Respiratory

Respiratory complications (e.g., neurogenic pulmonary edema [up to 23%], pneumonia, ARDS, PE) are the most common nonneurologic causes of death following SAH. Pulmonary aspiration may have occurred as the result of a neurological deficit from an intracranial hemorrhage.

Tests: As indicated from H&P. Elevated cTnI may predict pulmonary complications.

Cardiovascular

Generally, these patients do not have other cardiovascular diseases, although intracerebral aneurysms occur more commonly in patients with certain congenital disorders, such as polycystic disease of the kidneys, coarctation of the aorta, fibromuscular hyperplasia, and Marfan or Ehlers-Danlos syndromes. Patients who have had a recent intracranial hemorrhage (ICH) are prone to develop systemic HTN, hypovolemia, ↓ Mg⁺⁺ and ECG abnormalities. The HTN is thought to be due to autonomic hyperactivity and is generally treated with antihypertensive medication, which should be continued up to the time of anesthesia and surgery. ECG abnormalities occur in many patients following ICH and may represent subendocardial injury 2° catecholamine release from intracardiac nerve terminals (contraction band injury). Dysrhythmias (most commonly PVCs) occur in 30-80% of patients, and ischemic changes (typically T-wave inversion and S-T-segment depression) are seen in > 50%. Appropriate preop preparation includes ECG characterization of the abnormality. If patient has Hx of ischemic heart disease, ECHO and cardiac enzyme studies may be helpful in determining whether the myocardial injury and consequent ECG changes are likely to be of clinical significance.

Tests: ECG; others (e.g., cardiac enzymes) as indicated from H&P

Neurological

Occasionally unruptured aneurysms produce neurological Sx by enlarging to the point that they compress adjacent neural tissue or cause ↑ ICP. If ICH occurs, the neurological dysfunction will vary, depending on the site and extent of the hemorrhage. Typically, SAH → ↑↑ ICP → sudden severe HA ± confusion and disorientation, ± motor deficit, ± coma. Admission GCS < 12 predicts ↑ mortality. Subsequent cerebral vasospasm (˜70% incidence) and delayed cerebral ischemia (DCI) may cause worsening of the neurological deficits. Clinically detectable vasospasm commonly begins on day 1 reaching a maximum at 5-14 d and usually is resolved within 2-4 wk. The precipitating agent is believed to be free Hb → release of vasospastic substances from brain tissue. Treatment of vasospasm usually involves support of BP (occasionally, induced HTN), euvolemia, and systemic Ca⁺⁺ antagonists (e.g., nimodipine (60 mg PO q 4 h) or iv (3-15 mg/h iv)). Triple H therapy (↑ volume, ↑ BP, ↓ Hct) should be avoided in favor of euvolemia and a trial of ↑ BP for DCI. Control of BP is important: any substantial ↑ BP may → serious rebleed, permanent neurological deficits or death; any substantial ↓ BP may → cerebral ischemia and infarction. Arterial catheterization and continuous beat-to-beat monitoring of BP prior to induction of anesthesia is essential in these patients.

Tests: CT; MRI; CTA, which the anesthesiologist should examine preop to identify the nature and site of the aneurysm. DSA is the gold standard for detection of vasospasm.

Hydrocephalus

Acute hydrocephalus occurs in 15-20% of patients within 24 h of SAH. External ventricular drainage may be necessary.

Hematologic

Thrombocytopenia may develop following SAH. DVT prophylaxis (e.g., SCD) is beneficial.

Tests: Hct; PT; PTT

Radiographic findings

CT: Blood in basal cisterns (˜95% of patients) or ventricles; CTA (replacing conventional angiography): anatomical characteristics of the aneurysm.

Laboratory

Cardiac enzymes if ECG changes observed (↑ cTnI predicts ↓ neurologic outcome and ↑ mortality); serum Mg⁺⁺ and glucose; others as indicated from H&P. Hyponatremia may be 2° SIADH or CSW. In contrast to SIADH, patients with CSW are hypovolemic (↓ plasma volume, ↓ CVP, ↓ PCWP), ± ↑ K⁺.

Hepatic

Hepatic dysfunction following SAH is not uncommon (24% in one series).

Tests: LFTs, as indicated from H&P.

Premedication

Small doses of midazolam 1-3 mg iv are preferable to opiates. Detailed discussion with the patient about the anesthetic plan, with appropriate reassurance, is essential. Should an intracranial aneurysm leak or rupture in the immediate preop period, its signs may be difficult to distinguish from those associated with excessive response to premedication.

Induction

Smooth induction is essential. Propofol 1-2 mg/kg iv to provide amnesia and ↓ cerebral blood volume by inducing cerebral vasoconstriction. Fentanyl 7-10 mcg/kg iv to blunt response to intubation and provide analgesia for the first hours of surgery. Vecuronium 0.15 mg/kg, or rocuronium 0.6-1.2 mg/kg to provide muscle relaxation for tracheal intubation and positioning. Patients on nimodipine may require pressors (e.g., phenylephrine) during and after induction. Poor H-H grade patients (IV-V) may not tolerate ↓ MAP during induction. These patients may benefit from moderate hyperventilation during induction.

Maintenance

Isoflurane or sevoflurane (1/2 MAC if EP monitoring is used), inspired with O₂. Avoid N₂O > 50% and entirely in patients with ↑↑ ICP. Propofol (75-100 mcg/kg/min) may be used to further ↓ cerebral blood volume, ↓ cerebral metabolism, and ↓ CMRO₂. If movement is of concern, rocuronium 7 mcg/kg/min will provide adequate neuromuscular blockade. A remifentanil infusion (0.05-0.2 mcg/kg/min) can be used to supplement the anesthetic without interfering with EP monitoring. TIVA is not necessary for monitoring SSEPs or MEPs.

Emergence

H-H grade IV-V patients are not extubated and should be kept sedated on ventilator support postop. For grade I-III patients, with the start of dural closure, consider using low-dose sevoflurane (e.g., 0.5%) in 50% N₂O, supplemented with a low-dose remifentanil infusion (e.g., 0.05 mcg/kg/min). As recovery from anesthesia occurs, the patient’s BP generally will increase in response to the emergence stimuli. Titration of β-adrenergic blocking drugs (e.g., labetalol and esmolol) with vasodilators (e.g., SNP) may be needed; if so, the dose should be stabilized before transport to ICU. (See Control of BP, below.) The inhalation agent can be D/C’d at the time of dressing application. Most patients will breathe spontaneously and can be extubated uneventfully while on the remifentanil infusion. If the brain has not been injured by the surgical procedure, the patient should awaken within 10 min after cessation of remifentanil administration. As the patient is awakening, it is important to ensure full reversal from neuromuscular blockade and close regulation of BP. If the patient begins to cough on ETT, either it should be removed or cough reflex suppressed with iv lidocaine (0.5-1 mg/kg). Patient is placed in bed in a 30° head-up position and transported to ICU for monitoring overnight. Supplemental O₂ should be administered and close regulation of BP maintained. Prophylactic antiemetics (e.g., metoclopramide 10-20 mg and ondansetron 4-8 mg) should be given 30 min before extubation. Consider iv acetaminophen (1 g) and/or local anesthetic scalp infiltration for postop analgesia.

Blood and fluid requirements

IV: 14-18 ga × 2 NS @ < 10 mL/kg + UO

Maintain euvolemia. If blood volume is normal, crystalloid fluid should not exceed 10 mL/kg beyond that required to replace UO. Rapid, massive blood loss is possible.

Expand blood volume with albumin 5% if Hct > 30%. Albumin + PRBC if Hct < 30% Maintain colloid oncotic pressure

If blood volume is low because of vasospasm or prolonged bed rest, albumin 5% is given if Hct > 30%; combinations of albumin and blood, if Hct is < 30%.

Hetastarch may → coagulopathy.

Hetastarch 6% may be used in place of albumin, but limit use because of potential for coagulopathy.

Brain relaxation

Hyperventilate to PaCO₂ = 35 mm Hg (PetCO₂ = 30 mm Hg). PaO₂ > 100 mm Hg

↓PaCO₂ → ↓ cerebral vascular volume (better surgical access) + ↑ CBF to ischemic areas (“Robin Hood” effect) + ↓ anesthetic requirements + ↑ lactic acid buffering.

Consider propofol infusion to replace N₂O

↓ isoflurane/sevoflurane to < 1/2

MAC

Mannitol 0.5-1 g/kg

± Furosemide 0.3 mg/kg

± Steroids

± Lumbar CSF drain

Head up to provide venous drainage

Minimize neck flexion/rotation

Propofol → cerebrovasoconstriction → ↓ ICP

Remifentanil infusion (0.05-0.2 mcg/kg/min) may then be required to provide adequate analgesia. Mannitol/furosemide → ↓ K⁺; monitor level and replace as necessary. If mannitol is administered too rapidly, ↓ BP may occur, 2° peripheral vasodilation. e.g., 8 mg dexamethasone

CSF drain may be placed after induction of anesthesia, avoid rapid drainage → rupture or remote hemorrhage

Otherwise → ↑ venous pressure → ↑ ICP and ↓ CBF

Monitoring

Standard monitors (see p. B-1). Arterial line

Bladder/esophageal temperature

Blood glucose (keep < 180 mg/dL)

UO (Foley catheter)

CVP line (subclavian preferred)

± Evoked potentials/EEG

Direct monitoring of arterial BP is essential for ABGs and because marked BP fluctuations may occur, necessitating drug therapy. Transducers should always be leveled at the head.

Monitoring CVP is desirable in virtually all patients to assess adequacy of fluid therapy, for infusion of vasoactive drugs both intraop and postop, and for aspiration of VAE. Localization of the catheter can be determined by CXR, ECG tracing (noting P-wave changes) or pressure-wave contour and value as the catheter is withdrawn from the right atrium.

Hypothermia

Water-circulating pads

Cold operating room

Bladder irrigation

Mild hypothermia (33-34°C) is used in some centers to ↓ CMRO₂ and to ↓ susceptibility to ischemic injury during temporary clip application. CMRO₂ decreases ˜30% @ 33°C. This level of hypothermia has minimal effect on coagulation or the incidence of cardiac dysrhythmias. Rewarming using surface means can be quite slow. The use of bladder irrigation (40-42°C saline) or an InnerCool®-type device is useful.

InnerCool® or equivalent

A heat-exchange catheter may be placed in the vena cava (via femoral vein) to facilitate patient cooling and rewarming.

IHAST Study¹³

Although it implied that mild hypothermia was not useful in aneurysm surgery, the IHAST study was not designed to assess the effectiveness of mild hypothermia in the patient group most likely to benefit: otherwise intact patients requiring long temporary clip times. Generalizing the IHAST findings to all aneurysm patients is an unfortunate disservice to many of them.

Delayed response to peripherally administered drugs

Administer drugs through CVP line in hypothermic patients to ensure prompt effect.

Single H therapy (for vasospasm)

Hypertension

Goal: SBP 120-150 mm Hg (preclipping); 160-200 mm Hg (postclipping)

Hypervolemia

No benefit. ↑ cardiopulmonary complications, ↑ infection. Euvolemia is recommended.

Hemodilution

Not recommended. Optimal Hct is difficult to predict but is probably 30-33% for most patients.

Control of BP

During application of head fixation device (Mayfield): remifentanil: 100-200 mcg iv bolus 1-2 min in advance.

During aneurysm exposure: ↓ MAP to ˜80% of baseline.

Temporary clipping: ↑ MAP to ˜120% of baseline.

Control of BP is critical to the successful outcome of the case. ↑↑ BP →↑↑ transmural pressure across the aneurysmal wall → rupture of the aneurysm. Many neurosurgeons apply a temporary clip on the major feeding vessel(s) in advance of clipping the aneurysm. This technique collapses the aneurysm and makes the clipping easier and less likely to cause inadvertent rupture. If this technique is used, it is essential for the anesthesiologist to ↑ BP ˜20% above baseline pressure to maximize collateral flow while the feeding vessel(s) is occluded. Phenylephrine is preferred because it has minimal dysrhythmogenic potential. EEG/EP monitoring can be useful to guide BP management.

Postclipping: MAP typically 70-90 mm Hg

If it becomes necessary to ↓ BP, use esmolol 50-200 mcg/kg/min to ↓ HR to 50-60, supplemented as necessary with SNP 0.1-4 mcg/kg/min to desired effect. Responses to vasoactive drugs are much easier to regulate if euvolemia has been established and maintained throughout the anesthetic period. Labetalol (5-100 mg total dose) is a useful adjunct for postop BP control.

Video Angiography

Indocyanine Green (ICG)

NB: Usually contains iodine

ICG is an iv fluorescent dye for video angiography using specially equipped microscopes. Usual dose is 2.5-7.5 mg depending on tissue thickness. Rarely anaphylactic or other allergic reactions may occur.

Aneurysmal rupture

↓ MAP to 40-50 mm Hg Consider carotid compression

Bolus SNP: MAP will ↓ ˜20 mmHg/15 mcg SNP. Ipsilateral or bilateral carotid occlusion is often effective in controlling hemorrhage while a temporary clip is applied.

Adenosine 12 mg iv (CVP line)

Adenosine will produce asystole, allowing time for the application of a temporary clip. An external pacemaker should be available for hypothermic patients.

Positioning

For most aneurysms: Supine, head turned Three-point fixation (beware of marked ↑ BP with use of pins). Use shoulder roll. [check mark] and pad pressure points [check mark] eyes

Anesthetic gas hoses and all monitoring and vascular catheter lines are directed to patient’s side or feet, where the anesthesiologist is positioned during surgery. SCDs used to minimize DVT. Shoulder roll to ↓ brachial plexus stretch. Remifentanil (100-200 mcg bolus) to minimize ↑ BP during skull pinning.

Complications

Aneurysm rupture (intraop) Hypothermia (mild)

DVT

6-18% incidence; up to 2% rupture during induction. Many patients can be extubated safely at core T ≥ 35°C with active rewarming in progress. SCDs should be used for DVT prophylaxis

Complications

Intracranial hemorrhage Stroke

New deficits or delayed emergence may necessitate urgent transport to CT scanner and/or return to the OR.

Cerebral vasospasm SIADH/CSW

Avoid prophylactic triple H therapy (↑ volume, ↑ BP, ↓ Hct).

Pain management

Meperidine (10-20 mg iv prn) Acetaminophen 1 g iv

Meperidine will ↓ postop shivering. Avoid oversedation → interferes with neuro exam.

Tests

CT scan, if any change in neurological status

Be prepared to re-secure airway.

Respiratory

None unless patient has Hx of smoking or has sustained pulmonary aspiration as a result of a neurological deficit from an intracranial hemorrhage.

Tests: As indicated from H&P; elevated cTnI may predict pulmonary complications.

Cardiovascular

Generally, these patients do not have other cardiovascular diseases. (See Anesthetic Considerations for Intracranial Aneurysms, p. 6.)

Tests: ECG; others as indicated from H&P

Neurological

These patients usually present with complaints of intermittent or persistent headaches or visual disturbances that are probably due to aneurysmal compression of adjacent neural tissue or ↑ ICP. If an intracranial hemorrhage occurs, neurological dysfunction varies, depending on site and extent of the hemorrhage. Cerebral vasospasm is a major complication of intracranial hemorrhage (see discussion in Anesthetic Considerations for Intracranial Aneurysms, p. 6).

Tests: CT; MRI; angiogram. The anesthesiologist should examine the cerebral angiogram preop to visualize the size and site of aneurysm.

Hematologic

T&C for 6 U PRBCs.

Tests: Hct; PT; PTT; hemogram; others as indicated from H&P

Laboratory

Other tests as indicated from H&P

Premedication

Premedication is usually desirable, with small doses of midazolam (e.g., 1-2 mg) preferable to opiates. Detailed discussion with patient about the anesthetic plan, with appropriate reassurance, is effective in reducing premedication requirements. Should an intracranial aneurysm leak or rupture in the immediate preop period, it may be difficult to distinguish this event from changes associated with excessive responses to premedication.

Induction

Propofol 2-3 mg/kg iv to provide anesthesia and ↓ CBV by inducing cerebral vasoconstriction. Fentanyl 7-10 mcg/kg iv to blunt the response to laryngoscopy/intubation, and provide analgesia for the first hours. Vecuronium 0.15 mg/kg or rocuronium 0.6-1.2 mg/kg to provide relaxation for intubation and positioning.

Maintenance

Propofol 100-200 mcg/kg/min administered by constant-infusion pump. These doses provide additional amnesia and ↓ CBV and CMRO₂. Isoflurane ≤ 1%. N₂O not used. An additional dose of NMB is administered just prior to the start of CPB.

Emergence

Because of the length and nature of the operation and the potential for temporary neurological injury, it is advisable to leave the ETT in place immediately postop and send patient to the ICU on controlled ventilation. If patient begins to cough, the reflex should be suppressed with opiates, NMBs, and/or LTA sprayed down the ETT. The patient is placed in bed in a 30° head-up position and transported to ICU for overnight monitoring. Supplemental O₂ should be administered and close regulation of BP maintained. Prophylactic antiemetic (e.g., droperidol 0.625 mg or metoclopramide 10-20 mg and ondansetron 4 mg) should be given 30 min before extubation. Consider iv acetaminophen and/or local anesthetic scalp infiltration for postop analgesia.

Blood and fluid requirements

IV: 14-16 ga × 2

NS @ 1-2 mL/kg/h

PRBC 4-6 U

Maintain euvolemia.

Cold NS up to 10 mL/kg, + a volume equal to UO, is administered during surgery.

Isovolemic hemodilution

5% albumin: 4-8 × 250 mL

NS: 2-4 × 1000 mL

Albumin and NS are placed in a refrigerator at 4°C the night before surgery to be used as necessary for cooling during isovolemic hemodilution.

CPD bags (for blood collection)

After induction of anesthesia, a 2nd arterial or largevein cannula is placed for removal of blood into CPD bags. Generally, about 1000 mL of blood are removed and replaced with 1 L of cold albumin 5%. This usually → ↓ Hct to 22-26%. Frequent intraop Hct checks are appropriate. The withdrawn blood is held for reinfusion at the conclusion of operation. In addition, the perfusate from the CPB unit is spun down, and packed cells are returned to patient.

Control of ICP (brain relaxation)

Hyperventilate to PaCO₂ = 25-30 mm Hg

Limit crystalloid < 10 mL/kg + UO

Limit isoflurane ≤ 1%.

± Mannitol 0.5-1 g/kg

± Furosemide 0.3 mg/kg

Dexamethasone 8-12 mg

± Lumbar CSF drainage

Position head to promote venous drainage.

Ventilation is controlled and TV and RR adjusted such that PaCO₂ = ˜35 mm Hg. There are some advantages to mild hypocarbia, including ↓ CBV; improving regional distribution of CBF by preferentially diverting blood to ischemic areas of the brain and better buffering of brain lactic acid that may form as a result of focal ischemia.

Elevate head of bed, and minimize neck flexion/ rotation if possible.

Monitoring

Standard monitors (see p. B-1). Temperature: esophageal, bladder and brain surface Arterial line

Frequent checks are made of Hct, electrolytes, and ACT values, before, during, and after CPB.

CVP (triple-lumen) line

CVP line is used for infusions of esmolol, SNP, and phenylephrine. Subclavian preferred.

Blood glucose UO

Keep glucose between 80 and 180 mg/dL. Keep UO > 0.5 mL/kg/h.

Control of BP

Maintain BP normal to 20% below normal.

BP control is critical to successful surgery. ↑ BP during induction or prior to CPB will ↑ transmural pressure across the aneurysmal wall and ↑ likelihood of rupture. Prior to CPB, BP is generally kept at normal to 20% below patient’s usual pressure, using anesthetic agents ± an esmolol infusion to ↓ HR to a range of 50-60 bpm. If desired level of BP is not achieved with this combination, SNP or propofol infusion may be added. SNP also facilitates both cooling and rewarming because of its peripheral vasodilatory effect.

Phenylephrine

If a vasoconstrictor is needed, particularly during CPB while patient is still cold, phenylephrine is preferred because of its minimal dysrhythmogenic potential.

Positioning

Shoulder roll

180° table rotation

[check mark] and pad pressure points

[check mark] eyes

Circuit extension tubes

SCD

Anesthetic gas hoses and all monitoring and vascular catheter lines are directed to patient’s feet. Make sure that all will reach the foot of operating table.

SCDs used to minimize DVT.

Deep hypothermia and CPB

Initial cooling:

Circulating water blankets

Ice packs

InnerCool®-type device

SNP infusion

Heparinization

ACT monitoring

Rewarming

Surface cooling and/or central cooling is begun as soon as induction is complete, using either a central venous heat exchange device (e.g., InnerCool®) or thermal blankets above and below patient, ice packs and infusion of cold fluids during establishment of isovolemic hemodilution.

An SNP infusion (if tolerated) will promote surface cooling.

Once the aneurysm is exposed and the decision is made that CPB is required, systemic heparinization (load: 300 U/kg; maintenance: 100 U/kg/h) is established, and patient is put on CPB using fem-fem bypass and cooled to ˜18°C. During CPB cooling, the heart will usually fibrillate between 22 and 26°C. After 18°C is reached, the CPB unit is shut off to deflate the aneurysm; it may be activated and shut off several times during clipping to evaluate adequacy of the surgical occlusion of the aneurysm and to apply additional clips. Total circulatory arrest time should not exceed 45 min.

When clipping is complete, CPB is resumed and warming instituted. Partial CPB is continued until normal cardiac rhythm is established and body temperature reaches ˜36°C. Once partial CPB is D/C, patient will tend to cool unless vigorous efforts at warming are continued. Warming the OR and iv fluids, use of a Bair Hugger, or an InnerCool®-type device will facilitate the warming process. ACT analysis is performed to establish that heparin reversal is complete 5-10 min after protamine (1 mg/100 U heparin activity). Blood is sent for clotting studies, and Plts, FFP, and calcium gluconate are administered as needed. Hetastarch is not used in these patients because of its potential for inducing a coagulopathy.

Complications

↓↓ BP 2° failure to maintain circulating volume

Dysrhythmias 2° ↓ K⁺ from diuresis and cold

Restore circulating volume.

[check mark] K⁺ level and replace as indicated.

Complications

HTN

Vasospasm

Intracranial hemorrhage, stroke

Hypothermia

Hypervolemia

Coagulopathy

DVT

Seizures

PE

HTN Rx: esmolol + SNP titrated to effect.

Vasospasm Rx: euvolemia, trial of ↑ MAP; consider nimodipine.

Patient should be rewarmed to 36-37°C before terminating CPB.

[check mark] coag status.

SCDs may be useful.

Sz Rx: Phenytoin (1 g iv slowly to avoid ↓BP).

NB: Phenytoin is incompatible with dextrose containing solutions.

Pain management

Meperidine (10-25 mg iv prn) Codeine (30-60 mg im q 4 h prn)

Meperidine reduces postop shivering.

Tests

CT scan

Coag panel

If any question about neurological status arises, a CT scan is performed postop.

Coagulation studies are needed early postop to assure normal coagulation.

Respiratory

Not usually significant unless patient has Hx of smoking, or has aspiration pneumonitis as a result of a neurological deficit from an intracranial hemorrhagic or ischemic event.

Tests: As indicated from H&P

Cardiovascular

Generally, these patients do not have other cardiovascular diseases. Occasionally, ECG changes are noted following intracranial hemorrhage and may represent subendocardial injury 2° catecholamine release.

Tests: ECG; others as indicated from H&P

Neurological

Presenting Sx depend on location and size of AVM and whether it is a low- or high-flow lesion. Hemorrhage with resultant headache and/or neurological deficit is the most common Sx, although patients also may present with intractable seizure disorder, recurrent HAs, or Sx of cerebral ischemia 2° high-flow AV shunts, causing an intracerebral steal. Surgical treatment is essential to prevent future hemorrhage (incidence of 2-4%/yr) with substantial mortality (6-30%) or severe morbidity (15-80%). Unlike hemorrhages from an intracerebral aneurysm (generally subarachnoid), hemorrhages from an AVM are usually ventricular or intraparenchymal; hence, they are seldom associated with cerebral vasospasm.

Tests: CTA; MRI; cerebral angiogram. Preop cerebral angiogram indicates size and location of the AVM and whether it is likely to be a low- or high-flow lesion.

Hematologic

After surgery for AVM, it is fairly common for surrounding brain tissue to swell and resection sites to bleed. The cause of this is unknown, but it may be related to diversion of former AVM blood flow into the surrounding vasculature, producing a fragile hyperemic state. Thus, it is advisable to attempt embolization of the lesion before surgery; obtain coag studies preop, and consider staging resection over more than one sitting when the residual AVM is large.

Tests: Hct; PT; PTT; Plt count

Laboratory

CBC; other tests as indicated from H&P

Premedication

If medication is desirable, small doses of midazolam (e.g., 1-3 mg iv) are useful. Detailed discussion with patient about the anesthetic plan, with appropriate reassurance, is essential.

Induction

Propofol 1-2 mg/kg iv provides amnesia and ↓ CBV by inducing cerebral vasoconstriction. Fentanyl 7-10 mcg/kg iv blunts the response to laryngoscopy and provides analgesia for the first hours. High-dose opiates used as a primary anesthetic technique do not alter CBF or CMRO₂ enough to provide any special benefits. Vecuronium (0.15 mg/kg) or rocuronium (0.6-1 mg/kg), provides muscle relaxation for intubation and patient positioning. Occasionally the patient may be in a stereotactic frame, and ET intubation must be accomplished before anesthesia is induced because the frame may partially occlude the mouth, making conventional laryngoscopy impossible. Awake oral fiberoptic intubation of the trachea is the easiest method for accomplishing this (see p. I-2).

Maintenance

Isoflurane ≤ 1% or sevoflurane ≤ 2% (limit to 1/2 MAC maximum if EP monitoring is used) with 1:1 O₂/N₂O. With EP monitoring, a remifentanil infusion (0.05-0.2 mcg/kg/min) may be necessary to supplement the anesthetic. Propofol (50-150 mcg/kg/min) by continuous infusion may be administered to provide ↓ CBV and ↓ CMRO₂ and allow for reduction in inhalation agent concentration or elimination of N₂O. Mild hypothermia (33°C) provides additional cerebral protection (see below). Additional neuromuscular blocking drugs are usually not necessary, but can be administered if patient movement is of concern. Induced mild hypotension is often useful during AVM resection. Following resection, induced brief hypertension (e.g., 90 mm Hg) may be requested to assess hemostasis.

Emergence

With the start of dural closure, consider changing the anesthetic to low-dose sevoflurane (e.g., 0.5%) in 50% N₂O, supplemented with a low-dose remifentanil infusion (e.g., 0.05 mcg/kg/min). A propofol infusion (if used) should be discontinued at the start of the scalp closure. The patient’s BP generally will increase, and titration of β-adrenergic blocking drugs (e.g., labetalol or esmolol) and/or vasodilators (e.g., SNP) may be needed. (See Control of BP, below.) The inhalation agents can be D/C’d at the time of dressing application. Most patients will breathe spontaneously and can be extubated uneventfully while on a 0.05 mcg/kg/min remifentanil infusion. If the brain has not been injured by the surgical procedure, the patient should awaken within 10 min after cessation of remifentanil administration. Close regulation of BP is essential. If the patient begins to cough on ETT, either it should be removed or cough reflex suppressed with iv lidocaine (1 mg/kg). Patient is placed in bed in a 20-30° head-up position and transported to ICU for monitoring overnight. Supplemental O₂ should be administered and close regulation of BP maintained (typically at ˜10% below baseline values). Prophylactic antiemetics (e.g., metoclopramide 10-20 mg and ondansetron 4 mg) should be given 30 min before extubation. Consider iv acetominophen (1g) and/or local anesthetic scalp infiltration for postop analgesia.

Blood and fluid requirements

IV: 14-16 ga × 2

NS @ < 10 mL/kg + UO

Massive blood loss possible

Maintain euvolemia

Maintain colloid oncotic pressure

If blood volume is normal, NS—not to exceed 10 mL/kg beyond that required to replace UO—is given. If hypovolemic, albumin 5% is given if Hct > 30%; combination of albumin and blood, if Hct < 30%.

Hypothermia

Water-circulating blankets

Cool air blower

Cold OR

InnerCool®-type device

Bladder irrigation

Mild hypothermia (33°-34°C) is used in some centers for cerebral protection and to ↓ brain size. This level of hypothermia does not interfere appreciably with coagulation, nor is it generally associated with cardiac dysrhythmias. Warming is begun as soon as possible after lesion resection and is greatly facilitated by the use of a central warming device (e.g., InnerCool®).

Brain Relaxation (control of ICP)

Hyperventilate to PaCO₂ = ˜35

mm Hg or PetCO₂ = 30 mm Hg.

Limit isoflurane ≤ 1%.

Maintain euvolemia.

Consider propofol infusion (50 mg/kg/min) to replace N₂O.

Mannitol 0.5-1 g/kg

Furosemide 10-20 mg q 6 h

Lumbar CSF drainage

↓ PaCO₂ →↓ cerebral vascular volume →↓ working space and lessens need for vigorous retraction of brain tissue. ↓ PaCO₂ may also improve the regional distribution of CBF by preferentially diverting blood to potentially ischemic areas of the brain.

If AVM is superficial, decreasing brain volume is less important, and the first four techniques listed (at left) are usually sufficient. If AVM is deep, the additional listed therapies may be needed.

Monitoring

Standard monitors (see p. B-1).

Core temp: deep esophageal best

Arterial line

CVP line, subclavian preferred

UO

Blood glucose (100-180 mg%)

Direct monitoring is essential for rapid control of BP. Transducer should always be placed at the level of the head rather than the heart because CPP is arterial pressure at the brain level minus CVP or ICP, whichever is higher. Monitoring CVP via a near right atrial catheter is desirable in virtually all patients to assess adequacy of fluid therapy, for infusion of vasoactive drugs and aspiration of VAE. Localization of the catheter can be determined by CXR, ECG tracing, noting P-wave changes or pressure-wave contour and value as the catheter is withdrawn from the right atrium. NB: If patient has a high-flow AVM causing a large AV shunt, venous blood may appear arterialized (bright red) during central venous catheterization.

Control of BP

Isoflurane/sevoflurane

Esmolol infusion

SNP infusion

Maintain normovolemia.

Labetalol (emergence)

Close regulation of BP during induction and prior to excision of AVMs is important, both to prevent bleeding (↑ BP) and to avoid ischemia 2° steal (↓ BP). After surgical excision is underway, however, modest decreases in MAP (≤ 20% below normal) using isoflurane, alone or in combination with esmolol and/or SNP, should be used to prevent excessive bleeding. Responses to vasoactive drugs are much easier to regulate if the patient is euvolemic.

Positioning

Shoulder roll

Three-point fixation (Mayfield)

[check mark] and pad pressure points

[check mark] eyes

180° rotation

SCDs

For most AVMs, patient is supine, head turned laterally in three-point fixation, a roll under shoulder on the side of operation (Fig. 1.1-5). Anesthetic hoses and all monitoring/vascular catheter lines are directed toward patient’s feet or side. Make sure that all will reach the foot of operating table. SCDs are used to minimize DVT. Remifentanil (2-4 mcg/kg iv bolus) should be used to minimize ↑ BP during skull pinning.

Complications

Neurological deficits

Cerebral edema and ↑ ICP

Intracerebral hemorrhage

Seizures

If these complications occur, the patient likely will have to be reintubated and transported to the CT scanner for further neurological evaluation or possible reoperation.

Careful regulation of BP is essential to avoid postop hemorrhage.

*Sz Rx: Phenytoin (1 g loading dose). NB: Incompatible with dextrose-containing solutions.

Pain management

Meperidine 10-20 mg iv/70 kg Codeine (30-60 mg im q 4 h prn)

At this dose, meperidine minimizes postop shivering without producing excessive sedation.

Tests

CT scan

If neurological status changes.