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Orthopaedics and Trauma Elsevier, ISSN: 1877-1327, http://www.sciencedirect.com/science/journal/18771327 Volume 25, Issue 3, Pages 161-234 (June 2011) 1
Editorial Board, Page i
Mini-Symposium from the Asia Pacific Region 2
(i) Tuberculosis of the spine, Pages 161-167 W.Y. Cheung, Keith D.K. Luk
3
(ii) Stem cell research in orthopaedic and trauma surgery, Pages 168-173 Seok-Jung Kim, Asode Ananthram Shettey
4
(iii) Peripheral nerve repair, Pages 174-180 Jaiyoung Ryu, Claire F. Beimesch, Trapper J. Lalli
5
(iv) Cervical spondylotic myelopathy: a brief review of its pathophysiology, presentation, assessment, natural history and management, Pages 181-189 Lushun Wang, Hwan Tak Hee, Hee Kit Wong
Shoulder 6
Superior Labrum Anterior to Posterior (SLAP) lesions of the shoulder, Pages 190-197 Bynvant Sandhu, Sanjay Sanghavi, Francis Lam
Foot and Ankle 7
“Not Plantar Fasciitis”: the differential diagnosis and management of heel pain syndrome, Pages 198-206 Munier Hossain, Nilesh Makwana
Quiz 8
Radiology quiz, Pages 207-213 S. Chaganti, N. Venkatanarasimha, S.P. Suresh
Trauma 9
Traumatic hip dislocation, Pages 214-222 O. Obakponovwe, D. Morell, M. Ahmad, T. Nunn, P.V. Giannoudis
Hip 10
Chronic painful conditions of the hip, Pages 223-229 Olivia Flannery, Connor Green, Dominic Harmon, Eric Masterson
CME Section 11
CME questions based on the Mini-Symposium on “Asia Pacific”, Pages 230-231
12
Answers to CME questions based on the Mini-Symposium on “The Shoulder”, Page 232
Book Reviews 13
14
15
Arthroscopic surgical techniques: anterior cruciate ligament reconstruction, Page 233 Ian D. McDermott The AAOS/AAHS surgical techniques in orthopaedics DVD “ Ligament Balancing for Total Knee Arthroplasty”, Page 233
Ian McDermott Joint Replacement Arthroplasty – Basic Science, Elbow and Shoulder. Fourth Centennial Edition, Pages 233-234 Adam Rumian
Orthopaedics and Trauma Orthopaedics and Trauma presents a unique collection of International review articles summarizing the current state of knowledge in orthopaedics. Each issue begins with a focus on a specific area of the orthopaedic knowledge syllabus, covering several related topics in a mini-symposium; other articles complement this to ensure that the breadth of orthopaedic learning is supplemented in a 4 year cycle. To facilitate those requiring evidence of participation in Continuing Professional Development there is a questionnaire linked to the mini-symposium that can be marked and certified in the Editorial office.
Editor-in-Chief D Limb BSc FRCS Ed (Orth) Leeds General Infirmary, Leeds, UK
Editorial Committee M A Farquharson-Roberts (Gosport, UK), I Leslie (Bristol, UK) M Macnicol (Edinburgh, UK), I McDermott (London, UK), J Rankine (Leeds, UK)
Editorial Advisory Board D C Davidson (Australia) J Harris (Australia) G R Velloso (Brazil) P N Soucacos (Greece) A K Mukherjee (India) A Kusakabe (Japan) M-S Moon (Korea) R Castelein (The Netherlands) R K Marti (The Netherlands) G Hooper (New Zealand)
Emeritus Editor Professor R A Dickson MA ChM FRCS DSc Leeds General Infirmary, Leeds, UK
A Thurston (New Zealand) E G Pasion (Philippines) L de Almeida (Portugal) G P Songcharoen (Thailand) R W Bucholz (USA) R W Gaines (USA) S L Weinstein (USA) M Bumbasirevic (former Yugoslavia)
MINI-SYMPOSIUM FROM THE ASIA PACIFIC REGION
(i) Tuberculosis of the spine
and subsequently the immune response is stimulated. A delayed hypersensitivity immune response produces cytokines which in turn leads to recruitment of monocytes, lymphocytes and macrophages. These infected inflammatory cells then form a granuloma and the macrophages differentiate into foam cells, giant cells and epithelioid cells. The centre of the granuloma then caseates and becomes necrotic. The infection can progress to destroy bone, cause pain and lead to collapse of the vertebral body(ies) and kyphosis. Tuberculosis abscesses containing necrotic debris expand following the path of least resistance and beneath the anterior and posterior longitudinal ligaments to the adjacent levels and skin sinuses may form and drain spontaneously. While nerve roots may be compressed causing pain or radiculopathy, more commonly spinal cord or cauda equina compression gives rise myelopathy or paraplegia. This may happen early in active disease due to spinal cord compression by inflammatory tissues, epidural abscess, protruded intervertebral discs, pachymeningitis or spinal subluxation. It may also happen years after the initial tuberculosis infection e late-onset paraplegia e due to severe kyphosis with chronic spinal cord compression and spinal cord atrophy, with or without reactivation of the infection. Late-onset paraplegia may also arise due to due to spinal stenosis above the healed kyphosis.5 To compensate for the kyphotic deformity as a result of the tuberculosis infection, patients hyper-extend their thoracic spine to achieve overall sagittal balance. Such hyper-extension of adjacent levels can lead to early degeneration, spinal stenosis and neurological deficits.
W Y Cheung Keith D K Luk
Abstract The incidence of spinal tuberculosis, which may lead to severe spinal deformity, early and late neurological complications, is increasing. This paper reviews its pathophysiology, clinical presentation, diagnosis and management.
Keywords
diagnosis;
management;
pathophysiology;
spine;
tuberculosis
Epidemiology Worldwide tuberculosis is the commonest infectious disease and about 95% of cases occur in developing countries. The World Health Organization estimates that in China alone there are 1.4 million new cases annually and 1.81 million deaths from tuberculosis in Asia each year. The US Center for Disease Control (CDC) has predicted that the number of new diagnoses of active tuberculosis worldwide will increase from 7.5 to 11.8 million per year. The prevalence will rise from 143 to 173 per 100 000 and deaths due to tuberculosis will climb from 2.5 to 3.5 million or more per year.1,2 This has been attributed partly to an increase in HIV infection because HIV disables and destroys the thymic lymphocytes and tissue macrophages that are the body’s main defence against tuberculosis making those who are HIV-positive extremely susceptible to the disease. In some African countries, the number of reported tuberculosis cases has doubled or even tripled from 2001 to 2003 because of the spread of HIV/AIDS.1,2 While tuberculosis most commonly infects the lungs, it affects the spine in three to five per cent of patients.3 Tuberculous spondylitis, although less common, is the most dangerous form of skeletal tuberculosis.4
Clinical presentation In the early stages of the disease, most commonly there are slowly progressive constitutional symptoms including generalized weakness, malaise, night sweats, fever, and weight loss. Pain is a late symptom associated with bone collapse. While patients may present with neurological symptoms and signs such as lower limb weakness and numbness (Pott’s paraplegia) due to spinal cord or cauda equina compression, with, in severe cases, loss of urinary and bowel control, usually neurological signs occur later in the disease; Jain et al. calculated that the spinal canal can accommodate 76% encroachment on CT scan without neurological abnormality.6 Rarely cervical involvement can cause hoarseness because of recurrent laryngeal nerve paralysis, dysphagia, and respiratory stridor (Millar asthma) due to anterior abscess formation in the neck (Figure 1). Sudden death due to erosion into the great vessels has also been reported in association with cervical disease.
Pathophysiology Tuberculosis of the spine is a potentially life threatening infection caused by Mycobacterium tuberculosis which is an aerobic, weakly Gram positive bacillus with a thick cell wall containing mycolic acid, which renders it acid fast. The bacteria commonly reach the spine by haematogenous spread, so it is the vertebral bodies that are usually affected. They are then phagocytosed by macrophages
Diagnosis Laboratory studies are suggestive of chronic infection, i.e. anaemia, hypoproteinemia, and an elevated ESR. Tuberculin skin testing may be helpful, but is not diagnostic especially in TB endemic areas where the population may have had subclinical exposures or have received BCG vaccination. Interferon gammarelease assays (IGRA) is a relatively new method for detecting T cells specific for Mycobacterium tuberculosis antigens. It has sensitivity about 80% and is more specific than the tuberculin skin test. Its sensitivity remains high in immune-compromised patients and is not confounded by BCG vaccination. The main
W Y Cheung FRCSEdOrth FHKAM Associate Consultant, The Department of Orthopedics & Traumatology, The University of Hong Kong, Pokfulam, Hong Kong SAR, China. Keith D K Luk MCh Orth FRCSEd FRACS FHKAM Tam Sai Kit Chair in Spine Surgery, Chair Professor and Head, The Department of Orthopedics & Traumatology, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.
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evaluation of the bony destruction and possible instability while MRI permits further delineation of the soft-tissue components, activity of the disease and status of the spinal cord (Figure 2). Gupta et al. noted that abscess formation and the presence of bone fragments on MRI helped distinguish spinal tuberculosis from neoplasia. However definitive diagnosis is dependant on culture of the organism, requiring biopsy of the lesion. Percutaneous biopsies under radiographic or CT control usually suffice. Francis et al. reported 29 patients with suspected spinal tuberculosis. Epithelioid granulomata were seen in 89%, positive acid-fast bacilli cultures in 83% and positive acid-fast bacilli smears in 52%. Percutaneous thoracoscopic or laparoscopic biopsy has been reported by Dusmet et al. Nonetheless, open biopsy may be necessary if needle biopsy is unsuccessful or during a definitive open procedure. Because Mycobacterium tuberculosis is difficult to culture due to its fastidious growth requirements and slow growth rate, there is a need for techniques that permit more effective and earlier diagnosis. Polymerase chain reaction (PCR), a non-culture, molecular diagnostic test, amplifies the DNA of the Mycobacterium tuberculosis for identification. This utilizes a primer pair targeting a 123 base pair segment of the repetitive sequence IS6110 of the M. tuberculosis complex which covers M. tuberculosis, M. africanum, M. bovis, M. canetti and M. microti. The amplified segment of the tuberculosis DNA is subsequently detected with the Southern Blot hybridization technique. PCR is highly sensitive (95e98%) for diagnosing tuberculosis from smear-positive and culture-positive cases, but it has lower sensitivity (57e78%) for smear-negative and culture-positive cases. This is an exciting development, allowing quicker diagnosis and has also been used as a marker to monitor response to treatment. With different primers, it has also been shown to provide rapid information on drug resistance and clonality in epidemiological investigations of outbreaks.7
Figure 1 Marked soft-tissue swelling at the cervical or upper thoracic region may cause airway obstruction (Millar asthma).
limitation of the test is it cannot differentiate active from latent infection. Early radiographic findings include a subtle decrease in one or more disc spaces with localized osteopenia. Later findings include vertebral collapse, described by Seddon, as “concertina collapse” because of its resemblance to an accordion. Soft-tissue swelling and later calcification are highly predictable radiographic findings. CT scanning, with contrast, allows better
Figure 2 Contrast MRI shows enhancement at L4 and L5 vertebral body and a rim enhancement lesion at epidural space with cauda equina compression.
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Treatment
Surgical treatment Surgical treatment is an important component in the treatment of spinal tuberculosis. In the presence of active disease surgery is indicated if: there is significant neurological deficit due to spinal cord or cauda equina compression, there is severe deformity that requires surgical stabilization, the diagnosis is uncertain and open biopsy is required, and if conservative treatment has failed and there is significant back pain. As the disease is usually in the anterior aspect of the spine, surgery is commonly performed via the anterior approach. This was first described by Ito et al. in 19349 and subsequently popularized by Hodgson and Stock in 1956.10 It allows direct access to the anterior disease focus and permits complete clearance of the abscess, tissue biopsy for diagnosis and, more importantly, insertion of strut grafts under compression at the kyphus. Various studies have shown that patients with Pott’s paraplegia due to active disease had better neurological recovery if treated with surgery compared with conservative treatment alone. Martin et al. reported 60% of patients with Pott’s paraplegia treated with surgery had neurological recovery compared with 48% of patients treated conservatively.11 Guirguis et al. reported an even higher success rate with 93% patients treated surgically having neurological recovery versus 40% of patients treated conservatively.12 The role of surgery for patients without significant neurological deficit is less well defined. To study the relative merits of the conservative and surgical approach to the treatment of TB spine in this group of patients, the Medical Research Council of the United Kingdom initiated and coordinated a series of important clinical trials. These were carried out from 1965 in multiple centres in the world where the disease was prevalent. The patients were carefully selected, documented and followed up for as long as 15 years prospectively. The results were published in a series of reports that should be mandatory reading for every spinal surgeon.13e17 The efficacy of surgical treatment was compared with that of conservative drug treatment. In Rhodesia (now Zimbabwe), Korea and Hong Kong, patients were randomly allocated to the drug treatment group, debridement group or radical debridement plus anterior spinal fusion group. The inclusion criterion was clinical or radiological evidence of tuberculosis at any level except the cervical spine. Patients with significant neurological deficit such that they could not walk across the room, those had been given anti-tuberculous drugs for more than 1 year, those that had significant extra-spinal disease and, for the fusion group, those that had more than three levels of vertebral destruction were excluded from the study. All patients were given 18 months of two or three drug combination chemotherapy. In the debridement group, the abscess, the sequestrum and the loose disc fragments were removed to achieve spinal cord decompression and no fusion was performed. In Hong Kong, the radical surgery group underwent radical debridement of the necrotic tissue until healthy bleeding bone was reached. This was then followed by an anterior strut graft fusion using autologous rib, iliac or fibula grafts. The results reported at the 5-, 10- and 15-year reports indicated that all three groups achieved the same 87% favourable outcome, defined as
Tuberculosis is usually considered to be cured when there are no clinical signs of infection, the patient is neurologically intact, has regained their previous activity level and does not suffer relapse. However, spinal tuberculosis presents some additional problems, kyphosis and delayed neurological deficit. Therefore modern treatment is also directed at correcting the kyphosis thereby restoring the balance of the spine, achieving early bony fusion (healing), preventing local recurrence of spinal tuberculosis, and thus preventing late neurologic complications. Medical treatment The main stay of treatment is chemotherapy. Since the advent of specific anti-tuberculous chemotherapy, patients rarely die from the disease, the period of infectivity is considerably reduced, relapses are avoided and chronicity reduced. With the increasing prevalence of drug-resistant tuberculosis worldwide, it is very important to know the bacterial sensitivities before commencing chemotherapy. By culture of aspirate or tissue specimens, sensitivity tests of the cultured tubercle bacilli against each drug can be ascertained. There are currently five first line anti-tuberculous drugs, isoniazid, rifampicin, pyrazinamide, streptomycin and ethambutol. Various treatment regimens have been described and generally 6e12 months of chemotherapy is required2,8 (Table 1). In our centre, the standard regimen is ethambutol, pyrazinamide, rifampicin and isoniazid for 2 months, followed by rifampicin and isoniazid for 4 months. Longer treatment may be necessary for elderly or immune-compromised patients. Drug-resistant tuberculosis is defined as resistance to one or more of the primary anti-tuberculous drugs. Its management is very complex, necessitating treatment with secondary chemotherapeutic agents, which include amikacin, capreomycin, ciprofloxacin, cycloserine, ethionamide, kanamycin, ofloxacin, and para-aminosalicylic acid. It is better not to just add a single drug to a failing regimen because that creates an ideal condition for the development of resistance to the new medication. Instead, expert opinion from a microbiologist should be sought. The most common causes of development of drug resistance are inadequate treatment and/or patient non-compliance. Preventative measures including directly observed therapy to maximize compliance are essential.
Anti-tuberculosis regimes Three drug regimes (months) Davies PC (1996): HRZ (2) HR (10) Upadhyay et al (1999): HPaS(3)Hpa(3) Moon et al (1987, 1995, 1997, 2004): RHE(Z)(12) Four drug regimes (months) Medical research council (1993): RHEZ(2) RH(4) Yilmaz et al (1999): SRHZ(2) RH(7) Metha IS et al (2001): RHEZ(2) RHE(4) RH(6) Govender et al (2003): RHZE(12) H: isoniazid, R: rifampicin, Z: pyrazinamide, Pa: P-aminosalicylic acid, S: streptomycin.
Table 1
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no evidence of central nervous system involvement, no sinus or clinically evident abscess, no radiological evidence of disease activity and no restriction of normal physical activity. However, when these data were analyzed in greater detail, it was evident that the radical surgery group treated in Hong Kong had distinct advantages over the other two groups. There was much quicker relief of pain, earlier resolution of the sinus tracts and abscesses, and there was no neurologic involvement during treatment. There was a much higher rate of bony fusion of 85% at 5 years, which rose to 94% at 15 years. This compared with 46% at 5 years and 72% at 15 years for the group treated conservatively in Korea. The progression of the deformity was also different between the three groups. In the conservatively treated group, there was an increase of 21 at 5 years, which further increased to 25 at 15 years. The corresponding figures for the debridement group were 8 and 11 respectively. In contrast, the radical surgery group showed an improvement of 3 at 5 years, and this was maintained at the final 15-years follow-up assessment. It is also worth noting that in 5% of the conservative group, there was an alarming increase of kyphosis from 51 to 70 . Based on the results of this series of studies, the Medical Research Council concluded in its 13th report16 that: Conservative drug treatment, debridement alone and radical debridement and fusion all achieved similar favourable outcome in the majority of patients. The excellent results at 10 years are sustained at 15 years with no late relapse or late-onset paraplegia. The only advantage of radical operation is less late deformity compared with debridement. A question therefore comes, who will develop severe kyphosis that may benefit from early surgical stabilization and fusion? Rajasekaran et al. tried to answer this question by identifying some risk factors in patients who developed severe angular kyphosis.18,19 They retrospectively reviewed 90 adult patients who had suffered from tuberculosis of the spine. The vertebral body loss at the start of treatment had a good correlation with the severity of the deformity at the 5-year follow-up. It was reported that the deformity at 5 years could be predicted with a fair level of accuracy by the calculation of the pretreatment vertebral body loss and the application of the formula
While early surgical Intervention for prevention of deformity is relatively simple, producing good results, and preventing additional deformity, surgery for established severe deformity is difficult, and hazardous with a relatively high complication rate. However, gross kyphotic deformities in the thoracic and thoracolumbar region can result in severe cardio-respiratory embarrassment and in the lumbar region, the kyphosis can cause severe postural imbalance and frequently results in severe foreshortening of the trunk. There can also be increased back pain due to muscle fatigue and impingement of the rib cage on the iliac crest as well as self-image and psychological problems. Previously single stage correction of deformity had an unacceptable rate of neurologic complications and achieved negligible correction, which was dissatisfying both to the surgeon and the patient. Additionally there was a significant risk of paraplegia because of the need for meticulous debridement of the tissues all around the spinal cord before osteotomy. Side-slip deformity at the apex of the kyphosis made the procedure even more dangerous, because of the difficulty in actually locating the spinal canal. To minimize the complications, Yau et al. advocated a staged sequential procedure, first fitting halo-pelvic distraction apparatus, followed by anterior spinal osteotomy and decompression of the spinal cord, slow and gradual spinal distraction, posterior osteotomy and fusion, additional spinal distraction, and anterior spine fusion after achieving maximum correction.20 (Figure 3) Even with this technique of staged procedures, there was a 10% mortality rate and the average amount of correction obtained was only 28%. Therefore this is only recommended for patients with severe deformity, active disease and imminent paraplegia or death from chest complications. Instrumentation: Oga et al. have shown that Mycobacterium tuberculosis is not adhesive to implant surfaces and does not form biofilms which means it is safe to use implants in the presence of active tuberculosis infection, provided intensive anti-tuberculosis therapy is given. Various studies also confirmed that spinal instrumentation is safe and effective in active tuberculosis infections.21,22 Recent advances in spinal instrumentation in recent years and intra-operative spinal cord monitoring techniques have made more aggressive kyphosis correction surgery possible. Rajasekaran et al. recently described a single-stage closing/ opening wedge osteotomy to correct severe tuberculous kyphosis.23 The procedure is performed through a single posterior approach, performing wide laminectomies and a wedge of vertebral column is excised. The anterior column is reconstructed with a cage and the deformity correction achieved by posterior closing and anterior opening, fulcruming at the cage. The merits of this procedure are that the spinal column is not excessively shortened or lengthened during the procedure, so the risk of neurological complication should be low. They reported 17 cases with average kyphosis correction of 57% and only one patient had deterioration of neurological status after the procedure. However care has to be taken regarding the flexibility of the compensatory hyper-lordosis proximal and distal to the kyphus before proceeding with this surgical procedure. Particularly if the thoracic lordosis is not reversible, any overcorrection of the thoraco-lumbar kyphosis may result in stresses being thrown into the cervical segment. Thus, the best candidates for this procedure would be for children or young adults without neurological symptoms or signs and the
Y ¼ a þ bX where Y is the deformity at 5-year follow-up, X is the pretreatment vertebral body loss, and a and b are constant values of 5.5 and 30.5. There was an average kyphus angle of 30 to 35 for the complete destruction of each vertebral body in the dorsal and dorso-lumbar region and approximately 20 for the complete loss of each vertebral body in the lumbar region. They recommended surgery for patients with loss of 0.75 thoracic or thoraco-lumbar vertebrae, or the loss of one lumbar vertebra to produce final kyphosis of less than 30 . In another study, they also identified some risk factors for severe kyphosis in paediatric patients, namely separation of facet joints, posterior retropulsion, lateral translation and toppling. Patients with more than two of these signs had progression of kyphosis more than 30 and a final kyphosis of more than 60 . Surgical treatment is therefore also recommended for this group of patients.
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Figure 3 a Severe tuberculosis kyphosis. b Treated with halo-pelvic traction and combined anterior, posterior spinal fusion. c Sagittal profile after treatment.
compensatory curves are still flexible and can be reversed with the segmental instrumentation.
by blunt dissection. Anterior to the transverse processes are the pedicles and the intervertebral foramina. The spinal canal is entered by tracing the intercostal nerves and removing the surrounding bone. Crowded pedicles at the apex are removed and the dura is exposed posterior to the posterior longitudinal ligament. Then excision of the internal kyphus is performed to decompress the spinal cord and anterior fusion carried out with strut grafts. Hsu et al. reported 80% of patients with active disease and 50% of patients with healed disease had neurological improvement with this procedure, but 10% of patients had neurological deterioration after the surgery.24 We recently published our 5-year results for patients with lateonset Pott’s paraplegia of healed disease and severe kyphosis treated by this method.25 Forty per cent of patients had neurological improvement and none had neurological deterioration after the surgery. Solid bone fusion was demonstrated in all patients at 5 years after surgery. While this surgical procedure is technically less demanding, it does not correct the kyphosis and sagittal mal-alignment. Thus it is particularly indicated for older patients with fixed compensatory lordosis or patients with multiple co-morbidities and high surgical risks.
Late-onset paraplegia: late-onset paraplegia with residual spinal deformity is one of the most disastrous complications of Pott’s disease and the prognosis is generally poor. Chronic spinal cord compression as a result of the severe kyphotic deformity, with or without reactivation of the tuberculosis infection, leads to spinal cord dysfunction and progressive neurological deficits. In our centre, we prefer to use anterior decompression and strut bone grafting via a costo-transversectomy approach to treat this group of patients (Figure 4). A curved longitudinal incision 6e8 cm lateral to the midline is created, centred over the kyphus. The paraspinal muscles are stripped and retracted medially from the lateral side to expose the transverse processes and the adjacent 5e6 cm ribs subperiosteally. Two to three transverse processes and the corresponding posterior end of the ribs including the rib heads are excised. Segmental intercostal nerves are identified and held with slings. Great care is taken to remain extra-pleural and extra-peritoneal. Soft tissue, pleura, and peritoneum are mobilized from the pedicles and the collapsed vertebral bodies
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Figure 4 a Severe post-tubercular kyphosis. b Internal kyphectomy for spinal cord (arrow) compression and anterior fusion with strut graft. c Postoperative X-ray showed internal kyphectomy and bone graft in position (arrow).
Conclusion
5 Luk KD, Krishua M. Spinal stenosis above a healed tuberculosis kyphosis. A case report. Spine 1996; 21: 1098e101. 6 Jain AK, Aggarwal A, Mehrotra G. Correlation of canal encroachment with neurological deficit in tuberculosis of spine. Int Orthop (SICOT) 1999; 23: 85e6. 7 Rattan A. PCR for diagnosis of tuberculosis: where are we now? Indian J Tuberculosis 2000; 47: 79e82. 8 Medical Research Council Working Party on Tuberculosis of the Spine. Controlled trial of short-course regimens of chemotherapy in ambulatory treatment of spinal tuberculosis. J Bone Joint Surg 1993; 75: 240e8. 9 Ito H, Tsuchiya J, Asami G. A new radical operation for Pott’s disease. J Bone Joint Surg 1934; 16: 499. 10 Hodgson AR, Stock FE. Anterior spinal fusion. Br J Surg 1956; 44: 266e75. 11 Martin NS. Pott’s paraplegia. A report on 120 cases. J Bone Joint Surg Br 1971; 53: 596e608. 12 Guirguis AR. Pott’s paraplegia. J Bone Joint Surg Br 1967; 49: 658e67. 13 Medical Research Council Working Party on Tuberculosis of the Spine. Five-year assessments of controlled trials of ambulatory treatment, debridement and anterior spinal fusion in the management of tuberculosis of the spine: studies in Bulawayo (Rhodesia) and in Hong Kong. J Bone Joint Surg Br 1978; 60: 163e77. 14 Medical Research Council Working Party on Tuberculosis of the Spine. A ten-year assessment of a controlled trial comparing debridement and anterior spinal fusion in the management of tuberculosis of the spine in patients on standard chemotherapy in Hong Kong. J Bone Joint Surg Br 1982; 64: 393e8. 15 Medical Research Council Working Party on Tuberculosis of the Spine. A ten-year assessment of controlled trials of inpatient and outpatient treatment and of plaster-of-Paris jacket for tuberculosis of the spine in children on standard chemotherapy. Studies in Masan and Pusan, Korea. J Bone Joint Surg Br 1985; 67: 103e10. 16 Medical Research Council Working Party on Tuberculosis of the Spine. A 15-year assessment of controlled trials of the management of
Tuberculosis infection of the spine is a serious clinical condition which may lead to severe deformity, early or late neurological complications and even mortality. Its incidence is increasing worldwide. Advances in laboratory testing allow more effective and earlier diagnosis of this condition. The aims of treatment are to cure the infection, prevent or correct kyphotic deformity and preservation of neurology. Though most infections can be cured by anti-tuberculosis chemotherapy, surgery is indicated for selected groups of patients. The majority of patients with early onset paraplegia due to active disease have a good neurological recovery with surgical decompression. Surgery should also be considered for patients at high risk of developing significant kyphosis which may lead to sagittal imbalance and late-onset paraplegia. Late-onset Pott’s paraplegia with severe kyphotic deformity is notoriously difficult to treat. Surgical decompression with or without correction of the kyphosis are the main stays of treatment but is technically demanding with high operative risks and should therefore not be attempted by the inexperienced. A
REFERENCES 1 Moon MS. Tuberculosis of the spine; controversies and new challenges. Spine 1997; 22: 1791e7. 2 Moon MS. Tuberculosis of the spine e contemporary thoughts on current issues and perspective views. Curr Orthop 2007; 21: 364e79. 3 Jutte PC, Van Loenhout-Rooyackers JH. Routine surgery in addition to chemotherapy for treating spinal tuberculosis. Cochrane Database Syst Rev 2006; doi:10.1002/14651858.CD004532.pub2. Issue 1: Art. No.: CD004532. 4 Watts HG, Lifeso RM. Tuberculosis of bone and joints. J Bone Joint Surg 1996; 78-A: 288e98.
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17
18
19
20
21 Oga M, Arizono T, Takasita M, Sugioka Y. Evaluation of the risk of instrumentation as a foreign body in spinal tuberculosis. Spine 1993; 18: 1890e4. 22 Moon MS, Woo YK, Lee KS, Ha KY, Kim SS, Sun DH. Posterior instrumentation and anterior interbody fusion for tuberculous kyphosis of dorsal and lumbar spine. Spine 1995; 20: 1910e6. 23 Rajasekaran S, Vijay K, Shetty AP. Single-stage closingeopening wedge osteotomy of spine to correct severe post-tubercular kyphotic deformities of the spine: a 3-year follow-up of 17 patients. Eur Spine J 2010; 19: 583e92. 24 Hsu LCS, Cheng CL, Leong JCY. Pott’s paraplegia of late onset: the cause of compression and results after anterior decompression. J Bone Joint Surg Br 1988; 70: 534e8. 25 Wong YW, Leong JCY, Luk KDK. Direct internal kyphectomy for severe angular tuberculosis kyphosis. Clin Orthop Relat Res 2007; 460: 124e9.
tuberculosis of the spine in Korea and Hong Kong. J Bone Joint Surg Br 1998; 80: 456e62. Medical Research Council Working Party on Tuberculosis of the Spine. A controlled trial of anterior spinal fusion and debridement in the surgical management of tuberculosis of the spine in patients on standard chemotherapy: a study in Hong Kong. Br J Surg 1974; 61: 853e66. Rajasekaran S, Shanmugasundaram TK. Prediction of the angle of gibbus deformity in tuberculosis of the spine. J Bone Joint Surg Am 1987; 69: 503e9. Rajasekaran S. The natural history of post-tubercular kyphosis in children: radiology signs which predict late increase in deformity. J Bone Joint Surg Br 2001; 83: 954e62. Yau ACMC, Hsu LCS, O’Brien JP, Hodgson AR. Tuberculosis kyphosiscorrection with spinal osteotomy, halo-pelvic distraction and anterior and posterior fusion. J Bone Joint Surg 1974; 56A: 1419e34.
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(ii) Stem cell research in orthopaedic and trauma surgery
More widely, however, the therapeutic use of stem cells is still at an early stage.
Stem cells Stem cells have the potential to divide indefinitely in culture and can differentiate into specialized cells. After fertilization, eggs form a single cell, the zygote. This initially divides into identical cells which are totipotent and have the potential to form entire organs.3 As development proceeds these totipotent cells form a hollow sphere of cells referred to as a blastocyst (Figure 1). The cells forming the inner part of this hollow sphere are pluripotent and can form many types of cells, but not all the types of cells required for foetal development. These pluripotent stem cells go through further stages of specialization, becoming more commited stem cells which are referred to as being multi-potent.3 Multi-potent stem cells have been detected in several adult tissues. Generally, they do not change their differentiation process to form different cells or tissue, but numerous studies have shown that inherent flexibility remains, even in those which have become specialized, and which may under some circumstances be able to differentiate into different types of cells. However, to date there have been a limited number of studies investigating adult stem cells and, as they are not found in all tissues and their number is very small, and as the differentiation of such pluripotent stem cells is already well advanced, it is difficult to investigate the initial stages of stem cell development.3
Seok-Jung Kim Asode Ananthram Shettey
Abstract Injection of bone marrow to induce bone healing was an early form of stem cell therapy in orthopaedic practice. Clinical trials of newer techniques including cell culture for bone and cartilage repair are at an early stage, but rapid developments can be anticipated.
Keywords biocytotherapy; bone; bone marrow; cartilage; mesenchymal stem cells; osteoblast
Introduction Human organs comprise cells within a bio-matrix formed by the cells during a process of repeated cell division, proliferation, and differentiation while maintaining homeostasis and metabolic processes. If an organ is injured, the basis of the healing process is that cells undergo division, produce matrix material and heal the injury. Recently techniques to restore the function of damaged tissue, or to improve or maintain its functions using biomaterials, have been developed. Current research has investigated PLA (PolyLactic Acid), PGA (PolyGlycolic Acid), collagen, hyaluronic acid, and several other materials.1 At the cellular level various cells of mesenchymal origin have been used, including marrow-derived stem cells and umbilical cord blood-stem cells. As well as using such undifferentiated cells, cells more differentiated towards the desired tissue could be used. Such therapy for the regeneration of injured skeletal tissue has been termed ‘biocytotherapy’, defined as therapeutic methods using either biomaterials single cells or both in combination. The selection of appropriate cells and biomaterials is key to tissue regeneration. While allogenic cells can theoretically be used, considerations of immune side effects, infection, etc., have meant that autologous cells have been generally regarded as better for this purpose. For example, autologous chondrocyte implantation (ACI) has already been commercialized and used worldwide.2
Mesenchymal stem cells Mesenchymal stem cells (MSC) are also often referred to as marrow stromal cells, CFU-F (colony-forming unit-f), etc. They have the potential for self-renewal and the capability to differentiate into several, distinct mesenchymal lineages such as bone, cartilage, adipose tissue, muscle and marrow stroma. Additionally, as they can also differentiate into non-mesodermal cells such as hepatocytes, neural cells, epithelial cells etc. Hence they can be regarded as pluripotent or multi-potent.4
Fertilization Morula Totipotent
Seok-Jung Kim MD PhD FRCS The Catholic University of Korea, Department of Orthopedic Surgery, Uijeongbu St. Mary’s Hospital, Kumoh-dong, Uijeongbu City, Gyeonggi-do 480-717, Republic of Korea.
Multipotent Figure 1 The potency of stem cells declines from the Morula of totipotent cells to the adult in which multipotent cells remain but are difficult to isolate and culture.
Asode Ananthram Shettey MD PhD FRCS University of London, Department of Surgery, Kings’ College, London SE1 1UL, UK.
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MSCs have been found in several types of tissue, most notably in bone marrow. There have been many attempts to use them clinically. One method is to induce proliferation of MSCs in a relatively undifferentiated state, obtaining as many cells as possible, and then to apply them to injured tissue in anticipation of their contribution to tissue healing. Another method is to induce the differentiation and proliferation of cells appropriate to the injured tissue, thus treating the injury with suitably differentiated cells. Apart from bone marrow, attempts have been made to obtain MSC’s from fat and muscle tissue. Adipose tissue has been used clinically, particularly by plastic surgeons. Recent studies have shown that large number of MSCs can be obtained from synovium and synovial fluid. Basic research studies continue.
There is ongoing active research into the use of synovial fluid derived (MSCs) since Jones et al.9 showed that there are stem cells present within the synovial fluid of arthritis patients. Studies have also suggested the possibility of using MSCs to treat ligament injuries as well as those of articular cartilage. Umbilical cord blood (UCB) is increasingly used to treat haematologic disorders, and it is recognized that as well as being a rich source of haematopoietic stem cells,10 primitive stromal cells separated from the umbilical cord have been shown to differentiate into osteoblasts, chondrocytes, adipocytes, cardiomyocytes, neurocytes, etc. Numerous studies are being conducted into the potential clinical applications. Osteoblast differentiation from MSCs in bone marrow Because the identification of stem cells can be difficult, it is very important to observe the cell differentiation process after inoculation to confirm the presence of stem cells. The process of development from a primitive, pluripotent stem cell to an undifferentiated, multi-potent mesenchymal cell is as yet unknown, but several mediating factors promoting the development of pluripotent cell to immature osteo-progenitor cell have been discovered. Nonetheless it is not yet possible to identify the osteo-progenitor cells before expression of the osteoblastic marker, and so an antibody to cell surface protein of marrow stromal cells is used to detect musculoskeletal stem cells. A monoclonal antibody, STRO1, identifies clonogenic bone marrow stromal cell progenitors, i.e. fibroblast colony-forming units [CFU-F], in adult human bone marrow.11 STRO-1 positive CFU-F cells have been reported to demonstrate the phenotype of fibroblasts, adipocytes, and smooth muscle cells. When STRO-1 positive cells were cultured in the presence of dexamethasone, ascorbic acid 2-phosphate and inorganic phosphate, alkaline phosphatase activity was detected and it was thus determined that osteogenic fractions were present.11 All osteo-progenitor cells are STRO-1 positive and express alkaline phosphatase on the surface prior to proliferation and before they become phenotypically recognizable osteoblasts. Bone marrow is presently the most important source of stem cells, multi-potential mesenchymal progenitor and osteoprogenitor cells. During the culture of marrow stromal cells, fibroblastic-type clonal colonies are formed, each colony originating from a single CFU/F cell. Such colonies are a heterogeneous population expressing diverse enzymes with the potential to differentiate to fibroblastic, reticular, adipocytic, and osteogenic populations. In culture, two types of osteo-progenitor cells are observed (Figure 1); colony-forming cells have increased proliferative potential. After incubation for approximately 7 days, they form colonies consisting of several hundreds of antigen positive cells. After 7 days’ incubation, more mature and less proliferative cluster-forming cells differentiate into colonies consisting of 20e50 bone protein antigen positive, e.g. osteocalcin, cells.12 In order to have osteogenic potential, colony-forming cells and cluster-forming cells require osteogenic growth factors, although their requirements differ slightly. Colony-forming cells respond to TGF-beta, basic fibroblast growth factor, BMP-2, and 1,25-OH D3. Cluster-forming cells are primarily controlled by 1,25-OH D3 and TGF-beta, but do not respond to the basic fibroblast growth factor.26 The fibroblast growth factor (bFGF) and transforming growth factor-b1 (TGF-b1) are potent mitogens for periosteal
MSCs from bone marrow MSCs were originally isolated from bone marrow, being described as stromal cells. As bone marrow or trabecular bone cells have great osteogenic potential, it has been practice for many years to obtain bone marrow from either the sternum or the iliac crest in order to stimulate bone healing. In the supine patient, bone marrow can be aspirated from the anterior superior iliac spine. If prone, it can be aspirated from the posterior superior iliac spine. It is important to aspirate under negative pressure in order to obtain the marrow components and not venous blood. To obtain marrow stromal cells, it is recommended that approximately 2e5 ml are aspirated from one site.5 If a greater volume is aspirated, there is a significant risk of contamination with haematopoietic cells. In a 2-ml, human bone marrow aspiration, an average of 92 65 106 nucleated cells are present, and for every 106 nucleated cells, an average 43 28 of alkaline phosphatase-positive colonies are present.6 These colonies can be considered as representing the number of osteo-progenitor cells. Bone marrow injection is based on the theory that osteoprogenitor cells within bone marrow will induce and accelerate bone formation. The principal advantage over autologous bone graft is that bone marrow injection is not a surgical procedure requiring an incision of the skin in the donor area and thus does not give rise to donor site problems; complications or side effects. However, the number of osteo-progenitor cells in bone marrow is very limited and the quantity of bone marrow obtained from one site is small, and thus effects of bone marrow injection also are uncertain. MSCs from other tissue Since Friedenstein et al. separated MSCs from bone marrow (BM), the stroma of the spleen and the thymus,7 MSCs have been isolated from many other tissues including adipose tissue, cartilage, periosteum, synovium, synovial fluid, muscle, tendons, umbilical blood, and blood vessels, all have been reported to contain MSCs. Of these, adipose tissue shows pluri-potency and proliferative efficiency comparable to bone marrow-derived MSCs and a donor site morbidity comparable to that of other donor sites.8 The multi-potent cell population obtained during liposuction is referred to as ‘processed lipo-aspirate (PLA) cells’.8 Since Lendeckel et al. first reported the clinical use of adipose-derived stem cells they have been investigated as a possible treatment for myocardial infarction, cerebral infarction and spinal cord injuries.
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osteo-progenitor cells and marrow stromal cells and they are expressed and produced by osteoblast lineage cells. Such growth factors are stored in the extracellular matrix of bones and thus provide the local mechanism which accelerates the proliferation of progenitor cells in the microenvironment of bone. If bone marrow cells are cultured in the presence of bFGF, as well as mitogenic effects, the expression of alkaline phosphatase is also elevated. bFGF(3 ng/ml) increases [3H] thymidine and [3H] proline incorporation and protein accumulation. Together with the enhancement of cAMP responsiveness, alkaline phosphatase activity, osteocalcin level, 45Ca2þ deposition, and mineralized-like tissue formation, it induces the earlier expression of such markers.13 Stem cell culture is a biphasic sequence. The characteristic of the first phase is cell proliferation and matrix deposition, which can be assessed by the enhancement of [3H] thymidine and [3H] proline incorporation and continues for 11 days. The second phase is characterized by the rapid reduction of cell proliferation and matrix deposition, but alkaline phosphatase activity, mineral deposition, and osteocalcin expression increase continuously. bFGF enhances both phases.13 Marrow stromal cells are a heterogeneous population composed of cells of diverse lineages. In the presence of ascorbic acid, sodium beta-glycerophosphate and dexamethasone, they form discrete nodules of mineralized, bone-like tissue. However, the number of nodules decreases as subcultures progress, and similarly the number of cells showing alkaline phosphatase activity decreases. Therefore, for the formation of nodules, osteogenic progenitor cells or other cell types must appear during the early culture period, as osteo-progenitor cells have a limited capacity for self-renewal. The last stage of the development of osteoblasts is defined by the formation and organization of the extracellular matrix of bone. When pre-osteoblasts cease to proliferate, they change from being spindle-shaped osteoblasts to large cuboidal osteoblasts. Osteoblasts secrete type 1 collagen and specific bone matrix proteins. The differentiation and function of osteoblasts are controlled by the interaction of cells with matrix proteins, and it appears that the interaction of cell and matrix, as well as cell to cell signalling is important in bone maturation.
conducted using mesenchymal stem cells (MSCs) or osteoblasts, not only to treat bony defects, but also for fracture non-union. Clinical stem cell applications in the treatment of fractures Ashton et al. have shown experimentally that bone marrow stem cells can differentiate to osteoblasts, chondroblasts, fibroblasts or adipocytes depending on the local environment.14 However, as there are relatively few bone marrow stem cells, cell culture is essential. It would be ideal if bone marrow stem cells with such differentiation capability could be numerically amplified and then grafted into a fracture site. Most of the clinical trials have used bone marrow aspirate or its concentrate. After Connolly reported a case of treatment of non-union using bone marrow aspirate,15 a successful trial of injecting 3e5ml of bone marrow aspirate into tibial non-union in 100 patients was reported.16 There have been several subsequent studies differing amounts of both aspirate and injection volume. Such can occur clinically because of variations in non-union sites and the leakage of injected bone marrow due to the resistance of fibrous and hard, non-union tissue. A trial using a concentrated bone marrow aspirate was reported by Herningou et al.17 who aspirated 300 ml of bone marrow and concentrated it to 50 ml. They quantified the number of injected MSC and 53 of 60 patients showed bone union in a mean of 12 weeks. Kim et al. showed in animal experiments that grafted, cultured, autologous osteoblasts effectively induced bone formation in bone defect areas.18 They then showed in a randomized clinical trial that autologous, cultured osteoblasts implanted into a fracture accelerated union rate by bone formation.19 They obtained 4.8 107 autologous osteoblasts by culturing bone marrow aspirate for 4 weeks culture. The autologous, cultured osteoblast injection group showed statistically significant acceleration of fracture healing, and there were no specific patient complications. They chose 6e8 weeks following fracture for injection as at that point fracture healing decreases and callus formation was relatively slow. They felt that if osteogenic cell groups are injected at that time, new tissue formation occurred because of these cells. Clinical stem cell research in osteonecrosis Avascular necrosis (AVN) of the femoral head can be a devastating disease leading to femoral head collapse and osteoarthritis in the third to fifth decades. Many attempts have been made in animals to induce osteonecrosis in the femoral head by direct injury, such as intravascular injection of Lipiodol, arterial ligation of the blood vessels supplying the femoral head, and the insertion of a wax or silicone tampon into the hip joint. However, it has not been possible to reproduce in an animal model, particularly one that maintains a necrotic area over an extended period of time, i.e. that reproduces the natural history of human avascular necrosis of the femoral head. This has hampered the evaluation of the effectiveness cell therapy in the treatment of osteonecrosis. In 2002, Hernigou and Beaujean reported the use of bone marrow concentrate to treat osteonecrosis of the femoral head20 and this may represent a new and successful treatment for this debilitating condition. In 2004, Gangji et al. published a controlled, double blind, prospective study in which they performed core decompression using a 5 mm trephine with the instillation of concentrated bone marrow aspirate as described by
Clinical trials Fracture non-union, delayed union, bone defects and bone diseases such as osteonecrosis have historically been treated surgically with autologous or allogenic bone graft, with autologous bone graft being favoured by most clinicians. Autologous bone graft has the disadvantage of requiring a second painful incision to harvest the graft, which lengthens hospital stay and recovery time. Additionally donor bone sites are limited. Thus allograft may be a better alternative to autograft. Quantity is not restricted and obviously there is no donor site morbidity. It does have shortcomings; the sterilization process weakens the bone, there may be rejection reactions and the graft may transmit infections such as hepatitis and HIV/AIDS. Thus culturing bone marrow stromal cells, inducing them to differentiate into autologous osteoblasts, inserting them into an appropriate skeleton, and transplanting it has been studied as a way of replacing conventional bone grafting. Many studies are being
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Hernigou. Nine of 10 hips showed good results.21 Several subsequent studies using bone marrow concentrate have been completed and there has been one study using bone marrow MSC and decalcified bone matrix. Recently a case has been reported of a remarkable result using cultured autologous osteoblasts. The patient had AVN of both hips at a similar stage of disease before collapse. This was treated using core decompression and allograft impaction to the left hip and core decompression and autologous cultured osteoblast injection to the right hip. Five-year follow-up showed complete healing in the osteoblast injected hip.22 Further properly conducted studies are required. Many studies have been reported without sufficient information on degree of bone marrow concentrate and cultured osteoblast density. Newly formed bone tissue derived from culture is similar to cancellous bone, and according to Vashishth, et al., osteocytes included in such bone tissue, if assumed to be evenly distributed and converted to volume units are calculated to be approximately 4.07 105 cells/1 cm3 bone.23 Thus, the theoretical bone volume that could be formed by 1 200 000 osteoblasts is approximately 30 cm3, which is equivalent to approximately half the volume of the femoral head, and even if 50% of the osteoblasts undergo resorption by remodelling, there should still be sufficient volume to fill a necrotic area.
the regenerative capacity of cartilage is limited and injury can lead to degeneration of the fibrillar collagen structure. The natural history after of articular cartilage injury is unclear. However, it is generally accepted that once articular cartilage is injured, its ability to regenerate is limited and that injury progresses to arthritis with time.24 The prevalence of chondral lesions is unknown. In patients presenting with knee joint problems, it has been estimated that approximately 5e10% have full-thickness cartilage lesions.24 Over the years various treatments have been developed and are used, such as arthroscopic debridement, microfracture, multiple drilling, osteochondral transfer, and Autologous Chondrocyte Implantation (ACI). Of these, arthroscopic debridement has been shown to have limited beneficial effects. The others can be divided into treatment methods which apply cells and those which apply tissue. The former include abrasion chondroplasty, microfracture, multiple drilling, and ACI. The latter include osteochondral transfer and allograft. Combination treatments using both cells and tissues are new-generation ACI and microfracture with biomaterials. Microfracture: in 1959, Pridie described subchondral drilling leading to the formation of cartilage in arthritic knees.25 Subsequently, Rodrigo et al. introduced arthroscopic microfracture using awls rather than drills to avoid thermal necrosis.26 This technique has been widely used to treat articular cartilage defects since the 1990’s. Numerous, successful results with relatively small articular cartilage defects were reported, but it was recognized that this treatment was restricted to the treatment of small defects.
Cartilage injury Cartilage cells, present in all articular cartilage, not only make the matrix but also maintain the tissue. As articular cartilage is avascular, superficial injury does not induce a sufficient inflammatory reaction that would, in other tissues, lead to repair. Thus
Colony forming cell alk –p (–) osteocalcin (–) osteocalcin (±) poor p (?)
Cluster forming cell alk –p (–) osteocalcin (–)
Growing nodule centeralk –p (–) osteocaltin (+)
Pre OB OB alk (+) osteocalcin (+)
Full mineralization alk –p (–) osteocalcin (–)
paripahery alk –p (–) osteocalcin (–) Proliferation
Proliferation Matrix mataration
Mineralization
1 Type I collagen 2 thrombospondin (+) 3 alk –p (–)
4 Bone sialoprotein (mineralization) Cellular expression
5 Osteonectin 6 Osteopontin 7 Osteocalcin
Figure 2 The differentiation pathway for osteoblasts.
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When subchondral bone is breached, clots are formed by leaking marrow components containing mesenchymal stem cells and these differentiate and form fibrocartilage. This differs from hyaline cartilage, containing abundant type I collagen, but with minimal proteoglycan content, thus having poor wear characteristics. Prior to tissue engineering, debridement or microfracture were the only techniques available. Many reports showed that for lesions larger than 2 cm2, results were poor, and this size has come to be regarded as the upper limit for microfracture treatment. Thus it is used as the treatment for small-size articular cartilage injury or for partial injury, and in view of the successful results reported, albeit after short follow-up, it is now regarded as the first-line treatment for post-traumatic femoral cartilage defects. Nonetheless despite reported poor outcomes, some surgeons use microfracture for relatively large lesions (Figure 2).
small defects (Figure 3). Despite this limitation, the short- and long-term results of this surgery are relatively successful. New-generation ACI’s: to address the limitations of ACI using periosteum, a collagen membrane has been used.29 Chondrocytes are seeded onto the membrane and cultured for several days before the membrane is cut to the size and shape of the defect. This eliminates the need for a second incision for periosteal harvest, reduces operative time and extensive suturing. The results are also encouraging.29 More recently a new cartilage cell graft technique using a cell/gel mixture, has been introduced, known as Gel-type Autologous Chondrocyte Implantation (GACI, ‘ChondronÔ’). Fibrin gel appears to be an excellent substrate for cartilage reconstruction. Fibrin has long been used clinically as it is highly biocompatible, non-toxic and biodegradable.2 As a three-dimensional scaffold the fibrin matrix has excellent cell attachment properties and cell proliferation and migration within the matrix occurs readily making it an ideal environment for cells to develop into mature tissue which, as it biodegrades, can be replaced by regenerated tissue.30 At operation, fibrin will maintain the shape of the articular surface within 5 min of injection, ensuring that the cells remain in place.2 The early results are encouraging.
Microfracture with bio-scaffold: microfracture continues to be used despite the regenerated cartilage not being hyaline cartilage but mechanically weaker fibrocartilage because the short-term results are good and it is a simple, cost effective technique. Efforts to improve outcomes by facilitating the regeneration of articular cartilage after microfracture using a bio-scaffold are being developed. One such procedure, known as Autologous Membrane Induced Chondrogenesis (AMIC), aims to improve chondrogenesis by covering the cartilage defect with a collagen membrane after microfracture. This encourages marrow-derived stem cells to remain in the cartilage defect after microfracture by using such a collagen scaffold and it also improves cartilage formation.27 It is suitable for the treatment for focal lesions including osteochondral defects. Atellocollagen covering for cartilage defects has been used both the in United Kingdom and Korea.
Conclusion Biocytotherapy is a term coined by the authors to describe the use of stem cell therapy combined with a bio-matrix. In an orthopaedic setting, successful stem cell therapy research suggests that both the cellular component and the bio-matrix are important. Ideally the bio-matrix itself should be able to maintain the three-dimensional structures as well as providing the properties required for the maintenance of cell survival, including cell attachment and growth. The clinical applications of stem cell therapy are still at an early stage, but shows much promise, particularly in the management of non-union and bone and cartilage defects. A
Autologous Chondrocyte Implantation (ACI) Conventional ACI: ACI by implanting periosteum was first introduced in 1987 in Sweden and has subsequently become widely used to regenerate articular cartilage.28 The technique involves debridement of the cartilage defect, harvesting of periosteum through a separate incision and suturing it over the defect, after which chondrocytes are implanted into the defect. Success is dependent on the attachment of the periosteum to ensure that there is no leakage of injected cells. To ensure satisfactory suturing of the periosteum around the lesion, the exposure often requires a significant incision, even for relatively
REFERENCES 1 Nehrer S, Breinan HA, Ramappa A, et al. Canine chondrocytes seeded in type I and type II collagen implants investigated in vitro. J Biomed Mater Res 1997; 38: 95e104. 2 Choi NY, Kim BW, Yeo WJ, et al. Gel-type autologous chondrocyte (Chondron) implantation for treatment of articular cartilage defects of the knee. BMC Musculoskelet Disord 2010 May 28; 11: 103. 3 Regenerative medicine glossary, vol. 4. Regenerative Medicine, July 2009; doi:10.2217/rme.09.s1. p. S30. 4 Jiang Y, Jahagirdar BN, Reinhardt RL, et al. Pluripotency of mesenchymal stem cells derived from adult marrow. Nature 2002; 418: 41e9. 5 Muschler GF, Boehm C, Easley K. Aspiration to obtain osteoblast progenitor cells from human bone marrow: the influence of aspiration volume. J Bone Joint Surg Am 1997 Nov; 79: 1699e709. 6 Majors AK, Boehm CA, Nitto H, Midura RJ, Muschler GF. Characterization of human bone marrow stromal cells with respect to osteoblastic differentiation. J Orthop Res 1997 Jul; 15: 546e57. 7 Friedenstein AJ, Piatetzky-Shapiro II, Petrakova KV. Osteogenesis in transplants of bone marrow cells. J Embryol Exp Morphol 1966; 16: 381e90.
Figure 3 Autogenous cartilage transplantation in progress.
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8 Zuk PA, Zhu M, Mizuno H, et al. Multilineage cells from human adipose tissue: implications for cell-based therapies. Tissue Eng 2001; 7: 211e8. 9 Jones EA, English A, Henshaw K, et al. Enumeration and phenotypic characterization of synovial fluid multipotential mesenchymal progenitor cells in inflammatory and degenerative arthritis. Arthritis Rheum 2004; 50: 817e27. 10 Gluckman E, Broxmeyer HA, Auerbach AD, et al. Hematopoietic reconstitution in a patient with Fanconi’s anemia by means of umbilical-cord blood from an HLA-identical sibling. N Engl J Med 1989; 321: 1174e8. 11 Gronthos S, Graves SE, Ohta S, Simmons PJ. The STRO-1þ fraction of adult human bone marrow contains the osteogenic precursors. Blood 1994 Dec 15; 84: 4164e73. 12 Long MW, Robinson JA, Ashcraft EA, Mann KG. Regulation of human bone marrow-derived osteoprogenitor cells by osteogenic growth factors. J Clin Invest 1995 Feb; 95: 881e7. 13 Pitaru S, Kotev-Emeth S, Noff D, Kaffuler S, Savion N. Effect of basic fibroblast growth factor on the growth and differentiation of adult stromal bone marrow cells: enhanced development of mineralized bone-like tissue in culture. J Bone Miner Res 1993 Aug; 8: 919e29. 14 Ashton BA, Allen TD, Howlet CR, Eaglesom CC, Hatori A. Maureen owen: formation of bone and cartilage by marrow stromal cells in diffusion chambers in vivo. Clin Orthop 1980; 151: 294e307. 15 Connolly JF, Shindell R. Percutaneous marrow injection for an ununited tibia. Nebr Med J 1986; 71: 105e7. 16 Connolly JF. Clinical use of marrow osteoprogenitor cells to stimulate osteogenesis. Clin Orthop Relat Res 1998;(suppl 355); S257e66. 17 Hernigou PH, Poignard A, Beaujean F, Rouard H. Percutaneous autologous bone-marrow grafting for nonunions: influence of the number and concentration of progenitor cells. J Bone and Joint Surg A 2005; 87: 1430e7. 18 Kim SJ, Jang JD, Lee SK. Treatment of long tubular bone defect of rabbit using autologous cultured osteoblasts mixed with fibrin. Cytotech 2007; 54: 115e20.
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19 Kim S-J, Shin Y-W, Yang K-H, et al. A multi-center, randomized, clinical study to compare the effect and safety of autologous cultured osteoblast(Ossron) injection to treat fractures. BMC Musculoskeletal Disorders 2009; 10. article 20. 20 Hernigou P, Beaujean F. Treatment of osteonecrosis with autologous bone marrow grafting. Clin Orthop Relat Res 2002; 405: 14e23. 21 Gangji V, Hauzeur JP, Matos C, De Maertelaer V, Toungouz M, Lambermont M. Treatment of osteonecrosis of the femoral head with implantation of autologous bone-marrow cells. A pilot study. J Bone Joint Surg Am 2004; 86-A: 1153e60. 22 Kim SJ, Bahk WJ, Chang CH, Jang JD, Suhl KH. Treatment of osteonecrosis of the femoral head using autologous cultured osteoblasts: a case report. J Med Case Reports 2008 Feb 25; 2: 58. 23 Vashishth D, Gibson G, Kimura J, Shcaffler MB, Fyhrie DP. Determination of bone volume by osteocyte population. Anat Rec 2002; 267: 292e5. 24 Curl WW, Krome J, Gordon ES, Rushing J, Smith BP, Poehling GG. Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy 1997; 13: 456e60. 25 Pridie KH. A method of resurfacing osteoarthritic knee joints. J Bone Joint Surg Br 1959; 41: 618e9. 26 Rodrigo JJ, Steadman JR, Silliman JF, Fulston HA. Improvement of full thickness chondral defect healing in the human knee after debridement and microfracture using continuous passive motion. Am J Knee Surg 1994; 7: 109e16. 27 Steinwachs MR, Guggi T, Kreuz PC. Marrow stimulation techniques. Injury 2008; 39: S26e31. 28 Marlovits S, Zeller P, Singer P, Resinger C, Vecsei V. Cartilage repair: generations of autologous chondrocyte transplantation. Eur J Radiol 2006; 57: 24e31. 29 Steinwachs M. New technique for cell-seeded collagen-matrix-supported autologous chondrocyte transplantation. Arthroscopy 2009; 25: 208e11. 30 Ho W, Tawil B, Dunn JC, Wu BM. The behavior of human mesenchymal stem cells in 3D fibrin clots: dependence on fibrinogen concentration and clot structure. Tissue Eng 2006; 12: 1587e95.
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(iii) Peripheral nerve repair
axon. At the end of the axon is the synapse, which is the means by which nerve cells project signals to target organs. As in other cells, the microtubule system transports signalling elements and nutritional elements from the cell body down the axon. The velocity of axonal transport is both temperature and oxygen sensitive to such an extent that when either of these parameters is decreased for a prolonged period, it can lead to cellular degeneration.1 From a histological standpoint, myelin is perhaps the most critical molecule in the nervous system. Myelin is composed of 30% protein and 70% lipids, with cholesterol predominating among the lipids. Throughout the peripheral nervous system are both myelinated and unmyelinated fibres, which can be motor, sensory, or autonomic. Glial cells (in the CNS) and Schwann cells (in the peripheral nervous system) ensheath axons in myelin at regular intervals and allow faster and more intense propagation of signals along the axon2 (Figure 2). Between the intermittent areas surrounded by myelin are unmyelinated nodes of Ranvier, which initiate and propagate action potentials. Myelinated axons conduct action potentials faster than unmyelinated fibres because the nodes of Ranvier serve as points along which electrochemical impulses can jump, like stones skipping across a pond; this phenomenon is called “saltatory conduction”, from the Latin word saltare, meaning “to dance or to jump”. In addition to the axons involved, there are four types of collagen-containing connective tissue that provide structure to the peripheral nervous system (Figure 3). Progressing from smallest to largest, they are the endoneurium, the perineurium, the epineurium, and the paraneurium/mesoneurium. The endoneurium surrounds an individual myelinated axon or a group of unmyelinated nerve fibres and it is composed of thin collagen strands. Nerve fibres and their associated endoneurium are, in turn, grouped together into fascicles. The perineurium surrounds these fascicles and is composed of collagen and perineural cells. The perineural cells provide a barrier between the nerve and its blood supply, while the collagen provides the nerve’s tensile strength.3 The epineurium is the most abundant type of connective tissue in the nerve and comprises 60e85% of the nerve surface area.4 Many fascicles are arranged in large bundles, which are surrounded by interfascicular epineurium, and finally, the
Jaiyoung Ryu Claire F Beimesch Trapper J Lalli
Abstract Peripheral nerve injuries affect all age groups and can be devastating to patients. A timely repair and thorough exam both preoperatively and intraoperatively can help increase the chances of a successful outcome. The technical aspects of peripheral nerve injury evaluation and repair must take into account the unique anatomy and function of the nervous system. Proper microsurgical techniques such as tension-free repair are a critical aspect of the repair process. Nerve grafts, conduits, and biotherapies are all viable ways to increase the odds of a meaningful repair. Proper immobilization, mobilization, and a targeted rehabilitation protocol are also important.
Keywords microsurgery; nerve conduit; nerve graft; peripheral nerve
Peripheral nerve injuries affect all age groups and can be devastating to patients, affecting their jobs and daily activities. These injuries are often the result of traumatic events, such as an open fracture or wound, but they can also present latently after a peripheral nerve block or while observing a compartment syndrome. From a surgical perspective, it may seem a relatively simple task to repair a nerve laceration compared to a vessel injury, since the nerve has fascicles but no lumen. However, the technical aspects of peripheral nerve injury evaluation and repair extend far beyond just suturing. It is a field which has fostered many new techniques that have been shown to improve patient outcomes. In addition to proper microsurgical techniques, there are several biotherapies detailed in recent literature which may have some applicability for the surgeon.
Anatomy & physiology The neuron is the fundamental building block of the central and peripheral nervous system (Figure 1). Its distinctive structure equips it to send and receive signals from target organs that lie physically far from the brain. Transportation of the action potential of the neuron begins at the cell body or perikaryon and extends down the long narrow projection of the cell called the
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Jaiyoung Ryu MD Department of Orthopaedics, Chief, Hand and Upper Extremity Service, West Virginia University, Health Sciences Center, Morgantown, WV, USA. Conflicts of interest: none declared.
B
Claire F Beimesch MD Resident, Department of Orthopaedics, West Virginia University, Morgantown, WV, USA. Conflicts of interest: none declared. Trapper J Lalli MD Resident, Department of Orthopaedics, West Virginia University, Morgantown, WV, USA. Conflicts of interest: none declared.
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Figure 1 The structure of a neuron A. terminal button B. myelin C. node of Ranvier D. cell body/perikaryon E. dendrite.
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their anatomic course, nerves can have one fascicle (monofascicular), a few fascicles (oligofascicular), or many different fascicles (polyfascicular). Also, given the extent of nerve excursion and gliding throughout the extremities e in particular the upper extremity e a nerve repair which tethers the nerve can delay or prevent functional repair and actually worsen outcomes by causing neuropathic pain.6 After an injury to a peripheral nerve, both mechanical and cell biological factors play a role in the degeneration of the proximal stump and the distally amputated end. From a mechanical standpoint, direct injury to the capillaries surrounding the nerve creates increased vascular permeability. The release of serotonin and histamine by immunologic mast cells, which reside in the endoneurium and epineurium, also causes increased vascular permeability locally.7 Wallerian degeneration refers to the cascade of cellular and molecular events that occurs with direct injury to the axon and ultimately causes conduction failure.8 This phenomenon occurs between 48 and 160 h after the initial insult.1 Myelin, microtubules, and neurofilaments all degenerate in the presence of extracellular calcium and calcium-sensitive proteases, which digest the proteins comprising neurons. Myelin is believed to be broken down by activation of the erbB2 receptor on Schwann cells. It is then phagocytized by macrophages over a period of 48e96 h. This breakdown progresses from proximal to distal and begins at the site of injury. While macrophages are responsible for the uptake of degenerated myelin, they also express interleukin-1, which is believed to stimulate the production of nerve growth factor (NGF) by Schwann cells. NGF is essential for axonal regeneration and myelin formation.9 Schwann cells themselves increase to a peak number about 3 days postinjury. They produce several substances which encourage axon growth, including fibronectin, laminin, and neurotrophins. Structurally, they can self-organize into tubes called Bands of Bugner and provide support to the proximal stump. Despite these extensive mechanical and biological factors working to regenerate the nerve, they are not sufficient; surgical repair is needed for re-innervation of the transected distal end. Without nerve repair, lack of conduction to target organs over time leads to the loss of motor end plates and muscle fibrosis.1 The use of neurotrophin-4 in fibrin glue has been shown to improve outcomes when used with nerve transection and direct repair.10
A
B C
E D
Figure 2 The structure of a Schwann cell A. axon B. fascicle C. myelin D. Schwann cell E. Schwann cell nucleus.
extrafascicular epineurium surrounds the entire nerve and anchors blood vessels to the nerve.5 At certain points along the nerve, vascular pedicles cross the paraneurium/mesoneurium to reach the nerve, and along this layer, gliding of the nerve across its surrounding anatomy also occurs. Identification of individual fascicles during nerve repair is critical for optimal outcomes. Along
A C D
B E
Classification Nerve injuries can be roughly classified as either temporary (neurapraxia, axonotmesis) or permanent (neurotmesis). Seddon first advocated this classification in 1948, which was modified a few years later by Sunderland.11 A Sunderland First Degree Injury corresponds to a neurapraxia, meaning a partial disruption in conduction at the site of injury. However, since the basic structure of the axon is preserved, Wallerian degeneration does not occur. Compression neuropathies such as carpal tunnel syndrome fall into this category. These injuries typically take 3e4 months to recover with treatment.12 Second, third, and fourth degree injuries all fall into the broader category of axonotmesis, where axons are damaged to such a degree that Wallerian degeneration does occur. In Second Degree Injuries, the endoneurial sheath and Schwann cells are left intact. Although recovery is lengthy, the intact endoneurium allows for regeneration in a directed fashion. Distal to the
F
H G
I
Figure 3 The structure of connective tissue in a peripheral nerve. A. axon B. node of Ranvier C. myelin D. endoneurium E. fascicle F. perineurium G. interfascicular epineurium H. extrafascicular epineurium I. paraneurium/ mesoneurium.
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site of injury, conduction velocity is slowed or absent. In Third Degree Injuries, the endoneurium is disrupted, although the perineurium is left intact. In such cases, fibrosis can occur intrafascicularly, causing suboptimal regeneration. Motor and sensory function both decrease, and the return of either is significantly delayed, if at all. In Fourth Degree Injuries, the epineurium is the only portion of the nerve still intact. Scarring and degeneration are more significant than with lower grade injuries, and more of the proximal stump undergoes degeneration. At this level, excision of the scar and surgical nerve repair are necessary for any successful regeneration. Finally, Fifth Degree Injuries are termed neurotmesis. Complete transaction of the nerve with scar formation, resulting in a neuroma at the proximal end and Wallerian degeneration at the distal end, mandates surgical repair.13,14
the course of the affected nerve will be positive at the site of the nerve injury. The appearance of the wound can affect the timing of nerve repair. In general, there are three types of wounds: tidy, untidy, and closed traction injuries. A tidy wound involves a sharp edge, such as one made by glass or a scalpel, and usually means that primary repair is a good option as the injury is confined to the wound edges. Open fractures or gunshot wounds will produce untidy wounds, where there is extensive tissue damage and often infection. Infection in the local soft tissue bed or systemic sepsis is contraindication to immediate nerve repair. Closed traction injuries produce the worst outcomes of all wounds due to the retraction of nerves and vessels, as well as the generally poor condition of the surrounding soft tissues. Electromyography and nerve conduction studies can be difficult to interpret in the setting of an acute nerve injury. Fibrillation potentials indicating motor injury may not appear until 10e14 days after injury, and stimulation of the distal nerve end can persist for several days following complete nerve transection.15 After a nerve injury, electromyographic findings can precede clinical improvement and may lead one to falsely predict full recovery. Electrodiagnostic studies can be most useful intraoperatively to check the presence or absence of an action potential in the nerve distal to the injury, especially when the nerve is not completely transected and has neuroma formation. One can even distinguish between an intact fascicle and a neuroma. Clinically, the size and hardness of the neuroma is a negative factor for recovery, but good amplitude signals distal to the nerve lesion indicate a better prognosis because they suggest that intact fascicles are traversing the lesion.1 If one must extend the incision past the initial wound, an incision should not be made directly over the site of the repair or conduit. Intraoperatively, one should begin by examining the soft tissue bed and ensuring that there are no signs of infection. The proximal and distal ends of the nerve should be mobilized if necessary, to help take tension off the repair as much as possible, but with minimal handling of the nerve ends to decrease fibrosis and damage to the remaining vascular pedicles. If there is tension on the repair, one should consider the possibility of using a nerve conduit or graft, as results with nerve grafting/conduit without tension produce better results than primary repair with tension. One should examine the proximal and distal stumps for scar tissue formation. The ends should be sharply cut with a razor blade to identify the individual fascicles or groups of fascicles. After mobilizing and preparing the nerve ends, a direct end-toend repair of the nerve ends should be attempted when there is no excessive tension. The ends should be repaired at the level of the epineurium with 8-0, 9-0, or 10-0 nylon depending on size of the nerve. If possible, groups of fascicles should be repaired individually, so long as this does not significantly lengthen the tourniquet time. Perineurial intrafascicular repair and epineurial repair have been shown in studies to have equivalent results.16,17 Using the epineurial blood vessels as one’s guide can help align individual fascicles. Accurate identification of motor and sensory fascicles can be aided by using intraoperative nerve stimulation or histochemical identification (carbonic anhydrase for sensory fibres and, acetylcholinesterase for motor fibres), the latter of which can take at least an hour.18 When using direct electrical stimulation, one can use methylene blue or 10-0 nylon to label individual fascicles. Early use of this technique showed
Evaluation and surgical repair The decision to repair a nerve takes into account both the condition of the nerve and the capabilities of the operating team. Nerve exploration and repair is indicated in the following settings: paralysis associated with a wound in the vicinity of a nerve; a closed injury with soft tissue damage; an open injury requiring open reduction and internal fixation.1 Other indications include nerve lesions with arterial injury, traction injuries to the brachial plexus, declining nerve function under observation, failure to improve neurologically after a closed injury, failure to improve after a conduction block within 6 weeks of injury, and persistent pain or neuroma formation. To be worthwhile, a reasonable chance of regaining motor and/or sensory function must exist through the use of direct nerve repair or nerve grafting, nerve allografts, or nerve conduits. If this is not possible, the surgeon should consider alternatives such as tendon transfers. When performing surgical repair, age is the most important prognostic factor. Younger patients consistently have better outcomes. Sharp transection injuries can be repaired more acutely, within 24 h, whereas crush or avulsion injuries should be repaired on a slightly delayed basis (5e7 days out) to allow for tissue planes to demarcate. This is particularly important in cases of gunshot wounds or saw wounds. Finally, in the case of pure sensory deficits, a longer delay is reasonable and can still have good outcomes. Nerve injuries associated with vascular injury or compartment syndrome should be explored urgently. One should delay or forgo nerve repair when the overall condition of the patient does not allow further surgery, when specialized equipment is unavailable, or when there is a high risk of infection. In rare cases, tendon transfer provides superior outcomes to peripheral nerve repair and therefore, attention should also be given towards those reconstructive efforts in appropriate cases. This is true in cases where the patient presents with a long-term neurologic deficit, rather than an acute injury, or where there is such a large deficit in the nerve that repair, even with grafting, will result in inferior motor and sensory recovery.1 Preoperatively, the patient should have a thorough exam detailing baseline motor and sensory deficits. Moving and static 2-point discrimination, sharp and dull discrimination, grading of grip and pinch strength, and condition of the surrounding soft tissue should all be tested and documented. In the cases of brachial plexus traction injuries, one should check for ecchymosis and swelling at the neck and shoulder. A Tinel’s sign over
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promising results in nine patients, although all were primary repairs.19 The increased handling required to identify various fascicles can lead to increased scar tissue formation and tourniquet time, which may theoretically negate the benefit of matching fascicles using electrical stimulation or histochemistry.
treated to maximize Schwann cell development, was used in rats after a spinal cord contusion as a local autograft. The rats treated with the graft fared better than those without, and the rats who received the treated Schwann cell grafts had the best results.24 Two novel grafting methods have suggested alternatives to the more traditional techniques just described. A rat peroneal nerve defect was treated by suturing the proximal and distal ends to the epineurium of the intact tibial nerve in an end-to-side fashion. This technique was shown to not injure the tibial nerve, and showed similar results to autografting.25 A helicoid method of repair also yielded superior histologic and muscle volume results when compared to a traditional end-to-side techniques in rat peroneal nerves.26
Nerve grafts Nerve grafts and conduits are helpful in cases where tension on the nerve repair is difficult to avoid. Most research on different types of nerve grafts shows that autografts are a superior choice for grafting, given the immunologic complications that arise in allografts, and the need for immunosuppressives.20 Although the authors do not have personal experience with allografts, one should not discount allografts out of hand, especially for shorter defects, given the recent developments in decreasing graft immunogenicity. Processing the graft to make it acellular removes Schwann cells, as well as debris and proteoglycans, which can inhibit nerve growth or produce an immunologic response.21 In a rodent model, the use of acellular allografts in short nerve defects produced a higher axon count than nerve conduits, but less than isografts. These encouraging results were not reproduced when a longer nerve defect model was employed.22 Finally, ten nerve defects from 0.5 to 3.0 cm which were repaired with acellular allograft showed acceptable 2-point discrimination recovery. Thus, allografts may be a reasonable choice in certain situations.23 With autografts, the best results have occurred with interfascicular grafting, where one dissects individual fascicles of the damaged nerve and graft and interposes them. This maximizes the surface area for healing. Free vascularized nerve grafts have the advantage of their own blood supply, but studies have not shown a definite benefit versus free nerve grafts. They are recommended in cases where there is a scarred wound bed and a long nerve defect.1 Simple end-to-end grafting with a free graft is often not successful because the graft will fibrose before regeneration has a chance to occur. Autografts should be expendable with minimal donor site morbidity, have a known ratio of axons to fibrous tissue, and be thin enough to survive free grafting. One can harvest 30e40 cm from certain nerves with minimal functional deficit. The sural, lateral antebrachial cutaneous, and terminal branch of the posterior interosseus nerve are common donor sites for nerve grafts. Owing to the dense numbness which occurs at the base of the thumb, one should avoid the superficial radial nerve if possible; its use is contraindicated with a median nerve deficit. The sural nerve should be approached from a posterior midline incision, beginning at the lateral malleolus and extending proximally, where it lies lateral to the short saphenous vein. The lateral cutaneous nerve of the forearm can be found lateral to the biceps tendon, between the biceps and the brachialis. The length of the nerve defect should be measured with the wrist in neutral position and the elbow in extension. The nerve graft must be 15e20% longer than the defect measured because of the predicted elastic recoil postoperatively. One should keep the graft prepared with gauze moistened with blood or lactated Ringer’s solution. Fresh synovium or fat are good tissue beds for nerve grafting, while muscle, bone, and implants are not. With larger nerves, one can use several segments from a single graft to reconstruct each fascicle, using sutures through the epineurium of the graft and the perineurium/internal epineurium of each fascicle. Absorbable sponges can be used as buttresses to hold the graft in place. A sciatic nerve graft, either on its own or
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Nerve conduits Nerve conduits, either using autologous or engineered tissue, are another option to aid in nerve repair. These tubes allow for directed Schwann cell growth and subsequent axonal growth into the distal end of the nerve. They can be used for gaps up to 3 cm in length, although some studies have shown good results with defects of up to 4 cm. Autologous choices include vein and skeletal muscle. Although veins have shown good results, their parameters are limited and should be used only in sensory nerves with a defect of less than 3 cm.27 A promising case series of muscle in vein conduits showed good to excellent results in 14 of 22 people treated for nerve defects averaging 2.2 cm in length.28 Histological analysis shows that Schwann cells migrate into the tube during week 2 after repair with axon formation following shortly thereafter at week 3 and myelination at week 4.29 Skeletal muscle has shown better results than direct repair in some cases, but their disadvantages include donor site morbidity and a blockage to nerve growth by the growth of new muscle fibres. Engineered nerve conduits are available in diameters ranging from 1.5 to 10 mm, as well as absorbable and nonabsorbable forms.30 Nonabsorbable conduits include Gore-Tex and silicone, which have had some promising results but do have irritation as a side effect.31 Absorbable conduits include the NeuroTube, which is comprised of polyglycolic acid (PGA) and has been approved for use since 1999 (Synovis, Birmingham, AL, USA). Studies have shown the NeuroTube to yield better results than direct repair in cases of gaps less than 4 mm, as well as better results than nerve grafting in gaps up to 30 mm. NeuroTubes are indicated in the case of digital nerve repairs as well as mixed motor and sensory nerves with a segmental defect of less than 2 cm. The NeuroTube is recommended for defects between 8 mm and 3 cm. Because it is made of polyglycolic acid, it can begin to break down around 3 months into nontoxic glycolic acid. Collagen conduits (NeuraGen e Integra LifeSciences, Plainsboro, NJ, USA) are derived from bovine deep flexor tendons. An animal study in 2001 showed collagen nerve tubes were effective in treating 20 mm nerve defects in rat sciatic nerves.32 In a series of 12 patients treated with collagen tubes, the nine patients available for follow-up at 1 year showed an 88% rate of good or excellent results for 2-point discrimination.33 All patients had a defect of 2 cm or less. Similarly, Lohmeyer et al. showed good to excellent results in 2-point discrimination in six patients treated with collagen conduits, after more than 6 months of follow-up.34 Collagen has the advantage of being semipermeable, allowing for the diffusion of nerve growth factors into the tube. In 2007, Waitayawinyu showed that repair with
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collagen tubes resulted in better muscle contraction than PGA, when used to treat 10 mm gaps in rat sciatic nerves.35 A biodegradable Neurolac (Polyganics B.V., Groningen, The Netherlands) tube, made of copolyester poly (DL-lactide-e-caprolactone), showed equivalent results to standard repair techniques in a clinical study, although there were more complications in the Neurolac group.36 Animal research on bioengineered conduits show that nerve/vein and muscle/vein grafts have better outcomes than single component conduits, and may even be able to increase the maximum length (3 cm) that can be bridged. These conduits can also be enriched with NGF, ciliary neurotrophic factor, glial growth factor, and Schwann cells. NGF was shown to double the size of the myelin sheath and the number of axons when used with silicone grafts. Ciliary neurotophic factor improved nerve growth and myelination in 10 mm rat sciatic nerve defects. When used with a vein conduit, Schwann cells helped bridge nerve defects in rabbits of up to 60 mm. 10 mm long rat sciatic nerve injuries treated with a collagen tube filled with Schwann cells showed similar results to a sural nerve graft.37 A similar rat study showed that Schwann cells in a TMC/CL conduit induced healing in a 2 cm median nerve defect.38
nerve is of paramount importance; a pulseless or dysvascular limb produces a worse soft tissue bed for nerve repair than a healthy one. Axonal regeneration proceeds at a rate of about 1 mm per day, although it is faster in children and after primary (versus secondary) repair. Surgically, the delay between injury and nerve repair, as well as the condition of the nerve ends prior to the repair, and the damage sustained to them during the nerve repair all contribute to the recovery of nerve function.45 In a study of upper extremity injury patients, nerve injuries associated with older patients had higher pain scores, and more proximal injuries (i.e., brachial plexus injuries versus peripheral nerve injuries) showed higher DASH (Disabilities of the Arm, Shoulder and Hand) scores and thus more long-term disability.46 Paediatric nerve injuries, as stated previously, have far better results than those of adults, with faster recovery and lower incidence of neuropathic pain.47,48 However, issues unique to paediatric nerve repair which can negatively affect their outcome need to be taken into consideration. Since myelination is not yet complete in the infant, the conduction velocity of both motor and sensory neurons is decreased, and injury to this developing system can be catastrophic. If a body part is insensate in a child, this organ may be functionally ignored, and disuse can subsequently contribute to a slow recovery. Nerve injury can also cause growth disturbance and muscular imbalance, which can in turn impair functions such as ambulation and grasp. Despite these factors, rapid treatment of nerve injuries where there is an identifiable cause, leads to better results. Fractures with nerve entrapment should be explored. Compartment syndrome should be watched closely for signs of nerve involvement (since this typically occurs after muscle injury), and vascular injuries in children should be repaired as completely as possible.49 Postoperatively, the degree of functional recovery can be assessed in many ways. The Medical Research Council (MRC) System grades both motor and sensory recovery. Motor recovery is graded as M0 (no contraction), M1 (contraction in muscles proximal to the lesion), M2 (contraction in muscles proximal and distal to the lesion), M3 (contraction in all important muscles), M4 (contraction in all muscles acting synergistically), and M5 (complete recovery).50 Of these, M4 or better is “good”, M3 is “fair”, M2 is “poor”, and M1 or worse is “bad”, when using the simplification by Birch.1 Sensory recovery is graded as S0 (absence of sensation in the area), S1 (recovery of deep pain), S2 (recovery of pain and light touch), S3 (recovery of pain and light touch with disappearance of hypersensitivity), S3þ (return of 2point discrimination), S4 (complete recovery). Of these, S3þ/4 is “good”, S3 is “fair”, S2 is “poor”, and S1/0 is “bad”. There are special scales for grading median and ulnar nerve function, which correspond accurately to the MRC system and to the patient’s own subjective sense of function.51 Rehabilitation of the patient begins with repair of the nerve. Rehabilitation goals should include the following: (a) an objective assessment of initial disability. (b) the lessening of disability with physical, occupational, and hand therapy. (c) the return of the patient to his or her previous or a modified work environment. (d) a return to his or her recreational activities. (e) independent mobility.
Nerve glue In addition to conduits, one can also consider the various fibrinbased “nerve glues,” which may decrease gapping at the repair site. According to a recent cadaver study, Tisseel, Evicel, and DuraSeal all helped prevent initial gapping but did not increase the load to failure of the repair.39 Other methods of nerve repair Other methods examined in nerve repair include freeze-thawed muscle graft, nerve transfer, and direct muscular neurotization. Thus far, freeze-thawed muscle graft has shown only equivocal results.40 Nerve transfer, where an uninjured nerve is transferred to the distal stump of an injured nerve, has had promising results but is not yet a primary method, in part because there is sometimes a need for sensory retraining.41 Direct muscular neurotization, where one takes the avulsed end of a nerve and implants it directly into the muscle, is also a viable option, although it is used mostly in more proximal injuries.42
Recovery and rehabilitation Postoperatively, tension must be taken off the repair by splinting the extremity in an appropriate position for 2e3 weeks. In the case of repair at or near the wrist, a dorsal blocking splint is then applied for 3 more weeks.30 The likelihood of a successful recovery depends on several factors, both in the patient and during surgery. According to several studies, patient age and time elapsed between injury and repair are the most important factors in prognosis. A delay in repair of 6 days produces a decrease in performance of 1% relative to maximal performance.43,44 In general, more distal lesions recover more quickly, although repair of certain trunks of the brachial plexus has produced excellent results. Nerves which supply one or two muscle bellies tend to fare better than nerves which have mixed sensory and motor components. Unfortunately, all median, radial, and ulnar nerves belong to the latter group. Finally, the condition of the tissue surrounding the injured
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REFERENCES 1 Birch R. Nerve repair. In: Green DP, Hotchkiss RN, Pederson WC, Wolfe SW, eds. Green’s operative hand surgery. Philadelphia: Elsevier Churchill Livingstone, 2005; 1075e1111. 2 Webster Hde F. Development of peripheral nerve fibers. In: Dyck PJ, Thomas PK, Griffin JW, et al., eds. Peripheral neuropathy. Philadelphia: WB Saunders, 1993; 243e266. 3 Lundborg G. The nerve trunk. Nerve injury and repair. London: Churchill Livingstone, 1988. 32e63. 4 Sunderland S. Peripheral nerve trunks. Nerve and nerve injuries. Edinburgh: Churchill Livingstone, 1978. 31e60. 5 Jabaley ME. Internal topography of peripheral nerves as related to repair. In: Gelberman RH, ed. Operative nerve repair and reconstruction. Philadelphia: JB Lippincott, 1991; 231e240. 6 Millesi H, Zoch G, Rath T. The gliding apparatus of peripheral nerve: its clinical significance. Ann Hand Surg 1990; 9: 87e97. 7 Rowshan K, Gupta R. Peripheral nerve physiology, injury, and repair. In: Trumble TE, Budoff JE, eds. Hand surgery update IV. Rosemont: American Society for Surgery of the Hand, 2007; 389e399. 8 Waller A. Experiments on the section of the glossopharyngeal and hypoglossal nerves of the frog, and observations of the alterations produced thereby in the structure of their primitive fibres. Philos Trans R Soc Lond 1850; 140: 423e9. 9 Golz G, Uhlmann L, Ludecke D, Markgraf N, Nitsch R, Hendrix S. The cytokine/neurotrophin axis in peripheral axon outgrowth. Eur J Neurosci 2006; 24: 2721e30. 10 Yin Q, Kemp GJ, Yu LG, Wagstaff SC, Frastick SP. Neurotrophin-4 delivered by fibrin glue promotes peripheral nerve regeneration. Muscle Nerve 2001; 24: 345e51. 11 Flores AJ, Lavernia CJ, Owens PW. Anatomy and Physiology of peripheral nerve injury and repair. Am J Orthop 2000; 39: 167e73. 12 Isaacs J. Treatment of acute peripheral nerve injuries: current concepts. J Hand Surg 2010; 35: 491e7. 13 Seddon HJ. Three types of nerve injury. Brain 1943; 66: 237e88. 14 Sunderland S. A classification of peripheral nerve injuries producing loss of function. Brain 1961; 74: 491e516. 15 Smith SJM. Electrodiagnosis. In: Birch R, Bonney G, Wynn Parry CB, eds. Surgical disorders of the peripheral nerves. London: Churchill Livingstone, 1998; 467e490. 16 Cabaud HE, Radkey WG, McCarroll Jr HR, Mutz SB, Niebauer JJ. Epineurial and perineurial fascicular nerve repairs: a critical comparison. J Hand Surg 1976; 1: 131e7. 17 Murray JA, Willins M, Mountain RE. A comparison of epineurial and perineurial sutures for the repair of a divided rat sciatic nerve. Clin Otolaryngol Allied Sci 1994; 19: 95e7. 18 He YS, Zhong SZ. Acetylcholinesterase: a histochemical identification of motor and sensory fascicles in human peripheral nerve and its use during operation. Plast Reconstr Surg 1988; 82: 125e32. 19 Hakistan RW. Funicular orientation by direct stimulation: an aid to peripheral nerve repair. J Bone Joint Surg Am 1968; 50: 1178e86. 20 Mackinnon SE, Doolabh VB, Novak CB, Trulock EP. Clinical outcome following nerve allograft transplantation. Plast Reconstr Surg 2001; 107: 1419e29. 21 Krekoski CA, Nebauer D, Zuo J, Muir D. Axonal regeneration into acellular nerve grafts is enhanced by degradation of chondroitin sulfate proteoglycan. J Neurosci 2001; 21: 6206e13. 22 Hudson TW, Zawko S, Deister C, et al. Optimized acellular nerve graft is immunologically tolerated and supports regeneration. Tissue Eng 2004; 10: 1641e51.
General issues addressed by rehabilitation include motor and sensory deficits, fixed deformities, and loss of confidence, balance, and endurance. One should also consider the difference between complex regional pain syndrome or neuropathic pain versus the extremely common phenomena of cold sensitivity and regenerative pain. Encouragement to return to activity is the most helpful advice in these circumstances. Finally, one must take into account a patient’s functional demands at work and train them with these in mind, with return to work as the ultimate goal. If retraining is necessary, it is important to broach this possibility with the patient at an early stage in the rehabilitation process, although to discuss it too early may lead to a “self-fulfilling prophecy” of continued disability and pain. Tests of function as well as sensation is important in obtaining a clinically relevant picture of a patient’s ultimate limitations. Future directions for peripheral nerve repair involve both surgical techniques and biotherapies, which are currently being studies in animal models. A rabbit study supported the use of progressive distraction with an external fixator as a way to allow for primary median nerve repair and simultaneously accommodate for a defect in the nerve length of up to 7 mm. The rabbits studied showed higher nerve conduction velocities at 6 months postoperatively, as well as a larger neuromuscular junction surface area in the group treated with progressively extended external fixator positioning versus autografting or brief immobilization followed by unprotected elbow motion.52 From an immunologic standpoint, rats with a sciatic nerve crush injury were treated with glatiramer acetate, a multiple sclerosis drug which activates T suppressor cells and thus aids in nerve regeneration. The rats treated with glatiramer acetate showed greater muscle responses and higher axon counts than control groups. In addition, T-cell deficient rats did not show an increased muscle response to glatiramer acetate, although they did have a delayed increase in axon counts at 6 weeks. This confirms that T-cell suppression is a critical mechanism behind glatiramer acetate’s promotion of peripheral nerve regeneration.53 Erythropoietin, when given to rats after a sciatic injury, led to improvement in sciatic function index. This occurred more quickly with early administration of erythropoietin, but administration after 1 week also showed benefits.54 A combination of a silicone nerve conduit filled with a fibrin-based delivery system which allowed for controlled release of glial-derived neurotrophic factor showed similar results to the use of an isograft, both histologically and functionally.55 Keratin hydrogel-filled silicone conduits showed equivalent results to sural nerve autografts at 6 months with 4 mm rat tibial nerve defects.56 Repairing peripheral nerves with the argon laser yielded better neuromuscular function at 6 months postoperatively in rabbit peroneal nerves when compared to epineural suture repair, but there are no comparable human studies to evaluate this technique in a clinical setting.57 Nitric oxide, when administered to rats after an ischaemic injury to the rat sciatic nerve, showed an improvement in histology and functional recovery when compared to controls or steroids.58 Ultimately, peripheral nerve injuries have a critical impact on patients’ lives and functioning. Sound microsurgical technique as well as a tension-free repair is an important factor in a successful outcome. Various products to bridge the defect can help optimize the chances of a meaningful recovery. A ORTHOPAEDICS AND TRAUMA 25:3
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23 Whitlock EL, Tuffaha SH, Luciano JP, et al. Processed allografts and type I collagen conduits for repair of peripheral nerve gaps. Muscle Nerve 2009; 39: 787e99. 24 Rasouli A, Bhatia N, Suryadevara S, Cahill K, Gupta R. Transplantation of preconditioned Schwann cells in peripheral nerve grafts after contusion in the adult spinal cord. J Bone Joint Surg Am 2006; 88: 2400e10. 25 McCallister WV, Cober SR, Norman A, Trumble TE. Using intact nerve to bridge peripheral nerve defects: an alternative to the use of nerve grafts. J Hand Surg Am 2001; 26A: 315e25. 26 Yan JG, Matloub HS, Sanger JR, Zhang LL, Riley DA, Jaradeh SS. A modified end-to-side method for peripheral nerve repair: large epineurial window helicoid technique versus small epineurial window standard end-to-end technique. J Hand Surg Am 2002; 27: 484e92. 27 Stahl S, Rosenberg N. Digital nerve repair by autogenous vein graft in high-velocity gunshot wounds. Mil Med 1999; 8: 603e4. 28 Ignazio M, Adolfo V. Muscle-in-vein nerve guide for secondary reconstruction in digital nerve lesions. J Hand Surg Am 2010; 35A: 1418e26. 29 Tseng CY, Hu G, Ambron RT, Chiu DT. Histologic analysis of Schwann cell migration and peripheral nerve regeneration in the autogenous venous nerve conduit (AVNC). J Reconstr Microsurg 2003; 19: 331e40. 30 Agnew SP, Dumanian GA. Technical use of synthetic conduits for nerve repair. J Hand Surg 2010; 35A: 838e41. 31 Lundborg G, Ros en B, Dahlin L, Danielsen N, Holmberg J. Tubular versus conventional repair of median and ulnar nerves in the human forearm: early results from a prospective, randomised clinical study. J Hand Surg Am 1997; 22: 99e106. 32 Yoshii S, Oka M, Ikeda N, Akagi M, Matsusue Y, Nakamura T. Bridging a peripheral nerve defect using collagen filaments. J Hand Surg Am 2001; 26A: 52e9. 33 Bushnell BD, McWilliams AD, Whitener GB, Messer TA. Early clinical experience with collagen nerve tubes in digital nerve repair. J Hand Surg 2008; 33A: 1081e7. 34 Lohmeyer J, Zimmerman S, Sommer B, Machens HG, Lange T, Mailander P. Bridging peripheral nerve defects by means of nerve conduits. Chirurg 2007; 78: 1152e3. 35 Waitayawinyu T, Parisi DM, Miller B, et al. A comparison of polyglycolic acid versus type 1 collagen bioabsorbable nerve conduits in a rat model: an alternative to autografting. J Hand Surg 2007; 32A: 1521e9. 36 Bertleff MJOE, Meek MF, Nicolai J-PA. A prospective clinical evaluation of biodegradeable neurolac nerve guides for sensory nerve repair in the hand. J Hand Surg Am 2005; 30A: 513e38. 37 Kim DH, Connolly SE, Kline DG, et al. Labeled Schwann cell transplants versus sural nerve grafts in nerve repair. J Neurosurg 1994; 80: 254e60. 38 Sinis N, Schaller HE, Schulte-Eversum C, et al. Nerve regeneration across a 2-cm gap in the rat median nerve using a resorbably nerve conduit filler with Schwann cells. J Neurosurg 2005; 103: 1067e76. 39 Isaacs JE, McDaniel CO, Owen JR, Wayne JS. Comparative analysis of biomechanical performance of available “nerve grafts”. J Hand Surg Am 2008; 33A: 893e9.
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40 Lawson GM, Glasby MA. A comparison of immediate and delayed nerve repair using autologous freeze thawed muscle grafts in a large experimental animal. J Hand Surg Br 1995; 20: 663e70. 41 Ozkan T, Ozer K, Gulgonen A. Restoration of sensibility in irreparable ulnar and median nerve lesions with use of sensory nerve transfer: long-term follow up of 20 cases. J Hand Surg 2001; 26: 44e51. 42 Brunelli G, Monini L. Direct muscular neurotisation. Proceedings of the second congress of the international federation of societies for surgery of the hand. J Hand Surg 1985; 10: 993e4. 43 Omer GE. Injuries to nerves of the upper extremity. J Bone Joint Surg 1974; 56: 1615e24. 44 VA Medical Monograph. In: Woodhall B, Beebe GW, eds. Peripheral nerve regeneration. Washington, DC: U.S. Government Printing Office, 1956. 45 Seddon HJ, ed. Medical Research Council Special Report Series No. 282. Peripheral nerve injuries. London: Her Majesty’s Stationery Office, 1954. 46 Novak CB, Anastaskis DJ, Beaton DE, Katz J. Patient-reported outcome after peripheral nerve injury. J Hand Surg Am 2009; 34A: 281e7. 47 Lundborg G, Rosen B. Sensory relearning after nerve repair. Lancet 2001; 358: 809e10. 48 Lundborg G, Rosen B. Hand function after nerve repair. Acta Physiol (Oxf) 2007; 189: 207e17. 49 Klink BK, Kleinart JM. Upper extremity vascular injuries. In: Gupta A, Kay SPJ, Sceker LR, eds. The growing hand. St. Louis: Mosby, 2000; 659e664. 50 Seddon HJ. Results of repair of the nerves. Surgical disorders of peripheral nerves. Edinburgh: Churchill Livingstone, 1975. 303e314. 51 Rosen B, Lundborg G. A model instrument for the documentation of outcome after nerve repair. J Hand Surg Am 2000; 25: 535e43. 52 Ruch DS, Deal DN, Ma J, et al. Management of peripheral nerve defects: external fixator-assisted primary neurorrhaphy. J Bone Joint Surg Am 2004; 86-A: 1405e13. 53 Luria S, Waitayawinyu T, Conniff J, et al. Glatiramer acetate immune system augmentation for peripheral nerve regeneration in rat model. J Bone Joint Surg Am 2010; 92-A: 396e403. 54 Elfar JC, Jacobson JA, Puzas JE, Rosier RN, Zuscik MJ. Erythropoietin accelerated functional recovery after peripheral nerve injury. J Bone Joint Surg Am 2008; 90: 1644e53. 55 Moore AM, Wood MD, Chenard K, et al. Controlled delivery of glial cell line-derived neurotrophic factor enhances motor nerve regeneration. J Hand Surg Am 2010; 35A: 2008e17. 56 Apel PJ, Garrett JP, Sierpinski P, et al. Peripheral nerve regeneration using a keratin-based scaffold: long-term functional and histological outcomes in a mouse model. J Hand Surg Am 2008; 33A: 1541e7. 57 Campion ER, Bynum DK, Powers SK. Repair of peripheral nerves with the argon laser. J Bone Joint Surg Am 1990; 72: 715e23. 58 Park JW, Qi WN, Cai Y, Nunley JA, Urbaniak JR, Chen LE. The effect of exogenous nitric oxide donor on motor functional recovery of reperfused peripheral nerve. J Hand Surg Am 2005; 30A: 519e27.
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canal (antero-posterior (AP) canal diameter <13 mm), cervical disc herniation, vertebral body osteophyte formation, degenerative osteophytosis of four articulations (two facet joints and two uncovertebral joints) and hypertrophy/infolding/ossification of the ligamentum flavum and posterior longitudinal ligaments. The spondylotic changes begin with disc degeneration leading to its dessication, fragmentation, herniations, and collapse. The loss of disc material and structure has been thought to increase stress forces across adjacent vertebral endplates with resultant hypermobility.3,4 Reactive subperiosteal bone formation subsequently occurs to stabilize adjacent vertebral bodies by increasing the weight bearing surface area of these endplates. Osteophytosis of joint articulations with ligamentous changes occur additionally as part of the degenerative process. Factors increasing the risk of spondylotic changes include repeated axial loading,5 genetic predisposition,6,7 and Down’s syndrome.8 Smoking9 is also linked indirectly to CSM by disc degeneration. Dynamic factors refer to abnormal compressive forces exerted on the cervical spinal cord initiated by static factors during physiologic flexion and extension of the cervical spine. Neck extension can result in cervical cord pinching between a degenerated disc and osteochondral bar anteriorly, and the hypertrophied facet joints and infolded ligaments posteriorly. Neck flexion normally increases the canal dimension slightly to relieve cord compressive pressures. However, in the presence of spondylosis, neck flexion can result in stretching of the spinal cord over the ventral osteophytic bars. The repeated trauma of such movements has been likened to the high shear forces seen in acute spinal cord injury.10 Mechanical compression can also produce disruptions to the vascular supply of the spinal cord in three ways. First of all, the large blood vessels such as the anterior spinal artery can be directly compressed. Secondly, penetrating small arteries and the pial plexuses may have reduced blood flow. Lastly, venous congestion can result from increased pressures. It is not surprising that the region of the cervical cord (C5eC7) most commonly implicated in CSM corresponds to the area of most tenuous blood supply.11 Pathological studies12e14 have shown that, over time, a pattern similar to that of a transient hypoperfusion syndrome was found with neuronal loss and atrophy in the gray matter and severe degeneration in the white matter columns. Specifically, gray matter infarction and cavitation were found together with white matter demyelination of the lateral and posterior columns. Wallerian degeneration can be found in tracts above and below the site of compression. The anterior columns of the cervical spinal cord are affected in rare instances.
(iv) Cervical spondylotic myelopathy: a brief review of its pathophysiology, presentation, assessment, natural history and management Lushun Wang Hwan Tak Hee Hee Kit Wong
Abstract Cervical spondylotic myelopathy (CSM) is a debilitating condition associated with spinal cord dysfunction. It frequently occurs in the elderly and accounts for the majority of non-traumatic spastic paraparesis and quadriparesis. Cervical myelopathy refers to the clinical syndrome of long-tract aberrations in both upper and lower extremities arising from cervical spinal cord compression. It is most commonly caused by degenerative spondylosis leading to circumferential compression of the cervical spinal cord, often in a congenitally narrowed spinal canal. This article summarizes the current evidence surrounding the pathophysiology, presentation, assessment, natural history, and management of patients with cervical spondylotic myelopathy.
Keywords cervical; diagnosis; myelopathy; natural history; spondylosis; treatment
Pathophysiology First described by Brain and his colleagues1 in 1952, the primary anatomical pathology of CSM is a reduction in the sagittal diameter of the cervical spinal canal. This can be caused by mechanical factors working statically or dynamically as categorized by White and Panjabi.2 Static factors include the presence of a congenitally stenotic cervical spinal Lushun Wang MBBS (S’pore) MRCS (Ed) University Spine Center, University Orthopedics, Hand and Reconstructive Microsurgery Cluster, National University Health System, Singapore. Conflicts of interest: none.
Clinical assessment The clinical picture of CSM is varied, with a protean array of symptoms and signs. No single finding is pathognomonic of CSM as it typically presents insidiously. Therefore, its diagnosis requires a high index of suspicion. Findings are dependent upon the anatomical site and the extent of cord compression. Crandall and Batzdorf15 formulated five categories of CSM in 1966 (Table 1) while Ferguson and Caplan16 reported four CSM syndromes (Table 2) more recently in 1985. CSM is a clinical diagnosis resulting from detailed historytaking, accurate physical examination, and supported by corroborating radiological evidence.
Hwan Tak Hee MBBS (S’pore) FRCS (Ed) FRCS (Glas) FAMS (Orth) University Spine Center, University Orthopedics, Hand and Reconstructive Microsurgery Cluster, National University Health System, Singapore. Conflicts of interest: none. Hee Kit Wong MBBS(S’pore) MMED(Surg) FRCS(Glas) MCh(Orth)Liv FAMS University Spine Center, University Orthopedics, Hand and Reconstructive Microsurgery Cluster, National University Health System, Singapore. Conflicts of interest: none.
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Crandal and Batzdorf categories of Cervical Spondylotic Myelopathy (CSM)15 Syndrome 1. Transverse lesion 2. 3. 4. 5.
Description Corticospinal, spinothalamic, and posterior cord tracts involved with almost equal severity. This syndrome is associated with the longest symptom duration, suggesting that this category may be an end-stage of the disease Corticospinal tracts and anterior horn cells involvement, resulting in spasticity Motor and sensory deficits affecting the upper extremities more severely than the lower extremities Ipsilateral motor deficits with contralateral sensory deficits. Least advanced form of the disease. Radicular pain in the upper extremity along with motor and/or sensory long-tract signs
Motor system Central Brown-S equard Brachialgia cord
Table 1
History In the earlier stages of myelopathy, patients may complain of subtle gait disturbances or problems with maintaining their balance. They can also present with neck stiffness because of advanced cervical spondylosis. Pain is a less frequently noted complaint but may occur in the neck, subscapular or shoulder areas. Loss of manual dexterity is also a common presentation and can be accompanied by abnormal sensations. Patients may encounter difficulty with daily actions such as writing, buttoning or unbuttoning of clothing or zippers, and they may complain of “numb and clumsy” hands. Numbness or paraesthesiae in the upper extremities is usually non-specific. Dermatomal distribution of symptoms may occur from a concomitant radiculopathy. No specific level of cervical cord compression is proven to account for loss of hand dexterity and fine movements. It is however believed to be associated with compression above the C6eC7 level.17 Lower limb symptoms include stiffness due to spasticity and weakness. These symptoms are commonly asymmetrical. Sensory changes in the lower limb are common and are due to involvement of the dorsal columns affecting proprioception. Motor weakness can occur in both the upper and lower extremities. Advanced myelopathic patients may present with a classic “spastic gait” that is broad-based, jerky and hesitant. Loss of sphincter control with bowel or urinary tract symptoms signify late stage myelopathy. Urinary retention is a common presentation of sphincter dysfunction. In a review of 1,076 cases of CSM, subtle gait disturbance was the most common presentation.18 This was followed by loss of fine motor control of the hands with numbness. Other authors have also reported similar findings.19
It should be borne in mind that spondylotic degeneration can give rise to concurrent stenosis of the lumbar and cervical portions of the spinal canal in tandem. This can give rise to the triad of intermittent neurogenic claudication, progressive gait disturbance, and findings of mixed myelopathy and poly-radiculopathy in both upper and lower extremities. Examination Upper motor neuron findings or “myelopathic signs” include hyperreflexia, spasticity, clonus, Hoffman and Babinski signs, and the inverted radial reflex. These signs predominate below the level of significant cord compression. Lower motor neuron signs such as hyporeflexia and atrophy can occur at the level of root pathology in coexisting radiculopathy. The sensitivity of the Hoffman sign can be increased by dynamic manoeuvres with full neck extensions and flexions during examination.20 Another useful clinical sign, testing for compression in the upper cervical spine at the C2eC4 levels, is the pectoralis muscle reflex. Adduction and internal rotation of the ipsilateral shoulder occur in hyperreflexia when the pectoralis tendon is tapped in the deltopectoral groove. In a clinical scenario of diffuse hyperreflexia, the absence of the jaw jerk reflex can help to point to a lesion below the level of the foramen magnum. The Lhermitte’s sign is suggestive but is not specific to CSM. It is classically due to posterior column abnormalities. The “finger escape sign” described by Ono21 in 1987 reflects weakness of the intrinsic hand muscles. Spontaneous small finger abduction occurs during prolonged (30 s) finger extension and adduction. Inability to perform 15e20 repetitions of hand grip and release in 10 s is also indicative of a myelopathic hand. Paradoxical wrist motions or “trick motions” are well known in CSM patients, but their presence does not correlate with severity. This was recently reported by Hosono et al.22 Tandem gait testing in patients should be closely supervised due to the risk of falls and may not be possible in patients with severe gait disturbances. A newly reported performance test for CSM by Mihara et al,23 named the Triangle Step Test, can be performed safely in the sitting position and assesses circular foot tapping motions in a three dimensional space. The authors have suggested that this test can reliably evaluate the disability of the lower extremity and its improvement following surgical treatment. Instruments measuring CSM outcomes include the widely used Nurick disability score and the modified Japanese Orthopaedic Association (mJOA) scale scores. Alternative instruments include the Cooper and the Harsh scale as well as the Medical
Ferguson and Caplan cervical spondylotic myelopathy syndromes16 Syndrome Medial Lateral Combined Vascular
Description Primarily long-tract symptoms Primarily radicular symptoms Combined medial and lateral syndrome. Most common clinical presentation Rapidly progressive myelopathy and is thought to represent vascular insufficiency of the cervical spinal cord
Table 2
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Outcomes Study Short Form-36 which assesses the quality of life experienced by myelopathic patients. Myelopathic signs are significantly more common in CSM patients but may be negative in approximately 20% of myelopathic patients,24 The absence of myelopathic signs cannot be used to rule out the diagnosis of CSM. In patients with suspected cervical myelopathy but with no positive signs of CSM, treatment decisions should be based upon symptom presentation corroborated by radiological evidence. Investigations Plain radiographs: cervical spine plain films (AP and lateral) are routine in the assessment of symptomatic spondylotic cervical disease. A narrowed sagittal spinal canal of less than 13 mm suggests spinal stenosis while a Pavlov ratio of <0.8 suggests developmental canal stenosis. The Pavlov ratio is the ratio of the AP diameter of the canal to the AP diameter of the vertebral body at the same level. Plain radiographs are inexpensive and universally available. However, the ubiquitous presence of radiographic spondylotic changes in elderly patients limits their value in diagnosing CSM. Lateral radiographs, however, easily shed light on sagittal alignment, while flexion-extension views can be used to diagnose cervical instability. Such information can influence the choice of surgical procedures in the treatment of CSM.
Figure 1 MRI T2 weighted image showing multi-level cervical canal stenosis, most severe at C5/6 and C6/7 levels with myelomalacia at the C6/7 level.
Magnetic Resonance Imaging (MRI): in clinically suspected CSM, MRI is the investigation of choice as it provides multiplanar imaging and excellent detail of the spinal cord and subarachnoid space. MRI is also very sensitive in detecting the existence of extradural pathology on the spinal cord due to its accuracy in differentiating neural, osseous and soft tissue structures with high-resolution. T2 hyperintensity of the cord suggests myelomalacia, demyelination, gliosis or microcavity formation. Cord inflammation and oedema are reflected by very intense T2 signals. T1 weighted images classically show low signal intensities at the site of cord compression (Figure 1). Current MRI technology can lead to false positives in detecting pathology in asymptomatic patients or in detecting pathology unrelated to symptoms. Teresi et al.25 reported this incidence in asymptomatic individuals, noting apparent spinal cord compression in 16% of patients younger than 64 years of age. This increased to 26% in those who were older than 64 years of age.
studies infrequently employed to exclude differential diagnoses of CSM such as peripheral neuropathy, multiple sclerosis, and amyotrophic lateral sclerosis (ALS). EMGs are useful in the diagnosis of cervical radiculopathy and can also determine the chronicity of a lesion. Electrodiagnostic studies help to evaluate spinal cord dysfunction and may be useful in determining the timing for intervention in early CSM. Differential diagnoses Myelopathic signs are not unique to CSM and have a variety of causes. Failure of neurological improvement after successful surgery can sometimes be explained by erroneous diagnoses of CSM. Furthermore, cervical spondylosis is almost universal in the elderly population and CSM may hence be over-diagnosed. A lack of correlation between neurological examination findings and radiological evidence should prompt the physician to consider other causes. In particular, demyelinating diseases such as multiple sclerosis should be entertained. In clinically myelopathic patients with a lack of extremity sensory changes, ALS should be excluded. Other conditions that can mimic CSM include spinal cord tumours, syringomyelia, subacute combined degeneration, cerebral hemisphere disease, normal pressure hydrocephalus, spinal cord infarction, and peripheral neuropathy. Most of these conditions can usually be distinguished from CSM on account of the characteristic MRI findings.
Computed Tomography (CT): CT scans offer excellent bony detail of the cervical spine. Osteophytes, calcified discs, ossified posterior longitudinal ligaments (Figure 2), and the dimensions of the spinal canal and neural foramina are clearly delineated by CT. CT scanning is often used to complement MRI while characterizing the offending lesion. CT myelography is now uncommonly used owing to the widespread availability and non-invasive nature of MRI. However, it may still be utilized when contraindications to MRI exist or in conjunction when the MRI results are inconclusive. It should be noted that CT myelography has the advantage of being less artefactual in post-operative patients with metal implants inserted.
Natural history The natural history of CSM is mixed and unpredictable. It may present as a gradual, stepwise decline in neurological function or it may present in a progressive manner but with a long period of quiescence.
Electrodiagnostic studies: Electromyography (EMG) and/or somatosensory evoked potentials (SSEPs) are electrodiagnostic
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Figure 2 Lateral X-ray of the cervical spine reveals an Ossified Posterior Longitudinal Ligament (OPLL) from C2 to C5 levels. A CT scan of the cervical spine confirms OPLL from C2 to C5.
Treatment
Early reports have suggested that CSM is often a progressive and irreversible disease. Clark and Robinson26 found that the majority (70%) of patients have a stepwise progression with variable periods of quiescent disease, while 20% of patients have a steady but gradual decline neurologically; 5% of patients will deteriorate acutely. Traditionally, surgical decompression has been the mainstay of treatment for CSM. The Cochrane review27 on the role of surgical treatment for CSM found that there was no reliable evidence to suggest that progressive disability was an inevitable outcome in untreated individuals. It was suggested that the disease may not only remain static for lengthy periods but may also improve without surgical management in patients suffering from severe disability. The review was unable to draw any conclusions regarding the risks and benefits of cervical spine surgery for CSM. Only one randomized controlled trial was found in the Cochrane review addressing the role of operative versus nonoperative treatment. That study28 found no differences in outcome at a 2-year follow-up. An update of that study29 reported compelling evidence that mild CSM may be successfully treated by conservative treatment and is as effective as operative decompression for a period of up to 3 years. It was further found that objective deterioration is uncommon in the acute situation with mild CSM in relatively younger patients (<75 years of age). Nakamura et al.30 reported a follow-up of 3e10 years in 64 patients with mild CSM. Thirty percent of patients reported no disability, and failure of conservative treatment requiring operative treatment occurred in only 30% of patients. It was hence recommended by Matz et al.31 that patients younger than 75 years of age with mild CSM (mJOA scale scores of >12) be offered both operative and non-operative management. Emphasis should be placed on the mixed and unpredictable natural history of CSM as well as the potential irreversibility of neurological dysfunction in long-standing myelopathy when management options are discussed with the patient presenting with mild myelopathy.
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Conservative Conservative treatment is reserved for patients with mild CSM or patients who refuse or are unfit for surgery. Management options include analgesia, physiotherapy, neck braces, as well as activity modification. A greater AP spinal canal diameter, larger transverse area of the spinal cord, and old age were associated with a better response to conservative treatment in a study by Kadanka et al.32 Close monitoring of these patients is necessary as neurological deterioration can occur. Surgical management It is generally accepted that operative therapy should be offered to patients with progressive disease, severe symptoms, or stable moderate myelopathy of short duration (<1 year). Surgery is also indicated for patients when a mild myelopathy cannot be tolerated during activities of daily living or occupation. Tanaka et al33 have proposed that surgery may even be attempted in surgically fit patients older than 80 years of age provided that the inability to walk has persisted fewer than 3 months and that the symptom duration is less than 3 years. Some authors also advocate surgery in long-standing severe disease as these patients have very low chances of improvement with conservative management.31 The primary goal of surgical intervention is to achieve adequate expansion of the cervical spinal canal. This allows for cord decompression and avoids further compression by static or dynamic factors. Secondary goals are to achieve successful fusions where abnormal segmental hypermobility may have caused repeated shearing injuries of the cord, or to prevent the development of late spinal deformities. There are two general approaches for the surgical treatment of cervical myelopathy, namely the anterior or posterior approach. The anterior approach includes anterior cervical discectomy and fusion (ACDF) or anterior cervical corpectomy and fusion
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(ACCF), while laminectomy or laminoplasty represents the posterior approach. There are multiple factors to be taken into account when considering anterior versus posterior approaches for spinal cord decompression surgery. The sagittal alignment is a key consideration determining the choice of approach. Kyphosis occurs when the dorsal aspect of any of the C3eC7 vertebral bodies crosses a line drawn on the mid-sagittal plain radiograph/MRI from the dorso-caudal aspect of the C2 vertebral body to the dorso-caudal aspect of the C7 vertebral body. In lordosis, this line is not crossed by the dorsal aspect of any of the C3eC7 vertebral bodies. The posterior approach is contraindicated in kyphotic spines as posterior decompression may worsen ventral cord compression as the dural sac is tethered over ventral osteophytes. A posterior decompression will not allow posterior translation of the spinal cord away from ventral compressive elements in a kyphotic spine. The kyphosis may also worsen over time following a posterior approach. Secondly, the relative location of the stenosis should be identified and the most direct route of decompression is preferred. Cervical stenosis that results primarily from posterior compression, such as that seen in facet arthropathy and/or hypertrophy and buckling of the ligamentum flavum, is more directly decompressed with a posterior approach. Likewise, anterior compression resulting from disc herniations and vertebral body osteophytes is more completely decompressed with an anterior approach. Anterior approaches allow good visualization of abnormalities that are located ventral to the cord and obviate the need to work around the cord. In extensive CSM where more than three levels are involved, the posterior approach is favoured due to increased complications with the anterior approach. Morbidity from dysphagia, instrumentation and graft-related complications increases significantly for the anterior approach when more than three levels are operated upon. The presence of
significant pre-operative axial neck pain is, however, a relative contraindication to posterior surgery. In revision procedures, an alternative approach should be chosen, thus avoiding dissection through scar tissue and disrupted anatomic planes. The final choice of surgical procedure should be made after careful consideration of these factors together with the surgeon’s preferred surgical method. To date, there are no randomized prospective studies comparing these two approaches and debate continues over which surgical approach will yield the best outcome with the least number of complications. Reports thus far are retrospective cohort studies. Anterior Cervical Discetomy and Fusion (ACDF): this procedure involves the removal of disc material and impinging posterior osteophytes at or in the immediate, adjacent level of the cord. Indirect decompression of the canal and neural foramina occurs during distraction of the disc space by bone graft insertion (Figure 3). Advantages include relative preservation of cervical spine stability and the low incidence of graft migration. It also requires less exposure of the spinal cord but may increase the risk of inadequate decompression as a result of reduced visualization. It is not recommended in congenital canal stenosis since ACDF does not increase the AP spinal canal diameter. ACDF is usually indicated for cervical myelopathy due to soft disc herniation or spondylosis limited to the disc level. If compression occurs from ossification in the posterior longitudinal ligament (OPLL) or other extensive retrovertebral disease, anterior cervical corpectomy and fusion (ACCF) is preferred. Anterior Cervical Corpectomy and Fusion (ACCF): corpectomy involves the removal of about 15e19 mm of the anterior midline trough in the vertebral body down to the posterior longitudinal
Figure 3 Anterior discectomy and fusion (ACDF) of both C4/5 and C5/6 levels using cages and an anterior plate was performed in this patient.
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ligament or dura, with removal of the upper and lower adjacent discs. The foramen transversarium containing the vertebral artery marks the lateral limit of the decompression. Anatomical landmarks such as the medial margin of the uncus, the medial margin of the longus colli muscle and the natural curve of the vertebral end plate can be used to maintain midline orientation and avoid inadvertent vertebral artery injury (Figure 4). ACCF thus allows for canal expansion and concomitant osteophyte removal from the endplates. ACCF provides improved visualization over ACDF in the removal of these osteophytes. The posterior longitudinal ligament normally contributes to the stability of the spinal cord and serves as a natural barrier in preventing graft migration posteriorly. A thickened and ossified posterior longitudinal ligament causing cord compression can be removed during ACCF but complete removal may increase the risks of complications such as cord damage and haematoma formation. Bone Graft Options for ACDF and ACCF e autogenous iliac crest bone has traditionally been the choice of bone graft for multiple-level ACDF and one to two levels ACCF. Allograft bone avoids donor-site morbidity but is associated with higher rates of non-union following arthrodesis involving more than one level. Metallic cages or synthetic spacers in conjunction with local autograft, or allograft, avoid donor-site morbidity and provide rigid immobilization. Long-term results have not been published. We have earlier reported our experience in the reconstruction of multi-level cervical corpectomies with titanium cages and plating34 where we found a 95% radiographic consolidation rate.
There was a high complication rate (33%), largely the result of cage and plate construct failures, especially in patients with osteopenic bone. Recent advances in biomaterial technology have led to the development of polyether ether ketone (PEEK) interbody spacers that hold tremendous promise. These polymers are non-resorbable and can be used to create a structural graft with a modulus of elasticity resembling bone. The bioelastic properties of PEEK cages result in less stress shielding with more graft contact area, increased fusion rates, decreased subsidence, and better longterm sagittal alignment. There is also improved assessment of bony fusion through the radiolucent PEEK polymer.35 A 93% fusion rate at 6 months was noted in our retrospective review of the 15 consecutive cases of single-level anterior cervical interbody fusion using the Solis cage (PEEK material) for cervical spondylotic radiculopathy or myelopathy.36 In longer corpectomy defects, a fibular strut is commonly used. A fibular allograft has low risk of disease transmission, avoids donor-site morbidity, reduces operative time and intraoperative blood loss, and has been found biomechanically superior to the iliac crest under axial load testing.37 Role of plate fixation: anterior plating improves the rate of fusion, reduces the length of post-operative immobilization, decreases graft-related complications, and leads to less postoperative kyphosis.38e40 However, plating can be difficult in osteoporotic bone. It also leads to increased surgical costs and duration of the operation. Loose implants can also migrate, risking airway or oesophageal injury.
Figure 4 Anterior corpectomies (both C5 and C6) and fusion using cage and anterior plate.
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Laminectomy and laminoplasty: laminectomy (Figures 5 and 6) is the original treatment for CSM. Historical results were disappointing and stimulated the evolution of anterior surgical approaches and posterior laminoplasty. Over the years, however, encouraging improvements have been made in laminectomy technique. The junction of the cervical lateral masses and laminae marks the margins of lateral resection in laminectomy. Foraminotomy may be considered in patients with foraminal stenosis with radiculopathy. Goat and cadaveric studies41 have shown increased biomechanical instability post-laminectomy with increased spinal column flexibility, particularly at the lower levels of the laminectomy. This instability is also noted to be worsened by removal of 25% or more of the facet joints. Kyphosis as a result of instability is a well established complication of laminectomy. Dural scar formation post-laminectomy has also been reported and results in the formation of a membrane over the spinal cord that retracts as the scar tissue matures. This can cause recurrent compression of the cervical cord, with late neurological deterioration. Laminoplasty has largely superseded laminectomy as the standard posterior approach for the treatment of multi-level cervical myelopathy. Laminoplasty is used to treat long-segment cervical stenosis as an alternative to the anterior approach. The technique of laminoplasty involves the shifting of spinal laminae posteriorly either with the use of a single door with a lateral hinge technique, or a double door with bilateral hinges. This increases the effective diameter of the spinal canal from C3eC7, producing spinal cord decompression. Unlike laminectomy, laminoplasty preserves the posterior laminae for load-bearing and the re-attachment of paraspinal muscles. The ligamentum flavum is also retained. This minimizes instability and obviates the need for fusion. By preserving
the laminae, laminoplasty also minimizes extradural scar formation. Comparative studies have found equal neurological outcomes following single or double door laminoplasties.42 Autogenous spinous process grafts, allograft bone, synthetic spaces, and miniplates are recent devices used to maintain door position and patency. Instrumentation and fusion after laminectomy and laminoplasty e Fusion after laminectomy and laminoplasty may be indicated for significant axial neck pain and segmental instability. Instrumentation increases fusion rates and provides immediate stability to the cervical spine. Sublaminar/facet wires, interspinous wires, lateral mass and cervical pedicle screw fixation systems are instrumentation options for post-laminectomy patients. Lateral mass plates can also be used after laminectomy or laminoplasty. Comparison of approaches: there are three recently published systemic reviews comparing the various approaches.43e45 Each review independently concluded that all surgical approaches yielded similar improvements in neurological function. Laminoplasty was noted to produce a significant incidence of axial neck pain31,45 while multi-level ACCF had significantly higher rates of graft, instrumentation, and approach-related complications.34,43e45 Cunningham et al.43 performed a systematic review of retrospective cohort studies comparing ACDF, ACCF, laminectomy, and laminoplasty from 1980e2008. The paper also reviewed case series of single treatment modalities with greater than 10-year follow-up. The authors concluded that all approaches yielded similar neurological recovery rates. Multi-level ACCF and laminectomy with fusion also led to significant decreases in range of motion in the neck, as compared with laminoplasty.
Figure 5 Laminoplasty C3eC7 levels.
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Figure 6 Laminectomy C3eC7 levels with posterior instrumentation. This patient subsequently underwent anterior corpectomies of C5 and C6 with fusion using cage and anterior plate.
Mummaneni et al.44 concluded in his review that all surgical techniques (ACDF, ACCF, laminoplasty, laminectomy with fusion) improved functional outcome in CSM. ACDF and ACCF appear to yield similar results in multi-level spine decompression for lesions at the disc level with equivalent fusion rates by the use of anterior plating. Without anterior fixation, ACCF may provide a higher fusion rate than multi-level ACDF. Laminectomy is also associated with late neurological deterioration due to the development of kyphosis. Mathew et al.45 noted that ACDF is an excellent choice for one or two level spondylosis without retrovertebral disease. ACCF using a strut graft provides an improved decompression, and is ideal for patients with kyphosis or neck pain. Laminectomy historically has poor results from late deformity and neurologic deterioration, but results have improved lately with better surgical technique. Laminoplasty also compares favourably with anterior corpectomy and fusion for neurologic recovery.
2 White AA, Panjabi MM. Biomechanical considerations in the surgical management of cervical spondylotic myelopathy. Spine 1988; 13: 856e60. 3 Hoff JT, Wilson CB. The pathophysiology of cervical spondylotic radiculopathy and myelopathy. Clin Neurosurg 1977; 24: 474e87. 4 Wilkinson M. The morbid anatomy of cervical spondylosis and myelopathy. Brain 1960; 83: 589e616. 5 Jumah KB, Nyame PK. Relationship between load carrying on the head and cervical spondylosis in Ghanaians. West Afr J Med 1994; 13: 181e2. 6 Yamada Y, Okuizumi H, Miyauchi A, Takagi Y, Ikeda K, Harada A. Association of transforming growth factor beta1 genotype with spinal osteophytosis in Japanese women. Arthritis Rheum 2000; 43: 452e60. 7 Yoo K, Origitano TC. Familial cervical spondylosis: case report. J Neurosurg 1998; 89: 139e41. 8 Olive PM, Whitecloud 3rd TS, Bennett JT. Lower cervical spondylosis and myelopathy in adults with Down’s syndrome. Spine 1988; 13: 781e4. 9 Hadley MN, Reddy SV. Smoking and the human vertebral column: a review of the impact of cigarette use on vertebral bone metabolism and spinal fusion. Neurosurgery 1997; 41: 116e24. 10 Ichihara K, Taguchi T, Sakuramoto I, Kawano S, Kawai S. Mechanism of the spinal cord injury and the cervical spondylotic myelopathy: new approach based on the mechanical features of the spinal cord white and gray matter. J Neurosurg Spine 2003; 99: 278e85. 11 Shimomura Y, Hukuda S, Mizuno S. Experimental study of ischemic damage to the cervical spinal cord. J Neurosurg 1954; 28: 565e81. 12 Ito T, Oyanagi K, Takahashi H, Takahashi HE, Ikuta F. Cervical spondylotic myelopathy. Clinicopathologic study on the progression pattern and thin myelinated fibers of the lesions of seven patients examined during complete autopsy. Spine 1996; 21: 827e33. 13 Ogino H, Tada K, Okada K, et al. Canal diameter, anteroposterior compression ratio, and spondylotic myelopathy of the cervical spine. Spine 1983; 8: 1e15.
Conclusion CSM is a debilitating condition that commonly affects the elderly. It occurs as a result of chronic spondylotic degenerative changes leading to cervical cord compression. A thorough understanding of its pathophysiology, presentation and investigation is essential in modern management of the condition. Spine surgeons should be aware of the current evidence regarding the natural history and various treatment outcomes of CSM in order to achieve the best surgical results with the least number of complications. A
REFERENCES 1 Brain WR, Northfield D, Wilkinson M. Neurological manifestations of cervical spondylosis. Brain 1952; 75: 187e225.
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14 Ono K, Ota H, Tada K, Yamamoto T. Cervical myelopathy secondary to multiple spondylotic protrusions. A clinicopathologic study. Spine 1977; 2: 109e25. 15 Crandall PH, Batzdorf U. Cervical spondylotic myelopathy. J neurosurgery 1966; 25: 57e66. 16 Ferguson RJ, Caplan LR. Cervical spondylotic myelopathy. Neurol Clin 1985 May; 3: 373e82 (Review). 17 Small JM, Dillin WH, Watkins RG. Clinical syndromes in cervical myelopathy. In: Herkowitz H, Garfin SR, Balderson RA, et al., eds. The spine. 4th edn. Philadelphia: W.B. Saunders Co., 1999: 465e74. 18 Gorter K. Influence of laminectomy on the course of cervical myelopathy. Acta Neurochir 1976; 33: 265e81. 19 Epstein N, Epstein J, Carras R. Cervical spondylostenosis and related disorders in patients over 65: current management and diagnostic techniques. Orthotransactions 1987; 11: 15. 20 Denno JJ, Meadows GR. Early diagnosis of cervical spondylotic myelopathy: a useful clinical sign. Spine 1991; 16: 1353e5. 21 Ono K, Ebara S, Fuji T, Yonenobu K, Fujiwara K, Yamashita K. Myelopathy hand. New clinical signs of cervical cord damage. J Bone Joint Surg Br 1987; 69: 215e9. 22 Hosono N, Makino T, Sakaura H, Mukai Y, Fuji T, Yoshikawa H. Myelopathy hand: new evidence of the classical sign. Spine (Phila Pa 1976) 2010; 35: E273e7. 23 Mihara H, Kondo S, Murata A, Ishida K, Niimura T, Hachiya M. A new performance test for cervical myelopathy: the triangle step test. Spine (Phila Pa 1976) 2010; 35: 32e5. 24 Rhee JM, Heflin JA, Hamasaki T, Freedman B. Prevalence of physical signs in cervical myelopathy: a prospective, controlled study. Spine (Phila Pa 1976) 2009; 34: 890e5. 25 Teresi LM, Lufkin RB, Reicher MA, et al. Asymptomatic degenerative disk disease and spondylosis of the cervical spine: MR imaging. Radiology 1987; 164: 83e8. 26 Clarke E, Robinson PK. Cervical myelopathy: a complication of cervical spondylosis. Brain 1956; 79: 483e510. 27 Fouyas IP, Statham PF, Sandercock PA. Cochrane review on the role of surgery in cervical spondylotic radiculomyelopathy. Spine 2002; 27: 736e47. 28 Nakamura K, Kurokawa T, Hoshino Y, Saita K, Takeshita K, Kawaguchi H. Conservative treatment versus surgery in spondylotic cervical myelopathy: a prospective randomised study. Eur Spine J 2000; 9: 538e44. 29 Kadanka Z, Mares M, Bednanık J, et al. Approaches to spondylotic cervical myelopathy: conservative versus surgical results in a 3-year follow-up study. Spine 2002; 27: 2205e11. 30 Nakamura K, Kurokawa T, Hoshino Y, et al. Conservative treatment for cervical spondylotic myelopathy: achievement and sustainability of a level of ‘‘no disability”. J Spinal Disord 1998; 11: 175e9. 31 Matz PG, Anderson PA, Holly LT, et al. The natural history of cervical spondylotic myelopathy. J Neurosurg Spine 2009; 11: 104e11. 32 Kadanka Z, Mares M, Bednarık J, et al. Predictive factors for spondylotic cervical myelopathy treated conservatively or surgically. Eur J Neurol 2005; 12: 55e63. 33 Tanaka J, Seki N, Tokimura F, Doi K, Inoue S. Operative results of canal-expansive laminoplasty for cervical spondylotic myelopathy in elderly patients. Spine (Phila Pa 1976) 1999; 24: 2308e12. 34 Hee HT, Majd ME, Holt RT, Whitecloud 3rd TS, Pienkowski D. Complications of multilevel cervical corpectomies and reconstruction with titanium cages and anterior plating. J Spinal Disord Tech 2003; 16: 1e8. discussion 8e9.
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35 Hee HT, Kundnani V. Rationale for use of polyetheretherketone polymer interbody cage device in cervical spine surgery. Spine J 2010; 10: 66e9. 36 Kulkarni AG, Hee HT, Wong HK. Solis cage (PEEK) for anterior cervical fusion: preliminary radiological results with emphasis on fusion and subsidence. Spine J 2007; 7: 205e9. 37 Wittenberg RH, Moeller J, Shea M, White 3rd AA, Hayes WC. Compressive strength of autologous and allogenous bone grafts for thoracolumbar and cervical spine fusion. Spine 1990; 15: 1073e8. 38 Connolly PJ, Esses SI, Kostuik JP. Anterior cervical fusion: outcome analysis of patients fused with and without anterior cervical plates. J Spinal Disord 1996; 9: 202e6. 39 Kaiser MG, Haid Jr RW, Subach BR, Barnes B, Rodts Jr GE. Anterior cervical plating enhances arthrodesis after discectomy and fusion with cortical allograft. Neurosurgery 2002; 50: 229e38. 40 Wang JC, McDonough PW, Endow KK, Delamarter RB. Increased fusion rates with cervical plating for two-level anterior cervical discectomy and fusion. Spine 2000; 25: 41e5. 41 Baisden J, Voo LM, Cusick JF, Pintar FA, Yoganandan N. Evaluation of cervical laminectomy and laminoplasty. A longitudinal study in the goat model. Spine 1999; 24: 1283e8. 42 Naito M, Ogata K, Kurose S, Oyama M. Canal-expansive laminoplasty in 83 patients with cervical myelopathy. A comparative study of three different procedures. Int Orthop 1994; 18: 347e51. 43 Cunningham MR, Hershman S, Bendo J. Systematic review of cohort studies comparing surgical treatments for cervical spondylotic myelopathy. Spine (Phila Pa 1976) 2010; 35: 537e43 (Review). 44 Mummaneni PV, Kaiser MG, Matz PG, et al. Joint Section on Disorders of the Spine and Peripheral Nerves of the American Association of Neurological Surgeons and Congress of Neurological Surgeons. Cervical surgical techniques for the treatment of cervical spondylotic myelopathy. J Neurosurg Spine 2009; 11: 130e41. 45 Geck MJ, Eismont FJ. Surgical options for the treatment of cervical spondylotic myelopathy. Orthop Clin North Am 2002; 33: 329e48 (Review).
Key points C
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Cervical spondylotic myelopathy is debilitating. It is the most common cause of spinal cord dysfunction in the elderly and is responsible for the majority of non-traumatic causes of spastic paraparesis and quadriparesis. The onset of CSM is typically insidious with no pathognomonic clinical finding. It is a clinical diagnosis based upon detailed history-taking, accurate physical examination and corroborating radiological evidence. Pathophysiologically, CSM is caused by static and dynamic compressive forces as well as cervical cord vascular ischaemia. The natural history of CSM is mixed and unpredictable. Neurological dysfunction is potentially irreversible, especially in long-standing myelopathy. Conservative treatment retains a role in the management of mild CSM but progress of symptoms has to be closely monitored. Established surgical methods in the treatment of CSM appear to yield similar improvements in neurological function. Surgery is recommended for patients with progressive disease, severe or intolerable symptoms and stable, moderate myelopathy of short duration (<1 year).
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Superior Labrum Anterior to Posterior (SLAP) lesions of the shoulder
incidence of SLAP lesions is much higher in patients with chronic shoulder instability and can occur in addition to other capsulolabral pathologies.6
Anatomy The glenoid labrum is a fibrocartilaginous rim around the glenoid fossa. It is triangular in profile, with the base attached to the margin of the fossa. The inner free edge projects into, and continues the curve of, the glenoid, thus deepening the cavity. This helps contain the relatively large humeral head, which outsizes the glenoid fossa by a ratio of four to one. The blood supply to the peripheral labrum includes branches from the suprascapular artery, circumflex branch of subscapular artery and posterior humeral circumflex artery. The inner zone of the labrum is avascular. The superior and anterosuperior labrum is relatively less vascular than the posterior and inferior regions. The fibrous capsule envelops the joint and is supported by the tendon of suprsapinatus superiorly, infraspinatus and teres minor posteriorly, subscapularis anteriorly and the long head of triceps inferiorly. The rotator interval is a triangular unsupported area of capsule medially, between the superior edge of subscapularis and the anterior edge of supraspinatus. The three glenohumeral ligaments e superior, middle and inferior, reinforce the joint capsule anteriorly and inferiorly. The superior glenohumeral ligament (SGHL) passes from the supraglenoid tubercle just anterior to the long head of biceps to the humerus on the medial ridge of the intertubercular (bicipital) groove. Along with the coraco-humeral ligament the SGHL suspends the humeral head and provides stabilization to inferior translation. The middle glenohumeral ligament (MGHL) arises from the anterior glenoid margin below SGHL and passes inferolaterally to attach to the lesser tubercle deep to the tendon of subscapularis. It acts as an important secondary stabilizer of the shoulder, providing anterior stability from 45 to 60 of abduction. The inferior glenohumeral ligament (IGHL) complex arises from the anterior, middle and posterior margins of the glenoid labrum and passes anteroinferiorly to the neck of the humerus. It comprises a superior band, an anterior band and an axillary pouch. The anterior band is the primary anterior stabilizer of the shoulder beyond 60 of abduction. The long head of biceps arises from the supraglenoid tubercle and superior labrum and passes through the joint, to exit by the bicipital groove. Studies have shown that the biceps contributes to stability in patients with a damaged rotator cuff or glenohumeral ligaments.7e9 There are several important anatomical variations, which must be appreciated when reviewing radiological investigations and at arthroscopy to avoid misinterpretation as pathological features.
Bynvant Sandhu Sanjay Sanghavi Francis Lam
Abstract Superior Labrum Anterior to Posterior (SLAP) lesions are an abnormality of the superior glenoid labrum and are a significant cause of shoulder pain and instability. Pathology of the superior labrum can pose a significant diagnostic challenge, and therefore a sound knowledge of the relevant anatomy and associated variants is essential in diagnosing and treating these patients. In this article the capsulolabral anatomy and pathomechanics of SLAP lesions are revised. We then review current concepts in the clinical and radiological diagnosis of SLAP lesions and discuss approaches to operative management.
Keywords glenoid labrum; shoulder arthroscopy; SLAP
Introduction Tears of the superior glenoid labrum account for a significant burden of shoulder pain and instability. In 1985, Andrews et al first described lesions of the glenoid labrum in their series of 73 throwing athletes, mostly occurring in the anterior-superior labrum.1 In 1990, Snyder et al. proposed the term SLAP (Superior Labrum Anterior to Posterior) for lesions involving the superior aspect of the glenoid labrum.2 In these injuries labral separation from the glenoid begins posteriorly and extends anteriorly to include the origin of the long head of the biceps. The reported incidence of SLAP lesions varies from 1.2% to 11.8%.3e5 Warner et al analyzed 585 consecutive shoulder clinic patients over a period of 3 years and found an incidence of 1.2%. In Snyder’s series of 700 shoulder arthroscopies, SLAP lesions were found in 3.9%. Maffet et al. reported a much higher incidence, with SLAP lesions accounting for 11.8% of the 712 consecutive shoulder arthroscopies performed. However, the
Bynvant Sandhu MBChB MRCS Core Surgical Trainee, Department of Orthopaedic Surgery, Hillingdon Hospital, Uxbridge, Middlesex, UK. Conflicts of interest: none.
Anatomical variants Buford complex A Buford complex is a large anterosuperior labral foramen occurring with a thickened, cord-like MGHL and is found in 1.5e10.2% of individuals.10e13 This can resemble an anterior labral avulsion or a superior labral tear on Magnetic Resonance Imaging (MRI), but is readily identifiable at arthroscopy. The presence of a Buford complex alone does not require surgical intervention, but if mistakenly repaired can lead to pain and restricted shoulder rotation and elevation.
Sanjay Sanghavi FRCS Registrar, Trauma and Orthopaedics Department of Orthopaedic Surgery, Hillingdon Hospital, Uxbridge, Middlesex, UK. Conflicts of interest: none. Francis Lam MSc FRCS (Orth) Consultant Orthopaedic Surgeon, Department of Orthopaedic Surgery, Hillingdon Hospital, Pield Heath Road, Uxbridge, Middlesex UB8 3NN, UK. Conflicts of interest: none.
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Sub-labral foramen A sub-labral foramen is typically located in the anterosuperior quadrant and has an incidence of 11.9e18.5% in patients undergoing shoulder arthroscopy.11,12 Rao et al. and Ilahi et al. concluded that a sub-labral foramina should not be repaired, particularly when found in isolation, as they do not contribute significantly to shoulder stability.11,12
MGHL variations The MGHL is absent in 30e40% of shoulders.14,15 When present, it can arise from the anterosuperior labrum, the supraglenoid tubercle or the scapular neck. It can also vary in its appearance from a cord-like to a sheet-like structure.16,17 The cord-like variant presents with a foramen between MGHL and IGHL and the sheet-like variant presents as a sheet merging with the anterior band of IGHL. Superior labral variations Variations of the superior labrum occur due to its loose attachment to the glenoid and its association with the long head of the biceps. Firstly, extensive variations in the origin and insertion of the long head of the biceps have been described.18 Secondly, the presence of a synovial recess between the superior labrum and the biceps tendon can be misinterpreted as a SLAP lesion.19 Finally, a meniscoid superior labrum is a normal anatomical variant and does not require repair.20,21
Figure 1 Schematic representation of SLAP type I lesion: superior labral fraying with an intact biceps tendon.
scapula cause increased glenohumeral angulation. This results in abnormal posterior compression and anterior tension, thereby increasing the risk of labral injury.28
Pathophysiology Several anatomical and biomechanical factors predispose to SLAP lesions. The strength of the superior labrum/biceps complex varies according to shoulder position. In the initial description of SLAP lesions, the pathophysiology was attributed to forces applied to the long head of biceps during the followthrough phase of throwing.1 However, subsequent studies have demonstrated that SLAP tears occur more commonly in the late cocking position of throwing.22,23 Kuhn et al. showed that tension in the biceps tendon was 20% less in the late cocking phase of throwing than in the early deceleration phase.22 This finding was confirmed by Shepard et al, who demonstrated that tension on the biceps anchor was almost doubled during the deceleration phase compared to the late cocking phase of throwing.23 Overhead throwing athletes have been shown to have an increased range of movement in external rotation, with a corresponding reduction in internal rotation.24,25 This has been attributed to a number of factors, including posterior capsular contracture, anterior capsular laxity and increased proximal humeral retroversion.26,27 A tight posterior capsule results in increased posterosuperior migration of the humeral head.26 Anterior capsular laxity along with proximal humeral retroversion results in greater external rotation of the shoulder. This causes increased torsional loads across the superior labrum from the more posteriorly positioned biceps tendon. This results in displacement of the labrum and biceps tendon medially over the glenoid rim, producing a ‘peel-back’ injury to the labrum. Another predisposing factor to increased labral injury is the presence of SICK (Scapula malposition/Inferior medial border prominence/Coracoid pain, dysKinesis) scapula. Scapular protraction and increased glenoid ante-tilting seen in SICK
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Classification Snyder et al initially classified SLAP lesions into four types based on arthroscopic findings in their study of 27 patients presenting with pain and/or clicking of the shoulder2 (Figures 1e4). Morgan et al.
Figure 2 Schematic representation of SLAP type II lesion: detached labralebicipital complex from the superior glenoid.
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Classification of SLAP lesions Type of lesion I
II
IIA IIB IIC III
IV
Figure 3 Schematic representation of SLAP type III lesion: bucket handle tear of the superior labrum with an intact biceps anchor.
further divided SLAP II lesions into three subtypes29 and in 1995, Maffet et al added three types to Snyder’s original classification.5 The classification system has continued to develop and there are now 10 types of SLAP lesion described in the literature (Table 1).
V
VI
Clinical features The clinical diagnosis of SLAP lesions can be challenging, as the symptoms are often non-specific. Patients often present with a history of pain and associated locking, clicking or snapping. The pain is particularly associated with overhead or cross-body motion and patients may also complain of weakness or instability.
VII
VIII IX X
Description Marked fraying of the free edge of the superior labrum, with an intact biceps tendon. These lesions are associated with age-related degeneration (Figure 1). Avulsion of the labralebicipital complex from the superior glenoid. These are the most common type of SLAP lesions and are associated with repetitive microtrauma (Figure 2). Anterosuperior labral lesion. Posterosuperior labral lesion. Superior labral lesion extending both anteriorly and posteriorly. Displaced bucket handle tears of the superior labrum with a preserved biceps anchor. These are associated with a fall on an outstretched arm (Figure 3). Bucket handle tear of the superior labrum, with extension into the fibers of the biceps tendon. A partially torn biceps tendon may displace the superior labral flap into the joint (Figure 4). Anteroinferior Bankart lesion that extends upward to include separation of the biceps tendon. Unstable radial or flap tears that are associated with separation of the biceps anchor. Extension of a type II or III SLAP lesion into the MGHL. However, extension into the MGHL can be difficult to ascertain on MRI due to the variable nature and redundant folding of MGHL. A SLAP II or III lesion plus a posterior labral tear. Circumferential labral tears with anterior and posterior labral involvement. Superior labral tears with extension into the rotator cuff interval through the SGHL.
Table 1
The patients may give a history of trauma. The two most common mechanisms of injury leading to SLAP lesions are avulsion of the labrum by the long head of the biceps, usually resulting from repetitive overhead throwing, and compression forces applied to the shoulder, typically resulting from a fall on an outstretched arm. Other mechanisms of injury include forceful traction loads to the arm, impaction loading on the shoulder when it is forward flexed and direct traction injury to the biceps tendon.
Examination A number of clinical tests have been described to determine the presence of SLAP lesions. These include O’Brien’s, the
Figure 4 Schematic representation of SLAP type IV lesion: bucket handle tear of the superior labrum with extension into the biceps tendon.
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compression rotation test, Speed’s, Clunk test, Crank test, Kibler’s, Kim’s Biceps Load Test I and II and Mimori’s test. However, no single test is diagnostic.
The sensitivity and specificity are reported as 44% and 68% respectively.34 Crank test: can be performed with the patient sitting or supine.40 With the shoulder elevated to 160 in the plane of the scapula, the examiner applies an axial load whilst internally and externally rotating the humerus. Typically, patients with SLAP lesions report pain on external rotation. The sensitivity and specificity vary from 39 to 91%31,41,42 and 56 to 93%31,41,42 respectively.
O’Brien’s active compression test: performed with the shoulder placed in 90 forward elevation and 30 horizontal adduction.30 The examiner then applies a downward force on the forearm, first while the forearm is pronated and then with the forearm supinated. The test is positive when pain is elicited with the forearm pronated (Figure 5) and relieved when the forearm is supinated (Figure 6). The sensitivity and specificity vary from 54 to 100%30,31 and 11 to 99.5%30,32 respectively.
Kibler’s anterior slide test: is performed with the hand on the ipsilateral hip with the thumb positioned over the anterior superior iliac spine.43 The scapula is stabilized and an anterosuperiorly directed axial load is applied to the humerus to reproduce pain. The sensitivity and specificity vary from 8 to 78%33,43,44 and 70 to 98%33,35,44 respectively.
Compression rotation/grind test2: with the patient in the supine position, the glenohumeral joint is compressed from the elbow through the long axis of the humerus as the shoulder is passively rotated. This attempts to grind the labrum between the glenoid and humeral head to elicit pain. The sensitivity and specificity vary from 24 to 73%33e35 and 54 to 100%33e35 respectively. Speed’s/Biceps tension test2: performed with the shoulder placed in 90 forward elevation, the elbow extended and forearm supinated. The examiner applies downward force to the arm against resistance to reproduce pain in patients with SLAP lesions (Figure 7). The sensitivity and specificity vary from 32 to 90%36e38 and 13 to 81%.36e39
Kim’s Biceps Load Test I: the biceps is contracted against resistance with the shoulder placed in 90 abduction, maximal external rotation and the forearm supinated.45 Deep shoulder pain on this manoeuvre indicates a SLAP lesion. Kim reported a sensitivity of 91% and a specificity of 97%.45 Further refinement of this test led to a description of Biceps Load Test II.46 This is performed in the same manner as the original test, with the shoulder abducted to 120 . The sensitivity and specificity vary from 30 to 90%35,46 and 78 to 97%35,46 respectively.
Clunk test1: performed with the patient supine. Anterior translation of the humeral head is performed using one hand, while externally rotating the shoulder at the elbow with the other hand. The presence of a clunk or grinding sound indicates a labral tear.
Mimori’s pain provocation test: the shoulder is abducted to 90 and externally rotated with forearm in full pronation.47 The presence of pain on pronation indicates the presence of a SLAP lesion. This has a reported sensitivity of 100% and a specificity of 90%.47
Figure 5 O’Brien’s active compression test e the test is positive when pain is elicited with the forearm in pronation.
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Figure 6 O’Brien’s active compression test e pain relieved when the forearm is supinated.
Imaging
arthrography. A normal superior glenoid labrum has low intensity signal on all MRI sequences. The superior glenoid labrum is associated with a significant number of anatomical variations, including Buford complexes, sub-labral foramen and sub-labral
If a SLAP lesion is clinically suspected, radiological investigation needs to be considered prior to planning surgical intervention. The most frequently used imaging modalities are MRI and MR
Figure 7 Speed’s/Biceps tension test e the shoulder is positioned in 90 of forward flexion with the elbow extended and forearm supinated. Pain is elicited when a downward pressure is applied to the arm.
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recesses, as discussed above. These can complicate the interpretation of MRI. Furthermore, MRI is unable to differentiate the different types of SLAP lesions. The use of a contrast medium is beneficial in distinguishing pathology from normal anatomical variants and in classifying the type of SLAP lesion. This can be achieved through either direct (intra-articular injection of contrast) or indirect (intravenous contrast) MR arthrography (Figures 8 and 9). Studies comparing MR arthrography with standard MRI have shown superior sensitivity and accuracy in favour of arthrography, without influencing specificity.48,49 Furthermore, using arthroscopy as the gold standard, MR arthrography has shown a sensitivity ranging from 82 to 89% and a specificity of 91e98% for the detection of SLAP lesions.50,51 If a SLAP lesion is identified on MRI or MR arthrography, further characterization of the abnormality is necessary to plan operative intervention. This involves assessment of the lesion for the presence of a bucket handle tear or flap fragment, involvement of the biceps anchor and adjacent structures. Any associated abnormalities such as glenohumeral osteoarthritis, para-labral cysts and glenoid fractures must also be identified.
Figure 9 Coronal oblique T1 weighted fat saturated MR arthrogram of the right shoulder demonstrates linear full thickness undisplaced tear of the superior labrum (thick arrow) and biceps labral anchor (thin arrow) in a type 2 SLAP tear.
Treatment The conservative management of symptomatic SLAP lesions is generally unsuccessful, particularly when associated with other pathologies such as rotator cuff tears and joint instability. At arthroscopy the superior labrum and the biceps anchor are evaluated with a hook probe to assess stability. Burkhart describes a ‘Peel-back’ sign, which is the detachment of the bicepsesuperior labral complex medially over the edge of the glenoid at 90 abduction and 90 external rotation.52 A positive ‘peel-back’ test indicates a posterior SLAP lesion. An anterior SLAP lesion is identified by a displaceable biceps root.
A combined anterioreposterior SLAP lesion demonstrates both a positive ‘peel-back’ test and a displaceable biceps root. Type I lesions do not ordinarily necessitate treatment unless symptoms continue to progress or there is significant fraying. In such cases, the lesion is debrided back to a stable labrum. When the labral ring is detached, as in a Type II lesion, arthroscopic repair involves re-attachment of the superior labrum to the glenoid and stabilizing the biceps anchor. Fixation techniques include bio-absorbable tacks, suture anchors and knotless fixation methods. Accurate portal placement is crucial in achieving good access for anchor placement, suture passing and knot-tying. A posterior portal is used for viewing while a high anterolateral portal is used for anchor placement. A further working portal is placed anteriorly through the rotator cuff interval. The suture anchor is inserted through the anterolateral portal below the biceps root. A suture-passer is used to pass the suture through the same portal to penetrate through the labrum and the sutures are then tied from anterior to posterior. Burkhart describes the ‘money stitch’, which is the suture placed just posterior to the biceps root. This is the most effective suture in resisting the ‘peel-back’ force.53 Type III, as for Type I lesions, should be debrided back to a stable labrum. The exemption to this is lesions involving a Buford complex which should be repaired using a method similar to that described above for a Type II tear. The treatment for Type IV lesions depends on the extent of biceps anchor involvement. If the biceps tendon tear is greater than 25% of the entire tendon, a biceps tenodesis is performed. In older patients with a substantial tear the labrum is debrided and a biceps tenotomy performed. Patients must also be assessed for concomitant rotator cuff pathology. Patients with SLAP tears may present with concurrent PASTA (Partial Articular Sided Tendon Avulsion) lesions. Treatment options include debridement of the PASTA lesion, typically when the tear is less than 6 mm of the thickness of the
Figure 8 Coronal oblique T1 weighted fat saturated MR arthrogram of the right shoulder demonstrates high signal within the superior labrum (arrows) consistent with a type 1 SLAP tear.
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11 Rao AG, Kim TK, Chronopoulos E, McFarland EG. Anatomical variants in the anterosuperior aspect of the glenoid labrum: a statistical analysis of seventy-three cases. J Bone Joint Surg Am 2003; 85-A: 653e9. 12 Ilahi OA, Labbe MR, Cosculluela P. Variants of the anterosuperior glenoid labrum and associated pathology. Arthroscopy 2002; 18: 882e6. 13 Ilahi OA, Cosculluela PE, Ho DM. Classification of anterosuperior glenoid labrum variants and their association with shoulder pathology. Orthopedics 2008; 31: 226. 14 Ferrari DA. Capsular ligaments of the shoulder. Anatomical and functional study of the anterior superior capsule. Am J Sports Med 1990; 18: 20e4. 15 Plausinis D, Jazrawi LM, Zuckerman JD, et al. Anatomy and biomechanics of the shoulder. In: Schepsis AA, Busconi BD, eds. Sports medicine. Philadelphia: Lippincott Williams and Wilkins, 2006: 180. 16 Cole BJ, Rios CG, Mazzocca AD, et al. Anatomy, biomechanics, and pathophysiology of glenohumeral instability. In: Iannotti JP, Williams GR, eds. Disorders of the shoulder: diagnosis & management. 2nd edn. Philadelphia: Lippincott Williams and Wilkins, 2007: 289. 17 O’Brien SJ, Neves MC, Arnoczky SP, et al. The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 1990; 18: 449e56. 18 Vangsness Jr CT, Jorgenson SS, Watson T, Johnson DL. The origin of the long head of the biceps from the scapula and glenoid labrum. An anatomical study of 100 shoulders. J Bone Joint Surg Br 1994; 76: 951e4. 19 Levine WN, Flatow EL. The pathophysiology of shoulder instability. Am J Sports Med 2000; 28: 910e7. 20 O’brien SJ, Arnoczky SP, Warren RF, et al. Developmental anatomy of the shoulder and anatomy of the glenohumeral joint. In: Rockwood CA, Matsen FA, eds. The shoulder. Philadelphia: Saunders, 1990: 1e33. 21 Lee SB, Harryman 2nd DT. Superior detachment of a glenoid labrum variant resembling an incomplete discoid meniscus in a wheelchair ambulator. Arthroscopy 1997; 13: 511e4. 22 Kuhn JE, Lindholm SR, Huston LJ, Soslowsky LJ, Blasier RB. Failure of the biceps superior labral complex: a cadaveric biomechanical investigation comparing the late cocking and early deceleration positions of throwing. Arthroscopy 2003; 19: 373e9. 23 Shepard MF, Dugas JR, Zeng N, Andrews JR. Differences in the ultimate strength of the biceps anchor and the generation of type II superior labral anterior posterior lesions in a cadaveric model. Am J Sports Med 2004; 32: 1197e201. 24 Brown LP, Niehues SL, Harrah A, Yavorsky P, Hirshman HP. Upper extremity range of motion and isokinetic strength of the internal and external shoulder rotators in major league baseball players. Am J Sports Med 1988; 16: 577e85. 25 Crockett HC, Gross LB, Wilk KE, et al. Osseous adaptation and range of motion at the glenohumeral joint in professional baseball pitchers. Am J Sports Med 2002; 30: 20e6. 26 Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology Part I: pathoanatomy and biomechanics. Arthroscopy 2003; 19: 404e20. 27 Chant CB, Litchfield R, Griffin S, Thain LM. Humeral head retroversion in competitive baseball players and its relationship to glenohumeral rotation range of motion. J Orthop Sports Phys Ther 2007; 37: 514e20. 28 Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology Part III: the SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy 2003; 19: 641e61.
rotator cuff, in-situ repair of the rotator cuff and completing the tear to full thickness and repairing it in the usual manner. Simultaneous repair of the SLAP and rotator cuff tears poses a high risk of post-operative stiffness. For this reason, it is the author’s preference to repair the rotator cuff combined with a biceps tenodesis. For the first 3 post-operative weeks the patient’s shoulder is immobilized in internal rotation in a sling. Thereafter, physiotherapy is commenced to restore stability and improve mobility of the joint.
Outcome The outcome following operative intervention for SLAP lesions depends on the method of treatment and the presence of coexisting pathology. Snyder et al. published a retrospective review of 140 patients who underwent arthroscopic SLAP repair.4 They found that repair with the suture anchor technique was successful in 80% of patients. In a recent prospective study by Brockmeier et al, excellent results were achieved in 74% of athletes undergoing arthroscopic suture anchor repair of Type II SLAP lesions.54
Summary SLAP lesions are a significant cause of pain and disability amongst those presenting to the shoulder clinic. Although the clinical diagnosis remains a challenge because of the lack of a single diagnostic test and the frequent presence of other lesions, advances in diagnostic imaging and arthroscopic techniques have led to a much improved outcome and restoration of function in this patient group. A
REFERENCES 1 Andrews JR, Carson Jr WG, McLeod WD. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med 1985; 13: 337e41. 2 Snyder SJ, Karzel RP, Del Pizzo W, Ferkel RD, Friedman MJ. SLAP lesions of the shoulder. Arthroscopy 1990; 6: 274e9. 3 Warner JJ, Kann S, Marks P. Arthroscopic repair of combined Bankart and superior labral detachment anterior and posterior lesions: technique and preliminary results. Arthroscopy 1994; 10: 383e91. 4 Snyder SJ, Banas MP, Karzel RP. An analysis of 140 injuries to the superior glenoid labrum. J Shoulder Elbow Surg 1995; 4: 243e8. 5 Maffet MW, Gartsman GM, Moseley B. Superior labrum-biceps tendon complex lesions of the shoulder. Am J Sports Med 1995; 23: 93e8. 6 Yiannakopoulos CK, Mataragas E, Antonogiannakis E. A comparison of the spectrum of intra-articular lesions in acute and chronic anterior shoulder instability. Arthroscopy 2007; 23: 985e90. 7 Rodosky MW, Harner CD, Fu FH. The role of the long head of the biceps muscle and superior glenoid labrum in anterior stability of the shoulder. Am J Sports Med 1994; 22: 121e30. 8 Pagnani MJ, Deng XH, Warren RF, Torzilli PA, Altchek DW. Effect of lesions of the superior portion of the glenoid labrum on glenohumeral translation. J Bone Joint Surg Am 1995; 77: 1003e10. 9 Kim SH, Ha KI, Kim HS, Kim SW. Electromyographic activity of the biceps brachii muscle in shoulders with anterior instability. Arthroscopy 2001; 17: 864e8. 10 Stoller DW. MR arthrography of the glenohumeral joint. Radiol Clin North Am 1997; 35: 97e116.
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29 Morgan CD, Burkhart SS, Palmeri M, Gillespie M. Type II SLAP lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy 1998; 14: 553e65. 30 O’Brien SJ, Pagnani MJ, Fealy S, McGlynn SR, Wilson JB. The active compression test: a new and effective test for diagnosing labral tears and acromioclavicular joint abnormality. Am J Sports Med 1998; 26: 610e3. 31 Guanche CA, Jones DC. Clinical testing for tears of the glenoid labrum. Arthroscopy 2003; 19: 517e23. 32 Myers TH, Zemanovic JR, Andrews JR. The resisted supination external rotation test: a new test for the diagnosis of superior labral anterior posterior lesions. Am J Sports Med 2005; 33: 1315e20. 33 McFarland EG, Kim TK, Savino RM. Clinical assessment of three common tests for superior labral anterioreposterior lesions. Am J Sports Med 2002; 30: 810e5. 34 Nakagawa S, Yoneda M, Hayashida K, Obata M, Fukushima S, Miyazaki Y. Forced shoulder abduction and elbow flexion test: a new simple clinical test to detect superior labral injury in the throwing shoulder. Arthroscopy 2005; 21: 1290e5. 35 Oh JH, Kim JY, Kim WS, Gong HS, Lee JH. The evaluation of various physical examinations for the diagnosis of type II superior labrum anterior and posterior lesion. Am J Sports Med 2008; 36: 353e9. 36 Karlsson J. Physical examination tests are not valid for diagnosing SLAP tears: a review. Clin J Sport Med 2010; 20: 134e5. 37 Ebinger N, Magosch P, Lichtenberg S, Habermeyer P. A new SLAP test: the supine flexion resistance test. Arthroscopy 2008; 24: 500e5. 38 Bennett WF. Specificity of the Speed’s test: arthroscopic technique for evaluating the biceps tendon at the level of the bicipital groove. Arthroscopy 1998; 14: 789e96. 39 Ben Kibler W, Sciascia AD, Hester P, Dome D, Jacobs C. Clinical utility of traditional and new tests in the diagnosis of biceps tendon injuries and superior labrum anterior and posterior lesions in the shoulder. Am J Sports Med 2009; 37: 1840e7. 40 Liu SH, Henry MH, Nuccion SL. A prospective evaluation of a new physical examination in predicting glenoid labral tears. Am J Sports Med 1996; 24: 721e5. 41 Dessaur WA, Magarey ME. Diagnostic accuracy of clinical tests for superior labral anterior posterior lesions: a systematic review. J Orthop Sports Phys Ther 2008; 38: 341e52.
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42 Stetson WB, Templin K. The Crank test, the O’Brien test, and routine magnetic resonance imaging scans in the diagnosis of labral tears. Am J Sports Med 2002; 30: 806e9. 43 Kibler WB. Specificity and sensitivity of the anterior slide test in throwing athletes with superior glenoid labral tears. Arthroscopy 1995; 11: 296e300. 44 Schlechter JA, Summa S, Rubin BD. The passive distraction test: a new diagnostic aid for clinically significant superior labral pathology. Arthroscopy 2009; 25: 1374e9. 45 Kim SH, Ha KI, Han KY. Biceps load test: a clinical test for superior labrum anterior and posterior lesions in shoulders with recurrent anterior dislocations. Am J Sports Med 1999; 27: 300e3. 46 Kim SH, Ha KI, Ahn JH, Kim SH, Choi HJ. Biceps load test II: a clinical test for SLAP lesions of the shoulder. Arthroscopy 2001; 17: 160e4. 47 Mimori K, Muneta T, Nakagawa T, Shinomiya K. A new pain provocation test for superior labral tears of the shoulder. Am J Sports Med 1999; 27: 137e42. 48 Herold T, Hente R, Zorger N, et al. Indirect MR arthrography of the shouldervalue in the detection of SLAP-lesions. Rofo 2003; 175: 1508e14. 49 Dinauer PA, Flemming DJ, Murphy KP, Doukas WC. Diagnosis of superior labral lesions: comparison of noncontrast MRI with indirect MR arthrography in unexercised shoulders. Skeletal Radiol 2007; 36: 195e202. 50 Bencardino JT, Beltran J, Rosenberg ZS, et al. Superior labrum anterior-posterior lesions: diagnosis with MR arthrography of the shoulder. Radiology 2000; 214: 267e71. 51 Waldt S, Burkart A, Lange P, Imhoff AB, Rummeny EJ, Woertler K. Diagnostic performance of MR arthrography in the assessment of superior labral anteroposterior lesions of the shoulder. AJR Am J Roentgenol 2004; 182: 1271e8. 52 Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology. Part II: evaluation and treatment of SLAP lesions in throwers. Arthroscopy 2003; 19: 531e9. 53 Burkhart S, Lo I, Brady P. SLAP repair. In: Burkhart’s view of the shoulder: a Cowboy’s guide to advanced shoulder arthroscopy. Philadelphia: Lippincott Williams and Wilkins, 2006: 238. 54 Brockmeier SF, Voos JE, Williams 3rd RJ, Altchek DW, Cordasco FA, Allen AA. Hospital for special surgery sports medicine and shoulder service. Outcomes after arthroscopic repair of type-II SLAP lesions. J Bone Joint Surg Am 2009; 91: 1595e603.
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“Not Plantar Fasciitis”: the differential diagnosis and management of heel pain syndrome
degeneration, inflammation of the plantar bursa, nerve entrapment, local bony pathology and enthesitis caused by seronegative arthritis.1 The term Plantar Fasciitis is often used interchangeably with PHP. However, the distinction between true “Plantar Fasciitis” and many of the other conditions that cause PHP is not always clear. We therefore consider it more appropriate that patients presenting with symptoms of PHP have an initial diagnosis of heel pain syndrome (HPS) (Table 1).
Munier Hossain Epidemiology
Nilesh Makwana
HPS is not uncommon. It is estimated that 1 in 10 people will develop HPS during their lifetime.2 HPS is more common in middle-aged obese females and young male athletes.3 It is likely that the incidence is higher in the athletic population but not all suffering present for medical treatment. A number of risk factors
Abstract Plantar heel pain (PHP) is a common orthopaedic presentation, but our understanding of this symptom is still limited. Multiple risk factors have been proposed but few substantiated. Obesity and foot pronation are known risk factors, whilst running or standing for long periods probably also contribute. There, however, is no relationship between heel spurs and PHP. As well as plantar fasciopathy, a number of different conditions can also give rise to PHP. It may be helpful to consider the differential diagnoses in terms of the structures that are symptomatic: the plantar aponeurosis, other soft tissues, the calcaneum and the peripheral nerves. The pathophysiology of PHP is still unclear but could be multi-factorial. Histological specimens show evidence of degeneration in the plantar aponeurosis but not inflammation. Seronegative arthritis should be excluded in cases of bilateral PHP. A number of different treatment options have been tried but very few have been rigorously investigated. Indeed, the overwhelming majority of cases will improve on conservative treatment. Shock wave therapy and surgery may be of use in selected subsets of patients who do not respond to other modes of conservative treatment.
Differential diagnoses of heel pain syndrome Site Plantar aponeurosis
Sub diagnosis Insertional Non-insertional
Plantar aponeurosis rupture Plantar fibromatosis Enthesopathy Other soft tissues Fat pad atrophy Bursitis Flexor Hallucis Longus tendonitis Calcaneum Traumatic Stress fracture Infective Osteomyelitis Inflammatory Seronegative arthropathy Inflammatory bowel disease Gout Rheumatoid arthritis Neoplastic: benign Unicameral bone cyst Osteoid osteoma Intraosseous lipoma Aneurysmal bone cyst Giant cell tumour Neoplastic: malignant Metastatic tumour Osteogenic sarcoma Chondrosarcoma Ewing’s sarcoma Metabolic Osteomalacia Paget’s disease Hyperparathyroidism Neurological Baxter’s nerve entrapment Medial calcaneal nerve entrapment Tarsal tunnel syndrome S1 radiculopathy
Keywords heel pain syndrome; Plantar Fasciitis; plantar fasciopathy; plantar fasciosis; plantar heel pain
Introduction Plantar heel pain (PHP) is a common presentation in foot and ankle clinics. Although Plantar Fasciitis is the most common cause of PHP a variety of other conditions can also be implicated. Several mechanisms have been proposed for PHP: chronic inflammation and microtrauma of the plantar fascia, mechanical overload, periosteal inflammation, increased calcaneal intraosseous pressure, peripheral nerve entrapment, fat pad
Munier Hossain FRCS(Glasg) PG Cert MSc(Ortho Eng) MSc(Oxon) Associate Specialist at the Department of Trauma and Orthopaedic Surgery, Betsy Cadwaladr University Local Health Board, Wrexham Maelor Hospital, Wrexham, UK. Nilesh Makwana FRCSEd FRCS(Glasg) FRCS(Orth) Consultant Orthopaedic Surgeon at the Department of Trauma and Orthopaedic Surgery, Betsy Cadwaladr University Local Health Board, Wrexham Maelor Hospital, Wrexham, UK.
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Diagnosis e primary Plantar fasciopathy
Table 1
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described, only the central band is constant. It is triangular in shape and arises from the medial process of the calcaneal tuberosity (Figure 1). The band diverges distally at mid-metatarsal level into five separate strands that are attached at the forefoot onto the plantar skin, the base of the proximal phalanges (via the plantar plate), the metatarsophalangeal joints via the collateral ligaments and the deep transverse metatarsal ligaments. Proximally the PA has direct a fibrocartilaginous attachment to the calcaneum e an enthesis. In the fibrocartilaginous enthesis fibrous tissue is gradually replaced by uncalcified fibrocartilage, calcified fibrocartilage and finally bone. This extraordinary degree of osseous interdigitation is able to withstand very significant tensile and shear stress that is in direct proportion to the degree of calcification of the cartilage and the extent of interdigitation. The transitional arrangement is also helpful to evenly dissipate stress.10 Researchers have found that the fibres of the Tendo Achilles are in direct continuity with the fibres of PA.11 This finding may explain the association between HPS and tight heel cord (and therefore reduced ankle dorsiflexion).
have been proposed but there is scant evidence to substantiate these assertions. There seems to be general agreement that obesity and increased pronation are definite risk factors for HPS.4e6 Reduced ankle dorsi-flexion and prolonged standing have been proposed4 and refuted by the same authors.5 Increased age and reduced metatarsophalangeal joint extension may also play roles.4 Both Pes Cavus and Pes Planus have been implicated.7 It is suggested, but not proven, that extensive running, wearing poorly constructed shoes and running on hard surfaces can cause PHP.8 The association between PHP and heel spurs remains a subject of controversy. Although it is tempting to speculate that heel spurs may result from traction of the plantar aponeurosis (PA), it is important to be aware that in fact heel spurs are not located in the PA, but more dorsally in the Flexor Digitorum Brevis (FDB) muscle. A number of papers have reported a positive association between heel spur and PHP.4 However, most of these are retrospective case series and as such do not indicate causation. Heel spur is actually fairly common in the general population and the presence or absence of a spur has not been found to correlate with the patients’ symptoms.9
Nerves The posterior tibial nerve is located in the tarsal tunnel. It usually divides into its three terminal branches in the tarsal tunnel: the medial plantar nerve, the lateral plantar nerve and the medial calcaneal nerve. The medial calcaneal nerve innervates the medial side of the heel, the medial plantar aspect of the foot and the AH muscle, which is the medial most muscle of the superficial layer of the foot. The first branch of the lateral plantar nerve (Baxter’s nerve) is particularly at risk. This branch comes off of the lateral plantar nerve near its origin and travels to supply the rest of the superficial layer muscle of the foot and the QP muscle. The nerve also gives a sensory supply to the calcaneal periosteum. This nerve travels between the AH muscle medially and the QP muscle laterally and can become trapped between the deep fascia of AH and the medial head of the QP muscle.1
Practice points C C C
C
Heel pain syndrome is common Obesity and increased foot pronation are known risk factors Reduced ankle dorsi-flexion and prolong standing have also been implicated, although the evidence is weak The common assumption of a positive association between heel spur and HPS remains unproven
Relevant anatomy Calcaneum An understanding of the local anatomy is helpful when considering the differential diagnoses of HPS. The posterior tuberosity of the calcaneum contributes to the bony architecture of the heel. The tuberosity has medial and lateral processes. The medial process gives attachment to the FDB, Abductor hallucis (AH) and the medial head of the Quadratus plantae (QP) muscles as well as the central band of the PA. The calcaneum is separated from the plantar skin by retrocalcaneal and plantar bursae and the heel fat pad. Plantar fat pad The plantar fat pad (PFP) is a complex multi-lobular fatty structure, whose anatomy and physiological role in HPS is poorly appreciated. The heel pad is uniquely designed to absorb shock and allow pain-free ambulation. The heel pad has a honeycombed structure and consists of fibroelastic septae extending from the calcaneum to the plantar skin. Enclosed between the septae are fat globules. Each fibroelastic chamber is further reinforced by diagonal and transversely running fibres. Plantar aponeurosis The PA is a fibro-aponeurotic structure, which is condensed deep fascia of the foot. Although a medial and lateral band has been
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Figure 1 Anatomy of the plantar aponeurosis.
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Practice points C
C
C
C
C
The PA shares a common origin with the muscles of the superficial layer of the foot The calcaneum is separated from the plantar skin by a complex honeycombed fibro-fatty fat pad that attenuates impact stress The PA has a fibrocartilaginous attachment to the calcaneum, which helps to dissipate stress Heel skin is supplied by the medial calcaneal nerve that, if compressed more proximally, may present with heel pain Baxter’s nerve is at risk of compression between the Abductor hallucis muscle and the medial belly of the Quadratus plantae muscle
Figure 2 Weight bearing loads the arch, compresses the struts and places tensile stress on the plantar aponeurosis.
Local biomechanics
rope”, or effectively shortens the PA and tightens it, thus elevating the medial arch by a windlass effect (Figure 3).12 During early stance phase there is coupled internal rotation of the leg and subtalar joint pronation. This “unwinds” the windlass and, as a result of elongation of the PA, lowers the arch via a “reverse windlass” mechanism. There is negative feedback in the system: lowering the arch tightens the PA that eventually prevents any further pronation. An adequately functioning windlass mechanism is essential to allow the foot to act as a propulsive lever. From heel strike to weight acceptance, subtalar joint pronation tenses the PA, which prevents excessive pronation and prepares the foot for supination from midstance onwards. Supination transforms the foot into a rigid lever ready for propulsion. From the foregoing discussion it is clear that excessive subtalar pronation during gait would prevent the medial arch from rising and affect the foot’s ability to propel forward.
Plantar aponeurosis Although the PA is thought of as being relatively inelastic, this premise is based on quasi-static tests performed on cadavers. Researchers have shown that the PA also has time-dependent visco-elastic properties, with a modulus of elasticity between 342 and 822 MPa.10 The PA supports the longitudinal arch of the foot. This was proved experimentally, with sectioning of the PA resulting in weakening of the arch.10 Plantar aponeurosis: truss and tie-beam: During static stance the biomechanical arrangement of the medial longitudinal arch has been likened to a truss, or more specifically, a uni-planar simple truss: a single triangular unit where the base is formed by the PA. Since the joints of this postulated truss are not fixed a better analogy may be a tie-bar connecting two compressive elements. It is useful to remember that the PA is the only element capable of elongation in this structure. Weight bearing transmits compressive force through the tarsi and the metatarsi. This tenses the PA, which resists further deformation of the arch (Figure 2). Variable elongation of the PA body can adjust the stiffness and height of the arch in response to the applied load. The clinical implication is that tension on the tie-beam may be higher in pes planus. Therefore, from a biomechanical point of view this lends credence to the clinical finding of increased risk of HPS in patients with foot pronation. The PA is also subject to tensile stress during different phases of the gait cycle. At the early part of stance phase, the longitudinal arch is lowered, which tenses the PA. Towards the end of the stance phase, the gastro-soleus complex lifts the heel off the ground for forward progression and generates a postero-superior torque on the calcaneus. The PA acts to counteract this torque, which places additional tensile stress upon itself.
Plantar heel pad Each heel strike generates a force through the heel pad of around 110% of the body weight. This can increase to 250% during running and the PHP is able to attenuate up to 80% of the strain to the lower leg. In comparison, insoles are able to attenuate less than 20% of the strain.13 It is therefore clear that a well cushioned heel is essential to absorb impact of heel strike. The PHP demonstrates visco-elastic behaviour under strain. The specialized macro and micro compartmentalized globular fat structure means that the fat cells are incompressible.14 The structure does not allow free fluid movement between the heel pad compartments. The fat globules in PHP are also specialized, with an altered ratio of saturated/unsaturated fat compared to normal
Plantar aponeurosis: the windlass mechanism: A windlass is a device designed to lift a heavy object by tightening a rope. It is proposed that the PA acts both as a windlass and reverse windlass. The anatomical basis for this analogy is that the PA has a broad insertion onto the forefoot. As such, dorsi-flexion of the metatarsophalangeal joints during terminal stance pulls or “winds” the PA over the metatarsal heads. This “shortens the
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Figure 3 Schematic diagram of a functioning windlass mechanism in the foot. Raising of the winch handle (hallux) results in shortening and tensioning of the rope and elevation of the arch.
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human adipose tissue.13 This means that the PHP has a lower viscosity compared to normal adipose tissue. There have been conflicting reports regarding the change in PHP thickness in HPS, with claims and counter-claims of thinning and thickening of the pad.14 However, it is agreed that loss of heel pad elasticity is a crucial factor in HPS.14 With ageing there is alteration in collagen and elastin content as well as changes in the thickness of the heel pad. This results in reduced shock absorbing capacity and could explain the increased risk of HPS with ageing.
Practice points C C
C
The plantar “fascia” is a fibro-aponeurotic structure Histological changes of the PA in HPS are suggestive of degeneration rather than inflammation Repetitive microtrauma is widely believed to initiate plantar fasciopathy but there is no strong evidence that supports this theory
Practice points C C C
C
C
The PA is not inelastic, it has visco-elastic properties The PA supports the longitudinal arch of the foot The PA acts like a tie-beam and resists flattening of the arch on weight bearing A functioning windlass mechanism of the PA allows the foot to act as an efficient propulsive lever Excessive pronation of the subtalar joint prevents the arch from rising and turns the foot into an inefficient lever
The problem with “Plantar Fasciitis”: a misnomer
Figure 4 Area of tenderness: IPF: insertional PF, NIPF: non-insertional PF, MCN: medial calcaneal nerve compression, BN: Baxter’s nerve compression, TTS: tarsal tunnel syndrome, MM: medial malleolus.
The term “Plantar Fasciitis” implies that the plantar fascia is subject to inflammation. Actually the plantar fascia is not a fascia at all but a fibro-aponeurotic structure and there is no evidence that inflammation occurs in HPS. Current research indicates that “Plantar Fasciitis” may in fact be a degenerative condition. Classic signs of inflammation e swelling, erythema, leucocytic or macrophage infiltration e are absent. Histological analysis of resected specimens has instead shown tissue changes suggestive of chronic degeneration: myxoid degeneration and fibroblast necrosis, chondroid metaplasia, angiofibroblastic proliferation, collagen degeneration, altered ratio of Type III to Type I collagen, increased numbers of abnormal fibroblasts with mitochondrial defects etc.15 A number of authors have also found thickening of the PA in HPS, with a mean reported thickness exceeding 4 mm.16 It has therefore been suggested that a more appropriate term might be “Plantar Fasciosis” (PF) or “plantar fasciopathy”. It is widely believed that mechanical overload of the PA causes repeated microtrauma and, eventually, a mechanical type of PHP, although the actual evidence for this is tenuous.10 Mechanical stress, however, appears to be concentrated at the calcaneal attachment of the PA and could explain HPS. Some studies have shown the area of tendon most often affected in “degenerative” tendinopathy is not the area of the tendon that is subjected to the highest mechanical force.3 Such findings have led others to question repetitive trauma as a causative factor. Loss of the cushioning effect of plantar fat pad could be responsible in some patients. Researchers have found evidence that changes in heel pad thickness, especially with ageing, may result in loss of elasticity of the heel pad and HPS.17 There is certainly evidence of degeneration of the fat pad with ageing and this could explain the late onset of HPS in the nonathletic population.
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Clinical features Presentation Patients usually present with plantar heel pain. HPS is typically worse early in the morning, especially for the first few steps after arising, gets better after some time but returns towards the end of the day. Some patients with tarsal tunnel syndrome by contrast complain of pain that is worse in bed and is relieved by weight bearing. An appropriate clinical history should ascertain the
Baxter’s nerve Calcaneus
Quadraus plantae Abductor hallucis Flexor digitorum brevis
Plantar aponeurosis
Figure 5 Palpation of the medial border of heel will compress the Baxter’s nerve between the belly of AH and QP muscles.
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Useful clinical tests in HPS Tests Passive toe dorsi-flexion Silfverskiold’s test Resisted great toe flexion Dorsi-flexioneeversion test
Mechanism Tightens the Windlass mechanism and exacerbates pain Increased passive ankle dorsi-flexion with the knee flexed to 90 Strains the FHL and reproduces pain Dorsi-flexioneeversion of ankle with extension of MTP joints strains the tibial nerve and causes pain/dysaesthesia
Diagnosis Plantar fasciopathy Tight Tendo Achilles FHL tendonitis Tarsal tunnel syndrome
Table 2
Clinical examination A thorough clinical examination is essential. It may be useful to inspect the footwear first, provided they are not brand new, and observe the pattern of wear. One should specifically inspect for heel pad atrophy, pes planus or pes cavus, hindfoot deformity, overpronation during gait and check for ankle range of motion and posterior tibial tendon dysfunction. If ankle dorsi-flexion appears limited one should perform Silfverskiold’s test to assess if this is due to a tight gastrocnemius. Other tests that are of use include passive dorsi-flexion of the toes, which tightens the windlass mechanism and exacerbates the pain in PF. Resisted flexion of the toe will exacerbate HPS in case of Flexor Hallucis Longus (FHL) tendonitis (Table 2).
duration of symptoms, occupational activities, current footwear, any recent increase in activity etc. An enquiry into systemic health is also important, as bilateral HPS is likely to be due to spondyloarthropathy.8 Patients should be asked about any history of back pain, urethritis, uveitis, bowel disturbance etc. Unrelenting pain, even at rest, should alert one to the possibility of infection or tumour, whilst sensory disturbance suggests a neurological pathology. It is also useful to remember that patients may have multiple pathologies and present with a number of different presenting features. PF may be combined with entrapment of Baxter’s nerve or tarsal tunnel syndrome. There have been reports of a small series of patients presenting with a combination of PF, posterior tibial tendon dysfunction and tarsal tunnel syndrome.18 The authors postulated that the failure of both static and dynamic arch support led to traction injury to the posterior tibial nerve in these patients.
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Site of tenderness The site of tenderness may be useful in informing the definitive diagnosis (Figure 4): the medial calcaneal tubercle is usually tender in PF but the calcaneal tuberosity may also be tender. Pain may also be present more distally over the central PA. We like to differentiate between the central pain and tenderness that is found in non-insertional PF and the medial calcaneal tenderness of insertional PF. In the case of plantar fibromatosis there may be a palpable nodule and pain/tenderness over the midpart of the PA. If there is compression of the Baxter’ nerve then pain is more proximal and dorsal. Palpating the medial aspect of the heel in line with the posterior border of the medial malleolus will compress the Baxter’s nerve between the AH and QP muscle and reproduce the symptoms (Figure 5). This is a useful sign, as patients with Baxter’s nerve compression usually do not complain of any sensory disturbance. Compression of the medial calcaneal nerve in the tarsal tunnel may also give rise to medial heel discomfort. This may also be associated with a positive Tinel’s sign and altered sensation of medial side of the heel. Tenderness, if present, is usually more posterior and dorsal to the area of tenderness in Baxter’s nerve compression. Diffuse pain and tenderness of the calcaneum is suggestive of a calcaneal stress fracture. Patients with plantar calcaneal bursitis or ‘Policeman’s heel’ present with burning, aching or a throbbing type of pain. The heel may or may not feel warm to touch, but is usually tender on direct compression. Pain due to PA rupture is more proximal and may be associated with a palpable gap.
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C C C
C
C
Patients usually complain of heel pain immediately after waking up in the morning that gets better after a while but returns towards the end of the day Bilateral HPS is likely to be due to spondyloarthropathy Infection or tumour should be excluded if pain is unrelenting The medial calcaneal tubercle is tender in insertional plantar fasciopathy Tenderness over the medial aspect of the heel in line with the posterior border of the medial malleolus is suggestive of Baxter’s nerve compression Diffuse heel tenderness may suggest a calcaneal stress fracture
Investigations Blood tests Investigations may not always be necessary in routine practice. If symptoms are bilateral but there is no obvious previous systemic history then blood tests should be performed to rule out gout, spondyloarthropathy etc. However, blood tests, including HLA-B27, might be entirely normal in many patients with spondyloarthropathy.19 Plain radiology When radiology is performed a weight bearing lateral radiograph of the ankle should be the first investigation. This will help to rule out stress fracture or tumour (Figure 6a, b) but should not be performed in search of a heel spur.7,9,11 There are also reports
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Figure 7 Ultrasound shows thickening and hypo-echoic signal from the affected PA compared to the normal side.
diagnosis is unclear.7 Ultrasound is useful in detecting abnormalities of the PA (Figure 7). A thickened PA of more than 4 mm thickness, as well as areas of hypo-echoic abnormality within the PA, may be found in case of PF.20 The addition of Doppler may give additional information regarding local hyperaemia. Magnetic Resonance Imaging (MRI) MRI may be helpful in evaluating patients who have an atypical presentation, who fail conservative management or are suspected of other causes of heel pain, such as tarsal tunnel syndrome, ganglion, osteomyelitis or tumour.6 MRI is more useful to rule out other causes of HPS than to confirm a diagnosis of PF. Usual MRI findings include thickening of the plantar aponeurosis, periaponeurotic oedema, bone marrow oedema of the calcaneus, stress fracture, frank tear of the PA etc (Figure 8a, b). Electrophysiology Electromyography (EMG) and nerve conduction studies (NCS) can be performed and are useful for suspected tarsal tunnel syndrome. However, they are operator-dependent and Baxter’s nerve compression is difficult to examine with NCS. a Plain X-ray of the ankle shows a radio-lucent appearance of the calcaneum. b MRI demonstrates intraosseous cystic lesion with a peripheral rim of fat characteristic of intraosseous lipoma.
Practice points C
Figure 6
C
that a non-weight bearing lateral X-ray of the ankle has high sensitivity and specificity to rule out PF based on the assessment of the thickness of the PA and the quality of the fat pad.16 Periosteal reaction may be evident in infection or spondyloarthropathy.8 If there is strong suspicion of a stress fracture but X-ray is negative then further imaging is useful.
Treatment HPS is generally a self-limiting condition and an overwhelming majority are likely to report resolution of symptoms with conservative management alone.11 There is general agreement that if conservative treatment is started soon after the onset of HPS then this is likely to lead to improvement or recovery in most patients. However, the time to resolution is
Ultrasonogram Ultrasound examination is operator-dependent, but if available is considered by many to be the investigation of choice when the
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Get to know your radiologist If the diagnosis is unclear a discussion with the radiologist will help in planning appropriate modes of investigation
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a MRI scan showing incomplete stress fracture of the calcaneal tuberosity with surrounding bone oedema, sagittal section (blue arrow). b Stress fracture of calcaneum, coronal section. Figure 8
variable and around 10% of all cases fail to respond to conservative treatment.21 HPS can cause a significant deterioration in health related quality of life in patients with recalcitrant symptoms.22
friction massage have been tried, without any evidence of useful effect. Night splints are designed to prevent overnight ankle plantarflexion. Plantarflexion of the ankle relaxes the PA and allows it to contract. There is evidence that night splint is useful in improving symptoms although the strength of this recommendation is weak in view of poor internal validity of the studies.25 These studies also suggest that patient compliance with night splints is likely to be low.
A number of treatment options A number of different treatment modalities are available: rest, ice, heat, nonsteroidal anti-inflammatory drugs (NSAIDs), heel cushions, heel cups, magnetic insoles, taping, Achilles and plantar fascia-specific stretching exercises, night splints, walking cast, ultrasound, laser treatment, iontophoresis, steroid injections, extra-corporeal shock wave therapy and surgery.6 None have unequivocally proven benefit and very few have been assessed via well designed randomized controlled trials.23 Some of the interventions are assessed in combination with other interventions and this makes it difficult to comment on the usefulness of individual interventions. If there are modifiable external risk factors then these should be addressed. It is logical to advise patients to modify their physical activities, to change trainers or shoes if their own are less than ideal and to lose weight. A step-wise treatment approach is recommended: with simpler options tried first.
Physiotherapy Physiotherapy is recommended for tightness of the Tendo Achilles, and incorporates calf stretching as well as plantar fascia-specific stretching exercises. Tendo Achilles stretching is performed by leaning against a wall with the affected side is placed behind the normal side. The heels are kept firmly on the ground and knee fully extended on the affected side (Figure 9a). Passive extension of the metatarsophalangeal joints will specifically stretch the plantar aponeurosis. DiGiovanni et al were the first to publish the results of tissue specific plantar fascia-stretching exercise and found them to be superior to Achilles tendon stretching in a randomized trial.26 In a recently published study Rompe et al found plantar fascia-specific stretching (Figure 9b) to be superior to repeated low dose shock wave therapy for the treatment of acute symptoms of proximal PF at early follow-up, but there was no difference at 15 months.23 This study reinforces the generally agreed guideline that ESWT be used only in chronic cases.
Physical therapy Heel cups and gel heel pads provide cushioning. They are also inexpensive and readily available. Foot orthotics may provide short-term benefit but are not useful over the long term.24 If a patient is deemed to require an orthosis (if they have pes planus or hindfoot varus/valgus) off-the-shelf orthotics should be tried. They are less expensive and there is no evidence that custom-made orthotics give better results.1 Orthotics support the medial longitudinal arch. Corrective orthotics can protect the foot from excessive pronation. There is no role for magnetic insoles.25 Taping of the foot is postulated to provide arch support but there is no strong evidence that it works.25 Ultrasound and deep
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Anti-inflammatory medication NSAID’s are often used in clinical practice and may be helpful to relieve acute symptoms of HPS but are unlikely to be effective alone and have not been adequately investigated. There is limited evidence to support the effectiveness of local corticosteroid injection. The rationale of injecting an anti-inflammatory agent in what is essentially a degenerate condition is not entirely clear. A recently withdrawn Cochrane review had found that steroid
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approach and placed deep to the PA. The medial approach is likely to be less painful than a direct plantar approach. Injecting deep to the PA ensures adequate spread of the corticosteroid preparation and reduces the risk of fat pad atrophy. Ultrasound guidance may prove to be an useful adjunct for accurate needle placement. Extra-corporeal Shock Wave Therapy (ESWT) ESWT involves the delivery of what are essentially rapidly pressurized sound waves. They are generated via a Lithotripsy unit that converts electrical energy into mechanical energy. ESWT can be of high or low energy. Local anaesthesia is usually required for high energy ESWT. ESWT application results in a positive pressure and a shock wave effect at the interface of two different types of tissues with different acoustic impedance.6 ESWT application also creates a tensile wave and a tissue cavitation effect. How ESWT works at tissue level is not fully understood but two different mechanisms have been proposed. It has been claimed that the deep tissue cavitation effect causes microrupture of capillaries, leakage of chemical mediators and promotion of neovascularization of the damaged tissue. The alternative theory is that ESWT works by depleting local sensory nerve fibres of substance P and calcitonin gene related peptide and thereby desensitises the area.23 ESWT is contra-indicated in bleeding diatheses. There have been a number of trials investigating its role but results are conflicting. This may be because of the heterogeneity of intervention and outcome measures employed. A Canadian Health Technology Assessment did not recommend the use of ESWT for PF.21 In the UK, the National Institute for Health and Clinical Excellence (NICE) recommends that ESWT should be used within a framework of audit after informed patient decision.27 ESWT is not recommended as a first line of management but textbooks recommend ESWT for symptoms lasting for more than 6 months where at least three different modes of conservative therapy have already been tried. In our practice we found ESWT useful for refractory cases of HPS. We are presently auditing our results. Surgery Open or endoscopic PA release may be suitable for a small subset of carefully selected patients in whom symptoms persist in spite of all other modes of conservative management. The procedure of choice is open partial PA release with simultaneous release of the Baxter’s nerve. The aim of surgery is to partially release the medial PA (<50%) and divide both superficial and deep fasciae of AH. Endoscopic PA release may appear to be attractive but there is concern that the procedure carries an unacceptably high rate of complications. Visualization is poor with the endoscopic technique and there is poor control of the extent of PA release. Other complications that have been reported include pseudoaneurysm of the lateral plantar artery and nerve injury. It is not possible to decompress Baxter’s nerve with the endoscopic technique and the American Orthopaedic Foot and Ankle Society (AOFAS) recommends that in case of suspected nerve compression endoscopic release should not be performed.8 It is not clear if the heel spur should be concurrently removed. Studies have reported complete/partial/no removal of the heel spur along with PA release.
a Tendo Achilles stretching: the stickman is leaning against the wall, keeping the front knee bent and the affected back knee completely extended, both heels are firmly on the ground. He should feel his calf muscles getting tight. b Plantar fascia-specific stretching is performed by passive extension of the toes until the PA feels taut. It is advisable to confirm that PA is correctly stretched by palpating the tension in the PA with the contralateral hand while stretching. Figure 9
injection had short-term benefit compared to control.2 This would suggest that the margin of benefit from corticosteroid injection is likely to be small. Nevertheless, corticosteroid injection remains a useful item in the orthopaedic armoury. There is a risk of fat pad atrophy and iatrogenic PA rupture with local corticosteroid injection. We suggest that the needle be introduced via the medial
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11 McPoil TG, Martin RL, Cornwall MW, Wukich DK, Irrgang JJ, Godges JJ. Heel pain e plantar fasciitis. J Orthop Sports Phys Ther 2008; 38: A1e17. 12 Hicks JH. The mechanics of the foot: the plantar aponeurosis. J Anat 1954; 88: 25e30. 13 Miller-Young JE, Duncan NA, Baroud G. Material properties of the human calcaneal fat pad in compression: experiment and theory. J Biomech 2002; 35: 1523e31. 14 Tong J, Lim CS, Goh OL. Techinque to study the biomechanical properties of the human calcaneal heel pad. The Foot 2003; 13: 83e91. 15 Lemont H, Ammirati KM, Usen N. Plantar fasciitis: a degenerative process (fasciosis) without inflammation. J Am Podiatr Med Assoc 2003; 93: 234e7. 16 Osborne HR, Breidahl WH, Allison GT. Critical differences in lateral Xrays with and without a diagnosis of plantar fasciitis. J Sci Med Sport 2006; 9: 231e7. € € o € yu €ncu € Y, Ozg €rgen M, Dabak K. Effects of changes in 17 Ozdemir H, So heel fat pad thickness and elasticity on heel pain. J Am Podiatr Med Assoc 2004; 94: 47e52. 18 Labib SA, Gould JS, Rodriguez-Del-Rio FA, Lyman S. Heel pain triad (HPT): the combination of plantar fasciitis, posterior tibial tendon dysfunction and tarsal tunnel syndrome. Foot Ankle Int 2002; 23: 212e20. 19 Lehman TJA. Enthesitis, arthritis and heel pain. J Am Podiatr Med Assoc 1999; 89: 18e9. 20 McMillan AM, Landorf KB, Barrett JT, Menz HT, Bird AR. Diagnostic imaging for chronic plantar heel pain: a systematic review and metaanalysis. J Foot Ankle Res 2009; 2: 32. 21 Extracorporeal shock wave treatment for chronic plantar fasciitis. Canadian Agency for Drugs and Technologies in Health 2007; vol. 96. http://www.cadth.ca/media/pdf/E0009_chronic-plantar-fasciitispart1_cetap_e.pdf [accessed 19.12.10]. 22 Irving DB, Cook JL, Young MA, Menz HL. Impact of chronic plantar heel pain health related quality of life. J Am Podiatr Med Assoc 2008; 98: 283e9. 23 Rompe JD, Cacchio A, Weil Jr L, et al. Plantar fascia-specific stretching versus radial shock-wave therapy as initial treatment of plantar fasciopathy. J Bone Joint Surg Am 2010; 92: 2514e22. 24 Landorf KB, Keenan AM, Herbert RD. Effectiveness of foot orthoses to treat plantar fasciitis: a randomized trial. Arch Intern Med 2006; 166: 1305e10. 25 Stuber K, Kristmanson K. Conservative therapy for plantar fasciitis: a narrative review of randomized controlled trials. J Can Chiropr Assoc 2006; 50: 118e33. 26 DiGiovanni BF. Tissue-specific plantar fascia stretching exercise enhances outcomes in patients with chronic heel pain. J Bone Joint Surg Am 2003; 85-A: 1270e7. 27 Extracorporeal shockwave therapy for refractory plantar fasciitis. National Institute for Health and Clinical Excellence. 2009. http:// guidance.nice.org.uk/IPG311 [accessed 19.12.10] 28 Riley G. Tendinopathydfrom basic science to treatment. Nat Clin Pract Rheumatol 2008; 4: 82e9.
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C
C
C
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Although a myriad of treatment options are available very few have been assessed via well designed trials Plantar fascia-specific stretching exercise appears to be useful in an acute setting Steroid injection should be attempted via the medial approach, with the needle placed deep to the PA Ultrasound guided injection may assist accurate needle placement ESWT may be useful in chronic recalcitrant cases although how ESWT works are subject to speculation Surgery should only be attempted in a selected subset of patients after all modes of conservative therapy have been tried Open partial PA release and decompression of the Baxter’s nerve is the procedure of choice
Conclusion It will be useful if future trials include placebo or no treatment arms to investigate the self-limiting nature of HPS. More trials are also needed to better understand the doseeresponse relationship and the appropriate combination of energy, frequency and duration of treatment of ESWT to determine if this has a place in management plans. Advances in the future treatment of HPS are likely to come from improvements in our understanding of the pathomechanics of HPS. There is evolving interest in the role of metalloproteinase enzymes in tendinopathy in general and they may well have a role to play in HPS.28 Unlocking the cellular secrets of HPS may also help to advance more specific cell-based treatment options in future. A
REFERENCES 1 Lee T, Maurus PB. Plantar heel pain. In: Coughlin MJ, Mann RA, Saltzman CL, eds. Surgery of the foot and ankle. Philadelphia: Mosby Elsevier, 2007: 689e707. 2 Crawford F, Thomson CE. Interventions for treating plantar heel pain. Cochrane Database Syst Rev 2003; 3: CD000416. 3 Juliano PJ, Harris TG. Plantar fasciitis, entrapment neuropathies, and tarsal tunnel syndrome: current up to date treatment. Curr Opin Orthop 2004; 15: 49e54. 4 Irving DB, Cook JL, Menz HB. Factors associated with chronic plantar heel pain: a systematic review. J Sci Med Sport 2006; 9: 11e22. 5 Irving DB, Cook JL, Young MA, Menz HB. Obesity and pronated foot type may increase the risk of chronic plantar heel pain: a matched caseecontrol study. BMC Musculoskelet Disord 2007; 8: 41. 6 Puttaswamaiah R, Chandran P. Degenerative plantar fasciitis: a review of current concepts. Foot 2007; 17: 3e9. 7 Alvarez-Nemegyei J, Canoso JJ. Heel pain: diagnosis and treatment, step by step. Cleve Clin J Med 2006; 73: 465e71. 8 Buchbinder R. Plantar fasciitis. N Engl J Med 2004; 350: 2159e66. 9 Thomas JL, Christensen JC, Kravitz SR, et al. The diagnosis and treatment of heel pain: a clinical practice guideline e revision 2010. J Foot Ankle Surg 2010; 49: S1e19. 10 Wearing SC, Smeathers JE, Urry SR, Henning EM, Hills AP. The pathomechanics of plantar fasciitis. Sports Med 2006; 36: 585e611.
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Acknowledgement The authors would like to thank Dr. HJ Patel, Consultant Radiologist, Wrexham Maelor Hospital for providing the radiological images.
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QUIZ
Radiology quiz Questions
Case 2 A 35-year-old male presented with an inversion injury. Plain radiography of the ankle was performed and is shown below. Describe the lesion and give a differential.
Case 1 A 50-year-old male presented to the emergency department with neck pain following a road traffic accident. Clinical examination revealed tenderness at the C3/C4 level. What do these radiographs show and what will you do next?
S Chaganti MBBS MRCSEd Department of Radiology, Derriford Hospital, Plymouth, UK. N Venkatanarasimha MBBS MRCP FRCR Department of Radiology, Derriford Hospital, Plymouth, UK. SP Suresh MBBS MRCP FRCR Department of Radiology, Derriford Hospital, Plymouth, UK.
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QUIZ
Case 3 A 20-year-old male presented to the emergency department following a fall onto the left shoulder. A plain radiograph of the left shoulder was performed. What are the findings and what would you do next?
Case 5 A 30-year-old male was reviewed at the Orthopaedic OPD with worsening chronic back pain. What is the diagnosis?
Case 4 A 26-year-old male had a plain radiograph for shoulder pain evaluation. What does the radiograph demonstrate? What would you do next to confirm the diagnosis?
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Answers
Case 6 A 15-year-old boy presented to his GP with a 6-month history of knee pain and swelling. What do these radiographs show? What will you do next?
Case 1 Description: There are flowing osteophytes (arrows) involving the anterior aspect of the cervical vertebral bodies with preservation of intervertebral disc spaces and unfused facet joints consistent with diffuse idiopathic skeletal hyperostosis (DISH).
In the context of trauma, Multi Detector Computerised Tomography (MDCT) was performed which confirmed the diagnosis of DISH and no fractures were demonstrated. Patients with DISH are prone to cervical spine fractures following trivial injuries and the fractures are often missed on plain radiographs.
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More information: DISH is a common musculoskeletal disorder of unknown aetiology. It commonly involves the anterolateral vertebral bodies of the thoracic spine but can also involve cervical, lumbar spine and other joints. It is more common in men than women and the prevalence increases with age. Currently, the diagnosis of DISH is based on plain radiographic appearances. Resnick and Niwayama set criteria for the diagnosis of DISH, which requires involvement of at least four contiguous vertebrae of the thoracic spine. The following features help to distinguish DISH from spondyloarthropathy: a) Preservation of the intervertebral disc space b) Absence of apophyseal joint involvement c) Preserved sacroiliac joints
Case 3 Description: The AP view demonstrates the light bulb sign (arrows) indicating a posterior shoulder dislocation.
Case 2 Description: There is a well circumscribed radiolucent lesion marginated by a thin well defined sclerotic border in the body of calcaneum (arrows) with central ossified matrix consistent with an intraosseous lipoma. The differential diagnosis includes simple bone cyst.
The axial view confirms the diagnosis of posterior shoulder dislocation. If pain and muscle spasm do not allow enough abduction to obtain a satisfactory axillary view, a modified axillary lateral or scapular views (“Y” view) may help. A modified axillary view demonstrated a reverse Hille Sachs lesion (arrow) in this patient.
More information: Posterior shoulder dislocation is an uncommon injury and accounts for 2e4% of shoulder dislocations. Several signs on the AP radiograph can suggest a posterior dislocation which include the light bulb (as demonstrated) and rim signs. However, caution is needed when these signs are used, as the “light bulb” and rim signs can be absent in reverse HilleSachs injury. The reverse HilleSachs lesion is a compression fracture of the anteromedial humeral head. CT is very useful for evaluating the size of the defect in the humeral head and associated glenoid changes. Suspected capsular or ligamentous injuries are more readily investigated by CT- or MR-arthrography.
More information: Intraosseous lipoma is an uncommon benign bone tumour consisting of mature adipose tissue and accounts for 0.1% of all bone tumours. The most common site for intraosseous lipoma is the intertrochanteric and subtrochanteric regions of the femur, followed by the calcaneum. There is a slight male predominance with predilection in the 4the6th decades. Plain radiographic appearances are diagnostic. In the absence of cortical bone expansion and intra-lesional calcification, intraosseous lipomas may closely resemble unicameral bone cysts. In these cases CT or MR may help to differentiate between the two by demonstrating fat within the lesion.
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Case 4 Description: The plain radiograph shows round equal sized calcified bodies in the joint consistent with the diagnosis of primary synovial osteochondromatosis.
More information: Primary Synovial Osteochondromatosis (SOC) is an uncommon benign neoplasm caused by synovial metaplasia. Synovial Osteochondromatosis commonly affects the knee, hip and elbow joints and rarely involves the shoulder and ankle joints. It is more common in males and is frequently seen between the 2nd and 5th decades of life. Secondary SOC occurs in joints with degenerative changes. Plain radiographs show multiple calcific densities within the joint space in 70e95% of cases. The MR appearances of SOC depend on the composition of the cartilaginous loose bodies and on the severity of synovitis. Purely cartilaginous loose bodies are hypointense (dark) on T1W sequence and hyperintense (bright) on T2W sequences; when the intraarticular bodies are ossified they are predominantly of low signal intensity (dark) on all pulse sequences. In addition when the ossified loose bodies are mature, fatty marrow (seen as bright signal on T1W and T2W sequences) may be seen in the centre of the loose bodies.
MR arthrography was performed to demonstrate the unossified synovial lesions and to quantify the extent of disease. The MR arthrogram demonstrates multiple similar sized loose bodies within the anterior recess of the shoulder joint which are hypointense on T1 with fat suppression sequences (arrows).
Case 5 The radiographic features are consistent with Ankylosing spondylitis (AS). Description: The spine radiographs demonstrate: a) On the lateral view: squaring of the vertebral bodies, syndesmophytes (vertical bony projections bridging adjacent vertebral bodies anteriorly and laterally to form a “bamboo-spine”) (arrow). b) On the AP view: The ossification of the interspinous and supraspinous ligaments can result in a vertical radioopaque stripe in the midline on antero-posterior spinal radiographs and this is known as the “tram-track” and “dagger” sign (long arrow) and complete fusion of the sacroiliac joints (small arrow). More information: MRI is the preferred imaging modality in patients with suspected early AS. The main differential considerations include DISH and HLA-B27 negative
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Case 6 Description: Plain radiographs: There is a well defined lucency in the medial femoral condyle seen on the AP and lateral views (arrows). This was further investigated with an MRI scan which demonstrated a hyperintense lesion in the medial femoral condyle corresponding to the plain radiographic location on STIR images (long arrows) which was communicating with a small collection in the posterior aspect of the knee (small arrow) and also gross soft tissue oedema (arrow heads), consistent with osteomyelitis.
inflammatory arthropathies like psoriatic and Reiter’s. Bilaterally symmetrical sacroiliitis, involvement of apophyseal joints (costovertebral and costo-transverse joints) can usually differentiate AS from the above described differentials. Hip arthropathy (requiring replacement) in a young male should always suggest ankylosing spondylitis.
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More information: Plain radiographs can be normal initially and show bone destruction or periosteal reaction only after 7e10 days. Bone scintigraphy and ultrasound are useful in establishing the diagnosis of osteomyelitis but the sensitivity and specificity are poor. MRI is considered as the investigation of choice for osteomyelitis. It is very sensitive and can demonstrate the subtle changes in the soft tissue as well as the bone marrow. Hyperaemia in an infected bone can be seen 24e48 h after the onset of symptoms with the administration of gadolinium. Findings of marrow hypointensity on T1 weighted images, hyperintensity on T2, and enhancement after gadolinium administration are considered indicative of osteomyelitis.
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TRAUMA
Traumatic hip dislocation
Dislocation of the hip is a true orthopaedic emergency, requiring prompt reduction to reduce the risk of avascular necrosis (AVN) of the femoral head.1e4 The hip joint is inherently very stable, with a high degree of bony conformity and stout surrounding capsular and ligamentous structures. A considerable amount of force, acting across the joint, is required to dislocate the joint. Posterior dislocations of the hip represent 85e90% of all THD. Anterior and central dislocations constitute the rest, with a further sub-classification of anterior dislocations into superior type(10%) and inferior type(90%).5 Central (acetabular) dislocations are rare and are associated with a poor prognosis. Historically mining accidents, in the form of a roof collapse onto a kneeling miner, were a potent source of THD. An impacting force was directly applied to the lumbar region whilst the hips were flexed, resulting in hip dislocation, and it was in dealing with these accidents that reduction and treatment methods were pioneered. Currently, falls from a height are the second most common cause of THDs whilst sporting injuries are a rarer cause, accounting for 2e5%.6 THD is more common in younger patients, most frequent in men between 20 and 30 years of age.7 The most common contemporary mechanism of injury associated with traumatic hip dislocations is road-traffic accidents. Over the years, although the safety profile of the motor vehicle industry has improved, the incidence of THD has risen due to the increased rate of motor vehicle collisions.1 As previously mentioned, a large amount of energy is required to cause a THD, therefore associated injuries, sometimes severe, are common in this patient group.4,8e10 Up to 50% of these patients suffer other fractures at the time of dislocation.10 In addition to the obvious joint disruption and soft tissue injury to the hip, associated fractures of the femur, acetabulum and chondral disruptions of the femoral head are also common.5 These associated injuries not only compromise joint integrity but also inhibit joint recovery, leading to chronic morbidity of the affected joint. Associated injuries from a dashboard impact also include soft tissue knee injuries. These are estimated to occur in up to 30% of THD. The classic association is posterior cruciate ligament rupture accompanying posterior hip dislocation, the force being applied to the flexed knee, displacing the proximal tibia posteriorly.
O Obakponovwe D Morell M Ahmad T Nunn P V Giannoudis
Abstract Traumatic dislocations of the native hip are a relatively rare injuries resulting from high-energy mechanisms producing grossly abnormal force vectors acting across the hip joint. Road-traffic collisions are the main cause and the affected patients have a high incidence of associated injuries. A thorough trauma assessment should be undertaken and, in simple dislocations, immediate reduction should be attempted before considering operative measures. An optimal outcome is achieved when reduction is achieved within 6 h, which has been shown to minimize the incidence of ensuing avascular necrosis. Open reduction is necessary when concentric reduction is not achieved by closed manipulation due to the interposition of soft tissue, cartilage or bone. Surgical fixation of the acetabulum and femoral head, in complex cases, is necessary to maintain joint congruity and reduce the risk of late post-traumatic arthrosis. The management of patient expectations and adequate surveillance for avascular necrosis is necessary in treating these relatively rare injuries.
Keywords fracture-dislocation of the hip; hip dislocation; hip reduction; Pipkin fracture; traumatic dislocation
Introduction Traumatic hip dislocation (THD) is a relatively rare injury, representing about 5% of all traumatic joint dislocations.1
O Obakponovwe MBChB Clinical Research Fellow, Academic Unit of Orthopaedic Surgery, Leeds General Infirmary, Leeds LS2 9NS, UK. Conflict of interest: none.
Anatomy of the hip The hip joint is one of the most mobile joints in the human body despite being heavily stabilized by both ligaments and a capsule. The acetabulum encloses just over half of the femoral head and is further deepened by the fibrocartilagenous acetabular labrum. The adult femoral neck projects at a mean angle of 126 to the axis of the femoral shaft, with anteversion of 15 . The ball and socket design allows the hip a large arc of rotation.11 The hip capsule consists of a strong but slack collection of fibrous tissue, composed of both circular and longitudinal fibres. The circular fibres form a band around the femoral neck; the zona orbicularis. The longitudinal fibres support the blood vessels that supply the hip joint and travel along the neck. The laxity of the tissue forming the capsule acts to allow some degree of relaxation with all ranges of movements of the hip.12 The hip joint is reinforced by five ligaments, of which four are extracapsular and one intracapsular .The extracapsular ligaments
D Morell BSc MBChB Clinical Research Fellow, Academic Unit of Orthopaedic Surgery, Leeds General Infirmary, Leeds LS2 9NS, UK. Conflict of interest: none. M Ahmad MBBS MRCS Registrar, Academic Unit of Orthopaedic Surgery, Leeds General Infirmary, Leeds LS2 9NS, UK. Conflict of interest: none. T Nunn FRCS (Orth) Specialist Registrar, Academic Unit of Orthopaedic Surgery, Leeds General Infirmary, Leeds LS2 9NS, UK. Conflict of interest: none. P V Giannoudis BSc MB MD FRCS(Orth) Consultant Orthopaedic Surgeon, Academic Unit of Orthopaedic Surgery, Leeds General Infirmary, Leeds LS2 9NS, UK. Conflict of interest: none.
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include the ischiofemoral, iliofemoral and pubofemoral ligaments, which attach to the ischium, ilium and pubis respectively. The zona orbicularis, or annular ligament, is formed by the circular fibres of the anterior capsule. The Y-shaped iliofemoral ligament (of Bigelow) is one of the strongest ligaments in the human body and, upon standing, prevents hyperextension of the hip and splints the anterior capsule. It is rarely disrupted in trauma, therefore acts as a reliable fulcrum for joint relocation. The pubofemoral ligament acts to restrict hip abduction, whilst the ischiofemoral ligament prevents internal rotation. Attached to a depression in the acetabulum lies the ligamentum teres, which projects into a depression in the femoral head. It acts to prevent displacement of the femoral head and contains the foveolar artery. This vessel is a branch of the obturator artery and may anastomose with the main vessels supplying the femoral head, which arise from the circumflex femoral arteries. However, this anastomosis is never established in 20% of the population and the patency of the foveolar artery decreases with advancing age.12 The dominant arterial supply of the adult hip joint arises from the medial circumflex femoral artery, which is a branch of the profunda femoris artery. It is the major contributor to the trochanteric anastamosis, which ultimately supplies the subcapsular retinacular vessels that are at risk of disruption during femoral head dislocation.
injuries in patients with THD has been quoted to range from 70% to 95%, depending on the cited literature.4,8,9 Sciatic nerve damage is a serious complication of THD, especially in central dislocations, where it can be anticipated in 10e20% of cases.21,22 Hak et al.23 reviewed THDs presenting to a level I trauma centre and found a 95% rate of associated injuries. 33% of these injuries were orthopaedic in nature and a 67% were non-orthopaedic. Of the non-orthopaedic injuries, closed head injuries represented 24%, thoracic injuries 21% and abdominal injuries 15%. Considering the portion of patients with associated orthopaedic injuries, 70% had an associated acetabular fracture, 23% also sustained a lower-extremity fracture, 21% an additional upper-extremity fracture and 14% sustained an associated femoral head fracture. Another study by Dreinhofer et al.7 looked at the demographic characteristics of 50 patients diagnosed with THD in Germany. Associated injuries were present in 86% of the cases, with 74% suffering head injuries, 66% lower-limb, 44% upper-limb and 20% abdominal injuries. Both of these publications highlight the high incidence of associated injuries with THD.
Classification The classification of THD is based on the direction of dislocation and the degree of joint disruption including any associated joint fractures. All three commonly used classification systems; the Epstein classification of anterior hip dislocation,18 the Thompsone Epstein classification24 of posterior dislocations and the Pipkin subclassification25 of ThompsoneEpstein grade V fractures, are ranked such that there is a worse prognosis with increasing classification grade (Tables 1, 2 and 3).
Mechanism of injury Several studies have shown “dashboard” impact to be the most common cause of THD, in which an axial load is transmitted from the knee, through the distal to the proximal femur and across the hip joint.7,13e16 The type of dislocation experienced depends on the position of the femur in relation to the pelvis at the time of impact and the direction of force vectors. Anterior dislocations may occur in automobile accidents, in falls from a height or secondary to a blow to the back of a squatted patient.17e19 The mechanism producing an anterior dislocation is force transmitted through an abducted and externally rotated hip. The neck of the femur impinges on the rim of the acetabulum, levering the head of the femur out of the acetabulum through a tear in the anterior capsule. The degree of flexion of the femur determines whether a superior or inferior anterior dislocation results. Posterior dislocations usually result from an impact onto a flexed knee with the hip in adduction and flexion and may be associated with acetabular fractures. A simple posterior dislocation, without a fracture, is usually the outcome if the hip is in a neutral or adducted position at the time of impact. Slight hip flexion in these circumstances is associated with a fracture of the posterior rim of the acetabulum.8,19,20
Patient evaluation As previously mentioned, a variety of concomitant injuries; pelvic, thoracic and/or abdominal, may exist alongside the THD. Therefore, good clinical acumen is essential for appropriate diagnosis and management. An altered level of consciousness is not uncommon in patients with THD. This may be due to hypovolaemia, hypoxia or the presence of an associated head injury. A history of the trauma mechanism, subsequent management and a careful multi-system evaluation in such cases is invaluable. Patients presenting with an acute dislocation of their native hip are typically in severe pain and are unable to move the affected lower extremity. The position of the limb and the history are usually highly suggestive of the diagnosis. A limb with an anterior dislocation of the hip may reveal slightly shortening on physical examination. In the superior dislocation subtypes, the hip appears extended and externally rotated, whilst with the inferior sub-type the hip may appear flexed, abducted and externally rotated. In both cases the fullness of the femoral head may be palpable; in the vicinity of the anterior-superior iliac spine or in the groin respectively. In posterior dislocations, the affected limb is classically shortened, internally rotated and adducted. Associated musculoskeletal injuries are common and the published risk of sciatic nerve injury with posterior dislocations ranges from 10% to14%.10,18,26e28 The presence of an ipsilateral concomitant extremity injury in both types of THDs can significantly alter the appearance of a limb and this should be taken into consideration by the attending clinician.
Associated injuries Hip dislocations are frequently associated with severe concomitant injuries due to the massive impact forces involved.4,8,9 Therefore, the attending clinician has to bear this in mind during the initial assessment and management of these patients. Advanced Trauma Life Support principles; a primary survey and initial imaging are employed to identify and treat life-threatening injuries first. Associated injuries may be in close proximity to the hip joint or involve other body regions. The incidence of associated
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Epstein classification of anterior hip dislocation Type I IA IB IC Type II IIA IIB IIC
Pipkin sub-classification of fracture-dislocation of the hip
Superior dislocations, including pubic and subspinous No associated fractures Associated fracture or impaction of the femoral head Associated fracture of the acetabulum Inferior dislocations, including obturator and perineal No associated fractures Associated fracture or impaction of the femoral head Associated fracture of the acetabulum
Type I Type II
Type III Type IV
Table 3
Table 1
increasing, in-line traction with the patient in the supine position and the knee and hip flexed is usually successful. Of paramount importance is the function of the assistant, who must stabilize the pelvis whilst the reduction occurs.30
A careful distal neurovascular examination should be undertaken and documented at the time of admission and repeated subsequently, due to the risk of damage to the sciatic and rarely, the femoral neurovascular structures.
Methods of reduction The Bigelow and reverse Bigelow methods were first described in 1869 by Henry Jacob Bigelow in his book ‘The mechanism of dislocation and fracture of the hip: with the reduction of the dislocations by the flexion method’.31 The method originally describes the use of a continuous movement of circumduction which can be divided in five stages: 1) Full hip flexion; 2) Abduction; 3) Smooth external rotation; 4) Gradual extension, and finally 5) Correction of the external rotation to a neutral position. The reverse Bigelow method is used for reduction of anterior dislocations and consists of the opposite (Longitudinal traction, adduction, internal rotation followed by extension and neutralization of the hip). Iatrogenic fractures of the neck of femur have been reported with this latter manoeuvre.32 Oscar H Allis described his method of hip relocation in 1895 in his monograph ‘Obstacles to the dislocation of the hip’.33 The patient is placed in the supine position as low to the floor as possible. In-line traction is applied to the affected side whilst the assistant stabilizes the pelvis. As traction is gradually applied with increasing force the degree of hip flexion is increased to 70 . Minimal rotational movements are made with slight adduction of the hip, resulting in the head of the femur passing over the labrum into the acetabulum.34 The Stimson gravity technique was first published by Lewis A Stimson in his book ‘A practical treatise on fractures and dislocations’ in 1900.35 The patient is placed in a prone position with their legs hanging over the end of the table. The unaffected limb is then held by the assistant, with the pelvis being supported by the end of the table. The knee and hip are flexed to 90 and direct pressure is applied to the posteriorly dislocated head of femur. To assist, downward pressure can also be directed to the upper calf until relocation occurs.32 Numerous other techniques have been described with variable degrees of popularity. Certain methods work on the concept of a fulcrum being used to exaggerate the forces applied for reduction. One such technique is the Rochester method. This allows for controlled rotational manipulation with traction applied through the surgeon’s forearm, which is used as
Hip reduction Early reduction of the uncomplicated hip dislocation is of vital importance if complications are to be minimized. A delay in reduction of the joint has been shown to increase the risk of avascular necrosis of the femoral head. Historically, this has been reported to be as high as 21% in groups treated by both closed and open techniques, with delays in reduction of up to 21 days.29 The hip reduction can be performed by either closed or open techniques, as promptly as possible. All methods of closed reduction should ideally be performed in the operating theatre with adequate analgesia and relaxation under general anaesthesia. Several methods of closed reduction for both posterior and anterior hip dislocation are reported and practiced, including Bigelow, Allis and Stimsen’s methods. Regardless of the method of reduction used, complete muscle relaxation is the key to success and therefore a general anaesthetic and closed reduction in theatre is preferable. Whatever the direction of dislocation (posterior, central or anterior), reduction using gradually
ThompsoneEpstein classification of posterior hip dislocation Type I Type II Type III Type IV Type V
Simple dislocation with or without an insignificant posterior wall fragment Dislocation associated with a single large posterior wall fragment Dislocation with a comminuted posterior wall fragment Dislocation with fracture of the acetabular floor Dislocation with fracture of the femoral head
Table 2
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Posterior dislocation of the hip with fracture of the femoral head caudal to the fovea centralis Posterior dislocation of the hip with fracture of the femoral head cephalad to the fovea centralis Type I or Type II with associated fracture of the femoral neck Type I, II or III with associated fracture of the acetabulum.
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a fulcrum. The assistant needs only stabilize the flexed knee on the uninjured side by holding the ankle (Figure 1).36 An interesting technique is the “Piggyback” method, described by Mayra and Samuel in 1994, and is perhaps one for the readers arsenal. Here the surgeon uses his shoulders as the fulcrum for reduction. The patient is positioned supine at the end of the table and the affected leg is passed over the surgeons shoulder. Downward traction is applied to the tibia and the limb is adducted as an anterior traction force is applied to the hip.37 Following successful closed relocation of a dislocated hip joint, the hip must be assessed for stability, much easier if the procedure has been carried out under anaesthesia in an operating theatre environment. Stability is tested by flexing the hip to 90 , applying internal rotation, adduction and a posterior directed force. The degrees of flexion, adduction and internal rotation needed to dislocate the hip should be documented. Appreciation of dislocation may not be easy in the presence of large posterior wall fractures. Rarely a detached or torn labrum may be responsible for joint instability. In this case, MRI is the gold standard to confirm this diagnosis and if confirmed, surgical stabilization by arthroscopic techniques may be indicated.
The use of distal femoral skeletal traction may be required, especially in cases which appear to be unstable. After closed reduction, more detailed imaging in the form of a CT scan is needed for detailed definition of the anatomy of the joint to ensure concentric reduction and exclude incarcerated fragments.
Operative management The indications for operative treatment following a hip dislocation include: 1. An irreducible hip dislocation. 2. Dislocation in association with a femoral neck fracture. 3. Interposed fragments (bone or cartilage) within the hip joint. 4. Large femoral head splitting fracture. 5. Incongruent reduction of the hip joint. 6. An unstable hip following reduction. Hip dislocations are considered an orthopaedic emergency due to the serious long-term sequelae that can result from the injury, which may be lessened by early reduction. The operative approach used for an irreducible hip dislocation depends on the direction of the dislocation, the related injuries and the preferences of the surgeon.38 In femoral head fractures, small osteochondral fragments of bone should be excised whereas larger fragments should fixed in place with a cancellous screw.32 All associated fractures should be either fixed or stabilized at the time of open reduction. Anterior dislocations can be accessed via the anterior (SmithPetersen) or anterolateral (Watson-Jones) approaches. These approaches are useful for visualizing reduction and fixation of femoral head fractures, which tend to be located on the anteromedial aspect and attached to the ligamentum teres. The Smith-Petersen approach utilizes the interval between sartorius and tensor fascia lata superficially, and deep to that between the rectus femoris and gluteus medius. Care must be taken to avoid damage to the lateral femoral cutaneous nerve of the thigh and femoral nerve, as well as the ascending branch of the lateral femoral circumflex artery. The Watson-Jones approach identifies the interval between the tensor fascia lata and gluteus medius. The anterior third of gluteus medius and minimus are raised as a flap to allow exposure of the hip capsule. This approach allows access to the posterior aspect of the hip if required. The potential danger of this approach is denervation of the abductor musculature. In the case illustrated, a 45-year-old lady presented with hip pain and shortening of the leg having been thrown from a horse (Figure 2). Radiographs demonstrated a Pipkin 2 fracture dislocation. A CT was obtained which confirmed a rotated anterior medial head fracture fragment, which remained within the acetabulum (Figure 3). There was no associated acetabular bony lip injury. Emergent open reduction of the head fragment (Figure 4) via a lateral approach was performed. Anatomical reduction necessitated detaching the fragment from the ligamentum teres and it was fixed with countersunk 3.5 mm screws (Figure 5). Even though reduction was performed within 6 h the prognosis is guarded due to the associated severe chondral damage. Complex posterior dislocations are best accessed via the Kocher-Langenbeck approach.39 This approach to the posterior acetabular column allows direct inspection of the femoral head for osteochondral defects, the acetabulum for any loose bodies
Figure 1 Rochester method. The patient is placed in the supine position and the uninjured hip and knee are flexed and stabilized by an assistant. The surgeon then places their forearm underneath the flexed knee on the injured side with the hand coming to rest on the knee of the uninjured side. Traction is then applied by pushing down upon the ankle. Reduction is achieved by traction, controlled internal rotation and once the hip relocates, by external rotation.
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Figure 4 Intraoperative image showing split to the femoral head.
can also be utilized for irreducible dislocations with an associated anterior femoral head fracture. The presence of small loose bony fragments needs to be identified as removal is necessary, to prevent abrasive damage to the articular surface. CT is ideal for identifying such fragments. Small fragments present in the fovea and not causing any impingement do not require excision.8 The preferred surgical approach to remove incarcerated fragments is the KocherLangenbeck approach, as this allows the best visualization of the acetabulum and skeletal traction can be used to dislocate the hip joint if required. The anterior approaches are indicated only when fragment(s) are located anteriorly. Modern arthroscopic techniques can also be used to excise fracture fragments. If the reduction of the dislocated hip is incongruent clinically, interposed soft tissues or a fracture of the weight-bearing portion of the acetabulum or femoral head, are the usual offending suspects and all these are indications for surgery.
Figure 2 Image of the leg position on presentation.
and the posterior acetabular wall for fractures. The short external rotators are detached to allow exposure of the posterior acetabulum and hip joint. The sciatic nerve needs to be identified and carefully protected during this approach as does the medial circumflex femoral artery. The Pipkin 4 injury with an associated posterior wall acetabular fracture deserves particular mention. This can be tackled by performing two separate approaches to the hip. Alternatively, this problem has been addressed by combining a Kocher-Langenbeck approach, set up in the lateral position, with a trochanteric digastric flip osteotomy, as is performed in the Ganz surgical dislocation. Using this approach allows visualization and fixation of the posterior acetabular wall and the anterior femoral head using the same incision and may be beneficial in helping to preserve femoral head vascularity.40 It
Aftercare There is still much debate as to the correct method of postreduction aftercare. Some advocate splinting or traction for up
Figure 3 Coronal CT reconstruction image showing hip fracture dislocation.
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Figure 5 Intraoperative image following fixation of the femoral head.
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to 4 weeks and a delay in weight-bearing of up to 6 weeks to minimize complications.32 Others claim that this delay in mobilization increases the incidence of intra-articular adhesions and therefore should be avoided.30 Certainly, there has been some evidence historically that early protected weight-bearing does not have any significant impact on the development of complications such as avascular necrosis of the femoral head, but it does reduce the severity of the disease.1 It has been shown that in those patients whose hip is reduced more than 6 h after injury have the highest rate of avascular necrosis. It may therefore be justifiable in these cases to delay weight-bearing for 8e12 weeks.34 However, current management practises are moving towards a more dynamic approach, with shorter immobilization and early physiotherapy. If the hip dislocation is reduced within 6 h then a brief period of immobilization is advisable, between several days and 2 weeks, before full mobilization. Continuous passive movements of the hip should be carried out to prevent intra-articular adhesions from occurring.41 Any extremes of motion should be avoided until up to 6e8 weeks allowing the hip capsule to heal.34 In general, early mobilisation from bed to chair, within a few days, is preferable. Initial weight-bearing should be toe touch, progressing to full weight-bearing by the 6th week.34
of the nerve is indicated if, following reduction, there is a decline in neurological status.34 Short-term complications associated with hip dislocation are related to pain and decreased mobility. If there has been an open reduction then there are complications secondary to surgery, such as infection and bleeding. Until mobility returns to normal there is an increased risk of thromboembolic events. Avascular necrosis, post-traumatic osteoarthritis and heterotopic ossification are the main long-term complications following traumatic dislocation of the hip. The incidence of avascular necrosis has been shown to be 4.8% in those individuals whose hip has been reduced in less than 6 h. This is increased to 52.9% in those whose hip is reduced after 6 h. As previously discussed, early weight-bearing has not been shown to influence the development of avascular necrosis but may affect its rate of progression.45 The cause of avascular necrosis of the femoral head is multifactorial. There may be injury to the cervical vessels to the femoral head and its contributions from ligamentum teres. There is also a resulting ischaemia to head for the period of dislocation.34 Studies on the dislocated femoral head of rabbits have shown that tearing of the cervical vessels is rare and therefore it is the period of ischaemia that is the cause of avascular necrosis,46 at least in this animal model. Radiographic findings for avascular necrosis usually appear within 2 years but can present as late as 5 years postinjury.34 Post-traumatic arthritis is very common and can occur in up to 24% of patients.30 Arthritis is more common after posterior than anterior dislocation. In those with associated femoral head fractures this rises to almost 50%.34 This higher rate is believed to be directly related to chondrocyte death during the initial trauma. In vitro analysis by Repo and Finley on articular cartilage showed that chondrocyte injury can occur with as little as 20e30% strain and this threshold may be breached even in simple THDs.47 The diagnosis of true primary arthritis can be complicated, as any case of avascular necrosis will progress to secondary arthritis. True primary arthritis is also associated with the more severely injured patients.34 Heterotopic ossification (HO) commonly occurs following posterior dislocation of the hip, especially when there is a fracture of the posterior wall. It is also associated with the need to carry out an open reduction of the hip and can in some cases lead to hip fusion. Treatment modalities have included the use of indomethacin and radiation therapy, which may decrease the rate of HO. Associated femoral head fractures also increase the risk of HO, and it can develop in up to 58% of patients when explored through an anterior approach.34
Complications There are a multitude potential of complications associated with traumatic dislocation of the hip. These can be divided into immediate, short- and long-term complications. In 2e15% of cases the hip cannot be reduced by closed means and needs to go to theatre for open reduction.38 In posterior dislocations the piriformis, gluteus maximus, ligamentum teres, capsule, labrum or a bony fragment may interpose and prevent concentric reduction. In anterior dislocations the reduction may be prevented by the labrum, psoas or in-folding of the capsule.42 Prior to open reduction it is important to obtain inlet, outlet and Judet views of the pelvis or a CT to visualize the location of any bony fragments.30 The methods of open reduction have been discussed in more detail elsewhere in this review. Complications such as AVN of the femoral head, post-traumatic arthritis and heterotopic ossification are also common with THD. The incidence of these complications is known to increase with more severe hip injuries, as disruption of the circumflex vessels, which supply the femoral head, is proportionally greater. Indeed, in some cases these vessels are irreversibly damaged. Other factors which can affect the management and outcome of patients with THD range from nerve injuries, such as sciatic or femoral nerve trauma, to small cartilage or osseous fragmentation, which may inhibit congruent reduction and predispose the joint to posttraumatic arthritis.18,19,43,44 Sciatic nerve damage is a serious complication of THDs and should be anticipated in 10e20% of cases.21,22 Therefore appropriate patient counselling must be undertaken. This figure is significantly higher if there is an associated bony injury. It is important to examine the neurological status of the patient preand post-reduction and if there are any discrepancies there is a risk that the nerve may be trapped. Functional recovery following sciatic nerve injury occurs in 70% of cases; however, this is dependent of the severity of injury.34 Surgical exploration
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Outcomes The clinical outcome after THD depends on a variety of factors. The magnitude of the initial insult and the amount of disruption of the hip joint, along with the effects of associated injuries, all have a bearing on patient outcome. Therefore, the type of dislocation and the classification grade of the injury should always be considered. Simple posterior dislocations are often associated with acetabular fractures and have a worse prognosis than anterior dislocations without femoral head fractures.5,7 Femoral head fractures occur in 7%e16% of patients with posterior
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Traumatic Simple Hip dislocation
ATLS + CT Pelvis
Polytrauma
Isolated Injury
Temporary stabilisation of multiple injuries Closed Reduction of dislocation within 6 hours Fracture Dislocation
Successful
Simple Dislocation
Unsuccessful Expertise available
Expertise unavailable
Stabilise with ExFix or traction Proceed to Open Reduction +/- Open Reduction Internal Fixation
Consider fixation or secondary reconstruction
Successful
MUA for stabilisation
Stable
Bed Rest 1/52
Transfer to Specialist centre for definitive care
Toe-touch weight bearing
Unstable
Bed Rest 2/52
Toe-touch weight bearing
Figure 6 Suggested algorithm of management for traumatic hip dislocation.
dislocations44,48 and in these cases are a significant poor prognostic feature.2,44 The timing of dislocation to relocation is also an important prognostic factor affecting long-term prognosis,2,8 as the risk of AVN of the femoral head and degenerative arthritis increases with increased dislocation time, as previously intimated. The long-term complications of THD are generally believed to result from insufficient blood flow to the femoral head due to vascular injury. Prompt reduction serves to restore adequate femoral blood flow by reducing this disruption by relieving compression, spasm and traction on any remaining intact vessels. Work by Duncan et al. showed blood flow to the femoral head reached a minimum within 24 h of continued dislocation in rabbit models. Complete recovery was only achieved after early relocation, with irreversible compromise to blood flow associated with reduction after 12 h of dislocation.49
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The landmark study by Hougaard et al. is usually quoted; a retrospective case series on 137 consecutive hips, which inferred that reduction within 6 h from time of injury is associated with a lower incidence of complications (AVN) but also showed that the risk of AVN was greater in the group of cases with severe dislocations. This study had no outcome data for reductions performed within 12 h of dislocation.45 Other clinical studies on human subjects also indicate that prompt reduction is the most important factor in the initial management, with a critical delay being reported as a 12 h interval.1,19 However, more recent studies have confirmed recommendations that reduction within 6 h should be attempted for improved outcomes. Again, an increased frequency of AVN occurred after delays in reduction greater than this.2,50 THDs are frequently associated with multiple injuries.9 Multiple injuries in turn affect a patients general mobility and
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6 Schuh A, Doleschal S, Schmickal T. Anterior hip dislocation in a football player: a case report. Case Report Med 2009; 2009: 363461. 7 Dreinhofer KE, Schwarzkopf SR, Haas NP, Tscherne H. Isolated traumatic dislocation of the hip. Long-term results in 50 patients. J Bone Joint Surg Br 1994; 76: 6e12. 8 Rosenthal RE, Coker WL. Posterior fracture-dislocation of the hip: an epidemiologic review. J Trauma 1979; 19: 572e81. 9 Suraci AJ. Distribution and severity of injuries associated with hip dislocations secondary to motor vehicle accidents. J Trauma 1986; 26: 458e60. 10 Stewart MJ, McCarroll Jr HR, Mulhollan JS. Fracture-dislocation of the hip. Acta Orthop Scand 1975; 46: 507e25. 11 Faulkner KG, Cummings SR, Black D, Palermo L, Gluer CC, Genant HK. Simple measurement of femoral geometry predicts hip fracture: the study of osteoporotic fractures. J Bone Miner Res 1993; 8: 1211e7. 12 Parke WW. The anatomy of the hip. In: Balderston RA, Rothman RH, Booth RE, Hozack WJ, eds. The hip. 1st edn. Pennsylvania: Lea and Febiger, 1992: 3e40. 13 Martinez AA, Gracia F, Rodrigo J. Asymmetrical bilateral traumatic hip dislocation with ipsilateral acetabular fracture. J Orthop Sci 2000; 5: 307e9. 14 Dudkiewicz I, Salai M, Horowitz S, Chechik A. Bilateral asymmetric traumatic dislocation of the hip joints. J Trauma 2000; 49: 336e8. 15 Kaleli T, Alyuz N. Bilateral traumatic dislocation of the hip: simultaneously one hip anterior and the other posterior. Arch Orthop Trauma Surg 1998; 117: 479e80. 16 Lam F, Walczak J, Franklin A. Traumatic asymmetrical bilateral hip dislocation in an adult. Emerg Med J 2001; 18: 506e7. 17 Aggarwal ND, Singh H. Unreduced anterior dislocation of the hip. Report of seven cases. J Bone Joint Surg Br 1967; 49: 288e92. 18 Epstein HC. Traumatic dislocations of the hip. Clin Orthop Relat Res 1973; 92: 116e42. 19 Epstein HC. Traumatic dislocation of the hip. Baltimore: Williams & Wilkins, 1980. 20 Reigstad A. Traumatic dislocation of the hip. J Trauma 1980; 20: 603e6. 21 Pickett JC. Injuries of the hip. Clin Orthop 1954; 4: 64e75. 22 Helfet DL, Schmeling GJ. Somatosensory evoked potential monitoring in the surgical treatment of acute, displaced acetabular fractures. Results of a prospective study. Clin Orthop Relat Res 1994; 301: 213e20. 23 Hak DJ, Goulet JA. Severity of injuries associated with traumatic hip dislocation as a result of motor vehicle collisions. J Trauma 1999; 47: 60e3. 24 Thompson VP, Epstein HC. Traumatic dislocation of the hip; a survey of two hundred and four cases covering a period of twenty-one years. J Bone Joint Surg Am 1951; 33: 746e92. 25 Pipkin G. Treatment of grade IV fracture-dislocation of the hip. J Bone Joint Surg Am 1957; 39: 1027e197. 26 Hunter GA. Posterior dislocation and fracture-dislocation of the hip. A review of fifty-seven patients. J Bone Joint Surg Br 1969; 51: 38e44. 27 Peet MM. Fracture of the acetabulum with intrapelvic displacement of the femoral head. Ann Surg 1919; 70: 296e304. 28 Seddon H. Surgical disorders of the peripheral nerves. Edinburgh: Churchill-Livingstone, 1972. 29 Stewart MJ, Milford LW. Fracture-dislocation of the hip; an end-result study. J Bone Joint Surg Am 1954; 36: 315e42.
hence the ability of a patient to perform activities of daily living independently. Studies by Dreinhofer et al. and Yang et al. drew such conclusions.4,7 The issue of time to weight-bearing after the reduction of THD has long been contentious, with some authors recommending an extended period of non-weight-bearing in order to allow restoration of blood flow to the femoral head, reducing the risk of AVN. Hougaard et al. did not identify weightbearing as a significant risk factor for subsequent development of AVN of the femoral head.2 In a proportion of cases, the delay in weight-bearing is primarily due to the presence of associated injuries, inhibiting mobilization. Post-traumatic arthritis is a very common complication of THD. Its incidence is believed to be related to the severity of the initial insult to the joint, in the form of chondrocyte damage and the disruption of joint congruity. Post-traumatic arthritis also increases in observed incidence with increased time of followup.5 After a 14-year follow-up period, patients with sedentary lifestyles have a lower incidence, 24%, compared with patients known to perform heavy, physical jobs, 37.5%.51
Conclusion THDs are relatively rare injuries resulting from large forces acting across and disrupting the hip joint. Due to the nature and mechanism of the injury, associated injuries are common and the attending medical doctor should perform a thorough trauma assessment and initiate appropriate acute management, which must include immediate reduction of the joint whenever possible. We propose an algorithm, Figure 6, which is simple and easily implemented for the management of these high-energy injuries, which frequently occur in the polytrauma settings. To re-iterate, early reduction, within 6 h of dislocation, should be the target and ideally performed for all cases, followed by operative intervention, to restore anatomical bony union, joint congruity and reduce the risk of long-term complications, where necessary. It is important to counsel patients about the incidence of long-term sequelae, such as AVN and post-traumatic arthritis and the likely necessity of future interventions, should these complications develop. AVN generally occurs within 2 years of the injury, but has been reported as up to 5 years post-injury. Therefore, an appropriate length of clinical and radiological follow-up and surveillance should be arranged. A
REFERENCES 1 Brav EA. Traumatic dislocation of the hip: army experience and results over a twelve-year period. J Bone Joint Surg Am 1962; 44: 1115e34. 2 Hougaard K, Thomsen PB. Coxarthrosis following traumatic posterior dislocation of the hip. J Bone Joint Surg Am 1987; 69: 679e83. 3 Jacob JR, Rao JP, Ciccarelli C. Traumatic dislocation and fracture dislocation of the hip. a long-term follow-up study. Clin Orthop Relat Res 1987; 214: 249e63. 4 Yang RS, Tsuang YH, Hang YS, Liu TK. Traumatic dislocation of the hip. Clin Orthop Relat Res 1991; 265: 218e27. 5 DeLee JC. Fractures and dislocations of the hip. In: Rockwood C, Green DP, Buckholz RW, Heckman JD, eds. Fractures in Adults. Vol 2., 4th edn. Philadelphia: Lippincott-Raven, 1996: 1756e1803.
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30 Sanders S, Tejwani N, Egol KA. Traumatic hip dislocationea review. Bull NYU Hosp Jt Dis 2010; 68: 91e6. 31 Bigelow HJ. The true neck of the femur: its structure and pathology. 1875. Clin Orthop Relat Res 1997; 344: 4e7. 32 McRae R, Esser M. Practical fracture treatment. 4th edn. ChurchillLivingstone, 2002: 280e286. 33 Allis OH. The hip. 1st edn. Philadelphia: Dornan, 1895. 34 Kain MSH, Tornetta 3rd P. Hip dislocations and fractures of the femoral head. In: Bucholz RW, Heckman JD, Court-Brown CM, eds. Rockwood & Green’s fractures in adults. 6th edn. Philadelphia: Lippincott Williams & Wilkins, 2006: 1716e1752. 35 Stimson LA. A practical treatise on fractures and dislocations. Lea Brothers, 1900. 36 Stefanich RJ. Closed reduction of posterior hip dislocation: the Rochester method. Am J Orthop (Belle Mead NJ) 1999; 28: 64e5. 37 Goulet JA. Hip dislocations. In: Browner BD, Levine AM, Jupiter JB, Trafton PG, Krettek C, eds. Skeletal trauma: basic science, management and reconstruction. 4th edn. Philidelphia: Saunders-Elsevier, 2009: 1781e1818. 38 Tornetta 3rd P, Mostafavi HR. Hip dislocation: current treatment regimens. J Am Acad Orthop Surg 1997; 5: 27e36. 39 Von langenbeck B. Ueber die Schussverletzungen des Huftgelenks. Arch Klin Chir 1874; 16. 40 Siebenrock KA, Gautier E, Ziran BH, Ganz R. Trochanteric flip osteotomy for cranial extension and muscle protection in acetabular fracture fixation using a Kocher-Langenbeck approach. J Orthop Trauma 1998; 12: 387e91.
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41 Torzilli PA, Grigiene R, Borrelli Jr J, Helfet DL. Effect of impact load on articular cartilage: cell metabolism and viability, and matrix water content. J Biomech Eng 1999; 121: 433e41. 42 Canale ST, Manugian AH. Irreducible traumatic dislocations of the hip. J Bone Joint Surg Am 1979; 61: 7e14. 43 Epstein HC, Wiss DA. Traumatic anterior dislocation of the hip. Orthopedics 1985; 8: 130, 132e4. 44 Epstein HC, Wiss DA, Cozen L. Posterior fracture dislocation of the hip with fractures of the femoral head. Clin Orthop Relat Res 1985; 201: 9e17. 45 Hougaard K, Thomsen PB. Traumatic posterior dislocation of the hipeprognostic factors influencing the incidence of avascular necrosis of the femoral head. Arch Orthop Trauma Surg 1986; 106: 32e5. 46 Shim SS. Circulatory and vascular changes in the hip following traumatic hip dislocation. Clin Orthop Relat Res 1979; 140: 255e61. 47 Repo RU, Finlay JB. Survival of articular cartilage after controlled impact. J Bone Joint Surg Am 1977; 59: 1068e76. 48 Brumback RJ, Kenzora JE, Levitt LE, Burgess AR, Poka A. Fractures of the femoral head. Hip 1987; 181e206. 49 Duncan CP, Shim SS. Blood supply of the head of the femur in traumatic hip dislocation. Surg Gynecol Obstet 1977; 144: 185e91. 50 Jaskulka RA, Fischer G, Fenzl G. Dislocation and fracture-dislocation of the hip. J Bone Joint Surg Br 1991; 73: 465e9. 51 Upadhyay SS, Moulton A, Srikrishnamurthy K. An analysis of the late effects of traumatic posterior dislocation of the hip without fractures. J Bone Joint Surg Br 1983; 65: 150e2.
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Chronic painful conditions of the hip
genes associated with OA include the interleukin 1 gene, the matrilin 3 gene, the IL-4 receptor alpha-chain gene, the secreted frizzled-related protein 3 gene, the metalloproteinase gene ADAM12 and the asporin gene (ASPN).2 There are two different types of osteoarthritic pain, identified by Hawker et al.3 The first type of pain is a constant, dull, aching pain but does not affect activities of daily living. The second type of pain includes episodes of unpredictable, intense pain resulting in the avoidance of activities. Pain is not the sole complaint of patients with hip OA. They frequently complain of the sensation of instability or giving way. This sensation does not necessarily lead to a fall but it may do so. There may be a difference in the symptom severity of hip OA between males and females, with women having a higher prevalence of hip OA, more severe symptoms and a greater disability. Examination findings will vary depending on the severity of pain but there will be some degree of pain and restriction in range of movement of the hip joint, in particular affecting internal rotation. A patient is classified as having hip OA when they have hip internal rotation < 15 and hip flexion 115 , when the erythrocyte sedimentation rate (ESR) is 45mm/hr.4 Other reliable findings include a leg length discrepancy and a positive Thomas test for flexion contracture. Radiological features of hip OA include osteophytes on the joint margins, narrowing of the joint cartilage, subchondral cysts and sclerosis and an altered shape of the femoral head (Figure 1). The non-operative management of patients with hip osteoarthritis includes both non-pharmacological and pharmacological therapies. The Osteoarticular Research Society International (OARSI) group has produced guidelines for the management of OA.4,5 Non-pharmacological therapy includes patient education,
Olivia Flannery Connor Green Dominic Harmon Eric Masterson
Abstract Hip pain is a common complaint with many causes. Pathology in the hip can present with pain referred to sites other than the hip and pain in the hip may result from pathology elsewhere. An accurate history and examination is paramount. Chronic painful conditions of the hip summarised in this paper can be classified into three main groups: intra-articular, extraarticular and hip mimickers. The intra-articular conditions include osteoarthritis, rheumatoid arthritis, femoroacetabular impingement, labral tears and snapping hip secondary to loose bodies, synovial chondromatosis or labral tears. Extra-articular conditions include snapping hip, iliopsoas bursitis, piriformis syndrome and greater trochanteric pain syndrome. Hip mimickers include myofascial pain syndrome, osteitis pubis, sacroiliac joint pain and nerve entrapment syndromes.
Keyword chronic hip pain
Osteoarthritis Osteoarthritis (OA) is a common cause of hip pain, with a mean prevalence of 8% (range 0.9e27%) in the general adult population.1 The primary change in OA is loss of hyaline articular cartilage. Secondary changes include osteophyte formation (see Figure 1), bony remodelling and changes of the synovium, capsule, ligaments and muscles. Primary OA is the term given when no specific disease or anatomical abnormality is found. When conditions, such as osteonecrosis, Paget’s disease, inflammatory arthropathy, traumatic remodelling, degenerative dysplasia of the hip or slipped capital femoral epiphysis have resulted in degenerative change, this is termed “secondary OA”. Risk factors for developing OA include age, genetic predisposition, postmenopausal hormone deficiency and obesity. The Olivia Flannery MB ChB MRCSI MCh SpR Orthopaedics, Department of Orthopaedics, Croom Orthopaedic Hospital, Croom, Limerick, Ireland. Connor Green MB BCh BOA MRCSI MSc MCh SpR Orthopaedics, Department of Orthopaedics, Croom Orthopaedic Hospital, Croom, Limerick, Ireland. Dominic Harmon MD FCARCSI Consultant in Anaesthesia and Pain Medicine, Department of Anaesthesia and Pain Medicine, Croom Orthopaedic Hospital, Croom, Limerick, Ireland. Eric Masterson BSc MCh FRCSI FRCS (Orth) Consultant Orthopaedics, Professor of Orthopaedic Science, Department of Orthopaedics, University of Limerick, Croom Orthopaedic Hospital, Croom, Limerick, Ireland.
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Figure 1 Severe osteoarthritis of the left hip, with loss of joint space, osteophytes, subchondral cysts and sclerosis.
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health professional social support via telephone contact, weight loss, occupational therapy and physiotherapy which incorporates aerobic aquatic exercise programs, thermal modalities, walking aids, transcutaneous electrical nerve stimulation (TENS) and acupuncture.5 Pharmacological therapy includes non-opioid analgesia (e.g. Paracetamol), oral and topical non-steroidal anti-inflammatory drugs (NSAIDs), opioid analgesia and intraarticular injections of corticosteroids and hyaluronates.5 Surgical options for hip OA include osteochondroplasty (early OA only), osteotomy, resurfacing hip replacement, cemented, uncemented or hybrid total hip arthroplasty, arthrodesis and resection arthroplasty as a salvage procedure. The best predictor of outcome at 6 months following THR is the patient’s baseline pain and function. However, not only pre-operative bodily pain and physical function, but also demographic characteristics and social support correlate significantly with improvements in outcome, indicating the THR should be performed before symptoms are too severe.
are required to evaluate instability. Up to 61% of patients with RA can have radiological evidence of cervical spine instability, with 50% of those having no relevant signs or symptoms.8 Resurfacing, cemented, uncemented or hybrid total hip arthroplasty can be performed depending on the bone stock and quality and good results are reported for all.
Femoroacetabular impingement (FAI) Femoroacetabular impingement is defined as the abutment between the proximal femur and the acetabular rim, which arises from morphologic abnormalities affecting the acetabulum or the proximal femur or both. The abnormal contact results in anterior hip pain, tears of the labrum, damage to the articular cartilage and progressive degenerative changes leading to osteoarthritis. Two types of FAI have been described: cam-type impingement and pincer type impingement. Cam-type impingement (Figure 2) is caused by jamming a non-spherical femoral head with an increased femoral neck radius (Figure 2), and usually a prominence at the anterosuperior headeneck junction, into the acetabulum.9,10 Damage is thought to takes place during flexion and internal rotation of the hip where shear forces are generated against the cartilage of the anterosuperior quadrant of the acetabulum. Pincer type impingement results from a prominent acetabular rim abutting against the femoral headeneck junction. It occurs because of overcoverage of the acetabulum where the acetabulum has overhanging edges or is too deep, and is seen in conditions such as acetabular retroversion, coxa profunda or protrusio acetabuli. The mixed type impingement, being the most common, contains features of both the cam and pincer types.9 FAI occurs in active young and middle-aged adults, and can be precipitated by minor trauma. Patients typically complain of
Rheumatoid arthritis Rheumatoid arthritis (RA) is a chronic systemic inflammatory autoimmune disease involving the synovium. As the disease progresses there is a decreasing functional capacity, which is related to the degree of early activity of the disease and determined by joint destruction later in the disease. Although joint destruction increases as time passes, the progress is slower later in the disease. Early adequate medical treatment has been shown to be beneficial. Treatment goals include reducing pain, control of disease activity, maintaining daily functionally activity and work, and maximizing quality of life. The mainstay of treatment is medication, which is managed by Rheumatologists and includes NSAIDs, glucocorticosteroids and disease modifying anti-rheumatoid drugs (DMARD). The hip can be involved in 15% of cases at 1 year and 28% at 5 years after the onset of disease.6 Patients with hip involvement usually present with pain in the groin, buttock or thigh but occasionally can present with knee pain. The level of functional activity and mobility depends on the number of involved joints. Patients may present using various walking aids or may be confined to a wheelchair. Examination reveals a painful and restricted range of motion of the affected hip joint. There may be flexion and adduction contractures. Both upper and lower limbs should be examined for contractures, deformities and range of motion. Radiological findings include periarticular osteopenia and generalized osteoporosis, erosions, cysts and concentric joint space narrowing. As the disease progresses protrusio acetabuli may develop and then medial migration progresses at an average of 2.65 mm a year and superior migration progresses at an average of 4 mm a year.7 When hip symptoms are severe enough to warrant surgery, a thorough pre-operative general assessment is required. Patients with RA often have co-morbidities and impaired physical function. There is an increased risk of delayed wound healing and deep infection so any pre-existing source of infection needs to be eliminated prior to surgery. The cessation of DMARD therapy may lower the risk of subsequent prosthesis infection but not significantly. Lateral flexion and extension cervical spine radiographs
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Figure 2 Cam lesion of the right hip in a young male.
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degeneration.11 Traumatic tears are rare but can occur following a high or low velocity injury with or without subluxation or dislocation of the hip. As previously mentioned, morphologic abnormalities affecting the acetabulum or the proximal femur, or both can result in FAI, which can crush the labrum on movement resulting in a labral tear. Capsular laxity can lead to increased pressure on the anterosuperior labrum as the head moves anterior in the joint.11 Dysplasia can cause localized anterior, posterior or diffuse tears as a result of increased stresses on the labrum because of the abnormal position of the femur within the acetabulum. A high percentage of labral abnormalities have been found in cadavers, suggesting degeneration with increasing age.11 Labral tears are more common in females. The most common complaint is of groin or anterior hip pain. Pain can occur in the buttock or lateral hip region but is less common. Anterior or groin pain is more likely to indicate an anterior labral tear whereas buttock pain suggests a posterior labral tear. A high percentage of patients complain of night pain and pain when sitting. Mechanical symptoms, such as clicking, locking and giving way have been reported, with clicking being the most consistent.12 Examination findings may reveal a mild limp and positive Trendelenburg sign and there may be slight reduction in range of movement. The most reliable and consistent finding is a positive impingement test, in which pain is elicited when the hip is flexed beyond 90 , adducted and internally rotated. Plain radiographs will not show a labral tear but AP and lateral views should be performed to exclude any bony abnormality such as degenerative changes, coxa profunda, protrusio acetabuli, acetabular retroversion, abnormal femoral headeneck offset or femoral head asphericity. The investigation of choice is a magnetic resonance arthrogram (MRA) which has a high sensitivity and specificity. Labral detachments are well demonstrated using contrast.11 However, the gold standard remains hip arthroscopy, where tears can be directly visualized and treated accordingly. Non-surgical treatment for labral tears should be attempted first and includes a restriction in physical activity, NSAIDs and physiotherapy. Physiotherapy should be directed towards aligning the hip joint, optimizing the hip abductors, external rotators, gluteus maximus and iliopsoas muscles to avoid excessive forces into the anterior hip joint. If pain persists then surgery, arthroscopic or open, can be performed. Open procedures include surgical dislocation, osteoplasty and labral debridement. Arthroscopic options, which are gaining popularity and include labral repair or labral debridement, have been shown to be as successful as open procedures.
the gradual onset of groin or hip pain, which can be exacerbated by athletic activities or by prolonged walking or sitting. Examination reveals restriction in flexion, adduction and internal rotation and a positive impingement test in which pain is experienced when the hip is flexed to 90 , adducted and internally rotated with the patient supine. Cam-type FAI is more prevalent in young males whereas the pincer type is more prevalent in middle-aged females. If FAI is suspected a true AP and lateral X-ray are required. Pistol grip deformity of the proximal femur, herniation pits, reduced offset of the femoral headeneck junction, hip dysplasia, acetabular retroversion, coxa profunda or protrusio acetabuli are some radiological findings that may be present. The alpha angle which measures cam-type impingement can be measured by drawing a best fit circle over the femoral head and two lines: the first from the centre of rotation of the femoral head to the femoral neck and the second from the centre of rotation of the femoral head to the first point of the femoral neck junction which lies outside the circle.10 The angle sustained between these two lines is the alpha angle, the upper limit of normal ranging from 50.5 to 55.5 .10 More accurate evaluation is obtained with magnetic resonance imaging (MRI) or magnetic resonance arthrography (MRA) in which not only will the above-mentioned radiological findings will be more easily identified, but labral and chondral lesions can be detected. Non-operative management of FAI includes modification of athletic activities and non-steroidal anti-inflammatory drugs. However, surgical management is usually required due to the patient’s high level of activity. Operative treatment can be performed by either open or arthroscopic means. The aim of surgery is to clear the abutment of the proximal femur against the rim of the acetabulum to allow an unrestricted range of movement. This includes excision osteoplasty, femoral osteotomy, resection of excessive anterior acetabular rim, periacetabular osteotomy, reverse periacetabular osteotomy, repair or partial resection of labral tears and chondral lesions. The early diagnosis of FAI is of paramount importance before the onset of degenerative changes necessitating hip arthroplasty.
Labral tears Labral tears are more common than previously thought, having a prevalence between 22% and 55% in patients with groin or hip pain.11 The labrum stabilizes the hip joint by deepening and increasing the surface area of the acetabulum by approximately 21% and 28% respectively.11 The labrum acts as a seal maintaining hydrostatic pressure, which may enhance joint lubrication.12 Tears in the labrum would disrupt the labral seal, destabilize the hip joint, decrease contact area and increase the stresses across the joint leading to degenerative changes.12 Tears are most frequent in the anterior portion of the labrum, known as the watershed lesion, as a result of a sharp and abrupt chondrolabral zone anteriorly.12 Controversy remains over the healing potential of labral tears. The majority of the labrum is avascular with blood vessels only penetrating the outer one-third of the labrum. Although neovascularization has been shown to occur within the labrum following a tear, some believe that the labrum has no healing potential. Five aetiologies of labral tears have been proposed: trauma, femoroacetabular impingement, capsular laxity, dysplasia and
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Coxa saltans Coxa saltans (CS), also known as snapping hip, is a benign condition characterized by an audible and sometimes painful snapping, which occurs with flexion and extension of the hip. There are three types of coxa saltans: (a) external (b) internal and (c) intra-articular. The external type is the most common and is caused by movement of the iliotibial band (ITB) over the greater trochanter, formed from the tensor fascia anteriorly and the gluteus maximus posteriorly, it can also occur as a complication following total hip arthroplasty, however any swelling or anatomic change can result in snapping over the greater trochanter because the ITB remains taut throughout range of movement of the hip. Internal snapping is usually a result of the iliopsoas tendon moving over the iliopectineal eminence, the
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femoral head, the lesser trochanter or the anterior hip capsule but it can also be related to the iliopsoas bursa.13 Intra-articular type snapping can be caused by loose bodies, synovial chondromatosis or idiopathic recurrent subluxation of the hip. However, it is usually caused by acetabular labral tears.13 Snapping hip typically occurs in females ranging from the mid-teens to early forties. There may be a history of trauma but this is usually associated with the intra-articular type of CS. Patients will present with a painful snapping sensation localized over the greater trochanter in external snapping, or over the anterior hip in internal snapping. Intra-articular lesions present mainly with pain, however, the patient usually describes a clicking rather than a snapping sensation.13 Patients with external type snapping can demonstrate the tendon snapping over the greater trochanter, either when standing or lying on their side with the affected leg abducted. The snap can be felt during active flexion of the hip or passive internal and external rotation of the abducted leg. For the internal type, the snapping can be demonstrated with the patient supine and by moving the hip from a position of flexion or flexion with abduction, to extension or extension with adduction.13 The only investigation worth doing for external type snapping is dynamic ultrasound, where the ITB can be visualized snapping over the greater trochanter. For internal type snapping, dynamic and static ultrasound demonstrate the abnormal movement of the iliopsoas tendon, a thick iliopsoas muscle, an enlarged bursa as well as peritendinous fluid collections. Bursography and tendonography have also been described for detecting internal snapping.13 The only role for CT is to compare the iliopectineal eminences on each side.13 Plain radiographs and MRI are useful in the diagnosis of intra-articular type snapping by demonstrating any loose bodies, synovial chondromatosis, acetabular labral tears or osteochondral fractures. Treatment is only required for painful snapping and usually non-operative management is successful. Non-operative modalities include rest, avoidance of movements that produce the snap, NSAIDs, steroid injection and physiotherapy. Physiotherapy involves stretching of the ITB for external type and for the internal type, hip flexor stretching and strengthening, pelvic and peripelvic mobilization and alignment exercises. In the rare case where non-operative management is unsuccessful, surgical options are available. Z-plasty of the ITB, for external type snapping has good results. For the internal type, release or lengthening the iliopsoas muscle is worthwhile. Intra-articular type snapping may require the removal of large loose bodies or excision of synovial chondromatosis.14 Arthroscopy is used for the debridement of acetabular labral tears and removal of small loose bodies. More recently arthroscopy has also been shown to be successful in the treatment of internal and external types of snapping, where iliopsoas tenotomy, release of the tensor fascia lata and trochanteric bursectomy can be performed.
beneath the musculotendinous part of the iliopsoas. Bursitis can be caused by a variety of sporting activities as a result of excess activity but can also be caused by trauma, rheumatoid arthritis or total hip arthroplasty.15 Trauma to the bursa may be a result of sudden hyperextension of the hip from a flexed position, which stretches the iliopsoas muscle and bursa.15 Pain may also be the result of an inflamed iliopsoas tendon snapping over the femoral head and anterior capsule.15 Iliopsoas bursitis usually affects younger adults of average age 25 years.15 There may be a history of trauma or prior orthopaedic surgery but usually the onset of pain follows some form of athletic activity. Patients complain of anterior hip pain, which can radiate into the thigh. The pain is aggravated by activity and relieved with rest. Palpable inguinal masses with compression of neighbouring structures and lower leg oedema have been reported.15 There may be little to find on examination. Possible positive findings include a positive Thomas test, weak resisted external rotation with the hip in flexion, and a snapping hip sign. Tenderness may be elicited on deep palpation in the femoral triangle with the patient supine or palpating the lesser trochanter with the patient prone. Abnormalities on plain radiographs are non-specific.16 Iliopsoas bursography involves injecting contrast into the bursa and this can confirm the presence of bursitis. Iliopsoas bursitis can also be demonstrated using ultrasound (U/S), computed tomography (CT) or MRI, which provides the most accurate data.16 However, US is the quickest, simplest and most costefficient method and allows for dynamic assessment.16 Non-operative management should be initiated on diagnosis and includes a period of rest, NSAIDs and physiotherapy. An exercise program of hip rotation and extension exercises and stretching is effective. Stretching exercises of hip flexors, glutei, quadriceps and hamstring are also recommended.15 Injection of local anaesthetic and steroids into the bursa under ultrasound guidance can provide short-term pain relief.15 If non-operative management fails, surgical options include release or lengthening of the iliopsoas tendon. However, complications have been reported, which include subjective weakness of hip flexion, haematoma formation and loss of sensation in the distribution of the lateral cutaneous nerve of the thigh.15
Piriformis syndrome Piriformis syndrome (PS) is a rare condition causing posterior hip and buttock pain that may radiate to the thigh. The diagnosis is difficult and usually one of exclusion. The piriformis muscle was recognized as a potential source of sciatic type pain in 1928.17 The piriformis syndrome was described as periarthritis involving the anterior sacroiliac ligament, piriformis muscle and adjacent branches of the sciatic nerve. The piriformis muscle originates from the pelvic surface of the sacrum, exits through the greater sciatic notch and inserts onto the apex of the greater trochanter of the femur. It functions as an external rotator of the hip when the hip is extended and as a hip abductor when the hip is flexed at 90 . In the majority of cases the sciatic nerve runs distal to the piriformis muscle. However, there are variations involving a split or single sciatic nerve passing proximal, through or distal to a split or single piriformis muscle.17 PS is more common in females and is believed to result from an haematoma following trauma, the commonest mechanism
Iliopsoas bursitis The psoas muscle arises from the lumbar vertebrae and the origin of iliacus is the internal wall of the iliac wing. Both insert into the anteromedial aspect of the lesser trochanter of the femur. They function as a hip flexor and external rotator of the femur. The iliopsoas bursa is the largest synovial bursa in humans and lies
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lower limb biomechanics.19 True bursitis, which may be due to repeated microtrauma, acute injury, overuse or regional muscle dysfunction is commonly misdiagnosed as magnetic resonance imaging demonstrates bursitis in only 8% of cases.19 GTPS is characterized by a continuous greater trochanteric or gluteal pain exacerbated by prolonged standing, lying on the affected side, sitting with the affected leg crossed and high impact activities. Pain may mimic lumbar radiculopathy with patients describing pain along the lateral aspect of the thigh to the knee, and sometimes below the knee. On examination there is point tenderness in the posterolateral area of the greater trochanter. Apart from this there are no specific signs. Ege et al described the two main criteria as lateral hip pain and tenderness over the greater trochanter, both of which have to be present. They added three minor criteria, one of which had to be present.20 A positive Trendelenburg’s test is the most accurate, with a sensitivity of 73% and a specificity of 77%.19 Non-operative intervention is successful in the majority of cases. Such measures include NSAIDs, weight loss and physiotherapy to improve flexibility and muscle strength. Patients who do not respond should have a steroid and local anaesthetic injection into the region of pain and may be repeated for recurrence. This has been shown relieve pain in 60e100% of cases.19 If symptoms persist after injection an alternate source for the pain should be considered. Where non-operative intervention fails surgery may be considered, particularly for a true trochanteric bursitis where a bursectomy and/or iliotibial band release may be performed.
being compression or scarring of the sciatic nerve following a simple fall onto the buttocks. Patients present with pain in the buttock, in the posterior hip or lower back. This pain may radiate into the thigh or lower leg, and there is an intolerance to sitting on the affected side.17 The pain can be aggravated by activity or standing and is often relieved on lying down. There may be associated numbness or paraesthesia radiating distally in the distribution of the sciatic nerve. Three signs have been described on physical examination. Lasegue’s sign, which is pain over the greater sciatic notch on palpation and when the hip is flexed to 90 with the knee extended, Freiberg’s sign, which is pain on passive internal rotation of the hip, and Pace’s sign, where pain and weakness are elicited on resisted abduction and external rotation of the thigh. The most consistent findings on physical examination are tenderness on palpation of the greater sciatic notch and pain with maximum flexion, adduction and internal rotation.17 Plain radiographs will not assist in the diagnosis of PS. Electromyograms (EMGs) may reveal abnormalities in the tibial and peroneal divisions of the sciatic nerve. CT and MRI can help differentiate PS from other possible causes of sciatica and can be used to directly determine the diagnosis of PS by revealing an enlarged piriformis muscle. The non-operative management of PS involves the use of NSAIDs to reduce prostaglandin-mediated inflammation, pain and spasms. Abnormal biomechanics caused by pelvic obliquities, leg length discrepancies and posture need to be corrected. Physiotherapy treatments include cryotherapy, ultrasound, stretching and strengthening exercises and heating modalities. If non-invasive measures fail, local anaesthetic and corticosteroid injections can be tried. Despite the use of bony landmarks and contrast, most of the fluoroscopically attempted piriformis injections are placed superficially within the gluteus maximus and so ultrasound should be considered to ensure correct needle placement. Failure of conservative measures may require open or arthroscopic surgical release of the piriformis muscle/tendon. Sciatic neurolysis has had encouraging results, although in order to avoid recurrence, it is suggested that polytetrafluoroethylene pledgets be placed around the sciatic nerve to avoid compression and entrapment by scar tissue.17,18 It is important to differentiate between a myofascial pain syndrome of the piriformis muscle causing posterior hip pain and piriformis syndrome with concomitant sciatic type pain.
Myofascial pain Myofascial pain is a major cause of musculoskeletal pain. It is described as a pain that arises from trigger points which are focal, tender areas within a taut band of skeletal muscle that may produce pain, vasoconstriction or vasodilation in a distant region either by local pressure or spontaneously.21,22 This is known as the trigger point phenomena.21 Multiple precipitating factors have been suggested, which include trauma, poor posture, degeneration, nerve root compression, endocrine, metabolic and nutritional deficiencies, chronic infection emotional psychological stress, and sleep disturbance.22 Myofascial pain is a great mimicker and in the lower limb can present as pain in the hip or knee. It needs to be considered once more serious pathologies such as infection, fractures, malignancy and neurological injuries have been excluded. Myofascial pain from the iliopsoas, piriformis, tensor fascia lata, pectineus, quadriceps and sartorius can be referred to the groin or thigh.22 Patients who have myofascial pain may have asymmetry of their posture and gait due to muscular pain and tightness. However, the main finding on examination is tenderness on palpation of the specific muscle. A local twitch response can be elicited by snapping palpation or needling of the trigger point.22 Radiological investigations are useful only to exclude other causes of pain. Myofascial pain itself will not show up on any investigation. Ultrasound guided specific muscle injections of small amounts of local anaesthetic are helpful in diagnosis. The treatment of myofascial pain is mainly simple analgesia such as paracetamol, NSAIDs or narcotic analgesia, depending on the severity of pain. Physiotherapy modalities include massage, ultrasonography, acupuncture, transcutaneous electric
Greater trochanteric pain syndrome The trochanteric bursae which overlie the lateral aspect of the greater trochanter are commonly implicated as a cause of lateral hip pain. This condition was originally described by Stegemann in 1923. However, the term “greater trochanteric pain syndrome” (GTPS) is the contemporary term to cover pain and tenderness in the greater trochanteric, gluteal or lateral thigh regions. There is a broad spectrum of causes, including tendinopathies, gluteal muscle tears and iliotibial band disorders. GTPS describes a chronic, intermittent pain and tenderness overlying the greater trochanteric region. It is probably best described as a regional pain syndrome that often mimics pain generated from other sources such as the spine or hip joint.19 There is an increased frequency of association with age, female gender, knee OA, obesity, low back pain and altered
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nerve stimulation and application of ice and or heat. If non-invasive treatment fails then trigger point injections can be used. Options include dry needling or the use of local anaesthetics, corticosteroid or botulinum toxin.
pregnancy. Presenting complaints are pain or discomfort in the inguinal and suprapubic region. Hyper- or hypoaesthesia may also be present. Diagnosis is difficult due to the small area of sensory supply and the overlap between it and the ilioinguinal and genitofemoral nerves. Infiltration of local anaesthetic can be diagnostic.
Osteitis pubis Ilioinguinal nerve The ilioinguinal nerve originates from the T12 and L1 nerve roots. The pubic symphysis and the superomedial aspect of the femoral triangle receive a sensory supply from this nerve. The ilioinguinal nerve can be injured during surgical approaches to the lower abdomen, during pregnancy and bone graft harvesting from the iliac region. Entrapment of the nerve can occur at the point where it passes through the transversus abdominis and internal oblique muscles medial to the anterosuperior iliac spine (ASIS). Nerve injury can also occur with tearing of the lower external oblique aponeurosis, an injury described in hockey players. The diagnosis of this condition is made clinically. Neuropathy of the ilioinguinal nerve has three characteristics; pain, altered sensation and the presence of a trigger point.26 Pain occurs in the iliac fossa and radiates to the groin, scrotum or labia majora, the proximal medial aspect of the thigh and the back.26 Altered sensation may be hyper-, hyo- or dysaesthesia and a trigger point is present medial and distal to the ASIS.26 The patient walks with a flexed trunk gait. Provocative testing involves hip extension. In addition palpation of the inguinal canal or medial to the ASIS may reproduce these symptoms. As with the iliohypogastric nerve, local aesthetic injection can aid diagnosis as it is difficult to differentiate the pain caused by the iliohypogastric, ilioinguinal and genitofemoral nerves due to the overlap of sensory innervation.
The pubic symphysis is a fibrocartilaginous joint. Osteitis pubis is a painful inflammatory condition of the pubic symphysis, which can be difficult to diagnose. It was first described in 1924 following suprapubic surgery. It most commonly occurs in 30e40 years old men who participate in football, basketball or long distance running.23 It is mainly caused by impaction trauma but may also be a result of primary inflammation, childbirth or secondary to infection.23 A sudden increase in the frequency, intensity or duration of training, limited range of motion of the hip, or weakness of the hip abductors or adductors, can result in osteitis pubis. The diagnosis is confirmed radiologically where on a plain AP X-ray of the pelvis, findings include bilateral subchondral irregularity, bone erosions and cysts. An isotope bone scan will show a localized increased uptake of the isotope and an MRI scan will demonstrate bone marrow oedema.23 Treatment options include physiotherapy for core stabilization, stretching and strengthening exercises of abdominal, hip adductor and abductor muscles, steroid and local anaesthetic or surgery. Operative procedures include wedge resection of the symphysis pubis, curettage or symphysiodesis.
Sacroiliac joint pain The sacroiliac joint (SIJ) is a synovial joint. The prevalence of sacroiliac joint pain in patients presenting with lower back pain ranges from 15% to 25%.24 SIJ pain can result from either intra-articular causes, for example arthritis or infection, or extraarticular causes, including enthesopathy, ligamentous injury, fractures or myofascial pain.24 SIJ pain cannot be diagnosed from history or physical examination alone, and X-ray and MRI are necessary. Initial treatment should involve non-invasive measures such as anti-inflammatory medications and physiotherapy, focussing on exercises to improve lumbopelvic stability. Invasive treatment, which involves injection of the SIJ, can also be used in the diagnosis of SIJ pain. Blind injections are unreliable and not recommended. Radiologically guided SIJ injections can provide pain relief for up to 1 year.24 These injections are performed under fluoroscopy or CT or MRI guidance or more recently, realtime, high-resolution ultrasound guidance.25
Genitofemoral nerve This nerve takes origin at the L1 and L2 level. At the inguinal ligament it forms two main branches, the genital and femoral branches. The femoral branch is of primary interest. It travels lateral to the femoral artery and gives sensory innervation to the femoral triangle, lateral to that described for the ilioinguinal nerve. As with the ilioinguinal nerve, injury is most commonly caused by surgical trauma. However, other causes reported include direct trauma to the inguinal region and tight clothing. The main presenting complaint is pain and a burning sensation in the groin, which radiates to the inner thigh. Aggravating factors including walking, stooping and hyperextension of the hip.27 Examination findings reveal tenderness and possible hyperaesthesia along the inguinal canal. Provocative testing involves internal or external rotation of the hip joint.
Nerve entrapment syndromes round the hip
Lateral cutaneous nerve of the thigh The lateral cutaneous nerve of the thigh (LCNT) can have one of three origins; L1 and L2, L2 and L3 or L3 alone.28 The LCNT divides into its anterior and posterior branches just distal to the inguinal ligament and supplies the anterolateral aspect of the thigh.28 Entrapment of the LCNT is named meralgia paraesthetica or Roth’s meralgia. It is known complication of several orthopaedic procedures. However, there are many non-surgical causes including seat belts, tight trousers, obesity, pregnancy, intraabdominal pathology, diabetes mellitus, alcoholism, lead poisoning or it can occur spontaneously.28
Entrapment of iliohypogastric, ilioinguinal, genitofemoral, lateral cutaneous nerve of the thigh and the obturator nerves can mimic hip pain. Iliohypogastric nerve The iliohypogastric nerve originates from the L1 nerve root with some contributing fibres from T12. The nerve divides into anterior and lateral cutaneous branches, supplying an area of skin in the upper buttock, groin and symphysis pubis. It is most commonly injured during surgical procedures by direct trauma or scar formation can be injured following a muscle tear or during
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HIP
The presenting complaints include pain, which may be worse on hip extension, paraesthesia and a reduced sensation to touch and temperature in the anterolateral aspect of the thigh. Examination findings include tenderness on palpation, reduced sensation and possibly a positive Tinel’s sign.28 Similar to the other nerve entrapments injection of local anaesthetic can be diagnostic.
6 7 8
Obturator nerve The obturator nerve takes its origins from L2, L3, and L4. It divides into an anterior and a posterior branch anterior to the internal obturator muscle. It gives a motor supply to the gracilis, adductor brevis and longus. The anterior nerve joins the femoral and saphenous nerves to form a sensory cutaneous plexus. Patient positioning during total hip replacement may result in nerve entrapment in the obturator canal.28 Other causes include childbirth, pelvic trauma, osteitis pubis and exercise. The main presenting complaints include hypoaesthesia, paraesthesia or pain in the medial thigh, groin or pubic bone.28 The patient may also complain of weakness and a feeling of leg instability. Examination findings may reveal a circumducting gait secondary to an externally rotated hip, weakness or wasting of the adductor muscles and a decrease in hip adduction and internal rotation of the hip.29 Nerve entrapment syndromes around the hip should be considered at the initial consultation but also where a cause for hip pain remains elusive. Treatment consists of activity modification to avoid the exacerbating movement. In the case of meralgia paraesthetica, symptoms can resolve spontaneously. The use of antiseizure medication such as gabapentin may also be useful.30 Injection at the point of entrapment with a local anaesthetic and steroid can be both diagnostic and therapeutic. Ultrasound guided injection is useful in the diagnosis of nerve entrapment. In cases where injections fail to relieve symptoms, or where symptoms recur, then surgical exploration for excision of scar tissue, neurolysis or excision of damaged nerve can be considered.
9 10
11 12 13 14
15 16
17
18 19 20
Conclusion 21
Hip pain can take origin from a myriad of pathological processes and can often be from more than one source. History and physical examination remains the cornerstone in determining the aetiology of the pain. However, if pain persists after treatment an alternate or co-existing pathology should be considered. A
22 23
24 REFERENCES 1 Dagenais S, Garbedian S, Wai EK. Systematic review of the prevalence of radiographic primary hip osteoarthritis. Clin Orthop Relat Res 2009; 467: 623e37. 2 Loughlin J. The genetic epidemiology of human primary osteoarthritis: current status. Expert Rev Mol Med 2005; 7: 1e12. 3 Hawker GA, Stewart L, French MR, et al. Understanding the pain experience in hip and knee osteoarthritisean OARSI/OMERACT initiative. Osteoarthritis Cartilage 2008; 16: 415e22. 4 Altman R, Alarcon G, Appelrouth D, et al. The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hip. Arthritis Rheum 1991; 34: 505e14. 5 Zhang W, Moskowitz RW, Nuki G, et al. OARSI recommendations for the management of hip and knee osteoarthritis, Part II: OARSI
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evidence-based, expert consensus guidelines. Osteoarthritis Cartilage 2008; 16: 137e62. Eberhardt K, Fex E, Johnsson K, Geborek P. Hip involvement in early rheumatoid arthritis. Ann Rheum Dis 1995; 54: 45e8. Ranawat CS, Dorr LD, Inglis AE. Total hip arthroplasty in protrusio acetabuli of rheumatoid arthritis. J Bone Joint Surg Am 1980; 62: 1059e65. Collins DN, Barnes CL, FitzRandolph RL. Cervical spine instability in rheumatoid patients having total hip or knee arthroplasty. Clin Orthop Relat Res 1991; 272: 127e35. Crawford JR, Villar RN. Current concepts in the management of femoroacetabular impingement. J Bone Joint Surg Br 2005; 87: 1459e62. Allen D, Beaule PE, Ramadan O, Doucette S. Prevalence of associated deformities and hip pain in patients with cam-type femoroacetabular impingement. J Bone Joint Surg Br 2009; 91: 589e94. Groh MM, Herrera J. A comprehensive review of hip labral tears. Curr Rev Musculoskelet Med 2009; 2: 105e17. Beaule PE, O’Neill M, Rakhra K. Acetabular labral tears. J Bone Joint Surg Am 2009; 91: 701e10. Allen WC, Cope R. Coxa saltans: the snapping hip revisited. J Am Acad Orthop Surg 1995; 3: 303e8. Provencher MT, Hofmeister EP, Muldoon MP. The surgical treatment of external coxa saltans (the snapping hip) by Z-plasty of the iliotibial band. Am J Sports Med 2004; 32: 470e6. Johnston CA, Wiley JP, Lindsay DM, Wiseman DA. Iliopsoas bursitis and tendinitis. A review. Sports Med 1998; 25: 271e83. Wunderbaldinger P, Bremer C, Schellenberger E, Cejna M, Turetschek K, Kainberger F. Imaging features of iliopsoas bursitis. Eur Radiol 2002; 12: 409e15. Benson ER, Schutzer SF. Posttraumatic piriformis syndrome: diagnosis and results of operative treatment. J Bone Joint Surg Am 1999; 81: 941e9. Kobbe P, Zelle BA, Gruen GS. Case report: recurrent piriformis syndrome after surgical release. Clin Orthop Relat Res 2008; 466: 1745e8. Williams BS, Cohen SP. Greater trochanteric pain syndrome: a review of anatomy, diagnosis and treatment. Anesth Analg 2009; 108: 1662e70. Ege Rasmussen KJ, Fano N. Trochanteric bursitis. Treatment by corticosteroid injection. Scand J Rheumatol 1985; 14: 417e20. Travel JG, Simons DG. Myofascial pain and dysfunction: the trigger point manual, vols. 1 and 2. Baltimore: Williams & Wilkins, 1999. Yap EC. Myofascial pain e an overview. Ann Acad Med Singapore 2007; 36: 43e8. Haider NR, Syed RA, Dermady D. Osteitis pubis: an important pain generator in women with lower pelvic or abdominal pain: a case report and literature review. Pain Physician 2005; 8: 145e7. Cohen SP. Sacroiliac joint pain: a comprehensive review of anatomy, diagnosis, and treatment. Anesth Analg 2005; 101: 1440e53. Harmon D, O’Sullivan M. Ultrasound-guided sacroiliac joint injection technique. Pain Physician 2008; 11: 543e7. Knockaert DC, D’Heygere FG, Bobbaers HJ. Ilioinguinal nerve entrapment: a little-known cause of iliac fossa pain. Postgrad Med J 1989; 65: 632e5. Starling JR, Harms BA. Diagnosis and treatment of genitofemoral and ilioinguinal neuralgia. World J Surg 1989; 13: 586e91. Grossman MG, Ducey SA, Nadler SS, Levy AS. Meralgia paresthetica: diagnosis and treatment. J Am Acad Orthop Surg 2001; 9: 336e44. Tipton JS. Obturator neuropathy. Curr Rev Musculoskelet Med 2008; 1: 234e7. Benito-Leon J, Picardo A, Garrido A, Cuberes R. Gabapentin therapy for genitofemoral and ilioinguinal neuralgia. J Neurol 2001; 248: 907e8.
Ó 2011 Elsevier Ltd. All rights reserved.
CME SECTION
CME questions based on the Mini-Symposium on “Asia Pacific” C Mycobacteria do not form biofilms D Staged correction of severe kyphotic deformity with halopelvic distraction has a 10% mortality E The use of metallic implants in actively infected bone is safe with concurrent antituberculous chemotherapy
The following series of questions are based on the MiniSymposium on ‘‘Asia Pacific”. Please read the articles in the Mini-Symposium carefully and then complete the selfassessment questionnaire by filling in the square corresponding to your response to each multiple-choice question. After completing the questionnaire, either post or fax the answer page to the Orthopaedics and Trauma Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Orthopaedics and Trauma. Replies received before the next issue of the journal is published will be marked and those reaching an adequate standard will qualify for three external CME points. You will be notified of your marks and a CME certificate will be despatched, via email, for your records.
5 In what period after nerve injury does Wallerian degeneration occur? A Within the first 6 hours B From immediately after injury until 6 months later C From 2 to 7 days after injury D From 1 month to 1 year after injury E Beyond 6 months after injury 6 What characteristic of first degree nerve injuries fundamentally differs from second, third and fourth degree injuries? A Only the epineurium remains intact B Schwann cells remain intact at the site of injury C The endoneural sheath remains intact D The perineurium remains intact E Wallerian degeneration does not occur
Questions 1 What component of the cell wall renders the bacteria responsible for tuberculosis acid fast? A Casein B Keratan sulphate C Mycolic acid D Polylactose E Tuberculin
7 Which of the following tissues is a source of mesenchymal stem cells that are equivalent in pluripotency and in proliferative efficiency to bone marrow? A Adipose tissue B Cartilage C Muscle D Periosteum E Tendon
2 Approximately what proportion of the cross sectional area of the spinal canal can be occupied by tuberculous material before neurological compromise begins to occur? A 33% B 50% C 60% D 75% E 90%
8 Below what anteroposterior dimension in the adult is the spinal canal deemed to be congenitally stenotic A 10 mm B 13 mm C 15 mm D 18 mm E 20 mm
3 In the treatment of spinal tuberculosis, what is the only advantage of radical debridement and strut grafting over drug treatment alone or simple debridement? A The ‘cure’ rate is higher B There is a lower rate of relapse after 10 years C There is a lower risk of chronic sinus formation D There is a lower risk of late kyphosis developing E There is a lower risk of the late development of paraplegia
9 Which of the following regions has the most tenuous blood supply to the spinal cord? A C1e2 B C3e4 C C5e7 D C8eT1 E T2e5
4 Which of the following statements concerning the surgical treatment of spinal tuberculosis is not true? A Cord monitoring is not useful in the treatment of kyphotic deformity B Mycobacteria do not adhere to implants
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CME SECTION
Responses
10 Which category of cervical spondylotic myelopathy is associated with the longest duration of symptoms? A Brown Sequard B Brachalgia cord C Central D Motor system E Transverse lesion
Please shade in the square for the correct answer. B C D E 1A 2A B C D E 3A B C D E 4A B C D E 5A B C D E 6A B C D E 7A B C D E 8A B C D E 9A B C D E 10 A B C D E 11 A B C D E 12 A B C D E
11 What marks the lateral limit for decompression of the cervical cord during anterior corpectomy and fusion? A Foramen transversarium B Lateral margin of posterior longitudinal ligament C Medial border of pedicle D Midpoint of the foramen below the pedicle E Uncovertebral joint
Your details (Print clearly)
12 What proportion of the facet joint can be removed during laminectomy before instability begins to develop? A 5% B 10% C 25% D 33% E 50%
NAME ............................................................................ ADDRESS ............................................. ........ ............................................. EMAIL ................................................. ........ RETURN THE COMPLETED RESPONSE FORM by fax to 113-392-3290, or by post to CME, Orthopaedics and Trauma, Academic Department of Orthopaedic Surgery, “A” Floor Clarendon Wing, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK.
Please fill in your answers to the CME questionnaire above in the response section provided to the right. A return address and fax number is given below the response section.
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CME SECTION
Answers to CME questions based on the Mini-Symposium on “The Shoulder” Please find below the answers to the Orthopaedics and Trauma CME questions from Vol. 25, issue 1 which were based on the Mini-Symposium on “The Shoulder”
Answers 1a
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2a
b
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3a
b
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4a
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BOOK REVIEWS
The lectures/demonstrations cover a large proportion of the issues that can be encountered in knee replacement surgery, focussing on how best to achieve equal tension/gaps in flexion and extension, how to avoid undue laxity and how best to deal with laxity when it does arise. Techniques shown include demonstration of the stepwise effects of sequential release of the medial or lateral structures, ways of releasing a tight PCL and when to consider a PCL substituting or additionally stabilized prosthesis. The DVD also demonstrates the use of computer navigation in knee arthroplasty. This DVD is very well made and is very clear to follow, and shows the various described techniques in a very easy to follow way. The clarity of the cadaveric and intra-operative views makes this DVD as useful, if not even more useful, than actually being there in theatre with some of the US’s most experienced and respected arthroplasty surgeons. This DVD should be mandatory viewing for all orthopaedic trainees considering a career that might include performing knee arthroplasties, and should be an extremely interesting and valuable educational tool even for experienced arthroplasty surgeons. This is yet another excellent DVD from the AAOS series that can be highly recommended. A
Arthroscopic surgical techniques: anterior cruciate ligament reconstruction Edited by Freddie Fu and Stephen Howell, Publisher: AAOS 2010; Resident price: $209; AAOS member $229, ISBN: 9780892036400
This two-DVD set was one of the very best CPD ‘experiences’ I’ve had to-date! The video presentations give an amazingly clear view as to how some of the US’s top knee surgeons perform ACL reconstruction surgery. The topics covered include the use of the most common graft types (patellar tendon and hamstring) as well as a number of grafts that are likely to be less familiar to most UK surgeons, such as Achilles tendon allografts and quadriceps tendon grafts. Furthermore, a variety of different fixation methods are shown in detail. Also included are very clear descriptions of double bundle techniques, revision techniques plus numerous invaluable pieces of advice. The discs are nicely compartmentalized into distinct separate presentations/videos, making the overall content (14 video presentations in all) very easy to view piecemeal (as and when one has the time), without ‘losing the thread’ of the topics. Watching the videos in combination with the very clear audio commentaries and the additional slides and explanatory images is actually as good if not better than being there in theatre, physically, directly watching ‘the masters’ at work (and is certainly a lot less hassle). Inevitably, there were some techniques that I did not necessarily entirely agree with and that I would not personally be adopting in my own practice. However, there were definite points of interest in each of the 14 presentations and some genuinely invaluable bits of golden advice. The highlight of both discs for me was the compelling description of how the ACL femoral tunnel position viewed from the lateral portal actually gives a false impression of the true angle of the graft (potentially giving a too vertical graft even when attempting to hit the 2 o’clock/10 o’clock position), and the advice was therefore to view the medial wall of the lateral femoral condyle via the notch but actually from the medial portal, with the femoral drill bit being passed from an accessory medial (further medial) portal. This two-DVD set from the AAOS is an absolute must-see for any knee surgeon performing ACL reconstruction surgery. A
Ian D McDermott
Ian McDermott
31 Old Broad Street, London EC2N 1HT, UK.
Joint Replacement Arthroplasty – Basic Science, Elbow and Shoulder. Fourth Centennial Edition Edited by Bernard Morrey, John Sperling and Kai-Nan An, Publisher: Lippincott Williams & Wilkins 2010; Price £146, 376 pages, ISBN: 9781608314676
The publication of the fourth edition of this textbook coincides with the 100th year anniversary of the Orthopaedic Department at the Mayo Clinic. It is the first of two volumes with the second volume concerning hip, knee and ankle arthroplasty due for publication in 2011. Although online access to the full text and image bank is included via an access code printed on the inside of the front cover, it was not yet operational at the time of this review. Nevertheless, this promises to be a valuable resource when it is up and running. The volume itself is divided into three main sections concerning the basic science behind joint replacement arthroplasty, elbow arthroplasty and shoulder arthroplasty. The basic science section is only available online and is not contained in the print version of this first volume, apart from its table of contents, and so has not been reviewed here. However, it appears to cover all the topics that a surgeon undertaking joint arthroplasty needs to be familiar with, including chapters on bone cement, bearing surfaces, dealing with patient co-morbidities and outcome measurement. The section concerning elbow arthroplasty starts with a chapter outlining the history of arthroplasty, followed by ones describing the anatomy, surgical approaches, biomechanics and prosthesis design. This provides a comprehensive overview of elbow arthroplasty, including discussion of why various designs have failed in the past and the relative merits of linked and unlinked
MB BS MS FRCS(Orth) FFSEM(UK)
Consultant Orthopaedic Surgeon and Honorary Professor Associate, Brunel University, UK and London Sports Orthopaedics, 31 Old Broad Street, London EC2N 1HT, UK.
The AAOS/AAHS surgical techniques in orthopaedics DVD “Ligament Balancing for Total Knee Arthroplasty” Edited by James B Stiehl and David C Ayers, Published: AAOS 2010; Price: AAOS member $149; Resident $129, ISBN: 9780892034604
This DVD is a series of cadaveric and intra-operative lectures/ demonstrations that predominantly covers the subject of ligament balancing in total knee replacements.
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MBBS MS FRCS(Orth) FFSEM(UK)
Consultant Orthopaedic Surgeon, London Sports Orthopaedics,
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BOOK REVIEWS
prostheses. The following chapters deal individually with arthroplasty in specific indications, for example in rheumatoid arthritis, fractures and non-unions. Elbow hemiarthroplasty, radial head and capitellar replacement are also covered. These chapters explain the rationale for performing the arthroplasty in any given situation, provide technical tips and expert advice to improve surgical technique and review the available results. Each chapter stands alone and is ideal for use as a quick reference by a surgeon looking for help in a specific case. Potential complications are then reviewed in depth, together with strategies on how to deal with them successfully. Finally, revision surgery and reconstructive procedures for when prosthetic elbow arthroplasty is not possible or contra-indicated are described. The section on shoulder arthroplasty follows a broadly similar structure, starting with the history, surgical approaches and biomechanics etc., followed by chapters describing arthroplasty in specific indications. Thus shoulder hemiarthroplasty, resurfacing, total, reverse and revision shoulder arthroplasty are all described, together with the treatment of rheumatoid arthritis, fractures, cuff tear arthropathy, fractures and complications. All the chapters are written in a clear and logical format, well supported by tables, figures and illustrations to explain specific points. Although the text draws heavily from the Mayo arthroplasty experience, controversial topics and alternative philosophies are appropriately acknowledged. The elbow arthroplasty section is more globally comprehensive in its coverage than the shoulder section, perhaps as would be expected from a book whose Editor-in-
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Chief is the internationally acclaimed elbow expert, Bernard Morrey. The only disappointments are the black and white line drawings in both of the anatomy and surgical approaches sections, which have been reproduced from older publications and do not appear as sharp as the beautiful colour illustrations and photographs in the rest of the text. The chapter on elbow interposition arthroplasty is also somewhat brief and surgeons contemplating the procedure may wish for greater explanation of the surgical technique. Overall, this is an excellent textbook that will appeal to all who practice shoulder and elbow arthroplasty or are looking to develop such an interest. Even experienced surgeons will find the chapters discussing revision surgery or newer techniques such as capitellar replacement of great benefit. The basic science section and the first few chapters of the shoulder and elbow sections would also be of interest to trainees wishing to further their understanding of the subject. Joint Replacement Arthroplasty e Basic Science, Elbow and Shoulder serves both as a ready reference tool when confronted by a specific case and also as a background reading text and the editors and authors are to be congratulated on their achievement.A
Adam Rumian
MD FRCS(Tr & Orth)
Consultant in Trauma and Orthopaedics, Lister Hospital, East and North Hertfordshire NHS Trust, Coreys Mill Lane, Stevenage, Herts SG1 4AB, UK.
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