Contents
- Pathophysiology
- Classification
- Primary Assessment
- Secondary Insults
- ICP Management — Stepwise Approach
- Key Trials
- Viva Questions
Pathophysiology
Monroe-Kellie Doctrine
The skull is a rigid fixed-volume compartment:
ICV = Brain parenchyma (~80%) + Blood (~10%) + CSF (~10%)
Compensatory mechanisms buffer rising intracranial volume:
- CSF displaced into the spinal subarachnoid space
- Venous blood displaced from the cranium
Once compensatory reserve is exhausted, intracranial compliance falls — small additional volume increments cause exponential ICP rises.
Cerebral Perfusion Pressure
CPP = MAP − ICP
- Normal ICP: <15 mmHg; treatment threshold: >22 mmHg (Brain Trauma Foundation 2016)
- Target CPP: 60–70 mmHg (below 50 mmHg causes ischaemia; above 70 mmHg risks forced hyperaemia and vasogenic oedema)
Cerebral Autoregulation
CBF is normally maintained at ~50 mL/100g/min across MAP 50–150 mmHg. In TBI, autoregulation is frequently impaired — CBF becomes pressure-passive. Both hypotension and hypertension become dangerous.
Primary vs Secondary Injury
| Type | Timing | Nature |
|---|---|---|
| Primary | At impact | Direct mechanical disruption — irreversible |
| Secondary | Hours–days | Ischaemia, hypoxia, oedema, excitotoxicity, raised ICP — preventable |
Prevention of secondary injury is the principal modifiable target.
Classification
Severity (GCS)
| Severity | GCS |
|---|---|
| Mild | 14–15 |
| Moderate | 9–13 |
| Severe | ≤8 |
Intracranial Lesion Types
| Lesion | CT appearance | Notes |
|---|---|---|
| Extradural haematoma (EDH) | Biconvex hyperdense collection | Middle meningeal artery; lucid interval then rapid deterioration; excellent prognosis if evacuated early |
| Subdural haematoma (SDH) | Crescent-shaped, crosses sutures | Bridging veins; elderly/anticoagulated; worse prognosis than EDH |
| Intracerebral contusion | Heterogeneous hyperdensity | May enlarge over 24–48h — rescan at 4–6h if clinical change |
| Diffuse axonal injury (DAI) | CT often normal; petechial bleeds at grey-white interface | Shearing forces; MRI more sensitive; poor prognosis in severe form |
| Traumatic SAH | Sulcal hyperattenuation | Associated with vasospasm risk |
Primary Assessment
- A: Cervical spine control; definitive airway if GCS ≤8 or airway at risk; RSI with inline stabilisation
- B: Target SpO₂ >95%, PaO₂ >60 mmHg; hypoxia doubles mortality
- C: Target SBP ≥110 mmHg (age 15–49 and ≥70 years) or ≥100 mmHg (age 50–69) — BTF 2016 updated thresholds
- D: GCS (document component scores), pupils (size, reactivity, symmetry), lateralising signs
- E: Identify all injuries; do not miss haemothorax, pelvic fracture
Non-contrast CT head immediately on stabilisation.
Secondary Insults — Prevention Targets
| Insult | Target | Rationale |
|---|---|---|
| Hypoxia | SpO₂ >95%, PaO₂ >60 mmHg | SaO₂ <90% in even a single episode associated with doubled mortality |
| Hypotension | SBP ≥100–110 mmHg | Single episode SBP <90 mmHg doubled mortality in BTF cohort data |
| Hyperthermia | ≤37.5°C | ↑ metabolic demand, worsens excitotoxicity; active cooling if needed |
| Hyperglycaemia | 6–10 mmol/L | Hyperglycaemia worsens neuronal injury; strict control causes harmful hypoglycaemia |
| Seizures | Levetiracetam or phenytoin ×7 days | Reduces early post-traumatic seizures; no evidence beyond 7 days for late epilepsy prevention |
| Hypercapnia | PaCO₂ 35–40 mmHg | Hypercapnia causes cerebral vasodilation → ↑ ICP; sustained hyperventilation causes ischaemia |
| Hyponatraemia | Na 140–150 mmol/L | Exacerbates cerebral oedema |
| Corticosteroids | Contraindicated | CRASH-1 trial (Roberts 2004, Lancet): methylprednisolone significantly increased mortality in TBI |
ICP Management — Stepwise Approach
Indications for ICP monitoring: GCS ≤8 with abnormal CT (haematoma, contusion, swelling, effaced cisterns, midline shift). An external ventricular drain (EVD) provides both monitoring and therapeutic CSF drainage.
Tier 1
- Head of bed 30°; head midline (avoid jugular venous compression)
- Adequate analgesia and sedation (propofol or midazolam + opioid analgesia)
- Normocapnia: PaCO₂ 35–40 mmHg
- Normothermia: ≤37.5°C
- CSF drainage via EVD: bolus or continuous to target ICP <22 mmHg
Tier 2
- Hyperosmolar therapy:
- Mannitol 0.25–1 g/kg IV: onset 15–30 min; osmotic diuresis + rheological improvement; hold if serum osmolality >320 mOsm/kg; causes volume depletion
- Hypertonic saline (3% or 23.4%): osmotic gradient without volume depletion; preferred in hypovolaemia or AKI risk; target serum Na 145–155 mmol/L
- Neuromuscular blockade: eliminates dyssynchrony and coughing-driven ICP spikes; use with TOF monitoring
Tier 3
- Hypothermia (32–35°C): reduces CMRO₂; not recommended as routine prophylaxis (POLAR, EUROTHERM3235 trials showed no benefit or harm); may be used as targeted rescue therapy
- Barbiturate coma: burst suppression → ↓ metabolic demand; significant cardiovascular depression; specialist centres only
- Decompressive craniectomy: see Key Trials; life-saving in refractory ICP but shifts outcomes from death to severe disability
Hyperventilation
- Transient only (PaCO₂ 30–35 mmHg) as a bridge to definitive intervention for impending herniation
- Sustained hyperventilation causes cerebral vasoconstriction and ischaemia — do not use routinely
Key Trials
| Trial | Question | Finding |
|---|---|---|
| CRASH-1 (Roberts, Lancet 2004) | Methylprednisolone vs placebo in TBI | Significantly increased mortality — corticosteroids absolutely contraindicated in TBI |
| DECRA (Cooper, NEJM 2011) | Early bifrontotemporoparietal craniectomy vs medical management in diffuse TBI with ICP >20 mmHg | Lower ICP in surgical group but significantly worse functional outcomes; more patients alive but in vegetative state |
| RESCUEicp (Hutchinson, NEJM 2016) | Decompressive craniectomy vs medical management for refractory ICP >25 mmHg | Surgical group: lower 6-month mortality (26.9% vs 48.9%) but more survivors in vegetative state (8.5% vs 2.1%); no improvement in rate of good neurological outcome |
| CRASH-3 (CRASH-3 Collaborators, Lancet 2019) | TXA within 3h of TBI | Reduced head-injury deaths in mild-moderate TBI when given within 3h; no benefit in severe TBI; no benefit if given after 3h |
| POLAR (Cooper, NEJM 2018) | Prophylactic hypothermia after severe TBI | No improvement in 6-month neurological outcome — prophylactic hypothermia not recommended |
| EUROTHERM3235 (Andrews, NEJM 2015) | Hypothermia for raised ICP in TBI | Worse 6-month outcomes with hypothermia — trial stopped early |
Viva Questions
1. Explain the Monroe-Kellie doctrine and how it explains ICP dynamics in TBI.
The skull is a fixed-volume rigid compartment containing brain parenchyma, blood, and CSF. When an expanding lesion (haematoma, oedema) increases intracranial volume, compensation occurs by displacing CSF into the spinal subarachnoid space and reducing venous blood volume. This produces an initial flat pressure-volume curve — ICP rises little despite volume accumulation. However, once compensatory reserve is exhausted, compliance falls dramatically and the curve becomes steep — small additional volume increments cause exponential ICP rises. This explains both why patients may tolerate relatively large haematomas initially, and why they can deteriorate rapidly once the threshold is crossed. It also explains the effectiveness of small interventions (a few mL of CSF drained, mannitol reducing brain water) when the patient is on the steep part of the curve.
2. What are the secondary insults in TBI and how do you prevent them?
Secondary injury is the main modifiable target. Hypoxia (even a single episode of SaO₂ <90% doubles mortality) — secure the airway early, target SpO₂ >95%; hypotension (SBP <90 mmHg associated with doubled mortality) — fluid resuscitation and vasopressors to maintain SBP ≥100–110 mmHg; raised ICP — stepwise protocol (sedation, osmotherapy, CSF drainage, craniectomy if refractory); hyperthermia (active cooling, paracetamol); hyperglycaemia (target 6–10 mmol/L); hypercapnia (normocapnia 35–40 mmHg; avoid sustained hyperventilation); hyponatraemia (target Na 140–150 mmol/L); early seizures (7-day antiepileptic prophylaxis). Corticosteroids are absolutely contraindicated based on CRASH-1 mortality data.
3. Interpret the DECRA and RESCUEicp trials — what is the clinical implication?
Both trials examined decompressive craniectomy for raised ICP, but in importantly different populations. DECRA enrolled diffuse TBI patients with relatively early and moderately raised ICP (>20 mmHg) and found worse functional outcomes in the surgical group — more patients were alive but vegetative. This raised concerns about early craniectomy for moderate ICP. RESCUEicp enrolled patients with truly refractory ICP (>25 mmHg despite aggressive tier 1-2 treatment) and found surgery significantly reduced mortality (26.9% vs 48.9%), but the survivors included more in a vegetative state, with no improvement in the rate of good neurological outcomes. The combined message is that craniectomy reduces mortality at the cost of shifting outcomes from death to severe disability. This is not straightforwardly beneficial — the decision requires careful integration of patient preferences, family values, and the clinical context. It should not be offered without exploring what outcome the patient themselves would find acceptable.
4. When and how would you use hyperosmolar therapy, and what are the differences between mannitol and hypertonic saline?
Both agents reduce cerebral oedema by creating an osmotic gradient that draws water from brain tissue across an intact blood-brain barrier into the intravascular compartment, acting within 15–30 minutes. Mannitol (0.25–1 g/kg) additionally causes an osmotic diuresis and improves blood rheology (reduced viscosity, better microcirculation). It is the best-studied agent. Limitations: volume depletion (contraindicated in hypovolaemia), hold if serum osmolality >320 mOsm/kg due to AKI risk. Hypertonic saline (3%, 7.5%, or 23.4%) achieves equivalent or superior ICP reduction while maintaining or expanding circulating volume, making it preferable in hypovolaemic patients or where avoiding volume depletion matters. The 23.4% solution can be given as a small bolus for rapid ICP reduction. There is no definitive RCT evidence of mortality superiority of either agent. Both should be used as bridges to definitive ICP control (surgical decompression, CSF drainage) rather than as indefinite therapy.