Key Facts

Intracerebral haemorrhage (ICH) is the deadliest form of stroke. Despite advances in acute care, mortality remains high. Early aggressive management of blood pressure and anticoagulant reversal are the key modifiable factors in the acute phase.

Epidemiology

~15% of all strokes (~15,000 per year in the UK). Incidence ~25 per 100,000 per year. Mortality ~40% at 30 days, ~55% at 1 year. Only 20% of survivors are functionally independent at 6 months. Incidence higher in Afro-Caribbean and South Asian populations. Rising incidence due to anticoagulant use in aging population.

Aetiology

• Hypertensive vasculopathy (~60%): deep locations (putamen 35%, thalamus 20%, pons 5%, cerebellum 10%)
• Cerebral amyloid angiopathy (~15-20%): lobar haemorrhages in elderly; sporadic or hereditary
• Anticoagulant-related (~10-15%): warfarin, DOACs, heparin
• Vascular malformations: AVM, cavernoma, dural AV fistula (younger patients)
• Other: brain tumour (metastasis, glioma), coagulopathy, vasculitis, cocaine/amphetamine use, haemorrhagic transformation of ischaemic stroke, venous sinus thrombosis

Pathophysiology

Hypertensive ICH: chronic hypertension damages small penetrating arteries → lipohyalinosis and Charcot-Bouchard microaneurysms → rupture → haematoma formation → mass effect, raised ICP, secondary injury from inflammation and oedema. Haematoma expansion occurs in ~30% within the first 3-6 hours ("spot sign" on CTA predicts expansion). CAA: amyloid-β deposition in cortical/leptomeningeal vessel walls → vessel fragility → lobar haemorrhage.

Presentation

• Sudden-onset severe headache ("worst headache" — less common than SAH but can occur)
• Rapid-onset focal neurological deficit (similar to ischaemic stroke but often more rapid)
• Vomiting (raised ICP)
• Decreased level of consciousness (earlier and more frequent than ischaemic stroke)
• Seizures (~10% at onset)

Location-Specific Features

• Putaminal: contralateral hemiparesis, hemisensory loss, gaze deviation
• Thalamic: contralateral sensory loss > motor, upgaze palsy, small pupils
• Pontine: quadriplegia, pinpoint pupils, coma (devastating)
• Cerebellar: sudden ataxia, headache, vomiting → rapid deterioration (hydrocephalus/brainstem compression)
• Lobar (CAA): cortical signs depending on location; seizures more common

Red Flags

• Decreasing GCS (haematoma expansion, hydrocephalus)
• Fixed dilated pupil (uncal herniation)
• Anticoagulated patient with sudden neurological deficit
• Young patient with lobar ICH (underlying vascular malformation)

Bedside

• GCS: baseline and serial monitoring
• Blood glucose: exclude hypoglycaemia
• BP: often markedly elevated

Imaging

• CT head (non-contrast): IMMEDIATE — acute blood appears hyperdense (bright white); identify location, volume (ABC/2 method), intraventricular extension, hydrocephalus
• CT angiography: spot sign (contrast extravasation within haematoma) predicts expansion; identify underlying vascular malformation
• MRI (GRE/SWI sequences): cerebral microbleeds (CAA pattern — lobar; hypertensive — deep); cortical superficial siderosis (CAA); identify underlying lesion
• CT/MR venography: if venous sinus thrombosis suspected
• Digital subtraction angiography (DSA): gold standard for AVM/aneurysm if suspected

Bloods

• FBC, coagulation (INR, APTT, fibrinogen): URGENT — guide reversal therapy
• U&Es, LFTs: baseline
• Group and save: for potential surgery
• Drug screen: if cocaine/amphetamine suspected

ICH Score

• ICH Score (Hemphill): predicts 30-day mortality; uses GCS, ICH volume, IVH, infratentorial origin, age >80
  • Score 0: ~0% mortality; Score 5: ~100% mortality

Acute

• Admit to hyperacute stroke unit/neurocritical care
• BP reduction: target <140 mmHg systolic within 1 hour (INTERACT-2 trial)
  • IV labetalol 10-20 mg bolus, repeat every 10-20 min (max 300 mg); or infusion 2 mg/min
  • IV GTN infusion 1-10 mg/hr
  • IV nicardipine infusion 5-15 mg/hr
• Anticoagulant reversal (URGENT):
  • Warfarin: IV vitamin K 5-10 mg + 4-factor PCC (Beriplex) 25-50 IU/kg (do NOT wait for INR result if strongly suspected); target INR <1.5
  • Dabigatran: idarucizumab 5 g IV (specific reversal agent)
  • Anti-Xa agents (rivaroxaban, apixaban, edoxaban): andexanet alfa if available; otherwise PCC 50 IU/kg
  • Heparin: protamine sulphate (1 mg per 100 units heparin given in last 2-3 hours)
• Tranexamic acid: TICH-2 trial showed no overall benefit on functional outcome; may reduce early haematoma expansion but not routinely recommended

Surgical/Interventional

• Neurosurgical referral: all patients with cerebellar haemorrhage (risk of hydrocephalus/brainstem compression), large superficial lobar haemorrhages, hydrocephalus
• External ventricular drain (EVD): for acute hydrocephalus (intraventricular extension)
• Surgical evacuation: cerebellar haematoma >3 cm with deterioration; large lobar haematoma with deterioration; STICH/STICH-2 trials showed no overall benefit of early surgery for supratentorial ICH but benefit in superficial lobar haematomas <1 cm from cortical surface
• Minimally invasive surgery: MISTIE III — stereotactic catheter + alteplase into haematoma; some benefit if residual clot reduced to <15 mL

Secondary Prevention

• BP control: long-term target <130/80
• Anticoagulation restart: controversial; consider restart at 4-8 weeks if high thromboembolic risk (e.g., mechanical valve, high-risk AF) after MDT discussion; LEFT-APPENDAGE CLOSURE (LAA occlusion) may be alternative
• Statin use: controversial after ICH; likely safe for non-CAA ICH
• Investigate underlying cause: AVM, aneurysm, tumour in young patients or atypical location

Referral Criteria

• Neurosurgery: all ICH (especially cerebellar, with hydrocephalus, young patients)
• Hyperacute stroke unit: all ICH patients
• Haematology: anticoagulant reversal advice

30-day mortality ~40%. 1-year mortality ~55%. Only 20% of survivors are functionally independent at 6 months. Haematoma volume >30 mL and GCS <8 predict poor outcome. Intraventricular extension doubles mortality. Cerebellar haemorrhage: rapid deterioration but good outcomes if promptly evacuated. CAA-related ICH has ~10% annual recurrence risk. Anticoagulant-related ICH has higher mortality than spontaneous ICH.

ICH Score (Hemphill)

Hypertensive vs CAA ICH