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hemorrhagic stroke (ich & sah)

acute neurological injury from intracerebral hemorrhage or subarachnoid hemorrhage, usually presenting with abrupt severe headache or focal deficits

neurologyless-commonemergency

About This Page

This is a clinician-written, evidence-based summary aligned to the USMLE Step 2 CK Content Outline. It is intended for medical students preparing for USMLE Step 2 CK. Management reflects current ACC/AHA, USPSTF, and APA guidelines. Always cross-reference with UpToDate, institutional protocols, and clinical judgment.

The Bottom Line

  • ICH is bleeding into brain parenchyma; SAH is bleeding into the subarachnoid space
  • Noncontrast CT head is first-line for both ICH and suspected SAH
  • Reverse anticoagulation immediately in anticoagulant-associated ICH
  • Aneurysmal SAH requires aneurysm securing plus nimodipine
  • LP for xanthochromia if CT is negative and SAH suspicion remains high

Overview

Hemorrhagic stroke includes spontaneous intracerebral hemorrhage and subarachnoid hemorrhage. ICH is commonly due to chronic hypertension, cerebral amyloid angiopathy, anticoagulation, vascular malformation, tumor, or hemorrhagic transformation. SAH is classically caused by rupture of a saccular aneurysm and presents with thunderclap headache. Rapid CT diagnosis, anticoagulant reversal, neurocritical care, and neurosurgical involvement are central.

Epidemiology

Hypertensive ICH commonly affects the basal ganglia, thalamus, pons, and cerebellum. Cerebral amyloid angiopathy causes lobar hemorrhage in older adults. Aneurysmal SAH risk factors include smoking, hypertension, family history, autosomal dominant polycystic kidney disease, and connective tissue disorders.

Clinical Features

Symptoms
Abrupt focal neurological deficit with headache, vomiting, or reduced consciousness
Thunderclap headache maximal within seconds to minutes
Neck stiffness, photophobia, syncope, or seizure in SAH
Warfarin, DOAC, antiplatelet therapy, or recent thrombolysis increases hemorrhage risk
Sentinel headache days to weeks before SAH may represent minor aneurysm leak
Signs
Hypertension with bradycardia and irregular respirations suggests raised ICP
Nuchal rigidity suggests SAH or meningitis
CN III palsy with dilated pupil suggests posterior communicating artery aneurysm
Cerebellar hemorrhage can cause ataxia, vomiting, gaze palsy, and brainstem compression
Rapid mental status decline is an emergency

Investigations

First-line
Noncontrast CT headFirst-line; acute blood is hyperdense
CTA head and neckAssesses aneurysm, AVM, spot sign, or vascular lesion
CBC, BMP, PT/INR, aPTT, platelet countIdentify coagulopathy, thrombocytopenia, and operative risk
Second-line
Lumbar punctureFor suspected SAH with negative CT; xanthochromia supports diagnosis
MRI brain with susceptibility sequencesIdentifies cavernoma, amyloid microbleeds, tumor hemorrhage, or subacute blood
Digital subtraction angiographyGold standard if CTA/MRA negative but aneurysm suspicion remains
Specialist
Serial CT headMonitors expansion, hydrocephalus, and mass effect
External ventricular drainFor acute hydrocephalus or elevated ICP
Transcranial DopplerMonitors vasospasm after SAH
1
Immediate management
  • Airway protection when consciousness or bulbar function is impaired
  • Neurocritical care admission and urgent neurosurgical consultation
  • Stop antithrombotics and reverse anticoagulation immediately
  • Elevate head of bed and manage fever, glucose, and ICP
2
Anticoagulant reversal
  • Warfarin: 4-factor PCC plus IV vitamin K
  • Dabigatran: idarucizumab
  • Apixaban/rivaroxaban: andexanet alfa where available or 4-factor PCC
  • Heparin: protamine sulfate
3
ICH BP and surgery
  • Carefully lower SBP toward 140 in many patients presenting 150-220 if no contraindication
  • Avoid excessive BP reduction causing hypoperfusion
  • Cerebellar hemorrhage with hydrocephalus or brainstem compression needs urgent decompression
  • Treat elevated ICP with hypertonic saline or mannitol when indicated
4
Aneurysmal SAH
  • Secure aneurysm early with coiling or clipping
  • Nimodipine for 21 days to reduce delayed ischemic deficits
  • Treat hydrocephalus with external ventricular drain
  • Monitor for vasospasm and delayed cerebral ischemia

Complications

  • Hematoma expansion: Highest early after onset
  • Hydrocephalus: Common with SAH or intraventricular hemorrhage
  • Herniation: Risk with mass effect or posterior fossa hemorrhage
  • Vasospasm: SAH days 3-14
  • Rebleeding: Before aneurysm is secured
USMLE Step 2 CK Exam Tips
  • 1Thunderclap headache = SAH until proven otherwise
  • 2Negative CT with high SAH suspicion = LP for xanthochromia
  • 3Basal ganglia/thalamus/pons/cerebellum = hypertensive ICH
  • 4Lobar hemorrhage in elderly = cerebral amyloid angiopathy
  • 5SAH + blown pupil CN III palsy = posterior communicating artery aneurysm
  • 6Nimodipine improves SAH neurological outcomes; it is not simply an antihypertensive
  • 7Warfarin-related ICH = PCC plus vitamin K
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Verified Sources & References

AHA/ASA Spontaneous ICH Guideline
AHA/ASA Aneurysmal SAH Guideline
Neurocritical Care Society Antithrombotic Reversal Guideline