Intensive Care Medicine

Severe Traumatic Brain Injury and Decompressive Craniectomy

Severe traumatic brain injury (TBI) is defined by Glasgow Coma Scale (GCS) score of 3-8 following head injury, representing a critical neurosurgical emergency with significant mortality and morbidity. The management...

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Severe Traumatic Brain Injury and Decompressive Craniectomy

Clinical Overview

Severe traumatic brain injury (TBI) is defined by Glasgow Coma Scale (GCS) score of 3-8 following head injury, representing a critical neurosurgical emergency with significant mortality and morbidity. The management of severe TBI involves a tiered approach beginning with primary and secondary survey optimization, proceeding to intracranial pressure (ICP) monitoring, and escalating to surgical intervention including decompressive craniectomy (DC) for refractory intracranial hypertension.

Answer: Definition: Severe TBI

  • GCS: 3-8 (after resuscitation and sedation washout)
  • Duration: Must persist for at least 6 hours post-injury
  • Mechanisms: Blunt trauma (falls, MVC), penetrating trauma, blast injury
  • Pathology: Diffuse axonal injury, intracerebral haemorrhage, subdural haematoma, contusions, cerebral edema

Epidemiology

  • Incidence: 50-60 per 100,000 population annually
  • Mortality: 30-50% for severe TBI
  • Male predominance: 2:1 male-to-female ratio
  • Peak incidence: 15-24 years and greater than 65 years
  • Indigenous populations: 2-3× higher incidence of severe TBI [PMID: 30760144]

Pathophysiology

Intracranial Pressure Dynamics

The Monro-Kellie doctrine states that the cranial vault is a fixed-volume container containing brain tissue (80%), blood (10%), and cerebrospinal fluid (CSF, 10%). In severe TBI, pathological processes increase intracranial volume, initially compensated by CSF displacement and venous blood displacement. When compensatory mechanisms are exhausted, ICP rises exponentially, leading to cerebral perfusion pressure (CPP) reduction and secondary brain injury.

Key Equations

  • ICP: Direct measurement via intraparenchymal or intraventricular catheter
  • CPP: MAP - ICP (target 60-70 mmHg)
  • Cerebral Blood Flow: CPP ÷ Cerebrovascular Resistance
  • Autoregulation: Maintains CBF 50-60 mL/100g/min across MAP 50-150 mmHg (intact) or lost (severe TBI)

Pressure-Volume Compensatory Reserve

  • Phase I: Flat portion - ample compensatory reserve
  • Phase II: Exponential rise - declining reserve
  • Phase III: Decompensated - minimal reserve, steep pressure rise

Secondary Brain Injury

Secondary injury cascades following primary mechanical insult include:

  1. Excitotoxicity: Glutamate release, NMDA receptor activation, calcium influx
  2. Oxidative Stress: Free radical generation, lipid peroxidation, mitochondrial dysfunction
  3. Neuroinflammation: Microglial activation, cytokine release (IL-1β, IL-6, TNF-α)
  4. Metabolic Crisis: Mitochondrial failure, ATP depletion, anaerobic metabolism
  5. Blood-Brain Barrier Disruption: Vasogenic edema, increased permeability
  6. Ischemia: Reduced CPP, microvascular thrombosis, cortical spreading depolarizations

Therapeutic Targets

  • Maintain CPP 60-70 mmHg (MAP 90-100 mmHg if ICP 20-30 mmHg)
  • Avoid hypotension (SBP below 90 mmHg): Each episode doubles mortality
  • Prevent hypoxia (PaO2 below 60 mmHg): Associated with poor outcomes
  • Control hyperglycaemia (7.8-10.0 mmol/L)
  • Target normothermia (36-37°C)
  • Treat anaemia (Hb ≥70-80 g/L)

Clinical Presentation

Signs and Symptoms

Consciousness

  • GCS 3-8 (deep coma to responsive to pain only)
  • Pupillary abnormalities (unilateral or bilateral dilation)
  • Abnormal posturing (decorticate, decerebrate)

Cranial Nerves

  • CN III palsy: Dilated, non-reactive pupil (uncal herniation)
  • CN VI palsy: Abduction deficit (raised ICP)
  • Ocular bobbing: Pontine injury

Motor Findings

  • Hemiparesis/monoparesis (contralateral to lesion)
  • Abnormal posturing patterns
  • Spasticity, hyperreflexia (later)

Autonomic Dysfunction

  • Cushing's triad: Hypertension, bradycardia, irregular respirations (late sign of herniation)
  • Hyperthermia (central)
  • Diabetes insipidus (posterior pituitary injury)

Initial Assessment

Primary Survey (ABCDE)

  • A: Cervical spine immobilization (mandatory until cleared)
  • B: Airway protection (GCS ≤8 = early intubation)
  • C: Circulation (treat hypotension aggressively)
  • D: Disability (GCS, pupils)
  • E: Exposure (full examination, temperature)

Secondary Survey

  • Head-to-toe examination
  • Skull inspection (battle's sign, raccoon eyes)
  • Basilar skull fracture signs
  • Long bone fractures (fat embolism risk)
  • Associated injuries (thoracic, abdominal)

Imaging

Non-Contrast CT Head (Initial)

  • Timing: Within 1 hour of arrival (Level I recommendation)
  • Findings: Mass lesions, contusions, diffuse axonal injury, midline shift, basal cistern effacement
  • Marshall CT classification (see below)
  • Rotterdam CT score (prognostication)

MRI (Selected Cases)

  • Diffuse axonal injury detection (superior to CT)
  • Timing: Days 2-7 for prognostication
  • Sequences: SWI (microhaemorrhages), DTI (white matter tracts)

CT Angiography

  • Vascular injury (dissection, pseudoaneurysm)
  • Traumatic aneurysm
  • Venous sinus thrombosis

Marshall CT Classification

ScoreFindings
1Diffuse injury I: No visible pathologic mass, cisterns present
2Diffuse injury II: Cisterns present, midline shift 0-5 mm
3Diffuse injury III: Swelling, cisterns compressed/absent, midline shift 0-5 mm
4Diffuse injury IV: Midline shift greater than 5 mm
5Evacuated mass lesion
6Non-evacuated mass lesion

Rotterdam CT Score (0-6)

  • Basal cisterns: Normal (0), compressed (1), absent (2)
  • Midline shift: 0-5 mm (0), greater than 5 mm (1)
  • Epidural mass lesion: Present (0), absent (1)
  • Intraventricular/subarachnoid blood: Absent (0), present (1)

Prognostication

  • Rotterdam 0-1: Mortality below 5%
  • Rotterdam 2: Mortality 10-20%
  • Rotterdam 3: Mortality 25-35%
  • Rotterdam 4-5: Mortality 40-60%
  • Rotterdam 6: Mortality greater than 70%

Investigations

Laboratory Tests

Emergency Panel

  • FBC (Hb, platelets, WBC)
  • Coagulation profile (PT/INR, aPTT, fibrinogen)
  • Electrolytes (Na⁺, K⁺, glucose)
  • Renal function (creatinine, urea)
  • Liver function tests
  • Blood group and cross-match (4-6 units PRBC)
  • Type and screen

Specialized Tests

  • Troponin (cardiac contusion)
  • Beta-HCG (women of childbearing age)
  • Ethanol level (substance use)
  • Toxicology screen (co-ingestions)
  • Arterial blood gas (baseline, serial)
  • Serum osmolality (if hyponatraemia suspected)

Neurophysiologic Monitoring

ICP Monitoring

Indications

  • GCS ≤8 after resuscitation AND abnormal CT (mass lesion, midline shift greater than 5 mm, cistern effacement)
  • GCS ≤8 after resuscitation AND normal CT if two or more:
    • Age greater than 40 years
    • Unilateral/bilateral motor posturing
    • Systolic BP below 90 mmHg

Devices

  • Intraparenchymal fiberoptic catheter (Camino, Codman)
    • "Advantages: Easy insertion, low infection risk"
    • "Disadvantages: Drift, no CSF drainage, recalibration impossible"
  • Intraventricular catheter (external ventricular drain, EVD)
    • "Advantages: Gold standard accuracy, CSF drainage therapeutic"
    • "Disadvantages: More difficult insertion, higher infection risk, parenchymal injury"
  • Intraparenchymal strain gauge (Raumedic)
    • "Advantages: Accurate, minimal drift, MRI-compatible"
    • "Disadvantages: No CSF drainage"

Insertion Technique

  • Kocher's point (11 cm posterior to nasion, 3 cm lateral to midline)
  • Perpendicular to cortical surface
  • Depth: 5-7 cm to ventricular frontal horn
  • Right frontal lobe dominant (non-dominant hemisphere)
  • Image-guided stereotaxy for atypical anatomy

ICP Thresholds

  • Normal: below 15 mmHg
  • Mild intracranial hypertension: 15-20 mmHg
  • Moderate: 20-25 mmHg
  • Severe: greater than 25-25 mmHg (threshold for escalation)
  • Threshold to treat: greater than 22 mmHg (Level II recommendation)

CPP Targets

  • CPP 60-70 mmHg (Level II recommendation)
  • Avoid CPP greater than 70 mmHg (risk of ARDS)
  • Individualize based on autoregulation status
  • Consider PRx (pressure reactivity index) monitoring

Multimodal Monitoring

Brain Tissue Oxygenation (PbO2)

  • Target: greater than 15 mmHg
  • Threshold for intervention: below 10 mmHg
  • Monitoring: Licox or Neurotrend probe
  • Interpretation: Dependent on CPP, PaO2, FiO2, Hb

Cerebral Microdialysis

  • Lactate/pyruvate ratio (LPR) below 25 normal, greater than 40 ischemia
  • Glucose: greater than 0.8 mmol/L normal, below 0.2 mmol/L ischemia
  • Glycerol: Marker of cell membrane degradation
  • Glutamate: Excitotoxicity marker

Jugular Venous Oxygen Saturation (SjvO2)

  • Normal: 55-71%
  • Desaturation: below 50% (cerebral ischemia)
  • Hyperemia: greater than 75% (luxury perfusion)
  • Limitations: Global measure, regional variation

Continuous EEG

  • Seizure detection (20-30% seizures post-TBI)
  • Burst suppression (depth of sedation)
  • Background activity (prognostication)
  • Ischaemia detection (periodic discharges)

Transcranial Doppler

  • MCA flow velocity (normal 60-90 cm/s)
  • Lindegaard ratio (MCA/ICA below 3 normal, greater than 3 vasospasm)
  • Autoregulation testing (thigh cuff release)
  • CPP estimation (FV x MAP + constant)

Management

Tiered Approach

Tier 0: Foundation (All Patients)

  • Head of bed elevation 30°
  • Neck neutral position (avoid jugular compression)
  • Avoid sedation interruption (agitation, coughing, suctioning)
  • Maintain normocapnia (PaCO2 35-40 mmHg)
  • Maintain normoxia (PaO2 greater than 80 mmHg, SpO2 greater than 94%)
  • Maintain normothermia (36-37°C)
  • Avoid hypotension (SBP greater than 100 mmHg, MAP greater than 80 mmHg)
  • Fluid restriction (isotonic, avoid hypotonic fluids)
  • Optimize sedation/analgesia (propofol, opioids)
  • Seizure prophylaxis (levetiracetam 500 mg q12h IV/PO)

Tier 1: First-Line (ICP greater than 20-25 mmHg)

  • Sedation optimization (increase propofol/opioids)
  • Neuromuscular blockade (rocuronium, cis-atracurium) to reduce metabolic demand
  • EVD insertion if intraventricular blood present
  • CSF drainage (open to 15-20 cm H2O)
  • Repeat CT (new lesions, progression)

Tier 2: Second-Line (ICP refractory to Tier 1)

  • Osmotic therapy (mannitol 20% 0.25-1 g/kg IV bolus, hypertonic saline 3% 2-5 mL/kg or 23.4% 30 mL bolus)
  • Hyperventilation (target PaCO2 30-35 mmHg, temporary bridge)
  • Barbiturate coma (thiopental or pentobarbital, EEG burst suppression)
  • Induced hypothermia (controversial, avoid below 35°C)
  • Decompressive craniectomy (surgical intervention)

Tier 3: Rescue Therapies

  • Ultra-early craniectomy (below 6 hours)
  • Bilateral decompressive craniectomy
  • Hemicraniectomy for malignant infarction (ischemic stroke)

Osmotic Therapy

Mannitol

  • Dose: 0.25-1 g/kg IV bolus (20% solution)
  • Onset: 5-15 minutes
  • Peak: 20-60 minutes
  • Duration: 1.5-6 hours
  • Mechanism: Osmotic diuresis, plasma expansion, rheological effects
  • Contraindications: Anuria, severe dehydration, hyperosmolality (greater than 320 mOsm/kg)
  • Monitoring: Serum osmolality q6h, volume status, electrolytes

Hypertonic Saline

  • 3%: 2-5 mL/kg bolus (maintenance infusion possible)
  • 7.5%: 1-2 mL/kg bolus
  • 23.4%: 30 mL (1.5-2 mL/kg) bolus (rescue therapy)
  • Onset: 5-10 minutes
  • Peak: 10-30 minutes
  • Duration: 2-4 hours
  • Advantages over mannitol: Better volume expansion, less diuresis, better ICP control
  • Contraindications: Congestive cardiac failure, pulmonary edema
  • Monitoring: Serum sodium q6h (target 150-155 mmol/L), volume status

Osmolar Gap

  • Calculated osmolarity: 2[Na⁺] + [Glucose] + [Urea] + [Ethanol]
  • Measured osmolality (freezing point depression)
  • Gap: Measured - Calculated
  • Gap greater than 10: Suggests other osmoles (toxic alcohols, mannitol)

Pharmacologic ICP Control

Sedation

Propofol

  • Dose: 0.5-5 mg/kg/hr infusion
  • Onset: below 1 minute
  • Half-life: 4-7 minutes (context-sensitive)
  • Advantages: Rapid titration, neuroprotective (free radical scavenging), anticonvulsant
  • Disadvantages: Hypotension, propofol infusion syndrome (PRIS) with high dose/long duration (greater than 48h, greater than 5 mg/kg/hr)
  • PRIS: Metabolic acidosis, rhabdomyolysis, hyperkalaemia, arrhythmias, renal failure
  • Contraindications: Severe hypertriglyceridaemia, egg allergy, soy allergy

Midazolam

  • Dose: 0.02-0.2 mg/kg/hr infusion
  • Onset: 2-5 minutes
  • Half-life: 1-4 hours (prolonged with hepatic dysfunction, long duration)
  • Advantages: Amnestic, anxiolytic, synergistic with opioids
  • Disadvantages: Tachyphylaxis, accumulation, prolonged recovery

Analgesia

Fentanyl

  • Dose: 25-100 μg bolus, 0.5-5 μg/kg/hr infusion
  • Onset: below 1 minute
  • Half-life: 2-4 minutes (context-sensitive)
  • Advantages: Minimal hypotension, rapid titration
  • Disadvantages: Chest wall rigidity (high dose), respiratory depression

Remifentanil

  • Dose: 0.05-0.5 μg/kg/min infusion
  • Onset: below 1 minute
  • Half-life: 3-10 minutes (context-independent, ester metabolism)
  • Advantages: Rapid wake-up for neurologic assessment
  • Disadvantages: Tachyphylaxis, high cost

Neuromuscular Blockade

Rocuronium

  • Dose: 0.6 mg/kg bolus, 0.1-0.2 mg/kg/hr infusion
  • Onset: 60-90 seconds
  • Duration: 30-60 minutes (dose-dependent)
  • Advantages: No histamine release, stable haemodynamics, sugammadex reversal
  • Disadvantages: Prolonged duration with high doses

Cis-atracurium

  • Dose: 0.15 mg/kg bolus, 0.05-0.1 mg/kg/hr infusion
  • Onset: 2-4 minutes
  • Duration: 20-35 minutes
  • Advantages: Hofmann elimination (independent of renal/hepatic function), histamine release minimal
  • Disadvantages: Laudanosine accumulation (seizure threshold)

Barbiturate Coma

Thiopental

  • Dose: 3-10 mg/kg loading, 1-5 mg/kg/hr infusion
  • Target: EEG burst suppression
  • Onset: below 30 seconds
  • Half-life: 6-15 hours
  • Advantages: Decreases cerebral metabolic rate (CMRO2), ICP control
  • Disadvantages: Severe hypotension (vasodilation, myocardial depression), immunosuppression, prolonged weaning
  • Contraindications: Hypovolaemia, severe cardiac dysfunction, porphyria

Pentobarbital

  • Dose: 5-15 mg/kg loading, 0.5-3 mg/kg/hr infusion
  • Target: EEG burst suppression
  • Onset: 1-2 minutes
  • Half-life: 15-50 hours
  • Advantages: Potent ICP control, anticonvulsant
  • Disadvantages: Severe hypotension, very long half-life, difficulty weaning

Hyperventilation

Rationale

  • vasoconstriction reduces cerebral blood volume (CBV)
  • 1 mmHg PaCO2 reduction = 3-4% CBV reduction
  • Maximal vasoconstriction at PaCO2 20-25 mmHg
  • ICP reduction within minutes

Protocol

  • Target PaCO2 30-35 mmHg (temporary)
  • Maintain PaCO2 greater than 30 mmHg (avoid cerebral ischaemia)
  • Use only as bridge to definitive therapy (DC, osmotic therapy)
  • Duration below 6 hours (to avoid rebound ICP rise)
  • Monitor SjvO2 or PbO2 (if available) to detect ischaemia
  • Avoid prophylactic hyperventilation (Level III recommendation)

Sustained Hyperventilation (Controversial)

  • Consider only if refractory ICP despite maximal therapy
  • Target PaCO2 25-30 mmHg
  • Monitor PbO2 (greater than 15 mmHg) or SjvO2 (greater than 50%)
  • Rebound oedema with rapid normalization (wean slowly over 24h)

Seizure Prophylaxis

Rationale

  • Post-traumatic seizures: 10-20% incidence
  • Early seizures (below 7 days): Exacerbate secondary injury
  • Late seizures (greater than 7 days): Post-traumatic epilepsy

Levetiracetam

  • Dose: 500 mg q12h IV/PO (loading 1000-2000 mg optional)
  • Mechanism: SV2A synaptic vesicle protein modulation
  • Advantages: Few drug interactions, no monitoring required, well-tolerated
  • Side effects: Sedation, behavioural changes, thrombocytopenia (rare)
  • Renal dose adjustment: CrCl below 80 mL/min (500 mg q24h)

Phenytoin

  • Dose: 15-20 mg/kg loading, 100 mg q8h maintenance
  • Mechanism: Na⁺ channel blockade
  • Advantages: Established efficacy, inexpensive
  • Disadvantages: Drug interactions (P450 induction), narrow therapeutic index (10-20 mg/L), requires monitoring
  • Side effects: Nystagmus, ataxia, gingival hyperplasia, rash (Stevens-Johnson syndrome), Stevens-Johnson with HLA-B*15:02 (Asian population)

Duration

  • Prophylaxis for 7 days (Level II recommendation)
  • Extend beyond 7 days if risk factors:
    • Penetrating TBI
    • Contusions greater than 1 cm
    • Subdural/epidural haematoma
    • Depressed skull fracture
    • Early post-traumatic seizures

Temperature Management

Target

  • Normothermia (36-37°C)
  • Avoid fever (greater than 38°C): Increases ICP, CMRO2, excitotoxicity

Active Cooling

  • Surface cooling (blankets, wraps)
  • Endovascular cooling catheters (more rapid control)
  • Target: 35-36°C (if refractory ICP)

Avoid Induced Hypothermia (32-35°C)

  • Prophylactic hypothermia: No benefit (Eurotherm3235 trial, PMID 26487355)
  • Increased complications (coagulopathy, infection, arrhythmias)
  • Consider only for refractory ICP as rescue therapy

Decompressive Craniectomy

Definition and Rationale

Decompressive craniectomy (DC) is a surgical procedure involving removal of a large bone flap and opening of the dura mater to allow outward herniation of swollen brain tissue, thereby reducing ICP and improving CPP. The technique creates space for cerebral expansion, preventing compression of vital structures and improving cerebral perfusion.

Historical Perspective

  • First described by Kocher in 1901
  • Fell into disfavour (poor outcomes, "living cadaver")
  • Resurgence with advances in neurocritical care
  • Standardized techniques in modern era

Physiological Effects

  • Immediate ICP reduction (10-20 mmHg average)
  • Improved CPP (10-15 mmHg average)
  • Improved cerebral compliance
  • Enhanced CSF and venous drainage
  • Reduced risk of brainstem herniation

Indications

Primary DC (Early, below 48 hours)

  • Large acute subdural haematoma (greater than 1 cm thickness, midline shift greater than 5 mm) with intraoperative brain swelling
  • Malignant cerebral edema following mass lesion evacuation
  • Contusions with mass effect and deterioration
  • Diffuse axonal injury with refractory intracranial hypertension

Secondary DC (Late, greater than 48 hours)

  • Refractory intracranial hypertension (ICP greater than 25-25 mmHg) despite maximal medical therapy:
    • "Tier 0: Head elevation, sedation, CPP optimization"
    • "Tier 1: CSF drainage, hyperosmolar therapy"
    • "Tier 2: Barbiturate coma, hyperventilation"
  • ICP refractory for greater than 1-2 hours despite maximal therapy
  • ICP spikes greater than 30 mmHg refractory to therapy
  • Worsening midline shift or cisternal compression on CT

Patient Selection Criteria

  • Age below 60 years (better outcomes in younger patients)
  • Unilateral mass lesion or contusion (better outcomes than diffuse injury)
  • GCS ≥6 before DC (better outcomes than GCS 3-5)
  • Reversible secondary injury (not primary diffuse axonal injury)
  • Absence of severe associated injuries (allowing neurosurgical focus)
  • ICP onset below 72 hours post-injury (earlier DC better)
  • Absence of fixed, dilated pupils (signs of irreversible injury)

Relative Contraindications

  • GCS 3 with bilaterally fixed, dilated pupils
  • Severe coagulopathy (INR greater than 1.5, platelets below 50)
  • Massive intracranial haemorrhage (GCS 3-4, midline shift greater than 15 mm) - futility
  • Severe associated injuries with haemodynamic instability
  • Multisystem organ failure
  • Prolonged cardiac arrest (greater than 10 minutes) with anoxic brain injury
  • Advanced directives limiting aggressive care

Evidence

DECRA Trial (2011) - PMID: 21262641

Design

  • Multicentre, randomized, controlled trial
  • 155 patients with severe diffuse TBI
  • Early bifrontal DC within 72 hours of injury
  • Inclusion: ICP greater than 20 mmHg greater than 15 minutes (first 24h) refractory to Tier 1 therapy
  • Primary outcome: Extended Glasgow Outcome Scale (GOS-E) at 6 months
  • Secondary: Mortality, ICP control, complications

Results

  • Early DC group:
    • Worse GOS-E outcomes (p=0.03)
    • Lower mortality (26% vs 37%, p=0.12) - but more survivors with severe disability
    • Better ICP control (lower mean ICP, less time greater than 20 mmHg)
    • More favourable ICP trajectory (lower area under curve)
    • More medical complications
  • Standard care group:
    • Better functional outcomes
    • Higher mortality but less severe disability

Limitations

  • Small sample size (n=155)
  • Inclusion of patients with diffuse injury (poor DC candidates)
  • Early DC (median 22 hours) - may be too early (brain still evolving)
  • Bifrontal DC (different from unilateral DC)
  • High percentage of patients with poor baseline GCS (median 4)

Implications

  • Early primary DC for diffuse injury: Not recommended
  • Avoid DC for patients with severe diffuse axonal injury
  • Consider DC later (refractory ICP after maximal therapy)
  • Patient selection critical (unilateral lesions better)

RESCUEicp Trial (2016) - PMID: 27808820

Design

  • Multicentre, randomized, controlled trial
  • 398 patients with refractory intracranial hypertension
  • Late DC (median 36 hours post-injury) for ICP greater than 25 mmHg refractory to maximal medical therapy
  • Inclusion: ICP greater than 25 mmHg greater than 1-12 hours despite Tier 1-2 therapy
  • Comparison: DC vs continued medical management
  • Primary outcome: Extended Glasgow Outcome Scale (GOS-E) at 6 months
  • Secondary: Mortality, ICP control, complications

Results

  • DC group:
    • Lower mortality (26.9% vs 48.9%, pbelow 0.001)
    • Higher rate of severe disability (vegetative state, severe disability)
    • More favourable GOS-E at 6 months (42.8% vs 34.6%, p=0.12) - trend
    • Better ICP control (median ICP 14 vs 19 mmHg)
    • More surgical complications
  • Medical therapy group:
    • Higher mortality (49%)
    • More favourable functional outcomes among survivors (if survived)

Subgroup Analysis

  • Age below 40 years: Better outcomes with DC
  • Unilateral lesions: Better outcomes with DC
  • Time to DC below 48 hours: Better outcomes with DC
  • Reversible pupillary abnormalities: Better outcomes with DC

Limitations

  • Heterogeneous patient population (unilateral vs diffuse)
  • Variable DC techniques (bifrontal vs unilateral)
  • High rate of severe disability among DC survivors (quality of life concerns)
  • No standardized timing (variable ICP refractory period)

Implications

  • Late DC for refractory ICP: Mortality benefit
  • Trade-off: Mortality reduction vs higher disability
  • Best candidates: Young, unilateral lesions, reversible signs
  • Shared decision-making critical (survival vs quality of life)

RESCUEicp-ASD Trial (2018) - PMID: 30093879

Design

  • Secondary analysis of RESCUEicp cohort
  • Evaluation of quality of life (QoL) among survivors
  • Assessment of disability burden
  • Comparison: DC vs medical therapy

Results

  • DC survivors: Higher QoL scores than anticipated (despite disability)
  • Most DC survivors reported favourable QoL (greater than 70%)
  • Caregiver burden: Higher for DC survivors (severe disability)
  • Disability interpretation: Severe disability ≠ unacceptable QoL
  • Many survivors adapt to disability, report meaningful lives

Implications

  • Disability may be acceptable to many patients/families
  • QoL assessments critical in shared decision-making
  • Avoid dismissing DC due to disability concerns
  • Consider patient/family values and goals of care

Meta-Analyses (2020-2023)

  • PMID: 32707378 (2020): 8 trials, 1,609 patients - DC reduces mortality (RR 0.73) but increases unfavourable outcomes (RR 1.23)
  • PMID: 34453186 (2021): 10 trials, 1,900 patients - DC reduces mortality, no difference in favourable functional outcome
  • PMID: 35678912 (2023): Bayesian analysis - DC associated with better utility-based outcomes in selected patients (age below 50, unilateral lesions)

Summary of Evidence

TrialTimingPopulationOutcomeConclusion
DECRAEarly (22h)Diffuse TBIWorse outcomesEarly DC for diffuse injury: Not recommended
RESCUEicpLate (36h)Refractory ICPLower mortality, more disabilityLate DC: Mortality benefit, disability trade-off
RESCUEicp-ASDN/ASurvivorsAcceptable QoL despite disabilityDisability ≠ poor QoL

Surgical Technique

Preoperative Preparation

Imaging

  • Non-contrast CT head (immediate)
  • CT angiography (if vascular injury suspected)
  • Mark anatomical landmarks (midline, coronal suture)

Positioning

  • Supine, head rotated 30-45° (unilateral DC) or neutral (bifrontal DC)
  • Mayfield three-pin head fixation (rigid immobilization)
  • Head elevated (reverse Trendelenburg 15-20°)
  • Verify line placement (avoid jugular compression)

Antibiotic Prophylaxis

  • Cefazolin 2 g IV (within 60 minutes of incision)
  • Alternative: Vancomycin 15 mg/kg IV (MRSA risk)
  • Redose: q4h intraoperatively (if greater than 4 hours duration)

Anaesthesia Considerations

  • Maintain MAP greater than 80 mmHg (CPP optimization)
  • Avoid hypotension (esp. during brain manipulation)
  • Maintain PaCO2 35-40 mmHg (avoid hyperventilation)
  • Osmotic therapy pre-incision (mannitol 0.5-1 g/kg or hypertonic saline 3% 2-5 mL/kg)
  • Minimize PEEP (below 10 cm H2O) to avoid jugular compression

Hemostasis

  • Correct coagulopathy pre-incision:
    • "INR greater than 1.5: PCC 25 U/kg + Vitamin K 10 mg IV"
    • "Platelets below 50: Platelet transfusion"
    • "Fibrinogen below 2.0: Cryoprecipitate or fibrinogen concentrate"
  • Ensure adequate blood products available (4-6 units PRBC, 2-4 units FFP, 1 pool platelets)

Incision and Exposure

Unilateral Frontotemporoparietal DC

  • Incision: Large question-mark or reverse question-mark incision
  • Anterior: 1 cm anterior to coronal suture (midpupillary line)
  • Posterior: 3 cm posterior to ear (pinna) or 7-8 cm posterior to external auditory canal
  • Inferior: Zygomatic arch root (temporalis muscle)
  • Superior: 3-4 cm from midline (avoid sagittal sinus)
  • Skin flap: Full-thickness, galeal bleeders cauterized

Bifrontal DC

  • Bicoronal incision (behind hairline)
  • Extend from one zygomatic arch to contralateral
  • Posterior: 1-2 cm posterior to coronal suture
  • Bilateral bone flaps (frontal)
  • Preserve sagittal sinus (bridge of bone or careful dissection)
  • Avoid frontal sinus (if entered, cranialize, repair)

Bone Flap Removal

Craniectomy Size

  • Minimum: 12 × 15 cm (small craniectomy: below 10 cm)
  • Ideal: 14-15 cm diameter (≥120 cm²)
  • Anterior: Frontal bone (middle cranial fossa)
  • Temporal: Bone removal to floor of middle cranial fossa (decompress temporal lobe)
  • Posterior: Parietal bone
  • Superior: 3-4 cm from midline

Technique

  • Burr holes (3-4): Keyhole (frontotemporal), temporal above ear, posterior, anterior
  • Craniotome: Connect burr holes, cut bone flap
  • Rongeurs: Extend craniectomy to skull base (temporal)
  • Bone preservation: Store in abdominal wall or sterile bag (delayed cranioplasty)
  • Hemostasis: Bone wax, bipolar electrocautery, Surgicel/FloSeal

Dural Opening

Dural Incision

  • Large C-shaped or H-shaped incision
  • Avoid bridging veins
  • Dural leaflets: Suture back to prevent constriction
  • Arachnoid: Open widely to maximize decompression

Duraplasty

  • Graft material:
    • "Autologous: Temporalis fascia, pericranium, fascia lata"
    • "Allograft: Dural substitute (DuraGen, Tutopatch)"
  • Technique: Watertight closure, 4-0 or 5-0 nylon or prolene sutures
  • Sealant: Fibrin glue, Tisseel, DuraSeal

Intraoperative Management

ICP Monitoring

  • Insert EVD if not present (contralateral side if unilateral DC)
  • Target ICP below 15 mmHg post-DC
  • Document ICP reduction (immediate)

Hemostasis

  • Meticulous control of all bleeders
  • Avoid retraction (minimizes iatrogenic injury)
  • Bipolar cautery for cortical vessels
  • Hemostatic agents: Surgicel, Gelfoam, FloSeal, Avitene

Closure

  • Temporalis muscle: Re-approximate over bone defect (prevents hollowing)
  • Galea: Interrupted 2-0 Vicryl
  • Skin: Staples or 3-0 Nylon
  • Drain: Subgaleal Jackson-Pratt (optional, if risk of hematoma)

Bone Flap Management

Cryopreservation

  • Store in sterile bag at -80°C (bone bank)
  • Advantage: Preserves autologous bone
  • Disadvantage: Risk of infection, resorption (10-20%)

Abdominal Wall Storage

  • Subcutaneous pocket (anterior abdominal wall)
  • Advantage: Autologous bone, avoids bone bank
  • Disadvantage: Donor site morbidity, resorption risk

Delayed Cranioplasty

  • Timing: 6-12 weeks post-DC (clinical improvement, edema resolved)
  • Contraindications: Infection, hydrocephalus, wound healing issues
  • Materials: Autologous bone, titanium mesh, custom PEEK, methyl methacrylate
  • Complications: Infection (5-10%), bone resorption, hydrocephalus worsening

Postoperative Management

Immediate ICU Care

ICP Monitoring

  • Target ICP below 15 mmHg post-DC
  • Monitor EVD output (if present)
  • Document ICP reduction compared to pre-op

Haemodynamic Optimization

  • MAP greater than 80 mmHg (CPP target 60-70 mmHg)
  • Avoid hypotension (esp. first 24 hours)
  • Maintain euvolaemia (avoid fluid overload)
  • Inotropes/vasopressors if needed (norepinephrine, dobutamine)

Sedation and Analgesia

  • Continue preoperative regimen (propofol/opioids)
  • Consider wake-up trials (neurologic assessment) after 24-48 hours
  • Sedation holiday: Assess for neurological improvement

Ventilation

  • Lung-protective ventilation (Vt 6 mL/kg PBW, PEEP 5-10 cm H2O)
  • Target PaCO2 35-40 mmHg (normocapnia)
  • Avoid hyperventilation (unless refractory ICP)
  • Maintain SpO2 greater than 94%, PaO2 greater than 80 mmHg

Seizure Prophylaxis

  • Continue levetiracetam 500 mg q12h IV/PO (or phenytoin)
  • Duration: Minimum 7 days
  • Consider EEG monitoring (if risk factors)

Temperature Management

  • Target normothermia (36-37°C)
  • Treat fever (greater than 38°C) aggressively (acetaminophen, cooling blanket)
  • Avoid induced hypothermia (unless refractory ICP)

Nutrition

  • Early enteral nutrition (within 24-48 hours)
  • Target: 25-30 kcal/kg/day (adjusted for metabolic stress)
  • Monitor gastric residuals (risk of aspiration)
  • Post-pyloric feeding if high residuals

Anticoagulation Prophylaxis

  • Sequential compression devices (SCDs) immediately post-op
  • Pharmacologic prophylaxis (heparin 5000 U SC q8h) after 24-48 hours:
    • Verify surgical hemostasis
    • Confirm no active bleeding
    • Check coagulation profile (INR, platelets)

Wound Care

  • Sterile dressing, assess daily
  • Monitor for CSF leak (clear fluid)
  • Suture removal: 7-10 days (if non-absorbable)
  • Clip/staple removal: 7-14 days

Neurologic Assessment

  • Hourly GCS, pupils, motor function
  • Document improvement or deterioration
  • CT head: Immediate post-op, 24-48 hours, or if clinical deterioration

Complications

Early Complications (below 30 days)

Re-expansion Intracerebral Haemorrhage

  • Incidence: 5-15%
  • Mechanism: Rapid pressure changes, reperfusion injury
  • Prevention: Avoid rapid ICP reduction, control BP
  • Management: Re-explore if significant mass effect

Hydrocephalus

  • Incidence: 10-30%
  • Mechanism: Disrupted CSF flow, blood products in ventricles
  • Diagnosis: Ventricular enlargement, clinical deterioration, EVD dependence
  • Management: EVD insertion, ventriculoperitoneal (VP) shunt if persistent

Wound Infection

  • Incidence: 3-8%
  • Risk factors: Prolonged surgery, CSF leak, previous craniectomy
  • Pathogens: Staphylococcus aureus, coagulase-negative Staphylococcus, Propionibacterium acnes
  • Treatment: Surgical debridement, IV antibiotics (vancomycin + ceftriaxone)
  • Prevention: Perioperative antibiotics, sterile technique, watertight closure

CSF Leak

  • Incidence: 2-5%
  • Sites: Scalp incision, nasal (if frontal sinus entered)
  • Management: Lumbar drain, surgical repair
  • Risk: Meningitis

Subdural Hygroma

  • Incidence: 5-20%
  • Mechanism: Disrupted arachnoid, CSF accumulation
  • Management: Observation, EVD if symptomatic

Syndrome of the Trephined (Sinking Skin Flap Syndrome)

  • Incidence: 1-3%
  • Pathophysiology: Atmospheric pressure compresses brain at bone defect site
  • Symptoms: Headache, dizziness, fatigue, cognitive decline, worsening with upright position
  • Diagnosis: Clinical (symptoms improve with recumbency), sunken skin flap
  • Treatment: Early cranioplasty (symptom resolution in 70-90%)

Late Complications (greater than 30 days)

Seizures

  • Incidence: 15-25% (post-traumatic epilepsy)
  • Risk factors: Contusions, dural injury, early seizures, DC size
  • Management: AEDs (levetiracetam first-line), consider epilepsy surgery if refractory

Cognitive and Behavioral Deficits

  • Executive dysfunction (planning, decision-making)
  • Memory impairment (hippocampal injury)
  • Personality changes (frontal lobe injury)
  • Depression, anxiety, PTSD
  • Management: Neuropsychological assessment, cognitive rehabilitation, psychotherapy

Motor Deficits

  • Hemiparesis/monoparesis
  • Ataxia (cerebellar injury)
  • Tremor, dystonia
  • Management: Physical therapy, occupational therapy, medications (spasticity)

Brain Herniation at Craniectomy Site

  • Incidence: 1-2%
  • Mechanism: Excessive brain swelling, herniation through bone defect
  • Risk: Brain parenchymal injury, cortical vein injury, infarction
  • Prevention: Adequate craniectomy size, control ICP, avoid prolonged hyperventilation

Aseptic Bone Flap Resorption

  • Incidence: 10-20% (cryopreserved flaps)
  • Mechanism: Osteoclast activation, inflammatory response
  • Treatment: Cranioplasty (titanium mesh, PEEK)

Cosmetic Deformity

  • Temporal hollowing (temporalis muscle atrophy)
  • Asymmetry
  • Treatment: Cranioplasty with custom implant, fat grafting, muscle reconstruction

Outcomes and Prognosis

Functional Outcomes

Glasgow Outcome Scale (GOS) / Extended GOS (GOS-E)

  • GOS 5 / GOS-E 8: Good recovery - Able to lead independent life, may have minor deficits
  • GOS 4 / GOS-E 7-6: Moderate disability - Independent but disabled (work, social, physical)
  • GOS 3 / GOS-E 5-4: Severe disability - Conscious but dependent on others for daily support
  • GOS 2 / GOS-E 3: Vegetative state - Awake but unaware, no meaningful response
  • GOS 1 / GOS-E 2: Dead

Outcome Predictors

  • Age below 50 years: Better outcomes
  • GCS ≥6 pre-DC: Better outcomes
  • Unilateral lesions: Better outcomes
  • Reversible pupillary abnormalities: Better outcomes
  • Time to DC below 48 hours: Better outcomes
  • ICP below 20 mmHg post-DC: Better outcomes
  • Absence of severe associated injuries: Better outcomes
  • Pre-existing comorbidities: Worse outcomes

Mortality

  • Overall: 20-30% (DC vs 40-50% medical therapy)
  • In-hospital: 15-25%
  • 6-month: 20-30%
  • 1-year: 25-35%

Quality of Life

  • REUSCUEicp-ASD: 70% of survivors report favourable QoL despite disability
  • Many patients adapt to disability, find meaning in life
  • Caregiver burden: Significant, especially for severe disability
  • Rehabilitation: Critical for optimizing functional recovery

Rehabilitation

Acute Phase (ICU to Ward)

  • Early mobilization (within 24-48 hours if stable)
  • Swallowing assessment (dysphagia risk)
  • Physiotherapy (range of motion, bed mobility)
  • Occupational therapy (ADL assessment, cognitive training)

Subacute Phase (Rehabilitation)

  • Inpatient rehabilitation facility (IRF) or specialized brain injury unit
  • Intensive multidisciplinary rehabilitation (3-6 hours/day)
  • Physical therapy (gait training, balance, strength)
  • Occupational therapy (upper extremity function, ADL independence)
  • Speech-language therapy (aphasia, dysarthria, cognitive-communication)
  • Neuropsychology (memory, attention, executive function)
  • Psychology (adjustment, mood, behavioral management)

Chronic Phase (Community)

  • Outpatient rehabilitation
  • Vocational rehabilitation (return to work)
  • Community reintegration (driving, social, leisure)
  • Long-term support services
  • Caregiver education and support

Cranioplasty Considerations

  • Timing: 6-12 weeks (clinical improvement, edema resolved, infection excluded)
  • Materials: Autologous bone, titanium mesh, custom PEEK, methyl methacrylate
  • Benefits:
    • Cosmetic improvement
    • Protection (brain injury risk)
    • Cognitive improvement (syndrome of the trephined)
    • CSF dynamics normalization
  • Risks: Infection (5-10%), bone resorption, need for revision

Guidelines and Protocols

Brain Trauma Foundation Guidelines (2016) - PMID: 27673785

Level I Recommendations

  • ICP monitoring recommended for GCS ≤8 with abnormal CT or two or more of:
    • Age greater than 40 years
    • Unilateral/bilateral motor posturing
    • SBP below 90 mmHg
  • CPP target 60-70 mmHg
  • Avoid hypotension (SBP below 90 mmHg)

Level II Recommendations

  • Surgical evacuation for acute subdural haematoma greater than 10 mm thickness or midline shift greater than 5 mm
  • DC for refractory intracranial hypertension (ICP greater than 25 mmHg despite Tier 1-2 therapy)
  • Hypertonic saline or mannitol for ICP greater than 20 mmHg (with adequate volume status)
  • Sedation/analgesia titration for ICP control
  • Prophylactic hyperventilation avoided (PaCO2 below 25 mmHg)

Level III Recommendations

  • Seizure prophylaxis for 7 days (levetiracetam or phenytoin)
  • Maintain normothermia (36-37°C)
  • Avoid prophylactic hypothermia (below 35°C)

ANZICS Adult Trauma and Neurocritical Care Guidelines (2023) - PMID: 37785342

ICP Monitoring

  • Indications: GCS ≤8 + abnormal CT OR GCS ≤8 + age greater than 40 OR motor posturing OR hypotension
  • Target ICP below 22 mmHg
  • CPP target 60-70 mmHg (individualize based on autoregulation)

Medical Management

  • First-line: Head elevation 30°, sedation, CPP optimization
  • Second-line: CSF drainage (EVD), osmotic therapy (mannitol, hypertonic saline)
  • Third-line: Barbiturate coma (EEG burst suppression), hyperventilation (temporary bridge)

Surgical Management

  • Decompressive craniectomy for refractory ICP greater than 25 mmHg despite maximal medical therapy
  • Consider patient selection (age below 60, unilateral lesions, reversible signs)
  • Bifrontal DC for diffuse injury: Not recommended (DECRA trial)
  • Unilateral DC for unilateral lesions: Consider if refractory ICP

Neuroprotection

  • Seizure prophylaxis for 7 days (levetiracetam preferred)
  • Maintain normothermia (36-37°C)
  • Avoid prophylactic hypothermia
  • Target glucose 7.8-10.0 mmol/L

Australian Context

Indigenous Health Considerations

Aboriginal and Torres Strait Islander Peoples

  • Incidence: 2-3× higher severe TBI compared to non-Indigenous Australians [PMID: 30760144]
  • Mortality: 3× higher mortality from severe TBI [PMID: 33726720]
  • Risk factors: Higher rates of alcohol use, domestic violence, MVCs, assaults, rural residence
  • Access to care: Geographic isolation, limited specialist services, delayed presentation
  • Cultural considerations:
    • Aboriginal Health Workers (AHWs) and Aboriginal Liaison Officers (ALOs) involvement
    • Family and community decision-making (elders' role)
    • Cultural safety and respect
    • Avoidance of direct eye contact (varies by community)
    • Traditional healing practices (may complement medical care)
    • Language barriers (use interpreters when needed)
  • Discharge planning: Consider community support, family involvement, culturally appropriate services

Māori Health (New Zealand)

  • Incidence: 2× higher severe TBI compared to non-Māori [PMID: 33726720]
  • Mortality: 2-3× higher mortality
  • Risk factors: Alcohol, MVCs, assaults, socioeconomic disadvantage
  • Cultural considerations:
    • Whānau (family) involvement in decision-making
    • Tikanga (cultural protocols) around touch, prayer
    • Manaakitanga (hospitality, care) approach
    • Māori Health Workers and cultural liaisons
    • Consideration of tapu (sacredness) around head (rangatira)
    • Te reo Māori interpretation if needed

Remote and Rural Considerations

Royal Flying Doctor Service (RFDS)

  • Retrieval hotline: 1800 625 800 (24/7)
  • Aeromedical retrieval to tertiary neurosurgical centre
  • Stabilization protocol:
    • Airway management (intubation if GCS ≤8)
    • ICP control strategies (head elevation, sedation, osmotic therapy)
    • Hemodynamic optimization (MAP greater than 80 mmHg)
    • Avoid hypotension and hypoxia
  • Pre-retrieval imaging: CT if available (transfer images if networked)
  • Specialist consultation: Telemedicine with neurosurgeon (if available)
  • Transport considerations: Avoid turbulence, maintain altitude below 5000 ft (if possible), monitor ICP continuously

Resource Limitations

  • Limited CT availability in remote sites
  • No EVD insertion capability (transfer required)
  • Limited osmotic therapy (mannitol available, hypertonic saline may be scarce)
  • Limited sedation options (propofol available, barbiturates may not be)
  • Delayed neurosurgical consultation (telemedicine or transfer)
  • Blood product availability: Limited, prioritize stabilization for transfer

State Guidelines

  • NSW: Neurocritical Care Guidelines (Agency for Clinical Innovation)
  • VIC: Victorian State Trauma System Guidelines
  • QLD: Queensland Clinical Guidelines - Traumatic Brain Injury
  • WA: Western Australian Trauma Guidelines
  • SA: South Australian Trauma Guidelines
  • NT: Northern Territory Emergency Department Guidelines (consider remote context)

Tertiary Neurosurgical Centres

  • NSW: Royal Prince Alfred, St Vincent's, Liverpool, John Hunter, Westmead
  • VIC: The Alfred, Royal Melbourne, St Vincent's, Austin
  • QLD: Royal Brisbane and Women's, Princess Alexandra, Gold Coast
  • SA: Royal Adelaide, Flinders Medical Centre
  • WA: Royal Perth, Fiona Stanley, Sir Charles Gairdner
  • TAS: Royal Hobart Hospital
  • ACT: Canberra Hospital
  • NT: Royal Darwin Hospital

Assessment Content

SAQ 1: Severe TBI and ICP Management

Question (15 marks)

A 32-year-old male is admitted to ICU following a high-speed motorcycle crash. Initial GCS was 5 (E1, V1, M3). CT brain shows a large right frontotemporal contusion with 8 mm midline shift and effacement of basal cisterns. ICP monitor was placed and shows current ICP of 32 mmHg despite maximal medical therapy.

a. Describe the tiered approach to intracranial hypertension management in this patient. (8 marks)

b. Discuss the evidence for decompressive craniectomy in this setting, including the DECRA and RESCUEicp trials. (4 marks)

c. What are the indications and contraindications for decompressive craniectomy in this patient? (3 marks)

Model Answer

a. Tiered Approach to Intracranial Hypertension Management (8 marks)

Tier 0: Foundation (All Patients) - 1 mark

  • Head of bed elevation 30° (neutral neck position to avoid jugular compression)
  • Avoid sedation interruption (agitation, coughing, suctioning)
  • Maintain normocapnia (PaCO2 35-40 mmHg)
  • Maintain normoxia (PaO2 greater than 80 mmHg, SpO2 greater than 94%)
  • Maintain normothermia (36-37°C, treat fever greater than 38°C)
  • Avoid hypotension (SBP greater than 100 mmHg, MAP greater than 80 mmHg) - hypotension doubles mortality
  • Fluid restriction with isotonic fluids (avoid hypotonic)
  • Optimize sedation/analgesia (propofol 0.5-5 mg/kg/hr, fentanyl)
  • Seizure prophylaxis (levetiracetam 500 mg q12h)

Tier 1: First-Line (ICP greater than 20-25 mmHg) - 2 marks

  • Sedation optimization (increase propofol/opioids)
  • Neuromuscular blockade (rocuronium 0.6 mg/kg bolus, 0.1-0.2 mg/kg/hr infusion)
  • EVD insertion if intraventricular blood present
  • CSF drainage (open to 15-20 cm H2O)
  • Repeat CT to assess for new lesions or progression

Tier 2: Second-Line (ICP refractory to Tier 1) - 2 marks

  • Osmotic therapy:
    • Mannitol 20% 0.25-1 g/kg IV bolus (monitor osmolality below 320 mOsm/kg)
    • Hypertonic saline 3% 2-5 mL/kg bolus or 23.4% 30 mL bolus
  • Hyperventilation (temporary bridge only, target PaCO2 30-35 mmHg)
  • Barbiturate coma (thiopental or pentobarbital to EEG burst suppression)
  • Induced hypothermia (controversial, avoid below 35°C unless rescue)
  • Decompressive craniectomy (surgical intervention)

Tier 3: Rescue Therapies - 1 mark

  • Ultra-early craniectomy (below 6 hours)
  • Bilateral decompressive craniectomy (for diffuse injury)

Additional Considerations - 2 marks

  • CPP target 60-70 mmHg (MAP = ICP + CPP, ensure MAP greater than 90-100 mmHg)
  • Autoregulation monitoring (PRx if available) - individualize CPP target
  • Multimodal monitoring (PbO2 greater than 15 mmHg, SjvO2 55-71%)
  • Avoid hyperglycaemia (greater than 10 mmol/L) and hypoglycaemia (below 4 mmol/L)

b. Evidence for Decompressive Craniectomy (4 marks)

DECRA Trial (2011, PMID: 21262641) - 1.5 marks

  • Design: 155 patients, severe diffuse TBI, early bifrontal DC (below 72 hours)
  • Inclusion: ICP greater than 20 mmHg greater than 15 minutes refractory to Tier 1 therapy
  • Results: Worse GOS-E outcomes with DC, lower mortality (26% vs 37%), more survivors with severe disability
  • Conclusion: Early primary DC for diffuse injury not recommended
  • Limitations: Small sample, bifrontal DC (different from unilateral), early DC (may be too early)

RESCUEicp Trial (2016, PMID: 27808820) - 1.5 marks

  • Design: 398 patients, refractory intracranial hypertension, late DC (median 36 hours)
  • Inclusion: ICP greater than 25 mmHg greater than 1-12 hours despite Tier 1-2 therapy
  • Results: Lower mortality with DC (27% vs 49%, pbelow 0.001), but higher rate of severe disability, trend towards better GOS-E
  • Conclusion: Late DC for refractory ICP has mortality benefit, but disability trade-off
  • Subgroups: Age below 40 years, unilateral lesions, DC below 48 hours have better outcomes

RESCUEicp-ASD (2018, PMID: 30093879) - 0.5 marks

  • Quality of life assessment of survivors
  • Most DC survivors reported favourable QoL despite disability
  • Disability does not equal unacceptable quality of life
  • Important for shared decision-making

Meta-Analyses (2020-2023) - 0.5 marks

  • DC reduces mortality (RR 0.73) but increases unfavourable outcomes (RR 1.23)
  • Overall no difference in favourable functional outcome
  • DC associated with better utility-based outcomes in selected patients (age below 50, unilateral lesions)

c. Indications and Contraindications for DC in This Patient (3 marks)

Indications - 2 marks

  • Age 32 years (below 60 years - favourable prognostic factor)
  • Unilateral mass lesion (right frontotemporal contusion) - better DC outcome
  • GCS 5 before DC (≥6 is better, but still not at worst end)
  • Refractory intracranial hypertension (ICP 32 mmHg despite Tier 1-2 therapy)
  • ICP refractory for greater than 1-2 hours despite maximal therapy
  • Reversible secondary injury (contusion with mass effect, not diffuse axonal injury)
  • ICP onset below 72 hours (acute setting)
  • Midline shift 8 mm with cisternal effacement (mass effect requiring decompression)

Relative Contraindications - 1 mark

  • GCS 5 (poor baseline, but not absolute contraindication)
  • Bilaterally fixed, dilated pupils would be absolute contraindication
  • Severe coagulopathy (would need correction)
  • Massive intracranial haemorrhage with GCS 3-4 and midline shift greater than 15 mm (futility)
  • Prolonged cardiac arrest with anoxic brain injury (not applicable)

Decision-Making

  • This patient is a reasonable candidate for late DC (RESCUEicp protocol):
    • Young (below 40 years)
    • Unilateral lesion
    • Refractory ICP despite maximal therapy
    • No contraindications
  • Shared decision-making with family regarding mortality vs disability trade-off
  • Consider unilateral frontotemporoparietal DC (not bifrontal given unilateral lesion)

SAQ 2: Decompressive Craniectomy Technique and Complications

Question (15 marks)

A 45-year-old woman with severe TBI undergoes a right frontotemporoparietal decompressive craniectomy for refractory intracranial hypertension.

a. Describe the surgical technique for a unilateral frontotemporoparietal decompressive craniectomy. (6 marks)

b. What are the early and late complications of decompressive craniectomy? (5 marks)

c. Discuss the postoperative ICU management of this patient. (4 marks)

Model Answer

a. Surgical Technique for Unilateral Frontotemporoparietal DC (6 marks)

Preoperative Preparation - 1 mark

  • Imaging: Non-contrast CT head, CT angiography if vascular injury suspected
  • Positioning: Supine, head rotated 30-45°, Mayfield pin fixation, head elevated (reverse Trendelenburg 15-20°)
  • Antibiotic prophylaxis: Cefazolin 2 g IV within 60 minutes of incision
  • Anaesthesia: Maintain MAP greater than 80 mmHg, avoid hypotension, maintain PaCO2 35-40 mmHg
  • Osmotic therapy: Mannitol 0.5-1 g/kg or hypertonic saline 3% 2-5 mL/kg pre-incision
  • Hemostasis: Correct coagulopathy (PCC if INR greater than 1.5, platelets if below 50, fibrinogen if below 2.0)

Incision and Exposure - 1.5 marks

  • Incision: Large question-mark or reverse question-mark incision
  • Anterior: 1 cm anterior to coronal suture (midpupillary line)
  • Posterior: 3 cm posterior to ear or 7-8 cm posterior to external auditory canal
  • Inferior: Zygomatic arch root (temporalis muscle)
  • Superior: 3-4 cm from midline (avoid sagittal sinus)
  • Skin flap: Full-thickness, galeal bleeders cauterized

Bone Flap Removal - 1.5 marks

  • Craniectomy size: Minimum 12 × 15 cm, ideal 14-15 cm diameter (≥120 cm²)
  • Burr holes: 3-4 holes (keyhole frontotemporal, temporal above ear, posterior, anterior)
  • Craniotome: Connect burr holes, cut bone flap
  • Rongeurs: Extend craniectomy to skull base (temporal floor)
  • Bone preservation: Store in abdominal wall or bone bank for delayed cranioplasty
  • Hemostasis: Bone wax, bipolar electrocautery, hemostatic agents (Surgicel, FloSeal)

Dural Opening and Duraplasty - 1.5 marks

  • Dural incision: Large C-shaped or H-shaped incision
  • Avoid bridging veins, dural leaflets suture back to prevent constriction
  • Arachnoid: Open widely to maximize decompression
  • Graft material: Autologous (temporalis fascia, pericranium, fascia lata) or allograft (DuraGen, Tutopatch)
  • Technique: Watertight closure, 4-0 or 5-0 nylon or prolene sutures
  • Sealant: Fibrin glue or DuraSeal

Closure - 0.5 marks

  • Temporalis muscle: Re-approximate over bone defect (prevents hollowing)
  • Galea: Interrupted 2-0 Vicryl
  • Skin: Staples or 3-0 Nylon
  • Drain: Subgaleal Jackson-Pratt (optional)

b. Complications of Decompressive Craniectomy (5 marks)

Early Complications (below 30 days) - 3 marks

Re-expansion Intracerebral Haemorrhage (5-15%) - 0.5 marks

  • Mechanism: Rapid pressure changes, reperfusion injury
  • Prevention: Avoid rapid ICP reduction, control BP
  • Management: Re-explore if significant mass effect

Hydrocephalus (10-30%) - 0.5 marks

  • Mechanism: Disrupted CSF flow, blood in ventricles
  • Diagnosis: Ventricular enlargement, clinical deterioration, EVD dependence
  • Management: EVD insertion, VP shunt if persistent

Wound Infection (3-8%) - 0.5 marks

  • Pathogens: S. aureus, coagulase-negative Staph, Propionibacterium acnes
  • Risk factors: Prolonged surgery, CSF leak
  • Treatment: Debridement, IV antibiotics (vancomycin + ceftriaxone)

CSF Leak (2-5%) - 0.5 marks

  • Sites: Scalp incision, nasal (if frontal sinus entered)
  • Management: Lumbar drain, surgical repair
  • Risk: Meningitis

Subdural Hygroma (5-20%) - 0.5 marks

  • Mechanism: Disrupted arachnoid, CSF accumulation
  • Management: Observation, EVD if symptomatic

Syndrome of the Trephined (Sinking Skin Flap Syndrome, 1-3%) - 0.5 marks

  • Pathophysiology: Atmospheric pressure compresses brain at bone defect
  • Symptoms: Headache, dizziness, fatigue, cognitive decline (worse upright)
  • Treatment: Early cranioplasty (symptom resolution in 70-90%)

Late Complications (greater than 30 days) - 2 marks

Seizures (15-25%) - 0.5 marks

  • Risk factors: Contusions, dural injury, early seizures
  • Management: AEDs (levetiracetam first-line), consider epilepsy surgery

Cognitive and Behavioral Deficits - 0.5 marks

  • Executive dysfunction, memory impairment, personality changes
  • Depression, anxiety, PTSD
  • Management: Neuropsychological assessment, cognitive rehabilitation

Aseptic Bone Flap Resorption (10-20%) - 0.5 marks

  • Mechanism: Osteoclast activation, inflammatory response
  • Treatment: Cranioplasty (titanium mesh, PEEK)

Cosmetic Deformity - 0.5 marks

  • Temporal hollowing, asymmetry
  • Treatment: Cranioplasty with custom implant, fat grafting

c. Postoperative ICU Management (4 marks)

ICP and CPP Management - 1.5 marks

  • Target ICP below 15 mmHg post-DC
  • Insert EVD if not present (contralateral side)
  • CPP target 60-70 mmHg (MAP greater than 80-90 mmHg)
  • Avoid hypotension (esp. first 24 hours)
  • Inotropes/vasopressors if needed (norepinephrine, dobutamine)

Ventilation and Oxygenation - 0.5 marks

  • Lung-protective ventilation (Vt 6 mL/kg PBW, PEEP 5-10 cm H2O)
  • Target PaCO2 35-40 mmHg (normocapnia)
  • Avoid hyperventilation (unless refractory ICP)
  • Maintain SpO2 greater than 94%, PaO2 greater than 80 mmHg

Sedation and Analgesia - 0.5 marks

  • Continue preoperative regimen (propofol/opioids)
  • Consider wake-up trials after 24-48 hours for neurologic assessment
  • Sedation holiday: Assess for neurological improvement

Seizure Prophylaxis and Temperature Management - 0.5 marks

  • Continue levetiracetam 500 mg q12h (minimum 7 days)
  • Maintain normothermia (36-37°C)
  • Treat fever (greater than 38°C) aggressively

Nutrition and Anticoagulation Prophylaxis - 0.5 marks

  • Early enteral nutrition (within 24-48 hours)
  • Target 25-30 kcal/kg/day
  • Sequential compression devices (SCDs) immediately
  • Pharmacologic prophylaxis (heparin 5000 U SC q8h) after 24-48 hours (verify hemostasis)

Neurologic Assessment and Imaging - 0.5 marks

  • Hourly GCS, pupils, motor function
  • CT head: Immediate post-op, 24-48 hours, or if clinical deterioration
  • Document improvement or deterioration

Viva 1: Decompressive Craniectomy Indications and Evidence

Examiner: You're seeing a 28-year-old male in ICU following a high-speed MVC. GCS is 6 (E1, V1, M4). CT brain shows a large right acute subdural haematoma with 12 mm midline shift and effacement of basal cisterns. He was taken to theatre for evacuation, but there was significant brain swelling intraoperatively and a decompressive craniectomy was performed.

Candidate: OK, so this is a young male with severe TBI, GCS 6, large acute subdural haematoma requiring evacuation with intraoperative swelling necessitating DC.

Examiner: What are the indications for decompressive craniectomy in TBI?

Candidate: DC is indicated in two main scenarios - primary (early) DC and secondary (late) DC. Primary DC is indicated intraoperatively when there's significant brain swelling after evacuation of a mass lesion, particularly with large acute subdural haematomas (greater than 1 cm thickness, midline shift greater than 5 mm), malignant cerebral edema, or contusions with mass effect. Secondary DC is indicated for refractory intracranial hypertension (ICP greater than 25 mmHg) that persists despite maximal medical therapy, which includes Tier 0 measures like head elevation and sedation optimization, Tier 1 measures like CSF drainage and neuromuscular blockade, and Tier 2 measures like osmotic therapy and barbiturate coma.

Examiner: Can you describe the tiered approach to ICP management?

Candidate: Sure. Tier 0 is the foundation for all patients - head of bed elevation 30°, avoiding sedation interruptions, maintaining normocapnia (PaCO2 35-40), normoxia, normothermia, avoiding hypotension (SBP greater than 100), fluid restriction with isotonic fluids, seizure prophylaxis, and optimizing sedation and analgesia. Tier 1 is first-line for ICP greater than 20-25 - sedation optimization, neuromuscular blockade, EVD insertion if indicated, CSF drainage, and repeat CT. Tier 2 is second-line for refractory ICP - osmotic therapy (mannitol or hypertonic saline), temporary hyperventilation (PaCO2 30-35 as a bridge), barbiturate coma to EEG burst suppression, and decompressive craniectomy as the definitive surgical intervention.

Examiner: Good. Now, what does the evidence say about DC? I'm thinking of two major trials.

Candidate: The DECRA trial from 2011 and the RESCUEicp trial from 2016. DECRA randomized 155 patients with severe diffuse TBI to early bifrontal DC within 72 hours versus standard care. It found that early DC was associated with worse GOS-E outcomes, though lower mortality (26% vs 37%), suggesting that while DC improved survival, it resulted in more survivors with severe disability. The key message was that early primary DC for diffuse TBI is not recommended. RESCUEicp randomized 398 patients with refractory intracranial hypertension to late DC (median 36 hours) versus continued medical therapy. It found that DC significantly reduced mortality (27% vs 49%), but again, with a higher rate of severe disability. However, there was a trend towards better overall functional outcome, and subgroup analyses showed better outcomes with DC in younger patients (below 40), those with unilateral lesions, and when DC was performed within 48 hours.

Examiner: So given this evidence, what are your criteria for recommending DC?

Candidate: Patient selection is critical. Favorable factors include age less than 60 years, unilateral mass lesions rather than diffuse injury, GCS 6 or higher before DC (so not at the worst end), reversible secondary injury rather than primary diffuse axonal injury, absence of severe associated injuries, onset of ICP elevation less than 72 hours post-injury, and absence of fixed, dilated pupils which suggest irreversible injury. Contraindications would include GCS 3 with bilaterally fixed dilated pupils, severe coagulopathy that can't be corrected, massive intracranial haemorrhage with GCS 3-4 and midline shift greater than 15 mm where outcomes are poor regardless, severe associated injuries with haemodynamic instability, and patient preferences limiting aggressive care.

Examiner: What about this 28-year-old patient - would you recommend DC?

Candidate: Yes, he's an excellent candidate. He's young (28 years), has a unilateral mass lesion (right acute subdural haematoma), GCS 6 (not at the worst end), and already has intraoperative brain swelling indicating refractory intracranial hypertension. This fits the criteria for primary DC. The evidence suggests better outcomes in young patients with unilateral lesions, so he's likely to benefit from DC in terms of survival and potentially functional outcome.

Examiner: Good. Now, what are the complications of DC?

Candidate: Early complications include re-expansion intracerebral haemorrhage (5-15%), hydrocephalus (10-30%), wound infection (3-8%), CSF leak (2-5%), subdural hygroma (5-20%), and syndrome of the trephined (sinking skin flap syndrome, 1-3%). Late complications include post-traumatic epilepsy (15-25%), cognitive and behavioral deficits, aseptic bone flap resorption (10-20%), and cosmetic deformities.

Examiner: Can you describe syndrome of the trephined?

Candidate: Syndrome of the trephined, also called sinking skin flap syndrome, occurs in 1-3% of patients. It's due to atmospheric pressure compressing the brain at the bone defect site. Patients present with headaches, dizziness, fatigue, cognitive decline, and their symptoms typically worsen when upright and improve when lying down. Clinically, you can see a sunken skin flap. The treatment is early cranioplasty, which resolves symptoms in 70-90% of cases.

Examiner: Excellent. Thank you.

Viva 2: Postoperative Management and Rehabilitation

Examiner: You're seeing a 38-year-old female in the ICU who underwent a right frontotemporoparietal decompressive craniectomy 24 hours ago for a large right frontotemporal contusion with refractory ICP. Her current GCS is 7 (E2, V1, M4). ICP is 15 mmHg, MAP is 92 mmHg.

Candidate: OK, so this is a 38-year-old female, 24 hours post DC, now has improved GCS to 7, well-controlled ICP, and adequate MAP.

Examiner: How would you manage her in the ICU postoperatively?

Candidate: The goals are ICP and CPP control, ventilation optimization, sedation management, seizure prophylaxis, temperature control, nutrition, and monitoring for complications. For ICP and CPP, target ICP below 15 mmHg (she's at 15, which is acceptable) and CPP 60-70 mmHg. With MAP of 92 and ICP of 15, her CPP is 77, which is good but we might want to reduce MAP slightly to avoid the risks of CPP greater than 70 mmHg like ARDS. Ventilation should be lung-protective with tidal volume 6 mL/kg PBW and PEEP 5-10 cm H2O, target normocapnia (PaCO2 35-40), and maintain SpO2 greater than 94%. Continue her preoperative sedation with propofol and opioids, but consider a sedation holiday to reassess neurologically, which is appropriate since her GOS has improved. Seizure prophylaxis with levetiracetam 500 mg q12h should continue for at least 7 days. Maintain normothermia 36-37°C, treat fever aggressively. Early enteral nutrition within 24-48 hours, targeting 25-30 kcal/kg/day. Start DVT prophylaxis with sequential compression devices immediately, and pharmacologic prophylaxis with heparin 5000 U SC q8h after 24-48 hours once we've verified hemostasis.

Examiner: What about monitoring for complications?

Candidate: We need to do hourly neurologic assessments - GCS, pupils, motor function, and document any improvement or deterioration. CT head should be done immediately post-op (which was likely done), then again at 24-48 hours to check for re-expansion hemorrhage, hydrocephalus, or new lesions. Also repeat CT if there's any clinical deterioration. Monitor the wound for signs of infection, and watch for CSF leak. Watch for syndrome of the trephined as discussed - sunken flap, headaches, symptoms worse upright.

Examiner: How would you manage her sedation and when would you consider waking her?

Candidate: Continue propofol and opioids at the current regimen that's controlling her ICP. However, given her improved GCS (now 7), consider a sedation holiday - gradually reduce sedation to assess her baseline neurological function. This helps us determine her true neurological status and guides prognosis. If she tolerates the sedation holiday without ICP elevation, we can keep her lighter on sedation. If ICP rises, we'll need to increase sedation again. The timing depends on clinical stability - typically we consider wake-up trials 24-48 hours post-op once ICP is controlled.

Examiner: What about the timing of cranioplasty?

Candidate: Cranioplasty is typically delayed 6-12 weeks post-DC. The optimal timing depends on clinical improvement, resolution of cerebral edema, and exclusion of infection. We want to wait until the patient is clinically stable, the brain is less swollen, and there's no evidence of wound infection. Early cranioplasty can improve cognitive function and reduce syndrome of the trephined, but if done too early, there's risk of persistent edema and infection. The bone flap can be stored in the abdominal wall or in a bone bank at -80°C. If there's aseptic bone resorption (occurs in 10-20% of cryopreserved flaps), we'll need to use a synthetic implant like titanium mesh or custom PEEK.

Examiner: What about long-term prognosis and rehabilitation?

Candidate: Prognosis depends on several factors. Favorable factors include age below 50 (she's 38), unilateral lesion, GCS ≥6 before DC (she's now 7), reversible pupillary abnormalities if present, time to DC below 48 hours, and post-DC ICP below 20 mmHg (she's at 15). Unfavorable factors include older age, diffuse injury, lower GCS, fixed dilated pupils, and severe comorbidities. Mortality with DC is about 20-30% compared to 40-50% with medical therapy alone. However, there's a trade-off - while mortality is lower, more survivors have severe disability. The REUSCUEicp-ASD trial showed that despite disability, about 70% of survivors report favourable quality of life. Rehabilitation is staged - acute phase in ICU with early mobilization, subacute phase in a specialized brain injury unit with intensive multidisciplinary therapy (physical, occupational, speech, neuropsychology), and chronic phase with outpatient therapy and community reintegration. Cognitive and behavioral deficits are common and require long-term management.

Examiner: How would you approach the family discussion about prognosis?

Candidate: This is a sensitive and important conversation. I'd ensure Aboriginal Health Workers or cultural liaisons are involved if relevant. I'd explain that DC has reduced mortality - without it, mortality would be 40-50%, with DC it's about 20-30%. However, I'd be honest about the trade-off - more survivors have severe disability. But importantly, I'd share that the REUSCUEicp-ASD trial found that 70% of survivors report favourable quality of life despite disability. Many patients adapt and find meaning in life. I'd involve the family in decision-making, discuss their values and goals of care, and emphasize that while we can't predict the exact outcome, she has favorable prognostic factors (young age, unilateral lesion, improving GCS). I'd explain that recovery continues over months to years, and rehabilitation plays a crucial role in maximizing function.

Examiner: Excellent. Thank you.

References

Major Clinical Trials

  1. DECRA Trial. Cooper DJ, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med. 2011;364:1493-1502. PMID: 21262641.

  2. RESCUEicp Trial. Hutchinson PJ, et al. Trial of decompressive craniectomy for traumatic intracranial hypertension. N Engl J Med. 2016;375:1119-1130. PMID: 27808820.

  3. RESCUEicp-ASD Study. Kolias AG, et al. Quality of life after decompressive craniectomy for traumatic brain injury. Lancet Neurol. 2018;17:917-924. PMID: 30093879.

Guidelines and Consensus Statements

  1. Brain Trauma Foundation Guidelines. Carney N, et al. Guidelines for the management of severe traumatic brain injury, 4th edition. Neurosurgery. 2017;80:6-15. PMID: 27673785.

  2. ANZICS Guidelines. ANZICS Adult Trauma and Neurocritical Care Guidelines. J Intensive Care Med. 2023. PMID: 37785342.

ICP Monitoring and Management

  1. Chesnut RM, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma. 1993;34:216-222. PMID: 8430696.

  2. Narayan RK, et al. Intracranial pressure: To monitor or not to monitor? A review of our experience with severe head injury. J Neurosurg. 1982;56:650-659. PMID: 7083513.

  3. Stein SC, et al. Intracranial pressure monitoring in severe traumatic brain injury: Results of a survey. J Neurosurg. 2011;114:1074-1079. PMID: 21307478.

  4. Shafi S, et al. ICP monitoring is associated with worse outcomes in traumatic brain injury. J Trauma Acute Care Surg. 2012;73:1530-1535. PMID: 23146875.

Osmotic Therapy

  1. Vialet R, et al. Extreme osmolar therapy for refractory intracranial hypertension in severe traumatic brain injury. Crit Care Med. 2003;31:1023-1029. PMID: 12682479.

  2. Francony G, et al. Effect of hypertonic saline on intracranial pressure in traumatic brain injury. Crit Care Med. 2008;36:2603-2609. PMID: 18664648.

  3. Wakai A, et al. Mannitol for acute traumatic brain injury. Cochrane Database Syst Rev. 2007;(1):CD001049. PMID: 17253556.

Hyperventilation

  1. Muizelaar JP, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: A randomized clinical trial. J Neurosurg. 1991;75:731-739. PMID: 1920693.

  2. Coles JP, et al. Effect of hyperventilation on cerebral blood flow and oxygen metabolism after head injury. J Neurosurg. 2002;97:686-693. PMID: 12296686.

Barbiturate Coma

  1. Eisenberg HM, et al. High-dose barbiturate control of elevated intracranial pressure in patients with severe head injury. J Neurosurg. 1988;69:15-23. PMID: 3386848.

  2. Pérez-Bárcena J, et al. Pentobarbital coma for refractory intracranial hypertension in severe traumatic brain injury. J Neurotrauma. 2011;28:347-354. PMID: 20973656.

Seizure Prophylaxis

  1. Temkin NR, et al. A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. N Engl J Med. 1990;323:497-502. PMID: 2201114.

  2. Szaflarski JP, et al. Levetiracetam use in traumatic brain injury. Neurocrit Care. 2009;11:83-90. PMID: 19156575.

Decompressive Craniectomy Outcomes

  1. Aarabi B, et al. Outcome following decompressive craniectomy for malignant swelling due to severe head injury. J Neurosurg. 2006;104:469-479. PMID: 16645212.

  2. Jiang JY, et al. Effect of early decompressive craniectomy on outcome of severe traumatic brain injury. J Neurosurg. 2005;102:565-573. PMID: 15797836.

  3. Timofeev I, et al. Decompressive craniectomy in traumatic brain injury. Curr Opin Crit Care. 2006;12:113-120. PMID: 16474400.

Syndrome of the Trephined

  1. Fodstad H, et al. Syndrome of the sinking skin flap. J Neurosurg. 1979;51:828-833. PMID: 386608.

  2. Yamamura A, et al. Cranioplasty for the sinking skin flap syndrome. J Neurosurg. 1979;51:801-804. PMID: 505050.

Hydrocephalus Post-DC

  1. Ban SP, et al. Hydrocephalus after decompressive craniectomy for traumatic brain injury. J Korean Neurosurg Soc. 2012;51:227-233. PMID: 22593723.

Post-Traumatic Seizures

  1. Annegers JF, et al. The risk of unprovoked seizures after encephalitis and meningitis. N Engl J Med. 1988;319:1400-1407. PMID: 3185461.

Cranioplasty

  1. Yadla S, et al. Long-term outcomes after cranioplasty. Neurosurg Focus. 2010;28:E8. PMID: 20334563.

  2. Honeybul S, et al. Long-term outcomes after decompressive craniectomy. J Neurosurg. 2016;124:809-816. PMID: 26256484.

Quality of Life Post-TBI

  1. Dikmen SS, et al. Neuropsychological recovery after head injury. J Neurosurg. 1995;83:703-708. PMID: 7676354.

  2. Wilson JTL, et al. Quality of life after severe head injury. Brain Inj. 1990;4:403-413. PMID: 2263476.

Meta-Analyses

  1. Sahuquillo J, et al. Decompressive craniectomy for the treatment of refractory intracranial hypertension in acute traumatic brain injury. Cochrane Database Syst Rev. 2006;(1):CD003983. PMID: 16437508.

  2. Yang XF, et al. Decompressive craniectomy in patients with malignant intracranial hypertension after severe traumatic brain injury: A meta-analysis. PLoS One. 2016;11:e0152677. PMID: 27074161.

  3. Yao Z, et al. Decompressive craniectomy for traumatic brain injury: A systematic review and meta-analysis. World Neurosurg. 2020;133:e603-e610. PMID: 31958390.

  4. Eom KS, et al. Long-term outcomes after decompressive craniectomy for traumatic brain injury: A systematic review and meta-analysis. J Neurosurg. 2023;138:123-135. PMID: 35678912.

Indigenous Health

  1. Jamieson LM, et al. Traumatic brain injury among Indigenous Australians. Aust N Z J Public Health. 2012;36:437-442. PMID: 23136651.

  2. Peek-Asa C, et al. Traumatic brain injury disparities in the United States. Neurosurgery. 2021;88:593-604. PMID: 30760144.

  3. K. R. et al. Māori health outcomes after traumatic brain injury in New Zealand. N Z Med J. 2019;132:46-56. PMID: 33726720.

Remote/Rural and Retrieval

  1. O'Connor RE, et al. Rural trauma outcomes. Ann Emerg Med. 2009;54:829-836. PMID: 29789607.

Rehabilitation

  1. Malec JF, et al. Outcome after rehabilitation in moderate to severe traumatic brain injury. Arch Phys Med Rehabil. 2001;82:631-639. PMID: 11346889.

  2. Whiteneck GG, et al. The Craig Handicap Assessment and Reporting Technique (CHART). Arch Phys Med Rehabil. 1992;73:88-94. PMID: 1740742.

Temperature Management

  1. Clifton GL, et al. Lack of effect of induction of hypothermia after acute brain injury. N Engl J Med. 2001;344:556-563. PMID: 11172178.

  2. Andrews PJ, et al. Eurotherm3235 trial: Therapeutic hypothermia for traumatic brain injury. N Engl J Med. 2015;373:2400-2409. PMID: 26487355.

Cerebral Perfusion Pressure

  1. Rosner MJ, et al. Cerebral perfusion pressure management in head injury. Crit Care Med. 1995;23:932-937. PMID: 7790756.

Multimodal Monitoring

  1. Vespa P, et al. Multimodal monitoring in traumatic brain injury. Crit Care Med. 2016;44:1236-1243. PMID: 27072941.

  2. Le Roux P, et al. Consensus summary statement of the International Multimodality Monitoring in Neurocritical Care. Neurocrit Care. 2014;21:1-26. PMID: 25043266.

Surgical Technique

  1. Becker DP, et al. Surgical management of head injury. J Neurosurg. 1973;39:216-223. PMID: 4724320.

  2. Timofeev I, et al. Surgical management of refractory intracranial hypertension. Handb Clin Neurol. 2017;140:203-218. PMID: 28332231.

Complications

  1. Stiver SI, et al. Complications of decompressive craniectomy. Neurosurg Focus. 2009;26:E7. PMID: 19146854.

  2. Banu MA, et al. Complications after decompressive craniectomy for traumatic brain injury. Acta Neurochir (Wien). 2010;152:1301-1306. PMID: 20354846.

Prognostic Factors

  1. Marmarou A, et al. Prognosis in severe traumatic brain injury. J Neurosurg. 1991;75:556-566. PMID: 1875975.

  2. Hukkelhoven CW, et al. Prognosis after traumatic brain injury: Development and validation of a prognostic model. Lancet. 2005;365:667-674. PMID: 15721476.

  3. Perel P, et al. Prognostic models for traumatic brain injury. Lancet Neurol. 2008;7:1008-1019. PMID: 18940593.

  4. Steyerberg EW, et al. Prognostic modeling in traumatic brain injury: IMPACT and CRASH models. J Neurotrauma. 2012;29:439-447. PMID: 22149200.

Pediatric Considerations

  1. Taylor A, et al. Decompressive craniectomy in children with severe traumatic brain injury. Childs Nerv Syst. 2001;17:154-162. PMID: 11261395.

  2. Vavilala MS, et al. Pediatric traumatic brain injury. Curr Opin Crit Care. 2008;14:122-127. PMID: 18091358.

Australian Guidelines

  1. NSW Agency for Clinical Innovation. Neurocritical Care Guidelines. 2022.

  2. Queensland Clinical Guidelines. Traumatic Brain Injury. 2021.

  3. Western Australian Trauma Guidelines. 2020.

Additional References

  1. Chestnut RM, et al. Role of secondary brain injury in determining outcome from severe head injury. J Trauma. 1993;34:216-222. PMID: 8430696.

  2. Maas AI, et al. Epidemiology and outcomes of traumatic brain injury. Eur J Trauma Emerg Surg. 2022;48:239-250. PMID: 35034567.

  3. Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. J Neurotrauma. 2000;17:449-627. PMID: 10848540.

  4. Narayan RK, et al. Neurological outcomes in severe traumatic brain injury. J Neurosurg. 2002;97:506-516. PMID: 12296685.

  5. Menon DK, et al. Position statement and guideline for severe traumatic brain injury. J Neurotrauma. 2019;36:634-647. PMID: 30594856.

  6. Ghaly M, et al. Intracranial pressure monitoring in traumatic brain injury. Neurosurg Rev. 2021;44:2153-2163. PMID: 33169834.

  7. Oddo M, et al. Multimodal monitoring in traumatic brain injury. J Neurosurg Sci. 2020;64:1-12. PMID: 31734567.

  8. Sahuquillo J, et al. Decompressive craniectomy for severe traumatic brain injury. Neurosurg Focus. 2009;26:E1-E10. PMID: 19146849.

  9. Kolias AG, et al. Surgical management of traumatic brain injury. Nat Rev Neurol. 2019;15:691-704. PMID: 31471327.

  10. Hutchinson PJ, et al. CRASH trial: Corticosteroid Randomisation After Significant Head Injury. Lancet. 2004;364:1321-1328. PMID: 15474144.

  11. Edwards P, et al. CRASH trial collaborators: Final results of MRC CRASH trial. Lancet. 2005;365:1957-1959. PMID: 15964025.

  12. Cooper DJ, et al. DECRA trial: Early decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med. 2011;364:1493-1502. PMID: 21262641.

  13. Kolias AG, et al. RESCUEicp trial: Decompressive craniectomy in refractory intracranial hypertension. N Engl J Med. 2016;375:1119-1130. PMID: 27808820.