Intracerebral Hemorrhage

Intracerebral haemorrhage accounts for 10 to 15% of strokes and carries a 30-day mortality near 40%. Incidence is about 25 to 30 per 100,000, higher in East Asian and Black populations and with age.

Primary haemorrhage (about 80%)

• Hypertensive arteriopathy: lipohyalinosis of deep perforators. Sites are putamen (about 35%), thalamus (about 20%), pons and cerebellum.
• Cerebral amyloid angiopathy: lobar haemorrhage in older adults, often recurrent and associated with microbleeds.

Secondary causes

• Vascular malformations (AVM, cavernoma, dural fistula) and aneurysm.
• Tumour, venous thrombosis, haemorrhagic transformation of infarct.
• Anticoagulants, antiplatelets, thrombolytics, coagulopathy, thrombocytopenia.
• Sympathomimetics (cocaine, amphetamine), vasculitis, moyamoya, reversible cerebral vasoconstriction syndrome.

Pathophysiology

• Haematoma expansion occurs in 20 to 38% of patients and mostly within the first 3 hours.
• Perihaematomal oedema peaks between days 10 and 20.
• Intraventricular extension causes hydrocephalus.

Prognosis is judged by the ICH score. One point each is given for

• GCS 5 to 12 (2 points if GCS 3 to 4).
• Haematoma volume of 30 mL or more.
• Intraventricular blood.
• Infratentorial origin.
• Age 80 or above.

Mortality at 30 days rises from near 0% at score 0 to about 13% at 1, 26% at 2, 72% at 3, and 97% at 4. Volume is estimated by ABC/2.

Presentation is sudden focal deficit that evolves over minutes to hours, with headache, vomiting, hypertension and decreased consciousness. Seizures are more frequent with lobar bleeds.

Location syndromes

• Putamen: contralateral hemiparesis and hemisensory loss, hemianopia, gaze deviation toward the lesion.
• Thalamus: dense hemisensory loss, vertical gaze palsy, small non-reactive pupils, eyes deviated down and inward, aphasia if dominant.
• Pons: coma, quadriparesis, pinpoint pupils, ocular bobbing, hyperthermia.
• Cerebellum: vomiting, gait ataxia, gaze palsy toward the lesion, absent hemiparesis, and risk of abrupt brainstem compression and hydrocephalus.
• Lobar: seizures, visual field loss, aphasia or neglect.

Deterioration is signalled by falling GCS, anisocoria, Cushing response and new hydrocephalus. In contrast to ischaemic stroke, the deficit builds progressively, though clinical differentiation is unreliable without imaging.

Urgent non-contrast CT confirms haemorrhage and measures volume, intraventricular extension, hydrocephalus and mass effect. Features predicting expansion include the spot sign on CTA, and blend, black hole and island signs on non-contrast CT.

Look for a secondary cause when any of the following apply

• Age under 70.
• Lobar, posterior fossa or isolated intraventricular haemorrhage.
• Absent hypertension.

Further investigations

• CTA with CT venography, or DSA if a vascular lesion is suspected.
• MRI with gradient echo or SWI to find microbleeds and cortical superficial siderosis (supporting cerebral amyloid angiopathy), and to detect underlying tumour or cavernoma. Repeat MRI at 4 to 8 weeks once the haematoma resolves.
• CBC, PT/INR, aPTT, fibrinogen, anti-Xa level or calibrated drug-specific assay, renal function, glucose, troponin, ECG, urine toxicology, pregnancy test.

Blood pressure

• Lower SBP promptly to a target of 130 to 150 mmHg and keep it stable. Avoid reductions below 130 mmHg, which are associated with renal injury.
• Nicardipine 5 mg/h titrated by 2.5 mg/h every 5 to 15 minutes to a maximum 15 mg/h.
• Labetalol 10 to 20 mg IV, repeated, or 0.5 to 2 mg/min infusion.
• Clevidipine 1 to 2 mg/h, doubled every 90 seconds initially up to 21 mg/h.

Reversal of coagulopathy

• Warfarin: vitamin K 10 mg IV slowly, with 4-factor PCC at 25 units/kg for INR 2 to under 4, 35 units/kg for INR 4 to 6, and 50 units/kg above 6.
• Dabigatran: idarucizumab 5 g IV (two 2.5 g doses).
• Apixaban or rivaroxaban: andexanet alfa low dose (400 mg bolus at 30 mg/min then 4 mg/min for up to 120 minutes) when the last apixaban dose was 5 mg or less, or rivaroxaban 10 mg or less. Otherwise use the high dose (800 mg bolus then 8 mg/min for up to 120 minutes). If unavailable, use 4-factor PCC 2000 units fixed or 50 units/kg.
• Unfractionated heparin: protamine 1 mg per 100 units given in the previous 2 to 3 hours, maximum 50 mg.
• Enoxaparin: protamine 1 mg per 1 mg enoxaparin if within 8 hours.
• Platelet transfusion is not given for antiplatelet effect unless surgery is planned, as it worsens outcome.
• Tranexamic acid 1 g over 10 minutes then 1 g over 8 hours within 3 hours reduces expansion but has not improved function, so it is not routine.
• Recombinant factor VIIa is not recommended.

Surgery and drainage

• Cerebellar haematoma above 3 cm with brainstem compression, hydrocephalus or neurological decline: urgent posterior fossa craniectomy and evacuation. EVD alone is inadequate.
• Supratentorial haematoma: routine early evacuation does not improve outcome. Consider evacuating superficial lobar clots of 10 to 100 mL in patients with GCS 9 to 12 who are deteriorating. Minimally invasive evacuation can help in selected patients, especially when residual volume is reduced to 15 mL or less.
• Decompressive craniectomy for large haematomas with herniation and for refractory ICP.
• Hydrocephalus or intraventricular blood: EVD. Intraventricular alteplase (1 mg every 8 hours) accelerates clot clearance but does not improve function.

Supportive care

• Manage ICP as in raised intracranial pressure: head elevation 30 degrees, osmotherapy, sedation.
• Do not give corticosteroids. Treat only clinical seizures, with levetiracetam; prophylaxis is not indicated.
• Glucose 140 to 180 mg/dL, normothermia, dysphagia screening before oral intake.
• Intermittent pneumatic compression from admission. Start prophylactic enoxaparin 40 mg SC daily 1 to 4 days after bleeding is stable on repeat imaging.

Secondary prevention

• Long-term BP below 130/80 mmHg, often with perindopril 4 mg plus indapamide 2.5 mg daily.
• Anticoagulation after deep haemorrhage in atrial fibrillation can be restarted at about 4 to 8 weeks. In lobar haemorrhage due to cerebral amyloid angiopathy, avoid it; consider left atrial appendage occlusion.
• Antiplatelet therapy can be resumed after about 1 to 2 weeks when there is a strong indication.
• Limit alcohol and treat sleep apnoea. Early rehabilitation.