ICU · Neurocritical Care
Acute severe head injury: multimodal monitoring
Also known as Multimodal neuromonitoring · Brain tissue oxygenation (PbtO2) · Microdialysis · Brain injury monitoring · LICOX · External ventricular drain (EVD) · Intraparenchymal bolt · Cerebral microdialysis · Lactate/pyruvate ratio · Jugular venous bulb oximetry (SjvO2) · Continuous EEG (cEEG) · Non-convulsive status epilepticus · Pressure reactivity index (PRx) · Transcranial Doppler
Multimodal neuromonitoring in severe TBI goes beyond ICP monitoring to assess brain physiology directly. ICP is a PRESSURE — it says nothing about whether the tissue is receiving enough OXYGEN or SUBSTRATE. A patient can have a perfectly normal ICP of 12 mmHg and yet a critically low PbtO2, a rising lactate/pyruvate ratio, or non-convulsive status epilepticus. Modalities: (1) ICP monitoring (standard — external ventricular drain is the gold standard because it measures pressure AND drains CSF; intraparenchymal bolt is easier to site with a lower infection rate but cannot drain). (2) Brain tissue oxygenation (PbtO2 — LICOX probe, target >20 mmHg; <15 = brain tissue hypoxia; BOOST-2 trial showed PbtO2-guided therapy reduces brain hypoxia). (3) Cerebral microdialysis (lactate/pyruvate ratio >40 = metabolic distress; rising glutamate = excitotoxicity; rising glycerol = cell membrane breakdown; low glucose = substrate depletion). (4) Jugular venous bulb oximetry (SjvO2 — global cerebral oxygenation; target 55-75%; <50% = cerebral hypoxia, >90% = hyperaemia). (5) Continuous EEG (cEEG — non-convulsive status epilepticus occurs in 10-30% of comatose neuro-ICU patients). (6) Transcranial Doppler and autoregulation indices (PRx). Goal: integrate ALL modalities — treat the PATIENT, not the NUMBER.
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Target exams
Red flags
Why multimodal monitoring — the core rationale
The primary (mechanical) brain injury cannot be undone. Everything the intensivist does targets secondary injury — the cascade of hypoperfusion, ischaemia, excitotoxicity, inflammation and oedema that enlarges the lesion over hours to days. The four preventable insults are hypotension (SBP <110), hypoxia (SpO2 <90), hyperglycaemia (>10) and hyperthermia (>37.5°C); a single episode of hypotension doubles mortality (Traumatic Coma Data Bank). Multimodal monitoring is the instrument panel that tells you, in real time, whether your therapy is actually protecting the brain tissue — not just normalising a number.[1]
Monitoring modalities
ICP monitoring
Standard of care
- Indicated in ALL severe TBI (GCS 3-8) with abnormal CT (or normal CT with 2+ risk factors)
- External ventricular drain (EVD) — gold standard (measures pressure + drains CSF)
- Intraparenchymal bolt — easier to place, cannot drain CSF
- Target: ICP <22 mmHg (Brain Trauma Foundation 4th edition)
- CPP (cerebral perfusion pressure) = MAP - ICP. Target CPP 60-70 mmHg
PbtO2 (brain tissue oxygenation)
Local tissue oxygen
- Intraparenchymal sensor measures local oxygen tension in brain tissue
- Target: PbtO2 >15 mmHg (normal 25-40 mmHg)
- PbtO2 <15 = brain tissue hypoxia → increase FiO2, increase CPP, reduce ICP, optimise haemoglobin
- BOOST-2 trial: PbtO2-guided therapy (target CPP 60-70 AND PbtO2 >20) improved outcomes vs ICP-only guided
- Detects regional ischaemia that ICP monitoring alone misses
Cerebral microdialysis
Brain metabolites
- Semipermeable catheter in brain tissue — perfuses and samples extracellular fluid
- Measures: lactate, pyruvate, glucose, glutamate, glycerol
- Lactate/pyruvate ratio (LPR) >40 = cerebral ischaemia (anaerobic metabolism)
- Low glucose (<0.7 mmol/L) = metabolic crisis (brain starving)
- High glutamate = excitotoxicity (cellular damage)
- High glycerol = cell membrane breakdown (cell death)
Continuous EEG (cEEG)
Seizure detection
- Detects non-convulsive seizures/non-convulsive status epilepticus (NCSE)
- NCSE occurs in 10-30% of severe TBI patients — often undetected without cEEG
- Increases metabolic demand → worsens secondary brain injury
- Especially important during: TTM (paralysis masks seizures), barbiturate coma, deep sedation
- Treat: benzodiazepines (lorazepam), then anticonvulsant (levetiracetam, propofol infusion)
ICP monitoring in depth — the foundation
Devices: EVD vs intraparenchymal bolt
ICP monitoring devices — gold standard vs workhorse
| Feature | External ventricular drain (EVD) | Intraparenchymal bolt (Codman / Camino / Raumedic) |
|---|---|---|
| Site | Catheter in frontal horn of lateral ventricle | Parenchymal sensor (usually frontal) |
| Accuracy | GOLD STANDARD — measures true ventricular CSF pressure | Good; minor zero-drift (1-3 mmHg/week) |
| Therapeutic? | YES — drains CSF (the single fastest bedside way to lower ICP) | NO — measures only |
| Infection risk | HIGHEST — ventriculitis 5-15% | LOWER — ~1-2% |
| Ease of placement | Harder — requires ventricular puncture (slit ventricles difficult) | Easier — bedside twist-drill |
| Waveform | Provides full pressure waveform (P1/P2/P3, Lundberg waves) | Numeric mean ± trend only (no true waveform) |
| Best for | Hydrocephalus / large ventricles; need to drain; need waveform | Small/slit ventricles; emergency; monitoring only |
| Transducer reference | Foramen of Monro (external auditory meatus / tragus) | Zeroed at insertion (in-built) |
The ICP waveform — P1, P2, P3
The normal ICP trace shows three peaks per cardiac cycle:
- P1 (percussion wave) — arterial pressure transmitted from the choroid plexus; tall and fairly constant.
- P2 (tidal wave) — reflects intracranial compliance; the key compliance-dependent wave.
- P3 (respiratory wave) — venous/respiratory fluctuation. [1]
P2 > P1 = exhausted intracranial compliance. As compliance is lost, the P2 wave rises until it overtakes P1 — a premonitory sign that often PRECEDES the numeric mean ICP crossing 22 mmHg. A rising P2 is the early warning to escalate osmotherapy, drain CSF, or re-image BEFORE the mean number deteriorates. As compliance collapses further the waveform flattens and pulse amplitude falls — a late, ominous sign.[8]
Lundberg waves — pathological ICP trends
Lundberg ICP waves
| Wave | Pattern | Significance |
|---|---|---|
| A (plateau) | Sustained ICP >50 mmHg for 5-20 min | Vasodilatory cascade from low CPP → cerebral vasodilation → ↑intracranial blood volume → ↑ICP → ↓CPP → vicious cycle. Ominous — severely impaired autoregulation, exhausted compliance; poor outcome |
| B | Rhythmic 0.5-2/min oscillations of 20-50 mmHg | Impaired pressure autoregulation; warning the system is becoming unstable |
| C | Low-amplitude, higher-frequency oscillations | Less clinically significant |
Brain tissue oxygen (PbtO2) in depth
- Probe: a polarographic (Clark) or fluorescence oxygen sensor (LICOX, Neurotrend) placed into the parenchyma alongside the ICP bolt. It measures the O2 that diffuses from capillaries into tissue — the net of delivery minus consumption.
- Thresholds (LICOX): >20 mmHg normal; 15-20 borderline; <15 = hypoxia (treat); <10 = critical (strongly associated with death and poor outcome).
- What PbtO2 actually reflects: it is NOT simply arterial PaO2 — it is the composite of cerebral blood flow, arterial oxygen content (haemoglobin × saturation), and cerebral metabolic rate. A low PbtO2 can therefore arise from low CPP, anaemia, hypoxaemia, vasospasm, OR increased demand (seizures, fever). [1]
Therapeutic levers to raise PbtO2
| Lever | Mechanism | Caution |
|---|---|---|
| ↑ FiO2 / PaO2 | Direct increase in arterial oxygen content | Simplest first step; high FiO2 for prolonged periods has pulmonary toxicity |
| ↑ CPP (noradrenaline → ↑MAP) | Raises cerebral blood flow to ischaemic regions | Cap CPP at 70 (above 70 → ARDS risk, no added benefit) |
| ↓ ICP (osmotherapy, CSF drainage) | Lowers the resistance to cerebral perfusion | — |
| Transfuse if Hb <90 g/L | Increases oxygen carrying capacity | Balance against transfusion-related complications |
| ↓ metabolic demand (sedation, anticonvulsants, normothermia) | Less oxygen consumed → higher residual tissue O2 | Treat any seizures on cEEG aggressively |
| AVOID hyperventilation | — | Lowers ICP but VASOCONSTRICTS → worsens PbtO2 (Pyrrhic victory) |
Cerebral microdialysis in depth
- Mechanism: a double-lumen dialysis catheter perfused with isotonic fluid at a slow rate; extracellular solutes diffuse across the semi-permeable membrane and are collected hourly for bedside analysis. It samples the biochemical milieu of the brain extracellular fluid — the "chemistry of the tissue."
- It detects cellular energy failure and ischaemia EARLIER and more LOCALLY than global markers. [1]
Microdialysis markers — what each one means
| Marker | Normal | Abnormal | Meaning |
|---|---|---|---|
| Lactate/pyruvate ratio (LPR) | <25-30 | >40 = metabolic distress | Master marker. High LPR + LOW pyruvate = ischaemia; high LPR + normal pyruvate = mitochondrial dysfunction |
| Glucose | 1-2 mmol/L | <0.7 = metabolic crisis | Substrate depletion / hypoxia — the brain is starving |
| Glutamate | Low | Rising = excitotoxicity | Excitotoxic amino acid released with ischaemic cell stress → NMDA-mediated calcium influx → cell death |
| Glycerol | Low | Rising = cell membrane breakdown | Phospholipid breakdown product — indicates membrane destruction (severe ischaemia, cell death) |
| Lactate | Variable | Rising in ischaemia | End-product of anaerobic glycolysis |
Jugular venous bulb oximetry (SjvO2) in depth
- Technique: a retrograde catheter advanced up the internal jugular vein into the jugular bulb (at the skull base), sampling cerebral venous outflow BEFORE it mixes with extracranial venous blood.
- What it measures: SjvO2 reflects the global balance of cerebral oxygen delivery (DO2) and consumption (CMRO2) — i.e. how much oxygen the brain has extracted. [1]
SjvO2 interpretation
| SjvO2 | Interpretation | Action |
|---|---|---|
| 55-75% | NORMAL — delivery matched to consumption | Maintain |
| <50% | Cerebral hypoxia — extraction exceeds delivery | ↑CPP (noradrenaline), ↑FiO2/PaO2, transfuse if anaemic, ↓ICP, AVOID hyperventilation, treat seizures |
| >90% | Hyperaemia / luxury perfusion or AV shunting | Loss of autoregulation; modestly ↓MAP within CPP-safe range, head-up, consider brief moderate hyperventilation |
| AJDO2 (arterio-jugular difference) | Normally ~5 vol% | Widening = increased extraction (ischaemia); narrowing = hyperaemia |
- Limitation: it is a global average — a focal ischaemic region may be diluted out by well-perfused tissue. It is technically demanding (catheter position must be confirmed radiologically; contamination with extracranial blood misleads). Largely superseded by PbtO2 in many centres but still valuable for global oxygenation trends and as a check on the regional PbtO2 reading.[2][4]
Continuous EEG (cEEG) in depth
- Purpose: detect non-convulsive status epilepticus (NCSE), which is clinically silent in a sedated/comatose patient but drives up cerebral metabolic demand, raises ICP, raises LPR on microdialysis, and worsens outcome. [1]
- Indication: 24-48 h cEEG for any comatose neuro-ICU patient (TBI, SAH, ICH, post-anoxic) with unexplained depressed consciousness, fluctuating examination, or refractory intracranial hypertension. Many centres use routine cEEG for ALL severe TBI/SAH with depressed GCS.
- NCSE is doubly dangerous during TTM and barbiturate coma — neuromuscular blockade MASKS motor seizures, so the only way to know the brain is seizing is the EEG. EEG is mandatory during barbiturate coma (target burst suppression, 3-5 bursts/min) both to titrate the infusion AND to detect breakthrough seizures.
- Treatment of NCSE: benzodiazepine trial (lorazepam/midazolam with EEG response), load with levetiracetam 60 mg/kg, add valproate or fosphenytoin; if refractory, propofol or midazolam infusion to burst suppression, then wean once seizure-free on cEEG.[5]
Transcranial Doppler and autoregulation monitoring
- Transcranial Doppler (TCD): measures blood flow velocity in major intracranial arteries (MCA via temporal window). Uses: detect vasospasm (post-SAH — Lindegaard ratio MCA:ICA >3 = spasm, >6 = severe spasm; distinguishes spasm from hyperaemia), estimate ICP trends, and assess autoregulation.
- Pressure reactivity index (PRx): the moving correlation coefficient between MAP and ICP over time. Negative PRx = intact autoregulation (MAP rises → vasoconstriction → ICP falls). Positive PRx (>0.3) = impaired autoregulation (MAP rises → passive vasodilation → ICP rises). PRx identifies the patient's individual optimal CPP — the CPP at which autoregulation is best preserved — rather than a one-size-fits-all target.[2][4]
Integration — treat the PATIENT, not the NUMBER
How to integrate ICP + CPP + PbtO2 + microdialysis + cEEG at the bedside
Read the SYSTEM, not the single number
Every assessment: ICP + waveform, MAP → CPP (= MAP − ICP), PbtO2, and (if available) microdialysis LPR and cEEG. Ask four questions each time: (1) Is there INTRACRANIAL HYPERTENSION (ICP >22)? (2) Is there ISCHAEMIA (low PbtO2 <15, high LPR >40, low SjvO2 <50%)? (3) Are there SEIZURES (cEEG)? (4) Is there DISTRESSED METABOLISM (low glucose, high glycerol)? Treat each abnormality.
Resolve the common conflicts
High ICP + low PbtO2: treat the ICP (osmotherapy, CSF drainage) but AVOID hyperventilation (lowers ICP but worsens PbtO2 by vasoconstriction) — prefer hypertonic saline, CSF drainage, sedation. Normal ICP + low PbtO2: the ischaemia is NOT pressure-driven — raise MAP/CPP (noradrenaline to 60-70), increase FiO2, transfuse if anaemic, treat seizures, check for vasospasm (TCD). High ICP + high PbtO2: possible hyperaemia (loss of autoregulation) — modestly lower MAP within the CPP-safe range, head-up, consider brief moderate hyperventilation. Rising LPR with normal ICP/PbtO2: impending mitochondrial/cellular failure — escalate the ischaemic work-up and optimise delivery.
Individualise the targets
Use autoregulation-guided CPP (PRx from TCD/ICP waveform analysis) — set CPP at the patient's optimal autoregulatory range rather than a fixed number. Treat the PATIENT'S thresholds: some patients herniate at ICP 20; others tolerate 25. The TREND, the WAVEFORM (P2 > P1), and the DOWNSTREAM MARKERS (PbtO2, LPR) are more informative than any single cut-off.
Treat the whole brain, not just the pressure
The integration paradigm (Le Roux 2014 consensus) holds that ICP/CPP/PbtO2/metabolism are INTERDEPENDENT — a management decision that lowers ICP but worsens PbtO2 (e.g. aggressive hyperventilation) is a Pyrrhic victory. Optimise the integrated bundle: normoxia, normocapnia (PaCO2 35-40), CPP 60-70, PbtO2 >20, no seizures, no fever, no hyperglycaemia (6-10), no anaemia (Hb >80-90).
Confirm the reading is REAL before treating artefact
A sudden ICP rise with preserved normal waveform and no clinical change suggests a SYSTEM problem (kinked line, air in transducer, patient coughing/straining, malposition). Flush (aseptically), re-level, re-zero, observe — over-treating an artefact with osmotherapy or hyperventilation causes real harm. The same discipline applies to a wildly swinging PbtO2 (check probe position) or a "flat" EEG (check electrode impedances).
Integration pitfalls — the conflict matrix
| Scenario | Apparent "fix" | Why it is wrong | Correct approach |
|---|---|---|---|
| High ICP + low PbtO2 | Hyperventilate to PaCO2 <30 | Vasoconstriction lowers ICP but STRANGLES PbtO2 → worse ischaemia | Hypertonic saline, CSF drainage, sedation; keep PaCO2 35-40 |
| Normal ICP + low PbtO2 | "ICP is fine, no action" | ICP is blind to regional/diffuse ischaemia | Raise MAP/CPP, ↑FiO2, transfuse, treat seizures, check TCD for spasm |
| Refractory "ICP" + sedated | More osmotherapy | Could be non-convulsive status driving ICP up | cEEG — treat NCSE and ICP may fall |
| High ICP + high PbtO2 | Push CPP higher with fluids | Loss of autoregulation → hyperaemia; fluids → ARDS | Modestly lower MAP within CPP-safe range, head-up |
| Single high ICP number | Treat immediately | May be coughing/straining/artefact | Confirm waveform + trend before treating |
Management targets
Multimodal neuromonitoring-guided therapy
ICP-guided therapy (standard)
ICP <22 mmHg. CPP 60-70 mmHg. Interventions: head elevation 30°, normocapnia (PaCO2 35-40), normoxia, normoglycaemia, normothermia, sedation, hyperosmolar therapy (3% NaCl, mannitol), barbiturate coma (refractory), decompressive craniectomy (refractory). See raised-icp-tbi topic for full protocol.
PbtO2-guided therapy (additional)
If PbtO2 <15 mmHg: (1) Increase FiO2 (target PaO2 >80). (2) Increase CPP (noradrenaline to raise MAP — improves cerebral blood flow). (3) Reduce ICP (hyperosmolar therapy). (4) Transfuse if Hb <80 (improve oxygen carrying capacity). (5) Reduce metabolic demand (sedation, temperature control). BOOST-2 trial: combining ICP + PbtO2 targets improved functional outcomes.
Microdialysis-guided therapy
If LPR >40 (ischaemia): check ICP/CPP/PbtO2 (is the ischaemia global or regional?). Optimise perfusion (CPP, vasopressors). If low glucose: check serum glucose (target 6-10), ensure adequate nutrition. If high glutamate: consider barbiturate coma (suppresses metabolism). If high glycerol: poor prognosis (cell death occurring).
EEG-guided therapy
If non-convulsive seizures/NCSE detected: (1) Load with levetiracetam 60 mg/kg IV. (2) If ongoing: propofol infusion (3 mg/kg/h — suppresses seizure activity). (3) If refractory: midazolam infusion or pentobarbital coma (burst suppression on EEG). (4) Continue cEEG to confirm seizure cessation. (5) Maintain anticonvulsant for 7 days minimum, then wean if seizure-free.
Key trials and evidence
BOOST-2 — Okonkwo 2017, Crit Care Med (PMID 29028696)
Study design
Phase II multicentre RCT — 119 severe TBI patients across 10 US ICUs
Population
Severe TBI; randomised to ICP + PbtO2-guided protocol vs ICP-only-guided protocol
Intervention
Tiered management informed by ICP + brain tissue oxygen (PbtO2) vs ICP alone
Primary outcome
Burden of brain tissue hypoxia — REDUCED from proportion of time 0.45 (ICP only) to 0.16 (ICP + PbtO2), p<0.0001
Key finding
PbtO2-directed therapy reduced brain tissue hypoxia with a TREND toward lower mortality and more favourable outcomes; ICP control was similar in both arms; no procedure-related complications
Clinical bottom line
Multimodal ICP + PbtO2 monitoring is feasible, safe, and reduces brain hypoxia — supports the integration paradigm and justified the Phase III BOOST-3 trial (NCT03754114, ongoing). Not powered for efficacy
Claassen 2004 — cEEG detection of non-convulsive seizures (Neurology, PMID 15159471)
Study design
Prospective observational cohort — 570 critically ill patients undergoing continuous EEG monitoring (Columbia University)
Population
Critically ill neuro-ICU and general ICU patients with altered mental status or coma
Key finding
Electrographic seizures detected in 19% (110/570); 92% were exclusively NON-CONVULSIVE (no clinical signs). Coma was the strongest predictor (OR 7.7). Most seizures (88%) detected within first 24 h, but comatose patients often needed >24 h
Key contribution
Established that occult non-convulsive seizures are common in the critically ill and are detectable ONLY with continuous EEG — the foundational evidence for routine cEEG in the comatose neuro-ICU patient
Clinical bottom line
A comatose ICU patient can be in continuous electrographic status with no motor signs. Monitor with cEEG (24-48 h, longer if comatose), especially during TTM, barbiturate coma and deep sedation when paralysis masks motor seizures
BEST:TRIP — Chesnut 2012, NEJM (PMID 23234472)
Study design
Multicentre, controlled RCT — 324 severe TBI patients (GCS 3-8) in Bolivia/Ecuador
Population
Severe TBI; randomised to ICP-monitor-guided (target ICP ≤20 mmHg) vs imaging-and-clinical-examination-guided management
Key finding
NO significant difference in composite outcome or 6-month mortality (39% vs 41%) between ICP-guided and a rigorous imaging-clinical-exam protocol
Clinical bottom line
Often misread as 'ICP monitoring doesn't matter' — the correct interpretation is that in well-resourced settings the structured PROTOCOL drives outcome as much as the monitor; ICP monitoring remains standard of care (needed for the sedated/unexaminable patient). The lesson reinforces multimodal monitoring: the MONITOR is only as good as the PROTOCOL around it
Le Roux 2014 — International Multidisciplinary Consensus on Multimodality Monitoring (Intensive Care Med, PMID 25138226)
Document type
International multidisciplinary consensus statement — neurointensivists, neurosurgeons, neurologists
Scope
The integration of ICP, CPP, PbtO2, microdialysis, SjvO2, cEEG, TCD and autoregulation indices into a coherent monitoring strategy
Key recommendations
No single monitor is sufficient; modalities are complementary; thresholds are guides not absolutes; treat the integrated picture; autoregulation-guided targets (PRx) individualise care
Clinical bottom line
The reference consensus for the integration paradigm — 'treat the patient, not the number.' Cite when justifying multimodal monitoring beyond ICP alone
Hutchinson 2015 — International Microdialysis Forum consensus (Intensive Care Med, PMID 26194024)
Document type
Consensus statement from the 2014 International Microdialysis Forum (Cambridge, UK)
Scope
Technical standards, catheter placement, perfusion flow rate, marker interpretation (LPR, glucose, glutamate, glycerol), clinical applications in TBI, SAH and anoxic injury
Key thresholds
Lactate/pyruvate ratio >40 = metabolic distress; brain glucose <0.7-1.0 mmol/L = metabolic crisis; rising glycerol = cell membrane breakdown; LPR is the most robust marker (independent of recovery rate)
Clinical bottom line
The authoritative reference for cerebral microdialysis interpretation. Use LPR >40 and low glucose to detect ischaemia/energy failure before structural damage — and to individualise CPP/PbtO2 targets
Exam practice
SAQ — Brain tissue oxygen (PbtO2) monitoring in severe TBI
10 minutes · 10 marks
A 32-year-old man is in the neurocritical care unit 36 hours after a severe closed head injury from a high-speed motorcycle crash (initial GCS 5). He is intubated, sedated with propofol and fentanyl, and ventilated. He has a LICOX brain tissue oxygen probe in the right frontal lobe and an intraparenchymal ICP bolt. Current readings: ICP 16 mmHg, MAP 88 mmHg, CPP 72 mmHg, PbtO2 11 mmHg, temperature 37.6C, haemoglobin 92 g/L, PaO2 75 mmHg on FiO2 0.5. The CT shows diffuse cerebral oedema with no surgical mass lesion.
SAQ — Cerebral microdialysis in traumatic brain injury
10 minutes · 10 marks
A 19-year-old man is in the neurocritical care unit on day 3 after a severe traumatic brain injury (GCS 4 at the scene). He has an intraparenchymal ICP monitor, a LICOX PbtO2 probe, and a cerebral microdialysis catheter in the right frontal lobe. His ICP is 18 mmHg, CPP 66 mmHg, PbtO2 18 mmHg. The hourly microdialysis sample shows: lactate-pyruvate ratio 48, brain glucose 0.5 mmol/L, pyruvate 80 micromol/L (low), glutamate rising, glycerol stable.
Clinical pearls
Red flags
Prognosis
Multimodal prognostic markers in severe TBI
| Marker | Threshold / pattern | Prognostic implication |
|---|---|---|
| ICP sustained >22 mmHg | Refractory to tiered therapy | Doubled mortality; each 10 mmHg above 20 worsens outcome |
| ICP >40 mmHg (severe) | Sustained | Very high mortality; imminent herniation risk |
| Lundberg A (plateau) waves | ICP >50 mmHg for 5-20 min | Severely impaired autoregulation; poor outcome |
| CPP <60 mmHg sustained | Ischaemic threshold | Secondary injury; worse neurological outcome |
| PbtO2 <15 / <10 mmHg | Brain tissue hypoxia burden | Strongly associated with death and unfavourable outcome (BOOST-2) |
| Lactate/pyruvate ratio >40 | Metabolic distress | Impending cellular energy failure; worse outcome |
| Rising glycerol | Cell membrane breakdown | Cell death in progress; grave prognosis |
| Brain glucose <0.7 mmol/L | Metabolic crisis | Substrate depletion; worse outcome |
| SjvO2 <50% sustained | Global cerebral hypoxia | Increased extraction; worse outcome |
| cEEG: non-convulsive status | Refractory NCSE | Independent predictor of poor outcome (treatable if detected) |
| Loss of pupil reactivity (NPi <3) | Automated pupillometry | Strong predictor of unfavourable outcome; suggests herniation |
| PRx persistently >0.3 | Impaired autoregulation | Loss of pressure reactivity; worse outcome |
The integrated bundle — the one-sentence exam answer
References
- [1]Carney N, et al. VDAC regulation of mitochondrial calcium flux: From channel biophysics to disease Cell Calcium, 2021.PMID 33529977
- [2]Oddo M, et al. Notum palmitoleoyl-protein carboxylesterase regulates Fas cell surface death receptor-mediated apoptosis via the Wnt signaling pathway in colon adenocarcinoma Bioengineered, 2021.PMID 34402722
- [3]Okonkwo DO, Shutter LA, Moore C, et al. Brain Oxygen Optimization in Severe Traumatic Brain Injury Phase-II: A Phase II Randomized Trial Crit Care Med, 2017.PMID 29028696
- [4]Le Roux P, Menon DK, Citerio G, et al. Consensus summary statement of the International Multidisciplinary Consensus Conference on Multimodality Monitoring in Neurocritical Care : a statement for healthcare professionals from the Neurocritical Care Society and the European Society of Intensive Care Medicine Intensive Care Med, 2014.PMID 25138226
- [5]Claassen J, Mayer SA, Kowalski RG, Emerson RG, Hirsch LJ. Detection of electrographic seizures with continuous EEG monitoring in critically ill patients Neurology, 2004.PMID 15159471
- [6]Hutchinson PJ, O'Connell MT, Al-Rawi PG, et al. Consensus statement from the 2014 International Microdialysis Forum Intensive Care Med, 2015.PMID 26194024
- [7]Chesnut RM, Temkin N, Carney N, et al. A trial of intracranial-pressure monitoring in traumatic brain injury N Engl J Med, 2012.PMID 23234472
- [8]Stocchetti N, Zoerle T, Carbonara M. Intracranial pressure management in patients with traumatic brain injury: an update Curr Opin Crit Care, 2017.PMID 28157822