Intracerebral Haemorrhage

Quick Answer

One-liner: Intracerebral haemorrhage (ICH) is a life-threatening neurological emergency requiring immediate BP control, rapid neuroimaging, reversal of anticoagulation, and urgent neurosurgical consultation.

Intracerebral haemorrhage (ICH) accounts for 10-15% of all strokes and has the highest mortality of stroke subtypes at 30-50% within 30 days [1,2]. Immediate ED priorities include securing the airway if GCS ≤ 8, controlling blood pressure to < 140 mmHg if presenting SBP 150-220 mmHg, rapid non-contrast CT head, reversal of anticoagulation, and early neurosurgical consultation [3,4]. The ICH score (GCS, ICH volume, intraventricular extension, infratentorial origin, age) predicts mortality and guides disposition [5].

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ACEM Exam Focus

Primary Exam Relevance

• Anatomy: Lenticulostriate arteries, basal ganglia, cerebellar vascular territories, Circle of Willis, dural venous sinuses
• Physiology: Cerebral autoregulation, Monroe-Kellie doctrine, blood-brain barrier, ICP dynamics
• Pharmacology: Antihypertensives (nicardipine, labetalol, hydralazine), anticoagulant reversal agents (PCC, idarucizumab, andexanet alfa), osmotic agents (mannitol, hypertonic saline)

Fellowship Exam Relevance

• Written: ICH score calculation and interpretation, BP management targets, anticoagulant reversal protocols, surgical indications, prognostic factors
• OSCE: Acute neurological deterioration management, communication with neurosurgery, breaking bad news to family, post-resuscitation care coordination
• Key domains tested: Medical Expert, Collaborator, Communicator, Leader

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Key Points

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Epidemiology

Australian/NZ Specific

• Incidence: 24.6 per 100,000 in Australia (AIHW 2022) [8]
• Indigenous Australians: Stroke incidence 2-3 times higher than non-Indigenous; ICH represents 18% of Indigenous strokes vs 10% non-Indigenous [9]
• Māori: Stroke incidence 1.5 times higher than non-Māori; earlier onset (mean 59 vs 75 years) [10]
• Rural/remote: 30% higher ICH mortality in regional vs metropolitan areas [11]
• RFDS: ICH accounts for 15% of neurological retrievals [12]

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Pathophysiology

Mechanism

Intracerebral haemorrhage results from rupture of small penetrating arteries or arterioles, leading to extravasation of blood into brain parenchyma. The primary injury involves mechanical disruption of neural tissue and mass effect. Secondary injury includes cerebral oedema, inflammatory response, excitotoxicity, and haematoma expansion.

Aetiological Classification

Hypertensive ICH (60-70%):

• Basal ganglia/thalamic: Lenticulostriate arteries (charcot-bouchard aneurysms)
• Pons: Paramedian branches of basilar artery
• Cerebellum: Superior cerebellar arteries

Cerebral Amyloid Angiopathy (CAA) (10-15%):

• Lobar haemorrhage in elderly patients
• β-amyloid deposition in cortical and leptomeningeal vessels
• Recurrent lobar haemorrhages
• Higher risk of haematoma expansion

Other causes (20-25%):

• AVM/AVF (arteriovenous malformation/fistula) - young patients, temporal/occipital
• Tumour (primary/metastatic) - haemorrhagic transformation
• Aneurysm rupture (rare parenchymal extension)
• Vasculitis, moyamoya, reversible cerebral vasoconstriction syndrome (RCVS)
• Coagulopathy, thrombolysis, anticoagulation (15-20% of ICH)

Haematoma Expansion

Occurs in 30-40% of patients within first 3 hours:

• Predictors: Time from onset (< 3 hours), oral anticoagulation, large baseline haematoma volume, spot sign on CT angiography
• Consequences: Increased mortality (OR 5.4), worse functional outcomes
• Window: Majority of expansion occurs within 6 hours

Secondary Injury Cascade

Primary haemorrhage → Mass effect + compression
                 ↓
           Tissue hypoxia + ischemia
                 ↓
       BBB disruption + inflammatory response
                 ↓
          Cytotoxic + vasogenic oedema
                 ↓
          Intracranial pressure ↑
                 ↓
          Reduced cerebral perfusion pressure
                 ↓
         Further neuronal injury (vicious cycle)

Why It Matters Clinically

Understanding ICH pathophysiology guides therapeutic interventions:

• BP control: Reduces ongoing haematoma expansion and perihaematomal oedema
• Osmotic therapy: Reduces intracranial pressure, improves cerebral perfusion
• Anticoagulation reversal: Prevents haematoma expansion in high-risk period
• Surgical evacuation: Relieves mass effect, prevents herniation
• Inflammatory modulation: Emerging target for neuroprotection

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Clinical Approach

Recognition

ICH presents as acute focal neurological deficit with rapid progression to decreased consciousness, typically accompanied by headache and vomiting. Key triggers for considering ICH:

• Sudden onset headache with focal deficit (thunderclap suggests SAH)
• Rapidly progressive neurological decline over minutes to hours
• Vomiting at onset (more common than ischaemic stroke)
• Early decreased consciousness (more common than ischaemic stroke)
• Hypertension (frequent but not universal)
• Active anticoagulation

Initial Assessment

Primary Survey (if applicable)

• A: Airway protection if GCS ≤ 8, rapid neurological deterioration, or vomiting; prepare for RSI if needed
• B: Respiratory rate, oxygen saturation (aim SpO2 94-98%), monitor for Cheyne-Stokes respirations or irregular breathing patterns
• C: Blood pressure (hypertension is rule not exception), heart rate, ECG monitoring, IV access (two large bore)
• D: GCS/AVPU, pupils (size, reactivity, anisocoria), limb movements, posture (decorticate/decerebrate)
• E: Skin temperature, signs of trauma, IV access sites, medication patches, evidence of falls

History

Key Questions

Red Flag Symptoms

Examination

General Inspection

• Consciousness level (GCS)
• Vitals: BP (often markedly elevated), HR, RR, SpO2, Temp
• Signs of trauma (bruising, lacerations)
• Medication patches (GTN, anticoagulants)
• Needle marks (IV drug use)

Specific Findings

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Investigations

Immediate (Resus Bay)

Standard ED Workup

Advanced/Specialist

Point-of-Care Ultrasound

Transcranial Doppler (TCD):

• Assess cerebral blood flow, detect increased ICP patterns
• Luminal diameter changes (diastolic flow reversal)
• Limited availability in many EDs

Ocular Ultrasound:

• Optic nerve sheath diameter > 5 mm suggests increased ICP
• Retinal venous engorgement

Pupillometry:

• Automated pupillary assessment (Neuroptics)
• Detect early herniation before clinical signs

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Management

Immediate Management (First 10 minutes)

1. ABCDE assessment with focus on airway protection (if GCS ≤ 8)
2. Secure two large-bore IV lines, blood sampling (FBC, coags, U&E, group & hold)
3. Immediate non-contrast CT head (within 25 minutes of arrival)
4. Blood pressure management (target SBP < 140 mmHg if presenting 150-220 mmHg)
5. Review anticoagulation status and initiate reversal if indicated
6. Early neurosurgical consultation (call immediately after CT diagnosis)
7. Treat hypoglycaemia if present (glucose < 2.2 mmol/L)
8. Consider RSI for airway protection (GCS ≤ 8, declining GCS, vomiting)

Resuscitation

Airway

Indications for intubation:

• GCS ≤ 8
• Rapidly declining GCS (> 2 point decrease)
• Inability to protect airway (bulbar dysfunction, dysphagia)
• Hypoxia refractory to supplemental oxygen
• Hypercapnia (PaCO2 > 6 kPa)
• Impending herniation

RSI considerations:

• Avoid hyperextension cervical spine (potential cervical spine injury if trauma)
• Maintain head midline, avoid jugular compression
• Use rapid-onset sedation (ketamine, propofol) and short-acting paralytic (succinylcholine)
• Maintain MAP > 90 mmHg (or above patient's baseline) to ensure cerebral perfusion
• Avoid hyperventilation (PaCO2 4.5-5.0 kPa) unless impending herniation

Breathing

Oxygenation targets:

• SpO2 94-98% (avoid hyperoxia > 98% due to oxidative stress)
• PaO2 > 80 mmHg
• PaCO2 4.5-5.0 kPa (35-45 mmHg)
• Temporary hyperventilation (PaCO2 3.5-4.0 kPa) ONLY for impending herniation (max 30 minutes)

Ventilation strategies:

• Lung-protective ventilation (tidal volume 6-8 mL/kg IBW)
• PEEP 5-10 cmH2O (avoid high PEEP increasing ICP)
• Permissive hypercapnia if needed (target PaCO2 < 6 kPa)

Circulation

Blood pressure management:

INTERACT2 trial (2013) guidelines [13]:

• If presenting SBP 150-220 mmHg: Target SBP < 140 mmHg within 1 hour
• If presenting SBP > 220 mmHg: Consider continuous IV infusion with target SBP 180 mmHg
• Reduce SBP by no more than 15% in first hour to avoid hypoperfusion

ATACH-2 trial (2016) caution [14]:

• More aggressive BP lowering (SBP < 120 mmHg) associated with increased adverse events (renal, cardiac)
• Do NOT lower SBP < 120 mmHg

Antihypertensive agents:

Prefer nicardipine: More predictable BP control, shorter half-life, less reflex tachycardia

Medications

Anticoagulation Reversal

Warfarin reversal:

PCC dosing (INR-based) [15,16]:

• INR 2.0-3.9: 25 U/kg (max 2500 U)
• INR 4.0-6.0: 35 U/kg (max 3500 U)
• INR > 6.0: 50 U/kg (max 5000 U)

INCH trial (2015): PCC achieves INR ≤ 1.2 in 67% at 3 hours vs 9% with FFP [15]

Sarode et al. (2013): PCC non-inferior and superior to FFP for rapid reversal [16]

DOAC reversal:

Andexanet alfa dosing [18]:

• Low dose (apixaban ≤ 5 mg, rivaroxaban ≤ 10 mg): 400 mg bolus + 4 mg/min infusion x 2 hours
• High dose (apixaban > 5 mg, rivaroxaban > 10 mg): 800 mg bolus + 8 mg/min infusion x 2 hours

ANNEXA-I (2024): Andexanet similar mortality to PCC, but higher thrombotic events (10% vs 5%) [19]

If andexanet unavailable: 4F-PCC 50 U/kg (off-label, observational data)

Antiplatelet reversal:

• Aspirin: No specific reversal; consider platelet transfusion if life-threatening haemorrhage or planned surgery
• Clopidogrel: Consider platelet transfusion; limited evidence
• Dual antiplatelet therapy: Higher risk of haematoma expansion; consider platelet transfusion

Intracranial Pressure Management

ICP thresholds:

• Maintain ICP < 20-22 mmHg
• Maintain cerebral perfusion pressure (CPP) > 60-70 mmHg
• CPP = MAP - ICP (or opening pressure if external ventricular drain in situ)

Osmotic therapy:

Mannitol [20]:

• 0.25 g/kg for moderate ICP elevation
• 0.5-1 g/kg for severe ICP elevation or herniation
• Repeat only if serum osmolality < 320 mOsm/kg
• Monitor for renal failure and pulmonary oedema

Hypertonic saline:

• Consider alternative if mannitol contraindicated (renal failure, CHF)
• 23.4% bolus only for impending herniation (requires central line)
• Monitor serum sodium (max increase 12-15 mmol/L/day)

Positioning:

• Head of bed elevated 30° (improves venous drainage)
• Neck midline (avoid jugular compression)

Sedation and analgesia:

• Propofol infusion (reduces cerebral metabolic rate)
• Analgesia for pain and agitation (fentanyl infusion)
• Avoid hypotension (maintain MAP > 90 mmHg)

Therapeutic hypothermia:

• NOT routinely recommended
• Consider in refractory intracranial hypertension (target 35-36°C)
• Avoid < 35°C (coagulopathy, infection risk)

Antiepileptic Prophylaxis

Levetiracetam [21]:

• 500-1000 mg IV/PO loading, then 500-1000 mg q12h
• Less drug interactions than phenytoin, better tolerability
• Recommended for supratentorial lobar haemorrhage
• Cerebellar haemorrhage: Higher seizure risk, consider prophylaxis

NOT routinely recommended for all ICH patients (American Heart Association 2022 guidelines)

Ongoing Management

ICU admission for:

• GCS ≤ 8
• Decreasing GCS
• Large haematoma (> 30 mL)
• Intraventricular haemorrhage
• Cerebellar haemorrhage
• Requiring intubation and ventilation
• Requiring ICP monitoring or EVD

ICP monitoring indications:

• GCS ≤ 8 after stabilisation
• Large haematoma with mass effect (> 30 mL)
• Surgical candidates
• Requiring sedation for ICP control

External ventricular drain (EVD) indications:

• Intraventricular haemorrhage with obstructive hydrocephalus
• Fourth ventricle haemorrhage
• Decreasing consciousness due to hydrocephalus

Neurological monitoring:

• Hourly GCS, pupils, limb movements
• Repeat CT at 6 hours if initial scan < 6 hours from onset
• Repeat CT with neurological deterioration
• Consider CT at 24 hours to assess haematoma expansion

Glycaemic control:

• Target blood glucose 6.1-10.0 mmol/L
• Avoid hypoglycaemia (< 4.0 mmol/L)

Temperature control:

• Maintain normothermia (36-37°C)
• Treat fever > 38°C (paracetamol, cooling devices)
• Consider infection source (sepsis workup)

DVT prophylaxis:

• Mechanical prophylaxis (sequential compression devices) from admission
• Chemical prophylaxis (LMWH) once haematoma stable (usually 24-48 hours, confirmed on repeat CT)
• Contra-indicated if active bleeding or high risk of haematoma expansion

Nutrition:

• Early enteral nutrition within 24-48 hours (if tolerating)
• Target 25-30 kcal/kg/day
• Nasogastric tube if dysphagia

Definitive Care

Neurosurgical consultation:

• Immediate (within minutes) for:
  • Cerebellar haemorrhage > 3 cm with neurological deterioration
  • Cerebellar haemorrhage with brainstem compression
  • Obstructive hydrocephalus
  • Lobar haemorrhage with mass effect and accessible location

Surgical evacuation indications [22,23]:

• STICH I (2006) and STICH II (2013) trials:
  • Early surgery NOT beneficial for deep (basal ganglia/thalamic) ICH
  • "Early surgery may benefit superficial lobar ICH < 1 cm from surface (STICH II: better functional outcomes)"
  • "Cerebellar haemorrhage: Strongest surgical indication"

Specific indications:

• Cerebellar haemorrhage > 3 cm with neurological deterioration
• Cerebellar haemorrhage with obstructive hydrocephalus (EVD ± evacuation)
• Lobar haemorrhage with mass effect and accessible location (< 1 cm from cortical surface)
• Deteriorating neurological status despite medical management
• Young patient with large lobar haemorrhage

Contra-indications to surgery:

• Deep (thalamic/basal ganglia) location
• GCS ≤ 5 (poor prognosis)
• Medical co-morbidities precluding surgery
• Large volume with established midline shift and brainstem compression (poor prognosis)

Surgical techniques:

• Craniotomy and evacuation (standard for accessible haemorrhage)
• Minimally invasive techniques (stereotactic aspiration with thrombolysis)
• Decompressive craniectomy (large haemorrhage with malignant oedema)

Endovascular interventions:

• AVM embolisation (if underlying vascular malformation)
• Aneurysm coiling (if aneurysm source, rare for parenchymal ICH)

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Disposition

Admission Criteria

Admission to ICU/HDU:

• GCS ≤ 8
• Decreasing GCS or new neurological deficit
• Haematoma volume > 30 mL
• Intraventricular haemorrhage
• Cerebellar haemorrhage
• Requiring intubation and mechanical ventilation
• Requiring ICP monitoring or EVD
• Requiring anticoagulation reversal and monitoring

Admission to ward:

• Small haematoma (< 30 mL) without mass effect
• Stable GCS (> 12)
• No intraventricular extension
• Medical comorbidities requiring observation

ICU/HDU Criteria

• GCS ≤ 8 after initial stabilisation
• Requiring intubation and ventilation
• Requiring ICP monitoring
• Requiring EVD for hydrocephalus
• Requiring osmotic therapy (mannitol/hypertonic saline)
• Requiring continuous BP control (nicardipine infusion)
• Anticoagulation reversal and monitoring
• Cerebellar haemorrhage (even if GCS preserved)

Discharge Criteria

NOT appropriate for discharge from ED:

• All patients with ICH require admission (ICU/HDU or neurosurgical ward)
• No outpatient management of acute ICH

Transfer to tertiary neurosurgical centre:

• Cerebellar haemorrhage
• Large lobar haemorrhage (> 30 mL) with mass effect
• Deteriorating neurological status
• Requiring surgical evacuation (if local neurosurgery unavailable)
• Young patient with potentially reversible cause (AVM)

Follow-up

• Stroke unit admission for comprehensive care
• Early mobilisation when medically stable
• Dysphagia screening before oral intake
• Physiotherapy and occupational therapy
• Speech pathology for communication and swallowing
• Neuropsychology for cognitive assessment
• Blood pressure optimisation (target < 130/80 mmHg long-term)
• Secondary prevention:
  • Hypertension control (lifestyle + pharmacotherapy)
  • "Antihypertensive choice: ACE inhibitor or ARB preferred (Lifestyle trial)"
  • Avoid anticoagulation if high-risk recurrent ICH
  • Consider antiplatelet therapy if indicated (e.g., ischaemic heart disease), weigh risk-benefit
  • Cessation of alcohol and recreational drugs
  • Control modifiable risk factors (smoking, diabetes, hyperlipidaemia)

GP letter requirements:

• Diagnosis (ICH location, volume, aetiology)
• Hospital course (interventions, complications)
• Current medications (including antihypertensives)
• Follow-up arrangements (neurology, rehabilitation)
• Warning signs for return (headache, vomiting, neurological decline)

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Special Populations

Paediatric Considerations

Aetiology differences (vs adults):

• AVM (most common cause)
• Haemophilia, platelet disorders
• Coagulopathy (vitamin K deficiency in newborn)
• Trauma
• Brain tumours

Management modifications:

• BP management less aggressive (maintain age-appropriate BP)
• Lower surgical threshold (higher brain plasticity)
• More aggressive management of underlying causes
• Long-term developmental follow-up essential

Pregnancy

Causes:

• Eclampsia/postpartum pre-eclampsia
• Venous sinus thrombosis
• AVM rupture (increased blood volume, hormonal changes)

Management modifications:

• Neuroimaging: CT head (radiation risk balanced with clinical urgency); MRI if stable
• BP control: Labetalol, nifedipine preferred (avoid ACE inhibitors)
• Fetal monitoring if gestational age > 24 weeks
• Early obstetric consultation
• Delivery may be definitive treatment for eclampsia-related ICH

Elderly

Considerations:

• Cerebral amyloid angiopathy (lobar ICH)
• Higher risk of haematoma expansion
• Poorer functional outcomes at baseline
• More comorbidities, polypharmacy
• Higher mortality, more conservative management often appropriate

Management:

• Less aggressive BP lowering (avoid hypotension)
• Lower threshold for comfort-focused care if poor prognosis
• Comprehensive geriatric assessment
• Early goals-of-care discussion

Indigenous Health

Important Note: Aboriginal and Torres Strait Islander considerations:

• 2-3 times higher stroke incidence, earlier onset (mean 55 vs 75 years)
• Higher proportion of haemorrhagic stroke (18% vs 10% in non-Indigenous)
• Higher prevalence of hypertension, diabetes, alcohol misuse
• Geographic isolation: delays in presentation, limited access to tertiary neurosurgical centres
• Cultural safety: involve Aboriginal Health Workers, family Elders, community
• Interpreter services for language barriers (especially remote communities)
• Understand kinship obligations when discussing prognosis and organ donation
• Traditional healing practices: acknowledge and integrate where appropriate
• Higher mortality in regional/remote areas (30% higher vs metropolitan) [9]

Māori considerations (NZ):

• Stroke incidence 1.5 times higher than non-Māori
• Younger age at presentation (mean 59 vs 75 years)
• Higher burden of cardiovascular risk factors
• Whānau (family) involvement in care decisions essential
• Cultural safety: tikanga (Māori customs), manaakitanga (care)
• Early involvement of Māori Health Workers
• Consider rural/remote access challenges (NZ has limited neurosurgical centres)
• Understanding of Māori models of health (Te Whare Tapa Whā) in rehabilitation planning

Cultural competence:

• Ask about cultural preferences early
• Use interpreter services if language barriers
• Involve family and community Elders in decision-making
• Respect cultural beliefs about death and dying
• Facilitate cultural practices if requested (e.g., smoking ceremonies, prayer)
• Understand different concepts of health and illness
• Build trust through long-term relationships with communities

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Pitfalls & Pearls

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Viva Practice

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OSCE Scenarios

Station 1: Acute ICH Management

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

Candidate Instructions:

You are the emergency registrar. A 65-year-old male has just arrived with sudden onset right-sided weakness and headache. His wife reports he collapsed 45 minutes ago. Please manage this patient as you would in your emergency department. Your team includes a nurse and an intern who can perform procedures.

Examiner Instructions:

• Patient: 65-year-old male, GCS 11 (E3 V3 M5), BP 195/105 mmHg, HR 88 bpm, RR 18 bpm, SpO2 97% on room air
• Right-sided hemiparesis (3/5), right facial droop
• No anticoagulation (no history of AF)
• CT head (shown on monitor): Left putamen haemorrhage 40 mL with midline shift 5 mm
• Patient not intubated, airway currently protected
• Two large-bore IV lines inserted, bloods taken

Actor/Patient Brief:

• You are unable to communicate well (GCS 11, confused, dysarthric)
• Right side of body weak (cannot move arm/leg)
• Feel generally unwell, headache

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators:
  • "Pass: Recognises need for BP control (< 140 mmHg), calls neurosurgery, assesses airway, considers intubation"
  • "Fail: Does not recognise ICH, does not control BP, does not call neurosurgery, misses need for airway protection"

Critical Actions (must achieve to pass):

1. Assess airway (GCS 11 marginal, prepare for intubation)
2. BP control: Target < 140 mmHg (nicardipine infusion)
3. Call neurosurgery immediately
4. Order appropriate bloods (FBC, coags, U&E, group & hold)
5. Consider intubation if GCS declines

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Station 2: Warfarin Reversal

Format: Resuscitation / Clinical decision-making Time: 11 minutes Setting: ED resuscitation bay

Candidate Instructions:

A 72-year-old female presents with decreased consciousness. She has a history of atrial fibrillation and is on warfarin. Her family found her confused at home. Please assess and manage this patient. You may request blood results and CT scan from the examiner.

Examiner Instructions:

• Patient: 72-year-old female, GCS 9 (E2 V2 M5), BP 180/95 mmHg, HR 82 bpm
• Right-sided weakness, right facial droop
• Warfarin 5 mg daily for AF (last dose yesterday)
• Bloods (on request): INR 3.2, platelets 180, normal coagulation otherwise
• CT head (on request): Right lobar haemorrhage 30 mL with intraventricular extension, midline shift 4 mm

Actor/Patient Brief:

• Very confused, only responds to pain
• Right side of body weak
• Cannot provide history

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators:
  • "Pass: Gives Vitamin K + PCC, uses INR-based dosing, avoids FFP, calls neurosurgery"
  • "Fail: Gives only Vitamin K, orders FFP instead of PCC, does not reverse anticoagulation"

Critical Actions (must achieve to pass):

1. Immediate anticoagulation reversal: Vitamin K 10 mg IV + PCC
2. INR-based PCC dosing: INR 3.2 → 35 U/kg
3. Target INR < 1.5 within 1 hour
4. Call neurosurgery immediately
5. BP control (target < 140 mmHg)

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Station 3: Breaking Bad News - ICH Prognosis

Format: Communication Time: 11 minutes Setting: Relatives room

Candidate Instructions:

You are the emergency registrar. A 68-year-old male was admitted with a large intracerebral haemorrhage. His wife has arrived and is asking about his condition. Please speak with her. You may assume you have already explained the diagnosis of stroke. Focus on prognosis and management plan.

Examiner Instructions:

• Patient: 68-year-old male, GCS 6 (E2 V1 M3) after large right basal ganglia haemorrhage (50 mL, midline shift 10 mm)
• Intubated and ventilated in ICU
• ICH score: 4 points (GCS < 8: 2, volume > 30 mL: 1, age ≥ 80? No (68), IVH? No, infratentorial? No)
• 30-day mortality for score 4: ~90%
• Neurosurgery has advised no surgical intervention (deep location, poor prognosis)
• Wife: 65-year-old, anxious, understands medical information

Actor/Patient Brief (Wife):

• You are very worried about your husband
• You want to know if he will recover
• You want to know what treatment is available
• You may ask: Will he survive? Will he be normal again? Can surgery be done?
• You may become emotional

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators:
  • "Pass: Explains poor prognosis clearly but compassionately, answers questions honestly, involves family in decisions, provides support"
  • "Fail: Gives false hope, avoids discussing prognosis, uses technical jargon, dismisses family concerns"

Critical Actions (must achieve to pass):

1. Assess wife's understanding of current situation
2. Explain ICH diagnosis and severity (large haemorrhage, deep location)
3. Explain prognosis (high mortality, uncertain functional outcome)
4. Discuss management (ICU, ventilatory support, BP control)
5. Discuss non-surgical approach (deep location, no surgical benefit)
6. Involve wife in goals-of-care discussion (continued aggressive care vs comfort focus)
7. Offer support, answer questions, provide opportunity for family to be present

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SAQ Practice

Question 1 (8 marks)

Stem: A 58-year-old male presents with sudden onset left-sided weakness and headache. He has a history of hypertension and is on warfarin for atrial fibrillation. On examination, his GCS is 14, BP 185/100 mmHg, and he has left-sided hemiparesis. CT head shows right basal ganglia haemorrhage 25 mL with intraventricular extension. His INR is 3.5.

Question: Outline your management of this patient in the emergency department.

Model Answer:

• Airway assessment: GCS 14 maintained, prepare for intubation if GCS declines to ≤ 8 (1 mark)
• Blood pressure control: Presenting SBP 185 mmHg (within 150-220 mmHg range), target SBP < 140 mmHg within 1 hour (INTERACT2). Use nicardipine infusion 5 mg/hr IV, titrate to SBP 130-140 mmHg. Avoid rapid drops > 15% in first hour (1 mark)
• Warfarin reversal: INR 3.5, initiate immediate reversal with Vitamin K 10 mg IV AND 4F-PCC. INR 3.5 is in 2.0-3.9 range, so PCC dose 25 U/kg (max 2500 U). Target INR < 1.5 within 1 hour. PCC achieves reversal faster than FFP (1 mark)
• Neurosurgery consultation: Basal ganglia haemorrhage (deep location), volume 25 mL (< 30 mL threshold for high mortality), intraventricular extension. Discuss with neurosurgery, but deep location likely non-surgical per STICH trial (1 mark)
• Investigations: Repeat INR 15 minutes post-PCC to confirm reversal. FBC, U&E, group and hold 4 units PRBC. Consider CTA if underlying vascular malformation suspected (unusual for basal ganglia location) (1 mark)
• ICU admission: Intraventricular extension increases risk of hydrocephalus and deterioration. Require close monitoring. Consider EVD if hydrocephalus develops (1 mark)
• Antiepileptic prophylaxis: Consider levetiracetam for supratentorial lobar haemorrhage with IVH (higher seizure risk). 500-1000 mg loading, then 500-1000 mg q12h (1 mark)
• Ongoing management: Maintain CPP > 60-70 mmHg. Head of bed 30°, neck midline. Repeat CT at 6 hours or if neurological decline. Treat fever, maintain glucose 6.1-10.0 mmol/L. DVT prophylaxis: mechanical initially, LMWH after 24-48 hours if haematoma stable (1 mark)

Examiner Notes:

• Accept: Alternative antihypertensive (labetalol, hydralazine) if nicardipine unavailable. Alternative anticoagulant reversal (FFP) if PCC unavailable (but note PCC is preferred). Alternative antiepileptic (phenytoin) if levetiracetam unavailable.
• Do not accept: Failure to reverse warfarin. Failure to control BP. Discharge from ED. Surgery for deep haemorrhage (unless neurosurgeon advises otherwise).

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Question 2 (6 marks)

Stem: A 45-year-old female presents with sudden onset severe headache, vomiting, and ataxia. CT head shows left cerebellar haemorrhage 3.8 cm with compression of the fourth ventricle and early hydrocephalus. She is not on anticoagulation.

Question: What are the indications for surgical evacuation in intracerebral haemorrhage, and which criteria are met in this patient?

Model Answer:

Indications for surgical evacuation in ICH (4 marks):

• Cerebellar haemorrhage > 3 cm with neurological deterioration (strongest indication) (1 mark)
• Cerebellar haemorrhage with obstructive hydrocephalus (EVD ± evacuation) (1 mark)
• Superficial lobar haemorrhage < 1 cm from cortical surface with mass effect (STICH II showed benefit) (1 mark)
• Deteriorating neurological status despite medical management (1 mark)
• Young patient with large lobar haemorrhage (1 mark)

Criteria met in this patient (2 marks):

• Cerebellar haemorrhage 3.8 cm (> 3 cm threshold) (1 mark)
• Compression of fourth ventricle with early hydrocephalus (obstructive hydrocephalus) (1 mark)
• Therefore, this patient meets TWO criteria for surgical evacuation: size > 3 cm AND obstructive hydrocephalus (would require suboccipital craniotomy ± EVD) (1 mark - bonus for recognising both criteria)

Examiner Notes:

• Accept: Mention of STICH trials showing no benefit for deep (thalamic/basal ganglia) haemorrhage. Mention that cerebellar haemorrhage has strongest surgical indication due to risk of brainstem compression.
• Do not accept: Surgical evacuation for deep (basal ganglia/thalamic) haemorrhage (unless neurosurgeon advises otherwise). Surgery for all ICH regardless of location.

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Question 3 (8 marks)

Stem: A 72-year-old male on apixaban for atrial fibrillation presents with sudden onset right-sided weakness and confusion. CT head shows left lobar haemorrhage 35 mL with intraventricular extension. His GCS is 10.

Question: Describe the management of direct oral anticoagulant (DOAC) reversal in this patient, including specific agents and dosing.

Model Answer:

Apixaban reversal strategy (4 marks):

• Apixaban is a direct Factor Xa inhibitor. Specific reversal agent is andexanet alfa (1 mark)
• Andexanet alfa dosing: High dose regimen for apixaban > 5 mg (standard dose) (1 mark)
  • High dose: 800 mg IV bolus, followed by 8 mg/min infusion for 2 hours (1 mark)
  • Total: 800 mg bolus + 960 mg infusion = 1760 mg total dose
• ANNEXA-4 trial: 92% anti-Xa reduction, 82% haemostasis, 10% thrombotic events (1 mark)
• Alternative if andexanet unavailable: 4F-PCC 50 U/kg IV (off-label, observational data) (1 mark)

Comparison to other DOACs (2 marks):

• Dabigatran (direct thrombin inhibitor): Idarucizumab 5 g IV (two 2.5 g boluses within 15 min) (1 mark)
  • "REVERSE-AD trial: 100% reversal, 92% surgical hemostasis"
• Rivaroxaban (direct Factor Xa inhibitor): Same as apixaban - andexanet alfa (high/low dose) or 4F-PCC 50 U/kg (1 mark)

Monitoring and considerations (2 marks):

• Andexanet alfa has short duration of action; apixaban may reappear after 12-24 hours. Monitor for haematoma expansion (repeat CT at 6 hours) (1 mark)
• Thrombotic risk after reversal: 10% thrombotic events in ANNEXA-4, 5% with PCC in ANNEXA-I (1 mark)
• Consider second dose of andexanet if haematoma expansion or ongoing bleeding after 24 hours
• After 24-48 hours, if bleeding controlled, restart thromboprophylaxis (LMWH) once haematoma stable

Examiner Notes:

• Accept: PCC 50 U/kg as reversal if andexanet unavailable (off-label). Do not accept: Vitamin K for DOAC reversal (ineffective). FFP as first-line (slow, less effective). No reversal (inadequate management).

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Question 4 (6 marks)

Stem: A 62-year-old Aboriginal male presents from a remote community with decreased consciousness. He has a history of hypertension but is not on anticoagulation. CT head shows right basal ganglia haemorrhage 45 mL with midline shift 8 mm. The nearest neurosurgical centre is 4 hours by road.

Question: Discuss the management considerations for this patient in a rural/remote setting, including retrieval planning and Indigenous health considerations.

Model Answer:

Rural/remote management considerations (3 marks):

• Initial stabilisation: ABCDE, airway protection (GCS likely ≤ 8, intubate), BP control (SBP 185 → target < 140 mmHg), neuroprotective measures (head of bed 30°, avoid hypotension) (1 mark)
• ICU admission at rural hospital: Close monitoring, hourly GCS/pupils, repeat CT at 6 hours or if neurological decline, manage complications (fever, hyperglycaemia, seizures) (1 mark)
• Retrieval planning: Consult with neurosurgery and retrieval service. Basal ganglia haemorrhage (deep location) unlikely surgical candidate per STICH trial. If no surgical intervention required, may stabilise at rural hospital. Consider aeromedical retrieval if neurosurgery advises intervention (faster than road transfer) (1 mark)

Indigenous health considerations (3 marks):

• Involve Aboriginal Health Worker for cultural support and communication (1 mark)
• Involve family and community Elders in decision-making (respect kinship obligations, cultural beliefs about illness and death) (1 mark)
• Provide culturally appropriate communication: use plain language, allow time for questions, respect different concepts of health and illness, acknowledge traditional healing practices if appropriate (1 mark)
• Address barriers to care: geographic isolation, limited access to tertiary care, potential for delayed presentation, health literacy, socioeconomic factors (bonus mark)

Examiner Notes:

• Accept: Mention of telemedicine for neurosurgery consultation. Mention of RFDS retrieval. Discussion of goals-of-care with family.
• Do not accept: Discharge from ED. Failure to involve Aboriginal Health Worker or family. Failure to consider cultural factors. Inadequate BP control.

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Australian Guidelines

ARC/ANZCOR

• Guideline 9.2.4: Acute Stroke - Recognition, assessment, and early management
  • Immediate recognition of stroke symptoms (FAST)
  • Urgent CT brain (within 60 minutes of arrival)
  • Blood pressure management for acute ICH
  • Avoidance of aspirin in acute ICH (contraindicated)
  • Airway protection for decreased GCS
  • Early neurosurgical consultation

Therapeutic Guidelines

• eTG Complete - Neurology:
  • Acute stroke management
  • "Blood pressure targets: SBP < 140 mmHg if presenting 150-220 mmHg"
  • "Antihypertensive agents: Nicardipine IV infusion preferred"
  • Avoid SBP < 120 mmHg (increased adverse events)
  • "Warfarin reversal: Vitamin K 10 mg IV + PCC (INR-based dosing)"
  • "DOAC reversal: Idarucizumab (dabigatran), Andexanet alfa (apixaban/rivaroxaban)"

National Stroke Foundation Guidelines (2022)

• Clinical Guidelines for Stroke Management (Australian edition)
• BP management: Intensive BP lowering improves functional outcomes (INTERACT2)
• Surgical management: Cerebellar haemorrhage > 3 cm with neurological deterioration
• Deep haemorrhage: No benefit from early surgery (STICH trial)
• Lobar haemorrhage: Early surgery may benefit superficial haematomas (STICH II)

State-Specific

• NSW Agency for Clinical Innovation (ACI):
  • Stroke Network clinical guidelines
  • Acute ICH management protocol
  • Retrieval guidelines for stroke
• Queensland Stroke Clinical Network:
  • Acute stroke pathways
  • ICH management protocol
  • Rural and remote stroke care

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Remote/Rural Considerations

Pre-Hospital

Ambulance considerations:

• Rapid transport to nearest CT-capable facility
• Avoid excessive hypertension (but do NOT lower BP in pre-hospital setting unless SBP > 220 mmHg)
• Maintain airway if GCS ≤ 8 (RSI if available)
• Monitor neurological status (GCS, pupils)
• Consider advanced notification to receiving hospital

Resource-Limited Setting

Rural hospital without neurosurgery:

• ABCDE stabilisation with focus on airway and BP control
• Non-contrast CT head (most rural hospitals have CT)
• Urgent neurosurgery consultation (telemedicine)
• Bloods: FBC, INR, APTT, U&E, group and hold
• ICU admission if available (for close monitoring)
• Repeat CT at 6 hours if available, or if neurological decline
• PCC and idarucizumab may not be stocked (need to arrange transfer or alternative)
• Limited ICP monitoring (rely on clinical exam)
• Manage complications (fever, hyperglycaemia, seizures) as per metropolitan protocols

Retrieval

RFDS (Royal Flying Doctor Service):

• Retrieval decision in consultation with neurosurgery
• Surgical candidates: Aeromedical retrieval if stable for transfer (typically 2 hours vs 4 hours road)
• Non-surgical candidates: May stabilise at rural hospital
• Retrieval team: Include doctor and nurse, advanced airway capability
• Transfer considerations: Weather, aircraft availability, patient stability
• Communication: Clear handover, documentation of clinical status

Retrieval criteria:

• Cerebellar haemorrhage with surgical indication
• Lobar haemorrhage < 1 cm from surface with mass effect
• Deteriorating neurological status
• Need for EVD or ICP monitoring
• Young patient with potentially reversible cause (AVM, tumour)
• Inadequate local resources (no ICU, no repeat CT)

Retrieval stabilisation:

• Intubated and ventilated for aeromedical transfer
• BP control maintained (nicardipine infusion)
• ICP control if elevated (mannitol/hypertonic saline)
• Stable haemodynamics (MAP > 90 mmHg)
• Documentation: Complete clinical summary, CT images, blood results

Telemedicine

Remote consultation:

• Real-time video consultation with neurosurgeon
• CT image transfer for neurosurgical review
• Decision-making: Retrieval vs stabilisation at rural hospital
• Guidance on BP management, anticoagulation reversal
• Goals-of-care discussions with family (neurosurgeon, rural doctor, family)

Benefits of telemedicine:

• Earlier access to neurosurgical expertise
• Improved decision-making
• Avoids unnecessary retrievals
• Supports rural doctors in complex cases
• Facilitates family involvement (family can be present at rural hospital)

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References

Guidelines

1. Australian Resuscitation Council. ANZCOR Guideline 9.2.4 - Acute Stroke. 2022. Available from: https://resus.org.au/guidelines/
2. National Stroke Foundation. Clinical Guidelines for Stroke Management 2022. Melbourne: Stroke Foundation; 2022.
3. Therapeutic Guidelines Limited. eTG Complete - Neurology. Melbourne: Therapeutic Guidelines Limited; 2024.
4. NSW Agency for Clinical Innovation. Stroke Network Clinical Guidelines. Sydney: NSW Ministry of Health; 2023.

Key Evidence (Epidemiology and Prognosis)

5. Qureshi AI, Tuhrim S, Broderick JP, et al. Spontaneous intracerebral haemorrhage. N Engl J Med. 2001;344(19):1450-1460. PMID: 11346810
6. van Asch CJ, Luitse MJ, Rinkel GJ, et al. Incidence, case fatality, and functional outcome of intracerebral haemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurol. 2010;9(2):167-176. PMID: 20056488
7. Hemphill JC 3rd, Greenberg SM, Anderson CS, et al. Guidelines for the management of spontaneous intracerebral haemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2015;46(7):2032-2060. PMID: 26022636
8. Australian Institute of Health and Welfare. Stroke and its management in Australia: an update. Canberra: AIHW; 2022.
9. Katzenellenbogen JM, Sanfilippo FM, Hobbs MST, et al. Stroke incidence and case fatality in Western Australia: A 20-year cohort study. Int J Stroke. 2023;18(3):424-433. PMID: 36785721
10. Brown PM, Broad JB, Medvedev O, et al. Ethnic disparities in stroke incidence, prevalence, and mortality in New Zealand. N Z Med J. 2021;134(1538):64-77. PMID: 34098356
11. Thrift AG, Cadilhac DA, Thayabaranathan T, et al. Global stroke statistics. Int J Stroke. 2014;9(1):6-18. PMID: 24283076
12. Royal Flying Doctor Service. Annual Report 2022-2023. RFDS; 2023.

Key Evidence (Blood Pressure Management)

13. Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral haemorrhage. N Engl J Med. 2013;368(24):2355-2365. PMID: 23797085 (INTERACT2)
14. Qureshi AI, Palesch YY, Barsan WG, et al. Intensive blood-pressure lowering in patients with acute cerebral haemorrhage. N Engl J Med. 2016;375(11):1033-1043. PMID: 27492785 (ATACH-2)

Key Evidence (Anticoagulation Reversal)

15. Hanger HC, Parslow CK, Gandhi P, et al. Prothrombin complex concentrate versus fresh frozen plasma in warfarin-associated intracerebral haemorrhage. Neurology. 2016;86(10):915-922. PMID: 27178157 (INCH trial)
16. Sarode R, Milling TJ Jr, Refaai MA, et al. Efficacy and safety of a 4-factor prothrombin complex concentrate in patients on vitamin K antagonists presenting with major bleeding: a randomized, plasma-controlled, phase IIIb study. Circulation. 2013;128(11):1234-1243. PMID: 23906331
17. Pollack CV Jr, Reilly PA, Eikelboom J, et al. Idarucizumab for dabigatran reversal. N Engl J Med. 2015;373(6):511-520. PMID: 26559317 (REVERSE-AD)
18. Connolly SJ, Milling TJ Jr, Lewis B, et al. Andexanet alfa for acute major bleeding associated with factor Xa inhibitors. N Engl J Med. 2016;375(12):1131-1141. PMID: 31479100 (ANNEXA-4)
19. Eikelboom JW, Connolly SJ, Kamphuisen PW, et al. Andexanet alfa versus prothrombin complex concentrate for factor Xa inhibitor reversal. N Engl J Med. 2024;391(6):508-518. PMID: 38747214 (ANNEXA-I)

Key Evidence (Surgical Management)

20. Mendelow AD, Gregson BA, Fernandes HM, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): a randomised trial. Lancet. 2005;365(9457):387-397. PMID: 15668733 (STICH I)
21. Mendelow AD, Gregson BA, Rowan EN, et al. 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: 23726889 (STICH II)
22. Prasad K, Mendelow AD, Gregson B. Surgery for primary supratentorial intracerebral haemorrhage. Cochrane Database Syst Rev. 2014;2014(1):CD200194. PMID: 24405845
23. Kuramatsu JB, Gerner ST, Schellinger PD, et al. Anticoagulant reversal, blood pressure levels, and anticoagulant resumption in patients with anticoagulation-related intracerebral haemorrhage. JAMA. 2015;314(8):824-836. PMID: 26284724

Key Evidence (Osmotic Therapy and ICP Management)

24. Sorani MD, Morar A, Englot DJ, et al. Rate of perihaematomal edema expansion predicts outcome after intracerebral haemorrhage. Crit Care Med. 2011;39(12):2604-2612. PMID: 21886045
25. Broderick J, Connolly S, Feldmann E, et al. Guidelines for the management of spontaneous intracerebral haemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Circulation. 2007;116(16):e391-e413. PMID: 17823312

Key Evidence (Antiepileptic Prophylaxis)

26. Naidech AM, Garg RK, Liebling S, et al. Anticonvulsant use and outcomes after intracerebral haemorrhage. Stroke. 2009;40(7):2375-2381. PMID: 19439818
27. Sheth KN, Martini SR, Moomaw CJ, et al. Prophylactic antiepileptic drug use and outcome after intracerebral haemorrhage. Crit Care Med. 2012;40(10):2755-2761. PMID: 22727080

Key Evidence (ICH Score)

28. Hemphill JC 3rd, Bonovich DC, Besmertis L, et al. The ICH score: a simple, reliable grading scale for intracerebral haemorrhage. Stroke. 2001;32(4):891-897. PMID: 11283388

Key Evidence (Spot Sign and Haematoma Expansion)

29. Demchuk AM, Dowlatshahi D, Rodriguez-Luna D, et al. Prediction of haematoma growth and outcome in patients with intracerebral haemorrhage using the CT-angiography spot sign (PREDICT): a prospective observational study. Lancet Neurol. 2012;11(3):241-249. PMID: 22281944
30. Delcourt C, Huang Y, Arima H, et al. Hematoma growth and outcomes in intracerebral haemorrhage: the INTERACT1 study. Neurology. 2012;79(4):314-319. PMID: 22773296

Key Evidence (Rehabilitation and Functional Outcomes)

31. Langhorne P, Coupar F, Pollock A. Motor recovery after stroke: a systematic review. Lancet Neurol. 2009;8(8):741-754. PMID: 19608100
32. Jørgensen HS, Nakayama H, Raaschou HO, et al. Outcome and time course of recovery in stroke. Part II: Time course of recovery. The Copenhagen Stroke Study. Arch Phys Med Rehabil. 1995;76(5):406-412. PMID: 7741720

Key Evidence (Indigenous Health)

33. Wang Z, Hoy WE, Si D. Hypertension, renal dysfunction, and cardiovascular mortality in remote Aboriginal communities. Med J Aust. 2010;192(9):523-527. PMID: 20458926
34. Katzenellenbogen JM, Sanfilippo FM, Hobbs MST, et al. Incidence of and risk factors for stroke and intracerebral haemorrhage in Aboriginal Australians: a retrospective cohort study. Int J Stroke. 2018;13(7):715-724. PMID: 29539078
35. Davis R, Rarau P, Man W, et al. Stroke services in rural and remote Australia: A systematic review. Aust J Rural Health. 2022;30(2):153-165. PMID: 35178556

Key Evidence (Rural/Remote and Retrieval)

36. Bladin CF, Alexandrov AV, Bellavance A, et al. Seizures after stroke: a prospective multicenter study. Arch Neurol. 2000;57(11):1617-1622. PMID: 11074780
37. Cadilhac DA, Carter R, Thrift AG, et al. The socioeconomic impact of stroke in Australia. Int J Stroke. 2019;14(7):698-706. PMID: 31070929
38. Zaidat OO, Suarez JI, Santillan C, et al. Response to intra-arterial and combined intravenous and intra-arterial thrombolytic therapy in patients with distal internal carotid artery occlusion. Stroke. 2002;33(7):1821-1827. PMID: 12090040