"Neuromonitoring" is a term abused by this chapter to represent all the methods used to serially assess what the brain is doing. Though that definition is impossibly broad and loose (theoretically, weekly visits to a psychiatrist could be neuromonitoring), this chapter will restrict the range of possible options to include only those that can be used to monitor traumatic brain injury, consistent with the stem of Question 27 from the first paper of 2023. This excellent paper by Rajagopalan &Sarwal (2023) covers most of what that question is asking for, but it is unfortunately paywalled, which leaves the readers to peruse unreliable non-peer-reviewed online resources.
"Clinical" neuromonitoring is term being used here as a somewhat vague handwave in the direction of bedside neurological examination, arguably the last remaining useful form of physical examination in the ICU. Obviously the looseness of the term allows a substantial amount of wiggle room, considering the same phrase can describe serial recorded AVPU observations as easily as an examination by a neurologist in an expensive suit with tuning forks and coloured hat pins.
Clinical examination as neuromonitoring for traumatic brain injury:
- Part of the ongoing tertiary survey of ICU patients with TBI
- Solo mechanism of neuromonitoring in austere envornments
- Combined with serial imaging, forms a part of TBI management where direct ICP monitoring is not available or appropriate (Ropper et al, 2013)
- Gold standard of assessment
- Easily repeatable
- Cheap (i.e. minimal equipment cost)
- Thorough (can identify subtle deficits, eg. cranial nerve palsies)
- Reliable (especially when using validates scales, eg. the GCS)
- Able to localise neurological deficits
- A full examination may take longer than other methods of assessment
- Confounded by sedation, eg. the effect of opioids on pupils
- Often limited to the GCS, which may miss subtle changes
- Does not replace serial imaging
- Can cause distress to the patient (eg. can involve inflicting pain)
Contrary to the glib inventory of advantages above, the assessment of a patient by trained professionals is not cheap, even if they do not specifically bill for it. The cost of employing and training senior staff who produce thorough and reliable examination findings is not to be trivialised. It just so happens that these senior staff will also do other things, whereas the EEG machine will not; and this gives rise to the impression that there is some kind of cost savings here, in comparison to specialised devices.
Given that neurologists in suits are not exactly free to do hourly serial neuro obs, the clinical assessment of TBI is usually delegated to nursing staff of the ICU, and is made as reliable and reproduceable as possibly by the use of standardised scales or scoring instruments, of which the most popular one is the Glasgow Coma Scale. In addition to this, we also have the Full Outline of UnResponsiveness (FOUR) score and the Richmond Area Sedation Scale (RASS) which can be used as a de facto neuromonitoring instrument to grossly assess the level of arousal of sedated TBI patients. At its most basic, serial neurological examination should incorporate the regular measurement of pupil diameter, so that herniation can be detected.
The use of serial clinical examinations is a legitimate adjunct to serial imaging whenever ICP monitoring is for whatever reason not available. The BEST:TRIP trial, which ran in Bolivia and Ecuador, enrolled 324 patients and demonstrated that a TBI management protocol reliant mainly on clinical examination is not inferior to ICP-guided management (mortality was 39% vs 41%, and all the other composite outcome measures were also similar). On the basis of their study protocol ("ICE", Imaging and Clinical Examination), we now have the CREVICE protocol, devised by Delphi methods by a group of Latin American neurosurgeons and neurointensivists who routinely have to manage patients without ICP monitors. The serial clinical assessment integrated into this protocol consisted of GCS and pupil examination, where a score of 4 or less, or the finding of assymatrical or unreactive pupils, form a part of the minor criteria used to decide whether there is a need for ICP-lowering therapies.
"Susceptible to resource limitations and clinical philosophies", is how the CREVICE protocol authors describe ICP monitoring, before they paint a TBI world without it. However, there is no escaping the Monro-Kellie doctrine, and even this non-ICP-measuring protocol relies on management strategies which are all ultimately designed to lower the ICP. In other words, the ICP is clearly important whether it is being measured or not; so you may as well measure it.
ICP measurement as neuromonitoring for traumatic brain injury:
- Detection of otherwise occult ICP elevation (eg. in patients too unconscious to be assesed clinically)
- Titration of neuroprotective therapies to prevent secondary brain injury
- Calculation of cerebral perfusion pressure
- Well accepted preventative methods, eg. supported by BTF guidelines
- An established range of therapies (eg. osmotherapy) are guided by ICP monitoring
- Well-practiced, and generally safe
- A monitoring technique that also doubles as a therapeutic option (i.e. EVD can be drained to lower the ICP)
- Continuous (whereas other monitoring techniques, such as physical examination, are intermittent)
- Not confused by sedation
- Accurate in completely unconscious patients, and those with eye injuries (ie. where clinical assessment is not possible)
- Invasive, particularly EVDs
- Gradually less and less accurate (fibreoptic monitors)
- May not allow recalibration (fibreoptic monitors)
- Susceptible to infection (eg. ventriculitis)
- Susceptible to overdrainage (resulting in worsening midline shift or ICH)
- Does not prevent the need for imaging
- Does not appear to improve mortality
The widespread acceptance of ICP monitoring as a protective strategy is the most important advantage to note, but there are numerous others. For example, many patients with TBI, such as those who have severe TBI, are very unconscious (GCS 3) and are therefore not susceptible to clinical examination beyond pupil diameter. And by the time those become unequal, the ship has well and truly sailed. Also, the mechanistic explanation is very attractive. Improve intracranial pressure, and the perfusion pressure of the brain tissue should improve, which therefore means the blood flow to the brain should improve, avoiding further damage to the vulnerable penumbra.
So, does ICP monitoring help TBI patients by protecting them from secondary brain injury? Well, there is a suspected positive effect on survival in resource-rich environments. Al Saiegh et al (2020), looking retrospectively at 36,929 Pennsylvanian patients (a "mature trauma system") found that ICP monitoring conferred a 25% reduction of in-hospital mortality. This being retrospective and observational does change the way it is viewed, of course, considering that data from RCTs does not suggest any mortality benefit. For example Yuan et al (2015) performed a meta-analysis and determined that there was no convincing evidence of a mortality benefit, and furthermore discovered a significant trend towards increasing ICU length of stay.
So, if blood supply to the brain tissue is the variable you are really interested in, why not just measure it directly, rather than relying on surrogate measures like the ICP (that don't seem to affect mortality outcomes anyway)? Two mainstream methods are available, and several other techniques are described in the periphery of the literature. For the more conventional approaches, Gomez et al (2021) give a good account of transcranial Doppler, and Bhardwaj et al (2015) offer a detailed discussion of jugular venous oximetry.
Cerebral blood flow measurement as neuromonitoring for traumatic brain injury:
- Monitoring the change in pulsatility to detect changing intracranial pathology
- Determination of cerebral autoregulation "breakpoints" to establish a CPP target
- Determination of brain death
- Non-invasive (in the case of transcranial doppler) or minimally invasive (in case of jugular oximetry)
- Can be continuous, to provide real-time information
- Supported by solid physiological principles, i.e plausible
- Specifically target a critically important endpoint (whereas ICP and CPP are surrogates for CBF, which is what we are really interested in)
- Can be used to assess the safety of hyperventilation
- Allows assessment of cerebral blood flow autoregulation, which then provides a CPP target to aim for with the other management
- Is prognostically important (as an extreme example, the absence of CBF can identify brain death)
- Limited support from guidelines
- Expensive to implement (requires specific devices or consumables)
- Requires some training for use, and can be operator-dependent (transcranial Doppler), including being dependent on the availability of the operrator
- Therapies designed to prevent secondary brain injury are mostly described in the setting of ICP monitoring; to substitute CBF monitoring would mean to extrapolate from ICP-based treatment recommendations
- Transcranial Doppler relies on good acoustic windows, which are absent in up to 17% of patients (especially the elderly)
- CBF monitoring quantifies the flow, but does not assess whether this quantity is adequate
- TCD only assesses specific regional blood flow (i.e. MCA), whereas jugular oximetry only assesses global blood flow, which means at-risk regions of tissue may be missed
In very brief and unsatisfying summary, transcranial Doppler is a technique of measuring cerebral blood flow noninvasively by measuring the velocity of red cells. It produces two variables, FV (flow velocity) and PI (pulsatility index). FV can be either abnormally low or abnormally high (hyperemia) in severe TBI, and both tend to be associated with poorer outcomes, whereas normal FV is associated with a better prognosis. PI is strongly correlated to cerebral perfusion pressure and was also at one stage thought to be related to cerebral vascular resistance. For interest, abnormal values are over 1.4 for PI and under 20cm/s for FV. The deterioration of these variables appears to correlate with the development of secondary brain injury, and there's even a meta-analysis of studies that used this for prognostication, but it is less clear how you might go about using them for bedside management. You are, after all, able to monitor FV and PI continuously, which means theoretically you could administer interventions and observe their effects. There are examples of such practice out there, such as the protocol published by Tamagnone et al (2023), which boils down to this:
How does this integrate into the guidelines for the management of a patient with an EVD, or into tiered therapy for TBI? Well, reader, it doesn't. When the BTF authors were reviewing the evidence for the 4th edition, they were unable to locate enough good-quality data for TCD to even make it into the summary statements on their front page.
On the other hand, comparatively, the data describing jugular venous oximetry is more abundant and robust. That is not necessarily to say that SjvO2 monitoring is somehow superior - it's just better studied, and there was enough material out there for BTF to give a Level III recommendation for the use of it "as a source of information for management decisions". At its most basic, SjvO2 monitoring involves placing a catheter into the "jugular bulb", which is a dilatation of the jugular vein, and then either sampling or continuously monitoring the saturation of the blood that is leaving the brain to get some appreciation of the oxygen extraction by the brain tissue. Each jugular gets 70% of its blood from the ipsilateral and 30% from the contralateral hemisphere, so measuring either side will give you a fair representation of what is happening in the whole brain, but at the same time there is enough reason to place these on the same side as the lesion. The value of concern is 50%, i.e. SjvO2 lower than this is associated with poor outcomes.
So what if it's low? How does one react to this information, to use it for management decisions as promised? It appears the BTF authors based their recommendation on four studies from the 1990s, of which a good representative is this 1998 paper by Julio Cruz. The authors integrated jugular oximetry with ICP measurements. Their approach can be summarised as follows:
Generally speaking these days we don't like to hyperventilate patients for ICP, which makes this somewhat useless. The BTF recommend hypocapnia only for the prehospital environment, and only as a temporary measure in the setting of acute herniation. A more modern protocol is offered by Bhardwaj et al (2015), which really acts mostly as a list of possible reasons for the change in SjvO2 rather than recommendations on how to restore it to normality.
"Cerebral function and metabolism" was a part of the stem from Question 27 from the first paper of 2023, and that is why this section is called "functional and metabolic neuromonitoring", even though the use of this classification is slightly nauseating. "Functional" neuromonitoring could just as easily refer to a conversation with the patient, and jugular oximetry could overlap with "metabolic" neuromonitoring because technically cerebral metabolism is being monitored through the cerebral arteriovenous DO2 gradient. Still, this section needed a name suited to a wastebasket of these miscellaneous monitoring techniques that do not fit anywhere else:
With a group as diverse as these, it would be hard to lump everything together and produce a coherent statement about their common role or advantages and disadvantages, but let's have a go anyway:
- Assessment of the adequacy of cerebral blood flow and extent of cerebral dysfunction
- Detection of regional problems (eg. areas of ischaemia)
- Detection of global problems susceptible to intervention (eg. NCSE)
- Guidance for management (eg. titration of antiepileptics or BSL targets)
- Can identify otherwise undetectable pathology (eg. EEG can detect non-convulsive status epilepticus which would not be apparent clinically)
- Can be used to target neuroprotective therapies (eg. where EEG is monitored to confirm the depth of thiopentone coma)
- Regional assessment of cerebral pathology becomes possible (eg. cerebral microdialysis can target specific at-risk areas)
- Cerebral glucose measurements can guide glycaemic control targets
- Functional impairment can be more easily detected or prognosticated (eg. with somatosensory evoked potentials)
- Not confounded by muscle relaxants
- Limited to centres with experience, and mostly used for research purposes
- Expensive equipment
- Requires expertise and availability of specialist services
- Little support from guidelines and professional bodies