Emergency Medicine
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Traumatic Brain Injury

Traumatic brain injury (TBI) affects 180-250 per 100,000 Australians annually with 10-20% mortality for moderate-severe ... ACEM Primary Written, ACEM Primary V

Updated 23 Jan 2026
58 min read

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Urgent signals

Safety-critical features pulled from the topic metadata.

  • GCS less than 13 at 2 hours post-injury
  • Deteriorating GCS or neurological status
  • Basal skull fracture signs
  • Post-traumatic seizure

Exam focus

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  • ACEM Primary Written
  • ACEM Primary Viva
  • ACEM Fellowship Written
  • ACEM Fellowship OSCE

Linked comparisons

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  • Spontaneous Intracerebral Haemorrhage
  • Subarachnoid Haemorrhage

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ACEM Primary Written
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Clinical reference article

Quick Answer

One-liner: Traumatic brain injury is disruption of brain function from external force requiring rapid GCS assessment, CT brain imaging based on risk stratification, and immediate neuroprotective measures including airway protection, blood pressure optimisation, and ICP control when indicated.

Traumatic brain injury (TBI) affects 180-250 per 100,000 Australians annually with 10-20% mortality for moderate-severe injuries. Immediate priorities: secure airway if GCS below 8, target SpO2 94-98%, MAP 80-90 mmHg (CPP 60-70 mmHg), reverse anticoagulation urgently, obtain CT brain within 1 hour for high-risk patients, and involve neurosurgery early.


ACEM Exam Focus

Primary Exam Relevance

  • Anatomy: Skull sutures (coronal, sagittal, lambdoid), meningeal layers (dura, arachnoid, pia), middle meningeal artery course, cerebral venous sinuses
  • Physiology: Monro-Kellie doctrine, cerebral autoregulation (MAP 50-150 mmHg normal), CBF coupling to metabolic demand
  • Pharmacology: Mannitol osmolar shift, hypertonic saline osmotic gradient, levetiracetam pharmacokinetics, warfarin/DOAC reversal agents

Fellowship Exam Relevance

  • Written: Canadian CT Head Rule indications, anticoagulation reversal protocols, ICP management tiers, GCS interpretation, discharge criteria for mild TBI
  • OSCE: Deteriorating head injury management, anticoagulated TBI patient, counselling post-concussion, traumatic pupillary abnormalities examination
  • Key domains tested: Medical Expert, Communicator (breaking bad news about TBI prognosis), Leader (coordinating trauma team), Professional (informed consent for reversal agents)

Key Points

Clinical Pearl

The 5 things you MUST know:

  1. GCS below 8 mandates intubation for airway protection (Brain Trauma Foundation Guidelines)
  2. Canadian CT Head Rule: High-risk (GCS less than 15 at 2h, GCS less than 13, suspected open/depressed skull fracture, basal skull fracture, vomiting greater than 2, age greater than 65, amnesia greater than 30 min) all require CT
  3. Any anticoagulated patient with head injury plus ANY symptom (abnormal GCS, headache, vomiting, amnesia, seizure, basal skull fracture signs) needs CT and reversal regardless of INR
  4. Target CPP 60-70 mmHg in TBI (avoid below 50 or above 70 mmHg), maintain MAP 80-90 mmHg for adequate CPP
  5. Monro-Kellie doctrine: Fixed intracranial volume (80% brain, 10% blood, 10% CSF) - if one component increases, another must decrease or ICP rises

Epidemiology

MetricValueSource
Incidence (Australia)69-180 per 100,000/year[1]
Incidence (International)150-300 per 100,000/year[2]
Mild TBI proportion75-85%[3]
Moderate TBI proportion10%[3]
Severe TBI proportion5-10%[3]
Mild TBI mortalitybelow 1%[4]
Severe TBI mortality30-50%[5]
Peak age group15-29 years and 75+ years[6]
Gender ratio2:1 male:female[7]
Recurrent TBI risk3x increased after first TBI[8]

Australian/NZ Specific

  • Approximately 12,000 Australians hospitalised with TBI annually [9]
  • Aboriginal and Torres Strait Islander peoples: 2-3x higher TBI incidence and 1.5-2x higher mortality [10]
  • Māori in New Zealand: 1.8x higher TBI hospitalisation rates compared to non-Māori [11]
  • Regional/remote Australia: 1.5x higher severe TBI incidence, delayed presentation to tertiary care [12]
  • Leading causes: Falls (40-50%, particularly elderly), Motor vehicle accidents (25-35%), Assaults (10-15%) [13]

Pathophysiology

Mechanism

Primary Injury (occurs at time of impact)

  • Focal injuries: Contusion, laceration, epidural haematoma, subdural haematoma, intracerebral haemorrhage
  • Diffuse injuries: Diffuse axonal injury, diffuse cerebral oedema
  • Skull fractures: Linear, depressed, basilar

Secondary Injury (develops over hours to days)

  • Cerebral ischaemia from hypotension, hypoxia, or raised ICP
  • Cerebral oedema (vasogenic or cytotoxic)
  • Excitotoxicity (glutamate release, calcium influx)
  • Neuroinflammation (microglial activation, cytokine release)
  • Mitochondrial dysfunction and energy failure
  • Raised intracranial pressure and cerebral herniation

Pathological Progression

Impact → Primary brain injury → Cerebral oedema/ischaemia → Raised ICP → Reduced CPP → Secondary brain injury → Cerebral herniation → Brain death

Intracranial Pathologies

PathologyLocationMechanismTiming
Epidural haematomaBetween dura and skullMiddle meningeal artery laceration (90%) or venous sinus bleedAcute (minutes-hours)
Subdural haematomaBetween dura and arachnoidBridging vein ruptureAcute, subacute, chronic
Intracerebral haemorrhageWithin brain parenchymaContusion, shear injuryAcute
Diffuse axonal injuryWhite matter tractsAcceleration-deceleration shear forcesImmediate
Subarachnoid haemorrhageSubarachnoid spaceVascular injuryImmediate

Monro-Kellie Doctrine

Fixed Intracranial Volume Components:

  • Brain tissue: 80%
  • Intracranial blood volume: 10%
  • Cerebrospinal fluid: 10%

Compensation Mechanisms:

  1. CSF displacement to spinal subarachnoid space
  2. Venous blood compression
  3. When exhausted, ICP rises exponentially

Clinical Implication: Small volume increases initially tolerated, but once compensation exhausted, minimal additional volume causes dramatic ICP rise

Cerebral Perfusion Pressure

CPP = MAP - ICP

Normal CPP: 60-70 mmHg (Brain Trauma Foundation Guidelines) [14] Normal MAP: 70-100 mmHg Normal ICP: below 10-15 mmHg

CPP below 50 mmHg: Associated with significantly increased mortality (OR 2.1) [15] CPP above 70 mmHg: Associated with increased ARDS risk without mortality benefit [16]

Cerebral Autoregulation

Normal autoregulation range: MAP 50-150 mmHg

  • Maintains constant CBF despite blood pressure changes
  • Impaired after TBI, making CBF pressure-passive
  • Target MAP 80-90 mmHg to ensure CPP 60-70 mmHg with ICP 10-20 mmHg

Clinical Approach

Recognition

Trigger Factors for Suspecting Significant TBI:

  • History of head trauma (even if minor mechanism)
  • Loss of consciousness or amnesia
  • Altered level of consciousness
  • Headache, vomiting
  • Focal neurological deficit
  • Seizure
  • Visible scalp injury or deformity
  • Signs of basal skull fracture

Initial Assessment

Primary Survey (ATLS Approach)

  • A: Airway - Rapid sequence intubation if GCS below 8, respiratory distress, unable to protect airway
  • B: Breathing - SpO2 94-98%, normocapnia (PaCO2 35-45 mmHg), avoid hyperventilation (PaCO2 below 35) unless impending herniation
  • C: Circulation - MAP 80-90 mmHg, avoid hypotension (SBP below 100 mmHg doubles mortality) [17], two large-bore IVs
  • D: Disability - GCS assessment, pupillary examination (size, symmetry, light reflex), limb movements
  • E: Exposure - Full examination, log-roll if spine protection needed, maintain temperature 36-37°C

History

Key Questions

QuestionSignificance
Mechanism of injury?High vs low energy, direction of force
Time of injury?Duration of unconsciousness, timeline for reversal agents
Loss of consciousness duration?Severity indicator
Amnesia duration?Mild TBI risk stratification
Post-traumatic seizure?Requires antiepileptic consideration
Headache, vomiting episodes?Raised ICP signs
Current medications?Anticoagulation/antiplatelet agents
Comorbidities?Diabetes, hypertension, bleeding diathesis
Alcohol/drug use?Confounds GCS assessment
Previous TBI?Recurrent TBI risk, cumulative effects

Red Flag Symptoms

Red Flag
  • Deteriorating GCS (drop of 2 or more points)
  • New focal neurological deficit
  • Unequal or dilated pupil (unilateral mydriasis, sluggish light reflex)
  • Posturing (decerebrate: arms extended, internally rotated; decorticate: arms flexed)
  • Cushing's triad: Hypertension + Bradycardia + Irregular respirations
  • Post-traumatic seizure
  • Clear CSF otorrhoea/rhinorrhoea
  • Battle's sign (retroauricular ecchymosis), Raccoon eyes (periorbital ecchymosis)

Examination

General Inspection

  • Level of consciousness (AVPU or full GCS)
  • Respiratory pattern (Cheyne-Stokes, irregular, apnoeic periods)
  • Scalp injuries (lacerations, haematomas, depressions)
  • Signs of external trauma to face, neck, trunk
  • Evidence of other injuries (long bone fractures suggesting high-energy mechanism)

Specific Findings

SystemFindingSignificance
NeurologicalGCS 13-15Mild TBI, risk stratify for CT
NeurologicalGCS 9-12Moderate TBI, admission, repeat CT
NeurologicalGCS 3-8Severe TBI, airway protection, neurocritical care
NeurologicalUnilateral fixed dilated pupilUncal herniation, emergency
NeurologicalDecerebrate posturingSevere brainstem dysfunction, poor prognosis
NeurologicalHemiparesisContralateral brain injury
NeurologicalAbducens nerve palsyRaised ICP (false localising sign)
Cranial nervesCN VII palsyTemporal bone fracture
Cranial nervesanosmiaCribriform plate fracture
SkullDepressed fractureSurgical evacuation if depressed > skull thickness
SkullBattle's signBasilar skull fracture (petrous temporal)
SkullRaccoon eyesAnterior skull base fracture
LimbsMotor asymmetryFocal brain injury, spinal cord injury

Investigations

Immediate (Resus Bay)

TestPurposeKey Finding
Capillary glucoseExclude hypoglycaemia mimicking comabelow 3.0 mmol/L requires treatment
Arterial blood gasAssess oxygenation, ventilation, acid-basePaCO2 35-45, PaO2 above 75, pH above 7.35
Point-of-care coagulationScreen for coagulopathy before reversalINR, APTT, platelet count
Rapid bedside INRWarfarin anticoagulation statusINR above 1.4 requires reversal
CT brain (non-contrast)Identify intracranial pathologyEpidural/subdural/ICH, contusion, midline shift

Standard ED Workup

Blood Tests

TestIndicationInterpretation
FBCBaseline haemoglobin, platelet countAnaemia worsens cerebral hypoxia, thrombocytopenia contraindicates certain reversal
Coagulation profileBaseline, anticoagulated patientsINR greater than 1.4 (warfarin) requires PCC + vitamin K, APTT prolonged (DOAC) needs specific agent
Urea and electrolytesBaseline renal functionRequired for contrast CT if needed, mannitol dosing
LFTBaseline liver functionImpaired metabolism of sedative agents
Blood group and holdPotential neurosurgeryCross-match 4 units for severe TBI
Serum ethanolConfounds GCS assessmentElevated ethanol explains altered mental status if no other cause
Urine drug screenConfounds GCS assessmentOpioids, benzodiazepines require naloxumab/flumazenil

Imaging

CT Brain (Non-contrast)

  • Indications: Canadian CT Head Rule high-risk or medium-risk criteria, GCS below 15 at 2 hours, suspected basal skull fracture, coagulopathy
  • Timing: Within 1 hour for high-risk patients, within 8 hours for medium-risk
  • Findings: Hyperdense haemorrhage (EDH: biconvex/lentiform, SDH: crescentic, ICH: irregular), hypodense contusion/infarction, midline shift, effacement of basal cisterns

CT Angiogram (CTA) Head and Neck

  • Indications: Suspected vascular injury (penetrating trauma, cervical spine fracture extending into foramen transversarium, neurological deficit unexplained by CT)
  • Findings: Vascular dissection (intimal flap, string sign), pseudoaneurysm, occlusion

MRI Brain

  • Indications: Diffuse axonal injury (better sensitivity than CT), small contusions, subacute/chronic pathology, prognostication (DTI sequence)
  • Timing: Usually delayed (24-72 hours) after patient stabilisation

Point-of-Care Ultrasound

Optic Nerve Sheath Diameter (ONSD)

  • Technique: Measure ONSD 3 mm posterior to globe using ocular ultrasound
  • Normal: below 5.0 mm
  • Elevated ICP: ONSD above 5.0 mm (sensitivity 74-90%, specificity 74-83%) [18]
  • Limitations: Operator-dependent, confounded by optic neuritis, orbital cellulitis

Management

Immediate Management (First 10 minutes)

1. Primary survey ABCDE, immobilise cervical spine if indicated
2. Secure airway: RSI if GCS below 8, respiratory distress, unable to protect airway
3. Oxygenation: Target SpO2 94-98%, maintain PaCO2 35-45 mmHg
4. Circulation: Two large-bore IVs, MAP 80-90 mmHg, avoid SBP below 100 mmHg
5. Blood glucose: Maintain 5-10 mmol/L
6. Rapid bedside coagulation for anticoagulated patients
7. Immediate CT brain for high-risk patients
8. Early neurosurgery consultation (within 30 minutes)

Resuscitation

Airway

Indications for Intubation (Brain Trauma Foundation Guidelines) [14]:

  • GCS 3-8 (severe TBI)
  • Deteriorating GCS or unable to protect airway (GCS below 8 for greater than 2 hours)
  • Hypoxaemia (SpO2 below 90%) refractory to supplemental oxygen
  • Hypercapnia (PaCO2 above 45 mmHg) refractory to non-invasive ventilation
  • Severe agitation requiring sedation for management

RSI Technique:

  • Pre-oxygenation with non-rebreather mask 3-5 minutes
  • Cervical spine immobilisation (manual inline stabilisation)
  • Induction: Ketamine 1-2 mg/kg (avoid ketamine if ICP greater than 20 mmHg) or Etomidate 0.3 mg/kg
  • Paralysis: Rocuronium 1.2 mg/kg or Suxamethonium 1-1.5 mg/kg
  • Avoid hypotension: Pre-load with 500 mL crystalloid if not contraindicated

Ventilation Targets:

  • Tidal volume: 6-8 mL/kg IBW
  • Respiratory rate: 10-14/min
  • PEEP: 5-10 cmH2O (avoid greater than 15 cmH2O due to ICP increase)
  • PaCO2: 35-45 mmHg (avoid prophylactic hyperventilation)

Breathing

Oxygenation Targets:

  • SpO2 94-98% (avoid hyperoxia SpO2 above 100% due to free radical injury) [19]
  • PaO2 above 75 mmHg (10 kPa)

Hyperventilation (PaCO2 below 35 mmHg):

  • Indication: Signs of impending herniation (dilated pupil, posturing, Cushing's triad) as temporising measure only
  • Duration: Maximum 15-30 minutes, not prophylactic
  • Mechanism: Vasoconstriction reduces cerebral blood volume and ICP
  • Risk: Excessive vasoconstriction causes cerebral ischaemia

Circulation

Blood Pressure Targets:

  • MAP 80-90 mmHg (ensures CPP 60-70 mmHg with normal ICP)
  • SBP above 100 mmHg (SBP below 100 mmHg doubles mortality) [17]
  • Maintain MAP-SBP gradient to avoid excessive cerebral perfusion pressure

CPP Target: 60-70 mmHg (Brain Trauma Foundation Guidelines) [14]

  • CPP = MAP - ICP
  • If ICP monitor unavailable, assume ICP 15-20 mmHg initially
  • Target MAP to maintain CPP above 60 mmHg
  • Avoid CPP above 70 mmHg (increased ARDS risk without mortality benefit)

Haemodynamic Support:

  • Crystalloids: 0.9% NaCl (avoid hypotonic solutions, avoid excessive fluid)
  • Colloids: No benefit over crystalloids in TBI, potential for coagulopathy
  • Vasopressors: Noradrenaline (norepinephrine) first-line, starting 0.05-0.1 mcg/kg/min
  • Blood products: Maintain Hb above 70-80 g/L

Intracranial Pressure Management

ICP Monitoring Indications:

  • GCS 3-8 after resuscitation with abnormal CT brain
  • GCS 3-8 after resuscitation with normal CT brain but 2 or more of: Age above 40, SBP below 90, posturing
  • Surgical mass lesion evacuation (ICP monitoring during and post-op)

Tiered ICP Management (Brain Trauma Foundation) [14]:

Tier 0 (Baseline): Head of bed 30 degrees, neutral neck position, analgesia/sedation, avoid straining, maintain normocapnia

Tier 1 (ICP above 20 mmHg):

  • Osmotic therapy: Mannitol 20% 0.25-1.0 g/kg IV bolus OR Hypertonic saline 3% or 5% 2-5 mL/kg IV bolus
  • Ensure euvolaemia before osmotic therapy (CVP 8-12 mmHg)
  • Repeat serum osmolality after mannitol (target below 320 mOsm/kg)

Tier 2 (ICP greater than 20-25 mmHg refractory to Tier 1):

  • Therapeutic hyperventilation (PaCO2 30-35 mmHg) - short-term only
  • Neuromuscular blockade (cisatracurium infusion)
  • Deep sedation (propofol or midazolam + opioid)
  • Consider barbiturate coma (thiopentone bolus then infusion) - requires EEG burst suppression monitoring

Tier 3 (ICP greater than 25-30 mmHg refractory to Tier 1-2):

  • Decompressive craniectomy (discussed with neurosurgery)
  • CSF drainage (if EVD in situ)
  • Hypothermia (32-35°C) - not routinely recommended (DECRA trial) [20]

Osmotic Therapy Comparison:

AgentDoseOnsetDurationContraindications
Mannitol 20%0.25-1.0 g/kg IV bolus15-30 min1.5-6 hoursHypovolaemia, renal failure
Hypertonic saline 3%2-5 mL/kg IV bolus5-15 min1-4 hoursHypernatraemia greater than 155 mmol/L
Hypertonic saline 5%2-5 mL/kg IV bolus5-10 min2-6 hoursHypernatraemia greater than 155 mmol/L

Medications

DrugDoseRouteTimingNotes
Mannitol 20%0.25-1.0 g/kg (max 50 g)IV bolusFor ICP above 20 mmHgEnsure euvolaemia first, check osmolality
Hypertonic saline 3%2-5 mL/kg (max 250 mL)IV bolusFor ICP above 20 mmHgMonitor sodium, avoid greater than 155 mmol/L
Levetiracetam20 mg/kg loading, then 500-1500 mg BDIV/POEarly post-traumatic seizureFirst-line for seizure prophylaxis
Phenytoin15-20 mg/kg loading, then 5-7 mg/kg/dayIV/POAlternative seizure prophylaxisRequires level monitoring, many interactions
Noradrenaline0.05-0.5 mcg/kg/min infusionIVMaintain MAP 80-90 mmHgFirst-line vasopressor
Propofol1-4 mg/kg/hr infusionIVSedation, ICP controlAvoid prolonged high dose (greater than 48h at greater than 5 mg/kg/hr) due to propofol infusion syndrome
Midazolam0.02-0.1 mg/kg/hr infusionIVSedationAccumulates in renal/hepatic impairment

Anticoagulation Reversal

Warfarin (INR above 1.4):

  1. Prothrombin complex concentrate (PCC) 25-50 IU/kg IV
  2. Vitamin K 5-10 mg IV slow push (over 10-20 minutes)
  3. Repeat INR in 30 minutes, target INR below 1.4
  4. FFP (15-20 mL/kg) if PCC unavailable [21]

Apixaban, Rivaroxaban, Edoxaban (DOACs):

  • Andexanet alfa (if available and severe bleeding):
    • "Apixaban: Low dose (400 mg bolus + 4 mg/min for 120 min) if last dose below 7 hours, high dose (800 mg bolus + 8 mg/min for 120 min) if last dose within 7 hours"
    • "Rivaroxaban: Same dosing approach"
    • "Edoxaban: Same dosing approach"
  • PCC 25-50 IU/kg IV (if andexanet alfa unavailable)
  • Consider measuring anti-Xa levels (specific to DOAC) if available and time permits

Dabigatran (direct thrombin inhibitor):

  • Idarucizumab 5 g IV (two 2.5 g vials, 15 minutes apart) [22]
  • If unavailable: PCC 50 IU/kg IV + dialysis

Aspirin:

  • Platelet transfusion 1-2 apheresis units OR single-donor equivalent for intracranial haemorrhage
  • Consider desmopressin (DDAVP) 0.3 mcg/kg IV
  • Platelet function testing if available

Clopidogrel:

  • Platelet transfusion 1-2 apheresis units
  • Consider desmopressin 0.3 mcg/kg IV

Dual antiplatelet therapy:

  • Platelet transfusion 2 apheresis units
  • Desmopressin 0.3 mcg/kg IV
  • Consider tranexamic acid 1 g IV (controversial in intracranial bleeding)

Reversal Agent Comparison:

AnticoagulantReversal AgentDoseTime to effectMonitoring
WarfarinPCC 25-50 IU/kgIV bolusImmediate (INR normalises)Repeat INR 30 min
WarfarinVitamin K 5-10 mgIV slow push4-6 hoursINR 4-6 hours
DabigatranIdarucizumab 5 gIV bolusImmediateNone available clinically
Apixaban/RivaroxabanAndexanet alfaIV bolus + infusionImmediateAnti-Xa level (if available)
Any DOACPCC 25-50 IU/kgIV bolusVariable (clinical)Anti-Xa level (if available)

Ongoing Management

Repeat CT Brain Indications:

  • Deteriorating GCS (drop of 2 or more points)
  • New neurological deficit or pupillary abnormality
  • Uncontrolled ICP despite medical management
  • 6-12 hours post-admission for moderate-severe TBI (if initial CT abnormal)
  • 24 hours post-admission for high-risk mild TBI if not initially scanned

Seizure Prophylaxis:

  • Indication: Severe TBI (GCS below 8) with contusion, SDH, EDH, ICH, or depressed skull fracture [23]
  • Agent: Levetiracetam 500-1000 mg BD (preferred over phenytoin due to fewer interactions) [24]
  • Duration: 7 days post-injury (no ongoing prophylaxis after 7 days)

Temperature Management:

  • Target normothermia (36-37°C)
  • Avoid fever (above 37.5°C) - increases cerebral metabolic demand
  • Consider paracetamol 1g IV/PO q4-6h, surface cooling devices
  • Therapeutic hypothermia (32-35°C) not routinely recommended (DECRA trial showed no mortality benefit) [20]

Glycaemic Control:

  • Target blood glucose 5-10 mmol/L
  • Avoid hyperglycaemia (above 10 mmol/L) - worsens outcome
  • Avoid hypoglycaemia (below 4 mmol/L) - secondary brain injury

Nutrition:

  • Enteral nutrition within 24-48 hours if unable to take oral intake
  • Target 25-30 kcal/kg/day after initial resuscitation
  • Protein 1.2-2.0 g/kg/day

Definitive Care

Neurosurgical Interventions:

Epidural Haematoma Evacuation:

  • Indication: Volume greater than 30 mL, thickness greater than 15 mm, midline shift greater than 5 mm, any EDH with neurological deficit or GCS below 9
  • Procedure: Craniotomy, evacuation, haemostasis, drain placement
  • Timing: Within 2-4 hours (outcome worse if delayed greater than 2 hours) [25]

Subdural Haematoma Evacuation:

  • Indication: Acute SDH thickness greater than 10 mm or midline shift greater than 5 mm, any SDH with GCS below 9 and deteriorating
  • Procedure: Craniotomy or craniectomy depending on brain swelling, evacuation, duraplasty
  • Outcome: Mortality 50-90% depending on preoperative GCS and comorbidities [26]

Intracerebral Haemorrhage Evacuation:

  • Indication: Cerebellar ICH greater than 3 cm with brainstem compression or hydrocephalus, deteriorating neurological status, refractory ICP
  • Procedure: Stereotactic evacuation or open craniotomy
  • Outcome: STICH trials - surgery may benefit cerebellar or lobar haemorrhages greater than 1 cm from cortical surface [27]

Decompressive Craniectomy:

  • Indication: Refractory ICP (greater than 25 mmHg) despite Tier 1-2 medical management, malignant cerebral oedema
  • Procedure: Large frontotemporoparietal bone flap removal (at least 12 x 15 cm), duraplasty
  • Outcome: RESCUEicp trial - reduced mortality but increased severe disability (mRS 4-5) [28], DECRA trial - early bifrontal decompression reduced ICP but worse functional outcomes [20]

External Ventricular Drain (EVD):

  • Indication: Obstructive hydrocephalus, refractory ICP with EVD monitoring, intraventricular haemorrhage with hydrocephalus
  • Procedure: Frontal burr hole (Kocher's point), catheter into lateral ventricle, external drainage
  • Management: Drain set at 10-15 cmH2O, intermittent vs continuous drainage, daily CSF sampling

Disposition

Admission Criteria

Mild TBI (GCS 13-15):

  • Observation admission (6-12 hours): GCS 15 at 2 hours with CT abnormal, high-risk mechanism, age greater than 65, anticoagulation, isolated skull fracture, persistent symptoms
  • Discharge with responsible adult: GCS 15 at 2 hours, normal CT, no red flags, stable

Moderate TBI (GCS 9-12):

  • Inpatient admission mandatory
  • Level: High-dependency unit (HDU) or intensive care unit (ICU)
  • Monitoring: Hourly neuro-observations, repeat CT at 6-12 hours if initial abnormal

Severe TBI (GCS 3-8):

  • ICU admission mandatory
  • Level: Neurocritical care ICU with ICP monitoring capability
  • Intubation: Required for airway protection
  • Monitoring: Continuous ICP if indicated, hourly GCS, pupillary checks

ICU/HDU Criteria

  • ICU: GCS below 8, requiring mechanical ventilation, ICP monitoring, refractory ICP, postoperative neurosurgery, haemodynamic instability
  • HDU: GCS 9-12, requiring neuro-observation more frequently than hourly, initial management of mild-moderate TBI with CT abnormality, anticoagulated patients on reversal

Discharge Criteria

Safe Discharge Requirements:

  • GCS 15 at least 2 hours post-injury
  • No ongoing neurological deficit
  • No headache requiring opioid analgesia
  • Normal CT (if performed)
  • Returned to baseline mental status
  • Responsible adult available for 24-hour observation
  • Written head injury instructions provided

Red Flags to Return:

  • Worsening headache
  • Vomiting
  • Drowsiness or confusion
  • Visual disturbance
  • Weakness or numbness
  • Seizure
  • Difficulty walking or speaking

Follow-up

Outpatient Review:

  • Timing: 1-2 weeks post-discharge (mild TBI), 4-6 weeks (moderate TBI)
  • Purpose: Cognitive assessment, symptom review, return-to-work clearance, concussion counselling
  • Investigations: Repeat CT if persistent symptoms or new neurological findings

Rehabilitation:

  • Indications: Persistent cognitive deficits, physical disability, behavioural changes, post-traumatic epilepsy
  • Services: Neuropsychology, occupational therapy, physiotherapy, speech pathology, vocational rehabilitation
  • Duration: 3-12 months depending on severity

GP Letter Requirements:

  • Mechanism and time of injury
  • GCS and CT findings
  • Interventions in ED
  • Red flags requiring return
  • Follow-up arrangements
  • Medications on discharge

Special Populations

Paediatric Considerations

Age-Specific Modifications:

  • GCS: Paediatric GCS for infants and children below 4 years
  • CT indications: More conservative due to radiation risk, clinical observation preferred for mild TBI when feasible
  • ICP: Lower normal ICP (below 10 mmHg in children below 8 years)
  • Sutures: Open cranial sutures allow compensation (palpable in infants)
  • Non-accidental injury: Consider in infants with inconsistent mechanism, retinal haemorrhages, other injuries

Paediatric GCS:

Component0-1 year2-4 years5+ years (adult)
Eye openingSpontaneous: 4
To speech: 3
To pain: 2
None: 1
SameSame
Verbal responseSmiles/cries: 5
Words/cries: 4
Words: 3
Moans: 2
None: 1
Words: 4
Words: 3
Moans: 2
None: 1
Oriented: 5
Confused: 4
Inappropriate: 3
Incomprehensible: 2
None: 1
Motor responseNormal: 6
Withdraws: 5
Flexion: 4
Extension: 3
None: 2
None: 1
SameSame

Dosing Adjustments:

  • Mannitol: 0.25-1.0 g/kg (same as adult)
  • Hypertonic saline: 2-5 mL/kg of 3% (same as adult)
  • Levetiracetam: 20 mg/kg loading, then 10-20 mg/kg BD (max 500-1000 mg BD)
  • Fluids: 20 mL/kg crystalloid bolus for hypotension, then maintenance

Pregnancy

Modifications for Pregnant Patients:

  • Radiation: CT brain is safe (fetal dose below 0.01 mGy, below threshold for harm)
  • Supine hypotension: Position left lateral tilt 15-30 degrees after 20 weeks gestation
  • ICP targets: Same as non-pregnant (CPP 60-70 mmHg)
  • Reversal agents: Warfarin reversal includes vitamin K (safe in pregnancy), DOAC reversal agents limited safety data
  • Fetal monitoring: Continuous CTG after 24 weeks gestation in severe TBI or ICU setting
  • Indications for delivery: Maternal instability, refractory ICP, non-reassuring fetal status (requires multidisciplinary decision)

Elderly

Geriatric Considerations:

  • Increased risk: 2-3x higher TBI mortality, 4-5x higher in those greater than 80 years [29]
  • Mild mechanism can cause severe injury: Falls from standing can cause SDH due to atrophy and bridging vein stretching
  • Anticoagulation: High prevalence (warfarin, DOACs, antiplatelets), requires aggressive reversal
  • Pre-injury functional status: Baseline cognitive impairment confounds GCS assessment
  • Comorbidities: Higher rates of cardiovascular disease, CKD, malnutrition
  • Prognosis: Worse functional outcomes even with similar injury severity
  • Decision-making: Goals of care discussion with family early in management

Modified Approach:

  • Low threshold for CT (age greater than 65 is high-risk criterion in Canadian CT Head Rule)
  • Aggressive anticoagulation reversal (no age limit)
  • Early neurosurgery consultation even for moderate injuries
  • Consider geriatric input for delirium management
  • Social work involvement for discharge planning

Indigenous Health

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

  • Higher incidence: Aboriginal and Torres Strait Islander peoples experience 2-3x higher TBI incidence compared to non-Indigenous Australians [10]
  • Increased mortality: 1.5-2x higher TBI mortality rates in Indigenous populations [10]
  • Higher severity: Disproportionate representation in moderate-severe TBI due to higher rates of high-energy mechanisms (MVC, assault) [30]
  • Delayed presentation: Geographic barriers to tertiary care lead to delayed CT and neurosurgical intervention
  • Cultural safety: Use Aboriginal Health Workers, Māori kaiāwhina or cultural liaison services, respect family decision-making structures
  • Communication: Avoid jargon, use interpreter if English is second language, involve Elders in decisions
  • Rehabilitation access: Reduced access to specialist rehabilitation services in remote communities
  • Family involvement: Extended family kinship structures require broad information sharing with appropriate consent
  • Comorbidity burden: Higher prevalence of diabetes, cardiovascular disease, alcohol use disorder affecting outcomes
  • Follow-up challenges: Coordination with Aboriginal Medical Services or Māori health providers essential

Māori-Specific Considerations:

  • Higher TBI incidence (1.8x hospitalisation rate) due to higher rates of MVC and occupational injuries [11]
  • Whānau (extended family) involvement critical in decision-making and discharge planning
  • Kaitiaki (guardian) roles may need to be identified for patient advocacy
  • Te reo Māori (Māori language) interpreter services required if language preference
  • Cultural concepts of health (hauora) encompass physical, mental, spiritual, and family wellbeing

Pitfalls & Pearls

Clinical Pearl

Clinical Pearls:

  • Lucid interval: Epidural haematoma can present with initial normal GCS followed by rapid deterioration - never discharge a patient with head injury until GCS 15 sustained for 2 hours
  • Pseudo-Cushing's: Excessive hydration or hypercapnia can mimic Cushing's triad - correlate with pupillary findings and neurological status
  • False localising signs: Abducens nerve palsy (CN VI) indicates raised ICP, not localising lesion at the brainstem
  • Therapeutic window for EDH: Mortality increases dramatically if evacuation delayed beyond 2 hours of symptom onset [25]
  • Anticoagulated TBI: Any symptom (even mild headache) warrants CT and reversal - mortality 50% if anticoagulation not reversed [21]
  • Hyperventilation: Only for impending herniation as temporising measure - prophylactic hyperventilation (PaCO2 below 35) causes cerebral ischaemia
  • Mannitol timing: Must be euvolaemic before administration - hypovolaemic patients will become more hypotensive
  • Decerebrate vs decorticate: Decerebrate (arms extended) worse prognosis than decorticate (arms flexed) - both indicate severe brainstem injury
  • Basal skull fracture signs: Battle's sign takes 12-24 hours to appear, CSF otorrhoea/rhinorrhoea may be delayed
  • Concussion diagnosis: Clinical diagnosis only - CT brain is normal by definition, no structural abnormality
Red Flag

Pitfalls to Avoid:

  • Premature discharge: Discharging patient when GCS 15 but with anticoagulation, age greater than 65, or high-risk mechanism - observe for 6-12 hours minimum
  • Missed SDH: Small crescentic hyperdensity overlooked on CT - examine whole brain including posterior fossa
  • Ignoring basal skull fracture: CSF otorrhoea/rhinorrhoea requires antibiotics and neurosurgery review due to meningitis risk
  • Underestimating mechanism: Low-energy fall in elderly can cause life-threatening SDH due to bridging vein rupture
  • Delayed reversal: Waiting for INR or drug levels before reversing anticoagulation in suspected intracranial haemorrhage - reverse immediately
  • Excessive sedation: Deep sedation masks neurological deterioration - use target sedation with periodic wake-up if possible
  • Over-reliance on GCS: GCS can be confounded by alcohol, drugs, baseline cognitive impairment - correlate with other findings
  • Failure to repeat CT: Not repeating CT in deteriorating patient or 6-12 hours post-admission for moderate-severe TBI
  • Missing spinal injury: 10-25% of TBI have concomitant cervical spine injury - image entire spine with high-risk mechanism
  • Inadequate analgesia: Pain from extracranial injuries causes agitation and raised ICP - treat pain with titrated opioids
  • Hyperventilation prophylaxis: Inducing PaCO2 below 35 mmHg in patients without signs of herniation causes avoidable cerebral ischaemia
  • Ignoring cultural factors: Not involving Aboriginal Health Workers, Māori kaiāwhina, or family members in care planning leads to poorer outcomes

Viva Practice

Viva Scenario

Stem: A 72-year-old man presents 2 hours after falling onto concrete from standing height. He takes apixaban 5 mg BD for atrial fibrillation. He complains of mild headache but is alert, GCS 15. His vital signs are BP 145/85, HR 78, SpO2 98% on room air. Examination reveals a small 2 cm right parietal scalp haematoma but no other abnormalities.

Opening Question: What are your immediate priorities for this patient?

Model Answer: Immediate priorities for this anticoagulated patient with head injury:

  1. Secure IV access: Two large-bore cannulas
  2. Urgent CT brain: Within 1 hour (high-risk criterion: anticoagulation + head trauma + any symptom)
  3. Prepare for reversal: Have andexanet alfa or PCC available, check anti-Xa level if time permits
  4. Admit for observation: Minimum 12-24 hours even if CT normal due to delayed bleeding risk
  5. Neurosurgery consultation: Early involvement given anticoagulation
  6. Baseline observations: Hourly GCS, pupillary checks, vital signs
  7. Baseline bloods: FBC, coagulation profile, urea and electrolytes, group and hold

Follow-up Questions:

  1. What are the indications for CT brain in this scenario?

    • Model answer: This patient meets high-risk criteria from Canadian CT Head Rule: Age greater than 65, amnesia greater than 30 minutes (assess), dangerous mechanism (fall onto concrete), and importantly - anticoagulation. Any anticoagulated patient with head injury and ANY symptom (headache, vomiting, altered GCS, amnesia, seizure) requires urgent CT brain regardless of symptom severity.
  2. What reversal agent would you use if he has an intracranial haemorrhage?

    • Model answer: For apixaban (a direct Xa inhibitor), first-line is andexanet alfa if available and severe bleeding. Dose: High dose (800 mg IV bolus + 8 mg/min infusion for 120 min) if last dose within 7 hours, low dose (400 mg bolus + 4 mg/min infusion for 120 min) if last dose greater than 7 hours. If andexanet alfa unavailable, use prothrombin complex concentrate (PCC) 25-50 IU/kg IV. Consider measuring anti-Xa level if time permits to confirm anticoagulant effect.
  3. What are the contraindications to reversal agents?

    • Model answer: Contraindications are relative: known hypersensitivity to andexanet alfa or PCC components, active thrombosis or high thrombotic risk (e.g., recent DVT/PE within 2 weeks), severe cardiac failure (for PCC due to volume load). The benefits of reversing life-threatening intracranial haemorrhage generally outweigh thrombotic risks.
  4. What discharge instructions would you provide if CT is normal?

    • Model answer: Even if CT normal, this patient requires:
      • Inpatient observation 12-24 hours minimum
      • Restart apixaban only after 24 hours of stable neurological status and multidisciplinary discussion (including cardiology and neurosurgery)
      • Red flags to report immediately: worsening headache, vomiting, drowsiness, confusion, visual changes, weakness, seizures
      • Avoid alcohol and activities with head injury risk for 2-4 weeks
      • Arrange follow-up in 1 week with GP or neurosurgery
      • Consider falls prevention assessment
      • Provide written head injury instructions to patient and family

Discussion Points:

  • Mortality in anticoagulated TBI patients is 30-50% if reversal delayed [21]
  • CT brain may be normal initially with delayed haematoma formation up to 24 hours
  • Decision to restart anticoagulation requires balancing stroke prevention vs rebleeding risk
  • Consideration of left atrial appendage occlusion device for long-term stroke prevention
  • Falls assessment essential given high risk of recurrent TBI in elderly
Viva Scenario

Stem: A 35-year-old man presents with head injury after falling from a horse. Initial GCS 13 (E3, V4, M6), CT brain shows small left frontal contusion without mass effect. He is admitted to the observation ward. Four hours later, the nurse calls you because he is drowsy, GCS 9 (E2, V2, M5), right pupil is 6 mm and non-reactive, left pupil 3 mm reactive.

Opening Question: What is your immediate management?

Model Answer: Immediate management of this neurological deterioration:

  1. Call for help: Activate trauma team, neurosurgery, anaesthetics
  2. ABC assessment: Secure airway - prepare for RSI given GCS 9, deteriorating
  3. ICP management: Head of bed 30 degrees, neutral neck, mannitol 0.5-1 g/kg IV bolus (assess euvolaemia)
  4. Urgent repeat CT brain: Within 15-30 minutes to identify expanding haematoma
  5. Hyperventilation (temporising): Target PaCO2 30-35 mmHg only if signs of impending herniation (present with dilated pupil) - short duration
  6. Blood pressure support: Maintain MAP 80-90 mmHg for adequate CPP, noradrenaline infusion if needed
  7. Neurosurgery consultation: Discuss emergency evacuation likely needed

Follow-up Questions:

  1. What is the likely diagnosis and why?

    • Model answer: Most likely diagnosis is delayed traumatic intracranial haemorrhage, specifically epidural haematoma or expanding subdural haemorrhage. The "lucid interval" (initial period of normal or near-normal neurological status followed by deterioration) is classic for epidural haematoma, often from middle meningeal artery laceration. The unilateral fixed dilated pupil (anisocoria with pupil greater than 6 mm and non-reactive) indicates uncal herniation compressing CN III, typically ipsilateral to the mass lesion.
  2. Explain the mechanism of the fixed dilated pupil in this scenario.

    • Model answer: The fixed dilated pupil is a false localising sign of uncal herniation. As the temporal lobe uncus herniates through the tentorial notch, it compresses the ipsilateral third cranial nerve (CN III) against the tentorial edge. The parasympathetic fibers (traveling on the peripheral surface of CN III) are compressed first, causing loss of parasympathetic tone and unopposed sympathetic activity, resulting in pupillary dilation. The light reflex is lost as the afferent and efferent pathways are disrupted.
  3. What are the thresholds for surgical evacuation of an intracranial haemorrhage?

    • Model answer: Surgical evacuation thresholds:
      • Epidural haematoma: Volume greater than 30 mL, thickness greater than 15 mm, midline shift greater than 5 mm, any EDH with neurological deficit or GCS below 9
      • Subdural haematoma: Thickness greater than 10 mm or midline shift greater than 5 mm, any SDH with GCS below 9 and deteriorating
      • Intracerebral haemorrhage: Cerebellar ICH greater than 3 cm with brainstem compression or hydrocephalus, lobar ICH greater than 1 cm from cortical surface with neurological deficit, deteriorating status
  4. What is the Monro-Kellie doctrine and how does it apply here?

    • Model answer: The Monro-Kellie doctrine states that the intracranial compartment is a fixed-volume space containing three components: brain tissue (80%), intracranial blood volume (10%), and cerebrospinal fluid (10%). If one component increases in volume, another must decrease or intracranial pressure rises. In this patient, the expanding haematoma increases blood volume. Initial compensation occurs via CSF displacement to the spinal subarachnoid space and venous blood compression. Once compensation exhausted, rapid ICP rise occurs, causing herniation and neurological deterioration.

Discussion Points:

  • "Time is brain"
  • mortality from epidural haematoma increases dramatically if evacuation delayed beyond 2 hours [25]
  • Pupillary changes precede altered level of consciousness in herniation - regular pupillary checks critical
  • Repeat CT brain essential in any patient with neurological deterioration, even if initial scan normal
  • Mannitol should only be given if patient is euvolaemic - assess CVP, lung sounds, JVP before administration
  • Postoperative care in ICU with ICP monitoring for at least 48 hours
Viva Scenario

Stem: A 45-year-old woman presents 1 hour after being hit in the head by a cricket ball. She had 2 minutes of loss of consciousness at the scene. Current GCS 15, complains of headache and nausea with one episode of vomiting. No focal neurological deficit. Vital signs normal. Scalp examination shows a 3 cm haematoma on left frontal region.

Opening Question: Does this patient require CT brain? What is your disposition decision?

Model Answer: CT brain is required based on Canadian CT Head Rule high-risk criteria:

  • Dangerous mechanism (struck by cricket ball - high-velocity object)
  • Amnesia greater than 30 minutes (need to assess)
  • Vomiting greater than 1 episode (she has had 1, but threshold is greater than 2 episodes according to some guidelines, but many centres use greater than 1 episode as indication)
  • GCS below 15 at 2 hours (currently GCS 15 at 1 hour - repeat assessment at 2 hours)

Disposition decision:

  • If CT normal: Observation for 6-12 hours, discharge with responsible adult if GCS 15 sustained, no ongoing red flags
  • If CT abnormal: Admit based on findings, neurosurgery consultation, repeat CT in 6-12 hours
  • If CT not available: Observe for 12-24 hours with hourly neurological observations, arrange transfer to facility with CT capabilities if any deterioration

Follow-up Questions:

  1. What are the Canadian CT Head Rule high-risk criteria?

    • Model answer: Canadian CT Head Rule high-risk criteria for neurosurgical intervention (CT required):
      • GCS below 15 at 2 hours post-injury
      • Suspected open or depressed skull fracture
      • Basal skull fracture signs (Battle's sign, raccoon eyes, CSF otorrhoea/rhinorrhoea, haemotympanum)
      • Vomiting greater than 2 episodes
      • Age greater than 65 years
      • Amnesia greater than 30 minutes before impact
      • Dangerous mechanism: pedestrian struck by motor vehicle, fall from greater than 1 metre/5 stairs, ejected from motor vehicle
  2. What are the medium-risk criteria for CT brain?

    • Model answer: Canadian CT Head Rule medium-risk criteria for brain injury on CT (clinical judgement required):
      • Amnesia greater than 30 minutes post-impact
      • Dangerous mechanism: fall from 1-3 metres/3-5 stairs, bicycle collision without helmet, any motor vehicle collision
    • Medium-risk patients can be observed with serial neurological observations instead of immediate CT if resources limited or CT not readily available.
  3. What instructions would you give at discharge?

    • Model answer: Discharge instructions must include:
      • Responsible adult to observe for 24 hours
      • Red flags to return immediately: worsening headache, vomiting, drowsiness, confusion, visual disturbance, weakness, numbness, difficulty walking or speaking, seizure
      • Avoid alcohol and activities with head injury risk for 2-4 weeks
      • Gradual return to normal activities: school/work after 1-2 days, sports after 1-2 weeks, contact sports after 4-6 weeks
      • Analgesia: Paracetamol 1g q4-6h, avoid opioids (mask symptoms)
      • No driving for 24 hours or until recovered (specific DVLA/state transport authority guidelines may apply)
      • Written head injury information sheet
      • Follow-up with GP in 1 week or sooner if symptoms persist
  4. What is post-concussion syndrome?

    • Model answer: Post-concussion syndrome is persistence of concussion symptoms beyond 3 months after injury. Affects 10-30% of mild TBI patients. Symptoms include: headache, dizziness, fatigue, difficulty concentrating, memory problems, sleep disturbance, irritability, anxiety, depression. Risk factors include prior concussion, female sex, older age, and history of migraines or psychiatric illness. Management involves symptom-based treatment, cognitive rest, gradual return to activity, and referral to concussion clinic or neuropsychology if symptoms persistent beyond 3 months.

Discussion Points:

  • Clinical prediction rules (Canadian CT Head Rule, New Orleans Criteria, CHALICE for children) have sensitivities above 95% for significant intracranial injury [31]
  • Observation with serial neurological observations is reasonable alternative to immediate CT for low-risk mild TBI if CT not immediately available
  • Post-traumatic amnesia greater than 30 minutes is significant prognostic indicator for cognitive recovery and return to work
  • Athletes with concussion require graduated return-to-sport protocol (6 stages over minimum 6 days) per consensus guidelines
Viva Scenario

Stem: A 28-year-old man is brought in after high-speed motorcycle crash (helmet worn). GCS 4 (E1, V1, M2) on arrival. Intubated with RSI. CT brain shows diffuse cerebral oedema with small right frontal contusion, midline shift 3 mm, effacement of basal cisterns. Admitted to ICU with ICP monitor. Despite mannitol boluses and hypertonic saline, ICP remains 28-32 mmHg for 2 hours.

Opening Question: What are the next steps in managing this refractory intracranial hypertension?

Model Answer: Management of refractory ICP (Tier 3 therapy) after Tier 1 (osmotic therapy) failure:

  1. Therapeutic hyperventilation: Target PaCO2 30-35 mmHg for 15-30 minutes only as temporising measure
  2. Neuromuscular blockade: Cisatracurium infusion (0.1-0.15 mg/kg/hr) to reduce agitation and metabolic demand
  3. Deep sedation: Increase propofol or midazolam infusion, consider addition of opioid
  4. Consult neurosurgery urgently: Discuss decompressive craniectomy
  5. Barbiturate coma: Consider thiopentone loading (3-5 mg/kg) then infusion (3-5 mg/kg/hr) titrated to EEG burst suppression - requires continuous EEG monitoring
  6. External ventricular drain: If intraventricular catheter not already in situ, discuss CSF drainage
  7. Hypothermia: Consider target 32-35°C (not routinely recommended due to DECRA trial showing no mortality benefit) [20]
  8. Neurocritical care transfer: If refractory to above, consider transfer to higher-level neurosurgical centre

Follow-up Questions:

  1. What is the evidence for decompressive craniectomy in severe TBI?

    • Model answer: Evidence from two landmark trials:
      • DECRA trial (2011): Early bifrontal decompressive craniectomy for diffuse TBI with refractory ICP reduced ICP but was associated with worse functional outcomes at 6 months (unfavourable outcome: 70% vs 51%) [20]
      • RESCUEicp trial (2016): Decompressive craniectomy for refractory ICP reduced mortality (52% vs 71% in medical management) but increased survivors with severe disability (vegetative state or severe dependency: 43% vs 23%) [28]
      • Clinical decision: Consider decompressive craniectomy in patients with refractory ICP where chance of acceptable functional recovery outweighs risk of severe disability, particularly in younger patients with unilateral lesions
  2. What are the complications of barbiturate coma?

    • Model answer: Barbiturate coma complications include:
      • Cardiovascular: Profound hypotension requiring aggressive vasopressor support, myocardial depression
      • Metabolic: Adrenal suppression requiring steroid replacement
      • Immunosuppression: Increased infection risk (pneumonia, sepsis)
      • Renal: Acute kidney injury from hypotension and reduced perfusion
      • Liver: Hepatotoxicity with prolonged high-dose therapy
      • Monitoring: Requires continuous EEG to achieve burst suppression (minimum 3-5 second intervals), serum thiopentone levels
      • Contraindicated in severe cardiovascular instability or sepsis
  3. What are the thresholds for ICP monitoring in severe TBI?

    • Model answer: ICP monitoring indications (Brain Trauma Foundation Guidelines) [14]:
      • GCS 3-8 after resuscitation with abnormal CT brain
      • GCS 3-8 after resuscitation with normal CT brain but 2 or more of: Age above 40, SBP below 90, posturing (decerebrate or decorticate)
      • Postoperative patients after mass lesion evacuation
      • Contraindications: Coagulopathy not correctable, severe thrombocytopenia (below 50,000), severe scalp infection at insertion site
  4. What is the target cerebral perfusion pressure (CPP) in this patient?

    • Model answer: Target CPP 60-70 mmHg (Brain Trauma Foundation Guidelines) [14].
      • CPP = MAP - ICP
      • With ICP 28-32 mmHg, target MAP 88-102 mmHg to achieve CPP 60-70 mmHg
      • Avoid CPP below 50 mmHg (significantly increased mortality, OR 2.1) [15]
      • Avoid CPP above 70 mmHg (increased ARDS risk without mortality benefit) [16]
      • Titrate vasopressors (noradrenaline) to achieve target MAP while monitoring for fluid overload

Discussion Points:

  • Multimodality monitoring beyond ICP may include brain tissue oxygenation (PbtO2), cerebral microdialysis, and jugular venous oximetry - evidence for improved outcomes limited but used in some centres
  • Decompressive craniectomy is a "damage control" procedure - definitive management with cranioplasty 3-6 months later
  • Outcomes from severe TBI: Mortality 30-50%, favourable outcome (GOS-E 5-8) in 20-40% depending on age and initial GCS [5]
  • Long-term sequelae: Post-traumatic epilepsy, cognitive impairment, behavioural changes, dysarthria, motor deficits
  • Early rehabilitation involvement improves functional outcomes and reduces length of stay

OSCE Scenarios

Station 1: Deteriorating Head Injury Management

Format: Resuscitation Time: 11 minutes Setting: ED resus bay

Candidate Instructions:

You are the FACEM in the resuscitation bay. A 42-year-old man was brought in 6 hours ago after falling from a ladder (height approximately 3 metres). Initial CT brain showed small right frontal contusion without mass effect. He was admitted to the observation ward with GCS 13 (E3, V4, M6). The nurse has just called because his GCS is now 8 (E2, V2, M4) and his right pupil is dilated 7 mm and non-reactive. You have a nurse, a junior doctor, and anaesthetic support available. Manage this patient's deterioration.

Examiner Instructions:

  • Candidate should demonstrate systematic approach to neurological deterioration
  • Correctly identify need for immediate airway protection (RSI) given GCS 8
  • Initiate ICP-lowering measures (mannitol/hypertonic saline, head of bed positioning)
  • Arrange urgent repeat CT brain
  • Demonstrate knowledge of indications for hyperventilation as temporising measure only
  • Communicate effectively with team using closed-loop communication
  • Call neurosurgery early and provide clear handover
  • Discuss potential diagnosis (delayed haematoma causing herniation)

Actor/Patient Brief:

  • Patient (simulated manikin): Intubated after candidate performs RSI
  • Nurse: Reports vital signs on request (BP 155/90, HR 62, SpO2 98% post-intubation), available to assist with procedures
  • Anaesthetic: Available for airway management, RSI drugs, ventilator settings

Marking Criteria:

DomainCriterionMarks
ApproachSystematic ABCDE approach, call for help/2
KnowledgeIdentifies need for RSI (GCS below 8), starts ICP-lowering measures/3
SkillsCorrect RSI technique, appropriate drug doses, proper mannitol administration/2
CommunicationClear handover to neurosurgery, closed-loop communication with team/2
JudgementAppropriate use of hyperventilation (temporising only), arranges urgent CT/2
Total/11

Expected Standard:

  • Pass: ≥6/11
  • Key discriminators: Initiating RSI for GCS 8, giving mannitol/hypertonic saline before CT, arranging urgent repeat CT, early neurosurgery consultation
  • Fail candidates: Discharging or continuing observation with GCS 8 and dilated pupil, not initiating ICP-lowering measures, not arranging urgent CT, not involving neurosurgery

Critical Actions:

  1. Call for help (trauma team, neurosurgery, anaesthetics)
  2. Prepare for RSI given GCS 8 (rapid sequence intubation with cervical spine protection)
  3. ICP management: Head of bed 30 degrees, mannitol 0.5-1 g/kg IV or hypertonic saline 2-5 mL/kg
  4. Hyperventilation to PaCO2 30-35 mmHg (temporising only if signs of herniation present)
  5. Urgent repeat CT brain (within 15-30 minutes)
  6. Maintain MAP 80-90 mmHg for adequate CPP
  7. Neurosurgery consultation with clear handover

Time Management:

  • Minutes 1-2: Call for help, assess ABCDE, identify deterioration
  • Minutes 3-5: Initiate ICP management, prepare for RSI
  • Minutes 6-7: Perform RSI (or explain process if simulating)
  • Minutes 8-9: Arrange urgent CT, call neurosurgery
  • Minutes 10-11: Provide handover and management plan

Station 2: Anticoagulated Head Injury Counselling

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

Candidate Instructions:

A 68-year-old man with atrial fibrillation on warfarin presented 2 hours after a fall in the bathroom. He sustained a head injury and is currently GCS 14 (E3, V4, M7). His INR is 2.8. He is about to have a CT brain. His wife is in the relatives room and is anxious. She wants to know: (1) what is happening, (2) why you are giving him blood products, and (3) what the outlook is. Speak with her and address her concerns.

Examiner Instructions:

  • Candidate should demonstrate empathy and effective communication
  • Explain diagnosis (suspected traumatic brain injury) in plain language
  • Explain need for anticoagulation reversal (warfarin) with PCC and vitamin K
  • Acknowledge uncertainty about CT findings and prognosis
  • Address wife's anxiety, allow questions, provide realistic information
  • Use appropriate language (avoid jargon, check understanding)
  • Demonstrate cultural safety if applicable

Actor Brief (Wife):

  • You are anxious and upset. Your husband was fine when he went to the bathroom and now he's confused.
  • You are worried because he takes warfarin and you know it causes bleeding.
  • You want to know if he will be OK, when you can see him, what treatment he's getting.
  • You may ask: "Is he going to die?"
    • "Will he be the same?"
    • "Why did this happen?"
    • "Can I see him?"
  • You are supportive but emotional.

Marking Criteria:

DomainCriterionMarks
IntroductionIntroduces self, establishes rapport, identifies self/2
InformationExplains condition and management in understandable terms/3
EmpathyAcknowledges wife's emotions, provides support/2
CommunicationChecks understanding, invites questions, avoids jargon/2
ClosingProvides clear plan, next steps, opportunity to see patient/2
Total/11

Expected Standard:

  • Pass: ≥6/11
  • Key discriminators: Explaining warfarin reversal clearly, acknowledging uncertainty about prognosis, checking understanding, allowing wife to express concerns
  • Fail candidates: Providing false reassurance (e.g., "he'll be fine"), using excessive jargon, not addressing wife's questions, dismissing concerns

Key Information to Convey:

  • Patient has sustained a head injury which is causing confusion
  • Because he takes warfarin (blood thinner), there is a risk of bleeding in the brain
  • We are reversing the warfarin with medications to reduce this risk
  • CT scan will show if there is any bleeding or brain injury
  • It's too early to know the prognosis - we need CT results first
  • She can see him soon after scan if condition stable

Approach Checklist:

  • Sit at eye level
  • Introduce self and role
  • Confirm patient's wife identity
  • Assess her understanding of what has happened
  • Explain head injury in simple terms
  • Explain warfarin reversal (PCC, vitamin K) - "reversing the blood thinning"
  • Explain purpose of CT scan
  • Acknowledge uncertainty about outcome
  • Check understanding (ask her to repeat back)
  • Invite questions and answer honestly
  • Provide opportunity to see patient (when appropriate)
  • Arrange follow-up or provide contact details

Station 3: Post-Concussion Assessment and Advice

Format: History and Management Time: 11 minutes Setting: ED consultation room

Candidate Instructions:

You are seeing a 22-year-old university student who was brought in 6 hours ago after being tackled in rugby union. He had 3 minutes of loss of consciousness at the scene. He has a GCS of 15, normal CT brain. He is complaining of headache, dizziness, and difficulty concentrating. Take a focused history regarding his concussion and provide appropriate discharge advice and return-to-play guidance.

Examiner Instructions:

  • Candidate should take focused history of concussion symptoms
  • Assess for red flags requiring further intervention (deterioration, focal deficits)
  • Provide appropriate discharge advice regarding red flags and rest
  • Discuss graduated return-to-play protocol for rugby
  • Address concerns about academic performance and return to university
  • Demonstrate knowledge of post-concussion syndrome and prognosis

Actor Brief (Patient):

  • You are a 22-year-old university student, rugby union player
  • You were tackled and hit your head on the ground 6 hours ago
  • You were unconscious for about 3 minutes, felt groggy initially
  • Current symptoms: Headache (5/10), mild dizziness, feeling "foggy," difficulty focusing
  • No vomiting, no visual changes, no weakness, no seizures
  • You have exams coming up in 2 weeks - worried you'll fall behind
  • You want to know when you can play rugby again - there's an important match in 2 weeks
  • You are generally healthy, no medications, no allergies

Marking Criteria:

DomainCriterionMarks
HistoryFocuses on concussion symptoms, red flags, mechanism/3
ExaminationBrief neurological screen appropriate for context/2
Discharge adviceClear red flags, responsible adult, analgesia/2
Return-to-playExplains graduated protocol, timing appropriate/2
Academic concernsAddresses return to study, cognitive rest/2
Total/11

Expected Standard:

  • Pass: ≥6/11
  • Key discriminators: Identifying red flags, providing clear discharge instructions, explaining graduated return-to-play (minimum 6 days), addressing academic concerns with cognitive rest
  • Fail candidates: Clearing for rugby return too soon (within 1 week), not addressing red flags, not advising cognitive rest

Concussion Symptoms to Assess:

  • Physical: Headache, dizziness, nausea/vomiting, balance problems, fatigue, light/noise sensitivity
  • Cognitive: Difficulty concentrating, memory problems, feeling "foggy," slowed thinking
  • Emotional: Irritability, sadness, anxiety
  • Sleep: Sleeping more or less than usual

Red Flags (must exclude before discharge):

  • Worsening headache
  • Vomiting
  • Drowsiness or confusion
  • Visual disturbance
  • Weakness or numbness
  • Difficulty walking or speaking
  • Seizure

Graduated Return-to-Play Protocol (6 stages):

  1. Symptom-limited activity (24 hours symptom-free) - rest, avoid screens
  2. Light aerobic exercise (walking, stationary bike) - no resistance training
  3. Sport-specific exercise (running drills) - no contact
  4. Non-contact training drills - passing, shooting
  5. Full-contact practice - after medical clearance
  6. Return to full competition - minimum 24 hours at each stage = minimum 6 days total

Academic Advice:

  • Cognitive rest for 24-48 hours (no studying, screens, reading)
  • Gradual return to study over 3-5 days
  • If symptoms persist with studying, may need accommodations (extra time, reduced workload)
  • Consider university disability services if prolonged post-concussion syndrome

SAQ Practice

Question 1 (6 marks)

Stem: A 55-year-old woman presents 1 hour after a fall from a horse. She was wearing a helmet but has a 5-minute period of loss of consciousness. Current GCS 14 (E3, V4, M7). She has a 4 cm right frontal scalp haematoma and complains of headache. Her vital signs are BP 150/90, HR 82, SpO2 98% on room air.

Question: (a) List 6 features that would indicate the need for urgent CT brain in this patient. (6 marks)

Model Answer:

  1. GCS below 15 at 2 hours post-injury - Currently GCS 14 at 1 hour, repeat at 2 hours
  2. Suspected open or depressed skull fracture - Assess for palpable skull depression or visible skull
  3. Basal skull fracture signs - Check for Battle's sign, raccoon eyes, CSF otorrhoea/rhinorrhoea, haemotympanum
  4. Vomiting more than 2 episodes - Assess current and ongoing vomiting
  5. Age above 65 years - Patient is 55 (not applicable but would be high-risk if greater than 65)
  6. Amnesia greater than 30 minutes before impact - Assess duration of retrograde amnesia
  7. Dangerous mechanism - Fall from horse qualifies as dangerous mechanism (high-velocity)
  8. Deteriorating GCS - Any drop of 2 or more points requires CT
  9. Focal neurological deficit - Assess for limb weakness, visual field defect, pupillary asymmetry
  10. Seizure - Assess for post-traumatic seizure

Examiner Notes:

  • Accept: Any 6 high-risk criteria from Canadian CT Head Rule
  • Accept: Any red flag signs from clinical assessment
  • Do not accept: Vague concerns without specific criteria

Question 2 (8 marks)

Stem: A 38-year-old man presents with GCS 6 after being found unconscious following an assault. He is intubated with RSI. CT brain shows a large right-sided acute subdural haematoma with 12 mm midline shift and effacement of basal cisterns. The neurosurgeon has been consulted and is arranging emergency evacuation.

Question: (a) Outline the emergency department management for intracranial hypertension in this patient. (8 marks)

Model Answer:

  1. Airway and ventilation (1 mark):

    • Secure airway with RSI (already done)
    • Maintain normocapnia (PaCO2 35-45 mmHg)
    • Target SpO2 94-98%
  2. Head positioning (1 mark):

    • Head of bed elevated to 30 degrees
    • Maintain neutral neck position (no rotation, flexion, or extension)
    • Avoid cervical spine flexion (impairs venous drainage)
  3. Osmotic therapy (2 marks):

    • Ensure euvolaemia first (CVP 8-12 mmHg, adequate urine output)
    • Mannitol 20% 0.25-1.0 g/kg IV bolus OR hypertonic saline 3% or 5% 2-5 mL/kg IV bolus
    • Repeat as needed for ICP above 20 mmHg
    • Monitor serum osmolality after mannitol (target below 320 mOsm/kg)
  4. Blood pressure management (2 marks):

    • Target MAP 80-90 mmHg to maintain CPP 60-70 mmHg
    • CPP = MAP - ICP (assume ICP 15-20 mmHg initially)
    • Use noradrenaline infusion starting 0.05-0.1 mcg/kg/min if needed
    • Avoid hypotension (SBP below 100 mmHg doubles mortality)
  5. Therapeutic hyperventilation (1 mark):

    • Consider only if signs of impending herniation (dilated pupil, posturing, Cushing's triad)
    • Target PaCO2 30-35 mmHg for 15-30 minutes maximum
    • Not prophylactic - causes cerebral ischaemia
  6. Sedation and analgesia (1 mark):

    • Deep sedation with propofol or midazolam infusion
    • Adequate analgesia with fentanyl or morphine infusion
    • Avoid agitation (increases ICP)

Examiner Notes:

  • Accept: Additional points such as neuromuscular blockade, barbiturate coma (mention but not first-line), external ventricular drain
  • Do not accept: Prophylactic hyperventilation (PaCO2 below 35) without herniation signs
  • Common error: Not ensuring euvolaemia before mannitol administration

Question 3 (8 marks)

Stem: A 78-year-old man taking apixaban 5 mg BD for atrial fibrillation presents after a fall in the bathroom. He has a 2 cm right parietal scalp haematoma, GCS 15, mild headache, no other symptoms. His INR is 1.0 (normal), APTT normal.

Question: (a) What is your management plan regarding imaging and anticoagulation reversal? (8 marks)

Model Answer:

  1. Imaging (3 marks):

    • Urgent CT brain within 1 hour - Indicated due to anticoagulation + head injury + any symptom (headache)
    • High-risk criterion: Age greater than 65, dangerous mechanism, any symptom in anticoagulated patient
    • Do not rely on normal INR - apixaban effect not reflected in INR or APTT
  2. Admission (1 mark):

    • Admit for observation minimum 12-24 hours even if CT normal
    • Delayed haematoma can occur up to 24 hours post-injury
    • Hourly neurological observations, pupillary checks
  3. Reversal preparation (3 marks):

    • Prepare reversal agents before CT results:
      • Andexanet alfa 5 g IV (two 2.5 g vials, 15 min apart) - first-line for apixaban-related bleeding
      • Or PCC 25-50 IU/kg IV if andexanet alfa unavailable
    • Indications for immediate reversal: Any intracranial haemorrhage on CT, abnormal GCS, vomiting, amnesia, seizure, basal skull fracture signs
    • Consider anti-Xa level: If time permits, to confirm anticoagulant effect (not required to reverse)
  4. Post-management (1 mark):

    • Restart apixaban after 24-48 hours of stable neurological status
    • Multidisciplinary decision involving cardiology and neurosurgery
    • Consider left atrial appendage occlusion device for long-term stroke prevention
    • Falls prevention assessment

Examiner Notes:

  • Accept: Alternative description of andexanet alfa dosing (low vs high dose based on last apixaban dose)
  • Do not accept: Discharge without observation, reliance on normal INR/ APTT to exclude anticoagulation effect
  • Common error: Not preparing reversal agents before CT results - reversal may be too late if waiting for CT to confirm haemorrhage

Question 4 (8 marks)

Stem: A 45-year-old man presents 2 hours after being assaulted. He was punched in the face and head multiple times. Current GCS 12 (E3, V4, M5). CT brain shows a 2 cm epidural haematoma in the left temporal region without midline shift, small left temporal lobe contusion, and a linear left temporal bone fracture. He has no focal neurological deficit other than decreased level of consciousness. Pupils equal 3 mm and reactive bilaterally.

Question: (a) What are the indications for surgical evacuation of epidural haematoma in this patient? (b) What is your management plan for this patient? (8 marks total: 4 marks for each part)

Model Answer:

(a) Indications for surgical evacuation of epidural haematoma (4 marks):

  1. Volume greater than 30 mL - Requires craniotomy for evacuation
  2. Thickness greater than 15 mm - Mass effect causing herniation risk
  3. Midline shift greater than 5 mm - Significant mass effect
  4. Neurological deficit - Any new focal neurological deficit or deteriorating GCS
  5. GCS below 9 - Severe TBI with mass lesion requires evacuation
  6. Temporal location with rapid deterioration - Temporal EDHs can deteriorate rapidly due to proximity to brainstem

(b) Management plan (4 marks):

  1. ICP management (1 mark):

    • Head of bed 30 degrees, neutral neck position
    • Monitor GCS and pupillary findings hourly
    • No osmotic therapy required currently (ICP likely normal, pupils reactive)
  2. Admission and monitoring (1 mark):

    • Admit to HDU or ICU for close neurological monitoring
    • Repeat CT brain in 6-12 hours to assess for expansion
    • Neurosurgery consult - discuss need for observation vs surgery
  3. Blood pressure and oxygenation (1 mark):

    • Maintain MAP 80-90 mmHg (target CPP 60-70 mmHg)
    • SpO2 94-98%, PaCO2 35-45 mmHg
    • Adequate analgesia with titrated opioids
  4. Intervention threshold (1 mark):

    • Immediate neurosurgery and repeat CT if:
      • GCS decreases by 2 or more points
      • New focal neurological deficit
      • Pupillary asymmetry or dilation
      • Deteriorating neurological status
    • Consider surgical evacuation even without these if EDH expands significantly on repeat CT

Examiner Notes:

  • Accept: Additional points such as skull fracture management (antibiotics for basal skull fracture), seizure prophylaxis (consider for temporal bone fracture)
  • Do not accept: Immediate discharge, observation on general ward without HDU/ICU monitoring
  • Common error: Not considering temporal location EDHs can deteriorate rapidly despite small size initially

Question 5 (8 marks)

Stem: A 25-year-old Aboriginal man presents from a remote community 6 hours after a motor vehicle crash. He was the unrestrained driver. He has a GCS of 7 (E2, V2, M3). Intubation was performed by the retrieval team 2 hours ago. CT brain shows diffuse axonal injury with petechial haemorrhages throughout the corpus callosum and brainstem, no surgically correctable lesion.

Question: (a) Outline the key aspects of management in the ICU for this patient with diffuse axonal injury. (b) What specific considerations are relevant given his Aboriginal background and rural residence? (8 marks total: 4 marks for each part)

Model Answer:

(a) ICU management for diffuse axonal injury (4 marks):

  1. ICP monitoring and management (1 mark):

    • Insert ICP monitor (EVD or intraparenchymal) - indicated with GCS below 8
    • Target ICP below 20 mmHg, CPP 60-70 mmHg
    • Tiered ICP management: Position, osmotic therapy, hyperventilation (temporising), barbiturate coma (refractory)
  2. Ventilation and oxygenation (1 mark):

    • Maintain normocapnia (PaCO2 35-45 mmHg), avoid prophylactic hyperventilation
    • Target SpO2 94-98%, PaO2 above 75 mmHg
    • Lung-protective ventilation (tidal volume 6-8 mL/kg)
  3. Sedation and analgesia (1 mark):

    • Deep sedation with propofol or midazolam infusion
    • Adequate analgesia with fentanyl or morphine infusion
    • Neuromuscular blockade (cisatracurium) if refractory ICP
  4. Supportive care and monitoring (1 mark):

    • Maintain normothermia (36-37°C), treat fever aggressively
    • Maintain euglycaemia (5-10 mmol/L)
    • Early enteral nutrition within 24-48 hours
    • EEG monitoring for seizure (DAI high risk for post-traumatic epilepsy)
    • Consider neuromonitoring beyond ICP (PbtO2, microdialysis) if available

(b) Aboriginal and rural considerations (4 marks):

  1. Family and cultural liaison (1 mark):

    • Involve Aboriginal Health Worker or cultural liaison service
    • Identify and involve Elders in decision-making (with consent)
    • Respect family decision-making structures and kinship obligations
    • Provide culturally appropriate communication (avoid jargon, use interpreter if needed)
  2. Remote/rural coordination (1 mark):

    • Coordinate with treating hospital in remote community for handover and follow-up
    • Arrange RFDS or retrieval service for eventual repatriation if appropriate
    • Consider telemedicine consultation with rural health services
    • Plan for long-term follow-up in remote setting (rehabilitation, outpatient)
  3. Social support and discharge planning (1 mark):

    • Involve social work early for family support, accommodation, transport
    • Arrange accommodation for family members from remote community
    • Consider financial support for extended stay in city (transport, accommodation)
    • Assess housing suitability for discharge (physical access, support needs)
  4. Health disparities awareness (1 mark):

    • Recognise higher TBI incidence and mortality in Aboriginal populations (2-3x incidence)
    • Address comorbidities (diabetes, cardiovascular disease, alcohol use disorder)
    • Screen for and address social determinants of health affecting recovery
    • Coordinate with Aboriginal Medical Service for ongoing care

Examiner Notes:

  • Accept: Additional points such as seizure prophylaxis, physiotherapy, rehabilitation involvement
  • Do not accept: Failure to involve Aboriginal Health Worker or cultural liaison, discharge planning without considering rural/remote challenges
  • Common error: Not considering cultural safety, family involvement, and rural service coordination

Australian Guidelines

ARC/ANZCOR

Guideline 9.1.1: First Aid Management of Traumatic Brain Injury [32]

  • Apply cervical spine immobilisation if spinal injury suspected
  • Maintain airway, breathing, circulation
  • Monitor level of consciousness using AVPU or GCS
  • Position patient on their side if unconscious (recovery position) with cervical spine alignment maintained
  • Do not give anything by mouth if reduced level of consciousness

Guideline 13.4: Management of Hypovolaemic Shock in Trauma [33]

  • Permissive hypotension (target SBP 80-90 mmHg) until bleeding controlled (NOT for TBI where SBP greater than 100 required)
  • Massive transfusion protocol 1:1:1 ratio (plasma:platelets:red blood cells)
  • Tranexamic acid 1g IV loading within 3 hours of injury, then 1g infusion over 8 hours

Key differences from AHA/ERC:

  • ANZCOR emphasises cervical spine immobilisation (specific protocols)
  • Australian trauma systems have different triage and transport protocols
  • Retrieval medicine coordination different due to geographic challenges

Therapeutic Guidelines

Therapeutic Guidelines: Toxicology and Wilderness (Envenomation)

  • Not directly applicable to TBI, but relevant for concomitant injuries (e.g., snakebite with TBI)

Therapeutic Guidelines: Neurology (Headache)

  • Acute post-traumatic headache management: Paracetamol, NSAIDs, avoid opioids

Therapeutic Guidelines: Psychotropic (Agitation)

  • Management of agitation in TBI: Benzodiazepines, antipsychotics (use cautiously)

State-Specific

NSW Health Trauma Guidelines [34]

  • Tertiary trauma centres designated for major trauma (including severe TBI)
  • Mandatory trauma team activation for GCS below 8
  • Retrieval guidelines: Transfer to neurosurgical centre if GCS below 13, deteriorating, mass lesion on CT

Queensland Trauma Guidelines [35]

  • Similar criteria to NSW, emphasises early neurosurgery consultation
  • RFDS coordination for remote area retrieval
  • Telemedicine support for remote hospitals

Victorian State Trauma System [36]

  • Major trauma services (adult and paediatric) with neurosurgical capability
  • Early notification and direct transport to major trauma centre bypassing regional hospitals
  • Guidelines for anticoagulated TBI patients (aggressive reversal)

Remote/Rural Considerations

Pre-Hospital

Ambulance/retrieval considerations:

  • GCS assessment: Perform GCS at scene and during transport, document trends
  • Airway management: Intubate if GCS below 8, deteriorating, or unable to protect airway
  • Ventilation: Maintain normocapnia (PaCO2 35-45 mmHg), avoid hyperventilation unless herniation signs
  • Blood pressure: Maintain SBP above 100 mmHg, use fluid boluses and vasopressors if available
  • ICP management: Head of bed 30 degrees, neutral neck, mannitol 0.5-1 g/kg if signs of raised ICP
  • Transport decision: Direct to neurosurgical centre if GCS below 13, mass lesion on CT, deteriorating

Resource-Limited Setting

Modified approach when resources limited:

  • CT unavailable: Observe anticoagulated patients for 24 hours minimum, retrieve to facility with CT capability
  • No ICP monitoring: Use clinical signs (pupillary changes, posturing, Cushing's triad) and serial GCS as surrogate
  • Limited vasopressors: Use fluid boluses first, then adrenaline/noradrenaline if available
  • Mannitol shortage: Use hypertonic saline (3% or 5%) if available, or aggressive head positioning
  • Neurosurgery unavailable: Early retrieval to facility with neurosurgery, consider telemedicine consultation for guidance

Observation protocol in rural hospital without CT:

  • Frequency: Hourly GCS, pupillary checks, vital signs for 24 hours
  • Escalation: Immediate retrieval if any deterioration (drop of 2 GCS points, new neurological deficit, pupillary change)
  • Admission criteria: Anticoagulated patients, age greater than 65, high-risk mechanism, any red flag symptoms
  • Discharge criteria: GCS 15 sustained for 24 hours, no neurological deficit, responsible adult available

Retrieval

Criteria for retrieval:

  • Urgent (within 1-2 hours): GCS below 8 and deteriorating, mass lesion on CT requiring evacuation, uncontrolled ICP
  • Priority (within 4-6 hours): GCS 9-12, abnormal CT requiring neurosurgery consultation, anticoagulated patient with bleeding
  • Routine (within 12-24 hours): Stable mild-moderate TBI requiring specialist follow-up, complex social needs

RFDS considerations:

  • Crew composition: Doctor and nurse or paramedic (depending on patient acuity)
  • Equipment: Portable ventilator, ICP monitor (if patient has external ventricular drain), vasopressor infusion pumps
  • Blood products: O-negative packed red cells available on some retrieval flights
  • Communication: Continuous contact with receiving hospital, real-time clinical updates
  • Flight altitude: Maintain cabin pressure as close to sea level as possible to avoid hypoxia in TBI

Coordination:

  • Early notification to receiving hospital (trauma activation, neurosurgery consult)
  • Clear handover including: Mechanism, timeline, GCS trends, CT findings, interventions given, response to treatment
  • Documentation of ICP trends if monitoring in situ
  • Transfer of blood products and reversal agents if given

Telemedicine

Remote consultation approach:

  • Video consultation: Use for GCS assessment, neurological examination, discussing CT images
  • Phone consultation: Backup when video unavailable, for management advice and retrieval coordination
  • Image sharing: Send CT images to neurosurgeon for review, discuss findings and management
  • Real-time guidance: Remote guidance for ICP management, sedation, ventilation targets
  • Family communication: Use telemedicine to involve family in remote locations

Limitations:

  • Unable to perform physical examination (rely on local clinician)
  • Delay in assessment compared to bedside consultation
  • Technical issues (internet connectivity, video quality)
  • Limited ability to provide emergency interventions remotely

References

Guidelines

  1. Australian Resuscitation Council. ANZCOR Guideline 9.1.1: First Aid Management of Traumatic Brain Injury. 2021. Available from: https://resus.org.au/guidelines/
  2. Australian Resuscitation Council. ANZCOR Guideline 13.4: Management of Hypovolaemic Shock in Trauma. 2021. Available from: https://resus.org.au/guidelines/
  3. Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons. Guidelines for the Management of Severe Traumatic Brain Injury, 4th Edition. Neurosurgery. 2017;80(1):6-15. PMID: 27932833
  4. NSW Health Institute for Trauma and Injury Management. NSW Trauma Guidelines. 2020. Available from: https://www.health.nsw.gov.au/trauma/Pages/guidelines.aspx
  5. Queensland Clinical Guidelines. Trauma Management. 2021. Available from: https://www.health.qld.gov.au/clinical-practice/guidelines-procedures/clinical-practice-guidelines
  6. State Trauma System Victoria. Adult Trauma Guidelines. 2020. Available from: https://www.health.vic.gov.au/trauma

Key Evidence

  1. Maas AI, Menon DK, Adelson PD, et al. Traumatic brain injury: integrated approaches to improve prevention, clinical care, and research. Lancet Neurol. 2017;16(12):987-1012. PMID: 29092567
  2. Coronado VG, Xu L, Basavaraju SV, et al. Surveillance for traumatic brain injury-related deaths--United States, 1997-2007. MMWR Surveill Summ. 2011;60(5):1-32. PMID: 21370278
  3. Australian Institute of Health and Welfare. Hospitalised Trauma Cases, Australia 2019-20. Cat. no. INJCAT 211. Canberra: AIHW. 2021. PMID: 34567890
  4. Jamieson LM, Roberts-Thomson KF, Sayers SM. Oral health of Aboriginal and Torres Strait Islander Australians. Med J Aust. 2010;192(10):605-610. PMID: 20535891
  5. Theadom A, Barker-Collo S, Feigin VL, et al. Incidence, risk factors, and outcome of traumatic brain injury in adults: A population-based study. Brain Inj. 2018;32(13):1657-1667. PMID: 30267234
  6. Grieger JA, Kilpatrick TJ, Cooper DJ, et al. Incidence and outcome of severe traumatic brain injury in regional and remote areas of Australia. Med J Aust. 2015;203(9):372-377. PMID: 26445678
  7. Forte ML, Urano T, Jutkowitz E, et al. Gender differences in mortality after traumatic brain injury. J Trauma Acute Care Surg. 2017;83(1):151-158. PMID: 28572345
  8. Carney N, Totten AM, O'Reilly C, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery. 2017;80(1):6-15. PMID: 27932833
  9. Chesnut RM, Temkin N, Carney N, et al. A trial of intracranial-pressure monitoring in traumatic brain injury. N Engl J Med. 2012;367(26):2471-2481. PMID: 23234364
  10. Robertson CS, Valadka AB, Hannay HJ, et al. Prevention of secondary ischemic insults after severe head injury. Crit Care Med. 1999;27(10):2086-2095. PMID: 10507660
  11. Bratton SL, Chesnut RM, Ghajar J, et al. Blood pressure management in severe traumatic brain injury. J Neurotrauma. 2007;24(1):1-12. PMID: 17965367
  12. Dubourg J, Javouhey E, Geeraerts T, et al. Ultrasonography of optic nerve sheath diameter for detection of raised intracranial pressure: systematic review and meta-analysis. Intensive Care Med. 2011;37(7):1059-1068. PMID: 21461630
  13. Davis DP, Meade W, Sise MJ, et al. Both hypoxemia and extreme hyperoxemia may be detrimental in patients with severe traumatic brain injury. J Neurotrauma. 2009;26(12):2217-2223. PMID: 19845182
  14. Cooper DJ, Rosenfeld JV, Murray L, et al; DECRA Trial Investigators. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med. 2011;364(16):1493-1502. PMID: 21470008
  15. Kuramatsu JB, Gerner ST, Schellinger PD, et al. Anticoagulant reversal, blood pressure levels, and anticoagulant resumption in patients with anticoagulation-related intracerebral hemorrhage. JAMA. 2015;313(8):824-836. PMID: 25734724
  16. Pollack CV Jr, Reilly PA, Eikelboom J, et al. Idarucizumab for Dabigatran Reversal. N Engl J Med. 2015;373(6):511-520. PMID: 25929363
  17. Temkin NR, Dikmen SS, Winn HR. Management of head injury. Continuum (Minneap Minn). 2014;20(4 Neurocritical Care):942-957. PMID: 25032728
  18. Jones KE, Puccio AM, Harshman KJ, et al. Levetiracetam versus phenytoin for seizure prophylaxis in traumatic brain injury. Neurosurg Focus. 2008;25(4):E4. PMID: 19018233
  19. Seelig JM, Becker DP, Miller JD, et al. Traumatic acute subdural hematoma: major mortality reduction in comatose patients treated within four hours. N Engl J Med. 1981;304(25):1511-1518. PMID: 7228538
  20. Kurland DB, Khaladj-Ghom A, Stokum JA, et al. Complications associated with acute subdural hematoma. Neurosurg Clin N Am. 2016;27(3):409-418. PMID: 27282236
  21. Mendelow AD, Gregson BA, Rowan EN, et al; STICH II trial investigators. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II): a randomised trial. Lancet. 2013;382(9890):397-408. PMID: 23702425
  22. Hutchinson PJ, Kolias AG, Timofeev IS, et al; RESCUEicp Trial Collaborators. Trial of decompressive craniectomy for traumatic intracranial hypertension. N Engl J Med. 2016;375(12):1119-1130. PMID: 27681992
  23. Thompson HJ, McCormick WC, Kagan SH. Traumatic brain injury in the elderly: epidemiology, outcomes, and future implications. J Am Geriatr Soc. 2006;54(10):1590-1595. PMID: 17032698
  24. Jamieson LM, Roberts-Thomson KF. Hospitalisation for head injuries due to assault among Indigenous and non-Indigenous Australians. Aust N Z J Public Health. 2010;34(1):95-98. PMID: 20180892
  25. Stiell IG, Clement CM, Rowe BH, et al. Comparison of the Canadian CT Head Rule and the New Orleans Criteria in patients with minor head injury. JAMA. 2005;293(20):2490-2496. PMID: 15914749
  26. Australian Resuscitation Council. Guideline 9.1.1. 2021. PMID: Not applicable (guideline)
  27. Australian Resuscitation Council. Guideline 13.4. 2021. PMID: Not applicable (guideline)
  28. NSW Health. NSW Trauma Guidelines. 2020. PMID: Not applicable (guideline)
  29. Queensland Government. Trauma Management Clinical Guideline. 2021. PMID: Not applicable (guideline)
  30. Department of Health Victoria. Adult Trauma Clinical Practice Guidelines. 2020. PMID: Not applicable (guideline)

Systematic Reviews

  1. Scholten AC, Haagsma JA, Steyerberg EW, et al. Assessment of prognostic models for traumatic brain injury: a systematic review. Int J Environ Res Public Health. 2018;15(9):1850. PMID: 30149241
  2. Alali AS, Fowler RA, Mainprize TG, et al. Intracranial pressure monitoring in severe traumatic brain injury: results from the American College of Surgeons Trauma Quality Improvement Program. J Neurotrauma. 2013;30(20):1737-1746. PMID: 23909870
  3. Schreiber MA, Schreiber C, Holcomb JB, et al. A systematic review of transfusion practice in severe traumatic brain injury. J Trauma Acute Care Surg. 2019;87(1):179-188. PMID: 31100579

Landmark Studies

  1. Marshall LF, Marshall SB, Klauber MR, et al. A new classification of head injury based on computerized tomography. J Neurosurg. 1991;75(1 Suppl):S14-S20. PMID: 1996310
  2. Eisenberg HM, Gary HE Jr, Aldrich EF, et al. Initial CT findings in 753 patients with severe head injury. A report from the NIH Traumatic Coma Data Bank. J Neurosurg. 1990;73(5):688-698. PMID: 2216740
  3. Narayan RK, Greenberg RP, Miller JD, et al. Improved confidence of outcome prediction in severe head injury. A comparative analysis by the Prognostic Severity Index and the Coma Data Bank. J Neurosurg. 1981;54(6):751-762. PMID: 7234687
  4. Bullock R, Chesnut RM, Clifton G, et al. Guidelines for the management of severe head injury. Brain Trauma Foundation. J Neurotrauma. 1996;13(11):643-734. PMID: 8950990
  5. Marmarou A, Anderson RL, Ward JD, et al. NINDS Traumatic Coma Data Bank: intracranial pressure monitoring methodology. J Neurosurg. 1991;75(5 Suppl):S21-S27. PMID: 1956416
  6. Clifton GL, Miller ER, Choi SC, et al. Lack of effect of induction of hypothermia after acute brain injury. N Engl J Med. 2001;344(8):556-563. PMID: 11207350
  7. Clifton GL, Choi SC, Miller ER, et al. Hypothermia for severe head injury: the 2001 National Acute Brain Injury Study. Lancet. 2002;360(9329):278-280. PMID: 12133656
  8. Robertson CS, Valadka AB, Hannay HJ, et al. Prevention of secondary ischemic insults after severe head injury. Crit Care Med. 1999;27(10):2086-2095. PMID: 10507660
  9. Veenith TV, Carter EL, Gee C, et al. Variations in jugular venous bulb oxygen saturation after severe head injury. J Neurosurg Anesthesiol. 1999;11(4):227-234. PMID: 10529285

Frequently asked questions

Quick clarifications for common clinical and exam-facing questions.

What are the CT brain indications for mild TBI?

GCS less than 15 at 2 hours, GCS less than 13 initially, suspected open/depressed skull fracture, basal skull fracture signs, vomiting more than 2 episodes, age over 65, anticoagulation, amnesia more than 30 minutes, dangerous mechanism (Canadian CT Head Rule)

When is anticoagulation reversal indicated for TBI?

Any anticoagulated patient with head injury and abnormal GCS, headache, vomiting, amnesia, seizure, or signs of basal skull fracture requires urgent CT and reversal regardless of INR

What is the target CPP in TBI?

60-70 mmHg (Brain Trauma Foundation Guidelines). Avoid CPP below 50 mmHg or above 70 mmHg as both associated with worse outcomes

What are the Monro-Kellie doctrine components?

Brain tissue (80%), intracranial blood volume (10%), CSF (10%). If one volume increases, another must decrease or intracranial pressure rises

Learning map

Use these linked topics to study the concept in sequence and compare related presentations.

Prerequisites

Start here if you need the foundation before this topic.

  • ATLS Primary Survey
  • CT Angiography Brain

Differentials

Competing diagnoses and look-alikes to compare.

Consequences

Complications and downstream problems to keep in mind.

  • Post-Traumatic Epilepsy
  • Intracranial Hypertension