CHAPTER SYNOPSIS
Neurovascular injuries are rare after total hip arthroplasty but can result in considerable functional impairment. Total hip arthroplasty nerve injuries are reported in 1% to 2% of primary hip arthroplasties and as many as nearly 8% in revision cases. Vascular injuries, although more rare, are reported at 0.2% to 0.3%. The patient’s anatomy, including dysplasia and scarring around the neurovascular bundle in revision cases, can predispose the patient to these injuries. Furthermore, intraoperative dissection, preparation, and hardware placement can place these neurovascular bundles at risk.
IMPORTANT POINTS
- 1
Anatomy and classifications
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Neurovascular anatomy associated with total hip arthroplasty
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Seddon classification of neurovascular injury
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- 2
Etiology
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Predisposing factors and patient positioning
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- 3
Surgical techniques
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Smith-Peterson anterior approach
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Watson-Jones anterolateral approach
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Direct lateral approach
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Southern Moore posterior approach
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- 4
Evaluation and treatment of neurovascular injuries
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Intraoperative diagnostic evaluation of suspected neurovascular injuries
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Electromyographic analysis, education, physical therapy, and orthoses
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CLINICAL/SURGICAL PEARLS
- 1
Surgical approaches and respective dangers
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Smith-Peterson anterior: lateral femoral cutaneous nerve injury 2.5 cm distal to the anterior superior iliac spine, femoral nerve during anterior capsulotomy and retractor placement
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Watson-Jones anterolateral: lateral femoral cutaneous nerve injury 2.5 cm distal to the anterior superior iliac spine, superior gluteal nerve and artery and femoral nerve and artery injury with sharp retractor and aggressive capsule release
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Hardinge modified direct lateral: superior gluteal nerve and artery 3 to 5 cm proximal to the greater trochanter and femoral nerve injury with anterior capsulotomy and acetabular preparation at 2.3%
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Southern Moore posterior: sciatic nerve with posterior acetabular retractor placement
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- 2
Operative fixation
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Avoid screw placement when possible in the following zones of the acetabulum: anterosuperior (damage to the external iliac artery and vein) and anteroinferior (damage to obturator nerve and artery)
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- 3
Postoperative assessment
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Documentation of initial neurovascular deficit
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Appropriate physical therapy and rehabilitation
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Fitted orthoses to prevent equinus and foot drop
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Time-relevant diagnostic evaluation at 6 weeks to 3 months
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CLINICAL/SURGICAL PITFALLS
- 1
Patient population and inadequate risk factor evaluation
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Revision total hip arthroplasty with resultant scar tissue
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Developmental dysplasia of the hip or chronic lower extremity shortening
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Female gender prevalence
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- 2
Initial preoperative education
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Discussion with patient regarding risks/benefits depending on risk factors
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- 3
Inadequate patient positioning
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Upper extremity brachial plexus injuries
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Ulnar nerve
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Lower extremity injuries
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Deep peroneal nerve (fibular neck)
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- 4
Surgical limb overlengthening and nerve injury
- 5
Inadequate postoperative assessment
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Subgluteal hematoma and sciatic nerve deficit
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Postoperative abduction pillow or positioning and peroneal nerve injury
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Postoperative total hip arthroplasty dislocation and sciatic nerve compression
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INTRODUCTION
Total hip arthroplasty (THA) is considered one of the most clinically effective and cost-effective interventions in orthopedic surgery. Although many studies have reported greater than 90% survivorship at 15 years of follow-up and validated the cost effectiveness for quality-adjusted life-years in performing primary THA, neurovascular injuries represent a devastating complication that can result in a less than satisfactory outcome. A patient’s body habitus, hip deformity, sex, and number of previous hip surgeries are all factors that can influence the risk of neurovascular injury. In general, the risk of nerve injury is quite low at 1% to 2% for primary THA, but the incidence is as high as 8% for revision THA. Although the overall risk of a vascular injury is low at 0.2% to 0.3%, a review of the literature by Shoenfeld et al revealed a higher incidence in primary surgeries compared with revision cases. Of the reported 68 vascular injuries associated with THA, 61% of all documented cases occurred during primary procedures and the remainder occurred in revision cases. This chapter reviews current literature that identifies and supports the known neurovascular complications that can occur during a THA and discusses the strategies to prevent, identify, and treat neurovascular injuries.
ANATOMY
The functional unit of the neuromuscular system is composed of the lower motor neuron in the anterior horn of the spinal cord, the axon of the respective neuron, and the muscle group that it acts on. Peripheral nerves are composed of three primary components: a nerve fiber, the myelin sheath, and the accompanying Schwann cell. Within a nerve fiber exist nerve cells, which are composed of a cell body, axon, and both presynaptic and postsynaptic dendrites. The cell body contains the nucleus and houses the remainder of the organelles that allow the cell to survive. The axon provides the conduit for the electrical impulse and action potential to be transmitted and also allows the transport of vesicles and synthetic needs for the distal dendrites. Within a nerve exists a sensory (afferent) system, a motor (efferent) system, or both. The afferent conduction system is modulated by mechanoreceptors and nociceptors distally within the tissues; they send signals to the dorsal root ganglions, which can then be processed in a feedback or reflex circuit as applicable. The efferent system delivers an action potential from the anterior horn cells and acts on a distal motor group to contract the muscle. As nerve fibers are grouped into larger fascicles, which ultimately form what is seen in the operating theatre as a nerve, it is important to remember that important connective tissue surrounds each of these constituents. Many times the presence or absence of the connective tissue determines the capacity of a nerve to regenerate if damaged. As seen in Figure 27-1 , the endoneurium surrounds each nerve fiber, the perineurium surrounds each nerve fascicle, and the epineurium encompasses each nerve in its entirety. When a nerve is damaged, severely contused to prevent distal flow of metabolic products through the axon, or even severed, the intact endoneurium allows regeneration of the nerve. However, the initial insult causes Wallerian degeneration to the level of the localized injury. What is seen on a microscopic level regarding which layer of the connective tissue is damaged can also be seen at a clinical level regarding loss of motor or sensory function. Seddon has defined three levels of peripheral nerve damage: neuropraxia, axonotmesis, and neurotmesis ( Fig. 27-2 ). Neuropraxia is defined as the condition in which a nerve is anatomically intact but physiologically nonfunctional, usually the result of a contusion, localized pressure, or traction injury. Axonotmesis is viewed as a physiologically nonfunctional nerve with anatomic disruption at the level of the axon but with preservation of the epineurium and perineurium. This is vital for nerve survival because it allows regeneration at approximately 1 mm/day. Finally, neurotmesis is defined as a complete disruption of the axon without preservation of the endoneurium, which leaves the nerve anatomically and physiologically nonfunctional. This requires surgical repair of the nerve if any true regeneration of the nerve is to be expected.
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The sciatic nerve has been shown to be at most risk for injury during THA. Barrack reviewed 28 studies totaling more than 25,000 patients with 243 nerve injuries, 79% of which were sciatic. The femoral nerve was solely injured in 13%, and a combined femoral and sciatic nerve injury was present in 6%. The obturator nerve was the least injured at 1.6%. His review also reported that the cause was unknown in 47% of cases; however, the most common cause was found to be to the result of stretching in 20%, contusion in 19%, hematoma compression in 11%, and complete transection of the nerve in 1%.
The sciatic nerve (composed of both tibial and peroneal divisions) is the most common nerve injured during a primary THA. This nerve is at greatest risk during the surgical approach, soft tissue retraction, component implantation, and lengthening of the limb. Schmalzreid et al reported that more than 90% of 53 nerve injuries, diagnosed in a series of 3000 primary THAs, were sciatic. The sciatic nerve typically originates from the L4 through S3 nerve roots and is located within the pelvis, exiting deep to the piriformis and between the gluteal muscle bellies and short external rotators of the hip. Much less frequently, the peroneal division can pierce the piriformis, loop around it, or the entire sciatic nerve can pierce the piriformis. After exiting the sciatic notch, it courses along the ischial tuberosity and distally past the lesser trochanter, where it can be visualized between the adductor magnus and the long head of the biceps femoris. The sciatic nerve, and more specifically the tibial branch, supplies the long head of the biceps, the semitendinosus, and the semimembranosus above the level of the knee. The only muscle innervated proximal to the level of the knee by way of the peroneal division of the sciatic nerve is the short head of the biceps femoris. (This distinction will become relevant later in the chapter in the section describing postoperative peroneal nerve dysfunction and determining the etiology by electromyographic analysis.) As the nerve traverses the proximal aspect of the popliteal space, it divides into the tibial and common peroneal branch divisions and dives deep to the lateral head of the gastrocnemius. The tibial nerve then supplies the superficial posterior compartment of the leg and all the muscles within it: the gastrocnemius, the soleus, and the plantaris. It also innervates the deep posterior compartment muscles, including the flexor hallucis longus, the posterior tibialis, the flexor digitorum longus, and the popliteus. Both compartments are involved in ankle plantar flexion and heel/foot inversion. The tibial nerve also gives sensory innervation to the plantar aspect of the foot, which ends as the medial and lateral plantar nerves. The common peroneal nerve exits laterally distal to the popliteal space and courses around the fibular neck and then divides into its terminal branches, the deep and superficial divisions. The superficial nerve supplies the muscles of the lateral compartment of the leg, causing ankle/foot eversion, which are the peroneus longus and brevis. It then crosses from the lateral compartment into the anterior compartment through the intermuscular septum between 3 cm and 18 cm proximal to the ankle joint and terminates supplying the sensory innervation of the dorsum of the foot as the lateral and intermediate divisions. The deep peroneal branch dives deep into the intermuscular septum and crosses into the anterior compartment to supply the muscles of ankle dorsiflexion, including the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and the peroneus tertius. Finally, it exits into the foot deep to the dorsalis pedis and supplies motor innervation to the extensor digitorum brevis and sensory innervation to the first dorsal webspace. Both the tibial and common peroneal nerves give off branches to the sural nerve, which supplies the posterolateral cutaneous innervation of the calf.
Although most case series report sciatic nerve injuries at approximately 1.5% for primary THA, Weber et al reported a rate of 0.7% of more than 2000 patients. However, this group believed that these are likely only the functionally impaired injuries that are clinically apparent during the postoperative period. Their study evaluated preoperative and postoperative sciatic nerve electromyography and found some form of sciatic nerve dysfunction by conduction delay in 70% of their case series; however, nearly all were subclinical by examination. When differentiating between the tibial or peroneal divisions of the sciatic nerve, Schmalzreid et al reported peroneal nerve injury to be much higher than tibial at 94% of all injured sciatic nerves. One reason for the increased peroneal division nerve damage could be linked to its anatomic course as it leaves through the sciatic notch and courses distally to wrap around the fibular head/neck, thus tethering it and predisposing it to injury during traction and dislocation/reduction maneuvers. Furthermore, in a cross-sectional area, the peroneal nerve has more fascicles and less connective tissue than the tibial division, once again predisposing it to injury when stretched (see Fig. 27-2 ). Lastly, the peroneal division is more lateral than the tibial division within the sciatic nerve as it exits the greater sciatic notch; this also can predispose the nerve to injury during component trialing, with dislocation and relocation and posterior acetabulum retractor placement. Even suture placement, electrocautery, and cement-curing heat dissipation may damage the sciatic nerve.
The femoral nerve, superior gluteal nerve, and obturator nerve are all at risk depending on the placement of retractors and final screw placement to secure the acetabular shell. The femoral nerve, composed of the L2 through L4 nerve roots, pierces the psoas muscle and lies between the muscles bellies of the psoas and iliacus, exiting below the inguinal ligament to become the most lateral structure within the femoral triangle. It innervates the iliopsoas, which allows hip flexion, and the knee extensor mechanism, the quadriceps group. The femoral nerve also supplies the sartorius and pectineus as well as the sensory innervation to the medial aspect of the thigh and leg as the saphenous nerve. The superior gluteal nerve arises from the branches of the L4 through S1 nerve roots. It exits the greater sciatic notch, innervating the hip abductors: the gluteus medius, gluteus minimus, and tensor fascia lata. It is at its greatest risk with more of the lateral transtrochanteric approach than screw placement. Furthermore, violation of the 3 to 5cm “safe zone” above the tip of the greater trochanter described by Arbitbal also places the superior gluteal nerve and artery at risk. Finally, the obturator nerve (L2 through L4 roots) arises from the posterior aspect of the psoas and travels distally over the sacral ala and along the iliopectineal line. Exiting the pelvis through the superior aspect of the obturator foramen, it supplies the hip adductors, including the obturator externus, adductor magnus, adductor longus, adductor brevis, and the gracilis. The obturator nerve also provides distal medial thigh sensory innervation, which often can be seen clinically as referred knee pain after THA.
Deep placement of acetabular retractors along the anterior brim has been associated with femoral nerve neuropraxia. However, posterior acetabular retraction can result in sciatic nerve compression. In revision THA, Satcher et al found that hip flexion during acetabular retraction was associated with decreased motor evoked potentials, suggesting that hip flexion should be avoided during preparation of the acetabulum ( Fig. 27-3 ). Wasielewski et al evaluated cadaveric specimens to determine the least dangerous zones to place screws for transacetabular fixation of uncemented acetabular shells. Their research produced a four-quadrant zone system based on the results of perforation or proximity to neighboring neurovascular structures ( Fig. 27-4 ). By drawing a line from the anterior superior iliac spine through the acetabulum just posterior to the fovea and through the ischium and a second line perpendicular to the first, the quadrants are visualized. The posterosuperior and posteroinferior regions were found to have more substantial bone stock for screw placement and thus less risk of aberrant screw placement and damaging nerves. That being said, the posterosuperior quadrant places the superior gluteal nerve at risk while the posteroinferior quadrant places the sciatic, internal pudendal, and inferior gluteal nerves at risk. Although screws directed toward the latter do carry risk, it is minimized by bone stock that usually is greater than 25 mm in depth, robust soft tissue, the mobility of these structures, and the surgeon’s ability to palpate the sciatic nerve through the sciatic notch. The two danger zones described were the anterosuperior and anteroinferior quadrants. The external iliac vein and artery were placed at risk with anterosuperior screw placement, and the obturator nerve was at risk with anteroinferior placement. Although the greatest risk of obturator nerve injury was as the neurovascular structures exited through the obturator foramen, variants of the obturator vein anatomy (aberrant obturator vein) existed just to the anteroinferior wall of the acetabulum. The limited amount of bone (only 6 to 12 mm) in this zone and the paucity of soft tissue interposition between screw, bone, and nerves also contribute to the risk of neurovascular injury.
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