73: Anesthesia for Craniotomy

Published on 06/02/2015 by admin

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CHAPTER 73 Anesthesia for Craniotomy

Daniel J. Janik, MD [Colonel (Retired), USAF, MC]

1 Are there particular anesthetic problems associated with intracranial surgery?

Space-occupying intracranial lesions are associated with disturbed autoregulation in adjacent tissue; vascular malformations and aneurysms are accompanied by altered vasoreactivity (particularly if preceded by subarachnoid hemorrhage [SAH]); and traumatic injuries sometimes require contradictory efforts to minimize brain swelling while maximizing systemic resuscitation. In addition, there are specific neurophysiologic concerns: control of cerebral blood flow and volume, anticipation of the effects of surgery and anesthetic management on intracranial pressure (ICP) dynamics, and maintenance of perfusion. In addition, as for any operative procedure, the patient should be unconscious and remain unaware of intraoperative stimuli; adrenergic responses of the patient to intraoperative events should be attenuated; and the surgeon’s approach to the operative site should be facilitated.

2 How is the anesthetic requirement different in the brain and related structures?

During anesthesia for craniotomy the level of nociceptive stimulus varies greatly. Laryngoscopy and intubation require deep levels of anesthesia to block potentially harmful increases in heart rate, blood pressure, and brain metabolic activity, which may increase cerebral perfusion and brain swelling. Except for placement of pins in the skull for head positioning, considerable time may pass during positioning and operative preparation with no noxious stimulus. Incision of scalp, opening of the skull, and reflection of the dura provide increased surgical stimulus, only to be followed by dissection of the brain or pathologic tissue, which is almost completely free of nociceptive nerve fibers. Occasionally vascular structures of the brain may respond with an adrenergic surge during surgery, particularly if an SAH has occurred in the region of the procedure.

3 Should monitoring be different during a craniotomy?

The usual noninvasive monitors are used for every patient, including pulse oximetry, stethoscope, noninvasive blood pressure cuff, temperature, electrocardiogram, end-tidal and inspired gas monitors, and peripheral nerve stimulator. End-tidal anesthetic agent monitoring has some theoretic value, particularly in managing emergence. Continuous arterial pressure monitoring is often used to assess hemodynamic changes, which may develop acutely with cranial nerve root stimulation or slowly because of minimal intravascular volume repletion. Some forego the radial artery catheter for very superficial craniotomies such as mapping of the seizure focus directly with cortical electrodes; few anesthesiologists would use a central venous catheter unless there were a high risk of air entrainment in the venous system or a likelihood of using vasoactive infusions perioperatively. Occasionally continuous electroencephalography is used, not so much as an intraoperative monitor but rather as a means for the surgeon to localize diseased tissue. The various forms of processed electroencephalogram (EEG) monitors may facilitate the use of total intravenous anesthesia when indicated. Comparison of ipsilateral and contralateral evoked potentials has been reported during aneurysm surgery. Jugular bulb venous oxygen saturation and transcranial oximetry have been described as monitors of oxygen delivery and metabolic integrity of the brain globally but are not used regularly in intraoperative settings. Some patients, especially after trauma, have subdural, intraventricular, or cerebrospinal fluid pressure monitors in use intraoperatively.

4 Discuss the considerations for fluid administration during craniotomy

Volume depletion from overnight fasting and volume redistribution from vasodilating anesthetic agents result in relative hypovolemia. Each patient should be evaluated individually to ensure adequate myocardial, central nervous system, and renal perfusion. Special attention must be directed toward stability of intracranial volume. Before opening of the dura, sudden increases in intravascular volume may cause deleterious increases in ICP, especially in situations involving intracranial masses or contusions or intraparenchymal, subdural, or epidural hematomas. Therefore, although fluids must be given to avoid hypovolemia and hypotension, exuberant bolus administration is to be avoided.

The content of the fluids used during a craniotomy is also important. An isosmolar intravenous fluid should be chosen. Unless hypoglycemia is documented, glucose-containing solutions should be avoided. In both clinical and experimental settings in which glucose is used in the resuscitation fluids after head injury, outcome is worse. Saline is the appropriate fluid for use during craniotomy. Balanced salt solutions may be used if their osmolarity approximates or exceeds that of the serum. Ringer’s lactate has a slight theoretic disadvantage because lactate is metabolized and the solution becomes hypotonic. Colloid solutions such as 5% albumin or 3% NaCl are equivalent solutions for acute volume replacement before packed red cell administration. Often 25% albumin is used for pressure support when blood replacement is not needed. Hetastarch solutions should be limited to 15 to 20 ml/kg body weight during craniotomies because of concerns that larger quantities are associated with impaired coagulation in vitro.

5 When are measures for brain protection required?

Brain protection refers to the maneuvers by the anesthesiologist to maintain a balance between brain metabolism and substrate delivery and to prevent secondary injury to regions of the brain after an episode of ischemia. The need for brain protection should be anticipated after head trauma and brain contusion and during procedures for the correction of intracranial aneurysms or arteriovenous malformations. Of primary importance is adequate delivery of oxygen and energy substrates to brain tissue by ensuring optimal blood oxygen content and cerebral blood flow.

6 How can the brain be protected?

Historically long-acting barbiturates have been used for metabolic suppression for refractory intracranial hypertension. The goal is suppression of brain activity with resultant reduction of metabolism, which is reflected by a flat EEG.

In the intraoperative setting metabolic suppression is needed when a major artery is temporarily clipped to facilitate access to an aneurysm. The EEG correlate is “burst suppression” in which the typical anesthetic slow-wave activity slows to random bursts of electrical activity. Burst suppression can be achieved by rapid infusion of thiopental, propofol, or etomidate. Hypothermia has long been known to reduce brain metabolism (and to slow the EEG). Mild to moderate hypothermia (32.5° to 34° C) has not been found to be useful for intraoperative brain protection. The global metabolic suppression secondary to hypothermia decreases not only neuronal electrical activity but also housekeeping

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