Hemorrhagic stroke
(Redirected from Hemorrhagic Stroke)
Background
- Spontaneous (nontraumatic) intracerebral hemorrhage accounts for 10-15% of all strokes
- Second most common cause of stroke after ischemic stroke
- 30-day mortality: 40-50% — highest acute mortality of all stroke subtypes[1]
- Only 20% of patients are functionally independent at 6 months
Etiology
- Hypertensive hemorrhage (most common — 55-70%):
- Typically in basal ganglia (putamen), thalamus, pons, cerebellum
- Chronic hypertension → lipohyalinosis of small penetrating arteries → rupture
- Cerebral amyloid angiopathy (CAA):
- Most common cause of lobar ICH in elderly
- Amyloid deposition in cortical/leptomeningeal vessel walls
- Recurrent lobar hemorrhages
- Anticoagulation-related: warfarin, DOACs (hematoma expansion more common)
- Vascular malformations: AVM, cavernoma (consider in young patients without hypertension)
- Other: cocaine/amphetamine use, hemorrhagic transformation of ischemic stroke, tumors, coagulopathies, cerebral venous sinus thrombosis
Clinical Features
- Sudden onset focal neurologic deficit with headache (worse than ischemic stroke)
- Nausea, vomiting (raised ICP)
- Progressive deterioration (hematoma expansion occurs in ~30% within first 3 hours)
- Cannot reliably distinguish from ischemic stroke clinically — neuroimaging is required
Location-Specific Findings
- Putaminal (35-50%): contralateral hemiparesis, hemisensory loss, aphasia (dominant) or neglect
- Thalamic (15-20%): contralateral hemisensory loss, upgaze palsy, small pupils
- Cerebellar (5-10%): ataxia, vertigo, vomiting, headache → rapid deterioration from brainstem compression or hydrocephalus; SURGICAL EMERGENCY
- Pontine (5-10%): coma, quadriplegia, pinpoint pupils; high mortality
- Lobar (20-30%): symptoms depend on lobe; seizures more common; consider amyloid angiopathy
Differential Diagnosis
- Ischemic stroke (MUST image to distinguish)
- Subarachnoid hemorrhage
- Subdural hemorrhage / epidural hemorrhage
- Hemorrhagic tumor (metastasis, GBM)
- Cerebral venous sinus thrombosis
- Seizure with postictal deficit (Todd paralysis)
- Hypoglycemia
Evaluation
Imaging
- Non-contrast CT head (first-line — immediate): hyperdense (white) lesion
- Detects hemorrhage with ~100% sensitivity in first hours
- Evaluate for: hematoma size, location, midline shift, intraventricular extension, hydrocephalus
- CT angiography (CTA): identify spot sign (contrast extravasation = active bleeding, predicts hematoma expansion)[2]
- Also evaluates for underlying vascular malformation
- MRI/MRA: after stabilization to evaluate for underlying cause (especially if atypical location or age <50)
Labs
- Coagulation studies: PT/INR (warfarin), PTT (heparin), thrombin time (dabigatran)
- CBC with platelets
- BMP, glucose
- Type and screen
- Toxicology screen if cocaine/amphetamine use suspected
ICH Score (Prognosis)
- GCS 3-4 (+2), 5-12 (+1), 13-15 (0)
- ICH volume ≥30 cm3 (+1)
- Intraventricular hemorrhage (+1)
- Infratentorial origin (+1)
- Age ≥80 (+1)
- Score 0: ~0% 30-day mortality; Score 5: ~100% mortality
- Should NOT be used to limit care (self-fulfilling prophecy concern)
Management
Blood Pressure
- AHA/ASA Guidelines[3]:
- If SBP 150-220 mmHg: target SBP 140 mmHg is safe and may improve outcomes (INTERACT2 trial)
- If SBP >220 mmHg: aggressive reduction with continuous IV infusion and frequent monitoring (target 140-160)
- Nicardipine infusion (5-15 mg/hr) or clevidipine preferred
- Labetalol IV as alternative
- Avoid SBP <120 mmHg (risk of renal injury)
Anticoagulation Reversal
- Warfarin (elevated INR):
- 4-factor PCC (Kcentra) 25-50 units/kg IV (preferred — rapid, complete reversal)
- + Vitamin K 10 mg IV (takes hours but provides sustained reversal)
- FFP is second-line (requires thawing, large volume, incomplete reversal)
- Dabigatran: idarucizumab (Praxbind) 5g IV (immediate reversal)
- Rivaroxaban/Apixaban: andexanet alfa (Andexxa) if available; otherwise 4-factor PCC 50 units/kg
- Heparin: protamine sulfate
- Antiplatelet agents: platelet transfusion is NOT recommended (PATCH trial showed harm)
Seizure Management
- Treat clinical seizures with benzodiazepines, then AEDs (levetiracetam preferred)
- Prophylactic AEDs are NOT routinely recommended
- Consider continuous EEG for patients with AMS out of proportion to hemorrhage
Cerebellar Hemorrhage
- Neurosurgical EMERGENCY
- Surgical evacuation for hematoma >3 cm OR evidence of brainstem compression OR hydrocephalus
- EVD (external ventricular drain) for obstructive hydrocephalus
- These patients can deteriorate rapidly to death without surgery
Increased ICP Management
- Elevate HOB to 30°
- EVD for hydrocephalus or IVH with acute hydrocephalus
- Osmotic therapy: mannitol or hypertonic saline
- Consider surgical hematoma evacuation (benefit primarily for superficial lobar hemorrhages)
Disposition
- All patients with ICH require ICU admission in a stroke center/neurosurgical center
- Neurosurgery consultation for: cerebellar hemorrhage, large hematoma with mass effect, hydrocephalus, young patient with suspected vascular malformation
- Goals of care discussion early — but avoid early withdrawal of care (ICH score is imperfect)
- Transfer to stroke center if local neurosurgical capability unavailable
See Also
- Ischemic stroke
- Subarachnoid hemorrhage
- Subdural hemorrhage
- Anticoagulation reversal
- Intracerebral hemorrhage
References
- ↑ van Asch CJ, et al. Incidence, case fatality, and functional outcome of intracerebral haemorrhage over time. Lancet Neurol. 2010;9(2):167-176. PMID 20056489
- ↑ Demchuk AM, et al. Prediction of haematoma growth and outcome in patients with intracerebral haemorrhage using the CT-angiography spot sign (PREDICT). Lancet Neurol. 2012;11(4):307-314. PMID 22405630
- ↑ Greenberg SM, et al. 2022 Guideline for the management of patients with spontaneous intracerebral hemorrhage. Stroke. 2022;53(7):e282-e361. PMID 35579034
- Hemphill JC 3rd, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: AHA/ASA guideline. Stroke. 2015;46(7):2032-2060. PMID 26022637
- Anderson CS, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage (INTERACT2). N Engl J Med. 2013;368(25):2355-2365. PMID 23713578
- Baharoglu MI, et al. Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy (PATCH). Lancet. 2016;387(10038):2605-2613. PMID 27178479
