Epidemiology

• ICH accounts for 10–15% of all strokes but carries the highest mortality (~40% at 30 days)
• Incidence: ~25 per 100,000 person-years in the U.S.; higher in Asian and Black populations
• Median age of onset: 60–70 years
• ICH is the most common type of hemorrhagic stroke (more common than SAH)
• Only ~20% of ICH patients are functionally independent at 6 months

Risk Factors

Modifiable

• Hypertension — #1 risk factor overall (accounts for 60–70% of spontaneous ICH); chronic HTN → lipohyalinosis of small penetrating arteries
• Anticoagulation: Warfarin-associated ICH carries ~50% mortality; DOACs have lower ICH risk than warfarin
• Antiplatelet agents: Modestly increase ICH risk, especially dual antiplatelet therapy
• Heavy alcohol use: >2 drinks/day increases ICH risk 2–4 fold
• Cocaine / amphetamines / sympathomimetics: Acute hypertensive surge → ICH; often in younger patients; consider in any young patient with ICH
• Smoking: Independent risk factor; synergistic with HTN

Non-Modifiable / Structural

• Cerebral amyloid angiopathy (CAA): Leading cause of lobar ICH in elderly; recurrent lobar hemorrhages
• Vascular malformations: AVMs, cavernous malformations, dural AVFs — especially in young patients with lobar ICH
• Brain tumors: Primary (GBM, oligodendroglioma) and metastatic (melanoma, RCC, choriocarcinoma, thyroid) — hemorrhagic metastases
• Coagulopathies: Thrombocytopenia, DIC, hemophilia, liver disease
• Cerebral venous thrombosis: Venous infarction with secondary hemorrhagic conversion — often bilateral, near sinuses
• Moyamoya disease: ICH from fragile collateral vessels in young Asian patients
• Vasculitis / mycotic aneurysm: Infective endocarditis → septic emboli → mycotic aneurysm rupture

Hypertensive ICH Mechanism

• Chronic hypertension → lipohyalinosis (fibrinoid necrosis) of small perforating arteries (lenticulostriates, thalamoperforators, pontine perforators)
• Lipohyalinosis → weakening of vessel wall → formation of Charcot-Bouchard microaneurysms
• Acute BP surge or sustained HTN → rupture of microaneurysms → parenchymal hemorrhage
• Typical locations: putamen (35–50%), thalamus (10–15%), cerebellum (5–10%), pons (5–10%), caudate (5–7%)
• The same small vessel disease causes lacunar infarcts — ICH and lacunar strokes share a common vascular pathology

Hematoma Expansion

• Occurs in ~30–38% of patients within the first 3–6 hours (most within 1–3 hours)
• Defined as >33% increase in volume or >6 mL absolute growth from baseline CT
• Strongest modifiable predictor of early neurological deterioration and death
• Risk factors for expansion: early presentation (<3h from onset), anticoagulation, large initial volume, irregular hematoma shape, CTA “spot sign”
• Mechanism: ongoing bleeding from ruptured arteriole + secondary mechanical disruption of surrounding vessels (“avalanche model”)

Perihematomal Edema

• Surrounds the hematoma; peaks at ~10–14 days
• Mechanisms: clot retraction, thrombin-mediated inflammation, red blood cell lysis → iron and hemoglobin toxicity
• Contributes to secondary brain injury, mass effect, and clinical deterioration
• Target of emerging therapies (e.g., deferoxamine for iron chelation — i-DEF trial)

• Rule of thumb: Deep/infratentorial ICH = hypertensive etiology until proven otherwise
• Lobar ICH in elderly (>55) without HTN: Think CAA first
• Lobar ICH in young patient: Think AVM, cavernous malformation, tumor, drug use, venous thrombosis
• Any atypical location or age: Pursue further workup — CTA, MRI with GRE/SWI, catheter angiography if needed

Overview

• Deposition of amyloid-beta (Aβ) protein in the walls of small- to medium-sized cortical and leptomeningeal vessels
• Causes progressive vessel wall weakening → recurrent lobar hemorrhages
• Prevalence increases with age: found in ~50% of autopsies in patients >80 years
• Most cases are sporadic; rare hereditary forms (Dutch, Flemish, Iowa, Italian types with APP mutations)
• NOT the same as Alzheimer disease, but shares amyloid pathology; ~80% of AD patients have concurrent CAA

APOE Associations

• APOE ε2: Associated with CAA-related vasculopathy (vessel wall cracking/splitting) → increased risk of ICH and hematoma expansion
• APOE ε4: Associated with increased amyloid deposition in vessel walls → more microbleeds and recurrent lobar ICH
• APOE ε4 also the major genetic risk factor for Alzheimer disease
• APOE ε2/ε4 genotype carries the highest CAA-related ICH risk

Modified Boston Criteria 2.0 (2022)

Probable CAA

• Age ≥50 years
• At least 2 of the following hemorrhagic markers on MRI (strictly lobar distribution):
  • Lobar ICH (including in cerebellar cortex)
  • Lobar cerebral microbleeds (on GRE/SWI)
  • Cortical superficial siderosis (cSS) — focal or disseminated
• OR: 1 hemorrhagic marker + 1 non-hemorrhagic marker (white matter hyperintensities in a multispot pattern, perivascular spaces in centrum semiovale >20)
• Absence of other cause of hemorrhage

Possible CAA

• Age ≥50 years
• 1 hemorrhagic marker (single lobar ICH, lobar microbleeds, or cSS) in a strictly lobar location
• Absence of other cause

Definite CAA

• Full postmortem examination demonstrating lobar ICH + severe CAA with vasculopathy on histopathology
• Congo red staining: Apple-green birefringence under polarized light = amyloid

Key Imaging Features

• Lobar microbleeds (GRE/SWI) — strictly cortical/subcortical; spare deep structures (deep microbleeds suggest hypertensive small vessel disease)
• Cortical superficial siderosis (cSS): Hemosiderin lining the cortical surface; seen as curvilinear hypointensity on GRE/SWI; disseminated cSS = high risk of future ICH
• Convexity subarachnoid hemorrhage: Non-aneurysmal SAH localized to cortical sulci (NOT basal cisterns) — CAA is the most common cause in the elderly
• White matter hyperintensities: Posterior-predominant in CAA (vs. periventricular in hypertensive SVD)
• Enlarged perivascular spaces in centrum semiovale (characteristic of CAA)

CAA-Related Inflammation (CAA-ri)

• Autoimmune/inflammatory response to amyloid in vessel walls
• Presentation: Subacute cognitive decline, seizures, headache, focal deficits
• MRI: Asymmetric white matter hyperintensities (often patchy, extending to subcortex) + lobar microbleeds + leptomeningeal enhancement
• Key distinction: Resembles vasculitis or tumor but responds dramatically to immunosuppression (corticosteroids)
• CSF may show elevated protein and anti-Aβ antibodies
• Biopsy (if performed): Perivascular inflammation with granulomatous or lymphocytic infiltration

Putaminal Hemorrhage

• Most common location for hypertensive ICH (35–50%)
• Artery: lateral lenticulostriates (from MCA M1)
• Presentation: Contralateral hemiparesis (face/arm/leg), hemisensory loss, homonymous hemianopia
• Dominant hemisphere: Global aphasia (if large); may mimic MCA stroke
• Nondominant hemisphere: Hemispatial neglect, anosognosia
• Eyes deviate TOWARD the lesion (away from the hemiparesis) — same as cortical stroke; opposite of pontine hemorrhage
• Extension into internal capsule → dense hemiplegia
• Extension into ventricles → IVH → hydrocephalus

Thalamic Hemorrhage

• Second most common hypertensive ICH location (10–15%)
• Artery: thalamogeniculate and thalamoperforating arteries (from PCA)
• Presentation: Contralateral hemisensory loss (often predominant), contralateral hemiparesis (if extends to internal capsule)
• Classic eye findings:
  • Eyes deviate downward and inward (“peering at the nose”) — due to compression/damage of dorsal midbrain (upgaze center)
  • Wrong-way eyes: Eyes deviate AWAY from the lesion (toward the hemiparesis) — distinguishes from putaminal hemorrhage
  • Miotic (small) pupils that are poorly reactive
• Dominant thalamic hemorrhage: Transcortical aphasia (especially with pulvinar involvement)
• Frequently ruptures into the third ventricle → obstructive hydrocephalus (common reason for EVD)
• Late complication: Dejerine-Roussy syndrome — central thalamic pain with allodynia and hyperpathia

Cerebellar Hemorrhage

• 5–10% of ICH; usually from SCA or PICA perforators
• Presentation: Sudden occipital headache, vomiting, truncal ataxia (unable to sit/stand), vertigo, dysarthria
• NO limb weakness initially (distinguishes from supratentorial ICH)
• Danger: Posterior fossa is a confined space → rapid brainstem compression:
  • Progressive obtundation → coma
  • Ipsilateral CN VI and VII palsies
  • Obstructive hydrocephalus (compression of fourth ventricle)
• Surgical emergency if >3 cm or evidence of brainstem compression or hydrocephalus — suboccipital decompressive craniectomy + clot evacuation
• One of the few ICH locations where surgery is clearly life-saving

Pontine Hemorrhage

• 5–10% of ICH; basilar paramedian perforators
• Presentation (massive): Coma, quadriplegia, decerebrate posturing, loss of all brainstem reflexes, hyperthermia
• “Pinpoint pupils” (bilateral miotic but reactive — sympathetic disruption with intact parasympathetics)
• Ocular bobbing: Rapid downward conjugate eye movements with slow return — characteristic of pontine lesion
• Eyes midline and cannot cross midline (loss of horizontal gaze from bilateral PPRF/CN VI destruction)
• Small lateral pontine hemorrhage may present as ataxic hemiparesis or dysarthria-clumsy hand
• Prognosis: Massive pontine hemorrhage carries >80% mortality; very poor surgical candidacy

Lobar Hemorrhage

• 20–30% of ICH; cortical / subcortical white matter
• Etiologies: CAA (elderly), AVM (young), tumor, anticoagulation, occasionally hypertensive
• Presentation varies by lobe:
  • Frontal: Contralateral hemiparesis, abulia, headache
  • Parietal: Contralateral hemisensory loss, hemineglect (nondominant)
  • Temporal: Wernicke-type aphasia (dominant), agitation, superior quadrantanopia
  • Occipital: Contralateral homonymous hemianopia, headache
• Seizures more common with lobar ICH than deep ICH (~15–28% incidence)
• Higher tendency for IVH extension if near ventricular system

Caudate Hemorrhage

• 5–7% of ICH; recurrent artery of Heubner or lenticulostriates
• Presentation: Headache, confusion, memory impairment, abulia (behavioral changes predominate over motor deficits)
• Frequently ruptures into lateral ventricle due to proximity → IVH → hydrocephalus
• May mimic SAH clinically (sudden headache, stiff neck from IVH-related meningism)

ICH Score (Hemphill, 2001)

• Most widely used prognostic grading scale for ICH
• Predicts 30-day mortality
• Components (total 0–6 points):

ICH Score & 30-Day Mortality

FUNC Score (Rost, 2008)

• Predicts functional independence at 90 days (more useful than mortality prediction for patient/family counseling)
• Components: ICH volume, age, ICH location, GCS, pre-ICH cognitive impairment
• Score range 0–11; higher score = better functional prognosis
• FUNC score ≤4 → virtually no chance of functional independence

Self-Fulfilling Prophecy & Early Care Limitation Bias

• Critical concept: Early withdrawal of care or do-not-resuscitate orders based on initial prognostic scores may cause the predicted mortality rather than predict it
• Studies show that early DNR orders within 24h are independently associated with mortality after adjusting for severity
• AHA guidelines recommend: Full aggressive care for at least the first 24–48 hours; defer major goals-of-care decisions until trajectory is established
• Prognostic scores (ICH score, FUNC) were derived from populations with high rates of early care limitations — may overestimate mortality in aggressively treated patients

Initial Stabilization

• ABCs: Secure airway if GCS ≤8 or unable to protect airway; intubation with rapid sequence induction
• Stat NCCT head — differentiate ICH from ischemic stroke (ICH = hyperdense on CT)
• CTA: Assess for spot sign (active contrast extravasation), vascular malformation, or aneurysm
• Establish IV access, continuous monitoring, ICU admission
• Labs: CBC, BMP, coagulation studies (PT/INR, aPTT), fibrinogen, type and screen, toxicology screen in young patients
• Reverse any anticoagulation immediately (see below)

Blood Pressure Management

Key Trials

• INTERACT2 (2013):
  • Intensive BP lowering (<140 mmHg systolic within 1 hour) vs. guideline-recommended (<180 mmHg)
  • Primary outcome (death or major disability): No significant difference by ordinal analysis; however, shift analysis showed improved functional outcomes with intensive lowering
  • Intensive lowering appeared safe with no increase in adverse events
  • Basis for AHA guideline recommendation of SBP <140 mmHg target
• ATACH-2 (2016):
  • Intensive (<140 mmHg within 2 hours) vs. standard (<180 mmHg) using IV nicardipine
  • No benefit from intensive BP lowering; primary outcome (death or disability at 3 months) was similar
  • Increased renal adverse events in the intensive group (9% vs. 4%)
  • Possible explanation: achieved SBP was ~129 in intensive arm (too aggressive?) vs. ~141 in standard arm

Current AHA/ASA Guidelines (2022)

• SBP 150–220 mmHg: Acute lowering to <140 mmHg is safe (Class IIa, Level B-R)
• SBP >220 mmHg: Consider aggressive reduction with continuous IV infusion and frequent monitoring (Class IIb)
• Avoid SBP drops below 130 mmHg — ATACH-2 suggested potential harm with over-aggressive lowering
• Agents of choice:
  • Nicardipine: 5 mg/hr IV, titrate by 2.5 mg/hr q5–15 min (max 15 mg/hr) — preferred for precise titration
  • Labetalol: 10–20 mg IV bolus q10–20 min (max 300 mg); avoid in asthma, bradycardia, heart block
  • Clevidipine: 1–2 mg/hr IV, titrate rapidly; ultra-short half-life
• Avoid nitroprusside (raises ICP) and sublingual nifedipine (unpredictable drops)

Reversal of Anticoagulation

Seizure Management

• Clinical seizures occur in 5–16% of ICH patients (higher with lobar location)
• Subclinical/electrographic seizures may occur in up to 28–31% on continuous EEG monitoring
• AHA guidelines: Prophylactic antiepileptic drugs are NOT recommended (no proven benefit; potential harm from side effects)
• Treat clinical seizures when they occur with standard AEDs (levetiracetam preferred — no drug interactions, IV formulation)
• Continuous EEG monitoring recommended for patients with depressed mental status out of proportion to the degree of brain injury
• Avoid phenytoin — associated with worse outcomes in some ICH studies

ICP Management

• Indications: GCS ≤8, clinical signs of herniation, large ICH with significant mass effect, hydrocephalus
• General measures: Head of bed 30°, midline head position, avoid jugular vein compression, pain/agitation control, avoid hyperthermia
• Osmotherapy:
  • Mannitol 20%: 1–1.5 g/kg IV bolus; follow serum osmolality (hold if >320 mOsm/L); watch for rebound edema
  • Hypertonic saline (23.4%, 3%): 30 mL bolus of 23.4% via central line, or 250 mL of 3% NaCl; target Na 145–155 mEq/L; no osmol gap concern
• EVD: For IVH with hydrocephalus or ICP monitoring (target ICP <20 mmHg, CPP >60 mmHg)
• Hyperventilation: Temporary bridge only (target pCO₂ 30–35 mmHg); causes vasoconstriction → reduced CBF; rebound increase in ICP when discontinued

Other Acute Care Measures

• Glucose: Target 140–180 mg/dL; avoid hyperglycemia (worsens edema/outcomes) and hypoglycemia
• Temperature: Target normothermia; treat fever aggressively (acetaminophen, cooling blankets); fever is independently associated with worse outcomes
• DVT prophylaxis:
  • Intermittent pneumatic compression (IPC): Start on admission
  • Pharmacologic prophylaxis: Low-dose subcutaneous UFH or LMWH can be started at 24–48 hours after hemorrhage stabilization (AHA Class IIb) — ICH patients are at very high DVT/PE risk
• Stress ulcer prophylaxis: Consider PPI or H2-blocker in ICU patients
• Nutrition: Early enteral nutrition preferred; dysphagia screening mandatory

CTA Spot Sign

• Definition: One or more foci of active contrast extravasation within the hematoma on CTA source images
• Appears as 1–2 mm enhancing foci (density ≥120 HU) within the hematoma, discontinuous from normal vasculature
• Sensitivity ~50–60%, specificity ~85–90% for predicting hematoma expansion
• Number and size of spot signs correlate with expansion risk and mortality
• Best detected on CTA source images or delayed-phase CTA (1–3 minutes post-injection)

Predicting & Preventing Hematoma Expansion

• Predictors of expansion:
  • CTA spot sign (strongest imaging predictor)
  • Early presentation (<3 hours from onset)
  • Anticoagulant use
  • Large initial hematoma volume
  • Irregular / heterogeneous hematoma shape (“blend sign,” “swirl sign,” “black hole sign” on NCCT)
• Strategies to prevent expansion:
  • Aggressive BP lowering (INTERACT2 target <140 mmHg)
  • Rapid anticoagulation reversal
  • Tranexamic acid — TICH-2 trial (2018): Reduced hematoma expansion at 24h but no improvement in 90-day functional outcome
  • Recombinant factor VIIa — FAST trial: Reduced expansion but increased thromboembolic events with no clinical benefit; NOT recommended

Supratentorial ICH — Key Trials

STICH (2005)

• Design: Early surgical evacuation (within 24h) vs. initial conservative treatment for supratentorial ICH
• Result: No overall benefit of early surgery; trend toward benefit in lobar (superficial) hemorrhages <1 cm from cortical surface
• Deep hemorrhages did NOT benefit from surgery

STICH II (2013)

• Design: Specifically tested early surgery for lobar ICH (within 1 cm of cortical surface, 10–100 mL volume) without IVH
• Result: No statistically significant benefit of early surgery over conservative management
• However, 21% of the conservative group crossed over to surgery, diluting the effect
• Interpretation: Early surgery may benefit patients who deteriorate, but routine early surgery for all lobar ICH is NOT supported

MISTIE III (2019)

• Design: Minimally invasive surgery with stereotactic catheter placement + alteplase irrigation (to dissolve and drain clot) vs. standard medical care for ICH ≥30 mL
• Result: Did NOT meet primary endpoint (mRS 0–3 at 365 days)
• Key finding: Patients whose hematoma was reduced to <15 mL had significantly better outcomes → suggests surgical volume reduction may matter if sufficient clot removal is achieved

ENRICH (2024)

• Design: Early minimally invasive parafascicular surgery (using BrainPath device) + medical care vs. medical care alone for lobar ICH ≥30 mL
• Result: Met primary endpoint — improved utility-weighted mRS at 180 days with surgery
• First RCT to show benefit of surgical evacuation for supratentorial ICH
• Mainly in lobar ICH; confirms that technique and patient selection matter

Cerebellar Hemorrhage — Surgical Indications

• Surgical evacuation (suboccipital craniectomy) is indicated for:
  • Hematoma >3 cm in diameter
  • Neurological deterioration (declining GCS)
  • Brainstem compression (absent brainstem reflexes, new cranial nerve palsies)
  • Obstructive hydrocephalus from fourth ventricle compression
• Class I recommendation per AHA/ASA guidelines
• EVD alone may be insufficient — does not address mass effect from the hematoma itself; clot evacuation should be performed
• Patients can have excellent outcomes if surgery is performed before irreversible brainstem damage

EVD for IVH with Hydrocephalus

• Indications: IVH causing obstructive hydrocephalus with acute neurological decline or GCS ≤8
• Usually placed in the frontal horn of the lateral ventricle (Kocher’s point)
• Monitor ICP (target <20 mmHg, CPP >60 mmHg)
• Risk of ventriculitis with prolonged EVD (~5–10%)

Decompressive Craniectomy

• May be considered for large supratentorial ICH with refractory elevated ICP as a life-saving measure
• Limited evidence; SWITCH trial is evaluating this approach
• May reduce mortality but potentially at the cost of survival with severe disability — requires goals-of-care discussion

IVH Overview

• IVH occurs in ~45% of ICH patients (secondary extension from parenchymal hemorrhage)
• Independent predictor of poor outcome — included in the ICH Score
• Mechanisms of harm: obstructive hydrocephalus, direct ependymal injury, inflammation, impaired CSF absorption
• Thalamic and caudate hemorrhages most commonly extend into the ventricular system

CLEAR III Trial (2017)

• Design: Low-dose intraventricular alteplase (1 mg q8h, max 12 doses) via EVD vs. saline in patients with IVH and obstructive hydrocephalus
• Primary outcome: mRS 0–3 at 180 days — NOT significantly different (48% vs. 45%, p=0.48)
• Key secondary finding: Alteplase significantly reduced mortality (18% vs. 29%, p=0.006) without increasing serious adverse events
• Interpretation: Alteplase improved clot lysis and reduced mortality, but survivors had more severe disability → net functional outcome was neutral
• Greater clot removal (>80% of IVH removed) was associated with better functional outcomes
• Safe — no increase in symptomatic bleeding or ventriculitis

EVD Management Principles

• Place at Kocher’s point (1 cm anterior to coronal suture, mid-pupillary line, ~11 cm from entry to target)
• Set drainage height at 10–20 cmH₂O above the external auditory meatus
• Monitor ICP continuously; target ICP <20 mmHg, CPP >60 mmHg
• Weaning: Gradually raise the EVD (by 5 cmH₂O increments) and clamp trial for 24–48 hours before removal; repeat CT to assess ventricle size
• If patient cannot be weaned from EVD → consider VP shunt (needed in ~20% of IVH patients)
• Ventriculitis risk: ~5–10%; prophylactic antibiotics are controversial; daily CSF sampling for cell count, glucose, culture

Mortality & Functional Outcomes

• 30-day mortality: ~40% (highest among all stroke subtypes)
• 1-year mortality: ~50–60%
• Only ~12–20% achieve functional independence (mRS 0–2) at 6 months
• Most recovery occurs in the first 3–6 months; slow continued improvement possible up to 12 months
• Predictors of worse outcome: Larger hematoma volume, lower GCS, IVH, infratentorial location, older age, hematoma expansion, anticoagulant-related ICH
• Predictors of better outcome: Younger age, smaller volume, lobar location (if not CAA), preserved consciousness, absence of IVH

Restarting Anticoagulation After ICH

• Deeply contested and highly tested topic
• For patients with atrial fibrillation:
  • Risk of recurrent ICH (especially in CAA) must be balanced against risk of ischemic stroke/systemic embolism
  • Lobar ICH (likely CAA) = higher recurrent ICH risk (~7–14%/year) → more caution about restarting
  • Deep ICH (hypertensive) = lower recurrent ICH risk (~2–4%/year) → restarting anticoagulation may be more favorable
• SoSTART trial (2021): Observational data suggested starting OAC after ICH may reduce all-cause stroke without significantly increasing recurrent ICH risk
• Timing: If decision is to restart, generally 4–8 weeks after ICH (AHA/ASA); earlier for mechanical heart valves (higher embolic risk)
• DOACs preferred over warfarin if restarting (lower ICH risk: ~0.3–0.5%/year vs. ~0.5–1%/year)
• Left atrial appendage occlusion (LAAO / Watchman device): Alternative to long-term anticoagulation in AF patients with prior ICH; avoids ongoing bleeding risk
• Decision requires shared decision-making considering CHA₂DS₂-VASc score, ICH location, CAA status, functional status, patient preferences

Secondary Prevention After ICH

• Blood pressure control: Most important modifiable factor; target <130/80 mmHg (SPS3, PROGRESS trials support intensive BP control to reduce recurrent stroke)
• Statin use after ICH:
  • SPARCL trial raised concern about increased ICH risk with high-dose atorvastatin, particularly in patients with prior ICH
  • AHA: Statins can be continued in patients with strong indications (coronary artery disease), but may consider avoiding in lobar ICH / probable CAA
• Antiplatelet agents: RESTART trial (2019) showed restarting antiplatelets after ICH was NOT associated with increased recurrent ICH; may be reasonable when indicated
• Lifestyle: Smoking cessation, limit alcohol, regular exercise, healthy diet

• Step 1: ABCs, airway protection if GCS ≤8, stat NCCT head
• Step 2: Confirm ICH on CT; obtain CTA (spot sign, vascular malformation); stat labs including coagulation studies
• Step 3: Reverse anticoagulation immediately (4F-PCC for warfarin, idarucizumab for dabigatran, andexanet alfa or 4F-PCC for Xa inhibitors)
• Step 4: Lower SBP to <140 mmHg (nicardipine infusion preferred); avoid below 130 mmHg
• Step 5: ICU admission, continuous monitoring, ICP management if indicated (EVD for hydrocephalus)
• Step 6: Cerebellar ICH >3 cm or brainstem compression → urgent surgical evacuation
• Step 7: Treat clinical seizures (levetiracetam preferred); do NOT give prophylactic AEDs
• Step 8: DVT prophylaxis with IPC devices; start pharmacologic prophylaxis at 24–48 hours
• Step 9: Repeat imaging at 6–24 hours to assess for expansion
• Step 10: Goals-of-care discussion — defer major decisions for at least 24–48 hours; avoid self-fulfilling prophecy
• Step 11: MRI with GRE/SWI when stable to assess for microbleeds (CAA vs. hypertensive SVD), underlying lesion
• Step 12: Secondary prevention: BP <130/80, reassess anticoagulation/antiplatelet needs, statin risk-benefit, rehabilitation