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Anesthetic Management of Intracranial Aneurysms

The anesthetic and perioperative management of the surgical and endovascular treatment of intracranial aneurysms is designed to facilitate the conduct of the procedure and the patient's recovery and minimize the risk of aneurysmal rupture, cerebral ischemia, neurologic deficit, and associated systemic morbidity to improve functional survival.

I. Aneurysms


 Saccular aneurysms (<2.5 cm in diameter) are formed by the disintegration of the artery's elastic layer at the flow separator region from the pounding of the arterial pulse wave.
 Giant aneurysms measure up to 10 cm in diameter and represent 5% of all aneurysms.
Other types of aneurysms include fusiform (associated with severe atherosclerosis or degenerative processes in childhood), dissecting (from a tear in the luminal endothelium that permits a blood column to dissect between the endothelium and the media), traumatic (developing in the 2 to 3 weeks after severe head injury), and mycotic (infectious).


Ninety percent of aneurysms occur on the anterior circulation, most commonly the internal carotid-posterior communicating artery (more common in women), anterior communicating artery (more common in men), and middle cerebral artery (MCA) bifurcation. Ten percent occur on the posterior circulation, most commonly at the basilar apex. The internal carotid artery bifurcation is affected in children.


The annual incidence of aneurysmal subarachnoid hemorrhage (SAH) is approximately 6 to 8/100,000 in most western populations. The rate of rupture of an intracranial aneurysm is 0.05% to 6% per year, depending on the size and location of the aneurysm. Aneurysms are 11 times more likely to rupture in patients who have had a previous SAH than in those who have an asymptomatic aneurysm. Smoking and hypertension are risk factors. The incidence in men outnumbers women until age 50; women predominate thereafter; and aneurysms commonly present in the sixth decade of life. Approximately 20% of patients have more than one aneurysm.
Aneurysmal SAH accounts for 10% of all cerebrovascular accidents.


Table -1. Predictors of mortality after subarachnoid hemorrhage

Poor neurologic condition at hospital admission, a function of rate and volume of bleed
Depressed level of consciousness after initial bleed
Older age
Preexisting illness
Elevated blood pressure
Thick clot in the brain substance or ventricles on initial computed tomographic scan
Repeat hemorrhage
Basilar aneurysmal location

Natural history.

One patient in six will die within minutes of an SAH. Of the patients who survive to be admitted to the hospital, 25% will die thereafter, and just over 50% will recover completely. Without treatment, at least 50% of ruptured aneurysms will rerupture within 6 months and then at a rate of 3% per year.

Prognostic factors.

The rate and volume of bleeding affect the patient's neurologic condition at hospital admission and determine outcome. Patients who remain conscious and complain only of severe headache after SAH do better than patients who are comatose upon arrival at the hospital. Older age, poor general health, evidence of clots in either the brain substance or the ventricles, and repeat hemorrhage all affect outcome adversely (Table -1).

Genetics and associated diseases.

Of patients who have SAH, 5% to 10% will have one or more first-order relatives who have also had a ruptured aneurysm. The inheritance is probably dominant with variable penetrance. Conditions associated with intracranial aneurysms include polycystic kidney disease (5% of aneurysms series, 33% of polycystic kidney series), coarctation of the aorta (1% of aneurysm patients, 5% of coarctation patients, all of whom are hypertensive), sickle cell disease, drug abuse (cocaine: generalized vasoconstriction and hypertension; intravenous use: mycotic aneurysms), and hypertension (30% to 40% of patients with SAH). Rarer associations are with fibromuscular dysplasia, Marfan's syndrome, tuberous sclerosis, Ehlers-Danlos syndrome, hereditary hemorrhagic telangiectasia, moyamoya disease, and pseudoxanthoma elasticum. Choriocarcinoma and cardiac myxomas are associated with multiple cerebral aneurysms.


Rupture of an intracranial aneurysm causes the sudden onset of an excruciating headache. Patients may also complain of malaise and be irritable, combative, and uncooperative.


History includes the patient's report that this is the "worst headache of my life" as well as malaise, nausea, and vomiting.
Physical examination identifies change in level of consciousness, focal neurologic deficits, fever, meningismus, nuchal rigidity (may be absent early after SAH), photophobia, ophthalmic hemorrhages (poor prognostic sign), fluid (hypovolemia), and electrolyte (hyponatremia) imbalance.
Imaging should be performed: computed tomographic (CT) scan for amount of subarachnoid, intracerebral, and intraventricular blood; cerebral angiography for exact location and configuration of aneurysm and neck.
Lumbar puncture is recommended for analysis of cerebrospinal fluid (CSF) if the CT scan is negative.
Common misdiagnoses include flu, meningitis, cervical disc disease, migraine, myocardial infarction, malingering, and intoxication.


Botterell in 1956 introduced a system for grading patients after SAH to facilitate assessment of surgical risk, prediction of outcome, and prompt evaluation of the patient's condition. The Grades I to V describe the patient's level of consciousness and degree of neurologic impairment, with each higher grade representing greater severity.
Hunt and Hess modified Botterell's system in 1968 to include a provision for the effect of serious systemic illness (Table -2a).
The World Federation of Neurological Surgeons (WFNS) 1988 grading scale, based on the Glasgow Coma Scale, demonstrated that the preoperative level of consciousness correlated most directly with outcome (Table -2b).


Table -2a. Clinical grading after subarachnoid hemorrhage: Hunt and Hess modification

Grade Description Mortality (%)
Grade 0 Unruptured aneurysm -
Grade I Asymptomatic or minimal headache with normal neurologic examination 2
Grade II Moderate to severe headache, nuchal rigidity, no neurologic deficit other than cranial nerve palsy 5
Grade III Lethargy, confusion, or mild focal deficit 15-20
Grade IV Stupor, moderate to severe hemiparesis, possible early decerebrate rigidity, vegetative disturbances 30-40
Grade V Deep coma, decerebrate rigidity, moribund appearance 50-80

Serious systemic diseases (hypertension, coronary artery disease, chronic pulmonary disease, diabetes) and severe vasospasm on angiography cause assignment of the patient to the next less favorable category.


Table-2b. World Federation of Neurological Surgeons Clinical Grading Scale

WFNS Grade GCS Score Motor Deficit
I 15 Absent
II 14-13 Absent
III  14-13 Present
IV 12-7 Present or absent
V 6-3 Present or absent

WFNS, World Federation of Neurological Surgeons; GCS, Glasgow Coma Scale.

III. Complications of SAH (Table -3)

Rebleeding, the occurrence of further hemorrhage after the initial SAH, is one of the major causes of neurologic deterioration after SAH. The cardinal signs are deterioration in the level of consciousness, development of focal neurologic deficits (aphasia, hemiplegia), abnormal vital signs (hypertension, bradycardia, arrhythmias, irregular respirations), and the presence of hemorrhage on ophthalmic examination.
These subsequent episodes of aneurysmal rupture are usually more severe than the first hemorrhage. The mortality associated with a second hemorrhage rises precipitously with significant morbidity in the surviving patients. Late rebleeding is fatal in 67% of cases. All rebleeding accounts for 22% of the mortality from SAH.
The incidence of rebleeding is highest (4%) during the first 24 hours after SAH and then declines to 1% to 2% per day for the next 13 days. Approximately 20% to 30% of ruptured aneurysms rebleed within the first 30 days after SAH. The cumulative risk of rebleeding is 19% at 2 weeks, 50% at 6 months, and then decreases to 3% per year for up to 15 years. During the ensuing 5 months after the initial SAH, 10% to 15% of patients will rebleed. The overall incidence of rebleeding is 11%.
The incidence of aneurysmal rupture during induction of anesthesia is 0.5% to 2% and carries a mortality of 75%. The incidence of intraoperative aneurysmal rupture varies from 6% to 18%, depending on the institution and the size and location of the aneurysm. In order of decreasing incidence, the causes of rupture during operation include aneurysmal dissection, brain retraction, hematoma evacuation, and dural and arachnoid opening.


Table -3. Complications of aneurysmal subarachnoid hemorrhage

Central nervous system
Disordered autoregulation
Intracranial hypertension
Systemic disorders
Hyponatremia, hypokalemia, hypocalcemia
Electrocardiographic abnormalities
Respiratory abnormalities: pulmonary edema, pneumonia, pulmonary embolus
Hepatic dysfunction
Renal dysfunction
Gastrointestinal bleeding

Pathophysiologic sequelae of rebleeding include intracranial hypertension and compromised cerebral perfusion; acute hydrocephalus from the sudden deposition of subarachnoid clot that obstructs the flow of CSF through the basal cisterns; cerebral infarction from either direct, hematoma-induced destruction of tissue or shifts in the intracranial contents with vascular compromise; impaired autoregulation (the ability of the normal brain to maintain cerebral blood flow [CBF] at a fairly constant level between a mean arterial pressure [MAP] of 50 and 150 mm Hg); and a reduction in the cerebral metabolic rate for oxygen consumption (CMRo2).
Predisposing factors for rebleeding:
1. Large volume of blood in the subarachnoid space from the initial SAH
2. Poor neurologic status owing to the devastation caused by the initial SAH
3. Short interval from the initial hemorrhage
4. Female gender: women rebleed twice as frequently as men
5. Older age and poor general medical condition
6. Systemic hypertension: the risk of rebleeding is directly related to the patient's systolic blood pressure
7. Multiple previous episodes of rebleeding that increase the likelihood of subsequent rupture and death
8. Presence of either an intracerebral or intraventricular hematoma
9. Abnormal clotting parameters
10. Posterior circulation aneurysms
The size of the hematoma from the episode of rebleeding is the most critical factor in determining outcome. Patients who have a large subdural hematoma and a marked midline shift on CT scan have a poorer prognosis, as do those who have associated intracerebral and intraventricular hemorrhage.
Early surgical or endovascular obliteration of the aneurysm is the only definitive means to prevent rebleeding. Either operation or endovascular obliteration within 24 to 48 hours of SAH is therefore favored because of the association with improved outcome. At 1-year follow-up, the results of the International Subarachnoid Aneurysm Trial comparing operative aneurysmal clip ligation with endovascular metal coiling demonstrated that the risk of rebleeding was low in both groups: 1% for the surgical group and 2.4% for the endovascular group. The effects of rebleeding were taken into account in determining that the relative risk of either death or significant disability for endovascular patients is 22.6% lower than for surgical patients. This represented an absolute risk reduction of 6.9%. Most of the 2,143 patients randomized into the trial were in good condition (WFNS Grades I and II) after SAH and had small anterior-circulation aneurysms (92% <11 mm in size) for which endovascular coiling and neurosurgical clipping were both considered therapeutic options.
Prevention of rebleeding. The following are preferred methods:
1, Control systolic hypertension and increases in transmural pressure (MAP minus intracranial pressure [ICP]).
2. Administer short-acting antihypertensive drugs (esmolol, labetalol) to control either labile hypertension or transient spikes in blood pressure from therapeutic interventions.
3. Maintain the patient's "normal" blood pressure as the lower acceptable limit to avoid either initiation or exacerbation of vasospasm from a decrease in cerebral perfusion pressure (CPP), the difference between MAP and ICP.
4. Administer narcotic analgesics and sedatives in titrated doses to reduce pain and anxiety while avoiding oversedation and hypoventilation.
5. Avoid the rapid drainage of CSF from lumbar or ventricular puncture, which may lead to a fall in ICP, a relative rise in transmural pressure, and the potential for aneurysmal rerupture. CSF drainage may be instituted to lower ICP, however, if cerebral perfusion is seriously compromised because of intracranial hypertension.
6. Maintain euvolemia.
7. Avoid seizures that may themselves lead to hypertension.
8. Maintain transmural pressure across the wall of the aneurysm during the induction of anesthesia for aneurysmal clip ligation by the prevention of sudden increases in systemic blood pressure and decreases in ICP. Adjust ventilation to maintain normocapnia (Paco2 of 35 to 40 mm Hg) until the dura is opened. The presence of a large hematoma may mandate hyperventilation to improve intracranial compliance during induction. Give mannitol and begin spinal drainage after the bone flap has been turned.
9. Decrease the turgor of the aneurysmal sac during manipulation of the aneurysm by the neurosurgeon's temporary proximal occlusion of the parent vessel. The patient's blood pressure is maintained in the high-normal range to enhance distal and collateral perfusion. The blood pressure is quickly returned to the patient's low-normal range if the temporary clip is removed before the aneurysm has been secured to prevent aneurysmal rupture. Hypotension induced with either isoflurane or sodium nitroprusside (SNP) is not favored, however, because the CBF-lowering effect of the hypotension may adversely affect patients who have developed or are in the process of developing cerebral vasospasm.
10. Control blood pressure during emergence from anesthesia to prevent bleeding from other unsecured aneurysms, muslin-wrapped aneurysms, and sites of surgical hemostasis.
Management of rebleeding after SAH is designed to maintain CPP, limit intracranial hypertension, decrease intracranial volume, control systemic blood pressure, reduce transmural pressure across the wall of the aneurysm, and optimize cerebral oxygen delivery through the maintenance of normal arterial oxygen saturation and normal hemoglobin concentration.
1. If the aneurysm bleeds before, during, or after the induction of anesthesia, the patient is hyperventilated with 100% oxygen. Thiopental lowers the blood pressure and affords some cerebral protection, but excessive lowering of the systemic pressure at this juncture can be detrimental if it interferes with cerebral perfusion. Immediate craniotomy to accomplish "rescue clipping" after rupture during induction of anesthesia has been successful.
2. Intraoperative rupture of the aneurysm mandates rapid surgical control. The MAP may be reduced to 50 mm Hg briefly to facilitate temporary proximal and distal control of the parent vessel in preparation for clip ligation of the neck of the aneurysm. Once the parent vessel is controlled, the blood pressure is increased to normal to enhance collateral circulation during the period of temporary occlusion. Alternatively, the ipsilateral carotid artery may be manually compressed for up to 3 minutes to produce a bloodless field. Blood loss is replaced immediately because it is essential to maintain normovolemia if the blood pressure needs to be reduced.
Emergency reoperation may be necessary for evacuation of a hematoma or to control postsurgical bleeding or ventricular drainage. In an emergency, an external ventricular drain may be inserted at the patient's bedside to decompress the ventricles.
Although the use of epsilon-aminocaproic acid and other antifibrinolytic drugs halved the rebleeding rate in the initial 2 weeks after SAH, the incidence of vasospasm and hydrocephalus increased, resulting in no improvement in overall outcome. Instead of using antifibrinolytic drugs, neurosurgeons use either early endovascular obliteration or early operation with definitive clipping of the aneurysm. This mandates the rapid and efficient accomplishment of diagnosis, evaluation, and initial treatment.

Vasospasm or delayed ischemic deficit

Vasospasm is the reactive narrowing of the larger conducting arteries in the subarachnoid space that are surrounded by clots after SAH and affected by spasmogenic breakdown products of the red blood cells within the clot. The subsequent delayed ischemic deficit and infarction caused by vasospasm are major causes of disability and death after SAH, accounting for 30% of SAH-induced morbidity and mortality. Vasospasm has been considered the causative factor in 28% of all deaths and 39% of all disability after SAH and is therefore responsible for the great human cost and extensive utilization of limited health care resources.
1. Patients of all neurologic grades have a 50:50 chance of developing significant angiographic vasospasm. Symptoms of delayed ischemia occur in 20% to 25% of patients, and 30% to 50% of patients have evidence of infarction from vasospasm on CT scan. Death from vasospastic infarction occurs in 5% to 17% of patients.
2. The incidence of vasospasm peaks between the 4th and 9th day after SAH and decreases over the next 2 to 3 weeks.
3. Vasospasm is directly related to the severity of the hemorrhage from the aneurysmal rupture which correlates well with the location and volume of blood noted on the post-SAH CT scan. The risk of vasospasm is increased by SAH-induced cerebral dysautoregulation and abnormal carbon dioxide (CO2) responsiveness, a Glasgow Coma Scale score of <14 on hospital admission, an early increase in mean MCA flow velocity on transcranial Doppler (TCD) ultrasonography, and anterior cerebral and internal carotid artery aneurysms. The timing of surgery and the method of occlusion "surgical versus endovascular" have no effect on the subsequent development of vasospasm. The intraoperative transfusion of packed red blood cells is a risk factor for poor outcome, and postoperative transfusion is correlated with the development of angiographically confirmed vasospasm. The mechanism may involve either the depletion or the inactivation of nitric oxide, an endogenous vasodilator, which transfused red cells lack.
Diagnosis of vasospasm
1. Clinical signs include either progressive impairment in the level of consciousness or the appearance of new focal neurologic deficits >4 days after the initial SAH that are not associated with any other structural or metabolic cause. The onset may be either sudden or insidious and accompanied by increased headache, meningismus, and fever. It is important to rule out other causes of clinical deterioration after SAH including rebleeding, hydrocephalus, subdural hematoma, cerebral infarction and edema, meningitis, seizures, electrolyte and acid-base disturbances, and adverse reactions to medications.
2. TCD ultrasonography may be used to determine the efficacy and duration of treatment. Both a large increase in blood flow velocity (MCA velocity >120 cm/second) and a rapid rise in blood flow velocity (>50 cm/second in 24 hours) reflect a reduction in vessel caliber. A peak flow velocity of 140 to 200 cm/second indicates moderate vasospasm; a peak flow velocity >200 cm/second is associated with severe vasospasm. Critically high blood flow velocities (>120 cm/second) correlate strongly with vasospasm on angiography. Because TCD is operator dependent and reflects technical factors, ICP, cardiac output, and the artery being assessed, it is important to correlate TCD results with sequential neurologic examination and ICP, blood pressure, and cardiac output.
3. Cerebral angiography is the most reliable modality for diagnosing and evaluating vasospasm. Although some angiographic evidence of vasospasm occurs in 70% to 80% of cases, only one-third of patients develop the clinical picture. Signs and symptoms of decreased CBF usually occur when the reduction in the diameter of the arterial lumen exceeds 50%, the definition of angiographically severe vasospasm.
4. Xenon-enhanced CT, a relatively inexpensive technique, demonstrates the decrease in regional cerebral blood flow (rCBF) in patients who have clinical vasospasm. This technique can quantify rCBF accurately, be repeated within 20 minutes, fuse rCBF data with conventional CT scan anatomy, and distinguish ischemia from other causes of neurologic deterioration after SAH.
5. Jugular bulb oximetry detects changes in cerebral oxygen extraction (AVDo2). Patients who develop clinical vasospasm have a significant rise in AVDo2 approximately 1 day before the onset of signs of neurologic deficit. Increases in AVDo2 may therefore predict impending clinical vasospasm while an improvement in AVDo2 reflects the patient's response to treatment.
6. CBF-measuring modalities include positron emission tomography, which demonstrates a fall in CMRo2 after SAH and single-photon emission computed tomography (SPECT). Angiographic vasospasm, delayed ischemic deficit, and increased TCD velocities are associated with regions of hypoperfusion on SPECT.
Treatment of vasospasm involves pharmacologic and mechanical modalities.
1. Early operation for clip ligation of the aneurysmal neck permits the removal of a fresh clot by irrigation and suction. The surgeon may instill recombinant tissue plasminogen activator (rTPA) directly into the subarachnoid space to dissolve the remaining clot. This fibrinolytic drug can reduce vasospasm, but it also may cause bleeding by dissolving normal clots. Therefore, only patients at great risk of developing clinically significant vasospasm are candidates for this treatment.
2. Early operative clip ligation and endovascular occlusion of the aneurysm both facilitate the subsequent treatment of vasospasm. While patients who had better clinical grades (WFNS Grades I to III) on hospital admission and whose aneurysms were occluded with endovascular coils were less likely to develop symptomatic vasospasm as compared with those undergoing surgical clip ligation, there was no significant difference in overall outcome between those two groups at the longest follow-up period.
3. The prophylactic use of the calcium antagonist nimodipine within 96 hours of SAH is now a standard aspect of care after SAH. Although nimodipine reduces the incidence of vasospasm, the improvement in mortality has not been statistically significant when compared with control groups. Because nimodipine tends to decrease blood pressure, patients may require hydration and the administration of pressor drugs during the induction of anesthesia and careful attention to fluid balance intra- and postoperatively.
4. Enoxaparin, a low-molecular-weight heparin given as one subcutaneous injection of 20 mg/day, has been shown to improve overall outcome at 1 year after SAH by reducing delayed ischemic deficit and cerebral infarction. Patients receiving enoxaparin also had fewer intracranial bleeding events and a lower incidence of severe shunt-dependent hydrocephalus.
5. Other drugs used to treat vasospasm include tirilazad, an antioxidant and free radical scavenger whose clinical trials have demonstrated mixed results; nicaraven, a free radical scavenger associated with a trend toward improved mortality, good outcome, and smaller infarct size at 3 months; ebselen, an antioxidant and anti-inflammatory drug whose neuroprotective properties have caused it to be effective in the treatment of acute stroke; and fasudil, a kinase inhibitor used intra-arterially to treat vasospasm. The use of endothelin antagonists has been associated with an increase in the incidence of pneumonia and hypotensive episodes.
6. "Triple-H therapy". hypertensive hypervolemic hemodilution, augments cerebral perfusion in vasospastic areas of the brain in which autoregulation is impaired through increases in blood pressure, cardiac output, and intravascular volume. Relative hemodilution to a hematocrit of 30% to 35% promotes blood flow through the cerebral microvasculature. The early institution of triple-H therapy is crucial to prevent the progression from vasospasm-induced mild ischemia to infarction. The expansion of intravascular volume is important after SAH because the total circulating blood volume and total circulating red cell volume are reduced secondary to supine diuresis, peripheral pooling, negative nitrogen balance, decreased erythropoiesis, iatrogenic blood loss, and increased natriuresis from the elaboration of natriuretic hormone.
  (a) The guidelines for optimal volume expansion include a central venous pressure (CVP) of 10 mm Hg and a pulmonary capillary wedge pressure (PCWP) of 12 to 16 mm Hg. The vagal and diuretic response to intravascular volume augmentation may necessitate the administration of atropine, 1 mg intramuscularly (i.m.) every 3 to 4 hours, and aqueous vasopressin (Pitressin), 5 units i.m., to reduce urine output to <200 mL/hour. Hydrocortisone has also been used to attenuate the excessive natriuresis and consequent hyponatremia seen in patients after SAH and to prevent the decrease in total blood volume. The use of albumin to augment intravascular volume after the administration of normal saline has failed to increase the CVP above 8 mm Hg may improve clinical outcome at 3 months and reduce hospital costs.
  (b) Vasopressor drugs, including dopamine, dobutamine, and phenylephrine, may be necessary to increase blood pressure. If the aneurysm has not been secured, systolic pressure is maintained at 120 to 150 mm Hg. After the aneurysm has been secured, systolic blood pressure may be increased to 160 to 200 mm Hg. Invasive hemodynamic monitoring including the direct measurement of systemic arterial blood pressure, CVP, pulmonary artery pressure, PCWP, and cardiac output improves the safety and efficacy of treatment with induced hypertension.
  (c) The complications of triple-H therapy include rebleeding, transformation to hemorrhagic infarction, cerebral edema, intracranial hypertension, hypertensive encephalopathy, myocardial infarction, pulmonary edema, congestive heart failure, coagulopathy, dilutional hyponatremia, and the complications of central catheterization.
Transluminal balloon angioplasty, the mechanical dilatation of a cerebral vessel at a segment of spastic narrowing by the use of an inflatable intravascular balloon, may effect improvement in the patient's level of consciousness and focal ischemic deficits. Early intervention is crucial to success. The superselective intra-arterial infusion of papaverine has also been successful in dilating distal vessels, but because papaverine can be neurotoxic, verapamil, nimodipine, and nicardipine have been used instead. The complications of angioplasty include rupture of the aneurysm, rupture of intracranial vessels, intimal dissection, and cerebral ischemia and infarction.
Prevention of vasospasm requires attentive critical care, maintenance of normovolemia and electrolyte balance, monitoring of the level of consciousness and neurologic function in a critical care area until the peak time for the development of vasospasm has passed, and prevention of secondary cerebral insults and medical complications. After SAH, patients require 3 to 4 L of fluid per day to maintain normovolemia. Hypotonic solutions (e.g., lactated Ringer's solution) are avoided and hyponatremia is treated with either normal or hypertonic saline as necessary. The blood pressure is controlled before the aneurysm has been secured but not treated thereafter unless the elevation reaches critically high levels. Mannitol, ventricular drainage (with avoidance of a sudden drop in ICP and consequent rise in transmural pressure), and mild hyperventilation are used to maintain ICP in the normal range. The goal is to keep the CPP above 60 to 70 mm Hg.

IV. Central nervous system (CNS) complications

The CNS is directly affected by SAH and the resultant hematoma, vascular disruption, and edema, all of which decrease CBF and CMRo2. The patient's clinical grade correlates with the extent of neurologic impairment caused by the intracranial pathophysiology.
The cerebral vasculature's responsiveness to changes in CO2 tension (Paco2) is preserved after SAH. A decline in CO2 reactivity usually does not occur without extensive disruption of cerebral homeostasis.
SAH interferes with cerebral autoregulation. The upper and lower limits of autoregulation are higher in hypertensive patients.
Intracranial aneurysms themselves, particularly giant ones, and the SAH-induced hematoma and edema all have the potential for causing intracranial hypertension with a resultant decrease in the patient's level of consciousness and the potential for brain stem herniation and death. After SAH, the patient's Hunt and Hess clinical grade reflects the ICP. Grade I and II patients have normal ICP (but not necessarily normal elastance), whereas Grades IV and V patients have intracranial hypertension.
Hydrocephalus occurs in 10% of patients after SAH from obstruction of the CSF drainage pathways by either intraventricular or intraparenchymal blood and the subsequent development of arachnoidal adhesions that prevent reabsorption of CSF. Whether the aneurysm has been occluded by either surgical or endovascular means does not affect the patient's subsequent risk for the development of hydrocephalus.
Acute hydrocephalus occurs in 15% to 20% of patients. It is characterized by the onset of lethargy and coma within 24 hours of SAH and is associated with poor clinical grade on admission, either thick subarachnoid blood or intraventricular hemorrhage on initial CT scan, alcoholism, female gender, older age, increased aneurysm size, pneumonia, meningitis, and a preexisting history of hypertension. The development of acute ventricular dilatation immediately after SAH, a cause of the assignment of a spuriously poor neurologic grade, may require external ventricular drainage (EVD) to normalize ICP, especially if the patient's level of consciousness is depressed. Good results have been achieved when EVD is performed in conjunction with early occlusion of the aneurysm. While half of the patients who develop acute hydrocephalus go on to require a ventriculoperitoneal shunt, EVD can reduce the need for permanent shunting. Other predictors of the need for permanent shunting are poor grade on admission, rebleeding, and intraventricular hemorrhage.
Chronic hydrocephalus, which develops weeks later in 25% of patients who survive SAH, is an important cause of failure to improve in patients who are initially comatose and of secondary slow decline in those who were originally in good condition. Symptoms include impaired consciousness, dementia, gait disturbance, and incontinence. A CT scan is indicated a month after SAH to ascertain ventricular size.
The post-SAH incidence of seizures ranges from 3% to 26%. Early seizures occur in 1.5% to 5% of patients; late seizures occur in 3%. Seizures are detrimental to patients after SAH because they increase CBF and CMRo2 and may precipitate rebleeding from the attendant rise in blood pressure. Patients at highest risk for the development of seizures have either thick cisternal blood or lobar intracerebral hemorrhage on CT scan. Other risk factors include rebleeding, vasospasm and delayed ischemic deficit, MCA aneurysms, subdural hematoma, and chronic neurologic impairment. The value of prophylactic anticonvulsant therapy is controversial, however, because most seizures occur in the first 24 hours after SAH and frequently before hospitalization. Neurosurgeons usually institute seizure prophylaxis with phenytoin, fosphenytoin, or levetiracetam for 1 to 2 weeks after SAH. Patients who have either an intracranial hemorrhage or more than one early seizure receive anticonvulsants for at least 6 months.

V. Systemic sequelae of SAH

Fluid and electrolyte balance
Most patients (30% to 100%) develop a decrease in intravascular volume after SAH that correlates with clinical grade and the presence of intracranial hypertension.
Hyponatremia occurs from the release of atrial natriuretic factor from the hypothalamus. Treatment includes hydration with either normal or hypertonic (3%) saline to improve cerebral perfusion.
Many patients (50% to 75%) develop hypokalemia and hypocalcemia and require replacement.
Cardiac sequelae
Electrocardiographic (ECG) abnormalities occur in 50% to 100% of patients after SAH. The most common are T-wave inversion and ST segment depression. Other changes include U waves, QT interval prolongation, and Q waves. These abnormalities are similar to those seen with cardiac ischemia and infarction and may predispose the patients to life-threatening arrhythmias. Prolongation of the corrected QT interval (QTc) makes patients particularly vulnerable to ventricular arrhythmias. The routine measurement of QTc may identify patients at risk for potentially lethal arrhythmias, a risk exacerbated by hypokalemia.
Rhythm disturbances, seen in 30% to 80% of patients, include premature ventricular complexes (most commonly), sinus bradycardia and tachycardia, atrioventricular dissociation, atrial extrasystole, atrial fibrillation, brady- and tachyarrhythmias, and ventricular tachycardia and fibrillation. Arrhythmias occur most frequently within the first 7 days of SAH. The peak occurrence is between the 2nd and 3rd day.
The etiology has been attributed to injury to the posterior hypothalamus with release of norepinephrine and resultant subendocardial ischemic changes and electrolyte disturbances. This increase in sympathetic tone can persist for the first week after SAH.
The extent of myocardial dysfunction correlates with the severity of the neurologic injury after SAH.
Prophylactic adrenergic blockade has improved cardiac outcome in some patients.
In determining whether to proceed with surgery on an emergent basis after SAH, the measurement of serial cardiac isoenzymes and the assessment of ventricular function by echocardiography help elucidate the degree of ischemia.
The use of a pulmonary artery catheter to monitor PCWP and cardiac output may facilitate management of both the patient's cardiac dysfunction and the response to triple-H therapy for the treatment of vasospasm.
The presence of either a severe arrhythmia, as occurs in 5% of the patients who have arrhythmias, or significant cardiogenic pulmonary edema may necessitate the postponement of surgery until treatment has been instituted although delay could put patients at risk for rebleeding and compromise the treatment of vasospasm.
Respiratory system
Pulmonary conditions including cardiogenic and neurogenic pulmonary edema, pneumonia, adult respiratory distress syndrome, and pulmonary emboli account for 50% of deaths from medical complications at 3 months after SAH. Medical complications themselves cause 23% of all deaths.
The majority (60%) of patients become symptomatic from pulmonary edema between days 0 and 7 after SAH; the largest number of cases presents on day 3. The incidence of pulmonary edema is greater in patients older than 30 years. Poor clinical grade at the time of admission also correlates with more respiratory dysfunction, suggesting neurogenic influences.
Treatment includes antibiotics, supportive care, and correction of intracranial (intracranial hypertension, cerebral edema, hydrocephalus) and fluid and electrolyte abnormalities.
Other medical complications
Hepatic dysfunction (hepatic failure and hepatitis) occurs in 25% of patients after SAH, correlates positively with poor clinical grade, and is frequently observed in patients who develop pulmonary edema.
Renal dysfunction is noted in 8% of patients after SAH and occurs more frequently in septic patients who are receiving antibiotics.
Thrombocytopenia occurs in 4% of patients after SAH and is associated with sepsis, severe neurologic deficits, and antibiotic use. Disseminated intravascular coagulation and leukocytosis have also been reported.
Gastrointestinal bleeding occurs in almost 5% of patients and should be part of the differential diagnosis of any unexpected episode of hypotension and tachycardia.

VI. Surgical intervention

Early aneurysmal clip ligation in the first 24 to 48 hours after SAH has advantages: prevention of rebleeding, reduction in vasospasm from removal of blood from the subarachnoid space ("intracranial toilet"), and ability to treat vasospasm through volume expansion and deliberate hypertension with relative safety. Other advantages include reductions in medical complications, patient anxiety, and the cost of hospitalization.
The International Study on the Timing of Aneurysm Surgery, published in 1990, documented that early (0 to 3 days after SAH) and late (11 to 14 days) surgery yielded similar overall morbidity and mortality. The fact that results were better in the subset of North American patients who were alert and underwent early operation has made early surgical intervention a common practice.

VII. Anesthesia for surgical intervention

Preoperative evaluation includes the following:
Review of neurodiagnostic studies (magnetic resonance imaging, CT scan, and cerebral angiogram)
History and focused physical and neurologic examination
Notation of ward blood pressures and association between blood pressure decrease and neurologic deterioration
Assessment of fluid and electrolyte balance
Cardiac history and ECG with determination of need for echocardiogram, cardiac isoenzymes, cardiac nuclear scanning, perioperative cardiovascular monitoring
Notation of current drug regimen
Premedication includes the following:
Calcium channel-blocking drugs, anticonvulsants, and steroids are continued.
Drugs to reduce gastric acidity (cimetidine, ranitidine) and speed gastric emptying (metoclopramide) are given before the induction of anesthesia.
Sedatives, hypnotics, anxiolytics, and narcotics are used sparingly to avoid respiratory depression and the masking of neurologic deterioration. The anesthesiologist can administer small doses of intravenous narcotic (morphine, 1 to 4 mg; fentanyl, 25 to 50 mcg) and benzodiazepine (midazolam, 1 to 2 mg) to good-grade patients under direct supervision. Poor-grade patients do not receive premedication unless an endotracheal tube is in place, in which case they could require muscle relaxation, sedation, and blood pressure control.
Monitoring during anesthesia includes:
1. Cardiac rate, rhythm, and ischemia via ECG with V5 lead
2. Direct intra-arterial blood pressure with pressure transducer at brain level to reflect cerebral perfusion
3. CVP through the antecubital, jugular, or subclavian route
4. PCWP and cardiac output in patients who have cardiac compromise or severe vasospasm
5. Intermittent arterial blood gases, glucose, electrolytes, osmolality, hematocrit
6. Brain temperature by tympanic or nasopharyngeal thermistor
7. CBF velocity by TCD ultrasonography
8. Electrophysiologic monitors: electroencephalogram (EEG); brain stem, auditory, somatosensory, and motor-evoked potentials
9. Jugular bulb venous oxygen saturation
10. Neuromuscular blockade, oxygen saturation, urine output, end-tidal CO2
Intravenous access. The need for adequate intravenous access mandates the insertion of two large-bore intravenous catheters in addition to the CVP or pulmonary artery catheter before (a) positioning for operation, which may limit access to arteries and veins, and (b) interventions that will affect blood pressure, ICP, and transmural pressure.
Induction of Anesthesia
The induction period is critical because the rupture of the aneurysm at this juncture can be fatal. A smooth induction requires limitation of the hypertensive response to laryngoscopy and intubation, obliteration of coughing and straining on the endotracheal tube, and maintenance of adequate CPP while minimizing the change in transmural pressure across the wall of the aneurysm.
The ICP of good-grade patients (Grades 0, I, II) is usually normal; a decrease in blood pressure of 20% to 30% below the patient's normal value is not detrimental in the absence of evidence of cerebral ischemia. Poor-grade patients (Grades IV and V) already have the potential for ischemia secondary to intracranial hypertension and impaired perfusion. Decreasing the blood pressure of these patients may exacerbate the cerebral ischemia. Measures are still necessary, however, to blunt the sympathetic response to laryngoscopy and intubation.
Good-grade patients do not require hyperventilation during induction (Paco2 35 to 40 mm Hg) because they have normal intracranial elastance. Poor-grade patients who have intracranial hypertension benefit from moderate hyperventilation to a Paco2 of 30 mm Hg during induction.
The intravenous induction of anesthesia confers loss of consciousness while maintaining cardiovascular and intracerebral homeostasis during catechol-releasing maneuvers by the administration of thiopental, 3 to 5 mg/kg, etomidate, 0.1 to 0.3 mg/kg, or propofol, 1 to 2 mg/kg; fentanyl, 3 to 5 mcg/kg, or remifentanil, 0.5 mcg/kg; lidocaine, 1.5 mg/kg; and midazolam, 0.1 to 0.2 mg/kg. The patient is ventilated by mask with 100% oxygen (Table -4).
If the patient does not have an increase in intracranial elastance, the introduction of isoflurane or sevoflurane before laryngoscopy deepens the anesthesia.
Additional fentanyl, 1 to 2 mcg/kg; propofol, 0.5 mg/kg; or lidocaine, 1.5 mg/kg, is given before brief gentle laryngoscopy and intubation to preserve hemodynamic and intracranial stability.
Muscle relaxants
Vecuronium, 0.1 mg/kg, a nondepolarizing muscle relaxant of intermediate duration, does not increase the heart rate (and blood pressure) or the ICP in the presence of a reduction in intracranial compliance.
Succinylcholine has increased ICP and caused ventricular fibrillation in patients after SAH. Susceptible patients include those who are comatose but nonparetic; have flaccid paralysis, spasticity, or clonus after head injury; or move their extremities in response to pain but not command. For these patients, rocuronium, 0.6 mg/kg, which does not adversely affect CBF or ICP, is useful for rapid-sequence induction.


Table-4. Induction of anesthesia for endovascular and operative treatment of intracranial aneurysms

Optimal head position
Deep plane of anesthesia
Fentanyl 0.5-1 mcg/kg
Remifentanil 0.5 mcg/kg
Thiopental 3-5 mg/kg
Propofol 1-2 mg/kg
Vecuronium 0.1 mg/kg
Low-dose inhaled anesthetic 0.5 minimum alveolar concentration
Controlled ventilation 100% oxygen
Paco2 35-40 mm Hg (normal ICP)
Paco2 30-35 mm Hg (elevated ICP)
Before laryngoscopy
Lidocaine 1.5 mg/kg
Thiopental 2-3 mg/kg
Propofol 0.5 mg/kg
Brief, gentle laryngoscopy  
ICP, intracranial pressure.

Cardioactive drugs
Cardioactive drugs counteract the hypertensive response to laryngoscopy and intubation. Esmolol, 0.5 mg/kg, and labetalol, 2.5 to 5 mg, block the chronotropic and inotropic effects of sympathetic stimulation without affecting CBF or ICP. Intravenous lidocaine is also useful for this purpose.
SNP, a direct-acting cerebral vasodilator, increases cerebral blood volume (CBV) and ICP. Although SNP, 100 mcg intravenously (i.v.), can prevent the hypertensive response to laryngoscopy and intubation, it may be detrimental in patients who have a reduction in intracranial compliance.
Nitroglycerin also increases CBV from the dilatation of capacitance vessels and therefore may increase ICP.
The calcium channel-blocking drugs nicardipine, 0.01 to 0.02 mg/kg, and diltiazem, 0.2 mg/kg or 10 mg, facilitate rapid control of hypertension intraoperatively. Neither drug decreases local CBF or blood flow velocity.
Intravenous drugs including propofol, narcotics, and nondepolarizing muscle relaxants are used together or in combination with 0.5 minimum alveolar concentration (MAC) of a volatile anesthetic for maintenance of anesthesia. It is important to be able to manipulate blood pressure, minimize brain retractor pressure through cerebral relaxation, and facilitate rapid emergence and timely neurologic assessment.
All inhalational anesthetics are cerebral vasodilators and have the potential for increasing ICP; all of them, with the exception of nitrous oxide (N2O), depress cerebral metabolism. N2O should be avoided, especially during the induction of anesthesia, in patients who have decreased intracranial compliance. It is introduced only after giving cerebral vasoconstricting drugs and establishing hypocapnia. Alternatively, the use of N2O may be dispensed with altogether, especially if there is concern about the possibility of venous air embolism.
Isoflurane increases CBF minimally but has increased ICP despite hypocapnia in patients who have space-occupying lesions. Isoflurane is therefore used in low concentrations or avoided altogether in patients known to have a decrease in intracranial compliance. The cerebral vascular effects of desflurane (4% to 6%) are similar to those of isoflurane. Sevoflurane is also a cerebral vasodilator but might not increase ICP when administered after the establishment of hypocapnia. The low blood-gas solubility coefficient of desflurane and sevoflurane permits rapid emergence and prompt postoperative neurologic evaluation.
Fentanyl and remifentanil improve cerebral relaxation during craniotomy in hyperventilated patients receiving isoflurane. Either fentanyl, bolus: 25 to 50 mcg i.v.; infusion: 1 to 2 mcg/kg/hour, or remifentanil, bolus: 0.25 mcg/kg; infusion: 0.05 to 2 mcg/kg/hour (depending on whether remifentanil is combined with 60% N2O, 0.4 to 1.5 MAC of isoflurane, or propofol, 100 to 200 mcg/kg/minute) may be combined with isoflurane or sevoflurane or administered with an infusion of either thiopental, 1.0 to 1.5 mg/kg/hour, or propofol, 40 to 60 mcg/kg/minute, for the maintenance of anesthesia.
Thiopental may be useful as the primary anesthetic in a dose of up to 3 mg/kg/hour when the brain is "tight." The disadvantages of this approach are the potential for a slow recovery from anesthesia and the potential for systemic hypotension, which may be counteracted by volume expansion and enhancement of cardiac performance by monitoring pulmonary artery pressure and cardiac output.
Good-grade patients may be awakened in the operating room and their tracheas extubated at the end of the operation. The avoidance of coughing, straining, hypercarbia, and hypertension is essential. Hypertension in the immediate postoperative period, secondary to preexisting hypertension, pain, urinary retention from a malfunctioning catheter, and CO2 retention from residual anesthesia usually returns to normal within 12 hours. Antihypertensive drugs are administered as necessary.
If patients have received remifentanil intraoperatively, longer-acting narcotics are administered before the conclusion of the operation to confer analgesia in the immediate postoperative period.
The blood pressure of patients whose aneurysms have been wrapped rather than clipped or who have other untreated aneurysms is maintained within 20% of their normal range (120 to 160 mm Hg systolic) to avoid rupture during emergence.
Hypervolemia and relative hemodilution are maintained in the postoperative period.
Both poor preoperative status (Grade III to V) and a catastrophic intraoperative event (e.g., brain swelling, aneurysmal rupture, ligation of a feeding vessel) mandate continued intubation, sedation, and postoperative ventilatory support.
When the patient either fails to awaken or has a new neurologic deficit at the conclusion of the operation, the residual effects of sedatives, narcotics, muscle relaxants, and inhalational drugs should be reversed or dissipated, the Paco2 normalized, and other causes of depressed consciousness (e.g., hypoxia, hyponatremia) ruled out or treated. Both the persistence of diminished responsiveness and a new neurologic deficit for 2 hours after surgery require a CT scan to diagnose the presence of hematoma, hydrocephalus, pneumocephalus, infarction, or edema. An angiogram is helpful in demonstrating vascular occlusion.

VIII. Intraoperative management

Fluid administration
Patients have an SAH-induced decrease in circulating blood volume and therefore require hydration with isotonic crystalloid solution before the induction of anesthesia to preserve cerebral perfusion.
Full restoration of the intravascular volume to a state of modest hypervolemia occurs after the aneurysm has been clipped. Glucose-free crystalloid solutions are administered because both focal and global ischemic deficits can be exacerbated by hyperglycemia. Normal saline and other isotonic solutions are preferable to lactated Ringer's solution, which is hypo-osmolar to plasma and can lead to cerebral edema if the blood-brain barrier is disrupted.
Blood and blood products are indicated to maintain the hematocrit at 30% to 35%. Blood is available in the operating room when the dissection of the aneurysm commences. The use of 5% albumin can confer some rheologic advantage. The administration of >500 mL of hetastarch can, however, interfere with hemostasis and cause intracranial bleeding.
Cerebral volume reduction
The volume of the intracranial contents is reduced and brain relaxation improved to facilitate the surgical approach to the aneurysm after the opening of the dura.
Moderate hyperventilation to a Paco2 of 30 to 35 mm Hg is maintained until the dura is incised at which time the Paco2 is reduced to 25 to 30 mm Hg to decrease CBF, CBV, and brain bulk. With a preoperative increase in intracranial elastance, the Paco2 is reduced to 25 to 30 mm Hg during induction. Higher Paco2 values are necessary in patients who have vasospasm and during the period of induced hypotension.
Mannitol starts working within 10 to 15 minutes of the administration of 0.25 to 1 gm/kg, which should occur after turning the bone flap to avoid any decrease in CBV and ICP. Furosemide, 0.25 to 1.0 mg/kg, potentiates the action of mannitol and diminishes the dose.
CSF may be drained through a lumbar subarachnoid catheter inserted after the induction of anesthesia, a ventricular catheter, or intraoperative cannulation of the basal cisterns. Leakage of CSF is avoided while the cranium is closed to prevent a decrease in ICP and the concomitant rise in transmural pressure. If the ICP is elevated preoperatively, the escape of CSF from the subarachnoid puncture before craniotomy may also cause tonsillar herniation.
Temporary proximal occlusion
Controlled hypotension during microscopic dissection of the aneurysm with SNP, esmolol, or isoflurane has been advocated in the past to reduce the risk of rupture by decreasing aneurysmal wall tension and augmenting the malleability of the aneurysmal neck. Such artificial lowering of the blood pressure also decreases bleeding. Controlled hypotension can, however, compromise rCBF in patients who have SAH-induced dysautoregulation. Because patients with SAH have a higher incidence of cerebral ischemia, infarction, and postoperative neurologic deficit, neurosurgeons prefer to avoid the use of induced hypotension. An exception may be made to gain control of the parent vessel if the aneurysmal sac ruptures during surgical manipulation. Relative contraindications to induced hypotension include the presence of intracerebral hematoma, occlusive cerebrovascular disease, coronary artery disease, renal dysfunction, anemia, and fever.
Neurosurgeons now favor temporary proximal occlusion of the aneurysm's parent vessel to reduce the risk of rupture during aneurysmal manipulation. The application of temporary clips decreases the turgor of the aneurysmal sac through "local hypotension" and a reduction in blood flow.
The risks of distal ischemia and infarction, cerebral edema, and damage to the parent vessel are directly related to the duration of temporary occlusion and the integrity of the collateral circulation. The chance of developing a new neurologic deficit after temporary proximal occlusion is exacerbated by older age, poor preoperative neurologic status, and aneurysms involving the distributions of the basilar and middle cerebral arteries.
Drugs suggested for cerebral protection during temporary occlusion include mannitol, vitamin E, and dexamethasone. Thiopental, 3 to 5 mg/kg, may be administered as a bolus immediately before temporary occlusion.
Mild hypothermia to 32C to 34C has been investigated as a cerebral protective adjunct during aneurysm surgery. The preliminary results from the International Hypothermia in Aneurysm Surgery Trial, completed in 2003, failed to demonstrate any alteration in outcome for patients who were cooled before aneurysmal clip ligation.
The duration of temporary occlusion is 20 minutes or less because studies have shown a higher incidence of neurologic deficit and infarction postoperatively when the duration exceeds that limit. Some neurosurgeons even recommend removal of the temporary clip at 10 minutes of occlusion to reestablish perfusion and then reapplication after an additional dose of thiopental.
To enhance collateral circulation during temporary proximal occlusion, the patient's blood pressure is maintained in the high-normal range. This may require dopamine or phenylephrine, although patients who have coronary artery disease may be at risk for the development of cardiac ischemia.
Intraoperative aneurysmal rupture
Rupture of the aneurysm during induction of anesthesia and operation (7% before dissection, 48% during dissection, 45% during clip ligation) markedly increases mortality and morbidity because of the ischemia attendant upon the hypotension and surgical maneuvers to secure the aneurysmal neck including temporary proximal and distal occlusion. Normotension is maintained during this time to maximize collateral perfusion.
Diagnosis of rupture during or after induction is based on an abrupt increase in blood pressure with or without bradycardia. The ICP might increase as well. The TCD may demonstrate the rupture and the efficacy of management.
Therapy is designed to maintain cerebral perfusion, control ICP, and reduce bleeding by lowering the systemic pressure with thiopental or SNP after restoring the intravascular volume with crystalloid, colloid, blood, and blood products.
Intraoperative rupture of the aneurysm requires rapid surgical control. After restoration of intravascular volume, the MAP may be reduced briefly to 40 to 50 mm Hg to facilitate clip ligation of the aneurysmal neck or temporary proximal and distal occlusion of the parent vessel. Once the parent vessel is occluded, the blood pressure is increased to enhance collateral circulation.

IX. Endovascular treatment.

Interventional neuroradiologists are now able to treat aneurysms with endovascular technology as an alternative to operation, depending on the age of the patient and the size and location of the aneurysm. Most commonly, the Guglielmi detachable metal coil is threaded into the aneurysmal sac through a catheter inserted into the cerebral vascular tree through the femoral artery, cannulation of which can be extremely stimulating.
For good-grade patients who have small, anterior-circulation aneurysms, endovascular coil treatment is significantly more likely than neurosurgical treatment to result in survival free of disability 1 year after the SAH. Institutions that offer endovascular services also have lower rates of in-hospital mortality for both endovascular and surgical cases. Long-term follow-up data are necessary to determine whether endovascular or operative treatment is safer and more effective in this subgroup of patients.
The challenges of anesthesia for interventional neuroradiology include work in a location remote from the operating room, the need for communication with a team perhaps unfamiliar with the requirements of patients undergoing anesthesia for neurosurgical procedures, and the need for the anesthesiologist to have a thorough understanding of the technicalities, pace, and interventions planned by the interventional neuroradiologists. The anesthesiologist must also be familiar with the plan for anticoagulation (degree, duration, timing of reversal) and the potential intraprocedural requirement for induced hypotension, hypertension, and hypercapnia. Above all, the attention to the patient's comfort and safety, the precautions (two large-bore intravenous catheters, comfortable pillow, padding of all pressure points), and the monitoring (standard monitors plus direct intra-arterial blood pressure measurement when manipulation of blood pressure is required) for both conscious sedation and general anesthesia in the interventional suite must be identical to those indicated when patients are anesthetized in the operating room.
Anesthesia for endovascular procedures includes conscious sedation and general anesthesia. Conscious sedation offers the advantage of conferring the ability to perform intermittent neurologic examination. Some interventional neuroradiologists prefer general anesthesia because the quality of the images improves when patients are rendered motionless. Because access to the airway is limited, it is important to secure the airway before the procedure begins. Endotracheal intubation offers the combination of absolute control of ventilation, adequate conditions for intracranial manipulation, and excellent images. The choice of anesthetic drugs includes either total intravenous anesthesia or a combination of intravenous and inhalational anesthetics with or without muscle relaxation. The rapid return to consciousness at the conclusion of the procedure is important to facilitate neurologic evaluation.
Complications include both hemorrhagic and occlusive catastrophes. Differentiation between the two is important. If the problem is hemorrhagic, immediate administration of protamine to reverse the anticoagulation and maintenance of the blood pressure in the low-normal range are indicated. Occlusive problems require deliberate hypertension titrated to the neurologic examination either with or without direct thrombolysis. Other emergent interventions include volume expansion, head-up tilt, hyperventilation, diuretics, anticonvulsant drugs, hypothermia to 33C to 34C, and the infusion of thiopental to achieve encephalographic (EEG) burst suppression.

X. Hypothermic circulatory arrest for giant and vertebrobasilar aneurysms

Giant cerebral aneurysms are larger than 2.5 cm in diameter, lack an anatomic neck, and have perforating vessels traversing the aneurysmal wall. They represent 5% of all aneurysms and cause headache, visual disturbance, cranial nerve palsies, and signs and symptoms of an intracranial mass lesion.
Surgical treatment of giant aneurysms, associated with significant perioperative morbidity and mortality, uses proximal and distal temporary occlusion to collapse the aneurysm and empty the aneurysmal sac during circulatory arrest with adenosine under profound hypothermia. Circulatory arrest affords good visualization, a bloodless field, and easy aneurysmal manipulation and clip placement. Endovascular techniques may be an option only if the aneurysm is not wide necked and there is no need to debulk it.
Decreasing the cerebral metabolic rate for oxygen consumption affords cerebral protection during circulatory arrest. Barbiturates reduce the active component (maintenance of neuronal activity) of the cerebral metabolic rate and may be administered before cooling and arrest as either a single dose of 30 to 40 mg/kg over 30 minutes or as a continuous infusion. Hypothermia reduces the active and basal (maintenance of cellular integrity) components of cerebral oxygen consumption and confers protection during anoxic conditions. The tolerable period of circulatory arrest doubles for every 8C temperature reduction. At 15C to 18C, clinical circulatory arrest has been used safely for up to 60 minutes.
Brain temperature may be measured directly and correlates closely with esophageal, tympanic membrane, and nasopharyngeal thermistors but not rectal or bladder temperatures.
Hypothermia increases blood viscosity with the sludging of red blood cells. The deliberate lowering of the hematocrit through phlebotomy and simultaneous volume repletion with crystalloid avoids this complication while preserving platelet-rich autologous blood for transfusion during rewarming.
Monitors include direct arterial and CVP measurement, EEG to indicate burst suppression, somatosensory evoked potentials to measure sensory conduction to the cortex, brain stem auditory evoked potentials, and transesophageal echocardiography to assess ventricular function.
The major postoperative complications associated with hypothermic circulatory arrest are coagulopathy and intracranial hemorrhage. Risks may be reduced by the following:
The surgeon dissects the aneurysm and achieves hemostasis before the initiation of hypothermic circulatory arrest.
The activated clotting time (ACT) is maintained between 400 and 450 seconds after heparinization. After rewarming, protamine is used to reverse heparinization to achieve an ACT of 100 to 150 seconds.
Previously phlebotomized blood is transfused, and additional blood products (fresh frozen plasma, cryoprecipitate, platelets) are given as needed.
Hemostasis is achieved before dural closure.


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