Postoperative neuropathy

When a patient complains of pain, weakness, or numbness/paresthesia, the first question is whether the symptom began before or after surgery. A thorough preoperative history is necessary for any known preoperative neuropathy to be able to discern new from prior symptoms. If present prior to surgery, the diagnosis and management is beyond the scope of this chapter. A new-onset symptom, however, requires a thorough stepwise assessment that begins with a physical exam. The exam should elucidate the nature of the complaint (e.g. numbness, weakness, tingling) as well as the distribution. Symptoms in a specific dermatome or in the distribution of one or more peripheral nerves may aid in localization of the insult. The next step is to attempt to determine whether the paresthesia was caused by surgical manipulation or by some other event in the operating room.

Surgically related postoperative neuropathy

Certain surgical procedures have known implications for neuropathy, and it is helpful to have a high-yield summary of some known associations. For any patient work-up, a discussion with the surgical team regarding their exposure, retraction, and surgical manipulation would likely be of benefit.

In cardiac cases, sternal retraction during median sternotomy has been associated with brachial plexus injuries of variable severity based on location and extent of retraction.^[4] Sensory deficits may occur in the leg after saphenous vein harvesting during coronary artery bypass graft (CABG).^[5]

During a neck lift, the great auricular nerve can be injured, resulting in decreased sensation in the lower ear with or without paresthesias.^[6] During mandibular osteotomies/genioplasty, the mental nerve can be injured, resulting in paresthesias affecting the skin in the anterior aspects of the chin and oral mucosa of the inferior lip.^[6,7] For reconstructive surgery for sleep-disordered breathing including uvulopalatopharyngoplasty (UPPP), uvulopalatal flap (UPF), uvulopalatopharyngoglossoplasty (UPPGP), and laser midline glossectomy (LMG), paresthesias can be a complication of the surgical manipulation.^[6]

For orbital blow-out fracture repairs, paresthesia due to infraorbital nerve dysfuction was a frequent complication noted.^[8] For LeFort osteotomy, paresthesia of the forehead and upper cheek can be due to partial paralysis of cranial nerve II, and V1 and V2 as a result of displacement of bony fragments into the cavernous sinus. These symptoms resolved with a steroid taper.^[9]

After dental work, oral paresthesia can be a presenting symptom and may be due to mechanical trauma resulting in damage to the inferior alveolar nerve, a pressure phenomenon due to obturation material or endodontic instruments within the inferior alveolar canal, neurotoxic effects related to solutions used to clear the root canal or solutions used as sealants, or thermal injury.^[10] The paresthesia associated with these injuries usually resolves over time with conservative treatment, but in some cases microneurosurgical interventions may be appropriate.^[11]

In lumbar spine surgery such as discectomy or microdiscectomy, paresthesias may occur owing to nerve-root irritation from the surgery that may be improved by analgesics and/or muscle relaxants.^[6] In lumbar spine or hip surgeries, lateral femoral cutaneous nerve (LFCN) injury may result in an altered sensation known as meralgia paresthetica, described as persistent pain referred to the lateral thigh caused by direct nerve injury or neural ischemia.^[12,13] If physical examination suggests compression of the LFCN, then neurolysis of this nerve may be all that is needed. If block of the LFCN eliminates all the pain, both a neurolysis of the LFCN and resection of its posterior branch would be indicated.^[13]

This is by no means an exhaustive list, but highlights how surgical manipulation or retraction may risk peripheral nerve injury. Communication with the surgeon may be important in revealing a surgical etiology for a new postoperative neuropathy. In rare cases, the patient may need to return to the operating room to prevent permanent neurological damage.

Non-surgically related postoperative neuropathy

Non-surgically related postoperative neuropathy refers to all other causes that are not directly related to the surgical procedure. Occasionally, these can be related to anesthetic procedures. Transient hypoglossal nerve paralysis has been reportedly caused by endotracheal tube cuff compression.^[14] Difficult placement of intravenous or intraarterial catheters may result in direct nerve trauma. As with surgical manipulation, any procedure performed on the patient has the potential for causing a nerve injury. Other non-surgical causes can be due to neuraxial/regional anesthesia blocks, patient positioning, medications, and electrolyte abnormalities.

Neuraxial/regional anesthesia and postoperative neuropathy: Neuropathic issues following neuraxial anesthesia (i.e. epidural, spinal, combined spinal–epidural) may include backache that can be persistent and is possibly related to needle trauma, local anesthetic irritation, or ligamentous strain. Patients may present with postdural puncture headache requiring possible medical management or epidural blood patch. Symptoms concerning for spinal hematoma require prompt diagnosis as emergent spinal decompression increases odds of a good prognosis.^[15]

Regional anesthesia blocks may be performed for a variety of surgical procedures as the primary anesthetic or as an adjunct for postoperative analgesia. Assessment of paresthesia in this setting requires knowledge of the intended effects of the regional blockade and identification of any abnormal or unanticipated effects. For upper extremity procedures, where a brachial plexus block is performed, persistent paresthesia can be a complication of the block itself and may last 6 weeks or more.^[6] An association has been noted between incidental elicitation of paresthesias and postoperative neurological complications; therefore, it is recommended that intentional elicitation of paresthesia as a neurolocalization technique should be avoided.^[16] Nerve injuries in this setting are often multifactorial and involve nerve anatomy, needle insertion site, bevel type, needle tip location, injection pressures, and underlying patient nerve pathology.^[17] Regional anesthesia techniques may have further undesired neurological complications due to accidental intravenous, intraarterial, intraneural, or neuraxial injections.

Positioning and postoperative neuropathy: Patient positioning is a collaborative effort between the surgical, anesthesia, and nursing teams in the operating room. Patients under anesthesia are unable to safely adjust their own position, rendering them susceptible to positional nerve injury.

In the supine position, the brachial plexus may be injured at various levels by stretching or compression at the axilla based on head and arm position, especially if the head is abnormally rotated or arms abducted >90 degrees. Padding is required to prevent ischemia from point pressure at bony prominences (e.g. occiput, elbows, heels, sacrum) that may lead to radial, ulnar, or median nerve dysfunction. Appropriate mattress pads are required to disperse point pressure and support the spine, where loss of lumbar curvature or hyperlordosis may result in backache and spinal nerve ischemia, respectively.^[15]

In the lateral position, improper positioning may lead to compression of the common peroneal nerve by the legs, poor alignment of the head with the cervical and thoracic spines, or compression of the shoulder and neurovascular bundle in the axilla. Injury to the long thoracic nerve by positioning may lead to serratus anterior muscle dysfunction and winged scapula. Inadequate chest support in the lateral position may lead to suprascapular nerve injury causing shoulder pain.^[15]

In the prone position, the eyes and ears are susceptible to injury. Neck pain or limitation of cervical motion can result from unnatural stretch of neck muscles and ligaments. Inappropiate head flexion/extension can compromise cerebral vascular flow. Brachial plexus injuries remain a concern, as is compression of the chest and abdomen.^[15]

The lithotomy position, common in urological and gynecological procedures, is associated with paresthesias in the distribution of the obturator, lateral femoral cutaneous, sciatic, and peroneal nerves that were noted within 4 hours of surgery and resolved within 6 months.^[18] A motor symptom of common peroneal nerve involvement may be foot drop. Prevention measures that can be taken include minimizing the time in the lithotomy position; using two assistants to coordinate the simultaneous movement of both legs to and from the lithotomy position; avoiding excessive flexion of the hips, extension of the knees, or torsion of the lumbar spine; and avoiding excessive pressure on peroneal nerve at the fibular head.^[18]

In any patient position, hemodynamic influences can contribute to ischemic neuropathy. Poor perfusion to a peripheral nerve can be caused by systemic hypotension, compression of an extremity or point pressure at a bony prominence, or a raised limb where arterial pressure is unable to sufficiently perfuse the distal extremity.^[15]

Drug-induced postoperative neuropathy: Local anesthetics have been implicated in instances of postoperative neuropathy. Articaine and prilocaine have been associated with persistent paresthesia of the lips, tongue, and oral tissues with slow, incomplete, or no recovery; studies are inconclusive as to the cause.^[19] Theories include neurotoxicity from the local anesthetic and needle trauma resulting in nerve injury.^[19,20] Systemic local anesthetic toxicity results from systemic absorption, possibly by accidental intravenous or intra-arterial injection, and has a dose-dependent range of symptoms that may begin with circumoral numbness, facial tingling, and tinnitus. Central nervous system (CNS) symptoms progress from irritability, restlessness, vertigo, and slurred speech to tonic-clonic seizures.^[20] CNS effects may progress to cardiovascular effects with cardiac arrest that can be refractory to treatment. Vigilance during block placement, frequent aspirations during injection, and close patient monitoring are essential to diagnose local anesthetic toxicity and intervene early to minimize CNS or cardiovascular complications. The American Society of Regional Anesthesia and Pain Medicine Practice Advisory (ASRA) emphasizes primary prevention in reducing the frequency and severity of local anesthetic toxicity.^[21]

Nitrofurantoin is another medication that has been associated with paresthesia as reported in case studies. Patients had normal nerve conduction studies, but skin biopsies showed normal intra-epidermal nerve fiber density but with clustered swellings of terminal nerve fibers. Medications such as gabapentin and duloxetine provided some relief.^[22]

Immunosuppression is present in many patients undergoing surgical procedures, and may be associated with viral-induced neuropathies. Anesthetics, blood products, and other medications (e.g. antibiotics) have been shown to result in varying degrees of immunosuppression in some patients.^[15]

Electrolyte abnormalities and postoperative neuropathy: After a total thyroidectomy or parathyroidectomy, hypocalcemia (total calcium <8.4 mg/dl) in the immediate postoperative period can present with paresthesias as one of the signs and symptoms in addition to muscle spasms, Trousseau’s sign, Chvostek’s sign, tetany, laryngospasm, bronchospasm, and apnea. Treatment of the hypocalcemia includes 10 to 20 ml calcium gluconate 10% over 10 minutes. Following blood levels and repeating therapy until the clinical signs of hypocalcemia are controlled are key to treating this condition. Continuous positive airway pressure is effective for associated airway obstruction.^[6,23]

Severe hypophosphatemia (serum phosphorus <2 mg/dl) is another common postoperative electrolyte abnormality. The two most common causes are intravenous glucose administration and septicemia.^[24,25] Symptoms, in addition to paresthesia, can include muscle weakness, lethargy, confusion, disorientation, generalized or Guillain–Barré-like ascending paralysis, seizures, coma, and even death. Treatment involves treating hypocalcemia first, if present, and considering the patient’s renal function. The dose of intravenous phosphate should be decreased by 50% if serum creatinine is >2.5 mg/dl. For serum phosphate <2.5 mg/dl, administer 2 mmol/hr over 6 hours. For serum phosphate <0.5 mg/dl, administer 4 mmol/hr over 6 hours. For serum phosphate <1 mg/dl, administer 8 mmol/hr over 6 hours. While treating hypophosphatemia, one needs to monitor serum levels of both phosphate and calcium.^[25]