Motor deficits caused by surgery

Direct trauma to the spinal cord or a peripheral nerve may occur with procedures of the spine or limbs. Surgical injury to nerves can be cause by transection, ischemia, compression, or stretching. Nerves in or near the operative field are at greatest risk of surgical injury. Total hip replacement produces an incidence of postoperative nerve palsy in the range of 0.6% to 3.7%.^[1] Sciatic nerve injuries are most common and may impair leg flexion and dorsiflexion of the foot. Femoral nerve injuries occur with an incidence of 0.1% to 0.4%^[1] and may impair leg extension and hip flexion. The vast majority of nerve palsies associated with hip replacement are noted in the early postoperative period. A small subset of nerve injury may present several weeks after surgery with new-onset leg weakness and pain. Some of these may be caused by a post-inflammatory neuropathy.^[2] Abdominal hysterectomy may be associated with 10% incidence of postoperative femoral neuropathy, especially if self-retaining retractors are used for surgical exposure.^[3] Brachial plexus injuries occur with a frequency of 0.1% to 4% during shoulder surgery depending upon the particular procedure.^[4]

Management: New weakness after limb or spinal surgery needs to be brought to the attention of the surgeon. Post-inflammatory neuropathy may respond to intravenous (IV) methylprednisolone.^[2]

Regional anesthesia

Regional anesthesia produces motor blockade in addition to anesthesia. While this is anticipated, motor blockade occasionally causes concern for patients, family, or healthcare providers. The duration of expected blockade is dependent upon several factors including whether it is a “single shot” or continuous infusion, the pharmacokinetics of the local anesthetic, the dose administered and the use of adjuvants in the block, such as epinephrine. Actual nerve injury from regional anesthesia is rare, but may occur from neural toxicity of local anesthetic solutions, mechanical trauma to the nerve from the needle, intraneural injection, and tourniquet-induced nerve compression or ischemia.^[5] The incidence of nerve injury after brachial plexus blockade is very low and reported to be about 1.5 per 10,000 blocks,^[6] but severe motor damage is occasionally reported.^[7]

Management: Spontaneous recovery is typical, although the presence of a motor deficit is more ominous than is an isolated paresthesia. Concerns for either residual paresthesia or motor deficits in a patient receiving regional anesthesia should be referred to the anesthesiologist.

Compression neuropathy

Injury to peripheral nerves may occur because of stretch or compression. The most common nerve injury after surgery is ulnar neuropathy. Compression of the ulnar nerve in the olecranon fossa is the most commonly cited etiology, but the true etiology of ulnar neuropathy is probably multifactorial and more complex. The incidence of ulnar neuropathy after non-cardiac surgery is 1 in 2,729 procedures.^[8] Half of these patients will be asymptomatic at one year. Cardiac procedures carry an increased risk of both ulnar and brachial plexus injury with an incidence range of 1.5% to 24% between studies.^[9] The risk of brachial plexus injury is also increased for procedures in the lateral position including thoracotomy. Motor neuropathy is also seen after surgery in the lithotomy position with an incidence of 1 in 3,608 procedures.^[10] The risk of motor neuropathy increases by two orders of magnitude for every hour in lithotomy position.

Management: Compression neuropathy limited purely to sensory deficits usually has a good prognosis with most patients achieving complete recovery after several weeks. Motor deficits are more ominous and although complete recovery is possible, consultation with a neurologist is prudent.

Compartment syndrome: Acute compartment syndrome may develop in a limb when elevated compartment pressure impairs perfusion. The compartmental pressure needed to cause cellular injury is therefore dependent upon systemic blood pressure, but compartmental pressure may become injurious when it approaches 20 mmHg^[11] to 30 mmHg^[12] of diastolic blood pressure. Compartment syndrome may develop in the perioperative period. Signs and symptoms of compartment syndrome may be remembered by the mnemonic of the 6 Ps: pain, paresthesia, paralysis, pallor, pulselessness, and poikilothermia (referring to cooling of the affected limb). While paralysis is a sign of compartment syndrome, it typically is a late finding. Paresthesia, severe pain exacerbated by passive movement of the limb, and pallor occur earlier and before pulselessness or paralysis develop.

Acute compartment syndrome is most frequently observed in trauma patients with either long bone fractures or crush injuries, or may occur after reperfusion of an ischemic limb.^[13] Vascular puncture causing bleeding into the limb may cause acute compartment syndrome, especially in patients with pre-existing coagulopathy. Acute compartment syndrome may occur as a complication of intraoperative positioning, particularly for procedures performed in lithotomy syndrome.^[14–17] Mean arterial pressure decreases 2 mmHg for each inch above the level of the heart,^[18] so higher positioning of the legs when combined with intraoperative reduction in blood pressure may place the legs at risk. Longer surgeries (>4–6 hours) and higher patient body mass index also appear to carry increased perioperative risk. Although some clinicians have expressed concern that calf compression devices may cause compartment syndrome in conjunction with lithotomy positioning,^[14,16] these devices have been found to reduce compartment pressures in non-anesthetized healthy volunteers in lithotomy position.^[19]

Compartment syndrome may develop after infiltration of an IV catheter, particularly if the infusion is administered under pressure,^[20,21] or mannitol^[22] or IV contrast dye^[23] has been administered. Intraosseous fluid administration has rarely been associated with the subsequent development of compartment syndrome. This infrequent complication has been reported primarily among pediatric patients,^[24–29] who typically receive intraosseous administration more frequently than do adult patients. However, intraosseous administration of fluids and medications for the resuscitation of the unstable adult patient without IV access has been recommended by the American Heart Association since 2010.^[30] More recently, compartment syndrome has been reported in an adult patient in the intraosseous line.^[31] The development of compartment syndrome with intraosseous fluid administration has been associated with greater volumes and rates of fluid infusion, the use of hypertonic crystalloids, needle malposition, bone fracture, or recent (<48 hours) prior intraosseous infusion in the same bone.^[32] It should be emphasized that although fluid extravasation occurs in as many as 22% of pediatric patients with intraosseous fluid infusions,^[33] development of compartment syndrome is a rarely observed complication. Compartment syndrome has been very rarely reported with IV regional anesthesia (Bier block) of the upper^[34] or lower extremity.^[35] Compartment syndrome may occur at any point during the postoperative period, but is most typically recognized within 24 hours of surgery.^[36,37]

Management: The management of acute compartment syndrome is surgical. Best outcomes for limb function are achieved when fasciotomy is performed within 12 hours. Delayed diagnosis is limb-threatening, and compartment syndrome lasting more than 4 hours may result in acute kidney injury from rhabdomyolysis. Intravenous hydration and alkalization of the urine may be renal protective.

Quadriplegia

New-onset quadriplegia after surgery is rare and terrifying. If surgery involved the cervical spine, neurological deficits may be secondary to direct cord trauma, cord ischemia, or epidural hematoma. However, quadriplegia has been reported after procedures remote from the cervical spine including procedures of the lumbar spine, ophthalmological, cardiac, thoracic, and general surgical procedures. The diagnosis of the etiology of quadriplegia after procedures distant from the spinal cord is clinically challenging. Postoperative quadriplegia has been reported in patients with known cervical spine pathology, subclinical pathology, and in patients without pre-existing pathology.

Quadriplegia related to pre-existing spine pathology: Atlanto-axial instability is a feature of numerous diseases and syndromes, most notably rheumatoid arthritis and Down’s syndrome. While there is anecdotal evidence of injury to the cervical spinal cord from airway management in patients with unstable cervical spines either due to trauma or medical co-morbidity, these reports are rare, and causality is uncertain.^[38–43]

Pre-existing cervical spondylosis or spinal stenosis may create increase risk for cord injury during laryngoscopy or surgical positioning. Transient quadriplegia has been reported after endotracheal intubation in two patients with stable cervical spines who had cervical spondylosis.^[44] The mechanism of injury was presumably neck extension during laryngoscopy, although causality was not proven, and unrecognized disturbances of spinal cord perfusion during surgery could also have been contributory. Fortunately, outcome for both these patients was excellent and symptoms resolved within 24 hours. Undiagnosed cervical spondylosis and spinal stenosis contributed to permanent quadriplegia after lengthy neck extension for dental extractions under general anesthesia.^[45]

Central cord syndrome may also be triggered by neck hyperextension in the presence of spondylosis or spinal stenosis. Central cord syndrome presents as incomplete quadriplegia, usually with greater motor impairment of the upper extremities and spasticity of the lower extremities. It may be seen as a complication of neck extension of laryngoscopy.^[46,47] It may also occur as a consequence of the surgical procedure and has also been reported after cervical decompression.^[48] Spinal cord injury with the edematous changes to spinal cord gray matter has been implicated in central cord syndrome, so it may present in the early postoperative period or in some cases be a delayed finding. Prognosis is variable, but recovery is common.

Prolonged neck flexion has been associated with midcervical quadriplegia secondary to stretch of the cervical spinal cord. This rare injury has been most frequently reported from intracranial surgery in the sitting position with neck flexion.^[49,50] Prolonged neck flexion during any surgery imparts some risk, and midcervical quadriplegia has been reported from tracheal resection in a young woman maintained with neck flexion after surgery.^[51] Phrenic nerve function may be spared, but overall prognosis for neurological recovery is generally poor. Extreme neck extension in a crime victim who was bound with his head between his ankles for 12 hours resulted in an incomplete cervical injury with recovery at 8 weeks.^[52] This suggests this is a positioning injury and not attributable solely to other variables during surgery.

Management: Management is determined by the underlying etiology. High-dose IV steroid protocols used in other forms of spinal cord injury have been utilized with good results in some patients.

Quadriplegia unrelated to pre-existing spine pathology: Disruption of the anterior spinal artery may cause anterior spinal cord ischemia and subsequent damage to the corticospinal and spinothalamic tracts, with impairment of motor function and pain/temperature sensation and relative sparing of proprioception and vibratory sense. The majority of reported cases have resulted in paraplegia, but quadriplegia may result from more cephalad disruptions of the vasculature.^[53–55]

Cervical spinal hematoma is a feared complication that may rapidly cause spinal cord ischemia in the confined space of the vertebral column. Most perioperative cases can be attributed to surgical complications. Spinal hematoma very rarely develops after injections of the cervical spine. Spontaneous spinal hematoma is possible, and most reported cases have been associated with coagulopathy.^[56] Although coincidental cervical spinal hematoma would seem very unlikely in the postoperative period, coincidental lumbar hematoma related to perioperative dilutional thrombocytopenia has been reported.^[57]

An interesting cause of transient postoperative quadriplegia is hypokalemic periodic paralysis. This typically presents as episodic subjective muscle weakness. However, transient quadriplegia has been reported among individuals with periodic paralysis due to Addison’s disease^[58] and hyperthyroidism.^[59] A single report of postoperative hypokalemic periodic paralysis presented as transient quadriplegia.^[60] In distinction to high cervical cord injury, patients with periodic paralysis have intact phrenic nerve function and are able to breathe normally and phonate. Periodic paralysis results from a number of different channelopathies and may also be associated with eukalemia or hyperkalemia, so acute electrolyte testing during an episode of paralysis may or may not aid in diagnosis.

Management: Cervical epidural hematomas require immediate surgical decompression. Episodes of periodic paralysis are self-limited, and management is supportive. General medical management includes treatment of a causative co-morbidity (e.g. thyrotoxicosis) and avoidance of triggers such as carbohydrate loading, stress, or sudden changes in temperature.^[61] Surgery has not been implicated as a trigger to date.

Paraplegia

New-onset paraplegia after surgery is more common than quadriplegia and usually related to direct surgical injury to the spine. Major vascular and orthopedic procedures have been associated with a low incidence of postoperative paraplegia.

Anterior spinal cord syndrome is an important cause of postoperative paraplegia. Thoracic aortic and thoracoabdominal surgery are the most common causes of postoperative spinal cord ischemia resulting in paralysis. In most people, the artery of Adamkiewicz arises from the aorta between the T₈ and L₁ vertebral bodies, but significant variation in normal anatomy exists.^[62] This vessel is at risk during abdominal aortic aneurysm repair, and subsequent paraplegia has been observed.^[63–67] Aortic dissection may sometimes cause anterior spinal cord syndrome, whether it occurs spontaneously or is caused by the presence of an intra-aortic balloon pump.^[68,69] Anterior spinal cord syndrome has been infrequently reported after other non-vascular procedures including procedures of the thorax.^[70]

Spinal hematoma may be caused by either surgery or neuraxial anesthesia and results in postoperative paraplegia. Spinal hematoma occurs after 1 in 150,000 epidural anesthetics and 1 in 222,000 spinal anesthetics.^[71] More than half of the cases of neuraxial anesthesia in the American Society of Anesthesiologists (ASA) Closed Claims Database arise from vascular procedures with the second most common procedure being orthopedic.^[72] Back pain is the cardinal symptom of spinal hematoma and has been reported in approximately 80% of the more than 600 case reports in the literature.^[73] Interestingly, back pain was present in only 25% of the cases in the ASA Closed Claims Database. This may reflect a decreased incidence of back pain in perioperative hematomas (secondary to opioids, sedation, or distracting pain) or bias for abnormal presentations of spinal hematoma having delayed diagnosis and worse clinical outcomes.^[74] Bowel or bladder incontinence with motor impairment were the most common clinical presentations.

The accumulation of air in the epidural space from the injection of air during epidural catheter placement has been implicated in a variety of neurological deficits including, in very rare cases, transient paraplegia.^[75,76] Inadvertent injection directly into the spinal cord during spinal or epidural anesthesia can cause paraplegia. These injections are typically performed in awake patients who should be able to report pain during injection, but intracord injection with permanent paraplegia has been reported despite this precaution.^[77]

Transverse myelitis has been reported after both spinal and epidural injections.^[78–83] The etiology is unknown and causality unproven. In most of these reports, symptoms appeared between 6 hours and 2 days after injection, but may be delayed for 1 to 2 weeks. Adhesive arachnoiditis has been reported after injection with tainted pharmaceuticals. In most cases the symptoms are after an interval of weeks to months,^[84] but in a single report developed within six hours of injection.^[85]

Management: Acute-onset paraplegia needs rapid imaging (CAT scan or MRI). Management of paraplegia is dependent upon etiology, but radiographic imaging should be obtained without delay to make the diagnosis of spinal hematomas. Hematomas need prompt surgical decompression, with the best results usually obtained if performed within 8 to 12 hours from the onset of symptoms.

Stroke

Acute ischemic or hemorrhagic cerebrovascular events may occur after procedures that do not involve intracranial trespass or manipulation of cerebral vasculature. Cardiac procedures are at increased risk because of embolic events related to cardiopulmonary bypass. While the clinical presentation of stroke is varied, it may include limb weakness or hemiplegia. The incidence of stroke within 30 days of non-cardiac, non-neurological surgery is between 0.05% and 7.4%.^[86] Since these incidences are derived from retrospective review of databases of postoperative complications, they may underestimate the actual incidence of neurological events, owing to underreporting of transient events such as transient ischemic attacks or reversible ischemic neurological defects. The proinflammatory effects of surgery are implicated in the etiology of postoperative ischemic stroke after general surgery, with interleukin-6 appearing to be a significant mediator.^[87] While perioperative hypotension could cause cerebral ischemia, patient co-morbidities including chronic obstructive pulmonary disease, prior cerebrovascular accident, and peripheral vascular disease appear to be more important than hypotensive episodes.^[88] Advanced age, atrial fibrillation, and renal disease have also been identified as important predictors of perioperative stroke.^[86]

Management: A head computed tomography scan or diffusion-weighted MRI (if available) should be obtained without delay if stroke is suspected. Management in consultation with the neurologist is based upon the etiology of the event and on institutional resources and protocols for stroke management.