Neurologic Events

Definition

A central nervous system (CNS) injury is any new neurologic deficit presenting after anesthesia that can be localized anatomically to the brain or spinal cord.

Etiology

• Cerebral ischemia

  • Global

  • Focal

• Cerebral hemorrhage

• Cerebral embolism

• Increased ICP

• Hypoglycemia

• Direct trauma or surgical injury to CNS

• Injection of neurolytic solutions into the cerebrospinal fluid or into CNS

• Epidural or subdural hematoma

Typical Situations

• In patients with diseases predisposing to cerebral ischemia or embolism

  • AF

  • Endocardial mural thrombus following a MI

  • Known cerebrovascular disease

    • Previous stroke or transient ischemic attacks (TIAs)

    • Hypertension

    • Smoking history

    • Diabetes mellitus

    • Dyslipidemia

    • Obesity

  • Pregnancy-induced hypertension

• Following surgery that carries a high risk of CNS injury

  • Carotid endarterectomy or carotid stenting

  • Procedures requiring CPB

    • Cardiac surgery

    • Repair of descending thoracic aneurysm or dissection (impaired blood flow to the spinal cord)

  • Craniotomy or procedures on or near the spinal cord

• Following an intraoperative catastrophe with hypotension or cardiac arrest

• In patients with raised ICP

• In patients positioned with traction on or compromise of blood flow to the spinal cord

  • Procedures in the sitting position

• In patients with anatomic abnormalities of the bony covering of the CNS

  • Congenital (Down syndrome, Klippel-Feil syndrome)

  • Acquired (rheumatoid arthritis with cervical instability)

  • Spinal stenosis

• Following neuraxial anesthesia (especially in patients taking anticoagulants and antiplatelet agents)

Prevention

• Identify patients with conditions that predispose to CNS injury

  • Optimize treatment of medical conditions (hypertension, diabetes mellitus)

  • Monitor neurologic function in patients at risk

    • EEG

    • Evoked potentials

• Position patients carefully and reassess during long cases

  • Avoid extreme rotation, flexion, or extension of the cervical spine

  • In the sitting position, support patients adequately to prevent traction on the spinal cord or cervical spine

• Maintain an adequate cerebral perfusion pressure

  • Measure BP at the level of the brain

• Maintain adequate perfusion pressure of the spinal cord

  • Consider placement of a lumbar drain during thoracic aortic surgery

• In patients with raised ICP

  • Avoid obstruction to cerebral venous outflow

  • Maintain the head in an elevated position

  • Ventilate the patient to maintain PaCO ₂ of 30 to 35 mm Hg

• Avoid neuraxial regional anesthesia in patients with a bleeding diathesis

Manifestations

• Cerebral injuries may be manifested by

  • Delayed recovery from anesthesia

  • A new focal motor or sensory deficit

  • Seizures

  • Subarachnoid hemorrhage

    • Severe headache, stiff neck, or neurologic deficit

• SCI may be manifested by

  • Failure of the sensory or motor level to recede after neuraxial block

  • Motor and/or sensory deficits

  • Cauda equina syndrome

    • Loss of bowel and/or bladder function, saddle anesthesia, lower extremity pain and/or weakness

Similar Events

• Inadequate reversal of neuromuscular blockade (see Event 56, Postoperative Failure to Breathe )

• Slow resolution of spinal or epidural block

• Drug administration errors (see Event 63, Drug Administration Error )

• Delayed recovery from general anesthesia (see Event 55, Postoperative Alteration in Mental Status )

• Transient neurologic deficits secondary to metabolic disorders (see Event 55, Postoperative Alteration in Mental Status , and Event 54, Peripheral Nerve Injury )

• Seizure (see Event 57, Seizure )

• In patients with prior stroke, there may be a temporary exacerbation of previously compensated stroke symptoms in the recovery period after general anesthesia

• Psychosomatic neurologic deficit

Management

• Ensure adequate oxygenation and ventilation (see Event 10, Hypoxemia , and Event 32, Hypercarbia )

  • Mild hypoxemia can cause obtundation but more often causes restlessness, which may be mistakenly treated with further sedation and result in respiratory depression

  • Severe hypoxemia can cause coma

  • Hypercarbia generally causes obtundation

• Check that all volatile and IV anesthetics have been discontinued

  • Administer 100% O ₂ with high flows into the breathing circuit to enhance elimination of inhalation anesthetics

  • Check expired anesthetic gas concentrations

• Stimulate the obtunded patient

  • Use verbal or tactile stimuli and gentle suctioning of the upper airway

• Perform a neurologic examination

  • Check pupillary diameter and reaction to light

    • Anesthetic or ophthalmic drugs may affect pupillary size or response to light

  • CNS injury may alter pupillary size or might manifest as a blown pupil

  • Check for the presence of corneal and gag reflexes

  • Test the response to physical stimulation or deep pain

  • Check the limb reflexes and plantar responses (Babinski reflex)

• If abnormalities on neurologic examination are evident, inform the surgeon

  • Assume cerebral ischemia, infarction, embolism, or hemorrhage has occurred

  • Obtain an immediate neurology or neurosurgery consultation

  • Obtain a CT scan of the head or spinal cord if the patient can be moved safely

    • Hypertension and hypotension should be managed cautiously in consultation with the neurologist

  • Other imaging studies may be needed to determine cause of abnormality

  • Further therapy depends on the diagnosis but may include

    • Thrombolytics or anticoagulation for cerebral thromboembolism

    • Surgical decompression of intracranial hemorrhage

    • External ventricular drain placement for ICP management

  • For acute, nonpenetrating SCI, consider administering high-dose corticosteroids

    • Methylprednisolone IV, 30 mg/kg, followed by 5.4 mg/kg/day for 24 or 48 hours

    • Use of steroids in acute SCI remains controversial

• Rule out a metabolic etiology

  • Send blood and urine samples to the laboratory

    • Treat hypoglycemia with 50% dextrose IV, 1 mL/kg, or rapid infusion of D5W (see Event 41, Hypoglycemia )

    • Treat hyperglycemia, DKA, and hyperosmolar nonketotic coma with insulin therapy IV and volume resuscitation (see Event 39, Diabetic Ketoacidosis )

    • Treat hyponatremia (see Event 43, Hyponatremia and Hypo-osmolality )

    • Treat metabolic acidosis (see Event 46, Metabolic Acidosis )

• Send urine or blood for toxicology screens

• Check for drug administration errors (see Event 63, Drug Administration Error )

Complications

• Hypoxemia, hypercarbia

• Cardiovascular instability

• Inability to maintain or protect the airway

• Aspiration of gastric contents

• Extension of neurologic injury

• Permanent CNS injury

• Metabolic abnormalities (e.g., hyperglycemia)

• Seizures

• Death

Definition

Local anesthetic systemic toxicity (LAST) is an adverse systemic effect of high blood concentrations of local anesthetics.

Etiology

• Direct intravascular injection of local anesthetic solution

• Excessive amount of local anesthetic absorbed into the circulation over a short period

Typical Situations

• During regional anesthesia in which large volumes of local anesthetic are administered or when there is significant potential for intravascular injection

  • Epidural anesthesia

  • Intercostal nerve blocks

  • Paravertebral block

  • Lumbar plexus block

  • Brachial plexus block

  • Femoral nerve block

  • Paracervical block for gynecologic procedures

  • IV regional anesthesia (Bier block)

  • Pain-related blocks (e.g., stellate ganglion block, lumbar sympathetic block, etc.)

• During IV lidocaine infusion

• During topicalization of the nasopharynx with local anesthetic

Prevention

• Create “LAST Treatment Kit” and notify personnel as to its contents and location

• Post a LAST treatment cognitive aid at locations where high volumes and concentrations of local anesthetics are used (e.g., block areas, ORs, PACUs, labor and delivery)

• Pretreating the patient with a benzodiazepine will increase the seizure threshold but may mask early LAST neurologic symptoms

• Where large volumes of local anesthetic are administered, use standard American Society of Anesthesiologists (ASA) monitoring during and after the block for 30 minutes

• Use the following techniques during regional blockade to minimize risk of intravascular injection:

  • Ultrasound guidance

  • Assess the patient’s response to a test dose of local anesthetic; consider using epinephrine (5 µg/mL) as a marker for intravascular injection

  • Use an incremental aspiration and injection technique, looking for blood prior to injecting local anesthetic

  • Continuously assess patient’s mental, neurologic, and cardiovascular status during and after block

  • Any abnormality in patient status should be considered LAST until proven otherwise

  • Use the least amount of local anesthetic for desired effect

  • Do not administer more than the maximum recommended dose

• Monitor the surgeon’s use of local anesthetic for infiltration and in surgical packing

• Use appropriate bolus doses and infusion rates for IV lidocaine therapy

  • Check blood lidocaine levels during prolonged infusions

Manifestations

• CNS abnormalities

  • Tinnitus

  • Circumoral numbness, heavy tongue, metallic taste

  • Nystagmus, diplopia, difficulty in focusing

  • Mental status change: agitation, confusion, obtundation, coma

  • Preseizure motor irritability (twitching), followed by overt seizure

• Airway and respiratory abnormalities

  • Airway obstruction

  • Loss of airway reflexes

  • Respiratory depression followed by apnea

• Cardiovascular abnormalities

  • Initially may be hyperdynamic (hypertension, tachycardia, ventricular arrhythmias)

  • Conduction abnormalities (e.g., increased PR interval, T wave changes, bradycardia, asystole)

  • Progressive hypotension

  • Ventricular arrhythmias (VT, VF, torsades de pointes)

  • Cardiovascular collapse—cardiac arrest

    • Bupivacaine is the local anesthetic most likely to produce cardiovascular collapse, as the cardiovascular collapse:convulsion dosage ratio is lower for bupivacaine than for other local anesthetics

    • Patients with low cardiac ejection fraction are more susceptible to the cardiotoxic effects of local anesthetics

    • Acidosis and hypoxemia markedly potentiate the cardiotoxicity of bupivacaine

Similar Events

• Hyponatremia (see Event 43, Hyponatremia and Hypo-osmolality )

• IV injection of epinephrine

• Hypoxemia (see Event 10, Hypoxemia )

• Inadvertent neuromuscular blockade (see Event 63, Drug Medication Error )

• High spinal/epidural block (see Event 89, Total Spinal Anesthesia )

• Primary seizure disorder (see Event 57, Seizures )

• Anaphylaxis (see Event 16, Anaphylactic and Anaphylactoid Reactions )

• AFE (see Event 81, Amniotic Fluid Embolism )

• Panic reaction

Management

Intra-arterial injection into the carotid or vertebral arteries will result in immediate CNS toxicity, even with small volumes of local anesthetic.

• Stop injection of local anesthetic at the first indication of toxicity

• Call for help, get LAST Treatment Kit, and use the cognitive aid

  • Severe cases of LAST may require prolonged treatment

  • Patients who are healthy at the initiation of the event usually can be resuscitated

• If respiratory distress, apnea, or loss of consciousness occurs

  • Establish bag valve mask airway

  • Deliver 100% O ₂ , assist ventilation as necessary

  • Do not hyperventilate the patient, as this decreases the seizure threshold, but ensure adequate ventilation, as hypercapnia and hypoxemia exacerbate toxicity

• Ensure adequate IV access

• If there is preseizure motor irritability or seizure activity

  • Administer

    • Midazolam IV, 0.5 to 1 mg increments

    • Propofol IV, 10 to 20 mg (higher doses can further depress cardiac function)

      • Seizures are often exquisitely sensitive to these drugs

• If seizures occur, cardiovascular collapse may be imminent

  • Immediately administer lipid emulsion (20%)

    • Bolus 1.5 mL/kg over 1 minute (approximately 100 mL)

    • Continuous infusion 0.25-0.5 mL/kg/min until stable

    • Can repeat bolus dose if symptoms persist or if progresses to cardiac arrest

    • Recommended upper limit: 10 mL/kg in first 30 minutes

    • Continue infusion for at least 10 minutes after attaining circulatory stability

• If seizures do not resolve rapidly

  • Intubate the patient’s trachea using a short-acting muscle relaxant

  • Administer higher doses of midazolam

  • Administer other anticonvulsant drugs (see Event 57, Seizures )

    • Phenytoin IV, loading dose, 10 mg/kg, administered slowly (may cause hypotension)

    • Levetiracetam IV, 1000 mg

  • Administer muscle relaxant after the airway is protected to minimize peripheral O ₂ consumption and resultant acidosis during seizures

    • Assess ongoing seizure activity using an EEG monitoring device

• Management of Cardiac Instability

  • If patient arrests

    • Prolonged resuscitation efforts may be necessary

    • CPR as per BLS/ACLS with these modifications (see Event 94, Cardiac Arrest , and Event 82, Cardiac Arrest in the Parturient )

    • Medications:

      • Reduce epinephrine doses to < 1 μg/kg initially; high-dose epinephrine (1 mg) might impair resuscitation and efficacy of lipid rescue

      • Administer lipid emulsion (20%) as stated previously

      • AVOID vasopressin, calcium channel blockers, beta blockers, local anesthetics, and higher doses of propofol

      • Consider CPB for refractory cardiac arrest

        • Notify the necessary personnel (cardiac surgeon, perfusionist)

        • Transferring any patient in cardiac arrest within a hospital is VERY difficult; consider initiation of CPB at the location where the cardiac arrest occurred

        • If CPB is not available, alert the nearest facility with CPB capability and arrange transfer of the patient

• Monitor patient in the ICU for at least 12 hours, as LAST can persist or recur after initial treatment

• Obtain a consultation from a neurologist if seizures do not resolve

Complications

• Cardiovascular collapse

• Hypoxic brain injury

• Status epilepticus

• Recurrence of systemic toxicity

• Aspiration

• Death

NOTE: Infusion of lipid emulsion has proved useful in the treatment of overdose of other lipid-soluble medications (tricyclic antidepressants and sodium channel blockers). Consider the use of lipid emulsion where overdose is a possibility.

Definition

Perioperative visual loss (POVL) is permanent, partial, or total loss of vision during or after general anesthesia.

Etiology

• Ischemic optic neuropathy (ION)

  • Anterior ION

  • Posterior ION

• Central retinal artery occlusion (CRAO)

• Direct mechanical trauma to optic nerve or compression from retrobulbar hematoma (e.g., during sinus surgery)

• Retinal arterial or venous hemorrhages involving the macula or leading to optic nerve atrophy

• Acute closed-angle glaucoma

• Cortical blindness

• Photic injury from laser techniques

• Direct ocular trauma