73: Anesthesia for Craniotomy

Published on 06/02/2015 by admin

Filed under Anesthesiology

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 2064 times

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 functions, including cellular homeostasis and membrane integrity. Production of excitatory neurotransmitters during reperfusion of ischemic tissue may also be suppressed by modest hypothermia.

Much attention has been directed to suppression of the neuroexcitation that occurs with reperfusion after regional or global brain ischemia. Calcium influx into glial cells and vascular smooth muscle may be suppressed by calcium channel blockade; free radicals that are generated may be scavenged by mannitol, and increased intracellular hyperglycemia may be prevented by avoiding systemic hyperglycemia. Cerebral protection remains a fruitful area of investigation.

7 How is the choice of anesthetic agent made?

Choice of anesthesia for craniotomy is based on an understanding of the pharmacologic properties of hypnotic agents, inhalation agents, opioids, and muscle relaxants and on a balancing of beneficial and potentially adverse effects. Whichever agents are chosen, the goals are postoperative hemodynamic stability associated with an awake, neurologically assessable patient.

image Hypnotic agents: Thiopental effectively blocks conscious awareness and reduces the functional activity of the brain, ICP, cerebral blood flow, and brain metabolism. Propofol has similar effects and is eliminated more rapidly. Etomidate and midazolam are only slightly less effective in metabolic suppression. An agent is selected on the basis of associated hemodynamic effects, anticipated difficulty of regaining consciousness, and cost.
image Inhalation agents: The differences between isoflurane, desflurane, and sevoflurane concerning metabolic suppression and cerebral blood flow are slight. All cause suppression of brain activity while preserving or enhancing cerebral blood flow. Cost and speed of elimination are concerns in selection. Nitrous oxide has been shown to increase ICP and cerebral blood flow in humans, although this effect is modified by the prior administration or coadministration of other hypnotic, analgesic, and anesthetic agents.
image Opioids: All opioids have negligible effects on cerebral blood flow and small effects on cerebral metabolism. Chiefly they block adrenergic stimulation, which increases brain activity. They are useful as part of a balanced anesthesia. More fat-soluble opioids such as morphine and hydromorphone may be eliminated so slowly that they cause respiratory depression after the procedure is completed. Respiratory depression that causes hypercarbia results in undesirable increases in cerebral blood flow and potentially ICP, which is to be avoided after a craniotomy. Newer short-acting synthetic opioids may also cause residual respiratory depression after prolonged infusion.
image Muscle relaxants: Depolarizing muscle relaxants are generally not used in the setting of intracranial pathology unless emergent control of the airway is necessary. Although theoretic hemodynamic differences exist among the nondepolarizing muscular relaxants, these are of little importance during a craniotomy. The main criteria for choosing a nondepolarizing muscular relaxant are the duration of neuromuscular blockade desired, route of elimination, and cost.

8 What are the concerns for patient positioning during a craniotomy?

Because craniotomies tend to be lengthy procedures, protecting vulnerable peripheral nerves and pressure-prone areas from injury is essential. Provisions must be made to prevent preparation solutions from entering the eyes. Generally the head is fixed in position with pins clamped against the outer table of the skull. Because the head is held in a fixed position, any patient movement will stress the cervical spine. Muscle paralysis must be maintained all the time the head is secured in the holding device.

In every craniotomy the risk of air entrainment into the venous system must be estimated. Whenever the head is positioned 10 cm above the midthorax (>20-degree elevation), a potential negative pressure exists between the venous sinuses of the head and the central venous system. Air entrained in the central venous system may collect in the right side of the heart and interfere with preload and pulmonary flow. Air can potentially cross the intra-atrial septum and, if a patent foramen ovale is present (20% of patients), become a paradoxical air embolus to the systemic circulation. This risk is very significant in sitting-position craniotomies. End-tidal CO2, end-tidal nitrogen, transesophageal echocardiography, and precordial Doppler are sensitive indicators of venous air. In high-risk situations a multiorificed right atrial catheter should be placed for removal of air bubbles.

9 Why do some patients awaken slowly after a craniotomy?

Continuous infusion of opioid as part of balanced anesthesia leads to prolonged redistribution and persistent sedation. Residual volatile anesthetic or barbiturate may contribute to slow awakening. However, all these residual anesthetic effects are overcome simply by waiting and providing respiratory support. Use of agents of short duration is beneficial. Slow awakening that persists for more than 2 hours is rarely an effect of residual anesthesia. The patient who is unresponsive for several hours after a craniotomy should be evaluated for increased ICP, embolic phenomenon, brainstem ischemia, or intracranial masses. Evaluation should be a joint effort of the neurosurgeon and anesthesiologist. The anesthetic technique should be tailored to facilitate a rapid emergence for early testing of neurologic function.

KEY POINTS: Anesthesia For Craniotomy image

1. Always maintain a cerebral perfusion pressure of at least 50 mm Hg but preferably 70 mm Hg or higher.
2. If ICP is high, as evidenced by profound mental status changes of radiologic evidence of cerebral swelling, avoid volatile anesthetics and opt instead for a total intravenous anesthetic technique.
3. Remember that patients with profound mental status changes require little or no sedation before induction of general anesthesia.
4. Ensure deep anesthesia before intubation to avoid abrupt increases in cerebral blood flow.
5. Patients with large mass lesions may exhibit cardiovascular instability on induction of anesthesia because of intravascular volume reduction as a consequence of aggressive treatment of intracranial hypertension.
6. Rapid emergence from anesthesia facilitates early testing of neurologic function.

10 What anesthesia problems are unique to surgery on the intracranial blood vessels?

image SAH: Aneurysms of the intracerebral arteries may be diagnosed after SAH. Neurologic impairment after SAH ranges from headache and stiff neck (Hunt-Hess grade I) to deep coma (Hunt-Hess grade V). Initial resuscitation includes observation, tight control of blood pressure, and support of intravascular volume (hypervolemic, hyperosmolar, normotensive). The optimal time for surgical clipping of the aneurysm is within the first few days of hemorrhage. After 5 to 7 days following SAH the risk of rebleeding remains high, but the risk of vasospasm of the vessel feeding the aneurysm markedly increases because of irritation from the breakdown of old blood. Invasive monitoring of arterial pressure and central venous pressure is required to facilitate maintenance of hemodynamic stability and guide volume replacement. The minimal approach to brain protection is to maintain normal oxygen delivery to the brain tissue. Metabolic suppression by electroencephalographic burst suppression may be done at the time of temporary vessel clipping but may result in poor outcome when accompanied by hypotension.
image Rebleeding: Approximately 30% of intracranial aneurysms that have bled will rebleed at some time if untreated. In the initial few days the hydrodynamic forces on the aneurysm wall are caused by the systolic blood pressure resisted by the tension of the aneurysmal wall. Larger aneurysms have less wall tension for any part of the aneurysmal surface. Rebleeding of the aneurysm before the opening of the dura is catastrophic, requiring the surgeon to approach the bleeding vessel blindly, perhaps temporarily clipping major feeding vessels. Although it might seem reasonable to induce hypotension during the opening of the dura, should a rebleed occur hypotension adversely affects regional perfusion and may promote vasospasm.
image Vasospasm: Vasospasm can occur after any SAH, regardless of clinical stage. The end result of persistent vasospasm is ischemic stroke in the region of distribution of the aneurysmal artery, resulting in permanent neurologic damage after SAH. Diagnosis is by angiography, and many times an angiogram is requested on the first postoperative day to guide therapy. Maintaining hypervolemic normotensive hemodynamic status is the first line of prevention of vasospasm and should be maintained intraoperatively. Physiologically vasospasm is caused by mediator release in the vascular smooth muscle in response to hemoglobin in the interstitium, ending in calcium influx into the cellular walls of the artery and causing persistent vasoconstriction. Calcium channel blockade has been advocated but has shown mixed results. Thromboplastin activators have been used experimentally by irrigation in the region of the aneurysmal bleed with some success. The main lines of prevention are intraoperative irrigation of the hematoma early in the SAH course and maintenance of favorable hemodynamics after surgery.

11 Are there special anesthetic problems associated with brain tumors?

Mass lesions of the brain cause problems for the anesthesiologist because of their size and location. Frontal tumors grow to large size without producing neurologic symptoms or increased ICP. Supratentorial tumors of the motor and sensory cortical regions present with seizures, localizing neurologic signs, and increased ICP. Posterior fossa masses in adults cause disturbances in gait, balance, proprioception, or cranial nerve impingement. There is a penumbra around all intracranial tumors where the adjacent brain loses autoregulatory function. Thus on induction regional blood flow in these areas may increase in response to aggressive fluid replacement or increased systolic blood pressure. After the resection is completed, this penumbra may respond to reperfusion with swelling. The end result may be either preincisional or postoperative increases in ICP. Infratentorial posterior fossa tumors cause particular problems for the anesthesiologist. Tumors are generally small but may surround complex vascular channels of the basilar, posterior communicating, and cerebellar arteries. Tumors may arise from the glia surrounding the cranial nerve roots or impinge on them. Simple dissection of a brainstem tumor can cause disturbance of heart rate and rhythm or blood pressure when nerve roots are retracted. The surgical approach to the posterior fossa involves awkward positioning, from sitting to lateral to prone to park bench. At the least, any of these positions requires careful attention to the position of the endotracheal tube to avoid migration to an endobronchial position or out of the glottis. Venous air embolism must be anticipated. The plan for anesthesia must also allow for intraoperative monitoring of auditory-evoked potentials, somatosensory-evoked potentials, or motor-evoked potentials if indicated. Any of these evoked potentials can be suppressed by hypnotic and inhaled anesthetic agents.

12 Are there other anesthetic concerns during craniotomies?

Transsphenoidal surgery, although not strictly a craniotomy, involves manipulation of ventilation to raise the PaCO2 and ICP, which forces the pituitary into a more easily visualized position.

Rapidly deteriorating neurologic status after closed head injury often leads to emergency intubation, neuroradiologic studies, and emergent craniotomy. The increase in ICP that causes the clinical deterioration sometimes progresses to involve brainstem compression. The physiologic response to increased ICP is systemic hypertension and in the late stages bradycardia, known as the Cushing reflex. This reflex should be anticipated and treated by measures to reduce ICP rather than pharmacologic treatment of the hypertension per se. Typically, when the cranium is opened and brainstem pressure is reduced, the blood pressure decreases, but if aggressive treatment of elevated blood pressure has been undertaken, the drop in blood pressure may have disastrous consequences.

Craniotomies in pediatric patients are in principle the same as in adults but fortunately rarer. The intracranial pathology that is most common in the pediatric group is the posterior fossa tumor, particularly cerebellar astrocytoma. Positioning, cranial nerve root stimulation, and venous air embolus are concerns during posterior fossa resections in children.

SUGGESTED READINGS

1. Avitsian R., Schubert A. Anesthetic considerations for intraoperative management of cerebrovascular disease in neurovascular surgical procedures. Anesthesiol Clin. 2007;25:441-463.

2. Drummond J.C., Patel P.M. Neurosurgical anesthesia. In Miller R., editor: Anesthesia, ed 6, Philadelphia: Churchill Livingstone, 2005.

3. Pasternak J.J., Lanier W.L.Jr. Diseases affecting the brain. In Hines R.L., Marschall K.E., editors: Stoelting’s anesthesia and coexisting diseases, ed 5, Philadelphia: Churchill Livingstone, 2008.

4. Rozet I., Vavilala M.S. Risks and benefits of patient positioning during neurosurgical care. Anesthesiology Clin. 2007;25:631-653.

Related posts:

58: Congenital Heart Disease 59: Fundamentals of Obstetric Anesthesia 34: Heart Failure 66: Epidural Analgesia and Anesthesia 15: Inotropes and Vasodilator Drugs 41: Acute Respiratory Distress Syndrome (ARDS)