Spontaneous Nontraumatic Intracranial Hemorrhage


KEY FACTS

Terminology

  • Primary intraparenchymal hemorrhage (pICH)

  • Acute nontraumatic intracranial hemorrhage (ICH)

Imaging

  • Acute round or oval intracerebral hematoma

  • Subcentimeter “microbleeds” to massive ICH

  • Hematoma location for common causes of pICH

    • HTN: Basal ganglia > thalamus > pons > cerebellum

    • Amyloid angiopathy: Lobar

    • Arteriovenous malformation: Any location

    • Cavernous malformation: Any location

    • Venous sinus thrombosis: Subcortical white matter

    • Neoplasm: Any location

  • Recommended imaging: Begin with NECT

    • If HTN with striatocapsular hematoma → stop

    • If atypical hematoma → CTA or MR/MRA

    • Atypical hematoma or unclear history: MR (T2*, DWI, C+)

    • If standard study suggests vascular etiology → CTA/MRA

    • If concern for venous infarct → CTV/MRV

Pathology

  • Pediatric patients, < 18 years old: Vascular malformation (~ 50%) > hematologic disorders, vasculopathy, venous infarct, neoplasm

  • Young adults, < 45 years old: Vascular malformation, drug abuse, venous thrombosis, PRES, vasculitis, neoplasm

  • Adults > 45 years old: HTN, amyloid > neoplasm (primary or metastatic), venous infarct, coagulopathy

Clinical Issues

  • ICH causes ~ 15% of acute strokes

  • Treatment: Control of intracranial pressure, hydrocephalus

  • Surgical evacuation when clinically indicated

  • If positive spot sign indicates active bleeding, predicts hematoma expansion and poor outcome

  • 1-year mortality approaches 60%

Axial NECT in an elderly hypertensive patient shows a hyperdense hematoma centered in the left external capsule and putamen
with intraventricular extension of hemorrhage
. This is the most common location for a hypertensive hemorrhage.

Axial CT in this 5 year old shows a large frontal lobe hemorrhage
with surrounding edema and mass effect. Additional imaging revealed an underlying cavernous malformation. In children, vascular lesions represent ~ 50% of all intracranial hemorrhages.

Axial NECT in a 73-year-old hypertensive anticoagulated man with sudden onset of right hemiparesis shows a mixed-density hematoma centered in the lateral putamen/external capsule
.

CTA in the same case shows 2 enhancing foci (spot sign)
within the clot, which also is expanding
and demonstrates a fluid-fluid level
. All are dire prognostic indicators. The patient expired shortly after the scan was obtained.

TERMINOLOGY

Synonyms

  • Primary intraparenchymal hemorrhage (pICH), hemorrhagic stroke

Definitions

  • Acute nontraumatic intracranial hemorrhage (ICH)

    • Etiology often initially unknown

IMAGING

General Features

  • Best diagnostic clue

    • Acute nontraumatic intracerebral hematoma

  • Location

    • Varies with etiology

      • Hypertension (HTN): Deep gray matter (basal ganglia, thalamus), pons, cerebellar hemisphere

      • Amyloid angiopathy: Lobar

      • Arteriovenous malformation (AVM): Any location

      • Cavernous malformation: Any location, common in brainstem

      • Venous sinus thrombosis: Subcortical white matter (WM) adjacent to occluded sinus

      • Neoplasm: Any location, posterior fossa common

  • Size

    • Subcentimeter “microbleeds” to massive hemorrhage

  • Morphology

    • Typically round or oval; often irregular when large

    • Patterns with HTN and amyloid angiopathy

      • Acute parenchymal hematoma

      • Multiple subacute/chronic “microbleeds” in deep gray matter (HTN > amyloid) &/or subcortical white matter (amyloid > HTN)

      • Microbleeds often seen only on GRE or SWI MR

CT Findings

  • NECT

    • Acute hyperdense round/elliptical mass

    • May be mixed iso-/hyperdense

    • May have fluid-fluid level

      • Coagulopathy

      • Brisk bleeding

      • Bleed into cystic mass

    • Peripheral low density (edema)

    • Deep (ganglionic) ICH may rupture into ventricles

  • CTA

    • Often nonrevealing

    • ± underlying vascular malformation (AVM, aneurysm)

    • Look for dural sinus venous thrombosis

MR Findings

  • T1WI

    • Hyperacute (< 24 hours)

      • Isointense center (oxygenated Hgb)

      • Isointense periphery (deoxygenated Hgb, clot-tissue interface)

      • Hypointense rim (vasogenic edema)

  • T2WI

    • Hyperacute (< 24 hours)

      • Hyperintense, heterogeneous center

      • May have subtle hypointense periphery

      • Hyperintense rim of edema

  • T2* GRE

    • Hypointense

    • Multifocal hypointense lesions (“black dots”)

      • Basal ganglia (BG) and thalami suggests HTN

      • Subcortical WM suggests amyloid angiopathy

  • DWI

    • T2 shine through common; may see “DWI restriction” in core

  • T1WI C+

    • Often none in acute hematoma

    • May enhance if underlying neoplasm, vascular malformation

  • MRA

    • Often normal, look for vascular lesion

  • MRV

    • Look for dural sinus thrombosis

Angiographic Findings

  • DSA, often negative

    • Look for dural sinus occlusion, “stagnating vessels” (thrombosed AVM)

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