Anesthesia for Neurosurgery

An understanding of neuroanatomy is essential for all who care for patients with disease of the central nervous system (CNS) (Dagal A, Lam AM. Anesthesia for neurosurgery. In: Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Ortega R, Stock MC, eds. Clinical Anesthesia. Philadelphia: Lippincott Williams & Wilkins; 2013:996–1029).

I. Neuroanatomy

The brain and spinal cord are surrounded by protective but nondistensible bony structures that surround them and provide protection.
The intracranial volume is fixed, thereby providing little room for anything other than the brain, cerebrospinal fluid (CSF), and blood contained in the cerebral vasculature. It is in the context of the restrictive nature of the space in which the CNS is housed that all interventions must be considered.
The anterior cerebral circulation originates from the carotid artery, the posterior circulation results from the vertebral arteries, and the system of collateralization is known as the circle of Willis (Fig. 36-1).
The spinal column is the bony structure made up of the seven cervical, 12 thoracic, and five lumbar vertebrae, as well as the sacrum.
- The spinal cord exits the skull through the foramen magnum and enters the canal formed by the vertebral bodies. In adults, the spinal cord typically ends at the lower aspect of the first lumbar vertebral body.
- The anterior spinal artery arises from the vertebral arteries and supplies the anterior two thirds of the spinal cord. This vessel runs the length of the cord, receiving contribution from radicular arteries via intercostal vessels. The artery of Adamkiewicz is the most important radicular vessel.
- The posterior third of the cord is supplied by two posterior spinal arteries, which arise from the vertebral arteries and also receive contribution from radicular arteries.

Figure 36-1. The circle of Willis, which supplies blood flow to the brain.

II. Neurophysiology

Cerebral metabolism is directly related to the number and frequency of neuron depolarizations (activity or stimulation increases the metabolic rate). Cerebral blood flow (CBF) is tightly coupled to metabolism.
The CSF occupies the subarachnoid space, providing a protective layer of fluid between the brain and the tissue that surrounds it. It maintains a milieu in which the brain can function by regulating pH and electrolytes, carrying away waste products, and delivering nutrients.
Intracranial pressure (ICP) is low except in pathologic states. The volume of blood, CSF, and brain tissue must be in equilibrium. An increase in one of these three elements, or the addition of a space-occupying lesion, can be accommodated initially through displacement of CSF into the thecal sac but only to a small extent. Further increases, as with significant cerebral edema or accumulation of an extradural hematoma, quickly lead to a marked increase in ICP because of the low intracranial compliance (Fig. 36-2).
Many factors affect CBF because of their effect on metabolism. (Stimulation, arousal, nociception, and mild hyperthermia elevate metabolism and flow, and sedative–hypnotic agents and hypothermia decrease metabolism and flow.)
A number of other factors govern CBF directly without changing metabolism.
- A potent determinant of CBF is PaCO₂. CBF changes by approximately 3% of baseline for each 1 mm Hg of change in PaCO₂ (Fig. 36-3).
  
  Figure 36-2. Intracranial compliance (elastance) curve.
  
  Figure 36-3. Cerebrovascular response to a change in arterial carbon dioxide partial pressure (PaCO₂) from 25 to 65 mm Hg.
- As CBF changes, so does cerebral blood volume (CBV), which is the reason hyperventilation can be used for short periods of time to relax the brain or to decrease ICP. This effect is thought to be short lived (minutes to hours) because the pH of CSF normalizes over time and vessel caliber returns to baseline.
In contrast to PaCO₂, PaO₂ has little effect on CBF except at abnormally low levels (Fig. 36-4). When PaO₂ decreases below 50 mm Hg, CBF begins to increase sharply.

CBF remains approximately constant despite modest swings in arterial blood pressure (autoregulation) (Fig. 36-5).

As cerebral perfusion pressure (CPP), defined as the difference of mean arterial pressure (MAP) and ICP, changes, cerebrovascular resistance (CVR) adjusts in order to maintain stable flow.

The range of CPP over which autoregulation is maintained is termed the autoregulatory plateau. Although this range is frequently quoted as a MAP range of 60 to 150 mm Hg, there is significant variability between individuals, and these numbers are only approximate.

At the low end of the plateau, CVR is at a minimum, and any further decrease in CPP compromises CBF.

Figure 36-4. Cerebrovascular response to a change in arterial oxygen partial pressure (PaO₂). The response of cerebral blood flow to change in PaO₂ is flat until the PaO₂ decreases below about 50 mm Hg.

Figure 36-5. Cerebral autoregulation maintains cerebral blood flow constant between 60 to 160 mm Hg. These are average values, and there is considerable variation in both the lower and upper limit of cerebral autoregulation among normal individuals.

At the high end of the plateau, CVR is at a maximum, and any further increase in CPP results in hyperemia.

Anesthetic Influences
- Anesthetic agents have a variable influence on CBF and metabolism, carbon dioxide reactivity, and autoregulation.
- Inhalation anesthetics tend to cause vasodilation in a dose-related manner but do not per se uncouple CBF and metabolism. Thus, the vasodilatory influence is opposed by a metabolism-mediated decrease in CBF.
- The resultant effect is that during low-dose inhalation anesthesia, CBF is either unchanged or slightly increased. Compared with other inhaled agents, sevoflurane in clinically relevant doses does not increase CBF. Furthermore, sevoflurane is associated with profound regional and global reductions in cerebral metabolic rate.
- Intravenous (IV) agents, including thiopental and propofol, cause vasoconstriction coupled with a reduction in metabolism. Ketamine, on the other hand, increases CBF and metabolism.
- Cerebrovascular carbon dioxide reactivity is a robust mechanism and is preserved under all anesthetic conditions. Cerebral autoregulation, on the other hand, is abolished by inhalation agents in a dose-related manner but is preserved during propofol anesthesia.

III. Pathophysiology

The homeostatic mechanisms that ensure protection of the brain and spinal cord, removal of waste, and delivery of adequate oxygen and substrate to the tissue can be interrupted through a multitude of mechanisms (Table 36-1).

Table 36-1 Events that May Interrupt Homeostatic Mechanisms for Brain Protection

Traumatic Insults
Contusion with edema formation
Depressed skull fractures
Rapid deceleration

Mass Lesions
Tumors (compress adjacent structures, increase ICP, and obstruct normal flow of CSF)

Hemorrhage (spontaneous or traumatic)

CSF = cerebrospinal fluid; ICP = intracranial pressure.

Table 36-2 Monitoring Central Nervous System Function

EEG: depolarization of cortical neurons provides a pattern of electrical activity that can be measured on the scalp
BIS uses a computer-processed EEG to derive a dimensionless number to monitor the degree of hypnosis (40–60 considered optimal for prevention of awareness, yet end-tidal anesthetic monitoring may be equally effective)
Evoked potential monitoring detects signals that result from a specific stimuli

SSEP requires intact sensory pathway, spine surgery when the dorsal column of the spinal cord may be at risk
BAEP: acoustic neuroma surgery
VEP: difficult to record during anesthesia
MEP monitors descending motor pathways, complements SSEP during spine surgery, signals sensitive to volatile anesthetics and IV anesthetics may be preferred

sEMG detects injury to nerve roots in the surgical area; muscle relaxants must be avoided
Electromyography: cranial nerve monitoring

BAEP = brain stem auditory evoked potential; BIS = bispectral index; EEG = electroencephalography; IV = intravenous; MEP = motor evoked potential; sEMG = spontaneous electromyography; SSEP = somatosensory evoked potential; VEP = visual evoked potential.

IV. Monitoring

The integrity of the CNS needs to be evaluated intraoperatively with monitors that specifically detect CNS function, perfusion, or metabolism.

Central Nervous System Function (Tables 36-2 to 36-4)
Influence of Anesthetic Technique (Table 36-5)

V. Cerebral Perfusion

Although adequate CBF does not guarantee the well-being of the CNS, it is an essential factor in its integrity.

Laser Doppler flowmetry requires a burr hole and measures flow in only a small region of the brain.

Transcranial Doppler ultrasonography (TCD) is a noninvasive monitor for evaluating relative changes in flow through the large basal arteries of the brain (often flow velocity in the middle cerebral artery) (Fig. 36-6).

Table 36-3 Electroencephalogram Frequencies

	Frequency (Hz)	Description
Delta	0–3	Low frequency, high amplitude Present in deep coma, encephalopathy, deep anesthesia
Theta	4–7	Not prominent in adults May be seen in encephalopathy
Alpha	8–12	Prominent in the posterior region during relaxation with the eyes closed
Beta	>12	High frequency, low amplitude Dominant frequency during arousal

In addition to the measurement of flow velocity, TCD is useful for detecting emboli (Fig. 36-7).
Specific applications for intraoperative use of TCD include carotid endarterectomy (CEA), nonneurologic surgery and cerebral autoregulation in patients with traumatic brain injury (TBI), and surgical procedures requiring cardiopulmonary bypass.
An important use of TCD is to monitor the development of vasospasm in patients who have experiences a subarachnoid hemorrhage (SAH).

Intracranial Pressure Monitoring

Although monitoring ICP does not provide direct information about CBF, it allows calculations of CPP (the difference between MAP and ICP).

Within a physiologic range of CPP, CBF should remain approximately constant. A CPP that is too low results in

cerebral ischemia, and a CPP that is too high causes hyperemia.

Table 36-4 Indications for Electroencephalographic Monitoring

During anesthesia	Carotid endarterectomy
	Cardiopulmonary bypass
	Cerebrovascular surgery (temporary clipping, vascular bypass)
Intensive care unit	Barbiturate coma for patients with traumatic brain injury
	Subclinical seizures suspected

Table 36-5 Influence of Anesthetic Technique on Central Nervous System Monitoring

Inhalation agents (including nitrous oxide) generally have more depressant effects on evoked potential monitoring than IV agents.

Whereas cortical evoked potentials with long latency involving multiple synapses (SSEP, VEP) are exquisitely sensitive to the influence of anesthetic, short-latency brain stem (BAEP) and spinal components are resistant to anesthetic influence.

Monitoring of MEP and cranial nerve EMG in general preclude the use of muscle relaxants. Use of a short-acting neuromuscular blocking agent for the purpose of tracheal intubation is acceptable.

MEP is exquisitely sensitive to the depressant effects of inhalation anesthetics, including nitrous oxide. Total IV anesthesia without nitrous oxide is the recommended anesthetic technique for monitoring of MEP.

Opioids and benzodiazepines have negligible effects on recording of evoked potentials.

Propofol and thiopental attenuate the amplitude of virtually all modalities of evoked potentials but do not obliterate them.

During crucial events when part of the central neural pathway is specifically placed at risk by surgical manipulation, as in placement of a temporary clip during aneurysm surgery, change in “anesthetic depth” should be minimized to avoid misinterpretation of the changes in evoked potential.

BAEP = brain stem auditory evoked potential; IV = intravenous; MEP = motor evoked potential; SSEP = somatosensory evoked potential; VEP = visual evoked potential.

Only gold members can continue reading. Log In or Register to continue