Neurology · Cerebrovascular Disease
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Chronic hypertension is the most common cause of nontraumatic intracerebral hemorrhage (ICH), typically occurring in the basal ganglia, thalamus, pons, or cerebellum.
Non-contrast head CT is the gold standard initial imaging modality to rapidly differentiate hemorrhagic stroke from ischemic stroke.
Cerebral amyloid angiopathy is the most common cause of lobar (cortical) hemorrhage in elderly patients without a history of hypertension.
Acute blood pressure management in ICH targets a systolic blood pressure of 130 to <140 mmHg for at least 7 days in patients presenting with SBP 150-220 mmHg, and should not be lowered below 130 mmHg, to limit hematoma expansion.
Reversal of anticoagulation is mandatory for patients on warfarin using prothrombin complex concentrate (PCC) and intravenous vitamin K.
Cerebellar hemorrhage presents with occipital headache, vomiting, and ataxia/gait instability, and requires urgent neurosurgical consultation for potential decompression.
Intraventricular extension of an ICH is a poor prognostic indicator that may lead to obstructive hydrocephalus, requiring external ventricular drain (EVD) placement.
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A 72-year-old male is brought to the emergency department after a sudden onset of severe headache, nausea, and vomiting. His medical history is significant for long-standing hypertension and atrial fibrillation on warfarin. On examination, he is lethargic with left-sided hemiparesis and conjugate eye deviation toward the side of the lesion. A non-contrast head CT reveals a large hyperdense mass in the right basal ganglia with surrounding edema.
What is the most appropriate next step in the management of this patient's coagulopathy?
Administration of prothrombin complex concentrate (PCC) and intravenous vitamin K.
The patient has an ICH secondary to anticoagulation; immediate reversal of warfarin using PCC and vitamin K is required to limit hematoma expansion as per current guidelines.
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High yield triage
Etiology / Epidemiology
Primary cause is chronic hypertension leading to vessel rupture. Other causes include cerebral amyloid angiopathy and anticoagulant use.
Clinical Manifestations
Sudden severe headache, focal neurologic deficits, and altered mental status (thunderclap headache is most characteristic of subarachnoid hemorrhage). Look for nuchal rigidity in subarachnoid hemorrhage.
Diagnosis
Non-contrast CT head is the gold standard for initial diagnosis. Lumbar puncture for xanthochromia applies only to suspected subarachnoid hemorrhage with a negative noncontrast CT, and is not part of the intracerebral hemorrhage workup.
Treatment
Strict blood pressure control (target SBP 130 to <140 mmHg for at least 7 days; do not go below 130 mmHg). Avoid anticoagulants; reverse warfarin with 4-factor PCC plus Vitamin K (PCC preferred over FFP).
Prognosis
High 30-day mortality (up to 50%). Increased intracranial pressure is the primary cause of early death.
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Epidemiology & Etiology
Intracerebral hemorrhage (ICH) is most commonly caused by hypertensive vasculopathy of small penetrating arteries. Cerebral amyloid angiopathy is the leading cause in elderly patients without hypertension. Use of antiplatelets or warfarin significantly increases risk of expansion.
Pertinent Anatomy
The basal ganglia (specifically the putamen) is the most common site for hypertensive hemorrhage. Hemorrhage in the cerebellum or brainstem carries a higher risk of rapid deterioration due to compression of the fourth ventricle.
Pathophysiology
Chronic hypertension causes lipohyalinosis of small vessels, leading to microaneurysms (Charcot-Bouchard aneurysms). Rupture results in a hematoma that causes direct tissue compression and secondary excitotoxicity. The resulting vasogenic edema increases intracranial pressure, potentially leading to herniation.
Clinical Manifestations
Patients present with a rapidly progressive neurologic deficit. Thunderclap headache is the hallmark of subarachnoid hemorrhage. Cushing's triad (bradycardia, irregular respirations, hypertension) indicates impending herniation and is a critical emergency.
Diagnosis
A non-contrast CT head is the gold standard for immediate triage. If subarachnoid hemorrhage is suspected but CT is negative, lumbar puncture showing xanthochromia is diagnostic. CT angiography is indicated to rule out underlying vascular malformations.
Treatment
Immediate management focuses on blood pressure reduction using nicardipine or labetalol. Avoid nitroprusside as it increases intracranial pressure. In selected patients with spontaneous supratentorial lobar ICH of 30-80 mL and GCS 5-14, early minimally invasive hematoma evacuation within 24 hours improved 180-day functional outcome and reduced 30-day mortality; no benefit was shown for anterior basal ganglia hemorrhage. If coagulopathy is present, give 4-factor prothrombin complex concentrate (PCC) plus IV vitamin K for warfarin (PCC preferred over FFP), andexanet alfa for factor Xa inhibitor-associated ICH, and idarucizumab for dabigatran-associated ICH.
Prognosis
Hematoma expansion occurs in 30% of patients within the first 24 hours. Hydrocephalus is a common complication requiring external ventricular drainage. Seizures are a frequent sequela, but prophylactic antiseizure medication is not recommended; treat only clinically evident or electrographically confirmed seizures.
Differential Diagnosis
Ischemic stroke: sudden focal deficits typically without severe headache or vomiting
Subdural hematoma: usually follows trauma with a slower, venous bleed
Epidural hematoma: classic lucid interval following temporal bone trauma
Meningitis: presents with fever and photophobia, not focal deficits
Brain tumor: presents with subacute, progressive neurologic decline