Anesthesia for Craniotomy



Providing an anesthetic for neurosurgical procedures that include a craniotomy can involve unique anesthetic goals otherwise not encountered in routine practice. For example, tight hemodynamic control and cerebral protection techniques during aneurysm clipping or providing moderate sedation during intracranial tumor resection allow patients to cooperate during speech mapping. Anesthesiologists have suggested numerous dosing regimens to meet these goals. This chapter will briefly summarize a few of those designed for aneurysm clipping and awake procedures for tumor resection.



The incidence of unruptured intracranial aneurysms is thought to be near 2%. Approximately 10 in 100,000 people suffer a brain aneurysm rupture, making it frequently encountered problem in the operating room. The prognosis is poor; 40% of ruptured brain aneurysms are fatal and of those that survive, about two thirds have permanent neurologic deficits.1,2

Perioperative management of these patients focuses on 5 potentially conflicting goals:

  1. Maintain adequate cerebral perfusion pressure (CPP) to prevent cerebral ischemia and cerebral vasospasm.

  2. Maintain a low transmural pressure (TMP) gradient to prevent rupture of the aneurysm.3

  3. Minimize brain swelling.

  4. Minimize large swings in intracranial pressure (ICP).

  5. Provide an anesthetic that allows for a rapid emergence.

To accomplish this goal, a basic understanding of the aneurysm’s TMP is useful. TMP (the equivalent of the CPP) is defined by Equation 35–1.

(35–1)TMP = CPP = MAP – ICP or CVP

where MAP is the mean arterial pressure and CVP is the central venous pressure. Normal values for MAP, ICP, CVP, and CPP are presented in Table 35–1. The higher value between ICP and CVP is used. TMP describes the relationship between the pressure within the aneurysm (arterial blood pressure) and the pressure surrounding the aneurysm. Abrupt increases in the transmural pressure gradient may lead to aneurysmal rupture and poor outcomes.

Table 35–1Normal values for pressures that influence aneurysm transmural pressures.

Subarachnoid hemorrhage (SAH) associated with aneurysmal rupture can be linked with numerous physiologic derangements (Table 35–2) that should be considered when formulating an appropriate anesthetic as well as drugs that may be used in the perioperative period to manage these derangements.

Table 35–2Physiologic derangements associated with subarachnoid hemorrhage.


With this hemodynamic goal in mind, premedication to treat anxiety and pain should be considered for each patient, keeping in mind that no specific agent or combination of agents is applicable for all patients. It may be useful to consider the clinical grade of SAH, patient comorbidities, cardiac and pulmonary status, and ICP when formulating the premedication plan to put into perspective the amount of drug if any that will be required. Tables 35–3 and 35–4 present two grading systems used to classify SAHs (ie, the Hunt and Hess grading scale for SAH and the World Federation of Neurological Surgeons Grading Scale for aneurysmal SAH)5,6; these events can be associated with significant cardiac and pulmonary morbidity.

Table 35–3Hunt and Hess grading scale for subarachnoid hemorrhage5.

Table 35–4World federation of neurological surgeons grading scale for aneurysmal subarachnoid hemorrhage.6

Although anxiety can lead to worrisome hypertension, possibly resulting in aneurysmal rupture, oversedation may cause respiratory depression and unwanted increase in ICP and increased cerebral blood flow with rising arterial PCO2 levels. Careful titration of benzodiazepines and/or opioids is warranted given that many patients present in the preoperative period already on medications such as calcium channel blockers (ie, nimodipine to minimize cerebral vessel vasospasms), anticonvulsants, steroids, and possible analgesics (to treat severe headaches). These medications should be continued throughout the perioperative period. Special care should be taken when administering a benzodiazepine in the presence of an opioid, as each drug can enhance the effects of one another in a synergistic fashion.


As with premedication, a major goal of induction is to properly manage blood pressure. A primary focus is to limit the hypertensive response to laryngoscopy while at the same time maintaining appropriate CPP to minimize changes in the TMP gradient across the aneurysm. The depth of anesthesia should match the stimulation associated with laryngoscopy, tracheal intubation, and subsequent 3-point rigid cranial fixation. This can be accomplished using multiple techniques, and achieving these goals is more imperative than the actual drugs used. Amnesia can be induced by thiopental 2 to 5 mg/kg (where available), propofol 1 to 2 mg/kg, or etomidate 0.1 to 0.3 mg/kg. Adrenal suppression with etomidate should be considered when selecting an induction agent in critically ill patients.7,8 These induction agents all decrease cerebral blood flow and subsequently ICP. An opioid is necessary to blunt the sympathetic stimulation and hypertensive response to laryngoscopy and intubation. Fentanyl 3 to 5 mcg/kg or remifentanil 0.25 to 1 mcg/kg will achieve this goal. Fentanyl and remifentanil should be administered 3 to 5 minutes and 1 minute, respectively, before laryngoscopy and tracheal intubation to allow effect-site concentrations to reach their maximal level (Figure 35–1). Caution should be exercised when administering remifentanil in large bolus doses, as it is vagotonic and may cause bradycardia. Muscle relaxation for intubation and patient positioning is typically accomplished with a nondepolarizing muscle relaxant. Succinylcholine causes an undesirable increase in ICP, while nondepolarizing muscle relaxants do not. Rocuronium 0.7 to 1.2 mg/kg or vecuronium 0.15 mg/kg is typically used to achieve adequate muscle relaxation. Additionally, lidocaine 1.5 to 2 mg/kg or esmolol 0.5 mg/kg can be administered to further blunt the hemodynamic response to laryngoscopy and intubation.

Figure 35–1

Simulation of an induction with midazolam (2 mg), fentanyl (2 mcg/kg), and propofol (2 mg/kg). The top plot presents the predicted effect-site concentration (Ce) levels, and the bottom plot presents the predicted loss of response to laryngoscopy and tracheal intubation. Simulations used published pharmacokinetic and pharmacodynamic models to predict effect site concentrations and effects.9,10,11,12,13, and 14 The top plot illustrates the differences between drugs in the time required to reach the peak Ce (approximately 6 minutes for midazolam, 4 minutes for fentanyl, and 1.5 minutes for propofol). The timing of each bolus was such that each drug reached a peak concentration at nearly the same time to provide maximal effect during laryngoscopy (midazolam, followed 2 minutes later by fentanyl, followed 2.5 minutes later by propofol). The bottom plot presents the difference in the duration of effect for all 3 drugs combined, for propofol and fentanyl, for propofol alone, and for fentanyl alone. Of note, the midazolam prolonged the duration of effect (no response to laryngoscopy and tracheal intubation) for approximately 1 minute. Propofol administered without an opioid provided a shorter window of no response to laryngoscopy (4–5 versus 2–3 minutes above a 95% probability of no response for propofol alone and propofol combined with fentanyl and midazolam).

As is common with induction, hypotension may occur and should be treated promptly to maintain the TMP. A reasonable goal is to maintain the mean arterial blood pressure within 10% to 20% of baseline pressures.

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Dec 30, 2018 | Posted by in ANESTHESIA | Comments Off on Anesthesia for Craniotomy
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