Timing of symptoms

Most symptoms of ulnar neuropathy develop during the postoperative, not the intraoperative, period. Data support the finding that most surgical patients who develop ulnar neuropathy experience their first symptoms at least 48 h postoperatively, suggesting that the mechanism of acute injury occurs primarily outside the operating room. Nonsurgical medical patients also develop ulnar neuropathies during hospitalization.

Impact of elbow flexion

The ulnar nerve is the only major peripheral nerve in the body that always passes on the extensor side of a joint, in this case, the elbow. All other major peripheral nerves primarily pass on the flexion side of joints (e.g., median and femoral nerves). This difference in anatomy may play a role in some perioperative ulnar neuropathies. In general, peripheral nerves begin to lose function and develop foci of ischemia when they are stretched by 5% or more of their resting lengths. Elbow flexion, particularly more than 90 degrees, stretches the ulnar nerve. Prolonged elbow flexion and stretch of the ulnar nerve can result in sufficient ischemia to cause symptoms in awake and sedated patients and potential long-lasting damage in all patients.

Anatomy and elbow flexion

Prolonged elbow flexion of more than 90 degrees increases intrinsic pressure on the nerve and may be as important an etiologic factor as is prolonged extrinsic pressure. The ulnar nerve passes behind the medial epicondyle and then runs under the aponeurosis that holds the two muscle bodies of the flexor carpi ulnaris together. The proximal edge of this aponeurosis is sufficiently thick, especially in men, to be separately named the cubital tunnel retinaculum. This retinaculum stretches from the medial epicondyle to the olecranon. Flexion of the elbow stretches the retinaculum and generates high pressures intrinsically on the nerve as it passes underneath the retinaculum (Figure 244-1).

Forearm supination and ulnar neuropathy

Supination of the forearm and hand does not, by itself, reduce the risk of ulnar neuropathy. The action of forearm supination occurs distal to the elbow. Supination is typically used when positioning the patient’s arms on armboards or at the patient’s sides because of the impact it has on humerus rotation. That is, supination is uncomfortable for most patients, and they will externally rotate their humerus to increase comfort. It is this external rotation of the humerus that lifts the medial aspect of the elbow, including the ulnar nerve, and prevents it from directly resting on the surface of the table or armboard. This rotation helps reduce extrinsic pressure on the ulnar nerve.

Outcomes of ulnar neuropathy

Approximately 40% of sensory-only ulnar neuropathies resolve within 5 days; 80% resolve within 6 months. Few combined sensorimotor ulnar neuropathies resolve within 5 days; only 20% resolve within 6 months, and most result in permanent motor dysfunction and pain. The motor fibers in the ulnar nerve are primarily located in the middle of the nerve. Injury to these fibers is likely associated with more significant ischemia or pressure insult to all of the ulnar nerve fibers, and recovery may be prolonged or not possible.

Brachial plexopathies

Brachial plexopathies occur most often in patients undergoing sternotomies. The risk for this plexopathy in patients undergoing sternotomy is particularly high in those who undergo mobilization of the internal mammary artery, which is presumed to be associated with excessive concentric retraction on the chest wall and potential compression of the plexus between the clavicle and rib cage or stretch of the plexus. In general, patients in prone and lateral positions have a higher risk of developing this problem than do those in supine positions, except in patients having a sternotomy, as mentioned previously.

Anatomy of shoulder abduction

Abduction of a shoulder of 90 degrees or more places the distal plexus on the extensor side of the joint and potentially stretches the plexus (Figure 244-2). Therefore, it is prudent to avoid abduction of more than 90 degrees, especially for extended periods of time.

Impact of hip abduction on the obturator nerve

Hip abduction of more than 30 degrees results in significant strain on the obturator nerve. The nerve passes through the pelvis and out the obturator foramen. With hip abduction, the superior and lateral rim of the foramen serves as a fulcrum (Figure 244-3). The nerve stretches along its full length and is also compressed at this fulcrum point. Thus, excessive hip abduction should be avoided whenever possible. With obturator neuropathy, motor dysfunction is common, and approximately 50% of patients who have motor dysfunction in the perioperative period will continue to have it 2 years later. The dysfunction is usually not painful, but it can be debilitating.

Impact of hip flexion on the lateral femoral cutaneous nerve

Prolonged hip flexion of more than 90 degrees increases ischemia on fibers of the lateral femoral cutaneous nerve. One third of the fibers of this nerve pass through the inguinal ligament as the fibers pass into the thigh (Figure 244-4). Hip flexion of more than 90 degrees results in lateral displacement of the anterior superior iliac spine and in stretch of the inguinal ligament. The lateral femoral cutaneous nerve is compressed by the stretched inguinal ligament and, with time, becomes ischemic and dysfunctional. The lateral femoral cutaneous nerve carries only sensory fibers, so no motor disability occurs when this nerve is injured. However, patients with this perioperative neuropathy can have disabling pain and dysesthesias of the lateral thigh. Approximately 40% of these patients have dysesthesias that last for more than a year.

Follow-up care

If your patient develops a peripheral neuropathy and the neural loss is only sensory, it is reasonable to follow the patient’s condition daily for up to 5 days. Many sensory deficits in the immediate postoperative period will resolve during this time. If the deficit persists longer than 5 days, it is likely that the neuropathy will have an extended impact. It is appropriate if the sensory deficit lasts longer than 5 days to request that a neurologist become involved to provide an evaluation and long-term care.

If the loss is only motor or combined sensory and motor, it would be prudent to request that a neurologist become involved earlier. Patients with motor or combined sensory and motor loss likely have a significant neuropathy and will need prolonged postoperative care.

Thoracic outlet obstruction

Thoracic outlet obstruction, a rare event, occurs when patients with this syndrome are positioned prone or, less commonly, laterally. In almost all reported cases, the shoulder had been abducted more than 90 degrees. In that position, the vasculature to the upper extremity is compressed either between the clavicle and rib cage or between the two heads of the sternocleidomastoid muscle. This entrapment of the vasculature leads to upper-extremity ischemia. When ischemia is prolonged, the results range from minor disability to severe tissue ischemia or infarction that requires forequarter amputation. A simple preoperative question, such as “Can you use your arms to work above your head for more than a minute?” can elicit a history of thoracic outlet obstruction and reduce the risk of this potentially devastating complication occurring.

Steep trendelenburg position

As surgeons gain experience with new technologies (e.g., robotics for use in pelvic procedures), they often request that the patient be placed in a steep Trendelenburg position. These positions can be associated with cephalad shifting of anesthetized patients on operating room tables. Patients often are fixed to the table with draw sheets and other retaining devices (e.g., shoulder braces). Cephalad shifting can lead to cervical plexopathies from stretch and to subclavian vessel obstruction from compression. Although intracranial pressure also increases, it rarely results in a negative outcome. However, if orofacial edema occurs, careful attention to the airway is required.

Postoperative visual loss

Loss of vision when the patient emerges from an anesthetic following a cardiac or spinal surgical procedure is a devastating event for both the patient and the anesthesia provider. Because postoperative vision loss (POVL) occurs infrequently, it has not been possible to identify the cause, which most authorities agree is multifactorial. Review of the POVL registry of the American Society of Anesthesiologists demonstrates that 67% of patients who developed POVL had undergone a surgical procedure on the spine when they were in the prone position, so it is safe to say that positioning definitely plays a role. In those patients who did develop POVL, the majority had spine procedures that lasted between 5 and 9 h. Many authorities assume that, when the patient is in the prone position, edema in the retina and optic head leads to ischemia. POVL occurs in all age groups but appears to be more common in older patients; however, this may be a reflection more on the number of older patients who have cardiac and spinal surgical procedures or this may also be due to the fact that older patients are more likely to have peripheral vascular disease. Atherosclerosis, then, along with hypotension and anemia, may also play an important role in the development of POVL in these patients.

For patients having spinal surgical procedures that will be performed when the patient is in the prone position, the neck should be maintained in the neutral position with the forehead resting on a pad without any pressure whatsoever on the orbits. Though there is no evidence of benefit to this recommendation, many authorities endorse maintaining a mean arterial blood pressure of greater than 70 mm Hg and a perioperative hemoglobin level of 8 g/dL or higher. Attention to detail in this respect may be beneficial both in terms of patient outcome and, if medical negligence is claimed, if there is an adverse outcome.