General
- The bulk of neuromonitoring literature deals with intracranial pressure (ICP).
- Other parameters that can be monitored include:
- Jugular venous oxygen monitoring
- Regional CBF
- Brain tissue oxygen tension
- Brain metabolites (pyruvate, lactate, glucose…)
- The role of adjunctive monitoring is currently unknown.
- Unanswered questions include:
- Should neuromonitoring be disease specific (e.g. is SAH different from TBI),
- Which monitors provide additional unique information,
- What are the critical values of the monitored entity,
- What interventions should be undertaken to correct abnormalities?
- Other than ICP monitoring which shows to have some benefit in reducing mortality other types of intracranial monitoring does not have enough evidence backing its use.
Summary of techniques
Technique | Monitored variable(s) | Indications in TBI | Advantages | Disadvantages |
Intracranial pressure Intraparenchymal or subdural microsensor | ICP, CPP, Autoregulatory indices | To allow CPP optimization through derivation of PRx and ORx | Relatively easy insertion Low procedural complication rate Low infection risk | In vivocalibration not possible Measures localized pressure Small zero-drift with time |
Ventricular catheter | As above | As above, plus: To allow therapeutic drainage of CSF | Measures global ICP Therapeutic CSF drainage In vivocalibration possible | More difficult insertion Risk of procedure-related haemorrhage Risk of catheter-related ventriculitis |
Cerebral blood flow Transcranial Doppler ultrasonography | Blood flow velocity, Pulsatility index, Autoregulatory indices | May detect cerebral hypoperfusion and facilitate early goal-directed therapy | Noninvasive Can be used on an intermittent or continuous basis Good temporal resolution | Measures relative (not absolute) CBF Operator dependent Failure rate in 5–10% of patients (absent acoustic window) Little evidence base in TBI |
Cerebral oxygenation Jugular venous oximetry | Jugular venous oxygen saturation, Arterio-venous oxygen content difference | To evaluate the adequacy of cerebral perfusion and oxygen delivery To supplement ICP/CPP-guided therapy To assist titration of medical and surgical therapies to guide ICP/CPP therapy | Global assessment of balance between CBF and metabolism | Non-quantitative assessment of cerebral perfusion Insensitive to regional ischemia Risk of extracranial contamination of samples |
Brain tissue pO₂ | Brain tissue oxygen partial pressure, Oxygen reactivity | As for jugular venous oximetry, plus: To allow CPP optimization through derivation of ORx | Regional assessment of balance between CBF and metabolism Continuous Ischaemic ‘thresholds’ defined | Minimally invasive Measures oxygenation within a small region of interest One hour run-in period limits intraoperative applications |
Near infrared spectroscopy (cerebral oximetry) | Regional cerebral oxygen saturation, Autoregulatory indices | As for jugular venous oximetry, plus: Detection of intracranial haematoma | Noninvasive Real time Multisite measurement | rScO₂-derived ‘ischaemic’ threshold not defined Readings affected by the presence of intracranial haematoma and ‘contamination’ of signals by extracranial tissue Little evidence base in TBI |
Cerebral microdialysis | Glucose, Lactate, pyruvate, and LPR, Glycerol, Glutamate, Multiple biomarkers for research purposes | To detect cerebral ischaemia, hypoxia, cellular energy failure, and glucose deprivation To predict the development of secondary injury before it is detectable clinically or by other monitoring modalities To optimize CPP To assist titration of medical therapies such as systemic glucose control | Assessment of cerebral glucose metabolism Detection of hypoxia/ischemia Assessment of non-ischemic causes of cellular bioenergetic dysfunction | Focal measure Thresholds for abnormality unclear Not continuous Labour-intensive |
Electrophysiology EEG | Seizures, Diagnosis-specific EEG patterns, Some evidence that detection of SDs might be possible | To detect convulsive and non-convulsive seizures To diagnose characteristic EEG patterns to facilitate prognostication | Noninvasive Detection of non-convulsive seizures Correlates with cerebral ischaemic and metabolic changes | Skilled interpretation required Affected by anaesthetic and sedative agents |
ECoG | Cortical SDs | To detect spreading cortical depolarizations | Currently the only method to identify SDs accurately | Highly invasive No evidence that treatment of SDs improves outcome Little evidence base in TBI and currently remains a research tool |
For developing countries
Crevice protocol Chesnut 2020
Crevice protocol Chesnut 2020
The criteria for defining high risk of IC hypertension
- Intracranial hypertension is suspected, and treatment is recommended in the presence of one major or two minor criteria.
- Major criteria are:
- Compressed cisterns (computed tomographic [CT] classification of Marshall diffuse injury III).
- Midline shift >5 mm (Marshall diffuse injury IV)
- Non-evacuated mass lesion.
- Minor criteria are:
- Glasgow Coma Scale (GCS) motor score ≤4
- Pupillary asymmetry
- Abnormal pupillary reactivity
- CT classification of Marshall diffuse injury II (i.e., basal cisterns are present with midline shift 0–5 mm and/or high- or mixed-density lesion ≤25 cm³)
Performance of the rule in a LATAM Cohort of sTBI
- When high ICP is defined as >22mm Hg
Performance | High ICP | Normal ICP |
Rule positive | 61 | 49 |
Rule negative | 4 | 36 |
Sensitivity | 93.9% (95% Confidence Interval [CI]: 85.0–98.3%) | 93.9% (95% Confidence Interval [CI]: 85.0–98.3%) |
Specificity | 42.4% (95%CI: 31.7–53.6%) | 42.4% (95%CI: 31.7–53.6%) |
Positive predictive value | 55.5% (95%CI: 50.7–60.2%) | 55.5% (95%CI: 50.7–60.2%) |
Negative predictive value | 90.0% (95%CI: 77.1–96.0%) | 90.0% (95%CI: 77.1–96.0%) |
Positive likelihood ratio | 1.6 (95%CI: 1.3–2.0) | 1.6 (95%CI: 1.3–2.0) |
Negative likelihood ratio | 0.2 (95%CI: 0.1–0.4) | 0.2 (95%CI: 0.1–0.4) |
Definition of neuroworsening and protocol activation indications
- Escalation of therapy (or adding another treatment) was considered if:
- Neuroworsening:
- Decrease in the motor GCS of 1 or more points
- New loss of pupil reactivity.
- Interval development of pupil asymmetry of >2 mm or bilateral mydriasis
- New focal motor deficit
- Herniation syndrome (e.g., Cushing's triad)
- No improvement or worsening on follow-up CT imaging
- No acceptable response to initial therapy
- The “modified definition of neuroworsening” includes signs of the herniation syndrome (e.g. Cushing’s triad) and a lower threshold for GCS motor score deterioration (≥ 1 point).
- Neuroworsening requires an immediate therapeutic response.
CT time
- The consensus modified the ICE protocol CT imaging schedule.
- If the initial CT is obtained within 4h of injury, a second CT is indicated within the next 12h.
- In all cases, follow-up CT imaging is recommended at 24 and 72h after injury, and as needed based on the clinical situation or to facilitate decision making.
Tier therapy
- Tier 1
- Scheduled hypertonic saline (for example, every 4 hours)
- Scheduled Mannitol (for example, every 4 hours)
- Maintain normothermia (threshold = 37.5º)
- Tier 2
- Hyperventilation, PaCO₂ = 30–35 mmHg, corrected for altitude
- Hypertonic saline 3% by continuous infusion
- Increase in sedation
- Tier 3
- Decompressive craniectomy
- High dose IV barbiturates
- Hypothermia (central temperature range <37ºC)