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Patients with neurologic disease undergoing surgical procedures have increased risk of ischemic/hypoxic damage to the central nervous system (CNS). This risk may be related to hemodynamic/embolic events associated with a non-neurosurgical operation (e.g., patients with significant carotid stenosis undergoing cardiopulmonary bypass [CPB] procedures) or the risk may be inherent in the neurosurgical procedure itself (e.g., temporary clipping of feeding artery during cerebral aneurysm surgery). Intraoperative neurophysiologic monitoring may improve patient outcome by (a) allowing early diagnosis of ischemia/hypoxia before irreversible damage occurs and (b) enabling surgeons to provide optimal operative treatment as indicated by the monitoring parameter.
Although not universally adopted, neurophysiologic monitoring has become routine for some surgical procedures in many centers.
Broadly speaking, the brain can be monitored in terms of (a) function, (b) blood flow, and (c) metabolism (Tables-1, 2 and 3).

I. Monitoring of function

Electroencephalography. Summation of the excitatory postsynaptic potential generated by the pyramidal cells of the cerebral cortex gives rise to the electrical activity of the brain, which can be recorded as an electroencephalogram (EEG). The EEG comprises many underlying components with different frequencies and harmonics. The component waves are typically classified according to the respective frequencies (Table-4). This electrical activity is volume conducted and can be recorded from the scalp and forehead, using surface or needle electrodes.
Recording techniques. Because the scalp has no electrically neutral area, EEG is typically recorded using a montage (electrode arrangement) with bipolar recording. Thus, both electrodes are active, and the polarity of the signal recorded depends on the arbitrary designation of recording versus referential electrode. Other electrical activities generated in the body such as electromyographic and electrocardiographic potentials are minimized but not eliminated using common-mode rejection which rejects the electrical signals that are measured in both recording sites (common) in comparison to a third ground electrode. The number of channels used and the placement of electrodes determine the specificity of the EEG as a monitor of the occurrence of regional ischemia. The gold standard for raw EEG recording is 16-channel recording (eight channels for each hemisphere) with electrodes placed according to the International 10-20 System (Figure-1). With the exception of monitoring in carotid endarterectomy (CEA) in some centers, 16-channel EEG recording is seldom performed intraoperatively because of its relative complexity and the inaccessibility of recording sites in intracranial surgical procedures.

Table-1. Monitoring of function
Raw electroencephalogram
Computerized processed
  Compressed spectral array
  Density spectral array
  Aperiodic analysis
Bispectral Analysis
Evoked potentials
Sensory evoked potentials:
  Somatosensory EP
  Brain stem auditory EP
  Visual EP
Motor evoked potentials
  Transcranial magnetic MEP
  Transcranial electric MEP
  Direct spinal cord stimulation
Cranial nerve functions (V, VII, IX, X, XI, XII)
EP: evoked potential; MEP: motor evoked potential.

To simplify recording and interpretation of EEG, most EEG machines designed for intraoperative monitoring use two- to four-channel recording with computer processing to simplify the output. Although different vendors use different algorithms, the basic premise is to filter out the high frequency activity (likely to be artifacts or interference), typically at 30 Hz. The raw EEG is then separated into its component waves using Fast Fourier Transform and then they are grouped together according to the frequency spectrum. Thus, raw EEG recorded in a time domain is displayed in a frequency domain. The resultant power (square of the amplitude of the EEG wave) spectrum can be displayed in a number of ways, the most common ones being compressed spectral array or density spectral array with either the peaks and valleys or the density of the gray scale representing the power of the spectrum. Aperiodic analysis is another method of EEG processing that tracks each wave and plots it as a telephone pole with its height representing the amplitude or power of the wave.

Table -2. Monitoring of flow/pressure
Cerebral blood flow
Nitrous oxide wash-in
Radioactive xenon clearance
Laser Doppler blood flow
Transcranial Doppler
Intracranial pressure
Intraventricular catheter
Fiberoptic intraparenchymal catheter
Subarachnoid bolt
Epidural catheter


Table-3. Monitoring of metabolism
Invasive monitor
Intracerebral Po2 electrode (Paratrend, Licox)
Noninvasive monitor
Transcranial cerebral oximetry (near-infrared spectroscopy)
Jugular venous oximetry

Interpretation of EEG
The EEG is a random activity reflecting the state of arousal and metabolic activity. The generation of electrical activity is an energy-requiring process that depends on an adequate supply of substrates including oxygen and glucose. Thus, significant reductions of blood flow, oxygen, or glucose all lead to depression of EEG activity. Gradual reduction of cerebral blood flow (CBF) can be correlated with characteristic changes in EEG and constitutes the most frequent underlying indication for EEG monitoring.

Table-4. Electroencephalogram
Beta 13-30 Hz High frequency, low amplitude, dominant during awake state
Alpha 9-12 Hz Medium frequency, higher amplitude seen in occipital cortex with eyes closed while awake
Theta 4-8 Hz Low frequency, not predominant in any condition
Delta 0-4 Hz Very low frequency, low to high amplitude signifies depressed functions, consistent with deep coma (cause can be anesthesia, metabolic, or hypoxia)


Figure-1. The International 10-20 System for placement of EEG electrodes. It is based on dividing each head circumference (anteroposterior from nasion to inion over the vertex, coronal from tragus of one ear to the other) into two halves and then subdividing each half (50%) into 10%, 20%, 20% sectors. Fp, frontal pole; F, frontal; C, central; P, parietal; T, temporal; A, ear lobe; M, mastoid (not shown). Odd number subscripts denote the left hemisphere, and even numbers denote the right hemisphere.

Awake EEG is dominated by beta activity with high-frequency and low-amplitude waves. With the onset of ischemia/hypoxia, initially a transient increase in beta activity occurs, followed by development of slow waves (theta and delta) with large amplitude, disappearance of beta activity, and eventually the occurrence of delta waves with low amplitude. The ischemic changes can progress to suppression of electrical activity with an occasional burst of activity (burst suppression) and finally to complete electrical silence with flat EEG, signaling the onset of irreversible damage. Thus, the sudden development of delta waves coincident with a surgical maneuver such as cross-clamping of the common carotid artery would warn the anesthesiologist and the surgeon that the patient is at risk of cerebral injury. In the region of the ischemic penumbra where blood flow is inadequate to generate electrical activity but sufficient to maintain neuronal viability for a period of time, EEG has poor predictive power for brain damage. Thus, EEG is sensitive to the occurrence of ischemia but lacks specificity as a diagnostic test for irreversible damage. In general, the quicker the onset of the ischemic EEG changes, the higher the probability for irreversible damage.
Confounding factors. The observed changes in EEG with ischemia/hypoxia are not unique, and similar changes occur with anesthetic-induced metabolic depression, albeit in a reversible manner. Most intravenous (with the exception of ketamine) and inhalation anesthetics cause a dose-dependent depression of EEG and virtually all of them can produce a burst-suppression pattern on EEG. Similarly, hypothermia decreases cerebral metabolism and causes slowing of the EEG. EEG changes, therefore, should always be interpreted in concert with other physiologic variables, not in isolation.
Indications for EEG monitoring
All surgical procedures that potentially place the brain at risk are theoretically amenable to EEG monitoring. In practice, EEG monitoring is often difficult to perform during intracranial procedures because of the lack of access to scalp recording. The use of needle electrodes may ameliorate this problem. CEA, which places the ipsilateral hemisphere at risk during cross-clamping of the common carotid artery, is the most frequent indication for EEG monitoring. When EEG changes indicate that CBF is inadequate, the placement of an intraluminal shunt restores blood flow.
Some anesthesiologists and surgeons utilize anesthesia-induced metabolic suppression to provide cerebral protection during risky procedures. EEG monitoring in these circumstances allows optimal metabolic suppression with anesthesia administered by titration to achieve burst suppression. The main indications for EEG monitoring are listed in Table-5.

Table -5. Indications for electroencephalogram monitoring
Carotid endarterectomy
Cerebral aneurysm surgery when temporary clipping is used
Cardiopulmonary bypass procedures
Extracranial-intracranial bypass procedures
Deliberate metabolic suppression for cerebral protection

Although uncommon in the anesthetized patient, occult seizures occur frequently in patients with head injury in the intensive care unit (ICU). These seizures, which may worsen the outcome, may be detectable only with continuous EEG monitoring. Although treatment of these seizures is likely beneficial, it is yet to be determined whether continuous EEG monitoring in the ICU will improve outcome in a cost-effective manner.
Bispectral analysis. The bispectral index is a derived EEG parameter designed not to detect ischemia but to monitor the degree of hypnosis. Based on both power spectrum analysis and phase change or coherence of the different frequencies, the value is normalized to a range of 0 to 100. A value between 40 and 60 is considered adequate hypnosis to prevent possible recall, whereas a value above 80 is consistent with impending emergence from anesthesia. Strictly speaking, this is not a parameter used to preserve the integrity of the CNS but is derived from the raw EEG and, as such, it is potentially influenced by the occurrence of ischemia that results in changes in the EEG. The frontal location of electrode placement, however, renders the bispectral index less sensitive to development of regional ischemia.

Evoked potential monitoring
Sensory evoked potentials (SEPs). SEP is a time-locked, event-related, pathway-specific electroencephalographic activity generated in response to a specific stimulus such as electrical stimuli applied to the median nerve. The typical peaks and troughs are described by their polarity and latency (Figure-2). For example, the cortical negative peak that typically occurs 20 msec after stimulation of the median nerve is called N20. Alternatively, it is numbered according to the sequence in which it is generated; thus, the first positive wave that occurs following posterior tibial nerve stimulation is called P1. The amplitude of evoked potential waves is small relative to conventional EEG and is not easily visualized without computer averaging of repetitive stimuli. SEPs are anatomically pathway specific and theoretically assess only the integrity of the pathway monitored. The contrast between conventional EEG and SEP is summarized in Table -6.

Figure -2. Common modalities of sensory evoked responses. BAEP: brain stem auditory evoked potential; SSEP-median n, somatosensory evoked potential with median nerve stimulation; SSEP-post tibial n, somatosensory evoked potential with posterior tibial nerve stimulation; VEP-goggles, visual evoked potential in response to stimulation with light-emitted diode goggles.

SEP can be recorded in response to stimulation of any sensory nerve, cranial or peripheral. The common modalities of evoked potentials used in clinical practice are (a) somatosensory evoked potentials (SSEPs), (b) visual evoked potentials (VEPs), and (c) brain stem auditory evoked potentials (BAEPs). Of these three, VEP is profoundly influenced by inhalation anesthesia, is difficult to perform, and is seldom utilized as an intraoperative monitor. The SSEPs recorded in response to stimulation of the median nerve, ulnar nerve, and posterior tibial nerve monitor the integrity of the respective pathways from the periphery to the cortex. They are a routine monitor for surgical procedures on the spinal column with potential risk to the spinal cord such as scoliosis surgery.

Table -6. Difference between sensory evoked potential (SEP) and electroencephalogram (EEG)

Event-related Random
Anatomically pathway specific Primarily cortical activity
Monitors integrity of the pathway Monitors only the cortex
Small amplitude Large amplitude
Requires computer averaging No averaging required
Resistant to intravenous anesthetics, recordable during inhaled anesthetics Abolished by high dose intravenous or inhalation anesthetics

SEPs are also used during CEA and cerebral aneurysm surgery with the theoretical advantage over EEG that even subcortical ischemia can be detected. Indications for different SEP-monitoring modalities are summarized in Table-7.

Table-7. Indications for sensory evoked potential (SEP) monitoring

SSEP monitoring
Spinal column surgery
Carotid endarterectomy
Cerebral aneurysm surgery
BAEP monitoring
Acoustic schwannoma
Vertebral-basilar aneurysms
Other posterior fossa procedures
SSEP, somatosensory evoked potential; BAEP, brain stem auditory evoked potential.

BAEPs include a series of seven short-latency peaks generated in response to stimulation of the auditory (VIII) nerve, typically with repetitive clicks delivered to the ears with a head phone or ear-inserted transducers. A specific neurogenerator produces each peak, numbered with a Roman numeral. Examination of the change in latency interval between various peaks can localize the specific site of the injury. Monitoring BAEPs during acoustic schwannoma surgery, when feasible, has been shown to help preserve the integrity of the auditory nerve. Although the neurogenerators are specific to the VIII nerve, BAEP monitoring has also been used to reflect the general well-being of the brain stem in posterior fossa procedures.
Interpretation of evoked potentials. As with EEG, ischemia/hypoxia leads to depression of conduction with resultant decrease in amplitude and increase in latency of the specific peaks. For SSEPs, 50% reduction in amplitude from baseline in response to a specific surgical maneuver is generally accepted to be a significant change warranting alteration of surgical strategy to avert potential damage. Some centers also consider a 10% increase in latency of SSEP signals to be significant. For BAEP, an increase in latency of more than 1 msec, particularly in wave V, is considered to be clinically significant. In addition, a 50% decline in amplitude is a concern, and a loss of wave V is strongly predictive of postoperative hearing loss.
Confounding factors. As with EEG, anesthetic agents influence cortical evoked potentials. Unlike EEG, SSEPs resist the influence of intravenous agents. Although the amplitude may be slightly reduced and the latency increased, cortical SSEPs can be recorded even during deep barbiturate-induced coma with isoelectric EEG. In contrast, inhalation anesthetics cause a dose-related decrease in amplitude and increase in latency. With high doses, SSEP can become unrecordable. Nitrous oxide also has a profound depressant effect on the amplitude of SSEP, particularly when used in combination with an inhalation anesthetic. Therefore, the combination of inhalation anesthetic and nitrous oxide is avoided. Intraoperative recording of SSEP is best accomplished using an intravenous anesthetic technique or low-dose inhalation anesthetic (<1 minimum alveolar concentration [MAC]). Opioids have negligible effects on SSEP. Ketamine and etomidate have a paradoxical effect of augmenting the amplitude of SSEP and could make monitoring possible in patients with otherwise unrecordable SSEP. BAEP, unlike cortical SSEP, resists the influence of anesthetic agents and can be recorded even during high-dose inhalation anesthetics. For surgical procedures on the spinal column, evoked potentials can also be recorded directly from the epidural space; these potentials are robust and can be recorded regardless of anesthetic agents used. As with EEG, hypothermia also decreases amplitude and increases latency.
Motor evoked potentials. Because SSEP monitors only the integrity of the sensory pathway, it is theoretically possible to miss an injury specifically affecting the motor pathway but sparing the sensory tracts. Thus, motor evoked potential (MEP) recording was introduced into clinical practice to complement SSEP recording. The MEP is basically an electromyographic potential recorded over muscles in the hand or foot in response to depolarization of the motor cortex (Figure-3). Depolarization can be achieved using transcranial magnetic or electrical stimulation.
Unfortunately, anesthetic agents profoundly influence both modalities, rendering the transcranial magnetic stimulation essentially unrecordable during anesthesia and the electrical stimulation recordable only during total intravenous anesthesia. The use of a train-of-four stimuli has augmented MEP and makes it easier to record under general anesthesia. In contrast to SSEP, the relatively large voltage of MEP abrogates the need for averaging and provides almost instant feedback. In many centers, MEP monitoring is used in addition to SSEP during operations on the spinal column. MEPs cannot be recorded in the presence of neuromuscular blockade.

Figure-3. Motor evoked potential from stimulation of left cranium.

Spontaneous electromyography. Although not technically an evoked potential, spontaneous electromyography (EMG) is frequently recorded during surgical procedures of both the cervical spine and lumbar spine. Irritation of peripheral nerves, such as spinal nerve roots, invokes immediate motor activity in muscles that should otherwise be silent under general anesthesia. Spontaneous EMG is particularly useful when the surgeon is working around nerve roots and needs immediate feedback regarding injury or irritation to them.
Monitoring cranial nerve functions. Operations in the posterior fossa and the lower brain stem are associated with potential injury to the cranial nerves. Monitoring the electromyographic potential of the cranial nerves with motor components (V, VII, IX, X, XI, XII) can preserve the integrity of these cranial nerves. Two types of potentials can be recorded: spontaneous and evoked activity. Measuring spontaneous activity can detect injury potential, signifying accidental surgical trespass. Evoking the nerve with electrical stimulation facilitates identification and thus preservation of the cranial nerve. Although EMG theoretically can be recorded during partial neuromuscular blockade, it is best not to administer any muscle relaxants during cranial nerve monitoring.

II. Monitoring of CBF and intracranial pressure (ICP)

Absolute CBF. Most methods of CBF measurement are not applicable to intraoperative monitoring. Nitrous oxide wash-in is the classic method of measuring global hemispheric CBF, but it necessitates cannulation of the jugular bulb and clinically is cumbersome to use. Radioactive xenon clearance is a method that allows noninvasive measurement of regional CBF. Although some centers use it clinically to determine adequacy of hemispheric CBF during CEA, it is primarily a research tool.
Relative CBF. Other tools used for real-time evaluation of relative changes in CBF include laser Doppler flowmetry (LDF) and transcranial Doppler (TCD) sonography.
LDF. This tool is a parenchymal or surface Doppler probe that measures tissue local CBF in a quantitative manner. However, the flow can be expressed only in a relative manner in arbitrary units. Because the volume of tissue monitored is limited to 1 mm, its clinical use, both in the operating room (OR) and the ICU, remains limited. Its insertion also requires a burr hole. Its incorporation into the intracranial monitor may increase its functionality.
TCD sonography. This procedure allows measurement of CBF velocity in the major vessels of the Circle of Willis noninvasively and continuously. For intraoperative purposes, velocity in the middle cerebral artery (Vmca) is measured transtemporally over the zygomatic arch. Although it does not derive the absolute CBF, it can measure relative changes in CBF in a quantitative manner. The waveform profile also provides a qualitative assessment of ICP/cerebral perfusion pressure (CPP). In addition, the occurrence of air or particulate emboli can be detected. TCD can be used to determine cerebral autoregulation and carbon dioxide (CO2) reactivity.
Physiological principles of TCD
(1) The diameter of the basal cerebral arteries is constant. Flow velocity is proportional to CBF only when the diameter of the insonated vessel and the angle of insonation remain constant. There is considerable evidence to suggest that the basal cerebral arteries, as conductance vessels, do not dilate or constrict as the vascular resistance changes. Angiographic and CO2 reactivity studies confirm that changes in CO2 tension and blood pressure have negligible influence on the diameter of the proximal basal arteries. Intravenous and inhaled anesthetic agents do not constrict or dilate the middle cerebral artery (MCA) appreciably. Probably the only clinically important situation in which the basal cerebral vessels vasoconstrict is when vasospasm occurs as a complication of a subarachnoid hemorrhage. Vasospasm renders the relationship between CBF velocity and CBF invalid; as the vessel constricts, the flow velocity increases but the CBF actually decreases. This increase in flow velocity with constriction of the basal cerebral artery represents one of the most important and established uses of the TCD. Once angiography confirms the diagnosis of vasospasm, TCD can track the patient's response to therapy and the time course of resolution of the vasospasm.
(2) Changes in CBF velocity reflect relative changes in CBF. Although correlation between absolute flow velocity and CBF in any given population is poor, good correlation exists between relative changes in flow velocity and CBF.
Clinical applications of intraoperative TCD monitoring
(1) Carotid endarterectomy
(a) Detection of ischemia. TCD monitoring during CEA can detect cerebral ischemia during cross-clamping of the carotid artery and allows selective shunting. The correlation between changes in flow velocity and in EEG appears to be excellent in many studies. A decrease in Vmca of more than 60% compared to preclamped baseline suggests inadequate CBF and the need for an intraluminal shunt. TCD can also detect malfunctioning shunts due to kinking or thrombosis.
(b) Detection of microemboli. Microemboli occur frequently during CEA; embolic events may outweigh hemodynamic events as an etiology of perioperative stroke. TCD can detect both air and particulate emboli.
(c) Diagnosis and treatment of postoperative hyperperfusion syndrome. Approximately 1% of patients develop hyperperfusion syndrome following CEA, resulting in cerebral hemorrhage. TCD monitoring allows this diagnosis to be made and treatment to be implemented. Patients who develop the hyperperfusion syndrome show sustained elevation of flow velocities after release of carotid occlusion and often develop headaches. Prompt reduction of blood pressure is effective in normalizing the ipsilateral flow velocity and alleviating symptoms.
(d) Diagnosis and treatment of postoperative intimal flap or thrombosis. Occlusion of the carotid artery postoperatively can occur due to clot formation or the presence of an intimal flap. Sudden development of clinical symptoms in the post-anesthesia care unit should prompt an immediate TCD examination. A prompt exploration may prevent an impending stroke.
(2) Cardiac surgery. Stroke as a complication of cardiac surgical procedures occurs in up to 10% of patients. More subtle neurologic and cognitive dysfunction has been reported in 30% to 70% of patients.
Adverse cerebral outcomes are due either to embolic events or hypoperfusion, or both.
(a) Cerebral emboli during CPB. There is considerable evidence to suggest that the delivery of microemboli (air, platelet aggregate, and thrombus) into the cerebral circulation is responsible for the neuropsychologic deterioration seen after bypass procedures. Patients with the highest emboli counts have been observed to have greater neurologic deterioration. Other studies have shown that the presence of arterial line filters reduces the incidence of emboli detected by TCD. Despite these published findings, TCD monitoring of emboli is still evolving and faces a number of technical challenges.
(b) Cerebral perfusion during CPB. Brain injury during CPB may also occur as a result of hypoperfusion. TCD has been used as a noninvasive tool for examining CBF in patients having cardiac surgical procedures performed under CPB. The validity of TCD as a surrogate estimate of CBF during CPB is unclear at present, however.
(3) Closed head injury. TCD can be used to assess autoregulation and diagnose hyperemia and vasospasm as well as intracranial circulatory arrest. With elevation of ICP and cessation of CBF (intracranial circulatory arrest), a characteristic oscillating pattern is evident on TCD, with forward flow during systole and backward flow during diastole. In this context, although not widely used intraoperatively, TCD may be useful in monitoring patients with head injuries undergoing non-neurosurgical procedures.
(4) Diagnosis of brain death. When the oscillating pattern is persistent and reproducible, the American Academy of Neurology accepts it as a useful adjunct for the confirmation of brain death.
Limitations of TCD as a routine intraoperative monitor
(1) Most TCD monitors are designed for diagnostic rather than monitoring purposes. A fixation device is needed to allow continuous, reliable recording that does not interfere with the surgical procedure.
(2) Although most TCD equipment is fairly easy to operate, skill and training are nevertheless required.
(3) The successful transmission of ultrasound through the skull depends on the thickness of the skull, and the temporal bone thickness varies with gender, race, and age. The failure rate can be anywhere from 5% to 20%, depending on the patient population.

ICP. Monitoring ICP allows optimization of CPP and possibly prevents herniation. Monitoring methods currently available include ventriculostomy, subarachnoid bolt, epidural sensor, and fiberoptic intraparenchymal monitor; the latter is the most commonly used. The fiberoptic ICP monitors may allow simultaneous measurement of brain temperature, a function that is particularly useful in the ICU where fever exacerbates secondary injury. In addition, some incorporate LDF, partial pressure of arterial oxygen (Pao2), partial pressure of arterial carbon dioxide (Paco2), and pH monitoring.
Although its use is fairly common in the management of patients with head injury in the ICU, the ICP monitor is available only as an intraoperative monitor when placed preoperatively by the neurosurgeon.

III. Monitoring cerebral oxygenation and metabolism

Invasive monitoring
Brain tissue oxygenation (Po2). In the setting of head injury, where secondary injury from ischemia/hypoxia is of concern, maintaining a reasonable CPP may not be adequate for brain preservation. Significant inter-patient variability exists with respect to the CPP below which brain hypoxia is encountered. In this situation, a tissue Po2 monitor is useful for assessing the balance between oxygen supply and demand.
When a miniature Clarke-type polarographic electrode originally designed for continuous intra-arterial monitoring is used, the tissue Po2 monitor is placed intraparenchymally, typically in conjunction with an ICP monitor. As such, the monitor reveals regional or local, rather than global, oxygen levels. An oxygen tension of 10 mm Hg is considered the threshold for brain hypoxia. This value can be increased either by increasing supply of oxygen (supplemental O2, raising CPP, treating anemia) or by decreasing demand (propofol or barbiturate therapy). In addition to identifying inadequate cerebral Po2, this monitor may demonstrate hyperoxia that could occur with absolute or relative cerebral hyperemia such as from loss of cerebral autoregulation.
Some controversy exists regarding whether tissue Po2 monitors should be placed within a region of normal brain parenchyma or adjacent to the injured brain area.
Jugular bulb venous oximetry monitoring. In contrast to the regional information that the tissue Po2 monitor provides, the jugular bulb oximeter allows continuous or intermittent estimate of the global balance between cerebral oxygen demand and supply. Provided the cerebral metabolic rate for oxygen consumption (CMRo2) remains constant, calculation of the arteriovenous oxygen content allows estimation of the relative CBF. Even if CMRo2 does not stay constant, the arteriovenous oxygen content difference always reflects the balance between the brain's oxygen demand and supply. Because arterial oxygenation is usually 100%, provided that hematocrit remains constant, the jugular venous oxygen saturation (Sjvo2) equally reflects this balance. The physiological principle behind jugular venous oximetry is shown in Figure-4. Thus, intraoperative cerebral ischemia from inadequate perfusion pressure or excessive hyperventilation can be diagnosed readily. The influence of jugular venous desaturation on prognosis in patients with a head injury has been documented, and continuous jugular venous oximetry has become a routine monitor in many neurointensive care units. The thermistor-tipped catheter also measures temperature approximating that of the brain. Its major limitations include its global nature and therefore inability to detect focal cerebral ischemia and its invasive nature. Its reliability during CPB is also controversial.

Figure-4. Physiologic principles of jugular venous oximetry.

CMRo2 =


AVDo2 =


AVDo2 =

arterialO2 content (Cao2) - jugular venous O2 content (Cjvo2)

  = (Hgb x 1.39 x Sao2 + 0.003 x Pao2) - (Hgb x 1.39 x Sjvo2 + 0.003 x Pjvo2)
  = Hgb x 1.39 (Sao2 - Sjvo2) + 0.003 (Pao2 - Pjvo2)
  = Hgb x 1.39 (Sao2 - Sjvo2) (ignoring the amount of dissolved O2)

Interpretation of Sjvo2 values. The normal arterio-jugular difference for O2 (AVDo2) value is 2.8 mcmol/mL or 6.3 vol% of oxygen. (Range 2.2 to 3.3 mcmol/mL, or 5 vol% to 7.5 vol%), and Sjvo2 is between 60% and 70%. When oxygen delivery is higher than oxygen demand, as in hyperemia, AVDo2 decreases and Sjvo2 increases. During periods of global cerebral ischemia, AVDo2 widens and Sjvo2 decreases.
(1) Increased values. An Sjvo2 value of more than 90% indicates absolute or relative hyperemia. This can occur as a result of a reduced metabolic need (e.g., a comatose or brain-dead patient) or from excessive flow (e.g., severe hypercapnia). Patients with cerebral arteriovenous malformations have a direct arterial shunt into the venous circulation and thus have abnormally increased Sjvo2 values. Extracranial contamination, either from the facial vein or from rapid withdrawal in blood sampling (intermittent measurement), also results in an elevated value.
(2) Normal values. Although a normal balance between flow and metabolism results in a normal Sjvo2, it does not exclude the presence of focal ischemia. Because the blood in the jugular veins drains all areas of the brain, a discrete area of ischemia or infarction might not influence the overall level of saturation.
(3) Decreased values. On the other hand, Sjvo2 is sensitive to global cerebral ischemia. A value of <50% reflects increased O2 extraction and indicates a potential risk of ischemic injury. This may be due to increased metabolic demand, as in fever or seizure, not matched by an equivalent increase in flow, or due to an absolute reduction in flow. A significant decrease in O2-carrying capacity due to a decrease in hematocrit also leads to desaturation. Ischemia may also alter CMRo2 measurements and affect the interpretation of Sjvo2. As ischemia progresses to infarction, oxygen consumption decreases and Sjvo2 normalizes.
Microdialysis catheters. A small catheter, typically inserted in conjunction with an ICP or tissue Po2 monitor, allows sampling of small molecules in the interstitial fluid. The catheter, 0.6 mm in diameter, has a 10-mm dialysis membrane. Artificial cerebrospinal fluid (CSF) circulates through the catheter, allowing equilibration with the extracellular fluid and subsequent analysis of its chemical composition. This monitor's value is in determining the metabolic state of the brain and assessing the local cellular integrity. Three markers are thought to be valuable for these purposes. An increasing lactate/pyruvate ratio is sensitive to the onset of ischemia. High levels of glycerol suggest inadequate energy to maintain cellular integrity and the resultant membrane breakdown. Finally, excitatory amino acids, such as glutamate, are both a marker for neuronal injury and a factor in its exacerbation.
Currently, the microdialysis catheter is primarily used in two situations: (a) extensive subarachnoid hemorrhage where subsequent vasospasm is likely and (b) traumatic brain injury (TBI) of sufficient severity to warrant ICP/CPP monitoring. In either situation, a significant risk exists for the development of secondary injury due to cerebral ischemia.
Location of the microdialysis catheter is important because it provides information regarding only a small surrounding region of brain. With subarachnoid hemorrhage, the catheter should be placed in the region of the brain perfused by the vessel most likely at risk for vasospasm. Placement in TBI depends on the nature of the injury. With diffuse injury, the recommendation is to place the catheter in the right frontal region. A focal contusion warrants one catheter in the pericontusional area but not within the contusion and a second catheter in the normal brain.

Noninvasive monitoring. Near-infrared spectroscopy (NIRS) or transcranial oximetry measures cerebral regional oxygen saturation by measuring near-infrared light reflected off the chromophobes in the brain, the most important of which are oxyhemoglobin, deoxyhemoglobin, and cytochrome A3. NIRS has been studied in a variety of clinical settings including CEA and hypothermic circulatory arrest. Its major limitations include the intersubject variability, the variable length of the optical path, the potential contamination from extracranial blood, and most important, the lack of a definable threshold. Because of the thin scalp and skull in the neonate and infant, NIRS holds promise in this patient population but remains an investigative tool in its present form.


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