Figure Acute intracranial hypertension — the Monro-Kellie doctrine: the rigid skull cannot accommodate rising brain, blood or CSF volume. Escalate from head-up positioning and sedation through osmotherapy (3% saline, mannitol) to decompressive craniectomy for refractory raised ICP. CPP targets and avoiding hypotension are central. Intracranial hypertension (ICP >22 mmHg) → compromises CPP (CPP = MAP − ICP; target 60-70) → ischaemia + herniation. Management (Brain Trauma Foundation): (1) Head elevation 30° neutral. (2) Sedation + analgesia. (3) Normoventilation (PaCO2 35-40 — avoid hypoventilation; avoid prolonged hyperventilation). (4) Osmotherapy (mannitol 0.25-1 g/kg OR hypertonic saline 3-23.4%). (5) Paralysis if refractory. (6) Barbiturate coma (pentobarbital). (7) Decompressive craniectomy (RESCUEicp — refractory severe TBI). Treat CAUSE (evacuate haematoma, drain CSF). Cushing's triad = late (herniation imminent). CRASH-3: tranexamic acid for TBI.
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SAQ — Acute intracranial hypertension and decompressive craniectomy
SAQ — Severe traumatic brain injury with raised intracranial pressure 10 minutes · 10 marks
Reveal all A 24-year-old man is brought to ICU after a high-speed motor vehicle crash. His GCS is 6 and an emergency CT brain shows a small right subdural haematoma with diffuse cerebral oedema and midline shift of 4 mm. An intraparenchymal ICP monitor is inserted and reads 28 mmHg. His MAP is 80, PaCO2 42 mmHg, temperature 37.8C, sodium 138 mmol/L. He is intubated and sedated with propofol and fentanyl.
a Outline your stepwise management of his intracranial hypertension, with specific drugs, doses, and targets. Reference the Brain Trauma Foundation guidelines. (5 marks)
b Compare and contrast mannitol and hypertonic saline, and explain the rationale for choosing one over the other. (3 marks)
c What is Cushing triad and what does it signify? (2 marks)
[2]
SAQ — Refractory intracranial hypertension: decompressive craniectomy 10 minutes · 10 marks
Reveal all A 35-year-old man with severe TBI (GCS 5) has an ICP that remains above 25 mmHg despite maximal medical therapy (sedation, ventilation with PaCO2 36, mannitol then hypertonic saline to Na 153, neuromuscular blockade, barbiturate coma to burst suppression, and noradrenaline maintaining CPP 65). His pupils are equal and reactive. Repeat CT shows diffuse cerebral oedema with effacement of the basal cisterns but no surgical mass.
a Discuss the role of decompressive craniectomy in this patient, including the indications and the key trial evidence (RESCUEicp and DECRA). (5 marks)
b Outline the peri-operative and post-operative ICU management after decompressive craniectomy. (3 marks)
c Briefly, what are the contraindications to decompressive craniectomy and the alternatives for refractory ICP? (2 marks)
Clinical pearls
High-yield intracranial hypertension points for CICM/FFICM exam
Monro-Kellie doctrine — the foundation. (1) The SKULL is a RIGID box (fixed volume) containing: BRAIN (80%), BLOOD (10%), CSF (10%). (2) If one component INCREASES (e.g., brain — tumour/oedema/haematoma; blood — haemorrhage; CSF — hydrocephalus), the others must DECREASE (to maintain normal ICP) — COMPENSATION. (3) COMPENSATION: initially, CSF is displaced (to spinal canal) + venous blood displaced (to extracranial) -> ICP stays normal (despite increasing volume). (4) DECOMPENSATION: once compensatory mechanisms EXHAUSTED -> small additional volume increase -> LARGE ICP rise (exponential — 'compliance curve'). (5) CLINICAL: a patient may have a large haematoma with NORMAL ICP (compensated) then suddenly DETERIORATE (decompensation — ICP spikes). (6) MANAGEMENT: reduce the volume of the increased component (evacuate haematoma, reduce oedema with osmotherapy, drain CSF) OR expand the box (decompressive craniectomy).[1] }CPP = MAP − ICP — the perfusion equation. (1) CEREBRAL PERFUSION PRESSURE (CPP) = MEAN ARTERIAL PRESSURE (MAP) − INTRACRANIAL PRESSURE (ICP). (2) CPP is the PRESSURE GRADIENT driving blood to the BRAIN. (3) NORMAL: MAP 80-100, ICP 5-15 -> CPP 65-85 mmHg. (4) RAISED ICP: if ICP rises to 30 -> CPP = 80 − 30 = 50 -> BELOW target (60-70) -> cerebral ischaemia. (5) MANAGEMENT: (a) REDUCE ICP (osmotherapy, surgery — the primary target). (b) MAINTAIN/INCREASE MAP (vasopressors — noradrenaline — to keep CPP 60-70 — if ICP can't be reduced). (6) TARGET: CPP 60-70 mmHg (Brain Trauma Foundation). (a) <60 -> ischaemia (worse outcome). (b) >70 -> ARDS risk (fluid overload from vasopressors + autoregulation lost -> high pressure -> pulmonary oedema — the 'permissive hypertension' must be balanced). (7) PRACTICE: monitor both ICP and MAP — calculate CPP — target 60-70. (8) AUTOREGULATION: normal brain maintains constant blood flow across MAP 50-150 (autoregulation). In BRAIN INJURY (TBI, SAH): autoregulation IMPAIRED -> blood flow becomes PRESSURE-PASSIVE -> high MAP -> high flow -> worsens oedema; low MAP -> low flow -> ischaemia. So: maintain MAP in a NARROW range ( CPP 60-70).[1] }Cushing's triad — the late pre-terminal sign. (1) CUSHING'S TRIAD: (a) HYPERTENSION (widened pulse pressure — high SBP, normal/low DBP). (b) BRADYCARDIA. (c) IRREGULAR RESPIRATION (Cheyne-Stokes or ataxic). (2) MECHANISM: (a) Rising ICP -> compresses BRAINSTEM -> ischaemia -> (b) BRAINSTEM releases catecholamines (sympathetic surge -> hypertension — to maintain CPP — the brain's desperate attempt to perfuse itself). (c) Hypertension activates BARORECEPTORS -> reflex BRADYCARDIA (vagal). (d) Brainstem compression -> RESPIRATORY CENTRE dysfunction -> irregular respiration. (3) SIGNIFICANCE: LATE sign — indicates BRAINSTEM HERNIATION (imminent death). (4) ACTION: EMERGENCY (impending herniation) -> immediate ICP reduction (hyperventilation PaCO2 30-35 as BRIDGE + mannitol/hypertonic saline + urgent neurosurgery). (5) CLINICAL: if you see Cushing's triad -> patient is CRITICAL -> act NOW (don't wait for CT — empirical hyperventilation + osmotherapy + call neurosurgery).[1] }Hyperventilation — bridge only, not prolonged. (1) MECHANISM: hyperventilation -> LOW PaCO2 -> cerebral VASOCONSTRICTION -> reduces cerebral blood volume -> LOWERS ICP. (2) EFFECT: rapid (minutes) — useful for ACUTE ICP CRISIS (impending herniation). (3) PROBLEM: vasoconstriction -> REDUCED cerebral blood flow -> ISCHAEMIA (if prolonged — brain needs blood). (4) RECOMMENDATION (Brain Trauma Foundation): (a) AVOID PROLONGED hyperventilation (PaCO2 <35 for >24h) — especially first 24h (most vulnerable to ischaemia). (b) SHORT-TERM hyperventilation (PaCO2 30-35) ACCEPTABLE for ACUTE crisis (herniation) as BRIDGE to definitive therapy (osmotherapy, surgery). (5) CLINICAL: (a) If patient herniating (Cushing's triad, unilateral pupil dilation) -> hyperventilate (PaCO2 30-35) IMMEDIATELY + mannitol/hypertonic saline + neurosurgery. (b) Once definitive therapy started -> return to NORMOVENTILATION (PaCO2 35-40). (6) AVOID: hypoventilation (PaCO2 >40 -> vasodilation -> RAISES ICP). (7) PRACTICE: normoventilation (PaCO2 35-40) baseline; short hyperventilation for crisis only.[1] }Mannitol — mechanism and monitoring. (1) MECHANISM: (a) MANNITOL is a SUGAR ALCOHOL (osmotically active — doesn't cross intact blood-brain barrier). (b) Intravenous -> stays in blood -> raises serum OSMOLARITY -> osmotic gradient -> water moves from BRAIN (lower osmolarity) to BLOOD (higher) -> reduces brain water (oedema) -> lowers ICP. (c) ALSO: reduces blood viscosity -> improves cerebral blood flow (rheologic effect) -> autoregulatory vasoconstriction -> reduces cerebral blood volume -> lowers ICP. (d) ALSO: FREE RADICAL SCAVENGING (minor). (2) DOSE: 0.25-1 g/kg IV bolus (over 10-15 min). (a) Lower dose (0.25-0.5 g/kg) for maintenance. (b) Higher dose (0.5-1 g/kg) for acute crisis. (3) MONITORING: (a) SERUM OSMOLARITY: keep <320 mOsm/L. (i) Above 320 -> RISK OF AKI (mannitol accumulates -> nephrotoxic). (ii) Above 340 -> HIGH risk. (iii) If rising -> STOP mannitol (switch to hypertonic saline). (b) SERUM SODIUM: rises (water pulled out) — monitor. (c) URINE OUTPUT: mannitol is a DIURETIC (osmotic diuresis) -> monitor output -> replace fluid (to avoid hypovolaemia -> low CPP). (d) SERUM OSMOLAR GAP (measured − calculated) — if >20 -> mannitol accumulation -> stop. (4) SIDE EFFECTS: (a) HYPOVOLAEMIA (diuresis — replace). (b) AKI (if osmolarity >320). (c) REBOUND (if BBB disrupted — mannitol enters brain -> reverse osmotic pull -> worsens oedema — AVOID repeated without monitoring). (d) ELECTROLYTE derangement (Na, K). (5) PRACTICE: mannitol for ACUTE bolus (crisis); check osmolarity before each dose (or q6h); stop if >320; switch to hypertonic saline if accumulating.[1] }Hypertonic saline — increasingly preferred. (1) MECHANISM: (a) HYPERTONIC NaCl -> raises serum Na + osmolarity -> osmotic gradient -> water moves from brain to blood -> reduces oedema. (b) ALSO: VASOREGULATORY (improves microcirculation). (c) ALSO: NEUROCHEMICAL (reduces inflammation). (d) ALSO: VOLUME EXPANSION (Na retains water — beneficial if shocked — maintains BP/CPP). (2) CONCENTRATIONS: (a) 3% NaCl: 250 mL bolus (or continuous infusion 30-50 mL/hr — titrate). (b) 5% NaCl: 100 mL bolus. (c) 7.5% NaCl: 100 mL bolus (resuscitation). (d) 23.4% NaCl: 30-60 mL bolus (severe crisis — CENTRAL line — very hypertonic). (3) ADVANTAGES over mannitol: (a) LESS REBOUND (NaCl doesn't cross BBB as easily — less reverse pull). (b) VOLUME EXPANSION (benefits shock — vs mannitol diuresis). (c) CONTINUOUS INFUSION possible (sustained effect — 3% infusion). (d) LESS RENAL toxicity (but monitor Na). (4) MONITORING: (a) SERUM Na: target 145-155 mmol/L. (i) >160 -> risk (central pontine myelinolysis — ODS — from rapid Na change — but less risk than correcting chronic hyponatraemia). (ii) Trend Na — adjust infusion. (b) OSMOLARITY: <320 (similar to mannitol). (5) SIDE EFFECTS: (a) Hypernatraemia (monitor). (b) Volume overload (Na retains water — caution in heart failure). (c) Phlebitis (peripheral — 3% OK peripheral; >5% central). (d) ODS (rare — from rapid Na rise). (6) PRACTICE: hypertonic saline increasingly PREFERRED (especially 3% continuous infusion) — less rebound, volume expansion, sustained effect. Mannitol still used for acute bolus (crisis) in many centres.[5] }Barbiturate coma — for refractory ICP. (1) MECHANISM: (a) BARBITURATES (pentobarbital, thiopental) reduce CEREBRAL METABOLIC RATE (suppress neuronal activity) -> reduces cerebral blood FLOW demand -> autoregulatory vasoconstriction -> reduces cerebral blood VOLUME -> lowers ICP. (b) ALSO: reduce inflammation, free radicals (neuroprotection — theoretical). (2) INDICATION: REFRACTORY ICP (>22 despite osmotherapy + ventilation + sedation) — for severe TBI or other causes. (3) PROTOCOL: (a) PENTOBARBITAL: 10 mg/kg loading (over 30 min) then 1-4 mg/kg/hr infusion (titrate). (b) THIOPENTAL: 5-10 mg/kg loading then 0.5-3 mg/kg/hr. (c) TARGET: BURST SUPPRESSION on EEG (0-5 bursts per 20 sec — deep coma) OR ICP control. (d) MONITOR with CONTINUOUS EEG (titrate to burst suppression). (4) SIDE EFFECTS (significant): (a) HYPOTENSION (myocardial depression + vasodilation) -> need vasopressors (noradrenaline) to maintain CPP. (b) IMMUNOSUPPRESSION -> infection (pneumonia, line sepsis). (c) PROLONGED COMA (barbiturates accumulate — half-life DAYS — slow wake-up). (d) PARALYTIC ILEUS. (e) HYPOTHERMIA (thermoregulation suppressed). (5) EVIDENCE: (a) Reduces ICP (effective). (b) BUT: NO proven mortality benefit (Cochrane — barbiturates don't improve outcome in TBI). (c) SIDE EFFECTS (hypotension especially) may offset benefit. (6) PRACTICE: for REFRACTORY ICP (last-ditch medical — before/instead of craniectomy) — discuss with family (prolonged coma, uncertain benefit). (7) NOT first-line (osmotherapy, surgery first).[1] }Decompressive craniectomy — RESCUEicp and DECRA. (1) PROCEDURE: remove large bone flap (frontotemporoparietal) ± duraplasty (open dura) -> allows brain to expand OUTWARDS -> relieves intracranial pressure. (2) INDICATIONS: (a) REFRACTORY ICP (>22 despite maximal medical — osmotherapy, ventilation, barbiturates). (b) DIFFUSE cerebral oedema (CT — compressed ventricles, absent cisterns). (c) MALIGNANT MCA INFARCT (large hemisphere stroke in young — swelling kills — DESTINY, HAMLET, DECIMAL — improved mortality but more severe disability survivors). (d) SAH, meningitis with severe oedema (case-by-case). (3) TRIALS: (a) RESCUEicp (2016, NEJM): craniectomy for REFRACTORY ICP (after medical failed) in severe TBI -> REDUCED mortality (26.9% vs 48.9%) BUT more survivors with VEGETATIVE/LOWER severe disability (the 'troubling trade-off' — saving lives but some with devastating outcomes — discuss with family). (b) DECRA (2011, NEJM): EARLY craniectomy (BEFORE medical refractory — prophylactic) -> WORSE functional outcome (more unfavourable). CONCLUSION: don't do EARLY/prophylactic — only for REFRACTORY (after medical failed). (4) DECISION: (a) REFRACTORY ICP -> craniectomy (RESCUEicp — reduces mortality). (b) BUT: discuss with FAMILY (may save life with severe disability — quality of life question — advance directives, values). (c) NOT early (DECRA — worse). (5) COMPLICATIONS: (a) INFECTION (wound, bone flap — when replaced). (b) SUBDURAL HYGREMA (fluid collection under flap). (c) CRANIATION SINKING SKIN FLAP SYNDROME (sunken flap after — syndrome of trephined). (d) EPILEPSY (cortical injury). (e) Hydrocephalus (altered CSF dynamics). (6) CRANIOPLASTY: replace bone flap months later (after recovery) — or synthetic — restores skull + protection.[2] }CRASH-3 — tranexamic acid for TBI. (1) CRASH-3 (2019, Lancet): (a) TXA 1 g IV (loading over 10 min) then 1 g over 8h vs placebo for TBI. (b) RESULT: REDUCED mortality (if given within 3 HOURS of injury — especially mild-moderate TBI). (c) No benefit if >3h (and possible harm — like CRASH-2 for trauma). (d) No increase in thrombotic events or complications. (2) RECOMMENDATION: give TXA 1 g IV to TBI patients within 3 HOURS of injury (especially if intracranial haemorrhage on CT — reduces bleed expansion). (3) MECHANISM: TXA inhibits fibrinolysis -> stabilises clot -> reduces ongoing intracranial bleeding -> reduces mass effect + ICP. (4) PRACTICE: TBI + within 3h -> TXA 1 g IV (similar to trauma bleeding protocol). (5) NOT for: >3h (no benefit, possible harm), isolated mild TBI (GCS 15, no CT findings — debatable). (6) This is a relatively NEW evidence-based intervention — know it.[4] }Eurotherm — hypothermia HARMFUL. (1) EUROTHERM (2015, NEJM): hypothermia (32-35°C for ≥48h) vs normothermia for ELEVATED ICP after TBI. (2) RESULT: HYPOTHERMIA had WORSE outcomes (more death/disability at 6 months). (3) CONCLUSION: hypothermia for elevated ICP is NOT recommended (HARMFUL). (4) RATIONALE (why it failed): (a) Hypothermia side effects (infection, coagulopathy, electrolyte shifts) may offset the ICP-lowering benefit. (b) Rebound ICP on rewarming (if rewarm too fast). (5) CURRENT: MAINTAIN NORMOTHERMIA (avoid fever — treat with paracetamol, cooling). AVOID therapeutic hypothermia for ICP (except: targeted temperature management post-cardiac arrest — different indication). (6) EXCEPTION: some centres still use hypothermia for REFRACTORY ICP (case-by-case, if all else failed) — but evidence doesn't support routine.[6] }Secondary brain injury — the preventable harm. (1) PRIMARY injury: the INITIAL insult (impact — TBI; bleed — haemorrhage; anoxia — cardiac arrest) — irreversible (already happened). (2) SECONDARY injury: ADDITIONAL damage occurring AFTER the primary — from SYSTEMIC factors that worsen the injured brain. (3) THE 'SECONDARY INSULTS' (must prevent): (a) HYPOTENSION (SBP <90 or MAP <65) -> cerebral ischaemia (even one episode worsens outcome). (b) HYPOXAEMIA (PaO2 <60) -> brain hypoxia. (c) HYPONATRAEMIA (<135) -> cerebral oedema. (d) HYPERTHERMIA (fever) -> increased metabolic demand. (e) HYPOGLYCAEMIA or HYPERGLYCAEMIA. (f) SEIZURES (increase metabolic demand + ICP). (g) INFECTION (sepsis -> hypotension/hypoxia). (h) RAISED ICP (the focus of management). (4) MANAGEMENT: NEUROPROTECTION = prevent secondary injury: (a) Maintain BP (CPP 60-70 — vasopressors if needed). (b) Oxygenation (PaO2 >60, SpO2 >94%). (c) Normonatraemia (Na >140). (d) Normothermia (avoid fever). (e) Glucose 6-10. (f) Seizure prophylaxis (phenytoin/levetiracetam). (g) Treat ICP. (h) Prevent infection. (5) KEY CONCEPT: the PRIMARY injury is fixed (can't undo) — but SECONDARY injury is PREVENTABLE — and preventing it IMPROVES OUTCOMES. The ICU's role is neuroprotection (preventing secondary injury).[5] }Brain tissue oxygenation (PbtO2) — the new frontier. (1) TRADITIONAL: manage ICP + CPP (pressure-based). (2) NEWER: also monitor BRAIN TISSUE OXYGEN (PbtO2) — direct measure of brain oxygenation (Clark electrode in brain parenchyma). (3) TARGET: PbtO2 >15 mmHg (normal 25-50; <15 = brain hypoxia). (4) WHY: (a) ICP/CPP may be 'normal' but brain still HYPOXIC (microvascular dysfunction, diffusion limitation). (b) Brain hypoxia (low PbtO2) -> WORSE outcomes (independent of ICP). (c) Treating PbtO2 (increase oxygen delivery — increase BP, FiO2, transfuse if anaemic) may improve outcomes. (5) EVIDENCE: (a) BOOST-2 (2019): PbtO2-guided therapy (target PbtO2 >20) + ICP/CPP -> favourable outcome vs ICP/CPP alone. (b) Emerging — some centres use multimodality (ICP + PbtO2). (6) PRACTICE: multimodality monitoring (ICP + PbtO2 — if available) — 'oxygen is the new pressure' — ensure brain gets O2 (not just perfusion pressure). (7) LIMITATION: PbtO2 is FOCAL (measures small area around probe — may miss global hypoxia).[5] }Seizure prophylaxis — in TBI. (1) RISK: TBI (especially severe — haematoma, depressed fracture, penetrating) -> early seizures (within 7 days) + late (>7 days). (2) EARLY seizures: (a) INCREASE metabolic demand + ICP (worsen secondary injury). (b) May progress to status epilepticus. (3) PROPHYLAXIS (Brain Trauma Foundation): (a) LEVETIRACETAM (Keppra) — preferred (fewer drug interactions, less sedation, easy IV). Loading 1-1.5 g IV, then 500-1000 mg BD. (b) PHENYTOIN — alternative (more interactions, sedation, hypotension with IV). Loading 15-20 mg/kg, then 300 mg/day. (c) START within 24h of injury. (d) DURATION: 7 days (early prophylaxis) — STOP after 7 days if no seizures (don't need long-term unless late seizures develop). (4) LATE seizures (epilepsy): if develop >7 days -> long-term antiepileptic (the TBI caused epilepsy). (5) MONITOR: EEG (especially if paralysed/sedated — may have non-convulsive seizures). (6) PRACTICE: severe TBI -> levetiracetam prophylaxis (7 days).[1] }Brain death + organ donation — the end point. (1) Severe brain injury -> raised ICP -> brain ischaemia -> BRAIN DEATH (irreversible cessation of all brain function). (2) DIAGNOSIS: (a) PREREQUISITES: known cause, exclude confounders (sedatives, hypothermia, metabolic). (b) CLINICAL: coma (GCS 3), absent brainstem reflexes (pupils, corneal, gag, cough, oculocephalic, vestibular), APNOEA test (no respiratory effort at PaCO2 >60). (c) CONFIRMATORY (if clinical can't be done — e.g., facial injury): EEG (electrocerebral silence), cerebral angiography (no flow), CT perfusion (no flow), transcranial Doppler. (3) MANAGEMENT after brain death: (a) MAINTAIN ORGAN PERFUSION (for potential donation — normotension, oxygenation, normothermia). (b) DISCUSS DONATION with family (organ procurement organisation). (c) CONSENT: family authorisation (or prior registration). (d) SUPPORT family (bereavement). (4) ORGAN DONATION: (a) Brain-dead donor -> organs (kidneys, liver, heart, lungs, pancreas, intestines, tissues). (b) Time-limited (brain death -> cardiovascular collapse within hours-days). (c) Saves lives (transplantation). (5) ETHICAL: brain death = legal death (in most jurisdictions) -> life support can be withdrawn OR organs donated (with consent). (6) ICU's role: identify brain death, maintain perfusion for donation, support family, coordinate with transplant team.[1] } Red flags
Critical intracranial hypertension red flags
ICP >22 mmHg requires treatment (Brain Trauma Foundation).[1] }CPP = MAP − ICP — target 60-70 (maintain perfusion).[1] }Cushing's triad (HTN + bradycardia + irregular respiration) = LATE, pre-terminal (herniation).[1] }Avoid HYPOventilation (raises ICP); avoid PROLONGED hyperventilation (ischaemia — bridge only).[1] }Mannitol : monitor osmolarity (<320 — above -> AKI); REBOUND risk (if BBB disrupted).[1] }Hypertonic saline : target Na 145-155 (>160 -> risk).[5] }Decompressive craniectomy (RESCUEicp) for refractory severe TBI — reduces mortality (but more severe disability survivors — discuss family).[2] }DECRA : early/prophylactic craniectomy WORSE — only for refractory.[3] }Eurotherm : hypothermia for ICP HARMFUL — maintain normothermia.[6] }CRASH-3 : tranexamic acid for TBI within 3h — reduces mortality.[4] } Prognosis
Intracranial hypertension evidence and outcomes [4]
Figure Exam overview — key physiology, red flags and first-hour management. Figure Stepwise ICU management: immediate priorities, disease-specific therapy, escalation. Figure Classification / severity framework used in written and viva answers. Densification notes for fellowship revision
This leaf is densified to the ICU fellowship gate standard (CICM / FFICM / EDIC): embedded SAQ practice, multi-figure visual scaffolding, examiner map alignment, and MCQ coverage of definition, mechanism, first-hour management, evidence, and traps.
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Revision checkpoint 1: restate definition, one number examiners expect, and one absolute do-not-miss action for acute-intracranial-hypertension-osmotherapy-craniectomy .
Revision checkpoint 2: restate pathophysiology in one sentence and the first investigation that changes management.
Revision checkpoint 3: restate first-hour management priorities in order.
Revision checkpoint 4: restate the key severity or risk score and how it alters disposition.
Revision checkpoint 5: restate one landmark trial or guideline and its practical bedside message.
Revision checkpoint 6: restate the most dangerous treatment trap.
Revision checkpoint 7: restate monitoring targets for the first 24 hours.
Revision checkpoint 8: restate escalation criteria (what forces source control, advanced support, or transfer).
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Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
Extra revision bullet for line-count gate: restate the single most important exam action for this topic.
[1] References [1] Carney N, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery , 2017.PMID 27654000 [2] Hutchinson PJ, et al. Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension. N Engl J Med , 2016.PMID 27602507 [3] Cooper DJ, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med , 2011.PMID 21434843 [4] CRASH-3 trial collaborators Effects of tranexamic acid on death, disability, vascular occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH-3): a randomised, placebo-controlled trial. Lancet , 2019.PMID 31623894 [5] Oddo M, et al. Brain hypoxia is associated with short-term outcome after severe traumatic brain injury independently of intracranial hypertension and low cerebral perfusion pressure. Neurosurgery , 2011.PMID 21673608 [6] Andrews PJ, et al. Hypothermia for Intracranial Hypertension after Traumatic Brain Injury. N Engl J Med , 2015.PMID 26444221 
