Hemorrhagic (Intracerebral) Stroke
Non-traumatic bleeding into brain parenchyma; higher mortality than ischemic stroke.
Also known as: ICH, intracerebral hemorrhage, intraparenchymal hemorrhage, hypertensive hemorrhage
Overview
Spontaneous (non-traumatic) bleeding into the brain parenchyma, with or without extension into the ventricles or subarachnoid space. Distinguished from subarachnoid hemorrhage and traumatic hemorrhage.
Epidemiology
~10-15% of all strokes but accounts for ~40% of stroke mortality. 30-day mortality 30-50%. More common in Black, Hispanic, and Asian populations.
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Risk factors
- Chronic hypertension (most common cause, ~50% — typically deep structures: basal ganglia, thalamus, pons, cerebellum)
- Cerebral amyloid angiopathy (elderly, lobar hemorrhages, often recurrent)
- Anticoagulant or antiplatelet therapy
- Arteriovenous malformation, cavernoma (younger patients)
- Hemorrhagic transformation of ischemic stroke
- Tumor (primary or metastatic — melanoma, RCC, choriocarcinoma, thyroid, lung)
- Sympathomimetic drugs (cocaine, methamphetamine)
- Coagulopathy, thrombocytopenia, vasculitis
Pathophysiology
Rupture of small perforating arteries (lipohyalinosis from chronic HTN) or amyloid-laden cortical vessels causes blood to dissect into surrounding brain tissue. Mass effect, perihematomal edema, and toxic effects of blood breakdown products drive secondary injury. Hematoma expansion in the first 6 hours is the strongest predictor of poor outcome.
Clinical presentation
Symptoms
- Sudden focal neurologic deficit (similar to ischemic stroke)
- Headache (more common and severe than ischemic stroke)
- Nausea/vomiting
- Decreased level of consciousness, often progressive over minutes-hours
- Seizures in ~10% (especially lobar hemorrhage)
Signs / physical exam
- Markedly elevated blood pressure (often >180/110)
- Focal deficit by hematoma location: putaminal (contralateral hemiparesis, gaze deviation), thalamic (contralateral sensory loss, vertical gaze palsy), pontine (coma, pinpoint pupils, quadriparesis), cerebellar (ataxia, vertigo)
- Signs of elevated ICP: Cushing triad (HTN, bradycardia, irregular respirations), papilledema, fixed/dilated pupil (uncal herniation)
Classic findings
Hypertensive ICH classically in basal ganglia (putamen most common), thalamus, pons, or cerebellum. ICH score predicts 30-day mortality.
Differential diagnosis
- Ischemic stroke — Indistinguishable clinically — CT differentiates; ICH more often presents with headache, vomiting, depressed consciousness, and very high BP
- Subarachnoid hemorrhage — Thunderclap headache, meningismus, blood in basal cisterns rather than parenchyma
- Traumatic ICH / contusion — History of trauma; coup-contrecoup pattern; often frontal or temporal poles
- Brain tumor with hemorrhage — Surrounding edema disproportionate to hematoma size; heterogeneous enhancement; metastatic primaries above
- Hemorrhagic transformation — Recent ischemic stroke, classic arterial territory of hypodensity with petechial or confluent hemorrhage
- Cerebral venous sinus thrombosis — Lobar hemorrhage in non-arterial territory; risk factors (OCPs, pregnancy, thrombophilia); empty delta sign on CTV/MRV
Diagnostic workup
Labs
- CBC, platelets, PT/INR, PTT — assess coagulopathy
- BMP, glucose, troponin
- Toxicology screen (cocaine, methamphetamine in young patients)
- Type and screen
Imaging
- Non-contrast head CT — high-density acute hematoma; immediately diagnostic
- CT angiography — 'spot sign' (contrast extravasation) predicts hematoma expansion; rules out underlying vascular lesion
- MRI with susceptibility-weighted imaging — chronic microbleeds suggest cerebral amyloid angiopathy or hypertensive disease
- Catheter angiography if AVM, aneurysm, or vasculitis suspected (especially lobar hemorrhage in young patient)
Diagnostic algorithm
| Location | Typical Etiology | Classic Signs |
|---|---|---|
| Putamen / basal ganglia | Hypertension | Contralateral hemiparesis, eyes deviate toward lesion |
| Thalamus | Hypertension | Contralateral sensory loss, eyes deviate down and in |
| Pons | Hypertension | Coma, pinpoint reactive pupils, quadriparesis |
| Cerebellum | Hypertension | Ataxia, vomiting, occipital headache — surgical if >3 cm |
| Lobar (cortex) | Amyloid angiopathy, AVM, tumor | Variable by lobe; seizures common |
Treatment
First-line
- ABCs, intubation if GCS ≤8 or aspiration risk
- BP control: target SBP 130-150 within first hour (INTERACT2, ATACH-2). Agents: IV nicardipine, clevidipine, labetalol
- Reverse anticoagulation immediately: warfarin → 4-factor PCC + vitamin K 10 mg IV; dabigatran → idarucizumab 5 g IV; factor Xa inhibitors → andexanet alfa or 4-factor PCC; heparin → protamine
- Platelet transfusion NOT routinely beneficial (PATCH trial) unless platelet count <50k or surgery planned
- Reverse coagulopathy: FFP, vitamin K, platelet transfusion for thrombocytopenia
- Manage ICP: head of bed 30°, normocapnia, avoid hyponatremia and hyperglycemia, mannitol or 3% saline if herniating
Second-line / adjunct
- Surgical evacuation: cerebellar hemorrhage >3 cm or with brainstem compression/hydrocephalus (life-saving)
- Lobar ICH within 1 cm of cortex and 10-100 mL in deteriorating patient (selected cases — STICH/STICH II were equivocal)
- Ventriculostomy/EVD for hydrocephalus from IVH
- Seizure prophylaxis only if clinically apparent seizures (not routine)
- Long-term BP control (goal <130/80), AVM treatment if identified, avoid future anticoagulation if amyloid angiopathy
Complications
- Hematoma expansion (first 6 h)
- Cerebral edema, mass effect, herniation
- Intraventricular extension with hydrocephalus
- Seizures (early or late)
- Recurrent hemorrhage (especially amyloid angiopathy)
- DVT/PE, aspiration pneumonia, pressure ulcers
- Permanent disability, vascular dementia
PANCE pearls
- ICH score (GCS, age ≥80, ICH volume ≥30 mL, infratentorial, IVH): each point predicts ~30% mortality.
- Cerebellar hemorrhage >3 cm is a NEUROSURGICAL EMERGENCY — risk of brainstem compression and hydrocephalus.
- Cerebral amyloid angiopathy: elderly patient, lobar hemorrhages, normal BP, recurrent microbleeds on SWI/GRE MRI — avoid anticoagulation.
- Hypertensive bleeds favor deep structures (putamen, thalamus, pons, cerebellum). Lobar bleeds in elderly suggest amyloid angiopathy.
- Avoid corticosteroids — no benefit and harm shown in older trials.
References
- AHA/ASA 2022 — 2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage (Greenberg et al., Stroke 2022)
- INTERACT2 — Rapid Blood-Pressure Lowering in Patients with Acute Intracerebral Hemorrhage (Anderson et al., NEJM 2013)
- ATACH-2 — Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage (Qureshi et al., NEJM 2016)
- PATCH Trial — Platelet Transfusion versus Standard Care after Acute ICH Associated with Antiplatelet Therapy (Baharoglu et al., Lancet 2016)
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