Total hip arthroplasty (THA) remains one of the most successful orthopaedic procedures due to its predictable relief of pain and improvement in patient function. For these reasons, coupled with the growing population of elderly patients, the demand for THA is expected to dramatically increase in the near future. Therefore, an understanding of the surgical complications of this procedure is paramount. While neurovascular complications in THA are relatively uncommon, they can be potentially devastating when they occur. The close proximity of major nerves and vessels encountered in the various surgical approaches to the hip make a thorough knowledge of patient risk factors, conventional and aberrant anatomy, and surgical technique an absolute requirement to perform the operation safely. Prevention is the primary tenet of neurovascular injury; however, when injuries do occur, understanding how to properly diagnose and treat these injuries is of utmost importance.
The purpose of this chapter is to review the neurovascular injuries most commonly associated with THA, including relevant clinical anatomy, diagnosis, and treatment.
The incidence of nerve injury in primary THA ranges in the literature from 0.17% to 3.7%, and has been reported to be as high as 7% for revisions. The most common nerves injured are, in order, the sciatic, femoral, and superior gluteal nerves , ( Fig. 20.1 ). The most common identifiable cause of nerve injury is compression by a retractor, but neurologic insult from direct surgical trauma, traction, extremity positioning, limb lengthening, ischemia, and thermal injury can also occur.
The sciatic nerve is the most commonly injured nerve following THA. The sciatic nerve leaves the pelvis as two distinct nerves in 30% of the specimens studied by Sunderland et al. When this occurs, the tibial division commonly enters the gluteal region distal to the piriformis, and the peroneal division enters the gluteal region proximal or through the piriformis. The peroneal division is the more lateral division of the nerve; for this reason, it is more prone to injury. This anatomic relationship accounts for the high rate of isolated peroneal palsies and low rate of isolated tibial palsies. Weber et al. reported on electromyography findings after THA, finding evidence of sciatic nerve injury in up to 70% of extremities. They concluded that although frank neuropathy may be rare, subclinical injury to the sciatic nerve is common, further emphasizing the importance of retractor placement and limb position to minimize nerve insult.
Reports suggest that of patients 50 years old and younger undergoing THA, 20% are related to arthritis from developmental dysplasia of the hip (DDH). DDH presents a unique set of anatomic challenges during THA, especially with regard to the sciatic nerve. Rates of sciatic nerve palsy have been reported to be as high as 13% following THA in DDH patients, as the nerve is often chronically shortened. , For patients with advanced DDH, changes to the hip center of rotation can significantly lengthen the operative limb, and lengthening greater than 3 to 4 cm has been shown to be a risk factor for sciatic nerve injury due to excessive nerve stretch. In these cases, a shortening subtrochanteric osteotomy is often employed.
Femoral nerve palsy is a relatively uncommon complication following THA. However, this injury may become more common with the increasing popularity of anterior approaches. Fleischman et al. reported the overall incidence of femoral nerve palsy to be 0.21%, with the incidence 14.8 times higher in patients undergoing anterior hip surgery using either a direct anterior (0.40%) or anterolateral (0.64%) approach. The femoral nerve lies near the anterior joint capsule, running just anteromedial to the iliopsoas muscle and tendon. It can be injured by retractors placed anterior to the iliopsoas, during anterior capsulectomy, or with anterior soft-tissue retraction for acetabular preparation. Femoral nerve palsies have also been reported after the correction of a severe preoperative flexion contracture. In general, femoral nerve palsies are avoided by ensuring that anterior retractors are blunt tipped and carefully placed on the bony rim of the acetabulum while not allowing them to slip anteromedially. Care must be taken in releasing the anterior capsule, especially in the presence of extensive scarring, and in dividing these soft tissues to correct a flexion contracture. The prognosis for recovery after a femoral nerve palsy is good. However, because injury to the femoral nerve is uncommon, it can be easily overlooked in the early postoperative period, leading to a delayed diagnosis.
The superior gluteal nerve is most vulnerable to injury with anterolateral and direct lateral approaches that split the gluteus medius muscle. It arises from the dorsal branches of the L4-L5 and S1-S2 ventral rami and leaves the pelvis with its accompanying vessels via the greater sciatic foramen above the piriformis. , , It divides into superior and inferior branches and innervates the gluteus medius, gluteus minimus, and tensor fasciae latae. A safe zone has been described for splitting the muscle no more than 5 cm proximal to the greater trochanter, but variations in anatomy have been reported. , Ince et al. found that the distance from the greater trochanter to the superior gluteal nerve was, on average, 3.3 cm. Other studies report that distances from the greater trochanter to the superior gluteal nerve ranged from as close as 2 to 3 cm to as far as 6 to 8 cm. , The nerve may be injured by mechanisms other than direct injury from proximal dissection, including vigorous acetabular retraction for component insertion and extreme leg positioning for femoral preparation. The exact incidence of permanent damage to the superior gluteal nerve is not known, in part because it is often unclear as to whether the main manifestation of its injury, abductor insufficiency with Trendelenburg gait, is due to muscle or nerve injury. , , Picado et al. prospectively studied 40 patients who had THAs using the direct lateral approach. They found that 42.5% of patients had damage to the superior gluteal nerve visible on the first electromyographic evaluation performed 4 weeks postoperatively. Over time, the damage resolved in all but 7.5% of these patients when reevaluated 6 months postoperatively, and only 1 of the 3 patients had a positive Trendelenburg test 1 year postoperatively. Their results suggest that there are frequent electromyographic signs of damage to the superior gluteal nerve using the direct lateral approach to the hip, though the damage tends to improve spontaneously in most instances.
Initial assessment of any abnormal nerve findings postoperatively should include a thorough sensory and motor examination of both lower limbs to delineate whether the clinical presentation is consistent with a peripheral nerve injury rather than the manifestation of more central lesions such as an epidural hematoma. , It is important to note the presence of regional nerve blocks, which, when active, can confound an accurate diagnosis. Additionally, the postoperative examination should be compared with the preoperative examination to account for any preexisting neurologic deficits. The operative extremity should be assessed for obvious features of dislocation, and the operative notes should be reviewed for complications such as fractures or reduction issues. The surgeon should have a low threshold to obtain a hip radiograph to better assess for hip dislocation, fracture, cement extrusion, aberrant screw placement, or component loosening to explain abnormal nerve findings.
Sciatic nerve injuries typically present as foot drop. A foot drop present upon awakening from anesthesia is likely due to stretch or retractor compression on the peroneal division of the sciatic nerve, which is most vulnerable because of its lateral location. A foot drop that presents a short period of time after surgery, rather than immediately after surgery, may be due to an evolving hematoma that gradually increases compression on the nerve. If an evolving hematoma is suspected, an urgent MRI of the lumbar spine and hip is warranted. Workup of late sciatic nerve palsy diagnoses can include a computed tomography (CT) scan to evaluate screw position, lumbar spine imaging to evaluate for double-crush syndrome, electromyography (EMG), and/or neurology referral.
Femoral nerve injuries will present with some degree of weakness to the quadriceps muscle group. Diagnosing femoral nerve injuries after THA can be difficult. Often, patients with femoral nerve palsy, particularly incomplete palsy, may be able to stand and walk on flat surfaces with assistive devices due to the stabilizing effects of other muscle groups. Preexisting physical limitations in elderly patients with hip arthritis and the relatively low overall incidence can also make femoral nerve palsy easier to overlook. It is important to have an increased awareness of this complication, especially for anterior hip surgeons, to ensure prompt treatment and minimize fall risk in the early postoperative period if diagnosed.
Damage to the superior gluteal nerve during THA may cause abductor insufficiency and Trendelenburg gait. The etiology of superior gluteal nerve injuries is often confounded by normal postoperative abductor weakness, which can lead to a delayed diagnosis. Additionally, a superior gluteal nerve palsy may look clinically similar to an abductor avulsion injury. Suspicion for a nerve palsy should be heightened following a lateral approach to the hip, especially if the incision was extended greater than 5 cm proximal to the greater trochanter. Magnetic resonance imaging (MRI) with metal subtraction may have a role in differentiating between superior gluteal nerve palsy and abductor avulsion when the etiology of the abductor weakness is unclear. Electrophysiologic studies can aid in confirming the diagnosis in any nerve palsy but are particularly useful when the diagnosis remains uncertain, as is often the case with superior gluteal nerve injuries.
The treatment of any postoperative nerve injury should first aim at removing identifiable mechanical factors: screw or component malpositioning, cement extrusion, excessive limb lengthening, entrapment by cerclage wire or suture, or rapidly expanding hematomas may need to be addressed surgically in an urgent manner. The vast majority of postoperative nerve injuries, however, are palsies secondary to excessive intraoperative nerve compression or traction and require watchful waiting with thorough patient education. Temporary nonoperative measures such as bracing and physical therapy are vital in maintaining functional independence, range of motion, and preventing uninvolved muscle atrophy until palsy resolution. In rare cases, patients may experience excessive pain with nerve injury, requiring referral to pain management specialists who are well suited to prescribe therapies such as gabapentin, pregabalin, or nerve blocks.
If a sciatic nerve injury is identified in the immediate postoperative period, the operative limb should be positioned to take tension off the nerve: the hip should be extended and the knee flexed. In the setting of any sciatic nerve palsy, patients should be neurologically examined frequently and counseled about their injury so that surgical urgencies, such as an expanding hematoma, can be properly addressed with timely surgical evacuation. Postoperative radiographs should be compared with preoperative radiographs to determine whether the procedure resulted in excessive leg lengthening. If an over-lengthening is found to be the causative factor, revision surgery—including acetabular revision, modular head exchanges, or femoral revision—may result in symptom resolution. If a component or screw is thought to be the cause of a sciatic nerve palsy, a CT scan can be useful for better hardware visualization. Injuries to the peroneal division of the sciatic nerve that present with a postoperative foot drop require an ankle/foot orthosis to keep the ankle in neutral position and a physical therapy prescription to maintain range of motion. These measures decrease the chance of an Achilles tendon contracture. EMGs may be indicated if the palsy persists 6 weeks postoperatively in order to quantify the nerve injury.
In cases of femoral nerve palsy following THA, conservative treatment remains the mainstay. Especially in the elderly, muscles innervated by the femoral nerve undergo significant atrophy and fibrosis and femoral nerve palsy patients can become quickly deconditioned. Physical therapy to prevent muscle atrophy, including stretching and passive exercise, is paramount. A long leg drop lock brace or knee immobilizer is beneficial to maintain patient activities of daily living and functional independence until motor function returns. Using modalities such as knee extension bracing and physical therapy, prior reports have suggested that patients can expect a full recovery. Often, significant demonstrable progress does not begin until 6 months postsurgery; thus, patient education and counseling on this matter is important. , After return of muscle strength, muscle balance must also be restored with continued physical rehabilitation. Functional improvements have been reported up to 2 years postsurgery, which is considered the physiologic limit for nerve regeneration. ,
Similar to sciatic and femoral nerve palsy secondary mechanical issues, if a superior gluteal nerve palsy is suspected to be from hardware impingement, reoperation in an acute setting should be considered. Otherwise, superior gluteal nerve palsies should be treated with close observation, physical therapy with ambulatory aids, and patient education until function is restored.
Vascular complications in THA are less common than nerve injuries, with reported incidences of 0.04% in primary THA and 0.2% in revision THA. , However, the proximity of major vessels to the hip poses a more immediate and serious threat to the life and limb of the patient. Mortality rates after vascular injury in THA have been reported in the literature, ranging from 7% to 9%, with 15% risk of amputation and 17% chance of permanent disability. There are two main reasons that vascular-related morbidity and mortality are so high during THA. First, bleeding is contained within the pelvis, which disguises severity and can prevent immediate recognition. Second, proper vascular access is often restricted and efforts directed toward hemostasis require patient repositioning and difficult exposure. Risk factors for vascular injury in THA include revision surgery and intrapelvic migration of components. , , , , Vascular structures at risk when operating around the proximal femur and acetabulum include internal and external iliac, femoral, internal pudendal, obturator, and superior and inferior gluteal vessels, with the external iliac and femoral vessels being the most commonly injured ( Fig. 20.2 and Fig. 20.3 ). Vessels can be injured by laceration, traction, or retraction of the surrounding soft tissues. Direct trauma or compression from screws, cement, cables, cages, or structural allografts can also occur.