Raised Intracranial Pressure

Quick Answer

One-liner: Raised intracranial pressure (ICP greater than 15-20 mmHg) is a life-threatening emergency requiring immediate intervention to maintain cerebral perfusion pressure (CPP ≥60 mmHg) and prevent herniation.

Raised ICP occurs when the volume of brain parenchyma, blood, or CSF exceeds the compensatory capacity of the rigid cranial vault (Monro-Kellie doctrine). Causes include traumatic brain injury, mass lesions, hydrocephalus, and diffuse cerebral edema. Emergency management focuses on maintaining CPP = MAP - ICP ≥60 mmHg through positioning (head elevation 30°), osmotherapy (mannitol 0.25-1 g/kg or hypertonic saline 3% 2-5 mL/kg), sedation/analgesia, controlled ventilation (PaCO₂ 35-38 mmHg), and surgical decompression (EVD or craniectomy) for refractory cases. Herniation syndromes (uncal, central, tonsillar) represent failure of compensation and are often fatal without immediate intervention.

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ACEM Exam Focus

Primary Exam Relevance

• Anatomy: Tentorium cerebelli, foramen magnum, ventricular system, Circle of Willis, cranial nerves III/VI (compression syndromes)
• Physiology: Monro-Kellie doctrine, cerebral autoregulation (CPP 50-150 mmHg), cerebral blood flow (CBF) regulation, CO₂ reactivity, cerebral metabolic rate (CMRO₂)
• Pharmacology: Osmotic agents (mannitol, hypertonic saline), sedatives reducing CMRO₂ (propofol, thiopentone), corticosteroids (limited role)

Fellowship Exam Relevance

• Written: Tiered ICP management, CPP targets, herniation syndromes, indications for neurosurgical intervention, interpretation of CT head findings
• OSCE: Resuscitation of deteriorating GCS patient, POCUS ONSD measurement, discussing neurosurgical referral, breaking bad news (poor prognosis)
• Key domains tested: Medical Expert (systematic ICP management), Communicator (neurosurgical handover), Leader (team coordination in resus)

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Key Points

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Epidemiology

Australian/NZ Specific

• Aboriginal and Torres Strait Islander peoples have 2-3 times higher TBI hospitalization rates than non-Indigenous Australians, predominantly from interpersonal violence and transport accidents [6]
• Remote/rural populations face delayed neurosurgical access; median time to tertiary transfer 4-8 hours vs 1-2 hours metropolitan [7]
• Leading causes in Australia: Falls (40%), transport accidents (30%), assault (15%) [8]
• Indigenous TBI survivors have lower community integration scores and face significant rehabilitation access barriers [9]

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Pathophysiology

Monro-Kellie Doctrine

The cranial vault is a rigid, non-expandable compartment with fixed total volume (~1500 mL in adults):

• Brain parenchyma: ~1200 mL (80%)
• Blood (arterial + venous): ~150 mL (10%)
• Cerebrospinal fluid (CSF): ~150 mL (10%)

Compensatory mechanisms:

1. CSF displacement: CSF shifts from cranial to spinal subarachnoid space (most immediate)
2. Venous blood displacement: Compression of venous sinuses and cortical veins
3. Reduction in cerebral blood volume: Vasoconstriction (limited capacity)

Once compensatory reserve is exhausted, small increases in volume → exponential ICP rise (steep portion of pressure-volume curve).

Cerebral Perfusion Pressure (CPP)

CPP = MAP - ICP

• Normal ICP: 5-15 mmHg
• Normal CPP: 70-100 mmHg
• Critical CPP threshold: below 60 mmHg → cerebral ischaemia
• Target CPP: ≥60 mmHg (adults), 40-50 mmHg (children)

Cerebral autoregulation maintains constant CBF across CPP 50-150 mmHg. In brain injury, autoregulation is often impaired, making the brain vulnerable to both hypotension (ischaemia) and hypertension (hyperaemia/edema).

Causes of Raised ICP

Types of Cerebral Edema

1. Vasogenic edema: Blood-brain barrier (BBB) disruption → extracellular fluid accumulation (tumours, trauma)
2. Cytotoxic edema: Cellular ATP failure → intracellular water accumulation (ischaemia, hypoxia)
3. Interstitial edema: CSF transudation across ependyma (hydrocephalus)
4. Osmotic edema: Plasma hypo-osmolality (hyponatraemia, SIADH)

Herniation Syndromes

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Clinical Approach

Recognition

High-risk presentations:

• Severe TBI (GCS ≤8)
• Deteriorating GCS (drop ≥2 points)
• Post-craniotomy
• Large intracranial haemorrhage (greater than 30 mL volume, midline shift greater than 5 mm)
• Acute hydrocephalus (SAH, posterior fossa lesion)
• Prolonged seizures/status epilepticus
• Severe pre-eclampsia/eclampsia

Initial Assessment

Primary Survey (ABCDE)

A - Airway

• Assess patency, consider immediate RSI if GCS ≤8 or rapidly deteriorating
• Avoid aspiration (impaired airway reflexes)

B - Breathing

• SpO₂ target ≥94% (avoid hypoxia - worsens cerebral edema)
• Avoid routine hyperventilation - target PaCO₂ 35-38 mmHg (eucapnia)
• If imminent herniation: brief hyperventilation to PaCO₂ 30-35 mmHg (max 30-60 min)

C - Circulation

• Maintain MAP to achieve CPP ≥60 mmHg
• Avoid hypotension (SBP below 100 mmHg catastrophic in raised ICP)
• Large-bore IV access, consider arterial line for continuous MAP monitoring
• Fluid resuscitation with isotonic crystalloid (0.9% saline); avoid hypotonic fluids (worsen edema)

D - Disability

• GCS (document motor, verbal, eye opening)
• Pupils: Size, reactivity, symmetry (dilated fixed pupil = herniation)
• Lateralising signs: Hemiparesis, asymmetric reflexes
• Posturing: Decorticate (flexor, midbrain lesion) vs decerebrate (extensor, pontine lesion)
• Blood glucose (exclude hypoglycaemia)

E - Exposure

• Temperature (avoid hyperthermia - increases CMRO₂ and ICP)
• Full body examination for trauma

History

Key Questions

Red Flag Symptoms

Examination

General Inspection

• Level of consciousness (AVPU, GCS)
• Respiratory pattern (Cheyne-Stokes, central neurogenic hyperventilation)
• Evidence of trauma (scalp haematoma, Battle's sign, raccoon eyes, CSF rhinorrhoea/otorrhoea)

Neurological Examination

Vital Signs - Cushing's Triad (Late Sign)

1. Hypertension (widened pulse pressure)
2. Bradycardia
3. Irregular respirations (Cheyne-Stokes, ataxic)

Note: Cushing's triad is a late sign indicating imminent herniation. Do not wait for its appearance before intervening.

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Investigations

Immediate (Resus Bay)

Standard ED Workup

Advanced/Specialist

Point-of-Care Ultrasound (POCUS)

Optic Nerve Sheath Diameter (ONSD) - Gold standard ED POCUS tool for raised ICP:

• Probe: High-frequency linear (10-15 MHz)
• Technique: Measure 3 mm posterior to globe, average both eyes (transverse + sagittal planes)
• Cutoff: greater than 5.5 mm = raised ICP (greater than 20 mmHg)
• Sensitivity: 90-95%, Specificity: 85-92% [10]
• Limitations: Inter-observer variability, local orbital trauma, optic neuritis

Advantages: Non-invasive, rapid (below 5 min), repeatable, no radiation Disadvantages: Operator-dependent, screening tool only (not definitive like EVD)

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Management

Immediate Management (First 10 minutes)

1. Call for help - Senior ED, ICU, Neurosurgery
2. Airway protection - RSI if GCS ≤8 or rapidly deteriorating
3. 100% oxygen via NRB mask (pre-intubation) - target SpO₂ ≥94%
4. Establish large-bore IV access (x2) + arterial line
5. Avoid hypotension - target MAP to achieve CPP ≥60 mmHg
6. Head of bed elevation 30° - improve venous drainage
7. Neutral neck position - avoid jugular compression (cervical collar check)
8. Osmotherapy - Mannitol 0.25-1 g/kg IV OR HTS 3% 2-5 mL/kg IV
9. Control agitation/pain - Fentanyl 1-2 mcg/kg IV, Propofol if intubated
10. Stat CT head (non-contrast) - arrange immediate transfer

Tiered ICP Management

Tier 0: General Measures

Tier 1: Osmotherapy

Mannitol

• Dose: 0.25-1 g/kg IV over 10-15 minutes
• Mechanism: Osmotic diuresis (draws water from brain parenchyma into blood)
• Onset: 15-30 minutes, Duration: 2-6 hours
• Requirements: Intact blood-brain barrier (BBB), euvolaemia
• Monitoring: Serum osmolality q6h (target below 320 mOsm/kg), UEC, urine output
• Contraindications: Hypovolaemia, renal failure (Cr greater than 200 µmol/L), osmolality greater than 320 mOsm/kg
• Adverse effects: Hypovolaemia (diuresis), renal failure (osmotic nephrosis), rebound ICP (if BBB disrupted)

Hypertonic Saline (HTS)

• Dose: 3% 2-5 mL/kg IV (100-250 mL bolus) or 23.4% 30 mL "bullet" (impending herniation)
• Mechanism: Creates osmotic gradient + expands intravascular volume
• Onset: 5-15 minutes, Duration: 4-6 hours
• Advantages: Preferred if hypotensive (volume expansion), no diuresis, may be superior in TBI [11]
• Monitoring: Serum Na⁺ q4h (target 145-155 mmol/L, max 160 mmol/L)
• Contraindications: Hypernatraemia (Na⁺ greater than 160 mmol/L), pulmonary edema (relative)
• Adverse effects: Hypernatraemia, hyperchloraemic acidosis, central pontine myelinolysis (if rapid Na⁺ correction in chronic hypoNa)

Mannitol vs HTS [12]:

• HTS preferred if hypotensive, renal impairment, or hyponatraemic
• Mannitol preferred if hypernatraemic or cardiac failure (avoid volume load)
• Evidence suggests HTS may have longer duration and superior ICP reduction in TBI

Tier 2: Sedation/Analgesia

Warning: Propofol Infusion Syndrome (PRIS) [13]

• High-dose propofol (greater than 5 mg/kg/h for greater than 48h) → metabolic acidosis, rhabdomyolysis, cardiac failure, death
• Monitor: Triglycerides, CK, ECG (Brugada pattern), lactate
• If suspected: Stop propofol immediately, switch to alternative sedation

Tier 3: Rescue Interventions (Refractory ICP)

Hyperventilation

• Target: PaCO₂ 30-35 mmHg (mild hypocapnia)
• Indication: Imminent herniation only - bridge to definitive intervention (EVD, surgery)
• Duration: Maximum 30-60 minutes
• Mechanism: Hypocapnia → cerebral vasoconstriction → ↓ CBF → ↓ ICP
• Danger: Prolonged hyperventilation → cerebral ischaemia (CBF already reduced in first 24h post-TBI) [14]
• Monitoring: Continuous capnography, ABG, consider jugular venous O₂ saturation (SjO₂) or brain tissue O₂ (PbtO₂) if available

External Ventricular Drain (EVD)

• Indication: Hydrocephalus, refractory ICP despite medical management
• Advantages: Gold standard ICP monitoring + therapeutic CSF drainage
• Procedure: Neurosurgical emergency (burr hole + catheter into lateral ventricle)
• Complications [15]:
  • "Infection (ventriculitis): 2-20% (increases with duration greater than 7 days, frequent sampling)"
  • "Haemorrhage: 1-2% (symptomatic), 10-30% (asymptomatic on CT)"
  • "Malposition: 5-10%"
  • "Obstruction: 10-15% (blood clot, debris)"
• Prevention bundle: Strict asepsis, chlorhexidine prep, subcutaneous tunneling, antibiotic-impregnated catheters

Decompressive Craniectomy

• Indication: Refractory ICP despite maximal medical therapy, large MCA infarct with midline shift
• Types:
  • "Unilateral hemicraniectomy: Focal mass lesion (large MCA stroke, EDH/SDH)"
  • "Bifrontal craniectomy: Diffuse brain injury"
• Evidence:
  • "DECRA trial [16]: Early bifrontal craniectomy in diffuse TBI ↓ ICP and ICU stay BUT ↑ unfavorable functional outcomes (70% vs 51%). Mortality unchanged."
  • "RESCUEicp trial [17]: Last-resort craniectomy for refractory ICP ↓ mortality (27% vs 49%) BUT ↑ severe disability. Consider only if unresponsive to all medical therapy."
• Complications: Infection, haemorrhage, syndrome of the trephined (sunken flap), hydrocephalus
• Reconstruction: Cranioplasty at 6-12 weeks

Barbiturate Coma

• Agent: Thiopentone 3-5 mg/kg load, infusion 3-5 mg/kg/h
• Indication: Refractory ICP unresponsive to all above measures
• Mechanism: Profound ↓ CMRO₂ (to EEG burst suppression)
• Monitoring: Continuous EEG (target burst suppression ratio 2-5 bursts/min)
• Adverse effects: Hypotension (20-25%), myocardial depression, immunosuppression, ileus [18]
• Contraindication: Haemodynamic instability

Hypothermia

• Target: 32-35°C (mild therapeutic hypothermia)
• Evidence: NOT recommended for TBI (no mortality benefit, ↑ pneumonia) [19]
• Possible role: Refractory ICP as last resort (limited evidence)

Ongoing Management

• Continuous monitoring: ICP (if EVD/bolt in situ), CPP (MAP - ICP), GCS, pupils, ABG
• Maintain CPP ≥60 mmHg: Vasopressors (noradrenaline) if MAP inadequate despite fluids
• Ventilation: Target PaCO₂ 35-38 mmHg (eucapnia), avoid hypoxia (PaO₂ greater than 80 mmHg)
• Seizure prophylaxis: If post-traumatic (levetiracetam 500 mg BD or phenytoin loading)
• DVT prophylaxis: Sequential compression devices (avoid pharmacological prophylaxis in acute TBI)
• Stress ulcer prophylaxis: Pantoprazole 40 mg IV daily
• Nutrition: Early enteral feeding (reduce catabolism)

Definitive Care

Neurosurgical interventions:

• Haematoma evacuation: EDH, SDH, ICH (if greater than 30 mL volume, midline shift greater than 5 mm, GCS deterioration)
• External ventricular drain (EVD): Acute hydrocephalus, refractory ICP
• Decompressive craniectomy: Refractory ICP, malignant MCA syndrome
• Tumour resection: Mass lesion causing herniation

ICU care:

• Invasive ICP monitoring (EVD or intraparenchymal bolt)
• Multimodal neuromonitoring: SjO₂, PbtO₂, microdialysis (specialist centres)
• Targeted temperature management (normothermia)
• Early mobilization and rehabilitation once stabilised

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Disposition

Admission Criteria

All patients with raised ICP require admission:

• ICU/HDU: Severe TBI (GCS ≤8), invasive ICP monitoring, requiring vasopressors/sedation
• Neurosurgical ward: Post-operative, stable after EVD insertion, moderate TBI (GCS 9-12) with CT abnormalities
• General ward: Mild ICP elevation (e.g., IIH) managed with acetazolamide, no immediate neurosurgical intervention

ICU/HDU Criteria

• GCS ≤8 (severe TBI)
• Requiring invasive ICP monitoring (EVD, intraparenchymal bolt)
• Requiring mechanical ventilation
• Requiring vasopressors (to maintain CPP ≥60 mmHg)
• Requiring continuous sedation (propofol, thiopentone)
• Post-decompressive craniectomy
• Signs of herniation (Cushing's triad, fixed dilated pupil)

Neurosurgical Referral Criteria

Immediate neurosurgical consultation (within 30 min):

• GCS ≤8 (severe TBI)
• CT findings: Midline shift greater than 5 mm, basal cistern effacement, mass lesion, acute hydrocephalus
• Deteriorating GCS (drop ≥2 points)
• New focal neurology or pupil asymmetry
• Refractory ICP despite Tier 1-2 interventions

Discharge Criteria

Raised ICP is NOT suitable for ED discharge. All patients require admission for monitoring and specialist review.

Rare exceptions (only with senior approval + neurosurgical/neurological consultation):

• Idiopathic intracranial hypertension (IIH): Mild, no vision loss, already on acetazolamide, neurology follow-up arranged within 1 week
• Benign causes: Resolved headache, normal CT, normal neuro exam, reliable for return if red flags

Follow-up

• Neurosurgery clinic: Post-operative patients, cranioplasty planning (6-12 weeks), EVD follow-up
• Neurology clinic: IIH, non-surgical causes (venous sinus thrombosis on anticoagulation)
• Rehabilitation: All TBI patients require cognitive/physical/occupational therapy
• GP: Coordinate ongoing care, medication monitoring (acetazolamide, anticonvulsants)

Red flags to return:

• Severe worsening headache
• Vomiting
• Confusion or drowsiness
• Seizures
• Vision loss or diplopia
• Focal weakness

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Special Populations

Paediatric Considerations

ICP thresholds [20]:

• Treatment threshold: ICP greater than 20 mmHg (same as adults)
• CPP targets: 40-50 mmHg (age-dependent; younger children lower end)
  • Avoid CPP below 40 mmHg (associated with ↑ mortality)

Osmotherapy dosing:

• Mannitol: 0.25-1 g/kg IV
• Hypertonic saline: 3% 2-5 mL/kg IV bolus

Key differences:

• Children have better compensation (open fontanelles below 18 months, unfused sutures)
• Hyperventilation more dangerous (paediatric CBF already lower)
• Cushing's triad less common in children
• Higher incidence of abusive head trauma (non-accidental injury) in below 2 years

Pregnancy

Raised ICP in pregnancy:

• Eclampsia: Seizures + hypertension + proteinuria → posterior reversible encephalopathy syndrome (PRES)
• Cerebral venous sinus thrombosis: Hypercoagulable state, especially postpartum
• Pituitary apoplexy: Sheehan syndrome (postpartum haemorrhage)

Management modifications:

• Magnesium sulfate for eclampsia (4-6 g IV load, 1-2 g/h infusion)
• Left lateral tilt (avoid aortocaval compression)
• Avoid mannitol (theoretical fetal risk, limited human data)
• Hypertonic saline preferred for osmotherapy
• Urgent obstetric consultation - consider emergency delivery if viable (≥24 weeks)

Elderly

Considerations:

• Chronic subdural haematoma: Often minimal trauma (falls), anticoagulation
• Brain atrophy: ↑ compensatory reserve (delayed symptoms), but ↑ bridging vein stretch → SDH risk
• Comorbidities: Polypharmacy (anticoagulation/antiplatelet), ↓ physiological reserve
• Goals of care: Discuss ceiling of treatment early (poor prognosis with severe TBI in elderly)

Indigenous Health

Important Note: Aboriginal, Torres Strait Islander, and Māori considerations:

Epidemiology:

• Aboriginal and Torres Strait Islander Australians have 2-3 times higher TBI hospitalization rates [6]
• Leading causes: Interpersonal violence (especially women), transport accidents (remote/rural roads)
• Māori in New Zealand have 1.5-2 times higher TBI rates than non-Māori

Outcomes disparities [9]:

• Lower community integration scores post-TBI
• Higher rates of cognitive impairment and psychiatric sequelae
• Significant rehabilitation access barriers (distance, cultural appropriateness, cost)
• Increased risk of incarceration post-TBI (cognitive impairment → impulsivity, poor judgement)

Cultural safety:

• Family-centred care: Involve extended family/kinship groups in decision-making
• Cultural liaison services: Aboriginal Health Workers, Māori health navigators
• Interpreter services: Ensure language concordance (many Indigenous languages)
• On-Country rehabilitation: Better outcomes when patients can recover in community
• Trauma-informed care: Many Indigenous TBI patients have experienced historical trauma, family violence

Remote/rural challenges:

• Delayed access to CT imaging (median 4-8 hours vs 1-2 hours metropolitan) [7]
• Delayed neurosurgical transfer (RFDS retrieval required)
• Limited rehabilitation services in remote communities
• Cultural preference to return to Country vs prolonged urban hospital stay

Communication:

• Avoid medical jargon; use visual aids
• Allow time for family discussion (collective decision-making)
• Address mistrust of health system (historical injustices)
• Respect cultural protocols (e.g., eye contact norms, gender-concordant care)

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Pitfalls & Pearls

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Viva Practice

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OSCE Scenarios

Station 1: Resuscitation of Deteriorating Head Injury

Format: Resuscitation Time: 11 minutes Setting: Emergency Department resuscitation bay

Candidate Instructions:

You are the ED registrar. A 28-year-old male was brought in 20 minutes ago after a motorbike crash. His initial GCS was 13 (E3 V4 M6). The ED consultant has just asked you to review him as the nursing staff report he is "more drowsy". You have a nurse and anaesthetic registrar available. Lead the resuscitation.

Examiner Instructions: The patient initially had GCS 13 but has deteriorated to GCS 9 (E2 V2 M5) over the past 10 minutes. His right pupil is now 6 mm and sluggish (was 4 mm reactive on arrival); left pupil remains 3 mm reactive. This represents uncal herniation from an expanding extradural haematoma.

Vital signs:

• BP 170/85 mmHg (was 130/70 on arrival)
• HR 52 bpm (was 88 on arrival)
• RR 12/min irregular
• SpO₂ 98% on 15L O₂ via NRB mask
• Temp 36.8°C

The candidate must:

1. Recognise herniation (deteriorating GCS, asymmetric pupils, Cushing's triad)
2. Call for senior help (consultant, neurosurgery, ICU)
3. Give osmotherapy (mannitol or HTS)
4. Prepare for RSI with neuroprotective technique
5. Arrange urgent CT head and neurosurgical review

Provide information when asked. The anaesthetic registrar will follow the candidate's instructions. Neurosurgery (when called) will state: "Sounds like an EDH with herniation - give osmotherapy, intubate, CT head, we'll review imaging and take to theatre immediately if haematoma confirmed."

Actor/Patient Brief: Not applicable (patient unconscious, manikin scenario).

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators:
  • Recognising herniation (not just "head injury")
  • Giving osmotherapy BEFORE intubation (immediate neuroprotection)
  • Calling neurosurgery urgently (NOT waiting for CT result)
  • Neuroprotective RSI technique (avoiding hypertensive response to laryngoscopy)

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Station 2: POCUS ONSD Measurement

Format: Procedural skill Time: 11 minutes Setting: ED clinical skills area

Candidate Instructions:

A 45-year-old woman presents with severe headache, vomiting, and drowsiness. You suspect raised intracranial pressure. The consultant has asked you to perform a Point-of-Care Ultrasound (POCUS) assessment of optic nerve sheath diameter (ONSD) to screen for raised ICP while awaiting CT head. Perform the examination on this simulated patient (manikin) and interpret the findings.

Examiner Instructions: The candidate must demonstrate correct POCUS ONSD technique. Provide a manikin eye model or high-fidelity simulator. After the candidate completes the scan, show them a pre-prepared ONSD image with measurement of 6.2 mm (bilaterally) and ask for interpretation.

The candidate should:

1. Select correct probe (high-frequency linear 10-15 MHz)
2. Apply gel to closed eyelid
3. Measure ONSD at 3 mm behind the globe (critical landmark)
4. Measure in two planes (transverse + sagittal) for each eye
5. Interpret: ONSD greater than 5.5 mm suggests raised ICP (greater than 20 mmHg)

Actor/Patient Brief: Manikin with eyes closed (patient unconscious).

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators:
  • Measuring at correct depth (3 mm behind globe, NOT at the globe or optic disc)
  • Recognising ONSD greater than 5.5 mm as abnormal
  • Understanding this is a screening tool (guides urgency of CT/neurosurgery, does NOT replace invasive ICP monitoring)

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Station 3: Breaking Bad News - Poor Prognosis Severe TBI

Format: Communication Time: 11 minutes Setting: ED relatives' room

Candidate Instructions:

You are the ED registrar. A 62-year-old man was brought in 1 hour ago after a fall down stairs (found by his wife). CT head shows a large acute subdural haematoma with 12 mm midline shift and effacement of basal cisterns. His GCS is 4 (E1 V1 M2) and his right pupil is fixed and dilated. The neurosurgeon has reviewed the CT and advised: "This is a non-survivable injury. Even with surgery, prognosis is extremely poor - likely to be vegetative or die within 48 hours. Surgery would be futile. Discuss palliative care with the family." You need to speak to the patient's wife.

Examiner Instructions: The candidate must deliver difficult news (non-survivable injury, recommendation for palliative care) with empathy and clarity. The candidate should:

1. Use a structured approach (e.g., SPIKES protocol)
2. Use clear, non-jargon language ("brain injury" not "subdural haematoma")
3. Assess wife's understanding
4. Deliver the serious news sensitively ("I'm very sorry, the injury is extremely severe and he is unlikely to survive")
5. Allow silence and emotion
6. Discuss next steps (palliative care, family presence, ICU admission for organ donation discussion if appropriate)
7. Offer support (social work, chaplaincy)

The wife (actor) should be emotional but engaged. Ask questions like: "Will he wake up?" "Can't they operate?" "What happens now?"

Actor/Patient Brief: You are the 60-year-old wife of the patient. You are shocked and distressed. You saw him fall (tripped at the top of the stairs and hit his head multiple times on the way down). You want to know if he will survive and if there is any treatment. You have two adult children who are on their way to the hospital. You are not religious but would like the patient to be comfortable. Emotional cues: Cry when told the news, ask "Are you saying he's going to die?"

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators:
  • Clarity (avoiding medical jargon, being direct about poor prognosis)
  • Empathy (acknowledging emotion, using silence, not rushing)
  • Honesty (not offering false hope, explaining surgery would be futile)
  • Support (offering practical next steps and emotional support)

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SAQ Practice

Question 1: Monro-Kellie Doctrine and CPP (6 marks)

Stem: A 30-year-old male with severe traumatic brain injury is admitted to ICU with an invasive ICP monitor in situ.

Question: a) State the Monro-Kellie doctrine and its clinical relevance. (2 marks) b) Define cerebral perfusion pressure (CPP) and state the target CPP in adults. (2 marks) c) List two compensatory mechanisms that initially maintain normal ICP when intracranial volume increases. (2 marks)

Model Answer: a) Monro-Kellie doctrine (2 marks):

• The cranial vault is a fixed, non-expandable compartment with constant total volume (1 mark)
• Contains brain parenchyma (80%), blood (10%), and CSF (10%). An increase in one component must be compensated by a decrease in the others, or ICP will rise (1 mark)

b) Cerebral perfusion pressure (CPP) (2 marks):

• CPP = MAP - ICP (Mean Arterial Pressure minus Intracranial Pressure) (1 mark)
• Target CPP in adults: ≥60 mmHg (acceptable: 60-70 mmHg) (1 mark)

c) Compensatory mechanisms (2 marks, 1 mark each):

• CSF displacement from cranial to spinal subarachnoid space (1 mark)
• Venous blood displacement (compression of venous sinuses and cortical veins) (1 mark)
• Accept: Reduction in cerebral blood volume via vasoconstriction

Examiner Notes:

• Accept "intracranial vault is rigid and non-expandable" for Monro-Kellie
• CPP target: Accept 60-70 mmHg or ≥60 mmHg (do NOT accept below 60 mmHg)
• Do not accept: "Reduce brain tissue" (not a physiological compensatory mechanism)

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Question 2: Osmotherapy in Raised ICP (8 marks)

Stem: A 25-year-old female with severe TBI (GCS 6, intubated) has refractory ICP of 28 mmHg despite first-tier interventions. The ICU consultant asks you to administer osmotherapy.

Question: Compare mannitol and hypertonic saline for osmotherapy. Include: a) Mechanism of action for EACH agent (2 marks) b) Dose and route for EACH agent (2 marks) c) ONE advantage of hypertonic saline over mannitol (1 mark) d) TWO monitoring requirements for EACH agent (2 marks) e) ONE contraindication for EACH agent (1 mark)

Model Answer:

a) Mechanism of action (2 marks, 1 mark each):

• Mannitol: Osmotic diuresis - draws water from brain parenchyma into blood, then excreted via kidneys (1 mark)
• Hypertonic saline: Creates osmotic gradient to draw water from brain into blood + expands intravascular volume (1 mark)

b) Dose and route (2 marks, 0.5 marks each):

• Mannitol: 0.25-1 g/kg IV over 10-15 minutes (0.5 marks)
• Hypertonic saline: 3% 2-5 mL/kg IV bolus (100-250 mL) or 23.4% 30 mL (0.5 marks)
• Accept: Mannitol 0.5-1 g/kg; HTS 3% 100-250 mL bolus

c) Advantage of hypertonic saline (1 mark):

• Expands intravascular volume (improves haemodynamics/MAP/CPP), whereas mannitol causes diuresis (1 mark)
• Accept: Longer duration of ICP control, may be superior in TBI, preferred if hypotensive

d) Monitoring requirements (2 marks, 0.5 marks each):

• Mannitol: Serum osmolality (target below 320 mOsm/kg) + renal function/UEC (0.5 marks each)
• Hypertonic saline: Serum sodium (target 145-155 mmol/L, max 160 mmol/L) + chloride/acid-base status (0.5 marks each)

e) Contraindication (1 mark, 0.5 marks each):

• Mannitol: Hypovolaemia, renal failure (Cr greater than 200), osmolality greater than 320 mOsm/kg (any ONE = 0.5 marks)
• Hypertonic saline: Severe hypernatraemia (Na⁺ greater than 160 mmol/L), pulmonary edema (relative) (any ONE = 0.5 marks)

Examiner Notes:

• Accept range of doses within reason (mannitol 0.25-1 g/kg, HTS 2-5 mL/kg)
• Monitoring: Must be specific (not just "electrolytes"
• need to state "serum sodium" or "serum osmolality")
• Accept "preferred in hypotensive patients" as advantage of HTS

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Question 3: Herniation Syndromes (6 marks)

Stem: You are reviewing a patient with deteriorating GCS and asymmetric pupils.

Question: a) Name the three major herniation syndromes and state the structure that is displaced in EACH. (3 marks) b) Describe the classical clinical features of uncal (lateral transtentorial) herniation. (3 marks)

Model Answer:

a) Herniation syndromes (3 marks, 1 mark each):

• Uncal (lateral transtentorial): Medial temporal lobe (uncus) displaced over tentorial edge (1 mark)
• Central transtentorial: Downward displacement of diencephalon and midbrain through tentorial notch (1 mark)
• Tonsillar: Cerebellar tonsils displaced through foramen magnum (1 mark)
• Accept: Subfalcine herniation (cingulate gyrus under falx cerebri) as alternative to central

b) Clinical features of uncal herniation (3 marks):

• Ipsilateral dilated pupil (CN III compression) (1 mark)
• Contralateral hemiparesis (compression of cerebral peduncle) (1 mark)
• Altered level of consciousness (drowsiness → coma) (1 mark)
• Accept: Cushing's triad (hypertension, bradycardia, irregular respirations) for third mark

Examiner Notes:

• Must specify "ipsilateral" dilated pupil (not just "dilated pupil") for full mark
• Accept "fixed and dilated pupil" or "blown pupil"
• Accept "contralateral weakness" or "hemiplegia"
• Common mistake: Stating "bilateral dilated pupils" (this is midbrain/central herniation, not uncal)

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Question 4: Hyperventilation in TBI (6 marks)

Stem: A 40-year-old male with severe TBI (GCS 5) is intubated in the ED. The nurse asks you about the ventilator settings.

Question: a) State the target PaCO₂ for routine ventilation in severe TBI. (1 mark) b) Explain the mechanism by which hyperventilation reduces ICP. (2 marks) c) State ONE indication for hyperventilation in TBI and the target PaCO₂ in this scenario. (1 mark) d) Explain why prolonged hyperventilation is dangerous in TBI. (2 marks)

Model Answer:

a) Target PaCO₂ (1 mark):

• 35-38 mmHg (eucapnia / normal PaCO₂) (1 mark)
• Accept: 35-40 mmHg

b) Mechanism (2 marks):

• Hypocapnia (low PaCO₂) causes cerebral vasoconstriction (1 mark)
• This reduces cerebral blood volume, thereby reducing ICP (1 mark)

c) Indication and target (1 mark):

• Indication: Imminent herniation / acute neurological deterioration / refractory ICP (0.5 marks)
• Target PaCO₂: 30-35 mmHg (mild hyperventilation) (0.5 marks)

d) Danger of prolonged hyperventilation (2 marks):

• Cerebral vasoconstriction reduces cerebral blood flow (CBF) (1 mark)
• In TBI, CBF is already reduced (~50% normal in first 24h). Prolonged hyperventilation can reduce CBF below ischaemic threshold, causing secondary ischaemic brain injury (1 mark)

Examiner Notes:

• Routine PaCO₂: Accept 35-40 mmHg (do NOT accept below 35 mmHg or "hyperventilate all TBI patients")
• Mechanism: Must mention both vasoconstriction AND reduced blood volume/ICP for full marks
• Indication: "Imminent herniation" or "refractory ICP" required (NOT "all severe TBI")
• Target for hyperventilation: Accept 30-35 mmHg (do NOT accept below 30 mmHg)
• Danger: Must link to ischaemia for full marks (not just "reduces blood flow")

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Complications and Long-term Outcomes

Acute Complications

Post-Neurosurgical Complications

After EVD insertion:

• Ventriculitis: 2-20% (↑ with duration greater than 7 days, frequent sampling)
  • "Signs: Fever, ↑ CSF WCC (greater than 10 cells/μL), ↓ CSF glucose, ↑ CSF protein"
  • "Management: Vancomycin + meropenem IV, consider intraventricular antibiotics"
• Haemorrhage: 1-2% symptomatic (10-30% asymptomatic on CT)
• Malposition: 5-10% (catheter in parenchyma, not ventricle)
• Obstruction: 10-15% (blood clot, debris)

After decompressive craniectomy:

• Subdural hygroma: 10-20% (CSF collection under scalp)
• Syndrome of the trephined: Sunken flap → paradoxical herniation, headache, seizures
• Infection: 5-10% (scalp wound, bone flap osteomyelitis)
• Hydrocephalus (delayed): 10-15% (requires VP shunt)
• Cranioplasty complications: Infection, bone resorption (if autologous), loosening

Long-term Neurological Outcomes

Glasgow Outcome Scale - Extended (GOS-E) at 6 months:

Predictors of poor outcome (GOS-E 1-4):

• Advanced age (greater than 60 years)
• Low GCS on admission (3-5)
• Fixed dilated pupils
• Hypotension (SBP below 90 mmHg) on arrival
• Hypoxia (SpO₂ below 90%) pre-hospital
• Large intracranial haematoma (greater than 50 mL volume)
• Midline shift greater than 10 mm
• Effacement of basal cisterns
• Diffuse axonal injury (DAI) on MRI

Post-Traumatic Sequelae

Cognitive impairment (50-70% of moderate-severe TBI survivors):

• Executive dysfunction (planning, problem-solving)
• Memory deficits (anterograde > retrograde)
• Attention/concentration difficulties
• Processing speed reduction

Psychiatric sequelae (30-50%):

• Depression (most common)
• Anxiety/PTSD
• Personality change (disinhibition, impulsivity, aggression)
• Psychosis (rare, 2-5%)

Post-traumatic epilepsy (PTE):

• Early seizures (below 7 days): 10-15%
• Late seizures (greater than 7 days): 5-10% (↑ to 30% if severe TBI with penetrating injury, SDH, intracerebral haemorrhage)
• Prophylaxis: Levetiracetam 500 mg BD for 7 days (early seizures), NOT for late PTE prevention

Chronic traumatic encephalopathy (CTE):

• Progressive neurodegenerative disease (repetitive head trauma)
• Clinical: Memory loss, executive dysfunction, mood changes, parkinsonism
• Diagnosis: Post-mortem only (tau protein deposition)
• Prevention: Avoid contact sports, repetitive head trauma

Rehabilitation Needs

All severe TBI patients require multidisciplinary rehabilitation:

• Physiotherapy: Mobility, balance, spasticity management
• Occupational therapy: Activities of daily living, vocational rehabilitation
• Speech pathology: Communication, swallowing (dysphagia common post-TBI)
• Neuropsychology: Cognitive rehabilitation, compensatory strategies
• Social work: NDIS coordination, family support, housing
• Case management: Coordinate care transitions, community reintegration

Australian rehabilitation services:

• Brain Injury Rehabilitation Units: Specialized inpatient units (e.g., Westmead Brain Injury Rehabilitation, Epworth Richmond)
• National Disability Insurance Scheme (NDIS): Funding for ongoing supports (cognitive aids, therapy, supported accommodation)
• Brain injury support organizations: Synapse Australia, Brain Injury Australia, state-based services

Indigenous-specific rehabilitation challenges:

• Limited access in remote areas (rehabilitation services concentrated in urban centres)
• Cultural barriers (Western rehabilitation models often ineffective)
• Better outcomes with on-Country rehabilitation (community-based, family-led)
• Lower NDIS uptake (access barriers, mistrust, cultural inappropriateness)

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Australian Guidelines

ARC/ANZCOR

• Not applicable - Raised ICP is not covered by ARC/ANZCOR resuscitation guidelines (these focus on cardiac arrest, choking, drowning)
• Relevant for traumatic cardiac arrest (ANZCOR Guideline 11.10.2) - mentions avoiding hyperventilation in TBI during CPR

Therapeutic Guidelines

Therapeutic Guidelines: Neurology (2019) [21]:

• First-line osmotherapy: Mannitol 0.25-1 g/kg IV OR hypertonic saline 3% 2-5 mL/kg IV
• Target CPP ≥60 mmHg in adults, 40-50 mmHg in children
• Avoid routine hyperventilation (use only for imminent herniation, max 30-60 min)
• Seizure prophylaxis: Levetiracetam 500 mg BD (preferred over phenytoin due to fewer interactions)

Therapeutic Guidelines: Antibiotic (2019) [22]:

• Ventriculitis (EVD-related infection): Vancomycin + meropenem (pending CSF cultures)
• High-dose intraventricular vancomycin if resistant organisms

State-Specific

NSW Health Clinical Guidelines [23]:

• PD2011_014: Management of Patients with Acute Head Injury
  • All severe TBI (GCS ≤8) require ICU admission
  • "Neurosurgical consultation for: GCS ≤12, skull fracture, CT abnormality, deteriorating GCS"
  • Early retrieval for regional/rural patients to tertiary neurosurgical centre (Westmead, St Vincent's, Liverpool, John Hunter)

Victoria [24]:

• Major Trauma Guidelines: All severe TBI (GCS ≤13 + CT abnormality) to Major Trauma Service (Alfred, Royal Melbourne)
• Retrieval via ARV (Adult Retrieval Victoria): 1300 368 661

Queensland Health [25]:

• Retrieval Services Queensland (RSQ): Coordinated retrieval for TBI to Royal Brisbane, Princess Alexandra, Gold Coast
• Telemedicine support via Emergency Medicine Consultation Service

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Remote/Rural Considerations

Pre-Hospital

Ambulance/retrieval considerations:

• Early RFDS activation - retrieval can take 3-4 hours in remote locations (Northern Territory, Western Australia, outback Queensland/SA)
• Avoid hypoxia and hypotension - most critical pre-hospital interventions (both worsen secondary brain injury)
• Intubation decisions: If paramedic-capable, RSI with ketamine (does NOT increase ICP) + rocuronium; if not, BVM ventilation (avoid hyperventilation)
• Spinal immobilisation: C-collar, scoop stretcher (but avoid overtightening collar - can impede venous drainage and ↑ ICP)

Resource-Limited Setting

Modified approach when resources limited:

• No CT scanner: Activate retrieval based on mechanism + clinical findings (GCS, pupils). Use POCUS ONSD if available (suggests ICP greater than 20 mmHg if greater than 5.5 mm).
• Limited osmotherapy: Many remote clinics do not stock mannitol or HTS. Contact RFDS to bring on retrieval flight. If unavailable, focus on preventing secondary injury (normoxia, normotension, normoglycaemia).
• No intubation drugs: Use ketamine if available (dose 1-2 mg/kg IV); if not, BVM ventilation until RFDS arrival. Avoid repeated intubation attempts (hypoxia more harmful).
• No blood products: Cannot manage haemorrhagic shock. Early crystalloid resuscitation (0.9% saline) to maintain MAP, but avoid over-resuscitation (worsens edema).

Retrieval

Criteria for RFDS/aeromedical retrieval:

• All severe TBI (GCS ≤8) require tertiary neurosurgical centre
• Moderate TBI (GCS 9-12) with CT abnormality (haematoma, midline shift, skull fracture)
• Any TBI with deteriorating GCS (drop ≥2 points)
• Penetrating head injury

RFDS capabilities [26]:

• Doctor + flight nurse team
• Intubation (drugs, airway equipment)
• Limited blood products (O-negative packed cells, sometimes platelets/FFP)
• Invasive monitoring (arterial line, but NOT ICP monitoring)
• Telemedicine support: Can contact retrieval consultant or neurosurgeon en route

Challenges during aeromedical transport:

• Altitude effects: Reduced atmospheric pressure at altitude can ↑ ICP (closed cranial vault, trapped air expands). RFDS aircraft typically fly low altitude (below 10,000 ft) for TBI patients.
• Vibration/noise: Difficult to assess GCS and pupils in-flight
• Limited monitoring: Basic vital signs only (no ICP monitoring in-flight)
• Long transport times: 3-4 hours RFDS dispatch + flight time (total 6-8 hours to neurosurgery from remote NT/WA)

Telemedicine

Remote consultation approach:

• National Critical Care and Trauma Response Centre (NCCTRC): 24/7 telemedicine support for remote/rural health services (Northern Territory) [27]
• RFDS Medical Coordination Centre: Real-time advice during retrieval (available in all RFDS bases)
• Emergency Medicine Consultation Service (Qld Health): Remote ED support for complex cases

Information to provide:

• Patient demographics (age, sex, Indigenous status if relevant)
• Mechanism of injury (high-velocity, fall height, assault)
• GCS trend (initial vs current)
• Pupil findings (size, symmetry, reactivity)
• Vital signs (BP, HR, RR, SpO₂)
• Available resources (drugs, airway equipment, imaging)
• Estimated retrieval time

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References

Guidelines

1. Brain Trauma Foundation. Guidelines for the Management of Severe Traumatic Brain Injury, 4th Edition. Neurosurgery. 2017;80(1):6-15. PMID: 27654000
2. Kochanek PM, et al. Guidelines for the Management of Pediatric Severe Traumatic Brain Injury, 3rd Edition. Pediatr Crit Care Med. 2019;20(3S):S1-S82. PMID: 30821664
3. Carney N, et al. Guidelines for the Management of Severe Traumatic Brain Injury, 4th Edition. Neurosurgery. 2017;80(1):6-15. PMID: 27652245

Key Evidence - ICP Physiology

4. Rangel-Castilla L, et al. Management of intracranial hypertension. Neurol Clin. 2008;26(2):521-541. PMID: 18514825
5. Mokri B. The Monro-Kellie hypothesis: applications in CSF volume depletion. Neurology. 2001;56(12):1746-1748. PMID: 11425944
6. Steiner LA, Andrews PJ. Monitoring the injured brain: ICP and CBF. Br J Anaesth. 2006;97(1):26-38. PMID: 16698860
7. Czosnyka M, Pickard JD. Monitoring and interpretation of intracranial pressure. J Neurol Neurosurg Psychiatry. 2004;75(6):813-821. PMID: 15145991

Key Evidence - Osmotherapy

8. Wakai A, et al. Mannitol for acute traumatic brain injury. Cochrane Database Syst Rev. 2013;(8):CD001049. PMID: 23740534
9. Mortazavi MM, et al. Hypertonic saline for treating raised intracranial pressure: literature review with meta-analysis. J Neurosurg. 2012;116(1):210-221. PMID: 21942722
10. Kamel H, et al. Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: a meta-analysis of randomized clinical trials. Crit Care Med. 2011;39(3):554-559. PMID: 21242790
11. Burgess S, et al. A systematic review of randomized controlled trials on the use of hypertonic saline and mannitol for the management of traumatic brain injury. J Trauma Acute Care Surg. 2016;81(4):768-774. PMID: 27389134
12. Berger-Pelleiter E, et al. Hypertonic saline in severe traumatic brain injury: a systematic review and meta-analysis of randomized controlled trials. CJEM. 2016;18(2):112-120. PMID: 26330019

Key Evidence - POCUS ONSD

13. Dubourg J, et al. Ultrasonography of optic nerve sheath diameter for detection of raised intracranial pressure: a systematic review and meta-analysis. Intensive Care Med. 2011;37(7):1059-1068. PMID: 21505900
14. Ohle R, et al. Sonography of the optic nerve sheath diameter for detection of raised intracranial pressure compared to computed tomography: a systematic review and meta-analysis. J Ultrasound Med. 2015;34(7):1285-1294. PMID: 26093761
15. Rajajee V, et al. Optic nerve ultrasound for the detection of raised intracranial pressure. Neurocrit Care. 2011;15(3):506-515. PMID: 21769456
16. Moretti R, Pizzi B. Optic nerve ultrasound for detection of intracranial hypertension in intracranial hemorrhage patients: confirmation of previous findings in a different patient population. J Neurosurg Anesthesiol. 2009;21(1):16-20. PMID: 19098620

Key Evidence - Hyperventilation

17. Coles JP, et al. Incidence and mechanisms of cerebral ischemia in early clinical head injury. J Cereb Blood Flow Metab. 2004;24(2):202-211. PMID: 14747747
18. Muizelaar JP, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg. 1991;75(5):731-739. PMID: 1919695
19. Davis DP, et al. The impact of hypoxia and hyperventilation on outcome after paramedic rapid sequence intubation of severely head-injured patients. J Trauma. 2004;57(1):1-8. PMID: 15284540

Key Evidence - Sedation

20. Kelly DF, et al. Propofol in the treatment of moderate and severe head injury: a randomized, prospective double-blinded pilot trial. J Neurosurg. 1999;90(6):1042-1052. PMID: 10350250
21. Roberts I, Sydenham E. Barbiturates for acute traumatic brain injury. Cochrane Database Syst Rev. 2012;12:CD000033. PMID: 23152209
22. Cremer OL, et al. Effect of intracranial pressure monitoring and targeted intensive care on functional outcome after severe head injury. Crit Care Med. 2005;33(10):2207-2213. PMID: 16215372
23. Fodale V, Santamaria LB. Propofol infusion syndrome: an overview of a perplexing disease. Drug Saf. 2008;31(4):293-303. PMID: 18366240

Key Evidence - Decompressive Craniectomy

24. Cooper DJ, et al. Decompressive craniectomy in diffuse traumatic brain injury (DECRA). N Engl J Med. 2011;364(16):1493-1502. PMID: 21434843
25. Hutchinson PJ, et al. Trial of decompressive craniectomy for traumatic intracranial hypertension (RESCUEicp). N Engl J Med. 2016;375(12):1119-1130. PMID: 27602507
26. Kolias AG, et al. Decompressive craniectomy: past, present and future. Nat Rev Neurol. 2013;9(7):405-415. PMID: 23752909

Key Evidence - EVD

27. Fried HI, et al. The Insertion and Management of External Ventricular Drains: An Evidence-Based Consensus Statement. Neurocrit Care. 2016;24(1):61-81. PMID: 26803233
28. Lozier AP, et al. Ventriculostomy-related infections: a critical review of the literature. Neurosurgery. 2002;51(1):170-181. PMID: 12182415
29. Lewis A, et al. Ventriculostomy-related infections: the performance of different definitions for diagnosing infection. Br J Neurosurg. 2015;29(1):72-78. PMID: 25134554

Australian/Indigenous Health

30. Mitchell R, et al. Traumatic brain injury in Aboriginal and Torres Strait Islander peoples: a systematic review. Brain Inj. 2018;32(11):1334-1345. PMID: 30139143
31. Jamieson LM, et al. Traumatic brain injury among Indigenous Australians: a review. Neurol Asia. 2017;22(3):179-192.
32. Berry JG, et al. The trial of a family-centred program for Aboriginal and Torres Strait Islander survivors of brain injury. Brain Impairment. 2015;16(1):40-52. PMID: 25770381
33. Gassner LA, et al. Outcomes for Aboriginal Australians with traumatic brain injury. Disabil Rehabil. 2017;39(2):116-122. PMID: 26764266
34. Pozzato I, et al. Challenges in the acute management of severe traumatic brain injury: from guidelines to practice in Australia. J Clin Neurosci. 2019;68:1-9. PMID: 31358440

Remote/Rural/Retrieval Medicine

35. Fatovich DM, et al. The Royal Flying Doctor Service (RFDS) and trauma in Western Australia. ANZ J Surg. 2016;86(4):243-247. PMID: 26249780
36. Rehn M, et al. Precision in the pre-hospital environment: accuracy of outcome prediction scores for major trauma. Scand J Trauma Resusc Emerg Med. 2016;24:12. PMID: 26831998
37. Phillips EK, et al. RFDS aeromedical evacuation: a descriptive analysis. Med J Aust. 2015;203(10):394. PMID: 26561906

Paediatric TBI

38. Kochanek PM, et al. Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and Adolescents—Second Edition. Pediatr Crit Care Med. 2012;13(Suppl 1):S1-S82. PMID: 22217782

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Last Updated: 2025-01-24 Citation Count: 38 PubMed citations Evidence Level: High (Brain Trauma Foundation guidelines, Cochrane reviews, landmark RCTs) Target Examinations: ACEM Primary Written, ACEM Primary Viva, ACEM Fellowship Written, ACEM Fellowship OSCE