Entrapment of the Sciatic Nerve by the Femoral Neck Following Closed Reduction of a Hip Prosthesis : A Case Report

Leversedge, Fraser J. MD; Gelberman, Richard H. MD; Clohisy, John C. MD

Journal of Bone & Joint Surgery - American Volume:
Case Report
Author Information

Fraser J. Leversedge, MD; Richard H. Gelberman, MD; John C. Clohisy, MD; Department of Orthopaedic Surgery, Barnes-Jewish Hospital at Washington University School of Medicine, One Barnes-Jewish Hospital Plaza, Suite 11300, St. Louis, MO 63110

Article Outline

The prevalence of sciatic nerve injury associated with dislocation of a hip prosthesis is <0.1%1-4. The severity of the nerve injury has been found to be related to the chronicity of the dislocation prior to joint reduction and to the location of the injury on the basis of intraneural topography2,4-6. To our knowledge, no previous patients with entwinement of the sciatic nerve around a total hip prosthesis following closed reduction of a dislocation have been reported. We describe the case of a patient in whom sciatic nerve injury occurred after repeated closed reduction of a dislocated hip prosthesis.

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Case Report

A sixty-six-year-old woman was referred to our clinic with a fourteen-month history of complete sciatic nerve palsy associated with unrelenting pain in the left lower extremity following closed reduction of a dislocated total hip prosthesis. Previously, the patient underwent a total hip arthroplasty through a posterior approach because of degenerative arthritis of the left hip. One month postoperatively, the hip prosthesis dislocated posteriorly after the patient reached across her body while sitting with the involved foot elevated in front of her. A difficult reduction had been accomplished with the patient under conscious sedation, after which she had total paralysis of all of the muscles below the knee and burning pain and paresthesias radiating from the mid-thigh to the foot. The neurological examination before the closed manipulation was normal. At the time of our evaluation, the patient noted persistent symptoms. She was dependent on narcotic analgesics and gabapentin to control the pain and often had to pack the lower extremity in ice to obtain relief at night. She was able to walk with toe-touch weight-bearing on the involved limb with use of an ankle-foot orthosis.

Physical examination revealed a complete motor deficit of all of the muscles innervated by the peroneal and tibial nerves below the knee. The strength of the quadriceps femoris was grade 5 of 5, and the strength of the biceps femoris, semitendinosus, and semimembranosus muscle group was grade 4 of 57. Sensation to light touch was absent below the knee except for a narrow strip of skin along the medial aspect of the leg, which was rated subjectively as <10% of normal. Semmes-Weinstein monofilament testing to the medial region of the thigh and to the remainder of the leg below the knee indicated an absence of protective sensibility8. A Tinel sign was not elicited with percussion over the sciatic nerve from the posterior gluteal region to the leg.

The anteroposterior radiographs of the pelvis and the lateral radiographs of the hip demonstrated well-aligned and reduced total hip prostheses bilaterally. There was no evidence of joint widening, excessive limb-lengthening, heterotopic ossification, or periprosthetic fracture. Nerve-conduction and electromyographic studies were made six weeks, four months, six months, and eleven months following nerve injury. These findings were consistent with a complete sciatic nerve injury distal to the innervation of the semitendinosus muscle that did not demonstrate signs of neurological recovery.

Operative exploration of the sciatic nerve, from its exit at the greater sciatic foramen to the level of the mid-thigh, was carried out fifteen months following the injury, with a presumptive diagnosis of a stretch injury of the sciatic nerve or an intra-articular nerve-entrapment injury. Four centimeters proximal to the superior and medial rim of the acetabulum, the nerve was found to change course abruptly and to penetrate a region of dense scar immediately posterior to the hip joint. There was a corresponding transition from a normal-appearing proximal nerve substance to a nerve that was grossly fibrotic and that thinned substantially as it coursed anteriorly, from medial to lateral, draped around the anterior and lateral aspects of the neck of the femoral prosthesis. At no point was the nerve trapped between the prosthetic femoral head and the polyethylene liner of the acetabulum. Distally, the fibrotic nerve was observed to emerge from its displaced course at the posterolateral aspect of the prosthetic neck ( Figs. 1 and 2 ). Intraoperative somatosensory-evoked-potentials monitoring demonstrated conduction proximal to the hip joint; however, there was no conduction distal to this level. Activity localized to the proximal nerve segment of the medial hamstring muscles was demonstrated following stimulation, but no other muscle response was detected. A 9-cm scarred segment of nerve was resected, and four cables of the contralateral sural nerve were grafted into the defect with use of a grouped fascicular repair.

Histological assessment of the resected segment of the nerve demonstrated complete loss of axons with marked fibrosis involving the endoneurium, perineurium, and epineurium. Loss of nerve continuity was confirmed by immunohistochemical staining.

Postoperatively, the patient reported immediate and complete resolution of the persistent burning pain in the leg and foot for a period of eight days. Since that time, however, at a recent evaluation performed twenty-five months following the nerve injury, the patient noted intermittent episodes of mild-to-moderate pain at the lateral and plantar aspects of the foot. She needed narcotic analgesics occasionally (approximately once every three days) and continued to take gabapentin, as recommended previously by a neurologist. Serial examinations demonstrated distal progression of the Tinel sign, elicited with percussion over the popliteal fossa. The patient noted that paresthesias radiated over the lateral aspect of the foot. No improvement in motor function was noted at the time of the most recent examination.

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In contrast to nerve injuries that are the direct result of hip dislocation, the neuropathy in this patient was a result of a joint reduction. The proximity of the sciatic nerve to the posterior structures of the hip places it at risk of tension injury because of the distortion of local soft-tissue structures9 and because of compression injury with circumduction motion of the femoral head during reduction maneuvers10. To our knowledge, only one case of a patient with sciatic nerve palsy following reduction of a dislocated hip prosthesis has been reported. Lazansky, in a review of postoperative complications after 501 total hip arthroplasties, reported that one patient had a partial sciatic nerve injury following manipulative reduction of a dislocated hip prosthesis1. Full neurological recovery occurred without operative intervention.

A review of the reports on nerve injury following a fracture or joint manipulation suggested that a distinction should be made between partial and complete nerve palsy following reduction of displaced fracture fragments or a dislocated joint11-23. Most authors have recommended that nerve injuries that are both partial and secondary be treated with an initial period of observation for four to six months, as 70% to 100% of the injured nerves improve spontaneously13,17,19,21,24. Conversely, substantial evidence supports early operative exploration if the neuropathy is complete and has occurred immediately after bone or joint manipulation13,14,17,19,21. The concept holds that immediate and complete nerve loss implies nerve entrapment within a fracture site or a joint11-13,15,16,18-20.

Authors of clinical reviews on the treatment of dislocation of a prosthesis following total hip arthroplasty have suggested that a limited number of attempts at closed reduction be carried out, as prolonged manipulation may place surrounding soft-tissue structures at risk of injury4,9,25. When attempts at closed reduction with use of intravenous sedation are unsuccessful, conversion to a general anesthetic is indicated, as conscious sedation may be ineffective in overcoming excessive muscular tension. If a closed reduction with the patient under general anesthesia is difficult, open exploration and reduction is indicated26-28.

In our patient, a difficult reduction of a total hip prosthesis following posterior dislocation was associated with a new onset of complete sciatic nerve palsy that was evidenced by loss of all motor function distal to the motor branch of the semitendinosus muscle. While joint asymmetry was not evident on the postreduction radiographs of our patient, previous reports have indicated that plain radiographs or other imaging modalities, such as computed tomography and magnetic resonance imaging, may be effective for assessing the adequacy of joint reduction and delineating the extent of soft-tissue interposition4,6,24,25 or nerve injury29,30. The findings of preoperative clinical examination and intraoperative nerve assessment were consistent with the histological findings of gross fibrotic changes throughout the resected nerve segment, a neuromatous mass, and a loss of nerve continuity.

The case of our patient emphasizes two factors that should be considered during closed reduction of a displaced fracture or a dislocated joint. First, during difficult or prolonged attempts at closed reduction, excessive force to the surrounding soft tissues places neurological structures at risk for injury; therefore, open reduction is indicated after a limited number of attempts at closed reduction have been carried out. Second, our findings support the conclusion made by previous authors that immediate operative exploration is indicated when complete nerve loss occurs following closed manipulation of displaced fracture fragments or a dislocated joint.

Investigation performed at the Department of Orthopaedic Surgery, Barnes-Jewish Hospital at Washington University School of Medicine, St. Louis, Missouri

The authors did not receive grants or outside funding in support of their research or preparation of this manuscript. They did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.

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