Neurology · PANCE / PANRE

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

Anatomic distribution of intracerebral hemorrhage by etiology.

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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