Due to the high turnover of CSF, obstruction of CSF flow may cause ICH within a few hours, necessitating emergency treatment.
1) ICP and ICH
a) When growth of an intracranial lesion is slow, ICP will remain stable for a while because of shunting of CSF into spinal reservoirs and blood into the central vascular system.
b) When an increase in volume can no longer be accommodated, ICP will increase rapidly with any small change in volume of any of the three components (Fig. 75-1).
Figure 75-1 Idealized ICP/Volume Curve
From Kass IS. Physiology and metabolism of the brain and spinal cord. In: Newfield P, Cottrell JE, eds. Handbook of Neuroanesthesia. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007:21M
.c) ICP above 20 mm Hg will reduce cerebral perfusion pressure (CPP) (CPP = MAP – ICP), and thus needs to be treated.
i) When local tissue pressure exceeds perfusion pressure of the arterioles, the resultant ischemia can cause endothelial injury and increased transudation across capillary membranes, leading to cerebral edema.
ii) If ICH remains untreated, CBF will be low due to maximal arterial constriction, and death will quickly ensue due to limited CBF and/or herniation.
iii) ICH is associated with poor outcome after traumatic brain injury (TBI), and uncontrolled rise in ICP is the most common cause of death in these patients (1).
d) Conditions in which ICH may occur:
i) Parenchymal volume increase due to hemorrhage, tumor, TBI, edema following ischemic events, encephalopathies, and idiopathic ICH (IIH, also called pseudotumor cerebri).
ii) Hydrocephalus due to absolute or relative excess of CSF. Causes include:
(1) Increased CSF production (meningeal disease, CP tumor, or cyst)
(2) Obstruction to CSF flow (Arnold–Chiari malformation, mass effect from tumors, blood in the ventricles from subarachnoid hemorrhage)
(3) Normal pressure hydrocephalus
(a) Characterized by near-normal ICP that slowly increases due to gradually worsening obstruction of flow
(b) Patients are typically older than 60, and develop a triad of dementia, gait problems, and incontinence; etiology is unknown.
iii) Increased cerebral blood volume
(1) Cerebral arterial dilation (hypoxemia, arterial hypertension, volatile anesthetic administration, hypoventilation with resultant hypercapnia)
(2) Increased venous pressure (venous sinus thrombosis, right sided heart failure, or obstruction of jugular or great thoracic veins)
4) CSF leak
a) May occur from several sites, including the nose (rhinorrhea), external auditory canal (otorrhea), or traumatic or operative defects in the skull or spine
b) Causes
i) CSF rhinorrhea may follow trauma and skull base surgery (e.g., transsphenoidal resection of pituitary tumor, translabyrinthine acoustic neuroma resection, mastoid surgery).
ii) Otorrhea can be seen in perforated tympanic membrane with fracture of the petrous or temporal bone, and mastoid or translabyrinthine surgery.
iii) Spinal CSF leak may be seen in trauma, lumbar puncture (LP), inadvertent “wet tap” during epidural placement, Valsalva or nose-blowing, or postoperatively.
iv) Spontaneous CSF leak
(1) Rare and may be difficult to diagnose and treat
(2) Recent research indicates that 90% of these patients have ICH, and often the best closure success is with endoscopic repair.
c) Depending on the cause, epidural blood patch may be used as in therapy for post-dural puncture headache.
d) If unplanned durotomy is suspected intraoperatively, one may differentiate between CSF and other fluids by using a urine test strip to test for the presence of glucose.
5) Diagnosis of ICH
a) Symptoms may be subtle, depending on the etiology and anatomy involved, and include decreased level of consciousness, breathing irregularities, visual problems, headache, nausea and vomiting, irritability and personality changes, memory loss, ataxia, and weakness.
b) Signs include papilledema, neurologic deficit, and unstable vital signs (hyper- or hypotension, arrhythmias)
c) Diagnostic imaging
i) May be normal or show enlarged ventricles and/or lateral shift.
ii) Evaluate scan for CVA, mass effect from tumor or hemorrhage, as well as signs of impending herniation.
d) If patient is pregnant, preeclampsia should be ruled out.
Signs and symptoms of increased ICP are diminished consciousness, nausea/vomiting, visual problems, and headache.
6) Monitoring
a) Monitoring of ICP assists in determining optimal therapy and may prevent herniation.
b) Direct ICP monitoring is performed via ventriculostomy and manometry.
i) An external ventricular drain (EVD) or lumbar drain can be placed pre- or intraoperatively when anticipated that brain relaxation could be needed during the case, or if potential for postoperative CSF leak exists (see above).
ii) Removal of 3 to 5 mL can be quickly accomplished and may be sufficient to treat acute ICH.
c) Measurement of ICP
a) ICP is measured relative to a reference level, above which positive ICPs will result in CSF flow if the system is open.
b) Zero the catheter at the level of the external auditory meatus, then raise the top of the reservoir to a height above the ear that equals the acceptable ICP; CSF will flow into the reservoir bag once the ICP exceeds this level.
(1) Care must be used in determining the height at which to hang the reservoir bag as it is possible to over-drain CSF, with potential complications such as SDH, intracranial hypotension, rupture or re-bleed of an aneurysm, or even herniation (2).
(2) Volume-limited (20 to 30 mL) CSF drainage systems have been recently introduced.
d) Other types of ICP monitors (subarachnoid bolt, epidural sensor, fiberoptic direct tissue monitor (intraparenchymal) with a pressure transducer) are used primarily in the ICU.
e) Patients in whom ICP therapy is ongoing may need CVP and arterial line to optimize volume status and CPP.
Lumbar puncture, used to diagnose various neurologic conditions, may induce herniation and should not be perfrmed if ICH is suspected.
An extraventricular drain should be zeroed at the level of the external auditory meatus.
7) Medical treatment of ICH
a) Elevation of the patient’s head up to 30 degrees is rapidly effective.
b) Ensure there is no obstruction to venous drainage from the head.
c) Hyperventilate patient to ETCO2 of 25 to 30.
i) ETCO2 will return to normal via bicarbonate buffering after 4 to 8 hours of hyperventilation.
ii) Over-ventilation to ETCO2 < 25 may cause ischemia secondary to severe vasoconstriction.
d) Control BP to maintain systolic BP 110 > MAP > 70
e) Treat hypoxia
f) IV fluids should be isotonic or hypertonic to avoid further increase in brain water
g) Osmotic or loop diuretics
i) Mannitol is currently the first line agent at a dose of 0.25 to 1 g/kg.
ii) Hypertonic saline (HS) may be more effective than mannitol (3,4–5) with fewer side effects.
(1) There are few studies of intraoperative HS use (6,7), and none show a difference in effectiveness between HS and mannitol.
(2) HS expands plasma volume and may increase CPP, unlike mannitol which can decrease intravascular volume (4,8,9–10).
(3) A reasonable starting dose would be 30 mL of 23.4% HS via central venous catheter over 15 to 20 minutes, after which 3% HS may be infused at 30 to 50 mL/h to keep serum Na+ at 140 to 145 (checked with osmolality at least every 4 hours) (9).
h) Prevent shivering, muscle movements, pain, and seizures with narcotics, paralytics, anti-epileptics, sedatives or barbiturates as necessary, once appropriate ventilation is assured.
Dextrose-containing fluids should not be administered to patients with ICH because once the dextrose is metabolized, free water remains which can worsen brain edema.
Patients with ICH should get little or no preoperative sedation.
8) Surgical treatment of ICH
a) Preoperative planning
i) Patients with ICH who are awake and responsive should get little or no preoperative sedation because hypoventilation can further increase ICP, possibly causing herniation.
ii) ABG after induction may be helpful in determining the best ventilatory parameters in patients where significant end-tidal to arterial CO2 gradient may exist.
b) Intraoperative technique
i) Voluntary hyperventilation while awake followed by early mask hyperventilation during anesthetic induction may assist in minimizing changes in ICP or CPP during induction and intubation.
ii) Assurance of anesthetic depth before intubation is important.
iii) Anesthetic agents
1) Propofol, thiopental, and etomidate decrease ICP.
2) Ketamine recently shown to be safe in patients with ICH under certain conditions, although its use is still controversial (11).
1) Volatile anesthetic agents may cause a small increase in ICP via cerebral vasodilation, but this effect may be overcome by mild hyperventilation.
4) The effects of N2O on ICP vary with concentration.
(a) Increase in ICP has been shown in humans but is largely attenuated with prior hyperventilation or administration of induction agents which cause decreased ICP.
(b) N2O should not be used when there is a chance of intracranial air and some anesthesiologists do not use it at all for intracranial procedures.
5) Narcotics have no direct effect on ICP but may cause hypoventilation leading to ICH.
6) Barbiturates are occasionally administered to prevent brain herniation upon dural opening if the dura looks “tight” upon turning the bone flap.
Extreme care should be taken when intubating a patient with ICH as hypertension on laryngoscopy can cause uncal herniation.
c) Surgical procedures
i) Shunt procedures
1) For urgent but non-emergent increases in ICP due to obstruction of CSF flow (patient symptomatic but herniation not imminent)
2) Shunts are silastic catheters used to drain CSF from an area of high pressure (ventricles or cistern) to one of lower pressure
1) The proximal end is most often placed in the right lateral (intracranial) ventricle
4) The distal end is tunneled under the skin to one of several locations (the right atrium via the internal jugular vein, pleural cavity, peritoneal cavity, gall bladder)
a) Venous placement of the distal end is most often used if the patient is obese, has peritonitis or previous abdominal surgery.
b) The hypertensive response frequently seen with skin tunneling of the catheter should be forestalled by increasing anesthetic depth (narcotics, propofol, sevoflurane) or β adrenergic antagonists.
5) If there is free communication between intracranial and spinal CSF, an LP shunt may be used instead (from lumbar subarachnoid space into peritoneum).
6) For shunt removal due to infection, hold antibiotics until cultures are taken.
7) No special intraoperative monitoring is necessary for a shunt procedure.
VP Shunts have a fairly high failure rate over time and are frequently revised, or may be removed and subsequently replaced if infection develops.
ii) Minimally invasive neuroendoscopic surgery for treatment of CSF obstruction
1) Used effectively to treat many types of obstructive hydrocephalus, and may be lower risk than craniotomy or shunt procedures (12).
2) Infection rate of endoscopic third ventriculostomy for resection of colloid cyst is lower than with transcallosal craniotomy (13).
1) Aqueductoplasty and aqueductal stenting are examples of other therapeutic options afforded with the endoscope.
4) Long-term patency rates are as yet unknown and require follow up studies.
iii) Emergency craniotomy for refractory ICH
1) Decompressive craniectomy solely for ICH is still somewhat controversial.
2) Rarely, surgical resection of brain tissue may be necessary.
1) If ICP remains elevated at the end of a craniotomy (surgeon unable to put on bone flap without compressing brain tissue), the bone may be frozen and replaced at a later date.
9) Postoperative care
a) Maintain slight head up position.
b) If an ICP monitor or EVD is in place, watch the level of the bag and ICP as the patient is moved and transported.
c) Carry sedative agent, vasoconstrictors, and vasodilators with you during transport in case needed urgently to keep patient sedated or manipulate BP.
Chapter Summary for the Patient with Increased ICP
ICP, intracranial pressure; CPP, cerebral perfusion pressure; CSF, cerebrospinal fluid; MAP, mean arterial pressure; ICH, intracranial hypertension; ETCO2, end-tidal carbon dioxide.
References
1. Grande PO, Bentzer P. Hypertonic saline: a marker for discrimination between a disrupted and intact blood-brain barrier? Crit Care Med 2006;34(12):3057–3058.
2. Muraskin SI, Roy RC, Petrozza PH. Overdrainage of cerebrospinal fluid during central venous catheter exchange in a patient with an external ventricular drain. Anesth Analg 2007;105(5):1519–1520.
3. Qureshi AI, Wilson DA, Traystman RJ. Treatment of elevated intracranial pressure in experimental intracerebral hemorrhage: comparison between mannitol and hypertonic saline. Neurosurgery 1999;44(5):1055–1063; discussion 1063–1064.
4. Levine JM. Hypertonic saline for the treatment of intracranial hypertension: worth its salt. Crit Care Med 2006;34(12):3037–3039.
5. Battison C, Andrews PJ, Graham C, et al. Randomized, controlled trial on the effect of a 20% mannitol solution and a 7.5% saline/6% dextran solution on increased intracranial pressure after brain injury. Crit Care Med 2005;33(1):196–202; discussion 257–258.
6. Gemma M, et al. 7.5% hypertonic saline versus 20% mannitol during elective neurosurgical supratentorial procedures. J Neurosurg Anesthesiol 1997;9(4):329–334.
7. Rozet I, et al. Effect of equiosmolar solutions of mannitol versus hypertonic saline on intraoperative brain relaxation and electrolyte balance. Anesthesiology 2007;107(5):697–704.
8. Bentsen G, Breivik H, Lundar T, et al. Hypertonic saline (7.2%) in 6% hydroxyethyl starch reduces intracranial pressure and improves hemodynamics in a placebo-controlled study involving stable patients with subarachnoid hemorrhage. Crit Care Med 2006;34(12):2912–7.
9. Qureshi AI, Suarez JI. Use of hypertonic saline solutions in treatment of cerebral edema and intracranial hypertension. Crit Care Med 2000;28(9):3301–3313.
10. Schwarz S, Georgiadis D, Aschoff A, et al. Effects of hypertonic (10%) saline in patients with raised intracranial pressure after stroke. Stroke 2002;33(1):136–140.
11. Himmelseher S, Durieux ME. Revising a dogma: ketamine for patients with neurological injury? Anesth Analg 2005;101(2):524–534.
12. Schroeder HW, Oertel J, Gaab MR. Endoscopic treatment of cerebrospinal fluid pathway obstructions. Neurosurgery 2007;60(2 Suppl 1): ONS44–ONS51; discussion ONS51–ONS52.
13. Horn EM, Feiz-Erfan I, Bristol R, et al. Treatment options for third ventricular colloid cysts: comparison of open microsurgical versus endoscopic resection. Neurosurgery 2007;60(4):613–618; discussion 618–620.
Anesthesia and Diseases of the Nervous System
Divya Chander, MD, PhD
Assessment of underlying neurological disease in the patient undergoing anesthesia is critical. The nervous system exerts control over all physiological systems affected by anesthesia, including the respiratory and cardiac systems. The autonomic branch controls compensatory mechanisms to anesthetic perturbations, and all three branches contribute to maintenance of intact reflex systems, most notably, airway reflexes. Certain motor system diseases share susceptibility to malignant hyperthermia triggers. Anatomically, the nervous system is vulnerable to injury with delivery of anesthetics, especially when regional or neuraxial techniques are used. Finally, the nervous system itself is the target of anesthetics; cerebral vasoregulation, cerebral excitatory and inhibitory balance, traffic along peripheral nerves, and proper function of the neuromuscular junction are altered. Anesthesia also modulates the global arousal system and may therefore have long-lasting cognitive effects in select, vulerable patient populations. Therefore, knowledge of how to manage patients with neurological derangements contributes to the safety of anesthetic delivery.
1) Motor System Diseases
a) Motor system dominated diseases include myopathies and muscular dystrophies, motor end-plate denervation, motor neuron degeneration, spinal motor tract disorders, and disuse atrophy. Motor system disease involving other branches of the nervous system includes peripheral nerve disease, polyneuropathies, and spinal cord injury.
b) Amyotrophic lateral sclerosis (ALS)
i) Progressive loss of both upper and lower motor neurons leading to fasciculations, flaccid paralysis, hyperreflexia, and spasticity.
ii) Treatment
(1) There are no effective therapies at this time.
(2) Patients may be on a number of experimental treatments that rarely have anesthetic interactions (e.g. high dose antioxidants, or riluzole, an anti-glutamatergic drug).
c) Duchenne muscular dystrophy (DMD)
i) X-linked disorder of the dystrophin gene leading to muscle wasting and weakness, dilated cardiomyopathy (in 50% of patients by age 15), ultimately resulting in early death (1).
ii) Administration of malignant hyperthermia (MH) triggers can lead to perioperative, hypermetabolic complications reminiscent of MH (1–3).
d) Central core disease (muscle channelopathy)/King Denborough syndrome (myopathy)
i) A group of rare muscle disorders directly linked to MH (3).
e) Anesthetic management
i) Preoperative considerations
(1) Risk of aspiration and requirement for postoperative ventilatory support should be rigorously assessed.
(2) Regional anesthesia is not contraindicated, though nervous system deficits should be meticulously documented and risks explained thoroughly to patients so pre-existing deficits are not confused with nerve injury.
(3) Prepare an anesthesia machine free of MH-triggering agents for those disorders that are MH-susceptible (3,4).
ii) Induction
(1) Succinylcholine should be avoided secondary to muscle denervation and up-regulation of extrajunctional receptors in all motor neuron diseases. Severe hyperkalemia my lead to intractable bradycardia and/or cardiac arrest.
(2) Patients may be more sensitive to non-depolarizing muscle relaxants.
(3) In the dystrophies and myopathies such as central core disease and King Denborough syndrome, both succinylcholine and potent volatile anesthetics should be avoided because they may lead to rhabdomyolysis or hypermetabolic states reminiscent of MH (1,3).
iii) Maintenance and emergence
(1) A total intravenous anesthetic (TIVA) technique and a “clean” machine are recommended for the dystrophies and myopathies (2,3).
(2) In all motor system diseases, monitoring of muscle twitch with a nerve stimulator should be on an unaffected limb, if one is available.
(3) Autonomic nervous system (ANS) is typically not impaired in pure motor diseases, and hemodynamic responses will be more stable.
(4) In peripheral nerve disease, polyneuropathies (see below) and spinal cord injury, the ANS may show variable impairment and could alter hemodynamics significantly.
iv) Postoperative considerations
(1) Preparation for postoperative ventilatory support should be undertaken in select populations.
(2) Suspicion of hypermetabolic syndromes or rhabdomyolysis should be monitored appropriately in the PACU (e.g. serial serum potassium and creatine kinase levels, urine myoglobin).
When performing a history and physical in any patient with neurologic disease, rigorous documentation of pre-existing deficits, and a full risk-benefit discussion of anesthetic technique with patients is mandatory.
Neurologic diseases resulting in muscle denervation secondary to disuse atrophy or lower motor neuron denervation (e.g. ALS, post-polio syndrome, tetanus, MS, or GBS with motor involvement) can cause a proliferation of extrajunctional receptors and an exaggerated release of extra-cellular potassium in response to sub-paralytic doses of succinylcholine.
2) Peripheral Demyelinating Diseases: Guillian-Barré syndrome (GBS)
a) Demyelinating diseases typically have motor and sensory nervous system involvement; sometimes autonomic nervous system involvement is also present.
b) Guillain–Barré syndrome (GBS): Acute inflammatory demyelinating polyneuropathy (AIDP)
i) GBS is an infrequent, autoimmune response against peripheral nerves, triggered 60–70% of the time by an acute viral respiratory or gastrointestinal infection.
ii) Sequelae occur days to weeks after exposure to infection.
iii) GBS is characterized by an ascending paralysis, affecting limbs before trunk, and loss of deep tendon reflexes.
(1) Cranial nerves are involved 50% of the time.
iv) Treatment for acute episodes is via IV-IG or plasmapheresis exchange. Steroids are not considered useful.
c) Anesthetic management
i) Preoperative considerations
(1) A focused understanding of involved systems is imperative to managing the patient safely – a thorough chart review and patient history must be taken. Targets with important anesthetic implications include:
(a) Autonomic/cardiac system
(i) BP lability in the absence of compensatory cardiovascular reflexes, requiring vasoactive treatment at various intraoperative time points
(ii) Dysrhythmias and possibly cardiac arrest
(b) Brainstem
(i) Compromised pharyngeal reflexes which may contribute to reflux or inability to protect the airway, necessitating unplanned intubation or tracheostomy
(ii) Disordered swallowing
(iii) Vocal cord paralysis
(c) Respiratory system
(i) Increased risk of pulmonary embolus
(ii) Diaphragmatic paralysis necessitating intubation or tracheostomy
(d) Secondary skeletal muscle denervation or atrophy
(2) Regional and neuraxial anesthesia are not contraindicated; there are several case reports of safe neuraxial anesthesia undertaken in GBS patients (5–9).
(a) There is an increased risk of complications due to exaggerated hemodynamic responses in patients with autonomic involvement (10).
(b) There is the potential for exaggerated receptor responses to local anesthetics.
(c) Use of regional techniques should be balanced against the other risks and benefits of such approaches in these patients.
(d) These techniques may have increased benefit in the GBS parturient, but increased risk in the patient with lung disease.
(e) A detailed discussion of these risks should be undertaken with the patient and all pre-existing neurological deficits should be meticulously documented so pre-existing deficits are not confused with nerve injury.
(f) The choice must be made on a case-by-case basis.
ii) Induction
(1) Stress-dose steroids are only required in patients on long-term steroids, which is unusual in this population.
(2) Autonomic involvement will lead to exaggerated responses to:
(a) Induction agents (hypotension, brady- or tachycardia)
(i) Anticipate and consider pre-treatment with vasoactive agents as necessary
(b) Direct laryngoscopy (hypertension, tachycardia)
(i) Consider pre-medication (e.g. 3–5 mcg/kg fentanyl) prior to laryngoscopy to blunt autonomic responses
(3) Bulbar involvement may increase risk of aspiration – anticipate and use a modified rapid sequence technique with cricoid pressure if deemed necessary.
(4) Skeletal muscle denervation, even subclinical, can lead to an up-regulation of extrajunctional receptors. Avoid succinylcholine because of the risk for hyperkalemic bradycardia or cardiac arrest.
(5) There are no known contraindications to use of non-depolarizing muscle relaxants, though there is the potential for increased sensitivity and delayed recovery.
iii) Maintenance/Emergence
(1) Autonomic instability will lead to exaggerated responses to:
(a) addition of PEEP (hypotension)
(b) surgical stimulation (hypertension)
(c) blood loss (hypotension)
(d) changes in posture (hypo- and hypertension)
(2) Invasive arterial monitoring can assist management in patients with autonomic instability.
(3) Indirect-acting vasopressors may elicit exaggerated responses secondary to up-regulation of postsynaptic receptors.
(4) Myocardial irritants or sensitizers should be avoided (e.g. halothane).
(5) Wildly fluctuating blood pressure responses during emergence should be anticipated and pre-treated if possible (e.g. β-adrenergic antagonists).
(6) If there is motor involvement, monitoring of muscle twitch with a nerve stimulator should typically be on an unaffected limb.
(7) Careful attention to extubation criteria must be followed:
(a) Appropriate respiratory mechanics (11)
(b) Return of airway reflexes
(c) Full recovery of neuromuscular tone
(d) A warmed patient
(e) Recovery of mental status
(f) Normalized blood gases
(g) Minimal intraoperative hemodynamic shifts
(h) Normal electrolytes
iv) Postoperative
(1) Depending on severity of disease and involvement of the respiratory system, the GBS patient may require post-surgical ventilatory support.
Demyelinating diseases can affect both peripheral and central nervous system, and central nervous system, and involve all three branches – motor, sensory and autonomic. When multiple peripheral nerves are involved the disease is considered a polyneuropathy.
Patients with GBS are at high risk for autonomic instability and respiratory failure.
1) Central demyelinating diseases: Multiple sclerosis
a) Multiple sclerosis (MS)
i) Autoimmune disorder against CNS myelin.
ii) Has a relapsing and remitting course, with variable periods of latency in-between.
iii) Disease severity and expression is based on the burden and distribution of CNS lesions.
iv) Sensory, motor, and autonomic nervous system involvement is possible.
b) Treatment includes
i) Chronic immunosuppressive therapies (e.g. cyclophosphamide, azathioprine).
ii) Steroid treatment during acute flares.
iii) Intravenous ACTH if afflicted with optic neuritis.
iv) Antispasmodics if suffering severe spasticity or bladder involvement.
c) Anesthetic management
i) Preoperative considerations
1) As with GBS, a focused but thorough chart review and patient history must be taken. Central white matter loss may affect critical targets with anesthetic implications:
a) Autonomic/cardiac system resulting in blood pressure lability with poor compensatory reflexes
b) Brainstem nuclei affecting respiration, pharyngeal reflexes, swallowing or vocal cord function
c) Secondary skeletal muscle denervation or atrophy
2) Regional and neuraxial anesthesia are not contraindicated though controversial. Retrospective studies have not found an increase in MS exacerbations or documented neurotoxicity with neuraxial anesthesia or nerve blocks (12).
a) There is a theoretical risk of increased sensitivity of nerve conduction to either single or repeated doses of local anesthetics, particularly with intrathecal administration (13), or concern for secondary crush injury to already compromised nerves (14–15).
b) There is the potential for exaggerated receptor responses to local anesthetics.
c) Use of regional techniques should be balanced against the other risks and benefits of such approaches in these patients. The benefits may be more strongly seen in the MS parturient; increased caution should be exercised in the patient with documented spinal cord lesions. The decision to use regional techniques should be made on a case-by-case basis.
d) A detailed discussion of these risks should be undertaken with the patient, and all pre-existing neurological deficits should be meticulously documented so pre-existing deficits are not confused with nerve injury.
e) If utilized, one should consider use of lower local anesthetic doses, supplemented with opioids.
ii) Induction
1) Stress-dose steroids are only required in patients on long-term steroids, which is unusual in this population.
2) Autonomic involvement will lead to exaggerated responses to:
a) Induction agents (hypotension, brady- or tachycardia)
(i) Anticipate and consider pre-treatment with vasoactive agents as necessary
b) Direct laryngoscopy (hypertension, tachycardia)
(i) Consider premedication (e.g. 3–5 mcg/kg fentanyl) prior to laryngoscopy to blunt autonomic responses
1) Bulbar involvement may increase risk of aspiration – anticipate and use a modified rapid sequence technique with cricoid pressure if deemed necessary.
4) Skeletal muscle denervation, even subclinical, can lead to an up-regulation of extrajunctional receptors. Avoid succinylcholine because of the risk for hyperkalemic bradycardia or cardiac arrest.
5) There are no known contraindications to use of non-depolarizing muscle relaxants, though there is the potential for increased sensitivity and delayed recovery.
iii) Maintenance/Emergence
1) Autonomic instability will lead to exaggerated responses to:
a) Addition of PEEP (hypotension)
b) Surgical stimulation (hypertension)
c) Blood loss (hypotension)
d) Changes in posture (hypo- and hypertension)
2) Invasive arterial monitoring can assist management in patients with autonomic instability
1) Indirect-acting vasopressors may elicit exaggerated responses secondary to up-regulation of postsynaptic receptors.
4) Wildly fluctuating blood pressure responses during emergence should be anticipated and pre-treated if possible (e.g. β-adrenergic antagonists).
5) If there is motor involvement, monitoring of muscle twitch with a nerve stimulator should typically be on an unaffected limb.
6) Careful attention to extubation criteria must be followed:
a) Appropriate respiratory mechanics
b) Return of airway reflexes
c) Full recovery of neuromuscular tone
d) A warmed patient
e) Recovery of mental status
f) Normalized blood gases
g) Minimal intraoperative hemodynamic shifts
h) Normal electrolytes
iv) Postoperative
1) Depending on severity of disease and involvement of the respiratory system, the MS patient may require post-surgical ventilatory support.
Neuraxial and other regional techniques are generally safe in patients with peripheral nervous or neuromuscular involvement. However, the decision to perform these techniques should be made on a case-by-case basis with thorough discussion of risks and benefits with the patient.
4) Inflammatory neurologic disease
a) Lyme disease
i) Poly-inflammation of multiple organ systems (joints, heart, muscle, central and peripheral nervous system) is the hallmark of the disease.
ii) Early manifestations include erythema migrans and influenza-like symptoms.
iii) Later systemic manifestations can masquerade as many other diseases.
iv) As many as 10% of cases can have significant cardiac involvement (18), complicating anesthetic management.
1) Most common problem is atrioventricular block; other dysrhythmias/conduction abnormalities are possible.
2) Rarer cardiac manifestations include pericarditis, myocarditis, cardiomyopathy and degenerative valvular disease.
1) Unstable patients may require temporary pacing (18).
Up to 10% of cases of Lyme disease have significant cardiac involvement.
b) Neurologic Lyme disease (neuroborreliosis)
i) Occurs 1 to 4 weeks after initial infection in 10% to 15% of cases.
ii) Causes inflammation of the peripheral nerves, meningeal lining, or brain parenchyma.
iii) Manifestations include meningitis, meningoradiculitis, cranial neuritis, encephalopathy, peripheral neuropathy, encephalitis, and encephalomyelitis (19).
c) Treatment
i) Nervous system infection responds well to parenteral high-dose penicillin, ceftriaxone, and cefotaxime in both adults and children.
ii) Oral doxycycline is often used in adults with meningitis, cranial neuritis, and radiculitis (14).
d) Anesthetic Management
i) Preoperative considerations
1) Anesthetic risk depends on the portion of the nervous system involved. As with GBS and MS, an extremely thorough preoperative evaluation is needed to identify these affected systems to develop an anesthetic plan. Any system can be involved in Lyme Disease.
a) Cardiac involvement most prominently leads to dysrhythmias, and can result in arrest.
b) Myelitis can result in weakness, sensory loss, and dysautonomia, leading to autonomic lability. Denervation can affect the neuromuscular junction and respiratory muscles.
c) Cranial neuritis may affect airway reflexes, cause vocal cord paralysis, and impact the ability to protect the airway.
d) Management of peripheral neuritis depends on severity and distribution of lesions. It has maximal impact if autonomic fibers or muscles of respiration are affected.
e) In rare cases, vasculitic involvement can lead to stroke (see Ischemic Vascular Disease/CVA).
f) Parenchymal involvement can infrequently lead to seizures (see Epilepsy/Seizure Disorder).
2) Similar considerations (ALS, GBS, MS patients) for the use of neuraxial anesthesia in neuroborreliosis with peripheral neuritis hold. A strict risk-benefit analysis and meticulous documentation of pre-existing deficits should be performed.
ii) Induction
1) Cardiac and autonomic involvement may lead to dysrhythmias or exaggerated responses to:
a) Induction agents (hypotension, brady- or tachycardia)
(i) Anticipate and consider pre-treatment with vasoactive agents as necessary
b) Direct laryngoscopy (hypertension, tachycardia)
(i) Consider pre-medication (e.g. 3–5 mcg/kg fentanyl) prior to laryngoscopy to blunt autonomic responses.
2) Cranial neuritis and/or bulbar involvement may increase risk of aspiration – anticipate and consider using a modified rapid sequence technique with cricoid pressure.
1) Myelitis leading to muscle denervation carries high risk of hyperkalemia-induced bradycardia or arrest. Motor compromise may be impossible to document, so it is safer to avoid succinylcholine.
4) There are no contraindications to non-depolarizing muscle relaxants, though sensitivity to them may be slightly increased.
iii) Maintenance/Emergence
1) Autonomic instability will lead to exaggerated responses to:
a) Addition of PEEP (hypotension)
b) Surgical stimulation (hypertension)
c) Blood loss (hypotension)
d) Changes in posture (hypo- and hypertension)
2) Invasive arterial monitoring can assist management in patients with autonomic instability.
1) Indirect-acting vasopressors may elicit exaggerated responses secondary to up-regulation of postsynaptic receptors.
4) Myocardial irritants or sensitizers should be avoided (e.g. halothane).
5) Wildly fluctuating blood pressure responses during emergence should be anticipated and pre-treated if possible (e.g. β-adrenergic antagonists).
6) If there is motor involvement, monitoring of muscle twitch with a nerve stimulator should typically be on an unaffected limb.
7) Careful attention to extubation criteria must be followed (see ALS, GBS, MS).
iv) Postoperative considerations
1) If myelitis or cranial neuritis affects the respiratory system or ability to protect the airway, the patient with Lyme Disease may require post-surgical ventilatory support.
5) Cerebral disease: Epilepsy
a) Epilepsy/seizure disorder
i) Seizures are paroxysmal, transient disturbances of brain function characterized by excessive or hypersynchronous discharge of neurons.
ii) The electrical signature of seizures can be measured by surface scalp electrodes (EEG).
iii) The clinical manifestations can be sensory, motor, or psychic, and be accompanied by loss of consciousness.
iv) The hypermetabolic activity of brains undergoing seizure discharge necessitates supportive function, especially if seizure activity is not self-limited (status epilepticus).
v) Epilepsy is a chronic disorder characterized by recurrent seizures.
b) Pro- and anti-convulsant effects of anesthetic drugs
i) Many anesthetic agents have dose-dependent paradoxical pro- and anticonvulsant effects (21).
1) Lower doses are more likely to be proconvulsant.
2) Higher doses or infusions (propofol, ketamine, thiopental) are more likely to be anticonvulsant.
ii) The opposing effects may be related to dose-dependent effects on differential recruitment of GABAergic circuits.
iii) Narcotics may show the reverse effect (22–23).
Patients with seizure foci in a speech or other eloquent sensory center may require awake craniotomy for resection of seizure focus.
c) Anesthetic management of the patient for intracranial resection of seizure focus
i) Preoperative considerations
1) May require an awake craniotomy if the seizure focus overlaps with speech (motor or receptive), sensory, or motor (“eloquent”) centers.
a) Only motor centers can be tested with the patient asleep.
2) Benzodiazepines are usually avoided as pre-medication in both awake and asleep craniotomies
a) They raise the seizure threshold
b) They may interfere with intraoperative assessment during awake craniotomies
1) IV access is obtained on the side of the patient not involved with (motor) seizures.
ii) Induction
1) Choose a method of sedation that:
a) Provides patient comfort
b) Is rapidly titratable/reversible
c) Does not interfere with the seizure threshold
d) Does not induce profound apnea
(i) Adjuncts often include propofol, remifentanil, and dexmetetomidine
2) Have a carefully thought out back-up plan in case of loss of airway, especially since the patient’s head may be far from the anesthesiologist, fixed (i.e. pins), and difficult to access.
a) Discuss this airway plan with the surgeon if necessary, especially in high-risk patients (e.g. craniofacial compromise, obesity)
iii) Maintenance
1) Intraoperative brain mapping is common
a) May be done with electrocorticography (ECoG) , electrodes placed directly on the cortical surface overlying the focus, or with intracranial depth electrodes in the region of interest
b) The neurosurgeon may ask for pharmacological adjuncts for stimulation of the epileptogenic focus.
(i) Methohexital: 10 to 50 mg IV
(ii) Propofol: 10 to 20 mg IV
(iii) Thiopental 25 to 50 mg IV
(iv) Etomidate 2 to 8 mg IV
For awake craniotomies requiring adjunct sedation, have a carefully thought out back-up plan in case of loss of airway, especially since the patient’s head may be far from the anesthesiologist, fixed (i.e., pins), and difficult to access; discuss plan with the surgeon if necessary, especially if the patient has predictable airway difficulties (e.g., craniofacial compromise, obesity).
d) Anesthetic management of the epileptic patient undergoing non-epilepsy surgery
i) Preoperative evaluation
1) Thoroughly assess co-morbidities, including psychiatric illnesses, head trauma, or associated syndromes, some more common in childhood.
a) West syndrome, Lennox–Gastaut syndrome, mitochondrial syndromes such as MERRF and MELAS, neurofibromatosis, tuberous sclerosis, multiple endocrine adenomatosis.
2) Knowledge of the patient’s anticonvulsant therapy and associated complications is imperative.
a) Phenytoin: gum disease/poor dentition, airway management issues.
b) Valproate: altered platelet function, thrombocytopenia.
c) Carbamazepine: bone marrow suppression, cardiac toxicity.
Patients on antiseizure medication may require increased dose and frequency of medications.
ii) Maintenance
1) Avoid anesthetic agents that potentiate the seizure threshold such as etomidate and methohexital.
2) Avoid hypocapnia (through hyperventilation and control of minute ventilation)
a) Potentiates the seizure threshold and decreases cerebral blood flow through vasoconstriction.
1) For long intraoperative procedures, ongoing anticonvulsant therapy may need to be administered. Consult with the surgical team to determine the patient’s dosing schedule.
4) Most anticonvulsants (especially phenytoin and phenobarbital) undergo hepatic transformation and up-regulate the P450 enzyme system.
a) This usually necessitates an increased amount or frequency of dosing of many anesthetic drugs, especially the muscle relaxants.
In any setting where a seizure takes place, the first goal is to ensure a patent airway, administer supplemental O2, and maintain adequate perfusion (ABCs).
e) Anesthetic management of the epileptic patient in status epilepticus
i) Status epilepticus is ongoing, intractable seizure activity, either convulsive or non-convulsive.
1) Status epilepticus is a neurological emergency
ii) Treatment
1) Primary goal is prevention of brain damage.
2) Secondary goal is prevention of injury due to involuntary convulsions.
1) Brain damage prevention includes:
(a) ABC: Secure the airway, provide supplemental O2, maintain adequate perfusion/circulation.
(b) Decrease or silence neuronal activity.
(i) Decreases neuronal metabolism and secondary glutamate excitotoxicity.
(c) If hypoglycemia has not been ruled out and cannot be ruled out quickly, supplement with D50 as a slow IV push.
(i) Dextrose 50% = 25 g d-glucose in 50 mL water.
(d) Commonly used medications to decrease convulsive activity include:
(i) Benzodiazepines
(ii) Barbiturates
(iii) Propofol
(iv) Phenytoin
(e) Most intravenous anesthetics have anticonvulsant properties when used at adequate dosages as infusions.
(i) Anticonvulsant therapy can be titrated to a simultaneously monitored EEG.
Hypoglycemia should always be considered and treated in a patient who is seizing.
6) Cerebral disease: Ischemia
a) Ischemic vascular disease/cerebrovascular accident CVA
i) Rupture or obstruction of a blood vessel feeding the brain parenchyma that results in sudden impairment of consciousness, sensory, or motor function.
b) Treatment
i) Medical
1) Multifactorial treatment
a) Anticoagulation (if ischemic disease)
b) Decrease the risk of the associated comorbidities
i) Hypertension, dyslipidemia, tobacco use, diabetes
ii) Surgical
1) Open or endovascular carotid endarterectomy (CEA).
a) Performed to correct stenosis of the carotid artery in ischemic disease.
2) Open clipping or endovascular coiling treatment of aneurysm or AVMs is performed for hemorrhagic strokes.
c) Anesthetic implications
i) Anesthetic management of the patient with ischemic vascular disease undergoing non-CEA surgery
(1) Preoperative considerations
a) Meticulous attention should be paid to multiple comorbidities. These patients are generally pan-vasculopaths with small and large vessel atherosclerosis. They present with associated pro-inflammatory conditions including:
i) Hypertension
ii) Diabetes
iii) Coronary artery disease
iv) Obesity
v) Obstructive lung disease
b) History should emphasize exercise tolerance, use of home O2, symptoms of chest pain, orthopnea, dyspnea on exertion, and those consistent with obstructive sleep apnea.
i) Pre-existing neurological deficits should be documented.
c) Medications, electrolyte abnormalities (especially glucose, potassium, bicarbonate), coagulopathies, and anemia should be noted.
i) The ECG should be examined, and compared to prior ECGs if available.
d) Physical exam should focus on thorough airway and cardiopulmonary evaluation, including carotid auscultation.
(2) Intraoperative management
a) Induction
i) Minimize significant hemodynamic swings during induction and direct laryngoscopy.
(1) β-adrenergic antagonists, opioids or lidocaine may blunt tachycardia associated with direct laryngoscopy.
ii) A slow, controlled induction is preferred (with or without etomidate) supplemented by pressor support (e.g. phenylephrine) as necessary.
iii) If significant cardiac comorbidities or autonomic instability exist, pre-induction invasive arterial monitoring may be necessary to ensure rapid responses to hemodynamic shifts.
b) Heart rate is the most significant driver of myocardial O2 consumption.
i) Therefore strict control of heart rate (<80 bpm) is important to preventing transient myocardial ischemia by balancing O2 supply and demand.
c) Blood pressure (BP) should be kept within 20% of baseline mean arterial pressure (MAP) or systolic pressure to prevent further cerebral ischemia.
i) The cerebral autoregulation curve is generally shifted to the right; higher MAPs are required to maintain cerebral perfusion.
ii) Choice of pressor is based on baseline heart rate and other co-morbid conditions.
iii) Note: If these patients have associated elevations in intracranial pressure (ICP), elevated MAPs are required to maintain cerebral perfusion (CPP).
(1) CPP = MAP – ICP
d) Hypocapnia/hyperventilation should be avoided except to acutely decrease brain swelling.
i) May cause cerebral vasculature constriction and contribute to cerebral ischemia.
ii) PaCO2 should be kept within 5 mm Hg of the patient’s baseline.
(1) This can be determined by comparing the ETCO2 with a PaCO2 from an arterial blood gas.
(2) The PaCO2 gradient will allow the anesthesiologist to optimize ventilation to maintain cerebral perfusion.
(3) Emergence/postoperative management
a) Avoid sympathetic surges (hypertension, tachycardia) associated with emergence by having β-adrenergic antagonists readily available.
b) This elevated sympathetic drive may continue into the postoperative period in recovery, and up to 24 hours following the procedure. The perioperative risk for myocardial events and elevated ICP also continues well into this period.
c) IV or tracheal lidocaine can be used to blunt the response to extubation.
d) Adequate pain control is imperative to blunt sympathetic overdrive.
7) Cerebellar and basal ganglia diseases: Dementia and cognitive decline
a) Dementia and cognitive decline refer to a mixed group of disorders that represent a global decline in cognitive processing, and may result from a global cerebral insult or neurodegenerative process.
i) Well-known neurodegenerative dementias include Parkinson’s and Alzheimer’s Disease.
ii) Global ischemic or hypoglycemic insults may occur during development (e.g. cerebral palsy) or in adulthood (e.g. following a seizure or secondary to traumatic brain injury).
b) Anesthetic management
i) Preoperative
(1) Document pre-existing neurological and cognitive defecits.
(2) A large subset of these patients are older; a thorough preoperative evaluation to assess for co-morbidities is imperative.
(3) Familiarize yourself with the patient’s targeted medication list; many of the drugs alter cholinergic (e.g. donepezil, a reversible acetylcholinesterase inhibitor) and dopaminergic (L-DOPA) balance.
(a) Side effects should be anticipated.
(b) Interactions with anesthetic medications (e.g. neostigmine, metoclopramide) should be considered.
(4) Regional anesthesia may be preferred in this population (where appropriate) to decrease exposure to general anesthesia (24).
ii) Induction
(1) Hemodynamic swings to induction and laryngoscopy should be anticipated and managed appropriately (see Cerebral disease: Ischemia).
iii) Maintenance/Emergence
(1) There is increasing evidence that pre-existing cognitive decline may predispose to delayed emergence and postoperative cognitive worsening. This postoperative decline may be irreversible (24).
(2) One approach is to minimize depth of anesthesia and length of procedure/anesthetic exposure time; the evidence for this approach is suggestive but not conclusive (24).
(a) The patient should be kept just beyond a level of MAC aware.
(b) Autonomic responses and pain should be appropriately blunted by pharmacological intervention, judicious use of regional anesthesia, etc.
iv) Postoperative
(1) Cognitive engagement/enrichment during this period may hasten recovery and increase the likelihood that the patient will return to their preoperative baseline.
(2) Restart any critical medications that enhance cognitive performance.
Diphenhydramine and other anticholinergics can be used for decrease of tremor in awake patients with PD, and may ease IV placement if given as preoperative medication.
Patients on l-dopa for PD are at increased risk of catecholamine-induced tachyarrhythmias.
8) Cerebellar & basal ganglia diseases: Parkinson’s Disease
a) Parkinson’s Disease (PD)
i) Neurodegenerative disease that causes a relative deficiency of dopamine relative to acetylcholine (ACh) in the basal ganglia. In addition to bradykinetic manifestations, it may also result in dementia (see Cerebral disease: demntial and cognitive decline).
ii) Treatment
1) Patients are usually on medications that increase dopamine (DA) delivery or prevent its degradation.
2) Chronic increase in DA delivery can result in myocardial irritability, decreased intravascular volume, orthostatic hypotension, or nausea and vomiting.
1) Anticholinergic therapy may be added to decrease dyskinesias from dopaminergic therapy.
b) Anesthetic management
i) Preoperative considerations
1) Therapeutic agents should be continued through the morning of surgery.
2) IV access may be more difficult secondary to tremor.
1) Note baseline neurological defecits and any concomitant dementia (see Cerebral disease: dementia and cognitive decline).
ii) Induction
1) Hypotension may occur secondary to relative hypovolemia
a) Consider fluid-loading prior to giving an induction agent
b) Treat with direct-acting pressors (phenylephrine rather than ephedrine).
2) Succinylcholine and nondepolarizing neuromuscular blockers are generally considered acceptable.
a) If muscle denervation secondary to disuse atrophy is suspected, succinylcholine should be avoided because of the potential for hyperkalemic bradycardia and arrest.
iii) Maintenance/Emergence
1) Maintain euvolemia to prevent hypotension.
2) Avoid medications that can precipitate extra-pyramidal symptoms:
a) Phenothiazines
(i) chlorpromazine, promethazine
b) Butryophenones
(i) droperidol, haloperiodol
c) Benzamides
(i) Metoclopramide
1) There is an increased potential for catecholamine-induced tachyarrhythmias with L-DOPA.
a) Use epinephrine with extreme caution in these patients.
b) Avoid myocardial irritants or sensitizers (e.g. halothane).
4) Although these medications are generally used safely in PD, there are isolated case reports suggesting:
a) exaggerated hypertensive responses to ketamine
b) increased rigidity to fentanyl and inhaled anesthetics
c) increased predisposition toward dyskinesias with high dose morphine).
iv) Postoperative considerations
1) Propofol may block PD tremors in the immediate post-operative period.
2) Resume the patient’s therapeutic medications as soon as possible.
a) Brian death is defined as the absence of cerebral function (unresponsiveness/coma), absence of brainstem function, and loss of respiratory drive (apnea). Absence of cerebral function (unresponsiveness/coma).
b) Diagnosis
i) Two independent exams must be conducted by two physicians at least six hours apart.
ii) Absence of cerebral function can only be diagnosed when the cause of coma is identified and conditions that mimic brain death have been ruled out.
(1) Brain death mimicking conditions
(a) Drug overdose
(i) Includes drugs of abuse, anesthetic agents, neuromuscular blockers
(b) Hypothermia
(c) Locked-in syndrome
(d) Stroke variants that may prevent a patient from responding
(e) Shock/hypotension
(f) Guillain–Barré syndrome
(g) Encephalitis/encephalopathy
iii) Brainstem reflexes (sequential cranial nerve testing) (Table 76-1)
Table 76-1
Criteria for Diagnosis of Brain Death in Adults and Children
iv) Apnea test
(1) Absence of respiratory drive with a PaCO2 ≥ 60 mm Hg or 20 mm Hg above normal baseline (25).
(2) Connect pulse oximeter.
(3) Disconnect the patient from the ventilator.
(4) Deliver apneic oxygenation (6 L/min flow) into trachea.
(a) Can be done via catheter through the endotracheal tube to the level of the carina.
(5) Observe for spontaneous ventilation (abdominal, chest excursions).
(6) A PaCO2 rise of 3 mm Hg/min of apnea is expected.
(a) Therefore, 8 to 10 minutes is usually sufficient for assessment of the return of respiratory drive.
(b) Reconnect the patient to the ventilator after obtaining arterial blood gas for assessment of PaCO2, PaO2, and pH.
v) Ancillary testing for diagnosing brain death (if complete brainstem evaluation not possible)
(1) Isoelectric EEG for at least 30 minutes.
(2) Absence of cerebral perfusion as demonstrated by angiography, T-99 scan, or transcranial Doppler ultrasound (usually of the middle cerebral artery).
(3) Absence of somatosensory and brainstem auditory evoked potentials.
c) Organ donation (27)
i) If designated for organ donation, the brain dead patient must be optimally cared for to preserve remaining organ function.
ii) Brain death is often accompanied by dysautonomia.
(1) Loss of systemic sympathetic tone and relative or absolute hypovolemia.
(2) Causes fast deterioration of donor organ viability.
iii) Perioperative monitoring
(1) Standard ASA monitors
(2) Temperature
(3) Urine output
(4) Invasive arterial pressure
(5) Central venous/pulmonary artery pressure
iv) Physiological goals are geared toward maintaining normal parameters.
(1) Oxygen saturation 97% to 100%
(2) HR 60 to 100 beats per minute, sinus rhythm
(3) MAP 60 to 80 mm Hg
(4) CVP 8 to 12 mm Hg
(5) Pulmonary artery wedge 10 to 15 mm Hg
(6) CI > 2.1 L/min/m2
(7) Urine output 1 to 2 mL/kg/h
(8) Volume replacement approximately 50 mL/h > urine output
10) Summary Considerations
a) A systematic approach can assist the anesthesiologist in management of patients with neurological diseases, and can simplify the understanding of how to care for the patient with uncommon nervous system disorders as well.
i) Which branches of the nervous system are involved: sensory, motor or autonomic? (Table 76-2)
Table 76-2
Anesthetic Risk Associated with Disorders of the Nervous System
ii) What treatment or drug therapy is the patient on that can interact with anesthetic management and anesthetic drugs?
iii) How can baseline nervous system function be preserved?
iv) How can baseline organ function be preserved?
b) Disuse atrophy is often overlooked in bed-ridden (e.g. ICU), wheelchair bound, or young, healthy, but casted patients who have been unable to use limbs for longer than 3 days. These conditions predispose toward succinylcholine-induced hyperkalemia and cardiac arrest.
c) Rigorous documentation of pre-existing deficits and attention to the full risk-benefit discussion with patients must be undertaken.
i) The decision to use epidural, spinal or nerve block anesthetics should be made on a case-by-case basis.
Chapter Summary for Anesthesia and Diseases of the Nervous System
References
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Suggested Readings
28. Gupta AK, Gelb AW, eds. Essentials of Neuroanesthesia and Neurointensive Care. Elsevier Saunders; 2008.
29. Newfield P, Cottrell JE, eds. Handbook of Neuroanesthesia. 4th ed. Lippincott Williams & Wilkins; 2006.
30. Pasternak JJ, Lanier WJ. Diseases affecting the brain. In: Hines RL, Marschall KE, eds. Stoelting’s Anesthesia and Co-Existing Disease. 5th ed. Churchill Livingstone; 2008:199–238.
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