Figure 1.1-1. Locations of aneurysms of the circle of Willis and their relative occurrence. (Reproduced with permission from Greenfield LJ, Mulholland MW, Lillemore KD, et al:Surgery: Scientific Principles and Practice, 3rd edition. Lippincott Williams & Wilkins, Philadelphia: 2001.)

Table 1.1-1 Hunt-Hess Grading System for Aneurysmal SAH*

Anterior Circulation Aneurysms

Posterior Circulation Aneurysms

Circulatory Arrest (CPB) W/Deep Hypothermia

Position

Supine, head in Mayfield headrest, turned 30–45° to side away from aneurysm, vertex dropped (Fig. 1.1-5)

⇐ Or lateral decubitus, head lateral in Mayfield headrest

⇐ + Both groins must be accessible for arterial + venous cannulation; access to chest for defibrillation

Incision

Frontotemporal

⇐ Or temporal, temporosuboccipital, or suboccipital

⇐

Special instrumentation

Operating microscope; aneurysm clips; radiolucent table, and headrest for intraop angiography

⇐ + Aperture clips to accommodate cranial nerves and critical vessels

⇐ + CPB pump; femoral cannulae; defibrillator; CUSA for partially thrombosed aneurysms

Unique considerations

Temporary arterial clipping; mild hypothermia (33°C); intraop angiography with access to femoral artery; electrophysiological monitoring (SEPs, BAERs); brain relaxation; ± lumbar subarachnoid CSF drainage; dexamethasone 8–12 mg iv

⇐

⇐ + No manipulation of brain retractors after systemic heparinization; meticulous attention to hemostasis

Antibiotics

Ceftriaxone 1–2 g iv q d (avoid Ca⁺⁺ containing solutions)

⇐

⇐

Surgical time

3–5 h

3–6 h

6–8 h

Closing considerations

Rewarming

⇐

⇐

EBL

250–1000 mL

⇐

2000–4000 mL

Postop care

ICU 1–7 d; postop CBF monitoring. Transcranial Doppler (TDC) monitor

⇐

⇐ + ICP monitoring

Mortality

Unruptured: 0.5%
Ruptured: Hunt and Hess grades I–III:< 10% (See Table 1.1-1.)Hunt and Hess grades IV–V:20–40% (See Table 1.1-1.)

1.5%

15%

20–50%

5–10% (giant aneurysms)

5–15%

15–50%

Morbidity

Neurological: 5–20%
Cranial nerve injury
Stroke
Hydrocephalus: 15–25%
Hyponatremia
Respiratory failure: Rare
Seizures: 2–20%
Thromboembolism: Rare
CSF leak: Rare
Infection: Rare
Massive blood loss: Rare

10–30%
⇐
⇐
⇐
⇐
⇐
⇐
⇐
⇐
⇐
⇐

10–50%
⇐
⇐
⇐
⇐
⇐
⇐
⇐
⇐
⇐
⇐

Pain score

3–4

3–4

4–5

Age range

30–70 yr (Peak incidence in 5th and 6th decades)

Male:Female

44:56

Incidence

8–16/100,000/yr for ruptured aneurysms with SAH (highest in Japan and Finland)
Overall incidence of rebleeding is ~11% (4% in the first 24 h).

Etiology

Idiopathic (probably acquired and related to hemodynamic stress at arterial branch points, although may have congenital predisposition to loss of internal elastic lamina); traumatic; infectious; familial

Associated conditions

Polycystic kidney disease; coarctation of the aorta; Marfan syndrome; Ehlers-Danlos syndrome; intracranial AVMs; aortic aneurysm; fibromuscular dysplasia; pseudoxanthoma elastica; Rendu-Osler-Weber syndrome; cocaine/amphetamine use

Respiratory

Respiratory complications (e.g., neurogenic pulmonary edema (up to 23%), pneumonia, ARDS, PE) are the most common non-neurologic 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 and Ehlers-Danlos syndromes. Patients who have had a recent intracranial hemorrhage from leaking or rupture of a cerebral aneurysm are prone to develop systemic HTN, hypovolemia, 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. Why hypovolemia occurs following SAH is not clear, but may be due in part to cerebral vasospasm and to sustained bed rest. ECG abnormalities occur in most patients following an intracranial hemorrhage and may represent subendocardial injury 2° catecholamine release. 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

Seldom do aneurysms produce neurological Sx by enlarging to the point that they compress adjacent neural tissue or cause ↑ ICP. If an intracranial hemorrhage 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) may cause worsening of the neurological deficits. Clinically detectable vasospasm commonly begins on day 1 reaching a maximum at 6–8 d, and usually is resolved within 2–3 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), hydration to normovolemia, 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) does not appear to confer any additional advantage in most patients. 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.

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.
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); others as indicated from H&P.

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. STP 2–5 mg/kg (or 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. Pancuronium 0.1 mg/kg, vecuronium 0.15 mg/kg, or rocuronium 0.7–1 mg/kg to provide muscle relaxation for tracheal intubation and positioning patient. 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. Generally, if pancuronium is used, no additional NMBs are needed; however, if movement is of concern, rocuronium 10 mcg/kg/min will provide adequate neuromuscular blockade. A remifentanil infusion (0.05–0.1 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 or 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 assure 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 mg or dolasetron 12.5 mg) should be given 30 min before extubation.

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 = 30 mmHg (PetCO₂ = 25 mmHg). PaO₂ > 100 mmHg

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

↓ fluids < 10 mL/kg + UO
Consider propofol infusion to replace N₂O

↓ isoflurane/sevoflurane to < 1/2 MAC

Remifentanil infusion (0.05–0.2 mcg/kg/min) may be required to provide adequate analgesia

Mannitol 0.5–1 g/kg

Mannitol/furosemide →↓K⁺; monitor level and replace as necessary. If mannitol is administered too rapidly, ↓ BP may occur, probably from peripheral vasodilation.

± Furosemide 0.3 mg/kg
± Steroids (e.g., 8 mg dexamethasone)

± Lumbar CSF drain
Head up to provide venous drainage
Minimize neck flexion/rotation

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

Monitoring

Standard monitors (see p. B-1). Arterial line
Bladder temperature
Blood glucose (100–180 mg/dl)

Direct monitoring of arterial BP is essential because marked fluctuations may occur, necessitating drug therapy, as well as need for ABGs. Transducers should always be at the level of the head rather than the heart.

CVP line

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.

UO (Foley catheter) ± Evoked potentials

Hypothermia

Water-circulating pads
Cold OR
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°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 Study

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: patients requiring temporary clip times > 3 min. Generalizing the IHAST findings to all aneurysm patients is an unfortunate disservice to many of them.

↓ superficial blood flow

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

Triple H therapy
(if requested)

Hypervolemia
Hypertension

Hemodilution

Goal: CVP = 10–12; PCWP = 12–16
Goal: SBP 120–150 mmHg (preclipping); 160–200 mmHg (postclipping)
Goal: HCT = 30–35%

Control of BP

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

Postclipping: MAP typically 70–90 mmHg

If it becomes necessary to ↓ BP, use esmolol 50–200 mcg/kg/min to ↓ HR to ~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 a normal blood volume has been established and maintained throughout the anesthetic period.
Labetalol (5–100 mg total dose) is a useful adjunct for postop pressure control.

Aneurysmal rupture

↓ MAP to 40–50 mmHg, if necessary.
Consider carotid compression

Bolus SNP: ~20 mmHg ↓ MAP/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 for a temporary clip. An external pacemaker should be available.

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)

6–18% incidence; up to 2% rupture during induction.

Hypothermia (mild)

Many patients can be extubated safely at core T ≤ 35°C with active rewarming in progress.

Complications

Intracranial hemorrhage
Stroke
Cerebral vasospasm

New deficits or delayed emergence may necessitate urgent transport to CT scanner and/or return to the OR
Prophylactic triple H therapy (↑ volume, ↑ BP, ↓Hct) may have no advantage over simple euvolemia.

Pain management

Meperidine (10–20 mg iv prn)
Codeine (30–60 mg im q 4 h prn)

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

If premedication is desirable, small doses of midazolam (e.g., 1–2 mg) are 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

STP 2–5 mg/kg or propofol 2–3 mg/kg iv to provide amnesia and ↓ CBV by inducing cerebral vasoconstriction. Fentanyl 7–10 mcg/kg iv to provide analgesia for the first hours. Vecuronium 0.15 mg/kg or rocuronium 0.7–1 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.

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 8 × 250 mL
NS 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

After induction of anesthesia, a 2nd arterial or large-vein 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 at room temperature 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 mmHg
Limit crystalloid < 10 mL/kg + UO
Limit isoflurane ≤ 1%.
Mannitol 0.5–1 g/kg
± Furosemide 0.3 mg/kg
Dexamethasone 8–12 mg

Ventilation is controlled and TV and RR adjusted such that PaCO₂ ranges from 25–30 mmHg. There are several advantages to hypocarbia, including: ↓ CBV to provide more surgical working space, thereby lessening the need for vigorous retraction of brain tissue; improving regional distribution of CBF by preferentially diverting blood to potentially ischemic areas of the brain; better buffering of brain lactic acid that may form as a result of focal ischemia; and decreasing anesthetic requirement.

± Lumbar CSF drainage
Position head to promote venous drainage

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

Monitoring

Standard monitors (seep. B-1).
Temperature = esophageal, bladder and brain surface
Arterial line

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

CVP (triple-lumen) line

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

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 to normal-to-20% below normal for patient, using anesthetic agents alone or with 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 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

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.

SCD

SCDs used to minimize DVT.

Deep hypothermia and CPB

Initial cooling:
Circulating water
Thermal blankets
Ice packs
SNP infusion

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.

Innercool-type device

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

ACT monitoring

Heparinization

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 22–26°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.

Rewarming

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, and use of warming lights, Bair-Hugger, and 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 6% 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

Complications

HTN
Vasospasm
Intracranial hemorrhage, stroke
Hypothermia
Hypervolemia
Coagulopathy
DVT
Seizures
PE

HTN Rx: esmolol + SNP titrated to effect.
Vasospasm Rx: fluid-loading

Patient should be rewarmed to 36–37°C before terminating CPB.
[check mark] coag status.

Sz Rx: Phenytoin (1 g iv slowly to avoid ↓BP).
WB: Phenytoin is incompatible with dextrose containing solutions.

Pain management

Meperidine (10–20 mg iv prn)
Codeine (30–60 mg im q 4 h prn)

Meperidine minimizes 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.

Position

Supine or lateral decubitus

Incision

Frontal, temporal, or occipital

Special instrumentation

Microscopic instruments (fine forceps, miniature vascular clips, operating microscope)

Unique considerations

Neuroprotective agents during arterial segment occlusion (barbiturates, mannitol), mild hypothermia (33°C)

Antibiotics

Ceftriaxone 1–2 gm iv (avoid Ca⁺⁺ containing solutions)

Surgical time

3–4 h

Closing considerations

Avoid ↓BP (MAP 80–100 mmHg). Induced mild HTN (MAP 90–110) during temporary arterial occlusion.

EBL

100–250 mL

Postop care

Control BP (MAP 80–100 mmHg); start aspirin postop d 1; ICU: 1–2 d.

Mortality

5–10%

Morbidity

Intracerebral hemorrhageStroke
MI: Rare
Thromboembolism: Rare
Respiratory failure: Rare
Infection: Rare

Pain score

3–4

Figure 1.1-2. Middle cerebral artery (MCA) embolectomy. Exposure of right MCA in the sylvian fissure and removal of an embolus from the MI segment. (Reproduced with permission from Ojemann RG, Ogilvy CS, Crowell RM, et al: Surgical Management of Neurovascular Disease, 3rd edition. Williams & Wilkins, Philadelphia: 1995.)

Age range

50–80 yr

Male:Female

1:1

Incidence

Rare

Etiology

Atherosclerosis; carotid artery disease; atrial fibrillation; iatrogenic endovascular catheter complication

Associated conditions

HTN; CAD; PVD; carotid artery disease; hyperlipidemia; smoking; alcohol abuse; obesity; atrial fibrillation

Standard Craniotomy (High-Flow AVM)

Stereotactic Craniotomy (Low-Flow AOVM)

Brain Stem/ Thalamic Vascular Malformations

Position

Supine, lateral, Concorde (modified prone) (Fig. 1.1-3)

⇐

Lateral, Concorde, or semisitting (Fig. 1.1-4)

Incision

Frontal, temporal, parietal, occipital, suboccipital, or combination

⇐

Suboccipital (midline), paramedian or occipital

Special instrumentation

Operating microscope; irrigating bipolar coagulation; radiolucent table and headrest. Sundt mini aneurysm and micro AVM clips. Access to femoral artery for intraop angiography.

⇐ + Surgical navigation system

⇐

Unique considerations

Induced hypotension (MAP 60–65 mmHg) during resection, use of neuroprotective agents (see Craniotomy for Aneurysms, pp. 6–7). Relaxed brain. Mild hypothermia (33°C); ± lumbar CSF drain.

Use of neuroprotective agents and relaxed brain (seeCraniotomy for Aneurysms, pp. 8–9).

⇐

Antibiotics

Ceftriaxone 1 gm iv (avoid Ca⁺⁺-containing solutions)

⇐

⇐

Surgical time

4–10 h

2–5 h

3–6 h

Closing considerations

Maintain MAP 65–75 mmHg.
Avoid ↑ venous pressure.
For supratentorial vascular malformations, administer additional anticonvulsants; give loading dose of phenytoin (1 g iv for adults) if not previously on anticonvulsants.

Keep MAP 70–90 mmHg.
⇐
⇐

⇐

⇐
No anticonvulsants necessary

EBL

500–3000 mL

< 250 mL

⇐

Postop care

ICU × 1–2 d. Maintain MAP 65–75 mmHg for 1 d. ICP monitoring, ventricular drain; normovolemic in ICU.

ICU × 1 d; normovolemic in ICU

⇐

Mortality

1–10%, depending on AVM size, location, and venous drainage pattern

< 0.5%

< 2%

Morbidity

Overall: 5–30%
Breakthrough bleeding: < 5%
Intracranial hemorrhage
Cerebral edema
Stroke < 15%
Hydrocephalus
Massive blood loss: Occasional
Thromboembolism: Rare
Infection: Rare

< 5%
⇐
⇐
⇐
⇐
⇐
⇐
⇐

10–50% (transient)
< 5%
⇐
⇐
⇐
⇐
⇐
⇐
⇐

Pain score

3–4

3–4

3–4

Figure 1.1-3. Concorde (modified prone) position for resection of posterior fossa vascular malformations.

Figure 1.1-4. Semisitting position for resection of deep posterior corpus callosum or thalamic vascular malformations.

Age range

15–40 yr (most common), 41–60 yr (less frequent)

Male:Female

1:1

Incidence

0.5–1% of the U.S. population

Etiology

Congenital; traumatic for dural AVM

Associated conditions

Intracranial aneurysm (~10% of AVM patients [up to 58% in some studies]); Von Hippel-Lindau disease; Rendu-Osler-Weber syndrome; familial cavernous malformation syndrome

Respiratory

Not usually significant unless patient has Hx of smoking, or has pulmonary aspiration as a result of a neurological deficit from an intracranial hemorrhage.
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 obtain coag studies preop and stage excision over more than one sitting when the 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

STP 2–5 mg/kg or propofol 2–3 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), rocuronium (0.6–1 mg/kg), or pancuronium (0.1 mg/kg), provide 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 partially occludes the mouth, making conventional laryngoscopy impossible. Awake oral fiber optic intubation of the trachea is the easiest method for accomplishing this (see p. B-5).

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 (0.05–0.15 mcg/kg/min) may be necessary to supplement the anesthetic. Propofol (75–150 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 hypotension is often useful during AVM resection. Following resection, induced hypertension (e.g., 90 mmHg) may be requested to inspect 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 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. 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 (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 (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.

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%; combinations of albumin and blood, if Hct < 30%.

Hypothermia

Thermal 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 = ~30
mmHg or PetCO₂ = 25 mmHg.
Limit isoflurane ≤ 1%.
Maintain euvolemia
Consider propofol infusion to replace N₂O
Mannitol 0.5–1 g/kg
Furosemide 0.3 mg/kg
Lumbar CSF drainage

↓ PaCO₂ →↓ cerebral vascular volume →↑ working space and lessens need for vigorous retraction of brain tissue. ↓ PaCO₂ also improves 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, triple lumen
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, since 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.
Labetolol (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 under way, 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
[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

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.

Cerebral edema and ↑ ICP
Intracerebral hemorrhage

Careful regulation of BP is essential to avoid postop hemorrhage.

Seizures

*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.

Figure 1.1-5. Supine position, head elevated above heart, turned 30–45° to side, vertex dropped for approach to anterior circulation aneurysms and frontal vascular malformations. (Reproduced with permission from Long DM: Atlas of Operative Neurosurgical Technique, Vol 1. Williams & Wilkins, Philadelphia: 1989.)

Figure 1.1-6. Typical skin incision for EC-IC bypass. The main incision is planned over the superficial temporal artery (STA) with a T extension to allow exposure of the bone. (Reproduced from Chang SD, Steinberg GK: Superficial temporal artery to middle cerebral artery anastomosis. Tech Neurosurg 2000; 6(2):86–100.)

Figure 1.1-7. After the STA is dissected out, the temporalis muscle is divided and the bone flap is made to allow exposure of the brain over the anterior sylvian fissure. (Reproduced from Chang SD, Steinberg GK: Superficial temporal artery to middle cerebral artery anastomosis. Tech Neurosurg 2000; 6(2):86–100.)

Figure 1.1-8. A middle cerebral artery (MCA) recipient vessel is identified. The sylvian fissure can be split to allow identification of a larger, more proximal branch of the MCA, preferably an M3 branch. (Reproduced from Chang SD, Steinberg GK: Superficial temporal artery to middle cerebral artery anastomosis. Tech Neurosurg 2000; 6(2):86–100.)

Figure 1.1-9. When the anastomosis is complete, the vascular clips are removed. (Reproduced from Chang SD, Steinberg GK: Superficial temporal artery to middle cerebral artery anastomosis. Tech Neurosurg 2000; 6(2):86–100.)

Figure 1.1-10. The completed anastomosis shows the STA positioned such that flow is directed toward the proximal portions of the MCA. (Reproduced from Chang SD, Steinberg GK: Superficial temporal artery to middle cerebral artery anastomosis. Tech Neurosurg 2000; 6(2):86–100.)

EC-IC Bypass

EC-IC Bypass with Vein Graft

Indirect Procedures

Position

Supine or lateral decubitus

⇐

⇐

Incision

Frontal, parietal, temporal, occipital, or a combination of these, depending on area to be vascularized.

⇐ + Medial aspect of leg and thigh for harvesting greater saphenous vein

⇐ + possible abdominal incision for harvesting omentum and chest/ neck incision for tunneling

Special instrumentation

Microscopic instruments; microvascular Doppler to identify scalp donor artery course and confirm graft patency.

⇐ + Tunneling instruments

⇐

Unique considerations

Neuroprotective agents (barbiturates, mannitol) and induced mild HTN (MAP 90–110 mmHg) during cross-clamp of recipi-
ent intracranial artery. Avoid excessive brain relaxation. Mild hypothermia (33°C). Dexamethasone 8–12 mg iv.

⇐ + Attention to proper alignment of vein when tunneled, to avoid kinking; heparinization if major cervical artery (carotid, vertebral) is temporarily occluded.

⇐ + Avoid devascularizing source tissue during dissection or compromise to blood supply during closure.

Antibiotics

Ceftriaxone 1–2 gm iv q d (avoid Ca⁺⁺ containing solution)

⇐

⇐

Surgical time

3–5 h

⇐

⇐

Closing considerations

Careful attention to hemostasis. Avoid compromise of graft with dural closure, bone replacement or scalp closure.

⇐

⇐

EBL

< 100 mL

⇐

100–500 mL

Postop care

Start aspirin on POD 1; monitor for subdural hygroma (CSF fluid collection in subdural space); ICU × 1 d.

⇐

⇐

Mortality

< 0.5%

⇐

⇐

Morbidity

Transient neurologic deficit:
~20–40% Subdural hygroma: Rare
Wound infection: Rare
Stroke: Rare

⇐

⇐
⇐

⇐
⇐
Abdominal hernia: Rare

Pain score

3

3

3

Age range

40–80 yr; 2–20 yr for moyamoya disease

Male:Female

1:1 for atherosclerotic disease; 1:1.4 for moyamoya disease

Incidence

Thromboembolic stroke common, but indications for EC-IC bypass rare; 1/million/yr for moyamoya disease

Etiology

Atherosclerosis; embolism from heart or carotid artery

Associated conditions

HTN; CAD; PVD; hyperlipidemia; smoking; alcohol abuse; obesity; moyamoya disease

Respiratory

None unless patient has Hx of smoking or has sustained pulmonary aspiration 2° neurological deficit.
Tests: As indicated from H&P.

Cardiovascular

HTN is a common adaptive mechanism to maintain cerebral perfusion; therefore “normalization” of BP preop may be undesirable. Adult patients may have generalized vascular disease, including CAD, so a careful cardiac Hx, physical exam, and ECG analysis should be done. If findings are positive, consider a more complete evaluation, including ECHO and coronary angiography. Be aware that cardiac insufficiency is the cause of about half of the deaths in patients with cerebrovascular disease.
Tests: Consider ECG, others as indicated from H&P.

Neurological

Patients present with Sx of focal ischemic lesions. Cerebral angiography is necessary to r/o other causes of TIAs and characterize collateral circulation. Regional CBF studies are generally not helpful, because measurement does not distinguish between low flow due to cerebrovascular obstruction from that due to low metabolic demands 2° prolonged cerebral ischemia. Pre-existing deficits should be well-characterized.
Tests: CTA; MRI; angiogram

Hematologic

For most patients: a platelet-suppressive dose of aspirin should be continued through the day of surgery; drugs affecting PT/PTT should be D/C'd at least 1 wk before surgery to avoid excessive bleeding; Clopidogrel (Plavix) should be D/C'd 5 d before surgery.
Tests: Hct; PT; PTT; hemogram

Laboratory

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 the patient about the anesthetic plan with appropriate reassurance is essential.

Induction

STP 2–5 mg/kg (or 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. Pancuronium (0.1 mg/kg; helps offset ↓ HR/BP 2° induction drugs), vecuronium 0.15 mg/kg, or rocuronium 0.7–1.0 mg/kg to provide muscle relaxation for tracheal intubation. Bolus ephedrine and/or phenylephrine are often necessary to maintain CPP during induction.

Maintenance

Isoflurane ≤ 1% or sevoflurane ≤ 2% (1/2 MAC maximum if EP monitoring is used) with 1:1 O₂/N₂O. A phenylephrine infusion is usually necessary to maintain CPP during the procedure. STP (2–5 mg/kg) is given just before surgical occlusion of the cerebral vessel in preparation for anastomosis. A bolus dose of phenylephrine and/or ephedrine is often given concomitantly to offset the hypotensive effects of STP. If mild hypothermia was employed, rewarming should start as soon as revascularization is complete.

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 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. 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 (0.5–1.0 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 (typically at ~10% below baseline values). Prophylactic antiemetics (e.g., metoclopramide 10–20 mg, ondansetron 4 mg) should be given 30 min before extubation.

Blood and fluid requirements

IV: 18 ga × 2
NS @ < 10 mL/kg + UO

In hypothermic patients, IV drugs should be administered through the central line to ensure timely entry into the central circulation.

CVP (triple-lumen)

CVP use low volume (1 mL) extension for drug infusions. Reserve distal lumen for pressure monitoring and air aspiration.

Control of brain volume (ICP)

Avoid hypovolemia
↓ isoflurane ≤0.5%, or sevoflurane < 1%
N₂O ≤ 50%
± Furosemide 10–20 mg iv
± Mannitol 0.5–1.0 g/kg

Maintain normovolemia. Generally, vigorous control of brain volume is not necessary since surgeon is working with cerebral vessels on the surface of the brain. Keep PaCO₂ = ~30 mmHg. Excessive hypocarbia may cause unwanted cerebral vasoconstriction in these patients.

Monitoring

Standard monitors (seep. B-1).
Core temperature
Arterial line
CVP (triple-lumen catheter)
UO

Core temperature is best approximated by a deep esophageal temperature probe. Bladder temp tends to lag behind core temp.
The distal CVP lumen is used for pressure monitoring.

Control of BP

Maintain normal BP (MAP).
Phenylephrine infusion

Maintenance of normal MAP is important because cerebral autoregulation is often impaired in these patients, particularly during temporary occlusion of the surgical vessel being anastomosed. If a vasoconstrictor is needed, a pure α-adrenergic agonist, such as phenylephrine, is preferred because it has minimal dysrhythmogenic potential.

Normovolemia

Responses to vasoactive drugs are much easier to regulate if a normal blood volume has been maintained throughout the anesthetic period.

Positioning

[check mark] and pad pressure points.
[check mark] eyes.
Shoulder roll
SCDs

Anesthetic hoses and monitoring and vascular lines directed to patient's feet where anesthesiologist is positioned during surgery.
Used to minimize DVT.

Hypothermia

Cold-water circulating blankets.
Core temp goal: 33–34°C.
InnerCool-type device
Bladder irrigation

Surface cooling is quite effective in patients with high surface-to-volume ratios, and should be started as soon as induction of anesthesia is complete, using a cold-water circulating blanket underneath and above the patient. When anastomosis is nearly complete, vigorous efforts at warming, including bladder irrigation, are initiated. Cooling, and especially rewarming are greatly facilitated by the use of a central heat-exchange device (e.g., InnerCool) placed in the inferior vena cava through a femoral vein introducer.

Complications

Seizures
Stroke
Hemorrhage at anastomosis

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

Brain swelling

May be 2° hyperemia in revascularized territory.

Complications

Localized scalp necrosis

Major complications uncommon; localized scalp necrosis unique to this procedure.

Brain swelling

May be 2° to delayed hyperemia. Careful control of BP is important.

Pain management

Meperidine (10–20 mg iv prn)
Codeine (30–60 mg im q 4 h prn)

Useful to suppress shivering
Postop pain is usually not severe.

Tests

Cerebral angiogram

Cerebral angiography documents patency of graft and collateral flow.

Regional blood flow studies

Some centers have the capability of performing regional blood flow studies.

CT scan

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

Table 1.1-2. Common Tumor Location (Supratentorial vs Infratentorial)

Table 1.1-3. Intraaxial (Within-the-Brain Parenchyma) vs Extraaxial (Outside-the-Brain Parenchyma)

Table 1.1-4. Common Patient Positions Based on Tumor Location

Position

Supine, lateral, prone, or sitting, based on location of tumor

Incision

Linear or curvilinear, based on location of tumor

Special instrumentation

Operating microscope, laser, CUSA, electrophysiologic monitoring, image-guided navigation, lumbar drain, ventriculostomy

Unique considerations

ETT must be taped securely in a location satisfactory to the surgeon; anode or RAE tube is helpful in certain situations. Decadron is usually given preoperatively and dosed every 6 h to minimize brain edema. Brain relaxation techniques may be required. The patient with ↑ ICP may require special consideration for induction of anesthesia. Awake craniotomy (see p. 34) may be required for tumors involving eloquent brain areas.

Antibiotics

Ceftriaxone 1–2 g iv (avoid Ca⁺⁺ containing solutions)

Surgical time

3–5 h typically

Closing considerations

Possible requirement for dural graft. Drain often left in the epidural or subgaleal space. Good BP control during closing and extubation to prevent hemorrhage into tumor resection bed.

EBL

50–500 mL (Meningiomas and renal cell mets are highly vascular tumors and blood loss may be substantial.)

Postoperative care

ICU or close observation unit X 1–3 d. Fluid and electrolytes require frequent monitoring. BP may need to be controlled with antihypertensives.

Mortality

0–5% (mortality higher for tumors in critical locations)

Morbidity

Infection: 1%
Neurological: neurologic disability, nerve injury: 0–10%
CSF leak: 1–3%
Venous sinus injury, air embolus
Endocrine disorder
Massive blood loss

Pain score

2–7

Age range

Infant to 85 yr (usually 20–60 yr)

Male:Female

~1:1

Incidence

Common neurosurgical procedure (~40,000 dx/yr in the United States)

Etiology

Neoplastic

Respiratory

Occasionally neurogenic pulmonary edema may occur. H/o chemotherapy or radiation therapy may affect pulmonary function and airway management. Otherwise no special considerations, unless indicated from H&P.

Cardiovascular

Benign or malignant brain tumors cause edema formation in adjacent normal brain tissue, which may →↑ ICP. If ICP increases sufficiently to cause herniation of the brain stem, patients develop the “Cushing triad” of HTN, bradycardia, and respiratory irregularity. These changes will resolve when ICP is reduced, so vigorous attempts to regulate BP and HR prior to craniotomy are not warranted. After the diagnosis of brain tumor is made, most patients are placed on high-dose steroid therapy to lessen edema in surrounding normal brain. Steroids are extremely effective in this setting, and Sx of ↑ ICP will often abate.
Tests: Consider ECG; others as indicated from H&P.

Neurological

Patients may present with complaints related to ↑ ICP (e.g., HA, N/V, visual changes, recent onset of Sz), neurological deficits from compression of motor area, or as a result of hemorrhage from the tumor or edema in surrounding normal brain. Document preop physical findings.
Tests: A CT scan or MRI will delineate the site and size of the tumor, especially if iv contrast material, such as gadolinium, is administered to enhance the margins of the tumor. for intracranial mass effects: midline shift, ↓ ventricular volume, ↓ peri-brainstem (basal cisterns) CSF space, obstructive hydrocephalus.

Laboratory

Coags should be normal. Hct, electrolytes, and other tests as indicated from H&P.

Premedication

Standard premedication (except for patients with the possibility of ↑ ICP: no sedation).

Induction

If the patient is in a stereotactic frame, or a difficult intubation is anticipated, orotracheal intubation will need to be accomplished before induction of GA. Awake fiber optic intubation (see p. B-5) is the best choice, because fitting a mask on the face with the stereotactic frame in place is impossible. After the airway is secured, anesthesia usually is induced with STP (2–5 mg/kg) or propofol (1–3 mg/kg) and fentanyl (3–5 mcg/kg) in combination with a NMR (e.g., vecuronium 0.1 mg/kg or rocuronium 0.6 mg/kg). To minimize ↑↑ BP and ↑ ICP with ET intubation, it is important that the patient be well anesthetized (and paralyzed) before undertaking laryngoscopy. Induction doses of STP, propofol, or midazolam may not be sufficient to abolish increases in MAP, CPP, and, hence, ↑ ICP is associated with laryngoscopy and tracheal intubation. Consider hyperventilating the patient and using remifentanil (2–3 mcg/kg) as part of the induction technique to further blunt the response to laryngoscopy in patients with ↑ ICP.

Maintenance

Isoflurane or sevoflurane ≤1 MAC (≤1/2 MAC if EP monitoring is used), inspired with 50:50 O₂/N₂O. Propofol (50–100 mcg/kg/min) can replace N₂O and may be used to further ↓cerebral blood volume, ↓ cerebral metabolism, and ↓ CMRO₂. Generally, if pancuronium is used, no additional NMBs are needed; however, if movement is of concern, rocuronium 10 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.

Emergence

Surgeons should request transient ↑ MAP to 90–100 mmHg to test hemostasis after the tumor has been resected. With the start of dural closure, consider changing the anesthetic to low-dose sevoflurane (e.g., 0.5%) with 50% N₂O (or propofol replacement), supplemented with a low-dose remifentanil infusion (e.g., 0.05 mcg/kg/min). 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.) Reverse NMB as necessary. The anesthetic agent can be D/C'd at the time of dressing application while continuing the remifentanil infusion. Most patients will breathe spontaneously and can be extubated uneventfully while on 0.05 mcg/kg/min remifentanil. If the brain has not been injured by the surgical procedure, the patient should awaken within 10 min after cessation of remifentanil administration. Keep close regulation of BP. 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 BP control maintained. Prophylactic antiemetics (e.g., metoclopramide 10–20 mg and ondansetron 4 mg) should be given iv ~30 min before extubation.

Blood and fluid requirements

IV: 16–18 ga × 2
NS @ 2–3 mL/kg/h

Brain tumors (e.g., meningioma) can be highly vascular. To minimize postop cerebral edema, limit NS to ≤ 10 mL/kg + replacement of UO. If volume is needed, administer albumin 5% as required.

Monitoring

Standard monitors (seep. B-1).
Arterial line
CVP line
± Precordial

If the head of the OR table is significantly elevated (≤ 30°) or if the patient is in the seated position, a precordial Doppler monitor is necessary to monitor for VAE.

Doppler
± BAER, SSEP, MEP
UO

Evoked potentials can be monitored in the presence of inhaled anesthetics (e.g. ≤ 0.6% isoflurane with 50% N₂O).

Positioning

Supratentorial: supine/lateral
Posterior fossa: prone/sitting
[check mark] and pad pressure points.
[check mark] eyes.

For brain tumors in the frontal, parietal, or temporal lobes, patient will be supine with head in Mayfield-Kees skeletal fixation, turned to the side and a roll under the shoulder on the operative side (Fig. 1.1-5). For occipital or posterior fossa tumors, patient may be prone or, occasionally, sitting (see Anesthetic Considerations for Cervical Neurosurgical Procedures, Positioning, p. 109). Acoustic neuromas are generally most easily removed with patient in the lateral (“park-bench”) position with a roll under the axilla. The patient generally lies on a “bean bag” which holds her/him firmly in the lateral position.

Control of ICP

Maintain normovolemia
Control BP in normal range for patient
PaO₂ > 100 mmHg
Limit isoflurane or sevoflurane to 1/2 MAC
Steroids: 8–12 mg decadron iv

Patients with intracranial tumors may be on the steep portion of the intracranial compliance curve such that any increase in intracranial volume may →↑↑ ICP. Transient increases in ICP—even up to 50–60 mmHg—are tolerated, provided they are promptly terminated. Sustained increases in ICP > 25–30 mmHg are associated with severe neurologic injury and poor outcome.

PaCO₂ = 25–30 mmHg

↓ PaCO₂ →↓ CBV (providing better surgical access) + ↑ CBF to ischemic areas (“Robin Hood” effect) + ↓ anesthetic requirements.

Replace N₂O with propofol infusion

If further reduction in ICP is needed consider replacing N₂O with a propofol infusion.

Mannitol 0.5–1.0 g/kg
± Furosemide 10–20 mg

Mannitol/furosemide →↓ K⁺; monitor level and replace as necessary. If mannitol is administered too rapidly, profound ↓ BP will occur, probably from peripheral vasodilation.

± Lumbar CSF drain
Head up 20–30°

CSF drain often placed after induction of anesthesia, and may be opened as required to ↓ CSF volume and pressure.

Complications

Seizures
Neurologic deficits
Tension pneumocephalus
Hemorrhage requiring reexploration
Edema and ↑ ICP

* Sz Rx: Phenytoin (1 g loading dose). NB: Incompatible with dextrose-containing solutions.
In seated position, additional rare, but possible complications include quadriplegia from excessive flexion of head or tension pneumocephalus from air in cerebral cavities. Severe tension pneumocephalus may delay emergence from anesthesia or cause postop neurologic deficits. CT scan may be necessary for Dx.

Pain management

Meperidine (10–20 mg iv prn)
Codeine (30–60 mg im q 4 h)

Meperidine minimizes postop shivering. Avoid excessive sedation.

Tests

CT scan

If patient exhibits any delay in emergence from anesthesia and surgery, or any new neurologic deficits emerge postop, a CT scan is invariably obtained.

Premed

Midazolam 1–3 mg iv is usually tolerated. Beware of respiratory depression →↑ ICP.
Antiemetic: e.g., ondansetron 4 mg iv slowly and q 2–3 h during the procedure

Premapping

Most patients with space-occupying lesions will benefit from the early administration of mannitol 0.5 gm/kg by slow iv infusion (check with surgeon for possible contraindications). With the patient in a beach-chair position and following the application of standard monitors and nasal prong O₂, initial sedation is provided by incremental midazolam titrated by effect (1–10 mg iv). A loading dose of dexmedetomidine (1 mcg/kg iv over 10–15 min as tolerated) is given while the sites for arterial line and central line (subclavian or antecubital long-line) placement are infiltrated with local anesthetic. Following the loading dose, a maintenance infusion of dexmedetomidine (0.2–0.7 mcg/kg/h) typically 0.4 mcg/kg/h is started. The dexmedetomidine produces cooperative sedation and analgesia without respiratory depression. A ↓ BP and ↓ HR are common and occasionally will require treatment with vagolytics and/or pressors. If necessary the sedation can be deepened with a propofol infusion (25–75 mcg/kg/min) to cover the more painful aspects of the procedure. A nasal airway may be useful in some patients. Scalp blocks (supraorbital, temporal, and occipital nerves) are placed using 0.5% bupivacaine with epinephrine.
Arterial line, cerebral line, and Foley catheter are placed. Pin sites for the Mayfield skull clamp are infiltrated with local anesthetic and the clamp is applied. The incision is infiltrated with local anesthetic and, after patient comfort has been assured, the craniotomy is allowed to proceed. Drapes should be arranged so that the anesthesiologist and neuromonitoring team have an unobstructed view of, and access to, the patient's face and airway.

Mapping

The dexmedetomidine (and propofol) infusions are stopped at the end of the craniotomy. Initial mapping (e.g., phase-reversal localization) can be accomplished while the patient is recovering from the sedation. Some direct cortical stimulation can produce seizures; it is important that sterile, iced saline be immediately available for cortical irrigation to suppress the seizure activity. If seizure activity spreads, it will be necessary to administer a bolus dose of STP (25–75 mg iv) through the central line. Airway support (e.g., LMA) may be necessary in the post-ictal phase.
The patient should be awake and cooperative ~20 min after the dexmedetomidine and propofol infusions have stopped. Occasionally, flumazenil may be necessary to remove residual midazolam effects. Detailed speech-mapping can then be readily accomplished. We use a miniature wireless microphone taped below the patient's mouth to amplify the patient's voice during testing and tumor resection.

Resection

If the lesion is located safely away from the mapped speech areas, the resection can be accomplished after reinstituting the dexmedetomidine and propofol infusions. Otherwise, the patient must be kept awake and talking throughout the resection. Often the patient will benefit from a low-dose remifentanil infusion (e.g., < 0.05 mcg/kg/min) to improve ability to tolerate positional discomfort.

Closing

Closing is best accomplished by resuming the previously effective infusions of dexmedetomidine and propofol. The infusions should be stopped during the final phase of wound closure. Careful control of BP may require the use of labetalol, esmolol, and SNP, which should be titrated during emergence. Typically, the patient will be awake and alert for transport to the ICU.

Position

Supine, lateral, prone, or sitting, based on the location of the tumor

Incision

Dependent on location of tumor

Special instrumentation

Neuro drill, craniotome, image-guided navigation (if intracranial)

Unique considerations

ETT must be taped securely in a location satisfactory to the surgeon. Anode or RAE tube may be helpful in certain situations.

Antibiotics

Cefazolin 1 g iv (if dura not opened)

Surgical time

1–4 h

Closing considerations

Drain often left in epidural space. Surgeon often requests control of BP to avoid hemorrhage into the bed of tumor.

EBL

25–500 mL

Postop care

ICU or close observation unit

Mortality

0–2% (higher for tumors in critical locations)

Morbidity

Usually < 5%
Infection
Neurological disability
CSF leak
Massive blood loss 2° venous sinus injury

Pain score

2–5

Age range

Infant–85 yr (usually 20–60 yr)

Male:Female

~1:1

Incidence

Unknown

Etiology

Neoplastic

Figure 1.1-11. In an acute subdural hematoma: A: burr hole is made, followed by craniectomy, and the incision is extended upward to form a large question mark, the medial extent of which follows the midline. B: Additional burr holes are made, with the medial ones 1.5 cm off the midline to avoid injury to the major venous structures and granulations. The anterior burr hole is placed above the frontal sinus (the size of which can be estimated from preop radiographs). C: The dura can be opened with a Y- or X-shaped incision, with a flap being based on the superior sagittal sinus. (Reproduced with permission from Grossman RG, Loftus CM: Principles of Neurosurgery, 2nd edition. Lippincott-Raven, Philadelphia: 1999.)

Figure 1.1-12. Precautions to be taken during a craniotomy for subdural hematoma. (Reproduced with permission from Grossman RG, Loftus CM: Principles of Neurosurgery,2nd edition. Lippincott-Raven, 1999.)

Position

Supine, lateral, prone, or sitting, depending on site of injury

Incision

Varies with location of injury (typical incision shown in Fig. 1.1-11)

Unique considerations

The patient may have ↑↑ ICP. Because incipient herniation and/or associated injuries may be a concern, timing is critical. C-spine precautions may be necessary. Patients may also be on anticoagulation medications, necessitating transfusions of blood products or recombinant activated factor VII.

Antibiotics

Ceftriaxone 1 g iv (avoid Ca⁺⁺ containing solutions)

Surgical time

1.5–6 h

Closing considerations

Application of head dressing may jostle ETT at end of case →↑ BP. Patient may stay intubated postop. ICP monitor or external ventricular drain may be placed. Antiepileptic medications may be given for prophylaxis, if the patient had a seizure.

EBL

25–500 mL

Postop care

ICU or close observation unit until stable. Fluid and electrolytes require frequent monitoring, as the patient may develop SIADH. BP may need to be controlled with vasodilator and β-blocker infusions.

Mortality

10–50%, depending on lesion; higher for acute subdural hematomas, lower for epidural hematomas.

Morbidity

Morbidity depends on lesion; morbidity from craniotomy itself is low. Infection
Neurologic disability
Nerve injury
CSF leak
Endocrine disorders:
SIADH
Panhypopituitarism
Diabetes insipidus (DI)
Massive blood loss: venous sinus injury

Pain score

2–4

Age range

Infant–85 yr (usually 15–40 yr)

Male:Female

2:1

Incidence

Relatively common

Etiology

Trauma

Associated conditions

Abdominal injuries; C-spine fractures

Respiratory

Ensure a secure airway and adequate ventilation. Localized injuries to the frontal or parietal lobes may not cause any respiratory changes. If ↑ ICP, respirations may become slow (< 10 min) and deep, and result in substantial hypocapnia. Many patients with head injuries demonstrate partial airway obstruction from the tongue falling back into the posterior pharyngeal space. If this occurs, or if the patient is comatose and unable to protect the airway and prevent aspiration of gastric contents, immediate tracheal intubation should be performed. Head injuries in the region of the occipital lobes may → hypoventilation or apnea. Neurogenic pulmonary edema may occur in up to 20% of TBI patients.
Tests: As indicated from H&P and as time allows.

Cardiovascular

Most patients with head injuries evidence ↑ BP and ↑ HR. Relative hypotension (SBP < 90 mmHg) →↑ morbidity and mortality. If ICP increases sufficiently to cause herniation of brain stem, patients develop the “Cushing triad” of ↑ BP, ↓ HR and irregular respiration. These changes resolve when ↑ ICP is relieved, so vigorous attempts to regulate BP prior to craniotomy are not warranted. However, the patient should be taken to OR as quickly as possible.
Tests: As indicated from H&P, and as time allows.

Neurological

Neurological evaluation of the head-injured patient is based on the Glasgow Coma Scale (Table 1.1-5). The scale involves evaluation of three functions: eye opening, verbal response, and motor response. Using this scoring system, the severity of brain injury may be classified as mild (13–15 points), moderate (9–12 points), or severe (8 points or less). By definition, any patient having 8 points or less is in coma. Additional useful neurological examinations include assessment of pupillary size and reactivity to the light, reflex responses, and evidence of asymmetry or flaccidity of the extremities or decerebrate (e.g., rigid arm extension) or decorticate (e.g., rigid arm flexion) posturing. Head-injured patients whose neurological function is deteriorating rapidly, and in whom an epidural or subdural hemorrhage is suspected, should be taken to OR immediately. Hyperventilation is appropriate if herniation is eminent.
Tests: CT scan

Hematologic

Severe head injury may be associated with a progressively worsening coagulopathy, resulting in a clinical picture similar to that of DIC. The reason for this is not known, but the brain is rich in thromboplastin and other coagulation factors.
Tests: Hct; PT; PTT; others as indicated from H&P.

Associated Injuries

Multiple organ system injury must be considered. Evidence of intrathoracic or intraperitoneal hemorrhage should be sought and repaired first if the patient is hemodynamically unstable.
Tests: may include MRI, CT, ultrasound and others as indicated.

Laboratory

Other tests as indicated from H&P, and as time permits.

Premedication

Usually none

Table 1.1-5. Glasgow Coma Scale (GCS)

Induction

↑ ICP is likely in most patients with head injury requiring operation, and induction of anesthesia is best accomplished with drugs that ↓ ICP. A mannitol infusion (0.25–1 mg/kg iv over 20 min) may be necessary to control ICP. If the patient is hemodynamically stable and not hypovolemic, titrated induction with STP (2–5 mg/kg) or propofol (1.5–3 mg/kg) + fentanyl (2–5 mcg/kg) is satisfactory. If hemodynamically unstable, etomidate (0.1–0.4 mg/kg) is suitable for induction. Ketamine is not used because of its ability to ↑ ICP. If the patient is comatose, anesthetic requirement is less, needing only O₂ and muscle relaxant, or low-dose isoflurane (0.5%) or sevoflurane (< 1%). A nondepolarizing muscle relaxant (vecuronium [0.1 mg/kg] or rocuronium [1 mg/kg]) is administered for ET intubation. Succinylcholine may ↑ ICP transiently, but is still appropriate for emergency airway management. A defasciculating dose of a non-depolarizing NMB may attenuate the ICP ↑. Nasotracheal intubation is not recommended for patients with the possibility of maxillary and/or basilar skull fractures because of the potential for inserting the tube through the fracture site into the brain. To minimize ↑↑ BP and ↑↑ ICP with ET intubation, consider bolus remifentanil (2–5 mcg/kg iv) 1–2 min before laryngoscopy. In hypovolemic patients, hydration with a mixture of crystalloid (e.g., NS) and colloid (e.g., 5% albumin) should be initiated prior to induction.

Maintenance

The ideal drug for maintenance of anesthesia decreases ICP and CMRO₂, maintains cerebral autoregulation, redistributes flow to potentially ischemic areas, and provides protection for the brain from focal ischemia. Unfortunately, there is no ideal anesthetic.
Both isoflurane and sevoflurane are good choices for patients undergoing neurosurgical procedures. Although these agents cause dose-dependent increases in CBF and volume, and hence ↑ ICP, these effects tend to be mitigated by the prior administration of STP (or propofol), hyperventilation, and by limiting the inspired concentrations to < 1 MAC. At these concentrations, CBF responses to changes in PaCO₂ are maintained, and cerebral autoregulation remains intact.
N₂O is best avoided in patients with significantly elevated ICP. A propofol infusion is a reasonable alternative although its use has been associated with a ↓ CBF >↓ CMRO₂ →↑ potential for ischemia. Jugular bulb O₂saturation may be reduced during propofol anesthesia, consistent with an unfavorable supply-demand balance.
BP Goals: Keep SBP ~90 mmHg and CPP 60–70 mmHg. Avoid prophylactic hyperventilation. Mild hypothermia may be beneficial if maintained > 48 h. DVT prophylaxis is recommended. High-dose steroid administration is associated with worsened outcomes. Muscle relaxation can be maintained as necessary.

Emergence

Because recovery from head injury is so unpredictable, it is generally advisable to leave the ETT in place and maintain controlled ventilation until there is sufficient clinical evidence that normal neurological recovery is occurring. Postop sedation can be accomplished using propofol (20–75 mcg/kg/min) not to exceed 5 mg/kg/h to minimize the occurrence of propofol-related infusion syndrome (including: metabolic acidosis, ↑ K⁺, rhabdomyolysis).

Blood and fluid requirements

Possible marked blood loss
IV: 14–16 ga × 1
NS @ 2–4 mL/kg/h
± Albumin 5%

Blood transfusion to keep Hct > 30. Minimize postop cerebral edema by limiting crystalloid volume to < 10 mL/kg + replacement of UO. Glucose-containing solutions should be avoided; blood glucose levels should be maintained between 80–180 mg%. If volume is needed, albumin 5% should be administered.

Control of blood loss

Keep CPP 60–70 mmHg
Keep SBP > 90 mmHg
Maintain normovolemia

Controlled hypotension generally is not used unless bleeding becomes profuse and difficult to control. ↓ BP is better treated initially with volume replacement than vasopressors.

Monitoring

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

If the injury is extensive or unknown, or if the patient is unstable, invasive monitoring is mandatory. Monitor for VAE if head is elevated above heart. Level the arterial line at the head. EEG, EP, and SjO₂ monitoring may be desirable.

Positioning

[check mark] and pad pressure points.
[check mark] eyes.

For occipital or posterior fossa lesions, patient may be prone or sitting (see Anesthetic Considerations for Cervical Neurosurgical Procedures, Positioning, p. 107). Otherwise, patient will be supine with head in Mayfield-Kees skeletal fixation and turned to the side, and a roll placed under the shoulder on the operative side.

Control of ICP

Adequate anesthesia
Head up 20–30°
Keep SBP ≤ 90 mmHg
STP or propofol infusion

Transient increases in ICP—even up to 50–60 mmHg—are generally tolerated, provided they are promptly terminated. Sustained increases in ICP > 25–30 mmHg are associated with severe neurologic injury and poor outcome. Patients with skull fractures or intracranial bleeding may be on the steep portion of intracranial compliance curve such that any increase in intracranial volume may cause↑↑ ICP.

Hyperventilation to
PaCO₂ = 25–30 mmHg
PaO₂ > 100 mmHg

↓ CO₂ → cerebral vasoconstriction →↓ CBV, ↓ CBF, and ↓ ICP. Patients with diffuse brain injury may have lost cerebrovascular sensitivity to PaCO₂. Despite maintaining adequate ventilation, oxygenation and BP, patients with diffuse head injury often exhibit arterial and CSF lactic acidosis, a further indication of the metabolic derangement that exists in the brain from the injury.

Keep CPP 60–70 mmHg

Control MAP and cerebral venous pressure so that CPP = 60–70 mmHg. In severe, diffuse head injury with loss of autoregulation, some parts of the brain may exhibit ‘luxury perfusion’, while other areas exhibit severe ischemia.

Mannitol 0.25–1.0 g/kg

Vigorous diuresis will commence in about 30 min (if blood volume is adequate) and brain shrinkage will follow. It is often necessary to provide supplemental potassium (20–30 mEq iv slowly).

Furosemide 10–20 mg

Simultaneous administration of furosemide (10–20 mg) is recommended to avoid the transient ↑ CBV and ↑ ICP following mannitol. If mannitol is administered too rapidly, profound hypotension will occur, probably from peripheral vasodilatation.

Complications

Seizures

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

Neurologic deficits
Hemorrhage
SIADH/DI

NPE
↑ICP
DIC

Some patients with severe head injury remain unconscious for weeks or months, without evidencing any substantial neurological recovery. A late complication of head injury is hydrocephalus requiring a shunt procedure.
Neurogenic pulmonary edema may result from massive sympathetic discharge 2° ↑↑ ICP. Rx: ↓ ICP, alpha-blockers to control BP, respiratory support.
TBI is a risk factor for DIC.

Pain management

Fentanyl/propofol infusion

Most patients will remain intubated and sedated postop.

Tests

CT scan
ICP monitor

Unless neurological recovery is rapid, periodic CT scans are obtained postop to follow the intracranial changes. In addition, in many institutions, a device for monitoring ICP postop is placed at the time of operation.

Figure 1.1-13. Microvascular decompression: A. Location of incision. B. Enlargement of burr holes into craniectomy with a rongeur. C. Dural opening on the left side. Note position of venous sinuses. (Reproduced with permission from Wilson CB: Neurosurgical Procedures: Personal Approaches to Classic Operations. Williams & Wilkins, Philadelphia: 1992.)

Position

Normally, lateral (“park-bench”), head elevated 30°; upper shoulder retracted caudally

Incision

Retroauricular (mastoid) (See Fig. 1.1-13A.)

Special instrumentation

Operating microscope; cranial perforator; ± facial nerve monitoring; ± EMG; ± BAER

Unique considerations

Risk of air embolus in head-elevated positions

Antibiotics

Ceftriaxone 1–2 gm iv q d (avoid Ca⁺⁺-containing solutions)

Surgical time

2–3 h

EBL

25–250 mL

Postop care

ICU or close observation unit. Observe for change in neurologic status (e.g., level of alertness, response to commands), usually for 12–24 h.

Mortality

0.2–2%

Morbidity

Facial sensory deficit: 25% (often transient)
Aseptic meningitis: ≤ 20%, usually occurring 3–7 d postop
Hearing loss: 3%
Diplopia (usually transient)
Facial weakness: 2%
Deafness: 1%
Infection
CSF leak
Massive blood loss due to vertebral artery injury or sinus laceration

Pain score

4–6

Age range

40–85 yr (usually 60–70 yr)

Male:Female

~2:3

Incidence

4/1,000,000 (trigeminal neuralgia); 0.06/100,000 (glossopharyngeal neuralgia)

Etiology

Vascular compression of cranial nerve; multiple sclerosis plaque

Associated conditions

HTN; multiple sclerosis

Respiratory

None unless the patient has a long-standing Hx of smoking and has COPD.

Cardiovascular

Many patients will have Hx of idiopathic HTN requiring antihypertensive medications. Good preop control of BP is important because it will make intraop and postop management of BP easier. Anticipate exaggerated hemodynamic response to anesthetic medications.

Neurological

The presenting symptom is pain ± muscle spasm in the maxillary and/or mandibular division of the trigeminal nerve, unaccompanied by any motor or sensory deficits. Identify trigger points so that they may be avoided during mask placement and induction.

Laboratory

None, except for routine preop studies.

Premedication

Generally, patients for these procedures are elderly and do not require any special premedication. Midazolam 1–3 mg iv will provide amnesia for the preop events, if that is desired by patient or surgeons.

Induction

Induction is best accomplished with drugs that cause brain volume reduction, including STP (2–5 mg/kg) or propofol (1–2 mg/kg), followed by neuromuscular blockade and ET intubation.

Maintenance

Standard maintenance (p. B-2) is usually satisfactory. Desflurane has been associated with ↑ PONV. BP is maintained in the normal range during the operation. Hyperventilation to achieve a PaCO₂ of 25–30 mmHg is helpful to ↓ brain volume and ↑ workspace. Once the nerve has been isolated, stop hyperventilation. A spinal drain may be used to remove CSF during the operation and improve exposure. The drain usually is opened at the time of dural opening and closed as soon as surgery on the nerve is complete.

Emergence

The ETT is removed at the conclusion of operation. Postop HTN may need to be controlled with esmolol and/or SNP by continuous pump infusion. Prophylactic antiemetic (e.g., metoclopramide 10 mg and ondansetron 4 mg) should be given 30 min before extubation. The incidence of PONV is high following this procedure.

Blood and fluid requirements

Large blood loss is rare
IV: 18 ga × 1
NS @ 2–4 mL/kg/h

Mannitol 0.5–1 mg/kg is sometimes necessary to provide sufficient brain volume reduction to permit adequate surgical exposure.

Monitoring

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

Invasive monitoring will facilitate intraop and postop BP management.

± EMG and/or SSEP

Sometimes EMG and/or SSEP monitoring of the facial nerve is performed.

Positioning

Lateral, “park bench”
Pillow between legs
[check mark] and pad pressure points.
[check mark] eyes.

Patients usually will be positioned laterally in the “park-bench” position. Padding of the axillae and elbows and placing a pillow between the legs are necessary. A bean bag is often used to hold patient stable in the lateral position.

Complications

PONV
Bleeding
Brain edema

PONV is common and usually requires multimodal treatment (see p. C-1).
Major complications from this operation are uncommon, and postop recovery is usually uneventful. On rare occasion, significant brain edema or bleeding may be experienced.

Pain management

Codeine (30–60 mg im q 4 h)

Tests

CT scan, if neurological recovery is delayed.

Figure 1.1-14. Patient positioning for bifrontal craniotomy with bicoronal skin incision outlined. This position allows the frontal lobes to separate from the anterior cranial fossa with minimal retraction on the frontal lobes. (Reproduced with permission from Tindall GT, Cooper PR, Barrow DL: The Practice of Neurosurgery. Williams & Wilkins, Philadelphia: 1996.)

Position

Supine

Incision

Bicoronal (Fig. 1.1-14); Transnasal for endoscopic

Special instrumentation

Operating microscope; endoscope; image-guidance system

Unique considerations

Brain relaxation desired; lumbar subarachnoid catheter; fascia lata graft

Antibiotics

Ceftriaxone 1–2 g iv q d (avoid Ca⁺⁺ containing solutions)

Surgical time

2–3.5 h, depending on extent of leak or lesion

Closing considerations

Drain often left in epidural space. Anticipate that the application of a full head dressing will jostle patient and ETT →↑ BP + coughing/bucking.

EBL

75–500 mL

Postop care

ICU or close observation unit; Valsalva maneuver, coughing and vomiting can cause ↑↑↑ ICP → recurring CSF leak

Mortality

≤ 5%

Morbidity

Usually < 5% for all complications
Infection (ascending meningitis)
Recurrent CSF leak
Neurologic disability
Nerve injury
Massive blood loss: venous sinus injury

Pain score

3–5

Age range

15–65 yr

Male:Female

~3:2

Incidence

Relatively uncommon neurosurgical procedure

Etiology

Traumatic (73%); congenital; neoplastic

Figure 1.1-15. Inferior exposure of the clivus and chordoma. (Reproduced with permission from Grossman RG, Loftus CM: Principles of Neurosurgery, 2nd edition. Lippincott-Raven, Philadelphia: 1999.)

Figure 1.1-16. A. Basilar impression. The dens has moved superiorly into the foramen magnum (arrow). B. Removal of the dens with a drill. The arch of C1 and a portion of the clivus have been removed. (Reproduced with permission from Donald PJ: Surgery of the Skull Base. Lippincott-Raven, Philadelphia: 1998.)

Figure 1.1-17. A. Pannus formation in a patient with rheumatoid arthritis. B. Removal of pannus. (Reproduced with permission from Donald PJ: Surgery of the Skull Base.Lippincott-Raven, Philadelphia: 1998.)

Position

Supine; head in traction or pins

Incision

Back of oropharynx

Special instrumentation

Operating microscope; I.I.; intraop monitoring = SSEP or BAER; micro drill; intraoral retractors for exposure; image-guided navigation system (optional)

Unique considerations

FOL may be necessary. ETT must be taped securely in a location satisfactory to surgeon. Anode or RAE tube may be helpful. Occasionally, a tracheostomy is performed in advance.

Antibiotics

Ceftriaxone 1g iv (avoid Ca⁺⁺ containing solutions)

Surgical time

2.5–3 h

Closing considerations

Patient may remain intubated postop. C-spine precautions may be necessary.

EBL

25–250 mL

Postop care

ICU or close observation unit; monitor airway for swelling ([check mark] for stridor).

Mortality

0–3%

Morbidity

All < 5%:
Infection
CSF leak
Neurological
Massive blood loss

Pain score

2–4

Age range

18–85 yr (usually 20–60 yr)

Male:Female

~1:2

Incidence

Rare

Etiology

Neoplastic; traumatic; congenital; degenerative

Associated conditions

Rheumatoid arthritis (atlantoaxial subluxation in 25%; basilar compression in 8%); traumatic injury

Figure 1.1-18. The transnasal/transsphenoidal removal of a pituitary tumor. A. The rostrum of the sphenoid is removed (upper). The floor of the sella is removed, the dura opened, and the tumor removed using microcurettes (middle and lower). B. Fat taken from the subcutaneous tissue at the time of the fascial resection is utilized to fill the sphenoid and hold the graft material in position. (Reproduced with permission from Grossman RG, Loftus CM: Principles of Neurosurgery, 2nd edition. Lippincott-Raven, Philadelphia: 1999.)

Position

Supine, head elevated 20–30°

Incision

Endonasal; + abdomen (or thigh) for fat graft; occasionally sublabial, maxillary gingiva;

Special instrumentation

Operating microscope; operating endscope; micro drill; neuronavigation (image guidance)
Throat packs may be used but are usually unnecessary.

Unique considerations

ETT must be taped securely in a location away from the surgeon (usually left side of mouth). Anode or RAE tube may be helpful but is not essential. The generous use of topical vasoconstrictors and the injection of epinephrine-containing solutions may→↑ BP and dysrhythmias. Dissection in the nasal cavity can be painful →↑ BP and ↑ ICP. There is a risk of VAE following inadvertent entry into the cavernous sinus. Valsalva maneuver, jugular compression, or injection of saline through a lumbar intrathecal catheter may be requested to facilitate tumor exposure. Injuries to sphenopalatine or carotid arteries are rare but may be dramatic when they occur.

Antibiotics

Ceftriaxone 1 g iv (avoid Ca⁺⁺ containing solutions)

Surgical time

2.5–3 h

Closing considerations

Possible abdominal or thigh-fat graft. Closure quite fast. Avoid straining and bucking if there has been an intraoperative CSF leak. Remove throat pack before operation.

EBL

25–250 mL

Postop care

Close observation of fluid and electrolytes require frequent monitoring as the patient may develop diabetes insipidus (DI), usually transient, following this procedure.

Mortality

1%

Morbidity

Anterior pituitary insufficiency: 19.4%
DI: 0.5–31%; SIADH: 9–25%
Sinusitis: 8.5%
Septum perforation: 3%
CSF leak: 3.5%
Epistaxis: 3.0%
Loss of vision: 1.8%
Meningitis: 1.5%
Carotid artery injury: 1.1% stroke (rare)
Prolactin Secreting: Few anesthetic implications beyond possible mass effect and ↑ ICP
ACTH Secreting: HTN is very common and is often associated with diastolic dysfunction. OSA is common and may have implications for postop airway management. Hyperglycemia is common and should be treated if blood glucose > 180 mg/dL. ↑ cortisol→ fragile skin and veins → difficult iv access.
Growth Hormone Secreting: Hypertrophy of the mandible, tongue and other facial tissues is common and complicates airway management. Hoarseness suggests laryngeal stenosis or recurrent laryngeal nerve dysfunction. OSA is very common with its attendant risk of postop airway compromise. HTN and diastolic dysfunction (with a need for ↑ filling pressure) are very common. The incidence of intraop ventricular ectopy and SVT is higher in these patients. ECG changes (e.g., ST/T wave changes, conduction abnormality) are common.
Pituitary Apoplexy: Acute hemorrhagic infarction of the pituitary → severe HA, shock, coma, death. Urgent surgical decompression required.

Pain score

2–4

Age range

18–85 yr (usually 30–50 yr)

Male:Female

2:3 (microadenomas)

Incidence

16.7% (autopsy studies); 1.5/100,000/yr diagnosed

Etiology

Neoplastic; traumatic

Associated conditions

Cushing's disease (ACTH); acromegaly (GH); amenorrhea/galactorrhea (prolactin); hyperthyroidism (TSH); hypergonadotropism (FSH; LH); multiple endocrine neoplasia I

Endocrine

Tumors of the pituitary gland are either nonfunctional or secretory. If nonfunctional, they will produce Sx either by their mass effect on adjacent pituitary tissue, or because of extension outside of the sella turcica. Rarely, the mass effect may cause the clinical picture of panhypopituitarism requiring preop treatment with thyroxine, glucocorticoid, and vasopressin. Functional tumors commonly secrete prolactin (→ lactation), ACTH (→ adrenal hyperplasia), or growth hormone (→ acromegaly). Hyperprolactinemia may occur with any tumor 2° loss of inhibition of prolactin secretion.
Tests: Preop endocrine studies, including serum and urinary levels of pituitary, thyroid, and adrenal hormones; appropriate replacement therapy established before proceeding with surgery. “Stress-dose” hydrocortisone (e.g., 100 mg iv q.8.h) is often unnecessary; treatment should be guided by symptoms and periop cortisol levels. Dexamethasone will not interfere with cortisol assays.

Respiratory

No special requirements, unless patient has acromegaly, in which case large facial features, long neck, large tongue, and redundant soft tissue in the oropharynx may make mask fit and ET intubation difficult. If these patients evidence hoarseness or inspiratory stridor, they should have a full clinical and radiological evaluation of the upper airway.
Tests: As indicated from H&P.

Cardiovascular

No special requirements unless patient has acromegaly, in which case they may have HTN, ischemic heart disease, and diabetes.
Tests: As indicated from H&P.

Neurological

Secretory tumors of the pituitary are usually small, confined to the sella, rarely cause ↑ ICP (2° direct tumor effects or by obstruction of 3rd ventricle), and commonly produce Sx of endocrine dysfunction early in their growth. In contrast, nonfunctional pituitary tumors may not produce Sx until they extend beyond the boundaries of the sella, causing HA's (the most common presenting symptom) or compression of the optic chiasm, producing visual field defects (temporal or bitemporal hemianopsia).
Tests: A CT or MRI will delineate the site and size of the tumor, especially if iv contrast material, such as gadolinium, is administered to enhance the margins of the tumor.

Musculoskeletal

If growth hormone is the primary secretant, patient will exhibit Sx of acromegaly, including large hands, feet, head, and tongue. Cushing's myopathy (UE proximal muscle weakness) may affect apparent recovery from muscle relaxant.
Tests: As indicated from H&P.

Laboratory

Metabolic panel, HCT, and others as indicated from H&P. ↓ Na⁺ may indicate DI; ↑↑ Ca⁺⁺ may indicate MEN I.

Premedication

If ↑ ICP is not a concern, patients may benefit from midazolam 1–2 mg iv. In patients with ↑ ICP consider pretreatment with mannitol (e.g., 0.25 gm/kg 20 min before induction). Acromegalic patients may develop airway obstruction following even small doses of sedatives or narcotics.

Induction

If a difficult intubation is anticipated (e.g., severe acromegalic patients), orotracheal intubation will need to be accomplished before induction of GA. LMA placement may be difficult and awake FOL is often the best choice (see p. B-5). Because pituitary tumors generally are confined to the sella turcica and, hence, ICP usually is not increased, a standard induction technique with standard ETT is appropriate (see p. B-2). An oral RAE tube may be preferred by oral surgeons. If increased ICP is of concern, induction should be similar to that used for patients with other kinds of brain tumors (see Anesthetic Considerations for Craniotomy for Tumor, p. 31). Because the surgeon will be working from the patient's right side, the ETT must be positioned at the far left side of the mouth. The surgeon may infiltrate the nasal mucosa with lidocaine and epinephrine →↑ BP + dysrhythmias → possible myocardial ischemia.

Maintenance

Standard maintenance with sevoflurane (or propofol infusion) supplemented with remifentanil (see p. 1539). Generally, no further NMBs are administered beyond ET intubation. With adequate anesthesia, and the head in Mayfield clamp, patient movement of any consequence is highly unlikely. Ventilation is controlled with PaCO₂ maintained in the normal range. Hyperventilation is not desirable, because it makes it more difficult to access the tumor in the sella and establish that it has been removed in its entirety. Following the resection, the surgeon may request a Valsalva maneuver to check for CSF leak.

Emergence

If the patient evidences normal emergence from anesthesia, the ETT should be removed before vigorous coughing ensues. Before removing the ETT, however, make certain that all blood accumulated in the back of the throat is suctioned out, and that oropharyngeal packs which may have been placed in the back of the throat have been removed. An OG tube should be used to suction out the stomach. The surgeon may have packed the nose at the end of operation, forcing the patient to be an obligatory mouth breather. If there is any question about airway patency because of a large tongue, small mouth, or soft-tissue redundancy in the oropharynx, the ETT should be left in place until patient is fully awake from anesthesia. Prophylactic antiemetics (e.g., metoclopramide 20 mg and ondansetron 4 mg) should be given 30 min before extubation.

Blood and fluid requirements

Minimal blood loss usual
Potential large blood loss
IV: 16–18 ga × 1
NS @ 4–8 mL/kg/h

Blood loss is minimal, unless the surgeon inadvertently enters the internal carotid artery or cavernous sinus. Additional iv access may be necessary.

Monitoring

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

± CVP line
± precordial Doppler

Monitor for VAE in semisitting position if > 30°.
Ulnar artery flow may be compromised in acromegaly—document Alan test before placing radial artery catheter.
CVP line should be placed in patients at significant risk for VAE or as medically indicated.

Positioning

[check mark] and pad pressure points.
[check mark] eyes.
Shoulder roll
Table turned 90–180°

The surgeon will use an operating microscope or endoscope, which means that the anesthesiologist will be positioned at the side or foot. Anesthetic hoses and intravascular lines must be long enough to be accessible.

Complications

Carotid injury
VAE

Potential for large volume hemorrhage and intraop stroke. Deliberate hypotension may facilitate repair. Carotid compression may →↓ CBF → ischemia.

Complications

Hypopituitarism
Diabetes insipidus (24–48h postop)
CSF leak
SIADH
Cranial nerve injury

Replacement therapy with steroids is necessary in hypopituitary patients until normal pituitary function returns. Occasionally, patients will develop DI postop → polyuria and ↓ urine specific gravity < 1.005. Rarely, this may occur in the PACU necessitating fluid replacement and/or DDAVP.

Pain management

Codeine (30–60 mg im q 4 h)

HA is the most common complaint.

Tests

CT scan
Serum cortisol
Visual acuity/fields

If a patient exhibits any delay in emergence from anesthesia and surgery, or any new neurologic deficits emerge postop, a CT scan is ordinarily obtained.

Figure 1.1-19. Pathways of CSF flow and potential sites of obstruction. (Reproduced with permission from Tindall GT, Cooper PR, Barrow DL: The Practice of Neurosurgery, Vol III. Williams & Wilkins, 1996. Orig. from Scott RM: Hydrocephalus. Concepts in Neurosurgery, Vol III. Williams & Wilkins, Philadelphia: 1990.)

Figure 1.1-20. A. The catheter is threaded from the abdominal incision to the cranial incision. B. Insertion of the ventricular catheter. (Reproduced with permission from Meyer FB: Atlas of Neurosurgery: Basic Approaches to Cranial and Vascular Procedures. Churchill Livingstone, 1999).

VP Shunt

VA Shunt

ETV

Position

Supine, with head turned to contralateral side

⇐

Incision

Scalp, either coronal and retroauricular, or parietal; + neck and abdomen

Scalp, either coronal and retroauricular or parietal; + neck

Special instrumentation

Ventricular endoscope (optional)

⇐ + I.I.

Unique considerations

Patient to be treated as if there is ↑ ICP.

⇐

Antibiotics

Ceftriaxone 1–2 g iv q d (avoid Ca⁺⁺ containing solutions)

⇐

Surgical time

1 h

⇐

EBL

5–25 mL

⇐

Postop care

PACU → room; usually kept flat for 24 h.

⇐

Mortality

< 1%

⇐

Morbidity

Infection: < 15%
Neurological:
Intracranial bleed: < 1%
Subdural hematoma: < 1%
Hardware failure: < 1%

⇐

Basilar artery injury
↑↑ ICP →↓↓ HR or asystole

Pain score

4–6

2–4

Age range

Newborn-elderly

Male:Female

1:1

Incidence

Common

Etiology

Congenital (3–4/1000 live births); acquired; neoplastic; infectious; posthemorrhagic

Associated conditions

Subarachnoid hemorrhage; myelodysplasia; spina bifida (95% incidence); intraventricular hemorrhage; intraventricular tumor

Cardiovascular

↑ ICP →↑ BP + ↓↓ HR (Cushing's response)
Tests: As indicated from H&P.

Neurological

The most common presenting Sx is HA. If hydrocephalus is severe, Sx of ↑ ICP (> 15 mmHg) (e.g., N/V, drowsiness, papilledema, Sz, and focal neurological defects) develop.

Laboratory

Tests as indicated by H&P.

Premedication

Usually not required; should be avoided in patients with ↑ ICP.

Induction

If ↑ ICP, iv induction with STP (2–5 mg/kg) or propofol (1–2 mg/kg) is preferred, because of their ability to decrease cerebral blood volume and, hence, to decrease ICP. ET intubation is accomplished with the use of a NMB (e.g., vecuronium [0.1 mg/kg]; or rocuronium [0.6–1 mg/kg]).

Maintenance

Isoflurane ≤ 1% or sevoflurane < 2%, inspired with 50:50 N₂O/O₂ mixture. Depending on duration of operation, additional doses of vecuronium (0.1 mg/kg) or rocuronium (0.2 mg/kg) may be needed. Maintain normal temperature in children by keeping OR warm (78F) and using a forced-air warming blanket. Ventilation should be controlled. TV and frequency should be adjusted such that the PetCO₂ = 35–40 mmHg. Hyperventilation and hypocarbia are undesirable because they make cannulation of the ventricle(s) more difficult. Maintain normotension. During endoscopic 3rd ventriculostomy (ETV), puncture of the floor of the 3rd ventricle may be associated with significant ↓↓ HR or asystole. The surgeon should be immediately informed if bradycardia occurs.

Emergence

ETT is removed at the conclusion of the anesthetic. Prophylactic antiemetic (e.g., metoclopramide 10–20 mg and ondansetron 4 mg) should be given 30 min before extubation.

Blood and fluid requirements

IV: 18–20 ga × 1
NS @ 4–6 mL/kg/h

Administer crystalloid, usually NS. Blood is rarely, if ever, necessary.

Monitoring

Standard monitors (see p. B-1).

Invasive monitors as indicated

Positioning

Table turned 180°
[check mark] and pad pressure points.
[check mark] eyes.

Supine with a bolster under the shoulder on the operative side. The head, chest, and abdomen are prepped, so all anesthesia equipment and lines must be at the sides of the patient.

Complications

Valve malfunction

↓↓ HR or asystole
Basilar artery injury

Major intraop complications from this operation are rare.
ETV may be associated with severe bradycardia and injury to the basilar artery or its branches.

Pain management

Children < 2 yr: Tylenol suppositories
(10–15 mg/kg q 4 h)
Adults: meperidine 10–20 mg iv prn

Figure 1.1-21. A. A Y-shaped dural incision is made through the occipital craniectomy and laminectomy. B. Opening the arachnoid mater to gain access to the cerebellar tonsils and fourth ventricle. C. Loose closure of dura with graft. (Reproduced with permission from Meyer F: Atlas of Neurosurgery: Basic Approaches to Cranial and Vascular Procedures. Churchill Livingstone, 1999.)

Position

Prone or sitting

Incision

Midline posterior, posterolateral thigh for fascia lata graft (optional)

Special instrumentation

Operating microscope

Unique considerations

Risk of air embolus; brain stem manipulation can cause BP and pulse instability; dural patch used to expand dura at foramen magnum

Antibiotics

Ceftriaxone 1–2 g iv q d (avoid Ca⁺⁺ containing solutions)

Surgical time

2.5–3.5 h

Closing considerations

BP control to ensure adequate hemostasis

EBL

25–250 mL

Postop care

ICU or constant observation unit; neurological function monitored.

Mortality

0–3% (usually respiratory arrest)

Morbidity

Respiratory depression: 14% up to 5 d postop
All others < 5%:
Infection
Neurological: dysphagia and ↓ gag reflex

Aseptic meningitis
CSF leak
Massive blood loss; vertebral artery or transverse sinus injury

Pain score

5–7

Age range

Infant–70 yr; Chiari I: average age = 41 yr

Male:Female

~1:1

Incidence

Relatively rare neurosurgical procedure

Etiology

Congenital; acquired, S/P lumboperitoneal shunting

Associated conditions

Hydrocephalus; syringomyelia; scoliosis; myelodysplasia

Figure 1.1-22. OR layout for frameless stereotactic surgery.

Frame-Based Stereotaxy

Frameless Stereotaxy

Radiosurgery

Functional Neurosurgery

Position

Supine or prone

Sitting, supine, prone, or lateral

Supine or prone

Supine, head fixed to floor stand

Incision

0.5–2 cm, scalp

1–12 cm, scalp

None

1–3 cm, scalp

Special instrumentation

Stereotactic treatment arc

Sensor array, pointer, computer, monitor, dynamic reference frame

Linear accelerator (LINAC)
Cyberknife

Electrophysiologic monitoring equipment, image-guided navigation, C-arm

Unique considerations

Key for emergency: removal of frame

1. Minimize brain shift.
2. No patient movement during registration.
3. Clear line-of-sight between camera and dynamic reference frame.

Extended anesthesia in several different locations

Patient must be awake, able to cooperate with testing.

Antibiotics

Ceftriaxone 1g iv (avoid Ca++ containing solutions)

Ceftriaxone 1g iv (avoid Ca⁺⁺ containing solutions)

None

Ceftriaxone 1g iv (avoid Ca++ containing solutions)

Surgical time

0.5–1.5 h

2–6 h

5–8 h

2–6 h

EBL

< 10 mL

20–1000 mL

None

< 100 mL

Postop care

PACU

ICU

PACU

Neuroobservation unit

Mortality

< 0.5%

1%

None

< 1%

Morbidity

Overall: < 1% Symptomatic intracerebral hemorrhage

InfectionAir emboliHemorrhageStrokeSzWorsening edema

N/V: 2–3%

N/ V: 1–10%
Intracerebral hemorrhageNew neurologic deficits

Pain score

2

4

2

2

Age range

All ages

⇐

0–12 yr

18–90 yr

Male:Female

1:1

⇐

⇐

⇐

Incidence

Uncommon

Unusual

⇐

Rare

Etiology

Tumor; infection; AIDS; demyelinating syndromes

Tumor; vascular malformations; epilepsy

⇐

Parkinson's disease; pain syndromes; psychiatric syndromes

Neurological

Neurological Sx vary (depending on site and size of the lesion) and they should be carefully documented. In addition to the usual tests, a CT or MRI scan is obtained preop with the frame in place to determine stereotactic coordinates. Once the coordinates are established, the frame or fiducial markers must not be moved until the operation is complete.

Laboratory

Tests as indicated from H&P.

Induction

If MAC is planned, O₂ by nasal prongs is administered, and the patient is lightly sedated with combinations of propofol 25–50 mcg/kg/min ± midazolam 1–4 mg/kg in divided doses to provide amnesia ± remifentanil 0.02–0.05 mcg/kg/min to provide analgesia. It is important that the patient be able to communicate with the surgeon as needed throughout the operation. For functional neurosurgery (e.g., pallidotomy), sedation should be minimized to preserve normal electrophysiological activity essential for mapping. If GETA is needed in a framed stereotactic procedure, FOL is necessary before inducing anesthesia because the frame precludes intubation by direct laryngoscopy (see p. B-5). After ET intubation is established, anesthesia may be induced with STP 2–5 mg/kg or propofol 1–2 mg/kg, followed by a nondepolarizing NMB to facilitate positioning of patient.

Maintenance

If GA is used, maintenance is the same as for a tumor (see Anesthetic Considerations for Craniotomy for Tumor, p. 31) or AVM (see Anesthetic Considerations for Craniotomy for Intracranial Vascular Malformations, p. 19). If children are to be transported from the site of placement of the stereotactic frame to the radiologic suite and then to the OR, it is best to use a propofol infusion (e.g., 75–150 mcg/kg/min) with spontaneous or controlled ventilation to assure adequate ventilation and oxygenation during transport and study. Opiates and nondepolarizing NMBs should not be administered until the child is in the operating suite.

Emergence

ETT generally is removed at the conclusion of the operation. Prophylactic antiemetic (e.g., metoclopramide 10–20 mg and ondansetron 4 mg) in adults should be given 30 min before extubation.

Blood and fluid requirements

IV: 16–18 ga × 2 (adults); 20–22 ga (children)
NS @ 4–6 mL/kg/h

Blood loss is minimal because the volume of tissue removed is small.

Monitoring

If local anesthesia: standard monitors (see p. B-1).
If GA:
Arterial line
CVP line
UO

Positioning

[check mark] and pad pressure points.
[check mark] eyes.

Complications

Bleeding

Focal bleeding may occur postop, causing onset of a neurological deficit.

Pain management

Vicodin (1–2 mg po q 4 h prn)

Tests

CT or MRI scan, if a new neurological deficit occurs.