Everything You Need to Know About Hemorrhagic stroke (ICH, SAH) for Step 1

Hemorrhagic stroke questions on Step 1 love to test “where is the blood?” and “why did it bleed?”—then make you pick the correct imaging, complication, or next step. This post breaks hemorrhagic stroke into its two highest-yield buckets: intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH), with the classic presentations, pathophysiology, diagnostics, and management moves you’re expected to know cold.

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Big picture: Hemorrhagic stroke vs ischemic stroke

Hemorrhagic stroke = neurologic deficit from bleeding, not vessel occlusion.

• ICH (intracerebral hemorrhage): bleeding into brain parenchyma
  → mass effect, increased ICP, focal deficits
• SAH (subarachnoid hemorrhage): bleeding into subarachnoid space
  → meningeal irritation + high risk of vasospasm

First Aid cross-ref: Neurology → Cerebrovascular disease; Intracranial hemorrhage; Berry aneurysm; Charcot-Bouchard microaneurysms.

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High-yield anatomy: Where the blood goes (and why it matters)

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Intracerebral Hemorrhage (ICH)

Definition

Bleeding within brain parenchyma, often causing mass effect and elevated intracranial pressure.

Pathophysiology (what Step 1 tests)

Most common cause (overall): chronic hypertension leading to Charcot-Bouchard microaneurysms of small penetrating arteries.

• Hypertension → lipohyalinosis of small vessels → rupture
• Typical sites (classic Step list):
  • Basal ganglia (putamen) — most common
  • Thalamus
  • Pons
  • Cerebellum

Other high-yield etiologies:

• Cerebral amyloid angiopathy (CAA)
  • Elderly; amyloid deposition in cortical/leptomeningeal vessels
  • Causes lobar hemorrhages (cortical) with recurrent bleeds
• Anticoagulation / coagulopathy
• Vascular malformations (AVM, cavernous malformation)
• Tumor hemorrhage (e.g., metastases)
• Cocaine/amphetamine use (acute severe HTN)

First Aid cross-ref: Charcot-Bouchard microaneurysms (HTN) vs Berry aneurysm (SAH). Cerebral amyloid angiopathy.

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Clinical presentation

ICH often presents with:

• Sudden focal neurologic deficits (like ischemic stroke) plus:
  • Headache
  • Nausea/vomiting
  • Decreased level of consciousness (mass effect/↑ICP)
• Rapid deterioration can occur with expanding hematoma.

Clues for specific locations (high yield):

• Pontine hemorrhage: coma, pinpoint pupils, abnormal posturing
• Cerebellar hemorrhage: ataxia, vertigo, vomiting; can compress 4th ventricle → hydrocephalus

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Diagnosis

Noncontrast head CT is the first test.

• Acute blood = hyperdense (bright) on CT.

If concern for underlying structural cause (esp. lobar hemorrhage in younger patient):

• CT angiography or MRI/MRA can be considered after initial stabilization.

Pearl: In suspected stroke, the “door” question is usually CT head without contrast to distinguish hemorrhagic from ischemic before thrombolysis.

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Treatment (Step-level priorities)

Immediate management

• ABC + neuro checks
• Reverse anticoagulation if applicable
  • Warfarin: vitamin K + PCC (prothrombin complex concentrate)
  • Dabigatran: idarucizumab
  • Factor Xa inhibitors: andexanet alfa (commonly tested conceptually)
• Control blood pressure (carefully; institution-specific targets, but know BP control is crucial)
• Manage ↑ICP when present: head-of-bed elevation, hyperosmolar therapy (mannitol or hypertonic saline), consider intubation if needed

Neurosurgical considerations

• Some patients need hematoma evacuation, especially:
  • Cerebellar hemorrhage with brainstem compression/hydrocephalus
  • Large lobar hematomas with mass effect in selected cases

Avoid: tPA (contraindicated in hemorrhage).

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High-yield associations (ICH)

• Chronic HTN → Charcot-Bouchard microaneurysms → deep hemorrhages (basal ganglia, thalamus, pons, cerebellum)
• Elderly + recurrent lobar hemorrhages ± dementia → CAA
• Sudden neuro deficit + severe headache + hyperdense bleed on CT → think ICH
• Intraventricular extension can worsen prognosis and raise ICP

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Subarachnoid Hemorrhage (SAH)

Definition

Bleeding into the subarachnoid space, mixing with CSF → meningeal irritation and high risk of cerebral vasospasm.

Pathophysiology (classic causes)

1) Ruptured saccular (berry) aneurysm (most tested)

• Occurs at branch points in the Circle of Willis
• Common locations:
  • Anterior communicating artery (ACom) (very common)
  • Posterior communicating artery (PCom)
  • MCA bifurcation

Associations (memorize):

• ADPKD
• Ehlers-Danlos (type III)
• Marfan
• Family history, smoking, HTN (risk factors)

First Aid cross-ref: Berry aneurysm; ADPKD; Ehlers-Danlos/Marfan associations.

2) AVM rupture

• Often younger patients; can cause intracerebral and/or subarachnoid bleeding.

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Clinical presentation (what the vignette screams)

• Thunderclap headache: “worst headache of my life,” maximal at onset
• May have:
  • Neck stiffness (meningismus)
  • Photophobia
  • Nausea/vomiting
  • Brief loss of consciousness
• Focal deficits may or may not be present.

SAH vs meningitis quick contrast:

• SAH: abrupt thunderclap, often exertion/sex, rapid onset
• Meningitis: progressive headache/fever; not usually instantaneous “peak at onset”

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Diagnosis (the Step algorithm)

Step 1: Noncontrast CT head

• Best initial test; sensitivity is highest early.

Step 2: Lumbar puncture if CT is negative but suspicion remains

LP findings in SAH:

• Xanthochromia (yellow CSF from bilirubin breakdown)
• RBCs that do not clear between tubes (vs traumatic tap)
• Elevated opening pressure may be seen

Key differentiator: Xanthochromia suggests true SAH, not a traumatic tap.

Step 3: Identify aneurysm source

• CT angiography (often used) or conventional cerebral angiography.

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Treatment (acute + prevention of complications)

Acute stabilization

• ABC
• BP management (avoid extremes; prevent rebleeding while maintaining perfusion)

Prevent delayed ischemia from vasospasm

• Nimodipine (a dihydropyridine calcium channel blocker)
  • High yield: given to reduce neurologic deficits from vasospasm after SAH

Secure the aneurysm

• Endovascular coiling or surgical clipping (definitive prevention of rebleeding)

Manage hydrocephalus if present

• Blood can obstruct arachnoid granulations or ventricles → communicating hydrocephalus
• May require ventricular drainage/shunting depending on severity

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HY complication: Cerebral vasospasm after SAH

This is a Step favorite.

• Occurs days after SAH (classically around day 3–14)
• Leads to delayed cerebral ischemia: new focal deficits, worsening mental status
• Diagnosed clinically; can be supported by transcranial Doppler (in real life)
• Prevent/treat: nimodipine

Mechanism (conceptual): blood breakdown products irritate vessels → vasoconstriction → ischemia.

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HY complication: Rebleeding (SAH)

• Highest risk early if aneurysm not secured
• Worsening headache, sudden decline
• Definitive prevention: coiling/clipping

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ICH vs SAH: rapid-fire differentiation table

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First Aid-style “buzzword” snapshots

• Elderly + recurrent lobar hemorrhages → cerebral amyloid angiopathy
• Long-standing HTN + basal ganglia hemorrhage → Charcot-Bouchard microaneurysm
• “Worst headache of my life” → SAH
• SAH + ADPKD → berry aneurysm association
• SAH + new deficits days later → vasospasm → treat/prevent with nimodipine
• Stroke symptoms → CT head without contrast first (don’t give tPA until hemorrhage excluded)

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USMLE-style mini-checkpoints (self-test)

1. Sudden severe headache, neck stiffness; CT negative; next step?
   → Lumbar puncture (look for xanthochromia)

2. Older patient with dementia has repeated cortical hemorrhages. Underlying pathology?
   → Amyloid deposition in vessel walls (CAA)

3. Long-standing HTN; acute contralateral weakness; CT shows deep hemorrhage in putamen. Cause?
   → Charcot-Bouchard microaneurysm rupture

4. SAH patient worsens on hospital day 6 with new neuro deficits. Best prevention/therapy?
   → Nimodipine (vasospasm)