The prevalence of sciatic nerve injury following acetabular trauma and acetabular surgery has been reported to be as high as 30%1-3. This injury can result in a broad range of clinical symptoms: posterior thigh pain at the level of the sciatic notch, radicular pain along the sciatic nerve distribution with motion of the hip and knee, or weakness of muscles innervated by the sciatic nerve1,4,5. The peroneal division of the sciatic nerve is usually affected, with resultant weakness of the tibialis anterior, extensor hallucis longus, peroneus longus, and peroneus brevis6,7. These symptoms have been mistakenly interpreted as originating from the spine and have resulted in inappropriate lumbar decompression8,9.
Several factors associated with the initial acetabular injury and surgical intervention can result in sciatic neuropathy. The injury, especially when associated with a posterior hip dislocation, may result in blunt contusion, laceration, or stretch neurapraxia of the sciatic nerve1-6,10. An associated head injury may result in heterotopic ossification, which can encase and tether the sciatic nerve, restricting its excursion10-12. Certain extensile surgical exposures, such as the iliofemoral approach, are associated with a higher prevalence of heterotopic ossification13,14. Failure to provide prophylaxis against heterotopic ossification with postoperative radiation and/or indomethacin can result in a higher rate of nerve entrapment14-17. Iatrogenic injury can result from placement of posterior retractors with the hip in flexion, malreduction of the fracture, or poor placement of hardware1,5,18,19. Postoperatively, a developing hematoma may progressively compress the nerve, resulting in paralysis20,21. Months to years after surgery, capsular and muscular scarring and hardware debris or migration can irritate the sciatic nerve and present as a delayed neuropathy8,9,11,22-25.
The purpose of this retrospective study was to determine if surgical release of the sciatic nerve from scar tissue, heterotopic bone, and impinging implants is successful for the treatment of sciatic neuropathy after acetabular fractures.
Materials and Methods
Between 2000 and 2004, ten patients with a sciatic nerve injury following an acetabular fracture were treated by the senior author (D.L.H.) with sciatic nerve release from scar tissue and heterotopic bone (see Appendix). Institutional review board approval was obtained for this study. All patients were followed at regular intervals by the senior author. The average age of the patients was 42.7 years (range, fifteen to seventy-six years). There were eight male and two female patients. The average duration of neurologic symptoms prior to the nerve release was 6.5 months (range, one day to twenty-two months). The duration of follow-up after the release was twenty-six months (range, twelve to forty-two months).
In three patients (Cases 2, 3, and 4; see Appendix), the sciatic nerve deficit was a result of the original injury and was documented prior to open reduction and internal fixation of the acetabulum. All three of these patients had pain along the sciatic nerve distribution, and two had a footdrop. In four patients (Cases 5, 6, 7, and 9), the sciatic nerve injury was first noted following open reduction and internal fixation of an acetabular fracture. All of these four patients had pain in the sciatic nerve distribution; in addition, one had weakness of muscles innervated by the peroneal division (grade 3 [of 5] weakness of the extensor hallucis longus). In two patients (Cases 1 and 8), symptoms presented in a delayed manner, weeks after the acetabular fracture was sustained but prior to open reduction and internal fixation. These two patients presented for surgical treatment of the acetabular fracture and sciatic nerve release at five weeks and three months after the injury, respectively. The first patient had diminished sensation to light touch in the sciatic nerve distribution and a footdrop. The second patient had paresthesias in the distribution of the sciatic nerve and severe weakness of muscles innervated by the peroneal division (grade-1 weakness of the extensor hallucis longus). In the remaining patient (Case 10), it was unclear if the nerve injury was posttraumatic or postoperative. This patient presented with diminished sensation to light touch in the sciatic nerve distribution and a footdrop.
In addition to sciatic nerve release, five patients underwent open reduction and internal fixation of the acetabulum, three patients underwent removal of hardware and a total hip arthroplasty, and one patient underwent removal of hardware alone. Preoperative diagnoses included an acute acetabular fracture requiring open reduction and internal fixation in three patients; a case in which the nerve injury was not diagnosed until five weeks after the patient sustained the acetabular fracture (the patient presented to us late); acetabular malunion in three patients, two of whom also had posttraumatic arthritis; acetabular nonunion and posttraumatic arthritis in one patient; impinging hardware with extensive heterotopic ossification after acetabular open reduction and internal fixation in one patient; and extensive heterotopic ossification after acetabular open reduction and internal fixation in one patient. A Kocher-Langenbeck surgical approach was used in eight patients; a triradiate approach, in one patient; and a combined Kocher-Langenbeck and ilioinguinal approach, in one patient.
The types of acetabular fractures included posterior column/posterior wall (one), posterior wall (two), transverse (one), T-type (one), both-column (two), transverse-posterior wall (two), and anterior column/posterior hemitransverse (one). The mechanisms of the original injury included a fall (two patients), a motor-vehicle accident (two), a motorcycle accident (one), a pedestrian struck by a motor vehicle (three), a tractor accident (one), and a snowboarding accident (one). Five patients had undergone one prior open reduction and internal fixation of the acetabulum. No patient had an associated pelvic ring fracture.
Eight patients had electromyography before the sciatic nerve release, and four of them had findings suggestive of sciatic neuropathy. One of them demonstrated neuropathy involving the peroneal division of the sciatic nerve, one demonstrated neuropathy of the tibial division of the sciatic nerve, and two demonstrated denervation of both divisions of the sciatic nerve. The remaining electromyographic studies were nondiagnostic. Preoperative computed tomography was performed for six patients to delineate the acetabular fracture pattern. One computed tomography scan demonstrated heterotopic ossification under the abductors, one demonstrated an acetabular nonunion, and one demonstrated degenerative arthritis of the hip joint. Eight patients had preoperative magnetic resonance imaging, and four of these scans demonstrated abnormal findings related to the sciatic nerve: two demonstrated heterotopic bone encasing the sciatic nerve, one demonstrated scarring around the sciatic nerve, and one demonstrated an intra-articular screw touching the sciatic nerve.
The Kocher-Langenbeck approach was used to gain access to the sciatic nerve in all patients. The procedure was performed with use of intraoperative spontaneous electromyography and/or intraoperative somatosensory evoked potential monitoring2,26,27. A skin incision was made extending from 5 cm distal to the posterior superior iliac spine to the greater trochanter and then along the femoral shaft distally. Subcutaneous tissue and then the iliotibial band and the fascia over the gluteus maximus were divided in line with the skin incision. The trochanteric bursa was carefully dissected off the external rotators. In most cases, the sciatic nerve was identified distally by locating the tendon of the quadratus femoris and following this posteriorly until fibers of the sciatic nerve were identified. A combination of microdissecting scissors and osteotomes was used to free the sciatic nerve from scar tissue and encasing heterotopic bone. All heterotopic bone entrapping the nerve was removed. This procedure requires careful dissection and takes a considerable amount of time to avoid further injury to the sciatic nerve. The nerve decompression extended from below the gluteus maximus insertion on the femur to the greater sciatic notch. Decompression was performed until the nerve could be freely mobilized within this area. No attempt was made to explore the nerve proximal to the greater sciatic notch. Abnormal somatosensory evoked potential or electromyographic responses prompted a brief halt in the dissection, with reassessment of limb positioning and extension of the hip and flexion of the knee as necessary. Dissection resumed when somatosensory evoked potential and electromyographic activity returned to normal. Acetabular open reduction and internal fixation or total hip arthroplasty was then performed.
Postoperatively, the patients walked with toe-touch weight-bearing for three months. Prophylaxis against heterotopic ossification included indomethacin alone or in combination with irradiation.
Sensory symptoms included radicular pain or paresthesias (seven patients) and decreased sensation (three patients). All patients with sensory symptoms obtained some degree of relief following sciatic nerve release (Table I). Of the seven patients with radicular pain or paresthesias, four had complete relief of symptoms and the remainder had partial relief. Of the three patients with diminished sensation, one had complete improvement and two had partial improvement. Motor symptoms included weakness without a footdrop (two patients) and a footdrop (five patients). None of the patients with motor symptoms demonstrated complete resolution of those symptoms following decompression (Table I). Both of those with motor weakness and no footdrop had partial improvement in motor function. Three of the five patients with a footdrop demonstrated no improvement in motor function, and the remaining two had only partial improvement. No patient had worse neurologic function after the nerve decompression.
Sciatic nerve entrapment was observed intraoperatively in all patients. Sites of nerve entrapment included the obturator and piriformis tendons (one patient), scar tissue over the quadratus femoris muscle (one patient), hemorrhagic tissue over the quadratus femoris muscle (one patient), heterotopic bone and scar tissue at the acetabular fracture site (two patients), heterotopic bone under the abductors (one patient), scar tissue at the level of the lesser trochanter (one patient), and global scar tissue from the greater sciatic notch to the ischium (three patients).
Preoperatively, hip flexion averaged 82° (range, 60° to 90°); internal rotation, 3° (range, 0° to 10°); external rotation, 9° (range, 0° to 20°); abduction, 21° (range, 10° to 35°); and adduction, 13° (range, 5° to 20°). Postoperatively, hip flexion averaged 98° (range, 90° to 120°); internal rotation, 11° (range, 10° to 30°); external rotation, 25° (range, 10° to 40°); abduction, 32° (range, 20° to 40°); and adduction, 20° (range, 10° to 30°). One patient, a twenty-one-year-old woman (Case 5; see Appendix) who had had a preoperative sciatic neuropathy, underwent a revision total hip arthroplasty, because of aseptic loosening, thirty-nine months after a primary total hip arthroplasty. No further release of the sciatic nerve was performed at the time of the revision arthroplasty. There was one deep venous thrombosis, which was treated with long-term Coumadin (warfarin) therapy.
All patients were in general satisfied with the result of the procedure and stated that they would undergo such surgery again under similar circumstances. However, nine of the ten patients in our series underwent procedures in addition to the sciatic nerve release, including open reduction and internal fixation of the acetabulum and total hip arthroplasty, so it is difficult to assess how much of this patient satisfaction was related to the nerve release and sensory improvement and how much was related to improved mobility and function after successful hip reconstruction.
There are only a few reports in the literature describing sciatic neuropathy following severe acetabular trauma. In these reports, the neuropathy presented in a delayed fashion, concurrent with the development of heterotopic bone around the sciatic nerve10,28,29. Kleiman et al. reported a case in which sciatic nerve pain and weakness of ankle dorsiflexion developed 4.5 months after open reduction and internal fixation of a posterior fracture-dislocation of the hip28. Sciatic neurolysis with excision of heterotopic bone resulted in normal sensation but no improvement in motor function28. Thakkar and Porter reported on a patient in whom pain and paresthesias along the medial side of the leg and a footdrop developed after a fall on the buttock three years after open reduction of a posterior hip dislocation10. Surgical exploration revealed heterotopic bone encasing the sciatic nerve; surgical release of the nerve decreased sensory symptoms, but the footdrop remained unchanged at the time of follow-up, two years postoperatively. Hirasawa et al. reported a case in which sciatic neuropathy with paresthesias and motor loss developed progressively over four months following open reduction of a posterior hip dislocation29. At that point, sciatic nerve release was performed to free the nerve from encasing heterotopic bone. Sensory function was almost completely restored and motor function improved to a grade of 4 (of 5) at fifteen months after the release. Taken together, these case reports seem to suggest that, at least in cases of chronic nerve entrapment such as heterotopic bone encasement, lost motor function is less likely to be recovered fully following sciatic nerve decompression, which is consistent with our observations.
Surgical releases of the sciatic nerve have also been reported for treatment of complications related to implants following total hip arthroplasty8,9,23-25. Uchio et al. reported a case of bilateral sciatic neuropathy occurring four and six years following bilateral cementless total hip arthroplasty23. A hypertrophic posterior aspect of the hip capsule and a tense piriformis muscle were found intraoperatively. The neuropathy resolved after sectioning of each piriformis muscle and release of both sciatic nerves. Stiehl and Stewart reported a case of delayed sciatic neuropathy after loosening of a pelvic plate following complex acetabular reconstruction in hip arthroplasty25. Progressive neurologic signs of sciatic nerve compression developed six months following reconstruction of a pelvic discontinuity. Sciatic nerve exploration at one year identified a screw impinging on the nerve. The symptoms decreased substantially following hardware removal and sciatic nerve release. Isiklar et al. reported a case of delayed sciatic neuropathy resulting from intrapelvic migration of an acetabular cup9. This patient had undergone a laminectomy, without relief of the symptoms, before the cup migration was noted to be the problem. Removal of the protruding cup and cement and acetabular revision resulted in complete resolution of the sciatic neuropathy. Intraoperatively, the nerve was noted to be flattened at the greater sciatic notch.
The question arises of whether surgical release of the sciatic nerve from scar tissue and heterotopic bone improves neurologic outcomes compared with the natural course of this disorder. Reports on the natural history of posttraumatic or postoperative sciatic nerve palsies have provided conflicting results. Letournel and Judet reported on thirty-four sciatic nerve injuries that had occurred after surgical treatment of 569 acetabular fractures (a rate of 6.0%)19. The sciatic nerve injuries were noted immediately postoperatively, but it was unclear if some of the deficits simply had not been detected preoperatively. Eighteen of these palsies involved the peroneal division. One was a complete lesion secondary to iatrogenic intraoperative nerve transection, and the remainder were patchy lesions or pure sensory lesions. Nine palsies resolved fully, and twelve decreased substantially. Two-thirds of the patients had no sequelae. The recovery period extended up to three years.
Other surgeons have also reported favorable natural history. Epstein noted that 60% of thirty-eight sciatic nerve injuries associated with posterior fracture-dislocation of the hip resolved fully within three years after the injury30. Schmeling et al. observed that 100% of severe postoperative sciatic nerve palsies involving the peroneal division resolved fully31. Similarly, Tile noted that 75% of posttraumatic sciatic nerve injuries and 100% of postoperative sciatic nerve injuries resolved partially or fully32.
Fassler et al. reported on fourteen patients with a displaced acetabular fracture and a sciatic nerve injury1. Eleven injuries were posttraumatic, and three were iatrogenic. The authors classified the injuries as mild (grade-3 or 4 [of 5] motor weakness or predominantly sensory abnormalities) or severe (grade-0, 1, or 2 motor weakness with a marked decrease or absence of sensation). They also divided injuries according to whether there was involvement of the peroneal or tibial division. They observed that patients with a mild peroneal nerve, mild tibial nerve, or severe tibial nerve injury had substantial recovery at two years. When the peroneal injury was severe, however, recovery was poor; only three of ten patients with peroneal nerve injury had a satisfactory result, and one of these patients was seventeen years old. There were seven footdrops, five of which did not resolve.
Taken together, the conflicting results from the above studies suggest that there are several confounding factors, including the anatomic location of the lesion (peroneal or tibial division), severity of the trauma to the nerve (neurapraxia, axonotmesis, or neurotmesis), impairment of sensory or motor function, timing (posttraumatic or iatrogenic), chronicity of the lesion, and patient age, that determine nerve recovery.
Our study had several limitations. It was a retrospective analysis of a small number of symptomatic patients. There was no control group (i.e., no similar cohort treated without nerve release). Thus, it is unclear if the surgical release improved the neurologic outcomes of these patients compared with the natural history of posttraumatic or postoperative sciatic nerve palsies. While our findings suggest that motor function is less likely than sensory function to return after nerve release, the average duration of follow-up in our series was less than three years. As the peroneal division of the sciatic nerve has been reported to exhibit recovery for up to three years after injury19, it is possible that some of the footdrops in our series will yet improve. Certainly, a larger randomized study categorizing patients on the basis of potential confounding factors such as age, location of the lesion, nature of the nerve injury, impairment of sensory or motor function, degree of involvement, and timing of decompression will allow a more objective assessment of the benefits of surgical release.
A potential diagnostic problem encountered during the examination of a patient with an acetabular fracture and a sciatic nerve injury is the identification of the contribution of preexisting lumbosacral degenerative disease or pelvic or spine trauma to the neurologic findings. While there are reports in the literature of inappropriate lumbar decompression for extraspinal sciatic nerve entrapment8,9, the reverse—sciatic nerve decompression in the pelvis when the neurologic symptoms are caused predominantly by nerve root compression in the lumbar spine—may also occur. While a careful physical examination, with assessment for localized tenderness, step-off, and myelopathy, was performed on the patients in this series, the lumbar spine was not routinely imaged with computed tomography, magnetic resonance imaging, or computed tomography-myelography to objectively quantify lumbar degenerative disease. However, the absence of substantial spinal trauma or pelvic ring disruption in our patients at the time of the acetabular fracture and the temporal relationship between the onset of sciatic nerve-related symptoms and the acetabular trauma or reconstructive surgery suggest that the etiology of the neurologic symptoms was more likely related to the sciatic nerve injury than to lumbosacral nerve-root injury. Nevertheless, prospective studies in which cases of spinal trauma and spinal stenosis either are excluded or are randomized as confounding variables will allow a more scientific evaluation of the role of surgical release on nerve recovery.
Our experience indicates that careful release of the sciatic nerve from the greater sciatic notch to below the insertion of the gluteus maximus tendon during reconstructive acetabular surgery results in a marked decrease in preoperative sensory sciatic neuropathic symptoms, including radicular pain, paresthesias, and diminished sensation.
We did not explore the sciatic nerve proximal to the greater sciatic notch because of the difficulty with accessing the intrapelvic portion of the nerve. Compression of the sciatic nerve within the pelvis may compromise the result achieved by decompression of the extrapelvic portion of the nerve. Osteotomy of the greater sciatic notch can improve access to the nerve, but it is a dangerous procedure and can result in further sciatic nerve or superior gluteal vessel trauma. While the majority of patients with motor symptoms demonstrated improvement, footdrop was less likely to completely resolve after nerve release. None of the patients in our series had worse neurologic function following nerve decompression. However, rigorous determination of whether sciatic nerve release improves neurologic outcome compared with the natural history of sciatic nerve injuries will require prospective, randomized, controlled studies.
A table showing clinical details on all study patients is available with the electronic versions of this article, on our web site at jbjs.org (go to the article citation and click on “Supplementary Material”) and on our quarterly CD-ROM (call our subscription department, at 781-449-9780, to order the CD-ROM). ▪
Disclosure: The authors did not receive any outside funding or grants in support of their research for or preparation of this work. Neither they nor a member of their immediate families received 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, division, center, clinical practice, or other charitable or nonprofit organization with which the authors, or a member of their immediate families, are affiliated or associated.
Investigation performed at The Hospital for Special Surgery, New York, NY
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