Chapter 18
Clinical Monitoring III
Neurologic System
The practice of anesthesia requires constant vigilance and evaluation of the patient. Historically, early anesthetists such as John Snow and Arthur Guedel proposed the use of clinical and neurologic signs to evaluate and determine the depth of anesthesia. Snow described the “five stages of narcotism” for chloroform anesthesia.1 Guedel further refined these signs of anesthesia by developing a table of “clinical signs and stages of anesthesia” the patient passes through during anesthesia.2 Guedel used neurologic signs such as respiratory rate and rhythm, ocular movement, pupillary size, and reflexes to evaluate the depth of ether anesthesia.1,2
1. Possessing a thorough knowledge of the monitors and modalities available for neurologic monitoring
2. Selecting appropriate neurologic monitor(s) for data acquisition and patient management
3. Understanding the various pathologic and anesthetic effects on patients’ response with neurologic monitors
4. Managing neurologic changes during periods of surgical stimulation
5. Recognizing data changes that reflect neurologic changes and ischemia
The neurophysiologic parameters of interest that are monitored during surgery include brain function, blood flow, and metabolism. Monitoring of function is performed by measurement of electrical activity in the brain by means of electroencephalography (EEG), sensory and motor evoked potentials (EPs), and electromyography (EMG). Monitoring of blood flow/pressure is achieved by nitrous oxide wash-in, radioactive xenon clearance, laser Doppler blood flow, and transcranial Doppler sonography. Intracranial pressure can be determined by means of intraventricular catheters, fiberoptic intraparenchymal catheters, subarachnoid bolts, and epidural catheters. Lastly, brain metabolism can be measured either through invasive techniques such as placement of intracerebral Po2 electrodes or noninvasive techniques, such as transcranial cerebral oximetry and jugular venous oximetry.3 Select methods for monitoring neurologic functions are given in Box 18-1.
This chapter examines the monitors currently used in clinical practice and managing the neurologic function of patients during the perianesthetic period. Brain monitoring methods and their indications, advantages, and disadvantages are noted in Table 18-1.
TABLE 18-1
Adapted from Rabinstein AA. Principles of neurointensive care. In Daroff et al, eds. Bradley’s Neurology in Clinical Practice. 6th ed. Philadelphia: Saunders; 2012;805.
Intracranial Pressures and Jugular Venous Oxygenation
Recently the ICP, in conjunction with the jugular venous oxygenation (SjvO2) monitoring, has been used to evaluate intracranial injury with some success. A SjvO2 that ranges between 55% and 75% has been found to be a reasonable predictor of positive outcomes for traumatic brain injury (TBI) if the ICP is also maintained within a normal range. Those patients with a SjvO2 less than 55% or above 75% and an elevated ICP had poor outcomes.4,5
Electroencephalogram
The brain is an electrochemical organ generating electrical signals in a specific pattern. The electrical activity displayed through an EEG is sometimes called electrical brainwaves. The EEG is actually a measurement of differences in electrical potentials in groups of neurons between brain regions rather than the brain emitting electrical waves.6 Electrodes used to produce the EEG are placed on the patient in a standardized sequential configuration (or montage) that examines known electrical potentials. This configuration was internationally standardized by Jasper in 1958 as the 10-20 system and is usually used to record the spontaneous EEG. With this system, 21 electrodes are placed on the surface of the scalp. The positions of the electrodes are determined by following three primary reference points: (1) the nasal-frontal angle, which is the depression at the top of the nose; (2) the level aligning with the eyes; and (3) the inion, which is the bony lump at the base of the skull on the midline at the back of the head. These reference points allow the practitioner to measure the skull perimeters in the transverse and median planes. Electrode locations are determined by dividing these perimeters into 10% and 20% intervals.6 Freeman7 suggested that the electrodes should be placed in areas that emit similar signals to concentrate and better record the electrical activity.
Generally, the basic parameters of the EEG include frequency, amplitude, shape (amplitude and shape constitute morphology of the wave), and time of each of these electrical discharges. The waveforms are then arranged in the following manner. Four common types of brainwaves are noted on the EEG; they are alpha, beta, delta, and theta waves. There are also several variants or subgroups of waves noted during specific activities. Some of these waveform variants are gamma, mu, and lambda waves. Gamma waves are typically seen with high-order activity such as problem solving and analytic thinking. The amplitude of the mu wave is about one half that of the beta wave and is seen more frequently over the motor areas of the brain.8–10 Lambda waves occur in the awake patient and are usually present when staring, reading, or looking at objects for long periods, as happens with videogames and TV.11 It can be difficult to distinguish artifact and normal variations of the EEG from the four common types of known brainwaves.12–14
Monitoring the EEG intraoperatively for the development of delta waves allows for the recognition of an increased risk of ischemic damage to the brain. To simplify EEG interpretation, the anesthetic delivery should ideally be “stable” and not changing during the critical surgical portions of the case. Also, any changes in anesthetic delivery should be communicated to the EEG technician. The EEG can only provide information of the cerebral cortex function, and not much information on the subcortical brain, spinal cord, or the cranial and peripheral nerves.3,15,16
Anesthetic Effects on EEG
Induction doses of etomidate and propofol all cause similar effects on the EEG by increasing the frequency of beta waves and decreasing their amplitude. This beta-rhythm EEG activity correlates with the patient losing consciousness after drug administration; a dose-related depression is seen with anesthetic drugs.17,18
One difference noted with the administration of etomidate is that myoclonus, frequently seen with its use, is not reflected on EEG signals.19 Coincidently, the EEG frequency decreases as the serum levels of etomidate rise, thereby leading to burst suppression. Burst suppression can be achieved with both of these induction agents in their higher dosage ranges. Burst suppression is an alternating high-frequency activity with 0.5- to several-second periods of electrical suppression. This type of electrical activity is unpredictable, and the duration constantly varies. Burst suppression is also typically seen with a decrease in cerebral circulation and oxygenation, as well as with hypothermia, particularly during cardiopulmonary bypass surgery. Many of these effects can be additive. Burst suppression EEG patterns remain somewhat controversial relative to cardiopulmonary bypass surgery. However, to reduce cerebral oxygen requirements and provide neuroprotective properties, burst suppression may be desirable during manipulation of brain tissues.20–22 Burst suppression can be achieved during anesthesia using a variety of anesthetic agents. These agents include etomidate, propofol, and the inhalation agents, which all provide varying levels of suppression of electrical activity with increasing depth; effects usually remain bilateral and uniform.17,19,23 Unilateral burst suppression is usually indicative of ischemia or injury to the brain. Forethought should be given to the use of sevoflurane in patients with known epileptiform EEG activity; the activity may be accentuated by these inhalation agents in their lower concentrations.18,24,25
Processed Eeg Waveforms
The interpretation of a raw EEG can many times be difficult and depend on the quality of the waveform, lead placement, any artifact or electrical interference that might be present, and the skill level of the clinicians in interpreting the waveforms. To further analyze the EEG, multiple methods are used, including compressed spectral array (CSA) and density spectral array (DSA). The CSA and DSA are obtained, calculated, and displayed by collecting, assessing, and providing a summary of each of the waves (alpha, beta, theta, delta) over a period of time. A mathematical description for the timeframe, using the amplitude and frequency of the waves, is accomplished by using a fast Fourier transform (FFT) algorithm. Applying an FFT algorithm is typically thought of as breaking down a signal into a variety of components and then reconstructing the useful information into an analysis of the complex signals. The cell phone, TV, and radio are examples of devices in which this technology is best known. The Fourier analysis also results in a compressed view of EEG waveforms. The compressed data are presented in a two- or three-dimensional graph. Depending on the display used, these data appear as either a compressed spectral array (CSA) or a dot matrix called a density spectral array (DSA), as seen in Figure 18-1.26
The processed information collected and displayed for the CSA and DSA is analyzed for the waveform relationships using the amplitude and frequency and illustrated in two- or three-dimensional graphs. These relationships are expressed as the spectral edge frequency (SEF), median frequency (MF), and relative delta power (RDP). Most commonly, the SEF is used and represented by the EEG frequency and power activity, which falls below 90% (SEF90).27,28 Figure 18-2 shows an EEG power spectrum demonstrating the SEF of waveforms within 90% of power and frequency. As frequency declines below a predetermined power, the spectral edge changes. In the presence of general anesthesia or injury, frequency and power decline, thereby causing a change in the spectral edge. The modern EEG calculates the computerized spectral array, which is then used during anesthesia to determine the “depth of anesthesia” or unilateral injury, based on the processed results. The compressed spectral array (CSA) in Figure 18-3 shows the spectral edge shifted to the right, indicating lower power and frequency in brainwave activity. This pattern is typically found during deep sedation and sleep, and in Figure 18-3 is produced by the presence of 0.2% isoflurane anesthesia, indicating the patient’s brainwave activity is suppressed. General anesthesia produces a reduction in high-frequency waves and an increase in low-frequency amplitudes. In Figure 18-2, the spectral edge is positioned well to the left, indicating a higher power and frequency, suggesting that the patient is awake.29–31
Considerations for Inhalation Anesthetics and EEG Interpretation
Interpreting the EEG in the presence of anesthetic drugs can be confounding because the different drug classes used for anesthesia may affect the EEG in different ways. Instead, generalized assumptions can be made from the interpretation of the EEG. There are two major reasons the EEG remains difficult to correlate with the course of the anesthetic and patient outcomes. The first major variable preventing exact correlation between the EEG and anesthetic depth is the combination of the many different drugs used to induce and maintain general anesthesia. Dose-related effects are seen with each general inhalation and intravenous anesthetic. The inhalation agents affect the frequency and amplitude of the EEG waveforms (Table 18-2).29–34 Alpha waves seen primarily in the occipital and posterior lobes are increasingly abolished with inhalation anesthesia. Beta activity is usually seen in the frontal lobe and typically increases slightly with general anesthesia. The second major variable involves environmental factors and manipulation of the brain intraoperatively, adding to the complexity of interpretation. Extensive research with bispectral analysis (BIS) has sought to clarify EEG interpretation by analyzing the EEG electrical signals, processing them, and displaying the result as a final numeric value of 0 to 100. BIS measurement is effective in determining the level of anesthesia produced with inhalation agents but remains less predictable with pediatric patients and during regional and intravenous anesthesia.35
TABLE 18-2
Effects of Inhalation Anesthetics on EEG
↑, Increase; 0, no effect; MAC, minimum alveolar concentration; EEG, electroencephalogram.
Adapted from Seubert CN, Mahla ME. Neurologic monitoring. In Miller RD, ed. Miller’s Anesthesia. 7th ed. Philadelphia: Churchill Livingstone; 2010:1477-1514.