Neurologic Events

Central Nervous System Injury


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.


  • 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)


  • 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


  • 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


  • 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 urine or blood for toxicology screens

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


  • 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

Suggested Reading

  • 1. Stahel P.F., VanderHeiden T., Finn M.A.: Management strategies for acute spinal cord injury: current options and future perspectives. Curr Opin Crit Care 2012; 18: pp. 651-660.
  • 2. Mashour G.A., Shanks A.M., Kheterpal S.: Perioperative stroke and associated mortality after noncardiac, nonneurologic surgery. Anesthesiology 2011; 114: pp. 1289-1296.
  • 3. Davis M.J., Menon B.K., Baghirzada L.B., et. al.: Anesthetic management and outcome in patients during endovascular therapy for acute stroke. Anesthesiology 2012; 116: pp. 396-405.

  • Local Anesthetic Systemic Toxicity


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


    • 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


    • 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


    • 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


    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


    • 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.

    Suggested Reading

  • 1. Neal J.M., Bernards C.M., Butterworth J.F., et. al.: ASRA practice advisory on local anesthetic systemic toxicity. Reg Anesth Pain Med 2010; 35: pp. 152-161.
  • 2. Neal J.M., Mulroy M.F., Weinberg G.L.: American Society of Regional Anesthesia and Pain medicine checklist for managing local anesthetic systemic toxicity: 2012 version. Reg Anesth Pain Med 2012; 37: pp. 16-18.
  • 3. Neal J.M., Hsiung R.L., Mulroy M.F., et. al.: ASRA checklist improves trainee performance during a simulated episode of local anesthetic systemic toxicity. Reg Anesth Pain Med 2012; 37: pp. 8-15.
  • 4. Wolfe J.W., Butterworth J.F.: Local anesthetic systemic toxicity: update on mechanisms and treatment. Curr Opin Anesth 2011; 24: pp. 561-566.
  • 5. Mercado P., Weinberg G.L.: Local anesthetic systemic toxicity: prevention and treatment. Anesthesiol Clin 2011; 29: pp. 233-242.

  • Perioperative Visual Loss


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


    • 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

    Typical Situations

    • Prolonged spine or other surgery in the prone position

    • Procedures with substantial blood loss or hypotension

    • Procedures performed in the steep Trendelenburg position (e.g., robotic prostatectomy or robotic gynecology cases)

    • Perioperative globe compression

    • Procedures requiring CPB

    • Retrobulbar or peribulbar block administration

    • Male gender

    • Obesity


    Not all of the causative factors in POVL are known, the following are based on current recommendations.

    • Consider “staging” long, complex spine procedures as two or more separate operations

    • Maintain head in neutral position

      • Avoid head below heart position

      • Avoid use of Wilson positioning frame

    • Maintain BP within 20% of baseline

    • Avoid deliberate hypotension

    • Avoid hemodilution

      • Balance crystalloid administration with colloid

      • Monitor hematocrit at frequent intervals

        • Discuss transfusion threshold with patient and surgeon

    • Avoid direct pressure on globe and reassess at frequent intervals

      • Consider using mirrored headrest in prone cases

    • Avoid prolonged CPB times

    • Avoid N 2 O during and after intraocular sulfur hexafluoride (e.g., surgery for detached retina)

    • Cover patient’s eyes with appropriate goggles during nonocular laser surgery

    • Monitor visual-evoked potentials in procedures that affect the ophthalmic artery or optic nerve


    • Loss of vision evident after recovery from anesthesia

      • Bilateral or unilateral

      • Partial or total

    • Periorbital edema and chemosis

    • Decreased ocular movements

    • Nystagmus

    • Ocular pain

    • Abnormal fundoscopic examination

    • Loss of or abnormal pupillary reflexes

    • CRAO

      • Unilateral vision loss or changes in light perception, decreased extraocular movements

      • Periorbital edema and chemosis

      • Cherry-red spot and pale, edematous retina on fundoscopic examination

      • Afferent pupillary defect

    • Anterior ION

      • Painless visual loss

      • MRI evidence of enlarged optic nerve

      • Afferent pupillary defect

    • Posterior ION

      • Bilateral visual loss or changes

      • Onset may be delayed a few days

      • Afferent pupillary defect or nonreactive pupil

    • Cortical blindness

      • Normal pupillary response and fundoscopic examination results

      • Occipital infarction on MRI

    • Acute closed-angle glaucoma

      • Presents as ocular pain and blurred vision with a red eye

      • Raised intraocular pressure (IOP)

      • Fixed, dilated pupil

    Similar Events

    • Residual petroleum-based ophthalmic ointment

    • Corneal abrasion

    • Photophobia

    • Residual anticholinergic medication effects

    • Glycine toxicity during TURP


    • Examine the patient and evaluate the severity of visual impairment or ocular trauma

      • Check visual fields

      • Check pupillary responses to light

    • If examination is abnormal, obtain urgent ophthalmologic consultation

    • Obtain MRI examination

    • Manage patient with ophthalmology

      • In the absence of a treatable cause, visual loss is likely to be permanent

      • The ASA Task Force on Perioperative Blindness found that there is no role for antiplatelet agents, steroids, or IOP-lowering agents in the treatment of ION

    • The following therapies have been attempted, but efficacy has not been proved.

      • Head-up position

      • Hyperbaric O 2

      • Augmenting O 2 delivery (optimization of BP, hematocrit, and arterial oxygenation)

      • Acetazolamide to lower IOP

      • Diuretics

      • Steroids

      • Anterior chamber paracentesis

      • Ocular massage to lower IOP and possibly dislodge emboli

      • Inhaled CO 2 in O 2 to enhance retinal artery dilation

      • Endovascular fibrinolysis of the ophthalmic artery for retinal artery occlusion

      • Optic nerve sheath decompression


    Partial or total permanent visual loss

    Suggested Reading

  • 1. Roth S.: Perioperative visual loss: what do we know, what can we do?. Br J Anaesth 2009; 103: pp. i31-i40.
  • 2. Practice advisory for perioperative visual loss associated with spine surgery: an updated report by the American Society of Anesthesiologists Task Force on Perioperative Visual Loss. Anesthesiology 2012; 116: pp. 274-285.
  • 3. Lee L.A., Roth S., Posner K.L., et. al.: The American Society of Anesthesiologists Postoperative Visual Loss Registry: analysis of 93 spine surgery cases with postoperative visual loss. Anesthesiology 2006; 105: pp. 652.
  • Only gold members can continue reading. Log In or Register to continue

    Feb 22, 2019 | Posted by in ANESTHESIA | Comments Off on Neurologic Events
    Premium Wordpress Themes by UFO Themes