Summary
Intracerebral haemorrhage (ICH) is bleeding directly into the brain parenchyma, accounting for 10-15% of all strokes but 40-50% of stroke mortality. It is a neurological emergency requiring immediate blood pressure control, reversal of anticoagulation, and neurosurgical evaluation. Primary ICH results from hypertensive arteriopathy or cerebral amyloid angiopathy, while secondary ICH has identifiable structural causes. Mortality is 40% at 30 days, with only 20% achieving functional independence at 6 months. [1,2]
Key Facts
| Fact | Detail | Exam Relevance |
|---|---|---|
| Incidence | 10-30 per 100,000/year | Know UK/global epidemiology |
| Mortality | 40% at 30 days; 54% at 1 year | Quote in viva scenarios |
| Primary causes | Hypertension (50-70%), CAA (20-30%) | Common exam question |
| Location | Basal ganglia (50%), lobar (35%), cerebellum (10%), brainstem (5%) | Correlate with aetiology |
| BP target | SBP 130-140 mmHg within 1 hour | INTERACT2 evidence |
| Haematoma expansion | 30-40% expand in first 24 hours | Explains early deterioration |
| INR reversal | Target <1.5 within 4 hours | Critical for anticoagulated patients |
| Surgical indications | Cerebellar ICH >3cm, hydrocephalus, herniation | Know surgical criteria |
| ICH score | Predicts 30-day mortality (0-6) | Must know components |
| Functional outcome | Only 20% independent at 6 months | Important for prognosis discussions |
Clinical Pearls
High-Yield Fact: Haematoma volume is the strongest predictor of outcome. Every 1mL increase in volume increases mortality by 5%.
Exam Tip: Lobar ICH in elderly without hypertension suggests cerebral amyloid angiopathy (CAA) - presents with recurrent lobar bleeds and associated dementia.
Clinical Pearl: The "spot sign" on CT angiography (contrast extravasation into haematoma) predicts haematoma expansion with 91% specificity.
Pitfall Warning: Do NOT attribute altered consciousness to "stroke" alone - check for hydrocephalus, midline shift, or herniation requiring urgent intervention.
Mnemonic: ICH Score components: GCS, Age, Volume, IVH, Infratentorial - each scores 0-1 (age/volume/GCS can score 2).
Why This Matters Clinically
ICH is the deadliest stroke subtype with limited treatment options. Early aggressive blood pressure control and anticoagulant reversal are the only proven interventions to reduce haematoma expansion. Neurosurgical decompression is life-saving for posterior fossa bleeds. For examinations, ICH tests knowledge of stroke classification, BP management evidence, reversal agents, and prognostic scoring. Medico-legally, failure to reverse anticoagulation rapidly or delayed neurosurgical referral for posterior fossa bleeds are significant issues. [3,4]
Incidence & Prevalence
- Incidence: 10-30 per 100,000 population per year (varies by region) [PMID: 20413592]
- Proportion of stroke: 10-15% of all strokes (higher in Asian populations: 20-30%)
- Trend: Increasing due to aging population and anticoagulant use
- Geographic variation: Higher in East Asia (Japan, China) - 2-3x Western rates
- Seasonal variation: Higher incidence in winter months (BP fluctuation)
- Economic burden: Higher than ischaemic stroke due to severe disability
Demographics
| Factor | Details | Clinical Significance |
|---|---|---|
| Age | Incidence doubles each decade >55 years | Median age 65-70 years |
| Sex | Male:Female ~1.3:1 | Males have higher incidence |
| Ethnicity | 2x higher in Black and Asian populations | Genetic and BP control factors |
| Hypertension | Present in 70-80% of ICH patients | Most important modifiable risk |
| Anticoagulation | 12-20% of ICH is anticoagulant-related | Rising with DOAC prescribing |
| Socioeconomic | Higher in lower socioeconomic groups | Access to healthcare, BP control |
Risk Factors
Non-Modifiable Risk Factors:
| Factor | Relative Risk (95% CI) | Mechanism |
|---|---|---|
| Age >55 years | RR 2.0 per decade | Arteriopathy, amyloid deposition |
| Male sex | RR 1.3 (1.1-1.6) | Hormonal, lifestyle factors |
| Black ethnicity | RR 2.0-2.5 | Higher BP, genetic factors |
| Asian ethnicity | RR 1.5-2.0 | Genetic, dietary factors |
| Prior ICH | RR 2.1 (1.5-3.0) | Underlying arteriopathy persists |
| Family history stroke | RR 1.5 (1.2-1.9) | Genetic predisposition |
Modifiable Risk Factors:
| Risk Factor | Relative Risk (95% CI) | Evidence Level | Intervention Impact |
|---|---|---|---|
| Hypertension | RR 3-5 | Level 1a | BP control reduces risk 50% |
| Anticoagulation (warfarin) | RR 5-10 | Level 1b | INR monitoring critical |
| DOACs | RR 0.5 vs warfarin for ICH | Level 1a | Lower ICH risk than warfarin |
| Antiplatelet therapy | RR 1.5-2.0 | Level 1b | Smaller effect than anticoagulants |
| Heavy alcohol (>2 drinks/day) | RR 2.0-4.0 | Level 2a | Abstinence reduces risk |
| Cocaine/amphetamines | RR 5-10 | Level 2b | Acute hypertensive crisis |
| Smoking | RR 1.5 (1.2-1.8) | Level 2a | Cessation reduces risk |
| Low cholesterol | RR 1.2-1.5 | Level 2b | Controversial; benefit of statins outweighs |
Mechanism
Step 1: Vascular Pathology Development (Years)
- Hypertensive arteriopathy: Chronic hypertension causes lipohyalinosis and fibrinoid necrosis of small penetrating arteries (lenticulostriate, thalamoperforating)
- Cerebral amyloid angiopathy (CAA): Beta-amyloid deposition in cortical and leptomeningeal vessel walls causing fragility
- Microaneurysm formation: Charcot-Bouchard aneurysms develop at bifurcation points
- Vessel wall weakening: Progressive structural damage predisposes to rupture
Step 2: Vessel Rupture (Seconds)
- Initiating event: Acute BP surge or minor trauma in weakened vessel
- Arterial bleeding: High-pressure arterial blood extravasates into brain parenchyma
- Initial haematoma: Blood dissects along white matter tracts, path of least resistance
- Mass effect begins: Immediate compression of adjacent brain tissue
Step 3: Haematoma Expansion (Minutes to Hours)
- Active bleeding continues: 30-40% of haematomas expand in first 24 hours, mostly within 6 hours
- Multiple bleeding points: Satellite haemorrhages develop around primary bleed
- Coagulopathy contribution: Anticoagulation prevents clot formation, allows expansion
- Volume increase: Each 10% volume increase associated with 5% mortality increase
Step 4: Secondary Brain Injury (Hours to Days)
- Mass effect: Rising ICP, midline shift, herniation risk
- Perihematomal oedema: Cytotoxic and vasogenic oedema peaks at 3-7 days
- Blood breakdown products: Iron, haemoglobin degradation causes oxidative damage
- Inflammation: Microglial activation, cytokine release, BBB disruption
- Neuronal death: Combination of mechanical damage, ischaemia, and neurotoxicity
Step 5: Resolution or Progression (Days to Weeks)
- Clot organisation: Macrophage infiltration begins clearing haematoma
- Cavity formation: Residual hemosiderin-lined cavity in chronic phase
- Functional recovery: Depends on location, volume, and perilesional plasticity
- Complications: Hydrocephalus (from IVH), seizures, infections
Classification
By Aetiology:
| Type | Prevalence | Key Features |
|---|---|---|
| Primary - Hypertensive | 50-70% | Deep structures (basal ganglia, thalamus, pons), associated with chronic HTN |
| Primary - CAA | 20-30% | Lobar location, elderly, recurrent, associated dementia |
| Secondary - Vascular malformation | 5-10% | AVM, cavernoma, aneurysm, younger patients |
| Secondary - Tumour | 2-5% | Metastases (melanoma, RCC, lung), primary brain tumours |
| Secondary - Coagulopathy | 5-10% | Anticoagulation, thrombocytopenia, DIC |
| Secondary - Drug-related | 2-5% | Cocaine, amphetamines, sympathomimetics |
| Secondary - Venous | 1-2% | Cerebral venous thrombosis with haemorrhagic conversion |
By Location:
| Location | Proportion | Typical Aetiology | Clinical Features |
|---|---|---|---|
| Basal ganglia/Putamen | 35-50% | Hypertension | Contralateral hemiparesis, sensory loss |
| Thalamus | 10-15% | Hypertension | Sensory loss, vertical gaze palsy, small pupil |
| Lobar | 20-35% | CAA, tumour, AVM | Depends on lobe; headache prominent |
| Cerebellum | 5-10% | Hypertension | Ataxia, vertigo, rapid deterioration |
| Brainstem/Pons | 5-10% | Hypertension | Quadriparesis, coma, poor prognosis |
Symptoms
Cardinal Symptoms (Onset):
| Symptom | Frequency | Characteristics |
|---|---|---|
| Headache | 40-50% | Sudden, severe ("worst headache"); more common than ischaemic stroke |
| Focal weakness | 70-80% | Contralateral hemiparesis; face, arm, leg |
| Speech disturbance | 30-40% | Dysarthria or aphasia depending on location |
| Visual disturbance | 20-30% | Hemianopia, gaze deviation toward lesion |
| Altered consciousness | 30-50% | Drowsiness to coma; correlates with volume/IVH |
| Vomiting | 40-50% | Due to raised ICP; more common than ischaemic stroke |
| Seizures | 10-15% | At onset or within first 24 hours |
Differentiating Features from Ischaemic Stroke:
Red Flags
| Red Flag | Significance | Immediate Action |
|---|---|---|
| Decreasing GCS | Haematoma expansion, raised ICP, herniation | Repeat CT, neurosurgery review |
| Cushing's triad | Critically raised ICP | Osmotherapy, emergency decompression |
| Fixed dilated pupil | Uncal herniation | Emergency neurosurgery |
| Bilateral fixed pupils | Brainstem compression | Usually terminal |
| Anticoagulated patient | Risk of ongoing bleeding | Immediate reversal protocol |
| Posterior fossa signs | Risk of rapid deterioration and hydrocephalus | Urgent neurosurgery |
Examination Approach
Structured Neurological Examination:
- General observation: GCS, posturing, pupil size/reactivity
- Eye movements: Gaze deviation (toward lesion), vertical gaze palsy (thalamic)
- Motor examination: Hemiparesis pattern, pronator drift
- Sensory examination: If patient conscious
- Cerebellar signs: Ataxia (cerebellar ICH)
- Signs of raised ICP: Papilloedema, Cushing's response
Key Examination Findings
| Finding | Interpretation | Location Indication |
|---|---|---|
| Gaze deviation toward lesion | Frontal eye field involvement | Supratentorial |
| Wrong-way eyes | Gaze away from lesion | Thalamic haemorrhage |
| Vertical gaze palsy | Midbrain/thalamic involvement | Thalamic ICH |
| Pinpoint pupils | Pontine haemorrhage | Brainstem |
| Ipsilateral dilated pupil | Uncal herniation | Large supratentorial with mass effect |
| Bilateral dilated fixed | Severe brainstem involvement | Terminal sign |
| Contralateral hemiparesis | Motor pathway involvement | Any supratentorial location |
| Quadriparesis | Bilateral or brainstem involvement | Pontine ICH |
| Ataxia + vertigo | Cerebellar involvement | Cerebellar ICH |
Detailed Examination by Location
Putaminal/Basal Ganglia ICH:
- Contralateral hemiparesis (face, arm, leg)
- Conjugate gaze deviation toward the lesion (away from hemiparesis)
- Contralateral hemisensory loss
- Homonymous hemianopia (if extends posteriorly)
- Dysarthria
- Large lesions: Decreased consciousness, transtentorial herniation signs
Thalamic ICH:
- Contralateral hemisensory loss (prominent feature)
- Contralateral hemiparesis (milder than sensory findings)
- Downgaze palsy ("setting sun" appearance)
- Small reactive pupils (miosis)
- Wrong-way eyes (gaze toward hemiparesis - unique feature)
- Extension into third ventricle common → hydrocephalus
Lobar ICH:
- Deficits depend on lobe affected:
- Frontal: Contralateral leg weakness, personality change, expressive aphasia (dominant)
- Parietal: Contralateral sensory loss, neglect (non-dominant), receptive aphasia (dominant)
- Temporal: Wernicke's aphasia (dominant), memory impairment
- Occipital: Contralateral homonymous hemianopia
- Headache often prominent
- Seizures more common (cortical involvement)
Cerebellar ICH:
- Acute onset vertigo, vomiting, headache
- Truncal ataxia, dysmetria
- Gaze palsies (sixth nerve, horizontal gaze)
- Neck stiffness (irritation of meninges)
- CRITICAL: Can deteriorate rapidly
- Fourth ventricle compression → hydrocephalus
- Brainstem compression signs: Decreasing GCS, posturing
Pontine ICH:
- Quadriparesis (bilateral motor involvement)
- Bilateral pinpoint pupils (sympathetic pathway disruption)
- Internuclear ophthalmoplegia
- Ocular bobbing
- Hyperthermia
- Decerebrate/decorticate posturing
- Coma
- Very poor prognosis
Glasgow Coma Scale Assessment
GCS Components (Total 3-15):
| Component | Response | Score |
|---|---|---|
| Eye Opening | Spontaneous | 4 |
| To voice | 3 | |
| To pain | 2 | |
| None | 1 | |
| Verbal Response | Oriented | 5 |
| Confused | 4 | |
| Inappropriate words | 3 | |
| Incomprehensible sounds | 2 | |
| None | 1 | |
| Motor Response | Obeys commands | 6 |
| Localises pain | 5 | |
| Withdraws from pain | 4 | |
| Abnormal flexion (decorticate) | 3 | |
| Extension (decerebrate) | 2 | |
| None | 1 |
GCS Interpretation in ICH:
- GCS 13-15: Mild impairment - may deteriorate
- GCS 9-12: Moderate impairment - close monitoring
- GCS 3-8: Severe - consider intubation, ICU
- Trend more important than single value
- Motor score most predictive of outcome
Pupillary Assessment
Systematic Pupil Examination:
- Size (measure in mm)
- Shape (round, irregular, ovoid)
- Reactivity to light (direct and consensual)
- Symmetry (compare both sides)
Pupillary Signs by Location:
| Pupil Finding | Lesion Location | Mechanism |
|---|---|---|
| Unilateral fixed dilated | Ipsilateral third nerve (uncal herniation) | CN III compression |
| Bilateral pinpoint | Pons (pontine ICH) | Sympathetic pathway disruption |
| Small reactive | Thalamus | Horner's-like (ipsilateral) |
| Bilateral mid-fixed | Midbrain (tectal) | Aqueduct/tectal compression |
| Bilateral dilated fixed | Severe bilateral or terminal | Complete loss of function |
Herniation Syndromes
Types of Herniation:
| Type | Mechanism | Clinical Signs |
|---|---|---|
| Uncal (transtentorial) | Temporal lobe through tentorium | Ipsilateral pupil dilation, contralateral hemiparesis, then bilateral signs |
| Central (transtentorial) | Diencephalon through tentorium | Bilateral pupil changes, bilateral posturing, Cushing's triad |
| Subfalcine | Cingulate gyrus under falx | Contralateral leg weakness (ACA territory) |
| Tonsillar | Cerebellar tonsils through foramen magnum | Sudden respiratory arrest, neck stiffness |
| Upward | Cerebellum through tentorial notch | Midbrain signs, bilateral pupil dilation |
Cushing's Triad (Late Sign of Raised ICP):
- Hypertension (widened pulse pressure)
- Bradycardia
- Irregular/agonal respiration
- Indicates impending brainstem herniation
- Emergency intervention required
Laboratory Investigations
| Investigation | Key Findings | Clinical Significance |
|---|---|---|
| FBC | Platelet count | Thrombocytopenia increases bleeding risk |
| Coagulation | PT/INR, APTT | Identify anticoagulation, guide reversal |
| U&E | Baseline renal function | For contrast, osmotherapy |
| Glucose | Hypo/hyperglycaemia | Affects outcome, requires treatment |
| Troponin | Cardiac injury | Stress cardiomyopathy common |
| Toxicology | Cocaine, amphetamines | Young patient with unexplained ICH |
Comprehensive Blood Panel:
| Test | Rationale | Action if Abnormal |
|---|---|---|
| Full blood count | Anaemia, thrombocytopenia | Transfuse if indicated |
| PT/INR | Warfarin monitoring | Reverse with PCC + Vitamin K |
| APTT | Heparin effect | Protamine if on heparin |
| Fibrinogen | Coagulopathy assessment | Cryoprecipitate if <1.5g/L |
| Thrombin time | DOAC detection | Suggests dabigatran if prolonged |
| Anti-Xa level | Quantify Xa inhibitor | Guide andexanet dosing |
| Creatinine | Renal function | Caution with contrast, osmotherapy |
| Electrolytes | Sodium for osmotherapy monitoring | Target sodium 145-155 if using HTS |
| Glucose | Glycaemic control | Target 6-10 mmol/L |
| Liver function | Synthetic function | May affect coagulation factor production |
| Troponin | Cardiac injury | ECG, cardiology if elevated |
| Lactate | Shock, hypoperfusion | Indicates severity |
| Arterial blood gas | Oxygenation, pH, CO2 | Guide ventilation |
Point-of-Care Testing:
- Thromboelastography (TEG) or ROTEM: Real-time coagulation assessment in massive haemorrhage
- INR point-of-care: Rapid warfarin reversal guidance
- i-STAT: Rapid haemoglobin, electrolytes, gases
Imaging
CT Head (Non-contrast) - FIRST LINE:
- Hyperdense (white) lesion in acute phase
- Assess location, volume, midline shift
- Intraventricular extension (IVH)
- Hydrocephalus
- Volume calculation: ABC/2 method (A x B x C / 2 in cm = mL)
CT Interpretation Details:
| Finding | Description | Significance |
|---|---|---|
| Hyperdensity | 60-90 HU in acute phase | Fresh blood |
| Location | Deep vs lobar | Suggests aetiology |
| Volume | ABC/2 formula | >30mL associated with poor outcome |
| Shape | Round vs irregular | Irregular suggests expansion |
| Surrounding hypodensity | Oedema | Peaks 3-7 days |
| Midline shift | >5mm concerning | May need surgery |
| IVH | Blood in ventricles | Adds 1 point to ICH score |
| Hydrocephalus | Dilated ventricles | May need EVD |
| Mass effect | Effacement of sulci, cisterns | Indicates raised ICP |
Volume Calculation (ABC/2 Method):
- A = Maximum haematoma diameter on largest slice (cm)
- B = Diameter perpendicular to A on same slice (cm)
- C = Number of CT slices with blood × slice thickness (cm)
- (Count slices where blood is >50% of largest area)
- Volume (mL) = A × B × C ÷ 2
- Example: A=4cm, B=3cm, C=4cm → Volume = 24mL
CT Angiography:
- "Spot sign" - contrast extravasation predicting expansion
- Identify underlying vascular lesion (AVM, aneurysm)
- Venous imaging if CVT suspected
Spot Sign Details:
- Definition: Focal enhancement within haematoma on CTA source images
- Sensitivity 51%, Specificity 85% for haematoma expansion
- Associated with:
- 3x increased risk of haematoma expansion
- 2x increased mortality
- 6x increased risk of poor outcome
- Multiple spot signs indicate higher risk
- Used in clinical trial selection for haemostatic agents
When to Perform CTA:
- All patients with ICH (to detect spot sign and underlying lesion)
- Especially if:
- Lobar location
- No history of hypertension
- Age <45 years
- Unusual location
- SAH component
MRI Brain:
- More sensitive for underlying lesion (tumour, cavernoma)
- Gradient echo (GRE) or SWI shows microbleeds (CAA marker)
- Not first-line in acute setting
MRI Sequences and Findings:
| Sequence | Acute (<12h) | Subacute (2-14d) | Chronic (>14d) |
|---|---|---|---|
| T1 | Isointense | Hyperintense (peripheral then central) | Hypointense |
| T2 | Hypointense (rim) | Hyperintense | Hypointense (hemosiderin rim) |
| FLAIR | Variable | Hyperintense | Variable |
| GRE/SWI | Hypointense (bloom) | Hypointense | Hypointense (hemosiderin) |
| DWI | Variable | Hyperintense ring | Variable |
Microbleed Pattern (SWI/GRE) and Aetiology:
- Strictly lobar: Cerebral amyloid angiopathy (Boston criteria)
- Deep/infratentorial: Hypertensive arteriopathy
- Mixed: Either or both pathologies
- Lobar microbleeds predict future lobar ICH recurrence
Digital Subtraction Angiography (DSA):
- Gold standard for vascular malformations
- Indications:
- CTA/MRA negative but high clinical suspicion
- Young patient with lobar ICH
- Unusual location or multiple haemorrhages
- Planning for intervention
- Can perform embolisation if AVM/aneurysm identified
Prognostic Scoring
ICH Score (Hemphill):
| Component | Criteria | Points |
|---|---|---|
| GCS 3-4 | Yes | 2 |
| GCS 5-12 | Yes | 1 |
| GCS 13-15 | Yes | 0 |
| ICH volume ≥30mL | Yes | 1 |
| IVH present | Yes | 1 |
| Infratentorial origin | Yes | 1 |
| Age ≥80 years | Yes | 1 |
| Total | 0-6 |
30-Day Mortality by ICH Score:
- Score 0: 0%
- Score 1: 13%
- Score 2: 26%
- Score 3: 72%
- Score 4: 97%
- Score 5-6: 100%
Other Prognostic Scores:
| Score | Components | Use |
|---|---|---|
| FUNC Score | Age, ICH volume, location, GCS, pre-ICH cognitive impairment | Predicts functional independence at 90 days |
| ICH-GS | GCS, volume, IVH, hydrocephalus | Predicts 30-day mortality |
| max-ICH | Age, NIHSS, IVH, blood glucose | Mortality prediction |
| BRAIN Score | ICH volume, age, GCS, glucose | Functional outcome |
FUNC Score for Functional Independence:
| Component | Criteria | Points |
|---|---|---|
| ICH volume | <30mL | 4 |
| 30-60mL | 2 | |
| >60mL | 0 | |
| Age | <70 | 2 |
| 70-79 | 1 | |
| ≥80 | 0 | |
| Location | Lobar | 2 |
| Deep | 1 | |
| Infratentorial | 0 | |
| GCS | ≥9 | 2 |
| <9 | 0 | |
| Pre-ICH cognitive impairment | No | 1 |
| Yes | 0 | |
| Total | 0-11 |
FUNC Score Interpretation:
- Score 0-4: 0% chance of functional independence
- Score 5-7: 1-13%
- Score 8-10: 29-82%
- Score 11: 82-100%
Management Algorithm
SUSPECTED ICH Presentation
↓
┌─────────────────────────────────────────┐
│ IMMEDIATE ACTIONS │
│ - ABC assessment, GCS monitoring │
│ - IV access, bloods (FBC, coag, G&S) │
│ - Urgent CT head within 1 hour │
└─────────────────────────────────────────┘
↓
┌─────────────────────────────────────────┐
│ ICH CONFIRMED ON CT │
├─────────────────────────────────────────┤
│ → Blood pressure control immediately │
│ → Reverse anticoagulation if applicable │
│ → Neurosurgery referral │
│ → ICU/HASU admission │
└─────────────────────────────────────────┘
↓
┌─────────────────────────────────────────┐
│ BLOOD PRESSURE MANAGEMENT │
│ Target SBP 130-140 mmHg within 1 hour │
│ IV labetalol or nicardipine infusion │
│ Avoid rapid drops and hypotension │
└─────────────────────────────────────────┘
↓
┌─────────────────────────────────────────┐
│ ANTICOAGULATION REVERSAL │
├─────────────────────────────────────────┤
│ Warfarin: IV Vit K + PCC (target INR<1.5│
│ Dabigatran: Idarucizumab 5g IV │
│ Xa inhibitors: Andexanet or PCC │
│ Heparin: Protamine sulfate │
└─────────────────────────────────────────┘
↓
┌─────────────────────────────────────────┐
│ NEUROSURGICAL DECISION │
├─────────────────────────────────────────┤
│ Cerebellar ICH >3cm: SURGERY │
│ Hydrocephalus: EVD │
│ Lobar ICH <1cm from surface: Consider │
│ Deep ICH: Usually conservative │
└─────────────────────────────────────────┘
↓
┌─────────────────────────────────────────┐
│ ONGOING MANAGEMENT │
│ - Neurocritical care monitoring │
│ - ICP management if required │
│ - DVT prophylaxis (timing considered) │
│ - Rehabilitation planning │
└─────────────────────────────────────────┘
Medical Management
Blood Pressure Control:
- Target: SBP 130-140 mmHg within 1 hour (INTERACT2 evidence)
- First-line: IV labetalol 10-20mg bolus, then infusion
- Alternative: IV nicardipine 5mg/hr, titrate by 2.5mg/hr
- Avoid: Rapid BP drops (>60mmHg/hr), hypotension (SBP <110)
- Duration: Maintain for at least 7 days
Antihypertensive Drug Details:
| Drug | Class | Dose | Onset | Advantages | Disadvantages |
|---|---|---|---|---|---|
| Labetalol | Alpha/beta blocker | 10-20mg bolus, then 1-2mg/min | 5-10 min | Widely available, titratable | Bradycardia, bronchoconstriction |
| Nicardipine | CCB (dihydropyridine) | 5mg/hr, titrate 2.5mg/hr q5-15min | 5-15 min | No reflex tachycardia | Requires infusion pump |
| Clevidipine | CCB (ultrashort) | 1-2mg/hr, double q90sec | 2-4 min | Rapid offset, precise control | Lipid emulsion formulation |
| GTN | Nitrate | 5-100mcg/min | 1-2 min | Rapid onset | ICP concern (venodilator) |
| Sodium nitroprusside | Direct vasodilator | 0.5-10mcg/kg/min | Immediate | Powerful | Cyanide toxicity, ICP concern |
| Hydralazine | Direct vasodilator | 10-20mg IV q4-6h | 10-20 min | Alternative if others unavailable | Reflex tachycardia, unpredictable |
BP Monitoring Protocol:
- Arterial line placement recommended for continuous monitoring
- Target SBP 130-140 mmHg (not <130 per ATACH-2)
- Avoid MAP <70 mmHg (risk of cerebral hypoperfusion)
- Reassess if patient deteriorates neurologically
- Continue intensive BP management for 7 days minimum
Anticoagulation Reversal:
| Anticoagulant | Reversal Agent | Dose | Target |
|---|---|---|---|
| Warfarin | IV Vitamin K + 4-factor PCC | Vit K 10mg IV + PCC 25-50 u/kg | INR <1.5 in 4 hours |
| Dabigatran | Idarucizumab | 5g IV | Complete reversal |
| Rivaroxaban/Apixaban | Andexanet alfa OR PCC | Andexanet or PCC 50 u/kg | Stop anticoagulant effect |
| Heparin | Protamine sulfate | 1mg per 100 units heparin | Normalise APTT |
| LMWH | Protamine (partial) | 1mg per 1mg enoxaparin | 60% reversal |
Warfarin Reversal Protocol:
- Stop warfarin immediately
- IV Vitamin K 10mg (slow infusion over 10-20 minutes)
- 4-factor PCC: Dose based on INR and weight
- INR 2-4: 25 units/kg
- INR 4-6: 35 units/kg
- INR >6: 50 units/kg
- Recheck INR at 30 minutes and 4 hours
- Target INR <1.5
- FFP only if PCC unavailable (slower, volume overload risk)
DOAC Reversal Protocol:
- Dabigatran: Idarucizumab 5g IV (two 2.5g vials)
- Immediate reversal, lasts 24 hours
- Can redose if needed
- Factor Xa inhibitors (rivaroxaban, apixaban, edoxaban):
- Andexanet alfa (if available): High-dose or low-dose based on time since last dose and specific drug
- 4-factor PCC 50 units/kg if andexanet unavailable
- No specific reversal agent for all Xa inhibitors
General Supportive Care:
- Head of bed 30° elevation
- Avoid hyperthermia (target normothermia)
- Glycaemic control (target glucose 6-10 mmol/L)
- Seizure management if seizures occur (no prophylactic anticonvulsants routinely)
- DVT prophylaxis (IPC immediately, pharmacological 24-48 hours if stable)
- Nutrition assessment and support
- Stress ulcer prophylaxis if ventilated
Surgical Management
Indications for Surgery:
- Cerebellar haemorrhage >3cm diameter or causing brainstem compression
- Cerebellar haemorrhage with hydrocephalus
- Lobar ICH >30mL and <1cm from cortical surface with deterioration
- Hydrocephalus requiring EVD
Surgical Options:
- Craniotomy and haematoma evacuation
- Minimally invasive surgery (endoscopic, stereotactic)
- EVD for hydrocephalus
- Decompressive craniectomy (limited evidence)
Craniotomy Technique:
- Open surgical evacuation via bone flap
- Best for accessible lobar haematomas
- Allows direct visualisation and haemostasis
- Higher morbidity than minimally invasive approaches
- Evidence: STICH I and II showed no overall benefit vs conservative
Minimally Invasive Surgery (MIS):
- Stereotactic aspiration with thrombolysis (rtPA)
- Endoscopic evacuation
- Smaller incision, less tissue disruption
- May improve outcomes (MISTIE III showed trend to benefit)
- Emerging as preferred technique in selected patients
EVD Placement:
- Indication: Obstructive hydrocephalus from IVH
- Usually Kocher's point (frontal) approach
- Allows CSF drainage and ICP monitoring
- Intraventricular thrombolysis (rtPA) can be given to clear IVH
- Risk: Ventriculitis (5-10%), haemorrhage
Decision Algorithm for Surgery:
| Scenario | Recommendation |
|---|---|
| Cerebellar ICH >3cm, deteriorating | Emergency craniotomy |
| Cerebellar ICH with hydrocephalus | EVD +/- craniotomy |
| Lobar ICH <1cm from surface, deteriorating | Consider craniotomy |
| Deep basal ganglia ICH | Usually conservative |
| Pontine ICH | Conservative (surgery not beneficial) |
| IVH with hydrocephalus | EVD +/- intraventricular thrombolysis |
Immediate Complications (0-24 hours)
| Complication | Incidence | Prevention/Management |
|---|---|---|
| Haematoma expansion | 30-40% | BP control, reversal, INTERACT2 |
| Raised ICP/herniation | 20-30% | Osmotherapy, surgery |
| Hydrocephalus | 15-20% (with IVH) | EVD |
| Seizures | 10-15% | Antiepileptics if occur |
| Aspiration | 20-30% | Swallow assessment, NBM |
Early Complications (1-7 days)
| Complication | Incidence | Prevention/Management |
|---|---|---|
| Perihematomal oedema | Peak 3-7 days | Monitor, osmotherapy if severe |
| Hospital-acquired pneumonia | 20-30% | Aspiration precautions |
| DVT/PE | 10-20% | Prophylaxis timing controversial |
| Fever | 30-40% | Antipyretics, infection screen |
Late Complications
| Complication | Incidence | Management |
|---|---|---|
| Post-stroke epilepsy | 5-10% | Long-term AEDs |
| Depression | 30-50% | Screening, treatment |
| Recurrent ICH | 2-4% per year | BP control, avoid anticoagulation |
| Cognitive impairment | 50%+ | Rehabilitation, support |
Mortality
- 30-day mortality: 40% (range 30-50%)
- 1-year mortality: 54%
- Factors: Volume, GCS, IVH, age, location
Functional Outcomes
- Independent at 6 months (mRS 0-2): 20%
- Dependent (mRS 3-5): 40%
- Dead: 40%
Predictors of Poor Outcome
- Large haematoma volume (>30mL)
- Low GCS at presentation
- Intraventricular extension
- Infratentorial location
- Older age
- Anticoagulation-related ICH
- Haematoma expansion
Key Guidelines
AHA/ASA Guidelines (2022):
- Target SBP 130-140 mmHg (Class IIa, Level B)
- Rapid reversal of anticoagulation (Class I, Level C)
- Cerebellar haematoma >3cm: surgical evacuation (Class I)
- VTE prophylaxis with IPC immediately, pharmacological 1-4 days
NICE Guidelines (2022):
- Immediate BP lowering for SBP 150-220 mmHg
- Imaging within 1 hour of presentation
- Admission to stroke unit
- Reverse anticoagulation urgently
Landmark Trials
INTERACT2 (2013):
- Population: n=2,839, ICH within 6 hours
- Intervention: Intensive BP lowering (SBP <140) vs guideline (<180)
- Result: Trend to reduced death/disability (OR 0.87); improved functional outcomes
- Impact: Changed practice to target SBP 130-140 mmHg
- PMID: 23713578
ATACH-2 (2016):
- Population: n=1,000, ICH with SBP >180
- Intervention: SBP 110-139 vs 140-179 mmHg
- Result: No difference in outcome; more renal AE in intensive arm
- Impact: Avoid target SBP <130 mmHg
- PMID: 27276234
STICH I (2005) and STICH II (2013):
- Population: Supratentorial ICH
- Intervention: Early surgery vs initial conservative
- Result: No overall benefit from early surgery
- Impact: Surgery reserved for specific indications
- PMID: 15680007 / PMID: 23245604
Explanation
"You have had a bleed inside your brain, called an intracerebral haemorrhage. This happens when a blood vessel in the brain bursts and blood spills into the brain tissue. The most common cause is high blood pressure over many years, which weakens the small blood vessels. The blood pressing on the brain causes the symptoms you are experiencing like weakness on one side or difficulty speaking. We need to control your blood pressure very carefully to try to stop the bleeding getting bigger. If you were on blood thinners, we need to reverse those quickly. Some people need an operation if the bleed is in a dangerous location or causing too much pressure. The first few days are critical because the bleeding can get worse. Recovery takes many months and involves rehabilitation to regain as much function as possible."
-
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: 20056489
-
Qureshi AI, Mendelow AD, Hanley DF. Intracerebral haemorrhage. Lancet. 2009;373(9675):1632-1644. PMID: 19427958
-
Hemphill JC 3rd, Greenberg SM, Anderson CS, et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage. Stroke. 2015;46(7):2032-2060. PMID: 26022637
-
Greenberg SM, Ziai WC, Cordonnier C, et al. 2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage. Stroke. 2022;53(7):e282-e361. PMID: 35579034
-
Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013;368(25):2355-2365. PMID: 23713578
-
Qureshi AI, Palesch YY, Barsan WG, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med. 2016;375(11):1033-1043. PMID: 27276234
-
Mendelow AD, Gregson BA, Fernandes HM, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas (STICH). Lancet. 2005;365(9457):387-397. PMID: 15680007
-
Mendelow AD, Gregson BA, Rowan EN, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II). Lancet. 2013;382(9890):397-408. PMID: 23726393
-
Hemphill JC 3rd, Bonovich DC, Besmertis L, et al. The ICH score: a simple, reliable grading scale for intracerebral hemorrhage. Stroke. 2001;32(4):891-897. PMID: 11283388
-
Goldstein JN, Fazen LE, Snider R, et al. Contrast extravasation on CT angiography predicts hematoma expansion in intracerebral hemorrhage. Neurology. 2007;68(12):889-894. PMID: 17372123
-
Pollack CV Jr, Reilly PA, van Ryn J, et al. Idarucizumab for Dabigatran Reversal - Full Cohort Analysis. N Engl J Med. 2017;377(5):431-441. PMID: 28693366
-
Connolly SJ, Crowther M, Eikelboom JW, et al. Full Study Report of Andexanet Alfa for Bleeding Associated with Factor Xa Inhibitors. N Engl J Med. 2019;380(14):1326-1335. PMID: 30730782
-
Viswanathan A, Greenberg SM. Cerebral amyloid angiopathy in the elderly. Ann Neurol. 2011;70(6):871-880. PMID: 22190361
-
Davis SM, Broderick J, Hennerici M, et al. Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage. Neurology. 2006;66(8):1175-1181. PMID: 16636233
-
Steiner T, Al-Shahi Salman R, Beer R, et al. European Stroke Organisation (ESO) guidelines for the management of spontaneous intracerebral hemorrhage. Int J Stroke. 2014;9(7):840-855. PMID: 25156220
-
Frontera JA, Lewin JJ 3rd, Rabinstein AA, et al. Guideline for Reversal of Antithrombotics in Intracranial Hemorrhage. Neurocrit Care. 2016;24(1):6-46. PMID: 26714677
-
Sprigg N, Flaherty K, Appleton JP, et al. Tranexamic acid for hyperacute primary IntraCerebral Haemorrhage (TICH-2). Lancet. 2018;391(10135):2107-2115. PMID: 29778325
-
Al-Shahi Salman R, Frantzias J, Lee RJ, et al. Absolute risk and predictors of the growth of acute spontaneous intracerebral haemorrhage. Brain. 2018;141(10):2857-2865. PMID: 30192917
Common Exam Questions
Questions that frequently appear in examinations:
-
MRCP Part 1: "A 72-year-old man on warfarin (INR 3.8) presents with sudden left-sided weakness and headache. CT shows right basal ganglia haemorrhage. What is the most appropriate reversal strategy?"
-
MRCP Part 2/PACES: "Describe the ICH score and how it predicts mortality."
-
FRCS Neurosurgery: "What are the indications for surgical intervention in spontaneous ICH?"
-
Emergency Medicine: "A patient with cerebellar haemorrhage is deteriorating rapidly. Describe your immediate management."
-
Viva: "Compare the evidence for blood pressure targets in acute ICH - discuss INTERACT2 and ATACH-2."
Viva Points
Opening Statement:
"Intracerebral haemorrhage accounts for 10-15% of strokes but has the highest mortality at 40% at 30 days. It is classified as primary (hypertensive or CAA) or secondary (vascular malformation, tumour, anticoagulation). Management priorities are BP control to target 130-140 mmHg within 1 hour (INTERACT2 evidence), anticoagulation reversal, and neurosurgical evaluation - with cerebellar ICH >3cm being an indication for emergency surgery."
Key Facts to Mention:
- Mortality 40% at 30 days; only 20% functionally independent at 6 months
- ICH Score predicts mortality (GCS, volume, IVH, infratentorial, age)
- Haematoma expansion occurs in 30-40% within 24 hours
- BP target: SBP 130-140 mmHg (not <130 - ATACH-2)
- Spot sign on CTA predicts expansion
Classification to Quote:
- "Primary ICH includes hypertensive (deep, basal ganglia) and CAA (lobar, elderly)"
- "ICH Score: 0-6 points; score of 3 = 72% 30-day mortality"
Evidence to Cite:
- "INTERACT2 showed intensive BP lowering (target <140) improved functional outcomes"
- "ATACH-2 showed no benefit and potential harm from targeting SBP <130"
- "STICH trials showed no overall benefit from early surgery for supratentorial ICH"
Common Mistakes
What fails candidates:
- ❌ Not knowing BP targets (too high or too low)
- ❌ Forgetting reversal agents for specific anticoagulants
- ❌ Not knowing surgical indications (especially cerebellar >3cm)
- ❌ Confusing ICH with SAH management
- ❌ Not knowing ICH score components
Dangerous Errors to Avoid:
- ⚠️ Delaying anticoagulant reversal
- ⚠️ Over-aggressive BP lowering (SBP <130)
- ⚠️ Missing posterior fossa ICH needing urgent surgery
- ⚠️ Attributing GCS drop to "stroke" without considering herniation
MCQ Practice Questions
Question 1: According to INTERACT2, what is the target systolic blood pressure for acute ICH? A. <120 mmHg B. 130-140 mmHg C. 140-160 mmHg D. <180 mmHg E. No BP lowering needed Answer: B - INTERACT2 showed improved functional outcomes with target SBP <140 mmHg within 1 hour. ATACH-2 showed harm with <130 mmHg.
Question 2: A 75-year-old on dabigatran presents with acute ICH. What is the specific reversal agent? A. Vitamin K B. Fresh frozen plasma C. Idarucizumab D. Protamine sulfate E. Tranexamic acid Answer: C - Idarucizumab (Praxbind) is the monoclonal antibody specific for dabigatran reversal. Dose is 5g IV.
Question 3: Which ICH location is most strongly associated with cerebral amyloid angiopathy? A. Basal ganglia B. Thalamus C. Lobar (cortical) D. Pons E. Cerebellum Answer: C - CAA causes lobar haemorrhages due to amyloid deposition in cortical vessels. Recurrent lobar bleeds in elderly without hypertension is classic.
Question 4: An ICH patient has GCS 5, haematoma volume 45mL, IVH present, located in cerebellum, age 82. What is their ICH score? A. 3 B. 4 C. 5 D. 6 E. 7 Answer: C - GCS 5 (1 point), volume ≥30mL (1 point), IVH (1 point), infratentorial (1 point), age ≥80 (1 point) = 5 points. 30-day mortality approaches 100%.
Question 5: A patient with a 4cm cerebellar haemorrhage and decreasing GCS. What is the most appropriate next step? A. IV mannitol and observe B. Emergency surgical evacuation C. Repeat CT in 6 hours D. Start tranexamic acid E. Transfer to stroke unit Answer: B - Cerebellar haemorrhage >3cm with clinical deterioration is an indication for emergency surgical evacuation due to risk of brainstem compression.
OSCE Station Guidance
Station: Acute ICH Management (8 minutes)
Scenario: You are the medical registrar. A 68-year-old man on warfarin for AF presents with sudden severe headache and right-sided weakness. GCS 12, BP 195/110. CT confirms left basal ganglia ICH with INR 4.2.
Expected Actions:
- Recognise anticoagulant-related ICH requiring urgent reversal
- Order IV Vitamin K 10mg AND 4-factor PCC 25-50 units/kg
- State INR target <1.5 within 4 hours
- Lower BP to target SBP 130-140 (IV labetalol)
- Contact neurosurgery for review
- Explain need for repeat CT to monitor for expansion
- Discuss prognosis sensitively with family
Differential Diagnosis
Conditions Mimicking ICH:
| Condition | Distinguishing Features | Key Investigation |
|---|---|---|
| Ischaemic stroke | Less headache/vomiting, CT initially normal or hypodense | CT/MRI - no blood |
| Subarachnoid haemorrhage | Thunderclap headache, meningism, blood in subarachnoid space | CT - basal cistern blood |
| Subdural haematoma | Crescent-shaped collection, history of trauma | CT - extra-axial blood |
| Epidural haematoma | Biconvex shape, lucid interval history | CT - lens-shaped |
| Brain tumour with haemorrhage | May have preceding symptoms, ring enhancement | MRI with contrast |
| Cerebral venous thrombosis | Headache, seizures, young women, postpartum | CT/MR venography |
| Hypertensive encephalopathy | PRES pattern on MRI, reversible | MRI - posterior white matter |
Secondary Causes to Exclude:
| Cause | Red Flag Features | Investigation |
|---|---|---|
| AVM | Young patient, lobar location | CT/MR angiography, DSA |
| Cavernoma | Multiple bleeds, family history | MRI with GRE/SWI |
| Aneurysm | SAH component, suprasellar | CT angiography |
| Tumour | Gradual symptoms, surrounding oedema | MRI with contrast |
| Coagulopathy | Known anticoagulation, liver disease | Coagulation screen |
| Cocaine/amphetamines | Young patient, drug history | Toxicology screen |
Special Populations
Anticoagulant-Related ICH:
- Higher mortality (50-67% vs 35% for non-anticoagulated)
- Larger haematomas, more expansion
- Urgent reversal is critical intervention
- Warfarin: INR-guided PCC + IV vitamin K
- DOACs: Specific reversal agents available
- Resume anticoagulation timing: individualised decision (often 4-8 weeks if high thrombotic risk)
- Consider left atrial appendage occlusion for AF patients with prior ICH
Pregnancy and ICH:
- Rare but devastating (incidence ~5-10 per 100,000 pregnancies)
- Causes: Eclampsia, HELLP, AVM rupture, CVT
- Management similar but multidisciplinary
- Foetal monitoring essential
- Delivery decision based on gestational age and maternal stability
- Eclampsia: Magnesium sulfate, delivery
Elderly Patients:
- Higher mortality at any given ICH score
- More likely CAA-related (lobar)
- Frailty and premorbid function important
- Goals of care discussion critical
- Avoid nihilistic approach - treatment still beneficial
- Age alone not contraindication to intervention
Young Patients (<45 years):
- Higher suspicion for secondary causes (AVM, aneurysm, coagulopathy)
- Drug use (cocaine, amphetamines) common cause
- Better recovery potential
- More aggressive investigation warranted
- Consider DSA if no cause on CTA
ICP Management
Indications for ICP Monitoring:
- GCS ≤8 and concern for raised ICP
- Intraventricular haemorrhage with hydrocephalus
- Post-operative monitoring after evacuation
ICP Management Steps:
| Intervention | Threshold | Details |
|---|---|---|
| Head elevation | ICP any | 30° head-up, neutral position |
| Sedation | ICP >20 | Propofol, midazolam |
| Osmotherapy | ICP >20 | Mannitol 0.5-1g/kg or hypertonic saline 23.4% 30mL |
| Hyperventilation | ICP >25 emergency | Target PaCO2 30-35 (temporary only) |
| CSF drainage | ICP >20 with EVD | Continuous or intermittent drainage |
| Neuromuscular blockade | Refractory | Paralysis reduces ICP |
| Decompressive surgery | Refractory | Last resort |
Osmotherapy Comparison:
| Agent | Dose | Onset | Duration | Considerations |
|---|---|---|---|---|
| Mannitol 20% | 0.5-1g/kg IV | 15-30 min | 2-6 hours | May cause AKI, monitor osmolar gap |
| Hypertonic saline 23.4% | 30mL bolus | 5-10 min | 2-4 hours | Requires central line, check sodium |
| Hypertonic saline 3% | 250mL bolus | 15-30 min | 2-4 hours | Can use peripheral, less effective |
Rehabilitation and Recovery
Acute Rehabilitation:
- Swallow assessment within 24 hours
- Physiotherapy and occupational therapy early
- Speech therapy if dysphasia/dysarthria
- Positioning to prevent contractures
- DVT prophylaxis (IPC, then pharmacological when safe)
Long-term Rehabilitation:
- Inpatient rehabilitation if potential for recovery
- Community rehabilitation and support
- Spasticity management (botox, baclofen)
- Cognitive rehabilitation
- Mood assessment and treatment
- Return to work/driving assessment
Prognosis by Location:
| Location | Mortality | Good Recovery (mRS 0-2) | Key Determinants |
|---|---|---|---|
| Putaminal | 30-40% | 25-35% | Volume, IVH |
| Thalamic | 40-50% | 15-25% | IVH common, hydrocephalus |
| Lobar | 25-35% | 30-40% | Better if superficial |
| Cerebellar | 30-40% | 40-50% | Surgery if >3cm |
| Pontine | 60-80% | 5-10% | Very poor prognosis |
Prevention
Secondary Prevention:
- Blood pressure control (target <130/80 mmHg)
- Avoid anticoagulation if possible (LAA occlusion for AF)
- Reduce alcohol intake
- Smoking cessation
- Statin therapy (CAA concern theoretically but benefit outweighs)
- Control modifiable risk factors
BP Target Post-ICH:
- Long-term: SBP <130 mmHg (PROGRESS trial)
- Reduces recurrence by 50-70%
- All major guidelines recommend aggressive BP control
Ethical Considerations
Prognostication:
- ICH score is guideline, not absolute
- Early withdrawal of care may be self-fulfilling prophecy
- Recommend aggressive early treatment for at least 24-48 hours
- Involve palliative care early for comfort measures discussions
- Family meetings crucial for shared decision-making
Goals of Care:
- Discuss DNAR status appropriately
- Consider premorbid function and patient wishes
- Advance directive relevant if available
- Time-limited trial of treatment reasonable approach
- Avoid both therapeutic nihilism and futile intervention
Quality Indicators
Hospital Metrics:
- Time to CT (<1 hour from presentation)
- Time to anticoagulation reversal (<4 hours for INR <1.5)
- BP control within 1 hour
- Stroke unit admission rate
- Neurosurgery referral for surgical indications
- DVT prophylaxis within 24-48 hours
- Swallow screen within 24 hours
- Rehabilitation referral
Outcome Metrics:
- 30-day mortality
- 90-day functional outcome (mRS)
- Length of stay
- Discharge destination
- Readmission rate
- Recurrent ICH rate
Comparison with Other Stroke Types
| Feature | ICH | Ischaemic Stroke | SAH |
|---|---|---|---|
| Proportion of stroke | 10-15% | 80-85% | 3-5% |
| Mortality (30-day) | 40% | 10-15% | 30-40% |
| Headache at onset | 40-50% | 15-20% | 90%+ |
| Vomiting | 40-50% | 10-15% | 70%+ |
| Decreased consciousness | 30-50% | 10-20% | 30-50% |
| CT appearance (acute) | Hyperdense | Normal/hypodense | Subarachnoid blood |
| Key treatment | BP control, reversal | Thrombolysis, thrombectomy | Aneurysm securing |
Historical Perspective
Evolution of ICH Management:
- 1960s-70s: Surgical evacuation primary treatment
- 1980s: Medical management emerged
- 1990s: Risk factor identification
- 2000s: STICH trials changed surgical practice
- 2010s: INTERACT changed BP management
- 2020s: Focus on reversal agents, MIS
Key Historical Figures:
- Charcot and Bouchard: Described microaneurysms (1868)
- Cushing: Described Cushing response
- Hemphill: Developed ICH score (2001)
- Anderson: INTERACT trials changing BP targets
Future Directions
Research Areas:
- Minimally invasive surgery (MISTIE, ENRICH trials)
- Novel haemostatic agents
- Neuroprotection strategies
- Biomarkers for expansion prediction
- Precision medicine approach
- AI-assisted prognostication
- Gene therapy for CAA
Emerging Therapies:
- Tranexamic acid (TICH-2 negative, but role debated)
- Deferoxamine (iron chelation, neuroprotection)
- Anti-inflammatory agents
- Stem cell therapy (experimental)
- Blood pressure targets refinement
Extended MCQ Practice
Question 6: A 58-year-old man with no significant past medical history presents with sudden onset headache and left arm weakness. CT shows a 2cm lobar haemorrhage in the right parietal lobe. What investigation should be performed next? A. Lumbar puncture B. CT angiography C. Transthoracic echocardiogram D. 24-hour tape E. Carotid Doppler Answer: B - Young patient with lobar ICH and no hypertension needs investigation for secondary causes. CT angiography can identify AVM, aneurysm, or other vascular malformation.
Question 7: A 78-year-old woman with known AF on apixaban (last dose 6 hours ago) presents with acute ICH. What is the most appropriate reversal strategy? A. Vitamin K 10mg IV B. FFP 15mL/kg C. 4-factor PCC 25-50 units/kg D. Andexanet alfa E. Tranexamic acid Answer: D - Andexanet alfa is the specific reversal agent for factor Xa inhibitors (apixaban, rivaroxaban). If unavailable, 4-factor PCC (C) is an alternative.
Question 8: Which of the following imaging findings is most predictive of haematoma expansion? A. Midline shift >5mm B. Intraventricular extension C. Spot sign on CT angiography D. Surrounding oedema E. Volume >30mL Answer: C - The "spot sign" represents active contrast extravasation into the haematoma and predicts expansion with 91% specificity. This has implications for prognosis and potential trial eligibility.
Question 9: A patient with a 4.5cm pontine haemorrhage is in coma with bilateral pinpoint pupils. The family asks about prognosis. What is the approximate 30-day mortality for this presentation? A. 10-20% B. 30-40% C. 50-60% D. 70-80% E. >90% Answer: D or E - Pontine haemorrhage has the worst prognosis of all ICH locations, with mortality 60-80% and functional independence extremely rare. Large volume with coma suggests prognosis at the worse end.
Question 10: A 65-year-old with ICH and IVH has decreasing consciousness. CT shows hydrocephalus. What is the most appropriate immediate intervention? A. IV mannitol B. External ventricular drain C. Decompressive craniectomy D. Lumbar puncture E. High-dose methylprednisolone Answer: B - Obstructive hydrocephalus from IVH requires CSF diversion. EVD allows drainage and ICP monitoring. Mannitol may help temporarily but doesn't address the obstruction.
Additional Viva Scenarios
Scenario 1: Young Patient with ICH
"A 32-year-old man presents with sudden severe headache and right-sided weakness. CT shows left frontal lobar haemorrhage. No history of hypertension. How do you approach this case?"
Model Answer:
- "This is atypical ICH - young patient, lobar location, no hypertension. I am suspicious of secondary cause."
- "Initial management: ABC, secure IV access, urgent bloods including toxicology screen"
- "Blood pressure control to <140 systolic"
- "Investigations for underlying cause: CT angiography urgently to look for AVM, aneurysm, or DAVF. Consider MRI with contrast for tumour."
- "If CTA negative and clinical suspicion high, would consider DSA (gold standard for vascular malformations)"
- "Ask about drug use - cocaine and amphetamines are important causes in young patients"
- "Discuss with neurosurgery for possible intervention if vascular malformation found"
Scenario 2: Posterior Fossa ICH
"A 70-year-old man with hypertension presents with acute onset vertigo, vomiting, and ataxia. CT shows a 3.5cm cerebellar haemorrhage with early hydrocephalus. GCS is 13. What is your management?"
Model Answer:
- "This is a surgical emergency. Cerebellar haemorrhage >3cm with hydrocephalus and neurological symptoms requires urgent intervention."
- "Immediate actions: Airway protection if GCS deteriorates, IV access, bloods"
- "Blood pressure control to SBP 130-140"
- "Urgent neurosurgical referral for posterior fossa decompression and haematoma evacuation"
- "May need EVD for hydrocephalus"
- "Close monitoring for deterioration - can deteriorate rapidly from brainstem compression"
- "Surgery is life-saving in this scenario - studies show improved outcomes vs conservative management"
Scenario 3: Anticoagulated Patient
"A 75-year-old woman on rivaroxaban for AF presents with acute left hemiparesis. CT confirms right basal ganglia ICH. Her CHA2DS2-VASc is 5. Discuss your management and long-term anticoagulation strategy."
Model Answer:
- "Anticoagulant-related ICH is a medical emergency with higher mortality"
- "Immediate: Andexanet alfa if available, otherwise 4-factor PCC 50 units/kg. Stop rivaroxaban."
- "Blood pressure control to 130-140 systolic"
- "Neurosurgery referral for consideration of intervention"
- "Long-term anticoagulation decision: Complex - high stroke risk (CHA2DS2-VASc 5) but now history of ICH"
- "Options: Left atrial appendage occlusion (Watchman device), antiplatelet therapy alone, or cautious re-anticoagulation after 4-8 weeks with DOAC (lower ICH risk than warfarin)"
- "Multidisciplinary decision involving stroke, cardiology, and patient preferences"
Last Reviewed: 2025-12-27 | MedVellum Editorial Team
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists and current guidelines.