngeal or tracheal avulsion is usually fatal, but surviving dogs and cats typically show massive amounts of mediastinal air. Intrapulmonary or extrapulmonary bronchial “fractures” can lead to a large-volume pneumomediastinum. Air from recently created traumatic lung spaces can dissect along the pulmonary veins into the mediastinum—a proposed mechanism to explain a so-called spontaneous pneumomediastinum. Occasionally a foreign body spontaneously perforates the esophagus and causes a pneumomediastinum

464

SECTION V ❚❚❚ The Throat, Neck, and Thorax

A

C

B

Figure 46-14 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a dog with disseminated blastomycosis show an oval shaped mass superimposed on the caudal vena cava immediately cranial to the diaphragm. C, A frontal oblique sonogram of the eye shows a spherical mass against the caudolateral surface of the retina.

(and potentially a mediastinitis). Attempting to extract an esophageal foreign body by mouth or forcing an esophageal foreign body into the stomach with a stomach tube can have equally disastrous results.

with varying degrees of pleural hemorrhage, secondary pulmonary atelectasis, and intrapulmonary bleeding.16 Diagnosis is based on an abnormal coagulation profile.17

In my experience a pneumomediastinum does not lead to a pneumothorax, nor does a pneumothorax result in a pneumomediastinum.

❚❚❚ MEDIASTINAL BLASTOMYCOSIS

❚❚❚ MEDIASTINAL HEMORRHAGE (HEMOMEDIASTINUM) Forceful chest injuries can rupture one of the large cranial mediastinal veins, causing blood to accumulate in the cranial (and occasionally the middle) mediastinum. In my experience, most such hemorrhage is self-limiting but may exert enough pressure on the trachea to cause dyspnea. Both fatal and nonfatal thymic hemorrhage have been reported in young dogs and attributed to a rather vague “loss of vascular support in the involuting thymus.”15 Hemomediastinum is an oft-reported feature of warfarin poisoning and usually occurs in conjunction

Occasionally, fungal granulomas develop in the mediastinum. Their clinical importance usually is determined by their physical effect on adjacent structures, particularly the esophagus, trachea, bronchi, and large blood vessels (Figure 46-14, A and B). Once mycotic disease has been identified, other areas of potential involvement, such as the eye, also should be investigated (Figure 46-14, C).

References 1. Meyer W: Radiography review: the mediastinum. J Am Vet Rad Soc 19:197, 1978. 2. McGuire NC, Williams J, Marks SL: What is your diagnosis? J Am Vet Med Assoc 214:1158, 1999.

CHAPTER 46 ❚❚❚ Mediastinal Disease

3. Blocker TL, Roberts BK: Acute tracheal obstruction associated with anticoagulant rodenticide intoxication in a dog. J Small Anim Pract 40:577, 1999. 4. Stowater JL, Lamb CR: Ultrasonography of noncardiac thoracic disease in small animals. J Am Vet Med Assoc 195:514, 1989. 5. Konde LJ, Spaulding K: Sonographic evaluation of the cranial mediastinum in small animals. Vet Rad 32:178, 1991. 6. Atwater SW, Powers BE, et al: Thymoma in dogs: 23 cases (1980-1991). J Am Vet Med Assoc 205:1007, 1994. 7. Cantwell HD: Radiographic diagnosis. Vet Rad 27:189, 1986. 8. Hunt GB, Churcher RK, et al: Excision of a locally invasive thymoma causing cranial vena caval syndrome in a dog. J Am Vet Med Assoc 210:1628, 1997. 9. Sottiaux J, Frank M: Cranial vena caval thrombosis secondary to invasive mediastinal lymphosarcoma in a cat. J Small Anim Pract 39:352, 1998. 10. Starrak GS, Berry CR, et al: Correlation between thoracic radiographic changes and remission/survival duration in 270 dogs with lymphosarcoma. Vet Radiol Ultrasound 38:411, 1997.

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11. Shaiken LC, Evans SM, Goldschmidt MH: Radiographic findings in canine malignant histiocytosis. Vet Rad 32:237, 1991. 12. Lord PF, Dubielzig RR: Radiographic diagnosis. Vet Rad 32:17, 1991. 13. Ellison GW, Garner MM, Ackerman N: Idiopathic mediastinal cyst in a cat. Vet Radiol Ultrasound 35:347, 1994. 14. Barrett RJ, Mann FA, Aronson E: Use of ultrasonography and secondary wound closure to facilitate diagnosis and treatment of a cranial mediastinal abscess in a dog. J Am Vet Med Assoc 203:1293, 1993. 15. Coolman BR, Brewer WG, et al: Severe idiopathic thymic hemorrhage in two littermate dogs. J Am Vet Med Assoc 205:1152, 1994. 16. Berry CR, Gallaway A, et al: Thoracic radiographic features of anticoagulant rodenticide toxicity in fourteen dogs. Vet Radiol Ultrasound 34:391, 1993. 17. What is your diagnosis? J Small Anim Pract 40:464, 1999.

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Disorders of the Thoracic Esophagus ❚❚❚ ESOPHAGEAL FOREIGN OBJECT (BODY) Background Bone fragments, especially if irregularly shaped, such as vertebrae, may become lodged in the esophagus. The longer an irregular bone fragment is trapped in the esophagus, the greater the potential for injury such as perforation or stricture. Shiroma and Anderson described the appearance of a 100-mg amoxicillin tablet, found incidentally in the thoracic esophagus of a cat undergoing an unrelated preanesthesia workup, which included thoracic radiography. The medication, which later passed into the stomach, was described as a “mineral opacity” and initially was believed to be located in the cranial mediastinum.1

Imaging Findings High-density foreign bodies, such as bone fragments, usually can be identified readily in thoracic radiographs (Figure 47-1). Low-density objects, such as gristle, fruit fragments and pits, and various synthetics, also may be visible, as sometimes is the case when the esophagus is distended with air (Figure 47-2). Just as bladder stones appear dark when seen against a background of diagnostic iodine solution, so most esophageal foreign bodies appear in esophagrams as filling defects.

❚❚❚ ESOPHAGEAL PERFORATION Esophageal perforation is most often the result of a trapped foreign body, often irregularly shaped, such as a vertebra. Although the popular conception is that only sharp objects such as chicken bones are likely to penetrate the esophagus, the reality is that all sorts of objects are potentially capable of causing esophageal perforation, most likely as a result of ischemic necrosis. Sometimes, but not always, air escapes from the esophagus and accumulates in the mediastinum. 466

Because most such air is atmospheric, the more the animal swallows, the greater the degree of pneumomediastinum. Mediastinitis may or may not develop, depending in part on the size of the perforation, the presence (or absence) of a pleural seal, and the contents of the esophagus.

❚❚❚ ESOPHAGEAL ENLARGEMENT (MEGAESOPHAGUS) Some degree of esophageal enlargement accompanies most esophageal foreign bodies as well as both primary and secondary esophageal transport disorders. Regional or generalized esophageal enlargement is also a feature of certain systemic diseases, such as myasthenia gravis (Figure 47-3).2 It is important to be aware that megaesophagus resulting from myasthenia may or may not be associated with generalized weakness (the supposedly classic feature of this disease).3 Megaesophagus is also a feature of dysautonomia in cats, along with regurgitation, vomiting, dilated pupils, and dry mucous membranes (Figure 47-4).4 I have also observed esophageal enlargement and atony in dogs with severe head injuries, following tracheal wash (Figure 47-5), and after inhaling vomit (Figure 47-6). Radiographing or otherwise manipulating dogs with megaesophagus, especially if much restraint is required, can result in regurgitation and inhalation, leading to pneumonia.

❚❚❚ ESOPHAGEAL TRANSPORT DISEASE (DELAYED ESOPHAGEAL TRANSPORT, ESOPHAGEAL MOTILITY DYSFUNCTION, ESOPHAGEAL MOTILITY DISORDER) Indications The evaluation of esophageal transport in dogs or cats usually is prompted by the presence of esophageal

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467

A

Figure 47-1 • Esophageal foreign body: Lateral thoracic view of a dog with a bone fragment caught in its cervical esophagus shows an irregularly shaped, high density object in the caudal esophageal field. Note: More often than not, esophageal foreign bodies, even bones, lack specific features.

enlargement (megaesophagus) identified in an earlier radiographic examination. Occasionally, similar examinations are prompted by unexplained vomiting (regurgitation?) or recurrent pneumonia. B

Fluoroscopic Evaluation

Figure 47-2 • Esophageal foreign body: A, Lateral thoracic ra-

Esophageal transport is best evaluated fluoroscopically, after administration of a small amount of barium. It is best to allow the animal to sit or stand when administering the contrast because swallowing is often delayed when the animal is on its side and being restrained. Forcing a dog to swallow while on its back is dangerous and should not be done. I usually do my initial evaluation with barium alone. If I have reason to believe that barium is being transported differently than food is, I repeat the study using a mixture of barium and food (preferably similar in consistency to that which the animal normally eats). Seen fluoroscopically, the normal barium swallow consists of one or more tapered oval barium boluses passing directly or in a stepwise fashion, through the esophagus, to the stomach. In most dogs, a small amount of residual barium coats the longitudinal folds of the esophagus for a few minutes after the initial swallow. If high-viscosity barium paste is used, it generally persists longer than liquid barium. Barium powder mixed with water appears more varied in density than commercially prepared barium suspensions. Generally, contrast clumping (flocculation) is not a problem in esophagography, but it has negative connotations when observed in barium films of the stomach or bowel.

Figure 47-3 • Dysautotonia: Lateral close-up view of the thoracic esophagus in a cat shows marked distension with vertically oriented folds over the caudal heart base and cranial to the diaphragm. Typically, the trachea and heart are displaced ventrally.

diograph of a dog with a piece of apple caught in its caudal esophagus, which is distended with a combination of air and fluid, and is displacing the trachea and heart ventrally. B, Close-up barium film shows the head of the barium column conforming to the leading edge of the apple fragment.

468

SECTION V ❚❚❚ The Throat, Neck, and Thorax

A

B

C Figure 47-4 • Megaesophagus induced by tracheal wash: Lateral (A) and ventrodorsal (B) thoracic radiographs of a dog with

pneumonia, made immediately following a tracheal wash. In addition to pneumonia, there is a pneumomediastinum and mild esophageal distension. A second thoracic examination, made an hour later after the dog developed difficulty drinking, shows that the esophageal dilation has markedly worsened (C).

Nonfluoroscopic Evaluation

Figure 47-5 • Megaesophagus induced by inhaling vomit: Lateral thoracic radiograph of a dog made 18 hours after choking on semisolid vomit while being anesthetized. There is a esophageal dilation, secondary to chemical esophagitis, and underinflation of the caudal lobes caused by bronchial obstruction, spasm, and bronchiolitis.

If fluoroscopy is not available, sequential films can be substituted. I prefer to make three consecutive lateral views of the thorax (following a single dose of barium), including as much of the neck as possible. If I see a persistent bolus or esophageal dilation, I repeat the sequence. If a focal or regional abnormality persists, I make a ventrodorsal or dorsoventral view of the suspect area. I continue filming or not, based on what it is I am looking for and what the most recent film has shown. In other words, each examination is customized, depending on the animal’s suspected disease and the goals of the study. If I am unable to be present during a nonfluoroscopic examination, the technicians are instructed to use a standard protocol, which I provide, again, based on anticipated pathology.

Cats Moses and co-workers reported on a series of 44 cats with abnormal esophageal transport. They concluded

CHAPTER 47 ❚❚❚ Disorders of the Thoracic Esophagus

469

A

B C Figure 47-6 • A, Lateral view of a dog with acquired megaesophagus and secondary bronchopneumonia. B, Postural film (standing patient position with a horizontally directed x-ray beam) shows a dark, compressed, oval-shaped object in the caudodorsal lung field representing an air-fluid level within the esophagus. C, A subsequent postural esophagram shows an enlarged, flaccid, barium and air-filled esophagus.

that about 40% of these cases were of an unknown cause, and the remaining 60% were either congenital or related to a concurrent disease known to cause abnormal esophageal function5 (Table 47-1).

Imaging Findings Potential Problems. Generally, I do not perform esophageal assessment on fractious animals. Muzzles are dangerous and can lead to inhalation pneumonia if an animal regurgitates and chokes. Tranquilization or sedation of such individuals often results in esophageal flaccidity and concomitant delay in transport. Performing esophagography under such conditions can be diagnostically frustrating and often poses more questions than it provides answers. Radiographic Disease Indicators. As mentioned, a barium bolus should pass through the esophagus into the stomach shortly after contrast administration. It is abnormal for a bolus to persist beyond a few minutes. Likewise, the esophagus should fully contract after

Table 47-1 • CONDITIONS KNOWN TO CAUSE ABNORMAL ESOPHAGEAL TRANSPORT Disease

Comment

Dysautotonia Esophageal stricture Gastroesophageal reflux

Atony Focal internal obstruction Walker and co-workers reported gastroesophageal reflux in a middleaged dog with a sliding hiatal hernia, an ulcerated antral carcinoma, and chronic suppurative gastritis.5 Transient megaesophagus and loss of normal esophageal motility also were reported in a dog that refluxed stomach contents into its esophagus during surgery (Figure 47-3). External obstruction and deformity Incoordination Regional external compression Atony Focal external compression

Hiatal hernia Laryngeal paralysis Mediastinal mass Myasthenia Vascular ring

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completion of the swallow. When barium paste is used, small amounts sometimes are retained for a brief time on the surface of the tongue and pharynx. As a result, a fresh bolus may be generated in the course of making sequential films and must not be mistaken for a retained bolus. Immediately thereafter, the film in question under such circumstances should be repeated; in most instances, the bolus will have disappeared. Dogs with esophageal motility disorders may (Figure 47-7) or may not also have related inhalation pneumonia.

Chinese Sharpei Using barium esophagography, Stickle and co-workers documented abnormal esophageal transport in 29 clinically normal 3-month-old Chinese Sharpei puppies, which they monitored radiographically until the dogs were at least 18 months of age, whenever possible. Of these dogs, 69% had delayed formation of secondary esophageal waves, 48% exhibited delayed bolus transport (“poor motility or tone”), and 38% possessed an anatomically abnormal esophagus featuring a ventrally directed half-loop, located at or near the thoracic inlet, which the authors termed “esophageal redundancy.” As many of the animals matured, their esophageal motility improved or became completely normal, but dogs that had esophageal redundancy, in addition to decreased motility, showed little or no improvement.6

❚❚❚ ESOPHAGITIS In my experience, radiographically demonstrable esophagitis is unusual. Most cases I have seen have been caused by protracted contact with stomach acid (in some instances, presumed), usually while unconscious during surgery. Plain films rarely show any indication of disease. Sometimes a small amount of gas accumulates in the damaged portion of the esophagus, but this is an inconsistent finding. Only rarely is there any distension, and when present it is minimal and thus hard to detect. Barium films potentially can reveal esophagitis, typically in the form of a localized narrowing, seen against a backdrop of uneven and incomplete mucosal folds. Small amounts of barium often are retained at the lesion site for short periods.

❚❚❚ ESOPHAGEAL STRICTURE (ESOPHAGEAL STENOSIS) Esophageal stricture or stenosis may occur as a result of external or internal compression or disfigurement. For example, a persistent right or left aortic arch causes a focal esophageal constriction that prevents the passage of solid food beyond the base of the heart.7 It should be noted, however, that not all abnormal blood vessels are harmful, for example, a persistent left cranial vena cava.8

Figure 47-7 • Lateral close-up view of an enlarged esophagus in a dog with myasthenia.

A mass in the wall of the esophagus, such as a granuloma caused by Spirocerca lupi or rarely, a tumor, occludes the adjacent esophageal lumen. Chemical, physical, or vascular damage to the esophageal lining can result in esophagitis, which, if severe enough, can lead in turn to scarring, deformity, and stenosis.9 Causes of esophagitis include the following: • Chemical injury (consumption of caustic substances) • Chronic vomiting • Foreign bodies: (1) direct injury to surrounding esophagus, (2) iatrogenic injury related forced extraction, and (3) ischemic injury secondary to esophageal spasm attempting to dislodge foreign object • Gastroesophageal reflux or peptic esophagitis (presumably related to a loss of tone or excessive relaxation in the caudal esophageal sphincter during anesthesia) • Hiatal hernia • Megaesophagus • Trauma (related to forceful passage of stomach tube, or chronic abrasion by indwelling feeding tube)

❚❚❚ RADIOGRAPHIC AND FLUOROSCOPIC EVALUATION OF THERAPEUTIC ESOPHAGEAL DILATION Sooy and co-workers described treating esophageal strictures in dogs with balloon catheter dilation while using esophagography and fluoroscopic monitoring.10

❚❚❚ ESOPHAGEAL TUMOR Background Primary esophageal tumors are rare in dogs and even more so in cats.11 Leiomyoma, leiomyosarcoma,

CHAPTER 47 ❚❚❚ Disorders of the Thoracic Esophagus

471

fibrosarcoma, osteosarcoma, and squamous cell carcinoma are among the most often-reported cell types. Esophageal plasmacytoma is comparatively less common, but affected animals have been surgically cured.12

Imaging Findings As previously noted, esophageal tumors are rare; consequently, comparatively few published reports contain medical images. Nevertheless, because most esophageal tumors impede flow, one can use this feature to reliably predict their probable appearance, especially as seen with barium films. Typically, esophagrams show tapered or abrupt narrowing at the tumor site. Cranial to the lesion, the esophagus usually is dilated and may contain filling defects representing stalled foodstuff.

A

❚❚❚ ESOPHAGEAL FISTULA Background Both esophagobronchial and esophagotracheal fistulae have been reported in pet animals.13 Circumstantially, esophageal foreign bodies often are incriminated. The most characteristic clinical sign of this disease is coughing in association with eating or drinking. The resultant contamination of the associated airway usually leads to localized bronchitis or tracheitis and later to pneumonia or pulmonary abscess formation.

B Figure 47-8 • An uncommon view of a common event.

Imaging Findings Plain films may show nothing, especially when there is no associated pneumonia. I have seen a single case in which air was intermittently observed in the central portion of the thoracic esophagus, a location later determined to be the point of communication between the esophagus and the left mainstem bronchus. Most cases of suspected communication between the esophagus and proximal airways are confirmed with esophagography using a water-soluble contrast agent administered orally.

A, Lateral thoracic radiograph made just as dog began to vomit shows food in the caudal part of a dilated esophagus. B, Moments later, the vomiting completed, the dilated esophagus disappeared.

was observed. Given shape and location of the lesion, it was believed to have originated in the esophageal wall, an assumption that was later confirmed at necropsy.14

❚❚❚ ESOPHAGEAL HEMATOMA

❚❚❚ VOMITING AND ITS TEMPORARY EFFECT ON THE ESOPHAGUS

Bree and co-workers reported a case of esophageal hematoma in a dog causing partial obstruction. The authors speculate that the lesion was the result of a previous injury, speculation supported by the presence of a fractured first right rib.14 Plain films showed air in the cervical portion of the esophagus, which suggested an abnormality but provided no clue as to its nature. It was not until esophagography was performed that an eccentric filling defect

Sometimes, when a dog is having its chest radiographed, it vomits just at the moment of exposure. In such circumstances, the esophagus often appears distended with gas and vomit, the latter often appearing surprisingly discrete given its liquid or semisolid state (Figure 47-8). If there is any doubt that the appearance of the esophagus is a transient finding related to vomiting, then it can be resolved easily by radiographing the thorax.

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❚❚❚ ESOPHAGEAL GAS IN HEALTHY DOGS Gas is often present in the esophagus of an unconscious dog (Figure 47-9) or one that has struggled during radiography (Figure 47-10).

References

Figure 47-9 • Normally invisible, the esophagus of this dog is seen because of its relaxed state during anesthesia, a situation that encourages gas accumulation (emphasis zone).

Figure 47-10 • Standing lateral thoracic radiograph of a tranquilized dog with aortic stenosis shows incidental esophageal gas.

1. Shiroma JT, Anderson SE: Esophageal foreign body. Vet Radiol Ultrasound 40:126, 1999. 2. Shelton GD: Myasthenia gravis: lesions from the past 10 years. J Small Anim Pract 39:368, 1998. 3. Shelton GD, Schule A, Kass PH: Risk factors for myasthenia gravis in dogs: 1,154 cases (1991-1995). J Am Vet Med Assoc 211:1428, 1997. 4. Guilford WG, O’Brien, et al: Diagnosis of dysautonomia in a cat by autonomic nervous system function testing. J Am Vet Med Assoc 193:823, 1988. 5. Moses L, Harpster NK, et al: Esophageal motility dysfunction in cats: a study of 44 cases. J Am Anim Hosp Assoc 36:309, 2000. 6. Stickle R, Sparschu G, et al: Radiographic evaluation of esophageal function in Chinese Shar Pei pups. J Am Vet Med Assoc 201:81, 1992. 7. Hurley K, Miller MW, et al: Left aortic arch and right ligamentum arteriosum causing esophageal obstruction in a dog. J Am Vet Med Assoc 203:410, 1993. 8. Buchanan JW: Persistent left cranial vena cava in dogs: angiography, significance, and coexisting anomalies. J Am Vet Rad Soc 4:1, 1963. 9. Weyrauch EA, Willard MD: Esophagitis and benign esophageal strictures. Comp Cont Educ 20:203, 1998. 10. Sooy TE, Adams WM, et al: Balloon catheter dilation of alimentary tract strictures in the dog and cat. Vet Rad 28:131, 1987. 11. Gualtieri M, Monzeglio MG: Esophageal squamous cell carcinoma in 2 cats. J Small Anim Pract 40:79, 1999. 12. Hamilton TA, Carpenter JL: Esophageal plasmacytoma in a dog. J Am Vet Med Assoc 204:1210, 1994. 13. Thrall DE: Esophagobronchial fistula in a dog. J Am Vet Rad Soc 14:22, 1973. 14. Bree H van, Rick A De, Vandenberghe L: Partial esophageal obstruction by an intramural hematoma in a dog. Vet Rad 22:267, 1981.

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Diaphragmatic Hernia

❚❚❚ DIAPHRAGMATIC VARIATION, VISIBILITY, DISPLACEMENT, AND DISFIGURATION The first thing to bear in mind about the diaphragm is that it is radiographically invisible. What is commonly described as the diaphragm is actually the interface (or junction) between the caudal aspect of the lung field and the cranial portion of the liver. Sometimes, when the stomach is partially full of food and air, its cranial boarder is superimposed on the pulmonary-hepatic junction, mimicking the diaphragm (Figure 48-1). In reality, the only time the diaphragm becomes visible is when there is free air in either the pleural or peritoneal cavities. The radiographic appearance of the diaphragm is influenced by the following factors: • The animal’s position while being radiographed: In the dorsoventral projection, the diaphragm usually appears as a single large asymmetric arch; in the ventrodorsal view, the diaphragm typically appears as three small, partially superimposed arches. Oblique positioning causes the diaphragm to appear asymmetric—a potentially deceptive finding, especially if a diaphragmatic hernia is being considered. • Beam centering. When the x-ray beam is decentered (not positioned directly over the heart), the shape of the cardiac silhouette is slightly changed. Most of the time, this is not a problem, but caution should be exercised when assessing the heart under such circumstances. • The depth of breathing affects both the shape and position of the diaphragm. Shallow breathing generally is associated with an undulant, cranially positioned diaphragm, usually around the seventh or eighth rib. Conversely, deep breathing usually results in a relatively straight diaphragm located in the caudal aspect of the rib cage.

• The force with which the animal is being restrained, especially cats, which have a relatively flexible thorax, can radically change the appearance of the diaphragm compared with a cat that is not resisting. Extreme traction typically produces the most abnormal appearing diaphragm. • A tension pneumothorax can cause the diaphragm to assume a reversed curvature so that it becomes convex toward the abdomen. Conversely, an acutely collapsed caudal lobe usually is associated with a cranially displaced hemidiaphragm (diaphragmatic crus). • A large volume of pleural fluid usually results in cranial displacement of the diaphragm. • A large cranial abdominal mass may displace as well as disfigure the nearby hemidiaphragm (Figure 48-2). • Congenital sternal deformities and old fracturedislocations can straighten or displace the diaphragm. • Surgery to correct a diaphragmatic hernia or to remove a caudal parasternal mass often results in diaphragmatic straightening (Figure 48-3).

❚❚❚ DIAPHRAGMATIC TEARING WITH PASSAGE OF ONE OR MORE ABDOMINAL ORGANS INTO THE THORAX (DIAPHRAGMATIC RUPTURE, DIAPHRAGMATIC HERNIA) Trauma is the leading cause of diaphragmatic hernias in dogs and cats. The resultant intrathoracic mass effects (organs and fluid) often substantively reduce lung inflation. Liver, spleen, stomach, omentum, and small intestine are all prime candidates for herniation because of their proximity to the diaphragm and thorax.1 The right kidney of a cat has been reported to herniate into the caudodorsal thorax after presumed trauma.2 473

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SECTION V ❚❚❚ The Throat, Neck, and Thorax

A

B Figure 48-1 • A, Close-up view of the normal composite shadow created by the contiguous surfaces of the dorsal aspect of the diaphragm and stomach wall. Also note the abnormally small intervertebral disk in the 11-12 spinal unit, the result of a recent traumatic rupture. B, Close-up view of normal diaphram made visible by adjacent stomach gas.

C

A

B

D

Figure 48-2 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a dog with a massive tumor of the right kidney causing diaphragmatic displacement and disfiguration. Lateral (C) and ventrodorsal (D) abdominal films show the diseased kidney filling most of the ventral half of the abdomen.

CHAPTER 48 ❚❚❚ Diaphragmatic Hernia

475

A

A

B Figure 48-3 • Lateral view of a bulging ventral diaphragmatic mass centered just caudal to the sternum (A). Immediate postoperative view (B) shows overly straight diaphragm, the result of having to close the resultant surgical defect.

B Figure 48-4 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a dog with a severe diaphragmatic hernia (rupture, tear), in which the stomach, spleen, and a portion of the liver have moved into the thorax, displacing the heart to the right and compressing much of the left half of the lung.

Imaging Findings Diaphragmatic hernias range from the obvious to the obscure. When large, solid abdominal organs pass into the chest through a rent in the diaphragm, they are usually obvious (Figure 48-4). An exception to this generality is when there is accompanying caudal lobe consolidation and hemothorax, conditions that often create a measure of diagnostic uncertainty. In such circumstances, barium often clarifies the situation (Figure 48-5). In some instances, initial films are confusing, suggesting but not confirming a hernia. Provided the animal is stable, progress films may be made later, which may resolve the question (Figure 48-6, A to D).

Ultrasound can be helpful in identifying displaced abdominal viscera secondary to diaphragmatic rupture; however, it is rarely capable of precisely locating a diaphragmatic tear. Caution: In severe hernias with extensive visceral displacement, secondary fluid formation, and compression atelectasis, ultrasound is often inadvisable because it invariably leads to additional patient manipulation and stress and can aggravate an already compromised respiratory system. If ultrasound is absolutely necessary, it should be done with the animal standing, sitting, or on its sternum, which should be less painful and make breathing easier (Figure 48-6, E).

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SECTION V ❚❚❚ The Throat, Neck, and Thorax

A

B Figure 48-5 • Diaphragmatic hernia: Lateral plain film (A) of an injured cat shows what appears to be the stomach, and much of the intestine ventral to a dorsally displaced heart, observations that were confirmed with a barium marking study (B). The liver has also been displaced into the caudal part of the thorax, accounting for the abnormal heart shape.

❚❚❚ POSITIVE AND NEGATIVE CONTRAST PERITONOGRAPHY Positive contrast peritonography is capable of providing indirect evidence of a diaphragmatic hernia in the form of opacification of the pleural space, indicating abnormal communication between the abdominal and thoracic cavities, presumably through a tear in the diaphragm.3 Apositive contrast pneumoperitoneogram is also capable of outlining a herniated liver lobe, as exemplified in a case report by Park.4 Caution: One of the dangers of positive contrast peritonography is that, depending on the contrast medium employed (ionic or nonionic), additional pleural fluid may form, causing further compression atelectasis of the lung. Likewise, a medium to large volume of air can be injected into the peritoneal cavity with the same intent

(diagnostic pneumoperitoneum); however, the procedure is also risky because it will cause a pneumothorax if the presumptive diagnosis is correct, potentially making the dog’s condition worse. Kopler and co-workers described using mesenteric arteriography to diagnose experimentally created diaphragmatic hernias in dogs.5 Table 48-1 specifically describes their findings.

❚❚❚ PLEUROPERITONEAL DIAPHRAGMATIC HERNIA (TRUE DIAPHRAGMATIC HERNIA) In cats, pleuroperitoneal diaphragmatic hernias may be congenital or traumatic (acquired) and usually result in displacement of liver into the ventral aspect

A

B

C

E

D

Figure 48-6 • Conformation of suspected hernia: Diaphragmatic hernia was strongly suspected in these initial chest films, based on what appeared to be an incomplete diaphragm in the lateral projection (A), and intrathoracic intestine in the ventrodorsal view (B). The owner took the cat home, but returned in 2 weeks when the cat began to vomit. The thorax was reradiographed (C, D), again revealing intrathoracic intestine. A hernia was confirmed sonographically (E, sitting position).

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SECTION V ❚❚❚ The Throat, Neck, and Thorax

Table 48-1 • OBSERVATIONS AFTER MESENTERIC ARTERIOGRAPHY IN DOGS WITH VARIOUS TYPES OF EXPERIMENTALLY CREATED DIAPHRAGMATIC HERNIAS Herniated Organ

Opacified Vessel Observed in Thorax

Liver Omentum Small intestine

Common hepatic artery Left gastroepiploic artery Jejunal branches of the cranial mesenteric artery

of the caudal mediastinum. Radiographically, the displaced liver has a nonspecific appearance, often appearing as a small to medium-sized soft tissue mass. When examined sonographically, however, hepatic masses reveal their true nature in the form of characteristic echo texture and portal veins.6 Voges and colleagues also described such a hernia in a cat involving the falciform fat and closely resembling a lung mass.7 A pleuroperitoneal hernia also has been described in a dog in which a hernial sac containing a portion of the stomach, the spleen, and two liver lobes moved into the caudal mediastinum through a diaphragmatic opening adjacent to the esophagus.8

❚❚❚ DIAPHRAGMATIC EVENTRATION An eventration, as commonly used in human medicine (and occasionally in veterinary medicine), refers to an elevated segment of the diaphragm (a focal convexity as seen in an upright frontal radiographic projection), which is caused by a congenital weakness or absence of a portion of the diaphragmatic musculature; this results in poor contractility of the abnormal segment, and inability to resist pressure from adjacent abdominal viscera.9

❚❚❚ PERITONEOPERICARDIAL DIAPHRAGMATIC HERNIA (PERICARDIOPERITONEAL DIAPHRAGMATIC HERNIA) Background Peritoneopericardial hernia is a congenital malformation in which the pericardium becomes a thoracic extension of the peritoneal cavity. This is made possible by the embryologic joining of the pericardium with the peritoneum through a central defect in the diaphragm. As a consequence of this abnormal thoracoabdominal communication, one or more abdominal organs may enter the pericardium, which already is being occupied by the heart. The results of this visceral migra-

tion vary from inconsequential to fatal, depending largely on what, if any, effect there is on the systemic circulation or that of the translocated viscus. The condition occurs in both dogs and cats but is more common in dogs.10,11 In my experience, the liver and intestine are the organs most often found in the pericardial sac, although there are reports of other displaced viscera, including the uterine horn of a pregnant dog, which contained a radiographically visible fetus.12 Although I am unable to cite any prevalence statistics, most of the peritoneopericardial hernias I have seen have been incidental radiographic findings. Those who are unaware of the condition (or fail to consider it when examining thoracic films) are likely to mistake the resultant silhouette effect (the combined shadow of the heart plus contiguous viscus) for an enlarged heart. Evans and Biery published an excellent review of the subject.13

Imaging Findings It has been my observation that many of the hearts of cats with peritoneopericardial hernias resemble mildly enlarged dog hearts. That is to say, the normally small, oval-shaped heart of the cat, combined with whatever abdominal viscera are in the pericardium, assumes a more spherical shape characteristic of dogs. Bierry and co-workers reported the discovery of a discrete tissue fold (as seen in a lateral thoracic radiograph), which is present in many cats with peritoneopericardial hernias. They assert that this pleural-like remnant that spans the caudal edge of the heart and adjacent surface of the diaphragm, just below the caudal vena cava, can be used as a reliable radiographic indicator of peritoneopericardial hernia in the cat. The authors caution, however, that pleural thickening or pleural fluid may mimic this finding.14

References 1. Worth LT, Pugh CR: What is your diagnosis? J Am Vet Med Assoc 210:29, 1997. 2. Rochat MC, Aronson E: Radiographic diagnosis. Vet Rad 32:110, 1991. 3. Rendano VT: Positive contrast peritonography: an aid in the radiographic diagnosis of diaphragmatic hernia. J Am Vet Rad Soc 20:66, 1979. 4. Park RD: Radiographs presented as part of the 1992 A.C.V.R. oral certification examination: thoracic section. Vet Radiol Ultrasound 34:239, 1993. 5. Koper S, Habil MM, et al: Selective abdominal angiography as a diagnostic method for diaphragmatic hernia in the dog: an experimental study. Vet Rad 23:50, 1982. 6. Smith SA, Goggin JM, Kraft SL: What is your diagnosis? J Am Vet Med Assoc 214:480, 1999. 7. Voges AK, Bertrand S, et al: True diaphragmatic hernia in a cat. Vet Radiol Ultrasound 38:116, 1997. 8. Berry CR: Answers for film reading session: 1995 A.C.V.R. annual meeting. Vet Radiol Ultrasound 36:449, 1995. 9. Marchiori DM: Chest disease patterns. In Marchiori DM: Clinical imaging: pattern differentials. St. Louis, 1999, Mosby.

CHAPTER 48 ❚❚❚ Diaphragmatic Hernia

10. Clinton JM: A case of congenital pericardio-peritoneal communication in a dog. J Am Vet Rad Soc 8:57, 1967. 11. Barrett RB, Kittrell JE: Congenital peritoneopericardial diaphragmatic hernia in a cat. J Am Vet Rad Soc 7:21, 1966. 12. Iwasaki M, Sterman F, Carolina A: What is your diagnosis? J Am Vet Med Assoc 1775:214, 1999.

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13. Evans SM, Biery DN: Congenital peritoneopericardial diaphragmatic hernia in the dog and cat: a literature review and 17 additional case histories. Vet Rad 21:108, 1980. 14. Berry CR, Koblik PD, Ticer JW: Dorsal peritoneopericardial mesothelial remnant as an aid to the diagnosis of feline congenital peritoneopericardial diaphragmatic hernia. Vet Rad 31:239, 1990.

S E C T I O N

V I

The Heart

C h a p t e r

4 9

Heart and Circulatory Variations and Radiographic Disease Indicators ❚❚❚ VARIATIONS Normal Physiologic Variants That May Resemble Cardiac Radiographic Disease Indicators The Respiratory Cycle. Breathing is associated with thoracic movement, which may result in blurring of the heart and lungs, especially when longer exposure times are used (Figure 49-1). This motion unsharpness, as it is termed, can be mistaken for heart or lung disease, particularly pulmonary edema or pleural fluid. Even when exposure times are brief enough to ensure crisp intrathoracic imagery, breathing still can influence radiographic appearances, depending on whether the radiograph was made during inspiration or expiration. In an inspiratory film, the heart usually appears both relatively and absolutely smaller than during expiration. Conversely, during expiration, the heart appears larger than it does during inspiration. These differences pertain to all standard thoracic projections: lateral, dorsoventral, and ventrodorsal (Figure 49-2). Of equal importance, especially when attempting to render a judgment on heart failure, is the appearance of the lung,

which appears relatively dense during expiration, often resembling pulmonary edema. The Cardiac Cycle. Just as breathing influences the appearance of the heart, cardiac emptying and filling likewise can be appreciated radiographically, especially in dorsoventral projections of large dogs with slow heart rates. To generalize: the heart appears mild to moderately larger and rounder during maximal filling (ventricular end diastole), whereas during emptying (end ventricular systole), the heart appears relatively smaller, often featuring prominent atria and tapered ventricles. Toal and co-workers described the effect of variations in the cardiac cycle (systole and diastole) on the radiographic appearance of the feline heart.1 Somewhat surprisingly, they discovered that the dorsoventral position was associated with the greatest difference in cardiac size and shape, whereas the ventrodorsal and left lateral views proved less variable. In no view, however, were the anatomic disparities marked. The authors concluded that although minor anatomic differences occurred with differences in patient positioning, none of the variations resembled heart disease. 481

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SECTION VI ❚❚❚ The Heart

A A

B Figure 49-1 • Light (A) and dark (B) lateral thoracic radiographs

B

of a healthy dog show mild vascular blurring, the result of motion unsharpness caused by prolonged exposure time (0.1 sec).

Normal Anatomic Variants That May Mimic Cardiac Radiographic Disease Indicators Rib Cage and Sternum. The rib cage of the Bulldog often causes the heart and lung to appear unusually tall and tapered in the lateral projection, especially during expiration (Figure 49-3, A). In the dorsoventral or ventrodorsal views, the heart often appears disproportionately wide and flattened ventrally, especially during expiratory filming (the norm for a Bulldog). The ribs flare cranially, suggesting a chronic respiratory disease such as emphysema; in human radiology, this is referred to as the crawfish sign (Figure 49-3, B). In Bassett Hounds, the ventrodorsal view often shows what appear to be symmetric fluid accumulations located in the lateral aspects of the pleural space (Figure 49-4). In reality, this is not fluid but rather the superimposition of portions of the lateral chest wall on the outer margins of the lung, the result of the recurved shape of the Bassett Hound’s ribs and costochondral connections. Severe congenital caudal sternal indentation (L. pectus excavatum), which almost never causes illness

C Figure 49-2 • Close-up dorsoventral views of the hearts of three dogs: one healthy (A) and two with mitral insufficiency (B, C) showing how both the depth of inspiration and the size of the heart can influence the cardiac thoracic ratio.

in dogs and cats, can force the heart to one side or another, often changing its orientation in the process. In the latter context, the heart may appear enlarged and misshapen, mimicking heart disease (Figures 49-5 and 49-6).

CHAPTER 49 ❚❚❚ Heart and Circulatory Variations and Radiographic Disease Indicators

483

A

B Figure 49-3 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a healthy Bulldog show characteristically tall heart and tapered lung in the lateral projection and a wide, squatty heart in the opposite view.

A

B

Figure 49-4 • Orientation (A) and close-up ventrodorsal (B) views of the thorax of a normal Bassett Hound shows breed-specific rib curvature that can mimic pleural fluid or lung consolidation, especially when the thorax is obliqued.

484

SECTION VI ❚❚❚ The Heart

A A

B Figure 49-5 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a dog show right cardiac shift caused by a congenital deformity of the sternum (pectus excavatum).

B Figure 49-6 • Lateral (A) and ventrodorsal (B) thoracic

Mediastinal Fat Cranial Mediastinum. The accumulation of fat in the cranial mediastinum causes widening, which in some cases is pronounced, and has been misdiagnosed as tumor or hemorrhage. In a cardiovascular context, mediastinal fat may be misinterpreted as an enlarged cranial vena cava. Obese animals are most likely to have these mass-like fat accumulations (Figure 49-7). Middle Mediastinum. Pericardial and extrapericardial fat can mimic heart enlargement (see later) or, more often, pleural fluid. In questionable cases, either postural radiography or ultrasound should resolve the issue. Enlarged Aortic Root (False Aortic Aneurysm). Moon and colleagues reported what appear to be two normal anatomic variants in the hearts of older cats, usually 10 years of age or older.2 The first of these is a localized bulge in the proximal part of the aortic arch, which

radiographs of a cat show left cardiac shift caused by a congenital deformity of the sternum (pectus excavatum).

is appreciable in all standard thoracic projections (Figure 49-8). The second variant has to do with the forward inclination of the heart as seen in lateral projection; specifically, in some cats, this angle of cranial inclination gradually becomes smaller. The significance of these normal variations is that they can mimic heart disease: increased sternal contact in the lateral view and cardiac remodeling in the dorsoventral or ventrodorsal view.

The Double Cardiac Silhouette Sign Litster and Buchanan described how pericardial fat can falsely create the impression of cardiomegaly in obese but otherwise healthy cats, an error most commonly made by novice film readers (Figure 49-9).3 It was further determined that cats with a large amount of falciform fat tended to have the most pericardial fat.

CHAPTER 49 ❚❚❚ Heart and Circulatory Variations and Radiographic Disease Indicators

485

A

Figure 49-7 • Ventrodorsal view of the thorax of an overweight dog shows a widened, indistinct cranial mediastinum, the result of fat accumulation.

Cats with questionable heart enlargement (disease or fat?) or a double cardiac silhouette sign can be reevaluated in a subsequent pair of thoracic films made with contrast-enhancing technique (increased mAs, decreased kilovoltage potential). These additional high-contrast images, especially the lateral view, should enable the observer to see the true heart margins as distinct from surrounding pericardial fat and thus simplify the decision. If additional films fail to resolve the question, ultrasound predictably will reveal the actual heart size. Another indication that perceived cardiomegaly is actually due to pericardial fat is the presence of a blocked or squared-off right cranial heart margin, sometimes seen in ventrodorsal thoracic projections of fat cats.4

Positional Variants That Resemble Thoracic Radiographic Disease Indicators Dorsoventral Versus Ventrodorsal Projections. Generally, the heart appears longer and narrower when projected ventrodorsally than when projected dorsoventrally (Figure 49-10). This difference results in large part from caudal displacement of the cardiac apex, owing to its relatively weak moorings compared with that of its base. For the same reason, the heart often tips to the right or left of midline, in some instances markedly altering its radiographic profile. Overall, the dorsoventral projection more accurately portrays the cardiac anatomy than does the ventrodorsal view.

B Figure 49-8 • Lateral (A) and ventrodorsal (B) views of the thorax of an aged cat with thyroid-induced myopathy show an enlarged aortic root (emphasis zones).

Right Versus Left Lateral Projections. In the right lateral projection, the cardiac apex appears conical, and the caudal vena cava appears to blend imperceptibly with the caudal border of the left ventricle (Figure 49-11). In contrast, the left lateral projection features a relatively rounded cardiac apex and a distinctive cardiocaval overlap. With practice, a right lateral projection can be readily differentiated from a left lateral view provided the heart is centered on the middle of the film. Postural Projections. Postural projections, such as the standing (Figure 49-12) or erect (Figure 49-13) views, can look very different from conventional projections, to the extent that care must be taken when analyzing

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Figure 49-9 • Lateral thoracic radiograph of a healthy cat in which the heart appears falsely enlarged because of surrounding fat.

such images. Unlike oblique projections, however, most postural films can be standardized so that it is possible to compare them with normal films (when adjusted for breed variations). Oblique Projections. Oblique ventrodorsal or dorsoventral views of the heart are usually of little or no diagnostic value because they are impossible to standardize. When made accidentally, such projections often give the false impression of extreme right-sided or left-sided heart enlargement, depending on which direction the dog or cat is tipped. Holmes and co-workers investigated the effects of patient rotation on the appearance of the canine heart in the ventrodorsal position. Not surprisingly, they concluded that the cardiac silhouette changed more as obliquity increased. They considered images diagnostically unreliable when the dorsal spinous processes were projected outside either lateral margin of the spine.5 In my opinion, this is an overly cautious view; however, I do agree with the basic premise that oblique views of the heart can be diagnostically misleading. I must add here that thoracic films made in dogs that are in heart failure or that have sustained serious chest injuries are often obliqued and frequently cannot repeated. Standard projections are undoubtedly highly desirable, but film quality must never take precedence over patient well-being. Learn to read obliqued chest films under such circumstances. Optimally positioned films can be made later after emergency treatment has been instituted and the animal has been stabilized.

❚❚❚ CARDIOVASCULAR RADIOGRAPHIC DISEASE INDICATORS The following abnormalities are reliable indicators of cardiac or circulatory disease.

A

B Figure 49-10 • Ventrodorsal image (A) of the heart of a healthy dog appears relatively elongated compared with a dorsoventral projection (B). In the latter view, the heart hangs naturally in the chest; in the ventrodorsal projection, the heart tips caudally and sometimes laterally, casting a longer shadow.

Decreased Heart Size In my experience, the most common causes of diminished heart size are blood loss and shock; the latter condition functionally resembles blood loss inasmuch as blood trapped in the stagnant abdominal capillary beds is temporarily unavailable to the general circulation. The pattern of diminished heart size, pulmonary oligemia, and reduced caval dimensions is often termed hypovolemia (Figure 49-14).6

B

A Figure 49-11 • Right (A) and left (B) lateral thoracic radiographs of a healthy dog show small but consistent differences in the heart shape, sternal contact, and caval overlap.

Figure 49-12 • Standing lateral thoracic radiograph of a healthy dog.

Figure 49-13 • Erect lateral radiograph of a healthy dog.

A

B

Figure 49-14 • Lateral and ventral thoracic films of a dog recently hit by a car show a small heart and overinflated lungs, often seen in shocky animals and sometimes mistaken for pneumothorax.

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SECTION VI ❚❚❚ The Heart

A

A

B B

Figure 49-16 • A, Lateral view shows severe mitral

radiographs of a cat with thyroid-induced cardiomyopathy (TIM) show an enormous heart and enlargement of the caudal vena cava. Caution: The combination of expiratory filming and a relatively light exposure mimic pleural fluid, a potentially critical finding that would signal heart failure.

insufficiency characterized by a distinctive left atrial dome, which is being enhanced by the superimposition of distended pulmonary veins (lateral view). B, Seemingly mismarked dorsoventral view showing cardiac apex shifted from its normal left-sided location to the right half of the chest cavity.

Increased Heart Size

Abnormal Cardiac Contour

Increased heart size is usually the result of cardiac remodeling in response to primary heart disease (Figure 49-15). Less commonly, fluid accumulates in the pericardial sac, mimicking heart enlargement. Occasionally, the heart enlarges because of chronic lung disease (cor pulmonale) or high blood pressure. Some diaphragmatic hernias and congenital pericardioperitoneal hernias also can simulate cardiomegaly.

Mitral insufficiency, especially if severe, characteristically alters the caudal heart base (as seen in lateral projection) by creating a large left atrial dome (Figure 49-16). Hager and co-workers described a case of right atrial hemangiosarcoma in a dog creating a small but distinct bulge in the cranial margin of the heart (in the left but not the right lateral view).7 Such subtle changes in cardiac contours may be the only detectable abnor-

Figure 49-15 • Lateral (A) and ventrodorsal (B) thoracic

CHAPTER 49 ❚❚❚ Heart and Circulatory Variations and Radiographic Disease Indicators

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Figure 49-17 • Lateral radiograph of a 6-year-old Golden Retriever being screened for metastasis after finding a small perianal lump believed to be a tumor. Although no metastases were found, the shape of the heart appeared abnormal. Cardiac evaluation, including ultrasound, was normal. The lump was removed and proved to be benign.

Figure 49-18 • Oblique ventrodorsal thoracic radiograph of a cat

mality related to the heart in some diseases and, as such, warrant further diagnostic consideration in the form of sonography. This case report also points out the occasional value of alternate-side radiography (right and left lateral views) for the detection of heart disease as well as lung lesions. Not all misshapen hearts are abnormal, however, as evidenced by some medium- to large-sized breeds that have what I term “sagging hearts” as seen in lateral projection but are clinically and sonographically normal in all respects (Figure 49-17). Occasionally, nonstandard positioning is responsible for an abnormalappearing cardiac silhouette, exemplified by the cat in Figure 49-18.

made just as it was twisting shows a striking opaque trough on the right side of the heart. Other than the fact that there is no heart disease with this appearance, the most persuasive argument against this being heart or lung disease is the relative difference in right- versus left-sided lung inflation and density, findings typical of oblique positioning and, less often, postural atelectasis secondary to anesthesia.

Positional Abnormality Large cardiac displacements are most often the result of a unilateral volume loss in one or more adjacent lung lobes. Less often, the heart is pushed out of position by a mass, such as a primary lung tumor, or by a mass effect, such as a herniated stomach. Occasionally, the apex of the heart shifts from its normal position on the left side of the thorax to the opposite side of the chest. Displacements of this sort are often of an accommodative nature, providing growing room for a diseased heart. When displacements of this sort are accompanied by projectional obliquity, the effect can be quite pronounced (Figure 49-19).

Aortic or Main Pulmonary Arterial Enlargement Enlargement of the aortic base in young dogs with heart disease usually is caused by a persistent arterial duct

Figure 49-19 • Ventrodorsal radiograph of a dog with a patent arterial duct shows a shift of the cardiac apex from the left to right side of the thorax, apex shifted to right side, accentuated by oblique positioning.

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SECTION VI ❚❚❚ The Heart

A A

B Figure 49-21 • A, Pulmonary congestion secondary to chronic

B Figure 49-20 • Lateral (A) and dorsoventral (B) views of the heart of a dog with a persistent arterial duct show massive dilation of the aortic root.

(Figure 49-20) or aortic stenosis, whereas enlargement of the main pulmonary artery is typically the result of pulmonic stenosis or pulmonary overcirculation secondary to a ventriculoseptal defect (VSD).

Pulmonary Hyperemia Pulmonary hyperemia or excessive lung blood (synonyms: pulmonary plethora, pulmonary congestion, overcirculated lung, hypervascular lung, pulmonary hyperperfusion) is most often seen as a result of heart failure (Figure 49-21). Less commonly, the lung may become overcirculated because of a cardiac anomaly, such as a VSD, which reroutes freshly oxygenated blood destined for the systemic circulation back through the lung. Abnormally large volumes of intravenous fluids can effect a similar appearance. Heartworm disease selectively causes pulmonary arterial enlargement, often accompanied by vascular disfigurement, including an undulant profile and abrupt, nontapered termination (vascular blunting). These changes are especially striking when viewing pulmonary arteriograms of infected dogs and cats.8

mitral regurgitation shows an increased number of lung vessels. B, In the cranioventral close-up, vessels extend much further into the lung periphery than normal.

Pulmonary Oligemia Pulmonary oligemia or diminished lung blood (synonyms: undercirculated lung, hypovascular lung, pulmonary underperfusion) is most often the result of blood loss or shock. In the context of heart disease, pulmonary undercirculation is a feature of cardiac tamponade, Ebstein’s malformation (Figure 49-22), tetralogy of Fallot, and other right-to-left shunts. Individuals with pulmonic stenosis often have reduced peripheral lung circulation.

Pleural Fluid Pleural fluid, in the form of a transudate, is most often the result of heart disease, especially in cats, where it is the prime radiographic indicator of failure (Figure 49-23). Pleural hemorrhage usually is caused by lung injury and occasionally by a poison such as warfarin. Chyle may accumulate in the pleural space secondary to rupture of the thoracic duct or secondary to lymphatic obstruction, usually by a mediastinal tumor. Heart failure in cats also may cause lymphatic backup, resulting in a pleural fluid laced with chyle. Pleural

CHAPTER 49 ❚❚❚ Heart and Circulatory Variations and Radiographic Disease Indicators

491

A

Figure 49-23 • Heart failure in a cat with hypertrophic cardiomyopathy, as indicated by pleural fluid, pulmonary hyperemia, and heart enlargement. It is notable that this cat was referred by another specialist with a diagnosis of congestive cardiomyopathy, an extremely rare disease in cats, based on “a globose heart and dilated vena cava.”

exudates (pyothorax) are now relatively rare. Diaphragmatic hernias can be associated with large volumes of pleural fluid, especially where portions of the liver and spleen are involved. The omentum, although possessing little mass, is still sufficiently vascular that when displaced into the thorax it produces a surprisingly large amount of fluid.

B

Pneumopericardium

C Figure 49-22 • A, Close-up lateral radiograph of a 1-year-old Boxer with Ebstein’s anomaly (elongated tricuspid valve). B, Close-up view of the cranioventral lung shows abnormally small vessels. A dorsoventral view completes the examination.

Pneumopericardium (air within the pericardial sac) is a rare radiographic finding. Precisely how and why pneumopericardium develops is uncertain, but radiologists have observed this phenomenon in a relatively small situational cluster, including (1) thoracic injury (especially cavitary lung lesions), (2) neck and throat injuries (particularly to the larynx and trachea), (3) bronchitis and bronchiectasis, (4) chronic pericardial disease, and (5) following tracheotomy or endotracheal tube injury. Although I have seen fewer than a dozen cases of pneumopericardium in nearly three decades, most have been associated with pneumomediastinum (both “spontaneous” and traumatic). This latter observation suggests that pneumopericardium is caused by air escaping from ruptured alveoli, dissecting along the adventitial planes of the pulmonary vasculature, most probably the pulmonary veins, into the middle mediastinum, and eventually the pericardial sac. More important than the mechanism of pneumopericardium are its consequences. Theoretically, a rapidly developed medium- or large-volume pneu-

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SECTION VI ❚❚❚ The Heart

mopericardium can lead to a serious or even fatal circulatory deficiency secondary to cardiac compression. I must hasten to point out, however, that I have never observed a tamponade in such circumstances, except diagnostic pneumopericardium, an outdated special procedure that has long since been replaced by cardiac ultrasound. Furthermore, I have yet to appreciate any related clinical signs as described in a recent case report.9

References 1. Toal RL, Losonsky JM, et al: Influence of cardiac cycle on the radiographic appearance of the feline heart. Vet Rad 26:63, 1985. 2. Moon ML, Keene BW, et al: Age related changes in the feline cardiac silhouette. Vet Radiol Ultrasound 34:315, 1993.

3. Litster AL, Buchanan JW: Radiographic and echocardiographic measurement of the heart in obese cats. Vet Radiol Ultrasound 41:320, 2000. 4. Litster AL, Buchanan JW: Radiographic and echocardiographic measurement of the heart in obese cats. Vet Radiol Ultrasound 41:320, 2000. 5. Holmes RA, Smith FG, et al: The effects of rotation on the radiographic appearance of the canine cardiac silhouette in dorsal recumbency. Vet Rad 26:98, 1985. 6. Thrall DE: Radiographic diagnosis. Vet Rad 22:87, 1981. 7. Hager D, Ackerman N, Spencer CP: Radiographic diagnosis. Vet Rad 28:32, 1987. 8. Donahoe JM, Kneller SK, Lewis RE: In vivo pulmonary arteriography in cats infected with Dirofilaria immitis. J Am Vet Rad Soc 17:147, 1976. 9. Capizzi PJ, Martin M, Bannon MP: What is your diagnosis? J Am Vet Med Assoc 1377:212, 1998.

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Cardiac Silhouette Analysis

Traditionally, veterinarians and physicians alike have attempted to diagnose heart disease by considering the size and shape of each part of the heart separately (left atrium, left ventricle, and so forth) and then attempting to integrate the results. Although of some value, this reductionist approach to radiographic analysis of the heart rarely generates a specific diagnosis. Worse, it may blind the evaluator to the presence of a more informative global deformity that, at the very least, can be used to determine which side of the heart is diseased and malfunctioning. Using a holistic, gestalt-like approach to the diagnosis of heart disease in pets need not supplant the more traditional piecemeal approach to cardiac radiology currently used by most veterinarians. It can supplement it, however. As for the novice, this method is far simpler, one in which there is a clear observational focus: the overall size and shape of the heart compared with normal (the cognitive strategy used by most radiologists).

appears to be the source of enlargement, the heart is described as cardiomegaly, left-sided emphasis. If each side of the heart appears to be making an equal contribution to the enlargement, the heart enlargement is simply described as generalized.

Enlarged Aorta or Pulmonary Artery Once the heart has been assessed, the aorta and pulmonary artery are evaluated. Each then is declared to be normal, enlarged, or diminished. In general, such observations should be noted only if clear-cut.

Increased or Decreased Lung Vessels The size and number of visible lung vessels can provide information about the heart, lung, and general circulation (Figure 50-1). As a diagnostic point of departure, the following generalities pertain, shown in Table 50-1.

❚❚❚ METHODOLOGY

Left-sided Cardiac Emphasis

Radiographic assessment of the heart should focus on three things: (1) the size and shape of the heart, (2) the presence of aortic or pulmonary arterial enlargement or diminishment, and (3) the circulatory status of the lung. By combining the observed abnormalities, it is often possible to predict which side of the heart is diseased and the effect on the pulmonary circulation (and, by inference, the systemic circulation as well).

In middle-aged and older dogs, cardiomegaly with left-sided emphasis most often is seen with mitral regurgitation secondary to endocardiosis. In puppies or young adult dogs, this pattern is more apt to reflect aortic stenosis or a persistent arterial duct (patent ductus arteriosus), especially if accompanied by enlargement of the aortic base. The quality of the heart murmur usually can be used to choose between these possibilities.

Heart Size: Left, Right, or Generalized

Right-sided Cardiac Emphasis

If the heart appears enlarged on plain films, is it the right or left side that is the major contributor? If the principal enlargement appears to be on the right, the enlarged heart is described as follows: cardiomegaly, right-sided emphasis. If, on the other hand, the left side

In puppies and young adult dogs, right-sided emphasis most often is seen with pulmonary stenosis and ventricular septal defect. Heartworm disease (in appropriate geographic locales) can produce similar cardiac remodeling. 493

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SECTION VI ❚❚❚ The Heart

Table 50-1 • POTENTIAL DIAGNOSTIC RELATIONSHIPS BETWEEN THE HEART AND PULMONARY VASCULATURE Normal vessels

Normal Heart

Small Heart

Large Heart

Normal cardiovascular system

Probable normal variation Decreased functional blood volume due to shock or blood loss Addison disease Chronic obstructive lung disease, e.g., emphysema Inspiratory radiograph

Probable heart disease; no indication of current failure; endurance-conditioned dog, e.g., sled dog Cardiac compression caused by pericardial fluid (tamponade) Congenital heart diseases such as pulmonic stenosis, Ebstein’s malformation, tetralogy of Fallot

Small vessels

Large vessels

Possible inflammatory hyperemia, e.g., early pneumonia Systemic hypertension

Heart failure if accompanied by lung edema; possible future failure if not; most commonly due to mitral insufficiency in the dog and thyroidinduced myopathy in the cat Heartworm disease. Congenital heart diseases such as PDA, aortic stenosis, and VSD Expiratory radiograph

PDA, Patent ductus arteriosus; VSD, ventriculoseptal defect.

is calculated by dividing the widest part of the heart by the width of the thorax at the same level (as measured in the frontal view). In dogs, cardiac measurement never has achieved clinical popularity in veterinary medicine, largely because of breed variation and low overall sensitivity. If measurements are to be used, it is prudent to use a large control base for each breed of dog evaluated.

Cats

Figure 50-1 • Lateral radiograph of a dog with a patent ductus arteriosus (PDA) shows generalized heart enlargement and vascular congestion. Note that the blood vessels in the midcranial thorax (emphasis zone) are about the same size as the ribs they cross, indicative of pulmonary hyperemia.

No Emphasis, Generalized Enlargement Generalized cardiomegaly can be anticipated in dogs with bilateral atrioventricular insufficiency secondary to endiocardiosis. When generalized cardiomegaly is accompanied by pulmonary hyperemia, future heart failure is likely. Generalized enlargement is also seen with dilated cardiomyopathy in dogs.

❚❚❚ CARDIAC MEASUREMENTS (CARDIAC RADIOMETRICS) Dogs In humans, in whom cardiac measurements are used routinely as a screening method, the cardiothoracic ratio

Ahlberg and co-workers established that the volume of a cat’s heart can be accurately and reliably measured from ventrodorsal and left lateral radiographs.1 Litster and Buchanan devised a comparative method of measuring heart size in cats,2 similar to a previously published technique designed for dogs.3 In my experience, the use of cardiac-thoracic ratios, measured from frontal, dorsoventral, or ventrodorsal views, has both low sensitivity and specificity and is generally unreliable in cats unless cardiac remodeling is advanced.

Judging Heart Size in the Context of a Large Volume of Pleural Fluid Judging the size of the heart when it is surrounded by a large amount of fluid can be difficult. Not only does fluid conceal much of the heart, but the associated flotational effect exerted by the lung as it attempts to reach the surface of the fluid usually leads to some degree of tracheal displacement, falsely suggesting a taller than normal heart. Cardiac measurements performed in this context are typically unreliable.4 Postural radiography can be used to move pleural and mediastinal fluid away from the heart, but one must become familiar with the normal appearance of the heart as seen in the standing lateral, ventrodorsal erect, lateral erect, and lateral decubitus projections.

CHAPTER 50 ❚❚❚ Cardiac Silhouette Analysis

References 1. Ahlberg N-E, Hansson K, et al: Radiographic heart-volume estimation in normal cats. Vet Rad 30:253, 1989. 2. Litster AL, Buchanan JW: Measurement of the normal feline cardiac silhouette on thoracic radiographs. J Am Vet Rad Assoc 216:210, 2000.

495

3. Buchanan JW, Buchler JB: Vertebral scale system to measure canine heart size in radiographs. J Am Vet Med Assoc 206:194, 1995. 4. Snyder PS, Sato T, et al: The utility of thoracic radiographic measurement for the detection of cardiomegaly in cats with pleural effusion. Vet Rad 31:89, 1990.

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Angiography and Angiocardiography ❚❚❚ BACKGROUND Buchanan, Patterson, and others in the Comparative Cardiovascular Studies Unit of the University of Pennsylvania School of Veterinary Medicine published extensively on the use of angiocardiography in the diagnosis of congenital and acquired canine heart disease.1,2 Bohn and Rhodes, from the same institution, published one of the earliest reports on the diagnostic versatility of angiography. They gave examples of an aortic aneurysm caused by Spirocerca, caudal aortic thrombi in a dog and cat, an aortic body tumor occluding the cranial vena cava, and valvular disfiguration secondary to endocarditis.3 Kneller and co-workers later showed that both carotid and femoral aortography are capable of accurately and completely depicting the abdominal vasculature of cats, although the former catheterization site sometimes left the animal with an ipsilateral Horner syndrome.4 Gomez and co-workers made similar observations in the dog, but because they used the femoral artery exclusively, they reported no harmful side effects.5 Cantwell described the use of selective right and left-sided ventriculography in the angiographic diagnosis of an aortic body tumor in a dog.6 Suter also contributed much to the literature, largely in the form of a pair of excellent textbooks, which regrettably are no longer in print. Lord and co-workers published their findings on feline congestive cardiomyopathy, emphasizing the diagnostic role played by selective angiocardiography, a role that has now largely been assumed by echocardiography.7 Likewise, ultrasound machines have assumed the calculation of ventricular volumes, which is welcome because the required computations were tedious and time consuming.8 Stickle and Anderson asserted that nonselective angiocardiography is within the capability of veterinarians in general practice. They also stated that, along with thoracic radiographs, it can be used to diagnose common congenital heart diseases, including per496

sistent arterial duct, ventricular septal defect, tetralogy of Fallot, pulmonic stenosis, and aortic stenosis.9 They caution, however, that the superimposition of one contrast-filled heart chamber on another can be confusing and can make the identification of some left-to-right shunts difficult or impossible. I would add to this an additional warning: obtaining one or more images at just the right time to appreciate a particular lesion can be extremely difficult (and frustrating). Barthez and co-workers described the angiographic and sonographic appearance of an anomalous caudal vena cava in a dog in which the posthepatic portion was absent. To compensate for the missing segment, the remaining caudal vena cava was joined to the azygos vein at the level of the right kidney, forming a single vascular conduit to the right side of the heart. This type of caval malformation is called azygos continuation of the caudal vena cava.10 Del Palacio and coworkers described the angiographic and sonographic appearance of a persistent left cranial vena cava and associated dilated coronary sinus.11 Physician radiologists have described the use of CO2 in canine angiocardiography, claiming that it is as effective as organic iodine solutions in identifying pericardial disease, intracardiac shunts and valvular obstructions, cardiac tumors, and heartworms.12

❚❚❚ RISKS ASSOCIATED WITH CARDIAC CATHETERIZATION Selective cardiac catheterization is a potentially risky and occasionally fatal procedure, especially when performed by novices or unpracticed experts. Although the veterinary literature contains few descriptions of such injuries—often sanitized in the literature as “complications” or “untoward events”—there seems little doubt that such hazards exist.13 For example, the catheter may whip during a pressurized injection, causing a myocardial hematoma, injection of contrast into the myocardium, catheter puncturing the heart

CHAPTER 51 ❚❚❚ Angiography and Angiocardiography

497

Table 51-1 • POTENTIAL CATHETER-RELATED INJURIES TO THE HEART Catheter Injury

Comments

Bruising or lacerating ventricle wall

Usually caused by catheter whip related to excessive injection pressure; Caution: Can lead to arrhythmias Also caused by catheter whip, this injury is compounded by the hyperosmolar nature of many contrast media, which potentially prolongs bleeding; Caution: Can lead to arrhythmias A knotted catheter cannot be retrieved until it is first unknotted, a procedure that can be time-consuming Usually the result of inexperience, impatience, or both; Caution: Can result in serious regurgitation through the damaged valve Typically occurs from not verifying the location of the catheter before attempting to advance it, especially if excessive resistance is encountered; Caution: Can lead to hemopericardium and tamponade As above. Be especially careful when attempting to catheterize a PDA; Caution: Can lead to hemopericardium and tamponade Again, usually a novice mistake, caused by the forceful advance of relatively rigid, snouted catheter; Caution: Can lead to hemopericardium and tamponade

Injecting ventricular wall with contrast solution Knotting catheter Lacerating heart valve Punctured atrium Punctured coronary artery Punctured ventricle

Table 51-2 • PROS (+) AND CONS (-) OF SELECTIVE VERSUS NONSELECTIVE ANGIOCARDIOGRAPHY Selective Angiocardiography

Nonselective Angiocardiography

+Fully delineates the interior of individual heart chambers and associated vessels +Allows for test injection +Maximizes radiographic contrast at suspected lesion site by using pressure injector +Minimizes contrast dilution at suspected lesion site by using pressure injector +Simplifies film timing +Allows for concurrent oximetry and pressure measurements -Potentially dangerous -Time consuming -Requires specialized training and experience -Requires specialized equipment: cinefluoroscopy with image intensification, rapid film changer, pressure injector, blood oxygen and pressure measuring equipment, a large variety of catheters and and a surgically clean environment

+ Safe +Fast +Inexpensive +Can be performed without any additional equipment +Requires no specialized training -Poorly delineates the interior of the heart -Images are usually of low contrast and poor detail owing to hemodilution of contrast agent related to hand injection -Image timing is usually hit and miss -Disallows test injection -Intracardiac blood pressure and oxygen tension measurements impossible

wall and causing hemopericardium, catheter tearing a valve cusp, and catheter inadvertently placed into coronary artery, which ruptures with high-pressure injection, causing hemoperitoneum. Some potential catheter-related injuries of the heart are listed in Table 51-1.

❚❚❚ METHODS OF CATHETERIZATION: WHICH IS BEST? The pros and cons of selective versus nonselective angiocardiography are listed in Table 51-2.

Dosage and Opacification Times for the Dog and Cat in Nonselective Angiocardiography: Fixed or Flexible Dosages Wise determined that 200 mg of iodine per 0.45 kg of body weight produces optimal opacification of the heart

Table 51-3 • NORMAL NONSELECTIVE OPACIFICATION TIMES IN THE DOG Good Visualization

Time from Start of Injection (sec)

Aorta Cranial vena cava Left atrium Left ventricle Pulmonary arteries Pulmonary outflow tract Fair visualization Heart valves Papillary muscles Right atrium Right ventricle

4.5-6.5 1-2.5 5-5.5 4.5-6 2-3 2-3 Variable Variable 1-1.5 1.5-2.5

Modified from Wise M: Non-selective angiocardiography in the normal dog and cat. Vet Rad 23:144, 1982.

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Table 51-5 • OPTIMAL CONTRAST DEPLOYMENT IN SELECTIVE ANGIOCARDIOGRAPHY Heart Chamber or Artery

Suspected Lesion

Left atrium

Thrombus, tumor, atrial septal defect, mitral stenosis secondary to dysplasia Mitral insufficiency secondary to dysplasia, aortic stenosis, combined aortic stenosis and mitral dysplasia, ventricular septal defect and left-to-right shunting Persistent arterial duct Abnormal pulmonary arteries (e.g., dirofilariasis, Eisenmenger syndrome) Tricuspid stenosis secondary to dysplasia, thrombus, tumor Pulmonic stenosis, tetralogy of Fallot, ventricular septal defect with right to left shunting (Eisenmenger syndrome)

Left ventricle

Proximal aorta Proximal pulmonary artery Right atrium Right ventricle

Figure 51-1 • Lateral nonselective cardiac angiogram in a cat with thyroid-induced cardiomyopathy shows opacification of the caudal vena cava, right atrium and ventricle, and pulmonary arteries. The limitation of this procedure lies in the fact that the left atrium and ventricle, the focus of the examination, are not yet seen; even when they do become visible, superimposition by the contrast-filled right heart will make assessment difficult or impossible.

Table 51-4 • NORMAL NONSELECTIVE OPACIFICATION TIMES IN THE CAT Good Visualization

Time from Start of Injection (s)

Aorta Cranial vena cava Left atrium Left ventricle Pulmonary arteries Pulmonary outflow tract Fair visualization Heart valves Papillary muscles Right atrium Right ventricle

5-7 0.5-1.5 4.5-7 5-7 1.5-2.5 (Figure 51-1) 1.5-2.5 Variable Variable 1-1.5 1.5-2

Modified from Wise M: Non-selective angiocardiography in the normal dog and cat. Vet Rad 23:144, 1982.

chambers during nonselective angiocardiography in both dogs and cats.14 In my experience, a patienttailored dose, estimated from an initial test injection, is superior to a fixed dose rate, which often underopacifies or overopacifies the hypertrophied or dilated heart. Additionally, a customized dose avoids total body opacification (resulting from excessive circulating contrast solution), which can obscure anatomic detail, especially of the aortic and pulmonic valves (Tables 51-3 to 51-5).

References 1. Buchanan JW, Patterson DF: Selective angiography and angiocardiography in dogs with congenital cardiovascular disease. J Am Vet Rad Soc 6:21, 1964. 2. Buchanan JW: Selective angiography and angiocardiography in dogs with acquired cardiovascular disease. J Am Vet Rad Soc 6:5, 1965. 3. Bohn Fk, Rhodes WH: Angiograms and angiocardiograms in dogs and cats: some unusual filling defects. J Am Vet Rad Soc 11:21, 1970. 4. Kneller AK, Barrett RB, Lewis RE: Abdominal aortography in cats: comparison of carotid and femoral technics. J Am Vet Rad Soc 12:65, 1971. 5. Gomez JA, Lawson TL, et al: Selective abdominal angiography in the dog. J Am Vet Rad Soc 14:72, 1973. 6. Cantwell HD: Radiographic diagnosis. Vet Rad 27:121, 1986. 7. Lord PF, Tilley LP, et al: Radiography and angiocardiography of feline cardiomyopathy. J Am Vet Rad Soc 15:56, 1974. 8. Lord PF: Quantitative left ventricular cineangiocardiography in the dog: measurement and usefulness of left ventricular volume. J Am Vet Rad Soc 18:51, 1977. 9. Stickle RL, Anderson LK: Diagnosis of common congenital heart anomalies in the dog using survey and nonselective contrast radiography. Vet Rad 28:6, 1987. 10. Barthez PY, Seimens LM, Koblik PD: Azygous continuation of the caudal vena cava in a dog: radiographic and ultrasonographic diagnosis. Vet Radiol Ultrasound 37:354, 1996. 11. Del Palacio MJF, Bayon A, Agut A: Dilated coronary sinus in a dog with persistent left cranial vena cava. Vet Radiol Ultrasound 38:376, 1997. 12. Viamonte M: CO2 angiocardiography in dogs. J Am Vet Rad Soc 4:18, 1963. 13. Robertson SA, Fowler D: A complication of cardiac catheterization in the dog. Vet Rad 29:202, 1988. 14. Wise M: Non-selective angiocardiography in the normal dog and cat. Vet Rad 23:144, 1982.

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Cardiac Ultrasound (Echocardiography)

❚❚❚ NORMAL APPEARANCES AND MEASUREMENTS Dogs O’Grady and co-workers described the normal sonographic appearance of the canine heart, including normal measurements.1 Snyder and colleagues, however, determined that such “one size fits all” measurements may not be reliable in all breeds. Nonracing Greyhounds, for example, have been shown to have breed-specific values for left ventricular volume and wall thickness, fractional shortening, and systolic intervals.2 Thomas and co-workers proposed a set of specific terms to describe echocardiography and echocardiograms in dogs and cats.3 Loyer and Thomas described the technique of transesophageal echocardiography in the dog, including specific imaging planes and resultant sonographic anatomy.4 They assert that the described technology is capable of providing unique cardiac images that are often superior to those obtained by conventional sonographic means. Kienle and co-workers published similar data for the cat.5 Later, St.-Vincent and Pharr repeated the work of Loyer and Thomas, drawing similar conclusions.6 Using transesophageal echocardiography in an acutely dyspneic dog with renal amyloidosis, Venco and co-workers reported finding an enormous thrombus, which nearly occluded the main pulmonary artery.7 Little detailed information has been published on the subject of fetal sonology (canine or feline) and, in particular, whether it is a reliable means of detecting congenital heart disease. A fetal echocardiogram is shown in Figure 52-1.

Cats DeMadron and co-workers described the normal sonographic appearance of the feline heart, including normal measurements.8 Soderberg and colleagues

were among the first to describe the use of M-mode echocardiography in the diagnosis of feline cardiomyopathy.9 Schille and Skrodzki published the normal M-mode values for kittens (2 to 12 weeks old).10

❚❚❚ OVERALL APPROACH Based on personal experience, I recommend the following tactical considerations when using ultrasound in a dog or cat with suspected congenital (or acquired) heart disease: • Use an anatomic checklist. • Examine the entire heart, even after finding a probable cause of disease. • Check all valves for competency using continuousor pulsed-wave Doppler (the latter is more precise, but it is not capable of assessing abnormally high blood flows caused by valvular stenosis or regurgitation without aliasing (separation of Doppler waveforms into two parts, above and below the baseline). • Exercise caution when judging the following: heart wall or septal thickness, chamber dilation, contractility. • If the heart is abnormal, but it is not possible to make a precise diagnosis, consider continuing the examination at a later time. This provides time to review the sonographic data, read the relevant literature, and simply ponder the problem. I am often pleasantly surprised at how a good night’s sleep can provide new diagnostic insights. • Avoid prolonged examinations wherever possible. Given that the theoretical attention span of most people is between 15 and 20 minutes (less in a darkened room), two 30-minute examinations are likely to be more rewarding than a 1-hour session. • Do not forget the animal. Puppies are often impatient, a quality that needs to be acknowledged with briefer examination periods. Sick animals may have difficulty with temperature regulation and will 499

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rapidly lose body heat to a table surface that is not insulated. Some scan positions are uncomfortable for the animal and should not be maintained for longer than necessary. • Above all, do your utmost to avoid a preconceived diagnosis. Diagnostic bias of this type is capable of severely limiting one’s thinking. • Do not become overly reliant on published scanning techniques. Scan planes illustrated in almost all articles and textbooks on the subject are highly stylized and presume that the sagittal plane of the heart lies parallel to the surface of the examination table. This is often untrue, especially in animals that are sedated or under general anesthesia. In these instances, the heart rapidly shifts to the dependent side of the chest (toward the table surface) as a result of postural atelectasis, often rendering the recommended scan planes useless. • Another common problem is that enlarged, remodeled hearts often are not where they should be, frequently moving caudally or to the right or left sides of the thorax to accommodate their increased bulk. Anticipate such phenomena. Be flexible. Establish the location of one or two reliable anatomic landmarks, such as the left ventricle or aorta, and proceed accordingly.

❚❚❚ EVALUATING THE PLACEMENT OF INTRAVASCULAR EMBOLIZATION COILS An increasing number of puppies are being treated for persistent arterial duct (patent ductus arteriosus) with intravascular embolization coils. Intraprocedural assessment is largely done fluoroscopically, whereas postoperative and follow-up evaluations may be both radiographic and sonographic.11

Unneeded Jargon Thomas provided an excellent echocardiographic description of the normal canine heart along with anatomic correlations and scanning directions, one I strongly recommend reading.12 It appears, however, that he has fallen prey to the bane of specialists everywhere (myself included): the use of unnecessary and often confusing jargon. For example, the preceding reference is entitled TwoDimensional, Real-Time Echocardiography in the Dog. Although it is possible to perform three-dimensional reconstruction on a sonogram, conventional ultrasound machines are rarely equipped with this capability. Thus, it is unnecessary to use the expression two-dimensional when describing echocardiography because it is already understood that this is how the image will be displayed. Likewise, the term real time is superfluous because rapid monitor refresh rates featured in contemporary ultrasound machines provide the viewer with a realistic sense of viewing the heart as it is actually beating (even though this is not quite true), much like watching commercial television. My point is this: echocardiography is already challenging enough (especially for the novice) without adding unnecessary terms to an already complex lexicon.

Anatomic (Two-dimensional) Assessment of the Heart Assessing the interior of the heart sonographically is a straightforward endeavor that can be mastered with practice. The ultrasound scanner, referred to by some as a transducer or probe, is moved along the right and left craniolateral aspects of the sternum, at a point just behind the elbow, until the desired image is obtained.

Interpreting Intracardiac Blood Flow The movement of blood into, through, and out of the heart can be tracked with Doppler ultrasound. In addition, the speed with which the blood travels, and the nature of its flow, can be assessed.

❚❚❚ UNDERSTANDING AND INTERPRETING THE DOPPLER TRACING Determining the Direction of Intracardiac Blood Flow

Figure 52-1 • Four-chamber view of the heart of a near-term German Shepherd fetus shows individual atria and ventricles (emphasis zone).

Intracardiac blood flow moving toward the ultrasound scanner (the top of the ultrasound image) is represented on the Doppler tracing by multiple waves appearing above the baseline. Conversely, blood moving away from the scanner (toward the bottom of the ultrasound sector) is represented by multiple waves appearing below the baseline. Waveforms lying beneath the baseline also are termed negative, and those above baseline are referred to as positive.

CHAPTER 52 ❚❚❚ Cardiac Ultrasound (Echocardiography)

Determining the Speed and Duration of Intracardiac Blood Flow Intracardiac blood flow ebbs and wanes with the pulsation of the heart, hydraulic events that are depicted by the shape and size of the individual waves composing the Doppler tracing.

Determining the Character of Intracardiac Blood Flow Normal Doppler Waveforms. Transvalvular Doppler waveforms recorded in an adult Labrador Retriever illustrate the similarities and differences between normal heart valves. As a reminder, the mitral and tricuspid waveforms appear above the baseline, whereas the aortic and pulmonic traces appear below the baseline, reflecting the direction of blood flow in conjunction with the positions of the dog and scanner (Figure 52-2). The traces on the opposite side of the baselines are artifactual. Kirberger and co-workers published a graphic description of normal Doppler flow patterns in dogs, followed later by an article discussing the factors influencing the speed of blood movement, particularly that occurring within the right and left sides of the heart.13,14

Color Doppler Color Doppler, or color Doppler mapping as it is also known, is an excellent means of screening specific areas of the heart for disturbed blood flow. For example, the aortic or pulmonic outflows can be checked for abnormally high velocities, supporting valvular or subvalvular stenosis. The atria can be scrutinized for regurgitation in cases of endocardiosis. The dorsal part of the right ventricle can be examined for transseptal blood flow indicating a ventriculoseptal defect.

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assessments. For my part, I agree that M-mode has its place, albeit a limited one, in sonographic diagnosis. Adding M-mode to routine two-dimensional Doppler assessments undoubtedly will prolong examination time, however. Thus, the true value of M-mode will lie in its diagnostic contribution, whatever that may be, something that is probably best left up to the individual examiner to decide, depending on the individual case.

❚❚❚ ATHLETIC HYPERTROPHY Lonsdale and co-workers showed that regimented athletic conditioning in racing Greyhounds results in adaptive hypertrophy of the left ventricle, including the interventricular septum.16 Specific increases in ventricular wall thickness and chamber diameters observed in conditioned male and female Greyhounds (compared with nonconditioned Greyhounds) were as follows: • Female Greyhounds showed increased ventricular thickness during diastole. • Male dogs had increased left ventricular internal dimension during systole. • Male dogs had increased left ventricular wall thickness during systole. • Male dogs showed increased ventricular thickness during systole. The authors also noted that training Greyhounds have a larger fractional shortening than nontraining Greyhounds. I would like to note at this point that the cardiac remodeling described in the preceding, at least in my experience, is usually mild, often lying just beyond the upper limits of measured normal. Thus, when hypertrophy is detected, especially if the dog is not highly conditioned, it must not be summarily dismissed as athletic hypertrophy simply because the dog appears fit or regularly exercises.

❚❚❚ M-MODE ECHOCARDIOGRAPHY Academic cardiologists, and others, often use M-mode echocardiography for a variety of clinical and research purposes, including the determination of cardiac output, a value that was previously calculated using other means, such as thermodilution, dye dilution, the Fick method, and conventional or radionuclide angiography. Knowing cardiac output, in particular whether it is increased or decreased, is useful in assessing treatment effectiveness or prognosis in diseases such as cardiomyopathy.15 Novice sonographers often find M-mode an attractive option for two reasons. First, interior cardiac measurements can be compared with normal reference tables, which requires far less experience than a visual assessment of the heart. Second, advocates of sonographic measurement argue that it is more objective— and by inference, more scientific—than visual

❚❚❚ CONGENITAL MUSCULAR DYSTROPHY Berry and colleagues reported hypertrophic muscular dystrophy in a pair of 5-month-old kittens, a disease that is brought about by a complex congenital absence of the protein dystrophin. In addition to heart muscle change, there were also esophageal, pulmonary, diaphragmatic, hepatic, splenic, renal, and adrenal abnormalities. Specifically, thoracic radiographs showed progressive cardiomegaly, ventral diaphragmatic deformity, and megaesophagus with secondary aspiration pneumonia. Echocardiographically, the left ventricle was dilated, thickened, and abnormally echogenic. Abdominal films revealed enlargement of the liver, kidneys, and spleen; mineralization of the adrenal

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A

B

C

D

Figure 52-2 • Normal Doppler waveforms. A, Continuous-wave, left-sided, mitral outflow recorded from a normal adult Retriever. B, Pulsed-wave, left-sided, tricuspid outflow recorded from a normal adult Retriever. C, Continuous-wave, right-sided, pulmonic outflow Recorded from a normal adult Retriever. D, Pulsed-wave, right-sided, pulmonic outflow recorded from a normal adult Retriever. E, Continuous-wave, left-sided, aortic outflow recorded from a normal adult Retriever.

E glands; hypertrophy of the paralumbar musculature; and peritoneal fluid. Sonography confirmed the earlier radiographic observations and in addition showed increased echogenicity of the liver and renal cortex.17

References 1. O’Grady MR, Bonagura JD, et al: Quantitative cross-sectional echocardiography in the normal dog. Vet Rad 27:34, 1986. 2. Snyder PS, Sato T, Atkins CE: A comparison of echocardiographic indices of the non-racing healthy Greyhound to reference values from other breeds. Vet Radiol Ultrasound 36:387, 1995.

3. Thomas WP, Gaber GJ, et al: Recommendations for standards in transthoracic two-dimensional echocardiography in the dog and cat. Vet Radiol Ultrasound 35:173, 1994. 4. Loyer C, Thomas WP: Biplane transesophageal echocardiography in the dog: technique, anatomy and imaging planes. Vet Radiol Ultrasound 36:212, 1995. 5. Kienle RD, Thomas WP, Rishniw M: Biplane transesophageal echocardiography in the normal cat. Vet Radiol Ultrasound 38:288, 1997. 6. St.-Vincent RS, Pharr JW: Transesophageal ultrasonography of the normal canine mediastinum. Vet Radiol Ultrasound 39:197, 1998. 7. Venco L, Calzolari D, Morini S: Pulmonary thromboembolism in a dog with renal amyloidosis. Vet Radiol Ultrasound 39:564, 1998.

CHAPTER 52 ❚❚❚ Cardiac Ultrasound (Echocardiography)

8. DeMadron E, Bonagura JD, Herring DS: Two-dimensional echocardiography in the normal cat. Vet Rad 26:149, 1985. 9. Soderman SF, Boon JA, et al: M-mode echocardiography as a diagnostic aid for feline cardiomyopathy. Vet Rad 24:66, 1983. 10. Schille S, Skrodzki M: M-mode echocardiographic reference values in cats in the first three months of life. Vet Radiol Ultrasound 40:491, 1999. 11. Fellows CG, Lerche P: Traetment of patent ductus arteriosus by placement of 2 intravascular embolization coils in a puppy. J Small Anim Pract 39:196, 1998. 12. Thomas WP: Two-dimensional, real-time echocardiography in the dog. Vet Rad 25:50, 1984. 13. Kirberger RM, Bland-van den Berg P, Grimbeek RJ: Doppler echocardiography in the normal dog: part 1 velocity findings and flow patterns. Vet Radiol Ultrasound 33:370, 1992.

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14. Kirberger RM, Bland-van den Berg P, Grimbeek RJ: Doppler echocardiography in the normal dog: part II factors influencing blood flow velocities and a comparison between left and right heart blood flow. Vet Radiol Ultrasound 33:380, 1992. 15. Atkins CE, Curtis MB, et al: The use of M-mode echocardiography in determining cardiac output in dogs with normal, low, and high output states: comparison to thermodilution method. Vet Radiol Ultrasound 33:297, 1992. 16. Lonsdale RA, Labuc RH, Robertson ID: Echocardiographic parameters in training compared with nontraining greyhounds. Vet Radiol Ultrasound 39:325, 1998. 17. Berry CR, Gaschen FP, Ackerman N: Radiographic and ultrasonographic features of hypertrophic feline muscular dystrophy in two cats. Vet Radiol Ultrasound 33:357, 1992.

C h a p t e r

5 3

Congenital Heart Disease

❚❚❚ ANOMALOUS VESSELS Sammarco and co-workers reported a case of anomalous venous return in a 1-year-old dog, in which most of the blood from the abdomen and hindquarters was returned to the heart by an anomalous left azygos vein instead of the caudal vena cava. An abnormal blood vessel was identified in a lateral thoracic radiographic, which in a subsequent nonselective angiogram proved to be a left azygos. Additionally, the dog was found to have a vestigial caudal vena cava and a mild aortic stenosis.1

❚❚❚ DEFECTS AND SHUNTS Atrial Septal Defect Background. Atrial septal defects (ASDs) are classified into four types according to location.2 Compared with ventricular septal defects (VSDs), abnormal interatrial communications are uncommon, especially as solitary lesions. Persistence of the foramen ovale (patent foramen ovale) is not a true defect, although occasionally it behaves as one. The Latin designations septum primum and septum secundum are used to indicate the dorsal or ventral location of the defect. Because left atrial pressure exceeds that in the right atrium, interatrial shunting is from left to right.

or partition between the right and left ventricles. The uppermost portion, the so-called membranous septum, differs from the rest, being composed of a short, thin layer of connective tissue, Unfortunately, many VSDs are located in the latter region, which can be diagnostically ambiguous because of its poor, often inconsistent sonographic visibility (see caution segment on p. 505). In my experience, VSD is the most common congenital heart disease of cats and one of the most common in dogs. VSDs usually occur as solitary or “isolated” lesions; less frequently, they are identified in combination with another anomaly, such as patent ductus arteriosus (PDA) or as part of a specific group of defects, such as tetralogy of Fallot. Radiology. A classic VSD features (1) cardiomegaly with right-sided emphasis in both the lateral and dorsoventral (DV)/ventrodorsal (VD) views, (2) an enlarged main pulmonary artery, and (3) small or invisible peripheral lung vessels. The central pulmonary arteries are variably enlarged.

Ventricular Septal Defect (Incomplete Interventricular Septum, Defective Interventricular Septum)

Ultrasound. A large dorsally located VSD usually can be readily identified during an anatomic (twodimensional) assessment; medium-sized VSDs are sometimes seen, and small defects are rarely visible. Most such defects, irrespective of size or location, usually can be detected with Doppler by scanning along an imaginary line connecting the tricuspid and aortic valves (Figure 53-1). Sonographic characterization of VSDs, like most congenital anomalies, should focus on the location and size of the defect. With respect to size, I prefer to describe the length of the VSD (as seen in long section) in comparison to the width of the aorta at the level of the aortic valve. Although not a strong prognostic indicator, the relative size of the VSD compared with the aortic base is superior to simply describing the size of the defect.

Background. Most of the interventricular septum is made up of a thick muscular band that serves as a wall

Caution: In some normal animals, depending on the scanning plane, the upper part of the ventricular septum appears

Radiology and Ultrasound. Hamlin and co-workers described the characteristic radiographic appearance of ASD as featuring (1) cardiomegaly with right-sided emphasis, (2) a small aortic root, and (3) variable pulmonary hyperemia.3 Sonographically, the left atrium is typically dilated as a result of left-to-right shunting. The key diagnostic feature is, of course, the identification of an ASD using Doppler.

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505

defective, simulating a large VSD. This is an illusion, often termed dropout. Rescanning such areas from different angles and confirming the suspected lesion with Doppler can avoid misdiagnosis.

Persistent Arterial Duct (Patent Ductus Arteriosus) Background. Normally, blood flow through a persistent arterial duct is from left to right, reflecting the nearly fivefold difference between left and right interventricular blood pressures; however, with sustained high-volume left-to-right shunting, pulmonary vascular resistance may equal or exceed that of the systemic circulation, causing unsaturated blood to flow from the pulmonary artery to the aorta, often leading to cyanosis in the caudal half of the dog.

A

Imaging Findings

B

C Figure 53-1 • A, Cardiac sonogram (right-sided long section) in a cat with a ventral septal defect (VSD) shows a large proximal septal defect. B, Gray-scale Doppler mapping shows blood flow within the VSD. Color (not shown) indicated left-to-right direction. C, Continuous-wave Doppler shows tall narrow waveforms representing individual systolic pulses of blood passing through the VSD.

Radiology. Usually, PDAs show generalized cardiomegaly when viewed laterally. The enlarged aortic base typically extends obliquely into the precardiac portion of the mediastinum, widening the heart base and causing the heart margins to appear parallel (Figure 53-2, A). In the opposite imaging plane, the heart often appears long and lumpy as a result of atrial, aortic, and pulmonary arterial enlargements (Figure 53-2, B). The supposed classic, oft-illustrated DV or VD film featuring three consecutive bulges along the upper right heart margin—the enlarged aorta, pulmonary artery, and left atrial appendage—are rarely present at the same time. If such findings are to be found, however, it is most likely to be with a penetrated view. This is an image made with a 20% increase in kilovoltage peak (kVp) for the purpose of revealing the margins of the aorta and main pulmonary artery, which normally are lost in the interior of the cardiac silhouette (Figure 53-2, C). The size and shape of a surgically corrected PDA differ little from their preoperative appearance, unlike the pulmonary vasculature, which quickly resumes a normal or nearly normal appearance (Figure 53-2, D). Occasionally a surgically occluded PDA recannulates. If it is not reclosed, the reopened duct can cause pulmonary hypertension secondary to increased vascular resistance, leading to reversed, right-to-left blood flow (Eisenmenger reaction) and eventual heart failure. Radiographically, a right-to-left shunting ductus (reversed PDA) is supported by an increased number of enlarged, irregular pulmonary arteries, the result of chronic pulmonary hyperemia (Figure 53-3). In such cases, right ventriculography reveals enlarged, tortuous pulmonary arteries and concurrent movement of contrast solution into the aorta.

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A

C

D B Figure 53-2 • A, Close-up lateral view of a dog with a persistent arterial duct shows moderate generalized cardiomegaly, a widened heart base, left atrial enlargement, parallel heart margins, and pulmonary hyperemia. B, A dorsoventral close-up made at standard technique shows an elongated heart but no interior arterial detail. C, A penetrated view made with a 20% increase in kilovoltage peak (kVp) clearly reveals enlargement of both the proximal aorta and main pulmonary artery, characteristics of a patent ductus arteriosus (PDA). D, One month after surgery, the lung vessels are substantially smaller; however, the heart appears unchanged.

Ultrasound. Left atrial and ventricular dilation are typically present in a measure consistent with the size and duration of the shunt. Conclusively proving the presence of an open duct is often difficult; however, a characteristic Doppler profile demonstrating continuously disturbed, high-velocity blood flow in the main pulmonary artery provides a strong circumstantial case. Doppler evaluation is best done from the right side, using a cross-section view of the right ventricular outflow tract at the level of the aorta. Right ventricular hypertrophy is often present when ductal flow becomes reversed. Goodwin and Holland described the use of contrast echocardiography

(described later) in the diagnosis of persistent arterial duct, a technique that also can be used to confirm right-to-left shunting resulting from a hypertensive PDA.4 Technique of Contrast Echocardiography. Evaluating for right-to-left intracardiac shunt (VSD, ASD) involves the following steps: 1. The sonographer continuously scans the right atrium and ventricle (in long section). 2. An assistant rapidly injects 3 to 4 mLof agitated (vigorously shaken) isotonic saline via a cephalic catheter.

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A

C

B

Figure 53-3 • A, Close-up lateral view of the heart made 1 year after surgical closure of a patent ductus arteriosus (PDA) shows enlarged undulant cranial lobe blood vessels suggesting pulmonary hypertension. B, Ventrodorsal close-up shows enlargement of the aorta and main pulmonary artery in the context of generalized heart enlargement. Recanalization of the ductus with a subsequent reversal of blood flow (right-to-left) was responsible. C, Following a second surgical closure, the ductus remained shut, eventually leading to a more normal pulmonary circulation a reduction in heart size, as seen in this ventrodorsal view.

3. The sonographer looks for characteristic appearance of microbubbles in the right atrium and ventricle. Also check left atrium, left ventricle, and proximal aorta to ensure that there are no microbubbles in these locations. Evaluating for right-to-left extracardiac shunt (PDA) involves the following steps: 1. The sonographer continuously scans the abdominal aorta (in long section). 2. An assistant rapidly injects 3 to 4 mL of agitated (vigorously shaken) isotonic saline via a cephalic catheter. 3. The sonographer looks for the characteristic appearance of microbubbles in abdominal aorta.

For a thorough review on the subject of ultrasound contrast media, see the article by Schmid and Lang.5

Aortic-Pulmonary Arterial Communication through Common Wall Defect (Aorticopulmonary Window) Functionally, a persistent arterial duct and aorticopulmonary window are the same, both leading to pulmonary overcirculation, systemic oligemia, and eventually congestive heart failure. From a surgical standpoint, however, the aorticopulmonary window is far more difficult to close than an arterial duct. The

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radiographic and sonographic findings are similar to those described for PDA.

Pulmonic Stenosis Background. In this relatively common form of congenital heart disease, deformity of the pulmonic valve (valvular dysplasia) and the resultant circulatory deficiency are responsible for the animal’s illness. Only rarely does obstruction occur away from the valve, in which case it is referred to as subvalvular or supravalvular stenosis, according to its anatomic relationship to the pulmonic valve.6 Pulmonary stenosis can lead indirectly to cyanosis when accompanied by a VSD.7 Reversal of transseptal, left-to-right blood flow occurs when the right ventricular pressure exceeds that of the left, a consequence of restricted pulmonary outflow. Combined congenital heart defects capable of producing cyanosis include the following: • Eisenmenger complex • Eisenmenger syndrome (VSD with reversed rightto-left shunting) • Patent arterial duct with reversed right-to-left shunting • Pulmonic stenosis, ASD, with right-to-left shunting • Pulmonic stenosis, patent foramen ovale, with rightto-left shunting • Pulmonic stenosis, VSD, with right-to-left shunting

cardiac defect in large breeds. The disease can be inherited in Newfoundlands; German Shepherds, Boxers, Golden Retrievers, and Rottweilers are predisposed to this anomaly. Subaortic stenosis is far and away the most common variant, with valvular and supravalvular stenosis being rare. Structurally, subaortic stenosis is often characterized by a discrete fibrous tissue band located in the distal part of the left ventricular outflow tract, immediately ventral to the aortic valve. The resulting back pressure (pressure overload) leads to varying degrees of left ventricular hypertrophy, coronary artery injury, and myocardial ischemia. Prognosis depends on the degree of outflow obstruction, with a transvalvular gradient of 80 or more characterizing serious disease (a high-risk patient). Predicted life expectancy is approximately 11/2 to 2 years; dogs with this disease may die suddenly. Cats with aortic stenosis have an even worse prognosis than dogs, with most dying within a year of their first signs of illness.8 Surgical repair potentially can prolong the life of dogs with aortic stenosis, but it is not curative. Surgical injuries to the septal cusp of the mitral valve and the aortic valve constitute the most serious operative risks.9 Another form of congenital aortic stenosis is aortic coarctation (cinching tight), a thickening of the muscular layer of the aorta beyond the aortic valve, causing a reduction in luminal diameter, and, as a consequence, localized aortic dilation and left ventricular enlargement.10 Imaging Findings

Imaging Findings Radiology. Aclassic pulmonic stenosis features (1) cardiomegaly with right-sided emphasis, (2) an enlarged main pulmonary artery, (3) large or normal-sized central pulmonary arteries, and (4) small central and peripheral pulmonary arteries (Figure 53-4, A and B). These abnormal findings generally become more pronounced as the disease worsens. Cardiac Catheterization. Catheterization of the right ventricle in a dog with pulmonic stenosis typically reveals (1) narrowing of the pulmonic valve, (2) dilation of the main pulmonary artery, and (3) right ventricular hypertrophy (Figure 53-5, C and D). Ultrasound. Sonographically, pulmonic stenosis is characterized by (1) a thickened right ventricle, (2) abnormally high pulmonic blood flow, and (3) an increased transvalvular pressure gradient (Figure 536). Doppler evaluation is best done from the right side using a cross-section view of the right ventricular outflow tract at the level of the aorta.

Aortic Stenosis Background. Aortic stenosis is the third most common congenital heart disease in dogs and the most common

Radiology. Extension of the dilated aortic root into the precardiac portion of the cranial mediastinum in a dog with aortic stenosis causes the heart to appear elongated in the ventrodorsal projection, similar to a PDA. Unlike a ductus, the lung is not overcirculated because there is no left-to-right shunting. The bottom half of the left ventricle may or may not bulge, depending on the degree of stenosis. In the lateral view, the heart often appears abnormally tall and forwardly inclined, in large part because of superimposition of the bulging aorta. The overall impression is that of cardiomegaly with left-sided emphasis. These features are illustrated in Figure 537, A and B. Cardiac Catheterization. Catheterization of the left ventricle in a dog with aortic stenosis typically reveals (1) narrowing of the left ventricular outflow tract just below the valve or a band-like filling defect in the same location, (2) dilation of the proximal aorta, and (3) left ventricular hypertrophy (Figure 53-7, C and D). Ultrasound. Sonographically, aortic stenosis is characterized by (1) a thickened left ventricle, (2) abnormally high aortic blood flow, and (3) an increased transvalvular pressure gradient (Figures 53-8 and 539). Doppler evaluation is best done from the left side using a four-chamber view.

A

B

C

D Figure 53-4 • A, Close-up lateral view of the heart in a dog with a pulmonic stenosis shows cardiomegaly with right-sided emphasis, an enlarged main pulmonary artery, and small peripheral lung vessels. B, Ventrodorsal close-up shows right-sided cardiomegaly, enlarged pulmonic trunk, and right and left pulmonary arteries. Close-up lateral angiogram following right ventricular injection, without (C) and with (D) lesion enhancement, shows narrowing of the right ventricular outflow tract at the level of the pulmonic valve consistent with pulmonic stenosis.

Figure 53-5 • Lateral close-up view of the heart of a dog with pulmonic stenosis shows mild to moderate cardiomegaly with right-sided emphasis, small central lung vessels, and no visible main pulmonary artery.

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A

B

C Figure 53-6 • Right-sided cardiac sonogram (A) (long section) of a dog with pulmonary stenosis shows a severely hypertrophied right ventricle. Right-sided, cross-sectional sonogram (B) of a dog with pulmonic stenosis shows a hyperechoic, thickened, and deformed pulmonic valve (emphasis zone, above small diamond). Pulsed-wave Doppler spectrum (C) revealed high-velocity outflow characteristic of stenosis and a moderate transvalvular pressure gradient.

CHAPTER 53 ❚❚❚ Congenital Heart Disease

511

A B

C

D Figure 53-7 • A, Close-up lateral view of the heart in a dog with subaortic stenosis shows an abnormally tall, forwardly inclined heart. An enlarged aortic root causes the increased density in the precardiac portion of the mediastinum. B, Ventrodorsal close-up of the heart shows an elongated heart with a bulging proximal aorta and left ventricle. A left ventricular angiocardiogram (C) and close-up (D) show a band-like subaortic filling defect and a dilated proximal aorta, the result of subaortic stenosis.

Mitral and Tricuspid Stenosis In my experience, mitral and tricuspid stenoses are rare compared with most other congenital heart diseases. Of the few I have seen in living animals (all cats), a perforated left atrioventricular membrane is the most common. In this anomaly, the mitral valve consists of a single, centrally perforated membrane rather than individual cusps, which may or may not be attached to the papillary muscles by one or more rudimentary cords. The appearance can be deceptive sonographically because the membrane usually is quite mobile, in many ways resembling a normal atrioventricular (AV) valve. Radiographically, the cats I have seen with perforated AV membranes have had enlarged left atria, causing the heart to resemble thyroid-induced myopa-

thy, but unlike cats with thyroid-induced myopathy (TIM), these animals are usually young and have different murmurs.

Tetralogy of Fallot Background. Tetralogy of Fallot (pulmonic stenosis, secondary right ventricular hypertrophy, large VSD, and abnormal aortic positioning) typically is associated with cyanosis, fatigue, and a lack of endurance, secondary to a right-to-left shunt. Radiology. Atetralogy of Fallot can be difficult to diagnose; often it is confused with pulmonic stenosis, which it resembles radiographically. If a VSD is also detected,

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Figure 53-9 • Continuous Doppler tracing made in a healthyappearing 6-month-old German Shepherd puppy with a faint murmur, but normal chest films revealed mild subaortic stenosis.

Ultrasound. The sonographic features of a tetralogy are (1) right ventricular hypertrophy, (2) abnormally high pulmonary blood flow, with an increased transvalvular pressure gradient, (3) a VSD, typically featuring right-to-left shunting and (4) an abnormally positioned aorta.

A

Congenital Mitral and Tricuspid Insufficiency

B Figure 53-8 • A, Close-up, left-sided, four-chamber cardiac sonogram in a dog with subaortic stenosis shows a thickened left ventricle. B, Continuous-wave Doppler tracing through the aortic outflow and valve indicates abnormally high blood flow.

there is an excellent chance that the dog has a tetralogy because a tetralogy is more common than a simple combined anomaly. Ettinger and Suter described the typical radiographic appearance of a dog with a tetralogy as having cardiomegaly with right-sided emphasis, enlargement of the ascending aorta, and pulmonary oligemia.11 In some of the cases I have seen, the aorta has been small, difficult to identify without the aid of a penetrated view, and occasionally positioned on the right side of the cardiac silhouette as seen in a DV or VD view.

Various types of valvular malformations cause congenital mitral or tricuspid insufficiency, for example, two instead of three valve cusps, fusion of two or more valve cusps, and replacement of individual valve cusps by a single immobile membrane with a small hole in its center (Figure 53-10). In many dogs and cats with congenital mitral or tricuspid deformity, the resultant regurgitation is so small that even though there is an audible murmur, there is little or no cardiac remodeling and thus no radiographic evidence of disease (Figure 53-11).

Ebstein Anomaly Extension of an abnormally long tricuspid valve down into the right ventricle (Ebstein anomaly)—functionally increasing the volume of the right atrium and proportionately decreasing the volume of the right ventricle—is one of the most severe forms of tricuspid dysplasia (Figure 53-12). Not only does this anomaly affect relative chamber volumes on the right side of the heart, but it also causes abnormal forward and reversed blood flows.

Congenital Aortic and Pulmonic Insufficiency Primary congenital aortic or pulmonic insufficiency is rare in dogs and cats (Figure 53-13). Secondary aortic

CHAPTER 53 ❚❚❚ Congenital Heart Disease

513

Figure 53-10 • Sonographic long-section of the dilated left atrium and ventricle of a cat with a congenital mitral membrane instead of a normal left atrioventricular valve (emphasis zone).

B

A

Figure 53-11 • Thorax of a 2-year-old Old English Sheepdog with congenital tricuspid insufficiency shows mild-to-moderate right-sided heart enlargement in the lateral projection (A) but a normal-appearing heart in the ventrodorsal view (B).

insufficiency can result from endocarditis, and pulmonary insufficiency may be identified with pulmonic stenosis.

❚❚❚ ARTERIAL MALFORMATIONS Common Arterial Trunk (Truncus arteriosis) Rarely, a single valved artery is the only exit from the heart. This common arterial trunk—lying above a

sizable VSD—must provide the systemic, pulmonary, and coronary circulations. Although this vascular anomaly can assume a variety of forms, the most common is likely a solitary trunk featuring either a single or paired branching pulmonary arteries. To date, all my experience with this rare disease has been with cyanotic newborn calves and a single llama, none of which have survived beyond a few days. Radiographically, these hearts appeared large and the lungs hyperemic. Sonographically, a VSD and only one exit valve were noted.

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SECTION VI ❚❚❚ The Heart

A

C

B

D Figure 53-12 • A, Lateral view of the thorax of a dog with Ebstein anomaly shows cardiomegaly with right-sided emphasis and a small volume of pleural fluid, accentuated by expiratory filming. B, Underexposed ventrodorsal view, which was not repeated because of patient distress, reveals similar findings. C, Right-sided cardiac sonogram (long section) in a dog with pulmonic stenosis shows a severely hypertrophied right ventricle and elongated tricuspid valve leaflets extending deeply into the right ventricle. D, Doppler tracing of transvalvular tricuspid blood flow shows protracted, poorly defined forward flow and regurgitation.

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515

A

C

B

Figure 53-13 • A, Close-up lateral view of the heart of a dog with congenital aortic insufficiency resembles mitral insufficiency, which is commonly seen in older dogs. B, Ventrodorsal view shows bulging of the left ventricle. C, An inadvertently oblique dorsoventral projection falsely suggests right-sided enlargement.

Transposition of the Aorta and Pulmonary Arteries (Complete Transposition of the Great Arteries) In this rare condition, the aorta and pulmonary artery occupy the positions normally assumed by each other. The aorta originates from the right ventricle, and the pulmonary artery arises from the left ventricle. Under such conditions, systemic oxygenation is provided by a patent foramen ovale, VSD, or PDA. Resulting cyanosis is usually severe. Diagnosis is based on sonographic recognition of the characteristic bifurcation of the pulmonary artery exiting the left ventricle.

Isolated Nonvalvular Aortic Stenosis (Aortic Coarctation) In this context, coarctation refers to a severe stenosis, a malformation of the proximal aorta. More commonly

encountered as a component of a tetralogy or other complex congenital heart disease, aortic coarctation is rarely encountered alone. Herrtage and co-workers reported such a case in a middle-aged Great Dane with a swelling on the side of its thorax, eventually diagnosed as a chondrosarcoma. Incidentally, what was at first believed to be a large middle mediastinal mass was discovered. Later, aortography determined that the “mass” was in reality an aortic aneurysm located immediately distal to the stenosis.12

Partitioned Atrium Partitioning either atrium into two communicating chambers, anatomic abnormalities also known by their rather cumbersome Latin names, cor triatrium sinister, when referring to the left atrium and cor triatrium

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Table 53-1 • GENERALITIES RELATED TO COMMON CONGENITAL HEART DISEASE Defect

Type

Effect

Breed Incidence

Clinical Signs

Aortic stenosis

Subvalvular lesion

Left ventricular outflow obstruction

Exercise intolerance, fainting

Pulmonic stenosis

Valvular lesion

Right ventricular outflow obstruction

Newfoundland, Golden Retriever, Rottweiler, Boxer, German Shepherd Beagle, Chihuahua, English Bulldog, Keeshond, Samoyed, Mastiff, Boxer

Tricuspid dysplasia

Valvular lesion

Right ventricular backflow due to valvular incompetency

Labrador Retriever

Exercise intolerance

Ebstein malformation Mitral dysplasia

Valvular lesion Valvular lesion

Left ventricular backflow due to valvular incompetency

Exercise intolerance

Persistent arterial duct (patent ductus arteriosus)

Vascular lesion

Abnormal left (systemic) to right (pulmonary) extracardiac blood flow or shunting

Very common in cats, Great Dane, German Shepherd, Bull Terrier, Golden Retriever, Newfoundland Poodle, Pomeranian, Springer, Bichon Frise, Yorkshire Terrier, Maltese, Shetland Sheepdog

Ventricular septal defect Eisenmenger syndrome Tetralogy of Fallot

Septal lesion

Many dogs are asymptomatic Exercise intolerance, fainting

Cough, shortness of breath

Primary septal lesion Primary valvular and septal lesions with secondary right ventricular disease

dexter when referring to the right atrium, restricts blood flow and produces clinical signs similar to those of mitral stenosis. This unusual form of congenital heart disease is rare in dogs and exceptionally rare in cats13 (Table 53-1).

References 1. Sammarco CD, Regan J, et al: Caudal venous return through a left azygos vein in a dog. Vet Radiol Ultrasound 36:517, 1995. 2. Monnet E, Orton EC, et al: Diagnosis and surgical repair of partial atrioventricular septal defects in two dogs. J Am Vet Med Assoc 211:569, 1997. 3. Hamlin RL: Ostium secundum interatrial septal defects in the dog. J Am Vet Med Assoc 143:149, 1963. 4. Goodwin J-K, Holland M: Contrast echocardiography as an aid in the diagnosis of right-to-left shunting patent ductus arteriosus. Vet Radiol Ultrasound 36:157, 1995.

5. Schmid V, Lang J: Intravascular ultrasound contrast media. Vet Radiol Ultrasound 36:307, 1995. 6. Anderson M, Mann FA, Aronson E: What is your diagnosis? J Am Vet Med Assoc 200:2013, 1992. 7. Lombard CW, Ackerman N, et al: Pulmonic stenosis and right-to-left atrial shunt in three dogs. J Am Vet Med Assoc 194:71, 1989. 8. Stepien RL, Bonagura JD: Aortic stenosis: clinical findings in six cats: J Small Anim Pract 32:341, 1991. 9. Monnet E, Orton EC, et al: Open resection for subvalvular aortic stenosis in dogs. J Am Vet Med Assoc 209:1255, 1996. 10. Berry CR: Answers for film reading session: 1995 A.C.V.R. annual meeting. Vet Radiol Ultrasound 36:449, 1995. 11. Ettinger SJ, Suter PF: Congenital heart disease. In Canine cardiology. Philadelphia, 1970, WB Saunders. 12. Herrtage ME, Gorman NT, Jefferies AR: Coarctation of the aorta in a dog. Vet Radiol Ultrasound 33:25, 1992. 13. Koie H, Sato T, et al: Cor triatrium sinister in a cat. J Small Anim Pract 41:128, 2000.

C h a p t e r

5 4

Acquired Heart Disease

❚❚❚ BENEFITS OF PRESURGICAL THORACIC SCREENING Although there is no consensus as to what precisely constitutes an “old” dog, the practice of presurgical screening of such animals is practiced in some North American veterinary teaching hospitals. Proponents of presurgical screening claim that it may reveal otherwise undetectable abnormalities, such as heart or lung disease. What is the likelihood, however, of finding occult thoracic disease under such circumstances? To my knowledge, only one publication exists that addresses this question; the results of that study are presented in Table 54-1.1

❚❚❚ ENDOCARDIOSIS OF THE MITRAL AND TRICUSPID VALVES (ATRIOVENTRICULAR INSUFFICIENCY, ATRIOVENTRICULAR REGURGITATION, CHRONIC VALVE DISEASE) Mitral Endocardiosis (Mitral Insufficiency, Mitral Regurgitation) Background. Mitral endocardiosis is the most common form of acquired heart disease in dogs. It gradually thickens and deforms the atrioventricular (AV) valves of older dogs, particularly the mitral valve, so that eventually the valves no longer function properly. The result is that during systole, although the AV valves are closed, their imperfect fit allows blood to flow back into the atrium. If severe and prolonged enough, such regurgitant flow will raise blood pressure in the lung to a dangerous level, potentially leading to heart failure. Additional names for endocardiosis of the mitral and tricuspid valves are mitral or tricuspid insufficiency

and mitral or tricuspid regurgitation, with the former referring to the inability of the mitral valve to prevent the backflow of blood into the left atrium during systole and the latter making reference to the actual backflow of blood (the source of the characteristic mitral murmur). In advanced cases, the left atrium may become so severely dilated that the endocardium splits, and the resultant hemorrhage causes hemopericardium. Imaging Findings Radiology. Mitral insufficiency results in gradual leftsided heart enlargement, beginning with widening of the heart base, progressing to left atrial doming, and culminating in cardiomegaly with left-sided emphasis, dorsal displacement of the trachea and caudal vena cava, and pulmonary hyperemia (Figures 54-1 to 543). Heart failure is signaled by pulmonary edema (Figure 54-4). Ultrasound. The sonology of mitral and tricuspid insufficiency secondary to endocardiosis is straightforward. Characteristic features include (1) atrial and ventricular dilation (left- or right-sided, depending on whether one or both AV valves are affected); (2) mitral or tricuspid thickening, deformity, and increased echogenicity; (3) asynchronous leaflet motion; (4) atrial inversion; and (5) varying degrees of atrial regurgitation. In my experience, the degree of mitral or tricuspid deformity does not always correlate with the amount of regurgitation. Lombard and Spencer reported good correlation between the radiographic and sonographic findings in advanced mitral endocardiosis.2 I agree with the authors’ conclusions regarding the radiographic predictability of mitral insufficiency; however, I have not found radiographs to be a reliable predictor of combined or predominantly right atrial disease (Figure 54-5). Concerning mitral insufficiency and its principal sign of left atrial doming, Buchanan and Kelly, in a published report on atrial splitting causing hemopericardium in 517

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SECTION VI ❚❚❚ The Heart

Table 54-1 • PROBABILITY OF DETECTING OCCULT THORACIC DISEASE IN DOGS OLDER THAN SEVEN YEARS OF AGE USING PRESURGICAL RADIOGRAPHIC SCREENING Radiographic Observation

Probability

Heart enlargement with normal lung vascular Heart and pulmonary vascular enlargement. Note: In no instance was heart failure missed on presurgical physical examination Major noncardiovascular abnormality such as primary lung tumor, pulmonary metastases, or diaphragmatic hernia

1 in 5 1 in 100 1 in 500

a dog, described other sources of left atrial enlargement and the means by which they might be differentiated radiographically.3 I have used these signs and found them to be helpful, especially when ultrasound is unavailable, as when reading referral films. Tricuspid insufficiency due to endocardiosis is much less common than mitral insufficiency, but it can occur alone or in combination with mitral disease. The contribution made by the tricuspid valve in combined AV valvular endocardiosis usually must be determined sonographically (because films are of little value for this purpose). Distinguishing Between Left Atrial Hemorrhage, Benign Pericardial Effusion, and Heart Base Tumor. At least half of the heart-base tumors I have seen to date featured a distinctive right-sided bowing of the trachea over the center of the heart as seen in either dorsoventral (DV) or ventrodorsal (VD) projection (Table 54-2 and Figure 54-6). Based on the identification of a regurgitant murmur, the prevalence of endocardiosis is estimated to be 5% in middle-aged dogs (defined by authors as 5 to 7 years old) and 35% in older dogs (defined by authors as 12 years or older). Not so surprisingly, however, when based on necropsy findings, these percentages increase.4 Some breeds, such as King Charles Spaniels, appear to develop endocardiosis at a much younger age than others, with prevalences of 9% in dogs less than a year of age, 56% in dogs 4 years and older, and 100% in dogs of 10 years or older (Figure 54-7).5 Pederson and colleagues graphically defined varying degrees of mitral prolapse in the breed.6 The presence of concurrent thyrotoxicosis has been shown to aggravate mitral insufficiency secondary to endocardiosis, increasing the potential of heart failure.7

❚❚❚ DILATED CARDIOMYOPATHY Background Dilated cardiomyopathy occurs regularly in dogs but rarely in cats. It typically affects the left ventricle, eventually leading to left-sided heart failure. Occasionally, the disease is confined to the right ventricle, causing

A

B Figure 54-1 • A, Close-up lateral view of the heart of a dog with endocardiosis shows cardiomegaly with left-sided emphasis. B, A second lateral close-up made 3 months later shows progressive enlargement.

right-sided failure. In the latter instance, there also may be a related chylothorax.8 Certain breeds of dogs are more likely to develop cardiomyopathy than others, for example, Irish Wolfhounds. In one study of Wolfhounds, cardiac abnormalities were found in about 42% of the 500 dogs examined, with approximately one quarter of these showing dilated myopathy accompanied by atrial fibrillation. Surprisingly, 27 of the dogs with abnormal ultrasounds were judged clinically normal. Following diagnosis, 39 dogs were dead within about 5 months (5.1 months’ median survival); 59 remained alive (15.7 months’ median survival ).9 Text continued on p. 523

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519

A B

D

C Figure 54-2 • A and B, Lateral and ventrodorsal views of a dog in heart failure resulting from severe mitral insufficiency show multidimensional heart enlargement, capped by a large, offset left atrial dome. A pair of close-up views show the characteristic vascular enlargement that is typically seen with this disease: surrounding the left atrium (C) and immediately cranial to the heart (D).

Table 54-2 • DISTINGUISHING BETWEEN LEFT ATRIAL HEMORRHAGE, BENIGN PERICARDIAL EFFUSION, AND HEART BASE TUMOR Heart Disease

Usual Presenting Signs

Heart Sounds

RDIs

Comments

Left atrial hemorrhage

Dyspnea, cough, abnormal lung sounds, cyanosis

Medium-intensity mitral murmur Diastolic gallop

Benign pericardial hemorrhage

Venous congestion, hepatomegaly, ascites

Muffled

Large hemispheric left atrium located over caudal aspect of spherically enlarged heart Large spherical heart, without visible mass

Heart-base tumor

Venous congestion and edema, especially of head and neck Ascites and liver enlargement

Muffled

Reported in old male dogs, none of which were brachycephalic All died within 2 days of diagnosis, likely due to rapid pericardial fluid buildup Adults of any age or breed, typically featuring gradual fluid accumulation Most common in Boxers and other middle-aged to older brachycephalic breeds

Large spherical heart, sometimes with visible mass overlying cranial aspect of heart base

Modified from Buchanan JW, Kelly AM: Endocardial splitting of the left atrium in the dog with hemorrhage and hemopericardium. J Am Vet Rad Soc 5:28, 1964. RDI, Radiographic disease indicators.

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SECTION VI ❚❚❚ The Heart

A

B

C Figure 54-3 • Congestive heart failure in a dog caused by severe endocardiosis. Lateral (A) and lateral close-up (B) images show an abnormally tall heart with severe left atrial doming, pulmonary hyperemia, and edema. Note how in the close-up view axial edema (fluid within the bronchovascular connective tissue sheaths) falsely makes the bronchial cross-sections appear thickened. Left-sided sonograms of the mitral valve (C) recorded during diastole (left) and systole (right) show extreme valvular deformity, and atrial inversion during systole.

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521

A

B

C

D Figure 54-4 • A, Close-up lateral view of a dog in heart failure secondary to mitral endocardiosis shows cardiomegaly with left-sided emphasis, a broad-based atrial dome, tracheal lift, and lung vessels that extend abnormally far into the lung periphery but are not enlarged centrally. B, A left-sided, four-chamber sonogram shows severe left ventricular and atrial dilation, and a moderately deformed mitral valve. C, Continuous-wave Doppler tracing shows high-velocity mitral regurgitation. D, Seventy-two hours after treatment, the heart remains enlarged although slightly smaller. Elimination of lung of edema combined with improved inflation have sharpened the borders of the heart considerably, making it seem smaller compared with pretreatment films.

522

SECTION VI ❚❚❚ The Heart

A

B C Figure 54-5 • A, Left-sided, four-chamber view of a dog in heart failure as a result of mitral and tricuspid endocardiosis shows severe dilation of all heart chambers, resembling dilated myopathy. B, The tricuspid valve failed to close completely during systole, allowing extensive right atrial backflow. The mitral valve was also incompetent but not to the same extent (C).

CHAPTER 54 ❚❚❚ Acquired Heart Disease

Another high-risk breed is the Doberman, not only for cardiomyopathy but also from sudden death caused by undiscovered disease. Remote heart monitoring (Holter Performer Manufacturer) has shown that dogs that had periods of sustained ventricular tachycardia lasting longer than 30 seconds were especially vulnerable.10

523

With regard to evaluating Dobermans (or other breeds with a high incidence of cardiomyopathy) for subclinical heart disease, it may become feasible to assess pulmonary venous and transmitral blood flow (using pulsed Doppler ultrasound) with the aim of detecting characteristic disease patterns. To this end, Schober and co-workers have been developing the technique of measuring venous flow patterns in normal dogs for comparison with different heart diseases.11

Imaging Findings Radiology Generalized Myopathy. In the advanced stages of disease, most myopathic hearts feature fairly typical radiographic disease indicators (RDIs): cardiomegaly with left-sided emphasis, pulmonary hyperemia, and, in the case of failure, pulmonary edema (Figure 54-8). Early disease, on the other hand, is more difficult to detect (Figure 54-9), almost always requiring sonographic confirmation. Sonographically, the myopathic heart gradually dilates, with a concurrent loss of contraction (Figure 54-10). In the later stages of the disease, the AV valves become distorted and leak, leading to atrial regurgitation (Figure 54-11).

Figure 54-6 • Ventrodorsal view of a Boston Bull Terrier with a heart base tumor shows characteristic right lateral bowing of the trachea over the central part of the heart.

Figure 54-7 • Left-sided, fourchamber sonogram (left) of a 3year-old King Charles Spaniel with mitral endocardiosis shows moderate left atrial regurgitation, indicated by wide and deep negative waveforms (right) recorded during continuous-wave Doppler assessment.

Isolated Right Ventricular Myopathy. Radiographically, isolated right ventricular myopathy (dilated) shows cardiomegaly with right-sided emphasis. Sonographically, isolated right ventricular cardiomyopathy (dilated) is characterized by an enlarged right atrium and ventricle, bowing of the interventricular septum to the left, and a normal left ventricle. Over the course of the disease, cardiac contraction gradually lessens until it eventually leads to failure.

524

SECTION VI ❚❚❚ The Heart

A Figure 54-9 • Lateral thoracic radiograph of a dog with early cardiomyopathy shows a taller than normal heart with an abnormally widened base. Initially, the case was misdiagnosed as endocardiosis.

reduced capacity, and abnormal filling (diastolic dysfunction) attributable to decreased distensibility and a resultant increase in filling pressure. If severe, hypertrophic cardiomyopathy results in heart failure as evidenced radiographically by pulmonary edema in dogs and pleural fluid in cats. Although hypertrophic cardiomyopathy is the most common heart disease of cats, it is rare in dogs.13 Hypertrophic cardiomyopathy can lead to the formation of thrombi, which may form in the heart or peripheral arteries, especially the distal aorta. Less often, these thrombi lodge in the right brachial, renal, and mesenteric arteries.14

Imaging Findings B Figure 54-8 • A, Lateral view of a Doberman Pinscher with dilated cardiomyopathy shows a tall, deformed heart appearing to explode with engorged blood vessels. Increased background lung density is due to a combination of congestion, edema, and expiratory filming. B, The opposite dorsoventral view is also abnormal (cardiomegaly, hyperemia, edema, and a small amount of pleural fluid) but less ominous.

Nuclear Medicine. Daniel and co-workers investigated the use of instantaneous ejection-volume images to produce ventricular volume curves from an equilibrium radionuclide ventriculogram.12

❚❚❚ HYPERTROPHIC CARDIOMYOPATHY Background Hypertrophic cardiomyopathy is a primarily a disease of the left ventricle characterized by thickening,

Radiology. Mild feline cardiomyopathy can be difficult to diagnose radiographically. Subtle disease-related changes in the size and shape of the heart differ little from the vagaries of form often seen with expiratory films. Lateral oblique images often make the heart appear overly tall, whereas VD obliques falsely accentuate the right or left side of the heart. Forceful restraint or resistance by the cat typically will result in excessive stretching, which in the lateral view appears as increased sternal contact and, in the VD projection, relative cardiomegaly related to narrowing of the rib cage. Moderate feline cardiomyopathy usually takes one of two forms: (1) a generalized enlargement with increased forward inclination, causing increased sternal contact and intercostal width (Figure 54-12) and bulging of the dorsal aspect of the heart, sometimes creating a distinctive bilobed appearance in the lateral view; and a (2) a bloated triangular shape in the opposite plane (Figure 54-13). Severe feline cardiomyopathy shows the same abnormalities seen in moderately diseased hearts (enlarge-

CHAPTER 54 ❚❚❚ Acquired Heart Disease

525

A

Figure 54-11 • Left-sided, four-chamber view of the heart of a dog with dilated myopathy shows massive left atrial and ventricular dilation.

the heart, provided the cat does not become overly stressed during positioning. Failure as mentioned previously, is signaled by pleural fluid, typically in the context of cardiomegaly and enlarged central lung vessels (Figures 54-15 to 54-18).

B

C Figure 54-10 • A left-sided four-chamber view (A) of the heart of a Pointer with dilated cardiomyopathy shows the enormity of the expansile changes caused by this disease. Right-sided systolic (B) and diastolic (C) long sections indicate reduced wall movement indicative of poor contractility.

ment and basilar deformity) but to a greater degree (Figure 54-14). When failure occurs, which in most cats is indicated by pleural fluid rather than pulmonary edema as in dogs, the heart may be so obscured that assessment is not possible. In such circumstances, postural films can be used to relocate the fluid away from

Ultrasound. As with radiographic diagnosis, sonographically detecting early myopathy in cats is often difficult. Not only is the cardiac image quality in cats usually inferior to that in dogs, but also cats tend to resist more; as a result, examination times tend to be briefer and less detailed. In my experience, interior measurement (e.g., chamber wall thickness, shortening fraction) are often ambiguous and generally have high margins of error. In such cases, I recommend that such examinations be considered nondiagnostic or uncertain rather than “suspicious,” as some seem to prefer, and repeated later if the cat remains ill. Moderate and severe cases are more straightforward, with affected hearts typically featuring a small, thickened left ventricle and an enlarged left atrium. In both long and cross-sections, the ventricular wall is often so thick that it obliterates the chamber during systole.

❚❚❚ MYOCARDITIS In my experience, myocarditis can be an extremely difficult diagnosis, even with sophisticated forms of medical imaging. Often I have suspected myocardial inflammation based on increased or decreased echogenicity in the heart wall (with or without dilation), but I have only rarely been able to confirm my

526

SECTION VI ❚❚❚ The Heart

A

B C Figure 54-12 • Lateral thoracic radiograph (A) of a cat with thyroid-induced myopathy (TIM) shows moderate cardiac enlargement with a widened base, giving the heart a bilobed appearance. Right systolic long (B) and cross-section (C) sonograms show left ventricular thickening and reduced chamber volume.

CHAPTER 54 ❚❚❚ Acquired Heart Disease

A

527

B

C

D Figure 54-13 • A, Lateral thoracic radiograph of a cat with thyroid-induced myopathy (TIM) shows an enlarged, forwardly inclined heart with very large central lung vessels but no pleural fluid. Unlike some cats with this ubiquitous disease, the heart is proportionally enlarged rather than bilobed. Because this cat with TIM could not be handled, it was sedated 15 minutes before being radiographed. B, A ventrodorsal view shows a severe right lateral cardiac shift (nonspecifically termed a mediastinal shift), making it difficult to separate possible heart enlargement from right-sided postural atelectasis. Right-sided, long-axis, systolic (C) and diastolic (D) sonograms reveal ventricular hypertrophy and partial obstruction of the left ventricular outflow tract by a bulging septum. Caution: Lateral images made during expiration or ventrodorsal views made with excessive traction can mimic TIM owing to a falsely increased cardiac-thoracic ratio.

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depression, weight loss, and anorexia found in advanced cases. Middle-aged male dogs are most often affected and possibly German Shepherds more than other breeds. Twenty-five percent of affected dogs also have congenital heart disease. Venous blood cultures are often positive (70%), typically revealing Corynebacterium, Erysipelothrix, Streptococcus, Staphylococcus species, or Escherichia coli. Endocarditis is often fatal, regardless of treatment; 50 to 75% of dogs die within 6 months after diagnosis. In addition to causing valvular insufficiency and heart failure, bacteria from the cardiac vegetations can spread to other organs, such as the kidneys, intestine, brain, or joints, causing infarction, abscess, or infection. Dogs with undiagnosed endocarditis may present with illness seemingly unrelated to the heart, the result of bacterial emboli spawned by aortic vegetations, for example, intestinal colic caused by mesenteric thrombosis.

A

Imaging Findings

B Figure 54-14 • Lateral (A) and ventrodorsal (B) close-up views of the heart of a cat with thyroid-induced myopathy (TIM) show an immense heart that fills nearly half the thorax.

suspicions. This has been especially true of dogs exhibiting the so-called “Swiss-cheese” myocardium, a pattern often seen in older dogs, which I now consider to be of dubious diagnostic value; others have apparently fared better. Trypanosomiasis (T. cruzi) was reported as a cause of predominantly right-sided heart disease in a small series of dogs in Texas. Thoracic radiography showed generalized or right-sided heart enlargement in six of eight dogs.15

❚❚❚ ENDOCARDITIS Background Dogs. Bacterial endocarditis can range from clinically silent in its earliest stages to the classic signs of fever,

Radiology and Ultrasound. Radiographically, the heart usually appears normal (Figure 54-19) or mildly enlarged; sonographically, the valves (usually the aortic or mitral), their cords, and sometimes the papillary muscles may contain bacterial colonies embedded in variably sized and shaped lumps of granulation tissue (so-called vegetations or vegetative lesions) characteristic of the disease. Occasionally, dogs with endocarditis are first examined while already in heart failure, in which case they usually have enlarged hearts, pulmonary vasculature, and lung edema (Figure 54-20).16 Most dogs with severe aortic or mitral endocarditis reveal some degree of regurgitation on Doppler. Occasionally, vegetations obstruct aortic outflow, leading to accelerated blood flow (Figure 54-21). Sottiaux and Franck reported abnormal aortic valve motion in a dog with endocarditis.17 In my view, it seems probable that most, if not all, endocarditic valves likely move abnormally, a sort of abbreviated “sea anchor” created by projecting vegetations being buffeted in the hemic torrent. Rarely, bacteria residing on the aortic valve may “tunnel” through the wall of the nearby left atrium, creating an internal communication with the left ventricular outflow tract. Simplistically, this may be thought of as an intracardiac fistula.18 Cats. Endocarditis is rare in cats, although some cases have been reported. As in dogs, the aortic valve is most often affected, followed by the mitral valve. Sonographically, the infected valve cusps appear lumpy and hyperechoic, lesions that often are referred to as vegetations. Occasionally, the deformed valves calcify, in which case they potentially can be seen on radiographs.19 Text continued on p. 533

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529

A

B

C Figure 54-15 • Lateral (A) and ventrodorsal (B) views of a cat in heart failure resulting from thyroid-induced myopathy (TIM) show cardiomegaly with characteristic remodeling and pleural fluid. The widened cranial mediastinum, seen best in the ventrodorsal projection, was an unsuspected tumor. C, Right-sided four-chamber sonogram shows a small, thickened left ventricle and dilated atrium. D, Continuous-wave Doppler showed severe, prolonged mitral leakage, depicted by downwardly directed waveforms.

D

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SECTION VI ❚❚❚ The Heart

B

A Figure 54-16 • Before and after: A, Lateral view of a cat in heart failure caused by hypertrophic cardiomyopathy shows a taller than normal heart, pulmonary hyperemia, pulmonary edema, and pleural fluid. B, A subsequent image made following successful medical treatment shows disappearance of the pulmonary edema, pleural fluid, and hyperemia but not cardiomegaly.

A

B Figure 54-17 • A, Lateral thoracic radiograph of an aged cat in heart failure caused by thyrotoxicosis shows a taller than normal heart that is largely concealed by a medium volume of pleural fluid and pulmonary atelectasis due to the same cause. B, Right-sided oblique cardiac sonogram shows a dilated left atrium (lower center), indicative of increased left ventricular pressure.

CHAPTER 54 ❚❚❚ Acquired Heart Disease

531

A

C

B

Figure 54-18 • Lateral (A) and ventrodorsal (B) views of a dyspneic cat in heart failure resulting from thyroid-induced myopathy (TIM) show a large volume of pleural fluid, which has partially collapsed the caudal lung lobes and conceals much of the heart. This appearance often is mistaken for a cranial mediastinal mass. Caution: A dorsally displaced trachea, as seen in a lateral thoracic radiograph, is an unreliable indicator of a cranial mediastinal mass (see flotation effect in text). Left-sided long-axis cardiac sonogram (C) shows massive left ventricular hypertrophy and associated atrial dilation.

A

B

Figure 54-19 • A, Lateral thoracic radiograph of a dog with endocarditis shows a slightly taller than normal heart and increased hilar and caudal lung lobe densities. B, A sonographic cross-section through the aortic valve shows multiple hyperechoic objects characteristic of infected vegetations at the edges of the valve cusps.

A

B

Figure 54-20 • A, Lateral thoracic radiograph of a dog with

C

A

endocarditis shows heart enlargement (left-sided emphasis), pulmonary hyperemia, and edema. B, The ventrodorsal view shows a heart with vague ventral borders and a cloudy lung caused by edema. C, A right-sided sonographic long section of the aortic outflow tract shows a grossly deformed, triangular aortic valve cusp, the result of endocarditis.

B Figure 54-21 • A, A right-sided cross-sectional sonogram shows multiple bright objects within the aorta, consistent with endocarditis. B, Blood flow through the aorta, as recorded with pulse-wave Doppler, was greatly accelerated because of a narrowed outflow caused by the projecting vegetations.

CHAPTER 54 ❚❚❚ Acquired Heart Disease

❚❚❚ PERICARDIAL DISEASE

533

• Cranial vena cava height divided by right fourth rib = 3.5

Pericardial Fluid: Causes and Consequences

Fluoroscopy

Capillary leakage results in the accumulation of fluid within the pericardial sac. Loss of capillary integrity can result from a variety of local and systemic diseases, including infectious and noninfectious pericarditis, pericardial tumor, some forms of heart failure, and coagulopathies. Rarely, rat poisons, such as brodifacoum, can cause pericardial hemorrhage and tamponade as a result of their intense anticoagulant properties.20

Pneumopericardiography. When pericardial fluid is present, it is possible to define the pericardium radiographically by performing a transthoracic pericardial puncture, removing fluid, and instilling air (pneumopericardiography). If a discrete intrapericardial lesion is present, postural radiography often can be used to optimize its appearance. Both normal and abnormal pneumopericardiograms have been described.22,23

Imaging Methods Plain Films. Other than by inference, it is usually impossible to distinguish small and medium volumes of pericardial fluid from uncomplicated cardiomegaly using plain films. Large volumes of pericardial fluid usually cause marked cardiac enlargement, however, accentuated by an exaggerated rounding giving rise to a bevy of descriptors such as “soccer-ball” and “pumpkin-shaped.” Another unpublished radiographic feature of large pericardial fluid volumes is what I term the “object within an object” sign. This abnormal appearance—a relatively high-density interior heart shadow superimposed on a larger, lighter one— is largely the result of the spherical shape of the fluidfilled pericardium. The compressive nature of the fluid-distended pericardium, particularly to the right side of the heart, reduces pulmonary blood flow and backs up venous return to the heart. These circulatory derangements are depicted radiographically by pulmonary oligemia and enlargement of the caudal vena cava. Furthermore, the globally enlarged heart often causes secondary respiratory distress by displacing and compressing the overlying trachea and extrapulmonary bronchi (Figure 54-22). Determination of Caval Size. Lehmkuhl and coworkers described how an enlarged caudal vena cava, as measured from a left lateral radiograph, can be related to right heart failure by using a left lateral thoracic radiograph.21 Specifically, they proposed comparing the height of the cranialmost portion of the caudal vena cava to one of three nearby structures: (1) the height of the aorta, (2) the length of the thoracic vertebra dorsal to the carina, and (3) the width of the right fourth rib just as it passes the ventral edge of the associated vertebra. The resultant measurements then were used to calculate ratios, which, if exceeded, indicated an increase in caval volume and the possibility of right heart failure. The upper limits of normal for the described ratios were as follows. • Cranial vena cava height divided by aortic height = 1.5 • Cranial vena cava height divided by vertebral length = 1.3

Ultrasound Constrictive/Restrictive Pericarditis. Based on the few published reports, constrictive pericarditis is relatively rare in dogs. Male dogs are three times more likely to be affected than are female dogs. Reported causes of restrictive pericarditis include traumatic, infectious (Coccidioidomycosis, Mycobacteriosis, Actinomycosis organisms), parasitic (Dirofilariasis sp.), metaplastic (osseous), and idiopathic.24 In some cases, constrictive pericarditis may lead to chylothorax by way of elevated right atrial and ventricular pressures, increased central venous pressure, dilation of the thoracic duct, and leakage of chyle (Figure 54-22, D and E).25

Intrapericardial Cyst Large intrapericardial cysts can compress the heart, particularly its right side, secondarily causing an increase in right ventricular filling pressure. In turn, this can lead to a dangerous decrease in cardiac output (cardiac tamponade). Plain-film findings are similar to those seen with large volumes of free pericardial fluid, namely, moderate to severe cardiomegaly with exaggerated rounding of the cardiac silhouette. Sonographically, it can be difficult to distinguish a large intrapericardial cyst from free pericardial fluid unless the cyst wall can be positively identified.26

Pericardial Hematoma Pericardial hemorrhage can be benign or malignant. In the former instance, the cause of the bleeding usually is not determined, but postdrainage recurrence is common. As indicated by its name, the malignant form typically is associated with a discrete pericardial or cardiac tumor. Hematomas are rare (Figure 54-23).

❚❚❚ HEARTWORM DISEASE Dogs Background. The severity of heartworm disease in dogs and cats depends on the following factors: (1) the duration of the infection, (2) the number of

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A

C

B

E

D Figure 54-22 • Lateral (A), lateral hilar close-up (B), and dorsoventral (C) thoracic radiographs of a dog with a large volume of pericardial

fluid causing the heart to appear distinctively spherical. Trachial and main-stem bronchial displacement is severe, and the lung is oligemic. Sonograms show a large intrapericardial tumor, labeled “mass” (D) and a large volume of pericardial fluid (E).

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A

B C Figure 54-23 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a dog with benign pericardial hemorrhage show a rounded heart with an “object within an object” appearance and a lung devoid of peripheral vasculature. Sonogram (C) shows a large, lobulated intrapericardial mass, which proved to be a hematoma.

mature worms in the right ventricle and pulmonary arteries, (3) the functional and mechanical effects of microfilaria on the lung vasculature, and in particular the development of pulmonary hypertension, (4) the effectiveness of the animal’s immune system in combating the parasites’ metabolic byproducts, and (5) the harmful side effects of treatment such as pneumonia, thromboembolism, and granulomatosis.26a Imaging Findings Radiology. The radiographic appearance of naturally occurring and experimentally created heartworm disease has been exhaustively studied. For example, Carlisle, Losonsky, and co-workers described the

general radiographic appearance of canine dirofilariasis.27,28 Thrall and Calvert reported the appearance of heartworm disease causing right heart failure.29 Calvert and colleagues and others have correlated the radiographic, electrocardiographic, and sonographic findings associated with right heart enlargement caused by dirofilariasis.30 The RDIs of canine heartworm disease are as follows: 1. Early cardiac remodeling: Mild cardiomegaly with right-sided emphasis, with or without central arterial enlargement (Figure 54-24) 2. Later changes: Overt righted-sided heart enlargement, including the main pulmonary artery (MPA) and its principal branches

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5. Posttreatment appearance: The appearance of the heart and central pulmonary arteries following successful treatment usually differs little from its pretreatment look. Pulmonary Arteriography. Thrall and co-workers described the angiographic appearance of the pulmonary arteries in dogs experimentally infected with dirofilariasis.31 In addition, they discovered that a direct relationship existed between the type and severity of pulmonary arterial abnormalities and the number of adult heartworms infecting a dog. Later, the same authors described the collateral pulmonary circulation that develops from the bronchial and esophageal branches of the left gastric arteries as a consequence of heartworm infection.32

A

Ultrasound. Baderscher and co-workers reported the sonographic appearance of Dirofilaria in dogs. The parasites appear as multiple short, stratified echogenic bands, which represent portions of one or more worms as they coil in and out of the ultrasound beam.33 Nuclear Imaging. Daniel and Allhands reported using Dirofilaria immitis–specific, technetium-99m–labed, monoclonal antibodies to diagnose heartworm disease in dogs.34

Cats Background. The radiographic signs of feline dirofilariasis are far more variable than in dogs. Some, but not all, cats with heartworm disease cough or are dyspneic; others appear outwardly normal.35 Imaging Findings

B Figure 54-24 • Lateral (A) and ventrodorsal oblique (B) thoracic radiographs of a dog with mild-to-moderate heartworm disease shows cardiomegaly with right-sided emphasis.

3. Advanced disease: Marked right-sided heart enlargement, bulging MPA, obviously thickened central arteries, with or without undulation or abrupt termination, also termed arterial pruning, implying embolization. 4. Related noncardiac disease: Eosinophilic “pneumonitis,” a form of allergic pneumonia caused by migrating pulmonary microfilaria, may occur in dogs but is less common in cats. Variable degrees of pulmonary hypertension occur in most animals with dirofilariasis, which if it becomes severe, is usually termed cor pulmonale. Secondary liver disease, termed the caval syndrome, has been described as the cause of sudden death in dogs with heartworm disease.

Radiology. Selcer and co-workers determined that the radiographic abnormalities that develop in the lungs of cats experimentally infected with heartworms change over time and, in some cases, disappear altogether. Specifically, (1) abnormal lung density, termed by the authors bronchointerstitial lung disease, persisted throughout the study period, (2) lobar arterial enlargement slowly resolved, and (3) pulmonary hyperinflation tended to worsen. Heart enlargement was present in fewer than half of the infected cats, and adult heartworms were sonographically detectable in only about 40% of the animals. The authors pointed out the radiographic similarities between heartworm disease and allergic bronchitis (asthma).36 Vascular alterations resulting from experimental D. immitis infection in cats include pulmonary arterial enlargement, tortuosity, and loss of normal tapering. These abnormalities are usually most obvious in the VD projection. Enlargement of the main pulmonary artery, a highly reliable sign of heartworm disease in dogs, is usually absent in affected cats as a result of cardiac superimposition.37 In naturally occurring heartworm infections, the primary divisions of the pulmonary artery usually are enlarged by about 50% in

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most affected cats.38,39 Unlike the dog, cardiomegaly is typically absent in the cat.40 Pulmonary Arterial Measuration. Schaffer and Berry described a simplified method of measuring the pulmonary arteries to the caudal lung lobes as seen in ventrodorsal projection, measurements that they contend can reliably identify cats with heartworm disease.41 • Pulmonary arterial width greater than 5 mm measured at the center of the seventh intercostal space • Pulmonary arterial width greater than 4 mm measured at the center of the ninth intercostal space • An AC (arterial-chondral) ratio of greater than 1.6 (left pulmonary artery measured at center of ninth intercostal space and width of ninth rib)

A

In my experience (largely gained in Oklahoma and Texas), a normal thoracic radiograph does not exclude dirofilariasis. The earliest abnormality that I have observed is an increase in the size of the right of the heart as viewed laterally, which may or may not be accompanied by enlargement of the second and third divisions of the pulmonary arteries. Later, cardiomegaly with right-sided emphasis may become evident in both the VD and lateral views (Figure 54-25). I have observed unequivocal cardiomegaly and pulmonary hyperemia on only a few occasions, and in each instance the cat later proved to be severely hypertensive as a result of its advanced infection. Occasionally, infected cats with minimal cardiovascular enlargement may show an increase in their caudal lobe density, in which case dirofilariasis should be considered (presuming this occurs in an endemic area).42 Ultrasound. When associated with pulmonary hypertension, heartworms sometimes are detected sonographically.43 Typically, the worms appear as a pair of closely approximated, parallel, linear, or curvilinear echogenicities.44 Occasionally, a clump of worms may be encountered, appearing as an echogenic mass, its movement orchestrated by the rhythm of the heart. As spectacular as the finding of a heartworm is, it occurs infrequently, often because of the inaccessibility of the worms or a suboptimal scanning angle. Thus, most such searches are futile, even though worms may be present.

❚❚❚ THIRD-DEGREE HEART BLOCK Background Third-degree AV heart block refers to the lack of neuroelectrical transmission or conduction between the atria and ventricles. In such circumstances, the ventricles are independently paced at a point beyond the blockage, producing an electrocardiographic tracing that features an abnormal relationship between the P waves and QRS complexes. In other words, the atria and ventricles are beating independently.

B Figure 54-25 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a cat with heartworm disease show mild to moderate cardiomegaly with right-sided emphasis (exaggerated by surrounding fat) and enlarged central vasculature.

Causes of a third-degree block are varied and include (1) bacterial endocarditis, (2) hypertrophic cardiomyopathy, (3) infiltrative cardiomyopathy, (4) myocardial ischemia, (5) myocardial infarction, (6) myocardial fibrosis, (7) digitalis poisoning, (8) myasthenia gravis, and (9) potassium toxicity. Clinical indicators of thirddegree block relate to insufficient circulation caused by an underperforming heart and include weakness, fainting, heart failure, and sudden death.45

Imaging Findings Radiography. Dogs with complete or third-degree heart block typically have an enlarged heart with leftsided emphasis (Figure 54-26).

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mitral insufficiency secondary to endocardiosis. Sonographically, the disease is characterized by a massively dilated, immobile left atrium with an incompetent mitral valve and left ventricular enlargement (Figure 54-27). Ventricular contraction is typically poor. Left atrial tearing is an ever-present danger in such circumstances.

❚❚❚ INHERITED VENTRICULAR TACHYCARDIA IN GERMAN SHEPHERDS Inherited ventricular tachycardia, potentially causing sudden death at a comparatively young age (4 to 18 months), has been reported in German Shepherds. Animals in which abnormal electrocardiograms were obtained had normal thoracic radiographs and nearnormal sonograms.47 A

❚❚❚ ISCHEMIC HEART DISEASE (ARTERIOSCLEROSIS)

B Figure 54-26 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a dog with a third-degree heart block show moderate cardiomegaly and an oligemic lung.

Ultrasound. Sonographically, dogs and cats with this conduction disorder show left-sided atrial and ventricular dilation, often leading to marked chamber rounding. Doppler typically reveals severe mitral backflow that is often diastolic in nature.46

❚❚❚ ATRIAL STANDSTILL Radiography and Ultrasound Dogs with atrial standstill generally have cardiomegaly with left-sided emphasis, which can closely resemble

Falk and Jonsson asserted that arteriosclerosis may be responsible for sudden death and death during general anesthesia. Moreover, they contend that arteriosclerosis should also be a consideration in the clinical evaluation of dilated myopathy and may contribute to decreased myocardial contractility in dogs with mitral regurgitation secondary to endocardiosis.48 As described by the authors, arteriosclerosis is a vascular disease that causes coronary arterial wall thickening secondary to proliferative and degenerative noninflammatory changes and, in the process, results in luminal narrowing and reduced myocardial blood flow. The resultant myocardial pathology is believed to occur in the following sequence: (1) intramural coronary arterial lesions, (2) myocardial infarct, (3) myocardial necrosis, and (4) myocardial fibrosis (or scarring). Although individual infarcts in dogs are usually small and unlikely to result in serious heart disease, multiple healed infarcts have the potential to cause substantial myocardial scarring. In addition, myocardial ischemia secondary to arteriosclerosis can lead to myocardial atrophy and further fibrosis. Sonographically, affected dogs showed a moderate decrease in muscular contractility (hypokinesia); fractional shortening, admittedly only a limited indicator of contractility, ranged from 15 to 30%, with a mean value of 22%.

❚❚❚ CENTRAL AND PERIPHERAL ARTERIAL THROMBOSIS Background Arterial thrombosis can occur in large centrally located blood vessels like the aorta and pulmonary artery or in the more peripheral vessels, such as the iliac or

A

B

C

D Figure 54-27 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a dog in heart failure caused by atrial standstill show severe cardiomegaly with left-sided emphasis and a medium volume of pleural fluid. C, Right-sided, long-axis sonogram shows severely dilated left ventricle. D, Normal left ventricular systole (reader’s right) and diastole (reader’s left) are provided for comparison. Continued

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F

E Figure 54-27 • cont’d E, Color mapping displayed in gray scale shows mitral regurgitation in a four-chamber view from the left side. F, Continuous-wave Doppler tracing illustrates high velocity atrial backflow.

femoral arteries. Thrombosis can attend a variety of diseases, including (1) cardiomyopathy in cats, (2) hyperadrenocorticism, (3) disseminated intravascular coagulopathy (DIC), (4) autoimmune hemolytic anemia, (5) and some forms of cancer. Disturbances in one or more of the following mechanisms are thought to be the prime initiators of arterial thrombosis: blood flow, endothelial integrity, coagulation, and fibrinolysis.49 Aortic thrombosis also has been reported in association with a gunshot wound, specifically a BB lodged in the caudal aspect of the abdominal aorta. The presenting clinical signs in this cat were similar to those exhibited with embolic cardiomyopathy.50

❚❚❚ AORTIC SINUS RUPTURE (RUPTURED SINUS OF VALSALVA) Abbott and Porzio described a case of probable left aortic sinus rupture in an 18-month-old Dalmatian, which fistulated into the adjacent main pulmonary artery.52 The presumptive diagnosis was based on a combination of sonographic and angiographic evidence.

❚❚❚ COR PULMONALE Background

Imaging Findings Most of what has been published about pulmonary thrombosis has been based on a single case report, a small case series, or limited postmortem data. Theoretically, one might expect that a large thrombosed lung vessel would appear blunted, much like those seen with advanced heartworm disease, and that the affected lobe distal to the obstruction would appear oligemic. In cats, peripheral thrombi, particularly those located in the distal aortic and iliac arteries, have been identified using angiography and ultrasound. Nuclear Medicine. Daniel and co-workers described the use of radionuclide angiography to diagnose aortic thromboembolism in two dogs. Using a cephalic injection of 99mtechnetium pertechnetate, the authors were able to demonstrate an absence of activity beyond the point of aortic obstruction, such that the terminal aorta and iliac bifurcation could not be identified.51

Pulmonary hypertension, either primary or secondary, causing secondary right ventricular disease is termed cor pulmonale or pulmonary-induced lung heart disease. Congenital heart diseases such as ventricular septal defect (VSD) or patent ductus arteriosus (PDA), which cause excessive pulmonary blood flow and eventually can lead to increased vascular resistance, abnormal back pressure, and secondary right ventricular hypertrophy. Heartworms and systemic hypertension can cause similar disease. Insofar as I am aware, the true incidence and prevalence of cor pulmonale in pets are not known, with many case reports being based almost entirely on circumstantial evidence. Chronic bronchial disease, especially bronchiectasis, also can lead to pulmonary hypertension and cor pulmonale.

Imaging Findings Radiology and Ultrasound. Neither radiographic nor sonographic findings are conclusive. Suggestive

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541

A

C

B

Figure 54-28 • Lateral (A) and ventrodorsal (B) close-up views of the heart and hilar region of a dog with bronchiectasis show dilation of the visible portion of the trachea and associated principal bronchi. Cor pulmonale was diagnosed sonographically based on right ventricular hypertrophy, labeled RV (C).

abnormalities include cardiomegaly with right-sided emphasis; an enlarged main pulmonary artery; and widened, sometimes tortuous, central pulmonary arteries (Figure 54-28). Sonographic findings include right ventricular hypertrophy, right atrial dilation, and an increased pulmonic valve pressure gradient.

References 1. Farrow CS: Critical thinking: benefits of presurgical thoracic screening. Can Vet J 35:723, 1994. 2. Lombard CW, Spencer CP: Correlation of radiographic, echocardiographic, and electrocardiographic signs of left heart enlargement in dogs with mitral regurgitation. Vet Rad 26:89, 1985. 3. Buchanan JW, Kelly AM: Endocardial splitting of the left atrium in the dog with hemorrhage and hemopericardium. J Am Vet Rad Soc 5:28, 1964. 4. Detweiler DK, Patterson DF: The prevalence and types of cardiovascular disease in dogs. Ann NY Acad Sci 127:481, 1965.

5. Beardow AW, Buchanan JW: Chronic mitral valve disease in Cavalier King Charles Spaniels: 95 cases (1987-1991: J Am Vet Med Assoc 203:1023, 1993. 6. Pederson HD, Lorentzen KA, Kristensen BO: Observer variation in the two dimensional echocardiographic evaluation of mitral valve prolapse in dogs. Vet Radiol Ultrasound 37:367, 1996. 7. Reid CF, Pensinger RR, et al: Functioning adenocarcinoma of the thyroid gland in a dog with mitral insufficiency. J Am Vet Rad Soc 4:36, 1963. 8. McIntosh J, Bright MS, McEntee M: Isolated right ventricular cardiomyopathy in a dog. J Am Vet Med Assoc 207:64, 1995. 9. Vollman AC: The prevalence of cardiomyopathy in the Irish Wolfhound: a clinical study of 500 dogs. J Am Anim Hosp Assoc 36:125, 2000. 10. Calvert CA, Hall G, et al: Clinical and pathologic findings in Doberman Pinschers with occult cardiomyopathy that died suddenly or developed congestive heart failure: 54 cases (1984-1991). J Am Vet Med Assoc 210:505, 1997.

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11. Schober KE, Fuentes VL, et al: Pulmonary venous flow characteristics as assessed by transthoracic pulsed Doppler echocardiography in normal dogs. Vet Radiol Ultrasound 39:33, 1998. 12. Daniel GB, Tucker RL, et al: Utilization of instantaneous ejection volume images to produce ventricular volume curves from an equilibrium radionuclide ventriculogram. Vet Radiol Ultrasound 34:276, 1993. 13. Marks CA: Hypertrophic cardiomyopathy in a dog. J Am Vet Med Assoc 203:1020, 1993. 14. Venco G: Left ventricular thrombus in a cat with hypertrophic cardiomyopathy. Vet Radiol Ultrasound 38:467, 1997. 15. Meurs KM, Anthony MA, et al: Chronic Trypanosoma cruzi infection in dogs: 11 cases (1987-1996). J Am Vet Med Assoc 213:497, 1998. 16. Toal R: Radiographic diagnosis. Vet Radiol Ultrasound 33:348, 1992. 17. Sottiaux J, Franck M: Echocardiographic appearance of flail aortic valve in a dog with infective endocarditis. Vet Radiol Ultrasound 39:436, 1998. 18. Smith AN, Finn-Bodner, et al: Left ventricular outflow tract to left atrial fistula associated with endocarditis in a dog. J Am Anim Hosp Assoc 36:133, 2000. 19. Malik R, Church DB, et al: What is your diagnosis? J Am Vet Med Assoc 200:1391, 1992. 20. Petrus DJ, Henik RA: Pericardial effusion and cardiac tamponade secondary to brodifacoum toxicosis in a dog. J Am Vet Med Assoc 215:647, 1999. 21. Lehmkuhl LB, Bonagura JD, et al: Radiographic evaluation of caudal vena cava size in dogs. Vet Radiol Ultrasound 38:94, 1997. 22. Reed JR, Thomas WP, Suter PF: Pneumopericardiography in the normal dog. Vet Rad 24:112, 1983. 23. Thomas WP, Reed JR, Gomez JA: Diagnostic pneumopericardiography in dogs with spontaneous pericardial effusion. Vet Rad 25:2, 1984. 24. Wright KN, DeNovo RC, et al: Effusive-constrictive pericardial disease secondary to osseous metaplasia of the pericardium in a dog. J Am Vet Med Assoc 209:2091, 1996. 25. Campbell SL, Forrester D, et al: Chylothorax associated with constrictive pericarditis in a dog. J Am Vet Med Assoc 206:1561, 1995. 26. Less RD, Bright JM, et al: Intrapericardial cyst causing cardiac tamponade in a cat. J Am Anim Hosp Assoc 36:115, 2000. 26a. Suter PF: Cardiac diseases in thoracic radiography. Zurich, Switzerland, 1984, Wettswil, p 439. 27. Carlisle CH: Canine dirofilariasis: its radiographic appearance. Vet Rad 21:123, 1980. 28. Losonsky JM, Thrall DE, Lewis RE: Thoracic radiographic abnormalities in 200 dogs with spontaneous heartworm infestation. Vet Rad 24:120, 1983. 29. Thrall DE, Calvert CA: Radiographic evaluation of canine heartworm disease coexisting with right heart failure. Vet Rad 24:124, 1983. 30. Calvert CA, Losonsky JM, et al: Comparisons of radiographic and electrocardiographic abnormalities in canine heartworm disease. Vet Rad 27:2, 1986. 31. Thrall DE, Badertscher RR, et al: The pulmonary arterial circulation in dogs experimentally infected with Dirofilaria immitis: its angiographic evaluation. J Am Vet Rad Soc 20:74, 1979.

32. Thrall DE, Badertscher RR, Lewis RE, McCall: Collateral pulmonary circulation in dogs experimentally infected with Dirofilaria immitis: its angiographic evaluation. Vet Rad 21:131, 1980. 33. Baderscher RR, Losonsky JM, et al: Two-dimensional echocardiography for diagnosis of dirofilariasis in nine dogs. J Am Vet Med Assoc 193:843, 1988. 34. Daniel GB, Allhands RV: In-vivo testing of technetium99m-labeled monoclonal antibodies specific for Dirofilaria immitis. Vet Rad 30:74, 1989. 35. Atkins CE, DeFrancesco TC, et al: Prevalence of heartworm infection in cats with signs of cardiopulmonary abnormalities. J Am Vet Med Assoc 212:517, 1998. 36. Selcer BA, Newell SM, et al: Radiographic and 2-D echocardiographic findings in eighteen cats experimentally exposed to D. immitis via mosquito bites. Vet Radiol Ultrasound 37:37, 1996. 37. Donahoe JM, Kneller SK, Lewis RE: In vivo pulmonary arteriography in cats infected with Dirofilaria immitis. J Am Vet Rad Soc 17:147, 1976. 38. Schafer M, Berry CR: Cardiac and pulmonary artery measuration in feline heartworm disease. Vet Radiol Ultrasound 36:499, 1995. 39. Atkins CE, DeFrancesco TC, et al: Heartworm infection in cats: 50 cases (1985-1997). J Am Vet Med Assoc 217:355, 2000. 40. Wong MM, Pederson NC, Cullen S: Dirofilariasis in cats. J Am Anim Hosp Assoc 19:855, 1983. 41. Schafer M, Berry CR: Cardiac and pulmonary artery measuration in feline heartworm disease. Vet Radiol Ultrasound 36:499, 1995. 42. Farrow CS: The thorax. In Farrow CS, ed: Radiology of the cat. St. Louis, 1994, Mosby. 43. Boon JA: Acquired heart disease. In Boon JA, ed: Manual of Veterinary Echocardiography, Philadelphia, 1998, Williams & Wilkins. 44. Dvorak LD, Preziosi DE, Hitchcock LS: What is your diagnosis? J Am Vet Med Assoc 217:180, 2000. 45. Hackett TB, Van Pelt DR, et al: Third degree atrioventricular block and acquired myasthenia gravis in four dogs. J Am Vet Med Assoc 206:1173, 1995. 46. Rosenthal SL, Fox PR: Diastolic mitral regurgitation detected by pulsed wave Doppler echocardiography and color flow Doppler mapping in five dogs and two cats with second- and third-degree atrioventricular block. Vet Radiol Ultrasound 36:152, 1995. 47. Moise NS, Gilmore RF, et al: Diagnosis of inherited ventricular tachycardia in German Shepherd dogs. J Am Vet Med Assoc 210:403, 1997. 48. Falk T, Jonsson L: Ischemic heart disease in the dog: a review of 65 cases. J Small Anim Pract 41:97, 2000. 49. Boswood A, Lamb CR, White RN: Aortic and iliac thrombosis in 6 dogs. J Small Anim Pract 41:109, 2000. 50. Whigham HM, Ellison GW, Graham J: Aortic foreign body resulting in ischemic neuromyopathy and development of collateral circulation in a cat. J Am Vet Med Assoc 213:829, 1998. 51. Daniel GB, Wantsschek L, et al: Diagnosis of aortic thromboembolism in two dogs with radionuclide angiography. Vet Rad 31:182, 1990. 52. Abbott JA, Porzio P: Rupture of the left aortic sinus into the pulmonary artery in a Dalmatian dog. Vet Radiol Ultrasound 39:544, 1998.

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5 5

Patterns of Heart Failure

Numerous patterns of heart failure are illustrated throughout this section. The most common of these occurs in dogs and is characterized by the following radiographic disease indicators (RDI’s) large heart; large, numerous lung vessels; and bilateral pulmonary edema. Occasionally, a variation of this pattern occurs, featuring a single but notable difference: the lung edema is unilateral, usually right sided. The cause or causes for this unusual distribution of abnormal lung water is unknown (Figure 55-1). In cases in which medical treatment proves ineffective, the edema eventually spreads to the unaffected half of the lung. Another occasional failure pattern consists of heart enlargement, increased lung vasculature, diffuse lung edema, and ascites, the latter indicating right- as well as left-sided failure.

The most common failure pattern in cats is a large volume of pleural fluid that obscures much of the heart and most of the pulmonary vasculature. Often assessment can be improved by making postural films, provided they are not too stressful to the animal. The pattern of a large heart, small vessels, and ascites strongly suggests cardiac compression (particularly right-sided) secondary to a medium or large volume of pericardial fluid. Caution: Heart failure, or more specifically the edema caused by heart failure, can be mimicked by a variety of noncardiac diseases: neurogenic edema from a severe head injury, strangulation, smoke inhalation, near drowning, warfarin poisoning, disseminated intravascular coagulopathy, pulmonary

A

B Figure 55-1 • Lateral (A) and dorsoventral (B) thoracic radiographs of dog in heart failure attributable to severe mitral endocardiosis in which the pulmonary edema is predominantly right sided and the lung appears oligemic.

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A

B

C

Figure 55-2 • Lateral (A), lateral close-up (B), and ventrodorsal (C) views of a dog with bilateral caudal lobe pneumonia, secondary to a lung abscess (emphasis zone, ventrodorsal projection). Even though the localization of lung consolidation in this case is not typical of most dogs in heart failure, the presence of unrelated cardiomegaly helps to create the illusion of heart failure.

interstitial edema, and some forms of pulmonary metastasis and pneumonia. The illusion is made even more realistic when there is unrelated heart enlargement, for example, in endocardiosis in older dogs (Figure 55-2). Right-sided heart failure is typically characterized by (1) cardiomegaly, (2) diminished lung vasculature, and (3) ascites (Figure 55-3).

Figure 55-3 • Lateral thoracic radiograph of a dog with a right atrial hemangiosarcoma causing pericardial bleeding shows an enlarged, but not spherical, heart. Resultant right ventricular compression led to a marked reduction in visible lung vessels.

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5 6

Cardiac Tumors and Thrombi

❚❚❚ BACKGROUND Compared with metastatic tumors, primary heart tumors are uncommon in dogs. The most common primary heart tumor in dogs is hemangiosarcoma, a tumor usually found in the right atrium or right auricular appendage, but it also has been reported in the left ventricle and main pulmonary artery.1,2 Other reported primary heart tumors include fibroma, fibrosarcoma, hemangioma, rhabdomyoma, chondroma, myxofibroma, myxoma, mesothelioma, neurofibroma, teratoma, lipofibroma, lymphangioendothelioma, and mixed spindle and round cell sarcomas.3 Intracardiac tumors exert a variety of harmful effects on the heart, including (1) obstruction of the right or left cardiac outflow tracts, (2) valvular incompetence, and (3) reduced atrial or ventricular volume, secondary to the space-occupying effect of the tumor. Accordingly, signs of right-sided or left-sided heart failure may be present. If the tumor has grown into the heart wall, arrhythmia, tachycardia, or heart block may be present, which also can lead to heart failure. The diagnosis of intracardiac tumors is often difficult because of the broad and inconsistent spectrum of clinical signs but inevitably must rely on sonography, especially when there are signs of possible or probable heart disease (Table 56-1).

❚❚❚ ATRIAL AND AURICULAR TUMORS Background Atrial and auricular masses, primarily hemangiosarcomas, can indirectly cause pericardial fluid. Although conflicting reports exist regarding the difficulty in detecting such tumors, there appears to be general consensus that right auricular tumors are harder to identify than those located in the right atrium. The right auricular appendage is more difficult to image than the right atrium, and right auricular tumors are relatively smaller than those found in the right atrium.4,5

Radiology Atrial and auricular masses such as tumors and thrombi are radiographically invisible. Related pericardial hemorrhage, if in sufficient quantity, will cause the heart to become enlarged and rounded.

Ultrasound Ultrasound, as mentioned previously, is capable of identifying these tumors, but only if they are sufficiently large and in a sonographically accessible region (Figure 56-1). In this regard, I should mention that the routine examination of the heart in dogs with splenic hemangiosarcoma rarely reveals an atrial or auricular mass; I would estimate it does so less than 1% of the time. For a detailed account of this tumor type, see the article by Thomas and co-workers describing the sonographic appearance of right atrial and auricular hemangiosarcoma.6

❚❚❚ ATRIAL THROMBUS Thrombi can develop in the atria for a variety of reasons: For example, an atrial thrombus was reported in a dog with blastomycosis that was traced to a hilar lymph node. The same authors reported that they observed abnormally echogenic blood in the atria, a phenomenon they termed spontaneous contrast.7 I, too, occasionally have made such an observation in dogs with hemagglutination (Figure 56-2).

❚❚❚ VENTRICULAR TUMORS AND THROMBUS In my experience, ventricular chamber masses are rare. The only proven example I have is a thrombus, found in a cat with thyroid-induced myopathy believed to have originated in the associated left atrium (Figure 56-3). By way of a precautionary note, dogs with severe 545

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SECTION VI ❚❚❚ The Heart

Table 56-1 • LOCATION OF CARDIAC TUMORS RELATED TO RADIOGRAPHIC APPEARANCE OF HEART Tumor Location

Heart Appearance

Heart base tumors: Chemodectoma Ectopic thyroid tissue Ectopic parathyroid tissue

May not alter heart sufficiently to be detected radiographically. May be associated with ill-defined mass at base of heart, which can make heart appear taller or mistaken for atrial enlargement. May displace or deform distal aspect of trachea or associated bronchi. May be associated with pleural fluid.

Outer surface (epicardial) tumors: Mesothelioma Hemangiosarcoma Metastases

May not alter heart sufficiently to be detected radiographically. May increase cranial to caudal dimension as viewed laterally, which can lead to the erroneous conclusion that one or both ventricles are enlarged. Can cause heart to appear uniformly enlarged and distinctly rounded if associated with a medium or large volume of pericardial fluid.

Cardiac wall (intramural) tumors: Cardiac metastases Hemangiosarcoma Lymphosarcoma

These are relatively rare tumors and unless quite large can be difficult to diagnose.

Inner surface (endocardial) tumors, which usually extend into the nearest atrium or ventricle: Hemangiosarcoma Myxoma Sarcoma

Right atrial and auricular hemangiosarcomas are the most common of these tumors, with the latter often escaping detection because of sonographic inaccessibility or lying outside the standard scanning planes.

Modified from Suter PF: Thoracic radiography. A text atlas of thoracic diseases of the dog and cat. Zurich, Switzerland, 1984, Wettswil, p 427.

A

B

Figure 56-1 • Lateral (A) and ventrodorsal (B) thoracic radiographs of a dog with multiple diseases: (1) a right atrial sarcoma, (2) pericardial hemorrhage, (3) pulmonary metastasis, and (4) disseminated intravascular coagulation. The left cardiac shift seen in the ventrodorsal view is postural atelectasis related to prolonged left lateral recumbency before radiographic examination.

CHAPTER 56 ❚❚❚ Cardiac Tumors and Thrombi

547

A Figure 56-2 • Sonographic long section through the right and left atria and ventricles (four-chamber view) shows excessive blood echogenicity, particularly evident in the right atrium and ventricle, the result of hemagglutination.

endocarditis sometimes develop large vegetative lesions on one or more of their papillary muscles that can mimic an intraventricular mass.

❚❚❚ PERICARDIAL TUMORS Mesothelioma Background. Mesotheliomas form on the serosal lining of body cavities such as the pericardium, pleura, and peritoneum. Their most visible by-product is fluid, which in the case of the pericardium, may result in severe cardiac compression (tamponade) and a dangerous decrease in cardiac output. Fortunately, pericardial mesotheliomas are rare in both dogs and cats. Pericardiectomy, combined with chemical treatment, has been reported as curative, although this is an exceptional result.8 Imaging Findings. The radiographic detection (by inference) of pericardial mesothelioma depends on the amount of pericardial fluid produced. Small amounts of fluid cause little or no increase in heart size or shape. Medium volumes of fluid enlarge the cardiac silhouette but do little to alter its shape. Large quantities of fluid enlarge and round the heart in a characteristic fashion. Unless a discrete mass can be identified on or in the pericardium, it is difficult to differentiate a pericardial mesothelioma from benign pericardial fluid, even with the aid of cytologic analysis. In dogs with survival times longer than 4 months that were treated by pericardiectomy (but not chemotherapy), the probability of benign pericardial effusion exceeded that of mesothelioma. Dogs that suf-

B Figure 56-3 • Right-sided, long (A) and cross-sectional (B) sonograms of a cat show a sizable thrombus (emphasis zones) in the left ventricle.

fered a recurrence of their disease, as evidenced by the re-formation of pericardial fluid or constrictive pericarditis, were most likely to have mesothelioma.9

References 1. Keene BW, Rush JE, et al: Primary left ventricular hemangiosarcoma diagnosed by endometrial biopsy in a dog. J Am Vet Med Assoc 197:1501, 1990. 2. Pharr JW, Holmberg DL, Clark EG: Hemangiosarcoma in the main pulmonary artery of a dog. Vet Radiol Ultrasound 33:78, 1992. 3. Krotje LJ, Ware WA, Niyo Y: Intracardiac rhabdomyosarcoma in a dog. J Am Vet Med Assoc 197:368, 1990. 4. Berg RJ, Wingfield W: Pericardial effusion in the dog: a review of 42 cases. J Am Anim Hosp Assoc 20:721, 1984. 5. Fruchter AM, Miller CW, O’Grady MR: Echocardiographic results and clinical considerations in dogs with right atrial/auricular masses. Can Vet J 33:171, 1992. 6. Thomas WP, Sisson D, et al: Detection of cardiac masses in dogs by two-dimensional echocardiography. Vet Rad 25:65, 1984.

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7. Ware WA, Fenner WR: Atrial thromboembolic disease in a dog with blastomycosis localized in a hilar lymph node. J Am Vet Med Assoc 193:847, 1988. 8. Closa JM, Font A, Mascort J: Pericardial mesothelioma in a dog: long-term survival after pericardectomy in combination with chemotherapy. J Small Anim Pract 40:383, 1999.

9. Stepien RL, Whitley NT, Dubiezig RR: Idiopathic or mesothelioma-related pericardial effusion: clinical findings and survival in 17 dogs studied retrospectively. J Small Anim Pract 41:342, 2000.

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Cardiac Trauma

❚❚❚ TRAUMATIC PNEUMOPERITONEUM

❚❚❚ PERICARDIAL RUPTURE AND ADHESIONS1

Most forms of cardiac injury are difficult or impossible to detect using radiology or ultrasound, but there are a few exceptions. The first of these is traumatic pneumopericardium, which is depicted radiographically as one or more fine, gently curved lines partially surrounding the heart that typically disappear in a day or two. Pneumopericardium may or may not be accompanied by a pneumomediastinum, but in the few cases I have observed, it has not led to a cardiac tamponade (although theoretically it might).

I previously reported a case of coronary arterial stricture following traumatic pericardial hernia in a police dog. Specifically, the ventral pericardium split open and the heart passed through the resultant defect, stopping at a point just below the circumflex coronary artery. Eventually the torn surface of the pericardium adhered to the epicardial surface, gradually shutting off the blood flow to the downstream portion of the myocardium in the process. The effect was disastrous, being similar to a heart attack in a human, and resulted in the dog’s death. Radiographically the dog was in heart failure, as indicated by cardiomegaly with left-sided emphasis, pulmonary hyperemia, and edema (Figure 57-1). Cardiac ultrasound showed dilation of the left ventri-

❚❚❚ MYOCARDIAL CONTUSION Theoretically, myocardial bruising can be seen with ultrasound but, practically speaking, is rarely diagnosed. Previously, it was believed that a well-defined interventricular notch, as seen in a lateral thoracic radiograph in a recently injured dog, supported myocardial injury, but I never have been able to confirm the specificity of this finding.

❚❚❚ TRAUMATIC PERICARDIAL HEMORRHAGE Pericardial hemorrhage is surprisingly rare, especially given the fact that dogs and cats are often forcefully stuck by motor vehicles. Perhaps the reason for this is that, when formed rapidly, even small volumes of pericardial fluid can prove fatal, compared with larger volumes, which form gradually, allowing for some measure of adaptation.

Figure 57-1 • Lateral thoracic radiograph of a dog with a traumatic pericardial hernia shows cardiomegaly, pulmonary hyperemia, and edema.

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SECTION VI ❚❚❚ The Heart

cle, a motionless septum, and poor contraction overall—findings mistakenly attributed to cardiomyopathy.

❚❚❚ PERICARDIAL ADHESIONS OBSTRUCTING CAUDAL VENA CAVA Pericarditis may affect not only the heart, but also its major feeder vessels. For example, the caudal vena cava

may become constricted at or near where it enters the right atrium, reducing blood flow and promoting thrombus formation—a combination of lesions that can often prove deadly.

Reference 1. Farrow CS: Have you ever, and if you have, would you. Vet Radiol Ultrasound 35:139, 1994.

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Pulmonary-Induced Heart Disease (Cor Pulmonale)

❚❚❚ CONCEPTUALIZING COR PULMONALE Thickening of the muscular layer of the pulmonary arteries resulting from increased vascular resistance can cause varying degrees of pulmonary hypertension, which if severe can lead to enlargement of the main pulmonary artery (MPA) and hypertrophy of the right ventricle. Because the initiating cause of the described cardiovascular abnormalities is typically diffuse lung disease, the condition is known by its Latin name, cor pulmonale, or in English, pulmonary-induced heart disease.

Congenital Cor Pulmonale Congenital lung cysts and congenital lobar emphysema have been reported to cause secondary right-sided heart enlargement (including the main pulmonary artery).1

Acquired Cor Pulmonale Chronic interstitial pneumonia has been reported to cause pulmonary hypertension, leading to MPA and RV enlargement1 (Figure 58-1).

Figure 58-1 • Close-up ventrodorsal view of the heart shows a pneumopericardium (a pair of fine curved lines lying outside the lateral heart margins). The diminished, rounded heart shape and notched lower right border are the results of a recent auto accident, fracture, and blood loss.

Reference 1. Berry CR: Answers for film reading session: 1995 A.C.V.R. annual meeting. Vet Radiol Ultrasound 36:449, 1995.

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Radiographic Evaluation of Cardiac Pacemakers

❚❚❚ BACKGROUND

❚❚❚ IMAGING FINDINGS

Cardiac pacemakers are used widely in people and sparingly in pets to correct cardiac arrhythmias and conduction disorders. Echo-Doppler is used to determine pacemaker type and settings required to optimize hemodynamic performance in many such patients. The two pacing techniques that improve cardiac function over and above that seen with ventricular demand are (1) dual-chamber pacing and (2) variable rate pacing.1 Dual-chamber pacing provides rate responsiveness and arteriovenous (AV) synchrony, whereas variable rate pacers temporarily increase heart rate to meet increased physical demand. Patients benefiting from dual-chamber pacing include those with sinus node disease or chronic atrial fibrillation. Alternatively, individuals suffering from reduced ventricular function may find rate demand pacing superior. Complications2 potentially associated with pacemaker installation include:

The tip of a cardiac pacemaker is typically positioned in the apex of the right ventricle or, if atrial pacing is desired, the coronary sinus.3 Accurate pacemaker placement can be assessed with either radiology (Figure 59-1) or ultrasound. Dual-plane imaging is mandatory irrespective of the mode of imaging.

• Electrode displacement • Broken wires • Twiddler’s syndrome: rotation of the pulse generator due to manipulation • Incorrect location

552

Caution: Magnetic resonance imaging (MRI) is generally contraindicated in patients with cardiac pacemakers.

References 1. Thoreau WA, Harrigan PH, Weyman AE: The echocardiogram in disorders of cardiac rhythm and conduction. In Weyman AE, ed: Principles and Practice of Echocardiography, ed 2. Philadelphia, 1994, Lea & Febiger. 2. Weissleder R, Rieumont MJ, Wittenberg J: Cardiac imaging. Primer of Diagnostic Imaging, ed 2. St. Louis, 1997, Mosby, p. 103. 3. Fox PR, Moise NS, et al: Techniques and complications of pacemaker implantation in four cats. J Am Vet Med Assoc 199:1742, 1991.

CHAPTER 59 ❚❚❚ Radiographic Evaluation of Cardiac Pacemakers

553

A

B Figure 59-1 • Lateral (A), lateral ultraclose (B), and ventrodorsal (C) views of the heart of a dog containing a pacemaker to treat atrial standstill. The tip of the pacemaker is situated in the right ventricle (emphasis zones in A and C), whereas the coupling element appears in the right atrium (B).

C

S E C T I O N

V I I

The Abdomen

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6 0

Abdominal Radiographic Disease Indicators The following radiographic abnormalities, radiographic disease indicators, or RDIs, are indicative of abdominal disease.

❚❚❚ PERITONEAL FLUID (INTRAPERITONEAL FLUID, PERITONEAL EFFUSION, ABDOMINAL FLUID, ASCITES) Large volumes of peritoneal fluid have two principal effects on the radiographic appearance of the abdomen: increased density and decreased detail (Figure 60-1). Medium amounts of peritoneal fluid are usually detectable radiographically, but the effects are less pronounced (Figures 60-2 and 60-3). Small quantities of peritoneal fluid often go unrecognized. As pointed out by Thrall, the extent to which the margins of the abdominal viscera become indistinct depends on the amount of abdominal fat compared with the volume of peritoneal fluid.1 The distribution of abdominal fluid and the position of the animal while being radiographed also strongly influence visceral clarity, forming the basis for postural radiography.

Types of abdominal fluid include (1) blood, (2) urine, (3) chyle, (4) transudate, and (5) exudate. The causes of peritoneal fluid are diverse, ranging from the commonplace (traumatic bladder rupture) to the obscure (peritoneal tapeworm infection).2 Broadly speaking, escaped bile, stomach juices, and unformed bowel content also fall into the category of peritoneal fluids. Possible causes of peritoneal fluid are listed in Table 60-1. In one study, Wright and co-workers calculated that the most likely causes of peritoneal fluid in cats were, in order of greatest probability, (1) cardiovascular disease (before the discovery that taurine deficiency was the primary cause of dilated cardiomyopathy in cats) and neoplasia thereafter, (2) hepatic disease, (3) renal disease, (4) feline infectious peritonitis, (5) peritonitis from a variety of other causes, and (6) urinary tract injury.3 Henley and co-workers compared the relative abilities of radiography and sonography to detect small amounts of peritoneal fluid in healthy dogs. Predictably, sonography proved more sensitive but not by a great deal (3 versus 4 mL/lb). Also as expected, the lateral radiographic projection proved 555

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SECTION VII ❚❚❚ The Abdomen

A

A

B B Figure 60-1 • A, Lateral abdominal radiograph of a dog recently struck by an automobile shows a large volume of peritoneal fluid (later determined to be blood from a ruptured liver lobe) as indicated by a combination of increased abdominal density and decreased visceral detail. B, Abdominal sonogram of the caudal abdomen shows a cross-section of an intact urinary bladder surrounded by blood.

more revealing (Table 60-2).4

than

the

ventrodorsal

view

❚❚❚ PERITONEAL AIR (PNEUMOPERITONEUM) Most dogs with readily appreciable free air in the peritoneal cavity that have not had recent abdominal surgery are likely to have a serious disease.5 Peritoneal air, like fluid, is most detectable when present in large quantities but, unlike peritoneal fluid, which obscures the abdominal viscera, peritoneal air enhances it. Medium volumes of peritoneal air may outline otherwise invisible organs, such as the diaphragm or uterus. Small amounts of peritoneal air sometimes appear as sharply marginated, triangular gas pockets interspersed among the small intestine. Mixed with fluid,

C Figure 60-2 • Lateral abdominal radiograph (A) of a bleeding hepatic hemangiosarcoma shows a vague mass immediately caudal to a gas-filled stomach. The remaining viscera are difficult to assess because of a medium volume of peritoneal fluid and visceral crowding. Abdominal sonograms show a spherical, hypoechoic intrahepatic mass (B) and a normal spleen (C).

CHAPTER 60 ❚❚❚ Abdominal Radiographic Disease Indicators

557

A

B

C

Figure 60-3 • Lateral (A) and ventrodorsal (B) abdominal radiographs of a dog with a medium volume of peritoneal fluid show increased density and decreased detail. A cranial abdominal sonogram (C) shows a portion of a liver lobe being outlined by peritoneal fluid.

free abdominal air usually appears in clusters of small bubbles (Table 60-3).

❚❚❚ INTRAVISCERAL GAS Liver Gas Filamentous gas accumulations are usually indicative of air in conduits such as blood vessels or bile ducts, whereas gas bubbles are more likely to represent a cavitated abscess. Lord and colleagues, reporting an emphysematous hepatic abscess in a dog, described the liver as containing “a bubbly accumulation of gas.”6 Sato and Solano reported a case of an acute torsion of the quadrate lobe of the liver. The displaced organ became trapped (incarcerated) between the pylorus and the hepatogastric ligament, causing it to distend with blood and eventually rupture. It later became abscessed. Radiographs showed a large gas-containing mass in the right parasagittal plane, immediately cranial and ventral to the pyloric part of the stomach.7

Gas in the Gallbladder Gas in the wall or lumen of the gallbladder (emphysematous cholecystitis) is most likely to be the result of

infection, which may be associated with necrosis and localized peritonitis. The radiographically or sonographically observed gas typically is produced by clostridial organisms.8 Alpha-hemolytic Streptococcus and Escherichia coli also were isolated from an emphysematous gallbladder unassociated with peritonitis.9 Affected dogs may or may not be diabetic.10

Splenic Gas Splenic gas usually is located in the vasculature, often as a result of torsion. Splenic gas also was reported in a dog with splenic hemangiosarcoma, ruptured gallbladder, and peritonitis. The asserted relationship was that intestinal bacteria had reached the peritoneal cavity via the necrotic gallbladder and then proceeded to colonize the cancerous spleen—producing gas in the process.11

Intestinal Gas Gas in the wall of the small intestine (pneumatosis intestinalis) is rare. In most instances, the cause of intramural gas is unknown, with ischemia, bacteria, and antigens the most commonly proposed causes. In my experience, regional or generalized intestinal dilation

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SECTION VII ❚❚❚ The Abdomen

Table 60-1 • POSSIBLE CAUSES OF PERITONEAL FLUID Possible Causes of Peritoneal Fluid

Comment

Abdominal tumor

Most abdominal tumors are discrete masses associated with one or more abdominal organs. Occasionally, large numbers of cancer cells invade the peritoneum, forming numerous small neoplastic islands on its surface and promoting the formation of peritoneal fluid. Because these tumors are often carcinomas, the disease has been termed carcinomatosis.a In cats, chylous ascites may be associated with a variety of abdominal tumors including intestinal lymphosarcoma, hemangiosarcoma, and paraganglioma of the mesenteric root.b Clinical signs often indicate the probable point of caval obstruction.c • Hind leg edema—blockage caudal to the renal veins • Kidney disease—blockage between hepatic and renal vein • Liver failure and high protein ascites—blockage cranial to the liver

Chyle Extrinsic neoplastic obstruction of the caudal vena cava (anaplastic sarcoma) Heart disease • Cardiomyopathy • Pericardial fluid • Restrictive pericarditis • Right atrial thrombus • Right atrial tumor • Tricuspid dysplasia Hepatic failure (biliary cirrhosis) with secondary hypoalbuminemia Intrinsic neoplastic obstruction of the caudal vena cava (adrenal tumor) Peritonitis • Bacterial • Chemical (urine, bile) • Parasitic • Viral (FIP) Portal hypertension Postcaval syndrome (seen in some cases of dirofilariasis) Posttraumatic caval scaring

Protein-losing enteropathy Protein-losing nephropathy Thrombosis of caudal vena cava

The radiographic combination of abdominal fluid and a possible intestinal foreign body or impaction (with or without a small volume of free peritoneal air) should prompt the consideration of intestinal perforation and peritonitis. Usually resulting from a congenital portosystemic shunt, in combination with reduced serum albumind A Budd-Chiari–like syndrome (obstruction of hepatic venous outflow causing postsinusoidal hypertension and development of ascitic fluid with a high protein concentration) has been reported in a dog six months following chest injury. At surgery the dog was found to have partial obstruction of the caudal vena cava, secondary to a ruptured pericardium with adhesions to the caudal vena cava.e Abnormalities caused by obstruction of the caudal vena cava depend on the level of obstruction. In general, the closer the blockage is to the right atrium, the more likely the development of ascites.f

FIP, Feline infectious peritonitis. a From Root CR, Lord PF: Peritoneal carcinomatosis in the dog and cat: its radiographic appearance. J Am Vet Rad Soc 12:54, 1972. b From Gores BR, Berg J, et al: Chylous ascites in cats: nine cases (1978-1993). J Am Vet Med Assoc 205:1161, 1994. c From Wallace KD, Losonsky JM: Radiographic diagnosis. Vet Rad 26:159, 1985. d From Landers EA, Mitten RW: Intrahepatic arteriovenous fistula with portosystemic communications: a case report. J Am Vet Rad Soc 19:70, 1978. e From Fine DM, Oliver NB, et al: Surgical correction of late-onset Budd-Chiari syndrome in a dog. J Am Vet Med Assoc 212:835, 1998. f From Mitten RW, Riedesel DH, Deyoung DW: Thrombosis of the caudal vena cava in a dog. J Am Vet Rad Soc 19:192, 1978.

and atony typically are not found in dogs and cats (including puppies and kittens), although this is a common early finding in premature infants suffering from necrotizing enterocolitis.12 Large flattened, cyst-like gas accumulations in the colonic wall (pneumatosis coli, pneumatosis cystoides) are usually benign and relatively harmless. Possible causes include the following:

More serious causes of pneumatosis, often characterized by a series of small bubbles or linear gas accumulations, include the following:

• Chronic obstructive pulmonary disease • Recent assisted ventilation • Iatrogenic mucosal injury resulting from a rectal tube or proctoscope • Colon or rectal surgery

Gas in the Urinary Bladder

• • • •

Intestinal infarction Deep perianal bite wounds Septicemia Severe perianal fistulas

Gas in the wall or lumen of the urinary bladder is usually the result of infection, often, but not always, occurring in diabetic dogs. Gas also may be injected

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559

Table 60-2 • CLASSIFICATION OF PERITONEAL FLUID Fluid Type

Pure Transudate

Modified Transudate

Exudate

Protein content Nucleated cell count Echogenicity

<2.5 g/dL <500-1000?mL Anechoic

~2.5 g/dL <5000/mL Anechoic/mildly echogenic

Common etiologies

Congestive heart failure Diaphragmatic hernia Hepatopathies Hypoproteinemia (proteinlosing enteropathies or nephropathies) Lymphangiectasia Lymphatic obstruction Neoplasia Portal venous obstruction Urinary tract rupture

Budd-Chiari–like syndrome Caval syndrome Chronic hepatic failure Chronic right heart failure Feline infectious peritonitis Pericardial disease

>3 g/dL >5000/mL Usually echogenic, may be complex with fibrous strands Purulent exudate Gastric perforation Incarcerated contents in a hernia Intestinal perforation Pancreatitis Penetrating wounds Steatitis Serosanguinous exudate Bile peritonitis Feline infectious peritonitis Gastric peritonitis Pancreatic peritonitis Steatitis Urine peritonitis Hemorrhagic exudate Bleeding disorder Bowel torsion Gastric torsion Ruptured tumor Splenic torsion Thrombosis Trauma

Modified from Spaulding KA: Sonographic evaluation of peritoneal effusion in small animals. Vet Radiol Ultrasound 34:427, 1993.

Table 60-3 • POTENTIAL SOURCES OF PNEUMOPERITONEUM IN THE DOG AND CAT Source of Pneumoperitoneum

Comment

Clostridial peritonitis

Usually secondary to perforation of the stomach or proximal small intestine where clostridia may normally reside Occasionally air escapes from the stomach, presumably due to increased permeability, but can also result from perforation secondary to focal or regional ischemic necrosis. Dog or cat attempts to remove. Usually poor or incorrect installation Occasionally air escapes from the bowel, presumably due to increased permeability, but can also result from perforation secondary to focal or regional ischemic necrosis. Bite wounds most commonly, gunshot or stab wound This injury is usually iatrogenic, caused by trying to force a feeding tube into a torsed stomach. Typically, the perforation occurs between the diaphragmatic opening and the cardia of the stomach and produces a large volume of peritoneal air. Cecal perforation is rare, but when it does occur it is usually the result of chronic impaction, usually with bone fragments. Presumably, intestinal perforation is pressure related, leading to ischemia, anoxia, and eventually necrosis, not simply by a sharp object piercing the bowel. Ulcerative colitis, iatrogenic colonoscope injury, overinflation of Bardex catheter (used for barium enemas); perforation attempting to extract impacted stool The intestinal blood supply is surprisingly fragile, and rather limited. Thus, a single small thrombus can lead to infarction, and in turn, perforation. Bacterial thrombi originating from an infected aortic valve (endocarditis) occasionally cause such lesions. Mesenteric avulsion, secondary to trauma, leads to a similar but larger area of devitalized bowel Perforating ulcers can be caused by certain medications such as aspirin and antiinflammatory medications. Gastric carcinomas may also become ulcerated, leading to perforation. Overly long, rigid indwelling feeding tubes can abrade the inner surface of the stomach, occasionally causing perforation. Gastropexy following torsion, if not done properly, may lead to a tear in the stomach wall, spillage of stomach contents, and peritonitis. The most common source of peritoneal air is recent abdominal surgery, in which case atmospheric contamination can persist for over a week or more, especially if the peritoneum is diseased or there is peritonitis. Ruptured lung: pneumothorax: overflow into peritoneal cavity made accessible by a diaphragmatic hernia.

Gastric torsion Incompletely sealed abdominal drain Incompletely sealed stomach tube Intestinal torsion Penetrating abdominal wound Perforated abdominal esophagus Perforated cecum Perforated colon Perforated small intestine

Perforated stomach

Recent abdominal surgery Secondary pneumomediastinum

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SECTION VII ❚❚❚ The Abdomen

inadvertently into the bladder wall during pneumocystography, especially if a rigid catheter is used. In this regard, never attempt to inject air into the bladder when there is abnormally high injection pressure. Radiographically identified intravisceral and intravascular gas (diagnostic CO2) has been reported in a cat within a few minutes of pneumoperitonography, a potentially dangerous special procedure that is rarely performed since the advent of ultrasonography. In the described case, the cat died.13 If ultrasound is not available and it is decided to perform diagnostic peritonography, an appropriate organic iodine solution should be considered instead of air. Bear in mind, however, that such contrast media will produce a transient increase in abdominal fluid and a corresponding degree of dehydration.14

Figure 60-4 • Lateral abdominal radiograph of a healthyappearing 15-year-old dog with a fatty liver. The wire fragments are incidental.

Uterine Gas Uterine gas (physometra) most often is identified in dogs with open pyometra, the result of retrograde atmospheric contamination owing to an incompetent cervix. Uterine gas also may be seen in conjunction with a dead fetus but only rarely with infection.

Retroperitoneal Air The most common cause of retroperitoneal gas is deep wounds. Atmospheric gas usually reaches the retroperitoneal space indirectly, first entering the deep fascial planes of the neck, chest, and abdomen and then proceeding to the retroperitoneal space. Gas also may reach the retroperitoneal space via the deep fascial planes of the neck and the mediastinum following a deep throat wound. In a similar fashion, gas may migrate to the retroperitoneal space from deep perianal bite wounds. Occasionally, gas enters the mediastinum subsequent to an intrapulmonary or bronchial rupture and then enters the retroperitoneal space. Gas occasionally enters the retroperitoneal space as a result of penetrating bite wounds, but this is unusual. Rarely, gas enters the retroperitoneal space through a draining sinus, the result of a suture abscess following spaying or a nephrectomy. I also have seen retroperitoneal gas after surgical repair of a torn bladder neck or ureteral transplant. To reiterate: The discovery of retroperitoneal air should prompt an immediate search for its source. High-probability sites of origin include the pharynx, larynx, trachea, bronchi, and lung. Air also may enter the retroperitoneum via deep perianal wounds as well as some rectal or vaginal tears.

❚❚❚ RETROPERITONEAL FLUID In recently injured dogs and cats, especially those with caudal rib fractures (indicating the force of the blow), the primary sources of retroperitoneal fluid are blood

Figure 60-5 • Close-up lateral view of the cranial abdomen of a dog with an enlarged liver resulting from lymphosarcoma.

from a ruptured or avulsed kidney and urine from a torn or avulsed ureter. Obviously, a combination of the two fluids is also possible. Occasionally, a ureteral stone blocks, dilates, and subsequently perforates the ureter, causing a uroretroperitoneum. Less common sources of retroperitoneal fluid include infection following a penetrating wound and iatrogenic hemoretroperitoneum following unsuccessful transabdominal cystocentesis.

❚❚❚ INCREASED ORGAN SIZE Increased organ size is not always a reliable indicator of disease, for example, a fatty liver (Figure 60-4), but neither should hepatomegaly be dismissed, as exemplified by this case of lymphosarcoma (Figure 60-5). When enlargement is combined with deformity, however, the probability is much greater that serious disease is present.

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Figure 60-6 • Close-up lateral view of the cranial abdomen of a dog with a small liver due to a congenital liver shunt.

❚❚❚ DECREASED ORGAN SIZE

Figure 60-7 • Close-up lateral projection of the liver of a dog with dystrophic calcification of the bladder wall secondary to chronic catheter abrasion (emphasis zone).

Like organomegaly, diminished organ size cannot always be construed as certain evidence of disease, although it may, as in this case of hepatic dysplasia, result from a portacaval shunt (Figure 60-6). Chronic disease, especially of the liver, can lead to cirrhosis, typified by shrinkage and an irregular contour.

❚❚❚ ABDOMINAL CALCIFICATION Calcification may be found anywhere in the abdomen: individual organs, the mesentery or omentum, blood vessels, or peritoneal cavity. Etiologic considerations are best based on a combination of (1) lesion configuration, (2) lesion location, (3) knowledge of related diseases known to be associated with calcification in that locale, and (4) past medical and surgical history. Intraabdominal calcification is usually due to one of three causes: (1) tissue death or dystrophic calcification (Figure 60-7), (2) metabolic disorders resulting in metaplastic calcification (Figure 60-8), and (3) some types of cancer. Furthermore, calcification may occur in the walls of cysts or in the tissue surrounding a peritoneal foreign body (Figure 60-9). Stones (calculi) may form in the kidneys (Figure 60-10), ureters, or urinary bladder. Bone fragments are regularly identified in the stomach and intestine of dogs, with cats being more inclined toward the skeletal remnants of birds and mice. Some medications, in particular enteric protectants, can mimic mucosal mineralization, as can the denser sediments of sandy soils. Gallstones are extremely rare in dogs and cats. Calcification associated with the caudal aspects of the costochondral junctions can resemble gallstones (Figure 60-11), while nipples projected end-on can mimic intestinal foreign bodies, and calculi in the urinary tract (Figure 60-12). Sources of organ calcification are listed in Table 60-4.

Figure 60-8 • Ventrodorsal view of the abdomen of a dog with metaplastic calcification of the stomach wall.

Alternatively, a lesion-specific approach can be used (Table 60-5) in which the morphologic features of a specific calcific lesion are used to categorize it as a (1) stone (concretion), (2) conduit (a tubular structure through which fluid runs), (3) cyst, or (4) mass. For further graphic examples of abdominal mineralizations, see the article by Lamb and colleagues.15 Artifactual mineralization, in the form of spilled contrast solutions (Figure 60-13), some medicaments, and wet hair are also potential sources of misdiagnosis (Table 60-6).

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SECTION VII ❚❚❚ The Abdomen

A

Figure 60-10 • Close-up ventrodorsal radiograph of the renal fields of a dog shows bilateral kidney stones (emphasis zones).

that can serve as the circumstantial basis for a diagnosis. In this regard, it is of interest to note that as the availability of abdominal ultrasound has increased, the ability of many veterinarians to diagnose abdominal films has decreased. Presumably this is because less time is being spent trying to interpret abdominal radiographs knowing that a subsequent ultrasound examination will likely reveal any abnormalities.

❚❚❚ ABNORMAL BOWEL DISTRIBUTION PATTERN B Figure 60-9 • Lateral (A) and ventrodorsal (B) views of a calcified, peanut-shaped mass located in the ventral aspect of the caudal abdomen, the result of a surgical sponge fragment inadvertently left in the abdomen following a spay.

❚❚❚ ABDOMINAL MASSES Most abdominal masses, especially cancers, develop within existing viscera, causing enlargement or deformity in the process. Hollow organs such as the stomach, intestine, and urinary bladder may resemble masses when they become extremely enlarged, a phenomenon known as a mass effect (Figures 60-14 and 60-15). Root advocated a systematic approach to the radiographic diagnosis of abdominal masses in dogs and cats.16 Root’s methods are quite straightforward; they emphasize how neighboring organs accommodate the spatial demands of a developing mass by virtue of their predictable displacement, positional rearrangements

I have described a strategy for diagnosing abdominal masses in the preceding section. For the most part, it focused on identifying abdominal masses based on the relative positions of the surrounding organs. Although this is an excellent method, it can be enhanced by placing greater emphasis on the behavior of the surrounding intestine, or more particularly, its pattern of distribution. Such patterns are often organ specific, thus allowing an observer to incriminate or exclude a particular organ as the source of an observed abdominal mass. Figure 60-16 illustrates the abnormal bowel distribution that is most often associated with acute splenic torsion.

❚❚❚ VISIBLE ABDOMINAL LYMPH NODES Pugh mapped and described the sonographic appearance (including normal variations) of the abdominal

CHAPTER 60 ❚❚❚ Abdominal Radiographic Disease Indicators

563

Figure 60-11 • Close-up lateral view of the caudoventral aspect of the rib cage of a dog shows metaplastic calcification of the costochondral junctions (emphasis zone), a frequent normal finding in dogs.

Figure 60-13 • Close-up view of the caudoventral abdomen of a dog undergoing retrograde urethrography shows contrast spillage cranial to the penis, appearing as multiple, wispy, medium gray strands.

Figure 60-12 • Ventrodorsal view of the abdomen shows regularly spaced, similar sized, spherical opacities in both the right and left parasagittal planes. These are nipples, which because of their perpendicular projection from the surface of the abdomen and their being surrounded by air on all but one side, appear with a radiographic density comparable to bone.

lymph nodes in the dog.17 Additionally, a primary lymphatic drainage scheme was developed, indicating the relationship between the regional nodes and the organs they drain. For organizational purposes, lymph nodes were grouped into lymphocenters according to their primary afferent drainage.

Lymphocenters of the Abdominal Viscera and Abdominal/Pelvic Wall of the Dog Visceral Nodes. Cranial mesenteric lymphocenter Jejunal lymph nodes Colic lymph nodes Right colic Middle colic Caudal mesenteric lymphocenter Caudal mesenteric lymph nodes (left colics) Celiac lymphocenter Hepatic lymph nodes Splenic lymph nodes Gastric lymph node (variably present) Pancreaticoduodenal lymph nodes

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SECTION VII ❚❚❚ The Abdomen

Table 60-4 • SOURCES OF ORGAN CALCIFICATION Calcified Organ or Appearance of Calcified Organ

Disease or Other Explanation

Adrenal gland Gallbladder Intestine

Tumor (especially pheochromocytoma) Gallstone, calcified wall (porcelain gallbladder) Bone fragments, some medications, some foreign bodies or materials, diagnostic opaque (barium, iodine) Kidney stone, renal calcification, tumor, residual iodine following urography Gallstone, cyst, abscess, hematoma, tumor Chronic infection Chronic infection (especially of fat), idiopathic nodular fat necrosis, enveloped surgical sponge Chronic pancreatitis, cyst or tumor, peripancreatic inflammation Calcified surgical sponge, calcified internal (intestine) or external (abdominal wall) foreign body, chronic sinus tract, leaked barium or surgical talcum powder Prostatitis, tumor, stone from urinary tract, residual iodine following urography or cystography Abscess, hematoma, tumor, regenerative nodule Uremia, chronic infection, bone fragments, some medications, some foreign bodies or materials, diagnostic opaque (barium, iodine) Ureteral stone Bladder stone, dystrophic calcification following catheter injury, tumor, residual iodine following urography, cystography, or urethrography Pregnancy (6 wks or more), fetal remnant, uterine body remnant

Kidney Liver Lymph node Omentum and mesentery Pancreas Peritoneal cavity Prostate Spleen Stomach Ureter Urinary bladder Uterus

Modified from Bromel C, Smeak DP, Leveille R: Abdominal calcification in the dog. J Am Vet Med Assoc 213:1137, 1999.

Table 60-5 • A MORPHOLOGIC APPROACH TO THE IDENTIFICATION OF ABDOMINAL CALCIFICATION IN THE DOG AND CAT Lesion Feature

Stone

Conduit

Cyst

Mass

Border

Smooth

Smooth

Irregular

Margin Matrix

Continuous Usually homogeneous

Smooth or irregular Usually continuous None

Continuous Less dense

Shape

Oval or round, excepting some kidney stones

Tracklike (in long section) and circular in cross section

Oval or round

Interrupted Heterogeneous, featuring a wide variety of patterns: speckled, mottled, whorled, streaky, hatched Varied

Table 60-6 • SOURCES OF ARTIFACTUAL OR PSEUDOMINERALIZATION Source of Pseudomineralization

Comment

Engorged ticks

Engorged ticks may become quite large and protrude well off the skin surface, resulting in a surprisingly dense, radiographic cross-section. Clumps of hair are capable of producing cloudlike abdominal densities, which if extensive enough, can resemble abdominal fluid, peritonitis, or in extreme cases, a mass.

Matted, dirty hair Muddy hair Nipples Radiographic contrast media on hair: barium paste, liquid barium, and diagnostic iodine solution Small skin tumors Some medicaments, including intestinal protectants Twigs or bush fragments caught in hair Wet hair

Muddy hair can appears as linear, band-like, or blotchy surface densities depending on the combination of hair and mud. Surrounded on all but one side by air, thoracic nipples may resemble lung metastases. The resultant artifacts are quite variable, depending mostly on the amount of barium and the extent to which it disperses within the hair coat. Thickness and the extent to which the tumor projects from the skin surface determine visibility. Generally, such densities are faint. These artifacts can be surprisingly varied, ranging from nearly imperceptible to strikingly dense. Wet hair usually produces streaky linear densities.

Modified from Britt LG, Barbee DD, et al: Engorged ticks appearing as distinct radiographic opacities. Vet Radiol Ultrasound 41:145, 2000.

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565

A A

B Figure 60-14 • Lateral abdominal radiograph (A) of a dog that began vomiting 3 days earlier shows a gas- and fluid-distended small intestine and a spherical object in the caudal abdomen. A close-up compression view (B) revealed an oddly shaped mass immediately ventral to the colon that later proved to be a piece of hard rubber obstructing the distal part of the small intestine.

B Figure 60-15 • Lateral abdominal radiograph (A) of a vomiting dog shows a cigar-shaped mass in the ventral part of the cranial abdomen (emphasis zone) and a lumpy, right-sided spherical mass in the opposite view (B), which was eventually found to be a rubber toy lodged in the proximal duodenum. In the ventrodorsal projection, the kidney can be seen faintly superimposed on the center of the dilated intestine, creating the illusion of a second mass.

Figure 60-16 • Close-up lateral view of the central abdomen of a dog with a splenic torsion shows most of the intestine displaced into the caudal abdomen and a secondarily displaced, dilated fluid- and air-filled stomach. Part of the spleen can be seen in the bottom center of the photograph to the immediate left of the gas-filled bowel.

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SECTION VII ❚❚❚ The Abdomen

Parietal Nodes (Abdominal and Pelvic Walls). Lumbar lymphocenter Lumbar aortic lymph node Renal lymph nodes Iliosacral lymphocenter Medial iliac lymph nodes (external iliac nodes) Sacral lymph nodes (variably present) Hypogastric lymph nodes (internal iliac nodes)

❚❚❚ ADDITIONAL CONSIDERATIONS IN THE DIAGNOSIS OF ABDOMINAL DISEASE Acute Abdominal Colic Acute abdominal pain regularly accompanies a variety of diseases in dogs and cats, although the term colic is not widely used by small animal veterinarians. This is in marked contrast to equine veterinarians, who regularly use the terms colic or colicky to describe horses with painful abdomens. Ljunggren published a schedule of abdominal disorders that potentially produce colic in dogs (Box 60-1).18

❚❚❚ COMPUTED TOMOGRAPHIC APPEARANCE OF THE NORMAL CANINE ABDOMEN Smallwood and George described the computed tomographic (CT) appearance of the Beagle abdomen in a pair of publications.19,20 Samii and co-workers provided the same information for the cat.21 These publications are highly recommended for those desiring a better understanding of the normal cross-sectional anatomy of the dog and cat as depicted by CT.

❚❚❚ MAGNETIC RESONANCE APPEARANCE OF THE NORMAL CANINE ABDOMEN

B o x

6 0 - 1

Diseases Causing Acute Abdominal Colic Liver

Cholelithiasis Acute hepatitis Liver trauma Stomach and Bowel

Gastric foreign body Gastric torsion Intestinal obstruction: foreign body, tumor, intussusception, incarceration, volvulus, intestinal necrosis from trauma, stool impaction (coprostasis) Pancreas

Acute pancreatitis (including localized peritonitis) Pancreatic trauma Spleen

Ruptured hemangiosarcoma Traumatic rupture Splenic torsion Urinary Tract

Traumatic kidney rupture Ureteral calculi Ureteral abscess Ruptured urinary bladder Urethral rupture Female Reproductive Tract

Endometritis Pyometra Uterine rupture Uterine torsion Male Reproductive Tract

Samii and co-workers have also described the normal magnetic resonance imaging (MRI) appearance of the feline abdomen, correlating it with the normal crosssectional anatomy of cadavers.22

Prostatitis Prostatic abscess Testicular torsion

❚❚❚ RELATIVE SIGNAL STRENGTHS EMITTED BY THE ABDOMINAL ORGANS OF HEALTHY CATS

Intraabdominal segment of the esophagus Stomach (including gastric ulcer) Small intestine (including duodenal ulcer) Cecum and colon (including colonic ulcer) Gallbladder Urinary tract Prostatic abscess Uterus

Newell and colleagues described what they refer to as quantitative MRI of the cranial abdomen of healthy cats.23 On T1 images, the epaxial muscle had the lowest signal intensity, followed by the renal medulla, spleen, renal cortex, pancreas, liver, and fat. On T2 images, epaxial muscles had the lowest signal intensity, followed by liver, spleen, fat, and gallbladder lumen.

Diffuse Peritonitis Secondary to Perforation or Rupture

Modified from Ljunggren LV: The radiological diagnosis of some acute abdominal disorders in the dog. J Am Vet Rad Soc 5:5, 1964.

CHAPTER 60 ❚❚❚ Abdominal Radiographic Disease Indicators

Abdominal Applicability Muleya and co-workers studied the use of low-fieldstrength MRI in a small series of dogs with abdominal tumors, concluding that MRI was comparable to images obtained with ultrasound.24 Their specific comments regarding abdominal MRI were as follows: • Most (but not all) tumors appeared dark (hypointense) on T1 and light (hyperintense) on T2 images compared with normal parenchyma. • Sometimes MRI was better able to resolve the edges of a tumor compared with ultrasound. • Splenic tumors were difficult to detect with MRI because of the similarity between tumor and normal tissue. • The pancreas enjoys signal intensity comparable to that of the intestine, making it difficult to distinguish between the two. • A primary renal tumor in one kidney and metastasis in the opposite kidney appeared hypointense in both T1 and T2. • MRI was able to clearly identify a caudal sublumbar melanoma that extended into the pelvic canal. The following were some technical considerations related to abdominal MRI: • Respiratory and bowel motion (peristalsis) degrade image quality but can be overcome by physiologic gating. • A strong signal is emitted by subcutaneous tissue, which also can be dealt with by gating. • The stomach and especially the bowel can mask adjacent lesions. • Intravenous injection or oral administration of contrast media improves lesion contrast

❚❚❚ PHYSICAL REVERSAL OF THE ABDOMINAL VISCERA Reversal of the abdominal organs so that those normally on the right are located on the left and those on the left are located on the right is a congenital anomaly that may or may not affect the health of the affected individual. The former instance, situs inversus, as it is known in Latin, is found in conjunction with sinusitis and bronchiectasis, disorders emanating from defective ciliary transport, and is termed Kartagener syndrome, after its initial descriptor. Reversal of the abdominal viscera may be incidental, however, and carries no clinical consequences.25

References 1. Thrall DE: Intraperitoneal vs. extraperitoneal fluid. Vet Radiol Ultrasound 33:138, 1992. 2. Crosbie PR, Boyce WM, et al: Diagnostic procedures and treatment of eleven dogs with peritoneal infections caused by Mesocestoides spp. J Am Vet Med Assoc 213:1578, 1998.

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3. Wright KN, Gompf RE, DeNovo RC: Peritoneal effusion in cats: 65 cases (1981-1997). J Am Vet Med Assoc 214:375, 1999. 4. Henley RK, Hager DA, Ackerman N: A comparison of two-dimensional ultrasonography and radiography for the detection of small amounts of free peritoneal fluid in the dog. Vet Rad 30:1321, 1989. 5. Lonsdale RA, Richardson JL: Pneumoperitoneum and gastric perforation in a minimally clinically affected dog. Vet Radiol Ultrasound 40:120, 1999. 6. Lord PF, Carb A, et al: Emphysematous hepatic abscess associated with trauma, necrotic nodular hyperplasia and adenoma in a dog: a case history report. Vet Rad 23:46, 1982. 7. Sato AF, Solano M: Liver lobe entrapment and associated emphysematous hepatitis. Vet Radiol Ultrasound 39:123, 1998. 8. Hawe RS: What is your diagnosis? J Am Vet Med Assoc 197:1653, 1990. 9. Lord PF, Wilkins RJ: Emphysema of the gall bladder in a diabetic dog. J Am Vet Rad Soc 13:49, 1972. 10. Burk RL, Johnson GF: Emphysematous cholecystitis in the nondiabetic dog: three case histories. Vet Rad 21:242, 1980. 11. Ramirez O: What is your diagnosis? J Am Vet Med Assoc 214:625, 1999. 12. Weissleder R, Rieumont MJ, Wittenberg J: Primer of diagnostic imaging, 2nd ed, St Louis, 1997, Mosby. 13. Childers HE: What is your diagnosis? J Am Vet Med Assoc 203:508, 1993. 14. Rendano VT: Positive contrast peritonography: an aid in the radiographic diagnosis of diaphragmatic hernia. J Am Vet Rad Soc 20:66, 1979. 15. Lamb CR, Kleine LJ, et al: Diagnosis of abdominal calcification on abdominal radiographs. Vet Rad 32:211, 1991. 16. Root CR: Abdominal masses: the radiographic differential diagnosis. J Am Vet Rad Soc 15:26, 1974. 17. Pugh CR: Ultrasonographic examination of abdominal lymph nodes in the dog. Vet Radiol Ultrasound 35:110, 1994. 18. Ljunggren LV: The radiological diagnosis of some acute abdominal disorders in the dog. J Am Vet Rad Soc 5:5, 1964. 19. Smallwood JE, George TF: Anatomic atlas for computed tomography in the mesaticephalic dog: thorax and cranial abdomen. Vet Radiol Ultrasound 34:65, 1993. 20. Smallwood JE, George TF: Anatomic atlas for computed tomography in the mesaticephalic dog: caudal abdomen and pelvis. Vet Radiol Ultrasound 34:143, 1993. 21. Samii VF, Biller DS, Koblik PD: Normal cross-sectional anatomy of the feline thorax and abdomen: comparison of computed tomography and cadaver anatomy. Vet Radiol Ultrasound 39:504, 1998. 22. Samii VF, Biller DS, Koblik PD: Magnetic resonance imaging of the normal feline abdomen: an anatomic reference. Vet Radiol Ultrasound 40:486, 1999. 23. Newell SM, Graham JP, et al: Quantitative magnetic resonance imaging of the normal feline cranial abdomen. Vet Radiol Ultrasound 41:27, 2000. 24. Muleya JS, Taura Y, et al: Appearance of canine abdominal tumors with magnetic resonance imaging using a low field permanent magnet. Vet Radiol Ultrasound 38:444, 1997. 25. Choi M, Hwang G, et al: Radiographic diagnosis: situs inversus of abdominal organs in a dog. Vet Radiol Ultrasound 42:423, 2001.

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Abdominal Wall Injury, Infection, and Tumor

❚❚❚ BRUISING AND HEMATOMA Abdominal wall bruising typically appears as a diffuse, nondescript swelling that often obscures or eliminates individual muscle layers, the so-called abdominal belly stripes. Such swelling is diagnostically useful insofar as it often coincides with the point of impact in the case of an animal that has been struck by an automobile, warranting especially close inspection of the immediately underlying viscera for further evidence of injury. Hematomas of the abdominal wall, like most such lesions, undergo a gradual and predictable series of changes from their creation to their eventual demise. Most develop immediately beneath the skin or between muscle layers. True intramuscular hematomas are rare. Those that are located just under the skin may persist for some time or in some instances become larger, owing to serum supplementation by nearby damaged tissues. These hybrid serohematomas (as I prefer to term them) appear as large fluctuant surface masses and have a uniform lacy appearance sonographically. Intermuscular hematomas are often short-lived because of their rapid indirect breakdown and dispersal by the compressive effect of the bordering muscle. Intramuscular hematomas are usually quite small but, as with all such compressive lesions, require early regular surveillance, lest they lead to ischemic myolysis.

❚❚❚ POSTOPERATIVE EVALUATION Normally healing and infected incision sites potentially share a number of common sonographic features, including (1) fluid pockets, with and without associated far-field enhancement; (2) abnormal muscle pattern (“disrupted muscle fibers”); and (3) gas pockets. Ultrasound-guided fluid sampling is recommended as the best means of discriminating between infection and 568

inflammation. Hematomas can be confirmed in a similar manner.1

❚❚❚ TRAUMATIC DISRUPTION (ABDOMINAL HERNIA) Full-thickness tearing of a portion of the abdominal wall may allow extrusion of abdominal content, an injury that is often termed an abdominal hernia. In such circumstances, a radiographic diagnosis may be based on what is seen outside the abdomen or, alternatively, what is not seen inside the abdomen. For example, when one or more gas-filled intestinal segments lie between the abdominal wall and skin, they usually appear as distinctive dark bands or spheres and as such are readily recognized (Figure 61-1).2 A gas-filled stomach located outside the margins of the abdominal silhouette is even more striking.3 By way of contrast (or more to the point, a lack of it), many inguinal hernias containing fluid-filled bowel show only as a bulging groin (Figure 61-2).

❚❚❚ PENETRATING WOUND Gunshots Background. Exploratory laparotomy has been advocated for all dogs and cats with abdominal gunshot wounds based on the high potential for serious visceral injury and secondary complications, such as bacterial or chemical peritonitis and intractable hemorrhage.4 High-volume peritoneal lavage, followed by sample retrieval and cytologic/bacteriologic analysis, also has been recommended as a relatively noninvasive means of determining whether the stomach or bowels have been punctured. Imaging Findings. Abdominal gunshot wounds are most easily recognized when a bullet, pellet, or shot is

CHAPTER 61 ❚❚❚ Abdominal Wall Injury, Infection, and Tumor

569

A A

B Figure 61-2 • Lateral (A) and ventrodorsal (B) radiographs of a dog with a ventrolateral abdominal hernia: Unlike the dog in Figure 61-1, where the herniated bowel is immediately recognizable because of its gas content, the fluid-filled bowel in this dog provides no hint as to its true nature.

B Figure 61-1 • Lateral (A) and ventrodorsal (B) radiographs of a cat with a caudal ventrolateral abdominal hernia show elements of both the small and large intestine located outside the body wall.

present. In general, higher-velocity bullets pass completely through the abdomen, leaving spilled bodily fluids or free air in their wake. Resultant peritonitis may be bacterial or chemical. Transabdominal aspiration or combined lavage/aspiration may indicate which is the case. Both low- and high-velocity bullets typically leave small circular entry wounds, resembling those left by a biopsy punch.

❚❚❚ DRAINING ABDOMINAL SINUSES Nonabsorbable sutures (silk, nylon, cotton, polyester) remaining from a previous ovariohysterectomy are the most common cause of abdominal draining sinuses.

Other sources of sinus formation and drainage include (1) bacterial and fungal infections; (2) foreign bodies, such as plant awns, porcupine quills, pieces of wood, wooden splinters, and surgical sponges; and (3) some types of tumor.5-7 As discussed earlier, sinography is the optimal means of evaluating a draining sinus. Ultrasound usually provides considerably less information about the sinus tract but is very useful in a contextual sense because it allows a detailed assessment of the surrounding tissues and organs. Sinography will usually establish whether or not there is fistulation, organ effacement, or filling defects suggesting a foreign body. Additionally, sinography will create a detailed “map” of the sinus system and its points of communication (Figures 61-3 and 61-4).

❚❚❚ MUSCLE AVULSION Avulsion of part of the abdominal wall from the caudolateral rib cage occurs most commonly in cats

570

SECTION VII ❚❚❚ The Abdomen

A

Figure 61-3 • Peritoneal abscess: Lateral sinogram centered over the cranioventral aspect of the abdomen shows a complex network of communicating channels extending from the caudal edge of the liver to the cranial edge of the spleen. The air-filled catheter cuff is partially visible lying in a pool of contrast solution just beneath the skin.

and may be associated with a paracostal hernia. Avulsion of the prepubic tendon from the cranioventral aspect of the pelvic canal, with or without visceral displacement, is more common in dogs (Figure 61-5).

❚❚❚ ABSCESS In my experience, most abdominal wall abscesses are related to foreign bodies or surgical infections. Abscesses are radiographically nonspecific, appearing as a localized swelling and affecting the visibility of the belly stripes according to the depth of the lesion. B

❚❚❚ EXTRAABDOMINAL TUMOR Tumors of the abdominal wall usually visibly distort or destroy the muscle in which they grow; but extraabdominal tumors, such as lipomas, typically displace the adjacent muscle, features that are readily appreciable using a high-frequency ultrasound scanner. Some extraabdominal tumors, such as hemangiosarcomas, appear to erase the belly stripes when imaged radiographically, but when ultrasound was done, show only inward displacement of the abdominal muscles. In this later regard, an extraabdominal tumor, such as a hemangiosarcoma, can be mistaken for a hematoma or abscess (Figure 61-6).

Figure 61-4 • Deep suture abscesses: Lateral sinogram (A) with close-up (B) of an elaborate network of communicating channels that join encapsulated foreign bodies, appearing as oblong filling defects, to a large subsurface contrast-filled cavity.

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571

A A

B Figure 61-5 • A, Lateral radiograph of the caudal abdomen of a dog with an avulsion fracture of the prepubic eminence and rupture of the prepubic tendon. B, The displaced fracture fragment appears as a small irregularly shaped bone fragment superimposed on the upper edge of the forward-most femur.

References 1. Trout NJ, Penninck DG, et al: Early postoperative ultrasonic evaluation of incisional sites in dogs: 15 cases (1990-1992). J Am Vet Med Assoc 205:1565, 1994. 2. Henry CJ: What is your diagnosis? J Am Vet Med Assoc 201:1773, 1992. 3. Corn L: What is your diagnosis? J Am Vet Med Assoc 212:957, 1998. 4. Fullington RJ, Otto CM: Characteristics and management of gunshot wounds in dogs and cats: 84 cases (1986-1995). J Am Vet Med Assoc 210:658, 1997. 5. Matteucci ML, Spaulding K, et al: Intra-abdominal wood foreign body. Vet Radiol Ultrasound 40:513, 1999. 6. Zeltsman PA, Downs MO, Girard EM: What is your diagnosis? J Am Vet Med Assoc 212:193, 1998. 7. Murphy ST, Newell SM, Burrows CE: What is your diagnosis? J Am Vet Med Assoc 212:196, 1998. 8. Lamb CR, White RN, McEvoy FJ: Sinography in the investigation of draining tracts in small animals: retrospective review of 25 cases. Vet Surg 23:129, 1994.

B Figure 61-6 • A, After it collapsed, this dog was hospitalized, radiographed, and diagnosed by the resident on emergency duty as having an enlarged spleen, probably a bleeding hemangiosarcoma. B, A subsequent ultrasound examination showed a large, cavitated mass lying along the left flank, outside the body wall. The biopsy diagnosis was extraabdominal hemangiosarcoma. Also noteworthy was that fact that the dog had been operated on earlier for what was presumptively diagnosed as an arteriovenous fistula in the same location. The resident had not reviewed the medical record, nor had the owner mentioned the previous surgery.

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6 2

Peritonitis

❚❚❚ CHEMICAL PERITONITIS Chemical peritonitis results from the leakage of bile or urine into the peritoneal cavity (Figure 62-1). Strictly speaking, leakage of pancreatic enzymes secondary to pancreatic inflammation or injury is also a form of chemical peritonitis, although generally it is confined to the tissues immediately surrounding the pancreas. Theoretically, the leakage of stomach or bowel content also may be considered a type of chemical peritonitis, although bacterial peritonitis is probably a more appropriate designation (see later discussion).

❚❚❚ BACTERIAL PERITONITIS Leakage from the abdominal portion of the esophagus, stomach, intestine, or an abscessed prostate is the usual source of bacterial peritonitis. Deep bite wounds are another potential source of bacterial peritonitis, especially in cases in which one or more large dogs attack a smaller one. Likewise, cats often sustain multiple penetrating wounds to both pleural and peritoneal cavities after being mauled by one or more large dogs. Other sources of bacterial peritonitis include (1) ischemic perforation secondary to prolonged intussusception (Figure 62-2), (2) ischemic perforation following bone impaction or another kind of intestinal foreign body, and (3) perforation resulting from mesenteric emboli due to aortic endocarditis.

❚❚❚ FELINE INFECTIOUS PERITONITIS Background Feline infectious peritonitis (FIP) is a fatal infectious disease of young cats caused by coronavirus, which affects wild cats (cougars, lions, cheetahs, jaguars, bobcats, and lynx) as well as domestic cats. Immune572

mediated vasculitis is the core pathology of FIP, which manifests itself systemically in one of two ways: an effusive or “wet” form and a noneffusive or “dry” form. The effusive form of the disease outnumbers the noneffusive form by nearly 3 : 1. A fibrinous pleuritis or peritonitis characterizes the effusive form of the disease, often accompanied by large volumes of pleural or peritoneal fluid. Pyogranulomas of the abdominal viscera, lungs, nerve tissues, and eyes characterize the noneffusive form of the disease. The signs of FIP are nonspecific, including fever, vomiting, diarrhea, weakness, pale mucous membranes, and loss of appetite. Medium and large abdominal fluid accumulations cause abdominal distension; similar fluid build-ups in the chest hamper breathing. The pyogranulomatous form of the disease may cause a particular organ or organ system to malfunction, but not in any characteristic way. Histologic examination is the most reliable means available for definitive diagnosis.1

Imaging Findings The radiology of FIP is nonspecific and highly variable, ranging from normal to massive fluid distension of the abdomen. Sonographically, the effusive form of the disease is characterized by abdominal fluid, fibrin, and adhesions. In some instances, the small intestine becomes tightly bunched, resembling a fixed linear foreign body.2 Currently, I see very little FIP in my practice.

❚❚❚ STEATITIS Background Steatitis (yellow fat disease) is a comparatively rare dietary disease of cats in which the intraabdominal fat initially becomes inflamed and later becomes

CHAPTER 62 ❚❚❚ Peritonitis

Figure 62-1 • Lateral abdominal radiograph of a dog recently struck by a car shows increased abdominal density and decreased visceral detail caused by a large volume of urine that had leaked from a ruptured bladder.

necrotic. The disease is caused by diets that contain an excessive amount of fish, particularly red tuna. Clinically steatitis is characterized by fever, lack of appetite, lethargy, abdominal pain (especially on palpation), and an elevated white cell count.

Imaging Findings The radiographic disease indicators of steatitis are nonspecific, resembling a small to medium volume of peritoneal fluid. They include increased abdominal detail

573

Figure 62-2 • Peritonitis secondary to a perforated ileocolic intussusception: Lateral abdominal radiograph of a dog shows enlargement, increased density, an absence of detail, and multiple gas-distended bowel segments.

(regional or generalized) and increased abdominal density. In general, the fatter the cat, the more pronounced the described radiographic abnormalities.3

References 1. Everman JE, Henry CJ, Marks SL: Feline infectious peritonitis. J Am Vet Med Assoc 206:1130, 1995. 2. Barr F: Feline infectious peritonitis. J Small Anim Pract 39:501, 1998. 3. Root CR: Steatitis in cats: its radiographic appearance. J Am Vet Rad Soc 12:60, 1971.

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Using Vascular Maps to Navigate the Abdomen

Spaulding produced a prodigious paper on the sonographic navigation of the interior abdomen using the vascular system.1 With the thoroughness of a textbook chapter, the author illustrates (literally and figuratively) how to use the abdominal vasculature to locate hard-to-find organs such as the abdominal esophagus, pancreas, adrenal glands, and mesenteric lymph nodes. Like many good ideas, the concept behind this work is deceptively simple: Abdominal blood vessels can be used to locate nearby organs. Most of us are inclined to do it the other way around, that is, find the organ and

574

then the adjacent vessel. My point is that, by learning Spaulding’s vascular navigational method, which is clearly more difficult than a traditional organ-based approach, one can develop an integrated style that is more versatile than either of the other techniques used alone.

Reference 1. Spaulding KA: A review of sonographic identification of abdominal blood vessels and juxtavascular organs. Vet Radiol Ultrasound 38:4, 1997.

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6 4

Liver Disease

❚❚❚ RADIOLOGY OF THE LIVER Accurately judging liver size in dogs is hazardous business. Although it is conceded that marked departures from the norm are easily recognized—liver dysplasia in dogs with congenital hepatic shunts or lymphocytic engorgement in lymphoma—less pronounced alterations are more difficult or even impossible to appreciate. Some factors that can affect the estimation of liver size include the following: • • • • • • • • •

Radiographic projection X-ray beam centering Radiographic technique Splenic clarity Phase of respiration Stomach contents Obesity Age Concomitant disease, especially Cushing disease

Liver size is much easier to assess in recumbent lateral than in ventrodorsal or dorsoventral projections. The standing lateral position is best, but most veterinarians are unfamiliar with this view. As with any curved surface, the caudal liver margins are easier to estimate in lighter rather than in darker images, where edges are typically less well defined. Because the spleen may lie in close contact with the caudoventral edge of the liver (as seen in lateral view), the two organs may be indistinguishable from one another, resulting in an overestimation of liver size. Thus, the clearer the spleen, the less likely it will be mistaken for part of the liver. During full inspiration, the caudal liver margin will be positioned more caudally than during exspiration. This effect is more pronounced in lateral than in ventrodorsal views. Much of the caudal liver margin is defined by the adjacent stomach; accordingly, the fuller the stomach, and the more visible its

contents, the easier it is to outline the caudal reaches of the liver. As a generality (but no more) the older a dog is, the larger its liver. This is due to at least four factors: (1) the livers of older dogs tend to be fatty and thus are actually larger; (2) the hepatic ligaments of older dogs stretch with age, resulting in greater caudal displacement; (3) the muscle tone of older animals is often reduced, causing the abdomen to be more pendulous and, accordingly, the liver is positioned more caudally than usual; and (4) older animals tend to exercise less and thus tend to gain weight, resulting in a generalized sagging of the viscera, including the liver. Cushing disease often leads to reduced muscle tone, which in the case of the abdomen can lead to a potbelly. In such circumstances, the liver usually relocates to the lowest point in the abdomen, falsely giving the impression of enlargement.

Other Considerations for Estimating Liver Size In a lateral projection, the combination of a large liver and urinary bladder may cause the splenic triangle to appear tipped on end, a normal variant sometimes termed a bookend spleen (Figure 64-1). When comparing progress films of the liver, it is important to consider carefully the many anatomic, physiologic, and technical variations that can influence the perceived size of the liver (Figure 64-2). The caudoventral liver margin of normal dogs may appear sharply angled, gently rounded, or blunted (Figure 64-3). In some normal dogs, the caudoventral corner of the liver is invisible. Hepatic measurement using surrounding anatomy, for example, lateral liver length in terms of intercostal spaces, is unreliable. In dogs with extremely tapered abdomens, for example, Doberman Pinschers, Great Danes, and Afghans, the caudal liver margin often has a decided upward inclination, a normal breed variant that must not be mistaken for disease. 575

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A

A

B

B

Figure 64-1 • Unusual splenic orientation: A, Occasionally, the combination of an enlarged liver and full bladder will cause the splenic triangle to appear vertically rather than horizontally oriented in a lateral projection, a so-called bookend spleen. B, Companion ventrodorsal projections usually are not affected.

❚❚❚HEPATIC ULTRASOUND Nyland and Park were among the first to demonstrate the diagnostic capabilities of sonography in detecting a wide variety of liver diseases, including metastases, abscess, necrosis, hematoma, and cyst (Figures 64-4 to 64-6). To this list can be added calcification (Figures 64-7 and 64-8). Notably, the authors also concluded that hepatic ultrasound “has proved of little value” in diagnosing hepatitis, cirrhosis, lymphoma, or fatty infiltration, although increased hepatic echogenicity can be suggestive of these disorders (Figures 64-9 and 64-10).1 England described the normal sonographic appearance of the liver of puppies. He reported the following:2

Figure 64-2 • Lateral views of the cranial abdomen of a dog made 3 weeks apart: initial (A) and subsequent (B) views illustrate how anatomic (full versus empty stomach), physiologic (inspiration versus expiration), and technical (light versus dark film) variations all can influence the estimation of liver size in dogs.

• Hepatic echo texture (interior appearance) was finer (less coarse) for the first 2 months after birth. • Portal veins were less distinct (less well delineated) for the first 2 months after birth. • Measures of hepatic length were inaccurate for the first month after birth as a result of changing body proportions. • From 2 to 6 months of age, liver length was proportionate to body size, although the ratios differed from adult dogs.

❚❚❚ “IMAGING” LIVER FUNCTION Bahr and co-workers described the use of technetium99m (99mTC)-mebrofenin to quantitatively assess hepa-

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B A

D

C Figure 64-3 • Considerable variability exists in the appearance of the caudoventral margin of the liver (size, shape, and orientation) as seen in the lateral radiographs of four dogs with no clinical evidence of liver disease.

tocyte function (extraction fraction) in healthy dogs. The authors theorize that, based on human experience, this test could be used to monitor liver function in dogs receiving hepatotoxic drugs.3

❚❚❚ LIVER DISEASE: A REALISTIC APPROACH From the radiologist’s perspective, the simplest way to approach the diagnosis of liver disease initially is to put forth the following questions: Is the liver normal or abnormal in appearance? If the answer is “abnormal,” then the second question to ask is, To what extent is the liver affected? If the entire liver appears diseased, then terms such as hepatitis, cholangitis, cholangiohepatitis, and so forth may be appropri-

ate; however, in most instances, such diagnostic refinement is not possible (or at least it is not likely to be accurate) and must await laboratory and biopsy input. Much the same also can be said of many solitary lesions, although the identification of metastasis is often comparatively clear. Radiographic and sonographic diagnosis notwithstanding, it behooves the medical imager to be conversant with the pathophysiology of liver disease, and to this end the article by Center is highly recommended.4 Furthermore, I recommend that the initial radiographic or sonographic diagnosis in the case of diffuse nonstructured liver disease simply be hepatitis, at least until more information is forthcoming. Modifiers such as active/nonactive, suppurative/nonsuppurative, and chronic/acute are for the most part presumptuous and better left to the pathologist’s report.

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Figure 64-4 • Hepatic sonogram shows a very large hemangiosarcoma with extensive cavitation.

Figure 64-5 • Hepatic sonogram shows a metastatic pancreatic carcinoma in a cat (electronic cursors).

Figure 64-7 • Hepatic sonogram (transverse plane) in a dog shows multiple areas of calcification. Figure 64-6 • Hepatic sonogram in a cat shows multiple cysts.

Figure 64-8 • Hepatic sonogram shows extensive calcification in the wall of the gallbladder.

Figure 64-9 • Hepatic sonogram in a dog, interpreted as normal, but later fine-needle biopsy showed that the dog had diffuse cholangiohepatitis.

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579

6 4 - 1

Histologic Subsets of Hepatitis in the Cat • Biliary cirrhosis • Chronic, progressive, nonsuppurative lymphocytic cholangitis/cholangiohepatitis • Chronic, progressive, nonsuppurative lymphocyticplasmacytic cholangitis/cholangiohepatitis • Sclerosing cholangitis • Sclerosing lymphocytic cholangitis • Suppurative cholangitis/cholangiohepatitis

The cats with cholangiohepatitis revealed similar findings. Sonographically, most cats with either subtype of inflammatory liver disease exhibit a coarse or nodular hepatic echo texture, with normal attenuation.7 For more information on the subject of sonographic beam attenuation, see the article by O’Brien.8

A

Feline Hepatic Lipidosis (Fatty Liver) Background. Feline hepatic lipidosis is the name given to fatty cat livers in which the amount of intrahepatocytic fat has become sufficiently great that it interferes with normal cellular function and in severe instances causes liver failure.

B Figure 64-10 • Close-up lateral radiograph (A) of the cranial abdomen of a dog with severe liver enlargement due to fatty infiltration, which is also shown in a companion sonogram (B).

Diffuse or Predominantly Diffuse Liver Diseases Feline Cholangitis, Cholangiohepatitis, and Cholangiohepatitis Complex Background. In cats, hepatitis is exceeded in incidence only by hepatic lipidosis. The disease has been subdivided histologically according to the type of cellular infiltration and the degree of periportal fibrosis (Box 64-1). Recently the histologic classification of feline hepatitis was simplified, and now consists of only two categories: (1) lymphocytic portal hepatitis and (2) cholangiohepatitis (acute and chronic).5 Clinically, affected cats appear listless, anorexic, and have been vomiting; as a result, they lose weight. Some have fever, and most have elevated liver enzymes. Some (but not all) are jaundiced. Weiss and co-workers showed that about 40% of cats with cholangiohepatitis also have severe inflammatory bowel disease and mild pancreatitis.6 Imaging Findings. Radiographically, about half of the cats with lymphocytic portal hepatitis had liver enlargement, and the remaining cats had normal or small livers.

Imaging Findings. In the context of medical imaging, in particular, ultrasound, the term lipidosis often is used as a differential explanation for a diffusely hyperechoic liver, especially one that is brighter than adjacent falciform fat (as typically observed using a 7.5-MHz transducer). At one time, it was claimed that such an observation was strongly indicative of lipidosis: 91% sensitivity, 100% specificity, and 100% positive predictive value.9 Such diagnostic adamance no longer exists, however, in light of the work by Nicoll and O’Brien, which demonstrated that the livers of healthy but obese cats were normally hyperechoic compared with nearby falciform fat (Figures 64-10 and 64-11).10 Lymphosarcoma Radiology. Hepatic lymphosarcoma, depending on its form and extent, may or may not enlarge the liver sufficiently to be detected radiographically. Even when obviously enlarged, it is not possible to differentiate most lymphomas from many benign causes of hepatomegaly, such as a fatty liver. Ultrasound. Hepatic lymphomas lack a characteristic appearance. According to Nyland, canine hepatic lymphosarcoma may appear in at least three different ways, one diffusely involving the liver and the other two producing discrete individual lesions: (1) diffuse normal or slightly reduced echogenicity, (2) poorly marginated hypoechoic lesions, and (3) well-marginated hyperechoic lesions featuring a hypoechoic rim.11 The diffuse form of hepatic lymphosarcoma may not discernibly alter the sonographic appearance of the

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Figure 64-12 • Hepatic sonogram shows a lumpy, hyperechoic liver swimming in a sea of peritoneal fluid, the result of cirrhosis.

Figure 64-11 • Close-up lateral view of the cranial abdomen of a cat with a large amount of fat beneath its liver that was misinterpreted as fluid by an emergency clinic veterinarian.

liver. Alternatively, the liver may appear slightly decreased in echogenicity, a determination that is difficult to make with a high degree of confidence. The second and third pattern types are relatively straightforward, although I have seen hypoechoic lesions that were just barely visible. Displaying considerably less diagnostic optimism, Lamb and co-workers have largely dismissed ultrasound, terming it an unreliable and inconsistent means of diagnosing diffuse hepatic lymphosarcoma after it failed to identify 11 of 14 histologically proven cases.12 Nuclear Imaging. Steyn and Ogilvie described the use of 99mTc-sestamibi for the diagnosis and pretreatment staging of malignant canine lymphoma involving the liver.13 Hepatic Congestion. Severe hepatic congestion leading to surface transudation (“hepatic sweating”) is most likely to occur under two circumstances: (1) primary right-sided heart disease and (2) large-volume pericardial fluid accumulation. Radiographically, chronic hepatic congestion is marked by peritoneal fluid, with or without hepatomegaly. Sonographically, the hepatic veins are both enlarged and more numerous, although this is not always immediately evident, especially when the examination is hurried. Hepatic Cirrhosis. Cirrhosis of the liver is usually the result of chronic hepatitis, specific etiology notwithstanding. Contrary to what was reported by Nyland and co-workers, I usually have found the sonographic

diagnosis of cirrhosis to be relatively straightforward, typically characterized by (1) marked parenchymal shrinkage, (2) increased and often uneven echogenicity, (3) lumpy margins, and (4) the presence of peritoneal fluid (Figure 64-12). Hepatic Dysplasia. Abnormal liver development, primarily in the form of reduced size and curtailed function, is usually the result of a lack of hepatic growth factors caused by a rerouting of the normal intrahepatic blood flow through an anomalous vessel. Such vascular bypasses are often termed intrahepatic or extrahepatic shunts, depending on their location relative to the liver. Liver Disease and Canine Superficial Necrolytic Dermatitis (Hepatocutaneous Syndrome). Canine superficial necrolytic dermatitis is a relatively new, or at least newly discovered, skin disease of dogs that causes ulcers on the footpads, genitals, elbows, hocks, and mucocutaneous junctions. Because most affected dogs also have liver or pancreatic disease, a causal relationship is strongly suggested, although its precise nature remains a mystery. Nyland and coworkers reported on the sonographic appearance of liver disease seen in association with necrotic dermatitis, describing it as having a unique honeycomb pattern.14

Regional and Localized Liver Disease Nodular Hyperplasia. Hepatic nodular hyperplasia is a benign condition of older animals, not a disease, whose importance lies in the fact that these small, discrete masses resemble some forms of liver cancer. Unrelated to illness or specific etiology, these “lesions” may or may not be detected during routine abdominal sonography because they may not differ sufficiently from the normal hepatic parenchyma. Because of the difficulty in distinguishing hyperplastic nodules from

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A

C

B

Figure 64-13 • Lateral (A) and ventrodorsal (B) views of the abdomen of a dog with diffuse liver cancer. Because of the large volume of associated fluid, it is difficult to see much of the viscera, especially in the cranial half of the abdomen. Hepatic sonogram (C) shows numerous circular objects featuring thick, well-defined margins and dark (hypoechoic) interiors.

hepatic metastases, Stowater and colleagues recommend fine-needle biopsy.15 Liver Tumors Radiology. The radiographic detection of a hepatic tumor depends on one of two factors: liver enlargement or distortion. Thus, a hepatic tumor must become quite large before it can achieve either of these qualities. When multiple small nodular tumors are present, the possibility of enlargement exists, but detectable distortion is rare. Tumor detection becomes even more difficult when there is a medium-sized or large volume of peritoneal blood, as often is the case with a ruptured hemangiosarcoma. Of course, any hepatic tumor is potentially capable of obstructing a sufficient number of hepatic or portal veins, leading to ascites. Because many dogs with liver tumors are older, and thus are susceptible to having larger livers as a result of other causes,

diagnostic conformation nearly always requires ultrasound. Ultrasound. To be detected sonographically, solitary or multiple liver tumors must fulfill two basic requirements: They must contrast with the surrounding normal liver (assuming there is some normal liver), and they must have sufficient detail to be recognized as a discrete nodule or mass (a nodule is 0.5 cm in diameter or smaller, whereas a mass is characterized by a width greater than 0.5 cm). Individual tumor types are variable, with interiors ranging from light (hyperechoic) to dark (hypoechoic) and possessing margins ranging from discrete to vague (Figures 64-13 and 64-14). Primary Liver Tumors. Evans characterized the radiographic appearance of primary liver tumors in dogs, most of which were mass lesions (thus the reason for their being considered under this heading). Most of the animals were older, with an average age of 11 years,

582

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A

B

D

C Figure 64-14 • Four hepatic sonograms showing the variability of diffuse liver cancer in dogs.

presenting with a combination of abnormalities including seizures, vomiting, anorexia, and malaise. Cell types included hepatoma, bile duct cystadenoma, hepatocellular carcinoma, and cholangiocellular carcinoma, with individual tumor masses ranging from 0.5 to 18 cm. Four of the five diffuse tumors were cholangiocellular carcinomas (see the following section on biliary tumors for further details). The most common radiographic appearance for any type of primary liver tumor was a right cranial abdominal mass causing caudolateral displacement of the stomach. About half the dogs had peritoneal fluid or signs (not specified) suggesting carcinomatosis, but only three (of 22) had signs of pulmonary metastasis.16

Biliary Cystadenoma and Cystadenocarcinoma Biliary cystadenomas are uncommon benign liver tumors that often affect older cats. They typically appear

as solitary or multiple cysts lying inside or just outside the liver in the extrahepatic bile ducts. Although cystadenomas usually do not cause visible signs of illness, they may appear on abdominal radiographs as liver enlargement or, in some cases, as a discrete cranial abdominal mass. Nyland and colleagues reported on a variety of sonographic appearances featuring varying degrees and types of cavitation: (1) multilocular masses containing thin-walled cysts, (2) hyperechoic masses with cystic components, and (3) masses of mixed echogenicity with cystic components. Some multifocal lesions featured two or more of the preceding variants.17 In my limited experience with biliary cystadenocarcinoma, large size and cavitation are the most consistent features of this tumor type (Figure 64-15). To date, I have seen these tumors only in older dogs, one of which has survived for nearly a year following removal and chemotherapy.

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system became dilated, beginning with the common duct and gradually extending to the peripheral intrahepatic ducts. Common duct enlargement was first evident 1 to 2 days after ligation, with peripheral ducts appearing dilated 5 to 7 days after surgery. Dilated biliary ducts were distinguishable from hepatic and portal veins by their tortuosity and irregular branching patterns. These findings are consistent with what has been reported in a naturally occurring case of extrahepatic biliary duct obstruction in a cat.20 Hepatic Cyst. Most hepatic cysts are 1 cm or smaller, are solitary, and are incidental sonographic findings (see Figure 64-6). As a matter of caution, many such cysts are examined subsequently and, in my experience, usually do not change. Figure 64-15 • Hepatic sonogram shows a huge hepatic cystadenocarcinoma in a dog featuring extensive cavitation, the tumor type’s most defining feature.

Hepatic Hemangiosarcoma Background. In my experience, hepatic hemangiosarcoma is much less common than splenic hemangiosarcoma, especially as a source of acute abdominal hemorrhage. Combined hepatic-splenic lesions also occur, but they do so less frequently than isolated splenic lesions. Radiography. Large hepatic hemangiosarcomas often enlarge the liver so that in a lateral radiograph the stomach, spleen, and intestinal mass appear displaced caudally. If the dog has collapsed recently, the visceral margins are likely to appear vague as a result of related peritoneal hemorrhage. For the same reason, thoracic films often show a small heart and an oligemic, hyperinflated lung (Figure 64-16). Ultrasound. Like their splenic counterparts, hepatic hemangiosarcomas appear sonographically as large spherical cavitated lesions (Figure 64-17). Alternatively, the disease may assume an appearance resembling hepatic metastasis: multiple, vaguely marginated, variably sized, hypoechoic spherical masses (Figure 64-18). Hepatic Tumors and Related Biliary Obstruction Background. Cholangiocarcinoma (cholangiocellular carcinoma, bile duct carcinoma) is an uncommon tumor of dogs and cats (usually females) that originates from the intrahepatic bile duct epithelium. Often only a single liver lobe is affected, similar to an abscess, cyst, or granuloma. Even without evidence of spread, the prognosis is poor, with about half of the diagnosed dogs dead within a year.18 Imaging Findings: Ultrasound. Experimental ligation of the common bile duct has been performed in dogs, and the effects of extrahepatic biliary obstruction have been observed sonographically.19 Predictably, the biliary

Hepatic Abscess Background. Hepatic abscesses are rare. Farrar and coworkers reported on a series of 14 cases of hepatic abscesses in dogs.21 The most common presenting complaints were lack of appetite and decreased physical activity, followed by vomiting and diarrhea. Abnormal physical findings included fever, abdominal pain, palpable liver enlargement, mucosal bleeding, and dehydration. The white blood cell count was elevated, whereas platelets and red blood cells were decreased. Bilirubin, alkaline phosphatase, and alanine aminotransferase were increased. Bacteria isolated from the described hepatic abscesses included Escherichia coli, Clostridium species, Klebsiella pneumoniae, Enterococcus organisms, Staphylococcus epidermidis, and S. intermedius. Concurrent infections were identified in the biliary tract, spleen, endocardium, lung, prostate, brain, salivary glands, lymph nodes, and blood of several dogs. Radiology. Radiologic abnormalities varied, but the most common appearance consisted of (1) liver enlargement, (2) decreased visceral detail, and (3) a hepatic mass or splenomegaly. Six of the 14 dogs radiographed also had abnormal chest films, described by the authors as “alveolar consolidation or mixed bronchial/interstitial pulmonary patterns.” Ultrasound. Only 9 of the 14 dogs studied underwent ultrasound examination. All had liver lesions, which were subsequently confirmed as abscesses. The lesions were highly variable in appearance, ranging from hypoechoic, to mixed, to hyperechoic. The authors speculated that this variability might reflect the maturity of a particular abscess. Follow-up ultrasound examinations were done in selected cases to determine whether there was a reduction in lesion size following antibiotic treatment. Schwarz and co-workers also reported on the sonographic appearance of hepatic abscesses in 13 dogs.22 The observed lesions were characterized as follows: (1) solitary more common than multiple, (2) often poorly echogenic, (3) frequently featuring central cavitation, (4) showing far enhancement, and

584

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A

B

C

D

E Figure 64-16 • A, Hepatic hemangiosarcoma appears as a large opaque sphere in the cranial abdomen as seen in this lateral projection. The remaining viscera are difficult to assess because of mass-related displacement and resultant crowding in the central abdomen. B and C, Sonograms made through different sections of the tumor show a wide variation in appearance including cavitation, and a large volume of peritoneal fluid, which is probably blood. D and E, Screening thoracic films fail to reveal metastasis but do show reduced cardiovascular dimensions and pulmonary hyperinflation secondary hypovolemia.

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Ultrasound Standard Examination. Ultrasound has replaced cholecystography as the principal means of imaging and assessing the gallbladder. Astandard examination focuses on (1) the overall appearance of the gallbladder (i.e., size, shape, position), (2) the size and shape of the bile duct, (3) wall thickness, (4) wall echo texture, (5) content, and (6) the immediately surrounding tissue and spaces. Spaulding succinctly described the sonographic appearance of the normal and abnormal gallbladder wall, indicating that this is one of the most frequently detected abnormalities.29 Figure 64-17 • Hepatic sonogram shows large cavitated hemangiosarcoma in a dog.

Combined Ultrasound and Cholecystography. Cholecystography and sonography have been combined to evaluate the ability and rapidity of the gallbladder to empty, prompted by an intravenous injection of synthetic cholecystokinin.30 In particular, this procedure can assist in the diagnosis of outlet obstruction based on the findings of a dilated common bile duct and an emptying time of 20% or less (a normal gallbladder empties at least 40% of its volume within an hour, as does a nonobstructed gallbladder in an icteric dog).

Gallbladder Sludge (Sludge, Sediment, Inspissated Bile)

Figure 64-18 • Hepatic sonogram shows primary hepatic hemangiosarcoma featuring multiple lesions that resemble hepatic metastasis.

(5) variably shaped (round, oval, or irregular). Some lesions were associated with regional hyperechoic fat or adenopathy. Abscess was confirmed in most cases by ultrasound-guided biopsy; four of the dogs were treated by ultrasound-guided, percutaneous drainage.

❚❚❚ GALLBLADDER DISEASE Cholecystography Cholecystography has been used to characterize the normal anatomy of the gallbladder of the dog and cat and, to a lesser extent, assess its physiology. Compared with other special procedures in veterinary medicine, cholecystography never has achieved everyday status, largely because of its inconsistent ability to image the gallbladder. With the advent of ultrasound, cholecystography is now little more than a historical curiosity, albeit one that is periodically revisited.23-28

Background. Sludge is a partially solidified form of bile that appears as a granular echogenic layer in the dependent part of the gallbladder. Some healthy dogs and most anorexic dogs have “sludge” in their gallbladders, the result of not eating (or eating less) rather than of biliary disease. Bromel and co-workers showed that the presence of sludge is usually an incidental finding, unrelated to disease, including that of the liver and gallbladder.31

Gallstones (Cholelith, Cholelithiasis, Choledocholithiasis) Stones in the gallbladder or bile ducts of dogs are rare. Although choleliths are theoretically capable of obstructing a portion of the biliary system (obstructive cholangitis), the extent to which they actually do so is not known. Likewise, ureteral colic, associated with trying to pass a small kidney stone, is also a rare occurrence in dogs.

Cholecystitis Unlike people, dogs rarely have inflammation of the gallbladder, or cholecystitis. The incidence and prevalence of acute and chronic cholecystitis in dogs are not known.32 Although there are no completely reliable sonographic signs of cholecystitis, edema of the gallbladder wall is a frequent finding.

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Cystic Hyperplasia (Benign Cystic Hyperplasia) Cystic hyperplasia of the mucus-producing glands of the gallbladder (also termed benign cystic hyperplasia) was described by Partington and Biller as occurring in older dogs but having no clinical significance. In some instances, discrete polyps are also present, which the authors caution cannot be sonographically discriminated from early cancer.32 Thus, biopsy or recheck is in order.

Necrosis In my experience, infectious necrosis of the gallbladder is most common in Cocker Spaniels and usually is related to so-called mucoceles. Additional information on biliary mucoceles follows.

A

Calcification Calcification of the wall of the gallbladder, as observed radiographically or sonographically, can be a feature of adenocarcinoma. In humans, this observation is termed porcelain gallbladder and is considered a precancerous lesion, necessitating surgical removal. Differential radiographic diagnosis should include (1) calcified gallbladder, (2) choleliths, (3) concentrated mineral salts in the bile, (4) contiguous hepatic calcification, (5) calcified nearby lymph nodes, (6) calcified pancreatic cysts, (7) superimposition of calcified costochondral rib junctions, and (8) mineralized surface lesions, such as tumoral calcinosis or calcinosis cutis. Sonographically, mural calcification should be distinguishable from gallbladder stones on the basis of dependency: Bladder stones should move to the dependent portion of the gallbladder as the animal is moved, whereas mural calcification remains fixed.33

Duplication and Absence Both duplication and absence of the gallbladder are rare. Moentk and Biller reported duplication of the gallbladder of a cat and described its sonographic appearance.34 The absence (aplasia) of the gallbladder has been reported in a dog.35

Biliary Mucocele Background. Mucinous distension of the gallbladder has been termed a mucocele. A mucocele differs from routinely encountered hyperechoic bile (sludge) insofar as it is immobile, failing to relocate when the animal is repositioned during a sonographic examination. Moreover, whereas biliary sludge often fills much of the gallbladder and is of uniform or near-uniform echogenicity, a mucocele is typically a distinctly shaped or patterned object, located within what otherwise appears to be normal bile. Affected dogs, often middle-aged and older Cocker Spaniels, typically present as obviously ill, often

B Figure 64-19 • Long (A) and cross-sectional (B) hepatic sonograms show a hypoechoic gallbladder containing a large, ill-defined object characteristic of a mucocele.

vomiting and lethargic. Many appear icteric and exhibit pain with cranial abdominal palpation (colic). Abnormal laboratory indices include elevations of total bilirubin, alkaline phosphatase, alanine aminotransferase, and gamma glutamyl transferase. The authors postulate that the primary causes of the mucoceles are biliary stasis and mucosal hypertrophy, often, but not invariably, associated with aerobic infection.36 In my experience, true mucoceles, at least insofar as the term is commonly used in human medicine, are uncommon in dogs. Many infected and necrotic gallbladders, identified sonographically and confirmed at surgery or necropsy, actually contain sloughed mucosa, blood, pus, and congealed bile rather than a purely mucinous substance. Only occasionally have I observed what I believed to be a true mucocele. Imaging Findings. In my experience, canine “mucoceles” (primarily involving Cocker Spaniels) appear as variably shaped, variably defined, relatively hyperechoic objects within the lumen of the gallbladder (Figures 64-19 to 64-21). The gallbladder itself is often asymmetric or overtly deformed, and the immediate surrounding tissue may be abnormally echogenic.

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Besso and co-workers reached similar conclusions, describing the appearance of gallbladder mucoceles in 14 dogs, 50% of which had perforated or ruptured. Sonographic features include (1) the presence of a mucocele; (2) the absence of positional relocation; (3) variable wall thickness, and (4) in the case of perforation or rupture, bladder wall discontinuity.36

❚❚❚ PORTOSYSTEMIC SHUNTS (PORTAL VEIN ANOMALIES. PORTACAVAL SHUNTS, ABNORMAL PORTOSYSTEMIC COMMUNICATIONS, LIVER SHUNTS)

A

Background Abnormal vascular communication between the portal vein and the caudal vena cava is termed a portacaval shunt. Occasionally, the portal vein communicates with the azygos vein instead of the portal vein, in which case it is termed a portoazygous shunt. As a result of these abnormal vascular communications, portal hypertension may develop, causing a reversal of blood flow away from the liver and back toward the stomach and intestine, where it originated. Most importantly, this leads to an increase in potentially toxic metabolites accumulated in the stagnant visceral circulation and physically to an enlargement of surrounding systemic veins, called portosystemic collaterals. Associated signs of illness include (1) hepatoencephalopathy, (2) weight loss, (3) poor growth, and (4) cystitis secondary to ammonium biurate crystalluria. Serum bile acids (postprandial) are typically greater than 25 mM per liter. In one comparatively small anecdotal study of 20 dogs operated on to correct portosystemic shunts, most owners reported that their dogs improved, especially if the shunt was occluded before 1 year of age.37

B Figure 64-20 • Long (A) and cross-sectional (B) hepatic sonograms show a hypoechoic gallbladder containing a mediumsized, poorly defined object suggesting a mucocele.

Imaging Findings Radiology Plain Films. Asmall (atrophic or dysplastic) liver suggests, but does not confirm, a hepatic shunt. Likewise, small stones or crystals in the kidneys or urinary bladder support, but do not confirm, a shunt. Also, some dogs with normal-sized livers and no urinary tract abnormalities have liver shunts. Portal Angiography. Portal angiography or, more simply, portography, was pioneered, perfected, and widely promoted by Suter in a number of publications and presentations. One of the first of these was published in Veterinary Radiology in 1975, in which seven distinct types of portacaval shunts were described, most of which were unknown to most veterinarians at the time, including many radiologists.38

Figure 64-21 • Sonographic long-section of a colicky Cocker Spaniel shows a misshapen gallbladder containing a complex gangrenous mucocele. The gallbladder was later removed when it was found to be gangrenous, although this was not hinted at sonographically.

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Table 64-1 • ARRANGEMENT OF PORTAL AND HEPATIC VEINS IN THE CANINE LIVER Portal Vein

Hepatic Vein

Liver Lobe

Branch Arrangement

Branch Number

Branch Arrangement

Branch Number

Caudate process

Separate (see right lateral above)

1-4 large

Separate (see above)

Left lateral Left medial

Separate Separate vessel in a majority of dogs, but occasionally originates in common with the quadrate vein Separate multiple

1-4 large 1-6 large

Separate Separate

Usually 1 large, but may be as many as 4 1-5 large 1-5 large

Inconsistent origins, but may be as many as 1-7 branches each 1 large > 3 small

Separate (if multiple)

Usually 1 large 1 large > 3 small

1-4 large, plus up to 6 smaller vessels

Common origin with right medial vein 0.3 cm long Separated from caudate by 1/2-11/2 cm

1 large > 5 small

Common with quadrate

Papillary process Quadrate Right lateral Right medial

Usually a separate vessel located 1-4 cm from right medial vein Originates with caudate vein but then immediately separates Usually separate

1-3 large vessels with up to 5 smaller veins 1 large > 5 small

Carlisle and co-workers produced what I consider the definitive article on the anatomy of the portal and hepatic veins of the dog, appropriate to a detailed sonographic assessment of the portal system.39 In a follow-up article, the authors described the sonographic appearance of the canine portal system using their previously published, anatomic guidelines (Table 64-1).40 Types of Portography. Schmidt and Suter reviewed the various angiographic methods currently used in the investigation of suspected hepatic shunts in dogs and cats, in addition to the direct and indirect means of determining portal pressure.41,42 Operative Portography. Although not always convenient, it is extremely important to make both lateral (preferably left lateral) and ventrodorsal views when performing operative portography.42a This minimizes the risk of missing an anomalous communication due to vascular superimposition, as reported by Wilson and co-workers in a case of combined portacaval and portoazygous shunts.43 Subtraction radiography is especially helpful in the case of complex central shunts complicated by multiple large portosystemic collaterals. In addition to revealing the precise nature and location of a suspected hepatic shunt, portography occasionally serves to identify calculi located within the urinary tract as the contrast medium is eliminated. Specifically, stones in the kidneys, ureters, or bladder are characterized by variably sized and shaped, dark filling defects seen against a relatively light background of iodine-laden urine.44 The sonographic and angiographic features of typical central hepatic shunts are shown in Figures 64-22 and 64-23, C.

A

B Figure 64-22 • A, Portoazygous shunt: Hepatic sonogram in a cat shows a large, abnormal blood vessel lying just along the surface of the liver that was diagnosed as a probable portacaval shunt. B, Lateral operative mesenteric portogram shows contrast solution flowing from the catheter to the mesenteric vein, through the portal vein, and into the azygous vein.

CHAPTER 64 ❚❚❚ Liver Disease

589

B

A1

C

A2

D Figure 64-23 • A, Portacaval shunt: Operative lateral (A1) and ventrodorsal (A2) portograms of a large extrahepatic portacaval shunt in a dog. B, Portacaval shunt: Hepatic sonogram of a large intrahepatic portacaval shunt in a dog (top), and associated Doppler profile showing reversed (hepatofugal) blood flow. C, Portacaval shunt: Hepatic sonogram of what was presumed to be an enormously dilated patent ductus venosus. D, Long sectional sonogram of an adjustable vascular clamp (arrow) surrounding a portacaval shunt vessel.

Nonoperative Portography. Mesenteric arterial portography,45 even when pharmacologically enhanced, is often very difficult to interpret because of a combination of extensive vascular superimposition and faint opacification. Even with digital subtraction, identification of the primary shunt vessel can be problematic.

Percutaneous Transsplenic Portography. Herrgesell and co-workers published a technique for percutaneously placing a catheter into a splenic vein and from there continuing into the portal vein, where contrast solution was injected. After evaluating a number of different types and sizes of catheter and needle combinations, a 17-gauge spinal needle combined with a

590

SECTION VII ❚❚❚ The Abdomen

19-gauge through-the-needle-catheter produced the best results.46 In my experience, this skill requires considerable practice to master and continued practice to maintain. Furthermore, it can lead to prolonged, often undetected splenic hemorrhage due to the anticoagulant properties of the contrast solution and lack of visibility related to the percutaneous technique. Subtraction Portal Venography. Wrigley and coworkers reported that subtraction portal venography not only improved the visibility of portosystemic shunts and intrahepatic portal veins but also detected shunts not appreciated in preliminary, nonsubtraction venograms.47 Most modern portable x-ray machines equipped with fluoroscopy (often termed “C-arms”) have the ability to perform digital subtraction on acquired images, displaying them either on a dedicated monitor or as hardcopy. Ultrasound Anatomic Assessment. The sonographic assessment of hepatic shunts in small dogs with small livers can be difficult, in some cases impossible, especially if the animal is uncooperative. Even under optimal conditions, using both an abdominal and an intercostal approach and searching for and precisely locating a shunt can require an hour or more. There are few quick studies. Bostwick and Twedt proposed a presonographic workup designed to predict shunt location. Before sonographic examination of the liver and its surroundings for a hepatic shunt is done, the animal’s body size and its blood glucose and serum alkaline phosphatase values should be considered as potential predictors of shunt type: intrahepatic versus extrahepatic.48 Theoretically, this advance knowledge may reduce examination time. Portal Blood Flow Assessment. Kantrowitz and coworkers described the evaluation, using Doppler ultrasound, of portal blood flow in healthy dogs.49 Nyland and Fisher followed with a comparable Doppler assessment of portal blood flow in experimental dogs whose common bile ducts had been ligated to induce liver cirrhosis and portosystemic shunts. Predictably, portal flow was reduced by nearly half.50 Lamb and Mahoney compared three different methods of determining the speed of portal blood flow using Doppler ultrasound51: 1. Sampling portal blood flow from the center of the portal vein, then manually selecting data points on the resultant blood flow spectrum and correcting the calculated maximum velocity to mean velocity (using a factor of 0.57) 2. Using a small, centrally located sample volume to calculate maximum blood flow (again using a correction factor of 0.57) 3. Using a relatively large sample volume that overlaps the outer margins of the portal vein to compute the mean velocity of portal blood flow

Although there was no statistical difference in the results obtained using these three techniques, the authors considered the third method the easiest.51 In cases in which an adjustable clamp is used to reduce blood flow through a central extrahepatic shunt gradually, sonography can be used to assess the position of the device and to obtain a Doppler reading in the abnormal vessel (Figure 64-23, D). Diagnostic Accuracy. Using combined anatomic and Doppler assessments to diagnose congenital portacaval shunts in a medium-sized group of dogs, Lamb and Mahoney claimed a diagnostic accuracy rate of 94%, featuring a sensitivity of 95% and a specificity of 98%.52,53 Nuclear Imaging. Quantitative nuclear imaging (a form of nuclear medicine) has been used to evaluate the effectiveness of portosystemic shunt ligation.54 An enema solution containing 123I-iodoamphetamine has been used to identify the presence, but not the physical nature, of portosystemic shunts in dogs.55 McEvoy and co-workers reported the use of rectally administered 99mTc-pertechnetate to determine normal feline portal blood flow56 and shunt fractions in cats with portosystemic shunts.57 Portocaval shunt fraction (shunt index) using transcolonic 123I-iodoamphetamine and 99mTc-macroaggregated albumin was compared in dogs with experimentally induced liver cirrhosis and secondary portosystemic shunts. Results obtained from the two described methods were comparable.58 Daniel and co-workers carried out a similar experiment comparing rectally administered 99mTC with cerium141 labeled microspheres (injected into a mesenteric vein). They also found the results comparable.59 Magnetic Resonance Imaging. Seguin and coworkers reported the use of magnetic resonance angiography (MRA) in the diagnosis of portosystemic shunts in dogs by using a customized protocol based on a gradient echo sequence that was modified to enhance the signal intensity emitted from the portal system and caudal vena cava.60 Based on the evaluation of 10 normal dogs and 23 dogs with one or more portacaval shunts, the authors concluded the following: • Sensitivity in diagnosing a shunt (healthy and sick dogs): 80% • Specificity in diagnosing a shunt (healthy and sick dogs): 100% • Sensitivity in diagnosing multiple extrahepatic shunts (in abnormal dogs): 63% • Specificity in diagnosing multiple extrahepatic shunts (in abnormal dogs): 97% • Sensitivity in diagnosing single congenital shunts (in abnormal dogs): 79% • Specificity in diagnosing single congenital shunts (in abnormal dogs): 100%

CHAPTER 64 ❚❚❚ Liver Disease

Portosystemic Collaterals (Acquired Portosystemic Shunts) The expression acquired portosystemic shunt or shunts is often misunderstood because it implies the creation of an abnormal vein that reroutes venous blood from the splanchnic circulation, around the liver, to the caudal vena cava or azygos vein, much like a congenital shunt. In reality, however, there is no “new” blood vessel; rather, it is a recruitment process in which normal resident veins become enlarged to accommodate a reversal of portal blood flow. Thus, for the sake of both clarity and understanding, the term portosystemic collaterals seems the better descriptor.

B o x

591

6 4 - 2

Normal Doppler Blood Flow Values Obtained from the Common Hepatic Artery of Normal Dogs (Adults and Puppies) Adult • Velocity (mean): 1.5 m/s (range, 1.1-2.3) • Resistive Index (mean): 0.68 (range, 0.62-0.74) Puppy • Velocity (mean): 1.0 m/s (range, 0.8-1.3) • Resistive Index (mean): 0.59 (range, 0.46-0.65) No differences were noted between preprandial and postprandial data.

Hepatic Microvascular Dysplasia Hepatic microvascular dysplasia, as the name implies, is a disease of the intrahepatic portal vasculature, in particular, its inability to prevent the “leakage” of enteric breakdown products into the systemic circulation. What makes this recently discovered disorder problematic is that it may or may not be associated with a congenital portosystemic shunt. Further complicating diagnosis is that isolated portosystemic shunt, hepatic microvascular dysplasia, and combined portosystemic shunt/microvascular dysplasia all share similar clinical signs. Radiographically, various combinations of abnormalities, including a small liver, kidney enlargement, renal calculi, and bladder stones, usually characterize liver shunts. Sonographically, a portosystemic shunt typically is confirmed by the identification of an anomalous intrahepatic or extrahepatic blood vessel. Existing shunts may go undetected, however, especially in small dogs with small livers and a large amount of stomach and bowel gas. Regrettably, from a diagnostic perspective, microvascular dysplasia may be associated with many of the same findings as a portosystemic shunt, with the exception of the anomalous blood vessel. Thus, if no shunt is found, it may be impossible to distinguish between the two diseases or to know whether they coexist. The veterinary literature is ambiguous with respect to the sensitivity of portography. One group has claimed that dogs with microvascular dysplasia can be discriminated from normal dogs on the basis of a stunted portal system,61 whereas another asserts that they were unable to detect any distinguishing portographic features in a series of histologically proven cases.62 The reader is referred to the work of Allen and co-workers for the biochemical particulars of these diseases.62

Portal Vein Thrombosis Background. Portal vein thrombosis is a clinical rarity that has been reported in conjunction with a number of diseases including the following63,64:

• Acute necrotizing pancreatitis • Hypercoagulability (as in chronic glomerular disease) • Immune-mediated hemolytic anemia • Myeloproliferative disease • Steroid therapy • Thrombocytopenia (secondary to disseminated abdominal cancer) Imaging Findings Ultrasound. Lamb and co-workers reported the sonographic identification of portal vein thrombosis in four dogs, lesions that were variously attributed to coagulopathy, vasculitis secondary to ehrlichiosis, and invasive duodenal cancer. The authors recommend using the right tenth, eleventh, or twelfth intercostal spaces to view the portal vein, pointing out the relative merits of various types of sonographic assessment: anatomic, spectral, and color Doppler.65

Hepatic Arterial Blood Flow Lamb and co-workers described a sonographic method of evaluating hepatic arterial blood flow in dogs.66 They used Doppler to measure blood flow in the common hepatic artery of normal puppies and adults (before and after eating), resulting in the hemodynamic data in Box 64-2.

References 1. Nyland TG, Park RD: Hepatic ultrasonography in the dog. Vet Rad 24:74, 1983. 2. England GCW: Renal and hepatic ultrasonography in the neonatal dog. Vet Radiol Ultrasound 37:374, 1996. 3. Bahr A, Daniel GB, et al: Quantitative hepatobiliary scintigraphy with deconvolutional analysis for the measurement of hepatic function in dogs. Vet Radiol Ultrasound 37:214, 1996. 4. Center SA: Chronic liver disease: current concepts of disease mechanisms. J Small Anim Pract 40:106, 1999. 5. Gagne JM, Weiss DJ, Armstrong PJ: Vet Pathol 33:521, 1996.

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6. Weiss DJ, Gagne JM, Armstrong PJ: Relationship between inflammatory hepatic disease and inflammatory bowel disease, pancreatitis, and nephritis in cats. J Am Vet Med Assoc 214:514, 1999. 7. Gagne JM, Armstrong PJ, et al: Clinical features of inflammatory liver disease in cats: 41 cases (1983-1993). J Am Vet Med Assoc 214:513, 1999. 8. O’Brien RT: Attenuation: the clinical utility of subjective sonographic assessment. Vet Radiol Ultrasound 39:234, 1998. 9. Yeager AE, Mohammed H: Accuracy of ultrasonography in the detection of severe hepatic lipidosis in cats. Am J Vet Res 53:597, 1992. 10. Nicoll RG, O’Brien RT, Jackson MW: Qualitative ultrasonography of the liver in obese cats. Vet Radiol Ultrasound 39:47, 1998. 11. Nyland TG: Ultrasonic patterns of canine hepatic lymphosarcoma. Vet Rad 25:167, 1984. 12. Lamb CR, Hartzband LE, et al: Ultrasonographic findings in hepatic and splenic lymphosarcoma in dogs and cats. Vet Rad 32:117, 1991. 13. Steyn PF, Ogilvie G: 99mTc-methoxy-isobutyl-isonitrile (sestamibi) imaging of malignant canine lymphoma. Vet Radiol Ultrasound 36:411, 1995. 14. Nyland TG, Barthez PY, et al: Hepatic ultrasonographic and pathologic findings in dogs with canine superficial necrolytic dermatitis. Vet Radiol Ultrasound 37:200, 1996. 15. Stowater JL, Lamb CR, Schelling SH: Ultrasonographic features of canine hepatic nodular hyperplasia. Vet Rad 31:268, 1990. 16. Evans SM: The radiographic appearance of primary liver neoplasia in dogs. Vet Rad 28:192, 1987. 17. Nyland TG, Koblik PD, Tellyer SE: Ultrasonographic evaluation of biliary cystadenomas in cats. Vet Radiol Ultrasound 40:300, 1999. 18. Ball SM: What is your diagnosis? J Am Vet Med Assoc 213:1707, 1998. 19. Nyland TG, Gillett NA: Sonographic evaluation of experimental bile duct ligation in the dog. Vet Rad 23:252, 1982. 20. Frenier SL: Radiographic diagnosis. Vet Rad 31:200, 1990. 21. Farrar ET, Washabau RJ, Saunders HM: Hepatic abscesses in dogs: 14 cases (1982-1994). J Am Vet Med Assoc 208:243, 1996. 22. Schwarz LA, Penninck DG, Leveille-Webster C: Hepatic abscesses in 13 dogs: a review of the ultrasonographic findings, clinical data and therapeutic options. Vet Radiol Ultrasound 39:357, 1998. 23. Allan GS, Dixon RT: Cholecystography in the dog: the choice of contrast media and optimum dose rates. J Am Vet Rad Soc 16:3, 1975. 24. Carlisle CH: Radiographic anatomy of the cat gallbladder. J Am Vet Rad Soc 18:170, 1977. 25. Carlisle CH: A comparison of technics for cholecystography in the cat. J Am Vet Rad Soc 18:173, 1977. 26. Allan GS, Dixon RT: Cholecystography in the dog: assessment of radiographic positioning and the use of a double-contrast examination by visual and densitometric methods. J Am Vet Rad Soc 18:177, 1977. 27. Wrigley RH, Reuter RE: Percutaneous cholecystography in normal dogs. Vet Rad 23:239, 1982. 28. Fugita M, Hiromitsu O: Effect and safety of melamine iotroxate for cholangiocystography in normal cats. Vet Radiol Ultrasound 35:79, 1994. 29. Spaulding KA: Gallbladder wall thickness. Vet Radiol Ultrasound 34:270, 1993.

30. Finn St, Park RD, et al: Ultrasonic assessment of Sinclade-induced canine gallbladder emptying: an aid to the diagnosis of biliary obstruction. Vet Rad 32:269, 1991. 31. Bromel C, Barthez PY, et al: Prevalence of gall bladder sludge in dogs as assessed by ultrasonography. Vet Radiol Ultrasound 39:206, 1998. 32. Partington BP, Biller DS: Liver. In Green RW, ed: Small animal ultrasound. Philadelphia, 1996, LippincottRaven. 33. Bromel C, Smeak DD, Leveille R: Porcelain gallbladder associated with primary biliary adenocarcinoma in a dog. J Am Vet Med Assoc 213:1137, 1998. 34. Moentk J, Biller DS: Bilobed gallbladder in a cat: ultrasonographic appearance. Vet Radiol Ultrasound 34:354, 1993. 35. Liptak JM, Swinney GR et al: Aplasia of the gallbladder in a dog. J Small Anim Pract 41:175, 2000. 36. Besso JG, Wrigley RH, et al: Ultrasonographic appearance and clinical findings in 14 dogs with gallbladder mucocele. Vet Radiol Ultrasound 41:261, 2000. 37. Lawrence D, Bellah JR, Diaz R: Results of surgical management of portosystemic shunts in dogs: 20 cases (19851990). J Am Vet Med Assoc 201:1750, 1992. 38. Suter PF: Portal vein anomalies in the dog: their angiographic diagnosis. J Am Vet Rad Soc 16:84, 1975. 39. Carlisle CH, Wu J-X, Heath TJ: Anatomy of the portal and hepatic veins of the dog: a basis for systematic evaluation of the liver by ultrasonography. Vet Radiol Ultrasound 36:227, 1995. 40. Wu J-X, Carlisle CH: Ultrasonographic examination of the canine liver based on recognition of hepatic and portal veins. Vet Radiol Ultrasound 36:234, 1995. 41. Schmidt S, Suter PF: Angiography of the hepatic and portal venous system in the dog and cat: an investigative method. Vet Rad 21:57, 1980. 42. Schmidt S, Suter PF: Indirect and direct determination of the portal vein pressure in normal and abnormal dogs and normal cats. Vet Rad 21:246, 1980. 42a. Scrivani PV, Yeager AE, et al: Influence of patient positioning on sensitivity of mesenteric portography for detecting an anomalous portosystemic blood vessel in dogs: 34 cases (1997-2000). J Am Vet Med Assoc 219:1251, 2001. 43. Wilson K, Scrivani PV, Leveille R: What is your diagnosis? J Am Vet Med Assoc 211:415, 1997. 44. Tillson M, Layton CE, Godshalk CP: What is your diagnosis? J Am Vet Med Assoc 209:561, 1996. 45. Hornof WJ, Suter PF: The use of prostaglandin E1 and tolazoline to improve cranial mesenteric arterial portography in the dog. J Am Vet Rad Soc 20:15, 1979. 46. Herrgesell EJ, Hornoff WJ, Koblik PD: Percutaneous ultrasound-guided trans-splenic catheterization of the portal vein in the dog. Vet Radiol Ultrasound 40:509, 1999. 47. Wrigley RH, Park RD, et al: Subtraction portal venography. Vet Rad 28:208, 1987. 48. Bostwick DR, Twedt DC: Intrahepatic and extrahepatic portal venous anomalies in dogs: 52 cases (1982-1992). J Am Vet Med Assoc 206:1181, 1995. 49. Kantrowitz BM, Nyland TG, Fisher P: Estimation of portal blood flow using duplex real-time and pulsed Doppler ultrasound imaging in the dog. Vet Rad 30:223, 1989. 50. Nyland TG, Fisher PE: Evaluation of experimentally induced canine hepatic cirrhosis using duplex Doppler ultrasound. Vet Rad 31:189, 1990.

CHAPTER 64 ❚❚❚ Liver Disease

51. Lamb CR, Mahoney PN: Comparison of three methods for calculating portal blood flow velocity in dogs using duplex Doppler ultrasonography. Vet Radiol Ultrasound 35:190, 1994. 52. Lamb CR: Accuracy of ultrasonographic diagnosis of congenital portocaval shunt in the dog. Vet Radiol Ultrasound 36:439, 1995. 53. Lamb CR: Ultrasonic diagnosis of congenital portosystemic shunts in dogs: results of a prospective study. Vet Radiol Ultrasound 37:281, 1996. 54. Koblik PD, Hornof WJ, Brezock EM: Use of quantitative hepatic scintigraphy to evaluate spontaneous portosystemic shunts in 12 dogs. Vet Rad 24:232, 1983. 55. Koblick PD, Yen C-K, et al: Use of transcolonic 123Iiodoamphetamine to diagnose spontaneous portosystemic shunts in 18 dogs. Vet Rad 30:67, 1989. 56. McEvoy FJ, Forster-van Hijfte, White RN: Detection of portal blood flow using per-rectal 99mTc-Pertecnetate scintigraphy in normal cats. Vet Radiol Ultrasound 39:234, 1998. 57. Forster-van Hijfte, McEvoy FJ, et al: Per rectal portal scintigraphy in the diagnosis and management of feline congenital portosystemic shunts. J Small Anim Pract 37:7, 1996. 58. Koblik PD, Yen C-K, et al: Comparison of transcolonic 123 I-iodoamphetamine and portal vein injection of 99m Tc-macroaggregated albumin shunt fraction calculations in experimental dogs with acquired portosystemic shunts. Vet Rad 31:170, 1990.

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59. Daniel GB, Bright R, et al: Comparison of perrectal portal scintigraphy using 99mtechnetium pertechnetate to mesenteric injection of radioactive microspheres for quantification of portosystemic shunts in an experimental dog model. Vet Rad 31:175, 1990. 60. Seguin B, Tobias K, et al: Use of magnetic resonance angiography for diagnosis of portosystemic shunts in dogs. Vet Radiol Ultrasound 40:251, 1999. 61. Schermerhorn T, Center SA, et al: J Vet Int Med 10:219, 1996. 62. Allen L, Stobie D, et al: Clinicopathologic features of dogs with hepatic microvascular dysplasia with and without portosystemic shunts: 42 cases (1991-1996). J Am Vet Med Assoc 216: 533, 1997. 63. Espineira MMD, Vink-Nooteboom M, et al: Thrombosis of the portal vein in a miniature schnauzer. J Small Anim Pract 40:540, 1999. 64. LeGrange SN, Fossum TW, et al: Thrombosis of the caudal vena cava presenting as an unusual cause of an abdominal mass and thrombocytopenia in a dog. J Am Anim Hosp Assoc 36:143, 2000. 65. Lamb CR, Wrigley RH, et al: Ultrasonographic diagnosis of portal vein thrombosis in four dogs. Vet Radiol Ultrasound 37:121, 1996. 66. Lamb CR, Burton CA, et al: Doppler measurement of hepatic arterial blood flow in dogs: technique and preliminary findings. Vet Radiol Ultrasound 40:77, 1999.

C h a p t e r

6 5

Stomach Disorders

❚❚❚ PLAIN FILMS Positional and Functional Variations The pyloric antrum changes quite dramatically, depending on how it is positioned when a dog is being radiographed. In the right lateral projection, the antrum is usually lowermost and, as a result, fills with fluid, appearing as an opaque sphere in a radiograph. In the left lateral view, however, the antrum is uppermost and accordingly fills with air, appearing as a lucent circular object.1 Additionally, the pyloric antrum and gastric body are repeatedly swept by contractile waves, regularly changing the shape of these areas, a potentially valuable observation when considering the possibility of atony. The pyloric canal is also quite variable in appearance, but these differences can be appreciated only when the stomach contains barium or some other diagnostic opaque.

❚❚❚ BARIUM EXAMINATION Although the interior of the stomach can be viewed using a variety of diagnostic opaques (as well as with air), barium is by far the most popular. I previously advocated the use of low-dose, patient-tailored gastrointestinal (GI) examinations in both dogs and cats.2-4 Others, for the most part, continue to recommend older, more traditional contrast protocols.5-7

Types of Barium Studies Patient Tailored. Ideally, every examination should be tailored to the individual patient. The radiographer must begin the study by ascertaining (1) the express purpose of the radiographic examination in this animal and (2) precisely what needs to be shown. Once these objectives are clear in the mind of the radiographer, 594

the examination can be optimized to the specific needs of the patient. For the veterinarian requesting a particular examination, this means that his or her instructions to the radiographer must be specific. For example, “suspect osteochondritis of the coronoid process” is more specific than “rule out osteochondritis; radiograph the shoulder and elbow.” Or, in the case of a vomiting dog believed to have pyloric stenosis, it is gastrography, with an emphasis on gastric emptying, that should be ordered, not merely an “upper GI.” In this latter example, most images should be made when pyloric emptying can best be evaluated, not hours later. The appropriate filming interval is best determined by what the preceding radiograph has shown (or not shown). The opportunity to reimage questionable or abnormal GI anatomy is often fleeting and must not be lost to an inflexible protocol. For another example: What about the eccentric bone lesion that fails to be profiled in either standard view? This problem can be resolved by ignoring the standard projections and tailoring the examination to present needs by making a pair of custom right-angle projections, in one of which the x-ray beams are directed tangentially to the lesion.8

Protocol (Predetermined Film Sequence) Most radiographic examinations are performed according to widely accepted, published recommendations, termed protocols. Typically, such instructions indicate the manner in which the animal is to be positioned, the center point of the x-ray beam, and the number of projections required. In general, the more anatomically complex the part, the greater the number of views required for a particular examination. More elaborate protocols exist for so-called special procedures such as gastroenterography and urography, in which contrast media and dosages are described in addition to image sequencing.

CHAPTER 65 ❚❚❚ Stomach Disorders

Only rarely are modifications to these protocols mentioned, although they may seem advisable. Usually of a practical nature, and thus easily committed to memory, most protocols are optimized for the so-called average patient but are often ill suited to the needs of the particular patient. Most veterinarians seem to hold the view that, because most of these protocols are quite effective and have gone unmodified, in some instances for decades, no further refinement is necessary (or for that matter possible). To paraphrase the lateral-thinking guru Edward deBono on the perils of adequacy, “Good is the single greatest obstacle to best!” Many barium protocols have been published previously. When forced by circumstances to perform a protocol-based GI study, I prefer the contrast dosages recommended by Riedesel (the lowest number in each range).9 My preferred filming sequence for such examinations, consisting at the very least of right lateral and ventrodorsal projections, is as follows: Survey films, immediate postcontrast administration, 5, 15, 30 minutes; 1, 3, and 5 hours, and supplementary films thereafter as required depending on the rate of contrast passage. Again, I would like to stress to the reader the absolute superiority of a patient-tailored examination over a fixed protocol study, provided there is time to supervise it (Table 65-1). Morgan proposed the barium protocol for use in cats.10 As with the previous protocol, I recommend using the lowest number in the dose range, or if the

Table 65-1 • RECOMMENDED DOSE RATE OF DIAGNOSTIC OPAQUES FOR DOGS AND CATS Contrast Medium

Dog

Cat

Barium sulfate suspension (undiluted) Diagnostic organic iodine solution (undiluted) Nonionic diagnostic organic iodine solution (240-300 mg I/mL) Barium-impregnated microspheres

6-12 mL/kg

12-16 mL/kg

2-3 mL/kg

2 mL/kg

10 mL/kg (1 : 2 dilution)

10 mL/kg (1 : 2 dilution)

Ten 5-mm and thirty 1.5-mm spheres

Ten 5-mm and thirty 1.5-mm spheres

595

cat is vomiting frequently, a flat dose of 20 mL of fullstrength barium, which is usually more than enough to diagnose most foreign bodies in cats (Table 65-2). Double Contrast: Barium and Air. Evans described double-contrast gastrography in normal dogs11 and later in normal cats,12 pointing out its advantage in identifying mucosal lesions, a point reiterated in a subsequent article comparing single- and double-contrast gastrography in the dog and cat.13 In my experience, the greatest problem with this method is keeping the air in the stomach long enough to complete the examination. Acarbonated beverage (as a source of gas) combined with full-strength barium is another possibility but might result in frothy images. Effect of Barium Temperature on Gastric Motility. Eville and Ackerman demonstrated that temperature has no effect on gastric or esophageal motility. Normal motility values for these organs were reported as 4- to 10-second transit times for the esophagus and four contractions per minute for the stomach.14 Consequences of Barium Entering the Lung. For most dogs and cats, the accidental placement of a small volume of barium or diagnostic iodine solution into the lung causes little or no harm, although it may result in a short-term cough. Clearance in a fully conscious dog with a healthy lung is usually rapid, especially if the contrast gets no farther than a primary bronchus (Figure 65-1). Inhalation of diagnostic opaque usually is related to the forced administration of the contrast medium combined with the animal’s struggles. Using a feeding tube to administer contrast under such circumstances is risky and in the worst case may add a gastric or even tracheal foreign body to the animal’s problems.

❚❚❚ NORMAL GASTRIC EMPTYING TIME Dogs With some exceptions, if the stomach of a dog or cat is contracting normally and the pyloric canal is unobstructed, most of the barium should pass into the duodenum by the end of an hour. This is especially true of cats where barium is often in the colon by 30 minutes.

Table 65-2 • PROTOCOL FOR CONTRAST RADIOGRAPHY IN THE CAT Barium Concentration 30% (wt/wt)

Dose

Timing

Views

12-16 ml/kg body weight

5, 30, and 60 min after administration of contrast and hourly thereafter until barium reaches the colon

Right and left laterals, plus ventrodorsal projection initially; right lateral and ventrodorsal views thereafter

Modified from Morgan JP: The upper gastrointestinal tract in the cat: a protocol for contrast radiography. J Am Vet Rad Soc 18:134, 1977.

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A

B C Figure 65-1 • A, Close-up view of the stomach and caudal lung field of a dog immediately before beginning gastroenterography. B, Close-up lateral view of the stomach made 10 minutes after oral administration of barium shows barium filling a nearby bronchus. C, Subsequent image made 30 minutes later shows that the bronchial barium has disappeared.

Miyabayashi and Morgan described the gastric emptying time in normal Beagles using a variety of food and barium combinations: solid kibble, semisolid kibble, and a mixture of semisolid kibble and barium suspension. Reported complete gastric emptying times were (1) solid food, about 7.5 hours; (2) semisolid food, 7 hours; and (3) semisolid food and barium, 4.5 hours. Allan and co-workers also reported their experience with gastric emptying time in healthy dogs but with

barium-impregnated, polyethylene spheres (1.5 and 5.0) mixed with canned dog food. The authors contend that they have developed a practical technique with clinical potential, but as yet they have no patient data. Normal percent emptying times (based on hourly films) were 4.85 hours (25%), 6.05 hours (50%), and 8.32 hours (75%). Individual plus-minus variations were extreme, being nearly half the mean in the case of the 25% and 50% times.15

CHAPTER 65 ❚❚❚ Stomach Disorders

597

Kunze and co-workers tested numerous radioactive labeling compounds, so-called radiolabels, to determine which was best for scintigraphically evaluating gastric emptying in dogs. Of the five radiopharmaceuticals tested, 99mTc-mebrofenin was determined to be the superior product for radioactively labeling solid-phase test meals.16 Lester and co-workers simultaneously compared radiography and nuclear imaging to evaluate solidphase gastric emptying in normal dogs, using a combination of 30 small barium-impregnated polyethylene spheres mixed with a radiolabeled test meal (99mTcsulfur colloid). Following serial imaging over an 8-hour period (or until 95% of the barium spherules had exited the stomach) and the subsequent construction and statistical analysis of the resultant data, it was determined that gastric emptying, as evaluated scintigraphically, could be assessed in approximately one third of the time it took to obtain similar data by radiographic means.17

bowel, and colon. Four more or less distinct tissue layers and one surface were described: (1) mucosal surface, (2) mucosa, (3) submucosa, (4) muscularis, and (5) serosa-subserosa. Stomach-wall thickness measured 3 to 5 mm; the small and large intestines measured 2 to 3 mm. Peristalsis occurred in the stomach and small bowel but not in the colon.22 Examining the stomach under less than ideal conditions can lead to misdiagnosis and sometimes, as a result, unnecessary biopsy or surgery. In describing such a case, Lamb and Forster-van Hijfte recommend the following patient preparation:23 Partially filling the stomach with water before scanning improves overall visibility by displacing gas, evening out and thinning the stomach wall, and maximizing ultrasound transmission. Withholding food for 12 hours before examination reduces or eliminates solid and semisolid luminal content, which occasionally is mistaken for disease.

Cats

Cats

Using nuclear imaging, Goggin and co-workers determined that gastric emptying in cats is influenced by (1) meal size, (2) meal composition, and (3) concurrent water intake.18 Chandler and co-workers reported the use of radiopaque markers to determine the gastric emptying time (GET) and small intestinal transit time (SITT) of healthy cats fed a low-fiber diet.19 In a followup article, the authors reported that a low dose of diazepam (used to stimulate appetite), administered to healthy cats before being fed a high-fiber diet containing barium-impregnated, polyethylene markers, had little or no effect on gastric emptying times. Highfiber meals emptied more rapidly than low-fiber ones.20 Goggin and co-workers simultaneously compared gastric emptying times in healthy cats fed Tc-disofeninlabeled catfood, which also contained bariumimpregnated polyethylene spheres. They also concluded that radiolabeling is superior to radiopaque marking for the following reasons21:

Newell and colleagues described the normal sonographic appearance of the feline stomach, small intestines, and large intestines.24 Surprisingly, the stomach wall measurements did not fluctuate with volume variations, ranging from full to empty: rugal fold, ~4.38 mm, interrugal cleft, ~2.0 mm.

• Nuclear imaging was potentially less stressful than radiography; thus, stress-related emptying delays were less likely. • Both large and small radiopaque markers tended to precipitate out of the food mass and clump, causing them to be retained in the stomach after the base meal (including the radiolabels) had passed. • Large numbers of radiopaque markers mixed into a test meal reduce its palatability.

❚❚❚ NORMAL SONOGRAPHIC APPEARANCE OF THE STOMACH Dogs Penninck and colleagues characterized the normal sonographic appearance of the canine stomach, small

Gastrointestinal Nuclear Medicine Koblik and Hornof described the uses of nuclear imaging in diagnosing GI disease.25 Specific disorders discussed include esophageal and gastric motilitytransport disorders, gastroesophageal reflux, disturbances in the gastric secretory mechanisms, GI hemorrhage, and various kinds of inflammatory stomach and bowel disease. Hornof and Koblik developed a nuclear imaging technique for quantifying solid-phase emptying time in the dog. They claim that the procedure is capable of identifying which individuals potentially will benefit from corrective pyloric surgery, even though earlier gastrograms were normal.26 Steyn and co-workers reported a similar procedure for use in cats.27 Additionally, the same group determined that intravenous diazepam, a central nervous system appetite stimulant used to “encourage” consumption of foodcontrast mixtures in cats, delays gastric emptying, although it remains uncertain whether the drug directly affects gastric emptying or, alternatively, the delay relates to increased meal size.28

❚❚❚ GASTRIC ENLARGEMENT Gastric enlargement, in the worst-case scenario, can be the result of obstruction, but it is more likely to be incidental, the result of a recent meal or drinking water. The stomach often becomes enlarged during the course of prolonged surgery, a circumstance that potentially

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Table 65-3 • CAUSES OF BENIGN GASTRIC ENLARGEMENT IN DOGS Explanations

Comment

Recent large meal

Caution: A food- or fluid-distended stomach, which contains little or no gas, may be mistaken for liver enlargement (Figure 65-2) See above Rompun (xylazine hydrochloride) has been reported to cause both gastric and intestinal dilation in dogs* Animals with diabetes may regularly overeat, increasing the capacity of the stomach

Consumption of a large amount of water Recent sedative Diabetes

*Modified from Bargai U: The effect of xylozine hydrochloride on the radiographic appearance of the stomach and intestine in the dog. Vet Rad 23:60, 1982.

can lead to postsurgical regurgitation or displacement. Certain diseases, such as diabetes, also can result in enlargement of the stomach. The point is that diagnostic caution needs to be exercised when gastric enlargement is seen (Table 65-3).

❚❚❚ FOREIGN OBJECTS AND MATERIALS Background The radiographic detectability of an abnormal object or foreign material in the stomach depends on three factors: (1) the density of the object or material; (2) the size of the object or material; and (3) the amount of air, fluid, and food in the stomach. The last of these in turn will depend on the dog’s position during imaging. Thus, strategic positioning can be used to demonstrate some foreign bodies that are not visible in standard paired projections.

A

Imaging Findings Radiology Opaque Foreign Body. Opaque foreign bodies such as bone fragments, rocks, wires, and coins are readily appreciated on abdominal films as well as on widefield thoracic images (Figures 65-3 and 65-4). Most pass without incident. Surprisingly, even fishing lures, some with treble hooks, can transit the bowel without apparent adverse effect. Some coins, U.S. pennies, for example, are made of almost pure zinc, a poisonous metal. In their description of such a case, Ackerman and co-workers recommended that objects known to contain zinc be removed from the stomach immediately.29 Some rubber balls appear opaque, whereas others are invisible; the same is true of plastics (Figure 65-5).

❚❚❚ HAIRBALLS AND OTHER LOW-DENSITY MATERIALS IN THE STOMACH Radiographing a cat for hairballs (trichobezoars) is usually unproductive, although occasionally they can be seen in the stomach when surrounded by air (Figure

B Figure 65-2 • A, For a variety of reasons (many of which have little or nothing to do with disease), stomachs may become much larger than normal and, if filled with fluid, can resemble a liver mass. B, Marking the stomach with a small amount of barium and then radiographing it again often resolves suspicious findings such as these.

65-6, A). Likewise, materials such as Styrofoam (Figure 65-6, B), carpet (Figure 65-6, C), paper, and leaves may be detected under similar radiographic circumstances.

❚❚❚ NONOPAQUE FOREIGN BODY Nonopaque gastric foreign bodies usually are suspected based on circumstantial evidence. That is to say, the

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diagnosis usually is based on the acute onset of vomiting in an otherwise healthy dog, an absence of radiographic abnormality in abdominal films, and lack of response to symptomatic treatment. Provided they are surrounded by ample fluid, large and medium-sized fabric foreign bodies can be detected sonographically (Figure 65-7, A, B). Smaller nonopaque objects are difficult to detect under any circumstances.

❚❚❚ SECOND FOREIGN BODY Occasionally, two or more foreign bodies are present in the same animal.30 If one of these is outstanding, especially if is located in the stomach, there is a high probability that a second, less visible but clinically more important object in the intestine will be missed. Conversely, the situation may be reversed, with one or more highly visible intestinal foreign bodies and a relatively faint foreign object in the stomach (see Figure 65-4). Omissions of this sort can be reduced by always conducting a thorough search of the GI tract, even after an obvious foreign body has been found. Admittedly, such a strategy can be time consuming and thus costly; alternatively, some choose to stop filming once an obstruction has been identified, leaving the remaining bowel to be assessed manually at the time of surgery.

A

❚❚❚ GASTRITIS Background Imaging Findings Radiology. Plain films do little to elucidate the interior surface of the stomach, even when ample gas is present. Rugal size is at its maximum when the stomach is empty and gradually becomes smaller as the stomach distends. When a portion of the stomach wall (to include the associated rugae) fails to change in sequential radiographs, it suggests, but does not confirm, a lesion at this point. It most cases, however, gastritis involves the entire stomach. Occasionally, severe gastritis may cause ulceration, which later may lead to perforation. This condition is called ulcerative gastritis and has been described by Barber and Lorenz.31 Ultrasound. In most cases, gastritis can be readily discriminated from an advanced stomach cancer by its diffuse and nondisruptive nature; however, severe gastritis and an early carcinoma may share similar features, making discrimination difficult or impossible.

❚❚❚ UNUSUAL GASTRIC DISORDERS

B Figure 65-3 • Lateral (A) and ventrodorsal (B) radiographs show a cluster of safety pins in the antral region of the stomach of a dog.

(3) distortion and reduced definition of the layers of the stomach wall.32

Stomach Worms Astomach worm, Aonchotheca putorii, has been reported to cause delayed gastric emptying and rigidity of the pylorus and duodenal bulb in a cat. Gastritis and a perforated pyloric ulcer were found in the same animal during exploratory surgery.33 The stomach fluke, Ollulanus tricuspis, is capable of causing a fibrotic form of gastritis in cats that leads to chronic intermittent vomiting.

Uremic Gastritis Dogs and cats with gastritis secondary to renal failure show a wide variety of sonographic lesions, including (1) mural thickening, (2) mucosal mineralization, and

Gastrointestinal Pythiosis Graham and co-workers described the sonographic appearance of canine GI pythiosis (pronounced pith”

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C

A

D

B E Figure 65-4 • Lateral (A) and ventrodorsal views (B) show multiple high-density objects in the gastrointestinal tract: one in the stomach (C) and three in the small intestine (D, E). Additionally, there is an interrupted intestinal gas pattern suggesting bunching of the bowel, similar to what is often seen in cats with fixed linear foreign bodies such as thread or string.

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B o x

601

6 5 - 1

Risk Factors for Gastric Dilation in Irish Setters Aerophagia Age Once-daily feeding Recent car ride Recent kenneling Single food type

B o x

6 5 - 2

Nonrisk Factors for Gastric Dilation in Irish Setters Appetite Body temperature Dry dog food Excitement Intensity or duration of exercise Speed of eating Vomiting or diarrhea

Figure 65-5 • Ventrodorsal view of the abdomen shows golf ball fragments in the left half of the stomach and a low-density, spherically shaped object superimposed on a pair of bowel segments (the rubber center of the golf ball) just to the right of L2.

e-o’sis).34 The disease, caused by a mold, which grows in warm, standing water; attacks the stomach and much of the intestine; and produces many of the same sonographic signs customarily associated with neoplasia: wall thickening, loss of layering, and regional adenopathy.

Gastric Dilation (Gastric Dilation, Gastric Distension, Bloat) Background. In my experience, gastric dilation as a result of overeating is far more common than gastric torsion; this experience challenges the widespread belief that gastric enlargement inevitably leads to displacement (torsion).Although dilation presumably precedes torsion in some dogs, it does not necessarily follow that dilation leads to torsion. Risk factors for gastric displacement have been reported for dogs in general and also for specific breeds.35 Predictive data for the Irish Setter, a typical deep-chested breed, are presented in Boxes 65-1 and 65-2. Imaging Findings. The food-, fluid-, or gas-distended stomach resembles the torsed stomach insofar as both appear extremely large and displace the bowel and spleen caudally; however, simple distension usually does not cause the stomach to fold on itself (resulting

in a distinctive compartmentalized appearance) or result in marked pyloric displacement (usually dorsally). In addition, torsion typically causes extreme degrees of splenic engorgement and dislocation, features uncharacteristic of simple bloat.

Gastric Torsion (Gastric Volvulus, Gastric Dilation-Volvulus) Background. Gastric torsion may follow gastric distension, particularly in certain breeds of dogs, such as Great Danes, German Shepherds, Weimaraners, Saint Bernards, Gordon and Irish Setters, and Standard Poodles. Torsion does not invariably follow dilation, however, and for this reason, the expression gastric dilation/volvulus syndrome can be misleading or in some instances inaccurate. Other risk factors include (1) advanced age, (2) increased weight, and (3) body type.36 Gastric torsion is for the most part a disorder of adult dogs, but it has been reported in a 5-week-old Labrador Retriever puppy.36a Most veterinarians believe that gastric torsion is a physical disorder of large, deep-chested breeds, triggered by rapidly eating a large meal either immediately before or after vigorous exercise. Many contend that drinking a large volume of water after a meal increases the risk of torsion. This view, however widely held, may be too simplistic, failing to take into consideration important physiologic changes related to eating, exercise, excitement, and body type. Using thoracic radiographs from 437 dogs, including 17 different breeds, Glickman and co-workers calculated the depth/width ratios of the caudal ribcage, and concluded that the greater this ratio, the greater the risk of gastric torsion.37 Although fatality rates as high as 60% have been reported in dogs, large studies with standardized

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B

A

C Figure 65-6 • A, Close-up ventrodorsal view of the abdomen of a cat shows a large, irregular object (or objects) in the stomach characteristic of a hairball. B, Close-up ventrodorsal view of the abdomen of a cat shows a vague, medium-sized irregular object (or objects) in the stomach that later proved to be Styrofoam. C, Close-up ventrodorsal view of the abdomen of a cat shows a large, patterned object (or objects) in the stomach, later found to be carpeting.

methods of diagnoses and treatment have generated far more optimistic numbers (~85% survival).38 Bear in mind, however, that the available resources in a university veterinary teaching hospital are far greater than those available to most private practices. Imaging Findings Radiology. Traditionally, radiographic assessment of gastric dilation, gastric torsion, and combined gastric dilation and torsion has been based on lateral and ventrodorsal films made of a recumbent animal. Radiographic variations have included decompressing the stomach before radiography, omitting the ventrodorsal image, and adding a left lateral view.

In previous publications, I advocated use of the standing lateral projection (postural film) in dogs thought to have a gastric torsion because it is less stressful and less dangerous than a conventional recumbent view.39 As I have also shown, the standing lateral position is nearly always more conclusive than a recumbent view, provided that the person making the judgment is familiar with the postural projection. The following are radiographic indicators of gastric dilation:40 • A greatly enlarged stomach, filled with a combination of food, fluid, and air (Figure 65-8). • Aright-sided antral/duodenal junction (“pylorus”) as seen in ventrodorsal projection.

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603

A

Figure 65-8 • Lateral close-up view of a dilated (but not torsed) stomach.

B Figure 65-7 • A, Transverse sonogram of the body of the stomach shows multiple hyperechoic surfaces that are producing intense acoustic shadows, compatible with a foreign body (athletic sock). B, Sonographic cross-section of the pyloric antrum of a dog shows a bright object casting a strong acoustic shadow, which subsequently proved to be a chunk of plastic.

Figure 65-9 • Lateral close-up view of a bloated stomach that

• A normal-appearing antral/duodenal junction (“pylorus”) as seen in a right or left lateral projection (Figure 65-9).

• A dorsally located antral/duodenal junction (“pylorus”) as seen in right lateral projection. • Pneumoperitoneum strongly suggests either iatrogenic injury caused by a stomach tube, or spontaneous gastric perforation.41

I also observed a case of severe gastric dilation (bloat), which developed during an extended spinal surgery (6 hours) and subsequently led to splenic rupture, hemoperitoneum, and death as a result of vascular obstruction (Figure 65-10). The following are radiographic indicators of gastric torsion (volvulus): • Greatly enlarged, compartmentalized stomach, which is filled with a combination of food, fluid, and air (Figure 65-11).

developed during surgery, causing dyspnea.

Barium Films. Generally, barium films are unnecessary because a diagnosis of gastric displacement usually can be easily made from plain films. Occasionally, the body of the stomach may become secondarily twisted, in which case it can be difficult or impossible to locate. In such circumstances, a barium marking study can be quite useful (Figure 65-12). Strange Twists. Yeager published a highly unusual case of gastric torsion in which a 9-year-old Gordon

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Figure 65-10 • Ventrodorsal view of a severely dilated stomach in a dog, which secondarily caused splenic torsion, rupture of multiple splenic blood vessels, and a hemoperitoneum.

Figure 65-12 • Lateral close-up view of the abdomen following barium marking shows twisted stomach, an unusual form of torsion. Note that the stomach is capable of receiving barium but not expelling it.

showed an air-filled, characteristically deformed stomach, clearly indicative of torsion. Because there was no discussion as to what the author thought of this unusual turn of events, readers can only speculate as to when and why the stomach became displaced.42 I recently observed a gastric torsion in a dog in which the stomach appeared to have turned end-for-end, something I had never seen before. As a result, the bowel mass was displaced cranial to the stomach instead of caudally and the spleen lay almost entirely in the right cranial part of the abdomen. Other than the stomach, the only organs remaining in the caudal two thirds of the abdomen were the distal colon and bladder (Figure 65-13). Figure 65-11 • Lateral view of the abdomen shows a distended, displaced, compartmentalized stomach and duodenum (upper left) characteristic of torsion, which developed shortly after the dog ate a dead bird.

Setter was first seen for behavioral changes and possible colic (2 weeks’ duration). Abdominal radiographs showed caudolateral bowel displacement inferring an enlarged and possibly displaced stomach, although the stomach itself could not be identified with certainty. Unspecified medical treatment was given and the animal sent home. Four days later, the dog was brought back with a painful, distended abdomen and attempting (unsuccessfully) to vomit. This time, abdominal radiographs

The Posttorsional Stomach Gastropexy. The goal of incisional gastropexy is to attach the antral portion of the stomach to the adjacent right abdominal wall and thus prevent torsion from recurring. To ensure permanency, the sutures used to join the two surfaces must be replaced eventually by connective tissue adhesions. The presence and effectiveness of such adhesions are best evaluated sonographically by demonstrating the (1) continuity and (2) simultaneous movements of the antrum and right abdominal wall.43 Caution: Apyloric gastropexy may sonographically resemble an intussusception.

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A

Figure 65-14 • Ventrodorsal gastrogram of a 12-month-old Airedale that has been vomiting persistently since it was a small puppy shows the intestine abnormally distributed in the right half of the abdomen, dominated by one or more large gas-filled objects cranially. Subsequent surgery revealed herniation and entrapment (incarceration) of the pyloric antrum through the foramen of Winslow.

B Figure 65-13 • Close-up lateral and ventrodorsal views of a highly unusual gastric torsion in a dog in which the stomach has rotated in the long rather than the short access of the torso. In this type of displacement, the intestine is located cranial to the stomach instead of caudally.

Gastric Tube Position and Possible Leakage. The location of a stomach tube can be reliably established in two views (but not in one view) of the cranial abdomen. The patency of a gastric tube requires the injection of a diagnostic iodine solution into the tube and subsequent biplanar demonstration of contrast in the stomach. In my experience, small leaks combined with small amounts of contrast solution often go undetected, at least in initial films. It is good practice always to make a second set of films at least 10 minutes following the first. Postcorrectional Vomiting. In my experience, some dogs operated on for a gastric torsion vomit persistently following surgery, irrespective of diet or feeding schedule. I hypothesize that this may be due to one of two possible causes: ischemia and the resultant tissue

anoxia associated with gastric torsion can damage or destroy the cells of the gastric pacemaker located in the cardia, upsetting the coordination between gastric contraction and pyloric opening. Alternatively, when gastropexy is performed, it can affect the contractility of the pyloric antrum, in turn leading to pyloric insufficiency. Pyloric Entrapment. Partial outlet obstruction may develop secondary to pyloric entrapment (“incarceration”), in conjunction with proximal duodenal atony (Figure 65-14). A form of pyloroduodenal fixation can also develop following pancreatitis and inflammation of the pancreatic mesentery, with or without resultant GI blockage.

Gastric Ulcers Background. Common clinical signs associated with gastric ulcers include (1) vomiting, (2) hematemesis, (3) melena, (4) weight loss, and (5) anemia. Additionally, most dogs with ulcers exhibit some degree of colic that usually is exacerbated by eating. Ibuprofen has been reported to cause gastric ulcers in dogs, which potentially can perforate and result in suppurative peritonitis.44 In such cases, one can expect

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not only the radiographic indicators of peritonitis (increased abdominal density and decreased visceral detail) but also a large volume of peritoneal air, suggesting gastric or esophageal perforation. Imaging Findings. Barber described the radiographic features of gastric ulcers in dogs as exemplified in Figure 65-15.45 Edwards reported a case of a house cat with acute, severe abdominal distension, subsequently discovered to be the result of pneumoperitoneum. Postmortem examination revealed a perforating gastric ulcer. Surprisingly (and inexplicably), there was no evidence of peritonitis.46 Penninck described the sonographic appearance of gastric ulcers in dogs, pointing out the following salient features47:

A

• Focal echogenicity associated with the ulcer crater, representing trapped air (microbubbles) • Frequent loss of normal wall architecture (individual layers) • Localized thickening of the stomach wall: 9-16 mm, often featuring a centrally located ulcer • Presence of an ulcer crater or stomach wall defect related to ulceration

Stomach Tumors (Gastric Tumors, Gastric Neoplasia) Background. A variety of stomach tumors have been reported in dogs, including lymphoma, leiomyoma, leiomyosarcoma, and adenocarcinoma. The last of these often has been associated with gastric ulcers.48 Penninck and colleagues, in a description of 16 dogs with gastric epithelial tumors, reported vomiting, anorexia, and weight loss as common, and melena and hematemesis as infrequent.49 Imaging Findings Plain Films. Survey radiographs occasionally suggest a gastric tumor, especially bulky wall tumors such as lymphoma, leiomyoma, leiomyosarcoma, and some adenocarcinomas, where the stomach may appear to contain an usually shaped or oriented “gas bubble” positioned deep in its interior, which persists relatively unchanged through a number of subsequent films (Figure 65-16, A, B).50 Gastrography. Small and medium-sized stomach tumors are usually best seen using a combination of air and barium (double contrast). Large tumors are usually seen equally in either single- or doublecontrast studies (Figure 65-16, C, D). In my experience, a relatively immobile area (or areas) of thickened stomach wall, as seen in sequential barium films, strongly suggests a tumor. Survey films rarely reveal such lesions. Ultrasound. The single most defining quality of a malignant stomach tumor is its anatomically disruptive

B Figure 65-15 • Ventrodorsal (A) and close-up (B) views of the stomach of a dog with a duodenal ulcer show a bilobed filling defect within a pool of barium.

nature, as reported by Lamb and Grierson. A mass in the wall of the stomach is likely cancerous when it exhibits one or more of the following sonographic abnormalities51: • • • • • •

Absence of discrete stomach layers Disruption of normal stomach layers Surrounding adenopathy Thickened stomach wall Ulceration Region of relative immobility

Kaser-Hotz and co-workers also observed that (1) stomach wall thickening, (2) lack of definable wall layers, and (3) enlargement of nearby lymph nodes are sonographic features characteristic of stomach tumors. Echogenicity, either increased or decreased, did not prove to be a reliable indicator of cancer.52 Penninck and colleagues touted the diagnostic value of pseudolayering, a term proposed by Johnston53 to describe a dark-light-dark, banded appearance of the affected portion of the stomach, often identified with gastric tumors.54

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A

C

D B Figure 65-16 • Plain lateral (A) and ventrodorsal (B) abdominal radiographs and lateral (C) and ventrodorsal (D) barium films show massive dilation of the stomach as a result of a leiomyoma (seen best in the ventrodorsal gastrogram as an enormous gastric filling defect).

Predicting Specific Cancers. According to Pinninck, carcinoma and lymphoma are usually hypoechoic. Carcinomas often extend beyond the stomach surface, whereas lymphomas typically remain within the confines of the serosa. Leiomyosarcoma is typically heterogeneous, sometimes associated with anechoic foci believed to be necrosis. Other features of the leiomyosarcoma include (1) its appearance as a focal mass, (2) a thickened muscularis, and (3) an antral location. The following features, although compatible with a primary stomach tumor, do not reliably discriminate between the various cell types: • Degree of echogenicity • Magnitude of wall thickening

• Presence of regional adenopathy • Presence of ulceration

Pyloric Obstruction Background. Obstruction of the pylorus may be due to a variety of causes55: • • • • • • •

Acquired hypertrophy Asynchronous opening Congenital hypertrophy Foreign body Pyloric inversion (gastrogastric intussusception) Pyloric tumor Pancreatitis, pancreatic cancer

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A Figure 65-17 • Lateral view of the abdomen shows enormous object filling much of the cranial two thirds of the abdomen. The object in question is actually a mass effect caused by a fluid-filled stomach obstructed by a pyloric tumor. The bone fragments were presumed to be either incidental or too large to pass through the narrowed pylorus.

• Pyloric ulcer • Pylorospasm • Extrinsic compression secondary to pancreatitis Imaging Findings Radiology. Rhodes and Brodey described the radiographic differentiation of pyloric obstructions in dogs resulting from congenital or acquired hypertrophy and pylorospasm.56 Huml and co-workers described a rare case of gastrogastric intussusception in a 3-year-old Rottweiler with acute vomiting. Plain films of the abdomen showed a large spherical mass in the fundic region of the stomach, outlined by gas. Sonography confirmed the presence of a large partially lobulated, intraluminal stomach mass, featuring a poorly defined hyperechoic center, which gradually become hypoechoic toward the periphery. The dog went to surgery with a diagnosis of stomach mass, probably a tumor. In retrospect, the authors believe that had the stomach wall not been so edematous, its characteristic layers would have been identified, and the “mass” would have been appreciated for what it was: part of the stomach.57 In plain images, the combination of a large fluidfilled stomach and one or more foreign bodies, especially bone fragments, suggests physical blockage of the pylorus (Figure 65-17). Barium films are capable of demonstrating pyloric-filling defects caused by tumors, but because of the highly variable nature of the pyloric part of the stomach, lesions in this location must be demonstrated repeatedly to be diagnosed with confidence (Figure 65-18). Ultrasound. Biller and co-workers reported the sonographic appearance of chronic pyloric hypertrophy in six dogs, most of which were older, smaller breeds.

B

C Figure 65-18 • Orientation (A) and close-up ventrodorsal views (B, C) of the pylorus show only a very faint band of communicating barium between the antrum and duodenum approximately 1 hour after the beginning of the examination. This finding is compatible with obstruction from sources such as tumor, large ulcer, and, less often, benign hypertrophy. A large pyloric tumor was diagnosed surgically.

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The authors assert that if the pyloric wall, which sonographically appears as a thick dark ring (in crosssection), equals or exceeds 9 mm in width, the dog likely has pyloric stenosis.58 A close-up profile view of a normal pyloric antrum featuring a characteristic pyloric “nipple” is shown in Figure 65-19 (Table 65-4).

Hiatal Hernia Background. The incidence of hiatal hernia is unknown, but English Bulldogs appear to be at relatively greater risk than other breeds.59 The two types of hiatal hernia are sliding and stationary. In the sliding type, the abdominal portion of the esophagus and a small portion of the stomach pass back and forth into the caudal mediastinum through the esophageal opening in the diaphragm.60 In the stationary form of hiatal hernia, the displaced abdominal esophagus and stomach remain in the thorax. Hiatal hernias have been reported in cats,61 but most appear to be of an incidental nature.62 Hiatal hernias may or may not be associated with gastroesophageal reflux. Hiatal hernia has also been reported to be a complication of chronic diaphragmatic hernia/surgical repair, developing about a week after surgery.63 Imaging Findings. Nontraumatic hernias of the stomach through the opening in the diaphragm intended for the esophagus can be partial or complete, permanent or temporary, the latter often being described as sliding, referring to their back-and-forth movement from the abdomen to the thorax. In my experience, such dislocations are often of no consequence and as such are incidental findings, especially in older cats (Figure 65-20). I have seen one referral case in which an asymptomatic, presumably fixed hiatal hernia in a dog initially was mistaken for a lung mass. Fortunately, a barium marking study was performed, which revealed the true nature of the abnormality. Left lateral images of the thorax can be mistaken for hiatal hernias, especially when the stomach is fully or partially air-filled. Consequently, gastric marking studies are advisable whenever the diagnosis is in doubt.

Gastroesophageal Intussusception Background. Displacement of the stomach into the caudal part of the esophagus is an unusual occurrence that may affect young male German Shepherd puppies with megaesophagus. Clinical signs include regurgitation, vomiting, dyspnea, hematemesis, colic, and varying degrees of shock.64 Van Camp described a similar clinical profile in a cat.65 Imaging Findings. Many gastroesophageal intussusceptions can be diagnosed on plain radiographs, especially if a postural film is included (supported sternal position with horizontal x-ray beam). An esophagram

Figure 65-19 • Close-up sonographic long section of the pyloric antrum of a healthy dog shows a characteristic pyloric nipple (center left) representing the pyloric canal.

is also usually diagnostic but often adds to the animal’s swallowing difficulties and may cause aspiration. Plain thoracic films typically show esophageal enlargement. Abdominal images may reveal cranial displacement of the stomach, depending on the size of the intussusception. One report described both the stomach and the spleen lodged within the caudal aspect of the esophagus.66 A postural radiograph usually shows a dilated esophagus, a lengthy fluid level, and a caudal esophageal mass effect. An esophagram typically shows a generalized esophageal enlargement with a large oval-shaped filling defect caudally. No barium or iodine solution appears in the stomach.67 Occasionally, a gastroesophageal invagination will resolve spontaneously but may leave the esophagus partially incapacitated (Figure 65-21). In my experience, most such abnormalities resolve within a few weeks but may recur, depending on what led to the original dislocation.

Chronic Lymphocytic/Plasmacytic Gastritis Chronic lymphocytic/plasmacytic gastritis occurs in both dogs and cats, typically manifesting as gradual weight loss accompanied by intermittent vomiting. The disease can be very difficult to diagnose with medical imaging (plain and contrast radiography or sonography) because it produces only subtle irregularities in the lining of the stomach and causes negligible thickening. In most cases, an endoscopic or surgical gastric biopsy is required for diagnosis.68

Gastric Perforation and Rupture In my experience, gastric rupture occurs most often following a gastric torsion (although this is by no means

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Figure 65-20 • Close-up lateral view of a hiatal hernia in a cat as depicted by a portion of the barium-containing stomach passing through the esophageal opening in the diaphragm (far left center).

Table 65-4 • DIFFERENTIAL CONSIDERATIONS IN CANINE PYLORIC OBSTRUCTION Form of Pyloric Obstruction

Onset of Signs

Nature of Vomiting

RDIs

Acquired pyloric hypertrophy Congenital pyloric stenosis

Older dogs

Varying intervals after eating

Puppies: coincides with change over to solid food

Projectile; occurs at regular intervals following eating

Pylorospasm

Any age

Varying intervals after eating

Marked delay in gastric emptying that is not relieved by spasmolytic drugs Marked delay in gastric emptying Fluoroscopically, pylorus may be abnormally shaped as indicated by “beak,” “string,” or “teat” signs (see Figure 65-19), depending on the extent of pyloric blockage Delayed gastric emptying, which becomes normal after administration of spasmolytic drugs

RDIs, Radiographic disease indicators.

a certainty). Other causes of gastric rupture or perforation include the following: 1. Dehiscence of a gastric biopsy, GI anastomosis, or exploratory gastrotomy site 2. Dislodged gastrotomy tube 3. Penetrating wound, especially gunshot 4. Perforated ulcer 5. Procedural injury: perforation with a stomach tube 6. Tumor necrosis or fistulation

Gastrobronchial Fistula Background. Gastrobronchial fistula is rare. Possible precipitating causes include left-sided diaphragmatic hernia, gastric ulcer (primary or secondary to tumor), diaphragmatic or paradiaphragmatic abscess, migrating foreign body (lung to stomach, or stomach to lung), and caudal or accessory lung lobe abscess.

Imaging Findings Radiology. Pulmonary abnormalities, which can be anticipated in a gastrobronchial fistula, include focal or regional lung consolidation, cavitation, volume loss, and bronchial dilation. Abdominal films are usually unremarkable, although cranial displacement of the pyloric part of the stomach has been reported.69 Gastrography. When an abnormal opening in the stomach is suspected, for example, a fistula, sinus, or perforated ulcer, only iodine-based contrast agents should be used, ideally ones that are nonionic. Because such lesions are highly unpredictable with respect to when and how they will fill with contrast, standard filming protocols are often inadequate and instead should be replaced with patient-tailored examinations. In this method of examination, the x-ray beam is centered over the stomach and duodenum, and right and left laterals, dorsoventral, and ventrodorsal views

CHAPTER 65 ❚❚❚ Stomach Disorders

611

A

A

B Figure 65-21 • A, Lateral view of the thorax of a dog with a gastroesophageal intussusception, which is apparent as an oval, air-containing object in the caudal esophagus. Fluid and air cranial to the displaced stomach have created sufficient mass to displace the trachea and heart ventrally. B, A 24-hour progress film shows that although the stomach has returned to the abdomen, the esophagus remains distended with air and fluid.

are made immediately following contrast administration. All subsequent views (and their timing) are predicated on what is seen in the preceding images. The examination is complete once the question of leakage has been resolved. Other than the proximal duodenum, the remaining bowel is not examined because that is not the purpose of the examination.

Gastric Calcification Localized or regional calcification of the stomach wall is a rare finding that is usually related to a physical or chemical injury leading to tissue death (dystrophic calcification), abnormal mineral deposition related to a variety of disease-related metabolic disturbances, neoplasia, or the metaplastic conversion of one tissue type into another. In the stomach, calcified tissue is more readily appreciated than in most other locations because of its characteristic banded appearance corresponding to the

B Figure 65-22 • Lateral (A) and ventrodorsal (B) views of the abdomen show a large calcified mass occupying the pyloric and antral regions of the stomach and protruding into the adjacent airfilled lumen.

rugal folds and the high contrast between the calcified stomach tissue and the gastric air bubble. As a generality, the more the calcification conforms to the normal rugal pattern stomach, the more likely it is to be benign. Conversely, the more amorphous the calcification, the greater the likelihood that it is malignant (Figure 65-22).

Gastric Atony (Immobility) and Its Diagnostic Implications In my experience, gastric immobility is most often the result of nongastric disease. Less often, atony

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results from muscular fatigue brought about by prolonged pyloric (outlet) obstruction. I have also seen gastric stasis in dogs with parvoviral enteritis, even though the disease causes no stomach lesions. Occasionally, stomachs that have been dilated or torsed go through a brief period of atony following decompression. Some dogs undergoing GI contrast examinations may initially show what appears to be atony, but later in the study a full range of stomach sizes and shapes is revealed. In my experience, volume, consistency, temperature, and route of administration all potentially affect gastric emptying time using either barium or diagnostic iodine solutions; however, these differences are usually minor. With respect to the relationship between gastrography, atony, and obstruction, I hold the following view: If in a dog barium fails to leave the stomach within an hour of administration, and interim images show little or no change in the appearance of the stomach, I begin with the premise that the stomach is atonic. Conversely, if barium fails to leave the stomach within an hour, but the intervening images of the stomach show normal variability, and thus infer normal contraction, I start with the idea that there is probable pyloric obstruction.

References 1. Love NE: The appearance of the canine pyloric region in right versus left lateral recumbent radiographs. Vet Radiol Ultrasound 34:169, 1992. 2. Farrow CS: Tailoring radiographs to fit the patient. Waltham Focus 6:25, 1996. 3. Farrow CS: The abdomen. In Farrow CS, ed: Radiology of the cat. St. Louis, 1994, Mosby. 4. Farrow CS: The stomach. In Farrow CS, ed: Emergency radiology in small animal practice. Toronto, 1988, BC Decker. 5. Riedesel EA: The small bowel. In Thrall DE, ed: Textbook of veterinary diagnostic radiology. Philadelphia, 2002, WB Saunders. 6. Morgan JP: The upper gastrointestinal examination in the cat: normal radiographic appearance using positive contrast medium. Vet Rad 22:159, 1981. 7. Kleine LJ, Lamb CR: Comparative organ imaging: the gastrointestinal tract. Vet Rad 30:133, 1989. 8. Farrow CS: Tailoring radiographs to fit the patient. Waltham Focus 6:25, 1996. 9. Riedesel EA: The small bowel. In Thrall DE: ed: Textbook of veterinary diagnostic radiology. Philadelphia, 2002, WB Saunders. 10. Morgan JP: The upper gastrointestinal tract in the cat: a protocol for contrast radiography. J Am Vet Rad Soc 18:134, 1977. 11. Evans SM, Laufer I: Double contrast gastrography in the normal dog. Vet Rad 22:2, 1981. 12. Evans SM, Biery DN: Double contrast gastrography in the cat. Vet Rad 24:3, 1983. 13. Evans SM: Double versus single contrast gastrography in the dog and cat. Vet Rad 24:6, 1983. 14. Eville P, Ackerman N: The effect of barium temperature on esophageal and gastric motility in dogs. Vet Rad 25:233, 1984.

15. Allan FJ, Guilford WG, et al: Gastric emptying of solid radiopague markers in healthy dogs. Vet Radiol Ultrasound 37:336, 1996. 16. Kunze CP, Hoskinson JJ, et al: Evaluation of solid phase radiolabels of dog food for gastric emptying. Vet Radiol Ultrasound 40:169, 1999. 17. Lester NV, Roberts GD, et al: Assessment of barium impregnated polyethylene spheres (BIPS) as a measure of solid-phase gastric emptying in normal dogs: comparison to scintigraphy. Vet Radiol Ultrasound 40:465, 1999. 18. Goggin JM, Hoskinson JJ, et al: Scintigraphic assessment of gastric emptying of canned and dry diets in healthy cats. Am J Vet Res 159:388, 1998. 19. Chandler ML, Guilford WG: Assessment of gastric emptying and small intestinal transit in cats using radiopaque markers. J Vet Intern Med 11:361, 1997. 20. Chandler ML, Guilford WG, et al: Gastric emptying and intestinal transit times of radiopaque markers in cats fed a high-fiber diet with and without low-dose intravenous diazepam. Vet Radiol Ultrasound 40:3, 1999. 21. Goggins JM, Hoskinson JJ, et al: Vet Radiol Ultrasound 40:89, 1999. 22. Penninck DG, Nyland TG, et al: Ultrasonography of the normal canine gastrointestinal tract. Vet Rad 30:272, 1989. 23. Lamb CR, Forster-van Hijfte M: Beware the gastric pseudomass. Vet Radiol Ultrasound 35:398, 1994. 24. Newel SM, Graham JP, et al: Sonography of the normal feline gastrointestinal tract. Vet Radiol Ultrasound 40:40, 1999. 25. Koblik PD, Hornof WJ: Gastrointestinal nuclear medicine. Vet Rad 26:138, 1985. 26. Hornof WJ, Koblik PD, et al: Scintigraphic evaluation of solid-phase gastric emptying in the dog. Vet Rad 30:242, 1989. 27. Steyn PF, Twedt D, Toombs W: The scintigraphic evaluation of solid phase gastric emptying in normal cats. Vet Radiol Ultrasound 36:327, 1995. 28. Steyn PF, Twedt D, Toombs W: The effect of intravenous diazepam on solid phase gastric emptying in normal cats. Vet Radiol Ultrasound 38:469, 1997. 29. Ackerman N, Spencer CP, et al: Zinc toxicosis in a dog secondary to ingestion of pennies. Vet Rad 31:155, 1990. 30. Scrivani PV, Miyabayashi T, et al: What is your diagnosis? J Am Vet Med Assoc 207:1409, 1995. 31. Barber DL, Lorenz MD: Radiographic diagnosis. Vet Rad 22:118, 1981. 32. Grooters AM, Miyabayashi T, et al: Sonographic appearance of uremic gastrography in four dogs. Vet Radiol Ultrasound 35:35, 1994. 33. Curtsinger DK, Carpenter JL, Turner JL: Gastritis caused by Aonchotheca putori in a domestic cat. J Am Vet Med Assoc 203:1151, 1993. 34. Graham JP, Newell SM, et al: Ultrasonographic features of canine gastrointestinal pythiosis. Vet Radiol Ultrasound 41:273, 2000. 35. Elwood CM: Risk factors for gastric dilation in Irish Setters. J Small Anim Pract 39:185, 1998. 36. Glickman LT, Glickman NW, et al: Analysis of risk factors for gastric dilation and dilatation-volvulus in dogs. J Am Vet Med Assoc 204:1465, 1994. 36a. Mazin RM, Christman A, Pasek A: What is your diagnosis? J Am Vet Med Assoc 221:489, 2002. 37. Glickman L, Glickman N, et al: Radiological assessment of the relationship between thoracic conformation and the risk of gastric dilatation-volvulus in dogs. Vet Radiol Ultrasound 37:174, 1996.

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38. Brockman DJ, Washabau RJ, Drobatz KJ: Canine gastric dilatation/volvulus syndrome in a veterinary critical care unit: 295 cases (1986-1992). J Am Vet Med Assoc 213:515, 1993. 39. Farrow CS: Tailoring radiographs to fit the patient. Waltham Focus 6:25, 1996. 40. Hathcock J: Radiographic view of choice for the diagnosis of gastric volvulus: the right lateral recumbent view. J Am Anim Hosp Assoc 20:967, 1984. 41. Probst CW, Bright RM, et al: Spontaneous pneumoperitoneum subsequent to gastric volvulus in two dogs. Vet Rad 25:37, 1984. 42. Yeager AE: Radiographs presented as part of the 1995 A.C.V.R. oral certification examination: abdomen section. Vet Radiol Ultrasound 37:181, 1996. 43. Wacker CA, Weber WT: Ultrasonic evaluation of adhesions induced by incisional gastropexy in 16 dogs. J Small Anim Pract 39:379, 1998. 44. Godshalk CP, Roush JK, et al: Gastric perforation associated with administration of ibuprofen in a dog. J Am Vet Med Assoc 201:1734, 1992. 45. Barber DL: Radiographic aspects of gastric ulcers in dogs. Vet Rad 23:109, 1982. 46. Edwards NJ, Mead WW, Haviland DG: Spontaneous pneumoperitoneum in a cat. Vet Radiol Ultrasound 35:428, 1994. 47. Penninck D, Tidwell A: Ultrasonography of gastric ulceration in the dog. Vet Radiol Ultrasound 38:308, 1997. 48. Berg P, Rhodes WH, O’Brien JB: Radiographic diagnosis of gastric adenocarcinoma in a dog. J Am Vet Rad Soc 5:47, 1964. 49. Penninck DG, Moore AS, Gliatto J: Ultrasonography of canine gastric epithelial tumors. Vet Radiol Ultrasound 39:342, 1998. 50. Cantwell HD: Radiographic diagnosis. Vet Rad 28:1987. 51. Lamb CR, Grierson J: Ultrasonic appearance of primary gastric neoplasia in 21 dogs. J Small Anim Pract 40:211, 1999. 52. Kaser-Hotz B, Hauser B, Arnold P: Ultrasographic findings in canine gastric neoplasia in 13 patients. Vet Radiol Ultrasound 37:51, 1996. 53. Johnston BA: A proposed new sonographic sign to aid in further differentiation of gastric neoplasms. Diagn Med Sonogr 3:21, 1987.

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54. Penninck DG, Moore AS, Gliatto J: Ultrasonography of canine gastric epithelial tumors. Vet Radiol Ultrasound 39:342, 1998. 55. Douglas SW: Lesions involving the pyloric region of the canine stomach. J Am Vet Rad Soc 9:89, 1968. 56. Rhodes WH, Brodey RS: The differential diagnosis of pyloric obstructions in the dog. J Am Vet Rad Soc 6:65, 1965. 57. Huml RA, Konde L, et al: Gastrogastric intussusception in a dog. Vet Radiol Ultrasound 33:150, 1992. 58. Biller DS, Partington BP, et al: Ultrasonographic appearance of chronic hypertrophic pyloric gastrography in the dog. Vet Radiol Ultrasound 35:30, 1994. 59. Lorinson D, Bright RM: Long-term outcome of medical and surgical treatment of hiatal hernias in dogs and cats: 27 cases (1978-1996). J Am Vet Med Assoc 213:381, 1998. 60. Ackerman N, Millman T: Esophageal hiatal hernia in a dog. Vet Rad 23:107, 1982. 61. Rossmeisel JH, Blevins WE, Widmer WR: What is your diagnosis? J Am Vet Med Assoc 215:782, 1999. 62. Farrow CS: The abdomen. In Farrow CS, ed: Radiology of the cat. St. Louis, 1994, Mosby. 63. Pratschke KM, Huges JML: Hiatal herniation as a complication of chronic diaphragmatic herniation. J Small Anim Pract 39:33, 1998. 64. Clark GN, Spodnick GJ, Rush JE, Keyes ML: Belt loop gastropexy in the management of gastroesophageal intussusception in a pup. J Am Vet Med Assoc 201:739, 1992. 65. Van Camp S, Love NE, Kumarasan S: Gastroesophageal intussusception in a cat. Vet Radiol Ultrasound 39:190, 1998. 66. Masloski A, Besso J: What is your diagnosis? J Am Vet Med Assoc 212:23, 1998. 67. Pollock S, Rhodes WH: Gastroesophageal intussusception in an Afgan Hound: a case report. J Am Vet Rad Soc 11:5, 1970. 68. Huang-Kornic E: Chronic intermittent vomiting in a cat: a case of chronic lymphocytic-plasmacytic gastritis. Can Vet J 40:196, 1999. 69. Silverstone AM, Adams WM: Gastrobronchial fistula in a dog. Vet Radiol Ultrasound 40:477, 1999.

C h a p t e r

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❚❚❚ NORMAL PLAIN FILM VARIATIONS

notoriously unreliable physical finding—it should be verified sonographically.

Bowel Gas

Bowel Distension

The amount of gas in the small intestine of normal dogs is extremely variable, in abdominal films ranging from barely perceptible to the major radiographic observation. In general, the greater the volume of intestinal gas, the more concern it engenders in the observer. Although excessive bowel gas can be an important feature of some common intestinal disorders, such as foreign-body obstruction or intussusception, it also may be an incidental finding: the result of a dog or cat that became excited during its lengthy journey to the hospital, an encounter with another pet in the reception room, or the animal’s struggles while being radiographed. The point is that, on a probability basis, large amounts of intestinal gas are not a reliable indicator of intestinal disease and rarely provide a specific diagnosis. Accordingly, caution should be exercised before pronouncing that an animal has a “surgical abdomen.” Finally, the presence of an inordinate volume of bowel gas does not constitute an ileus, which means intestinal obstruction, nor can gas alone be taken as prima facie evidence of an intestinal blockage.

The following are some generalities:

Bowel Fluid Although far more common than bowel gas, intestinal fluid usually has to be extreme before it attracts notice, even though in my experience it is a more reliable indicator of bowel obstruction than is gas. As with gas, fluid distension alone is usually not enough for a high level of diagnostic confidence. When excessive fluid is combined with an abnormal bowel distribution pattern, however, the probability of blockage rises.

Bowel-wall Thickness Bowel-wall thickness cannot be reliably estimated from radiographs. If the intestine seems palpably thickened—a 614

• An abrupt change in intestinal diameter from large to small (Figure 66-1) is more likely to indicate obstruction than a gradual change, provided the observation persists over time; otherwise, it is difficult to differentiate these sudden differences from normal peristalsis. • Regional distension is more likely the result of a localized obstruction, whereas generalized distension is more likely to be an intestinal volvulus, entrapment, or atony with or without blockage (Figure 66-2). • Canine parvoviral enteritis (CPE) produces such a severe net influx of fluid and related distension that in many instances the diameters of the small and large bowel become comparable.

Bowel Distribution An abnormal bowel distribution pattern is often the best way to determine the most probable origin of an abdominal mass. For example, a splenic tumor predictably displaces the small intestine dorsally and caudally (as observed in a lateral radiograph), whereas an enlarged left kidney is most likely to push the colon ventrally. Keep in mind when using this technique that an enlarged fluid-filled stomach or full bladder is also capable of creating an abnormal bowel distribution pattern and, as such, must be differentiated from an actual mass.

Bowel Content In general, bowel content is not as specific appearing as many believe. Most nonfood substances, such as fabrics, Styrofoam, leaves, wood chips, paper, and carpeting, provide few visual clues as to their actual nature.

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including the composition, amount, and viscosity of the contrast agent. Not all individuals pass barium at the same rate or show the same degree of peristalsis. Excited or fearful animals often handle barium differently from calm, cooperative animals. Cats pass barium up to 10 times faster than dogs. Barium films made of puppies (and, in my experience, kittens as well) differ from those of adult dogs. The following observations were made in four normal Beagle puppies given barium and barium food mixtures at a dose of 10 mL/kg (60% wt/vol).1

Figure 66-1 • Long-axis sonogram of an obstructed bowel segment in the proximal jejunum of a dog shows an abrupt change in the diameter of the fluid-filled intestine as it encounters a foreign body.

Figure 66-2 • Long-axis sonogram of a distended jejunal segment caused by severe enteritis.

Thus, most are overlooked or dismissed as feces. On the other hand, bone fragments, rocks, metallic foreign bodies, and some medications usually are readily recognized. Empty areas within the intestine, so-called filling defects, are most often gaseous in nature, randomly situated, and usually of little or no consequence. Most do not persist in the same location over the course of an examination. Unchanging filling defects, especially those encountered during gastroenterography, may warrant further consideration, especially when obstruction by a radiolucent foreign body or intussusception or tumor is being sought.

❚❚❚ NORMAL BARIUM FILM VARIATIONS Considerable variation exists in the appearance of the opacified bowel, depending on many different factors,

• The stomach was consistently located to the left of midline. • The pylorus was located on or near midline (as determined by ventrodorsal (VD) projection). • The stomachs of puppies emptied more rapidly than did those of adults. • Repetitive, focal duodenal disfigurations (pseudoulcers), the result of normal lymphoid tissue (Peyer patches) embedded in the intestinal wall, were present in straight barium studies but not when barium and food were combined. • Gastric emptying was usually progressive, as noted in consecutive films, irrespective of contrast composition. • The maximum intestinal diameter was 13 mm with barium suspension and slightly smaller with a barium and food mixture. • Predictably, with barium alone, luminal opacification was uniform; but when barium and food were mixed together, the food caused numerous filling defects. • The cecum filled fully with a barium and food mixture but only partially with barium alone.

❚❚❚ NORMAL IODINE FILMS Diagnostic iodine solutions often are used instead of barium when perforation is suspected or when a speedier transit time is desired. Ionic compounds attract water, distend the bowel, and as a result move through the intestine more rapidly than barium, but at a cost of decreased luminal visibility caused by dilution of the contrast medium and a transient dehydration. Nonionic iodine solutions also pass more rapidly than barium, but without as much dilution and dehydration, and thus are a better choice for seriously ill animals.

Ionic Compositions Ionic compounds are not used nearly as much as barium, for the most part because of their inferior mucosal coating qualities and poor overall visibility. Furthermore, diagnostic iodine solutions, both ionic and nonionic alike, have a highly objectionable taste, even when flavored. Cats in particular resist the oral administration of these diagnostic opaques. Allan and co-workers

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reported contrast examination of the feline gastrointestinal tract using a dedicated organic iodine solution.2

they have in dogs, see above) and recommend the following protocol.6

Nonionic Compositions

Dose: 875 mg iodine per kg of body weight: A stock solution of iohexol containing 300 mg of iodine per milliliter was used to arrive at the calculated dose; then water was added until a final volume of 10 mL/kg was obtained. Film Times: (1) Survey (precontrast), (2) immediately following contrast administration, (3) 5 minutes, (4) 10 minutes, (4) 15 minutes, (6) 20 minutes, (7) 30 minutes, and then (8) every 15 minutes for an hour. Films then should be made every 30 minutes until contrast is seen in the colon.

The recent trend in the examination of dogs and cats suspected of having a perforated esophagus or gastrointestinal tract has been toward the use of nonionic contrast media and away from the older, potentially harmful ionic media. Some specific research in this area follows. Dogs. Agut and co-workers investigated the use of iohexol as a gastrointestinal contrast agent in dogs and recommend the following protocol.3 Dose: 700 or 875 mg iodine per kilogram of body weight: A stock solution of iohexol containing 300 mg of iodine per milliliter was used to arrive at the calculated dose; then water was added until a final volume of 10 mL/kg was obtained.4 Film Times: (1) Survey (precontrast), (2) immediately following contrast administration, (3) 15 minutes, (4) 30 minutes, and (5) every 30 minutes thereafter until contrast is seen in the colon. Contrast is predicted to begin leaving the stomach immediately and to reach the large intestine in 1 1/2 to 2 hours in a normal dog. The authors recommend the use of gastrointestinal iohexol when there appears to be a risk of perforation and leakage of contrast into the peritoneal cavity. Cats. Williams and co-workers described the use of iohexol as a gastrointestinal contrast agent in normal cats.5 Dose: A stock solution of iohexol containing 240 mg of iodine per milliliter was used. 1. 10 mL/kg, diluted 1 : 3 with water (one part contrast, three parts water) for routine gastrointestinal examinations 2. 10 mL/kg, diluted 1 : 2 with water (one part contrast, two parts water) for animals with large amounts of fluid in the gastrointestinal tract Advantages of using iohexol (according to the authors) are (1) safety in the event of leakage into the peritoneum, (2) rapid transit time, (3) absence of luminal dilution, which degrades image quality, (4) acceptable image quality, and (5) low osmolality. In my view, the disadvantages of using iohexol are (1) it is more costly than barium, (2) images are inferior to those obtained with barium, (3) iohexol has an objectionable taste even when diluted with water, and (4) some cats will vomit immediately after receiving iohexol, even when it is administered by stomach tube. Agut and co-workers also investigated the use of iohexol as a gastrointestinal contrast agent in cats (as

Gastric reflux occurred in three of four cats. Gastric emptying commenced immediately and was complete by 30 minutes. Iohexol reached the colon by 30 minutes and in some cases in as little as 10 minutes. Forty percent of the healthy cats examined showed intestinal absorption of contrast, as indicated by opacification of the urinary bladder. Mucosal evaluation was impossible because of very poor detail.

❚❚❚ BOWEL DISTRIBUTION PATTERN As mentioned previously, abnormally distributed intestine often provides the best clue as to the most probable origin of an abdominal mass.

Normal The intestine, more than any other organ in the abdomen, is subject to displacement by an intraabdominal mass. Lesser rearrangements also can be prompted by (1) increased or decreased liver size, (2) increased or decreased stomach volume, (3) splenomegaly secondary to tranquilization or sedation, (3) cecal and colonic size, and (4) bladder fullness. Physiologic enlargements of this latter sort are termed mass effects and occasionally can be quite pronounced.

Characteristic Abnormal Bowel Distribution Patterns The concept underlying the diagnostic use of abnormal bowel distribution patterns (BDPs) is that a mass originating from a resident abdominal organ will characteristically displace one or more neighboring organs.7 • Liver:Aliver mass or enlargement (lymphoma, fatty liver) will originate in the cranial-most abdomen, typically on the right where most of the liver is situated, and displace the bowel caudally. • Stomach: A mass effect created by gastric enlargement, typically on the left where the most of the stomach is located, will displace the intestine caudally.

CHAPTER 66 ❚❚❚ Small Intestinal Disease

• Spleen: Most splenic tumors (hemangiosarcomas) will displace the intestine caudally and toward the center line in the VD projection and dorsally and caudally in a lateral view. • Pancreas: A pancreatic mass or enlargement (pancreatitis) will displace the bowel variably depending mostly the size of the stomach. Generally, the degree of associated bowel displacement is not predictive. • Right kidney: A right renal mass or enlargement (lymphoma, hydronephrosis) will displace the right side of the bowel mass caudally in a VD projection and ventrally in a lateral view. Right adrenal and ovarian tumors do likewise. • Left kidney: A left renal mass or enlargement (lymphoma, hydronephrosis) will displace the left side of the bowel mass caudally in a VD projection and ventrally in a lateral view. Left adrenal and ovarian tumors do likewise. • Uterus: Uterine enlargement (pregnancy, pyometra) will displace the bowel cranially in a VD projection and cranially and dorsally in a lateral view. • Bladder: A mass effect created by a full bladder will displace the bowel cranially in a VD projection and cranially and dorsally in a lateral view. Most bladder tumors do not create sufficient bladder enlargement or disfiguration to be recognized on plain films. • Prostate:An enlarged prostate (hypertrophy/hyperplasia, prostatitis, adenocarcinoma) will displace the bladder and bowel cranially in a lateral projection and cranially and laterally in a VD view.

❚❚❚ NORMAL SONOGRAPHIC APPEARANCE OF THE INTESTINE As mentioned, intestinal-wall thickness cannot be reliably determined from either plain or barium films; however, it can be accurately measured sonographically.

Dog Penninck and Nyland described the normal sonographic appearance of the canine stomach and bowel.8 Wall thickness in normal dogs may vary somewhat with transducer frequency, but the differences are negligible. Normal small intestinal-wall thickness has been reported to range from 2 to 4 mm using 5- to 7.5-MHz transducers.9

Cat Newell and colleagues described the normal sonographic appearance of the feline bowel.10 The duodenal wall was thicker than any other part of the intestine, a difference that became even more pronounced during anesthesia. Goggin and colleagues described the normal ileocolic region in the same species (Table 66-1).11

617

Table 66-1 • SONOGRAPHICALLY MEASURED FELINE INTESTINAL WALL THICKNESS Intestinal Region

Intestinal Wall Thickness (mm)

Duodenal thickness (nonsedated) Duodenal thickness (sedated) Mean small intestinal wall thickness Mean colonic wall thickness

2.4 2.7 2.1 2.1

❚❚❚ POTENTIAL SONOGRAPHIC INDICATORS OF SMALL INTESTINAL DISEASE Penninck and co-workers described the ultrasound features of a wide variety of intestinal disorders. Potential sonographic observations include abnormalities involving (1) wall thickness, (2) wall layer definition and identification, (3) wall symmetry, (4) lesion extension, (5) intestinal content, (6) intestinal motility or lack thereof, and (7) related findings such as regional adenopathy.

❚❚❚ DUODENAL ULCER Background Duodenal ulcers may be superficial, deep, or perforating. As might be imagined, perforating ulcers are the most serious, potentially leading to peritonitis. Histamine-releasing tumors such as mastocytomas are capable of causing both gastric and duodenal ulcers, which may subsequently perforate.12

Imaging Findings Barium duodenography may not reveal leakage, even though a perforated ulcer is present.13 Ionic contrast media distend the bowel more than barium, potentially increasing the prospects for leakage, but iodine compounds are much fainter and disappear soon after entering the peritoneal cavity. In general, the larger the ulcer crater (and its surrounding mound), the greater the chance of demonstrating it with barium.

❚❚❚ DUODENAL THICKENING, DEFORMITY, AND DECREASED MOTION SECONDARY TO PANCREATITIS Pancreatitis has been reported to cause thickening, persistent dilation, and rigidity of the proximal duodenum in dogs with pancreatitis. These observations have been made directly using sonography and indirectly using radiography (Figure 66-3).14 In my experience, plain radiography (with or without sequential filming) rarely contributes significantly to a diagnosis of pan-

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A

B Figure 66-3 • Ventrodorsal (A) and lateral (B) views of the abdomen of a vomiting dog show a markedly distended, static (based on this and subsequent films) pyloric antrum and proximal duodenum, the result of chronic pancreatitis after allowing passage through the foramen of Winslow.

creatitis. Even when the pyloric antrum and proximal duodenum are opacified with barium, radiographs typically prove woefully insensitive. Ultrasound, on the other hand, can often detect pancreatic disease provided the pancreas has become enlarged and is not being obscured by stomach or bowel gas.

❚❚❚ INFLAMMATORY BOWEL DISEASE Radiographically, the intestines of most cats with inflammatory bowel disease (IBD) appear normal. Sonographically, the intestines of most cats with moderate or severe IBD appear thickened, often in association with mesenteric adenopathy.15

❚❚❚ INFILTRATIVE BOWEL DISEASE Sensitivity of Barium Studies Weichselbaum and co-workers examined the sensitivity of gastroenterography in detecting specific types of enteritis in dogs and cats.16 The following aspects of small intestinal morphology and function were evaluated in both survey and barium films: • Volume of gas (relative to normal expectations for dogs and cats) • Diameter (in millimeters) • Gastric emptying time (in minutes) • Intestinal peristalsis (graded 1 to 4 according to magnitude and extent)

• Mucosal fimbriation (in millimeters) • Small intestinal transit time (from proximal duodenum to proximal colon) • Volume of fluid (relative to normal expectations for dogs and cats) Based on the correlation (or lack thereof) between radiographic and histologic diagnoses, certain tendencies were noted (Table 66-2, modified from author’s original table for clarity).16 Phycomycosis Background. Phycomycosis is a general term that refers to fungal infections caused by various filamentous organisms. Affected dogs are often very thin and have palpably thickened intestines. Clinical signs related to the gastrointestinal form of the disease include vomiting, diarrhea, and weight loss. Prognosis is poor. Imaging Findings. Because thickened intestine cannot be radiographically appreciated, radiographs are nondiagnostic. Sonography, on the other hand, will readily identify thickened bowel walls. Intestinal lymphosarcoma, another disease that causes intestinal thickening, can be differentiated from phycomycosis by its characteristic obscuring of the various layers of the bowel.17

❚❚❚ ENTERITIS Imaging Generalities Plain Films. With perhaps the exception of canine parvovirus, which causes a massive influx of fluid

CHAPTER 66 ❚❚❚ Small Intestinal Disease

619

Table 66-2 • DISEASE TENDENCIES SUGGESTED BY BARIUM ENTEROGRAPHY Plain film findings warrant contrast examination • Decreased gas/fluid ratio in dogs • Increased gas • Increased gas/fluid ratio in cats

Barium film findings that favor cancer • Focal convexities (thumb printing) originating on bowel surface and extending into the opacified lumen • Highly irregular contours (inferred spasticity) • Marked luminal narrowing

into the small intestine, most types of enteritis offer few plain film indications of either their presence or their nature. When the intestine is distended with fluid, it becomes turgid and is forced to fold repeatedly on itself to accommodate its increased volume. The close proximity of the various fluid-distended bowel segments results in a loss of definition and an increase in density, not unlike that caused by peritoneal fluid. Underexposed films produced under such conditions often appear extremely abnormal (a so-called surgical abdomen), so much so that affected animals may be subjected to unnecessary surgical exploration (Figure 66-4). Hemorrhagic enteritis also causes moderate intestinal distension causing a similar loss in visceral definition (Figure 66-5). Enterography. In general, the worse the enteritis, the more likely that barium films will appear abnormal; unfortunately, with the exception of CPE, I am unaware of any enterographic disease pattern that is consistently associated with a particular form of enteritis. Thus, my preference is simply to describe the abnormal intestinal examination as compatible or consistent with enteritis (Figures 66-6 and 66-7). In my experience, dehydration, intestinal bleeding, or extremes of pH rarely produce more than subtle changes in the appearance of the intestinal lining, although excessive luminal acidity or alkalinity may lead to flocculation (clumping of barium particles). Canine Parvoviral Enteritis. Canine parvoviral enteritis is the only form of enteritis of which I am aware that consistently produces a characteristic enterographic pattern. Specifically, the lining of the CPE intestine appears distinctively wrinkled and in severe cases overtly corrugated. Most of the small bowel becomes affected, although not always to the same degree.

Barium film findings that favor enteritis

Barium film findings that favor neither cancer nor enteritis

• Persistence of barium on mucosal surface (contrast “adhesion”)

• Abnormal straightening of the bowel or lack of normal contour variations; sometimes referred to as plasticity • Barium flocculation • Decreased fimbriation (normal is 1-2 mm) • Extraluminal distortion • Gallbladder reflux • Increased or decreased intestinal transit time • Increased or decreased peristalsis • Increased or decreased gastric emptying time • Luminal dilation • Mucosal scalloping

Intestinal Cryptococcosis Intestinal cryptococcosis varies in both its onset and duration. A yeast-like fungus, the organism also may result in nasal, pulmonary, and meningeal lesions. Cryptococcal infection of the small intestine has also been reported in dogs, associated with mesenteric lymphadenopathy.18

❚❚❚ INTESTINAL FOREIGN BODY Foreign Bodies as Incidental Findings Abdominal imaging in vomiting dogs (and less often cats) sometimes reveals one or more gastrointestinal foreign bodies, bone fragments, for example, which then invites the seemingly straightforward argument of cause and effect. Although such relatively simplistic (in the good sense of the word) thinking is often justified, occasionally it is not. As a safeguard against misdiagnosis under such circumstances, I recommend that a brief list of other common causes of vomiting also be considered before beginning treatment, especially if it is surgical.

Metallic Foreign Bodies Metallic objects or material in the gastrointestinal tract are typically outstanding on radiographs. In addition to the usual concerns about intestinal obstruction, there is the additional problem of potential toxicity, especially where lead is suspected. In such circumstances, it is important to observe the dog closely for signs of lead poisoning: colic, vomiting, ataxia, head pressing, depression or stupefaction, and seizures. Hematologic support for lead poisoning includes a large number of nucleated erythrocytes without severe anemia, hypochromasia, basophilic stippling, and anisocytosis.19

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A

Figure 66-5 • Lateral close-up view of the cranial abdomen shows a fluid-distended small intestine in a dog with hemorrhagic gastroenteritis, a disease that can be fatal. The bone fragments in the stomach were incidental.

B Figure 66-4 • A case of mistaken identity. Emergency veterinarian and physician-owner agreed that this vomiting dog had a “surgical abdomen” on the basis of lateral (A) and ventrodorsal (B) radiographs, which unfortunately neither recognized as being badly underexposed (too light). At surgery, the stomach and bowel appeared hyperemic, consistent with acute gastroenteritis. On recovery from the effects of anesthesia and surgery, the vomiting subsided, and the dog was discharged.

Obstructive Foreign Bodies Nonlinear Foreign Bodies Background. Intestinal foreign bodies, like their gastric counterparts, may appear opaque or translucent, depending on their ability to absorb radiation. Those of high density show on x-ray, whereas those of low density do not. Some low-density foreign bodies, such as peach or plum pits, have a characteristic striped appearance, which sometimes can be recognized radiographically. Likewise, the density of corncobs and wine corks may differ enough from their intestinal backgrounds that they can be detected in plain films.20 Fabrics, plastics, and foam rubber are usually invisible.21

Bone fragments are seen commonly but often prove incidental. Small rocks are often found in dogs kept in gravel-covered runs and, again, like bone fragments, are often incidental. Coins are usually immediately obvious and, in my experience, often persist in one location for a few days and then move on, eventually to pass. Flat, smooth rocks seem to have difficulty getting out of the stomach into the intestine and are not readily vomited. Surprisingly, some fishing lures make their way through the intestine, especially when they are ushered along by a large, high-fiber meal. Although it is generally believed that younger animals are more likely to consume nonfood objects and materials than older (wiser?) animals, age should not be a basis for diagnostic exclusion. Plain Films. Plain film diagnosis of intestinal obstruction is based almost entirely on the presence of intestinal distension, either with gas or fluid, and usually involving a portion of the small bowel. Occasionally, a foreign object is also visible (Figure 66-8). Lacking experience, a fledgling film reader may be hard pressed to recognize all but the most extreme examples. Lacking reliable mental images of normal and distended small intestine (or unable to recall them), a novice can turn to comparative measurement as an objective means to determine the obstructive potential of a dilated bowel segment. The use of both right and left lateral views (alternate-side radiography), in the case of suspected intestinal foreign body, has a greater diagnostic potential than using only a single right or left lateral view. This is because the fluid-filled portion of the intestine tends naturally to fall toward the tableside of the abdomen, whereas the air-filled segments rise toward the tube

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A

A

B Figure 66-7 • A, Lateral abdominal radiograph of a dog with

B

diarrhea shows a moderately distended, fluid-filled small intestine. B, A barium film shows excessively roughened interior margins compatible with nonspecific enteritis.

side of the animal. Thus, the distribution and clarity of the various portions of the bowel will appear differently in each of the two lateral views, providing a greater opportunity to detect a lesion, which otherwise might have been obscured by overlying tissue or gas.22 The vertical diameters of the suspect small intestinal segment and L5 vertebral body are measured and compared. If the diameter of the questionable small intestinal segment is 1.6 times (or less than) that of the body of L5, obstruction is unlikely. If, however, the intestinal diameter exceeds 1.6, the probability of obstruction becomes more likely.23 Graham recommends that the 1.6 L5-SI ratio be used cautiously because its sensitivity is only 88%. Additionally, dogs with nonobstructive diseases, such as gastritis and intestinal atony, also may have L5-SI ratios that exceed 1.6.24 C Figure 66-6 • Lateral (A), lateral close-up (B), and ventrodorsal (C) barium films (A, B) made of a dog with diarrhea show excessively irregular intestinal lining that is best seen in a lateral close-up (C). Bowel biopsies were consistent with enteritis.

The “Obstructive Pattern” and “Surgical Abdomen”: Do They Exist? The capacity of plain-film radiology to diagnose intestinal foreign-body obstruction is, in my opinion, exaggerated. The false perception that the mere presence of a fluid- and gas-distended intestine in a vomiting dog with a painful abdomen is sufficient to diagnose bowel obstruction has given rise to the unfortunate clinical expressions “obstructive pattern”

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A

C B Figure 66-8 • Lateral (A) and lateral close-up (B) views of the abdomen of a dog that began vomiting 3 days earlier show a gas- and fluid-distended small intestine, and a large, oddly shaped opacity in the caudal abdomen. A sonogram (C) shows that the object is within the distal jejunum, abutting the cranial aspect of the urinary bladder. The latter proved to be a piece of hard rubber lodged in the distal part of the small intestine.

Table 66-3 • CAUSES OF INTESTINAL DISTENSION OTHER THAN FOREIGN BODY OBSTRUCTION Cause of Excess Bowel Gas and Fluid

Comment

Dyspnea

Generally, dyspnea results in large amounts of stomach and bowel gas; with obstruction, gas is usually concentrated in the small intestine Especially canine parvoviral enteritis Some dogs and cats become extremely nervous when they travel in a car or go to a strange place, such as an animal hospital. This often leads to more swallowed gas and bowel distension than normal Endocarditis Severe shock often causes intestinal atony Vomiting causes most dogs to swallow air

Enteritis Excitement Mesenteric thrombi Shock Vomiting

and, even worse, “surgical abdomen.” Granted, intestinal enlargement is a feature of most obstructions,25 but it is not the only explanation for such a finding. Table 66-3 lists alternative explanations of intestinal distension. Barium/Diagnostic Iodine Films. The proximal duodenum (also termed the duodenal bulb) varies considerably, sometimes moment to moment, during the

course of a contrast examination. Sometimes it appears fully open, at other times partially or completely closed. Its shape is rarely the same in consecutive films. Consequently, a suspected lesion in this location, just as with the pylorus, usually requires repeated demonstration to be diagnostically convincing (Figures 66-9 and 66-10). Foreign bodies located deeper in the small bowel are in general more consistent in appearance, although

A

B

C

D

E

Figure 66-9 • Lateral (A) and ventrodorsal (B) radiographs of a vomiting dog eventually found to have a rubber toy lodged in its proximal duodenum. These films provide no indication as to the nature of the dog’s illness. Seven close-up barium films (C-I) centered on the proximal duodenum and made over a span of 90 minutes show the considerable variability of fixed intestinal foreign bodies located in this highly dynamic portion of the small intestine. Continued

SECTION VII ❚❚❚ The Abdomen

624

F G

H

I

Figure 66-9 • cont‘d Seven close-up barium films (C-I) centered on the proximal duodenum and made over a span of 90 minutes show the considerable variability of fixed intestinal foreign bodies located in this highly dynamic portion of the small intestine.

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A

B

D

C Figure 66-10 • Ventrodorsal plain film (A) shows distension and distortion of the proximal duodenum (emphasis zone). Barium films: ventrodorsal (B), ventrodorsal close-up (C), and lateral (D) show an irregularly shaped, proximal duodenal filling defect compatible with a mass or mass effect, which in this instance was a piece of gristle.

multiple-film confirmation is often necessary. Three different foreign bodies and their effects on the appearance of the small intestine are shown in Figures 66-11 to 66-13. Cautions 1. If a dog or cat is to be operated on to remove a radiographically identified foreign body believed to be obstructing the stomach or bowel, an additional film should be made just before the animal is anesthetized to verify that the location of the foreign body has not changed. This is especially important in cases in which the radiographic diagnosis is made on one day, but surgery is not to be performed until the next day. 2. The mere presence of a bone fragment or small rock in the stomach or intestine does not establish causation, although it may be inferred.

Intestinal Ultrasound. Tidwell and Penninck described the sonographic appearance of a variety of gastrointestinal foreign bodies in dogs and cats: mostly objects or parts of objects like balls, toys, and string. Although these objects appeared differently, depending on their size, shape, composition, and location, many shared the common sonographic characteristic of a brilliant white surface, configured as either a thick linear or arched band, representing the surface of the foreign body. Some objects, rubber balls for example, were readily recognizable when surrounded by fluid in the stomach. Others, such a strings, were invisible, and could be inferred only from their characteristic disfiguration of the host bowel (plicated bowel around ragged, often interrupted, echogenic band).26 Barium and diagnostic iodine solutions have little effect on the sonographic appearance of intestinal foreign bodies.

A

C

B

D Figure 66-11 • Lateral (A), lateral close-up (B), and ventrodorsal (C) views of the abdomen of a vomiting dog show gaseous distension of a portion of the small intestine, in the middle of which is an unusual density suggesting a foreign body. Lateral barium film (D) shows an object within the dilated small intestine partially outlined by contrast.

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E

F Figure 66-11 • cont‘d A long-sectional sonogram (E) shows a segment of small intestine containing an irregular echoic band (part of the foreign body) surrounded by fluid. An athletic headband was surgically removed from the intestine (F).

Linear Foreign Bodies Background. Root and Lord were among the first to characterize the distinctive radiographic appearance of the so-called linear foreign body in dogs and cats,27 which was later subclassified as free or fixed.28 Free Linear Foreign Bodies. Free linear foreign bodies are those that reside in the intestine, free of any physical attachment, although they may be firmly wedged in the lumen of the bowel, causing obstruction. Most involve at least one bowel segment, with some involving an entire region of the intestine. Fixed Linear Foreign Bodies. A fixed linear intestinal foreign body is anchored in position, usually within the gastrointestinal tract, by a second, nonlinear object typically located in the stomach. For example, a dog may swallow a child’s pull-toy, which remains in the stomach while the attached cord trails out into the duodenum. The intestine then “ascends” the cord, becoming tightly bunched as it moves toward the tether point in the stomach, giving the affected bowel its distinctive plicated or ribbon-candy appearance when filled with barium. Intestinal disfigurement of this sort can be difficult to appreciate sonographically, although it usually is not difficult to identify the offending foreign body (Figure 66-14).29

Cats, on the other hand, rarely swallow toys, preferring instead thread, yarn, and occasionally string or cassette tape. Thread has a penchant for wrapping around and sometimes becoming embedded in the base of the tongue, creating an anchor point, before trailing off into the esophagus, stomach, and proximal small intestine. Over a period of 2 to 3 days, the bowel gradually becomes bunched around the thread, eventually forming a clump of plicated bowel in the right cranial or central part of the abdomen. Because of the highly segmented nature of the intestine, the gas content is divided into many small pockets, creating a highly suggestive interrupted gas pattern. In my experience, associated peritonitis is uncommon. If an anchored thread is cut and marked with a metallic vascular clip, it usually passes within a day or so; however, the bowel distribution typically requires at least 3 days to become radiographically normal.

Intussusception Background. The telescoping or sliding of the intestine into itself is termed an intussusception. Typically, a cranial bowel segment enters a caudal one, with the former being described as the inner, penetrating element and the latter as the outer, receiving element. In my

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A

C

D

B Figure 66-12 • Close-up lateral (A) and ventrodorsal (B) views of the cranial abdomen of a vomiting dog show increased density and decreased detail compatible with peritoneal fluid. What appears to be a foreign object or material is present in the small intestine (emphasis zones), with air and fluid distending the small intestine proximally (C, D). These findings, combined with colic and a fever, suggest peritonitis. Five minutes after oral administration of a diagnostic nonionic iodine solution, the background density of the abdomen has increased as a result of intestinal leakage of the contrast medium into the peritoneal cavity. A perforating chunk of hard plastic was surgically removed from the jejunum.

opinion, archaic terms like intussusceptum (inner intestinal element) and especially intussuscipiens (outer intestinal element) are too unwieldy for everyday usage. Inner and outer elements are far easier. The cause (or causes) of intussusception is (are) not known, but speculation traditionally has focused on “intestinal irritation.” Clinical indicators of intussusception include (1) a palpable (and often painful) intraabdominal mass, (2) vomiting, and (3) diarrhea, often containing blood and mucus. Most intussusceptions occur in the distal third of the small bowel of puppies and young dogs and appear to be functional in nature. Although ileocolic and cecocolic sites are less common in my experience, there are reports to the contrary.30 Ileocolic intussus-

ception with cecal inversion (cecum inverted through the cecocolic opening into the proximal colon) is rare.31,32 Pure cecocolic intussusceptions have been reported but are also infrequently encountered. Empirically, there is an association between prolonged surgical handling of the intestine and subsequent intussusception. Recently created anastomotic sites, as well as other surface alterations to the bowel, are considered potential lead points for mechanical intussusception. I have not found an association between enteritis and intussusception and never have seen an intussusception in a dog with parvovirus. Most intussusceptions cause acute intestinal colic, but occasionally some do not, with clinical signs as long

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A

C

D

B Figure 66-13 • Lateral (A) and ventrodorsal (B) survey radiographs of a vomiting cat show abnormal fluid-distended bowel. In a subsequent contrast study (C, D), no barium had passed beyond the middle of the small intestine by an hour. Considering that the stomach still contained a large amount of barium and that the proximal bowel was gradually becoming increasingly distended, intestinal obstruction appeared likely. A rubber mouse head was surgically removed from the ileum.

as 5 months having been reported.33 Most affected dogs have a palpable abdominal mass. Recurrent intussusception occurs occasionally, with or without surgical stabilization of the affected gut.34 When performing ultrasound on a postoperative case for reintussusception, it is important to determine precisely what surgery was performed, especially with respect to intestinal plication, which under certain circumstances resembles an intussusception.35 Imaging Findings Plain Films. Occasionally, an intussusception is apparent as a discrete mass or an obviously dilated small intestinal segment. More often, however, the intussuscepted bowel blends in with the surrounding fluidfilled intestine, making it largely invisible. If the

adjacent bowel is gas filled, the intussusception may cause an abnormal bowel distribution pattern, suggesting a mass or mass effect (Figure 66-15, A, B). Radiographically visible bowel distension varies with content (food, fluid, or air), point of blockage, and whether the intestine is completely or partially obstructed. Occasionally, small bands of sediment can be trapped between the telescoped portions of the intestine (Figure 66-15, C). For example, a complete cecocolic intussusception with a predominantly fluid-filled bowel may resemble ascites, all but erasing any traces of the intestine.36 Conversely, an air-filled proximal jejunal intussusception may appear as one or two dilated bowel segments. Ultrasound. Classically, an intussuscepted bowel appears as a series of closely approximated light and

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air and bowel, compared with that of barium and bowel. • If a contrast enema fails to identify a suspected intussusception, gastroenterography can be performed using barium or a nonionic iodine solution if perforation is suspected, cutting the calculated dose of barium by at least one half, which will result in less gastrointestinal distension and make vomiting less likely. Paired lateral and VD views on a patienttailored basis can be made until the diagnosis is confirmed or denied.

Figure 66-14 • Cross-sectional sonogram of a portion of a vomiting dog’s small intestine shows a pair of centrally located hyperechoic objects, parts of a leather leash swallowed 2 days earlier.

dark concentric rings or bands, depending on whether it is scanned in cross or long-section (Figure 66-15, D, E). If fluid is present between the inner and outer intestinal elements, the intussusception is likely fresh and accordingly has a better prognosis. Contrast Examinations. Typically, an intussuscepted bowel appears as an intraluminal filling defect, which may or may not prevent the further flow of barium distally. The coiled spring sign, although visually quite spectacular, is inconsistently seen (Figure 66-15, F, G).37 Diagnostic Strategy • Plain films are often confusing because of the accumulated gas and fluid secondary to the obstructive nature of the lesion. If a mass can be palpated, it should be gently compressed and radiographed because this greatly enhances lesion visibility. Apostural radiograph (standing lateral with horizontally directed x-ray beam centered on the midabdomen) often provides the best view of both the intussusception (mass) and surrounding distended bowel loops. • If ultrasound is available, it should precede barium films because it is faster and more specific. A careful check for peritoneal fluid often indicates severe vascular obstruction (related to the compressed mesenteric blood supply) or peritonitis. • If sonography is not available, a barium enema should be done, or if intestinal perforation is suspected, a nonionic, iso-osmolar diagnostic iodine solution can be substituted. If an ionic solution is used and there is a perforation, the animal is at risk of developing a serious electrolyte disturbance because the contrast medium will be absorbed from the peritoneum. • Gas enemas are also a possibility, but I rarely use them because distinguishing relevant from irrelevant bowel gas is difficult. Radiographic technique also becomes much more critical under such circumstances because of the diminished contrast between

Pitfalls • Not all intussusceptions cause complete intestinal obstruction; consequently, gastroenterography conducted with long filming intervals may fail to uncover an existing lesion. • Plicated bowel, viewed early in the postoperative period, can mimic intussusception. Alternative Diagnoses • Enteritis with inflamed, thickened bowel mimicking an intussusception on palpation • Fluid-distended bowel mimicking intussusception • Intestinal entrapment • Intestinal foreign body • Intestinal impaction • Intestinal torsion • Malignant hyperthermia secondary to ingestion of hops38 • Mesenteric infarction secondary to endocarditis • Paralytic ileus related to systemic disease

❚❚❚ SMALL INTESTINAL TUMORS Background Fewer than 1% of animal tumors involve the intestine. In dogs, the colon and rectum are most often involved, whereas in cats, the small bowel is usually affected. Adenocarcinoma is the most common cell type in dogs; lymphosarcoma is most prevalent in cats. Other kinds of intestinal tumor include sarcomas (fibrous, muscular, undifferentiated), leiomyoma, leiomyosarcoma, plasmacytoma, and argentaffin cell tumor (carcinoid).39,40 Most intestinal tumors develop either spontaneously or as a result of metastasis. Occasionally, however, intestinal tumors develop as a result of a specific stimulus. An example of this phenomenon is described in a report by Pardo and co-workers, in which a primary jejunal osteosarcoma was discovered in conjunction with a gauze surgical sponge inadvertently left in the abdomen 6 years earlier.41

Imaging Findings Radiology. In my experience, most intestinal tumors are invisible on plain abdominal films. Where there

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A

C

B

E

D Figure 66-15 • Lateral (A) and ventrodorsal (B) views of the abdomen of a dog with abdominal colic, scant bloody stools, and an

intermittently palpable abdominal mass show displacement of much of the small bowel to the left side of the abdomen. A ventrodorsal close-up of the right cranial part of the abdomen (C) shows a small amount of sediment, appearing as a faint curved line perpendicular to the spine, just caudal to the last rib. Long (D) and cross-sectional (E) sonograms of the mass show the characteristic appearance of an intussusception. Continued

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F

G

Figure 66-15 • cont‘d Ventrodorsal (F) and ventrodorsal close-up (G) views of the affected part of the bowel, following administration of barium, show the concentric rings (coiled spring sign) that typify an intussusception.

is an abnormality, it is usually of an indirect nature, most typically, distension of the bowel immediately proximal to the lesion as a result of the obstructive effect of the tumor on intestinal transit. Affected bowel segments are most likely to appear as elongated ovals or rounded rectangles in lateral perspective, lying in the center of smaller-caliber intestine. Dilated bowel located in the cranial part of the abdomen, especially if ventrally positioned, can be mistaken for an enlarged spleen or liver lobe (Figure 66-16). Barium Films. Patient-tailored examinations will uncover more intestinal tumors than will fixed protocols. As when searching for a foreign body, each film set should dictate the timing of the next, depending on what is or is not seen. The best time to reexamine a suspicious finding is shortly after it is initially observed, not an hour later, as often is the case when protocols are used. Ultrasound. The larger the dog and the smaller the tumor, the less likely it is to be identified sonographically. A large volume of bowel gas further decreases the probability of finding anything and will greatly prolong the examination time. A more efficient approach is to attempt to find only those lesions that have first been identified by some other means, for example, by palpation or with barium films. The socalled tumor search, often based on nonspecific laboratory data, is typically unrewarding.

Figure 66-16 • Ventrodorsal close-up view of the cranial abdomen of a persistently vomiting dog shows deformity and displacement of the proximal duodenum caused by a large intestinal adenocarcinoma.

❚❚❚ SPECIFIC TUMOR TYPES Lymphosarcoma Ultrasound. Penninck and colleagues described the sonographic appearance of feline gastrointestinal lymphosarcoma in cats. Individual wall lesions were classified according to the symmetry, extent, and nature

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A Figure 66-18 • Close-up long-sectional sonogram of thickened bowel in a dog with diffuse intestinal lymphosarcoma.

• The presence of localized or regional thickening, combined with abnormal architecture and echogenicity (compared with the surrounding intestine), strongly suggests intestinal adenocarcinoma. • Some forms of lymphosarcoma closely resemble intestinal adenocarcinoma.

B Figure 66-17 • Intestinal lymphosarcoma: Long (A) and crosssectional (B) views of the small intestine of a cat severely infiltrated by lymphocytes.

of involvement: (1) transmural-circumferential, symmetric, (2) transmural-circumferential, asymmetric, (3) transmural-bulky, (4) transmural-nodular, (5) transmural-segmental, and (6) mucosal infiltration.42 Figures 66-17 and 66-18 illustrate the sonographic appearance of intestinal lymphosarcoma in a cat and dog. Grooters and co-workers also characterized the sonographic appearance of feline gastrointestinal lymphosarcoma.43 Stomach lesions assumed two forms (both hypoechoic), either focal masses or diffuse, unevenly thickened areas of the stomach wall. Intestinal lesions appeared for the most part as symmetric, hypoechoic thickening of the bowel wall. Rivers and co-workers reported on a small series of intestinal adenocarcinomas in cats, describing their sonographic appearance as well as emphasizing how they can be differentiated from intestinal lymphosarcoma. Their findings follow: • Sonography is more sensitive than either abdominal palpation or plain film radiography in detecting intestinal adenocarcinoma. • Sonography is superior to radiography as a medical imaging screening procedure in cats with clinical signs suggesting intestinal adenocarcinoma.

Note: Intestinal leiomyoma and leiomyosarcoma also share some or all of the features attributed to adenocarcinoma but warrant secondary consideration because of their much lower frequency. Caution: Some forms of enteritis may appear sonographically similar to intestinal tumors.

Leiomyosarcoma and Leiomyoma Meyers and Penninck described the radiographic and sonographic appearance of intestinal leiomyosarcoma and leiomyoma in dogs.44 Not surprisingly, ultrasound was nearly twice as sensitive as plain film in detecting abdominal masses, most of which were not large enough to be palpable. The authors claimed that they were able to identify an abdominal “mass effect” in half of the dogs they studied and either free fluid or air in a third of the dogs (Figure 66-19). Gastroenterography was not performed in any of these animals in lieu of ultrasound. No radiographs appeared in the article, and no mention was made of how long the examinations took. The sonographic diagnosis of an intestinal mass in the described cases was usually of an inferential nature, based on finding gas in or adjacent to the lesion. The tumors, for the most part leiomyosarcomas, appeared as large masses, eccentrically projecting from the bowel wall and frequently containing hypoechoic or anechoic areas.

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B o x

6 6 - 1

Possible Sources of Intestinal Perforation • • • • • • • • • • •

A

• • • • • •

B Figure 66-19 • Lateral (A) and ventrodorsal (B) views of the abdomen of a dog show a medium-sized mass in the midventral abdomen, which eventually proved to be an intestinal leiomyosarcoma.

Intestinal Perforation Background. Intestinal perforation can come about in a variety of ways, some of which are direct (penetrating foreign bodies) and some of which are indirect (mesenteric thrombosis). Numerous possibilities are listed in Box 66-1. Imaging Findings. The hallmark of intestinal perforation is peritoneal gas, which in large volumes is not difficult to recognize but in small amounts may be difficult or impossible to differentiate from intestinal gas. One means by which extraluminal gas often can be differentiated from that found inside the bowel is its shape. Intestinal gas often appears circular or oval, whereas peritoneal gas tends to be more angular as it effaces

Wound dehiscence following intestinal biopsy Wound dehiscence following intestinal anastomosis Deep bite wounds Bullet and stab wounds Perforation by an intestinal foreign body Bowel necrosis secondary to intestinal cancer Bowel necrosis secondary to severe enteritis Chronic impaction leading to ischemia, anoxia, and necrosis of the surrounding bowel wall Traumatic mesenteric avulsion Intestinal torsion (volvulus) cutting off mesenteric blood supply Intestinal herniation (diaphragmatic, abdominal, inguinal) cutting off mesenteric blood supply Intestinal entrapment (incarceration) cutting off blood supply Chronic intussusception cutting off mesenteric blood supply Endocarditis generating infective emboli leading to mesenteric thrombosis Nonspecific thromboembolic disease causing mesenteric infarction Perforated duodenal ulcer induced by some antiinflammatory drugs Some uncoated oral medications, potassium, for instance, are capable of causing intestinal perforation if they remain in direct contact with the mucosal surface too long

small portions of the exterior surfaces of various abdominal organs. In some instances, large surfaces may become coated with gas, enough that a particular organ or tissue becomes recognizable, the upper portion of the diaphragm or a corner of the liver or spleen, for example. If peritonitis has developed, especially if there is a large amount of related peritoneal fluid, small clusters of bubbles may form, especially in and around the mesentery and omentum. As mentioned, intestinal perforation is rarely imaged directly, even with the aid of opaque media; thus, inference is a staple of the diagnostic process. For example, where a discernible mass with gas pockets is present, possible explanations include (1) abscess secondary to a perforating foreign body, (2) a perforating bowel tumor, or (3) a necrotic tumor that has been colonized by gas-forming bacteria.45 Diagnostic Strategies. The scenario: A standard twofilm abdominal series shows a number of small angular gas pockets suggesting peritoneal gas. Faced with this possibility, the following should be considered: • Repetition of the original two projections, adding two opposite views. If right lateral and VD projections were made originally, they can be supplemented with left lateral and dorsoventral (DV) views. After inspection of the repeated views (in this

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635

example, the right lateral and VD) to see whether the questionable gas pockets have persisted, the additional views (left lateral and DV) should be reviewed for any additional signs of extraluminal gas. • If the issue of peritoneal gas remains unresolved, right and left decubitus views can be made and a search done for gas immediately beneath the uppermost body wall. • Using the same decubitus views, the lowermost body wall is checked for adjacent fluid, keeping in mind that unless there are huge amounts of free fluid and air in the peritoneal cavities, there will be no fluid lines (other than those normally found in the stomach and bowel).

A

❚❚❚ INTESTINAL TORSION (VOLVULUS) Background Intestinal torsion is typically an acute event in which most or all of the small intestine rotates around its mesenteric axis, obstructing the intestine in at least two points and effectively isolating the intervening section of bowel. The cause is unknown. Like most such intestinal catastrophes, the most immediate concern is for the concurrently compromised vasculature: cranial mesenteric artery and branches, cranial pancreatic-duodenal, jejunal, ileocolic, and right/middle colic arteries. If the obstructed arterial circulation is not quickly reestablished, the resultant intestinal ischemia will rapidly lead to necrosis, sepsis, and death. Affected dogs, often German Shepherds, appear extremely sick. They are reluctant to move, have distended abdomens and pale gums, and periodically vomit. Bloody diarrhea may or may not be present. Most die within 12 to 18 hours from a combination of septicemia (Escherichia coli and Clostridia organisms) and hypovolemic shock.46

B Figure 66-20 • Lateral (A) and ventrodorsal (B) views of the abdomen of a dog with an acute axial torsion of the small intestine.

Imaging Findings Radiographs made shortly after the bowel becomes displaced may show only mild to moderate fluid distension. Later films typically reveal progressive gaseous distension involving most of the intestine (Figures 6620 and 66-21). The appearance of the stomach varies from unremarkable to moderately gas/fluid-distended, depending on the degree of distress experienced by the animal. Still later, as bacteria begin to leak through the wall of the dying intestine, peritonitis develops, accompanied by varying volumes of peritoneal fluid.47 Precautionary Note: Large, closely approximated, fluidfilled bowel segments often produce increased abdominal density and decreased visceral detail, just as abdominal fluid does. Therefore, it is strongly recommended that a diagnosis of possible peritoneal fluid be sonographically confirmed before attempting an abdominal puncture.

Not only can ultrasound (1) confirm the presence of abdominal fluid, (2) establish its location, and (3) estimate its amount, but it can also (4) assist in avoiding an intestinal puncture when performing an abdominocentesis. Plain Films. Classically, a lateral projection shows multiple large, gas- and fluid-filled bowel segments, often associated with varying degrees of associated visceral displacement. A VD view may reveal a predominantly left-sided distribution. Ascertaining whether peritoneal fluid is present is difficult owing to the large amount of fluid contained within the distended bowel. Contrast Examinations. Barium or diagnostic iodine solutions (1) would have to be given in unacceptably large volumes, (2) promote further vomiting, (3)

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SECTION VII ❚❚❚ The Abdomen

❚❚❚ INTRAABDOMINAL INTESTINAL ENTRAPMENT (INCARCERATION) Background

Figure 66-21 • Lateral abdominal radiograph of a dog with a mesenteric volvulus shows (1) intestinal layering, (2) fluid and air distension of the small bowel, (3) splenomegaly, and (4) peritoneal fluid.

progress very slowly (assuming enough remains in the stomach), and (4) likely only add to the animal’s already substantial discomfort. In this situation, a contrast examination is too time consuming and is unlikely to be diagnostic. Ultrasound. Ultrasound is diagnostically impractical (as well as dangerous) under these circumstances, other than for the purposes of identifying peritoneal fluid for the purpose of microscopic analysis.

Diagnostic Strategy • Intestinal torsion is a rarity. Bear this in mind when considering differential diagnostic probabilities. • Nearly all intestinal torsion involves the entire bowel, resulting in massive distension as a result of accumulating air, fluid, or a combination of the two. • Dogs with intestinal torsion are extremely ill and usually exhibit some degree of shock.

Pitfalls Enteritis can cause severe fluid and gas distension of the entire small intestine resembling intestinal torsion or entrapment. For this reason, a diagnosis of “surgical abdomen” can be both hazardous and shortsighted.

Alternative Diagnoses • • • • • • •

Atypical gastric torsion Intestinal entrapment (incarceration) Some distally located intestinal foreign bodies Diffuse mesenteric infarction Some forms of infectious enteritis Peritonitis Addison disease

The small intestine is necessarily exceedingly mobile, a fact that is borne out by the wide variety of bowel distribution patterns regularly encountered in abdominal films. Such displacements are quite normal and serve to accommodate the ebb and flow of the gastrointestinal contents and, to a lesser extent, the regular expansion and contraction of the urinary bladder. Occasionally, however, the intestine may pass through a natural or unnatural mesenteric or omental opening and become trapped.48 Likewise, it is possible (but fortunately rare) for the bowel to become entangled in one of the visceral ligaments. The consequence of such entrapments, mesenteric or ligamentous, is often intestinal strangulation. Most intestinal entrapments, spontaneous or traumatic, occur acutely and typically are associated with varying degrees of intestinal vascular occlusion. The resulting ischemia rapidly leads to intestinal anoxia, dilation, atony, permeability, and eventually necrosis and peritonitis. Affected animals often show severe abdominal colic, vomiting, and later profound shock. If most of the intestine is involved, the abdomen may be markedly distended, resembling gastric dilation or torsion. If not treated soon after it develops, intestinal entrapment is often fatal.

Imaging Findings Plain Films. Classically, an intraabdominal intestinal entrapment shows as multiple gas-distended bowel segments, many of which are arranged in parallel. In some animals, particularly those in which the onset of vascular occlusion is more gradual, the bowel initially appears fluid filled and later assume a more typical gaseous distension. The “stacked” appearance of the affected intestine is of no particular diagnostic significance, other than reflecting the cramped circumstances of the distended bowel. Likewise, fluid levels (as demonstrated in postural films) do little more than remind the viewer that the bowel contains fluid as well as air. Barium Films. Because of secondary atony, orally administered barium often remains in the stomach for a protracted period before sluggishly moving along the intestinal tract. The result is that transit times under such circumstances often are numbered in days rather than in hours. Ultrasound. When the intestine contains a large amount of gas, sonography often proves futile. Even if the bowel is fluid filled, ultrasound usually fails to identify a specific intraabdominal entrapment site.

CHAPTER 66 ❚❚❚ Small Intestinal Disease

❚❚❚ ABDOMINAL HERNIAS: EXTRAABDOMINAL INTESTINAL DISPLACEMENT Background Sometimes, as a result of severe injury, the diaphragm or abdominal wall becomes torn, allowing a portion of the bowel to pass through these normally impenetrable barriers. Once displaced, the dislocated intestine is likely to swell and increase in volume, making escape more difficult. In the worst instance, the bowel (and its associated vasculature) becomes strangulated, which eventually leads to necrosis and perforation. Less common potential extraabdominal entrapment sites include the inguinal rings, retroperitoneum, and congenital peritoneal-diaphragmatic-pericardial fusion defects, which may allow a portion of the small intestine to reside in a greatly enlarged pericardial sac along with the heart.

Imaging Findings The key feature of an abdominal hernia is the presence of intestine outside the peritoneal cavity. In some cases, the dislocated bowel contains sufficient gas that there is little or no doubt as to its true nature. In other instances, particularly where the intestine is fluid filled, it can be difficult to separate bowel from its soft tissue surroundings. Hematomas, seromas, and unabsorbed pockets of subcutaneously administered fluids can be difficult to distinguish from small intestinal hernias. If plain films are inconclusive, barium can be given with the intent of opacifying the herniated bowel; however, precisely when this will occur is often a matter of speculation, which can result in exhaustive and inefficient filming times in an effort to capture the event. Ultrasound usually can confirm the presence of intestine outside the body wall, although demonstration of the muscular tear through which the bowel has passed is often surprisingly elusive. A rapid method of checking a suspicious object under the skin (bowel?) is to grasp it between the thumb and forefinger of one hand while scanning with the other. The areas on either side of the presumably immobilized intestine should also be examined, as they are more likely to contain telltale gas.

❚❚❚ INTESTINAL IMPACTION AND PERFORATION Most intestinal impactions in dogs are primary, resulting from eating something unusual, such as straw, leaves, fabric, or large quantities of bone. Secondary impactions usually occur just proximal to a point of luminal stenosis, for example, a colonic tumor. Sand and clay impactions, on the other hand, are more likely to occur in the cecum. Cats often suffer long-term colonic impaction after displaced fractures of the

637

sacrum and tail. Many Manx cats are plagued by chronic constipation related to a variety of inbred neuropathies. Long-standing impaction occasionally leads to mural ischemia in the distended segment, potentially leading to anoxia, necrosis, and perforation. Bone fragments sometimes take days to negotiate the intestinal tract completely but rarely injure the bowel in the process and rarely perforate (contrary to popular belief). The keys to radiographically identifying an intestinal impaction are (1) persistence of the suspected lesion over time, (2) luminal distention, and (3) unusually high density. Although ultrasound is capable of identifying an impaction site, barium is far better, particularly as concerns the establishment of the beginning and the end of the obstruction and the degree to which it blocks the bowel (Figure 66-22).

❚❚❚ INTESTINAL PARASITISM Most parasites do not greatly affect the radiographic appearance of the bowel as seen with plain films. Large worms, however, will cause characteristic filling defects that are easily identified in barium films. Hookworms (in conjunction with specific bacteria) can result in typhlitis that may or may not be consistently recognizable radiographically.

❚❚❚ INTESTINAL MALABSORPTION In my experience, it is not possible consistently to recognize diseases of the small intestine that cause malabsorption. Most published cases are typically retrospective studies based almost entirely on stool composition and volume, laboratory data, and histologic assessment of biopsy specimens and not on predictable radiographic signs. Like many other biochemical disorders, intestinal malabsorption seems better suited to the functional talents of nuclear medicine.

❚❚❚ PROTEIN-LOSING ENTEROPATHY Protein-losing enteropathy is not so much a disease as it is a symptom of (bowel) disease. In reality, most types of enteritis cause some loss of protein but in most cases not enough to deplete serum levels notably. It is only when protein escapes in large volumes or when there is sustained leakage that clinical signs develop. Bowel diseases noted for causing protein loss include histoplasmosis, plasmocytic-lymphocytic enteritis, eosinophilic enteritis, and lymphosarcoma. Using healthy dogs, Berry and co-workers performed a feasibility study on the effectiveness of 111 indium-labeled transferrin (111In-TF) in establishing the presence of intestinal protein loss. The authors concluded that 111In-TF is an effective and sensitive means of detecting intestinal protein loss but withheld further judgment pending the completion of clinical trials.49

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SECTION VII ❚❚❚ The Abdomen

A

B Figure 66-22 • A, Lateral view of the abdomen of a rapidly deteriorating Dalmatian 1 hour after being given a diagnostic nonionic iodine solution. Most of the contrast remains in the stomach, but some has accumulated in and around a vague caudal abdominal mass (emphasis zone). A transverse sonogram (B) of the enlarged part of the bowel, as determined by abdominal palpation, shows a distended small intestine filled with some sort of material, which does not resemble formed stool or liquid feces. Exploratory surgery performed a short time later revealed a distal jejunal impaction (straw) that had resulted in intestinal perforation and peritonitis.

❚❚❚ “SHORT-BOWEL SYNDROME”

fluid content. Barium films reveal similar findings in addition to a predictable decrease in transit time.50

Background Short-bowel syndrome is the medical expression used to describe the adverse effects, particularly intractable diarrhea and related weight loss, caused by the surgical removal of a large percentage of the bowel (usually the small intestine). It is not so much a disease as it is a surgical complication. Congenital intestinal hypoplasia is rare in dogs and cats, and little or nothing has been attempted in the way of corrective action.

Imaging Findings Radiographic findings range from the specific: a less than normal number of visible bowel segments to the nonspecific: intestinal dilation, and excessive gas, or

❚❚❚ CONGENITAL INTESTINAL MALFORMATION Various intestinal malformations have been described in dogs and, to a lesser extent, cats. Broadly speaking, these anomalies encompass (1) abbreviated intestinal length (typically involving the small bowel), (2) blind pouches, (3) abnormal connections, and (4) duplications. Classification notwithstanding, these embryologic errors are rare. As might be expected, animals with these maladies usually, but not always puppies and kittens, show disease signs related to their digestive tracts and, as a

CHAPTER 66 ❚❚❚ Small Intestinal Disease

639

A

B Figure 66-23 • Lateral abdominal radiograph of a dog initially thought to have endocarditis (fever and heart murmur). Following a cardiac workup, which proved normal, other possible sources of illness were investigated. Lateral (A) and lateral compression close-up (B) abdominal radiographs showed a uniformly thickened intestinal segment, which was at first thought to be an intussusception but was later found to be a rare intestinal wall abscess.

result, often appear small, frail, and undernourished. Antemortem diagnosis typically is based on barium films, which usually correlate well with later surgical or postmortem assessments.51

Duplications Background. Very rarely, kittens and puppies are born with extra or duplicate portions of their intestine. Some authorities prefer the terms blind sac, blind pouch, or duplication cyst for such anomalies. In veterinary practice, most such findings have been of an incidental nature, discovered at necropsy. Radiography. Spaulding and co-workers described the sonographic appearance of intestinal duplication cysts in two dogs.52 Radiographically, duplications cysts can resemble an abdominal mass on plain films, whereas a barium study may reveal a localized narrowing of the bowel similar to some tumors (barium rarely enters

a duplication cyst). Afluid level sometimes can be identified in postural films if the cyst communicates with the nearby intestine. Ultrasound. Typically, the wall of duplication cysts comprises three discrete coats: inner and outer hyperechoic layers and an intermediate hypoechoic layer. The interior contains fluid, which may be uniformly black or filled with numerous small intermediate strength echoes. In some respects, these cysts resemble abscesses or a pyometra in cross section.

❚❚❚ INTESTINAL TRAUMA Background If blunt abdominal trauma is severe enough, it can potentially cause a variety of intestinal injuries, including bruising, mesenteric avulsion leading to devascularization, and rupture. Some of these injuries do not

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SECTION VII ❚❚❚ The Abdomen

A

B

D

C Figure 66-24 • Lateral (A) and ventrodorsal (B) views of the abdomen of a vomiting student-surgery dog 1 month after an ovariohysterectomy. The bowel distribution pattern is abnormal, residing mainly in the cranial third of the abdomen. Additionally, there is a large gas- and fluid-distended bowel segment, which resembles the colon, but actually is part of the small intestine, as indicated by later barium films (C, D). Surgical exploration revealed numerous intestinal adhesions, some of which were partially obstructing the bowel.

CHAPTER 66 ❚❚❚ Small Intestinal Disease

become fully developed for a few days and may thus be overlooked initially.

Imaging Findings I know of no published case series dealing with the specific radiographic or sonographic signs of mesenteric avulsion. In about half of the confirmed cases I have seen, the major radiographic observation was some degree of paralytic ileus. Caution: Lamb and Boswood showed that intestinal discontinuity can be mimicked sonographically as a result of differences in sound transmission through partially overlying organs such as the spleen, making it falsely appear as though two halves of the same object, in this example the intestine, are located at different depths. This phenomenon is termed a propagation speed error artifact.53 In my experience, such artifacts are invariably uniplanar, so that with customary biplanar imaging, one is not apt to be fooled.

❚❚❚ BOWEL ABSCESS Intestinal abscesses have no distinguishing radiographic features per se; however, a bowel abscess occasionally becomes large enough that it appears as a nonspecific mass. Using compression radiography, it is possible to show a physical connection between a previously identified mass and the nearby intestine (Figure 66-23). If the mass effect is substantial, it make cause partial obstruction, which is potentially detectable using barium. Ultrasound is the best method of identifying an intestinal abscess, but locating an otherwise invisible lesion can be difficult and time consuming.

❚❚❚ INTESTINAL ADHESIONS Intestinal adhesions are difficult to detect irrespective of the type of imaging used. In most cases, the best that can be hoped for is to establish a persistent physical relationship between two or more bowel segments, abnormal connections that can sometimes be established with postural films, compression radiography, barium, or ultrasound (Figure 66-24).

References 1. Miyabayashi T, Morgan JP: Upper gastrointestinal examinations: a radiographic study of clinically normal beagle puppies. J Small Anim Pract 32:83, 1991. 2. Allan GS, Rendano VT, et al: Gastrografin as a gastrointestinal contrast medium in the cat. Vet Rad 20:110, 1979. 3. Agut A, Sanchez-Valverde MA, et al: Use of iohexol as a gastrointestinal contrast medium in the dog. Vet Radiol Ultrasound 34:171, 1992. 4. Ginai AZ: Experimental evaluation of various available contrast agents for use in the gastrointestinal tract in case of suspected leakage: effects on the peritoneum. Br J Radiol 58:969, 1985.

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5. Williams J, Biller DS, et al: Evaluation of iohexol as a gastrointestinal contrast medium in normal cats. Vet Radiol Ultrasound 34:310, 1993. 6. Agut A, Sanchez-Valverde MA, et al: Iohexol as a gastrointestinal contrast medium in the cat. Vet Radiol Ultrasound 35:164, 1994. 7. Root CR: Abdominal masses. In Thrall DE, ed: Textbook of veterinary diagnostic radiology, ed 4. Philadelphia, 2002, WB Saunders. 8. Penninck DG, Nyland T, et al: Ultrasonography of normal canine gastrointestinal tract. Vet Radiol 30:272, 1989. 9. Riedesel EA: The small bowel. In Thrall DE, ed: Textbook of veterinary diagnostic radiology, ed 4 Philadelphia, 2002, WB Saunders. 10. Newel SM, Graham JP, et al: Sonography of the normal feline gastrointestinal tract. Vet Radiol Ultrasound 40:40, 1999. 11. Goggin JM, Biller DS, et al: Ultrasonographic measurement of gastrointestinal wall thickness and the ultrasonic appearance of the ileocolic region in healthy cats. J Am Anim Hosp Assoc 36:224, 2000. 12. Zontine WJ, Mierhenry EF, Hicks RF: Perforated duodenal ulcer associated with mastocytomas in a dog: a case report. J Am Vet Rad Soc 18:162, 1977, 13. Ackerman N, Root C: Benign duodenal ulceration and perforation in a dog. Vet Rad 22:19, 1981. 14. Penninck DG, Nyland TG, et al: Ultrasonic evaluation of gastrointestinal diseases in small animals. Vet Rad 31:134, 1990. 15. Baez JL, Hendrick MJ, et al: Radiographic, ultrasonographic, and endoscopic findings in cats with inflammatory bowel disease of the stomach and small intestine: 33 cases (1990-1997). J Am Vet Med Assoc 215:349, 1999. 16. Weichselbaum RC, Feeney DA, Hayden DW: Comparison of upper gastrointestinal radiographic findings to histopathologic observations: a retrospective study of 41 dogs and cats with suspected small bowel infiltrative disease (1985-1990). Vet Radiol Ultrasound 35:418, 1994. 17. Hayes-Fowler SD, Homco LD: What is your diagnosis? J Am Vet Med Assoc 209:563, 1996. 18. Malik R, Hunt GB, et al: Intra-abdominal cryptococcosis in 2 dogs. J Small Anim Pract 40:387, 1999. 19. Huerter L: Lead toxicosis in a puppy. Can Vet J 41:565, 2000. 20. Lamb CR, Hansson K: Radiological identification of nonopaque intestinal foreign bodies. Vet Radiol Ultrasound 35:87, 1994. 21. Downs MO: What is your diagnosis? J Am Vet Med Assoc 197:119, 1990. 22. Dodd VM: Radiographic diagnosis. Vet Rad 28:230, 1987. 23. Graham JP, Lord PF, Harrison JM: Quantitative estimation of intestinal dilation as a predictor of obstruction in the dog. J Small Anim Pract 39:521, 1998. 24. Graham JP: Radiographic criteria for intestinal diameter in suspected small intestinal obstruction in the dog. Vet Radiol 35:238, 1994. 25. Ackerman N, Spencer CP, Schaer M: Radiographic diagnosis. Vet Rad 24:237, 1983. 26. Tidwell AS, Penninck DG: Ultrasonography of gastrointestinal foreign bodies. Vet Radiol Ultrasound 33:160, 1992. 27. Root CR, Lord PF: Linear radiolucent gastrointestinal foreign bodies in cats and dogs: their radiographic appearance. J Am Vet Rad Soc 12:45, 1971.

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28. Farrow CS: Linear intestinal foreign body. In Farrow CS, ed: Emergency radiology in small animal practice. Toronto, 1988, BC Decker. 29. Barber DL, Rakich PM: Radiographic diagnosis. Vet Rad 22:170, 1981. 30. Sardinas J, Fagin B: What is your diagnosis? J Am Vet Med Assoc 198:1435, 1991. 31. Houston DM: What is your diagnosis? J Am Vet Med Assoc 198:1061, 1991. 32. Carrig C: Radiographs presented as part of the 1992 A.C.V.R. oral certification examination: abdomen section. Vet Radiol Ultrasound 34:188, 1993. 33. Lamb CR, Mantis P: Ultrasonic features of intestinal intussusception in 10 dogs. J Small Anim Pract 39:437, 1998. 34. Sivasankar M: Recurrent intussusception in a 14-monthold, spayed, female German shepherd cross. Can Vet J 41:407, 2000. 35. Oakes MG, Lewis DD, et al: Enteroplication for the prevention of intussusception recurrence in dogs: 31 cases (1978-1992). J Am Vet Med Assoc 205:72, 1994. 36. Carrig C: Radiographs presented as part of the 1992 A.C.V.R. oral certification examination: abdomen section. Vet Radiol Ultrasound 34:188, 1993. 37. Gellasch KL, Spackman CAJ, Thomas M: What is your diagnosis? J Am Vet Med 216:1065, 2000. 38. Duncan KL, Hare WR, Buck WB: Malignant hyperthermia-like reaction secondary to ingestion of hops in five dogs. J Am Vet Med Assoc 210:51, 1997. 39. Kropp KE, Michelotti MF: What is your diagnosis? J Am Vet Med Assoc 214:1482, 1999. 40. Biery DN, Berg P: Duodenal leiomyosarcoma: a case report. J Am Vet Rad Soc 7:34, 1966.

41. Pardo AD, Adams WH, et al: Primary jejunal osteosarcoma associated with a surgical sponge in a dog. J Am Vet Med Assoc 196:935, 1990. 42. Penninck DG, Moore AS, et al: Ultrasonography of alimentary lymphosarcoma in the cat. Vet Radiol Ultrasound 35:299, 1994. 43. Grooters AM, Biller DS, et al: Ultrasonic appearance of feline alimentary lymphoma. Vet Radiol Ultrasound 35:468, 1994. 44. Meyers NC, Penninck DG: Ultrasonic diagnosis of gastrointestinal smooth muscle tumors in the dog. Vet Radiol Ultrasound 35:391, 1994. 45. Gustafson BW, Godshalk CP: What is your diagnosis? J Am Vet Med Assoc 197:1515, 1990. 46. Cairo J, Font J, et al: Intestinal volvulus in dogs: a study of 4 clinical cases. J Small Anim Pract 40:136, 1999. 47. Harvey HJ, Rendano VT: Small bowel volvulus in dogs— clinical observations. Vet Surg 13:91, 1984. 48. Hosgood G, Bunge M, Dorfman M: Jejunal incarceration by an omental tear in a dog. J Am Vet Med Assoc 200:947, 1992. 49. Berry CR, Guilford WG, et al: Scintigraphic evaluation of four dogs with protein-losing enteropathy using 111indiumlabeled transferrin. Vet Radiol Ultrasound 38:221, 1997. 50. Ansari MM, Stickle R: What is your diagnosis? J Am Vet Med Assoc 199:1779, 1991. 51. Zenger E, Evering WN, Willard MD: Chronic diarrhea associated with intestinal anomalies in a six-year-old dog. J Am Vet Med Assoc 201:1737, 1992. 52. Spaulding KA, Cohn LA, et al: Enteric duplication in two dogs. Vet Rad 31:83, 1990. 53. Lamb CR, Boswood A: An artifact resulting from propagation speed error. Vet Radiol Ultrasound 36:549, 1995.

C h a p t e r

6 7

Cecum, Colon, and Rectum

❚❚❚ NORMAL APPEARANCE Cecum and Colon On plain films, the canine cecum usually appears as a medium-sized, bilobed, air-filled object in the upper portion of the right middle abdomen. When the bladder is full, the cecum often lies to the left of midline. Together with the cecum, the colon resembles a question mark as seen in the ventrodorsal projection. The feline cecum is invisible in plain films and only barely evident when opacified with barium. In the latter context, the cecum appears as a small, wrinkled, roughly triangular structure about the size of a pencil eraser.

Rectum The rectum lies entirely within the pelvic canal, beginning at the pelvic inlet and ending with the anus. As such, a portion of the rectum is concealed by the pelvis and distal spine irrespective of projection. Barium studies of the colon in which a Bardex catheter is used often fail to portray much of the rectum because of the enormous size of the catheter cuff and rectal spasm caused by its inflation.

❚❚❚ BARIUM COLONOGRAPHY (BARIUM ENEMA) Although the colon can be assessed at the conclusion of an upper gastrointestinal (upper GI) examination, it is often far better evaluated with a barium enema. Specific lesions best evaluated with barium colonography include (1) intussusception in the region of the cecum, (2) stenosis, (3) hernia, and (4) diverticula. Normal valves at the intestinal transition zone can appear ominous to the uninitiated (Figure 67-1).

❚❚❚ COLONIC TRANSIT TIME USING SYNTHETIC MARKERS (BARIUM-IMPREGNATED POLYETHYLENE SPHERES) Bruce and co-workers determined the mean colonic filling and mean colonic residence times in normal dogs of various ages fed barium-impregnated polyethylene spheres (BIPS).1 Two sizes of spheres (1.5 and 10 mm) were mixed with commercial dog food and fed to the animals. Abdominal radiographs then were made every 2 hours until 90% of the spheres had left the colon and entered the rectum. The mean colonic filling time differed for spheres of different sizes. The mean time for 90% of the small spheres to enter the colon was 14 hours, with a range of 10 to 19.3 hours; the mean time for larger spheres was 16.6 hours (range, 12 to 22 hours). Roles were reversed, however, with respect to mean residence times. Larger spheres spent less mean time in the colon than smaller ones: 11.5 compared with 12 hours (ranges: 5.2 to 26.6 and 5.5 to 28.1 hours, respectively). Author’s note: In my experience, intestinal transit time, including separate values for the small or large bowel, has limited clinical value, irrespective of the contrast medium or carrier used.

❚❚❚ AIR COLONOGRAPHY (DIAGNOSTIC PNEUMOCOLON) Nyland and Ackerman described the use of colonic air in the diagnosis of large-bowel disease.2 Barber and Campbell also touted pneumocolonography as the best method of identifying a high-density object such as a bone or a rock, although it may be argued that such procedures are superfluous in these situations.3 643

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SECTION VII ❚❚❚ The Abdomen

larity of the procedure in humans and the fact that many of the early veterinary radiologists received a part of their training in medical schools. Others and I have published textbooks and case reports explaining the technique and showing colonic diseases that were diagnosed in this manner. Over the past decade or so, however, colonography has fallen from favor, largely being replaced by proctoscopy and fine-needle biopsy. As a footnote to the gradual demise of colonography, I have noted that the technical quality of the outside examinations that I receive is steadily decreasing (primarily overfilling with barium and underfilling with air), probably because of a lack of practice. A

❚❚❚ COLONIC MARKING Colonic making is safer, cheaper, faster, and, most importantly, less uncomfortable than a barium enema. The procedure consists of gently injecting liquid barium into the distal part of the intestine using a soft, medium-sized, well-lubricated catheter or, alternatively, a nasal bulb syringe. The intent is to add sufficient barium to the bowel that it becomes visible in a subsequent radiograph, not to distend it with contrast. The technique is especially useful in differentiating between the large and small intestines in cases in which obstruction is suspected based on suspicious plain films (Figure 67-2).

❚❚❚ POTENTIAL HARM RESULTING FROM COLONOGRAPHY B Figure 67-1 • A, Lateral barium film of the mid-abdomen of a healthy dog shows the intestinal transition zone, where the ileum, cecum, and colon join together. B, In the ventrodorsal close-up, the ileocolic valve appears as a thin band at the top center of the image, with the partially empty cecum appearing below. The rough triangular part of the cecum is a normal variation related to incomplete filling.

Although pneumocolonography is capable of identifying a mass or stricture, the injected air is highly mobile (especially when the dog is being repositioned for additional views), making all but general comparisons difficult or impossible. In conscious animals, the air often is rapidly expelled around all but the largest rectal catheters. Generally, I use pneumocolonography only to mark the location of an otherwise invisible or only partially visible colon.

❚❚❚ DOUBLE-CONTRAST COLONOGRAPHY Double-contrast colonography was once quite popular in veterinary radiology, reflecting both the popu-

The most common injury to the distal part of the intestine related to colonography, of which I am aware, is perforation of the rectal or colonic wall by the catheter. In the few cases I am familiar with, one or more of the following conditions pertained: (1) an attempt was made to forcibly move the catheter beyond a point of stoppage, (2) the catheter was unusually small and/ or rigid, (3) lubrication was not used, (4) the dog struggled during the examination, or (5) fresh blood was present in the stool. The lessons from these observations appear to be that when performing colonography: (1) make every effort to insure that the examination is pain free by using sedation and a well-lubricated, soft catheter, (2) keep in mind that a bleeding and inflamed bowel is especially fragile, and, most importantly, (3) avoid forcing the catheter.

❚❚❚ CECOCOLIC INTUSSUSCEPTION Cecocolic intussusceptions are rare compared with those occurring entirely within the small intestine. Most are characterized by the absence of a normal cecal shadow (bilobed lucency) in plain films and a sizable filling defect in the proximal colon in a

A

Figure 67-2 • A case of mistaken identity: Lateral (A) and ventrodorsal (B) views of the abdomen of a dog show what appear to be a pair of small intestinal segments entering the pelvic canal. A barium marking study (C, D) of the rectum and colon reveals that the suspect gas accumulations were actually in the colon.

B

C

D

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SECTION VII ❚❚❚ The Abdomen

barium examination. Any associated mass affect is usually negligible.

stool is enough to make a diagnosis (Figure 67-5). Most such lesions are cancerous.

❚❚❚ ILEOCOLIC INTUSSUSCEPTION

❚❚❚ ABNORMAL COLONIC DISTENSION (MEGACOLON)

Ileocolic intussusceptions are also rare compared with those that exclusively involve the distal third of the small intestine; however, they may resemble a purely small intestinal intussusception, including the presence of a coil-spring sign. As with most distal intestinal invaginations, such lesions are best and most rapidly demonstrated with barium colonography.

❚❚❚ ULCERATIVE COLITIS The appearance of ulcerative colitis on either plain or barium films depends on its severity. In its worst form, the disease may result in a distinctively crinkled mucosa, a mix of ulcers, edema, and spasm, an observation made possible only when sufficient gas is present to create the needed luminal contrast in plain films. Colonography is usually more dramatic, with lesions being best depicted using a double-contrast technique consisting of a light coat of undiluted barium followed by a large volume of air (Figure 67-3). As mentioned earlier, the ulcerated colon is typically quite friable, and thus every precaution must be taken not to injure it further. Theoretically, this includes perforation and air or barium emboli.

❚❚❚ NONULCERATIVE COLITIS Most cases of nonulcerative colitis lack any specific appearance on either plain or barium films. Occasionally, an inflamed colon may appear corrugated, inferring spasticity; however, some healthy dogs occasionally exhibit highly irregular colonic margins, casting doubt on the reliability of this finding.

❚❚❚ COLONIC IMPACTION Colonic impaction is usually a diagnosis of context and circumstance, with the former being a colon full of high-density stool and the latter being a dog that is straining in an unsuccessful effort to defecate (Figure 67-4). As a generality, the longer the colon remains unemptied, the more difficult it will be for the animal to defecate and the more likely it is that diarrhea will develop. Temporary colorectal flaccidity often marks the relief of longstanding impactions, especially those found in cats.

❚❚❚ COLONIC STENOSIS Colonic stenosis, as with most large-bowel disease, is best appreciated with barium films, although occasionally the natural contrast provided by backed-up

The cause of colonic distension (megacolon), especially in cats, is often difficult or impossible to determine. Generally, primary colonic atony is separable from simple impaction by its much greater size and recurrence, even in the face of dietary modification. Subtotal colectomy (including postoperative radiographic evaluation) has been performed in dogs and cats to treat chronic colonic distension or atony as well as a variety of other diseases of the large bowel, including the following: • Persistent colonic dilation of undetermined cause (termed colonic or spontaneous or idiopathic megacolon) • Rectal neuropathy • Distal colonic and rectal strictures • Distal colonic and rectal tumors • Mass-related extraluminal obstruction • Selected endocrine disease

❚❚❚ RECTAL DIVERTICULAR DISEASE Weakening of the lateral rectal wall occasionally results in an outpouching or diverticulum that can interfere with defecation. These sacs are best demonstrated by filling the rectum with barium; however, distension is unnecessary. Alubricated nasal bulb syringe is the most effective way to deliver rectal barium and rarely requires sedation.

❚❚❚ COLONIC CANCER Colonic and rectal tumors are often malignant, and most stenose or otherwise deform the affected portion of the bowel. Medium-sized and large tumors often can be directly seen on plain films or inferred from backedup or deformed stool (see Figure 67-5). Others will require barium. Ultrasound may or may not be informative, depending on the accessibility of the lesion and the amount of surrounding gas. Ultrasound-guided fine-needle biopsy also can be useful.

❚❚❚ COLONIC AND RECTAL PERFORATION Other than from gunshots, my experience with colonic perforation has been extremely limited. To date, all those I have seen have been iatrogenic. The most common of these have been related to the forceful extraction of hardened stools using surgical instruments, especially from cats with chronic megacolon. I

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B A

C Figure 67-3 • A, Ventrodorsal view of the abdomen of a dog with blood in its stool, thought to be originating in the colon. B, Barium film shows a normal colon, but a double-contrast study (C, D) reveals numerous small ulcers compatible with ulcerative colitis.

D

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A A

B Figure 67-5 • Lateral (A) and lateral close-up (B) views of the abdomen of a dog show abrupt narrowing and malalignment of the distal part of the colon, the result of a napkin-ring carcinoma.

common radiographic features, they should be easily distinguishable on the basis of associated illness (or lack thereof).

B Figure 67-4 • Lateral (A) and ventrodorsal (B) views of a chronically constipated cat show the colon distended with high-density stools and an old thoracolumbar spinal fracture. Additional pelvic films (not shown) showed a collapsed pelvic canal as a result of numerous old fractures.

also have seen a rectal perforation following removal of an anal gland using electrocautery.

❚❚❚ COLONIC TORSION AND COLONIC REVERSAL In my experience, isolated colonic torsion is among the rarest of bowel disorders (Figure 67-6). Burk and Ackerman reported the following potential abnormalities resulting from torsion of the large intestine: (1) extreme displacement and (2) marked gaseous distension.4 In addition to torsion, a displaced colon also may be the result of colonic reversal, an embryologic error found in a small number of otherwise normal dogs and cats.5 Even though colonic torsion and reversal share

❚❚❚ PNEUMATOSIS COLI Pneumatosis coli, also termed pneumatosis intestinalis and pneumatosis cystoides intestinalis, is a rare colonic condition characterized by the presence of multiple contiguous air-filled cysts located beneath either the serosal or mucosal layers of the colon. Little hard information exists as to the cause of these gas accumulations, with current speculation focusing on noninfectious causes. At least one affected animal has recovered spontaneously.5 Radiographically, pneumotosis usually appears as broken bands of gas flanking the colonic lumen (Figure 67-7).

❚❚❚ REDUNDANT COLON (ABNORMALLY LONG COLON) In the current edition of Thrall’s Veterinary Diagnostic Radiology, Biery describes what he terms an excessively long or redundant appearing colon, a finding that he

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A

C

B

Figure 67-6 • Lateral (A) and ventrodorsal (B) views of the abdomen of a dog with acute colic show a greatly dilated and ventrally displaced colon. The lack of visceral detail is due to the thinness of the animal. At surgery, the colon was torsed, and much of it was ischemic, requiring excision. Peritonitis developed following surgery, the result of wound dehiscence, shown in this colonogram as a small plume of iodinated contrast solution escaping from the ventral aspect of the operative site (C).

says “seems to be a variant of normal and not clinically significant.”6 In some respects, this description resembles the so-called inchworm colon, a transient half-loop sometimes observed in the caudal part of the large intestine of otherwise normal dogs.

References

Figure 67-7 • Pneumotosis coli: Lateral view of the abdomen of a dog suspected of being septicemic shows air in both the wall and the lumen of the colon, rectum, and cecum.

1. Bruce SJ, Guilford WG, et al: Development of reference intervals for the large intestinal transit of radiopaque markers in dogs. Vet Radiol Ultrasound 40:472, 1999. 2. Nyland TG, Ackerman N: Pneumocolon: a diagnostic aid in abdominal radiography. J Am Vet Rad Soc 19:203, 1978. 3. Barber DL, Campbell K: Radiographic diagnosis. Vet Rad 23:250, 1982. 4. Burk RL, Ackerman N: The abdomen. In Burk RL, Ackerman N, eds: Small animal radiology and ultrasound. Philadelphia, 1996, WB Saunders. 5. Morris EL: Pneumotosis coli in a dog. Vet Radiol Ultrasound 33:154, 1992. 6. Biery DE: The large bowel. In Thrall DE, ed: Textbook of veterinary diagnostic radiology. Philadelphia, 2002, WB Saunders.

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Pancreatic Disease

In general, pancreatitis is an acute disease in dogs and a chronic one in cats. In dogs, the disease usually is confined to the pancreas and immediate surroundings; in cats, neighboring organs such as the duodenum, liver, gallbladder, and bile duct also are likely to be affected. Unlike dogs with acute pancreatitis, which commonly vomit and are colicky, cats often have no localizing signs and are not vomiting.1

❚❚❚ ACUTE PANCREATITIS Background Acute pancreatitis, as previously mentioned, is common in dogs and uncommon in cats. In the acute form of the disease, the pancreas becomes acutely inflamed, edematous, hemorrhagic, and to varying degrees necrotic. Related enzymatic leakage often causes a localized aseptic peritonitis with resultant duodenal atony and dilation. Abdominal colic, vomiting, and weakness usually accompany pancreatitis. Pulmonary edema and disseminated intravascular coagulopathy also have been reported in association with acute pancreatitis, but they are rare. In most instances, the precise cause (or causes) of acute pancreatitis is unknown. Reported risk factors in dogs include (1) advanced age (i.e., 7 years or older), (2) neutering (spay or castration), (3) breed susceptibility (terriers and nonsporting breeds), and (4) the presence of one or more additional diseases.2

Imaging Findings Radiographic. In my experience, there are no consistent and reliable radiographic indicators for acute pancreatitis in dogs and cats. Burk and Ackerman expressed a similar sentiment in their textbook, Small Animal Radiology and Ultrasound.3 For many years, it was asserted—and generally accepted—that the following radiographic signs were reliable indicators of acute pancreatitis in dogs4: 650

• Indistinctness in “the right cranial quadrant” • Gaseous distension of the stomach, proximal duodenum, or transverse colon • Gastric displacement • A vaguely defined paraduodenal mass constituted radiographic evidence of pancreatitis Many of these findings, however, are routinely present in healthy dogs. Additionally, many animals with pancreatitis lack any loss of abdominal clarity and do not exhibit gastrointestinal distension. Thus, it appears that the so-called classic signs of acute pancreatitis lack both radiographic sensitivity and specificity. Unfortunately, some review articles continue to promote and perpetuate the belief that pancreatitis is a radiographic diagnosis, albeit from dated references.5 Ultrasound. The sonographic appearance of both experimentally produced and naturally occurring acute pancreatitis has been reported repeatedly.6-9 Miles and co-workers showed that diagnostic hydroperitoneum, performed in conjunction with sonography, improves pancreatic visualization in normal dogs, and, presumably, those with pancreatic disease, although the advisability of doing so is questionable given the discomfort levels typically associated with pancreatitis.10 When the pancreas is readily imaged in the vicinity of the stomach (the right pancreatic limb between the right kidney and duodenum and the left pancreatic limb along the caudal edge of the pyloric antrum), it is nearly always diseased, although the cause is often a source of speculation because inflammation, infection, and cancer all can assume a similar sonographic appearance.11,12 Diagnostic ambiguity notwithstanding, however, acute pancreatitis remains the most commonly diagnosed pancreatic malady (Figures 68-1 and 68-2). The sonographic features of acute pancreatitis include the following: • Pancreatic enlargement often associated with marginal irregularity

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A

Figure 68-2 • A long-sectional view of a dog with acute pancreatitis shows moderate to severe enlargement but only a mild increase in echogenicity.

B Figure 68-1 • Sonographic long (A) and cross-section (B) of the pancreas of a vomiting dog shows mild to moderate enlargement combined with a generalized increase in echogenicity compatible with acute pancreatitis.

• Variable pancreatic echogenicity: hyperechoic or hypoechoic, depending on the amount of associated hemorrhage, edema, and necrosis • Increased echogenicity in the surrounding pancreatic mesentery (evidence of fat saponification) • Thickened duodenal wall (evidence of duodenitis) • Evidence of extrahepatic biliary obstruction and occasionally pleural fluid Morita and co-workers reported on the endoscopic sonographic appearance of the pancreas in healthy dogs.13 Although the published pancreatic images were vivid and far more detailed than what can be obtained transabdominally, the required equipment is costly and requires considerable practice to master, in particular, locating and aligning the pylorus and negotiating the pyloric canal.

❚❚❚ CHRONIC PANCREATITIS Radiographically, chronic pancreatitis is no more easily detected than the acute form of the disease; however, using ultrasound, it is often possible to diagnose a

Figure 68-3 • Sonographic image of an inflamed pancreas in a dog shows the undulating margins often seen with chronicity.

chronically diseased pancreas based on its swollen, mottled appearance. Additional signs of chronicity include calcification and cavitation. In general, the larger, more irregular, and echogenic the pancreas, the more likely it is to be chronically diseased, although, as mentioned earlier, it may be impossible to differentiate inflammation, infection, and cancer (Figure 68-3).

❚❚❚ PANCREATIC PHLEGMON Dorland’s defines a pancreatic phlegmon as a solid, swollen, inflamed mass of pancreatic tissue occurring as a complication (result) of acute pancreatitis, which may subside spontaneously or become secondarily

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Figure 68-4 • Sonographic image of a pancreatic phlegmon in a dog.

Figure 68-5 • Sonographic cross-section of a large pancreatic cyst in a dog.

infected and develop into an abscess.14 A phlegmon may share both physical and etiologic features with a pancreatic pseudocyst, but it is usually much larger and more complex (Figure 68-4).

❚❚❚ PANCREATIC PSEUDOCYST According to Dorland’s, a pancreatic pseudocyst is a cystic collection of fluid and necrotic debris whose walls are formed by the pancreas and other surrounding organs.14 Like a phlegmon, a pseudocyst typically occurs as an aftermath of acute pancreatitis, but it is physically smaller and more discrete. Most pancreatic pseudocysts are diagnosed sonographically, typically featuring a small to medium-sized spherical mass surrounded by a well-marginated, fluid-filled cavity (Figure 68-5). In some larger abscesses, it is possible to demonstrate an interior shimmering-like movement characteristic of pus.

A

❚❚❚ PANCREATIC ABSCESS Like the phlegmon and pseudocyst, the pancreatic abscess follows on the heels of acute pancreatitis. For the most part, reports of pancreatic abscesses have been of individual cases, typically describing varying degrees of cavitation. In most instances, the border of the abscess is smooth and its echogenic content uniform or slightly speckled. As expected with pus, far enhancement is usually present (Figure 68-6).15

❚❚❚ PERIPANCREATIC MASSES Pancreatic pseudocyst, phlegmon, and abscess also can originate in the pancreatic mesentery rather than in the pancreas itself. Most such masses are likely caused by ongoing pancreatitis, although proof of such a relationship is often based on circumstantial evidence. There is a single report of a chyle-filled peripancreatic abscess in a dog that was sonographically diag-

B Figure 68-6 • A, A presumed pancreatic abscess in a dog is marked by an arrow. B, A later image shows the tip of a hypodermic needle used to aspirate the lesion.

CHAPTER 68 ❚❚❚ Pancreatic Disease

nosed as a fluid-filled mass. When abdominal lymphangiography was performed, no contrast medium was observed within the mass. The authors speculated that following chronic pancreatitis, a peripancreatic abscess developed and led to localized peritonitis. They continue their hypothesis by suggesting that regional lymphatics then were incorporated into an inflammatory fibrous mass surrounding a portion of the nearby colon; the lymphatic walls became eroded or were made abnormally permeable; as a result, they spilled their contents into the mass.16

❚❚❚ OTHER FORMS OF PANCREATITIS Surgical Pancreatitis Student surgeons often manipulate the pancreas excessively during laparotomy, causing mild postoperative pancreatitis. The pancreas usually appears both radiographically and sonographically normal under such circumstances, although affected dogs may have abdominal colic, vomit, and refuse to eat. Pancreatic enzymes may be mildly elevated.

Traumatic Pancreatitis Varying degrees of pancreatitis can result from blunt trauma, for example, that sustained in car accidents. Small dogs may receive abdominal bite wounds when attacked by larger dogs. Cats that fall from window ledges and balconies are subject to a hemorrhagic form of pancreatitis, which can be overlooked because of more obvious injuries. Radiographically, traumatic hemorrhagic pancreatitis is initially hard to detect. Later, on average 3 to 5 days, abnormalities begin to appear in abdominal films. These include (1) increased density and decreased detail in the region of the pancreas, (2) mottled fat, and (3) abnormal duodenal contours and medial displacement, as seen in barium films. As time passes, the entire abdomen becomes involved as indicated by a generalized loss of organ clarity.17

Drug-induced Pancreatitis Pancreatitis has been reported in epileptic dogs treated with a combination of potassium bromide/ phenobarbital.18

❚❚❚ PANCREATIC TUMORS Unfortunately, from a diagnostic standpoint, pancreatic inflammation and neoplasia share a number of common sonographic features (although not in any consistent fashion): reduced echogenicity, hyperechoic masses, cavitations, and thickened adjacent duodenal wall. Lamb and McEvoy, however, showed that even though pancreatitis and pancreatic tumors have common sonographic features, they also exhibit differences, or at least a tendency to differ, which can be diagnostically exploited: Pancreatitis is most likely to

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appear as a diffusely hypoechoic structure, whereas neoplasia is more likely to be represented by a hypoechoic mass19 (Figure 68-7).

❚❚❚ INSULINOMAS Background Insulinomas are beta cell tumors of the pancreas that cause an increase in insulin production, often leading to hypoglycemia. In dogs, most insulinomas are malignant (45% show visible metastasis at the time of surgery, most often to surrounding lymph nodes and liver). Typically, there is only a single pancreatic mass, with multiple masses or diffuse infiltration occurring with a much lower frequency. Surgical resection is reported to prolong survival time, which averages about 14 months. About one in four operated-on dogs remain hypoglycemic.20

Imaging Findings Radiology. At diagnosis, most pancreatic insulinomas are only 2 to 3 cm in diameter, too small to be detected radiographically. Provided the procedural expertise is available, retrograde arteriography is potentially useful because of the hypervascular nature of insulinomas. Ultrasound. Although transabdominal sonography has a relatively greater chance of identifying a typically sized pancreatic insulinoma than radiography does, most such lesions still are likely to go undetected unless endoscopic transducers are available. Nuclear Medicine. Lester and co-workers reported on the scintigraphic appearance of a pancreatic insulinoma in a dog by using somatostatin receptor scintigraphy (indium-111 pentetreotide).21

❚❚❚ PANCREATIC CARCINOMAS Homco described the appearance of pancreatic carcinoma as echogenically variable and differing considerably in size and location within the pancreas. The liver and regional lymph nodes are mentioned as likely metastatic sites.15

References 1. Swift NC, Marks SL, MacLachlan, Norris CR: Evaluation of serum feline trypsin-like immunoreactivity for the diagnosis of pancreatitis in cats. J Am Vet Med Assoc 217:37, 2000. 2. Cook AK, Breitschwerdt EB, et al: Risk factors associated with acute pancreatitis in dogs: 101 cases (1985-1990). J Am Vet Med Assoc 203:673, 1993. 3. Burk RL, Ackerman N: The abdomen. In Burk RL, Ackerman N, eds: Small animal radiology and ultrasound. Philadelphia, 1996, WB Saunders. 4. Klein LJ, Hornbuckle WE: Acute pancreatitis: the radiographic findings in 182 dogs. J Am Vet Rad Soc 19:102, 1978. 5. Schaer M: Acute pancreatitis in dogs. Comp Cont Ed 13:1769, 1991.

A

C

B Figure 68-7 • Fixed Pylorus: Close-up lateral (A) and ventrodorsal (B, emphasis zone) views of the stomach of a dog show an unusually shaped pyloric antrum, a configuration that persisted in all subsequent films, suggesting it was not merely a chance finding. A sonogram shows a lobulated, hypoechoic mass adjacent to the pyloric region of the stomach (C). A dorsoventral (D) view of the thorax shows a spherical area of consolidation in the right caudal lung labe. A large pancreatic adenocarcinoma was found at necropsy, distorting the pyloric region of the stomach and rendering it nearly immobile.

6. Nyland TG, Mulvany MH, Strombeck DR: Ultrasound features of experimentally induced, acute pancreatitis in the dog. Vet Rad 24:260, 1983. 7. Murtaugh RJ, Herring, et al: Pancreatic ultrasonography in dogs with experimentally induced acute pancreatitis. Vet Rad 26:27, 1985. 8. Hess RS, Saunders HM, et al: Clinical, clinicopathologic, radiographic, and ultrasonographic abnormalities in dogs with fatal acute pancreatitis: 70 cases (1986-1995). J Am Vet Med Assoc 213:665, 1998. 9. Lamb CL, Simpson KW: Ultrasonographic findings in cholecystokinin-induced pancreatitis in dogs. Vet Radiol Ultrasound 36:139, 1995. 10. Miles KG, Lattimer JC, et al: The use of intraperitoneal fluid as a simple technique for enhancing sonographic visualization of the canine pancreas. Vet Rad 29:258, 1988. 11. Yeager AE: Sonograms presented as part of the 1994 A.C.V.R. oral certification examination: ultrasound section. Vet Radiol Ultrasound 36:243, 1995. 12. Salisbury SK, Lantz GC, et al: Pancreatic abscess in dogs: six cases (1978-1986). J Am Vet Med Assoc 193:1104, 1988.

D

13. Morita Y, Takiguchi M, et al: Endoscopic ultrasonography of the pancreas in the dog. Vet Radiol Ultrasound 39:552, 1998. 14. Dorland’s Illustrated Medical Dictionary, ed 28. Philadelphia, 1994, WB Saunders. 15. Homco L: Pancreas. In Green RW, ed: Small animal ultrasound. Philadelphia, 1996, Lippincott-Raven. 16. Barnhart MD, Smeak D: Pericolonic mass containing chyle as a presumed sequela to chronic pancreatitis in a dog. J Am Vet Med Assoc 212:70, 1998. 17. Suter PF, Olsson S-E: Traumatic hemorrhagic pancreatitis in the cat: a report with emphasis on the radiological diagnosis. Vet Rad 10:4, 1969. 18. Gaskill CL, Cribb AE: Pancreatitis associated with potassium bromide/phenobarbital combination therapy in epileptic dogs. Can Vet J 41:555, 2000. 19. Lamb CR, McEvoy FJ: Comparison of ultrasonographic findings in canine pancreatitis and pancreatic neoplasia. Vet Radiol Ultrasound 36:434, 1995. 20. Lester NV, Newell SM, et al: Scintigraphic diagnosis of insulinoma in a dog. Vet Radiol Ultrasound 40:174, 1999.

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Splenic Disease

❚❚❚ VARIATIONS IN SPLENIC VISIBILITY AND ESTIMATED SIZE Splenic visibility in the dog depends on a variety of factors, including breed, spleen size, and the size of the immediately surrounding viscera. Generally, the more caudally positioned the spleen, the larger it appears. Thus, dogs with large livers or more caudally positioned livers will appear to have larger spleens than dogs with small livers. The same holds true for the stomach. A large, food-filled stomach displaces the spleen into the central part of the abdomen, where splenic visibility is improved, potentially resulting in a misdiagnosis of splenomegaly. Breeds with highly tapered abdomens, Dobermans, for example, often are judged to have small spleens, whereas dogs with symmetric torsos, such as Bassetts, may be deemed to have splenic enlargement.

❚❚❚ SPLENIC CONGESTION Splenic enlargement caused by vascular congestion is common in tranquilized, sedated, and anesthetized dogs (Figure 69-1).

❚❚❚ PREVALENCE OF SPLENIC DISEASE IN DOGS AND CATS Dogs Hyperplastic nodules and nontraumatic hematoma were the most common splenic abnormalities based on histologic examination of nearly 1500 tissue specimens submitted to a veterinary pathology laboratory in California from 1985 to 1989. Because nontraumatic hematomas often are found in the presence of hyperplastic nodules, it is hypothesized that hyperplastic nodules are the precursors to splenic hematomas in the dog.

Hemangiosarcoma is the most common splenic tumor in dogs, but it cannot be grossly distinguished from nontraumatic splenic hematoma. According to the literature, German Shepherds rank first in breed prevalence, followed by Golden and Labrador Retrievers. Splenic lymphosarcoma is seen with only about one quarter the frequency of hemangiosarcoma.1 In my sonographic experience, medium and large cavitary splenic lesions, with or without associated peritoneal hemorrhage, are nearly always hemangiosarcomas.

Cats According to Spangler and Culbertson, mast cell tumor is the most common source of splenomegaly in cats, followed by lymphosarcoma, nonspecific congestion, diffuse lymphoid hyperplasia, myeloproliferative disease, and hemangiosarcoma.2 Hanson and co-workers, speaking from an ultrasonic perspective, reached a somewhat different conclusion, ranking lymphosarcoma first, followed closely by mast cell tumor and extramedullary hematopoiesis/lymphoid hyperplasia.3 Much less frequent sources of sonographically identified splenic disease (six or fewer cases) in cats were epithelial tumors, mesenchymal tumors, malignant histiocytosis, myeloproliferative disease, pyogranulomatous inflammation, erythroleukemia, eosinophilic syndrome, hematoma, and granulomatous splenitis. Regrettably, the authors were unable to identify any specific sonographic features for the described splenic disorders.

❚❚❚ NODULAR HYPERPLASIA, HYPERPLASTIC NODULE, REGENERATIVE NODULE According to Hudson, nodular hyperplasia is common in the spleens of old dogs, with most lesions being true 655

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Figure 69-1 • A lateral abdominal radiograph shows splenic enlargement secondary to tranquilization.

Figure 69-3 • Sonographic close-up of the spleen of a dog shows a 0.5-cm isoechoic regenerative nodule surrounded by an anechoic ring (arrow).

Figure 69-2 • Sonographic close-up of the spleen of a dog shows a spherical, 1-cm hypoechoic regenerative nodule (arrow), an incidental finding during a pregnancy evaluation.

Figure 69-4 • Sonographic close-up of the spleen of a dog with a presumed myelolipoma.

nodules (0.5 cm or smaller), but some reach up to 5 cm in diameter. Most such nodules appear hypoechoic. Some regenerative nodules appear to have the potential of becoming necrotic and later may result in a splenic hematoma. When similar-appearing lesions are present in the liver, the possibility of cancer exists.4 Although regenerative nodules potentially exhibit considerable sonographic variability, most appear hypoechoic with vague margins (Figure 69-2). The remaining nodules are either hyperechoic (compared with the surrounding spleen) or appear as “an object within an object” (Figure 69-3). Rarely are more than one or two nodules found.

❚❚❚ EXTRAMEDULLARY HEMATOPOIESIS AND SPLENIC MYELOLIPOMAS Extramedullary hematopoiesis can closely resemble nodular hyperplasia, with both lesions typically

appearing as hypoechoic splenic nodules. Concurrent bone marrow disease may or may not be present.5 Echogenic splenic nodules may be due to the localized accumulation of fat and accordingly are described as myelolipomas or lipomatosis (Figure 69-4). According to Schwarz and co-workers, myelolipomas can range in size from millimeters to centimeters. As yet there is no known disease associated with these “lesions.”6

❚❚❚ CANINE ABDOMINAL MALIGNANT HISTIOCYTOSIS Canine abdominal malignant histiocytosis has been reported to cause nodules and small masses in the liver, spleen, and kidney as well as mesenteric and medial iliac lymphadenopathy. Sonographically, the lesions appear highly variable, including hypoechoic, hyperechoic, and of mixed echogenicity.7 In my experience,

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the spleens of dogs with histiocytosis may also feature a distinctive lacelike appearance.

❚❚❚ SPLENITIS AND SPLENIC ABSCESS Splenitis is a somewhat ambiguous term that is only occasionally found in the veterinary literature. Citing human literature, Hudson seems to suggest that the term be used literally. No characteristic appearance is mentioned.8 Konde and co-workers described the sonographic appearance of a variety of abdominal abscesses involving the liver, spleen, kidney, uterine stump, and mesentery.9 Although the abscesses featured in the cited report were variable, most, including the splenic lesion, appeared dark overall with a roughed, relatively hyperechoic border.

A

❚❚❚ SPLENIC TUMORS Hemangiosarcoma Background Dogs. Hemangiosarcoma is the most common splenic tumor in dogs. Many affected animals present with a classic history of having recently collapsed (owners frequently describe this as “fainting”) and are now profoundly weak, which usually indicates that the tumor has ruptured and bled into the abdominal cavity. Golden and Labrador Retrievers are affected far more than any other breeds, including German Shepherds. Most dogs with a sonographically visible hemangiosarcoma do not have concurrently detectable atrial or auricular metastasis. Affected dogs rarely live beyond 5 months after their spleens have been removed. Imaging Findings Radiography. Radiographically, a large spherical mass (representing the cancerous spleen) is often present in the ventral abdomen, caudal to the stomach. If there has been extensive bleeding—unfortunately, a common occurrence—the tumor may be vague or invisible. Even so, it is often possible to infer a splenic mass based on the characteristic displacement of the surrounding viscera, especially air-filled stomach and bowel. Figures 69-5 to 69-7 illustrate the typical appearance of splenic hemangiosarcoma in the dog. Following substantial bleeding from a ruptured splenic hemangiosarcoma, the pulmonary vasculature may become abnormally small (pulmonary oligemia) until the blood volume returns to normal (Figure 69-8). Ultrasound. Sonographically, hemangiosarcoma of the spleen has a characteristic appearance: (1) regional splenic enlargement, (2) replacement of normal uniform

B Figure 69-5 • Close-up abdominal radiographs of a dog with a splenic hemangiosarcoma, which in the lateral projection (A) appears as a large spherical object in the ventral abdomen and in the ventrodorsal view (B) shows as a large oval mass displacing the stomach to the right.

texture by uneven blotchy white (hyperechoic) areas, (3) multiple variably sized and shaped fluid-filled cavities (some often quite large), and (4) if the tumor ruptures, peritoneal hemorrhage (Figure 69-9, A-C).10 Occasionally, splenic hemangiosarcomas resemble cysts or, in the case of acute injury, hemorrhage in the splenic interior (Figure 69-9, D). Cats. Hemangiosarcoma is rare in cats. Radiographically, it may or may not be distinguishable, depending on the extent to which it alters the caudal margins of the liver. Detection is further hampered when medium or large volumes of abdominal fluid are

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A

A

B Figure 69-7 • Bleeding splenic hemangiosarcoma: A, Lateral radiograph shows (1) increased density in the ventral two thirds of the abdomen caused by an enlarged cancerous spleen surrounded by blood, (2) displacement of the intestine away from the tumor (termed an abnormal bowel distribution pattern), and (3) decreased visceral detail resulting from peritoneal hemorrhage. B, A sonographic cross-section of the radiographically identified mass shows a large cavitated object in the tail of the spleen surrounded by fluid (blood).

B Figure 69-6 • Lateral (A) and ventrodorsal (B) close-up views of the cranial abdomen of a dog that collapsed 1 week ago show a predominantly left-sided splenic hemangiosarcoma.

present. Sonographically, hepatic hemangiosarcoma is characterized by regional or generalized enlargement, ill-defined areas of increased echogenicity, and cavitation. Abdominal fluid may or may not be present. Prognosis is poor because of the high and rapid rate of metastasis.11

❚❚❚ LYMPHOSARCOMA Background Imaging Findings Radiography. Moderate to severe splenomegaly in dogs that have not been tranquilized, sedated, or anes-

thetized is suggestive of lymphosarcoma, especially if there is a peripheral adenopathy. Splenic enlargement in cats that also have large a large liver and kidneys is very suggestive of lymphosarcoma. Ultrasound. Feeney, and later Hering, likened some forms of splenic lymphosarcoma to “Swiss cheese” because of the numerous small, ill-defined areas of decreased echogenicity.12,13 Lamb and co-workers described the sonographic appearance of splenic lymphosarcoma in a small number of dogs and cats. Sonographic disease indicators were (1) diffuse decreased echogenicity; (2) multiple roughly spherical, hypoechoic lesions of varying size; and (3) a single large, cavitated mass. Based on the sonographic identification of one or more of these abnormalities in five of six cases, the authors rather optimistically determined that ultrasound was a sensitive means of diagnosing this disease.14

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A

B C Figure 69-8 • Screening thoracic films (A-C) of a dog show no evidence of metastasis but do reveal pulmonary oligemia (best seen in lateral close-up view), suggesting tumor-related abdominal hemorrhage.

In my experience, a lymphomatous spleen is just as likely to look normal as not, although most show some degree of enlargement. Unlike the previously cited authors, I have encountered no consistent (and thus reliable) pattern for this form of splenic cancer.

❚❚❚ SPLENIC TORSION Background Splenic torsion is a rare disorder in dogs, associated with a wide spectrum of nonspecific abnormalities. These include disinterest in play or exercise, decreased

or absent appetite, vomiting, extreme weakness (including inability to stand unassisted), collapse, pallor, and shock. Barnes likened the more serious signs to those often seen with a ruptured hemangiosarcoma. and I agree.15 Splenic malpositioning that occurs in conjunction with a gastric torsion is not a true torsion; rather, it is a secondary displacement. Occasionally, gastric torsion occurs in dogs that have had a previous splenic torsion. A causative relationship has been suggested, namely, that the gastrosplenic ligaments become stretched when the spleen becomes twisted, which in turn leads to greater gastric mobility and, under certain circumstances, torsion.16 However, given the relatively inelastic nature of

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A

B

D

C Figure 69-9 • Four sonograms (A-D) illustrating the variability of cavitary lesions typically seen with splenic hemangiosarcoma in dogs.

ligaments,—a ligament sets limits to a given normal range of motion—this hypothesis seems unlikely.

Imaging Findings Radiography. An acute splenic torsion typically presents as a large central abdominal mass, which typically displaces the intestinal mass caudally. In most instances, the stomach becomes secondarily displaced and usually is filled with a combination of gas and fluid. If the thorax is radiographed, the heart and lung vessels often appear small because of shock. Occasionally, the enlarged spleen may appear to be originating from the caudal part of the abdomen as indicated by a cranially displaced bowel and in this respect can resemble pyometra or uterine torsion.17 Examples of splenic torsion are shown in Figures 69-10 to 69-12. Ultrasound. Konde and co-workers reported on the sonographic signs of splenic torsion, including (1) splenic enlargement; (2) an abnormally dark and

coarse echo texture attributable to the spreading apart of the brighter elements in the parenchyma caused by a hyperemic pulp, sometimes described as a lacyappearing spleen; and (3) enlargement of hilar vessels.18 As mentioned previously, malignant histiocytosis may also appear sonographically as an enlarged lacelike spleen. Saunders and co-workers retrospectively analyzed spectral and color Doppler data in 15 confirmed cases of splenic torsion in dogs and found that all the animals lacked demonstrable splenic blood flow. Additional sonographic findings included thrombi, presumably caused by vascular stasis in two dogs in which the splenic echo texture appeared normal. Given the latter finding, the authors recommend that both anatomic and blood flow assessments be performed in such cases.19 Although splenic hyperemia has been a widely reported sign of torsion in dogs, I have found this to be an inconsistent sonographic sign that appears to be largely dependent on the duration of the disease. Perhaps more disturbingly, I have found dogs that did not have splenic torsion exhibiting marked splenic vein

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A Figure 69-11 • Combined acute gastrosplenic torsion: Lateral radiograph of a dog with an acute splenic torsion shows gastric dilation and displacement, splenic enlargement, and displacement of the bowel mass.

B Figure 69-10 • A, Close-up lateral view of the cranial abdomen of a dog with a splenic torsion shows displacement of both the stomach and spleen (emphasis zone shows cranial aspect of spleen) seen against a backdrop of peritoneal hemorrhage. B, A ventrodorsal view shows displacement of the small intestine to the left lateral side of the abdomen and right-sided splenic margin (emphasis zone).

distension. Likewise, I have recorded splenic blood flow (using Doppler ultrasound) in surgically confirmed cases of splenic torsion.

❚❚❚ SPLENIC NECROSIS SECONDARY TO SPLENIC INFARCTION Background Splenic necrosis, although an inarguable indication of splenic injury, remains a nonspecific finding (with respect to etiology). Diseases capable of causing splenic necrosis include (1) infarction, (2) abscess, and (3) primary and secondary tumors.

Imaging Findings Schilling and colleagues described splenic infarction in dogs as having at least three different appearances (described echogenicity is relative to the liver).20

Figure 69-12 • Close-up lateral view of the cranial abdomen of a dog with an acute splenic torsion shows enlargement and displacement of both stomach and spleen and caudal displacement of the bowel mass. The small heart and hyperlucent lung reflect secondary vascular obstruction.

1. Focal hypoechoic lesions located in the splenic interior 2. Focal hypoechoic or isoechoic lesions that lie just below the splenic surface, causing it to bulge outwardly 3. Coarse, regional or diffuse, hypoechoic or heteroechoic echogenicity that was described by the authors as having a “lacy” appearance

❚❚❚ TRAUMATIC HEMATOMA Like hematomas located anywhere in the body, the sonographic appearance of a splenic hematoma

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Figure 69-13 • Sonogram showing numerous small areas (“islands”) of decreased echogenicity within the spleen of a dog with immune-mediated thrombocytopenia.

depends mostly on its age: Recently formed hematomas usually appear dark and become lighter with time. Likewise, the uniform hypoechoic appearance that typically characterizes a fresh hematoma is soon replaced by a variety of hyperechoic patterns, ranging from striated to speckled as the torn and bruised splenic pulp heals.21 This time-related variability can be used in serial examinations to support an otherwise uncertain diagnosis of hematoma.22 Because the spleen is a long, flat organ resembling the torso of a fish, large hematomas usually produce localized or regional splenic enlargement, which unfortunately is also a physical quality shared by other splenic lesions: hemangiosarcoma, hemangioma, abscess, infarct, or unusually large hyperplastic nodule. Accordingly, a diagnosis of splenic hematoma is typically contextual, rendered in light of recent trauma.

❚❚❚ SPLENOMEGALY SECONDARY TO AUTOIMMUNE HEMOLYTIC ANEMIA OR THROMBOCYTOPENIA Splenic enlargement often occurs in autoimmune diseases that modify, damage, or destroy red blood cells to the extent that they are selectively filtered out of the general circulation by the spleen. This process, also known as splenic sequestration, can be inferred radiographically (Figure 69-13) and diagnosed specifically using nuclear imaging.23

References 1. Spangler WL, Culbertson MR: Prevalence and type of splenic diseases in dogs: 1,480 cases (1985-1989). J Am Vet Med Assoc 200:829, 1992.

2. Spangler WL, Culbertson MR: Prevalence and type of splenic diseases in cats: 455 cases (1985-1991). J Am Vet Med Assoc 201:773, 1992. 3. Hanson JA, Papageorges M, et al: Ultrasonographic appearance of splenic disease in 101 cats. Vet Radiol Ultrasound 42:347, 2001. 4. Hudson JA: The spleen. In Cartee RE, ed: Practical veterinary ultrasound. Philadelphia, 1995, Lea & Febiger. 5. Hudson JA: The spleen. In Cartee RE, ed: Practical veterinary ultrasound. Philadelphia, 1995, Lea & Febiger. 6. Schwarz LA, Penninck DG, et al: Canine splenic myelipomas. Vet Radiol Ultrasound 42:347, 2001. 7. Ramirez S, et al: Ultrasonic features of canine abdominal malignant histiocytosis. Vet Radiol Ultrasound 43:167, 2002. 8. Hudson JA: The spleen. In Cartee RE, ed: Practical veterinary ultrasound. Philadelphia, 1995, Lea & Febiger. 9. Konde LJ, Lebel JL, et al: Sonographic application in the diagnosis of intraabdominal abscess in the dog. Vet Rad 27:151, 1986. 10. Hahn KA, Widmer WR, et al: What is your diagnosis? J Am Vet Med Assoc 200:222, 1992. 11. Spangler WL, Culbertson MR: Prevalence and type of splenic diseases in cats: 455 cases (1985-1991). J Am Vet Med Assoc 201:773, 1992. 12. Feeney D, Johnston G, et al: Two-dimensional, gray-scale ultrasonography for assessment of hepatic and splenic neoplasia in the dog and cat. J Am Vet Med Assoc 184:68, 1984. 13. Hering DS: Abdominal ultrasound: theory and practice. Semin Vet Med Surg (Small Anim) 1:102, 1986. 14. Lamb CR, Hartzband LE, et al: Ultrasonographic findings in hepatic and splenic lymphosarcoma in dogs and cats. Vet Rad 32:117, 1991. 15. Barnes EA: What is your diagnosis? J Small Anim Pract 40:251, 1999. 16. Mills DL, Nemzek J, et al: Gastric dilatation-volvulus after splenic torsion in two dogs. J Am Vet Med Assoc 207:314, 1995. 17. Thomas WB, Hudson JA, Cartee RE: Ultrasonic diagnosis. Vet Rad 32:227, 1991. 18. Konde LK, Wrigley RH, et al: Sonographic and radiographic changes associated with splenic torsion in the dog. Vet Rad 30:41, 1989. 19. Saunders HM, Neath PJ, Brockman DJ: B-mode and Doppler ultrasound imaging of the spleen with canine splenic torsion: a retrospective evaluation. Vet Radiol Ultrasound 39:349, 1998. 20. Schelling CG, Wortman JA, Saunders HM: Ultrasonic detection of splenic necrosis in the dog. Vet Rad 29:227, 1988. 21. Hanson JA, Penninck DG: Ultrasonic evaluation of a traumatic splenic hematoma and literature review. Vet Radiol Ultrasound 35:463, 1994. 22. Farrow CS: Musculoskeletal system. In Green RW, ed: Small animal ultrasound. Philadelphia, 1996, LippincottRaven. 23. Berry CR, Kuperus JH, Malone D: Splenic sequestration scintigraphy in the dog: a comparison of denaturing techniques. Vet Radiol Ultrasound 36:57, 1995.

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Kidney, Ureteral, Bladder, Prostatic, and Urethral Disease ❚❚❚ KIDNEY DISEASE (RENAL DISEASE) Diagnostic Approach Practically speaking, the kidneys, ureters, bladder, and urethra are an integral unit; thus, what affects one part of the system is likely to affect another. Although arguably more a part of the reproductive tract than of the urinary tract, an enlarged prostate gland may cause full or partial obstruction of the urinary bladder, and an infected or cancerous prostate can be responsible for blood in the urine. Because of its anatomic intimacy with the caudal part of the urinary tract and its potentially influential role on urinary dysfunction, I have chosen to include the prostate in this chapter.

Ultrasound-Guided Biopsy Hager and co-workers reported on the successful biopsy diagnosis of liver, kidney, and prostate diseases of dogs.1 In the case of the kidney, diagnostic samples were obtained 88% of the time with a maximum of two attempts. For best results and the lowest probability of collateral kidney damage and postprocedural hemorrhage, general anesthesia is recommended. In regard to the issue of procedural safety, Drost and co-workers found that renal biopsy in healthy sedated cats has only minimal effect on renal function as determined by quantitative renal scintigraphy: 99mTc-DTPA to evaluate the glomerular filtration rate (GFR) and 99m Tc-MAG3 to assess effective renal blood flow (ERBF).2

Imaging Strategy Radiography. Abdominal radiography, with an emphasis on the urinary tract, usually follows the palpation of enlarged kidneys or an abnormal urinalysis (Box 70-1). In such circumstances, the kidneys typically are evaluated for absolute and relative size.

Absolute Kidney Size. Most North American veterinarians consider a dog’s kidney to be radiographically normal when its length measures somewhere between 2.5 and 3.5 times the length of its second lumbar vertebra (in ventrodorsal projection). A cat’s kidney is smaller, however, measuring only 2.4 to 3.0 the length of the second lumbar vertebra (Table 70-1). Relative Kidney Size. As first described by a physician radiologist and later adapted to veterinary radiology by others and myself, relative renal assessment (comparing the size, shape, and contour of one kidney with another) is arguably of greater clinical utility than knowing the absolute size of each kidney.3–5 For example, the renal tandem (my term) of one large and one small kidney is often the result of unilateral chronic nephritis and contralateral compensatory hypertrophy, whereas the combination of two large, smooth kidneys is more likely to be due to lymphoma (Table 70-2). Renal Volume. Radiographic measurements of the kidneys are often inaccurate because of a combination of geometric distortion and magnification. Urography can overcome some of the problems associated with plain film assessment but also can add to the dilemma by increasing kidney size secondary to osmotic diuresis. Nyland and co-workers reported the volumetric assessment of normal canine kidneys using ultrasound. Because of a systematic underestimation of actual renal volume (as determined by measuring the extirpated kidney), it was necessary to manipulate the raw data mathematically to achieve the desired results.6 Felkai and co-workers also described the sonographic determination of renal volumes based on linear and area measurements applied to a geometric model of the kidney (prolate ellipsoid).7 Experience with such calculations appears to be based largely on human renal transplant work, with animal applications remaining largely theoretic at this time. 663

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B o x

7 0 - 1

Diseases Potentially Causing Bilateral Kidney Enlargement Acromegaly Acute nephritis Amyloidosis Feline infectious peritonitis Hydronephrosis Lymphoma • 50% of cats with lymphoma are positive for feline leukemia virus • 40% of dogs with lymphoma have hypercalcemia Metastasis Perirenal pseudocysts Polycystic kidneys Pyelonephritis

Table 70-1 • RADIOGRAPHIC ASSESSMENT OF NORMAL KIDNEY SIZE IN THE DOG AND CAT Species

Kidney Size

Dog Cat

2.5 to 3.5 times the length of L2 2.4 to 3.0 times the length of L2

Table 70-2 • RENAL DISEASE TANDEMS: PREDICTORS OF KIDNEY DISEASE IN DOGS AND CATS Renal Disease Tandem

Possible Explanations

Two small kidneys Two normal kidneys

Chronic interstitial nephritis Normal, acute nephritis, acute ethylene glycol poisoning, glomerulonephritis, chronic interstitial nephritis Polycystic disease, lymphoma (and occasionally some other cancers), hydronephrosis, kidney worms Chronic interstitial nephritis with compensatory hypertrophy of the opposite kidney Tumor, trauma, perirenal cyst, hydronephrosis

Two large kidneys One small and one large kidney One normal and one large kidney

Canine Neonatal Kidneys. England described the sonographic appearance of the kidneys of puppies from birth to 6 months of age. He reported the following 8: • Cortical echogenicity was increased for the first 2 weeks of life. • Renal size (compared with body size) was increased for the first 3 months of life. • Renal size became proportional to body size after 3 months of age. Excretory Urography Method. It is best to obtain urine specimens intended for culture and sensitivity before performing urography because Ruby and co-workers showed that iodine

Table 70-3 • KIDNEY SIZE OF CATS: REPRODUCTIVE STATUS VS. RENAL LENGTH Reproductive Status

Renal Length (Times L2)

Intact Neutered

2.1–3.2 1.9–2.6

concentrations typically used in urography inhibit the growth of Proteus mirabilis, a potential source of urinary tract infection (although Escherichia coli and Staphylococcus aureus are not affected). Anatomic Assessment. Shiroma and co-workers showed that renal length in healthy cats depends on whether or not the animals are neutered.9 Specifically, the kidneys of cats neutered before reaching maturity are smaller than those of intact animals (Table 70-3). Functional Assessment. Although the primary purpose of urography is to assess the kidneys and ureters anatomically, it also can be used to draw some general conclusions about renal function.10 Specifically, renal opacification, or more specifically the time to maximum renal opacification, once contrast has been administered, can potentially predict disorders of (1) renal perfusion, (2) glomerular filtration, (3) intrarenal or extrarenal obstruction, (4) tubular necrosis, and (5) contrast toxicity. Risks. Fortunately, harmful effects related to excretory urography in dogs and cats—so-called contrast reactions—are rare. Carr and co-workers reported persistent renal opacification in a cat during intravenous urography, attributing it to either acute renal failure or contrast medium–induced hypotension.11 Some dogs retch or vomit shortly after contrast injection but recover quickly.

Ultrasound The Rim Sign: Is It a Sign of Disease? Konde and coworkers described the normal sonographic appearance of the canine kidney (Figure 70-1).12 Biller and coworkers reported observing the medullary rim sign in dogs and cats, a previously reported sonographic finding in people and animals consisting of an echogenic band in the outer part of the renal medulla paralleling the corticomedullary junction, but they stopped short of calling it a reliable sonographic disease indicator (Figure 70-2). Instead, they showed the rim sign in conjunction with a variety of canine renal disorders, repeatedly pointing out that it might be an incidental finding and also indicating that rim signs have been described in normal cats. After a discussion of the human pathophysiology (apparently there is little such information on dogs), the authors closed their report with the following statement: “The medullary rim sign provides an additional

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A

Figure 70-2 • Renal sonogram in a healthy donor cat shows an unusual appearance, which I term the renal rim sign and others have termed the medullary rim sign or simply the rim sign. To date, I have been unable to establish any consistent relationship between this appearance and any specific renal disease in cats or dogs.

described the use of 99mTc-DTPAtransit times in healthy dogs as a potential means of evaluating animals with renal disease.17 B

Compensatory Renal Hypertrophy Figure 70-1 • Renal sonograms from a normal dog show: renal arteries (A) and associated arterial blood flow (B).

ultrasonic change indicating primary renal damage in some patients (my italics).”13 In a later communication, Mantis and Lamb suggested that the rim sign was, at the least, nonspecific and in some instances probably insignificant; however, the authors did leave the interpretive door open by concluding, “The possibility cannot be excluded that it (the rim sign) is a sentinel sign of subclinical renal disease.”14 In my experience, the medullary rim sign has usually proven to be an incidental finding that subsequently could not be histologically or biochemically related to any past or present kidney disease. Influences of Diet and Age. Churchill and co-workers investigated the influence of age and diet on relative renal echogenicity (kidney compared with adjacent liver and spleen) in a group of uninephrectomized but otherwise normal 7- and 8-year-old female Beagles observed over a 4-year period. It was determined that these factors exerted only a minimal effect on renal appearance.15

Renal Nuclear Medicine Daniel and co-workers recently reviewed the subject of renal nuclear medicine.16 Barthez and co-workers

Boag and co-workers showed that after removal of a single kidney in a healthy dog, the remaining kidney will enlarge (compensatory hypertrophy) by as much as 40% within 3 weeks after nephrectomy.18 Churchill and co-workers, studying the effects of unilateral nephrectomy on 11- and 12-year-old healthy female Beagles over a 4-year period, found that the remaining normal kidney grew in length by 10 to 15%, mostly in the first 3 months.19

Congenital Renal Disease Polycystic Kidney Disease. Polycystic kidney disease is one of those curious disorders about which much is taught, but little is experienced; in other words, it is rare. In radiographs, two large, smoothly bordered kidneys usually characterize severe cases (Figure 703). Sonographically, the defining feature of this disease is the presence of multiple asymmetric cavitary lesions. Some forms of polycystic disease, however, more closely resemble the appearance of normal kidneys distended by intravenous fluids.20 Polycystic kidney disease has been reported in association with renal lymphoma in a cat.21 Renal Ectopia, Fusion, and Duplication. Renal ectopia, or crossed renal ectopia, is an extremely rare congenital disorder in which one kidney crosses to the opposite side of the abdomen and fuses with the other.

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A A

B Figure 70-4 • Close-up ventrodorsal urogram (A) and ultraclose view (B) of left renal pelvis show an angular filling defect in the context of mild to moderate ureteral dilation.

B Figure 70-3 • Polycystic kidneys: Lateral and ventrodorsal radiographs in a cat show enormously enlarged kidneys displacing the bowel ventrally.

This prenatal collation may result in later functional abnormalities, including renal failure, as described in a middle-aged cat by Allworth and Hoffman.22 Fusion and duplication rarely occur in dogs and cats. Renal Infection. Typically, renal infections are diagnosed by urinalysis, culture, and sensitivity, not by medical imaging. This being said, there appears to be no dearth of requests at our hospital for sonographic examination of suspected renal infections, most of which are negative. It is disappointing, however, that urographic assessment fares only somewhat better than plain films in diagnosing renal infection. Generalities Concerning Renal Infections • Most acute renal infections are associated with normal radiographic and sonographic appearance. • Some subacute infections may cause dilation of the renal pelvis, pelvic recesses, and ureters (Figure 70-4).

• Chronic renal disease can lead to marked renal shrinkage, loss of corticomedullary distinction, increased echogenicity, and irregular margins (Figures 70-5 and 70-6).

Leptospirosis Canine leptospirosis is caused by a spirochete that primarily infects the liver and kidneys and, less often, the lung.23 Renal failure may result. I am unaware of any consistent plain film abnormalities associated with this disease. Forrest and co-workers described the sonographic appearance of leptospirosis in 20 dogs.24 Abnormalities (in order of frequency of appearance) included (1) increased cortical echogenicity, (2) increased renal size, (3) mild pelvic dilation, (4) an outer rim or band of increased medullary echogenicity (renal rim sign), and (5) perirenal fluid.

Renal Obstruction and Hydronephrosis Terminology. Pugh and co-workers challenged the use of the term hydronephrosis, as veterinarians typically use it, saying that the term is a specific one that is appro-

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Figure 70-5 • Chronic nephritis: Lateral sonogram in an elderly cat shows a small, shrunken hyperechoic kidney, the result of chronic nephritis.

Figure 70-7 • Sonographic long section of a hydronephrotic kidney shows moderate dilation of the renal pelvis, pelvic recesses, and associated ureter.

Giant Kidney Worm (Dioctophyme renale) Kidney worms affect a variety of mammals including the dog, eventually causing hydronephrosis. Adiseased kidney may become two to three times its normal size and contain a female worm that is more than a yard in length that can be detected sonographically.

Kidney Stones (Renal Calculi) and Crystals

Figure 70-6 • Sonographic long section of a chronically infected kidney (electronic cursors) shows substantial shrinkage, marginal deformity, lack of corticomedullary definition, and a diminished collecting system.

priate only for describing dilation of the renal pelvis and pelvic recesses secondary to ureteral obstruction. Except for diseases that dilate the renal collecting system, and not caused by ureteral blockage, the authors propose the term pyelectasia, contending that is more appropriate for such conditions as urinary tract infections and high-volume hydration, conditions that can cause renal dilation.25 Felkai and co-workers, although they do not quarrel with the term hydronephrosis, do find it limiting in some circumstances; consequently, they proposed a subclassification (Table 70-4).26 My own view in this matter is simply to state the observation, clearly and unequivocally: pelvic dilation, mild, moderate, or severe. After this should be comments on any inferred implications, particularly with respect to ureteral obstruction (Figure 70-7).

The radiographic identification of kidney stones depends on a number of factors: (1) the size of the stone, (2) its chemical composition, and (3) the quality of the radiograph (Figure 70-8). Sometimes there are also ureteral stones in the same individual (Figure 70-9). Renal sonography typically results in a higher diagnostic yield than does radiography (Figure 70-10) but can have difficulty in distinguishing small stones or crystals from pelvic fat (Figure 70-11). Fat in the renal sinus can resemble crystals or stones in the renal pelvis, as can focal dystrophic calcification in the nearby parenchyma.27 Osseous metaplasia has been reported in association with hydronephrosis in a dog.28

Perirenal Pseudocyst (Perinephric Pseudocyst, Perirenal Cyst) Perirenal or perinephric pseudocysts are large fluid accumulations that completely or partially surround the kidney (Figure 70-12). Thought to be a consequence of renal disease or injury, these cysts may leak fluid into the peritoneal or retroperitoneal spaces, causing abdominal distension. This unusual disease is occasionally found in cats but only rarely in dogs.29–31 Perirenal cysts can be subtyped according to content and presumed cause: (1) urine-containing, (2) lymphcontaining, (3) blood-containing, and (4) transudatecontaining cysts. Cysts that contain urine (also termed uriniferous perirenal cysts) are presumed to be the result

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Figure 70-8 • Sonographic long section of a nephritic kidney shows a number of variably defined acoustic shadows caused by kidney stones.

Table 70-4 • SUBCLASSIFICATION OF SONOGRAPHICALLY DIAGNOSED HYDRONEPHROSIS IN DOGS

Type of Renal Pelvic Dilation Advanced hydronephrosis Dilation with stasis Functional dilation Mild hydronephrosis

Sonographic Features (in addition to pelvic enlargement) Parenchyma is markedly thinned and no longer recognizable Parenchymal structure is retained No retention of urine and of brief duration Parenchymal narrowing is present, but still recognizable

of leakage of urine from the underlying kidney. Lymphfilled cysts are believed to be caused by inflammation or obstruction of the hilar lymphatics. Hemorrhagic cysts have been reported secondary to injury, neoplasia, blood dyscrasias, and after some renal transplants. The precise cause of transudate-containing cysts is usually unknown.32 Rishniw and colleagues reported a case of hydrothorax in a cat caused by a communicating perinephric psudocyst.33 Specifically, a fistula had formed between the described pseudocyst and the diaphragmatic opening for the caudal vena cava (foramen venae cavae), allowing fluid from the cyst to drain into the pleural space. Injecting a radioisotope into the cyst and scintigraphically tracking it toward the thorax established the probability of a communicative relationship between the nephrocyst and the pleural space preoperatively.

Comment

This type of mild dilation is most likely to be encountered during intravenous fluid administration

Table 70-5 • CANINE PRIMARY RENAL NEOPLASMS Tumor Type Primary renal cell carcinoma Transitional cell carcinoma Renal adenoma, papilloma Renal sarcoma Nephroblastoma Fibroma Lymphoma

Relative Percentage 69 9 7 7 4 2 2

lecting system. Multiple renal cysts sometimes are difficult to differentiate from congenital polycystic disease.

Renal Tumors Intrarenal Cysts Typically, intrarenal cysts are located in the renal interior, and unless they are extremely large, they are of little clinical consequence (Figure 70-13). Less often, renal cysts are found on the cortical surface, where they may appear as small marginal blebs. Occasionally, large renal cysts may compromise the renal col-

Background. Eighty-five percent of canine renal tumors are reported to be metastatic, spreading to the kidneys by the blood, lymph, or direct extension. Primary renal tumors, on the other hand, are found only occasionally, and most are malignant. Benign primary renal tumors, such as hemangioma, are rare (Table 70-5).34

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B

A

C

D Figure 70-9 • Lateral (A) and ventrodorsal (B) urograms featuring multiple abnormalities: (1) persistence of contrast solution in the circulatory system (12 hours after intravenous injection) resulting from poor renal function, (2) bilateral kidney stones, and (3) a possible right ureteral stone. Sonograms (C, D) (1) show bilateral hydronephrosis and hydroureter, (2) confirm the presence of a stone in the right ureter, and (3) reveal a medium-sized bladder stone, previously concealed by contrast solution.

Imaging Findings Radiography. Other than enlargement, there is little to indicate the presence of a renal tumor, and even this is not foolproof because obstruction and compensatory hypertrophy can result in a similar appearance. Depending on the capacity of a particular tumor to distort or obstruct the renal pelvis or pelvic recesses or to substantially disrupt renal circulation, urography may offer little advantage over plain radiography in the diagnosis of kidney cancer. Ultrasound. Konde and co-workers described the sonographic appearance of a variety of canine renal tumors.35 In most instances, sonography leaves little doubt about the neoplastic nature of the lesion;

however, it is often unclear as to its cell type and whether it is benign or malignant.

Specific Renal Tumors Lymphoma. Typically, renal lymphoma is characterized by bilateral enlargement of the kidneys and may enlarge the kidneys by as much as twice.36 Alternatively, what initially appears as renal enlargement actually may be a subcapsular hematoma, which may accompany renal lymphoma and may be present in one or both kidneys.37 Sonographically, a lymphomatous kidney often appears to have a dark, thickened cortex and lacks a discernible medulla (Figure 70-14). The true size of the kidney usually can be determined

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Figure 70-12 • Cross-sectional sonogram of a large perirenal cyst with the cranial pole of the kidney positioned at the lower right of the photograph.

Figure 70-10 • Sagittal sonogram shows acoustic shadowing originating from numerous small centrally located kidney stones.

Figure 70-13 • Sagittal sonogram shows a medium-sized intrarenal cyst.

Figure 70-11 • Sonogram of a normal canine kidney shows echogenic fat in the renal sinus, which must be distinguished from pelvic crystals and small stones.

Figure 70-14 • Lateral sonogram of a dog with bilateral renal lymphoma.

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sonographically or urographically. If doubt remains, renal angiography,* either selective or nonselective, should resolve any question. Nephroblastoma. Renal nephroblastoma is a malignant tumor of puppies and young dogs. Affected dogs often present with abdominal distension caused by ascites. Radiographs often reveal a large, vaguely outlined cranial abdominal mass and peritoneal fluid. Using the associated bowel distribution pattern, it is often possible to determine that the mass is retroperitoneal in origin. Sonographically, nephroblastomas often appear cystic and, when right-sided, may invade the nearby caudal vena cava. Metastatic spread is usually to nearby lymph nodes, the liver, and the lungs.38 Hereditary Multifocal Renal Cystadenocarcinomas. Renal cystadenoma is a hereditary disease of relatively young German Shepherds (4 to 5 years of age) that causes multifocal renal tumors and cysts. Moe and Lium described the tomographic (computed) appearance of typical kidney lesions in a group of Shepherds born and raised in Norway. The authors advocate CT for detection of small lesions not readily demonstrable with radiography or urography and for screening of suspected carriers before breeding.39

Chronic Renal Failure Background. Chronic renal failure is somewhat of a misnomer because it can be argued that once the kidneys fail, without dialysis or transplant, the individual will die. More correctly, this term refers to the gradual process of failure, that is, the slipping away of nephrons, and with them, renal function. Imaging Findings. Theoretically, the greater the degree of renal degeneration (morphologically speaking), the smaller the kidney becomes. Concurrent scarring, which is typically nonuniform, is likely to bring about varying degrees of tissue contraction that can lead to marginal irregularity. Varying types and degrees of associated renal calcification and stone formation are further indications of chronicity.40

Antifreeze Poisoning The deposition of calcium oxalate crystals in the renal tubules results in a marked increase in cortical echogenicity, which in some cases verges on brilliance. It is this unique characteristic of ethylene glycol toxicity that sets it apart from all other renal disease.41 Similar renal changes have been observed in the kidneys of a pregnant cat and her unborn kittens.42 *Renal angiography is now largely limited to experimental settings, having been supplanted by sonography. For an excellent pictorial discussion of the subject, see Barber DL: Renal angiography in veterinary medicine. J Am Vet Rad Soc 16:187, 1975.

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Hypercalcemic Nephropathy Background. Persistent hypercalcemia in the dog may develop as a side effect of cancer and, as such, is termed a paraneoplastic syndrome. Other causes of hypercalcemia include hyperparathyroidism, hypervitaminosis D, renal disease, and some diffuse skeletal diseases. Chronic calcium deposition in the kidneys eventually leads to tubular injury and renal dysfunction, some of which may be irreversible. Imaging Findings. Typically, the amount of calcium deposited in the kidneys is insufficient to detect radiographically. Using sonography, however, one often can identify an increase in renal cortical echogenicity compared with the liver (normally, the renal cortex should be slightly less echogenic than the liver).43

Renal Transplant Rejection Nyland and co-workers sonographically chronicled the gradual demise of rejected renal transplants in healthy dogs; their intention was to determine the best means of sonographically monitoring acute allograft rejection in this species.44 These authors recommend that, based on their experience, renal transplants be sonographically monitored using cross-sectional area measurements. Their observations are as follows: • Transplanted kidneys undergoing rejection rapidly increased in volume and cross-sectional area: more than 100% increase in volume and more than 80% increase in excess area (by 17 days). • Increased renal size was ascribed to a combination of hypertrophy and acute rejection. • Renal volume then began to decrease, being only 35% greater than normal by day 34. • Concurrently, the sonographic appearance of the dying kidneys changed, showing in order of appearance: (1) increased medullary volume with decreased echogenicity, (2) increased cortical thickness and echogenicity, and (3) decreased corticomedullary definition.

❚❚❚ URETERAL DISEASE: OBSTRUCTION AND ECTOPIA Ureteral Obstruction Ureteral obstruction may be due to a variety of causes, and, if unrelieved, leads to secondary ureteral and renal dilation. Potential sources of luminal blockage include stones, abscesses, blood clots, and, very rarely, tumors. Ureteral stenosis per se is rare. Ureteral outlet obstruction is most often the result of trigonal cancer, whereas extraneous blockage is usually secondary to accidental ligation or postsurgical scarring following hysterectomy.45–47 Occlusion also can follow ureteral transplantation in the case of ectopic ureter.

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Table 70-6 • CAUSES OF URETERAL OBSTRUCTION Cause

Comment

Bladder tumor at or very near vesicoureteral junction Congenital ureteral malpositioning (ectopic ureter)

Exterior surface, intramural, and luminal tumors are all potentially capable of ureteral blockage Resistances to urine flow and infection have been suggested as possible causes of ureteral and renal pelvic–pelvic recess distension A ureterocele is a dilation of the distal ureter within the bladder wall, resembling the inflated cuff on a Foley catheter; diagnosis is usually made with urography, sonography, or a combination of the two* Tumors need not invade the ureter or kidney to cause significant disease, although some do; in fact, merely occluding the ureter is often sufficient to incapacitate one or both kidneys† Relatively rare and almost always associated with renal fracture and related hematoma; blockage is usually near kidney; often subsides spontaneously after a few days Rare‡ Rare Accidental ureteral ligation typically occurs during ovariohysterectomy Calcium oxalate ureteroliths, diagnosed sonographically, have been reported in both a cat and a dog.§ Accidental ureteral transection may lead to the formation of a urinoma Many surgically repositioned ureters, although functional, never regain their original form

Congenital ureterocele Dorsal peritoneal or retroperitoneal midline tumors Extraluminal hemorrhage Ureteral abscess Ureteral hemorrhage Ureteral ligation Ureteral stones (calculi) Ureteral transection Vesicoureteral stenosis following surgical repositioning of an ectopic ureter

*From Takiguchi M, Yasuda J, et al: Ultrasonographic appearance of orthotopic ureterocele in a dog. Vet Radiol Ultrasound 38:308, 1997. † From Forrest LJ, Galbreath EJ, et al: Peripheral neuroblastoma in a dog. Vet Radiol Ultrasound 39:337, 1998. ‡ From Kleine LJ: An unusual case of pyelonephritis in a cat. J Am Vet Rad Soc 5:54, 1964. § Form Forrest Armbrust L, Kraft SL, et al: Canine ureteral calculus. Vet Radiol Ultrasound 38:360, 1997.

Complete ureteral obstruction leads to a characteristic enlargement of the ureter proximal to the point of blockage (hydroureter) and later enlargement of renal pelvis and pelvic recesses (hydronephrosis). Some or all of these changes can be appreciated with both radiology and ultrasound (Table 70-6).48 Imaging Findings Ureteral Enlargement (Megaureter). As already mentioned, ureteral enlargement can be detected radiographically, although it is difficult. If sufficiently enlarged, the ureter appears as a thick band, not unlike the profile of a blood vessel, extending caudally from the kidney to the dorsal aspect of the bladder neck (Figure 70-15, A). Sonographically, identification of an enlarged ureter is more straightforward, with the diseased ureter often resembling a tortuous blood vessel (Figure 70-15, B). Ureteral Stones (Ureteral Calculi). Ureteral stones are rare and, when present, are difficult to detect, even assuming that ureteral calculi are being diagnostically considered (Figure 70-16, A,B). If the colon is full, detection becomes even more problematic. Confirmation requires urography or sonography (Fig. 70-16, C-E).

Retrograde Urography As with gastroenterography, I prefer the patient-tailored examination to a strict protocol study. Accordingly, once I see the ureters are beginning to opacify, I film the retroperitoneal region at brief intervals until filling is complete and I have been able to establish whether

any blockage is present. I may supplement the examination with ultrasound, especially if I want to observe the ureteric jets emptying into the bladder. In general, the larger and the more tortuous the ureters, the more likely there is to be distension of the renal collecting system (renal pelvis and pelvic recesses). Figure 70-17 provides an excellent example of bilateral ureteral enlargement caused by obstructive trigonal cancer. Blockage of one ureter was so complete that it caused proximal ureteral sacculation. When a ureter is accidentally ligated during spaying, it rapidly dilates, and unless quickly relieved, it results in permanent enlargement, urine stasis, and a tendency to become infected (Figure 70-18). Ultrasound Diagnostic Value of Resistive Index in Dogs. Nyland and co-workers have reported that using Doppler ultrasound to determine the resistive index (RI) of experimentally obstructed canine kidneys has a falsepositive rate of nearly 30%, making it unsuitable for clinical diagnosis.49 Morrow and co-workers differ, however, pointing out that although the sensitivity of the renal RI is admittedly low, its high specificity is valuable in the early identification of kidney disease, which cannot be detected by sonographic or laboratory means.50 With regard to the influence of anesthesia on the accuracy of sonographically measured resistive and pulsatile indices, Mitchell and co-workers determined that in cats the results are likely to be unreliable because of an anesthesia-related increased intrarenal vascular resistance and decreased renal blood flow.51

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673

A

B Figure 70-15 • Lateral view (A) of the abdomen of a dog with a faintly visible right hydroureter, which was later confirmed sonographically (B).

Congenital Ureteral Malpositioning (Ectopic Ureter, Ureteral Ectopia) Background. Congenital malpositioning is the most commonly diagnosed primary ureteral disease in the dog (ectopic ureter). Females are 20 to 25 times more likely to be affected than males. The owners of affected dogs usually seek veterinary advice because their pets are continuously dribbling urine (urinary incontinence) and have done so since they were puppies. In most instances, the incontinence is due to one or two ectopic ureters. Less often, the problem of dribbling is attributed to ineffective bladder control, especially after an ectopic ureter has been ruled out. This type of presumptive diagnosis is sometimes referred to as an “immature” bladder or “immature” bladder sphincter. Dribbling also may be the result of congenital

urogenital malformations, deformities that may involve the bladder, urethra, and vagina as well as the ureters and kidneys.52 Imaging Findings. Traditionally, ectopic ureters have been diagnosed by excretory urography (Figure 70-19). Many centers now supplement this basic examination, or have replaced it altogether, with retrograde vaginourethrocystography, whereas others prefer to rely totally on ultrasonography (Figure 70-20), especially with respect to the evaluation of ureteric jets, a reliable sonographic indicator of normal ureteral positioning (Figure 70-21). Although it may occasionally be possible to identify very distended ureters on plain films, it is impossible to determine their precise termination point; thus, noncontrast films do very little to confirm or deny a diagnosis of ectopic ureter.

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A

D

B

C

E Figure 70-16 • Lateral (A) and close-up lateral (B) views of the abdomen of a dog with a pear-shaped left kidney and a small pair of ureteral stones. Surprisingly, lateral (C) and ventrodorsal (D) urograms reveal no ureteral enlargement, even though the right kidney is hydronephrotic. The ureteral calculi appear as a pair of small filling defects surrounded by an abnormally angular ureter; the collecting system of the deformed left kidney appears normal. A close-up sonogram (E) shows that the stones are currently lodged within, but not obstructing, the midureter.

A

B Figure 70-17 • Bilateral hydroureter secondary to bladder tumor: Lateral (A) and ventrodorsal (B) urograms show severe sacculation of the left renal pelvis and proximal ureter, and moderate, more uniform enlargement of the right renal collecting system.

Figure 70-18 • Accidental ureteral ligation: Sagittal sonogram of a dilated left renal pelvis and proximal ureter in a dog, inadvertently incorporated into an arterial ligature during a spay.

Figure 70-19 • Close-up lateral urethrogram shows a faintly opacified ectopic ureter gently arching over the bladder neck before entering the proximal urethra within the pelvic canal.

B

A Figure 70-20 • A, Sonographic long-section view of the left kidney shows dilation indicative of hydronephrosis. B, Three anechoic spheres are located nearby, representing individual cross-sections of the coiled left hydroureter.

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A

Figure 70-21 • Sonographic cross-section through the bladder neck shows a ureteric jet appearing as a short white band (arrow), representing a small volume of urine entering the bladder.

Intravenous Urography Standard and Modified Protocols. As repeatedly mentioned, contrast protocols of the urinary tract and elsewhere are clearly inferior to patient-tailored examinations. If there are insufficient personnel to oversee customized studies, however, some or all of the following additions should be considered: • Begin examination by making three consecutive lateral films centered on the dog’s hips, taking care to use skeletal technique. This method affords the evaluator the best chance of seeing a dislocated ureter before the bladder becomes distended with contrast-laden urine and intensely opaque. • Make paired lateral oblique projections to separate overlapping distal ureters. • Add air to urinary bladder to enhance ureteral contrast.53 • Use localized compression over the trigone region to eliminate confusing overlying tissues. • Include the vagina in the radiographic field to allow for the detection of contrast solution, which often accompanies an ectopic ureter.

Antegrade Ureterography Ackerman and co-workers recommend antegrade ureterography in cases in which excretory urography provides insufficient ureteral detail.54 Fox and coworkers described the use of antegrade ureterography instead of excretory urography in a dog with a retroperitoneal carcinoma, one of the few clinical reports recounting the use of this procedure.55 I would not recommend attempting this technique without expert training and regular subsequent practice.

B Figure 70-22 • A, Retrograde vaginourethrography: Close-up lateral retrograde vaginourethrogram shows a large, dilated ectopic ureter passing ventral to the vagina and dorsal to the urethra. B, Retrograde vaginourethrography: Close-up lateral retrograde vaginourethrogram shows a faint, normally sized ectopic ureter passing ventral to the vagina and dorsal to the urethra.

Pneumovaginography Adams and Biery described the pneumovaginographic appearance of a large fibroleiomyoma.56 As might be imagined, the challenge in performing pneumovaginography is to fill the vagina with air and then to keep it there long enough to make a pair of radiographs. Again, this technique should be practiced and perfected before being tried on a patient.

Retrograde Vaginourethrocystography Although retrograde vaginourethrography is growing in popularity, it has yet to receive the widespread acceptance enjoyed by intravenous urography. Supporters of vaginourethrography point out that this method of detecting ectopic ureter is not subject to the ambiguity that has plagued intravenous urography, namely, whether or not a seemingly normal ureter is not tunneling through the bladder wall without actually entering the bladder lumen but instead is emptying downstream into the urethra (Figure 70-22, A, B).

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On the other hand, Feeney and Johnston criticized vaginourethrography for (1) failing to allow predictably for identification of ureters that do not terminate in the vagina and (2) its inability to assess the competency of the urethral sphincter (because the bladder is not filled physiologically). They also correctly point out that the procedure usually requires a general anesthetic (or at least deep sedation), whereas urography does not.57

Sonographic Identification of Ureteric Jets The first sonographic description of ureteric jets, including the method of identification, was published in 1993 in Veterinary Radiology and Ultrasound,58 followed later by a second report describing the sonographic appearance of ectopic ureter in 14 dogs.59 In the hands (and eyes) of an experienced radiologist, this is a nearly foolproof method of establishing that both ureters enter the urinary bladder normally. Caution: When assessing ureteric jets in a dog suspected of having one or two ectopic ureters, take care not to mistake a crossover jet, a jet that originates on one side of the bladder but then skims along the dependent surface of the bladder to the opposite side as if it had originated there.

Computed Tomography Barthez and co-workers described the tomographic (computed) appearance of diagnostically opacified ureters in healthy dogs, specifically with regard to contrast dose and image timing.60 Optimal ureteral opacification was reported to occur with a contrast dose of 400 mg iodine per kilogram of body weight; the most favorable imaging was obtained anywhere between 3 and 60 minutes after contrast administration, providing time for at least two acquisitions.

677

the effect can be striking, appearing as a broad, high-density band spanning the length of the upper abdomen. Tidwell and co-workers described the radiographic and sonographic appearance of urinoma.61 Radiographically, the cyst appeared as a medium-sized, oval mass resembling a kidney, but it was located more caudally. Sonographically, the urinoma, like most cysts, looked a lot like the bladder but with a brighter, more homogeneous wall.

Lithotripsy In dogs, ureteral and kidney stones have been therapeutically disintegrated using shock waves. Initially, radiographs are used to locate the stones and ultrasound or urography is used to evaluate the relevant portions of the urinary tract. After the initial shocks, the stones are radiographed again to determine the extent of fragmentation. If this is insufficient, the animal is shocked again, often with a change in machine settings (e.g., number of shocks and kV value) until the fragmentation is judged to be satisfactory. Ideally, the remnants of the original stone now can be passed in the urine, negating the need for surgery.62

❚❚❚ URETERAL DIVERTICULA (URETERAL DIVERTICULOSIS) Background Ureteral diverticula are a rarity. One proposed pathogenesis is as follows: ureteral transitional cell hyperplasia and mucinous metaplasia result in submucosal proliferation of the “urothelium” and the formation of crypts and small cysts. Presumably, these changes are initiated by the presence of inflammation or infection.

Imaging Findings

❚❚❚ URETERAL INJURY Background Following a forceful blow to the high flank, the kind incurred in a car accident, for example, the kidney or ureter may be ruptured or avulsed, causing perirenal hemorrhage and leakage of urine into the retroperitoneal space. The accidental ligation or transection of a ureter during ovariohysterectomy not only leads to hydronephrosis but also can result in the formation of a urinoma, an encapsulated accumulation of escaped urine.

Excretory Urography. Jakovljevic and co-workers reported a pair of dogs with ureteral diverticula. Apair of lateral urograms in one dog showed a series of beadlike densities, presumably opacified diverticula, superimposed on the proximal ureter. Unfortunately, a single lateral urogram of the second dog was too small, too dark, and lacked sufficient contrast for the described lesions to be appreciated.63

❚❚❚ BLADDER DISEASE Background

Imaging Findings Radiographically, ureteral injury with associated urine leakage is suggested by opacification of the retroperitoneal space accompanied by loss of renal detail. When large volumes of blood or urine collect in this location,

Terminology. Bladder disease in dogs, and particularly in cats, has been of ongoing interest to veterinarians since the advent of pet animal practice. Originally termed cystitis, the disease has since undergone numerous etymologic makeovers, including manda-

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tory abbreviations as the descriptions became longer and more unwieldy, especially over the past 10 to 15 years: feline urologic syndrome (FUS), feline urologic signs (also FUS), feline “lower” urinary tract disease (FLUTD), and feline interstitial cystitis (FIC). Recently, Buffington and co-workers have argued that interstitial cystitis should be considered a disease in its own right and proposed the diagnostic means by which FIS could be discriminated clinically from other forms of cystitis.64 Additionally, bladder and urethral disease has been categorized according to (1) whether or not it caused obstruction: obstructive or nonobstructive “lower” urinary tract disease (OLUTD) and (2) its relationship to what are broadly termed behavioral disorders, for example, a cat that is refusing to use its litter box. Of course, there is the idiopathic category for urinary tract disease without known cause. In my opinion, the terminology has become unnecessarily complex, to the extent that it is more likely to confuse than to inform. Therefore, I propose a return to the original term, cystitis, modified judiciously if need be, according to individual circumstances. Purposes of Cystography. The diagnostic superiority of ultrasound over cystography is, for most bladder diseases, unchallenged; however, not every veterinary practice is equipped with an ultrasound machine, nor is every veterinarian proficient in its use. Thus, cystography continues to enjoy considerable popularity, especially in small rural practices, where it may be used to diagnose or infer tumors, inflammation and infection, calculi, and trauma, and to differentiate the bladder from its surroundings.

Imaging Findings Radiography. The radiographic abnormalities typically found in canine and feline cystitis are shown in Box 70-2. Of course, not all abnormalities are found in each case. I have placed question marks after “bladder wall thickening” to indicate that I do not believe it is possible to render such a judgment from plain films, although not everyone shares this opinion. In any event, if one attempts to make such an evaluation, I strongly advise sonographic confirmation. If sonography is not available, then double-contrast cystography can be used, taking care not to mistake pseudo-wall thickening for genuine mural pathology. Pseudo-wall thickening is the illusion that the bladder wall is thickened, when in reality it is not. This illusion occurs when air and fluid are projected on one another as they lie within a highly deformable organ such as the bladder, stomach, or intestine. Under such circumstances, these organs typically assume a broad oval shape with what appears to be a thickened wall. Cantwell and others have illustrated this phenomenon in case reports and textbook chapters on the subject.65 Cystography. Cystography may be performed with air, diagnostic organic iodine solution (ionic or

B o x

7 0 - 2

Potential Plain-Film Findings Found in Canine and Feline Cystitis • Presence or absence of a bladder shadow • Bladder stone or stones of sufficient density to be radiographically visible • Air bubble or bubbles in bladder lumen (usually from an earlier attempt at urine sampling) • Calcified bladder wall (rare) • Gas in bladder wall (rare) • Bladder wall thickening (?)

nonionic), or a combination of the two. These special procedures are referred to as negative, positive, and double-contrast cystography, respectively. Double-contrast cystography provides the greatest amount of information unless one is attempting to confirm that the bladder is ruptured, in which case a straight diagnostic iodine solution is better because it is easier to detect than air once it is outside the bladder. Potential Injury Related to Cystography. In my experience, overdistension of the urinary bladder is by far the leading cause of bladder injury during cystography. In general, the more inflamed the bladder, the greater the potential harm related to overdistension. Specifically, an inflamed bladder—one with bacterial cystitis, for example—is less distensible than normal. This is one of the reasons for an increased urinary frequency. When the inflamed, hyperemic bladder is overinflated with air, its mucosa often cracks, tearing capillaries, resulting in luminal bleeding. Deeper tears may extend into the bladder wall, causing mural hemorrhage. When full-strength (or even half-strength) iodinated contrast media are introduced into the bladder, the mucosal surface becomes further inflamed, often causing mild hemorrhage, even before any air is added. Distension usually aggravates the bleeding (as described previously), which is often protracted owing to the anticoagulant properties of the diagnostic iodine solution. In such a fragile environment, even the softest of urinary catheters may bruise or lacerate the bladder lining. Likewise, manual compression, advocated by some as a means to determine when enough air has been added, may bruise, lacerate, or rupture the bladder. Fatal air embolism has been reported in both dogs and cats, but in my estimation it is an extremely rare occurrence.66,67 To Distend or Not to Distend. Mahaffey and coworkers showed that maximal distension of the bladder is unnecessary to achieve a diagnostic cystogram.68 Furthermore, it has been demonstrated that overdistension of the bladder may conceal experimentally created mucosal abnormalities, especially if they are not pronounced (Box 70-3).69

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B o x

679

7 0 - 3

Potential Cystographic Abnormalities • Bladder stones • Blood clots • Deformity (as in that caused by an encroaching contiguous mass or mass effect) • Dislocation (as in retroflexion related to perineal hernia) • Extraluminal mass • Intraluminal mass • Irregular bladder wall • Mass in bladder wall • Perforation • Specific location (for the purpose of differentiating the bladder from an adjacent object such as a prostatic cyst) • Thickened bladder wall

Figure 70-23 • Chronic cystitis: Pneumocystogram (fully but not overly distended) shows abnormally thickened bladder wall consistent with cystitis.

Types of Cystography Negative-Contrast Cystography (Pneumocystography, Air Cystography). Although many case reports, articles, and textbook chapters have been devoted to the subject of pneumocystography, one of the earliest, an article by Rhodes and Biery, remains a classic.70 In addition to clearly exemplifying a wide range of bladder lesions, the authors also offer this valuable technical advice: • The best studies are performed in tranquilized or anesthetized dogs, especially if they have cystitis with painful bladder distension. • Catheters passed too far into the bladder are capable of injuring the mucosa, knotting, or perforating the bladder wall.71 • Catheterization should be as aseptic and as gentle as possible. • The volume of air or diagnostic iodine solution injected into the bladder cannot be prescribed. Rather, the appropriate contrast volume should be tailored to the individual patient and predicated on a combination of factors, including (1) the specific objective of the study, (2) the probable disease, (3) the size of the animal, (4) past experience, and (5) good judgment. Figure 70-23 exemplifies an abnormal negativecontrast cystogram. Positive-Contrast Cystography. Breton and coworkers showed that even relatively low concentrations of diagnostic iodine solutions (ionic) cause mild cystitis. In general, as the concentration of iodine increases, so do its inflammatory effects.72 In my experience, the harmful effects of positive-contrast cystography are lessened when nonionic contrast is used. Irrespective of the chemical properties of the contrast solution, however, full distension of the bladder usually aggravates existing disease and increases the prospects of postprocedural bleeding. Figure 70-24 exemplifies a normal but overfilled positive-contrast cystogram.

Figure 70-24 • Normal lateral cystogram, fully distended, with air-filled catheter cuff appearing as a circular lucency lodged in the neck of the bladder.

Double-Contrast Cystography. Scrivani and coworkers demonstrated the influence of patient positioning in demonstrating or concealing bladder wall lesions.73 Specifically, they showed that in both a cadaver (with an experimentally created lesion) and a naturally occurring case, lesion-related filling defects were visible only when the lesion was surrounded by iodine solution. Double-contrast cystography (and cystoscopy) has been proposed as a reliable means of differentiating between the idiopathic and behavioral forms of cystitis.74 Figures 70-25 and 70-26 show examples of doublecontrast cystography, and the cystographic features of cystitis and potential diagnostic errors are shown in Tables 70-7 and 70-8.

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Figure 70-27 • Close-up lateral sonogram of the bladder of a dog Figure 70-25 • Close-up lateral, double-contrast cystogram shows moderate mucosal thickening and irregularity typical of cystitis.

shows mild cystitis as indicated by mucosal thickening and irregularity.

body weight and thinned with increasing distension. Measurements made during minimal distension were the most variable, whereas those obtained from the caudoventral aspect of the bladder were slightly less than at other locations (Table 70-9). Full bladder distension was not evaluated in this study based on mounting evidence that this is a potentially harmful procedure, one that may hide small lesions.76

Figure 70-26 • Normal double-contrast cystogram performed with a rigid metallic catheter shows unnecessary overdistension and an excessive amount of diagnostic iodine solution. A series of air bubbles featuring characteristically blunted interfaces appear along the lower right margin of the bladder, the result of failing to fill the catheter with contrast solution before injection.

Ultrasound. Ultrasound, where available, has largely replaced cystography, except for the purposes of marking the location of the bladder or establishing its integrity in cases of suspected rupture. Additionally, ultrasound has become an increasingly popular alternative to conventional (nonimaging) cytocentesis, especially when the latter is repeatedly unsuccessful. The classic indication of cystitis is mucosal thickening and irregularity, the degree of which generally correlates with the severity of the disease (Figure 70-27). Evaluating Bladder Wall Thickness. Geisse and coworkers measured the bladder wall of normal dogs in four locations (craniodorsal, caudodorsal, cranioventral, and caudoventral) and with variable degrees of distension (minimal, mild, and moderate).75 They found that the bladder wall thickened with increasing

Sonographic Evaluation of Bladder Volume. The precise calculation or, alternatively, an estimation of bladder volume in the dog, has been the subject of numerous scientific articles and textbook chapters.77-79 Asimilar sonographic procedure has been used in people for more than 25 years.80 Although such information undoubtedly has theoretic value, and possibly some clinical usefulness as well (a predictor of severe obstruction, dysfunctional voiding, and neurogenic bladder disorders), these numbers are not routinely used in most clinical setting.81,82 Accordingly, I do not engage the reader in a literary discussion of the merits of various methods. Suffice it to say, those who require such information should review the included reference material and proceed according to individual needs. For those so inclined, I first recommend reading the article by Atalan and colleagues, which contains a detailed account of the relevant sonography, supported by sonographic-pathologic correlation.83 Computed Tomography. Computed tomography (CT) is the method of choice for radiotherapy treatment planning, but it is unnecessary for most other purposes.

❚❚❚ SUBCATEGORIES OF CYSTITIS Feline Idiopathic Cystitis The diagnosis of feline idiopathic cystitis is one of exclusion and is used when no cause of their disease can be

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Table 70-7 • RADIOGRAPHIC INDICATORS OF CYSTITIS AS IDENTIFIED IN DOUBLECONTRAST CYSTOGRAPHY Radiographic Indicator

Comment

Absorption of contrast by bladder wall Contrast medium in adjacent portion of peritoneal cavity Irregularity of interior bladder margin

This finding is most often seen following a catheter abrasion Presumed escape of contrast through bladder wall into peritoneal cavity When localized consider the additional possibility of tumor, and check lesion in the future to see if it has changed Presumably blood May be generalized, regionalized, or localized Most often seen in chronic cystitis reflecting the fact the not all mucosal surfaces are affected to the same extent Most commonly seen in cats with chronic cystitis, especially when bladder is overfilled; either air or diagnostic iodine solution may be seen in one or both ureters in such cases

Luminal filling defects Thickening of bladder wall Variations in mucosal contrast Vesicoureteral reflux

Table 70-8 • POTENTIAL INTERPRETIVE ERRORS ASSOCIATED WITH DOUBLE-CONTRAST CYSTOGRAPHY Radiographic Observation

Erroneous Interpretation

Iodinated contrast medium free in the peritoneal cavity

Ruptured bladder (actually may be due to one or more microscopic holes in the bladder or, alternatively, permeation of contrast through bladder wall) Bleeding related to cystitis (may actually be due to iodinated contrast and air distension) Inflammation (may actually be due to optical illusion) Mucosal ulceration or erosion (may actually be small defects related to localized hemorrhage or edema) Abnormal vesicoureteral junctions (may actually be due to overdistension of inflamed bladder)

Luminal filling defects Mild thickening of bladder wall Uneven “coating” of the inner lining by iodinated contrast Vesicoureteral reflux

Table 70-9 • BLADDER WALL MEASUREMENTS DURING VARYING AMOUNTS OF DISTENSION Degree of Bladder Distension

Minimal Distension

Mild Distension

Moderate Distension

Mean bladder wall thickness

2.3 mm (0.5 mL/kg saline)

1.6 mm (2 mL/kg saline)

1.4 mm (4 mL/kg saline)

found. Double-contrast cystography is usually negative when performed at the time of initial consultation, but it may become positive in subsequent studies. Radiographic abnormalities reported in cats diagnosed with idiopathic cystitis include (1) varying degrees of generalized bladder wall thickening, (2) focal or multifocal bladder wall thickening, (3) interior marginal irregularity, (4) variations in bladder wall density, (5) various luminal filling defects most likely representing blood clots, and (6) vesicoureteral reflux of contrast-containing urine. Absorption of iodinated contrast by the bladder wall and free peritoneal contrast, presumably having permeated the bladder wall, also has been reported in cats with idiopathic cystitis following double-contrast cystography.84

in the bladder lumen (presumed to have come from ruptured intramural gas vesicles). Some but not all of these animals also are diabetic, strongly suggesting that gas-forming bacteria are using glucose as a growth medium; however, emphysematous cystitis has been reported in nondiabetic dogs, with and without concurrent bladder abnormalities.85

Diverticula For the most part, nonsurgical diverticula of the bladder are confined to persistent urachus. Although much speculation exists concerning the role of this congenital abnormality in bladder infection, I know of no certain linkage between the two.

Retroflexion Emphysematous Cystitis Occasionally, bladder infections are accompanied by gas in the bladder wall and, in advanced stages, gas

Retroflexion of the urinary bladder through a peritoneal tear (also termed a peritoneal hernia or rupture) occurs most often in intact male dogs. The cause is unknown.

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The peritoneal rent typically is located between the levator ani and coccygeus muscles and the external anal sphincter. With loss of lateral support, there is progressive rectal enlargement and dilation. Peritoneal and pelvic fat and occasionally portions of the small intestine also may accompany the displaced bladder. Clinical signs may include (1) perineal swelling (bilateral or unilateral), (2) straining to urinate, (3) straining to defecate, and (4) uremia (if unable to urinate).86

Intrapelvic Bladder and Infective Foci I am aware of no clear-cut evidence that cystitis is in any way linked to the position of the urinary bladder with respect to the pelvic canal, in either male or female dogs. In my opinion, this is not an issue. Bacterial cystitis may spread to one or more joints, presumably by way of the bloodstream, causing infectious arthritis.87 Evidence to date, however, is that this outcome is exceptional and as such can be anticipated only rarely.

A

Bladder Tumors Most bladder tumors are located in the trigone and usually cause some measure of ureteral or urethral obstruction once they become large enough. Most of these are lobulated or spherical, although the margins of some appear quite irregular, depending on the projection angle (Figure 70-28). Plain films are of no use other than possibly to infer obstruction based on increased size. Sonographically, small malignant bladder tumors can resemble benign polyps and vice versa (Figures 70-29 and 70-30). Leveille and co-workers determined that sonography is far superior to either double-contrast cystography or intravenous urography in the detection of transitional cell carcinoma of the urinary bladder; accordingly, they advise that ultrasound be the first form of medical imaging used in evaluation of possible caudal urinary tract tumors in dogs or cats.88

B Figure 70-28 • Long (A) and cross-sectional (B) sonograms of a caudally located transitional cell carcinoma in the bladder of a dog. What make this neoplasm especially interesting are its smooth margins in one view and bumpy border in the other.

Caution: The ureteral papillae may resemble very small mucosal lesions, including some types of tumor. Located in the caudal aspect of the bladder, just at the mouth of the trigone, these paired structures are inconsistently found in dogs. Papillae are most likely to be encountered during excretory urography, when the ureters are distended with urine; in this regard, they serve as valuable anatomic landmarks when searching for ureteric jets. Others and I have published this observation.89

Bladder Stones Bladder stones come in a variety of shapes and sizes, but spherical is most common (Figures 70-31 and 7032). A stool-filled colon superimposed on the bladder may hide a calculus from view but can be easily displaced with compression radiography (Figure 70-33). The appearance of small or faint bladder stones can be enhanced in the same fashion.

Figure 70-29 • Close-up sonographic long section of urinary bladder shows a small object attached to the interior wall. It was surgically removed and found to be a benign polyp.

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Figure 70-30 • Close-up sonographic long section of the urinary bladder shows a small lobulated object attached to the interior wall. It was surgically removed and found to be a transitional cell carcinoma.

Figure 70-32 • Close-up view of the caudal abdomen of a dog shows three large bladder stones, two of which are unusually shaped.

Weichselbaum and co-workers compared the relative sensitivities of various types of medical imaging (i.e., plain radiography, pneumocystography, doublecontrast cystography, and ultrasonography) in detecting nine different types of bladder stones contained in a phantom.90 It was concluded that doublecontrast cystography (using an iodine concentration of 200 mg/mL) and ultrasonography (using a 7.5-MHz transducer) were diagnostically equivalent. Decreasing iodine content below 200 mg/mL or using a lower-frequency transducer (5 or 3.5 MHz) resulted in decreased accuracy, especially with respect to the numbers of stones and, in some instances, a falsenegative diagnosis. A

Caution: When scanning the bladder of a dog or cat, be aware that colonic gas can mimic a large calculus. Termed by Berry a phantom calculus, the bright irregular arch, seemingly a large stone lying on the floor of the urinary bladder, is actually colonic gas. The validity of this conclusion can be readily tested by digitally disturbing the bladder and its contents or by inverting the dog to see whether the “stone” changes position as predicted if it is in fact genuine.91

B Figure 70-31 • A, Close-up lateral view of the caudal abdomen of a dog with bladder stones, the largest of which resembles a colonic segment viewed in cross-section. High-density stool interferes with the radiographic assessment of this portion of the abdomen, making it difficult to determine the number of stones. B, A sonogram confirms that the object in question is indeed a bladder stone.

Weichselbaum and co-workers also reported a variety of contrast medium–related artifacts encountered when using a bladder phantom to evaluate the sonographic visibility of various types of calculi using different concentrations of iodine. Among the more unusual described artifacts were (1) contrast medium adhesion, primarily in sodium acid urate, and cystine calculi, and, less commonly; and (2) bubble adhesion or bubble accumulation in close proximity to stones, primarily in cystine or silica calculi. The clinical implications of these experimental findings have yet to be determined.92 Again in an experimental setting, the same authors determined that the architectural features of individual calculi, such as size, shape, and exterior topogra-

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A

C

B

D

E Figure 70-33 • A series of radiographs, including close-up, showing a single medium-sized bladder stone and how its appearance can be enhanced with compression radiography: conventional lateral abdominal radiograph (A), close-up of uncompressed bladder stone (B), lateral abdominal radiograph with caudal compression (C), and close-up of compressed bladder show one large and one small stone (D). A sonogram shows the characteristic acoustic shadowing produced by the larger stone (E).

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phy, are unlikely to serve as accurate predictors of chemical composition.93 Finally, in a follow-up communication (again related to their original data), the authors asserted that existing ultrasound transducers lacked sufficient resolving power to relate the surface features of bladder stones to their chemical composition.94

Ruptured Bladder Background. The most common cause of bladder rupture is trauma, usually forceful enough to also cause pelvic or upper hindlimb fractures. Less frequently, a urinary catheter may accidentally punch through the cranial bladder wall. Occasionally, a low-velocity projectile such as an air gun pellet or BB will penetrate the abdominal wall, enter the bladder, and cause leakage. I also have seen the bladder of a cat ruptured by someone attempting to obtain a urine sample and in another instance by someone attempting compressioninduced voiding cystography. I also have been bedeviled by pinhole-sized leaks in the neck of the bladder, which I have been able to demonstrate only as a vague cloud of escaped contrast solution surrounding the bladder trigone (usually the source of the leak or leaks). As mentioned elsewhere, positive-contrast cystography is, in my opinion, the easiest and fastest way to determine conclusively that the bladder is or is not intact; however, if an ionic iodine compound is used, it may aggravate bleeding in the case of a recent injury. Once into the peritoneal cavity, it will attract body water and thus potentially worsen shock.

Figure 70-34 • Close-up lateral cystogram (made at the completion of contrast injection) of a dog suspected of having a ruptured bladder shows diagnostic iodine solution escaping from the bladder and filling much of the peritoneal cavity.

Caution: If ultrasound is used to assess the integrity of the bladder, watch out for a pseudodefect in the cranial wall, termed a pseudolesion by Douglas and Kremkau.95 Imaging Findings. Diagnosing a ruptured urinary bladder needs to be rapid and, if at all possible, unequivocal; thus, it is best done using a nonionic diagnostic iodine solution administered via the urethra. Nonionic media are superior to their ionic counterparts because they are not hyperosmolar and do not aggravate bleeding or cause significant dehydration (Figure 70-34). When using intravenous urography, bear in mind that if bladder leakage is present, it often takes 5 or 10 minutes to demonstrate. Do not be too quick to declare the study negative if leakage is not seen immediately (Figures 70-35 and 70-36). A similar degree of caution should be exercised when searching for suspected leaks in the kidney, ureter, or urethra.

Bladder Hemorrhage, Mural Hematomas, and Contrast-Related Hematuria Hemorrhage in the bladder wall is often iatrogenic as a result of a failed attempt(s) at transabdominal cystocentesis. Mural hemorrhage also may result from

A

B Figure 70-35 • Lateral urograms made 5 (A) and 10 (B) minutes after intravenous injection of iodinated contrast medium. The initial film shows opacification of the kidneys, ureters, and bladder but no leakage. Shortly thereafter, contrast fills the abdominal cavity, presumably as a result of leakage from the bladder.

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A

Figure 70-36 • Lateral urogram (A) and close-up (B) made 15 minutes after an intravenous injection of diagnostic iodine solution in a dog suspected of having a catheter injury shows contrast outside the cranial aspect of the bladder, the result of a slow leak.

B injury, particularly that of an extremely forceful nature, such as being struck by a motor vehicle. O’Brien and Wood also reported intramural bladder hemorrhage secondary to systemic bleeding disorders, such as immune-mediated thrombocytopenia and vitamin K antagonist toxicity, noting whether the resolution (return to normal wall thickness) occurred at a rate of 1 mm per day.96 Iatrogenic Mural Hematomas. Luminal hematomas occur most often as a result of failed transabdominal cystocentesis. Recognized risk factors include (1) obesity, (2) inadequate restraint or pain relief, (3) small bladder, (4) repeated unsuccessful attempts to obtain urine, and (5) operator inexperience (Figure 70-37).97 I was not aware of how often the bladder is injured in an attempt to obtain a urine sample until I started assisting those who were unsuccessful. Using ultrasound guidance, it soon became apparent that cysto-

centesis is not an innocuous procedure, especially when performed by novices, for example, veterinary students. Based on hundreds of first-hand sonographic observations, I have concluded that most bladder wall injuries are caused by an overly tentative operator who tries to advance the needle gradually though the bladder wall into the lumen. This technique often results in the bladder being impaled but not penetrated. In such circumstances, the razor-sharp needle bevel can act like a scalpel blade, lacerating the bladder wall as the animal moves in pain. Quickly puncturing the bladder wall, once encountered, usually proves far more effective and is likely to result in little or no injury in the process. Contrast-Induced Hematuria. Positive contrast cystography performed with full-strength diagnostic iodine solution may cause the mucosa to ooze blood for a day or two. The probability of postprocedural

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A

B

C

D

E

F Figure 70-37 • A, Sonographic long section of the urinary bladder made shortly after repeated unsuccessful attempts at obtaining urine. A fresh hematoma is present on the caudolateral aspect of the bladder wall, presumably the result of a needle wound. B, Sonographic long section of the urinary bladder shows a small peanut-shaped hematoma, the result of an unsuccessful attempt at obtaining a urine sample. C, Sonographic long section of the urinary bladder shows a medium-sized hematoma on the inner surface of the bladder wall secondary to an unsuccessful attempt at obtaining urine. D, Sonographic long section of the urinary bladder shows a large hematoma in the bladder wall, secondary to an unsuccessful attempt at obtaining a urine sample. E, Sonographic long section of the urinary bladder shows multiple echogenic crescent-shaped objects: hematomas from an earlier failed cystocentesis. F, Sonographic long section of the urinary bladder shows bloody sediment accumulated on the floor of the bladder shortly after a failed cystocentesis.

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Table 70-10 • NORMAL PROSTATIC SIZE AS A FUNCTION OF AGE AND BODY WEIGHT: MAXIMUM PROSTATIC LENGTH IN THE SAGITTAL PLANE (TO NEAREST TENTH) Age (years) Weight (kg) 2 4 5 6 8 10 12

5

10

15

20

25

30

35

40

45

50

3.9 4.2 4.3 4.4 4.7 5 5.3

4.2 4.4 4.6 4.7 5 5.3 5.6

4.4 4.7 4.9 5 5.3 5.6 5.9

4.7 5 5.1 5.3 5.6 5.8 6.1

5 5.3 5.4 5.5 5.8 6.1 6.4

5.3 5.5 5.7 5.8 6.1 6.4 6.7

5.5 5.8 6 6.1 6.4 6.7 7

5.8 6.1 6.2 6.4 6.7 7 7.2

6.1 6.4 6.5 6.6 6.9 7.2 7.5

6.4 6.6 6.8 6.9 7.2 7.5 7.8

Table 70-11 • NORMAL PROSTATIC SIZE AS A FUNCTION OF AGE AND BODY WEIGHT: MAXIMUM PROSTATIC HEIGHT IN THE SAGITTAL PLANE (TO NEAREST TENTH) Age (years) Weight (kg) 2 4 5 6 8 10 12

5

10

15

20

25

30

35

40

45

50

3.1 3.2 3.3 3.3 3.5 3.6 3.7

3.3 3.4 3.5 3.6 3.7 3.8 4

3.5 3.7 3.7 3.8 3.9 4.1 4.2

3.7 3.9 4 4 4.2 4.3 4.4

4 4.1 4.2 4.2 4.4 4.5 4.7

4.2 4.3 4.4 4.5 4.6 4.8 4.9

4.4 4.6 4.6 4.7 4.8 5 5.1

4.7 4.8 4.9 4.9 5.1 5.2 5.4

4.9 5 5.1 5.2 5.3 5.4 5.6

5.1 5.3 5.3 5.4 5.5 5.7 5.8

hematuria increases further if the animal has moderate or severe cystitis and if the bladder is distended.

Bladder Wall Calcification Bladder wall calcification is usually dystrophic in nature and in my experience is most often the result of mucosal injury caused by an indwelling semirigid catheter placed in “blocked” cats. I have also observed calcification following bladder surgery, marsupialization of paraprostatic cysts, and bladder tumors.

male dogs age, their prostates become enlarged under the influence of dihydrotestosterone, a metabolite of testosterone. Prostatic adenocarcinoma, the most common form of prostatic neoplasia, is not hormone dependent and thus can develop in either castrated or noncastrated dogs. Prostatitis often occurs in enlarged, cystic glands as a result of infection by resident urethral bacteria.99 As in humans, prostatic enlargement of any kind frequently leads to protracted small-stream urination resulting from compression of the prostatic urethra.

Prostatic Measuration

❚❚❚ PROSTATE DISEASE (PROSTATIC DISEASE) Background The prostate gland functions by producing a specialized fluid that transports and supports sperm through the urethra during ejaculation. Smoothly symmetric, the prostate varies in shape, ranging from almost spherical to bilobed or pear-shaped. Sonographic measurements may be used to determine whether the prostate is normal in size.98 Prostatic hypertrophy, cystic hyperplasia, and bacterial prostatitis are the most common prostatic diseases reported in dogs. Many authors use the modifier benign when writing of prostatic hypertrophy, a carryover from human medicine where the malignant form of the disease is far more common than in the dog. As intact

Radiography. Atalan and co-workers determined that prostatic length, as measured in a lateral abdominal radiograph, which then is compared with the distance between the sacral promontory and the pubic brim, provides a more accurate estimate of overall prostatic size than does prostatic height measured under comparable circumstances. A value of 70% or greater is considered indicative of enlargement. Comparative prostatic length also was considered the preferred measurement for sonographic assessment of prostatic size.100 Ultrasound. Feeney and co-workers assert that prostatic size can be better evaluated with ultrasonography than with radiography.101 Table 70-10 demonstrates normal prostatic size as a function of age and body weight, and Table 70-11 demonstrates maximum prostatic height in the sagittal plane.

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Kamolpatana and co-workers also described the use of transabdominal ultrasound to measure prostatic height, width, and length. From these values, prostatic volume can be calculated. Because of the bilobed nature of the canine prostate (compared with the spherical shape of the human prostate), the formulas used in this study that treat the prostate as if it were rectangular or elliptical in configuration consistently overestimated prostatic volume.102 Prepubic Versus Transrectal Scanning of the Canine Prostate. Zohil and Castellano used transabdominal and intrarectal scanners to image a comparatively small series of dogs with prostatic disease. Predictably, they determined that transabdominal scanners did a superior job of imaging cranially located lesions; conversely, transrectal scanning was best for identifying caudally situated disease. Similar observations were made with respect to ultrasound-guided biopsy.103 The most common prostatic lesion reported in dogs is cystic hyperplasia. Cavitation, although it is readily identified sonographically, is not necessarily an indication of active disease. Some prostatic abscesses and tumors are associated with cavitation resembling prostatic cysts. In such instances, diagnosis usually depends on cytologic analysis of the cyst contents, obtained by ultrasound-guided aspiration.104 Loss of marginal smoothness has been reported as an inconsistent finding in prostatic cancer.105 When scanning the prostate based on the earlier radiographic identification of prostatic enlargement and colonic displacement or deformity, particularly in dogs presented for tenesmus, it is advisable to always scan well into the caudodorsal part of the abdomen on the chance that another mass may be present.106

❚❚❚ SPECIFIC PROSTATIC DISEASES Prostatic Hypertrophy (Benign Prostatic Hypertrophy) Background. Prostatic hypertrophy may be associated with one or more of the following clinical signs: (1) urethral bleeding, (2) dysuria, (3) hematuria, (4) constipation, and (5) dyschezia. Physical examination often reveals a symmetrically enlarged, nonpainful prostate.107 Imaging Findings Radiography. Radiographically, the hypertrophied prostate is by definition enlarged, usually exceeding 70% of the distance between the pubic bone and the sacral promontory as seen in lateral projection.108 As a result, the full bladder is often displaced cranially and the colon dorsally (Figure 70-38). Retrograde urethrography often shows narrowing and elongation of the prostatic portion of the urethra, frequently the cause of protracted, small-stream urination (Figure 70-39).

Figure 70-38 • Close-up lateral view of the caudal abdomen shows from front to rear: (1) a full bladder just beneath the airand stool-filled colon, (2) an enlarged prostate, and (3) the leading edges of the thigh muscles.

Retrograde Urethrography. Retrograde urethrography in a male dog can be performed in at least three different ways, each of which is associated with procedurally based variability, especially in the diameter of the urethra: 1. For maximum urethral distension, the bladder is first filled with contrast, with films being made subsequently during a second contrast injection. With this type of examination, the prostatic portion of the urethra normally has a larger diameter than the membranous portion.109 2. For moderate urethral distension, the bladder is not filled, but films are made during contrast injection. 3. For minimal urethral distension, the bladder is not filled; the urethral contrast is injected, and then films are made. Prostatic Reflux. The presence of contrast (iodine solution) in the prostate gland, as seen in a retrograde urethrogram, is abnormal and is termed prostatic reflux (Figure 70-40). Although reflux may be associated with a number of different prostatic disorders—hypertrophy, infection, and cancer—it is specific for none. Occasional prostatic reflux is observed in dogs with normal prostate glands, especially if the contrast injection is made under a head of pressure created by first filling the bladder.110 Personal Preferences. As previously mentioned, I prefer not to fill the bladder before contrast injection. Additionally, I always make at least two lateral projections of the urethra: one made during injection, the other following injection. This is done to take full advantage of the distensibility of the normal urethra compared with the diseased urethra, which may lose some or all of its distensibility when diseased, a conclusion that is often best drawn by comparing images before and after injection. Ultrasound. Sonographically, the noncystic hypertrophied prostate has a uniform echo texture.111

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A Figure 70-40 • Prostatic reflux: Close-up lateral urethrogram (centered over the prostate) made as contrast solution is being injected into the urethra. Instead of passing directly through the prostatic into the bladder, a portion of the contrast has entered the prostate gland, filling various sized cystic cavities.

B Figure 70-39 • Obstructive prostatic hyperplasia: Lateral (A) and ventrodorsal close-up (B) views of the prostatic field (recall that a radiographic field is where an organ is normally located but not necessarily seen) made during urethral contrast injection: The prostatic portion of the urethra is severely narrowed (best seen in lateral projection), and the adjacent urethral segment is dilated as a result of the resultant back pressure. Note that even with this degree of urethral narrowing, contrast solution was still able to reach the bladder.

Prostatic Cysts Most prostatic cysts develop within the gland (intraprostatic cysts) in association with its gradual enlargement related to increasing age. Prevailing theory holds that this type of prostatic cavitation most likely results from ductal obstruction. Any relationship between prostatic cysts and infection remains the subject of speculation, although there is theoretic support for such a viewpoint. Ruel and co-workers reported that 14% of healthy intact dogs have prostatic cysts.112 Some hypertrophied prostates become so extensively cystic that they resemble tumors (Figure 70-41), pointing out the necessity for histologic confirmation in such instances.

Figure 70-41 • Close-up lateral sonogram of the bladder and prostate of a dog shows severe, compressive, prostatic hypertrophy associated with extensive cyst formation. This rather ominous appearance, although benign, resembles some forms of prostatic cancer.

Paraprostatic Cysts Background. Some prostatic cysts develop on the surface of the prostate (rather than in the interior of the gland) and may become so large that they reach beyond the urinary bladder into the middle of the abdomen. These are termed paraprostatic cysts. Occasionally, a paraprostatic cyst may relocate to the perineal region, resembling a retroflexed bladder, perineal hernia, perineal abscess, or tumor.113 Most paraprostatic cysts occur in older, large-breed animals that are brought to the hospital because of depression, lack of appetite, stranguria, tenesmus, and bloody penile discharge. A palpable abdominal mass may or may not be detected during physical examination.

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Imaging Findings Radiography. Radiographically visible mineralization (osseous metaplasia) of paraprostatic cysts has been reported in dogs, but appears to have no specific prognostic value.114 I have occasionally seen calcification in the remnants of a paraprostatic cyst (Figure 70-42). Occasionally, a tumor adjacent to the bladder may be mistaken for a paraprostatic cyst on plain films; this misconception is readily clarified once the lesion is examined sonographically (Figure 70-43). Ultrasound. Stowater and Lamb described the sonographic appearance of paraprostatic cysts in the dog.115 Sonographic findings included (1) large size, (2) absence of internal echogenicity, (3) internal septa, and (4) communicating intraprostatic cysts. It was not possible to determine whether the cysts were infected. In my experience, paraprostatic cysts often lack a visible wall (although they obviously must have one), are of medium or large size, and are sonographically transparent (Figure 70-44).

A

Prostatitis, Prostatic and Paraprostatic Abscesses Background. Most but not all dogs with prostatitis show glandular enlargement, which may or may not be asymmetric. Likewise, most but not all dogs with prostatitis exhibit pain when palpated or forcefully scanned. Abscess is an inconstant feature of prostatitis. Diagnosis is confirmed by aerobic bacterial culture of seminal fluid. Occasionally, a prostatic abscess may rupture, causing peritonitis. Imaging Findings Radiography. Prostatitis radiographically.

cannot

be

diagnosed

Ultrasound. Although sonography allows for characterization of the interior of the prostate gland, including the prostatic portion of the urethra, it typically is incapable of doing more than suggesting prostatitis (Figure 70-45). On the other hand, large intraprostatic or paraprostatic abscesses are usually obvious and can be readily confirmed with ultrasoundguided aspiration (Figure 70-46). Newell and co-workers described the pulsed Doppler appearance of chronic lymphocytic and lymphoplasmacytic prostatitis in dogs and compared it with spectral waveforms obtained from normal control dogs.116 No differences were found.

Prostatic Cancer Background. Prostatic adenocarcinoma in dogs has no distinguishing radiographic or sonographic features. Like prostatitis, the gland is usually enlarged, asymmetric, possesses an uneven echo texture, and may

B Figure 70-42 • Close-up (A) and ultra close-up (B) compression view radiographs of the bladder field show amorphous calcification in, or superimposed on, the neck of the urinary bladder. Surgical exploration showed that the calcification was in the stump of a paraprostatic cyst, removed 2 months earlier.

show vague calcification. Palpation and forceful scanning are not usually painful. Carcinoma is the most frequently described prostatic disease of cats. Characteristically, the tumor replaces portions of the normal prostate gland (with or without visible enlargement) and eventually invades the urethra, leading to dysuria and hematuria.

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Figure 70-43 • Cross-sectional sonogram of the caudal abdomen of a dog shows a solid spheric mass gently compressing the left side of the bladder that subsequently proved to be a carcinoma unrelated to the bladder or prostate.

Figure 70-45 • Sonographic long section of a large paraprostatic abscess that reaches nearly to the cranial end of the bladder.

Figure 70-44 • Sonographic cross-section of the caudal abdomen of a dog shows a hypertrophied, mildly cystic prostate (PROST) and an adjacent paraprostatic cyst (PPCYST).

Figure 70-46 • Sonographic long section of the prostate

Imaging Findings Radiography. Radiography often reveals prostatomegaly (Figure 70-47), whereas retrograde urethrography often shows narrowing and distortion of the intraprostatic portion of the urethra. As a personal observation, I found the great majority of large and medium-sized prostatic cancers to be unusually hard and unyielding when being scanned. Additionally, and further to their rigid nature, many large prostatic cancers severely compress the distal colon, rectum, and bladder, often producing changes in defecation and urination that prompt owners to seek veterinary advice (Figure 70-48). Ultrasound. In my experience, there is no typical sonographic appearance for canine prostatic cancer; however, some such tumors may have a disorganized appearance, suggesting malignancy (Figure 70-49).

(electronic cursors) and caudal bladder shows abnormal but nonspecific echogenicity, later shown to be the result of a prostatic abscess.

Although found only inconsistently, some prostatic tumors also show partially calcified interiors, but without any consistent pattern, thus rendering this little more than suggestive. In cats, prostatic carcinoma has been reported as smoothly marginated, with multiple predominantly hypoechoic lesions, featuring bright and dark internal foci.117

❚❚❚ URETHRAL DISEASE Background Often urethral diseases are classified initially as either nonobstructive or obstructive. An inability to urinate

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Figure 70-47 • Close-up lateral, compression-induced, voiding cystourethrogram in a dog.

A

B

Figure 70-48 • Close-up lateral (A) and ventrodorsal (B) views of caudal abdomen shows what at first appears to be an enlarged bladder but in reality is a hard cancerous prostate, which is interfering with the dog’s ability to urinate and defecate.

(or perceived inability to urinate) is generally considered strong presumptive evidence of urethral obstruction and often prompts radiographic examination. Some potential causes of urethral obstruction are presented in Box 70-4.

Imaging Findings

Figure 70-49 • Close-up cross-sectional view of an enlarged partially mineralized prostatic carcinoma in a dog.

An Overview of Methods. Other than the identification of visible (radiodense) urethral calculi or a metallic foreign body such as a BB, shotgun/airgun pellet, or bullet, plain radiography contributes little to the diagnosis of urethral blockage.118 Sonography fares little better, usually failing to assess more than the cranial aspect of the urethra. Antegrade, compressioninduced cystourethrography (often mistakenly termed

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B o x

7 0 - 4

Causes of Urethral Obstruction • • • • • • • • • • •

Acute obstruction secondary to a fractured os penis Catheter injury Foreign body Frostbite Late-developing obstruction caused by callus from fracture of os penis Postinflammatory scar Spasm Trauma Tumor Ulcer Urethral calculi

voiding cystography) is technically difficult and more often than not fails (see Figure 70-47). Accordingly, retrograde urethrography is the simplest and fastest means available to image the urethra in a male dog or cat. In a female dog, vaginourethrocystography is often a better procedural choice because it potentially allows an unobstructed view of the entire urethra.119 With retrograde urethrography, either a cuffed or a noncuffed catheter must be used to inject the diagnostic iodine solution into the urethra. If a noncuffed catheter is used, unwanted backflow is inevitable, potentially creating questions regarding urethral diameter. AFoley catheter eliminates backflow of the contrast medium, but it obscures much of the urethra resulting from the filling defect created by the inflated cuff and, to a lesser extent, from the associated urethral spasm.

A

B Retrograde Urethrography. Ticer and co-workers described the radiographic appearance of the normal canine urethra and most of the commonly encountered urethral disorders.120 Figures 70-50 and 70-51 illustrate the characteristic appearance of some of the described lesions. In a subsequent publication, the same authors described the characteristic appearance of transitional cell carcinoma in four female dogs.121 Johnson and co-workers advocated distending the bladder with contrast medium during retrograde urography.122 They justify their recommendation on the basis that this will better standardize the examination and thus reduce or eliminate artifacts and procedurerelated variations in urethral diameter.123 Personal Preference. By first distending the urinary bladder, it is a near certainty that the urethra also will become distended, especially if the exposure is made during contrast. The result is that some types of stenoses may be concealed or appear understated. A better method is not to distend the bladder but instead produce two sets of urethrograms: one while injecting the contrast solution, the other immediately afterward. Three views are best: a lateral and two 30-degree ventrodorsal obliques (necessary to avoid spinal superimposition). In this way, there will be a greater opportunity to dynamically evaluate suspicious

Figure 70-50 • Lateral (A) and lateral close-up (B) retrograde urethrograms in a dog show urethral stenosis just caudal to the ileal neck.

areas of both the interior and exterior surfaces of the urethra.

Sources of Misdiagnosis When an exposure is made while contrast solution is being injected into the urethra, it is common to see varying amounts of dilation in the urethra up to and sometimes beyond the ischial arch. This is especially true of male dogs with moderate to severe prostatic hypertrophy. It is important to recognize that this finding reflects prostatic compression and not primary urethral stenosis. Scrivani and co-workers warned of possible urethral misdiagnosis in cats with nonobstructive lower urinary tract disease.124

❚❚❚ SPECIFIC URETHRAL DISEASES Urethral Carcinoma Background. The size and precise location of primary urethral tumors—most often squamous cell and

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A

Figure 70-51 • Close-up lateral retrograde urethrogram in a dog shows complete obstruction at the level of the hips.

transitional cell carcinomas—can be quite variable, but in general transitional cell carcinomas tend to grow in the cranial urethra, whereas squamous cell carcinomas are more likely to develop in the caudal two thirds of the urethra. Either tumor can be focally constrictive or regionally invasive. Transitional cell carcinomas originating in the proximal urethra may grow into and around the trigone of the bladder, occluding one or both ureters.125 Both cell types can metastasize, usually to the regional lymph nodes or lungs, which in the latter case are most likely to appear as a subtle increase in overall lung density (as opposed to discrete lung nodules).126 Imaging Findings Radiography. The urethra is radiographically invisible unless a diagnostic opaque is used; thus, plain films are limited to identifying stones and occasionally gas related to an earlier catheterization. Retrograde Urethrography. Because most urethral carcinomas result in some measure of obstruction, this is typically the major radiographic observation. As mentioned previously, however, the nature of such blockages is extremely varied, to the extent that no single disease configuration predominates. Ultrasound. Hanson and Tidwell described the sonographic appearance of urethral transitional cell carcinoma in seven female and three male dogs.127 Specifically, they reported the appearance of a welldefined, nonshadowing echogenic line (smooth or irregular) located on the interior surface of the urethra,

B Figure 70-52 • Lateral (A) and lateral close-up (B) views of the caudal paraabdominal region show callus-like new bone on the os penis (thought to have developed as a result of a previous injury, which in a subsequent urethrogram was shown to be partially obstructing the urethra).

accompanied by variable degrees of hypoechoic thickening of the underlying urethra. With respect to the diagnostic reliability of the line sign, the authors cautioned that similar line signs were also observed in two dogs that did not have urethral cancer: one that had transitional cell dysplasia and another with a urethral stricture.

Urethral Inflammation and Stenosis Indwelling catheters are capable of causing abrasive type injury to the urethral lining, which in some instances may lead to scarring and eventual stenosis. Displaced fractures of the os penis can be associated with urethral laceration and also can lead to later stenosis as a result of callus impingement (Figure 70-52).

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SECTION VII ❚❚❚ The Abdomen

Urinary Incontinence In incontinent male dogs, clinical attention is usually first directed to the urethral sphincter mechanism, the means by which urine either remains stored in the bladder or is eliminated. Anatomically, the focus is on three factors: (1) bladder neck position, (2) proximal urethral length, and (3) whether or not the dog has been castrated.128 In most such cases, diagnostic confirmation requires the construction of a urethral pressure profile.

Uterus Masculinus Background. Cystic uterus masculinus, a congenital form of paraprostatic mass, potentially causes a variety of clinical signs in affected male dogs, most related to pressure on the nearby rectum and bladder. With large cystic lesions, a midcaudal abdominal mass is usually evident or may be inferred by a dorsally displaced colon or ventrally displaced bladder. Positive-Contrast Retrograde Urethrocystography. Various disease patterns indicative of uterus masculinus can potentially be identified with retrograde urethrography.129 These include (1) ventral displacement of an opacified bladder and urethra; (2) demonstration of a pair of roughly cylindrical, irregular, contrast-filled structures caudal to the opacified bladder; and (3) opacification of a bladder-like structure caudal and somewhat dorsal to the bladder.

References 1. Hager DA, Nyland TG, Fisher P: Ultrasound-guided biopsy of the canine liver, kidney, and prostate. Vet Rad 26:82, 1985. 2. Drost WT, Henry GA, et al: The effects of a unilateral ultrasound-guided renal biopsy on renal function in healthy sedated cats. Vet Radiol Ultrasound 41:57, 2000. 3. Davidson AJ: Radiologic diagnosis of renal parenchymal disease, Philadelphia, 1977, WB Saunders. 4. Farrow CS: The abdomen. In Farrow CS, ed: Radiology of the cat, St Louis, 1994, Mosby. 5. Ackerman N: Radiology of urogenital diseases in dogs and cats, Davis, Calif, 1983, Venture Press. 6. Nyland TG, Kantrowitz BM, et al: Ultrasonic determination of kidney volume in the dog. Vet Rad 30:174, 1989. 7. Felkai CS, Vorus K, et al: Ultrasonic determination of renal volume in the dog. Vet Radiol 33:292, 1992. 8. England GCW: Renal and hepatic ultrasonography in the neonatal dog. Vet Radiol Ultrasound 37:374, 1996. 9. Shiroma JT, Gabriel JK, et al: Effect of reproductive status on feline renal size. Vet Radiol Ultrasound 40:242, 1999. 10. Feeney DA, Barber DL, Osborne CA: The functional aspects of the nephrogram in excretory urography: a review. Vet Rad 23:42, 1982. 11. Carr AP, Reed AL, Pope ER: Persistent nephrogram in a cat after intravenous urography. Vet Radiol Ultrasound 35:350, 1994. 12. Konde LJ, Wrigley RH, et al: Ultrasonic anatomy of the normal canine kidney. Vet Rad 25:173, 1984. 13. Biller DS, Bradlet GA, Partington BP: Renal medullary rim sign: ultrasonographic evidence of renal disease. Vet Radiol Ultrasound 33:286, 1992.

14. Mantis P, Lamb CR: Most dogs with medullary rim sign on ultrasonography have no demonstrable renal dysfunction. Vet Radiol Ultrasound 41:164, 2000. 15. Churchill JA, Feeney DA, et al: Age and diet effects on relative renal echogenicity in geriatric bitches. Vet Radiol Ultrasound 40:642, 1999. 16. Daniel GB, Mitchell SK, et al: Renal nuclear medicine: a review. Vet Radiol Ultrasound 40:572, 1999. 17. Barthez PY, Wisner ER, et al: Renal transit time of 99mTcDTPAin normal dogs. Vet Radiol Ultrasound 40:649, 1999. 18. Boag BL, Atilola M, Pennock P: Renal sonographic measurements in the dog preceding and following unilateral nephrectomy. Vet Radiol Ultrasound 34:112, 1993. 19. Churchill JA, Feeney DA, et al: Effects of diet and aging on renal measurements in uninephrectomized geriatric bitches. Vet Radiol Ultrasound 40:233, 1999. 20. Burk RL, Ackerman N: The Abdomen. In Burk RL, Ackerman N, eds: Small animal radiology ultrasound. Philadelphia, 1996, WB Saunders. 21. Podell M, DiBartola, Rosol TJ: Polycystic kidney disease and renal lymphoma in a cat. J Am Vet Med Assoc 201:906, 1992. 22. Allworth MS, Hoffman KL: Crossed renal ectopia with fusion in a cat. Vet Radiol Ultrasound 40:357, 1999. 23. Baumann D, Fluckiger M: Radiographic findings in the thorax of dogs with leptospiral infections. Vet Radiol Ultrasound 42:305, 2001. 24. Forrest LJ, O’Brien RT, et al: Sonographic renal findings in 20 dogs with leptospirosis. 39:337, 1998. 25. Pugh CR, Schelling CG, et al: Iatrogenic renal pyelectasia in the dog. Vet Radiol Ultrasound 35:50, 1994. 26. Felkai C, Vorus K, Fenyves B: Lesions of the renal pelvis and proximal ureter in various nephro-urological conditions: an ultrasonographic study. Vet Radiol Ultrasound 36:397, 1995. 27. Green RW: Kidneys. In Green RW, ed: Small animal ultrasound, Philadelphia, 1996, Lippincott-Raven. 28. Miller JB, Sande RD: Osseous metaplasia in the renal pelvis of a dog with hydronephrosis. Vet Rad 21:146, 1980. 29. Hill TP, Odesnik JO: Omentalisation of a perinephric pseudocyst in a cat. J Small Anim Pract 41:115, 2000. 30. Ochoa VB, DiBartola SP: Perinephric pseudocysts in the cat: a retrospective study and review of the literature. J Vet Intern Med 13:47, 1999. 31. Miles KG, Jergans AE: Unilateral perinephric pseudocyst of undetermined origin in a dog. Vet Radiol Ultrasound 33:277, 1992. 32. Essman SC, Drost WT, et al: Imaging of a cat with perirenal pseudocysts. Vet Radiol Ultrasound 41:320, 2000. 33. Rishniw M, Weidman J, Hornof WJ: Hydrothorax secondary to a perinephric pseudocyst in a cat. Vet Radiol Ultrasound 39:193, 1998. 34. Klein LJ: Canine primary renal neoplasms: a retrospective review of 54 cases. J Am Vet Med Assoc 24:443, 1988. 35. Konde LJ, Wrigley RH, et al: Sonographic appearance of renal neoplasia in the dog. Vet Rad 26:74, 1985. 36. Smith J: What is your diagnosis? J Small Anim Pract 39:157, 1998. 37. Bush M, Montali RJ, James AE: Subcapsular hematomas associated with renal lymphoma in a cat: a radiographic study. J Am Vet Rad Soc 14:27, 1973. 38. Frimberger AE, Moore AS, Schelling SH: Treatment of nephroblastoma in a juvenile dog. J Am Vet Med Assoc 207:596, 1995.

CHAPTER 70 ❚❚❚ Kidney, Ureteral, Bladder, Prostatic, and Urethral Disease

39. Moe L, Lium B: Computed tomography of hereditary multifocal renal cystadenocarcinomas in German Shepherd dogs. Vet Radiol Ultrasound 38:335, 1997. 40. Barber DL, Rowland GN: Radiographically detectable soft tissue calcification in chronic renal failure. Vet Rad 20:117, 1979. 41. Stanton ME, Toal R: Radiographic diagnosis. Vet Rad 27:15, 1986. 42. Adams WH, Toal RL, Breider MA: Ultrasonic findings in ethylene glycol (antifreeze) poisoning in a pregnant queen and 4 fetal kittens. Vet Rad 31:60, 1991. 43. Barr FJ, Patteson MW: Hypercalcemic nephropathy in three dogs: sonographic appearance. Vet Rad 30:169, 1989. 44. Nyland TG, Fisher PE, et al: Ultrasonographic evaluation of renal size in dogs with acute allograft rejection. Vet Radiol Ultrasound 38:55, 1997. 45. Jergens AE, Miles KG, Turk M: Bilateral pyelonephritis and hydroureter associated with metastatic adenocarcinoma in a dog. J Am Vet Med Assoc 193:961, 1988. 46. Ruiz de Gopequi R, Espada V, Majo N: Bilateral hydroureter and hydronephrosis in a nine-year-old female German shepherd dog. J Small Anim Pract 40:224, 1999. 47. Lamb CR: Acquired ureterovaginal fistula secondary to ovariohysterectomy in a dog: diagnosis using ultrasound-guided nephropyelocentesis and antegrade ureterography. Vet Radiol Ultrasound 35:201, 1994. 48. Moon ML, Dallman: Calcium oxalate ureterolith in a cat. Vet Rad 32:261, 1991. 49. Nyland TG, Fisher PE, et al: Diagnosis of urinary tract obstruction in dogs using duplex Doppler ultrasonography. Vet Radiol Ultrasound 34:348, 1993. 50. Morrow KL, Salman MD, et al: Comparison of the resistive index to clinical parameters in dogs with renal disease. Vet Radiol Ultrasound 37:193, 1996. 51. Mitchell SK, Toal RL, et al: Evaluation of renal hemodynamics in awake and isoflurane-anesthetized cats with pulsed-wave Doppler and quantitative renal scintigraphy. Vet Radiol Ultrasound 39:451, 1998. 52. Bargai U, Bark H: Multiple congenital urinary tract abnormalities in a bitch: a case history report. Vet Rad 23:10, 1982. 53. Anderson CC, Cook CR, Pope ER: What is your diagnosis? J Am Vet Med Assoc 214:1321, 1999. 54. Ackerman N, Ling GV, Ruby AL: Percutaneous nephropyelocentesis and antegrade ureterography: a fluoroscopically assisted diagnostic technic in canine urology. Vet Rad 21:117, 1980. 55. Fox LE, Ackerman N, Buergelt CD: Urinary obstruction secondary to a retroperitoneal carcinoma in a dog. Vet Radiol Ultrasound 34:181, 1993. 56. Adams WM, Biery DN, Miller HC: Pneumovaginography in the dog: a case report. J Am Vet Rad Soc 19:80, 1978. 57. Feeney DA, Johnston GR: The kidneys and ureters. In Thrall DA, ed: Textbook of diagnostic radiology, Philadelphia, 2002, WB Saunders. 58. Farrow CS: Ureteric jets: evaluation of ectopic ureters using sonography. Vet Radiol Ultrasound 34:134, 1993. 59. Lamb CR, Gregory SP: Ultrasonic findings in 14 dogs with ectopic ureter. Vet Radiol Ultrasound 39:218, 1998. 60. Barthez PY, Begon D, Delisle F: Effect of contrast medium dose and image acquisition timing on ureteral opacification in the normal dog as assessed by computed tomography. Vet Radiol Ultrasound 39:524, 1998.

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61. Tidwell AS, Ullman SL, Schelling SH: Urinoma (para-ureteral pseudocyst) in a dog. Vet Rad 31:203, 1990. 62. Baily G, Burk RL: Dry extracorporeal shock wave lithotripsy for treatment of ureterolithiasis and nephrolithiasis in a dog. J Am Vet Med Assoc 207:592, 1995. 63. Jakovljevic S, Van Alstine WG, Adams LG: Ureteral diverticula in two dogs. Vet Radiol Ultrasound 39:425, 1998. 64. Buffington T, Chew DJ, Woodworth: J Am Vet Med Assoc 215:682, 1999. 65. Cantwell HD: Radiographic diagnosis. Vet Rad 28:205, 1987. 66. Ackerman N, Wingfield WE, Corley EA: Fatal air embolism associated with pneumourethrography and pneumocystography in a dog. J Am Vet Med Assoc 160:1616, 1972. 67. Zontine WZ, Andrews L: Fatal air embolization as a complication of pneumocystography in two cats. J Am Vet Rad Soc 19:8, 1978. 68. Mahaffey MB, Barber DL, et al. Simultaneous doublecontrast cystography and cystometry in dogs. Vet Rad 25:254, 1984. 69. Mahaffey MB, Barsanti JA, et al: Cystography: effect of technique on diagnosis of cystitis in dogs. Vet Rad 30:261, 1989. 70. Rhodes WH, Biery DN: Pneumocystography in the dog. J Am Vet Rad Soc 8:45, 1967. 71. Buchanan JW: Kinked catheter: a complication in pneumocystography. J Am Vet Rad Soc 8:54, 1967. 72. Breton L, Pennock PW, Valli VE: The effects of Hypaque 25% and sodium iodine 10% in the canine urinary bladder. J Am Vet Rad Soc 19:116, 1978. 73. Scrivani PV, Leveille R, Collins RL: The effect of patient positioning on mural filling defects during double contrast cystography. Vet Radiol Ultrasound 38:355, 1997. 74. Buffington CA, Chew DJ, et al: Clinical evaluation of cats with nonobstructive urinary tract diseases. J Am Vet Med Assoc 210:46, 1997. 75. Geisse AL, Lowry JE, et al: Sonographic evaluation of urinary bladder wall thickness in normal dogs. Vet Radiol Ultrasound 38:132, 1997. 76. Mahaffey MB, Barber DL, et al: Cystography: effect of technique on diagnosis of cystitis in dogs. Vet Radiol Ultrasound 30:261, 1989. 77. Hackenberg OW, Ryall RI, et al: The estimation of bladder volume by sonocystography. J Urol 130:249, 1983. 78. Atalan G, Barr FJ, Holt PE: The assessment of bladder volume by means of linear ultrasonographic measurements. Am J Vet Res 59:10, 1998. 79. Barr F: Diagnostic ultrasound in the dog and cat, Oxford, 1990, Blackwell Scientific. 80. Pederson JF, Bartum JK, Grytter RJ: Residual urine determination by ultrasonic scanning. AJR Am J Roentgenol 125:474, 1975. 81. Moreau PM: Neurogenic disorders of micturition in the dog and cat. Compend Contin Educ 4:12, 1982. 82. Voros K, Felkai CS, et al: Ultrasonic examination of the canine and feline urinary tract. Eur J Comp Anim Pract 1:56, 1995. 83. Atalan G, Barr FJ, Holt PE: Estimation of bladder volume using ultrasonographic determination of crosssectional areas and linear measurements. Vet Radiol Ultrasound 39:446, 1998. 84. Scrivani PV, Chew DJ, et al: Results of double-contrast cystography in cats with idiopathic cystitis: 45 cases (1993-1995). J Am Vet Med Assoc 212:1907, 1998.

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SECTION VII ❚❚❚ The Abdomen

85. Lobetti RG, Goldin JP: Emphysematous cystitis and bladder trigone diverticulum in a dog. J Small Anim Pract 39:144, 1998. 86. Niles JD, Williams JM: Perineal hernia (rupture) with bladder retroflexion in a female cocker spaniel. J Small Anim Pract 40:92, 1999. 87. Morrow M: Urinary tract infection as nidus for systemic spread and septic arthritis. Can Vet J 40:666, 1999. 88. Leveille R, Biller DS, et al: Sonographic investigation of transitional cell carcinoma of the urinary bladder in small animals. Vet Radiol Ultrasound 33:103, 1992. 89. Douglass JP: Bladder wall mass effect caused by the intramural portion of the canine ureter. Vet Radiol Ultrasound 34:107, 1993. 90. Weichselbaum RC, Feeney DA, et al: Urocystolith detection: comparison of survey, contrast radiographic and ultrasonographic techniques in an in vitro bladder phantom. Vet Radiol Ultrasound 40:386, 1999. 91. Berry CR: Differentiating cystic calculi from the colon. Vet Radiol Ultrasound 33:283, 1992. 92. Weichsel RC, Feeney DA, et al: Contrast medium-related artifacts observed during in vitro radiographic characterization of urocystolith mineral composition. Vet Radiol Ultarsound 41:235, 2000. 93. Weichsel RC, Feeney DA, et al: Loss of urocystolith architectural clarity during in vivo radiographic simulation versus in vitro visualization. Vet Radiol Ultrasound 41:241, 2000. 94. Weichsel RC, Feeney DA, et al: Relevance of sonographic artifacts observed during in vitro characterization of urocystolith mineral composition. Vet Radiol Ultrasound 41:241, 2000. 95. Douglas JP, Kremkau FW: The urinary bladder wall hypoechoic pseudolesion. Vet Radiol Ultrasound 34:45, 1993. 96. O’Brien RT, Wood EF: Urinary bladder mural hemorrhage associated with systemic bleeding disorders in three dogs. Vet Radiol Ultrasound 39:54, 1998. 97. Farrow CS: Bladder injury resulting from failed transabdominal cystocentesis in dogs and cats. Can Vet J 2002 (in press). 98. Atalan G, Holt PE, Barr FJ: Ultrasonic estimation of prostate size in normal dogs and relationship to body weight and age. J Small Anim Pract 40:119, 1999. 99. Krawiec DR: Canine prostatic disease. J Am Vet Med Assoc 204:1561, 1994. 100. Atalan G, Barr FJ, et al: Comparison of ultrasonographic and radiographic measurements of canine prostatic dimensions. Vet Radiol Ultrasound 40:408, 1999. 101. Feeney DA, Johnston GR, et al: Canine prostatic disease: comparison of ultrasonographic appearance with morphologic and microbiologic findings. J Am Vet Med Assoc 190:1027, 1987. 102. Kamolpatana K, Johnston GR, Johnston SD: Determination of canine prostatic volume using transabdominal ultrasonography. Vet Radiol Ultrasound 41:73, 2000. 103. Zohil AM, Castellano MC: Prepubic and transrectal ultrasonography of the canine prostate: a comparative study. Vet Radiol Ultrasound 36:393, 1995. 104. Ramirez O, Homco LD: Cystic prostatic hyperplasia. Vet Radiol Ultrasound 36:146, 1995. 105. Cartee RE, Rowles T: Transabdominal sonographic evaluation of the canine prostate. Vet Rad 24:156, 1983. 106. Delger JM, Hedland CS, et al: Radiographic diagnosis. Vet Radiol Ultrasound 33:87, 1992.

107. Kustritz MVR, Merkel L: Theriogenology question of the month. J Am Vet Med Assoc 213:807, 1998. 108. Feeney DA, Johnston GR, et al: Canine prostatic disease: comparison of ultrasonographic appearance with morphologic and microbiologic findings: 30 cases (19811985). J Am Vet Med Assoc 190:1018, 1987. 109. Feeney DA, Johnston GR, et al: Dimensions of the prostatic and membranous urethra in normal male dogs during maximum distension retrograde urethrocystography. Vet Rad 25:249, 1984. 110. Ackerman N: Prostatic reflux during positive contrast retrograde urethrography in the dog. Vet Rad 24:251, 1983. 111. Feeney DA, Johnston GR, et al: Canine prostatic diseasecomparison of radiographic appearance with morphologic and microbiologic findings: 30 cases (1981–1985). J Am Vet Med Assoc 190:1027, 1987. 112. Ruel Y, Barthez PY, et al: Ultrasonographic evaluation of the prostate in healthy intact dogs. Vet Radiol Ultrasound 39:212, 1998. 113. Welsh EM, Kirby BM, et al: Surgical management of perineal, paraprostatic cysts in 3 dogs. J Small Anim Pract 41:358, 2000. 114. Girad C, Despots J: Mineralized paraprostatic cyst in a dog. Can Vet J 36:573, 1995. 115. Stowater JL, Lamb CR: Ultrasonographic features of paraprostatic cysts in nine dogs. Vet Rad 30:232, 1989. 116. Newell SM, Neuworth L, et al: Doppler ultrasound of the prostate in normal dogs and in dogs with chronic lymphocytic-lymphoplasmocytic prostatitis. Vet Radiol Ultrasound 39:332, 1998. 117. Caney SMA, Holt PE: Prostatic carcinoma in 2 cats. J Small Anim Pract 39:140, 1998. 118. Barry SE: What is your diagnosis? J Am Vet Med Assoc 193:857, 1988. 119. Eslinger LI, Byers MA, Kantrowitz: What is your diagnosis? J Am Vet Med Assoc 206:31, 1995. 120. Ticer JW, Spencer CP, Ackerman N: Positive contrast retrograde urethrography: a useful procedure for evaluating urethral disorders in the dog. Vet Rad 21:2, 1980. 121. Ticer JW, Spencer CP, Ackerman N: Transitional cell carcinoma of the urethra in four female dogs: its urethrographic appearance. Vet Rad 21:12, 1980. 122. Johnston GR, Jessen CR, Osborne CA: Effects of bladder distention on canine and feline retrograde urethrography. Vet Rad 24:271, 1983. 123. Johnston GR, Feeney DA: Comparative organ imaging. Vet Rad 25:146, 1984. 124. Scrivani PV, Chew DJ, et al: Results of retrograde urethrography in cats with idiopathic, nonobstructive lower urinary tract disease and their association with pathogenesis: 53 cases (1993–1995). J Am Vet Med Assoc 211:741, 1997. 125. Pollock SP: Urethral carcinoma in the dog: a case report. 9:95, 1968. 126. Healy BE: Radiographic diagnosis. Vet Rad 28:213, 1987. 127. Hanson JA, Tidwell AS: Ultrasonic appearance of urethral transitional cell carcinoma in ten dogs. Vet Radiol Ultrasound 37:293, 1996. 128. Power SC, Eggleton KE: Urethral sphincter mechanism in the male dog: importance of bladder neck position, proximal urethral length and castration. J Small Anim Pract 39:69, 1998. 129. Atilola MAO, Pennock PW: Cystic uterus masculinus in the dog. Vet Rad 27:8, 1986.

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7 1

Adrenal Gland Disorders

❚❚❚ BACKGROUND The adrenal gland, like other hormone-producing organs in the body, functions as a physiologic regulator. As such, an excess or deficiency of either of its secretions, aldosterone or cortisol, signals its malfunction. Hyperadrenocorticism, common in mature dogs but comparatively rare in cats, refers to diseases caused by an excess of cortisol in the blood. There are two principal causes of naturally occurring hyperadrenocorticism: (1) macroadenoma and microadenoma of the pituitary gland, each of which produces excessive adrenocorticotropic hormone (ACTH), which prompts the adrenal gland to produce excessive cortisol (accounting for about 80% of cases), and (2) adrenal tumors such as adrenocortical carcinoma (accounting for the remaining 20%). Hyperadrenocorticism also can occur as a result of chronic glucocorticoid administration prescribed for the treatment of unrelated disorders. Abnormalities commonly associated with hyperadrenocorticism include excessive water consumption and urination, abdominal distension, dermatitis, muscle atrophy, and weakness. Cats with hyperadrenocorticism are also often diabetic. A low-dose dexamethasone suppression test is claimed to identify hyperadrenocorticism accurately in 95% of affected dogs but is not as sensitive in cats.1 Although it is only inconsistently found, some prostatic tumors show partially calcified interiors but without any consistent pattern; thus, such a finding is merely suggestive.

❚❚❚ IMAGING FINDINGS Radiography Adrenal gland enlargement usually is considered when a perirenal mass is identified. When such masses are partially calcified (a characteristic of about half of all adrenal tumors), the probability of adrenal disease

increases. I have seen adrenal tumors that so closely resembled a normal kidney that it was radiographically impossible to determine which was the mass and which was the kidney without the use of urography or ultrasound. Diffuse pulmonary calcification also has been reported, as has pulmonary metastasis.2

Ultrasound In the case of pituitary-dependent hyperadrenocorticism, bilateral adrenomegaly should be anticipated. Alternatively, if an adrenal tumor is present, it will likely suppress the opposite adrenal gland, making it difficult or impossible to locate. Some right adrenal tumors may grow into the nearby caudal vena cava, causing varying amounts of obstruction. Dogs. Grooters and co-workers described the sonographic appearance of the adrenal glands in healthy dogs.3 The morphology of the right adrenal differs from that of the left, with both glands appearing relatively dark (relatively hypoechoic) compared with the nearby renal cortices. Douglas and co-workers investigated the correlative nature of canine adrenal glands, presumed normal based on a lack of clinical evidence to the contrary, with respect to body weight, body surface area, age, and sex, and found it to be generally poor.4 Adrenal measurements, obtained from 193 dogs, were as follows: Left adrenal gland • Length: 10.7 to 50.2 mm • Caudal pole width: 1.9 to 12.4 mm Right adrenal gland • Length: 10 to 39.3 mm • Caudal pole width: 3.1 to 12 mm Recommended strategies for scanning the adrenal glands are as follows. 699

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SECTION VII ❚❚❚ The Abdomen

Note: Typically, the right adrenal is more difficult to image than the left. Right adrenal 1. With dog on its back, place the scanner just medial to the costal arch at the level of the 12th right intercostal space. 2. Alternatively, the scanner is placed 2 to 3 cm dorsolateral to the costal arch at the 11th or 12th right intercostal space. 3. Locate the caudal vena cava in the transverse plane at the level of the portal vein. 4. Follow the vena cava caudally until the right adrenal gland comes into view along the right lateral edge of the vena cava. 5. The right adrenal resembles a long, narrow oval viewed in lateral profile and an asymmetric, blunted arrowhead as seen from above. Left adrenal 1. With the dog on its back, place the scanner just medial to the costal arch at the level of the 12th left intercostal space. 2. Alternatively, the scanner can be placed 2 to 3 cm dorsolateral to the costal arch at the 11th or 12th left intercostal space. 3. Locate the aorta adjacent to the cranial pole of the left kidney in the sagittal plane. 4. Move the scanner slightly in a craniolateral direction and examine the area just craniomedial to the kidney and ventrolateral to the aorta. 5. Like the right adrenal, the left resembles a long, narrow oval viewed in lateral profile and a peanut shell seen from above. 6. Alternatively, the left adrenal gland can be found just cranial to the point where the left renal artery leaves the aorta. Hyperplastic adrenals are usually easier to locate than normally sized glands and are darker (hypoechoic) than normal. Nodular hyperplasia causes the normally smooth adrenal margin to become roughened or bumpy and may affect one or both glands. Lack of sonographic visualization does not eliminate the possibility of disease, especially if the gland is only mildly altered.5

Adrenal Tumors Adrenal tumors are well known for their invasive tendencies, particularly with respect to the caudal vena cava and adjacent kidney. Rupture of a pheochromocytoma may result in retroperitoneal hemorrhage.6 Besso and co-workers showed adrenal tumors to be highly variable in their sonographic appearance; however, they did identify some tendencies. Pheochromocytoma, adenocarcinoma, and neuroblastoma

tended to be large, rounded masses; adenoma and hyperplasia often appeared mildly enlarged with disfiguring bulges. Surprisingly, mineralization was absent in the pheochromocytomas, but it was present in two cases of hyperplasia.7,8 Cats. In cats, adrenal masses and general enlargement (adenoma, hyperplasia, and adenocarcinoma) have been associated with both hyperadrenocorticism and hyperaldosteronism.9 The mean length of hyperplastic adrenal glands in a series of cats with hyperadrenocorticism has been reported as 1.8 cm, with normal controls having a mean measurement of 1.0 cm.10 Zimmer and co-workers recently reported that the left adrenal gland in normal cats measures about 10% less than the right (0.89 cm versus 0.98 cm) but that both are similar in width (0.39 cm).11 The optimal scanning planes for imaging the adrenal glands have been described previously. Spaulding described techniques for detecting and differentiating between the caudal abdominal aorta and the vena cava, important landmarks for sonographically locating the adrenal glands.12

Nuclear Medicine 123

I-MIGB (iodine 123-labelled metaiodobenzylguanidine) has been used to diagnose a pheochromocytoma in a dog.13

Magnetic Resonance Imaging (MRI) Hypoadrenocorticism also has been reported in two cats with adrenal lymphoma. One cat had a 1-week history of intermittent vomiting, lack of appetite, and lassitude; the other had acute collapse and weakness. In one cat, the diseased right adrenal gland appeared as an indistinct noncalcified soft tissue mass that displaced the right kidney caudally and the stomach to the left. In the other, a nonspecific, cranial abdominal mass was identified.14

References 1. Widmer WR, Guptill L: Imaging techniques for facilitating diagnosis of hyperadrenocorticism in dogs and cats. J Am Vet Med Assoc 206:1857, 1995. 2. Selcer BA, Jacobs G, Nuehring L: Radiographic diagnosis. Vet Rad 29:37, 1988. 3. Grooters AM, Biller DS, Merryman J: Ultrasonographic parameters of normal canine adrenal glands: comparison to necropsy findings. Vet Radiol Ultrasound 36:126, 1995. 4. Douglas JP, Berry CR, James S: Ultrasonographic adrenal gland measurements in dogs without evidence of adrenal disease. Vet Radiol Ultrasound 38:124, 1997. 5. Kantrowitz BM, Nyland TG, Feldman EC: Adrenal ultrasonography in the dog. Vet Rad 27:91, 1986. 6. Schermerhorn T, McNamara PS: Cullen’s sign and hemaglobinuria as presenting signs of retroperitoneal hemorrhage in a dog. J Small Anim Pract 39:490, 1998.

CHAPTER 71 ❚❚❚ Adrenal Gland Disorders

7. Besso J, Penninck D: Ultrasonographic evaluation of adrenal masses in dogs: correlation with pathological findings in a retrospective study of 20 cases. Vet Radiol Ultrasound 36:433, 1995. 8. Besso JG, Penninck DG, Gliatto: Retrospective ultrasonographic evaluation of adrenal lesions in 26 dogs. Vet Radiol Ultrasound 38:448, 1997. 9. Moore LE, Biller DS, Smith TA: Use of abdominal ultrasonography in the diagnosis of primary hyperaldosteronism in a cat. J Am Vet Med Assoc 217:213, 2000. 10. Watson PJ, Herrtage ME: Hyperadrenocorticism in 6 cats. J Small Anim Pract 39:175, 1998.

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11. Zimmer C, Horauf A, Reusch C: Ultrasonic examination of the adrenal gland and evaluation of the hypophysealadrenal axis in 20 cats. J Small Anim Pract 41:156, 2000. 12. Spaulding KA: Helpful hints in identifying the caudal abdominal aorta and caudal vena cava. Vet Radiol Ultrasound 33:90, 1992. 13. Berry CR, Wright KN, et al: Use of 123iodine metaiodobenzylguanidine scintigraphy for the diagnosis of a pheochromocytoma in a dog. Vet Radiol Ultrasound 34:52, 1993. 14. Parnell NK, Powell LL, et al: Hypoadrenocorticism as the primary manifestation of lymphoma in two cats. J Am Vet Med Assoc 214:1208, 1999.

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7 2

Normal and Abnormal Pregnancy

❚❚❚ OVARIAN CHANGES RELATED TO OVULATION Silva and co-workers described the sonographic appearance of ovaries during the canine heat cycle. They focused on ovulation and related their findings to hormonal changes and the physical appearance of the ovaries as determined laparoscopically.1 Their observations were as follows: • Five days before the estimated luteinizing hormone (LH) peak (presumed ovulation), the ovaries appeared anechoic and thereafter gradually became larger. • The greatest changes occurred between 2 and 4 days after the LH peak: echogenicity varied unpredictably from animal to animal, day by day, ranging from anechoic to hyperechoic. • Six days after the LH peak, the ovaries consistently appeared hypoechoic. The authors concluded that neither ultrasonography nor laparoscopy was capable of determining precisely when ovulation took place; however, it did appear that ovulation was related to changes in ovarian echogenicity: the period in which follicles became corpora lutea, 2 to 4 days after the LH peak.

❚❚❚ NORMAL PREGNANCY Imaging Findings Radiography. The earliest radiographic indicator of pregnancy in dogs and cats is uterine enlargement (Figure 72-1), followed by fetal mineralization (Figure 72-2). Rendano and colleagues reported that the uterus first becomes visible 35 days before delivery, gradually changing from a circular to an oval-shaped cylinder.2 The fetal skeletons become radiographically visible between the 36th and 45th days of gestation, 702

with an average identification time of 43 days for puppies and 37 days for kittens. Ossification of the limbs occurs nonuniformly from proximal to distal, with the fetal metacarpal and metatarsal bones usually becoming apparent by the 59th day (dogs). The deciduous teeth typically become visible at about the same time.3 Ultrasound. Although numerous published reports have stated that pregnancy can be accurately determined at 3 weeks, I often find examinations at this time to be equivocal, in large part because of the small size of the conceptus and to a lesser extent because of overlying bowel gas. Therefore, my preference is to examine dogs at about 30 days, the presumed time since impregnation (Figure 72-3). If a dog is examined at 3 weeks and is not found to be pregnant, it is my recommendation that the examination be repeated at 1 month (at which time I have found examination sensitivity and specificity to be extremely high (>95%). The ultrasonographic appearances of normal canine and feline gestation are presented in Table 72-1. Normal Sonographic Appearance of Fetal Organs in Dogs and Cats. Individual fetal organs are conventionally situated but often differ in echogenicity from that observed postpartum. The uninflated fetal lung is visible in its entirety, appearing relatively hyperechoic compared with the nearby heart and liver. As the fetus matures and the skeleton ossifies, portions of the heart and lung will become concealed from view by the acoustic shadows cast by the thoracic vertebrae and ribs. The fetal heart, appearing internally dark with a bright exterior, typically signals its presence with a characteristic, rapid blinking movement. The fetal liver appears large, hypoechoic, and relatively asymmetric to the right. The contiguous stomach is usually distinctly anechoic as a result of the ingestion of amniotic fluid. At about 7 weeks, the aorta and caudal vena cava

CHAPTER 72 ❚❚❚ Normal and Abnormal Pregnancy

703

Figure 72-3 • Cross-sectional sonogram of the uterine horns of a pregnant dog shows normal 30-day fetuses. Figure 72-1 • Close-up view of the uterus of a pregnant dog at about 5 weeks, before fetal mineralization, shows the characteristic lobular appearance of the uterus.

become discernible as thick, anechoic bands in the central thorax. Once ossified, the fetal skull assumes a distinctive spherical appearance and casts a broad acoustic shadow. Likewise, the strongly reflective mineralized spine assumes a distinctive segmented appearance. Davidson and co-workers have described the sonographic appearance of normal fetal development in both the dog and the cat. Estimating Litter Size. In my experience, the radiographic estimation of litter size (Table 72-2) is far more accurate than a sonographic estimate, an impression that has been confirmed by Toal and colleagues.4 Imaging Strategies. When radiographing the abdomen of a dog or cat for the purpose of estimating litter size, it is highly advisable to obtain both lateral and ventrodorsal or dorsoventral views. The field of view should extend from the diaphragm cranially to at least the hips caudally. In large dogs, separate films of the cranial and caudal parts of the abdomen may be required to cover the desired field or to compensate for marked regional differences in abdominal thickness. Fetuses should be counted at least twice, first using fetal skulls and then spines. If a second person is available, he or she should conduct a second set of independent counts. Then the results should be compared, with recounts and discussion as needed. In large dogs with half a dozen fetuses or more, it is sometimes useful to use small bits of opaque tape to identify individual skulls or spines to avoid missing a fetus or counting the same one twice.

A

B Figure 72-2 • Lateral (A) and close-up lateral (B) views of the abdomen of a pregnant dog show a single normal-appearing fetus in the caudal abdomen.

Estimating Fetal Age (Gestational Age), Estimating Delivery Dates. Fetal measurement, as performed sonographically, can be used to estimate gestational age, although some breed-related adjustments may be necessary.5 Beck and co-workers showed that single transverse measurements of the skull and central torso of fetal kittens are capable of predicting delivery dates with a moderate degree of accuracy.6

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Table 72-1 • INITIAL APPEARANCE TIMES OF FETAL ORGANS IN THE DOG AND CAT Sonographic Observation

Time of 1st Appearance in Dogs (days)

Time of 1st Appearance in Cats (days)

Fetal membranes Fetal motion Fetal pole (embryoblast); appears hyperechoic Gestational sac (blastocyst); appears anechoic Identification of individual fetal organs Visible heartbeat

Variable 24-28 20-26

21-24 28-30 15-17

17-23

11-14

38-45

Variable

24-28

16-20

Modified from Miles K: Imaging pregnant dogs and cats. Comp Cont Educ 17:1217, 1995.

Table 72-2 • RELATIVE SENSITIVITIES OF RADIOGRAPHY, ULTRASOUND, AND PALPATION IN DETECTING PREGNANCY AND DETERMINING LITTER SIZE IN DOGS Imaging Method or Palpation Palpation (performed over entire pregnancy) Radiography (performed during last 3 wks of pregnancy) Ultrasound (performed over entire pregnancy)

Pregnancy Detection Accuracy (%)

Litter Size Accuracy (%)

88

12

100

93

94

36

In my experience, long-section measurements in fetal puppies and kittens are often inaccurate (as high as 25%) as a result of fetal obliquity. This problem usually can be overcome by making multiple measurements from different angles, but the time required for such exhaustive studies may prove prohibitive.

❚❚❚ INCOMPLETE FETAL RESORPTION AND PREMATURE PLACENTAL SEPARATION Imaging Findings Radiographically, a partially reabsorbed fetus may or may not be suggested, depending on its size, the presence or absence of skeletal mineralization, the size of the uterus in which it resides, the surrounding bowel content, and distribution. Compression radiography greatly increases the chances of identifying a reabsorbed fetus or regional uterine enlargement, compatible with a partial fetal resorption. Sonographically, a partially reabsorbed fetus usually resembles a small hyperechoic mass lodged within a tubular organ containing varying amounts of fluid. It may be present in conjunction with endometritis (Figure 72-4). Hypercalcemia has been reported in a dog with a retained partially reabsorbed fetus and endometritis.7 Recent premature placental separation appears sono-

Figure 72-4 • Close-up cross-sectional sonogram of the uterus of a dog shows a partially reabsorbed fetus.

CHAPTER 72 ❚❚❚ Normal and Abnormal Pregnancy

705

graphically as a band of fluid between the uterine wall and placental tissue.

❚❚❚ LATE-TERM FETAL DEATH Imaging Findings Radiography. Late-term fetal death can be detected radiographically, especially if the skull of a questionable fetus can be relatively isolated using compression. In such circumstances, the presence of overlapping cranial bones strongly suggests a dead fetus. Intrafetal gas is also a reliable indicator of fetal death but is considerably more difficult to demonstrate conclusively because of interference by overlying bowel gas. Fetal motion may be inferred from radiographs by comparing films for substantial differences in fetal positioning, for example, a reversed or inverted position in one radiograph compared with another.8,9

A

Ultrasound. Judging fetal viability is comparatively simple using ultrasound. Specifically, the heart of each fetus is initially judged for its characteristic movement (rapid blinking). This will indicate whether or not the fetus is alive. Determining the heart rate (it should be between 120 and 140 beats per minute) provides further information relating to the circulatory status of the fetus and, by inference, its overall well-being; lower than normal suggests failing health.

❚❚❚ ECTOPIC PREGNANCY Background Three possible causes have been recently proposed to explain ectopic pregnancy in cats10: • Traumatic or iatrogenic dislodgment of the fetus from the uterus to the abdominal cavity • Direct or induced movement of a fertilized ovum from the fallopian tube directly into the abdominal cavity, bypassing the uterus • Abnormal reproductive anatomy, such as a persistent urachus

B Figure 72-5 • Lateral (A) and ventrodorsal (B) close-up views show the head of a mature fetus wedged against the pelvic inlet.

Imaging Findings A nonmineralized ectopic fetus, at best, appears as a nonspecific soft tissue mass. On the other hand, a mineralized fetus is often outstanding.

❚❚❚ PREDICTING MECHANICAL DYSTOCIA More than two decades ago, I first published my radiographic observations on predicting mechanical dystocia in the dog, based on the relative size of the

fetal skull compared with that of the maternal pelvic canal (Figures 72-5 and 72-6).11 Later, I published similar findings in the cat, including pertinent radiometrics.12 Recent communications have drawn attention to the fact that this technique can be applied to specific, dystocia-prone breeds, such as Boston Bull Terriers, with the aim of predicting mechanical dystocia before parturition. Moreover, it may prove feasible to select prime breeding stock based on similar radiographic criteria.13

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Figure 72-6 • Close-up lateral view of an abnormally large fetus in a cat that, even with normal cranial molding, will be unable to pass through the pelvic canal.

Table 72-3 • TIME-SPECIFIC UTERINE APPEARANCES Postwhelping Period

Uterine Appearance

Early postwhelping (1-4 days)

1. At day 1 post partum, uterine diameter was similar in all dogs, irrespective of litter size. 2. Uterine contents were described as being of mixed echogenicity, compatible with both fluid and solids, theorized to represent a combination of blood clots and remnants of both fetal and maternal membranes. 3. Placentation sites were nearly twice the size (2.2-2.8 cm) of the flanking interplacental zones (1.01.5 cm). 4. In the longitudinal imaging plane, the placentation sites appeared ovoid. 5. If echogenic content was located near the inner surface of the uterus (endometrium), the latter was difficult to define. 6. The uterine wall appeared thickened, moderately irregular, and echogenic, sometimes featuring blood vessels. 1. The uterine wall gradually thinned and became smoother. 2. There were two types of uterine content: (1) predominantly hypoechoic and (2) predominantly hyperechoic—the former having a “target-like” appearance when scanned in cross-section. 3. In some dogs, cross-sections of the uterus revealed a second dark ring just outside the myometrium, believed to represent a combination of subserosal fat and connective tissue. 4. Although it was maintained throughout the period of observation, the difference in uterine diameter between the larger placentation sites and the smaller adjacent interplacental zones gradually diminished. 5. Distinguishing between small intestine and uterus was possible throughout the study, based on (1) the greater echogenicity and resultant acoustic shadowing of bowel content compared with that of the uterus and (2) the expected absence of uterine peristalsis. 6. Uterine discharge (placental remnants and blood clots) may normally persist beyond 3 wks in some normal dogs.

Late postwhelping (8-24 days)

❚❚❚ THE POSTWHELPING (POSTPARTUM) UTERUS Pharr and Post described both the radiographic and the sonographic appearance of the postwhelping uterus in the dog.14 Radiographically, five dogs (young, medium-sized, cross-bred females) were monitored from 24 hours to 18 days after the birth of normal litters. The uterus was visible in all dogs at 1 and 4 days, but by day 8 only three of five animals had a visible uterus, and by day 12, the uterus could not be identified in any of the dogs. The same five dogs described above were examined by ultrasound at 1, 4, 8, 12, 18, and 24 days after the

birth of their puppies (two to nine pups per litter), with the uterus remaining visible for the entire period. Timespecific uterine appearances (described by the authors as “early and late postwhelping states”) are given in Table 72-3. The value of knowing the sonographic appearance of the postwhelping uterus, the authors point out, is when trying to assess the importance of a vaginal discharge in a dog that has recently given birth. Further to such ends, this article draws attention to the considerable variability noted in this study, especially with respect to uterine content and the potential difficulty in distinguishing between a retained placenta and normal placental remnants/blood clots. Finally, the

CHAPTER 72 ❚❚❚ Normal and Abnormal Pregnancy

authors counsel that using persistent uterine enlargement, as observed in serial sonographic examinations, may be the more reliable means of detecting uterine disease.

References 1. Silva LDM, Onclin K, Verstegen JP: Assessment of ovarian changes around ovulation in bitches by ultrasonography, laparoscopy and hormonal assays. Vet Radiol Ultrasound 37:313, 1996. 2. Rendano VT, Lein DH, Concannon PW: Radiographic evaluation of prenatal development in the beagle. Vet Rad 25:132, 1984. 3. Miles K: Imaging pregnant dogs and cats. Comp Cont Educ 17:1217, 1995. 4. Toal RL, Walker MA, Henry GA: A comparison of realtime ultrasound, palpation and radiography in pregnancy detection and litter size determination in the bitch. Vet Rad 27:102, 1986. 5. Luvoni GC, Grioni A: Determination of gestational age in medium and small size bitches using ultrasonic fetal measurements. J Small Anim Pract 41:292, 2000.

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6. Beck KA, Baldwin CJ, Bosu WTK: Ultrasound prediction of parturition in queens. Vet Rec 31:32, 1990. 7. Hirt RA, Kneissl S, Teinfalt M: Severe hypercalcemia in a dog with a retained fetus and endometritis. J Am Vet Med Assoc 216:1423, 2000. 8. Farrow CS, Morgan JP, Story EC: Late-term fetal death in the dog: early radiographic diagnosis. Vet Rad 17:11, 1976. 9. Farrow CS: Abdominal compression radiography in the dog and cat. J Am Anim Hosp Assoc 14:337, 1978. 10. Nack RA: Theriogenology question of the month. J Am Vet Med Assoc 217:182, 2000. 11. Farrow CS: Maternal-fetal evaluation in suspected canine dystocia: a radiographic perspective. Can Vet J 19:24, 1978. 12. Farrow CS: The abdomen. In Farrow CS, ed: Radiology of the cat. St. Louis, 1994, Mosby. 13. Eneroth A, Linde-Forsberg C, et al: Radiographic pelvimetry for assessment of dystocia in bitches: a clinical study in two terrier breeds. J Small Anim Pract 40:257, 1999. 14. Pharr JW, Post K: Ultrasonography of the canine postpartum uterus. Vet Radiol Ultrasound 33:35, 1992.

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Uterine Disease

❚❚❚ RADIOGRAPHIC APPEARANCE OF UTERINE ENLARGEMENT Normally, the uterus is radiographically invisible, even when a dog or cat is in heat. When moderately enlarged, the uterus typically appears as one or more serpentine bands located in the caudal part of the abdomen that displace the bowel cranially. When viewed in cross-section, these same uterine segments often appear circular. As with the intestine, these radiographic observations (a broad band in one plane and a sphere in the other) lead to the conclusion that the organ in question is cylindrical and thus anatomically compatible with the uterus. Such reasoning (three-dimensional reconstruction) underlies the commonly used descriptive phrase tubular structure, which so often appears in radiographic descriptions of uterine enlargement.

❚❚❚ POSSIBLE CAUSES OF UTERINE ENLARGEMENT The most common cause of radiographically visible uterine enlargement in a mated dog or cat is pregnancy. In an unmated dog or cat, pyometra is most likely, followed by mucometra and hydrometra.1 After a normal and complete delivery, uterine enlargement may be due to hemometra secondary to incomplete placental involution.

❚❚❚ CYSTIC ENDOMETRIAL HYPERPLASIA: PRECURSOR TO INFECTION Proposed as an ideal “prepyometra environment” and by some described as part of the so-called pyometra complex, cystic uterine hyperplasia can exist (and 708

persist) as a clinical entity in its own right, causing chronic vaginal discharge. Sonographically, cystic endometrial hyperplasia is characterized by regional and, less often, diffuse thickening of the uterine wall, multiple small intramural cysts, with or without luminal fluid.2

❚❚❚ PYOMETRA Background Progesterone stimulates the development of cystic endometrial hyperplasia and the formation of intrauterine fluid. In such an environment, infection may occur, typically by Escherichia coli. As the magnitude of infection grows, so does the uterus. Untreated, the disease may be fatal, usually as a result of endotoxic shock. The clinical signs of pyometra, polydipsia and vomiting, typically develop in diestrus. An enlarged uterus—presumed on the basis of palpating a large tubular object in the caudal abdomen—often is detected during physical examination. Vulval discharge occurs in 85% of affected dogs, but only 40% of these have a fever. Animals with a closed cervix, and thus the inability to drain the infection, are more likely to become toxic. It is important to note that near-identical clinical signs to those described for pyometra can develop in pregnant dogs with fetal, placental, or uterine infection. Fetal death also may produce similar signs.3

Imaging Findings Uterine disease is best assessed sonographically, which allows for evaluation of both the exterior, as is the case with radiography, and the interior. If ultrasound is unavailable, radiography can be used to reliably detect moderate and severe uterine enlargement, but not a mild increase in uterine size.

CHAPTER 73 ❚❚❚ Uterine Disease

709

A Figure 73-1 • Lateral view of the abdomen of a dog initially thought to be in the advanced stage of pregnancy shows uniform uterine enlargement, uncharacteristic of pregnancy, which usually appears lobulated. Pyometra was diagnosed sonographically.

B Figure 73-3 • A, Lateral view of a dog with pyometra shows characteristic craniodorsal displacement of the bowel caused by uterine enlargement. B, A diagnostic pneumoperitoneum shows the uterine horns coiled in the central abdomen, pushing the colon dorsally and the small intestine cranially.

Figure 73-2 • Close-up lateral view of a moderately swollen uterus in a dog with pyometra.

Radiography Moderate to severe uterine enlargement is characterized by a substantial mass effect, which typically pushes the intestinal mass forward (Figures 73-1 to 73-4).

Ultrasound Early Pyometra. Early pyometra is often characterized by mild, segmental uterine dilations containing hypoechoic fluid. The presence of one or more circular echogenic masses suggests reabsorbing placental tissue.4 As such, it is unlikely plain films will be of any diagnostic use, and one should proceed directly to ultrasound to obtain confirmation. Advanced Pyometra. Advanced pyometra is characterized by cylindrical enlargement of the uterus, in

Figure 73-4 • Lateral close-up view of the central abdomen of a dog with pyometra shows a large coiled uterine segment, which along with the rest of the diseased uterus is displacing the bowel mass cranially. Sonographic cross-section of the uterus in a dog with pyometra shows (1) thickening of the uterine wall, (2) mucosal irregularity, and (3) a highly echogenic content (pus). The urinary bladder lies just above and to the left.

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SECTION VII ❚❚❚ The Abdomen

A

Figure 73-5 • Sonographic cross-section of the uterus in a dog with pyometra shows (1) thickening of the uterine wall, (2) mucosal irregularity, and (3) a highly echogenic content (pus). The urinary bladder lies just above and to the left.

particular, one or usually both of its horns. The uterine wall typically appears thickened and the mucosa roughened. Uterine content varies with the amount and consistency of pus but usually appears as a lighter shade of gray (Figure 73-5). B

❚❚❚ STUMP GRANULOMA Ackerman, in his review of uterine disease, indicates that the diagnosis of stump granuloma is difficult.5 He continues, “The granuloma may produce a mass which compresses the urinary bladder or colon and may also cause ureteral obstruction.” Special procedures like cystography and urography may provide indirect evidence of a stump granuloma in the form of a mass effect but are unlikely to achieve more. “Survey abdominal radiographs are usually of little value.” In my experience, it is sometimes possible to identify a large stump granuloma in plain films, especially if compression is used (Figure 73-6). Confirmation then can be made by using a combination of ultrasound and fine-needle biopsy.

❚❚❚ RETAINED SURGICAL SPONGE Background Merlo and Lamb described the radiographic and sonographic appearance of retained surgical sponge in eight dogs, most of which had had a recent elective or therapeutic ovariohysterectomy.6 On average, diagnosis occurred 91/2 months after surgery; however, the associated range was extraordinarily wide (4 days to 38 months), rendering this figure of dubious predictive worth. Five dogs had a draining sinus; four had palpable abdominal masses.

Figure 73-6 • A, Close-up lateral view of the caudal abdomen of a dog shows a vague circular mass beneath the bladder. B, A compression film of the same area reveals a sharply marginated mass, which subsequently proved to be a stump granuloma.

Imaging Findings Radiography. Intraabdominal sponges (with and without encapsulating soft tissue) exhibited a variety of radiographic appearances, including (1) a soft tissue mass; (2) an ill-defined area of increased soft tissue density; and (3) various gas/soft tissue patterns: speckled, pocked, lined, and banded. Sinography. Sinographically, a retained surgical sponge usually appears as a medium-sized, spherical filling defect found at the base of an opacified drainage channel. The defect is usually larger than the sponge because some form or another of connective tissue often coats the latter. In some instances, multiple drainage channels will be present that often exhibit cross drainage. Ultrasound. For the most part, sponges usually appeared as hypoechoic masses with bright-banded centers; less often, it was possible to see the individual layers of the sponge, represented as two or more undulant, roughly parallel lines.

CHAPTER 73 ❚❚❚ Uterine Disease

711

Figure 73-7 • Close-up view of an unhealthy fetus (abnormally low heart rate) seen in an ultrasound examination performed about 30 minutes after a car struck the dog. Other than a small amount of peritoneal fluid, thought to be blood, everything else appeared normal. Subsequent surgery showed a large uterine tear.

Table 73-1 • CAUSES OF INTRAUTERINE MASS Cause

Sonographic Comment

Adenomyosis Chronic pyometra

May resemble endometrial polyp but with smaller, more deeply embedded cysts Less interior complexity than polyps or adenomyosis; lesion characterized by distended uterine lumen with uniform, hypoechoic content Sonographically, a uterine cyst typically appears as a round or oval-shaped, fluid-filled structure protruding from the interior surface of the uterine wall Benign, variably sized, often cystic, solitary masses originating from the endometrial lining of the uterus in older dogs and cats; may become very large and extend through cervical canal into vagina; no malignant potential; rarely associated with pyometra or uterine torsion Rare Rare Rare Developing pregnancy is associated with one or more fetuses and their related placental structures May resemble endometrial polyp but is typically more diffuse; sometimes seen with false pregnancy Occasional finding: leiomyomas appear as solid, well-demarcated, mural masses, which bulge into the uterine lumen; lymphosarcoma, hemangiosarcoma, and fibrosarcoma are rare

Cyst Endometrial polyp Granuloma Mesonephric duct remnant Mural abscess Pregnancy Segmental endometrial hyperplasia Tumor

Modified from Schlafer DH, Yeager AE, Concannon RW: Theriogenology question of the month. J Am Vet Med Assoc 210:759, 1997.

❚❚❚ UTERINE RUPTURE In my experience, the combination of advanced pregnancy and a serious injury is the principal circumstance surrounding a uterine rupture in a cat or dog. Plain film diagnosis may be straightforward if one or more fetuses are found free in the peritoneal cavity, but this is not always the case. Sometimes the uterus is split open, but the fetus remains within the uterine lumen. Under such circumstances, it can be difficult or impossible to confirm a rupture. Feeney and Johnston described peritoneal fluid (blood) as a potential radiographic/sonographic finding relating to uterine rupture, but they failed to mention the likelihood of such an occurrence.7 If the dam is in shock, the fetal circulation, particularly the fetal heart rate, may decrease (Figure 73-7). Traumatic placental avulsion is often hard to diagnose

sonographically. A uterus and fetuses, which initially appear normal, may not remain so for long and always should be rechecked at least once and preferably more than that in the days following the initial evaluation.

❚❚❚ CONTRAST EVALUATION OF THE UTERINE INTERIOR The uterine interior can be visualized radiographically by injecting nonionic, diagnostic iodine solution into the uterus, a special procedure referred to as hysterography.8 With the ubiquity of ultrasound, this procedure has been largely abandoned, but it does provide some recourse for isolated practices with limited referral options.

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❚❚❚ INTRAUTERINE MASSES Uterine masses are rare compared with masses in other commonly examined abdominal organs. A list of possible causes is presented in Table 73-1.9

❚❚❚ CYSTIC UTERINE REMNANT Typically, cystic uterine remnants are located between the caudal part of the colon and the trigone of the bladder, often causing tenesmus or stranguria. If sonography is available, it is the superior means of diagnosis; if not, either pneumocolonography or air cystography will help to outline the dorsal and ventral aspects of the mass, respectively.10

References 1. von Reitzenstein M, Archbald LF, Newell SM: Theriogenology question of the month. J Am Vet Med Assoc 216:1221, 2000.

2. Voges AK, Neuwirth L: Cystic uterine hyperplasia. Vet Radiol Ultrasound 37:131, 1996. 3. Memon MA, Mickelsen WD: Diagnosis and treatment of closed-cervix pyometra in a bitch. J Am Vet Med Assoc 203:509, 1993. 4. Fayrer-Hosken RA, Mahaffey M, et al: Early diagnosis of canine pyometra using ultrasonography: radiographic diagnosis. Vet Rad 32:287, 1991. 5. Ackerman N: Radiographic evaluation of the uterus: a review. Vet Rad 22:252, 1981. 6. Merlo M, Lamb CR: Radiographic and ultrasonographic features of retained surgical sponge in eight dogs. Vet Radiol Ultrasound 41:279, 2000. 7. Feeney DA, Johnston GR: The uterus, ovaries, and testes. In Thrall DE, ed: Textbook of veterinary diagnostic radiology. Philadelphia, 2002, WB Saunders. 8. Funkquist B, Lagerstedt A-S, et al: Hysterography in the bitch. Vet Rad 26:12, 1985. 9. Schlafer DH, Yeager AE, Concannon RW: Theriogenology question of the month. J Am Vet Med Assoc 210:759, 1997. 10. Franklin RT, Prescott JVB: Tenesmus and stranguria from a cystic uterine remnant. Vet Rad 24:139, 1983.

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Ovarian Disorders

❚❚❚ NORMAL OVARY Like the pancreas, adrenal glands, and uterus, the ovaries typically are not seen during a routine ultrasound examination of the abdomen. During heat, however, they become more visible because of a notable increase in size. The ovaries normally are found immediately caudal to the kidney and occasionally one or two centimeters caudally.

❚❚❚ OVARIAN TUMORS Background Canine ovarian tumors are rare, representing only about 1% of all canine neoplasms. Unilateral and bilateral ovarian tumors have been reported, with the latter usually being adenomas or adenocarcinomas. Ovarian adenocarcinoma is noted for its spread to peritoneal lymphatics, where it obstructs lymph flow, causing ascites. Granulosa cell tumors are usually unilateral and are reported to occur in conjunction with endometrial hyperplasia. Occasionally, a dog develops an ovarian tumor after being spayed; possible explanations include (1) incomplete surgical excision of one or both ovaries and (2) the presence of an accessory ovary that was overlooked at the time of surgery. Residual ovarian tissue most commonly is found near the right ovary, presumably because the right ovary is more difficult to visualize through a small abdominal incision than is the left. Accessory ovarian tissue usually is located near the normal ovary, but it tends to be overlooked because the possibility is not considered and the surgery is often performed without regional exploration.1 Clinical signs associated with ovarian tumors usually are caused by one or more of the following factors: (1) physical effects related to the tumor mass, (2) hormonal disturbances, and (3) metastasis. Ovarian teratomas may be either benign or malignant and are

composed of tissue types from one or more of the three germ cell layers.

Imaging Findings Radiography. If an ovarian tumor becomes large enough to be radiographically identified, it will likely appear as a midabdominal mass. If it becomes large enough, a cancerous or cystic ovary may be mistaken for a diseased kidney. Bone-containing teratomas are often quite distinctive, vaguely resembling bone fragments in the stomach but with a more dispersed appearance.2 Ultrasound. The ovaries are found caudal to the kidneys, the latter serving as reliable anatomic landmarks. Normal ovaries can be as long as 2.5 cm, depending on the size of the dog and the current status of the reproductive cycle.3 Sonographically, bilateral ovarian adenocarcinomas appear as irregularly marginated echogenic masses con-

B o x

7 4 - 1

Aids to the Diagnosis of Benign and Malignant Ovarian Tumors • Masses that do not exceed 6 cm in length are most apt to be recognized as ovarian in origin. • Ovarian masses associated with peritoneal fluid are often cancerous. • Ovarian masses associated with regional adenopathy are often cancerous. • The more cystic an ovarian mass, the more likely it is to be benign. • The presence of a mass caudal to a kidney suggests an ovarian origin. • The presence of bilateral masses caudal to the kidneys strongly suggests an ovarian origin. • The smoother the border of an ovarian mass, the more likely it is benign. 713

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SECTION VII ❚❚❚ The Abdomen

incidental findings observed during an abdominal examination (Figure 74-1). Cysts may or may not have a visible wall, but most exhibit far-field enhancement. Ovarian cysts may resemble normal follicles or related postovulatory structures such as (1) follicles that failed to ovulate, (2) corpora hemorrhagica, (3) fluid-filled corpora lutea, or (4) cystic luteinized follicles.6 Thus, differentiating ovarian cysts from other sources of ovarian change always must take into consideration the animal’s heat cycle.

References

Figure 74-1 • Celebrity cyst: Ovarian cyst in a dog resembles the widely recognized frontal silhouette of the famed cartoon character Mickey Mouse. (Courtesy Dr. Kim Tryon.)

taining a number of small interior cysts.4 Diez-Bru and co-workers reported the ultrasonic findings in 10 dogs with ovarian tumors and arrived at the conclusions listed in Box 74-1.5

❚❚❚ OVARIAN CYSTS Ovarian cysts typically appear as small circular, oval, and occasionally lobulated anechoic cavities; most are

1. Pluhar GE, Memon MA, Wheaton LG: Granulosa cell tumor in an ovariohysterectomized dog. J Am Vet Med Assoc 207:1063, 1995. 2. Meyer W: Radiographs presented as part of the 1994 A.C.V.R. oral certification examination: abdomen section. Vet Radiol Ultrasound 36:30, 1995. 3. Wallace SS, Mahaffey MB, et al: Ultrasonographic appearance of the ovaries of dogs during the follicular and luteal phases of the estrous cycle. Am J Vet Res 53:209, 1992. 4. Goodwin J-K, Hager D, et al: Bilateral ovarian adenocarcinoma in a dog: ultrasonic-aided diagnosis. Vet Rad 31:265, 1990. 5. Diez-Bru N, Garcia-Real I, et al: Ultrasonographic appearance of ovarian tumors in 10 dogs. Vet Radiol Ultrasound 39:226, 1998. 6. Mahaffey MB, Selcer BA, et al: The reproductive system. In Cartee RE, ed: Practical Veterinary Ultrasound. Philadelphia, 1995, Lea & Febiger.

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7 5

Urethral and Vaginal Disease

❚❚❚ CONGENITAL DEFORMITIES

• Uterine hypoplasia • Vaginal hypoplasia or absence

Vaginal Septa Background. Clinical signs associated with vaginal septa include (1) an inability to breed naturally, (2) infertility, (3) urinary incontinence, (4) dysuria, (5) chronic or recurrent vaginitis, and (6) abnormal or ambiguous genitalia.1 Diagnosis and surgical planning are best achieved through a combination of direct observation (vaginoscopy) and vaginography. Imaging Findings. Typically, vaginal septa are oriented longitudinally or diagonally. Vaginography is necessary to detect vaginal septa, which typically appear in ventrodorsal projection as longitudinally oriented linear or curved filling defects. Most septa are located centrally and run the entire length of the vagina. Some are only partial length and are positioned diagonally within the vagina.

Urethral Hypoplasia Urethral underdevelopment has been reported in conjunction with urine dribbling attributed to an incompetent urethral sphincter in both dogs and cats, with the former more commonly afflicted. Other regional congenital anomalies associated with urinary incontinence include the following2: • • • • •

Colorectal fistula Hypoplastic urinary bladder Ureteral misplacement Urethral hypoplasia or absence Urethrorectal fistula

Annular Strictures Vaginal strictures are associated with the same clinical signs as vaginal septa. Like vaginal septa, vaginal strictures are not apparent on plain radiographs without the aid of a diagnostic contrast solution.

❚❚❚ EFFECT OF SPAY OR CASTRATION ON URETHRAL DIAMETER IN CATS Root and colleagues investigated the influence of prepubertal and postpubertal spay and castration on urethral diameter in cats. Based on measured urethral diameters obtained by compression-induced, voiding cystourethrography, the diameter of the prepelvic urethra of female cats spayed at 7 weeks of age was smaller than the urethra in nonspayed controls. The urethras of prepubertal and postpubertal castrated males did not differ from controls.3

References 1. Root MV, Johnston SD, Johnston GR: Vaginal septa in dogs: 15 cases (1983-1992). J Am Vet Med Assoc 206:56, 1995. 2. Baines SJ, Speakman AJ, et al: Genitourinary dysplasia in a cat. J Small Anim Pract 40:286, 1990. 3. Root MV, Johnston SD, et al: The effect of prepuberal and postpuberal gonadectomy on penile extrusion and urethral diameter in the domestic cat. Vet Radiol Ultrasound 37:363, 1996.

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Scrotal, Testicular, and Penile Disease

❚❚❚ TESTICULAR DISEASE Normal Testicle (Testes) and Associated Diseases Pugh and co-workers described the sonographic appearance of the normal testicle, which was followed later by a catalog of testicular and scrotal abnormalities: testicular tumors (seminoma, Sertoli cell, interstitial cell), hydrocele, orchitis, and epididymitis.1,2

Testicular Tumors Sonography can readily localize most scrotal tumors to the testis or epididymis for the purpose of biopsy or surgical planning. Where an undescended, intraabdominal testis is suspected of being cancerous, sonography can be used to check adjacent lymph nodes for tumor extension and more distant organs for metastasis. A difference of opinion exists as to whether or not specific testicular tumors have characteristic appearances. Burk and Ackerman contend they do not3 (Table 76-1), whereas Johnston and colleagues believe otherwise.4 Cartee cautioned that the intratesticular septum is capable of producing a circular hypoechoic attenuation artifact that resembles a Sertoli cell tumor.5

Testicular Trauma In my experience, the most common types of scrotal injuries in dogs are bite wounds, followed by crushing and bruising related to being hit by a motor vehicle. In most instances, there is massive swelling, especially of the scrotum (as opposed to the testicles themselves). Infection with abscess following one or more puncture wounds is frequent. Localized, extratesticular, loculated fluid accumulations form occasionally and are composed of serum (hydrocele), blood (hematocele), and pus (pyocele). The last of these can be quite difficult to differentiate from an abscess, although it may be argued that they are fundamentally similar (Figure 76-1). 716

Testicular Torsion Testicular torsion usually involves a testicle located within the scrotum; swelling and pain are typical. Sonographically, there is usually testicular and epididymal enlargement, marked hyperemia, and intrascrotal edema. Blood will be diminished or static, depending on the completeness of the degree of vascular strangulation. Without rapid relief, the ischemic testicle will soon become necrotic, sonographically assuming the characteristic appearances of tissue death, including disruption of internal architecture and loss of normal echogenicity. Seminoma in an undescended testicle has been reported in conjunction with torsion of the associated scrotal testicle.6

Retained Testicle (Undescended, Nondescended Testicle) According to Burk and Ackerman—and in keeping with my own experience—a retained testicle is difficult (Figure 76-2) or impossible to detect radiographically.3 The exception to this generality is the palpable intraabdominal testicle, which usually can be imaged radiographically, especially if compression is used. Sonography is an even more effective way to view a suspected undescended testicle, especially if it can be first digitally immobilized, which greatly cuts down on search time. Most retained testicles are small and tend to be more spherically shaped than a normal testicle, although they typically retain their usual interior features.7

Testicular and Epididymal Infection (Orchitis, Epididymitis) Pugh summarized the sonographic features of testicular infections in five dogs, as follows, warning that Brucella canis is often responsible.7 1. Testicular enlargement 2. Epididymal enlargement

CHAPTER 76 ❚❚❚ Scrotal, Testicular, and Penile Disease

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Figure 76-1 • Cross-sectional sonogram of a dog’s testicles shows a left-sided hydrocele depicted by fluid surrounding a relatively small testicle.

A

B Figure 76-2 • Lateral (A) and close-up (B) views of the abdomen of a dog show a vague mass that later proved to be a retained testicle.

Table 76-1 • TESTICULAR TUMORS AND THEIR SONOGRAPHIC APPEARANCE Testicular Tumor Type

Sonographic Appearance

Focal seminomas and interstitial cell tumors (>3 cm) Focal seminomas and interstitial cell tumors (<3 cm) Sertoli cell tumor (>5 cm) Tumors of multiple cell types (>5 cm)

Mixed echogenicity: hypoechoic-hyperechoic Hypoechoic Sonographically variable; accordingly, no characteristic appearance Mixed echogenicity: hypoechoic-hyperechoic

Modified from Burk RL, Ackerman N: The abdomen. In Burk RL, Ackerman N, eds: Small animal radiology and ultrasound. Philadelphia, 1996, WB Saunders.

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3. Abnormal echo texture: diffuse, patchy, and hypoechoic 4. Scrotal fluid 5. Loss or disfigurement of the intratesticular septum (a normal echogenic band located in the center of the testicle, also known as the mediastinum testis)

of the considerable variation in the appearance of the os penis, which can be mistaken for infection. In a similar regard, the os penis may form from more than a single ossification center, in which case the caudalmost element may resemble a fracture fragment, especially when seen in the context of a recent injury.

References

❚❚❚ PENILE DISEASE Injury Potential injuries to the penis include abrasion, bruising, laceration, puncture, and occasionally fracture of the os penis. Urethral injury may accompany penile trauma but usually requires a urethrogram to be seen. Severe swelling can secondarily occlude the urethra, which then must be kept open with an indwelling catheter until the inflammation subsides. A precautionary urethrogram should be performed whenever the os penis is fractured, irrespective of the dog’s urinary pattern. Although I have seen a case of osteomyelitis following deep penile bite wounds, this is an exceptionally rare occurrence. I raise the issue of infection because

1. Pugh CR, Konde LJ, Park RD: Testicular ultrasound in the normal dog. Vet Rad 31:195, 1990. 2. Pugh CR, Konde LJ: Sonographic evaluation of canine testicular and scrotal abnormalities: a review of 26 case histories. Vet Rad 32:243, 1991. 3. Burk RL, Ackerman N: The abdomen. In Burk RL, Ackerman N, eds: Small animal radiology and ultrasound. Philadelphia, 1996, WB Saunders. 4. Johnson GR, Feeney DA, et al: Ultrasonographic features of testicular neoplasia in dogs: 16 cases (1980-1988). J Am Vet Med Assoc 198:1779, 1991. 5. Cartee RE: The testicles and epididymis. In Cartee RE, ed: Practical veterinary ultrasonology. Philadelphia, 1995, Lea & Febiger, p 259. 6. Hathaway JE: Seminoma of an undescended testicle: a case report. J Am Vet Rad Soc 6:75, 1965. 7. Pugh CR: Testes. In Green RW, ed: Small animal ultrasound. Philadelphia, 1996, Lippincott-Raven.

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Fluoroscopic, Ultrasonic, and Computed Tomography– Guided Biopsy, and Fine-Needle Aspiration ❚❚❚ ULTRASOUND-GUIDED, FREEHAND BIOPSY The following stepwise account of how to perform an ultrasound-guided biopsy in a dog or cat is taken (with some personal modifications regarding the need for sedation) from an article by Menard and Papageorges1: 1. Localize the lesion sonographically, taking care to view it from as many different angles as possible, to estimate its true height, width, and depth. 2. Consider potential needle routes to the lesion, paying particular attention to avoiding the gallbladder/bile duct, pancreas, intestine, and blood vessels. 3. Sedate/tranquilize the animal to the extent that it will neither feel pain nor, as a result, move during the biopsy. 4. The use of local anesthesia is a matter of personal preference; however, I disagree with the authors’ view (or possibly their technique) that “Local anesthesia is never used because it causes more discomfort than the biopsy itself.” Rather than adhering to a blanket policy on local anesthesia, I advise dealing with each case on an individual basis. 5. Clip hair from the biopsy site and wipe with alcohol; briefly rescan to confirm the availability of the target and planned needle track. 6. Surgically clean the skin and scanner (especially its contact surface). 7. I prefer regular ultrasound gel to sterile K-Y gel, but again this is a matter of personal choice. In either case, no more than necessary should be used. 8. Use 22-gauge needles of variable lengths (2.5 to 8.9 cm), depending on the target depth, connected to a 12-cc syringe (partially air-filled) by a lengthy extension tube. Positioning the beveled surface of the needle toward the ultrasound beam improves

9.

10. 11.

12. 13.

the visibility by producing a relatively stronger reverberation artifact than the nonbeveled side. Once the needle tip is identified, advance it well into the target tissue, which should move perceptibly, confirming that the needle has actually penetrated the lesion rather than merely being superimposed on it. Once in the lesion, move the needle tip rapidly back and forth half a dozen times without applying negative pressure. Withdraw the needle and expel its contents on a glass microscope slide, which then is immediately air-dried and submitted to the laboratory for staining and evaluation. Repeat biopsy at least twice more, preferably from different areas of the lesion. Bear in mind, especially in the case of nondiagnostic biopsies, that a tumor, for example, may contain areas of hemorrhage, necrosis, and normal tissue, in addition to neoplastic cells. Thus, the more times a lesion is sampled, the greater the probability of a diagnosis.

❚❚❚ COMPUTED TOMOGRAPHY– GUIDED BIOPSY Differentiating Between True and False Needle Tips Tidwell and Johnson devised a method of visually distinguishing between the actual and simulated tips of biopsy needles seen in computed tomography (CT) images (Table 77-1).2

Biopsy Technique Tidwell and Johnson described a technique for freehand, CT-guided biopsy in the dog.3 The method of free-hand CT-guided biopsy (modified after Tidwell and Johnson) is as follows: 719

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Table 77-1 • DIFFERENTIATING BETWEEN TRUE AND FALSE NEEDLE TIPS Distinguishing Tip Feature

True Biopsy Needle Tip

False Biopsy Needle Tip

Clarity Leading edge Associated flame artifact

Distinct Abrupt Present

Indistinct Tapered Present

1. Obtain CT images of the lesion using a level table (0-degree gantry tilt). Identify target tissue on one transverse image, noting the table position. Inject a bolus of diagnostic iodine solution to estimate the vascularity of the lesion and its immediately surrounding tissues. 2. Withdraw the patient from the gantry and clip the biopsy site. 3. Return the patient to the previously marked table position. 4. Mark the skin with indelible ink along the transverse plane of the gantry’s laser marker. 5. Apply several (e.g., five) strips of barium paste along the longitudinal plane. 6. Obtain a transverse CT image (barium strips will appear as white dots). 7. Choose the best skin puncture site (between two of the white dots), and mark with indelible ink or sterile suture. 8. Prepare the biopsy site. 9. Adjust the stopper on the calibrated needle to correspond with lesion depth. 10. Insert the needle to the level of the stopper, taking care to remain within the transverse plane (facilitated by using the shortest needle possible). If the needle’s pathway is angled, use a protractor as a guide. 11. Move the table so that the biopsy needle is centered in the gantry’s laser beam. 12. Obtain a transverse CT image. 13. Verify that the “true” needle tip is within the lesion and perform the biopsy.

❚❚❚ FALSE ABDOMINAL LESIONS Weber and Spaulding described how parahepatic organs and tissues can mimic liver masses during sonographic examination, potentially leading to unnecessary and potentially dangerous biopsy attempts.4 • The cranial pole of the right kidney could appear as a hepatic mass during a transverse scan of the right dorsal aspect of the liver. • Fat adjacent to the portal vein also may resemble an intrahepatic mass. • Fat investing the gastrosplenic ligament, falciform ligament, and lesser omentum also can mimic a hepatic mass.

• When the gallbladder is filled with dehydrated bile, it sometimes creates the illusion of a mass in the nearby right cranioventral aspect of the liver.

❚❚❚ BIOPSY NEEDLE ENHANCEMENT Allen and Kramer described improving the sonographic appearance of a biopsy needle by roughening its tip with a file. The physical basis for this recommendation lies in the fact that with standard, smoothsurfaced biopsy needles, only the needle tip is visible with ultrasound, with echoes from the needle’s shaft being reflected away from the scanner’s transducer. When the tip of the needle is scarified, air becomes trapped in its pits and furrows, improving its reflectivity, and thus its sonographic visibility in tissue.5

❚❚❚ TECHNIQUES Papageorges and co-workers described a simple modification to the standard technique of ultrasoundguided, fine-needle aspiration and fluid sampling.6 Two people, a sonologist and an assistant, perform the procedure on a sedated dog or cat. 1. A 22-guage needle is attached to an 84-cm extension tube, which is fixed to a medium-sized syringe. 2. The sonologist locates the target tissue. 3. The immediate area around the target tissue is scanned, and a safe approach (i.e., the most direct line to the target that avoids other organs and blood vessels) is selected. 4. The sonologist then punctures the target tissue, holding the scanner in one hand and the needle in the other. 5. The assistant then creates a vacuum by pulling the plunger on the syringe, taking care not to move or jerk the needle, which is being held by the sonologist. 6. The sonologist then moves the needle gently back and forth within the tissue, and the assistant maintains the vacuum. 7. On the word of the sonologist, the vacuum is released, and the needle is withdrawn. 8. The aspirated material is expelled onto glass slides, air-dried rapidly, and submitted for cytologic evaluation. Large-sized fluid samples are placed in edathamil (EDTA) tubes and then submitted to the laboratory. 9. The process is repeated to increase the probability of diagnosis. 10. The target tissue is checked for hemorrhage.

❚❚❚ PRACTICE Spaulding published a description of how to make and use an ultrasound biopsy phantom, an excellent learning and practice device for beginners.7

CHAPTER 77 ❚❚❚ Fluoroscopic, Ultrasonic, and Computed Tomography–Guided Biopsy, and Fine-Needle Aspiration

Table 77-2 • CONSIDERATIONS IN SAFELY OBTAINING AN ULTRASOUND-GUIDED BIOPSY OF ABDOMINAL ORGANS AND MASSES Consideration Technical skill Operator experience Painless procedure Rapid procedure

Supervised procedure

Patient immobility

Comment

Imagine this being done to you The shorter the time the needle is in the tissue being biopsied, the less needle movement and the less unnecessary tissue injury Novices should not be sent to do a biopsy without an experienced person on hand to assist or take over in the event of problems If the dog or cat moves while the needle is in the abdomen, not only may the organ being biopsied be unnecessarily damaged, but adjacent tissues also can be injured

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❚❚❚ POTENTIAL INJURIES Hemorrhage is of course the most serious risk attending ultrasound-guided intraabdominal biopsy. Nyland and co-workers reported the inadvertent seeding of the ventral abdominal wall with cancer cells while performing ultrasound-guided biopsies on three dogs with separate transitional cell carcinomas of the bladder, urethra, and prostate. The authors point out that, based on the human literature as well as their own experience, the likelihood of implantation is remote and thus should not unduly influence the decision to perform fine-needle biopsies on lesions of this nature.12 Berry and co-workers reported a biliary pseudocyst (biloma), which they believe resulted from a liver biopsy.

❚❚❚ BIOPSY OF SPECIFIC ORGANS Gastrointestinal Tract

❚❚❚ BODY REGIONS Thoracic Cavity McMillan and co-workers described fluoroscopy guided, transthoracic biopsy in 48 dogs.8 One of the animals was under general anesthesia, and the rest were sedated. Thirty-five lung and 13 mediastinal lesions were sampled. Pneumothorax occurred in eight dogs, one of which died as a result; 77% of the biopsies were diagnostic.8

Abdominal Cavity Background: Ensuring Safety. Based on published reports, ultrasound-guided biopsy of abdominal organs and masses appears to be a relatively safe procedure.9 My observations regarding this type of biopsy are that skill and operator experience are the two most important factors in safely obtaining a diagnostic sample (Table 77-2).

❚❚❚ CHOOSING A BIOPSY DEVICE Hoppe and co-workers compared the performances of a manually manipulated biopsy needle and an automated, purpose-built biopsy device that were used while under fluoroscopic control. They concluded that the automated device was superior by virtue of its obtaining larger and higher-quality tissue samples.10 Even using an automatic biopsy needle, success is not guaranteed, as indicated by published failure rates (absence of tissue contained in biopsy device) as high as 18%.11

Penninck and co-workers described the techniques and application for fine-needle and automatic microcore ultrasound-guided biopsy of the gastrointestinal tract of the dog and cat.13,14 De Rycke and colleagues reported the following success rates in ultrasoundguided, tissue-core biopsies in normal dogs: spleen (90%), liver (77%), left kidney (54%), and right kidney (40%).11

References 1. Menard M, Papageorges M: Technique for ultrasoundguided fine needle biopsies. Vet Radiol Ultrasound 36:137, 1995. 2. Tidwell AS, Johnson KL: Computed tomography-guided percutaneous biopsy: criteria for accurate needle tip identification. Vet Radiol Ultrasound 35:440, 1994. 3. Tidwell AS, Johnson KL: Computed tomography-guided percutaneous biopsy in the dog and cat: description of technique and preliminary evaluation in 14 patients. Vet Radiol Ultrasound 35:445, 1994. 4. Weber WJ, Spaulding KA: Hepatic pseudomasses caused by normal anatomic structures in the dog. Vet Radiol Ultrasound 35:307, 1994. 5. Allan JK, Kramer RW: Enhanced sonographic visualization of biopsy needles. Vet Radiol Ultrasound 34:359, 1993. 6. Papageorges M, Gavin P, et al: Ultrasound-guided fineneedle aspiration. Vet Rad 29:269, 1988. 7. Spaulding KA: Use of an ultrasound phantom. Vet Radiol Ultrasound 33:199, 1992. 8. McMillan MC, Klein LJ, Carpenter JL: Fluoroscopically guided percutaneous fine-needle aspiration biopsy of thoracic lesions in dogs and cats. Vet Rad 29:194, 1988. 9. Leveille R, Partington BP, et al: Complications after ultrasound-guided biopsy of abdominal structures in dogs and cats: 246 cases (1984-1991). J Am Vet Med Assoc 203:413, 1993. 10. Hoppe FE, Hager DA, et al: Acomparison of manual and automatic ultrasound-guided biopsy techniques. Vet Rad 27:99, 1986.

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11. de Rycke LMJH, van Bree HJJ, et al: Ultrasoundguided tissue-core biopsy of liver, spleen and kidney in normal dogs. Vet Radiol Ultrasound 40:294, 1999. 12. Nyland TG, Wallack ST, et al: Needle-tract implantation following US-guided fine-needle aspiration biopsy of transitional cell carcinoma of the bladder, urethra, and prostate. Vet Radiol Ultrasound 43:50, 2002.

13. Penninck DG, Crystal MA, et al: The technique of percutaneous ultrasound-guided fine-needle aspiration biopsy and automated microcore biopsy in small animal gastrointestinal diseases. Vet Radiol Ultrasound 34:433, 1993. 14. Crystal MA, Penninck DG, et al: Use of ultrasound-guided fine-needle aspiration biopsy and automated core biopsy for diagnosis of gastrointestinal disease of small animals. Vet Radiol Ultrasound 34:438, 1993.

Index

A A-mode ultrasound of eye, 236 Abdominal calcification, 561-563f, 564t Abdominal colic, 566, 566b, 650 Abdominal drain, 559t Abdominal fluid, 555-556, 556-557f, 558t, 559t Abdominal hernia, 568, 569f, 637 Abdominal imaging, 555-722 abdominal radiographic disease indicators in, 555-567 abdominal calcification in, 561563f, 564t abdominal masses in, 562, 565f abnormal bowel distribution pattern in, 562, 565f acute abdominal colic and, 566, 566b computed tomographic appearance of normal canine abdomen and, 566 decreased organ size in, 561, 561f increased organ size in, 560, 560f intravisceral gas in, 557-560 magnetic resonance appearance of normal canine bowel and, 566 peritoneal fluid in, 555-556, 556557f, 558t, 559t physical reversal of abdominal viscera and, 567 pneumoperitoneum in, 556-557, 559t relative signal strengths emitted by abdominal organs of cats and, 566-567 retroperitoneal fluid in, 560 visible abdominal lymph nodes in, 562-566 of abdominal wall, 568-571 abscess of, 570 bruising and hematoma of, 568 draining sinuses of, 569, 570f extraabdominal tumor of, 570, 571f gunshot wound to, 568-569

Abdominal imaging—cont’d of abdominal wall—cont’d muscle avulsion of, 569-570, 571f postoperative evaluation of, 568 traumatic disruption of, 568, 569f of adrenal gland, 699-701 of bladder, 677-688 abnormal bowel distribution patterns and, 617 calcification of, 561f, 564t, 688 calculi of, 682-685, 683-684f cystography in, 678-679, 679b, 679680f, 681t diverticula of, 681 emphysematous cystitis and, 681 feline idiopathic cystitis and, 680681 gas in, 558-560 hemorrhage of, 685-688, 687f intrapelvic, 682 plain films in, 678, 678b retroflexion of, 681-682 rupture of, 322, 685-686f tumor of, 671, 675, 682-683f ultrasound in, 680, 680f, 681t of colon, 643-649 abnormal distention of, 646 abnormally long, 648-649 air colonography in, 643-644 barium enema in, 643, 644f cancer of, 646, 648f cecocolic intussusception and, 644-646 colonic marking of, 644, 645f colonic transit time using synthetic markers, 643 double-contrast colonography in, 644 ileocolic intussusception and, 646 impaction of, 646, 648f normal appearance of, 643 perforation of, 559t, 646-648 pneumatosis coli and, 648, 649f stenosis of, 646

Abdominal imaging—cont’d of colon—cont’d torsion of, 648, 649f ulcerative colitis and, 646, 647f of kidney, 663-671 antifreeze poisoning and, 671 chronic renal failure and, 671 compensatory renal hypertrophy and, 665 congenital kidney disorders and, 665-666, 666f giant kidney worm and, 667, 667f hypercalcemic nephropathy and, 671 imaging strategy in, 663-664, 664b, 664t infection and, 666-667f intrarenal cysts and, 668, 670f kidney stones and, 667-670f leptospirosis and, 666 nuclear medicine in, 665 perirenal cysts and, 667-668, 670f renal obstruction and hydronephrosis and, 666-667, 668t renal transplant rejection and, 671 tumors and, 668t, 668-671, 670f ultrasound-guided biopsy in, 663 ultrasound in, 664-665, 665f of liver, 575-593 abscess in, 583-585 biliary cystadenoma and cystadenocarcinoma and, 582, 583f diffuse liver disease and, 579b, 579f, 579-580, 580f gallbladder disease and, 585-587, 586-587f hemangiosarcoma in, 583, 584f, 585t hepatic mass versus parahepatic organs in, 720 hepatic radiology in, 575, 576f, 577f

Note: Page numbers followed by “f” refer to illustrations; page numbers followed by “t” refer to tables; page numbers followed by “b” refer to boxes.

723

724

Index ❚❚❚

Abdominal imaging—cont’d of liver—cont’d hepatic ultrasound in, 465, 578579f imaging of liver function in, 576577 portosystemic shunts in, 587-588f, 587-591, 588t, 591b regional and localized hepatic disease and, 580-582, 581-582f tumors and biliary obstruction in, 583 of ovary, 713b, 713-714, 714f of pancreas, 650-654 abscess in, 652, 652f acute pancreatitis in, 650-651, 651f cancer in, 587f, 653 chronic pancreatitis in, 651, 651f insulinoma in, 653 pancreatic phlegmon in, 651-652, 652f peripancreatic mass in, 652-653 pseudocyst in, 652, 652f tumor in, 653 of penis, 718 in peritonitis, 572-573, 573f in pregnancy, 702-707 abnormal bowel distribution patterns in, 617 ectopic, 705 incomplete fetal resorption and premature placental separation in, 704f, 704-705 intrauterine mass and, 711t late-term fetal death and, 705 mechanical dystocia and, 705-706f normal, 702-704, 703f, 704t ovarian changes related to ovulation, 702 postwhelping uterus and, 706t, 706-707 of prostate, 688-692 abnormal bowel distribution patterns and, 617 benign prostatic hypertrophy and, 689-690f calcification and, 564t cancer of, 691-692, 693f cyst of, 690, 690f measurement of, 688t, 688-689 paraprostatic cysts and, 690-691, 691-692f prostatitis and, 691, 692f of small intestine, 614-642 abscess in, 639f, 641 adhesion in, 640f, 641 bowel distribution pattern and, 616-617 calcification in, 564t congenital malformations in, 638639 displacement in abdominal hernia, 637 duodenal thickening secondary to pancreatitis in, 617-618, 618f duodenal ulcer in, 617 enteritis in, 618-619, 620-621f

Abdominal imaging—cont’d of small intestine—cont’d foreign body in, 565f, 619-627, 622t, 622-630f gas in, 557-558 impaction in, 637, 638f incarceration in, 636 infiltrative bowel disease and, 618, 619t inflammatory bowel disease and, 618 intussusception in, 627-630, 631632f leiomyosarcoma and leiomyoma in, 633, 634f lymphosarcoma in, 632-633, 633f normal barium film variations in, 615 normal iodine films in, 615-616 normal plain film variations in, 614-615, 615f normal sonographic appearance in, 617, 617t parasitic infection in, 637 perforation in, 559t, 634b, 634-635 potential sonographic indicators of, 617 protein-losing enteropathy in, 637 short-bowel syndrome in, 638 torsion in, 635-636, 635-636f trauma and, 639-641 tumor in, 630-632, 632f of stomach, 594-613 abdominal hernia and, 568, 569f abnormal bowel distribution patterns in, 616 acute abdominal colic and, 566b barium examination in, 594-595, 595t, 596f calcification in, 561f, 564t, 611, 611f chronic lymphocytic-plasmacytic gastritis in, 609 diaphragmatic hernia and, 475f, 476f dilation in, 601, 601b enlargement in, 597-598, 598f, 598t fetal stomach and, 702 foreign objects and materials in, 598, 599-601f gastric atony and, 611-612 gastric dilation in spinal fracture and, 275 gastritis in, 599 gastrobronchial fistula in, 610-611 gastroesophageal intussusception in, 609, 611f gastrointestinal pythiosis in, 599601 hairballs in, 598, 602f herniated stomach and, 382f hiatal hernia and, 609, 610f nonopaque foreign body in, 598599, 603f normal barium film variations in, 615 normal gastric emptying time in, 595-597

Abdominal imaging—cont’d of stomach—cont’d normal sonographic appearance in, 597 perforation and rupture in, 559t, 609-610 plain films in, 594 posttorsional stomach and, 604605, 605f pyloric obstruction in, 607-609, 608f, 609f, 610t second foreign body in, 599 tumor in, 606-607, 607f ulcer in, 605-606, 606f uremic gastritis in, 599 volvulus in, 601-604, 602-604f worms in, 599 of testes, 716-718, 717f, 717t ultrasound-guided, free-hand biopsy and, 719, 721 of ureter, 671-677 antegrade ureterography and, 676 calcification in, 564t computed tomography in, 677 diverticula in, 677 ectopic ureter and, 673, 675-676f injury and, 677 intravenous urography and, 676 lithotripsy and, 677 obstruction and, 671-672, 672t, 673-674f pneumovaginography and, 676 retrograde urography and, 672, 675f retrograde vaginourethrocystography and, 676f, 676-677 ultrasound in, 672 ureteric jets and, 676f, 677 of urethra, 692-696, 693-694f, 694b, 715 carcinoma of, 694-695 hypoplasia of, 715 inflammation and stenosis of, 695, 695f trauma to, 718 urinary incontinence and, 696 of uterus, 708-712 contrast evaluation of interior uterus and, 711 cystic endometrial hyperplasia and, 708 cystic uterine remnant and, 712 enlargement and, 708 masses and, 711t, 712 pyometra and, 617, 708-710, 709f, 710f retained surgical sponge and, 710 rupture and, 711, 711f stump granuloma and, 710, 710f of vagina, 715 vascular mapping and, 574 Abdominal lymph node, 562-566 Abdominal mass, 562, 565f Abdominal pain, 566

❚❚❚ Index

Abdominal radiographic disease indicators, 555-567 abdominal calcification in, 561-563f, 564t abdominal masses in, 562, 565f abnormal bowel distribution pattern in, 562, 565f acute abdominal colic and, 566, 566b computed tomographic appearance of normal canine abdomen and, 566 decreased organ size in, 561, 561f in gastric torsion, 603, 604f increased organ size in, 560, 560f intravisceral gas in, 557-560 magnetic resonance appearance of normal canine bowel and, 566 peritoneal fluid in, 555-556, 556-557f, 558t, 559t physical reversal of abdominal viscera and, 567 pneumoperitoneum in, 556-557, 559t in pyloric obstruction, 610t relative signal strengths emitted by abdominal organs of cats and, 566-567 retroperitoneal fluid in, 560 visible abdominal lymph nodes in, 562-566 Abdominal sinus, 569, 570f Abdominal surgery, postoperative pneumoperitoneum and, 559t Abdominal tumor, 558t Abdominal vascular mapping, 574 Abdominal viscera intravisceral gas and, 557-560 lymphocenters of, 563-566 physical reversal of, 567 Abdominal wall, 568-571 abscess of, 570 bruising and hematoma of, 568 draining sinuses of, 569, 570f extraabdominal tumor of, 570, 571f gunshot wound to, 568-569 lymphocenters of, 563-566 muscle avulsion of, 569-570, 571f postoperative evaluation of, 568 traumatic disruption of, 568, 569f Abnormal bowel distribution patterns, 562, 565f, 614, 616-617 Abrasion corneal, 238 penile, 718 Abscess, 23-27, 27f abdominal wall, 570 brain, 226, 226t deep paraspinal, 308, 308f dental, 212-213, 214f, 215f extremital, 119, 119f, 120f hepatic, 557, 583-585 in hip infection, 353 intestinal, 639f, 641 laryngeal, 360, 360f mandibular bone loss in, 194 mediastinal, 463 mural, 711t pancreatic, 652, 652f

Abscess—cont’d parapharyngeal, 305 paraprostatic, 691, 692f pleural, 411f prostatic, 689, 691, 692f pulmonary in foreign body pneumonia, 416, 417f pyothorax and, 420f retrobulbar, 242, 242f scrotal, 716 splenic, 657 sternal or suprasternal, 399, 399f ureteral, 672t Absolute kidney size, 663, 664t Accessory ovarian tissue, 713 Acetabular component in hip replacement, 350, 350f Acetabulum dysplastic versus normal, 348f fracture of, 329, 330f Legg-Calv[ac]e-Perthes disease and, 325, 326f osteoarthritis in, 95, 103f relocation for hip dysplasia, 349, 349t Achilles tendon rupture, 25f, 26, 27f, 179, 179f Acquired heart disease, 517-542 aortic sinus rupture in, 540 arterial thrombosis in, 538-540 atrial standstill in, 538, 539f benefits of presurgical thoracic screening and, 517, 518t cor pulmonale in, 540-541, 541f dilated cardiomyopathy in, 518, 523524, 524-525f endocardiosis in, 517-518, 517-523f, 519t endocarditis in, 528, 531-532f heartworm disease in, 533-537 canine, 533-536, 536f feline, 536-537, 537f hypertrophic cardiomyopathy in, 524-525, 526-531f inherited ventricular tachycardia in German shepherds in, 538 ischemic, 538 myocarditis in, 525-528 pericardial disease in, 533, 534f, 535f third-degree heart block in, 537-538, 538f Acquired portosystemic shunt, 591 Acquired pyloric hypertrophy, 610t Actinomycosis, 408, 415 Acute abdominal colic, 566, 566b Acute cor pulmonale, 444 Acute pancreatitis, 650-651, 651f Acute pneumonia, 407 Acute respiratory distress syndrome, 443 after smoke inhalation, 438 in paraquat poisoning, 440 Acute subperiosteal hematoma, 196197 Adaptive hypertrophy of left ventricle, 501

725

Adenitis, salivary, 361 Adenocarcinoma adrenal, 700 gastric, 606-607, 607f intestinal, 630, 632f mammary gland, 427f, 429 nasal, 207f, 208f ovarian, 713 prostatic, 617, 691-692, 693f pulmonary, 423, 424t tracheal, 451 Adenoma ovarian, 713 parathyroid, 362-363 pituitary, 222-223, 223-224f Adenomyosis, 711t Adenopathy hilar, 387-388, 390f false radiographic disease indicator of, 374f in nocardiosis, 415 retropharyngeal, 362 Adhesion intestinal, 640f, 641 pericardial, 549f, 549-550 Adrenal gland, 699-701 calcification of, 564t tumor of, 617 Adrenocorticotropic hormone, 600 Age-related pulmonary fibrosis, 395396 Aggressive bone lesion, 10-15, 13f, 14f Aging new bone, 4-5 Air-bronchogram sign, 380, 384f in paraquat poisoning, 440 in pneumonia, 408 Air colonography, 643-644 Air cystography, 679, 679f Air embolism, cystography-related, 678 Airflow obstruction in facial depression fracture, 195 Airway disease, 449-455 abnormal tracheal distention in, 450451 bronchial foreign body in, 451 bronchiectasis in, 453-454, 453-454f, 541f bronchitis in, 451-453 bronchocutaneous fistula in, 451 emphysema in, 454 laryngeal paralysis in, 449, 450t mass versus nodule in, 451 tracheal and bronchial parasites in, 451 tracheal collapse in, 449-450, 450b tracheal hypoplasia in, 449 tracheal polyps in, 451 tracheal tumors in, 451 tracheitis in, 449 Allergic bronchitis, 436, 437f, 452 Allergic pneumonia, 445f Alternate-side radiography in chest trauma, 400-404, 403f, 404f in intestinal obstruction, 620-621 in lung screening for cancer, 423-426 Alveolar consolidation, 380-383, 384f

726

Index ❚❚❚

Alveolar pattern, 395 Amputation arteriovenous fistula after, 180 mimicking thoracic radiographic disease indicator, 371f traumatic, 58, 61t Analog versus digital hip images, 351 Anatomic variations in anconeal process, 139-140, 139143f brain disease and injury and, 228 in coronoid process, 140f in lung patterns, 394 resembling cardiac radiographic disease indicators, 482, 483f, 484f resembling spinal radiographic diagnostic indictors, 251t resembling thoracic radiographic disease indicators, 368, 369t, 369-371f sternal, 398 Anconeal process anatomic variations in, 139-140, 139143f nonunion fracture of, 76f osteoarthritis in, 96, 97f osteochondritis in, 152, 154-155f Anemia, myelophthisic, 180 Aneurysmal bone cyst, 133t Angiocardiography, 496-498, 497t, 498f, 498t Angiography, 496-498, 497t, 498f, 498t in arteriovenous fistula, 180, 182f, 183f cerebral, 218, 219f portal, 587-590, 588f, 588t, 589f of soft tissue tumor, 137 subtraction, 67 Angiomatosis, vertebral, 264 Angiostrongylus vasorum, 408-409 Angular limb deformity, 17, 19f, 188f Ankylosis of head, 195, 196f, 197f Annular stricture, 715 Annulus fibrosus, 285 Anomalous blood vessels, 504 Anoxia, 21 Antegrade, compression-induced cystourethrography, 693-694 Antegrade ureterography, 676 Anterior chamber hyphema and, 239f, 240 sonography of, 237t Antifreeze poisoning, 671 Aonchotheca putorii, 599 Aorta coarctation of, 508, 515 enlargement of, 489-490, 490f, 493 fetal, 702-703 normal nonselective opacification time of, 497t, 498t optimal contrast deployment in selective angiocardiography, 498t thrombosis of, 538-540 transposition of great arteries and, 515

Aortic insufficiency, 512-513, 515f Aortic root enlargement, 484, 485f Aortic sinus rupture, 540 Aortic stenosis, 508, 511-512f, 516t Aorticopulmonary window, 507-508 Aortoiliac thrombus, 183-184 Aplasia of dens, 259f gallbladder, 586 Apophyseal fracture, 40, 43f Apophysis, 40 Arachnoid cyst, 227, 263 ARDS. See Acute respiratory distress syndrome. Arterial blockage by heartworms, 180 Arterial malformations, 513-516 Arterial thrombosis, 383t, 538-540 Arteriosclerosis, 538 Arteriovenous fistula, 180, 181-183f of ear, 235 exophthalmia and, 242 intraosseous, 133 Arthritic stifle, 36, 36f immune-mediated, 99, 99f osteophytes in, 13f, 94f posttraumatic, 95f Arthritis facetal, 303, 304f in osteoarthritis, 93-105 articular fracture and, 40 avascular necrosis and, 96-98, 97f capital physeal fracture and, 329 categorization of, 93, 94f, 95f in congenital elbow dislocation, 186 in dysplastic hip, 343-345f generative nature of, 93 gout and pseudogout and, 101, 105 hip dysplasia and, 94-96, 95f in injured stifle, 36, 36f intraarticular calcification, ossification, and fragmentation in, 98t, 98-99, 100f in Legg-Calv[ac]e-Perthes disease, 325 magnetic resonance imaging appearance of, 93 osteochondritis and, 96, 96f, 97f, 145, 145f, 146f periarticular osteophytes in, 9, 12f postsurgical, 99-101, 101-104f posttraumatic, 80f primary bone tumor versus, 119 radiographic appearance of, 93, 94f storage disease and, 105, 105f synovitis and, 93 septic, 117-118 Arthrography of bicipital tenosynovitis, 178, 179f of congenital elbow dislocation, 189f of coxal joint, 343f of osteochondritis in femoral condyle, 165f of shoulder, 159-161, 160-162f

Articular cartilage erosive lesions in, 98 MRI appearance of osteoarthritis and, 93 periarticular osteophytes in, 9, 13f Articular fracture, 40-41, 44f, 45f, 64t Artifactual mineralization, 561, 563f, 564t Artificial hip, 349-350, 350f Arytenoid, 356 Ascites, 543, 555-556, 556-557f, 558t, 559t Aspergillosis, 205t, 225, 225f, 412 Aspiration pneumonia, 408 Asthma, 436, 437f Atelectasis, 383, 385f, 395 cardiac shift and, 383t in chest trauma, 399-400, 401f, 404f compression, 381f postural, 368, 373f thyrotoxicosis and, 530f Athletic hypertrophy, 501 Atlantoaxial dislocation, 258, 259f Atony, gastric, 611-612 Atrial septal defect, 504, 506-507 Atrial standstill, 538, 539f Atrial thrombus, 545, 547f Atrial tumor, 545, 546f Atrioventricular heart block, 537-538, 538f Atrioventricular insufficiency, 517-518, 517-523f Atrioventricular regurgitation, 517518, 517-523f Atrium catheter-related injury of, 497t normal nonselective opacification time of, 497t, 498t optimal contrast deployment in selective angiocardiography, 498t Aural canalography, 231 Aural polyp, 234-235, 235f Aural tumor, 235 Auricular tumor, 545, 546f Autoimmune hemolytic anemia, 662, 662f Automatic biopsy needle, 721 Avascular necrosis of femoral head, 325, 326-327f osteoarthritis and, 96-98, 97f of subphyseal bone of femoral neck, 329 Avulsion of abdominal wall, 569-570, 571f of gastrocnemius, 178-179, 179f mesenteric, 639, 641 Avulsion fracture, 41, 45t, 46f differential diagnosis in, 98t dislocation and hip and, 333 patella and, 177 of long digital extensor tendon, 23 of prepubic eminence, 571f Azygous continuation of caudal vena cava, 496-497, 497t

❚❚❚ Index

B B-mode ultrasound of eye, 236, 237b Baby teeth, 213, 213f Back pain in spinal tumor, 317 Bacterial infection of bladder, 682 extremital, 107, 107f, 109t of hip, 353 new bone production in, 245f in peritonitis, 572 in pleuritis, 378f in pneumonia, 408-412f in tracheitis, 449 Bacteriologic analysis in abdominal gunshot wound, 568 Ballooning of trachea, 364 Barium colonography, 643, 644f Barium enema, 643, 644f Barium film of abdominal hernia, 637 of duodenal ulcer, 617 in esophageal transport disease, 467 gastric, 594-595, 595t, 596f in gastric torsion, 603-604, 604f, 605f in infiltrative bowel disease, 618, 619t of intestinal intussusception, 630 in intestinal obstruction, 622-625, 623-629f in intestinal torsion, 635-636 of intraabdominal intestinal entrapment, 636 iodine film versus, 616 normal intestinal variations in, 615 of pyloric obstruction, 608, 608f of small intestine tumor, 832 of ulcerative colitis, 647f Barium impregnated polyethylene spheres, 643 BB pellet, radiographic and sonographic features of, 41t Belly stripes, 568 Benign bone tumor, 121, 122t Benign cystic hyperplasia of gallbladder, 586 Benign lung tumor, 431 Benign pericardial effusion, 518, 519t, 523f Benign prostatic hypertrophy, 689-690f Biceps brachii tendon mineralization, 178 Bicipital tenosynovitis, 178, 178f, 179f Bile duct carcinoma, 583 Bile duct cystadenoma, 582 Bile leakage into peritoneal cavity, 572 Biliary atresia, 186 Biliary cystadenocarcinoma, 582, 583f Biliary cystadenoma, 582, 583f Biliary mucocele, 586-587, 586-587f Biliary obstruction, 583 Biliary pseudocyst, 721 Biopsy brain, 228-229 choosing device for, 721 computed tomography-guided, 719720, 720t

Biopsy—cont’d needle enhancement in, 720 potential injuries in, 721 renal, 663 thoracic, 390-391 ultrasound-guided, free-hand, 719 Bipartite sesamoids, 54, 60f Biplanar endplate fracture, 280, 281f Bite wound arteriovenous fistula after, 180 gas pockets in, 23f infection and, 106, 107, 107f penile, 718 peritonitis and, 572 in punctured or ruptured trachea, 364 retroperitoneal air and, 560 scrotal injury in, 716 soft tissue swelling in, 19f Bladder, 677-688 abnormal bowel distribution patterns and, 617 calcification of, 561f, 564t, 688 calculi of, 682-685, 683-684f cystography of, 678-679, 679b, 679680f, 681t diverticula of, 681 emphysematous cystitis and, 681 feline idiopathic cystitis and, 680-681 gas in, 558-560 hemorrhage of, 685-688, 687f intrapelvic, 682 pelvic fracture and, 322 plain films of, 678, 678b retroflexion of, 681-682 rupture of, 685-686f tumor of, 682-683f hydroureter secondary to, 675 ureteral outlet obstruction in, 671 ultrasound of, 680, 680f, 681t Bladder volume, 680 Bladder wall thickness evaluation, 680, 681t Blastomycosis, 111, 115, 115f, 116f chylothorax in, 422t intracranial, 226 mediastinal, 464, 464f pulmonary, 412-415f Bleb, 386 Bleeding into anterior chamber, 239f, 240 Blind pouch, 639 Blind sac, 639 Bloat, 601, 601b Block vertebrae, 249, 253f, 256, 256t, 258 Blood in consolidated lung, 382 in pleural fluid, 377t Blood flow, intracardiac, 500-501, 502f Blood supply fracture nonunion and, 70 to proximal femoral growth plate, 329 Bloody tap, 291 Blooming of lateral ventricle, 220

727

Blunt trauma intestinal, 639-641 mediastinal bleeding in, 456 Bone abscess, 119, 119f, 120f Bone cyst, 133, 133f Bone density cranial, 194 differential diagnosis for, 98t of jaw, 193-194 of new bone, 5 tenosynovitis and, 178 Bone disease congenital and developmental, 167176 disseminated idiopathic hyperostosis in, 176 hypertrophic pulmonary osteoarthropathy in, 168-169, 173f, 174f hypochondroplastic dwarfism in, 173, 174t, 175f hypothyroidism in, 176 metaphyseal osteopathy in, 167168, 171f, 172f nutritional secondary hyperparathyroidism in, 175 panosteitis in, 167, 168-170f partial absence of distal limb in, 167 retained cartilage core in ulnar metaphysis in, 169, 173, 175f role of dietary calcium in, 167, 168b Scottish fold osteodystrophy in, 175-176 skeletal and ocular dysplasia in, 176 in osteochondritis, 138-166 of anconeal process, 152, 154-155f classification schemes in, 163t, 163-165, 165t, 166t commonly affected breeds, 138 differential diagnosis in intraarticular bone or bone-like densities, 98t of distal humeral epiphysis, 152, 156, 157f of elbow, 138-152. See also Elbow. osteoarthritis and, 96, 96f, 97f of shoulder, 156-161, 157-162f of stifle, 162-163, 165f of tarsal joint, 161-162, 162-164f unusual locations of, 9, 10f sacral, 268 Bone infarct, 180 Bone infection, 106-120 abscess and, 119, 119f, 120f blastomycosis in, 111, 115, 115f, 116f cancer versus, 118-119 chronicity of, 116-117, 116-119f coccidioidomycosis in, 111, 114f hepatozoonosis in, 107-111 histoplasmosis in, 115-116 new bone formation and, 4f nonspecific bacterial, 107, 107f, 109t nuclear imaging of, 107, 108t pathologic fracture and, 116, 116f

728

Index ❚❚❚

Bone infection—cont’d Phialemonium ovatum in, 116 radiographic disease indicators of, 107 radiology of, 106-107 septic arthritis and, 117-118 surgical, 107, 110-114f terminology in, 106 Bone lesion in leishmaniasis, 180-181 periosteal new bone and, 4, 4f, 5f radiation-induced, 180 as radiographic disease indicator, 10-15 aggressive, 10-15, 13f, 14f nonaggressive, 15, 15f tumorlike, 133t, 133-134, 134f Bone loss in digital tumor or inflammation, 132 in mandibular infection, 244 in mandibular tumor, 199, 202f in osteogenesis imperfecta, 190 in osteomyelitis, 107 as radiographic disease indicator, 10-15 aggressive lesions and, 10-15, 13f, 14f nonaggressive lesions and, 15, 15f of spine, 254-256, 255f, 256f in renal osteodystrophy, 194 Bone reaction, 1 Bone scan in hip infection, 353 for metastatic bone tumor, 124 in osteomyelitis, 107, 109t Bone tumor, 121-136 aggressive bone lesion in, 14f benign, 121 digital tumor versus infection, 131133 increased cranial bone density in, 194 infarct and, 180 invading soft tissue tumor and, 134135, 134-136f of joint, 124, 130, 132f localized bone loss in vertebra in, 255, 255f metastatic melanoma in, 130 new bone deposition in, 13f osteomyelitis versus, 118-119 parosteal sarcoma in, 130-131 periosteal new bone and, 4, 4f, 5f primary, 121-123, 122t, 123-129f primary hemangiosarcoma in, 131 pulmonary metastasis in, 426, 426f radiologic findings in, 123-124, 129-131f secondary, 123 skull, 199-203, 200-203f, 203b tumorlike bone lesions and, 133t, 133-134, 134f Bony union, 63, 67, 68f Bookend spleen, 575, 576f

Bowel, 614-642 abscess of, 639f, 641 adhesion of, 640f, 641 bowel distribution pattern and, 616617 calcification of, 564t congenital malformations of, 638-639 diaphragmatic hernia and, 475f, 477f, 478t displacement of by abdominal hernia, 637 by pyometra, 709f distention of, 614, 615f duodenal thickening secondary to pancreatitis, 617-618, 618f duodenal ulcer and, 617 enteritis and, 618-619, 620-621f foreign body in, 565f, 619-627 barium and iodine films of, 622625, 623-629f fixed, 627, 630f free linear, 627 as incidental finding, 619 metallic, 619 obstructive pattern and, 621-622, 622t plain films of, 620-621, 622f sonography of, 625 gas in, 557-558 impaction of, 637, 638f incarceration of, 636 infiltrative bowel disease and, 618, 619t inflammatory bowel disease and, 618 intussusception of, 627-630, 631-632f leiomyosarcoma and leiomyoma of, 633, 634f lymphosarcoma of, 632-633, 633f normal barium film variations of, 615 normal iodine films of, 615-616 normal plain film variations of, 614615, 615f normal sonographic appearance of, 617, 617t parasitic infection of, 637 perforation of, 634b, 634-635 peritonitis and, 572 pneumoperitoneum in, 559t potential sonographic indicators of disease, 617 protein-losing enteropathy and, 637 short-bowel syndrome and, 638 torsion of, 559t, 635-636, 635-636f trauma to, 639-641 tumor of, 630-632, 632f Bowel content, 614-615 Bowel distribution pattern, 616-617 Bowel fluid, 614 Bowel-wall thickness, 614 Brain disease and injury, 218-230 abscess in, 226, 226t aspergillosis in, 225, 225f biopsy in, 228-229 blastomycosis in, 226 cerebrovascular accident in, 228

Brain disease and injury—cont’d choice of imaging study in, 220, 220t computed tomographic evaluation of postoperative brain in, 229 computed tomography in, 219, 220t craniocerebral trauma in, 220-221, 221b cysts in, 227-228 encephalitis in, 224-225, 225b focal granulomatous meningoencephalitis in, 221, 221b hydrocephalus in, 226-227, 227f magnetic resonance imaging in, 219220, 220t necrotizing meningoencephalitis in, 225 normal anatomic variants and, 228 normal ventricular variation and, 220 nuclear medicine imaging in, 218 seizure in, 221 sonography in, 218, 219t special radiographic procedures in, 218, 219f tumor in, 221-224, 222t, 223-224f Branchial cyst, 362, 462 Breathing effects on diaphragm, 473 normal physiologic variants resembling cardiac radiographic disease indicators and, 481, 482f Brodifacoum, 533 Bronchial fracture, 405 Bronchial obstruction, 383t Bronchial parasites, 451 Bronchial pattern, 395 Bronchiectasis, 453-454, 453-454f, 541f Bronchiole-alveolar cell carcinoma, 424t Bronchitis, 451-453 allergic, 436, 437f Bronchocutaneous fistula, 451 Bronchography in bronchiectasis, 453 in chronic bronchitis, 452-453 in pneumomediastinum, 405 Bronchointerstitial lung disease, 536 Bronchopneumonia, 469f Bronchoscopic evaluation in tracheal collapse, 450, 450b Brucella canis, 306 Bruising, 21 of abdominal wall, 568 of chest wall, 397 cystography-related, 678 intracerebral, 220-221 myocardial, 549 penile, 718 Budd-Chiari-like syndrome, 558t Bulging disk, 272t, 300 Bulla, 386 chest trauma and, 399-400, 401f inflammatory disease of, 231-234, 232f inflammatory polyps and, 234-235, 235f

❚❚❚ Index

Bulla—cont’d normal, 232-234f otolith and, 235 Bursitis, 23, 26f Butterfly fragment, 42f Butterfly vertebra, 258

C Calcaneus dislocation of superficial digital flexor tendon and, 180 longitudinal fracture of, 58f nonunion of fracture, 71f Calcification abdominal, 561-563f, 564t bladder, 688 in chronic pancreatitis, 651 of disk, 252f in disseminated idiopathic hyperostosis, 176 in feline primary lung tumor, 423 gallbladder, 586, 587f gastric, 611, 611f hepatic, 587f intestinal, 564t in osteoarthritis, 98t, 98-99, 100f of paraprostatic cyst, 691f prostatic, 564t pulmonary, 445, 445f, 446 pulmonary artery, 446 soft tissue, 22-23, 25f, 26f ureteral, 564t Calcifying tendinopathy, 178 Calcinosis circumscripta, 264, 265t Calcium pyrophosphate dihydrate deposition disease, 101, 105 Calcium role in bone disease, 167, 168b Calculi biliary, 561, 585 bladder, 682-685, 683-684f lithotripsy for, 677 morphology of, 564t renal, 561, 562f ureteral, 672, 672t, 674f Callus fracture healing and, 63 in secondary ankylosis, 195 Callus impingement, 695, 695f Canalogram, 231 Cancer biopsy-related seeding in, 721 cause of peritoneal fluid, 558t chronic nasal disease in dogs and, 205t colonic, 646, 648f disseminated intravascular coagulation versus, 441 extremital infection versus, 117f, 118119 gastric, 606-607, 607f intraabdominal calcification in, 561, 561f liver, 581-582, 581-582f nasal cavity, 204-210 computed tomography in, 208209, 209b, 209t

Cancer—cont’d nasal cavity—cont’d deviation and destruction of vomer in, 193 evaluation of postoperativepostradiation nasal radiographs in, 206-208, 209f fluid, bone destruction, and nasal conchal pattern in, 204-205, 206b, 207-208f infection versus, 205-206, 206t magnetic resonance imaging in, 209-210 nasal septum and cribriform plate and, 204 rhinography in, 208 pancreatic, 587f, 653 prostate, 691-692, 693f ureteral outlet obstruction and, 671, 672t Cancer bone, 4 Canine abdominal malignant histiocytosis, 656-657 Canine leukocyte adhesion deficiency, 244 Canine parvoviral enteritis, 614, 619 Canine superficial necrolytic dermatitis, 580 Cannulation of salivary duct, 361 Capital physeal fracture, 329, 331-332f Capsulitis, traumatic, 34f Carcinoma choroid plexus, 223-224 mammary, 429 pancreatic, 653 prostatic, 691-692, 693f tracheal, 451 urethral, 694-695 Carcinomatosis, 558t Cardiac catheterization, 496-498, 497t in aortic stenosis, 508, 511f in pulmonic stenosis, 508, 509f Cardiac compression, 543 Cardiac cycle, 481, 482f Cardiac edema, 433 Cardiac output M-mode echocardiography of, 501 mesothelioma and, 547 Cardiac pacemaker, 552, 553f Cardiac radiographic disease indicators, 485-492 abnormal cardiac contour in, 488489, 488-489f aortic or main pulmonary arterial enlargement in, 489-490, 490f decreased heart size in, 486, 487f in dilated cardiomyopathy, 523 in heart failure, 543-544f, 543-545 in heartworm disease, 535 increased heart size in, 488, 488f normal anatomic variations resembling, 482, 483f, 484f normal physiologic variants resembling, 481, 482f pleural fluid in, 490-491, 491f pneumopericardium in, 491-492 positional abnormality in, 489-489f

729

Cardiac radiographic disease indicators—cont’d positional variants resembling, 485486, 487f in pulmonary embolism, 444 pulmonary hyperemia in, 490, 490f pulmonary oligemia in, 490, 491f Cardiac shift, 380, 381f, 382f, 383t chest trauma and, 399 interior atelectasis and, 385f in lung-lobe torsion, 436 pectus excavatum and, 484f pneumonia and, 407 postural atelectasis and, 368, 372f, 373f in thyroid-induced myopathy, 527f Cardiac silhouette analysis, 493-495, 494f, 494t Cardiac tamponade, 533 Cardiac trauma, 549f, 549-550 Cardiac tumor, 545-548, 546-547f Cardiac ultrasound, 499-503 of aortic stenosis, 508, 512f athletic hypertrophy and, 501 of atrial septal defect, 504 of atrial tumor, 545, 547f congenital muscular dystrophy and, 501-502 interpretation of Doppler tracing in, 500-501, 502f M-mode echocardiography and, 501 normal appearances in, 499, 500f overall approach in, 499-500 of patent ductus arteriosus, 506 placement of intravascular embolization coils in, 500 of pulmonic stenosis, 508, 510f in tetralogy of Fallot, 512 of ventricular septal defect, 504-505, 505f Cardiomegaly in atrial septal defect, 504 in atrial standstill, 538, 539f cardiac edema and, 433 as cardiac radiographic disease indicator, 488, 488f cardiac silhouette analysis and, 493495, 494f, 494t double cardiac silhouette sign versus, 484 in Ebstein anomaly, 514f in heartworm disease, 535, 536f in mitral endocardiosis, 517, 518f, 521f in patent ductus arteriosus, 506f in pulmonic stenosis, 508, 509f in ventricular septal defect, 504 Cardiomyopathy chylothorax and, 422t dilated, 518, 523-524, 524-525f hypertrophic, 491f, 524-525, 526-531f Cardiopulmonary silhouette sign, 377f, 434f Cardiothoracic ratio, 494 Cardiovascular disease, 517-542 angiocardiography in, 496-498, 497t, 498f, 498t

730

Index ❚❚❚

Cardiovascular disease—cont’d aortic sinus rupture in, 540 arterial thrombosis in, 538-540 atrial standstill in, 538, 539f benefits of presurgical thoracic screening and, 517, 518t cardiac radiographic disease indicators in, 485-492 abnormal cardiac contour in, 488489, 488-489f aortic or main pulmonary arterial enlargement in, 489-490, 490f decreased heart size in, 486, 487f in dilated cardiomyopathy, 523 in heart failure, 543-544f, 543-545 in heartworm disease, 535 increased heart size in, 488, 488f normal anatomic variations resembling, 482, 483f, 484f normal physiologic variants resembling, 481, 482f pleural fluid in, 490-491, 491f pneumopericardium in, 491-492 positional abnormality in, 489-489f positional variants resembling, 485-486, 487f in pulmonary embolism, 444 pulmonary hyperemia in, 490, 490f pulmonary oligemia in, 490, 491f cardiac silhouette analysis in, 493495, 494f, 494t cardiac ultrasound in, 499-503 athletic hypertrophy and, 501 congenital muscular dystrophy and, 501-502 interpretation of Doppler tracing in, 500-501, 502f M-mode echocardiography and, 501 normal appearances in, 499, 500f overall approach in, 499-500 placement of intravascular embolization coils in, 500 congenital, 504-516, 516t anomalous vessels in, 504 aortic and pulmonic insufficiency in, 512-513, 515f aortic stenosis in, 508, 511-512f aorticopulmonary window in, 507-508 atrial septal defect in, 504 Ebstein anomaly in, 512, 514f mitral and tricuspid insufficiency in, 512, 513f mitral and tricuspid stenosis in, 511 patent ductus arteriosus in, 505507, 506f pulmonic stenosis in, 508, 509f, 510f tetralogy of Fallot in, 511-512 truncus arteriosus in, 513-514 ventricular septal defect in, 504505, 505f cor pulmonale in, 540-541, 541f dilated cardiomyopathy in, 518, 523524, 524-525f

Cardiovascular disease—cont’d endocardiosis in, 517-518, 517-523f, 519t endocarditis in, 528, 531-532f heartworm disease in, 533-537 canine, 533-536, 536f feline, 536-537, 537f hypertrophic cardiomyopathy in, 524-525, 526-531f inherited ventricular tachycardia in German shepherds in, 538 ischemic, 538 myocarditis in, 525-528 pericardial disease in, 533, 534f, 535f peritoneal fluid in, 558t pulmonary-induced, 551, 551f third-degree heart block in, 537-538, 538f Cardiovascular imaging, 481-553 in acquired heart disease, 517-542 aortic sinus rupture in, 540 arterial thrombosis in, 538-540 atrial standstill in, 538, 539f benefits of presurgical thoracic screening and, 517, 518t cor pulmonale in, 540-541, 541f dilated cardiomyopathy in, 518, 523-524, 524-525f endocardiosis in, 517-518, 517523f, 519t endocarditis in, 528, 531-532f heartworm disease in, 533-537, 536f, 537f hypertrophic cardiomyopathy in, 524-525, 526-531f inherited ventricular tachycardia in German shepherds in, 538 ischemic, 538 myocarditis in, 525-528 pericardial disease in, 533, 534f, 535f third-degree heart block in, 537538, 538f angiocardiography in, 496-498, 497t, 498f, 498t cardiac radiographic disease indicators in, 485-492 abnormal cardiac contour in, 488489, 488-489f aortic or main pulmonary arterial enlargement in, 489-490, 490f decreased heart size in, 486, 487f in dilated cardiomyopathy, 523 in heart failure, 543-544f, 543-545 in heartworm disease, 535 increased heart size in, 488, 488f normal anatomic variations resembling, 482, 483f, 484f normal physiologic variants resembling, 481, 482f pleural fluid in, 490-491, 491f pneumopericardium in, 491-492 positional abnormality in, 489-489f positional variants resembling, 485-486, 487f pulmonary hyperemia in, 490, 490f pulmonary oligemia in, 490, 491f

Cardiovascular imaging—cont’d cardiac silhouette analysis in, 493495, 494f, 494t in congenital heart disease, 504-516, 516t anomalous vessels in, 504 aortic and pulmonic insufficiency in, 512-513, 515f aortic stenosis in, 508, 511-512f aorticopulmonary window in, 507-508 atrial septal defect in, 504 cardiac ultrasound in, 499-500 Ebstein anomaly in, 512, 514f mitral and tricuspid insufficiency in, 512, 513f mitral and tricuspid stenosis in, 511 patent ductus arteriosus in, 505507, 506f pulmonic stenosis in, 508, 509f, 510f tetralogy of Fallot in, 511-512 truncus arteriosus in, 513-514 ventricular septal defect in, 504505, 505f echocardiography in, 499-503 athletic hypertrophy and, 501 of cardiac pacemaker, 552 congenital muscular dystrophy and, 501-502 contrast, 506-507 interpretation of Doppler tracing in, 500-501, 502f M-mode, 501 normal appearances in, 499, 500f overall approach in, 499-500 placement of intravascular embolization coils in, 500 of heart trauma, 549f, 549-550 of heart tumor, 518, 519t, 523f, 545548, 546t, 546-547f of pacemaker, 552, 553f patterns of heart failure and, 543544, 543-544f in pulmonary embolism, 444 of pulmonary-induced heart disease, 551, 551f Carpal sprain, 27-28, 28-34f, 29t posttraumatic osteoporosis in, 15, 17f Carpus extraskeletal chondroma of, 134f immunoarthritis in, 99, 99f location of sesamoid bones in, 45t new bone after infection, 7f synovial sarcoma of, 132f Cartilage, retained, 169, 173, 175f Cartilaginous bone tumor, 122t Castration, 715 Casts, 62-64f Cat absolute kidney size of, 663, 664t biliary cystadenoma in, 582, 583f cardiac measurements in, 494 dental disease in, 212-216, 213b, 213216f

❚❚❚ Index

Cat—cont’d diffuse liver disease in, 579, 579b elbow sprain, fracture, and dislocation in, 18f endocarditis in, 528 esophageal transport disease in, 468469, 469t hip dysplasia in, 351, 351f hypertrophic cardiomyopathy in, 524-525, 526-531f infectious peritonitis in, 572 lesion prevalence in intervertebral disk disease, 286, 286f loose joint bodies in, 9 nasopharyngeal polyps in, 234-235, 235f normal appearances in cardiac ultrasound, 499 normal gastric emptying time in, 597 normal intestinal iodine films of, 616 normal nonselective opacification times in, 498t normal sonographic appearance of intestine, 617, 617t normal sonographic appearance of stomach, 597 peritoneal effusion in, 555 primary lung tumor in, 423, 424t protocol for contrast radiography in, 595t pulmonary embolism in, 444 splenic disease in, 655 splenic hemangiosarcoma in, 657658 steatitis in, 572-573 thyroid masses and hyperthyroidism in, 363-364 toxoplasmosis in, 411 Cataracts, 236-238, 237b, 237t, 237-239f Catheter, intravenous fragment of, 184, 184f Cauda equina syndrome, 268b, 268t, 268-270, 270-271f, 272t, 273t Caudal cervical spondylomyelopathy, 264-267, 265-268f Caudal cruciate ligament, 98t Caudal lumbarization, 262 Caudal mediastinal compartment, 456 Caudal vena cava adrenal tumor and, 700 azygous continuation of, 496-497, 497t fetal, 702-703 obstruction from pericardial adhesions, 550 pericardial disease and, 533 thrombosis of, 558t Caval syndrome, 536 Cavernous sinus venography, 218, 219f, 241 Cavitary lung lesion, 386, 387t, 388f in chest trauma, 399-400, 401f in lung tumor, 427 Cavitation in biliary cystadenocarcinoma, 582, 583f in chronic pancreatitis, 651

Cavitation—cont’d prostatic, 689 in splenic hemangiosarcoma, 660f Cavities, 215 Cecocolic intussusception, 644-646 Cecum normal appearance of, 643 perforation of, 559t Cellulitis of hip, 353 Cement coverage in hip replacement, 350, 350f Central arterial thrombosis, 538-540 Central cord injection in myelography, 299 Central lymphangiography, 422 Cephalhematoma, 197 Cephalic vein, intravenous catheter fragment in, 184, 184f Cephalic venography, 459 Cerebral angiography, 218, 219f Cerebral infarction, 228 Cerebrospinal fluid analysis after myelogram, 291, 291f spinal arachnoid cyst and, 263 Cerebrovascular accident, 228 Certification programs in hip dysplasia, 339 Cervical diskography, 300 Cervical mass, 358, 358f, 359f Cervical spine abscess of, 308f block vertebrae in, 253f, 256f, 258 discospondylitis of, 252f dislocation of, 259f, 276 double line sign in, 297f fracture of, 275-276, 276-278f hypervitaminosis A and, 319 intervertebral disk disease in, 286 oblique view of, 250f osteosarcoma of, 255f spondylopathy of, 264-267, 265-268f tumor of, 315f, 316f, 317f Chemical peritonitis, 572 Chemodectoma, 546t Chest drain, 403-404 Chest trauma, 397-406 as cause of pleural fluid, 376t cavitary lung lesions and, 386 chest wall injury in, 397, 398f diaphragmatic rupture in, 473, 475477f gunshot wounds in, 404-405, 405f, 406f lung injury in, 399-404 intrapulmonary hemorrhage in, 399, 400f laceration, collapse, and cavitary lesions in, 399-400, 401f posttraumatic pneumothorax in, 400, 401-403f postural radiography in, 400-404, 403f, 404f mediastinal injury in, 405-406 pleural hemorrhage and hematoma in, 399 sternal fracture in, 397-398, 398f sternal tumors, infections, and gas in, 398-399, 399f

731

Chest wall injury, 397, 398f Chisel fracture, 41, 46f, 59f Cholangiocarcinoma, 583 Cholangiocellular carcinoma, 582, 583 Cholangiohepatitis, 579, 579b, 587f Cholecystitis, 585 Cholecystography, 585 Choledocholithiasis, 585 Cholelithiasis, 585 Cholestasis, 186, 187f Chondrium, 2 Chondroma, tracheal, 451 Chondrosarcoma, 123 periosteal new bone and, 4 spinal, 317 sternal, 398-399, 399f tracheal, 451 Choroid, 237t Choroid plexus tumor, 223-224 Chronic bacterial pleuritis, 378f Chronic bronchitis, 452 Chronic cor pulmonale, 444 Chronic cystitis, 679 Chronic interstitial pneumonia, 551, 551f Chronic lymphocytic-plasmacytic gastritis, 609 Chronic nephritis, 667f Chronic pancreatitis, 651, 651f Chronic pneumonia, 407 Chronic polyostotic immunoarthritis, 98 Chronic renal failure, 671 Chronic valve disease, 517-518, 517523f Chronicity of extremital infection, 116117, 116-119f Chyle, 377t, 378f, 490 in peripancreatic abscess, 653 in peritoneal fluid, 558t Chylothorax, 421, 422t, 518 Chylous ascites, 558t Chylous effusion, 459 Ciliary body, 237t Cirrhosis, 580, 580f Cisternal puncture in myelography, 291, 295-298, 298f Closed fracture, 41 Clostridium gas in gallbladder and, 557 in hepatic cyst, 583 in peritonitis, 559t Coccidioidomycosis, 111, 114f, 412-415, 416f Coccygeal fibrosarcoma, 255f Coccygeal fracture, 280 Coccygeal nerve, 268t Coiled spring sign, 630, 632f, 646 Colic, acute abdominal, 566, 566b Colitis, 646, 647f Collapse of trachea, 449-450, 450b Colon, 643-649 abnormal distention of, 646 abnormally long, 648-649 air colonography of, 643-644 barium enema and, 643, 644f cancer of, 646, 648f

732

Index ❚❚❚

Colon—cont’d cecocolic intussusception and, 644646 colonic marking of, 644, 645f colonic transit time using synthetic markers, 643 double-contrast colonography of, 644 ileocolic intussusception and, 646 impaction of, 646, 648f normal appearance of, 643 perforation of, 559t, 646-648 pneumatosis coli and, 648, 649f stenosis of, 646 torsion of, 648, 649f ulcerative colitis and, 646, 647f Colonic marking, 644, 645f Colonography air, 643-644 barium, 643, 644f double-contrast, 644 Color Doppler, 502 of spinal cord, 319 Combined laryngeal-pharyngealesophageal foreign body, 360 Combined linear tomography and cisternography in brain disease and injury, 218, 219f in pituitary adenoma, 222 Comminuted fracture, 41, 47f, 66f, 67f Common arterial trunk, 513 Common pharynx, 355 Communicating syringomyelia, 264 Compartmental syndrome, 21-22 Compensatory bronchiectasis, 453 Compensatory renal hypertrophy, 665 Complex multilocular bone cyst, 133t Compression cardiac, 543 epiphysis and, 40 spinal cord, 263-274 cauda equina syndrome in, 268b, 268t, 268-270, 270-271f, 272t, 273t in cervical spinal fracture, 276 dermoid sinus in, 263 epidermoid cyst in, 263 facetal, juxtaarticular, synovial, and ganglion cysts in, 264 in histiocytosis, 462 hydromyelia in, 264 in intravertebral disk herniation, 300 meningocele in, 264 meningomyelocele in, 264 spinal arachnoid cyst in, 263 in spinal tumor, 310, 311-313f syringomyelia in, 264, 265t tumoral calcinosis in, 264, 265t vertebral angiomatosis in, 264 Wobbler syndrome in, 264-267, 265-268f Compression atelectasis, 381f Compression fracture, 41, 47f congenital hemivertebra versus, 256t of thoracic spine, 279f Compression stress maneuver, 37

Computed tomography of bladder, 680 in brain disease and injury, 219, 220t of cataracts, 237-238 in cauda equina syndrome, 273t in cervical spinal fracture, 275, 276 in cervical spondylopathy, 267 of cranial tumor, 199, 200f, 203b of craniomandibular osteopathy, 244 in discospondylitis, 306 in encephalitis, 224, 225b of facial tumor, 199, 200f, 201f, 203b in focal granulomatous meningoencephalitis, 221b of hip infection, 353 of inflammatory polyp of ear, 235 in lumbosacral stenosis, 269-270, 270b, 273t of meningioma, 221 myelography with, 298-299 of nasal cavity tumor, 208-209, 209b, 209t in necrotizing meningoencephalitis, 225 of normal canine abdomen, 566 in orbital disease, 241 in osteochondritis, 147, 147b, 152, 153f in otitis media, 231 of pituitary adenoma, 222-223 in pneumonia, 408 of pneumothorax, 379 positional variants resembling thoracic radiographic disease indicators and, 368 of postoperative brain, 229 of spinal arachnoid cyst, 263 in spinal survey, 319 of spinal tumor, 310, 315 in spondylosis, 303 in stroke, 228 of ureter, 677 Computed tomography-guided biopsy, 719-720, 720t Concha aspergillosis and, 225, 225f radiographic disappearance of, 193 Conduit, 564t Condylar deformity, 195-196, 197f Condyloid process fracture, 195, 196f Configuration of new bone, 5 Congenital bone disease, 167-176 disseminated idiopathic hyperostosis in, 176 hypertrophic pulmonary osteoarthropathy in, 168-169, 173f, 174f hypochondroplastic dwarfism in, 173, 174t, 175f hypothyroidism in, 176 metaphyseal osteopathy in, 167-168, 171f, 172f nutritional secondary hyperparathyroidism in, 175 panosteitis in, 167, 168-170f partial absence of distal limb in, 167

Congenital bone disease—cont’d retained cartilage core in ulnar metaphysis in, 169, 173, 175f role of dietary calcium in, 167, 168b Scottish fold osteodystrophy in, 175176 skeletal and ocular dysplasia in, 176 Congenital brain cyst, 227 Congenital cor pulmonale, 551 Congenital disease of eye, 241 Congenital epiphyseal dysplasia, 325328, 328f, 332-333, 333f Congenital heart disease, 504-516, 516t anomalous vessels in, 504 aortic and pulmonic insufficiency in, 512-513, 515f aortic stenosis in, 508, 511-512f aorticopulmonary window in, 507508 atrial septal defect in, 504 cardiac ultrasound in, 499-500 Ebstein anomaly in, 512, 514f mitral and tricuspid insufficiency in, 512, 513f mitral and tricuspid stenosis in, 511 patent ductus arteriosus in, 505-507, 506f pulmonic stenosis in, 508, 509f, 510f tetralogy of Fallot in, 511-512 truncus arteriosus in, 513-514 ventricular septal defect in, 504-505, 505f Congenital hemivertebra, 256t, 256-257 Congenital intestinal hypoplasia, 638 Congenital malformations orofacial, 244, 246f of small intestine, 638-639 spinal, 258-262 atlantoaxial dislocation in, 258, 259f blocked vertebrae in, 258 hemivertebra in, 258, 259-261f lumbarization in, 258-262, 261f sacralization in, 261f, 262 spinal disease versus, 256t temporomandibular, 195-196, 197f ureteral, 673, 675-676f urethral and vaginal, 715 Congenital muscular dystrophy, 501502 Congenital pulmonary cyst, 446 Congenital pyloric stenosis, 610t Congenital renal disease, 665-666, 666f Congenital ureterocele, 672t Congestive heart failure in aorticopulmonary window, 507 in atrial standstill, 539f cardiac edema in, 433 cardiac tumor and, 545 as cause of pleural fluid, 376t chylothorax in, 422t cor pulmonale and, 541f expiratory film mimicking of, 368, 371f, 374f in mitral endocardiosis, 517, 519-522f in patent ductus arteriosus, 505 patterns of, 543-544, 543-544f

❚❚❚ Index

Congestive heart failure—cont’d in pericardial rupture, 549, 549f pleuropneumonia versus, 420 Consolidation, pulmonary, 380-383, 384f after near drowning, 439, 439f after near strangulation, 439, 439f, 440f in bronchiectasis, 454f chest trauma and, 403f in electric shock, 440 in lung-lobe torsion, 436 in pneumonia, 407-408 pulmonary metastasis versus, 427f in warfarin poisoning, 440 Constricted pericarditis, 533 Contextual diagnosis, 194, 393 Continuous-wave Doppler in atrial standstill, 540f in mitral endocardiosis, 521-523f in thyroid-induced myopathy, 529f Contrast backup phenomenon, 294 Contrast echocardiography, 506-507 Contrast media, 361 Contrast pleurography, 420 Contrast reaction in excretory urography, 664 Contrast-related hematuria, 685-688, 687f Contrecoup injury, 220 Contusion lung, 399, 400f myocardial, 549 Cor pulmonale, 444, 536, 540-541, 541f, 551, 551f Cor triatrium dexter, 515-516 Cor triatrium sinister, 515 Coracoid process osteochondritis, 160 Coralization, 116-117, 117f in hypertrophic pulmonary osteoarthropathy, 175f in osteosarcoma, 122, 122f Cord/canal ratio, 267 Cord compression in cervical spinal fracture, 276 in intravertebral disk herniation, 300 in spinal tumor, 310, 311-313f Cord edema, 300 Cord swelling in disk disease, 298, 299 Core decompression, 97 Cornea abrasion of, 238 sonography of, 237t Corner fracture, 46, 48f Corniculate process, 356 Coronary artery, catheter-related injury of, 497t Coronary sinus, pacemaker and, 552 Coronoid process anatomic variations in, 140f osteochondritis in, 94f, 96f, 138-140, 144-146f, 145, 150f Cortical bridge, 111, 114f, 115f Costochondral junction calcification, 563f Cough in primary lung tumor, 423 in tracheal collapse, 450

Coup injury, 220 Coxal arthroplasty, 349-350, 350f Coxal joint, 321-353 avascular necrosis of femoral head and, 325, 326-327f congenital epiphyseal dysplasia and, 325-328, 328f digital versus analog images of, 351 fractures and dislocations of, 329337, 334-337f acetabular, 329, 330f capital physeal, 329, 331-332f epiphysiolysis of femoral head and, 329-332 femoral head, 332-333, 333f femoral neck, 333, 334f multiple injuries in, 323f paracoxal mass in Doberman pinchers and, 337 postoperative assessment of femoral ostectomy muscle flap and, 334-337 proximal femoral, 329 spinal cord malacia and, 319 trochanteric, 333, 334f infections of, 353 normal canine, 339, 340-341f radiographic disease indicators of, 321 sacroiliac diastatic fracture and, 49f soft tissue sarcoma of, 136f traumatic deformities of, 90f Coxofemoral joint. See Coxal joint. Cranial cruciate ligament avulsion fracture of, 41 differential diagnosis in intraarticular bone or bone-like densities, 98t naturally occurring sprain in dog, 36f, 36-37, 37f rupture of, 29 dislocation and, 12f experimental destabilization of, 35-36 postsurgical osteoarthritis in, 104f surgical infection of, 118f Cranial lumbarization, 262 Cranial mediastinum, 456 mediastinal fat in, 484, 485f tumor of, 460f, 4570459 Cranial nerve sheath tumor, 223 Cranial sinus venography, 241 Cranial sternal adenopathy, 387-388, 390f Cranial vena cava normal nonselective opacification time of, 497t, 498f pericardial disease and, 533 thymoma and, 457, 459 Cranial vena cava syndrome, 459 Craniocerebral trauma, 220-221, 221b Craniomandibular osteopathy, 244 Cranium bone density of, 194 hydrocephalus and, 226-227, 227f injuries to, 196-198, 198f osteosarcoma of, 223f tumors of, 199, 200f, 203b

733

Crawfish sign, 482, 483f Cribriform plate, 204 Cricoid, 356 Cricopharyngeal achalasia, 358, 358t Crossed renal ectopia, 665-666 Crush fracture, 46, 48f Cryptococcosis, 415, 619 CT. See Computed tomography. Cubital joint infection of, 114f loose intra-articular bodies in, 7 Cuneiform process, 356 Cushing’s disease liver displacement in, 575 pulmonary calcification secondary to, 446 Cutback zones, 7, 8f Cyanosis, 508 Cyst bone, 133, 133f brain, 227-228 branchial, 462 congenital pulmonary, 446 duplication, 639 epidermoid, 263 hepatic, 583, 587f intrapericardial, 533 intrarenal, 668, 670f intrauterine, 711t laryngeal, 360 lung, 551 mediastinal, 462 morphology of, 564t ovarian, 714, 714f pancreatic, 652, 652f paraprostatic, 690-691, 691-692f parathyroid, 363 perirenal, 667-668, 670f in pneumatosis cystoids intestinalis, 648 prostatic, 690, 690f spinal, 263 Cystadenocarcinoma biliary, 582, 583f renal, 671 Cystadenoma biliary, 582, 583f renal, 671 Cystic endometrial hyperplasia, 708 Cystic hyperplasia, 586, 689 Cystic pulmonary lesion, 386, 387t, 388f Cystic uterine remnant, 712 Cystic uterus masculinus, 696 Cystitis, 677-678, 679f, 680f emphysematous, 681 feline idiopathic, 680-681 Cystography, 678-679, 679b, 679-680f, 681t in stump granuloma, 710 voiding, 693-694 Cytologic analysis in abdominal gunshot wound, 568

D Dacryocystitis, 242 Dacryocystorhinography, 242

734

Index ❚❚❚

Deciduous teeth, 213, 213f Decreased density, 1 Decreased organ size as abdominal radiographic disease indicator, 561, 561f Deep intramuscular gas, 397, 398f Deep muscle abscess, 119 Deep paraspinal abscess, 308, 308f Deep puncture wound, 26, 27f Deep suture abscess, 570f Defective interventricular septum, 504505, 505f Defensive bone, 4 Deforming spondylosis, 303, 304f Deformity. See Malformation. Degenerative disk disease, 285-302 anatomy in, 285 bulging disk in, 300 cord swelling in, 299 diagnostic terminology in, 285-286 diskography in, 300 epidurography in, 299 intraosseous vertebral venography in, 300 lesion prevalence in, 286, 286f magnetic resonance imaging in, 272t, 300-301 myelography in, 288-299, 295-297f background and beginnings of, 288 computed tomography with, 298299 epidural injection in, 291, 291t, 292f failure of contrast flow in, 295-298, 298f fat complications in, 293, 293f magnetic resonance imaging with, 299 needle placement in, 293, 294f patient positioning in, 293 postural maneuvers in, 298 risks in, 290-291, 291t test injection in, 294 timing of, 288-290 plain radiography in, 286-288, 287290f ruptured disk in, 300 Degenerative joint disease, 93 Degenerative lumbosacral stenosis, 268b, 268t, 268-270, 270-271f, 272-273t Delayed esophageal transport, 466-470, 469t, 470f Delayed fracture healing, 62-72, 69-76f Delayed growth plate closure, 186 Delivery day estimation, 703 Dens aplasia or hypoplasia of, 259f fracture of, 275, 276f, 277f mucopolysaccharidosis and, 319 Density cranial, 194 differential diagnosis for intraarticular bone or bone-like densities, 98t of jaw, 193-194

Density—cont’d of new bone, 5 tenosynovitis and, 178 Dental abscess, 212-213, 214f, 215f Dental disease, 212-216, 213b, 213-216f Dental fracture and dislocation, 215, 215f Dental tumor, 216, 216f Dentition, 213, 213f Depression fracture, 46, 49f cranial, 197 facial, 195, 196f of zygoma, 195, 196f, 197f Dermatitis, canine superficial necrolytic, 580 Dermoid cyst, 227 Dermoid sinus, 263 Derotational osteotomy, 94 Developing new bone, 5, 7f Developmental bone disease, 167-176 disseminated idiopathic hyperostosis in, 176 hypertrophic pulmonary osteoarthropathy in, 168-169, 173f, 174f hypochondroplastic dwarfism in, 173, 174t, 175f hypothyroidism in, 176 metaphyseal osteopathy in, 167-168, 171f, 172f nutritional secondary hyperparathyroidism in, 175 panosteitis in, 167, 168-170f partial absence of distal limb in, 167 retained cartilage core in ulnar metaphysis in, 169, 173, 175f role of dietary calcium in, 167, 168b Scottish fold osteodystrophy in, 175176 skeletal and ocular dysplasia in, 176 Developmental osteoarthritis, 93, 94f, 95f Developmental spinal disorders, 263274 cauda equina syndrome in, 268b, 268t, 268-270, 270-271f, 272t, 273t dermoid sinus in, 263 epidermoid cyst in, 263 facetal, juxtaarticular, synovial, and ganglion cysts in, 264 hydromyelia in, 264 meningocele in, 264 meningomyelocele in, 264 spinal arachnoid cyst in, 263 syringomyelia in, 264, 265t tumoral calcinosis in, 264, 265t vertebral angiomatosis in, 264 Wobbler syndrome in, 264-267, 265268f Diabetes mellitus gas in urinary bladder and, 558 gastric enlargement in, 598 Diagnostic hydroperitoneum, 650 Diagnostic pneumocolon, 643-644 Diagnostic pneumoperitoneum, 476 Diaphragmatic deformity, 388-390, 391f

Diaphragmatic eventration, 478 Diaphragmatic hernia, 473-479 cardiac shift and, 383t as cause of pleural fluid, 376t chylothorax and, 422t diaphragmatic variation, visibility, displacement, and disfiguration in, 473, 474f, 475f imaging findings in, 475-477f peritoneopericardial, 478 pleuroperitoneal, 476-478 positive contrast peritonography in, 476, 478t Diastatic fracture, 46, 49f Diastole, 481 DIC. See Disseminated intravascular coagulation. Diet, relative renal echogenicity and, 665 Diffuse bone loss, 255f, 255-256 Diffuse liver disease, 579b, 579f, 579580, 580f Diffuse lung disease, 393-396 Digit ectrodactyly and, 186 squamous cell carcinoma of, 134f traumatic amputation of, 61f tumor versus infection of, 131-133 Digital extensor tendon, 98t Digital versus analog hip images, 351 Dilated cardiomyopathy, 518, 523-524, 524-525f Dilation bronchial, 453-454, 453-454f esophageal, 386-387, 389f, 390f gastric, 275, 601, 601b right atrial, 444 tracheal, 364, 450-451 Diminished disk size, 249, 250f, 251t, 252-254f Dioctophyma renale, 667, 667f Discospondylitis, 249, 252f, 255, 306, 306t, 307-308f blocked vertebra versus, 256t endplate destruction in, 257t Discovertebral complex, 285 Disk blocked vertebra versus fenestration of, 256t diminished size of, 249, 250f, 251t, 252-254f discospondylitis and, 306, 306t, 307308f new bone deposition in, 254, 254f, 259 normal anatomic variant resembling spinal radiographic diagnostic indictor, 251t traumatic rupture of, 280, 284f vertebral new bone deposition and, 254, 254f, 259 Disk disease, 285-302 anatomy in, 285 bulging disk in, 300 cord swelling in, 299 diagnostic terminology in, 285-286 diskography in, 300

❚❚❚ Index

Disk disease—cont’d epidurography in, 299 intraosseous vertebral venography in, 300 lesion prevalence in, 286, 286f magnetic resonance imaging in, 272t, 300-301 myelography in, 288-299, 295-297f background and beginnings of, 288 computed tomography with, 298299 epidural injection in, 291, 291t, 292f failure of contrast flow in, 295-298, 298f fat complications in, 293, 293f magnetic resonance imaging with, 299 needle placement in, 293, 294f patient positioning in, 293 postural maneuvers in, 298 risks in, 290-291, 291t test injection in, 294 timing of, 288-290 plain radiography in, 286-288, 287290f ruptured disk in, 300 Disk herniation, 249, 252f Diskectomy, 301 Diskoepidurography, 269 Diskography, 273t, 300 Dislocation, 27-39 angular limb deformity and, 188f atlantoaxial, 258, 259f carpal, 27-28, 28-34f cervical spine, 259f, 276 congenital elbow, 186, 188-190f dental, 215, 215f genual joint, 43f hip, 329-337, 334-337f acetabular, 329, 330f capital physeal, 329, 331-332f epiphysiolysis of femoral head and, 329-332 femoral head, 332-333, 333f femoral neck, 333, 334f paracoxal mass in Doberman pinchers and, 337 postoperative assessment of femoral ostectomy muscle flap and, 334-337 proximal femoral, 329 trochanteric, 333, 334f hip dysplasia with, 321, 342f, 346 of implant in hip dysplasia, 69f intercarpal, 28, 29f mandibular, 195 patella, 177, 178f as radiographic disease indicator, 15-17, 18f, 19f shoulder, 28, 35f sternal, 397-398, 398f superficial digital flexor tendon, 180 surgical pin, 184, 184f tarsal sprain and, 39, 40f temporomandibular joint, 195-196, 196f, 197f

Disseminated idiopathic hyperostosis, 176 Disseminated infection, 106 Disseminated intravascular coagulation, 441-443, 650 Distal femoral growth plate, 50f Distal femur growth plate fracture of, 51f, 52f, 80f gunshot fracture of, 55f metaphyseal osteopathy in, 171f nonunion of fracture, 76f osteosarcoma of, 128t soft tissue sarcoma of, 135f Distal humerus congenital elbow dislocation and, 188f displaced articular fracture of, 44f growth-plate fracture of, 49, 51-52f gunshot fracture of, 54f, 55f osteoarthritis with osteochondritis in, 145, 145f osteochondritis in, 152, 156, 157f panosteitis in, 155f posttraumatic osteoarthritis of, 80f primary bone tumor of, 125f secondary bone tumor of, 129f synovial storage disease in, 105f Distal interphalangeal joint carcinoma, 134f Distal radial growth plate, 50f Distal radius arteriovenous fistula and, 183f blastomycosis of, 115f carpal sprain and, 31f chronic osteomyelitis of, 119f divided, 190, 190f growth plate fracture of, 87-88f healing of fracture, 64f hypertrophic pulmonary osteoarthropathy and, 173f, 175f impaction fracture of, 56f limb deformity secondary to growth plate fracture and early closure, 72, 80-91f medial bowing of, 79f metaphyseal osteopathy in, 171f nonunion of fracture, 72f panosteitis in, 169f pathologic fracture of, 57f retained cartilage core in, 175f rickets and, 187f sequestrum deformity of, 89f Distal tibia growth plate fracture of, 68f, 88f osteosarcoma of, 126f Distal ulna arteriovenous fistula and, 183f chronic osteomyelitis of, 119f hypertrophic pulmonary osteoarthropathy and, 173f, 175f impaction fracture of, 56f limb deformity secondary to growth plate fracture and early closure, 72, 80-91f nonunion of fracture, 72f panosteitis in, 169f pathologic fracture of, 57f

735

Distal ulna—cont’d retained cartilage core in, 175f rickets and, 187f segmental fracture of, 60f sequestrum deformity of, 89f transverse fracture of, 63f Distal ulnar growth plate, 50f Disuse osteoporosis, 15 Diverticular disease bladder, 681 rectal, 646 ureteral, 677 Divided distal radius, 190, 190f Dog adrenal gland of, 600-700 canine superficial necrolytic dermatitis and, 580 cardiac measurements in, 494 cauda equina syndrome in, 268b, 268t, 268-270, 270b, 270-271f, 272t, 273t chronic nasal disease in, 205t dental disease in, 212-216, 213b, 213216f endocarditis in, 528, 531-532f experimental destabilization of genual joint, 35-36 gastric enlargement in, 597-598, 598t, 5978f hip dysplasia in, 338-352 acetabular relocation for, 349, 349t artificial hip for, 349-350, 350f early detection of, 339 explanations for owners, 346-347, 347-348f femoral head relocation for, 348 historical background of imaging in, 338 implant dislocation in, 69f normal breed hip variations and, 339 Orthopedic Foundation for Animals certification and, 339 osteoarthritis and, 94-96, 95f, 103f postoperative assessment of, 350 previously injured hip versus, 346, 346f prognosis for, 348 progress examinations in, 350 radiographic features of, 339-342, 340-341f radiographic indicators of infectious surgical failure in, 351 radiographic indicators of noninfectious surgical failure in, 350-351, 351f role of stress radiography in, 338 sonographic evaluation in puppy, 351, 351f stressing of suspicious hip, 342, 345f, 346f unilateral, 342, 344, 345f leptospirosis in, 666 lesion prevalence in intervertebral disk disease, 286 location of sesamoid bones in, 45t

736

Index ❚❚❚

Dog—cont’d loose intra-articular bodies in, 7-9, 9f naturally occurring cruciate sprain in, 36f, 36-37, 37f neonatal kidney of, 664 normal appearances in cardiac ultrasound, 499, 500f normal gastric emptying time in, 595-597 normal intestinal iodine films of, 616 normal nonselective opacification times in, 497t normal sonographic appearance of intestine, 617 normal sonographic appearance of stomach, 597 osteochondritis in, 138-166 anconeal process and, 152, 154155f classification schemes in, 163t, 163-165, 165t, 166t differential diagnosis in intraarticular bone or bone-like densities, 98t distal humeral epiphysis and, 152, 156, 157f in dysplastic hip, 343-345t elbow and, 138-152. See also Elbow. osteoarthritis and, 96, 96f, 97f shoulder and, 156-161, 157-162f stifle and, 162-163, 165f tarsal joint and, 161-162, 162-164f unusual locations of, 9, 10f peritoneal effusion in, 555 pituitary tumor in hyperparathyroidism, 222 primary lung tumor in, 423, 424-426f pulmonary thromboembolism in, 444 renal tumor in, 668f, 668-671, 670t resistive index in, 672 secondary bone tumor in, 123 spinal infection in, 305-309 deep paraspinal abscess in, 308, 308f discospondylitis in, 306, 306t, 307308f spondylitis in, 305 vertebral physitis in, 306-308 splenic disease in, 655 splenic hemangiosarcoma in, 657658, 657-660f sprain, fracture, and dislocation of radiocarpal joint, 19f thyroid masses and hyperthyroidism in, 363, 363f Doppler blood flow analysis, hepatic, 591, 591b Doppler tracing interpretation, 500501, 502f Doppler ultrasound in atrial standstill, 540f of fracture healing, 67 in mitral endocardiosis, 521-523f in pulmonary embolism, 444 of spinal cord vasculature, 319

Dorsoventral versus ventrodorsal projection, 485, 486f Double cardiac silhouette sign, 484485, 486f Double-contrast barium examination, 595 Double-contrast colonography, 644 Double-contrast cystography, 679, 680f, 681t Double growth plate sign, 167 Double-heart sign, 423 Double line sign, 294-295, 297f Double-marking in dental radiography, 213, 2123f Drain, chest, 403-404 Draining sinus in abdominal wall, 569, 570f in paraspinal foreign body, 305 Dribbling, 673 Drug-induced pancreatitis, 653 Dual-chamber pacing, 552 Duodenal bulb, 622 Duodenum foreign object in, 565f thickening secondary to pancreatitis, 617-618, 618f ulcer of, 606f, 617 Duplication of gallbladder, 586 renal, 665-666 Duplication cyst, 639 Dural laceration, 284 Dural ossification, 304 Dural tail sign, 222 Dwarfism, hypochondroplastic, 173, 174t, 175f Dysautonomia, 466, 467f, 469t Dysgenesis, epiphyseal, 176 Dysplasia congenital epiphyseal, 325-328, 328f, 332-333, 333f hepatic, 561, 561f, 580, 591 hip, 338-352 acetabular relocation for, 349, 349t artificial hip for, 349-350, 350f in cat, 351, 351f early detection of, 339 explanations for owners, 346-347, 347-348f femoral head relocation for, 348 historical background of imaging in, 338 implant dislocation in, 69f normal breed hip variations and, 339 Orthopedic Foundation for Animals certification and, 339 osteoarthritis and, 94-96, 95f, 103f postoperative assessment of, 350 previously injured hip versus, 346, 346f prognosis for, 348 progress examinations in, 350 radiographic features of, 339-342, 340-341f radiographic indicators of infectious surgical failure in, 351

Dysplasia—cont’d hip—cont’d radiographic indicators of noninfectious surgical failure in, 350-351, 351f role of stress radiography in, 338 sonographic evaluation in puppy, 351, 351f stressing of suspicious hip, 342, 345f, 346f unilateral, 342, 344, 345f ocular, 176 skeletal and ocular, 176 temporomandibular, 195-196, 197f Dyspnea intestinal distention in, 622t in pleural fluid accumulation, 421 in primary lung tumor, 423 in tracheal hypoplasia, 449 Dystocia, mechanical, 705-706f Dystrophic calcification, 177, 179f, 611 Dystrophin, 501

E Ear, 231-235 aural tumors of, 235 inflammation and infection of, 231234, 232-234f inflammatory polyps of, 234-235, 235f otoliths of, 235 Eardrum, 231 Ebstein’s anomaly, 491f, 512, 514f, 516t Eburnation, 1 Echocardiography, 499-503 athletic hypertrophy and, 501 of cardiac pacemaker, 552 congenital muscular dystrophy and, 501-502 contrast, 506-507 interpretation of Doppler tracing in, 500-501, 502f M-mode, 501 normal appearances in, 499, 500f overall approach in, 499-500 placement of intravascular embolization coils in, 500 Ectopic kidney, 665-666 Ectopic parathyroid tissue, 546t Ectopic pregnancy, 705 Ectopic thyroid tissue, 546t Ectopic ureter, 672t, 673, 675-676f Ectrodactyly, 167, 186 Edema extrapleural, 369 malfunction of lymph system in, 421 in mediastinal lymphosarcoma, 460 pulmonary, 433-435 in acute pancreatitis, 650 after near strangulation, 439 after smoke inhalation, 438, 438f cardiac, 433 disseminated intravascular coagulation versus, 441 in electric shock, 440, 442f in endocarditis, 532f heart failure and, 543, 543f

❚❚❚ Index

Edema—cont’d pulmonary—cont’d in hypertrophic cardiomyopathy, 530f lymphosarcoma versus, 429, 431f in mitral endocardiosis, 517, 520f neurogenic, 444-445, 445b noncardiac, 433-435, 433-435f, 435t spinal cord, 300 in dermoid sinus, 263 in disk disease, 298, 299 in vascular mediastinal tumor, 462 Efferent vagal reflex, 362 Eisenmenger reaction, 505 Eisenmenger syndrome, 516t Elbow canine, 50f location of sesamoid bones in, 45t panosteitis in, 168f postsurgical osteoarthritis in, 102f tumoral calcinosis in, 179f congenital dislocation of, 186, 188190f dysplasia of, 138, 166 feline articular fracture of, 44f gunshot fracture of, 54f sprain of, 18f fungal osteomyelitis of, 116f hairline fracture of, 55f immunoarthritis in, 100-101f osteoarthritis in, 96f, 97f osteochondritis in, 96f, 138-152 anconeal process and, 152, 154-155f computed tomography of, 147, 147b, 152, 153f early disease in, 145, 147-149f false disease in, 145-147, 152f late disease in, 145, 150-151f lesion development and progression in, 140, 144-146f, 145 magnetic resonance imaging of, 152 medial coronoid process and, 138139 normal anatomic and radiographic variations in, 139140, 139-143f shortcomings associated with lateral view of, 139 Elbow Dysplasia Score, 163, 165t Electric shock, 440, 442f Electronic database for fracture classification, 58 Embedded disk content, 300 Embolism air, 678 pulmonary, 443-444 Emphysema, 454 orbital, 241b, 241-242 Emphysematous cholecystitis, 557 Emphysematous cystitis, 681 Encephalitis, 224-225, 225b Enchondroma, 121 tracheal, 451 Endocardiosis, 517-518, 517-523f, 519t

Endocarditis, 528, 531-532f Endometrial hyperplasia, 708 Endometrial polyp, 711t Endometritis, 704 Endosteal bone deposit, 5 Endosteum, 2 Endplate of intervertebral disk, 285 abnormalities of, 257, 257t fracture of, 280, 280f, 281f magnetic resonance imaging indicators of disk disease and, 272t Enlargement of aorta and pulmonary artery, 489490, 490f of aortic root, 484, 485f cardiac, 363 esophageal, 450, 466, 467-469f gastric, 597-598, 598f, 598t splenic, 655, 656f ureteral, 672, 673f uterine, 708 Enteritis, 618-619, 620-621f, 622t Enterococcus in hepatic cyst, 583 Enterography, 619, 619t, 621f Enthesiophyte, 9-10 Entrapment intestinal, 636 pyloric, 605, 605f Eosinophilia, pulmonary infiltrates with, 445, 445f Eosinophilic granulomatosis, 447, 454 Eosinophilic pneumonitis, 536 Ependymitis, 226 Epidermoid cyst, 227-228 intraosseous, 133-134 spinal cord, 263 Epididymitis, 716-718 Epidural myelogram, 291, 291f, 292f Epidurography, 269, 273t, 299 Epiglottis, 356 cyst of, 360 Epiphyseal dysgenesis, 176 Epiphyseal dysplasia, 325-328, 328f, 332-333, 333f Epiphysiolysis of femoral head, 329332 Epiphysis, compression and, 40 Erosive polyarthritis, 98 Erythrocyte pyruvate kinase deficiency, 191 Escherichia coli in discospondylitis, 306 gas in gallbladder and, 557 in hepatic cyst, 583 in pyometra, 708 Esophageal phase of swallowing, 356357 Esophageal transport disease, 466-470, 469t, 470f Esophagitis, 470 Esophagus, 466-472 combined laryngeal-pharyngealesophageal foreign bodies and, 360 dilated, 386-387, 389f, 390f effect of vomiting on, 471, 471f

737

Esophagus—cont’d enlargement of, 450, 466, 467-469f esophageal transport disease and, 466-470, 469t, 470f esophagitis and, 470 fistula of, 471 foreign object in, 457, 459f, 466, 467f gas in, 472, 472f gastroesophageal intussusception and, 609 hematoma of, 471 perforation of, 466 mediastinal infection and, 462463 pneumomediastinum in, 463-464 pneumoperitoneum in, 559t stricture of, 470 tumor of, 470-471 Eventration, diaphragmatic, 478 Everted laryngeal saccule, 360 Excellent conformation of hip, 339, 340f Excretory urography, 664, 664t, 677 Exophthalmia, 242 Experimental destabilization of canine genual joint, 35-36 Experimental pneumothorax, 404 Expiratory film, 368, 371f, 372f, 374f, 375f Exploratory laparotomy, 568 Expression fracture, 46 cranial, 197 Exterior atelectasis, 383, 385f Exterior foreign body causing partial strangulation, 358 External bars, 62, 67f Extraabdominal tumor of abdominal wall, 570, 571f Extraarticular osteophyte in immunoarthritis, 99, 100f as radiographic disease indicator, 9, 13f Extraaxial trauma, 220, 221b Extracerebral hematoma, 220 Extradural degenerative disease, 285302 anatomy in, 285 bulging disk in, 300 cord swelling in, 299 diagnostic terminology in, 285-286 diskography in, 300 epidurography in, 299 intraosseous vertebral venography in, 300 lesion prevalence in, 286, 286f magnetic resonance imaging in, 300301 myelography in, 288-299, 295-297f background and beginnings of, 288 computed tomography with, 298299 epidural injection in, 291, 291t, 292f failure of contrast flow in, 295-298, 298f fat complications in, 293, 293f

738

Index ❚❚❚

Extradural degenerative disease—cont’d myelography in—cont’d magnetic resonance imaging with, 299 needle placement in, 293, 294f patient positioning in, 293 postural maneuvers in, 298 risks in, 290-291, 291t test injection in, 294 timing of, 288-290 plain radiography in, 286-288, 287290f ruptured disk in, 300 Extradural myelogram, 291, 291f Extrahepatic biliary atresia, 186 Extrahepatic shunt, 580 Extraluminal hemorrhage, 672t Extramedullary hematopoiesis, splenic, 656, 656f Extramedullary plasmacytoma, tracheal, 451 Extrapleural air, 400, 401-403f Extrapleural hematoma, 399 Extrapleural lesion, 369 Extrapleural swelling, 369 Extraskeletal chondroma, 133, 134f Extrathoracic hematoma, 397 Extremities, 1-191 arteriovenous fistula and, 180, 181183f bicipital tenosynovitis, 178, 178f, 179f bone infarct and, 180 bone tumors of, 121-136 benign, 121 digital tumors versus infections and, 131-133 invading soft tissue tumors and, 134-135, 134-136f of joints, 124, 130, 132f metastatic melanoma in, 130 parosteal sarcoma in, 130-131 primary, 121-123, 122t, 123-129f primary hemangiosarcoma in, 131 radiologic findings in, 123-124, 129-131f secondary, 123 tumorlike bone lesions and, 133t, 133-134, 134f calcaneal dislocation of superficial digital flexor tendon and, 180 congenital and developmental bone disease in, 167-176 disseminated idiopathic hyperostosis in, 176 hypertrophic pulmonary osteoarthropathy in, 168-169, 173f, 174f hypochondroplastic dwarfism in, 173, 174t, 175f hypothyroidism in, 176 metaphyseal osteopathy in, 167168, 171f, 172f nutritional secondary hyperparathyroidism in, 175 panosteitis in, 167, 168-170f partial absence of distal limb in, 167

Extremities—cont’d congenital and developmental bone disease in—cont’d retained cartilage core in ulnar metaphysis in, 169, 173, 175f role of dietary calcium in, 167, 168b Scottish fold osteodystrophy in, 175-176 skeletal and ocular dysplasia in, 176 dislocation of patella, 177, 178f dislocation of surgical pin in, 184, 184f gastrocnemius avulsion and, 178179, 179f hindquarter weakness and pain in aortoiliac thrombus, 183-184 iliopsoas muscle strain and, 180 infections of, 106-120 abscess and, 119, 119f, 120f blastomycosis in, 111, 115, 115f, 116f cancer versus, 118-119 chronicity of, 116-117, 116-119f coccidioidomycosis in, 111, 114f hepatozoonosis in, 107-111 histoplasmosis in, 115-116 nonspecific bacterial, 107, 107f, 109t nuclear imaging of, 107, 108t pathologic fracture and, 116, 116f Phialemonium ovatum in, 116 radiographic disease indicators of, 107 radiology of, 106-107 septic arthritis and, 117-118 surgical, 107, 110-114f terminology in, 106 injury to, 21-92 apophyseal fracture in, 40, 43f articular fracture in, 40-41, 44f, 45f avulsion fracture in, 41, 45t, 46f bruise in, 21 carpal sprains in, 27-28, 28-34f, 29t chisel fracture in, 41, 46f closed fracture in, 41 comminuted fracture in, 41, 47f compartmental syndrome and, 2122 compression fracture in, 41, 47f corner fracture in, 46, 48f crush fracture in, 46, 48f delayed fracture healing and, 6272, 69f, 70-76f depression fracture in, 46, 49f diastatic fracture in, 46, 49f dislocated shoulder in, 28, 35f distal humeral growth-plate fracture in, 49, 51-52f elbow sprains in, 28, 34f, 35f experimental destabilization of canine genual joint and, 35-36 expression fracture in, 46 fabella injuries in, 38, 38f, 39f fault-line fracture in, 46-47 fracture classification using electronic databases and, 58

Extremities—cont’d injury to—cont’d fracture repair and, 58-63, 62-67f fracture union and, 63, 67, 68f greenstick fracture in, 47, 49f growth plate fracture in, 47b, 4748, 48b, 50f gunshot fracture in, 49, 53-55f hairline fracture in, 49, 55f hematoma in, 21, 22f high-density foreign bodies and, 23, 26f impacted fracture in, 49, 56f incomplete fracture in, 49, 57f insufficiency fracture in, 53, 57f intercondylar stenosis and, 37 limb deformity secondary to growth-plate fracture and early closure in, 72, 80-91f longitudinal fracture in, 53, 58f magnetic resonance arthrography of, 38, 39b magnetic resonance imaging of, 37-38 major tears, laceration, and trauma-related infection and abscess in, 23-27, 27f meniscal injuries in, 34-35 naturally occurring cruciate sprains in dogs and, 36f, 36-37, 37f oblique fracture in, 53, 58f open fracture in, 53, 59f pathologic fracture in, 53, 59f regeneration and, 72 segmental fracture in, 53, 60f sesamoid fracture in, 53-54, 60f simple fracture in, 54, 61f soft tissue calcification and, 22-23, 25f, 26f soft tissue foreign bodies and, 3940, 41t soft tissue gas and, 22, 23f, 24f spiral fracture in, 54, 61f stifle sprains in, 29, 34 strains, tendonitis, and bursitis in, 23, 26f stress fracture in, 54 T, Y, and V fractures in, 53, 57f talar neck fracture in, 54, 58 tarsal sprains in, 39, 40f transverse fracture in, 54, 61f traumatic amputation in, 58, 61t ultrasound of, 37 intravenous catheter fragments in, 184, 184f ischemia of, 182 lameness secondary to arterial blockage by heartworms, 180 mineralization of biceps brachii tendon and, 178 supraspinatus tendon and, 177178 neuroma and, 181 osteoarthritis in, 93-105 articular fracture and, 40 avascular necrosis and, 96-98, 97f

❚❚❚ Index

Extremities—cont’d osteoarthritis in—cont’d categorization of, 93, 94f, 95f generative nature of, 93 gout and pseudogout and, 101, 105 hip dysplasia and, 94-96, 95f in injured stifle, 36, 36f intraarticular calcification, ossification, and fragmentation in, 98t, 98-99, 100f magnetic resonance imaging appearance of, 93 osteochondritis and, 96, 96f, 97f periarticular osteophytes in, 9, 12f postsurgical, 99-101, 101-104f posttraumatic, 80f primary bone tumor versus, 119 radiographic appearance of, 93, 94f storage disease and, 105, 105f synovitis and, 93 osteochondritis of, 138-166 anconeal process, 152, 154-155f classification schemes in, 163t, 163-165, 165t, 166t commonly affected breeds, 138 differential diagnosis in intraarticular bone or bone-like densities, 98t distal humeral epiphysis, 152, 156, 157f elbow, 138-152. See also Elbow. osteoarthritis and, 96, 96f, 97f shoulder, 156-161, 157-162f stifle, 162-163, 165f tarsal joint, 161-162, 162-164f unusual locations of, 9, 10f osteopetrosis secondary to myelophthisic anemia and, 180 peripheral nerve sheath tumor and, 181 radiation-induced bone lesion of, 180 radiographic disease indicators of, 120 dislocation as, 15-17, 18f, 19f enthesiophyte as, 9-10 extraarticular osteophyte as, 9, 13f joint body as, 7-9, 9-12f limb deformity as, 17, 19f localized bone deposition as, 15, 15f localized bone loss as, 10-15, 1315f metaphyseal lysis as, 15, 16f, 17f osteopenia as, 15, 17f, 18f periarticular osteophyte as, 9, 12f periosteal new bone as, 1-7, 2-8f soft tissue swelling as, 17, 19f skeletal deficiencies of, 186-191 congenital elbow dislocation and, 186, 188-190f in delayed growth plate closure in castrated and spayed cats, 186 divided distal radius and, 190, 190f

Extremities—cont’d skeletal deficiencies of—cont’d ectrodactyly and, 186 in erythrocyte pyruvate kinase deficiency in basenjis, 191 incomplete ossification of humeral condyle and, 190 osteogenesis imperfecta and, 190 rickets secondary to cholestasis and, 186, 187f skeletal leishmaniasis and, 180-181 soft tissue tumors of, 137 tumoral calcinosis and, 179, 179f villonodular synovitis and, 182-183 Exudate peritoneal, 559t pleural, 377t Eye, 236-243 cataracts and, 236-238, 237b, 237-239f congenital disease of, 241 dacryocystitis and, 242 exophthalmia and, 242 foreign body in, 240, 240f infection of, 240 injury to, 238-240, 239f, 240f magnetic resonance imaging of, 236, 237b orbital and periorbital disease and, 241 orbital emphysema and, 241b, 241242 retrobulbar abscess and, 242, 242f sonography of, 236, 237b tumor of, 240-241, 241f

F Fabella injury, 38, 38f, 39f Facetal arthritis, 303, 304f Facetal cyst, 264 Facial bone destruction, 193 Facial injuries, 195, 196f Facial nerve tumor, 223 Facial tumor, 199, 200f, 201f, 203b Failed back surgery syndrome, 300-301 False abdominal lesion, 720 False aneurysm, 22 aortic, 484, 485f False biopsy needle tip, 719, 720t False disease in osteochondritis, 145147, 152f False radiographic disease indicators, 368, 369t False ridge sign, 140, 141-143f Fat complications in myelography, 293, 293f cranial mediastinal widening and, 456, 457f hepatic mass versus, 720 in renal sinus, 667, 670f Fatty bone tumor, 122t Fatty liver, 560f, 579, 579f, 580f, 616 Fault-line fracture, 46-47 Feeding stress maneuver, 266, 266f, 267f Feline asthma, 436, 437f Feline cholangitis, 579, 579b

739

Feline endogenous lipid pneumonia, 443 Feline hepatic lipidosis, 579, 579f, 580f Feline idiopathic cystitis, 680-681 Feline infectious peritonitis, 572 Feline osteochondromatosis, 133 Femoral arteriography, 22 Femoral component in hip replacement, 350, 350f Femoral fracture articular, 45f callus formation in, 3f comminuted, 43f, 66f effect on hip, 346, 346f growth plate, 51f, 52f, 78f, 80f gunshot, 55f long oblique, 65f malunion of, 77f mature new bone after, 8f nonunion of, 75f simple oblique, 61f Femoral head avascular necrosis of, 325, 326-327f congenital epiphyseal dysplasia and, 325-328, 328f epiphysiolysis of, 329-332 fracture of, 332-333, 333f capital physeal, 329, 331-332f epiphysiolysis and, 329-332 hip dysplasia and, 95, 348 Legg-Calv[ac]e-Perthes disease and, 96-98, 97f Femoral neck fracture, 333, 334f Femoral ostectomy muscle flap, 334337 Femur dislocation of patella and, 177 dysplastic versus normal, 347f metaphyseal osteopathy in, 171f osteomyelitis of, 112f osteosarcoma of, 128t soft tissue sarcoma of, 135f tumor versus infection of, 117f Fetal age, 703 Fetus incomplete fetal resorption, 704f, 704-705 late-term death of, 705 normal sonographic appearance of, 702-703, 704t Fibrosarcoma, 123 coccygeal, 255f esophageal, 471 maxillary, 201f new bone deposition in, 4, 13f orbital, 241 Fibrosing lung disease, 440, 442f Fibrosis pulmonary, 440 in radiation pneumonitis, 446 Fibrous bone tumor, 122t Fibula coccidioidomycosis of, 114f growth plate fracture of, 81f metastatic sarcoma of, 130t spiral fracture of, 61f Fifth metacarpal malunion, 79f

740

Index ❚❚❚

Fifty percent rule, 339 Filaroides hirthi, 409-411 Filaroides osleri, 451 Filling defects, 615 Fine-needle aspiration, 720 First-degree carpal sprain, 29t Fissure lines, 407 Fistula arteriovenous, 133, 180, 181-183f bronchocutaneous, 451 esophageal, 471 gastrobronchial, 610-611 intracardiac, 528 in traumatic pharyngeal perforation, 359 Fixed linear foreign body, 627, 630f Flaccid esophagus, 387, 389-390f Flail chest, 397 Flap, femoral ostectomy muscle, 334337 Flotational effect, 376, 377f cardiac silhouette analysis and, 494 in lung-lobe torsion, 436 Fluke, 599 Fluoroscopy in esophageal transport disease, 467 in pericardial disease, 533 in tracheal collapse, 450 Focal granulomatous meningoencephalitis, 221, 221b Foreign body acute abdominal colic in, 566b bronchial, 451 chronic nasal disease in dog and, 205t combined laryngeal-pharyngealesophageal, 360 esophageal, 386-387, 389f, 466, 467f mediastinal mass versus, 457, 459f exterior, causing partial strangulation, 358 fractured tooth as, 215 gastric, 598-599, 599-601f, 603f high-density, 23, 26f intestinal, 565f, 619-627 barium and iodine films of, 622625, 623-629f fixed, 627, 630f free linear, 627 as incidental finding, 619 metallic, 619 obstructive pattern and, 621-622, 622t plain films of, 620-621, 622f sonography of, 625 ocular, 240, 240f paraspinal, 305 pharyngeal, 359, 359f pneumonia related to, 416, 417f soft tissue, 39-40, 41t tracheal, 365, 451 Forelimb location of sesamoid bones in, 45t superimposition in thoracic radiography, 374f traumatic deformities of, 91f Forestier’s disease, 176

Fourth ventricle choroid plexus tumor of, 224 hydromyelia and, 264 Fracture, 40-72 angular limb deformity and, 188f apophyseal, 40, 43f articular, 40-41, 44f, 45f avulsion, 41, 45t, 46f differential diagnosis in, 98t of hip, 333 of long digital extensor tendon, 23 of patella, 177 of prepubic eminence, 571f blocked vertebra versus, 256t bone deposit in previous injury, 7f bronchial, 405 cervical spine, 275-276, 276-278f chisel, 41, 46f classification using electronic databases, 58 closed, 41 comminuted, 41, 47f compression, 41, 47f congenital hemivertebra versus, 256t of thoracic spine, 279f corner, 46, 48f cranial, 197, 198f crush, 46, 48f delayed healing of, 62-72, 69f, 7076f dental, 215, 215f depression, 46, 49f diastatic, 46, 49f expression, 46 facial depression, 195 fault-line, 46-47 femoral articular, 45f callus formation in, 3f comminuted, 43f, 66f effect on hip, 346, 346f growth plate, 51f, 52f, 78f, 80f gunshot, 55f long oblique, 65f malunion of, 77f mature new bone after, 8f nonunion of, 75f simple oblique, 61f greenstick, 47, 49f growth plate, 47b, 47-48, 48b, 50f distal humeral, 49, 51-52f femoral, 329, 331-332f limb deformity secondary to, 72, 80-91f malunion of, 78f metaphyseal lysis in, 15, 16f, 17f gunshot, 49, 53-55f hairline, 49, 55f hip, 329-337, 334-337f acetabular, 329, 330f capital physeal, 329, 331-332f epiphysiolysis of femoral head and, 329-332 femoral head, 332-333, 333f femoral neck, 333, 334f multiple injuries in, 323f

Fracture—cont’d hip—cont’d paracoxal mass in Doberman pinchers and, 337 postoperative assessment of femoral ostectomy muscle flap and, 334-337 proximal femoral, 329 radiographic disease indicators of, 321 trochanteric, 333, 334f impacted, 49, 56f incomplete, 49, 57f insufficiency, 53, 57f longitudinal, 53, 58f malunion of, 70-72, 77-80f mandibular, 194, 195, 196f nonunion of, 68-70, 69-76f of facial depression fracture, 195 of pelvic fracture, 324f oblique, 53, 58f open, 53, 59f osteochondritis versus, 164f pathologic, 53, 59f pelvic, 321-324, 323-324f repair of, 58-63, 62-67f rib, 397, 398f segmental, 53, 60f sesamoid, 53-54, 60f simple, 54, 61f skull, 198f spiral, 54, 61f sternal, 397-398, 398f stress, 54 T, V, and Y shaped, 53, 57f talar neck, 54, 58 temporomandibular joint, 195 tracheal, 405 transverse, 54, 61f vertebral endplate abnormalities versus, 257t of zygoma, 195, 196f, 197f Fracture union, 63, 67, 68f Fragmented coronoid process, 138, 140 Free disk fragments, 287-288, 288-289f Free-hand CT-guided biopsy, 719-720, 720t Free linear foreign body, 627 Free mediastinal air, 379-380, 381f Free pleural air, 378-379, 380f, 381f, 401f Fremitus, 180 Frontal sinus depression fracture of, 196f inflammatory disease of, 210, 210f mucopolysaccharidosis and, 319 nasal tumor and, 207f normal radiology of, 204, 206f Functional variations of stomach, 594 Fungal infection in discospondylitis, 306, 306t extremital, 115-116, 116f in osteomyelitis, 111, 245f pulmonary, 412-415 aspergillosis in, 412 blastomycosis in, 412-415f coccidioidomycosis in, 412-415, 416f

❚❚❚ Index

Fungal infection—cont’d pulmonary—cont’d cryptococcosis in, 415 histoplasmosis in, 415 Fusing the joint, 27

G Gallbladder, 585-587, 586-587f calcification of, 564t, 587f gas in, 557 Gallstones, 561, 585 Ganglial ischemia, compressioninduced, 269 Ganglion cyst, 264 Gas as abdominal radiographic disease indicator, 557-560 colonic, 683 esophageal, 472, 472f in gallbladder, 557 intestinal, 557-558 abdominal hernia and, 568 plain film of, 614 intrafetal, 705 sternal, 398-399, 399f Gas enema in intestinal intussusception, 630 Gas pocket, 22, 23f, 24f, 568 Gastric atony, 611-612 Gastric dilation in spinal fracture, 275 Gastric emptying, 595-597 normal barium film variations of, 615 Gastric enlargement, 597-598, 598f, 598t Gastric motility, effect of barium temperature on, 595 Gastric reflux, iohexol-induced, 616 Gastric torsion, 559t, 601-604, 603-604f, 659 Gastric tube, 605 Gastric tumor, 606-607, 607f Gastritis, 599 chronic lymphocytic-plasmacytic, 609 Gastrobronchial fistula, 610-611 Gastrocnemius avulsion, 178-179, 179f Gastrocnemius rupture, 38f Gastroenterography in infiltrative bowel disease, 618, 619t of leiomyosarcoma and leiomyoma, 633 Gastroesophageal intussusception, 609, 611f Gastroesophageal phase of swallowing, 357 Gastroesophageal reflux disease abnormal esophageal transport in, 469t hiatal hernia and, 609 Gastrogastric intussusception, 608 Gastrography in gastric tumor, 606 in gastrobronchial fistula, 610-611 Gastrointestinal pythiosis, 599-601

Gastrointestinal tract, 594-649 abdominal hernia and, 568, 569f abnormal distention of colon and, 646 abnormally long colon and, 648-649 acute abdominal colic and, 566b air colonography of, 643-644 barium examination of, 594-595, 595t, 596f, 643, 644f biopsy of, 721 bowel distribution patterns and, 616-617 chronic lymphocytic-plasmacytic gastritis and, 609 colon cancer and, 646, 648f colonic impaction of, 646, 648f colonic marking of, 644, 645f colonic perforation of, 559t, 646-648 colonic stenosis of, 646 colonic torsion of, 648, 649f colonic transit time using synthetic markers, 643 congenital malformations of, 638-639 diaphragmatic hernia and, 475-477f, 478t displacement by abdominal hernia, 637 double-contrast colonography of, 644 duodenal thickening secondary to pancreatitis, 617-618, 618f duodenal ulcer and, 617 enteritis and, 618-619, 620-621f fetal stomach and, 702 foreign body in, 565f, 619-627 barium and iodine films of, 622625, 623-629f fixed, 627, 630f free linear, 627 gastric, 598, 599-601f as incidental finding, 619 metallic, 619 obstructive pattern and, 621-622, 622t plain films of, 620-621, 622f sonography of, 625 gas in, 557-558 gastric atony and, 611-612 gastric calcification and, 561f, 564t, 611, 611f gastric dilation and, 275, 601, 601b gastric enlargement and, 597-598, 598f, 598t gastric herniation and, 382f gastric perforation and rupture and, 559t, 609-610 gastric plain films of, 594 gastritis and, 599 gastrobronchial fistula and, 610-611 gastrointestinal pythiosis and, 599601 hairballs in, 598, 602f hiatal hernia and, 609, 610f infiltrative bowel disease and, 618, 619t inflammatory bowel disease and, 618

741

Gastrointestinal tract—cont’d intestinal abscess of, 639f, 641 intestinal adhesion of, 640f, 641 intestinal calcification of, 564t intestinal impaction of, 637, 638f intestinal incarceration of, 636 intestinal leiomyosarcoma and leiomyoma of, 633, 634f intestinal lymphosarcoma of, 632633, 633f intestinal perforation of, 634b, 634635 peritonitis and, 572 pneumoperitoneum in, 559t intestinal torsion and, 559t, 635-636, 635-636f intestinal tumor of, 630-632, 632f intussusception of, 627-630, 631-632f cecocolic, 644-646 gastroesophageal, 609, 611f ileocolic, 646 normal appearance of, 643 normal barium film variations of, 615 normal gastric emptying time and, 595-597 normal iodine films of, 615-616 normal plain film variations of, 614615, 615f normal sonographic appearance of, 597, 617, 617t parasitic infection of, 637 pneumatosis coli and, 648, 649f posttorsional stomach and, 604-605, 605f potential sonographic indicators of disease, 617 protein-losing enteropathy and, 637 short-bowel syndrome and, 638 trauma to, 639-641 ulcerative colitis and, 646, 647f Gastropexy, 604 Gastrosplenic torsion, 661f Generalized pulmonary calcification secondary to Cushing’s disease, 446 Generative joint disease, 93 Genu valgum deformity, 177 Genual joint dislocation of, 43f experimental destabilization of, 3536 fracture-related deformities of, 84-86f loose intra-articular bodies in, 7 pin trauma in, 95f polyarthritis in, 99f sprain to, 29, 34 Geriatric fibrosis, 395-396 Gestational age, 703 Giant kidney worm, 667, 667f Glass, radiographic and sonographic features of, 41t Glenoid articular fracture of, 44f condylar displacement and deformity and, 196 osteochondritis of, 160

742

Index ❚❚❚

Glioma, 222, 222t Glossal tumor, 216-217 Gout, 101, 105 Granuloma in actinomycosis, 408 intrauterine mass and, 711t stump, 710, 710f Granulomatosis, pulmonary, 446f, 447, 447f Granulosa cell tumor, 713 Gravel, radiographic and sonographic features of, 41t Greater trochanter fracture, 333, 334f Greater tubercle osteochondritis, 160 Greenstick fracture, 47, 49f Growth plate delayed closure of, 186 fracture of, 47b, 47-48, 48b, 50f femoral, 329, 331-332f limb deformity secondary to, 72, 80-91f malunion of, 78f metaphyseal lysis in, 15, 16f, 17f Gum squamous cell carcinoma of, 199 tumor of, 216-217 Gun pellet, 26f Gunshot wound to abdominal wall, 568-569 arteriovenous fistula after, 180 fracture from, 49, 53-55f to head, 197-198, 198f thoracic, 404-405, 405f, 406f

H Hairball, 598, 602f Hairline fracture, 49, 55f Head, 193-247 ankylosis and impingement exostosis and, 195, 196f, 197f brain disease and injury and, 218-230 aspergillosis in, 225, 225f blastomycosis in, 226 brain abscess in, 226, 226t brain biopsy in, 228-229 brain cysts in, 227-228 brain tumor in, 221-224, 222t, 223224f cerebrovascular accident in, 228 choice of imaging study in, 220, 220t computed tomographic evaluation of postoperative brain in, 229 computed tomography in, 219, 220t craniocerebral trauma in, 220-221, 221b encephalitis in, 224-225, 225b focal granulomatous meningoencephalitis in, 221, 221b hydrocephalus in, 226-227, 227f magnetic resonance imaging in, 219-220, 220t necrotizing meningoencephalitis in, 225

Head—cont’d brain disease and injury and—cont’d normal anatomic variants and, 228 normal ventricular variation and, 220 nuclear medicine imaging in, 218 seizure in, 221 sonography in, 218, 219t special radiographic procedures in, 218, 219f congenital orofacial deformity and, 244, 246f congenital temporomandibular deformity and dislocation and, 195-196, 197f cranial injuries and, 196-198, 198f craniomandibular osteopathy and, 244 dental disease and, 212-216, 213b, 213-216f ear disorders and, 231-235 aural tumors in, 235 inflammation and infection in, 231-234, 232-234f inflammatory polyps in, 234-235, 235f otoliths in, 235 eye disorders and, 236-243 cataracts and, 236-238, 237b, 237239f congenital disease of eye in, 241 dacryocystitis and, 242 exophthalmia and, 242 infection in, 240 injury in, 238-240, 239f, 240f magnetic resonance imaging of, 236, 237b ocular foreign body in, 240, 240f orbital and periorbital disease and, 241 orbital emphysema and, 241b, 241242 retrobulbar abscess and, 242, 242f sonography of, 236, 237b tumor in, 240-241, 241f facial injuries and, 195, 196f gum and tongue tumors and, 216217 mandibular and maxillary injuries and, 195 mandibular infection and, 244, 245246f nasal cavity diseases and, 204-211, 205t nasal cavity tumor and, 204-210 computed tomography in, 208209, 209b, 209t evaluation of postoperativepostradiation nasal radiographs in, 206-208, 209f fluid, bone destruction, and nasal conchal pattern in, 204-205, 206b, 207-208f infection versus, 205-206, 206t magnetic resonance imaging in, 209-210

Head—cont’d nasal cavity tumor and—cont’d nasal septum and cribriform plate and, 204 normal radiology in, 204, 206f rhinography in, 208 radiographic disease indicators of skull, 193-194 sinonasal inflammatory disease and, 210, 210f skull tumors and, 199-203, 200-203f, 203b temporomandibular joint injuries and motion impairing disorders and, 195, 196f trauma to, 220-221, 221b, 390f Healing in avascular necrosis, 97 of fracture, 67-72f, 73 delayed, 67-72, 69-76f soft tissue viability and, 67 Heart, 481-553 cardiac shift and, 380, 381f, 382f, 383t cardiac silhouette analysis of, 493495, 494f, 494t double cardiac silhouette and, 484485, 486f echocardiogram of, 499-503 athletic hypertrophy and, 501 congenital muscular dystrophy and, 501-502 interpretation of Doppler tracing in, 500-501, 502f M-mode echocardiography and, 501 normal appearances in, 499, 500f overall approach in, 499-500 placement of intravascular embolization coils in, 500 enlargement in feline hyperparathyroidism, 363 fetal, 702 mediastinal fat and, 484, 485f normal anatomic variants resembling cardiac radiographic disease indicators, 482, 483f, 484f normal physiologic variants resembling cardiac radiographic disease indicators, 481, 482f positional variants resembling thoracic radiographic disease indicators, 485-486, 486f, 487f potential catheter-related injuries to, 496-498, 497t radiographic evaluation of pacemaker and, 552, 553f thymoma and, 459 trauma to, 549f, 549-550 tumor of, 518, 519t, 523f, 545-548, 546-547f Heart block, 537-538, 538f Heart disease, 517-542 angiocardiography in, 496-498, 497t, 498f, 498t aortic sinus rupture in, 540 arterial thrombosis in, 538-540

❚❚❚ Index

Heart disease—cont’d atrial standstill in, 538, 539f benefits of presurgical thoracic screening and, 517, 518t cardiac radiographic disease indicators in, 485-492 abnormal cardiac contour in, 488489, 488-489f aortic or main pulmonary arterial enlargement in, 489-490, 490f decreased heart size in, 486, 487f in dilated cardiomyopathy, 523 in heart failure, 543-544f, 543-545 in heartworm disease, 535 increased heart size in, 488, 488f normal anatomic variations resembling, 482, 483f, 484f normal physiologic variants resembling, 481, 482f pleural fluid in, 490-491, 491f pneumopericardium in, 491-492 positional abnormality in, 489489f positional variants resembling, 485-486, 487f in pulmonary embolism, 444 pulmonary hyperemia in, 490, 490f pulmonary oligemia in, 490, 491f cardiac silhouette analysis in, 493495, 494f, 494t cardiac ultrasound in, 499-503 athletic hypertrophy and, 501 congenital muscular dystrophy and, 501-502 interpretation of Doppler tracing in, 500-501, 502f M-mode echocardiography and, 501 normal appearances in, 499, 500f overall approach in, 499-500 placement of intravascular embolization coils in, 500 congenital, 504-516, 516t anomalous vessels in, 504 aortic and pulmonic insufficiency in, 512-513, 515f aortic stenosis in, 508, 511-512f aorticopulmonary window in, 507-508 atrial septal defect in, 504 Ebstein anomaly in, 512, 514f mitral and tricuspid insufficiency in, 512, 513f mitral and tricuspid stenosis in, 511 patent ductus arteriosus in, 505507, 506f pulmonic stenosis in, 508, 509f, 510f tetralogy of Fallot in, 511-512 truncus arteriosus in, 513-514 ventricular septal defect in, 504505, 505f cor pulmonale in, 540-541, 541f dilated cardiomyopathy in, 518, 523524, 524-525f

Heart disease—cont’d endocardiosis in, 517-518, 517-523f, 519t endocarditis in, 528, 531-532f heartworm disease in, 533-537 canine, 533-536, 536f feline, 536-537, 537f hypertrophic cardiomyopathy in, 524-525, 526-531f inherited ventricular tachycardia in German shepherds in, 538 ischemic, 538 myocarditis in, 525-528 pericardial disease in, 533, 534f, 535f peritoneal fluid in, 558t pulmonary-induced, 551, 551f third-degree heart block in, 537-538, 538f Heart failure in aorticopulmonary window, 507 in atrial standstill, 539f cardiac edema in, 433 cardiac tumor and, 545 as cause of pleural fluid, 376t chylothorax in, 422t cor pulmonale and, 541f expiratory film mimicking of, 368, 371f, 374f in mitral endocardiosis, 517, 519-522f in patent ductus arteriosus, 505 patterns of, 543-544, 543-544f in pericardial rupture, 549, 549f pleuropneumonia versus, 420 Heart valve catheter-related injury of, 497t normal nonselective opacification time of, 497t, 498t Heartworm disease, 533-537 arterial blockage in, 180 canine, 533-536, 536f chylothorax in, 422t feline, 536-537, 537f pulmonary hyperemia in, 490 Hemangiopericytoma, mediastinal, 462 Hemangiosarcoma, 546t of abdominal wall, 570, 571f cardiac, 488, 544, 545 hepatic, 556f, 583, 584f, 585t, 587f mediastinal, 462 primary, 131 pulmonary, 429-430 right atrial, 433f spinal, 315-317, 317f splenic, 617, 655, 657-658, 657-660f Hemarthrosis, 182 Hematocele, 716 Hematoma, 21, 22f of abdominal wall, 568 esophageal, 471 extraabdominal hemangiosarcoma versus, 570 extracerebral, 220 extrathoracic, 397 mural, 685-688, 687f pericardial, 533, 535f pleural, 399 splenic, 655, 661-662

743

Hematoma—cont’d in stroke, 228 subperiosteal, 196-197 Hematopneumatocele, 400 Hemilaminectomy blocked vertebra versus, 256t failed back surgery syndrome in, 301 ultrasound during, 276 Hemivertebra, 256t, 256-257, 314f Hemolytic anemia erythrocyte pyruvate kinase deficiency and, 191 splenomegaly secondary to, 662, 662f Hemomediastinum, 405f, 464 Hemopneumothorax, 399 Hemoptysis, 423 Hemoretroperitoneum, 560 Hemorrhage biopsy-related, 721 bladder, 685-688, 687f compartmental syndrome and, 21 cystography-related, 678 hyphema and, 239f, 240 intrapulmonary, 399, 400f left atrial, 518, 519t, 523f mediastinal, 458f, 464 pericardial, 535f, 549 pleural, 399 in splenic hemangiosarcoma, 658f in sternal fracture, 398 thymic, 456, 457f, 458f ureteral, 672t in warfarin poisoning, 440 Hemorrhagic enteritis, 619, 620f Hemorrhagic exudate, 559t Hepatic abscess, 557, 583-585 Hepatic congestion, 580 Hepatic cyst, 583, 587f Hepatic dysplasia, 561, 561f, 580 Hepatic failure, 558t Hepatic hemangiosarcoma, 556f, 583, 584f, 585t, 587f Hepatic lymphosarcoma, 560f, 579-580 Hepatic microvascular dysplasia, 591 Hepatic nodular hyperplasia, 580-581 Hepatic sweating, 580 Hepatic ultrasound, 465, 578-579f Hepatic vein, 588t Hepatitis, feline, 579, 579b Hepatocellular carcinoma, 582 Hepatocutaneous syndrome, 580 Hepatoma, 582 Hepatomegaly, 560, 560f Hepatozoan canis, 180 Hepatozoonosis, 107-111 Hereditary multifocal renal cystadenocarcinoma, 671 Herniation abdominal, 568, 569f diaphragmatic, 473-479 cardiac shift and, 383t as cause of pleural fluid, 376t chylothorax and, 422t diaphragmatic variation, visibility, displacement, and disfiguration and, 473, 474f, 475f

744

Index ❚❚❚

Herniation—cont’d diaphragmatic—cont’d imaging findings in, 475-477f peritoneopericardial, 478 pleuroperitoneal, 476-478 positive contrast peritonography in, 476, 478t disk, 249, 252f hiatal, 469t, 609, 610f pericardial, 383t, 549f, 549-550 peritoneal, 681 stomach, 382f Hiatal hernia, 469t, 609, 610f High-density foreign body, 23, 26f Hilar adenopathy, 387-388, 390f false radiographic disease indicator of, 374f in feline primary lung tumor, 423 in mediastinal disease, 456, 459f in nocardiosis, 415 Hindlimb location of sesamoid bones in, 45t traumatic deformities of, 90f Hip, 321-353 avascular necrosis of femoral head and, 325, 326-327f congenital epiphyseal dysplasia and, 325-328, 328f digital versus analog images of, 351 fractures and dislocations of, 329337, 334-337f acetabular, 329, 330f capital physeal, 329, 331-332f epiphysiolysis of femoral head and, 329-332 femoral head, 332-333, 333f femoral neck, 333, 334f multiple injuries in, 323f paracoxal mass in Doberman pinchers and, 337 postoperative assessment of femoral ostectomy muscle flap and, 334-337 proximal femoral, 329 spinal cord malacia and, 319 trochanteric, 333, 334f infections of, 353 normal canine, 339, 340-341f radiographic disease indicators of, 321 sacroiliac diastatic fracture and, 49f soft tissue sarcoma of, 136f traumatic deformities of, 90f Hip dysplasia, 338-352 acetabular relocation for, 349, 349t artificial hip for, 349-350, 350f in cat, 351, 351f early detection of, 339 explanations for owners, 346-347, 347-348f femoral head relocation for, 348 historical background of imaging in, 338 implant dislocation in, 69f normal breed hip variations and, 339 Orthopedic Foundation for Animals certification and, 339

Hip dysplasia—cont’d osteoarthritis and, 94-96, 95f, 103f postoperative assessment of, 350 previously injured hip versus, 346, 346f prognosis for, 348 progress examinations in, 350 radiographic disease indicators of, 321 radiographic features of, 339-342, 340-341f radiographic indicators of infectious surgical failure in, 351 radiographic indicators of noninfectious surgical failure in, 350-351, 351f role of stress radiography in, 338 sonographic evaluation in puppy, 351, 351f stressing of suspicious hip, 342, 345f, 346f unilateral, 342, 344, 345f Histiocytic sarcoma, 461-462, 463f Histiocytoma, malignant fibrous, 429 Histiocytosis, 461-462, 463f, 656-657 Histoplasmosis, 115-116, 415 Hookworms, 637 Hot spot, 124 Humeral joint congenital elbow dislocation and, 188f loose intra-articular bodies in, 7-9 retained cartilage core in ulnar metaphysis and, 169, 173, 175f Humeral shaft fracture, 43f Humeral theory of hypertrophic pulmonary osteoarthropathy, 168 Humerus abnormalities found in computed tomography of lameness, 147b comminuted fracture of, 59f congenital elbow dislocation and, 186 fibrosarcoma of, 127f incomplete ossification of condyle, 190 metaphyseal osteopathy in, 171f metastatic carcinoma of, 131f osteochondritis in, 152, 156, 156f, 157f osteosarcoma of, 123, 123f panosteitis in, 155f, 168f, 170f postoperative infection of, 111f posttraumatic osteoarthritis of, 80f primary bone tumor of, 125f secondary bone tumor of, 129f sterile abscess of, 119f synovial storage disease in, 105f tenosynovitis and, 178f Y-fracture of, 57f Hydrocele, 716, 717f Hydrocephalus, 218, 226-227, 227f Hydromyelia, 264, 299 Hydronephrosis, 617, 666-667, 668t, 672, 673f Hydrosyringomyelia, 264

Hydroureter, 672, 673f, 674f Hyoid bone, mucopolysaccharidosis and, 319 Hyperadrenocorticism, 600 Hypercalcemia, 704 Hypercalcemic nephropathy, 671 Hyperemia pulmonary in atrial septal defect, 504 cardiac edema and, 433 as cardiac radiographic disease indicator, 490, 490f in endocarditis, 532f in hypertrophic cardiomyopathy, 530f in mitral endocardiosis, 517, 520f in patent ductus arteriosus, 506f splenic, 660 Hyperostosis, 221 Hyperparathyroidism nutritional secondary, 175 osteopenia and, 194 pituitary tumor and, 222 Hyperperfusion, pulmonary, 490, 490f Hyperplasia adrenal, 700 cystic endometrial, 708 Hyperplastic nodule, splenic, 655-656, 656f Hyperplastic synovium, 105 Hypertension, pulmonary, 540-541, 541f cor pulmonale and, 551 in heartworm disease, 537 Hyperthyroidism, 363f, 363-364 Hypertrophic cardiomyopathy, 491f, 524-525, 526-531f Hypertrophic nonunion, 70f, 76f Hypertrophic osteodystrophy, 15, 17f, 167-168, 171f, 172f Hypertrophic osteopathy, 168 Hypertrophic pulmonary osteoarthropathy, 122, 168-169, 173f, 174f Hypertrophy benign prostatic, 689-690f compensatory renal, 665 Hypervascular lung, 490, 490f Hypervitaminosis A, 319 Hyphema, 239f, 240 Hypochondroplastic dwarfism, 173, 174t, 175f Hypoglycemia, 653 Hypokinesis, 444 Hypophosphatemic oncogenic osteomalacia, 397 Hypoplasia congenital intestinal, 638 of dens, 259f tracheal, 449 urethral, 715 Hypoproteinemia, 376t Hypothyroidism, 176, 450t Hypovascular lung, 490, 491f Hypovolemia, 486 Hysterography, 711

❚❚❚ Index

I Iatrogenic mural hematoma, 686, 687f Idiopathic pulmonary fibrosis, 440 Idiopathic pulmonary ossification, 445f, 445-446 Ileocolic intussusception, 646 Ileum, plate and screw fixation of, 69f Iliopsoas muscle strain, 180 Immature new bone, 5, 6f Immune-mediated osteoarthritis, 9899, 99f, 100f Immune-mediated vasculitis, 572 Immunoarthritis, 98-99, 99f, 100f extraarticular osteophyte in, 13f rickets versus, 186, 187f Impacted fracture, 49, 56f Impaction colonic, 646, 648f intestinal, 637, 638f Impingement exostosis, 195, 196f, 197f Implant dislocation in hip dysplasia, 69f Implant misapplication, 70 Incarceration, intestinal, 636 Inchworm colon, 649 Incision site, postoperative evaluation of abdominal wall, 568 Incisional gastropexy, 604 Inclusion cyst, 263 Incomplete fetal resorption, 704f, 704705 Incomplete fracture, 49, 57f Incomplete interventricular septum, 504-505, 505f Incomplete ossification of humeral condyle, 190 Increased density, 1 Increased organ size as abdominal radiographic disease indicator, 560, 560f Indium-labeled transferrin, 637 Infarction bone, 180 cerebral, 228 splenic, 660, 661 Infection in abdominal wall after surgery, 568 after facial depression fracture, 195 arteriovenous fistula and, 180 congenital hemivertebra versus, 256t cranial density in, 194 digital tumor versus, 131-133 of ear, 231-234, 232-234f extremital, 106-120 abscess and, 119, 119f, 120f blastomycosis in, 111, 115, 115f, 116f cancer versus, 118-119 chronicity of, 116-117, 116-119f coccidioidomycosis in, 111, 114f hepatozoonosis in, 107-111 histoplasmosis in, 115-116 nonaggressive bone lesions in, 15, 15f nonspecific bacterial, 107, 107f, 109t nuclear imaging of, 107, 108t

Infection—cont’d extremital—cont’d pathologic fracture and, 116, 116f Phialemonium ovatum in, 116 radiographic disease indicators of, 107 radiology of, 106-107 septic arthritis and, 117-118 as stimulus for new bone formation, 2-4, 4f surgical, 107, 110-114f terminology in, 106 trauma-related, 23-27, 27f fungal in discospondylitis, 306, 306t extremital, 115-116, 116f in osteomyelitis, 111, 245f pulmonary, 412-415, 412-416f hip, 351, 353 mandibular, 194, 244, 245-246f mediastinal, 462-463 nasal cavity lesions in dog and, 205t nasal neoplasia versus, 205-206, 206t ocular, 240 renal, 666-667f scrotal, 716 spinal, 305-309 deep paraspinal abscess in, 308, 308f discospondylitis in, 306, 306t, 307308f spondylitis in, 305 vertebral physitis in, 306-308 sternal, 398-399, 399f testicular and epididymal, 716-718 in tracheitis and tracheobronchitis, 364-365 uterine, 708 Infiltrative bowel disease, 618, 619t Inflammation in bronchitis, 452 of ear, 231-234, 232-234f of tear sac, 242 urethral, 695, 695f Inflammatory bowel disease, 618 Inflammatory polyp in ear, 234-235, 235f Inflammatory rhinitis, 205t Inhalation pneumonia, 384f, 407 Inherited ventricular tachycardia, 538 Injury biopsy-related, 721 cardiac, 549f, 549-550 chest, 397-406 as cause of pleural fluid, 376t cavitary lung lesions and, 386, 399-400, 401f chest wall injury in, 397, 398f diaphragmatic rupture in, 473, 475-477f gunshot wounds in, 404-405, 405f, 406f intrapulmonary hemorrhage in, 399, 400f lung laceration and collapse in, 399-400, 401f mediastinal injury in, 405-406

745

Injury—cont’d chest—cont’d pleural hemorrhage and hematoma in, 399 posttraumatic pneumothorax in, 400, 401-403f postural radiography in, 400-404, 403f, 404f sternal fracture in, 397-398, 398f sternal tumors, infections, and gas in, 398-399, 399f chronic nasal disease in dog and, 205t chylothorax following, 422t congenital hemivertebra versus, 256t craniocerebral, 220-221, 221b cystography-related, 678 endplate destruction in, 257t extremital, 21-92 apophyseal fracture in, 40, 43f articular fracture in, 40-41, 44f, 45f avulsion fracture in, 41, 45t, 46f bruise in, 21 carpal sprains in, 27-28, 28-34f, 29t chisel fracture in, 41, 46f closed fracture in, 41 comminuted fracture in, 41, 47f compartmental syndrome and, 2122 compression fracture in, 41, 47f corner fracture in, 46, 48f crush fracture in, 46, 48f delayed fracture healing and, 6272, 69f, 70-76f depression fracture in, 46, 49f diastatic fracture in, 46, 49f dislocated shoulder in, 28, 35f in dislocation of patella, 177 distal humeral growth-plate fracture in, 49, 51-52f elbow sprains in, 28, 34f, 35f experimental destabilization of canine genual joint and, 35-36 expression fracture in, 46 fabella injuries in, 38, 38f, 39f fault-line fracture in, 46-47 fracture classification using electronic databases and, 58 fracture repair and, 58-63, 62-67f fracture union and, 63, 67, 68f greenstick fracture in, 47, 49f growth plate fracture in, 47b, 4748, 48b, 50f gunshot fracture in, 49, 53-55f hairline fracture in, 49, 55f hematoma in, 21, 22f high-density foreign bodies and, 23, 26f impacted fracture in, 49, 56f incomplete fracture in, 49, 57f infection-related to, 23-27, 27f insufficiency fracture in, 53, 57f intercondylar stenosis and, 37 limb deformity secondary to growth-plate fracture and early closure in, 72, 80-91f longitudinal fracture in, 53, 58f

746

Index ❚❚❚

Injury—cont’d extremital—cont’d magnetic resonance arthrography of, 38, 39b magnetic resonance imaging of, 37-38 major tears, laceration, and trauma-related infection and abscess in, 23-27, 27f meniscal injuries in, 34-35 naturally occurring cruciate sprains in dogs and, 36f, 36-37, 37f oblique fracture in, 53, 58f open fracture in, 53, 59f pathologic fracture in, 53, 59f regeneration and, 72 segmental fracture in, 53, 60f sesamoid fracture in, 53-54, 60f simple fracture in, 54, 61f soft tissue calcification and, 22-23, 25f, 26f soft tissue foreign bodies and, 3940, 41t soft tissue gas and, 22, 23f, 24f spiral fracture in, 54, 61f stifle sprains in, 29, 34 strains, tendonitis, and bursitis in, 23, 26f stress fracture in, 54 T, Y, and V fractures in, 53, 57f talar neck fracture in, 54, 58 tarsal sprains in, 39, 40f transverse fracture in, 54, 61f traumatic amputation in, 58, 61t ultrasound of, 37 head ankylosis and impingement exostosis and, 195, 196f, 197f congenital temporomandibular deformity and dislocation and, 195-196, 197f cranial injuries and, 196-198, 198f facial injuries and, 195, 196f mandibular and maxillary injuries and, 195 megaesophagus following, 390f temporomandibular joint injuries and motion impairing disorders and, 195, 196f hip, 329-337, 334-337f acetabular fracture in, 329, 330f capital physeal fracture in, 329, 331-332f dysplasia versus, 346, 346f femoral head fracture in, 332-333, 333f femoral neck fracture in, 333, 334f multiple injuries in, 323f proximal femoral fracture in, 329 radiographic disease indicators of, 321 trochanteric fracture in, 333, 334f intestinal, 639-641 mediastinal, 405-406 ocular, 237t, 238-240, 239f, 240f

Injury—cont’d pelvic fracture-associated, 322-324 penile, 718 pharyngeal perforation in, 358-359 spinal, 275-284 blocked vertebra versus, 256t cervical spinal fracture in, 275-276, 276-278f disk rupture in, 280, 284f dural laceration in, 284 thoracic spinal fracture in, 276, 279-284f, 280 as stimulus for new bone formation, 2, 3f testicular, 716, 717f thoracic, 397-406 chest wall injury in, 397, 398f gunshot wounds in, 404-405, 405f, 406f intrapulmonary hemorrhage in, 399, 400f lung laceration, collapse, and cavitary lesions in, 399-400, 401f mediastinal injury in, 405-406 pleural hemorrhage and hematoma in, 399 posttraumatic pneumothorax in, 400, 401-403f postural radiography in, 400-404, 403f, 404f sternal fracture in, 397-398, 398f sternal tumors, infections, and gas in, 398-399, 399f ureteral, 677 urethral, 718 Instability cervical vertebral, 264-267, 265-268f lumbosacral, 268 Insufficiency fracture, 53, 57f Insulinoma, 653 Intercapital ligament, 286 Intercarpal dislocation, 28, 29f Intercondylar stenosis, 37 Interior atelectasis, 383, 385f Interior bone deposit, 5 Interlobar fissures, 407 Interlobar hematoma, 399 Intermuscular hematoma, 21, 568 International Elbow Working Group, 163, 163t Intersternal gas, 399 Interstitial cystitis, 678 Interstitial fibrosis, 446 Interstitial pattern, 395 Interstitial pneumonia, 408, 551, 551f Intertarsal joint calcaneal longitudinal fracture and, 58f impaction fracture of, 56f Intertrochanteric osteotomy, 348 Intervertebral disk diminished size of, 249, 250f, 251t, 252-254f discospondylitis and, 306, 306t, 307308f fenestration of, 256t

Intervertebral disk—cont’d normal anatomic variant resembling spinal radiographic diagnostic indictor, 251t vertebral new bone deposition and, 254, 254f, 259 Intervertebral disk disease, 285-302 anatomy in, 285 bulging disk in, 300 cord swelling in, 299 diagnostic terminology in, 285-286 diskography in, 300 epidurography in, 299 intraosseous vertebral venography in, 300 lesion prevalence in, 286, 286f magnetic resonance imaging in, 272t, 300-301 myelography in, 288-299, 295-297f background and beginnings of, 288 computed tomography with, 298299 epidural injection in, 291, 291t, 292f failure of contrast flow in, 295-298, 298f fat complications in, 293, 293f magnetic resonance imaging with, 299 needle placement in, 293, 294f patient positioning in, 293 postural maneuvers in, 298 risks in, 290-291, 291t test injection in, 294 timing of, 288-290 plain radiography in, 286-288, 287290f ruptured disk in, 300 Intestinal cryptococcosis, 619 Intestinal fluid, 614 Intestinal gas, 557-558 abdominal hernia and, 568 plain film of, 614 Intestinal transition zone, 644f Intestinal ultrasound, 625 Intestine, 614-642 abscess of, 639f, 641 adhesion of, 640f, 641 bowel distribution pattern and, 616617 calcification of, 564t congenital malformations of, 638-639 diaphragmatic hernia and, 475f, 477f, 478t displacement of by abdominal hernia, 637 by pyometra, 709f duodenal thickening secondary to pancreatitis, 617-618, 618f duodenal ulcer and, 617 enteritis and, 618-619, 620-621f foreign body in, 565f, 619-627 barium and iodine films of, 622625, 623-629f fixed, 627, 630f free linear, 627

❚❚❚ Index

Intestine—cont’d foreign body in—cont’d as incidental finding, 619 metallic, 619 obstructive pattern and, 621-622, 622t plain films of, 620-621, 622f sonography of, 625 gas in, 557-558 impaction of, 637, 638f incarceration of, 636 infiltrative bowel disease and, 618, 619t inflammatory bowel disease and, 618 intussusception of, 627-630, 631-632f normal barium film variations of, 615 normal iodine films of, 615-616 normal plain film variations of, 614615, 615f normal sonographic appearance of, 617, 617t parasitic infection of, 637 perforation of, 572, 634b, 634-635 colonography-related, 644 impaction and, 637, 638f peritonitis and, 572 pneumoperitoneum in, 559t potential sonographic indicators of disease, 617 protein-losing enteropathy and, 637 short-bowel syndrome and, 638 torsion of, 559t, 635-636, 635-636f trauma to, 639-641 tumors of, 630-632, 632f leiomyosarcoma and leiomyoma in, 633, 634f lymphosarcoma in, 419f, 618, 632633, 633f Intraabdominal calcification, 561, 561f Intraabdominal intestinal entrapment, 636 Intraabdominal sponge, 710 Intraaxial trauma, 220, 221b Intracardiac blood flow, 500-501, 502f Intracardiac fistula, 528 Intracardiac tumor, 545 Intracondylar femoral fracture, 329 Intracranial lesion, 218-230 in aspergillosis, 225, 225f in blastomycosis, 226 in brain abscess, 226, 226t brain biopsy in, 228-229 in brain cyst, 227-228 in brain tumor, 221-224, 222t, 223224f cerebrovascular accident in, 228 choice of imaging study in, 220, 220t computed tomographic evaluation of postoperative brain in, 229 computed tomography in, 219, 220t in craniocerebral trauma, 220-221, 221b in encephalitis, 224-225, 225b in focal granulomatous meningoencephalitis, 221, 221b

Intracranial lesion—cont’d in hydrocephalus, 226-227, 227f magnetic resonance imaging in, 219220, 220t in necrotizing meningoencephalitis, 225 normal anatomic variants and, 228 normal ventricular variation and, 220 nuclear medicine imaging in, 218 seizure in, 221 sonography in, 218, 219t special radiographic procedures in, 218, 219f Intradiskal osteomyelitis, 306, 306t, 307-308f Intrafetal gas, 705 Intrahepatic shunt, 580 Intramedullary pin dislocation, 184, 184f Intramuscular hematoma, 21, 22f, 568 Intranasal tumor, 204-210 computed tomography in, 208-209, 209b, 209t deviation and destruction of vomer in, 193 evaluation of postoperativepostradiation nasal radiographs in, 206-208, 209f fluid, bone destruction, and nasal conchal pattern in, 204-205, 206b, 207-208f infection versus, 205-206, 206t magnetic resonance imaging in, 209210 nasal septum and cribriform plate and, 204 normal radiology in, 204, 206f rhinography in, 208 Intraosseous arteriovenous fistula, 133 Intraosseous epidermoid cyst, 133-134 Intraosseous vertebral venography, 269, 300 Intrapelvic bladder, 682 Intrapericardial cyst, 533 Intraperitoneal fluid, 555-556, 556-557f, 558t, 559t Intraprostatic cyst, 690 Intrapulmonary hemorrhage, 399, 400f Intrarenal cyst, 668, 670f Intrauterine mass, 711t, 712 Intravascular embolization coil, 500 Intravenous catheter fragment, 184, 184f Intravenous urography, 676, 685 Intravertebral disk herniation, 300 Intravisceral gas, 557-560 Intussusception cecocolic, 644-646 gastroesophageal, 609, 611f ileocolic, 646 intestinal, 627-630, 631-632f peritonitis and, 572, 573f Involucrum, 2, 4f Iodine film in intestinal obstruction, 622-625, 623-629f in intestinal torsion, 635-636 of normal intestine, 615-616

747

Iodine solutions, 615 Iohexol, 290, 616 Ionic compositions, 615-616 Iopamidol, 290 Iridocyclochoroiditis, 411 Iris, 237t Ischemia, 21 extremital, 182 in hematoma, 21 as stimulus for new bone formation, 2 Ischemic heart disease, 538 Ischemic myolysis, 568 Ischium avulsion fracture of, 66f chondrosarcoma of, 127f Isolated nonvalvular aortic stenosis, 515 Isolated right ventricular myopathy, 523

J Jaw bone density of, 193-194 mandibular and maxillary injuries of, 195, 196f Jaw locking, 195-196, 197f Jejunal impaction, 638f Joint body, 7-9, 9-12f Joint fusion, 195, 196f, 197f Joint pain, 325 Joint tumor, 124, 130, 132f Jugular catheterization, 422t Juxtaarticular cyst, 264 Juxtacortical osteosarcoma, 130-131

K Kartagener syndrome, 210, 567 Kidney, 663-671 abnormal bowel distribution patterns and, 617 adrenal tumor and, 700 antifreeze poisoning and, 671 calcification of, 564t canine abdominal malignant histiocytosis and, 656-657 chronic renal failure and, 671 compensatory renal hypertrophy and, 665 congenital renal disease and, 665666, 666f giant kidney worm in, 667, 667f hypercalcemic nephropathy and, 671 imaging strategy for, 663-664, 664b, 664t infection in, 666-667f intrarenal cysts in, 668, 670f leptospirosis and, 666 nuclear imaging of, 665 perirenal cysts in, 667-668, 670f renal calculi and, 561, 562f, 667-670f renal obstruction and hydronephrosis and, 666-667, 668t transplant rejection in, 671 tumor of, 668t, 668-671, 670f ultrasound-guided biopsy of, 663 ultrasound of, 664-665, 665f

748

Index ❚❚❚

Kidney stones, 561, 562f, 667-670f Klebsiella pneumoniae, 583

L L5-SI ratio, 621 Laceration, 23-27, 27f cystography-related, 678 penile, 718 pulmonary, 399-400, 401f traumatic dural, 284 Lameness in calcaneal dislocation of superficial digital flexor tendon, 180 in capital physeal fracture, 329 in congenital elbow dislocation, 186 in metaphyseal osteopathy, 167 in nonunion, 70 in panosteitis, 167 secondary to arterial blockage by heartworms, 180 synovial tumors and, 130 Laminectomy blocked vertebra versus, 256t failed back surgery syndrome in, 301 Larynx abnormal, 359 combined laryngeal-pharyngealesophageal foreign bodies and, 360 cyst of, 360 everted laryngeal saccules and, 360 normal imaging findings, 356 paralysis of, 449, 450t, 469t polyps and abscesses of, 360, 360f tumor of, 360, 360t Late-term fetal death, 705 Lateral collateral ligament, 98t Lateral decubitus radiography, 400404, 403f, 404f Lateral ridge of anconeal process, 139, 141f Lateral ventricle, 220 Lead poisoning, 619 Left atrial doming, 488f, 517-518, 519520f Left atrium catheter-related injury of, 497t hemorrhage of, 518, 519t, 523f normal nonselective opacification time of, 497t, 498t optimal contrast deployment in selective angiocardiography, 498t Left lateral projection, 485, 487f Left-sided cardiomegaly, 493 Left-sided heart failure, 518, 523-524, 524-525f Left-to-right shunt, 505 Left ventricle adaptive hypertrophy of, 501 catheter-related injury of, 497t dilated cardiomyopathy and, 518, 523-524, 524-525f hypertrophic cardiomyopathy and, 524-525, 526-531f isolated right ventricular myopathy and, 523

Left ventricle—cont’d normal nonselective opacification time of, 497t, 498t optimal contrast deployment in selective angiocardiography, 498t pacemaker and, 552, 553f third-degree heart block and, 537 Legg-Calv[ac]e-Perthes disease, 96-98, 97f, 325, 326-327f Leiomyoma esophageal, 470 gastric, 606-607, 607f intestinal, 633, 634f tracheal, 451 Leiomyosarcoma esophageal, 470 gastric, 606-607, 607f intestinal, 633, 634f soft tissue swelling in, 19f Leishmaniasis, 180-181 Lens, 237t Leptospirosis, 666 Lesion superimposition in pulmonary metastasis, 428f Ligament carpal sprain and, 27-28, 28-34f, 29t dislocated shoulder and, 28, 35f elbow sprain and, 28, 34f, 35f meniscal injuries and, 34-35 naturally occurring cruciate sprains in dog, 36f, 36-37, 37f tarsal sprain and, 39, 40f Ligation, ureteral, 672, 672t, 675f Limb deformity as radiographic disease indicator, 17, 19f secondary to growth-plate fracture and early closure, 72, 80-91f Limb edema, 322 Linear intestinal foreign body, 627 Lipid pneumonia, 415-416, 443 Lipoma, 137 Liposarcoma, 137 Lithotripsy, 677 Litter size estimation, 703, 704t Liver abnormal bowel distribution patterns and, 616 biopsy of, 721 calcification of, 564t decreased size of, 561, 561f diaphragmatic hernia and, 475f, 476f, 478, 478t disease of, 575-593 acute abdominal colic in, 566b biliary cystadenoma and cystadenocarcinoma in, 582, 583f diffuse, 579b, 579f, 579-580, 580f gallbladder disease and, 585-587, 586-587f hepatic abscess in, 583-585 hepatic hemangiosarcoma in, 583, 584f, 585t hepatic radiology in, 575, 576f, 577f

Liver—cont’d disease of—cont’d hepatic ultrasound in, 465, 578579f imaging of liver function in, 576577 portosystemic shunts in, 587-588f, 587-591, 588t, 591b regional and localized, 580-582, 581-582f tumors and biliary obstruction in, 583 enlargement of, 560, 560f failure of, 558t fetal, 702 gas in, 557 mass in canine abdominal malignant histiocytosis and, 656-657 parahepatic organs in sonographic examination versus, 720 Lobar emphysema, 551 Lobar tracing, 376 Lobster claw, 186 Local anesthesia in ultrasound-guided, free-hand biopsy, 719 Localized bone deposition, 15, 15f Localized bone infection, 106 Localized bone loss, 10-15 aggressive lesions and, 10-15, 13f, 14f nonaggressive lesions and, 15, 15f of spine, 254, 255, 255f Localized liver disease, 580-582, 581582f Long digital extensor tendon avulsion fracture, 23 Longitudinal fracture, 53, 58f Lordosis, 263 Lumbar spine fracture of, 280, 281-284f intervertebral disk disease in, 286, 286f multiple myeloma and, 255f spondylosis of, 303, 304f tumor of, 315f Lumbarization, 258-262, 261f Lumbosacral spine dermoid sinus of, 263 discospondylitis of, 307f, 308f fracture of, 284f intervertebral disk disease in, 286, 286f oblique view of, 250f spondylosis of, 254f, 303 stenosis of, 268b, 268t, 268-270, 270271f, 272t, 273t Luminal hematoma, 686, 687f Lung abscess of in foreign body pneumonia, 416, 417f pyothorax and, 420f calcification of, 445f, 445-446 canine osteosarcoma metastasis to, 123 consequences of barium in, 595, 596f fetal, 702

❚❚❚ Index

Lung—cont’d foreign body in, 447 hemorrhage in warfarin poisoning, 440, 441f pulmonary metastasis in osteosarcoma and, 122 trauma to, 399-404 intrapulmonary hemorrhage in, 399, 400f laceration, collapse, and cavitary lesions in, 399-400, 401f posttraumatic pneumothorax in, 400, 401-403f postural radiography in, 400-404, 403f, 404f Lung consolidation, 380-383, 384f after near drowning, 439, 439f after near strangulation, 439, 439f, 440f in bronchiectasis, 454f chest trauma and, 403f in electric shock, 440 in lung-lobe torsion, 436 in pneumonia, 407-408 pulmonary metastasis versus, 427f in warfarin poisoning, 440 Lung disease, 436-448 acute respiratory distress syndrome in, 443 allergic bronchitis in, 436, 437f congenital pulmonary cysts in, 446 disseminated intravascular coagulation in, 441-443 electric shock in, 440, 442f generalized pulmonary calcification secondary to Cushing’s disease in, 446 idiopathic pulmonary fibrosis in, 440 idiopathic pulmonary ossification in, 445f, 445-446 lung-lobe torsion in, 436 near drowning in, 438-439, 439f near strangulation in, 439, 439f, 440f neurogenic pulmonary edema in, 444-445, 445b paraquat poisoning in, 440, 442f pleuritis in, 419-420, 419-420f pneumonia in, 407-418 in actinomycosis, 408, 415 Angiostrongylus vasorum in, 408409 in aspergillosis, 412 bacterial, 408-412f in blastomycosis, 412-415f classification of, 407 in coccidioidomycosis, 412-415, 416f computed tomography in, 408 in cryptococcosis, 415 expiratory film mimicking of, 368, 372f feline endogenous lipid, 443 Filaroides hirthi in, 409-411 foreign body, 416, 417f in histoplasmosis, 415 hypertrophic pulmonary osteoarthropathy and, 168

Lung disease—cont’d pneumonia in—cont’d lipid, 415-416 in nocardiosis, 415 in paragonimiasis, 411 Pneumocystis carinii, 447 radiography in, 407-408 in Rocky Mountain spotted fever, 411-412 secondary to megaesophagus, 384f Toxoplasma gondii in, 411 ultrasound in, 408 pulmonary arterial and parenchymal calcification in, 446 pulmonary foreign body in, 447 pulmonary granulomatosis in, 446f, 447, 447f pulmonary infiltrates with eosinophilia in, 445, 445f pulmonary patterns in, 393-396 pulmonary thrombosis, embolism, and thromboembolism in, 443444 radiation pneumonitis in, 446 smoke inhalation in, 438, 438f thoracic radiographic disease indicators in, 368-392 cardiac shift in, 380, 381f, 382f, 383t cystic and cavitary lung lesions in, 386, 387t, 388f diaphragmatic deformity in, 388390, 391f dilated esophagus in, 386-387, 389f, 390f extrapleural lesion in, 369 hilar and cranial sternal adenopathy in, 387-388, 390f large thoracic masses in, 386, 387f multiple lung nodules in, 384-386, 386f normal anatomic variants resembling, 368, 369t, 369-371f normal physiologic variants resembling, 368, 371-373f pleural fluid in, 376t, 376-378, 377t, 377-378f, 379t pneumomediastinum in, 379-380, 381f pneumothorax in, 378-379, 380381f positional variants resembling, 368, 370t, 373f, 374f pulmonary atelectasis in, 383, 385f pulmonary consolidation in, 380383, 384f solitary lung nodule in, 384 technical variants resembling, 368, 375f ultrasound-guided thoracic biopsy and, 390-391 warfarin poisoning in, 439-440, 441f, 442f Lung edema, 433-435 in acute pancreatitis, 650 after near strangulation, 439

749

Lung edema—cont’d after smoke inhalation, 438, 438f cardiac, 433 disseminated intravascular coagulation versus, 441 in electric shock, 440, 442f in endocarditis, 532f heart failure and, 543, 543f in hypertrophic cardiomyopathy, 530f lymphosarcoma versus, 429, 431f in mitral endocardiosis, 517, 520f neurogenic, 444-445, 445b noncardiac, 433-435, 433-435f, 435t Lung-lobe torsion, 436 Lung mass, 386, 387t cardiac shift and, 383t hilar adenopathy and, 388 mediastinal mass versus, 456 Lung nodule multiple, 384-386, 386f solitary, 384 Lung tumor, 386, 387f, 423-432 benign, 431 cardiac shift and, 383t cavitation in, 427 chylothorax and, 422t hemangiosarcoma as, 429-430 judging growth of, 427 lateral views of, 424-426 malignant fibrous histiocytoma as, 429 mammary carcinoma as, 429 mast cell tumor as, 430-431 mediastinal lymphosarcoma versus, 461 nonstructured or poorly structured pulmonary metastasis in, 429, 431f primary, 423, 424t, 424-426f pulmonary lymphosarcoma as, 431 pulmonary metastases and, 426-427, 426-430f secondary, 423-424 spontaneous regression of, 429 Lungworm, 409-411 Luteinizing hormone, ovulation and, 702 Luxation, 15-17, 18f, 19f Lymph node abdominal, 562-566 calcification of, 564t Lymph system, 421 Lymphangiography, 422 Lymphocytic portal hepatitis, 579 Lymphoma adrenal, 700 gastric, 606-607, 607f hepatic, 616 ocular, 241f renal, 617, 669-671, 670f spinal canal, 310 Lymphomatoid granulomatosis, 447 Lymphosarcoma cardiac, 546t chylothorax and, 422t hepatic, 560f, 579-580

750

Index ❚❚❚

Lymphosarcoma—cont’d intestinal, 419f, 618, 630, 632-633, 633f mediastinal, 459-461, 461-462f pulmonary, 431 pulmonary edema versus, 429, 431f splenic, 658-659

M M-mode echocardiography, 501 Macroadenoma, 222-223, 223-224f, 600 Magnetic resonance arthrography of stifle sprain, 38, 39b Magnetic resonance imaging of avascular necrosis, 97-98 in brain disease and injury, 219-220, 220t of cataracts, 237-238 of cranial nerve sheath tumor, 223 in discospondylitis, 306 in encephalitis, 225 of eye, 236, 237b of facetal cysts, 264 of feline organs, 566-567 in focal granulomatous meningoencephalitis, 221b of glioma, 222, 222t of hip infection, 353 in hydrocephalus, 227 in intervertebral disk disease, 300301 in lumbosacral stenosis, 270-271f, 272t, 273t of meningioma, 221, 222t myelography with, 299 in nasal cavity tumor, 209-210 in necrotizing meningoencephalitis, 225 of normal canine bowel, 566 in orbital disease, 241 of orbital tumor, 242 of osteoarthritis, 93 of osteochondritis, 152 in otitis media, 234 of pituitary adenoma, 223-224f of portosystemic shunt, 590 relative signal strengths emitted by abdominal organs of cats, 566567 of spinal arachnoid cyst, 263 of spinal tumor, 315, 316t in spondylosis, 303 of stifle sprain, 37-38 in stroke, 228 in traumatic cervical dislocation, 276 Magnetography, 700 Malformation diaphragmatic, 388-390, 391f in hip dysplasia, 321 orofacial, 244, 246f of small intestine, 638-639 spinal, 258-262 atlantoaxial dislocation in, 258, 259f blocked vertebrae in, 258 hemivertebra in, 258, 259-261f lumbarization in, 258-262, 261f

Malformation—cont’d spinal—cont’d sacralization in, 261f, 262 spinal disease versus, 256t temporomandibular, 195-196, 197f ureteral, 673, 675-676f urethral and vaginal, 715 Malignant bone tumor, 121-131 of joint, 124, 130, 132f metastatic melanoma in, 130 parosteal sarcoma in, 130-131 periosteal new bone and, 4, 4f, 5f primary, 121-123, 122t, 123-129f primary hemangiosarcoma in, 131 radiologic findings in, 123-124, 129131f secondary, 123 Malignant fibrous histiocytoma, 429 Malignant histiocytosis, 461-462, 463f Malignant schwannoma, 181 Malignant synovioma, 124, 130, 132f Malignant transformation, 180, 317 Malunion, 70-72, 77-80f hip dysplasia and, 346f Mammary carcinoma, 427f, 429 Mammary gland adenocarcinoma, 427f, 429 Mandible bone loss in renal osteodystrophy, 194 craniomandibular osteopathy and, 244 infection of, 244, 245-246f injuries to, 195, 196f tumors of, 199, 202f, 203f Mandibular osteopathy, 244 increased jaw density in, 193 new bone in, 193-194 Margination of new bone, 5 Mass abdominal, 562, 565f abdominal organ versus, 721 cervical, 358, 358f, 359f hepatic canine abdominal malignant histiocytosis and, 656-657 parahepatic organs in sonographic examination versus, 720 lung, 386, 387f, 423 cardiac shift and, 383t hilar adenopathy and, 388 mediastinal versus, 456 mediastinal abnormal esophageal transport and, 469t pulmonary versus, 456 tracheal collapse and, 450 ultrasound of, 457, 460f morphology of, 564t nasal, 193 obesity versus, 369f ovarian, 713b paracoxal, 337 in paraprostatic cyst, 690 parathyroid, 362-363 peripancreatic, 652-653 thyroid, 363f, 363-364

Mass—cont’d tracheal, 451 tumoral calcinosis and, 179, 179f uterine, 711t, 712 in villonodular synovitis, 182 Mass effects, 616 abdominal, 562 mediastinal, 456-457, 456-460f of pyloric tumor, 608f stump granuloma and, 710 uterine, 709 Mast cell tumor, 430-431 splenic, 655 tracheal, 451 Mastocytoma, 617 Mature new bone, 5-7, 7f, 8f Maxilla dental abscess in, 214f, 215f dental and periodontal tumors and, 216, 216f dentition and, 213f fibrosarcoma of, 201f injuries of, 195 Maxillary gland mucocele, 362 Mean colonic filling time, 643 Mean colonic residence times, 643 Mechanical dystocia, 705-706f Mechanical forces in new bone deposition, 3f Mechanical intussusception, 628 Medial collateral ligament, 98t Medial coronoid process osteochondritis, 138-139, 144f, 150f, 157f Medial epicondyle avulsion fracture, 46f Medial malleolar lesion, 161-162 Mediastinal air, 463-464 Mediastinal blastomycosis, 464, 464f Mediastinal disease, 456-465 abscess in, 463 approach to mediastinal masses, 456 blastomycosis in, 464, 464f cysts in, 462 hemomediastinum in, 464 histiocytosis in, 461-462, 463f lymphosarcoma in, 459-461, 461462f mass effects in, 456-457, 456-460f mediastinitis in, 462-463 pneumomediastinum in, 463-464 pulmonary versus mediastinal mass in, 456 thymoma in, 457-459, 460f vascular tumors in, 462 Mediastinal fat, 456, 457f, 484, 485f Mediastinal fluid, 463 Mediastinal hemorrhage, 464 Mediastinal injury, 405-406 Mediastinal mass abnormal esophageal transport and, 469t approach to, 456 in thymoma, 459 tracheal collapse and, 450 ultrasound of, 457, 460f

❚❚❚ Index

Mediastinal shift, 380, 381f, 382f, 383t chest trauma and, 399 in lung-lobe torsion, 436 in thyroid-induced myopathy, 527f Mediastinal tumor as cause of pleural fluid, 376t chylothorax and, 422t Mediastinitis, 462-463, 466 Medullary bone deposit, 5 Medullary rim sign, 664-665, 665f Megacolon, 646 Megaesophagus, 386-387, 389f, 390f, 466, 467-469f chest trauma and, 403f pneumonia secondary to, 384f Megaureter, 672, 673f Melanoma, 130 Membranous septum, 504 Meningeal tail, 222 Meningioma, 221, 222t, 317 Meningitis, 263 Meningocele, 264 Meningoencephalitis focal granulomatous, 221, 221b necrotizing, 225 Meningomyelocele, 264 Meniscal injury, 34-35 Meniscal ossification, 98t Meniscus, 98t Mesenteric arterial portography, 588 Mesenteric arteriography, 478t Mesenteric avulsion, 639, 641 Mesenteric calcification, 564t Mesenteric thrombus, 622t Mesenteric volvulus, 636 Mesonephric duct remnant, 711t Mesothelioma, 546t, 547 Metabolic disorders, intraabdominal calcification in, 561 Metacarpal bite wound-related osteomyelitis of, 107f displaced short oblique fracture of, 48f enchondroma of, 121 malunion of, 79f osteosarcoma of, 126f Metallic intestinal foreign body, 619 Metaphyseal deformity in rickets, 186 Metaphyseal lysis as radiographic disease indicator, 15, 16f, 17f in vertebral physitis, 308 Metaphyseal osteopathy, 7f, 15, 17f, 167-168, 171f, 172f increased jaw density in, 193 Metaphysis primary bone tumor in, 121 retained cartilage core in, 169, 173, 175f Metastasis cardiac, 546t in chondrosarcoma, 123 in osteosarcoma, 122 pulmonary, 426-427, 426-431f, 429 skip, 131f Metastatic bone tumor, 123

Metastatic carcinoma pancreatic, 587f spinal, 315f Metastatic melanoma, 130 Metatarsal enchondroma of, 121 oblique fracture of, 58f Metatarsophalangeal joint, 45t Metrizamide, 290, 291 Microadenoma, 222-223, 223-224f, 600 Microchip, migration of, 39 Microlithiasis, pulmonary, 445f Micrometastasis, 121 Middle ear disease, 231-234, 232-234f Middle mediastinal compartment, 456 tumor of, 457-459, 460f Milk teeth, 213, 213f Mineralization of biceps brachii tendon, 178 of cartilage fragment, 98t of supraspinatus tendon, 177-178 Misplaced coronoid process, 195-196, 197f Mitral endocardiosis, 517-518, 517523f Mitral insufficiency, 512, 513f, 516t, 517-518, 518-521f abnormal cardiac contour in, 488, 488f Mitral regurgitation, 517-518, 518-521f Mitral stenosis, 511 Monteggia’s fracture, 102f Motility dysfunction, esophageal, 466470, 469t, 470f Motion impairing disorders of temporomandibular joint, 195, 196f Motion unsharpness in thoracic radiography, 48 MRI. See Magnetic resonance imaging. Mucocele biliary, 586-587, 586-587f salivary, 362 Multicameral bone cyst, 133t Multicompartmental mediastinal lesion, 456 Multiple cartilaginous exostoses, 317 Multiple exostosis in cat, 133 Multiple fracture, 53, 60f Multiple lung nodules, 384-386, 386f Multiple myeloma localized bone loss in, 255f spinal, 315 Mural abscess, 711t Mural hematoma, 685-688, 687f Muscle mimicking of thoracic radiographic disease indicators and, 370f trauma to, 21-23 bruise in, 21 compartmental syndrome and, 2122 hematoma in, 21, 22f soft tissue calcification and, 22-23, 25f, 26f soft tissue gas and, 22, 23f, 24f

751

Muscle—cont’d trauma to—cont’d strains, tendonitis, and bursitis and, 23, 26f tears, laceration, infection, and abscess in, 23-27, 27f tumor of, 137f Muscle avulsion of abdominal wall, 569-570, 571f Muscle flap, femoral ostectomy, 334337 Muscular atrophy in capital physeal fracture, 329 in pelvic fracture, 322 Muscular dystrophy, 501-502 Myasthenia gravis abnormal esophageal transport in, 469t megaesophagus and, 466, 470f Mycotic infection in discospondylitis, 306, 306t extremital, 115-116, 116f in osteomyelitis, 111, 245f pulmonary, 412-415 aspergillosis in, 412 blastomycosis in, 412-415f coccidioidomycosis in, 412-415, 416f cryptococcosis in, 415 histoplasmosis in, 415 Myelitis, 263 Myelographic contrast media, 290 failure of flow, 295-298, 298f postmyelographic removal of, 291 subdural and central cord injections of, 299 test injection of, 294 Myelographic filling defects, 299 Myelography in cervical spinal fracture, 275-276 in cervical spondylopathy, 266 in dermoid sinus, 263 in discospondylitis, 306 in intervertebral disk disease, 288299, 295-297f background and beginnings of, 288 computed tomography with, 298299 epidural injection in, 291, 291t, 292f failure of contrast flow in, 295-298, 298f fat complications in, 293, 293f magnetic resonance imaging with, 299 needle placement in, 293, 294f patient positioning in, 293 plain radiography versus, 286-288, 287-290f postural maneuvers in, 298 risks in, 290-291, 291t test injection in, 294 timing of, 288-290 in lumbosacral stenosis, 269, 273t in spinal arachnoid cyst, 263 spinal cord malacia-induced by, 319 in spinal tumor, 310, 311t, 311-315f

752

Index ❚❚❚

Myelolipoma, splenic, 656, 656f Myelomalacia, spinal cord, 319 Myelophthisic anemia, 180 Myocardial contusion, 549 Myocarditis, 525-528 Myositis ossificans, 2 Myxoma, cardiac, 546t

N Nail, radiographic and sonographic features of, 41t Nailbed carcinoma, 134f, 134-135 Napkin-ring carcinoma, 648f Nasal bone destruction, 193 Nasal cavity aspergillosis and, 225, 225f diseases of, 204-211, 205t facial depression fracture and, 195 gunshot wound and, 197-198 normal radiology of, 204, 206f sinonasal inflammatory disease of, 210, 210f tumor of, 204-210 computed tomography in, 208209, 209b, 209t deviation and destruction of vomer in, 193 evaluation of postoperativepostradiation nasal radiographs in, 206-208, 209f fluid, bone destruction, and nasal conchal pattern in, 204-205, 206b, 207-208f infection versus, 205-206, 206t magnetic resonance imaging in, 209-210 nasal septum and cribriform plate and, 204 rhinography in, 208 Nasal fluid, 193 Nasal mass, 193 Nasal septum, 204 Nasopharyngeal foreign body, 359, 359f Nasopharyngeal polyp, 234-235, 235f Nasopharynx, 355 Near drowning, 438-439, 439f Near strangulation, 439, 439f, 440f Neck, 355-367 abnormal larynx and, 359 cervical masses and, 358, 358f, 359f combined laryngeal-pharyngealesophageal foreign bodies and, 360 everted laryngeal saccules and, 360 exterior foreign body causing partial strangulation and, 358 fracture of, 275-276, 276-278f laryngeal cyst and, 360 laryngeal polyps and abscesses and, 360, 360f laryngeal tumors and, 360, 360t larynx and, 356 parathyroid masses and, 362-363 pharyngeal foreign body and, 359, 359f pharynx and, 355-356, 356-357f

Neck—cont’d punctured or ruptured trachea and, 364 retropharyngeal adenopathy and, 362 salivary gland disease and, 361-362, 362f swallowing process and, 356-358, 358t thyroid masses and hyperthyroidism and, 363f, 363364 tracheal dilation and, 364 tracheal foreign body and, 365 tracheal stenosis and, 364 tracheitis and tracheobronchitis and, 364-365 traumatic pharyngeal perforation and, 358-359 tumors of, 365, 365f, 366f Necrosis of gallbladder, 586 in hematoma, 21 salivary, 361-362 spinal cord, 319 splenic, 661 Necrotizing encephalitis, 225 Necrotizing infection, 180 Necrotizing meningoencephalitis, 225 Needle enhancement in biopsy, 720 Needle placement in myelography, 293, 294f Negative-contrast cystography, 679, 679f Neocortex, 180 Nephroblastoma, 671 Nephropathy, hypercalcemic, 671 Nerve root compression in intravertebral disk herniation, 300 spinal cord, 263-274 cauda equina syndrome in, 268b, 268t, 268-270, 270-271f, 272t, 273t dermoid sinus in, 263 epidermoid cyst in, 263 facetal, juxtaarticular, synovial, and ganglion cysts in, 264 hydromyelia in, 264 meningocele in, 264 meningomyelocele in, 264 spinal arachnoid cyst in, 263 syringomyelia in, 264, 265t tumoral calcinosis in, 264, 265t vertebral angiomatosis in, 264 Wobbler syndrome in, 264-267, 265-268f in spondylosis, 303 Nerve root signature, 300 Nerve sheath tumor, 181 cranial, 223 spinal, 315, 316f Neurilemoma, 315, 316f Neurinoma, 315, 316f Neuroblastoma, 700 Neurofibroma, 223 Neurofibrosarcoma, 223

Neurogenic pulmonary edema, 444445, 445b Neuroma, 181 Neuronal theory of hypertrophic pulmonary osteoarthropathy, 168 New bone, 1-7 chronic infection and, 118f in craniomandibular osteopathy, 244 estimating age of, 5-7, 6-8f in hip infection, 353 in hypertrophic pulmonary osteoarthropathy, 169 increased cranial density and, 194 in mandibular infection, 244, 245f in mandibular osteopathy, 193-194 morphologic observations of, 5 origins of, 2 in panosteitis, 167 in plant awn-induced paraspinal infection, 305 stimuli of, 2-5, 2-5f terminology in, 1-2 vertebral, 249, 253f, 254, 254f in vertebral physitis, 308 Nipple, 563f Nocardiosis, 415 Nodular hyperplasia hepatic, 580-581 splenic, 655-656, 656f Nodule multiple pulmonary, 384-386, 386f in pulmonary hemangiosarcoma, 429-430 solitary lung, 384 splenic, 655-656, 656f tracheal, 451 Nonaggressive bone lesion, 15, 15f Noncardiac edema, 433-435, 433-435f, 435t, 439 Noncommunicating syringomyelia, 264 Nondescended testicle, 716, 717f Nonionic compositions, 616 Nonlinear intestinal foreign body, 620627, 622t, 622-630f Nonopaque foreign body in stomach, 598-599, 603f Nonoperative portography, 588 Nonselective angiocardiography, 497t, 497-498 Nonulcerative colitis, 646 Nonunion, 68-70, 69-76f of facial depression fracture, 195 of pelvic fracture, 324f Nose aspergillosis and, 225, 225f nasal cavity tumor and, 204-210 computed tomography in, 208209, 209b, 209t deviation and destruction of vomer in, 193 evaluation of postoperativepostradiation nasal radiographs in, 206-208, 209f fluid, bone destruction, and nasal conchal pattern in, 204-205, 206b, 207-208f

❚❚❚ Index

Nose—cont’d nasal cavity tumor and—cont’d infection versus, 205-206, 206t magnetic resonance imaging in, 209-210 nasal septum and cribriform plate and, 204 normal radiology in, 204, 206f rhinography in, 208 Notch width index, 37 Nuclear imaging in atrial standstill, 540 in brain disease and injury, 218 in dilated cardiomyopathy, 524 in extremital infection, 107, 108t in feline hyperparathyroidism, 364 gastrointestinal, 597 in heartworm disease, 536 of hepatic lymphosarcoma, 580 in hip infection, 353 of insulinoma, 653 of kidney, 665 of metastatic bone tumors, 124 of normal gastric emptying time, 597 in osteomyelitis, 107, 109t of pheochromocytoma, 700 of portosystemic shunt, 590 in pulmonary thromboembolism, 444 in thyroid masses and hyperthyroidism, 363 Nutritional secondary hyperparathyroidism, 175

O Obesity, 369f Oblique fracture, 53, 58f, 65f Oblique view of bulla, 231 of heart, 486 of spine, 250f Obstruction airflow, 195 biliary, 583 bronchial, 383t, 451 of caudal vena cava, 550 exterior, causing partial strangulation, 358 foreign body acute abdominal colic in, 566b chronic nasal disease in dog and, 205t combined laryngeal-pharyngealesophageal, 360 esophageal, 386-387, 389f, 457, 459f, 466, 467f fractured tooth as, 215 gastric, 598, 599-601f high-density, 23, 26f ocular, 240, 240f paraspinal, 305 pharyngeal, 359, 359f pneumonia related to, 416, 417f pyloric, 607-609, 608f, 609f, 610t renal, 666-667, 668t soft tissue, 39-40, 41t tracheal, 365, 451

Obstruction—cont’d intestinal, 565f, 619-627 barium and iodine films of, 622625, 623-629f fixed, 627, 630f free linear, 627 as incidental finding, 619 intussusception as, 627-630, 631632f metallic, 619 obstructive pattern and, 621-622, 622t plain films of, 620-621, 622f sonography of, 625 pyloric, 607-609, 608f, 609f, 610t ureteral, 671-672, 672t, 673-674f urethral, 695f Obstructive cholangitis, 585 Obstructive prostatic hyperplasia, 690f Ocular disorders, 236-243 cataracts in, 236-238, 237b, 237-239f congenital disease of eye in, 241 dacryocystitis in, 242 exophthalmia in, 242 eye infection in, 240 eye injury in, 238-240, 239f, 240f eye tumor in, 240-241, 241f foreign body in, 240, 240f magnetic resonance imaging of, 236, 237b orbital and periorbital disease in, 241 orbital emphysema in, 241b, 241242 retrobulbar abscess in, 242, 242f sonography of, 236, 237b Ocular dysplasia, 176 Odontoid process fracture, 276f Oil-based dewormers, 415 Olecranon fracture, 155f Ollulanus tricuspis, 599 Omental calcification, 564t Omnipaque, 290 Opacity, 1 Open fracture, 53, 59f Operative portography, 588, 588f, 589f Optic nerve, 237t Orbit disease of, 241 emphysema of, 241b, 241-242 magnetic resonance imaging of, 236, 237b Orbital venography, 241 Orchitis, 716-718 Organ calcification of, 561f, 563f, 564t mass versus, 721 Orofacial deformity, 244, 246f Oropharyngeal phase of swallowing, 356 Oropharynx, 355 Orthopedic Foundation for Animals certification, 339 Orthopedic imperative, 67, 69f Os penis, 695f, 718 Osseous bone tumor, 122t Osseous sinus venography, 273t

753

Ossification disseminated idiopathic hyperostosis and, 176 dural, 304 idiopathic pulmonary, 445f, 445-446 incomplete humeral condyle, 190 in osteoarthritis, 98t, 98-99, 100f role of calcium in, 167 Osteitis, 106 Osteoarthritis, 93-105 articular fracture and, 40 avascular necrosis and, 96-98, 97f capital physeal fracture and, 329 categorization of, 93, 94f, 95f in congenital elbow dislocation, 186 in dysplastic hip, 343-345f generative nature of, 93 gout and pseudogout and, 101, 105 hip dysplasia and, 94-96, 95f in injured stifle, 36, 36f intraarticular calcification, ossification, and fragmentation in, 98t, 98-99, 100f in Legg-Calv[ac]e-Perthes disease, 325 magnetic resonance imaging appearance of, 93 osteochondritis and, 96, 96f, 97f, 145, 145f, 146f periarticular osteophytes in, 9, 12f postsurgical, 99-101, 101-104f posttraumatic, 80f primary bone tumor versus, 119 radiographic appearance of, 93, 94f storage disease and, 105, 105f synovitis and, 93 Osteoarthrosis, 93 Osteochondral fragment, 158f Osteochondritis, 138-166 of anconeal process, 152, 154-155f classification schemes in, 163t, 163165, 165t, 166t commonly affected breeds, 138 differential diagnosis in, 98t of distal humeral epiphysis, 152, 156, 157f of elbow, 138-152 anconeal process and, 152, 154155f computed tomography in, 147, 147b, 152, 153f early disease in, 145, 147-149f false disease in, 145-147, 152f late disease in, 145, 150-151f lesion development and progression in, 140, 144-146f, 145 magnetic resonance imaging in, 152 medial coronoid process and, 138139 normal anatomic and radiographic variations, 139140, 139-143f osteoarthritis and, 96, 96f, 97f sacral, 268 of shoulder, 156-161, 157-162f

754

Index ❚❚❚

Osteochondritis—cont’d of stifle, 162-163, 165f of tarsal joint, 161-162, 162-164f unusual locations of, 9, 10f Osteochondroma, 121 spinal, 317 tracheal, 451 Osteochondromatosis, 98t Osteochondrosis, 138 Osteodystrophy hypertrophic, 15, 17f, 167-168, 171f, 172f radiation, 180 renal, 194 Scottish fold, 175-176 Osteogenesis imperfecta, 190 Osteomalacia, 397 Osteomedullography, 70 Osteomyelitis, 106-120 abscess and, 119, 119f, 120f blastomycosis and, 111, 115, 115f, 116f cancer versus, 118-119 chronicity of, 116-117, 116-119f coccidioidomycosis and, 111, 114f digital tumor versus, 135 following deep penile bite wound, 718 hepatozoonosis and, 107-111 histoplasmosis and, 115-116 mycotic, 245f new bone formation and, 4f nonspecific bacterial, 107, 107f, 109t nuclear imaging of, 107, 108t pathologic fracture and, 116, 116f Phialemonium ovatum in, 116 radiographic disease indicators of, 107 radiology of, 106-107 septic arthritis and, 117-118 surgical, 107, 110-114f terminology in, 106 vertebral, 305-309 deep paraspinal abscess in, 308, 308f discospondylitis in, 306, 306t, 307308f spondylitis in, 305 vertebral physitis in, 306-308 Osteopathy craniomandibular, 244 hypertrophic, 168 mandibular, 244 increased jaw density in, 193 new bone in, 193-194 metaphyseal, 7f, 15, 17f, 167-168, 171f, 172f Osteopenia, 53 hyperparathyroidism and, 194 in immunoarthritis, 98 in nutritional secondary hyperparathyroidism, 175 as radiographic disease indicator, 15, 17f, 18f Osteopetrosis erythrocyte pyruvate kinase deficiency and, 191

Osteopetrosis—cont’d secondary to myelophthisic anemia, 180 Osteophyte in disseminated idiopathic hyperostosis, 176 in immunoarthritis, 99, 100f in osteoarthritis, 93, 94f in osteochondritis, 145, 150f, 151f as radiographic disease indicator, 9, 12f, 13f Osteosarcoma, 122f, 122-123, 208f aggressive bone lesion in, 14f cervical spine, 255f esophageal, 471 juxtacortical, 130-131 micrometastasis and, 121 new bone deposition in, 13f orbital, 241 parosteal, 317 periosteal new bone and, 4, 4f, 5f pulmonary metastasis in, 426, 426f skull, 199-203, 200-203f, 203b, 223f sternal, 398-399, 399f tracheal, 451 Osteosclerosis, 191 Osteotomy intertrochanteric, 348 triple pelvic, 349, 349f Otitis media, 231-234, 232-234f Otolith, 235 Otoscopic assessment, 231 Ovary, 713-714 changes related to ovulation, 702 cyst of, 714, 714f normal, 713 tumor of, 617, 713b, 713-714 Overhydration, 376t Ovulation, 702

P Pacemaker, 552, 553f Pachymeningitis, 304 Pain in hematoma, 21 in nonunion, 70 in panosteitis, 167 in spinal fracture, 275 in spinal tumor, 317 in traumatic disk rupture, 280 in vertebral angiomatosis, 264 Palisade, 5 Pancreas, 650-654 abscess of, 652, 652f acute pancreatitis and, 650-651, 651f calcification of, 564t cancer of, 587f, 653 chronic pancreatitis and, 651, 651f insulinoma and, 653 pancreatic phlegmon and, 651-652, 652f peripancreatic mass and, 652-653 pseudocyst of, 652, 652f tumor of, 653 Pancreatitis abnormal bowel distribution patterns in, 617

Pancreatitis—cont’d acute, 650-651, 651f acute abdominal colic in, 566b chronic, 651, 651f duodenal thickening secondary to, 617-618, 618f Panosteitis, 5, 8f, 167, 168-170f in distal humerus, 155f leishmaniasis versus, 181 Pantopaque, 290 Papilloma, choroid plexus, 223-224 Paracoxal mass, 337 Paradoxic breathing in rib fracture, 397 Paragonimiasis, 411 Paralaryngeal abscess, 360f Paralysis in caudal lumbar fracture, 280 laryngeal, 449, 450t, 469t in spinal tumor, 317 in traumatic disk rupture, 280 in vertebral angiomatosis, 264 Paraneoplastic syndrome, 671 Parapharyngeal abscess, 305 Paraprostatic cyst, 690-691, 691-692f Paraquat poisoning, 440, 442f Parasitic infection intestinal, 637 tracheal, 451 Parasitic pneumonia, 408-412 Angiostrongylus vasorum in, 408-409 Filaroides hirthi in, 409-411 paragonimiasis in, 411 Rickettsia rickettsii in, 411-412 Toxoplasma gondii in, 411 Paraspinal abscess, 308, 308f Paraspinal foreign body, 305 Paraspinal tumor, 310 Parathyroid mass, 362-363 Paresis, diaphragmatic, 391f Parietal nodes, 566 Paronychia, 135 Parosteal osteosarcoma, 317 Parosteal sarcoma, 15f, 130-131 Partial absence of distal limb, 167 Partial cruciate tear, 34 Partitioned atrium, 515-516 Patella avulsion fracture of, 46f dislocation of, 177, 178f nonunion fracture of, 76f osteochondritis of, 162 Patent ductus arteriosus, 505-507, 506f, 516f aortic base enlargement in, 489-490, 490f intravascular embolization coils in, 500 radiography of, 494f Patent foramen ovale, 504 Pathologic fracture, 53, 59f extremital infection and, 116, 116f rib, 397 Pectus carinatum, 398 Pectus excavatum, 398, 482, 484f Pelvic nerve, 268t Pelvis, 321-353

❚❚❚ Index

Pelvis—cont’d avascular necrosis of femoral head and, 325, 326-327f chondrosarcoma of, 127f congenital epiphyseal dysplasia and, 325-328, 328f fracture of, 321-324, 323-324f hip and digital versus analog images of, 351 infections of, 353 normal canine, 339, 340-341f sacroiliac diastatic fracture and, 49f soft tissue sarcoma of, 136f traumatic deformities of, 90f hip dysplasia and, 338-352 acetabular relocation for, 349, 349t artificial hip for, 349-350, 350f in cat, 351, 351f early detection of, 339 explanations for owners, 346-347, 347-348f femoral head relocation for, 348 historical background of imaging in, 338 implant dislocation in, 69f normal breed hip variations and, 339 Orthopedic Foundation for Animals certification and, 339 osteoarthritis and, 94-96, 95f, 103f postoperative assessment of, 350 previously injured hip versus, 346, 346f prognosis for, 348 progress examinations in, 350 radiographic features of, 339-342, 340-341f radiographic indicators of infectious surgical failure in, 351 radiographic indicators of noninfectious surgical failure in, 350-351, 351f role of stress radiography in, 338 sonographic evaluation in puppy, 351, 351f stressing of suspicious hip, 342, 345f, 346f unilateral, 342, 344, 345f hip fractures and dislocations and, 329-337, 334-337f acetabular, 329, 330f capital physeal, 329, 331-332f epiphysiolysis of femoral head and, 329-332 femoral head, 332-333, 333f femoral neck, 333, 334f paracoxal mass in Doberman pinchers and, 337 postoperative assessment of femoral ostectomy muscle flap and, 334-337 proximal femoral, 329 trochanteric, 333, 334f lymphocenters of, 563-566

Pelvis—cont’d radiographic disease indicators of, 321 sacroiliac diastatic fracture and, 49f traumatic deformities of, 90f Pencil lead, radiographic and sonographic features of, 41t Penetrated view of patent ductus arteriosus, 505, 506f Penetrating wound abdominal to abdominal wall, 568-569 pneumoperitoneum and, 559t arteriovenous fistula after, 180 infection and, 106 ocular, 238-240 Penis contrast spillage in, 563f disease of, 718 Percutaneous transplenic portography, 589-590 Perforation abdominal, 559t acute abdominal colic in, 566b colonic and rectal, 646-648 of duodenal ulcer, 617 esophageal, 466 mediastinal infection and, 462-463 pneumomediastinum in, 463-464 gastric, 609-610 intestinal, 572, 634b, 634-635 colonography-related, 644 impaction and, 637, 638f peritonitis and, 572 pneumoperitoneum in, 559t pharyngeal, 358-359 tracheal, 364 Perianal bite wound, 560 Periarticular osteophyte in disseminated idiopathic hyperostosis, 176 in osteoarthritis, 93, 94f as radiographic disease indicator, 9, 12f Pericardectomy as cause of pleural fluid, 376t for mesothelioma, 547 Pericardial adhesion, 549f, 549-550 Pericardial disease, 533, 534f, 535f Pericardial effusion, 518, 519t, 523f Pericardial fluid causes and consequences of, 533 hepatic congestion and, 580 mesothelioma and, 547 Pericardial hematoma, 533, 535f Pericardial hemorrhage, 535f, 549 Pericardial hernia, 383t Pericardial rupture, 549f, 549-550 Pericardial tumor, 547 Pericardioperitoneal diaphragmatic hernia, 478 Pericarditis, 550 Pericardium, 478 Perinephric pseudocyst, 667-668, 670f Periodontal tumor, 216, 216f Periodontitis, 205t, 212 Periorbital disease, 241

755

Periosteal new bone, 1-7 estimating age of, 5-7, 6-8f morphologic observations of, 5 origins of, 2 in panosteitis, 167 stimuli of, 2-5, 2-5f terminology in, 1-2 Periosteum, 2 Periostitis, 106, 109f Peripancreatic mass, 652-653 Peripheral arterial thrombosis, 538-540 Peripheral lymphangiography, 422 Peripheral nerve sheath tumor, 181 Perirenal cyst, 667-668, 670f Perirenal pseudocyst, 667-668, 670f Peristalsis magnetic resonance imaging of, 567 in swallowing process, 356-357 Peritoneal abscess, 570f Peritoneal air, 556-557, 559t Peritoneal cavity calcification, 564t Peritoneal effusion, 555-556, 556-557f, 558t, 559t Peritoneal fluid, 555-556, 556-557f, 558t, 559t Peritoneal gas, 634 Peritoneal hernia, 681 Peritoneal lavage, 568 Peritoneal tumor, 672t Peritoneopericardial diaphragmatic hernia, 478 Peritonitis, 572-573, 573f in abdominal gunshot wound, 569 acute abdominal colic in, 566b in acute pancreatitis, 650 clostridial, 559t in duodenal ulcer perforation, 617 in intestinal perforation, 634 in intestinal torsion, 635 peritoneal fluid in, 558t Peritonography, 476, 478t Persistent arterial duct, 505-507, 506f, 516f Peyer patches, 615 Pharynx combined laryngeal-pharyngealesophageal foreign bodies and, 360 foreign body in, 359, 359f normal imaging findings, 355-356, 356-357f retropharyngeal adenopathy and, 362 traumatic perforation of, 358-359 Phase-one oropharyngeal dysphagia, 357 Pheochromocytoma, 700 Phialemonium ovatum, 116 Phycomycosis, 618 Physical reversal of abdominal viscera, 567 Physiologic variations in lung patterns, 394 resembling cardiac radiographic disease indicators, 481, 482f resembling thoracic radiographic disease indicators, 368, 371-373f

756

Index ❚❚❚

Physitis, vertebral, 306-308 Physometra, 560 PIE syndrome, 445, 445f Pigmented villonodular synovitis, 182 Pinning, 62, 64-66f for surgically infected fracture, 116 trauma from, 95f Pituitary adenoma, 222-223, 223-224f Placenta, premature separation of, 704f, 704-705 Plain film of abdominal hernia, 637 of bladder, 678, 678b in brain imaging, 218 of dermoid sinus, 263 of enteritis, 618-619, 620f in feline hyperparathyroidism, 364 of gastric tumor, 606, 607f in gastritis, 599 of gastroesophageal intussusception, 609 in intervertebral disk disease, 286288, 287-290f, 293, 293f of intestinal foreign body, 620-621, 622f of intestinal intussusception, 629, 630-631f in intestinal torsion, 635 of intraabdominal intestinal entrapment, 636 in lumbosacral stenosis, 269, 269t, 273t normal intestinal variations in, 614615, 615f of pericardial fluid, 533 of portosystemic shunt, 587 of prostate, 688 of pyloric obstruction, 608, 608f of small intestine tumor, 630-632, 632f of spinal tumor, 310, 311t of stomach, 594 in thyroid masses and hyperthyroidism, 363, 363f of urethral carcinoma, 695 Plant awn in foreign body pneumonia, 416, 417f nasal cavity lesions in dog and, 205t in paraspinal infection, 305 Plasma cell tumor, 423, 425f spinal, 315 Plasmacytoma, esophageal, 471 Plastic, radiographic and sonographic features of, 41t Plate and screw, 62-63, 67f Pleural abscess, 411f Pleural fissure, 376 in pleuritis, 419 in pneumonia, 407 Pleural fluid actinomycosis and, 415 as cardiac radiographic disease indicator, 490-491, 491f in displacement of diaphragm, 473 feline primary lung tumor and, 423 heart failure and, 543

Pleural fluid—cont’d heart size in context of, 494 hypertrophic cardiomyopathy and, 525, 529-531f in mediastinitis, 463 pleuritis and, 419-420, 419-420f in pulmonary thromboembolism, 444 secondary lung-lobe torsion and, 436 as thoracic radiographic disease indicator, 376t, 376-378, 377t, 377-378f, 379t in thymoma, 459 in vascular mediastinal tumor, 462 Pleural hematoma, 399 Pleural hemorrhage, 399, 404f Pleural mesothelioma, 376t Pleural peal, 378f Pleuritis, 378f, 383t, 419-420, 419-420f, 463 Pleurography, 420 Pleuroperitoneal diaphragmatic hernia, 476-478 Pleuropneumonia, 407, 411f, 420 Plexiform vascularization, 362 Pneumatocele, 400 Pneumatocyst, 411 Pneumatosis coli, 558, 648, 649f Pneumatosis cystoids, 558, 648, 649f Pneumatosis intestinalis, 557-558, 648, 649f Pneumocystis carinii pneumonia, 447 Pneumocystography, 679, 679f Pneumomediastinum, 379-380, 381f, 405-406, 463-464 chest injury and, 403f esophageal perforation and, 466 pneumopericardium versus, 491 pneumoperitoneum and, 559t tracheal perforation and, 364 Pneumonia, 407-418 in actinomycosis, 408, 415 after near drowning, 439, 439f after smoke inhalation, 438, 438f allergic, 445f Angiostrongylus vasorum in, 408-409 in aspergillosis, 412 bacterial, 408-412f in blastomycosis, 412-415f bronchiectasis with, 453 classification of, 407 in coccidioidomycosis, 412-415, 416f computed tomography in, 408 in cryptococcosis, 415 expiratory film mimicking of, 368, 372f feline endogenous lipid, 443 Filaroides hirthi in, 409-411 foreign body, 416, 417f in histoplasmosis, 415 hypertrophic pulmonary osteoarthropathy and, 168 lipid, 415-416 in nocardiosis, 415 in paragonimiasis, 411 Pneumocystis carinii, 447

Pneumonia—cont’d pulmonary hypertension in, 551, 551f pulmonary metastasis versus, 429, 431f radiography in, 407-408 in Rocky Mountain spotted fever, 411-412 secondary to megaesophagus, 384f Toxoplasma gondii in, 411 ultrasound in, 408 Pneumonitis, 407, 408 radiation, 446 Pneumopericardiography, 533 Pneumopericardium, 364, 491-492, 551f Pneumoperitoneum as abdominal radiographic disease indicator, 556-557, 559t traumatic, 549 Pneumoretroperitoneum, 364 Pneumothorax, 378-379, 380-381f bulla and, 386 cardiac shift and, 383t experimental, 404 false radiographic disease indicator of, 373f in pleural abscess, 411f posttraumatic, 400, 401-403f progressive, 404f in rib fracture, 397, 398f in sternal fracture, 398 Pneumovaginography, 676 Poisoning antifreeze, 671 paraquat, 440, 442f warfarin, 439-440, 441f, 442f Polyarthritis, 98, 99f Polycystic kidney disease, 665, 666f Polydipsia, 708 Polyostotic development, 123 Polyp bladder, 682f of ear, 235 endometrial, 711t laryngeal, 360, 360f tracheal, 451 Popliteal sesamoid, 9f Porcelain gallbladder, 586 Porcupine quill, 117 in canine neck, 359f in ocular injury, 240, 240f in paraspinal infection, 305 in substernal abscess, 399f Portal angiography, 587-590, 588f, 588t, 589f Portal blood flow assessment, 590 Portal hypertension, 558t, 587 Portal vein, 588t anomalies of, 587-588f, 587-591, 588t, 591b thrombosis of, 591 Portoazygous shunt, 587, 588f Portocaval shunt, 587-588f, 587-591, 588t, 591b Portocaval shunt fraction, 590 Portography, 587-590, 588f, 588t, 589f Portosystemic collaterals, 587, 591

❚❚❚ Index

Portosystemic shunt, 587-588f, 587-591, 588t, 591b Positional abnormality of heart, 489, 489f Positional variants cardiac, 485-486, 487f gastric, 594 spinal, 251t thoracic, 368, 370t, 373f, 374f Positioning in myelography, 293 for spinal radiograph, 249, 250f, 251t Positive-contrast cystography, 679, 679f Positive-contrast peritonography, 476, 478t Positive-contrast retrograde urethrocystography, 696 Postcaval syndrome, 558t Postcorrectional vomiting, 605 Posterior chamber sonography, 237t Postoperative assessment of abdominal wall, 568 in back surgery, 300-301 in brain surgery, 229 of femoral ostectomy muscle flap, 334-337 in hip dysplasia, 350 magnetic resonance imaging indicators of disk disease and, 272t Postpartum uterus, 706t, 706-707 Postsurgical osteoarthritis, 99-101, 101104f Posttorsional stomach, 604-605, 605f Posttraumatic caval scarring, 558t Posttraumatic lung spaces, 399-400, 401f Posttraumatic osteoarthritis, 80f, 93, 95f Posttraumatic osteoporosis, 15 Posttraumatic pneumothorax, 400, 401403f Postural atelectasis, 368, 373f, 383t Postural maneuvers in myelography, 298 Postural radiography of cavitary lung lesions, 386, 388f in cervical spondylopathy, 266, 266f, 267f in foreign body pneumonia, 416 in gastric torsion, 602 in gastroesophageal intussusception, 609 of heart, 485-486, 487f, 494 in lumbosacral stenosis, 269, 273t in thoracic trauma, 400-404, 403f, 404f Postwhelping uterus, 706t, 706-707 Predetermined film sequence, 594-595 Pregnancy, 702-707 abnormal bowel distribution patterns in, 617 ectopic, 705 incomplete fetal resorption and premature placental separation in, 704f, 704-705 intrauterine mass and, 711t late-term fetal death and, 705

Pregnancy—cont’d mechanical dystocia and, 705-706f normal, 702-704, 703f, 704t ovarian changes related to ovulation, 702 postwhelping uterus and, 706t, 706707 Premature physeal closure, 2f Premature placental separation, 704f, 704-705 Prepubic eminence avulsion fracture, 571f Prepubic scanning of prostate, 689 Presumptive contextual diagnosis, 381 Presurgical thoracic screening, 517, 518t Primary ankylosis, 195 Primary craniocerebral trauma, 220 Primary hemangiosarcoma, 131 Primary lung-lobe torsion, 436 Primary tumor bone, 121-123, 122t, 123-129f aggressive bone lesion in, 14f new bone deposition in, 13f osteomyelitis versus, 118-119 pulmonary metastasis in, 426, 426f cardiac, 545-548, 546t, 546-547f hepatic, 581-582 pulmonary, 423, 424t, 424-426f Procedural risks in myelography, 290291, 291t Progress examinations in hip dysplasia, 350 Progressive pneumothorax, 404f Propagation speed error artifact, 641 Prostate, 688-692 abnormal bowel distribution patterns and, 617 benign prostatic hypertrophy and, 689-690f calcification of, 564t cancer of, 691-692, 693f cyst of, 690, 690f measurement of, 688t, 688-689 paraprostatic cysts and, 690-691, 691-692f prostatitis and, 691, 692f Prostatic hypertrophy, 689-690f Prostatic reflux, 689, 690f Prostatitis, 617, 691, 692f Prosthesis, hip, 349-350, 350f Protein-losing enteropathy, 558t, 637 Protein-losing nephropathy, 558t Protocol in gastric barium examination, 594595 in intravenous urography, 676 Protozoal disease, 180-181 Proximal displacement of anconeal process, 152, 154f Proximal femur blastomycosis of, 115f blood supply to, 329 dysplastic versus normal, 347f fracture of, 329 gunshot fracture of, 53f infection of, 113f

757

Proximal femur—cont’d long oblique fracture of, 65f tumor versus infection of, 117f Proximal fibula coccidioidomycosis, 114f Proximal humerus coccidioidomycosis of, 114f fibrosarcoma of, 127f metastatic carcinoma of, 131f osteochondritis of, 156-161, 157-162f osteosarcoma of, 123, 123f Proximal intertarsal joint calcaneal longitudinal fracture and, 58f impaction fracture of, 56f Proximal olecranon fracture, 155f Proximal radius angular limb deformity and, 188f arteriovenous fistula and, 183f congenital elbow dislocation and, 188f limb deformity secondary to growth plate fracture and early closure, 72, 80-91f metaphyseal osteopathy in, 171f panosteitis in, 169f periostitis of, 109f Proximal tibia coccidioidomycosis of, 114f growth plate fracture of, 51f metaphyseal osteopathy in, 171f soft tissue sarcoma of, 135f Proximal ulna arteriovenous fistula and, 183f congenital elbow dislocation and, 186, 188f false ridge sign in, 141f healing of fracture, 64f lateral articular margin of anconeal process in, 141f limb deformity secondary to growth plate fracture and early closure, 72, 80-91f panosteitis in, 169f short oblique fracture of, 35f synovial storage disease in, 105f Pseudo-wall thickening of bladder, 678 Pseudoarthrosis in disseminated idiopathic hyperostosis, 176 of distal femur, 76f Pseudocyst biliary, 721 pancreatic, 652, 652f perinephric, 667-668, 670f Pseudogout, 101, 105 Pseudolayering, 606 Pseudomineralization, 564t Pseudoulcer, 615 Pudendal nerve, 268t Pullback view, 399, 400f Pulmonary abscess in foreign body pneumonia, 416, 417f pyothorax and, 420f Pulmonary arteriography, 536

758

Index ❚❚❚

Pulmonary artery calcification of, 446 cor pulmonale and, 551, 551f enlargement of, 493 heartworm disease and, 536-537, 537f normal nonselective opacification time of, 497t, 498t optimal contrast deployment in selective angiocardiography, 498t thrombosis of, 538-540 transposition of great arteries and, 515 Pulmonary atelectasis, 383, 385f Pulmonary calcification, 445, 445f Pulmonary consolidation, 380-383, 384f after near drowning, 439, 439f after near strangulation, 439, 439f, 440f in bronchiectasis, 454f chest trauma and, 403f in electric shock, 440 in lung-lobe torsion, 436 in pneumonia, 407-408 pulmonary metastasis versus, 427f in warfarin poisoning, 440 Pulmonary contusion, 399, 400f Pulmonary cyst, 446 Pulmonary disease, 436-448 acute respiratory distress syndrome in, 443 allergic bronchitis in, 436, 437f congenital pulmonary cysts in, 446 disseminated intravascular coagulation in, 441-443 electric shock in, 440, 442f generalized pulmonary calcification secondary to Cushing’s disease in, 446 idiopathic pulmonary fibrosis in, 440 idiopathic pulmonary ossification in, 445f, 445-446 lung-lobe torsion in, 436 near drowning in, 438-439, 439f near strangulation in, 439, 439f, 440f neurogenic pulmonary edema in, 444-445, 445b paraquat poisoning in, 440, 442f pleuritis in, 419-420, 419-420f pneumonia in, 407-418 in actinomycosis, 408, 415 Angiostrongylus vasorum in, 408409 in aspergillosis, 412 bacterial, 408-412f in blastomycosis, 412-415f classification of, 407 in coccidioidomycosis, 412-415, 416f computed tomography in, 408 in cryptococcosis, 415 expiratory film mimicking of, 368, 372f feline endogenous lipid, 443 Filaroides hirthi in, 409-411 foreign body, 416, 417f

Pulmonary disease—cont’d pneumonia in—cont’d in histoplasmosis, 415 hypertrophic pulmonary osteoarthropathy and, 168 lipid, 415-416 in nocardiosis, 415 in paragonimiasis, 411 Pneumocystis carinii, 447 radiography in, 407-408 in Rocky Mountain spotted fever, 411-412 secondary to megaesophagus, 384f Toxoplasma gondii in, 411 ultrasound in, 408 pulmonary arterial and parenchymal calcification in, 446 pulmonary foreign body in, 447 pulmonary granulomatosis in, 446f, 447, 447f pulmonary infiltrates with eosinophilia in, 445, 445f pulmonary thrombosis, embolism, and thromboembolism in, 443444 radiation pneumonitis in, 446 smoke inhalation in, 438, 438f thoracic radiographic disease indicators of cardiac shift in, 380, 381f, 382f, 383t cystic and cavitary lung lesions in, 386, 387t, 388f diaphragmatic deformity in, 388390, 391f dilated esophagus in, 386-387, 389f, 390f extrapleural lesion in, 369 hilar and cranial sternal adenopathy in, 387-388, 390f large thoracic masses in, 386, 387f multiple lung nodules in, 384-386, 386f normal anatomic variants resembling, 368, 369t, 369-371f normal physiologic variants resembling, 368, 371-373f pleural fluid in, 376t, 376-378, 377t, 377-378f, 379t pneumomediastinum in, 379-380, 381f pneumothorax in, 378-379, 380381f positional variants resembling, 368, 370t, 373f, 374f pulmonary atelectasis in, 383, 385f pulmonary consolidation in, 380383, 384f solitary lung nodule in, 384 technical variants resembling, 368, 375f ultrasound-guided thoracic biopsy and, 390-391 warfarin poisoning in, 439-440, 441f, 442f

Pulmonary edema, 433-435 in acute pancreatitis, 650 after near strangulation, 439 after smoke inhalation, 438, 438f cardiac, 433 disseminated intravascular coagulation versus, 441 in electric shock, 440, 442f in endocarditis, 532f heart failure and, 543, 543f in hypertrophic cardiomyopathy, 530f lymphosarcoma versus, 429, 431f in mitral endocardiosis, 517, 520f neurogenic, 444-445, 445b noncardiac, 433-435, 433-435f, 435t Pulmonary embolism, 443-444 Pulmonary eosinophilic granulomatosis, 447 Pulmonary fibrosis, 440 Pulmonary foreign body, 447 Pulmonary granulomatosis, 423, 446f, 447, 447f Pulmonary hyperemia in atrial septal defect, 504 cardiac edema and, 433 as cardiac radiographic disease indicator, 490, 490f in endocarditis, 532f in hypertrophic cardiomyopathy, 530f in mitral endocardiosis, 517, 520f in patent ductus arteriosus, 506f Pulmonary hyperperfusion, 490, 490f Pulmonary hypertension, 540-541, 541f cor pulmonale and, 551 in heartworm disease, 537 Pulmonary-induced heart disease, 551, 551f Pulmonary infiltrates, 407 Pulmonary infiltrates with eosinophilia, 445, 445f Pulmonary lymphomatous granulomatosis, 447 Pulmonary lymphosarcoma, 431 Pulmonary mass, 456 Pulmonary metastasis, 426-427, 426430f lung screening for, 423-426 nonstructured or poorly structured, 429, 431f in osteosarcoma, 122 Pulmonary oligemia, 490, 491f Pulmonary ossification, 445f, 445-446 Pulmonary patterns, 393-396 Pulmonary thromboembolism, 443-444 Pulmonary underperfusion, 490, 491f Pulmonic insufficiency, 512-513, 515f Pulmonic stenosis, 508, 509f, 510f, 516t Pulse-wave Doppler, 499, 502f, 532f Puncture wound ocular, 238-240 penile, 718 Punctured trachea, 364 Puppy strangles, 15 Puppy teeth, 213, 213f Purulent exudate, 559t

❚❚❚ Index

Push-pull maneuver, 342 Pyelectasia, 667 Pyloric antrum, 594 Pyloric canal, 594 Pyloric entrapment, 605, 605f Pyloric gastropexy, 604 Pyloric nipple, 609, 609f Pyloric obstruction, 607-609, 608f, 609f, 610t Pylorospasm, 610t Pyocele, 716 Pyogranuloma, 572 Pyometra, 617, 708-710, 709f, 710f Pyothorax, 377f, 419, 420f, 434f

Q Quantitative computed tomography of brain, 219, 220t Quantitative magnetic resonance imaging, 566-567 Quantitative nuclear imaging of portosystemic shunt, 590 Quantitative thyroid imaging, 364

R Radiation-induced bone lesion, 180 Radiation osteodystrophy, 180 Radiation pneumonitis, 446 Radiocarpal joint sprain, fracture, and dislocation of, 19f traumatic capsulitis of, 34f Radiodensity, 2 Radiographic disease indicators abdominal, 555-567 abdominal calcification in, 561563f, 564t abdominal masses in, 562, 565f abnormal bowel distribution pattern in, 562, 565f acute abdominal colic and, 566, 566b computed tomographic appearance of normal canine abdomen and, 566 decreased organ size in, 561, 561f in gastric torsion, 603, 604f increased organ size in, 560, 560f intravisceral gas in, 557-560 magnetic resonance appearance of normal canine bowel and, 566 peritoneal fluid in, 555-556, 556557f, 558t, 559t physical reversal of abdominal viscera and, 567 pneumoperitoneum in, 556-557, 559t in pyloric obstruction, 610t relative signal strengths emitted by abdominal organs of cats and, 566-567 retroperitoneal fluid in, 560 visible abdominal lymph nodes in, 562-566 cardiac, 485-492 abnormal cardiac contour in, 488489, 488-489f

Radiographic disease indicators—cont’d cardiac—cont’d aortic or main pulmonary arterial enlargement in, 489-490, 490f decreased heart size in, 486, 487f in dilated cardiomyopathy, 523 in heart failure, 543-544f, 543-545 in heartworm disease, 535 increased heart size in, 488, 488f normal anatomic variations resembling, 482, 483f, 484f normal physiologic variants resembling, 481, 482f pleural fluid in, 490-491, 491f pneumopericardium in, 491-492 positional abnormality in, 489-489f positional variants resembling, 485-486, 487f in pulmonary embolism, 444 pulmonary hyperemia in, 490, 490f pulmonary oligemia in, 490, 491f of cystitis, 681t extremital, 1-20 aggressive lesions in, 10-15, 13f, 14f dislocation in, 15-17, 18f, 19f enthesiophyte in, 9-10 extraarticular osteophyte in, 9, 13f in infection, 107 joint body in, 7-9, 9-12f limb deformity in, 17, 19f localized bone deposition in, 15, 15f metaphyseal lysis in, 15, 16f, 17f nonaggressive lesions in, 15, 15f osteopenia in, 15, 17f, 18f periarticular osteophyte in, 9, 12f soft tissue swelling in, 17, 19f in tenosynovitis, 178 of pelvis and hips, 321 in avascular necrosis, 325 periosteal new bone in, 1-7 estimating age of, 5-7, 6-8f morphologic observations of, 5 origins of, 2 stimuli of, 2-5, 2-5f terminology in, 1-2 of skull, 193-194 spinal, 249-257 altered vertebral shape in, 256f, 256t, 256-257, 257t diffuse bone loss in, 255f, 255-256 diminished disk size in, 249, 250f, 251t, 252-254f localized bone loss in, 254, 255f new bone deposition in, 249, 254, 254f positioning and comparative assessment and, 249, 250f, 251t in spinal tumors, 311t vertebral endplate alterations in, 257, 257t thoracic, 368-392 cardiac shift in, 380, 381f, 382f, 383t cystic and cavitary lung lesions in, 386, 387t, 388f

759

Radiographic disease indicators—cont’d thoracic——cont’d diaphragmatic deformity in, 388390, 391f dilated esophagus in, 386-387, 389f, 390f in esophageal transport disease, 469-470, 471f extrapleural lesion in, 369 hilar and cranial sternal adenopathy in, 387-388, 390f large thoracic masses in, 386, 387f multiple lung nodules in, 384-386, 386f normal anatomic variants resembling, 368, 369t, 369-371f normal physiologic variants resembling, 368, 371-373f pleural fluid in, 376t, 376-378, 377t, 377-378f, 379t pneumomediastinum in, 379-380, 381f pneumothorax in, 378-379, 380381f positional variants resembling, 368, 370t, 373f, 374f pulmonary atelectasis in, 383, 385f pulmonary consolidation in, 380383, 384f solitary lung nodule in, 384 technical variants resembling, 368, 375f ultrasound-guided thoracic biopsy and, 390-391 Radiographic indicators of surgical failure infectious, 351 noninfectious, 350-351, 351f Radiography in acute pancreatitis, 650 of adrenal gland, 600 in aortic stenosis, 508 of atrial septal defect, 504 of atrial tumor, 545, 546f in benign prostatic hyperplasia, 689 of cardiac pacemaker, 552, 553f in cardiac silhouette analysis, 493495, 494f, 494t of cavitary lung lesions, 386, 388f in cervical spondylopathy, 265, 265f, 266f in cor pulmonale, 540-541, 541f of cranial nerve sheath tumor, 223 in dilated cardiomyopathy, 523, 524525f of duplication cyst, 639 in endocarditis, 528, 531-532f in feline hyperparathyroidism, 364 in gastric torsion, 602-603, 603-604f of gastric tumor, 606, 607f of gastric ulcer, 606, 606f in gastritis, 599 of gastrobronchial fistula, 610 in heartworm disease, 535-537, 536f, 537f in hepatic hemangiosarcoma, 583, 584f

760

Index ❚❚❚

Radiography—cont’d in hypertrophic cardiomyopathy, 524-525, 526-531f in insulinoma, 653 laryngeal, 356 of laryngeal tumor, 360, 360t of late-term fetal death, 705 in liver abscess, 583 lung patterns in, 393-396 of mediastinal abscess, 463 in mitral endocardiosis, 517, 518-521f of multiple lung nodules, 386, 386f of normal pregnancy, 702-704, 703f, 704t of ovarian tumor, 713 of paraprostatic cyst, 691-692f of patent ductus arteriosus, 505-506, 506f of pericardial fluid, 533 pharyngeal, 355, 356-357f of pleural fluid, 376, 377f, 377t, 378f in pleuritis, 419-420, 419-420f in pneumonia, 407-408 of pneumothorax, 379, 380f, 381f in prostate cancer, 692, 693f of pulmonary atelectasis, 383, 385f in pulmonic stenosis, 508, 509f of punctured or ruptured trachea, 364 of pyloric obstruction, 608, 608f of pyometra, 709, 709f in renal disease, 663, 664b, 664t of renal tumor, 669 in retained surgical sponge, 710 of small intestine tumor, 630-632, 632f of splenic hemangiosarcoma, 657659f of splenic lymphosarcoma, 658 in splenic torsion, 660, 661f in tetralogy of Fallot, 511-512 in third-degree heart block, 537, 538f in thyroid masses and hyperthyroidism, 363, 363f in tracheal collapse, 450 of ventricular septal defect, 504 Radiolabels, 597 Radiolucency, 2 Radiolucent band in hip replacement, 350 Radionuclide imaging in atrial standstill, 540 in brain disease and injury, 218 of metastatic bone tumors, 124 in osteomyelitis, 107, 109t Radiopharmaceuticals, 107 Radioulnar subluxation, 166 Radius abnormalities found in computed tomography of lameness, 147b arteriovenous fistula and, 183f chronic osteomyelitis of, 119f congenital elbow dislocation and, 188f dislocation of, 35f divided, 190, 190f fungal osteomyelitis of, 116f

Radius—cont’d greenstick fracture of, 49f growth plate fracture of, 87-88f hairline fracture of, 55f hypertrophic pulmonary osteoarthropathy and, 173f, 175f hypochondroplastic dwarfism and, 175f impaction fracture of, 56f, 56t incomplete fracture of, 57f, 63f limb deformity secondary to growth plate fracture and early closure, 72, 80-91f malunion-related deformity of, 80f medial bowing of, 79f metaphyseal osteopathy in, 171f nonunion of fracture, 70f, 72f, 73f osteosarcoma of, 122f panosteitis in, 168f, 169f pathologic fracture of, 57f repair of fracture, 62f retained cartilage core in, 175f rickets and, 187f sequestrum deformity of, 89f Ranula, 362 Reactive bone, 2 Rectum diverticular disease of, 646 normal appearance of, 643 perforation of, 646-648 Redundant colon, 648-649 Reexpansion lung edema, 421 Reflux, prostatic, 689, 690f Regeneration, 72 Regenerative nodule, splenic, 655-656, 656f Regional infection, 106 Regional liver disease, 580-582, 581582f Regional spinal bone loss, 255-256 Relative renal assessment, 663, 664t Remodeling of dysplastic acetabulum, 95 Renal adenocarcinoma, 180 Renal calculi, 561, 562f, 667-670f Renal disease, 663-671 antifreeze poisoning in, 671 chronic renal failure in, 671 compensatory renal hypertrophy in, 665 congenital, 665-666, 666f giant kidney worm in, 667, 667f hypercalcemic nephropathy in, 671 imaging strategy in, 663-664, 664b, 664t infection in, 666-667f intrarenal cysts in, 668, 670f kidney stones in, 667-670f leptospirosis in, 666 nuclear medicine in, 665 perirenal cysts in, 667-668, 670f renal obstruction and hydronephrosis in, 666-667, 668t renal transplant rejection in, 671 tumors in, 668t, 668-671, 670f ultrasound-guided biopsy in, 663 ultrasound in, 664-665, 665f

Renal duplication, 665-666 Renal ectopia, 665-666 Renal failure, 671 Renal fusion, 665-666 Renal nuclear medicine, 665 Renal osteodystrophy, 194 Renal tandem, 663, 664t Renal volume, 663 Repair of fracture, 58-63, 62-67f Repetitive implant movement, bone abscess from, 119 Residual ovarian tissue, 713 Resistive index, 672 Respiratory failure, 399 Restoration of fractured bone, 63, 67, 68f Restrictive pericarditis, 533 Retained cartilage core in ulnar metaphysis, 169, 173, 175f Retained dental root, 216, 216f Retained surgical sponge in uterus, 710 Retained testicle, 716, 717f Retina detachment of, 237, 239f, 240, 240f sonography of, 237t Retrobulbar abscess, 242, 242f Retroflexion of bladder, 681-682 Retroglenoid process, condylar displacement and deformity and, 196 Retrograde urethrography, 694-695f, 695 in benign prostatic hyperplasia, 689 in prostate cancer, 692 Retrograde urography, 672, 675f Retrograde vaginourethrocystography, 673, 676f, 676-677 Retroperitoneal air, 560 Retroperitoneal fluid, 560 Retroperitoneal midline tumor, 672t Retropharyngeal adenopathy, 362 Reversal of colon, 648, 649f Reversed patent ductus arteriosus, 505-506 Rhabdomyosarcoma, 317 Rhinitis chronic nasal disease in dog and, 205t magnetic resonance imaging of nasal cavity in, 210f Rhinography, 208 Rib fracture of, 397, 398f superimposition in pulmonary metastasis, 429f Rib cage, 482, 483f, 484f Rickets secondary to cholestasis, 186, 187f Rickettsia rickettsii, 411-412 Ridge sign in osteochondritis, 147-149f Right atrium catheter-related injury of, 497t dilation of, 444 hemangiosarcoma of, 433f normal nonselective opacification time of, 497t, 498t

❚❚❚ Index

Right atrium—cont’d optimal contrast deployment in selective angiocardiography, 498t thymoma and, 457 Right lateral projection, 485, 487f Right-sided cardiomegaly, 493 Right-sided heart failure characteristics of, 544, 544f chylothorax and, 518 hepatic congestion in, 580 in trypanosomiasis, 528 Right-to-left shunt, 505-506 Right ventricle catheter-related injury of, 497t isolated right ventricular myopathy and, 523 normal nonselective opacification time of, 497t, 498t optimal contrast deployment in selective angiocardiography, 498t pacemaker and, 552, 553f Right ventricular hypertrophy in patent ductus arteriosus, 506 in pulmonary stenosis, 510f Rim sign, 664-665, 665f Ring enhancement, 228 Rock, radiographic and sonographic features of, 41t Rocky Mountain spotted fever, 411-412 Root fragments, 216, 216f Root resorption, 215 Rotary intraarticular dislocation, 177 Routes of infection, 106 Rupture aortic sinus, 540 bladder, 322, 685-686f cranial cruciate ligament, 12f diaphragmatic, 473, 475-477f disk, 280, 284f, 296f, 300 cauda equina syndrome and, 271f magnetic resonance imaging indicators of, 272t spinal cord malacia and, 319 gastric, 609-610 pericardial, 549f, 549-550 thoracic duct, 376t tracheal, 364 uterine, 711, 711f

S Sacculation, 453 Sacral fracture, 280 Sacral osteochondritis, 268 Sacralization, 261f, 262 Sacroiliac diastatic fracture of, 49f plate and screw fixation of, 69f Salivary gland disease, 361-362, 362f Salter-Harris classification of growth plate fractures, 47, 47b Sand bronchogram, 439 Sarcoma cardiac, 546f, 546t hemangiosarcoma, 546t

Sarcoma—cont’d hemangiosarcoma—cont’d of abdominal wall, 570, 571f cardiac, 488, 544, 545 hepatic, 556f, 583, 584f, 585t, 587f mediastinal, 462 primary, 131 pulmonary, 429-430 right atrial, 433f spinal, 315-317, 317f splenic, 617, 655, 657-658, 657-660f histiocytic, 461-462, 463f lymphosarcoma cardiac, 546t chylothorax and, 422t hepatic, 560f, 579-580 intestinal, 419f, 618, 630, 632-633, 633f mediastinal, 459-461, 461-462f pulmonary, 431 pulmonary edema versus, 429, 431f splenic, 658-659 osteosarcoma, 122f, 122-123, 208f aggressive bone lesion in, 14f cervical spine, 255f esophageal, 471 juxtacortical, 130-131 micrometastasis and, 121 new bone deposition in, 13f orbital, 241 parosteal, 317 periosteal new bone and, 4, 4f, 5f pulmonary metastasis in, 426, 426f skull, 199-203, 200-203f, 203b, 223f sternal, 398-399, 399f tracheal, 451 parosteal, 130-131 soft tissue, 135-136f subcervical, 365f synovial, 124, 130, 132f Scapula chondrosarcoma of, 124f gunshot wound to, 53f osteosarcoma of, 124f transverse fracture of, 61f Scar formation after spinal fracture, 280, 283f disk herniation versus, 301 magnetic resonance imaging indicators of disk disease and, 272t Schmorl’s nodes, 300 Schwannoma cranial, 223 spinal, 315, 316f Sciatic nerve, 268t Sclera, 237t Sclerosis, 1 endplate destruction in, 257t Scoliosis, 263 Scottish fold osteodystrophy, 175-176 Screening, presurgical thoracic, 517, 518t Scrotal injury, 716, 717f Second-degree carpal sprain, 29t Second foreign body in stomach, 599

761

Second metacarpal fracture, 48f Secondary ankylosis, 195, 196f, 197f Secondary bone tumor, 14f, 123 Secondary craniocerebral trauma, 220 Secondary lung-lobe torsion, 436 Secondary lung tumor, 423-424 Sedation in transthoracic biopsy, 721 in ultrasound-guided, free-hand biopsy, 719 Seeding, biopsy-related, 721 Segmental endometrial hyperplasia, 711t Segmental fracture, 53, 60f Seizure, 221 Selective angiocardiography, 497t Seminoma, 716, 717t Septal defect atrial, 504 ventricular, 504-505, 505f Septic arthritis, 117-118 Septum primum, 504 Septum secundum, 504 Sequestrum deformity, 89f Serohematoma, 568 Serosanguineous exudate, 559t Sertoli cell tumor, 716, 717t Sesamoid avulsion fracture versus, 41 fracture of, 53-54, 60f location in dog, 45t loose joint body versus, 7, 9f Sewing needle foreign body, 359, 359f Shifting leg lameness, 167 Shock, 622t Short-bowel syndrome, 638 Shoulder dislocation of, 28, 35f mineralization of supraspinatus tendon and, 177-178 osteochondritis of, 156-161, 157-162f Shunt extrahepatic or intrahepatic, 580 left-to-right, 505 portosystemic, 587-588f, 587-591, 588t, 591b right-to-left, 505-506 Shunt index, 590 Sialadenosis, 242 Sialography, 361 Simple bone cyst, 133t Simple fracture, 54, 61f Sinography of deep muscle abscess, 119, 119f in draining abdominal sinus, 569 of intraabdominal sponge, 710 Sinus dermoid, 263 in paraspinal foreign body, 305 Sinus injury, 195, 196f Sinus of Valsalva rupture, 540 Sinusitis after sinus injury, 195, 196f magnetic resonance imaging of nasal cavity in, 210f nasal cavity lesions in dog and, 205t

762

Index ❚❚❚

Situs inversus, 567 Skeletal deficiencies, 186-191 congenital elbow dislocation and, 186, 188-190f in delayed growth plate closure in castrated and spayed cats, 186 divided distal radius and, 190, 190f ectrodactyly and, 186 in erythrocyte pyruvate kinase deficiency in basenjis, 191 forelimb abnormalities in, 174b incomplete ossification of humeral condyle and, 190 osteogenesis imperfecta and, 190 rickets secondary to cholestasis and, 186, 187f Skeletal dysplasia, 176 Skeletal leishmaniasis, 180-181 Skin canine superficial necrolytic dermatitis and, 580 intraosseous epidermoid cyst and, 133-134 Skin folds, 369f, 379 Skin sinus, infected mandibular fracture and, 246f Skiodan, 290 Skip metastasis, 131f Skull facial length differences and, 205f fetal, 703 fracture of, 198f hydrocephalus and, 226-227, 227f radiographic disease indicators of, 193-194 tumor of, 199-203, 200-203f, 203b Sliding type hiatal hernia, 609 Sludge, gallbladder, 585 Small intestine, 614-642 abscess of, 639f, 641 adhesion of, 640f, 641 bowel distribution pattern and, 616617 calcification of, 564t congenital malformations of, 638639 diaphragmatic hernia and, 475f, 477f, 478t displacement by abdominal hernia, 637 duodenal thickening secondary to pancreatitis, 617-618, 618f duodenal ulcer and, 617 enteritis and, 618-619, 620-621f foreign body in, 565f, 619-627 barium and iodine films of, 622625, 623-629f fixed, 627, 630f free linear, 627 as incidental finding, 619 metallic, 619 obstructive pattern and, 621-622, 622t plain films of, 620-621, 622f sonography of, 625 gas in, 557-558 impaction of, 637, 638f

Small intestine—cont’d incarceration of, 636 infiltrative bowel disease and, 618, 619t inflammatory bowel disease and, 618 intussusception of, 627-630, 631632f leiomyosarcoma and leiomyoma of, 633, 634f lymphosarcoma of, 632-633, 633f normal barium film variations of, 615 normal iodine films of, 615-616 normal plain film variations of, 614615, 615f normal sonographic appearance of, 617, 617t parasitic infection of, 637 perforation of, 634b, 634-635 peritonitis and, 572 pneumoperitoneum in, 559t potential sonographic indicators of disease, 617 protein-losing enteropathy and, 637 short-bowel syndrome and, 638 torsion of, 559t, 635-636, 635-636f trauma to, 639-641 tumor of, 630-632, 632f Small parts transducer, 363 Smoke inhalation, 438, 438f Soft tissue calcification of, 22-23, 25f, 26f foreign body in, 39-40, 41t fracture healing and, 67 gastrocnemius avulsion and, 178179, 179f iliopsoas muscle strain and, 180 infection of, 4, 4f mineralization of biceps brachii tendon and, 178 supraspinatus tendon and, 177178 sarcoma of, 135-136f swelling of in acute cruciate sprain, 36, 36f in bone tumor, 132 in bruise, 21 in calcaneal dislocation of superficial digital flexor tendon, 180 in chest wall bruise, 397 in osteomyelitis, 107 as radiographic disease indicator, 17, 19f in scrotal injury, 716 in spondylitis, 305 tumor of, 137 extradural cervical spine, 317f gum and tongue, 216-217 invasion into bone, 134-135, 134136f tumoral calcinosis and, 179, 179f Soft tissue gas, 22, 23f, 24f Solitary lung nodule, 384 Solitary osteochondroma, 317

Spaulding’s vascular navigational method, 574 Spay effect on urethral diameter in cats, 715 ovarian tumor after, 713 paraspinal abscess after, 308 Sphenoid sinus, mucopolysaccharidosis and, 319 Spinal arachnoid cyst, 263 Spinal cord color Doppler of, 319 compression of, 263-274 cauda equina syndrome and, 268b, 268t, 268-270, 270-271f, 272t, 273t in cervical spinal fracture, 276 dermoid sinus in, 263 epidermoid cyst in, 263 facetal, juxtaarticular, synovial, and ganglion cysts in, 264 in histiocytosis, 462 hydromyelia in, 264 in intravertebral disk herniation, 300 meningoceles and meningomyeloceles in, 264 spinal arachnoid cyst in, 263 in spinal tumor, 310, 311-313f syringomyelia in, 264, 265t tumoral calcinosis in, 264, 265t vertebral angiomatosis in, 264 Wobbler syndrome in, 264-267, 265-268f necrosis of, 319 swelling of in dermoid sinus, 263 in disk disease, 298, 299 Spinal cord malacia, 319 Spinal disease congenital blocked vertebrae versus, 256t congenital hemivertebra versus, 256t facetal arthritis in, 303, 304f hypervitaminosis A in, 319 intervertebral, 285-302 anatomy in, 285 bulging disk in, 300 cord swelling in, 299 diagnostic terminology in, 285286 diskography in, 300 epidurography in, 299 intraosseous vertebral venography in, 300 lesion prevalence in, 286, 286f magnetic resonance imaging in, 300-301 myelography in, 288-299, 291t, 292-294f, 295-298f plain radiography in, 286-288, 287-290f ruptured disk in, 300 mucopolysaccharidosis in, 319 spinal cord malacia in, 319 spondylosis in, 303, 304f Spinal pulse, 276

❚❚❚ Index

Spinal radiographic disease indicators, 249-257 altered vertebral shape in, 256f, 256t, 256-257, 257t diffuse bone loss in, 255f, 255-256 diminished disk size in, 249, 250f, 251t, 252-254f localized bone loss in, 254, 255f new bone deposition in, 249, 254, 254f positioning and comparative assessment and, 249, 250f, 251t vertebral endplate alterations in, 257, 257t Spine, 249-320 computed tomographic survey of, 319 congenital malformations of, 258262 atlantoaxial dislocation in, 258, 259f blocked vertebrae in, 258 hemivertebra in, 258, 259-261f lumbarization in, 258-262, 261f sacralization in, 261f, 262 developmental disorders of, 263-274 cauda equina syndrome in, 268b, 268t, 268-270, 270-271f, 272t, 273t dermoid sinus in, 263 epidermoid cyst in, 263 facetal, juxtaarticular, synovial, and ganglion cysts in, 264 hydromyelia in, 264 meningocele in, 264 meningomyelocele in, 264 spinal arachnoid cyst in, 263 syringomyelia in, 264, 265t tumoral calcinosis in, 264, 265t vertebral angiomatosis in, 264 Wobbler syndrome in, 264-267, 265-268f dural ossification of, 304 facetal arthritis of, 303, 304f infection of, 305-309 deep paraspinal abscess in, 308, 308f discospondylitis in, 306, 306t, 307308f spondylitis in, 305 vertebral physitis in, 306-308 injury of, 275-284 blocked vertebra versus, 256t cervical spinal fracture in, 275-276, 276-278f disk rupture in, 280, 284f dural laceration in, 284 thoracic spinal fracture in, 276, 279-284f, 280 spinal radiographic disease indicators, 249-257 altered vertebral shape in, 256f, 256t, 256-257, 257t diffuse bone loss in, 255f, 255-256 diminished disk size in, 249, 250f, 251t, 252-254f localized bone loss in, 254, 255f

Spine—cont’d spinal radiographic disease indicators—cont’d new bone deposition in, 249, 254, 254f positioning and comparative assessment and, 249, 250f, 251t vertebral endplate alterations in, 257, 257t spondylosis of, 303, 304f survey radiography of, 286-288, 287290f tumor of, 310-318 chondrosarcoma as, 317 computed tomography in, 310, 315 hemangiosarcoma as, 315-317, 317f localized bone loss in, 254, 255f magnetic resonance imaging in, 315, 316t meningioma as, 317 multiple myeloma as, 315 myelography in, 310, 311t, 311-315f neurilemoma as, 315, 316f osteochondroma as, 317 parosteal osteosarcoma as, 317 rhabdomyosarcoma as, 317 tumoral calcinosis versus, 179 Spiral fracture, 54, 61f Spleen, 655-662 abnormal bowel distribution patterns and, 617 abscess of, 657 calcification of, 564t canine abdominal malignant histiocytosis of, 656-657 diaphragmatic hernia and, 475f enlargement caused by vascular congestion, 655, 656f extramedullary hematopoiesis and myelolipomas of, 656, 656f lymphosarcoma of, 658-659 necrosis secondary to infarction of, 661 nodular hyperplasia of, 655-656, 656f radiologic relationship to liver, 575, 576f splenomegaly secondary to autoimmune hemolytic anemia and, 662, 662f torsion of, 565f, 659-661, 661f traumatic hematoma of, 661-662 tumor of, 657-658, 657-660f variations in visibility and size, 655 Splenic gas, 557 Splenic sequestration, 662 Splenitis, 657 Splenomegaly secondary to autoimmune hemolytic anemia, 662, 662f Splints, 62-64f Split-paw deformity, 186 Spondylitis, 254, 254f, 305 Spondylopathy, cervical spine, 264-267, 265-268f

763

Spondylosis, 303, 304f diminished disk size in, 249, 250f, 251t, 252-254f new bone deposition in, 253f, 254, 254f, 259 Spondylotic bridge, 254f Spontaneous pneumomediastinum, 463 Spontaneous regression of lung tumor, 429 Sprain, 27-39 carpal, 27-28, 28-34f, 29t differential diagnosis in, 98t dislocation of patella and, 177 elbow, 24f, 25f, 28 stifle, 29, 34 tarsal, 39, 40f Spur in spondylosis, 303 Squamous cell carcinoma aural, 235 in canine foot, 132 of distal interphalangeal joint, 134f esophageal, 471 in feline primary lung tumor, 424t of gum and tongue, 216-217 mandibular, 199, 202f urethral, 694-695 Staging of brain abscess, 226t Standing position radiograph in cervical spondylopathy, 265f, 266f in gastric torsion, 602 of heart, 485-486, 487f of spine, 287-288, 287-290f of stifle, 37f Staphylococcus aureus discospondylitis, 306 Staphylococcus epidermidis in hepatic cyst, 583 Stationary type hiatal hernia, 609 Steatitis, 572-573 Steel wire, radiographic and sonographic features of, 41t Stenosis aortic, 508, 511-512f, 516t colonic, 646 congenital pyloric, 610t esophageal, 470 inflammatory ear canal, 231 intercondylar, 37 mitral and tricuspid, 511 pulmonic, 508, 509f, 510f, 516t tracheal, 364 urethral, 695, 695f Sternum fracture of, 397-398, 398f infection of, 398-399, 399f normal physiologic variants resembling cardiac radiographic disease indicators and, 482, 483f, 484f Stick impalation, 305 pharyngeal, 358-359 tracheal, 365 Stifle arthritic, 36, 36f immunoarthritis in, 99, 99f osteophytes in, 13f

764

Index ❚❚❚

Stifle—cont’d dislocation of patella and, 178f gas pockets in, 59f growth plate fracture of, 82-83f location of sesamoid bones in, 45t magnetic resonance arthrography of, 38, 39b magnetic resonance imaging of, 37-38 metastatic fibrosarcoma of, 129f muscle tumor of, 137f nonunion fracture of, 76f optimal imaging planes for, 39b osteochondritis of, 162-163, 165f osteosarcoma of, 128t sprain of, 29, 34, 36f standing position radiograph of, 37f traumatic deformities of, 90f ultrasound of, 37 Stomach, 594-613 abdominal hernia and, 568, 569f abnormal bowel distribution patterns and, 616 acute abdominal colic and, 566b barium examination of, 594-595, 595t, 596f calcification of, 561f, 564t, 611, 611f chronic lymphocytic-plasmacytic gastritis and, 609 diaphragmatic hernia and, 475f, 476f dilation of, 601, 601b enlargement of, 597-598, 598f, 598t fetal, 702 foreign objects and materials in, 598, 599-601f gastric atony and, 611-612 gastric dilation in spinal fracture, 275 gastritis and, 599 gastrobronchial fistula and, 610-611 gastroesophageal intussusception and, 609, 611f gastrointestinal pythiosis and, 599601 hairballs in, 598, 602f herniated, 382f hiatal hernia and, 609, 610f nonopaque foreign body in, 598-599, 603f normal barium film variations of, 615 normal gastric emptying time of, 595-597 normal sonographic appearance of, 597 perforation and rupture of, 559t, 609-610 plain films of, 594 posttorsional, 604-605, 605f pyloric obstruction in, 607-609, 608f, 609f, 610t second foreign body in, 599 tumor of, 606-607, 607f ulcer of, 605-606, 606f uremic gastritis and, 599 volvulus of, 601-604, 602-604f worms in, 599

Stones biliary, 561, 585 bladder, 682-685, 683-684f lithotripsy for, 677 morphology of, 564t renal, 561, 562f ureteral, 672, 672t, 674f Storage disease, 105, 105f, 319 Strain, 23, 26f dystrophic calcification and, 179f iliopsoas muscle, 180 Strangulation, 439, 439f, 440f exterior foreign body causing, 358 Streptococcal infection, 557 hepatic cyst and, 583 Stress as stimulus for new bone formation, 2, 2f, 3f Stress fracture, 54 Stress myelography, 266-267, 267-268f Stress radiography in cervical spondylopathy, 266, 266f, 267f in hip dysplasia, 338 in lumbosacral stenosis, 269 of suspicious hip, 342, 345f, 346f Stricture annular, 715 esophageal, 469t, 470 Stroke, 228 Structural adaptation of bone, 2f Structured interstitial pattern, 395 Stump granuloma, 710, 710f Subacute hematoma, 22f Subaortic stenosis, 508, 511-512f Subarachnoid myelogram, 291, 291f Subcervical sarcoma, 365f Subchondral bone cyst, 133t Subchondral sclerosis, 93 Subcutaneous gas in chest wall injury, 397, 398f Subdural contrast injection, 299 Sublingual gland mucocele, 362 Subluxation patellar, 177, 178f as radiographic disease indicator, 15-17, 18f, 19f Submandibular swelling, 242 Subperiosteal hematoma, 196-197 Substernal abscess, 399f Subtotal colectomy, 646 Subtraction angiography, 67 Subtraction portal venography, 590 Subtraction radiography, 241 Subtrochanteric fracture, 329 Subungual carcinoma, 134f, 134-135 Sulcus, periodontal disease and, 212 Summation phenomenon, 386f Superficial digital flexor tendon dislocation, 180 Superficial gas in chest wall injury, 397, 398f Supracondylar femoral fracture, 329 Supraglenoid, osteochondritis of, 160, 161f Supraspinatus tendon mineralization, 177-178 Suprasternal abscess, 399, 399f

Surgical abdomen, 621-622, 622t Surgical failure in hip replacement, 349-351, 351f Surgical infection, extremital, 107, 110114f, 118f Surgical injury chronic nasal disease in dog and, 205t retained surgical sponge and, 710 Surgical pancreatitis, 653 Surgical pin, dislocation of, 184, 184f Surgical treatment of hip dysplasia, 348-351, 349-351t of proximal growth-plate fracture of femoral head, 329, 331-332f Survey radiography filming sequence in, 595 in intervertebral disk disease, 286288, 287-290f, 293, 293f Swallowing process, 356-358, 358t Swelling soft tissue in acute cruciate sprain, 36, 36f in bone tumor, 132 in bruise, 21 in calcaneal dislocation of superficial digital flexor tendon, 180 in chest wall bruise, 397 in osteomyelitis, 107 as radiographic disease indicator, 17, 19f in scrotal injury, 716 in spondylitis, 305 spinal cord in dermoid sinus, 263 in disk disease, 298, 299 Synovial cyst, spinal, 264 Synovial osteochondromatosis, 9, 11f Synovial sarcoma, 124, 130, 132f Synovitis osteoarthritis and, 93 villonodular, 182-183 Syringohydromyelia, 264 Syringomyelia, 264, 265t Systole, normal physiologic variants resembling cardiac radiographic disease indicators and, 481

T T fracture, 53, 57f Tachycardia, ventricular, 538 Talar lesion, 161, 162-164f Talar neck fracture, 54, 58 Target lesion in multiple myeloma, 255f Tarsal joint osteochondritis, 161-162, 162-164f Tarsocrural joint fracture-related deformities of, 84-86f impaction fracture of, 56f osteochondritis of, 163f posttraumatic osteoarthritis in, 81f sprain of, 39 Tarsometatarsal joint location of sesamoid bones in, 45t sprain-fracture-dislocation of, 48f

❚❚❚ Index

Tarsus fracture of corner, 48f impacted, 56t immunoarthritis in, 99, 100-101f osteochondritis of, 161-162, 162-164f soft tissue sarcoma of, 135f sprain of, 39, 40f, 48f posttraumatic osteoporosis in, 15, 17f torn Achilles tendon and, 25f tumoral calcinosis in, 26f Tear, 23-27, 27f Tear sac inflammation, 242 Technical variations in lung patterns, 395 resembling thoracic radiographic disease indicators, 368, 375f Temporomandibular dysplasia, 195196, 197f Temporomandibular joint congenital deformity and dislocation of, 195-196, 197f injuries and motion impairing disorders of, 195, 196f Tendon dystrophic calcification of, 23 injury of avulsion fracture of long digital extensor tendon, 23 calcaneal dislocation of superficial digital flexor tendon, 180 ruptured Achilles, 25f, 26, 27f, 179, 179f Tendon sheath, fluid distention of, 26f Tendonitis, 23, 26f Tenosynovitis bicipital, 178, 178f, 179f focal bone deposits in, 11f Tension pneumothorax, 382f, 383t, 473 Tentorium cerebelli osseum, 228 Teratoma, ovarian, 713 Test injection in myelography, 294 Testicular disease, 716-718, 717f, 717t Testicular torsion, 716 Tetralogy of Fallot, 511-512, 516t Third-degree carpal sprain, 29t Third-degree heart block, 537-538, 538f Third metacarpal displaced short oblique fracture of, 48f osteosarcoma of, 126f Thoracic cavity biopsy, 721 Thoracic drain, 403-404 Thoracic duct ligation of, 421 lymphangiography of, 422 rupture of, 376t Thoracic esophagus, 466-472 effect of vomiting on, 471, 471f enlargement of, 466, 467-469f esophageal transport disease and, 466-470, 469t, 470f esophagitis and, 470 fistula of, 471 foreign object in, 466, 467f gas in, 472, 472f

Thoracic esophagus—cont’d hematoma of, 471 perforation of, 466 stricture of, 470 tumor of, 470-471 Thoracic imaging, 355-479 in airway disease, 449-455 abnormal tracheal distention in, 450-451 bronchial foreign body in, 451 bronchiectasis in, 453-454, 453454f, 541f bronchitis in, 451-453 bronchocutaneous fistula in, 451 emphysema in, 454 laryngeal paralysis in, 449, 450t mass versus nodule in, 451 tracheal and bronchial parasites in, 451 tracheal collapse in, 449-450, 450b tracheal hypoplasia in, 449 tracheal polyp in, 451 tracheal tumor in, 451 tracheitis in, 449 in chest trauma, 397-406 cavitary lung lesions and, 386 chest wall injury in, 397, 398f diaphragmatic rupture in, 473, 475-477f gunshot wounds in, 404-405, 405f, 406f intrapulmonary hemorrhage in, 399, 400f lung laceration, collapse, and cavitary lesions in, 399-400, 401f mediastinal injury in, 405-406 pleural fluid and, 376t pleural hemorrhage and hematoma in, 399 posttraumatic pneumothorax in, 400, 401-403f postural radiography in, 400-404, 403f, 404f sternal fracture in, 397-398, 398f sternal tumors, infections, and gas in, 398-399, 399f in chylothorax, 421, 422t in diaphragmatic hernia, 473-479 cardiac shift and, 383t as cause of pleural fluid, 376t chylothorax and, 422t diaphragmatic variation, visibility, displacement, and disfiguration and, 473, 474f, 475f imaging findings in, 475-477f peritoneopericardial, 478 pleuroperitoneal, 476-478 positive contrast peritonography in, 476, 478t of lung, 436-448 in abscess, 416, 417f, 420f in acute respiratory distress syndrome, 443 in allergic bronchitis, 436, 437f in congenital pulmonary cysts, 446

765

Thoracic imaging—cont’d of lung—cont’d in disseminated intravascular coagulation, 441-443 in electric shock, 440, 442f in generalized pulmonary calcification secondary to Cushing’s disease, 446 in idiopathic pulmonary fibrosis, 440 in idiopathic pulmonary ossification, 445f, 445-446 in lung-lobe torsion, 436 in near drowning, 438-439, 439f in near strangulation, 439, 439f, 440f in neurogenic pulmonary edema, 444-445, 445b in paraquat poisoning, 440, 442f in pleuritis, 419-420, 419-420f in pulmonary arterial and parenchymal calcification, 446 in pulmonary calcification, 445f, 445-446 in pulmonary foreign body, 447 in pulmonary granulomatosis, 446f, 447, 447f in pulmonary infiltrates with eosinophilia, 445, 445f pulmonary patterns in, 393-396 in pulmonary thrombosis, embolism, and thromboembolism, 443-444 in radiation pneumonitis, 446 in smoke inhalation, 438, 438f in warfarin poisoning, 439-440, 441f, 442f of lung trauma, 399-404 intrapulmonary hemorrhage in, 399, 400f laceration, collapse, and cavitary lesions in, 399-400, 401f posttraumatic pneumothorax in, 400, 401-403f postural radiography in, 400-404, 403f, 404f of lung tumor, 386, 387f, 423-432 benign, 431 cardiac shift and, 383t cavitation in, 427 chylothorax and, 422t hemangiosarcoma as, 429-430 judging growth of, 427 lateral views of, 424-426 malignant fibrous histiocytoma as, 429 mammary carcinoma as, 429 mast cell tumor as, 430-431 mediastinal lymphosarcoma versus, 461 nonstructured or poorly structured pulmonary metastasis in, 429, 431f primary, 423, 424t, 424-426f pulmonary lymphosarcoma as, 431 pulmonary metastases and, 426427, 426-430f

766

Index ❚❚❚

Thoracic imaging—cont’d of lung tumor—cont’d secondary, 423-424 spontaneous regression of, 429 in mediastinal disease, 456-465 abscess in, 463 approach to mediastinal masses, 456 blastomycosis in, 464, 464f cysts in, 462 hemomediastinum in, 464 histiocytosis in, 461-462, 463f lymphosarcoma in, 459-461, 461462f mass effects in, 456-457, 456-460f mediastinitis in, 462-463 pneumomediastinum in, 463-464 pulmonary versus mediastinal mass in, 456 thymoma in, 457-459, 460f vascular tumors in, 462 in pleuritis, 378f, 419-420, 419-420f in pneumonia, 407-418 in actinomycosis, 408, 415 Angiostrongylus vasorum in, 408409 in aspergillosis, 412 bacterial, 408-412f in blastomycosis, 412-415f classification of, 407 in coccidioidomycosis, 412-415, 416f computed tomography in, 408 in cryptococcosis, 415 expiratory film mimicking of, 368, 372f feline endogenous lipid, 443 Filaroides hirthi in, 409-411 foreign body-related, 416, 417f in histoplasmosis, 415 hypertrophic pulmonary osteoarthropathy and, 168 lipid, 415-416 in nocardiosis, 415 in paragonimiasis, 411 Pneumocystis carinii in, 447 pulmonary hypertension in, 551, 551f pulmonary metastasis versus, 429, 431f radiography in, 407-408 in Rocky Mountain spotted fever, 411-412 secondary to megaesophagus, 384f Toxoplasma gondii in, 411 in pulmonary edema, 433-435 in acute pancreatitis, 650 after near strangulation, 439 after smoke inhalation, 438, 438f cardiac, 433 disseminated intravascular coagulation versus, 441 in electric shock, 440, 442f in endocarditis, 532f heart failure and, 543, 543f in hypertrophic cardiomyopathy, 530f

Thoracic imaging—cont’d in pulmonary edema—cont’d lymphosarcoma versus, 429, 431f in mitral endocardiosis, 517, 520f neurogenic, 444-445, 445b noncardiac, 433-435, 433-435f, 435t of pulmonary mass, 386, 387t cardiac shift and, 383t hilar adenopathy and, 388 mediastinal mass versus, 456 multiple nodules, 384-386, 386f solitary nodule, 384 of thoracic esophagus, 466-472 effect of vomiting on, 471, 471f enlargement of, 466, 467-469f esophageal transport disease and, 466-470, 469t, 470f esophagitis and, 470 fistula of, 471 foreign object in, 466, 467f gas in, 472, 472f hematoma of, 471 perforation of, 466 stricture of, 470 tumor of, 470-471 thoracic radiographic disease indicators in, 368-392 cardiac shift in, 380, 381f, 382f, 383t cystic and cavitary lung lesions in, 386, 387t, 388f diaphragmatic deformity in, 388390, 391f dilated esophagus in, 386-387, 389f, 390f extrapleural lesion in, 369 hilar and cranial sternal adenopathy in, 387-388, 390f large thoracic masses in, 386, 387f multiple lung nodules in, 384-386, 386f normal anatomic variants resembling, 368, 369t, 369-371f normal physiologic variants resembling, 368, 371-373f pleural fluid in, 376t, 376-378, 377t, 377-378f, 379t pneumomediastinum in, 379-380, 381f pneumothorax in, 378-379, 380381f positional variants resembling, 368, 370t, 373f, 374f pulmonary atelectasis in, 383, 385f pulmonary consolidation in, 380383, 384f solitary lung nodule in, 384 technical variants resembling, 368, 375f ultrasound-guided thoracic biopsy and, 390-391 of throat and neck, 355-367 abnormal larynx and, 359 cervical masses and, 358, 358f, 359f combined laryngeal-pharyngealesophageal foreign bodies and, 360 everted laryngeal saccules and, 360

Thoracic imaging—cont’d of throat and neck—cont’d exterior foreign body causing partial strangulation and, 358 laryngeal cyst and, 360 laryngeal polyps and abscesses and, 360, 360f laryngeal tumors and, 360, 360t larynx and, 356 parathyroid masses and, 362-363 pharyngeal foreign body and, 359, 359f pharynx and, 355-356, 356-357f punctured or ruptured trachea and, 364 retropharyngeal adenopathy and, 362 salivary gland disease and, 361362, 362f swallowing process and, 356-358, 358t thyroid masses and hyperthyroidism and, 363f, 363364 tracheal dilation and, 364 tracheal foreign body and, 365 tracheal stenosis and, 364 tracheitis and tracheobronchitis and, 364-365 traumatic pharyngeal perforation and, 358-359 tumors of, 365, 365f, 366f Thoracic mass, 369f, 386, 387f Thoracic radiographic disease indicators, 368-392 cardiac shift in, 380, 381f, 382f, 383t cystic and cavitary lung lesions in, 386, 387t, 388f diaphragmatic deformity in, 388390, 391f dilated esophagus in, 386-387, 389f, 390f in esophageal transport disease, 469470, 471f extrapleural lesion in, 369 hilar and cranial sternal adenopathy in, 387-388, 390f large thoracic masses in, 386, 387f multiple lung nodules in, 384-386, 386f normal anatomic variants resembling, 368, 369t, 369-371f normal physiologic variants resembling, 368, 371-373f pleural fluid in, 376t, 376-378, 377t, 377-378f, 379t pneumomediastinum in, 379-380, 381f pneumothorax in, 378-379, 380-381f positional variants resembling, 368, 370t, 373f, 374f pulmonary atelectasis in, 383, 385f pulmonary consolidation in, 380383, 384f solitary lung nodule in, 384 technical variants resembling, 368, 375f ultrasound-guided thoracic biopsy and, 390-391

❚❚❚ Index

Thoracic spine fracture of, 276, 279-284f, 280 hemivertebra of, 259f intervertebral disk disease in, 286 spondylotic bridge in, 254f tumor of, 314f vertebral angiomatosis in, 264 Thoracic trauma, 397-406 chest wall injury in, 397, 398f diaphragmatic rupture in, 473, 475477f gunshot wounds in, 404-405, 405f, 406f lung injury in, 399-404 intrapulmonary hemorrhage in, 399, 400f laceration, collapse, and cavitary lesions in, 399-400, 401f posttraumatic pneumothorax in, 400, 401-403f postural radiography in, 400-404, 403f, 404f mediastinal injury in, 405-406 pleural hemorrhage and hematoma in, 399 sternal fracture in, 397-398, 398f sternal tumors, infections, and gas in, 398-399, 399f Thoracolumbar spine calcified disk in, 252f compression fracture of, 279f intervertebral disk disease in, 286 new bone deposition in, 252f spondylosis of, 303, 304f tumor of, 311f Thorax biopsy of thoracic cavity, 721 presurgical screening of, 517, 518t ultrasound-guided biopsy of, 390391 Three-window approach in spine radiography, 287f, 288f, 298 Throat and neck, 355-367 abnormal larynx and, 359 cervical masses and, 358, 358f, 359f combined laryngeal-pharyngealesophageal foreign bodies and, 360 everted laryngeal saccules and, 360 exterior foreign body causing partial strangulation and, 358 laryngeal cyst and, 360 laryngeal polyps and abscesses and, 360, 360f laryngeal tumors and, 360, 360t larynx and, 356 parathyroid masses and, 362-363 pharyngeal foreign body and, 359, 359f pharynx and, 355-356, 356-357f punctured or ruptured trachea and, 364 retropharyngeal adenopathy and, 362 salivary gland disease and, 361-362, 362f

Throat and neck—cont’d swallowing process and, 356-358, 358t thyroid masses and hyperthyroidism and, 363f, 363364 tracheal dilation and, 364 tracheal foreign body and, 365 tracheal stenosis and, 364 tracheitis and tracheobronchitis and, 364-365 traumatic pharyngeal perforation and, 358-359 tumors of, 365, 365f, 366f Thrombocytopenia, 662, 662f Thromboembolism, pulmonary, 443444 Thrombus aortoiliac, 183-184 arterial, 524, 538-540 atrial, 545, 547f cardiac, 545-548, 546t, 546-547f cardiac shift in, 383t caudal vena cava, 558t as cause of pleural fluid, 376t obstructed caudal vena cava and, 550 pulmonary, 443-444 ventricular, 545-547, 547f Thymic hemorrhage, 456, 457f, 458f Thymic sail, 457f Thymoma, 457-459, 460f Thyroid, 356 cancer of, 424 mass in, 363f, 363-364 Thyroid-induced cardiomyopathy, 526529f, 531f atrial doming in, 488f nonselective angiocardiogram of, 498f Thyrotoxicosis heart failure and, 530f mitral insufficiency and, 518 Tibia coccidioidomycosis of, 114f dislocation of patella and, 177 fracture of avulsion, 43f comminuted, 42f, 67f growth plate, 51f, 68f, 81f, 87f, 88f pathologic, 59f related deformities in, 84-86f spiral, 61f metaphyseal osteopathy in, 171f, 172f metastatic sarcoma of, 130t osteosarcoma of, 126f postsurgical osteoarthritis in, 104f soft tissue sarcoma of, 135f Tibial tuberosity congenital overgrowth of, 165f dislocation of patella and, 177 infection of, 110f osteochondritis of, 162-163, 163f Tongue carcinoma, 199 Tooth, 212, 213f abscessed, 212-213, 214f, 215f cavities and root resorption, 215

767

Tooth—cont’d fracture and dislocation of, 215, 215f retained roots and root fragments, 216, 216f Torsion colonic, 648, 649f gastric, 601-604, 603-604f, 659 intestinal, 559t, 635-636, 635-636f lung-lobe, 436 splenic, 659-661, 661f testicular, 716 Total hip replacement, 349-350, 350f Toxoplasma gondii, 411 Trachea, 449-455 abnormal distention of, 450-451 bronchiectasis and, 453-454, 453454f, 541f bronchitis and, 451-453 bronchocutaneous fistula and, 451 collapse of, 449-450, 450b dilation of, 364, 450-451 emphysema and, 454 foreign body in, 365, 451 hypoplasia of, 449 kink mimicking thoracic radiographic disease indicator, 370f laryngeal paralysis and, 449, 450t mass versus nodule in, 451 parasitic infection of, 451 polyp of, 451 punctured or ruptured, 364 sonogram of, 359f stenosis of, 364 tracheitis and, 449 tracheitis and tracheobronchitis of, 364-365 tumor of, 360t, 451 Tracheal fracture, 405 Tracheal wash, 463 Tracheitis, 364-365, 449 Tracheobronchitis, 364-365 Traction apophysis and, 40 as false radiographic disease indicator, 373f Traction-induced stimulation in disk rupture, 300 Traction-stress maneuver, 196 Transection, ureteral, 672t Transesophageal echocardiography, 499 Transient bronchiectasis, 453 Transitional cell carcinoma, 424 ultrasound of, 682f, 683f urethral, 694-695 Transitional vertebra, 258 Transmissible venereal tumor, 241 Transosseous vertebral venography, 300 Transplant rejection, renal, 671 Transposition of great arteries, 515 Transrectal scanning of prostate, 689 Transthoracic biopsy, 721 Transudate peritoneal, 559t pleural, 377t, 378f, 490, 491f

768

Index ❚❚❚

Transverse fracture, 54, 61f Trauma biopsy-related, 721 cardiac, 549f, 549-550 chest, 397-406 as cause of pleural fluid, 376t cavitary lung lesions and, 386, 399-400, 401f chest wall injury in, 397, 398f chylothorax following, 422t diaphragmatic rupture in, 473, 475-477f gunshot wounds in, 404-405, 405f, 406f intrapulmonary hemorrhage in, 399, 400f lung laceration and collapse in, 399-400, 401f mediastinal injury in, 405-406 pleural hemorrhage and hematoma in, 399 posttraumatic pneumothorax in, 400, 401-403f postural radiography in, 400-404, 403f, 404f sternal fracture in, 397-398, 398f sternal tumors, infections, and gas in, 398-399, 399f chronic nasal disease in dog and, 205t congenital hemivertebra versus, 256t craniocerebral, 220-221, 221b cystography-related, 678 endplate destruction in, 257t extremital, 21-92 apophyseal fracture in, 40, 43f articular fracture in, 40-41, 44f, 45f avulsion fracture in, 41, 45t, 46f bruise in, 21 carpal sprains in, 27-28, 28-34f, 29t chisel fracture in, 41, 46f closed fracture in, 41 comminuted fracture in, 41, 47f compartmental syndrome and, 2122 compression fracture in, 41, 47f corner fracture in, 46, 48f crush fracture in, 46, 48f delayed fracture healing and, 6272, 69f, 70-76f depression fracture in, 46, 49f diastatic fracture in, 46, 49f dislocated shoulder in, 28, 35f in dislocation of patella, 177 distal humeral growth-plate fracture in, 49, 51-52f elbow sprains in, 28, 34f, 35f experimental destabilization of canine genual joint and, 35-36 expression fracture in, 46 fabella injuries in, 38, 38f, 39f fault-line fracture in, 46-47 fracture classification using electronic databases and, 58 fracture repair and, 58-63, 62-67f fracture union and, 63, 67, 68f

Trauma—cont’d extremital—cont’d greenstick fracture in, 47, 49f growth plate fracture in, 47b, 4748, 48b, 50f gunshot fracture in, 49, 53-55f hairline fracture in, 49, 55f hematoma in, 21, 22f high-density foreign bodies and, 23, 26f impacted fracture in, 49, 56f incomplete fracture in, 49, 57f infection-related to, 23-27, 27f insufficiency fracture in, 53, 57f intercondylar stenosis and, 37 limb deformity secondary to growth-plate fracture and early closure in, 72, 80-91f longitudinal fracture in, 53, 58f magnetic resonance arthrography of, 38, 39b magnetic resonance imaging of, 37-38 major tears, laceration, and trauma-related infection and abscess in, 23-27, 27f meniscal injuries in, 34-35 naturally occurring cruciate sprains in dogs and, 36f, 36-37, 37f oblique fracture in, 53, 58f open fracture in, 53, 59f pathologic fracture in, 53, 59f regeneration and, 72 segmental fracture in, 53, 60f sesamoid fracture in, 53-54, 60f simple fracture in, 54, 61f soft tissue calcification and, 22-23, 25f, 26f soft tissue foreign bodies and, 3940, 41t soft tissue gas and, 22, 23f, 24f spiral fracture in, 54, 61f stifle sprains in, 29, 34 strains, tendonitis, and bursitis in, 23, 26f stress fracture in, 54 T, Y, and V fractures in, 53, 57f talar neck fracture in, 54, 58 tarsal sprains in, 39, 40f transverse fracture in, 54, 61f traumatic amputation in, 58, 61t ultrasound of, 37 head ankylosis and impingement exostosis and, 195, 196f, 197f congenital temporomandibular deformity and dislocation and, 195-196, 197f cranial injuries and, 196-198, 198f facial injuries and, 195, 196f mandibular and maxillary injuries and, 195 megaesophagus following, 390f temporomandibular joint injuries and motion impairing disorders and, 195, 196f

Trauma—cont’d hip, 329-337, 334-337f acetabular fracture in, 329, 330f capital physeal fracture in, 329, 331-332f femoral head fracture in, 332-333, 333f femoral neck fracture in, 333, 334f multiple injuries in, 323f proximal femoral fracture in, 329 radiographic disease indicators of, 321 trochanteric fracture in, 333, 334f intestinal, 639-641 mediastinal, 405-406 ocular, 237t, 238-240, 239f, 240f pelvic fracture-associated, 322-324 penile, 718 pharyngeal perforation in, 358-359 spinal, 275-284 blocked vertebra versus, 256t cervical spinal fracture in, 275-276, 276-278f disk rupture in, 280, 284f dural laceration in, 284 thoracic spinal fracture in, 276, 279-284f, 280 as stimulus for new bone formation, 2, 3f testicular, 716, 717f thoracic, 397-406 chest wall injury in, 397, 398f gunshot wounds in, 404-405, 405f, 406f intrapulmonary hemorrhage in, 399, 400f lung laceration, collapse, and cavitary lesions in, 399-400, 401f mediastinal injury in, 405-406 pleural hemorrhage and hematoma in, 399 posttraumatic pneumothorax in, 400, 401-403f postural radiography in, 400-404, 403f, 404f sternal fracture in, 397-398, 398f sternal tumors, infections, and gas in, 398-399, 399f ureteral, 677 urethral, 718 Traumatic amputation, 58, 61t Traumatic bulla, 386, 399-400, 400f Traumatic capsulitis, 34f Traumatic disk rupture, 285 Traumatic disruption of abdominal wall, 568, 569f Traumatic hematoma of spleen, 661662 Traumatic pancreatitis, 653 Traumatic respiratory distress syndrome, 443 Triceps calcification, 25f Trichobezoar, 598, 602f Tricuspid endocardiosis, 517-518, 522f Tricuspid insufficiency, 512, 513f, 516t

❚❚❚ Index

Tricuspid stenosis, 511 Trigeminal nerve tumor, 223 Tripartite sesamoids, 54, 60f Triple pelvic osteotomy, 94, 349, 349f Trochanteric fracture, 333, 334f Trough effect, 266 True biopsy needle tip, 719, 720t True diaphragmatic hernia, 476-478 Truncus arteriosus, 513-514 Trypanosomiasis, 528 Tumor abdominal wall, 570, 571f adrenal, 700 arteriovenous fistula and, 180 aural, 235 bladder, 682-683f bone, 121-136 benign, 121 cranial bone density in, 194 digital tumors versus infections and, 131-133 infarct and, 180 invading soft tissue tumors and, 134-135, 134-136f of joints, 124, 130, 132f localized bone loss in vertebra in, 255, 255f metastatic melanoma in, 130 parosteal sarcoma in, 130-131 primary, 121-123, 122t, 123-129f primary hemangiosarcoma in, 131 radiologic findings in, 123-124, 129-131f secondary, 123 skull, 199-203, 200-203f, 203b tumorlike bone lesions and, 133t, 133-134, 134f brain, 221-224, 222t, 223-224f cardiac, 545-548, 546t, 546-547f dental and periodontal, 216, 216f esophageal, 470-471 facial, 199, 200-201f, 203b gastric, 606-607, 607f gum, 216-217 heart base, 518, 519t, 523f hepatic, 581-583 infection versus, 117f, 118-119 intestinal, 630-632, 632f laryngeal, 360, 360t lung, 386, 387f, 423-432 benign, 431 cardiac shift and, 383t cavitation in, 427 chylothorax and, 422t hemangiosarcoma as, 429-430 judging growth of, 427 lateral views of, 424-426 malignant fibrous histiocytoma as, 429 mammary carcinoma as, 429 mast cell tumor as, 430-431 mediastinal lymphosarcoma versus, 461 nonstructured or poorly structured pulmonary metastasis in, 429, 431f primary, 423, 424t, 424-426f

Tumor—cont’d lung—cont’d pulmonary lymphosarcoma as, 431 pulmonary metastases and, 426427, 426-430f secondary, 423-424 spontaneous regression of, 429 mediastinal as cause of pleural fluid, 376t chylothorax and, 422t nasal cavity, 204-210 computed tomography in, 208209, 209b, 209t deviation and destruction of vomer in, 193 evaluation of postoperativepostradiation nasal radiographs in, 206-208, 209f fluid, bone destruction, and nasal conchal pattern in, 204-205, 206b, 207-208f infection versus, 205-206, 206t magnetic resonance imaging in, 209-210 nasal septum and cribriform plate and, 204 normal radiology in, 204, 206f rhinography in, 208 ocular, 237t, 240-241, 241f ovarian, 713b, 713-714 pancreatic, 653 peripheral nerve sheath, 181 renal, 668t, 668-671, 670f spinal, 310-318 chondrosarcoma as, 317 computed tomography in, 310, 315 hemangiosarcoma as, 315-317, 317f localized bone loss in, 254, 255f magnetic resonance imaging in, 315, 316t meningioma as, 317 multiple myeloma as, 315 myelography in, 310, 311t, 311-315f neurilemoma as, 315, 316f osteochondroma as, 317 parosteal osteosarcoma as, 317 rhabdomyosarcoma as, 317 tumoral calcinosis versus, 179 splenic, 617, 657-658, 657-660f sternal, 398-399, 399f testicular, 716, 717t in throat and neck, 365, 365f, 366f tongue, 216-217 tracheal, 451 uterine, 711t Tumor bone, 4 Tumoral calcinosis, 23, 26f, 264, 265t Tumorlike bone lesion, 133t, 133-134, 134f Tunnel view, 37 Twiddler’s syndrome, 552 Two-dimensional echocardiography, 500 Tympanic membrane, 231

769

U Ulcer duodenal, 606f, 617 gastric, 605-606, 606f Ulcerative colitis, 646, 647f Ulcerative gastritis, 599 Ulna abnormalities found in computed tomography of lameness, 147b angular limb deformity and, 188f arteriovenous fistula and, 183f cancerous, 129f chronic osteomyelitis of, 119f congenital elbow dislocation and, 186, 188f, 189f fracture of hairline, 55f healing of, 64f impaction, 56f, 56t limb deformity in, 72, 80-91f malunion-related deformity of, 80f nonunion of, 70f, 72-74f pathologic, 57f repair of, 62f segmental, 60f fungal osteomyelitis of, 116f hypertrophic pulmonary osteoarthropathy and, 173f, 175f hypochondroplastic dwarfism and, 175f panosteitis in, 169f retained cartilage core in ulnar metaphysis, 169, 173, 175f rickets and, 187f sequestrum deformity of, 89f synovial storage disease in, 105f Ultrasound abdominal of abdominal hernia, 637 in acute pancreatitis, 650-651, 651f in diaphragmatic hernia, 475 in draining abdominal sinus, 569 of duplication cyst, 639 in gallbladder disease, 585 of gastrointestinal lymphosarcoma, 632-633, 633f of insulinoma, 653 of intestinal intussusception, 629630 in intestinal torsion, 635, 636 of intraabdominal intestinal entrapment, 636 of phycomycosis, 618 adrenal gland, 600-700 in arteriovenous fistula, 180 bladder, 680, 680f, 681t of bone tumor, 121 in brain disease and injury, 218, 219t cardiac, 499-503 in aortic stenosis, 508, 512f athletic hypertrophy and, 501 of atrial septal defect, 504 of atrial tumor, 545, 547f congenital muscular dystrophy and, 501-502 in endocarditis, 528, 531-532f

770

Index ❚❚❚

Ultrasound—cont’d cardiac—cont’d in hypertrophic cardiomyopathy, 525 interpretation of Doppler tracing in, 500-501, 502f M-mode echocardiography and, 501 in mitral endocardiosis, 517, 522f normal appearances in, 499, 500f overall approach in, 499-500 in patent ductus arteriosus, 506 in pericardial disease, 533, 534f placement of intravascular embolization coils in, 500 in pulmonic stenosis, 508, 510f in tetralogy of Fallot, 512 in third-degree heart block, 538 of ventricular septal defect, 504505, 505f of cataracts, 236-237, 237-239f of cervical mass, 358, 358f, 359f cystography versus, 678 of deep muscle abscess, 120f of deep puncture wound, 26, 27f in feline hyperparathyroidism, 364 of gastric tumor, 606 in heartworm disease, 536, 537 of hematoma, 22f during hemilaminectomy, 276 hepatic, 465, 578-579f of hepatic hemangiosarcoma, 583, 585f of hepatic lymphosarcoma, 579580 of hepatic shunt, 590 of hepatic tumor, 581-582f, 583 in liver abscess, 583-585 of portal vein thrombosis, 591 of hip dysplasia, 96, 351, 351f in hydrocephalus, 226-227 of incomplete fetal resorption, 704f intestinal, 625 of abscess, 638f, 641 normal, 617, 617t of tumor, 832 of intraabdominal sponge, 710 laryngeal, 356, 360 of late-term fetal death, 705 of normal pregnancy, 702, 703f, 704t ocular, 236, 237b orbital in orbital disease, 241 of tumor, 242 of ovarian tumor, 713b, 713-714 pharyngeal, 355-356 prostatic, 688t, 688-689 in benign prostatic hyperplasia, 689 of paraprostatic cyst, 691, 692f in prostate cancer, 692, 693f in prostatitis, 691, 692f of pyloric obstruction, 608-609, 609f of pyometra, 708, 709-710, 710f renal, 664-665, 665f of kidney stones, 667, 670f of tumor, 669

Ultrasound—cont’d of salivary gland, 361 splenic of hemangiosarcoma, 657, 660f of lymphosarcoma, 658 in splenic torsion, 660-661 of stifle sprain, 37 of stomach, 597 in testicular disease, 716, 717f, 717t thoracic in cor pulmonale, 540-541, 541f in foreign body pneumonia, 416 of mediastinal mass, 457, 460f of pleural fluid, 378, 378f in pleuritis, 420 in pneumonia, 408 in pulmonary embolism, 444 of torn muscle, 27f of transitional cell carcinoma, 682f of ureter, 672 of ureteric jets, 676f, 677 of urethral carcinoma, 695 Ultrasound-guided biopsy free-hand, 719, 721 renal, 663 thoracic, 390-391 Undescended testicle, 716, 717f Unger system, 58 Unicameral bone cyst, 133t Unilateral hip dysplasia, 342, 344f, 345f Union of fracture, 63, 67, 68f Unstructured interstitial pattern, 395 Ununited anconeal process, 152 Ununited coronoid process, 138 Uremic gastritis, 599 Ureter, 671-677 antegrade ureterography and, 676 calcification of, 564t computed tomography of, 677 diverticula of, 677 ectopic, 673, 675-676f injury of, 677 intravenous urography and, 676 lithotripsy and, 677 obstruction of, 671-672, 672t, 673674f papillae of, 682 pneumovaginography and, 676 retrograde urography and, 672, 675f retrograde vaginourethrocystography and, 676f, 676-677 ultrasound of, 672 ureteric jets and, 676f, 677 Ureteral sacculation, 672 Ureteric jets, 673, 676f, 677 Ureterocele, 672t Ureterography, antegrade, 676 Urethra, 692-696, 693-694f, 694b carcinoma of, 694-695 hypoplasia of, 715 inflammation and stenosis of, 695, 695f trauma to, 718 urinary incontinence and, 696 Urethrography, 694-695f, 695, 718

Urinary bladder, 677-688 abnormal bowel distribution patterns and, 617 calcification of, 561f, 564t, 688 calculi of, 682-685, 683-684f cystography of, 678-679, 679b, 679680f, 681t diverticula of, 681 emphysematous cystitis and, 681 feline idiopathic cystitis and, 680-681 gas in, 558-560 hemorrhage of, 685-688, 687f intrapelvic, 682 plain films of, 678, 678b retroflexion of, 681-682 rupture of, 322, 685-686f tumor of, 682-683f hydroureter secondary to, 675 ureteral outlet obstruction in, 671 ultrasound of, 680, 680f, 681t Urinary incontinence, 696 in ectopic ureter, 673 in urethral and vaginal disease, 715 Urinary tract disorders, 663-698 bladder disease in, 677-688 abnormal bowel distribution patterns and, 617 calcification in, 561f, 564t, 688 calculi in, 682-685, 683-684f cystography in, 678-679, 679b, 679680f, 681t diverticula in, 681 emphysematous cystitis in, 681 feline idiopathic cystitis in, 680681 gas in, 558-560 hemorrhage in, 685-688, 687f intrapelvic bladder and, 682 plain films in, 678, 678b retroflexion in, 681-682 rupture in, 322, 685-686f tumor in, 671, 675, 682-683f ultrasound in, 680, 680f, 681t kidney disease in, 663-671 antifreeze poisoning in, 671 chronic renal failure in, 671 compensatory renal hypertrophy in, 665 congenital, 665-666, 666f giant kidney worm in, 667, 667f hypercalcemic nephropathy in, 671 imaging strategy in, 663-664, 664b, 664t infection in, 666-667f intrarenal cysts in, 668, 670f kidney stones in, 667-670f leptospirosis in, 666 nuclear medicine in, 665 perirenal cysts in, 667-668, 670f renal obstruction and hydronephrosis in, 666-667, 668t renal transplant rejection in, 671 tumors in, 668t, 668-671, 670f ultrasound-guided biopsy in, 663 ultrasound in, 664-665, 665f

❚❚❚ Index

Urinary tract disorders—cont’d prostate disease in, 688-692 abnormal bowel distribution patterns and, 617 benign prostatic hypertrophy in, 689-690f calcification in, 564t cancer in, 691-692, 693f cyst in, 690, 690f measurement of, 688t, 688-689 paraprostatic cysts and, 690-691, 691-692f prostatitis in, 691, 692f ureteral disease in, 671-677 antegrade ureterography and, 676 calcification in, 564t computed tomography and, 677 diverticula in, 677 ectopic ureter in, 673, 675-676f injury in, 677 intravenous urography and, 676 lithotripsy and, 677 obstruction in, 671-672, 672t, 673674f pneumovaginography and, 676 retrograde urography and, 672, 675f retrograde vaginourethrocystography and, 676f, 676-677 ultrasound in, 672 ureteric jets in, 676f, 677 urethral disease in, 692-696, 693-694f, 694b carcinoma in, 694-695 hypoplasia in, 715 inflammation and stenosis in, 695, 695f trauma and, 718 urinary incontinence and, 696 Urine leakage into peritoneal cavity, 572, 573f Uriniferous perirenal cyst, 667 Urinoma, 677 Urography excretory, 664, 664t, 677 intravenous, 676, 685 retrograde, 672, 675f in stump granuloma, 710 Uroretroperitoneum, 560 Uterine gas, 560 Uterus, 708-712 abnormal bowel distribution patterns and, 617 calcification of, 564t contrast evaluation of interior, 711 cystic endometrial hyperplasia and, 708 cystic uterine remnant in, 712 enlargement of, 708 masses in, 711t, 712 postwhelping, 706t, 706-707 pyometra and, 617, 708-710, 709f, 710f retained surgical sponge in, 710 rupture of, 711, 711f stump granuloma and, 710, 710f

Uterus masculinus, 696 Uveitis, 237t

V V fracture, 53, 57f Vacuum phenomenon, 159, 160f, 399 Vagina pneumovaginography and, 676 retrograde vaginourethrocystography and, 676f, 676-677 stricture of, 715 Vaginal septa, 715 Vaginography, 715 Vaginourethrocystography, 694 Valgus deformity, 91f Valvular heart disease, 517-518, 517523f Variable rate pacing, 552 Vascular blunting, 490 Vascular congestion, splenic, 655, 656f Vascular maps, 574 Vascular mediastinal tumor, 462 Vascular pressure tracing, 67 Vascular ring, 469t Vegetations in endocarditis, 531f, 532f Vena cava caudal azygous continuation of, 496-497, 497t obstruction from pericardial adhesions, 550 pericardial disease and, 533 thrombosis of, 558t cranial normal nonselective opacification time of, 497t pericardial disease and, 533 thymoma and, 457, 459 obstruction from pericardial adhesions, 550 Venography in brain disease and injury, 218, 219f intraosseous vertebral, 300 in lumbosacral stenosis, 269, 273t in orbital disease, 241 Venous thrombosis, 422t Ventilation/perfusion mismatching, 399 Ventral segment disease, 285-302 anatomy in, 285 bulging disk in, 300 cord swelling in, 299 diagnostic terminology in, 285-286 diskography in, 300 epidurography in, 299 intraosseous vertebral venography in, 300 lesion prevalence in, 286, 286f magnetic resonance imaging in, 300301 myelography in, 288-299, 295-297f background and beginnings of, 288 computed tomography with, 298299

771

Ventral segment disease—cont’d myelography in—cont’d epidural injection in, 291, 291t, 292f failure of contrast flow in, 295-298, 298f fat complications in, 293, 293f magnetic resonance imaging with, 299 needle placement in, 293, 294f patient positioning in, 293 postural maneuvers in, 298 risks in, 290-291, 291t test injection in, 294 timing of, 288-290 plain radiography in, 286-288, 287290f ruptured disk in, 300 Ventricle, cardiac catheter-related injury of, 497t normal nonselective opacification time of, 497t, 498t optimal contrast deployment in selective angiocardiography, 498t thrombus of, 545-547, 547f tumor of, 545-547, 547f Ventricle, cerebral choroid plexus tumor of, 224 hydromyelia and, 264 normal variation in, 220 Ventricular septal defect, 504-505, 505f, 516t contrast echocardiography in, 506507 pulmonary hyperemia in, 490 Ventricular tachycardia, 538 Ventriculography, 218 Ventrodorsal versus dorsoventral projection, 485, 486f Vertebra altered shape of, 256f, 256t, 256-257, 257t compression fracture of, 47f endplate alterations of, 257, 257t facetal arthritis and, 303, 304f localized bone loss in, 255, 255f new bone deposition in, 254, 254f, 259 Vertebral angiomatosis, 264 Vertebral osteomyelitis, 305-309 deep paraspinal abscess in, 308, 308f discospondylitis in, 306, 306t, 307308f spondylitis in, 305 vertebral physitis in, 306-308 Vertebral physitis, 306-308 Vertebral tumor, 310-318 chondrosarcoma as, 317 computed tomography in, 310, 315 hemangiosarcoma as, 315-317, 317f localized bone loss in, 254, 255f magnetic resonance imaging in, 315, 316t meningioma as, 317 multiple myeloma as, 315 myelography in, 310, 311t, 311-315f

772

Index ❚❚❚

Vertebral tumor—cont’d neurilemoma as, 315, 316f osteochondroma as, 317 parosteal osteosarcoma as, 317 rhabdomyosarcoma as, 317 tumoral calcinosis versus, 179 Vertical ramus fracture, 195, 196f Vesicoureteral stenosis, 672t Vestibulocochlear nerve tumor, 223 Villonodular synovitis, 182-183 Viral tracheitis, 449 Viscera, physical reversal of, 567 Visceral leishmaniasis, 180-181 Visceral node, 557 Vitamin A, hypervitaminosis A and, 319 Vitreal degeneration, 237, 238f, 239f Vitreous chamber, 237t Voiding cystography, 693-694 Volvulus gastric, 601-604, 602-604f intestinal, 635-636, 635-636f

Vomer, 204 deviation and destruction of, 193 Vomiting in acute pancreatitis, 650 after correction of gastric torsion, 605 effect of thoracic esophagus, 471, 471f intestinal distention in, 622t megaesophagus induced by, 468f in pyloric obstruction, 610t in pyometra, 708 von Willebrand disease, 337 Vulval discharge, 708

W Warfarin poisoning, 376t, 439-440, 441f, 442f, 456 Washout in brain imaging, 219, 220t Weakness in acute pancreatitis, 650 in hematoma, 21 Wedge radiography, 338

Wedged vertebrae, 256t, 256-257 Weight-bearing ring, 322 Wiring, 62, 64-66f Withdrawal myelogram, 291 Wobbler syndrome, 258, 264-267, 265268f Wood, radiographic and sonographic features of, 41t Worm infestation gastric, 599 renal, 667, 667f

Y Y fracture, 53, 57f Yellow fat disease, 572-573

Z Zygoma depression fracture of, 49f, 195, 196f, 197f squamous cell carcinoma of, 201f, 203b, 203f