CENTRAL NERVOUS SYSTEM DISEASE

CENTRAL NERVOUS SYSTEM DISEASE
Dr Abdollahi 9/19/2018

9/19/2018 Anesthesia for neurosurgery requires an understanding of the physiology of the central nervous system (CNS). The anesthesia provider must control the physiologic and pharmacologic factors that influence cerebral blood flow (CBF), cerebral metabolic rate for oxygen consumption (CMR02), and intracranial pressure (ICP). The selection of drugs, ventilation techniques, and monitors have important implications in the care of patients with diseases of the CNS.

9/19/2018 NEUROANATOMY Conceptually, the cranium is divided into supratentorial and infratentorial compartments. The supratentorial compartment contains the cerebral hemispheres and diencephalon (thalamus and hypothalamus); the brainstem and cerebellum make up the infratentorial compartment.

9/19/2018 The location of intracranial pathology can have significant implications, particularly if eloquent areas such as the language centers and motor cortex of the brain are at risk.

9/19/2018 Arterial blood supply The arterial blood supply to the brain is through the left and right internal carotid arteries and the vertebrobasilar system. Anastomoses between these vessels form the circle of Willi and create a collateral blood supply to protect against ischemia. The classic depiction of this ring is found in fewer than half of human brains and collateralization may not be complete in all individuals.

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Blood-brain barrier (BBB)
9/19/2018 Blood-brain barrier (BBB) Many of the physiologic properties of the central nervous system are dependent on an intact blood-brain barrier. The blood-brain barrier is composed of capillary endothelial cells with tight junctions that prevent extracellular passage of macromolecules, such as proteins.

9/19/2018 In contrast, lipid-soluble substances (carbon dioxide, oxygen, anesthetics) cross the blood-brain barrier easily. The blood- brain barrier may be disrupted in the event of acute systemic hypertension, trauma, infection, arterial hypoxemia, severe hypercapnia, tumors, and sustained seizure activity.

9/19/2018 NEUROPHYSIOLOGY Cerebral Blood Flow Normal CBF is approximately 50 mL/100 g/min and represents 15% of cardiac output. The brain receives a disproportionately large share of cardiac output due to its high metabolic rate and inability to store energy.

Determinants of CBF include
9/19/2018 Determinants of CBF include (1) CMR02, (2) cerebral perfusion pressure (CPP) and autoregulation, (3) PaC02 (4) Pa02 (5) Anesthetic drugs The impact of autonomic system innervation on CBF is small.

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Cerebral Metabolic Rate
9/19/2018 Cerebral Metabolic Rate Cerebral blood flow in the brain is heterogeneous and directly influenced by CMR02 through cerebral flow metabolism coupling. Increases or decreases in CMR02 result in a proportional increase or decrease in CBF.

9/19/2018 CMR02 is reduced by hypothermia and most anesthetic drugs and produces a coupled reduction in CBF in healthy brains (CBF decreases 7% for every 1 o C decrease in body temperature below 37° C). In contrast, CMR02 and CBF may be dramatically increased by seizure activity.

Cerebral Perfusion Pressure and Autoregulation
9/19/2018 Cerebral Perfusion Pressure and Autoregulation CPP is the difference between mean arterial pressure (MAP) and ICP or central venous pressure (CVP), whichever is greater. Autoregulation is a protective mechanism that maintains a constant CBF in the presence of a changing CPP and reflects the ability of cerebral arterioles to constrict or relax in response to changes in perfusion pressure.

9/19/2018 This response normally requires 1 to 3 minutes to develop, so a rapid increase or decrease in MAP causes a brief period of cerebral hyperperfusion or hypoperfusion, respectively

9/19/2018 Autoregulation maintains CBF relatively constant between a CPP of 50 and 150 mm Hg in normotensive, healthy individuals. Cerebral blood flow varies directly with cerebral perfusion pressures above or below this range. Chronic uncontrolled hypertension or sympathetic stimulation shifts the autoregulatory curve to the right, and these patients require a higher minimum CPP to maintain adequate CBF.

9/19/2018 The anesthetic state shifts the autoregulatory response to the left, which may provide some safety from the decreases in MAP that can occur intraoperatively.

9/19/2018 Autoregulation may be impaired in specific circumstances. Autoregulation can be abolished following traumatic brain injury and intracranial surgery. As a result, CBF becomes directly proportional to MAP which has important clinical implications in the management of these patients.

9/19/2018 Autoregulation may also be impaired in the proximity of intracranial tumors. Inhaled anesthetics are potent cerebral vasodilators and impair autoregulation to varying degrees at high doses.

9/19/2018 Although autoregulation is maintained at anesthetic concentrations less than 1 minimum alveolar concentration (MAC) higher concentrations abolish autoregulation, and CBF becomes proportional to MAP. In contrast, intravenous anesthetics do not disrupt autoregulation.

Effects of PaC02 and Pa02 on CBF
9/19/2018 Effects of PaC02 and Pa02 on CBF Changes in PaC02 produce corresponding directional changes in CBF between a PaC02 of 20 to 80 mm Hg CBF increases or decreases 1 mL/100 g/min for every 1-mm Hg increase or decrease in PaC02 from 40 mm Hg.

9/19/2018 Such changes in CBF reflect the effect of carbon dioxide- mediated alterations in perivascular pH and lead to dilation or constriction of cerebral arterioles.These changes in CBF are transient because of an increase in cerebrospinal fluid (CSF) HC03 concentrations.

9/19/2018 CBF returns to normal in 6 to 8 hours, even if the altered PaC02 levels are maintained.Aggressive or prolonged hyperventilation (PaC02 < 30 mm Hg) should be avoided because of the risk of cerebral ischemia. Prolonged aggressive hyperventilation following traumatic brain injury is probably associated with poorer neurologic outcome

9/19/2018 Decreases in Pa02 (less than a threshold value of about 50 mm Hg) result in an exponential increase in CBF.

Effect of Anesthetic on CBF
9/19/2018 Effect of Anesthetic on CBF Intravenously administered anesthetics, such as thiopental, propofol, and etomidate, are cerebral vasoconstrictors and reduce CMR02 and CBF in parallel and are therefore used frequently for anesthesia for neurosurgery. There is controversy about the effects of ketamine, which probably reflects differences in the conditions of the research study.

9/19/2018 KETAMINE When ketamine is given on its own without control of ventilation, PaC02, CBF, and ICP all increase, whereas when given in the presence of another sedative/ anesthetic drug in patients whose ventilation is controlled, these increases do not occur. Because of this controversy, however, ketamine is not usually selected for patients with known intracranial disease.

Benzodiazepines and opioids
9/19/2018 Benzodiazepines and opioids Benzodiazepines and opioids decrease CMR02 and CBF, analogous to thiopental and propofol, although to a lesser extent. However, associated respiratory depression and elevation of PaC02 may produce the opposite effect.

9/19/2018 Opioid Opioids should be used with caution in patients with intracranial disease because of their (1) depressant effects on consciousness, (2) production of miosis, and (3) depression of ventilation with associated increases in ICP from PaC02 increases.

9/19/2018 a2-agonists a2-agonists (clonidine and dexmedetomidine) are unique sedatives in that they do not cause significant respiratory depression. They reduce arterial blood pressure, CBF, and CPP with minimal effects on ICP. a2-Agonists can be used intraoperatively to reduce the dose of other anesthetics and analgesics or postoperatively as sedatives and to attenuate postoperative hypertension and tachycardia.

9/19/2018 Volatile anesthetic Volatile anesthetic drugs are potent cerebral vasodilators. When administered during normocapnia at concentrations higher than 0.5 MAC destlurane, sevoflurane, and isoflurane rapidly produce cerebral vasodilation and result in dose- dependent increases in CBF. CBF remains increased relative to CMR02 despite concomitant decreases in CMR02• When used in isolation, nitrous oxide increases CBF and possibly CMR02, but these effects appear to be attenuated by co-administration of other anesthetics.

INTRACRANIAL PRESSURE
9/19/2018 INTRACRANIAL PRESSURE Intracranial Pressure-Volume Relationship The intracranial compartment is composed of three substances: (1) brain matter, (2) cerebral spinal fluid, and (3) blood. Increases in any of the these substances can result in elevated intracranial pressure, defined as a sustained increase above 15 mm Hg.

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9/19/2018 The pressure-volume compliance curve depicts the impact of increasing intracranial volume on intracranial pressure (ICP). As volume increases from point 1 to point 2 on the curve, ICP does not increase because cerebrospinal fluid is shifted from the cranium into the spinal subarachnoid space. Patients with intracranial tumors who are between point 1 and point 2 on the compliance curve are unlikely to manifest clinical symptoms of increased ICP. Patients who are on the rising portion of the pressure-volume curve (point 3) can no longer compensate for increases in intracranial volume, and ICP begins to increase. Clinical symptoms attributable to increased ICP are likely at this stage. Additional increases in volume at this point, as produced by increased CBF during anesthesia, can precipitate abrupt increases in ICP (point 4).

Methods to Decrease Intracranial Pressure
9/19/2018 Methods to Decrease Intracranial Pressure

Effect of Anesthetic on ICP
9/19/2018 Effect of Anesthetic on ICP Most intravenous anesthetic drugs reduce CMR02 and CBF, and this decrease is associated with a reduction in ICP. The effects of ketamine are controversial and were discussed earlier. These drugs may be administered to patients with intracranial hypertension to decrease ICP.

9/19/2018 However, this must be done carefully as large doses of propofol or thiopental may decrease systemic blood pressure and CPP. An increased frequency of excitatory peaks on the electroencephalogram of patients receiving etomidate, as compared with thiopental, suggests caution in the administration of etomidate to patients with a history of epilepsy

9/19/2018 Opioids and benzodiazepines reduce ICP through reductions in CBF and CMR02 although this benefit will be offset if respiratory depression and increases in PaC02 occur.

9/19/2018 Cerebral vasodilators and produce dose-dependent increases in ICP that parallel the increases in CBF and CBV. Hyperventilation to decrease PaC02 to less than 35 mm Hg attenuates the tendency for volatile anesthetics to increase ICP.

9/19/2018 Neuromuscular blocking drugs do not usually affect ICP unless they induce release of histamine or hypotension. Histamine can cause cerebral vasodilation, leading to a small increase in ICP. Succinylcholine may increase ICP through stimulation of muscle spindles, which in tum either directly or indirectly results in increased CMR02.

9/19/2018 NEUROPROTECTION Many anesthetics may act as neuroprotectants given their potential to reduce cerebral metabolic rate and excitotoxicity during oxygen deprivation. In animal studies, many anesthetics, including barbiturates, volatile anesthetics, xenon, and propofol, provide neuroprotection although human outcome data are lacking. Hypothermia has been described as a method for cerebral protection during acute injury.

NEUROPHYSIOLOGIC MONITORING
9/19/2018 NEUROPHYSIOLOGIC MONITORING Neurophysiologic monitoring is employed during neurosurgery with increasing frequency due to minimal risk to patients and the potential to reduce neurologic deficits. An understanding of the effects of anesthetic agents on somatosensory and motor evoked potentials is critical in neuroanesthesia. In general, nitrous oxide and volatile anesthetics have a greater effect on motor and sensory evoked potentials than intravenous anesthetics.

Electrocorticography
9/19/2018 Electrocorticography Electrocorticography (ECG) is another intraoperative mapping technique used to identify epileptic foci for resection and is sensitive to anesthetic drugs that change the seizure threshold (e.g., benzodiazepines and volatile anesthetic agents).

Anesthesia For Neurosurgery
9/19/2018 Anesthesia For Neurosurgery Preoperative Assessment Patients presenting for neurosurgical procedures can have a wide range of symptoms. Patients with intracranial mass lesions may present with seizures, altered level of consciousness, headaches, cranial nerve abnormalities, and motor or sensory deficits. Aneurysms and arteriovenous malformations (AVMs) can present with a severe ("thunderclap") headache if ruptured, and focal deficits or visual impairment from compression of the optic chiasm when unruptured.

9/19/2018 Evidence of increased ICP should be elicited during the preoperative visit. Clinical signs may be consistent with but do not reliably indicate, the level of ICP .

Preoperative Evidence of Increased Intracranial Pressure
9/19/2018 Preoperative Evidence of Increased Intracranial Pressure

9/19/2018 Imaging may reveal a midline shift of more than 0.5 cm, encroachment of expanding brain on cerebral ventricles, cerebral edema, hydrocephalus, or any combination of these signs. In symptomatic patients, preoperative medications that cause sedation or depression of ventilation are usually avoided.

9/19/2018 Drug-induced depression of ventilation can lead to increased PaC02 and subsequent increases in ICP. In alert patients, small doses of benzodiazepines may provide useful relief of anxiety.

9/19/2018 Monitoring In addition to standard monitors, continuous monitoring of arterial blood pressure via a peripheral arterial catheter is recommended because of hemodynamic perturbations occurring during induction of anesthesia, tracheal intubation, surgery, and emergence from anesthesia, all of which may compromise cerebral perfusion.

9/19/2018 These catheters also allow for arterial blood gas sampling and accurate determination of PaC02.Central venous catheters are not routinely used and employed for patient indications, such as anticipated need for vasoactive infusions. Measurement of the end-tidal carbon dioxide concentration (capnography) is used to determine ventilation parameters.

9/19/2018 The electrocardiogram (ECG) allows prompt detection of cardiac dysrhythmias caused by surgical manipulation of cardiovascular centers. Neuromuscular blockade is monitored with a peripheral nerve stimulator. Because of the length of these surgical procedures and the use of diuretics, a bladder catheter is often necessary and helps in guiding intravenous fluid therapy. A continuous monitor of ICP is helpful but rarely used

9/19/2018 There are two main monitors for ICP inserted by neurosurgeons. The intraventricular catheter or external ventricular dvice (EVD) permits direct measurement of ICP and drainage of CSF. The subarachnoid or subdural bolt is placed through a burr hole and can be inserted quickly in an emergency setting, but it does not allow for CSF drainage.

9/19/2018 Positioning Resection of supratentorial tumors and intracranial vascular lesions is typically accomplished with the patient in the supine or lateral position. Resection of posterior fossa/infratentorial tumors frequently requires placement of the patient in the sitting or prone position .

Management of Anesthesia for Patients with Intracranial Masses
9/19/2018 Management of Anesthesia for Patients with Intracranial Masses

9/19/2018 The sitting position facilitates surgical exposure of posterior fossa tumors, but because of the high risk for venous air embolism (25% incidence), many neurosurgeons prefer the prone position. Other risks associated with the sitting position include upper airway edema as a result of venous obstruction from excessive cervical flexion and quadriplegia from spinal cord compression and ischemia, especially in the presence of preexisting cervical stenosis.

9/19/2018 Another popular approach is the "park bench position" in which the patient is placed in a lateral position but rolled slightly forward with the head further rotated to "look" at the floor. This position allows the surgeon full access to the posterior fossa and minimizes the risk for venous air embolism.

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9/19/2018 The head is commonly fixed in a frame using pins (Mayfield head damp). Caution must be used to avoid bucking or movement while the patient is fixed in the frame to avoid injury to the patient. Compression of the internal jugular veins resulting in excessive venous pressure should also be avoided to minimize increases in ICP.

Induction of Anesthesia
9/19/2018 Induction of Anesthesia The goal of induction of anesthesia is to achieve a sufficient level of anesthesia to blunt the stimulation of direct laryngoscopy and tracheal intubation without compromising cerebral perfusion by increasing ICP or decreasing MAP. Intravenous induction with propofol ( 1.5 to 3 mg/kg), thiopental (3 to 6 mg/kg), or etomidate (0.2 to 0.5 mg/kg), produces reliable and prompt onset of unconsciousness and is unlikely to adversely increase ICP.

9/19/2018 Hemodynamic support with sympathomimetic drugs may be necessary and such drugs should be readily available, especially in cases in which CPP may already be compromised.

Neuromuscular blocking drug
9/19/2018 Neuromuscular blocking drug A neuromuscular blocking drug is used to facilitate tracheal intubation, mechanical ventilation of the lungs, and patient positioning on the operating table. Increases in ICP may occur after the administration of succinylcholine, but the extent of the increase is quite variable and usually short-lived. The trachea is intubated after a peripheral nerve stimulator confirms the establishment of skeletal muscle paralysis so that coughing is avoided, which may result in marked increases in ICP.

9/19/2018 Injection of additional intravenous doses of propofol, thiopental, opioids, or lidocaine 1 to 2 minutes before beginning direct laryngoscopy may be effective in attenuating the increase in arterial blood pressure and ICP that can accompany tracheal intubation.

9/19/2018 After tracheal intubation, ventilation of the lungs is controlled at a rate and tidal volume sufficient to maintain PaC02 between 30 and 35 mm Hg. There is no evidence of additional therapeutic benefit when PaC02 is decreased below this range. Use of positive end-expiratory pressure (PEEP) is not encouraged because it could impair cerebral venous drainage and increase ICP, but it can usually be counteracted by raising the head 10 to 15 cm above the level of the chest.

Maintenance of Anesthesia
9/19/2018 Maintenance of Anesthesia After tracheal intubation, measures should be taken to optimize CPP and minimize ICP. Maintenance of anesthesia is achieved with a combination of opioid (either bolus or infusion), continuous infusion of propofol, and inhalation of a volatile anesthetic with or without nitrous oxide. Volatile anesthetics must be used carefully because of their ability to increase ICP. Nevertheless, low concentrations of volatile anesthetics ( <0.5 MAC) may be useful for blunting the increases in systemic blood pressure evoked by surgical stimulation.

Direct-acting vasadilating drugs
9/19/2018 Direct-acting vasadilating drugs Direct-acting vasadilating drugs (hydralazine, nitroprusside, nitroglycerin, calcium channel blockers) increase CBF and ICP despite causing simultaneous decreases in systemic blood pressure; therefore, use of these drugs, particularly before the dura is open, is not encouraged.

9/19/2018 Movement, coughing, or reacting to the presence of the tracheal tube during intracranial procedures is avoided because these responses can lead to increases in ICP, bleeding into the operative site, and a brain that bulges into the operative site and makes surgical exposure difficult. Thus, maintenance of an adequate depth of anesthesia is important. Skeletal muscle paralysis is often used to provide added insurance against movement or coughing.

9/19/2018 If cerebral swelling occurs, administration of additional doses of diuretics can be given to decrease brain water. Mannitol (0.25 to 1 g/kg IV) is an osmotic diuretic and reduces cerebral water content. The onset of action is 5 to 10 minutes, maximum effects are seen in 20 to 30 minutes, and its effects last for about 2 to 4 hours.

9/19/2018 However, if administered rapidly, mannitol can also cause peripheral vasodilation (hypotension) and a shortterm increase in intravascular volume, which could result in increased ICP.

9/19/2018 Acute mannitol toxicity, as manifested by hyponatremia, high measured serum osmolality, and a gap between the measured and calculated serum osmolality of greater than 10 mOsm/kg, can also occur when large doses of the drug (2 to 3 g/kg IV) are given.

9/19/2018 Furosemide (0.5 to 1 mg/kg IV) is effective in decreasing ICP, though less so than mannitol.

9/19/2018 Intermittent intravenous injections of thiopental or propofol may also be effective in decreasing ICP, and if surgically possible, placing the patient in a head-up position also helps. Other useful measures include hyperventilation and discontinuing the administration of volatile anesthetics.

Intravenous Fluid Management
9/19/2018 Intravenous Fluid Management Maintaining euvolemia is recommended. Dextrose solutions are not recommended because they are rapidly distributed throughout body water, and if blood glucose concentrations decrease more rapidly than brain glucose concentrations, water crosses the blood-brain barrier and cerebral edema results. Furthermore, hyperglycemia augments ischemic neuronal cell damage by promoting neuronal lactate production, which worsens cellular injury.

9/19/2018 Therefore, crystalloid solutions such as normal saline and lactated Ringer's solution are recommended. Colloids, such as 5% albumin, are also an acceptable intravenous fluids, but no improvement in outcome has been shown as compared to crystalloids.

Postoperative Management
9/19/2018 Postoperative Management On awakening from anesthesia, coughing or straining by the patient should be avoided because these responses could increase the possibility of hemorrhage or edema formation. A prior intravenous bolus of lidocaine, opioid, or both may help decrease the likelihood of coughing during tracheal extubation.

9/19/2018 Postoperatively, assessing neurologic status frequently and providing adequate analgesia are important. Delayed return of consciousness postoperatively or neurologic deterioration in the postoperative period is evaluated by computed tomography (CT) or magnetic resonance imaging (MRI).

9/19/2018 Tension pneumocephalus as a cause of neurologic deterioration is a consideration, especially if nitrous oxide was administered during anesthesia. The postoperative stress response and resulting hyperdynamic events (e.g., hypertension, tachycardia) are attenuated with the use of hemodynamically active drugs and opioids. Labetalol is commonly used to treat hypertension prophylactically due to its ability to reduce MAP without cerebral vasodilation.

9/19/2018 Venous Air Embolism Neurosurgery that requires significant elevation of the head is associated with an increased risk for venous air embolism. Not only is the operative site above the level of the heart but the venous sinuses in the cut edge of bone or dura may not collapse when transected.

9/19/2018 Air enters the pulmonary circulation and becomes trapped in the small vessels, thereby causing an acute increase in dead space. Massive air embolism may cause air to enter and be trapped in the right ventricle and lead to right ventricular failure. Microvascular bubbles may also cause reflex bronchoconstriction and activate the release of endothelial mediators causing pulmonary edema. Death is usually due to cardiovascular collapse and arterial hypoxemia.

9/19/2018 Air may reach the coronary and cerebral circulations (paradoxical air embolism) by crossing a patent foramen ovale (a probe-patent foramen ovale is present in 20% to 30% of adults) and may result in myocardial infarction or stroke. Furthermore, transpulmonary passage of venous air is possible in the absence of a patent foramen ovale

9/19/2018 Transesophageal echocardiography is the most sensitive method to detect air embolism, but it is invasive and cumbersome. A precordial Doppler ultrasound transducer placed over the right side of the heart (over the second or third intercostal space to the right of the sternum to maximize audible signals from the right atrium) is the next most sensitive (detects amounts of air as small as 0.25 mL) and noninvasive indicator of the presence of intracardiac air.

9/19/2018 Sudden decrease in end-tidal concentration of carbon dioxide reflects increased dead space secondary to continued ventilation of alveoli no longer being perfused because of obstruction of their vascular supply by air bubbles. An increased end-tidal nitrogen concentration may reflect nitrogen from venous air embolism but is rarely available.

9/19/2018 Aspiration of air through a correctly positioned central venous catheter can also be used to diagnose air embolism. In this regard, a right atrial catheter with the tip positioned at the junction of the superior vena cava and the right atrium may provide the most rapid aspiration of air.

9/19/2018 During controlled ventilation of the lungs, sudden attempts (gasps) by patients to initiate spontaneous breaths may be the first indication of the occurrence of venous air embolism.

9/19/2018 Sings Hypotension, tachycardia, cardiac dysrhythmias, cyanosis, and a "mill wheel" murmur are late signs of venous air embolism. A pulmonary artery catheter may provide additional evidence that venous air embolism has occurred because of increases in pulmonary artery pressure. Additional signs in awake patients include chest pain and coughing.

9/19/2018 The surgeon should be notified immediately whenever a venous air embolism is suspected. Venous air embolism is treated by (1) Irrigation of the operative site with fluid, as well as the application of occlusive material to all bone edges so that sites of venous air entry are occluded; (2) Gentle compression of the internal jugular veins; (3) Placement of the patient in a head-down position.

9/19/2018 If nitrous oxide is being administered, it should be promptly discontinued to avoid the risk of increasing the size of venous air bubbles because of diffusion of this gas into the air bubbles.

9/19/2018 PEEP Despite the logic of positive end-expiratory pressure to decrease entrainment of air, the efficacy of this maneuver has not been confirmed. Furthermore, positive end-expiratory pressure could reverse the pressure gradient between the left and right atria and predispose to passage of air across a patent foramen ovale.

9/19/2018 COMMON CLINICAL CASES Intracranial Mass Lesions Intracranial masses (tumors) requiring surgery occur most often in patients 40 to 60 years of age, and the initial signs and symptoms reflect increases in ICP. Seizures that appear in a previously asymptomatic adult suggest the presence of an intracranial tumor, and such tumors are usually confirmed by CT or MRI. Avoidance of abrupt increases in intracranial pressure is an important anesthetic goal when managing patients with intracranial tumors.

9/19/2018 Posterior fossa masses have several additional considerations. In addition to an arterial line, monitoring for the sitting position should include a properly positioned central venous catheter and precordial Doppler given the high incidence of venous air embolism. Operations on posterior fossa tumors can injure vital brainstem respiratory and circulatory nuclei and result in intraoperative hemodynamic fluctuations and postoperative depression of ventilation.

9/19/2018 The cranial nerves can also be affected and lead to impairment of protective airway reflexes. Postoperatively, the patient should be assessed to determine whether the airway can be maintained, or whether tracheal intubation and mechanical ventilation should be continued in the intensive care unit.

Intracranial Aneurysms
9/19/2018 Intracranial Aneurysms Intracranial aneurysms are the most common cause of intracranial hemorrhage. They occur in 2% to 4% of the population, with 1 % to 2% rupturing per year. Although aneurysms may be found incidentally or appear as a slowly enlarging mass, they are most frequently manifested as hemorrhage together with a sudden, severe headache, nausea, vomiting, focal neurologic signs, and depressed consciousness.

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9/19/2018 complications Major complications of aneurysmal rupture include death, rebleeding, and vasospasm and they may be treated with either endovascular coiling or surgery. Short-term outcomes are similar in patients treated surgically versus endovascular insertion of platinum coils . Some patients are unsuitable candidates for insertion of platinum coils because of the anatomy and location of their aneurysms and they require surgery.

9/19/2018 Early treatment is advocated for prevention of rebleeding, but surgery may be associated with more technical difficulty because of a swollen inflamed brain, whereas delaying treatment increases the risk for rebleeding. Vasospasm of the cerebral arteries is generally manifested clinically 3 to 5 days after subarachnoid hemorrhage and is the foremost cause of morbidity and death.

9/19/2018 Transcranial Doppler and cerebral arteriography can detect cerebral vasospasm before clinical symptoms (worsening headache, neurologic deterioration, loss of consciousness) occur. Treatment of vasospasm includes "triple H" therapy . (hypervolemia, hypertension, hemodilution), which consists of the intravenous administration of fluids or inotropic drugs, or both.

9/19/2018 The intravenous administration of a calcium entry blocker, nimodipine, decreases the risk of morbidity and death from vasospasm. Other treatment modalities include selective intra-arterial injection of vasodilators and balloon dilation (angioplasty) of the affected cerebral vessels using interventional radiology.

9/19/2018 Other complications of subarachnoid hemorrhage include seizures (10%), acute and chronic hydrocephalus, and intracerebral hematoma. Changes on the ECG (T -wave inversions, U waves, ST segment depressions, prolonged QT interval, and rarely Q waves) and mild elevation of cardiac enzymes are frequent but do not usually correlate with significant myocardial dysfunction or poor outcome. .

9/19/2018 Hyponatremia is commonly seen after subarachnoid hemorrhage. Significant electrolyte imbalances, acid-base abnormalities, and hemodynamic derangements should be corrected if present, and a cardiac workup should ensue if Q waves are seen on the ECG.

9/19/2018 Management of anesthesia for resection of an intracranial aneurysm is designed to (1) prevent sudden increases in systemic arterial blood pressure, which would increase the aneurysm's transmural pressure and could result in rupture, (2) facilitate surgical exposure and access to the aneurysm .

Anesthetic Management of Patients with Intracranial Aneurysms
9/19/2018 Anesthetic Management of Patients with Intracranial Aneurysms

9/19/2018 Induction and maintenance of anesthesia must be designed to minimize the hypertensive responses evoked by noxious stimulation, such as direct laryngoscopy and placing the patient's head in immobilizing pins. Conversely, CPP must be maintained to prevent ischemia during retraction or temporary vessel occlusion or as a result of vasospasm.

9/19/2018 Hemodynamic control is important during dissection of the aneurysm to prevent intraoperative rupture. Temporary occlusive clips applied to the major feeding artery of the aneurysm can create regional hypotension without the need for systemic hypotension and its inherent risks on multiple organ systems. As a result, normal or even increased systemic arterial blood pressure should be instituted to facilitate perfusion through the collateral circulation.

9/19/2018 ln addition to maintaining collateral cerebral circulation via systemic hypertension, drugs such as thiopental may be administered in the hope that they can provide some protection from cerebral ischemia. Occasionally, hypothermic circulatory arrest may be used for very large complex aneurysms.

9/19/2018 The patient's trachea is generally extubated at the completion of surgery unless there is significant neurologic impairment. Measures to prevent vasospasm and seizures while maintaining adequate CPP should be continued during care of these patients postoperatively.

Arteriovenous Malformations
9/19/2018 Arteriovenous Malformations The incidence of arteriovenous malformations (AVMs) in the general population and annual rate of rupture is similar to that for aneurysms at 2% to 4% and 2%, respectively. Up to 1 % of patients diagnosed with an AVM have an associated aneurysm.

9/19/2018 Risk of hemorrhage is related to anatomic features of the AVM including size and characteristics of the feeding vessels. These patients may be treated several ways: expectantly, open resection, endovascular embolization, or with stereotactic radiosurgery (gamma knife). Preoperative embolization is frequently employed to reduce blood loss and facilitate surgical resection.

9/19/2018 Anesthesia for resection or embolization of A VMs is similar to that for aneurysms with a few distinct considerations. Because their flow characteristics (low-pressure, high-flow shunts), AVMs are unlikely to rupture during acute systemic hypertension, such as occurs during laryngoscopy.

9/19/2018 Despite this, hypertension should still be avoided during induction of anesthesia, given the frequent rate of associated aneurysms. Finally, anesthesia for intracranial AVMs must include preparation for massive, persistent blood loss and postoperative cerebral swelling.

9/19/2018 Carotid Disease A significant proportion of strokes are due to stenosis of the carotid artery and may result in severe disability and death. Randomized controlled trials have confirmed the benefit of carotid endarterectomy (CEA) in symptomatic patients with 70% to 99% stenosis.

9/19/2018 Although a perioperative risk of stroke and death (approximately 4% to 7%) must be taken into account, CEA may be beneficial in asymptomatic patients as well. Carotid stenting using interventional radiology is an alternative therapy for carotid stenosis and is increasing in popularity.

9/19/2018 CEA probably should be optimally performed within 2 weeks of the onset of symptoms given the presence of unstable atherosclerotic plaque. Preoperative assessment of patients undergoing CEA should focus on assessment of perioperative risk of cardiac ischemia as these patients typically have atherosclerotic disease . Either general or regional anesthesia (deep and superficial cervical plexus block) may be used for this procedure.

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9/19/2018 Even though an awake patient may provide a more accurate intraoperative assessment of the patient's neurologic status and more stable hemodynamic profile, the procedure requires a cooperative and motionless patient. Controversy remains on whether CEA is best performed under regional or general anesthesia.

9/19/2018 Goals of anesthesia for CEA include ( 1) prevention of cerebral ischemia through maintenance of adequate cerebral perfusion pressure (2) prevention of myocardial ischemia through avoidance of acute peaks in arterial blood pressure and heart rate. Invasive hemodynamic monitoring with a peripheral arterial catheter is indicated to ensure adequate cerebral perfusion pressure.

9/19/2018 This is especially important during intraoperative clamping of the carotid artery. The anesthesiologist should ensure that the MAP is maintained above the patient's baseline pressure (within 20%) to ensure adequate collateral flow through the circle of Willis. Hypocarbia should be avoided given the risk of cerebral vasoconstriction and ischemia.

9/19/2018 Many methods have been employed to detect intraoperative cerebral ischemia and need for shunting during clamping including EEG, transcranial Doppler, and stump pressure, although none have been shown to definitively improve outcome.

9/19/2018 Postoperative complications include cardiovascular ischemia and neurologic deficits secondary to intraoperative emboli. Hypertension may lead to neck hematoma with airway compromise and hyperperfusion syndrome and should be avoided.

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