Central Nervous System Injury
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
Suggested Reading
Local Anesthetic Systemic Toxicity
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.
Suggested Reading
Perioperative Visual Loss
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
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
Prevention
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
Manifestations
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
Management
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
Complications
Partial or total permanent visual loss
Suggested Reading
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