Intracerebral haemorrhage
Description
- Spontaneous bleeding into brain parenchyma, not due to trauma
- ~10-15% of all strokes but disproportionately high mortality/morbidity
- *Neurological deterioration in the first hours is the rule, not the exception* - haematoma expansion drives early decline
Epidemiology
- 30-day mortality ~40%; only ~20% functionally independent at 6 months
- Incidence rises steeply with age and uncontrolled hypertension
- Higher incidence in Asian populations and with anticoagulant use
Aetiopathogenesis
By location (guides likely cause)
- Deep (basal ganglia, thalamus, pons, cerebellum) - hypertensive small vessel disease (lipohyalinosis) - commonest overall
- Lobar - cerebral amyloid angiopathy (older patients, recurrent lobar bleeds, associated with cognitive decline) or structural lesion
Other causes
- Anticoagulant/antiplatelet-associated - major and increasing cause
- Vascular malformation (AVM, cavernoma) - consider in younger patients or atypical location
- Haemorrhagic transformation of ischaemic infarct
- Vasculitis, venous sinus thrombosis, tumour, illicit stimulant use (cocaine, amphetamines)
- Coagulopathy (liver disease, thrombocytopenia)
Diagnosis
A. Clinical
- Sudden focal neurological deficit, often with headache, vomiting, reduced consciousness, and hypertension more than in ischaemic stroke
- Progressive deterioration over minutes-hours (haematoma expansion) - unlike the typically static deficit of ischaemic stroke
B. Imaging
- Non-contrast CT brain - immediate, defines haemorrhage, volume, location, intraventricular extension, mass effect
- CT angiography "spot sign" - contrast extravasation within the haematoma predicts expansion and poor outcome
- MRI +/- vessel imaging if underlying structural lesion (AVM, tumour) suspected, especially in younger/lobar/atypical cases
- Coagulation studies, FBE, UEC, glucose, toxicology in selected cases
Management
A. Hyperacute care bundle - the biggest outcome driver, and now guideline-defining
- INTERACT3 goal-directed bundle: early intensive SBP lowering to target <140mmHg, glucose control (6.1-7.8mmol/L non-diabetic; 7.8-10.0mmol/L diabetic), temperature control (<=37.5C), and rapid anticoagulation reversal (INR <1.5) - this bundle improved functional outcome in a large RCT and is now the benchmark of hyperacute care
- Do not lower BP so aggressively/rapidly as to risk cerebral hypoperfusion - target reached smoothly, not by bolus overcorrection
B. Reverse coagulopathy immediately
- Warfarin: prothrombinex (4-factor PCC) + IV vitamin K, target INR <1.5 urgently
- DOAC (factor Xa inhibitor): andexanet alfa where available (ANNEXA-I showed improved haemostatic efficacy over usual care/PCC), or 4-factor PCC if unavailable
- Dabigatran: idarucizumab
- Antiplatelet-associated: platelet transfusion not routinely recommended (may worsen outcome) unless urgent neurosurgery planned
- Resume anticoagulation timing for AF post-ICH is individualised (typically weeks), balancing recurrent hemorrhage vs thromboembolism risk
C. Surgical/procedural
- Minimally invasive haematoma evacuation - ENRICH trial (2024) showed functional benefit for lobar haemorrhages 30-80mL evacuated within 24h; changes prior nihilism (STICH trials) about surgery for supratentorial ICH
- Cerebellar haemorrhage >3cm, brainstem compression, or hydrocephalus - urgent surgical evacuation/EVD - a long-standing, unambiguous indication
- External ventricular drain for hydrocephalus/intraventricular extension
- Decompressive craniectomy considered in selected large haematomas with mass effect
D. General supportive care
- ICU/stroke unit level monitoring, seizure treatment only if clinical/EEG-confirmed seizures occur (no role for prophylactic anticonvulsants)
- Avoid hyperglycaemia and hyperthermia (part of the bundle above)
- Early, cautious VTE prophylaxis (mechanical first; pharmacological once stability confirmed, usually 24-48h post-bleed)
E. Secondary prevention
- Long-term BP control is the single most important modifiable factor for recurrence
- Address underlying cause - treat structural lesion if found; caution with future antithrombotic use, especially lobar/amyloid-related ICH
Associations
- Hypertension (deep ICH)
- Cerebral amyloid angiopathy (lobar ICH, older patients, cognitive decline)
- Anticoagulant and antiplatelet therapy
- Vascular malformations (younger patients)
- Alcohol excess, illicit stimulant use
Natural history & complications
- Haematoma expansion in the first 24 hours is the dominant driver of early deterioration and mortality
- 30-day mortality ~40%; survivors often left with significant disability
- Recurrence risk highest in lobar/amyloid-related ICH
- Late complications: hydrocephalus, seizures, cognitive impairment (especially with amyloid angiopathy)
- Early, aggressive physiological control (bundle above) is now proven to shift the outcome curve - this is not a purely nihilistic diagnosis
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