Ankylosing Spondylitis in an Athlete With Chronic Sacroiliac Joint Pain

Ankylosing Spondylitis in an Athlete With Chronic Sacroiliac Joint Pain

Timothy L. Miller, MD; Nathan Cass, BS, MS; Courtney Siegel

Abstract

Ankylosing spondylitis is a disease in which inflammation of joints, most often in the axial skeleton, can lead to reactive fibrosis and eventual joint fusion with associated immobility and kyphosis. The disease often involves extra-articular features, such as uveitis and aortic regurgitation, as well as associated inflammatory conditions of the intestines. Its etiology is unknown. Ankylosing spondylitis most commonly presents in young males (15–30 years old) as persistent low back pain and stiffness that is worse in the morning and at night and improves with activity. The authors report the case of a young male athlete whose symptoms were initially incorrectly diagnosed as sacroiliac joint instability and dysfunction and later as a sacroiliac stress fracture before further workup revealed a seronegative spondyloarthropathy and the diagnosis of ankylosing spondylitis. The patient was prescribed oral indomethacin daily by the attending rheumatologist and started on a slow progression of return to running, jumping, and weight lifting. Within 4 weeks of beginning this treatment, the patient had complete cessation of pain with the medication. At follow-up 1 year after graduation from his university, the patient was nearly symptom free and working in a non-heavy labor job. The purpose of this case report is to remind sports medicine physicians of the prevalence of rheumatologic diseases in general and ankylosing spondylitis in particular and of the various ways in which spondyloarthropathies may present in athletes. Increased suspicion may lead to earlier diagnosis and treatment, potentially reducing illness severity and duration and improving the performance of athletes with this condition.


The authors are from the Sports Medicine Center, The Ohio State University, Columbus, Ohio.

The authors have no relevant financial relationships to disclose.

Correspondence should be addressed to: Timothy L. Miller, MD, Care Point Gahanna, 920 N Hamilton Rd, Gahanna, OH 43230 ( timothy.miller@osumc.edu).
Received: June 21, 2013
Accepted: October 09, 2013
Posted Online: February 07, 2014


Ankylosing spondylitis is a disease in which inflammation of joints, most often in the axial skeleton, can lead to reactive fibrosis and eventual joint fusion with associated immobility and kyphosis. Other musculoskeletal complications include spinal fractures, cauda equina syndrome, dactylitis, and peripheral asymmetric oligoarticular arthritis. The disease often involves extra-articular features, such as uveitis and aortic regurgitation, as well as associated inflammatory conditions of the intestines.1 The etiology is unknown but postulated to be of autoimmune origin, having a strong association with the B27 histocompatibility complex (HLA-B27).2

Ankylosing spondylitis most commonly presents in young males (15–30 years old) as persistent low back pain and stiffness that is worse in the morning and at night and improves with activity. This report describes a young male athlete whose symptoms were initially incorrectly diagnosed as sacroiliac joint instability and dysfunction and later as a sacroiliac stress fracture before further workup revealed a seronegative spondyloarthropathy and the diagnosis of ankylosing spondylitis.

Case Report

A 21-year-old male track and field long-jump athlete presented with the chief complaint of right hamstring tightness and sacroiliac pain of 1-week duration. The sharp pain was rated as 2 to 3 out of 10 (numeric pain scale: 0=no pain, 5=moderate pain, 10=worst pain imaginable) and occurred while running and jumping, but not while walking. There was no known mechanism of injury. The patient reported no weakness or numbness.

The patient had no history of previous spinal, pelvic, or hip trauma, although he had previously been diagnosed with ulcerative colitis. Surgical history included emergency subtotal colectomy at age 18 for intractable bleeding (subsequently diagnosed as ulcerative colitis), followed by mucosal proctectomy with ileal J-pouch anal anastamosis and loop ileostomy, an exploratory laparotomy and lysis of adhesions for small bowel obstruction, and later an ileostomy reversal.

On presentation, physical examination revealed tenderness to palpation along the right sacroiliac joint line. Hamstring and gluteal strength, as well as range of motion of the hip and back, were normal. The hamstring muscles were noted to have high tension bilaterally, which was normal for this athlete. The sacroiliac rotation stress test, long-sit test, and sacroiliac compression, distraction, and squish tests yielded negative results. The flexion, abduction, and external rotation test yielded positive results for pain.

A tentative diagnosis of sacroiliac joint instability and dysfunction was given. Therapy consisting of rest, scheduled anti-inflammatory medications, electrical muscle stimulation, osteopathic manipulative treatment, and physical therapy yielded no immediate improvement in symptoms. During 3 to 5 weeks, using regular physical therapy, prepractice heating and stretching, and postpractice icing and electrical muscle stimulation, the patient’s symptoms improved and he returned to full training and competition. However, on cessation of physical therapy, his symptoms returned. He continued to practice his exercises during the 6 months following initial presentation, through the end of his junior-year track season.

Ten months after initial presentation, and after a period without physical therapy, the patient presented with recurrence of sacroiliac joint pain of greatly increased severity. His training and competition were limited due to pain. Regular physical therapy was restarted. During the following week, the severity of his symptoms escalated to the point that he was completely unable to practice and the use of crutches to assist with walking, due to debilitating pain, was discussed. Anti-inflammatory medications were started, and a series of radiographs of the lumbar spine and sacrum were interpreted as revealing normal findings (Figure 1). Magnetic resonance images (MRI) revealed a right superior labral tear, right cam morphology of the femoral head, and right sacroiliitis (Figures 2–3). However, the patient was initially diagnosed as having a sacral stress fracture.


Figure 1:

Anteroposterior radiograph showing no abnormalities, including no inflammatory changes of the lumbar spine or sacroiliac joints.



Figure 2:

Coronal (A) and axial (B) T2 series magnetic resonance image sections showing increased signal medial and lateral to the sacroiliac joint.



Figure 3:

Coronal T2 magnetic resonance image showing increased T2 signal at the right inferolateral sacrum bordering the sacroiliac joint compared with normal T2 signal at the left sacroiliac joint.


A second opinion regarding the MRI prompted follow-up blood work to rule out a seronegative spondyloarthropathy, given the increased T2 signal medial and lateral to the sacroiliac joint. Anti-inflammatory medications were continued. The patient was instructed to continue exercising via nonimpact modalities such as pool running and elliptical training, without running or jumping, until the problem could be further elucidated. The patient had an erythrocyte sedimentation rate of 14 mm/hr, a C-reactive protein level of 1.36 mg/L, a serum calcium level of 9.7 mg/dL, and a serum 25-hydroxy vitamin D level of 49.6 ng/mL. The antinuclear antibody screen yielded negative results, and the histocompatibility antigen (HLA-B27) test had a positive result. Given the HLA-B27 results, the patient was referred to Rheumatology for further workup and treatment of suspected ankylosing spondylitis with sacroiliitis.

The patient was prescribed oral indomethacin daily by the attending rheumatologist and started on a slow progression of return to running, jumping, and weight lifting. Within 4 weeks of beginning this treatment, he experienced complete cessation of pain with the medication. He was able to compete and finish his senior-year indoor and outdoor track and field seasons without residual symptoms. He was further able to compete and score in the Big Ten Conference long-jump championships. Following completion of the outdoor track and field season, the patient graduated from the university and elected not to continue his athletic career. He also requested that indomethacin be discontinued.

At follow-up 1 year after graduation, the patient was nearly symptom free and working in a non-heavy labor job. He was taking no medications, including no anti-inflammatory medications, for the conditions. He reported that he was able to run 10 to 20 miles per week as well as lift weights 3 to 4 times per week without symptoms. He reported only occasional right sacroiliac joint pain when playing pick-up basketball. These symptoms required no medication for pain control and resolved within hours of participation.

Discussion

Ankylosing spondylitis is a rheumatologic condition in which immune-mediated inflammation induces fibrosis, bone remodeling, and new bone deposition.2 The disorder is not rare, with a recent study estimating a prevalence as high as 0.9% in the US population.3

Joints are most commonly affected in ankylosing spondylitis, although extra-articular symptoms exist as well. The axial skeleton is more often involved than the appendicular, where large, proximal, unilateral arthritis predominates. The sacroiliac joint is involved nearly 100% of the time, followed by the intervertebral joints (75%); unilateral involvement of the shoulders (30%) and knees (20%) and other joints, such as temporomandibular, also occurs. Extra-articular symptoms of ankylosing spondylitis commonly include uveitis, enthesitis, and fatigue. Long-term complications include spinal stenosis and fracture as well as restrictive pulmonary and cardiac sequelae resulting from pronounced kyphosis and spinal fusion.4 Classically, patients initially present with a history of dull, diffuse low back and buttock pain and stiffness, often unilateral or alternating, which are worse in the morning but improve with activity. The presentation and course of the condition may vary greatly between patients, and shoulder symptoms as the presenting feature may increase confusion and delay diagnosis.5

Clinically significant as well as more severe disease occurs more commonly in males.6 Age of onset is often in the second or third decade, with a mean of 25.6 years. Associations have also been reported in patients with ankylosing spondylitis and inflammatory bowel disease. Palm et al7 reported an overall prevalence of 2.6% of patients with ulcerative colitis having associated ankylosing spondylitis. Brophy et al,1 describing a series of 3287 patients with ankylosing spondylitis, reported an increased rate of coinflammatory disease including iritis, psoriasis, and inflammatory bowel disease. They concluded that psoriasis and inflammatory bowel disease are associated with increased severity of the condition and decreased function in patients with ankylosing spondylitis.

The differential diagnosis for the sacroiliitis and low back pain that often herald this condition includes stress fracture, muscle sprain or spasm, lumbar disk herniation, osteoarthritis, gout, neoplasia, infection, Whipple’s disease, inflammatory bowel disease, and rheumatologic diseases such as ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and rheumatoid arthritis. Magnetic resonance imaging is preferred for early detection of ankylosing spondylitis, especially when conventional radiographs are equivocal.8,9Conventional radiographs show structural damage in more advanced disease and can help monitor progress; MRI should be used instead to screen for ankylosing spondylitis.10,11

Treatment for ankylosing spondylitis has long been centered around nonsteroidal anti-inflammatory drugs and disease-modifying antirheumatic drugs. Newer agents such as tumor necrosis factor-alpha antagonists have been shown to have greater effect ameliorating symptoms; however, their impact in slowing or reversing the long-term sequelae of ankylosing spondylitis is unknown.12–14

A review of rheumatologic diseases presenting as sports-related injuries explored the temptation of sports medicine physicians to diagnose every joint complaint as mechanically induced injury.15 It also highlighted the importance of having a high index of suspicion for rheumatologic diseases such as spondyloarthropathies, rheumatoid arthritis, gout, pseudogout, and systemic lupus erythematosus in athletes presenting with joint symptoms.

The current patient had a fairly classic presentation, with right hamstring tightness and unilateral low back pain centered on the sacroiliac joint. Although he was a long jumper, he had experienced no known mechanical injuries. He had a history of ulcerative colitis requiring partial bowel resection. Other than tenderness to palpation along the joint line of the right sacroiliac joint, results of the physical examination were normal. After 10 months of remitting and relapsing symptoms treated with intermittent physical therapy and use of nonsteroidal anti-inflammatory drugs, the patient experienced a progressive escalation of symptoms and deterioration in functional capability and athletic performance.

The patient’s history of ulcerative colitis, sacroiliac joint tenderness and pain, age, and sex placed him at moderate risk for having a spondyloarthropathy. A possible factor contributing to the delay in reaching the conclusive diagnosis in this case, and probably in other cases, is the individual sports medicine provider’s version of selection bias. Physicians who see only a specific subset of patients who are more likely to have joint complaints due to injury may unreasonably narrow the differential diagnosis. This may result in the inadvertent omission of rheumatologic conditions from consideration. Physicians must keep in mind that the population at risk for diseases that mimic sports injuries is the very cohort being seen most often: young, otherwise healthy males and, to a lesser extent, females. Other historical features that may increase or decrease the index of suspicion for rheumatologic disease and that should be screened for in every athletic patient presenting with joint complaints are morning stiffness lasting more than 1 hour that improves with exercise but does not resolve with rest and personal and family history of rheumatologic diseases or inflammatory conditions.

Conclusion

Similar delays in reaching diagnoses have occurred in other case reports of athletes with rheumatic diseases.5 The purpose of the current case report is to increase awareness among sports medicine physicians, athletic trainers, and other medical staff of the prevalence of rheumatologic diseases in general and ankylosing spondylitis in particular and of the various ways in which spondyloarthropathies may present among athletes. The authors hope that this increased awareness will lead to earlier diagnosis and treatment, potentially reducing illness severity and duration and improving the performance of athletes with this condition.

References
Brophy S, Pavy S, Lewis P, et al. Inflammatory eye, skin, and bowel disease in spondyloarthritis: genetic, phenotypic, and environmental factors. J Rheumatol. 2001; 28:2667–2673.
Ronneberger M, Schett G. Pathophysiology of spondyloarthritis. Curr Rheumatol Rep. 2011; 13:416–420. doi:10.1007/s11926-011-0202-x[CrossRef]
Reveille JD, Witter JP, Weisman MH. Prevalence of axial spondylarthritis in the United States: estimates from a cross-sectional survey. Arthritis Care Res (Hoboken). 2012; 64:905–910. doi:10.1002/acr.21621 [CrossRef]
Spondylitis Association of America. (2012). Complications.http://www.spondylitis.org/about/complications.aspx. Accessed June 21, 2013.
Hill JA, Lombardo SJ. Ankylosing spondylitis presenting as shoulder pain in an athlete: a case report. Am J Sports Med. 1981; 9:262–264. doi:10.1177/036354658100900416 [CrossRef]
Sieper J, Braun J, Rudwaleit M, Boonen A, Zink A. Ankylosing spondylitis: an overview. Ann Rheum Dis. 2002; 61(suppl 3):iii8–iii18.
Palm O, Moum B, Ongre A, Gran JT. Prevalence of ankylosing spondylitis and other spondyloarthropathies among patients with inflammatory bowel disease: a population study (the IBSEN study). J Rheumatol. 2002; 29:511–515.
Ostergaard M, Lambert RG. Imaging in ankylosing spondylitis. Ther Adv Musculoskelet Dis. 2012; 4:301–311. doi:10.1177/1759720X11436240[CrossRef]
Maksymowych WP. Controversies in conventional radiography in spondyloarthritis. Best Pract Res Clin Rheumatol. 2012; 26:839–852. doi:10.1016/j.berh.2012.10.003 [CrossRef]
Braun J, Bollow M. Imaging of inflammatory rheumatic diseases of the axial skeleton (sacroiliitis): when and how should we use MRI?J Clin Rheumatol. 2000; 6:339–349. doi:10.1097/00124743-200012000-00008 [CrossRef]
Blum U, Buitrago-Tellez C, Mundinger A, et al. Magnetic resonance imaging (MRI) for detection of active sacroiliitis: a prospective study comparing conventional radiography, scintigraphy, and contrast enhanced MRI. J Rheumatol. 1996; 23:2107–2115.
Braun J, Sieper J. Therapy of ankylosing spondylitis and other spondyloarthritides: established medical treatment, anti-TNF-alpha therapy and other novel approaches. Arthritis Res. 2002; 4:307–321. doi:10.1186/ar592 [CrossRef]
Braun J, Pham T, Sieper J, et al. International ASAS consensus statement for the use of anti-tumour necrosis factor agents in patients with ankylosing spondylitis. Ann Rheum Dis. 2003; 62:817–824. doi:10.1136/ard.62.9.817[CrossRef]
Dougados M. Treatment of spondyloarthropathies: recent advances and prospects in 2001. Joint Bone Spine. 2001; 68:557–563. doi:10.1016/S1297-319X(01)00328-1 [CrossRef]
Jennings F, Lambert E, Fredericson M. Rheumatic diseases presenting as sports-related injuries. Sports Med. 2008; 38:917–930. doi:10.2165/00007256-200838110-00003 [CrossRef]

http://www.tigenix.com/es/page/243/cartilago-de-la-rodilla

Cartílago de la rodilla

El cartílago articular es un tejido altamente estructurado responsable del funcionamiento óptimo de la articulación, gracias a su capacidad para absorber la tensión de una carga específica y al proporcionar una interfaz uniforme para el movimiento de la articulación. El cartílago articular tiene una capacidad limitada de autocuración, esto se debe principalmente al hecho de que es avascular, y una vez resulte gravemente dañado, las lesiones del cartílago articular no se regenerarán. (1)

Curl et al. revisaron retrospectivamente 31.516 artroscopias de rodilla en pacientes de todas las edades, e informaron sobre lesiones condrales en 19.827 (63%) de los pacientes. (2) Una revisión de 1.000 artroscopias por Hjelle et al., reportó una incidencia del 5% de lesiones de grado III y IV. (3) En una revisión de 993 artroscopias en pacientes con una edad media de 35 años, hubo una incidencia del 11% de lesiones del cartílago de espesor completo (ICRS grado III y IV), que podrían haberse beneficiado de un tratamiento quirúrgico. (4) Por último, en un análisis de 25.124 artroscopias de rodilla realizadas desde 1989 hasta 2004, se encontraron lesiones condrales en el 60% de los pacientes. Las lesiones de cartílago documentadas se clasificaron como lesiones condrales u osteocondrales focales localizadas en el 67%, osteoartritis en el 29%, osteocondritis disecante en el 2% y otros tipos en el 1% de los casos. Las lesiones de cartílago no aisladas representaron el 70%, y las lesiones aisladas el 30%. La superficie articular patelar y el cóndilo femoral medial fueron la localización más frecuente de las lesiones del cartílago. (5)

Las lesiones de cartílago con frecuencia provocan dolor, hinchazón y síntomas mecánicos como bloqueo “ catching” (mínimo bloqueo de la articulación) que reducen sustancialmente la calidad de vida del paciente. (6) La articulación de la rodilla es una de las zonas del cuerpo que resultan más comúnmente lesionadas durante actividades deportivas y recreativas. (7) Las lesiones en las articulaciones con frecuencia conducen a la degeneración progresiva de las articulaciones y a osteoartritis postraumática. (8) La prevalencia global de lesiones en rodilla en el adolescente, oscila entre 10-25%.
Los traumas, sobre todo en los hombres, se asocian con la progresión hacia la osteoartritis. (9; 10)

Hay una fuerte evidencia de que las lesiones del cartílago predisponen a la osteoartritis, cuando no son tratadas.(1,11-13) La osteoartritis (OA), el síndrome de dolor en las articulaciones y la disfunción causada por la degeneración de las articulaciones, afecta a más personas que cualquier otra enfermedad de las articulaciones. En la mayoría de los casos, la degeneración articular se desarrolla en ausencia de una causa identificable; sin embargo, el riesgo de OA aumenta con la edad, la carga excesiva en la articulación, anomalías en las articulaciones y debido a un trauma. El estrés debido al contacto de la superficie articular, el cual causa un daño tisular y compromete la capacidad de los condrocitos para mantener y restaurar el tejido, tiene un papel notable en que se produzca la degeneración de la articulación. (14) La incidencia acumulada de osteoartritis de rodilla hasta los  65 años, fue del 13,9% en los participantes que tuvieron una lesión en la rodilla durante la adolescencia y en la edad de adulto joven, y del 6,0% en aquellos que no tuvieron lesión (p = 0,0045).

Las afecciones musculoesqueléticas, como la osteoartritis, representan una carga económica importante para las personas, los sistemas de salud y los sistemas de asistencia social, con costes indirectos, siendo estos predominantes. (9) Se estima que 1,6 millones de personas se encuentran limitadas en sus trabajos debido a la osteoartritis y trastornos relacionados, lo que representa el 8,3% de todas las afecciones principales. (15)

Numerosos experimentos con animales y estudios clínicos han demostrado que la reconstrucción temprana biológica de los defectos del cartílago circunscritos en la rodilla, es superior al tratamiento quirúrgico conservador o diferido. Esta superioridad no sólo se refiere a una deficiencia de cicatrización, sino también a la eliminación de los cambios que siguen a la osteoartritis secundaria. (16)

Teniendo en cuenta el hecho de que las lesiones no tratadas de cartílago pueden predisponer a la OA, y debido a que representan una importante morbilidad para el paciente, el tratamiento de estas lesiones debería ser una prioridad.

(1) Messner K, Maletius W. Pronóstico a largo plazo de los daños graves en los cartílagos que soportan peso en la rodilla: un seguimiento clínico de 14 años y radiográfico en 28 atletas jóvenes. Acta Orthop Scand 1996 Abril;67(2):165-8.

(2) Curl WW, Krome J, Gordon ES, Rushing J, Smith BP, Poehling GG. Lesiones del cartílago: una revisión de 31.516 artroscopias de rodilla. Arthroscopy 1997 Agosto;13(4):456-60.
(3) Hjelle K, Solheim E, Strand T, Muri R, Brittberg M. Defectos del cartílago articular en 1.000 artroscopias de rodilla. Arthroscopy 2002 Septiembre;18(7):730-4..
(4) Aroen A, Loken S, Heir S, Alvik E, Ekeland A, Granlund OG, et al. Lesiones del cartílago articular en 993 artroscopias de rodilla consecutivas. Am J Sports Med 2004 Enero;32(1):211-5.
(5) Widuchowski W, Widuchowski J, Trzaska T. Defectos del cartílago articular: estudio de 25.124 artroscopias de rodilla. Knee 2007 Junio;14(3):177-82..
(6) Minas T. Implante de condrocitos autólogos para los defectos condrales focales de la rodilla. Clin Orthop Relat Res 2001 Octubre;(391 Suppl):S349-S361.
(7) Louw QA, Manilall J, Grimmer KA. Epidemiología de las lesiones de rodilla entre adolescentes: una revisión sistemática. Br J Sports Med 2008 Enero;42(1):2-10.
(8) Martin JA, Brown T, Heiner A, Buckwalter JA. Osteoartritis postraumática: el papel de la senescencia acelerada de los condrocitos. Biorheology 2004; 41 (3-4) :479-91.
(9) Woolf AD, Pfleger B. Carga de las principales afecciones musculoesqueléticas. Bull World Health Organ 2003;81(9):646-56.
(10) DG for Health & consumers. Enfermedad grave crónica - Report 2007. 2008.
(11) Gelber AC, Hochberg MC, Mead LA, Wang NY, Wigley FM, Klag MJ. Lesión de la articulación en adultos jóvenes y riesgo de posterior osteoartritis de rodilla y cadera. Ann Intern Med 2000 Septiembre 5;133(5):321-8.
(14) Buckwalter JA, Martin JA, Brown TD. Perspectivas sobre la mecanobiología de condrocitos y la osteoartritis. Biorheology 2006; 43 (3-4) :603-9.
(15) Stoddard S. Tabla sobre trabajo y discapacidad en los Estados Unidos. 1998. 

(16) Fritz J, Janssen P, Gaissmaier C, Schewe B, Weise K. Defectos del cartílago articular de la rodilla, terapias y resultados. Injury 2008 Abril;39 Suppl 1:S50-S57.

Uso correcto de las muletas

Los ortobilógicos son una gran promesa para el tratamiento de las fracturas de cadera /Orthobiologics have great promise for treatment of hip fractures

http://www.healio.com/orthopedics/trauma/news/online/%7Bc4cc9396-2b02-4804-9406-c46c70672536%7D/orthobiologics-have-great-promise-for-treatment-of-hip-fractures

Orthobiologics have great promise for treatment of hip fractures

WAILEA, Hawaii — Orthobiologics offer a faster track in hip fracture healing and show great promise for the future, according to a presenter, here.

“The most exciting thing is that everything is about to change. It is going to be exciting,” Thomas A. “Toney” Russell, MD, said here at Orthopedics Today Hawaii 2014.

Orthobiologics that are currently being used as implant surface enhancements have interference with fracture healing, he said. Numerous published studies have shown that orthobiologics have the ability to deliver materials and the biodegradability of the osteoconductive matrix, Russell noted.

Orthobiologics applications now involve implant surface enhancements, hydroxyapatite coatings, systemic medication delivery, parathyroid hormone, bisphosphonates and biomaterials. Present problems as well as the future options for orthobiologics may include the use of new calcium phosphate cements with increased porosity, proper insertion and positioning, as well as implant interface augmentation, he said. ─ by Kristine Houck, MA, ELS

Reference:

Russell TA. Will orthobiologics help fixation in hip fractures. Presented at: Orthopedics Today Hawaii 2014; Jan. 19-23, 2014; Wailea, Hawaii.

Disclosure: Russell receives a salary from Innovision Inc.; royalties from Smith & Nephew; is a patent holder for Innovision Inc., Smith & Nephew and Zimmer; and has ownership interest in Etex and Innovision Inc.

http://www.arthroscopyjournal.org/article/S0749-8063(13)01240-1/fulltext

Symptoms of Nerve Dysfunction After Hip Arthroscopy: An Under-Reported Complication?

Received 7 March 2013; accepted 13 November 2013.

Article Outline 

Purpose 

The primary purpose of this study was to analyze the rate, pattern, and severity of symptoms of nerve dysfunction after hip arthroscopy (HA) by reviewing prospectively collected data. The secondary purpose was to study whether symptoms of nerve dysfunction were related to traction time.

Methods 

From March to October 2010, 52 consecutive patients—27 male patients (mean age, 40 years; range, 21 to 63 years) and 25 female patients (mean age, 37 years; range, 15 to 60 years), underwent HA with labral repair, rim trimming, and osteoplasty. The patients received a follow-up questionnaire 1 year after HA concerning symptoms of nerve dysfunction, possible localization, and erectile dysfunction. Fifty patients participated and returned fully completed questionnaires. Patients reporting symptoms of nerve dysfunction 1 year after HA were re-examined.

Results 

Twenty-three of 50 patients (46%) reported symptoms of nerve dysfunction during the first week after HA; this was reduced to 14 patients (28%) after 6 weeks, 11 patients (22%) after 26 weeks, and 9 patients (18%) after 1 year. One patient experienced temporary erectile dysfunction. No difference in traction time between patients with symptoms of nerve dysfunction (n = 23) and patients without (n = 27) was found (98 minutes v 100 minutes; P = .88).

Conclusions 

Forty-six percent of patients undergoing HA reported symptoms of nerve dysfunction within the first 6 weeks after surgery. One year postoperatively, these symptoms remained in only 18% of all patients. Traction time during surgery was not different in patients with and those without symptoms of nerve dysfunction.

Level of Evidence 

Level IV, therapeutic case series.

Hip arthroscopy (HA) has become a standard procedure in addressing intra-articular pathologic conditions of the hip joint such as femoroacetabular impingement (FAI). Nerve affection is a known complication related to HA.¹, ²,³, ⁴, ⁵, ⁶, ⁷, ⁸, ⁹ Generally, there has been limited focus on complications after HA. In 2003, Clarke et al.² described an overall complication rate of 1.4% in a prospective study of 1,054 cases. Vascular lesions, postoperative infection, and postoperative nerve affection—whether described as neuropraxia, nerve injury, or dysesthesia—are the most common complications reported.¹, ², ⁷, ⁸ The rate of nerve complications published in the literature varies from 1.4% to 10%², ³,⁴, ⁶, ⁷, ⁸, ¹⁰ and is usually inconsistent regarding localization, duration, and type. Furthermore, it remains unclear if these complications were identified by the surgeons during follow-up examinations or if they were patient reported.The localization, degree, and duration of nerve affection may depend on the surgical setup, including the accumulated time of traction and traction force.There are no standards or consensus regarding the duration of traction, when and if traction-free intervals are needed, and how long they should last. Because it has been suggested that prolonged traction time and high traction force lead to increased risk of nerve injury,⁷ some authors have advocated that traction time should be reduced to 120 minutes,⁷, ¹¹ and others have favored average traction forces around 200 N.², ⁷, ¹¹, ¹² However, according to our literature review, this has not been the subject of research and is based only on expert opinion. Usually, 2 major sources of nerve injury in relation to HA have been described in the literature: pudendal nerve injury resulting from compression against the perineal post and sciatic or femoral neuropraxia (or both) resulting from traction, none of which have so far been objects of scientific interest. Only in the treatment of proximal femoral fractures using standard fracture tables and standard perineal posts is neuropraxia a well-known complication, in which dysesthesia of the pudendal nerve is found with a rate up to 17%.¹³, ¹⁴

The primary purpose of this retrospective study was to identify the self-reported rate of symptoms of nerve dysfunction after HA and their pattern in a consecutive series. Our secondary purpose was to study the influence of traction time and determine if this was related to the development of symptoms of nerve dysfunction. Our hypotheses were (1) that nerve dysfunction after HA is more common than previously reported in the literature and (2) that increased traction time would be associated with symptoms of nerve dysfunction.

Back to Article Outline

Methods  ;

All patients were scheduled for labral repair, rim trimming, and osteoplasty. All patients underwent these procedures, except 4 patients who did not undergo osteoplasty. Labral repair was not possible in one patient because of advanced degeneration, and a labral reconstruction with an iliotibial band autograft was performed. At the time of surgery for this investigation, both surgeons were experienced hip arthroscopists who performed more than 50 hip arthroscopies per year.

Before surgery, all patients underwent clinical examination, including an examination of sensibility around the index hip/groin, and completed a self-reported questionnaire regarding sensibility problems in the perineum and legs.They were told to notice if and how long any sensory disturbance lasted. Male patients were asked about erectile dysfunction. In our questionnaire, the patients had to answer 4 simple questions: (1) Do you have reduced sensibility (numbness, tingling, or pricking) in the hip/groin region? (2) Do you have reduced sensibility (numbness, tingling, or pricking) in the leg? (3) If any of the answers is “yes,” where and for how long? (4) Have you experienced erectile dysfunction?

No problems were reported at this point. Postoperatively, the questions in the questionnaire were: (1) Have you had reduced sensibility in the leg or the hip and groin region and did you have lacerations in your genitals? (2) If yes, how long?

Postoperatively, all patients were scheduled for follow-up examinations 6 to 12 weeks after surgery. All patients were examined fully, including examination for reduced sensibility. Not all patients completed a questionnaire at this point, but any alterations in sensibility were recorded in the patient records for later use. Furthermore, all patients were informed of the purpose of this study before surgery, at discharge, and at follow-up consultations (2 to 12 weeks postoperatively) and told that they would be contacted within a year to gather information regarding symptoms of nerve dysfunction and their pattern for the index leg.

One year after surgery, the patients received the same self-reported questionnaire regarding sensibility problems in the index leg after HA. In the questionnaire, the patients were asked if they had reduced sensation directly after surgery and how long this lasted. These results were compared with their previous findings. Patients described the localization in their own words or marked the area on an illustration, or both. Male patients were again asked to report any kind of erectile dysfunction postoperatively.

All patients reporting ongoing reduced sensation after 52 weeks were re-examined in the outpatient clinic by the surgeon. The area was examined manually and with the contralateral leg as reference. Subjective absence or reduction of tactile perception described as numbness, tingling, or pricking was defined as symptoms of nerve dysfunction. In the area of interest, light touch was tested digitally by light finger touch. In case the patient noticed a change in sensation in a certain area, he or she was re-examined by randomly alternating stimuli with the sharp or dull end of a safety pin. Afterward, the approximate extent of sensory disturbance was measured in centimeters.

A standard setup was used in all patients, focusing especially on the positioning of the patient and padding of the areas exposed to compression and traction.The patient was placed in the supine position on a fracture table using a perineal post to provide countertraction and as a fulcrum (Fig 1A). To reduce the risk of neuropraxia of the pudendal nerve we used a 23-cm–wide foam-padded perineal post (Bledsoe Brace Systems, Grand Prairie, TX). Both feet were placed in 1.5-cm–thick foam boots (Bledsoe Brace Systems) before they were mounted in the fracture table boots (Fig 1B). The genitals were checked at positioning and whenever traction was applied. For stabilization of the pelvis, the contralateral leg was mounted in a traction boot without regular traction. The traction force was not measured. To gain sufficient space for instrumentation in the central compartment, the joint was distracted by 10 to 15 mm with unknown traction force. Traction time was limited to 105 minutes. In case a second traction period was necessary, a 30-minute pause was mandatory.Traction times as well as traction-free intervals were noted. We only used 2 portals (anterolateral and inferior midanterior) (Fig 1C). No supplemental portals, e.g., posterior portals, were used. For instrumentation, slotted (half-pipe) cannulas were used as well as a cannula during labral repair. The labral repair, rim trimming, and osteoplasty were performed using the technique described by Philippon et al.¹⁵

• 

• Fig 1.  ;

  (A) The padded perineal post. (B) Padded boot under traction. (C) Placement of the anterolateral and midanterior portal. (D) Typical area of nerve dysfunction on the lateral thigh in relation to the portals.

Data Reduction and Statistical Analysis  ;

Descriptive statistics are given, including mean, range, and percentages.Analysis of traction time for patients with and those without symptoms of nerve affection was performed using statistical analysis for independent samples. Because data for traction times did not show a normal distribution, nonparametric statistics were used (Mann-Whitney U test for independent samples), with a significance level set at 5%. Medians and percentiles (25th to 75th) are given. SPSS, version 17 (SPSS, Inc, Chicago, IL) was used to calculate all statistics.

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Results  ;

The 52 HAs were performed in 27 male patients (mean age, 40 years; range, 21 to 63 years) and 25 female patients (mean age, 37 years; range, 15 to 60 years) at 2 separate institutions after the same surgical setup. Two patients (one woman and one man) were lost to follow-up, leaving 50 consecutive patients (26 men; mean age, 41 years; range, 21 to 63 years; and 24 women; mean age, 37 years; range, 15 to 60 years) to be included in this study. The physical activity level of the patients varied according to their jobs (white and blue collar workers as well as students) and the degree and amount of recreational sports activities. All patients were healthy individuals with a score 1 or 2 according to the American Society of Anesthesiologists.

Twenty-three patients (46%) reported symptoms of nerve dysfunction within the first week after surgery. The number of regions with reported symptoms of nerve dysfunction and the duration over time within the first year can be seen in Fig 2. Five patients had isolated symptoms at the index foot, 5 patients at the perineum, and 8 patients at the lateral thigh. Five patients experienced reduced sensibility at multiple locations: 4 patients had 2 areas of reduced sensibility (genitals/foot, lateral thigh/foot, erectile dysfunction/lateral thigh, and genitals/lateral thigh, respectively), and 1 patient had 3 different areas of reduced sensibility (genitals/foot/lateral thigh). One patient reported temporary erectile dysfunction within the first 7 weeks after surgery. Nine patients (18%) had symptoms after 1 year. The re-examination of these 9 patients showed that 8 of them had symptoms of nerve dysfunction at the lateral thigh, mainly located around the portals (Fig 1D), whereas one patient (2%) had symptoms of nerve dysfunction at the dorsal side of the first toe (Table 1). All 9 patients with reduced sensibility longer than 52 weeks had an HA with rim trimming and labral repair and all but one had a femoral osteoplasty. Among the 9 patients there were 4 women and 5 men, with an average age of 42 years (range, 22 to 63 years).

• 

• Fig 2.  ;

  The number of regions with symptoms of nerve dysfunction and the distribution over time as reported by the patients. Patients may have more than one region of nerve dysfunction.

Table 1. Localization of Permanent Nerve Affection 

Patient 1	10- × 10-cm reduced sensation at the lateral thigh
Patient 2	5- × 5-cm numbness around the stab incisions
Patient 3	5- × 15-cm reduced sensation at the lateral thigh
Patient 4	10- × 15-cm reduced sensation around the portals and down the lateral thigh
Patient 5	7- × 12-cm anterolateral, reduced sensation around the portals
Patient 6	10- × 7-cm reduced sensation anteroposterior at the level of the portals
Patient 7	3- × 10-cm reduced sensation distal from the portals
Patient 8	5- × 10-cm reduced sensation distal from the portals
Patient 9	1- × 1-cm at the index leg's left toe

The number of patients with symptoms of nerve dysfunction decreased within the first year, with the most rapid decrease within the first 6 weeks after surgery (Fig 2). The average age of patients with reduced sensibility (n = 23) was 36 years (range, 15 to 60 years): 14 female patients (average age, 34 years; range, 15 to 60 years) and 9 male patients (average age, 42 years; range, 23 to 63 years). The average age of patients with normal sensibility (n = 27) was 40 years (range, 21 to 61 years): 10 female patients (average age, 40 years; range, 15 to 50 years) and 17 male patients (average age, 40 years; range, 21 to 54 years).

To rule out bias from the fact that the procedures were performed by 2 surgeons, we analyzed their individual rates of patients with and those without reduced sensibility. Surgeon A performed 24 HAs with labral repair and osteoplasty.Among these patients, 8 had reduced sensibility, 4 cases of which lasted more than 52 weeks. Surgeon B performed 26 procedures, with 15 patients having reduced sensibility, 6 cases of which lasted more than 52 weeks.

Furthermore, there was no difference between the patients who underwent (n = 46) and those who did not undergo (n = 4) osteoplasty. Among the patients who did not undergo osteoplasty, 2 had symptoms of nerve dysfunction. One of these patients had symptoms for approximately 1 week at the index foot, whereas the other had symptoms of nerve dysfunction for more than 52 weeks at the lateral thigh. There was no significant difference in median traction time between the group with and the group without nerve dysfunction (98 minutes; range, 94 to 110 minutes [n = 23] v 100 minutes; range, 90 to 115 minutes [n = 27]; median, 25th to 75th percentiles; P = .884).

Two main subgroups of patients with symptoms of nerve dysfunction were identified: patients with isolated nerve dysfunction symptoms at the anterolateral thigh (n = 8) and patients with symptoms in the genitals or foot, or both (n = 15). Because symptoms at the anterolateral thigh are mainly located around the portal holes, and therefore may be assumed to be related to the surgical incision and instrumentation rather than traction, this type of nerve dysfunction is considered to have a different cause from that of nerve dysfunction in the genitals or foot, or both. We therefore decided in retrospect to perform a post-hoc analysis in which the traction time of a combined group of patients without symptoms of nerve dysfunction and patients with isolated symptoms of nerve dysfunction only at the anterolateral thigh (n = 35) was compared with the traction time of the patients with symptoms of nerve dysfunction in the genitals or foot, or both (n = 15). In this post-hoc analysis, there were no significant differences in median traction time between these groups (98 minutes; range, 90 to 110 minutes [n = 35] v 101 minutes; range, 95 to 120 minutes [n = 15]; P = .518).

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Discussion  ;

In patients undergoing HA, nerve injury is reported to be the most common postoperative complication, but the reported rate is low. The rate of nerve complications published in the literature varies from 1.4% to 10%², ³, ⁴, ⁵, ⁶, ⁷,⁸, ¹⁰ and is usually inconsistent regarding the localization, duration, and type of nerve affection.

In 2003, Clarke et al.² described 4 cases of neuropraxia (3 at the sciatic nerve and 1 at the femoral nerve) in 1,054 cases of HA. All resolved within the first 6 hours after surgery. Byrd et al.¹⁶ reported 3 nerve-related complications among the first 100 patients who underwent HA from 1993 to 2003: “a transient neuropraxia of the pudendal nerve and a transient neuropraxia of the lateral femoral cutaneous nerve, both of which resolved uneventfully.” Sampson et al.⁸ described 20 transient nerve injuries that resolved within the first week after HA. However, it remains unclear if these nerve injuries were identified by the surgeons during follow-up examinations or if they were patient reported. To our knowledge, the present study is the first in which all patients were asked about nerve affection before and after surgery and in which patients were re-examined when reporting such long-standing changes. This might be one reason why the number of patients describing nerve affection in our study is higher than that published in other studies about HA.

Access to the central compartment requires longitudinal traction that increases the risk of nerve dysfunction. Because midterm results indicate that labral repair is superior to debridement,¹⁰, ¹¹, ¹⁷, ¹⁸, ¹⁹, ²⁰ refixation of the labrum during traction is necessary. All our patients underwent HA with labral repair. We did not measure the traction force applied, but the force was sufficient to have the joint distracted 10 to 15 mm. According to our protocol, the traction time was limited to 105 minutes, and whenever a second traction period was needed, a 30-minute pause was mandatory. In our study, 15 patients (29%) reported nerve dysfunction located at the genitals and the foot. We believe that these are indirect lesions related to the traction force applied. Only one of these patients still had complaints after 1 year.

Permanent and temporary nerve injury has been described in other arthroscopic procedures as well. In ankle arthroscopy²¹ and knee arthroscopy,²² a 15% rate of nerve injury has been described. In an electrophysiologic study of 17 patients undergoing anterior cruciate ligament (ACL) reconstruction with a hamstring graft, Figueroa et al.²³ reported “hypoesthesia” in 77% of operated knees by the time of follow-up (>1 year). In our study, the incisions for the anterolateral and the inferior midanterior portal were longitudinal and followed by blunt dissection.

The most common interpretation of nerve injury as a complication after HA is a combination of traction and compression. Although known nerve complications by direct lesion (neurotmesis) have been described in many other arthroscopic procedures, in HA literature is sparse. Clarke et al.² described the overall rate related to nerve and vessel damage when entering the joint as low (0.6%). Larson reported a rate of “postoperative sensory disturbance adjacent to the portals or involving the distal anterolateral thigh, consistent with the lateral femoral cutaneous nerve” of 22.7% (C. Larson, personal communication, September 2012). Although it remains unclear how long these sensory disturbances lasted and if the patients or the surgeon reported them, the actual rates of nerve affection at the anterolateral thigh may be higher than previously reported.

We found symptoms of nerve dysfunction at the anterolateral thigh to be mainly located around the portals and they tended to be long lasting. All these patients had reduced sensation around the portals varying from 3 × 10 cm to 10 × 15 cm. None of these patients had a full lesion of the lateral femoral cutaneous nerve. Furthermore, the patients described these symptoms as negligible. We presume that these lesions were caused by a branch or branches of the lateral femoral cutaneous nerve being lacerated directly under portal placement or instrumentation (neurotmesis), or both, although we performed instrumentation with a standardized technique aimed at protecting nerves and vessels in the area. We made stab incisions only through the skin and used a switching stick or a half-pipe, or both, when changing instruments.

In the electrophysiologic study of Figueroa et al.²³ the average area of dysesthesia more than 1 year after ACL reconstruction was 36 cm² (1 to 120 cm²) and the patients were not impaired in daily life, although they were aware of “hypoesthesia.” Although the rate of nerve affection in the article of Figueroa et al. was higher, the size measured and the patients' estimations were comparable to our findings.

As a secondary purpose, we studied the influence of traction time and did not find a relation between traction time and nerve dysfunction. The post-hoc analysis we made hypothesizing that symptoms of nerve dysfunction at the lateral thigh are not related to traction did not show any significant difference between the traction times of these 2 groups (P > .518). Erectile dysfunction has not been described after HA before but has been published as a complication after intramedullary nailing of femoral fractures.²⁴, ²⁵ It is mainly transient but can affect up to 40% of the patients undergoing femoral nailing.²⁵ In our study, one patient had erectile dysfunction for approximately 7 weeks after surgery.

Overall, the patients were not impaired by these symptoms of nerve dysfunction; however, this might be influenced by the overall positive impact of the surgical FAI treatment and the postoperative rehabilitation and therefore considered of minor importance by the patients.

Limitations  ;

The fact that the clinical evaluation of the nerve dysfunction was performed by orthopaedic surgeons and not by a neurologist or an independent reviewer and the fact that no electromyography was performed could be a limitation of the study. Although examined and interviewed within the first 3 months after surgery, the long-term results were based on a retrospective patient-reported questionnaire, and only patients with symptoms at the 1-year follow-up questionnaire were examined clinically. This might introduce a recall bias. Furthermore, other factors apart from surgical setup and traction time may influence the development of symptoms of nerve dysfunction. However, these were not examined in this study.

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Conclusions  ;

Forty-six percent of patients undergoing HA reported symptoms of nerve dysfunction within the first 6 weeks after surgery. One year postoperatively, these symptoms remained in only 18% of all patients. Traction time during surgery was not different in patients with and those without symptoms of nerve dysfunction.

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