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Anesthesia & Analgesia:
doi: 10.1213/01.ANE.0000080203.58659.83
Regional Anesthesia: Case Report

Sciatic Nerve Palsy After Total Hip Arthroplasty in a Patient Receiving Continuous Lumbar Plexus Block

Ben-David, Bruce MD; Joshi, Rama MD; Chelly, Jacques E. MD, PhD, MBA

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Author Information

Department of Anesthesiology, University of Pittsburgh Medical Centers, Shadyside Hospital, Pittsburgh, Pennsylvania

Accepted for publication May 16, 2003.

Address correspondence and reprint requests to Bruce Ben-David, MD, Department of Anesthesiology, University of Pittsburgh Medical Centers, Shadyside Hospital, 5230 Centre Ave., Pittsburgh, PA 15232. Address e-mail to b.bendavid@verizon.net.

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Abstract

We report a case of late-onset postoperative sciatic palsy after total hip arthroplasty in a 30-yr-old man with congenital hip dysplasia. The patient was receiving continuous lumbar plexus blockade and had received low-molecular-weight heparin 3 h before the onset of symptoms. Anatomic distinction between the nerve block and the sciatic palsy facilitated rapid diagnosis and treatment of a periarticular hematoma, with resulting neurologic recovery. This case illustrates that, with the expanded role of regional anesthetic techniques in acute pain management, the finding of a new postoperative deficit must be jointly investigated by both anesthesiologists and surgeons. Timely and open communication between services is critical because rapid intervention may be essential to achieving full recovery of an affected nerve.

In recent years there has been increasing interest in the use of peripheral neural blockade (PNB), both as a primary anesthetic and as a postoperative analgesic technique. Persuasive evidence has accumulated as to the benefits that accrue to patients with these nerve blocks (1,2). However, there is the potential for complication after PNB, in particular, the risk of nerve injury (3). Nerve injuries may, however, also arise from, or be contributed to, by a variety of other causes, such as surgical complications (intraoperative and postoperative), patient disease (e.g., carpal tunnel or sulcus ulnaris syndrome, vascular disease, or diabetes), medications (e.g., cisplatin), patient positioning, or postoperative compression from dressings or compartment syndrome. Issues of diagnosis, acute and long-term management, and even of medicolegal ramifications are clouded by this potpourri of causation. We present here a case of postoperative sciatic nerve palsy after hip arthroplasty in a patient receiving continuous lumbar plexus block for postoperative analgesia.

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Case Report

A 30-yr-old man with congenital hip dysplasia and subluxation with secondary degenerative joint disease presented for left total hip arthroplasty. His medical history was significant for hypertension, scoliosis, nephrolithiasis, and neurofibromatosis. His surgical history included spinal fusion for scoliosis and renal calculi removal. He had no history of neurologic dysfunction or injury, no peripheral neuropathy related to his neurofibromatosis, and no history of metabolic or coagulation abnormality. His preoperative neurologic examination was normal. In the preoperative area, an IV infusion of lactated Ringer’s solution was begun, and automated blood pressure and pulse oximetry monitors were placed. After mild sedation with midazolam 2 mg IV, a psoas compartment/lumbar plexus block was performed, followed by the placement of a perineural catheter according to the following technique. The patient was placed in the right lateral decubitus position, and the landmarks for a psoas compartment/lumbar plexus block were drawn according to the description of Winnie et al. (4). The area was prepared with antiseptic solution and draped, and 3 mL of 1% lidocaine was injected into the skin. The lumbar plexus was identified with peripheral nerve stimulation (Stimuplex HNS 11; B. Braun, Melsungen, Germany) by using a 10-cm insulated Tuohy introducer needle (Contiplex; B. Braun). After positioning of the needle (depth of 8 cm from the skin) such that there was ipsilateral quadriceps contraction at 0.5 mA stimulation and negative aspiration for blood, 30 mL of 0.5% ropivacaine was injected in 5-mL increments. A 20-gauge catheter was inserted (depth of 13 cm at the skin) for postoperative continuous local anesthetic infusion and was taped into place. Paresthesiae were not elicited during the procedure, which proceeded easily and without significant patient discomfort.

Because of the patient’s history of congenital dysplasia and its association with an increased incidence of sciatic nerve injury during total hip arthroplasty, the surgery was scheduled to be performed under continuous somatosensory evoked potential monitoring of the sciatic nerve. Blockade of the sacral plexus would have interfered with this monitoring and was therefore not performed.

The patient underwent an uneventful total hip arthroplasty under general anesthesia. There were no intraoperative changes in the evoked potentials, and neurologic examination was normal in the recovery room, with the exception of decreased sensation in the distribution of the lumbar plexus. In the recovery room after surgery, his pain was minimal (0–2 out of 10 on a verbal pain analog scale), and a continuous infusion of 0.2% ropivacaine at 8 mL/h into the lumbar plexus catheter was begun. The first dose of enoxaparin 25 mg was given at 8:00 am the morning after surgery. According to our standard protocol, before discharge from the recovery room the patient was also given access to morphine patient-controlled analgesia (PCA). Because the patient’s overnight use of the PCA was minimal, this was discontinued at 10:00 am the following morning and was replaced by oral oxycodone as needed. At approximately 11:00 am, however, he started to complain of severe pain in the hip, and the PCA was reinstated. By noon, the patient complained of diminished sensory and motor function below the left knee, and this progressed to a complete loss of sensory and motor function over the next 30 min. Examination by the acute pain team verified profound loss of sensory and motor function in the distribution of both the tibial and common peroneal nerves. There was no pain on passive motion of the ankle or knee and no tenderness of the calf or posterior knee or thigh. There was diminished but present sensation over obturator, femoral, and lateral femoral cutaneous nerve distributions. Sensation over the ipsilateral abdomen was normal. The right leg had completely normal sensory and motor function. There was no visible swelling or discoloration of the left leg.

The lumbar plexus infusion was stopped to aid in further neurologic evaluation and to eliminate the very remote possibility of its involvement. The orthopedic surgical team was immediately consulted, was assured that there was little likelihood that this change was related to the nerve block, and was encouraged to consider an alternative explanation for the sudden loss of sciatic nerve function. An emergency computed tomography scan requested by the orthopedic surgeon revealed a hematoma in the hip with compression of the sciatic nerve. At 6:30 pm, the patient returned to the operating room, where a 300-mL hematoma was evacuated from the hip. After this operation, the patient was noted to have marked improvement in both sensory and motor function, and at 48 h he had nearly complete resolution of his sensory and motor deficits, with only mild weakness in his ability to fan out his toes.

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Discussion

With the expanded role of regional analgesic techniques for acute pain management, the finding of a new neurologic deficit in the postoperative period must be jointly investigated by anesthesiologists and surgeons. As illustrated by this case, timely and open communication between services is critical because rapid intervention may be essential to achieving full recovery of an affected nerve. It is all too easy for one service to reflexively dismisses a complication as a result of another service’s interventions. This is unfortunate, because it can delay proper management and possibly adversely affect the outcome. Of the several issues raised by this case, certainly foremost among them are the importance of understanding potential complications, not only of the analgesic technique, but also of the surgery, and the importance of communication between services.

The first sign of a developing problem in this patient was the sudden onset of severe pain in the operative hip despite a previously effective lumbar plexus block. Our first assumption was that this was a technical failure of the nerve block, perhaps related to the displacement of the perineural catheter, pump dysfunction, interruption of the infusion because of an empty bag, or disconnection of the catheter. However, examination revealed the catheter infusing normally, with no evidence of displacement and with decreased sensation to cold over the obturator, femoral, and lateral femoral distributions. Diagnosis was aided by the presence of a sciatic nerve deficit, which strongly suggested that the pain was of sciatic or gluteal nerve origin. Although the lumbar plexus ropivacaine infusion was stopped to aid in further neurologic evaluation, it was nevertheless believed to be extremely unlikely that it could account for this change. A surgical complication, such as dislocation of the prosthesis or an expanding hematoma, was considered the likely etiology, and appropriate action was immediately taken.

The reported incidence of nerve injury after total hip arthroplasty ranges from 0.7% to 3.0% for primary surgery and 2.9% to 7.6% for revision surgery (5). Schmalzried et al. (6) reviewed 3126 consecutive total hip replacements and found an overall 1.7% incidence of nerve injury—1.3% in primary arthroplasties, 3.2% in revisions, and 5.2% in cases of congenital dislocation or dysplasia. Between 80% and 90% of these nerve injuries are to the sciatic nerve, followed in frequency by femoral nerve injury (7) (estimated incidence of 0.1%–0.4%), with isolated case reports of obturator (8) or gluteal (9) nerve injury. Possible etiologies of intraoperative injury include direct trauma, retractor pressure or traction, stretch and/or compression of the nerve secondary to leg positioning, stretch due to excessive lengthening of the extremity, and local pressure or heat injury from extruded cement (5,6,10). Particularly disconcerting is a prospective study using electromyography before and after hip surgery, which showed a 70% incidence of subclinical nerve damage (11). Delayed postoperative nerve injury, as occurred in our case, is less likely but can be due to hematoma, cement fragment dispersion, excessively tight binding to an abduction pillow, dislocation and displacement of the prosthesis, compression over an osseous or prosthetic prominence, or migration of a trochanteric wire.

Given the relatively frequent risk of nerve injury in cases of congenital dysplasia, it is routine in many institutions to use, as we did, intraoperative neurophysiologic monitoring (5,12,13). Nevertheless, neurophysiologic monitoring does not carry over into the postoperative period and must be replaced by vigilance. Certainly vigilance is aided when the analgesic technique does not obscure clinical assessment. Our case demonstrates the value of using PNB isolated to a limited distribution. Given the great unlikelihood of causing dense unilateral sciatic blockade with the lumbar plexus infusion, the diagnosis and management of this patient was neither obscured nor delayed. The same principle of “isolated blockade” holds true with regard to the degree of blockade. Our goal is to maintain an analgesic sensory block, and we will routinely hold a continuous PNB infusion if more than a modest degree of motor blockade develops.

In addition to the risk of nerve injury from the hip surgery, PNBs also carry a risk of nerve damage. This is often expressed clinically as persistent dysesthesia (3,14,15). Although the incidence of these persistent dysesthesias 10 days after surgery has been reported to be as frequent as 14%(15), most reports suggest a much less frequent incidence, in the range of 2%–5%(3,14). Fortunately, in most cases, symptoms are mild, patients recover relatively quickly, and long-term complications are rare (3). However, consideration should be given to this issue when deciding on the use of a PNB for postoperative analgesia. In a case such as this, in which there was a substantial risk of operative sciatic nerve injury, it may have been wise to avoid sacral plexus blockade, even if we had not planned intraoperative evoked potential monitoring. Further, with the frequent incidence of electromyography-evidenced subclinical sciatic injury during hip surgery, there is the theoretical possibility that even subclinical injury to the nerve proximally as a result of sacral plexus block might predispose to distal injury. This concept of the “double crush syndrome” contends that axons injured at one site are far more susceptible to damage distally (16,17). Therefore, it is especially important to ask whether the addition of this block to a lumbar plexus block significantly contributes to postoperative analgesia after hip arthroplasty. This study is continuing.

In conclusion, we present a case of postoperative onset of sciatic palsy after total hip arthroplasty in a patient receiving continuous lumbar plexus blockade. The case illustrates the importance of communication between services, the value of selected or “isolated” neural blockade, and considerations in the choice of nerve block.

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References

1. Singelyn FJ, Deyaert M, Joris D, et al. Effects of intravenous patient-controlled analgesia with morphine, continuous epidural analgesia, and continuous three-in-one block on postoperative pain and knee rehabilitation after unilateral total knee arthroplasty. Anesth Analg 1998; 87: 88–92.

2. Chelly JE, Greger J, Gebhard R, et al. Continuous femoral blocks improve recovery and outcome of patients undergoing total knee arthroplasty. J Arthroplasty 2001; 16: 436–45.

3. Ben-David B. Complications of peripheral blockade. Anesthesiol Clin North Am 2002; 20: 457–69.

4. Winnie AP, Ramamurthy S, Durrani Z, Radonjic R. Plexus blocks for lower extremity surgery. Anesthesiol Rev 1974; 1: 11–6.

5. Stone RG, Weeks LE, Hajdu M, Stinchfield FE. Evaluation of sciatic nerve compromise during total hip arthroplasty. Clin Orthop 1985; 201: 26–31.

6. Schmalzried TP, Amstutz HC, Dorey FJ. Nerve palsy associated with total hip replacement: risk factors and prognosis. J Bone Joint Surg Am 1991; 73: 1074–80.

7. Simmons C Jr, Izant TH, Rothman RH, et al. Femoral neuropathy following total hip arthroplasty: anatomic study, case reports, and literature review. J Arthroplasty 1991; 6 (Suppl): 57–66.

8. Siliski JM, Scott RD. Obturator-nerve palsy resulting from intrapelvic extrusion of cement during total hip replacement: report of four cases. J Bone Joint Surg Am 1985; 67: 1225–8.

9. Donofrio PD, Bird SJ, Assimos DG, Mathes DD. Iatrogenic superior gluteal mononeuropathy. Muscle Nerve 1998; 21: 1794–6.

10. Edwards BN, Tullos HS, Noble PC. Contributory factors and etiology of sciatic nerve palsy in total hip arthroplasty. Clin Orthop 1987; 218: 136–41.

11. Weber ER, Daube JR, Coventry MB. Peripheral neuropathies associated with total hip arthroplasty. J Bone Joint Surg Am 1976; 58: 66–9.

12. Kennedy WF, Byrne TF, Majid HA, Pavlak LL. Sciatic nerve monitoring during revision total hip arthroplasty. Clin Orthop 1991; 264: 223–7.

13. Brown DM, McGinnis WC, Mesghali H. Neurophysiologic intraoperative monitoring during revision total hip arthroplasty. J Bone Joint Surg Am 2002; 84 (Suppl 2): 56–61.

14. Fanelli G, Casati A, Garancini P, Torri G. Nerve stimulator and multiple injection technique for upper and lower limb blockade: failure rate, patient acceptance, and neurologic complications. Anesth Analg 1999; 88: 847–52.

15. Borgeat A, Ekatodramis G, Kalberer F, Benz C. Acute and nonacute complications associated with interscalene block and shoulder surgery: a prospective study. Anesthesiology 2001; 95: 875–80.

16. Osterman AL. The double crush syndrome. Orthop Clin North Am 1988; 19: 147–55.

17. Upton AR, McComas AJ. The double crush in nerve entrapment syndromes. Lancet 1973; 18; 2: 359–62.

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