Patient positioning is a pivotal first step of lumbar surgery, which allows access to the cause of stenosis or radiculopathy. Lumbar surgery often requires positions that are not physiologic in an awakened patient and that last for a long period. Such positions can cause some advent events due to abnormal forces upon prominence of the patient’s anatomy[1]. In one study, the overall incidence of position-related upper extremity somatosensory evoked potential (SSEP) changes during spine surgery was 6.1%[2]. The lateral decubitus and prone superman positions were identified as having significantly more frequent incidences compared with other operative positions during spine surgery. Lasting surgery or improper positioning could therefore lead to perioperative peripheral nerve injury.
The incidence of perioperative peripheral nerve injury (PPNI) in a retrospective study of different surgeries during a 10-year period in one tertiary center has been reported as 0.03%-0.1%[3]. Neurosurgical and orthopedic procedures have a significant association with perioperative peripheral nerve injury. Female sex, old age (> 65 y/o), hypertension, tobacco use, diabetes mellitus and higher BMI also significantly increase the risk[3].
Ischemia is the most likely mechanism in patients with perioperative peripheral nerve injury. It has been revealed that the blood flow to peripheral nerves does not vary with even major changes in blood pressure, making peripheral nerves more vulnerable to systemic hypotension[1].
Apart from the potentially harmful influence of systemic hypotension on peripheral nerves[4], positioning-related factors can also aggravate ischemic damage. Direct pressure on peripheral nerves is the first mechanism causing neural dysfunction and ischemia. The second mechanism is latent but important, which is peripheral nerve stretching beyond its resting length. One experimental study reported that stretching peripheral nerves by as little as 6–11% may produce impaired signal transmission owing to mechanical injury and circulatory disturbance. Most peripheral nerves are intolerant of stretching beyond 10% of their normal length[5].
Lower extremity neuropathies may be related to direct operative injury, anesthetic techniques, or patient positioning. Perioperative lower extremity neuropathy owing to improper positioning in lumbar surgery is reported less commonly than those of the upper extremity. The lower extremities were typically placed in a near neutral body position and padded with pillows and fat pads, which eliminated direct pressure and strain on the peripheral nerves. To the best of our knowledge, the two peripheral nerves of the lower extremity passing near bony prominences and may therefore be vulnerable are the lateral femoral cutaneous nerve (LFCN) and the common peroneal nerve.
The LFCN is a pure sensory nerve that gives superficial innervation to the anterior lateral aspect of the thigh. LFCN palsy is commonly recognized as pain, numbness, or dysesthesia in this distribution, also known as meralgia paresthetica. The incidence of LFCN palsy has been reported to be 23.8% in posterior thoracolumbar spine surgery and is significantly associated with patients having a greater body mass index and prolonged surgical time. The clinical outcome is excellent, and most patients can anticipate complete recovery within 2 months.
The common peroneal nerve, also known as the common fibular nerve, is the smaller and terminal branch of the composed of the posterior divisions of L4, 5, S1, and 2. Near the distal thigh, just above or in the popliteal fossa, the sciatic nerve divides into the tibial and common peroneal nerves (CPNs). The CPN passes around the neck of the fibula, where it is most superficial and vulnerable to pressure or trauma. After entering the lateral leg compartment deep to the peroneus longus tendon, the CPN divides into deep and superficial peroneal branches.
Common peroneal nerve palsy could occur in any surgery adopting the lateral decubitus position because it is adjacent to the bony prominence of the fibular head. Several studies support that prolonged duration in the lithotomy position is associated with a higher risk of lower extremity neuropathy. Knee eversion and degenerative varus deformity could also lead to common peroneal nerve injury due to overstretching. Some case reports have proposed that postoperative common peroneal nerve palsy is related to prolonged surgery and systemic hypotension during the operation.
Due to the lack of clinical studies and rarity of perioperative lower extremity neuropathy, it is difficult to determine a specific mechanism of nerve injury. We assume that multiple factors, including a 4-hour surgery, patient positioning (prone position and tilted to the right side when performing unilateral laminotomy for bilateral decompression) and systemic hypertension as a risk factor for atherosclerosis, collectively led to common peroneal nerve palsy in this presented case. Lumbar MRI before surgery demonstrated a herniated intervertebral disc at the L4/5 level with impingement of the right L4 and L5 roots, which may be a predisposing factor. Additional factors, such as hypotension during surgery, type II diabetes mellitus and higher BMI, did not exist.
The development of perioperative common peroneal neuropathy is probably the result of the coincidence of several risk factors. It is more difficult to differentiate perioperative common peroneal injury, especially after lumbar surgery. Injury of the nerve root, epidural hematoma and inadequate decompression should be ruled out based on postoperative MRI. A detailed medical history and neurological examination before and after surgery, including the SLRT test, Tinel’s sign, dermatome of sensory impairment and muscle strength evaluation, may provide some hints of the etiology, but a definite diagnosis should rely on MRI and nerve conduction velocity (NCV) electromyography (EMG).
In view of prevention, intraoperative neuromonitoring is used for early detection of PPNI in patients with increased risks of comorbidity, such as systemic hypertension, type II diabetes mellitus, extreme higher or lower body weight, and prolonged surgery. Some studies have demonstrated that SSEP monitoring has an established role in the early detection of reversible positioning-related signal changes. Once the positioning is corrected and signals improve, most patients wake up without neurologic deficits. However, there are some factors other than patient positioning that cause changes in SSEP signals, such as spine instrumentation, hypoperfusion, hypothermia, anesthetic agents and depth, and operating room noise. The sensitivity and specificity of SSEPs for PPNI is yet to be determined, and it is also unclear whether SSEPs can decrease the incidence of PPNI.
The severity of peripheral nerve injury is the most important factor related to outcome. The most widely accepted classifications of nerve injuries are those described by Seddon (neuropraxia, axonotmesis, and neurotmesis) and by Sunderland (grade 1–5 nerve injuries). Nerve conduction studies (NCS) and needle EMG are the pivotal tests in the diagnosis of PPNI. These tests confirm the diagnosis, localize the lesion, determine the injury severity, predict outcome, and determine whether direct surgical repair should be performed. In the first 7 days after surgery, the NCS can localize the injury by identifying the site on a peripheral nerve where abnormal conduction is occurring.
If the NCS is postponed until 3–4 weeks after surgery, patients with neurapraxia usually have normal conduction due to remyelination. In patients with axonotmesis and neurotmesis, both proximal and distal conduction are lost due to Wallerian degeneration. Thus, electrophysiological exams at 3–4 weeks after surgery can distinguish the severity of PPNI.
Although most perioperative peripheral nerve injury due to positioning or hypoperfusion during surgery is classified as neuropraxia or axonotmesis, patients affected by PPNI might sustain long-term disability from motor deficits or chronic pain.
Surgical intervention is rarely required in patients with PPNI. Methylprednisolone has also been used as a medical treatment in several case reports, but its therapeutic effectiveness in treating PPNI remains unproven.
PPNI in spine surgery is a rare but important perioperative complication resulting in significant patient disability, functional loss, and the potential for litigation. It is most commonly caused by peripheral nerve ischemia due to abnormal nerve lengthening or pressure and can be exacerbated by systemic hypotension. Any diseases affecting microvasculature and anatomical differences may contribute to nerve injury or render patients more susceptible to nerve injury. Prevention and early detection and intervention are paramount to reducing PPNI and associated adverse outcomes. The use of intraoperative neuromonitoring (IONM) theoretically allows the surgical team to detect and intervene in impending PPNI during surgery.