Introduction
Monitoring systemic and central nervous system physiology is fundamental to the perioperative and critical care management of patients with neurologic disease. The clinical neurologic examination remains the cornerstone of neuromonitoring. In addition, several techniques are available for global or regional monitoring of cerebral hemodynamics, oxygenation, metabolism, and electrophysiology. The pathophysiology of acute brain injury (ABI) is complex, and involves changes in cerebral blood flow (CBF), oxygen and glucose delivery and utilization, and electrophysiological derangements (see Chapter 1 ). It is, therefore, not surprising that a single monitor is unable to detect all instances of cerebral compromise. Multi-modality monitoring, the measurement of multiple variables simultaneously, provides a more complete picture of the (patho) physiology of the injured brain and its response to treatment ( Fig. 8.1 ). Multimodal monitoring has allowed a move away from rigid physiological target setting towards an individually tailored approach to the management of ABI. Some monitoring modalities are well established, whereas others are relatively new to the clinical arena and their indications still being evaluated; all have advantages and disadvantages ( Table 8.1 ). The general indications for neuromonitoring are summarized in Box 8.1 .
| Technique | Monitored variable(s) | Advantages | Disadvantages |
|---|---|---|---|
| Intracranial Pressure | |||
| Intraparenchymal microsensor |
|
|
|
| Ventricular catheter |
|
|
|
| Cerebral Blood Flow | |||
| Transcranial Doppler ultrasonography |
|
|
|
| Thermal diffusion flowmetry |
|
|
|
| Cerebral Oxygenation | |||
| Jugular venous oximetry |
|
|
|
| Brain tissue pO 2 |
|
|
|
| Near infrared spectroscopy (cerebral oximetry) |
|
|
|
| Cerebral Microdialysis |
|
|
|
| Electrophysiology | |||
| Electroencephalography |
|
|
|
| Electrocorticography |
|
|
|
| Processed EEG |
|
|
|
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Monitoring the healthy but “at risk” brain:
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carotid surgery
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cardiac surgery
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surgery in the beach chair position
- –
- •
Early detection of secondary adverse events after acute brain injury:
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intracranial hypertension
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reduced cerebral perfusion
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impaired cerebral glucose delivery/utilization
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cerebral hypoxia/ischemia
- –
cellular energy failure
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nonconvulsive seizures
- –
cortical spreading depolarizations
- –
- •
Guiding individualized, patient-specific therapy after acute brain injury:
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optimization of ICP and CPP
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optimization of brain tissue PO 2
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optimization of cerebral glucose delivery/utilization
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monitoring cerebral vasospasm after subarachnoid hemorrhage
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prognostication
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This chapter will review the brain monitoring techniques applicable to the perioperative and critical care management of patients with neurologic disease. The use of evoked potential monitoring during spine surgery is covered elsewhere in this book ( Chapter 6 ) and will not be considered here.
Clinical assessment
Fundamental to neuromonitoring is serial clinical assessment of neurologic status. The Glasgow Coma Scale (GCS) is an easy to use and standardized method for evaluating a patient’s global neurologic status by recording best eye opening, and verbal and motor responses to physical and verbal stimuli. In combination with the identification and documentation of localizing signs such as pupil responses and limb weakness, the GCS has remained the mainstay of clinical assessment in the 40 years since its first description. The main limitations of the GCS are that verbal responses are not assessable in intubated patients, and brainstem function is not directly considered. The Full Outline of UnResponsiveness (FOUR) score, which provides a more complete assessment of brainstem function, has been designed and validated to overcome these issues. The FOUR score measures ocular (as well as limb) responses to command and pain, along with pupillary responses and respiratory pattern, and can be used to differentiate further patients with a GCS of 3. There is limited evidence that the FOUR score has greater prognostic value than the GCS alone.
Clinical assessment is limited in sedated patients or those with a decreased level of consciousness, and one or more neuromonitoring techniques can be used to identify or predict secondary brain insults and guide therapeutic interventions in such patients.
Clinical assessment
Fundamental to neuromonitoring is serial clinical assessment of neurologic status. The Glasgow Coma Scale (GCS) is an easy to use and standardized method for evaluating a patient’s global neurologic status by recording best eye opening, and verbal and motor responses to physical and verbal stimuli. In combination with the identification and documentation of localizing signs such as pupil responses and limb weakness, the GCS has remained the mainstay of clinical assessment in the 40 years since its first description. The main limitations of the GCS are that verbal responses are not assessable in intubated patients, and brainstem function is not directly considered. The Full Outline of UnResponsiveness (FOUR) score, which provides a more complete assessment of brainstem function, has been designed and validated to overcome these issues. The FOUR score measures ocular (as well as limb) responses to command and pain, along with pupillary responses and respiratory pattern, and can be used to differentiate further patients with a GCS of 3. There is limited evidence that the FOUR score has greater prognostic value than the GCS alone.
Clinical assessment is limited in sedated patients or those with a decreased level of consciousness, and one or more neuromonitoring techniques can be used to identify or predict secondary brain insults and guide therapeutic interventions in such patients.
Intracranial and cerebral perfusion pressures
Intracranial pressure (ICP) is the pressure inside the skull and thus in the brain tissue; it is synonymous with the cerebrospinal fluid (CSF) pressure in the lateral ventricles. In addition to the measurement of absolute ICP, ICP monitoring allows calculation of cerebral perfusion pressure (CPP), identification and analysis of pathologic ICP waveforms, and derivation of indices of cerebrovascular pressure reactivity.
Intracranial Pressure
The first clinical measurements of ICP were made in 1951 using an electronic transducer to measure ventricular fluid pressure signals. Refinements in technique, a low adverse effect profile, and the introduction of microtransducer technology have combined to facilitate the widespread adoption of ICP monitoring into clinical practice.
Technical Aspects
There are two main methods of monitoring ICP—an intraventricular catheter or parenchymal microtransducer device. Other techniques, such as subarachnoid or epidural devices, are less accurate and now rarely used.
Ventricular catheters measure global ICP (CSF pressure in the lateral ventricles) in one of two ways: using a standard catheter connected via a fluid-filled system to an external pressure transducer, or a catheter incorporating microstrain gauge or fiberoptic technology. In vivo calibration is possible with both methods. ICP monitoring via a ventricular catheter is the technique of choice in patients with established or incipient hydrocephalus as it allows therapeutic drainage of CSF. Ventricular catheter insertion can be difficult, and there is a risk of placement-related hemorrhage and catheter-associated ventriculitis. The risk of ventriculitis increases with the length of time since catheter insertion, and can be reduced but not abolished by the use of antibiotic-impregnated or silver-coated catheters.
Parenchymal microtransducer ICP monitoring systems are of two types. Solid-state piezoelectric strain gauge devices incorporate pressure-sensitive resistors which translate pressure generated changes in resistance to an ICP value. Fiberoptic devices transmit light via a fiberoptic cable towards a displaceable mirror at the catheter tip. Changes in ICP distort the mirror and the difference in intensity of reflected light is converted into an ICP value. Both systems are easy to insert and are usually placed about 2 cm into brain parenchyma through a cranial access device or at craniotomy when they can also be sited in the subdural space. While intraventricular catheters have historically been considered the “gold standard” for ICP monitoring, intraparenchymal devices provide equivalent pressure measurement and are safer. In particular, the risk of hematoma and infection is low. Microtransducer systems are considered reliable, but zero drift can result in measurement error over several days and in vivo calibration is not possible.
Several noninvasive ICP monitoring techniques, which would be applicable in broader patient groups than invasive monitoring, have been described. Transcranial Doppler (TCD) ultrasonography-derived pulsatility index is an imprecise assessment of ICP compared with invasively measured pressure, and there is large intra- and interoperator variability. Optic nerve sheath diameter (ONSD) can be measured using ultrasound or computed tomography (CT), and is able to predict intracranial hypertension. Although lacking the risks of invasive methods, noninvasive ICP monitoring techniques currently fail to measure ICP sufficiently accurately for routine clinical use. They are also unable to monitor intracranial dynamics continuously.
Indications
Despite the absence of high-quality evidence demonstrating outcome benefits of ICP-guided management, ICP monitoring has become a standard of care after traumatic brain injury (TBI). It can also provide valuable information in other brain injury types, as well as in patients with hydrocephalus (it can also be useful for chronic monitoring in normal pressure hydrocephalus), and those undergoing craniotomy for lesions producing mass effect.
The Brain Trauma Foundation (BTF) recommends ICP monitoring to guide ICP- and CPP-directed therapy after severe TBI in all salvageable patients with an abnormal cranial CT scan, as well as in those with a normal scan and two or more of: age > 40 years, unilateral or bilateral motor posturing, and/or systolic blood pressure < 90 mmHg. A recent expert statement provides more detailed and updated guidance. It recommends ICP monitoring in comatose TBI patients with cerebral contusions when interruption of sedation to check neurologic status is dangerous, or when the clinical examination is unreliable. ICP monitoring is also recommended following a secondary decompressive craniectomy and should be considered after evacuation of an acute supratentorial intracranial hematoma in salvageable patients at increased risk of intracranial hypertension, including those with a GCS motor score ≤ 5, pupillary abnormalities, prolonged/severe hypoxia and/or hypotension, cranial CT findings suggestive of raised ICP, or intraoperative brain swelling. The expert group recommended that ICP monitoring should also be considered in TBI patients with extracranial injuries requiring multiple surgical procedures and/or prolonged analgesia and sedation.
ICP monitoring is increasingly being incorporated into protocols for the critical care management of subarachnoid (SAH) and intracerebral hemorrhage (ICH), although these indications are not as well-defined or well-studied compared with TBI.
Thresholds for Treatment and Evidence
Normal ICP varies with age and body position; in healthy, resting supine adults, normal mean ICP is 5–10 mmHg. ICP greater than 20–25 mmHg is widely considered to require treatment after TBI, although higher and lower thresholds are described. The presence of intracranial hypertension is detrimental and the time spent above a defined ICP threshold, as well as absolute ICP, is an important determinant of poor outcome. Changes in the ICP waveform occur as ICP increases, and waveform analysis has been used to predict the development of intracranial hypertension. While indication of critical reductions in intracranial compliance, before intracranial compensatory mechanisms have become exhausted, would allow more timely clinical intervention, clinical translation of this technique remains elusive.
A meta-analysis of 14 studies and 24,792 patients with severe TBI found that ICP monitoring-guided management of intracranial hypertension had no significant mortality benefit overall compared with treatment in the absence of ICP monitoring, although mortality was lower in patients who underwent ICP monitoring in studies published after 2012. The only randomized controlled trial of ICP-guided management after TBI found no difference in 3- or 6-month outcomes in 324 patients in whom treatment was guided by ICP monitoring compared with imaging and clinical examination in the absence of ICP monitoring. The non-ICP monitoring group in this study received protocol-specified but empirical treatment on a fixed schedule basis, and the wider applicability of such an approach is questionable given evidence that one of the interventions (mannitol) has a more beneficial effect when directed by monitored rises in ICP. In contrast to previous studies, those undergoing ICP monitoring received significantly fewer days of ICP-directed treatment (hyperventilation, hypertonic saline/mannitol and barbiturates) than those in the ICP monitored group, although the length of intensive care unit (ICU) stay was similar. It remains to be seen whether the findings of this study, conducted in Bolivia and Ecuador, are applicable to populations with access to superior pre-hospital care and rehabilitation services. When interpreting this study it is also important to note that evaluation and diagnosis of intracranial hypertension, either by monitoring ICP or assessment of clinical and imaging variables, was fundamental to the management of all patients. It therefore reinforces the widely held view that assessment of ICP is an integral part of the monitoring and management of severe TBI.
Multimodal monitoring incorporating ICP, brain tissue partial pressure of oxygen (PbtO 2 ) and cerebral microdialysis (CMD) is significantly more accurate in predicting cerebral hypoperfusion than ICP monitoring alone, and ICP monitoring is, therefore, best regarded as one part of a multimodal monitoring strategy rather than as a monitoring modality in isolation.
Cerebral Perfusion Pressure
CPP and ICP monitoring are synonymous, as ICP must be measured to allow calculation of CPP.
Technical Aspects
CPP is calculated as the difference between mean arterial pressure (MAP) and ICP, and modifiable through this relationship. For the calculation of CPP to be accurate the arterial pressure transducer must be referenced at the level of the foramen of Monro (tragus of the ear), and the implications of failing to do this are profound. When the head of the bed is elevated, measuring arterial blood pressure (ABP) at the level of the heart results in a calculated CPP that is erroneously high; for example, a measured CPP reading of 60 mmHg may actually represent a “true” CPP of < 45 mmHg. Such measurement discrepancies are exacerbated in tall patients, with varying elevations of the head of the bed, and different sites of arterial cannulation.
Indications
The main indications for CPP monitoring are similar to those for ICP. Although CPP-guided management is primarily applied in patients with TBI there is emerging evidence for a role in other brain injury types. Postoperative ICP monitoring is indicated if there is a risk of intracranial hypertension, such as after surgery for large brain tumors with mass effect.
Thresholds for Treatment and Evidence
Recommendations for a CPP threshold have changed over time. Current BTF guidelines recommend that CPP be maintained between 50 and 70 mmHg after TBI, with evidence of adverse outcomes if CPP is lower or higher. While lower CPP risks cerebral ischemia, higher CPP does not necessarily achieve a favorable outcome, and the administration of large fluid volumes and inotropes/vasopressors to maintain CPP carries a substantial risk of acute lung injury. Rather than a single threshold for CPP, multimodal monitoring can be used to identify an “optimal” value for an individual, which aims to reduce the risks of an excessive CPP while minimizing the risks of cerebral hypoperfusion and worsening secondary brain injury. Optimal CPP (CPPopt) can be determined using autoregulatory indices, which are discussed in the next section.
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