Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
ROSEN'S EMERGENCY MEDICINE Concepts and Clinical Practice Sixth Edition
Editor-in-ChiefJohn A. Marx, MD, FAAEM, FACEP Chair and Chief, Department of Emergency Medicine, Carolinas Medical Center, Charlotte, North Carolina; Adjunct Professor, Department of Emergency Medicine, University of North Carolina School of Medicine, Chapel Hill, North Carolina; Senior EditorsRobert S. Hockberger, MD, FACEP, FAAEM Chair, Department of Emergency Medicine, Harbor–UCLA Medical Center, Torrance, California; Professor of Clinical Medicine, David Geffen School of Medicine at UCLA, Westwood, Los Angeles, California; Ron M. Walls, MD, FAAEM, FACEP, FRCPC Chair, Department of Emergency Medicine, Brigham and Women's Hospital; Associate Professor of Medicine (Emergency Medicine), Harvard Medical School, Boston, Massachusetts; James G. Adams, MD, FACP, FACEP Chair, Department of Emergency Medicine, Northwestern Memorial Hospital; Professor of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois; William G. Barsan, MD Professor and Chair, Department of Emergency Medicine, University of Michigan Medical School, Ann Arbor, Michigan; Michelle H. Biros, MD, MS, FAAEM, FACEP Research Director and Faculty Physician, Department of Emergency Medicine, Hennepin County Medical Center; Professor of Emergency Medicine, University of Minnesota Medical School, Minneapolis, Minnesota; Daniel F. Danzl, MD Professor and Chair, Department of Emergency Medicine, University of Louisville School of Medicine, Louisville, Kentucky; Marianne Gausche-Hill, MD, FACEP, FAAP Professor of Medicine, David Geffen School of Medicine at UCLA; Director of EMS and Pediatric Emergency Medicine Fellowship, Department of Emergency Medicine, Harbor –UCLA Medical Center, Torrance, California; Glenn C. Hamilton, MD, MSM Professor and Chair, Department of Emergency Medicine, Wright State University School of Medicine, Dayton, Ohio; Louis J. Ling, MD, FACEP, FACMT Professor of Emergency Medicine and Pharmacy, Associate Dean for Graduate Medical Education, University of Minnesota Medical School; Associate Medicine Director for Medical Education, Hennepin County Medical Center; Senior Associate Medical Director, Hennepin Regional Poison Center, Minneapolis, Minnesota; Edward J. Newton, MD, FACEP Chair, Department of Emergency Medicine, Los Angeles County and University of Southern California Medical Center; Professor of Clinical Emergency Medicine, University of Southern California Keck School of Medicine, Los Angeles, California;
Page 1
MOSBY ELSEVIER 1600 John F. Kennedy Boulevard, Suite 1800 Philadelphia, PA 19103-2899 ROSEN'S EMERGENCY MEDICINE: Concepts and Clinical Practice, 6th Editon Three-Volume Set 0-323-02845-4 Online Edition 0-323-03686-4 E-dition 0-323-04302-X Copyright © 2006, 2002, 1998, 1992, 1988, 1983 Mosby, Inc. All rights reserved. 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 storae 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) 215 239 3804; fax: (+1) 215 239 3805; e-mail:
[email protected] may also complete your request online via the Elsevier homepage ( http://www.elsevier.com.ezproxy.hsclib.sunysb.edu “Obtaining Permissions.”
. You
), by selecting “Customer Support” and then
Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment, and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Editors and Authors assume any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book.
Library of Congress Cataloging-in-Publication Data Rosen's emergency medicine : concepts and clinical practice.—6th ed. / editor-in-chief, John A. Marx ; senior editors, Robert S. Hockberger, Ron M. Walls ; editors, James Adams… [et al.] p. ; cm. Includes bibliographical references and index. ISBN 0-323-02845-4 1. Emergency medicine. I. Title: Emergency medicine. II. Marx, John A. III. Hockberger, Robert S. IV. Walls, Ron M. V. Adams, James. VI. Rosen, Peter Emergency medicine. [DNLM: 1. Emergencies. 2. Emergency Medicine. WB 105 E555 2006] RC86.7.E5784 2006 616.02′5—dc22 2005041694
Publisher's Team Acquisitions Editor: Todd Hummel Developmental Editor: Kimberly Cox Publishing Services Manager: Frank Polizzano
Page 2
Project Manager: Robin E. Hayward Cover Design Direction: Steven Stave Text Designer: Jayne Jones Marketing Manager: Dana Butler Printed in China Last digit is the print number: 9 8 7 6 5 4 3 2 1
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/1.htm l/top
Page 3
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
REFERENCES 1. Tobin MJ: Current concepts: Mechanical ventilation. N Engl J Med1994;330:1056. 2. Bone RC, Eubanks DH: The basis and basics of mechanical ventilation. Dis Mon1991;37:321. 3. Kacmarek RM, Hess DR: Essentials of Mechanical Ventilation, New York, McGraw-Hill/Appleton & Lange, 2002. 4. Banner MJ, Lampotang S: Mechanical ventilators: Fundamentals. In: Stock MC, Perel A, ed.Handbook of Mechanical Ventilatory Support, 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 1997: 5. Slutsky AS: ACCP Consensus Conference: Mechanical ventilation. Chest1993;104:1833. 6. Irwin RS: Mechanical ventilation. In: Rippe JM, ed.Intensive Care Medicine, 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2003: 7. Rossi A, Polese G, De Sandre G: Respiratory failure in chronic airflow obstruction: Recent advances and therapeutic implications in the critically ill patient. Eur J Med1992;1:349. 8. Shivaram U: Cardiopulmonary responses to continuous positive airway pressure in acute asthma. J Crit Care1993;8:87. 9. IPPB Trial Group : Intermittent positive pressure breathing therapy of chronic obstructive pulmonary disease. Ann Intern Med1983;99:612. 10. Bersten AD: Treatment of severe cardiogenic pulmonary edema with continuous positive airway pressure delivered by face mask. N Engl J Med1991;325:1825. 11. Sullivan MP: Continuous positive airway pressure in the prehospital treatment of acute pulmonary edema. Ann Emerg Med1995;25:129. 12. Pollack CV, Torres M, Alexander L: A feasibility study of the use of bilevel positive airway pressure for respiratory support in the emergency department. Ann Emerg Med1996;27:189. 13. Keenan SP: Effect of noninvasive positive pressure ventilation on mortality in patients admitted with acute respiratory failure: A meta-analysis. Crit Care Med1997;25:1685. 14. Poponick JM, Renston JP, Bennett RP, Emerman CL: Use of a ventilatory system (BiPAP) for acute respiratory failure in the emergency department. Chest1999;116:166. 15. Fernandez MM: Noninvasive mechanical ventilation in status asthmaticus. Intens Care Med2001;27:486. 16. Soroksky A, Stav D, Shpirer I: A pilot prospective, randomized, placebo-controlled trial of bilevel positive airway pressure in acute asthmatic attack. Chest2003;123:1018. 17. Vitacca M: Non-invasive modalities of positive pressure ventilation improve the outcome of acute exacerbations in COPD patients. Intensive Care Med1993;19:450. 18. Carrey Z, Gottfried SB, Levy RD: Ventilatory muscle support in respiratory failure with nasal positive pressure ventilation. Chest1990;97:150. 19. Bott J, Carroll MP, Conway JH: Randomised controlled trial of nasal ventilation in acute ventilatory failure due to chronic obstructive airways disease. Lancet1993;341:1555. 20. Liesching T, Kwok H, Hill NS: Acute applications of noninvasive positive pressure ventilation. Chest 2003;124:699. 21. Freichels TA: Palliative ventilatory support: Use of noninvasive positive pressure ventilation in terminal respiratory insufficiency. Am J Crit Care1994;3:6. 22. Ambrosino N: Physiologic evaluation of pressure support ventilation by nasal mask in patients with stable COPD. Chest1992;101:385. 23. Dreyfuss D, Saumon G: Barotrauma is volutrauma, but which volume is the one responsible?. Intensive Care Med1992;18:139. 24. Manning HL: Peak airway pressure: Why the fuss?. Chest1994;105:242. 25. Tobin MJ, Fahey PJ: Management of the patient who is “fighting the ventilator”. In: Tobin MJ, ed.Principles and Practice of Mechanical Ventilation, New York: McGraw-Hill; 1994: 26. Hill NS: Noninvasive ventilation: Does it work, for whom, and how?. Am Rev Respir Dis1993;147:1050. 27. Honig EG: Chronic obstructive pulmonary disease and asthma. In: Stock MC, Perel A, ed.Handbook of Mechanical Ventilatory Support, 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 1997: 28. Tuxen DV: Permissive hypercapnic ventilation. Am J Respir Crit Care Med1994;150:870. 29. Van der Touw T: Cardiorespiratory consequences of expiratory chest wall compression during mechanical ventilation and severe hyperinflation. Crit Care Med1993;21:1908.
Page 4
30. Eichacker PQ: Meta-analysis of acute lung injury and acute respiratory distress syndrome trials with low tidal volumes. Am J Respir Crit Care Med2002;166:1510. 31. Cross AM: Non-invasive ventilation in acute respiratory failure: A randomised comparison of continuous positive airway pressure and bi-level positive airway pressure. Emerg Med J2003;20:531. 32. Antonelli M: A comparison of noninvasive positive-pressure ventilation and conventional mechanical ventilation in patients with acute respiratory failure. N Engl J Med1998;339:429. 33. Meyer TJ, Hill NS: Noninvasive positive pressure ventilation to treat respiratory failure. Ann Intern Med 1994;120:760. 34. Celikel T: Comparison of noninvasive positive pressure ventilation with standard medical therapy in hypercapnic acute respiratory failure. Chest1998;114:1636. 35. Keenan SP: Noninvasive positive pressure ventilation in the setting of severe, acute exacerbations of chronic obstructive pulmonary disease: more effective and less expensive. Crit Care Med2000;28:2094. 36. Wood KA: The use of noninvasive positive pressure ventilation in the emergency department: Results of a randomized clinical trial. Chest1998;113:1339. 37. Wang SH, Wei TS: The outcome of early pressure-controlled inverse ratio ventilation on patients with severe acute respiratory distress syndrome in the surgical intensive care unit. Am J Surg2002;183:151. 38. Sydow M: Long-term effects of two different ventilatory modes on oxygenation in acute lung injury: Comparison of airway pressure release ventilation and volume-controlled inverse ratio ventilation. Am J Respir Crit Care Med1994;149:1550. 39. Derdak S: High-frequency oscillatory ventilation for acute respiratory distress syndrome in adults: A randomized, controlled trial, Multicenter Oscillatory ventilation for Acute respiratory distress syndrome Trial (MOAT). Am J Respir Crit Care Med2002;166:801. 40. Burchardi H: New strategies in mechanical ventilation for acute lung injury. Eur Respir J1996;9:1063. 41. Herridge MS, Slutsky AS, Colditz GA: Has high-frequency ventilation been inappropriately discarded in adult acute respiratory distress syndrome?. Crit Care Med1998;26:2073. 42. Wrigge H: Proportional assist versus pressure support ventilation: Effects on breathing pattern and respiratory work of patients with chronic obstructive pulmonary disease. Intensive Care Med1999;25:790. 43. Pollack CV, Fleisch KB, Dowsey K: Treatment of acute bronchospasm with beta-adrenergic aerosols delivered via a Bi-PAP circuit. Ann Emerg Med1995;26:547.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/10.htm l/top
Page 5
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
Chapter 44 – Genitourinary System Robert E. Schneider
PERSPECTIVE Despite the advances in the initial management and treatment of the severely injured patient, confusion remains regarding the recognition and subsequent management of genitourinary trauma. Only main renal vein lacerations or a severely shattered kidney, both of which are rare, portend a rapid death. Thus, most genitourinary injuries pale in comparison to the immediate life threats posed by injuries to the chest and abdomen. Hence, the urinary tract as an anatomically injured system is by necessity relegated to a position of secondary importance. Nevertheless, to maintain excellence and expertise in the overall management of all injured patients, it is mandatory for the emergency physician to have a thorough understanding of the global spectrum of genitourinary injury and how it can affect eventual patient outcome. Genitourinary trauma commonly is a covert entity associated with a wide spectrum of injury. Approximately 10% of all multiply injured patients have some manifestation of genitourinary involvement.[1] Because of its uncommon occurrence and subtle presentation, it is often overlooked in the initial evaluation of the trauma victim. Nevertheless, after the primary survey for life-threatening injuries, Foley catheter placement as part of the secondary survey may disclose the first sign of urinary tract injury. The urinary tract is unique in that diagnostic evaluation is always done in a retrograde fashion; that is, suspicion and elimination of urethral injury before bladder injury before ureteral or renal injury. Adherence to this axiom will permit discovery of virtually any important urinary tract injury, even during the resuscitation of critically injured patients.
Definitions For purposes of investigation and staging of urologic injuries, genitourinary trauma is divided into lower tract (i.e., bladder or urethral injury), upper tract (i.e., renal or ureteral injury), and external genitalia (i.e., penile, scrotal, and testicular injury). Each category is further subdivided on the basis of a blunt or penetrating mechanism of injury.
Historical Perspective The basic tenets of lower urinary tract injury have not changed appreciably in the last 25 years. A thoroughly performed physical examination and the recognition of blood at the urethral meatus or gross hematuria will identify all significant lower urinary tract injuries. Major advances in the identification of significant upper tract genitourinary injuries, their clinical markers, and ultimate staging procedures have come to the forefront over the last 18 years. Before 1985, any trauma patient with any amount of microhematuria was described as “at risk” for genitourinary injury and underwent intravenous pyelography (IVP). This was neither diagnostically definitive nor cost-effective and simply perpetuated the existing confusion and controversy. In 1985, Nicolaisen and colleagues[2] published the first of a series of articles that established guide-lines to identify significant upper tract genitourinary injuries, their markers, and the diagnostic studies that would define the exact extent of these injuries and aid in subsequent patient management. In addition, the advent of ultrasonography and computed tomographic (CT) scanning has greatly simplified the diagnosis and management of external genitalia trauma.
CLINICAL FEATURES Signs and Symptoms The signs and symptoms of genitourinary trauma are varied and nonspecific. Acutely, these signs may include flank, abdominal, rib, back, or scrotal pain; urinary retention; and penile/urethral bleeding. Renovascular hypertension may be the only finding weeks to months after injury.
Physical Examination
Page 6
Examination of the torso and pelvis during the secondary survey is the first step in the evaluation for urologic injury. Any evidence of abdominal tenderness should alert the examining physician to the possibility of a bladder rupture in addition to other intra-abdominal injuries. This likelihood increases significantly in the presence of a pelvic fracture. Tenderness elicited by pelvic compression or palpation of the pelvic girdle or pubic symphysis supports the diagnosis of a potential pelvic fracture with possible lower urinary tract injury. Examination of the genitalia can be informative. The emergency physician should look for evidence of hematoma or ecchymosis of the penile shaft, scrotal skin, or perineum. Gross blood at the urethral meatus is diagnostic of a urethral injury and dictates the need for early retrograde urethrography. In circumstances in which emergency surgical exploration for life-threatening injuries is needed, the retrograde urethrogram can be performed in the operating room or after the operative procedure. A Foley catheter should never be introduced when there is suspected urethral trauma without first ensuring urethral integrity by retrograde urethrography. Failure to do this may convert a partial urethral tear into a complete disruption. Careful inspection for blood at the vaginal introitus is particularly important in the female patient known to have a pelvic fracture. A thorough vaginal examination will discern vaginal lacerations or urethral disruption caused by displaced bony pelvic fracture fragments. Unlike male urethral injuries, urethrography is not helpful in suspected female urethral injuries because of the urethra's short length. The inability to pass a Foley catheter in a young premenopausal female patient with a pelvic fracture signifies the potential for urethral injury and subsequent necessity for suprapubic urinary drainage. Successful passage of a Foley catheter in the same type of patient with blood at the vaginal introitus does not exclude urethral injury, and these worrisome physical examination findings must be conveyed to the urologist, who can plan subsequent urethral evaluation.[3] In an older postmenopausal female trauma patient, urethral injury must be distinguished from a superiorly retracted urethral meatus and accompanying meatal stenosis. These preexisting conditions are common in an atrophic vaginal setting, and a 12- or 14-Fr coudé or Foley catheter usually is required for successful bladder access. Rectal examination evaluates sphincter tone, bowel wall integrity, and most important, the position of the prostate. Normally, the posterior lobe of the prostate is palpable and well defined ( Figure 44-1 ). A pelvic fracture may disrupt the puboprostatic ligaments and the prostatomembranous urethra, resulting in significant retropubic venous bleeding. This may produce a large pelvic hematoma that can displace the prostate superiorly, resulting in a boggy, ill-defined mass on rectal examination ( Figure 44-2 ).
Figure 44-1 Anatom y of m ale genitalia.
Figure 44-2 Injury to the posterior (m em branous) urethra. The prostate has been avulsed from the m em branous urethra secondary to fracture of the pelvis. Extravasation occurs above the triangular ligam ent and is periprostatic and perivesical. ((From McAninch JW: In Tanagho EA, McAninch JW [eds]: Sm ith's General Urology, 14th ed. Norwalk, Conn, Appleton & Lange, 1995.)Appleton & Lange)
Foley Catheter In any trauma patient presenting with a major mechanism of injury and the absence of any findings suggestive of urethral injury, a Foley catheter should be passed into the bladder. The initial bladder effluent must be observed by the responsible physician. Because of its importance in dictating subsequent patient evaluation, observation of the initial bladder effluent should optimally not be relegated to any other member of
Page 7
the resuscitation team. Any color to the urine other than clear or yellow must be considered a sign of gross hematuria until proved otherwise. The presence of gross hematuria indicates urologic injury. Rarely, severe rhabdomyolysis produces large quantities of urine myoglobin, the gross appearance of which can be confused with gross hematuria. In these cases, urinalysis will document the absence of red blood cells (RBCs) consistent with myoglobinuria. Most significant lower urinary tract injuries will be accompanied by either the presence of a pelvic fracture with blood at the urethral meatus or gross hematuria on Foley catheter placement.[4] Upper tract trauma, however, tends to be more subtle. It is often coincident with nonurologic organ disruption, the bleeding from which can be life-threatening. These events may dictate rapid volume resuscitation that can clear gross hematuria quickly. Moreover, blunt injury to the renovascular pedicle or penetrating ureteral injury may not produce gross or even microscopic hematuria.
LOWER URINARY TRACT Urethral Trauma Anatomy The urogenital diaphragm divides the anterior (bulbous and pendulous) urethra from the posterior (membranous and prostatic) urethra. It is a 1.5 cm fascial layer that lies between the ischial rami. It attaches anteriorly to the symphysis, posteriorly to the perineal body and ischial tuberosity, and laterally to the inferior ischial pubic rami. It is traversed by the membranous urethra. The prostatic urethra is contiguous with the urogenital diaphragm and is attached to the posterior symphysis pubis by the puboprostatic ligaments. A fracture of the pelvis with displacement of the symphysis may result in a laceration or avulsion of the prostatic urethra because of the shearing force on the fixed prostatic and membranous urethra. Injuries to the anterior and posterior urethra are caused by different mechanisms, involve different symptoms, and are treated differently.
Pathophysiology Urethral disruption is the most significant injury that must be identified. Failure to do so may lead to significant morbidity (i.e., converting a partial urethral tear into a complete tear). Urethral manipulation can convert a partial urethral tear into a complete tear, thus precluding accurate assessment of urinary output, and subsequently potentiating the long-term complications of urethral trauma (e.g., urethral stricture formation and urinary incontinence). Pelvic fractures account for most posterior urethral injuries proximal to the urogenital diaphragm (see Figure 44-2 ).[5] Anterior urethral injuries distal to the urogenital diaphragm are most often caused by straddle injuries, falls, gunshot wounds, and self-instrumentation ( Figure 44-3 ).[6]
Figure 44-3 Injury to the bulbous urethra. Left: Mechanism : usually a perineal blow or fall astride an object; crushing of urethra against inferior edge of pubic symphysis. Right: Extravasation of blood and urine enclosed within Colles' fascia. ((From McAninch JW: In Tanagho EA, McAninch JW [eds]: Sm ith's General Urology, 14th ed. Norwalk, Conn, Appleton & Lange, 1995.)Appleton & Lange)
Clinical Features During the secondary survey, examination of the lower abdomen, pelvis, genitalia, and rectum provides both direct and indirect evidence to support or refute urethral injury. Lack of pelvic and suprapubic tenderness; absence of penile, scrotal, or perineal hematoma; and normal findings on rectal examination all support the integrity of the urethra. These physical findings permit the safe passage of a 14- or 16-Fr Foley catheter into the bladder if the patient is unable to void and provide a suitable specimen for evaluation.
Diagnostic Strategies Catheter Placement The following technique for catheter placement assumes a normal urethra and includes the use of sterile technique, proper control of the foreskin, the use of copious amounts of lubricating jelly, and the gentle passage of a 14- or 16-Fr Foley or coudé catheter into the bladder. In all uncircumcised patients, continuous foreskin retraction with a folded 4 × 4 inch gauze pad is necessary to control the foreskin during catheter
Page 8
placement ( Figure 44-4 ). Without this maneuver, the foreskin tends to repeatedly reduce itself over the glans penis, which contaminates the field and makes catheterization difficult or impossible. Slight resistance to the advancing catheter should be expected at the urogenital diaphragm secondary to voluntary contraction of the external sphincter. This is more apt to occur in a combative, anxious trauma patient than in a cooperative or unconscious patient. When this occurs, the patient should be reassured and asked to relax the perineum and rectal area while gentle advancing pressure is applied to the catheter. This combined approach allows the catheter to navigate the urogenital diaphragm successfully and pass easily into the bladder. If reassurance and relaxation do not allow easy passage of the catheter, it should be removed and a retrograde urethrogram performed. In all cases, the catheter must be passed to its fullest extent before the balloon can be inflated safely, then withdrawn to the point of catheter balloon approximation with the bladder neck and left to drain. Inflation of the catheter balloon under any other circumstances may result in iatrogenic urethral trauma.
Figure 44-4 A, A norm al uncircum cised m an. B, Foreskin has been retracted and a folded 4 × 4 inch gauge sponge wrapped around it to prevent foreskin reduction during instrumentation.
Successful passage of a Foley catheter precludes a complete urethral disruption. Nonetheless, the possibility of a partial urethral injury not manifested by history, mechanism of injury, presence of meatal blood, or other indirect signs on physical examination may exist. If this injury is suspected initially, a retrograde urethrogram should be obtained. The presence of urethral extravasation together with contrast material filling the bladder is diagnostic of a partial urethral injury ( Figure 44-5 ).[6] Identification of a partial urethral injury would permit one careful attempt at urethral placement of a 12- or 14-Fr Foley or coudé catheter, depending on the size of the patient. If any difficulty is encountered, the catheter should be removed and a urologist consulted. If a partial urethral tear is suspected subsequent to successful passage of a Foley catheter, a small feeding tube can be placed along-side the urethral catheter and a modified retrograde urethrogram performed.[4] In this circumstance, the urethrogram is for documentation and subsequent management purposes only because appropriate therapy has already been instituted (i.e., Foley catheter drainage). Under no circumstances should a successfully placed Foley catheter be removed to perform standard retrograde urethrography.
Figure 44-5 Retrograde urethrogram dem onstrates a partial urethral disruption. Note the elongation of the posterior urethra with filling of the bladder. ((From Spirnak JP: Pelvic fracture and injury to the lower urinary tract. Surg Clin North Am 68:1057, 1988.))
Radiology In all cases of suspected urethral injury, a retrograde urethrogram is the diagnostic procedure of choice.[] Retrograde urethrography is not an emergency and should always follow more critical resuscitative measures. In a patient with a pelvic fracture, the entire retrograde urethrogram should be conducted with the patient in a supine rather than oblique position. Certain authors recommend oblique films for portions of the retrograde urethrogram to enhance urethral definition.[] These views add little information to a good supine study. More
Page 9
important, pelvic fractures are often associated with significant retropubic venous bleeding and hematoma formation. Maintenance of this stable hematoma can be crucial in the initial hemodynamic resuscitation of the patient. Any patient movement from the supine to the oblique position has the potential to disrupt the organized hematoma with resultant significant and potentially lethal rebleeding. The entire urethral integrity can be defined with the patient in the supine position throughout the examination, aided by oblique stretching of the penis over the left or right thigh to promote necessary urethral unfolding. A preinjection kidney, ureter, and bladder (KUB) film is first obtained. A simple Christmas tree adapter, a Cooke adapter placed on the end of a 60 mL Toomey syringe, or a Toomey syringe alone is gently passed into the urethral meatus until a snug fit inside the meatus is confirmed ( Figure 44-6 ). Some authors have recommended inflation of a Foley catheter balloon just proximal to the fossa navicularis or the use of other cumbersome adjuncts to facilitate injection of contrast media.[] These techniques should be avoided, however, because they promote leakage of contrast material around the penis, which can simulate extravasation on the urethrogram and promote a spurious examination. Next, 60 mL (or 0.6 mL/kg) of full-strength or half-strength iothalamate meglumine (Conray II) is injected over 30 to 60 seconds. A radiograph is taken during the injection of the last 10 mL of contrast material. Retrograde flow through the urethra and into the bladder without extravasation ensures continuity of the urethra and absence of urethral injury ( Figure 44-7 ). Extravasation of contrast material outside the urethra with concomitant evidence of bladder filling distinguishes a partial urethral injury (see Figure 44-5 ) from a complete urethral disruption in which there will be absence of contrast material inside the bladder ( Figure 44-8 ).[] The latter situation requires immediate urologic consultation for appropriate surgical management. In the interim, if measurement of urinary output is essential, the bladder should be accessed by the suprapubic placement of a peel-away sheath and Foley catheter using the Seldinger technique ( Figure 44-9 ).
Figure 44-6 Christm as tree adapter on the end of a 60 m L syringe has been gently placed inside the fossa navicularis in preparation for retrograde urethrography.
Figure 44-7 Norm al anatom y is dem onstrated by a line drawing (A) and by dynam ic retrograde urethrography (B). Bladder (1), prostatic urethra (2), verum ontanum (3), m em branous urethra (4), position of the urogenital diaphragm (5), bulbous urethra (6), and penile urethra (7). The penile and bulbous urethra together are considered the anterior urethra; the prostatic and m em branous urethra com pose the posterior urethra. ((Adapted from McCallum RW, Colapinto V: Urological Radiology of the Adult Male Lower Urinary Tract. Springfield, Ill, Charles C Thomas, 1976.))
Figure 44-8 Retrograde urethrogram s dem onstrates com plete urethral disruption. Note the absence of bladder filling, a finding diagnostic of com plete disruption. ((From Spirnak JP: Pelvic fracture and injury to the lower urinary tract. Surg Clin North Am 68:1057, 1988.))
Page 10
Figure 44-9 Percutaneous placem ent of a suprapubic tube with peel-away sheath introducer. A, An 18-gauge needle is in the bladder. A guidewire is advanced through needle. B, A dilator and peel-away sheath are advanced over the guidewire. C, The dilator and guidewire are rem oved. Through the peel-away sheath, an appropriately sized catheter can be introduced into bladder. D, The balloon is inflated, and the sheath is pulled back and peeled away. ((From O'Brien WM: Percutaneous placem ent of suprapub ic with peel away sheath introducer. J Urol 145:1015, 1991.))
Management During physical examination, urethral injury is suggested by the presence of a pelvic fracture, blood at the urethral meatus, the presence of a high-riding or absent prostate on rectal examination, or evidence of a perineal, scrotal, or penile hematoma. Any one of these latter three findings necessitates a retrograde urethrogram to disclose the anatomy and integrity of the urethra. If these findings are absent or the urethrogram is normal, the urethra is intact and a Foley catheter can be passed into the bladder. If a partial urethral disruption is identified, one careful attempt to pass a 12- or 14-Fr Foley or coudé catheter can be undertaken. If a complete urethral disruption is identified, consultation with a urology specialist and placement of a suprapubic catheter for urinary drainage are necessary.
Bladder Trauma Anatomy When empty, the bladder lies retroperitoneally almost entirely within the bony pelvis. It rests on the pubis and adjacent pelvic floor parts. When full, the bladder can extend up to the level of the umbilicus, where it is most vulnerable to blunt and penetrating trauma. The bladder consists of an inner longitudinal, a middle circular, and an outer longitudinal muscle layer. These three layers constitute the detrusor muscle, which contracts to propel urine out the urethra. Blood is supplied to the bladder by the internal iliac artery and vein. The nerve supply comes from the lumbar and sacral segments of the spinal cord. It includes parasympathetic motor fibers to the detrusor muscle and sensory fibers to the detrusor that give rise to the sensation of fullness and urgency when the detrusor is stretched. The third nerve group, the sympathetic fibers, innervate the blood vessels of the bladder and the bladder neck musculature. The mechanism of injury with bladder trauma is usually severe. This is reflected in the high mortality rate of 22% to 44%.[7] There is a high incidence of associated life-threatening nonurologic injury, the treatment of which always takes precedence. The diagnostic evaluation of the bladder, like the urethra, can be accomplished quickly without elaborate radiographic equipment or can be part of the CT evaluation if other nonurologic injuries are being evaluated.
Pathophysiology Extraperitoneal bladder perforation, intraperitoneal bladder perforation, and a combination of the two are the significant injuries in bladder trauma. Proper classification is critical because treatment options are completely different.[8] Whereas most ruptures occur singly as extraperitoneal or intraperitoneal, their coexistence is being recognized more often as the mechanism for bladder injury becomes better understood. The time-honored explanation for extraperitoneal rupture has been pelvic fracture with subsequent bladder laceration from an errant bony fracture fragment. It has become apparent, however, that extraperitoneal perforation can result from blunt trauma alone and need not require a lacerating fracture bony fragment. Intraperitoneal bladder rupture has been ascribed to blunt lower abdominal trauma in a patient with a full bladder. These blunt forces are directed to the dome of the bladder where the urachus originates during embryonic life. Because of this developmental hiatus, the dome is attenuated and represents the anatomic area most susceptible to rupture from sudden rises in intravesical pressure associated with blunt trauma. The dome also is unique in its isolated peritoneal reflection so that rupture in this area most likely will result in intraperitoneal urinary contamination.
Clinical Features Lower abdominal or suprapubic pain, the inability to urinate, or the presence of blood at the urethral meatus
Page 11
may alert the physician to the possibility of lower urinary tract trauma.
Diagnostic Strategies Laboratory Gross hematuria in the initial bladder effluent is indicative of urologic injury. The literature clearly defines gross hematuria alone or in conjunction with a pelvic fracture as the absolute markers for significant bladder injury.[] Grossly clear bladder urine in a trauma patient without a pelvic fracture virtually eliminates the possibility of bladder rupture. The overwhelming majority (98%) of patients with bladder rupture have gross hematuria (JW McAninch, personal communication, 1998). The other 2% are representative of the select group of patients with a pelvic fracture and only microhematuria. Clinical judgment is required when deciding when these patients need a bladder evaluation.
Radiology Conventional retrograde cystography or retrograde CT cystography are the diagnostic procedures of choice for suspected bladder injury.[] It is key that these studies not be done in an antegrade fashion, as such procedures may produce incomplete and spurious findings (e.g., injecting intravenous contrast material, clamping the Foley catheter, and allowing the examination to be dependent on antegrade filling of the bladder from renal excretion of progressively dilute contrast material).
Conventional Retrograde Cystogram. Performance of either conventional or CT retrograde cystography assumes or follows exclusion of urethral trauma and the presence of an indwelling Foley catheter in the bladder. A Toomey syringe alone without its central piston is used for gravity instillation of contrast material ( Figure 44-10 ). Allowing the contrast material to freely infuse from a hanging bottle connected to an indwelling Foley catheter runs the risk of the tubing becoming disconnected with subsequent leakage of contrast material onto the examination table ( Figure 44-11A and B ). This may promote an inaccurate examination that results in an unnecessary operative procedure ( Figure 44-11C ). For patients with a pelvic fracture, it is imperative that they remain supine throughout the examination rather than be repositioned obliquely for selected radiographs. This lessens the potential for rebleeding from an organized retropubic hematoma.
Figure 44-10 Retrograde cystogram . A Toom ey syringe without its central piston is connected to the catheter and held by the exam iner while gravity-instilled contrast m aterial fills the bladder.
Figure 44-11 Spurious retrograde cystogram . This exam ination resulted when the tubing from the contrast bottle becam e disconnected from the Foley catheter after both were placed on the exam ination table, and bladder filling was com pleted without direct supervision. A, Kidney, bladder, ureter (KUB) film. B, Postinfusion KUB film interpreted as intraperitoneal bladder perforation. C, Intraoperative retrograde cystogram showing no evidence of extravasation.
A preliminary KUB or scout film is obtained to provide a baseline evaluation of the pelvis, abdomen, and surrounding bony structures. It will become the film of reference for the post-evacuation radiograph obtained after completion of the cystogram. Potential areas of extravasation on the post-evacuation film will be confirmed when compared with the preliminary KUB film ( Figure 44-12 ). Contrast material should not be instilled into the bladder until the quality and anatomic information on the preliminary KUB film are confirmed.
Page 12
Figure 44-12 Retrograde cystogram . A, Prelim inary kidney, bladder, ureter (KUB) film . B, Film of filled bladder. C, Postevacuation film com paring posterior extravasation with the prelim inary KUB film .
Full-strength iothalamate meglumine (Conray II) is instilled under gravity filling to one of three endpoints: (1) 100 mL with immediate fluoroscopic evidence of gross extravasation; (2) a total instillation of 300 to 400 mL in any patient 11 years of age or older; in patients younger than 11 years of age, the correct amount of contrast medium is determined by the formula (age in years + 2) × 30; or (3) the instillation of a lesser amount than 100 mL, which initiates a bladder contraction. This will become evident by the retrograde filling of the Toomey syringe with bladder contents. After a few minutes, the original contrast material can again be instilled to the point of stimulating a bladder contraction, at which time an additional 50 mL of full-strength iothalamate meglumine should be injected slowly but forcefully into the bladder. The Foley catheter should be clamped, and an anteroposterior radiograph should be taken of the filled bladder ( Figure 44-13A and B). A lateral film may help clarify any areas in question ( Figure 44-13C ). After the film of the filled bladder meets standards for quality and detail, the bladder should be completely evacuated into a large basin or, preferably, into an available bedside drainage bag. Any spillage of contrast material onto the pelvic genitalia or examination table may lead to false-positive findings on the postevacuation radiograph. The postevacuation film may disclose evidence of posterior bladder wall or extraperitoneal extravasation not seen on the anteroposterior radiograph of the filled bladder ( Figure 44-14 ).
Figure 44-13 Retrograde cystogram . A, Prelim inary kidney, bladder, ureter (KUB) film . B, Film of filled bladder showing extravasation that could be intraperitoneal, as well as extraperitoneal. C, Film of patient in a lateral position shows no evidence of intraperitoneal extravasation.
Figure 44-14 Retrograde cystogram . A, Film of filled bladder. B, Postevacuation film showing extensive extraperitoneal extravasation.
In cases of extraperitoneal bladder perforation, contrast material will be evident in the area of the pubic symphysis and pelvic outlet ( Figure 44-15 ). With intraperitoneal perforation, contrast material outlines intraperitoneal structures (e.g., loops of bowel, the liver, and spleen) ( Figure 44-16 ).
Figure 44-15 Cystographic appearance of extraperitoneal bladder perforation. A and B, Note the teardrop deform ity caused by extrinsic com pression by the pelvic hem atom a and the flam elike wisps of extravasation confined by the pelvis. The bladder itself
Page 13
is elongated by a collection of perivesicular fluid. ((From Spirnak JP: Pelvic fracture and injury to the lower urinary tract. Surg Clin North Am 68:1057, 1988.))
Figure 44-16 Cystographic appearance of intraperitoneal bladder perforation. Cystogram reveals m assive intraperitoneal perforation and extravasation. ((From Spirnak JP: Pelvic fracture and injury to the lower urinary tract. Surg Clin North Am 68:1057, 1988.))
Several studies have documented that false-negative results are associated with the use of less than 300 to 400 mL or an age-appropriate amount of contrast material for cystography.[] This has been seen primarily in penetrating bladder injuries in which the perforation from a small-caliber gunshot wound or a thin blade stab wound can be missed. The anatomically interlacing bladder wall muscle fibers are arranged such that these wounds lend themselves to immediate muscle fiber reapproximation and tenuous sealing of the wound by covering peritoneum and intra-abdominal mesentery. Unless an adequate amount of full-strength contrast material is used to fully distend or even overdistend the bladder, extravasation will not be evident, the injury will be missed, and there will be potential for significant morbidity.
Computed Tomography Retrograde Cystogram. The same anatomic information regarding bladder injury may be obtained using retrograde CT cystography rather than routine plain film radiography.[11] CT cystography is best done in trauma patients who are undergoing CT evaluation for other suspected injuries. In either study, undiluted iothalamate meglumine (Conray II) must first be instilled in a retrograde fashion. Intraperitoneal perforation will be disclosed on helical CT scan by the presence of extravasated contrast material throughout the abdominal cavity (i.e., contrast ascites). Extraperitoneal extravasation will be more difficult to visualize but can be appreciated on images taken through the pelvic area ( Figure 44-17A and B ).
Figure 44-17 Bladder rupture. A, Intraperitoneal rupture shows contrast m aterial extravasated from the bladder outlining loops of bowel in the lower abdom en. B, Extraperitoneal rupture shows contrast m aterial extravasating into the disrupted soft tissue plains of the anterior and left pelvic side wall. ((Courtesy of Charlotte Radiology, Em ergency Radiology Section, Charlotte, North Carolina.))
Management In cases of superficial mucosal bladder lacerations, bladder contusions, or simple bladder hematomas, there will be no evidence of extravasation on retrograde cystography. For these injuries, expectant management with or without Foley catheter drainage is the standard of care.[]
Extraperitoneal Bladder Rupture Extraperitoneal bladder rupture heals spontaneously in most circumstances after simple Foley catheter
Page 14
drainage for 7 to 14 days using a 20-Fr or larger Foley catheter.[] Care must be taken to ensure continuous bladder decompression and prevention of catheter occlusion by clot or debris. In a patient with known or suspected infected urine before the traumatic event, consideration must be given both to Foley or suprapubic catheter drainage and to surgical placement of drains in the perivesical space to prevent subsequent abscess formation. Primary surgical repair of extraperitoneal bladder rupture should be considered in any trauma patient whose bladder injury appears to extend into the bladder neck or proximal urethra.[] This is most important in the female trauma patient because the short length of the female urethra lends itself to a higher incidence of urinary incontinence after injury. This can hopefully be reduced by primary surgical repair. Any patient whose other associated nonurologic injuries dictate abdominal exploration is a candidate for primary surgical repair of the extraperitoneal bladder injury provided the bladder laceration is easily accessible and does not require operative exposure through a large, organized, stable retropubic hematoma.[]
Intraperitoneal Bladder Rupture Larger, gaping intraperitoneal bladder perforations will not heal spontaneously and always require operative repair.[6] Without operative intervention for intraperitoneal injury, lower urinary tract contamination will quickly infect initially sterile urine and promote the development of subsequent bacterial peritonitis. Bladder repairs are never emergencies and normally follow operative repair of more urgent life-threatening injuries.
UPPER TRACT TRAUMA Renal Trauma Perspective Renal trauma is a capricious injury that has no known identifiable markers. Mechanisms responsible for significant renal injury almost never affect the kidney alone, but most often disrupt and perforate other vital organs that can be solely responsible for the patients' death and may demand immediate operative intervention. Significant renal injuries define a small subset of the trauma population at large. This by itself promotes diagnostic uncertainty and causes some of these injuries to be overlooked initially. Renal injuries are graded 1 through 5 according to the Organ Injury Scale Committee Guidelines, which identifies most injuries requiring operative intervention.[14]
Complications Development of renovascular hypertension occurs in approximately 1% of cases and is the main complication associated with failed arterial repairs or missed pedicle injuries.[14] When associated with elevated renal vein renin levels, nephrectomy is curative. For these reasons, the issue of whether to actively pursue this diagnosis is debated. An isolated pedicle injury in a young, healthy trauma patient would seem to be the ideal circumstance in which an all-out attempt should be made to reconstruct the renal artery or vein.
Anatomy and Physiology The kidneys are located in the retroperitoneal space, are surrounded by adipose tissue and loose areolar connective tissue, and lie along the lower two thoracic vertebrae and the first four lumbar vertebrae. The left kidney is suspended slightly higher than the right ( Figure 44-18 ). The kidneys are not fixed. They move with the diaphragm and are supported by their renal arteries, veins, and adipose tissue, which is connected to a layer of fibrous tissue called the renal fascia, or Gerota's fascia.
Figure 44-18 Dissection of abdom en showing kidneys and ureters and their relationship to other anatomic features in the retroperitoneal space.
The indented medial border of the kidney is called the hilum. The major renal vessels and ureter make up the renal pedicle and enter and exit at the hilum. The longitudinal section of the kidney ( Figure 44-19 ) shows an outer renal cortex and an inner renal medulla with its columns of Bertin. Each column of Bertin forms a papilla that empties into the renal pelvis. The renal pelvis is a funnel-shaped sac with cup-shaped extensions called calyces, which receive urine from each papilla and are the important decompression areas for varied
Page 15
rises in intrapelvic pressure.
Figure 44-19 Longitudinal section of kidney.
The kidneys are perfused by 1200 mL of blood per minute, or 20% to 25% of cardiac output. Of this, 90% goes to the cortex and 10% to the medulla. Reduced blood flow to the kidney, whether from blunt or penetrating injury, causes renin to be released from the juxtaglomerular cells. Renin enters the bloodstream and combines with a plasma protein to form angiotensin. Angiotensin raises blood pressure by causing arteriolar vasoconstriction and acting on the adrenal cortex to augment aldosterone secretion. Aldosterone acts on the renal tubules to promote sodium reabsorption. Water follows passively with subsequent increase in blood volume. These changes increase blood flow to the kidney and other organs. The body requires only one third of normal renal function to sustain life. It is unusual in cases of genitourinary trauma to lose total renal function unless the patient's injured kidney is a solitary kidney, which carries a 1 in 1000 to 1 in 5000 incidence.[15]
Epidemiology Renal trauma represents the most common of all urologic injuries.[2] Blunt renal trauma accounts for 80% to 85% of all renal injuries and is five times more common than penetrating renal trauma.[2] With the increasing prevalence nationwide of gunshot and stab wounds in association with drug-related violence, the proportion of injuries due to penetrating trauma may rise. Blunt mechanisms are seen most often after motor vehicle crashes, domestic violence, and sporting injuries. The pathophysiologic mechanisms include rapid deceleration, displacement, and, rarely, an explosion-type injury of the ureteropelvic junction. Approximately 20% of blunt renal trauma cases are associated with intraperitoneal injury.[2] Penetrating renal trauma is associated with intraperitoneal injury in approximately 80% of cases.[2]
Diagnostic Strategies Laboratory No accurate markers for renal injury exist. In all types of renal trauma, the degree of hematuria is not indicative of the severity or extent of injury. Formerly, a trauma patient who exhibited gross or microscopic hematuria was labeled “at risk” for urologic injury and underwent intravenous pyelography. Experience has shown that most of the identifiable injuries were renal contusions that could be managed expectantly. Moreover, in a significant number of severely traumatized patients, vigorous initial fluid resuscitation precluded satisfactory contrast concentration in the kidney, yielding an incomplete, nondiagnostic initial radiographic examination. In 1989, Mee and associates[16] published the hallmark article that established guidelines for the evaluation and treatment of blunt renal trauma. Their 10-year prospective study clearly established that (1) major renal lacerations represent significant reparable renal injuries; (2) adult patients at risk for having sustained major lacerations have either gross hematuria or microhematuria (≥3 to 5 RBCs/hpf) with shock (systolic blood pressure ≤90 mm Hg) initially in the field or on arrival at an emergency department, or, rarely but importantly, a history of sudden deceleration without hematuria or shock; and (3) intravenous contrast-enhanced CT scan is the procedure of choice in identifying the full extent of urologic injury.[] These guidelines are not applicable for cases of penetrating renal trauma or in children.
Pediatrics. In children, the kidney is the most commonly injured genitourinary organ in blunt abdominal trauma.[18] Additionally, unlike adults, major renal injuries can occur in the presence of microhematuria without shock or even in the presence of a normal urinalysis. Prior meta-analyses defined 50 RBCs/hpf as the microscopic quantity below which imaging could be confidently deleted without missing significant injuries.[19] Current literature supports radiographic investigation based mainly on mechanism of injury and clinical suspicion, because no absolute parameters for excluding significant renal injury exist.[20] As with adults, intravenous
Page 16
contrast-enhanced helical CT scanning is the diagnostic imaging technique of choice.
Radiology Intravenous Pyelography. Whether simple, routine IVP is ever indicated in the initial evaluation of suspected renal trauma depends on the institution and the radiologist. At a center that does not have 24-hour availability of radiologists and technicians, bolus infusion IVP with nephrotomography rather than simple IVP is the initial study of choice.[] Bolus infusion denotes the rapid injection of 2 mL of contrast material per kilogram of body weight to a maximum of 150 mL after a preliminary KUB film has been obtained.[15] Immediately on completion of the injection, a postinfusion supine film is obtained, followed by 1-, 2-, and 3-minute supine films, specifically tailoring the study to identify both renal outlines and evidence that contrast is extending down the collecting system of the kidney and ureter to the bladder without extravasation. In fact, most authors propose bolus infusion IVP with nephrotomography as the initial study of choice for uncommonly encountered isolated renal injury, which can be difficult to identify prospectively.[16] In the spectrum of experience with bolus infusion IVP as a diagnostic tool for renal injury, most authors find this study adequate only 60% to 85% of the time.[21] Often, abnormal findings are nonspecific and require more sophisticated studies, such as CT scanning, to identify the full extent of the existing renal injuries. When immediate, life-saving, nonurologic surgical intervention is mandated or an expanding retroperitoneal hematoma with the potential for significant renal injury is encountered in the operating room, a 2 mL/kg intraoperative bolus infusion of contrast and a 10-minute film are recommended to ensure the presence of both kidneys before the retroperitoneum is opened and control of the renal pedicle is attempted. A “single-shot” IVP in the emergency department used as a screening examination before the patient is transported to the operating room is discouraged because of the equally unacceptable incidence of false-positive and false-negative results.[15]
Computed Tomography. An intravenous contrast-enhanced helical CT scan is the diagnostic radiographic procedure of choice in evaluating significant upper tract blunt renal trauma. It is more sensitive and specific than bolus infusion IVP with nephrotomography ( Figure 44-20A-E ).[]
Figure 44-20 A, Renal artery injury. The left kidney dem onstrates alm ost com plete acute devascularization. (Note the right flank hem atom a.) B, Subcapsular hem atom a. Deform ing renal parenchym a on the left. C and D, Renal laceration. These two images are of the sam e patient separated by several m inutes of delay. The wedge-shaped hypodensities in the left kidney on the first scan (C) indicate the lacerations. The delayed scan (D) shows extravasation of contrast material from the lacerated kidney. E, Collecting system injury. Extravasation of contrast m aterial from the lacerated right renal pelvis. (Hypodense areas of the kidney represent contusion.) ((Courtesy of Charlotte Radiology, Em ergency Radiology Section, Charlotte, North Carolina.))
Management Blunt Injury Both an adult blunt trauma patient with microhematuria (≥3 to 5 RBCs/hpf) but no shock (systolic blood pressure ≤90 mm Hg) in the field or in the emergency department and a pediatric blunt trauma patient with 50 RBCs/hpf or fewer and no other coexisting major organ injuries can be confidently discharged from the emergency department if no other complicating nonurologic injuries are present that would dictate observation or hospital admission. Outpatient follow-up with a urologist until the microhematuria has cleared is mandatory to be certain it does not represent another more serious underlying condition.[23] Renal artery avulsions, intimal tears, and renal venous injuries should be considered under the classification of significant injuries. Although only 1% to 2% of all renal injuries involve the renal pedicle, their evaluation and management remain a real dilemma based on the frustrating and dismal experience with pedicle injuries
Page 17
from major centers.[24] Experience has shown that even under the most ideal clinical circumstances (i.e., fortuitous early recognition and prompt surgical repair), the salvage rate at best for a life-sustaining functioning kidney approaches only 15% to 20%. Renal vein injuries are more common than renal artery avulsions or intimal tears. Both injuries are often associated with rapid deceleration events. Most venous injuries tend to be partial rather than complete tears, or they involve segmental renal vein branches and therefore often occur in the periphery of the vein (i.e., involving contiguous adrenal or gonadal attachments to the left renal vein rather than at the junction of the main renal vein with the vena cava). As expected, a venous injury can potentially contribute more to a patient's unstable hemodynamic status than an arterial injury. The protective secondary vasospasm following arterial disruption does not occur with venous injuries. Pedicle injuries rarely occur alone. Most often they are associated with other life-threatening, nonurologic injuries that require immediate surgical intervention. This delays their diagnosis and repair for up to 6 to 8 hours, which results in significant warm ischemia time with subsequent low salvageability rates. An intravenous contrast-enhanced helical CT scan will identify most renal artery disruptions, whereas renal vein injuries must be indirectly diagnosed by the presence of a normal-appearing kidney in association with a large hematoma disproportionate to the rest of the radiographic study. Major renal lacerations represent approximately 2% to 4% of all renal injuries, and by definition are associated with renal fractures extending deep into the renal medulla and collecting system ( Figure 44-21 ). They also are readily diagnosed by an intravenous contrast-enhanced helical CT scan. Immediate surgical treatment of these injuries is controversial and depends on the presence or absence of continued renal bleeding, the hemodynamic status of the patient, and the degree of continued urinary extravasation.[25] This injury is in sharp contrast to minor renal lacerations (8-15%) and renal contusions (85-92%) that do not extend into the renal medulla or collecting system, are not associated with extravasation of urine, and heal spontaneously ( Figure 44-22 ). These latter two injuries can be managed expectantly and rarely, if ever, require initial or subsequent operative intervention.[16]
Figure 44-21 Major renal lacerations. A, Deep medullary laceration. B, Laceration into collecting system . ((From Nicolaisen GS, et al: Renal traum a: Re-evaluation of the indications for radiographic assessm ent. J Urol 133:183, 1985.))
Figure 44-22 Minor renal injuries. A, Minor renal laceration. B, Renal contusion. ((From Nicolaisen GS et al: Renal traum a: Re-evaluation of the indications for radiographic assessm ent. J Urol 133:183, 1985.))
Penetrating Injury In cases of penetrating renal trauma, the presence or absence of hematuria is of no consequence in predicting upper urinary tract injury. Rather, the location of the penetrating wound in relation to the urinary tract is the most important determining factor in deciding the need for radiographic investigation. Therefore, the absence of hematuria in a patient with a gunshot or stab wound in proximity to the urinary tract does not eliminate the need for an intravenous contrast-enhanced CT scan as the initial diagnostic examination. Significant injuries to the kidney and ureter occur in penetrating trauma without hematuria.[3] The majority of pene-trating renal and ureteral injuries require surgical intervention.
Page 18
Ureteral Trauma Pathophysiology Ureteral injuries are rare. Most are traumatic in origin and tend to occur as a result of shootings or stabbings or during various intra-abdominal or retroperitoneal operations.[26] Penetrating ureteral injuries are twice as common as blunt ureteral injuries. Most are localized in the upper third of the ureter.[27] This diagnosis should be considered when patients seen in the emergency department have a recent history of penetrating trauma, fever, and a palpably tender flank mass. If the ureter is injured by blunt trauma, there are often multiple associated nonurologic injuries. The gastrointestinal tract is injured in more than 50% of cases.[28] In pelvic fractures, the ureter is most likely to be injured as it crosses the pelvic brim. The intimate relationship of the ureter to the pelvis at this point allows it to be crushed, causing a contusion, tear, transection, or puncture by sharp fracture spicules.
Clinical Features The clinical picture of blunt ureteral injuries includes hematuria, flank pain similar to renal colic, and a flank mass. These classic signs are often overlooked initially because of the striking abdominal findings caused by associated nonurologic injuries. Hematuria may be present in association with ureteral contusion or partial ureteral tear but is rarely present in cases of complete ureteral transection. Pain in the lower abdomen, a palpable mass containing blood or urine, chills, fever, urgency, frequency, and pyuria are all symptoms of this injury.
Diagnostic Strategies In a Parkland Memorial Hospital series of 71 penetrating ureteral injuries, 32% of patients had no hematuria, 40% had gross hematuria, and 28% had microscopic hematuria.[29] If the patient survived the original penetrating event, the injury usually manifested itself 10 days later with the appearance of urine at the entrance or exit wounds or on the surgical dressings. If there is no vent for extravasated urine, a retroperitoneal urinoma will develop. If the diaphragm or peritoneum has been violated, the urine may cause an empyema or peritonitis.
Radiology If a ureteral injury is suspected, a contrast-enhanced helical CT scan with delayed films or bolus infusion IVP with delayed films should be done.[30] The clarity of injury identification depends on renal function and the lapsed time from the injury. If the study is performed soon after the injury, extravasation often has a ground-glass or hazy appearance as a result of contrast dilution from fluid resuscitation. If the injury is near the ureteropelvic junction, the contrast may extend peripherally around the kidney, giving the appearance of a lacerated renal pelvis or kidney. If the initial study of delayed films is inconclusive, retrograde pyelography is indicated to delineate a ureteral laceration or avulsion ( Figure 44-23A and B ). The more concentrated contrast used in retrograde pyelography compared with that used with routine IVP and the adjunctive use of fluoroscopy promote rapid identification of ureteral injury. A
B
Figure 44-23 Ureteral injuries. A, Intravenous pyelography (IVP) of patient with upper ureteral injury demonstrating extravasation (arrow). B, Retrograde pyelogram dem onstrating extravasation at the ureteropelvic junction (arrow).C, Retrograde pyelogram dem onstrating extravasation into a urinom a in a patient with delayed diagnosis. ((From Presti JC Jr, Carroll PR, McAninch JW: Ureteral and renal pelvic injuries from external traum a: Diagnosis and m anagem ent. J Traum a 29:370, 1989.))
Page 19
Management All ureteral injuries must be repaired surgically. If these injuries are diagnosed early, the kidney and ureter can be saved in most cases. In cases of delayed diagnosis, the rate of nephroureterectomies dramatically increases.[31]
EXTERNAL GENITALIA TRAUMA Penile Trauma Anatomy The penis contains three masses of erectile tissue ( Figure 44-24 ). The two corpora cavernosa constitute the main bulk of the penis and lie in the center of the penis. The corpus spongiosum is smaller, lies on the ventral surface of the penis, encases the urethra, and expands at the penile tip to form the glans penis. The tunica albuginea is a dense fibrous envelope that surrounds the corpus spongiosum and each corpus cavernosum. Blood is supplied through arteries lying in each of the three erectile masses and two dorsal penile arteries. A single dorsal vein drains most of the penis.
Figure 44-24 Cross-sectional view of the penis.
Clinical Features Injuries to the penis range from small lacerations or contusions to skin degloving or amputation. Strangulation injuries of the penis with string or scalp hair tightly encircling the shaft of the penis are seen in children ( Figure 44-25 ). Adolescents as well as adults may have various objects of penile incarceration such as bottles, washers, and metal rings ( Figure 44-26 ). These objects are often used to facilitate masturbation, prevent detumescence, and heighten sexual pleasure. These constricting devices must be identified and removed, a procedure that can test the ingenuity of the most experienced physician. If the strangulation is prolonged or appears to be associated with necrosis, the constricting object must be removed on an emergency basis. Various creative techniques, using saws, metal cutters, or emery wheels, may be necessary to remove some metal objects. Plastic surgery repair of the penis may eventually be needed but should be delayed until penile tissue viability has clarified. Fortunately, each corpora body has a separate blood supply and may be preserved even though the penile skin may slough and require skin grafting.
Figure 44-25 Idiopathic foreskin edema. A, This is the sam e picture that can be seen with penile strangulation injuries in children. B, The edem atous foreskin m ust be retracted proxim ally and distally looking for encircling hair, string, or other objects that m ay lead to vascular comprom ise.
Figure 44-26 A, Self-induced priapism . This patient placed two steel washers (B) around the base of his penis to prolong his erection. Subsequent priapism developed and the incarceration necessitated em ergency intraoperative rem oval with a pneum atic orthopedic drill.
Page 20
Pediatrics In small children, penile trauma may be associated with possible child abuse, especially when the explanations given for the event do not match the type of injury and objective physical findings. Examples include bruises that look like pinches, cigarette burns, or an injury reportedly caused by a falling toilet seat in a child who is too small to stand unsupported.
Management Superficial lacerations of penile-scrotal skin may be primarily reapproximated with 4-0 chromic or Vicryl absorbable suture. Patients with degloving penile injuries and scrotal skin loss should be treated by a urologist and plastic surgeon in the operating room with cleansing, debridement, and skin flaps or skin grafts. Traumatic penile amputation can be handled by primary reanastomosis (replantation) or local reshaping of the amputated penis. A recovered amputated distal penis should be placed in a clean plastic bag then immersed in cold saline if available. If the proximal penile stump is hemorrhaging, direct pressure on the bleeding source may promote hemostasis. A circumferentially placed Penrose drain at the base of the penis can be used acutely to control blood loss but should not be used for extended periods. Reanastomosis of a severed penis is possible up to 6 hours after amputation. Beyond this period, local reshaping is recommended. Both a urologist and a plastic surgeon should be involved in the patient's management if reimplantation is considered. Traumatic rupture of the corpus cavernosum, or penile fracture, occurs when the tunica albuginea is torn ( Figure 44-27 ). This usually occurs during vigorous sexual intercourse. The patient may hear a snapping sound and experience localized pain, detumescence, and a slowly progressive penile hematoma. Voiding is possible if the urethra is not injured. Ultrasonography is not diagnostically helpful in this setting. Occasional nonoperative management includes bed rest and ice packs for 24 to 48 hours followed by local heat and a pressure dressing. Most injuries are treated surgically. The penile hematoma is evacuated, the torn penile tunica albuginea is sutured, and a pressure dressing is applied. Of patients with a fractured penis, 10% experience a permanent deformity, suboptimal coitus, or impaired erections, especially if managed nonoperatively.
Figure 44-27 Fracture of the penis. Traum atic rupture of the corpus cavernosum , usually associated with sexual activity, results in a profound penile hem atom a, m ost often requiring operative repair.
Traumatic lymphangitis of the penis is a self-limiting disease usually caused by vigorous or prolonged sexual intercourse or masturbation. It is seen as a translucent, firm, nodular, almost cartilaginous cordlike configuration beginning at the coronal sulcus in the subcutaneous tissue. It may involve one side of the penis or encircle it completely. It is usually not tender and is freely mobile. It is best treated by abstinence from sexual activity and resolves in 2 to 3 weeks. Nonsteroidal anti-inflammatory drugs (NSAIDs) may be of some benefit. Traumatic lymphangitis should not be confused with Peyronie's disease, which is caused by recurring microtrauma leading to the formation of plaquelike fibrosis in the dorsal aspect of the tunica albuginea between the two corpora cavernosa. This fibrotic area causes decreased penile distensibility with subsequent dorsal curvature of the penis leading to painful erections and difficult or unsuccessful vaginal penetration. Reassurance and daily doses of vitamin E (400 IU) are the initial modes of therapy with subsequent urologic follow-up evaluation. Thrombosis and thrombophlebitis of the dorsal vein of the penis are usually associated with a history of direct trauma, idiopathic thrombophlebitis, or thromboangiitis obliterans. The physical findings are much more striking than those of traumatic lymphangitis, and the condition is treated symptomatically with heat and NSAIDs. Most human bites to the penis are acquired during sexual activity and represent a potentially serious polymicrobial infection. With this history and an examination showing localized swelling or generalized edema of the penile shaft with erythema suggestive of cellulitis, an immunocompromised patient should be
Page 21
admitted to the hospital for broad-spectrum intravenous antibiotic coverage that is sensitive to both aerobic and anaerobic organisms. Careful observation for the development of bacteremia or septicemia must be part of the management plan. An immunocompetent patient can be treated as an outpatient with cephalexin, NSAIDs, and re-evaluation within 2 to 3 days.
TESTICULAR TRAUMA Clinical Features Testicular injuries are most often caused by a fall or kick, or they are incurred while playing a sport and result in a contusion, laceration, fracture, or dislocation. The symptoms include severe pain, faintness, nausea, vomiting, and occasionally urinary retention secondary to pain. On examination, a tender swollen testicle may be present, but often only a small hematoma is noted. Therefore, anyone with a remote history of testicular trauma should undergo testicular color Doppler ultrasonographic examination, the diagnostic procedure of choice, to evaluate the integrity of the testis.[32] It can disclose testicular disruption, extruded testicular parenchyma, or a fragmented testicle. Loss of the normal homogeneous testicular pattern and the presence of a heterogeneous testicular pattern are diagnostic of testicular injury and require urologic evaluation ( Figure 44-28 ). Benign trauma often acts as the inciting event that discloses testicular torsion or malignancy.
Figure 44-28 Testicular rupture. A, Testicular ultrasonogram dem onstrates the norm al hom ogeneous testicular pattern. B, The heterogeneous pattern of injury, tum or, or disruption.
Management Testicular contusions are treated conservatively with bed rest, ice packs, NSAIDs, and appropriate urologic follow-up evaluation. Testicular dislocation occurs as a result of excessive pressure on the scrotum or thigh. In 80% of cases, the testis lies under the abdominal wall. Associated injuries are common, such as a pelvic fracture, hip dislocation, or cutaneous contusions. On examination, the affected hemiscrotum is swollen and ecchymotic with an absent testis. Operative repair is required for testicular laceration, disruption, or dislocation. Hematoma evacuation, testicular parenchymal debridement, and primary closure of the tunica albuginea are the treatments of choice. Immediate surgery allows earlier resumption of daily activity, a shorter hospital stay, greatly reduced morbidity, and a lower orchiectomy rate. Infrequent dog bites to the scrotum occur most often in children.[33] Careful examination of the scrotal tunica vaginalis will disclose involvement of the intrascrotal contents that dictates operative evaluation and repair. All other bites can be washed out thoroughly and closed primarily with absorbable suture. Prophylactic antibiotics can be administered based on the extent of the bite, subsequent injury, and the patient's immune status.
KEY CONCEPTS {,
Diag nosti c eval uatio n of the urina ry tract is gene rally unde
Page 22
rtake n in retro grad e fashi on. That is, susp icion and elimi natio n of ureth ral injur y befor e blad der injur y befor e urete ral or renal injur y. {,
Uret hral injur y is sugg este d by the pres ence of a pelvi c fract ure, bloo d at the ureth ral meat us, the pres ence of a highridin g or abse
Page 23
nt prost ate on recta l exa mina tion, or evid ence of a perin eal, scrot al, or penil e hem atom a. {,
Gros s hem aturi a alon e or in conj uncti on with a pelvi c fract ure is the abso lute mark er for signi fican t blad der injur y. Gros sly, clear blad der urine in a trau ma
Page 24
patie nt with out a pelvi c fract ure virtu ally elimi nate s the poss ibility of blad der ruptu re. {,
Adult patie nts at risk for majo r renal lacer ation s have gros s hem aturi a or micr ohe matu ria (3-5 RBC s/hpf ) with shoc k (syst olic bloo d pres sure ≥90 mm Hg) initial ly in the field
Page 25
or the eme rgen cy depa rtme nt, or, rarel y, a histo ry of sudd en dece lerati on with out hem aturi a or shoc k. Pedi atric patie nts can suffe r majo r renal injuri es with out any hem aturi a. {,
If a urete ral injur y is susp ecte d, a contr ast-e nhan ced helic al CT scan with dela yed
Page 26
films or bolu s infus ion IVP with dela yed films shou ld be done . If the initial stud y of dela yed films is inco nclu sive, retro grad e pyel ogra phy is indic ated to delin eate a urete ral lacer ation or avul sion.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Page 27
Bookmark URL: /das/book/view/60636217-2/1365/100.html/top
Page 28
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
REFERENCES 1. McAninch JW: Injuries to the genitourinary tract. In: Tanagho EA, McAninch JW, ed.General Urology, Norwalk, Conn: Appleton & Lange; 1999: 2. Nicolaisen GS: Renal trauma: Re-evaluation of the indications for radiological assessment. J Urol 1985;133:183. 3. Perry MO, Husmann DA: Urethral injuries in female subjects following pelvic fractures. J Urol 1992;147:139. 4. Corriere JN: Trauma to the lower urinary tract. In: Gillenwater JY, ed.Adult and Pediatric Urology, 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2002: 5. Sandler CM, Goldman SM, Kawashima A: Lower urinary tract trauma. World J Urol1998;16:69. 6. Spirnak JP: Pelvic fracture and injury to the lower urinary tract. Surg Clin North Am1988;68:1057. 7. Cass AS, Luxenberg M: Features of 164 bladder ruptures. J Urol1987;138:743. 8. Vaccaro JP, Brody JM: CT cystography in the evaluation of major bladder trauma. Radiographics 2000;20:1373. 9. Hochberg E, Stone NN: Bladder rupture associated with pelvic fracture due to blunt trauma. Urology 1993;41:531. 10. Schneider RE: Genitourinary trauma. Emerg Med Clin North Am1993;11:137. 11. Deck AJ, Shaves S, Talner L, Porter JR: Computerized tomography cystography for the diagnosis of traumatic bladder rupture. J Urol2000;164:43. 12. Corriere Jr JrJN, Sandler CM: Mechanisms of injury, patterns of extravasation and management of extraperitoneal bladder rupture due to blunt trauma. J Urol1988;139:43. 13. Corriere Jr JrJN, Sandler CM: Bladder rupture from external trauma: Diagnosis and management. World J Urol1999;17:84. 14. Santucci RA, McAninch JW: Diagnosis and management of renal trauma: Past, present, and future. J Am Coll Surg2000;191:443. 15. Morey AF: Single shot intraoperative excretory urography for the immediate evaluation of renal trauma. J Urol1999;161:1088. 16. Mee SL: Radiographic assessment of renal trauma: A ten-year prospective study of patient selection. J Urol1989;141:1095. 17. Bretan PN: Computerized tomographic staging of renal trauma: 85 consecutive cases. J Urol 1986;136:561. 18. Brown SL, Elder JS, Spirnak JP: Are pediatric patients more susceptible to major renal injury from blunt trauma? A comparative study. J Urol1998;160:138. 19. Morey AF, Bruce JE, McAninch JW: Efficacy of radiographic imaging in pediatric blunt renal trauma. J Urol1996;156:2014. 20. Nguyen MM, Das S: Pediatric renal trauma. Urology2002;59:762. 21. Carroll PR, McAninch JW: Staging of renal trauma. Urol Clin North Am1989;16:193. 22. Goldman SM, Sandler CM: Upper urinary tract trauma: Current concepts. World J Urol1998;16:62. 23. Hardeman SW: Blunt urinary tract trauma: Identifying those patients who require radiological diagnostic studies. J Urol1987;138:99. 24. Cass AS, Luxenberg M: Management of renal artery lesions from external trauma. J Urol1987;138:266. 25. Tong YC: Use of hematoma size on CT and calculated average bleeding rate as indications for immediate surgical intervention in blunt renal trauma. J Urol1992;147:984. 26. Campbell EW, Filderman PS, Jacobs SC: Ureteral injury due to blunt and penetrating trauma. Urology 1992;40:216. 27. Rober PE, Smith JB, Pierce JM: Gunshot injuries of the ureter. J Trauma1990;30:83. 28. McAninch JW, Corriere Jr JrJN: Renal and ureteral injuries. In: Gillenwater JY, ed.Adult and Pediatric Urology, 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2002: 29. Brandes SB: Ureteral injuries from penetrating trauma. J Trauma1994;36:766. 30. Presti JC, Carroll PR, McAninch JW: Ureteral and renal pelvic injuries from external trauma: Diagnostic and management. J Trauma1989;29:370. 31. Palmer LS: Penetrating ureteral trauma at an urban trauma center: 10-year experience. Urology
Page 29
1999;54:34. 32. Fournier Jr JrGR, Laing FC, McAninch JW: Scrotal ultrasonography and the management of testicle trauma. Urol Clin North Am1989;16:377. 33. Cummings JM, Boullier JA: Scrotal dog bites. J Urol2000;164:57.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/101.html/top
Page 30
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
Chapter 45 – Peripheral Vascular Injury Edward J. Newton
PERSPECTIVE Injury to major arteries or veins invariably poses a threat to the viability of the affected limb and even to life. Historically, because of rapid blood loss, injury to major vessels was often quickly fatal in the field. Most patients who survived to reach a hospital had relatively minor limb injuries. However, with the advent of modern Emergency Medical Service systems with advanced extrication methods and rapid transport, more patients with major vascular injury reach the hospital alive.[1] In addition, the incidence of penetrating civilian injuries from interpersonal violence and blunt injuries from motor vehicle–related trauma in the United States has increased dramatically over the past 50 years. Consequently, emergency physicians are frequently confronted with critically ill patients harboring overt or occult vascular injuries. Management of vascular injuries has evolved with advances in diagnostic methods and surgical techniques. Treatment of vascular injuries before and during World War II was simple ligation of the peripheral artery or vein involved. This approach resulted in limb amputation rates ranging from 40% for axillary artery injuries to 72% for popliteal artery injuries. During the Korean War, routine attempts to repair injured arteries decreased the amputation rate for popliteal injuries to 32%.[2] During the Vietnam War, repair of axillary and popliteal artery injuries with routine angiography and improved surgical techniques decreased the amputation rate to as low as 5% and 15%, respectively, which approaches the current rate of amputation for civilian injuries.[] However, extrapolation of high-velocity military wound data to low-velocity civilian gunshot wounds may not be valid, and even lower rates might be expected with civilian wounds. Tremendous progress has been achieved in diagnostic and therapeutic techniques for dealing with peripheral vascular injuries, and several noninvasive diagnostic modalities have emerged as accurate alternatives to surgical exploration or angiography. These techniques are easily used in the emergency department, and the goal of timely detection and repair of serious vascular injuries is achievable in the vast majority of cases.
Epidemiology Throughout the world, the etiology of peripheral vascular injuries is divided almost equally between blunt and penetrating mechanisms.[4] In the United States, 70% to 90% of these injuries are due to penetrating wounds.[] Penetrating wounds are particularly common in inner-city urban areas, although the incidence of low-velocity gunshot wounds has decreased over the past several years.[7] Because of the increased use of percutaneous endovascular diagnostic and therapeutic procedures, the incidence of iatrogenic vascular injuries has increased and accounts for up to a third of all cases in some series.[8] Major venous injuries are present in 13% to 51% of cases, but more than 80% are associated with arterial injury as well.[9] Approximately 90% of patients with vascular injury are male, and most are younger than 40 years.[5]
PRINCIPLES OF DISEASE Pathophysiology Blunt and penetrating types of trauma result in a similar spectrum of vascular injuries, although the mechanisms of injury differ. Even though blunt vascular injuries are less common than penetrating injuries, they are often more severe and more commonly require amputation because of associated injuries to nerves, bone, and soft tissue. Certain mechanisms of injury, such as close-range shotgun wounds and animal bites that crush and lacerate vessels, routinely combine penetrating and blunt mechanisms.
Penetrating Trauma Penetrating trauma from gunshot wounds results in the formation of a temporary cavity within distensible soft tissues with almost immediate recoil of these tissues. The size of the cavity and hence the degree of
Page 31
soft tissue injury depend directly on the velocity of the missile, as well as the tumble and yaw of the bullet. Consequently, gunshot wounds can cause direct arterial laceration or transection in addition to vascular injury at some distance from the track of the bullet. The latter injuries tend to be tears in the intima of an artery with subsequent thrombosis that may not become apparent for hours to months after the injury. Stab wounds can cause vascular injury by complete or partial transection of vessels. Partial laceration of an artery may produce few symptoms of arterial insufficiency on initial evaluation but commonly results in delayed complications. The vascular structures at risk can be predicted more reliably with stab wounds than with gunshot wounds by taking into consideration the anatomic location, the depth and direction of the wound, and the implement involved. Shotgun wounds are less common than gunshot or stab wounds and cause injuries varying from minor soft tissue wounds to massive destruction of soft tissue and bone, depending primarily on the range from which the shotgun was fired. The presence of multiple missiles ranging from 9 or 10 (buckshot) to dozens (birdshot) also complicates the evaluation of these injuries because of the many potential sites for vascular injury to occur. In addition, close-range shotgun wounds can cause significant blunt trauma to blood vessels, as well as a higher rate of bone and nerve injury than occurs with gunshot wounds. Migration of pellets proximally through the venous system to the heart or migration through an artery with subsequent distal occlusion has been reported frequently as a delayed complication.
Blunt Trauma Blunt injury involves avulsion forces that can stretch vessels beyond their capacity or direct crushing injury that disrupts the vessel wall. Fracture fragments resulting from blunt extremity trauma can lacerate or entrap vessels. Vascular injury can range from small intimal tears to complete avulsion of arteries and nerves. Open avulsion injury of a limb is particularly severe because the skin is the final structure to tear, and once such tearing occurs, it is inevitable that vessels and nerves will be torn as well.[10] Vascular injury must also be suspected in patients with massive soft tissue avulsion or crush injury, displaced long bone fractures, electrical or lightning injuries, and severe burns, as well as in those with compartment syndrome from trauma or prolonged immobilization as a result of stroke, coma, drug overdose, or other causes.[] Dog bites that are inflicted by large animals, such as those used by law enforcement, are particularly prone to the development of arterial injury and wound complications.[] Collateral circulation may continue to perfuse the limb adequately, but injuries that occur proximal to the collateral branch point or that involve both the main trunk and collateral branches will preclude adequate flow. Distal ischemia results from the inability of tissues to continue aerobic metabolism. Eventually, anaerobic metabolism consumes all substrate, thereby resulting in the accumulation of lactic acid. As ischemia progresses, cellular integrity is lost and irreversible cell death occurs. A vicious cycle of tissue edema and further impairment of the blood supply occurs. When no specific measures are taken to cool the limb, it is said that the limb is undergoing “warm ischemia” at room temperature. Although individuals may vary, 6 hours of complete warm ischemia is generally considered the point at which irreversible nerve and muscle damage begins to occur. After 6 hours of warm ischemia, 10% of patients will have irreversible damage; by 12 hours, 90% will. Artificially cooling the limb to just higher than freezing temperature will reduce the metabolic demands of unperfused tissues and greatly prolong the tissue's tolerance of ischemia. Two main types of vascular injury can result from trauma: occlusive injury (transection, thrombosis, and reversible spasm), in which all effective perfusion distal to the occlusion is lost, and nonocclusive injury (intimal flap, arteriovenous fistula [AVF], and pseudoaneurysm), in which some arterial flow continues past the injury.
Complete Occlusive Injury Transection The most common vascular injury is complete transection in which distal flow is effectively eliminated. Cleanly transected arteries will often retract and undergo spasm so that blood loss is minimized. With longitudinal arterial lacerations and venous injuries, blood loss cannot be limited by this means, and such injuries tend to result in greater blood loss. Pulsatile bleeding may lead to exsanguinating hemorrhage and shock.
Thrombosis Intraluminal thrombosis ( Figure 45-1 ) may occur in an injured artery acutely (within 24 hours) or may be delayed for many months. Acute thrombosis is initiated by stasis resulting from compression of the artery or
Page 32
from a disruption in the intima of an artery that becomes a nidus for thrombus formation. As the thrombus propagates, complete occlusion of the vessel can occur. Delayed thrombosis can occur months to years after injury if the injured vessel heals with stricture formation and decreased blood flow distally, followed by stasis and clot formation.
Figure 45-1 Com plete throm bosis of the distal brachial artery after reduction of a posterior elbow dislocation. ((Courtesy of D. Dem etreades, MD.))
Reversible Arterial Spasm The precise cause and incidence of significant reversible arterial spasm after trauma are unknown. In many cases the spasm occurs at some distance from the site of traumatic injury. In response to a traumatic stimulus, segmental narrowing of an artery may occlude the artery and produce distal ischemia. The spasm usually reverses with conservative treatment (topical warm saline or topical nitroglycerin paste), but prolonged spasm may require infusion of vasodilators such as nitroglycerin, lidocaine, or saline.[14] In many series, segmental arterial spasm is the most common arteriographic finding. However, it should never be assumed on clinical grounds that symptoms of ischemia are due to arterial spasm; that diagnosis is based on arteriographic results only.
Nonocclusive Injuries Intimal Flap An intimal flap occurs when there is a break in the intima of a vessel, generally from excessive stretch or concussive forces. Although flow is not altered by small flaps and the associated soft tissue wounds often appear benign initially, these intimal flaps may become a nidus for thrombosis that can occur hours to months after the initial injury. However, most intimal flaps heal spontaneously, and asymptomatic injuries that do not disrupt perfusion of the limb can be treated conservatively.
Pseudoaneurysm A true aneurysm contains all three layers of the vessel wall (intima, media, and adventitia) and rarely is caused by trauma. A pseudoaneurysm is formed when hemorrhage from a vessel is contained by surrounding fascia and the resulting hematoma is gradually encased by a capsule of fibrous tissue, analogous in consistency to the adventitia of a normal vessel ( Figure 45-2 ). Because it is relatively thin walled, rupture of a pseudoaneurysm is a distinct possibility. In addition, because its diameter inevitably expands under arterial pressure over days to months, compression of adjacent tissue may result in neuropathy, venous obstruction with resultant peripheral edema and venous thrombosis, and even erosion into adjacent bone. The cavity of a pseudoaneurysm is in direct communication with the lumen of the vessel, so embolization of mural clots may produce distal arterial occlusion. Patients with pseudoaneurysm are commonly seen months to years later with symptoms of compression neuropathy or peripheral arterial embolism or for investigation of a soft tissue “tumor” that represents the growing aneurysm.
Figure 45-2 Multiple sm all pseudoaneurysm s of the axillary artery after penetrating injury. ((Courtesy of D. Dem etreades, MD.))
Page 33
Arteriovenous Fistula An AVF is formed when both the artery and an adjacent vein are injured. Higher-pressure arterial flow is directed into the lower-pressure vein, thereby diverting the blood supply to distal tissues and engorging the distal veins. Because the aperture of the fistula is often relatively narrow and thus results in turbulent flow, a bruit and palpable thrill are common diagnostic findings. Symptoms are primarily those of distal ischemia, but rarely, high-output congestive heart failure may occur when large central vessels are involved. Symptoms are often delayed for months because it takes time for the fistula to mature.
Compartment Syndrome Compartment syndrome is most common after crush injury or a long bone fracture but may also be seen after reperfusion of an ischemic limb. Initially, blood flow is diminished and the injury can be considered nonocclusive. Smaller-caliber vessels are compressed first whereas larger vessels remain relatively patent, so pulses may be palpable until late in the course. If allowed to progress, however, all blood flow may end and the injury is then an occlusive one. Progressive edema elevates tissue pressure above capillary pressure, thus ending arterial flow and initiating a cascade of events that results in compartment syndrome. The risk for this complication is increased when ischemia time is prolonged, in the presence of combined arterial and venous injury, after ligation or repair of a major artery or vein, or in the presence of significant soft tissue injury.[5] After restoration of arterial flow to a previously ischemic limb, a cascade of reperfusion injury has been identified that results from release of oxygen free radicals, lipid peroxidation, and influx of intracellular calcium. These mediators give rise to progressive cellular damage, edema, and necrosis, thereby propagating the vicious cycle that increases compartment pressure.[15] Consequently, frequent reexamination of the limb is indicated to assess compartment pressure after arterial repair.
CLINICAL FEATURES Detection and treatment of vascular injuries must take place within the context of the overall resuscitation of the patient according to established principles of trauma care.[16] If the source of bleeding is readily identifiable, it is compressed with digital pressure. Once control of active bleeding has been achieved in this manner, detection and treatment of other life-threatening injuries can proceed. Peripheral vascular injury can occur coincident with nonvascular life-threatening trauma, which takes higher priority in resuscitating the patient. In other cases, peripheral vascular injury may be the most serious or only injury, and evaluation and management of these injuries can proceed directly. Despite rapid transport to a hospital through a modern Emergency Medical Service, injury to large central arteries and veins is still often fatal, and many of these deaths occur before medical contact. Patients who survive to reach the hospital may have obvious exsanguinating hemorrhage or only very subtle signs of vascular injury. Many patients have no evidence of injury but are considered at risk for vascular injury because of penetrating wounds in close proximity to major neurovascular bundles or because they have sustained high-risk injuries such as posterior knee dislocation. Patients who remain hypotensive after an initial fluid challenge may harbor an occult vascular injury if no other cause is found. In addition, patients with symptoms of intermittent claudication or with unexplained peripheral embolization and a history of previous trauma to the limb should be suspected of having occult arterial injury. Peripheral vascular injury can be divided into three categories by physical examination: hard findings, soft findings, and asymptomatic high-risk wounds based on the mechanism of injury.
Hard Findings of Vascular Injury Most patients have the classic “hard” findings of arterial injury, including pulsatile bleeding, an audible bruit or palpable thrill indicative of an AVF, an expanding or pulsatile hematoma, or any combination of the “five P's” of arterial insufficiency: pain on passive extension of the muscle compartment involved, pulselessness, p aresthesias, pallor, and paralysis. In addition, cyanosis and decreased temperature are common in a poorly perfused extremity, and massive distention of distal superficial veins may indicate an AVF as arterial flow is directed into distensible veins. The incidence of arterial injury in patients with any hard finding is consistently greater than 90%,[17] and the presence of these findings requires either further investigation by emergency angiography or immediate surgical intervention, depending on the duration of warm ischemia and the overall status of the patient.
Soft Findings of Vascular Injury An additional group of patients have “soft findings” of vascular injury, including a palpable but diminished pulse in comparison to the uninjured extremity, isolated peripheral nerve injury, or a large nonpulsatile hematoma.[18] The significance of prolonged capillary refill is controversial; some experts find it to be a reliable sign of vascular injury (when combined with a pulse deficit) and consider delayed capillary refill to be
Page 34
a valid soft sign of vascular injury. Others have found this sign to be a nonspecific and unreliable predictor of arterial injury.[] Delayed capillary refill in itself is insufficient to diagnose arterial injury but, in combination with other physical signs, supports the diagnosis. Isolated penetrating injury to a peripheral nerve is commonly associated with vascular injury because of the close proximity of these structures within the neurovascular bundles. Vascular injury occurs in 8% to 45% of cases of penetrating peripheral nerve injury.[19] Conversely, vascular injuries have associated peripheral nerve injury in almost half the cases.[20] It is sometimes difficult to distinguish whether the pain, paresthesias, or paralysis is due to a primary nerve injury or to an associated vascular injury or compartment syndrome. In general, primary nerve injury occurs immediately at the time of injury, whereas vascular neuropathy occurs over minutes to hours after the injury.[21] Up to 35% of patients with “soft” findings of vascular injury have positive angiographic studies, although only a small proportion of these injuries require emergency repair.[17]
High-Risk Injuries The proximity of a penetrating wound to a neurovascular bundle is defined imprecisely. Various definitions include 1 cm, 1 inch, or 5 cm as constituting “proximity.” Certainly, penetrating wounds that occur within 1 cm of a major neurovascular bundle or whose presumed trajectory has crossed such a bundle (“proximity wounds”) are more likely to produce an occult vascular injury. Major neurovascular bundles include large limb arteries proximal to critical branch points, such as the axillary, brachial, common femoral, and popliteal arteries ( Figures 45-3 and 45-4 ).[22] In addition, a substantial minority of patients with high-risk injuries, such as bites from large dogs or other animals, severely displaced fractures, crush injuries, or major joint dislocations (especially knee dislocation), will initially have occult vascular injury that is not detected by physical examination. The risk of missing such injuries is that the traditional 6-hour window of “warm ischemia time” will be exceeded or the patient will experience delayed complications resulting in loss of the limb. For example, patients with intimal flaps may be completely asymptomatic initially but can subsequently be subject to arterial thrombosis. Similarly, pseudoaneurysms progressively enlarge to produce compression of adjacent structures but may be very small and undetectable on initial physical examination. Consequently, many centers routinely perform some ancillary confirmation of arterial patency in these cases.
Figure 45-3 Major arteries of the upper lim b. ((From Snell R, Sm ith M [eds]: Clinical Anatom y for Em ergency Medicine. St Louis, CV Mosb y, 1993.)CV Mosb y)
Figure 45-4 Major arteries of the lower limb. ((From Snell R, Sm ith M [eds]: Clinical Anatom y for Em ergency Medicine. St Louis, CV Mosb y, 1993.)CV Mosb y)
History In patients who achieve and maintain hemodynamic stability, a more comprehensive history can be obtained. Important historical points to note include the exact time and mechanism of the injury. The time of
Page 35
injury is important because of the limitations of warm ischemia time noted earlier. The mechanism is of clinical and often forensic importance in that the injury is frequently inflicted during an assault or other violent crime, in the context of domestic violence or physical abuse, or in association with work. Various mechanisms of injury may mandate special reporting and may alter the patient's ultimate disposition. Certain types of injuries, such as crush or bite wounds, are particularly prone to complications. The occupation, avocation, and hand dominance of the patient are pertinent because a more aggressive strategy may be indicated in certain cases. Medical conditions that pose a risk of complications are important to note. Patients who are immunocompromised because of diabetes, acquired immunodeficiency syndrome, asplenia, cancer, or steroid use are at increased risk for infection and impaired wound healing. Patients with previous vascular insufficiency have more tenuous perfusion, are more susceptible to ischemia from elevated compartment pressure, and have a higher incidence of complications.[23] As with most aspects of trauma care, patients whose sensorium is altered by head injury or intoxication, patients with spinal cord injury who cannot perceive pain, and those with significant painful distracting injuries will not reliably be able to report pain or paresthesias suggesting vascular insufficiency, so extra caution must be exercised in these cases.
Physical Examination Physical examination is directed at discovering evidence of local wound complications and distal ischemia suggestive of vascular injury. Palpation of pulses in the affected extremities is the initial step. A comparison of the strength and quality of the pulses between the injured limb and its uninjured counterpart is then made. Isolated detection of a pulse deficit distal to the site of injury is a finding that merits further investigation rather than immediate surgery because palpation of pulses is a relatively inaccurate means of predicting arterial injury. False-positive findings of a pulse deficit may occur because of shock, in which all pulses are diminished, congenital absence of a pulse in one extremity, preexisting vascular disease, or arterial spasm. A false-positive finding of a pulse deficit occurs in 10% to 27% of cases.[] False-negative findings can occur with transmission of the pulse through a “soft clot,” past an intimal flap, or through collateral circulation. Distal pulses can persist in 6% to 42% of patients despite significant arterial injury.[24] Compression of an artery by casts, splints, or dressings may produce a pulseless extremity, and these should be removed if evidence of ischemia occurs.[25] Finally, even though the pulse may be absent, the limb may be well perfused by collateral arterial supply, thus making repair of the arterial injury less compelling. Simultaneous palpation of the injured and unaffected limb can detect relatively small differences in skin temperature that may suggest hypoperfusion. Testing two-point discrimination on the injured and unaffected limbs is similarly an effective means of detecting sensory deficits. Auscultation over the site of injury is an often-ignored examination that may reveal a bruit suggestive of an AVF. A bruit is audible in more than half of patients with an AVF.[26] Repeated examination of the hematoma adjacent to the wound is indicated to determine whether it is expanding or pulsatile. Despite the limitations just noted, reliance on the history and physical examination to triage patients into immediate surgery, angiography, and observation groups has been found to be relatively dependable, with a sensitivity of 92% and a specificity of 95%.[17]
DIAGNOSTIC STRATEGIES The diagnostic strategy for detection of peripheral vascular injury must be tailored to the clinical situation. Patients with clearly evident major arterial injury (e.g., pulsatile hemorrhage from a penetrating wound with a cold, pulseless distal end of the extremity) may require emergency operative intervention without the benefit of any ancillary confirmation of their injury. At times, the use of an intraoperative angiogram may be helpful in delineating the exact location and nature of the injury in patients taken directly to the operating room. However, delaying definitive treatment of an obvious arterial injury that is approaching the 6-hour limit of warm ischemia time to obtain an arteriogram is ill advised.
Plain Radiography Plain radiographs of the affected extremity are indicated to detect fractures, joint penetration, and foreign bodies. With gunshot wounds, the sum of the number of intact bullets seen on x-ray and the number of wounds in the body must be an even number. Failure to locate a bullet can result in unexpected complications. Rarely, bullets or shotgun pellets can migrate distally and produce vascular occlusion or migrate proximally through the venous system to the heart. These emboli are readily detected on plain radiographs.[] Lead bullets retained within a synovial joint can result in systemic absorption and elevated lead levels and should be removed electively.[29]
Pulse Oximetry
Page 36
Several relatively simple, noninvasive maneuvers can be performed at the bedside to elicit evidence of arterial injury. The use of pulse oximetry has been suggested as a means of identifying limb ischemia after trauma, but its utility in this setting has not been well studied. Clearly, in the absence of a pulse, no reading can be obtained. As the technology of transcutaneous measurement of physiologic indices advances, measurement of tissue oxygenation by near-infrared spectroscopy to quantify muscle oxyhemoglobin may prove more useful in detecting vascular injury.[]
Hand-Held Doppler An inability to palpate pulses in an injured extremity should be verified by auscultation with a hand-held Doppler unit. Apart from the absence of any signal, arterial injury may be suggested by a change in the usual triphasic quality of the Doppler pulse to a biphasic or monophasic waveform as the pulse is “damped” by partial occlusion. Though more sensitive, auscultation of the pulse by Doppler is subject to the same types of limitations as is palpation of the pulse.
Ankle-Brachial Index and Arterial Pressure Index Determination of the ankle-brachial index (ABI) or the arterial pressure index (API) has been well studied and provides somewhat more accurate information than does physical examination alone. Systolic pressure is measured by inflating a standard blood pressure cuff proximal to the injury and recording hand-held Doppler systolic pressure distal to the injury. The process is repeated on the uninjured limb, and a ratio of injured to uninjured systolic pressure is calculated (API). Generally, a ratio less than 0.90 is considered abnormal and is an indication for further investigation. Unfortunately, there is no consensus on the appropriate cutoff ratio to consider abnormal, and figures ranging from 0.85 to 0.99 are cited in various studies.[] If an API less than 0.90 is used as the cutoff, sensitivity decreases slightly but specificity increases. In one series a cutoff of 0.90 resulted in a false-negative rate of almost 40%. In other studies, an API less than 0.90 yielded a sensitivity of 95%, specificity of 97%, positive predictive value of 100%, and negative predictive value of 96%. [] Using an API cutoff of less than 1 produced a sensitivity of 96% to 100% but included many false-positive results.[] Still, the use of an API ratio less than 0.90 can eliminate a large number of unnecessary angiograms for proximity wounds and increase the diagnostic efficiency of angiography by limiting its use to high-yield cases. Limiting angiography to patients with either an abnormal physical examination (primarily a pulse deficit) or an API less than 0.90 appears to be an effective and safe strategy for detecting arterial injury.[] Patients with an API of 0.90 to 0.99 merit observation for 12 to 24 hours for repeated physical examination and API measurements to detect evolving injury. Exclusive reliance on API to screen for arterial injury has significant limitations. Comparisons cannot be made when both limbs are injured or when severe soft tissue mangling precludes placing a blood pressure tourniquet or locating the artery to be measured with the Doppler unit.[39] As with physical examination, the sensitivity of API is limited when an intimal flap allows near-normal flow or when collateral circulation is sufficient to produce near-normal systolic pressure, as in proximal injuries to the subclavian or iliac vessels. Certain arteries (e.g., the profunda femoris, profunda brachii, and peroneal arteries) normally do not produce palpable pulses, and API is of limited utility in these injuries. Shotgun wounds often have normal APIs despite multiple small arterial wounds; angiography is the preferred diagnostic modality in this group. As with angiography, API cannot detect venous injuries. In spite of the limitations just noted, API has proved effective in screening patients with proximity wounds. The vast majority of injuries missed by API heal spontaneously. Those that do not heal are generally seen within 3 months with hard signs of arterial injury.
Ultrasound The development of relatively small portable ultrasound (US) units has made possible direct visualization of both arterial and venous flow in major vessels. There are several different types of US that can detect vascular injury, and newer, more accurate techniques are being developed rapidly. B-mode (real-time) ultrasound is the most readily available form of US in portable units. It can easily visualize arterial pulsation in major vessels. Loss of pulsation distal to an obstruction or thrombosis is readily apparent. However, B-mode US cannot visualize certain anatomic areas accurately (subclavian and iliac vessels) because of overlying gas and is unreliable in detecting a fresh, relatively nonechogenic thrombosis or hematoma. As blood liquefies within a hematoma, it becomes echolucent and more readily distinguishable from surrounding tissues. Doppler US interprets sound moving toward or away from the transducer as flow. Venous flow is heard as a
Page 37
low-pitched hum, whereas arterial flow has a higher-pitched triphasic quality. The combination of B-mode and Doppler US is called duplex US and has enhanced accuracy in examining blood vessels. Duplex scans showing a focal increase in peak systolic velocity suggest partial obstruction of the vessel. However, duplex scanning is slightly less accurate in detecting injuries that do not decrease flow, such as small pseudoaneurysms, AVF, and intimal flaps,[32] and it is technically limited in examining certain anatomic areas such as the profunda femoris and profunda brachii arteries and the iliac and subclavian vessels. Duplex US findings may be subtle, and as with other applications of US, its accuracy is highly operator dependent. Despite these limitations, the sensitivity of duplex US in comparison to angiography ranges from 83% to 100%, with a specificity of 99% to 100% and an accuracy of 96% to 100%.[] Color flow Doppler converts Doppler echoes into quantitated visual signals. Flow toward the transducer is seen as red, and flow away from the transducer is seen as blue. The intensity of the color (the number of pixels on the screen) is proportional to flow through the vessel. Small prospective studies have indicated a high rate of accuracy in detecting arterial injury.[42] Absence of flow is readily apparent, but more subtle injuries, such as intimal flaps and small pseudoaneurysms, are more difficult to identify.[39] In addition, color flow Doppler is more accurate than standard venography in detecting major venous injuries.[45] The overall sensitivity of color flow Doppler in detecting arterial injury is 50% to 90%, with a specificity of 95% to 99%. The sensitivity for detecting injuries requiring surgical repair is significantly higher. The use of intravascular US for examination of abdominal aortic aneurysms has been well documented. Though not yet applicable to smaller peripheral vessels, with further reduction in size of the transducers, this technique may eventually be applicable for peripheral vascular injury as well.
Computed Tomography and Magnetic Resonance Imaging Computed tomography with contrast enhancement has had limited utility in the past, but newer-generation helical computed tomographic angiography scans have proved accurate in several small series, with 100% accuracy when compared with angiography or surgical exploration.[] Magnetic resonance angiography has also been described and is highly accurate, but it has yet to prove clinically useful.[]
Arteriography The policy of routinely exploring proximity wounds greatly improved the preservation of injured limbs in World War II. With the advent of arteriography, it became apparent that many negative wound explorations could be avoided with routine arteriography. In a study using routine arteriography, the negative surgical exploration rate in patients with “soft signs” of arterial injury or with proximity wounds fell from 84% to 2%.[51] As a result, until recently standard contrast angiography has been the gold standard for diagnosing peripheral arterial injury. Beginning in the 1980s, the number of civilian penetrating wounds increased tremendously. Because of high cost, limited availability at all hours, and poor reimbursement rates, the policy of routine arteriography for proximity wounds has been questioned. From a practical perspective, the time required to mobilize the angiography team and perform the study may be several hours, thus making this option less desirable when dealing with the time limitations posed by arterial injury. In addition, arteriography has a small, but measurable complication rate, including allergic reactions to contrast media, renal complications, hematoma formation, and false aneurysm formation at the site of cannulation. Finally, the clinical utility of the information provided by arteriography has become increasingly suspect as more of these injuries are being managed expectantly in recent years. Routine “exclusion” arteriography for proximity wounds detects unsuspected arterial injury in 0% to 21% of cases.[] However, relatively few of these patients require emergency surgery. In a series of 284 patients who underwent routine angiography for proximity wounds, 17% had unsuspected arterial injury detected, but only 1.8% (5 patients) required emergency surgical repair.[53] In other series reporting on a total of 483 patients who underwent angiography for proximity wounds, only one arterial injury that required emergency repair was discovered.[] In the presence of “soft signs” of injury, the yield for angiograms increases to 29% to 35%, but many of these injuries do not require emergency repair and can be detected by noninvasive means.[53] In addition, angiography results in an approximately 5% false-positive and false-negative rate when compared with surgical exploration. Many of the injuries detected on angiography are due to reversible vasospasm or very small intimal defects that generally heal spontaneously. Consequently, angiography for proximity wounds can detect injury in up to 21% of cases but results in acute surgical intervention in only 0% to 4.4% of cases.[] Many centers now successfully manage proximity wounds by repeated physical examination over a 24-hour period and reserve angiography for those with abnormal physical findings or an ABI less than 0.9.[] Angiography is also limited in that it cannot detect major venous injuries, which are increasingly being repaired surgically. The use of angiography is difficult in
Page 38
children because of the small caliber of their vessels and a propensity for vasospasm induced by angiography. Consequently, physical examination and noninvasive methods are preferred for detection of vascular injury in young children.[] Digital subtraction angiography (DSA) has been used for detecting vascular injuries as well. DSA has been found to be more accurate than standard angiography for detection of extravasation and has the advantage of requiring the administration of a smaller load of contrast material. However, the field of view is much smaller with DSA than with standard angiography, thus making it technically difficult to study the entire course of a limb artery with DSA. Standard angiography is also more accurate than DSA in detecting intimal flaps and dissection. Emergency center angiography involves the administration of intra-arterial contrast in a single bolus with a single radiograph as a rapid bedside alternative to formal angiography. Although technical difficulties occasionally limit its usefulness, accuracy approaching that of formal angiography can be achieved.[]
TREATMENT Initial treatment is directed at ensuring a patent airway and adequate air exchange before assessing the circulation. Once this is accomplished, active hemorrhage is controlled by direct digital pressure. Blind clamping of a bleeding vessel is not recommended because of the risk of crushing adjacent nerves. The use of tourniquets is similarly discouraged because occlusion of veins results in increased compartment pressure and an increased risk for venous thrombosis.[5] In cases in which proximal and distal control cannot be readily achieved in the emergency department, insertion of a Foley catheter into the wound and inflation of the balloon with sterile water can temporarily tamponade the bleeding. Intravenous lines should not be started in the injured extremity because they may be ineffective in delivering resuscitation fluid and because extravasation from an injured vein may increase compartment pressure. Serial hemoglobin determinations may indicate unexpected blood loss from occult vascular injury. Patients with significant blood loss should have blood typed and crossmatched and may require immediate transfusion for stabilization. Patients with significant vascular injury often remain hypotensive despite such infusion and require further volume infusion or blood transfusion. Moribund patients with multiple severe injuries may require urgent amputation as part of their overall stabilization or extrication from wrecked automobiles. Between 50% and 70% of patients with severely mangled limbs require urgent amputation, especially if they have multisystem trauma. The issue of “hypotensive resuscitation” is controversial with major vascular injuries. A tenuous clot can form in injured arteries and prevent further blood loss as long as the patient remains hypotensive. Once arterial pressure reaches a critical, but variable point, the clot may be expelled and massive blood loss can ensue. Therefore, when the arterial injury is inaccessible for occlusion by direct pressure, the target blood pressure for resuscitation should be lowered to a systolic pressure of approximately 90 mm Hg. Overly aggressive and rapid fluid administration in the field or in the emergency department can produce transient intravascular hypervolemia and may ultimately increase the rate of blood loss. Close monitoring of vital signs and the total volume of fluid infused is indicated in these situations. Once a vascular injury is identified, a specific diagnostic and therapeutic strategy can be developed that is consistent with the severity of the injury, the presence of other injuries, and the resources available.
Major Vascular Injuries Major vascular injuries that compromise the viability of a limb must be repaired within 6 hours to avoid irreversible ischemic neuropathy and myonecrosis.[5] If other life-threatening injuries must be repaired first, a temporary polytetrafluoroethylene (PTFE) vascular shunt can be placed in the operating room to restore perfusion to a limb.[59] These temporary PTFE shunts can be left in place for up to 24 hours before thrombosis begins to occur within the shunt. Major arterial transection or thrombosis is ideally repaired by end-to-end reanastomosis if possible without placing undue tension on the suture line. If a larger segment of the artery is destroyed, interposition of a reverse saphenous vein graft is the preferred technique. PTFE grafts are suitable for grafting larger arteries if necessary, but they tend to occlude when used in smaller arteries (e.g., distal to the femoral or brachial arteries). Before completing the reanastomosis, a Fogarty catheter is passed through both ends of the repair to extract any thrombi that may have formed. The distal circulation is flushed with a dilute 1:10 solution of heparin or enoxaparin to prevent early clot formation.[60] Systemic administration of heparin is usually contraindicated in major trauma patients. Pretreatment with mannitol has been shown to reduce compartment pressure and may decrease the risk for compartment syndrome if given preoperatively.[15] Assessment of distal perfusion and, in particular, compartment pressures is indicated frequently after repair and reperfusion of the limb. The use of broad-spectrum
Page 39
antibiotics such as a first-generation cephalosporin is recommended before commencing a vascular repair. A course of hyperbaric oxygen therapy has been shown to increase the rate of primary wound healing in patients with severe crush injuries, but it is not standard clinical practice.[61] Apart from excision of the affected arterial segment and repair of the vessel, less invasive techniques have been developed to manage pseudoaneurysms. Percutaneous embolization with Silastic beads, gel clot emboli, or thrombogenic coils is often successful.[] Placement of an endovascular sleeve can exclude the aneurysm and is also a successful alternative to open repair.[63] Similarly, repair of an AVF can be undertaken through open surgical ligation of the fistulous connection, by endovascular placement of a sleeve to exclude the fistula, or by percutaneous embolization of the fistulous tract.[62]
Late Complications Despite timely optimal repair of arterial injuries, approximately 21% of patients experience delayed complications requiring further surgical intervention, even including delayed amputation. The most common of such complications is delayed thrombosis, which often occurs after many months as stenosis at the repair site progresses. Other complications include intermittent claudication, chronic pain or edema of the limb, and aneurysm formation in the graft.[64]
Venous Injuries Venous injuries may be primarily ligated if the condition of the patient cannot tolerate prolongation of surgery. However, the current trend is to repair major venous injuries if possible, particularly in the lower extremity, because wound healing is improved and the incidence of compartment syndrome, venous thrombosis, pulmonary embolism, and chronic edema is decreased.[65] Extensive venous collaterals in the upper extremity make surgical repair less compelling. The timing of repair of a vascular injury when associated with complex fractures requiring fixation is controversial. Historically, the fracture was repaired first to give a more accurate measurement of limb length and the length of graft required for vascular repair and because of fear that manipulation of long bones during reduction might damage the vascular repair. However, the need for postoperative fasciotomy is higher in these patients than in those who undergo vascular repair first (80% versus 36%).[66] Currently in most centers, vascular repair is prioritized over orthopedic repair.
Minor Vascular Injuries Increasingly, minor, nonocclusive vascular injuries are being treated expectantly. Criteria for observation of vascular injuries include low-velocity missile wounds, intact distal circulation, absence of active hemorrhage, and minimal arterial wall disruption on angiography if performed. Angiographic findings meeting these criteria include intimal flaps extending less than 5 mm and pseudoaneurysms smaller than 5 mm in diameter.[5] Follow-up of these injuries with repeat angiography or US reveals that approximately 85% resolve spontaneously.[53] Patients meeting these criteria can be monitored as outpatients for 3 months with repeat physical examination and US to detect delayed complications. Some authors suggest caution with this policy because of multiple cases in which conservative treatment failed after prolonged delay.[67] Others have reported large series demonstrating the safety of this approach.[] However, almost all pseudoaneurysms ultimately require repair and, once discovered, should be repaired electively. Failure to detect and repair occult arterial injuries in children often results in severe differential limb growth, and thus a more aggressive policy of repairing any arterial injury that causes even a relatively minor decrease in blood flow to a child's growing limb may be justified.
SPECIFIC INJURIES Upper Extremity Subclavian Artery and Vein Subclavian artery injuries represent 1% to 2% of all vascular trauma.[70] Isolated injury to the subclavian vein is more common than isolated arterial injury, but in almost half the cases both the vein and artery are injured. [71] The vast majority (95% to 99%) are penetrating wounds, and because of massive hemorrhage, these injuries are often lethal before arrival at a hospital. Mortality in those who reach the hospital alive averages 15%, but overall mortality as high as 75% has been reported.[] The right subclavian artery arises from the brachiocephalic artery, the left from the arch of the aorta. From their origin, they course posterior and inferior to the clavicles to the outer margins of the first ribs, where they become the axillary artery and vein. The left subclavian rises higher than the right and extends into the root of the neck.[22]
Page 40
The clinical manifestation is that of hemorrhagic shock in 77% of cases. Occasionally, unsuspected subclavian vascular injury is discovered at thoracotomy for excessive blood loss from a chest tube.[71] Approximately 60% have an associated pneumothorax or hemothorax, and additional injury to mediastinal and spinal structures is relatively common.[70] Symptoms of limb ischemia may be apparent with absent radial and brachial pulses. However, pulses are completely absent in only 33% of cases because collateral flow from the thyrocervical trunk may provide sufficient perfusion to avoid the symptoms and signs of ischemia.[71] Neurologic deficits in the upper extremity occur in more than half the patients. The most severe of these injuries is disruption of the brachial plexus, which occurs in almost 50% of patients.[71] In a series of 100 cases of subclavian artery injury, the combination of physical examination and chest x-ray findings suggestive of subclavian injury (hemothorax, pneumothorax, apical pleural cap, or wide mediastinum) was 100% sensitive and could have eliminated the need for 69% of the arteriograms obtained. [72] If the patient's clinical condition permits, angiography can provide an accurate diagnosis and can locate the injury precisely. APIs are relatively inaccurate with proximal thoracic outlet injuries because of collateral arterial flow. US techniques are also relatively inaccurate in detecting subclavian injuries because of interference by overlying gas-filled lung tissue. Therefore, in cases in which the clinical diagnosis is equivocal (“soft signs” of injury or proximity wounds), arteriography is required to detect the injury. Immediate proximal and distal control of the subclavian artery is very difficult. An incision along the course of the clavicle is recommended but often needs to be extended to a sternotomy.[74] If primary reanastomosis is not possible, synthetic grafts are usually successful. Blunt subclavian injuries are often associated with clavicular fracture or dislocation. Isolated first rib fracture is rarely combined with vascular injury unless posterior displacement has occurred. However, first rib fracture in association with other major injuries, a wide mediastinum on chest x-ray, an expanding hematoma, an upper extremity pulse deficit, or a brachial plexus injury is accompanied by arterial injury in 24% of cases and merits investigation by angiography.[75] Several cases of shear injury of the subclavian artery have been reported to result from a loose shoulder restraint of a seat belt during a motor vehicle accident. Overall, blunt subclavian artery injuries are more severe than penetrating injuries because of higher rates of mortality, limb amputation, and associated brachial plexus injury.[70] Subclavian vein injuries are even more lethal than those to the artery. In addition to massive blood loss, there is a relatively high risk of massive air embolism, which is frequently fatal in association with penetrating subclavian vein injuries.
Axillary Artery and Vein Injury to the axillary vessels constitutes 3% to 9% of all vascular injuries and is divided nearly equally between penetrating and blunt mechanisms.[3] Forceful reduction of a chronically dislocated shoulder is a common iatrogenic cause of axillary artery injury. The axillary artery courses from the lateral border of the first rib to the inferior border of the teres major muscle, where it becomes the brachial artery. The axillary vein runs medial to the artery. The extensive anastomotic arterial connections around the shoulder joint usually permit good collateral flow,[] and up to half of these patients will have palpable pulses as a result of collateral circulation.[76] Because of the close proximity of the brachial plexus and the axillary vessels, significant denervation of the upper extremity can occur. Near-avulsion injuries resulting in scapulothoracic dissociation invariably produce severe disruption of the brachial plexus and often ultimately result in amputation despite successful vascular repair. There is a high rate of amputation for the combination of axillary vascular and brachial plexus injury, mainly because the presence of a flail limb results in amputation for placement of a prosthesis. In addition, patients with a flail limb have a 40-fold increased rate of suicide.[10]
Brachial Artery The brachial artery continues from the lower border of the teres major muscle and divides into the radial and ulnar arteries at the level of the proximal aspect of the radial head. The median and ulnar nerves and the basilic vein are in close proximity to the brachial artery. The profunda brachii artery is a major branch that arises soon after the origin of the brachial artery and often contributes good collateral flow if the brachial artery is injured distal to this branch point.[] Brachial artery injuries occur as a result of penetrating trauma, humeral shaft fracture, elbow dislocation, or animal bites. They are the most common major vascular injuries in the upper extremity. In 75% of cases, the radial pulse is absent.[24] Repair is indicated in all cases because the amputation rate is high with ligation.
Forearm Arteries
Page 41
The radial artery begins in the cubital fossa and runs superficially to the distal end of the radius, where it ultimately joins the deep branch of the ulnar artery to form the deep palmar arch of the hand. The ulnar artery begins in the cubital fossa and runs with the ulnar nerve anterior to the flexor retinaculum, at which point it joins the radial artery to form the superficial palmar arch of the hand.[77] Injuries detected by arteriography or US that are below the bifurcation of the arterial supply in the upper extremity do not need to be repaired unless there are signs of ischemia in the hand; hard signs of arterial injury such as an expanding hematoma, pseudoaneurysm, or AVF; or injury to both the radial and ulnar arteries. Some authors recommend repairing all these injuries because of the risk of intermittent claudication or cold intolerance in patients who have one artery ligated. Certain patients are almost exclusively dependent on the ulnar arterial supply to the hand because of an underdeveloped deep palmar arch. These patients clearly must have ulnar artery injuries repaired. Compartment syndrome in the forearm is common after repair of proximal arteries and veins and may require fasciotomy.
Lower Extremity Iliac Artery and Vein Given the intra-abdominal course of the iliac vessels, virtually all these injuries have associated trauma to the small or large intestine, bladder, solid viscera, or bony pelvis. The common and external iliac arteries are injured with equal frequency and more often than the internal iliac vessels.[78] In moribund patients, an initial “damage control” laparotomy with temporary vascular shunting of the iliac vessels is often necessary as resuscitation continues. Once the patient has overcome lactic acidosis, hypothermia, and coagulopathy, a second definitive repair can be undertaken. Surprisingly, the incidence of infection of synthetic or autologous grafts is rather low despite the high degree of bacterial contamination associated with perforation of a hollow viscus. Distal ischemic complications occur in about a third of repaired iliac arteries, and subsequent amputations are required in up to 18%.[78]
Femoral Artery and Vein The external iliac vessels become the common femoral vessels at the inguinal ligament. After giving off the profunda femoris artery in the femoral triangle, the femoral artery continues as the superficial femoral artery almost vertically to the adductor tubercle of the femur and enters the popliteal fossa as the popliteal artery. There are extensive proximal collaterals around the hip joint, including the gluteal, obturator, and pudendal branches of the iliac artery.[22] Common femoral artery injury occurs as a result of intertrochanteric hip fracture, hip dislocation, and iatrogenic injury from the placement of arterial catheters or from hip replacement surgery. Ligation of the common femoral artery culminates in amputation of the lower extremity in 80% of cases, so repair should be attempted in all cases. Penetrating wounds of the thigh result in femoral artery injury in 6.2% of cases, and up to 40% of these injuries are clinically occult. A medial or anteromedial wound track is present in virtually all these cases, and many centers routinely perform angiography on these wounds.[79]
Popliteal Artery and Vein The popliteal artery gives off the genicular branches in the popliteal fossa and then divides into the anterior and posterior tibial arteries at the lower border of the popliteus muscle. The peroneal artery arises from the posterior tibial artery shortly after its origin. The anterior and posterior tibial arteries and the peroneal artery form the trifurcation of the popliteal artery, and each runs with a corresponding vein and nerve in different compartments of the leg.[22] Popliteal artery injury is relatively common and in most cases is due to blunt trauma. The most common cause is posterior knee dislocation in which bony elements directly lacerate or cause thrombosis of the artery, although displaced fractures of the knee may also result in popliteal artery injury. Anterior knee dislocations may cause excessive stretch on the popliteal vessels that can culminate in arterial thrombosis, but this injury is relatively rare. Overall, knee dislocation results in popliteal artery injury in 25% to 33% of cases.[80] Up to 40% of these injuries may be clinically occult, and diagnosis is delayed in up to 40% of cases,[2] although other series note that more than two hard signs of ischemia occur in 71% to 94%.[] Twenty-five percent of cases have an associated injury to the peroneal and posterior tibial nerves, and in half the cases the knee dislocation may reduce spontaneously so that there may be little evidence of the original trauma, particularly in obtunded patients.[81] Patients showing complete ligamentous disruption of the knee on physical examination should be suspected of having a spontaneously reduced knee dislocation. Hemarthrosis may be absent if the joint capsule is torn because blood can track into the fascial planes of the leg.
Page 42
No consensus has been reached on the diagnostic approach to detect popliteal artery injury resulting from knee dislocation. There are three possible strategies, and each has proponents and detractors. The first option is to perform routine arteriography on every case of knee dislocation. The second is to perform arteriography on selected cases in which vascular injury is not certain in spite of the combination of physical signs, abnormal ABI measurement, or findings on noninvasive tests such as color flow Doppler, duplex scan, or computed tomographic angiography. The third option is to rely completely on these physical findings and ABI. If both these findings are normal, advocates of this approach claim 100% negative predictive value for vascular injury that requires surgery.[] The choice of these options is institution specific, but most centers continue to use arteriography in selected cases. Abnormal ABI and US (duplex and color flow Doppler) have been found to be very accurate in detecting popliteal injuries, and many centers reserve arteriography for cases in which noninvasive tests result in equivocal findings. As a general rule, high-energy mechanisms of trauma (e.g., auto versus pedestrian, motor vehicle accident) and posterior knee dislocations are more likely to produce popliteal artery injury than low-energy mechanisms are (e.g., sports injuries), and a more aggressive diagnostic approach (i.e., arteriography) may be warranted in such cases. However, patients with penetrating trauma and more than one hard sign of popliteal artery injury can be taken directly to the operating room for repair because delaying these cases to obtain an angiogram is “superfluous, unnecessary, costly and potentially dangerous.”[87] Patients with blunt trauma can have false-positive hard findings generated by soft tissue swelling and external arterial compression, and these patients should undergo diagnostic testing first to confirm arterial injury. The amputation rate for popliteal injuries was as high as 40% in the past but has currently been reduced to zero in some series with modern diagnostic and repair techniques.[] Most amputations are due to blunt trauma with severe mangling of the extremity or delay in repair exceeding 8 hours of warm ischemia time.[81] Because of the high incidence of compartment syndrome with lower leg injuries, fasciotomy is required in 36% to 62% of cases, and some centers routinely perform fasciotomy in all such cases.[88] Approximately two thirds of patients with popliteal artery injury will have persistent deficits caused by peripheral nerve injury, chronic ischemia, or amputation.
Lower Leg Arteries The popliteal artery divides into three branches, the anterior and posterior tibial and the peroneal arteries at the inferior margin of the popliteal fossa. Injuries below the trifurcation at the knee may need repair if hard signs of arterial injury are apparent in the foot or if two of the three arteries are occluded on angiography.[18] However, vascular injuries in the lower part of the leg are notorious for causing compartment syndrome and need to be monitored closely. Amputation is usually due to a combination of soft tissue, nerve, and bone injuries. If significant injury to all three of these tissues is present, the amputation rate may reach 54%.[] The combination of orthopedic and vascular injury, particularly as a result of crush injury, and shock on initial evaluation culminates in amputation in 35% of cases and should be considered a poor prognostic sign for limb viability.[90]
DISPOSITION Patients with confirmed injury to major vessels, equivocal findings on diagnostic tests, or symptoms of limb ischemia must be admitted to the hospital for further investigation or observation. Consultation with a vascular surgeon is indicated as soon as vascular injury is confirmed and the need for emergency operative repair established. Patients who are unstable because of vascular or other injuries may undergo further investigation or exploration in the operating room. If the treating hospital is incapable of performing vascular surgery or appropriate investigations, transfer to a trauma center should be initiated. Delaying transfer for angiograms of proximity wounds in centers that are incapable of acting on positive results is unwise because it often delays definitive care beyond the safe limits of warm ischemia time.
KEY CONCEPTS {,
The over all cond ition of the patie nt deter mine
Page 43
s the exte nt of diag nosti c stud y and stabi lizati on in the eme rgen cy depa rtme nt. Criti cal patie nts may requi re imm ediat e surg ery, whic h shou ld not be dela yed for confi rmat ory stud y of obvi ous vasc ular injur y. {,
Arter ial injur y may be readi ly appa rent or
Page 44
clinic ally occu lt. Up to 21% of proxi mity wou nds sho w arteri al injur y on angi ogra phy. Simil arly, vario us US mod alitie s and abno rmal APIs frequ ently dete ct clinic ally inap pare nt vasc ular injuri es. {,
Sym ptom s of arteri al injur y may be dela yed by hour s to mont hs after
Page 45
the initial injur y. Late onse t of sym ptom s sugg ests dela yed thro mbo sis, pseu doan eury sm or AVF form ation , com part ment synd rom e, or inter mitte nt clau dicat ion resul ting from sten osis or relia nce on smal l-cali ber colla teral vess els for arteri al perfu sion. {,
Rep erfus ion
Page 46
injur y can occu r after resto ratio n of arteri al flow and resul t in com part ment synd rom e. Freq uent reex amin ation of the repe rfuse d limb is indic ated in the post oper ative perio d. {,
Com part ment synd rom e frequ ently deve lops in limb s with arteri al injur y, and fasci
Page 47
otom y is often requi red.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/102.html/top
Page 48
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
REFERENCES 1. Wall MJ: Penetrating thoracic vascular injuries. Surg Clin North Am1996;76:749. 2. Applebaum R: Role of routine arteriography in blunt lower extremity trauma. Am J Surg1990;160:221. 3. Martinez R: Endovascular management of axillary artery trauma. J Cardiovasc Surg1999;40:413. 4. Fitridge RA: Upper extremity arterial injuries: Experience at the Royal Adelaide Hospital, 1969 to 1991. J Vasc Surg1994;20:941. 5. Modrall JG, Weaver FA, Yellin AE: Diagnosis and management of penetrating vascular trauma and the injured extremity. Emerg Med Clin North Am1998;16:129. 6. Bynoe RP: Noninvasive diagnosis of vascular trauma by duplex ultrasonography. J Vasc Surg 1991;14:346. 7. Cherry D: Trends in nonfatal and fatal firearm-related injury rates in the United States, 1985-95. Ann Emerg Med1998;32:51. 8. Giswold ME: Iatrogenic arterial injury is an increasingly important cause of arterial trauma. Am J Surg 2004;187:590. 9. Zamir G: Results of reconstruction in major pelvic and extremity venous injuries. J Vasc Surg 1998;28:901. 10. Pretre R: Blunt injury to the subclavian or axillary artery. J Am Coll Surg1994;179:295. 11. Snyder KB, Pentecost MJ: Clinical and angiographic findings in extremity arterial injuries secondary to dog bites. Ann Emerg Med1990;19:983. 12. Hutson HR: Law enforcement K-9 dog bites: Injuries, complications, and trends. Ann Emerg Med 1997;29:637. 13. Fish RM: Electrical injury, part II: Specific injuries. J Emerg Med2000;18:27. 14. Gillespie DL: Role of arteriography for blunt or penetrating injuries in proximity to major vascular structures: An evolution in management. Ann Vasc Surg1993;7:145. 15. Perry MO: Compartment syndromes and reperfusion injury. Surg Clin North Am1988;68:853. 16. Advanced Trauma Life Support, 6th ed. Chicago, American College of Surgeons, 1997. 17. Gonzalez RP, Falimirski ME: The utility of physical examination in proximity penetrating extremity trauma. Am Surg1999;65:784. 18. Weaver FA, Papanicolaou G, Yellin AE: Difficult vascular injuries. Surg Clin North Am1996;76:843. 19. Howlett DC, Holemans JA, Downes MO: Case report: The role of arteriography in patients with isolated neurological deficit following a penetrating upper limb injury. Br J Radiol1995;68:764. 20. Nichols JS, Lillehei KO: Nerve injury associated with acute vascular trauma. Surg Clin North Am 1988;68:837. 21. Shaw AD: Vascular trauma of the upper limb and associated nerve injuries. Injury1995;26:515. 22. In: Snell R, Smith M, ed.Clinical Anatomy for Emergency Medicine, St Louis: CV Mosby; 1993: 23. Wilson RF: Pre-existing peripheral arterial disease in trauma. Crit Care Clin1994;10:567. 24. Fields EF, Latifi R, Ivatury RR: Brachial and forearm vessel injuries. Surg Clin North Am2002;82:105. 25. Odland MD: Combined orthopedic and vascular injury in the lower extremities: Indications for amputation. Surgery1990;108:660. 26. Illyevski N: Emergency surgery of acute arteriovenous fistulas. Cardiovasc Surg2000;8:181. 27. Bongard F: Peripheral arterial shotgun missile emboli: Diagnostic and therapeutic management—case reports. J Trauma1991;31:1426. 28. Michelassi F: Bullet emboli to the systemic and venous circulation. Surgery1990;107:239. 29. Meggs WJ: The treatment of lead poisoning from gunshot wounds with succimer (DMSA). J Toxicol Clin Toxicol1994;32:377. 30. Cohn SM, Crookes BA, Proctor KG: Near-infrared spectroscopy in resuscitation. J Trauma2003;54(5 Suppl):S199. 31. Velmahos GC, Toutouzas KG: Vascular trauma and compartment syndromes. Surg Clin North Am 2002;82:125. 32. Johansen K: Non-invasive vascular tests reliably exclude occult arterial trauma in injured extremities. J Trauma1991;31:515. 33. Schwartz MR: Refining the indications for arteriography in penetrating extremity trauma: A prospective
Page 49
analysis. J Vasc Surg1993;17:116. 34. Hood DB, Weaver FA, Yellin AE: Changing perspectives in the diagnosis of peripheral vascular trauma. Semin Vasc Surg1998;11:255. 35. Nassoura ZE: A reassessment of Doppler pressure indices in the detection of arterial lesions in proximity penetrating injuries of extremities: A prospective study. Am J Emerg Med1996;14:151. 36. Lynch K, Johansen K: Can Doppler pressure measurement replace exclusion arteriography in the diagnosis of occult extremity arterial trauma?. Ann Surg1991;214:737. 37. Gahtan V, Bramson RT, Norman J: The role of emergent arteriography in penetrating limb trauma. Am Surg1994;60:123. 38. Atteberry LR: Changing patterns of arterial injuries associated with fractures and dislocations. J Am Coll Surg1996;183:377. 39. Bergstein JM: Pitfalls in the use of color-flow duplex ultrasound for screening of suspected arterial injuries in penetrated extremities. J Trauma1992;33:395. 40. Fry WR: The success of Duplex ultrasonographic scanning in diagnosis of extremity vascular proximity trauma. Arch Surg1993;128:1368. 41. Kuzniec S: Diagnosis of limbs and neck arterial trauma using duplex ultrasonography. Cardiovasc Surg 1998;6:358. 42. Bynoe RP: Noninvasive diagnosis of vascular trauma by duplex ultrasonography. J Vasc Surg 1991;14:346. 43. Anderson RJ: Reduced dependency on arteriography for penetrating extremity trauma: Influence of wound location and noninvasive vascular studies. J Trauma1990;30:1059. 44. Knudson MM: The role of duplex ultrasound arterial imaging in patients with penetrating extremity trauma. Arch Surg1993;128:1033. 45. Gagne PJ: Proximity penetrating extremity trauma: The role of ultrasound in the detection of occult venous injuries. J Trauma1995;39:1157. 46. Soto JA: Diagnostic performance of helical CT angiography in trauma to large arteries of the extremities. J Comput Assist Tomogr1999;23:188. 47. Nunez Jr JrD: Helical CT of traumatic arterial injuries. AJR Am J Roentgenol1998;170:1621. 48. Busquets AR: Helical computed tomographic angiography for the diagnosis of traumatic arterial injury of the extremities. J Trauma2004;56:625. 49. James CA: Magnetic resonance angiography in trauma. Clin Neurosci1997;4:137. 50. Yaquinto JJ: Arterial injury from penetrating trauma: Evaluation with single-acquisition fat-suppressed MR imaging. AJR Am J Roentgenol1992;158:631. 50. Geuder JW: The role of arteriography in suspected arterial injuries of the extremities. Am Surg 1985;51:893. 51. Reid JDS: Assessment of proximity of a wound to major vascular structures as an indication for arteriography. Arch Surg1988;123:942. 52. Dennis JW: New perspectives on the management of penetrating trauma in proximity to major limb arteries. J Vasc Surg1990;11:85. 53. Weaver FA: Is arterial proximity a valid indication for arteriography in penetrating extremity trauma? A prospective analysis. Arch Surg1990;125:1256. 54. Gillespie DL: Role of arteriography for blunt or penetrating injuries in proximity to major vascular structures: An evolution in management. Ann Vasc Surg1993;7:145. 55. Rose SC, Moore EE: Trauma angiography: The use of clinical findings to improve patient selection and case preparation. J Trauma1988;28:240. 56. De Virgilio C: Noniatrogenic pediatric vascular trauma: A ten year experience at a level I trauma center. Am Surg1997;63:781. 57. Itani KM: Emergency center arteriography. J Trauma1992;32:302. 58. Itani KM: Emergency center arteriography in the evaluation of suspected peripheral vascular injuries in children. J Pediatr Surg1993;28:677. 59. Shah DM: Polytetrafluoroethylene grafts in the rapid reconstruction of acute contaminated peripheral vascular injuries. Am J Surg1989;148:229. 60. Chen LE: Effects of enoxaparin, standard heparin, and streptokinase on the patency of anastomoses in severely crushed arteries. Microsurgery1995;16:661. 61. Bouachour G: Hyperbaric oxygen therapy in the management of crush injuries: A randomized double-blind placebo-controlled trial. J Trauma1996;41:333. 62. Naidoo NM: Angiographic embolization in arterial trauma. Eur J Vasc Surg2000;19:77. 63. Criado E: Endovascular repair of peripheral aneurysms, pseudoaneurysms and arteriovenous fistulas. Ann Vasc Surg1997;11:256. 64. Rich NM: Complications of vascular injury management. Surg Clin North Am2002;82:143. 65. Kuralay E: A quantitative approach to lower extremity vein repair. J Vasc Surg2002;36:1213. 66. McHenry TP: Fractures with major vascular injuries from gunshot wounds: Implications of surgical sequence. J Trauma2002;53:717.
Page 50
67. Tufaro A: Adverse outcome of nonoperative management of intimal injuries caused by penetrating trauma. J Vasc Surg1994;20:656. 68. Frykberg ER: Nonoperative observation of clinically occult arterial injuries: A prospective evaluation. Surgery1991;109:856. 69. Dennis JW: Validation of nonoperative management of occult vascular injuries and accuracy of physical examination alone in penetrating extremity trauma: 5- to 10-year follow-up. J Trauma1998;44:243. 70. Cox CS: Blunt versus penetrating subclavian artery injury: Presentation, injury pattern, and outcome. J Trauma1999;46:445. 71. Demetriades D: Penetrating injuries to the subclavian and axillary vessels. J Am Coll Surg1999;188:290. 72. Gasparri MG: Physical examination plus chest radiography in penetrating periclavicular trauma: The appropriate trigger for angiography. J Trauma2000;49:1029. 73. McKinley AG, Carrim ATO, Robbs JV: Management of proximal axillary and subclavian artery injuries. Br J Surg2000;87:175. 74. Degiannis E: Penetrating injuries of the subclavian vessels. Br J Surg1994;81:5246. 75. Gupta A, Jamshidi M, Rubin JR: Traumatic first rib fracture: Is angiography necessary?. Cardiovasc Surg1997;5:48. 76. Gonzalez RP, Falimirski ME: The role of angiography in periclavicular penetrating trauma. Am Surg 1999;65:711.discussion 714 77. Gates JD: Penetrating wounds of the extremities: Methods of identifying arterial injury. Orthop Rev 1994;10(Suppl):2. 78. Woodman G, Croce MA, Fabian TC: Iliac artery ischemia: Analysis of risks for ischemic complications. Am Surg1998;64:833. 79. Shayne PH: A case-controlled study of risk factors that predict femoral arterial injury in penetrating trauma. Ann Emerg Med1994;24:678. 80. Trieman GS: Examination of the patient with knee dislocation: The case for selective arteriography. Arch Surg1992;127:1056. 81. Wascher DC: High-velocity knee dislocation with vascular injury. Clin Sports Med2000;19:457. 82. Mills WJ, Barei DP, McNair P: The value of ankle-brachial index for diagnosing arterial injury after knee dislocation: A prospective study. J Trauma2004;56:1261. 83. Abou-Sayed H, Berger DL: Blunt lower-extremity trauma and popliteal injuries: Revisiting the case for selective arteriography. Arch Surg2002;137:585. 84. Klineberg EO: The role of arteriography in assessing popliteal artery injury in knee dislocations. J Trauma2004;56:786. 85. Miranda FE: Confirmation of the safety of physical examination in the evaluation of knee dislocation for injury of the popliteal artery: A prospective study. J Trauma2002;52:247. 86. Stannard JP: Vascular injuries in knee dislocations: The role of physical examination in determining the need for arteriography. J Bone Joint Surg Am2004;86:910. 87. Frykberg ER: Popliteal vascular injuries. Surg Clin North Am2002;82:67. 88. Pretre R: Lower limb trauma with injury to the popliteal vessels. J Trauma1996;40:595. 89. Grossman MD: Gunshot wounds below the popliteal fossa: A contemporary review. Am Surg 1999;65:360. 90. Rowe VL: Shank vessel injuries. Surg Clin North Am2002;82:91.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/103.html/top
Page 51
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
Section III - Orthopedic Lesions Chapter 46 – General Principles of Orthopedic Injuries Joel M. Geiderman
MANAGEMENT PRINCIPLES Patients with orthopedic injuries and nontraumatic musculoskeletal disorders compose a large portion of the more than 100 million patients who present annually to U.S. emergency departments. Although only rarely life-threatening, orthopedic injuries may threaten a limb or its function, and accurate early diagnosis and treatment can avert long-term problems. Many of these injuries can and should be treated definitively by the emergency physician. Consultation with an orthopedist should be sought for the treatment of most long bone fractures, open fractures, and flexor tendon injuries and for follow-up of certain patients initially treated in the emergency department. Orthopedic injuries often occur as a result of accidents (industrial or otherwise) and frequently involve young, otherwise healthy, working individuals. Accurate initial diagnosis, treatment, and documentation assume great importance medically and economically. Many problems can be avoided if the following 10 general principles are kept in mind: 1. Most orthopedic injuries can be predicted by knowing the chief complaint, the age of the patient, the mechanism of injury, and an estimate of the amount of energy delivered. 2. A careful history and physical examination predict x-ray findings with a high degree of accuracy. Many fractures were accurately described before the advent of roentgenology ( Table 46-1 ). Table 46-1 -- Common Fracture Names and Their Origins Fracture Eponym
Description
Aviator's
Vertical fracture of the neck of the First described in flyers during World War I. talus with subtalar dislocation and Arises from forced dorsiflexion of the foot in backward displacement of the body flying accidents and in traffic accidents after a head-on collision Intra-articular fracture-dislocation of Considered complicated and unstable. the wrist Requires surgical reduction in most cases. Described by Barton in 1838 before the advent of radiography Oblique intra-articular fracture of Results from high-velocity impact across the the dorsal rim of the distal radius articular surface of the radiocarpal joint, with with displacement of the carpus the wrist in dorsiflexion at the moment of along with the fracture fragment impact Wedge-shaped articular fragment Similar mechanism as dorsal Barton's but with sheared off of volar surface of the wrist in volar flexion at time of injury. Also radius (volar rim fracture), referred to as a reverse Barton's. Much more displaced volarly along with the rare than dorsal Barton's carpus Oblique fracture through base of Usually produced by direct force applied to the the first metacarpal with dislocation end of the metacarpal. Dorsal capsular
Barton's
Dorsal Barton's
Volar Barton's
Bennett's
Comment
Page 52
of the radial portion of the articular surface Fracture of the neck of the fourth or fifth metacarpal
structures disrupted by the dislocation. Marked tenderness along medial base of thumb Boxer's Results from striking a clenched fist into an unyielding object, usually during an altercation, or against a wall, out of frustration or anger Bosworth Fracture-dislocation of the ankle Rare injury, produced by a severe external resulting in the fibula being rotation force applied to the foot. Physical entrapped behind the tibia examination reveals foot severely externally rotated in relation to the tibia Chance's Vertebral fracture, usually lumbar, Caused by simultaneous flexion and involving the posterior spinous distraction forces on the spinal column, usually process, pedicles, and vertebral associated with use of lap seatbelts. Anterior body column fails in tension along with the middle and posterior columns. May be misdiagnosed as a compression fracture Chauffeur's Solitary fracture of radial styloid Occurs from tension forces sustained during ulnar deviation and supination of the wrist. Name derives from occurrence in chauffeurs who suffered violent, direct blows to the radius incurred while turning the crank on a car, only to have it snap back, during previous eras Clay shoveler's Fracture of the tip of the spinous First described in Australian clay shovelers process of the sixth or seventh who sustained a fracture of the spinous cervical vertebra process by traction as they lifted heavy loads of clay Colles' Fracture of the distal radius with Most common wrist fracture in adults, dorsal displacement and volar especially in the elderly. Results from fall on an angulation; with or without an ulnar outstretched hand. Also known as silver fork styloid fracture deformity, which accurately describes the gross appearance in the lateral view. First described by Colles in 1814, before the advent of radiography Cotton's Trimalleolar fracture Fracture of the lateral malleolus, the posterior malleolus, and either a fracture of the medial malleolus or a disruption of the deltoid ligament with visible widening of the mortise on ankle radiograph Dashboard Fracture of the posterior rim of the Named for mechanism of injury: a seated fracture acetabulum passenger striking the knee on a dashboard, driving the head of the femur into the acetabulum Dupuytren's Fracture-dislocation of the ankle Results from a similar mechanism as the better known Maisonneuve fracture (i.e., external rotation of the ankle), resulting in either deltoid ligament rupture or medial malleolus fracture, diastasis of the inferior tibiofibular joint, and indirect fracture of the fibular shaft. Maisonneuve was the student of Dupuytren Essex-Lopresti Fracture of radial head with Results from longitudinal (axial) compression dislocation of distal radioulnar joint of the forearm Galeazzi's Fracture of the shaft of the radius Results from fall on outstretched hand, with with dislocation of the distal the wrist in extension and the forearm forcibly radioulnar joint. Ligaments of pronated. Inherently unstable with tendency to inferior radioulnar joint are ruptured redisplace after reduction and head of ulna displaced from ulnar notch of the radius Hangman's Fracture-dislocation of atlas and Results from extreme hyperextension during
Page 53
Hume
Jefferson
axis, specifically of pars interarticularis of C2 and disruption of C2–3 junction. Separation occurs between second and third vertebral bodies from anterior to posterior side Fracture of the proximal ulna associated with forward dislocation of the head of the radius Burst fracture of ring of C1, or atlas
abrupt deceleration. Most common cause is the forehead striking the windshield of a car during a collision. A bit of a misnomer in that hanging usually produces death by strangulation rather than cord damage Essentially a high Monteggia injury
Axial loading results in a shattering of the ring of the atlas. Decompressive type of injury. Associated with disruption of transverse ligament; an unstable injury Should not be confused with the more common avulsion fracture of fifth metatarsal styloid, produced by avulsion at the insertion of the peroneus brevis. Jones described the fracture that bears his name in 1902, after suffering the injury himself, while dancing Types I, II, and III (see Chapter 39 ) Rare pull-off injury of the fibular attachment of the anterior tibiofibular ligament Lisfranc, a field surgeon in Napoleon's army, described an amputation performed through the tarsometatarsal joint in a soldier who caught his foot in a stirrup when he fell off his horse. Since then, the joint has borne his name Results from external rotation of the ankle with transmission of forces through syndesmosis; proximally the force is relieved by fracture of the fibula. Described experimentally in 1840, before radiography Resultant pelvic injury is unstable. Described by Malgaigne, based on clinical findings, in 1847
Jones'
Transverse fracture of the metatarsal base, occurring at least 15 mm distal to the proximal end of the bone, distal to the insertion of the peroneus brevis
Le Fort Le Fort-Wagstaffe Lisfranc's
Maxillary fracture Avulsion fracture of the anterior cortex of the lateral malleolus Fracture located around the tarsometatarsal (Lisfranc's) joint, usually associated with dislocation of this joint
Maisonneuve
Fracture of proximal third of fibula associated with rupture of the deltoid ligament or fracture of the medial malleolus and disruption of the syndesmosis Fracture of the ilium near the sacroiliac joint with displacement of the symphysis; or a dislocation of the sacroiliac joint with fracture of both ipsilateral pubic rami Fatigue, or stress, fracture of the Arises from long marches or other repetitive metatarsal use trauma (e.g., marathon running) or less commonly from single stumbling movements Fracture of the junction of the Usually caused by fall on outstretched hand proximal and middle thirds of the along with forced pronation of forearm or by a ulna associated with anterior direct blow on the posterior aspect of the ulna. dislocation of the radial head Reported by Monteggia in 1814 Fracture of either ulna or radius, or Name derived from a citizen's attempt to both protect himself from a police officer's baton or “nightstick” by offering the forearm Closed fracture of the radius at the Named for a series of cases presented at the middle third/distal third junction, Piedmont Orthopaedic Society of Durham, without associated ulnar fracture North Carolina Definitions vary (see comment); The exact fracture Pott described in 1769 is most commonly a bimalleolar uncertain; clearly it referred to a fracture of the fracture or a fracture of the distal lower fibula, usually associated with other fibula, 4–7 cm above the lateral fractures or dislocations about the ankle malleolus Intra-articular fracture at base of Produced by an axial load with the metacarpal metacarpal. Frequently Y-or in partial flexion. Worse prognosis than a
Malgaigne
March
Monteggia's
Nightstick
Piedmont fracture Pott's
Rolando's
Page 54
Salter-Harris
Stener
Smith's
Teardrop
Thurston Holland's fragment Tillaux
T-shaped, or may be severely Bennett's fracture and, fortunately, more rare comminuted An epiphyseal fracture occurring in Graded I-V, depending on degree of children or adolescents involvement and/or displacement of epiphysis and metaphysis (see text dealing with Salter-Harris fractures and also Figure 46-1 ) Avulsion of the ulnar corner of the Bony equivalent of rupture of the ulnar base of the proximal phalanx of the collateral ligament, or “gamekeeper's thumb” thumb Extra-articular fracture of the distal Reverse of the Colles' fracture but much more radius with volar displacement of uncommon. Sometimes referred to as a distal fragment “garden spade” deformity. Usually results from fall with force to back of hand. First described by Smith in 1847 Wedge-shaped fracture of the Commonly involves a ligamentous injury and anteroinferior portion of the may produce neurologic injury vertebral body, displaced anteriorly Triangular metaphyseal fragment Described by Thurston Holland in 1929. that accompanies the epiphysis in Commonly hyphenated, although technically it Salter-Harris type II fractures should not be Isolated avulsion fracture of the Occurs in older adolescents (12–15 years old) anterolateral aspect of the distal after the medial parts of the epiphyseal plates tibial epiphysis close, but before the lateral part closes. External rotation force places stress on anterior talofibular ligament. Described by Tillaux in 1872
3. If a fracture is suspected clinically, but x-ray films appear negative, the patient initially should be managed with immobilization as though a fracture were present. 4. Criteria for adequate radiographic studies exist; inadequate studies should not be accepted. 5. X-ray studies should be performed before attempting most reductions except when a delay would be potentially harmful to the patient or in some field situations. 6. Neurovascular competence should be checked and recorded before and after all reductions. 7. Patients must be checked for the ability to ambulate safely before discharge from the emergency department and should not be discharged unless this can be established. 8. Patients should receive explicit aftercare instructions before leaving the emergency department, covering such areas as monitoring for signs of neurovascular compromise or increasing compartment pressure, cast care, weight bearing, crutch use, and an explicit plan and timing for follow-up. 9. In a patient with multiple trauma, noncritical orthopedic injuries should be diagnosed and treated only after other more threatening injuries have been addressed. 10. All orthopedic injuries should be described precisely and according to established conventions.
FRACTURES Fracture Nomenclature Describing orthopedic injuries using precise language according to established convention permits relevant information to be communicated clearly to other parties. Terms commonly used to describe a fracture are listed in Box 46-1 . A fracture is a break in the continuity of bone or cartilage. Clinically a history of loss of function, pain, tenderness, swelling, abnormal motion, and deformity suggests a fracture. X-ray studies are the mainstay of diagnosis and are usually, although not always, confirmatory. At times, special views, radionucleotide bone scans, computed tomography (CT) scans, or magnetic resonance imaging (MRI) studies are necessary to confirm a clinical suspicion. These studies should be considered when the clinical impression is at odds with the findings of routine radiography.
Page 55
BOX 46-1 Fracture Description
Identification Ope n vers us clos ed Exac t anat omic locat ion Dire ction of fract ure line Sim ple/c om minu ted Posit ion (disp lace ment , align ment )
Additional Modifiers Complete versus incomplete Involvement of articular surface (%) Avulsion Impaction Depr essi on Com pres sion
Special Situations
Page 56
Path ologi c Stre ss
General Descriptors Description of a fracture should begin by stating whether the fracture is closed or open (less desirable terms are simple or compound). In a closed fracture, the skin and soft tissue overlying the fracture site are intact. The fracture is open if it is exposed to the outside environment in any manner. This exposure may be as obscure as a puncture wound or as gross as splintered bone protruding through the skin. It is sometimes difficult to determine whether a small wound in proximity to a fracture actually communicates with that fracture. Some physicians advocate probing such a wound with a blunt sterile swab to establish a relationship; no study has established the safety, benefit, or accuracy of this maneuver. If doubt exists, an open fracture should be assumed to be present. The next item that should be noted in the description of a fracture is the exact anatomic location, including the name of the bone, left or right, and standard reference points, for example, the humeral neck or posterior tibial tubercle. Long bones can be divided into thirds—proximal, middle, or distal—and these thirds or the junction of any two of them (e.g., the junction of the middle and distal third of the tibia) are used to describe fractures. The most descriptive language possible should be used. It is better to say “closed fracture of the right ulnar styloid” than “closed fracture of the right distal ulna” because the former conveys more precise anatomic information. An additional modifier describes the direction of the fracture line in relation to the long axis of the bone in question. A transverse fracture occurs at a right angle to the long axis of the bone ( Figure 46-1A ), whereas an oblique fracture runs oblique to the long axis of the bone ( Figure 46-1B ). A spiral fracture results from a rotational force and encircles the shaft of a long bone in a spiral fashion ( Figure 46-1C ). A fracture in which there are more than two fragments present is termed comminuted ( Figure 46-1D ).
Figure 46-1 Types of fractures. A, Transverse. B, Oblique. C, Spiral. D, Com m inuted.
The position and alignment of the fracture fragments (i.e., their relationship to one another) should be described. Fragments are described relative to their normal position, and any deviation from normal is termed displacement. By convention, the position of the distal fragment is described relative to the proximal one. In Figure 46-2 , there is a dorsal displacement of the fractured radius, and in Figure 46-3 , there is lateral, or valgus, displacement of the distal tibia and fibula.
Figure 46-2 Dorsal displacem ent of distal radius.
Page 57
Figure 46-3 Valgus displacem ent of distal tibia and fibula. The distal segm ent is angled away from the m idline of the body.
The terms valgus and varus are sometimes confusing. Valgus denotes a deformity in which the described part is angled away from the midline of the body. Conversely, varus denotes a deformity in which the angulation of the part is toward the midline. Alignment refers to the relationship of the longitudinal axis of one fragment to another; deviation from the normal alignment is termed angulation. The direction of angulation is determined by the direction of the apex of an angle formed by the two fracture fragments ( Figure 46-4 ). This angle is opposite to the direction of displacement of the distal fragment.
Figure 46-4 Volar angulation of fractured radius.
Descriptive Modifiers A fracture is termed complete if it interrupts both cortices of the bone and incomplete if it involves only one. It should be noted whether a fracture extends into and involves an articular surface. Frequently the percentage of articular surface that is involved is estimated; in some cases, the percentage that is involved dictates the need to perform a surgical reduction. In general, it is important that the articular surface be restored to anatomic integrity. Avulsion fracture refers to a bone fragment that is pulled away from its normal position by either the forceful contraction of a muscle ( Figure 46-5A ) or the resistance of a ligament to a force in the opposite direction ( Figure 46-5B ). Impaction refers to the forceful collapse of one fragment of bone into or onto another. In the proximal humerus, this collapse typically occurs in a telescoping manner, particularly in elderly patients, whose bones are soft and brittle. In the tibial plateau, impaction occurs frequently in the form of a depression ( Figure 46-6A and B ), and in the vertebral bodies, impaction frequently occurs in the form of compression ( Figure 46-6C ).
Figure 46-5 Avulsion fractures.
Figure 46-6 A and B, Tibial plateau fracture. C, Vertebral body com pression fracture.
A fracture that occurs through abnormal bone is termed pathologic. A pathologic fracture should be suspected whenever a fracture occurs from seemingly trivial trauma. Diseases that cause structural weakness predisposing to injury include primary or metastatic malignancies, cysts, enchondromata, and giant cell tumors. In addition, osteomalacia, osteogenesis imperfecta, scurvy, rickets, and Paget's disease all weaken bones, making them susceptible to fracture. The term pathologic also is applied to fractures through osteoporotic bone when the demineralization is a result of disease, as in polio. Fractures through osteoporotic bone of the elderly usually are not described as pathologic. When fractures occur in normal bones and a history of “trivial trauma” is elicited, violence or battering should be suspected. Repeated
Page 58
low-intensity trauma may lead to resorption of normal bone, resulting in a stress fracture. Other names for this condition are fatigue fracture and march fracture (see Table 46-1 ). Most stress fractures occur in the lower extremities and commonly affect individuals involved in activities such as running, basketball, aerobics, and dancing. The tibia, fibula, metatarsals, navicular, cuneiform, calcaneus, femoral neck, or femoral shaft may be involved.[]
Fracture Eponyms Many fractures were described before the advent of radiography and are described by an eponym rather than the exact bony injury. These eponyms reflect the rich history of orthopedic care and, despite the objections of some, are still commonly used to describe orthopedic injuries (see Table 46-1 ).
Fractures in Children Certain features of children's bones distinguish pediatric fractures from adult fractures. Bones of children are necessarily soft and resilient and sustain numerous incomplete fractures. Greenstick fractures are incomplete angulated fractures of long bones. The resultant bowing of the bone causes an appearance resembling a moist, immature branch that breaks in a similar fashion when bent ( Figure 46-7A ). A torus fracture is another form of incomplete fracture, characterized by a wrinkling or buckling of the cortex. In Greek architecture, a torus is a bump at the base of a column, and these fractures, occurring at the end of long bones, take on such an appearance. These fractures may be extremely subtle on radiographs ( Figure 46-7B ).
Figure 46-7 A, Greenstick fracture of m idshaft of fem ur. B, Torus fracture of distal third of radius.
Another feature of growing long bones that is a frequent source of trouble and confusion is the presence of epiphyses, cartilaginous centers at or near the ends of bone that give rise to growth of the bone. Figure 46-8 is a schematic review of the anatomy of a growing bone. Because cartilage is radiolucent, the cartilaginous portion of an epiphysis is not visualized on radiographs. A tendency exists to consider only the ossified nucleus and to ignore the cartilaginous structure that bridges to the metaphysis. Cartilage is present even before an ossified nucleus is seen. Because the epiphyseal growth plate is represented by a radiolucent line, confusion may exist as to whether a fracture line is present. These complexities in interpreting radiographs in children sometimes, but not always, require comparison x-ray views of the noninjured side. Injuries to the epiphyses may result from either compressive or shearing forces. These injuries are relatively common during childhood as opposed to sprains or shaft fractures and must be considered in children with a “sprained ankle” because of the relative weakness of the cartilaginous growth zone, which separates before stronger ligaments and bones are torn or broken. Epiphyseal injuries should be described according to the Salter-Harris classification ( Table 46-2 ).
Figure 46-8 Anatom y of growing bone.
Table 46-2 -- Salter-Harris Classification
Page 59
Desc Diagram riptio n Type Fract I ure exten ds throu gh the epiph yseal plate, result ing in displ acem ent of the epiph ysis (this may appe ar merel y as wide ning of the radiol ucent area repre senti ng the growt h plate)
Page 60
Desc Diagram riptio n Type As II abov e; in additi on, a triang ular segm ent of meta physi s is fractu red
Page 61
Desc Diagram riptio n Type Fract III ure line runs from the joint surfa ce throu gh epiph yseal plate and epiph ysis
Page 62
Desc Diagram riptio n Type Fract IV ure line occur s as in type III, but also pass es throu gh adjac ent meta physi s
Page 63
Desc Diagram riptio n Type This V is a crush injury of the epiph ysis; it may be diffic ult to deter mine by x-ray exam inatio n
Type I injuries involve only a slip of the zone of provisional calcification. Comparison radiographs are usually necessary to detect small slips. A child with swelling and tenderness over an epiphysis (e.g., of the lateral ankle) and a negative x-ray should be suspected to have an epiphysis injury, rather than a sprain, because the epiphysis is weaker than the overlying ligaments. Type II injuries are similar to type I injuries, with a fracture extending into the metaphysis. The triangular metaphyseal fragment sometimes is referred to as the Thurston Holland sign (see Table 46-1 ). Type II injuries account for approximately three fourths of all epiphyseal fractures. Because the germinal layer is not involved, growth disturbance usually does not occur with type I and II injuries. Type III injuries are composed of a slip of the growth plate plus a fracture through the epiphysis, involving the articular surface. Because this fracture involves the germinal layer, growth may be disrupted. Anatomic reduction does not eliminate the possibility of growth disturbance. Type IV fractures are similar to type III fractures, with the additional involvement of a metaphyseal fracture. Anatomic reduction is essential and usually requires surgery. Growth disturbance occurs in a high proportion of patients. Type V fractures are crush injuries of the epiphyseal plate, usually produced by a compressive force.[3] This type of injury usually occurs in joints that move in one plane, most commonly the knee and ankle. Because this injury occurs in a radiolucent area, the injury may be difficult to diagnose on x-ray, but it should be suspected by mechanism of injury and pain over the epiphysis. The diagnosis can be established by MRI if hemorrhage or a hematoma is identified within the growth plate immediately after injury.[4] Also reported is loss of MRI signal from the cartilage.[5] Growth arrest, manifest by shortening or angulation, is the rule in this injury. Type V injuries are extremely rare.[6]
Page 64
In a study of 410 fractures in children, 16.3% were torus fractures, and 13.9% were epiphyseal injuries.[6] Dislocations and subluxations were rare (3%), and most involved the radial head or the patella. There were no shoulder dislocations. The most common sites were the bones of the distal forearm and the hands (usually the phalanges), each group accounting for 20% of the total. The clavicle was involved 13% of the time; the elbow, 8%; the ankle, foot, and femur, 7% each; and the midforearm, lower leg, and humerus, 4% to 6% each. Another study found an incidence of physeal injury of 18% in 2000 bony injuries in children.[7] The peak age at the time of injury was 12 years in boys and 11 years in girls. In this series, the incidence of injury by category was type I, 8.5%; type II, 73%; type III, 6.5%; type IV, 12%; and type V, 0.5%. The sole Salter-Harris type V injury in this series occurred in the proximal tibia. The most frequent sites of Salter-Harris type III fractures are the phalanges and distal tibia, and most type IV fractures occur in the distal humerus and distal tibia. The overall frequency of growth arrest in all injuries is 1.4%, whereas the frequency of serious complications is less than 0.6%. The prognosis depends more on the location of the fracture than the Salter-Harris classification. The proximal tibia is the most common site for growth disturbance. Because the epiphysis is closer to fusing, the chances of growth disturbance are less; this influences decision making in terms of surgical versus conservative management.
Diagnostic Modalities for Fracture Diagnosis Plain Radiography Plain radiography is the mainstay in diagnosing fractures. In addition to confirming or excluding fractures, other pathologic conditions can be identified. With penetrating trauma, foreign bodies, air, and gas also may be detected. With minor trauma, and when good follow-up monitoring is ensured, it is acceptable to delay x-ray films. Delay cannot be permitted, however, when the suspected injury is one that might be made worse by delayed diagnosis, such as a nondisplaced hip fracture. At least two views perpendicular to each other are mandatory in examining long bones, and an oblique view also is usually obtained. In certain locations, such as the phalanges, oblique views are necessary. If doubt still exists, the clinician should ask for more views in various degrees of obliquity to the other films. A fracture line is most visible when it is parallel to the x-ray beam and is invisible when it is exactly 90 degrees to the beam. The clinician should never accept a study that examines the bone in only one plane. When a long bone is found to be fractured, it is imperative that the bone be viewed radiographically in its entire length. Each film must be examined to ensure that proper technique is used and that no important area is omitted from the film. Overexposed films may fail to reveal an abnormality. Although there is some loss of fine detail on portable films, these are acceptable in unstable patients, in whom the risk of moving the patient does not outweigh the benefit of the more detailed study. Computed (digital) radiography is now in widespread use. An advantage of this technique is the ability to alter the image-processing parameters based on a specific clinical problem after an exposure has been made.[7] Disadvantages are that the spatial resolution of computed radiographs, and especially of computer monitor formats, is less than that of standard screen-film combinations and that minification is often necessary when larger body parts, such as the thoracic spine, lumbar spine, and pelvis, are being examined. Minification also may contribute to reduced accuracy in the diagnosis of subtle, high-frequency chest abnormalities, such as pneumothorax. Despite these considerations, computed radiography seems to be acceptable and does not seem to diminish reader performance significantly.[8] Even with good technique, some fractures are not visible initially and do not appear until the margins of the fracture absorb. Absorption widens the radiolucent line, and a defect appears in 7 to 10 days. At that time, new bone produced beneath the periosteum at the margins of the fracture accentuates the fracture. Accordingly, if a fracture is suspected but not visible at the initial visit, the injury should be treated as a fracture and re-examined clinically and radiographically in 7 to 10 days, and the patient should be informed of the rationale for this regimen. Stress views of joints are used in some instances to evaluate the degree of ligamentous injury. Some authors argue against the use of stress views, citing a risk of injuring further an already traumatized structure, additional radiation exposure to the patient and the technologist, and the possibility that pain may not allow sufficient stress to be applied. For these reasons, stress views should be used judiciously in circumstances when other methods of evaluating ligamentous injuries are not available. Comparison views are useful in selected situations, but should not routinely be performed in all pediatric examinations.[9] If a fracture is definitely present on the affected side, the comparison view exposes the child to radiation and adds expense with no benefit. Similarly, an experienced physician generally is able to read a normal film with
Page 65
reasonable certainty. It is rational to use comparison views in instances when radiographs are inconclusive and when the confusion arises specifically out of the need to distinguish between a possible fracture and normal developmental anatomy. Obtaining a wide field of the affected extremity is more useful than routine comparison views for a young child because the child often does not localize the pain well; this is especially true with regard to complaints of knee pain in cases of hip injury or wrist complaints in forearm and elbow injury. Comparison views sometimes are helpful in adults when a question of accessory ossicles or nonfused bones (e.g., bipartite patella) exists because these anomalies are usually bilateral. The bleeding that inevitably accompanies fractures may produce soft tissue swelling and may impinge on or obliterate overlying muscle planes. Fat pads, such as in the elbow, may be displaced. Another useful sign is the fat-fluid level, which may accompany fractures extending into the knee joint. The fat-fluid level is visible, however, only if the cross-table technique is used. The bones themselves should be examined systematically. Normal adult bones possess a smooth unbroken contour. A distinct angle is highly suggestive of a fracture. In an adult, the typical fracture is represented by a lucent line that interrupts the smooth contour and usually extends to the opposite side. Nutrient arteries may be confused with fractures, but have different radiographic characteristics: They are fine, sharply marginated, extend obliquely through the cortex, and are less radiolucent than fractures. Pseudofractures can be created by soft tissue folds, bandages or other overlying material, or a radiographic artifact called the Mach effect. If lucencies extend beyond the bones, the line is highly unlikely to represent a fracture. Anomalous bones and calcified soft tissue likewise may be mistaken for fractures. Avulsions and small fracture fragments have an irregular, uncorticated surface, and a defect in the adjacent bone is present, whereas anomalous ossification centers (accessory ossicles) and sesamoids are characterized by smooth cortical margins. Reference texts are useful in identifying and confirming these anomalies because they tend to occur in predictable locations.[10] Compression fractures are represented by increased density rather than a lucency. Finally, “the most commonly missed fracture is the second fracture.” One must be diligent in searching for a second fracture after discovering the first fracture on a study. In particular, certain paired fractures, such as the distal tibia and proximal fibula, should be sought out.
Special Imaging Techniques Radionucleotide Bone Scanning In the past, radionucleotide bone scanning was used to detect skeletal abnormalities not radiographically evident in children and adults.[11] Occult lesions, especially stress fractures, acute osteomyelitis, and tumors, can be detected on these scans, although there are problems with specificity and sensitivity. This modality has been largely supplanted by CT and MRI and now is seldom used.
Computed Tomography CT is used to confirm suspicious fractures or to define better displacement, alignment, or fragmentation of fractures. It also is useful in trauma to rule out cervical spine fracture when plain films are equivocal and in noncompressive vertebral fractures to assess the number of fragments and their spatial relationship to the spinal canal. A CT scan is used frequently to define the integrity of articular surfaces in the acetabulum, knee, wrist, or ankle and in Salter-Harris type IV fractures.[3]
Magnetic Resonance Imaging MRI constitutes the most advanced noninvasive examination of orthopedic structures, delineating lesions of bone, cartilage, ligaments, and other structures, such as menisci, disks, and epiphyseal structures. MRI is expensive and time-consuming and should be reserved for instances when the diagnosis is in doubt and specific findings would alter the treatment.
Complications of Fractures Infection (Osteomyelitis) Open fractures are treated as true orthopedic emergencies because of the risk of infection; the dreadful nature of the complication of osteomyelitis dictates that no time should be wasted in initiating therapy ( Box 46-2 ). Wounds should be covered with sterile dressings, and parenteral antibiotics should be instituted as early as possible. Currently, suggested therapy includes a first-generation cephalosporin, such as cefazolin, for all open fractures, with the addition of an aminoglycoside for types II and III fractures.[] Although the traditional recommendation has been to obtain culture and sensitivity before starting antibiotics, the usefulness of this approach has not been supported by a controlled study.[14] A retrospective analysis of perioperative cultures in open fractures in children failed to show any value in predicting the identity of subsequent infecting pathogens.[15] It is prudent to omit such cultures.[16] BOX 46-2
Page 66
Classification and Emergency Management of Open Fractures
Grades Grade I: Wound <1 cm long, punctured from below Grade II: Laceration 5 cm long; no contamination or crush, no excessive soft tissue loss, flaps, or avulsion Grade III: Large laceration, associated contamination or crush: frequently includes a segmental fracture IIIA: Invol ves exte nsiv e soft tissu e strip ping of bone IIIB: Peri oste al strip ping has occu rred IIIC: Majo r vasc ular injur y pres ent
Management
Page 67
1.
2.
3.
Cont rol hem orrh age in field with steril e pres sure dres sing after caref ully rem ovin g gros s debri s (e.g., woo d, cloth ing, leav es). Splin t with out redu ction , unle ss vasc ular com pro mise is pres ent. Irriga te with salin e and cove r with salin e-so aked spon
Page 68
4.
5.
ges after arriv al in the eme rgen cy depa rtme nt. Begi n intra veno us antib iotic prop hylax is, usua lly a firstgene ratio n ceph alos porin . Admi niste r tetan us prop hylax is, inclu ding tetan us imm une glob ulin, for large crus h wou nds.
Hemorrhage Because of the rich blood supply to the skeleton, fractures can result in large amounts of blood loss, shock, and death from exsanguination. In particular, certain pelvic fractures can cause great blood loss because adequate tamponade is not possible. In adults, blood loss can range from 100 mL from a forearm fracture to 3 L from a pelvis fracture ( Table 46-3 ). Table 46-3 -- Blood Loss Associated with Fracture in Adults
Page 69
Fracture Site
Amount of Blood Loss (mL)
Radius and ulna Humerus Tibia and fibula Femur Pelvis
150–250 250 500 1000 1500–3000
Vascular Injuries Vascular injuries characteristically are associated with certain fractures. Fractures and dislocations about the knee result from tremendous force that often injures the popliteal artery. In the extremities, assessment of vascular injuries may be difficult. The initial survey should note the presence or absence of pulses and the state of capillary filling. If an end artery is completely disrupted, the tissue distal to the injury may exhibit the classic five Ps: pain, pallor, pulselessness, paresthesias, and paralysis. Incomplete and subclinical injuries occasionally occur, however, that initially may be asymptomatic and nondetectable. Likewise, in an unconscious, multiply-injured patient, major vascular injuries may not be obvious. The mechanism of injury and anatomy dictate the need to assess the possibility of an injured vessel. If pulses cannot be palpated, a Doppler stethoscope should be used to listen for blood flow. Even palpable pulses may be misleading, however, because it has been shown that in 10% to 20% of significant arterial injuries, distal pulses may initially be normal. When pulses are present, but the mechanism of injury suggests the possibility of vascular injury, additional diagnostic studies or surgical exploration may be necessary. Late complications of undiagnosed vascular injuries include thrombosis, arteriovenous fistulae, aneurysm, false aneurysm, and tissue ischemia with limb dysfunction.
Nerve Injuries Nerves can be injured by either blunt or penetrating trauma. Neurapraxia is the contusion of a nerve, with disruption of the ability to transmit impulses. Paralysis, if present, is transient, and sensory loss is slight. Normal function usually returns to a neurapraxic nerve in weeks to months. Axonotmesis is a more severe crush injury to a nerve. The injury to nerve fibers occurs within their sheaths. Because the Schwann tubes remain in continuity, spontaneous healing is possible but slow. Neurotmesis is the severing of a nerve, usually requiring surgical repair. Because of proximity, specific nerve injuries characteristically accompany certain fractures ( Table 46-4 ). Table 46-4 -- Nerve Injuries Accompanying Orthopedic Injuries Orthopedic Injury
Nerve Injury
Elbow injury
Median or ulnar
Shoulder dislocation
Axillary
Sacral fracture
Cauda equina
Acetabulum fracture
Sciatic
Hip dislocation
Femoral nerve
Femoral shaft fracture
Peroneal
Knee dislocation
Tibial or peroneal
Lateral tibial plateau fracture
Peroneal
When the nerve is completely severed, all functions are absent, including superficial sensation to touch, pain, and temperature; deep sensation to muscle and joint movements, position, deep pressure, and vibration; motor supply and deep tendon reflexes (to distally innervated muscle groups); and response to electrical stimulation. For less severe injuries, any subjective change in sensation should be noted. Light touch is a good screening test. Two-point discrimination is a more sensitive examination and should be used routinely in evaluating digital nerves. Two-point discrimination may be of limited value in children in whom a subjective response may be misleading; this is also true in patients with calloused fingertips and in patients who are uncooperative, comatose, in severe pain, or intoxicated. Testing for sympathetic nerve function using the O'Riain wrinkle test may be helpful.[17] Soaking the normally innervated digits in warm saline for 20
Page 70
minutes causes the digital pulps to wrinkle through a mechanism that is not understood. The presence of wrinkling probably indicates the nerve is intact, whereas absence of wrinkling may be more difficult to interpret. The Ninhydrin test, another sudomotor test used to assess peripheral nerve integrity, is reportedly more reliable than the O'Riain test, but is not practical to perform in the emergency department.
Compartment Syndrome Compartment syndrome is a serious acute emergency complication that should be considered whenever pain and paresthesias occur in an extremity after a fracture within an enclosed osseofascial space ( Table 46-5 ). The immediate threat is to the viability of nerve and muscle tissue within the involved compartment, but infection, gangrene, myoglobinuria, and renal failure also may ensue. Compartment syndrome is associated most commonly with a closed long bone fracture of the tibia, but it also is well described in the thigh, forearm, arm, hand, and foot.[] In addition, compartment syndrome can occur with soft tissue trauma alone and even with open fractures. It also has been described in a host of unusual situations, including prolonged procedures in the lithotomy position, the tuck position (knees tucked to the chest for lumbar surgery), spontaneous hemorrhage, use of pneumatic antishock trousers, and the application of excessive traction in treatment of a fracture.[] Table 46-5 -- Life-Threatening or Limb-Threatening Emergencies Condition
Possible Adverse Outcome
Open fracture
Osteomyelitis
Fracture or dislocation with major vascular disruption Amputation (especially popliteal) Major pelvic fracture
Exsanguination
Hip dislocation
Avascular necrosis of femoral head
Compartment syndrome
Ischemic contracture; myoglobinuria, renal failure
Pathophysiology Increased pressure in a closed nonexpandable compartment essentially represents a mismatch between the volume of that space and its contents. As such, it may arise from one of three circumstances: (1) increased compartment contents, (2) decreased compartment volume, or (3) external pressure ( Box 46-3 ). As tissue pressure increases, so does venous pressure, resulting in compromise of the local circulation and tissue hypoxia; this is believed to occur at pressures that are above normal diastolic pressure but below systemic arterial pressure because of a reduced arteriovenous gradient at the tissue level. The body responds by releasing histamine in an attempt to dilate capillaries and increase blood flow to the affected area. Histamine also increases capillary membrane permeability, resulting in a leak of proteins and fluid into the surrounding tissue, further increasing compartment pressure. BOX 46-3 Causes of Compartment Syndrome
Increased Compartment Content Bleeding Majo r vasc ular injur y Coa gulat ion disor der Antic
Page 71
oagu lant thera py Increased capillary filtration Reperfusion after ischemia Arter ial bypa ss grafti ng Emb olect omy Ergo tami ne inge stion Card iac cath eteri zatio n Lyin g on limb Trauma Frac ture Con vulsi on Intensive use of muscle Exer cise Seiz ures Ecla mpsi a Teta ny Burns Ther mal Elect rical Intra-arterial drug injection Orthopedic surgery
Page 72
Tibia l oste otom y Hau ser's proc edur e Red uctio n and inter nal fixati on of fract ures Snakebite Increased capillary pressure Intensive use of muscles Venous obstruction Phle gma sia cerul ea dole ns (i.e., acut e infla mm ation and ede ma of the legs) Ill-fitti ng leg brac e Veno us ligati on Diminished serum osmolarity (i.e., nephritic syndrome)
Page 73
Decreased Compartment Volume Clos ure of fasci al defe cts Exce ssiv e tracti on on fract ured limb s
Miscellaneous Infiltr ated infus ion Pres sure trans fusio n Leak y dialy sis cann ula Mus cle hype rtrop hy Popli teal cyst
External Pressure Tight cast s, dres sing
Page 74
s, or air splin ts Lyin g on limb From Matsen FA III: Compartmental Syndromes. New York, Grune & Stratton, 1980.
As tissue pressure continues to increase, venous blood flow is impaired as capillary perfusion pressure is exceeded. Finally, arterial capillary blood flow falls to a point where the basic metabolic needs are no longer met, leading to ischemic necrosis of muscles and nerves within the compartment. An important concept in the management of compartment syndrome is that because local venous pressure cannot be significantly below local tissue pressure, and because elevation of a dependent limb decreases local arterial pressure by 0.8 mm Hg for each 1 cm of limb elevation, elevation of a limb with resultant reduction in the local arteriovenous gradient may be counterproductive and may exacerbate compartment syndrome. Vascular spasm seems to play an insignificant or minimal role in the development of compartment syndrome, as evidenced angiographically, where spasm has never been shown, and clinically, where it is observed that distal pulses usually are maintained until late in the course. Normal compartment pressure is 0 mm Hg. Microcirculation generally is impaired when tissue pressures reach 30 mm Hg or more; however, some patients can tolerate much higher compartment pressures without compartment syndrome developing. Controversy exists over attempts to define compartment syndromes on the basis of specific tissue pressure. The tolerance to tissue ischemia varies among individuals because of shock, compensatory hypertension, altered tone in resistance vessels, and other unknown factors. Inadequate perfusion and relative ischemia begin when tissue pressure within a closed compartment increases to within 30 mm Hg of a patient's diastolic pressure.[26] When tissue pressure equals or exceeds the patient's diastolic pressure, tissue perfusion effectively ceases. The development of muscle ischemia depends not only on the magnitude, but also on the duration of elevated pressure. Intracompartmental pressures do not measure muscle and nerve ischemia, but rather suggest the existence of the proper setting for compartment syndrome.[27]
Anatomic Considerations and Risk Factors Compartment syndrome theoretically can develop in any location where neuromuscular tissue is contained in a limiting envelope. The condition has been reported in the leg, thigh, buttock, arm, forearm, and hand ( Box 46-4 ). By virtue of its location and higher likelihood of sustaining high-energy trauma, the leg, particularly the anterior compartment, is most commonly involved. BOX 46-4 Reported Anatomic Locations of Compartment Syndromes
Lower Extremity Leg Ante rior com part ment Later al com part ment Dee p post erior
Page 75
com part ment Sup erfici al post erior com part ment Thigh Qua drice ps com part ment Buttock Glut eal com part ment
Upper Extremity Hand Inter osse ous com part ment Forearm Dors al com part ment Volar com part ment Arm Delt oid com part ment Bice ps com part ment
Page 76
In a study of 164 patients treated over an 8-year period in the United Kingdom, a fracture was present in 69%, and half of these involved the tibial shaft.[28] Perhaps more significant is that 31% of patients had only soft tissue injury without fracture. Most patients were men younger than age 35. Ten percent of patients either had a bleeding disorder or were taking anticoagulants. Traffic accidents and sports activities were the most common mechanisms of injury.
Clinical Presentation In a conscious and fully oriented patient, pain that is disproportionate to the injury or physical findings is a hallmark finding in compartment syndrome. Pain often is characterized as deep, burning, and unrelenting and is difficult to localize. The need for increasing amounts of analgesics should not lead the clinician automatically to the conclusion that the patient is drug seeking; rather, it should serve as a prompt to the possibility that a compartment syndrome is developing or is present. Pain on passive stretching of the muscle groups in the suspect compartment is an important finding. In addition, active flexion of involved muscles may produce pain. Other reliable suggestive signs and symptoms are hypoesthesias and paresthesias in the distribution of nerves crossing the compartment or tenderness, tenseness, or the sensation of tightness of the compartment. Skin color, temperature, capillary refill, and distal pulses all are unreliable monitors for compartment syndrome because the pressure necessary to produce compartment syndrome is well below arterial pressure. Pallor and loss of pulses are late and ominous signs. Diminished pulses should suggest concomitant pathologic conditions responsible for reduced arterial flow. Although it is still frequently taught that the five Ps—pain, pallor, pulselessness, paresthesias, and paralysis—are signs and symptoms of compartment syndrome, this is generally not true. Rather they are the signs of acute disruption of arterial flow. Subjective complaints are an important indicator of compartment syndrome. Patients who are not fully alert or cooperative must be assessed with particular care.
Diagnostic Tests If the history and examination suggest compartment syndrome, compartment pressures should be measured by using any of the commercially available monitors ( Figure 46-9 ). The Stryker device is a hand-held digital display that is easy to use with minimal training. Care must be taken to zero the monitor in the plane in which it will be inserted to account for the effects of gravity. It is also paramount that the appropriate compartment is measured. Pressures of less than 30 mm Hg generally do not produce compartment syndrome. Pressures exceeding 30 mm Hg or within 30 mm Hg of the patient's mean arterial pressure are an indication for fasciotomy. Serial or continuous pressure measurements should be performed in cases that are not clear-cut. Compartment syndrome can occur at pressures significantly below systemic pressure. Doppler ultrasound is not useful in evaluating these patients because excellent arterial blood flow may be documented even in the presencof a significant compartment syndrome.
Figure 46-9 A, Hand-held device for m easuring com partm ent syndrom e. B, Insert device perpendicular to skin.
Treatment, Complications, and Disposition Complete fasciotomy is the only treatment that can reliably normalize elevated compartment pressure. Preparation for surgery must be done as quickly as possible. Delaying fasciotomy for more than 12 hours often results in irreversible muscle and nerve damage. While the patient is awaiting definitive treatment, the affected part should not be elevated above the level of the heart because this maneuver does not improve venous outflow and reduces arterial inflow. Slight dependency has been suggested to maximize the pressure head in the extremity. Rhabdomyolysis, hyperkalemia, and myoglobinuria may occur and should be managed aggressively to avoid renal failure. Lactic acid also is released from necrotic muscle tissue. Other complications include infection and tissue loss. Delayed treatment results in loss of nerve and muscle function and eventual contracture formation. The magnitude of these disasters may be measured by the fact that in 1993, the average indemnity award in cases of missed compartment syndrome was nearly $280,000. For these reasons, when the diagnosis of compartment syndrome is confirmed, fasciotomy should be done without delay. Gulli and Templeman[26] advise, “The functional and cosmetic results are always acceptable if done early. The
Page 77
results of inadequate treatment of compartment syndrome are never satisfactory.”
Avascular Necrosis Because of their blood supply, certain bones may undergo avascular necrosis after fracture, especially if fractures are comminuted and go untreated for any length of time. The femoral head, talus, scaphoid, and capitate are particularly prone to this complication.[]
Complex Regional Pain Syndrome (Reflex Sympathetic Dystrophy and Causalgia) Definitions The terms reflex sympathetic dystrophy (RSD) and causalgia have been used to describe pain syndromes that sometimes follow fractures, orthopedic surgery, soft tissue injuries, and other unrecognized trauma to the limbs and their appendages. Other names previously used for this spectrum of posttraumatic injuries include Sudeck's atrophy, shoulder-hand syndrome, and postinfarction sclerodactyly. In an attempt to reduce misunderstanding about their etiology and treatment, the International Association for the Study of Pain issued a consensus statement renaming the syndromes formerly called RSD and causalgia.[] Complex regional pain syndrome type I (CRPS-I), replacing the term RSD, is a pain syndrome that develops after an initiating noxious event, extends beyond the distribution of a single peripheral nerve, and is usually disproportionate to the inciting event. The site is most often the distal end of the affected extremity, with a distal-to-proximal gradient. It is associated with edema, changes in blood flow to the skin, abnormal sudomotor activity in the region of the pain, allodynia (pain resulting from non-noxious stimulation to the skin), hyperpathia (pain persisting or increasing after mild or light pressure), or hyperalgesia. The presence of a condition that otherwise would explain the degree of pain and dysfunction excludes the diagnosis of CRPS-I. Because so much of the literature still refers to RSD, this chapter still uses the terms RSD and CRPS-I interchangeably. The definition of CRPS-II is the same as for CRPS-I except that there is demonstrable peripheral nerve injury. This term replaces causalgia under the International Association for the Study of Pain taxonomy.
Pathogenesis and Etiology The pathogenesis of CRPS-I has not been elucidated. The sympathetic nervous system seems to play a role in the maintenance of the symptoms in some, but not all, patients. Cases of CRPS-I have been reported after fractures and as iatrogenic complications of surgery or after minor procedures, including subcutaneous excision and intravenous injection. Forceful manipulations and tight casts also are alleged to have produced the syndrome. In 10% to 26% of patients, no inciting event is identified.[] Although malingering and secondary gain are suspected in some patients, they are not the causes in most patients, as evidenced by pathologic tissue changes in patients who actually have CRPS-I.[37] CRPS-I occurs in children and adolescents.[38] Girls are affected three times as often as boys, and the median age is 12 years. The lower limb is affected twice as often as the upper, and history of inciting trauma can be identified in only half the children with the disorder.
Diagnosis No correlation exists between the severity of the original trauma and the incidence, severity, and cause of the symptoms, making early diagnosis a challenge, especially after trivial injury. Early diagnosis is crucial because the earlier treatment is initiated, the better the response. The diagnosis is not always easy to make, however. An RSD score consisting of nine criteria has been proposed to aid in the diagnosis of RSD and to enhance comparisons of outcome studies.[39] The criteria are as follows: 1.
2. 3. 4. 5. 6.
Allodynia (pain resulting from non-noxious stimulation to the skin) or hyperpathia (pain persisting or increasing after mild or light pressure) Burning pain Edema Color or hair growth changes Sweating changes Temperature changes
Page 78
7. 8. 9.
Radiographic changes (i.e., demineralization) Quantitative measurement of vasomotor/sudomotor disturbance Triple-phase bone scan consistent with RSD
One point is given for each positive criterion, none if absent, and half a point if equivocal. Patients with more than five points are probable RSD patients. Pain that is abolished with temporary selective sympathetic blockade is another test that is highly suggestive of RSD.
Treatment Treatment of CRPS is controversial. Debate arises because randomized, placebo-controlled studies are lacking; individual response to treatment varies; and experts disagree regarding the pathogenesis of the disease. A multidisciplinary approach, including physical therapy and psychological counseling, is often necessary to treat CRPS.[40] For some patients, definitive treatment involves sympathetic blockade, usually with regional anesthesia and occasionally by surgical sympathectomy.[41] Oral medications, including calcitonin, indomethacin, tricyclic antidepressants, gabapentin, and others, have been used to treat RSD with variable success.[] In one study, vitamin C was shown to reduce the incidence of RSD after wrist fracture.[43]
Fat Embolism Syndrome Fat embolism refers to the presence of fat globules in the lung parenchyma and peripheral circulation after a long bone fracture or major trauma.[44] The phenomenon of fat embolization is probably common as a subclinical event after long bone fracture. Intravascular fat droplets appear in nearly one of five patients admitted with major trauma, although not all patients are symptomatic or require treatment. Fat embolism syndrome is a serious manifestation of fat embolism, occurring most commonly after long bone fractures (usually tibia and fibula) in young adults and after hip fractures in elderly patients. Symptoms usually appear 1 to 2 days after an acute injury or after intramedullary nailing. Respiratory distress syndrome is the earliest, most common, and most serious manifestation. Neurologic involvement, manifest as restlessness, confusion, or deteriorating mental status, also is an early sign, as are thrombocytopenia and a petechial rash. Fever, tachycardia, jaundice, retinal changes, and renal involvement may occur. Fat is seen in the urine in 50% of patients within 3 days of the injury. The incidence of full-blown fat embolism syndrome varies from 0.5% to 2% in patients with isolated long bone fractures to 5% to 10% in patients with multiple fractures. Management of fat embolism syndrome is primarily supportive, usually in an intensive care unit. No specific therapy has shown benefit.
Fracture Blisters Fracture blisters are tense blisters or bullae that accompany high-energy injuries in areas of relatively little skin coverage over a fracture site. The ankle, elbow, foot, and knee (in that order) are the most common sites; all of these contain fewer hair follicles and sweat glands to anchor together the epidermal-dermal junction than do other limb locations.[45] Fracture blisters are believed, in many cases, to occur in the setting of increased underlying tissue pressure and may be a harbinger of compartment syndrome. Early surgical intervention reduces the incidence of fracture blister formation.[45] In addition, the presence of a fracture blister requires an alteration of the surgical approach or a delay in surgery. Most experts discourage incisions through a fracture blister because such incisions seem to increase infection. Measures to perform early surgery after high-energy injuries and to minimize increases in tissue pressures might reduce the incidence of this complication. Intact blisters should be covered with povidone-iodine solution and a sterile dressing.
Complications of Immobilization Fractures frequently result in long periods of immobilization. Immobility may lead to multiple medical problems, especially in elderly patients, including pneumonia, deep venous thrombophlebitis, pulmonary embolism, urinary tract infection, wound infection, decubitus ulcers, muscle atrophy, stress ulcers, gastrointestinal hemorrhage, and psychiatric disorders ( Box 46-5 ). Early ambulation is a major goal of optimal orthopedic care. BOX 46-5
Page 79
Complications of Fractures and Immobility
Fractures Hem orrh age Vasc ular injuri es Nerv e injuri es Com part ment synd rom e Volk man n's isch emic contr actur e Avas cular necr osis Refl ex dystr ophy Fat emb olis m synd rom e
Immobility Pne umo nia Dee p veno us thro mbo sis
Page 80
Pul mon ary emb olis m Urin ary tract infec tion Wou nd infec tion Dec ubitu s ulcer s Mus cle atrop hy Stre ss ulcer s
Fracture Healing Specific fractures are discussed in subsequent chapters. In general, the goal is to realign bony fragments so that healing or union can take place, and normal function is restored. The process from fracture to union begins with a hematoma that bridges the fragments. The hematoma is followed by an inflammatory phase when granulation tissue forms on the fracture surfaces with resorption of the hematoma to provide the first continuity between the fragments. Callus subsequently is formed on the periosteal and endosteal surfaces of the bone, acting as a biologic splint. This area first becomes calcified by deposition of calcium phosphate, then undergoes osseous metaplasia. Callus is resorbed as the original fracture surfaces develop firm bony union. In some bones, such as the skull and the neck of the femur, where periosteum is deficient, there may be virtually no callus formation. The process finally ends with remodeling. On x-ray studies, at 10 to 14 days, the bone surrounding the fracture line becomes less dense because of localized bone resorption and hyperemia associated with the formation of granulation tissue. As a result, the fracture becomes considerably easier to visualize radiographically about 10 days after injury. After 2 to 3 weeks, soft tissue swelling has regressed, and callus first becomes visible, initially in a mottled pattern and then taking on a dense appearance. The callus undergoes organization, with peripheral margins becoming smooth. For a healthy adult, the whole process from injury to consolidation takes about 2 months for the humerus and about 4 months for a large bone such as the femur. Oblique fractures tend to heal more quickly than transverse fractures. Healing is quicker in children and slower in the elderly. The rate of fracture healing is affected by many factors, including the type of bone (cancellous bone heals faster than cortical bone); degree of fracture and opposition; and systemic states, such as hyperthyroidism or excess corticosteroidism. Exercise speeds healing, whereas chronic hypoxia has been known to slow repair. The presence of abundant callus seen on x-ray that is beginning to organize usually is associated with clinical union. If any suggestion of movement at the fracture site is noted on clinical examination, union must be regarded as inadequate. Several terms are used to denote abnormal union. Delayed union is union that takes longer than usual for a particular fracture location. Malunion occurs when a residual deformity exists. Nonunion is the failure of a fracture to unite. When nonunion results in a false joint, it is termed a pseudarthrosis. If the ends of the bone have remained constant on serial films and an adequate surrounding sheath of
Page 81
organizing callus can be seen, it is permissible for the patient to return to limited active use, even if the original fracture remains visible. The final process of consolidation develops later.
SUBLUXATION AND DISLOCATIONS Nomenclature Abnormal forces applied to joints may result in the loss of continuity between two articulating surfaces. Partial loss of continuity is termed subluxation, and complete loss is termed dislocation. In general, dislocations are named for the major joint involved, as in a dislocated shoulder or hip. In three-bone joints, the injury is named for the joint involved if the disturbance involves the two major bones, or, if the lesser bone is involved, the disturbance is named for that bone. Separation of the femur from the tibia is termed dislocation of the knee, whereas displacement of the patella from its normal articulation is termed dislocation of the patella ( Figure 46-10 ). At the elbow, separation of the olecranon from the humerus is a dislocation of the elbow, whereas separation of the radius from the humerus is termed radial head dislocation.
Figure 46-10 Dislocation of the patella.
Dislocations and subluxations should be described according to the direction of the distal segment relative to the proximal segment or of the displaced bone relative to the normal structures. The injury shown in Figure 46-11 is termed dorsal dislocation of the distal interphalangeal joint of the thumb. Disruption of articulation also may occur in combination with a fracture. The term fracture-dislocation is used to describe this combination. If the overlying skin is broken in any way, dislocations, subluxations, or fracture-dislocations are described as open and constitute the same emergency as does an open fracture alone.
Figure 46-11 Dorsal dislocation of the distal phalanx of the thum b.
Assessment In most cases of dislocation, severe to excruciating pain exists because the joint capsule is stretched or torn. Movement of the joint exacerbates the pain. This useful sign is lost in an obtunded, intoxicated, or unconscious patient and may lead to failure to diagnose if a careful survey is not performed. Some dislocations, such as anterior shoulder dislocation, have an obvious deformity, whereas others, such as posterior shoulder dislocation, may be subtle. Swelling of soft tissues also may obscure the diagnosis, such as in the tarsal-metatarsal region. Gentle passive testing of range of motion should be performed but never forced. Assessment for neurovascular function is similar to that for fracture. Certain dislocations (e.g., knee) are so commonly associated with vascular injuries that in many institutions arteriography is performed routinely in evaluating these injuries. Plain x-ray studies detect most dislocations, provided that the correct views are ordered. Radiographs should be performed before and after attempts at reduction of first-time or complicated dislocations to confirm the diagnosis and to ensure that associated fractures are documented before treatment is undertaken.
Treatment Methods of relocating specific joints are reviewed in subsequent chapters, but a few general principles apply. In general, the sooner a joint is relocated, the better. Later, swelling and muscle spasm make reduction more difficult. Also, pain is not adequately relieved until the dislocation is reduced. In the hip, early reduction is mandatory to restore vascular supply and to avert the complication of avascular necrosis. Before attempting relocation, adequate analgesia or conscious sedation should be used. Nerve blocks are
Page 82
especially useful on the digits. The general principle of reducing a dislocation is to recreate and reverse the mechanism of injury, pulling the proximal end of the dislocated bone out and away from whatever is trapping it in its final resting place. As this maneuver is accomplished, the disarticulated surface is manipulated back or may snap back spontaneously toward its normal anatomic position. If the reduction is difficult, it should not be forced. A single good attempt is better than repeated attempts in an inadequately relaxed patient. Some joints cannot be reduced in the emergency department because (1) the opposing muscles are contracting too forcefully and general anesthesia is necessary to overcome these forces or (2) mechanical obstruction by a bony fragment or a torn piece of cartilage, tendon, or joint capsule requires surgical removal for reduction to occur.[]
SOFT TISSUE INJURIES Sprains Nomenclature Ligamentous injuries resulting from an abnormal motion of a joint are termed sprains. A sprain is defined as injury to the fibers of a supporting ligament of a joint. Sprains may be graded according to the severity of pathologic findings; clinically, however, the grades are often indistinct. First-degree sprains are characterized by minor tearing of ligamentous fibers with resultant mild hemorrhage and swelling. Minimal point tenderness can be elicited. Stressing the ligament produces some pain, but there is no opening or abnormal joint motion. A second-degree sprain is a partial tear of a ligament, meaning more fibers are torn than in the first-degree injury. Clinical findings include moderate hemorrhage and swelling, tenderness, painful motion, abnormal motion, and loss of function. There may be a tendency toward persistent instability and recurrence, and prevention of these complications is a major goal of treatment. A third-degree sprain describes the complete tearing of a ligament. Signs include a further exaggeration of the signs mentioned for second-degree sprain. In addition, stressing the joint reveals grossly abnormal joint motion, provided that this is not limited by pain or swelling. Analgesia and the evacuation of a hemarthrosis may be used to allow a more complete diagnosis of these injuries. Chronic joint instability is the rule if severe ligamentous injuries do not heal properly.
Assessment The clinical presentation of a patient with a sprain of the extremity may be indistinguishable from that of a patient with a fracture. The injury frequently occurs during vigorous athletic activity when forces applied in opposite directions result in a joint being stressed in an abnormal or exaggerated direction. The patient may complain of hearing a “snap” or a “pop” at the moment of injury and conclude that a fracture must be present. Other patients report “seeing stars” or “almost passing out” at the moment the injury occurred and may still be in extreme pain, appearing pale and diaphoretic, if seen shortly after the injury. Analgesia should be provided to these patients. Evaluation should include a careful history of the exact sequence of events at the time of the injury and ascertaining the position of the extremity and the forces applied to it at that moment. A history of any audible sounds at the time of injury should be elicited. Examination of the joint should include stressing it to show abnormal motion. If radiographs are planned to rule out a fracture anyway or if exquisite pain is produced by mild attempts to apply stress, it is probably better to delay stressing until films have verified the absence of a significant fracture. Plain radiography is indicated in some, but not all, cases to rule out a fracture. It has been well shown that clinical decision rules can reduce the number of studies that are ordered without missing significant fractures.[] Avulsion fractures may occur concomitantly with sprains. In children, epiphyseal fractures occur more commonly than ligamentous disruption because of the relative ligamentous strength compared with the ease of disrupting the epiphyses. Arthroscopy or MRI is indicated in the follow-up evaluation of some of these injuries (e.g., for suspected cruciate tears) when significant pain or disability is present.[]
Treatment and Disposition Specific management of sprains varies depending on the location and severity of the injury. In general, initial measures should include the traditional recommendations of ice, elevation, and analgesia. Nonsteroidal anti-inflammatory drugs (NSAIDs) are effective analgesics in many patients, but their anti-inflammatory properties have never been shown to affect the underlying pathophysiology of, or recovery from, a sprain.[55] Immobilization is used to provide protection and comfort in the initial management of most injuries, using one of the following methods. Because the severity of injury is sometimes difficult to establish at the first visit, it is reasonable to immobilize the affected joint for the first 48 to 72 hours, after which the extent of injury can
Page 83
be better determined. At that time, early mobilization is often desirable, particularly in lateral ankle injuries because this leads to earlier return to work and athletic activities and better preservation of proprioceptive neuromuscular function.[] For lower extremity injuries, protected weight bearing with crutches provides patients with comfort and avoids motion of the impaired part. In elderly patients, safe ambulation sometimes cannot be accomplished, and a short hospitalization or admission to a skilled nursing facility may be necessary. For complete or nearly complete ligamentous disruption, urgent orthopedic consultation is usually mandatory. Less severe injuries can be followed up 3 to 7 days postinjury when acute swelling has subsided. Copies of x-ray films ordered in the emergency department should be sent with the patient if possible. Physical therapy and rehabilitative exercises sometimes are begun at these visits and carried on for several weeks. Because ligaments are relatively avascular, healing is slow, and patients with significant sprains should be informed of this. Sprains should be diagnosed as precisely as possible and should not be trivialized. Too often, after radiographs have ruled out fracture of an affected extremity, the term sprain is applied indiscriminately, or the patient is told that the injury is “only a sprain.” The expression “only a sprain” is misleading and should be avoided. Aside from creating false expectations regarding recovery, thoughtless mislabeling of injuries not in evidence may lead to missed occult fractures in adults or epiphyseal injuries in children.
Strains Nomenclature A strain is an injury to a musculotendinous unit resulting from violent contraction or excessive forcible stretch. The term pulled muscle sometimes is used interchangeably with muscle strain. These injuries are graded in a manner similar to sprains. A first-degree strain is a minor tearing of the musculotendinous unit, characterized by swelling, local tenderness, and minor loss of function. Findings increase along a continuum such that in a second-degree strain, more fibers are torn, but without complete disruption; swelling, ecchymosis, and loss of strength are more marked. In a third-degree strain, the muscle or tendon is completely disrupted, with resultant separation of muscle from muscle, muscle from tendon, or tendon from bone. An accompanying avulsion fracture may be present on radiographs in either second-degree or third-degree injuries.
Assessment Signs and symptoms include pain, ecchymosis, swelling, and loss of function. A force applied to the muscle, either passive stress or active contraction, produces sharp pain at the site of injury even as the injured muscle may be relatively comfortable at rest. A palpable defect sometimes is present at the site of a complete rupture, which usually involves the region of the muscle tendon junction, or a bunching up of the muscle may be appreciated.[] Among nonathletes, strains commonly are seen in patients who have either overstressed a muscle group or tried to generate excessive force in a nonconditioned muscle. Examples are the weekend gardener or mover who presents on Monday morning with lower back strain, the aerobics student who strains the rectus muscles, and the weightlifter who presents with chest wall pain resulting from pectoralis major strain. These are usually first-degree injuries, and the onset is slow. Rapid acceleration (e.g., in a tennis player) may result in a third-degree gastrocnemius or plantaris tear, whereas pushing off to jump is a common cause of ruptures of the Achilles tendon in a basketball player. A sudden violent attempt at lifting in an older individual can result in a complete biceps brachii disruption. Sudden generation of forces of which the thighs are capable results in second-degree strain of the hamstrings, quadriceps, or thigh abductor muscles. In athletes, generation of tremendous contraction forces coupled with excessive forcible stretching (while the body may be either accelerating or “planting”) results in severe strains. Involvement of almost any muscle group is possible, and the onset of such injuries is usually acute. Immediate removal from activity, application of ice, and rest of the affected limb for 48 to 72 hours usually are advised to prevent further injury. A competitive athlete usually is unable to continue anyway because of the accompanying loss of function. After a brief rest period, however, early mobilization and rehabilitation should be encouraged.
Treatment and Disposition Treatment depends on the degree of disruption, location, and functional loss. Most first-degree injuries respond in a few days to rest, application of ice, and, for some patients, analgesics. NSAIDs commonly are recommended and prescribed, although their efficacy for other than analgesic purposes is unproven. Second-degree strains are treated similarly, with protection against aggravating activity required for longer periods. Third-degree strains receive similar initial treatment in the emergency department plus early
Page 84
orthopedic consultation. Some of these injuries are amenable to surgical repair, whereas others may be treated with immobilization. The muscle affected and the age, occupation, and activity level of the patient all are factors in deciding whether surgical intervention is appropriate. Many athletes and their trainers believe and it is universally espoused that many strains can be prevented by proper training, warm-up, stretching exercises, and avoidance of overexertion, although limited scientific data exist to support these recommendations.[]
Tendinitis and Tendinosis Tendinitis is classically described as an inflammatory condition characterized by pain at tendinous insertions into bone, occurring in the setting of overuse.[] It is now believed that the pathophysiology of this condition is more complex than mere overuse, with the roles of load and use affecting cell-matrix interaction.[64] Etiologic factors are believed to include aging, with decreased blood supply and decreased tensile strength; muscle weakness and imbalance; insufficient flexibility; male gender; obesity (in weight-bearing joints); smoking; malalignments; training errors; and improper equipment.[] Additionally, certain systemic diseases, including diabetes mellitus, chronic renal failure, rheumatoid arthritis, and systemic lupus erythematosus; steroids; and occasionally fluoroquinolone use are associated with the development of tendinopathy.[67] With chronicity, involved tissues are characterized morphologically by signs of chronic rather than acute inflammation (infiltration by macrophages, plasma cells, and lymphocytes rather than leukocytes) and degeneration (cell atrophy). It also has been shown that prostaglandin E2 levels are normal.[68] This evolving understanding of tendinitis in the future should allow for more logical treatment of these injuries aimed at the underlying pathophysiology. It also has led some authors to propose that chronic painful conditions of the tendon should be referred to as tendinosis rather than tendinitis or other terms previously used to describe this condition, including tendonitis, degenerative changes, chronic tendonopathy, or partial rupture.[] In this chapter, tendinitis and tendinosis are used interchangeably. Common sites for tendinitis are the rotator cuff of the shoulder, the Achilles tendon, the radial aspect of the wrist (de Quervain's tenosynovitis), and the insertion of the hand extensors on the lateral humeral epicondyle (tennis elbow). Also commonly involved in athletes are the patellar tendon, particularly in athletes engaged in jumping sports; the biceps femoris, semitendinosus, and semimembranosus (hamstring syndrome); posterior tibial tendon (shin splint syndrome); the iliotibial band; and the common wrist flexors (medial epicondylitis) seen in little league pitchers and golfers.[64] In some locations, most commonly the shoulder, calcium deposition occurs along the course of the tendon, resulting in a painful condition termed calcific tendinitis. This condition also may occur in the wrist, hand, neck, hip, knee, ankle, or foot.[70] Physical examination reveals pain with motion and limitation of function and may include point tenderness and palpable crepitus over the involved tendon with motion. In general, a clinical test can be performed by forcible flexion of the involved muscle while keeping the point of insertion fixed or by operating the involved muscle against resistance. Either test should intensify the discomfort. Radiographs are usually negative. A small fleck of bone may suggest an avulsion, or the surface of the bone at the attachment may be roughened, indicating periostitis. As mentioned, there also may be calcium deposits along the course of the tendon, which should not be confused with an avulsion fracture. Ultrasound is sometimes useful in confirming the diagnosis of tendinitis. Although a normal tendon is characterized by a relatively homogeneous pattern, tendinitis is characterized by one or more of the following features: loss of the fibrillar echotexture, focal tendon thickening, diffuse thickening, focal hypoechoic area, irregular or ill-defined borders, or microruptures.[71] There is little evidence to support any specific treatment for tendinosis. The classic approach consists of rest, ice, and NSAIDs initially, followed by rehabilitation and training and control of force loads to prevent recurrences. Although NSAIDs may be useful for a brief period at the onset of symptoms for their analgesic effects, no evidence exists that they significantly alter the pathophysiology of this condition, and no rationale exists for ordering them in patients at any risk for complications from this class of drugs.[72] Peritendinous local infiltrations of anesthetics and corticosteroids may be useful, but should not be repeated too often because tendon rupture may occur. Injection therapy is especially useful in calcific tendinitis around the shoulder. Injection of steroids directly into the Achilles tendon should be avoided because of reports of partial or complete rupture after even a single injection. Some cases of calcific tendinitis that do not respond to conservative therapy may require either arthroscopic or open surgery.[]
Bursitis Bursitis is a painful inflammation of the bursa that may be either traumatic or infectious. Commonly involved
Page 85
sites include the olecranon, the greater trochanter of the femur, and the prepatellar and anserine bursae around the knee. Physical findings are tenderness and swelling over the involved bursa, whereas warmth and erythema may signal infection. If infection is suspected, aspiration with Gram stain and culture of the bursal fluid are recommended. Otherwise, treatment may be conservative and is similar to treatment for tendinitis. Most patients can be managed as outpatients.[75]
TREATMENT MODALITIES Splinting and Bandaging Fractures or dislocations that are suspected or confirmed should be splinted to avoid damage to muscles, nerves, vessels, and the skin. Splinting also may restore blood flow to ischemic tissue by removing pressure caused by a bone fragment resting against a blood vessel. Finally, splinting relieves pain; conversely, movement of fracture fragments results in severe pain.
Prehospital Care Splinting should begin in the prehospital setting. Numerous commercial devices are available, and most ambulances carry an assortment of immobilization devices ( Figure 46-12 ). Minimal equipment includes long and short backboards, cervical collars, sandbags, and extremity splints. A half-ring traction splint also is essential. Inflatable air splints are favored by some authors because they are convenient, easy to apply, transparent, and radiolucent and because they tamponade low-pressure bleeding. Other authors prefer to avoid these devices because theoretically they could contribute to the development of a compartment syndrome. If used, inflatable splints should be inflated only by mouth and to the point that still permits indentation by gentle finger pressure.
Figure 46-12 Com m ercial splints.
Field personnel should splint suspected fractures before the patient is moved. Severely angulated long bone fractures should be straightened in the prehospital setting before they are splinted. Splints should be applied in such a way as to immobilize the joints above and below the fracture site to avoid motion of the involved bone. The skin should be padded to avoid local necrosis, and the splint should be secured by a circumferential wrapping material. This material should allow for some expansion and should not be applied in a constricting manner.
Emergency Department Care In the emergency department, the indications for splinting are the same as in the field. All splints should be checked and, if properly applied, need not be changed. Splinting or other immobilization also is used after diagnosis and treatment of injuries. In some cases, a splint is all that is needed for definitive treatment. Injuries other than sprains and fractures (e.g., inflammatory and infectious processes, bites, burns, and repaired injuries of muscle bellies or tendons) also benefit from immobilization. Splints also can be used to improve function, such as with wristdrop that accompanies radial nerve palsy. When the injury is immobilized, it is important to stress elevation of the affected part to avoid edema formation. Many different devices and materials are available. Some devices that are commonly used are described next.
Upper Extremity Sling-and-Swathe and Velpeau Bandages Sling-and-swathe and Velpeau bandages are useful in immobilizing the shoulder, humerus, and elbow. They are commonly used after reduction of dislocated shoulders and to treat impacted fractures of the humeral neck. The axillae should be padded and powdered to avoid skin maceration. A commercial shoulder immobilizer also is available and is useful after reduction of a shoulder dislocation. Its advantages are ease of application and ease of removal and reapplication by the patient for bathing.
Clavicle Splint Historically, middle one third clavicle fractures routinely were initially treated with a figure-of-eight clavicle
Page 86
strap with or without the addition of a sling. This device is commercially available or can be fashioned from tubular stockinette. If used, a clavicle splint should be applied snugly enough to keep the shoulders back in the “at-attention” position, but not so tight as to compress the axillary artery or brachial plexus. Chafing of the skin can be avoided by padding and powdering the axillae. Superiority of the figure-of-eight clavicle strap over a simple sling has not been shown.
Plaster Splints Well-fitting, customized plaster splints can be fashioned easily to immobilize the elbow, forearm, wrist, and hand. The advantage of these splints is the ability to mold them to an exact size and shape (e.g., along the ulnar side of the forearm and hand to immobilize a midshaft fourth or fifth metacarpal fracture, the so-called gutter splint). Several commercially available products consist of multiple layers of plaster or fiberglass strips, inside a covering of foam and flannel, on a continuous roll that can be applied to any length. While the splint is still wet, a bandage is wrapped over it, and the splint is molded and held in the desired position as the plaster hardens.
Forearm and Wrist Splints Numerous preformed splints are available for splinting fractures of the distal forearm and wrist. They are lightweight, neat, and easy to apply and are easily removed and replaced by the patient ( Figure 46-13 ).
Figure 46-13 Wrist splints.
Lower Extremity Femur and Hip Fractures of the femoral shaft can be immobilized by using a traction device, such as the Hare traction splint or a similar appliance ( Figure 46-14 ). These devices should be applied in the prehospital setting if possible; most ambulances carry them. The principle is that a proximal ring engages the ischial tuberosity for countertraction while the longitudinal traction is applied through the ankle by means of an ankle hitch. A commercial ankle hitch is recommended, but if one is not available, an improvised hitch can be fashioned with a triangular bandage or a wide piece of cloth tied in a Collins hitch. The patient's ankle bones, Achilles tendon, and arch of the foot should be padded, and the circulation should be checked to ensure it is intact. A properly applied splinting device relieves pain from a fracture rather than exacerbating it.
Figure 46-14 A, Hare traction splint. B, This com m ercial hitch is designed to protect the ankle and heel during traction.
The Sager splint might offer advantages over other appliances in that it is applied to the medial and lateral aspect of the thigh, rather than having a half-ring posteriorly ( Figure 46-15 ). The Sager splint is more acceptable for use in the presence of pelvic fractures and avoids compression of the sciatic nerve. Because the half-ring devices may produce angulation at the fracture site, the Sager device is purported to result in better alignment, although this has never been measured. The Sager splint is shorter and more compact than the Hare traction splint, rendering it more acceptable for certain transport helicopters and body scanners. Also, the amount of traction is metered at the ankle, and overtraction can be avoided.
Page 87
Figure 46-15 A, Sager splint. B, Detail of distal splint end.
Skin traction using a pulley and hanging weights (Buck's traction and others) formerly was recommended for patients awaiting surgery for displaced hip fractures, allegedly to reduce pain and the need for analgesics. Studies have shown no benefit from this treatment, however, while citing risks to skin and soft tissue and noting that it is time-consuming to apply.[] Placing the affected leg in a comfortable position on a pillow provides more comfort.[76]
Knee Knee immobilizers are commercially available devices that can be used after acute injuries to provide firm but not rigid stabilization of the knee. The device is essentially a foam cylinder with medial and lateral aluminum stays, attached by Velcro straps, and spanning the upper thigh to upper ankle. This device is commonly used after trauma to let the knee “cool off” until a better physical examination or diagnostic study can be performed in a few days. Another dressing that may be applied at the knee is the Jones “compression” dressing. Some authors believe the word compression should not be used here to discourage application that is too tight. The Jones dressing is a bulky dressing that is used by some clinicians in situations when swelling is expected, including internal fixation procedures. The ability to flex and extend at the knee is maintained. The dressing consists of a thick layer of absorbent cotton bandage (Webril) wrapped with an elastic bandage, followed by another layer of cotton bandage, followed by an additional elastic wrap. If more stability is required, slabs of plaster can be placed on the medial and lateral side of the limb, just under the last bandage. Caution must be exercised because burns have been reported with this type of dressing when too many layers of plaster are used. A similar type of bulky dressing may be used for some injuries of the ankle and fractures of the calcaneus. In general, commercial knee immobilizers have replaced the Jones dressing in the treatment of acute knee injuries.
Ankle Immobilization of the ankle can be accomplished by numerous means. Plaster splints can be used temporarily for the treatment of nondisplaced ankle fractures or for the treatment of severe sprains. These can be fashioned in the same manner as described for the upper extremity. An alternative method is to apply a full circular cast, bivalve it on either side, discard the anterior piece, and affix the posterior mold with an elastic bandage or bias-cut stockinette. Most ankle injuries should be splinted with the patient's ankle in neutral position. Injuries to the Achilles tendon, plantaris muscle, or gastrocnemius muscle initially should be treated with the foot held in slight equinus (plantar flexion) for comfort. The toes should be free to move distal to the metatarsophalangeal joints, and the proximal border should end below the tibial tubercle to avoid pressure on the peroneal nerve. Adhesive strapping is an alternative method of ankle immobilization that provides good support and limitation of motion. Taping reportedly loses its “protective properties” with cyclic loading and sweating; although this is cited as a disadvantage, it may actually be helpful in encouraging and allowing early mobilization. This method is lightweight and not bulky, and a shoe can be worn over it. Tape is applied in a noncontinuous manner, which allows for swelling and avoids constriction. First, the hair is shaved. Next, strips of tape are measured and torn off; 1½-inch or 2-inch cloth-backed adhesive tape or Elastoplast is used. Elastoplast is an elastic-backed tape, constructed to stretch only in the longitudinal direction; this serves to spring the foot back automatically to a neutral position if the foot is plantar flexed for any reason. The tape should be applied directly to the skin after a skin adherent, such as tincture of benzoin, is applied. The tape should lie flat because wrinkles may damage the skin ( Figure 46-16 ).
Page 88
Figure 46-16 Application of adhesive strips to im m obilize the ankle.
A dome-paste bandage, or Unna's boot, is a bandage impregnated with zinc oxide, calamine lotion, glycerin, and gelatin that also is well suited to immobilize an ankle sprain.[79] This combination is gentle to the skin, which is especially important if atrophy or venous incompetence is present. In addition, hair need not be shaved, the bandage is easy to apply, and a shoe can be worn over it. Some patients complain about the sticky sensation against the skin, especially in warm weather. Another disadvantage is that it is applied concentrically, and problems can arise if the bandage is wrapped too tightly. The bandage should be applied directly to the skin, starting at the foot and working upward; it should overlap at each turn approximately half the width of the previous turn and continue up to just below the tibial tubercle. Then the bandage should be covered with either bias-cut stockinette or an elastic bandage. The dome-paste bandage hardens to about the consistency of sturdy cardboard and provides firm support. Removal is best accomplished with bandage scissors. An increasingly preferred device for moderate to severe lateral ankle sprains is a commercial support composed of molded plastic with Velcro straps (e.g., Air Cast, AirStirrup) ( Figure 46-17 ).[] This product may be worn in the patient's shoe and permits early weight bearing and return to activity. It is designed to permit dorsiflexion and plantar flexion but to limit inversion and eversion, a concept referred to as functional bracing. Some authors also find this device useful during athletic activities instead of adhesive taping to prevent recurrences.[] Although these orthoses are relatively expensive, the cost might be more than offset by their ease of application, their reusability, and the benefit derived from earlier return to work.[80]
Figure 46-17 Air cast. A, Lateral view. B, Anteroposterior view.
Severe ankle sprains also may benefit from immobilization in a cam walker, which is a commercial appliance consisting of a layer of padding extending from the tibial tubercle to the metatarsal heads, supported by metal plates along the length of the lower leg. These plates articulate with a molded hard plastic boot at the ankle. The position of the foot can be adjusted as desired, and when set, the ankle is kept firmly immobile. The rounded undersurface of the boot allows for ambulation without movement of the ankle joint.
Casts Plaster casts perform a function similar to splints in that they provide stability and pain relief. Casts sometimes are used in conjunction with internal stabilizing devices, such as Kirschner wires or Steinmann pins. Casts are not mandatory for all fractures, and in situations in which they are, application is usually not an immediate necessity. Swelling and subsequent pressure under the cast are highest during the first 24 hours after injury.[83] Plaster is applied as strips or rolls of cloth that are impregnated with a hemihydrate of calcium sulfate. When this cloth is dipped in lukewarm water, a creamy paste is formed that can be molded into a cast. An exothermic reaction takes place that causes the plaster to harden and can burn the skin.[84] Factors that have been shown experimentally to increase skin temperatures during plaster application are dip-water temperatures greater than 24°C, cast thickness greater than eight plies, and inadequate ventilation of the newly applied cast. Immersing the plaster in water for too short a time or squeezing too much water out also may lead to generation of excess heat. To avoid pressure on the skin and over bony prominences, stockinette and layers of cotton sheet wadding (Webril) are snugly applied first. Padding that migrates under a formed cast can be
Page 89
uncomfortable and result in pressure sores. Padding alone does not prevent burns.[85] Variations of the basic cast exist. A window may be placed in the cast, and the cutout area may be used as access to skin wounds that require care during immobilization. Walking heels may be worked onto a lower extremity cast and should be placed in the center of the foot. Synthetic casts (fiberglass and other materials) are lightweight, durable, and water resistant. In addition, their setting temperatures are significantly lower, and they are less likely to produce burns.[86] They are more expensive and more difficult to apply. Patients with casts may present to the emergency department for complaints related to their casts; these usually are pain, local irritation, swelling, or numbness of the distal part. A cast that is too tight results in swelling, pain, coolness, and change in skin color of the distal parts. Pain also may be caused by the initial injury or by local pressure, or it may be a result of a developing compartment syndrome or wound infection. The safest thing to do if a patient complains of pain is to bivalve the cast and inspect the extremity. This is done by cutting the plaster and the padding on each side and removing half the cast at a time, using the other half as a mold to keep the extremity immobile. Afterward, the bivalved cast can be held together with bias-cut stockinette or elastic wrap until a new cast is applied. If relieving external pressure does not alleviate symptoms, the diagnosis of compartment syndrome should be seriously considered. Casts may obscure wound infections, sources of sepsis, and even the source of tetanus. The clinician should not hesitate to bivalve the cast and inspect the extremity. The need for mandatory routine cast checks 1 day after initial application has been questioned.[87] In a retrospective study of 250 patients, none experienced problems from neurovascular compression, although 24% required some alteration of the cast. In the study, it may be simply that the casts were applied incorrectly in the first place. It is probably advisable to continue routine cast checks if casts are applied in the emergency department.
Thermal Therapy Some confusion exists as to the role of cryotherapy versus heat therapy in the treatment of acute orthopedic injuries, although the available literature uniformly favors cryotherapy. Part of this confusion arises because heat may be more soothing to the patient. Cryotherapy produces physiologic effects that favor a better prognosis. Cold causes vasoconstriction, limiting blood flow and hemorrhage into the traumatized area. Metabolic requirements are reduced in cooled tissues, as is histamine, and less capillary breakdown occurs as a result. Reduced blood flow also limits edema formation. Lower extravascular fluid pressure allows better lymphatic drainage of injured areas. Cryotherapy produces three, and perhaps four, stages of sensation of which the physician and the patient should be aware. In the first stage, a cold sensation is noted for 1 to 3 minutes. The second stage consists of a burning or aching sensation for 2 to 7 minutes after the application of cold. This stage is uncomfortable, but must be endured to receive the benefits of the next two stages. Heat therapy, by contrast, is soothing, and patients are likely to prefer this to the second stage of cryotherapy. The third stage begins 5 to 12 minutes after the application of ice and produces local numbness or anesthesia. The pain-spasm cycle is interrupted. While under this anesthetic effect, passive exercise may be desirable. This exercise helps to prevent atrophy, mobilize edema, clear injury debris, and reduce adhesions.[] A fourth stage sometimes occurs 12 to 15 minutes after intense cryotherapy is begun, consisting of reflex deep tissue vasodilation without a corresponding increase in metabolism (reminiscent of the situation in rewarming shock). Because of this, a maximum of 15 minutes of cold application per treatment usually is advised.[] An experimental study using triple-contrast bone scans compared the effect of icing times from 5 to 25 minutes on blood flow to the knee. Five minutes produced a measurable decrease in all tissues of the knee, whereas 25 minutes increased this effect fourfold and produced the overall maximal effects. A paradoxical increase in blood flow, perhaps reflecting reflex vasodilation, occurred at 10 minutes, but then reversed.[93] These results suggest that longer icing times than previously recommended may be beneficial. Absolute contraindications to cryotherapy include severe cold allergy (with hives and joint pain) and Raynaud's phenomenon. Relative contraindications include some rheumatoid conditions and paroxysmal cold hemoglobinuria with renal dysfunction and secondary hypertension. Anesthetic skin in a paralyzed or comatose patient is at risk with ice therapy. One case of gangrene has been reported, but in this instance cold was applied for 16 hours a day for 2 months.[94] These contraindications to cryotherapy are rare, especially in the athletic population most at risk for serious injuries. Heat increases blood flow and the inflammatory response and edema. Warm tissues and cells have a higher metabolic rate and increased requirements of nutrients and oxygen. Ice, rather than heat, is the method of choice of most authorities in the acute treatment and rehabilitation of acute orthopedic injuries and should be initiated as soon as possible for maximum benefit.
Page 90
KEY CONCEPTS {,
Com part ment synd rom e is asso ciate d most com monl y with a clos ed long bone fract ure of the tibia, but also is well desc ribed in the thigh , forea rm, arm, hand , and foot and can occu r with soft tissu e trau ma alon e. Elev ation of a limb with resul tant
Page 91
redu ction in the local arteri oven ous gradi ent may be coun terpr oduc tive and may exac erbat e com part ment synd rom e. {,
Bec ause of their bloo d supp ly, certa in bone s may unde rgo avas cular necr osis after fract ure, espe cially if fract ures are com minu ted and go untre ated
Page 92
for any lengt h of time. The femo ral head , talus , scap hoid, and capit ate are parti cular ly pron e to this com plica tion. {,
Fat emb olis m synd rom e is a serio us mani festa tion of fat emb olis m, occu rring most com monl y after long bone fract ures in youn g adult s (usu ally
Page 93
tibia and fibul a) and after hip fract ures in elder ly patie nts. Res pirat ory distr ess synd rom e is the earli est, most com mon, and serio us mani festa tion. Neur ologi c invol vem ent, mani fest as restl essn ess, conf usio n, or deter iorati ng ment al statu s, is also an early sign, as are
Page 94
{,
thro mbo cyto peni a and a pete chial rash. In child ren, epip hyse al fract ures occu r mor e com monl y than liga ment ous disru ption beca use of the relati ve liga ment ous stren gth com pare d with the ease of disru pting the epip hyse s.
Page 95
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/104.html/top
Page 96
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
REFERENCES 1. Courtenay BG, Bowers DM: Stress fractures: Clinical features and investigation. Med J Aust 1990;153:155. 2. Umans H, Pavlov H: Stress fractures of the lower extremities. Semin Roentgenol1994;29:176. 3. de Sancis N, Della Corte S, Pempinello C: Orthopaedics distal tibial and fibular epiphyseal fractures in children: Prognostic criteria and long-term results in 158 patients. J Pediatr Orthop2000;9:40. 4. Rogers LF, Poznanski AK: Imaging of epiphyseal injuries. Radiology1994;91:297. 5. Jaramillo D, Hoffer FA: Cartilaginous epiphysis and growth plate: Normal and abnormal MR imaging findings. AJR Am J Roentgenol1992;58:1105. 6. Reed MH: Fractures and dislocations of the extremities in children. J Trauma1977;17:351. 7. Mizuto T: Statistical analysis of the incidence of physeal injuries. J Pediatr Orthop1987;7:518. 8. Lund PJ: Comparison of conventional and computed radiography: Assessment of image quality and reader performance in skeletal extremity trauma. Acad Radiol1997;4:570. 9. Chacon D: Use of comparison radiographs in the diagnosis of traumatic injuries of the elbow. Ann Emerg Med1992;21:895. 10. Keats TE, Anderson MW: Atlas of Normal Roentgen Variants That May Simulate Disease, 7th ed. St Louis, Mosby, 2001. 11. Conway JJ: The role of bone scintigraph in detecting child abuse. Semin Nucl Med1993;23:321. 12. Sorger JI: Once daily, high dose versus divided, low dose gentamicin for open fractures. Clin Orthop 1999;366:197. 13. Vasenius J: Clindamycin versus cloxacillin in the treatment of 240 open fractures: A randomized prospective study. Ann Chir Gynaecol1998;87:224. 14. Patzakis MJ, Wilkins J, Moore TM: Considerations in reducing the infection rate in open tibial fractures. Clin Orthop1983;178:36. 15. Kreder HJ, Armstrong P: The significance of perioperative cultures in open pediatric lower-extremity fractures. Clin Orthop1994;302:206. 16. Juren CT, Di Stadio AJ: Treatment of grade IIIB and IIIC open tibial fractures. Orthop Clin North Am 1994;25:561. 17. O'Riain S: New and simple test of nerve function in hand. BMJ1973;3:615. 18. Good LP: Compartment syndrome. AORN J1992;56:904. 19. Weinstein SM, Herring SA: Nerve problems and compartment syndromes in the hand, wrist, and forearm. Clin Sports Med1992;11:161. 20. McGee DL, Dalsey WC: The mangled extremity: Compartment syndrome and amputations. Emerg Med Clin North Am1992;10:783. 21. Myerson M, Manoli A: Compartment syndromes of the foot after calcaneal fractures. Clin Orthop 1993;142:142-150. 22. Kahan JS: Acute bilateral compartment syndrome of the thigh induced by exercise. J Bone Joint Surg 1994;76A:1068. 23. Hastings II IIH, Misamore G: Compartment syndrome resulting from intravenous regional anesthesia. J Hand Surg1987;12A:559. 24. Reddy PK, Kaye KW: Deep posterior compartment syndrome: A serious complication of the lithotomy position. J Urol1984;132:144. 25. Aschoff A, Steiner-Milz H, Steiner HH: Lower limb compartment syndrome following lumbar discectomy in the knee-chest position. Neurosurg Rev1990;13:155. 26. Gulli B, Templeman D: Compartment syndrome of the lower extremity. Orthop Clin North Am 1994;25:677. 27. Whitesides Jr JrTE: Tissue pressure measurement as a determinant for the need of fasciotomy. Clin Orthop1975;113:43. 28. McQueen MM, Gaston P, Court-Brown CM: Acute compartment syndrome: Who is at risk?. J Bone Joint Surg Br2000;82:200. 29. Lu-Yao GL: Outcomes after displaced fractures of the femoral neck: A meta-analysis of one hundred and six published reports. J Bone Joint Surg1994;76:15.
Page 97
30. Coombs RR, Thomas RW: Avascular necrosis of the hip. Br J Hosp Med1994;51:275. 31. Proctor MT: Non-union of the scaphoid: Early and late management. Injury1994;25:15. 32. Yoo CI: Avascular necrosis after fracture-separation of the distal end of the humerus in children. Orthopedics1992;15:959. 33. Rowbotham M: Complex regional pain syndrome type I (reflex sympathetic dystrophy): More than a myth. Neurology1998;51:4. 34. Stanton-Hicks M, Janig W, Hassenbusch S: Reflex sympathetic dystrophy: Changing concepts and taxonomy. Pain1995;63:127. 35. Rogers JN, Valley MA: Reflex sympathetic dystrophy. Clin Podiatr Med Surg1994;11:73. 36. Veldman P, Reynan HM, Arntz IE: Signs and symptoms of reflex sympathetic dystrophy: Prospective study of 829 patients. Lancet1993;342:1012. 37. Van der Laan L: Complex regional pain syndrome type I (RSD): Pathology of skeletal muscle and peripheral nerve. Neurology1998;51:20. 38. Murray CS: Morbidity in reflex sympathetic dystrophy. Arch Dis Child2000;82:231. 39. Gibbons JJ, Wilson PR: RSD score: A criterion for the diagnosis of reflex sympathetic dystrophy and causalgia. Clin J Pain1992;8:260. 40. Oerlemans HM, Oosteodorp RA, de Boo T, Goris RJ: Pain and reduced mobility in complex regional pain syndrome I: Outcome of a prospective randomized, controlled clinical trial of adjuvant physical therapy versus occupational therapy. Pain1999;83:77. 41. Tountas AA, Noguchi A: Treatment of post-traumatic reflex sympathetic dystrophy (RSDS) with intravenous blocks of a mixture of corticosteroid and lidocaine: A retrospective review of 17 consecutive cases. J Orthop1991;5:412. 42. Kingery WS: A critical review of controlled clinical trials for peripheral neuropathic pain and complex regional pain syndromes. Pain1997;73:123. 43. Zolinger PE: Effect of vitamin C on frequency of sympathetic reflex dystrophy in wrist fractures: A randomized trial. Lancet1999;354:2025. 44. Bulger EM, Smith DG, Maier RV: Fat embolism syndrome: A 10 year review. Arch Surg1997;132:435. 45. Varela CD: Fracture blisters: Clinical and pathological aspects. J Orthop Trauma1993;7:417. 46. Rodriguez-Merchan EC: Controversies on the treatment of irreducible elbow dislocations with an associated nonsalvageable radial head fracture. J Orthop Trauma1995;9:341. 47. Sabapathy SR, Bose VC, Rex C: Irreducible dislocation of the interphalangeal joint of the thumb due to sesamoid bone interposition: A case report. J Hand Surg1995;20:487. 48. Stiell IG: A study to develop clinical decision rules for the use of radiography in acute ankle injuries. Ann Emerg Med1992;21:384. 49. Stiell IG: Decision rules for the use of radiography in acute ankle injuries: Refinement and prospective validation. JAMA1993;269:1127. 50. Stiell IG: Implementation of the Ottawa ankle rules. JAMA1994;271:827. 51. Stiell IG: Implementation of the Ottawa knee rule for the use of radiology in acute knee injuries. JAMA 1997;278:2075. 52. Maffulli N: Acute haemarthrosis of the knee in athletes: A prospective study of 106 cases. J Bone Joint Surg1993;75B:945. 53. Fanelli GC: Posterior cruciate ligament injuries in trauma patients. Arthroscopy1993;9:291. 54. Ruwe PA: Can MR imaging effectively replace diagnostic arthroscopy?. Radiology1992;183:335. 55. Dupont M, Beliveau P, Theriault G: The efficacy of antiinflammatory medication in the treatment of the acutely sprained ankle. Am J Sports Med1987;15:41. 56. Konradsen L, Holmer P, Sanderguard L: Early mobilizing treatment for grade III ankle ligament injuries. Foot Ankle1991;12:69. 57. Scheuffelen C: Orthotic devices in functional treatment of ankle sprain: Stabilizing effects of real movements. Int J Sports Med1993;14:140. 58. Safran MR: The role of warmup in muscular injury prevention. Am J Sports Med1988;16:123. 59. Garrett WE: The effect of muscle architecture on the biochemical failure properties of skeletal muscle under passive extension. Am J Sports Med1988;16:7. 60. Arrington ED, Miller MD: Skeletal muscle injuries. Orthop Clin North Am1995;26:411. 61. Worrell TW: Factors associated with hamstring injuries: An approach to treatment and preventative measures. Sports Med1994;17:338. 62. Guidotti TL: Occupational repetitive strain injury. Am Fam Physician1992;4:585. 63. Nirschl RP: Elbow tendinosis/tennis elbow. Clin Sports Med1992;11:851. 64. Leadbetter WB: Cell-matrix response in tendon injury. Clin Sports Med1992;11:533. 65. Alfredson A, Lorentzon R: Chronic achilles tendinosis: Recommendations for treatment and prevention. Sports Med2000;29:135. 66. Fenwick SA, Hazleman BL, Graham PR: The vasculatureand its role in the damaged and healing tendon. Arthritis Res2002;4:252. 67. Zabraniecki L: Fluoroquinolone induced tendinopathy: Report of 6 cases. J Rheumatol1996;23:516.
Page 98
68. Alfredson H: In situ microdialysis in tendon tissue: high levels of glutamate but not prostaglandin E2 in chronic Achilles tendon pain. Knee Sports Surg Traumatol Arthosc1999;7:378. 69. Maffulli N, Wong J, Almekinders LC: Types and epidemiology of tendinopathy. Clin Sports Med 2003;22:675. 70. Holt PD, Keats TE: Calcific tendinitis: A review of the usual and unusual. Skeletal Radiol1993;22:1. 71. Grassi W: Sonographic imaging of tendons. Arthritis Rheum2000;43:969. 72. Astrom M, Westlin N: No effect of piroxicam on Achilles tendinopathy: A randomized study of 70 patients. Acta Orthop Scand1992;63:631. 73. Weiler JM: Medial modifiers of sports injury: The use of nonsteroidal anti-inflammatory drugs in sports soft tissue injury. Clin Sports Med1992;11:625. 74. Read MTF, Motto SG: Tendo achillis pain: Steroids and outcome. Br J Sports Med1992;26:15. 75. Stell I: Management of acute bursitis: Outcome study of a structured approach. J R Soc Med 1999;92:5216. 76. Finsen V: Preoperative traction in patients with hip fractures. Injury1992;23:242. 77. Needoff M, Radford P, Langstaff R: Preoperative traction for hip fractures in the elderly. Injury 1993;24:317. 78. Anderson GH: Preoperative skin traction for fractures of the proximal femur: A randomized prospective trial. J Bone Joint Surg1993;75:794. 79. Pointer J: Using an Unna's boot in treating ligamentous ankle injuries. West J Med1983;139:257. 80. De Maio M, Paine R, Dreg Jr JrD: Chronic lateral ankle instability-inversion sprains: Part I. Orthopedics 1992;15:87. 81. Gross MT: Comparison of support provided by ankle taping and semirigid orthosis. J Orthop Sports Phys Ther1987;9:33. 82. Rovere GD: Retrospective comparison of taping and ankle stabilizers in preventing ankle injuries. Am J Sports Med1988;16:228. 83. Patrick JH, Levack B: A study of pressures beneath forearm plasters. Injury1987;13:37. 84. Kaplan SS: Burns following application of plaster splint dressings. J Bone Joint Surg1981;63:670. 85. Lavalette R, Pope MH, Dickstein H: Setting temperatures of plaster casts: The influence of technical variables. J Bone Joint Surg1982;64:907. 86. Pope MH, Callahan G, Lavalette R: Setting temperatures of synthetic casts. J Bone Joint Surg 1985;67:262. 87. Riding G, Edgel M, James M: Plaster checks: A waste of resources?. J Accid Emerg Med1994;11:266. 88. Hocutt JE: Cryotherapy in ankle sprains. Am J Sports Med1982;10:316. 89. McMaster WC: A literary review on ice therapy in injuries. Am J Sports Med1977;5:124. 90. Basur RL, Sheperd E, Mouzas GL: A cooling method in the treatment of ankle sprains. Practitioner 1976;216:708. 91. Riverburgh DW: Physical modalities in the treatment of tendon injuries. Clin Sports Med1992;11:645. 92. Ernot E, Fialka V: Ice freezes pain? A review of the clinical effectiveness of analgesic cold therapy. J Pain Symptom Manage1994;9:56. 93. Ho SS: Comparison of various icing times in decreasing bone metabolism and blood flow in the knee. Am J Sports Med1995;23:74. 94. Fye KH, Denkler K: Gangrene as a complication of topical ice therapy [letter]. J Rheumatol1993;20:1808.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/105.html/top
Page 99
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
Chapter 47 – Hand Everett Lyn Robert E. Antosia
PERSPECTIVE The hand is intricate, dynamic, and unique in function. It combines extreme mobility, precision, power, and sensation and is used to express and execute. Because the hands are more exposed to the environment than the rest of the body, they are commonly injured. Function depends on intact relationships between intrinsic structural components, musculotendinous units originating from more proximal areas, and motor and sensory connections with the central nervous system. Restoration of function rather than appearance is the primary goal in management of hand injuries and infections. Early recognition and timely initiation of therapy for limb-threatening conditions are essential to outcome. The fate of the hand largely depends on the physician who initially cares for it. Mismanagement may result in unnecessary functional loss that may not be recoverable, even with the best convalescent care. An understanding of the functional anatomy of the hand is necessary for the appropriate evaluation and management of these disorders.
Epidemiology Overall, hand injuries are reported to represent 5% to 10% of emergency department visits, and approximately 6% of these patients have deep, significant injuries.[1] Injuries have environmental, occupational, and recreational causes and are seen in all age groups. The spectrum of injury includes infections, lacerations, fractures, crush wounds, amputations, and burns. It is estimated that 10% of all patients with hand injuries require referral to a hand specialist, and most patients referred from emergency departments have fractures.[2] The disability potential of hand injuries is generally high and may result from loss of strength, flexibility, or sensation. Data suggest that hand injuries account for 19% of lost-time injuries and 9% of workers' compensation cases.[3] Approximately 3 to 4 million working days are lost each year as a result of hand injuries.[4] Overall, hand and fingers are the most frequent body parts injured in the workplace and cared for in emergency departments.[5]
PRINCIPLES OF DISEASE, FUNCTIONAL ANATOMY, PHYSIOLOGY, AND EXAMINATION OF THE HAND Terminology To avoid confusion, it is important that standard terminology for the surface anatomy of the hand be used ( Figure 47-1 ). The back of the hand and fingers is called the dorsal surface, and the palm side is called either the palmar or the volar surface. The borders of the hand are radial and ulnar. The five digits often are designated by numerals, but common names are preferable: I (thumb), II (index finger), III (long or middle finger), IV (ring finger), and V (little finger). Each finger has three joints: the metacarpophalangeal (MCP), the proximal interphalangeal (PIP), and the distal interphalangeal (DIP) joints. The thumb has an MCP joint and only one interphalangeal (IP) joint. There are proximal, middle, and distal phalanges in the fingers and only a proximal and a distal phalanx in the thumb. The thenar mass or eminence refers to the muscular area on the palmar surface overlying the thumb metacarpal. The hypothenar eminence is the muscle mass on the palmar surface overlying the little finger metacarpal.
Figure 47-1 .Surface anatom y of the hand. ((From Burton RI, et al: The Hand: Exam ination and Diagnosis, 3rd ed. New York,
Page 100
Churchill Livingstone, 1990, p 6.)Churchill Livingstone)
Hand and digit motion is standardized and is illustrated in Figures 47-2 through 47-6 . The carpometacarpal (CMC) joint is more mobile in the thumb than in the other fingers and is the key to the grasp and dexterity that characterize the human hand. Motions of this joint include palmar abduction (also called flexion), radial abduction, retroposition (extension), adduction, and opposition (see Figure 47-6 ). The IP joints are essentially hinge joints and are capable of only two motions: flexion and extension.
Figure 47-2 Pronation and supination of the hand.
Figure 47-3 Ulnar and radial deviation of the hand.
Figure 47-4 Wrist extension and flexion.
Figure 47-5 Finger flexion is volar and occurs at the m etacarpophalangeal joint; extension and hyperextension are as shown.
Figure 47-6 Perpendicular view of thum b m obility.
Page 101
Structural Framework Skin Cover The hand has two skin surfaces, each with differing functions. The skin of the palm is thick compared with the dorsal skin and is stabilized by fibrous connections on its deep surface. The skin creases in the palmar aspect of the hand are largely transverse and represent adherence between skin and underlying fascia, without intervening adipose tissue. These features facilitate flexion and limit the development of inflammatory edema in the palm.[6] The other noteworthy characteristic of the palmar skin is the unique arrangement of epithelial ridges of the dermis that form cutaneous striations. They have forensic importance in the pulp as “fingerprints” and play an important role in increasing friction when grasping objects.[7] The dorsal skin is relatively thin and mobile, permitting motion of the various joints. As a path of least resistance, the dorsum of the hand also swells easily after inflammation or trauma and may limit flexion of the MCP joints.[7] In addition, infection in the palmar aspect of the hand may cause dorsal swelling and can be misleading without a careful physical examination.
Skeleton The hand and wrist contain 27 bones: 14 phalangeal bones, 5 metacarpal bones, and 8 carpal bones ( Figure 47-7 ). There are eight small carpal bones in the region of the wrist that are strongly united to one another by ligaments. These bones form synovial joints and are arranged in two rows, proximal and distal, with four bones in each row. Together the bones of the carpus present a concavity on their volar surface, which is bridged by a strong membranous band, the flexor retinaculum. In this way, the bridge and the bones form a tunnel, known as the carpal tunnel, through which passes the median nerve and long flexor tendons of the fingers. The IP joints are inherently more stable than the MCP joint, by virtue of their bicondylar configuration, which gives a modified tongue-in-groove appearance ( Figure 47-8 ).
Figure 47-7 Posteroanterior radiograph of the wrist and hand with the forearm pronated. ((From Snell RS, Sm ith MS: Clinical Anatom y for Em ergency Medicine. St. Louis, Mosb y, 1993, p 650.)Elsevier Inc.)
Figure 47-8 The m etacarpophalangeal (MP) and proximal interphalangeal (PIP) joints are quite different structurally. The PIP joint has a bicondylar configuration, m aking it inherently m ore stable than the globular MP joint. ((From DeLee JC, Drez D Jr: Orthopedic Sports Medicine: Principles and Practice, 2nd ed. Philadelphia, Saunders, 2003.)Elsevier Inc.)
The soft tissue supporting these joints includes the capsular ligamentous structures, which afford stability, and the tendinous structures, which generate mobility. The metacarpal and IP joints are stabilized on both sides by collateral ligaments and anteriorly by a palmar fibrocartilaginous “volar plate.” Because of anatomic differences between the metacarpals and phalanges, the IP collaterals are tight throughout the entire range of motion, whereas the collaterals of the MCP joint are tightest in flexion ( Figure 47-9 ). The IP joints are hinges, but the MCP joint has additional side-to-side mobility and rotational movement to facilitate efficient grasp.[7] The clinical importance of these differences is that to minimize the development of contractures after joint injuries, the preferred position of immobilization of the PIP joints is extension, whereas the MCP joints are more properly placed in flexion.
Page 102
Figure 47-9 The shape of the m etacarpal head is eccentric, resulting in a cam effect that m akes the collateral ligam ents m ore taut in flexion than in extension. Distance A-A1 is less than A-A2. The cam effect is not present in the proxim al interphalangeal joint. ((From DeLee JC, Drez D Jr: Orthopedic Sports Medicine: Principles and Practice, 2nd ed. Philadelphia, Saunders, 2003.)Elsevier Inc.)
The structure and arrangement of the metacarpals are noteworthy. The metacarpals participate in three arches: the proximal (carpal) and distal (metacarpal) transverse arches and the longitudinal arch ( Figure 47-10 ).[8] The index and long finger metacarpals form a fairly immobile segment because of their ridged articulation with the carpals. The adjacent metacarpals are more mobile. This unique anatomy gives the human palm a longitudinal and transverse concavity when the thumb is alongside the index finger; however, this changes to an oblique gutter when the thumb is extended.
Figure 47-10 The three arches of the m etacarpals. A, Sagittal view. B, Transverse view. ((From Am erican Society for Surgery of the Hand: Regional Review Course in Hand Surgery Syllab us, 10th ed. Aurora, Colo, ASSH, 1990.)ASSH)
The small bones of the child's hand differ significantly from the bones of adults and from other long bones because of the presence of an epiphysis or growth plate at one end of the bone. The phalangeal epiphyses and the thumb metacarpal epiphysis occur at the proximal end, and the finger metacarpal epiphyses are located at the distal end of the bone ( Figure 47-11 ). In boys, the proximal phalangeal epiphysis appears at 15 to 24 months and fuses at 16 years. In girls, it appears at 10 to 15 months and fuses at 14 years.[9] The time of appearance and fusion are related to skeletal maturity and can be judged accurately until puberty from hand and wrist radiographs because the sequence of development is age specific.[10]
Figure 47-11 Norm al location of the epiphysis of the hand. All of the phalangeal epiphyses are located at the proximal end. The m etacarpophalangeal epiphyses all are distally situated, however, except for that of the wrist, which is proxim al. ((From Harris WH, Harris CC: The Radiology of Em ergency Medicine. Baltim ore, William s & Wilkins, 1993, p 440)William s & Wilkins)
Muscle and Tendon Function The muscles that power the hand may be divided into extrinsic and intrinsic muscles. The intrinsic muscles have their origins and insertions within the hand. The extrinsic muscles have origins in muscle bellies in the forearm and tendinous insertions on bones in the hand. They are divided further into extrinsic flexor and extensor muscles. The flexors of the digits in the hand lie on the volar surface of the forearm; the extensors
Page 103
are on the dorsal surface.
Intrinsic Musculature The intrinsic muscles of the hand include the muscles of the thenar and hypothenar eminences, the adductor pollicis, the interossei, and the lumbricals ( Figure 47-12 ). The thenar muscles cover the thumb metacarpal. This group includes the abductor pollicis brevis, opponens pollicis, and flexor pollicis brevis. These muscles originate in the flexor retinaculum and on the carpal bones and insert at the base of the first metacarpal and first proximal phalanx. They act in concert with the long flexors and extensors to carry the thumb through its intricate range of motion. The muscles are evaluated by palpating the thenar eminence for contraction as the patient touches the tips of the thumb and little finger. They also can be tested by asking the patient to place the dorsum of the hand on a flat surface and to raise the thumb up straight to form a 90-degree angle with the palm. The thenar muscles usually are innervated by the motor branch of the median nerve. In some cases, they may be partially innervated by the ulnar nerve.
Figure 47-12 Anterior view of the palm of the hand. The palm ar aponeurosis and the greater part of the flexor retinaculum have been rem oved to display the m edian nerve, the long flexor tendons, and the lum brical m uscles. Segm ents of the tendons of the flexor digitorum superficialis m uscle have been rem oved to show underlying tendons of the flexor digitorum profundus m uscles. ((From Snell RS, Sm ith MS: Clinical Anatom y for Em ergency Medicine. St. Louis, Mosb y, 1993, p 641.)Elsevier Inc.)
The adductor pollicis arises from the second and third metacarpals and inserts on the first proximal phalanx. This muscle is innervated by the ulnar nerve. Thumb adduction is tested separately by having the patient forcibly hold a piece of paper between the thumb and radial side of the index proximal phalanx. If the adductor pollicis is weak or nonfunctioning, the thumb IP joint flexes with this maneuver (Froment's paper sign).[11] In this evaluation, the two hands should be compared. The lumbrical muscles arise from the sides of the flexor digitorum profundus (FDP) tendons; the interossei muscles lie between the metacarpal bones and originate from them. Both of these muscle groups insert in the extensor expansions of digits II to V and act on the fingers to flex the MCP joints and extend the IP joints. The radial two lumbricals are innervated by the median nerve, and the ulnar two are innervated by the ulnar nerve. The seven interossei (three palmar and four dorsal) can be considered together. They lie on either side of the finger metacarpals and are innervated by the ulnar nerve. The dorsal interossei muscles abduct the fingers away from the midline; the volar muscles adduct the fingers. For an accurate test that isolates their function from the extrinsic muscles, the patient should place the palm flat on a table, extend the digit, and move it from side to side. The hypothenar group of intrinsic muscles includes the opponens digiti minimi, the flexor digiti minimi, and the abductor digiti minimi. These muscles arise from the carpal bones and in the flexor retinaculum and insert on the proximal phalanx and metacarpal of the little finger. The flexor and abductor flex the proximal phalanx and abduct the little finger. The three muscles are evaluated as a group by having the patient place the wrist in a neutral position and abduct the little finger (move it away from the other fingers) against resistance. This muscle mass is palpated at that time, and a dimpling of the hypothenar skin is noted. All the intrinsic muscles of the little finger are innervated by the ulnar nerve.
Extensor Tendons The extensor tendons are on the dorsal side of the forearm, wrist, and hand. The nine extensor tendons cross the wrist joint dorsal to its axis of rotation, pass under the extensor retinaculum, and are separated on the dorsum of the hand by a series of six fibro-osseous canals or compartments. Figure 47-13 outlines the compartments and their contents. The fibrous roof of these compartments prevents the tendons from bowstringing dorsally during active finger extension, particularly when the wrist also is extended.
Page 104
Figure 47-13 A, The extensor tendons gain entrance to the hand from the forearm through a series of six canals, five fibro-osseous and one fibrous (the sixth dorsal com partm ent, which contains the extensor digiti quinti proprius [EDQP]). The first com partm ent contains the abductor pollicis longus (APL) and extensor pollicis brevis (EPB); the second, the radial wrist extensors; the third, the extensor pollicis longus (EPL), which angles around Lister's tubercle; the fourth, the extensor digitorum com m unis (EDC) to the fingers and the extensor indicis proprius (EIP); the fifth, the EDQP; and the sixth, the extensor carpi ulnaris (ECU). The com m unis tendons are joined distally near the m etacarpophalangeal joints by fibrous connections called juncturae tendinum . Beneath the retinaculum , the extensor tendons are covered with a synovial sheath. B, The proprius tendons to the index and little fingers are capable of independent extension, and their function may be evaluated as depicted. With the m iddle and ring fingers flexed into the palm , the proprius tendons can extend the ring and little fingers. ECRB, extensor carpi radialis brevis; ECRL, extensor carpi radialis longus. ((From Doyle JR: In Green DP [ed]: Operative Hand Surgery. New York, Churchill Livingstone, 1993, p 1927.)Churchill Livingstone)
The first dorsal wrist compartment contains the tendons of the abductor pollicis longus, which inserts at the dorsal base of the thumb metacarpal, and the extensor pollicis brevis, which inserts on the proximal phalanx of the thumb. The abductor pollicis longus serves to abduct the first ray radially, and the extensor pollicis brevis acts primarily to extend the ray at the MCP joint. These tendons are evaluated by having the patient abduct and extend the thumb with resistance applied to the thumb; they can be palpated on the radial side of the wrist during this maneuver. Two tendons lie in the second compartment: the extensor carpi radialis longus and brevis. These tendons insert at the dorsal base of the index and middle metacarpals. They act primarily to extend and deviate the wrist radially. These tendons can be palpated by having the patient extend the wrist against resistance while making a fist. In the third compartment, a single tendon, the extensor pollicis longus, arises from the deep muscles of the midforearm, passes around a bony prominence on the dorsum of the wrist termed Lister's tubercle, and inserts on the base of the distal phalanx of the thumb. This tubercle can be palpated just proximal to the wrist joint. The extensor pollicis longus forms the dorsal border of the anatomic snuff-box, and the abductor pollicis longus forms the volar border ( Figure 47-14 ). The floor of this area contains the radial artery and two carpal bones, the scaphoid and trapezium. The extensor pollicis longus functions to extend and adduct the entire first ray and extend and hyperextend the IP joint of the thumb. This muscle is evaluated by placing the hand flat on a table and having the patient lift only the thumb off the surface. Because the abductor pollicis brevis and the adductor pollicis add terminal extension, complete laceration of the extensor pollicis longus tendon may not eliminate the patient's ability to extend the thumb.[12]
Figure 47-14 Surface anatom y of the wrist and hand. The tendons that are palpated with the thum b abducted and extended form an anatom ic snuff-box.
The tendons that extend the fingers—the extensor indicis proprius and the extensor digitorum communis— are in the fourth compartment. The extensor digitorum muscle divides into four tendons proximal to the wrist. In the dorsum of the hand, these tendons are connected by juncturae, which help stabilize them to their insertions in the extensor expansions of digits II to V. The tendon to the index finger is joined on its radial side by the tendon of the extensor indicis proprius. The tendon to the little finger is joined on its ulnar side by two slips from the extensor digiti minimi. The extensor digiti minimi is contained in the fifth dorsal compartment and lies ulnar to the small finger extensor. The extensor indicis lies ulnar and deep to the index extensor. The dual extensor system for the index and small fingers gives these two digits extension independent of the
Page 105
other digits. The middle finger and especially the ring finger have considerably limited independent extension. The restrictive motion is due to the junctura, which also prevents retraction of the proximal tendon end after distal division of an extensor. Complete division of an extensor proximal to the junctura can be associated with normal MCP joint extension.[7] This extension occurs through the junctura connection. The extensor digitorum communis tendons can be evaluated by asking the patient to straighten out all of the fingers. The function of the extensor indicis proprius can be isolated from the common extensors by asking the patient to make a fist and then to point the second digit. The extensor digiti minimi is examined by having the patient straighten the little finger while the hand is closed into a fist. The extensor mechanism of each digit is a complex interrelationship of muscle tendon units of the long extrinsic extensor tendons and the intrinsic system ( Figure 47-15 ). The extensor expansion divides into a central slip that attaches to the middle phalanx and two lateral bands that join with the tendons of the lumbrical and interosseous muscles and attach to the base of each distal phalanx. The interossei and lumbrical muscles insert in the lateral aspects of the dorsal hood. Most of the power of the common extensors serves to extend the MCP joint. Distal digit extension is provided by continuation of the lateral band mechanism and the oblique retinacular ligament. Because of this complex anatomy, injuries involving the extensor mechanism require meticulous repair.
Figure 47-15 The extensor tendon at the m etacarpophalangeal (MP) joint level is held in place by the transverse lamina or sagittal band, which tethers and centers the extensor tendons over the joint. This sagittal band arises from the volar plate and the interm etacarpal ligam ents at the neck of the m etacarpals. Any injury to the extensor hood or expansion m ay result in subluxation or dislocation of the extensor tendon. The intrinsic tendons from the lum brical and interosseous m uscles join the extensor m echanism at about the level of the proxim al and m idportion of the proxim al phalanx and continue distally to the distal interphalangeal (DIP) joint of the finger. The extensor m echanism at the proxim al interphalangeal (PIP) joint is best described as a trifurcation of the extensor tendon into the central slip, which attaches to the dorsal base of the m iddle phalanx and the two lateral bands. These lateral bands continue distally to insert at the dorsal base of the distal phalanx. The extensor m echanism is m aintained in place over the PIP joint by the transverse retinacular ligam ents. ((From Doyle JR: In Green DP [ed]: Operative Hand Surgery. New York, Churchill Livingstone, 1993, p 1928.)Churchill Livingstone)
The sixth compartment contains the extensor carpi ulnaris. This tendon passes distal to the head of the ulna on the ulnar aspect of the wrist and inserts on the base of the little finger metacarpal. The extensor carpi ulnaris functions to extend and deviate the wrist ulnarly. This tendon is evaluated by having the patient extend and push the hand to the ulnar side against resistance; the tendon can be palpated distal to the ulnar styloid process.
Flexor Tendons The flexor tendons reside on the volar side of the forearm and cross the wrist joint volar to its axis. Generally, 12 tendons function to flex the wrist and digits; 3 of them—the flexor carpi radialis, flexor carpi ulnaris, and palmaris longus—primarily flex the wrist and deviate the wrist radially or ulnarly ( Figure 47-16 ). The remaining tendons pass into the digits through the carpal tunnel. A single tendon, the flexor pollicis longus, inserts on the distal phalanx of the thumb, and two flexor tendons go to each remaining finger. The flexor digitorum superficialis (FDS) tendons bifurcate near the base of the proximal phalanges and surround the tendons of the FDP before inserting on the middle phalanges of digits II to V ( Figure 47-17 ). The FDS flexes all the joints it crosses, including the wrist, PIP joints, and MCP joints. The profundus tendons lie deep to the superficialis tendons over most of their course in the forearm. At the level of the MCP joint, they perforate the superficialis tendon to emerge to a superficial position. They insert at the base of the distal phalanx and act primarily to flex the DIP joint and all joints flexed by the FDS. From the level of the MCP joint distally, the two flexor tendons become enclosed in a fibrous flexor sheath lined by synovium. Regions of thickening in this sheath form pulleys that help prevent bowstringing of the flexor tendons across the joint and assist smooth, effective flexion ( Figure 47-18 ).
Page 106
Figure 47-16 Palm aris longus accentuation.
Figure 47-17 Anatom y of flexor digitorum superficialis (FDS) and profundus (FDP) in the finger. ((From Schneider LH: Flexor Tendon Injuries. Boston, Little, Brown, 1985.)Little, Brown)
Figure 47-18 The flexor pulley system . The pulleys are thickenings in the fibrous flexor sheath. There are five annular pulleys (transversely oriented fibers) (A). There are four cruciate pulleys (oblique with some crisscrossing fibers) (C). ((Courtesy of Kleinert, Kutz and Associates Hand Care Center.))
After observation, each muscle-tendon unit is tested with a functional examination. The flexor carpi radialis, palmaris longus, and flexor carpi ulnaris are tested together by having the patient flex the wrist against resistance while the examiner palpates the individual tendons. The tendon of the flexor pollicis longus attaches to the base of the distal phalanx of the thumb and flexes the thumb MCP and IP joints. This tendon is tested by having the patient bend the tip of the thumb against resistance. FDP function can be tested by having the patient flex the distal phalanx of each finger while the PIP is stabilized in extension by the examiner ( Figure 47-19 ). The FDS is tested individually by asking the patient to flex the PIP joint while the other fingers are held in extension to block the flexion produced by the profundus tendons ( Figure 47-20 ). This is a subtle but important distinction because lacerations of the digital creases can easily damage one or more of the tendons or adjacent neurovascular bundles. The FDP is more commonly lacerated in the finger because of its paradoxically superficial position. If movement against resistance is intact but accompanied by pain or diminished strength, the involved tendon may be partially disrupted. Pathologic nodular swelling of one of the long flexor tendons may result in intermittent catching, or “triggering,” on a thickened flexor sheath anterior to the MCP joint. This condition, known as trigger finger, may cause a palpable and sometimes audible snapping when a patient is asked to flex and extend the fingers.
Figure 47-19 To test for an intact profundus tendon, the examiner m aintains the digit in extension, while the patient attem pts to flex the term inal phalanx.
Page 107
Figure 47-20 Exam ination to assess function of the flexor digitorum superficialis.
Synovial Spaces Bursae are synovial sheaths that cover tendons as they pass through osseofibrous tunnels. They contain synovial fluid and serve two essential functions: They decrease friction during tendon movement, and they help supply nutrients to the relatively avascular tendons ( Figure 47-21 ). These sheaths also can provide pathways for spread of infection. Extensor tendons do not lie within definite sheaths and are afforded a greater resistance to infections. The synovial sheaths of the flexors in the index, middle, and ring fingers are enclosed from their insertion to approximately the level of the distal palmar crease. The sheath of the flexor pollicis longus extends from the tip of the thumb to the proximal volar wrist crease, where it communicates with the radial bursa in the palm and carpal tunnel. Similarly the synovial sheath of the little finger communicates with the ulnar bursa. Clinical features of flexor tenosynovitis are caused by inflammation and distention of these synovial sheaths. Kanavel[13] described the classic signs, including a flexed posture of the digits, pain on passive extension of the digits, incomplete flexion, and tenderness of the synovial sheath.
Figure 47-21 Radial and ulnar bursae and their relation to flexor tendons and to each other. Th, thumb; I, index finger; M, m iddle finger; R, ring finger; L, little finger. ((From Siegel DB, Gelb erm an RH: Infections of the hand. Orthop Clin North Am 19:779, 1988.))
Blood Supply Arterial System The hands and the digits have a dual blood supply ( Figure 47-22 ). The major blood supply to the hand is from the radial and ulnar arteries. The radial artery lies on the anterior aspect of the radius in the distal part of the forearm. It continues around the lateral side of the wrist onto the dorsum of the hand by passing deep to the tendons of the abductor pollicis longus and the extensor pollicis brevis. On entering the palm, the radial artery terminates as the deep palmar arch. The ulnar artery enters the hand anterior to the flexor retinaculum on the radial side of the ulnar nerve and pisiform bone. The artery gives off a deep branch, then continues into the palm as the superficial palmar arch. This complex arterial arch system anastomoses and sends branches to the individual digits and the deep palmar spaces. Because of extensive collateralization, the hand usually survives even if both vessels are transected at the wrist.[14] The circulation of the hand is evaluated by palpating the radial and ulnar artery on the volar aspect of the wrist, by noting the color and warmth of the skin, and by noting capillary refill. Because these findings vary among patients, the injured hand should be compared with the normal side.
Figure 47-22 Arteriogram of the hand. The ulnar artery is the principal contributor to the superficial palmar arch. ((Courtesy of Dr. D. Arm strong, Associate Professor of Radiology, University of Toronto, Ontario, Canada.))
Page 108
Although Allen's test is an imperfect predictor of vascular compromise, it is commonly used to determine the patency of the arteries supplying the hand and the contributions to the circulation of the hand derived from each of the major vessels. The radial and ulnar arteries are compressed by the examiner at the wrist ( Figure 47-23 ). The patient opens and closes the hand repeatedly to exsanguinate it, then maintains a relaxed position. The radial artery is released. If the palm and fingers fill immediately with blood, the radial artery is patent with good collateral flow into the ulnar artery system. To evaluate the ulnar artery, the same steps are repeated, but the ulnar artery is released. This method also can be used on a single digit to help evaluate the patency of each digital vessel to that finger. Similar to the hand, the digit usually survives even if both digital vessels are transected at the base of the finger; however, healing of associated injuries may be delayed or may be compromised by excessive scar formation because of associated, although relative, ischemia.[14]
Figure 47-23 Allen's test. ((From ASSH: The Hand: Exam ination and Diagnosis, 3rd ed. New York, Churchill Livingstone, 1990, p 46.)Churchill Livingstone)
Venous and Lymphatic Systems The veins generally follow the arterial pattern in the deep system. The abundant dorsal, superficial veins are more extensive than the deep system and drain most of the blood from this region. The lymphatic vessels essentially follow the veins, with most lymph flowing into channels in the dorsal subcutaneous space. This vascular anatomy and the laxity of the dorsal skin account for palmar infections causing swelling on the dorsum rather than the palmar surface of the hand.
Nerve Supply The nerve supply to the hand comes from the radial, ulnar, and median nerves. All three nerves control movement of the wrist, fingers, and thumb. In the hand, the ulnar and median nerves are mixed motor and sensory nerves, whereas the radial nerve is purely sensory. Each of the three major nerves passes through a muscle in the forearm, and each passes points of potential entrapment en route to the hand.
Motor Innervation The radial nerve (C6 through C8) passes through the supinator muscle and enters the dorsal aspect of the wrist between the radial styloid and Lister's tubercle. At this level, the nerve has a purely sensory function. Its important motor function is to innervate the dorsal extrinsic muscles in the forearm, which extend the wrist and MCP joints and abduct and extend the thumb. No intrinsic muscles in the hand are innervated by the radial nerve. Motor function in this nerve is tested by having the patient extend the wrist against resistance. Proximal injury to the radial nerve causes a condition known as wristdrop: The fingers are held in flexion at the MCP joints, and the thumb is adducted ( Figure 47-24A ).
Figure 47-24 Deform ities of the hand. A, Radial palsy—wrist drop. B, Ulnar nerve palsy—m ain en griffe (clawhand). C, Median nerve palsy—m ain en singe (m onkey hand). The shaded areas represent the usual distribution of anesthesia. ((From Ellis H: Clinical Anatom y: A Revision and Applied Anatom y for Clinical Students, 7th ed. Oxford, UK, Blackwell Scientific, 1983.)Blackwell Scientific)
The ulnar nerve (C7, C8, and T1) passes through the flexor carpi ulnaris muscle in the forearm and lies
Page 109
ulnar to the artery and superficial to the flexor retinaculum. It enters the hand at the wrist through a tunnel called the ulnar tunnel or Guyon's canal. The ulnar nerve innervates the hypothenar muscles, the seven interosseous muscles, the lumbrical muscles to the ring and little fingers, and the adductor pollicis. Innervation of the flexor pollicis brevis is variable. In the forearm, the flexor carpi ulnaris and the ulnar half of the FDP also are innervated by the ulnar nerve. Loss of motor function of the ulnar nerve results in inability to pinch a piece of paper tightly between the thumb and the index finger. A late characteristic of distal ulnar damage is Duchenne's sign, manifested by clawing of the ring and little fingers ( Figure 47-24B ). The ring and little fingers are hyperextended at the MCP joints by the extensor digitorum communis (radial nerve) and flexed at the IP joints by the FDP (intact proximal ulnar nerve). In addition, the interosseous and hypothenar muscles are atrophied. The median nerve enters the forearm through the pronator teres muscle. At that level, it innervates that muscle, the flexor carpi radialis, the FDS, the radial part of the FDP, the flexor pollicis longus, and the pronator quadratus. The branch of the median nerve that innervates the last three muscles is called the anterior interosseous nerve. The median nerve enters the hand through the carpal tunnel accompanied by the nine extrinsic flexor tendons of the digits. The thenar motor branch (recurrent median nerve) innervates the abductor pollicis brevis, the opponens pollicis variably, and the flexor pollicis brevis. Common digital branches innervate the lumbrical muscles to the index and long fingers. Injury to this nerve occurs most commonly at the level at the wrist, by laceration or by compression in the carpal tunnel. Motor function is tested by having the patient oppose the thumb to the index digit. Injury to the median nerve in the upper forearm or at the elbow usually results in weakness or absence of flexion of the index finger distal phalanx, the middle phalanx, and the thumb and weakness of thumb abduction and opposition.[15] With passage of time, the muscles of the thenar eminence atrophy, and the hand looks flattened and “apelike” ( Figure 47-24C ).
Sensory Innervation The typical distribution of the sensory nerves to the hand is shown in Figure 47-25 . Because some overlap occurs between various sensory nerves, it is preferable to test sensation in the areas least likely to have dual innervation. The anatomic area of least ulnar variation and overlap is the volar tip of the little finger. The median nerve exclusively innervates the volar tip of the index finger. The dorsal first web space is entirely within the radial nerve distribution.
Figure 47-25 The cutaneous nerve supply in the hand. M, m edian; R, radial; U, ulnar; PCM, palmar cutaneous branch of m edian nerve; DCU, dorsal cutaneous branch of ulnar nerve. ((Courtesy of Kleinert, Kutz and Associates Hand Care Center.))
Several methods exist to assess sensation. The preferred method, which is most accurate and objective, is comparative two-point discrimination. An uninjured hand is able to distinguish two points that are 2 to 5 mm apart at the fingertips and 7 to 10 mm apart at the base of the palm. The dorsum of the hand is the least sensitive region, with a normal threshold at 7 to 12 mm. Two-point threshold distances wider than these ranges indicate impaired sensory function.[15] The threshold and two-point discrimination tests may be of limited value in children, patients with heavily calloused fingertips, uncooperative patients, comatose patients, patients in severe pain, or suspected malingerers.
Fingertip The fingertip generally is defined as the area distal to the insertion of the flexor profundus and extensor tendons ( Figure 47-26 ). The pulp is the tissue of the fingertip between the volar skin and the distal phalangeal bone. The fingertip is well padded by adipose tissue and is covered by highly innervated skin that is tethered to the distal phalanx by a series of fibrosepta. The dorsal skin is thinner and less vascularized than the volar skin. Sensation is supplied by nerves that travel with arteries bilaterally along the radial and ulnar aspect of the fingers. The arteries branch to form volar anastomoses or arches similar to those in the palm. Dorsal branches supply the nail bed and matrix.
Page 110
Figure 47-26 Sagittal section of the distal finger. ((From Siegel DB, Gelb erm an RH: Infections of the hand. Orthop Clin North Am 19:779, 1988.))
Nail The nail (or nail plate) consists of compacted scales that originate from cornified epithelial cells. The proximal part of the nail is called the root; it emerges from a groove in the skin to form the body of the nail, which is exposed. The root of the nail is covered by a fold in the skin called the proximal nail fold. A small portion of the epidermis of the nail fold extends out over the proximal body of the nail to form the cuticle, or eponychium. The floor of the nail plate or nail bed is composed of tissue known as the nail matrix. The distal skin of the nail bed complex is called the hyponychium. The skin overlying the nail laterally is called the perionychium. The semicircular white crescent region near the nail fold is called the lunula. The nail bed complex on the dorsum of the fingertips is important in providing additional stabilization of the palmar soft tissues against compression and shear forces. The nail grows from the nail matrix along the nail bed and is firmly adherent to the bed. It is now believed that the entire nail bed is active in the generation and migration of the nail. As new nail forms, the nail glides forward over the nail bed at a rate of about 0.5 to 1.2 mm per week (toenails grow much more slowly). The nail itself is a hard, firm, and relatively translucent structure; the underlying vascular tissue showing through gives the nail its pink appearance. A smooth nail bed is essential to normal function. If the nail bed sustains injury that is not repaired accurately, granulation tissue forms scar that impedes normal nail production and growth. The result may be a split or absent nail that is cosmetically unappealing and sometimes functionally debilitating.[16]
CLINICAL FEATURES: SIGNS AND SYMPTOMS The initial evaluation of an acutely injured hand is crucial because it affords the best opportunity to assess accurately the extent of damage and to restore altered anatomy.[17] Evaluation of any hand injury should begin by obtaining the historical facts of the patient's age, occupation, hand dominance, and previous hand impairment or injury. In traumatic injuries, the time of occurrence, length of elapsed time since the injury, mechanism of injury, posture of the hand at the time of injury, and treatment before arrival in the emergency department all are useful data. In nontraumatic problems, pain, swelling, sensory change or contracture, timing of symptoms, presence of similar symptoms in other extremities, aggravating or alleviating factors, and functional impairment are useful historical points. A review of the medical history and a review of systems complete the evaluation. After a detailed history is taken, the entire extremity should be exposed and evaluated when the hand is examined. A system of priorities, based primarily on threat to ultimate function, should direct the sequence of the examination. In order of priority, the examination includes evaluation of vascular and neurologic integrity, skin cover, skeletal stability, and joint and tendon function ( Box 47-1 ). The general appearance of the hand should be noted with focus on its color, presence of swelling or edema, and any abnormal posture or position. In traumatic injuries, the precise area of maximal tenderness should be localized. Rotational, angular, and shortening deformities should be noted with regard to direction and extent. Angular deformity may be seen best with the fingers in full extension. Rotational deformity is best observed during digital flexion. Digital or wrist block anesthesia may be helpful in some cases to accurately assess fracture deformity and stability during digital motion and, if necessary, stress testing. Open wounds should be assessed with regard to location, relationship to skin creases, direction and viability of skin flaps, extent of skin loss, degree of contamination of the wound, and extent of soft tissue injury. The examiner must have a sterile field, good light, adequate exposure, and a nearly bloodless field for a thorough evaluation. The complete examination also may require an evaluation of active shoulder motion, elbow motion, and pronation and supination of the forearm and assessment of the contralateral hand. BOX 47-1 General Physical Examination of the Hand
I.
General appearance
Page 111
A.
B.
C.
II.
Skin A. B. C.
D.
E.
F. III.
Vascular A.
B. C.
D.
IV.
Activ e hem orrh age Amp utati ons or avul sion s Posit ion at rest Integ rity Mois ture Swel ling or ede ma Disc olora tion Infla mm ation Scar s Colo r and war mth Puls es Capil lary refill Allen 's test
Neurologic A. Motor function 1. Ulna r nerv e— finge r abdu ction
Page 112
B.
V.
and addu ction 2. Radi al nerv e— wrist exte nsio n 3. Medi an nerv e— flexio n of digit s I, II, and III; thum b oppo sitio n Sensory function 1. Ulna r nerv e— tip of digit V 2. Medi an nerv e— tip of digit II 3. Radi al nerv e— dors al first web spac e
Bone and joint A. Defo rmity B. Loca l tend erne ss
Page 113
C.
VI.
Pain with axial com pres sion D. Joint rang e of moti on E. Liga ment ous stabi lity: dista l inter phal ange al, proxi mal inter phal ange al, meta carp opha lang eal joint s Musculotendinous A. Func tion of each mus cle-t endo n grou p B. Stre ngth agai nst resis tanc e C. Pain with moti on
DIAGNOSTIC STRATEGIES: RADIOGRAPHIC EVALUATION Despite the development of numerous new and sophisticated imaging techniques, the plain radiograph
Page 114
remains the most important imaging modality for the hand and wrist. The standard radiographic series of the hand should include a posteroanterior, a true lateral, and an oblique projection ( Figure 47-27 ). With correct positioning, the bones do not overlap on the film, allowing complete evaluation of each area for visualization of fractures, subluxation, dislocation, deformities, and retained radiopaque foreign bodies.[18] On a hand series, the wrist is not properly positioned for radiographic examination, and vice versa; if the patient has injuries to the hand and wrist, separate radiographic series should be performed. For an adequate posteroanterior view, the forearm and hand should be fully pronated so that the palm rests flat on the film. This view forms the basis of all assessments, but is poor at showing fractures of the articular surface of the metacarpal head. The lateral view is normally a radioulnar projection and is made by positioning the palm and forearm at 90 degrees to the film with the fingers splayed. This view is essential to show displacement of fracture fragments and joint dislocations. If the projection is not a true lateral, joint dislocation, avulsion fractures, or fractures through the articular surface of the base of the phalanx may be missed. The oblique view is made with the hand and forearm pronated at 45 degrees to the film. It is particularly useful for assessing dislocation of the MCP and CMC joints and fractures at the base of the metacarpal bones. When injury is confined to the distal end of a single digit, radiography should be limited to that digit, but the same projections are used ( Figure 47-28 ).
Figure 47-27 Norm al hand radiographs. A, Anteroposterior view. B, Lateral view. C, Oblique view. The hand is routinely exam ined in three different planes to identify fractures that cannot be identified in two views because of overlapping bony structures. ((From Rosen P, et al: Diagnostic Radiology in Em ergency Medicine. St. Louis, Mosb y, 1992, p 179.)Elsevier Inc.)
Figure 47-28 Norm al radiographs of the finger.
Special views are used to diagnose specific injuries. The standard views of the hand do not give true posteroanterior and lateral projections of the thumb because the plane of the thumb is at 90 degrees to the fingers. Separate posteroanterior and lateral views of the thumb should be requested. The posteroanterior projection of the thumb is taken with the hand and forearm hyperpronated so that the dorsal surface of the thumb and first metacarpal rests flat on the film. The lateral view is obtained by pronating the hand and forearm to allow the lateral surface of the thumb to lie on the film. Stress views are used most often to rule out ligamentous injury to the first MCP joint. Localized widening of the joint space or subluxation may indicate a significant collateral ligament injury. Plain films taken in multiple projections can help detect and localize soft tissue foreign bodies. Whether an object is visualized on plain films depends on its composition, configuration, size, and orientation. Many foreign bodies encountered in the emergency department, including almost all glass, are more dense than soft tissue and can be readily seen on plain radiographs.[19]
MECHANISMS OF INJURY AND MANAGEMENT Trauma The bones of the hand are the most commonly fractured bones in the body. Radiographic evaluation of significant hand injuries is mandatory. Any hand injury that causes swelling should be evaluated radiographically with a minimum of three views. Although the classification of hand fractures is difficult and at times confusing, it is generally done according to the nature and site of the fracture line and whether the fracture is open or closed ( Figure 47-29 ).
Page 115
Figure 47-29 Fracture term inology. ((From Idler RS, et al [eds]: The Hand: Exam ination and Diagnosis, 3rd ed. New York, Am erican Society for Surgery of the Hand, 1990, p 64.)Am erican Society for Surgery of the Hand)
A fracture is unstable if it cannot be reduced or maintained in an anatomic or near-anatomic position without fixation when the hand is placed in the “safe” or functional position. The four principal determinants of fracture stability or instability are (1) fracture configuration, (2) integrity of the periosteal sleeve and surrounding soft tissues, (3) muscle balance or imbalance, and (4) external forces. In general, transverse fractures have a stable configuration. Spiral, oblique, and comminuted fractures are unstable. The degree of displacement also is an indicator of potential fracture instability. Fractures of unstable configuration may be stable if they are nondisplaced or only minimally displaced because the periosteum is undamaged or minimally disrupted. Displacement is defined by the deformity it creates and can result in rotation, angulation, shortening, or a combination of these fractures. Although shortening has an adverse effect on muscle tension, the hand accommodates more easily to this component of deformity than to others.[20] Definitive management of many hand fractures is controversial and beyond the scope of this text. The emphasis here is on appropriate initial interventions, including proper splinting techniques to minimize morbidity and understanding which fractures may require operative fixation and their potential complications. Most closed injuries may be treated initially in the emergency department. Most open, intra-articular, periarticular, and unstable fractures require operative management by a hand surgeon.[20]
Distal Phalanx Fractures Pathophysiology and Clinical Features Fractures of the distal phalanx are the most common fractures of the hand. They occur most often as a result of crush or shearing forces, usually as a sports-related injury in children and adolescents, industrial accidents in adults, or accidental falls in the elderly.[21] Distal phalangeal fractures are classified into extra-articular fractures (longitudinal, transverse, and comminuted) and intra-articular fractures. The most common location for fractures is the distal tuft ( Figure 47-30 ). Because the mechanism of injury is usually direct trauma, tuft fractures are often comminuted and usually associated with soft tissue injury to the nail, nail bed, and nail matrix.[22] Supporting fibrous septa that radiate from the bone to the skin prevent displacement of fracture fragments and contain soft tissue swelling, contributing to the severe pain that can accompany these fractures. Examination typically reveals tenderness and swelling over the distal phalanx, including the pulp.
Figure 47-30 Tuft fracture of the distal phalanx of the thum b, anteroposterior view. This radiograph reveals the com m inuted displaced fracture fragm ents and som e radiopaque foreign m aterial on the substance of the nail. ((From Rosen P, et al: Diagnostic Radiology in Em ergency Medicine. St. Louis, Mosb y, 1992, p 180.)Elsevier Inc.)
Fractures at the base of the distal phalanx may be associated with tendon avulsion. As previously mentioned, the flexor profundus tendon attaches to the volar aspect of digits II through V, and the terminal slip of the extensor tendon attaches on the dorsal surface of the distal phalanx. In the distal phalanx of the
Page 116
thumb, the flexor pollicis longus inserts on the volar base, and the extensor pollicis longus inserts on the dorsal base. These tendons can avulse when subjected to excessive stress. Clinically, loss of function is evident, and radiographically small avulsion fractures along the dorsal or volar surface may be seen. These fractures are considered intra-articular, and their management is considered with other tendon injuries.
Management Treatment of most fractures of the distal phalanges is directed toward the accompanying soft tissue injury. Closed tuft fractures need only symptomatic treatment with elevation (to reduce swelling) and analgesics. Fracture immobilization is rarely necessary; however, a short volar splint or hairpin splint ( Figure 47-31 ) is recommended for 2 to 3 days to protect the tip of the finger from further trauma and allow swelling without constriction. Immobilization should not include the PIP joint. Transverse shaft fractures with angulation or displacement may be irreducible because of interposition of soft tissue. Closed reduction may be attempted with dorsal traction on the distal fragment followed by immobilization with a volar splint and repeat radiographs for documentation of position. If this approach is unsuccessful, referral to a hand surgeon is indicated for Kirschner wire fixation.[22]
Figure 47-31 The hairpin splint used for distal phalangeal fractures. ((From Sim on RR, Koenigsknecht SJ: The hand. In Sim on RR [ed]: Em ergency Orthopedics: The Extrem ities, 2nd ed. Norwalk, Conn, Appleton & Lange, 1995, p 59.)Appleton & Lange)
Distal phalangeal fractures associated with nail bed laceration are considered open fractures. This may be obvious if the nail has been avulsed or torn, but the recognition of nail bed laceration is more difficult in closed tuft fractures with an intact nail and a subungual hematoma present. Subungual hematomas are often associated with occult lacerations of the nail bed, and such cases uncommonly may require removal of the nail for accurate assessment and laceration repair.
Complications Distal phalanx fractures are generally uncomplicated; however, distal phalanx fractures that appear apparently innocuous can result in prolonged morbidity, especially if there is concomitant soft tissue crush injury. In a long-term follow-up series, DaCruz and associates[23] showed that 31% of tuft fractures had not healed radiographically, and 70% of patients had bothersome symptoms at 6 months, including numbness, hyperesthesia, and cold sensitivity. Trauma to the nail bed may result in abnormal nail growth despite exact tissue approximation. Failure to recognize and extricate an entrapped nail bed in the fracture site may result in nonunion of the fracture. Osteomyelitis from open fractures is a rare but potentially serious complication.
Proximal and Middle Phalangeal Fractures Pathophysiology and Clinical Features Because the anatomy, mechanism of injury, and treatment of proximal and middle phalangeal fractures are similar, they are discussed together. The proximal phalanx has no tendinous attachments. Fractures in this region have a typical volar angulation resulting from forces exerted from the extensors and the interosseous muscles. The middle phalanx has two important insertions. The tendon of the FDS divides and inserts along nearly the entire volar surface of the phalanx, and the extensor tendon inserts on the proximal dorsal base of the middle phalanx. Because of this alignment, fractures at the base of the middle phalanx usually result in dorsal angulation, and fractures at the neck of the middle phalanx usually result in volar angulation.[24] The mechanism of injury often determines the nature of the fracture; a direct blow is more likely to cause a transverse or comminuted fracture, whereas a twisting injury more often results in an oblique or spiral fracture. Associated injuries may include contusion or transection of digital nerves, vascular disruption, and tendon rupture. Intra-articular fractures include condylar fractures; comminuted fractures; dorsal, volar, or lateral base fractures; fracture-dislocations; and shaft fractures involving the joint. Extra-articular fractures involve the
Page 117
neck, shaft, or base of the phalanx. Although most phalangeal fractures may be easily seen, condylar fractures and displaced neck fractures are not always apparent on anteroposterior radiographs; oblique views may be needed to identify them.[25] Rotational deformities are difficult to determine by x-ray study but may appear on the lateral view as discrepancies in the diameter of the shaft at the fracture site. Skeletal alignment can be assessed radiographically, but rotational alignment must be judged clinically by the relationship of the finger to adjacent normal fingers ( Figure 47-32 ). Symmetric flexion of adjacent injured and normal fingers at their MCP and PIP joints is the best possible guide to accurate rotational alignment of the injured segment.[26] Normally, all of the fingers of the closed fist except the thumb should point to the scaphoid. Alternatively, when the fingers are loosely flexed, the nails of opposing digits should lie in the same parallel plane ( Figure 47-33 ). The noninjured hand should be used for comparison.
Figure 47-32 Any m alrotation of a m etacarpal or phalangeal fracture must be corrected. A, Norm ally all fingers point toward the region of the scaphoid when a fist is m ade. B, Malrotation at fracture causes the affected finger to deviate. ((From Job e MT, Calandruccio JH: Fractures, dislocations and ligam entous injuries. In Canale ST (ed): Cam pb ell's Operative Orthopedics, 10th ed. St. Louis, Mosb y, 2003, p 3484.)Elsevier Inc.)
Figure 47-33 Observing the plane of the fingernails helps detect any m alrotation at the fracture. ((From Job e MT, Calandruccio JH: Fractures, dislocations and ligamentous injuries. In Canale ST (ed): Cam pb ell's Operative Orthopedics, 10th ed. St. Louis, Mosb y, 2003, p 3484.)Elsevier Inc.)
Management Similar to metacarpal fractures, phalangeal fractures require precise anatomic alignment to ensure a good result because of the intimate relationship of the flexor and extensor tendons to the phalanx.[27] Appropriate treatment selection depends on accurate assessment of fracture stability. The angle of the fracture is an important factor in determining this stability. Transverse fractures are usually stable, whereas oblique fractures are inherently unstable. It also is important to ascertain whether the fracture has been impacted or displaced and what deforming forces are acting on it. If there is any question of the fracture's stability, the digit should be anesthetized, and stress should be applied. Reduction of phalangeal fractures is not usually necessary because approximately 75% are stable and nondisplaced.[28] Such fractures should be started on early protected motion as soon as pain subsides (within the first 3 to 5 days). Protection is provided by taping the injured digit to an adjacent normal finger, a form of dynamic splinting. This technique, known as “buddy-taping,” encourages the patient to move the finger and use the hand as normally as possible while the fracture heals ( Figure 47-34 ).
Figure 47-34 The injured finger is splinted to the adjacent norm al finger. This splint provides support for the injured digit, while
Page 118
perm itting m otion of the m etacarpophalangeal joint and som e m otion at the interphalangeal joint. A piece of felt cut to the proper size is inserted between the fingers, and the two digits are taped together as shown. ((From Sim on RR, Koenigsknecht SJ: The hand. In Sim on RR [ed]: Em ergency Orthopedics: The Extrem ities, 3rd ed. Norwalk, Conn, Appleton & Lange, 1995, p 518.)Appleton & Lange)
If the fracture is displaced or unstable, it is not suitable for dynamic splinting. In general, treatment depends on the type of trauma and the ability to achieve a stable reduction. Phalangeal fractures that are satisfactorily managed by closed reduction can be immobilized by several methods. In such cases, it is advisable to immobilize the wrist and the injured finger. Specific types of immobilization include circular cast, the Böhler method of incorporating a cast with an outrigger, gutter splints, and anterior and posterior splints ( Figure 47-35 ). Immobilization of phalangeal fractures should not exceed 3 weeks to prevent stiffness and to minimize disability. In addition to temporary immobilization, emergency management includes ice for comfort, elevation, analgesics, and follow-up referral. Repeat radiographs in 7 to 10 days are recommended to ensure that there has been no delayed displacement.
Figure 47-35 Gutter splints are used for the treatm ent of phalangeal and m etacarpal fractures. A, Fractures of the ring and little fingers are im m obilized in an ulnar gutter splint. B, Fractures involving the index finger and the long finger are im m obilized in a radial splint. The splint is m ade by using plaster sheets cut to the proper size. The measurem ent should be from the tip of the finger to a point two thirds of the way up the forearm . ((From Sim on RR, Koenigsknecht SJ: The hand. In Sim on RR [ed]: Em ergency Orthopedics: The Extrem ities, 3rd ed. Norwalk, Conn, Appleton & Lange, 1995, p 519.)Appleton & Lange)
Unstable fractures that cannot be reduced by closed manipulation and maintained with external splinting require internal fixation. Midshaft transverse fractures tend not to be amenable to closed reduction; similarly, spiral oblique fractures and intra-articular fractures are inherently unstable and require surgical fixation if a significant portion of the articular surface is involved.[29] Intra-articular fractures of the proximal metaphysis of the middle phalanx that have extreme comminution may require treatment in static or dynamic traction or external fixation with or without ancillary Kirschner wire fixation.[29]
Complications Malunion is the most common bony complication of phalangeal fractures and may result from malrotation, volar or lateral angulation, or shortening. Malrotation usually is seen after oblique or spiral fractures of the proximal and middle phalanges and may require osteotomy through the phalanx or metacarpal for correction. Volar angulation of proximal phalangeal fractures greater than 25 to 30 degrees results in pseudoclawing. This deformity makes use of the hand awkward and esthetically unacceptable. Other potential complications include diminished motion resulting from tendon adhesions and stiffness of the PIP joint after intra-articular fractures with incongruity.[27]
Metacarpal Fractures Metacarpal fractures generally are divided into two groups: fractures involving the first metacarpal and fractures involving metacarpals II through V. This distinction is based on the fact that the base of the thumb metacarpal is biomechanically distinct from the remaining metacarpals because of its high degree of mobility. For this reason, these two groups are discussed separately.
Metacarpal Fractures of Digits II Through V The hand can adjust functionally to dorsal angulation in the metacarpal equal to its motion at the CMC joint, plus 10 to 15 degrees in some patients. Because the index and middle fingers are immobile at their CMC joints, they may accommodate 10 to 15 degrees of dorsal angulation. The ring finger usually has 20 to 30 degrees of mobility at its CMC joint and may accommodate 40 to 45 degrees of dorsal angulation. The small finger generally has 30 to 50 degrees of motion at its base and may accommodate 50 to 70 degrees of dorsal angulation. Finger metacarpals may tolerate 10 to 15 degrees of lateral angulation and 3 to 4 mm of shortening. Rotational deformity, most commonly seen in spiral and oblique fractures, is poorly tolerated. A
Page 119
small amount of rotational deformity can translate into a substantial digital overlap when the fingers are closed to form a fist. More than 5 degrees of malrotation may cause overlapping (scissoring) of the fingers during flexion.[20]
Metacarpal Head Fractures Pathophysiology. Fractures of the metacarpal head are rare. They usually occur secondary to direct trauma or crush injury and typically result in a comminuted fracture.[22] These fractures occur distal to the attachment of the collateral ligaments. Physical examination reveals tenderness and swelling over the involved MCP joint. Pain is increased if axial compression is applied along the extended digit. The presence of lacerations over the metacarpal heads is significant and suggests the possibility of an open fracture or human bite injury.
Diagnostic Strategies: Radiology. Although routine imaging of the injured hand reveals most fractures, the metacarpal heads can be difficult to assess because of overlap on the lateral view. In such cases in which clinical suspicion of a fracture exists and the initial views are normal, the Brewerton “ball-catcher's” view may be helpful.[30] This view is obtained with the digits in 65 degrees of flexion at the MCP joints and the x-ray beam angled 15 degrees radially, projecting the metacarpal heads in profile. Occasionally, computed tomography also may be required to evaluate accurately the degree of displacement of intra-articular fractures at the MCP level.
Management. Emergency management of closed metacarpal head fractures consists of elevation, ice for comfort, analgesics, and immobilization of the hand in the “safe” or functional position, which balances the forces of the intrinsic muscles. In this position, the wrist is extended 20 degrees, the MCP joints are flexed to 90 degrees, and the PIP and the DIP joints are extended ( Figure 47-36 ). Referral to a hand surgeon for management and follow-up evaluation is required in all cases. Because these are intra-articular fractures, displacement greater than 1 to 2 mm predisposes to a poor result; however, there is little consensus as to optimal definitive treatment.[31]
Figure 47-36 The “safe” position described by Jam es. ((Modified from Stern PJ: Fractures of the m etacarpals and phalanges. In Green DP [ed]: Green's Operative Hand Surgery, 4th ed. New York, Churchill Livingstone, 1999.)Churchill Livingstone)
Lacerations or puncture wounds over the dorsum of the MCP joint associated with a metacarpal head fracture should be considered open until proved otherwise. Such injuries often are caused by a clenched-fist injury and are highly contaminated wounds. Emergent consultation with a hand surgeon for operative debridement and irrigation is recommended. Prophylactic coverage with a cephalosporin is routinely recommended, although highly contaminated wounds also should receive penicillin and an aminoglycoside. Several studies have found preoperative wound cultures to be of no value in predicting the risk of infection or the nature of the likely pathogen, and some authors have abandoned their use.[]
Complications. Metacarpal head fractures may be associated with debilitating hand complications, including avascular necrosis, rotational malalignment, interosseous muscle fibrosis, extensor tendon injury or fibrosis, and chronic stiffness of the MCP joint. Many of these fractures also may require late arthroplasty.[22]
Metacarpal Neck Fractures Pathophysiology. Fractures of the metacarpal neck are among the most common fractures in the hand. The mechanism of injury is a direct impaction force (e.g., a punch with a closed fist). A boxer's fracture is a fracture of the neck of the fifth metacarpal ( Figure 47-37 ). Most metacarpal neck fractures have a typical apex dorsal angulation (palmar angulation of the distal fragment). They are inherently unstable because of the deforming muscle
Page 120
forces and frequent comminution of the volar cortex. Management generally is difficult because of this instability and the difficulty in maintaining reduction.
Figure 47-37 .
Management. For treatment purposes, metacarpal neck fractures are divided into two groups: fractures involving the ring and little finger metacarpals and fractures involving the index and long finger metacarpals. There is considerably more mobility of the metacarpals of the ring and little fingers compared with the index and long fingers. The greater mobility makes them more prone to fracture, and the immobility of the index and long finger metacarpals increases the need for accurate alignment after reduction. Generally less than 15 degrees is allowed in the index and long finger metacarpals; in the ring and little finger metacarpals, 35 degrees and 45 degrees of angulation is allowed. Any rotational malalignment must be completely corrected. Nondisplaced ring and little finger metacarpal fractures without angulation deformity can be treated initially with ice, elevation, analgesia, and immobilization in a gutter splint. Nondisplaced, nonangulated metacarpal fractures of the index and long finger metacarpals are treated similarly. The splint should be in standard position of function and extend from below the elbow up to, but not including, the PIP joint. Generally, it is recommended to begin PIP and DIP motion without delay. Protected MCP motion can begin in 3 to 4 weeks.[ 22] For isolated fractures of the little finger metacarpal neck, some authors advocate immediate mobilization of fractures regardless of the degree of angulation. These results show excellent function and early return to work and only minor cosmetic deformity. Early follow-up evaluation is advised to exclude residual angulation, rotational deformity, and delayed displacement.[34] Reducing ring and little finger metacarpal neck fractures with significant angulation or deformity may be attempted in the emergency department. After appropriate anesthesia, usually a hematoma block, traction is applied on the metacarpal to disimpact the fracture. The MCP joints and IP joints are flexed at 90 degrees, and simultaneous pressure is applied in a volar direction over the metacarpal shaft and in a dorsal direction over the flexed PIP joint ( Figure 47-38 ). This maneuver is termed the 90-90 method and should complete reduction. A gutter splint in position of function should be applied. Postreduction radiographs should be obtained immediately and after 1 week to ensure that reduction has not been lost. If closed reduction is unable to be achieved or maintained, pin fixation by a hand surgeon is necessary, and early referral is indicated.
Figure 47-38 The 90-90 m ethod for m etacarpal neck fracture reduction.
Displaced or angulated index or long finger metacarpal neck fractures commonly require anatomic reduction and surgical fixation. Emergency department management consists of ice, elevation, and the application of a volar splint. Prompt referral to a hand surgeon is mandatory.
Complications. Metacarpal neck fractures may have an associated rotational component that can impair function and result in overlapping of the affected finger over an adjacent finger. If excessive angulation is not corrected, the patient may experience forced hyperextension of the MCP joint and flexion of the PIP joint when extending the finger and pain when tightly grasping objects. Other complications include extensor tendon injury and
Page 121
collateral ligament damage. Nonunion is rare after closed metacarpal fractures.
Metacarpal Shaft Fractures Pathophysiology. There are three types of metacarpal shaft fractures: transverse, oblique or spiral, and comminuted. Transverse and comminuted fractures usually result from a direct blow and commonly exhibit dorsal angulation ( Figure 47-39 ). Indirect trauma or rotational torque applied to the finger may result in a spiral shaft fracture. These fracture fragments tend to shorten and rotate rather than angulate.
Figure 47-39 X-ray film shows the typical dorsal angulation of fractures of the m etacarpal shafts. These fractures are usually the result of a direct blow and generally angulate dorsally because of the interosseous muscles exerting a volar force. ((From Green DP, Rowland SA: Fractures and dislocations in the hand. In Rockwood CA Jr, Green DP [eds]: Fractures in Adults. Philadelphia, JB Lippincott, 1991, p 490.)JB Lippincott)
Management. Metacarpal shaft fractures are treated differently than fractures involving the neck because rotational deformity and shortening are more likely, and less angular deformity is acceptable. In general, any rotational deformity must be corrected. Angulation deformities are unacceptable in the index and long finger metacarpals, whereas a small amount of angulation may be compensated for in the ring and little finger metacarpals. Acceptable reduction is less than 10 degrees of angulation in the former and less than 20 degrees in the latter, with less than 3 mm of shortening and normal rotational alignment.[20] Most metacarpal shaft fractures can be managed initially with ice, elevation, analgesia, and immobilization in a gutter splint. The splint should include the wrist and the entire metacarpal shaft, but not the MCP joint if the fracture is proximal to the neck. Repeat radiographic examination and referral to a hand surgeon are recommended. If manipulative reduction is necessary, operative fixation usually is indicated. Multiple displaced metacarpal shaft fractures, oblique or spiral fractures with rotational deformity, irreducible transverse fractures, and displaced open fractures require internal fixation.[34]
Complications. Complications seen in metacarpal shaft fractures are similar to the complications described for other metacarpal fractures. In addition to malrotation, which can cause a chronic painful grip, limitation of extensor function and interosseous muscle fibrosis may develop.
Metacarpal Base Fractures Clinical Features. Fractures of the metacarpal base generally are stable and occur infrequently. They may result from either a direct blow over the base of the metacarpal or an axial force or torque applied along the digit. Examination reveals tenderness and swelling at the base of the involved metacarpal, and a significant degree of rotational deformity may be evident. Fractures at the base of the ring or little finger metacarpals may cause injury to the motor branch of the ulnar nerve and result in paralysis of the intrinsic hand muscles. In addition, they may be associated with a carpal bone fracture.
Management. Initial management in the emergency department consists of ice, elevation, analgesia, and immobilization in a bulky compressive dressing or volar splint with referral to a hand surgeon for definitive management.
Complications. Metacarpal base fractures may be associated with extensor or flexor tendon damage and significant rotational malalignment. Chronic CMC joint stiffness is often associated with intra-articular fractures and
Page 122
may necessitate arthrodesis or arthroplasty.
Thumb Metacarpal Fractures Fractures of the thumb metacarpal are relatively uncommon because of its high degree of mobility. Although the shaft occasionally may be involved, most fractures involve the base of the metacarpal. These fractures are classified into two groups: extra-articular and intra-articular. The two common types of intra-articular fractures of the thumb are Bennett's and Rolando's fractures.
Extra-articular Fractures. Extra-articular fractures are seen more commonly than intra-articular fractures and usually result from direct trauma or impaction. The three types of extra-articular fractures are transverse, oblique, and epiphyseal in children. Examination reveals localized pain and swelling over the fracture site. Mobility of the thumb metacarpal allows 20 to 30 degrees of angular deformity without functional impairment. Extra-articular fractures with a greater degree of angulation should undergo closed reduction, postreduction radiographs, and immobilization of the thumb in abduction with its IP joint extended using a thumb spica cast for 4 weeks. Transverse fractures are usually stable and can be managed with closed reduction and immobilization. If the fracture is oblique, it may require Kirschner wire fixation because of instability and a propensity for rotational deformity.[20]
Intra-articular Fractures Bennett's Fracture. Bennett's fracture is an intraarticular fracture at the base of the thumb metacarpal combined with a dislocation or subluxation of the CMC joint. The ulnar portion of the metacarpal remains in place, and the larger fragment subluxes dorsally because of the pulling force of the abductor pollicis longus and adductor pollicis muscle ( Figure 47-40 ). There is complete disruption of the ligaments about the CMC joint. Because stability is conferred mostly by the dorsal ligament (posterior oblique CMC ligament), dislocation ensues. The mechanism of injury usually involves an axial force acting on a partially flexed metacarpal (e.g., striking a rigid object with a closed fist). This is the most common fracture of the thumb base.[35]
Figure 47-40 Bennett's fracture, anteroposterior view. Avulsion fracture of the articular surface of the first metacarpal with subluxation at the carpom etacarpal joint. This fracture m ust be differentiated from Rolando's fracture and the m ore com m on extra-articular varieties. ((From Rosen P, et al: Diagnostic Radiology in Em ergency Medicine. St. Louis, Mosb y, 1992, p 181.)Elsevier Inc.)
Bennett's fracture requires an anatomic reduction. Treatment goals are to achieve stability of the CMC joint by rejoining the volar lip fragment to the first metacarpal and to restore articular congruity. Initial management consists of immobilization in a thumb spica splint, ice, elevation, and analgesia. Early referral to a hand surgeon is warranted because although closed reduction can be achieved, the fragments are difficult to hold in position as a result of the pulling forces of the abductor pollicis longus and adductor pollicis muscle. Definitive treatment consists of conservative management, closed reduction with percutaneous pinning, or, less often, open reduction and internal fixation.
Rolando's Fracture. Rolando's fracture is a comminuted fracture of the base of the thumb metacarpal. Various degrees of comminution occur, but the typical configuration is in a Y- or T-shaped pattern. The severity of comminution is often underrepresented on radiographic studies. The mechanism of injury is the same as in Bennett's fracture, but Rolando's fracture occurs much less commonly and generally has a much worse prognosis. Emergency department management of Rolando's fracture consists of immobilization in a thumb spica splint, ice, elevation, analgesia, and early referral to a hand surgeon for surgical reduction. Definitive
Page 123
treatment is controversial and depends on the severity of comminution of the base of the thumb and the degree of displacement. If open reduction is indicated, a plate is often placed dorsally to maintain the reconstruction; with severe comminution, Kirschner wire fixation, bone graft placement, and external fixation may be used for continued distraction until healing occurs.[35]
Complications. Complications include joint stiffness, degenerative arthritis, and malunion. Malunion is the most common late complication but is usually well tolerated at the thumb CMC joint.[36] Posttraumatic arthritis is more common after Rolando's fracture and may require arthrodesis or resection hemiarthroplasty. Nonunion is rare.
Pediatric Fractures of the Hand Pathophysiology and Assessment The hand is the most commonly injured body part in children.[37] In young children, the most common hand fracture involves a crush injury of the fingertip with an open fracture of the distal tuft.[34] The most distinctive feature of the immature skeleton is the presence of epiphyseal growth centers. Although the cartilaginous epiphysis is believed to be a weak link in the imma-ture skeleton, injuries involving this region reportedly account for only 18% of pediatric fractures.[38] The Salter-Harris classification of epiphyseal fractures is used to direct treatment and predict outcome. The injuries are classified numerically I through V, with higher numbers corresponding to an increased risk for growth disturbance.[39] The most common epiphyseal fracture in the hand is a Salter-Harris type II fracture of the proximal phalanx.[37] It usually results from a twisting or hyperextension mechanism and most often involves the ring and little fingers and the thumb. Although lack of cooperation may make examination difficult, the clinician should look for swelling, ecchymosis, and deformity. In addition, one should palpate for bony tenderness and for tenderness over the collateral ligaments. Persistent limitation of motion in a young child usually implies a significant injury of the bones or joints of the digit. Radiographic studies should be obtained and should include the same views that are obtained in an adult. In addition, comparison views may be helpful, particularly in subtle fractures. Epiphyseal fractures may be particularly difficult because they appear differently at different ages, and their varied radiographic appearance may be mistaken for a fracture.
Management Most pediatric hand fractures can be readily treated with either simple splinting or closed reduction, followed by brief immobilization, usually for no longer than 3 weeks. A plaster or fiberglass gutter splint incorporating the adjacent uninjured finger and including the wrist is the best means of immobilizing a child's finger fracture. The previously mentioned safe position still should be used whenever possible. Some authors advocate that even stable injuries that ordinarily would be treated by buddy splinting in an adult should be protected with full splinting for several weeks in children to prevent further injury. Open reduction and surgical fixation may be necessary for displaced intra-articular fractures, displaced Salter-Harris type III or IV fractures, and unstable fractures that cannot be maintained by closed methods.[40]
Complications Pediatric hand fractures heal more quickly compared with similar injuries in adults. In addition, remodeling allows correction of some step-offs or angular deformities in younger children, but does not correct rotational deformities. The ability of bone to correct angular deformities by remodeling is diminished with age and cannot be relied on in adolescents and adults. Residual deformity is the most commonly reported complication. Other complications, including joint stiffness, tendon adherence, and nonunion, are rarely seen.
Soft Tissue Injuries Soft tissue injuries of the hand are extremely common, accounting for 82% of hand injuries seen in the emergency department.[41] Trauma accounts for most of these injuries to the tendons, ligaments, and cartilage. Although such injuries are not life-threatening, they may result in potentially disabling complications, including joint laxity, loss of motion, chronic pain, swelling, and deformity.
Dislocations and Ligamentous Injuries Ligamentous injuries to the hand are common and often missed. Injury may range from mild sprain to complete rupture and may produce varying degrees of joint instability. Purely ligamentous injuries may be “tears in continuity” (grade I), partial tears (grade II), or complete tears (grade III). The disruption of joints may
Page 124
be complete, with the articular surfaces completely separated (a dislocation), or incomplete, leaving the articular surfaces in partial communication (a subluxation). Because the goal of treatment is to restore functional stability, it is essential to perform a systematic evaluation of joint stability. Functionally, stability may be determined by using a two-phase test of the IP and MCP joints of the hand. Because range of motion is heavily influenced by pain, accurate assessment generally requires digital or wrist block anesthesia in even the most cooperative patients. Active stability is tested by allowing the patient to move the digit through the normal range of motion. Completion of a full range without displacement indicates that adequate joint stability remains. Passive stability is assessed by applying gentle radial and ulnar stress to each collateral ligament and posteroanterior stress to assess volar plate integrity. Stress testing should be done in extended and moderately flexed positions to avoid the stabilizing effect of the volar plate. Comparisons with the same joint of the uninvolved hand may assist in the diagnosis. Supplemental stress radiographs also may be helpful in evaluating difficult cases.[42] The diagnosis of incomplete or partial ligamentous injuries is made when the joint is stable to active and passive stress but is significantly swollen, with pain elicited on stress and palpation of the involved ligament systems. The examiner should attempt to ascertain whether the most tender area is over the central slip (dorsal), collateral ligaments (radial and ulnar), or volar plate (volar). Grade I and II injuries exhibit pain with stability on stress testing. Grade III injuries show instability on stress testing. Stability of the joint provides strong evidence that optimal functional recovery would result from short-term immobilization rather than surgical intervention. Because of the three-dimensional boxlike configuration that the collateral ligaments and volar plate form around the joint, wide displacement indicates that at least two components of the ligament-box complex are disrupted ( Figure 47-41 ).[] Joints with demonstrable instability should be immobilized in a gutter splint and referred for assessment by a hand surgeon to determine whether surgical repair is necessary. Immobilization should be done with the IP joints splinted at 30 degrees of flexion and the MCP joints splinted at 45 to 50 degrees of flexion; when the thumb MCP is involved, it should be splinted in 30 degrees of flexion. Because the long-term effects of joint injuries are almost always joint stiffness and loss of flexion rather than persistent instability, immobilization is usually brief (2 to 3 weeks) and should be followed by a gradual procession of active range-of-motion exercises.[22]
Figure 47-41 The collateral ligam ents on either side of the joint and the volar plate form a boxlike support around the joint. ((From Sim on RR, Koenigsknecht SJ: In Sim on RR [ed]: Em ergency Orthopedics: The Extrem ities, 3rd ed. Norwalk, Conn, Appleton & Lange, 1995.)Appleton & Lange)
Distal Interphalangeal Joint The DIP joint structure is analogous to that of the PIP joint. Additional stability is provided by the adjacent insertions of the flexor and extensor tendons, and dislocations are uncommon. Most dislocations are dorsal and usually are associated with an open wound ( Figure 47-42 ). Routine radiographs are used more to rule out associated fractures than to confirm a suspected diagnosis. Treatment consists of closed reduction under digital or wrist block anesthesia, followed by active and passive stability testing. Reduction usually is accomplished easily by longitudinal traction and hyperextension to distract the bayonet-opposed distal phalanx followed by direct application of dorsal pressure to the base of the distal phalanx. Irreducible cases require surgery for open reduction. Irreducible cases may be caused by an avulsion fracture with interposition in the joint, entrapment of the profundus tendon, or buttonhole tear through the volar plate.[43]
Figure 47-42 Dorsal dislocation of the distal interphalangeal joint without associated fracture. ((From Harris JH Jr, et al: The Radiology of Em ergency Medicine. Baltim ore, William s & Wilkins, 1993, p 446.)William s & Wilkins)
Page 125
If the dislocation is open, the joint is contaminated, and treatment should include debridement and copious wound irrigation. The skin should be sutured and the joint splinted in slight flexion with a dorsal splint for 3 weeks. Most authors recommend prophylactic antibiotics.[]
Proximal Interphalangeal Joint Dislocations of the PIP joint are the most common ligament injuries in the hand. Stability is derived from the strong conjoined attachments of the paired collateral ligaments and the volar plate. Three types of displacement of the PIP joint may occur: dorsal, lateral, and volar. The mechanism of injury is usually sports related with a high-velocity blow to the end of the finger, which causes an axial load and hyperextension. Simple dorsal dislocations result when the volar plate ruptures and the middle phalanx assumes the position of bayonet opposition. Alternatively a lateral dislocation may result from a radially or ulnarly directed force on the joint that leads to rupture of one collateral ligament and at least partial avulsion of the volar plate from the middle phalanx. In lateral dislocations, the ratio of radial-to-ulnar collateral ligament (UCL) rupture is 6:1, and the digit is usually ulnarly deviated. Volar dislocation of the PIP joint is rare. The most common mechanism of injury is a rotary longitudinal compression force on a semiflexed middle phalanx that results in unilateral disruption of a collateral ligament and par-tial avulsion of the volar plate. Physical examination reveals swelling and tenderness over the PIP joint and inability to extend the joint. Routine radiographs of the injured digit reveal the type of dislocation and any associated avulsion fractures.
Management. Small bony fragments at attachment sites seen on radiographs are associated with avulsions of minor ligamentous attachment points and do not indicate the need for open repair. Avulsion fractures involving 33% or more of the articular surface are usually unstable and require surgery.[45] Most closed dorsal and lateral PIP dislocations are treated nonoperatively.[46] Reduction is facilitated by digital nerve block and usually can be accomplished by longitudinal traction and mild hyperextension followed by firm dorsal pressure on the proximal aspect of the middle phalanx. When reduction is achieved, active motion is tested. Reduction is stable if there is no displacement during active range of motion and passive stressing of the joint. More than 20 degrees of deformity and instability with lateral testing indicate a complete ligamentous injury.[47] If there is stability to active range of motion, treatment consists of 3 weeks of immobilization in 20 to 30 degrees of flexion, followed by active exercises. Although stiffness, pain, and swelling are likely to persist for months, the long-term prognosis is good, and subluxation usually does not recur unless the finger is hyperextended again.[20] If the joint is irreducible or there is evidence of complete ligamentous disruption with dislocation on active range of motion, operative repair is required. The management of volar dislocations of the PIP joint is controversial. The dislocation has been described as irreducible and requiring open reduction; however, some authors state that most volar dislocations can be reduced by a closed technique of applying gentle traction with MCP and PIP joints flexed.[48] A stable reduction with repair of the soft tissue structures and transarticular pinning in the fully extended position also has been recommended.[43]
Metacarpophalangeal Joint of the Fingers Pathophysiology. MCP dislocations are considerably less common than dislocations of the PIP joint. The MCP joints of the fingers are resistant to ligamentous injury and dislocation because of their inherent ligamentous structure, their surrounding supporting structures, and their protected position at the base of the fingers. Similar to the DIP and PIP joints, each MCP joint has two collateral ligaments and a volar fibrocartilaginous plate; however, the MCP joints are condyloid joints and permit, in addition to flexion and extension, 30 degrees of lateral motion while the joint is extended. Because of the shape of this articulation, the joint is more stable in flexion when the collateral ligaments are stretched than they are in extension. They are most vulnerable to injury from forces directed ulnarly and dorsally. Isolated injury to the collateral ligaments and volar plate of the MCP joint is rare. These injuries usually occur with hyperextension stress applied to the MCP joint with the finger extended. The patient has ecchymosis and swelling of the joint. Examination reveals tenderness along the joint and varying degrees of instability. Routine radiographs are usually normal, but some authors recommend a Brewerton view to show any evidence of avulsed bone fragments.[49] Treatment for most of these injuries is gentle compression dressing with light plaster reinforcement and early orthopedic referral. Dislocations of the MCP joints of the fingers are relatively rare injuries and are usually dorsal. The most
Page 126
common digit involved is the index finger, followed by the little finger. These dislocations result from hyperextension forces that rupture the proximal volar plate and are divided into simple and complex types. In the simple dislocation (subluxation), the joint appears to be hyperextended to 60 to 90 degrees, and the articular surfaces are in contact without interposed soft tissue. With complex (complete) dislocations, the MCP joint is in moderate hyperextension and angulated, the metacarpal head is prominent in the palm, and the distended palmar skin is dimpled. Complex dislocations have a less striking presentation but are a more severe injury; the volar plate is interposed in the MCP joint space, and closed reduction is not possible ( Figure 47-43 ). Radiographic examination shows an obvious dislocation in the lateral view. Posteroanterior views reveal widening of the joint space in complex dislocations. In addition, sesamoids may be seen in the joint and are a pathognomonic sign ( Figure 47-44 ).
Figure 47-43 The m ost im portant elem ent preventing reduction in a complex m etacarpophalangeal dislocation is interposition of the volar plate within the joint space. It m ust be extricated surgically. ((From Green DP, Rowland SA: Fractures and dislocations in the hand. In Rockwood CA Jr, Green DP [eds]: Fractures in Adults. Philadelphia, JB Lippincott, 1991, p 521.)JB Lippincott)
Figure 47-44 A pathognom onic radiographic sign of com plex m etacarpophalangeal dislocation is the presence of a sesamoid bone in the widened joint space, indicative of interposition of the entrapped volar plate. ((From DeLee JC, Drez D Jr, Miller MD: Orthopedic Sports Medicine: Principles and Practice, vol 2. 2nd ed. Philadelphia, WB Saunders, 2003, p 1387.)Elsevier Inc.)
Management. After appropriate anesthesia, simple dorsal dislocations should be reduced in a way that prevents entrapment of the volar plate in the joint. Reduction is accomplished by flexing the wrist to relax the flexor tendons and applying firm pressure over the dorsum of the proximal phalanx in a distal and volar direction. Excessive hyperextension or longitudinal traction should be avoided. The MCP joints should be splinted in flexion, and referral to a hand surgeon is necessary. Complex dorsal dislocations do not reduce with closed methods and require operative reduction. Volar dislocations are rare and generally require operative reduction.
Carpometacarpal Joints of the Fingers Pathophysiology. The CMC joints of the digit form the base of the transverse metacarpal arch of the hand. The metacarpal bases articulate with each other and with the distal carpal row in a complex interlocking structural arrangement. The joints are supported by strong dorsal, volar, and interosseous ligaments and are reinforced by the broad insertions of the wrist flexors and extensors ( Figure 47-45 ). Dislocations of the CMC joints are uncommon and often are missed.[50] Overall the most commonly injured CMC joint is the little finger, and most of these injuries are dorsal fracture-dislocations.[51] The injury occurs as a result of motor vehicle accidents, falls, crushes, and closed-fist trauma.
Page 127
Figure 47-45 The volar plates of four palm ar m etacarpals are held together firm ly by the deep transverse m etacarpal ligam ent, which is continuous with the volar plate. Eaton calls this the intervolar plate ligam ent. ((From Green DP, Rowland SA: Fractures and dislocations in the hand. In Rockwood CA Jr, Green DP [eds]: Fractures in Adults. Philadelphia, JB Lippincott, 1991, p 518.)JB Lippincott)
Clinical Features and Diagnostic Strategies. Clinically the patient has swelling on the dorsum of the hand and tenderness over the involved CMC joints. Routine radiographs must be viewed carefully because fracture lines may be subtle, and the metacarpals may be obscured by superimposition. Other radiographs that may be helpful include multiple oblique, forearm in 30-degree pronation, and Brewerton views.[51]
Management. Initial treatment consists of ice for comfort, elevation, and analgesia. Closed reduction of the dorsal fracture-dislocation may be attempted under adequate regional anesthesia. Traction and flexion with simultaneous longitudinal pressure on the metacarpal base, followed by extension of the metacarpal head when length has been restored, generally results in reduction. Even in cases in which reduction is achieved by closed means, early referral to a hand surgeon is needed because Kirschner wire fixation is advisable to ensure adequate stability. The late sequelae of fracture-dislocations include pain and weakness from traumatic arthritis secondary to imprecise alignment or chronic dislocation of the CMC joints.
Interphalangeal Joint of the Thumb The IP joint of the thumb is similar to a finger DIP joint except that the phalanges of the thumb are typically larger and stronger than the phalanges of the fingers. Even with the thumb's vulnerable position, IP dislocation is uncommon. Most dislocations are dorsal, and they often are associated with open injuries. Reduction is usually simple after a median nerve block. The joint usually remains stable because the volar plate remains attached to the distal phalanx, and immobilization in mild flexion for 3 weeks usually suffices.
Metacarpophalangeal Joint of the Thumb The MCP joint of the thumb is a condyloid joint that allows mainly flexion and extension; however, it also permits some degree of abduction, adduction, and rotation. Its volar plate and collateral ligaments are stronger than other MCP joints, but its vulnerable position leads to frequent traumatic injury. Overall, injury to the MCP joint of the thumb accounts for five times the injuries of all the other MCP joints combined. Most dislocations of thumb MCP joints are dorsal and result from a hyperextension force that ruptures the volar plate, joint capsule, and at least part of the collateral ligament. Similar to other dorsal MCP dislocations, displacement varies from subluxation of the phalanx to a complex dislocation with the proximal phalanx resting over the metacarpal head. The complex dislocation is not easily reduced because of volar plate entrapment in the joint. Clinically the complex dislocation may show a dimple over the thenar eminence. Radiographic studies confirm the dorsal dislocation and reveal the sesamoids in close proximity to the proximal phalanx.
Management. Closed reduction may be attempted under radial and median nerve wrist block anesthesia. Pressure is directed distally on the base of the proximal phalanx with the metacarpal flexed and adducted. If reduction is difficult, the IP joint and wrist can be flexed to relax the entrapped flexor pollicis longus tendon. When reduction is accomplished, the collateral ligaments should be tested, and reduction should be confirmed by radiography. Stability to active range of motion and stress testing suggest that immobilization in a thumb spica splint with the MCP joint in 20 degrees of flexion for 4 weeks is adequate. Nonreducible (complex) dislocations or dislocations with significant lateral instability require open reduction and operative repair. Hyperextension, instability, and chronic pain on pinching may occur after these injuries.
Ulnar Collateral Ligament Injuries (Gamekeeper's Thumb, Skier's Thumb) Pathophysiology
Page 128
Injury to the UCL was first described as an occupational hazard of Scottish gamekeepers who damaged their thumbs by repeatedly twisting the necks of hares.[52] Skiing is now the most common cause of acute and chronic injury to the UCL.[53] Skier's thumb is the most common upper extremity injury in skiing and results from interference with release of the pole at the moment of impact. UCL rupture occurs 10 times more often than radial collateral ligament injury.[42] The mechanism of injury is forced radial deviation (abduction), and the subsequent tear usually occurs at the insertion into the proximal phalanx. Stener[54] showed that in nearly two thirds of cases of complete UCL rupture, the adductor pollicis becomes interposed between the superficial proximal portion and the deep distal portion of the ligament (see Figure 47-45 ). Besides the collateral ligament, associated injuries of the dorsal capsule and volar plate are common.
Clinical Features. Physical examination reveals swelling and localized tenderness over the ulnar border of the joint and weakness of pinch. Complete and partial ruptures usually can be differentiated by clinical examination. Valgus stress testing of the UCLs is required and should be performed in full extension and in 30 degrees of flexion to avoid the stabilizing effect of the volar plate. If examination is accompanied by pain and guarding, the test should be done under median and radial nerve block at the wrist or local infiltration anesthesia. More than 35 degrees of joint laxity or 15 degrees more laxity than is present in the uninjured thumb is consistent with complete UCL rupture.[37] Routine radiographs should be taken before stressing the joint and may reveal a bony avulsion from the insertion of the UCL into the proximal phalanx or an associated condylar fracture. Radiographic findings of proximal phalanx volar subluxa-tion and radial deviation may indicate complete UCL rupture.[37] Because of the difficulty in diagnosing complete rupture, it is commonly misdiagnosed as a sim-ple sprain in the emergency department, resulting in chronic disability.[55]
Management. Acute partial ruptures of the UCL can be treated effectively by a 4-week period of immobilization in a thumb spica cast; full recovery is the rule. Complete ligament tears require surgical repair because a high percentage are associated with soft tissue interposition from the adductor aponeurosis (Stener's lesion) with limited predicted healing potential. Anatomic repair within 3 weeks of injury achieves good or excellent results in 90% of patients.[37] Long-term complications include chronic pain and instability with the loss of pinch strength, which may require arthrodesis.
Radial Collateral Ligament Injuries. Radial collateral ligament injuries of the MCP joint of the thumb are less common but equally debilitating.[56] The usual mechanism is forced adduction with or without hyperextension. Diagnosis and treatment are generally similar; however, anatomic differences between the two sides of the MCP joint do not allow a Stener-like lesion on the radial side, and the role of surgical repair is not well defined.[37]
Carpometacarpal Joint of the Thumb Injuries of the volar ligament of the thumb CMC joint, similar to in other joints of the hand, may be complete or partial. Complete rupture permits the entire thumb metacarpal to dislocate dorsally.[57] These dislocations are reduced easily but are unstable after reduction. Initial management consists of ice, analgesia, elevation, and application of a thumb spica splint. The patient should be referred to a hand surgeon promptly for possible operative repair of the ligament. If the capsule is allowed to heal with imperfect metacarpal reduction, joint instability may occur with progressive degenerative changes resulting in chronic pain.
Tendon Injuries Tendon injuries may involve one or more of the extensor or flexor tendons in the hand and encompass a spectrum of abnormalities, ranging from simple stretching of the fibers to complete tendon rupture with or without an associated avulsion fracture. The most common mechanisms of injury of tendons are lacerations, avulsions, and crush injuries. In a normal resting position, the fingers are flexed, with the little finger having the greatest degree of flexion and the index finger having the least. In the resting hand, a finger with greater or lesser degree of flexion than that of the opposite hand often indicates a tendon injury. This observation may be especially useful in an uncooperative patient or child. If the patient can move a joint, but active flexion or extension is limited or painful, a partial tendon laceration may be present. To assess the tendons adequately, motion should be tested against resistance. This testing may cause a partially ruptured tendon to rupture, but identifies a lesion that needs surgical repair. The tendon should be placed in maximal stretch before testing to provide for the greatest strength during contraction. As a general rule, extensor injury causes greater impairment of motion than does a similar flexor injury. Vessels and nerves travel
Page 129
closely with flexor tendons, particularly in the fingers. Damage to one of these structures is likely to be associated with damage to the other two. The position the hand was in when the injury occurred is important. When trauma occurs while the hand is held in flexion, the flexor tendons may be transected, and the distal stump would lie distal to the wound. If the hand is in the extended position, however, the tendon stumps would lie at wound edges. When the tendons are injured by a direct blow to the hand or the fingers, the closed injury may hide significant tissue damage. Partial tendon lacerations may be associated with small surface wounds. To help exclude injury, wounds and visible tendons should be inspected while the joints are taken through a full range of motion.
Extensor Tendon Injuries The most common site of tendon injury is the extensors over the dorsum of the hand. The extensors are predisposed to laceration because of their superficial location on the dorsum of the hand and the minimal amount of subcutaneous tissue between the tendon and overlying skin. This anatomic feature also predisposes the extensor mechanism to more complex ten-don injuries, including abrasion, crush, and avulsion. Because the extensor tendons are not constrained in tight fibro-osseous canals except in the wrist, they also are easily located and repaired. Injuries to the extensor tendons have been grouped into anatomic zones for easy understanding and classification. There are different systems for assigning zones, but the most widely accepted is that of Verdan[58] ( Figure 47-46 ). In this system, there are eight zones, from zone I at the DIP joint level to zone VIII at the distal forearm level. The use of zones is convenient for assessing injury patterns, repair techniques, and rehabilitation.
Figure 47-46 Zone classification for extensor tendon injuries. ((From Kleinert HE, et al: Flexor tendon injuries. Surg Clin North Am 61:267, 1981.))
Zone I Injuries Pathophysiology. Zone I is the area over the distal phalanx and DIP joint. In this region, the conjoint extensor tendon is well defined and dorsally positioned. Injuries that occur here disrupt the terminal extensor tendon; they may be open or closed and may occur with or without a fracture. Complete laceration of the conjoint tendon results in a flexed posture of about 40 degrees at the DIP joint. Partial transection results in a lesser extension lag and a decrease in the strength of extension against resistance from a flexed position. The extension lag may increase if the partial injury is not treated appropriately. For this reason, exploration of dorsal lacerations near the DIP joint is important. Mallet finger is the most common injury in zone I and refers to a closed disruption of the distal extensor apparatus.[22] As a result of loss of extensor tendon continuity to the distal phalanx, there is a flexion deformity of the DIP joint. The injury can be seen in any finger but is seen most commonly in the long, ring, and little fingers. Overall, mallet finger represents the most common tendon injury in the hand seen in athletes.[59] The mechanism of injury is often sudden forceful flexion of an extended finger when an object, such as a ball, strikes the tip of the finger. This mechanism is commonly encountered in athletes and is often described as “jamming” the finger. Other mechanisms include hyperextension with axial compression and direct crush injury at the DIP joint. Three types of injury patterns may occur: type 1 tendon rupture (no fracture), type 2 tendon avulsion with a small bone fragment, and type 3 tendon avulsion with a large bone avulsion (25% to 33% of the articular surface) ( Figure 47-47 ).[60] Fractures of varying size are seen in one fourth to one third of cases ( Figure 47-48 ). Small avulsion fractures are usually the result of hyperflexion injuries, whereas large fracture fragments usually result from a hyperextension mechanism.[61]
Page 130
Figure 47-47 Mallet finger occurs with loss of extensor function to the distal phalanx. This may be caused by a tear of the tendon itself or an avulsion fracture of the dorsal base of the distal phalanx.
Figure 47-48 Mallet finger fracture, lateral view. This is an intra-articular avulsion of the dorsal surface of the distal phalanx. ((From Rosen P, et al: Diagnostic Radiology in Em ergency Medicine. St. Louis, Mosb y, 1992, p 181.)Elsevier Inc.)
Clinical Features. In the acute injury, the patient has swelling, pain, and tenderness over the DIP joint. The distal phalanx is flexed because of the unopposed action of the FDP. There is usually complete passive but incomplete active extension at the DIP joint. Although the diagnosis is easily made, the patient often seeks treatment late because the functional disability is not great.
Management. The primary goal of treatment is the maintenance of continuous DIP joint extension until tendon healing occurs. Treatment of type 1 and 2 injuries is nonoperative. Immobilization can be accomplished with either a volar or a dorsal splint made from a variety of materials, including aluminum and plastic ( Figure 47-49 ). The DIP joint is immobilized in slight hyperextension for 6 to 8 weeks, but the PIP and MCP joints are allowed to move freely.[] Definitive treatment of a type 3 injury is controversial. Some authors recommend operative repair; others recommend conservative management with uninterrupted splinting of the digit.[12]
Figure 47-49 Only the distal interphalangeal joint is m obilized in treating m allet fingers. This m ay be done with a dorsal padded alum inum splint (A), a volar unpadded alum inum splint (B), a Stack splint (C), a m odified Stack splint (D), or an Abouna splint (E). Each of these splints uses a three-point fixation principle. ((From Green DP, Rowland SA: Fractures and dislocations in the hand. In Rockwood CA Jr, Green DP [eds]: Fractures in Adults. Philadelphia, JB Lippincott, 1991, p 450.)JB Lippincott)
Open zone I injuries that divide the extensor tendon are treated by suturing the cut ends ( Figure 47-50 ). Partial and compete lacerations are repaired with either a roll suture or figure-of-eight stitch using 5-0 nonabsorbable sutures. This repair should be followed by continuous splinting of the DIP joint in full extension for a minimum of 6 weeks.
Page 131
Figure 47-50 Lacerations of the extensor m echanism over the distal joint with mallet finger deform ity (A) can be repaired by a roll-type suture, which simultaneously approxim ates skin and tendon (B and C). A small dressing is applied with a splint to m aintain the joint in full extension. Sutures are rem oved at 10 to 12 days. A figure-of-eight vertical suture (D) also m ay be used, which sim ultaneously closes the defect in tendon and skin. Splinting is mandatory for 6 weeks. ((From Doyle JR: In Green DP [ed]: Operative Hand Surgery. New York, Churchill Livingstone, 1993, p 1939.)Churchill Livingstone)
Prognosis. The results of treatment of mallet fingers are not universally good by any method. Although most patients are improved, only 30% to 40% regain normal function in the DIP joint after treatment.[63] Possible delayed complications include dorsal deformity, cold intolerance, pain, and development of a swan neck deformity ( Figure 47-51 ). This abnormality develops when the lateral bands displace proximally and dorsally, resulting in increased extension forces on the PIP joint. Secondarily, the extensor lag at the DIP joint increases because the force of the FDP tendon is unopposed, and the tendon is functionally increased by the greater distance required to pass over the hyperextended PIP joint. The swan neck deformity is not seen acutely, unless the injured finger has a normally hyperextended PIP joint. Classically, this deformity occurs as a complication of a chronic untreated mallet finger.[63]
Figure 47-51 Swan neck deform ity of the fingers.
Zone II Injuries Zone II is the area over the middle phalanx. As the lateral bands blend dorsally to form the conjoint tendon, they are thin and oriented around the dorsal half of the middle phalanx. Injuries here are usually the result of simple lacerations that seldom transect all of the dorsal apparatus. Examination reveals a typical mallet deformity. The treatment is identical to that of open zone I injuries.
Zone III Injuries Pathophysiology. Zone III is the area over the PIP joint. The central tendon is the most commonly injured structure in this zone and represents the second most common closed tendon injury in athletes.[59] The mechanisms for closed rupture include forced flexion of an actively extended finger, a direct blow to the dorsum of the PIP joint, and hyperextension with volar dislocation of the PIP joint. It often results from a “jamming” injury. Lacerations that occur just distal to the PIP joint also may divide the central tendon and readily extend into the joint. Wounds must be carefully explored to define the status of the PIP joint capsule. Disruption of the central tendon causes an imbalance in the extensor mechanism. The FDS is now unopposed and flexes the PIP joint. The lateral bands displace volarly to the axis of the PIP joint and become flexors of the joint. In addition, the extensor hood retracts proximally, causing extension of the MCP and DIP joints. The resulting tendon imbalance leads to the so-called buttonhole, or boutonnière, deformity, with flexion of the PIP joint and hyperextension of the DIP and MP joints ( Figure 47-52 ). Although open injuries of the central tendon may cause an acute boutonnière deformity, this is usually delayed several weeks after a closed athletic injury.
Figure 47-52 Buttonhole (boutonnière) deform ity of the index finger with swan neck deform ity of other fingers.
Page 132
Clinical Features. Early diagnosis of a closed central tendon rupture or avulsion is difficult before the boutonnière deformity has developed. The patient typically has a history of trauma to the involved digit and a painful, swollen PIP joint. The finger is held in slight flexion at the PIP joint and slight extension at the DIP joint. Rupture of the central tendon may be differentiated from the more common injury to the collateral ligament by the location of the maximal area of tenderness of the dorsum rather than sides of the joint and by the patient's inability to extend the PIP joint actively. PIP joint extension can be tested by having the patient attempt to extend the fingers against slight resistance with the hand flat on the table and the PIP joint flexed 90 degrees over an edge of a table (the tabletop test). Radiographs are typically normal but may be diagnostic if an avulsion fracture of the volar base of the middle phalanx is visualized on the lateral view.
Management. Patients with suspected closed central tendon injuries should be treated with splinting of the PIP joint in full extension for 5 to 6 weeks. Only the PIP joint should be immobilized, and passive and active DIP joint flexion is encouraged from the outset. Operative repair may be required for an acute closed boutonnière injury associated with a displaced avulsion fracture and injury with volar PIP joint dislocation. Early referral to a hand surgeon is advised. When an acute boutonnière deformity is caused by an open injury, exploration of the central slip is mandatory, and a hand surgeon should be consulted. Primary repair of the tendon and Kirschner wire fixation of the PIP joint are often performed. If the joint capsule has been violated, the joint should be thoroughly debrided and irrigated, and the use of prophylactic antibiotics is recommended.
Zone IV Injuries Zone IV includes the area over the proximal phalanx. The clinical findings are similar to the findings of zone III injury, but are less severe because the PIP joint and lateral bands are intact. The resulting injury is usually partial, and the tendon ends usually do not retract appreciably. These injuries are treated with primary or delayed primary repair and appropriate splinting for 3 to 6 weeks. Simple injuries in this zone can be well approximated with 5-0 nonabsorbable sutures with buried knots. Immobilization should be done with maintenance of the wrist in extension and the MCP joints in about 15 degrees of flexion. Tendon adhesions are common in this zone because of associated damage to the periosteum.
Zone V Injuries Zone V injuries involve the areas over the MCP joint and should be presumed to be due to a human bite until proved otherwise. These injuries occur most commonly over the MCP joints of the long and ring fingers. Radiographs are mandatory and may include Brewerton views to assess the metacarpal head closely for injury. The clinical findings of injuries to the extensor tendon at this level are flexion of the MCP joint and inability to extend the joint fully. In an open joint injury caused by a human bite, the potential for mixed aerobic and anaerobic infections is high. Operative exploration, debridement, and irrigation are necessary. A combination of penicillin and antistaphylococcal agent or a single p -lactamase inhibitor drug is recommended empirically for infections related to human bites.[64] The wound is left open and may be closed at 4 to 5 days if free from infection. The resultant tendon injury is usually only a partial laceration and may be treated with primary or delayed primary repair. For simple lacerations at this level caused by a sharp, clean object, primary repair is indicated. The involved tendon ends do not retract and can be approximated with 4-0 nonabsorbable sutures. Sagittal bands also must be repaired if injured to prevent loss of extension or subluxation. The wrist and MCP joints should be immobilized. Early referral to a hand surgeon is advised.
Zone VI Injuries Zone VI includes the area of the dorsum of the hand. Although these injuries may have a similar clinical appearance to zone V injuries, the joint is not involved, and these injuries are generally not as severe. Because the extensor tendons are superficial at this level, a relatively trivial-appearing skin laceration may be associated with one or more tendon lacerations. If the injury is proximal to the junctura tendineae, the patient may be able to extend the involved MCP joint because weak extensor forces are transmitted to the junctura from adjacent extensor tendons. The tendons in this area are round or oval and easily exposed. Primary repair using a modified Kessler stitch with a 4-0 nonabsorbable material or a figure-of-eight stitch with a buried knot on the deep, palmar surface of the tendon suffices. This repair is followed by immobilization of the wrist at 30 degrees of extension and the
Page 133
MCP joint at neutral. Referral to a hand surgeon for delayed primary repair also is appropriate.
Zone VII and VIII Injuries Zone VII and VIII injuries involve the wrist and forearm. Management follows basic principles for tendon injuries.
Flexor Tendon Injuries Pathophysiology. Flexor tendon injuries are not as common as injuries to the extensor complex and are often subtle. The most common mechanism of injury is laceration, but closed traumatic disruption also may occur. FDP avulsion is the third most common tendon rupture in the hand in athletes.[59] This injury is usually sports related and involves a hyperextension force applied to an actively flexing digit; the classic example is a football player who grabs the jersey or pants of an opponent who is breaking free from a tackle. Although the reason is not clearly understood, more than 75% of these injuries involve the ring finger.[65] Because of the closed nature of these injuries, the patient may not seek immediate care, or the condition initially may be misdiagnosed.
Clinical Features. Careful assessment is necessary to diagnose flexor tendon disruption and associated neurovascular injury. With the normal hand at rest, there is a cascade of flexion of the digits, beginning with less flexion at the index finger and progressing to more flexion toward the little finger. An injury to a flexor tendon may be evident if the involved finger does not assume a naturally flexed position. Complete disruption of the profundus tendon results in an extended position of the DIP joint as a result of unopposed extensor forces. If the FDS is completely severed, or a partial tendon injury has occurred, the digit rests in less flexion than normal. An abnormal posture of the injured digit may suggest a flexor tendon injury; this is usually confirmed by a functional examination. The FDP and the FDS should be tested separately as previously described. This examination must be observed carefully because the patient may flex the distal tip with an intact profundus, but an injury to the FDS precludes flexion at the PIP joint. Disruption of the FDP tendon leads to loss of flexion at the DIP joint, instability in pinch, and loss of grip strength. Partial flexor tendon lacerations may be clinically occult. Because the tissue is torn and not lacerated, the degree of soft tissue injury and hemorrhage is greater than that seen with a laceration in the same zone. As a result, scarring within the sheath is often significant, and adjacent superficialis tendon may become secondarily involved.[62] Such injuries may be present if the patient complains of subjective weakness or if there is an abnormal position of the hand at rest. Clinically, injuries are associated with pain and weakness with flexion against resistance. Despite these findings, it may not be possible to arrive at a complete and accurate diagnosis until the wound is surgically explored. The palmaris longus, which is not present in approximately 15% of people, is not a functionally significant wrist flexor. Palmaris longus lacerations have tremendous diagnostic significance, however, because most (80% to 90%) have concomitant partial or complete median nerve lacerations. For this reason, all patients with palmaris longus lacerations should be assumed to have median nerve laceration until proved otherwise.[66]
Management. Flexor tendon repairs require the expertise of a hand surgeon. Immediate or delayed primary repair is now advocated for most acute flexor tendon injuries, including avulsions of the FDP and injuries involving the so-called no man's land, which extends from the distal palmar crease to the midportion of the middle phalanx. The advantages of primary repair with surgical reapproximation over secondary grafting for treatment of acute injuries have been well described in the literature.[67] Relative contraindications to immediate primary flexor repair are few and include crush wounds with poor skin coverage or tendon loss greater than 1 cm, possibly contaminated injuries over 12 hours that cannot be converted to clean wounds (human bites are not repaired initially), the presence of inadequate pulleys, an uncooperative patient, and surgical inexperience.[68] In such cases, a delayed primary repair can be performed 10 days after injury. Secondary repair of flexor tendons may be performed 4 weeks after injury but is considered late after that. Generally the results of primary, delayed primary, and early secondary repair are about equal. Treatment of partial flexor tendon lacerations is controversial, but referral to a hand surgeon for further exploration and possible repair is prudent. If a hand surgeon is not immediately available, open wounds should be copiously irrigated, closed with 5-0 nylon, and splinted with the wrist in 30 degrees of flexion—the MCP joints flexed approximately 70 degrees and the IP joint flexed 10 to 15 degrees. This flexion ensures that no further damage occurs to the tendon and that the tendon will not contract further on movement. The patient also should receive tetanus immunization as indicated, and most authors recommend empiric use of broad-spectrum antibiotics. Most
Page 134
closed tendon injuries require referral to a hand surgeon because of the risk of long-term disability.
Complications. With optimal management, 80% of patients with flexor tendon injuries have good to excellent results.[67] Injuries involving the no man's land may result in poor outcomes and occasionally require tendon grafting. Overall, adhesions remain the most significant problem after operative repair. Other complications include triggering, bowstringing, and intratendinous epidermoid cyst formation.[69]
Mutilating Injuries Mutilating injuries to the hand are encountered frequently in the emergency department. These are severe multistructural injuries that destroy the anatomy and functional integrity of the hand. Initial evaluation should focus on preservation of vital structures, analgesics, early consultation, wound care with debridement of devitalized tissue, and antibiotics. Evolving over recent years is a more aggressive push with respect to procedure timing regardless of being single stage or multistage.[70] Successful long-term clinical and socioeconomic outcomes have brought focused attention on procedure timing. The concept of early primary reconstruction with fast rehabilitation should be pursued based on case profile.[70] One such type is snowblower-associated or lawnmower-associated hand injuries, which can result in substantial deformity and disability. Snowblower injuries typically occur in clusters and are responsible for approximately 1000 amputations and 5000 emergency department visits annually.[71] The dominant hand is involved approximately 86% of the time, with middle and ring fingers most commonly injured. Phalangeal fractures are the most common type of injury.[72] Snowblower injuries are often managed as open fractures with intravenous antibiotics, irrigation, and debridement, with repair of bone, soft tissue, and nail bed structures.[ 72] Irreparable devascularization currently is considered the only absolute indication for immediate or early digital amputation after injury.[73] The concept and techniques for reimplantation and revascularization in mutilating injuries in children are similar to those of adults.[74]
Fingertip Injuries Fingertip injuries may involve any structures distal to the DIP joint, including the skin, volar pulp tissue, distal phalanx, nail, nail bed, and related structures. These are among the most common injuries of the upper extremity and, although usually minor, may be associated with significant long-term consequences. The goals of management are to maintain finger length and achieve good tissue coverage, near-normal sensibility, and early functional recovery.
Fingertip Amputations Classification. Fingertip amputations are the most common type of amputation of the upper extremity. In zone I injuries ( Figure 47-53 ), the proximal two thirds of the nail bed are preserved. In zone II injuries, bone is exposed, and in zone III injuries, the entire nail bed is lost.[75] Radiographic studies are indicated if bony avulsion injury or fracture cannot be excluded. Most of these fingertip injuries can be managed on an outpatient basis.
Figure 47-53 Classification of nail bed and fingernail injuries: zone I, distal to the bony phalanx; zone II, distal to lunula (between distal end of lunula and end of phalanx); zone III, proxim al to distal end of lunula. ((From Rosenthal EA: Treatm ent of fingertip and nail b ed injuries. Orthop Clin North Am 14:675, 1983.))
Management. Treatment of distal fingertip injuries is controversial; consequently, management must be individualized, and few guidelines are available. Generally, most hand surgeons try to maintain length of the thumb by whatever means possible.[75] The index finger is considered next before the other fingers. An intact pulp- to-pulp pinch mechanism is the principal goal. Other factors to consider include the patient's age, health, occupation, and handedness. In most fingertip amputations distal to the DIP joint, adequate care can be provided with conservative wound
Page 135
management. The simplest and often best method for managing a fingertip amputation is allowing the wound to heal by secondary intention. This method is generally effective and produces good results if the wound is less than 1 cm. Large dorsal wounds also heal well by this method. It is the treatment of choice in childhood fingertip amputations, particularly when no bone is exposed. In cases in which a small protuberance of phalangeal bone (<0.5 cm) is exposed, it may be trimmed back with a rongeur to just below skin level and allowed to heal by secondary intention; if the bone is left exposed without soft tissue coverage, the patient will need an operative procedure. In most cases, the wound heals through a process of granulation, wound contracture, and re-epithelialization within a few weeks. Initial management should include careful and meticulous wound cleansing, a nonadherent dressing, appropriate tetanus prophylaxis, and splinting to protect the tip. Amputations that involve the distal phalanx usually are treated as contaminated open fractures with an initial intravenous dose of a cephalosporin followed by an oral course. Patients should have appropriate follow-up care to ensure adequate healing and recovery. Fingertip injuries that involve significant soft tissue (especially volar) or bone loss usually require the expertise of a hand surgeon. Surgical management may include primary closure, full-thickness or partial-thickness skin grafts, composite grafts, adjacent flaps, regional flaps from the hand, distant flaps, and reimplantation. Most of these operative techniques are best performed as primary procedures under ideal circumstances or as a delayed procedure when necessary. A flap may be used to cover exposed bone or soft tissue avulsion and to add bulk to the tip. The nail bed tissues should be preserved because the presence of a nail affects the cosmetic result. At least 5 mm of healthy nail bed distal to the lunula is needed for nail adherence. Skin grafting is a common method for treating fingertip amputations with significant avulsed tissue and can provide a functional and an esthetic reconstruction.
Complications. These injuries commonly leave the patient with a painful, cold-intolerant fingertip; this complication occurs after primary closure, coverage with grafts or flaps, and healing by secondary intention. Skin grafting may result in induration, fissuring, and diminished sensibility. Nail deformity is common, particularly if there is considerable volar loss of tissue.[76]
Acute Nail Bed Injuries Injuries of the nail bed most commonly result from localized trauma to the nail with subsequent compression of the nail bed. The most common type of injury is the simple laceration followed by stellate laceration, crush, and avulsion.[77] The middle and distal thirds of the nail bed are the most common sites of injury, and 50% of injuries involve fractures of the distal phalanx or tuft.[78] Radiographs are required in most cases to show occult fractures and foreign bodies.
Subungual Hematoma. Subungual hematomas result from crush injury or blunt trauma to the nail bed with bleeding from the rich vascular bed. The nail bed is predisposed to injury because it is interposed between the firm nail and the distal phalanx. The injury is manifested by pain and dark red-to-black discoloration of the nail bed and is classified by the percentage of area beneath the nail that is involved. When the fingertip is unstable or the mechanism of injury suggests a significant distal phalanx fracture, a radiograph should be obtained to identify associated fracture.
Management. Small subungual hematomas do not require drainage; the blood is incorporated into the nail and eventually removed with the free edge. Large hematomas cause significant discomfort and should be removed by nail trephination with a heated paperclip or a hot microcautery unit. Some authors recommend a surgical scrub of the finger before perforation of the nail to prevent contamination of the subungual area and the subsequent risk of infection and potential osteomyelitis, but this is generally unnecessary. Anesthesia is not necessary, and pain relief is immediate with decompression. If a significant fracture is present, the digit should be splinted. Although a distal phalangeal fracture with a subungual hematoma is technically an open fracture, such injuries usually heal without problems. Ungual tuft fractures are not associated with osteomyelitis. The risk of infection with an open fracture of the phalanx proper must be considered, and a broad-spectrum antibiotic and close follow-up monitoring are recommended. Patients with significant hematomas should be informed that they may lose the nail. Simon and Wolgin[79] attempted to correlate the association between subungual hematomas, digital phalanx fractures, and occult nail bed lacerations. In their series, patients with a subungual hematoma greater than half the size of the nail had a 60% incidence of nail bed laceration requiring repair, and if there was an associated fracture of the distal phalanx, the incidence was 95%. If more than 25% to 50% of the visible
Page 136
portion of the nail is undermined by hematoma, many authors recommend removal of the nail, inspection of the nail bed, and repair of injuries.[77] Another study found no notable differences in outcome between nail trephination alone versus formal nail bed repair regardless of hematoma size in cases with an intact nail and nail margins.[80]
Nail Bed Lacerations. Lacerations of the nail bed should be repaired to minimize esthetic deformity and the duration of functional impairment. These injuries generally do well after primary repair, but late reconstruction of the nail bed is unpredictable, and usually little improvement is obtained. Simple and crushing lacerations should be repaired accurately with 5-0 or 6-0 absorbable suture, ideally under loupe magnification. The results for both should be satisfactory in more than 90% of cases.[80] After the nail bed is accurately approximated, a hole is burned through the nail to allow drainage of serum or hematoma from the subungual area after the nail is reinserted into the nail fold. The avulsed nail may be sutured in place or secured with tape. A single thickness of nail-shaped Adaptic or other nonadherent gauze may be placed in the nail fold if the nail is unavailable. The replaced nail or gauze is used as a temporary splint to help protect the integrity of the underlying nail bed and maintain the fold for new nail growth and help prevent synechiae and subsequent nail deformity. Complete nail growth takes 70 to 160 days, but after the injury the growth pattern often is changed. Nail bed avulsion commonly leaves fragments of nail bed attached to the undersurface of the avulsed nail.[81] In these cases, it is advisable to replace the nail as accurately as possible onto the avulsion site. Repair should be done using mattress sutures without attempting to separate the nail from the nail bed. If the tissue is not available and the defect is small, effective healing occurs by secondary intention.
Clenched-Fist Injuries All human bites should be considered serious and at risk for significant complications. Clenched-fist injuries, also called “fight bite,” are notorious for being the worst human bites. Inadequate initial management leads to significant morbidity. Misleading history, innocuous wound appearance, intoxication and lack of cooperation of the patient leading to inadequate examination, patient reluctance to admit the nature of the injury, delayed presentation, and inadequate exploration all may lead to mismanagement. Clenched-fist injuries have the highest incidence of complications of any closed-fist injury and of any type of bite wound.[82]
Clinical Features The classic injury is a bite wound over the third MCP joint, but injury can occur over any joint. Soft tissue injury is apparent with possible extensor tendon injury and violation of the joint capsule. The fist is subsequently opened, and the bacterial innoculum is dragged with the extensor tendon and soft tissue proximally into the dorsum of the hand.[82] Presentation may be acute or delayed. Swelling, limited range of motion, erythema, and pain out of proportion to severity of injury are typical findings. Pain is more severe with range of motion.
Management Aggressive management should be employed in all cases. Radiographs should be considered in all cases. Immediate consultation with a hand surgeon should be done. Analgesics, tetanus, cultures, intravenous antibiotics, appropriate wound care, elevation, and admission should be considered for all patients. Foreign bodies must be excluded with radiographic studies and possibly exploration. Tendon injuries must be ruled out with careful exploration. The hand should be splinted in the position of function. Pathogens are usually polymicrobial, with Staphylococcus aureus, streptococci, and anaerobes the predominant species. Multiple regimens are recommended with amoxicillin/clavulinic acid or penicillin with a first-generation cephalosporin commonly used.
High-Pressure Injection Injuries Epidemiology High-pressure injection injuries to the hand are uncommon, and most are occupation related. The usual cause is industrial equipment, with machinery such as grease guns, spray guns, and diesel engine injectors accounting for most of these injuries.[83] A wide variety of materials, including paint, paint thinner, grease, oil, hydraulic fluid, plastic, wax, water, and semifluid cement, have been reported to be injected. Generally, substances that are highly viscous (e.g., grease) require higher forces than do paint, oil, and solvents. The high pressures involved are sufficient to penetrate skin from a distance, and contact of the device with the hand is not a prerequisite for injury to occur. High-pressure injection injuries have been associated with
Page 137
amputation rates of 60% to 80%.[84] Early recognition and intervention is necessary. Even with early intervention, the injury leads to significant impairment. Amputation is more likely if debridement is delayed more than 6 hours.[84]
Pathophysiology Patient characteristics and injury circumstances are often similar in high-pressure injection injuries. The patient generally has a history of coming into close proximity to the jet stream during cleaning of the nozzle, testing, or operation of the equipment. The patient is usually a young working man, and the nondominant hand is most commonly involved, with the index finger the most common site. Operator inexperience has been cited as the most common cause of injury. Tissue injury from high-pressure injection generally depends on physical, chemical, and biologic factors. Of particular importance are the type, amount, and velocity of injected material and the anatomic location. The most important factor is the type of material injected. The material determines the likely tissue inflammatory response and the resulting fibrosis that develops during healing. Paint and paint thinner produce a large, early inflammatory response and result in a high percentage of amputations.[85] In contrast, grease injuries cause a small inflammatory response and have a lower amputation rate, but are associated with oleogranuloma formation, fistulae, scarring, and loss of digit function.[86] The amount of material injected into the confined space of the digits or palm determines the degree of mechanical distention and the potential for vascular compromise. The velocity of the injected material and the site of tissue penetration determine dispersion, which may include the digit, hand, and forearm.
Clinical Features The patient who seeks treatment early after injury may have minimal symptoms with either an innocuous entrance wound or no visible break in the skin. Fusiform swelling resulting from mechanical distention of the tissue by the injectant usually is apparent. Several hours later, the involved digit or palm becomes extremely painful, swollen, and pale because of vascular compromise and tissue necrosis. Careful examination is necessary to document the extent of injury and associated neurovascular function. Radiographs of the involved hand help determine the spread of material and the amount of debridement necessary because certain injected materials are radiopaque. In addition, they may reveal subcutaneous emphysema.
Management Initial emergency department management includes splinting, elevation, tetanus prophylaxis, analgesia, and broad-spectrum antibiotics. Digital blocks are contraindicated because of the potential for increased tissue pressure, which may aggravate vascular compromise. Urgent hand surgery consultation is warranted because most cases require early extensive surgical decompression and debridement. The keystone in treatment of these injuries is prompt recognition of the severe nature of the injury and aggressive early debridement. Current treatment methods using irrigation and wide debridement have reduced the amputation rate significantly.[87]
Complications Early recognition and treatment, including operative decompression and debridement, greatly influence outcome. Early amputation should be considered in cases in which the affected digit is initially cool or poorly perfused.[88] In most other cases, joint stiffness is a late sequela.
Amputations and Ring Avulsion Injuries Few epidemiologic studies have been done on amputation injuries. Amputations have been reported to constitute 0.1% to 1% of all hand injuries.[2] Amputation may be complete or partial. Injuries with interconnecting tissue between the distal and the proximal portions are considered incomplete, or partial, amputations. Complete amputations are replanted, whereas partial amputations are revascularized. Traumatic amputations most commonly result from local crush injuries and occur infrequently from a sharp guillotine mechanism. Partial and complete amputations reportedly occur with equal frequency. The former are often related to the use of power saws and lawnmowers. Ring avulsions include a spectrum of injuries from partial degloving of the skin of a finger to loss of the entire digit and entire length of a flexor tendon. These injuries usually occur when a ring on a finger catches on an object during a fall. In addition to neurologic and arterial injuries, there may be complete disruption of the venous return of the finger. Generally, these injuries represent complex management problems, and treatment may range from primary amputation to microvascular repair with reimplantation and free tissue transfer in addition to local flap, pedicle flap, or graft coverage.[89]
Page 138
The initial care and treatment of the patient who has a body part amputated are the same as care and treatment for any trauma patient. After the initial primary assessment and stabilization of the patient, the injured extremity should be examined carefully with documentation of neurologic, vascular, and musculotendinous function. Subsequent care should be directed toward preservation of the limb and its components. General management goals include the following: provide supportive care, such as control of hemorrhage with direct pressure and elevation; prolong the time that the amputated tissues remain viable; protect wounds from further injury; and arrange expeditious consultation by a surgical subspecialist. With few exceptions, all completely amputated parts should be considered for reimplantation, and all partially amputated parts should be considered for revascularization. In complete amputations, the proximal stump and the amputated part should be examined for the degree of tissue injury, contamination, and associated injuries. Gross contamination can be removed by irrigation with normal saline. Local antiseptics, especially hydrogen peroxide or alcohol, should not be used because they may damage viable tissues. The wound should not be manipulated, clamped, tagged, or traumatized further in any way. The stump should be covered with a saline-moistened sterile dressing to prevent further contamination and desiccation and elevated to help reduce edema and control bleeding. The amputated part requires minimal handling and should be cooled as soon as possible. After wrapping in saline-moistened gauze, the part is sealed in a dry plastic bag and placed in ice water. Ice should not come in direct contact with the tissue because this can cause local damage. Amputated parts should not be discarded or sent to the pathology department because even if they cannot be replanted, they may serve as a donor source for skin, bone, or vessel grafts. Radiographs of the amputated part and proximal stump should be obtained. The use of analgesic medications may be necessary, and appropriate tetanus prophylaxis may be administered. The use of prophylactic antibiotics is indicated in amputation injuries because significant devitalized tissue is often present. Most authors recommend empiric coverage for S. aureus with a combination of penicillin G and an antistaphylococcal antibiotic or first-generation cephalosporin. Treatment for partial amputations with vascular compromise is the same as that just described. The wound should be cleaned with normal saline irrigation, wrapped in a sterile moist dressing, and splinted to protect it from further injury. Cold packs are applied to the dressings to prevent warm ischemia. The time that an amputated part can survive before reimplantation has not been determined. As a general rule, the more proximal the amputation, the less ischemia time the amputated part can tolerate. Attempts to extend viability during ischemia have shown that the most important controllable factor is the temperature of the amputated part. Warm ischemia may be tolerated for 6 to 8 hours; cooling the part to 4° C extends this time to approximately 12 to 24 hours with distal amputations. There are reports of successful reimplantation of digits after 30 hours of warm ischemia.[90] The decision of whether to attempt reimplantation should be made by the surgeon who is responsible for performing the procedure. Patient selection generally is based on the nature and level of the injury and patient age and health-related factors. The classic indications and contraindications for reimplantation are listed in Box 47-2 . The thumb is required to preserve the function of opposition, and all such amputations should be considered for microvascular salvage regardless of the level of amputation or mechanism of injury. Loss of the thumb is equivalent to a 40% loss of function of the hand.[91] Similarly, all amputations in children should be considered for reimplantation. In reimplantation of digits amputated distal to the insertion of the FDS between the PIP joint and the DIP joint, good motor and sensory function is often achieved. If the amputated part is crushed, mangled, or amputated at multiple levels, however, reimplantation is usually contraindicated. Digits that cannot be replanted require skin coverage by flaps or ray resection. BOX 47-2 Classic Indications and Contraindications for Replantation
Indications Multi ple digit s Thu mb Wris t and
Page 139
forea rm Shar p amp utati ons with mini mal to mod erate avul sion proxi mal to the elbo w Singl e digit s amp utate d betw een proxi mal inter phal ange al joint and dista l inter phal ange al joint (dist al to flexo r digit oru m supe rficia lis inser tion) All pedi atric amp
Page 140
utati ons
Contraindications Amp utati ons in unst able patie nts seco ndar y to other life-t hreat enin g injuri es Multi ple-l evel amp utati ons Self-i nflict ed amp utati ons Singl e-dig it amp utati ons proxi mal to the flexo r digit oru m supe rficia lis inser tion Seri ous unde rlyin
Page 141
g dise ase, such as vasc ular dise ase, com plica ted diab etes melli tus, cong estiv e heart failur e Extr eme s of age
Complications Replanted fingers and hands never regain premorbid function. Replanted and revascularized parts may develop cold intolerance, stiffness, loss of sensation, pain, malunions, and nonunions. Even successful reimplantations may require repeated operative procedures and involve prolonged disability. Necrosis is an obvious sign of failure.
Vascular Injuries Significant vascular disorders of the hand are uncommon compared with other problems of the hand. The vascular supply to the hand and digits is duplicated so that isolated arterial injuries to either side seldom result in ischemia. Lacerations of the arteries of the hand may stop bleeding by the time the patient is evaluated; in these situations, a history of pulsatile bleeding is highly suggestive of an arterial injury. Although most arterial injuries are the result of penetrating trauma, blunt trauma to the hand occasionally can result in arterial thrombosis or a false aneurysm.[92] In addition, associated injuries should not be overlooked. Because digital nerves invariably cross with and are superficial to the digital artery, an arterial lesion should raise the possibility of an accompanying nerve injury. Circulatory status is assessed as previously described by observation for cyanosis or pallor, palpation of radial or ulnar pulses at the wrist, assessment of capillary refill, and the use of Allen's test. Ischemic pain is the most common initial complaint of vascular insufficiency, along with physical manifestations of pallor and gangrene. The presence of a mass, with or without pain and tenderness, is the second most common initial complaint.
Management Lacerations or amputations of the upper limb rarely cause life-threatening hemorrhage. Even a major vessel that is completely transected usually retracts, constricts, and clots. Major vessels often continue to bleed briskly, however, from partial transections with life-threatening hemorrhage. Usually, hemorrhage can be adequately controlled with direct pressure and elevation. If necessary, a proximally placed blood pressure cuff inflated to 30 mm Hg above systolic pressure can be used for short periods (<30 minutes) to control severe bleeding. Vascular clamps and hemostats should not be used in the emergency department to control bleeding in the hand because of the danger of inadvertently crushing nerves and tendons. Lacerated arteries should be repaired if symptoms of ischemia are present or if there is an associated nerve injury. Arterial repair is not mandatory in isolated arterial injuries with good distal vascularity because there is a high rate of thrombosis after reanastomosis. If the decision is made not to repair a lacerated artery, both stumps should be ligated to prevent further bleeding. Palmar arch lacerations may be difficult to visualize in the
Page 142
emergency department and usually require surgical exploration to control bleeding.
Compartment Syndrome in the Hand A compartment syndrome develops when elevated pressure within a closed fascial space reduces perfusion to the point of muscle and nerve dysfunction. In the hand, 10 compartments are visible on cross section through the palm ( Figure 47-54 ). In addition, the fingers are compartmentalized by fascia and skin at flexor creases. Because these compartments are not interconnected, each additional compartment must be surgically decompressed if muscle ischemia is suspected.[93]
Figure 47-54 Cross section through the palm showing com partm ents of the hand. ((From Rowland SA: In Green DP [ed]: Operative Hand Surgery, 3rd ed. New York, Churchill Livingstone, 1993, p 670.)Churchill Livingstone)
Nerve Injuries Nerve injuries may result from a direct blow, puncture or laceration, crush injury, injection injury, and amputation. These injuries are primarily divided into three groups: neurapraxia, axonotmesis, and neurotmesis. In neurapraxia, there is loss of function of the nerve, but the axon, Schwann's sheath, and endoneurium remain intact. Recovery in these cases is usually complete within days. In axonotmesis, the axon is severed within an intact endoneurial tube. The distal axon degenerates and is absorbed after disruption. The proximal portion of the severed axonal stump can regenerate along the intact endoneurial tube at a rate of approximately 1 to 3 mm/day. Neurotmesis refers to complete disruption of all nerve elements. Regrowth of the proximal axonal endings does not occur along the endoneurial tubes, unless the severed nerve endings are reapproximated.[94] Peripheral nerve injuries are diagnosed by physical examination by showing loss of motor or sensory function. Specific nerves at risk should be examined as previously outlined. Injury most commonly involves one of the digital nerves, but also may be localized to the median, radial, or ulnar nerves.[37]
Management Identification of the injury and proper referral are important aspects in the initial management of patients with nerve injuries in the hand. Patients with closed nerve injuries not associated with compartment syndromes should be referred to a hand specialist for serial examinations. All digits that have lost function as a result of a nerve injury should be splinted to prevent further inadvertent injury. If function does not return within 3 weeks, electromyograms and nerve conduction studies can help differentiate neurotmesis from axonotmesis and determine the need for surgical exploration.[95] Lacerated nerves require reapproximation by hand surgeons. In general, all motor branches of the ulnar and median nerves should be repaired. Additionally, digital nerve injuries proximal to the DIP crease on the radial aspect of the index finger, the ulnar aspect of the little finger, and both sides of the thumb should be considered for repair.[53] Clean, single-nerve lacerations should be repaired primarily when feasible. Complex nerve injuries may involve wound contamination or extensive tissue damage and are usually managed by delayed repair to allow for improved soft tissue conditions. Although the functional recovery is never complete, a good outcome can result from primary and delayed repair. In general, sensory recovery returns more often than does motor function.
Complications Complications of nerve injuries include motor and sensory loss, atrophy from denervation, chronic paresthesias, regrowth of painful neuromas, and sympathetic dystrophy.
Infections of the Hand The unique anatomic structures of the hand affect the nature of infections in this region of the body. In general, hand infections can be divided into infections involving the skin, subcutaneous tissues, fascial spaces, tendon, joint, and bone. Fibrous compartments of the distal fingertips contain the spread of infection, whereas flexor tendon sheaths allow infection to travel considerable distances along the lengths of
Page 143
the tendons from the original site. Infections in the deep spaces of the palm usually manifest on the dorsal surface of the hand.
Paronychia Pathophysiology A paronychia is a localized superficial infection or abscess involving the lateral nail fold. It is the most common infection in the hand and is thought to be caused by frequent trauma to the delicate skin around the fingernail and cuticle. Clinically, swelling and tenderness of the soft tissue along one or both sides of the lateral nail fold are evident. A paronychia begins as a cellulitis, but a frank abscess may form, and occasional extension to the overlying proximal nail (termed an eponychia) may occur. S. aureus is the most common isolate, followed by streptococci.[96] Paronychias in children are often caused by anaerobes, and it is believed that this is the result of finger sucking and nail biting.[97] Atypical mycobacteria and Candida albicans should be considered as etiologic agents in chronic cases.[98]
Management In the early cellulitis phase, management consists of frequent warm soaks, elevation, and administration of an oral antistaphylococcal antibiotic, such as dicloxacillin or cephalexin. When the area becomes fluctuant, drainage is necessary and is usually curative. Adequate drainage often can be obtained by lifting the skin edge off the nail to allow the pus to drain ( Figure 47-55 ). This can be accomplished without anesthesia in selected patients, but drainage for more extensive lesions is best carried out under digital block anesthesia. After softening the eponychium by soaking, a No. 11 blade scalpel or an 18-gauge needle may be advanced parallel to the nail and under the eponychium at the site of maximal swelling.[99] If the infection is more extensive, the lateral one fourth of the nail may be bluntly dissected from the underlying nail bed and germinal matrix and the lateral nail plate excised. After the cavity is irrigated, a small piece of packing gauze may be slipped under the eponychium for 24 hours to provide continual drainage. Cultures are not indicated. Antibiotics are commonly prescribed, although not essential if drainage is complete or if the surrounding area of cellulitis is minimal. Most paronychias resolve in 5 to 10 days, and patients are advised to have primary care follow-up evaluation. A well-known complication of even a properly drained paronychia is osteomyelitis of the distal phalanx. Patients with a chronic, indolent infection of the perionychium seldom respond to emergency department intervention. These patients should be referred to a dermatologist or hand surgeon because of the prolonged treatment required.
Figure 47-55 Drainage of paronychia. A, Eponychial fold is elevated from the nail for a sim ple paronychium . B, Lateral nail is rem oved if pus tracks under it. A sm all eponychial incision m ay be necessary. C, Proxim al nail is rem oved if pus tracks under it. Two incisions are needed to rem ove the proxim al nail. ((From Moran GJ, Talan DA: Hand infections. Emerg Med Clin North Am 11:601, 1993.))
Felon Pathophysiology A felon is an infection of the pulp of the distal finger or thumb. It differs from other types of subcutaneous abscesses because of the presence of multiple vertical septa that divide the pulp into small fascial compartments. The usual cause is penetrating trauma with secondary bacterial invasion. The most common pathogen is S. aureus, although gram-negative organisms also have been described.[98] Although the septa may facilitate an infection in the pulp and inhibit drainage after incomplete surgical decompression, they provide a barrier that protects the joint space and the tendon sheath by limiting the proximal spread of infection. Clinically a felon begins as an area of cellulitis and inflammation that progresses rapidly to severe throbbing, pain, swelling, and pressure in the distal pulp space.
Management Traditional management of felons emphasizes the need for early and complete incision through the septa to provide adequate drainage and to relieve pressure in septal compartments. Most felons can be drained by a
Page 144
single lateral incision.[100] The incision should be made along the ulnar aspect of digits II to IV and the radial aspects of digits I and V, avoiding pincher surfaces. The incision is begun approximately 0.5 cm distal to the DIP joint crease and dorsal to the neurovascular bundle of the fingertip. The incision is extended to the free edge of the nail ( Figure 47-56 ). The wound should be irrigated, loosely packed with gauze, and splinted. The packing is removed in 48 to 72 hours, and the wound is left to close secondarily. Most felons are treated empirically with an antistaphylococcal oral antibiotic for at least 5 days pending culture results. Some authors recommend draining this abscess where it points, using a volar midline incision that does not cross the distal flexion crease.[100]
Figure 47-56 Incision and drainage of felon using the unilateral longitudinal approach. Most felons should be drained via this incision. ((From Milford L: In Crenshaw AH [ed]: Cam pb ell's Operative Orthopedics, 8th ed. St. Louis, Mosb y, 1992.)Elsevier Inc.)
Complications If untreated, the expanding abscess can extend toward the phalanx, producing an osteitis or osteomyelitis, or toward the skin, causing necrosis and a sinus tract on the palmar surface of the digital pulp. Other complications include soft tissue and bony tuft necrosis, osteomyelitis, septic arthritis of the DIP joint, and flexor tenosynovitis from proximal extension. The lateral incision used to drain felons commonly leaves unstable finger pads or may result in painful neuromas or anesthetic fingertips. “Fish-mouth” incisions may destroy the blood supply to the fingertip.[100] Longitudinal midline incisions on the volar surface may leave scars over an important area for sensation, but do not have the other disadvantages of lateral incisions. Any incision that is made too deeply and proximally can injure the flexor tendon sheath and initiate a tenosynovitis.
Herpetic Whitlow Epidemiology and Pathophysiology Herpetic whitlow is a self-limited herpes simplex viral infection of the distal finger. It is the most common viral infection of the hand. Infection by herpes simplex virus type I or II is clinically indistinguishable.[101] Direct inoculation of the virus into an open wound or broken skin is the usual mechanism of primary infection. Herpetic whitlow is commonly reported in adult women with genital herpes and children with coexistent herpetic gingivostomatitis. Health care workers are at increased risk for developing this infection as an occupational hazard secondary to exposure to orotracheal secretions; however, a more recent review of herpes infection in the hand found that only 14% of adult cases are in health care workers.[102] The incidence has decreased probably as a result of heightened awareness of the condition and strict infection control precautions.
Clinical Features The infection usually involves a single finger and begins with localized pain, pruritus, and swelling, followed by the appearance of clear vesicles. Systemic symptoms are usually absent; however, secondary infection of the vesicles can occur.[103] More typically, the vesicles coalesce over 2 weeks to form an ulcer, which may develop a hemorrhagic base. At this stage, it may be difficult to distinguish herpes simplex infection of the hand from more common bacterial infections, such as felon or paronychia. The distinction is important because drainage of the herpetic lesions is contraindicated and may lead to viral dissemination and secondary bacterial infection. A careful history is important to determine risk of a possible herpetic etiology. On examination, tenderness is present but is noticeably less than that seen with bacterial infections. In addition, the pulp space remains soft and does not become tense, as it does in a bacterial felon.[104]
Diagnostic Strategies The diagnosis usually is made clinically based on the appearance of the lesion and the history of recurrence or potential sources of inoculation. The diagnosis may be confirmed by viral culture or a Tzanck test showing multinucleated giant cells in a scraping taken from the base of an unroofed vesicle.[105]
Page 145
Management Herpetic whitlow usually resolves spontaneously in 3 to 4 weeks. The main goals of treatment are to prevent oral inoculation or transmission of the infection and to provide symptomatic relief. The involved digit should be kept covered with a dry dressing. Oral acyclovir has a role in treatment of immunocompromised patients and patients with frequently recurring infections, but its role in nonimmunocompromised patients is less clear.[105] Topical acyclovir has not been shown to be effective in either the treatment or the prophylaxis of this disorder.
Tenosynovitis Pathophysiology Acute synovial space infections in the hand usually involve the flexor tendon sheaths and the radial and ulnar bursae. The tendon sheaths are double walled, with a visceral layer adherent to the tendon and a parietal layer extending from the midpalmar crease to just proximal to the DIP joint. The flexor tendon sheath of the thumb is continuous with the radial bursa of the palm, and the small finger sheath is continuous with the ulnar palmar bursae. The ulnar bursa surrounds the superficial and deep flexor tendons, and the radial bursa surrounds the flexor pollicis longus. These two bursae communicate in 80% of individuals; however, for most individuals, the tenosynovial coverings of digits II, III, and IV do not communicate. Infections in the synovial spaces in the hand tend to spread along the course of the flexor tendon sheaths and may spread to the midpalmar, thenar, and lumbrical compartments. Infections usually are caused by penetrating trauma to the sheath, but they occasionally result from hematogenous spread. The most commonly isolated organism is S. aureus.
Clinical Features Four cardinal signs of acute flexor tenosynovitis are usually present and help differentiate tenosynovitis from other soft tissue infections in the hand: (1) tenderness along the course of the flexor tendon, (2) symmetric swelling of the finger, (3) pain on passive extension, and (4) a flexed posture of the finger.[13] All four signs may not be present early in the course of infection. The third sign may be the most important. Early recognition and treatment are essential because elevated pressure within the enclosure of the flexor tendon sheath can occlude the already tenuous circulation to the tendon, resulting in necrosis and proximal spread.
Management All patients with flexor tenosynovitis require hospital admission and prompt consultation with a hand surgeon to determine whether open drainage or closed tendon sheath irrigation is indicated. In early cases or uncertain diagnoses, the hand should be splinted in a bulky dressing and elevated, and intravenous antibiotics should be initiated. Infections secondary to penetrating trauma should be treated with a penicillinase-resistant antistaphylococcal penicillin or first-generation cephalosporin. Disseminated gonorrhea must be considered in all sexually active individuals, especially if there is no apparent traumatic etiology of the infection. In such cases, some authors recommend empiric treatment with ceftriaxone until final cultures are available.[106] Surgical treatment is indicated for established cases or when improvement is not evident within 24 hours.
Deep Fascial Space Infections Anatomy and Pathophysiology The deep fascial spaces of the hand include the dorsal subaponeurotic space, the subfascial web space, the midpalmar space, and the thenar space ( Figure 47-57 ). The fascial spaces are potential rather than actual spaces in a normal hand.[107] These closed compartments are susceptible to infection from direct penetrating trauma, infection in contiguous compartments, or hematogenous seeding. The most commonly isolated pathogens are S. aureus, streptococci, and coliforms.
Figure 47-57 Potential m idpalm ar spaces. ((From Neviasser RJ: In Green DP [ed]: Operative Hand Surgery, 3rd ed. New York, Churchill Livingstone, 1993, p 1028.)Churchill Livingstone)
Page 146
Clinical Features The unique anatomic features of the deep fascial spaces lead to characteristic clinical findings when these regions are involved with pyogenic infection. The dorsal subaponeurotic abscess causes swelling and erythema on the dorsum of the hand. Pain with passive movement of the extensor tendons is often present, but it may be difficult to distinguish clinically from simple cellulitis on the dorsum of the hand. Subfascial web space infections commonly result when palmar blisters become secondarily infected. The infection tends to spread dorsally into the interdigital space and produce a characteristic hourglass configuration, or the so-called collar-button abscess ( Figure 47-58 ). Thenar space infections are characterized by pain and swelling of the thenar eminence and the first web space; the thumb is held in abducted and flexed position.[ 108] In midpalmar infections, there is loss of the normal hand concavity and tenderness of the central palm; movement of digits III and IV is painful. Suppurative tenosynovitis of the second digit can rupture proximally into the thenar space and create an abscess. Tenosynovitis of digits III, IV, and V may be responsible for a midpalmar space infection.
Figure 47-58 Collar-button abscess. The palmar space infection has spread to the dorsum of the hand. ((From Lewis RC Jr: Infections of the hand. Em erg Med Clin North Am 3:263, 1985.))
Management Treatment of all deep fascial space infections involves intravenous antibiotics and operative exploration and drainage by experienced surgeons. Most authors recommend broad-spectrum empiric coverage with a p -lactamase –resistant penicillin or a first-generation cephalosporin.
Septic Arthritis Pathophysiology Septic arthritis in the hand may involve the IP, MCP, CMC, or radiocarpal joints. These joints usually are infected by direct inoculation of bacteria from penetrating trauma or spread from contiguous infection, such as a felon or tenosynovitis. Hematogenous spread may occur but is less common than in other joints of the body. S. aureus is the most common cause; streptococci, Haemophilus influenzae, Pseudomonas aeruginosa, and coliforms are involved much less commonly.[109] Monarticular nontraumatic septic arthritis also may be caused by Neisseria gonorrhoeae.
Clinical Features Clinically the involved joint appears red and swollen and is extremely tender; an overlying puncture wound may be visible. The joint is held in a position that maximizes its volume, and passive motion of the joint, however slight, is painful. In contrast to flexor tenosynovitis, tenderness is localized to the involved joint.[110] Pain also may be elicited by axial compression of the joint. The diagnosis is made by arthrocentesis.
Management Treatment includes parenteral antibiotics with a semisynthetic antistaphylococcal penicillin and emergent drainage of the joint. Most infected joints require open drainage, but some hand surgeons may choose to manage certain cases with closed joint catheter irrigation and repeated aspiration.
Osteomyelitis Osteomyelitis in the hand occurs most commonly with open fractures or with secondary involvement of bone from soft tissue infections. The incidence of infection in open fractures of the hand is much lower than in open long bone fractures and is reported to be 1% to 11%. McLain and colleagues[111] found that injuries with severe skeletal trauma, gross contamination, and significant soft tissue injury have the highest risks for infection. The presentation of osteomyelitis is seldom rapid and fulminant, unless associated with septic arthritis or other deep space infection of the hand. Physical signs may include fever, localized redness, swelling, warmth, and tenderness. Children with osteomyelitis may have pseudoparalysis, which is refusal
Page 147
of the child to use the affected limb.[112] Radiographs may show bony destruction or periosteal elevation. Treatment includes debridement of infected bone and sequestra and parenteral antibiotics.
Nontraumatic Disorders of the Hand Stenosing Tenosynovitis The most common type of stenosing tenosynovitis in the hand involves the flexor tendons at the level of the MCP joint where the tendon passes through the pulley systems. Repetitive strain can result in tendon and pulley hypertrophy with localized tenderness. When there is painful blocking of flexion and extension at the involved joint, the syndrome is called trigger finger. The ring and long fingers are the most commonly involved digits. Injection therapy is recommended and works well in most patients. A mixture of 2 mL of lidocaine and 0.5 mL of steroid suspension is given through the web space and over the nodule.[113] After the injection, extension of the finger is usually possible. The finger should be splinted in extension, and referral to a hand surgeon is advised because multiple injections or surgical release may be required.
Ganglion A ganglion is the most common soft tissue tumor of the hand and consists of a synovial cyst from either a joint or the synovial lining of a tendon that has herniated. Ganglia contain a jelly-like fluid that is secreted by the synovial tissue. They are common in the wrist and the flexor tendon sheaths of the fingers and usually have an insidious onset. A specific traumatic event can be elicited from only 15% of patients, although most give a history of chronic stress.[114] Patients commonly complain of a dull ache or mild pain over the ganglion. Reassurance is important, and the patient should be informed of the benign nature of the lesion. A large or troublesome ganglion can be aspirated. Because of the high rate of recurrence, definitive treatment is operative excision, which is done on an elective basis.
Foreign Bodies in the Hand Penetrating trauma to the hand may result in a foreign body becoming lodged in the soft tissues. The presence of a foreign body should be considered in any wound regardless of its size. A detailed and accurate history of the injury should be obtained because the mechanism often gives clues to the possibility of a foreign body. The most common foreign bodies are pieces of wood, glass, or metal. Useful signs of occult foreign bodies include sharp pain with deep palpation over a puncture wound, pain associated with a mass, or a wound that fails to heal or continues to cause pain with movement.[115] Initial examination of hand wounds should include local exploration using sterile technique in a bloodless field. After exploration and removal of easily accessible foreign bodies, radiographs should be taken, using soft tissue technique with multiple views. Radiographs are the best method for detecting radiopaque foreign bodies and detect metals, most glass, many plastics, gravel, and sand.[115] Wooden foreign bodies are difficult to visualize radiographically.[116] Whether an object shows on plain films depends on its composition, configuration, size, and orientation. When a foreign body is clinically suspected and initial radiographic studies are negative, other imaging methods should be considered. The identification of nonmetallic objects such as splinters may be improved by the use of modalities including computed tomography, magnetic resonance imaging, and ultrasound.[]
Management Removal of embedded foreign bodies can be difficult and time-consuming, and potential damage to tissues caused by the procedure must be weighed against the risk posed by a particular foreign body. Generally, if a foreign body contaminating a wound is clearly visible and easily extracted during local exploration, it should be removed in the emergency department. In some cases, the entrance wound may need to be enlarged with a small skin incision. In general, foreign bodies should be removed only under direct vision. When the object is buried within the intricate anatomy of the hand, this procedure should be referred to a hand specialist. Decisions regarding the necessity and timeliness of removal of a foreign body are based on the size and the reactivity of the foreign body, proximity to vital structures, degree of wound contamination, and presence or absence of symptoms.[115] Foreign bodies that cause continued pain, interfere with hand function because of their size or their position, or cause local or systemic toxicity (e.g., paints or mercury) should be removed. Foreign bodies associated with fractures require prompt surgical debridement to prevent osteomyelitis.[118] Wounds that are grossly contaminated with soil or organic material require immediate irrigation, debridement, and removal of the foreign body. Foreign bodies near tendons, nerves, and vessels and foreign bodies causing ischemia or hemorrhage require cautious removal under optimal conditions.
Page 148
Patients who do not require immediate removal of the foreign body may be referred to a hand surgeon for delayed surgical exploration. If the hand specialist plans to remove the object within 3 to 4 days after injury, and there is minimal bacterial contamination, the wound may be closed primarily. Initial treatment also should include tetanus prophylaxis and an appropriate wound dressing. The patient should be informed about the presence of the foreign body and the reason for delayed removal. If no removal is planned, the physician should explain to the patient that the dangers of removal outweigh the benefits.
Complications Foreign bodies can damage soft tissues, provoke excessive inflammation with granuloma formation, predispose to infection, and cause systemic toxicity. Iatrogenic damage to tissue can result from blind probing or excessively aggressive searches for foreign bodies and should be avoided, particularly in the hand.
KEY CONCEPTS {,
Injuri es and infec tions of the hand are amo ng the most com monl y enco unter ed probl ems in the eme rgen cy depa rtme nt.
{,
An accu rate histo ry and caref ully perfo rme d phys ical exa mina tion of
Page 149
the hand have a centr al role in eval uatio n and treat ment . Han d radio grap hs shou ld be obtai ned if sugg estiv e sign s are pres ent. Highl y tech nical diag nosti c mod alitie s are rarel y indic ated. {,
The best funct ional outc ome s of hand injuri es usua lly are achi eved by
Page 150
{,
{,
accu rate initial eval uatio n and treat ment . A key facto r in the eval uatio n of hand injuri es is deter mini ng whic h entiti es requi re spec ialty refer ral or urge nt cons ultati on. Man age ment of the injur ed hand shou ld focu s on resto ratio n of funct ion and mini mizi ng longterm
Page 151
disa bility.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/106.html/top
Page 152
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
REFERENCES 1. Overton DT, Uehara DT: Evaluation of the injured hand. Emerg Med Clin North Am1993;11:585. 2. Atroshi I, Rosenberg H: Epidemiology of amputations and severe injuries of the hand. Hand Clin 2001;17:343-350. 3. Altman RS, Harris GD, Knuth CJ: Initial management of hand injuries in the emergency patient. Am J Emerg Med1987;5:400. 4. Chung K, Spilson S: The frequency and epidemiology of hand and forearm fractures in the United States. J Hand Surg2001;26A:1044-1053. 5. Sorock G: J Occup Environ Med2002;44:345. 6. Snell R, Smith M: The wrist and hand. Clinical Anatomy for Emergency Medicine, St. Louis: Mosby; 1993: 629-675. 7. Belliappa PP, Scheker LR: Functional anatomy of the hand. Emerg Med Clin North Am1993;11:557. 8. Ashkenaze DM, Ruby LK: Metacarpal fractures and dislocation. Orthop Clin North Am1992;23:19. 9. Graham TJ, O'Brien ET: Fractures of the hand and wrist region. In: Rockwood Jr CA, Wilkins KE, King RE, ed.Fractures in Children, 5th ed. Philadelphia: Lippincott-Raven; 2001: 655. 10. Hodgkinson DW: The hand: ABC of emergency radiology. BMJ1994;308:401. 11. American Society for Surgery of the Hand : The Hand: Examination and Diagnosis, 3rd ed. Edinburgh, Churchill Livingstone, 1990. 12. Doyle JR: Extensor tendons—acute injuries. In: Green DP, ed.Operative Hand Surgery, 4th ed. New York: Churchill Livingstone; 1999: 1950. 13. Kanavel AB: Infections of the Hand, 6th ed. Philadelphia, Lea & Febiger, 1993. 14. Hentz VR: Functional anatomy of the hand and arm. Emerg Med Clin North Am1985;3:197. 15. Sloan EP: Nerve injuries in the hand. Emerg Med Clin North Am1993;11:651. 16. Hart RG, Kleinert HE: Fingertip and nail bed injuries. Emerg Med Clin North Am1993;11:755. 17. Mark H: Fractures and dislocations in the hand. In: Rockwood Jr CA, Green DP, ed.Fractures in Adults, 5th ed. Philadelphia: Lippincott-Raven; 2001: 18. Wilson AJ, Mann FA, Gilula CA: Imaging the hand and wrist. J Hand Surg1990;15B:153. 19. Lammers RL, Magill T: Detection and management of foreign bodies in soft tissue. Emerg Med Clin North Am1992;10:767. 20. Freeland AE: Hand Fractures, Repair, Reconstruction, and Rehabilitation, New York, Churchill Livingstone, 2000. 21. DeJonge JJ: Phalangeal fractures of the hand: An analysis of gender and age-related incidence and aetiology. J Hand Surg1994;19B:168. 22. Simon RR, Koenigsknecht SJ: Emergency Orthopedics: The Extremities, 4th ed. New York, McGraw-Hill, 2001. 23. DaCruz DJ, Slade RJ, Malone W: Fractures of the distal phalanges. J Hand Surg1988;13B:350. 24. Bowman SH, Simon RR: Metacarpal and phalangeal fractures. Emerg Med Clin North Am1993;11:671. 25. Wayne PH: Radiology of the occupationally injured hand. Hand Clin1986;2:467. 26. Agee J: Treatment principles for proximal and middle phalangeal fractures. Orthop Clin North Am 1992;23:35. 27. Green DP: Complications of phalangeal and metacarpal fractures. Hand Clin1986;2:307. 28. Wilson RL, Carter MS: Management of hand injuries. In: Hunter JM, Schneider LH, Mackin EJ, ed. Rehabilitation of the Hand: Surgery and Therapy, St. Louis: Mosby; 1990: 284-294. 29. Stern PJ: Pilon fractures of the proximal interphalangeal joint. J Hand Surg1991;16A:844. 30. Margles SW: Intraarticular fractures of the metacarpophalangeal and proximal interphalangeal joints. Hand Clin1988;4:67. 31. Hastings H, Carroll C: Treatment of closed articular fractures of the metacarpophalangeal and proximal interphalangeal joints. Hand Clin1988;4:503. 32. Wolfe SW, Dick HM: Articular fractures of the hand: Part I. Guidelines for assessment. Orthop Rev 1991;20:27. 33. McLain RF, Steyers C, Stoddard M: Infections in open fractures of the hand. J Hand Surg1991;16A:108.
Page 153
34. Ashkenaze DM, Ruby LK: Metacarpal fractures and dislocations. Orthop Clin North Am1992;23:19. 35. Pellegrini VDJ: Fractures at the base of the thumb. Hand Clin1988;4:87. 36. Foster RJ, Hastings II IIH: Treatment of Bennett, Rolando, and vertical intraarticular trapezial fractures. Clin Orthop1987;214:121. 37. Graham TJ: Hand. In: Beaty JH, ed.Orthopaedic Knowledge Update 6: Home Study Syllabus, Rosemont, Ill: American College of Orthopaedic Surgeons; 1999: 38. Della-Guistina K, Della-Guistina DA: Emergency department evaluation and treatment of pediatric orthopedic injuries. Emerg Med Clin North Am1999;17:895. 39. Salter RB, Harris WR: Injuries involving the epiphyseal plate. J Bone Joint Surg1963;45A:587. 40. Stahl S, Jupitur JB: Salter-Harris types III and IV epiphyseal fractures in the hand treated with tension-band wiring. J Pediatr Orthop1999;19:233. 41. Clark DP, Scott RN, Anderson IWR: Hand problems in an accident and emergency department. J Hand Surg1985;10:297. 42. Hossfeld GE, Uehara DT: Acute joint injuries of the hand. Emerg Med Clin North Am1993;11:781. 43. Glickel SZ: Dislocations and ligament injuries in the digits. In: Green DP, ed.Operative Hand Surgery, 4th ed. New York: Churchill Livingstone; 1999: 772. 44. Thayer D: Distal interphalangeal joint injuries. Hand Clin1988;4:1. 45. Kahler D, McCue F: Metacarpophalangeal and proximal interphalangeal joint injuries of the hand, including the thumb. Clin Sports Med1992;11:57. 46. Freiberg A: Management of proximal interphalangeal joint injuries. J Trauma1999;46:523. 47. Kiefhaber TR, Stern PH, Grood ES: Lateral stability of the proximal interphalangeal joint. J Hand Surg 1986;11A:661. 48. Inoue G, Maeda N: Irreducible palmar dislocation of the proximal interphalangeal joint of the finger. J Hand Surg1990;15A:301. 49. Wilson RL, Liechty BW: Complications following small joint injuries. Hand Clin1986;2:329. 50. Henderson JJ, Arafa MAM: Carpometacarpal dislocation: An early missed diagnosis. J Bone Joint Surg 1987;69:212. 51. Gurland M: Carpometacarpal joint injuries of the fingers. Hand Clin1992;8:733. 52. Campbell CS: Gamekeeper's thumb. J Bone Joint Surg1955;37B:148. 53. Harrison BP, Hilliard MW: Emergency department evaluation and treatment of hand injuries. Emerg Med Clin North Am1999;17:793. 54. Stener B: Displacement of the ruptured ulnar collateral ligament of the metacarpophalangeal joint of the thumb. J Bone Joint Surg1962;44:869. 55. Heyman P: Injuries to the ulnar collateral ligament of the thumb: Metacarpophalangeal joint. J Am Acad Orthop Surg1997;5:224. 56. Durham JW, Khuri S, Kim MH: Acute and late radial collateral ligament injuries of the thumb metacarpophalangeal joint. J Hand Surg1993;18A:232. 57. Chen VT: Dislocation of the carpometacarpal joint of the thumb. J Hand Surg1987;12B:246. 58. Kleinert HE, Smith DJ: Primary and secondary repair of flexor and extensor tendon injuries. In: Flynn JE, ed.Hand Surgery, 4th ed. Baltimore: Williams & Wilkins; 1991: 241-261. 59. Pyne JI, Adams BD: Hand tendon injuries in athletics. Clin Sports Med1992;11:833. 60. Hart RG, Uehara DT, Kutz JE: Extensor tendon injuries of the hand. Emerg Med Clin North Am 1993;11:637. 61. Blair WF, Steyers CM: Extensor tendon injuries. Orthop Clin North Am1992;23:141. 62. Perron A, Brady W, Keats T, Hersh R: Orthopedic pitfalls in the emergency department: Closed tendon injuries of the hand. Am J Emerg Med2001;19:76-80. 63. Stern PJ, Kastrup JJ: Complications and prognosis of treatment of mallet finger. J Hand Surg 1988;13A:329. 64. Moran GJ, Talan DA: Hand infections. Emerg Med Clin North Am1993;11:601. 65. Steinberg DR: Acute flexor tendon injuries. Orthop Clin North Am1992;23:125. 66. Ablove RH, Moy OJ, Peimer CA: Pediatric hand disease diagnosis and treatment. Pediatr Clin North Am 1998;45:1507. 67. Strickland JW: Flexor tendons: acute injuries. In: Green DP, ed.Operative Hand Surgery, 4th ed. New York: Churchill Livingstone; 1999: 1851. 68. Kleinert HE, Smith DJ: Primary and secondary repairs of flexor and extensor tendon injuries. In: Jupiter JB, ed.Flynn's Hand Surgery, 4th ed. Baltimore: Williams & Wilkins; 1991: 241. 69. O'Hara JJ, Stone JH: An intratendinous epidermoid cyst after trauma. J Hand Surg1990;15:477. 70. Geissler GA, Erdmann D, Germann G: Soft tissue coverage in devastating hand injuries. Hand Clin 2003;19:63. 71. Proano L, Partridge R: Descriptive epidemiology of a cluster of hand injuries from snowblowers. J Emerg Med2002;22:341-344. 72. Chin G: Snowblower injuries to the hand. Ann Plast Surg1998;41:390. 73. Arellano A, Wegener E, Freeland A: Mutilating injuries to the hand: Early amputation or repair and
Page 154
reconstruction. Orthopedics1999;22:683. 74. Buncke G, Buntic R, Romeo O: Pediatric mutilating hand injuries. Hand Clin2003;19:121. 75. Louis DS: Amputations. In: Green DP, ed.Operative Hand Surgery, 4th ed. New York: Churchill Livingstone; 1999: 48. 76. Burkhalter WE: Fingertip injuries. Emerg Med Clin North Am1985;3:245. 77. Zook EG, Brown RE: The perionychium. In: Green DP, ed.Operative Hand Surgery, 4th ed. New York: Churchill Livingstone; 1999: 1353. 78. Guy RJ: The etiologies and mechanisms of nail bed injuries. Hand Clin1990;6:9. 79. Simon RR, Wolgin M: Subungual hematoma: Association with occult laceration requiring repair. Am J Emerg Med1987;5:302. 80. Roser SE, Gellman H: Comparison of nail bed repair versus nail trephination for subungual hematomas in children. J Hand Surg1999;24A:1166. 81. Shepard G: Perionychial grafts in trauma and reconstruction. Hand Clin2002;18:595. 82. Perron A, Miller M, Brady W: Orthopedic pitfalls in the ED: Fight bite. Am J Emerg Med2002;20:114. 83. Sirio CA, Smith Jr JrJS, Graham III IIIWP: High-pressure injection injuries of the hand: A review. Am Surg 1989;55:714. 84. Vasilevski D, Noorbergen M, Depierreux M, Lafontane M: High pressure injections injuries to the hand. Am J Emerg Med2000;18:820. 85. Neal NC, Burke FD: High-pressure injection injuries. Injury1991;22:467. 86. Curka PA, Chisholm CD: High-pressure water injection injury to the hand. Am J Emerg Med1989;7:165. 87. Schnall S, Mirzayan R: High pressure injections to the hand. Hand Clin1999;15:245. 88. Lewis HG: A 10-year review of high-pressure injection injuries to the hand. J Hand Surg1998;23B:479. 89. Kay S, Werntz J, Wolff TW: Ring avulsion injuries: Classification and prognosis. J Hand Surg 1989;14A:204. 90. Chiu Y, Chen MT: Revascularization of digits after thirty-three hours of warm ischemia time: A case report. J Hand Surg1984;9A:63. 91. Neumeister M, Brown R: Mutilating hand injuries: Principles and management. Hand Clin2003;19:1. 92. Komar LA: Vascular disorders. In: Green DP, ed.Operative Hand Surgery, 4th ed. New York: Churchill Livingstone; 1999: 2254. 93. Rowland SA: Fasciotomy: The treatment of compartment syndrome. In: Green DP, ed.Operative Hand Surgery, 4th ed. New York: Churchill Livingstone; 1999: 689. 94. Hainline B: Nerve injuries. Med Clin North Am1994;78:327. 95. Frykman GK, Wolf A, Coyle T: An algorithm for management of peripheral nerve injuries. Orthop Clin North Am1986;12:239. 96. Canales FL, Newmeyer III IIIWL, Kilgore ES: The treatment of felons and paronychias. Hand Clin 1989;5:515. 97. Brook I: Bacteriologic study of paronychia in children. Am J Surg1981;141:703. 98. Hausman MR, Lisser SP: Hand infections. Orthop Clin North Am1992;23:171. 99. Butler KH: Incision and drainage. In: Robert JR, Hedges JR, ed.Clinical Procedures in Emergency Medicine, 4th ed. Philadelphia: WB Saunders; 2004: 717. 100. Wright PE: Hand infections. In: Canale ST, ed.Campbell's Operative Orthopaedics, vol 4. 10th ed. St. Louis: Mosby; 2003: 101. Fowler JR: Viral infections. Hand Clin1989;5:613. 102. Gill MJ, Arlette J, Buchan K: Herpes simplex virus infection of hand: A profile of 79 cases. Am J Med 1988;84:89. 103. Haedicke GJ, Grossman JAI, Fisher AE: Herpetic whitlow of the digits. J Hand Surg1989;14B:443. 104. Mann RJ, Hoffeld TA, Farmer CB: Human bites of the hand: Twenty years of experience. J Hand Surg 1985;2:97. 105. Habif TP: Clinical Dermatology: Diagnosis and Therapy, 3rd ed. St. Louis, Mosby, 1996. 106. Levy CS: Treating infections of the hand: Identifying the organism and choosing the antibiotic. Instr Course Lect1990;39:533. 107. Lampe EW: Surgical anatomy of the hand. Clin Symp1988;40:1. 108. Siegel DB, Gelberman RH: Infections of the hand. Orthop Clin North Am1988;19:779. 109. Freeland AE, Senter BS: Septic arthritis and osteomyelitis. Hand Clin1989;5:533. 110. Schurman DJ, Smith RL: Surgical approach to the management of septic arthritis. Orthop Rev 1987;16:241. 111. McLain RF, Steyers C, Stoddard M: Infections in open fractures of the hand. J Hand Surg 1991;16A:1108. 112. Sonnen GM, Henry NK: Pediatric bone and joint infection: Diagnosis and antimicrobial management. Pediatr Clin North Am1996;43:4. 113. Newport ML: Treatment of trigger finger by steroid injection. J Hand Surg1990;15A:748. 114. Strickland JW, Rettig AC: Hand Injuries in Athletes, Philadelphia, WB Saunders, 1992. 115. Rudnitsky GS, Barnett RC: Soft tissue foreign body removal. In: Roberts JR, Hedges JR, ed.Clinical
Page 155
Procedures in Emergency Medicine, Philadelphia: WB Saunders; 1998: 116. Russell RC: Detection of foreign bodies in the hand. J Hand Surg1991;16A:2. 117. Gooding GAW: Sonography of the hand and foot in foreign body detection. J Ultrasound Med 1987;6:441. 118. Stein F: Foreign body injuries of the hand. Emerg Med Clin North Am1985;3:383.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/107.html/top
Page 156
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
Chapter 48 – Wrist and Forearm Karen G.H. Woolfrey Mary A. Eisenhauer
WRIST PERSPECTIVE The wrist is anatomically and biomechanically complex. This complexity allows for its diverse functional capabilities, but also puts it at risk for injury. Bony and ligamentous injuries are common, and a detailed knowledge of the anatomy and appropriate clinical evaluation and an understanding of mechanism of injury are essential for proper diagnosis and treatment of wrist injuries.[1] Although certain wrist injuries may provide a diagnostic challenge, most are evident on routine wrist views and can be diagnosed and treated by an emergency physician.
Anatomy By definition, the wrist includes the distal radioulnar joint (DRUJ), the radiocarpal joint, and the midcarpal joints. With these complex articulations, the wrist is capable of flexion, extension, and radial and ulnar deviation. Pronation and supination of the hand occur at the proximal radioulnar joint and DRUJ. The bones of the wrist joint include the distal articular surfaces of the radius and ulna and the bones of the carpus ( Figure 48-1 ). The distal radius articulates directly with the proximal carpal row, and the articular surface of the ulna is separated from direct contact with the carpus by the triangular fibrocartilage. The carpal bones are divided into two rows: a proximal row consisting of the scaphoid, lunate, triquetrum, and pisiform and a distal row consisting of the trapezium, trapezoid, capitate, and hamate.
Figure 48-1 .Bones of the wrist. The wrist joint includes the distal articular surfaces of the radius and ulna and the proxim al and distal carpal rows. ((Redrawn from Netter: Atlas of Hum an Anatom y, 3rd edition, Icon, 2003.))
The stabilizing ligaments of the wrist joint are divided into two major groups: the extrinsic ligaments and the intrinsic ligaments. The extrinsic ligaments link the carpal bones to the distal radius and ulna and the metacarpals, and the intrinsic ligaments interconnect the individual carpal bones. The extrinsic ligaments are divided further into a volar and a dorsal group. The volar extrinsic ligaments are divided into two V-shaped ligamentous bands called the proximal and distal arcades, which generally are thicker and stronger than the dorsal extrinsic ligaments and are the most important in providing ligamentous stability to the wrist. Between these volar arcades is an area relatively devoid of ligamentous support called the space of Poirier. This space enlarges when the wrist is dorsiflexed, and an injury to the joint capsule in this region can result in significant carpal instability ( Figure 48-2 ). The intrinsic ligaments interconnect adjacent carpal bones within each carpal row. The most important of these ligaments, in terms of maintaining carpal stability, are the scapholunate and lunotriquetral ligaments.[2]
Page 157
Figure 48-2 Ligam ents of the wrist. A, The volar extrinsic ligam ents are the m ost im portant ligam ents in providing stability to the wrist and include the radial collateral ligam ent, radiocapitate ligament, radioscaphoid ligam ent, radiotriquetral ligam ent, ulnotriquetral ligam ent, capitotriquetral ligam ent, and ulnar collateral ligament. The space of Poirier (*) is a gap in the volar ligam ents and the site of potential weakness. B, The intrinsic (intercarpal) ligam ents interconnect the individual carpal bones. The m ost im portant of these are the scapholunate ligam ent and the lunotriquetral ligam ent. ((Redrawn from Netter: Atlas of Hum an Anatom y, 3rd edition, Icon, 2003.))
Most structures that cross the wrist joint are contained within individual compartments formed by the deep fascia of the wrist. On the dorsal surface of the wrist, the extensor tendons are divided by the extensor retinaculum into six compartments, each having a separate synovial sheath that extends proximal and distal to the retinaculum. On the volar surface of the wrist, the flexors of the digits and the median nerve are contained within the carpal tunnel, which is formed by the flexor retinaculum and its attachments to the carpal bones. Radial to the carpal tunnel, the flexor carpi radialis tendon crosses the wrist joint in its own compartment. The vascular supply to the wrist is provided by the radial and ulnar arteries, which join in a series of dorsal and palmar arches to supply the bones of the carpus. The intrinsic blood supply to most carpal bones enters the distal portion of the bone, leaving the proximal portion at risk of devascularization and avascular necrosis when fractured. This is particularly true for the scaphoid, capitate, and lunate because they each receive their blood supply from a single vessel ( Figure 48-3 ).
Figure 48-3 Vascular supply to the wrist. Note the relationship of the wrist ligaments to the neurovascular supply to the wrist. ((Redrawn from Netter: Atlas of Hum an Anatom y, 3rd edition, Icon, 2003.))
The innervation of the wrist and hand is via the radial, median, and ulnar nerves. The radial nerve and the dorsal sensory branch of the ulnar nerve cross the dorsum of the wrist near the radial and ulna styloids. The median nerve crosses the volar radial aspect of the wrist within the carpal tunnel, just lateral to the palmaris longus tendon, and the ulnar nerve is within Guyon's canal between the pisiform and the hook of the hamate (see Figure 48-3 ).
CLINICAL FEATURES The clinical examination of the wrist begins with a complete history, including the mechanism of injury and the site of maximal pain or tenderness. Most wrist injuries are caused by a fall on the outstretched hand. The physical examination begins with inspection of the wrist, using the opposite noninjured wrist as the “normal” reference, and includes an assessment of the presence of swelling, discoloration or obvious deformity, and the ability of the patient to move the joint through a normal range of motion. On palpation, several bony prominences in the wrist act as useful landmarks, and the locations of these are best described in relation to the major reference points in the wrist—the radial and ulnar styloids. Lister's tubercle can be palpated on the dorsum of the wrist just ulnar to the radial styloid. This is an important landmark because just distal to the tubercle lies the scapholunate joint, an important site of ligamentous injury in the wrist. Just distal to the radial styloid is the anatomic snuffbox, bordered radially by the abductor pollicis longus and extensor pollicis brevis tendons and ulnarly by the extensor pollicis longus tendon. The body of the scaphoid is palpable within the snuffbox and is more prominent with the wrist in ulnar deviation.[3]
Page 158
The triquetrum is palpable just distal to the ulnar styloid in the proximal carpal row and can be made more prominent with radial deviation of the wrist. With the wrist in neutral position, the capitate is palpable in a small depression found midway between the base of the third metacarpal and Lister's tubercle. Bringing the wrist into flexion can bring the lunate forward into a palpable position at this same site. On the volar aspect of the wrist, the scaphoid tubercle is palpable just distal and palmar to the radial styloid. It is felt as a rounded prominence at the base of the thenar muscles and is especially prominent when the wrist is extended. On the ulnar border of the wrist, the pisiform is palpable at the base of the hypothenar muscles, just distal to the distal wrist crease. In addition, approximately 1 cm distal and radial to this point, one can palpate the prominence formed by the hook of the hamate. The clinical examination of the wrist includes an assessment of the neurovascular status. Radial and ulnar pulses are easily palpable on the volar surface of the wrist, and the presence of pulses should be documented in all injuries to the wrist.
DIAGNOSTIC STRATEGIES: RADIOLOGY Plain radiographs remain the cornerstone of diagnosis of fractures and dislocations of the wrist. Routine radiographic views include the posteroanterior, lateral, and oblique projections, each performed with the wrist in neutral position. Accurate interpretation of these views requires knowledge of the normal appearance and anatomic relationships of the distal radius, ulna, and carpal bones. On the posteroanterior view of the wrist, the radial styloid process extends beyond the end of the articular surface of the ulna by a normal distance of 9 to 12 mm. This normal difference in length is called the radial length measurement. The ulnar slant of the articular surface of the radius is visible on the posteroanterior view and normally should measure 15 to 25 degrees. Both of these measurements are important when assessing the degree of radial shortening seen in association with some fractures of the distal radius ( Figure 48-4 ).[4] The normal appearance of the carpus on the posteroanterior view shows an approximately equal distance (usually 1 to 2 mm) between each of the carpal bones, and opposing articular surfaces are parallel to one another, known as parallelism. Three smooth curves normally can be drawn along the carpal articular surfaces ( Figure 48-5 ). Disruption of these curves or widening of the carpal spaces is an indication of carpal ligament disruption and carpal instability.[5]
Figure 48-4 Norm al posteroanterior view of the wrist. A, Radial length m easurem ent. The radial styloid extends 9 to 12 m m beyond the articular surface of the distal ulna. B, The ulnar slant of the distal radius noram ally m easures 15 to 25 degrees. ((From Greenspan A: Orthopedic Radiology: A Practical Approach, 2nd ed. New York, Gower Medical Pub lishing, 1992.)Gower Medical Pub lishing)
Figure 48-5 Wrist arcs. On the normal posteroanterior view of the carpus, three arcuate lines can be drawn along the carpal articular surfaces. ((From Weissm an BN, Sledge CB: Orthopedic Radiology. Philadelphia, WB Saunders, 1986.)Elsevier Inc.)
On the lateral view of the wrist, the normal volar tilt of the distal radial articular surface is visible and normally measures between 10 and 25 degrees ( Figure 48-6 ). The normal alignment of the distal radius with the lunate and capitate also is seen on the lateral view and appears as two concentric cups, the cup of the distal radius containing the lunate and the cup of the distal lunate containing the capitate. Ideally the long axis of the radius, lunate, capitate, and third metacarpal should appear as a straight line on the lateral view, although the
Page 159
“normal” alignment is usually within 10 degrees of this ideal line ( Figure 48-7 ). The carpal alignment on the lateral view is defined further by the scapholunate angle, which normally measures 30 to 60 degrees, and the capitolunate angle, which is normally 0 to 30 degrees ( Figure 48-8 ). Abnormalities in these angles are seen in patients with carpal ligament injuries and carpal instability.
Figure 48-6 Norm al lateral view of the wrist. The distal radius has a norm al volar tilt of 10 to 25 degrees. ((From Greenspan A: Orthopedic Radiology: A Practical Approach, 2nd ed. New York, Gower Medical Pub lishing, 1992.)Gower Medical Pub lishing)
Figure 48-7 Norm al relationship of carpal bones on lateral view. Concavity of radius and lunate and convexity of capitate form three C-shaped areas (stippled) along a straight line that runs through the central axis of these bones.
Figure 48-8 A, The norm al scapholunate angle is formed by the intersection of the longitudinal axes of the scaphoid and lunate and norm ally m easures 30 to 60 degrees. B, The norm al capitolunate angle is formed by the intersection of the capitate and lunate central long axes and norm ally m easures 0 to 30 degrees. ((From Greenspan A: Orthopedic Radiology: A Practical Approach, 2nd ed. New York, Gower Medical Pub lishing, 1992.)Gower Medical Pub lishing)
The soft tissues of the wrist also offer valuable clues to the presence of underlying bony injuries. On the lateral view of the wrist, the pronator quadratus line is visible as a linear fat collection in the volar soft tissues just anterior to the distal radius and ulna ( Figure 48-9 ). Fractures of the distal radius or ulna result in volar displacement or complete obliteration of this line.
Figure 48-9 The pronator quadratus is a narrow fat stripe located 1 cm from the volar surface of the radius on the normal lateral wrist view. ((From Propp DA, Chin H: Forearm and wrist radiology—Part I. J Em erg Med 7:393, 1989.))
Additional radiographic views of the wrist include posteroanterior views in ulnar and radial deviation, lateral views in maximal flexion and extension, and the clenched fist anteroposterior view. These views are useful to delineate further abnormal motion of the carpus as a result of carpal ligament injuries. Specific scaphoid views, obtained with the wrist prone and in ulnar deviation, allow for better visualization of the scaphoid along its long axis. The carpal tunnel view is performed with the wrist hyperextended and provides an axial view of
Page 160
the bony margins of the carpal tunnel. This view and the reverse (supinated) oblique view help identify fractures involving the hamate, especially the hook of the hamate, and the pisiform ( Table 48-1 ).[6] Table 48-1 -- Additional Radiographic Wrist Views Radiographic View
Benefit
Clenched fist view
Exposes scapholunate ligament injury; pushes capitate into proximal carpal row
Scaphoid view
Elongates scaphoid; exposes waist fractures
Carpal tunnel view
Identifies fractures involving hamate and pisiform; identifies bony encroachment onto the carpal tunnel
CARPAL INJURIES Scaphoid Fractures The scaphoid is the most commonly fractured of the carpal bones and accounts for more than 60% of all carpal fractures.[7] It typically is seen in young adults age 15 to 30 and occurs after a fall on the outstretched hand. Scaphoid fractures in skeletally immature individuals are rare. Fractures of the scaphoid are classified by the anatomic location of the fracture line and may be divided into three groups: fractures of the tuberosity and distal pole, fractures of the waist, and fractures of the proximal pole. Fractures through the waist of the scaphoid are the most common of these three patterns and account for approximately 70% to 80% of all scaphoid fractures.[8] Clinically, patients complain of dorsal radial wrist pain just distal to the radial styloid, with limited range of motion of the wrist and thumb. Classically, physical examination reveals tenderness on palpation of the scaphoid and swelling within the anatomic snuffbox, but pain also may be elicited with palpation of the scaphoid tubercle volarly, with axial compression of the thumb metacarpal, or with resisted supination.[9] Radiographic diagnosis of scaphoid fractures is often difficult, and special scaphoid views should be requested when a fracture is suspected on clinical examination. A visible fracture lucency may be occult, and more subtle findings, such as obliteration or displacement of the scaphoid fat pad, may be the only clue to the presence of a fracture.[] Plain radiographs fail to detect 15% of scaphoid fractures.[12] For this reason, and the associated risk of nonunion when diagnosis and immobilization are delayed, patients clinically suspected of having a scaphoid fracture are treated with cast immobilization, with repeat radiographs in 10 to 14 days. If a fracture is present, it may be more evident on the repeat radiographs because of resorption associated with fracture healing. If radiographic results remain negative at 10 to 14 days, and clinical examination is still suggestive of fracture, a three-phase technetium bone scan or a computed tomography (CT) scan of the scaphoid should be obtained.[] More recent studies have shown that a negative bone scan 72 to 96 hours after injury accurately can exclude scaphoid fracture. These studies suggest that a patient can be immobilized for comfort, and a bone scan can be performed within the first few days of injury. A negative bone scan allows much earlier mobilization.[] Magnetic resonance imaging also can be used to detect these radiographically occult fractures, with sensitivities of 100%. High correlation has been shown between bone scan and magnetic resonance imaging of the scaphoid.[] Treatment of uncomplicated, undisplaced scaphoid fractures involves immobilization in a short arm thumb spica cast ( Figure 48-10 ), although some specialists prefer to use a long arm cast for the first 2 weeks of immobilization, replacing this with a short arm cast for the remainder of the immobilization period. The duration of immobilization varies relative to the location of the fracture, but averages 12 weeks, with the more proximal fractures requiring longer immobilization to ensure adequate healing. This variability in healing time is related directly to the pattern of blood supply to the scaphoid, which flows from the distal to proximal portion of the bone through the scaphoid tuberosity. This pattern of blood flow also accounts for the higher incidence of avascular necrosis and fracture nonunion in the more proximal fractures. Overall, avascular necrosis is seen in approximately 3% and nonunion in 5% to 10% of scaphoid fractures, with the risk of complications being greatest in fractures of the proximal pole.[] Any scaphoid fracture that is displaced more than 1 mm or is associated with an increase in the normal scapholunate or capitolunate angles requires prompt orthopedic referral for consideration of operative treatment.
Page 161
Figure 48-10 Thum b spica cast.
Lunate Fractures Fractures of the lunate are relatively uncommon, representing fewer than 3% of all carpal fractures. This injury occurs more commonly in individuals with a congenitally short ulna, owing to compromise of the normal triangular fibrocartilage support. The usual mechanism of injury involves a fall on the outstretched hand, causing extreme dorsiflexion, with the resultant force being transmitted from the capitate to the lunate. Patients have pain over the dorsum of the wrist, which is exacerbated by axial loading of the long finger metacarpal. On examination, tenderness may be elicited on palpation over the dorsum of the wrist in the depression felt just distal to Lister's tubercle. Fractures of the lunate may be difficult to see on plain radiographs because of overlap of the distal radius, ulna, and other carpal bones. For this reason, and because of the risk of avascular necrosis in missed injuries, patients suspected of having a lunate fracture should be immobilized in a short arm cast until a fracture can be confirmed or excluded by CT or technetium bone scan. Lunate fractures are treated with immobilization in a short arm cast, with orthopedic follow-up evaluation in 1 to 2 weeks. Complications include progression to carpal instability, nonunion, and avascular necrosis. Posttraumatic avascular necrosis is seen in 20% of fractures and is called Kienbock's disease. In well-established cases of Kienbock's disease, the lunate appears sclerotic and fragmented on x-ray, and ultimately the bone collapses with resultant proximal migration of the capitate. These changes cause secondary osteoarthritis of the radiocarpal joint and chronic wrist pain. Treatment involves operative intervention, with correction of the articular abnormalities either by lengthening the ulna or by shortening the radius. In more advanced cases, excision and prosthetic replacement of the lunate or arthrodesis may be necessary.[26]
Triquetral Fractures Fracture of the triquetrum, the second most common fracture of the carpals, usually results either from a direct blow to the bone causing a fracture of the body or from a fall on the outstretched hand. In the latter situation, the mechanism of fracture is believed to be impact of the ulnar styloid against the triquetrum, which results in a dorsal chip fracture.[] Patients have localized tenderness over the dorsum of the wrist just distal to the ulnar styloid. On physical examination, swelling may be noted in this same area, and wrist motion is limited because of pain. The fracture is best seen on the standard lateral view of the wrist as a small dorsal chip fragment, although a more oblique pronated lateral view may be necessary. Treatment with immobilization in a short arm cast or splint usually results in an uncomplicated course with prompt fracture healing over 4 to 6 weeks.
Pisiform Fractures The pisiform is a unique carpal bone because it is a sesamoid bone that lies within the flexor carpi ulnaris tendon and articulates on its dorsal surface with the triquetrum. Fractures of the pisiform usually occur from a fall on the outstretched hand, but also may be seen with direct blows to the hypothenar eminence. On clinical examination, there is tenderness over the ulnar aspect of the volar wrist crease, which may be exacerbated with wrist flexion and ulnar deviation.[29] Fractures of the pisiform can impinge on Guyon's canal, resulting in ulnar nerve injury. Paresthesias in the distribution of the ulnar nerve and hand clumsiness from intrinsic muscle dysfunction can occur. Pisiform fractures are poorly seen on routine wrist radiographs, so special views must be requested. A reverse (supinated) oblique view and the carpal tunnel view allow for better visualization of these fractures.[6] Fractures of the pisiform generally have an excellent prognosis and are treated with immobilization in a short arm cast or splint for 3 to 4 weeks. If evidence of nerve compromise exists, orthopedic consultation for possible urgent surgical decompression is indicated to restore nerve function. Fractures that are complicated by nonunion may require excision of the pisiform to prevent chronic pain.
Hamate Fractures
Page 162
Hamate fractures are rare and account for approximately 2% of all carpal bone fractures. The hook or hamulus is the most common site of fracture, although fractures through the articular surfaces or body also are seen. Fracture of the hook usually occurs from a fall on the outstretched hand or by a direct blow to the palm of the hand. Commonly, the use of hammers and vibration from equipment also can cause fractures. Patients present with pain over the hypothenar eminence with associated decreased grip strength. Pain may be localized on palpation of the hamate, 1 cm distal and radial to the pisiform. Fractures of the hamate body and articular surface usually are seen on posteroanterior views of the wrist, but fractures of the hook are seen best on the reverse oblique and carpal tunnel views.[6] When these views are inconclusive, plain tomography or a CT scan may allow confirmation of fracture.[30] Initial treatment is by immobilization in a short arm cast with orthopedic follow-up in 1 to 2 weeks. Fractures of the hook of the hamate often are complicated by associated ulnar nerve injury or progression to nonunion. In both cases, operative intervention with excision of the hook at the fracture site is necessary.[]
Trapezium Fractures Fractures of the trapezium are uncommon and represent only 1% to 5% of all carpal injuries. There are two main types of fractures: fractures involving the body and fractures involving the trapezial ridge. A direct blow to the adducted thumb causes fracture through the body of the trapezium with the force being transmitted by the base of the thumb metacarpal. Avulsion fractures of the trapezial ridge occur with forceful radial deviation or rotation of the wrist. On examination, patients complain of pain with movement of the thumb and on direct palpation of the trapezium just distal to the scaphoid in the anatomic snuffbox. Fractures are seen best on slightly pronated oblique views of the wrist, although a true anteroposterior view of the trapezium (Roberts' view) or CT scan may be necessary.[33] Patients are treated with immobilization in a thumb spica cast for 6 weeks, unless the fracture is displaced or involves the carpometacarpal joint, in which case referral for open reduction and fixation is indicated.
Capitate Fractures The capitate lies in a central position in the distal carpal row, and because of this protected location, it is rarely fractured. When fracture does occur, the mechanism is generally a direct blow to the dorsum of the wrist. Fracture also may be seen in association with a perilunate dislocation after a fall on the outstretched dorsiflexed hand. Clinical examination reveals dorsal wrist pain and swelling, with localized tenderness on palpation of the capitate. Fractures usually are visible on the standard posteroanterior view of the wrist, although the lateral view may be helpful in determining the presence of rotation or displacement of the fracture fragment. Undisplaced isolated fractures of the capitate may be managed with immobilization in a short arm cast for 6 weeks. Any fracture with displacement or associated carpal dislocation requires prompt orthopedic referral for open reduction and fixation. Complications of nonunion and avascular necrosis of the proximal fragment are rare, but do occur because the capitate receives its blood supply through its distal half.[29]
Trapezoid Fractures The trapezoid rarely is fractured and is said to account for fewer than 1% of all carpal bone fractures.[34] The typical mechanism of injury is a direct blow down the long axis of the index metacarpal, which may result in isolated fracture to the trapezoid or may cause a dorsal fracture-dislocation. On clinical examination, pain and tenderness are localized over the dorsum of the wrist at the base of the second metacarpal. The fracture may be visible on routine posteroanterior views of the wrist; however, oblique views or tomography may be necessary to visualize this injury. Undisplaced fractures are treated with immobilization in a short arm cast for 6 weeks, and fracture-dislocations need prompt orthopedic referral for reduction and fixation.[29]
Carpal Instability Mayfield and associates[35] described a progressive pattern of carpal ligamentous injury caused by wrist hyperextension, ulnar deviation, and intercarpal supination. Their studies of the pathomechanics of these injuries led to the classification of carpal instability into four distinct stages. Each stage represents a sequential intercarpal injury beginning with scapholunate joint disruption and proceeding around the lunate, creating progressive ligamentous injury and progressive carpal instability ( Figure 48-11 ). Each stage also may be associated with specific bony fractures, which if present should alert the physician to the possibility of an occult perilunate ligamentous injury. These associated fractures include fractures of the radial styloid, scaphoid, capitate, and triquetrum.
Page 163
Figure 48-11 Sequential stages of carpal dislocation. Each of four stages represents a sequential intercarpal ligam ent injury proceeding around the lunate. ((From Greenspan A: Orthopedic Radiology: A Practical Approach, 2nd ed. New York, Gower Medical Pub lishing, 1992.)Gower Medical Pub lishing)
A stage I injury, or scapholunate dissociation, results in a characteristic widening of the scapholunate joint on the posteroanterior view, which has been called the “Terry Thomas sign,” after the British comedian with a gap between his front teeth.[36] If associated with rotatory subluxation of the scaphoid, the scaphoid is seen end on with the cortex of the distal pole appearing as a ring shadow over the scaphoid; this is called the signet ring sign ( Figure 48-12 ). Routine radiographs may appear normal so that when a scapholunate ligament injury is suspected clinically, additional stress views should be obtained. Views taken with a clenched fist and ulnar deviation (the clenched fist anteroposterior view) accentuate widening of the scapholunate joint.
Figure 48-12 Scapholunate dissociation with scaphoid subluxation. Posteroanterior wrist view shows characteristic widening of the scapholunate joint and a ring shadow over the scaphoid (arrow). ((From Sonnenb erg J: Carpal injuries. Traum a Q 1:71, 1985.))
A stage II injury, or perilunate dislocation, is seen best on the lateral view of the wrist. Although the lunate remains in position relative to the distal radius, the capitate is dorsally dislocated. The posteroanterior view shows overlap of the distal and proximal carpal rows and may show an associated scaphoid fracture or subluxation ( Figure 48-13 ).[37]
Figure 48-13 Perilunate dislocation. Lateral view shows lunate in normal position and the capitate dorsally dislocated. ((From Propp DA, Chin H: Forearm and wrist radiology—Part I. J Em erg Med 7:393, 1989.))
A stage III injury appears identical to a stage II injury but includes a dislocation of the triquetrum that is seen best on the posteroanterior view, with overlap of the triquetrum on the lunate or hamate. This injury may be associated with a volar triquetral fracture. A stage IV injury, or lunate dislocation, results in a characteristic triangular appearance of the lunate on the posteroanterior view because of the rotation of the lunate in a volar direction. This triangular appearance is known as the “piece of pie sign.” This rotation also is visible on the lateral view of the wrist, where the lunate looks like a cup tipped forward and spilling its contents into the palm. This latter sign is called the “spilled
Page 164
teacup sign.” On the lateral view, the capitate is seen to lie posterior to the lunate and often migrates proximally to contact the distal radius ( Figure 48-14 ).
Figure 48-14 Lunate dislocation. A, Posteroanterior view shows the characteristic triangular shape of the lunate (arrow). B, Volar displacem ent of the lunate resem bles a spilled teacup on lateral view (arrow), with dorsal displacement of the capitate. ((From Propp DA, Chin H: Forearm and wrist radiology—Part I. J Em erg Med 7:393, 1989.))
Patients with these carpal dislocation injuries typically have a history of a fall on the outstretched hand. They complain of pain and swelling over the dorsum of the wrist, with limited range of motion. On physical examination, there is palpable tenderness over the dorsum of the wrist, particularly in the region of the scapholunate ligament. With perilunate and lunate dislocations, visible deformity of the wrist also is present, and diminished two-point sensation is often present in the median nerve distribution. Complications of carpal dislocation injuries include median nerve injury and chronic carpal instability with resultant degenerative arthritis. Carpal dislocation injuries require orthopedic consultation in the emergency department for reduction and stabilization. Either arthroscopically guided reduction and pinning or open reduction with ligament repair is now recommended for the optimal management of these acute injuries.
Intercalated Segment Instability Not all patterns of carpal instability follow the pattern described by Mayfield and associates.[35] Two other common types of carpal instability—dorsal intercalated segment instability (DISI) and volar intercalated segment instability (VISI)—are better understood as a pattern of midcarpal joint collapse ( Figure 48-15 ).[38] These patterns of carpal instability are recognized radiographically by specific deformities on the lateral view of the wrist ( Figure 48-16 ).
Figure 48-15 The wrist as a link m echanism . A, The wrist as a link m echanism in which the distal radius (R), proxim al carpal row (represented by the lunate [L]), and distal carpal row (represented by the capitate [C]) compose the individual links. B, With axial com pression (arrows), carpal collapse occurs in a zigzag pattern if there is loss of the carpal longitudinal supports (the scaphoid and ligam entous attachm ents). ((From Green DP: Operative Hand Surgery, vol 1, 3rd ed. New York, Churchill Livingstone, 1993.)Churchill Livingstone)
Figure 48-16 A, Dorsal intercalated segm ent instability (DISI). In this pattern of carpal instability, the scapholunate angle m easures m ore than 60 degrees, and the capitolunate angle m easures m ore than 30 degrees. B, Volar intercalated segment instability (VISI). In this pattern of carpal instability, the scapholunate angle m easures less than 30 degrees, and the capitolunate angle m easures m ore than 30 degrees. ((From Propp DA, Chin H: Forearm and wrist radiology—Part I. J Em erg Med 7:393, 1989.))
Page 165
With the DISI pattern of instability, there is dorsiflexion of the lunate relative to the capitate, which results in an increase in the scapholunate and capitolunate angles. With the VISI pattern of instability, there is volar flexion of the lunate relative to the capitate, with a decrease in the scapholunate angle and an increase in the capitolunate angle. These angles are best visualized on the lateral view radiograph and appear as if the articular surface of the lunate is tilting dorsally (DISI) or volarly (VISI). DISI is the most common pattern of carpal instability and may be seen after scapholunate dissociation or with scaphoid fractures with or without associated perilunate dislocation. VISI patterns of instability occur after lunotriquetral or triquetrohamate joint disruption. Either pattern may be seen in association with radiocarpal joint malalignment, as is seen in lunate collapse with Kienbock's disease, rheumatoid arthritis, or congenital carpal ligamentous laxity.[] Clinically, patients have chronic pain, weakness, and limited range of motion of the wrist and may complain of the wrist clicking with ulnar deviation. On physical examination, there is point tenderness over the area of primary injury, usually the scapholunate or lunotriquetral joints. Gross deformity of the wrist, resulting from subluxation, also may be apparent compared with the unaffected “normal” wrist. Patients should be referred to an orthopedic surgeon for definitive treatment of these injuries. Operative treatment involves reduction and stabilization, with ligamentous reconstruction or repair.
DISTAL RADIUS AND ULNA INJURIES Colles' Fracture Colles' fracture, first described in 1814, is the most common wrist fracture seen in adults.[40] It is a transverse fracture of the distal radial metaphysis, which is dorsally displaced and angulated. The fracture usually is located within 2 cm of the radial articular surface and may be associated with intra-articular extension into the radiocarpal or radioulnar joints. There is commonly an associated fracture of the ulnar styloid. Clinically, patients have a history of a fall on the outstretched hand and complain of immediate pain and swelling over the dorsum of the wrist. On examination, there is an obvious “dinner fork” deformity of the wrist caused by the dorsal displacement and angulation of the fracture. A neurovascular examination should be performed to exclude an associated median nerve injury or vascular compromise caused by this deformity. The posteroanterior and lateral views of the wrist show the fracture through the radial metaphysis. The posteroanterior view may show extension of the fracture into the radioulnar or radiocarpal joints and shows the amount of radial shortening present. The degree of dorsal displacement and angulation is seen best on the lateral view, with loss of the normal volar tilt of the distal radial articular surface ( Figure 48-17 ).
Figure 48-17 Colles' fracture. A, Posteroanterior view shows fracture and shortening of radius. B, Lateral view shows typical dorsal displacem ent and angulation of radial fracture. ((From Propp DA, Chin H: Forearm and wrist radiology—Part I. J Em erg Med 7:393, 1989.))
Colles' fracture requires prompt anatomic reduction in the emergency department, with full restoration of radial length and correction of the dorsal angulation either to a neutral position or ideally to the normal volar tilt position. Closed reduction, using local or regional anesthesia, with cast immobilization is successful in most cases ( Figure 48-18 ). An effective method of anesthesia is placing a 22-gauge needle in the dorsum of the distal radius, withdrawing until a hematoma is encountered, then instilling 5 to 10 mL of 2% lidocaine (Xylocaine) ( Figure 48-19 ). Finger traps also are an effective means of obtaining the reduction and allow positioning for casting ( Figure 48-20 ). The more comminuted and displaced the fracture, the more likely operative reduction will be necessary. Complicated fractures with significant displacement (<20 degrees of dorsal angulation), marked dorsal comminution, or intra-articular extension should be followed closely by an orthopedic specialist because loss of reduction often occurs and mandates early operative reduction with internal or external fixation. Immediate referral to an orthopedic surgeon should be considered if initial
Page 166
attempts at closed reduction are unsuccessful, if there is associated neurovascular compromise, or if the fracture is open.
Figure 48-18 Short arm cast.
Figure 48-19 Hem atom a block.
Figure 48-20 Finger traps.
Complications of Colles' fracture are seen most often in elderly patients and in patients with inadequate fracture reduction.[] Median nerve injury may be seen acutely either because of traction from the original fracture displacement or because of direct injury to the nerve by fracture fragments. Injury to the median nerve also has been described after closed reduction because of traction on the nerve, direct pressure from the cast or position of immobilization, or swelling causing compression in the carpal tunnel. Treatment is repositioning, decreasing the splint pressure, or occasionally carpal tunnel release. For this reason, it is important to document neurologic function before and after fracture reduction. A more common complication is malunion of the fracture, resulting in chronic wrist pain and limited range of motion. This complication is more likely to occur in cases of fracture involving the radiocarpal joint.
Smith's Fracture Smith's fracture is a transverse fracture of the metaphysis of the distal radius, with associated volar displacement and volar angulation. In some cases, the fracture may extend into the radiocarpal joint. Because the resultant deformity is opposite to that seen in Colles' fracture, Smith's fracture is often called a reverse Colles' fracture. The typical mechanism of injury involves a direct blow to the dorsum of the wrist or fall onto the dorsum of the hand, resulting in extreme palmar flexion. The fracture also may be seen after a fall backward on an outstretched hand with the forearm in supination. The patient has a swollen, painful wrist, which is deformed with fullness visible on the volar aspect. The fracture is visible on posteroanterior and lateral radiographs of the wrist, but the lateral view best shows the degree of volar displacement and angulation ( Figure 48-21 ).
Page 167
Figure 48-21 Sm ith's fracture. A, Posteroanterior view shows a metaphyseal fracture of the radius with shortening. B, Lateral view shows volar displacem ent of the distal fracture fragm ent along with the carpus. ((From Propp DA, Chin H: Forearm and wrist radiology—Part I. J Em erg Med 7:393, 1989.))
Treatment of this fracture involves closed reduction with cast immobilization for 6 to 8 weeks; however, molding of the cast to maintain the reduction can lead to median nerve compression. Orthopedic consultation is recommended because open reduction and internal fixation may be required. Complications include median nerve injury, malunion, and posttraumatic arthritis, especially in fractures with significant displacement or intra-articular extension. As with Colles' fracture, prognosis is most favorable in patients with successful reduction, with restoration of the normal radial length and volar tilt.[43]
Barton's Fracture Barton's fracture is an oblique intra-articular fracture of the rim of the distal radius, with displacement of the carpus along with the fracture fragment. The fracture may involve the dorsal rim of the radius with dorsal carpal subluxation (Barton's fracture), or it may involve the volar rim with volar carpal subluxation (volar Barton's fracture). These fractures are rare and account for only 1.2% to 4.2% of all distal radius fractures.[ 44] The volar-anterior margin fracture is seen more often than the dorsal-posterior margin fracture. The mechanism of injury for these fractures involves a high-velocity impact across the articular surface of the radiocarpal joint, with the wrist in either volar flexion (causing a volar rim fracture) or dorsiflexion (causing a dorsal rim fracture). Volar and dorsal rim fractures are easily visible on posteroanterior and lateral wrist radiographs; however, the lateral view best shows the degree of articular surface involvement and the amount of associated fracture displacement ( Figure 48-22 ).
Figure 48-22 Volar Barton's fracture. Lateral view shows typical oblique intra-articular fracture of the volar rim of the radius with associated volar displacem ent of the distal radial fragment along with the carpus. ((From Harris JH, et al: The Radiology of Em ergency Medicine, 3rd ed. Baltimore, William s & Wilkins, 1993.)William s & Wilkins)
Treatment of these fractures requires orthopedic consultation for reduction and stabilization. Closed reduction occasionally may be successful. Most authors now advocate early operative management, however, with either closed reduction under fluoroscopy followed by percutaneous pinning or open reduction and internal fixation to restore accurately the articular surface of the radius and stabilize the carpus.[44] Complications include posttraumatic arthritis of the radiocarpal joint and delayed carpal instability. Both complications are seen more commonly when reduction fails to achieve or maintain anatomic realignment of the radiocarpal joint surface.
Hutchinson's Fracture Hutchinson's fracture, or chauffeur's fracture, is an intra-articular fracture of the radial styloid. The mechanism of injury is usually a direct blow or fall resulting in trauma to the radial side of the wrist. The term chauffeur's fracture originated from the era of hand-cranked automobiles, when this injury occurred because of direct trauma to the radial side of the wrist from the recoil of the crank. The fracture is seen best on the posteroanterior view of the wrist, as a transverse fracture of the radial metaphysis with extension through the radial styloid into the radiocarpal joint ( Figure 48-23 ).
Page 168
Figure 48-23 Hutchinson's fracture. Posteroanterior view shows intra-articular fracture of the radial styloid. ((From Greenspan A: Orthopedic Radiology: A Practical Approach, 2nd ed. New York, Gower Medical Pub lishing, 1992.)Gower Medical Pub lishing)
Nondisplaced fractures may be immobilized in a short arm cast for 4 to 6 weeks; however, displaced fractures require open/closed reduction and fixation. Because the radial styloid is the primary site of attachment for many of the ligaments of the wrist, accurate fracture reduction and union are crucial.[45] Complications of radial styloid fracture include associated scapholunate ligament disruption and posttraumatic arthritis, both of which are more likely when there is fracture displacement.
Radioulnar Joint Disruption Dislocation of the DRUJ may be seen in association with distal radial fractures and Galeazzi's fractures. It also may be seen as an isolated injury without fracture. Diagnosis is often difficult because plain radiographs commonly are reported as normal, so a careful clinical examination looking for certain characteristic findings may be the only clue to the presence of this injury. The typical mechanism of injury is a fall on the outstretched hand with either hyperpronation, resulting in dorsal dislocation, or hypersupination, causing volar dislocation of the ulna. Another mechanism known to cause DRUJ dislocation occurs when the hand is caught in rotating machinery, resulting in the same forcible hyperpronation or supination. This forcible rotation of the wrist causes disruption of the triangular fibrocartilage complex, the major stabilizer of the DRUJ, and may result in an associated avulsion fracture of the ulnar styloid. Patients with this injury have a history of sudden onset of pain with a “snapping” sensation in the wrist, swelling, and limited range of motion. On examination, there is tenderness over the ulnar aspect of the wrist, with palpable crepitus on supination and pronation. With a dorsal dislocation of the ulna, the ulnar styloid appears more prominent than on the unaffected side, and there is significant pain and limitation of movement on supination of the wrist. With a volar dislocation of the ulna, there is loss of the normal ulnar styloid prominence, with pain and limitation of movement on pronation. These characteristic clinical findings should alert the physician to the possibility of DRUJ disruption and prompt the appropriate investigations to confirm the presence or absence of this injury. Plain radiographs of the wrist may show the presence of DRUJ dislocation, but pain and inability of the patient to rotate the wrist fully may cause a falsenegative result because a true lateral view cannot be obtained. It also is important to assess for radial head fractures because these fractures commonly are associated with DRUJ disruption. If there is significant clinical suspicion of injury and plain radiographs appear normal, a CT scan of the DRUJ is recommended.[] Treatment of these acute injuries requires orthopedic consultation for reduction and stabilization. Closed reduction with the forearm in supination and a long arm cast is often successful. Alternatively, open reduction is often necessary with volar dislocations because the ulnar head often is locked on the volar distal radius. Operative reduction also is necessary in dorsal dislocations to repair the associated injury to the triangular fibrocartilage complex. Immobilization in a long arm cast usually is maintained for 6 weeks.
Pediatric Fractures of the Distal Radius Fractures of the distal radius in children may be divided into two types: fractures involving the distal radial metaphysis and fractures involving the growth plate. They usually occur as a result of a fall on an outstretched hand with the wrist forcibly dorsiflexed. Fractures of the radial metaphysis are of three types: torus fractures, greenstick fractures, and complete fractures. The torus fracture is the most common of these fractures and results in a buckling of the radial cortex, which, because of the strong periosteum, is seen without significant displacement ( Figure 48-24 ). These fractures are treated with immobilization in a short arm cast with orthopedic follow-up. Healing usually occurs over 2 to 3 weeks, and complications are rarely seen.[48] Greenstick fractures also are incomplete metaphyseal fractures, with disruption of the cortex on one side and angulation or bowing on the opposite side. By definition, these fractures are displaced and require reduction with regional or general anesthesia if angulated more than 10 degrees. Angulations of less than 10 degrees usually remodel. Short arm well-molded cast immobilization is recommended, with close orthopedic follow-up to ensure maintenance of reduction. Complete fractures of the radial metaphysis involve complete disruption of both cortices of bone and usually result in significant displacement and angulation. These fractures also may be associated with a fracture of the distal ulna. Closed reduction by an orthopedic surgeon with regional or general anesthesia may be successful, but if alignment is unsatisfactory
Page 169
or if the fracture is unstable, open reduction with internal fixation may be necessary.[49]
Figure 48-24 Torus fracture of the distal radius. Anteroposterior and lateral views of a radial torus fracture with buckling of the radial cortex. ((From Dvorkin ML: Office Orthopaedics. Norwalk, Conn, Appleton & Lange, 1993.)Appleton & Lange)
In 1963, Salter and Harris classified growth plate injuries in children ( Table 48-2 ). Growth plate or physeal fractures of the distal radius are usually Salter-Harris type I or type II. Although these injuries result in disruption of the growth plate, they rarely result in growth disturbance.[50] Type I injuries cause pain and palpable tenderness over the distal radial physis, with the only radiographic abnormality being volar displacement of the pronator quadratus fat pad. These injuries may be treated with a short arm cast or splint immobilization for 3 to 4 weeks; orthopedic follow-up is suggested within 1 week of the injury. Type II injuries involve a fracture through the radial metaphysis and the physis and are visible on routine wrist radiographs as a triangular metaphyseal fragment on the dorsal surface of the radius ( Figure 48-25 ). These fractures may be complicated by displacement of the radial epiphysis or by an associated fracture of the distal ulna. If displaced, these injuries require orthopedic referral for closed reduction under general anesthesia and immobilization in a short arm cast for 6 weeks. Operative fixation may be necessary if adequate alignment can-not be achieved or maintained with closed reduction and casting. Table 48-2 -- Salter-Harris Classification Salter-Harris Type
Radiographic Finding
Complication
I
Epiphyseal and metaphyseal separation. No fracture on x-ray Fracture through metaphysis and physis (Thurston Holland sign) Fracture through epiphysis to physis Fracture from epiphysis through physis to metaphysis Severe crush force through epiphysis to an area of the physis. Initial x-rays are normal Peripheral bruise or injury to the perichondrial ring or periosteum at the edge of the physis
None
II
III IV V
VI (Rang)
Usually none
Concern with anatomic alignment. High rate of displacement while casted Early partial growth arrest. Surgical management recommended Severe growth arrest with progressive shortening or angular deformity. Premature or uneven physeal fusion Seve re grow th arre st, angu lar defor mity, or osse ous bridg e
Page 170
Salter-Harris Type
Radiographic Finding
Complication form ation betw een phys is and meta phys is. Oste ocho ndro ma form ation
Figure 48-25 Salter-Harris type II distal radial fracture showing typical triangular m etaphyseal fracture fragm ent, with associated epiphyseal fracture displacem ent. ((From Harris JH, et al: The Radiology of Em ergency Medicine, 3rd ed. Baltimore, William s & Wilkins, 1993.)William s & Wilkins)
SOFT TISSUE INJURIES OF THE WRIST Carpal Tunnel Syndrome Carpal tunnel syndrome is a neuropathy of the median nerve at the wrist that occurs as a result of compression of the median nerve within the carpal tunnel. The transverse carpal ligament and the volar surfaces of the carpal bones form the carpal tunnel. It is a rigid compartment that contains nine flexor tendons (the flexor pollicis longus tendon, four flexor digitorum superficialis tendons, and four flexor digitorum profundus tendons) and the median nerve. Any process (local or systemic) that results in an increase in pressure within this compartment may produce carpal tunnel syndrome. The most common causes of carpal tunnel syndrome are distal radius fractures and repetitive strain. Carpal tunnel syndrome also can be associated with rheumatoid arthritis, hypothyroidism, diabetes mellitus, and collagen vascular diseases. Each of these systemic diseases is thought to produce an increase in pressure within the carpal tunnel from thickening of the flexor synovia or transverse carpal ligament. Hormonal changes associated with pregnancy and menopause also are known to cause carpal tunnel syndrome, probably by retention of fluid in the soft tissues about the wrist.[51] The classic symptoms include a gradual onset of numbness, paresthesia, and pain in the thumb, index finger, and long finger. These symptoms are often bilateral and are worse during the night and after strenuous activities. Typically, patients report numbness and paresthesias on awakening that improves when the hands are shaken or held in a dependent position. On physical examination, the most sensitive provocative test is the wrist flexion test, or Phalen's test (sensitivity 76%, specificity 80%) ( Figure 48-26 ).[52] This test is performed by asking the patient to flex the wrists fully for 60 seconds while the forearms are held in a vertical position. The test is positive if paresthesias or numbness develops in the median nerve distribution. Another test, Tinel's sign, is positive if light tapping or percussion over the median nerve at the wrist produces pain or paresthesias in the median nerve distribution. Analysis of the literature suggests, however, that Tinel's sign (sensitivity 64%, specificity 55%) is not as powerful a test as Phalen's test in detecting median nerve compression, although neither is
Page 171
100% sensitive. Given that neither Phalen's test nor Tinel's sign is completely reliable in making the diagnosis of carpal tunnel syndrome, nerve conduction studies have been used to confirm the diagnosis, with reports of 90% sensitivity.[53] Conservative treatment for carpal tunnel syndrome has varying results. Treatment includes splinting the wrist in a neutral position and cortisone injections in the carpal tunnel. Splinting initially may be prescribed full-time for 3 or 4 weeks, then reduced to splinting at night only. Nonsteroidal anti-inflammatory drugs have proved to be of little benefit. Surgical release of the flexor retinaculum to unroof the carpal tunnel is indicated when nonoperative management fails.[]
Figure 48-26 Phalen's test.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/108.html/top
Page 172
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
FOREARM PERSPECTIVE Accurate evaluation of forearm injuries requires a thorough knowledge of the complex anatomic relationships between the radius and ulna. The ulna may be thought of as a stable structure around which the radius rotates, allowing supination and pronation to occur. With any injury to the forearm, the clinician should suspect an associated injury involving the elbow or wrist joints. The clinical and radiologic evaluation of forearm injuries should include the wrist and elbow. The biomechanical interdependence of the radius and ulna means that accurate reduction and fixation of forearm fractures is essential to maintain full pronation and supination.[55]
Anatomy The bones of the forearm consist of the radius and ulna, which articulate at each end at the proximal radioulnar joint and DRUJ. The capsule of the elbow joint and the annular ligament provide soft tissue support at the proximal articulation. Distally the anterior and posterior radioulnar ligaments and the triangular fibrocartilage complex support the radioulnar joint. Of all these soft tissue supports, the triangular fibrocartilage complex acts as the major stabilizer of the DRUJ. The interosseous membrane and the supinator, pronator teres, and pronator quadratus muscles join the shafts of the radius and ulna. These muscles act as important supports to the radial and ulnar shafts and are responsible for the significant bony displacement seen with some forearm fractures. The forearm is divided into two compartments, one volar to the forearm bones and interosseous membrane and one dorsal, and the antebrachial fascia encloses each compartment. The volar compartment contains the flexors and pronators of the wrist and hand, and the dorsal compartment contains the extensor muscles of the wrist and hand. The muscles of each compartment are divided further into a superficial and deep layer. The nerves and vessels of each compartment lie between the superficial and deep muscle layers ( Table 48-3 ). Table 48-3 -- Compartments of the Forearm Muscles
Nerves
Vessels
Median nerve (except flexor carpi ulnaris supplied by ulnar nerve)
Ulnar and radial arteries
Median nerve (except medial half of flexor digitorum profundus supplied by ulnar nerve)
Ulnar and radial arteries
Radial nerve
Ulnar artery
Volar compartment Superfici al layer
Deep layer
Pronator teres Flexor carpi radialis Palmaris longus Flexor carpi ulnaris Flexor digitorum superficialis Flexor pollicis longus Pronator quadratus Flexor digitorum profundus
Dorsal compartment Superfici al layer
Brachioradialis
Page 173
Extensor carpi radialis longus Extensor carpi radialis brevis Extensor digitorum Extensor digiti minimi Extensor carpi ulnaris Deep layer
Radial nerve
Ulnar artery
Supinator Abductor pollicis longus Extensor pollicis brevis Extensor pollicis longus Extensor indicis proprius
CLINICAL FEATURES The clinical assessment of forearm injuries begins with a detailed history of the mechanism of injury. The physical examination includes inspection of the injured forearm, taking note of any deformity or discoloration or lacerations of the overlying skin. Observation of the patient's attempts at range of motion at the wrist and elbow joints is important, and results can be compared with range of motion of the “normal” uninjured side. The site of maximal tenderness should be determined by palpation along the entire length of the radius and ulna and by palpation of the soft tissues over the dorsal and volar surfaces of the forearm. The neurovascular examination of the forearm should include evaluation of the brachial artery pulse proximally and the radial and ulnar pulses distally and an assessment of distal radial, median, and ulnar nerve function.
DIAGNOSTIC STRATEGIES: RADIOLOGY The routine radiographic views of the forearm are anteroposterior and lateral views and should include the wrist and elbow joints. The inclusion of the joint above and below the forearm is crucial because a fracture or dislocation at one end may be associated with a similar abnormality at the opposite end. The normal anatomic relationships between the distal radius and ulna, including the radial length measurement, the normal volar tilt of the radius, and the ulnar slant of the distal radial articular surface, have been described in the section on radiology of the wrist (see Figure 48-4 ). These same relationships are visible on the anteroposterior view of the forearm. The normal proximal radial alignment is seen best on the lateral view of the forearm, when a line drawn through the proximal radial shaft and radial head should intersect the capitellum ( Figure 48-27 ). This alignment is particularly important to assess when looking for the presence of a radial head dislocation.
Figure 48-27 Norm al lateral view of elbow. A line (dashed) bisecting the proxim al radial shaft bisects the capitellum . ((From Weissm an BN, Sledge CB: Orthopedic Radiology. Philadelphia, WB Saunders, 1986.)Elsevier Inc.)
Observing the orientation of several bony projections of the radius and ulna assesses normal alignment of the radial and ulnar shafts. On the normal anteroposterior view, the radial styloid should point in a radial direction, and the biceps tuberosity of the proximal radius should point in an ulnar direction. On the normal lateral view, the ulnar styloid should point dorsally, and the coronoid process of the proximal ulna should
Page 174
point volarly. Any alteration in these normal relationships implies an abnormal rotational or axial deformity ( Figure 48-28 ).
Figure 48-28 Norm al anteroposterior and lateral views of the forearm . Both bones should be visible their entire length and should include the wrist and elbow joints. ((From Propp DA, Chin H: Forearm and wrist radiology—Part I. J Em erg Med 7:393, 1989.))
FOREARM FRACTURES Shaft Fractures of Radius and Ulna Fracture of the radial and ulnar shafts usually occurs as a result of a direct blow to the forearm, but may be seen after a fall on the outstretched hand. In either case, the degree of force required to fracture both bones usually results in fracture displacement. Clinically, patients have obvious deformity of the forearm and pain and swelling at the fracture site. All movements of the forearm and hand are resisted because of pain. A neurovascular examination must be done to exclude associated neurologic impairment or early compartment syndrome. Anteroposterior and lateral radiographs of the forearm must include elbow and wrist joints to exclude an associated dislocation or articular fracture. Although these fractures are usually obvious on clinical examination, radiographs allow an accurate means of determining the amount of fracture displacement and comminution. Undisplaced fractures are rare in adults, but when they do occur, they are treated conservatively with immobilization in a long arm cast for a minimum of 8 weeks. Prompt orthopedic follow-up and repeat radiographs should be arranged within 1 week of injury to ensure that displacement does not occur after casting.[] Displaced fractures of the radial and ulnar shafts are treated surgically and should be splinted, and an orthopedic consultation should be obtained for open reduction and internal fixation. Fracture healing is usually complete in 6 months. Nonunion and malunion may occur in 3% to 5% of cases.[58] The most significant complication of this fracture is a compartment syndrome, which may result from the initial trauma or occur after surgery.
Ulnar Shaft Fractures Isolated ulnar shaft fractures, or nightstick fractures, are relatively common and usually are caused by a direct blow to the forearm. Patients have localized pain and swelling over the site of the fracture. Radiographs of the forearm show this fracture and depict the degree of fracture displacement if present. Undisplaced fractures of the distal third of the ulna may be treated with immobilization in a short arm cast for 6 to 8 weeks. Fractures of the middle or proximal third of the ulna require long arm cast immobilization. Weekly follow-up monitoring is recommended to confirm continued lack of displacement during the period of fracture healing. If loss of fracture position occurs, open reduction and internal fixation are necessary. Displaced fractures of the ulna are defined as fractures with greater than 10 degrees of angulation or fractures with displacement greater than 50% of the diameter of the ulna.[59] Whenever significant displacement is present, radiographs should be examined carefully to rule out an associated dislocation of the radial head (Monteggia's fracture). Isolated displaced ulnar shaft fractures should be referred to an orthopedic surgeon for open reduction and internal fixation. Most fractures heal uneventfully with excellent results. Fractures of the middle third of the shaft may be complicated by nonunion if reduction is not adequately achieved or maintained.[59]
Monteggia's Fracture In 1814, Monteggia described a fracture at the junction of the proximal and middle thirds of the ulna associated with anterior dislocation of the proximal radial head. This original description accounts for only 60% to 65% of proximal ulnar fractures with associated radial head dislocation. The entire spectrum of fracture-dislocations has since been classified by Bado[60] into four types of Monteggia lesions, depending on the site of the proximal ulnar fracture and the direction of fracture angulation and associated radial head
Page 175
dislocation. Overall, this injury is rare and accounts for only 7% of all fractures of the radius and ulna.[61] The mechanism of injury of Monteggia's fracture is forced pronation of the forearm during a fall on the outstretched hand or a direct blow to the posterior aspect of the ulna. On clinical examination, pain and tenderness are present at the fracture site, and range of motion is limited at the elbow joint. The forearm may appear shortened compared with the unaffected side, and the radial head dislocation may be palpable in the antecubital fossa. A complete neurovascular examination is essential to rule out an associated radial nerve injury, which may be present in 17% of cases. The proximal ulnar fracture is readily seen on anteroposterior and lateral radiographs of the forearm, but the elbow joint must be examined carefully to avoid missing the associated radial head dislocation ( Figure 48-29 ). This dislocation is commonly missed, and delayed diagnosis has been reported in 24% of cases.[62] To avoid missing the associated radial head dislocation, the alignment should be confirmed on anteroposterior and lateral radiographs. A line drawn through the radial shaft and head normally should intersect the capitellum on all views.
Figure 48-29 Monteggia's fracture-dislocation. Fractures of the ulna diaphysis with anterior angulation and associated anterior dislocation of the radial head. ((From Propp DA, Chin H: Forearm and wrist radiology—Part I. J Em erg Med 7:393, 1989.))
Treatment of Monteggia's fracture is surgical, and immediate orthopedic referral should be arranged for definitive open reduction and internal fixation. An exception may be made in a pediatric patient, in whom closed reduction followed by a long arm cast may be effective. Casts should be in a flexed and supinated position to maintain fracture position. Flexion should be as close to 90 degrees as possible while ensuring the maintenance of a good radial pulse. Common complications include malunion or nonunion of the ulna fracture with redislocation or subluxation of the radial head. These complications are more likely to occur when the diagnosis has been delayed or when fracture fixation has been inadequate.[62]
Galeazzi's Fracture Galeazzi's fracture involves the junction of the middle and distal thirds of the radius, with an associated dislocation or subluxation of the DRUJ. This rare injury accounts for only 7% of all fractures of the forearm. This injury occurs as a result of a fall on the outstretched hand, with the wrist in extension and the forearm forcibly pronated. Another less common but well-described mechanism of injury is a direct blow to the dorsoradial aspect of the wrist. Clinical examination is often the key to diagnosis because disruption of the DRUJ may not otherwise be apparent. The radial fracture causes obvious swelling and deformity on the radial side of the forearm, and pain is localized over the fracture site. In addition, the DRUJ is swollen and painful on palpation, and the ulnar head appears prominent compared with the unaffected wrist. On the anteroposterior radiograph, a transverse or short oblique fracture of the radius is visible at the junction of the middle and distal thirds of the radius. The radius appears shortened, and an increase in joint space may be visible between the distal radius and ulna. The lateral view shows dorsal angulation of the radial fracture, and the head of the ulna is displaced dorsally ( Figure 48-30 ). An associated ulnar styloid fracture is seen in approximately 60% of cases and should alert the physician to the presence of disruption of the DRUJ.[63]
Figure 49-30 Galeazzi's fracture-dislocation. An obvious fracture of the distal third of the radius with severe displacem ent and
Page 176
an associated dislocation of the distal radioulnar joint (open arrow). ((From Harris JH, et al: The Radiology of Em ergency Medicine, 3rd ed. Baltimore, William s & Wilkins, 1993.)William s & Wilkins)
Galeazzi's fractures are inherently unstable. Occasionally, if the radial fracture is distal, a closed reduction of the radius and reduction of the DRUJ in supination with a long arm cast can be successful. These fractures often require operative fixation, however. The instability is the result of several factors, including the distracting pull of the brachioradialis and pronator quadratus muscles and the associated disruption of the DRUJ. Operative treatment involves open reduction and internal fixation of the radial shaft fracture, with immobilization of the forearm in supination to maintain reduction of the DRUJ. Reports have suggested that failure of closed reduction of the DRUJ in some patients is due to soft tissue interposition, and in these cases open reduction and fixation of the DRUJ is recommended.[66] Complications of Galeazzi's fracture include malunion and nonunion of the radial fracture and recurrent subluxation or dislocation of the DRUJ. These complications result in chronic pain, with significant limitation of pronation and supination, and are thought to be largely avoidable with appropriate open anatomic reduction and rigid internal fixation of the fracture.[65]
Pediatric Forearm Fractures Shaft Fractures of Radius and Ulna In children, fractures to both bones of the forearm usually occur as a result of a fall on the outstretched hand. Fractures generally are classified into three types: buckle, or torus, fractures; incomplete, or greenstick, fractures; and complete fractures. The forearm fracture is usually obvious clinically, with significant pain, swelling, and visible deformity at the fracture site. Anteroposterior and lateral radiographs of the forearm distinguish whether fractures are complete or incomplete and show the degree of angulation and rotational deformity ( Figure 48-31 ).
Figure 48-31 Pediatric forearm fracture. Anteroposterior and lateral views of radial and ulnar shaft fractures with dorsal angulation. ((From Dvorkin ML: Office Orthopaedics. Norwalk, Conn, Appleton & Lange, 1993.)Appleton & Lange)
The objective of successful treatment of forearm fractures in children does not differ significantly from treatment in adults; the goal is successful reduction of fracture deformity. Nevertheless, in children, there is the potential for spontaneous correction of residual fracture angulation with bone remodeling. The younger the child (especially <10 years old), and the closer the fracture is to the growth plate, the greater the potential for remodeling. These principles govern the acceptability of fracture reduction, and generally angulations of less than 10 degrees are considered acceptable.[67] Greenstick and complete forearm fractures require orthopedic referral for closed reduction under deep procedural sedation or general anesthesia. Results are usually excellent if correction of angular and rotational deformity is achieved and maintained. Immobilization in a long arm cast is usually necessary for 7 to 8 weeks. Open reduction and internal fixation are occasionally necessary if closed reduction is unsuccessful or cannot be maintained with casting. Complications of malunion and nonunion are rarely seen because of rapid healing and a tremendous capacity for remodeling.[49]
Plastic Deformation The occurrence of plastic deformation of bone is unique to children and refers to a bending of the bone without overt fracture. Plastic deformation may be seen as an isolated injury to the radius or ulna, or it may be seen in one bone in combination with a fracture of the other bone. Clinically, this injury produces localized pain and deformity of the forearm, and radiographically it appears as a fixed curvature of the bone shaft ( Figure 48-32 ). If significant curvature is present, the deformity is obvious, and pronation and supination are
Page 177
significantly restricted. Treatment requires orthopedic referral for closed reduction under general anesthesia and immobilization in a long arm cast for 6 to 8 weeks.[68]
Figure 48-32 Acute plastic bowing fracture of the forearm. Anteroposterior and lateral views show broad volar bowing of the radial shaft with no visible fracture lucency. ((From Kom ara JS, et al: Acute plastic b owing fractures in children. Ann Em erg Med 15:585, 1986.))
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/109.html/top
Page 178
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
Chapter 3 – Monitoring the Emergency Patient Michael F. Murphy Timothy A.D. Graham
PERSPECTIVE To monitor means to measure or observe a physiologic parameter either continuously or intermittently. The monitoring device may provide a "snapshot in time" or may detect deterioration, track improvement, or measure the effects of interventions. Monitoring parameters, such as clinical observation, routine vital sign measurement, and electrocardiogram monitoring, are basic requirements in emergency medicine. This chapter addresses newer technologies, such as pulse oximetry, end-tidal carbon dioxide (CO2) measurement, sublingual capnography, and noninvasive blood pressure (BP) measurement. Fetal monitoring immediately after maternal trauma also is discussed briefly. The following questions are important with respect to monitoring: 1. 2. 3.
4.
5.
Which physiologic parameters are important indicators of status or progression? What technology monitors that parameter? Can the monitoring device be relied on to do so with precision and accuracy in this particular clinical situation? In other words, what are the limitations of the technology? (For example, is a noninvasive monitor of BP adequate for the management of a hypertensive crisis with sodium nitroprusside?) In which clinical situations are the data provided potentially inaccurate? What is the role of the emergency department in the management of this particular problem? The best example of this question relates to the appropriateness of inserting pulmonary artery catheters in the emergency department. Is the emergency department an extension of the intensive care unit (ICU)? Does the expected standard of care demand a certain level of monitoring?
NONINVASIVE BLOOD PRESSURE MEASUREMENT Automatic, noninvasive measurement has become a popular and, if applied to appropriate clinical situations, an accurate method of determining BP. Advantages include (1) more time for staff to attend to other tasks; (2) timed repetition of BP measurements; (3) continuous display of the systolic pressure; and (4) a display of other several parameters (e.g., systolic, diastolic, and mean BP; pulse rate), depending on the machinery. Noninvasive machines use a detection system based on auscultatory, oscillometric, or Doppler principles.[] Automatic oscillometric devices determine BP by electronically determining the pulse amplitude. This method and Doppler are the most accurate of the indirect methods. The cuff is automatically inflated at predetermined intervals to a preset level. As the machine gradually deflates the cuff, it senses the amplitude of the oscillations (pulsations) transmitted to the cuff by movement of the arterial wall under the cuff. An abrupt increase in the magnitude of the oscillation signals an opening of the artery and an increase in volume under the cuff; this is the systolic pressure. The magnitude of the oscillation increases to a peak, then falls rapidly. The point where there is no longer an alteration in the magnitude of the oscillation is the diastolic pressure. Some machines calculate the mean arterial pressure, identified as the cuff pressure at the point of largest oscillation.[1]
Limitations The shortcomings of noninvasive BP techniques are the same shortcomings of any cuff measurement technique, including patients with obese arms, uncoopera-tive moving patients, and patients with very high or very low BP. Even with these limitations, automatic machines are more accurate, precise, and reliable than auscultation in patients with very low or very high BP, primarily because the sensing devices are more
Page 179
sensitive than the human ear.[2] The cycle length of the inflation-deflation sequence of the older machines was exceedingly long and led to frequent failure. Newer machines have rectified this problem. The most accurate method of measuring BP is with an intra-arterial catheter transduced to an electronic display. The ability to identify beat-to-beat variability, respiratory variation, and longer trends is unsurpassed by any other currently available technology. In addition, the placement of the arterial catheter enables frequent sampling of arterial blood without additional arterial punctures. Arterial line pressure monitoring is used increasingly in emergency departments, particularly because lack of ICU bed availability mandates longer stays in the emergency department for critically ill patients. The risk of arterial injury or thrombosis related to arterial line insertion is low but real and can result in vascular compromise. Arterial line insertion should not delay transfer of patients to an operating room or critical care setting. Traditional methods of noninvasive BP measurement are often inadequate in the following situations, and invasive monitoring should be considered: 1.
2.
3.
4. 5.
Exceedingly high (>250 mm Hg systolic) or low (<80 mm Hg systolic) BPs. Although the invasive method also is less accurate at these extremes than in the physiologic range, the error is significantly less. Many clinicians believe that any patient receiving sodium nitroprusside should have continuous invasive monitoring because of rapid fluctuations in blood pressure, although this is unsupported in the literature. In a patient who is rapidly going into shock, the best chance to insert an arterial line may be in the emergency department while the arterial pulse is still palpable, although this should not be allowed to delay transfer to a more appropriate location for definitive care. Anatomic indications for invasive monitoring include patients who are critically ill and either have no limb or no have suitable limb (e.g., too obese) to undertake conventional measurement. Frequent arterial sampling is required. The requirement in such cases is for vascular access rather than the monitoring modality per se. Patients who are ill enough to require frequent arterial sampling usually benefit from continuous arterial BP monitoring.
BLOOD GAS MONITORING Although the ability to monitor oxygen usage at the level of the individual cell or group of cells might be considered ideal, current technology allows less precise measures of performance. Transcutaneous oxygen and CO2 monitoring, conjunctival oxygen pressure, pulse oximetry, and end-tidal CO2 measurements (capnography, capnometry) all are used to indicate the adequacy of pulmonary gas exchange and arterial blood gas tensions and to assess ventilatory efficacy. Sublingual capnography is emerging as a valuable modality in detecting early shock and visceral hypoperfusion.[3]
Transcutaneous and Conjunctival Monitors Transcutaneous (Ptco2) and conjunctival (Pcjo2) systems of oxygen pressure monitoring use the Clark polarographic oxygen electrode, the same device used in blood gas machines. The skin must be heated to obtain reliable Po2 readings with rapid response times when transcutaneous devices are used. The sensor actually measures epidermal tissue Po2. Conjunctival devices do not require heating.[4] Ptco2 and Pcjo2 are significantly influenced by cardiac output, local tissue metabolism, and capillary blood flow. The utility of these devices in emergency medicine has been mostly in relation to their ability to reflect tissue perfusion in situations of reduced or absent cardiac output as an early indicator of gas exchange difficulty and cardiopulmonary deterioration.[5] This modality has been used most extensively and appropriately in the neonatal ICU and in medical air transport.[4] Slow calibration and response times relative to other modalities (e.g., oximetry) make Ptco2 and Pcjo2 devices less useful for the noninvasive monitoring of arterial oxygen saturation in the emergency department. Ptco2 monitors generally use a miniature, heated electrode that is pH sensitive. The same technical limitations apply to these devices. Technologic developments should eliminate these shortcomings in the future to make these devices more useful in the emergency department and field environment.
Pulse Oximetry The pulse oximeter provides a noninvasive and continuous means of rapidly determining arterial oxygen saturation and its changes. The devices are easy to use and interpret, pose no risk to the patient, and are relatively inexpensive.[6] A reliable interpretation of the information given by these devices requires an appreciation of their limitations in certain situations.
Page 180
Transmission oximetry is based on differences in the optical transmission spectrum of oxygenated and deoxygenated hemoglobin. Specifically, the physics and physiology of oximetry are based on the Beer-Lambert law, which relates the concentration of a solute to the intensity of light transmitted through a solution.[7] Light absorption is related to the concentration of the solute and a constant called the extinction coefficient. This extinction coefficient is constant for a given solute at a specified wavelength. At the wavelength of red light (660 nm), reduced hemoglobin absorbs about 10 times as much light as oxyhemoglobin, whereas at the infrared (IR) wavelength (940 nm), the extinction coefficient of oxyhemoglobin is near that of reduced hemoglobin.[7] In addition to arterial hemoglobin, other absorbers in the light path include skin, soft tissue, and venous and capillary blood. Pulse oximeters measure red and IR light transmitted through a tissue bed and in particular the pulse variations in that transmission.[6] The light sources are light-emitting diodes, and the detectors are photodiodes.[7] The light absorption is divided into a pulsatile (AC) component related to the pulsatile arterial blood and a nonpulsatile (DC) component related to the tissue bed, including venous and capillary blood and nonpulsatile arterial blood. The digital microprocessor of the pulse oximeter first determines the AC component of absorbance at each wavelength and divides this value by the corresponding DC component to obtain a ‘opulse-added’ absorbance. The device calculates the ratio of these pulse-added absorbances, a nonlinear but reproducible function of the oxygen saturation of arterial blood. The microprocessor converts this pulse-added absorbance to saturation.[ 7] Data averaged over several arterial pulse cycles are presented as saturation (Spo2).[6] Studies have shown an excellent correlation between arterial hemoglobin oxygen saturation and Spo2.[] Limitations to the value of pulse oximetry exist with severe vasoconstriction (e.g., shock, hypothermia), excessive movement, synthetic fingernails and nail polish, severe anemia, or the presence of abnormal hemoglobins. The extinction coefficients for carboxyhemoglobin (COHb) and methemoglobin (MetHb) are not zero in the red and IR range. Their presence contributes to light absorption and causes errors in pulse oximetry readings.[7] The pulse oximeter senses COHb as though it were mostly oxyhemoglobin and provides a falsely high reading. The MetHb produces a large pulsatile absorbance signal at the red and the IR wavelengths. This signal forces the absorbance ratio toward unity, which corresponds to an Spo2 of 85%. [7] With high levels of MetHb, the Spo2 is erroneously low when the arterial saturation is greater than 85% and erroneously high when the arterial saturation is less than 85%. Erroneously high readings (about 3% to 5%) and a higher incidence of failure to detect signals have been reported in dark-skinned races.[6] In general, signals are weaker from ears than from fingers except in hypotension or peripheral vasoconstriction, but ear responses are faster. Nasal bridge probes have been reported to read falsely high. In children particularly, it is essential to be certain the signals are adequate; a valid pulse reading can be of some reassurance. Pulse oximetry is particularly useful in the emergency department evaluation of patients with acute cardiopulmonary disorders, such as bronchiolitis, asthma, heart failure, and chronic obstructive pulmonary disease (COPD), but is valuable in any patient for whom continuous knowledge of oxygen levels is of value in their management.[8] It is a standard monitoring parameter for patients undergoing procedural analgesia and sedation and in patients with a decreased level of consciousness, such as intoxication, overdose, and head injury.[] The ability of pulse oximetry to decrease the frequency with which arterial blood gas readings are obtained also has been shown.[8] Improvements in pulse oximeter technology have resulted in significantly better accuracy and reliability during patient motion. Continuous monitoring may indicate the insidious development of shock as vasoconstriction and deterioration of signal detection develops. Continuous oximetry is mandatory in patients requiring definitive airway management. This valuable device has become an established component of the monitoring armamentarium of the emergency physician.[] Adequate oxygen saturation does not ensure adequate ventilation, however, particularly in patients with decreased levels of consciousness. Also, a normal oxygen saturation does not preclude the presence of a pulmonary embolus.
Capnography/Capnometry: End-Tidal Carbon Dioxide CO 2 concentration in exhaled gases is intrinsically linked to tissue metabolism, systemic circulation, and ventilation.[12] Capnography is the graphic record of instantaneous CO2 concentrations (capnogram) in the respired gases during a respiratory cycle.[13] This record may be qualitative or quantitative, although typically only the end-tidal CO2 concentration is displayed quantitatively. Capnometry is the measurement and display of CO2 concentrations on a visual display; the usual concentration displayed is the end-tidal CO2. Although traditionally a parameter followed during general anesthesia in the operating room, end-tidal CO2 monitoring
Page 181
is becoming increasingly common in the emergency department and prehospital setting. More than 80% of emergency medicine training programs in the United States use CO2 monitoring, with colorimetric devices being the most frequently used.[14] The remaining programs did not use them, in direct conflict with what some authorities would say is the standard of care for the verification of tracheal placement of an endotracheal tube (ETT).[15] Four spectrographic methods are used to measure end-tidal CO2 concentration in expired gases: IR, mass, Raman, and photoacoustic spectrography.[] Most stand-alone units use the IR technique. CO2 selectively absorbs IR light with a wavelength of 4.26 p-m. The concentration of the CO2 in a gas can be determined by passing filtered IR light through the gas in question and comparing the amount of light that is absorbed with a reference light beam passing through a CO2-free chamber.[12] Capnometers are either sidestream or mainstream in design. Sidestream capnometers are more likely to be encountered in the emergency department and work by aspirating a sample of gas through a small catheter into a measuring chamber. They are lightweight, can be used in intubated and nonintubated patients, and have been incorporated into commercially available nasal prong oxygen delivery apparatus to facilitate CO2 monitoring during procedural sedation. Disadvantages include plugging by secretions, 2- or 3-second delays in response time, and air leaks, which can dilute the sample.[12] Mainstream capnometers are useful only in intubated patients; they are bulky and heavy; and because they must be heated to prevent condensation, they may burn patients. Colorimetric capnometers use color scales to estimate ranges of end-tidal CO2 but are not accurate enough to give quantitative measurements. They use pH-sensitive filter paper impregnated with metacresol purple, which changes color from purple (<4 mm Hg CO2) to tan (4 to 15 mm Hg CO2) to yellow (>20 mm Hg CO2) depending on the concentration of CO2, although there is some variability in absolute numbers based on the brand of device (see Chapter 1 , Figures 1-3 and 1-4 ).[] The indicator, housed in a plastic casing, is inserted between the ETT and the ventilator bag and responds quickly enough to detect changes on a breath-by-breath basis.[13] Colorimetric capnometers are inexpensive and easy to use and should be available in every emergency department for confirmation of ETT placement if quantitative methods are not available. Usually a close correlation exists between end-tidal CO2 and arterial CO2 partial pressure (Paco2). In patients who are otherwise healthy, the end-tidal CO2 is usually 2 to 5 mm Hg less than the Paco2 because of the contribution of physiologic dead space to the end-tidal gases.[] Many conditions that affect ventilation-perfusion ratios can widen the Paco2—end-tidal CO2 gradient, including pulmonary embolism, cardiac arrest, hypovolemia, asthma, COPD, and the lateral decubitus position.[] Although end-tidal CO2 may not always reflect the absolute Paco2 in critically ill patients accurately, it is still valuable in detecting trends and sudden airway events.
Phases A normal capnogram has four phases ( Figure 3-1A ). Phase A-B represents a CO 2-free portion of the respiratory cycle. Most often this is the inspiratory phase, although it may represent apnea or a disconnection of the device from the patient. Increase in this baseline implies rebreathing of CO2, as in increased dead space in the circuit, hypoventilation, or contamination of the sensor.[12]
Figure 3-1 Four phases of a norm al capnogram . A-B, The carbon dioxide—free portion of the respiratory cycle. B-C, The rapid upstroke of the curve, representing the transition from inspiration to expiration and the mixing of dead space and alveolar gas. C-D, The alveolar plateau, representing the alveolar gas rich in carbon dioxide and tending to slope gently upward with the uneven em ptying of the alveoli. D-E, The respiratory downstroke, which is a nearly vertical drop to baseline.
Phase B-C, the rapid upstroke of the curve, represents the transition from inspiration to expiration and the mixing of dead space and alveolar gas. Prolongation of phase B-C ( Figure 3-1B ) occurs with obstruction to
Page 182
expiratory gas flow (e.g., asthma, bronchospasm, COPD, kinked ETT[12]) or leaks in the breathing system. Phase C-D, the alveolar plateau, represents alveolar gas rich in CO2 and tends to slope gently upward with the uneven emptying of alveoli. The end-tidal CO2 that is measured and read by capnometry represents point D. The slope of this phase can be increased by the same obstructive factors that increase the slope of phase B-C and is a normal physiologic variation in pregnancy.[13] A dip in the plateau indicates a spontaneous respiratory effort during mechanical ventilation, as in hypoxia, hypercarbia, or oligoanesthesia ( Figure 3-1C ).[] Phase D-E, the inspiratory downstroke, is a nearly vertical drop to baseline. This slope can be prolonged and blend in with the expiratory phase with ETT cuff leaks ( Figure 3-1D ). Abnormal respiratory patterns that are fast or chaotic limit the usefulness of end-tidal CO2 monitoring.
Uses Capnography is used in the emergency department in several clinical scenarios. It can confirm ETT placement; estimate Paco2; monitor the effectiveness of cardiopulmonary resuscitation (CPR) and mechanical ventilation; and during procedural sedation. Capnography may be used in the future to diagnose asthma and pulmonary embolism and to measure cardiac output. Along with visualizing an ETT going through the vocal cords, capnometry is the other ‘gold standard’ used to confirm intubation of the trachea. Misleading end-tidal CO2 readings can occur with esophageal intubation after bag/mask ventilation and ingestion of carbonated beverages or antacids. These tracings usually resolve after six breaths and look abnormal.[] End-tidal CO2 also is falsely elevated for about 5 minutes after the injection of bicarbonate.[18] In nonarrest settings, the end-tidal CO2 approaches 100% sensitivity and specificity in confirming correct tube placement; conversely, it is also useful to monitor for accidental extubation. End-tidal CO2 can estimate Paco2 in hemodynamically stable patients who do not have rapidly progressive lung pathology.[18] The Paco2—end-tidal CO2 gradient is usually 2 to 5 mm Hg, but this may increase to 15 mm Hg in patients with hemodynamic instability and pulmonary complications.[] It may be helpful initially to compare a serum Paco2 determination with the end-tidal CO2 to determine what magnitude of gradient is present in a particularly unstable patient. With correction for this gradient, trends in end-tidal CO2 generally can be used as a substitute for Paco2 measurements. Sidestream sampling of spontaneously breathing nonintubated patients is a reliable technique for monitoring hypoventilation and apnea.[12] It can be used to monitor patients undergoing procedural sedation in the emergency department. Animal and human studies have shown that end-tidal CO2 is a useful noninvasive measurement that is highly correlated with cardiac output and can help in predicting return of spontaneous circulation in CPR.[19] Return of spontaneous circulation is heralded by an almost immediate increase in end-tidal CO2. Two studies showed that end-tidal CO2 has prognostic value in terms of mortality during CPR.[] No patient with an average end-tidal CO2 level less than 10 mm Hg during CPR survived, giving end-tidal CO2 measurement a high negative predictive value for failure of resuscitation. Capnography needs to be prospectively validated to confirm its utility as a monitor of adequacy of CPR and as a prognostic tool in prehospital arrest. Asthma-induced bronchospasm can cause upward slanting of the expiratory plateau of the capnogram. Changes in end-tidal CO2 over time have been shown to correlate well with 1-second forced expiratory volume measurements.[18] End-tidal CO2 has the advantage of being independent of effort, gender, age, and height and might be a useful objective measure in asthmatic patients who are unwilling or unable to cooperate with 1-second forced expiratory volume testing (e.g., children, ventilated patients). Pulmonary embolism results in the increase of the ratio of physiologic dead space in the lung to total tidal volume (VD /VT).[18] Hypovolemia, cardiac arrest, and the lateral decubitus position also increase VD /VT, but are uncommon ambulatory complaints. In the future, end-tidal CO2 measurements correlated with VD /VT may allow the emergency physician to provide bedside testing to rule in or rule out pulmonary embolism in the appropriate clinical setting.[]
Page 183
The measurement of cardiac output requires invasive placement of pulmonary arterial catheters and is rarely done in the emergency department. Using modified forms of the direct Fick equation, animal and human studies have shown excellent correlation of end-tidal co2 measurements and cardiac output over a wide range of values. These measurements seem independent of changes in dead space (hypovolemia) or shunt (pulmonary edema) and might be adaptable to nonintubated patients.[18]
Sublingual Capnography Studies in the mid-1990s identified that increases in esophageal and gastric Pco2 (‘gastric tonometry’) were associated with tissue hypoxia, most commonly found in low-flow states, such as shock.[21] This finding occurred early in the clinical course of shock before more conventional global measures of tissue oxygenation, such as heart rate, blood pressure, serum lactate, and arterial blood gases, heralded tissue hypoxia. Sublingual capnography (Pslco2) subsequently was found to correlate with gastric tonometry and to be a useful and noninvasive alternative to visceral Pco2 monitoring.[] Pslco2 is relatively simple to monitor. A noninvasive microelectrode CO2 probe is placed under the tongue. A hand-held device similar in appearance to a digital thermometer (Tycohealthcare, Hazelwood, MO) provides a continuous Pslco2 reading.[22] The device consists of three major components: a disposable CO2 sensor, a fiberoptic cable that connects the disposable sensor to a blood gas analyzer, and a blood gas monitoring instrument. Studies currently are under way to determine what absolute measures of Pslco2 or trends in Pslco2 would be useful in diagnosing early tissue dysoxia. One study of patients with penetrating torso trauma found that a Pslco2 less than 45 mm Hg accurately predicted hemodynamic stability.[23] This technology is likely to prove useful in emergency medicine and prehospital care, where the early detection of tissue hypoxia is important and currently imprecise.
FETAL MONITORING Trauma occurs in about 7% of pregnant women.[24] The maternal mortality in trauma is no different than that for nonpregnant women with comparable injury severity. The fetal mortality is increased, however, even with seemingly minor trauma. The American College of Obstetricians and Gynecologists recommends that a pregnant patient with a viable fetus undergo fetal monitoring for 2 to 6 hours after injury characterized as any degree of abdominal jarring.[25] Emergency physicians usually use fetal monitoring in the emergency department to detect occult fetal distress and to inform therapy and referral. A study found that 92% of emergency medicine residents were taught the cardiotocographic findings indicative of fetal distress, although only 15% of the programs have this monitoring equipment available in the emergency department; however, 51% of programs have the sonographic equipment available to permit monitoring.[24] Figure 3-2A depicts a normal fetal heart trace with good baseline fetal heart rate. Persistent fetal tachycardia ( Figure 3-2B ), bradycardia, loss of baseline variability ( Figure 3-2C ), or decelerations after uterine contractions ( Figure 3-2D ) (e.g., Braxton Hicks contractions), and uterine hyperactivity are indications for referral to an obstetrician. A
B
C
Page 184
Figure 3-2 Exam ples of cardiotachographs. A, Normal trace. The fetal heart rate is the top trace; the bottom trace shows uterine activity. B, Fetal tachycardia. C, Reduced baseline heart rate variability. D, Late heart rate decelerations. ((Courtesy Dr. C.J. Peters, Fetal Monitoring Tutorial, www.freeserve.co.uk))
KEY CONCEPTS {,
Moni tors do not repla ce the obse rvati ons mad e by clinic ians; thes e are deci sion supp ort devi ces for aidin g man age ment , ident ifying the impa cts of inter venti ons, predi
Page 185
{,
{,
cting deter iorati on, and follo wing the patie nt's clinic al cour se. Eme rgen cy pers onne l must kno w the limit ation s of the tech nolo gy and the mac hiner y in the clinic al setti ng in whic h they work . Alar m limit s shou ld be adju sted to ensu re reas onab le warn ings
Page 186
are deliv ered. Disa bling alar ms is dang erou s.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/11.htm l/top
Page 187
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
KEY CONCEPTS {,
{, {,
{, {,
{,
Plain radiographs fail to detect 15% of scaphoid fractures. For this reason, and the associated risk of nonunion when diagnosis and immobilization are delayed, patients clinically suspected of having a scaphoid fracture should be placed in a short arm thumb spica cast with repeat x-rays in 10 to 14 days. Triquetral fracture is best seen on the standard lateral view of the wrist as a small dorsal chip fragment, although a more oblique pronated lateral view may be necessary. Lunate dislocation results in a characteristic triangular appearance of the lunate on the posteroanterior view (piece of pie sign) because of the rotation of the lunate in a volar direction. This rotation also is visible on the lateral view of the wrist, where the lunate looks like a cup tipped forward and spilling its contents into the palm (spilled teacup sign). In carpal dislocations, the articular surfaces on the posteroanterior view form three parallel arcs. The articular surfaces between carpal bones are parallel and 1 to 2 mm apart (parallelism). Colles' fracture requires prompt anatomic reduction in the emergency department, with full restoration of radial length and correction of the dorsal angulation either to a neutral position or ideally to the normal volar tilt position. Closed reduction, using local or regional anesthesia, with cast immobilization is successful in most cases. Anteroposterior and lateral views of the forearm must include the wrist and elbow joints because radial and ulnar forearm fractures may be associated with proximal, radial, or DRUJ dislocations.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/110.html/top
Page 188
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
REFERENCES 1. Larsen CF, Lauristen J: Epidemiology of acute wrist trauma. Int J Epidemiol1993;22:911. 2. Bednar JM, Osterman AL: Carpal instability: Evaluation and treatment. J Am Acad Orthop Surg1993;1:10. 3. Watson HK, Weinzweig J: Physical examination of the wrist. Hand Clin1997;13:17. 4. Greenspan A: Orthopedic Radiology: A Practical Approach, 2nd ed. New York, Gower Medical Publishing, 1992. 5. Schreibman KL: Imaging of the hand and wrist. Orthop Clin North Am1997;28:537. 6. Lacey JD, Hodge JC: Pisiform and hamulus fractures: Easily missed wrist fractures diagnosed on a reverse oblique radiograph. J Emerg Med1998;16:445. 7. Amadio PC, Taleisnik J: Fractures of the carpal bones. In: Green DP, ed.Operative Hand Surgery, vol 1. New York: Churchill Livingstone; 1993: 799. 8. Cooney WP, Linscheid RL, Robyns JH: Fractures and dislocations of the wrist. In: Rockwood CA, Green DP, Bucholz RW, ed.Fractures in Adults, vol 1. 4th ed. Philadelphia: Lippincott-Raven; 1996: 563-678. 9. Parvizi J: Combining the clinical signs improves diagnosis of scaphoid fractures: A prospective study with follow-up. J Hand Surg1998;23B:324. 10. Kirk M, Orlinsky M, Goldberg R: The validity and variability of the navicular fat stripe as a screening test for the detection of navicular fractures. Ann Emerg Med1990;19:1371. 11. Mehta M, Brautigan MW: Fracture of the carpal navicular: Efficacy of clinical findings and improved diagnosis with six view radiography. Ann Emerg Med1990;19:255. 12. Tiel van Buul MMC: The value of radiographs and bone scintigraphy in suspected scaphoid fracture. J Hand Surg1993;18B:403. 13. Shewring DJ, Savage R, Thomas G: Experience of the early use of technetium 99 bone scintigraphy in wrist injury. J Hand Surg1994;19B:114. 14. Murphy DG, Eisenhauer MA: The utility of a bone scan in the diagnosis of clinical scaphoid fracture. J Emerg Med1994;12:709. 15. Tiel van Buul MMC: Significance of a hot spot on the bone scan after carpal injury: Evaluation by computed tomography. Eur J Nucl Med1993;20:159. 16. Jonsson K: CT of the wrist in suspected scaphoid fracture. Acta Radiol1992;33:500. 17. Bain GI: Longitudinal computed tomography of the scaphoid: A new technique. Skeletal Radiol 1995;24:271. 18. Kukla C: Occult fractures of the scaphoid. J Hand Surg1997;22B:810. 19. Murphy DG: Clincial scaphoid fracture: Can day four bone scans accurately predict the presence or absence of scaphoid fracture?. Ann Emerg Med1995;26:434. 20. Woolfrey K: Accuracy of day four bone scans and efficacy of clinical findings in the assessment of patient with clinical scaphoid fractures. Ann Emerg Med1999;34:544. 21. Breitenseher MJ: Radiographically occult scaphoid fractures: Value of MR imaging in detection. Radiology1997;203:245. 22. Hunter JC: MR imaging of clinically suspected scaphoid fractures. AJR Am J Roentgenol1997;168:1287. 23. Fowler C, Sullivan B, Williams LA: A comparison of bone scintigraphy and MRI in the early diagnosis of the occult scaphoid waist fracture. Skeletal Radiol1998;28:683. 24. Kerluke L, McCabe SJ: Non-union of the scaphoid: A critical analysis of recent natural history studies. J Hand Surg1993;18A:1. 25. Duppe H: Long term results of fracture of the scaphoid. J Bone Joint Surg1994;76A:249. 26. Salmon J, Stanley JK, Trail IA: Kienbock's disease: Conservative management versus radial shortening. J Bone Joint Surg Br2003;82:820. 27. Cohen MS: Fractures of the carpal bones. Hand Clin1997;13:587. 28. Hocker K, Menshik A: Chip fractures of the triquetrum: Mechanism, classification and results. J Hand Surg1994;19B:584. 29. Chin HW, Visotsky J: Wrist fractures. Emerg Med Clin North Am1993;11:703. 30. Andresen R: Imaging of hamate bone fractures in conventional x-rays and high resolution computed tomography. Invest Radiol1999;34:46.
Page 189
31. Whalen JL, Bishop AT, Linscheid RL: Nonoperative treatment of acute hamate hook fractures. J Hand Surg1992;17A:507. 32. Carroll RE, Lakin JF: Fracture of the hook of the hamate: Acute treatment. J Trauma1993;34:803. 33. Inston N, Pimpalnerkar AL, Avafa MA: Isolated fracture of the trapezium: An easily missed injury. Injury 1997;28:485. 34. Yasuwaki Y: Fracture of the trapezoid bone: A case report. J Hand Surg1994;19A:457. 35. Mayfield JK, Johnson RP, Kilcoyne RK: Carpal dislocations: Pathomechanics and progressive perilunar instability. J Hand Surg1980;5A:226. 36. Frankel VH: The Terry Thomas sign. Clin Orthop1978;135:311. 37. Herzberg G: Perilunate dislocations and fracture-dislocations: A multicenter study. J Hand Surg 1993;18A:768. 38. O'Heeghan CJ: The natural history of an untreated isolated scapholunate interosseous ligament injury. J Hand Surg2003;28B:307. 39. Watson HK, Weinzweig J, Zeppieri J: The natural progression of scaphoid instability. Hand Clin 1997;13:29. 40. Colles A: On the fracture of the carpal extremity of the radius. Edinb Med Surg J1814;10:182. 41. Aro HT, Koivunen T: Minor axial shortening of the radius affects outcome of Colles' fracture treatment. J Hand Surg1991;16A:392. 42. Trumble TE, Schmitt SR, Vedder NB: Factors affecting functional outcome of displaced intra-articular distal radius fractures. J Hand Surg1993;19A:325. 43. Mehta JA, Bain GI: An overview of distal radius fractures. Aust J Rural Health1999;7:121. 44. Mehara AK: Classification and treatment of volar Barton fractures. Injury1993;24:55. 45. Leibovic SJ, Geissler WB: Treatment of complex intra-articular distal radius fractures. Orthop Clin North Am1994;25:685. 46. Bruckner JD, Alexander AH, Lichtman DM: Acute dislocations of the distal radioulnar joint. Instr Course Lect1996;45:27. 47. Burk Jr JrDL, Kavasick D, Wechsler RJ: Imaging of the distal radioulnar joint. Hand Clin1991;7:263. 48. Dicke TE, Nunley JA: Distal forearm fractures in children. Orthop Clin North Am1993;24:333. 49. Wilkins KE, O'Brien ET: Fractures of the shafts of the radius and ulna. In: Rockwood CA, Wilkins KE, Beaty JH, ed.Fractures in Children, vol 3. 4th ed. Philadelphia: Lippincott-Raven; 1996: 415-508. 50. Salter RB, Harris WR: Injuries involving the epiphyseal plate. J Bone Joint Surg1963;45A:587. 51. Skandalakis JE: The carpal tunnel syndrome: Part I. Am Surg1992;58:72. 52. Kushner SH: Tinel's sign and Phalen's test in carpal tunnel syndrome. Orthopedics1992;15:1297. 53. Slater RR, Bynum DK: Diagnosis and treatment of carpal tunnel syndrome. Orthop Rev1993;22:1095. 54. Jimenez DF, Gibbs SR, Clapper AT: Endoscopic treatment of carpal tunnel syndrome: A critical review. J Neurosurg1998;88:817. 55. Graham TJ: Disorders of the forearm axis. Hand Clin1998;14:305. 56. Griggs SM, Weiss AC: Bony injuries of the wrist, forearm, and elbow. Clin Sports Med1996;15:373. 57. Schemitsch EH, Richards RR: The effect of malunion on functional outcome after plate fixation of fractures of both bones of the forearm in adults. J Bone Joint Surg1992;74A:1068. 58. Richards RR, Corley FG: Fractures of the shafts of the radius and ulna: Part II. In: Rockwood CA, Green DP, Bucholz RW, ed.Fractures in Adults, vol 1. 4th ed. Philadelphia: Lippincott-Raven; 1996: 869. 59. Villarin LA, Belk KE, Freid R: Emergency department evaluation and treatment of elbow and forearm injuries. Emerg Med Clin North Am1999;17:843. 60. Bado JL: The Monteggia lesion. Clin Orthop1967;50:71. 61. Boyd HB, Boals JC: The Monteggia lesion: A review of 159 cases. Clin Orthop1969;66:94. 62. Ring D, Jupiter JB, Simpson NS: Monteggia fractures in adults. J Bone Joint Surg1998;80A:1733. 63. Bruckner JD, Lichtman DM, Alexander AH: Complex dislocations of the distal radioulnar joint. Clin Orthop 1992;275:90. 64. Perron AD: Orthopaedic pitfalls in the ED: Galeazzi and Monteggia fracture-dislocation. Am J Emerg Med2001;19:225. 65. Beneyto FM: Treatment of Galeazzi fracture-dislocations. J Trauma1994;36:352. 66. Budgeon A: Irreducible Galeazzi injury. Arch Orthop Trauma Surg1998;118:176. 67. Price CT: Fractures of the shafts of the radius and ulna: Part II. In: Rockwood CA, Wilkins KE, Beaty JH, ed.Fractures in Children, vol 3. 4th ed. Philadelphia: Lippincott-Raven; 1996: 443. 68. Komara JS, Kottamasu L, Kottamasu SR: Acute plastic bowing fractures in children. Ann Emerg Med 1986;15:585.
Page 190
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/111.html/top
Page 191
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
Chapter 49 – Humerus and Elbow Joel M. Geiderman
PERSPECTIVE Injuries in the region of the elbow have a high potential for complications and residual disability. Early recognition of neurovascular and soft tissue complications has a salutary effect on the outcome in many of these injuries.
Anatomy The humerus is a long bone that articulates proximally, at the shoulder, with the glenoid of the scapula to form the glenohumeral joint and distally with the radius and ulna to form the three-way elbow joint. The upper end of the humerus, the humeral head, is shaped like a near-hemisphere. Adjacent to the humeral head are two bony prominences, the greater and lesser tuberosities. Between these, on the anterolateral aspect of the humerus, runs the bicipital groove. The shaft of the humerus extends from the upper border of the insertion of the pectoralis major muscle superiorly to the supracondylar ridges inferiorly. The shaft is cylindrical on cross section in the upper half and tends to become flat in the distal portion in an anteroposterior direction. Three surfaces are described. The anterolateral surface presents the deltoid tuberosity for the insertion of the deltoid muscle, and below this is the radial soleus, which transmits the radial nerve and profunda artery. The anteromedial surface forms the floor of the intertubercular groove, but it normally has no outstanding surface markings. An exception is when the supracondylar process is present. The posterior surface is the origin for the triceps and contains the spiral groove. The bony anatomy of the distal humerus and elbow is diagrammed in Figure 49-1 . The distal end of the humerus tapers into two columns of bone, the medial and lateral condyles. Between the condyles, the bone thins, and the recess created is the coronoid fossa. The more proximal nonarticular portions of the condyles are the epicondyles. Just proximal to the epicondyles, the supracondylar ridges run up each side of the humerus. Collectively, these areas serve as points of origin for the muscles of the forearm. The wrist flexors originate from the medial epicondyle, and the wrist extensors originate from the lateral epicondyle. Fractures of the distal humerus often result in fragment displacement because of the pull of these strong forearm muscles on attachment sites.
Figure 49-1 Bony anatom y of distal hum erus and elbow region. A, Anterior view. B, Posterior view. C, Posterior view, 90 degrees flexion. D, Lateral view. Right elbow is shown. ((Modified from Connolly JF: DePalm a's Managem ent of Fractures and Dislocations. Philadelphia, WB Saunders, 1981.)Elsevier Inc.)
The bony anatomy of the elbow allows for two complex motions: flexion-extension and pronation-supination. The elbow is composed of three articulations within a common joint cavity. The trochlea is the articular surface of the medial condyle and articulates with the deep trochlear notch of the ulna formed by the olecranon inferiorly and posteriorly and by the coronoid process anteriorly. This articulation permits hinged flexion and extension at the elbow. The articular surface of the lateral condyle is the capitellum, which permits the radius to hinge on the elbow. The proximal radius consists of a disklike head supported by the
Page 192
smooth narrow radial neck. The radial head articulates with the capitellum of the humerus and with the radial notch of the ulna. Four ligamentous structures are important in evaluating elbow injuries ( Figure 49-2 ). The radial head is held in place by the annular ligament and the radial collateral ligament. Rotation of the radial head within the annular ligament permits pronation and supination. In addition, the ulnar collateral ligament and anterior capsule add stability to the joint. These structures may be severely damaged with fracture or dislocation of the joint.
Figure 49-2 Ligam entous structures of elbow. ((From Sim on R, Koenigsknecht S: Emergency Orthopaedics: The Extrem ities, 2nd ed. Norwalk, Conn, Appleton & Lange, 1987.)Appleton & Lange)
The soft tissues of the upper arm are divided into two compartments, anterior and posterior. The anterior compartment contains three muscles—the biceps brachii, the brachialis, and the coracobrachialis—and the brachial artery, median nerve, musculocutaneous nerve, and ulnar nerve. The only two structures contained in the posterior compartment are the triceps brachii muscle and the radial nerve. The neurovascular structures of this area are diagrammed in Figure 49-3 . The brachial artery, the continuation of the axillary artery, travels with the median nerve in the anterior compartment of the upper arm. It enters the antecubital fossa as diagrammed and bifurcates into the radial and ulnar arteries.
Figure 49-3 Neurovascular structures of elbow region. Volar surface of left elbow is shown.
The median nerve runs with the brachial artery as diagrammed. One important anatomic variation is the presence of a supracondylar process just proximal to the medial epicondyle ( Figure 49-4 ). When present, the median nerve and brachial artery must traverse behind this process, then forward between a fibrous band connecting the process to the epicondyle. Median nerve symptoms may develop if this process is fractured or if an injury causes swelling in the vicinity of the supracondylar process.
Figure 49-4 Supracondylar process of the hum erus (arrow). Volar surface of right elbow is shown.
The radial nerve leaves the axilla and spirals posteriorly around the humerus between the heads of the triceps in the radial groove. It reenters the anterior compartment of the arm laterally, crossing the elbow anterior to the lateral epicondyle, to innervate the extensors of the wrist and fingers. Because of its close
Page 193
relationship to the shaft of the humerus, the radial nerve is particularly susceptible to injury with fractures of the midshaft of the humerus. Fixed in position by the intermuscular septum, the nerve may become trapped between fracture fragments, particularly when reduction is attempted. The ulnar nerve runs parallel to the median nerve. Halfway down the arm, it penetrates the intermuscular septum to run along the medial aspect of the triceps muscle in the posterior compartment. It enters the forearm by passing behind the medial condyle. Fractures in the vicinity of the medial condyle place this nerve at considerable risk for injury. Three elbow bursae are clinically important. The olecranon bursa is located between the olecranon and the skin posterior to the joint. This bursa provides protective padding and allows smooth movement of the skin over the olecranon. Because of its position, it is often a site of traumatic or infectious bursitis. The radiohumeral bursa provides for smooth movement over the radial head with supination and pronation. A third bursa cushions the biceps tendon from the radius during flexion of the elbow. As evident by the descriptions of these structures, all are vulnerable when significant skeletal injury occurs in this region.
CLINICAL FEATURES History A history detailing musculoskeletal complaints includes a description of any pain in terms of quality, duration, location, palliative and provocative activities, severity, and radiation. Past medical history and occupational features are important in chronic problems. For traumatic injuries, a complete account of the incident is important because it provides information as to the mechanism of injury and some estimate of the energy delivered. Subjective complaints of numbness or weakness distal to the injury are important clues to possible neurovascular injury. In dealing with injuries in children, the possibility of child abuse must be considered.
Physical Examination Inspection of the upper extremity is important, but manipulation of the painful extremity should be minimized and postponed to the end of the examination when possible. This is especially important with children. A great deal of useful information can be gathered by simple inspection. The position in which the extremity is held should be noted. Children with extension-type supracondylar fractures present with the arm held at the side with a characteristic S-shape configuration, whereas with flexion-type supracondylar fractures, the forearm is supported with the opposite hand with the elbow flexed to 90 degrees. Patients with radial head subluxation have the elbow only slightly flexed and hold the forearm in pronation. Deformity is evidence not only of significant injury, but also of the type of injury. Increased prominence of the olecranon suggests a posterior dislocation of the elbow or extension supracondylar fracture, whereas loss of the normal olecranon prominence indicates anterior dislocation or flexion supracondylar fracture. The extremity also should be inspected for wounds that may indicate an open fracture, evidence of swelling, and change in color of the distal extremity. One special aspect of the elbow examination is the determination of the carrying angle, the normal outward angulation of the extended forearm at the elbow. This angle allows the long axes of the humerus and forearm to become superimposed when the elbow is flexed ( Figure 49-5 ). This angle varies from 5 to 20 degrees in adults, with men having less angulation than women. Measurement of the carrying angle is helpful in assessing subtle supracondylar fractures in children. As shown in Figure 49-6 , lines drawn parallel to the shafts of the humerus and ulna intersect to form an angle with a mean measurement in children of 13 degrees, although this angle varies widely.[1] A difference in carrying angles of greater than 12 degrees (from one side to the other for a particular individual) is associated with fractures.
Figure 49-5 Carrying angle (3) is form ed by intersection of lines drawn parallel to long axis of hum erus (1) and ulna (2). ((Modified from Ruiz E, Cicero J: Em ergency Managem ent of Skeletal Injuries. St Louis, Mosb y, 1995.)Elsevier Inc.)
Page 194
Figure 49-6 A, The axis of the elbow joint bisects the angle form ed by the long axes of the hum erus and forearm . B, This allows these axes to becom e superim posed when the elbow is flexed. C, If the axis of the elbow joint was perpendicular to the long axis of the forearm , the respective axes would diverge when the elbow was flexed, as shown in D.
The vascular status of the extremity is of highest priority. Brachial, radial, and ulnar pulses should be palpated and documented. The ulnar pulse is not palpable in some normal people. Although brisk capillary refill suggests adequate tissue perfusion, a hand-held Doppler device often is required to evaluate major vessel flow if significant swelling is present or if the pulses are not palpable. Any suspicion of arterial injury requires immediate investigation. Poor perfusion may result from direct arterial injury, compression or kinking in the instance of significant displacement from a fracture or dislocation, or a compartment syndrome. Passive extension of the fingers produces severe pain in the forearm in the presence of flexor (volar) compartment ischemia. Of the five P s associated with arterial occlusion (pain, paresthesia, pallor, pulselessness, and paralysis), pain is the only dependable early sign of compartment syndrome. Orthopedic consultation and measurement of compartment pressures should be considered for patients who have pain disproportionate to their injury. Other modalities used to evaluate vascular status before calling in the orthopedist include measurement of the ankle-brachial index and color flow Doppler (see Chapter 45 for further details). Neurologic evaluation includes assessment of the radial, median, and ulnar nerves. After evaluation of neurovascular function, all bony prominences are palpated, and areas of tenderness are noted carefully and documented. Crepitus and bony deformities are highly suggestive of fracture or dislocation. The radial head specifically should be palpated for tenderness, and if present, an effusion should be noted. The range of motion of the elbow in all planes (i.e., flexion-extension and pronation-supination) should be determined and documented. With the forearm supinated, the normal range of motion is 0 degrees in full extension to 150 degrees in full flexion. A mild degree of hyperextension is found in some normal individuals and should be symmetrical. With the elbow flexed at 90 degrees and the thumb facing up, the forearm normally supinates and pronates 90 degrees. Range-of-motion testing may be impossible with severe injuries and can be postponed until after radiographic evaluation, avoiding manipulating fractures and dislocations. Any manipulation of the extremity must be followed by re-examination because neurovascular injury has been reported with nearly every therapeutic procedure.
Radiographic Findings It is not necessary to take x-ray films in all cases. Although clinical decision rules for the elbow have not been validated, it is reasonable to perform radiography when there is significant limitation in range of motion, obvious deformity, joint effusion, or significant tenderness over any of the bony prominences or the radial head. In the absence of these, it seems appropriate to omit radiography. Routine views of the elbow include at least the anteroposterior and lateral views, with consideration given to obtaining oblique views for certain injuries. Anteroposterior and oblique views are taken with the elbow extended. The lateral view is taken with the elbow in 90 degrees of flexion and the thumb pointing upward. Positioning of the elbow is important because anything but a true lateral view makes accurate interpretation of soft tissue findings and alignment difficult. Corresponding views of the opposite extremity may be helpful, especially for children, but should not be ordered routinely. Many fractures in the elbow region are obvious on x-ray film, with cortical disruption, angulation, or displacement of fragments. Minor fractures can be subtle and may be missed. Special attention to the contour of the radial head and the fat pads reduces the risk of missing fractures. The normal cortex of the radius is smooth and has a gentle continuous concave sweep. If consistent with history and physical findings, any disruption of this smooth arc is considered evidence of fracture. Abnormalities within the soft tissues on elbow films are particularly important and may be the only radiographic sign of a fracture. Normally, fat surrounding the proximal elbow joint is hidden in the concavity of the olecranon and coronoid fossae. The radiographically normal elbow has only a narrow strip of lucency anteriorly (the anterior fat pad), and a posterior fat pad is not visible. Injuries that produce intra-articular hemorrhage cause distention of the synovium and displace the fat out of the fossa, making the posterior fat pad visible on lateral x-ray views.
Page 195
The anterior fat pad also is altered by this swelling, becoming more prominent and taking the shape of a spinnaker sail from a boat ( Figure 49-7 ). In the setting of trauma, more than 90% of patients with the “posterior fat pad” sign have intra-articular skeletal injury. These soft tissue findings occur even with subtle fractures, and when present in the setting of trauma, an occult fracture is considered to be present even when not visible on the x-ray. In adults, a radial head fracture is implied, whereas in children, a supracondylar fracture is the probable underlying injury. In the absence of trauma, the presence of a fat pad suggests other causes of effusion (e.g., gout, infection, bursitis). The fat pad sign may be absent with a fracture if the injury is severe enough to have ruptured the capsule.
Figure 49-7 A, Anterior fat pad sign on lateral study (arrow). B, The anterior fat pad is norm ally a thin radiolucent stripe; the posterior fat pad is now seen. C, An effusion displaces both fat pads. This posterior fat pad is now visible.
The anterior humeral line is a line drawn on a lateral radiograph along the anterior surface of the humerus through the elbow. Normally this line transects the middle third of the capitellum ( Figure 49-8 ). With an extension supracondylar fracture, this line either transects the anterior third of the capitellum or passes entirely anterior to it. The abnormal relationship between the anterior-humeral line and capitellum may be the only evidence of a minimally displaced supracondylar fracture.
Figure 49-8 A, A line drawn down anterior surface of hum erus on lateral film should transect the m iddle of the capitellum . B, With extension supracondylar fracture, the line passes more anteriorly. ((From Sim on R, Koenigsknecht S: Emergency Orthopaedics: The Extrem ities, 2nd ed. Norwalk, Conn, Appleton & Lange, 1987.)Appleton & Lange)
Another diagnostic aid in evaluating radiographs of suspected supracondylar fractures in children is the determination of Baumann's angle. As shown in Figure 49-9 , the intersection of a line drawn on the anteroposterior film through the midshaft of the humerus and the growth plate of the capitellum defines an angle of approximately 75 degrees. In normal children, Baumann's angle is the same in both elbows, and it has been suggested that a comparison between the injured and uninjured sides be used to assess the accuracy of reduction. An increase in Baumann's angle indicates medial tilting of the distal fragment. Alteration in Baumann's angle is thought to predict the final carrying angle when the fracture heals, although there is controversy regarding its reliability.[2]
Figure 49-9 Worlock P: Baum ann's angle as m easured on anteroposterior film. ((From Supracondylar fractures of the hum erus. J Bone Joint Surg 68B:755, 1986.))
Page 196
Radiographic evaluation of the elbow in children is difficult because of the presence of multiple ossification centers ( Figure 49-10 ). Table 49-1 lists the typical age of first appearance and fusion of ossification centers. Comparison views of the uninjured elbow are often helpful in distinguishing fractures from the normal epiphyses and ossification centers.
Figure 49-10 Secondary growth centers of the elbow. 1, Capitellum; 2, radial head; 3, m edial epicondyle; 4, trochlea; 5, olecranon; 6, lateral epicondyle. ((From Townsend DJ, Bassett GS: Com m on elb ow fractures in children. Am Fam Physician 53:2031, 1996.))
Table 49-1 -- Ossification Centers of the Elbow: CRITOE Ossification Centers
Age of Appearance
Capitellum
1–2
Radial head
4–5
Internal (medial) epicondyle
4–5
Trochlea
8–10
Olecranon
8–9
External (lateral) epicondyle
10–11
Management General management principles for humerus and elbow injuries are similar to management principles for other orthopedic injuries. Limb-threatening conditions, such as vascular injury, must be addressed immediately by reduction of fractures or surgical exploration. The limb should be splinted in a position of comfort, and appropriate analgesia should be provided. Antibiotics are administered for suspected open fractures. Prolonged immobilization of the elbow frequently results in stiffness of the joint that requires extensive physiotherapy to restore normal function. For this reason, range-of-motion exercises are begun early in the convalescent period, often before a fracture has healed completely.
FRACTURES Injuries in the region of the shaft of the humerus and about the elbow fall into several categories ( Box 49-1 ). Emergency department management varies with location and type of fracture or dislocation. BOX 49-1 Classification of Fractures
I.
Humerus fractures A. Shaft of the humerus fractures B. Distal humerus fractures 1.
Supracondylar a. Exte nsio n b. Flexi on
Page 197
2.
Transcondylar a. Exte nsio n b. Flexi on
3.
Intercondylar a. Non displ aced b. Sep arate d c. Sep arate d and rotat ed d. Com binat ion with artic ular surfa ces
4.
Condylar a. b.
Medi al Later al
5.
Articular surface a. Capi tellu m b. Troc hlea
6.
Epicondylar a. Medi al b. Later al
II.
Radial head fracture A. Non displ aced B. Displ aced C. Com minu ted
III.
Ulnar fracture A. Olec rano n
Page 198
B.
fract ure Coro noid fract ure
Fractures of the Shaft of the Humerus Pathophysiology Fractures of the humeral shaft most often result from a direct blow to the arm, such as occurs during a fall or motor vehicle crash. Occasionally, severe twisting of the arm or a fall on an outstretched hand produces this type of fracture. Fractures produced by violent muscle contraction also are reported, such as when throwing a javelin or baseball.[3] Motion of the humerus is controlled by several muscle groups. These same muscle groups also influence the fracture pattern of the humeral shaft. If the fracture is located proximal to the attachment of the pectoralis major, the proximal fragment of the humerus abducts and rotates internally owing to the action of the rotator cuff, whereas the distal fragment is displaced medially by the pectoralis major ( Figure 49-11A ). If the fracture occurs below the pectoralis major insertion but above the deltoid insertion, the distal fragment is displaced laterally by the deltoid muscle, and the proximal fragment is displaced medially by the pull of the pectoralis major, latissimus dorsi, and teres major muscles ( Figure 49-11B ). In fractures occurring distal to the deltoid insertion, the proximal fragment is abducted by the deltoid, and the distal fragment is proximally displaced ( Figure 49-11C ). The shaft of the humerus most commonly fractures in the middle third in a transverse fashion.
Figure 49-11 Influence of m uscles on displacem ent of hum eral shaft fractures based on fracture location (see text).
Clinical Features The patient complains of localized pain. The arm is visibly swollen and cannot be used. When a fracture is complete, bony crepitus is felt in the shaft of the humerus with any manipulation of the arm. The arm may be shortened or rotated, depending on the displacement of the fracture fragments. When the fracture is incomplete, the skeleton is tender to palpation and swollen, but not otherwise deformed. A complete neurovascular examination is indicated. Attention should be directed to radial nerve function because injury to this nerve is the most common complication associated with humeral shaft fractures. X-ray findings are confirmatory. Studies routinely should include the shoulder and elbow joints. The humerus is a common site for benign tumors, unicameral cysts, and primary bone malignancies. The humeral shaft also is a common site for metastatic disease. Thinning of the cortex and abnormal osteoblastic or osteoclastic activity are evidence of a pathologic fracture. These fractures do not heal without concomitant treatment of the underlying pathologic condition.
Management Closed fractures that are isolated injuries are treated conservatively with a high degree of success. Elaborate attempts at fracture reduction and external immobilization are unnecessary and sometimes detrimental to healing. Humeral shaft fractures remain surrounded by a richly vascularized envelope of muscle so that fracture reduction is accomplished most easily with the aid of gravity and muscle balance. Fractures that are nondisplaced or minimally displaced are immobilized by adding a coaptation, or “sugar-tong” splint, to the sling and swathe ( Figure 49-12 ). This is accomplished by first padding the extremity, then carrying a long plaster splint from the lateral side of the shoulder, down the lateral aspect of the upper arm, around the elbow with the elbow flexed, and then up the inner aspect of the arm to the axilla. The sugar tong is wrapped in an elastic bandage, and a sling is used to support the arm in 90 degrees or less of flexion. The weight of the splint aided by gravity applies traction at the same time it immobilizes the fracture. Some authorities use the coaptation splint for only the first 10 to 14 days of treatment followed by a functional brace.
Page 199
Figure 49-12 Sugar-tong splint for hum eral shaft fractures. Gentle traction is applied (1) as the splint is placed (2) from over the deltoid laterally, under the elbow, and up into the axilla. An Ace wrap holds the splint in place (3). The axilla must be padded (4), and a sling is used (5). ((Modified from Connolly JF: DePalm a's Managem ent of Fractures and Dislocations. Philadelphia, WB Saunders, 1981.)Elsevier Inc.)
If the fracture is grossly displaced or comminuted, the hanging cast technique sometimes is used. This technique is especially effective with spiral fractures. The cast is lightweight, applied at least 1 inch proximal to the fracture site, and extends to the distal palmar crease of the hand. The elbow is flexed 90 degrees, and the wrist is placed in the neutral position. The sling is attached through a loop at the wrist. Angulation is corrected by placing the plaster loop on the dorsal aspect of the cast (to reduce lateral angulation) or on the volar side of the cast (to reduce medial angulation). Anterior or posterior angulation is corrected by altering the length of the sling apparatus ( Figure 49-13 ). Care must be taken not to make the cast too heavy because this would distract fracture fragments. The hanging cast has the disadvantage of requiring gravity for traction and requires that the patient remain upright at all times, including during sleep, a situation that many patients find intolerable. Neurovascular examination is repeated after the application of any splint or cast. Loss of nerve function from entrapment of the nerve between fragments can occur after these interventions.
Figure 49-13 Hanging cast technique.
Open reduction and internal fixation is necessary in certain circumstances, including open fractures, presence of multiple injuries that preclude mobilization, bilateral fractures, poor reduction, poor patient compliance, failure of closed treatment, and fractures through pathologic bone.[] Isolated radial nerve palsy usually is assumed to be a neurapraxia and is managed nonoperatively. Exploration and internal fixation are indicated, however, if the radial nerve palsy develops after manipulation because this is highly suggestive of nerve entrapment.[4] All patients with humeral shaft fractures should be referred to an orthopedic surgeon for close follow-up monitoring. When dependency casting is used, follow-up evaluation within 24 to 48 hours is recommended to be certain that the alignment has been maintained. Emergent referral to an orthopedist is recommended for patients with evidence of radial nerve injury, severely displaced or comminuted fractures, open fractures, or fractures associated with forearm fractures in the same extremity.
Complications The most common complication, radial nerve injury, occurs in 20% of humerus fractures. This nerve injury is most often a benign neurapraxia that resolves spontaneously in most patients, although recovery may take several months. Radial nerve injuries associated with penetrating trauma or open fractures are likely to be permanent and usually warrant operative exploration. Median and ulnar nerve injuries are rarely seen, usually in the presence of penetrating trauma. Injuries to the brachial artery occur rarely and, if suspected, angiography or other vascular studies should be considered.
Fractures of the Distal Humerus Supracondylar Fractures Distal humerus fractures that occur proximal to the epicondyles are called supracondylar fractures. This fracture is almost exclusively an injury of the immature skeleton. The peak incidence is in children 5 to 10
Page 200
years old; the average age in a large combined series was 6.7 years.[6] This injury occurs rarely after age 15. In children, the tensile strength of the collateral ligaments and joint capsule of the elbow is greater than that of bone. In adults, the reverse is true, and a posterior elbow dislocation is sustained instead. Supracondylar fractures are classified as either extension or flexion fractures, depending on the mechanism of injury and the displacement of the distal fragment. Of these injuries, 98% are of the extension type.
Extension Supracondylar Fractures Pathophysiology. Extension supracondylar fractures occur as a consequence of a fall on the outstretched arm, when the elbow is either fully extended or hyperextended. The elbow is likely to be in the latter position at the time of the fall because ligamentous laxity, with hyperextension of the joints, is a normal phenomenon in younger children. With the forearm acting as a lever, the ground reaction produces a moment of force at the elbow ( Figure 49-14 ).[7] Ultimately the distal humerus fails anteriorly in the supracondylar area. The strong action of the triceps tends to pull and displace the distal fragment in a posterior and proximal direction. There may be anterior angulation of the sharp distal end of the proximal fragment into the antecubital fossa, endangering the brachial artery and median nerve ( Figure 49-15 ). In most cases, however, the brachialis muscle protects the anterior neurovascular structures from injury.
Figure 49-14 Mechanism of injury, extension supracondylar fractures. A, Fall on outstretched arm produces hyperextension of elbow. B, Ulna levers against distal humerus. C, Hum erus fails, triceps exerts unopposed force. D, Distal fragm ent displaces.
Figure 49-15 Supracondylar fractures, extension and flexion. ((Adapted from Sim on R, Koenigsknecht S: Emergency Orthopaedics: The Extrem ities, 2nd ed. Norwalk, Conn, Appleton & Lange, 1987.)Appleton & Lange)
Clinical Features. A child with a complete fracture comes to the emergency department holding the upper extremity immobile in extension to the side, with a typical S-shaped configuration and tenderness and swelling in the region of the elbow. Prominence of the olecranon attached to the posteriorly displaced distal fragment is similar to that seen with posterior dislocation of the elbow. When an incomplete supracondylar fracture exists, the diagnosis may be less obvious, with an elbow effusion as the only clinical sign. A careful neurovascular examination is essential. Although palpation is useful in determining the site of injury, the examining physician should avoid manipulation of the injury to elicit crepitus because movement can cause further neurovascular damage. Alleviating pain often facilitates the examination.
Diagnostic Strategies. On x-ray examination, the distal fragment is often displaced on the lateral view. This displacement is most likely to occur with a complete fracture wherein the muscle activity results in proximal migration of the distal fragment. Because this fracture occurs in children, 25% of supracondylar fractures are of the greenstick variety with the posterior cortex remaining intact. Subtle changes (e.g., the presence of a posterior fat pad or an abnormal anterior humeral line) may be the only radiographic clues to the presence of a fracture. In displaced fractures on the anteroposterior view, the distal fragments may be displaced either medially or
Page 201
laterally in relationship to the humerus. Often, with minimally displaced fractures, the fracture line is transverse and not visible on the anteroposterior view. Based on radiographic findings, extension supracondylar fractures are classified into three types: type I, minimal or no displacement; type II, displaced fracture, posterior cortex intact; and type III, totally displaced fracture, anterior and posterior cortex disrupted.
Management. Nondisplaced fractures (type I) are immobilized primarily for comfort and protection because they are inherently stable. They are treated in a splint or cast flexed to 90 degrees with the forearm in neutral rotation. Protected active range of motion is begun in approximately 3 weeks. Even without definite radiographic findings, a child with localized tenderness consistent with a supracondylar fracture should be splinted and referred for follow-up examination. An x-ray study performed a few weeks after the injury may reveal periosteal new bone formation in the supracondylar region. Minimally displaced (type II) fractures that are stable after reduction can be treated with splinting or casting with the elbow flexed. Some authors recommend flexion to 110 to 120 degrees for this injury.[] This position uses the intact posterior periosteum as a tension band to hold the reduction; however, if swelling or circulatory obstruction prevents this much flexion, it cannot and should not be used. The greater the flexion at the elbow, the greater the chance of vascular impairment. When swelling peaks at 24 to 48 hours, the risks of vascular obstruction and compartment syndrome are the greatest. Occasionally, these injuries must be pinned percutaneously to maintain stability, especially if a significant rotational component is present. Percutaneous pinning of a fracture after reduction has grown in popularity in recent years.[10] Type III totally displaced fractures generally are the result of more severe injuries that produce more swelling than type I or type II injuries. Displacement necessitates the re-establishment of length, increases the chance of varus deformity, and increases the chances of interposed soft tissues and neurovascular injury. For all these reasons, type III fractures require immediate orthopedic consultation. The general principles that must be adhered to in treating these injuries are (1) achieving adequate reduction, (2) properly assessing reduction, and (3) maintaining the reduction. Closed reduction is attempted with the patient under anesthesia. If closed reduction is not possible or if the brachial artery seems to be trapped in the fracture site, open reduction may be necessary. When adequate reduction has been achieved, most authorities recommend percutaneous pin fixation to maintain the reduction.[] Reduction in the emergency department is indicated only when the displaced fracture is associated with vascular compromise that threatens the viability of the extremity. Under these conditions, closed reduction should be attempted. After appropriate conscious sedation, an assistant fixes the arm of the patient. The physician grasps the patient's wrist and applies steady, firm traction in line with the long axis of the limb ( Figure 49-16A ). The forearm is kept in the neutral, thumb-up position. While traction is maintained, correction of any medial or lateral displacement is accomplished with the other hand at the elbow ( Figure 49-16B ). If the distal fragment is displaced laterally, it is pushed inward; if it is displaced medially, it is pushed outward.
Figure 49-16 A-C, Steps in reduction of displaced supracondylar fracture (see text).
After length is restored and the angular deformity is corrected, the thumb of the free hand is placed over the anterior surface of the proximal fragment and the fingers behind the olecranon. While traction is maintained, the elbow is gently flexed to just beyond 90 degrees ( Figure 49-16C ). Angulation is corrected to a normal carrying angle. Medially displaced supracondylar fractures are most prone to tilt into cubitus varus and are immobilized with the forearm pronated to tighten the brachioradialis and common extensor muscles. This procedure closes the fracture laterally. The less common laterally displaced fracture is immobilized in supination to close the fracture medially.
Page 202
Only one attempt should be made at manipulation. Multiple attempts increase the likelihood of neurovascular injury and swelling. If reduction is unsuccessful, simple traction on the extended elbow may restore vascular supply. When reduction is performed, follow-up radiographs are obtained to ensure adequate reduc-tion. Neurovascular function is checked at frequent intervals. Cylinder casts are not applied initially because they increase the risk of forearm ischemia; a posterior plaster splint provides safe and adequate immobilization. Patients with type I fractures can be discharged safely from the emergency department with instructions to elevate the extremity and apply ice and have a follow-up evaluation in 1 to 2 days. Fractures that require manipulation usually warrant admission to the hospital to ensure compliance and for neurovascular monitoring.
Complications. Ten percent of children lose the radial pulse temporarily, most often as a result of swelling and not direct brachial artery injury. Reducing the fracture, avoiding flexing the elbow more than 90 degrees, and elevating the arm help prevent secondary obstruction to arterial flow. Compartment syndrome, or Volkmann's ischemic contracture as a result of prolonged ischemia of the forearm, is a dreaded complication but is rare in this era (reported incidence <0.5%).[10] The most common complication is the loss of the carrying angle, resulting in a cubitus varus or “gunstock” deformity. Measurement of Baumann's angle postreduction is predictive of the final carrying angle. Cubitus varus has been reported previously in 25% to 60% of patients, depending on the management used.[] This incidence has decreased significantly (<10%), with the use of percutaneous pinning. The distal humerus has little capacity to remodel because only 20% of the growth of the bone derives from the distal physis. A small amount of extension or flexion deformity produces little disability, has the greatest chance of remodeling, and is not a major cosmetic concern. Valgus or varus deformities, being in the coronal plane, have little or no chance of remodeling. Although cubitus varus is not a significant functional disability, it presents a significant cosmetic problem. In most cases, this complication can be corrected at a later time by an osteotomy.[15] Nerve injuries occurred in 7% of 4520 fractures compiled from 31 major reported series. The radial, median, and ulnar nerves all are commonly involved. Most deficits seen at the time of injury are neurapraxias that resolve with conservative management. Motor function returns within 7 to 12 weeks, whereas recovery of sensation may take more than 6 months.[16]
Flexion Supracondylar Fractures Pathophysiology. Flexion-type injuries are much less common, with a reported frequency of 1% to 10%; they account for 2% of all supracondylar fractures in a large pooled series of 7212 patients. The mechanism of injury is a direct blow to the flexed elbow. Energy is transferred from the posterior aspect of the proximal ulna to the distal humerus, resulting in a supracondylar fracture with anterior displacement of the distal fragment. As the fragment displaces, the periosteum is torn posteriorly.
Clinical and Radiographic Features. The elbow is usually held in flexion rather than the extremity presenting in the S-shaped configuration seen in extension-type injuries. In displaced fractures, the normal olecranon process is not palpable, in contrast to the increased prominence of the olecranon seen with extension injuries. Radiographically, these injuries can be classified into three types, similar to extension injuries: {, {, {,
Type I fracture—undisplaced or minimally displaced Type II fracture—incomplete fracture; anterior cortex intact Type III fracture—completely displaced; distal fragment migrates proximally and anteriorly
X-ray films may reveal a simple increase in the anterior angulation of the distal supracondylar fragment or gross displacement of the distal fragment proximal and anterior to the distal end of the proximal fragment. In the latter case, the distal end of the proximal fragment protrudes posteriorly. A line down the anterior humeral shaft intersects the capitellum either normally or posteriorly in these fractures, depending on whether there
Page 203
is anterior displacement.
Management. When the posterior periosteum is torn, the anterior periosteum functions as a tension band with the arm in extension. In type I fracture, the periosteum is minimally displaced. These injuries do not need to be immobilized in extension. The elbow can be comfortably flexed and should be immobilized in a splint as with extension injuries. Type II and III injuries should be referred to an orthopedist emergently. Type II injuries are manipulated into extension, then held either in a long arm cast or with percutaneous pins. Type III injuries often require open reduction.
Complications. The most common complication is injury to the ulnar nerve by the proximal fragment. The radial and median nerves are rarely injured. Stiffness of the elbow also may occur, especially after open reduction. Cubitus valgus may occur, but is not as cosmetically problematic as cubitus varus.
Transcondylar Fractures Transcondylar (or dicondylar) fractures have a fracture line, either transverse or crescent-shaped, that passes through both condyles within the joint capsule just proximal to the articular surface ( Figure 49-17 ). As with supracondylar fractures, two types have been described, extension and flexion, based on the position of the elbow when fractured, and extension types are the most common. The mechanism of injury is similar to that for supracondylar injuries. In contrast to supracondylar fractures, however, the injury is more common in elderly individuals with fragile, osteoporotic bone. These fractures generally are difficult to treat because the small distal fragment possesses little extra-articular bone, and only a small amount of bone contact is available for union.[17] During healing, excessive callus may form in the olecranon or coronoid fossae with residual loss of motion. Orthopedic consultation should be obtained for these injuries.
Figure 49-17 Transcondylar fracture of distal hum erus. ((Left from Ruiz E, Cicero J: Em ergency Managem ent of Skeletal Injuries. St Louis, Mosb y, 1995. Right m odified from Sim on R, Koenigsknecht S: Emergency Orthopaedics: The Extrem ities, 2nd ed. Norwalk, Conn, Appleton & Lange, 1987.)Appleton & Lange)
Intercondylar Fractures Intercondylar fractures are usually T-shaped or Y-shaped fractures with variable degrees of separation of the condyles from each other and from the proximal humerus fragment ( Figure 49-18 ). The distal portion of the fracture extends to the articular surface of the distal humerus. These injuries are rare and generally are seen in adults in their 50s and 60s.[18] The usual mechanism of injury is direct trauma to the elbow that drives the olecranon against the humeral articular surface and splits the distal end.
Figure 49-18 Intercondylar T fractures, types I, II, and III. ((From Connolly JF: DePalm a's Managem ent of Fractures and Dislocations. Philadelphia, WB Saunders, 1981.)Elsevier Inc.)
Clinical and Radiographic Features Patients with intercondylar fractures complain of pain at the elbow, which on examination is tender to palpation. Good-quality anteroposterior and lateral x-rays are essential in evaluating fracture displacement and comminution. A computed tomography scan may be used to delineate fracture patterns further. Neurovascular complications are not common with these injuries.
Management
Page 204
Intercondylar fractures are notoriously difficult and complicated to treat.[] The goal of treatment is to re-establish articular congruity and alignment and to begin active motion as soon as possible. Open reduction with rigid internal fixation is usually preferred. Closed treatment has been recommended for elderly patients, for patients with medical conditions that prohibit surgery, and historically for patients with nondisplaced fractures. These injuries all should be referred to an orthopedic surgeon emergently. Similar to supracondylar fractures, manipulation should be avoided, unless limb-threatening ischemia is present. Traction across the elbow with the arm extended is helpful in restoring blood flow to an ischemic forearm.
Complications Historically, loss of elbow joint function is the most common complication reported, although this now can be largely avoided with optimal surgical technique.[21] Any method of treatment that requires prolonged immobilization is likely to result in fibrosis or ankylosis of the joint. Neurovascular complications are rare.
Lateral Condyle Fractures in Children Lateral condyle fractures are the second most common fractures involving the elbow in children, after supracondylar fractures.[22] The fracture occurs after a fall on the outstretched hand, with a varus stress applied to the extended arm.
Clinical and Radiographic Features Tenderness and swelling are noted over the lateral aspect of the elbow. Generally, there is less swelling than with supracondylar fractures, and neurovascular compromise is uncommon. Diagnosis usually can be made on standard anteroposterior and lateral views, although an oblique view also may be helpful.
Management Fractures with less than 2 mm displacement can be treated closed in a cast, whereas fractures with greater displacement require either open or closed reduction with pin fixation for 3 to 4 weeks.[22]
Complications Fractures diagnosed and treated in a timely manner should have few complications, although historically, nonunion, valgus deformity, and avascular necrosis all have been reported.
Medial Condyle Fractures in Children Medial condyle fractures are rare, comprising 1% to 2% of pediatric elbow fractures.[23] These fractures are type IV Salter injuries with physeal injury a possible outcome. The mechanism of injury is believed to be a valgus force on the extended elbow.
Clinical and Radiographic Features The patient presents with tenderness and swelling over the medial aspect of the elbow. Anteroposterior, lateral, and oblique films may show the fracture in older children, but in children younger than age 9 the trochlea does not ossify until this time. Magnetic resonance imaging (MRI) may be necessary to confirm the diagnosis in these patients.
Management Operative treatment is indicated if displacement is greater than 2 mm; otherwise, conservative treatment is sufficient.
Complications A study of 21 patients with medial condyle fractures revealed a 33% complication rate.[23] Complications included loss of reduction requiring reoperation, avascular necrosis, nonunion, and cubitus varus. Most minimally displaced fractures healed uneventfully.
Condylar Fractures in Adults Condylar fractures are rare in adults and typically involve the articular surface and the nonarticular portion of the distal humerus, including the epicondyle ( Figure 49-19 ). The lateral trochlear ridge is the key to analyzing humeral condyle fractures. It may be involved with either medial or lateral condylar fractures and, when incorporated into the distal fragment, is far more likely to result in instability.
Page 205
Figure 49-19 Condylar fractures. A, Norm al anatom y. B, Lateral trochlear ridge not in fracture fragment (stable). C, Lateral trochlear ridge included with fracture fragm ent (unstable). ((Modified from Sim on R, Koenigsknecht S: Emergency Orthopaedics: The Extrem ities, 2nd ed. Norwalk, Conn, Appleton & Lange, 1987.)Appleton & Lange)
Pathophysiology Lateral condylar fractures are uncommon, although more common than medial condylar fractures. The mechanism of injury is either a direct blow to the lateral aspect of the flexed elbow or a force that results in adduction and hyperextension with avulsion of the lateral condyle. Medial condylar fractures are rare and result from either a direct blow to the apex of the flexed elbow or a fall on the outstretched arm with the elbow forced into varus.
Clinical and Radiographic Features The presentation of condylar fractures is similar to that of other distal humerus fractures, with swelling, tenderness, and crepitus localized over either the medial or the lateral elbow. On palpation, independent motion of the involved condyle may be appreciated. In lateral condylar fractures, findings may be accentuated with movement of the radius. On radiographic examination, lateral condylar fractures show a widening of the intercondylar distance. The distal fragment is often displaced, most commonly posteriorly and inferiorly. Because of the location of the ulnar nerve, it is imperative to test its function when this fracture is present. Medial condylar fractures are associated with tenderness over the medial condyle and pain with flexion of the wrist against resistance. On x-ray examination, displaced distal fragments tend to be anterior and inferior because of the pull of the forearm flexors.
Management Immediate treatment depends on x-ray findings. For undisplaced or minimally displaced condylar fractures, immobilization of the flexed elbow in a long arm posterior plaster splint is sufficient. For lateral condylar fractures, the forearm should be supinated and the wrist extended to relieve the tension on the extensor muscle attachments. For medial condylar fractures, the reverse is true (i.e., the forearm should be pronated and the wrist flexed). For fractures displaced greater than 3 mm, surgical fixation is required.
Complications Complications include nonunion, restricted range of motion, joint instability, cubitus valgus or varus deformity, arthritis, and ulnar neuropathy. Because of the high rate of complications, all condylar fractures should have orthopedic consultation.
Articular Surface Fractures Capitellum Fractures Pathophysiology Although fractures of the capitellum and trochlea do occur as isolated injuries, more often they occur as a result of posterior dislocation of the elbow. Injury to the capitellum occurs when the patient falls on an outstretched hand, jamming the radial head upward, similar to a piston, shearing off the capitellum into the radial fossa. Because the capitellum has no muscular attachments, the fragment may remain nondisplaced. More often, the fragment is displaced (usually anteriorly, but occasionally posteriorly). Because of this mechanism, a radial head fracture also may be present.
Clinical and Radiographic Features The development of significant signs and symptoms may be delayed with capitellum fractures. Eventually, swelling within the capsule results in severe pain that manifests as well-localized tenderness on examination. Flexion of the elbow increases pain. A true lateral x-ray film usually shows the fragment lying anterior and proximal to the main portion of the capitellum ( Figure 49-20 ).
Page 206
Figure 49-20 Fracture of the capitellum.
Management Treatment begins in the emergency department with a posterior splint, ice packs, elevation, compression, and analgesia. Accurate anatomic alignment, rigid internal fixation, and early mobilization are prerequisites for a good functional result.[24] Fractures of the articular surfaces can be treated nonsurgically only if x-rays show perfect anatomic alignment.
Complications Complications include posttraumatic arthritis, avascular necrosis of the fracture fragment, and restricted range of motion.
Trochlea Fractures Pathophysiology Isolated fractures of the trochlea are exceedingly rare because of the structure's protected position deep within the elbow joint. The shearing force of the ulna against the trochlea is associated more commonly with posterior elbow dislocation.
Clinical Features The elbow is painful, with an effusion and limited range of motion because this is an intra-articular injury. On x-ray, a fragment is seen lying on the medial side of the joint, just distal to the medial epicondyle, and signs of joint effusion are visible. The fracture may extend into the distal portion of the medial epicondyle.
Management Nondisplaced fractures may be treated with a posterior splint for 3 weeks followed by early range-of-motion exercises. Displaced fractures should be treated operatively; fragments that can be internally fixed are repaired, whereas small fragments are excised. Immobilization should be minimized to 10 to 14 days.[]
Epicondyle Fractures Most epicondylar fractures involve the medial epicondyle. Medial epicondyle fractures are most common in children and adolescents and often involve the apophysis, which is the last ossification center to fuse in the distal humerus, usually after age 15. Fractures through this ossification center usually occur in adolescence and compose 11% of pediatric elbow fractures.[27] These are not Salter injuries because the apophysis is involved rather than the physis. Because the lateral epicondyle is almost level with the flattened outer surface of the lateral condyle, it has only minimal exposure to a direct blow, and fracture is extremely rare.
Pathophysiology Medial epicondyle injuries occur from a variety of mechanisms. First, avulsion fractures are associated with posterior elbow dislocations in patients younger than 20 years old.[28] Second, repetitive valgus stress (as with throwing a ball) results in eventual avulsion fracture of the epicondyle (little leaguer's elbow). Another reported cause of fracture separation of the medial epicondyle, usually in adolescent boys, is from arm wrestling.[29] Violent muscular forces associated with a shifting center of gravity during this activity seem to produce an avulsion just before closure of the epiphyseal plate. Finally, a direct blow to the medial epicondyle can cause this injury.
Clinical and Radiographic Features The elbow is held in flexion, and any movement is resisted. Isolated fractures are associated with focal tenderness over the medial epicondyle. Use of the forearm flexors increases pain because their attachment is along the medial epicondyle. Ulnar nerve function should be evaluated. When associated with a posterior dislocation, the examination reveals a prominent olecranon.
Page 207
Simple fractures of the medial epicondyle are extra-articular injuries with limited soft tissue injury.[22] They generally do not produce a fat pad sign on the lateral x-ray view of the elbow. A posterior fat pad or significant swelling of the joint should suggest concurrent injuries, such as elbow dislocation. Careful radiographic evaluation is especially important because fracture fragments may migrate into the joint space. If the fragment is overlying the joint line on x-ray examination, it should be considered intra-articular ( Figure 49-21 ). Radiographic detection of the intra-articular fragment is often difficult.[28] Associated ulnar nerve palsy may be present with an entrapped fragment. Fragments may be difficult to see on radiographs, and a true anteroposterior view is difficult to obtain because of severe pain on extension. In an adolescent patient, there is a tendency to confuse the normal radiolucent epiphyseal growth plate with a fracture. Comparison films of the uninjured elbow may be useful. If dislocation is present, repeat radiographs taken after reduction should be evaluated for fragment location.
Figure 49-21 Fractures of m edial epicondyle. A, Minim al displacem ent. B, Marked displacem ent. C, Displacem ent into joint. ((From Connolly JF: DePalm a's Managem ent of Fractures and Dislocations. Philadelphia, WB Saunders, 1981.)Elsevier Inc.)
Management If the fracture fragment is minimally displaced, treatment with a posterior splint is appropriate. To minimize distraction of the fragment by the forearm flexors, the elbow and wrist are flexed with the forearm pronated. Treatment of displaced fractures is controversial.[30] In the past, the amount of displacement often dictated the need for surgery. Results of operative and nonoperative treatment seem to be good, however, regardless of the degree of displacement.[30] Some experts advocate surgery for patients who participate in high-performance athletic activities that involve the injured extremity, but controlled studies are lacking. Immediate orthopedic consultation should be sought for these injuries. Intra-articular fragments that cannot be removed from the joint by manipulation are an indication for surgery.[30] Treatment of the rare lateral epicondylar fracture in an adult involves simple immobilization until pain resolves.[31]
Little Leaguer's Elbow Little leaguer's elbow warrants special mention. An adolescent pitcher traumatizes immature epiphyses by repetitive throwing. Throwing the curve ball or breaking ball has been implicated as a particular culprit, although the most important factor is probably the number of innings pitched.[32] It has been shown in a group of highly competitive young baseball players that this injury also is common in catchers and fielders.[33 ] The adolescent bone structure cannot withstand the extreme loading produced by repetitive hard throwing. Avulsion of the medial epicondyle or compression fracture of the subchondral bone of the lateral condyle or radial head may result ( Figure 49-22 ). This diagnosis should be sought in an athletic adolescent with medial epicondyle or radial head pain in the absence of acute injury by history. Adolescents with this condition should be forced to rest the elbow if throwing causes pain. After healing occurs, the amount of throwing and technique should be monitored carefully.
Figure 49-22 Little Leaguer's elbow. Avulsion fracture of m edial epicondyle (1). Com pression fractures of the radial head (2) and capitellum (3). ((From Connolly JF: DePalm a's Managem ent of Fractures and Dislocations. Philadelphia, WB Saunders, 1981.)Elsevier Inc.)
Page 208
Olecranon Fractures Pathophysiology Fractures of the olecranon may result from one of several mechanisms. Most commonly, a direct blow as a result of a fall, a motor vehicle or motorcycle crash, or an assault produces this injury. Such injuries are frequently comminuted. Less commonly, indirect force applied by forceful contraction of the triceps while the elbow is flexed during a fall can cause a transverse or oblique fracture through the olecranon. A combination of direct and indirect forces is believed also to cause some of these fractures. Olecranon fractures occur in adults and less commonly in children.[34] The anatomic integrity of the olecranon is essential for triceps strength and normal function of the elbow, similar to the way intact patellar function is necessary for extension of the knee.
Clinical Features Physical findings may include tenderness and pain over the olecranon, a palpable separation at the fracture site, or the inability to extend the elbow against force. This last finding indicates complete discontinuity of the pulling mechanism and the consequent failure of triceps function. The neurovascular status should be examined, with special attention given to the ulnar nerve distribution because this structure is most vulnerable to injury in this location. Loss of sensation over the palmar aspect of the fifth digit and hypothenar eminence or motor weakness in the interossei muscles of the hand suggests ulnar nerve injury.
Diagnostic Strategies Lateral x-ray views are most helpful. In addition to noting the fracture, the degree of comminution, the extent of articular surface disruption, and the amount of displacement in the 90-degree flexion position should be noted. Nondisplacement in this position indicates that the triceps aponeurosis is intact, and prolonged immobilization is unnecessary. Displacement of more than 2 mm is considered an indication for surgery. A fracture line that increases in separation with flexion of the elbow also is considered a displaced fracture. When this fracture is associated with elbow dislocation, the plane of instability is located through the fracture site and the radiohumeral joint, resulting in posterior displacement of the proximal fragment of the ulna and anterior dislocation of the radius and ulna as a unit.
Management Undisplaced fractures can be treated conservatively on an outpatient basis with ice, compression, immobilization in 45 to 90 degrees of flexion, and analgesia. Follow-up films should be done at frequent intervals to ensure that subsequent displacement does not occur. Range-of-motion exercises can be started within 3 weeks in many cases. Displaced fractures or fracture-dislocations require open reduction and internal fixation and should be referred immediately to an orthopedic consultant. Displaced fractures in elderly patients sometimes are treated conservatively, but this should be left to the discretion of the consultant. Orthopedic referral also is necessary when ulnar nerve symptoms are present. These symptoms occur in 10% of patients, and in most cases the injury is an ulnar contusion that resolves spontaneously. The long-term outcome of treated olecranon fractures in adults is usually favorable with a low incidence of subsequent arthritis.[35]
Radial Head and Neck Fractures Pathophysiology Radial head and neck fractures generally are produced by an indirect mechanism, typically a fall on an outstretched hand. The radius transmits the force upward, drives the radial head against the capitellum, and results in fracture of the weaker radial head or neck. Although the fracture of the radial head may be the only radiographic finding, damage to the articular surface of the capitellum and injury to the collateral ligament commonly occur. Displacement of the radial head fragment suggests considerable force and significant soft tissue injury. This injury is characterized by localized tenderness over the radial head or pain with passive rotation of the forearm.
Diagnostic Strategies Radiographic findings range from a subtle disruption of the usual gradual sweep of the radial neck/head surface to an obvious displaced or comminuted fracture. Undisplaced fractures are notoriously difficult to see on radiographs. Tenderness coupled with a positive fat pad sign on x-ray should be treated as a radial head fracture even in the absence of a visible fracture. Radial head fractures are classified into four types: {, {,
Type I—undisplaced fractures Type II—marginal fractures
Page 209
{, {,
(involving <30% of the articular surface) with displacement, including impaction or angulation Type III—comminuted fractures of the entire radial head Type IV—any of the above with elbow dislocation
Management Type I nondisplaced fractures are treated symptomatically by a brief period of sling support and early range-of-motion exercises (within 24 to 48 hours). Aspiration of the hemarthrosis and injection of 0.5% bupivacaine into the joint space may give dramatic relief of pain and improve the range of motion.[36] Most patients with this injury recover well in 2 to 3 months. A few do poorly, however, with long-term pain, contracture, or inflammation. Type II injuries usually are treated similarly, with aspiration, instillation of bupivacaine, and immobilization in the emergency department, followed by a trial period of range of motion. In these cases, aspiration of the joint and instillation of bupivacaine not only improve pain, but also allow testing of the range of motion to identify entrapped fragments. Radial head excision sometimes is performed later if the patient fails to improve. Early excision is advised for type II fractures when a mechanical block is present and for most type III fractures. Long-term functional results after radial head excision are acceptable in most patients, although a few have some functional disability after this procedure.[] Type IV injuries are treated for the elbow dislocation as described next and for the specific radial head lesion that is present.
DISLOCATION AND SUBLUXATION Elbow Dislocation Because of its anatomic structure, the elbow is inherently subject to mechanical instability, and dislocations are common. The elbow is second only to the shoulder as the most commonly dislocated large joint. Elbow dislocation is a term usually used to describe a disruption of the relationship between the humerus and the olecranon. Generally the radius and ulna, bound together firmly by the annular ligament and interosseous membrane, displace as a unit. Most classifications refer to the abnormal position of the ulna relative to the humerus. The elbow most often dislocates posteriorly, although it may dislocate anteriorly, medially, or laterally ( Figure 49-23 ). A dislocation also may occur between the radius and ulna, and such dislocations rarely occur concurrently with the ulnohumeral type. The latter are termed divergent dislocations.
Figure 49-23 Elbow dislocation, posterior and anterior. ((Modified from Sim on R, Koenigsknecht S: Emergency Orthopaedics: The Extrem ities, 2nd ed. Norwalk, Conn, Appleton & Lange, 1987.)Appleton & Lange)
Dislocation of the elbow requires considerable energy, and it is not surprising that a significant number of dislocations are associated with fractures of adjacent bony structures. Immediate reduction of these dislocations is imperative to relieve pain and to prevent circulatory embarrassment or cartilaginous damage.
Posterior Elbow Dislocation Pathophysiology The mechanism of injury is a fall on the outstretched hand or wrist, the elbow being either extended or hyperextended at the time of impact. A valgus stress usually also occurs. The resultant forces lever the ulna from the trochlea and produce the dislocation.
Clinical and Radiographic Features Patients hold the elbow in flexion at approximately 45 degrees and have marked prominence of the olecranon. Some elbow dislocations reduce before examination in the emergency department, presenting a confusing picture. In any case, significant diffuse tenderness and swelling are present. Neurovascular status
Page 210
must be checked because brachial artery and median nerve injuries have been described. Neurovascular injury may occur from numerous mechanisms, including the initial traction, local swelling, and entrapment during reduction.[39] Repeat examinations are mandatory. A radiographic example of elbow dislocation is provided in Figure 49-24 . X-ray evaluation is crucial before manipulation to rule out fractures that can mimic dislocation on examination. Also, several fractures commonly occur in conjunction with dislocation, and these need to be identified and treated when present. These include fractures of the distal humerus, radial head, and coronoid process.
Figure 49-24 Posterior dislocation of elbow. Ligam ents and joint capsules are disrupted to the point that lateral displacement also is present.
Management Orthopedic consultation is usually not necessary to proceed. Reduction should be attempted immediately if there is vascular compromise. Conscious sedation is helpful in most cases. Regional blocks are useful in selected cases, and general anesthesia is rarely needed. Posterior dislocations are reduced with an assistant immobilizing the humerus while traction is applied distally at the wrist. The elbow is brought into flexion as steady countertraction is applied to the anterior surface of the distal humerus. When the capitellum slides over the coronoid process, a coupling sound occurs as the articular surfaces mesh. The joint is gently moved through its normal range of motion to check stability. If stable, the elbow is flexed to approximately 90 degrees and immobilized with posterior plaster mold. The neurovascular status should be rechecked. Postreduction radiographs are important to avoid missing concomitant fractures of the coronoid process or radial head or, in children, separation of the medial epicondylar apophysis. Postreduction management includes immobilization in a posterior splint with the elbow in as much flexion as circulation allows. The arm is suspended in a sling. Circular casting should be avoided initially. Patients can be discharged with instructions to apply ice, elevate, and watch for signs of vascular impairment. Patients should not be discharged until and unless they can follow such instructions. If the elbow is stable after reduction, gentle range-of-motion exercises may be initiated in 3 to 5 days. Unstable joints may require either prolonged immobilization in the presence of ligamentous instability or internal fixation for instability associated with fracture.[40]
Complications The most serious complication of elbow dislocation is vascular compromise. Severe disruption results in injury to the brachial artery in 8% of cases.[41] This injury should be sought when a wide opening between the tip of the olecranon and the distal humerus is palpated or seen on a radiograph. The presence of distal pulses is not proof of an intact artery, and if a question of vascular compromise exists, emergent vascular studies or consultation are indicated. Median nerve traction injuries and entrapment also have been reported. Loss of median nerve function after reduction should prompt immediate orthopedic consultation. Recurrent dislocation of the elbow is rare.
Medial and Lateral Dislocations Medial and lateral elbow dislocations are produced by a similar mechanism as in posterior dislocations with a vector of force displacing the ulna and radius as a unit either medially or laterally. The anteroposterior view is the key to determining these dislocations. Reduction is carried out with the arm in slight extension, but otherwise is similar to that for posterior dislocation. Care must be taken not to convert these to posterior dislocations during reduction. Complications and aftercare are the same as for posterior dislocations.
Anterior Elbow Dislocation Pathophysiology Anterior dislocations are rare and occur as a result of a blow from behind to the olecranon while the elbow is in the flexed position. Severe associated soft tissue trauma is present, including avulsion of the triceps mechanism or vascular disruption. These dislocations are frequently open.
Clinical Features
Page 211
The upper arm appears shortened and the forearm elongated. The elbow is fully extended, and the forearm is supinated. The olecranon fossa is palpable posteriorly.
Management Reduction of closed injuries is performed with distal traction of the wrist and a backward pressure on the forearm, while grasping the distal humerus. A click usually indicates that reduction has been achieved. These injuries have a higher incidence of vascular impairment than the more common posterior dislocation, but ulnar nerve injuries are unusual.[42] Emergent orthopedic referral is advised and is mandatory for open injuries or when vascular disruption is suspected.
Radial Head Subluxation Pathophysiology Subluxation of the radial head is a common injury, representing more than 20% of upper extremity injuries in children. Children age 1 to 3 years are most often affected, although cases have been reported in children 6 months to 15 years of age. Girls are affected more commonly than boys. This injury is called nursemaid's elbow or pulled elbow because it results from a sudden longitudinal pull on the forearm while the child's arm is in pronation. Stretching of the annular ligament allows fibers to slip between the capitellum and the head of the radius, resulting in an inability of the child to supinate the arm. There is a recurrence rate of about 20% for this injury.[43]
Clinical and Radiographic Features Clinically the arm is in passive pronation, with slight flexion at the elbow. The child is unable or unwilling to move the arm. Resistance to supination and tenderness on direct palpation over the head of the radius are present. Swelling, ecchymosis, and deformity are absent. X-rays are not required when the history suggests this injury. If there is swelling or deformity, if there is an uncharacteristic history, if the child does not resume use of the arm after reduction, or if there is a suspicion of child abuse, appropriate x-ray studies should be obtained. If palpation of the forearm, wrist, or humerus away from the elbow elicits reproducible tenderness, radiographs should be taken to exclude other diagnoses.
Management Radial head subluxations usually can be reduced by supination of the forearm while slight pressure on the radial head is applied with the examiner's thumb. In one continuous motion, the elbow is supinated and flexed. A click often, but not always, is felt as the radial head reduces ( Figure 49-25 ). If this method is unsuccessful, supination with extension also has been recommended.
Figure 49-25 Subluxation of the radial head. Method of reduction: (1) Apply pressure to radial head, (2) supinate the forearm, and (3) flex elbow, in one continuous m otion.
Many patients are asymptomatic within 5 to 10 minutes; 90% of patients regain use of the arm within 30 minutes. Hearing or palpating a click is associated with success. It is a good idea for the physician to leave the room and for parents to distract the child to show return of normal function. A fearful child often does not use even the successfully reduced limb. If function does not return within 24 hours, the patient should be re-evaluated. Immobilization after successful reduction is not necessary. A sling is often recommended, but most children do not keep it in place. Most of these injuries are unintentional on the part of the caregiver, but inflicted injury should be considered in suspicious cases.
SOFT TISSUE DISORDERS Epicondylitis (Tennis Elbow) Pathophysiology Tennis elbow is a term first introduced in the 1880s to describe an inflammatory process that involves the radiohumeral joint or lateral epicondyle of the humerus. It is a common exercise-related syndrome, and the mechanism is thought to be repetitive pronation and supination of the forearm. The actual pathologic nature of this syndrome is unclear. Radiohumeral bursitis or synovitis, tendinitis of the common extensor tendon,
Page 212
periostitis of the lateral epicondyle, and entrapment by scar tissue of the radial nerve all have been suggested as culprits in this syndrome. Histologically the abnormality has been described as angiofibroblastic hyperplasia, a term subsequently modified to angiofibroblastic tendinosis. The cause has been theorized to be a degenerative process because of the paucity of acute inflammatory cells seen histologically.[44] Medial tennis elbow and posterior tennis elbow have been reported, the former involving the pronator teres and flexor carpi radialis insertions and the latter involving the triceps tendon. The following discussion pertains to lateral tennis elbow.
Clinical and Radiographic Features Whatever the cause, the onset is usually gradual. Patients have complaints of dull pain over the lateral aspect of the elbow, increased by grasping or twisting motions. Tenderness is located over the lateral epicondyle or radiohumeral joint. Supination and pronation against resistance may be painful. Pain can be shown by stretching the wrist extensors. To test this, the elbow is extended, the forearm pronated, and the wrist fully dorsiflexed. X-ray findings may be normal, although with chronicity, calcifications may be present over the lateral epicondyle. Characteristic MRI findings also have been described, although MRI is not indicated and generally not available in the emergency department.[45]
Management Traditional treatment includes protection, rest, ice, compression, elevation, and medication. Initial therapy includes avoidance of the inciting activity and immobilization with a sling. Nonsteroidal anti-inflammatory drugs are often used, but their efficacy probably is limited to their analgesic rather than their anti-inflammatory properties.[46] Injection of a corticosteroid at the point of tenderness provides some relief of pain in most patients.[] Because corticosteroids weaken collagen, premature resumption of heavy loading of the tendon at the lesion should be avoided, as should injection directly into the tendon.[50] Patients with pain that persists despite treatment and a rehabilitation program should be referred for possible surgery.[51] Modification of athletic technique is recommended after the symptoms subside.
Olecranon Bursitis Pathophysiology Although several bursae are located in the elbow region, the olecranon bursa is the one most often involved in an isolated pathologic process. Olecranon bursitis commonly is caused by repetitive minor trauma, such as leaning on the elbow during work activities. It also may result from an inflammatory process, such as gout or an infectious process within the bursa (septic bursitis). Septic olecranon bursitis also occurs most commonly in patients engaged in work that predisposes to repetitive trauma to the elbow, such as gardening or plumbing.
Clinical Features Patients usually have progressive pain, tenderness, and swelling over the olecranon. Some patients with septic bursitis have an abrupt onset instead, with a rapid increase in pain over a few hours. On examination, the septic bursa is typically swollen, hot, erythematous, and tender. Flexion often is limited by pain brought on by tightening of the skin over the inflamed bursa. Minor breaks in the skin, frank abrasions, or healing lacerations over the bursa may be present. In one small series, 7 of 20 patients with septic olecranon bursitis were febrile (38.5° C to 40.3° C), 75% had cellulitis, and 25% had regional adenopathy. Noninfectious bursitis usually presents with less warmth and erythema. The skin is intact, and swelling may be the only finding. The most important aspect of evaluation is the differentiation of a septic process from a benign inflammatory process. This differentiation may be difficult on clinical grounds because considerable overlap exists in the histories and physical findings.
Diagnostic Strategies If doubt exists, aspiration of the bursa should be performed and the aspirate sent for crystals, white blood cell count, Gram stain, and cultures. Unless it is frankly bloody, traumatic nonseptic olecranon bursitis usually has a leukocyte count of less than 1000 cells/mm3, whereas septic bursal fluid usually has greater than 10,000 white blood cells/mm3.
Management Aspiration is diagnostic and therapeutic because relief of pressure relieves some of the pain. In cases of purulent bursitis, the bursa should be drained, and appropriate penicillinase-resistant antibiotics should be begun in the emergency department. Bursitis refractory to aspiration and penicillinase-resistant antibiotics
Page 213
may require incision and drainage. Noninfectious bursitis can be managed with a compression dressing, ice, nonsteroidal anti-inflammatory medications, and avoidance of the inciting activity. Patients who have had their bursa aspirated should be rechecked within 24 hours to verify culture results and monitor their response to treatment.
Biceps Tendon Rupture Pathophysiology Biceps tendon rupture occurs most commonly in the proximal portion of the long head of the biceps. It is most common in middle-aged athletes or physical laborers who sustain repetitive microtrauma to the tendon. Patients experience a snapping sound and pain in the anterior shoulder during strenuous activities that produce rapid loading of the muscle. Rupture also occurs distally, usually as an avulsion from the insertion on the radial tuberosity, although ruptures at the musculotendinous junction occasionally occur. Rupture of the distal biceps tendon occurs almost exclusively in men, most commonly between the ages of 40 and 60 and most often involving the dominant arm.[52] The inciting event is usually an unexpected extension force applied to the arm flexed at 90 degrees. The pathophysiology of tendon rupture is poorly understood, although tendon rupture generally occurs in the setting of underlying tendinosis. Diabetes, chronic renal failure, systemic lupus erythematosus, rheumatoid arthritis, and steroid or fluoroquinolone therapy all may result in tendinosis. Smoking has been shown to be strongly associated with distal biceps tendon rupture.[53]
Clinical Features The diagnosis is usually obvious. In proximal tendon rupture, the patient usually has a visible defect at the top of the bicipital groove with bunching of the muscle distally. Flexing of the elbow produces pain at the proximal insertion. Flexion remains intact, however, because the short head of the biceps usually maintains its integrity. With distal ruptures, the patient complains of pain and tearing in the antecubital region. There is a visible deformity and palpable defect of the biceps muscle belly with weakness of elbow flexion and supination. If the tendon is completely ruptured, there is a bunching up of the muscle, and this effect is accentuated when the patient attempts flexion. X-rays are not revealing and usually not necessary. MRI may be useful when a partial rupture is suspected.
Management All patients require urgent referral to an orthopedist. Early anatomic repair of complete ruptures usually is recommended. Partial ruptures occasionally respond to conservative treatment, but also may require surgical repair. Patients should be splinted and advised to apply ice and be given analgesics while awaiting orthopedic consultation.
KEY CONCEPTS {,
Clini cal deci sion rules for the elbo w joint have not been valid ated. It is reas onab le to perfo rm x-ray
Page 214
s whe n there is signi fican t limit ation in rang e of moti on, obvi ous defor mity, joint effus ion, or signi fican t tend erne ss over any of the bony pro mine nces or the radia l head . In the abse nce of thes e, it woul d see m appr opria te to omit x-ray s. {,
In the setti
Page 215
ng of trau ma, mor e than 90% of patie nts with the post erior fat pad sign of the elbo w have intraartic ular skel etal injur y. In adult s, a radia l head fract ure is impli ed, wher eas in child ren, a supr acon dylar fract ure is the prob able unde rlyin g injur y. In the abse nce
Page 216
of trau ma, other caus es of effus ion (e.g., gout, infec tion, or bursi tis) shou ld be cons idere d. {,
The most com mon com plica tion, radia l nerv e injur y, occu rs in 20% of hum erus fract ures. This is most often a beni gn neur apra xia that resol ves spon tane ousl y in most patie nts, altho
Page 217
ugh reco very may take seve ral mont hs. Radi al nerv e injuri es asso ciate d with pene tratin g trau ma or open fract ures are likely to be per man ent and usua lly warr ant oper ative expl orati on. {,
Gen erall y the radiu s and ulna, boun d toget her firml y by the annu lar liga ment
Page 218
and inter osse ous me mbr ane, displ ace as a unit and typic ally dislo cate post eriorl y, altho ugh anter ior, medi al, or later al dislo catio ns may occu r. {,
X-ra y studi es are not requi red whe n the histo ry sugg ests radia l head dislo catio n (nur sem aid's elbo w). If there is swell ing
Page 219
or defor mity, if there is an unch aract eristi c histo ry, if the child does not resu me use of the arm after redu ction , or if there is a susp icion of child abus e, appr opria te x-ray studi es shou ld be obtai ned. {,
Bice ps tend on ruptu re occu rs almo st excl usiv ely in men, most com monl y
Page 220
age 40 to 60, most often invol ving the domi nant arm and usua lly subs eque nt to an unex pect ed exte nsio n force appli ed to the arm flexe d at 90 degr ees. Smo king, diab etes, chro nic renal failur e, syst emic lupu s eryth emat osus , rheu mato id arthri tis, and stero id or fluor oqui nolo
Page 221
ne thera py may predi spos e to this injur y.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/112.html/top
Page 222
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
REFERENCES 1. Paraskevass G: Study of the carrying angle of the human elbow joint in full extension: A morphometric analysis. Surg Radiol Anat2004;26:19. 2. Mohammad S, Rymaszewski LA, Runciman J: The Baumann angle in supracondylar fractures of the distal humerus in children. J Pediatr Orthop1999;19:65. 3. Branch T: Spontaneous fractures of the humerus during pitching. Am J Sports Med1992;20:468. 4. Vander Griend R: Open reduction and internal fixation of humeral shaft fractures. J Bone Joint Surg 1986;68A:430. 5. Chiu FY: Closed humeral shaft fractures: A prospective evaluation of surgical treatment. J Trauma 1997;43:947. 6. Wilkins KE: Fractures and dislocations of the elbow region. In: Rockwood CA, Wilkins KE, King RE, ed. Fractures in Children, 4th ed. Philadelphia: JB Lippincott; 1996: 653. 7. Mikowitz B, Busch MT: Supracondylar humerus fractures. Orthop Clin North Am1994;25:581. 8. Williamson DM, Cole WG: Treatment of selected extension supracondylar fractures by manipulation and strapping in flexion. Injury1993;24:249. 9. Wilkins KE: Supracondylar fractures: What's new?. J Pediatr Orthop1997;6:110. 10. Harris IE: Supracondylar fractures of the humerus in children. Orthopedics1992;15:811. 11. Mehserle WL, Mechan PL: Treatment of displaced supracondylar fracture of the humerus (Type III) with closed reduction and percutaneous cross-pin fixation. J Pediatr Orthop1991;11:705. 12. Pirone AM, Graham HK, Krajbich JI: Management of displaced extension-type supracondylar fractures of the humerus in children. J Bone Joint Surg1988;70A:641. 13. Boyd DW, Aronson DD: Supracondylar fracture of the humerus: A prospective study of percutaneous pinning. J Pediatr Orthop1992;12:789. 14. Weiland AJ: Surgical treatment of displaced supracondylar fractures of the humerus in children: An analysis of fifty-two cases followed up for 5 to 15 years. J Bone Joint Surg1978;60A:657. 15. Gaddy BC: Distal humeral osteotomy for correction of post-traumatic cubitus varus. J Pediatr Orthop 1995;15:419. 16. Brown IC, Zinar D: Traumatic and iatrogenic neurological complications after supracondylar humerus fractures in children. J Pediatr Orthop1995;15:440. 17. Perry CR, Gibson CT, Kowalski MF: Transcondylar fractures of the distal humerus. J Orthop Trauma 1989;3:98. 18. Gupta R: Intercondylar fractures of the distal humerus in adults. Injury1996;27:569. 19. Hotchkiss RN, Green DP: Fractures and dislocations of the elbow. In: Rockwood CA, Wilkins KE, King RE, ed.Fractures, 4th ed. Philadelphia: JB Lippincott; 1996: 929. 20. Safran O: Surgical treatment of intercondylar fractures of the humerus in adults. Am J Orthop 1999;28:659. 21. Gupta R, Khanchandani P: Intercondylar fractures of the distal humerus in adults: A critical analysis of 55 cases. Int J Care Injured2002;33:511. 22. Skaggs D, Pershad J: Pediatric elbow trauma. Pediatr Emerg Care1997;13:425. 23. Leet AI, Young C, Hoffer M: Medial condyle fractures of the humerus in children. J Pediatr Orthop 2002;22:2. 24. McKee MG: Fractures of the capitellum and trochlea. Orthop Clin North Am2000;31:115. 25. Wang KC: Intercondylar fractures of the distal humerus: Routine anterior subcutaneous transposition of the ulna nerve in a posterior operative approach. J Trauma1994;36:770. 26. Foulk DA, Robertson PA, Timmerman LA: Fracture of the trochlea. J Orthop Trauma1995;9:530. 27. Case SL, Hennrikus WL: Surgical treatment of displaced medial epicondyle fractures in adolescent athletes. Am J Sports Med1997;25:682. 28. Fowles JV, Slimane N, Kasseb MT: Elbow dislocation with avulsion of the medial humeral epicondyle. J Bone Joint Surg1990;72B:102. 29. Ogawa K, Ui M: Fracture-separation of the medial humeral epicondyle caused by arm wrestling. J Trauma1996;41:494. 30. Farsetti P: Long-term results of treatment of fractures of the medial humeral epicondyle in children. J
Page 223
Bone Joint Surg2001;83A:12299. 31. Kobayashi Y, Oka Y, Munesada S: Avulsion fractures of the medial and lateral epicondyles of the humerus. J Shoulder Elbow Surg2000;9:59. 32. Green CP: The curve ball and the elbow. In: Zarins B, Andres JR, Carson WG, ed.Injuries to the Throwing Arm, Philadelphia: WB Saunders; 1985: 33. Hang DW, Chao CM, Hang YS: A clinical and roentgenographic study of little league elbow. Am J Sports Med2004;32:79. 34. Evans MC, Graham HK: Olecranon fractures in children: Part 1. A clinical review. Part 2. A new classification and management scheme. J Pediatr Orthop1999;19:559. 35. Karlsson MK: Fractures of the olecranon: A 15 to 24 year follow up of 73 patients. Clin Orthop 2002;403:205. 36. Dooley JF, Angus PD: The importance of elbow aspiration when treating radial head fractures. Arch Emerg Med1991;8:117. 37. Coleman DA, Blair WF, Shurr D: Resection of the radial head for fracture of the radial head. J Bone Joint Surg1987;69A:385. 38. Goldberg I, Peylan J, Yosipovitch Z: Late results of excision of the radial head for an isolated closed fracture. J Bone Joint Surg1986;68A:675. 39. Platz A: Posterior elbow dislocation with associated vascular injury after blunt trauma. J Trauma 1999;46:948. 40. Phillips CS, Segalman KA: Diagnosis and treatment of post-traumatic medial and lateral elbow ligament incompetence. Hand Clin2002;18:149. 41. Rao SB, Crawford AH: Median nerve entrapment after dislocation of the elbow in children: A report of two cases and review of the literature. Clin Orthop1995;312:232. 42. Skaggs D, Pershad J: Pediatric elbow trauma. Pediatr Emerg Care1997;13:425. 43. Teach SJ, Schutzman SA: Prospective study of recurrent radial head subluxation. Arch Pediatr Adolesc Med1996;150:164. 44. Nirschl RP: Elbow tendinosis/tennis elbow. Clin Sports Med1992;11:851. 45. Martin CE, Scweitzer ME: MR imaging of epicondylitis. Skeletal Radiol1998;27:133. 46. Labelle H, Guibert R: Efficacy of diclofenac in lateral epicondylitis of the elbow also treated with immobilization. Arch Fam Med1997;6:257. 47. Hay E, Paterson SM, Lewis M: Pragmatic randomized controlled trial of local corticosteroid injection and naproxen for treatment of lateral epicondylitis of elbow in primary care. BMJ1999;319:964. 48. Guidotti TC: Occupational repetitive strain injury. Am Fam Physician1992;45:585. 49. Hay EM: Pragmatic randomized controlled trial of local corticosteroid injection and naproxen for treatment of lateral epicondylitis of elbow in primary care. BMJ1999;319:964. 50. Sperryn PN: Overuse injury in sport. BMJ1994;308:1430. 51. Field LD, Savoie FH: Common elbow injuries in sport. Sports Med1998;26:193. 52. Ramsey ML: Distal biceps tendon injuries: Diagnosis and management. J Am Acad Orthop Surg 1999;7:199. 53. Safran M, Graham SM: Distal biceps tendon rupture: Incidence, demographics and the effect of smoking. Clin Orthop2002;404:275.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/113.html/top
Page 224
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
Chapter 50 – Shoulder Mohamud Daya
PERSPECTIVE The shoulder joint is a unique and complex articulation unit. It has the largest range of motion of any appendicular joint in the body and can be moved through a space that exceeds a hemisphere. The wide range of motion also predisposes the joint to instability and injury; this was depicted in 3000 b.c. in wall paintings of Egyptian tombs, which show accurate drawings of manipulations (similar to the Kocher technique) used to reduce shoulder dislocations.[1] Hippocrates may have been the first to outline extensively the diagnosis and treatment of shoulder dislocations.[2] Shoulder injuries are commonly encountered in emergency medicine. Statistical studies show that 8% to 13% of all athletic injuries involve the shoulder and that shoulder dislocations account for more than 50% of all major joint dislocations seen in the emergency department. Almost every major sport or athletic activity involves use of the shoulder joint in one way or another. The shoulder can be injured by trauma (indirect or direct) or by overuse. Traumatic injuries tend to occur in football and ice hockey, whereas overuse injuries (impingement syndromes) are more common in swimming and baseball. Shoulder injuries also are common in wrestling, tennis, volleyball, and javelin throwing.[3] In general, children are vulnerable to the same injuries as adults; however, the presence of the epiphysis and its growth plate changes the pattern of injuries.[4] The strength of the joint capsule and its ligaments is two to five times greater than that of the epiphyseal plate. An injury that produces a sprain or dislocation in an adult often causes a fracture through the hypertrophic zone of the growth plate in a child. The shoulder girdle has epiphyseal plates at the acromion process, proximal humeral head, coracoid process, glenoid cavity, and medial end of the clavicle. Complete or greenstick fractures of the clavicle and fractures of the proximal humeral epiphysis are encountered more commonly in the pediatric population. Most shoulder injuries in children can be treated conservatively with a good prognosis for full return of function.[4]
PRINCIPLES OF DISEASE Anatomy The shoulder girdle connects the upper extremity to the axial skeleton ( Figure 50-1 ). It consists of three bones (clavicle, humerus, and scapula), three joints (acromioclavicular, glenohumeral, and sternoclavicular), and one articulation (scapulothoracic). The clavicle is an S-shaped bone that acts as a strut to support the upper extremity and keep it away from the chest wall. The clavicle articulates medially with the sternum and laterally with the acromion process. The sternoclavicular joint (SCJ) represents the only true articulation between the upper extremity and the axial skeleton. The large articular surface of the sternal end of the clavicle fits poorly with the sloping narrow clavicular notch on the manubrium sterni. A circular flat fibrocartilaginous disk helps reduce the discrepancy between the two articular surfaces ( Figure 50-2 ). The stability of the joint largely depends on associated ligaments. A loose fibrous capsule whose expansions form the anterior and posterior sternoclavicular ligaments envelops the joint.[5] The interclavicular and costoclavicular ligaments are two additional structures that stabilize the joint. The costoclavicular ligament opposes the pull of the sternocleidomastoid and is the most important stabilizing ligament.[5] The SCJ participates in all movements of the upper extremity and is the most moved joint in the body.[6] The superior mediastinum with its great vessels, trachea, esophagus, and other important structures are immediately posterior to the joint.
Page 225
Figure 50-1 Anatom y of the shoulder girdle. ((From Roy S, Irwin R: Sports Medicine: Prevention, Evaluation, Managem ent and Rehab ilitation. Englewood, NJ, Prentice Hall, 1983.)Prentice Hall)
Figure 50-2 Ligam ents and the interarticular disk of the sternoclavicular joint. ((Redrawn from DePalm a AF: Surgery of the Shoulder, 3rd ed. Philadelphia, JB Lippincott, 1983.)JB Lippincott)
The tubular clavicle flattens laterally to provide attachment sites for the coracoclavicular and acromioclavicular ligaments ( Figure 50-3 ). The clavicle also protects the subclavian neurovascular bundle and provides the neck with an acceptable cosmetic appearance. The middle third of the clavicle, which is the most commonly fractured segment, is thin and untethered by any ligamentous structures.[7] Rotation around the long axis of the clavicle increases the range of motion of the glenohumeral joint and improves the strength of the arm-trunk mechanism.[7]
Figure 50-3 Ligam ents of the acrom ioclavicular joint. ((Redrawn from DePalm a AF: Surgery of the Shoulder, 3rd ed. Philadelphia, JB Lippincott, 1983.)JB Lippincott)
The acromioclavicular joint (ACJ) connects the lateral end of the clavicle with the medial aspect of the acromion process (see Figure 50-3 ). The bony configuration of the joint varies considerably and provides little or no stability.[8] Stability is a function of associated ligaments and muscles. The joint capsule is strengthened on all sides to form the relatively weak anterior, posterior, superior, and inferior acromioclavicular ligaments. The clavicular and acromial attachments of the deltoid and trapezius muscles provide additional static and dynamic support for the superior aspect of the joint. The powerful coracoclavicular ligament, which is the primary suspensory ligament of the upper extremity, also stabilizes the joint. The coracoclavicular ligament is composed of two parts—the trapezoid and conoid ligaments.[8] The trapezoid ligament arises from the shaft of the coracoid process and runs superiorly to insert onto the inferior surface of the lateral clavicle. The conoid ligament arises from the base of the coracoid process and inserts more medially on the inferior surface of the distal clavicle. The distance from the clavicle to the coracoid process varies from 1.1 to 1.3 cm in the standing adult. Although the ACJ itself has only 5 to 8 degrees of movement, it allows for 40 to 50 degrees of clavicular rotation. The latter is required to achieve a full range of motion at the glenohumeral joint. The scapula is a flat triangular bone that forms the posterior aspect of the shoulder girdle. The thin body of the scapula lies flat against the posterior thorax and widens laterally to form the glenoid fossa. A stable base from which glenohumeral motion can occur is provided by 18 muscular origins and insertions on the scapula.[9] The flat anterior surface of the scapula gives rise to the subscapularis muscle, whereas the serratus anterior muscle inserts onto its thickened medial border. Posteriorly the surface is divided into two parts by the scapular spine. The areas superior and inferior to the spine give rise to the supraspinatus and infraspinatus muscles. The teres minor and major muscles originate from the posterior aspect of the lateral border of the scapula. The thickened posteromedial border serves as the attachment site for the rhomboid and levator scapulae muscles.
Page 226
The superior border of the scapula gives rise to an anterior projection, the coracoid process (see Figure 50-1 ). As discussed, the coracoid provides attachment for numerous important ligaments and muscles that help stabilize the glenohumeral joint. The acromion, in conjunction with the strong coracoacromial ligament, forms the coracoacromial arch (see Figure 50-3 ). Muscles attached to the coracoid process include the short head of the biceps, coracobrachialis, and pectoralis minor. The neurovascular bundle is located beneath the coracoacromial arch, immediately posterior to the coracoid process. The glenohumeral articulation is a ball-and-socket–type joint ( Figure 50-4 ). The glenoid fossa is deepened by a rim of fibrocartilage (glenoid labrum) and provides a bearing surface for only half of the humeral head at any one time. The absence of congruent surfaces makes the bony joint mechanically unstable. The stability of the joint primarily depends on associated muscles and ligaments. A negative intracapsular pressure completes the stabilization mechanism.[] The absence of bony stability permits a range of motion, however, that is greater than that of any other joint in the body.
Figure 50-4 Anatom y of the glenohum eral joint.
A synovial membrane extends from the glenoid fossa to the humeral head. The membrane is large and redundant inferiorly to accommodate the extensive range of movement. The synovial membrane extends medially to form the subscapularis bursa and laterally to envelop the long head of the biceps. Overlying the synovial membrane is a loose and redundant fibrous capsule (see Figure 50-4 ). Anteriorly the capsule is thickened to form the superior, middle, and inferior glenohumeral ligaments. The inferior glenohumeral ligament is subdivided further into an anterior band, a posterior band, and an interposing pouch. The anterior band of the inferior glenohumeral ligament is the most important restraint to anterior glenohumeral dislocations.[] Superiorly the acromial process and the coracohumeral ligament (see Figure 50-4 ) protect the capsule. The proximal humerus articulates with the glenoid fossa and provides for the attachment of many important muscles. The supraspinatus, infraspinatus, and teres minor insert onto facets of the greater tuberosity, whereas the subscapularis inserts onto the lesser tuberosity. Together, this group of muscles forms the rotator cuff, which helps stabilize the humeral head within the glenohumeral joint ( Figure 50-5 ). The long head of the biceps tendon originates from the supraglenoid tubercle and ascends over the humeral head to enter the arm via the bicipital groove. The long head acts as an additional stabilizer for the superior and anterior aspect of the glenohumeral joint (see Figure 50-5 ). Long muscles that cross the articulation are involved primarily in movements of the glenohumeral joint. The pectoralis major, latissimus dorsi, and teres major muscles all insert into the humeral intertubercular groove. Displacements encountered with fractures of the humerus usually reflect the pull of these attached muscle groups. The proximal humerus is composed primarily of trabecular bone with a thin cortical shell. Changes in bone density with age (osteoporosis) greatly increase the risk of fractures in this area.[7]
Figure 50-5 The rotator cuff.
The blood supply of the articular surface of the humerus is derived from vessels contained in the rotator cuff tendons and from the anastomosis of the anterior and posterior circumflex humeral arteries. The neurovascular bundle runs anteriorly, and the axillary nerve is in close proximity to the inferior aspect of the joint. Movements of the glenohumeral joint include flexion, extension, abduction, adduction, internal rotation, external rotation, and circumduction.
Page 227
Four nerves supply most of the shoulder muscles. The axillary nerve supplies the deltoid and teres minor muscles; the suprascapular nerve, the supraspinatus and infraspinatus muscles; the subscapular nerve, the teres major and subscapularis muscles; and the musculocutaneous nerve, the proximal arm muscles. These nerves represent the final branches of the upper bracial plexus (nerve roots C5-8), and injuries to the brachial plexus invariably result in significant shoulder dysfunction.
CLINICAL FEATURES History Most complaints usually involve some combination of pain, stiffness, instability, and weakness. Pain can result from many different conditions extrinsic and intrinsic to the shoulder. Extrinsic sources of shoulder pain include disorders of the cervical spine, thoracic outlet syndromes, and Pancoast's tumors. In addition, pain can be referred to the shoulder from myocardial processes, diaphragmatic irritation (e.g., subphrenic abscess, lower lobe pneumonia, splenic hematoma, ruptured ectopic pregnancy, gallbladder disease), and gastric or pancreatic diseases. Acute intrinsic pain usually is associated with a traumatic event. The most important factors to determine are the time and mechanism of injury, its precise location, and the intensity of the pain. Occasionally the patient may have acute pain in the absence of associated trauma (e.g., calcific tendinitis). Shoulder pain also can present in an insidious manner, unrelated to any precipitating factor. In these instances, the duration, location, character, and aggravating and alleviating factors of the pain should be noted. Intrinsic shoulder pain in general does not radiate past the elbow. Stiffness usually signifies a restricted range of motion resulting from an underlying painful condition of the shoulder. Instability can be seen in the form of an obvious subluxation or dislocation. Alternatively the patient may relate the sensation of the shoulder almost going out. A rotator cuff tear or an underlying nerve lesion usually causes significant shoulder weakness.
Physical Examination The shoulder should be inspected from the anterior, posterior, and lateral positions. Any obvious deformity, ecchymosis, laceration, swelling, or hematoma should be noted. The masses of the trapezius, deltoid, infraspinatus, and supraspinatus muscles should be compared to detect any atrophy. Palpation of the shoulder should be performed systematically, beginning at the SCJ and moving laterally along the clavicle to the ACJ. Next the scapula, glenohumeral joint, and humerus are palpated. Any point tenderness, crepitus, swelling, or deformity should be noted. Active and passive ranges of motion should be tested. Active range of motion is best determined with the patient in the sitting position, which eliminates the contributions of the lumbar spine and lower extremity joints. Passive range of motion is best evaluated with the patient in the supine position. The degrees of abduction, forward flexion, extension, and internal and external rotation should be recorded and compared with the unaffected extremity. In addition, the motion of the scapulothoracic articulation should be observed carefully in all cases. After 45 degrees of abduction, the scapula moves approximately 1 degree for every 2 degrees of glenohumeral motion. A thorough neurovascular examination should be performed in all cases before and after all manipulations. The vascular status is checked by determining the brachial, radial, and ulnar pulses with the arms in various positions. A complete sensory (light touch and pinprick) and full motor examination also should be performed. The brachial plexus can be tested by evaluating the myotomes and dermatomes pertinent to each nerve root ( Table 50-1 ). In addition, the deep tendon reflexes should be evaluated in both upper extremities. Table 50-1 -- Sensory and Motor Components of the Brachial Plexus Level
Sensory Area
Muscle
C2–4 C5 C6 C7 C8 T1
— Lateral arm Lateral forearm Index fingertip Little fingertip Medial forearm
Trapezius Deltoid Biceps Thumb extensors Finger flexors Interossei
Page 228
Level
Sensory Area
Muscle
DIAGNOSTIC STRATEGIES Radiology The initial assessment of traumatic injuries includes a three-view series of radiographs consisting of true anteroposterior (45-degree lateral), transscapular lateral, and axillary lateral views ( Figures 50-6 and 50-7 ). The true anteroposterior view (see Figure 50-7B ) is preferred over standard anteroposterior views because it projects the glenohumeral joint without any bony overlap. Standard anteroposterior views taken in internal and external rotation profile the lesser and greater tuberosity and are more useful in the evaluation of soft tissue conditions.
Figure 50-6 Positions for the traum a series of shoulder radiographs. A Axillary view. B True anteroposterior (35-degree oblique) view. C Transscapular lateral view.
Figure 50-7 Norm al axillary (A), true anteroposterior (B), and transscapular lateral (C) views (trauma series) of the shoulder.
Acceptable orthogonal views include the axillary lateral, transscapular lateral, and apical oblique.[12] The preferred view is the axillary lateral (see Figure 50-7A ), which projects the glenohumeral joint in a cephalocaudal plane. This view is particularly useful for defining the relationship of the humeral head with the glenoid fossa and in identifying lesions of the coracoid process, humeral head, and glenoid rim.[13] Some degree of abduction is required to obtain the axillary view. Because this may not be possible with some injuries, a reverse projection or a modified axillary view ( Figure 50-8 ) may be considered. The difficulty in obtaining the axillary view has led to the popularity of the transscapular view (see Figure 50-7C ). Advantages of this projection include its simplicity and reproducibility and the clear delineation of anatomic structures. In this view, the scapula is projected as a Y, with the body forming the lower limb and the coracoid and acromion processes forming the upper limbs. The humeral head is normally superimposed over the glenoid, which is located at the junction of the three limbs. This view is particularly useful in identifying anterior and posterior glenohumeral dislocations. The apical oblique film (obtained by placing the injured shoulder in a 45-degree oblique position and angling the central ray 45 degrees caudally) provides a unique coronal view of the glenohumeral joint. The view can be obtained easily and painlessly and has been found to be more sensitive than the transscapular view for detecting bone and joint abnormalities in the injured shoulder.[14] Plain radiographs are the mainstay of the radiologic examination in the emergency department, but in selected circumstances, additional bone and soft tissue details may be obtained using computed tomography (CT) or magnetic resonance imaging (MRI).[15]
Figure 50-8 Modified axillary view of the shoulder.
Page 229
SPECIFIC INJURIES Fractures Clavicle Pathophysiology The clavicle accounts for 5% of all fractures and is the most commonly fractured bone in children. Epidemiologic studies in adults have documented an annual incidence rate of 30 to 50 per 100,000 population, with a 2:1 male-to-female ratio.[] Clavicular fractures are classified anatomically and mechanistically into three types. Fractures of the medial third are uncommon (5%) and occur as a result of a direct blow to the anterior chest. Fractures of the middle third are the most frequent ( Figure 50-9 ), accounting for 80% of all injuries. The usual mechanism of injury involves a direct force applied to the lateral aspect of the shoulder as a result of a fall, sporting injury, or motor vehicle accident. Fractures of the lateral third (15%) result from a direct blow to the top of the shoulder and are classified further into three subtypes.[ 18] Type I fractures are stable and occur lateral to the coracoclavicular ligaments. Type II fractures are medial to the coracoclavicular ligaments and have a tendency to displace because the proximal fragment lacks any stabilizing ligaments. Type III injuries involve the articular surface ( Figure 50-10 ).[18]
Figure 50-9 Displaced m idclavicular fracture.
Figure 50-10 Type III lateral clavicular fracture (intra-articular). ((Courtesy of David Nelson, MD.))
Clinical Features The patient has pain over the fracture site, and the affected extremity is held close to the body. With fractures of the middle third, the shoulder typically is slumped downward, forward, and inward. This is a result of the effect of gravity and the pull of the pectoralis major and latissimus dorsi on the distal fragment. The proximal fragment is often displaced upward by the action of the sternocleidomastoid. The head is often tilted toward the injured side in an attempt to relax the effects of these displacing muscular forces. Ecchymosis, crepitus, and a palpable or visible deformity may be present over the fracture site. Although associated neurovascular injury is rare, the close proximity of the subclavian vessels and brachial plexus demands a thorough assessment. Rarely, injury to the dome of the pleura may result in an associated pneumothorax.
Management Principles of initial management include pain control, immobilization, and proper follow-up. Fractures of the clavicle can be immobilized with supportive devices, such as a simple sling or sling and swathe ( Figure 50-11 ). Another immobilization technique for midclavicular fractures still recommended in the orthopedic literature is the clavicular (figure-of-eight) splint ( Figure 50-12 ). This splint is applied after closed reduction of the fracture, which is accomplished by pulling the shoulders up and back. Such reductions are difficult to maintain and may be associated with increased discomfort at the fracture site. Clavicular splints can lead to skin irritation and compression of the neurovascular bundle in the axilla. Because malunion and shortening are associated with an acceptable functional and cosmetic outcome, treatment with a simple sling is a valid and appropriate alternative to the clavicular splint in the emergency department.[]
Page 230
Figure 50-11 Shoulder im m obilization. A Sling over swathe. B Velpeau sling im m obilization.
Figure 50-12 Clavicular or figure-of-eight splint.
Disposition Immediate orthopedic consultation should be sought for open fractures or fractures associated with neurovascular injuries, skin tenting, or interposition of soft tissues. More urgent orthopedic consultation (before 72 hours) is recommended for type II lateral clavicle fractures because these fractures have a 30% incidence of nonunion and may require surgical repair.[18] Severely comminuted or displaced fractures of the middle third (defined as >20 mm of initial shortening) also may benefit from early orthopedic referral because these have been associated with a higher incidence of nonunion.[21] Greenstick fractures of the midclavicle are common in children ( Figure 50-13 ). Most of these fractures are nondisplaced and heal uneventfully. Initial radiographs may appear normal despite suggestive clinical findings. In these instances, the arm should be immobilized in a simple sling and the radiographs repeated in 7 to 10 days if symptoms persist.
Figure 50-13 Greenstick fracture of the clavicle (arrow).
Most fractures of the clavicle heal uneventfully and can be followed by a primary care physician. A sling should be worn until repeat radiographs show callus formation and healing across the fracture site. Passive shoulder range-of-motion exercises ( Figure 50-14 ) are encouraged to reduce the risk of adhesive capsulitis. Younger children generally require shorter periods of immobilization (2 to 4 weeks) than adolescents and adults (4 to 8 weeks). Vigorous competitive play should be avoided until the bone healing is solid.
Figure 50-14 Pendular shoulder exercises.
Complications Complications are unusual, with the most common ones being delayed union or nonunion.[] Complications after fractures of the medial third resemble complications associated with posterior sternoclavicular dislocations. Fractures of the middle third have been associated with injuries to the neurovascular bundle and the pleural dome. Articular surface injuries (type III lateral clavicle fractures) can lead to subsequent
Page 231
osteoarthritis of the ACJ.
Scapula Pathophysiology Fractures of the scapula are rare injuries, with an annual incidence of 10 to 12 per 100,000 population.[] They account for 1% of all fractures and occur primarily in men 30 to 40 years old.[9] A thick muscle coat and the ability to recoil along the chest wall protect the scapula from direct and indirect trauma. In general, considerable force and energy are required to fracture the scapula. Most fractures result from high-speed vehicular accidents, falls from heights, or crush injuries.[24] Coracoid process fractures are usually avulsive, and glenoid rim fractures are commonly associated with anterior glenohumeral dislocations. An acromial process fracture usually results from a direct blow applied to the top of the shoulder. The most important aspect of scapular fractures is the high incidence (75% to 98%) of associated injuries to the ipsilateral lung, chest wall, and shoulder girdle complex.[] The most common associated orthopedic injuries are fractures of the ribs, proximal humerus, and clavicle. Associated lung injuries include pneumothorax, hemothorax, and pulmonary contusion; these may be seen in a delayed fashion, 2 to 3 days after the initial injury. Associated injuries of the head, spinal cord, brachial plexus, and subclavian or axillary vessels are more significant but less common.[] Fractures of the scapula can be classified according to their anatomic location. In the system proposed by Ada and Miller,[25] type I fractures involve the acromion process, scapular spine, or coracoid process. Type II fractures involve the scapular neck, and type III injuries are intra-articular fractures of the glenoid fossa ( Figure 50-15 ). The most common are type IV fractures, which involve the body of the scapula.[25]
Figure 50-15 Com m inuted type III fracture of the scapular. ((Courtesy of David Nelson, MD.))
Clinical Features In a conscious patient, the shoulder is adducted, and the arm is held close to the body. Any attempts at movement result in significant pain. There may be associated tenderness, crepitus, or hematoma over the fracture site. The clinical findings occasionally mimic those seen with a rotator cuff tear. Hemorrhage into the rotator cuff associated with the scapula fracture can result in spasm and a temporary reflex inhibition of function (pseudorupture).[25] The presence of a scapula fracture mandates a thorough search for associated thoracic, intracranial, orthopedic, and neurovascular injuries.
Diagnostic Strategies The trauma series of shoulder radiographs identifies most fractures, as does careful examination of the scapula on the trauma chest radiograph. The axillary lateral view is especially useful in evaluating fractures of the glenoid fossa and the acromion or coracoid processes.[9] The os acromiale (unfused acromial process epiphysis) is present in 3% of the population and should not be confused with a fracture of the acromion.[7] A comparison film can be useful because the abnormality is present bilaterally in 60% of cases. In many patients, fractures of the scapula initially are overlooked because of the life-threatening nature of the associated injuries.[9]
Management Most fractures, including fractures with severe comminution and displacement, heal rapidly with conservative therapy.[] Initial therapy consists of analgesia and immobilization in a sling to support the ipsilateral upper extremity. Passive shoulder exercises (see Figure 50-14 ) are initiated as soon as discomfort subsides to reduce the risk of adhesive capsulitis. In general, patients require a sling for 2 to 4 weeks.[24]
Page 232
Fractures of the body and spine usually require no further therapy. Nondisplaced fractures of the acromion process also respond well to conservative therapy. Displaced acromial fractures that impinge on the glenohumeral joint require surgical management. Rarely the acromion is fractured as part of a superior dislocation of the humeral head. In these instances, an accompanying tear of the rotator cuff is invariably present and requires surgical repair. If the coracoclavicular ligaments remain intact, fractures of the coracoid process respond well to conservative therapy. Severely displaced coracoid fractures with ruptured coracoclavicular ligaments usually require open reduction and internal fixation.[6] Scapular neck and glenoid fossa fractures present the most difficult management issues. Although most of these injuries do well with conservative therapy, open reduction and internal fixation are recommended for severely displaced or angulated fractures.[]
Complications Associated injuries of the ipsilateral lung, chest wall, and shoulder girdle account for most complications after fractures of the scapula. A shear-type brachial plexus injury has been associated with fractures of the acromion process. Neurovascular (brachial plexus, axillary artery) injuries also have been reported with fractures of the coracoid process.[6] Scapular neck, body, or spine fractures that extend into the suprascapular notch can injure the suprascapular nerve.[6] Delayed complications include adhesive capsulitis and rotator cuff dysfunction.[24]
Proximal Humerus Pathophysiology Fractures of the proximal humerus are common and account for 4% of all fractures.[27] A prospective Swedish study reported an incidence of 114 per 100,000 with a mean age of 67 years and a female-to-male ratio of 3:1.[28] These fractures occur primarily in the older population, in whom structural changes associated with aging (osteoporosis) weaken the proximal humerus, predisposing it to injury. Although most of these injuries are minimally displaced and do well with conservative therapy, significantly displaced fractures may require operative intervention. Fractures of the proximal humerus separate along old epiphyseal lines, producing four distinct segments consisting of the articular surface (anatomic neck), greater tuberosity, lesser tuberosity, and humeral shaft (surgical neck). The Neer classification system ( Figure 50-16 ) is based on the relationship of these fracture fragments.[] In this system, a segment is considered displaced if it is angled greater than 45 degrees or separated more than 1cm from the neighboring segment. Because this classification system considers only displacement, the number of fracture lines is irrelevant. There are four major categories of fracture: minimal displacement ( Figure 50-17 ), two-part displacement ( Figure 50-18 ), three-part displacement, and four-part displacement. When present, anterior and posterior dislocations are included as part of the classification. Impaction and head-splitting fractures are classified separately.
Figure 50-16 Neer's classification of proxim al hum eral fractures. ((From Neer CS: Displaced proxim al hum eral fractures: Part 1. Classification and evaluation. J Bone Joint Surg Am 52:1077, 1979.))
Figure 50-17 Three-part m inim ally displaced fracture of the proxim al hum erus.
Page 233
Figure 50-18 Anteroposterior (A) and axillary (B) views of a two-part displaced fracture of the proximal hum erus. The degree of displacem ent often is visualized better on the axillary view. ((Courtesy of David Nelson, MD.))
The classic mechanism of injury involves a fall on an outstretched abducted arm. Concurrent pronation limits further abduction and levers the humerus against the acromial process; this produces a fracture or dislocation, depending on the tensile strengths of the bone and surrounding ligaments. Older patients are prone to fracture, whereas younger individuals are apt to dislocate. The combined injury (fracture and dislocation) may be seen in middle-aged individuals. Proximal humerus fractures also may result from a direct blow to the lateral side of the arm or from an axial load transmitted through the elbow. High-energy mechanisms and polytrauma are more common in younger individuals.
Clinical Features The affected arm is held close to the body, and all movements are restricted by pain. Tenderness, hematoma, ecchymosis, deformity, or crepitus may be present over the fracture site. Although usually normal, a thorough neurovascular examination helps identify associated injuries of the axillary nerve, brachial plexus, or axillary artery.
Management Minimally displaced fractures (see Figure 50-17 ) constitute 80% to 85% of all cases. No displacement or angulation is present, and the fracture segments are held together by the capsule, periosteum, and surrounding muscles. Initial treatment consists of adequate analgesia and immobilization with a sling and swathe device. As soon as clinical union is achieved (head and shaft move together), functional exercises are initiated. Initial passive exercises (see Figure 50-14 ) are slowly replaced by more active and resistive exercises. Most nondisplaced fractures heal over 4 to 6 weeks. The treatment of two-part, three-part, and four-part displaced fractures is beyond the scope of this discussion. An orthopedic surgeon should be consulted because many of these injuries require operative repair.[30] Fracture-dislocation injuries also may require an orthopedic surgeon. Care must be used because reductions of these injuries in the emergency department are often unsuccessful and can cause separation of previously undisplaced segments. Closed reduction under x-ray control and general anesthesia may be preferable.[31] Posterior glenohumeral dislocations usually are associated with anteromedial impression fractures of the articular surface. A similar fracture of the posterolateral aspect of the humeral head is present with anterior dislocations (Hill-Sachs deformity). Impression fractures involving less than 20% of the articular surface are usually stable. With more than 20% involvement, the reduction is usually unstable and requires surgical repair.
Complications The most common complication of proximal humeral fractures is adhesive capsulitis (“frozen or stiff shoulder”). This complication can be prevented by the early initiation of a thorough rehabilitation program. Two-part fractures of the articular surface and four-part fractures have a high incidence of avascular necrosis of the humeral head. Repeated forceful attempts at reduction of fracture-dislocations may be associated with subsequent heterotopic bone formation (myositis ossificans). Neurovascular injuries (axillary nerve, brachial plexus, and axillary artery) may be encountered with displaced surgical neck fractures and fracture-dislocations.
Proximal Humeral Epiphysis Pathophysiology Fractures of the proximal humeral epiphysis are uncommon and account for 10% of all shoulder fractures in children.[32] The injury can occur at any age while the epiphysis remains open but is most common in boys
Page 234
11 to 17 years old.[33] The most common mechanism of injury involves a fall onto the outstretched hand, and the fracture typically occurs through the zone of hypertrophy in the epiphyseal plate. Injuries can be classified according to their location (Salter system), stability, and degree of displacement.[6]
Clinical Features The patient has the injured arm held tightly against the body by the opposite hand. The area over the proximal humerus is swollen and extremely tender to palpation. Radiographs obtained at 90 degrees to each other confirm the diagnosis. Comparison views may be helpful with minimally displaced fractures.[33]
Management Fractures of the proximal humeral epiphysis should not be taken lightly because the potential for growth disturbance exists even under the most ideal conditions. The active healing process at the site of an epiphyseal injury makes delayed reduction extremely difficult. Early orthopedic consultation should be obtained for all such injuries. Children younger than 6 years old usually have Salter I epiphyseal injuries ( Figure 50-19 ) and can be treated conservatively with sling and swathe immobilization and analgesic agents. Children older than age 6 usually have a Salter II epiphyseal injury. Salter II injuries with greater than 20 degrees of angulation should be reduced.[34] Closed reduction is accomplished by reversing the mechanism of injury. Imperfect reductions are often acceptable because growth and remodeling correct the deformity with time. After reduction, unstable injuries should be immobilized in a shoulder spica cast, whereas stable lesions can be immobilized with a sling and swathe. Fractures of the proximal humeral epiphyses generally heal in 3 to 5 weeks.[34]
Figure 50-19 A Salter I injury of the right proximal hum eral epiphysis. B Norm al left side is included for com parison.
Complications Complications are rare and include malunion, growth plate disturbances, and injuries to the neurovascular bundle. Markedly displaced or angulated fractures are more likely to result in a residual loss of mobility.[32]
Dislocations Sternoclavicular Pathophysiology The SCJ is the least commonly dislocated major joint in the body. Significant forces are required to disrupt the strong ligamentous stabilizers of this joint. The most common causes are motor vehicle accidents and injuries sustained in contact sports, such as rugby or football. The SCJ can dislocate in an anterior or posterior direction. Anterior dislocations, which result from indirect forces, are more common (9:1 ratio).[5] The usual mechanism of injury ( Figure 50-20 ) involves an anterolateral force to the shoulder, followed by backward rolling, which levers the medial clavicle out of its articulation. Posterior dislocations ( Figure 50-21 ) can result from a direct blow to the medial clavicle (30%) or from a posterolateral force to the shoulder followed by inward rolling (70%). Posterior dislocations can be associated with life-threatening injuries within the superior mediastinum. Injuries to the SCJ can be graded into three types.[5] A grade I injury is a mild sprain secondary to stretching of the sternoclavicular and costoclavicular ligaments. A grade II injury is associated with subluxation of the joint (anterior or posterior) secondary to rupture of the sternoclavicular ligament. The costoclavicular ligament remains intact. Complete rupture of the sternoclavicular and costoclavicular ligaments results in a grade III injury (dislocation). In patients younger than age 25, these actually represent Salter Type I injuries because the medial epiphysis of the clavicle has not yet fused.[35]
Page 235
Figure 50-20 Mechanism s that produce anterior and posterior displacem ents of the sternoclavicular joint. A When the patient is lying on the ground and a com pression force is applied to the posterolateral aspect of the shoulder, the medial end of the clavicle is displaced posteriorly. B When the lateral compression force is directed from the anterior position, the medial end of the clavicle is dislocated anteriorly. The same m echanism could apply with any type of lateral compression injury of the shoulder. ((From Neer CS, Rockwood CA: Fracture and dislocations of the shoulder. In Rockwood CA, Green DP [eds]: Fractures in Adults, 4th ed. Philadelphia, JB Lippincott, 1984.)JB Lippincott)
Figure 50-21 CT scan shows posterior dislocation of the right sternoclavicular (arrow) joint with com pression of the superior m ediastinum . ((Courtesy of Donald Sauser, MD.))
Clinical Features Clinical suspicion is the most important factor in diagnosing these injuries, and prompt diagnosis is vital because it is associated with a better prognosis. Patients have the injured extremity foreshortened and supported across the trunk by the opposite arm. There is pain with any movement of the upper extremity or lateral compression of the shoulders. The SCJ is mildly swollen and tender to palpation. With an anterior dislocation, the displaced medial end of the clavicle may be palpable. Posterior dislocations are associated with more severe pain, and the neck is often flexed toward the injured side.[5] The clavicular notch of the sternum may be palpable, and there may be complaints of hoarseness, dysphagia, dyspnea, and weakness or paresthesias in the upper extremities. Rarely, airway complications can occur. These patients should be examined thoroughly to identify any injuries to superior mediastinal or intrathoracic structures. When necessary, appropriate consultation should be obtained immediately.
Diagnostic Strategies: Radiology Although the diagnosis of sternoclavicular dislocations can be made clinically, it should be confirmed radiologically. Standard anteroposterior, oblique, and specialized (40-degree cephalic tilt) views are often difficult to interpret because of overlapping rib, sternum, and vertebral shadows. CT is best to visualize these dislocations and associated injuries (see Figure 50-21 ) or MRI.[15] Ultrasound also may be a useful adjunct in some circumstances.[5]
Management Treatment of grade I injuries includes immobilization (simple sling), adequate analgesia, and primary care follow-up. Immobilization generally is maintained (1 to 2 weeks) until full painless motion is restored. Grade II injuries should be immobilized with a sling or soft clavicular (figure-of-eight) splint and referred for orthopedic follow-up. The figure-of-eight splint is preferred because it maintains the clavicle in a more anatomic position. Grade II injuries require a longer course of immobilization (3 to 6 weeks) and are more likely to be associated with persistent pain.[] All grade III injuries should be managed by closed reduction. Anterior dislocations may be reduced in the emergency department after orthopedic consultation and intravenous analgesia ( Figure 50-22 ). A rolled sheet is placed posteriorly between the shoulder blades to elevate both shoulders approximately 5 cm above the table. Traction is applied to the arm in an extended (10- to 15-degree) and abducted (90-degree) position. If reduction does not occur, an assistant can add inward pressure on the medial end of the clavicle. Stable reductions should be maintained in a clavicular splint and referred for orthopedic follow-up.[] Most reductions are unstable. Because the deformity is primarily cosmetic and not functional, the current treatment of choice for recurrent anterior dislocations is benign neglect.
Page 236
Figure 50-22 Reduction of dislocated sternoclavicular joints. ((From Sim on RR, Koenigsknecht SJ: Em ergency Orthopedics: The Extrem ities, 2nd ed. Norwalk, Conn, Appleton & Lange, 1987.)Appleton & Lange)
Posterior dislocations are true orthopedic emergencies and should be reduced expeditiously.[5] Ideally, reduction of posterior dislocations should be attempted in the operating room under general anesthesia, although it can be attempted in the emergency department under conscious sedation. Emergency reduction may be required for patients with airway obstruction or vascular compromise. The patient is positioned as described previously, and traction is applied in an extended and abducted position. If traction alone does not reduce the dislocation, concurrent clavicular manipulation may be helpful. The skin is sterilely prepared, and the clavicle shaft is grasped with a sterile towel clip and pulled out anterolaterally. When reduced, these injuries are generally stable and can be immobilized with a clavicular splint. Buckerfield and Castle[36] described an alternate method of reduction for posterior dislocations. In this technique, traction is applied to the adducted arm while both shoulders simultaneously are forced posteriorly using direct pressure. This technique levers the clavicle into place and requires much less force than the traditional abduction-extension method.
Complications Complications of anterior injuries are primarily cosmetic. Twenty-five percent of posterior dislocations may be complicated by life-threatening injuries to intrathoracic and superior mediastinal structures. A potential long-term complication of both is degenerative osteoarthritis.
Acromioclavicular Joint Pathophysiology Injuries of the ACJ occur primarily in men and account for 25% of all dislocations about the shoulder girdle.[28 ] The annual incidence is 15 per 100,000, and most injuries result from participation in contact sports, such as football, rugby, ice hockey, and wrestling.[28] A small percentage of injuries are caused by motor vehicle accidents and falls. The most common mechanism of injury involves a fall or direct blow to the point of the shoulder with the arm adducted. The resultant force drives the scapula downward and medially to produce the injury. The weak acromioclavicular ligaments rupture first. With increasing force, the coracoclavicular ligament ruptures, and the attachments of the deltoid and trapezius muscles are torn from the distal clavicle. The ACJ also can be injured after a fall onto the outstretched hand. In this instance, the force is transmitted to the acromioclavicular ligaments only, and the coracoclavicular ligament, which is relaxed, remains uninjured.[37] The three-part Tossy and Allman classification system is based on the degree of damage sustained by the acromioclavicular and coracoclavicular ligaments ( Figure 50-23 ).[8] Type I injuries are sprains of the acromioclavicular ligaments. Type II injuries are associated with disruption of the acromioclavicular ligaments. The joint space is widened, and the clavicle displaces slightly upward. There are minor tears in the attachments of the deltoid and trapezius muscles, but the coracoclavicular ligament remains intact, and the coracoclavicular distance is maintained. A type III injury is characterized by complete disruption of the acromioclavicular ligaments, coracoclavicular ligament, and muscle attachments. The joint space is widened, and the coracoclavicular distance is increased. The clavicle is displaced upward by the pull of the trapezius, and the shoulder is displaced downward by the effect of gravity. Rockwood modified this three-part classification system by describing three additional types (IV, V, and VI) of ACJ injuries.[35] In type IV and V injuries, the ligamentous and muscle disruptions are similar to the disruptions encountered in type III injuries, but the clavicle displaces either posteriorly into the trapezius (type IV) or superiorly in an exaggerated fashion (type V). In the rare type VI injury, the clavicle displaces inferiorly.
Page 237
Figure 50-23 Mechanism of injury and classification of acromioclavicular joint injuries. A The direct force is applied to the point of the shoulder (1); the scapula and attached clavicle are forced downward and m edially; the clavicle approaches the first rib (2). If the force continues, the first rib abuts the clavicle, producing a counterforce (3). Depending on the magnitude of the force, a grade I, II, or III sprain m ay occur. B Grade I sprain. A few fibers of the acromioclavicular ligam ent stretch, and a few tear (1); the acrom ioclavicular joint is stable (2); the coracoclavicular ligam ent is intact (3). C Grade II sprain (subluxation). The capsule and the acrom ioclavicular ligam ent rupture (1); the joint is lax and unstable (2); the end of the clavicle rides upward, usually less than half of the width of the end of the clavicle (3); the coracoclavicular ligam ent rem ains intact (4); the attachm ents to the trapezius and deltoid rem ain intact. D Grade III sprain (dislocation). The capsule and acromioclavicular ligam ents rupture (1); the coracoclavicular ligam ent ruptures (2); the insertions of the trapezius and deltoid tear away (3); the clavicle rides upward (4); the interval between the clavicle and the coracoid process is greatly increased (5). ((From DePalm a AF: Surgery of the Shoulder, 3rd ed. Philadelphia, JB Lippincott, 1983.)JB Lippincott)
Clinical Features Patients should be examined while they are in the sitting or standing position because the supine position can mask ACJ instability. Type I injuries are associated with mild tenderness and swelling over the ACJ margin. No deformity occurs, and a full range of motion is usually possible, although painful. Type II injuries produce moderate pain, and the distal end of the clavicle may lie slightly superior or posterior to the acromion. Patients with type III, IV, V, and VI injuries usually have severe pain and hold the arm tightly adducted to reduce traction stress across the joint. In type III injuries, the shoulder hangs downward, and the clavicle rides high, producing a visible clinical deformity. In type IV injuries, the clavicle may be palpable posteriorly, and in type V injuries, the clavicle may be palpable subcutaneously above the acromion. In type VI injuries, the shoulder assumes a flattened clinical appearance.
Diagnostic Strategies: Radiology The energy settings used for the radiographic trauma series overpenetrate the ACJ. Specific ACJ views that use one third to two thirds less intensity should be ordered. The recommended projections include an anteroposterior view of both joints on a single wide film, an axillary lateral view, and a 15-degree cephalic tilt view.[] The axillary lateral view is useful for identifying associated fractures and posterior dislocation of the clavicle. The normal coracoclavicular distance varies between 11 and 13 mm. A difference of more than 5 mm between the injured and uninjured sides is diagnostic of a complete coracoclavicular disruption. Type I injuries have essentially normal radiographs. Type II injuries show widening of the joint and a slight upward or posterior displacement of the clavicle but a normal coracoclavicular distance. Type III, IV, and V injuries have a widened joint, an increased coracoclavicular distance, and either superior or posterior displacement of the clavicle ( Figure 50-24 ). Historically, stress views of the ACJ have been recommended to differentiate between type II and III injuries. Such views lack efficacy for this purpose, and their routine use is unnecessary.[38]
Figure 50-24 Third-degree sprain of the acrom ioclavicular joint. The coracoclavicular distance measures 18 m m (arrow). ((Courtesy of David Nelson, MD.))
Management Type I and II injuries should be immobilized in a sling for comfort and to protect against further injury. These patients should be referred for follow-up with their primary care physician. When pain has subsided (1 to 3 weeks), the patient can begin range-of-motion and strengthening exercises with a return to sports when pain-free function has been achieved.[8] Type IV, V, and VI injuries require early surgical treatment. The management of type III injuries has changed dramatically since the 1980s. Most studies have concluded that conservative treatment provides equal or, in some cases, better functional results than surgical intervention. In addition, surgical patients have longer recovery times and higher complication rates.[8] The main complications of conservative therapy are the persistence of nuisance symptoms (clicking or pain) and a
Page 238
cosmetic deformity. Selected patients who are young, have severe displacement (>2 cm), and perform repetitive overhead activities may be candidates for surgical intervention.[8] Treatment of type III injuries in the emergency department should consist of sling immobilization and early (<72 hours) orthopedic referral. The initial therapy in all cases should include adequate analgesia.
Complications The most common concurrent injuries are associated fractures of the clavicle and coracoid process. Osteoarthritis of the ACJ is a potential long-term complication of an acute injury.[8] Acromioclavicular arthritis typically presents as an impingement syndrome with shoulder pain between 120 and 180 degrees of abduction.
Glenohumeral Dislocations Perspective The glenohumeral joint is the most commonly dislocated major joint in the body. The lack of intrinsic bony stability in conjunction with its wide range of motion predisposes the joint to dislocations. The annual incidence is 17 per 100,000, and there are two distinct age peaks. The first is in men age 20 to 30 years, and the second is in women age 61 to 80 years.[39] The glenohumeral joint can dislocate anteriorly, posteriorly, inferiorly, or superiorly. Anterior dislocations account for 95% to 97% of all glenohumeral dislocations. Posterior dislocations account for most of the remainder, whereas inferior and superior dislocations are rare.
Anterior Dislocations Pathophysiology. Anterior dislocations can result from indirect or direct forces. The most common mechanism of injury consists of an indirect force transferred to the anterior capsule from a combination of abduction, extension, and external rotation. In younger individuals, the injury usually is sustained during athletic activities. In older patients, a fall onto the outstretched arm is more common.[28] Rarely a direct force applied to the posterolateral aspect of the shoulder can force the humeral head out of the glenoid fossa anteriorly. Anterior dislocations can be classified according to their etiology (traumatic or nontraumatic), frequency (primary or recurrent), and the anatomic position of the dislocated humeral head.[39] After dislocation, the humeral head can assume a subcoracoid, subglenoid, subclavicular, or intrathoracic position ( Figure 50-25 ). The subcoracoid is the most common type of anterior dislocation. The head is displaced anteriorly and rests on the scapular neck inferior to the coracoid process. The next most common type is the subglenoid dislocation, in which the head is anterior and inferior to the glenoid fossa. Together the subcoracoid and subglenoid types account for 99% of all anterior dislocations. Subclavicular and intrathoracic dislocations are extremely rare and involve the addition of strong lateral to medial forces that push the humeral head medially.
Figure 50-25 Types of anterior dislocation. A Subcoracoid. B Subglenoid. C Subclavicular. D Intrathoracic. ((From DePalm a AF: Surgery of the Shoulder, 3rd ed. Philadelphia, JB Lippincott, 1983.)JB Lippincott)
Clinical Features. The patient is in severe pain with the dislocated arm held in slight abduction and external rotation by the opposite extremity. The lateral edge of the acromion process is prominent, and the normally rounded shoulder assumes a “squared-off” appearance. The coracoid process is indistinct, and the anterior shoulder appears full. The patient leans away from the injured side and cannot adduct or internally rotate the shoulder even slightly without severe pain. A neurovascular examination is performed to identify associated injuries of the brachial plexus, axillary nerve, radial nerve, or axillary artery. The reported incidence of axillary nerve injuries after anterior glenohumeral dislocation ranges from 5% to 54%.[] Axillary nerve function can be
Page 239
assessed by testing for sensation over the lateral aspect of the shoulder and by testing motor function of the teres minor and deltoid muscles. Deltoid function is tested by having the patient attempt shoulder abduction while the examiner feels for muscle contraction. Motor testing is more accurate because sensory testing can be misleading owing to the presence of overlapping cutaneous nerve root dermatomes. Axillary nerve injuries occur more frequently in patients older than age 50 years.[41]
Diagnostic Strategies: Radiology. The trauma series of radiographs confirms the clinical diagnosis and identifies the position of the humeral head ( Figure 50-26 ). Associated fractures may be present in 50% of cases. The most common of these is a compression fracture of the posterolateral aspect of the humeral head caused by forceful impingement against the anterior rim of the glenoid fossa. This defect in the humeral head, or Hill-Sachs deformity (see Figure 50-26 ), is reported to be present in 11% to 50% of all anterior dislocations. The actual incidence is probably much higher because minor compression fractures are difficult to visualize on plain radiographs. The defect is best visualized on an internal rotation anteroposterior view of the glenohumeral joint. A corresponding fracture of the anterior glenoid rim (Bankart's fracture) is present in approximately 5% of cases.[10] Avulsion fractures of the greater tuberosity are present in 10% to 15% of cases.[]
Figure 50-26 Recurrent anterior subcoracoid dislocation with Hill-Sachs deform ity of the hum eral head (arrow).
Management. Closed reduction of the dislocation should be accomplished expeditiously because the incidence of neurovascular complications increases with time.[41] Radiographic documentation of the type of dislocation and any associated fractures should be obtained before attempting reduction. Reduction can be accomplished using various techniques, most of which involve traction, leverage, or scapular manipulation principles.[42] There are no good comparative studies of one reduction technique over another.[42] The ideal method should be simple, quick, and effective; require little assistance; and cause no additional injury to the shoulder. It is wise to be familiar with several techniques of reduction because none is uniformly successful. Good muscle relaxation is the key to a successful reduction in most settings. Muscle relaxation can be achieved using conscious sedation or interscalene, supraclavicular, or suprascapular nerve blocks.[43] Occasionally, reductions can be accomplished without the use of any analgesia, especially if the time from injury to reduction is short or if the dislocation is a recurrent one. Muscle relaxation and analgesia also can be provided through intra-articular injection of a local anesthetic agent.[] This technique is especially useful when conscious sedation is contraindicated and is associated with a shorter length of stay in the emergency department after reduction.[44] The joint is entered under sterile technique 2 cm inferior to the lateral edge of the acromion using an 18-gauge or 20-gauge needle. Any associated hemarthrosis is aspirated, then 20 mL of 1% lidocaine is injected over 30 seconds. The patient is allowed to relax for 15 minutes before reduction is attempted. Gentle traction in various directions (forward flexion, abduction, overhead, lateral) is used to overcome the muscle spasm that holds the humeral head in its dislocated position.[42] In the Stimson or hanging weight technique ( Figure 50-27 ), the patient is placed prone with the dislocated arm hanging over the edge of the examining table. A 10- or 15-lb weight attached to the wrist or lower forearm provides traction in forward flexion. Reduction usually occurs over 20 to 30 minutes. In the traction-countertraction method ( Figure 50-28 ), traction is applied along the abducted arm while an assistant using a folded sheet wrapped across the chest applies countertraction. The forward elevation maneuver of Cooper and Milch is also simple and safe. The arm is initially elevated 10 to 20 degrees in forward flexion and slight abduction. Forward flexion is continued until the arm is directly overhead. Abduction is increased, and outward traction is applied to complete the reduction.[45]
Page 240
Figure 50-27 Stim son or hanging weight m ethod of reduction for anterior dislocations.
Figure 50-28 Traction-countertraction m ethod for reducing anterior shoulder dislocations.
Another simple and effective traction technique is the Snowbird technique.[46] In this method, the patient is seated in a chair, and the affected arm is supported by the patient's unaffected extremity. A 3-foot loop of 4-inch cast stockinet is placed along the proximal forearm of the involved extremity with the elbow at 90 degrees. The patient is assisted or instructed to sit up, and the physician's foot is placed in the stockinet loop to provide firm downward traction. The physician's hands remain free to apply any gentle external pressure or rotation as needed until reduction is accomplished. The most commonly recommended leverage technique is the external rotation method of Liedelmeyer.[47] With the patient in the supine position, the involved arm is slowly and gently adducted to the side. The elbow is flexed to 90 degrees, and slow, gentle external rotation is applied to achieve reduction ( Figure 50-29 ).
Figure 50-29 External rotation technique. The involved arm is slowly adducted to the patient's side, and the elbow is flexed 90 degrees. Gentle external rotation is applied to the forearm to achieve reduction. ((From Sim on RR, Koenigsknecht SJ: Em ergency Orthopedics: The Extrem ities, 2nd ed. Norwalk, Conn, Appleton & Lange, 1987.)Appleton & Lange)
Scapular manipulation accomplishes reduction by repositioning the glenoid fossa rather than the humeral head. The patient is placed in the prone position with the affected arm hanging off the table as for the Stimson technique. After the application of downward traction (manual or hanging weights), the scapula is manipulated by rotating the inferior tip medially ( Figure 50-30 ), while stabilizing the superior and medial edges with the opposite hand.[48] McNamara[49] also described a seated modification of the scapular method in which traction is applied in the forward horizontal position while an assistant manipulates the scapula. Scapular manipulation can be difficult in heavyset individuals, in whom it is difficult to palpate and grasp the inferior tip of the scapula. More traditional techniques, such as the Hippocratic method (traction with the foot in the axilla) and the Kocher maneuver (leverage, adduction, and internal rotation), are no longer recommended because of a high incidence of associated complications (axillary nerve injury, humeral shaft and neck fractures, capsular damage).
Page 241
Figure 50-30 Proper hand position and direction of rotation during shoulder relocation using the scapular m anipulation technique. ((From Kothari RU, Dronen SC: The scapular manipulation technique for the reduction of acute anterior shoulder dislocations. J Em erg Med 8:625, 1990.))
The neurovascular examination must be repeated after any attempt at reduction. It also is generally recommended that radiographs be repeated to confirm reduction and to identify any associated fractures not apparent on prereduction films. More recent studies have questioned the need and cost-effectiveness of routine postreduction radiographs.[] The authors of these studies did not find any new clinically significant fractures on postreduction radiographs and argued that in most instances a successful reduction can be determined clinically by the presence of a palpable clunk, decrease in pain, and improvement in the range of motion. These findings must be confirmed in larger prospective studies before they are adopted as a standard of care. After reduction, the affected extremity is immobilized using a sling and swathe bandage or a Velpeau sling (see Figure 50-11 ). Patients should be discharged with adequate analgesia and appropriate follow-up. Primary dislocations and complicated cases (associated fracture, rotator cuff tear, axillary nerve injury) should receive orthopedic follow-up. In uncomplicated cases, the shoulder is immobilized for 3 to 6 weeks in younger patients and 1 to 2 weeks in older (>40 years old) individuals.[10] The traditional position of immobilization is with the shoulder in internal rotation. Studies suggest that this positioning may delay healing and is associated with a higher recurrence rate.[53] In a randomized clinical trial, Itoi and coworkers[54 ] found that 3 weeks of immobilization in 10 degrees of external rotation was associated with a zero recurrence rate at 13 to 15 months compared with a 30% recurrence rate with sling immobilization in internal rotation. If these preliminary findings are confirmed by additional trials, sling immobilization may be replaced by external rotation splints. Regardless of the immobilization technique, early initiation of shoulder exercises (see Figure 50-14 ) helps reduce the risk of adhesive capsulitis. A meticulous rehabilitation program aimed at restoring the static and dynamic stabilizers of the glenohumeral joint follows the period of immobilization.[10]
Complications. Complications include the aforementioned fractures and neurovascular injuries. Most axillary nerve injuries are neurapraxic, and the prognosis for recovery of function is good.[41] Rotator cuff tears may be present in 10% to 15% of cases.[55] Rotator cuff tears are especially common in primary dislocations in patients older than age 40. In this setting, failure to abduct the arm often is misdiagnosed initially as an axillary nerve injury. Most of these individuals require tendon and capsular repair to restore shoulder stability.[55] Recurrence also is a common complication after anterior dislocation, and patients younger than age 30 have a reported recurrence rate of 79% to 100%.[39] A Hill-Sachs deformity or glenoid rim fracture is associated with increased risk of recurrence.[10] Studies suggest that the traditional method of treatment (immobilization followed by physical therapy) is ineffective in preventing redislocation in young, highly athletic individuals. Arthroscopic studies of primary anterior dislocations in young, highly athletic individuals have detected a high incidence of anteriorinferior capsulolabral avulsions (Perthes-Bankart lesion) from the glenoid rim. This avulsion is believed to be the primary predisposing factor for recurrence, and these individuals seem to benefit from early arthroscopic repair of the lesion.[56] Recurrence rates decline with increasing age and in the presence of a greater tuberosity fracture.[10]
Anterior Subluxation Transient anterior subluxation of the shoulder is encountered often in young athletic adults. The patient complains of sudden sharp shoulder pain and weakness (dead arm syndrome) while performing an abduction and external rotation maneuver. The patient also may relate a sensation of the shoulder slipping in and out. Radiographs are usually normal, and a positive apprehension sign confirms the diagnosis. The latter is performed by gently reproducing the injury motion, abduction, and external rotation of the arm while applying an anterior force to the posterior shoulder ( Figure 50-31 ). This maneuver increases the pain and may cause anterior displacement of the humeral head. A lax or redundant anterior capsule is thought to be responsible for this syndrome, and recurrent episodes are common. These patients should be referred for orthopedic follow-up because definitive therapy (capsulorrhaphy) is surgical.[57]
Page 242
Figure 50-31 Technique for perform ing the shoulder apprehension test. ((From Sim on RR, Koenigsknecht SJ: Em ergency Orthopedics: The Extrem ities, 2nd ed. Norwalk, Conn, Appleton & Lange, 1987.)Appleton & Lange)
Posterior Dislocation Pathophysiology. Posterior dislocations are rare and account for 2% of all glenohumeral dislocations.[58] This rarity is explained partly by anatomy of the shoulder girdle. The 45-degree angulation of the scapula on the thoracic cage positions the glenoid fossa posterior to the humeral head and serves as a partial buttress against posterior dislocation. Greater than 50% of posterior dislocations are missed on initial evaluation, and many remain unrecognized (“locked posterior dislocations”) for weeks and months.[] A posterior dislocation can result from several distinct mechanisms of injury. Convulsive seizures (epileptic or after electrical shock) often are associated with unilateral or bilateral posterior dislocations. In this instance, the larger and stronger internal rotator muscles (latissimus dorsi, pectoralis major, teres major, subscapularis) overpower the weaker external rotators (teres minor, infraspinatus) to produce the injury.[59] A posterior dislocation also can occur after a fall onto the outstretched hand with the arm held in flexion, adduction, and internal rotation or after a direct blow to the anterior aspect of the shoulder. Acute posterior dislocations are classified into three types (subacromial, subglenoid, subspinous) based on the final resting position of the humeral head. The subacromial variety accounts for 98% of all posterior dislocations.[58]
Clinical Features. Early diagnosis is essential to prevent long-term functional and therapeutic complications. As mentioned, the initial examining physician misses the diagnosis with some regularity, in part because of an overreliance on radiologic findings and an underreliance on the clinical examination. The most common misdiagnosis is adhesive capsulitis.[] The patient holds the affected arm across the chest in adduction and internal rotation. Although usually painful, the injury can be relatively painless.[59] The normal shoulder contour is replaced by a flat, squared-off appearance, and the coracoid process is prominent and easily palpated. The humeral head may be palpable posteriorly beneath the acromion process. Abduction is severely limited, and external rotation is completely blocked.
Diagnostic Strategies: Radiology. Standard anteroposterior radiographs can appear deceptively normal with posterior dislocations. The common inability to diagnose posterior dislocation in the frontal plane has led to the description of several characteristic radiographic findings. Standard anteroposterior films show loss of the half-moon elliptical overlap of the humeral head and glenoid fossa. In addition, the distance between the anterior glenoid rim and the articular surface of the humeral head is increased (“rim sign”). The humeral head is profiled in internal rotation and takes on a “light bulb” or “drumstick” appearance. A true anteroposterior film shows abnormal overlap of the glenoid fossa with the humeral head ( Figure 50-32 ). Finally, an impaction fracture of the anteromedial humeral head (reverse Hill-Sachs deformity) is invariably present ( Figure 50-33 ). This fracture may produce a curvilinear density on the frontal projection parallel to the articular cortex of the humeral head (“trough sign”). An orthogonal view, such as an axillary lateral, transscapular, or apical oblique, confirms the diagnosis. The axillary lateral view or apical oblique view also identifies associated fractures of the humeral head and posterior glenoid rim. CT may be helpful in some instances.[61]
Figure 50-32 Overlap of the glenoid rim associated with posterior dislocation.
Page 243
Figure 50-33 Anteroposterior and axillary views of a posterior glenohum eral dislocation. Note the widened joint space (rim sign), anterom edial im paction fracture of the hum eral head, and curvilinear density parallel (arrow) to the articular surface (trough sign). ((Courtesy of Donald Sauser, MD.))
Management. Orthopedic consultation should be obtained for all patients with posterior dislocations. Closed reduction may be attempted in the emergency department under conscious sedation. The technique of reduction incorporates axial traction in line with the humerus, gentle pressure on the posteriorly displaced head, and slow external rotation. If this technique fails, reduction with the patient under general anesthesia is indicated. After reduction, the shoulder should be immobilized in external rotation with slight abduction.[60] Cases that were missed initially and present as a chronic or locked posterior dislocation should be referred to the orthopedist for follow-up. Locked posterior dislocations usually require open reduction and internal fixation or arthroplasty.[]
Complications. Fractures of the glenoid rim, greater tuberosity, lesser tuberosity, and humeral head account for most associated injuries. Rarely the subscapularis muscle may be avulsed from its insertion site on the lesser tuberosity. Neurovascular injuries are uncommon because the anterior location of the neurovascular bundle protects it from injury. Recurrent posterior dislocations occur in 30% of patients and predispose the joint to degenerative changes.
Inferior Glenohumeral Dislocation (Luxatio Erecta) Pathophysiology. Luxatio erecta is a rare type of glenohumeral dislocation in which the superior aspect of the humeral head is forced below the inferior rim of the glenoid fossa. It is estimated that 0.5% of all shoulder dislocations are of this variety. The mechanism of injury involves either direct or indirect forces.[] Application of a direct axial load to an abducted shoulder can disrupt the weak inferior glenohumeral ligament and drive the humeral head downward. Most inferior dislocations result from indirect forces, however, that hyperabduct the affected extremity[62]; this causes impingement of the humeral head against the acromion process. Further levering of the humeral shaft against the acromion ruptures the capsule and dislocates the head inferiorly ( Figure 50-34 ).
Figure 50-34 Luxatio erecta. A The m echanism by which this injury occurs in hyperabduction. B This is always accom panied by disruption of the rotator cuff and tear through the inferior capsule. ((From Sim on RR, Koenigsknecht SJ: Em ergency Orthopedics: The Extrem ities, 2nd ed. Norwalk, Conn, Appleton & Lange, 1987.)Appleton & Lange)
Clinical Features. Clinically the patient has the arm locked overhead in 110 to 160 degrees of abduction. The elbow is usually flexed, and the forearm typically rests on top of the head. The shoulder is fixed in this position, and any attempts at movement result in significant pain. The inferiorly displaced humeral head may be palpable along the lateral chest wall. A thorough neurovascular examination is essential.
Diagnostic Strategies: Radiology. Many cases of luxatio erecta are mistakenly diagnosed and treated as subglenoid anterior dislocations because the radiographic features of these two clinical entities are remarkably similar. Standard anteroposterior radiographs show the superior articular surface inferior to the glenoid fossa ( Figure 50-35 ).
Page 244
In addition, the humeral shaft characteristically lies parallel to the spine of the scapula on the anteroposterior view.[63] This radiographic feature is useful in distinguishing luxatio erecta from a subglenoid anterior dislocation because in the latter, the humeral shaft lies parallel to the chest wall. Associated fractures of the acromion, coracoid, clavicle, greater tuberosity, humeral head, and glenoid rim are common.
Figure 50-35 Anteroposterior view of an inferior glenohumeral dislocation. The hum eral shaft lies parallel to the spine of the scapula.
Management. If possible, orthopedic consultation should be obtained before attempting closed reduction under conscious sedation in the emergency department. Reduction usually can be accomplished using traction-countertraction maneuvers. Traction is applied in line with the humeral shaft, while an assistant applies countertraction across the shoulder ( Figure 50-36 ). Gentle abduction usually reduces the dislocation, and the arm is brought down into an adducted position. In rare instances, buttonholing of the capsule prevents closed reduction, necessitating open reduction.
Figure 50-36 Traction-countertraction m ethod for reduction of luxatio erecta humeri. The initial m aneuver (1) includes steady axial traction in line with the hum eral shaft position followed by gentle abduction. This reduces the glenohum eral dislocation. At this point (2), the arm is brought down to a position of adduction and internal rotation. ((From Davids JR, Talb ott RD: Luxatio erecta hum eri. Clin Orthop 252:144, 1990.))
Complications. Neurapraxic lesions of the brachial plexus are common, and thrombosis of the axillary artery has been associated with luxatio erecta.[62] Tears of the rotator cuff almost always accompany luxatio erecta and may require surgical repair. Adhesive capsulitis is a common long-term complication of luxatio erecta.
Scapulothoracic Dislocation Scapulothoracic dissociation is a rare and severe injury characterized by complete disruption of the scapulothoracic articulation. The mechanism of injury involves a strong traction force applied to the upper extremity (e.g., motorcyclist hangs onto the handlebars while body is forced away). Massive local soft tissue swelling associated with lateral displacement of the scapula is seen on the chest radiograph. Additional osseous injuries include acromioclavicular separation, displaced fractures of the clavicle, and dislocations of the SCJ. Associated neurovascular (subclavian or axillary vessels, brachial plexus) injuries are common and account for the poor functional outcomes associated with this injury.[64]
Soft Tissue Conditions Subacromial Syndromes and Impingement (Rotator Cuff Tendinitis, Subdeltoid/Subacromial Bursitis) Pathophysiology Rotator cuff tendinitis and subacromial bursitis can be considered part of a pathophysiologic continuum whose endpoint is represented by complete rupture of the rotator cuff. These two conditions are common causes of shoulder pain and have similar clinical presentations.[65] A key feature of their clinical presentation
Page 245
is the presence of an impingement or painful arc syndrome ( Figure 50-37 ).
Figure 50-37 Arcs of painful abduction: subacromial painful arc, 60 to 120 degrees; acrom ioclavicular painful arc, 120 to 180 degrees. ((From DePalm a AF: Surgery of the Shoulder, 3rd ed. Philadelphia, JB Lippincott, 1983.)Appleton & Lange)
The subacromial space is the area between the coracoacromial arch and the greater tuberosity of the humerus. This space, which is only a few millimeters wide, contains the long head of the biceps, the rotator cuff, and the subacromial bursa. The last-mentioned acts as the gliding mechanism between the musculotendinous cuff and the coracoacromial arch. The functional arc of shoulder elevation is forward, which normally leads to impingement of the cuff and bursa under the anterior third of the coracoacromial arch. Similar impingement also occurs between 60 and 120 degrees of abduction and with the extremes of adduction. The critical wear from impingement is centered on the supraspinatus tendon, near its insertion on the greater tuberosity.[66] Micro-opaque injection studies also have shown a relative avascularity within this “critical” area. The hypovascularity in conjunction with repeated wear and age-related degenerative changes ultimately results in rotator cuff tendinitis. Narrowing of the subacromial space (anatomic variants of anterior acromion) and occupations that require excessive overhead activity accelerate the entire process. With time, the inflammatory reaction spreads to involve the adjacent bursa. This inflammation leads to edema, thickening, and fibrosis, further narrowing the subacromial space (secondary impingement); this is eventually followed by attritional changes within the rotator cuff. Because the rotator cuff is a primary humeral head depressor, loss of function adds to the secondary impingement process.[65] The impingement process also may involve the long head of the biceps. If so, bicipital tenosynovitis, degeneration, or rupture may be present. In some cases, osteoarthritis of the ACJ can narrow the subacromial space and accelerate the pathologic process. Impingement in this context occurs between 120 and 180 degrees of abduction (see Figure 50-37 ).
Clinical Features Neer[66] classified the progressive pathologic processes underlying subacromial syndromes into three stages ( Table 50-2 ). The impingement sign ( Figure 50-38 ) is positive in all three stages. Patients in stage 1 complain of a dull ache around the deltoid area after strenuous activity. On examination, tenderness is present over the supraspinatus and anterior acromion. A painful arc of abduction between 60 and 120 degrees is characteristic. Table 50-2 -- Three Progressive Stages of Impingement Lesions Stage
Pathology
Age (yr)
Course
Treatment
I II
Edema, hemorrhage <25
Reversible
Conservative
Fibrosis, tendinitis
Recurrent pain with Conservative, activity surgical
III
Bone spurs, tendon >40 rupture
25–40
Progressive disability
Surgical
Figure 50-38 Im pingem ent injection test. The im pingem ent sign is elicited with the patient seated and the exam iner standing. Scapular rotation is prevented with one hand, while the other hand raises the arm in forced forward elevation, causing the
Page 246
greater tuberosity to im pinge against the acrom ion. This m aneuver produces pain in patients with im pingem ent lesions of all stages. It also causes pain in m any other shoulder conditions. In the case of impingem ent lesions, the pain caused by this m aneuver is relieved by the injection of 10 m L of 1% lidocaine beneath the anterior acrom ion. This test is useful in separating im pingem ent lesions of all stages from other causes of shoulder pain. ((Redrawn from Neer CS: Im pingem ent lesions. Clin Orthop 173:70, 1983.))
Stage 2 is characterized by more persistent pain that is particularly severe at night. The inflammatory process within the bursa and tendons leads to the formation of minor adhesions. Disruption of these adhesions is thought to account for the nighttime pain. Physical findings are similar to those of stage 1. In addition, bursal thickening leads to increased soft tissue crepitus within the glenohumeral joint. The hallmark of stage 3 is significant tendon degeneration after a prolonged history of tendinitis and bursitis. Findings in this stage are discussed in the section on tears of the rotator cuff. Radiographs are usually normal in stages 1 and 2. Findings in stage 3 are similar to those seen with complete tears of the rotator cuff. The differential diagnosis of subacromial syndromes is extensive and includes intrinsic and extrinsic causes of shoulder pain. Extrinsic sources include the cervical spine, lung, heart, and diaphragm. Intrinsic conditions include acromioclavicular arthritis, adhesive capsulitis, calcific tendinitis, and traumatic anterior subluxation. A positive impingement sign may be present in many of these conditions. Relief of pain after the subacromial injection of 10 mL of 1% lidocaine (impingement test [see Figure 50-38 ]) helps localize the condition to the subacromial space.
Management Initial treatment in stage 1 is conservative and consists of rest, nonsteroidal anti-inflammatory drugs (NSAIDs), and modification of activities that produce impingement. In stage 2, emphasis is on maintaining flexibility and range of motion through physiotherapy and rotator cuff strengthening exercises. Patients with stage 1 and 2 disease who present to the emergency department reporting treatment failure with NSAIDs may benefit from a subacromial injection of corticosteroids. Refractory stage 2 and some stage 3 patients may require decompression surgery to control pain. Patients with stage 2 and 3 disease may benefit from referral to an orthopedist for more detailed evaluation and treatment.
Rotator Cuff Tears Pathophysiology The rotator cuff acts as a dynamic stabilizer of the glenohumeral joint.[67] Its primary function is to hold the humeral head in place throughout the full range of motion (see Figure 50-5 ). In addition, it contributes power in all directions and is responsible for specific movements. The infraspinatus and teres minor act as external rotators, whereas the subscapularis is an internal rotator. The supraspinatus is essential for the first 30 degrees of shoulder abduction. The tenuous blood supply of the rotator cuff, abusive tensile overload, and chronic wear under the coracoacromial arch predispose it to age-related degenerative changes. The advanced stage of this process is characterized by complete rupture of the rotator cuff. The role of impingement in the development of rotator cuff tears is controversial. Primary impingement (e.g., acromial variance) is uncommon, but when present accelerates the degenerative process. More often, weakening or rupture of the cuff with age allows for superior migration of the humeral head, which results in secondary impingement. This impingement produces secondary changes within the subacromial space and symptoms characteristic of the painful arc syndrome.[68] Most tears involve the dominant arm and occur in men older than age 40 years. The occupational history is significant for strenuous work requiring overhead activity. Most tears occur near the attachment of the supraspinatus and can extend anteriorly into the subscapularis or posteriorly into the infraspinatus. Tears can be classified according to their size, completeness, pattern location, or duration. A clinically useful system is to divide tears into acute or chronic types. Acute tears (10%) usually are associated with a specific traumatic event. Often no history of previous shoulder problems exists. The most common mechanism of injury is forced abduction associated with significant resistance; this usually occurs when the patient attempts to break a fall with an outstretched hand. Alternatively the tendon rupture may occur while lifting a heavy object or after falling directly onto an immovable object.[69]
Page 247
Clinical Features The patient complains of a sudden tearing sensation in the shoulder followed by severe pain that radiates into the arm. Pain and secondary muscle spasm limit shoulder motion. Physical findings depend on the completeness, size, and location of the tear. Point tenderness is usually present over the site of rupture (greater tuberosity). A palpable defect also may be present. Subacromial injection of 10 mL of 1% lidocaine eliminates pain and allows for proper evaluation of motor function. The patient with a large tear cannot initiate shoulder abduction. A discrepancy between active and passive range of motion is highly suggestive of a rotator cuff tear.[69] The drop-arm test, performed by passively abducting the arm to 90 degrees and asking the patient to hold the arm in this position, is positive with significant tears. Slight pressure on the distal forearm or wrist causes the patient to drop the arm suddenly. The acute pain resulting from hemorrhage and spasm subsides over a few days. Repeat examination at this point confirms the loss of function in significant tears. Chronic tears account for approximately 90% of all lesions. Chronic tears are attritional and more insidious in their presentation. Early findings include a painful arc syndrome as a result of secondary impingement. The pain is worse at night and interferes with sleep. Worsening pain is followed by the gradual onset of weakness in the arm. Flexion and abduction are affected first. The patient attempts to initiate abduction using scapulothoracic movement. Internal rotation is weakened by anterior extension of the tear. Posterior extension compromises external rotation. The drop-arm test is positive with large tears, and there may be atrophy of the supraspinatus and infraspinatus muscles.
Diagnostic Strategies: Radiology Radiographs may be normal in acute and chronic tears, but more often they show evidence of nonspecific degenerative changes within the glenohumeral joint and subacromial space. The greater tuberosity can have a sclerotic or cystic appearance. Osteophytic spurs and sclerosis of the undersurface of the acromion may narrow the subacromial space. The hallmark of a complete tear is superior displacement of the humeral head. This displacement is best seen on an external rotation view. The normal distance from the superior aspect of the humerus to the undersurface of the acromion varies from 7 to 14 mm. A distance of less than 6 mm is highly suggestive of a complete tear. Outpatient MRI, ultrasound, or an arthrogram can confirm the diagnosis.
Management Acute tears should be immobilized in a sling and referred promptly for orthopedic follow-up. Early surgical repair (<3 weeks) is preferred in these instances, especially for a young or active individual. The management of chronic tears includes pain control and a shoulder rehabilitation program. Painful arc symptoms may respond to the subacromial injection of a corticosteroid preparation. Orthopedic follow-up is essential because patients with persistent pain and weakness may require surgical repair.
Lesions of the Biceps Muscle The biceps is composed of two heads. The long head originates from the supraglenoid tubercle and glenoid labrum and ascends over the humeral head to enter the arm via the bicipital groove. The long head is covered by a synovial sheath and is held in place within the groove by the coracohumeral and transverse humeral ligaments. The short head of the biceps originates from the coracoid process and inserts with the long head onto the tuberosity of the radius. The biceps is responsible for flexion and supination at the elbow.
Bicipital Tenosynovitis Pathophysiology. Anatomically the long head of the biceps is subject to the same stresses as the rotator cuff within the subacromial space. Irritation and microtrauma as a result of repetitive elevation or abduction of the shoulder produce an inflammatory reaction within the synovial sheath. Bicipital tenosynovitis usually is associated with other acromial arch impingement conditions (e.g., subacromial bursitis and rotator cuff tendinitis).[70] The typical patient is middle-aged and involved in an occupation or recreational activity that requires overhead movement. The patient complains of pain in the anterior part of the shoulder that radiates into the upper arm. The pain usually is initiated by some minor traumatic event involving forceful contraction of the biceps. Pain increases with activity and decreases with rest. Abduction and external rotation in particular are painful. Pain increases at night and interferes with sleep.
Clinical Features On examination, tenderness is present over the biceps tendon as it passes through the bicipital groove. This is best shown with the arm in abduction and external rotation. Active range of motion is limited by pain, but
Page 248
the passive range remains intact. Supination against resistance (Yergason's test) with the arm adducted and the elbow flexed to 90 degrees reproduces the pain ( Figure 50-39 ). The biceps resistance test in which forward flexion of the shoulder (elbow extended and forearm supinated) is carried out against resistance also produces pain in the bicipital groove.
Figure 50-39 Yergason's test. Flexion of the elbow and supination of the forearm against resistance causes pain in the anterior and inner aspect of the shoulder. ((From DePalm a AF: Surgery of the Shoulder, 3rd ed. Philadelphia, JB Lippincott, 1983.)Appleton & Lange)
Diagnostic Strategies: Radiology. Radiographs may show evidence of subacromial space impingement by associated acromioclavicular arthritis, inferior subluxation of the clavicle, and inferior acromial osteophytes.
Management. Emergency treatment consists of immobilization in a sling and anti-inflammatory medication. Gentle stretching exercises are encouraged, and refractory or progressive cases should be referred to an orthopedic surgeon. Although the bicipital sheath can be injected with a corticosteroid preparation, the procedure is technically difficult. Subacromial decompressive surgery and biceps tenodesis may be necessary in patients who fail to respond to conservative therapy.[71]
Ruptures of the Biceps Tendon Pathophysiology. Ruptures of the biceps tendon can be classified into proximal and distal types. Distal ruptures are rare and are not discussed. Proximally, microtears and other age-related attritional changes within the long head predispose it to rupture.[69] The rupture can be spontaneous or may follow a traumatic event involving either forced extension or resisted supination and flexion.
Clinical Features. The classic history of an acute rupture is that of a sudden snap or pop, followed by pain and ecchymosis in the region of the bicipital groove. The tendon usually ruptures at its weakest point, which is just distal to the exit from the glenohumeral joint cavity. With a complete rupture, distal retraction of the muscle results in a “Popeye” appearance of the arm. A difference in muscle contour (Ludington's test) also may be seen when both arms are placed behind the head and the biceps muscles are contracted.[72] Functionally, forearm supination is weakened, but elbow flexion stays strong because the coracobrachialis and short head of the biceps remain intact. Most ruptures also are associated with a rotator cuff tear.
Diagnostic Strategies: Radiology. Radiographs are usually unremarkable, and the confirmatory test of choice is MRI.
Management. The injured arm should be immobilized in a sling with the elbow in 90 degrees of flexion. The local application of ice may provide temporary relief. Analgesia should be provided, and the patient should be referred to an orthopedic surgeon within 72 hours for further evaluation and treatment. Surgical repair is a consideration in young, active individuals. In older individuals, conservative therapy (range-of-motion and strengthening exercise) is preferred because the cosmetic deformity is minimal, and the mild functional loss is usually acceptable.
Subluxation and Dislocations of the Biceps Tendon Subluxations and dislocations of the biceps tendon usually are associated with a congenitally shallow bicipital groove or atraumatic (attritional) tears of the coracohumeral and transverse humeral ligaments. The
Page 249
patient complains of a snapping sensation in the upper arm with abduction and external rotation. External and internal rotation of the abducted shoulder shows dislocation and relocation of the tendon. With complete dislocation, the arm may reflexively drop to relocate the tendon. These conditions may require operative repair and should be referred to an orthopedist.
Calcific Tendinitis Pathophysiology Rotator cuff calcific tendinitis is encountered frequently in the emergency department. The condition occurs in the 40s and 50s and is rare in individuals younger than age 30 or older than age 60. Calcific deposits occur primarily in the supraspinatus tendon near its attachment to the greater tuberosity. Deposits also may involve the infraspinatus, teres minor, or subscapularis tendons. Initially the tendon undergoes fibrocartilaginous transformation. The precipitating factors for this change are unclear and may involve hypoxia or stress-related degenerative changes within the tendon.[73] Calcium crystals are deposited and coalesce within the matrix of the tendon. Subsequent invasion of vascular channels into the deposit allows for the influx of neutrophils and macrophages (inflammatory response), which remove the calcification through phagocytosis. Finally, fibroblasts migrate into the area to create a postcalcification scar.[74]
Clinical Features The clinical presentation can be divided into silent, subacute, and acute phases based on the physical characteristics of the calcific deposits and the nature of the inflammatory response within the tendon and subacromial bursa. The silent phase consists of a dry powdery deposit with no surrounding inflammatory reaction. It is usually an incidental diagnosis when shoulder radiographs are obtained for other purposes. The deposits may remain painless and eventually reabsorb. The painful arc syndrome is a hallmark of the subacute phase. Enlargement and softening of the deposit narrows the subacromial space, resulting in impingement under the acromial arch. Pain between 60 and 120 degrees of abduction (see Figure 50-37 ) is characteristic. A severe inflammatory reaction within and around the deposit produces the acute phase. The deposit becomes milky and has the appearance of an acute abscess. The patient has severe pain with the arm held close to the chest. Active and passive range of motion is severely limited. The shoulder is warm and extremely tender to the touch. Severe pain is related to increased intratendinous pressure, and spontaneous rupture of the deposit into the subacromial bursa can provide dramatic relief of symptoms.
Diagnostic Strategies: Radiology Radiographs show calcific deposits in the involved tendon. For the supraspinatus, calcific deposits are best seen on the internal and external rotation anteroposterior views. The axillary view is useful for showing calcification within the other tendons of the rotator cuff.
Management Subacute symptoms usually respond to NSAIDs and measures to limit any offending activity. The acute phase should be treated with sling immobilization, NSAIDs, and analgesia. Subacromial injection of a local anesthetic may provide dramatic temporary relief. Needle lavage (puncturing of the calcific deposits to decrease intratendinous pressure) also has been described as an effective treatment.[73] The subacromial injection of corticosteroids for impingement symptoms is controversial because these agents may delay the process of calcium resorption and interfere with the natural course of the condition. Patients with chronic symptoms may benefit from extracorporeal shock wave therapy or surgical removal of the calcific deposit.[75 ] Early shoulder range-of-motion exercises should be encouraged in all patients to minimize the risk of adhesive capsulitis. All symptomatic patients should receive orthopedic follow-up.
Adhesive Capsulitis Pathophysiology Adhesive capsulitis is a specific diagnostic entity characterized by an inflammatory reaction within the capsule and synovium of the glenohumeral joint. This inflammatory reaction results in the formation of adhesions within the capsule and inferior axillary fold. Adhesive capsulitis must be differentiated from other, more common causes of the painful stiff shoulder; this is important because any painful condition of the shoulder (e.g., calcific tendinitis, rotator cuff tear, osteoarthritis, or trauma) may be associated with decreased range of motion.[76] Although the cause of adhesive capsulitis is unknown, any condition associated with prolonged dependency of the arm can result in capsular contraction, including voluntary immobilization after calcific tendinitis, rotator cuff injury, mastectomy, or a distal upper extremity injury
Page 250
(Colles' fracture).
Clinical Features The typical patient is a woman between 40 and 60 years old. The nondominant arm is usually affected, and the patient has trouble with the activities of daily living. The pain is often severe at night and localized over the deltoid area. There is uniform limitation of all glenohumeral movement, especially abduction and internal and external rotation. On passive testing, a sense of mechanical restriction of joint motion is present. The shoulder radiographs are usually normal if there is no associated condition.
Management The best form of therapy is preventive. Prolonged immobilization must be avoided, and early motion of the shoulder should be encouraged in all instances (see Figure 50-14 ). Treatment of adhesive capsulitis in the emergency department consists of NSAIDs and referral to an orthopedic surgeon. The diagnosis usually is confirmed by an arthrogram, which shows obliteration of the axillary fold and a reduction in the joint volume. Initial therapy is usually conservative and consists of a gentle assisted exercise program. Some patients require shoulder manipulation under anesthesia to improve the range of motion.
Injection Therapy The local injection of corticosteroid preparations can be useful in many painful conditions that affect the shoulder, including rotator cuff tendinitis and subacromial bursitis. Evidence-based research that supports or refutes the use of injection corticosteroid therapy is limited.[77] Although useful for relieving the inflammatory reaction, corticosteroid injections in general do not alter the underlying disease process. Corticosteroids inhibit all phases of the inflammatory response, including leukocyte migration, edema formation, mediator release, vascular permeability, collagen deposition, and fibroblast proliferation. Systemic complications are rare after local injection therapy. Site-specific complications include articular cartilage damage and subcutaneous atrophy. The incidence of local complications correlates with the injection technique, dose used, and frequency of administration. Direct tendon injection must be avoided at all times, and the frequency of injections should be limited to four injections per year.[78] Numerous corticosteroid preparations are available on the market ( Table 50-3 ). Injection of a long-acting agent or a combination of a short-acting and long-acting agent is preferred. The dose used depends on the size of the joint or bursa and the response of the individual. Concurrent use of a local anesthetic agent may provide acute pain relief and allow for better diffusion of the steroid preparation. Table 50-3 -- Potency, Duration of Action, and Dose of Commonly Used Corticosteroid Preparations Preparation (Trade Relative Potency Name)
Duration of Action Preparation (Suspension) (mg/mL)
Subacromial Dose (mg)
Hydrocortisone acetate (Hydrocortone) Betamethasone sodium phosphate and acetate (Celestone Soluspan) Methylprednisolone acetate (Depo-Medrol) Triamcinolone acetonide (Kenalog-10) Triamcinolone hexacetonide (Aristospan) Triamcinolone diacetate (Aristocort)
1
Short
50 mg/mL
25–37.5
25
Short/long
6
6
5
Long
40
40–80
5
Long
10 mg/mL
10–20
5
Long
20 mg/mL
20
5
Long
25
25
Page 251
Preparation (Trade Relative Potency Name)
Duration of Action Preparation (Suspension) (mg/mL)
Subacromial Dose (mg)
Dexamethasone acetate (Decadron-LA)
Long
4–16
25
8
After injection, the shoulder should be immobilized, and activity should be limited for several days to protect against further injury. Improvement usually begins within 1 to 7 days and can last weeks to months, depending on the preparation and underlying condition. Local anesthetic injection may result in a dramatic temporary improvement in symptoms.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/114.html/top
Page 252
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
KEY CONCEPTS {, {, {,
{, {, {, {, {, {, {, {,
The most important aspect of scapular fractures is the high incidence of associated injuries to the ipsilateral lung, chest wall, and shoulder girdle complex. Posterior SCJ dislocations can be associated with life-threatening injuries within the superior mediastinum, and the preferred imaging technique is a CT scan. If the coracoclavicular distance exceeds 10 to 13 mm, or there is a difference of more than 5 mm in this distance between the injured and the uninjured sides, a grade III ACJ dislocation should be suspected. Most studies have concluded that conservative treatment of type III ACJ dislocations provides equal or, in some cases, better functional results than surgical intervention. A compression fracture of the posterolateral aspect of the humeral head (Hill-Sachs deformity) is present in a large percentage of anterior glenohumeral dislocations. Good muscle relaxation is the key to success in the reduction of anterior glenohumeral dislocations. Axillary nerve function is best evaluated by motor function of the deltoid muscle. Recurrence is a common complication after anterior dislocation, especially in patients younger than age 30 years, and such individuals may benefit from arthroscopic repair. A posterior dislocation should be suspected in any individual who complains of shoulder pain after a convulsive episode. It is important to evaluate the relationship between the spine of the scapula and the longitudinal axis of the humerus to avoid missing an inferior glenohumeral dislocation. Early initiation of passive shoulder range-of-motion exercises helps reduce the risk of adhesive capsulitis.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/115.html/top
Page 253
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
REFERENCES 1. Hussein MK: Kocher's method is 3,000 years old. J Bone Joint Surg Br1968;50:669. 2. Rowe CR: Historical development of shoulder care. Clin Sports Med1983;2:231. 3. Simon RR, Koenigsknecht SJ: Emergency Orthopedics: The Extremities, 4th ed. Norwalk, Conn, McGraw-Hill, 2001. 4. Tibone JE: Shoulder problems of adolescents: How they differ from those of adults. Clin Sports Med 1983;2:423. 5. Yeh GL, Williams GR: Conservative management of sternoclavicular injuries. Orthop Clin North Am 2000;31:189. 6. Neer CS, Rockwood CA: Fracture and dislocations of the shoulder. In: Rockwood CA, Green DP, ed. Fractures in Adults, 4th ed. Philadelphia: JB Lippincott; 1996: 7. McKoy BE, Bensen CV, Hartsock LA: Fractures about the shoulder: Conservative management. Orthop Clin North Am2000;31:205. 8. Clarke HD, McCann PD: Acromioclavicular joint injuries. Orthop Clin North Am2000;31:177. 9. Cole PA: Scapular fractures. Orthop Clin North Am2002;33:1. 10. Wen DY: Current concepts in the treatment of anterior shoulder dislocations. Am J Emerg Med 1999;17:410. 11. Cleeman E, Flatow EL: Shoulder dislocation in the young patient. Orthop Clin North Am2000;31:217. 12. Brems-Dalgaard E, Davidsen E, Sloth C: Radiographic examination of the acute shoulder. Eur J Radiol 1990;11:10. 13. De Smet AA: Axillary projection in radiography of the nontraumatized shoulder. AJR Am J Roentgenol 1980;134:511. 14. Kornguth PL, Salazar AM: The apical oblique view of the shoulder: Its usefulness in acute trauma. AJR Am J Roentgenol1987;149:113. 15. Ernberg LA, Potter HG: Radiographic evaluation of the acromioclavicular and sternoclavicular joints. Clin Sports Med2003;22:255. 16. Robinson CM: Fractures of the clavicle in the adult: Epidemiology and classification. J Bone Joint Surg Br1998;80:476. 17. Nowak J, Mallmin H, Larsson S: The etiology and epidemiology of clavicular fractures: A prospective study during a two-year period in Uppsala, Sweden. Injury2000;31:353. 18. Anderson K: Evaluation and treatment of distal clavicle fractures. Clin Sports Med2003;22:319. 19. Andersen K, Jensen PO, Lauritzen J: Treatment of clavicular fractures. Acta Orthop Scand1987;57:71. 20. Nordqvist A: Shortening of the clavicle after fracture: Incidence and clinical significance, a 5-year follow-up of 85 patients. Acta Orthop Scand1997;68:349. 21. Hill JM, McGuire MH, Crosby LA: Closed treatment of displaced middle-third fractures of the clavicle gives poor results. J Bone Joint Surg Br1997;79:537. 22. Nordqvist A, Petersson CJ: Incidence and causes of shoulder girdle injuries in an urban population. J Shoulder Elbow Surg1995;4:107. 23. Ideberg R, Grevesten S, Larsson S: Epidemiology of scapular fractures: Incidence and classification of 338 fractures. Acta Orthop Scand1995;66:395. 24. Zuckerman JD, Koval KJ, Cuomo F: Fractures of the scapula. Instr Course Lect1993;42:271. 25. Ada JR, Miller ME: Scapular fractures: Analysis of 113 cases. Clin Orthop1991;269:174. 26. Stephens NG: Significance of scapular fracture in the blunt trauma patient. Ann Emerg Med1995;26:439. 27. Court-Brown CM, Garf A, McQueen MM: The epidemiology of proximal humeral fractures. Acta Orthop Scand2001;72:365. 28. Nordqvist A, Petersson CJ: Incidence and causes of shoulder girdle injuries in an urban population. J Shoulder Elbow Surg1995;4:107. 29. Neer CS: Displaced proximal humeral fractures: Part 1. Classification and evaluation. J Bone Joint Surg Am1979;52:1077. 30. Williams GR, Wong KL: Two-part and three-part fractures: Open reduction and internal fixation versus closed reduction and percutaneous pinning. Orthop Clin North Am2000;31:1. 31. Ferkel RD, Hedley AK, Eckardt JJ: Anterior fracture-dislocation of the shoulder: Pitfalls in treatment. J
Page 254
Trauma1984;24:363. 32. Burgos Flores J: Fractures of the proximal humeral epiphysis. Int Orthop1993;17:16. 33. Williams DJ: The mechanisms producing fracture-separation of the proximal humeral epiphysis. J Bone Joint Surg Br1981;63:102. 34. DePalma AF: Surgery of the Shoulder, 3rd ed. Philadelphia, JB Lippincott, 1983. 35. Garretson RB, Williams GR: Clinical evaluation of injuries to the acromioclavicular and sternoclavicular joints. Clin Sports Med2003;22:239. 36. Buckerfield CT, Castle ME: Acute traumatic retrosternal dislocation of the clavicle. J Bone Joint Surg Am 1984;66:379. 37. Richards R: Acromioclavicular joint injuries. Instr Course Lect1993;42:259. 38. Bossart PJ: Lack of efficacy of weighted radiographs in diagnosing acute acromioclavicular separation. Ann Emerg Med1988;17:20. 39. Kroner K, Lind T, Jensen J: The epidemiology of shoulder dislocations. Arch Orthop Trauma Surg 1989;108:288. 40. Perron AD: Acute complications associated with shoulder dislocation at an academic emergency department. J Emerg Med2003;24:141. 41. Perlmutter GS: Axillary nerve injury. Clin Orthop1999;368:28. 42. Riebel GD, McCabe JB: Anterior shoulder dislocations: A review of reduction techniques. Am J Emerg Med1991;9:180. 43. Gleeson AP: Comparison of intra-articular lignocaine and a suprascapular nerve block for acute anterior shoulder dislocation. Injury1997;28:141. 44. Matthews DE, Roberts T: Intraarticular lidocaine versus intravenous analgesia for the reduction of acute anterior shoulder dislocations: A prospective randomized study. Am J Sports Med1995;23:54. 45. Janecki CJ, Shahcheragh GH: The forward elevation maneuver for reduction of anterior dislocation of the shoulder. Clin Orthop1982;164:177. 46. Westin CD: Anterior shoulder dislocation: A simple and rapid method for reduction. Am J Sports Med 1995;23:369. 47. Danzl DF: Closed reduction of anterior subcoracoid shoulder dislocation: Evaluation of an external rotation method. Orthop Rev1986;15:311. 48. Kothari RU, Dronen SC: The scapular manipulation technique for the reduction of acute anterior shoulder dislocations. J Emerg Med1990;8:625. 49. McNamara RM: Reduction of anterior shoulder dislocations by scapular manipulation. Ann Emerg Med 1993;22:1140. 50. Harvey RA, Trabulsy ME, Roe L: Are postreduction anteroposterior and scapula Y views useful in anterior shoulder dislocations?. Am J Emerg Med1992;10:149. 51. Hendey GW, Kinlaw K: Clinically significant abnormalities in postreduction radiographs after anterior shoulder dislocation. Ann Emerg Med1996;28:399. 52. Hendey GW: Necessity of radiographs in the emergency department management of shoulder dislocations. Ann Emerg Med2000;36:108. 53. Murrell GC: Treatment of shoulder dislocation: Is a sling appropriate?. Med J Aust2003;179:370. 54. Itoi E: A new method of immobilization after traumatic anterior dislocation of the shoulder: A preliminary study. J Shoulder Elbow Surg2003;12:413. 55. Neviaser RJ, Neviaser TJ, Neviaser JS: Anterior dislocation of the shoulder and rotator cuff rupture. Clin Orthop1993;291:103. 56. Taylor DC, Arciero RA: Pathological changes associated with shoulder dislocations: Arthroscopic and physical exam findings in first-time traumatic anterior dislocations. Am J Sports Med1997;25:306. 57. Rowe CR: Recurrent transient anterior dislocation of the shoulder. Orthop Clin North Am1988;19:767. 58. Heller KD: Posterior dislocation of the shoulder: Recommendation for a classification. Arch Orthop Trauma Surg1994;113:228. 59. Perrenoud A, Imhoff AB: Locked posterior dislocation of the shoulder. Bull Hosp Joint Dis1996;54:165. 60. Perron AD, Jones RL: Posterior shoulder dislocation: Avoiding a missed diagnosis. Am J Emerg Med 2000;18:189. 61. Wadlington VR, Hendrix RW, Rogers LF: Computed tomography of posterior fracture-dislocations of the shoulder: Case reports. J Trauma1992;32:113. 62. Grate Jr JrI: Luxatio erecta: A rarely seen, but often missed shoulder dislocation. Am J Emerg Med 2000;18:317. 63. Davids JR, Talbott RD: Luxatio erecta humeri. Clin Orthop1990;252:144. 64. Althausen PL: Scapulothoracic dissociation. Clin Orthop2003;416:237. 65. Morrison DS, Greenbaum BS, Einhorn A: Shoulder impingement. Orthop Clin North Am2000;31:285. 66. Neer CS: Impingement lesions. Clin Orthop1983;173:70. 67. SooHoo NF, Rosen P: Diagnosis and treatment of rotator cuff tears in the emergency department. J Emerg Med1996;14:309. 68. Nirschl RP: Rotator cuff surgery. Instr Course Lect1989;38:447.
Page 255
69. Brunelli MP, Gill TJ: Fractures and tendon injuries of the athletic shoulder. Orthop Clin North Am 2002;33:497. 70. Neviaser TJ, Neviaser RJ: Lesions of long head of biceps tendon. Instr Course Lect1981;30:250. 71. Curtis AS, Snyder SJ: Evaluation and treatment of biceps tendon pathology. Orthop Clin North Am 1993;24:33. 72. Travis RD, Doane R, Burkhead WZ: Tendon ruptures about the shoulder. Orthop Clin North Am 2000;31:313. 73. Hurt G, Baker Jr JrCL: Calcific tendinitis of the shoulder. Orthop Clin North Am2003;34:567. 74. Re LP, Karzel RP: Management of rotator cuff calcifications. Orthop Clin North Am1993;24:125. 75. Gerdesmeyer L: Extracorporeal shock wave therapy for the treatment of chronic calcifying tendonitis of the rotator cuff. JAMA2003;290:2573. 76. Neviaser RJ, Neviaser TJ: The frozen shoulder: Diagnosis and management. Clin Orthop1987;223:59. 77. Buchbinder R, Green S, Youd JM: Corticosteroid injections for shoulder pain. Cochrane Database Syst Rev2003;1:CD004016 78. Cardone DA, Tallia AF: Joint and soft tissue injections. Am Fam Physician2002;66:290.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/116.html/top
Page 256
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
Chapter 51 – Musculoskeletal Back Pain Michelle Lin
LOW BACK PAIN PERSPECTIVE Background Approximately 70% to 90% of adults during their lifetime experience acute low back pain, defined as pain lasting less than 6 weeks in duration.[] Frustrating for the medical practitioner and the patient, 85% of these patients have an unknown etiology for their pain.[3] These patients frequently are diagnosed with “acute lumbosacral strain,” “lumbago,” or “mechanical back pain.” These nonspecific, catch-all terms reflect the diagnostic challenge and lack of pathognomonic tests for low back pain. More accurately, these patients should be diagnosed with “idiopathic low back pain.” Regardless, most of these cases resolve spontaneously within 6 weeks. Based on more recent studies regarding the management of acute low back pain, the most significant discovery, contradictory to traditional teaching from the 1980s, is to avoid bed rest for these patients, including patients with sciatica symptoms.[] Management recommendations for chronic back pain remain controversial, however, and the condition accounts for a significant proportion of costs to the health care system.
Epidemiology In the ambulatory care setting, the medical complaint of back pain is the fifth most common reason for a visit to a physician's office, with 15 million annual visits in the United States.[6] Low back pain primarily affects adults 30 to 60 years old and has a tremendous impact on the economy and workforce productivity. Approximately 14% of all Americans take at least 1 day off of work secondary to back pain. For people younger than age 45 years, persistent chronic back pain ranks as the leading cause of disability among chronic ailments. For people age 45 to 64, it ranks third behind coronary disease and arthritis.[7] Patients with back pain generate an estimated $24 billion in annual medical expenses and $50 billion to $100 billion in total direct and indirect costs in the United States.[] The natural history of most cases of low back pain follows a benign and self-limited course. Approximately 70% to 90% of patients have complete resolution of pain within 6 weeks.[10] If the pain does not resolve within 3 months, however, it is unlikely to resolve after 12 months. The recurrence rate for pain is 66% to 84% within the first 12 months.[11] Risk factors for low back pain are continually being investigated. Data so far have been elusive and often contradictory.[] It seems that the most consistent risk factor for future back problems is a previous history of back problems. Heavy lifting, pushing and pulling, or vibration at work; poor job satisfaction; smoking; and family history all seem to predispose to future back problems, whether causal or merely linked.[] There also is early evidence of a genetic predisposition to lumbar disk disease.[17] Multiple other factors have been investigated, including body habitus, various occupations, and psychological profile, with conflicting results.[]
PRINCIPLES OF DISEASE Anatomy and Physiology The lumbosacral spine consists of five lumbar vertebrae and the sacrum. Moving from anterior to posterior, each vertebra can be divided into the cylindrical vertebral body, two pedicles, two transverse processes, two overarching laminae, and a spinous process. These structures surround the neural canal, which houses the spinal cord and nerve roots and has a midsagittal anteroposterior diameter of 15 to 23 mm. The paired superior and inferior articulating processes join the articulating processes one vertebral level above and below. Each articulation site is called a facet joint. An intervertebral disk interposes between each vertebral
Page 257
body, providing elasticity and stability to the vertebral column. Each disk consists of an inner colloidal gelatinous substance, the nucleus pulposus, and an outer capsule, the annulus fibrosus, which is thinner posteriorly than anteriorly ( Figure 51-1 ).
Figure 51-1 Lateral and axial views of lum bar vertebral anatom y.
Various ligaments and musculature also provide stability to the lumbosacral spine. The anterior and posterior longitudinal ligaments course along the anterior and posterior surfaces of the vertebral bodies. The posterior longitudinal ligament forms a border between the intervertebral disks and the neural canal. As expected, because this ligament thins as it runs inferiorly from L1 to S1, 95% of lumbar disk herniations occur at the L4-5 and L5-S1 levels, causing pain and neurologic deficit in the L5 and S1 distribution. Most herniations extrude posterolaterally to impinge a nerve root asymmetrically.[20] The ligamentum flavum courses just anteriorly to the laminae within the neural canal. With age, this ligament can thicken and cause spinal stenosis. The spinal cord ends at the L1-2 interspace and the lower cauda equina nerve roots extend inferiorly, exiting the sacral foramina as peripheral nerves to the lower extremity. Pain fibers supplying structures in the lumbosacral region primarily arise from the posterior rami and sinuvertebral nerves at each lumbar vertebral level. Uniquely the nucleus pulposus and inner annular fibers of the intervertebral disk lack any pain fibers.[21] This lack of pain fibers correlates consistently with magnetic resonance imaging (MRI) findings of disk pathology in 20% to 30% of asymptomatic patients. The significance of these findings is unclear.[]
Pathophysiology Most conditions of low back pain have no proven cause. It is estimated that 85% of patients have no definitive diagnosis and are presumed to have pain originating from the soft tissue, including the muscles and ligaments.[] The other 15% of patients with a known etiology have pain at the site of the (1) nerve root, (2) articular facets, or (3) bone itself. First, a spinal nerve root can become inflamed and painful with external impingement. Disk herniation, usually at the L4-5 and L5-S1 level, is the most common cause of sciatica (i.e., pain radiating down the posterior leg from sciatic nerve root irritation). As the disk starts to desiccate and degenerate, starting in the 30s, patients are more at risk for outward herniation of the nucleus pulposus and consequently nerve root impingement. With further aging, these disks progressively shrink in size. This corresponds to the finding that disk herniations typically are found in patients 30 to 50 years old. Local nerve ischemia from physical compression also may contribute to the inflammation and pain. Studies also show that the nucleus pulposus, when exposed during disk herniation, may directly cause local neural inflammation, leading to pain.[24] Nerve root impingement also can occur with spinal stenosis, a narrowing of the neural canal from congenital narrowing or, more often, from degenerative or hypertrophic changes of the disks, vertebrae, facet joints, and ligamentum flavum.[25] The two most emergent conditions causing nerve irritation are the cauda equina syndrome and a spinal epidural abscess. Cauda equina syndrome is a massive central disk herniation usually compressing multiple, bilateral nerve roots, causing back pain radiating to both legs, saddle anesthesia, and impaired bowel and bladder function. Emergent surgical decompression is indicated to preserve neurologic function. An epidural abscess similarly results in nerve root impingement, causing significant back pain. These rare infections develop most commonly from the hematogenous spread of Staphylococcus aureus.[20] Congenital and developmental spinal abnormalities also may cause back pain by nerve root inflammation in some cases, but much less frequently than was thought previously. Conditions such as kyphosis and scoliosis usually do not cause pain unless the degree of vertebral column misalignment is pronounced.[26] Similarly, spondylolisthesis (slippage of one vertebral body on another) does not usually cause pain if the slippage is less than 25% of the vertebral body depth. Even patients with higher grades of anterior slippage (anterolisthesis) rarely develop severe back pain. Although it is much less common, backward slippage (retrolisthesis) is almost always associated with back pain. Spondylolisthesis occurs most often at the
Page 258
L5-S1 level (82.1%), followed by the L4-5 level (11.3%) and the L3-4 level (0.5%).[27] Multifactorial causes of spondylolisthesis include degenerative changes and trauma. Spondylolisthesis is often associated with bilateral pars interarticularis defects in the affected vertebra (spondylolysis). Second, similar to any other joint in the body, degenerative changes of the synovial articular facets in the lumbosacral spine occur with age. The exact role of articular facet joints in back pain is unclear, however. Third, direct irritation of the vertebral bone and its periosteum can cause back pain. The causes for spondylitis (osteomyelitis of the axial skeleton) can range from a slowly progressing tuberculosis infection (Pott's disease) to a more acute bacterial infection. Typically, bacteria seed the bone from a hematogenous source, such as from a skin wound, urinary tract infection, or directly from intravenous drug use. The most common bacterial culprit is S. aureus. Primary and metastatic bone neoplasms can cause back pain from tumor infiltration into the bone. Primary bone tumors, such as multiple myeloma, are 25 times less frequent than metastatic disease.[28] Of the neoplasms, breast, lung, prostate, thyroid, lymphoma, and kidney are the most likely to metastasize to bone. Inflammatory conditions, such as ankylosing spondylitis and other arthropathies, and osteoporosis also can cause back pain. For osteoporosis, the generalized decrease in bone mineralization can cause pain from microfractures of the vertebral column. Referred pain, most commonly from intraperitoneal and retroperitoneal abdominal pathology, plays a significant role in back pain. Functional processes play a substantial role in back pain, especially for prolonged symptoms lasting more than 4 to 6 weeks. Functional causes range from fear, depression, and personality disorders to financial motivation. In such cases, there is no anatomic or pathophysiologic correlation with the reported pain. Chronic back pain is complex and multifactorial. Not only are the structural causes unclear,[29] but also the nonphysical factors are variable and difficult to determine. It is likely that many of these patients do have some kind of chronic pain. What is unknown is why chronic pain triggers depression, drug dependence, and malingering in some people but not others. One difference may be the degree of disruption that the condition causes in the patient's lifestyle. A normally active and athletic person who is incapacitated is more profoundly affected than someone who is normally sedentary. Psychological factors and compensation play a large role in the behavior of many patients with chronic back pain.[] Pediatric back pain results in a diagnosis more often than adult pain.[] Children complaining of back pain must be investigated. They may turn out to have spondylolysis with varying degrees of spondylolisthesis, Scheuermann's disease (kyphosis and osteochondritis of the vertebral end plates), infectious diseases, or neoplastic etiologies. Disk herniation in children is comparatively rare, but when it does occur, the presentation is similar to that seen in adults.[32]
CLINICAL FEATURES Signs and Symptoms A thorough history and physical examination are crucial in evaluating all patients with acute low back pain. The classic historical ( Table 51-1 ) and physical findings for various low back pain etiologies are reviewed in this section. Although most etiologies are benign, there are four that the Agency for Health Care Policy and Research has identified as “cannot miss” or “red flag” diagnoses—spinal fracture, cauda equina syndrome, spinal infection, and malignancy.[34] A methodical and focused approach to the history and physical examination can help assess the patient's pretest probability for each of these disease entities and determine whether further tests should be ordered. Table 51-1 -- Historical Clues for the Etiology of Low Back Pain Questions for Patient Potential Diagnosis Does the back pain radiate down past the knees? Is the pain worse with walking and better with bending forward and sitting? Do you have morning back stiffness that improves with exercise? Are you >50 years old? Has there been any recent history of blunt trauma?
Radiculopathy and likely a herniated disk Spinal stenosis Ankylosing spondylitis Osteoporotic fracture, spinal malignancy Fracture
Page 259
Questions for Patient
Potential Diagnosis
Do you take long-term corticosteroids? Do you have a history of cancer? Does your pain persist at rest? Has there been persistent pain for >6 weeks? Has there been unexplained weight loss? Is the pain worse at night? Are you immunocompromised? (HIV, alcoholic, diabetes) Have you had fevers or chills? Do you have pain, weakness, or numbness in both legs? Do you have bladder or bowel control problems?
Fracture, spinal infection Spinal metastatic malignancy Spinal malignancy, spinal infection Spinal malignancy Spinal malignancy Spinal malignancy, spinal infection Spinal infection Spinal infection Cauda equina syndrome Cauda equina syndrome
HIV, human immunodeficiency virus.
Uncomplicated Musculoskeletal Back Pain Most patients with back pain can be classified in the category of uncomplicated musculoskeletal back pain after excluding worrisome disease processes. Often, patients are unable to recall an inciting incident. The pain usually is characterized as an “ache” or “spasm” and is localized asymmetrically in the lumbar paraspinous muscle with radiation to the buttock or posterior thigh proximal to the knee. Movement exacerbates the pain, and rest relieves it. There is no associated deficit in sensation, strength, or bowel/bladder sphincter tone by history or examination. The only physical finding may be regional lumbosacral tenderness and a limited range of motion of the lower back. This diagnosis of exclusion is made only after ruling out the more worrisome causes of back pain.
Radiculopathy Approximately 1% of all low back pain patients exhibit signs of lumbar radiculopathy (i.e., nerve root irritation).[35] The most common etiology is a herniated lumbar disk; other causes include spinal stenosis, malignancy, and infection. The most common type of lumbar radiculopathy is sciatica—an L5 or S1 radiculopathy. Patients with sciatica describe their pain as radiating from the low back to the legs, distal to the knee. Such pain is characterized as “shooting,” “lancing,” “sharp,” or “burning.” Associated symptoms include focal numbness or weakness in one of the lower extremities. Exacerbating triggers include sitting, bending, coughing, and straining; relieving factors include lying supine and still. On physical examination, the patient frequently is tender in the sciatic notch. The straight leg raise (SLR) test is a fairly sensitive assessment tool to determine if the patient has sciatica. The SLR test is done with the patient supine and the legs extended. The symptomatic leg is passively raised, while keeping the knee straight. The presence of back pain, which radiates past the knee while the leg is elevated 30 to 70 degrees, suggests an L5 or S1 radiculopathy. If the SLR test results in isolated low back pain without radiation symptoms to the legs, however, it is considered to be a negative finding. A positive SLR test has a sensitivity of 80% but a low specificity of 40%, meaning that a negative result is fairly accurate in ruling out sciatica. Corroborative tests for sciatica include the “bowstring sign” (reproduction of pain with deep palpation in the midline popliteal fossa) and Laségue's sign (reproduction of pain with foot dorsiflexion while the leg is elevated just short of the pain threshold during the SLR test). As an alternative to the SLR test, with the patient in a seated position, the knee can be extended (“flip test”), which also should stretch the sciatic nerve. Reproduction of the pain often causes the patient to lean backward reflexively from the pain, almost “flipping” back into a supine position. A crossed SLR test is done by passively raising the patient's asymptomatic leg, while keeping the knee straight. The presence of pain radiating from the back to the opposite affected leg has a sensitivity of only 25% but a high specificity of 90% for sciatica, meaning that a positive crossed SLR result is almost pathognomonic for sciatica, whereas a negative result is nondiagnostic.[20] A reverse SLR test is performed to detect L3 or L4 radiculopathy. With the patient prone, each hip is
Page 260
passively extended. If there is irritation of the L3 or L4 nerve root, pain is elicited. In addition to stressing lumbar nerve roots, a thorough examination of the lower extremities detects subtle findings associated with radiculopathies. This examination includes mapping the distribution of pain and assessing individual nerve root function, specifically strength, sensation, and reflexes. For the sensory examination, the earliest deficit can be detected by examining the most distal aspect of the dermatome. Specifically, light touch and pinprick sensation should be tested in the medial foot (L4), the area between the great and second toe (L5), and the lateral foot (S1) ( Figure 51-2 ).
Figure 51-2 Physical exam ination findings for L3-S1 radiculopathy. The “X” m arks the ideal location to test for sensation for each nerve root. C-SLR, crossed straight leg raise; R-SLR, reverse straight leg raise; SLR, straight leg raise.
Herniated Disk Patients with herniated lumbar disks are usually 30 to 50 years old and often have a long history of recurrent nonradicular low back pain, theoretically from irritation of the outer annular fibers of the disk. When the nucleus pulposus of the disk prolapses through the annulus fibrosus, local nerve root inflammation and radiculopathy result. Coughing, sitting, and any movement in general exacerbate the patient's pain and radiculopathy symptoms. The severity of leg pain from radiculopathy often overshadows the back pain. Sciatica findings have a sensitivity of 95% for lumbar disk herniation, meaning that herniation is extremely unlikely in the absence of sciatica.[20] The physical examination should focus on lower extremity neurologic function and signs of radiculopathy. Weakness of ankle dorsiflexion, great toe extension, ankle plantar flexion, and knee extension have respective specificities of 70%, 70%, 95%, and 99% for lumbar disk herniation.
Spinal Stenosis Patients with spinal stenosis are typically older (mean age 55 years) and constitute only 3% of all low back pain patients.[] The classic history, found in 60% to 75% of patients with spinal stenosis, is one of subacute or chronic pain and lower extremity radiculopathy, which occurs with walking and is relieved with rest and, uniquely, leaning forward.[37] Because these symptoms mimic peripheral vascular claudication symptoms, pain from spinal stenosis is termed pseudoclaudication. Typically, vascular claudication lasts 5 minutes after resting, while pseudoclaudication lasts 10 to 15 minutes.[38] Patients with spinal stenosis have symptom relief with spine flexion and leaning forward because it increases spinal canal diameter and reduces spinal cord tension. Sitting improves the symptoms, in contrast to patients with herniated disks. A typical history involves a patient who walks uphill without pain but develops pain while walking downhill because the back is extended. On physical examination, most patients have a lumbar radiculopathy at one or multiple levels and increased back pain with extension.[37] Classically, patients with spinal stenosis walk with a slight bent-forward position. To help distinguish spinal stenosis from vascular claudication, peripheral pedal pulses and ankle-brachial indices should be checked.
Degenerative Spondylolisthesis Most cases of spondylolisthesis, forward displacement of one vertebral body over another, are caused by degenerative changes. This condition is most prevalent in adults older than age 40 and occurs most commonly at the L4-5 and L5-S1 junction. Two thirds of patients with radiographically documented degenerative spondylolisthesis are asymptomatic.[39] For patients with pain, bending, twisting, and lifting activities aggravate the symptoms. Radiculopathies, spinal stenosis symptoms, or both may coexist. On physical examination, patients may have a loss of lumbar lordosis, a step-off along the midline spine if the spondylolisthesis is severe, tight hamstrings, or a radiculopathy.
Arthropathies Inflammatory arthropathies, such as ankylosing spondylitis, rheumatoid arthritis, and psoriatic arthritis, all are
Page 261
associated with subacute and chronic low back pain. All of these patients exhibit a decreased range of spinal flexibility. Commonly with ankylosing spondylitis, patients complain of morning back stiffness and pain relief with exercise. On physical examination, these patients may have nonspecific findings, such as decreased spinal mobility, sacroiliac joint tenderness, and decreased chest expansion.
Red Flag Diagnosis: Fracture In all patients with significant blunt trauma to the back or with minimal trauma in the setting of osteoporosis, fractures of the spinal column must be considered. For patients taking long-term corticosteroids, who are predisposed to early osteoporosis, back pain had a specificity of 99.5% for a spinal fracture in one series.[20] This subpopulation of patients must be assessed for a fracture despite the absence of trauma. On examination, tenderness along the midline spine and paraspinous muscles from concurrent muscle spasm usually can be elicited.
Red Flag Diagnosis: Cauda Equina Syndrome Cauda equina syndrome results from a sudden compression of multiple lumbar and sacral nerve roots. Although it is an extremely rare presentation of back pain, it is a neurosurgical emergency. Usually caused by a massive central disk herniation, other etiologies include a spinal epidural abscess, hematoma, trauma, and malignancy. Patients with cauda equina syndrome present with back pain and multiple-level radiculopathies, often involving both legs. Patients may have difficulty with bladder or bowel function. Diagnostic dilemmas arise because patients can present atypically with equivocal neurologic compromise and only mild-to-moderate pain. The most consistent examination finding in cauda equina syndrome is urinary retention. With a high sensitivity of 90%, it is highly unlikely to have this disease process if the patient's postvoid residual urine volume is less than 100 to 200 mL. Saddle anesthesia, sensory deficit over the buttocks, upper posterior thighs, and perineal area, is frequently an associated finding with a sensitivity of 75%. In 60% to 80% of cases, the rectal examination reveals a decreased sphincter tone.[20]
Red Flag Diagnosis: Spinal Infection Epidural abscess and spondylitis (osteomyelitis of the vertebral bone) are two types of dangerous spinal infections. Patients at higher risk include injection drug users, alcoholics, immunocompromised patients (e.g., patients with human immunodeficiency virus, diabetes mellitus, chronic renal failure, long-term corticosteroid use), the elderly, patients recently sustaining blunt trauma to the back, patients with an indwelling catheter, and patients with a recent bacterial infection. For epidural abscesses, approximately 20% of patients have no comorbidities or risk factors. The most common bacterial culprit is S. aureus, spreading hematogenously from a remote site or from direct extension of a local infection, such as spondylitis or disk space infection. Less common culprits are streptococci strains and enteric gram-negative bacilli. Patient history reveals back pain even at rest and subjective fevers. On physical examination, midline spinal tenderness to percussion at the site of abscess is commonly present. What makes a spinal epidural abscess a diagnostic challenge is the fact that about 50% of the patients have no neurologic deficits, and 50% may be afebrile on initial presentation.[40] Nevertheless, it is essential to diagnose this neurosurgical emergency that entails a mortality as high as 23%.[] For spondylitis, infection often begins as a subtle hematogenous seeding of the disk space, causing diskitis. Subsequent contiguous spread of the disk space infection causes vertebral end plate erosion, leading to spondylitis. Similar to an epidural abscess, the most common bacterial culprit is S. aureus. Less commonly, enteric gram-negative bacilli and Mycobacterium tuberculosis (Pott's disease) are the infectious organisms. Injection drug users also are at risk for Pseudomonas spondylitis. Patient history typically reveals a more indolent course of back pain with subjective fevers. The physical examination findings can range from nonspecific tenderness of the spine to radiculopathy and cauda equina syndrome. Similarly nondiagnostic, the presence of fever has a sensitivity of only 27% to 50% for spondylitis.[20]
Red Flag Diagnosis: Malignancy Vertebral infiltration with a tumor can be caused by either a primary or, more commonly, a metastatic malignancy. These patients are generally older than age 50 and often complain of subacute or chronic back pain, which is worse at night. Risk factors include a history of known cancer (98% specificity), unexplained weight loss (94% specificity), persistent pain despite bed rest (90% specificity), and pain lasting more than 1 month (specificity 81%).[43] On examination, these patients typically have mild-to-moderate spinal tenderness. Examination of the organs most likely to metastasize to bone, including breast, prostate, and lung, may be indicated.
Page 262
Referred Back Pain Referred pain is often difficult to differentiate from pain originating from the lumbosacral structures. It is vital, however, to make the distinction. A sudden onset of severe, tearing back pain is classically an aortic dissection. Abdominal pain radiating to the back could be a ruptured abdominal aortic aneurysm in an elderly patient with atherosclerotic disease. Alternatively, abdominal pain radiating to the back could be pancreatitis in a chronic alcoholic. Unilateral paraspinal pain associated with fever and nausea in a young woman could be pyelonephritis. In all such cases, a thorough examination of the abdomen, genitourinary system, and cardiovascular system is essential. Distinguishing the primary cause of the pain radically alters the therapy for the patient.
Functional Back Pain Distinguishing functional pain from “real” pain is often difficult, but several clues can be elicited from the history. A prolonged history of nonanatomic pain complaints, vague pain descriptions without localization, multiple lawsuits over similar problems, and lack of coordinated care for a problem that otherwise seems to dominate the patient's life all suggest that a search for a physical cause would be fruitless. These patients are often thought to have secondary gains for their complaints. On physical examination, maneuvers can be performed to try to detect functional back pain, if a psychological overlay is suspected. The first is performing the SLR test from the sitting instead of the supine position. Seemingly focused on the knee examination, the physician extends the patient's knee; this physiologically reproduces the SLR by stretching the L5 and S1 nerve roots. A positive response includes reproduction of the patient's pain and extension of the back while seated to decrease traction on the sciatic nerve. A positive supine SLR test but a negative sitting SLR test suggests a nonphysiologic cause for the pain. A second sign involves superficial tenderness. Some patients, to impress the physician with their degree of pain, respond dramatically to superficial palpation. This response is atypical for patients with genuine back pain. Nondermatomal sensory loss and widespread nondermatomal pain complaints also are unlikely to be caused by physiologic processes. Third, back pain should not be elicited by pushing down on the patient's scalp against the cervical spine. This maneuver axially loads only the cervical and not the lumbar spine. Fourth, a patient who generally overreacts during the examination is probably not giving a true reflection of the actual discomfort. All of these signs are believed to correlate well with psychopathology but have poor prognostic value. They are suggestive of malingering and functional complaints, but are neither sensitive nor specific enough to rule out organic pathology.[]
Back Pain in the Elderly When the elderly experience back pain, musculoskeletal back pain and disk herniation are less likely the underlying etiology. Instead, spinal stenosis and degenerative spondylolisthesis should be considered. Also, the incidence of more worrisome diagnoses, such as an osteoporotic fracture, spinal infection, and malignancy, is much greater in this patient population. Consequently in these cases, the threshold for further investigation should be much lower.
Back Pain in Children The likelihood of congenital etiologies for back pain, such as leg-length discrepancy and spondylolisthesis, is greater for children compared with adults. Spondylolisthesis is diagnosed most often in patients older than age 10 years, who are involved heavily in sports and complain of low back pain worsened with activity. A history suggesting infection or malignancy in children is similar to that of adults. Radicular symptoms are relatively rare in children. Functional processes are suggested when the pain is present only with certain undesired activities, such as housework or chores.
DIAGNOSTIC STRATEGIES Laboratory Evaluation In the absence of historical and physical findings suggesting “red flag” diagnoses for low back pain, laboratory evaluation is unnecessary. When a patient presents with back pain suggesting a spinal infection or malignancy, however, laboratory studies may help with risk stratification. Specifically, a complete blood cell count, erythrocyte sedimentation rate (ESR), and urinalysis should be obtained. Additional laboratory studies should be tailored to the patient's history and physical examination. Liver function tests and amylase/lipase level may need to be checked for abdominal complaints.
Page 263
For a spinal infection, the ESR usually is elevated (>20 mm/hr), whereas the serum white blood cell (WBC) count may or may not be elevated.[46] In one study, 13 of 40 (32%) patients with an epidural abscess had a falsely reassuring WBC count less than 11,000/mL.[41] When patients are diagnosed with a spinal infection, blood cultures should be drawn because a single strain, most commonly S. aureus, can be isolated in 50% to 90% of the cases.[] Performing a lumbar puncture to evaluate the cerebrospinal fluid is unnecessary and is relatively contraindicated because of the risk of seeding the cerebrospinal fluid with bacteria. For a bony malignancy, the ESR also usually is elevated, whereas the WBC may be equivocal. The hematocrit may be low secondary to anemia of chronic disease. Other additional helpful laboratory tests include alkaline phosphatase, prostate-specific antigen concentrations, and serum immunoelectrophoresis and urine testing for light chains (for multiple myeloma).
Radiology Plain Radiograph The utility of “screening” lumbosacral plain radiographs for all patients with acute low back pain is extremely low. Plain radiographs contribute little to patient management in the absence of concerning red flag findings and needlessly expose the patient to irradiation.[48] Most patients with back pain do not need radiographs. Most films are normal, but they also may have incidental findings, which may not be the true cause of the patient's pain. These findings include spondylolisthesis, abnormal spinal curvature, disk space wedging, and degenerative changes.[8] Current indications for radiographs in back pain patients are listed in Box 51-1 . BOX 51-1 Indications for Plain Lumbosacral Films in Patients with Low Back Pain
{,
{,
{,
Age youn ger than 18 or older than 50 year s Any histo ry of mali gnan cy or unex plain ed weig ht loss Any histo ry of fever , imm unoc omp romi se, or injec tion
Page 264
{,
{,
{,
drug use Rec ent trau ma, other than simp le lifting Prog ressi ve neur ologi c defic its or other findi ngs cons isten t with caud a equi na synd rom e Prol onge d durat ion of sym ptom s great er than 4 to 6 wee ks
Patients with radiculopathy findings suggesting a herniated disk do not require radiographs. In addition to being radiographically undetectable on plain films, disk herniations resolve with conservative management in most cases. If radiographs are obtained, anteroposterior and lateral views are usually sufficient in the emergency department, although many centers also prefer a coned-down lateral sacral view. Oblique films are not necessary except in children, in whom spondylolysis and spondylolisthesis may be more prevalent.[49] On plain radiographs, spondylolisthesis, vertebral osteomyelitis, and vertebral metastatic disease have classic appearances. Spondylolisthesis ( Figure 51-3 ) is classified into grade 1 through grade 4 based on the severity of the anterior slippage of one vertebral body over another. Grade 1, which is often asymptomatic, involves less than 25% slippage. Grade 2 through grade 4 involve 25% to 50%, 50% to 75%,
Page 265
and at least 75% slippage, respectively.
Figure 51-3 Lateral plain radiograph and schematic diagram of grade 2 anterior spondylolisthesis of L5 on S1. Grading is based on the percentage of slippage with 0% to 25%, 25% to 50%, 50% to 75%, and greater than 75% corresponding to grades 1 to 4, respectively.
Spondylitis ( Figure 51-4 ) is characterized by erosion of contiguous vertebral endplates and a shortened disk space height, as best seen on the lateral view. Because the anterior subchondral vertebral bone and disk space are highly vascular, it follows that spondylitis has a predilection in these areas because of the hematogenous spread of infection. With more advanced disease, vertebral bony erosion and collapse may occur.
Figure 51-4 Lateral plain radiograph shows Staphylococcus aureus spondylitis of L3 and L4. There is narrowing of the L3-4 disk space and erosion of the vertebral end plates of L3 and L4 (sm all arrows). Notice the distinct vertebral end plate m argins in unaffected areas (large arrows).
Vertebral metastatic disease ( Figure 51-5 ) can present either as a blastic (hyperdense) or lytic (hypodense) lesion and has a predilection for the vertebral body and pedicles. In contrast to osteomyelitis, the intervertebral disk space is spared.
Figure 51-5 Anteroposterior plain radiograph shows blastic infiltration of m etastatic breast cancer to the pedicles of L3-5 (arrows).
If a red flag diagnosis is of concern, a plain radiograph may rule out a fracture but may not be adequate to rule out other pathologies, such as cauda equina syndrome, spinal infection, and malignancy. For cauda equina syndrome, patients more often have normal or nonspecific plain film findings because the most common etiology is a central disk herniation. For spinal infection and vertebral malignancy, the sensitivity of a plain radiograph is only fair at 82% and 60%.[48] In these cases, the patient subsequently should undergo MRI if there is a high clinical suspicion.
Computed Tomography and Magnetic Resonance Imaging For fractures and bony abnormalities of the vertebral column, computed tomography (CT) is superior to MRI. In the case of a fracture, CT helps to elucidate the integrity of the spinal canal and the risk for spinal cord impingement. For all other red flag diagnoses—cauda equina, spinal infection, and malignancy—MRI is the gold standard test. Its superior tissue resolution, especially of the spinal cord and intervertebral disks, and its ability to perform more accurate sagittal reconstructions make MRI the ideal imaging modality. MRI is able to differentiate subtle soft tissue pathology, such as a spinal epidural abscess ( Figure 51-6 ). There is no
Page 266
radiation with MRI, whereas CT exposes the patient to about 4 years' worth of natural background radiation.[ 50]
Figure 51-6 Axial T2-weighted m agnetic resonance im aging of Staphylococcus aureus L2 epidural abscess im pinging the dorsolateral aspect of the spinal canal. CSF, cerebrospinal fluid. (Im age contributed by Dr. Stephen Bretz.)
Although disk herniation is easily visualized on MRI, patients with findings consistent with an uncomplicated disk herniation (i.e., without objective neurologic findings on examination) should not routinely undergo MRI imaging because of the self-limited nature of the disease in most cases. Overimaging patients with lumbar radiculopathy may lead to an overdiagnosis of disk herniations because incidental MRI-documented herniations have been shown to occur in 20% to 30% of asymptomatic individuals. The result may be unnecessary surgical interventions.[]
Special Investigations Unless there is suspicion of a process other than uncomplicated back pain or disk herniation, other investigations are not required. MRI is the definitive test for most conditions. Radionuclide scans have been used for locating suspected malignancy, infectious foci, and occult fractures as in spondylolysis. Nuclear medicine scans are regarded as sensitive but nonspecific.
DIFFERENTIAL CONSIDERATIONS Nonspecific low back pain is in many ways a diagnosis of exclusion. In a typical patient, within the 18- to 50-year age range with acute low back pain and with no radiculopathy, prior malignancy, weight loss, or fever, the diagnosis is almost certainly uncomplicated musculoskeletal back pain. When the patient falls outside of the aforementioned parameters, a wide variety of differential diagnoses must be entertained. Almost anything can cause low back pain. Box 51-2 contains an extensive list of possible diagnoses, but it is useful to look at the most common and most serious causes of low back pain other than musculoskeletal lumbosacral pain. One of the most life-threatening causes of referred back pain is a leaking or ruptured abdominal aortic aneurysm. See appropriate chapters for further discussion of specific problems. BOX 51-2 Differential Diagnosis for Low Back Pain
Localized/Common Unc ompl icate d mus culo skel etal back pain Inter verte bral disk herni ation Spin al sten
Page 267
osis Spo ndyl olist hesi s Oste oarth ritis Frac ture
Localized/Uncommon Infection Spo ndylit is Epid ural absc ess Diski tis Herp es zost er
Malignancy Metastatic Brea st Lung Pros tate Kidn ey, thyro id, colo n (less com mon ) Primary Multi ple myel oma Lym pho ma
Page 268
Leuk emia Prim ary cord/ extra dural tumo rs Oste oid oste oma Othe r prim ary bone tumo rs
Pediatric Spo ndyl olist hesi s/sp ondy lolysi s Seve re scoli osis Sch euer man n's dise ase
Rheumatologic Anky losin g spon dyliti s Psor iatic arthri tis Poly myal
Page 269
gia rheu mati ca Reit er's synd rom e
Vascular Arter iove nous malf orm ation of spin al cord Epid ural hem atom a
Life-Threatening Referred Pain Abdo mina l aorti c aneu rysm
Gastrointestinal System Biliar y path olog y Pan creat itis Pepti c ulcer dise ase Dive
Page 270
rticul itis
Genitourinary System Ren al colic Pyel onep hritis Pros tatiti s Cysti tis
Gynecologic System Men strua l cra mps Spo ntan eous abort ion Labo r Ecto pic preg nanc y Pelvi c infla mm atory dise ase End omet riosi s Ovar ian cyst Ovar ian torsi on
Page 271
Hematologic System Sickl e cell crisi s
Functional Som atiza tion disor der Depr essi on Fibro sitis Malin gerin g
MANAGEMENT Because most patients with acute low back pain have symptomatic resolution within 4 to 6 weeks, only conservative management is needed. In general, MRI and surgery are reserved for the few patients who have concerning systemic signs and patients with refractory, debilitating back pain. Over the past few decades, the accepted practice has shifted 180 degrees from an overaggressive recommendation for invasive surgical intervention to the minimalistic recommendation of symptomatic pain control and early return to activity. The role of the physician in back pain management is to obtain a correct diagnosis, rule out significant pathology, avoid excessive investigation, provide analgesia, and educate the patient.[52] The management of various etiologies for low back pain is summarized in Figure 51-7 . For fractures and referred pain, refer to the appropriate chapters.
Figure 51-7 Algorithm for m anagem ent of low back pain. The patient's history m ay be concerning for m ore than one red flag diagnosis.
Uncomplicated Musculoskeletal Back Pain Besides a thorough history and physical examination, no further investigations are required for uncomplicated low back pain. Only pain control and patient education are indicated. Aside from an initial parenteral opioid or nonsteroidal anti-inflammatory drug, most patients can be managed with oral nonsteroidal medications.[52] Ibuprofen is an ideal choice because it is inexpensive, and various nonsteroidal anti-inflammatory drugs have been shown to have the same efficacy. It is unclear whether ibuprofen is superior to acetaminophen.[53] Short-term opioids also occasionally are needed for break-through pain in the acute setting. Various other medications have been advocated, including benzodiazepines and other muscle relaxants. Based on the current conflicting literature, these medications probably do not provide a significant
Page 272
added benefit, but they do increase the incidence of side effects such as drowsiness and drug dependence.[ 54] There is no role for corticosteroids in the treatment of uncomplicated low back pain. In terms of patient education, one of the outdated practices of back pain management was that physicians convinced patients that they were sick. This was done by overinvestigating, overtreating, putting patients to bed, and taking them off work. It now has been shown convincingly and repeatedly that all of those interventions are excessive. Instead, patients should be educated as to why they are not receiving plain films of their lumbosacral spine or laboratory tests and reassured on the likely benign course of the pain. Most patients can be convinced by education and an explanation of radiation dosing. A typical lumbosacral spine series involves as much gonadal radiation as a chest x-ray every day for 5 or 6 years.[55] Patients also are discouraged from the outdated recommendation of strict bed rest. Compared with patients who are prescribed strict bed rest, patients experience earlier resolution of pain and return to work sooner if they remain active.[4] Patients should be made aware, however, that the back pain has a 66% to 84% likelihood of recurring within 12 months.[11] Other supplemental treatment modalities have been shown to be of debatable efficacy in the management of acute and chronic low back pain. These include acupuncture, physiotherapy, chiropractic manipulation, massage, ultrasound, traction, and transcutaneous nerve stimulation.[]
Lumbar Disk Herniation Similar to patients with uncomplicated low back pain, patients with disk herniations and radiculopathy do not benefit from strict bed rest.[5] In the acute setting, these patients should receive analgesics, but further investigation with laboratory tests and radiographs is not necessary. Most of these patients have symptomatic resolution within 6 weeks with conservative, nonsurgical management.[] Corticosteroid injections into the epidural space have been advocated for sciatica in the belief that this helped relieve some of the inflammation associated with disk herniation. Although this treatment may offer some initial symptom improvement, there is no long-term benefit or reduction in the need for later surgery.[62] The use of systemic steroids in back pain and disk herniation remains controversial. It is difficult to argue their benefit in nonspecific low back pain, but the anti-inflammatory effects make empiric sense in the context of radiculopathy. A large retrospective review showed no definite benefit of systemic steroids in either setting, but the definitive trial is yet to be done.[54] When the pain from disk herniation persists for longer than 4 to 6 weeks, outpatient MRI is indicated. With a documented herniation, these patients benefit from surgical diskectomy. Other indications for surgery include intractable pain and worsening motor or sensory deficit. Although surgical patients tend to have earlier relief of pain compared with nonsurgical patients, the 4- and 10-year results are the same. Microsurgery techniques and laser therapy have not been shown to confer any advantage over conventional techniques.[63]
Spinal Stenosis Patients with spinal stenosis should be managed conservatively with pain medications. In the absence of alarming red flag findings, these patients do not require laboratory or radiographic studies in the emergency department. These patients may be candidates for surgery if they show any of the following conditions: progressive neurologic deficit, progressive reduction in ability to walk secondary to pseudoclaudication, evidence of cauda equina syndrome, or intractable pain. Elective surgical decompression is more controversial. A 10-year longitudinal study showed that no findings predicted which patients would benefit more from surgery versus conservative management.[64] The benefits of surgery also must be weighed against the risks of surgery itself because these patients are usually elderly.
Degenerative Spondylolisthesis Patients with symptomatic degenerative spondylolisthesis are managed conservatively with analgesia and lifestyle changes, which include the avoidance of repetitive bending, heavy lifting, and twisting at the waist. For refractory and severe back pain, patients should undergo outpatient MRI and receive neurosurgical follow-up for possible operative decompression.
Red Flag Diagnosis: Fracture See Chapter 40 , Spinal Injuries.
Red Flag Diagnosis: Cauda Equina Syndrome
Page 273
Cauda equina syndrome is a neurosurgical emergency that requires urgent operative decompression to help preserve distal neurologic function. All patients with concerning findings, such as saddle anesthesia or a large postvoid residual volume, require emergent MRI. On average, these patients may have an improved outcome if decompression takes place within 24 hours.[65] Early evidence exists, however, that shows delayed operative decompression under a more controlled setting may be performed without any adverse effects, particularly for patients who have overflow urinary incontinence.[66]
Red Flag Diagnosis: Spinal Infection If a patient's history or physical examination is worrisome for a spinal infection, further investigation is paramount. With a low index of suspicion, a normal serum WBC count, ESR, and lumbosacral plain film can safely rule out infection. If any of these tests are abnormal or if the patient has a moderate to high pretest probability for a spinal infection, the next step is to obtain emergent MRI. Pyogenic spinal infections should be treated with broad-spectrum intravenous antibiotics that cover at least for S. aureus and gram-negative bacilli until blood culture results return. Vancomycin should be added if the patient is at risk for methicillin-resistant S. aureus. For injection drug users, antibiotic coverage for Pseudomonas is necessary. For almost all epidural abscesses, treatment also requires neurosurgical drainage and decompression.
Red Flag Diagnosis: Malignancy An algorithmic guideline to the management of back pain, which is worrisome for malignancy, involves subdividing patients into two categories—patients with and patients without a history of prior cancer. Of cancer patients, 20% to 85% develop spinal metastasis.[] These patients are subdivided further into patients with and patients without evidence of a radiculopathy. Most patients fall into the classification of back pain without a history of cancer and without a radiculopathy. They have a history only suggestive of a malignancy, such as unexplained weight loss or back pain that is worse at night. These patients require further risk stratification with plain radiographs and laboratory tests, including a complete blood cell count and ESR. With normal results, these patients can be referred to their primary care physician for further workup. The physician should not feel completely reassured that malignancy has been ruled out, however, because plain films have a false-negative rate of 10% to 17% for vertebral bone metastasis. This false-negative rate is likely due to the fact that a cancer needs to erode at least 50% of the bone before becoming radiographically apparent.[69] With abnormal results, such as a bony lesion or extremely elevated ESR level (>100 mm/hr), these patients should receive urgent MRI as an outpatient within the next 3 to 7 days. For patients with no known history of cancer but with signs of radiculopathy, the workup also includes a plain radiograph, complete blood cell count, and ESR. If the test results are normal, the patients should be referred to their primary care physician for further evaluation for malignancy and other etiologies for radiculopathy, including spinal stenosis and disk herniation. If the workup shows a bony lesion on plain film or an extremely elevated ESR level (>100 mm/hr), these patients should undergo emergent MRI because (1) the presence of radiculopathy may be an early harbinger of impending spinal cord compression from a mass effect, and (2) it is often difficult to distinguish between a neoplasm from early spondylitis (especially tuberculous osteomyelitis) and an osteoporotic fracture causing a vertebral collapse on plain film.[70] For patients with a history of prior cancer and low back pain, all require MRI either emergently or urgently within 3 to 7 days. In the absence of radiculopathy findings, these patients should undergo outpatient MRI regardless of plain film and laboratory results. Plain radiography is too insensitive to rule out a vertebral neoplastic process definitively. If radiculopathy is present, however, these patients require emergent MRI regardless of plain radiography findings because of the concern for spinal cord compression. According to one study of known cancer patients with back pain and radiculopathy, the risk of epidural spinal cord compression was 25% despite normal films and 88% with films showing vertebral metastasis.[71] For all patients undergoing emergent MRI to evaluate for vertebral malignancy and cauda equina syndrome, dexamethasone should be administered to reduce the potential mass effect. In addition to high-dose corticosteroids, patients with a vertebral neoplasm also may benefit from radiation therapy.
Pediatric Back Pain Management of back pain in children is similar to management for adults and depends on the etiology. Spondylolisthesis is managed by observation, with only 4% to 5% of cases worsening. Progression usually stops as skeletal maturity is achieved in the late teens. Current recommendations are for limited contact
Page 274
sports in children with less than 30% to 50% slippage and surgical stabilization for children with slippage greater than 30% to 50%. Treatment becomes more aggressive if the child is symptomatic.[72]
Chronic Back Pain Patients with chronic back pain often are regarded as the most challenging of back pain patients. The cause of chronic back pain is complex and multifactorial and usually requires a multidisciplinary approach for the greatest chance for success. There is little doubt that psychosocial factors, including depression, drug dependence, and financial gain, play a significant role in the behavior of many of these patients, making proper assessment and treatment impossible for the emergency physician. After the emergency physician has made sure that no red flag condition exists, emergency management involves analgesia and follow-up. The main decision usually centers on the use of narcotics, which becomes an individual decision for the physician to make. Patients showing drug-seeking behavior classically are from out of town, have a physician who cannot be contacted, or are “allergic” to all nonopioid medications.
DISPOSITION Almost all patients with uncomplicated back pain can be discharged from the emergency department. In rare circumstances, severe pain or an unacceptable social situation may preclude discharge. For patients who have a red flag diagnosis of cauda equina syndrome or epidural abscess, an immediate neurosurgical consultation is required for emergent surgical decompression. For spondylitis, patients require hospital admission for intravenous antibiotics. For vertebral malignancy, the decision to hospitalize a patient for pain control, high-dose corticosteroids, and radiation therapy should be made in conjunction with a neurosurgeon, oncologist, and radiation therapist. One of the most important aspects in the management of patients with low back pain is the discharge instruction. Not only are clear and simple instructions useful to the patient, but they are also a medicolegal necessity for the physician. Physicians must avoid using medical terms. The discharge instructions should include the following: 1.
2.
3.
4.
Diagnosis: Distinguish between uncomplicated (musculoskeletal) back pain and diskogenic radiculopathy. Activity: Recommend maintaining active mobility as limited only by pain, avoiding heavy lifting until symptoms resolve, and getting back to work early. Reassurance: Educate patients on the likely benign etiology for the pain. Warnings: Instruct patients to return to the emergency department immediately if they have a fever; lose bladder or bowel control; have numbness or tingling around their anus, vagina, or penis; or have new pain or weakness down one or both legs.
Pediatric back pain is subject to the same discharge instructions as that of adults. In patients with pain secondary to spondylolisthesis, activity restrictions should be made in conjunction with an orthopedic surgeon. Emergency department disposition for a patient with chronic back pain is relatively simple: pain management with nonopioids, when possible, and follow-up with a primary care provider. The prognosis is guarded because patients who are off of work for 6 months are usually still off of work after 2 years.[30]
Page 275
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/117.html/top
Page 276
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
KEY CONCEPTS {, {, {, {, {,
{,
The key to differentiating between benign and serious pathology in low back pain is a focused and thorough history and physical examination. The absence of sciatica findings practically rules out a lumbar disk herniation. Screening laboratory tests and plain radiographs are not indicated for patients with uncomplicated low back pain or a simple disk herniation. The best treatment for uncomplicated back pain and disk herniation is analgesia and resumption of normal activities—not bed rest. Age younger than 18 or older than 50 years, fever, injection drug use, immunocompromised status, symptoms lasting more than 4 to 6 weeks, night pain, and prior malignancy all are red flag warnings of potentially serious causes of back pain and should be heeded and evaluated accordingly. Bilateral leg pain or weakness, bowel or bladder sphincter problems (especially urinary retention), and saddle anesthesia are worrisome for a cauda equina syndrome a neurosurgical emergency.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/118.html/top
Page 277
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
UPPER BACK PAIN PERSPECTIVE Background Thoracic pain is far less common than low back pain. Thoracic pain usually has a musculoskeletal origin, but other more emergent causes must be considered first, including thoracic aortic dissection, pulmonary embolism, and esophageal disease. Compared with lumbar disk herniation, which is fairly common, thoracic disk disease is extremely rare, difficult to diagnose, and difficult to treat.
Epidemiology The actual incidence of thoracic pain is unknown. The incidence of symptomatic thoracic disk disease is low, with estimates at 1 in 1 million.[73] The average age is in the 40s with equal gender distribution. Surgery for thoracic disks comprises less than 4% of all disk operations.[74] Metastases are more common in the thoracic spine than lumbar spine, with 60% to 70% of spinal metastases localizing there.[]
PRINCIPLES OF DISEASE Anatomy and Physiology The thoracic vertebral column can be regarded as an extension of the cervical column with the addition of ribs. There are 12 thoracic vertebrae, connected by the anterior and posterior longitudinal ligaments and the ligamentum flavum, similar to the lumbar vertebrae. Also similarly, intervertebral disks provide elasticity and stability to the thoracic column. The spinal canal diameter remains unchanged through the thoracic and lumbar levels, but at the thoracic level, the space around the spinal cord is smaller compared with the lumbar level. Because lumbar nerve fibers have not yet branched off from the spinal cord, the thoracic cord is thicker than the lumbar cord. Significant neurologic findings may result from minimal spinal canal impingement at the thoracic level.
Pathophysiology Common thoracic soft tissue pain is likely a combination of sprain and muscle inflammation. Similar to the lower back, innervation of the paravertebral area is provided by the sinuvertebral nerve, and any anatomic disruption of surrounding structures results in nonspecific pain. Thoracic disk herniations, which most commonly occur in the midthoracic to lower thoracic spine, cause pain and neurologic symptoms in much the same way as lumbar disks. It is not clear why their presentation is so varied, although a possible cause is a higher number of centrally herniated disks, resulting in much more frequent myelopathic symptoms.[74]
CLINICAL FEATURES Symptoms and Signs History Nondiskogenic thoracic back pain usually presents with paraspinal discomfort. There may or may not be a history of trauma or recent unusual activity preceding the onset of pain. Complaints with thoracic disk herniations are variable at best, but usually are associated with long-standing pain, neurologic symptoms, or both. Pain may be localized to one part of the thoracic vertebrae, it may radiate down to the sacrum, or it may have a radicular component along the ribs. Central disk herniation can present as diffuse abdominal and back pain or burning sensation in the lower extremities. Associated findings may include mild weakness, spasticity, gait disturbance, bowel or bladder dysfunction, or paraplegia. These usually progress until the condition is diagnosed. The average patient with thoracic disk disease is not diagnosed until 20 months after first presentation. Pain from other causes should be sought in the initial assessment. A history of trauma, fever, previous malignancy, cardiovascular disease, or gastrointestinal problems may indicate problems originating outside the thoracic spine and may warrant further investigation.
Physical Examination
Page 278
Patients with benign musculoskeletal pain have an unremarkable examination. They may exhibit mild to moderate paraspinal tenderness, pain with motion, and even discomfort from chest wall expansion with respirations, but objective findings are minimal. The physical examination for patients with thoracic disk herniations varies with the location and degree of herniation. Objective findings may range from a normal examination to a loss of posterior column function (position, touch, vibration) or unilateral or bilateral weakness. Gait and sensory abnormalities are common. Hypotonic abdominal reflexes may be present with distal hyperreflexia. A Babinski response may be present. Myelopathy may result in urinary retention. Muscle wasting may be present with chronic symptoms. The possibility of other pathologic conditions should be kept in mind during the physical examination, with appropriate assessment tailored to the presentation and clinical suspicion.
DIAGNOSTIC STRATEGIES Laboratory Evaluation In the face of an unremarkable history and physical examination, the likelihood of useful laboratory re-sults is extremely small. In appropriate clinical circumstances, assessment for malignancy, infection, and inflammation should be undertaken.
Radiology The usefulness of a radiograph is dubious in a patient with atraumatic acute thoracic back pain who has no other preexisting illness or neurologic findings. As a general guide, however, suspicion of other conditions; unexplainable symptoms; extremes of age; concern for trauma, tumor, infection, gastrointestinal pathology, or vascular pathology; or prolonged symptoms should prompt basic radiologic studies and appropriate further investigations. Similar to patients with lower back pain, patients with a history of cancer and upper back pain should undergo plain radiography and possibly MRI to assess for vertebral metastatic disease, especially because metastases have a predilection for the thoracic spine. MRI has become the modality of choice for evaluating a herniated thoracic disk. The incidence of asymptomatic disk herniations seen on MRI is 37%. Most herniated thoracic disks, whether symptomatic or not, have been seen to recede spontaneously.[73]
DIFFERENTIAL CONSIDERATIONS Although muscular back pain is extremely common, Box 51-3 lists the expansive differential diagnosis for thoracic back pain. BOX 51-3 Differential Diagnosis for Thoracic Back Pain
{, {, {, {, {, {, {, {, {, {,
Uncompliated musculoskeletal back pain Spinal cord and nerve root pathology (e.g., disk herniation, tumor, hematoma) Vertebral column disease (e.g., primary and metastatic malignancy and osteomyelitis) Disk infection Primary neurologic disease Degenerative and autoimmune arthropathies Herpes zoster Vascular disease (e.g., thoracic aortic dissection, acute coronary syndrome, pulmonary embolism) Thoracic cavity pathology (e.g., pleuritis, pericarditis, pneumonia, esophageal pathology) Intraperitoneal and retroperitoneal abdominal pathology (e.g., peptic ulcer disease, pancreatitis, hepatobiliary disease)
Page 279
MANAGEMENT Commonly, thoracic musculoskeletal pain is managed with analgesia. No studies show that there should be any difference in management compared with musculoskeletal low back pain. Thoracic disk disease is difficult to diagnose and manage. Symptomatic pain management and outpatient follow-up are recommended. Given the limited space in the spinal canal at the thoracic level compared with the lumbar level, spinal cord compression from a herniated disk is more likely at the thoracic level. Any herniated disk that precipitates an acute neurologic deficit warrants MRI and early neurosurgical evaluation.
DISPOSITION Patients with benign back pain in any part of the thoracic vertebral column can be discharged with follow-up by the primary care physician. Patients with a suspected thoracic disk require close outpatient follow-up. Most cases of subjective discomfort resulting from thoracic disks without objective neurologic findings resolve on their own, with one study showing a 77% improvement rate.[73] Although there are no clear guidelines as to when emergent neurosurgical consultation is required for thoracic disk herniation, patients with significant pain or neurologic compromise should be assessed rapidly. Radicular symptoms seem to respond better to surgery than nonradicular findings.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/119.html/top
Page 280
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
REFERENCES 1. Ng KG: Automated noninvasive blood pressure measurement. Intensive Care World1995;12:89. 2. De Jong JR, Ros HH, De Lange JJ: Noninvasive continuous blood pressure measurement during anaesthesia: A clinical evaluation of a method commonly used in measuring devices. Int J Clin Monit Comput1995;12:1. 3. Jin X: Decreases in organ blood flows associated with increases in sublingual Pco2 during hemorrhagic shock. J Appl Physiol1998;85:2360. 4. Isenberg SJ: Continuous oxygen monitoring of the conjunctiva in neonates. J Perinatol2002;22:46. 5. Abraham E, Ehrlich H: Conjunctival and transcutaneous oxygen monitoring during resuscitation. Ann Emerg Med1984;13:287. 6. Severinghaus JW: Oximetry: What does it tell you?. ASA Annual Refresher Course Lectures1991;266:1. 7. Tremper KK, Barker SJ: Pulse oximetry. Anaesthesiology1989;70:98. 8. Sinex JE: Pulse oximetry: Principles and limitations. Am J Emerg Med1999;17:59. 9. Cote CJ: Adverse sedation events in pediatrics: A critical incident analysis of contributing factors. Pediatrics2000;105:805. 10. Burillo-Putze G: Transcranial oximetry as a new monitoring method for HEMS (Helicopter EMS). Air Med J2002;21:13. 11. Macnab AJ: The cost-benefit of pulse-oximeter use in the prehospital environment. Prehospital Disaster Med1999;14:245. 12. Ward KR, Yealy DM: End-tidal carbon dioxide monitoring in emergency medicine: Part 1. Basic principles. Acad Emerg Med1998;5:628. 13. Buhre W, Rossaint R: Perioperative management and monitoring in anaesthesia. Lancet2003;29:1839. 14. Wang VJ, Krauss B: Carbon dioxide monitoring in emergency medicine training programs. Pediatr Emerg Care2002;18:251. 15. Schneider RE, Murphy MF: Bag mask ventilation and endotracheal intubation. In: Walls RM, ed.Manual of Emergency Airway Management, 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2004: 43-69. 16. Cardoso MM: Portable devices used to detect endotracheal intubation during emergency situations: A review. Crit Care Med1998;26:957. 17. Wahba RWM, Tessler MJ: Misleading end-tidal CO2 tensions. Can J Anaesth1996;43:862. 18. Ward KR, Yealy DM: End-tidal carbon dioxide monitoring in emergency medicine: Part 2. Clinical applications. Acad Emerg Med1998;5:637. 19. Ahrens T: End-tidal carbon dioxide measurements as a prognostic indicator of outcome in cardiac arrest. Am J Crit Care2001;10:391. 20. Wayne MA, Levine RL, Miller CC: Use of end-tidal carbon dioxide to predict outcome in prehospital cardiac arrest. Ann Emerg Med1995;25:762. 21. Marik PE: Sublingual capnography: A clinical validation study. Chest2001;120:923. 22. Boswell SA, Scalea TM: Sublingual capnography: An alternative to gastric tonometry for the management of shock resuscitation. AACN Clin Issues2003;14:176. 23. Baron BJ: Diagnostic utility of sublingual Pco2 for detecting hemorrhage in patients with penetrating trauma. Acad Emerg Med2002;9:492. 24. Kolb JC: Blunt trauma in the obstetric patient: monitoring practices in the ED. Am J Emerg Med 2002;20:524. 25. An educational aid to obstetrician-gynecologists: Trauma during pregnancy. ACOG Technical Bulletin 1991;161:1-5.
Page 281
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/12.htm l/top
Page 282
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
KEY CONCEPTS {,
{, {,
Although thoracic disk herniation can result in significant upper back pain, other, more dangerous etiologies must be considered first, such as an aortic dissection, pulmonary embolism, and acute coronary syndrome. The associated neurologic examination with thoracic disk hernations can be extremely variable, ranging from nonspecific paresthesias to significant upper motor neuron weakness. The incidence of vertebral metastatic malignancy is higher in the thoracic spine compared with the lumbar spine.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/120.html/top
Page 283
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
REFERENCES 1. Frymoyer J, Cats-Baril W: An overview of the incidence and costs of low back pain. Orthop Clin North Am 1991;22:263. 2. Deyo RA, Cherkin D, Conrad D, Volinn E: Cost, controversy, crisis: Low back pain and the health of the public. Annu Rev Public Health1991;12:141. 3. Deyo RA, Weinstein JN: Low back pain. N Engl J Med2001;344:363. 4. Malmivaara A: The treatment of acute low back pain: Bed rest, exercises, or ordinary activity?. N Engl J Med1995;332:351. 5. Vroomen PC: Lack of effectiveness of bed rest for sciatica. N Engl J Med1999;340:418. 6. Hart LG, Deyo RA, Cherkin DC: Physician office visits for low back pain: Frequency, clinical evaluation, and treatment patterns from a U.S. national survey. Spine1995;20:11. 7. Cunningham LS, Kelsey JL: Epidemiology of musculoskeletal impairments and associated disability. Am J Public Health1984;74:574. 8. Wipf JE, Deyo RA: Low back pain. Med Clin North Am1995;79:231. 9. Luo X: Estimates and patterns of direct health care expenditures among individuals with back pain in the United States. Spine2004;29:79. 10. Nordin M, Campello M: Physical therapy: Exercises and the modalities: When, what and why?. Neurol Clin North Am1999;17:759. 11. Pengel LH, Herbert RD, Maher CG, Refshauge KM: Acute low back pain: Systematic review of its prognosis. BMJ2003;327:323. 12. Adams MA, Mannion AF, Dolan D: Personal risk factors for first-time low back pain. Spine1999;24:2497. 13. Videman T, Battie MC: The influence of occupation on lumbar degeneration. Spine1999;24:1164. 14. Matsui H: Familial predisposition for lumbar degenerative disk disease: A case control study. Spine 1998;23:1029. 15. Feldman DE, Rossignol M, Shrier I, Abenhaim L: Smoking: A risk factor for development of low back pain in adolescents. Spine1999;24:2492. 16. Leboeuf-Yde C: Smoking and low back pain: A systematic literature review of 41 journal articles reporting 47 epidemiologic studies. Spine1999;24:1463. 17. Paassilta P: Identification of a novel common genetic risk factor for lumbar disk disease. JAMA 2001;285:1843. 18. Haldorsen EMH, Indahl A, Ursin H: Patients with low back pain not returning to work: A twelve month follow-up study. Spine1998;23:1202. 19. Croft PR: Short-term physical risk factors for new episodes of low back pain: Prospective evidence from the South Manchester Back Pain Study. Spine1999;24:1556. 20. Deyo RA, Rainville J, Kent DL: What can the history and physical examination tell us about low back pain?. JAMA1992;268:760. 21. Bogduk N: The lumbar disk and low back pain. Neurosurg Clin N Am1991;2:791. 22. Paajanen H: Magnetic resonance study of disk degeneration in young low-back pain patients. Spine 1989;14:982. 23. Jensen M: Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994;331:69. 24. Olmarker K: Radicular pain—recent pathophysiologic concepts and therapeutic implications. Schmerz 2001;15:425. 25. Thomas SA: Spinal stenosis: History and physical examination. Phys Med Rehabil Clin N Am 2003;14:29. 26. Ramirez N, Johnston CE, Browne RH: The prevalence of back pain in children who have idiopathic scoliosis. J Bone Joint Surg Am1997;79:364. 27. Nachemson AL: Newest knowledge of low back pain: A critical look. Clin Orthop1992;279:8. 28. McGowin PR, Borenstein D, Wiesel SW: The current approach to the medical diagnosis of low back pain. Orthop Clin North Am1991;22:315. 29. Mayer TG: Rehabilitation: What do we do with the chronic patient?. Neurol Clin North Am1999;17:131. 30. Andersson GB: Epidemiological features of chronic low-back pain. Lancet1999;354:581.
Page 284
31. Gatchel RJ, Gardea MA: Psychosocial issues. Neurol Clin North Am1999;17:149. 32. King HA: Back pain in children. Orthop Clin North Am1999;30:467. 33. Mason DE: Back pain in children. Pediatr Ann1999;28:727. 34. Bigos S: Acute Low Back Problems in Adults. Clinical Practice Guideline No. 14 (AHCPR Publication No. 95-0642), Rockville, Md, Agency for Health Care Policy and Research, Public Health Service, U.S. Department of Health and Human Services, 1994. 35. Frymoyer JD: Back pain and sciatica. N Engl J Med1998;318:291. 36. Turner JA, Ersek M, Herron L, Deyo R: Surgery for lumbar spinal stenosis: Attempted meta-analysis of the literature. Spine1992;17:1. 37. Radu AS, Menkes CJ: Update on lumbar spinal stenosis: Retrospective study of 62 patients and review of the literature. Rev Rhum Engl Educ1998;65:337. 38. Hawkes CH, Roberts GM: Neurogenic and vascular claudication. J Neurol Sci1978;38:337. 39. Kauppila LI: Degenerative displacement of lumbar vertebrae: A 25-year follow-up study in Framingham. Spine1998;23:1868. 40. Joshi SM, Hatfield RH, Martin J, Taylor W: Spinal epidural abscess: A diagnostic challenge. Br J Neurosurg2003;17:160. 41. Hlavin M, Kaminski HJ, Ross JS, Ganz E: Spinal epidural abscess: A ten-year perspective. Neurosurgery1990;27:177. 42. Darouiche R: Bacterial spinal epidural abscess: Review of 43 cases and literature survey. Medicine 1992;71:369. 43. Deyo RA, Diehl AK: Cancer as a cause of back pain: Frequency, clinical presentation, and diagnostic strategies. J Gen Intern Med1998;3:230. 44. Polatin PB, Cox B, Gatchel RJ, Mayer TG: A prospective study of Waddell signs in patients with chronic low back pain: When they may not be predictive. Spine1997;22:1618. 45. Main CJ, Waddell G: Behavioral responses to examination: A reappraisal of the interpretation of “nonorganic signs.”. Spine1998;23:2367. 46. Martin R, Yuan H: Neurosurgical care of spinal epidural, subdural, and intramedullary abscesses and arachnoiditis. Orthop Clin North Am1996;27:125. 47. Nussbaum ES: Spinal epidural abscess: A report of 40 cases and review. Surg Neurol1992;38:225. 48. Jarvik JG, Deyo RA: Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med 2002;137:586. 49. Boos N, Hodler J: What help and what confusion can imaging provide?. Baillieres Clin Rheumatol 1998;12:115. 50. Dixon AK: Imaging the bad back: Increasing reliance on MRI. Hosp Med1998;49:496. 51. Jarvik JG: Rapid magnetic resonance imaging vs radiographs for patients with low back pain: A randomized controlled trial. JAMA2003;289:2810. 52. Burton AK, Waddell G: Clinical guidelines in the management of low back pain. Clin Rheumatol 1998;12:17. 53. Van Tulder MW, Scholten RJ, Koes BW, Deyao RA: Nonsteroidal anti-inflammatory drugs for low back pain: A systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine 2000;25:2501. 54. Deyo R: Drug therapy for back pain: Which drugs help which patients. Spine1996;21:2840. 55. Frazier LM: Selective criteria may increase lumbosacral spine roentgenogram use in acute low-back pain. Arch Intern Med1989;149:47. 56. Koes BW: Physiotherapy exercises and back pain: A blinded review. BMJ1991;302:1572. 57. Cherkin DC: A comparison of physical therapy, chiropractic manipulation, and provision of an educational booklet for the treatment of patients with low back pain. N Engl J Med1998;339:1021. 58. Bronfort G: Spinal manipulation: Current state of research and its indications. Neurol Clin1999;17:91. 59. Van Tulder MW: The effectiveness of acupuncture in the management of acute and chronic low back pain: A systematic review within the framework of the Coch-rane Collaboration Back Review Group. Spine 1999;24:1113. 60. Vroomen PC, de Krom MC, Slofstra PD, Knottnerus JA: Conservative treatment of sciatica: A systematic review. J Spinal Disord2000;13:463. 61. Benoist M: The natural history of lumbar disc herniation and radiculopathy. Joint Bone Spine2002;69:155. 62. Carette S: Epidural corticosteroid injections for sciatica due to herniated nucleus pulposus. N Engl J Med1997;336:1634. 63. Gibson JN, Grant IC, Waddell G: The Cochrane review of surgery for lumbar disc prolapse and degenerative lumbar spondylosis. Spine1999;24:1820. 64. Amundsen T: Lumbar spinal stenosis: Conservative or surgical management? A prospective 10-year study. Spine2000;25:1425. 65. Shapiro S: Cauda equina syndrome secondary to lumbar disk herniation. Neurosurgery1993;32:743. 66. Gleave JR, Macfarlane R: Cauda equina syndrome: What is the relationship between timing of surgery and outcome?. Br J Neurosurg2002;16:325.
Page 285
67. Weigel B: Surgical management of symptomatic spinal metastases. Spine1999;24:2240. 68. Antunes NL, De Angelis LM: Neurologic consultations in children with systemic cancer. Pediatr Neurol 1999;20:121. 69. Schiff D: Spinal cord compression. Neurol Clin2003;21:67. 70. Laredo JD, el Quessar A, Bossard P, Vuillemin-Bodaghi V: Vertebral tumors and pseudotumors. Radiol Clin North Am2001;39:137. 71. Byrne T: Spinal cord compression from epidural metastases. N Engl J Med1992;327:614. 72. Lonstein JE: Spondylolisthesis in children: Cause, natural history and management. Spine1999;24:2640. 73. Wood KB: The natural history of asymptomatic thoracic disk herniations. Spine1997;22:525. 74. Stillerman CB: Experience in the surgical management of 82 symptomatic herniated thoracic disks and review of the literature. J Neurosurg1998;88:623. 75. Jennis LG, Dunn EJ, An HS: Metastatic disease of the cervical spine. Clin Orthop1999;359:89.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/121.html/top
Page 286
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
Chapter 52 – Pelvis A. Adam Cwinn
PERSPECTIVE In evaluating a trauma patient, a pelvic fracture or dislocation indicates the profound magnitude of disruptive energy at the time of injury. Significant pelvic injury alerts the physician to the likelihood of major injury to other body systems, and the pelvic injury itself poses diagnostic and therapeutic challenges.
Epidemiology Mechanisms of injury in pelvic fractures include motor vehicle crash in 57% to 71% of patients, collisions with pedestrians in 13% to 18%, motorcycle crashes in 5% to 9%, falls in 4% to 9%, and crushing forces in 4% to 5%.[] Depending on the size of the study group, the types of pelvic fractures included in the study, and the associated trauma to other body systems, reported mortality figures for pelvic injuries range from 8% to 13% in studies totaling 4621 patients with heterogeneous mechanisms of injury.[] The subsets of patients with high-energy pelvic injuries or open pelvic fracture from these studies have a much higher mortality rate. Pedestrians who are struck by motor vehicles and sustain pelvic trauma have a mortality rate of 23%.[5] Mortality in patients with blunt trauma who have the combination of pelvic ring fractures and hemorrhagic shock is approximately 50%.[] This chapter reviews the pertinent anatomic and radiologic anatomy and discusses pelvic trauma in three broad categories: (1) injury to the pelvic viscera and soft tissues, (2) bony injury, and (3) related hemorrhage. The term pelvic fracture includes fractures and dislocations.
Anatomy The bony pelvis is composed of the right and left innominate bones, the sacrum, and the coccyx ( Figure 52-1 ). The innominate bone is formed by three bones that fuse at the acetabulum: the ilium, the ischium, and the pubis. The bony pelvis provides protection for its visceral contents, serves as attachment points for muscles, and transmits weight from the trunk to the lower limbs. Strong posterior ligaments—the sacrospinous, sacrotuberous, iliolumbar, and anterior and posterior sacroiliac (SI) ligaments—provide considerable mechanical support, and disruption of these ligaments is the major cause of pelvic instability after injury.
Figure 52-1 Pelvic anatom y. A Anterior view of pelvis. B Lateral view of right innom inate bone. 1, Iliac fossa; 2, iliac crest; 3, anterior superior iliac spine; 4, anterior inferior iliac spine; 5, symphysis pubis; 6, body of pubis; 7, superior ram us of pubis; 8, inferior ram us of pubis; 9, ram us of ischium ; 10, ischial tuberosity; 11, obturator foram en; 12, ischial spine; 13, lesser sciatic notch; 14, acetabulum (14a, articular surface; 14b, fossa); 15, sacrum ; 16, anterior sacral foram ina; 17, sacroiliac joint; 18, anterior sacroiliac ligam ent; 19, sacrotuberous ligam ent (sacrum to ischial tuberosity); 20, coccyx; 21, sacrospinous ligam ent; 22, greater trochanter of fem ur; 23, lesser trochanter of fem ur; 24, iliofem oral ligam ent; 25, pubofem oral ligam ent; 26, arcuate line; 27, posterior or fem orosacral arch, through which m ain weight-bearing forces are transm itted; 28, anterior arch.
The main weight-bearing forces are transmitted through the posterior wall of the pelvis, called the posterior arch, which is composed of thick bone and ligaments. The rich network of major arteries, veins, and nerves that course adjacent to the anterior wall of the posterior arch may be injured concomitantly with forces causing bony injuries of this arch.
Vascular Anatomy and Pathophysiology
Page 287
Most of the blood supply to the pelvis comes from the left and right internal iliac arteries. The internal iliac arteries course at the level of the SI joints. The various arteries that derive from the internal iliac arteries initially run in close proximity to the posterior pelvic arch and eventually anastomose extensively with each other, forming a rich collateral network. The superior gluteal artery is the largest branch. Because it originates at right angles from the internal iliac artery and has little muscular protection, the superior gluteal artery is commonly injured in fractures of the posterior pelvic arch. The obturator and internal pudendal branches are often injured in fractures involving the pubic rami.[9] The venous system also has many collateral branches and is without valves, allowing bidirectional flow. The veins are arranged in a plexus that adheres closely to the pelvic walls. Because these veins are thin walled, they do not have the ability to constrict in response to damage.[9] This anatomic arrangement of the arteries and veins accounts for the hemorrhage seen with pelvic fractures. Without performing angiography, it is impossible to know clinically if a retroperitoneal hematoma is caused by disruption of major arteries or veins or smaller, unnamed blood vessels. Most pelvic hematomas are venous in origin, however, and are contained and tamponaded retroperitoneally by the intact peritoneum. Normal hemostatic mechanisms contain many hematomas, but some continue to enlarge, producing hemorrhagic shock. The hematoma also may dissect anteriorly to invade the anterior abdominal wall—to the chagrin of the unwary clinician who introduces a scalpel or peritoneal dialysis catheter. A retroperitoneal hematoma also may rupture through the peritoneum into the abdominal cavity, causing a loss of the tamponade effect. Hemorrhage from pelvic fractures results from lacerations of the rich vascular network supplying the pelvis and collects in the retroperitoneal space, but considerable bleeding also may occur from the marrow at the fracture sites.[9] Coagulopathy is another cause of persistent retroperitoneal bleeding and should be considered when the patient does not respond to fluid and blood replacement.
Neurologic Anatomy and Pathophysiology The cauda equina course through the sacral spinal canal and exit through the sacral neural foramina to form the lumbar and sacral plexus. Injury to the posterior bony pelvis and sacrum may result in neurologic deficits in the lower extremities and autonomic dysfunction involving the bowel, bladder, and genitalia.
CLINICAL FEATURES Prehospital Care Paramedics should recognize mechanisms of injury that may result in severe trauma to the pelvis, such as an automobile striking the pelvis of a pedestrian or heavy objects crushing the pelvis. On-scene times should be kept as short as possible in cases of severe pelvis injury. Paramedics should consider immobilizing the fractured pelvis using commercial pelvic binding devices or by wrapping the pelvis with a sheet and binding the legs together in cases of prolonged transit times of patients in shock with severe pelvis injury.[10]
History and Physical Examination As priorities permit, the emergency physician should obtain the following history: the mechanism of injury, location and radiation of pain, whether gross hematuria was present if voiding occurred after the injury, last menstrual period, and possibility of pregnancy. On inspection, rotation of the iliac crests indicates a serious pelvic fracture. Leg-length discrepancy may suggest a hip injury or cephalad migration of an unstable hemipelvis. The presence of tenderness on palpation of the sacrum and SI joints in patients with a Glasgow Coma Scale score of 12 or more is an important and reliable sign of injury to the posterior pelvis ring.[11] The integrity of the pelvic ring can be tested clinically by gentle lateral compression and distraction of the iliac crests and gentle inward compression of the symphysis pubis. Extensive movement of fracture fragments should be avoided when any instability is detected. Pain with axial percussion through the bottom of the foot may localize a hip injury or pelvic fracture site. Care must be exercised so that fractures are not displaced further by these maneuvers, which potentially could exacerbate pelvic fracture–related hemorrhage. Careful inspection of the skin and skin folds is necessary to identify open fractures. Perineal ecchymosis or hematoma may be observed, and in cases when many hours have elapsed since the injury, ecchymosis on the abdomen (Cullen's sign) or flanks (Grey Turner's sign) from retroperitoneal hemorrhage may be present. The penis should be milked to examine for blood at the meatus. The digital rectal examination should evaluate sensation, sphincter tone, position and consistency of the prostate, presence of a presacral hematoma, bony contour of the sacrum and coccyx, mucosal penetration of bony spicules, and presence of frank or occult blood. In the setting of a pelvic fracture, female patients should undergo a vaginal examination
Page 288
to diagnose an open fracture. Digital rectal and vaginal examinations must be performed carefully, especially in an unconscious patient who cannot localize pain, because it is possible to create an open fracture iatrogenically through the vaginal or rectal wall. The examiner should be mindful when performing these examinations that bony spicules can cause injury to self. Extravasated urine may be detected in the scrotum or the subcutaneous tissues of the penis, vulva, or abdominal wall. The presence and quality of pulses in the lower limb should be assessed, as should sensation, strength, and deep tendon reflexes.
Visceral and Soft Tissue Injuries Open Pelvic Fractures and Deep Perineal Laceration An open pelvic fracture is present when there is direct communication between the fracture site and a skin, rectal, or vaginal wound.[12] These are potentially lethal injuries, especially if the open nature is not recognized, with early mortality resulting from hemorrhage in the acute phase and sepsis and multiorgan failure in the delayed phase.[13] Even after introduction of an aggressive patient treatment protocol, the overall mortality rate of open pelvic fractures is 30% in several series and 78% in the subgroup of patients older than age 40.[] The patient must be rolled on his or her side and the skin over the posterior pelvis and gluteal area inspected carefully for wounds. Some fractures are open only by virtue of a bone spicule penetrating the vagina or rectum, but these must be identified by careful digital rectal and vaginal examinations. Hemorrhage from a large open laceration may be treated by external packing and application of a pressure dressing or packing followed by application of the pneumatic antishock garment.[] A perineal laceration should be inspected but not probed, for fear of disturbing hemostasis and introducing infection. The perineal wounds require aggressive operative debridement and irrigation, and in cases in which the rectum is violated, a diverting colostomy is required.[]
Urologic Injury The overall incidence of bladder or urethral disruption associated with pelvic fracture ranges from 7% to 25%. More than 80% of patients with lower urinary tract injury after blunt trauma have a pelvic fracture, however.[18] The length and tethered anatomy of the male urethra make it vulnerable to rupture in association with high-energy pelvic injuries. Urethral rupture in women with pelvic fractures is less common, but does occur.[19] Although there does not seem to be a significant relationship between the type of pelvic fracture and the type of bladder injury, fractures adjacent to or involving the symphysis pubis are associated most often with urologic injuries.[20] In 103 patients with pelvic fractures in whom cystography was performed, all patients with bladder rupture had fractures of the anterior pelvic arch.[21] It formerly was recommended that a pelvic fracture associated with gross or microscopic hematuria mandated cystourethrography; however, several studies show that microscopic hematuria is not associated with significant urologic injury in these patients.[] Urethrography and cystography are unnecessary in the absence of gross hematuria or clinical suspicion of bladder or urethral rupture.[] Blood at the urethral meatus necessitates a retrograde urethrogram followed by a cystogram. Gross hematuria is investigated by a combination of urethrography, intravenous pyelography, cystography, and computed tomography (CT). The sequence and types of examinations are individualized for each patient. Male sexual dysfunction is a recognized complication of pelvic trauma. The incidence of impotence associated with urethral rupture is significant. In the absence of urethral injury, impotence still may occur secondary to neurovascular disruption associated with the pelvic fracture.[24]
Neurologic Injury Neurologic injury occurs commonly in patients with pelvic ring fractures that have vertical sacral fractures as a component and with transverse fractures at or above the S3 level. Among patients with vertical fractures that involve the foramina, 28% have associated neurologic deficits. In patients with fractures medial to the foramina involving the spinal canal, 56% have neurologic deficits.[25] Autopsy and clinical studies performed on patients with pelvic fractures have documented disruptions by traction and compressive forces at many levels along the neural pathway: within the sacral spinal canal, within the neural foramina, distally in the roots and divisions that form the sacral and lumbar plexus, and to the various nerves derived from these plexus.[25 ]
Page 289
Cauda equina syndrome and various plexopathies and radiculopathies may occur as follows. Injury to the L5 root may cause weakness of muscles in the anterior tibial compartment and sensory deficits in the dorsum of the foot and lateral calf. Injury to S1 and S2 roots may cause weakness of hip extension, knee flexion, and plantar flexion and sensory deficits on the posterior aspect of the leg, sole and lateral foot, and genitalia. Injury to S2-5 roots and distal afferent, efferent, and autonomic fibers causes sensory deficits in the perineum, sexual dysfunction, and bowel and bladder dysfunction. Cauda equina syndrome may be fully or partially present with sacral fractures: There is hyperesthesia and later anesthesia in a saddle-shaped distribution in the groin; weakness of ankle plantar flexion, hamstrings, and gluteus muscles; and decreased or absent ankle jerk. With involvement of the lower sacral roots, a neurogenic bladder with overflow incontinence, motor and sensory deficits in the lower extremities, anal sphincter dysfunction, and sexual dysfunction may occur. All patients with neurologic deficits from sacral fractures require orthopedic or neurosurgical consultation.
Gynecologic Injury Vaginal bleeding may result from uterine or vaginal wall laceration secondary to deceleration forces or crush injury or, in a pregnant woman, secondary to abruptio placentae or uterine perforation. Most gynecologic injuries associated with pelvic fracture occur in pregnant patients; however, the nongravid uterus and the fallopian tube or ovary also may be injured.[] Dyspareunia may occur as a late sequela of pelvic fracture.[28] Sexual dysfunction in women also is reported as a sequela of pelvic fracture.[29] Gynecologic consultation is indicated when there is injury to the female reproductive tract in association with a pelvic fracture.
Thoracic Aorta There is a well-documented association between pelvic fracture and injury to the thoracic aorta.[30] This is presumably the result of the enormous forces required to produce either injury. In particular, anteroposterior compression fractures are associated with an eight times greater incidence of aortic rupture than is seen in the overall blunt trauma population.[30]
Penetrating Pelvic Trauma Because of the complex anatomy of the viscera, blood vessels, and nerves within the pelvis, penetrating trauma to this area presents a major challenge to the physician. Overall mortality in this group of patients has been reported to be 6% to 12%, but the mortality of patients in shock is 50%.[] At surgery, vascular injuries singly and in combination were found to involve the aorta; common iliac artery; and external, internal, and common iliac veins. Injuries to genitourinary structures and hollow viscera were common, and a particular concern was fecal contamination from colorectal injury. When present, the finding of blood on digital rectal examination is an important clue that rectal injury has occurred. Emergent surgical consultation is required in all cases of penetrating pelvic trauma.
DIAGNOSTIC STRATEGIES Radiology Routine radiographs of the pelvis are not necessary in asymptomatic, awake, alert blunt trauma patients who have a normal physical examination of the pelvis.[] The physician should obtain an anteroposterior plain radiograph of the pelvis early in the resuscitation phase, however, on all victims of severe blunt trauma who are symptomatic or have a compromised ability to perceive pain. Some sacral fractures and SI joint disruptions may not be well visualized on the anteroposterior view. In hemodynamically stable patients, two additional views—the inlet and outlet (tangential) projections—are often necessary to show these injuries. The anteroposterior, inlet, and outlet views identify virtually all clinically important bony injuries.[36]
Anteroposterior View The anteroposterior view of the pelvis identifies most pelvic fractures and dislocations but often does not show the degree of bony displacement. On the anteroposterior view, the symphysis pubis is normally no more than 5 mm wide, and a small (1 or 2 mm) vertical offset of the left and right pubic rami is normal.[37] Overlapping at the symphysis pubis is abnormal and is the result of a severe crushing injury. Normally the SI joint is approximately 2 to 4 mm wide.[37] On the anteroposterior view, the physician may judge the degree of pelvic rotation caused by technique and positioning by the presence of asymmetry in the size and shape of the left and right obturator foramina and iliac wings. Diastasis of the SI joint also causes an asymmetric appearance of the obturator foramina and the iliac wings: If there is displacement into external rotation, the affected iliac wing appears broader, and the anterior iliac spine appears more prominent.[37] Avulsion fracture of the fifth lumbar transverse process by
Page 290
the iliolumbar ligament often accompanies an SI joint disruption or a vertical sacral fracture and is a valuable clue to posterior arch injuries.[37]
Inlet View The inlet projection is obtained with the x-ray beam angled from the head toward the feet at 60 degrees to the plate such that it is perpendicular to the pelvic inlet ( Figure 52-2 ).[16] This view shows posterior and cephalic displacement of the fractures of the posterior arch, widening of the SI joint, and inward displacement of the anterior arch.
Figure 52-2 The inlet view. A Inlet x-ray projection of pelvis. 1, Beam is angled 60 degrees to plate. This view is possible with a portable m achine. B and C Inlet of pelvis is well shown in this radiograph of a unilateral vertical shear fracture with cephalad and posterior displacem ent of the left hem ipelvis (Tile type C1). 1, Norm al sacral ala on the right side; 2, left sacral ala is indistinct because of a vertical fracture, and the cephalad and posterior displacem ent of this hem ipelvis is shown by this inlet projection; 3, ischial spine on the left is partially obscured by bowel gas, but it is located m ore cephalad com pared with the right spine because of cephalad displacem ent of the left hem ipelvis; 4, fractured left superior pubic ram us with displacem ent cephalad; 5, on the inlet view, we are looking through the superior and inferior pubic ram i, which are superim posed so that the obturator foram ina are not seen.
Outlet View The opposite view is the outlet projection, in which the beam is at 30 degrees of cephalic angulation to the plate and is roughly perpendicular to the long axis of the sacrum. It is useful for showing sacral fractures and disruptions of the SI joints.[16] The inlet and outlet projections are performed by angling the beam, and they do not require the patient to be moved.
Computed Tomography Although anteroposterior, inlet, and outlet series detect most pelvic fractures and provide the necessary details for accurate classification,[36] CT has an important role in the planning of orthopedic treatment and the diagnosis of associated visceral injuries and hemorrhage. CT shows whether injuries to the posterior arch are impacted or unstable, or whether there is rotational deformity. CT has the added advantage of rapidly acquiring detailed information on the pelvic fracture and can be reconstructed from other studies, such as abdominopelvic CT scan. Because CT provides detailed information on injury to abdominal and pelvic visceral structures as well as the pelvic fracture, in many centers it has largely replaced plain radiography for suspected pelvic fracture in a hemodynamically stable patient.
Evaluation of Hemorrhage A high percentage of patients with retroperitoneal hemorrhage from pelvic fracture also have active intraperitoneal hemorrhage from coincident organ injury. In a hypovolemic patient with pelvic fracture, it is important to establish early on whether there is hemorrhage within the abdominal cavity necessitating laparotomy. Diagnostic strategies for evaluation of pelvic fracture–associated hemorrhage include diagnostic peritoneal lavage, ultrasound, and CT. Regardless of the modality of evaluation, it is crucial to avoid unnecessary laparotomy because of the higher mortality rate for hemodynamically unstable patients with pelvic fractures who undergo a negative abdominal exploration.
Diagnostic Peritoneal Lavage Diagnostic peritoneal lavage (DPL) is a widely accepted, rapid, and accurate means of establishing the presence of intra-abdominal hemorrhage. It has been largely supplanted in many centers by ultrasound, which is less invasive, and with CT in stable patients. Nevertheless, DPL is an important and effective tool to assist with difficult triage decisions in the trauma patient.[38] A pelvic fracture presents a special situation for DPL and requires an alteration in the technique and an understanding of the variables that can confound the result. DPL is safe and accurate in the presence of a pelvic fracture, provided that the fully open technique is employed (i.e., the peritoneum is entered under direct visual control).[39] If this requirement is met, the false-positive and false-negative rates are each 0.7%, which is comparable to the rates reported for DPL in
Page 291
patients without pelvic fractures.[39] Using the fully open technique prevents the operator from blindly entering a retroperitoneal hematoma that may have dissected into the anterior abdominal wall. The DPL may be performed in the infraumbilical location in most patients; however, the supraumbilical location should be employed if any of the following conditions are present: prior abdominal scars, time delay since the injury of more than 1 hour, or a hematoma encountered during the procedure.[39] DPL is useful in establishing the priorities for laparotomy, external fixation, and angiography in a hemodynamically unstable patient with major pelvic fractures, depending on whether the aspirate is negative or positive ( Figure 52-3 ).
Figure 52-3 Algorithm for initial m anagem ent of hem odynam ically unstable pelvic fractures. 10,45 Note: Ultrasound is in wide use in this setting, but its accuracy specifically in the presence of pelvic fracture–related hem orrhage has not been studied.
A negative peritoneal aspirate indicates that the peritoneal cavity is not a major source of bleeding or a significant contributor to hemorrhagic shock. Assuming that external and thoracic sources of blood loss have been eliminated as causes of hemodynamic instability, a negative DPL in a patient with a major pelvic fracture is evidence of the presence of a large retroperitoneal hematoma. Angiography with therapeutic embolization and mechanical fracture stabilization should be pursued aggressively. Gross aspiration of blood indicates possible major intra-abdominal hemorrhage. Immediate laparotomy is recommended for hemodynamically unstable patients with pelvic fractures.[] The lavage that is positive by cell count criteria alone is a special situation. If these patients are hemodynamically unstable, angiography with therapeutic embolization and external pelvis fixation should be performed before laparotomy.[]
Ultrasound (FAST) Focused assessment with sonography for trauma (FAST) is widely used to identify free intraperitoneal fluid rapidly in the trauma patient. The accuracy and safety of the FAST technique in evaluating patients with serious pelvic fractures who are hemodynamically unstable have not been published. Nevertheless, a positive FAST study that shows free fluid is widely used as a triage point to decide on laparotomy in a hemodynamically unstable patient with pelvic fracture. Important caveats relating to FAST in patients with pelvic fractures should be kept in mind. First, it is impossible to evaluate the retroperitoneum with diagnostic ultrasound. Second, there is a significant incidence of false-negative diagnostic ultrasound in patients with pelvic fractures.[42]
Computed Tomography If the patient is hemodynamically stable, CT of the abdomen may be undertaken to evaluate intraperitoneal and retroperitoneal injury. Additional cuts through the pelvis show the degree of displacement and rotation at the sites of pelvic fracture. CT scan with intravenous contrast often can distinguish a stable hematoma from ongoing bleeding from pelvic arteries.[43] The presence or absence of extravasated intravenous contrast material on CT scan of the pelvis is useful in predicting which patients will require therapeutic angiography.[] These comments on CT apply to a hemodynamically stable patient with pelvic injury; however, in a critically ill unstable patient, the value of FAST or DPL in quickly establishing treatment priorities should not be underestimated.
MANAGEMENT General Management Attempts should be made to stabilize the patient hemodynamically with crystalloid infusion. Transfusion of blood products should be initiated without delay in the presence of hypotension and a severe pelvic fracture.[ 10] Lower limb intravenous sites should be avoided in patients with severe pelvic fractures because the infused products may be delivered to the retroperitoneal space.[41] Wrapping the pelvis tightly with a sheet and securing this with towel clips or the use of a pelvic binder to splint the fracture temporarily and tamponade pelvic bleeding is recommended.[] Because many patients with severe pelvic fractures have concomitant injuries to other body systems, the potential need for and timing of laparotomy, angiography,
Page 292
and skeletal fixation must be considered early in the course of resuscitation. Figure 52-3 is an algorithmic representation of the investigation and resuscitation of a patient with pelvic injury.
Injury to Bone Classification Multiple classification schemes for pelvic fractures have been proposed. This chapter uses Tile's classification ( Box 52-1 ).[16] Tile's classification is based on the concepts of high-energy and low-energy forces, the mechanism of injury, and the biomechanical factors that together determine the need for external and internal fixation and predict the likelihood of serious hemorrhage and associated injuries. The biomechanical factors include the direction of forces applied to the pelvis, the concepts of rotational instability and vertical instability, and the importance of injury to the strong posterior ligaments of the pelvis.[] Fractures of the acetabulum are classified separately from other pelvic injuries. The terms unstable fracture (referring to mechanical stability) and unstable patient (referring to hemodynamic status) should not be confused, although a cause-and-effect relationship often exists. BOX 52-1 Tile's Classification of Pelvic Fractures
Type A—Stable pelvic ring injury A1— Avul sion fract ures of the inno mina te bone A2— Stabl e iliac wing fract ures or stabl e mini mall y displ aced ring fract ures A3— Tran sver se fract ures of the cocc yx
Page 293
and sacr um Type B—Partially stable pelvic ring injury (rotationally unstable, vertically stable) B1— Ope n book injur y— unila teral B2— Later al com pres sion injur y B3— Bilat eral type B injuri es Type C— Unstable pelvic ring injury (vertical shear) (rotationally and vertically unstable) C1 — Unila teral C2 — Bilat eral, one side type B, one side type C C3 — Bilat eral type C
Page 294
lesio ns From Tile M: Fractures of the Pelvis and Acetabulum, 2nd ed., Baltimore, Williams & Wilkins, 1995.
Low-Energy Fractures (Tile Type A) Stable Pelvic Ring Injury Fractures of individual bones without involvement of the pelvic ring represent one third of all pelvic fractures. In general, these are stable injuries that heal well with rest and analgesic drugs for pain control ( Figure 52-4 ).[16]
Figure 52-4 Fractures of individual pelvic bones. 1, Avulsion of anterosuperior iliac spine; 2, avulsion of anteroinferior iliac spine; 3, avulsion of ischial tuberosity; 4, fracture of superior pubic ram us; 5, fracture of inferior pubic ram us; 6, fracture of ischial ram us; 7, fracture of iliac wing; 8, transverse fracture of sacrum ; 9, fracture of coccyx.
Avulsion Fractures—Tile Type A1. Avulsion fractures (see Figure 52-4 ) usually occur during athletic activities and are the result of a sudden, forceful muscular contraction or excessive muscle stretch. They are seen more commonly in older children and teenagers before closure of the corresponding physis occurs; adults may have the same symptoms from ligamentous injury at these sites without radiographic abnormality. The ischial tuberosity may be avulsed during strenuous contraction of the hamstrings ( Figure 52-5 ). There is pain on palpation of the involved tuberosity, and this pain is increased by flexion of the hip with the knee in extension (hamstrings stretched), but not with the knee flexed (hamstrings relaxed). Ischial tuberosity avulsion also may cause chronic discomfort with no history of acute injury.
Figure 52-5 A and B Radiograph and interpretive drawing. 1, Avulsion of ischial tuberosity through epiphysis; 2, normal ischial epiphysis.
A portion of the iliac crest epiphysis may be avulsed by contraction of the abdominal muscles. Similarly, the anterior superior iliac spine may be avulsed by forcible contraction of the sartorius muscle. Forceful contraction of the rectus femoris (as in kicking a ball) can result in the less common injury of anterior inferior iliac spine avulsion; however, this radiographic finding must be distinguished from a normal variant, the os acetabuli, which is a secondary center of ossification at the superolateral margin of the acetabulum.[37] Clinical examination is similar in these injuries and reveals local pain, swelling, and limitation of motion. The conservative treatment of all these avulsion injuries is analgesia and bed rest in a position that avoids tension on the affected muscles. Orthopedic consultation is advised for follow-up care. Surgical treatment rarely is required.[48]
Stable, Minimally Displaced Fractures of the Pelvic Ring—Tile Type A2 The normal pelvis is not totally rigid because of the slight mobility at the SI joints and symphysis pubis and the inherent elasticity of bone. A single break in the ring is possible. Nevertheless, the pelvis is not totally
Page 295
forgiving, and identification of a single break in the ring should prompt a search for a second disruption.
Iliac Wing Fracture—Tile Type A2-1. Isolated fracture of the iliac wing was described by Duverney in 1751 and now bears his name. It is caused by direct trauma to the iliac crest, usually by lateral compression forces. Although displacement is usually minimal because of the arrangement of the muscle attachments of the abdominal wall, orthopedic consultation is recommended. The fracture may extend into the acetabulum, altering the treatment and prognosis. Severely displaced fractures of the iliac wing require open reduction and internal fixation.[16]
Stable Undisplaced or Minimally Displaced Fractures of the Pelvic Ring— Tile Type A2-2. An isolated fracture of the superior or inferior pubic ramus is the most common pelvic fracture. These fractures are stable and do not displace. They are common fractures in elderly people after a fall and must be considered in the evaluation of an acutely painful hip. Fracture of the body of the ischium is a rare injury that may result from a fall in the sitting position. These fractures around the obturator foramen are treated conservatively with bed rest, analgesia, and early mobilization. Fracture of the superior and inferior pubic rami on the same side is a commonly encountered injury after a fall or vehicular crash. These are generally stable fractures and are treated conservatively. The presence of significant displacement at the fracture site is an important finding and always indicates a second disruption elsewhere in the pelvic ring that must be diagnosed. Even in the absence of displacement, fractures of both rami on the same side may be associated with an unrecognized impaction fracture of the posterior pelvis. If the patient complains of pain in the posterior pelvis or if the radiograph is at all suspicious, further imaging is required. After a ramus fracture, some patients may complain of hip or SI pain despite plain radiographs of these areas that appear normal; these patients subsequently may develop symptoms and request re-evaluation. A study of patients who sustained apparently isolated pubic ramus fractures from simple falls showed increased uptake of radionuclides on bone scans in the acetabulum and SI joint, suggesting that occult bony or ligamentous injury accounted for the complaints of pain.[49] When such patients are evaluated, repeat plain radiographs should be performed. If radiographs are normal, symptomatic treatment, rest, and close follow-up can be prescribed. Radionuclide bone scan can be considered if confirmation of occult posterior injury is required. Stress fractures of the pelvis rarely have been reported with vigorous athletic or military training and in the last trimester of pregnancy.[] Pathologic fracture related to neoplasm, Paget's disease, or dietary osteomalacia is included in the differential diagnosis. Diagnosis of stress fractures is based on the clinical evaluation and can be confirmed by radionuclide bone scan if necessary.
Four-Pillar Anterior Ring Injuries—Tile Type A2-3. Also termed a straddle fracture, four-pillar injuries refer to fractures of both pubic rami on both sides of the symphysis pubis, causing the so-called butterfly segment ( Figure 52-6 ). The injury is produced by a direct blow with a straddle mechanism. Four-pillar injuries also commonly are associated with lateral compression or vertical shear forces, in which case there are concomitant injuries to the posterior pelvic arch, and the injury would be classified as a Tile type B or C. A CT scan of the pelvis is required in cases of four-pillar injuries to detect and classify precisely the posterior arch injury and plan orthopedic treatment.[16] The genitourinary tract frequently is injured concomitantly with this type of pelvic fracture and must be evaluated carefully (see Figure 52-6 ).
Figure 52-6 Four-pillar (straddle) fracture (Tile type A2-3). A and B Partial inlet view of pelvis shows straddle fracture. 1 and 2, Marked com m inution of left pubic bone and com m inuted right superior and inferior ram i. This partial inlet projection shows displacem ent of fragm ents into the pelvis, which is not evident on the anteroposterior view of the sam e patient in C and D. A true inlet projection and com puted tom ography scan (not available) would provide further inform ation about the posterior arch, which is injured frequently in straddle fractures and always should be imaged (see text). C and D Postvoid cystogram of the sam e patient with anteroposterior pelvis. 1, Fractures of pubic ram i are seen again, but do not appear to be as displaced compared
Page 296
with A and B because this projection is an anteroposterior view: Even m inor degrees of angulation of the x-ray beam can change the appearance of pelvic fracture displacem ent; 2, extravascular contrast indicates bladder rupture; 3, left acetabular fracture is seen in this projection but not in B because of the difference in projection. The acetabular fracture disrupts the ilioischial line (see also Figure 52-10) and is a posterior column fracture.
Transverse Fractures of the Coccyx and Sacrum—Tile Type A3 Coccygeal Fracture—Tile Type A3-1. Patients may present to the emergency department for evaluation of pain after direct trauma to the coccyx. The mechanism of injury is frequently a fall in the sitting position or a kick. Fracture and injury also may occur during parturition. Physical examination reveals local tenderness to palpation in the gluteal crease, with pain and, sometimes, abnormal motion of the coccyx during palpation on digital rectal examination. Normally the tip of the coccyx moves 30 degrees anteriorly and 1 cm laterally.[51] Displacement also is diagnosed on rectal examination, but attempts at reduction are not recommended. Radiographic confirmation of a coccygeal fracture is not always necessary. Displaced fractures often are seen on the lateral view, but the diagnosis is evident on rectal examination. Undisplaced fractures may be difficult to show radiographically. The physician must decide whether the knowledge gleaned from x-ray studies would alter the therapy to a degree that warrants radiation exposure to the pelvis, especially considering that most of these fractures occur in women. Treatment of coccygeal fracture consists of bed rest, stool softeners, analgesia, and sitz baths to relieve muscle spasm. As activity is increased, maneuvers that may minimize discomfort include using an inflatable rubber donut cushion, alternate sitting on the side of each buttock, slouching to displace body weight more proximally, and sitting on a hard chair rather than a soft one (sinking into a soft chair may distribute weight onto the coccyx).[51] Because of muscle action on the fragment, healing is slow and patients must be cautioned that discomfort may be prolonged. In the case of persistent severe disability, an orthopedic consultation is indicated for considerations of local steroid injection or possible coccygectomy.[52] Other causes of coccydynia (besides fracture) include trauma during parturition; faulty posture; midline disk herniations (caused by nonsegmental referral of pain from irritation of the dura); lumbar facet arthropathy; compression of the first, fourth, and fifth sacral roots; neuralgia from sacral plexopathy or sacrococcygeal neuropathy; infections; and local tumors.[51]
Sacral Fractures Several classification systems have been proposed for fractures of the sacrum and share a distinction between transverse and vertical fractures: The transverse fractures do not involve the pelvic ring, but vertical fractures of the sacrum do.[] The neurologic complication rate secondary to vertical sacral fractures and transverse fractures above the S4 level has been reported to be 21% to 34%[]; however, transverse fractures at or below S4 are unlikely to be accompanied by neurologic injury.[53] Orthopedic or neurosurgical consultation is warranted in all cases of sacral fracture.
Transverse Sacral Fracture—Tile Type A3-2 (Undisplaced), A3-3 (Displaced). An upper sacral transverse fracture is the result of a flexion injury, such as being struck on the lower back by a heavy load while bending over, or by direct forces to the sacrum, as in a fall from a great height.[53] The patient complains of pain in the buttocks, perirectal area, and posterior thighs. There may be local pain, swelling, and bruising overlying the sacrum, and on gentle bimanual rectal examination, severe pain, abnormal motion, and palpable hematoma may be elicited. Radiographically the fracture may be difficult to visualize on anteroposterior and lateral projections, in which case an outlet view may be helpful. Neurologic injuries also are common, with upper transverse sacral fractures necessitating careful clinical evaluation of sacral nerve root function. A lower sacral transverse fracture results from direct trauma to the area. Nerve injury is uncommon with this type of fracture.[53] The comments on general physical findings for upper transverse fracture are applicable here. Attempts at reduction of displaced sacral fractures bimanually through the rectum are discouraged because the injury may be converted to a contaminated open fracture, or an existing presacral hematoma may be enlarged. Surgery is commonly necessary for fractures associated with neurologic dysfunction.[] Simple lower transverse fractures with no associated injury are managed with bed rest and analgesia.
Vertical Sacral Fracture—Tile Type C1-3.
Page 297
Vertical sacral fractures are seen only as a component of high-energy fractures. Vertical fractures are classified further into three groups according to whether the fracture line extends lateral to the sacral foramina, through the foramina, or medial to them, involving the central spinal canal.[25] The diagnosis of this fracture on radiographs hinges on careful examination of the symmetrical cortical lines that are normally present at the superior margins of the sacral foramina on the anteroposterior view. Disruption, distortion, or asymmetry of these lines is an important marker of sacral fractures.[37]
High-Energy Fractures (Tile Types B and C) Transmission of high-energy forces to the pelvis causes injury to the posterior, weight-bearing arch resulting in double breaks in the pelvic ring. These are mechanically unstable fractures by definition, although the degree of instability varies with the pattern of the fractures. Because of the large amount of force required to produce these injuries, they commonly are associated with intraperitoneal injuries, retroperitoneal hemorrhage, and injuries to other body systems. A patient with a double break in the pelvic ring must be considered to be critically injured. Malgaigne first described these serious double-break fractures in 1859, defining the pattern of multiple fractures that included both pubic rami plus a constellation of posterior arch injuries on the same side. The term Malgaigne fracture is mentioned for its historical relevance; the newer classification allows for more precise descriptions of the injuries. The following discussion of high-energy injuries uses the Tile classification, which is based on the biomechanical concept that stability of the pelvis depends on an intact posterior weight-bearing arch whose tensile strength derives from the thick SI, sacrotuberous, and sacrospinous ligaments.[16] Important radiographic clues to the presence of serious posterior arch fractures are listed in Box 52-2 . BOX 52-2 Radiographic Clues to Posterior Arch Fractures
{,
Avul sion of L5 trans vers e proc ess[* ]
{,
Avul sion of ischi al spin e[*]
{,
Avul sion of lowe r later al lip of the sacr um (sac rotub erou s
Page 298
{,
{,
liga ment )[*] Displ ace ment at the site of a pubi c ram us fract ure Asy mm etry or lack of defin ition of bone corte x at supe rior aspe ct of the sacr al fora mina
* Always indicates m echanical instability.
Tile Type B: Partially Stable Pelvic Ring Injury (Rotationally Unstable but Vertically Stable) Open-Book—Tile Type B1 (Unilateral) and B3 (Bilateral). Severe anteroposterior compression forces result in disruption at or near the symphysis pubis. As the forces continue in the anteroposterior vector, external rotation of the hemipelvis occurs, and the anterior SI ligament and sacrospinous ligaments rupture. The SI joint rotates open as a hinge supported by the intact posterior SI ligament, and the resulting injury is aptly described as an open-book fracture.[16] The other ligaments also remain intact; the injury is rotationally unstable but vertically stable.[16] When diastasis of the pubic symphysis is greater than 2.5 cm on the anteroposterior radiograph, the posterior injury is usually evident (most often SI diastasis, but occasionally sacral or iliac fracture) ( Figure 52-7 ).[16] CT of open-book fractures shows the anterior part of the SI joint to be widened, but the posterior portion to be normal; however, if the injurious forces continue, they may separate the hemipelvis, and the SI joint is seen as widely separated on the plain anteroposterior radiograph and the CT scan.[16] The anteroposterior radiograph may be misleading in suggesting a pure open-book fracture in cases with symphysis disruptions greater than 2.5 cm. These cases commonly are associated with severe type C vertical shear fractures, and careful clinical and CT assessment for vertical instability is essential to classify the fracture properly and plan treatment.[16]
Page 299
Figure 52-7 A and B Interpretive drawing and radiograph. Severe unilateral open-book fracture (Tile type B1) from anteroposterior com pression forces that is also open (com pound). 1, Separated pubic sym physis with asym m etry of hem ipelvis; 2, norm al sacroiliac joint; 3, separated sacroiliac joint; 4, cystogram with displacem ent and abnorm ally elongated shape of bladder caused by retroperitoneal hematom a associated with separated left sacroiliac joint, which has pushed the bladder to the right; 5, extravasated contrast into perineum from urethral rupture; 6, soft tissue air indicating an open fracture.
These same forces also may injure the neurologic and vascular structures at the posterior arch; the overall volume of the pelvis is increased in the open-book injury, allowing the expansion of a retroperitoneal hematoma. In several studies of patients with major pelvic ring disruptions, patients with severe grades of anteroposterior compression injuries have the highest crystalloid and blood requirements.[]
Lateral Compression Injury—Tile Type B2. Severe forces applied sideways through the pelvis cause inward rotation of the hemipelvis and reduce the pelvic volume by causing the following lesions. In the anterior arch, the possibilities are double rami fractures on the same side as the posterior injury (Tile type B2-1); double rami fractures on the opposite side of the posterior injury, the so-called bucket-handle fracture (Tile type B2-2); or an overriding symphysis pubis. In the posterior arch, the possibilities are impacted vertical fracture through the sacrum, anterior crush of the SI joint with intact posterior ligaments, or an impacted posterior complex with disrupted posterior ligaments and severe rotational instability ( Figure 52-8 ).[16] Compared with anteroposterior compression and vertical shear fractures, lateral compression fractures are associated with the least requirement for fluid replacement in general.[55]
Figure 52-8 Lateral com pression fracture (Tile type B2). A and B Anteroposterior view of the pelvis. 1, Norm al sacral foram inal lines on the left; 2, sacral foram inal lines on the right are indistinct and do not m irror the norm al side, indicating the subtle second break in the pelvic ring; 3 and 4, fractures of the superior and inferior pubic ram i are overriding and displaced, indicating the lateral com pression forces (there m ust be a second break in the pelvic ring); 5, normal sacroiliac joints. C and D Com puted tom ography scan of sam e pelvis. 1, Norm al sacroiliac joints; 2, com pression fracture of the sacrum through the foram en corresponding to the loss of definition of the foram inal lines in A and B.
Tile Type C: Unstable Pelvic Ring Injury (Rotationally Unstable and Vertically Unstable) Vertical Shear. The forces transmitted through the pelvis causing the injury in type C fractures have sheared through the posterior ligamentous complex, tearing them completely, and across the bony trabecular pattern, causing that hemipelvis to displace posteriorly and possibly cephalad.[47] This is a mechanically unstable pelvic injury and doubly so if vertical shear occurs on each side of the sacrum ( Figure 52-9 ). Type C fractures may be unilateral (C1), bilateral (C3), or a combination of a type C on one side and a type B on the other (classified as C2). Anteriorly the symphysis pubis or two to four pubic rami may be disrupted. Posteriorly there is gross displacement and instability through the sacrum, the SI joint, or the ileum.[]
Page 300
Figure 52-9 A and B Vertical shear fractures bilaterally (Tile type C3). At first glance, the pelvis appears normal because of the sm ooth, uninterrupted arcuate line, but careful interpretation reveals the extremely critical nature of the injuries: 1, Fractures through the sacrum —note loss of definition and sym m etry of sacral foram ina indicating vertical fractures through both sides of the sacrum (see com puted tom ography scan in D). 2, Transverse process fragment from right L5 (iliolum bar ligam ent attachm ent) is pathognom onic for a vertical shear fracture through the right sacrum. 3, Transverse process fragm ent from left L5, pathognom onic for a vertical shear fracture through the left sacrum . 4, Both hem ipelves are dislocated cephalad because of the double-ring fractures through each side of the sacrum . This dislocation explains why the L5 transverse processes appear so close to the iliac crests (the body of L5 is obscured because of rotational dislocation of the central free sacral fragm ent posteriorly and because of technique). 5, Norm al sacroiliac joints. C and D Com puted tom ography scan of sam e pelvis. 1, Bilateral com m inuted fractures of sacrum with lateral displacem ent of both hem ipelves; 2, norm al sacroiliac joints.
Avulsion of the ischial spine, the lower lateral lip of the sacrum, or the transverse process of the fifth lumbar vertebra (sites of insertion of ligaments) (see Figure 52-9 and Box 52-2 ) are important clues to the presence of vertical shear fractures.[47] The vertical shearing forces that act on the bone also act on the rich vascular network and nerve plexus that are directly adjacent to the bone. This activity accounts for the major hemorrhage and neurologic injuries associated with vertical shear fractures.
Implications of High-Energy Pelvic Injuries The implications of these injuries reach far beyond the issue of mechanical stability of the pelvis. The mortality rate for patients with vertical shear fractures was 25% and for anteroposterior compression fractures was 14% to 26% in a series totaling almost 2900 patients.[] High-energy fractures also are associated with major blood transfusion requirements, with one series reporting an average of 14.8 U in the anteroposterior compression group, 9.2 U in the vertical shear group, and 3.6 U in the lateral compression group.[55] These serious fractures attest to the large magnitude of force at the time of injury. They mandate an aggressive search for associated trauma to other body regions and a timely use of blood products, especially in elderly patients. Orthopedic consultation should be obtained early in the care of these patients because surgical stabilization of the pelvis can reduce the amount of retroperitoneal bleeding and late sequelae.
Acetabular Fractures Many pelvic fractures in adults involve the acetabulum. The force of injury can be transmitted to the acetabulum through the femur (e.g., striking the dashboard in an automobile crash) or laterally through the side of the hip. On physical examination, hip pain with reproduction of these forces (percussing the sole of the foot and the greater trochanter) is a helpful finding. Tile has a widely accepted separate classification for acetabular fractures ( Box 52-3 ). These four types may occur in combination with each other or in association with a femoral head dislocation or fractures of the pelvic ring. The radiographic anatomy of the acetabulum is explained in Figure 52-10 . BOX 52-3 Acetabular Fractures
{,
{,
Post erior lip fract ure Cent ral or trans vers e fract
Page 301
{,
{,
ure Ante rior colu mn fract ure Post erior colu mn fract ure
Figure 52-10 Schem atic drawing of radiographic anatom y of acetabulum in anteroposterior pelvis projection. a, Arcuate (iliopubic) line. b, Ilioischial line. c, Radiographic U or teardrop caused by superim position of parasagittal surface of ileum onto anteroinferior portion of acetabulum. d, Acetabular roof. e, Anterior lip of acetabulum . f, Posterior lip of acetabulum . ((Redrawn from Rogers LF, Novy SB, Harris NF: Occult central fractures of the acetab ulum . AJR Am J Roentgenol 124:98, 1975.))
The posterior lip fracture is the first and the most common form of acetabular fracture and usually is associated with posterior dislocation of the femoral head.[16] The second fracture is the central or transverse fracture. On the anteroposterior view of the pelvis, the fracture line crosses the acetabulum horizontally or obliquely and usually is seen clearly (see Figure 52-6D ). Three separate centers of ossification join within the acetabulum to form the innominate bone. This junction, called the triradiate cartilage, is seen as a Y-shaped lucency in the acetabulum until solid bony union occurs around age 20. On radiographs, this normal anatomic feature may be mistaken for a central fracture, although true fractures also can occur through the triradiate cartilage. Comparison views with the uninjured side may be helpful in difficult cases. The third fracture type involves the anterior, or iliopubic, column, which is formed by bone extending from the ilium to the pubis. The fracture disrupts the arcuate line, and the iliopubic column and radiographic U are usually displaced medially, but the ilioischial line remains intact ( Figure 52-11 ; see Figure 52-10 ). In the case of central dislocation, the femoral head also is displaced medially.
Figure 52-11 A and B Interpretive drawing and radiograph. Acetabular fracture from lateral com pression forces in the third trim ester. 1, The fetus (cranium punctured by acetabular bone); 2, medial dislocation of fem oral head with acetabular fracture; 3, arcuate line (see Figure 52-10) disrupted with medial displacem ent of anterior (iliopubic) colum n; 4, ilioischial colum n fragm ent; 5, left superior and inferior pubic ram i fractures. Note: Fetal assessm ent and m anagem ent would take precedence in this case over m aternal m echanical skeletal dysfunction.
The fourth fracture type involves the posterior or ilioischial column, which is the bone extending from the ilium to the ischium. The entire posterior column becomes separated from the pelvis: The fracture line begins at the sciatic notch, traverses the acetabulum, and ends near the ischiopubic junction. In cases in which the acetabular component is not displaced, it may be difficult to diagnose a posterior column fracture
Page 302
on the anteroposterior radiograph. Two helpful radiographic clues are discontinuity of the ilioischial line and separation of the ilioischial line from the radiographic U. CT scan of the acetabulum is the most sensitive imaging modality for further delineation of an acetabular fracture. If CT is not readily available, the external and internal plain film oblique views, also called the Judet views, are useful for imaging the acetabulum and both columns. After a fall, some patients may complain of extreme hip pain and inability to bear weight despite normal anteroposterior pelvis and lateral hip radiographs. An occult acetabular fracture should be considered in this situation, and further imaging should be pursued.
Hemorrhage Mortality in patients with blunt trauma who have the combination of pelvic ring fractures and hemorrhagic shock is approximately 50%.[] In the emergency department phase of the care of patients with pelvic fractures, the goals in terms of hemorrhage are as indicated in Box 52-4 . Blood transfusion is essential treatment, particularly for a patient with anteroposterior compression or vertical shear fracture who is hypotensive and has not responded well to crystalloid infusion. Either of the following simple findings on the anteroposterior view of the pelvis is predictive of the need for major blood transfusions: (1) an open-book fracture or (2) displacement of 0.5 cm or more at any fracture site in the pelvic ring.[56] BOX 52-4 Pelvic Fracture–Related Hemorrhage: Goals in the Emergency Department
1.
Res usci tatio n: Rec ogni ze the patie nt who is in hem orrh agic shoc k, and initiat e bloo d trans fusio n early in the resu scita tion.
2.
Rec ogni tion: Reali ze that
Page 303
3.
patie nts with post erior arch injuri es may have a retro perit onea l hem atom a contr ibuti ng to their hypo vole mic state . Eval uati on: Ident ify the patie nt who, in addit ion to a poss ible retro perit onea l hem atom a, has intraabdo mina l blee ding that nece ssita tes lapar otom
Page 304
4.
5.
y. Stab ilizat ion: Mini mize mov eme nt of bone at the fract ure sites so as not to distu rb the hem ostat ic proc esse s. Emb oliza tion: Und ersta nd the role and timin g of angi ogra phy in man agin g the patie nt.
In addition to blood transfusion, two important therapeutic modalities for control of hemorrhage are mechanical stabilization of the pelvis and angiographic embolization. There has been some debate as to which of these modalities should take precedence, and this has been predicated on institutional availability. As a general rule, angiography with therapeutic embolization of bleeding arteries is more effective than and takes precedence over external fixation.[]
Mechanical Stabilization External Fixation Acute application of an external fixator has not been proved to decrease morbidity or mortality in a prospective study; however, there is evidence that this technique improves clinical outcome by limiting hemorrhage and restoring mechanical integrity.[57] Many experts believe that this is the preferred method of
Page 305
stabilizing the anterior arch of the pelvis to prevent movement at pelvic fracture sites and attendant bleeding.[ 16] Application of the fixator is time-consuming, however, and should not delay more definitive treatment of pelvic or other injuries. In many centers with a multispecialty trauma service, indications for and rapid access to external fixation are predetermined by protocol, which mandates orthopedic consultation as soon as a high-energy pelvic injury is identified. From a mechanical point of view, lower grades of anteroposterior and lateral compression fractures can be treated definitively by the external fixator.[16] In vertically unstable fractures and anteroposterior compression fractures with unstable posterior elements, the external fixator can assist in the correction of external or internal rotation, but does not provide definitive stabilization of the important vertical displacement. Its use in these injuries is as a temporizing measure initially or as an adjunct to traction or open reduction and internal fixation.[] The external fixator must be constructed and applied with consideration of the biomechanical properties of the fracture. Most fixators can be constructed to allow convenient surgical access to the abdomen and groin. The antishock pelvic clamp is a device that can be applied rapidly by the orthopedic surgeon in the emergency department to externally stabilize the posterior pelvic arch on an emergency basis.[] The mechanical design of this and similar devices and standards of practice in the use of these devices are evolving.
Open Reduction and Internal Fixation Indications and modalities of open reduction and internal fixation, either acute or delayed, vary depending on the patient's other injuries, the timing of other surgeries, and the surgeon's preference.[]
Angiography and Embolization The techniques of arteriography and venography have been investigated for their usefulness in managing hemorrhage associated with pelvic fractures. Most commonly, the source of retroperitoneal hemorrhage with pelvic fractures is the venous plexus or smaller veins; however, venography is not useful in managing these patients because even when venous bleeding points are localized, embolization is ineffective because of the extensive anastomoses and valveless collateral flow. In contrast, arteriography is a major diagnostic and therapeutic modality for a patient with severe pelvic hemorrhage from arterial sources. The arteriogram is performed with the contrast material injected through the femoral artery on the least-injured side or via the upper extremity. The examination starts above the level of the aortic bifurcation and proceeds to selective branches of the internal iliac (hypogastric) artery.[7] Transcatheter embolization using thrombogenic coils, foam, or spherules is employed to stop the hemorrhage from the branches of the internal iliac artery ( Figure 52-12 ). In one study, the average blood requirement per patient in the 48 hours or less before embolization was 32 U, but it decreased to 5 U in the 48 hours after embolization.[62]
Figure 52-12 Unilateral open-book fracture (Tile type B1) from anteroposterior com pression forces—pre-em bolization angiogram s. Despite external fixation and control of nonpelvic sources of bleeding, this patient required ongoing blood transfusion. A and B Angiography showed bleeding from a branch of the right iliolumbar artery (1). Extravasated dye reflects bleeding only at the instant of photograph; actual hematom a would be quite large. After em bolizing this artery, the opposite side was exam ined (B and C). On this side, arterial hem orrhage from the left internal pudendal artery (2) was identified and em bolized (postem bolization film s are not included because of space considerations). 3, Marked diastasis of sym physis pubis; 4, right sacroiliac joint diastasis; 5, fracture of inferior pubic ram us; 6, external fixator. ((Angiogram s courtesy of R.L. Desm arais, MD, and P. Rasuli, MD.))
Angiography is indicated when hypovolemia persists in a patient with a major pelvic fracture, despite control of hemorrhage from other sources. Recommended criteria for angiography are (1) more than 4 U of blood transfused for pelvic bleeding in less than 24 hours, (2) more than 6 U of blood transfused for pelvic bleeding in less than 48 hours, (3) large pelvic hematoma seen on CT scan, (4) hemodynamic instability and negative DPL or negative FAST, and (5) large and expanding retroperitoneal hematoma seen at the time of
Page 306
laparotomy.[63] Additionally, extravasated contrast blush at the time of contrast-enhanced CT is a marker of the need for angiography.[] The timing of angiography is individualized for each patient depending on priorities for treatment of concomitant injuries. While setting these priorities, physicians should remember that posterior arch disruptions are associated with the most severe hemorrhage; angiography should be considered at an early stage for these patients. Some patients require surgery for treatment of other injuries before undergoing angiography; others proceed directly to the angiography suite from the emergency department. A logistical delay often occurs in mobilizing the angiography team, so this intervention must be anticipated as early as possible. The transfer of the patient to the angiography suite also requires orchestrating the necessary personnel and equipment to care for the critically injured patient there.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/122.html/top
Page 307
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
KEY CONCEPTS {,
{,
{,
{,
{,
{,
The most serious high-energy pelvic injuries are anteroposterior compression fractures (open book) and vertical shear fractures. High-energy pelvic injuries can be diagnosed using anteroposterior, inlet, and outlet views. When the patient is hemodynamically stable, a CT scan should be obtained to identify associated injuries to viscera, to identify a retroperitoneal hematoma, and to plan definitive orthopedic care. The emergency physician should anticipate the need for large amounts of blood products. Concomitant injuries to the aortic arch, diaphragm, solid viscera, and genitourinary tract are common. Careful examination of the skin in the perineum and buttocks and digital rectal and vaginal examinations are necessary to diagnose open fractures because these have the highest mortality rates.
Page 308
{,
{,
{,
Trauma hospitals should have institutional guidelines and mechanisms to access angiography and external fixation. The combination of posterior arch fracture plus a hypotensive patient is potentially lethal, with a mortality rate of approximately 50%. Aggressive resuscitation with blood products is recommended. Decisions regarding the need for angiographic transcatheter embolization and external pelvic fixation must be made early in the course of care. Open-book fractures and displacement at any fracture site of more than 0.5 cm are predictors for major blood transfusion requirements.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/123.html/top
Page 309
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
REFERENCES 1. Dalal SA: Pelvic fracture in multiple trauma: Classification by mechanism is key to pattern of organ injury, resuscitative requirements and outcome. J Trauma1989;29:981. 2. Poole GV, Ward EF: Causes of mortality in patients with pelvic fractures. Orthopedics1994;17:691. 3. Pohlemann T: Pelvic fractures: Epidemiology, therapy and long term outcome: Overview of the multicenter study of the pelvis study group. Unfallchirurg1996;99:160. 4. Gansslen A: Epidemiology of pelvic ring injuries. Injury1996;27(Suppl 1):S-A13. 5. Eastridge BJ, Burgess AR: Pedestrian pelvic fractures: 5 year experience of a major urban trauma center. J Trauma1997;42:695. 6. Eastridge BJ: The importance of fracture pattern in guiding therapeutic decision making in patients with hemorrhagic shock and pelvic ring disruptions. J Trauma2002;53:446. 7. O'Neill PA: Angiographic findings in pelvic fractures. Clin Orthop1996;329:60. 8. Starr AJ: Pelvic ring disruptions: Prediction of associated injuries, transfusion requirement, pelvic arteriography, complications and mortality. J Orthop Trauma2002;16:553. 9. Maull KL, Sachatello CR: Current management of pelvic fractures: A combined surgical-angiographic approach to hemorrhage. South Med J1976;69:1285. 10. Biffl WL: Evolution of a multidisciplinary clinical pathway for the management of unstable patients with pelvic fractures. Ann Surg2001;233:843. 11. McCormick JP, Morgan SJ, Smith WD: Clinical effectiveness of the physical examination in diagnosis of posterior pelvic ring injuries. J Orthop Trauma2003;17:257. 12. Brenneman FD: Long-term outcomes in open pelvic fractures. J Trauma1997;42:773. 13. Jones AL: Open pelvic fractures: A multicenter retrospective analysis. Orthop Clin North Am 1997;28:345. 14. Birolini D: Open pelviperineal trauma. J Trauma1990;30:492. 15. Hanson P, Milne J, Chapman M: Open fractures of the pelvis. J Bone Joint Surg1991;73B:325. 16. Tile M: Fractures of the Pelvis and Acetabulum, 2nd ed. Baltimore, Williams & Wilkins, 1995. 17. Davidson BS: Pelvic fractures associated with open perineal wounds: A survivable injury. J Trauma 1993;35:36. 18. Watnik NF, Coburn M, Goldberger M: Urologic injuries in pelvic ring disruptions. Clin Orthop1996;329:37. 19. Diekmann-Guiroy B, Young D: Female urethral injury secondary to blunt pelvic trauma. Ann Emerg Med 1991;20:1376. 20. Cass AS: The multiple injured patient with bladder trauma. J Trauma1984;24:731. 21. Hochberg E, Stone NN: Bladder rupture associated with pelvic fracture due to blunt trauma. Urology 1993;41:531. 22. Fallon B, Wendt JC, Hawtrey CE: Urological injury and assessment in patients with fractured pelvis. J Urol1984;131:712. 23. Antoci JP: Bladder and urethral injuries in patients with pelvic fractures. J Urol1982;128:25. 24. Ellison M, Timberlake GA, Kerstein MD: Impotence following pelvic fracture. J Trauma1988;28:695. 25. Denis F, Davis S, Comfort T: Sacral fractures: An important problem. Clin Orthop1988;227:67. 26. Smith J: Avulsion of the nongravid uterus due to pelvic fracture. South Med J1989;82:70. 27. Doman AN, Hoekstra DV: Pelvic fracture associated with severe intra-abdominal gynecologic injury. J Trauma1988;28:118. 28. Wilkes RA, Seymour N: Dyspareunia due to exostosis formation after pelvic fracture. Br J Obstet Gynaecol1993;100:1050. 29. Kiely N, Williams N: Sexual dysfunction in women following pelvic fractures with sacro-iliac disruption. Injury1996;27:45. 30. Ochsner MG: Associated aortic rupture-pelvic fracture: An alert for orthopedic and general surgeons. J Trauma1992;33:429. 31. Duncan AO: Management of transpelvic gunshot wounds. J Trauma1989;29:1335. 32. Malangoni MA: The management of penetrating pelvic trauma. Am Surg1990;56:61. 33. Civil ID: Routine pelvic radiography in severe blunt trauma: Is it necessary?. Ann Emerg Med 1988;17:488.
Page 310
34. Salvino SK: Routine pelvic x-ray studies in awake blunt trauma patients: A sensible policy?. J Trauma 1992;33:413. 35. Koury HI, Peschiera JL, Welling RE: Selective use of pelvic roentgenograms in blunt trauma patients. J Trauma1993;34:236. 36. Resnick CS: Diagnosis of pelvic fractures in patients with acute pelvic trauma: Efficacy of plain radiographs. AJR Am J Roentgenol1992;158:109. 37. Rogers LF, Bradd FJ, Kennedy W: Radiology of Skeletal Trauma, New York, Churchill Livingstone, 1992. 38. Nagy KK: Experience with over 2500 diagnostic peritoneal lavages. Injury2000;31:479. 39. Mendez C, Gubler KD, Maier RV: Diagnostic accuracy of peritoneal lavage in patients with pelvic fractures. Arch Surg1994;129:477. 40. Moreno C: Hemorrhage associated with major pelvic fracture: A multispecialty challenge. J Trauma 1986;26:987. 41. Mucha P, Welch TJ: Hemorrhage in major pelvic fractures. Surg Clin North Am1988;68:757. 42. Ballard RB: An algorithm to reduce the incidence of false-negative FAST examinations in patients at high risk for occult injury. J Am Coll Surg1999;189:145. 43. Cerva DS: Detection of bleeding in patients with major pelvic fractures: Value of contrast enhanced CT. AJR Am J Roentgenol1996;166:131. 44. Stephen DJ: Early detection of arterial bleeding in acute pelvic trauma. J Trauma1999;47:638. 45. Miller PR: External fixation or arteriogram in bleeding pelvic fracture. J Trauma2003;54:437. 46. Routt MLC: Circumferential pelvic antishock sheeting: A temporary resuscitation aid. J Orthop Trauma 2002;16:45. 47. Tile M: Pelvic ring fractures: Should they be fixed?. J Bone Joint Surg1988;70B:1. 48. Lynch SA, Renstrom AFH: Groin injuries in sport: Treatment strategies. Sports Med1999;28:137. 49. Gertzbein SD, Chenoweth DR: Occult injuries of the pelvic ring. Clin Orthop1977;128:202. 50. Pavlov H: Roentgen examination of groin and hip pain in the athlete. Clin Sports Med1987;6:829. 51. Traycoff RB, Crayton H, Dodson R: Sacrococcygeal pain syndromes: Diagnosis and treatment. Orthopedics1989;12:1373. 52. Wray CC, Easom S, Hoskinson J: Coccydynia: Aetiology and treatment. J Bone Joint Surg 1991;73B:335. 53. Gibbons KJ, Soloniuk DS, Razazk N: Neurologic injury and patterns of sacral fractures. J Neurosurg 1990;72:889. 54. Schied DK, Tile M, Kellam JF: Open reduction internal fixation of pelvic ring fractures. J Orthop Trauma 1991;5:226. 55. Burgess AR: Pelvic ring disruptions: Effective classification system and treatment protocols. J Trauma 1990;30:848. 56. Cryer HM: Pelvic fracture classification: Correlation with hemorrhage. J Trauma1988;28:973. 57. Wolinsky PR: Assessment and management of pelvic fracture in the hemodynamically unstable patient. Orthop Clin North Am1997;28:321. 58. Kellam JF: The role of external fixation in pelvic disruptions. Clin Orthop1989;241:66. 59. Ganz R, Krushell RJ, Jakob RP: The antishock pelvic clamp. Clin Orthop1991;267:71. 60. Heini PF, Witt J, Ganz R: The pelvic C-clamp for the emergency treatment of unstable pelvic ring injuries: A report on clinical experience of 30 cases. Injury1996;27(Suppl 1):S-A38. 61. Gruen GS: The acute management of hemodynamically unstable multiple trauma patients with pelvic ring fractures. J Trauma1994;36:706. 62. Matalon TSA: Hemorrhage with pelvic fractures: Efficacy of transcatheter embolization. AJR Am J Roentgenol1979;133:859. 63. Henry SM, Tornetta P, Scalea TM: Damage control for devastating pelvic and extremity injuries. Surg Clin North Am1997;77:879.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/124.html/top
Page 311
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
Chapter 53 – Femur and Hip Michael A. Gibbs Edward J. Newton James F. Fiechtl
PERSPECTIVE Background Ancient Egyptian and Greek drawings depict a lame person afflicted with hip deformities ambulating with a cane. The first available written description of a hip fracture was by the 16th century French surgeon Ambroise Paré.[1] In 1850, Von Langenbeck was the first to attempt repair of a hip fracture with a nail for internal fixation. Later, Davis used ordinary wood screws in an attempt to aid the healing of femoral neck fractures.[2] With the advent of radiography in the 19th century, the types of fractures and dislocations became easily identifiable, thus allowing discussion and investigation of management strategies, classification systems, and prognosis.
Epidemiology Both age and gender are important predisposing factors for specific injury patterns and pathologic conditions occurring in the hip, femur, and thigh. As a whole, the elderly segment of society almost universally suffers from some type of hip pathology. Osteoarthritis of the hip may severely limit one's ability to perform activities of daily living. Approximately 6 million women in the United States suffer from osteoporosis, and an additional 17 million have osteopenia, both of which predispose to hip fracture.[3] During the late 1990s, approximately 250,000 patients a year sought treatment in emergency departments after sustaining a hip fracture.[4] As baby boomers mature, the number of hip fractures is expected to reach half a million a year by 2050.[5] Eighty percent of femoral neck fractures occur in men. The average age of patients with femoral neck fractures is 72 years for men and 77 years for women.[6] On average, intertrochanteric fractures occur 10 to 12 years later than those of the femoral neck, and women are afflicted eight times more often than men.[7] Overall, three quarters of all hip fractures occur in postmenopausal women older than 50 years.[3] Perthes' disease (avascular necrosis [AVN] of the femoral head) is four times more common in boys than girls and occurs between 3 and 12 years of age. Slipped capital femoral epiphysis (SCFE) is twice as common in boys and peaks at 13 years of age for boys and 11 years for girls in association with the onset of puberty.
PRINCIPLES OF DISEASE Anatomy of the Hip and Femur Skeletal Anatomy The femoral head is firmly seated in the acetabulum, which is reinforced by labral cartilage. The welldeveloped capsule, overlying ligaments, and proximal musculature of the lower extremity add strength to the joint ( Figure 53-1 ). The nearly spherical femoral head articulates with the acetabular cup in a variation of the “ball-and-socket” joint.
Figure 53-1 The ligam ents of the hip com bine to form a tough joint capsule as seen in both anterior (A) and posterior (B)
Page 312
views.
The femur is the longest and strongest bone in the human body and is routinely subjected to substantial forces produced during powerful muscle contraction and weight transmission. In an anatomic position, the two femurs extend obliquely from the pelvis medially to the knee and bring the legs closer to the midline, where they can best support the body. Structurally, the femoral neck serves as an oblique strut between the pelvis (the horizontal beam) and the shaft of the femur (the vertical beam) ( Figure 53-2 ). The length, angle, and narrow circumference of the femoral neck permit substantial range of motion at the hip, but these same characteristics subject the neck to incredible shearing forces. A fracture results when these forces exceed the strength of the bone. The intertrochanteric line, an oblique line connecting the greater and lesser trochanter, marks the junction of the femoral neck and its shaft.
Figure 53-2 Bony architecture of proxim al end of the fem ur.
The bone in the femoral head, neck, and intertrochanteric region is predominantly cancellous. This type of structural bone is less resistant to forces produced by torsion than is solid bone. Distal to the intertrochanteric region, the femur is composed predominantly of cortical bone. The subtrochanteric region extends from the superior aspect of the lesser trochanter distally to the center of the isthmus of the femoral shaft. The shaft is a nearly cylindrical tubular structure that flares posteriorly along the linea aspera (rough line) where the fascia inserts. The shaft becomes predominantly cortical and requires greater force to cause failure. The distal metaphysis widens into the condyles at the knee. As the cortex widens and thins, the stress forces increase at the supracondylar region.
Musculature The musculature of the hip and thigh is the largest and most powerful in the human body. The muscles in this region of the body are located within three different compartments, each containing associated nerves and vessels ( Table 53-1 ). The muscles are also grouped according to their primary action at the hip. Knowledge of the major muscle actions offers insight into the injury patterns and deformities commonly seen ( Figure 53-3 ). Table 53-1 -- Contents Found within the Compartments of the Thigh Compartme Muscles nt
Nerves
Vessels
Anterior
Quadriceps femoris, sartorius, iliacus, psoas, pectineus
Lateral femoral cutaneous
Femoral artery and vein
Medial
Gracilis, adductor longus and magnus, obturator externus
Obturator
Profundus femoris artery, obturator artery and vein
Posterior
Biceps femoris, semitendinosus, semimembranosus, adductor magnus
Sciatic, posterior femoral cutaneous
Profundus femoris branches
Figure 53-3 A and B, Anatom ic illustration of the m ajor m uscles acting about the hip and thigh.
Page 313
Vascular Anatomy Arterial Supply The arterial supply to the femoral head arises from three sources ( Figure 53-4 ). The major source is the ascending cervical arteries as they branch off the extracapsular ring and run along the femoral neck beneath the synovium. Some blood is supplied to the femoral head from the second source, which is within the marrow spaces as intraosseous cervical vessels. A third and dubious source is from the foveal artery as it lies within the ligamentum teres.
Figure 53-4 The arterial blood supply of the femoral neck and head is provided to varying degrees by three sources: the ascending cervical arteries, the arterial branches within the m arrow (not illustrated), and the dubious foveal artery within the ligam entum teres.
As the external iliac artery passes beneath the inguinal ligament, it forms the common femoral artery.[8] At this point the artery is located midway between the anterior superior spine of the ilium and the symphysis pubis. Approximately 3 to 4 cm distal to the inguinal ligament, the common femoral artery branches to form the superficial and deep femoral arteries. The larger superficial femoral artery passes along the anteromedial aspect of the thigh and terminates at the junction of the middle and lower thirds of the thigh. Here, the superficial femoral artery passes through the adductor hiatus and forms the popliteal artery. The deep femoral artery runs posterolateral to the superficial femoral artery, supplies the hamstrings, and terminates in the distal third of the thigh as small branches piercing the belly of the adductor magnus. These perforating branches are an additional site of potential injury. The abundant blood supply of the thigh aids in healing fractures of the femoral shaft.
Venous System In the proximal two thirds of the thigh, the common and superficial femoral veins lie adjacent to the common and superficial femoral arteries. At the inguinal ligament, the common femoral vein is posterior and medial to the common femoral artery and moves to the lateral position as it passes distally. The deep femoral vein and the greater saphenous vein are the two main tributaries to the common and superficial femoral veins. The deep femoral vein and artery run parallel as the vein joins the superficial femoral vein just distal to the inguinal ligament. The greater saphenous vein arises in the dorsum of the foot and ascends anterior to the medial malleolus. This vein is relatively superficial as it passes up the medial aspect of the leg to join the common femoral vein distal to the inguinal ligament.[8]
Nerves The femoral and sciatic nerves are the major nerves within the thigh. The femoral nerve is the largest branch of the lumbar plexus; it passes under the inguinal ligament lateral to the femoral artery and divides into anterior and posterior branches soon after entering the thigh. The sensory divisions of the anterior branch, the intermediate and medial cutaneous nerves, supply sensation to the anteromedial aspect of the thigh. The motor division of the anterior branch innervates the pectineus and sartorius muscles. The posterior femoral branch forms the saphenous nerve, which supplies sensation to the skin along the medial aspect of the lower part of the leg. The posterior branch also supplies motor function to the muscles of the quadriceps femoris group.[8] The sciatic nerve is the largest peripheral nerve in the body. It arises from the sacral plexus, the fourth and fifth lumbar nerve roots, and the first, second, and third sacral nerve roots. The sciatic nerve exits the pelvis through the greater sciatic foramen and travels through the posterior of the thigh; it extends from the inferior border of the piriformis to the distal third of the thigh. The sciatic nerve gives off articular branches that supply the hip joint. In the thigh, muscular branches innervate the adductor magnus and hamstring muscles. Just proximal to the popliteal fossa, the sciatic nerve divides and forms the tibial and common peroneal nerves.[8]
Pathophysiology Fractures of the Femur and Hip
Page 314
The pathophysiology of femur and hip fractures is discussed in the description of individual fractures. The vast majority of hip fractures occur in elderly patients with preexisting bone disease after relatively low-energy trauma, usually a ground-level fall. Major trauma such as motor vehicle crashes or falls from significant heights is responsible for the majority of fractures in young, otherwise healthy individuals.
Osteoarthritis of the Hip and Osteoporosis of the Femur As the population ages, a greater percentage of the population will suffer with the chronic pain associated with degenerative osteoarthritis of the hip. Disability often results from persistent pain and limited physical mobility. The progression of osteoarthritis can be demonstrated with serial radiographs of the affected hip ( Figure 53-5 ).
Figure 53-5 Radiographic evidence for the developm ent of osteoporosis or degenerative joint disease of the hip is dem onstrated with serial radiographs in the sam e patient over several years. A, The sym ptom s are initially m ore dram atic than the radiographic findings of increased sclerosis along the weight-bearing surface of the superior acetabulum . B, The joint space is lost. C, Erosion of the head and acetabular surfaces and reactive bony cystic changes develop.
Osteoporosis is the leading cause of hip fracture. The pathophysiology of osteoporosis is not completely understood, but there are strong associations with hormonal changes related to aging, genetic predisposition, vitamin D deficiency, lack of physical activity, and smoking.[9] Severe osteoporosis and hip fractures are most common in elderly white women. Radiography of the head of the femur can quantify the degree of osteoporosis, even in the nonfractured hip. The trabeculae of the femoral head and neck strengthen the bone and support the large mechanical forces produced across the hip joint. Singh and colleagues introduced a grading system involving the trabecular patterns of the proximal end of the femur that is useful in evaluating the degree of osteoporosis ( Figure 53-6 ).[10] The Singh score for the degree of osteoporosis uses five trabecular groups found within the head, neck, and proximal end of the femur of nondiseased bone. A healthy femur has all five of these groups represented on a plain anteroposterior (AP) radiograph. As osteoporosis begins and then progresses, the groups disappear one at a time in a predictable pattern. A
B
Figure 53-6 Singh score used to quantify the degree of osteoporosis as it develops. Six grades are differentiated by the presence or absence of trabecular groups. A, Grade VI. All normal trabecular groups are visible, and the upper end of the fem ur is occupied by cancellous bone. B, Grade V. The structures of the principal tensile and principal com pressive trabeculae are accentuated. Ward's triangle appears prom inent. C, Grade IV. The principal tensile trabeculae are m arkedly reduced but can still be traced from the lateral cortex to the upper part of the femoral neck. D, Grade III. A break in the continuity of the principal tensile trabeculae opposite the greater trochanter indicates definite osteoporosis. E, Grade II. Only the principal compressive trabeculae are prom inent; the others have been com pletely resorbed. F, Grade I. Even the principal compressive trabeculae are markedly reduced in num ber and are not prom inent. ((From Singh M, Nagrath AR, Maini PS: Changes in trab ecular patterns of the upper end of the fem ur as an index of osteoporosis. J Bone Joint Surg Am 52:457, 1970.))
Page 315
Avascular Necrosis Epidemiology and Pathophysiology When a patient has an increasingly painful hip, buttocks, thigh, or knee and no history of recent trauma, AVN of the femoral head should be considered. AVN has been referred to as aseptic necrosis, ischemic necrosis, and osteonecrosis. It is the result of ischemic bone death of the femoral head after compromise of its blood supply. AVN occurs bilaterally in 52% of patients. It is common in relatively young patients, the mean age being 37 years.[11] Although the specific cause is unknown in 20% of cases, known atraumatic causes include chronic corticosteroid therapy, chronic alcoholism, hemoglobinopathy (e.g., sickle cell anemia), dysbarism, and chronic pancreatitis.[11] Traumatic AVN is a subacute manifestation after hip dislocation or femoral neck fracture. It is more common in males and African Americans. The incidence of AVN as a subacute complication of hip dislocation can reach 40%. Its development is clearly related to both the initial degree of trauma and the amount of time that the femoral head remains out of joint. Reduction of the hip within 6 to 12 hours after dislocation significantly decreases the incidence of AVN.[12] For this reason, hip dislocation should be considered one of the few orthopedic emergencies. The emergency physician must be able to reduce the hip if there is any delay in orthopedic consultation. Even with optimal treatment, femoral neck fractures are complicated by AVN in 11% to 19% of cases ( Figure 53-7 ). Apart from direct injury to the key arteries supplying the femoral head, a second factor contributing to the development of AVN is its location within a joint. For all practical purposes, femoral neck fractures are effectively intra-articular fractures. Acutely, bleeding from the fracture site may cause high intracapsular pressure and a tamponade effect on the femoral head, thus further impairing the blood supply.[ 13] In addition, if the bony fragments are not impacted, synovial fluid will lyse the blood clot. Such lysis prevents the development of capillary buds and the scaffolding needed for osseous repair. These factors all contribute to make AVN of the femoral head a common complication.
Figure 53-7 Even with optim um treatm ent of fem oral neck fractures, avascular necrosis of the fem oral head still m ay occur as happened in the patient shown. The fracture was treated by open reduction and internal fixation with a sliding com pression screw and plate to m aintain alignm ent of the fracture while allowing loading across the site.
Intertrochanteric fractures are located in an area of rich blood supply provided by an extracapsular arterial supply. AVN therefore rarely complicates these fractures.
Classification Four stages are used in classifying the progression of AVN. Ischemia of the femoral head, regardless of cause, produces an increase in intramedullary pressure and results in bone death. Reactive bone growth, edema, and fibrosis result ( Box 53-1 ). BOX 53-1 Classification of Avascular Necrosis of the Femoral Head
Stag Isch e I: emia caus es incre ased pres sure, ede ma, and
Page 316
fibro sis. New bone form ation mas ks chan ges on plain film; com pute d tomo grap hy is requi red. Stag Addit e II: ional bone grow th appe ars as mottl ed dens ity and luce ncy. The femo ral head main tains its nor mal cont our. Stag Stru e III: ctura l colla pse of the head . “The cres cent sign” is
Page 317
pres ent. Stag Seve e IV: re colla pse of the femo ral head , irreg ular dens ities. From Harris JH, Harris WH, Novelline RA: The Radiology of Emergency Medicine, 3rd ed. Baltimore, Williams & Wilkins, 1993.
Calcifying Lesions of the Femur and Hip Myositis Ossificans Epidemiology and Pathophysiology Myositis ossificans (heterotrophic ossification) is pathologic bone formation at a site where bone is not normally found. Traumatic myositis ossificans results from a direct blow or occurs after a fracture. The thigh and hip muscles are most commonly involved. The incidence of myositis ossificans is approximately 2% after closed treatment of hip dislocation but rises to 34% when open reduction is required. These lesions are clinically significant in only 10% to 20% of cases.[14] Bleeding into the muscle after trauma produces a local hematoma with subsequent new bone formation within the hematoma. This inappropriate response may also result from repeated minor trauma for unknown reasons. Within a few weeks, a firm and often painful mass develops in the affected muscles. This lesion matures over a 12-month period.[15] Radiographically, myositis ossificans appears as irregularly shaped masses of heterogeneous bone in the soft tissues around the joint or along fascial planes. Its appearance may simulate primary bone neoplasm, especially when the periosteum is involved. Osteosarcoma and periosteal osteogenic sarcoma should be considered in the differential diagnosis. The ossific mass is often palpable and may limit motion, depending on its location. Operative removal of a mature lesion may be indicated if the lesion is near a joint or is causing permanent impairment ( Figure 53-8 ). A
B
Figure 53-8 Myositis ossificans of the proxim al end of the fem ur. A, Lesion seen along the lateral cortex of the proxim al fem oral shaft. B, Sagittal m agnetic resonance im aging (MRI) views identify calcification within the lateral m usculature of the proxim al end of the fem ur. C, Sam e lesion on an MRI axial view dem onstrating the extent of the lesion.
Page 318
Calcifying Peritendinitis and Bursitis Calcification surrounding tendons and bursae or occurring in the joint capsule is referred to as calcific bursitis or calcifying peritendinitis. The cause of these lesions is unknown but may be similar to that of myositis ossificans. There is no relationship between the radiographic findings and acute symptoms. Calcific bursitis is uncommon, but when it does occur, it most frequently affects the trochanteric bursa of the hip ( Figure 53-9 ). The bursal calcification is seen on radiographs as an amorphous, poorly marginated line that is clearly separate from the cortex of the femur.
Figure 53-9 Calcific trochanteric bursitis. Faint calcification (arrow) in the region of the trochanteric bursa is noted along the lateral cortex of the greater trochanter. ((From Harris JH, Harris WH, Novelline RA: The Radiology of Emergency Medicine, 3rd ed. Baltim ore, William s & Wilkins, 1993.)William s & Wilkins)
Neoplastic Disease in the Hip Benign neoplasms of the femur may produce pain severe enough to justify a visit to the emergency department. The most common of these neoplasms is osteoid osteoma. A solitary osteochondroma may be manifested as a large, bothersome mass. Primary malignant neoplasm is also common in the femur and may be osteoblastic or osteolytic. Solitary osteochondroma ( Figure 53-10 ), osteoid osteoma ( Figure 53-11 ), and metastatic lesions are relatively frequent in the femur. Primary malignant neoplasms may be localized (e.g., chondrosarcoma) or generalized (e.g., multiple myeloma).
Figure 53-10 Classic radiographic appearance of a solitary osteochondrom a of the fem ur as seen in the anteroposterior (A) and frog-leg lateral (B) views. This lesion is a cartilage-capped bony excrescence typically arising from the cortex of long tubular bones. ((From Harris JH, Harris WH, Novelline RA: The Radiology of Emergency Medicine, 3rd ed. Baltimore, William s & Wilkins, 1993.)William s & Wilkins)
Figure 53-11 Osteoid osteom a of the fem ur (closed arrow).A, A large focal area of greater density than that of the surrounding fem ur represents both cortical and endosteal proliferation. The new cortical bone is smooth and sharply delineated, indicative of a nonaggressive process. The open arrow represents a bone island. B, A frontal tomogram dem onstrates an oval central radiolucent nidus (closed arrow). ((From Harris JH, Harris WH, Novelline RA: The Radiology of Emergency Medicine, 3rd ed. Baltim ore, William s & Wilkins, 1993.)William s & Wilkins)
CLINICAL FEATURES History
Page 319
Age and gender are predisposing factors for certain injuries. A detailed description of any antecedent trauma or other precipitating events is often helpful. With trauma, details of the mechanism of injury may aid in predicting injury patterns. With stress fractures, an alteration in physical activity or exercise routine provides a clue to the diagnosis. Systemic illnesses or known metabolic disorders should be noted. Any past steroid use is important to know because it predisposes patients to AVN in the femoral head. There is a linear relationship between the cumulative steroid dose and the incidence and severity of osteoporosis and hip fracture.[16] Past cancer, irradiation, and chemotherapy are clues to pathologic fractures. A review of systems should include information that may help in ascertaining the cause of atypical groin pain. Pain here may be the result of nephrolithiasis, pelvic inflammation, infection or tumor, inguinal and femoral hernia, or adenopathy from genital or cutaneous infection. A history of low back pain may suggest radiculopathy as the cause of the patient's pain. Elderly patients with a hip fracture sustained in a fall at home may be unable to summon help for hours to days. They often have severe dehydration, electrolyte abnormalities, rhabdomyolysis, and renal insufficiency and require a thorough evaluation of these metabolic parameters before considering surgery.[17] In addition, the reason for the fall should be determined if possible because it may reveal other comorbid conditions (e.g., syncope, cardiac dysrhythmias, polypharmacy, alcoholism). Elderly patients may have additional painful injuries sustained in a fall, most commonly fracture of a vertebral body or wrist. A high suspicion for cervical spine and intracranial injuries must also be maintained. Young patients with a hip fracture as a result of high-energy mechanisms have concomitant injuries in 40% to 75% of cases.[12]
Physical Examination Management principles for injuries of the hip and femur are the same as those for trauma elsewhere. Hypotension is a problem commonly encountered during the initial resuscitation of a multitrauma patient; however, hemorrhagic shock from an isolated femoral fracture must be a diagnosis of exclusion. Although up to 3 L of blood may be lost into the thigh with a femoral shaft fracture and subsequent hypotension may result, cardiac, pulmonary, intra-abdominal, and pelvic trauma must first be considered and excluded. Hypotension, neurovascular compromise, or suspicion of multiple injury requires transfer to a trauma center after the patient has initially been stabilized in the emergency department. After other life-threatening conditions have been addressed, the injured extremity should be carefully evaluated. Visual inspection will reveal any pallor, ecchymosis, asymmetry, or deformity. Abrasions, lacerations, or open wounds are critical because their presence alters the management of concomitant fractures. The position that the leg assumes offers a clue to what may be found radiographically. In the presence of a displaced femoral neck fracture, the leg classically assumes the position of external rotation, abduction, and slight shortening. In intertrochanteric fractures, the leg is found in internal rotation with mild shortening. Shortening or a limb length discrepancy is found with fractures, dislocations, and osteoarthritis. Undisplaced fractures, including stress fractures, will not produce limb shortening or rotation but will be painful on passive range of motion, particularly internal and external rotation. These fractures will also prevent the patient from being able to perform a straight leg raise. In patients with obvious deformities, range of motion should be deferred until after radiographs. Systematic examination will reveal any tenderness or warmth. Active and passive range of motion and muscle strength, though offering important information, are often limited by pain. Detailed neurovascular assessment is vital. Femoral nerve and arterial injury often occurs with subtrochanteric and femoral shaft fractures or anterior hip dislocation. The sciatic nerve can be injured with a hip fracture or posterior hip dislocation. Neurologic examination includes light touch and pinprick sensation. Femoral, popliteal, dorsalis pedis, and posterior tibial pulses are assessed. Comparative blood pressures obtained by Doppler examination in the injured and uninjured extremities may be useful in diagnosing occult femoral arterial injuries. The ankle-brachial index offers useful information regarding arterial injury or insufficiency. An index less than 0.9 strongly suggests arterial injury or stenosis.[18]
DIAGNOSTIC STRATEGIES Radiographic Anatomy and Evaluation The normal radiographic and skeletal anatomy is familiar to emergency medicine physicians ( Figure 53-12 ). One common inaccuracy merits clarification: the soft tissue linear radiolucencies superolateral and inferomedial to the femoral head and neck do not represent the hip capsule as is commonly believed. Instead, they represent the fat within the fascial plane covering the gluteus minimus superiorly and the tendon of the iliopsoas muscle inferiorly.[19] Comparison of these lines on the symptomatic side with those on the unaffected side should not be used to determine whether an effusion of the hip is present.
Page 320
Figure 53-12 A, Norm al adult hip. The superior arrow indicates fatty tissue covering the gluteus minim us; the inferior arrow indicates the edge of the iliopsoas m uscle shadow. These m uscles lie im m ediately on the capsule of the hip joint. The sm all concavity in the center of the fem oral head is for the attachm ent of the ligam entum teres. B, Cross-table lateral view of the hip dem onstrating the norm al relationship of the fem oral head to the neck. The asterisk indicates the ischial tuberosity. ((From Harris JH, Harris WH, Novelline RA: The Radiology of Emergency Medicine, 3rd ed. Baltimore, William s & Wilkins, 1993.)William s & Wilkins)
True AP and lateral radiographs of the femur are usually adequate for the evaluation of potential fractures. The femur should be in as much internal rotation as possible. The fracture line may be very subtle, particularly with femoral neck fractures. The authors have found three methods useful in identifying inconspicuous fractures. The use of Shenton's line is described in the section on hip dislocations (see Figure 53-24 ). Lowell[20] described a second method, which is illustrated in Figure 53-16 . When searching for a fracture of the femoral neck, both the medial and lateral cortical margins of the femoral head and neck must be carefully examined for the normal S and reverse S curves found on nonfractured hips. The convex outline of a normal femoral head smoothly joins the concave outline of the femoral neck when in anatomic position. This produces an S and reverse S curve regardless of the angle of the x-ray. A fracture produces a tangential or sharp angle indicative of disruption of the normal anatomic relationship. A third method, useful in the evaluation of seemingly unremarkable hip films, is to trace the trabecular groups as they pass from the femoral shaft to the femoral head. These lines will be disrupted as they pass through the fracture site, and such disruption often provides the only subtle clue. If a fracture is found, radiographs of the knee should be taken as well. It is a basic orthopedic principle to image the joint above and below any fracture.[18]
Figure 53-24 Shenton's line is a sm ooth curved line drawn along the superior border of the obturator foram en and m edial aspect of the fem oral m etaphysis. Disruption of this line should raise suspicion of a fem oral neck fracture or hip dislocation.
Figure 53-16 Lowell20 described the normal anatom ic x-ray appearance of the fem oral head as a sm ooth S and reverse S lines drawn above. The concave outline of the femoral neck m eets the convex outline of the fem oral head in all views. Any tangential angle suggests a fracture.
Occult Hip Fracture If radiographs do not show a fracture, the patient must be observed while ambulating. An inability to ambulate heightens the suspicion of occult fracture. Approximately 5% of all hip fractures are radiographically “occult” on plain films. Failure to detect these injuries results in increased mortality, risk of
Page 321
subsequent displacement of the fracture, and a higher incidence of AVN.[21] It also affects patients' disposition, in keeping with the admonition “If they can't walk, they can't go home.” When a painful hip prevents ambulation and plain films do not reveal a fracture, magnetic resonance imaging (MRI) should be performed.[22] In addition, elderly patients with unexplained chronic hip pain for more than 3 weeks may harbor an occult fracture even if they continue to ambulate. T1-weighted MRI reveals a fracture that was imperceptible at the time of injury with 100% accuracy and has been found to be cost-effective when compared with other strategies.[21] Its use allows either earlier operative repair or physical therapy and immediate mobilization. Bone scans have been useful in these patients, yet such scans lack adequate sensitivity. To identify most occult fractures, the scan must be delayed 72 hours after the injury. These 3 days of bed rest and hospitalization while awaiting a bone scan are costly and not without risk (e.g., formation of deep venous thrombosis) ( Figure 53-13 ).
Figure 53-13 A, The patient com plained of hip pain and could not ambulate. Initial radiographs failed to dem onstrate a fracture. B, A radionuclide bone scan 72 hours after the fall provided no evidence of a fracture. C, A m agnetic resonance im age obtained 24 hours after the fall shows an altered signal in the intertrochanteric area, indicative of an acute fracture. (B and C, From Rockwood JC Jr, Green DP, Bucholz RW [eds]: Rockwood and Green's Fractures in Adults, vol 2, 4th ed. Philadelphia, JB Lippincott, 1996).
MANAGEMENT Patients with traumatic fracture of the hip or femur should have blood typed and crossmatched for administration of at least 2 U of blood. Hemodynamic instability may result from dehydration and blood loss of up to 3 U into the fracture site. The potential for significant blood loss and the multiple common associated injuries are important justifications for this recommendation. Currently, treatment of these fractures is hemiarthroplasty or open reduction and internal fixation for femoral neck fractures. Internal fixation with a sliding compression screw is generally used to treat intertrochanteric fractures. The goal is to promote immediate postoperative mobilization. It has become widely accepted that the risks of surgery in elderly patients are minimal when compared with the risks of prolonged bed rest, deep venous thrombosis, pulmonary embolism, pneumonia, and urosepsis from an indwelling Foley catheter. If possible, the repair is conducted under spinal anesthesia to decrease the operative risk. Care of an elderly patient with a hip fracture is a multidisciplinary effort and often requires coordination between the emergency physician, orthopedist, internist, neurologist, and cardiologist to stabilize the patient before surgery. Operative repair should be performed as soon as possible after the patient is resuscitated and is in optimal preoperative condition.
Traction and Immobilization Prehospital personnel often place a Hare splint or similar device that applies traction to the leg before transport if they suspect a femoral fracture. Although such management may provide pain relief and limit blood loss, great care must be given to the proper use of these devices. Prolonged traction during the assessment and management of other injuries can cause or worsen serious neurovascular injury in the thigh. The traction used in the field for transport will produce potentially damaging tension on the nerve and artery. The femoral and sciatic nerves are much more likely to be injured from traction or during surgery than they are from a femoral fracture.[23] Maintaining the leg in flexion at the hip reduces intracapsular pressure, whereas extension of the leg increases pressure and potential for ischemic necrosis of the femoral head. For these reasons, traction should be discontinued once the patient arrives in the emergency department. There are some contraindications to the use of traction. Providers should be instructed that traction should not be applied to any open fracture that has exposed bone. Such reduction pulls grossly contaminated bone fragments back into the wound before adequate debridement can be undertaken in the operating room. Traction should not be used in patients with any suggestion of neurologic involvement because it may worsen the injury. The injured extremity should be immobilized without traction when moving the patient. The leg may be supported in a position of comfort with a pillow placed under the thigh.
Page 322
Open Fracture Care By definition, an open fracture is any in which a break in the integrity of the skin and soft tissue allows communication with the fracture and its hematoma. Any wound or break in the skin in proximity must be considered to communicate with the fracture. Open fractures are divided into the three categories ( Table 53-2 ), the third of which may be subdivided according to the amount of nerve, arterial, or periosteal injury present. A bone piercing from the inside outward often causes only a small wound. The contaminated bone tip then slips deceptively back into the soft tissue; therefore, any break in the integrity of the skin makes the fracture an open one. Open wounds should be irrigated and then covered with sterile saline-moistened gauze. Table 53-2 -- Classification of Open Fractures Wound size Soft tissue damage
Type I
Type II
<1 cm Minimal, if any
>1 cm and <10 cm Moderate, without nerve, arterial, or periosteal stripping
Type III[*]
>10 cm Extensive muscle devitalization. Nerve and arterial involvement often classified as type IIIb Mechanism of injury Bone edge pierces Variable High-energy shotgun, outward high-velocity gunshots From Morris JM, Blickenstaff LP: Fatigue Fractures. Springfield, Ill, Charles C Thomas, 1967. Type I: endosteal or periosteal callus without a definite fracture line on plain radiographs; type II: a definite fracture is identified on plain radiographs, but no displacement; type III: the fracture is displaced. *
Any shotgun wound, high-velocity gunshot wound, segm ental fracture, farm yard injury, vascular injury, or crush injury is classified as type III, regardless of wound size.
For all type I open fractures, a first-generation cephalosporin should be administered intravenously. Types II and III require additional gram-negative coverage because of the amount of devitalized tissue and increased gram-negative skin flora found in the groin.[24] This additional coverage could be provided by an aminoglycoside such as gentamicin or tobramycin. The use of perioperative first-generation cephalosporins has been shown to reduce postoperative infection even in closed fractures that are to undergo surgery.[18] Great care should be taken to identify tetanus-prone wounds so that appropriate prophylaxis can be provided with penicillin and tetanus immune globulin when indicated.
Compartment Syndrome Because of its larger volume, compartment syndrome within the thigh is far less common than in the lower part of the leg. A large amount of bleeding into the compartment is required before the pressure rises above capillary perfusion pressure. It is difficult to clinically differentiate the expected swelling after an injury from early compartment syndrome. Clinical examination and the use of direct compartment pressure measurements can detect the development of compartment syndrome at an early stage.
Pain Management Systemic Analgesia It is well known that control of pain in emergency departments is often inadequate.[25] There may be greater reluctance to administer adequate doses of analgesics in the elderly because of possible respiratory depression. Nevertheless, pain control should be a high priority during the initial management period.
Femoral Nerve Block Femoral nerve blocks have been used to treat femoral shaft fractures for more than 50 years.[26] Despite proven effectiveness and a low complication rate, this technique has not been widely embraced by emergency physicians or surgeons.[27] Femoral nerve block is invaluable as an adjunct or alternative to systemic analgesics in those at risk for hypotensive side effects. For obvious reasons, careful neurovascular examination and consultation with the orthopedic surgeon involved should be carried out and documented before performing the procedure.
Page 323
If a long-acting anesthetic such as bupivacaine is used, the expected onset of analgesia is 15 to 30 minutes, and its duration is 6 to 8 hours.[28]
Hip Arthroplasty Background and Epidemiology Sir John Charnley first described the modern form of total hip arthroplasty (THA) in 1961. Despite many changes in both the design and materials used, Charnley's essential design has been established as the standard.[29] The incidence of THA in the United States rose from 65,000 per year in 1982 to more than 120,000 per year by the mid-1990s.[30] Women account for 62% of THA in the United States. The most common indication for THA is joint failure resulting from severe osteoarthritis. Other indications include rheumatoid arthritis, certain types of hip fracture, AVN, and certain tumors. Arthritis associated with Paget's disease, trauma, ankylosing spondylitis, and juvenile rheumatoid arthritis are also relative indications for total or partial hip arthroplasty.
Outcomes and Complications THA provides an immediate, substantial improvement in pain, functional ability, and overall quality of life. A 10-year follow-up of patient outcomes, including gait, perception of pain, physical mobility, sleep patterns, and energy scores, showed positive results in more than 90% of cases.[31] Despite the tremendous success of THA, there are numerous complications, aseptic loosening of the prosthesis being the most common. Other complications include component wear, infection, surrounding femoral fractures, and deep venous thrombosis. Postoperative dislocation of the femoral component occurs in 3% of patients. Generally, flexion past 90 degrees, adduction, and internal rotation place the hip at risk for dislocation. This combination can occur when patients bend at the waist (e.g., to sit on a normal low toilet or to get out of a chair) or cross their legs ( Figure 53-14 ).[32]
Figure 53-14 Dislocation of the fem oral prosthesis in a patient with a total hip arthroplasty. The fem oral head often becom es caught on the rim of the acetabular cup, thereby preventing reduction. Reduction may disrupt or dislocate the acetabular cup.
SPECIFIC INJURY PATTERNS Fractures of the Hip and Femur Avulsion Fractures The pain of avulsion injuries of the hip may be manifested as referred pain to the thigh and is most common in adolescents and young adult athletes. The muscular origin of this type of injury commonly involves the pelvic apophyses. Avulsion at the site of the growth plate is the result of sudden, maximal muscular exertion. It may occur with rapid acceleration or sudden changes in speed or direction. The athlete classically experiences a sudden piercing pain at the site of injury, describes a “snapping” or “popping” feeling, and frequently falls to the ground because of the intensity of this pain. Avulsion at the anterior superior iliac spine involves the separation of a thin piece of bone as the sartorius muscle suddenly contracts. The anterior inferior spine is avulsed by the rectus femoris, and the hamstring group may pull off the ischial tuberosity ( Figure 53-15 ).
Figure 53-15 Avulsion of the anterior inferior iliac spine by the rectus femoris produced a fracture.
Page 324
Proximal Femoral Fractures Classification Systems Fractures of the proximal end of the femur have been classified on the basis of their relationship to the hip capsule (e.g., intracapsular and extracapsular), geographic location (neck, trochanteric, intertrochanteric, subtrochanteric, and shaft fractures), and degree of displacement. A working knowledge of the classification system allows the emergency physician to communicate with the consulting orthopedist regarding the fracture's pattern, stability, and treatment options.
Femoral Neck Fractures Pathophysiology Many now refer to femoral neck fractures as insufficiency fractures in acknowledgment of the major role played by osteoporosis. Age-related bone loss is believed to be the most important factor in determining the incidence of femoral neck fractures.[33] The theory that these fractures result from primary skeletal pathology is supported by the fact that minimal or no injury is associated with most of these fractures. Pathologic fractures from metastatic carcinoma are well described.
Classification. Fractures of the femoral neck were originally divided by location into either subcapital or transcervical types. The subcapital fracture line lies just under the dome of the femoral head's articular surface. Although several classification systems were used to describe these fractures, they have been abandoned because of poor inter-rater reliability and limited clinical utility. Currently, femoral neck fractures should be classified as either nondisplaced or displaced fractures. Fifteen percent to 20% of all femoral neck fractures are nondisplaced fractures. The fracture line may often be very subtle. Techniques described for detection of subtle fracture lines may be useful for this reason. Evaluation of the continuity of the subcapital cortical lines, search for an indistinct broad band of increased subcapital density, and identification of the S and reverse S curves ( Figure 53-16 ) will lead to the correct diagnosis in most cases. In impacted femoral neck fractures, the neck cortex is driven into the cancellous femoral head. Bony impaction lends a certain inherent stability ( Figure 53-17 ). Because of this inherent stability, two different approaches have been advocated: early ambulation and internal fixation. AVN, the most common complication, occurs in 20% of patients regardless of the type of management.[23] The prognosis for nondisplaced fractures is excellent; 96% of patients heal without complication. Without impaction, a nondisplaced femoral neck fracture possesses no inherent stability and will become displaced without internal fixation.
Figure 53-17 A, Subtle nondisplaced im pacted fem oral neck fracture (Garden type I). Use of Lowell's S curves aids in identification. B, A nondisplaced fem oral neck fracture (Garden type II) possesses no stability without im paction. C, The sam e fracture after treatm ent with a sliding com pression screw and side plate.
On initial evaluation, a patient with a displaced fracture of the femoral neck lies with the limb externally rotated, abducted, and slightly shortened. The diagnosis is confirmed with plain hip films ( Figure 53-18 ). To avoid further disruption of the blood supply to the femoral head, range of motion should be deferred unless radiographs fail to reveal a fracture. In all displaced femoral neck fractures, the femoral head is rendered largely avascular, and subsequent signs of AVN and collapse may occur over the ensuing several years.
Figure 53-18 The num ber of parts that the fracture produced classifies intertrochanteric fractures. A, Two-part fractures have one part connected to the fem oral head and a second part attached to the shaft. B, The greater or lesser trochanter is also
Page 325
fractured with three-part fractures. A greater degree of instability is produced because the attached muscles continue to act on the fractured trochanter. C, Four-part intertrochanteric fractures involve both trochanters.
Treatment of these displaced fractures is either open reduction with internal fixation or hemiarthroplasty ( Box 53-2 ). BOX 53-2 Relative Indications for Hemiarthroplasty as Treatment of Displaced Femoral Neck Fractures
Parki nson 's dise ase Hem iplegi a or other neur ologi c dise ase Path ologi c fract ure or Pag et's dise ase Olde r than 70 (phy siolo gic age) Blind ness Seve re oste open ia Poor healt h that woul d prev ent a seco nd
Page 326
oper ation From Rockwood JL Jr, Green DP, Bucholz RW (eds): Rockwood and Green's Fractures in Adults, vol 2, 4th ed. Philadelphia JB Lippincott, 1996.
Outcome and Complications The mortality rate during the first year after a femoral neck fracture is 14%, as compared with 9% for the control population. Factors affecting mortality include age, male sex, psychiatric illness, end-stage renal disease, and congestive heart failure.[34] Institutionalized patients have a death rate three times higher.[35] Complications can be minimized by early reduction, stable internal fixation, and early ambulation. AVN and nonunion are the two major complications of femoral neck fractures. AVN is the most common complication, despite optimal treatment, because of the complex arterial anatomy. Deep infection in the form of osteomyelitis or septic arthritis is more common with femoral neck fractures because the fracture line extends into the joint. The rate of infection has been dramatically reduced with the use of perioperative antibiotics. Pulmonary embolism is another significant complication and is the leading cause of death 7 days after fracture in all orthopedic patients.
Intertrochanteric Fracture Anatomy The fracture line of intertrochanteric fractures extends between the greater and lesser trochanter of the femur. They are considered extracapsular fractures. The fracture line extends through cancellous bone and has an excellent blood supply. The hip's short external rotators remain attached to the proximal femoral neck, and the internal rotators are attached to the distal end of the femur, thus explaining the position that the leg assumes with this fracture.
Pathophysiology An intertrochanteric fracture in younger adults is usually the result of high-speed accidents or high-energy trauma, such as falls from heights. The elderly may sustain this injury during a fall from any height. The fracture lines are the result of both direct and indirect forces. The direct forces act along the axis of the femur and on the greater trochanter as it strikes the ground. Indirect forces are produced as the iliopsoas pulls the lesser trochanter and the abductors pull the greater trochanter; these forces often cause fractures at the site of insertion.
Classification A large number of classification systems for intertrochanteric fractures have been proposed to predict the possibility of achieving and maintaining stable reduction.[36] An oft-used system, and one sufficient for our use, designates the fracture according to the number of separate bone fragments produced (see Figure 53-18 ).
Management Intertrochanteric fractures carry particular pitfalls for the emergency physician. Great care must be taken to address the entire patient and not focus on the fracture alone. Hemodynamic instability may result from dehydration and blood loss of up to 3 U into the fracture site.[37] Poor nutrition before the fall, chronic diuretic use, and decreased oral intake in patients who have to wait until they are found contribute to the level of dehydration. Up to 70% of these patients are under-resuscitated.[17] Associated distal radial, proximal humeral, and rib fractures and compression fractures of the lumbar and thoracic spine are often overlooked because the femoral fracture distracts the attention of both the patient and physician. Spinal compression fractures most commonly involve T12 and L1. A substantial majority of intertrochanteric fractures require some type of internal fixation. Such fixation allows rapid mobilization, decreased hospital length of stay, reduced mortality, and improved function.[18] The procedure should be performed on an urgent, not an emergency basis. Although the patient's other medical conditions are unlikely to improve significantly, mortality is increased when the patient is taken to the operating room on the day of injury. If delayed longer than 48 hours, however, a 10-fold increase in mortality has been reported.
Outcomes Intertrochanteric fractures have an associated mortality rate of 10% to 30% in the first year. Life expectancy
Page 327
returns to normal in those who survive that year. Survival is most commonly related to the patient's age and preexisting medical conditions. Additional risks associated with operative treatment include mechanical failure (1% to 16%), implant migration (2% to 10%), and infection (2% to 8%).[] Mechanical failure and nonunion are much more common in unstable fractures and those that were not adequately reduced. Approximately only half of patients sustaining these fractures are able to eventually regain their original level of ambulation.
Pathologic Intertrochanteric Fractures Aggressive treatment of patients who have pathologic intertrochanteric fractures or impending fractures is indicated if their life expectancy is more than a few months. Such treatment with subsequent radiation therapy improves the patient's quality of life, decreases pain, and improves mobility.
Isolated Fracture of the Greater or Lesser Trochanter Fractures of the greater or lesser trochanter are rare. They occur in women more than in men and are the result of a fall directly onto the trochanter or avulsion by the iliopsoas muscle. There may be a comminuted fracture involving only part of the greater trochanter or more subtle impaction of the lateral cortex. If avulsed, the fragments are displaced superiorly and posteriorly ( Figure 53-19 ).[18]
Figure 53-19 Isolated fracture of the greater trochanter. Note that the trochanter is displaced in the typical posterior and superior direction.
Treatment consists of pain control and early mobilization with crutches; weight bearing is allowed as tolerated by pain. Outpatient management of this injury is possible with a satisfactory social situation. The prognosis is good, and healing is generally excellent.
Subtrochanteric Fracture Anatomy and Pathophysiology Subtrochanteric fractures occur between the lesser trochanter and the proximal 5 cm of the femoral shaft. They may accompany intertrochanteric fractures. The subtrochanteric region is composed almost entirely of cortical bone, which lacks the vascularity important to new bone growth and repair. When fractured, it is more likely to be comminuted than bone with a higher cancellous content. Additionally, the majority of the biomechanical forces of the femur are transmitted down the curved medial cortex of the femoral shaft. If this cortex is disrupted, the metal hardware undergoes the majority of the stress. This mechanism accounts for the increased incidence of hardware failure when the medial cortex is largely involved. These fractures are characteristically deformed because of the unbalanced muscle forces. The attachments of the iliopsoas, gluteal, and external rotator muscles consistently produce flexion, abduction, and external rotation of the proximal fragment.
Epidemiology Subtrochanteric fractures account for 11% of all fractures of the proximal end of the femur. Although 10% of these fractures are caused by gunshots, the mechanism of injury is usually direct blunt trauma.[40] They occur in a bimodal distribution. The first group consists of elderly patients after a fall. The fracture occurs through an area of weakened cortical bone. Pathologic fractures from metastatic lesions, Paget's disease, renal osteodystrophy, osteogenesis imperfecta, and osteomalacia are well recognized in this area. A second distribution of these fractures occurs in victims of extreme high-energy trauma. In this group of patients, the subtrochanteric fracture is rarely an isolated injury because of the tremendous force required to produce it. Associated thoracic and abdominal injuries are common and must be aggressively sought to adequately manage the patient. Thirty percent to 50% of patients with subtrochanteric fractures have associated fractures of the pelvis, spine, or other long bones. Stress fractures can occur in this region but are extremely uncommon.
Classification
Page 328
A variety of classification systems for these fractures have been proposed, although none are widely accepted.[36] From a practical standpoint, it is best to define and describe these fractures by location (proximal or distal), angle (transverse, oblique), and the presence of comminution ( Figure 53-20 ).
Figure 53-20 Variants of subtrochanteric fractures. A, Short oblique fracture. B, Short oblique fracture with com m inution. C, Long oblique fracture. D, Long oblique fracture with comm inution. E, High transverse fracture. F, Low transverse fracture.
Management Hemodynamic instability may result from blood loss of up to 3 U into the fracture site.[37] Although such blood loss can lead to hypovolemic shock, other causes of hypotension in a trauma patient must be investigated. Open fractures are rare and, when present, accompany significant soft tissue injury. Vascular and neurologic injuries are also uncommon. Definitive management of subtrochanteric fractures is a complex issue. Maintaining limb length and controlling rotation are difficult. Open reduction with internal fixation is generally the treatment of choice. However, in the rare case with severe comminution or an open, grossly contaminated fracture, nonoperative management may be preferable.[41] Children younger than 10 years may also be treated nonoperatively. The amount of remodeling and growth stimulation that occurs in children of this age usually ensures good results without internal fixation.
Outcomes The bone in the subtrochanteric region is largely cortical and relatively avascular when compared with the cancellous intertrochanteric region. It logically follows that healing is comparatively slow. Comminution is common and increases the likelihood of nonunion. Because of ample muscle coverage in this area, delayed union, nonunion, and hardware failure are rare. Comminuted and distal subtrochanteric fractures have a worse prognosis. Complications include fat embolism and the adverse effects of prolonged immobilization in the elderly. The reported mortality rate from subtrochanteric fractures ranges from 12.2% to 20.8%.[42] The violent force and common associated injuries contribute to the high mortality of patients who sustain these fractures.
Femoral Shaft Fractures Pathophysiology Femoral shaft fractures are common injuries in young adults after high-energy trauma. As is the case with other femoral cortical fractures, considerable violent force is required to produce a fracture in a normal shaft. Automobile and motorcycle accidents, falls, and pedestrian accidents account for the majority of femoral shaft fractures. The femoral shaft usually fails under tensile strain, and a transverse fracture results. Higher forces produce varying degrees of segmentation or comminution. Open fractures of the femoral shaft are less frequent and are often the result of a gunshot wound. Pathologic fractures occur from a torsional stress that produces a spiral fracture.[43]
Classification There is no commonly accepted or easily remembered classification for femoral shaft fractures. Location and geometry of the fracture line should be used to describe these fractures. Transverse, oblique, spiral, wedge, and comminuted are useful terms for describing these fractures.
Clinical Features Patients often arrive in the emergency department with the injured extremity immobilized by traction devices, which should be removed while maintaining immobilization of the limb. Neurovascular injuries are rarely associated with closed femoral shaft fractures.[44] Significant hemorrhage into the thigh can occur with a femoral shaft fracture, just as it can with intertrochanteric and subtrochanteric fractures. Injuries commonly
Page 329
occurring in the presence of femoral shaft fractures include hip fractures, fracture-dislocations, femoral neck fractures, supracondylar femoral fractures, and patellar fractures.[45] Almost half of femoral shaft fractures have associated ligamentous damage in the knee. If the patient has a femoral fracture, pain often prevents adequate evaluation of knee stability. Any attempt to evaluate the stability of the knee acutely will result in additional pain and hemorrhage without providing useful reliable information.
Management Internal fixation with intramedullary rods has been demonstrated to shorten both hospitalization and total disability time with most femoral shaft fractures. The vast majority of femoral shaft fractures heal well in time, regardless of the mode of treatment. Severely comminuted fractures are more likely to be treated by closed reduction.
Fractures with Minimal or No Trauma Most patients who arrive in the emergency department with hip or thigh pain will provide a clear history of a traumatic event. Hip or knee pain in the young, in athletes, and in the elderly deserves investigation, even when minimal or no trauma has been reported. This patient population commonly has occult hip pathology and occasionally femoral pathology. Although senile osteoporosis is the leading cause of femoral neck fractures after minor trauma, pathologic fractures of the femur may result from metastatic, metabolic, or endocrinologic disease.[46] The incidence of fracture in patients with hyperthyroidism is 12%.[47]
Outcomes Patients sustaining a femoral shaft fracture have close to a 100% union rate, and most are able to return to work after approximately 6 months. Nonunion is relatively uncommon and occurs in about 1% of patients. Even a minor degree of limb shortening or malalignment leads to posttraumatic arthritis.[48] Refracture is a rare occurrence that occurs at two times during the healing process. The leg can refracture during early healing and callus formation or during the brief period after the hardware is removed. After the hardware is removed, the unsupported bone is required to bear the entire weight of axial loading and is at risk for refracture.
Stress Fractures Biomechanics Stress fracture of the femoral neck was first reported in 1905 by Blecher.[49] Stress fractures occur when normal bone is repeatedly subject to submaximal forces. This recurring stress stimulates the bones to remodel and strengthen. In a stress fracture, osteoblasts are unable to lay down new bone and remodel fast enough, so the bone fails. Stress fractures can also occur in diseased bone when it is subjected to repeated minimal stress.[50]
Clinical Features The symptoms of a stress fracture of the femoral neck are often so subtle that they may be mistaken for muscle strain or an overuse injury. Early symptoms frequently include morning stiffness and aching in the hip on the first steps after a period of rest. The pain gradually increases during prolonged exercise and may reach the point at which bearing weight becomes impossible. Pain is felt in the groin or along the medial aspect of the thigh toward the knee. On examination, an obvious, painful limp is present. This painful or antalgic gait is characterized by shortening of the stance phase of the injured extremity. There is no obvious external rotation or shortening of the leg, only minor discomfort with active or passive motion, except at the extremes of flexion and internal rotation. Tenderness is minimal because of the large amount of soft tissue coverage at the femoral neck.
Diagnostic Strategies Radiographs are helpful if they demonstrate a fracture, but they are often negative until 10 to 14 days after the injury.[18] Endosteal or subperiosteal callus develops during this period and indicates the fracture site. In addition to the standard AP and lateral views of the hip, oblique views may delineate the fracture line. Close attention should be paid to the trabecular fibers of the femoral neck. Often, a stress fracture can be identified as an isolated disruption of either the compressive (medial aspect of the femoral neck) or the tensile (lateral aspect of the femoral neck) trabecular fibers. If a fracture is suspected clinically, negative radiographs should be followed by MRI or computed tomography (CT).[22] If a fracture is found, the other hip should be extensively evaluated because of the significant incidence of bilateral stress fractures.
Classification and Management
Page 330
Stress fractures are commonly separated into three classes. This division is used to guide management of stress fractures of the femoral shaft. A type I stress fracture is treated in the hospital with strict bed rest until the pain has subsided and the hip has full range of motion. Because of the tremendous disability associated with displaced fractures, types II and III are internally fixed.[5]
Other Causes of Pain Other considerations in the diagnosis of atraumatic pain of the hip and thigh are listed in Box 53-3 . BOX 53-3 Differential Diagnosis of a Painful Hip without Fracture
Refe rred pain (lum bar spin e, hip, or knee ) Avas cular necr osis of the femo ral head Deg ener ative joint dise ase or oste oarth ritis Hern iatio n of a lumb ar disk Diski tis Toxi c syno vitis of the hip Septi c
Page 331
arthri tis Burs itis Tend oniti s Liga ment ous injuri es of the knee or hip Occ ult fract ure Slipp ed capit al femo ral epip hysi s Pert hes' dise ase Tum or (lym pho ma) Dee p veno us thro mbo sis Arter ial insuf ficie ncy Oste omy elitis
Dislocations and Fracture-Dislocations of the Hip and Femur Injury Patterns Epidemiologists have identified injury patterns in victims according to the mechanism of injury.[51] Pedestrians who are struck by a car have head, chest, pelvic, arm, and femur injuries. Motorcyclists tend to sustain pelvic and ipsilateral leg injuries. A person who stumbles and falls seldom has major associated injuries. Each will be discussed in the following sections.
Page 332
Hip Dislocations Dislocations and fracture-dislocations of the hip are two of the few true orthopedic emergencies. The hip joint possesses impressive inherent strength and stability; thus, considerable force is required to produce these injuries. With this understanding, a hip dislocation serves as a “red flag” for multisystem injury and should prompt a diligent search for other occult injuries. Serious associated injuries are found in up to 95% of patients with a dislocated hip.[] Knee fractures, ligamentous injuries, and dislocations are present in up to 30% of patients sustaining a hip dislocation.[54] It is highly recommended that in the presence of this type of injury, patients be evaluated as major trauma victims.
Mechanism and Biomechanics Traumatic hip dislocations occur primarily in patients sustaining severe multisystem trauma, most often as a result of high-speed motor vehicle crashes. Failure to use seat belts is a significant risk factor. Other less common mechanisms include falls, sports injuries, and pedestrians struck by automobiles. Posterior dislocations are almost always the result of motor vehicle crashes. A seated vehicle occupant typically has the hip adducted, flexed, and internally rotated at the time of impact. As the knee strikes the dashboard, the force is transmitted through the femoral shaft to the femoral head. With sufficient force, the femoral head dislocates posteriorly. Anterior dislocations result from forceful extension, abduction, and external rotation of the femoral head. These forces lever the head up out of the acetabular cup. Such dislocation most often occurs after a motor vehicle crash when the occupant has the hip abducted and externally rotated at the time of impact. It may also result from a fall or sports injury when the hip is forcefully hyperextended.
Classification The relationship of the femoral head to the acetabulum is used to classify dislocations into anterior, posterior, central, and inferior types. A fracture-dislocation refers to an associated fracture of the acetabulum or femoral head. Posterior dislocations ( Figure 53-21 ) account for 80% to 90% of cases. Anterior dislocations ( Figure 53-22 ) are seen in 10% to 15% of patients. In anterior dislocations, the femoral head may dislocate medially toward the obturator foramen (obturator dislocation) ( Figure 53-23 ) or laterally toward the pubis (pubic dislocation). Central dislocations, which occur in 2% to 4% of cases, are not true dislocations because the entire femoral head is forced centrally through a comminuted fracture of the acetabulum. Inferior dislocation (luxatio erecta) of the hip is a very rare condition that occurs almost exclusively in children younger than 7 years.
Figure 53-21 In a posterior dislocation the hip is internally rotated and the lesser trochanter is superimposed on the fem oral shaft. Failure to visualize the lesser trochanter on the anteroposterior projection identifies a posterior dislocation.
Figure 53-22 In an anterior dislocation the hip is externally rotated, and the lesser trochanter appears in profile. The hip is further from the x-ray cassette than the unaffected side and may appear larger because of the beam 's projection.
Page 333
Figure 53-23 Radiograph of obturator dislocation.
Clinical Features. The position of the injured extremity may provide valuable clues when evaluating a hip dislocation. A patient with a posterior dislocation typically holds the hip flexed, adducted, and internally rotated. The knee of the affected extremity rests on the opposite thigh. The extremity is generally shortened, and the greater trochanter and buttock may be unusually prominent. In contrast, a patient with an anterior dislocation holds the hip in abduction, slight flexion, and external rotation. However, these physical findings may be absent in patients with an associated ipsilateral femoral shaft fracture. The neurovascular examination should focus on the sciatic nerve and femoral vessels. Sciatic palsy is present in about 10% of patients with hip dislocation and most commonly involves the peroneal nerve branch. The femoral vessels and nerve are particularly prone to injury after an anterior dislocation.
Diagnostic Strategies Radiologic investigation begins with an AP view of the pelvis. This view alone will identify the majority of hip dislocations. An AP pelvis film should be obtained in all trauma patients with the aforementioned deformities. The AP radiograph should include the entire pelvis and the proximal third of the femur to allow comparison of both hips. When a dislocation is found or suspected, a lateral view of the hip will provide additional definition of the injury. Although most hip dislocations are seen clearly with these two views, several more subtle radiographic signs may assist physicians in making a confident diagnosis. The first indicator involves the position of the lesser trochanter. Because a posteriorly dislocated hip is internally rotated, the lesser trochanter is superimposed on the femoral shaft and is not seen on the AP projection. In contrast, an anteriorly dislocated hip is externally rotated and the lesser trochanter appears in profile. The second clue is found in the size of the femoral head. Because a posteriorly dislocated hip is closer to the x-ray cassette than the unaffected side is, it appears smaller. The converse is true in anterior dislocations, where the hip is farther from the x-ray cassette than the contralateral side is and thus appears larger. The third finding relates to the integrity of Shenton's line ( Figure 53-24 ). This line is a smooth, curved line drawn along the superior border of the obturator foramen and medial aspect of the femoral metaphysis. Disruption of this line should raise suspicion of a femoral neck fracture or hip dislocation.[] An obvious dislocation may distract the physician from a search for concomitant fractures. Examination of the trabecular pattern can identify associated fractures of the acetabulum and femoral head, neck, or shaft. It is especially important to identify acetabular fractures before closed reduction is attempted because intra-articular bone fragments may interfere with effective reduction. Oblique radiographs (Judet views) or CT will help visualize the acetabulum and precisely define the injury.[57]
Management Hip dislocations are true orthopedic emergencies, and reduction should be performed as soon as possible. The earlier the reduction, the better the results. The incidence of AVN, traumatic arthritis, permanent sciatic nerve palsy, and joint instability logarithmically increases with the length of time that the hip remains dislocated[]; therefore, prompt anatomic reduction should be attempted. The timing and method of reduction are dependent on the overall condition of the patient, the type of dislocation, and the presence or absence of associated fractures. In cases of simple dislocation, closed reduction should be attempted first. Although some physicians recommend that this procedure be performed under general anesthesia, this delay and its associated increase in the rate of AVN are not warranted when conscious sedation in the emergency department is readily available. If the emergency physician chooses to attempt closed reduction, the principles of conscious sedation and monitoring should be followed. The primary contraindication to closed reduction is the presence of a femoral neck fracture. Other relative contraindications include coexistent fractures in the dislocated extremity because of an inability to apply traction to the limb. Techniques of closed reduction are described in the next section.
Reduction Techniques The Stimson technique and the Allis technique are the methods most commonly used for reduction of posterior hip dislocations ( Figure 53-25 ).[18] The Stimson technique ( Figure 53-26 ) uses the weight of the limb and the force of gravity to reduce the dislocation and is relatively atraumatic. Although the Stimson
Page 334
technique is generally effective, placing an acutely and often multiply injured trauma patient in the prone position to perform the procedure may be a challenge. Adequate radiographic clearance of the spine has usually not yet been accomplished, and the administration of sedatives and analgesics in a prone patient has inherent risks. The Stimson technique is performed as follows: {,
The patient is placed prone with the leg hanging over the edge of the bed. The hip and knee are flexed at 90 degrees
Figure 53-25 Radiograph of posterior dislocation identified by loss of the lesser trochanter on the anteroposterior view.
Figure 53-26 Stim son's technique for hip reduction. See the text for a description of this m ethod.
{, {, {,
{,
An assistant stabilizes the pelvis The operator applies steady downward traction in line with the femur The femoral head is gently rotated and the assistant pushes the greater trochanter anteriorly toward the acetabulum Once reduction is achieved, the hip is brought to the extended position while traction is maintained
In a patient who cannot assume the prone position, the Allis technique should be used ( Figure 53-27 ). This technique is usually effective for obturator dislocations. It is perhaps the most commonly used method for hip reductions in the emergency department and is performed as follows: {,
The patient is placed in the supine position, and the pelvis is stabilized by an assistant
Figure 53-27 The Allis technique for hip reduction. See the text for a description of this
Page 335
m ethod.
{,
With the knee flexed, the operator applies steady traction in line with the deformity The hip is slowly brought to 90 degrees of flexion while steady upward traction and gentle rotation are applied The assistant pushes the greater trochanter forward toward the acetabulum Once reduction is achieved, the hip is brought to the extended position while traction is maintained
{,
{,
{,
Other recently described techniques for closed reduction of posterior hip dislocations include the Rochester method[60] and the traction-countertraction technique.[61] Closed reduction of a pubic dislocation can be quite difficult. The anterior position of the femoral head will resist flexion and thus makes the Allis technique impossible. We recommend reduction with the following maneuvers: {, {, {,
The patient is placed in the supine position Longitudinal traction is applied in line with the deformity The hip is hyperextended and internally rotated as an assistant applies downward pressure on the femoral head
Although prompt anatomic reduction is clearly desirable, multiple attempts at reduction in the emergency department should be avoided. Difficulty with reduction is usually the result of incarceration of a tendon, capsular structure, or an unrecognized osteochondral fragment that is blocking reduction. In the case of an irreducible dislocation, closed reduction under general anesthesia or open reduction is often required.
Postreduction Management After closed reduction, the hip should be tested for stability, which is accomplished by gently placing it through a full range of motion to see whether it will redislocate. An AP radiograph of the pelvis should be obtained to verify the adequacy of reduction. The radiograph should be carefully inspected to verify that the femoral head is in the acetabulum, the shaft of the femur is in neutral position, Shenton's line is intact, and the profile of the lesser trochanter is well visualized. The intra-articular space should be symmetrical and, when measured, the same depth as the unaffected joint. Asymmetry signals an entrapped intra-articular fragment and is an indication for CT scanning ( Figure 53-28 ).
Figure 53-28 A, A fracture through the fem oral head is seen with this anterior hip dislocation. B, Incom plete reduction is identified by exam ination of the joint space. This space should be the sam e width as the unaffected joint. Asym m etry signals an entrapped intraarticular fragm ent, which should be verified by com puted tom ography.
In general, fracture-dislocations should be reduced by closed reduction under general anesthesia or by open
Page 336
reduction. Attempted closed reduction of a fracture-dislocation by an emergency physician is not recommended in view of the rate of complications and associated medicolegal risk.
Outcomes The precarious blood supply to the femoral head is particularly important with regard to the long-term consequence of hip dislocations. The development of AVN of the femoral head has been reported in 1% to 17% of dislocations. Reduction after 24 hours is correlated with a higher incidence of AVN of the femoral head and posttraumatic arthritis.[58] Other risk factors for the development of AVN include the total dislocation time, the severity of the injury, the number of reduction attempts, and patient comorbid conditions.
Fracture-Dislocation of the Femoral Head Epidemiology and Mechanism. A small subset of hip dislocations are associated with fractures of the femoral head ( Figure 53-29A ). Femoral head fracture occurs in 22% to 77% of anterior hip dislocations and in 10% to 16% of posterior hip dislocations.[62] These injuries are almost always the result of high-speed vehicular trauma. Because of the tremendous force required to produce this injury pattern, coexistent multisystem trauma is the rule.
Figure 53-29 A, Anterior hip dislocation is identified as the lesser trochanter is brought into profile. Note a fracture of the lateral aspect of the greater trochanter. B, A postreduction radiograph demonstrates adequate reduction with symm etrical joint spaces.
When a femoral head fracture and hip dislocation coexist, patients assume the position typical of the dislocation. Hip mobility is markedly reduced and pain is usually severe. After initial stabilization, the involved extremity should be carefully examined for associated fractures of the femoral shaft and knee. The neurovascular examination should assess for femoral or sciatic injury. Radiographs should be evaluated carefully for any femoral head fracture in all patients with hip dislocations. The fracture of the femoral head can be subtle. These fractures may be detected by following the curve of the dislocated head and the acetabular cup to search for a small fragment that may otherwise be overlooked. Known or suspected injuries can be further defined by CT or MRI.[62] In most cases, satisfactory results can be obtained by closed reduction (see Figure 53-29B ).[57] Several authors recommend obtaining a CT scan of the hip before closed reduction to further define the injury and locate fracture fragments.[57] If the hip cannot be reduced by manipulation or if there is an unsatisfactory reduction of the femoral head fragment, open reduction will be required.
Dislocation of Hip Prosthetics An increasing number of patients have undergone hip arthroplasty. In addition to those performed as treatment of femoral neck fractures, nearly 200,000 patients undergo elective primary THA each year.[63] Postoperative dislocation of the prosthesis is a common complication that occurs in 1.5% to 3% of patients.[] Although most dislocations take place within 3 months of surgery, “late dislocations” have been reported up to 10 years after the operative procedure; such dislocations can result from major trauma or from trivial events (e.g., rising from a seated position). Posterior dislocations account for 75% to 90% of cases (see Figure 53-14 ).[53] Reduction techniques for prosthetic hip dislocations are identical to those described earlier. Consultation with an orthopedic surgeon is essential for safe reduction and development of a long-term treatment plan for the patient. Reduction of the prosthesis does not carry the same urgency as reduction of a dislocated hip because there is no risk for the development of AVN once the femoral head has been replaced. However, traction on the sciatic nerve can occur and makes early reduction more compelling. In addition, the reduction itself carries the unique dangers of loosening of the components, fracturing of the surrounding bone, and movement of the acetabular cup; reduction is best deferred to an orthopedic consultant.
Soft Tissue Injuries Soft tissues may be subject to muscle or tendon strain or contusions from misuse, overuse, or accidental
Page 337
trauma. Rupture, hemorrhage, or myositis ossificans may develop in muscles.[65]
Muscular Injury Strenuous exercise in a poorly conditioned person, sudden exertion, and direct trauma may all traumatize soft tissues. Cold temperature, vascular or infectious disease, fatigue, and poor training are known predisposing conditions for this injury.[66] Infectious predisposing diseases include trichinosis, tuberculosis, and typhoid fever. A detailed classification system of muscular injuries has been devised, but it is of little clinical significance for the emergency physician. Classification of complete and partial tears is reasonable and of greater clinical utility. Partial tears are reversible injuries that are aggravated by movement or tension. Mild spasm, swelling, ecchymosis, and tenderness cause minor loss of function and strength. Complete tears produce a palpable depression, and the torn muscle edge is also often palpable. Severe spasm, swelling, ecchymosis, tenderness, and loss of muscle function occur. In significant muscle strains, radiographs are needed to evaluate the possibility of an accompanying bony avulsion injury. Initial management of incomplete tears traditionally includes the local application of ice for the first 48 hours, followed by heat. Compressive wraps cause distal venostasis with the potential for distal venous clot formation and do not significantly decrease recovery time. Nonsteroidal anti-inflammatory agents and sufficient analgesics are important for recovery and patient satisfaction. Muscle relaxants may be useful when the injury is accompanied by muscular spasm. In general, complete rest of the affected muscle should be maintained with the recommendation of “weight bearing as pain tolerated.” This progressive muscle loading can be started within 3 to 5 days. Any significant injury should be referred for physical therapy. A complete muscle tear is a serious condition. Consultation plus follow-up with an orthopedic surgeon or sports medicine specialist is vital for these patients.
Sports Injury Patterns Athletes commonly experience muscular injury from accidents and overtraining. The two most common injuries involve the hamstrings and the quadriceps.
The Hamstrings Hamstring muscle strains are common in sports involving running and sudden acceleration. The injury is accompanied by sudden, intense pain in the posterior of the thigh. Any active or passive motion at the hip is poorly tolerated because of the intense pain that movement causes. Crutches and toe-touch weight bearing are recommended until the patient is evaluated by a physician trained in sports medicine. Toe-touch weight bearing refers to walking with crutches while the toes of the injured extremity rest on the ground without placing any weight on it. Appropriate weight-training programs have been shown to speed rehabilitation of this injury.[65] Complete recovery from a hamstring muscle strain may take weeks to months.
The Quadriceps. The quadriceps is the most common muscular group to sustain complete tears. This injury occurs when the muscles are contracted suddenly against the body's weight, such as may occur when an athlete slips or stumbles and attempts to avoid a fall. Ambulation is significantly affected. There is pain with active and passive knee extension. In significant tears, the patient is able to neither actively extend the knee nor maintain its extension against gravity. A depression just proximal to the superior pole of the patella suggests a complete tear. A complete tear of the quadriceps most often requires surgical repair and extensive rehabilitation.
Iliopsoas Strain. Gymnasts and dancers are the most likely group of athletes to experience an injury to the iliopsoas as a result of sudden forceful hip flexion against resistance. Severe pain is often experienced in the groin, thigh, or low back region. Severe intra-abdominal pain is common at the muscle origin and may dominate the clinical picture. Examination reveals groin tenderness and pain with active hip flexion. Radiographs of the femur should be obtained to identify an avulsion fracture of the lesser trochanter. CT will frequently demonstrate a large hematoma. Bed rest with partial flexion at the knee and hip is generally required for 7 to 10 days. With severe strains, symptoms may persist for 2 to 3 months.
Hip Adductor Strain.
Page 338
Injury to the hip adductors occurs as the thigh is forcefully abducted, such as in a straddle injury. The patient complains of pain in the groin, the pubic region, and the medial proximal aspect of the thigh. Abduction and adduction are often limited because of pain. Swelling and skin discoloration confirm the tear. If the tear is complete, a defect in the muscle may be felt along the medial aspect of the thigh near the groin.
Gluteus Muscle Strain. The gluteus muscles may be injured with vigorous or forced hip extension as is seen in track-and-field jumping events. The pain is typically less severe than that associated with injuries to other muscle groups. The hip is tender when extended or abducted.
Tendon Injuries. Clinically, tendon strains tend to have a more insidious onset than muscle strains do. These strains may occur at the attachment of the muscles to the superior or inferior pubic ramus, the pubic symphysis, the ischium, and the femur. A groin pull is the layman's term referring to an injury to the tendons of the hip adductors. The injury usually involves only the adductor longus, yet the adductor magnus and brevis and the pectineus are often involved as well.[66] It commonly occurs in skaters and cross-country skiers when an accidental stress abducts the thigh during a powerful contraction of the adductors. These muscles may also be injured from overuse in an unconditioned patient. Local pain is noted at the inferior pubic ramus and the ischial tuberosity. Extension, abduction, and adduction of the hip are painful. The pain may radiate to the back of the thigh. Pain over the greater trochanter may represent tendon strain of the attachments of the gluteus medius, gluteus minimus, tensor fasciae latae, or piriformis. Pain is aggravated by resisted abduction. Tenderness in the groin and painful hip movement suggest a strain of the iliopsoas tendon at its attachment to the lesser trochanter. Trochanteric bursitis, peritendinitis, AVN, neoplasm, and other causes should be considered. Treatment of a tendon strain is similar to that for other soft tissue injuries. The use of crutches with weight bearing as tolerated by pain is helpful for the first 2 weeks. Opioid analgesics and a short course of anti-inflammatory agents should be given. Complete tendon disruption frequently requires surgical repair.
Vascular Injuries Hip dislocations and the various types of femoral fractures may have an associated arterial injury. The vessel may be partially lacerated, completely severed, or thrombosed. Lack of distal arterial flow may also represent a stretched vessel in spasm. The superficial femoral artery is most commonly injured with trauma to the hip and thigh. The common and the deep femoral arteries are less frequently injured. In the acute setting, penetrating trauma is the usual mechanism of injury. Arterial injury with femoral shaft fractures is rare and occurs in less than 2% of the cases reported.[67] Anterior- and superior-type dislocations may produce femoral artery injury.[18] Comparative examination of blood pressure, the ankle-brachial index, and Doppler pulses in the injured and uninjured extremity is critical if arterial injury is suspected. The need for ancillary studies in the evaluation of extremity trauma for vascular injury is somewhat controversial and dependent on the institution.[68] Diagnostic evaluation must not delay surgical exploration when clinical signs and symptoms of vascular injury are obvious.[69] Early restoration of blood flow is essential to prevent ischemic damage to the leg.
Neurologic Injury Trauma, infectious agents, and degenerative disease may all injure peripheral nerves. In trauma, nerves may be injured by a blunt object that causes a contusion, by a sharp penetrating object that produces a partial or complete tear, or by the stretch of a missile as it passes in proximity. Nerves are particularly vulnerable to prolonged ischemia, which can lead to necrosis. Compression of the nerve from a hematoma or a dislocated femoral head may also appear as a neurapraxia manifested by transient loss of conductivity. The femoral and sciatic nerves are rarely injured with femoral shaft fractures because they are encased in muscles throughout the length of the thigh. Treatment of neurovascular compromise and a hip dislocation or a displaced femoral fracture is immediate reduction to ensure limb viability. Reduction should be accomplished before transfer to another facility whenever possible.
Femoral Nerve
Page 339
When the femoral nerve is injured, the iliac and femoral arteries are commonly involved because of their anatomic proximity. If injured, the femoral nerve is most often traumatized in penetrating trauma of the pelvis, groin, or thigh. Femoral neuropathy can occasionally result from compression by a hematoma within the abdominal wall or the iliopsoas as a complication of hemophilia, anticoagulant therapy, or trauma.[70] The motor deficit in complete femoral neuropathy is manifested as marked weakness of knee extension. The patient is able to walk on level ground, yet has extreme difficulty walking up stairs or an incline. Patients cannot rise from a sitting position because of significant proximal muscle weakness. The sensory deficit varies, but is localized along the anterior aspect of the thigh and medial lower aspect of the leg. The most reliable spot for testing a sensory deficit is just superior and medial to the patella. The deep tendon reflex of the knee will be diminished or absent. If a traumatic neuropathy is suspected, immediate orthopedic consultation should be obtained. Nerve exploration and repair are generally preferred for penetrating trauma and when direct impingement on the nerve by bone fragments or hematoma is suspected. Surgical exploration and drainage of a hematoma that is impinging on the femoral nerve are appropriate. Progressive nontraumatic neuropathies require urgent neurologic consultation. When a chronic neuropathy exists, atrophy of the anterior aspect of the thigh will already have developed. The motor deficits have been discussed previously.
Sciatic Nerve Sciatic injury is rare with femoral fractures, but it may develop as a result of the traction used to stabilize the fracture during the initial management period. Complete traumatic injury may result from a deep penetrating wound in the hip, thigh, or buttock. Sciatic nerve palsy from both inadvertent injection into the nerve and intraneural or extraneural hemorrhage in patients taking anticoagulants has been described. Posterior hip dislocations and fracture-dislocations produce sciatic neurapraxia in 10% to 14% of these injuries.[] Patients with complete sciatic neuropathy have paralysis of the hamstring muscles and all muscles below the knee. With partial injury, a peroneal palsy with weakness of the extensor hallucis longus muscle is the most sensitive clinical sign. There is sensory loss below the knee and along the posterior of the thigh. The deep tendon reflex at the ankle is absent or diminished. Sciatic injury from posterior dislocations often consists of only transient loss of conductivity, particularly in its motor fibers. Unfortunately, the other injury patterns to the sciatic nerve carry the worst prognosis of all peripheral nerve injuries. The prognosis is poorest when the injury is proximal and complete. Even with optimal repair, recovery is often inadequate. Sciatic neuropathy is a disabling problem. Obvious atrophy of the lower part of the leg and foot develops, followed by ulceration of the sole of the foot and infection. A below-the-knee amputation is frequently necessary in these cases.
SPECIAL PEDIATRIC CONSIDERATIONS Anatomy Development of the femoral head and neck with its growth plates and two primary ossification centers is illustrated in Figure 53-30 . A significant proportion of the pediatric hip is radiopaque cartilage and developing new bone. For this reason, almost any type of trauma in this location carries the potential for premature growth arrest. Understanding that large portions of the pediatric hip are radiolucent will dissuade the tendency to focus attention on the ossified elements.
Figure 53-30 Developm ent of the fem oral head and neck with its growth plates and two prim ary ossification centers.
Hip Dislocation The incidence of hip fractures and dislocations is increasing in young patients, often as a result of high-energy trauma. Up to 50% of children with a hip dislocation will also have fractures elsewhere. In small children, dislocation of the hip is more common than femoral neck fractures. The force required to dislocate a pediatric hip is much less than that required in an adult because the acetabulum is less completely developed than in adults. Seemingly negligible trauma, such as tripping or a minor fall, may dislocate the femoral head in a young child. In a school-age child, athletic injuries are the major cause of traumatic hip
Page 340
dislocation. In the teenage years, motor vehicle accidents predominate as the cause of hip dislocations.
Femoral Fractures Unlike adults, the vast majority of pediatric hip fractures do not result from high-energy violent trauma. These fractures are usually the result of falling from heights, jumping out of a swing, being struck by a car, or having a bicycle accident. Child abuse must also be considered. Whereas a car commonly strikes an adult at the tibial level, a smaller child is most often hit at the level of the hip, which results in a fracture there. The classic Salter-Harris division of fractures in the pediatric population is not used in the hip. The Delbet classification is a well-accepted system used for pediatric femoral fractures.[72] This system separates fractures through the physis and the transcervical, cervicotrochanteric, and intertrochanteric regions ( Figure 53-31 ).
Figure 53-31 Pediatric proxim al fem oral fractures are classified by a system that separates fractures in the physis (A) the transcervical area (B), the cervicotrochanteric area (C), and the intertrochanteric region (D). ((From Canale ST, Beaty JH: Fractures of the pelvis. In Rockwood JC Jr, Green DP, Bucholz RW [eds]: Rockwood and Green's Fractures in Children, vol 3, 5th ed. Philadelphia, JB Lippincott, 2001, pp 883-911.)JB Lippincott)
Spiral Shaft Fractures If seemingly trivial trauma has resulted in a spiral femoral shaft fracture in a child, child abuse and pathologic fracture must be considered.[] Common causes of pathologic fracture include unicameral bone cysts, fibrous dysplasia, osteogenesis imperfecta, and malignancy.[]
Management Femoral fractures in children are so rare that most orthopedists treat only three or four in a career.[72] Although these pediatric injuries are extremely rare, their complications are significant. Unlike an adult, a child's femur has growth potential, and any disruption carries the possibility of lifetime disability. Treatment of femoral shaft fractures in adults is aimed at prevention of the complications of prolonged immobilization. Unlike adults, children tolerate bed rest well, which allows more treatment options. The primary goal in children is prevention of the many complications common with femoral fractures. Premature closure of the physeal plate results in a valgus deformity of the hip. AVN, malunion, nonunion, and limb length discrepancy are all complications frequently seen with pediatric femoral fractures. For all these reasons, referral to a pediatric orthopedist is recommended.[72]
The Child with a Limp A child who comes to the emergency department with a limp is a diagnostic challenge. Both life-threatening and benign disease processes can produce a limp. When the child is too young to give an adequate history, the etiology becomes more elusive. The attending physician should inquire about the chronology of the symptoms, the child's development (i.e., social milestones, weight gain, physical development), and diet. Associated illness and a family history may be helpful. Though challenging, the history and physical examination, combined with appropriate diagnostic modalities, will allow discovery of the cause in most patients. An important point to remember in the pediatric population is that the knee is a common site for referred hip pain. Proper follow-up is crucial to avoid additional morbidity in these children.
Evaluation of the Child's Gait Gait is a learned, complex combination of motions produced through coordination of the musculoskeletal, peripheral, and central nervous systems. A limp is produced by anything that alters this process and can be divided into categories according to the underlying abnormality. Pain, muscle weakness, structural alteration, peripheral sensory deficit, and cerebellar or vestibular imbalance are major categories. A limp caused by pain is referred to as an “antalgic” gait. Conditions that disturb the biomechanics of the hip or cause the child pain may affect any of the elements of gait. Other conditions such as cerebellar pathology or disease of the
Page 341
knee or foot are discussed in their appropriate sections.
Etiology of the Limp Inflammation and Infection Inflammation of the articular surface, the intraarticular synovium, or the joint capsule creates pain. Weight bearing increases the pain. The child limps in an attempt to limit the proportion of time that the affected hip bears the body's weight. Toxic synovitis is a common nonbacterial inflammatory clinical entity that can cause a limp. Little is known about its etiology. It develops most frequently in boys between 3 and 10 years of age. Clinically, the synovitis is manifested as pain in the hip or knee. An antalgic gait is present with minimal systemic symptoms. There is restriction of hip motion and associated muscle spasm, and the child will often refuse to bear weight on the hip. As the disease progresses, the joint capsule is increasingly stretched and intraarticular pressure rises. The potential volume of the joint capsule is largest with the hip flexed, abducted, and externally rotated. The child prefers to lie in this position as the capsule begins to bulge to minimize the tension and intra-articular pressure. The diagnosis of toxic synovitis must be one of exclusion of more serious diseases that mimic it. Acute joint inflammation and pain may be associated with juvenile rheumatic arthritis, systemic lupus erythematosus, Perthes' disease, septic arthritis, and tuberculous arthritis. Ultrasound of the hip joint will detect an effusion in 78% of cases of toxic synovitis but cannot distinguish this condition from septic arthritis.[76] Joint aspiration may be required when the diagnosis is in doubt. Distinguishing between toxic synovitis and septic arthritis can be a diagnostic dilemma. Recent work has illustrated four key predictors: temperature higher than 38.5° C in the preceding week, non–weight bearing (refusal or inability to bear weight even with support), erythrocyte sedimentation rate higher than 40 mm/hr, and a white blood cell count greater than 12,000 cells/mL. These four predictors were developed in a retrospective study and then validated in a prospective study.[] Based on the validation study, the probability of septic arthritis was 2% for zero predictors, 9.5% for one predictor, 35% for two predictors, 73% for three predictors, and 93% for four predictors.[79] These predictors should be used in conjunction with clinical assessment. Acute bacterial infections of the hip and femur require early identification and intervention to minimize their subsequent morbidity and disability.[79] Unfortunately, the diagnosis is often missed initially because the child may appear relatively nontoxic in the early phases of infection. Signs and symptoms of systemic illness usually accompany infection of the femur or hip. Fever, malaise, decreased oral intake, a limp, or refusal to bear any weight is common.[80] Whereas osteomyelitis most commonly develops in the metaphysis in adults, the physeal region is often the infected site in children. Pyarthrosis (septic arthritis) may result from hematogenous seeding or direct extension of osteomyelitis. The hip and the knee are the most common infected joints. The causative agent in osteomyelitis and pyarthrosis is nearly always a gram-positive organism, usually Staphylococcus. The incidence of Haemophilus influenzae infection has fallen as a direct result of its addition to the childhood immunization regimen. Neonates, asplenic children, and children with sickle cell anemia are at risk for infection with gram-negative organisms. Salmonella is also more often seen in sickle cell patients with osteomyelitis. Viral and rickettsial diseases (e.g., Lyme disease) have been known to be present in subacute cases.[81]
Radiographic Evaluation Identification of acute osteomyelitis by plain radiographs is difficult until 2 to 3 weeks after infection. Pyarthrosis may be manifested by widening of the space between the femoral head and the acetabular roof and bulging of the joint capsule and surrounding soft tissues. This is seen as a change in the contour of the gluteus minimus and iliopsoas fat stripes ( Figure 53-32 ). Care should be taken to distinguish the normal shadow of the muscles and the joint capsule as described earlier in this chapter (see Figure 53-12 ). Plain radiographs are seldom useful in the initial identification of infection because visualization of a joint effusion has low sensitivity for pyarthrosis. Bone scan, MRI, CT, and ultrasound-guided joint aspiration are appropriate to diagnose a septic joint.
Page 342
Figure 53-32 Prom inence of the soft tissue shadows about the right hip, including bulging of the obturator internus muscle and its aponeurosis (open arrows), indicates distention of the joint capsule. The opposite hip shows the norm al soft tissue shadows indicated by the closed arrows. ((From Harris JH, Harris WH, Novelline RA: The Radiology of Emergency Medicine, 3rd ed. Baltim ore, William s & Wilkins, 1993.)William s & Wilkins)
The inflammatory process involved in the immune system's attempt to eradicate the intruder also begins to destroy the body's own articular surface. Even with treatment, most children experience some arthritic disability.[82]
Slipped Capital Femoral Epiphysis Anatomy The capital femoral epiphysis appears during the first year of life. The epiphysis of the greater trochanter appears by the age of 5 and the lesser trochanter during the 13th year of life. All these structures unite during the 18th through 20th years. The anatomic relationship has been compared with a scoop of ice cream sitting on a cone. This relationship remains symmetrical on both AP and lateral radiographs ( Figure 53-33 ). Asymmetry in any view represents either SCFE or a subcapital fracture ( Figures 53-34 and 53-35 ).
Figure 53-33 An anteroposterior radiograph of a 10-year-old boy demonstrates the norm al anatom ic relationship of the capital fem oral epiphysis, the proximal physis, the apophysis of the lesser trochanter, and the triradiate synchondrosis.
Figure 53-34 Frank slipped capital fem oral epiphysis. The capital fem oral epiphysis is displaced m edially, inferiorly, and posteriorly. The inhom ogeneity of the fem oral neck is consistent with early avascular necrosis. ((From Harris JH, Harris WH, Novelline RA: The Radiology of Em ergency Medicine, 3rd ed. Baltimore, William s & Wilkins, 1993.)William s & Wilkins)
Figure 53-35 Right slipped capital femoral epiphysis. A, The slippage appears m inim al and m ay be overlooked; however, m edial displacem ent of the capital fem oral epiphysis with respect to the m etaphysis results in the lateral cortex of the fem oral neck and the epiphysis being in the same plane (open arrow). The capital fem oral epiphysis is flattened (arrow), and the right hip joint space is widened. B, Medial and posterior displacem ent of the capital fem oral epiphysis (arrow). ((From Harris JH, Harris WH, Novelline RA: The Radiology of Emergency Medicine, 3rd ed. Baltimore, William s & Wilkins, 1993.)William s & Wilkins)
Epidemiology and Pathophysiology
Page 343
SCFE occurs in approximately 5 people per 100,000 population per year. Twenty-five percent of cases are bilateral.[83] SCFE occurs twice as frequently in boys as in girls, with the respective peak incidence being 13 and 11 years old. Epidemiologic data have provided clues to the pathophysiology of this injury. SCFE is associated with the onset of puberty and rarely occurs before 10 years of age. It most commonly develops in boys 10 to 17 years of age during their period of rapid growth. It is believed to be the result of a structural weakness in physeal cartilage at the onset of pubescence.[84] The specific cause is not well understood. That SCFE occurs more frequently in male African Americans than in the white population supports the presence of a genetic element in the pathophysiology of this disease.[84] Other risk factors identified are obesity, previous irradiation or chemotherapy, renal osteodystrophy, hypothyroidism, and neglected septic arthritis.[85]
Clinical Features SCFE is usually an insidious process extending over a period of several weeks to months. Initially, there may be only slight discomfort in the groin, thigh, or knee after activity. Eventually, as slippage progresses, the pain occurs at rest as well. Referred pain to the knee is a classic manifestation. Frequently, the ectopic nature of the pain leads to delayed diagnosis, increased displacement, and a worsened prognosis.[86] As the epiphysis continues to slip, the pain increases. Parents often bring the child in for medical evaluation when they notice the child beginning to limp. Physical examination may reveal hip tenderness, decreased hip range of motion, and an abducted, externally rotated thigh.
Diagnostic Strategies Children with unexplained hip or knee pain merit clinical as well as radiographic evaluation. Initially, AP, lateral, and frog-leg lateral radiographs of the hip should be obtained. The frog-leg lateral projection shows the hip in a plane midway between the AP and lateral views. The earliest radiographic findings are subtle, with the abnormality visualized on only one projection. The most reliable initial finding of SCFE is asymmetry of the femoral epiphysis in relation to the neck. Small amounts of slippage can be detected by examining the epiphyseal edge as it becomes flush with the superior border of the femoral neck. This can be thought of as “the scoop slipping off the ice cream cone.” The dome of the epiphysis may be flattened. A line drawn along the medial aspect of the femoral shaft (Klein's line) should intersect some part of the normal femoral head. Failure of this line to intersect the head indicates medial and posterior movement of the head on the epiphysis.[83] Comparative views of the two hips are indicated if initial radiographs are equivocal. If occult fracture is suspected, MRI or CT should be performed.[] Surgery is required to anchor the epiphysis and prevent further slippage.
Perthes' Disease Perthes' disease is the name given to AVN of the pediatric femoral head. It has also been called LeggCalvé-Perthes and Calvé-Perthes disease. It occurs at a younger age than SCFE does—between the ages of 2 and 10. Its peak incidence is at 6 years, and it occurs five times more often in boys than girls. The disease affects both hips in 15% of patients.[88]
Isolated Fracture of the Greater or Lesser Trochanter in Children An isolated fracture of the greater trochanter is a rare injury. In children, a fracture occurs as the entire greater trochanteric epiphysis is avulsed from the femur. This type of fracture occurs in children and adolescents between 7 and 17 years of age. The mechanism of injury is generally a powerful muscular contraction of the lateral rotators of the hip joint during a twisting fall. If the fragment is large and displaced by more than 1 cm, open reduction and internal fixation may be indicated. An isolated fracture of the lesser trochanter occurs as a forceful contraction of the iliopsoas muscle avulses the lesser trochanter from the physis during sudden hip flexion ( Figure 53-36 ). Eighty-five percent of all cases occur in patients younger than 20 years, with a peak incidence between 12 and 16 years.[89] Marked tenderness in the femoral triangle is present, and hip flexion against resistance is painful. Clinically, a seated patient is unable to lift the foot of the affected leg from the floor.
Page 344
Figure 53-36 Forceful contraction of the iliopsoas m uscle results in avulsion of the lesser trochanter.
Treatment of an isolated lesser trochanter avulsion fracture usually involves bed rest and early mobilization. Painless active hip motion is achieved within 3 weeks.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/125.html/top
Page 345
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
KEY CONCEPTS {,
{, {, {,
{,
Hip dislocation: Hip dislocation is one of the few orthopedic emergencies. The likelihood of its complication, AVN, is related to both the initial degree of trauma and the amount of time that the femoral head remains out of joint. Reduction of the hip within 6 hours after dislocation significantly decreases the incidence of AVN. Hip fracture: When a painful hip prevents ambulation and plain films do not reveal a fracture, magnetic resonance imaging should be performed. Intertrochanteric fractures: Hemodynamic instability may result from dehydration and blood loss of up to 3 U into the fracture site. Up to 70% of these patients are under-resuscitated. Acetabular fractures: It is especially important to identify acetabular fractures before closed reduction is attempted because intra-articular bone fragments may interfere with effective reduction. Oblique radiographs (Judet views) or CT will help visualize the acetabulum and precisely define the injury. Slipped capital femoral epiphysis: This condition is most commonly seen in African American boys 10 to 17 years of age; 25% of cases are bilateral. The most reliable initial finding of SCFE is asymmetry of the femoral epiphysis in relation to the neck wherein small amounts of slippage give the appearance of “the scoop slipping off the ice cream cone.”
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60640736-2/1365/126.html/top
Page 346
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
REFERENCES 1. Pare A: The work of that famous chirurgeon, Ambrose Pare, translated out of Latin and compared with the French by Tho Johnson, Book XV, London, T Cotes & R Young, 1634. 2. Von Langenbeck B: Verhandl d, deutch, p 92. Gesellsch F, Chir 1878. As found in Davis GG: The operative treatment of intracapsular fracture of the neck of the femur. Am J Orthop Surg 1908-1909;6:481-483. 3. Gourlay M, Richy F, Reginster JV: Strategies for the prevention of hip fracture. Am J Med2003;115:309. 4. Koval KJ, Zuckerman JD: Functional recovery after fracture of the hip. J Bone Joint Surg Am1994;77:751. 5. AAOS Bulletin: Femoral Neck Fracture (Adult)., Chicago: American Academy of Orthopaedic Surgeons; 1989: 11-12. 6. Sernbo I, Johnell O: Changes in bone mass and fracture type in patients with hip fractures. Clin Orthop 1989;238:139. 7. Wadsworth CT: Manual Examination and Treatment of the Spine and Extremities, Baltimore, Williams & Wilkins, 1988. 8. Gray H: Anatomy, Descriptive and Surgical, revised from English 17th ed, New York, Bounty Books, 1997. 9. Brunner LC, Eshilian-Oates L: Hip fractures in adults. Am Fam Physician2003;67:537. 10. Singh M, Nagrath AR, Maini PS: Changes in trabecular patterns of the upper end of the femur as an index of osteoporosis. J Bone Joint Surg Am1970;52:457. 11. Learmonth ID, Maloon S, Dall G: Core compression of early atraumatic osteonecrosis of the femoral head. J Bone Joint Surg Br1990;72:287. 12. Sahin V: Traumatic dislocation and fracture dislocation of the hip: A long-term follow-up study. J Trauma 2003;54:520. 13. Bachiller FGC, Caballer AP, Portal LF: Avascular necrosis of the femoral head after femoral neck fracture. Clin Orthop2002;399:87. 14. Garland DE: A clinical perspective on common forms of acquired heterotrophic ossification. Clin Orthop 1991;263:13. 15. Booth DW, Westers BM: The management of athletes with myositis ossificans traumatica. Can J Sport Sci1989;14:10. 16. Vestergaard P: Corticosteroid use and risk of hip fracture: A population-based case-controlled study in Denmark. J Intern Med2003;254:486. 17. Koval K: Clinical pathway for hip fractures in the elderly. Clin Orthop2004;425:72. 18. DeLee JC: Fractures and dislocations of the hip. In: Rockwood Jr JC, Green DP, Bucholz RW, ed.Rockwood and Green's Fractures in Adults, vol 2. 4th ed. Philadelphia: JB Lippincott; 1996: 19. Harris JH, Harris WH, Novelline RA: The Radiology of Emergency Medicine, 3rd ed. Baltimore, Williams & Wilkins, 1993. 20. Rizzo PF, Gould ES, Lyden JP, Asnis SE: Diagnosis of occult fractures about the hip: Magnetic resonance imaging compared with bone scanning. J Bone Joint Surg Am1993;73:395. 21. Perron AD, Miller MD, Brady WJ: Orthopedic pitfalls in the emergency department: Radiographically-occult hip fracture. Am J Emerg Med2002;20:234. 22. Guanche CA: The use of MRI in the diagnosis of occult hip fractures in the elderly: A preliminary review. Orthopedics1994;17:327. 23. Needoff M, Radford P, Langstaff R: Preoperative traction for hip fractures in the elderly: A clinical trial. Injury1993;24:317. 24. Brillman J, Quenzer RW: Infectious Disease in Emergency Medicine, 2nd ed. Philadelphia, Lippincott-Raven, 1998. 25. Jones JS, Johnson K, McNinch M: Age as a risk factor for inadequate emergency department analgesia. Am J Emerg Med1996;14:157. 26. Ronchi L: Femoral nerve blockade in children using bupivacaine. Anesthesiology1989;70:622. 27. Fletcher AK, Rigby AS, Heyes FLP: Three-in-one femoral nerve block as analgesia for fractured neck of the femur in the emergency department: A randomized controlled trial. Ann Emerg Med2003;41:227.
Page 347
28. Dean E, Orlinsky M: Nerve blocks of the thorax and extremities. In: Roberts J, Hedges J, ed.Clinical Procedures in Emergency Medicine, 3rd ed. Philadelphia: WB Saunders; 1998: 29. Harkness JW: Arthroplasty of the hip. In: Canale ST, ed.Campbell's Operative Orthopaedics, 9th ed. St Louis: CV Mosby; 1998: 30. Cushner F, Friedman RJ: Economic impact of total hip arthroplasty. South Med J1988;81:1379. 31. Thomas BJ, Saa J, Lane JM: Total hip arthroplasty. Curr Opin Rheumatol1996;8:148. 32. Shaw JA, Greer RB: Complications of total hip replacement. In: Epps Jr CH, ed.Complications in Orthopedic Surgery, 3rd ed. Philadelphia: JB Lippincott; 1994: 33. Birge SJ: Osteoporosis and hip fracture. Clin Geriatr Med1993;9:69. 34. Clayer MT, Bauze RJ: Morbidity and mortality following fractures of the femoral neck and trochanteric region: Analysis of risk factors. J Trauma1989;29:1673. 35. Ahmad LA, Eckhof DG, Kramer AM: Outcome studies of hip fractures: A functional viewpoint. Orthop Rev1994;23:19. 36. De Boeck H: Classification of hip fractures. Acta Orthop Belg1994;60(Suppl 1):106. 37. Kovall KJ, Zuckerman JD: Hip fractures II: Evaluation and treatment of intertrochanteric fractures. J Am Acad Orthop Surg1994;2:150. 38. Sernbo I: Unstable trochanteric fractures of the hip: Treatment with Ender pins, compared with a compression hip-screw. J Bone Joint Surg Am1988;70:1297. 39. Davis TRC: Intertrochanteric femoral fractures: Mechanical failure after internal fixation. J Bone Joint Surg Br1990;72:26. 40. Russell TA, Taylor JC: Subtrochanteric fractures of the femur. In: Browner BD, ed.Skeletal Trauma, Philadelphia: WB Saunders; 1992: 41. Bajaj HN, Kumar B, Chacko V: Subtrochanteric fractures of the femur—an analysis of results of operative and non-operative management. Injury1988;19:169. 42. Velasco RU, Comfort TH: Analysis of treatment problems in subtrochanteric fractures. J Trauma 1978;18:513. 43. Arneson TJ: Epidemiology of diaphyseal and distal femoral fractures in Rochester, Minnesota, 1965-1984. Clin Orthop1988;234:188. 44. Kluger Y: Blunt vascular injury associated with closed mid-shaft femur fracture: A plea for concern. J Trauma1994;36:222. 45. Taylor MT, Banerjee B, Alpar EK: Injuries associated with a fractured shaft of the femur. Injury 1994;25:185. 46. Hofeldt F: Proximal femoral fractures. Clin Orthop1987;218:12. 47. Chalmers J, Irvine GB: Fractures of the femoral neck in elderly patients. Clin Orthop1988;229:125. 48. Bucholz RW, Brumback RJ: Fractures of the shaft of the femur. In: Rockwood Jr JC, Green DP, Bucholz RW, ed.Rockwood and Green's Fractures in Adults, vol 2. 4th ed. Philadelphia: JB Lippincott; 1996: 49. Blecher A: Über den Einflup des Parademarsches auf der Entstehung der Fup geschwulst. Med Klin 1905;1:305. 50. Clement DB: Exercise-induced stress injuries to the femur. Int J Sports Med1993;14:347. 51. Leung KS: Treatment of ipsilateral femoral shaft fractures and hip fractures. Injury1993;24:41. 52. Hak DJ, Goulet JA: Severity of injuries associated with traumatic hip dislocation as a result of motor vehicle collisions. J Trauma1999;47:60. 53. Morey BF: Instability after total hip arthroplasty. Orthop Clin North Am1992;23:237. 54. Ferguson KL, Harris V: Inferior hip dislocation in an adult: Does a rare injury now have a common mechanism?. Am J Emerg Med2000;16:117. 55. Sanville P, Nicholson DA, Driscoll PA: The hip: ABC of emergency radiology. BMJ1994;308:524. 56. Bassett LW, Gold RH, Epstein HC: Anterior hip dislocation: Atypical superolateral displacement of the femoral head. AJR Am J Roentgenol1983;141:385. 57. Hougaard K, Thomsen PB: Traumatic posterior fracture-dislocation of the hip with fracture of the femoral head or neck, or both. J Bone Joint Surg Am1988;70:233. 58. Dreinhofer KE: Isolated traumatic dislocation of the hip. J Bone Joint Surg Br1994;76:6. 59. Hillyard RF, Fox J: Sciatic nerve injuries associated with traumatic posterior hip dislocation. Am J Emerg Med2003;21:545. 60. Stefanich RJ: Closed reduction of posterior hip dislocation: The Rochester method. Am J Orthop 1999;28:401. 61. Dahner LE, Hundley JD: Reduction of posterior hip dislocations in the lateral position using traction-countertraction: Safer for the surgeon?. J Orthop Trauma1999;13:373. 62. Potter HG: MR imaging of acetabular fractures: Value of detecting femoral head injury, intraarticular fragments, and sciatic nerve injury. AJR Am J Roentgenol1994;163:881. 63. National Institutes of Health : Total hip replacement. NIH consensus statement online1999;12:1. 64. Yuan L, Shih C: Dislocation after total hip arthroplasty. Arch Orthop Trauma Surg1999;119:263. 65. Young JL, Laskowski ER, Rock MG: Thigh injuries in athletes. Mayo Clin Proc1993;68:1099.
Page 348
66. Renstrom AFH: Tendon and muscle injuries in the groin area. Clin Sports Med1992;11:815. 67. Barr H, Santes G, Stephenson I: Occult femoral artery injury in relation to fractures of the femoral shaft. J Cardiovasc Surg1987;28:193. 68. Austin OMB: Vascular trauma—a review. J Am Coll Surg1995;181:91. 69. Frykberg ER: The reliability of physical examination in the evaluation of penetrating extremity trauma for vascular injury: Results at one year. J Trauma1991;31:502. 70. D'Amelio LF, Musser DJ, Rhodes M: Bilateral femoral nerve neuropathy following blunt trauma. J Neurosurg1990;73:630. 71. Sunderland S: Repair of a transected sciatic nerve. J Bone Joint Surg Am1993;75:911. 72. In: Rockwood Jr JC, Green DP, Bucholz RW, ed.Rockwood and Green's Fractures in Children, vol 3. 4th ed. Philadelphia: JB Lippincott; 1996: 73. Dalton HJ: Undiagnosed abuse in children younger than 3 years with femoral fracture. Am J Dis Child 1990;144:875. 74. Azouz EM: Types and complications of femoral neck fractures in children. Pediatr Radiol1993;23:415. 75. Hughes LO, Beaty JH: Fractures of the head and neck of the femur in children. J Bone Joint Surg Am 1994;76:283. 76. Kermond S: A randomized clinical trial: Should the child with transient synovitis of the hip be treated with non-steroidal anti-inflammatory drugs?. Ann Emerg Med2002;40:294. 77. Kocher MS, Zurakowski D, Kasser JR: Differentiating between septic arthritis and transient synovitis of the hip in children: An evidence-based clinical prediction algorithm. J Bone Joint Surg Am1999;81:1662. 78. Kocher MS: Validation of a clinical prediction rule for the differentiation between septic arthritis and transient synovitis of the hip in children. J Bone Joint Surg Am2004;86:1629. 79. Dabney KW, Lipton G: Evaluation of limp in children. Curr Opin Pediatr1995;7:88. 80. Dressler F: Infectious diseases affecting the musculoskeletal system in children and adolescents. Curr Opin Rheumatol1993;5:651. 81. Dagan R: Management of acute hematogenous osteomyelitis and septic arthritis in the pediatric patient. Pediatr Infect Dis J1993;12:88. 82. Betz RR: Late sequelae of septic arthritis of the hip in infancy and childhood. J Pediatr Orthop 1990;10:365. 83. Perron AD, Miller MD, Brady WJ: Orthopedic pitfalls in the emergency department: Slipped capital femoral epiphysis. Am J Emerg Med2002;20:484. 84. Kelsey JL: The incidence of slipped capital femoral epiphysis in Connecticut. J Chronic Dis1997;23:567. 85. Canale ST, King RE: Fractures of the hip. In: Rockwood Jr CA, Wilkins KE, King RE, ed.Rockwood and Green's Fractures in Children, vol 3. 3rd ed. Philadelphia: JB Lippincott; 1991: 86. Ankarath S: Delay in the diagnosis of slipped capital femoral epiphysis. J R Soc Med2002;95:356. 87. Lang P, Genant HK, Jergesen HE: Imaging of the hip joint: Computed tomography versus magnetic resonance imaging. Clin Orthop1992;274:135. 88. McErlean MA: The child with a limp. In: Graff J, ed.Critical Decisions in Emergency Medicine, 18. Irving, Tex: ACEP; 2004: 1-10. 89. Poston HL: Traction fracture of the lesser trochanter of the femur. Br J Surg1921-1922;9:256.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyright © 2006 Elsevier Inc. All rights www.mdconsult.com reserved.
Bookmark URL: /das/book/view/60636217-2/1365/127.html/top
Page 349
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
Chapter 54 – Knee and Lower Leg Everett Lyn Daniel Pallin Robert E. Antosia
KNEE PERSPECTIVE More than 1 million patients are seen annually in North American emergency departments with complaints of acute knee injuries.[1] Injuries range from simple contusions to complete dislocations, which are true limb-threatening emergencies. The knee is the largest and most complicated joint in the body. Motion at the knee is a complex interaction of flexion, extension, rotation, gliding, and rolling. The knee joins the two longest mechanical levers in the body, the thigh and lower leg. The knee is subject to high forces during ambulation, sports, and blunt trauma and is a frequent site of acute or chronic injury. The knee joint also comprises an enormous synovial space and is frequently involved in infectious or autoimmune inflammatory conditions, ranging from septic arthritis to serum sickness.
PRINCIPLES OF DISEASE: ANATOMY AND PATHOPHYSIOLOGY The knee is a modified-hinge diarthrodial synovial joint that consists of the tibiofemoral and patellofemoral joints. The distal femur, proximal tibia, and patella compose the bony articulation. The head of the fibula, although not part of this articulation, is closely approximated laterally and provides a site for the attachment of muscles and ligaments. Joint stability is provided by the capsule, ligaments, and surrounding muscles; however, the stability mainly depends on the integrity of the ligamentous structures ( Figure 54-1 ).
Figure 54-1 Anterior and posterior views of the right knee.
The distal femur terminates in the medial and lateral condyles. The V-shaped femoral trochlea between them articulates with the patella. Small protuberances arise from each of the condyles and are called epicondyles. The medial and lateral epicondyles serve as important sites of origin for the medial collateral ligament (MCL) and lateral collateral ligament (LCL). The femoral condyles articulate with the superior surface of the tibia and the corresponding medial and lateral tibial condyles. Within the joint, medial and lateral menisci are interposed between the femoral and tibial condyles, providing a form of shock absorption. The cruciate ligaments are located in the intercondylar notch. Functionally the knee joint can be divided into three compartments: patellofemoral, medial tibiofemoral, and lateral tibiofemoral. These compartments, defined anatomically by the articulation of the bones, are contained within the same joint capsule. The patellofemoral compartment, located anteriorly, contains the quadriceps tendon, which envelops the patella, continues inferiorly as the patellar tendon, and terminates on the tibial tubercle. The fibers of the medial and lateral retinacula are found on either side of the patella, originating from the vastus medialis and vastus lateralis. The medial and lateral patella retinacula also are called extensor retinacula. Normally the patella glides in a rotational manner that increases the mechanical advantage of the quadriceps tendon. The quadriceps tendon is a continuation of the quadriceps femoris muscle, which consists of the rectus femoris, vastus medialis, vastus lateralis, and vastus intermedius, comprising the important extensor structures of the knee. Improper function or weakness may lead to patellar malalignment, which may manifest clinically by the development of chondromalacia patella and peripatellar pain.
Page 350
The medial tibiofemoral compartment is located on the medial aspect of the knee and consists of the medial femoral condyle, concave medial tibial condyle (plateau), medial meniscus, MCL, adductor tubercle, and pes anserinus. The pes anserinus (meaning “goose foot”) is a three-pronged tendinous structure that is the conjoined insertion of the sartorius, semitendinosus, and gracilis muscles. The lateral tibiofemoral compartment encompasses the lateral half of the knee joint and includes the lateral femoral condyle and epicondyle, lateral tibial condyle (plateau), LCL, lateral meniscus, and popliteus tendon. The fibular head can be palpated posterolaterally and inferiorly to the joint line but is not usually considered a structure of the lateral tibiofemoral compartment. There is no complete, independent fibrous capsule uniting the bone. Instead a thick ligamentous sheath constructed largely of tendons or expansions from them surrounds the knee joint. The capsule of the knee joint is reinforced at multiple sites: anteriorly, by the ligamentum patella; medially and laterally, by the medial and lateral patellar retinacula; and posterolaterally, by a combination of structures referred to as the posterolateral corner. The posterolateral corner includes the iliotibial band, biceps femoris, fibular collateral ligament, popliteus complex (tendon, tibial attachment, popliteofibular ligament, lateral meniscal attachments), arcuate complex, fabellofibular ligament, capsular ligament, and joint capsule. The popliteofibular ligament has been identified as an important contributor to posterolateral stability. The synovial capsule of the knee works in unison with the ligamentous structures in strengthening the knee. The capsule communicates with the suprapatellar bursa, which expands in conditions that cause knee effusion. Although the prepatellar bursa does not communicate with the joint space, prepatellar bursitis frequently is confused with a septic knee joint. The popliteal fossa is a rhomboid hollow in the posterior aspect of the knee. It is bounded by the biceps femoris laterally, the semimembranosus and semitendinosus muscles medially, and the two heads of the gastrocnemius muscle inferiorly. Found within the popliteal space are the popliteal artery, the popliteal vein, and the peroneal and tibial nerves. Pathologic conditions localized to this area include popliteal cysts and traumatic injuries to the neurovascular structures within the fossa. The popliteal artery is found deep within the popliteal fossa and represents the direct continuation of the femoral artery beyond the adductor hiatus. The popliteal artery descends across the posterior aspect of the knee joint and terminates at the level of the tibial tubercle, where it divides into the anterior and posterior tibial arteries. The popliteal artery is anchored firmly at the proximal and distal ends of the popliteal fossa, which explains the high incidence of arterial injury with knee dislocations. Blood supply to the knee joint comes from the popliteal artery via the geniculate arteries. Branches of the geniculate arteries interconnect with other vessels, forming a complex anastomosis around the knee. The circumflex fibular artery is a branch from the anterior tibial artery and is the main blood supply to the head of the fibula. Blood supply to the head of the tibia is derived in part from two branches of the anterior tibial artery: the anterior and posterior recurrent tibial arteries. The tibial nerve, along with one of its branches, the common peroneal nerve, is responsible for innervation of the knee. The tibial nerve joins the artery and vein in the popliteal fossa. It is not tethered proximally and seems to be injured less often than the popliteal artery. The common peroneal nerve wraps around the head of the fibula and continues inferiorly as the deep and superficial peroneal nerves. Common peroneal nerve injury may occur in association with injury to the fibula head or due to prolonged compression of the lateral aspect of the knee joint. This causes footdrop, in which dorsiflexion strength at the ankle is reduced. Knee and leg fractures are commonly treated with immobilization. A 19% risk of deep venous thrombosis has been seen with immobilization. Prophylactic treatment with low-molecular-weight heparin reduced this risk to 9%.[3]
CLINICAL FEATURES Presentation When a patient complains of a painful knee, the differential diagnosis must include the hip and lumbar nerve roots. This is especially true in children, in whom problems such as a septic hip or slipped capital femoral epiphysis commonly present as knee pain. A swollen knee may result from infection, hemarthrosis, or inflammatory arthritis, and arthrocentesis is commonly required for diagnosis. In the case of traumatic knee injury, mechanism of injury is more important than any other single piece of information in arriving at a correct diagnosis.[4] By noting the position of the body at the time of injury and the likely forces, predictable patterns of injury are found. High-energy trauma without knee swelling should raise the suspicion of disruption of the joint capsule with expulsion of joint fluid and hemorrhage into the thigh or lower leg. Lower energy injuries are more commonly associated with meniscal tears, patella dislocations,
Page 351
and less severe ligament injuries; in particular, activities with twisting and turning are associated with anterior cruciate tears and meniscal pathology. Immediate deformity, hemarthrosis, or instability suggests intra-articular fracture, major ligamentous injury, or vascular injury. In contrast, a torn meniscus may cause an acutely locked knee, but more commonly has delayed onset of swelling over 12 to 24 hours and intermittent locking associated with joint line pain. Locking of the knee is a symptom in which there is inability to extend the joint fully. It typically results from either a meniscal tear or a loose body catching in the joint and preventing full extension. A complaint of “giving way” may indicate instability or involuntary muscle inhibition secondary to pain. This is a nonspecific symptom and may be reported in association with arthritis or patellofemoral disorders when inhibition of quadriceps function occurs in association with episodic pain. Although pain remains a helpful indicator of injury, its absence should not be interpreted as proof that only minor injury is present. Partial ligamentous tears may be painful, whereas complete tears may not be because the completely disrupted ligament has no tension across the injured fibers.
Physical Examination Proper examination of the knee requires the patient to be supine on a stretcher with both legs exposed. The evaluation should begin with an assessment of the neurovascular integrity of the foot. The question of whether knee pain might be the result of hip or spine pathology should be raised early. Examination of the knee begins with visual inspection ( Box 54-1 ). Any obvious deformity, swelling, effusion, or ecchymosis should be noted. Localized swelling must be distinguished from the presence of a joint effusion, which may obliterate the normal contour of the knee. If a large effusion is present, the patella is elevated from the femur by the fluid; ballottement of the patella against the femur is possible by direct pressure on the patella. An effusion also may be shown by tapping the lateral retinaculum with a palpable fluid wave appreciated on the medial side. Loss of the medial peripatellar concavity may be the only sign of a small effusion. A small effusion may be shown by milking the suprapatellar pouch inferiorly to force fluid into the knee joint. BOX 54-1 Examination of the Knee
1.
2.
3.
Outli ne area s of tend erne ss. Note whet her any effus ion is pres ent. Che ck for rang e of moti on, valg us stres s at 0 and 30
Page 352
4.
5.
degr ees of flexio n, and varu s stres s at 0 and 30 degr ees of flexio n. Eval uate the patel lar and exte nsor mec hani sm of the knee (qua drice ps and patel la tend ons). Perf orm Lach man' s, anter ior draw er, post erior draw er, and pivot shift tests to chec k for anter
Page 353
6.
olate ral rotat ory insta bility and furth er delin eate poss ible injur y to the anter ior cruci ate liga ment . Perf orm meni scal exa mina tion with McM urray 's and Aple y's tests .
Precise localization of pain helps define the pathology. Palpation is most helpful in localizing the site of maximal tenderness ( Figure 54-2 ). In general, it is best to palpate areas of tenderness last because provocation of pain early in the examination may cause anxiety, and the patient may be unable to relax and cooperate fully. In the acute setting, the examination may be limited by the presence of muscle spasm, guarding, and effusion. The patella and the extensor mechanism should be palpated with attention to the superior pole. In the absence of trauma, tenderness localized here is consistent with quadriceps tendinitis. Warmth, erythema, and swelling over the anterior patella may result from prepatellar bursitis. Tenderness along the inferior pole of the patella is seen with peripatellar tendinitis. The insertion of the patellar tendon onto the tibial tubercle should be palpated. Pain at this location in an adolescent is the hallmark of Osgood-Schlatter disease. In an adolescent, pain along the femoral or tibial epiphysis after trauma may represent a nondisplaced fracture through the physis. The joint line should be palpated carefully. Pain along the joint line may indicate meniscal pathology. The posterior aspect of the knee should be examined for fullness, which may indicate a popliteal cyst or popliteal artery pseudoaneursym. Tenderness over the medial or lateral heads of the gastrocnemius may indicate tendinitis or muscle strain.
Page 354
Figure 54-2 Palpation of tenderness in the knee. 1, quadriceps tendinitis; 2, prepatella bursitis, patella pain; 3, retinacular pain after patella subluxation; 4, patella tendinitis; 5, fat pad tenderness; 6, Osgood-Schlatter disease (tibial tubercle pain); 7, m eniscus pain; 8, collateral ligam ent pain; 9, pes anserine tendinitis bursitis. ((Adapted from Cailliet R: Knee pain. In Soft Tissue Pain and Disab ility, 3rd ed. Philadelphia, FA Davis, 1976, p 411.)FA Davis)
The range of motion of the knee should be assessed. The knee can be viewed as a hinged joint, with range of motion from slight hyperextension to approximately 135 degrees of flexion. In addition to flexion and extension, complete knee function requires anterior and posterior motion and internal and external rotation. The anatomic arrangement of the knee normally allows the tibia to glide posteriorly and internally rotate about 15 to 30 degrees with knee flexion and move anteriorly and externally rotate with extension. In the extended position, tautness of the ligaments prevents rotary motion. At 90 degrees of flexion, rotation to 40 degrees is possible. Inward rotation is always greater than outward rotation. When range of motion is determined, stability or stress testing should be carried out. Generally the cruciate ligaments provide anteroposterior stability, and medial and lateral stability relies on the joint capsule and collateral ligaments. Range-of-motion evaluation of the knee should include active straight leg raising. Loss of active extension of the knee and inability to maintain the passively extended knee against gravity are the hallmarks of quadriceps and patellar tendon rupture, which otherwise may be clinically occult.
Stability Testing Stability testing seeks to identify disruption of the connective tissues supporting the knee joint. A progressive decrease in laxity occurs with age.[5] Comparison testing with the opposite knee is necessary because sideto-side differences are more important than absolute laxity. Stability to anterior stress means that the tibia cannot be moved anteriorly relative to the femur, and stability to posterior stress means the opposite. Stability to valgus stress means that the tibia cannot be bent laterally relative to the femur, and stability to varus stress means that the tibia cannot be bent medially. As noted earlier, specific diagnosis of ligamentous or meniscal injury is difficult in the acute setting, and the diagnosis ultimately is made later, during orthopedic follow-up. Nonetheless, familiarity with the standard diagnostic maneuvers is essential.
Anterior Drawer Test The anterior drawer test is a test for disruption of the anterior cruciate ligament (ACL). A positive test is defined as the ability of the tibia to move forward relative to the femur compared with the other knee. The test is performed with the patient in a supine position, the hip flexed at 45 degrees, and the knee flexed at 90 degrees. Foot and leg positions are stabilized by sitting on the foot. The examiner determines the amount of step-off between the femoral condyle and the tibial plateau by placing the thumbs over the joint line while exerting a smooth, gentle pull anteriorly on the tibia. The amount of forward displacement is compared with the normal side. The anterior drawer test is not reliable and is of little value in diagnosing acute ACL injuries. It is of more value in a chronic ACL-deficient knee.[6] False-negative findings may occur from an effusion preventing knee flexion to 90 degrees, hamstring muscle spasm caused by pain, or insufficient force applied during performance of the test. A false-positive test can be caused by posterior cruciate ligament (PCL) insufficiency, which allows the tibia to slip back on the femur, showing an abnormal amount of displacement when pulled forward.[7]
Lachman's Test Since the 1970s, Lachman's test has gained popularity in diagnosing ACL injury; before this, the anterior drawer test was used most often.[8] Lachman's test is currently the best clinical test for determining the integrity of the ACL and one of the only reliably performed tests for a patient with an acute hemarthrosis.[9] Accuracy in diagnosing ACL injury increases from 70% to 99% using Lachman's test rather than the anterior drawer test.[10] The test is especially useful for acute injuries, in which muscle spasm and the presence of an effusion often limit knee flexion. It also minimizes the blocking effect of the posterior horns of the menisci. Lachman's test is done with the knee flexed 20 to 30 degrees with one hand grasping the thigh and stabilizing it. The tibia is pulled forward with an anteriorly directed force, and the examiner notes tibial excursion. The examiner records “firmness” or a “soft endpoint.” The endpoint can be graded as 1+ (0 to 5mm more displacement than the normal side), 2+ (5 to 10mm), or 3+ (>10mm). The tibiofemoral joint should be in a neutral position before manipulation, and the PCL must be intact for the test to be valid. In an acute injury, any difference in translation or the feeling of a soft or indistinct endpoint may indicate a ligament tear. A PCL injury results in a false-positive test as the knee is pulled forward. Potential causes of false-negative tests include hamstring spasm, meniscal tears, and third-degree MCL tears with posterior
Page 355
medial extension. Specific limitations of Lachman's test include difficulty quantitating the amount of anterior translation and inability to limit motion of the femur. In addition, the detection of partial tears of the ACL is problematic and less reliable.[8] Lachman's test also may be difficult to perform if the examiner's hands are small relative to the patient's thigh.
Posterior Drawer Test The posterior drawer test remains the “gold standard” for evaluating PCL injury. The posterior drawer test can be accomplished with the patient's knee flexed at 90 degrees and the foot stabilized by the examiner's thigh. A smooth backward force is applied to the tibia. Posterior displacement of the tibia more than 5 mm, or a “soft” endpoint, indicates injury to the PCL. A normal knee should exhibit no significant posterior excursion. The posterior drawer test may be positive in only 85% of patients with PCL insufficiency documented operatively. The phenomenon of an absent or inconclusive posterior drawer test is believed to occur when the mechanism of injury does not stress, strain, or tear the posterolateral corner ligaments (arcuate complex).[11]
Posterior Sag Sign The posterior sag sign test is a second method of determining PCL integrity. The test can be done as follows. The patient is placed in a supine position, and a pillow is placed under the distal thigh for support while the heel rests on the stretcher. The knee is flexed to either 45 or 90 degrees, depending on which position provides the greatest muscle relaxation. If the tibia sags backward, the test is positive, indicating PCL insufficiency. If the posterior sag sign is not appreciated before the different drawer tests are performed, a false-positive anterior drawer test is misinterpreted as an ACL injury.[7] Posterior sag also may be shown by passive elevation of the leg in a fully extended position, with the examiner applying the elevating force at the ankle. As the leg is elevated, the tibia may fall back on the femur if the PCL is ruptured.
McMurray's Test McMurray's test is used to identify meniscal tears. The patient is placed in a supine position with the knee hyperflexed. The examiner grasps the lower leg, flexing and extending the knee while simultaneously internally and externally rotating the tibia on the femur with a smooth, firm, controlled movement. A positive test occurs when, with the other hand, a “clicking” sensation is felt along the joint line or the patient experiences pain during internal and external rotation. By twisting the leg into internal rotation, the posterior segment of the lateral meniscus is tested. External rotation tests the posterior segment of the medial meniscus. In the acute setting, limitation of range of motion may not allow sufficient hyperflexion to perform McMurray's test, and the test may be falsely negative.
Apley's Test Apley's test also aids in diagnosing meniscal tears. With the patient prone, the knee is flexed 90 degrees, and the leg is internally and externally rotated with pressure applied to the heel. Downward pressure eliciting pain suggests meniscal pathology. The pain should be relieved with distraction of the knee and rotation of the leg back to a neutral position.
Pivot Shift The pivot shift test, also called subluxation provocation or the “jerk” test, is performed to detect anterolateral rotatory instability associated with an injury to the ACL or lateral capsular structure. This test must be done carefully, if at all, in the acutely injured knee because the test maneuvers can exacerbate the initial injury. The pivot shift test is performed with the patient supine. The knee is examined in full extension. The tibia is internally rotated with one hand grasping the foot and the other hand applying a mild valgus stress at the level of the knee joint. Then, with flexion of the knee to approximately 20 to 30 degrees, a jerk is suddenly experienced at the anterolateral corner of the proximal tibia. In a positive test, the tibia subluxes when the knee is extended and relocates when it is flexed to 20 to 30 degrees. Grading of the relocation event is as follows: absent (0), rolling (1+), moderate (2+), or momentary locking (3+). Because of pain or spasm, the pivot shift test is unreliable without anesthesia.[6]
Collateral Ligament Stress Test The collateral ligament stress test is used to test the integrity of the MCL and LCL. The test is performed as follows. With the patient lying supine, the examiner applies varus and valgus stress with the knee at 0 and 30 degrees of flexion. Joint line opening is the amount of movement produced between the tibia and the femur; this can be palpated and estimated in millimeters. The normal knee should be subjected to the same amount of valgus and varus stress and joint line opening compared with the injured knee. Laxity in full extension implies complete collateral ligament tear, with injury to the secondary restraints, such as the ACL,
Page 356
PCL, and posteromedial or posterolateral corners. When the knee is flexed to 30 degrees, the stability provided by the cruciate ligaments to valgus and varus stress is removed. If the knee is stable to valgus stress with the knee in full extension but lax at 30 degrees of flexion, injury is limited to the superficial and deep MCLs. Varus stress at 0 degrees of flexion producing no instability but laxity present at 30 degrees indicates that at least part of the LCL and lateral stability complex has been injured. Laxity may be graded as follows: grade I, some laxity; grade II, marked laxity; and grade III, total laxity.
Instrument Testing More recent developments have seen the advent of instrument testing to evaluate ACL injury. The arthrometer gives numeric quantitative comparison of ACL laxity of the knee. Studies using commercially available arthrometers indicate that a side-to-side difference exceeding 3 mm anterior displacement at 20 lb is predictive of ACL with 94% accuracy.[12] Reports also indicate that quantitative laxity determination with such instruments can yield prognostic information and may aid clinicians in determining how aggressively to treat ACL injuries. However practical and useful such instruments may be, they have not gained widespread usage or acceptance at present.
DIAGNOSTIC STRATEGIES Radiographic Evaluation Plain Radiographs The traditional standard of care was to obtain anteroposterior and lateral radiographs of the knee in all cases of acute knee trauma. More recent work has led to validation of clinical decision rules that help decrease unnecessary radiography.[] The Ottawa Knee Rule states that radiography is necessary only if any one of five conditions is present: (1) age older than 55 years, (2) inability to transfer weight from one foot to the next four times at the time of injury and in the emergency department, (3) inability to flex the knee to 90 degrees, (4) patellar tenderness with no other bony tenderness, or (5) tenderness of the fibular head. Initial tests found that this rule detected 100% of fractures, while allowing significantly fewer radiographs to be done.[] Similarly the Pittsburgh Knee Rule was found to be 100% sensitive.[17] The Pittsburgh Knee Rule states that radiography is necessary only if the patient fell or sustained blunt trauma to the knee, and either of two conditions is present: (1) age younger than 12 or older than 50 or (2) inability to walk four full weight-bearing steps in the emergency department. One study compared these two decision rules and found that both had good sensitivity, but that the Pittsburgh rule was more specific, allowing fewer radiographs to be done without sacrificing sensitivity; in this study, the sensitivity of the Ottawa rule was 97% (95% confidence interval, 90% to 99%), and the sensitivity of the Pittsburgh rule was 99% (95% confidence interval, 94% to 100%).[13] Until further work determines the optimal approach, either rule may be used, but patients should be told that there is about a 1% chance of a missed fracture, and they should seek re-evaluation in the event of persistent or progressive symptoms. One study validated the Ottawa Knee Rule in children older than age 5, finding a sensitivity of 100%. The Ottawa Knee Rule permitted a 31% reduction in the number of radiographic evaluations.[18] In another pediatric study, of 13 fractures, 1 was missed, implying a sensitivity of only 92%, so application of the rule in children still requires clinical judgment.[19] In another approach, Verma and colleagues[20] recognized that fears of malpractice might limit implementation of decision rules and instead asked whether a single lateral x-ray could replace the traditional three-view “knee series” (anteroposterior, lateral, and tunnel views). These investigators found that a single lateral view could detect 100% of fractures identifiable on the full series.[20] Some clinicians may prefer this more conservative approach until the decision rules are validated further. Joint space narrowing, as seen in osteoarthritis, is easily discernible on erect standard views. Lateral views may reveal an abnormally low-riding or high-riding patella. Tangential, “sunrise,” or “skyline” views are especially good for delineating the patellofemoral joint.[21] Tangential views are useful to assess patella tracking or subluxation. Oblique x-ray studies are particularly useful when tibial plateau fractures are suspected but not seen on routine views.[22] “Tunnel” views, which image the intercondylar notch, are used to detect tibial spine fractures and loose bodies within the notch. Although most ligamentous injuries cannot be diagnosed by plain films, avulsion of the attachment site can be seen occasionally and provides indirect evidence of ligament disruption. Stress radiographs may aid in the diagnosis of collateral ligament disruption but generally are not used in the initial evaluation.
Computed Tomography
Page 357
Computed tomography (CT) is most useful in detecting and classifying tibial plateau fractures and usually is done when the diagnosis is unclear, or operative intervention is considered.
Ultrasound Ultrasound is useful in diagnosing several pathologic conditions of the knee. It has gained wide acceptance in the diagnosis of clinically suspected popliteal cyst, which appears as a nonechogenic mass with smooth walls lying medially within the popliteal fossa.[23] Small cysts can lead to false-negative ultrasound results. The popliteal artery is the most common site for peripheral aneurysms, yet the clinical diagnosis can be difficult.[21] Typically the aneurysm occurs just distal to the adductor hiatus in the proximal segment and midsegment of the artery and is bilateral in 50% of cases.[23] Realtime ultrasound is an excellent modality for diagnosing popliteal artery aneurysm and can differentiate aneurysm from cyst.[21]
Contrast Arteriography and Color-Flow Doppler Contrast arteriography and color-flow Doppler ultrasonography are used to evaluate the arteries of the knee and leg. Traditionally, arteriography was deemed mandatory in all cases of tibiofemoral knee dislocation and in all cases of penetrating trauma in close proximity to major arteries. More recently, serial examination and Doppler scanning have been studied and found to be acceptable alternatives to arteriography in patients with normal distal neurovascular examinations and low-risk mechanisms.[24]
Radionuclide Bone Scan A radionuclide bone scan can be used to detect osteomyelitis or occult bony injuries, such as stress fractures, osteochondritis dissecans, and avascular necrosis.
Magnetic Resonance Imaging Double-contrast arthrograms are of primarily historical interest because they have been largely replaced by magnetic resonance imaging (MRI).[21] Arthrography may be performed after prosthetic replacement of the knee to detect loosening. It also may be used if there is a contraindication to MRI, or if MRI is not available. MRI can be helpful to identify associated injuries to the menisci and articular cartilage when the clinical examination is limited because of pain and swelling. The diagnostic accuracy of MRI in detecting meniscal and capsuloligamentous injuries of the knee is well documented.[25] Although the sensitivity of MRI in identifying ACL injury may be high (90% to 98%), its specificity, particularly in differentiating partial from complete tears, is low (<50% in some series).[26] MRI is extremely sensitive for determining PCL injury; however, the diagnosis usually can be established by history and physical examination. Images with T1 and T2 weighting are required for optimal assessment. Sagittal images are best for evaluating menisci, cruciate ligaments, and articular surfaces; coronal images enable optimal assessment of the collateral ligaments. MRI has proved superior to other imaging modalities in the evaluation of osteonecrosis, osteochondritis dissecans, occult fractures, and bone contusion.[21] Advantages of MRI in evaluating soft tissue injury are that it is noninvasive and painless, and it does not require the use of ionizing radiation. Although MRI is a useful diagnostic tool, because of its high cost and limited availability, it should be used selectively, depending on the specific clinical situation and information desired.
Arthroscopy The most commonly performed orthopedic surgical procedure in the United States is arthroscopy of the knee.[27] It is useful in diagnosis and treatment of knee injuries, including injuries of the meniscus, cruciate ligaments, articular cartilage, capsule, and synovium. The superior diagnostic accuracy of arthroscopy compared with the clinical knee examination has been well documented. In particular, arthroscopy has increased the accuracy of diagnosis of ACL injuries and small capsular tears. It is especially helpful for children, in whom diagnoses can be difficult because of developing skeletal changes. Difficulties in visualization arise when the capsular structures are tight and when meniscal tears are situated posteriorly. Indications for arthroscopy are situation specific and include drainage of tense hemarthrosis, removal of osteochondral fragments (loose bodies), repair of meniscal tears, and reconstruction of ACLs or PCLs. Rapid rehabilitation and cost savings are two significant advantages over open-knee surgery.
Arthrocentesis Aspiration of fluid from the knee joint can be diagnostic and therapeutic, although there is no evidence-based support for therapeutic value.[28] Arthrocentesis should be performed if the injured knee is greatly distended with a tight effusion, and when the cause of the joint effusion is unknown. Aspiration of the joint and subsequent analysis can distinguish among hemarthrosis, sympathetic effusion, and septic arthritis. Joint
Page 358
aspiration is diagnostic of fracture if fat globules are present. Intra-articular injection of morphine and bupivacaine has been used for analgesia after traumatic knee injuries and elective knee arthroscopy. Several studies have shown that although both drugs reduce the need for systemic analgesia, morphine is more effective and can provide relief for 24 hours.[29] The typical dose is 1 to 5mg (1mg/mL diluted in normal saline solution to a total volume of 30 mL). Evidence suggests that analgesia is mediated by local action within the joint.
MECHANISMS OF INJURY AND MANAGEMENT Distal Femur Fractures Anatomy and Pathophysiology Distal femur fractures compose approximately 4% of all femoral fractures.[30] The mechanism of injury is often related to motor vehicle accidents or significant falls in which the force of impact is severe. An isolated fracture of the femoral condyle may occur, or the fracture may extend in a T or Y pattern to include the intercondylar or supracondylar region of the femur. Condylar fractures are intra-articular and may result in knee joint incongruity.
Clinical Features Patients with condylar or intercondylar fractures have pain and swelling in the distal femur and suprapatella region and are often unable to bear weight. Examination may reveal shortening, rotation, and angulation of the extremity and tenderness to palpation along the medial or lateral joint line. Acute hemarthrosis is common and may be secondary to intra-articular extension of the fracture or associated ligamentous injury. Careful assessment of the circulation and motor function of the limb should be documented. Any soft tissue defect in the region of the fracture is considered to be an open fracture until proved otherwise.
Diagnostic Strategies The diagnosis of a distal femoral fracture is made from radiographs. Routine anteroposterior and lateral radiographs should be obtained and usually show the fracture pattern and any significant displacement of fragments. In high-energy injuries, radiographs of the ipsilateral hip and tibia are required to exclude associated fractures. Occasionally, CT or MRI may be required to diagnose a nondisplaced fracture. If signs of vascular impairment are present, an arteriogram should be obtained promptly when surgical exploration is not being considered.
Management After the initial examination, the leg should be splinted to prevent excessive motion of the fracture site. Early orthopedic consultation is prudent. In a stable patient with an uncomplicated fracture, reduction may be done with skeletal traction followed by immobilization with a hinged fracture brace. If any degree of joint incongruity is detected on radiographs, the fracture should be treated with open reduction and internal fixation. Fractures of the distal femur are often difficult to fix securely because they must withstand forces from weight bearing and knee motion. Operative techniques include use of multiple fixation screws or a sliding compression screw with side plate, depending on the clinical circumstances and the preference of the orthopedic surgeon. Distal femoral fractures may be associated with several significant complications, including thrombophlebitis; fat embolus syndrome; delayed union or malunion if reduction is incomplete or not maintained; intra-articular or quadriceps adhesions if the fracture is intra-articular; angulation deformities; and osteoarthritis, particularly affecting the patellofemoral articulation.
Proximal Intra-articular Tibial Fractures Proximal intra-articular tibial fractures include condylar or plateau injuries, epiphyseal fractures, and fractures of the tibial spine. Extra-articular fractures are discussed in the section on the lower leg.
Tibial Plateau Fractures Anatomy and Pathophysiology The proximal end of the tibia is expanded into the medial and lateral condyles, the former having the greater surface of the two. Together they make up approximately three quarters of the proximal tibial surface, and their integrity is important for normal knee alignment, stability, and motion. The plateau normally slopes 10 degrees from anterior to posterior; on a straight anteroposterior view, the anterior and posterior portions of the plateau may not appear to be at the same level. In addition, the lateral plateau is slightly convex upward, whereas the medial is slightly concave upward.[22] Tibial plateau fractures represent 1% of all fractures and 8% of fractures in the elderly.[30] Tibial plateau
Page 359
fractures are intra-articular and result in loss of joint congruity. The forces that normally act on the tibial condyles include axial compression and rotation. The most common mechanism of injury is a strong valgus force with axial loading.[30] Severe high-energy tibial plateau fractures occur primarily in younger age groups and are often the result of motor vehicle accidents or falls from heights.[30] These fractures occur in concert with many other injuries and may be open. Fatigue stress fractures of the tibial plateau occur mostly in elderly persons. These low-energy fractures are the result of compression forces in osteoporotic bones. Tibial plateau fractures encompass many differing degrees of articular depression and displacement. Because the initial injury is usually a valgus stress with an abduction force on the leg, 55% to 70% of condylar fractures involve the lateral plateau. Medial plateau fractures typically result from adduction forces on the distal leg and account for 10% to 23% of these fractures; both plateaus are involved 11% to 31% of the time.[30] If the knee is extended at the time of injury, the fracture tends to be anterior. Posterior condylar fractures usually occur when the knee is flexed at the time of impact. The Segond fracture represents a bony avulsion of the lateral tibial plateau. The avulsion occurs at the site of attachment of the lateral capsular ligament. It appears as an oval-shaped fragment adjacent to the lateral tibial plateau and must be differentiated from an avulsion from the adjacent fibular styloid. The Segond fracture is an important marker of ACL disruption and anterolateral rotary instability.[31] Most Segond fractures are caused by sports injuries, and the mechanism is almost always knee flexion with excessive internal rotation and varus stress. Segond fractures can be detected on radiographs (lateral capsule sign) and, when seen, must be regarded as a strong indication that ligament rupture has occurred, and surgical repair may be needed ( Figure 54-3 ).[31]
Figure 54-3 Anteroposterior view of the left knee shows lateral curvilinear avulsion fracture (arrow) and joint effusion. ((From Kerr HD: Segond fracture, hem arthrosis, and anterior cruciate ligam ent disruption. J Em erg Med 8:29, 1990.))
Clinical Features Clinical signs of knee fractures are the presence of an effusion, inability to bear weight, severe joint line tenderness, ecchymosis, and localized soft tissue swelling and pain. Acute hemarthrosis, presenting with decreased range of motion, is the most sensitive predictor of a knee fracture.[] These findings are not specific for fracture, however, because they are often seen with ligament tears. Tenderness is present over the fracture, but also may be found near torn collateral ligaments. A valgus or varus limb deformity may be present and usually indicates a depressed fracture or concomitant ipsilateral leg fracture. The most important aspect of the initial examination is the neurovascular status. Tibial plateau fractures produce a high percentage of vascular complications. The popliteal artery is immobile in this region and branches into the anterior and posterior tibial artery at the upper edge of the interosseous membrane. The popliteal artery may be injured by fragments from bicondylar or comminuted fractures involving the subcondylar area. Vascular impairment may result in distal circulatory compromise. Displaced fractures of the lateral condyle may produce peroneal nerve paralysis in addition to injury to the anterior tibial artery. Stretch of the peroneal nerve is the usual cause of injury. Soft tissue injuries also may involve the capsuloligamentous structures of the knee. Ligamentous injuries accompany tibial plateau fractures in 20% to 25% of cases, most often involving the ACL and MCL.[] Although ligament injuries can occur with any type of tibial plateau fracture, they occur more commonly with local compression and split compression fractures ( Figure 54-4 ).[35]
Page 360
Figure 54-4 Hohl's revised classification of tibial plateau fractures: m inim ally displaced (22%), local com pression (28%), split com pression (18%), total com pression (13%), split (3%), rim avulsion or com pression (5%), and bicondylar (11%). ((Modified from Watson JT, Wiss AA: Fractures of the proximal tib ia and fib ula. In Rockwood CA Jr, Green DP [eds]: Fractures, vol 3, 5th ed. Philadelphia, JB Lippincott, 2001.)JB Lippincott)
Treatment of ligament injuries associated with tibial plateau fractures is controversial. There is no general consensus that the repair of associated ligament injuries at the time of fracture fixation is necessary or improves late instability after these fractures. Cruciate ligament injuries associated with tibial plateau fractures have an increased incidence of late traumatic arthritis and a poor prognosis.[35] Regardless of the type of treatment, operative or nonoperative, tibial plateau fractures with significant residual laxity fare poorly compared with stable fractures.[35] Most authors agree that four factors determine the prognosis of tibial plateau fractures: (1) degree of articular depression, (2) extent and separation of the condylar fracture lines, (3) diaphyseal-metaphyseal comminution and dissociation, and (4) integrity of the soft tissue envelope (i.e., open versus closed). Fractures of the tibial plateau generally have a good prognosis, with good to excellent results having been found in 90% of patients more than 20 years after injury; however, high-energy tibial plateau fractures generally have a more guarded prognosis.[36] In high-energy fractures, a large degree of articular depression, multiple displaced condylar fracture lines, and diaphyseal-metaphyseal extension and comminution in association with open injuries or an extensive internal degloving injury may occur and are poor prognostic signs.[37]
Diagnostic Strategies A plateau fracture is usually evident on routine anteroposterior and lateral radiographs. At times, however, the fracture itself may be difficult to identify on routine radiographs. In such cases, the presence of a fat-fluid level on a “cross-table” lateral radiograph is highly suggestive of an occult fracture; it is believed that the observed fat originates from the bone marrow. Because of the normal contour of the tibial plateau, oblique films usually are required to see a subtle fracture line and for more complete assessment of obvious fractures. All knee radiographs should be examined closely for bony avulsion fragments from the fibular head, femoral condyles, and intercondylar eminence because these may indicate ligamentous injury. Widened joint spaces associated with a fracture of the opposite condyle also may indicate concomitant ligamentous injury. Tomograms, CT, or MRI may be required in certain clinical situations, particularly nondisplaced or severely comminuted fractures. These studies are more sensitive than plain radiographs, help localize occult lesions, and help quantify the amount of depression in displaced fractures and the extent of articular surface involvement in comminuted fractures.[38] Bone scans also may help detect occult compression fractures. Several classification systems have been proposed. Most classification systems depend on the mechanism of injury (i.e., the location and force with which the femoral condyle is driven into the plateau). The revised Hohl classification is in common, although not universal, use.[30] As shown in Figure 54-4 , this system divides the plateau fractures into two categories: minimally displaced (<4 mm depression or displacement) and displaced. Displaced fractures are subdivided into six distinct types: local compression, split compression, total depression, splint, rim, and bicondylar.
Management As a rule, accurate reduction and prolonged non–weight bearing are the guidelines to be followed in tibial condylar fractures. The four most common treatment modalities are compression dressing, closed reduction and casting, skeletal traction, and open reduction with internal fixation. Regardless of which treatment is selected, the therapeutic goals include precise reconstruction of the articular surfaces, stable fragment fixation, and early knee motion to prevent stiffness. Weight bearing is generally delayed until healing is complete, usually 6 to 8 weeks. Consensus on the treatment of tibial plateau fractures is not completely uniform. Conservative treatment is acceptable in stable nondisplaced and stable bicondylar fractures. If displacement is minimal, and there is no significant disruption of the articular surface, initial management with a long leg cast or immobilizer is acceptable. In general, with more severely depressed fractures, operative treatment has better results than nonoperative therapy; however, no universal agreement exists on the acceptable amount of articular depression. Ranges from 4 to 10 mm have been described as tolerable. A long-term study with more than
Page 361
20 years' follow-up indicates a lack of correlation between residual osseous depression of the joint surface and the development of arthrosis.[37] If the joint deformity or depression is significant enough to produce joint instability, it is predictive of a poor result.[30] All authors agree that a depressed intraarticular surface will not reconstitute itself if treated by traction alone. Significantly depressed plateau surfaces require surgical elevation and support with bone graft. Early complications of tibial plateau fractures include wound infection, loss of reduction, and development of compartment syndrome. Compartment syndromes most commonly occur with high-energy fractures, typically within the first 24 to 48 hours after injury. Deep vein thrombosis also may occur. The most common late complication is the development of osteoarthritis in the affected compartment.
Fractures of the Intercondylar Eminence (Tibial Spine) Anatomy and Pathophysiology The intercondylar eminence, or tibial spine, is the central portion of the proximal tibial surface. The spine has two prominences: the medial and lateral tubercles. The medial tubercle is larger and located more anteriorly than the lateral tubercle. The ACL and the anterior horns of the medial and the lateral menisci attach in the anterior intercondylar fossa. The PCL and the posterior horns of the menisci attach in the posterior intercondylar fossa. Fractures of the intercondylar eminence (tibial spine) are commonly seen in children and adolescents, but a study suggests that these fractures occur more commonly in adults than previously thought.[38] Of cases previously reported in the literature, 40% of tibial spine fractures occurred in adults, and 60% occurred in children.[39] The injury is more common in children than adults because the ligaments are stronger than the adjacent physeal plates in the immature skeleton. A fracture of the anterior tibial spine in children is the equivalent of an ACL rupture in adults. Most tibial spine and intercondylar eminence fractures occur as the result of violent knee twisting, hyperflexion, hyperextension, or valgus-varus forces generated during motor vehicle accidents or athletic activities. The tibial spines are fractured by twisting knee movements, whereas hyperextension or hyperflexion forces may cause avulsion of the intercondylar eminence or of the cruciate ligaments from their tibial attachments.[40]
Clinical Features After tibial spine or intercondylar eminence fracture, the patient complains of pain and swelling of the knee and may be unable to bear weight on the affected extremity. Examination confirms acute hemarthrosis and may reveal a block to full knee extension. Tense effusion may limit range of motion, hinder physical examination, and mask ligament disruption. Definite ACL laxity is associated with this injury, and patients may exhibit an anterior drawer sign, positive Lachman's test, or other signs of ligamentous laxity. In the presence of open physes, tibial spine fractures are usually isolated injuries. Adults are more likely to have an associated tear of the MCL or associated intraarticular fracture and have a worse prognosis.[38]
Diagnostic Strategies Radiographic evaluation should include standard anteroposterior and lateral views, but a tunnel view provides a clearer look at the intercondylar area and may be necessary to confirm the diagnosis.[22] Joint margins should be examined closely for evidence of collateral or capsular bony avulsions. Tomograms or CT scans sometimes are required to show the location and displacement of the fracture. The fabella is an inconsistent sesamoid bone located in the lateral head of the gastrocnemius muscle. It should not be mistaken for an intra-articular loose body or fracture fragment. The classification of tibial spine fractures is based on the degree of displacement ( Figure 54-5 ). Type I involves incomplete avulsion of the tibial spine without displacement. In type II, there is an incomplete avulsion with minimal displacement of the anterior third of the fracture fragment, but the posterior portion remains adherent. Type III is characterized by complete separation of the fragment from its fracture bed and has a higher associated rate of collateral ligament injuries and peripheral meniscal tears.[39] Type III may be subdivided into type IIIA, fractures with complete displacement, and type IIIB, fractures with displacement and rotation (see Figure 54-5 ).
Page 362
Figure 54-5 Tibial em inence fracture classification. Type I, fracture elevated anteriorly only slightly; type II, anterior fracture fragm ent elevated with only m inim al posterior attachm ent; type IIIA, fracture fragment com pletely separated from tibia; type IIIB, fracture fragm ent com pletely separated and rotated. ((Modified from Meyers M, McKeever F: Fractures of the intercondylar em inence of the tib ia. J Bone Joint Surg 41:209, 1959.))
Arthroscopy is useful for diagnosis and treatment of tibial spine fractures. Arthroscopy allows drainage of tense hemarthrosis and enables precise diagnosis and classification, especially for children, in whom the diagnosis can be difficult because of developing skeletal changes.
Management Conservative treatment is effective for all type I injuries. Nondisplaced or incomplete tibial spine fractures generally heal well when treated with cast immobilization in full extension for approximately 6 weeks. Type I and II fractures may require arthroscopy for lavage and accurate classification. If satisfactory closed reduction cannot be obtained or there is associated ligamentous injury, open or arthroscopic reduction and internal fixation should be performed. To restore normal function of the ACL, displaced or rotated fragments must be reduced. Type III fractures usually require arthroscopic or open reduction; screws and tension band wiring techniques have yielded excellent results.[30] Most uncomplicated fractures of the tibial spine have good results when the fracture heals and restores function to the avulsed ACL. A poor outcome, with residual pain and instability, may be associated with additional intra-articular fractures and damage to the MCL.[40]
Epiphyseal Fractures Anatomy and Pathophysiology The physes, which occur at the end of the long bones, are primarily responsible for longitudinal growth through the process of endochondral ossification. The proximal tibia and distal femoral epiphyses are examples of pressure epiphyses and are the largest two in the body. From birth to skeletal maturity, the distal femoral growth plate contributes 70% of the growth of the femur and 37% of the growth of the lower extremity.[41] Likewise, the upper tibial epiphysis accounts for most of the long growth of the tibia. Biomechanical data and clinical studies in children and adolescents have confirmed that the ligaments and articular capsule are firmer than the bone and epiphyseal plate.[42] As a result, trauma to this region of the maturing skeleton usually injures the cartilaginous epiphyseal plate. In this way, the physis protects the joint surface from the grossly comminuted fractures seen in adults. Despite data showing that the physis is the weakest link in the immature skeletal unit, only 15% to 20% of all fractures in children occur through the growth plate.[43] The physes of the upper extremities are reported to be involved more often than the physes of the lower extremity, in a ratio of 3:1.[44] Epiphyseal fractures about the knee are even less common, with distal femur epiphyseal separations accounting for only 9% and proximal tibial epiphyseal fractures only 4% of lower extremity epiphyseal fractures.[45] The proximal tibial physis is far more resistant than other physes as a result of the unique anatomic features of this site.[41] The proximal tibial physis has no significant attachments to the collateral ligaments of the knee. The LCL inserts into the head of the fibula and has no tibial attachment, and the MCL has only a minor attachment to the epiphysis. The major portion of this ligament is attached to the tibial shaft well below the epiphysis. Varus or valgus stress is more likely to injure the distal femoral physis or the tibial metaphysis. Fracture-separation of the distal femoral growth plate and proximal tibial epiphysis is most often caused by an indirect mechanism, commonly related to athletic injuries.[41] The Salter and Harris classification of epiphyseal injuries is described in Chapter 46 .
Clinical Features Epiphyseal injuries should be suspected in a child or adolescent who has juxta-articular (growth plate) tenderness, limps, or refuses to or cannot bear weight. The degree of pain varies, but it is often severe. Depending on the mechanism of injury, the overlying soft tissue may be abraded or lacerated. Swelling is usual in the overlying soft tissue, and an effusion may be present. If the separation is displaced, there may be an angular deformity. Epiphyseal growth plate fractures in the lower extremity have a high incidence of associated injury. Physeal
Page 363
fractures in the region of the knee may be associated with ligament injuries, especially to the ACL and MCL in half of patients. The most serious injury associated with a proximal tibial physis fracture is neurovascular trauma. In particular, popliteal artery injuries have been associated with these fractures, especially when there is posterolateral or posteromedial displacement. Peroneal nerve injury also has been reported and may range from neurapraxia to complete disruption.[41]
Diagnostic Strategies Plain radiography remains the primary means for evaluating epiphyseal injuries. Diagnosis is based on epiphyseal displacement, widening of the physis, and obliteration or haziness of the normal sharply defined, fine, sclerotic opposing margins of the metaphysis and epiphysis. The latter may result from angulation at one or both sites. Oblique views may be required to show nondisplaced fractures of the epiphysis. CT or MRI can evaluate more fully or classify injuries that already are established on the basis of plain radiography.
Management The most common complication of fractures through the proximal tibial physis is growth disturbance.[42] When growth arrest occurs (approximately 1% of cases), it is usually partial and results from a bridge of bone forming from the metaphysis to the epiphysis, crossing the growth plate. Although shortening or deformity is less well tolerated in the lower extremity because of weight bearing, many of the growth disturbances do not prove clinically significant because of the ability of the immature skeleton to remodel; only 2% or less are reported to be sufficient to interfere with function.[43] With regard to treatment, important differences exist between fractures in children and fractures in adults. In general, fractures in children heal rapidly. The younger the child, the more rapidly the fracture heals. In newborn infants, callus forms within 1 week after a birth injury. During the first year, callus is established within 2 weeks; callus takes slightly longer to form in toddlers. Fracture modeling also is more extensive in younger children and when the fracture is closer to the end of the bone. Modeling is less perfect in fractures of the mid-diaphysis in older children. Reduction of fractures near the proximal or distal end of the bone need not be perfect. If a child has juxta-articular tenderness with a negative radiograph, a growth plate injury (Salter-Harris type I) should be assumed. If there is difficulty in deciding whether a line on the radiograph is an epiphyseal line or fracture, a comparison view should be obtained. Because epiphyseal growth centers ossify at different times, this technique of comparing the uninvolved limb is often of great assistance in confirming a suspected physeal injury. In such cases when a physeal injury is suspected, the extremity should be immobilized for approximately 2 weeks and re-evaluated with radiographic study, looking for periosteal new bone or physeal thickening. Generally, emergency management of most epiphyseal fractures of the distal femur or proximal tibia includes ice, elevation, immobilization with a long leg posterior splint, and early orthopedic consultation. Anatomic reduction is desirable for displaced fractures of the distal femur and proximal tibial epiphysis. Open reduction usually is required only for patients in whom closed reduction fails. Late complications include angular deformity, leg-length discrepancy, stiffness, quadriceps atrophy, and persistent instability of the knee. Delayed union or nonunion is almost never a problem except in a patient with an underlying neuropathy.[41] Because growth inhibition may follow even nondisplaced physeal fractures, long-term orthopedic follow-up is advisable.
Bone Bruise Bone bruise is a radiographic diagnosis, involving areas of cancellous bone with high signal intensity on MRI fat-suppression sequences. Bone bruise may be present in about half of acutely injured knees.[46] A high proportion of patients with bone bruise have significant soft tissue injury. Nearly all bone bruises resolve after 1 year.[46]
Osteochondritis Dissecans Osteochondritis dissecans is a rare orthopedic disorder of unknown etiology. The disorder is found mainly in adolescents and results in a segment of articular cartilage and subchondral bone becoming partially or totally separated from the underlying bone. A male predominance (2:1) is reported.[47] It is commonly unilateral, involving the non–weight-bearing lateral aspect of the medial femoral condyle, and it is thought to be related to acute or chronic trauma.[2] Occasionally the lateral femoral condyle or inferior patella pole is involved. Patients often have pain, swelling, and giving-way episodes without a history of trauma. Localized tenderness of the condyle is often the only physical finding. Routine radiographs are usually diagnostic, but occasionally a tunnel view may be needed. The osteochondral fragment appears separated from the condyle by a thin radiolucent line. Tomography may aid in determining the exact location and extent of the
Page 364
osteochondrotic lesion. Bone scanning may be useful in detecting a very early lesion. The management of these patients is based on the stability of the osteochondral fragment and the maturity of the skeleton.[48] If the epiphyses are open, conservative treatment with protective weight bearing usually results in healing of the lesion. When the epiphyses are closed, the prognosis for healing is guarded. If the fragments are detached, the loose fragments require surgery for removal or fixation. Protected range of motion with non–weight-bearing activity for 6 to 10 weeks is generally advised.
Osteonecrosis Osteonecrosis occurs when disruption of the blood supply to the bone causes infarction. The knee is a common site of involvement, particularly the weight-bearing surface of the medial femoral condyle.[21] Spontaneous osteonecrosis usually affects middle-aged and elderly patients, whereas secondary osteonecrosis may occur in younger patients related to steroid therapy or in association with sickle cell disease, lupus, or renal transplantation, among many other risk factors.[49] The exact etiology is unknown. The patient often has spontaneous onset of severe localized knee pain that may be accompanied by an effusion and loss of joint motion. The physical examination reveals point tenderness over the involved femoral condyle or tibial compartment. Radiographs performed at the onset of symptoms are usually normal, and the diagnosis is confirmed with technetium bone scanning, with increased activity noted. MRI also is diagnostic of acute osteonecrosis. Subchondral marrow signal abnormality is the earliest change of osteonecrosis; subchondral collapse and fracture may be seen in more advanced cases.[26] Initially, most patients should be treated conservatively with rest, protected weight bearing, and nonsteroidal anti-inflammatory drugs (NSAIDs). The outcome depends on the percentage of the weight-bearing surface involved with the process. If the lesion is small, no surgical treatment is required. Over the long term, degenerative changes develop in most patients, but initially the changes are not severe. For more advanced stages of femoral osteonecrosis, various surgical treatments have been proposed, including arthroscopic debridement, proximal tibial osteotomy, prosthetic replacement, and allografting.[49]
Extensor Mechanism Injuries Anatomy and Pathophysiology The extensor mechanism consists of the quadriceps muscles, quadriceps tendon, medial and lateral retinacula, patella, patellar tendon, and tibial tubercle ( Figure 54-6 ). Passive and dynamic stabilization of the patella are aided by the surrounding soft tissue. Although this anatomic complex encompasses the most superficial aspect of the knee, ruptures of the extensor mechanism are infrequent injuries relative to other types of injuries of the knee joint. Disruptions of the extensor mechanism may occur at any level from the quadriceps muscle to the insertion on the tibial tubercle. Injury generally occurs as a result of sudden vigorous contraction of the quadriceps muscle with the knee in a flexed position, laceration, or a direct blow. Rupture of the quadriceps tendon usually occurs at or just proximal to the patellar insertion. Occasionally the rupture may extend into the vastus intermedius tendon or transversely into the retinaculum. Most patellar tendon ruptures occur at the site of origin on the inferior pole of the patella.
Figure 54-6 Parasagittal section (lateral to m idline) of the knee showing extensor m echanism s.
Tendons of the extensor mechanism are extremely resistant to tensile loads and do not rupture under normal physiologic conditions, even with significant degrees of stress. Chronic systemic conditions, including rheumatoid arthritis, gout, systemic lupus erythematosus, hyperparathyroidism, and iatrogenic immunosuppression of organ recipients, may render the tendon vulnerable to rupture.[50] Several studies have implicated steroid use in tendon rupture.[51] Age also seems to be a factor, with quadriceps tendon rupture usually occurring in patients age 40 or older and patellar tendon rupture occurring in patients younger than 40. Overall, patellar tendon rupture is reported to occur one third as often as quadriceps tendon disruption.[52] In the pediatric population, quadriceps and patellar tendon ruptures are rare, and muscle tears seem to predominate.[2] In adolescents, patellofemoral dysplasia, chronic tendinitis, and the use of steroids
Page 365
seem to be predisposing factors. Dysplasia may cause extensor mechanism injury by repetitive tensile overloading, and corticosteroids seem to weaken collagen ultrastructure and impair the reparative process.
Clinical Features Clinical evaluation can elicit the correct diagnosis in most cases of complete disruption of the extensor mechanism.[52] Patients with extensor disruption may have the following signs and symptoms: (1) acute onset of pain, swelling, and ecchymoses over the anterior aspect of the knee and a palpable defect in the patella, quadriceps tendon, or patella tendon; (2) loss or limited ability for active leg extension (extension lag usually is seen when the last 10 degrees of extension are performed haltingly or with difficulty); (3) high-riding patella (patella alta) with patellar tendon rupture and superior retraction; and (4) low-riding patella (patella baja) with quadriceps tendon rupture and inferior retraction. Partial disruptions may be difficult to diagnose on clinical examination and may require imaging for confirmation.
Diagnostic Strategies Standard anteroposterior and lateral radiographs should be obtained and may reveal characteristic findings, possibly including obliteration of the quadriceps or patella tendon, a poorly defined suprapatellar or infrapatellar soft tissue mass, soft tissue calcific densities, or a displaced patella ( Figure 54-7 ). Patella alta may be sought on the lateral radiograph using a ratio of patellar tendon length to patellar length. If this ratio is greater than 1:2, patella alta is present.[53] The degree of flexion should not affect this ratio, which relies on the inelasticity of the patellar tendon. In patients with quadriceps rupture, there is commonly degenerative spurring of the patella evident on tangential views (tooth sign). Obliteration of the extensor tendons may be caused by a frayed tendon and surrounding hematoma. A soft tissue mass represents proximal or distal retraction of the torn tendon. Calcific densities may represent avulsed bone fragments of the patella or tibial tubercle or dystrophic calcifications in the substance of the tendons. Despite these multiple radiographic signs, the correct diagnosis is infrequently made by plain radiography in cases of complete quadriceps tendon rupture. MRI scan shows the entire extensor mechanism and is the best imaging modality for diagnosing pathology in this system, even in the acute phase. MRI usually is reserved for patients with possible incomplete disruption or patients with a complication of intra-articular derangements.
Figure 54-7 Rupture of the infrapatellar tendon, resulting in the high-riding patella in frontal (A) and lateral (B) projections. In the lateral projection (B), the norm ally lucent infrapatellar portion of the joint space is dense (asterisk), representing blood within the anterior com partm ent. ((From Harris JH, et al: The Radiology of Em ergency Medicine, 3rd ed. Baltimore, William s & Wilkins, 1993.)William s & Wilkins)
Management Treatment of acute extensor mechanism injuries produces a much better clinical outcome if instituted early, within 2 to 6 weeks of the initial injury. Accurate diagnosis at the time of injury is essential. Patients with delayed diagnosis of patellar tendon rupture may experience significant retraction of the patella proximally and subsequent development of quadriceps contractures or adhesions. If the tear is only partial, immobilization in full extension for 4 to 6 weeks is the treatment of choice.[54] Surgical intervention is required for reattachment of complete tendon ruptures and should be performed as soon as possible after injury to obtain the best results. Numerous techniques have been described for early and late repairs. The choice of repair depends on several factors, including location of the tear, lag time between injury and repair, and presence or absence of adhesions. After primary repair, the knee is immobilized in full extension with a long leg cast until healing is complete. Gradual active and passive range-of-motion exercises must follow to yield optimal results.
Patellar Fractures Anatomy and Pathophysiology The patella is the largest sesamoid bone in the body. It is held in place by the quadriceps tendon, the patellar ligament, and the medial and lateral retinacula. As an integral part of the extensor mechanism, the patella increases the effective lever arm of the quadriceps by providing anterior displacement of the quadriceps
Page 366
tendon.[30] Fractures of the patella, except for small avulsion fractures of the rim, are all intra-articular. Patellar fractures constitute approximately 1% of all skeletal injuries and occur in all age groups.[55] Patellar fractures are classified as transverse, stellate, or comminuted; longitudinal or marginal; proximal pole or distal pole; and rarely osteochondral. They may be either displaced or nondisplaced and occur either from direct or indirect forces or from dislocation. The most common fracture pattern is the transverse fracture (50% to 80%).[55] This type often is seen in young adults and usually results from a powerful contractile force transmitted from the quadriceps tendon. This force may pull the superior portion of the patella upward, leading to wide displacement. In such cases, the medial and lateral retinacula are usually disrupted, resulting in significant functional disability; active extension is impossible. Nondisplaced transverse patellar fractures usually are caused by a direct blow to the anterior aspect of the patella (e.g., a fall on the knee or a direct blow sustained in vehicular trauma). The retinaculum and extensor mechanism usually remain intact, and patients retain limited functional ability for active extension. Stellate and comminuted fractures account for 30% to 35% of all patellar fractures and commonly result from a direct impact.[55] The fracture elements often appear as separated fragments on plain radiography, but they are held in place and supported by the medial and lateral retinacula and the overlying soft tissues. Small proximal fragments are at risk for avascular necrosis because the patellar blood supply is central and inferior. Longitudinal or marginal vertical fractures constitute 12% to 17%, are usually the result of direct injury, and involve the lateral facet.[56]
Clinical Features On physical examination, pain, swelling, and ecchymosis over the patella and prepatellar bursa are present. Active extension may be limited or absent, depending on the fracture pattern and amount of fragment displacement. Associated injuries may include fractures of the femoral neck, dislocation of the hip, and acetabulum fractures.
Diagnostic Strategies Radiologic evaluation of patellar fractures should include standard anteroposterior, lateral, and sunrise views. Most patellar fractures are obvious on plain radiographs, but vertical marginal fractures may be difficult to identify; they are obscured by the femur on the anteroposterior view and not seen at all on the lateral view.[57] Close examination of sunrise (or equivalent) views may reveal an osteochondral avulsion fragment or marginal fracture ( Figure 54-8 ). Bipartite and multipartite patellas are common normal variants and should not be confused with fractures. Ossification centers are found at the upper outer quadrant of the patella and have smooth cortical margins. Comparison radiographs may be helpful because these anatomic anomalies are often bilateral. In some cases, MRI or arthroscopy may be needed to identify occult marginal fractures or free osteochondral fragments.
Figure 54-8 Patellar fracture, sunrise view. The sharp nonsclerotic margins identify this as an acute fracture and not a congenital finding. ((From Rosen P, et al: Diagnostic Radiology in Em ergency Medicine. St. Louis, Mosb y, 1992, p 196.)Elsevier Inc.)
Management If the patient can actively extend the knee without displacing the fracture, the retinaculum is intact, and the patient may be treated nonoperatively. Nondisplaced patellar fractures are usually treated with a long leg cast for 4 to 6 weeks and have uniformly good results. Casting the knee in full extension relieves the patella of almost all stress and allows ample time to heal. In the initial management, a knee immobilizer may be used. Patients should be instructed to use crutches with partial weight bearing as tolerated and orthopedic or primary care follow-up. For widely displaced transverse fractures, open reduction and internal fixation are necessary for optimal results. Although operative techniques vary among surgeons, tension band wire and suturing of the retinaculum are often used. A knee immobilizer or long leg posterior splint can be used initially to immobilize the extremity before definitive care. Treatment options for displaced comminuted fractures include open
Page 367
reduction and internal fixation and partial or complete patellectomy. With the patella removed, the patellar ligament is pulled upward and sutured to the quadriceps femoris tendon, and the retinaculum is repaired. After partial or complete patellectomy, patients generally experience good functional results, although with reduced active knee motion and isokinetic strength.[58] Fracture fragment separation and dehiscence of the fracture repair are uncommon. They generally result from inadequate internal fixation or, in some cases, an inadequate period of immobilization. Avascular necrosis is rare. Range of motion is generally good after all procedures. Persistent patellofemoral pain and osteoarthritic symptoms are reported as late sequelae of patellar fractures in 56% of patients.[55]
Patellar Dislocation Anatomy and Pathophysiology Traumatic patellar dislocation is a relatively common knee injury and can lead to recurrent patellar subluxation and dislocation. It is more common in children than in adults. In adults, patellar dislocation occurs almost exclusively in the setting of patellofemoral dysplasia.[59] Most cases are lateral extra-articular dislocations, and the mechanism of injury is usually a direct blow to the anterior or medial surface of the patella.[2] It may occur from an athletic injury caused by a valgus stress combined with flexion and external rotation. In nearly all cases, there is disruption or sprain in the medial patellar retinaculum caused by stretching of this structure as the patella subluxes laterally; subluxation usually indicates a stretched medial retinaculum, and dislocation suggests a tear. Although extra-articular patella dislocations are common, intra-articular dislocations are rare occurrences that must be considered in any patient with a locked knee. Intra-articular dislocations are usually vertical or horizontal, according to the axis of rotation.[60] Risk factors for partial or complete dislocations are listed in Box 54-2 . BOX 54-2 Risk Factors for Partial or Complete Patellar Dislocations
{,
{,
{,
{,
Laxit y of patel lofe mor al joint Gen u valg um (kno ck-k nee defor mity) Shall ow troch lear groo ve Decr ease d quad ricep s femo ris and vast
Page 368
{,
{,
{,
{,
us medi alis stren gth Previ ous patel lar dislo catio n or subl uxati on Medi al retin acul um path olog y Rupt ure of any porti on of the exte nsor mec hani sm Larg eQ angl e
The quadriceps angle (Q angle) is measured with the quadriceps contracted. The angle is formed by lines drawn from the tibial tubercle to the center of the patella and from the center of the patella to the anterior superior iliac spine. Normally this angle is 10 degrees or less in men; it may be 15 degrees in women. A Q angle exceeding these dimensions may predispose to patellofemoral problems.
Clinical Features Patients may complain of the knee giving out accompanied by pain and swelling. Inability to bear weight and inability to flex the knee are common complaints. There may be a history of previous dislocation. Examination reveals a defect anteriorly with the patella deviated laterally. Tenderness along the medial joint line usually can be elicited by palpation. An effusion also may be present. Acute hemarthrosis is seen most commonly if there is an associated osteochondral fracture. Osteochondral fractures typically occur on the articular surface of the patella and may involve only cartilage (chondral fractures) or include a piece of underlying cortical bone. Patellar dislocations may reduce spontaneously, or the patient may self-reduce the dislocation, usually followed by formation of a large effusion. The patellar apprehension test is used to aid the clinical identification of patients at risk for patellar dislocation or subluxation. The apprehension sign refers to the anxiety the patient exhibits when the examiner attempts to slide the nondisplaced patella laterally. When the patella is displaced laterally, the patient may experience pain and forcefully contract the quadriceps femoris muscle. This is a positive apprehension sign and indicates a tendency for patellar subluxation or dislocation. The test has no value and is not necessary in a patient with acute patellar dislocation, but it may be useful in establishing the diagnosis
Page 369
in patients who report an “event” that occurred and resolved spontaneously.
Diagnostic Strategies Standard anteroposterior and lateral views are used and are usually adequate. A sunrise (skyline) view usually is not possible because of pain and inability to flex the knee. Radiographic findings show the patella deviated laterally out of the trochlear groove, and an effusion is usually evident. Radiographs should be examined for evidence of avulsion fractures.
Management After dislocation is diagnosed, closed reduction should be attempted. Force or pressure should be directed anteromedially on the lateral patellar margin, while simultaneously attempting gentle extension of the leg. Postreduction radiographs are mandatory and should reveal the patella in the trochlear grove. Osteochondral avulsion fragments may be visualized radiographically, and postreduction radiographs should be examined carefully for their presence. Radiologically evident intra-articular loose bodies may require arthroscopic removal. Occasionally, patellar reduction may be difficult. Several cases have been reported in which the conventional method of reducing a laterally dislocated patella either has failed or has proved difficult.[61] In nearly all cases, there has been the suggestion of locking of the medial facet onto the lateral femoral condyle with internal rotation of the patella. Closed reduction can be achieved by applying downward pressure to the lateral aspect of the patella, creating an external rotational force that unlocks the medial patellar facet.[61] Typically, traumatic patellar dislocations occur with disruption of the medial retinaculum but an intact lateral retinaculum, preventing internal rotation. Dislocations that are irreducible by conventional methods may have significant internal rotation and lateral retinaculum pathology. After successful reduction, the knee should be immobilized in full extension for 3 to 6 weeks to allow adequate time for the medial retinaculum to heal. Ice, elevation, non–weight bearing, and analgesia provide additional benefit in the acute setting. The patient can be discharged with orthopedic or primary care follow-up within 2 weeks. Although the incidence of recurrence may be decreased with appropriate therapy and proper patient selection, at least 30% to 50% of all patients having sustained a primary patellar dislocation continue to have symptoms of instability or anterior knee pain. Recurrent patellar dislocations reportedly have a 15% incidence and may require surgical intervention, including release of the lateral retinaculum, reconstruction of the medial retinaculum, or tibial tuberosity transfer medially to decrease the Q angle. The most common surgical procedure is arthroscopic release of the lateral retinaculum. Incision of the lateral retinaculum results in decreased pull on the patella. If this is unsuccessful, other operative techniques include shortening of the medial patella retinaculum and tibial tuberosity transfer.
Patellofemoral Pain Syndrome Anatomy and Pathophysiology The patellofemoral pain syndrome refers to the clinical presentation of anterior knee pain related to changes in the patellofemoral articulation. Most authors refer to symptoms that result from pathologic changes on the surface of the patella as chondromalacia patellae. The term chondromalacia has been used imprecisely to define the syndrome of patellofemoral pain.[62] Chondromalacia is a pathologic term that refers to softening of the articular cartilage. Correlating pathologic changes on the surface of the patella and clinical symptoms has been difficult, and the pain mechanism has not been precisely defined.
Clinical Features Patellofemoral pain is the most common symptom complex in the knee joint. Patients are generally 10 to 20 years old and often have difficulty describing their symptoms clearly. A typical presentation is nonspecific anterior knee discomfort that is nonradiating and occurs in a teenage girl. The pain usually begins gradually and commonly is not related to trauma. One knee is usually more affected than the other. The knee is more painful with prolonged flexion, and the discomfort typically is accentuated by stair climbing and kneeling. The patient may have instability related to patellar subluxation or dislocation. The syndrome also may occur in athletes with patellofemoral pain induced by overactivity. At times, elderly patients may have arthritis affecting the patellofemoral joint. When arthritis is isolated to the patellofemoral joint, the symptoms are identical to symptoms in patients with patellofemoral syndrome pain; however, the response to treatment and prognosis are different. The differential diagnosis includes tears of the menisci, plica syndrome, inflammatory or degenerative arthritis, ligament injuries, and overuse syndromes (e.g., prepatella bursitis and patella tendinitis).
Page 370
The physical examination should begin with observation. The patient may ambulate with an antalgic gait. Any referred pain syndromes from hip or disk disease should be excluded. Direct knee examination should include documentation of the size of any effusion, palpation of the patella facets for any evidence of tenderness, and compression testing of the patella for apprehension to medial or lateral subluxation.
Diagnostic Strategies Radiographic examination of the patellofemoral joint is of limited value and relies for the most part on lateral and sunrise axial projections. The axial view can be obtained with the patient prone or supine. Merchant's projection is the most popular axial projection for the evaluation of patellofemoral congruency.[63] It is obtained with the knee flexed 45 degrees. Plain radiography helps rule out arthritic involvement and visualize any malalignment. Further evaluation may be undertaken with CT or MRI. MRI and the combination of CT and arthrography are sensitive in detecting abnormalities of the articular surface of the patella.[63]
Management Most patients, regardless of the cause of their condition, respond to a rehabilitation program. Conservative treatment for patellofemoral pain is usually effective, with most patients responding to one or more of four types of treatment, including (1) exercises to strengthen the quadriceps, (2) brace support of the patellofemoral mechanism, (3) activity modification limiting flexion, and (4) medications such as NSAIDs for pain. The initial goal is to reduce pain and improve function, with emphasis placed on strengthening the vastus medialis oblique muscle. The patient should receive appropriate referral to ensure that an appropriate rehabilitative scheme is designed.
Tibial Femoral Knee Dislocation Anatomy and Pathophysiology Tibial femoral knee dislocation is a severe injury and a limb-threatening emergency. This is a rare injury, but should be considered when an appropriate injury mechanism was present because half of all knee dislocations spontaneously reduce or are reduced in the field by emergency personnel.[64] Patients presenting with knee dislocations that have been reduced have similar risk of injury and coexisting trauma as patients who present with a dislocated knee.[65] Two thirds of all knee dislocations result from motor vehicle crashes, with the remainder occurring from falls, sports injuries, and industrial injuries. Of all knee dislocations, 50% to 60% are anterior.[1] Epidemiologic data show a peak incidence in the teens and 20s, with a male predominance of 3:1.[65] Dislocations invariably are associated with significant soft tissue and ligamentous injury. There is disruption of the joint capsule with accompanying trauma to the muscles and tendons. Vascular injury to the popliteal artery is the most severe complication and is the major cause of morbidity and limb loss. The neurovascular bundle, which is composed of the popliteal artery, popliteal vein, and common peroneal nerve, runs posteriorly behind all bony and ligamentous structures in the popliteal fossa. The popliteal artery is fixed in the fibrous tunnel of the adductor magnus hiatus proximally and traverses the fibrous arch of the soleus and interosseous membrane distally. In essence, it is tethered to the femur and the tibia, and its inherent immobility renders it susceptible to injury during dislocation. At that time, the popliteal artery may be stretched, lacerated, or contused. Because of the parallel course of the popliteal vein and peroneal nerve, they are vulnerable to a similar injury. Traumatic dislocation of the knee can be characterized by the mechanism of injury and the type of dislocation. The injury is most commonly sustained in high-velocity accidents, such as motor vehicle and motorcycle crashes, or in severe crush injuries.[24] Accidents associated with athletic activity (e.g., water skiing) also have produced dislocation. Anatomically, dislocations are described based on the relative displacement of the tibia with respect to the femur. They are classified into five types: anterior, posterior, medial, lateral, and rotary. Anterior dislocation is reported to be the most common type and usually is caused by hyperextension of the knee.[24] Posterior dislocations are the second most common type and usually result from high-velocity direct trauma to the flexed knee, often in association with vehicular trauma (dashboard-type injury). The remaining dislocations are lateral, medial, or rotary dislocations and result from direct or indirect trauma producing valgus, varus, or rotary forces.
Clinical Features The diagnosis of knee dislocation is based on the mechanism of injury and clinical and radiographic findings. Clinical deformity should be easily palpable when a dislocation is present. Swelling may be absent, however, because of the associated tearing of the capsular structures and dissipation of the acute hemarthrosis into
Page 371
the adjacent soft tissue. The initial evaluation may not reveal an obvious gross deformity because of the variable occurrence of spontaneous reduction. Some authors have advocated expanding the definition of knee dislocation to include patients who have a bicruciate (ACL and PCL) ligament injury, even when the knee is reduced on initial presentation.[65] For this reason, patients with grossly unstable knees but no proven dislocation and patients who have a bicruciate (ACL and PCL) ligament injury should be evaluated for concomitant injuries, similarly to patients with proven dislocation.[66] Regardless of the type of dislocation, patients usually have associated trauma with high injury severity, most commonly ipsilateral or contralateral lower extremity fractures.[65] Other injuries may include pelvic fractures, multiple rib fractures, skull fractures, and posterior dislocation of the hip. Vascular injury is a potential catastrophic complication of knee dislocation, and popliteal artery injury is reported in 14% to 65% of these patients.[64] Anterior dislocations usually lead to a severe stretch injury with damage to the long segment of the artery, whereas posterior dislocations produce an isolated transection of the artery.[64] The risk of vascular injury seems to be less when the dislocation is the result of relatively low-energy trauma (except with hyperextension), as might be encountered on the athletic field (5% to 50% in various series), than with high-energy trauma (20% to 50%).[9] The collateral geniculate arteries around the knee also may be damaged directly or secondarily compressed by hematoma formation after the dislocation. Direct arterial injury, decreased collateral circulation, and elevated compartment pressures all may compromise limb perfusion. In addition to being clinically occult, vascular injury in blunt trauma is more difficult to manage because of associated soft tissue injury and edema. Evaluation of the limb vascular status is the most important part of the initial physical examination of knee dislocation. All knee dislocations probably warrant surgical consultation, but the so-called hard signs of vascular injury mandate immediate surgical consultation.[67] These signs include absence of pulse, limb ischemia, rapidly expanding hematoma, pulsatile bleeding, and bruit or thrill over the wound, especially in penetrating injuries. When repair is delayed beyond 8 hours, the amputation rate may be 86%.[68] The posterior tibial and dorsal pedal pulses should be evaluated. Doppler pressure measurements and peripheral pulse determinations have been found to be highly predictive of major arterial trauma when diminished or absent, but normal values do not rule out vascular injury.[1] In all cases of extremity trauma with vascular injury, approximately 10% are associated with a normal pedal pulse.[69] Even in low-velocity dislocations, the possibility of vascular injury should not be overlooked. Vascular injury also should be sought in patients with ligamentous disruption only. There is no significant difference between patients with documented knee dislocation and patients with severe ligamentous disruption regarding the frequency of major (22% versus 18%) or minor (38% versus 36%) vascular abnormalities.[1] The treatment of minor vascular injuries is controversial. Intimal flap tears are undetectable by a physical examination and are identified by arteriography. Injuries to small branches of the popliteal artery can be managed by observation and serial examinations.[] These “minor” injuries may place the limb at risk if significant bleeding occurs predisposing to compartment syndrome. Any such injury mandates immediate vascular surgical consultation. Neurologic integrity in the limb also should be assessed because peripheral nerve injury may be associated with all types of dislocation. Peroneal nerve injury is the most common major neurologic problem associated with knee dislocation; some degree of dysfunction occurs in 40% of patients and is permanent in 78% of these.[1] The peroneal nerve should be evaluated by determining sensation of the dorsum of the foot and by having the patient dorsiflex the ankle. Less commonly, the posterior tibial nerve may be injured, manifesting as diminished plantar sensation and plantar flexion of the foot. The exact mechanism is unclear, but is thought to involve traction during displacement. Complete nerve palsy in the acute setting has been associated with a poor prognosis for recovery.[1] Knee dislocation may involve damage to other structures around the knee joint, including the cruciate ligaments, collateral ligaments, and menisci. Ligament injury is predictable as soon as the displacement exceeds 10% to 25% of the ligament resting length.[52] Classically, complete dislocation of the knee joint has been associated with complete tears of the ACL and PCL, resulting in complete disruption of the tibial femoral articulation. Most accounts of complete knee dislocation in the literature suggest that disruption of both cruciate ligaments is sufficient and necessary to make the diagnosis of knee dislocation; however, knee dislocation without disruption of both cruciate ligaments has been reported.[] No firm assumptions regarding the degree of associated ligamentous injury should be made.
Diagnostic Strategies
Page 372
Radiographic examination usually confirms the clinical findings ( Figure 54-9 ). In rare posterolateral and rotary dislocations, radiographic interpretation may be more difficult. Radiographic examination also serves to document associated fractures.
Figure 54-9 Anterior dislocation of the knee. A Anteroposterior view shows overlap of the fem ur and tibia, which is never seen under norm al circum stances. The anteriorly dislocated tibia is m agnified. B Lateral view shows anterior dislocation of the tibia in relation to the fem ur. The patella also is anteriorly dislocated. ((From Rosen P, et al: Diagnostic Radiology in Em ergency Medicine. St. Louis, Mosb y, 1992, p 194.)Elsevier Inc.)
There is a high incidence of popliteal artery injury with knee dislocations, and the longer repair is delayed, the more likely it is that amputation will be necessary. Contrast arteriography generally has been considered the standard of care.[] More recently, however, there has been debate in the trauma literature as to whether all patients with knee dislocations require arteriography. Some studies have found that serial examinations can detect all clinically significant injuries, whereas others have emphasized the occasional occurrence of an occult arterial injury.[] A meta-analysis found that absence of normal pulses had only 79% sensitivity for a surgical popliteal artery injury after knee dislocation, suggesting that the de-fault still should be to obtain angiography on these patients.[] Color-flow Doppler ultrasonography is gaining acceptance as an alternative to arteriography in some centers, but it may not be as readily available during off hours.
Management The dislocated knee should be reduced immediately by longitudinal traction using appropriate analgesia and sedation. Radiologic confirmation is not required before reduction. The neurovascular status should be checked before and after reduction is achieved. Reduction usually can be accomplished with simple traction-countertraction, preferably using intravenous conscious sedation; general anesthesia is rarely necessary. The limb should be immobilized in a long leg posterior splint with 15 to 20 degrees of flexion. Circumferential casting is avoided in the acute setting. When there is any suspicion for vascular injury or if immediate exploration is not planned, an arteriogram should be obtained. Current indications for immediate surgery include obvious vascular injury with a cool, cyanotic ischemic lower extremity and irreducible or open dislocations. Arthroscopy is contraindicated in the acute setting because of the risk of fluid extravasation secondary to capsular deficiencies. Prompt and accurate diagnosis of vascular trauma is essential to successful management and limb salvage. Early revascularization also is crucial because delay of more than 6 hours increases the risk of compartment syndrome and amputation. Rates of limb salvage have improved dramatically with widespread application of modern techniques of vascular repair.[72] A large prospective study of limb-threatening injuries (not limited to dislocations) cast doubt, however, on the superiority of reconstruction over amputation, finding equivalent long-term functional outcomes for patients treated with amputation and reconstruction, even though the amputation patients had more severe initial injuries.[79] In the specific case of dislocation, early operative intervention does seem to confer an advantage.[80] Loss and disability are minimized by expedient revascularization and primary arterial repair, local heparinization when not contraindicated, repair of popliteal venous injury, aggressive wound debridement, and early soft tissue coverage. Four-compartment fasciotomies are done routinely or selectively in various centers to minimize the consequences of reperfusion edema in patients who undergo vascular repair.[9] If the neurovascular structures remain intact after dislocation, the knee joint is reduced and allowed to rest for 2 to 3 days before reconstruction of the torn ligaments is considered. Although the management of ligament injuries secondary to knee dislocation is controversial, the long-term results of surgical repair of ligaments damaged during dislocations have been good. In follow-up studies, clinical instability is generally not a problem, but chronic pain and discomfort are present in almost half of patients. Loss of motion is a common complication, and extensive damage to the articular surfaces at the time of injury increases the risk of early osteoarthritis. Inability to achieve a closed reduction is uncommon; however, it may occur as a result of concomitant
Page 373
ligamentous injuries or femoral condyle herniation through a large capsular defect.[81] Complications associated with traumatic knee dislocations include the development of deep vein thrombosis, compartment syndrome, pseudoaneurysms, and arterial thrombosis. Compartment syndromes generally occur within 24 to 48 hours of the initial injury. Pseudoaneurysm formation may occur several hours to months after an undiagnosed acute popliteal artery injury. A review of the literature reveals the civilian incidence of posttraumatic pseudoaneurysms to be rare, accounting for only 0% to 3.5% of all popliteal aneurysms.[82] Heterotopic ossification is a poorly-understood syndrome of calcification of the soft tissues of the knee. It has been observed in uninjured knees of patients who sustained major trauma. In its severest form, heterotopic ossification can cause dramatic decreases in knee mobility. Almost half of dislocated knees go on to have heterotopic ossification, although the most function-limiting form may be limited to patients with severe trauma.[83]
Soft Tissue Injuries The knee is the most commonly injured joint in the human body, and the ligaments sustain damage in most cases. The incidence of knee ligament injuries in the United States has increased since the 1980s, possibly because of increased activity levels in middle-aged people and increased participation at all levels in a variety of sports.[9] The ligaments of the knee are the MCL, LCL, ACL, and PCL. They function in conjunction with the joint capsule to limit varus-valgus (medial-lateral) and anterior-posterior translations of the knee. Ligament injuries to the knee may involve any or all of the ligaments and may range from mild sprain to complete tears. Collateral ligament injury usually causes tenderness and pain along the joint line. Cruciate injuries pose more of a diagnostic dilemma because they are intra-articular structures.
Cruciate Ligament Injuries The cruciate ligaments are the primary stabilizers for anterior and posterior displacement of the tibia on the femur. They are so named because they cross each other between their attachments. They form the keystone of the “four-bar cruciate linkage.”[84] The ACL extends obliquely upward, medially, and backward from the anterior intercondylar area of the tibia to the medial side of the lateral femoral condyle. The ACL prevents excessive anterior displacement of the tibia on the femur and helps control rotation and hyperextension of the knee during cutting, twisting, and turning activities. It is the most commonly injured major ligament of the knee, with more than 200,000 new ACL tears occurring in the United States annually.[7] The PCL passes upward, laterally, and forward medial to the ACL from the posterior intercondylar area of the tibia to the lateral side of the medial condyle of the femur. The PCL prevents excessive posterior displacement of the tibia on the femur, especially during flexion. The PCL is extremely strong, and injuries are relatively uncommon. Isolated PCL injury accounts for 3.4% to 10% of all knee injuries.[85] The ACL is commonly injured in association with sporting activities, particularly skiing and football.[86] Numerous mechanisms of injury produce ACL disruption. Although ACL injuries can be caused by contact, they are more common in noncontact sports, with the plant-and-pivot or stop-and-jump mechanisms the predominant injuries.[9] A direct blow to the flexed knee, as might occur in motor vehicle crashes (dashboard), and turf injuries with the knee flexed and the ankle plantar flexed also can result in an ACL injury. Approximately 50% of patients with ACL injuries have associated meniscal tears.[9] The lateral menicus is torn more commonly than the medial meniscus in acute ACL injuries, but in chronic ACL tears, the medial meniscus is more commonly involved. Several studies suggest that the classically described “unhappy triad” of ACL, MCL, and medial meniscus injury is less common than the association of torn ACL, torn MCL, and torn lateral meniscus.[9] Acute or chronic ACL insufficiency is uncommon in children younger than age 14 years old with open epiphyses.[87] ACL insufficiency secondary to trauma in this age group most often is associated with avulsion of the intercondylar eminence of the tibia. Nonpathologic ligament laxity or congenital absence of the ACL must be considered in the differential diagnosis in children with suspected ligamentous injury. The diagnosis of ACL injury often can be made from the history alone. Most patients with acute ACL injury give a history of immediate disability and inability to continue activity, citing lack of confidence in their knee. Pain is the most common complaint with ACL rupture and is usually immediate and often accompanied by acute hemarthrosis. A history of audible “pop” at the time of injury is an important clue and occurs in about 70% of patients with ACL rupture. Reports of the knee giving out suggest ACL rupture or tear; giving out is reported in 17% to 65% of cases.[88] Patients also may complain of the knee buckling, locking, or collapsing and inability to bear weight. In one study of 40 patients with ACL, 86% complained of the knee giving way
Page 374
with strenuous activities.[88] Giving way is commonly associated with activities such as cutting and twisting maneuvers and rapid deceleration, but it may occur with daily activities. Patients with an ACL-deficient knee usually complain of repetitive episodes of buckling with activities. The diagnostic limitations of clinical knee examination compared with arthroscopy have been well documented. Although the diagnosis of collateral ligament injuries is usually made clinically, reports concerning ACL injury reveal much disparity in accuracy, ranging from 38% to 95%.[9] In the largest prospective study to date, the diagnostic accuracy of the clinical examination for intra-articular injuries of the knee compared with arthroscopy was 56%.[89] The lesions most difficult to diagnose were chondral fractures, tears in the ACL, loose bodies, and fibrotic fat pads. Immediate swelling and the presence of hemarthrosis indicate an ACL tear or other internal derangement of the knee. Acute hemarthrosis is a common and significant sign with acute ACL injury and occurs in approximately 70% of patients.[90] It is defined as rapid extravasation of blood into the joint and is an indication of significant intra-articular injury. Acute hemarthrosis also occurs in 10% to 15% of patellar subluxations or dislocations, 10% of peripheral meniscal tears, 2% to 5% of osteochondral fractures, and 5% of capsular tears and PCL injuries. The appearance of hemarthrosis of the knee in children usually signifies a serious knee injury and should be treated with the same importance as in adults.[91] The PCL is less commonly injured than the ACL and generally is injured more often outside of sporting activities.[9] Mechanisms of PCL injury include a fall onto the ground with the foot plantar flexed (striking the tibial tubercle), a direct posterior blow to a flexed knee (e.g., a dashboard injury), hyperflexion, hyperextension, severe varus or valgus loads after failure of the collaterals, and knee dislocations. Ninety-five percent of all PCL injuries are associated with other ligament injuries, including concurrent injuries of the MCL, ACL, or posterolateral complex.[11] PCL injuries are classified as partial (grade I or II) or complete (grade III) tears. Pain and swelling are common complaints with isolated PCL tears and with PCL tears having combined capsuloligamentous disruption. Popping or tearing sensations are infrequently noted, and instability usually is not immediately appreciated. Later the patient may complain of the femur falling off the tibia. The posterior drawer test is commonly done to assess for the integrity of the PCL. Careful inspection also may reveal a posterior sag sign.
Collateral Ligament Injuries The medial stabilizers of the knee are the joint capsule and the MCL. The semimembranosus and pes anserinus are medial dynamic stabilizers. These structures resist valgus laxity and medial rotary instability. The MCL is a two-part structure with a long superficial and a deep capsular component that attaches to the medial meniscus and acts as a stabilizer for this structure. The MCL usually is injured by a direct blow or impact to the lateral aspect of the knee, which imposes a valgus stress. Overall, MCL injury is the most common isolated knee ligament injury, and it is the injury most commonly associated with ACL injury. MCL injury does not require surgical treatment in most patients.[9] The lateral stabilizers of the knee are the LCL and the lateral joint capsule. Secondary contributors to lateral stability are supplied by the iliotibial band, biceps tendon, and popliteal arcuate complex in the posterolateral corner of the knee. Resistance to varus stress is provided mainly by the LCL. Fibers descend from the lateral femoral condyle and insert at the fibula head. The lateral ligaments are under tension during standing and walking, when they are at or near maximal extension. The LCL usually is injured by a mechanism of hyperextension with varus stress commonly accompanied by a direct blow or rotation. Injuries to the LCL are less common but more disabling than injuries of the medial side. The lower incidence of injury is attributed to the greater mobility of the LCL and overall greater stability of the lateral compartment. Varus injury is uncommon because the inner aspect of the knee is protected by the opposite leg. The forces necessary to produce LCL injury are usually greater than the forces required for medial injury, which partially explains the high frequency of associated injuries accompanying LCL injury. The tendon of the biceps femoris muscle attaches to the head of the fibula. Just below this juncture, the common peroneal nerve is close to the head of the fibula. Because of this relationship, common peroneal nerve injury and biceps femoris tendon injury must be considered in patients with LCL injury. The knee should be examined as soon as possible after an injury to exclude ligamentous damage. Focal tenderness at the origin or insertion sites suggests collateral ligament trauma, but also can occur with muscular injury, osseous pathology, or meniscal tear. Range of motion should be documented and stability testing done to assess ligamentous injury as outlined previously.
Diagnostic Strategies
Page 375
Plain radiography may be used in cases of suspected ligamentous injury before stress testing to rule out the possibility of an associated fracture. Although patients with isolated collateral ligament strain rarely show acute osseous pathology, the yield increases in cases with traumatic effusions and cases with suspected cruciate ligament injury. The initial radiographic evaluation should include anteroposterior, lateral, intercondylar notch, and sunrise views. Each radiograph should be evaluated for possible osteochondral injuries, loose bodies, or avulsion injuries at the attachment sites of ligaments. The lateral capsular sign (Segond fracture) is highly suggestive of injury to the ACL and is seen in approximately 6% of injuries.[31] Fracture of the posterior aspect of the lateral tibial plateau may represent another indirect radiographic sign of ACL tear.[92] The fracture may represent an injury at the capsular insertion analogous to the Segond fracture. MRI is an excellent modality for determining the status of the cruciate and collateral ligaments. MRI has been shown in a more recent study to be cost-effective by reducing the number of diagnostic arthroscopies.[93] In other cases, it may aid the orthopedic surgeon in planning therapeutic arthroscopy if a clinically significant, surgically correctable lesion is found. MRI is highly accurate for diagnosing ACL rupture, with reported sensitivity and specificity exceeding 90%.[94] The diagnosis is difficult when the ACL is incompletely torn and in chronic cases, when the ligament may scar down in near-anatomic position. MRI consistently shows the thick PCL and is reportedly 90% sensitive for documenting a PCL injury. Arthroscopy is unquestionably the best method for ascertaining the integrity of the ACL.[52] Arthroscopic observation of the PCL is more difficult, however, and probably not as reliable as MRI. Arthroscopy has the advantage of allowing simultaneous therapy via cruciate ligament debridement or reconstruction.
Management There is consensus that isolated grade I and II collateral ligament injuries should be managed conservatively, provided that the ACL is intact. The nonoperative approach should focus on pain control, restoring range of motion, regaining muscle strength, and protecting the knee from further injury. Appropriate initial therapy includes ice pack application, NSAIDs, and symptomatic immobilization with a knee immobilizer if necessary. Patients may be placed on a regimen of partial weight bearing or non–weight bearing using crutches. Orthopedic or primary care follow-up is advised, and a rehabilitative exercise program for quadriceps and hamstring strengthening may be instituted when the acute injury resolves. In isolated grade III collateral ligament injuries, nonoperative treatment also is the preferred method of treatment. Generally a completely torn LCL does not lead to significant instability or loss of function, unless associated with an ACL tear. Nonsurgical treatment of all degrees of isolated MCL injury is well established.[9] In cases in which there is a concomitant tear of the ACL and the MCL, the treatment plan may change from conservative management to operative repair.[95] Management of an ACL tear is controversial because of the variability of patient impairment after an ACL injury and the lack of documentation that operative repair prevents degenerative arthritis. The outcome for a patient with ACL disruption is most closely related to the level of activity. Most young patients with a complete ACL tear who are active in sports require reconstructive surgery to stabilize the knee. Usually surgery is performed arthroscopically after a delay of 2 to 3 weeks to allow swelling to subside. Older patients and patients who do not participate in active sports may be treated conservatively with muscle-strength training. If recurrent functional instability subsequently develops, reconstruction may be considered at a later date. The natural history of patients with isolated PCL varies. Instability is a less frequent complaint after isolated PCL injuries than after isolated ACL injuries. Isolated PCL injuries are more frequently associated with pain than instability. Some patients function relatively well with a good rehabilitative program that includes quadriceps strengthening and functional bracing. Over time (10 to 20 years), many patients develop disability related to degenerative changes of the articular surface with stiffness and pain. Although some controversy surrounds the natural history and treatment of true isolated PCL injuries, these injuries are usually partial tears and do not require surgery.[9] Nonsurgical treatment should focus on quadriceps rehabilitation. There is general agreement that PCL injuries with combined ligamentous injuries, especially injuries involving the posterolateral corner, should be treated operatively within 2 weeks.[9]
Meniscal Injuries Anatomy and Pathophysiology The menisci are of great clinical importance to the normal function and integrity of the knee joint. The medial and lateral menisci are crescent-shaped, semilunar fibrocartilaginous structures that sit on the superior articular surface of the tibia and provide a gliding surface for the femoral condyles. In this interposed position
Page 376
between the femur and tibia, they function as shock absorbers and aid in the distribution of stress across the joint surface by providing a larger area of contact. They also act as secondary stabilizers by deepening the tibial plateau. Normal tibial femoral articulation and function depend on meniscal integrity; damage or loss is associated with degenerative changes within the knee and the accelerated development of osteoarthritis. The medial meniscus is semilunar and firmly attached anteriorly and posteriorly to the joint capsule. The lateral meniscus is less firmly attached to the capsule and more mobile. During flexion and extension, the menisci migrate slightly forward with extension and backward with flexion. Because of the greater mobility, the lateral meniscus is less vulnerable to injury. The meniscus is avascular except at the peripheral one third, which has tremendous clinical importance in that it is this area that has the greatest potential to heal after injury. Injury to the menisci may be from a single traumatic episode, a degenerative process, or a combination. The mechanism usually involves a twisting maneuver on a weight-bearing knee. The force required sometimes can be as slight as that produced when a middle-aged person arises from a chair and turns to reach for an object. The associated compression and rotation of the knee joint can lead to abnormal shear forces that result in damage to the meniscus. The triad of meniscal tears comprises joint line pain, swelling, and “clicking” or locking of the knee. True locking may occur immediately after the injury, with the knee held at 30 degrees of flexion; this is primarily associated with a displaced meniscal fragment. In general, knee locking that occurs the day after injury is usually the result of “pseudolocking,” whereby full range of motion is limited by effusion, pain, and muscle spasm rather than a displaced meniscal fragment. Meniscal tears can be classified based on their description and orientation. They include radial, horizontal, longitudinal, and complex tears. Radial tears are tears that occur from the inner edge of the meniscus to the peripheral margin. The so-called bucket-handle tears are vertical longitudinal tears typically seen in younger patients in association with ACL insufficiency.[52] The bucket-handle tears are three times as common in the medial compared with the lateral meniscus and can displace into the knee, resulting in a “locked” knee. Complex meniscal injuries are the most common of all meniscal lesions and usually are seen in older individuals without associated ligamentous instability. Meniscal tears also can be classified based on their location and peripheral and central surface appearances.[96] Red-red tears are peripheral detachments that have a functional blood supply and the best prognosis for healing. Red-white tears have an active peripheral blood supply that is sufficient for healing if adequately repaired. The last category is the white-white tear, which is within the inner two thirds of the meniscus, has no true vascularity, and has minimal to no healing ability.
Clinical Features Meniscal injuries are unusual in children but become increasingly more common in adolescents and adults. An isolated meniscal tear should be suspected in a patient with a history of intermittent locking, effusion, giving way, and pain and physical examination findings of joint line tenderness and a positive McMurray's test.[97] Cruciate tears invariably result in immediate hemarthrosis; meniscal tears usually result in an effusion forming over 12 to 24 hours. A second, more common presentation is a patient with an unstable knee who has chronic ACL insufficiency and similar history and physical findings. The cardinal sign of a meniscal tear is local pain and tenderness along the joint line. Joint line pain and tenderness are especially apparent with extremes of flexion and extension. Specific joint line tenderness is helpful diagnostically, particularly in the posterior half of the menisci, because 81% of meniscal tears are located posteriorly.[96] Not all tears of the menisci are symptomatic. Degenerative lesions of the posterior horn are relatively common in middle age and later and may be asymptomatic. The differential diagnosis of a torn meniscus is extensive and includes loose bodies, osteochondrotic lesion, tibial spine fractures, patellofemoral pain syndrome, popliteal tendinitis, plica syndromes, inflammatory arthritis, and discoid menisci with or without a concurrent tear. Much evidence correlates an increased incidence of meniscal pathology with ACL rupture, with an overall incidence of meniscal tears with ACL rupture of 52%. Isolated medial meniscal tears are present in 22%, isolated lateral tears are present in 23%, and a combined meniscal lesion is present in 9% of cases.[98] PCL tears are uncommonly reported in association with meniscal pathology. The accuracy of clinical diagnosis for meniscal lesions has been well described in the literature.[99] The diagnosis can be made through a careful history and physical examination in 90% of patients.[9] No one specific test is predictive, however, and physical findings suggesting meniscal lesions have decreased reliability in patients with associated ACL tears.[99]
Diagnostic Strategies
Page 377
Although routine knee radiographs do not reveal direct evidence of injury to the cartilaginous menisci, they should be obtained to rule out other associated osseous injuries. The diagnosis of a meniscal injury may be confirmed by MRI or arthroscopy. The reported sensitivity of MRI for meniscal tears ranges from 87% to 97%, with specificity ranging from 91% to 95%.[] The negative predictive value of MRI for meniscal tears is approximately 95%. Arthroscopy is generally considered the gold standard for diagnosis with which other modalities are compared. It has the advantage of allowing direct visualization with diagnostic accuracy of 97% and can be therapeutic.
Management Definitive treatment of a meniscal injury is not an urgent concern. Unless the knee is locked and cannot be extended or flexed, a patient with a suspected torn meniscus should be treated initially with NSAIDs for analgesia, knee immobilization, ice, non–weight bearing, and orthopedic or primary care referral. Further management of a meniscal tear may include a conservative, nonoperative approach. Surgical treatment can be done with arthroscopic or open technique and may range from meniscal repair to partial meniscectomy. Current recommendations emphasize preserving as much normal meniscus as possible to decrease the risk of progressive osteoarthritis. The use of meniscal allograft tissue to reconstruct the knee has elicited a great deal of interest in recent years. The indications for meniscal allograft transplantation are currently being defined.[9] The lack of uniformity in patient selection, surgical technique, and follow-up criteria has made the results of clinical studies difficult to interpret, however. The management of meniscal lesions in a patient with ACL injury is generally influenced by the subsequent treatment of the ligament injury. ACL deficiency of the knee greatly increases the risk of meniscal repair failure. This failure can be obviated by concomitant repair of the ACL.
Overuse Injuries All overuse syndromes are associated with the development of inflammation. The common mechanism of injury is repetitive microtrauma to tissue, whereby the innate ability of the tissue to repair itself is outpaced by the repetition of the insult. Repetitive stress injury occurs commonly in sports, fitness, and training activities, but it is less commonly seen in free-play activities. These injuries have become more common in children and adolescents with the trend toward increased participation in organized sports. In general, the goal of treatment is to reduce inflammation through rest, activity modification, and medications. The typical complaint is knee pain, often localized to one of three particular areas: the medial aspect, the lateral aspect, or the peripatella region. Medial knee pain may be caused by subluxation of the patella, a stress fracture of the upper third of the tibia, pes anserine bursitis or tendinitis, and MCL strain related to excessive foot pronation. Lateral knee pain may be caused by iliotibial or popliteal tendinitis, LCL strain, or stress fracture of the fibula. Anterior pain is typical of lateral patellar compression syndrome, peripatellar tendinitis, and patellofemoral syndrome.
Iliotibial Band Syndrome The iliotibial band syndrome is the result of inflammation secondary to overuse and is most often described in high-mileage runners.[102] The iliotibial band is a thickened strip of fascia lata that extends from the iliac crest to the lateral tibial tubercle. This band serves as a ligament between the lateral femoral condyle and the lateral tibia and functions to stabilize the knee joint in extension. The irritation associated with overuse can cause inflammation of a bursa underlying the iliotibial band at the lateral femoral epicondyle. Symptoms generally include pain aggravated by repetitive knee movement associated with running or cycling. Discomfort typically appears after a consistent distance is covered. There is usually no history of direct trauma. Physical findings include localized tenderness to palpation of the lateral femoral epicondyle but an otherwise negative knee examination. Knee radiographs are normal. The differential diagnosis includes early degenerative joint disease, cystic or torn lateral meniscus, lateral capsular strain, lateral tibial or femoral condyle osteonecrosis, stress reactions, chondromalacia, and popliteus tendinitis. Treatment consists of rest or decreased distance, shoe changes, modification of exercise technique, anti-inflammatory medications, steroid injections, and stretching. Surgery is generally not required.[102]
Peripatellar Tendinitis Peripatellar tendinitis, or jumper's knee, refers to a spectrum of patellar tendon and extensor mechanism abnormalities that result from chronic repetitive stress.[103] The condition is commonly seen in athletes, especially athletes involved in some type of repetitive jumping, running, or cutting. The repetitive acceleration and deceleration that occur with jumping activities lead to overload on the extensor mechanism and
Page 378
microtears within the tendon matrix. In children and adolescents, biomechanical stresses are concentrated at the growth plates, which represent the weakest link in a closed system. In Sinding-Larsen-Johansson disease, stress concentrates at the accessory ossification center at the inferior pole of the patella and leads to a traction tendinitis and eventual fragmentation. Traction at the tibial tubercle and proximal tibial physis can result in the insidious development of an Osgood-Schlatter lesion or in an acute avulsion fracture of the tibial tubercle. The patient may have insidious onset of chronic, well-localized pain in the region of the patellar or quadriceps tendon before, during, or after participation. Complaints of weakness or giving way are common, although true locking, clicking, or effusion is rarely seen. Tenderness over the quadriceps tendon at the upper pole of the patella or the patellar tendon at the lower pole or at the tibial tuberosity is the hallmark of peripatellar tendinitis. The remainder of the examination usually reveals no additional findings. Radiographic changes have been documented but are rare before 6 months of symptoms. At that time, a radiolucency or elongation of the involved pole of the patella may be seen. Bone scans may show localization of tracer activity in the region of inflammation. Conservative therapy is the treatment of choice in the early stages. NSAIDs, rest, and activity modifications all have been successful. Local steroid injections have not proved to be of any long-lasting benefit, increase the risk of tendon rupture, and are not recommended.[103] For highly competitive athletes or for patients who fail conservative treatment, surgery with debridement of abnormal tissue may be performed.
Lateral Patellar Compression Syndrome Lateral compression of the patella is a clinical radiographic diagnosis characterized by knee pain and patellar tilt.[104] The syndrome usually becomes manifest during the growth period of adolescence. As body weight increases and growth occurs, the lateral stress on the patella increases, and lateral retinacular strain and lateral patella tilt may occur. Several theories have been proposed to explain the mechanism for pain, including subchondral microfractures, marginal synovitis, and excessive tension in the lateral retinacular structures.[104] The pain is classically anterior and is noticed with prolonged knee flexion, ascending or descending stairs, or athletics. The patient also may complain of giving way of the knee, crepitance, and intermittent swelling. Presentation may be similar to patellar subluxation.[104] Physical findings may reveal a slight effusion, marked tenderness on the articular surface of the patella, and crepitation in the patellofemoral joint. The diagnosis may be confirmed by an axial radiograph or a CT scan that reveals patellofemoral malalignment and abnormal patellar tilt. If the lateral compression forces are allowed to continue unabated, articular cartilage degeneration and subsequent patellofemoral osteoarthritis may occur. Nonoperative treatment consists of weight reduction, quadriceps strengthening, and oral anti-inflammatory medications. Surgical treatment involving lateral retinacular release is reserved for refractory cases.
Plica Syndrome The plica syndrome is an uncommon pathologic condition with symptoms that can be indistinguishable from symptoms of other internal derangements of the knee. Redundant folds of synovium, or plicae, found within the knee joint represent normal embryologic septa that persist into the adult knee. For reasons that are unclear, some plicae become symptomatic, and others remain quiescent. Repetitive bouts of synovitis within the plica may result in a tight, inelastic band and interfere mechanically with knee motion.[105] The constellation of symptoms seen in plica syndrome are generally nonspecific. Patients typically complain of pain over the region of the medial femoral condyle brought on by activity, but also occurring after sitting for prolonged periods. A snapping sensation is another commonly reported symptom as the plica sweeps across the femoral condyle. Other nonspecific symptoms supporting the diagnosis include intermittent swelling, locking, weakness, and stiffness. The physical examination often elicits tenderness over the medial femoral condyle but not the medial joint line, which is more typical of a medial meniscal lesion. An effusion, crepitus, loss of motion, quadriceps atrophy, and positive McMurray's test may be present as well. The diagnosis of plica syndrome can be made from the history alone and is supported by the physical examination. Plain radiographs are necessary to eliminate other causes of knee pain, but are of no value in diagnosing plica syndrome. Arthroscopy is most accurate in the diagnosis of this syndrome; however, the mere presence of a plica does not warrant intervention. Most plicae are incidental arthroscopic findings unrelated to underlying knee pathology.[105] Medial patella pain is more likely to be related to patellofemoral maltracking than to plica syndrome. Likewise, anteromedial joint line tenderness is more likely to be related to a meniscal tear than to a pathologic plica. Treatment is conservative, with a regimen including rest and NSAIDs. When the acute symptoms have resolved, a rehabilitation program is instituted to emphasize quadriceps strengthening and stretching.
Page 379
Arthroscopic excision of pathologic plica may be necessary if conservative treatment fails.
Popliteus Tendinitis Popliteus tendinitis is an uncommon and often misdiagnosed injury of the posterior aspect of the knee. The popliteus forms part of the floor of the popliteal fossa. It is a small, flat muscle that passes beneath the lateral head of the gastrocnemius and inserts onto the posterior aspect of the proximal tibia. This tendon is surrounded by a synovial bursa that separates it from the fibular collateral ligament, femoral condyle, and capsule. The popliteus muscle has two primary functions. First, it functions to internally rotate the tibia. Second, it acts to withdraw the meniscus during flexion to prevent impingement between the femur and the tibia. A third function, along with the quadriceps and PCL, is to stabilize the knee by preventing forward displacement of the femur on the tibia. Overuse injuries involving the popliteus are generally the result of quadriceps overuse. The condition usually occurs in athletes and often causes localized pain over the posterior or posterolateral aspect of the knee.[106] Running and walking downhill often initiate and later exacerbate symptoms caused by the excessive eccentric quadriceps load that occurs with this activity. Usually there is no history of recurrent effusions, locking, or buckling. On physical examination, point tenderness is noted along the lateral joint line on either side of the LCL or at the insertion point of the muscle. Because of its close relationship to other soft tissue structures, the diagnosis may be difficult. The Webb test is a specific provocation test to aid in the diagnosis.[107] This test is performed with the patient supine and the knee flexed 90 degrees. The leg is internally rotated, and the patient is asked to resist the examiner's attempt to externally rotate the leg. Such a maneuver reproduces symptoms and is the most reliable method to diagnose this condition. The differential diagnosis for popliteus tendinitis includes disorders involving structures of the popliteal fossa. Injuries of the iliotibial band, biceps femoris, and lateral head of the gastrocnemius may mimic popliteus tendinitis. In addition, injuries involving the lateral meniscus must be considered in the differential diagnosis; meniscoid pathology generally is associated with a history of locking, recurrent effusion, or recurrent episodes of giving way. Because popliteus tendinitis is almost always a result of quadriceps overuse, treatment requires relative rest and intensive quadriceps rehabilitation. NSAIDs, ice, and physical therapy may be useful adjuncts to treatment. A good response is the rule, and the athlete may return to activity gradually in 10 to 14 days.[106]
Bursitis of the Knee There are numerous bursae about the knee, some of which bear clinical significance. These function to decrease friction between adjacent moving structures. They are usually thin, but with repeated stress may become thickened and fluid filled. The anserine bursa separates the pes anserinus from the distal portion of the MCL and the medial tibial condyle. The prepatellar bursa is located between the patella and the overlying subcutaneous tissues. The superficial infrapatellar bursa is located between the tibial tubercle and the overlying skin. The deep infrapatellar bursa is located between the posterior margin of the distal part of the patellar tendon and the anterior aspect of the tibia. The suprapatellar bursa is not a true bursa, but is an extension of the synovial joint capsule. Bursae usually become inflamed or swollen as a result of repeated stress or infection, but inflammation may occur with local trauma, with crystal deposition, or in association with a systemic inflammatory arthropathy. Its presence must be differentiated from a knee effusion. Prepatellar bursitis is characterized by swelling with effusion of the superficial bursa overlying the lower pole of the patella. Passive motion usually is fully preserved, and the pain is generally mild. The disorder is usually caused by pressure from repetitive kneeling on a firm surface (housemaid's knee).[108] The prepatellar bursa is also a common site of septic bursitis. Suprapatellar bursitis usually is associated with synovitis of the knees. This may be traumatic in origin or may be associated with an inflammatory arthropathy. The superficial infrapatellar bursa is not a common site for bursitis, but may uncommonly follow direct trauma. Anserine bursitis occurs most commonly in obese women in association with osteoarthritis of the knee, but also may occur from overuse, especially in runners. It is characterized by a relatively abrupt onset of knee pain with localized tenderness and a puffy sensation on the anteromedial side of the knee. It may mimic a medial meniscal tear or injury of the MCL. Radiographic studies are usually normal. Ultrasound examination may be useful for the detection of a small fluid collection. MRI may be helpful if the diagnosis remains unclear. These lesions represent encapsulated fluid collections and exhibit low signal intensity on T1-weighted images and high signal intensity on T2-weighted images because of their high content of free water.[109] If there is any uncertainty regarding the
Page 380
possibility of infection, the bursa fluid should be aspirated, and a Gram stain and culture should be performed. Aseptic bursitis is self-limited and can be treated with usual nonoperative modalities, such as ice, rest, and anti-inflammatory medications. Local intrasynovial injection of lidocaine or corticosteroid preparations can be used as an adjunct in the management program to overcome refractory pain.[110] Contraindications to injection therapy are relative and include infections, either local or in the vicinity of the site of involvement, and hypersensitivity to any preparation or substance that might be injected. In septic bursitis, operative drainage may be required in addition to antibiotic therapy.
Osteoarthritis Osteoarthritis is the result of degenerative changes within the joint. The incidence increases with advancing age, obesity, and antecedent trauma. Knee injuries that most commonly cause early arthritic changes in the knee are ACL tears, meniscal damage, and direct injuries of the hyaline cartilage. Removal of the medial meniscus (meniscectomy) increases the risk of osteoarthritis fourfold.[27] Persistent or recurrent episodes of joint instability caused by ligamentous or bony abnormalities commonly result in accelerated arthritis of the knee. Pain is usually the initial complaint and often is aggravated by activity and relieved by rest. Associated complaints of locking, giving way, and a sensation of instability are often present. The physical examination may reveal a gross angular deformity—either genu valgum (knock-knee) or genu varum (bowed legs)—and an antalgic gait may be present. Pain is usually present at the joint line of the involved compartment. Osteoarthritis may involve one or all compartments of the knee. Standard anteroposterior weight-bearing radiographs may reveal narrowing of the joint spaces, peripheral osteophyte formation, subchondral sclerosis, and cyst formation; they also may show angular deformity of the knee. Lateral and oblique films may show the presence of peripheral osteophytes and loose bodies. Tangential sunrise views are needed to evaluate the patellofemoral joint for osteophytes, sclerosis, and maltracking. The treatment options for early arthritis in young patients are limited. Initial treatment consists of restricting activities, providing NSAIDs, bracing, and strengthening quadriceps and hamstrings. Ambulatory assistance with a cane may be helpful to unload the affected extremity and provide symptomatic relief. If the patient is obese, weight reduction is recommended. Surgical treatment is used for advanced cases and may involve high-tibial osteotomy, hemiarthroplasty, or total knee arthroplasty in selected cases. Currently, total knee replacement is contraindicated in persons younger than age 40 except for patients with rheumatoid arthritis.[ 27] Total knee replacement may provide excellent pain relief and improved range of motion but does not allow the patient to return to sports or heavy working activities because these contribute to early loosening and failure of the prosthesis.[111] Overall, longevity of the prosthesis is a major limitation, with most lasting only 10 to 15 years. Research has identified cartilage transplantation and use of biosynthetic cartilage as future options in degenerative knee arthritis, but more work is needed.
Septic Arthritis The most common joint affected with septic arthritis is the knee. The knee is involved 40% to 50% of the time, followed by the hip (20% to 25%) and the shoulder (10% to 15%).[112] Hematogenous seeding is the most common route of spread. The incidence of septic arthritis is higher in individuals with a history of trauma to the joint, especially individuals with penetrating injuries. Bacterial spread usually affects the vascular synovial membrane, then extends into the joint. Although Neisseria gonorrhoeae has been reported to be the most common organism causing septic arthritis, a study has suggested that Staphylococcus infection may occur more often.[113] Nongonococcal arthritis is more common at the extremes of age, often in an immunocompromised host. Gonococcal arthritis commonly affects young, sexually active adults, especially women.[114]
Popliteal (Baker's) Cyst A Baker's, or popliteal, cyst also may be considered in the differential diagnosis of pain in the popliteal region. This lesion of the posterior aspect of the knee is a herniation of the synovial membrane through the posterior aspect of the capsule of the knee, or it may occur through escape of fluid via the normal communication of an anatomic bursa adjoining the semimembranosus or gastrocnemius ( Figure 54-10 ). It is usually the result of an internal knee derangement with recurrent synovitis caused by a torn meniscus, loose body, instability, degenerative change, or other factors. This condition generally causes a mass of varying size occupying the posteromedial corner of the knee and often produces pressure, pain, and limitation of range of
Page 381
motion. Rupture of the bursa with resultant escape of fluid into the calf may produce a clinical picture similar to thrombophlebitis. Although a popliteal cyst can be treated by aspiration or even surgical excision, spontaneous disappearance is common, and no treatment is usually required. Differentiation from other clinical entities may require aspiration, ultrasound, or MRI. Management must be directed at the basic underlying intra-articular pathology to prevent recurrence.
Figure 54-10 Baker's cyst is an extension of the semim em branosus bursa posteriorly. This bursa often is connected with a joint cavity.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/128.html/top
Page 382
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
LOWER LEG PERSPECTIVE Bony and soft tissue injuries of the lower leg are common. The lower leg's vulnerable position to injury, in combination with specific anatomic features unique to the leg, results in various conditions, some of which occur acutely. Other conditions occur some interval of time after the injury itself.
PRINCIPLES OF DISEASE Anatomy and Pathophysiology The bony structure of the lower leg is relatively simple, consisting of the tibia and fibula. The tibia is the only weight-bearing bone. The shaft of the tibia is triangular in cross section and poorly covered with soft tissue over its anteromedial aspect. Given its subcutaneous course, it is not surprising that the tibia is the most common long bone to be fractured and to sustain open fracture. In addition, the lack of overlying musculature results in a tenuous blood supply, which increases the rate of osteomyelitis and contributes to the commonly observed delayed union and nonunion after tibial fractures. The distal end of the tibia is expanded and bears an additional surface, the fibula notch, for the lower tibiofibular joint. The medial malleolus projects from the distal medial aspect of the bone and is grooved posteriorly by the tibialis posterior tendon. The lower inferior surface of the distal tibia is covered with articular cartilage and forms the tibial plafond, the upper anterior surface of the ankle joint. The fibula, in contrast to the tibia, is well covered throughout most of its length except at the ankle, where it is subcutaneous and easily palpable. The fibula is composed of the head with a styloid process, the neck, the shaft, and the lower end or lateral malleolus of the ankle joint. The tibia and fibula are connected by a superior and inferior tibiofibular joint and an interosseous membrane. The latter is a fibrous band that has particular importance at the distal portion of the lower leg, where it is responsible for keeping the tibia and fibula closely approximated to provide a stable ankle mortise. Disruption of this membrane may have clinical significance because it may cause a widening of the distance between the tibia and the fibula and result in disrupted ankle joint function. The lower leg is divided into anterior, lateral, superficial posterior, and deep posterior compartments by deep partitions of the investing crural fascia. The anterior compartment contains the tibialis anterior, the long toe extensor muscles, the deep peroneal nerve, and the anterior tibial artery. The deep peroneal nerve supplies sensation to the first web space of the foot. The lateral compartment contains two muscles that evert the foot, the peroneus longus and brevis. No major arteries are contained in this compartment. The superficial peroneal nerve supplies sensation to the dorsum of the foot. The posterior compartment of the leg is divided into superficial and deep divisions. The superficial posterior compartment contains the strong plantar flexors of the ankle, the gastrocnemius, plantaris, and soleus muscles. The sural nerve passes through the superficial compartment for a variable distance before piercing the fascia to supply the lateral side of the foot and distal calf. The deep posterior compartment contains the tibialis posterior muscle, the long toe flexor muscles, the posterior tibial and peroneal arteries, and the tibial nerve, which supplies sensory function to the plantar aspect of the foot. Each compartment has a sensory nerve that runs through it, an anatomic fact that can be used to help diagnose an incipient compartment syndrome. The vascular supply of the lower leg develops from the popliteal artery, which trifurcates to form three branches: the anterior tibial artery, which passes into the anterior compartment; the posterior tibial artery; and the peroneal artery. The anterior tibial artery can be assessed by palpating the dorsalis pedis artery pulse over the dorsum of the foot, and the posterior tibial artery pulse can be palpated posterior to the medial malleolus.
MECHANISMS OF INJURY AND MANAGEMENT Proximal Extra-articular Tibial Fractures
Page 383
Subcondylar Tibial Fractures Isolated subcondylar fractures are not seen often, and most are associated with tibial plateau fractures, especially bicondylar fractures.[30] Subcondylar fractures involve the proximal tibial metaphysis and are typically transverse or oblique. The mechanism of injury involves a rotational or angular stress accompanied by vertical compression. Examination reveals tenderness and swelling of the involved area. A hemarthrosis may indicate extension of the fracture line into the joint or associated ligamentous injury. Routine radiographs are usually adequate in showing the fracture line. Subcondylar fractures are commonly associated with tibial plateau fractures and are subject to similar complications. Emergency department management includes ice and immobilization with a long leg posterior splint. Stable extra-articular nondisplaced transverse fractures usually are treated conservatively with a long leg splint followed by cylinder casting. Comminuted fractures or fractures associated with an intra-articular (condylar) component require open reduction and internal fixation or may be treated with traction.
Tibial Tubercle Fractures Anatomy and Pathophysiology Anatomically the tubercle of the tibia is at the proximal anterior border of the shaft and gives attachment to the ligamentum patella. The anterior aspect of this tubercle is subcutaneous except for the infrapatella bursa immediately in front of it. The proximal tibial epiphysis and the tibial tuberosity develop from two separate ossification centers that coalesce during adolescence. Epiphyseal ossification terminates in late adolescence. Avulsion fractures of the tibial tubercle are uncommon. They occur predominantly in adolescent boys, most commonly at age 15 or 16 years.[115] The injury typically occurs near the end of growth, when endochondral ossification of the physeal cartilage of the tibial tubercle occurs. Avulsion fractures mainly occur as an indirect injury during sporting activities or active play.[115] The mechanism of injury has been described as a violent flexion of the knee against a tightly contracted quadriceps muscle, and the injury may be a surrogate patellar tendon rupture. An avulsion fracture occurs when the tensile force brought about by the contraction of the quadriceps complex overcomes the cohesive force within the apophyseal cartilage. Watson-Jones described three grades of injury depending on the extent of displacement ( Figure 54-11 ). In type I injuries, the tubercle is hinged upward without displacement from the proximal base. The type II injury has a small portion of the tubercle avulsed, but it is retracted proximally. The articular surface is not involved. Type III fractures are more severe and extend across the articular surface. There is displacement of the fragment and often comminution.
Figure 54-11 Tibial tuberosity fractures.
Clinical Features Physical examination reveals acute tenderness and swelling at the anterior aspect of the knee and proximal tibia. Depending on the type of injury, there is functional disability ranging from extensor lag to complete loss of active extension. Hemarthrosis is evident with type III injury because of intra-articular fracture extension across the proximal epiphysis.
Diagnostic Strategies Plain radiographs generally confirm the clinical diagnosis. The lateral view shows the avulsion fracture, number of fragments, and amount of displacement. Swelling of the overlying soft tissue is evident. Comparison views may be necessary when a type I injury is suspected. The only differential diagnosis that may lead to confusion with avulsion fractures of the tibial tuberosity is Osgood-Schlatter disease; however, significant clinical and radiographic differences exist to distinguish the two pathologic conditions. Osgood-Schlatter disease typically is associated with chronic pain in the anterior tibial tuberosity in adolescents participating intensively in sports. Functional disability is never complete, and Osgood-Schlatter disease is never accompanied by hemarthrosis. Active extension of the knee is possible, although painful. Radiographs may show an irregularity or fragmentation of the tibial apophysis.
Management
Page 384
Treatment depends on the degree of displacement and the presence of joint involvement. Nondisplaced, type I avulsions are treated with cast immobilization with the knee in extension until healing results. Such treatment has consistently provided good results. Minimally displaced, type II avulsions may be treated similarly if the displacement can be reduced by external manual maneuvers. Displaced, type III fractures are treated by open reduction and internal fixation to restore proper biomechanics and joint congruity. Fixation screw and tension band wiring techniques have yielded excellent results. After a period of immobilization and progressive rehabilitation, most patients are able to return to full activity. Complications of tibial tubercle fractures include genu recurvatum, patella alta, meniscal tears, failure of surgical fixation, and subsequent heterotopic ossification and osteonecrosis of the tubercle.[2] Because the involved growth plates are closing at the time of injury, premature physeal closure rarely results in a significant recurvatum deformity.
Osgood-Schlatter Disease Anatomy and Pathophysiology Tibial tubercle apophysitis was first described by Osgood and Schlatter in 1903.[] Trauma was postulated to be the cause of this condition. Seventy years later, Ogden provided histologic support for a traumatic etiology. His work revealed evidence of repetitive microtrauma and subsequent healing of the develop-ing tibial tubercle. It is now believed that OsgoodSchlatter disease is an apophysitis caused by repeated traction to the anterior portion of the developing ossification center of the tibial tuberosity. This traction apophysitis affects pubescent children in the midst of the adolescent growth spurt. Organized sporting activities commonly are associated with the onset of symptoms, with a fivefold increase in the incidence of Osgood-Schlatter disease in athletically active boys compared with the incidence in nonathletic controls.[118] Past reports have suggested a large male predominance for the development of Osgood-Schlatter disease. As more girls and young women have joined competitive sports, however, no significant sex differences have been found.[118] The development of this disorder seems to depend on the degree of skeletal maturity and activity level rather than gender.
Clinical Features The disease is characterized by painful swelling over the tibial tubercle, which is exacerbated by activity, is relieved by rest, and is usually of several months' duration. The tubercle may appear abnormally prominent, often on both sides. There is pain on resisted extension of the flexed knee and occasionally an extensor lag. Tenderness is most noticeable at the insertion of the patellar tendon. Bilateral involvement is noted in 20% to 30% of patients.
Diagnostic Strategies The diagnosis of Osgood-Schlatter disease is based on clinical signs and symptoms. Radiographs of the knee may be useful to exclude other pathologic entities (e.g., tumors, infection, and avulsion fractures), but generally are not required. They typically reveal pretibial soft tissue edema or prominence of the tubercle. Fragmentation of the ossification center is an unreliable sign because ossification patterns of the tubercle are highly variable.
Management Treatment varies according to the acuteness of the symptoms and the skeletal age of the patient. Initially, rest, ice, and analgesics are the mainstays of therapy. As symptoms subside, a rehabilitation program that stretches and strengthens the quadriceps muscle unit should be instituted. Knee orthoses are used to dampen the pull of the extensor mechanism on the weakened tibial apophysis. Immobilization is reserved for the unreliable patient who will not or cannot comply with the program of relative rest in which aggravating activities are avoided. For children with severe symptoms, immobilization for 2 to 3 weeks may be used. Despite conservative management, some children continue to experience symptoms referable to the tibial tubercle. Surgery may be required if the conservative treatment fails, but it cannot be implemented until the epiphysis is closed, at which time the problem usually is resolved.
Tibial Shaft Fractures Anatomy and Pathophysiology Because the tibia and fibula run parallel and are tightly bound to each other, a displaced fracture of one bone typically is associated with an obligatory fracture or ligamentous injury of the other bone. The fibula remains intact in only 15% to 25% of tibial shaft fractures.[119] Similar to tibia plateau fractures, tibial shaft fractures can affect knee alignment, stability, and strength. Compared with other fractures, these are associated with
Page 385
a high incidence of infection, delayed union, nonunion, and malunion. Tibial diaphyseal fractures may result from either direct or indirect trauma and may be secondary to low-energy or high-energy mechanisms. Direct trauma, as seen with vehicular accidents and certain types of skiing injuries, is the most common mechanism of injury.[120] This typically results in transverse or comminuted fractures and reflects high-energy injury, particularly when the fracture is greatly displaced, severely comminuted, or associated with a fibular fracture. Indirect trauma is associated with low-energy rotatory and compressive forces, such as from skiing, a fall, or child abuse, and usually results in a spiral or oblique fracture.[120] Tibial fractures also may occur without antecedent trauma. Pathologic fractures are uncommon in the tibia but should be suspected when there is no significant mechanism of injury. Pathologic fractures may be caused by metabolic bone disease; osteomalacia; or benign, metastatic, or primary bone neoplasms. Stress fractures occur most commonly in the tibial shaft. Periosteal reaction is often delayed in such cases, and repeat radiography, bone scans, or tomography may be required to establish the diagnosis. A toddler's fracture is an often subtle, nondisplaced spiral fracture of the distal tibia in 9-month-old to 3-year-old children. [121] Children may have acute onset of a limp or refusal to bear weight. The classic distal fracture often relates to accidental trauma as opposed to a midshaft fracture, which correlates with nonaccidental trauma. Orthopedic differences in children revolve around two basic features in the immature or growing musculoskeletal system: the potential for growth and the greater elasticity of bone, cartilage, and soft tissue.[ 119] A child's bone is more porous than an adult's, permitting the bone to bend, buckle, and sustain a greenstick fracture, all of which are unknown in adults. Buckle fractures usually occur in the metaphysis of long bones, such as the tibia or fibula. Radiographically, they manifest as an often subtle buckling without angulation in contrast to the smooth line formed by the normal cortex. A greenstick fracture is a bending fracture, with a break in the periosteum and cortex of the convex side of the angulated bone. These fractures are stable with an intact periosteum so that swelling, crepitance, and mobility at the fracture site are minimal.
Clinical Features Tibial shaft fractures cause pain, swelling, and deformity of the leg, usually angulation or rotation of the foot. After visual inspection of the injured leg, determination of vascular integrity remains the highest priority. Distal dorsalis pedis and posterior tibial pulses should be assessed. Severe lower limb fractures complicated by vascular injuries are uncommon, with an incidence estimated at 0.1%.[122] Anterior compartment syndromes may follow tibial fractures and usually occur within the first 24 to 48 hours. A careful neurologic examination also must be documented because it serves as a baseline against which subsequent examinations can be compared. Because the peroneal nerve is commonly damaged in lower extremity injuries, its function must be assessed. Motor function of the peroneal nerve is checked by testing active ankle and toe dorsiflexion (deep peroneal nerve function) and active foot eversion (superficial peroneal nerve function). Sensory function of the peroneal nerve is documented by testing sensation in the first dorsal web space in the foot (deep peroneal nerve distribution) and sensation of the dorsal lateral foot (superficial peroneal nerve distribution). Integrity of the posterior tibial nerve is assessed by the presence or absence of plantar sensation. Significant soft tissue damage also may accompany tibial shaft fractures. One study finds a 22% incidence of injury to at least one ligament of the knee.[123] A thorough examination of knee stability is indicated after fracture stabilization, especially in high-energy injuries.
Diagnostic Strategies Anteroposterior and lateral x-ray studies are mandatory to document the fracture, define the fracture pattern, and identify any associated bone loss ( Figure 54-12 ). The knee and ankle must be included in both views, and additional x-ray studies of the pelvis and ipsilateral femur may be required to assess for associated injuries. Postreduction views should be taken after any manipulation of the extremity and should include the knee and ankle joints so that alignment of the proximal and distal joint surfaces can be determined.
Figure 54-12 Tibiofibular fracture. A Anteroposterior view. Com m inuted fractures of the tibial and fibular shafts are present. Note the obliteration of the normal soft tissue planes because of edem a or hem orrhage. B Lateral view. ((From Rosen P, et al:
Page 386
Diagnostic Radiology in Em ergency Medicine. St. Louis, Mosb y, 1992, p 198.)Elsevier Inc.)
Management Open tibial fracture usually is encountered in a multiply injured patient. Unstable high-energy fractures usually are associated with injuries of multiple organ systems and often occur in conjunction with multiple fractures. Open fractures may seem to be associated with more complications than closed fractures; however, closed fractures may be associated with more soft tissue damage. Classification of a tibial fracture as closed or open does not indicate its severity. One of the most prognostically important distinctions is between fractures produced from high-energy forces and fractures from low-energy forces. In all studies of tibial shaft fractures, the fractures that result from high-energy trauma always have a poorer prognosis than the fractures that result from low-energy trauma. After life-threatening injuries have been evaluated, fracture management should follow. The initial management of closed tibial shaft fractures consists of immobilization in a long leg posterior splint with 10 to 20 degrees of knee flexion. This may require analgesia and sedation. Generally, after fractures are immobilized, the pain decreases. If the patient complains of continued severe pain after immobilization, a complication such as nerve root compression or limb ischemia should be considered, and additional in-juries should be sought. A circumferential cast should be avoided in the acute setting because of the risk of compartment syndrome. Initial hospitalization is indicated for most patients with significant tibial shaft fractures for pain control, observation for compartment syndrome, long leg casting, and instruction in crutch walking. Emergency department treatment of open tibial shaft fractures should be directed at four interventions. First, open fractures should be covered with a sterile dressing. Second, a long leg posterior splint should be applied. Third, if tetanus immunization is not current, appropriate tetanus prophylaxis should be given. Fourth, most authors also recommend empiric antibiotics for open fractures. Intravenous antibiotic prophylaxis using a first-generation cephalosporin is recommended. In tibial fractures caused by highvelocity injuries that have extensive soft tissue defects and significant wound contamination, a loading dose of an aminoglycoside may be given in addition to the first-generation cephalosporin. Emergency operative debridement with external or internal fixation is recommended as soon as possible for open tibial fractures with significant soft tissue disruption. The incidence of osteomyelitis is related in part to the time between contamination and definitive debridement and stabilization of the open fracture site. Open tibial fractures have a fivefold increased risk of developing osteomyelitis, and the incidence of infection correlates directly with the extent of soft tissue damage and classification. In general, tibial fractures are slow to heal. Delayed union is generally applied to fracture segments that have not united after 20 weeks. The average time to union is approximately 20 weeks for stable tibial shaft fractures caused by a low-energy mechanism and more than 30 weeks for unstable fractures caused by a high-energy mechanism.[124] At times, nonunion may occur. Nonunion is a radiographic diagnosis, with a finding of rounded, well-corticated edges of the major fracture fragments. It is much more common in adult long bone fractures than childhood fractures, which generally are characterized by rapid healing. Delayed vascular injuries also may occur as a complication of tibial shaft fractures, including pseudoaneurysm, arteriovenous fistula, and deep vein thrombosis. Fat embolism also may occur. Additional late complications include malrotation of the leg, re-fracture, and reflex sympathetic dystrophy.
Proximal Fibula Fractures Anatomy and Pathophysiology Isolated proximal fibula and fibula shaft fractures are uncommon, and fibula fracture is usually seen in association with a tibial fracture. Clinically, fibula fractures are relatively unimportant because no significant weight is supported by the fibula. The mechanism of injury is usually a direct blow to the lateral aspect of the leg or an indirect varus stress to the knee. An exception to this is Maisonneuve fracture, which is a proximal fibula fracture with an associated ankle fracture or deltoid ligament tear ( Figure 54-13 ). The mechanism resulting in Maisonneuve fracture is often an external rotatory force applied to the ankle that results in partial or complete syndesmotic disruption.
Page 387
Figure 54-13 Maisonneuve's fracture, anteroposterior view. The rotatory force involved in this injury has caused fractures of the distal tibia and the proxim al fibula (arrows). ((From Rosen P, et al: Diagnostic Radiology in Em ergency Medicine. St. Louis, Mosb y, 1992, p 197.)Elsevier Inc.)
Clinical Features Isolated fibula shaft fractures cause lateral leg pain that is exacerbated by walking. Local pain, swelling, and tenderness at the fracture site may be elicited. Palpation of the proximal fibula should be performed whenever significant ankle injury is present to assess for a Maisonneuve fracture. A thorough evaluation should be done to exclude serious associated occult neurovascular or ligamentous injuries. The common peroneal nerve courses around the proximal neck of the fibula and may be contused or lacerated at the time of injury. The LCL may be ruptured or strained in association with the fracture, and anterior tibial artery injury with thrombosis may occur.
Diagnostic Strategies Radiographic evaluation should be undertaken in cases of suspected proximal fibula fracture. Anteroposterior and lateral radiographs should include the knee and ankle joints and confirm the fracture pattern. A bone scan may be required for diagnosis if a fibular stress fracture is in question.
Management Isolated uncomplicated fibula shaft fractures are treated symptomatically with ice, analgesia, and non– weight bearing. Immobilization in a long leg cast is rarely done but may provide symptomatic relief beginning 2 days after the acute injury. The patient should remain non–weight bearing until a small amount of weight can be tolerated. Weight bearing may be advanced progressively as tolerated. Patients with nondisplaced or minimally displaced fractures may have little pain and tolerate crutch walking without casting well. In general, isolated fibula shaft fractures can be managed on an outpatient basis and heal without complication. For severely displaced fibula shaft fractures or fractures with associated peroneal nerve deficit such as footdrop, orthopedic consultation is indicated. Cast immobilization is not recommended in cases with concomitant nerve damage, and follow-up is scheduled at a shorter interval from injury. Elective surgical repair may be indicated if function does not return. Maisonneuve fracture is associated with partial or complete syndesmotic diastasis and may result in an unstable ankle mortise. Stress radiographs are necessary, and operative repair may be indicated.
Proximal Tibiofibular Joint Dislocations Anatomy and Pathophysiology The proximal tibiofibular joint is a small synovial joint between a circular or oval facet on the head of the fibula and a similar facet on the inferior aspect of the lateral tibial condyle. The proximal tibiofibular joint is stabilized by the joint capsule and the anterior and posterior tibiofibular ligaments. Dislocation of the proximal tibiofibular joint is rare, occurring most commonly in adolescents and young adults because of its association with motor vehicle accidents and sporting injuries.[125] Several types of dislocations of the joint have been described; anterolateral dislocation is the most common and usually is caused by a fall on a flexed, abducted leg.[126] Posterior medial dislocation generally is caused by a direct blow to the flexed knee and is more often associated with peroneal nerve injury. Superior dislocation is associated with ankle diastasis and typically occurs simultaneously with an ankle fracture.
Clinical Features The patient may complain that the knee feels out of place, or if the problem is chronic, the knee may lock or give way periodically. Physical examination reveals tenderness and fusiform swelling over the proximal fibula and tibiofibular joint. In the absence of associated injury, the knee examination is normal, with full range of motion and no joint line tenderness or effusion.
Diagnostic Strategies
Page 388
Plain radiography may confirm the diagnosis. On the anteroposterior view, the fibula head is displaced laterally, and the interosseous space is widened. Comparison views of the uninjured knee may be necessary to appreciate these findings. If the diagnosis is still suspected but not confirmed by plain radiography, an axial CT scan may be obtained.
Management Traumatic proximal tibiofibular dislocation is treated initially with closed reduction. If the patient seeks treatment within a few days of injury, reduction of an anterior lateral dislocation can be accomplished in the emergency department by flexing the knee to 90 degrees, everting the ankle, and applying direct pressure to the head of the fibula.[126] Immobilization of the knee for a minimum of 3 to 6 weeks is necessary after reduction. Failure of closed reduction may require open reduction, with repair of the torn capsule ligaments and pinning. Recurrent cases or cases that do not respond to initial treatment may be treated with resection of the proximal fibula or arthrodesis.
Stress Fractures Anatomy and Pathophysiology Stress fractures are common skeletal lesions, and most involve the lower limbs. The specific anatomic sites vary depending on the athletic activity. The most common site of stress fracture in the athlete is the tibia, accounting for 50% of stress fractures in some series.[127] Usually the stress fracture occurs on the tibial shaft. Fractures are typically horizontal or oblique, with only 10% reported to be longitudinal.[128] Other sites include the femur, fibula, tarsal navicular, and metatarsal. Stress fractures result from repetitive cyclic and prolonged muscle force on bone and have been well described as overuse injuries in military recruits and athletes.[129] Fatigue fractures occur in normal bone because of abnormally increased stress and commonly are related to activities such as running, jumping, marching, or ballet dancing. Insufficiency fractures occur when normal stresses are applied to bone deficient in mineral content or abnormally inelastic bone. These injuries typically occur in postmenopausal, osteoporotic women, but also are found in patients with osteopenia of any cause, including renal osteodystrophy, rheumatoid arthritis, and diabetes mellitus. Stress fractures are distinguished from pathologic fractures, which occur through bone weakened by tumor. The incidence of stress fractures in the general population has not been studied. Most studies on stress fractures have concentrated on specific populations that are predisposed to their occurrence, particularly military recruits and athletes. These fractures may constitute 10% of all sports injuries and account for 5% to 15% of all running injuries.[129] Several factors have been associated with the development of stress fractures. Military recruits typically undergo a vigorous training program over a short period that does not allow sufficient time for proper bone remodeling. Women have been reported to have a higher incidence of stress fractures, which may be related to differences in bone mass, body mass, body habitus, musculoskeletal fitness, or endocrine factors. [130] Race also may play a role in the development of stress fractures. Several reports indicate a higher incidence of stress fractures in whites compared with African Americans. This difference has been attributed to the greater average bone mass in African Americans.
Clinical Features Clinically the patient exhibits bone pain and tenderness without a history of direct trauma. The diagnosis of stress fractures can be difficult because of limited presenting signs and minimal or no initial radiographic findings. The most important historical information includes a recent increase in physical activity, training on hard surfaces, and inadequate footwear. The pain is usually insidious in onset and progressive but may be sudden. Classically a patient with a stress fracture describes pain associated with a particular activity that is relieved with rest and worsened with continued activity. The relationship between bone pain and stress fractures has been studied using nuclear scintigraphy, and it seems that stress fractures may be present even when pain is poorly localized or absent. The differential diagnosis of lower leg pain also includes shin splints, exercise-induced compartment syndrome, contusion, muscle strains, tendinitis, periostitis, and interosseous membrane strains. The physical examination may reveal localized bony tenderness and swelling of the overlying soft tissues. Usually there is no muscle atrophy, weakness, or restriction of joint range of motion.
Diagnostic Strategies The radiographic findings vary depending on the location of the fracture and the stage in the repair process at which the radiograph is taken. Only 30% of stress fractures are evident radiographically at the time of initial diagnosis, whereas approximately 50% of treated stress fractures are associated with radiographic
Page 389
findings after 2 to 6 weeks. The radiographic findings are often subtle and may include periosteal new bone, sclerosis, and a lucent line perpendicular to the cortex. If a stress fracture of the lower extremity is suspected and initial plain radiography is unremarkable, a follow-up in 10 days to 2 weeks may detect radiographic signs of fracture after a period of inactivity. Evidence of healing in response to treatment usually suffices to confirm the diagnosis. If the patient cannot comply with a prescription of rest or if an urgent definitive diagnosis is needed, additional diagnostic studies may be done. Technetium diphosphate bone scintigraphy may be positive 3 days after the onset of symptoms of a stress fracture and has a sensitivity that approaches 100%. Typically, bone scans show a focal area of increased radiotracer uptake on the delayed images in the region of the stress fracture. Bone scintigraphy cannot distinguish fracture from infection or neoplasm and is less specific than plain radiography. The roles of plain tomography, CT scan, and MRI are uncertain at this time. These studies may be used to gain added specificity in cases that remain indeterminate on prior radiographic studies. Early detection and treatment of stress fractures before the development of cortical disruption prevent increased morbidity and possible disabling sequelae.
Management Most tibial and fibula stress fractures can be treated nonoperatively. Generally activities should be decreased for 3 to 6 weeks to allow for healing, and serial radiographs should be obtained. In rare instances in which walking causes pain, a cast and non–weight bearing may be required. Serial radiographs are used to evaluate healing. Surgery is reserved for rare patients with tibial stress fractures who have failed nonoperative treatment and have developed characteristic radiographic findings of nonunion.[129]
Compartment Syndrome in the Lower Leg Compartment syndrome is generally defined as the necrosis of muscle and nerve secondary to increased tissue pressure within an osteofascial compartment and is discussed in Chapter 46 .
Soft Tissue Injuries Involving the Lower Leg Strains Gastrocnemius Strain In the lower extremity, the medial head of the gastrocnemius muscle is especially prone to strain injury. A sudden push-off can tear the gastrocnemius muscle or musculotendinous junction, resulting in the so-called tennis leg. The mechanism of injury seems to be a sudden ankle dorsiflexion in the involved leg in which the knee has been previously extended and the ankle plantar flexed. This position is commonly encountered in the back leg of an athlete during the follow-through of a tennis serve. Predisposing factors include increasing age, inadequate stretching, fatigue, and previous muscle injury. The athlete experiences a sudden, intense pain in the posterior and medial aspect of the calf, swelling, diffuse tenderness, and variable loss of function. On physical examination, a palpable gap may be identified in the substance of the muscle, and point tenderness may be elicited in the medial and inferior borders of the muscle belly. Any attempted active or passive ankle dorsiflexion elicits severe pain. Gastrocnemius strain or rupture may be confused with rupture of the plantaris tendon, which causes tenderness, swelling, and ecchymosis in the proximal calf; rupture of a Baker's cyst, which may result in the escape of fluid into the calf, mimicking thrombophlebitis; and Achilles tendon rupture, which typically results in a palpable gap just proximal to the os calcaneus. If the diagnosis of a soft tissue injury is in doubt, imaging may be useful. Plain radiography is of no help except to exclude an avulsion fracture. MRI is superior to plain radiography and CT as an imaging modality for muscle strain injury. A mild partial rupture of the medial head of the gastrocnemius can be treated with rest and non–weight bearing for several days. Treatment for an incomplete rupture is casting in equinus position for 8 weeks. For a complete tear, most orthopedists recommend surgical repair to restore normal length and tensile strength. Acute compartment syndrome has been reported as a complication of gastrocnemius strain.[131]
Plantaris Strain and Rupture The plantaris is a small, variable, pencil-sized muscle that originates at the lateral condyle of the femur and passes beneath the soleus to attach on the Achilles tendon. It is a feeble flexor of the knee and plantar flexor of the ankle joint with little functional significance. Rupture may occur at the myotendinous junction with or without an associated partial tear of the medial head of the gastrocnemius muscle. A strain of the more proximal plantaris muscle also may occur as an isolated injury or in conjunction with injury to the ACL.[132]
Page 390
The patient may complain of a sudden sharp snap in the posterior calf followed by a duller deep ache, which may be disabling. Tenderness is greatest just lateral to the midline of the posterior calf. Repair is not needed here; only symptomatic treatment is indicated.[120]
Shin Splints The term shin splints refers to nonspecific, anterior lower leg pain, usually during or after exercise. The most common causes are a tibial stress reaction or periostitis. Tibial stress reactions are microfractures caused by stress placed on the tibia. The clinical spectrum may range from mild exertional lower leg pain to severe debilitating pain localized to the anterior tibia. The history is important in making the diagnosis of this overuse injury; it occurs most commonly in runners and is often bilateral. Bilateral symptoms are usually seen with chondromalacia, Osgood-Schlatter disease, and anterior tibialis syndrome. Other injuries, such as plantar fasciitis and Achilles tendinitis, are usually unilateral. Shin splints also can be confused with stress fractures. The physical examination reveals direct localized tenderness over the tibia or medial tibial crest, usually at the junction of the middle and lower thirds of the tibia. Radiographic studies are not helpful in the diagnosis of shin splints but may help exclude a tibial stress fracture. Shin splints, similar to other overuse injuries, are associated with the development of inflammation. The goal of treatment is to reduce inflammation through rest, use of NSAIDs, and alteration of activities. The duration of rest varies with the spectrum of the disease; however, several weeks is usually sufficient.
Foreign Bodies Soft tissue foreign bodies are a common cause of emergency department visits and may account for 4% of liability claims against emergency physicians.[] Early detection can be challenging, especially if a foreign body is small and radiolucent. Wood and plastic pieces can be elusive on plain films. Plain radiographs are 95% to 100% sensitive in detecting radiopaque objects but not as helpful in detecting radiolucent foreign bodies.[] Foreign bodies to the lower extremity are especially prevalent in children and adolescents. Missed retained foreign bodies to the lower leg can lead to devastating consequences, such as cellulitis, abscess formation, myonecrosis, necrotizing fasciitis, and gangrene. Plain films remain the standard, but when plain films are inconclusive, other modalities, such as ultrasound or CT, must be employed. Surgical exploration remains the diagnostic and therapeutic modality of choice.
About MD Consult | Contact Us | Terms and Conditions | Privacy Policy | Registered User Agreement Copyr ight © 2006 Elsevi er Inc. All rights reserv ed.
www.mdconsult.com
Bookmark URL: /das/book/view/60636217-2/1365/129.html/top
Page 391
Use of this content is subject to the Term s and Conditions of the MD Consult web site.
Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Copyright © 2006 Mosby, Inc.
Chapter 4 – Shock Alan E. Jones Jeffrey A. Kline
PERSPECTIVE In philosophic terms, shock can be viewed as a transition between life and death. Whether shock results from hemorrhage, sepsis, or cardiac failure, mortality rates exceed 20%.[] In scientific lexicon, shock results from the widespread failure of the circulatory system to oxygenate and nourish the body adequately. In the laboratory, the scientist defines the metabolic effect of shock quantitatively, by examining the mechanisms by which shock alters mitochondrial energy transfer, evokes the production of toxic chemicals, and reduces their removal. At the bedside, the clinician identifies shock by linking the clinical impression, synthesized from the patient's history of present illness, age, underlying health status, and general appearance, to quantitative data, including vital signs, blood chemistry, urine output, and direct measurements of oxygenation. When the clinical impression and the quantitative data suggest widespread inadequate organ perfusion, emergent resuscitation must restore normal tissue oxygenation and substrate delivery to prevent deterioration into systemic inflammation, organ dysfunction, and death.
Classification For years, shock has been classified into four broad categories based on Blalock's 1934 description: hematological, neurologic, vasogenic, and cardiogenic.[3] Although it seems archaic to classify a gunshot wound as “hematologic” shock, this basic organization scheme remains useful today. Box 4-1 outlines five categories of shock that generally have specific mechanisms and treatments. BOX 4-1 Categories of Shock According to Primary Treatment
Causes That Require Primarily the Infusion of Volume Hemorrhagic shock Traumatic Gastrointestinal Body cavity Hypovolemia Gastrointestinal losses Dehydration from insensible losses Third-space sequestration from inflammation
Causes That Require Improvement in Pump Function by Either Infusion of Inotropic Support or Reversal of the Cause of Pump Dysfunction Myocardial ischemia Coronary artery thrombosis Arterial hypotension with hypoxemia Cardiomyopathy Acute myocarditits
Page 392
Chronic diseases of heart muscle (ischemic, diabetic, infiltrative, endocrinologic, congenital) Cardiac rhythm disturbances Atrial fibrillation with rapid ventricular response Ventricular techycardia Supraventricular tachycardia Hypodynamic septic shock (late sepsis) Overdose of negative inotropic drug p -blocker Calcium channel antagonist overdose (e.g., verapamil) Structural cardiac damage Traumatic (e.g., flail mitral valve) Ventriculoseptal rupture Papillary muscle rupture
Causes That Require Volume Support and Vasopressor Support Hyperdynamic sepsis syndrome (early sepsis) Anaphylactic shock Central neurogenic shock Drug overdose (dihydropyridines, p 1-antagonists)
Problems That Require Immediate Relief from Obstruction to Cardiac Output Pulmonary embolism Cardiac tamponade Pneumothorax Valvular dysfunction Acute thrombosis of prosthetic valve Critical aortic stenosis Congenital heart defects in newborn (e.g., closure of patent ductus arteriosus with critical aortic coarctation) Critical idiopathic subaortic stenosis
Cellular Poisons That Require Specific Antidotes Carbon monoxide Methemoglobinemia Hydrogen sulfide Cyanide
Epidemiology The epidemiology of shock in the emergency department remains speculative because shock rarely is listed as a primary coding diagnosis and usually is hidden within another diagnosis. Patients presenting with traumatic, cardiogenic, or septic shock constitute about 1% of all emergency department visits. This chapter reviews the metabolic, systemic, and inflammatory responses that occur in all types of circulatory shock and discusses specific pathophysiology of the major causes of shock.
PATHOPHYSIOLOGY
Page 393
At the subcellular level, shock first affects the mitochondria. Mitochondria function at the lowest oxygen tension in the body, but paradoxically, they consume almost all the oxygen used by the body. More than 95% of aerobic chemical energy comes from mitochondrial combustion of fuel substrates (fats, carbohydrates, ketones) plus oxygen into carbon dioxide and water. Mitochondria have been referred to as the “canaries in the coal mine” because they are affected first in conditions of inadequate tissue perfusion.[] When mitochondria have inadequate oxygen, the cell converts fuels to lactate ( Figure 4-1 ), which accumulates and diffuses into the blood.
Figure 4-1 Energy m etabolism with special reference to the developm ent of lactic acidosis in shock. At site A, oxygen availability to the m itochondrial electron transport system decreases. In the tricarboxylic acid (TCA) cycle (site B), intermediary m etabolites accum ulate, including acetyl coenzym e A (AcCoA), which causes the pyruvate dehydrogenase enzyme com plex (site C) to shut down, leading to accum ulation in pyruvate. At site D, pyruvate is reduced to lactate, which generates oxidized nicotinam ide adenine dinucleotide (NAD+) to perm it anaerobic glycolysis to generate a marginal supply of adenosine triphosphate (ATP). Lactate can diffuse across the cell mem brane through a specific m onocarboxylase transporter in the cytosolic m em brane (dotted horizontal line). ADP, adenosine diphosphate; NADH, reduced nicotinamide adenine dinucleotide.
