October 02, 2020
4 min read

My Patient Has a Foot-Drop After Surgery. What Should I Do?

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Foot drop—the inability to dorsiflex the toes and ankle—is the most common clinical presentation of nerve injury after hip arthroplasty and represents failure of the peroneal division of the sciatic nerve. “Flail foot” is a rare devastating complication that results from complete sciatic nerve lesion with loss of both dorsiflexion and plantarflexion. Sensory loss may involve the entire foot and can lead to reflex sympathetic dystrophy-like changes, pressure sores, infections, and possibly amputations.

The etiology of nerve injury is multifactorial. When measured by electromyography (EMG), 70% of patients have subclinical sciatic nerve damage after total hip arthroplasty (THA). Over 50% of palsy patients have a pre-existing peripheral neuropathy.1 Patient populations at increased risk include patients with revisions, fibrotic ankylosis after joint sepsis, developmental dysplasia, limb lengthening, post-traumatic arthritis, cementless femoral implant fixation, and those with posterior approaches.2-4 Fortunately, the prevalence of clinically significant sciatic nerve palsy after hip arthroplasty is only about 0.1% to 0.2%.2 This rarity provides few evidence-based treatment recommendations. Timely diagnosis and early discussion of possible etiologies and outcomes increases trust in the physician, enhances patient satisfaction, and creates a more positive emotional response in the patient. It also may help minimize potential litigation. Describing the difference between loss of nerve function versus loss of nerve continuity provides a framework for understanding all possible outcomes.5

Some recovery of motor function in the first week or 2 after surgery indicates normal or near normal function is likely in longer term follow-up. Complete motor palsy, or complete motor and sensor palsy, indicates a poor prognosis. The largest series of complete nerve palsies noted approximately one-third recovered fully, one-third had partial recovery, and one third had no recovery. Maximal recovery averaged 1 to 2 years.2 The worst prognosis is found in palsy patients with dysesthesias that develop into complex regional pain syndrome (CRPS). Because most palsy patients enjoy partial or complete recovery, the surgeon should remain hopeful for the patient and the family. The physician should create a specific, proactive rehabilitation plan of care and recruit support of the patient (Figure 39-1).

Supportive care protocol to address clinical problems related to sciatic nerve palsy after total hip arthroplasty

Figure 39-1. Supportive care protocol to address clinical problems related to sciatic nerve palsy after total hip arthroplasty

When foot drop is encountered after THA, avoiding positions of hip flexion with knee extension may help reduce tension on the nerve. Perform a thorough exam and identify the extent of motor and sensory involvement as well as any skin hypersensitivity. Carefully review postoperative radiographs. Continue postoperative rehabilitation as normally as possible. Reviewing the many potential sources of palsy may help guide specific treatment (Table 39-1); however, the etiology is unknown in more than half of cases. When no cause is identified, supportive care of specific deficits is warranted. Motor deficits causing foot drop are best managed with an ankle-foot orthoses (AFO) to allow clearance during the swing phase of gait and to prevent late equinus deformity. Physical therapy is helpful to instruct patients on a home program of ankle dorsiflexor strengthening, plantarflexor stretching to prevent joint contractures, and skin desensitization in cases of causalgia. Sensory deficits demand diligence on the part of the patient to prevent heel ulcers and inadvertent foot trauma. Consultation with a skin care nurse as in patients with diabetic neuropathy may be worthwhile. Patients with dysesthesias and causalgic pain may benefit from pain management consultation and are often helped with gabapentin, antidepressants, and sympathetic nerve blocks.

Certain situations may encourage more immediate management. In the rare case where an obvious mechanical source of compression is identified, it should be removed. Postoperative radiographs can show unexpected posteriorly protruded cement, bony fragments, or proud screws, and exploration may be considered. If postoperative radiographs document excessive lengthening, consider shortening procedures.

A delayed onset of progressive neurologic symptoms after a normal postoperative check should alert the physician to consider correction of coagulation status and evacuation of a subfascial hematoma. Decreasing neurologic function and unexpected or increasing leg pain with significant buttock or thigh swelling suggest a hematoma in the region of the sciatic nerve. Cases recognized early, and promptly evacuated, show earlier and more complete recovery.6

Fortunately, serial examinations over time frequently show some recovery of nerve function. Electromyograms and nerve conduction velocity measurements 6 to 8 weeks after diagnosis provide a more objective measure of the level of injury, the degree of injury, and evidence of recovery of function. In patients whose palsy has not cleared, this also provides an opportunity to document and reinforce compliance with physical therapy, skin nurse, and pain management recommendations. Patients who had symptoms of stenosis prior to arthroplasty and have no recovery of their foot drop by 3 months may benefit from correcting coexisting spinal stenosis.7 If EMG shows no signs of nerve regeneration by 3 months, consider referral for late surgical exploration. Neurolysis, direct suture repair, and cable grafting techniques may have limited success if performed within 7 months after injury.8 Since maximal recovery of nerve palsy may take years, the late definitive reconstructive salvage procedures of tendon transfers (“bridle transfer”) or ankle fusions should be deferred at least 18 months.


As with all complications, prevention is preferable. Careful attention to detail, gentle handling of soft tissues, awareness of the anatomy, and experience are rewarded with fewer complications (Table 39-2).



1.  Dellon AL. Postarthroplasty “palsy” and systemic neuropathy: a peripheral-nerve management algorithm. Ann Plast Surg. 2005;55(6):638-642.

2.  Farrell CM, Springer BD, Haidukewych GJ, Morrey BF. Motor nerve palsy following primary total hip arthroplasty. J Bone Joint Surg. 2005;87(12):2619-2625.

3.  Pekkarinen J, Alho A, Puusa A, Paavilainen T. Recovery of sciatic nerve injuries in association with total hip arthroplasty in 27 patients. J Arthroplasty. 1999;14(3):305-311.

4.  Schmalzried TP, Amstutz HC, Dorey FJ. Nerve palsy associated with total hip replacement: risk factors and prognosis. J Bone Joint Surg Am. 1991;73(7):1074-1080.

5.  DeHart MM, Riley LH Jr. Nerve injuries in total hip arthroplasty. J Am Acad Orthop Surg. 1999;7:101-111.

6.  Butt AJ, McCarthy T, Kelly IP, Glynn T, McCoy G. Sciatic nerve palsy secondary to postoperative haematoma in primary total hip replacement. J Bone Joint Surg. 2005;87-B(11):1465-1467.

7.  Pritchett JW. Lumbar decompression to treat foot drop after hip arthroplasty. Clin Orthop Relat Res. 1994;303: 173-177.

8.  Kim DH, Murovic JA, Tiel R, Kline DG. Management and outcomes in 353 surgically treated sciatic nerve lesions. J Neurosurg. 2004;101(1):8-17.