Anesthesia for intracranial neurovascular procedures in adults

INTRODUCTION — Intracranial vascular lesions are relatively common abnormalities that may require elective or emergent intervention. This topic will discuss anesthetic management for craniotomy for unruptured and ruptured intracranial aneurysm clipping, resection of arteriovenous malformations, extracranial-to-intracranial bypass procedures, and interventional radiologic treatment of intracranial neurovascular lesions.

Epidemiology, evaluation, and management of subarachnoid hemorrhage (SAH) and the diagnosis and management of unruptured aneurysms and brain arteriovenous malformations (AVMs) are discussed separately. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis" and "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis" and "Unruptured intracranial aneurysms" and "Brain arteriovenous malformations" and "Treatment of cerebral aneurysms".)

INTRACRANIAL ANEURYSMS — Intracranial aneurysms may be treated with clipping via craniotomy, endovascular intervention, or with a combination of surgical and endovascular techniques. (See "Treatment of cerebral aneurysms".)

Anesthesia for craniotomy is discussed more fully separately. (See "Anesthesia for craniotomy in adults".)

The anesthetic concerns specific to craniotomy for aneurysm clipping are discussed here.

Planning the anesthetic — General anesthesia is performed for all intracranial vascular procedures. The plan for management of anesthesia should be discussed with the surgeon, including the following:

●Brain relaxation and management of intracranial pressure (ICP) including cerebral spinal fluid (CSF) drainage if external ventricular drain is in place.

Brain relaxation should be considered carefully because of potential risks in the setting of cerebral aneurysm. Use of osmotic agents (eg, mannitol or hypertonic saline) or aggressive drainage of CSF prior to dural opening may acutely decrease ICP, leading to an increased pressure gradient across the wall of the aneurysm and risk of rupture (transmural pressure [TMP] = mean arterial pressure – ICP).

In addition, excessive hyperventilation, which is often a component of brain relaxation, can result in cerebral ischemia. (See "Anesthesia for craniotomy in adults", section on 'Planned brain relaxation' and "Anesthesia for craniotomy in adults", section on 'Ventilation'.)

●Blood pressure (BP) goals. (See 'Blood pressure goals' below.)

●Plan for temporary aneurysm clipping. (See 'Temporary clipping' below.)

●Location of the aneurysm and patient positioning for surgery.

●Expected degree of surgical difficulty.

●The plan for management of intra-procedural rupture. (See 'Intraoperative aneurysm rupture' below and 'Adenosine-induced temporary flow arrest' below.)

●The use of neuromonitoring. (See "Neuromonitoring in surgery and anesthesia".)

Anesthetic management for craniotomy for aneurysm

Preparation for anesthesia

Preoperative evaluation — In addition to the usual preanesthesia evaluation, the neurologic status and physiologic effects of intracranial hemorrhage, ongoing treatment, and laboratory values may affect anesthetic management and should be reviewed:

●Neurologic status – Aneurysmal rupture usually results in subarachnoid hemorrhage (SAH), which can cause neurologic abnormalities ranging from mildly altered consciousness to coma. The patient may be intubated and ventilated for airway protection and ventilatory support. Neurologic evaluation and grading of hemorrhage severity are discussed separately. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis", section on 'Evaluation and diagnosis'.)

●Intracranial hypertension – Acute hydrocephalus and increased ICP are common after SAH. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Elevated intracranial pressure'.)

Management of anesthesia for patients with intracranial hypertension is discussed separately. (See "Anesthesia for craniotomy in adults", section on 'General concerns'.)

●Cardiac abnormalities – Various cardiac abnormalities may occur, including ischemia, arrhythmias, left ventricular dysfunction, and pulmonary edema. The preoperative electrocardiogram (ECG), echocardiogram if performed, and cardiac biomarkers should be reviewed. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Cardiopulmonary complications'.)

●Seizures – Acute seizures may occur with SAH. Antiepileptic drugs should be continued intraoperatively. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Seizures'.)

●Electrolyte abnormalities – Hyponatremia is relatively common after SAH, often due to inappropriate secretion of antidiuretic hormone (SIADH), particularly in patients with vasospasm. In this setting, hyponatremia is usually treated with hypertonic saline rather than fluid restriction, as fluid restriction may increase the risk of vasospasm related ischemic injury. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Hyponatremia'.)

●Vasospasm – Symptomatic vasospasm occurs in 20 to 30 percent of patients with SAH and may lead to delayed cerebral ischemia. Vasospasm rarely occurs immediately after SAH and typically occurs after day 3, reaching a peak at days 7 to 8 and continuing up to 21 days. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Vasospasm and delayed cerebral ischemia'.)

Hypovolemia may increase the risk of cerebral ischemia in the setting of vasospasm. The goal for fluid management for patients with vasospasm is euvolemia.

●Anemia – Anemia is common after SAH [1]; most studies suggest that anemia is associated with worse outcomes [2,3], though a goal hemoglobin for transfusion has not been defined for these patients. We aim for a hemoglobin of ≥8 g/dL, as outcomes appear to be optimal with a target hemoglobin of 8 to 11.5 g/dL [3,4]. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Acute care'.)

●Nimodipine therapy – Nimodipine (60 mg every four hours by mouth or nasogastric tube) is administered to all patients with SAH to improve outcomes and should be continued intraoperatively. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Nimodipine'.)

Vasoactive medications — A variety of vasoactive medications should be immediately available during craniotomy for aneurysm, including:

●Adenosine for temporary circulatory arrest to facilitate aneurysm clipping, or for management of intraprocedural aneurysm rupture

●Esmolol

●Labetalol

●Nicardipine

●Phenylephrine infusion, particularly for patients within the vasospasm period (ie, three to eight days)

Venodilators such as sodium nitroprusside are rarely used due to concerns about increasing intracerebral venous volume and ICP. (See "Anesthesia for craniotomy in adults", section on 'Vasoactive drugs'.)

Monitoring — An intra-arterial catheter should, if possible, be placed prior to induction of anesthesia to allow continuous BP monitoring and blood sampling. For elective aneurysm surgery, an arterial catheter may be deferred until post-induction for patient comfort or preference if the surgical and neuro-anesthesia team feel that there is low risk of aneurysm rupture during induction and intubation. Standard anesthesia monitors should also be applied (ie, ECG, pulse oximeter, temperature, end-tidal carbon dioxide [ETCO₂]). (See "Anesthesia for craniotomy in adults", section on 'Monitoring'.)

Patients may have other neurocritical care monitoring devices in place, such as an external ventricular drain (EVD), a jugular saturation (SjVO₂) catheter, or a brain tissue oxygen intraparenchymal probe. When possible, such monitoring should be continued throughout the perioperative period. (See "Anesthesia for patients with acute traumatic brain injury", section on 'Monitoring'.)

Neurophysiologic monitoring (ie, electroencephalography [EEG] and/or evoked potential monitoring) may be used and will affect the choice and timing of anesthetic drugs and neuromuscular blocking agents (NMBAs). (See "Neuromonitoring in surgery and anesthesia".)

Venous access — We place two intravenous (IV) catheters for intracranial aneurysm procedures, including at least one large-bore catheter (≥16 gauge).

Blood pressure goals — The optimal therapy for hypertension and goals for BP in patients with aneurysms are unclear. In patients with ruptured aneurysms, systemic hypertension may be a normal hemodynamic response, which maintains cerebral perfusion in the setting of increased ICP. One study showed a lack of association between variable EtCO₂ and BP values and neurologic outcome in patients with SAH [5]. However, it is likely, that participating anesthesiologists sought to maintain reasonable EtCO₂ and BP goals throughout endovascular coiling or clipping of the cerebral aneurysm in trial patients .

Our usual approach to BP management during induction and maintenance of anesthesia in these patients is as follows:

●Unruptured aneurysms and ruptured aneurysms with suspected normal ICP (ie, normal neurologic examination) – Aim for systolic BP ≤ the patient's normal systolic BP, maximum 140 mmHg, and mean arterial pressure (MAP) ≥60 mmHg.

●Ruptured aneurysms with suspected or known intracranial hypertension – Passive hypertension should not be treated. Hypertension in response to noxious stimulation and iatrogenic hypertension due to vasopressors should be avoided. If an ICP monitor is in place, cerebral perfusion pressure (CPP = MAP - ICP) ≥50 to 60 mmHg should be maintained.

Premedication — Anxiolytic premedication (eg, midazolam 1 to 2 mg IV, titrated to effect) is usually appropriate for elective aneurysm procedures. Premedication for patients with SAH should be tailored to the patient's mental status.

Induction of anesthesia — IV induction of anesthesia is usually performed for adult patients. The goal for induction for these procedures is to maintain hemodynamic stability. Drugs and doses should be selected to avoid hypertension and the risk of aneurysmal rupture, while avoiding hypotension, to maintain a stable CPP, particularly in patients with high-grade SAH who may not have normal autoregulatory capacity.

The choice of induction agents, adjuvant drugs for induction, and airway management strategies are discussed separately. (See "Anesthesia for craniotomy in adults", section on 'Induction of anesthesia' and "Induction of general anesthesia: Overview".)

Maintenance of anesthesia — A variety of anesthetic regimens may be used for craniotomy for aneurysm surgery, depending on the degree of preexisting intracranial hypertension, the need for brain relaxation during surgery, the use of neuromonitoring, and the patient's medical comorbidities. At the authors' institution, where neuromonitoring is routinely used for these procedures, the usual anesthetic includes a propofol infusion in conjunction with low-dose volatile anesthetics. (See "Neuromonitoring in surgery and anesthesia", section on 'Balanced anesthetic approach'.)

Maintenance of anesthesia for craniotomy is discussed in detail separately. Concerns specific to aneurysm surgery are discussed here. (See "Anesthesia for craniotomy in adults", section on 'Maintenance of anesthesia' and "Anesthesia for patients with acute traumatic brain injury", section on 'Choice of anesthetic agents'.)

Hemodynamic management during stages of surgery — BP management during aneurysm surgery must be dynamic, must respond to the surgical conditions, and requires close communication with the surgeon. Goals for anesthetic management and BP control for various stages of aneurysm surgery are as follows:

Skull pinning and incision — Skull pinning is a brief but highly painful stimulus, comparable to incision or laryngoscopy, that can result in sudden hypertension and tachycardia. Various strategies may be used to prevent a hemodynamic response to skull pinning, including IV medication (eg, lidocaine 1 mg/kg, fentanyl 100 mcg, propofol 20 to 50 mg, esmolol 0.5 to 1 mg/kg, doses adjusted for patient factors), local anesthetic infiltration at pin sites, and scalp blocks.

Skin incision and dural opening are other stimulating portions of surgery. (See "Anesthesia for craniotomy in adults", section on 'Skull pinning'.)

Dissection — A lighter plane of anesthesia may be used during dissection because brain tissue has no pain receptors. However, patient and iatrogenic movement must be strictly avoided during dissection of the aneurysm itself. (See 'Patient immobility' below.)

During delicate stages of dissection, the surgeon may request a reduced BP, though profound hypotension should be avoided, particularly in patients who have had an SAH. Induced hypotension has generally been replaced by the use of temporary clips placed on feeding vessels to facilitate manipulation of the aneurysm.

Temporary clipping — On occasion, the surgeon applies a temporary clip on a feeding artery proximal to the aneurysm to facilitate dissection. Prior to clip placement, decreased BP may help the surgeon manipulate the artery, though profound hypotension should be avoided. Specific, individualized goals should be discussed with the surgeon.

The temporary clip creates an area of focal ischemia, and neurologic outcomes are worse with prolonged occlusion times [6]. Neuromonitoring (eg, somatosensory evoked potential [SSEP], EEG) can be used to assess the adequacy of blood flow; when changes suggest ischemia, or during longer clip times, an increase in MAP of 10 to 20 percent may be appropriate. The authors routinely use neuromonitoring with SSEPs during temporary clipping, particularly for internal carotid artery or middle cerebral artery territory aneurysms. SSEPs are generally used rather than motor evoked potentials to allow for the use of neuromuscular blockade. Motor evoked potentials may be added for aneurysms placing certain vascular distributions at risk, including the internal capsule [7] . (See "Neuromonitoring in surgery and anesthesia", section on 'Evoked potentials'.)

Induced hypothermia and neuroprotective drugs have not been shown to be beneficial during temporary clipping. A post hoc analysis of the Intraoperative Hypothermia for Aneurysm Surgery Trial (IHAST) study, which was randomized for hypothermia but not for neuroprotective medications, found that anesthetic neuroprotective drugs and induced hypothermia (33.3 ± 0.8 degrees C) were not associated with improved outcomes in patients who had temporary clips applied [8]. (See 'Temperature management' below.)

Adenosine-induced temporary flow arrest — Adenosine may be administered to induce temporary bradycardia or cardiac arrest to reduce or suspend flow through the aneurysm. This technique can be used as an alternative to temporary clipping in selected patients, or in the event of aneurysmal rupture [9-13]. Adenosine should not be administered to patients with severe reactive airway disease, severe coronary artery disease, or cardiac conduction abnormalities.

The possible need for adenosine should be discussed in advance with the neurosurgeon. Transcutaneous pacing pads should be considered for possible temporary pacing or cardioversion for patients in whom adenosine is either planned or likely based on the risk for aneurysmal rupture. Optimal dosing for adenosine in this setting is unclear, and the dose response may vary. Escalating doses have often been administered, starting with an initial dose of 6 to 12 mg IV and adding increments of 6 mg. In one case series including 27 patients, adenosine doses between 0.24 and 0.42 mg/kg IV resulted in 30 to 60 seconds of asystole or hypotension [11]. If there is no time for dose escalation (eg, aneurysmal rupture), we administer an initial dose of adenosine 0.4 to 0.6 mg/kg IV, expecting asystole for 20 to 40 seconds, though it may last 60 seconds or more. If repeat adenosine induced flow arrest is required, it should be delayed until the patient returns to sinus rhythm and pre-adenosine BP.

In carefully selected patients, adenosine-induced flow arrest appears to be safe, with few complications. However, self-limited post-adenosine arrhythmias and ST segment depressions have rarely been reported [11,12,14].

Post-aneurysm clip — After the permanent clip is placed in the final position on the aneurysm, normal BP (ie, systolic BP <140 mmHg) is the goal. The surgeon may, on occasion, request a brief period of induced hypertension to confirm that there is no flow distal to the clip with increased BP.

Glycemic management — Hyperglycemia has been associated with a poor outcome after SAH. While both hyper- and hypoglycemia are associated with worse outcome after SAH, the optimal goal for blood glucose is unclear, and tight glycemic control in these patients is controversial. We monitor blood glucose during surgery, aim for a blood glucose between 80 and 180 mg/dL, and treat blood glucose >180 mg/dL with an insulin infusion. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Acute care'.)

Temperature management — Historically, mild hypothermia (33 to 35°C) was induced during aneurysm surgery in an attempt to reduce ischemic injury. However, a multicenter, randomized trial of patients who underwent aneurysm clipping after SAH, the IHAST, found no benefit from hypothermia (target temperature 33.5°C) compared with normothermia [15]. Induced hypothermia is now rarely used for these procedures, and consensus statements recommend targeted temperature management, with a goal of 36.5 to 37.5°C [16].

Fever worsens outcome after stroke and should be avoided and aggressively treated. We aim for a temperature from 36.5 to 37.5°C. (See "Anesthesia for patients with acute traumatic brain injury", section on 'Temperature management'.)

Patient immobility — Aneurysm dissection and clipping are delicate procedures performed under the operating microscope. Patient movement, and iatrogenic movement (eg, moving equipment, adjusting monitors) must be avoided during microdissection. We administer NMBAs to achieve complete paralysis unless neuromonitoring prohibits their use. An infusion of potent opiate may be used to achieve immobility in cases where NMBAs cannot be used.

Indocyanine green — The surgeon may ask for IV administration of indocyanine green, 25 mg, rapid IV injection, to visualize perfusion of the brain after the aneurysm is clipped. Indocyanine may cause a brief, artifactual reduction in the oxygen saturation, commonly to low 90s percent. Rarely, indocyanine green causes anaphylaxis.

Intraoperative aneurysm rupture — Intraoperative aneurysm rupture (IAR) may occur at any time from induction of anesthesia until the aneurysm is clipped, though it occurs most commonly during aneurysm dissection and clipping [17]. Neurologic outcomes are worse for patients who sustain IAR, and are particularly poor if IAR occurs prior to aneurysm dissection [18,19]. Risk factors for IAR unrelated to dissection are multifactorial and incompletely understood. Patient risk factors include characteristics of the aneurysm, poorly controlled hypertension [20,21], coronary artery disease, and chronic obstructive pulmonary disease (COPD) [22].

An increase in the aneurysm transmural pressure (TMP) is thought to increase the risk of rupture and should be avoided. An increase in TMP may be caused by hypertensive episodes (eg, during intubation, skull pinning, positioning, skin incision, dural opening, extubation) or by reductions in ICP (eg, rapid administration of mannitol, hyperventilation prior to dural opening or excessive CSF drainage via an EVD). (See 'Hemodynamic management during stages of surgery' above.)

Intraoperative rupture of the aneurysm is an emergency that requires a rapid, coordinated response. Options for management depend on when the rupture occurs and whether or not the aneurysm is exposed. Our strategy for anesthetic management after IAR is as follows:

Rupture with aneurysm exposed — The goals are to rapidly create a bloodless field to facilitate clipping and to protect the brain. The patient may then need volume resuscitation.

●Induce hypotension – Administer esmolol 10 to 20 mg IV as needed to achieve MAP of 50 to 60 mmHg to reduce bleeding and facilitate clip placement.

●Induce temporary flow arrest – In coordination with the surgeon, administer adenosine 0.4 to 0.6 mg/kg to achieve transient circulatory arrest (may repeat for re-rupture). (See 'Adenosine-induced temporary flow arrest' above.)

●Reduce cerebral metabolic rate – Administer propofol 20 to 60 mg IV. If using a propofol infusion for maintenance of anesthesia, increase the propofol rate to 125 to 200 mcg/kg/minute IV. If EEG monitoring is being used, propofol dosing can be titrated to achieve burst suppression.

●Volume resuscitate – After the clip is placed, administer IV fluid and blood products as required, aiming for euvolemia and hemoglobin ≥8 g/dL.

●Lighten anesthesia – After secure clipping, reduce propofol administration to discontinue EEG burst suppression.

Rupture prior to aneurysm exposure — In anesthetized patients, aneurysm rupture may be difficult to diagnose. IAR is usually heralded by an unexplained increase in BP and/or ICP [18,19]. If rupture is suspected, the team should rapidly decide whether to proceed with imaging, angiography, or proceed with surgery. The patient should be supported as follows:

●Optimize CPP – Allow permissive hypertension. Aim for a CPP 50 to 70 mmHg if an ICP monitor is in place or MAP >90 mmHg without ICP monitoring; administer vasopressors as necessary to increase BP. We prefer to use a titrated norepinephrine infusion in this setting.

●Manage intracranial hypertension (see "Anesthesia for craniotomy in adults", section on 'Intraoperative cerebral edema'):

•Optimize oxygenation and ventilation – Control ventilation with goals of PaO₂ >80 mmHg and PaCO₂ 32 to 38 mmHg.

•Administer osmotherapy – Administer mannitol 0.25 to 1 g/kg and/or hypertonic saline (ie, 100 mL of 3% sodium chloride [NaCl] or 30 mL of 23.4% NaCl), repeated if necessary, aiming for a serum sodium of ≤155 mmol/L or serum osmolality <320 mmol/L.

•Improve venous drainage – Elevate head to 15-degree head-up, neutral position. Tape rather than tie the endotracheal tube (ETT). ETT should be taped rather than tied so as not to contribute to occlusion of venous drainage from the cranium.

Ventriculostomy drainage of CSF may worsen bleeding as the transmural pressure gradient suddenly increases; beware of abruptly opening the ventriculostomy if one is in place as this can increase transmural gradient and, subsequently, the extent of bleeding.

●Induce neuroprotection – Administer propofol 20 to 60 mg IV. If using a propofol infusion for maintenance of anesthesia, increase the propofol rate to >125 mcg/kg/minute IV. If EEG monitoring is being used, propofol dosing can be titrated to achieve burst suppression. Whilst there are no data in support of burst suppression in this context, it can be used as a measurable endpoint of minimal intracerebral metabolism and hence the suggestion of neuroprotection.

Emergence and postoperative care — As usual, the goals for emergence from craniotomy include a smooth emergence, avoiding hypertension, coughing, and straining. Ideally, a rapid emergence should permit neurologic examination prior to leaving the operating room. Strategies for emergence and assessment of delayed emergence after craniotomy are discussed separately. (See "Anesthesia for craniotomy in adults", section on 'Emergence from anesthesia'.)

Patients should be admitted to the intensive care unit (ICU) after craniotomy for aneurysm clipping, to allow serial neurologic examination, continuous BP monitoring and control, and to facilitate treatment of pain and postoperative nausea and vomiting (PONV).

Endovascular therapy for intracranial aneurysm — Both ruptured and unruptured intracranial aneurysms may be amenable to endovascular treatment with coil embolism or a variety of newer techniques. (See "Treatment of cerebral aneurysms", section on 'Endovascular therapy'.)

Although monitored anesthesia care (MAC) may be suitable for diagnostic angiography to delineate aneurysmal anatomy, we prefer to administer general anesthesia with paralysis rather than MAC for endovascular aneurysm procedures. These are delicate procedures, and any patient movement can result in vessel rupture or dissection, aneurysm rupture, or displacement of coils into brain parenchyma.

Preparation for anesthesia — Endovascular procedures may be performed in an interventional radiology suite rather than an operating room. In addition to the usual preparation for anesthesia, the following concerns apply to these procedures:

●Before the procedure, the layout of the procedure room, position of the anesthesia machine for induction and for the procedure, expected movement of the fluoroscopy machine during the procedure, and availability of protective lead aprons and screen should all be determined. After induction and prior to draping, we move the fluoroscopy machine through its full range of motion, checking that all lines and tubes are out of the way.

●Monitors and the breathing circuit must be secured away from the radiograph field to avoid interference with images.

●The anesthesia machine may be positioned to one side of the patient without access to the airway; extensions may be required on IV tubing, arterial line pressure tubing, and the breathing circuit.

●In addition to the usual drugs that are prepared for anesthesia, phenylephrine infusion, nicardipine, norepinephrine, and vasopressin should be immediately available. Protamine should also be immediately available for heparin reversal in the event of aneurysm rupture.

●Patients on dual antiplatelet therapy should have platelets prepared in case of hemorrhage.

Induction and maintenance for endovascular therapy — The basic principles for anesthesia management are the same as they are for craniotomy for aneurysm, including avoidance of hypertension while maintaining cerebral perfusion. (See 'Anesthetic management for craniotomy for aneurysm' above.)

Concerns specific to endovascular procedures used to treat intracranial aneurysms include the following:

●Intra-arterial BP monitoring is required for these procedures. The femoral sheath placed for the procedure may be used for BP monitoring in lieu of a peripheral arterial catheter.

●Endotracheal intubation is often the most stimulating part of the case. Hypertension should be attenuated by deepening anesthesia with propofol (20 to 50 mg IV), lidocaine (1 mg/kg IV), or fentanyl (100 mcg IV), or by administering esmolol (0.5 to 1 mg/kg IV) prior to intubation.

●Patients are frequently heparinized for these procedures. The goal range for activated clotting time (ACT) and the procedure for performing ACTs should be established with the interventionist.

●Oral administration of antiplatelet medication may be required intraoperatively. An orogastric tube should be placed after intubation for administration of aspirin or clopidogrel.

●Aneurysmal rupture is uncommon during endovascular procedures but is most likely with deployment of the initial coil [23]. In the event of rupture, heparinization should be reversed with protamine. Patients should be managed as described above. (See 'Rupture prior to aneurysm exposure' above.)

●Downstream thromboembolism may complicate endovascular coiling and is detected by angiography.

If thromboembolism occurs during coiling, abciximab, a glycoprotein IIb/IIIa inhibitor, may be administered (bolus dose of 0.25 mg/kg IV, followed by an infusion of 0.125 mcg/kg/minute to a maximum dose of 10 mcg/minute). Some recommend inducing hypertension after the aneurysm is secured, as treatment for thromboembolism and resultant cerebral ischemia.

Anesthesia for vasospasm treatment — Endovascular therapy (ie, angioplasty and/or intra-arterial vasodilator therapy) may be used, in addition to medical therapy, to treat symptomatic vasospasm after SAH. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Vasospasm and delayed cerebral ischemia'.)

Patients who undergo intra-arterial therapy are critically ill and suffering from cerebral ischemia. They may require repeated procedures over days or weeks to treat vasospasm. Anesthetic concerns, in addition to those that relate to the systemic sequelae of SAH, include the following:

●These patients are intubated and mechanically ventilated, with intra-arterial and central venous catheters (CVCs) and often ICP monitoring and other advanced monitoring in place. They are often receiving high doses of vasopressors; transport between the ICU and the interventional radiology suite requires continuous monitoring. (See "Transport of surgical patients", section on 'Considerations for critically ill patients'.)

●The goal BP should be discussed before and during the procedure with the surgeon or interventionist. (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Vasospasm and delayed cerebral ischemia'.)

●Endovascular treatment may include angioplasty of larger vasospastic cerebral arteries and/or cerebral intra-arterial infusion of a variety of vasodilators (eg, nicardipine). The anesthesia clinician should be informed before vasodilator injection, as BP may be exquisitely sensitive to these small doses of vasodilator. Hypotension should be anticipated and treated immediately. High doses of vasopressors may be required to support BP after administration of intra-arterial vasodilators.

BRAIN ARTERIOVENOUS MALFORMATIONS — Brain arteriovenous malformations (AVMs) are rare congenital vascular malformation with potential to cause intracranial hemorrhage and epilepsy, generally presenting in young adulthood. Patients with brain AVMs may require anesthesia for angiography with or without embolization, surgical excision, or stereotactic radiosurgery (ie, gamma knife). Epidemiology, pathophysiology, diagnosis, and treatment decisions are discussed separately. (See "Brain arteriovenous malformations".)

Brain AVMs are often treated with combined therapy, including endovascular procedures designed to occlude feeder arteries and reduce the risk of intraoperative hemorrhage, followed by surgical resection of the lesion. Anesthetic management for these procedures is similar to management for cerebral aneurysm procedures. (See 'Anesthetic management for craniotomy for aneurysm' above.)

Concerns specific to brain AVMs include the following:

Hemorrhage — The expected degree of technical difficulty and potential for hemorrhage should be discussed with the surgeon preoperatively. Most patients with high-risk AVMs undergo serial preoperative endovascular intervention to minimize the risk of intraoperative hemorrhage. Nonetheless, preparation should be made for the possibility of significant, rapid hemorrhage, including large-bore IV access and blood type and cross. For high-risk cases, blood products should be in the operating room ready to transfuse. (See 'Venous access' above.)

The risk of intraoperative "rupture" is much less with a brain AVM than it is with a cerebral aneurysm. However, 20 to 25 percent of brain AVMs include aneurysms, and hypertension should be meticulously avoided. (See "Brain arteriovenous malformations", section on 'Pathogenesis and pathology'.)

Normal perfusion pressure breakthrough — After removal of an AVM from the cerebral circulation, patients are at risk for normal perfusion pressure breakthrough (NPPB), a poorly understood phenomenon that may include rapidly developing cerebral edema and hemorrhage, possibly as a result of penumbral sensitivity to increasing perfusion pressures as the AVM is resected. Anesthetic management to reduce the risk and complications of NPPB is controversial. While historical recommendations include mild volume restriction (or diuresis) and strict BP control, including BP reduction postoperatively [24], more recently, maintenance of normotension has been advocated [25].

In the event of postoperative hemorrhage, residual AVM should always be ruled out prior to invoking NPPB as a mechanism for hemorrhage.

Embolization for brain arteriovenous malformation — There are several unique considerations for patients undergoing endovascular embolization of an AVM. There are reports of transient desaturation following injection of ethylene vinyl alcohol polymer (ie, Onyx), a common embolizing agent [26]. There is also a low, but present, risk of the embolizing agent migrating through the AVM with possible occlusion of the distal venous circulation or entry into the right heart [27] and pulmonary circulation [28], with resultant pulmonary hypertension. The interventionalist may request hypotension (or adenosine induced asystole) during polymer injection to minimize passage into draining veins and the systemic circulation [29]. (See 'Adenosine-induced temporary flow arrest' above.)

Finally, it is interesting to note that patients undergoing Onyx embolization may have a distinctive smell following the procedure, which may persist into the next day [30].

EXTRACRANIAL-INTRACRANIAL BYPASS — Extracranial-intracranial (EC-IC) bypass involves the creation of an anastomosis between an extracranial artery and the middle cerebral artery (MCA) to improve MCA-distribution flow. EC-IC bypass is usually performed for patients with intracerebral atherosclerotic disease, moyamoya disease, or complex intracerebral aneurysms requiring aneurysm trapping (ie, permanent feeding and outflow arterial clipping) that results in permanent occlusion of the intracranial internal carotid artery. (See "Moyamoya disease and moyamoya syndrome: Treatment and prognosis".)

Extracranial-intracranial bypass procedures — A variety of EC-IC bypass procedures have been described. A direct anastomosis of either the superficial temporal or middle meningeal artery to a branch of the MCA can be considered in some patients, especially those requiring acute internal carotid artery occlusion for aneurysm trapping. However, given that the extracranial and intracranial vessels often have a small diameter (making direct anastomosis technically challenging), other indirect bypass procedures can be considered. Indirect procedures include encephalomyosynangiosis, where a branch of the superficial temporal artery is dissected along with its surrounding muscle and secured directly to the brain surface. In time, and in a brain with chronic hypoperfusion as is common in patients with Moyamoya disease, collateral vessels develop between the superficial temporal artery and branches of the MCA.

Anesthesia for extracranial-intracranial bypass — EC-IC bypass procedures require craniotomy, as a skull defect is produced to allow for the superficial temporal artery to enter the cranial vault. Anesthetic management for craniotomy is discussed separately. (See "Anesthesia for craniotomy in adults".)

Anesthetic considerations specific to patients having EC-IC bypass are discussed here.

●Blood pressure (BP) management – A primary goal for anesthesia for these procedures is to avoid cerebral ischemia or infarction by maintaining adequate cerebral perfusion pressure (CPP). Patients with intracranial vascular stenosis or Moyamoya disease are exquisitely sensitive to hypotension as it may precipitate cerebral ischemia. Mean arterial pressure (MAP) should be maintained at or above awake level at all times. An arterial catheter placed prior to induction of anesthesia is recommended to monitor for hypotension with induction of anesthesia. Hypovolemia should be avoided as it can contribute to hypotension.

●Ventilation – Hyperventilation should be avoided, as should hypoventilation because the resulting cerebral vasodilation can potentially lead to a steal physiology in the cerebral circulation, diverting blood flow away from ischemic vessels. Therefore, documented normocapnia should be maintained throughout the procedure.

●Neuromonitoring – Intraoperative electroencephalography (EEG) or evoked potential monitoring can be considered to detect cerebral hypoperfusion. If ischemia is detected, both surgeon and anesthesiologist should be notified. The anesthesiologist can increase BP, confirm normocapnia, ensure adequate arterial oxygen content, and treat anemia if present in an effort to try to improve cerebral oxygen delivery.

●Temporary arterial occlusion – In patients having direct EC-IC bypass, temporary arterial occlusion is often required for vessel anastomosis. If temporary clipping is planned, BP should be increased by 10 to 20 percent in an attempt to improve collateral blood flow while vessels are clamped. The use of anesthetics for neuroprotection during temporary clipping is discussed separately. (See 'Temporary clipping' above.)

SUMMARY AND RECOMMENDATIONS

●Intracranial aneurysm – Patients with aneurysmal subarachnoid hemorrhage (SAH) may exhibit physiologic derangements that affect anesthetic management, including neurologic dysfunction, cardiac abnormalities, electrolyte disturbances, anemia, and seizures. (See 'Preoperative evaluation' above.)

•Hemodynamic management – A primary goal for anesthesia for these procedures is hemodynamic stability, avoiding hypertension and aneurysmal rupture while maintaining cerebral perfusion. An arterial catheter should be placed prior to induction of anesthesia to allow continuous blood pressure (BP) monitoring. (See 'Monitoring' above.)

-Unruptured aneurysms and ruptured aneurysm with suspected normal intracranial pressure (ICP) (ie, normal neurologic examination) – Aim for systolic BP ≤ the patient's normal systolic BP, maximum 140 mmHg, and mean arterial pressure (MAP) ≥60 mmHg.

-Ruptured aneurysm with suspected or known intracranial hypertension – Passive hypertension should not be treated. Hypertension in response to noxious stimulation and iatrogenic hypertension due to vasopressors should be avoided, and cerebral perfusion pressure (CPP) ≥50 to 60 mmHg should be maintained. (See 'Blood pressure goals' above.)

•Temporary clipping – A temporary clip may be placed on a feeding vessel to facilitate dissection and permanent clipping. During longer clip times, or if neuromonitoring shows ischemic changes during temporary clipping, increasing MAP by 10 to 20 percent may be appropriate.(See 'Temporary clipping' above.)

Adenosine may be administered to induce temporary bradycardia or cardiac arrest to reduce or suspend flow through the aneurysm as an alternative to temporary clipping, or in the event of intraoperative aneurysm rupture. (See 'Adenosine-induced temporary flow arrest' above.)  

Induced hypothermia has not been shown to improve outcomes for patients who undergo aneurysm clipping. (See 'Temporary clipping' above.)

•Intraoperative aneurysm rupture – Intraoperative aneurysm rupture occurs most commonly during aneurysm dissection and clipping. Goals for management are to rapidly create a bloodless field to facilitate clipping, and to protect the brain. Our strategy is as follows (see 'Rupture with aneurysm exposed' above):

-Induce hypotension – Administer esmolol 10 to 20 mg intravenously (IV) as needed to achieve MAP of 50 to 60 mmHg.

-Induce temporary flow arrest – If necessary, administer adenosine 0.4 to 0.6 mg/kg IV, expecting 20 to 40 seconds of asystole or bradycardia. (See 'Adenosine-induced temporary flow arrest' above.)

-Reduce cerebral metabolic rate – Administer propofol 20 to 60 mg IV. If using a propofol infusion for maintenance of anesthesia, increase the propofol rate to >125 mcg/kg/minute IV. If electroencephalography (EEG) monitoring is being used, propofol dosing can be titrated to achieve burst suppression.

-Volume resuscitate – After aneurysm clipping, administer IV fluid and blood products to achieve euvolemia and hemoglobin ≥8 gm/dL.

If aneurysm rupture occurs prior to exposure of the aneurysm in an anesthetized patient, signs may include unexplained hypertension and/or ICP and a drop in heart rate. Management may include brain imaging, angiography, or continuation with surgery. Anesthetic management should include the following:

-Optimize CPP – Allow permissive hypertension. Aim for a CPP 50 to 70 mmHg if ICP monitor is in place, or MAP >90 mmHg without ICP monitoring; administer vasopressors as necessary to increase BP.

-Manage intracranial hypertension – Optimize ventilation, administer osmotherapy, and optimize venous drainage.

-Reduce cerebral metabolic rate – Administer propofol 20 to 60 mg IV to achieve EEG burst suppression. If using total IV anesthesia (TIVA), increase propofol rate as able to sustain burst suppression (typically >125 mcg/kg/minute IV).

●Brain arteriovenous malformations (AVMs) – AVMs are often treated with combined therapy, including endovascular procedures designed to occlude feeding arteries and reduce the risk of intraoperative hemorrhage, followed by surgical resection of the lesion. During and after resection, these patients are at risk for hemorrhage and normal perfusion pressure breakthrough (NPPB). (See 'Brain arteriovenous malformations' above.)

●Endovascular therapy – Goals for anesthesia for endovascular therapy for aneurysms and brain AVMs are similar to the goals for open procedures. (See 'Endovascular therapy for intracranial aneurysm' above and 'Embolization for brain arteriovenous malformation' above.)

●Extracranial-intracranial (EC-IC) bypass – A primary goal for anesthesia for these procedures is to avoid cerebral ischemia or infarction by maintaining adequate CPP. MAP should be maintained at or above awake level at all times, and hyperventilation should be avoided. (See 'Anesthesia for extracranial-intracranial bypass' above.)

Management during temporary clipping for these procedures is similar to management during aneurysm clipping. (See 'Temporary clipping' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Laurel E Moore, MD, who contributed to earlier versions of this topic review.