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Essentials of Multimodal Brain Monitoring 

Essentials of Multimodal Brain Monitoring
Chapter:
Essentials of Multimodal Brain Monitoring
Author(s):

Jennifer E. Fugate

DOI:
10.1093/med/9780190862923.003.0131
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date: 07 December 2019

Goals

  • Describe the physiologic principles of multimodal monitoring.

  • Describe the indications for multimodal monitoring.

  • Review the physiologic inferences that can be made from multimodal monitoring but not from traditional single monitors.

Introduction

Intensive care unit (ICU) clinicians spend a substantial amount of time monitoring patients and their organ systems. Staples of systemic monitoring include continuous electrocardiography, pulse oximetry, serum laboratory values of liver and kidney function, urinary output, and ventilator parameters. Monitoring methods for the brain have lagged somewhat in technologic advances. For years, the only brain monitoring system was the neurologic examination, and it is still the foundation of all neuromonitoring. Neurointensivists must have a thorough knowledge of the anatomy and physiology of the central nervous system and be able to correctly interpret changes in the neurologic examination. Neuroimaging is essential to supplementing the clinical examination, and the technology has become increasingly sophisticated. Although computed tomography (CT) and magnetic resonance imaging (MRI) are crucial to defining appropriate diagnoses and treatment plans for patients with acute brain injury, they are not covered in this chapter.

Several devices are available for monitoring parameters of brain physiology, including intracranial pressure (ICP), cerebral blood flow (CBF), autoregulation, brain oxygenation, and brain metabolism (Figure 131.1). The most robust data for these monitoring devices come from patients with severe traumatic brain injury (TBI) and aneurysmal subarachnoid hemorrhage (aSAH). The rationale for monitoring different aspects of brain physiology (ie, multimodal monitoring) is to allow clinicians to track, prevent, and treat secondary brain injury; to facilitate care according to protocols for pathophysiologic processes; to detect deterioration in heavily sedated patients (in whom the neurologic examination is nearly useless); and to provide information that can be used as prognostic markers.

Figure 131.1. Overview of Multimodal Monitoring of Brain Physiology. CPP indicates cerebral perfusion pressure; EVD, external ventricular drain; ICP, intracranial pressure; MAP, mean arterial pressure; Pbto2, partial pressure of oxygen in interstitial brain tissue; Spo2, oxygen saturation by pulse oximetry; TCD, transcranial Doppler ultrasonography.

Figure 131.1. Overview of Multimodal Monitoring of Brain Physiology. CPP indicates cerebral perfusion pressure; EVD, external ventricular drain; ICP, intracranial pressure; MAP, mean arterial pressure; Pbto2, partial pressure of oxygen in interstitial brain tissue; Spo2, oxygen saturation by pulse oximetry; TCD, transcranial Doppler ultrasonography.

Intracranial Pressure

When a person is lying in a supine position, normal ICP is less than 15 mm Hg. An ICP exceeding 20 to 25 mm Hg has surpassed a generally accepted threshold and should be treated. Sustained intracranial hypertension is strongly associated with increased mortality, particularly in patients with TBI. Cerebral perfusion pressure (CPP), a concept rather than a directly measured value, is equal to mean arterial pressure (MAP) minus mean ICP. CPP is used as a surrogate for CBF; in theory, when ICP is high, CPP may become compromised and the brain may be at risk of injury due to global cerebral ischemia. General guidelines for when to use an ICP monitor are shown in Table 131.1.

Table 131.1 Indications for Monitoring Intracranial Pressure

Acute Neurologic Disorder

Indicationsa

Traumatic brain injury

Coma and abnormal findings on CT of the head

Coma and normal findings on CT of the head and 2 of the following 3:

    Age >40 y

    SBP <90 mm Hg

    Motor posturing (decorticate or decerebrate)

Subarachnoid hemorrhage

Hydrocephalus

Diffuse brain edema and coma

Intracerebral hemorrhage

Hydrocephalus

Fulminant hepatic failure

Rapidly progressing grade 3 hepatic encephalopathy (incoherent speech and drowsy)

Grade 4 hepatic encephalopathy (comatose, unresponsive to pain, and motor posturing)

Diffuse brain edema

Acute bacterial meningitis

Diffuse brain edema

Other conditions with hydrocephalus (eg, cerebellar stroke, tumor)

Hydrocephalus

Abbreviations: CT, computed tomography; SBP, systolic blood pressure.

a Coma indicates Glasgow Coma Scale score less than 8.

The 2 reliable devices for measuring ICP are ventricular catheters (ie, external ventricular drains [EVDs]) and fiberoptic parenchymal monitors (Figure 131.2). Both are invasive, but the associated risks of infection and hemorrhage are minimal when the devices are placed and cared for by experienced operators. EVDs have the advantage that they can be used to treat increased ICP by diverting cerebrospinal fluid (CSF); EVDs are preferred for treatment of hydrocephalus. They produce a reliable measure of ICP, however, only when they are closed and not draining CSF. The benefit of parenchymal ICP monitoring is the relative ease of placement in addition to providing a continuous measure of ICP.

Figure 131.2. Intracranial Pressure Monitors. Axial noncontrast computed tomographic scans of the head show placement of intracranial pressure monitors. A and B, A patient with intraventricular hemorrhage (A) underwent placement of a right frontal external ventricular drain; the tip of the catheter is visualized in the right lateral ventricle (B). C and D, A patient with traumatic brain injury and right posterior subdural hematoma (C; arrows) underwent placement of a right frontal intraparenchymal fiberoptic intracranial pressure monitor (D; arrow).

Figure 131.2. Intracranial Pressure Monitors. Axial noncontrast computed tomographic scans of the head show placement of intracranial pressure monitors. A and B, A patient with intraventricular hemorrhage (A) underwent placement of a right frontal external ventricular drain; the tip of the catheter is visualized in the right lateral ventricle (B). C and D, A patient with traumatic brain injury and right posterior subdural hematoma (C; arrows) underwent placement of a right frontal intraparenchymal fiberoptic intracranial pressure monitor (D; arrow).

ICP measurements provide additional useful information because they are used to calculate secondary indexes of cerebral physiology. For example, the cerebrovascular pressure reactivity index (PRx), a moving correlation coefficient between mean ICP and slow fluctuations in MAP, reflects the ability of smooth muscle within cerebral arteriolar walls to react to changes in transmural pressure. Under normal circumstances, with increasing MAP, intact pressure reactivity will lead to vasoconstriction, a reduction in cerebral blood volume, and a reduction in ICP. Thus, as MAP increases, ICP decreases. PRx is calculated with a moving correlation coefficient between time-averaged values of ICP and MAP. A negative PRx reflects normal pressure reactivity of the blood vessels. A positive PRx signifies a nonreactive, passive arterial bed and dysfunctional cerebral autoregulation. Although PRx provides an indication of the status of cerebral autoregulation, it is not exact because other factors besides pressure reactivity contribute to autoregulation (eg, metabolic demand, Paco2, and autonomic nervous system input).

ICP has been the focus of monitoring in neurocritical care units for decades, but interest has increased in the use of CPP-directed therapy. Brain Trauma Foundation guidelines recommend that for patients with severe TBI, the target CPP should be 50 to 70 mm Hg, but much research is being conducted to determine whether an individualized CPP may be superior. In theory, if autoregulation is impaired, a CPP that would otherwise be considered a goal may be too high and result in worsening brain edema, higher ICP, and increased risk of hemorrhage. However, if autoregulation is intact, higher CPP levels may result in a compensatory vasoconstriction, reduced cerebral blood volume, and reduced ICP. Some research groups have proposed that an individualized “optimal CPP” may describe a target CPP at which autoregulation is optimal for each person. However, further large prospective studies are needed before this can be recommended for routine and widespread clinical use.

Brain Oxygenation

Adequate oxygenation is crucial to maintaining cell integrity. Hypoxia is defined as a reduction in tissue oxygenation to levels that are insufficient to maintain cellular metabolism and function. Inadequate oxygenation aggravates secondary brain injury, making detection and treatment of hypoxia (both brain and systemic) important in the care of critically ill patients. The introduction of monitoring the partial pressure of oxygen in interstitial brain tissue (Pbto2) and the jugular bulb venous oxygen saturation (Sjvo2) has allowed for continuous evaluation of the balance of oxygen delivery and use within the white matter of the brain. Brain Trauma Foundation guidelines recommend placement of brain oxygenation monitors when hyperventilatory strategies are used after TBI. More recent guidelines from various international ICU societies recommend monitor placement in any patient thought to be at risk for cerebral ischemia.

Monitoring Pbto2 requires an invasive probe that is placed through a bolt or through a craniotomy site. The probe provides a continuous measure of the partial pressure of oxygen within the adjacent white matter. Normal values for Pbto2 have been documented as 20 to 35 mm Hg, and recent guidelines suggest a treatment threshold of 20 mm Hg. Low levels of Pbto2 (<10 mm Hg) have been associated with morbidity, death, and extracellular evidence of metabolic crises. With the use of Pbto2 as a target in CPP-driven therapies and in a few preliminary small studies, outcomes have improved with this approach, but Pbto2 is not specific for failure of adequate perfusion. A product of both CBF and blood oxygen tension, Pbto2 provides information to assess for adequate oxygen delivery and to identify hypoxia not related to perfusion. Clinical data are still emerging. Retrospective studies have had mixed results, but more reliable information is awaited from an ongoing phase 3 trial, Brain Oxygenation Optimization in Severe TBI—Phase 3 (BOOST-3), which is comparing therapy directed by Pbto2 with therapy not directed by Pbto2 to determine whether Pbto2-directed therapy results in improved clinical outcomes.

In contrast to Pbto2, which provides regional information (within a diameter of about 5 mm of the probe), Sjvo2 provides a global measure of cerebral oxygen use. The monitoring of Sjvo2 requires central catheter placement, usually in the dominant internal jugular vein, and positioning superiorly in the jugular bulb. Normal values range between 55% and 75%. Sjvo2 levels less than 55% imply increased oxygen extraction and brain tissue possibly at risk for ischemia. These low values have been associated with poor outcomes, especially in patients with values that do not improve with treatment aimed at improving CBF. Sjvo2 levels greater than 75% may signify hyperemia, decreased metabolic demand, or cell death. The accuracy and safety of Sjvo2 monitoring is limited in comparison to Pbto2 monitoring, and it shares the similar limitation of providing nonspecific data. Enthusiasm for Sjvo2 monitoring has been limited because of the technical difficulties involved with placing and maintaining the device. Sjvo2 monitoring can be susceptible to positioning artifacts and complications associated with catheter insertion (eg, carotid puncture, infection, accidental misplacement, and jugular thrombosis).

Cerebral Microdialysis

Cerebral microdialysis allows the measurement of concentrations of interstitial markers of brain metabolism with a perfusion pump and a small 2-lumen probe inserted into the brain parenchyma. Microdialysis is recommended for patients who are at risk for (or already have) cerebral ischemia, hypoxia, energy failure, or glucose deprivation. Microdialysis should be used only in combination with other monitoring tools. A standard cerebral microdialysis membrane (with a 20-kDa molecular weight cutoff) can be used to recover glucose, pyruvate, lactate, glycerol, and glutamate. The rationale for collecting these substances is that they are useful for identifying a transition from aerobic to anaerobic metabolism, which may signify energy failure. These markers are not specific for ischemia alone but reflect overall energy metabolism in the brain. The most sensitive marker for ischemia is an increased lactate to pyruvate ratio (LPR). In observational studies, an LPR greater than 40 and persistently low brain glucose levels have been associated with unfavorable clinical outcomes. Microdialysis has also been used to monitor extracellular concentrations of neurotransmitters, such as glutamate and γ‎-aminobutyric acid, and markers of cellular damage, such as glycerol.

Microdialysis is used mostly as a research tool; it is performed as a routine part of clinical management in only a few centers in the world. One limitation of microdialysis is that data are delayed because fluid travels relatively slowly through the catheter and the collection occurs over approximately 60 minutes. This can be a labor- and resource-intensive process, further limiting its widespread applicability.

Cerebral Blood Flow

Thresholds of CBF that define ischemia have been derived from experimental models, and there is much interest in developing methods to monitor CBF in patients. Radiographic methods used to estimate CBF (eg, CT perfusion, MRI perfusion studies, arterial spin labeling, and positron emission tomography) are beyond the scope of this chapter, but they have shown that cellular injury can occur in the absence of traditionally defined thresholds for ischemia. CBF data should be interpreted in the clinical context and in combination with data from other monitoring devices.

Blood flow can be monitored continuously in a small region of the brain with invasive thermal diffusion flowmetry (TDF) or, less commonly, laser Doppler flowmetry. TDF uses an intraparenchymal probe with a thermistor and a temperature sensor. The distal thermistor is heated by 2°C, and the thermal gradient between the thermistor and the proximal temperature sensor is measured, providing a quantified regional CBF measurement in milliliters per 100 grams per minute. Mean values of 18 to 25 mL/100 g/min are considered normal; however, trends rather than absolute values may be better for detecting early neurologic deterioration or for assessing a response to therapy. The process has several limitations: 1) Reliability is decreased when patients have an elevated systemic temperature; 2) limited data correlate with clinical outcomes; 3) only a small region of the brain is monitored; and 4) the optimal placement site is uncertain.

Blood flow to larger regions of the brain can be estimated with transcranial Doppler ultrasonography (TCD). TCD provides information on flow velocity and direction of flow in a segment of blood vessel being investigated. Most centers use TCD as an intermittent study, but a head frame can be used for continuous monitoring. Generally when a head frame is used, the patient must be heavily sedated because small movements decrease the accuracy of the probe. Within the segment of artery studied, TCD provides beat-to-beat information from peak systole through end diastole and creates the spectral waveform (Figure 131.3).

Figure 131.3. Transcranial Doppler Ultrasonography. A, Spectral waveforms (reflecting arterial pulse waveforms) were obtained with transcranial Doppler ultrasonography of the left posterior cerebral artery (LPCA) (mean flow velocity, 42 cm/s). B, Spectral waveform of the left middle cerebral artery (LMCA) shows mean flow velocity of 112 cm/s.

Figure 131.3. Transcranial Doppler Ultrasonography. A, Spectral waveforms (reflecting arterial pulse waveforms) were obtained with transcranial Doppler ultrasonography of the left posterior cerebral artery (LPCA) (mean flow velocity, 42 cm/s). B, Spectral waveform of the left middle cerebral artery (LMCA) shows mean flow velocity of 112 cm/s.

In the ICU, TCD has been used primarily to monitor for vasospasm in aSAH and to identify hypoperfusion or hyperperfusion in patients with TBI. When monitoring for vasospasm, traditionally the mean blood flow velocity has been used to identify thresholds that correlate with the presence of angiographic vasospasm, and this is best studied in the proximal middle cerebral artery (MCA). A mean flow velocity less than 120 cm/s in the MCA is strongly suggestive of the absence of vasospasm. Values greater than 160 cm/s in the MCA are correlated with the presence of vasospasm, and values greater than 200 cm/s suggest the presence of severe vasospasm. The inclusion of the Lindegaard ratio (the ratio of the flow velocity in the MCA to the flow velocity in the extracranial internal carotid artery) or the relative rate of change of velocities improves accuracy. A Lindegaard ratio greater than 3 is consistent with the presence of intracranial vasospasm, and a ratio greater than 6 suggests severe vasospasm. As in any method of ultrasonography, the accuracy of TCD results is largely dependent on operator variability, which is a major limitation of this monitoring device. In addition, about 10% of patients have suboptimal bone windows for insonation.

Current Status

Devices are becoming more widely available to monitor various pathophysiologic parameters of the acutely injured brain (Table 131.2). These neurophysiologic data should always be integrated with the clinical examination and neuroimaging findings and should never be interpreted in isolation. The tremendous amount of data that can be generated with these monitors highlights the need for further development in bioinformatics, data acquisition, and data display techniques. Patient outcomes cannot be expected to be improved with the use of monitors alone but rather by the actions and changes in management that are provoked by data provided by the monitors. Much of the data for multimodal monitoring are from single-center observational studies, and prospective, multicenter, randomized trials are still needed.

Table 131.2 Brain Monitoring Modalities

Method

Variable Measured

Anatomical Resolution

Temporal Resolution

Advantages

Disadvantages

Fiberoptic catheter

ICP

Global

Continuous

Reliable

Quantitative

Allows calculation of secondary indexes

Invasive

EVD

ICP

Global

Intermittent or continuous

Reliable

Quantitative

Therapeutic

Allows calculation of secondary indexes

Invasive

Pbto2

Brain tissue oxygenation

Regional

Continuous

Sensitive

Quantitative

Invasive

Measures small region of brain

Sjvo2

Cerebral hemispheric oxygenation

Global

Continuous

Quantitative

Invasive

Susceptible to artifacts

Thrombosis

Microdialysis

Brain metabolism

Regional

Intermittent

Sensitive

Quantitative

Invasive

Labor intensive

Thermal diffusion flowmetry

Cortical CBF

Regional

Continuous

Robust information

Qualitative

Measures small region of brain

Not well standardized

TCD

CBF

Regional

Continuous

Noninvasive

Operator dependent

Difficult to keep probes in place

Abbreviations: CBF, cerebral blood flow; EVD, external ventricular drain; ICP, intracranial pressure; Pbto2, partial pressure of oxygen in interstitial brain tissue; Sjvo2, jugular bulb venous oxygenation saturation; TCD, transcranial Doppler ultrasonography.

Summary

  • A main goal of multimodal monitoring is to detect and limit secondary brain injury, an important cause of morbidity and death among patients with acute brain injury.

  • Measurement of ICP, the cornerstone of monitoring, is most accurate with an intraparenchymal fiberoptic catheter or, if hydrocephalus is present, with an EVD.

  • CPP should be between 50 and 70 mm Hg in most patients; individualized CPP values that reflect the patient’s autoregulation status are the subject of ongoing research.

  • Brain oxygen delivery and use can be measured regionally with an intraparenchymal catheter or globally with a probe that measures Sjvo2.

  • Cerebral microdialysis can assist in identifying neuroglycopenia and cellular metabolic crises.

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