Chapter 17 – Neuroanesthesia

Summary

Anesthesia for neurosurgical procedures is challenging. Understanding of neuroanatomy, physiology, and pharmacology gives anesthesiologists the opportunity to optimize patient care. Tailoring anesthesia, including medications, monitoring techniques, and physiologic manipulation, relates closely to the patient’s pathology and surgical procedure. Maintaining cerebral perfusion pressure (CPP), controlling the intracranial pressure (ICP), and preventing the progression of neurologic insults are an integral part of perioperative neuroanesthesia care.

Introduction

Neuroanatomy and Physiology

The central nervous system (CNS) comprises the brain and spinal cord. The brain, which includes the cerebral cortex (composed of the gray and white matter), brainstem (midbrain, pons, and medulla), and cerebellum, is covered by protective layers of the meninges (pia, arachnoid, and dura mater). The cerebral cortex is divided into frontal, parietal, temporal, and occipital lobes. While the cortex is responsible for processing information and thinking, the brainstem is responsible for vital functions of the body, including respiratory and hemodynamic control. The cerebrospinal fluid (CSF) in the subarachnoid (SA) space surrounds the brain and spinal cord, providing nutrition, waste management, and protection. It is produced by the choroid plexus in the lateral ventricles and absorbed by the arachnoid villi in cerebral venous sinuses. The CSF flows from the lateral ventricles to the third ventricle through the interventricular foramen (foramen of Monro), and then enters the fourth ventricle via the cerebral aqueduct. From the fourth ventricle, it reaches the SA space (foramina of Luschka and Magendie) to surround the brain and spinal cord.

The Monro–Kellie hypothesis states that the sum of the intracranial volumes (CSF, blood, and brain) and ICP are in equilibrium. An increase in one volume should cause a decrease in the other, with significant implications in the management of cerebral blood flow (CBF) and ICP (see Figure 17.1). The ICP is determined by several intracranial elements, including the CBF and CSF, and other intracranial contents, including space-occupying lesions and cerebral edema. The ICP can be increased by factors such as increase in intrathoracic pressure or intraabdominal pressure, pain, and shivering. It is often measured with an external ventricular drainage (EVD) catheter through a ventriculostomy or through an intraparenchymal catheter. Maintenance of a stable ICP is important, and while not routinely measured intraoperatively, it can often be gauged by neurosurgeons while operating. The anesthesiologist’s goal is to provide a “relaxed” brain, without sudden increases in intracranial pressure that can compromise operating conditions as well as the CPP. Maintenance of an adequate CPP is a critical and primary anesthetic goal, and it is defined as the mean arterial pressure (MAP) minus the ICP (or central venous pressure (CVP), whichever is higher). Through autoregulation, maintained by MAP, end-tidal carbon dioxide (ETCO₂), and PaO₂, the CBF is maintained relatively constant over a CPP of 50–150 mmHg (see Figure 17.2).

Figure 17.1 Intracranial pressure–volume curve. During a compensated phase, an increase in intracranial volume is compensated for, with minimal or no change in the ICP. Once it reaches the elbow of the ICP curve, this physiologic compensation is exhausted and a minimal increase in volume causes a significant and sharp rise in ICP.

Figure 17.2 Cerebral autoregulation. The CBF is maintained constant with the MAP (50–150 mmHg). An increase in PaCO₂ causes a marked increase in CBF (10 mmHg increase in CO₂ = 10 mL CBF increase/100 mg brain). The PaO₂ has minimal effect on the CBF (<50 mmHg PaO₂, higher CBF).

Monitoring – ASA Monitors, Neuromonitoring (EEG, ECoG, EMG, SSEP, MEP, BERA, VEP)

Monitoring of patients undergoing neurosurgical procedures depends on the complexity of the patient’s condition, surgical procedure, duration, blood loss, and intraoperative events. Standard American Society of Anesthesiologists (ASA) monitors, including ECG, SpO₂, ETCO₂, blood pressure, and temperature, are monitored for all neurosurgical procedures. Neuromuscular blockade is monitored closely and invasive arterial pressure (IAP) monitoring also facilitates frequent blood gas analysis. A CVP catheter is placed for fluid therapy and aspiration of air if a venous air embolus (VAE) arises, and for administration of vasopressors or other necessary medications. A urinary catheter is vital in guiding fluid management in many neurosurgical procedures, especially in patients receiving osmotic diuretics.

The anesthetic management of patients undergoing intraoperative neuromonitoring (IONM) requires close collaboration with neurosurgeons, neurophysiologists, and neurologists. Neuromonitoring assesses the functional integrity of structures (brain, brainstem, spinal cord, cranial nerves, and peripheral nerves) through the localization of anatomical structures, and reduces postoperative deficits. IONM is based on gauging spontaneous electrical activity through electromyography (EMG), EEG (electroencephalography), EcoG (electrocorticography), and evoked responses, through the stimulation of neural pathways. Evoked potentials (EPs) are divided into sensory (somatosensory evoked potentials (SSEPs), brainstem evoked response audiometry (BERA) or auditory evoked potentials (AEPs), visual evoked potentials (VEPs)) and motor (MEPs), based on stimulation and the recording site. The decision regarding the optimal type of IONM is based on the type of surgery and neural structures involved. Intraoperative EEG monitoring is primarily used for seizure surgery, whereas ECoG involves mapping the functional cortex, useful in cerebrovascular and CNS tumor surgery. Intraoperatively, anesthesiologists need to consider both physiologic and pharmacologic factors that affect IONM. Such physiologic factors include hypoxia, hypotension, hypothermia, and carbon dioxide (CO₂) levels. Pharmacologically, inhalational agents tend to affect EPs more than intravenous agents do. The most sensitive EPs to inhalational anesthetics are visual, whereas those the least affected are auditory (VEP > MEP > SSEP > AEP). Based on baseline IONM, inhalational agent use is typically limited (<0.3–0.5 minimum alveolar concentration (MAC)) and total intravenous anesthesia (TIVA) is commonly used during anesthetic management. Any changes in intraoperative monitoring (amplitude, latency, frequency, morphology, and threshold) should prompt evaluation as to whether the changes are localized or global, as well as prompt amelioration of insults to prevent postoperative neurological deficits.

Effects of Anesthetic Agents on Neurophysiology

The anesthesiologist plays a major role in maintaining optimal neurophysiology and facilitating optimal operating conditions, with a smooth anesthetic emergence that allows for a timely neurological examination postoperatively. In general, intravenous anesthetic agents decrease CBF and cerebral metabolic rate of oxygen (CMRO₂) in relative parallel, whereas the inhaled gases decrease CMRO₂, with a relative increase in CBF, with some nuances and exceptions discussed below.

Inhalational Agents

Inhalational anesthetics have the potential to increase ICP and reduce CMRO₂, with the exception of nitrous oxide (N₂O). The effect of inhalational anesthetics on CBF is a balance between a reduction in CBF caused by CMRO₂ suppression and increased CBF secondary to direct cerebral vasodilation. N₂O is shown to increase CBF and ICP, with a variable effect on CMRO₂. Furthermore, it can enlarge potential air space, and for this reason, N₂O is suboptimal for use in patients with the potential for intracranial or intravascular air. Sevoflurane tends to produce less vasodilation than isoflurane or desflurane, and preserves PaCO₂ reactivity the best. Its purported neuroprotective effect is similar to that seen with isoflurane. Moreover, its lower solubility in blood makes it a desirable choice for more rapid emergence from anesthesia. Desflurane is comparable to the aforementioned halogenated compounds in its potential neuroprotection, and while its low solubility in blood favors more rapid emergence from anesthesia, it tends to produce elevation in ICP, especially in patients with supratentorial lesions.

Intravenous Anesthetic Agents

Most of these medications will decrease both CBF and CMRO₂, and thus provide a favorable profile for ICP control and optimal neurosurgical conditions. Barbiturates offer neuroprotection, but ensuring stable hemodynamics can prove challenging, as can facilitation of an early postoperative neurological examination, given their slow metabolism and tissue accumulation. As such, propofol emerged with a better profile, dose-dependent 50–60% reduction in CBF, and a shorter context-sensitive half-life, as compared with barbiturates. Currently, propofol is a preferred choice in balanced neurosurgical anesthesia and it preserves CO₂ reactivity. Etomidate produces minimal cardiac side effects, with a parallel decrease of approximately 30–50% in CBF and CMRO₂, while largely preserving CO₂ vascular reactivity. Etomidate use is limited by the potential adverse effects of adrenocortical suppression and seizure activity in neurologically compromised patients. Ketamine increases CBF and ICP, and thus vigilance with CO₂ control is important as this can mitigate such issues to some extent. It has not traditionally been a first choice for anesthetic induction or maintenance for patients with reduced intracranial compliance, but has found a role for such patients who also have hemodynamic instability. Benzodiazepines, specifically midazolam, have a relatively similar effect to propofol on CBF and CMRO₂, and provide relative hemodynamic neutrality. Judicious use is recommended, as reversal with flumazenil in delayed emergence can risk the induction of seizures, increasing CBF and CMRO₂. As such, benzodiazepines do not typically form a core element of maintenance neuroanesthesia. Dexmedetomidine in animal models reduced global and regional CBF without a significant concomitant reduction in CMRO₂, raising concerns for reduced brain tissue oxygenation, but these results have not been clinically reproduced. Moreover, perioperative dexmedetomidine use has been shown to reduce intraoperative opioid consumption and reduces the odds of postoperative delirium in neurosurgical patients, so careful use of the medication may prove beneficial.

Opioids

The effects of opioids on CBF, CMRO₂, and ICP are variable, often dependent on other medications and elements. Fentanyl is one of the most commonly used perioperative opioids and, along with sufentanil, largely produces neutral effects on neurophysiology. It is important to consider the dosing of these medications, given their potentially prolonged effects resulting in delayed anesthetic emergence. Postoperative nausea, vomiting, and hypercarbia from respiratory depression can thus lead to increased ICP. Remifentanil is a commonly used synthetic opioid in neuroanesthesia, with a rapid-onset and -offset mechanism, particularly conducive as the analgesic component for TIVA. While its μ-receptor agonism can elicit nausea and vomiting, like other opioids, its ultrashort duration of action makes it a good choice for rapid emergence. Special attention should be paid to prevent postoperative hyperalgesia.

Neuromuscular Blockers

Succinylcholine, useful in the management of rapid sequence induction and difficult airway, is often avoided as a neuromuscular blocking agent (NMBA) in neurologically injured patients, given its tendency to increase ICP transiently through fasciculations. This can be attenuated through pretreatment with a nondepolarizing agent and careful control of PaCO₂ by ventilation. Nondepolarizing NMBAs (e.g., rocuronium, vecuronium) are the typical choice in neuroanesthetic care, with minimal effect on CBF, CMRO₂, and ICP. Rocuronium enjoyed widespread use, given its rapid onset of action and reversibility with sugammadex. Adequate depth of muscle relaxation during surgery is typically monitored with a train-of-four twitch monitor.

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