Intracerebral Hemorrhage

Quick Answer

Intracerebral hemorrhage (ICH) is bleeding directly into the brain parenchyma, accounting for 10-15% of all strokes but responsible for disproportionate mortality (40-50% at 30 days). Critical care management focuses on:

1. Blood pressure control: Target SBP 140-180 mmHg within 1 hour (INTERACT2), avoiding aggressive lowering to 110-139 mmHg (ATACH-2 showed no benefit and increased renal adverse events)
2. Reversal of coagulopathy: Warfarin requires immediate PCC 25-50 U/kg + vitamin K 10 mg IV; DOACs reversed with idarucizumab (dabigatran) or andexanet alfa (factor Xa inhibitors)
3. ICP management: Head of bed 30°, osmotherapy (mannitol 0.25-1 g/kg or hypertonic saline 3-23.4%), EVD for hydrocephalus, surgical evacuation for selected cases
4. Prognostication: ICH Score (GCS, volume greater than 30 mL, IVH, age greater than 80, infratentorial location) predicts 30-day mortality from 0% (score 0) to 100% (score 6)

Immediate neurosurgical consultation required for: GCS ≤8, volume greater than 30 mL, hydrocephalus, cerebellar hemorrhage, or clinical deterioration.

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CICM Exam Focus

What Examiners Expect

Primary Examination (Written)

• Pathophysiology of hematoma expansion and perihematomal edema
• Coagulation cascade and reversal agents (PCC vs FFP, mechanism of action)
• Cerebral perfusion pressure physiology, autoregulation failure

Second Part Fellowship (Written SAQ)

• Acute management of ICH in anticoagulated patient
• Blood pressure targets and evidence (INTERACT2, ATACH-2)
• Indications for surgical intervention (STICH-II, ENRICH, SWITCH trials)
• ICH Score calculation and prognostication

Second Part Fellowship (Viva/Hot Case)

• Systematic approach to deteriorating ICH patient
• Coagulopathy reversal protocols (warfarin, DOACs, antiplatelets)
• ICP management escalation (medical → surgical)
• Withdrawal of life-sustaining treatment discussions

Common Viva Stem

"A 68-year-old man on warfarin for atrial fibrillation presents with acute onset right-sided weakness and reduced GCS (E3V4M5 = 12). CT brain shows a 45 mL left basal ganglia hemorrhage with intraventricular extension. BP 190/110 mmHg, INR 3.2. How would you manage this patient?"

Expected approach:

1. ABCDE resuscitation (airway protection, intubation if GCS ≤8)
2. Immediate coagulopathy reversal (PCC + vitamin K, target INR below 1.5 within 4 hours)
3. Blood pressure control (IV nicardipine/labetalol, target SBP 140-180 mmHg)
4. ICP monitoring and management (EVD for hydrocephalus, osmotherapy)
5. Neurosurgical consultation (large volume, IVH, GCS ≤13)
6. Prognostication (ICH Score = 3: GCS 12 [1 point] + volume 45 mL [1 point] + IVH [1 point] → 26% 30-day mortality)

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Key Points

Key Points: - Primary brain injury occurs from mass effect and hematoma expansion (33% of patients in first 3 hours, 73% of growth in first hour). Secondary injury results from perihematomal edema, ICP elevation, seizures, and fever.

• Blood pressure management is time-critical: INTERACT2 showed intensive lowering (SBP below 140 mmHg within 1 hour) is safe and possibly beneficial for functional outcomes. ATACH-2 showed aggressive lowering (110-139 mmHg) offers no benefit and increases renal adverse events.
• Coagulopathy reversal is an emergency: Warfarin requires 4-factor PCC 25-50 U/kg (superior to FFP) + vitamin K 10 mg IV. DOACs: idarucizumab 5 g for dabigatran, andexanet alfa for factor Xa inhibitors (apixaban, rivaroxaban).
• ICP management follows tiered approach: Tier 1 (HOB 30°, analgesia/sedation, normothermia), Tier 2 (osmotherapy, EVD for hydrocephalus), Tier 3 (neuromuscular blockade, hyperventilation PaCO₂ 30-35 mmHg, decompressive craniectomy).
• ICH Score predicts 30-day mortality: GCS 3-4 (2 points), 5-12 (1 point); ICH volume ≥30 mL (1 point); IVH present (1 point); Infratentorial origin (1 point); Age ≥80 (1 point). Score 0 = 0% mortality, Score 6 = 100% mortality.

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Epidemiology

Incidence and Mortality

Intracerebral hemorrhage accounts for 10-15% of all strokes in Western populations but up to 30-40% in Asian populations (higher prevalence of hypertension and lower use of anticoagulation).[1] The annual incidence is 24.6 per 100,000 person-years, with significant geographic variation.[2]

Mortality is devastating:

• 30-day mortality: 40-50%
• 1-year mortality: 54-59%
• Only 12-39% achieve functional independence (mRS 0-3) at 90 days[3]

The majority of deaths (75%) occur within the first week, with early hematoma expansion and neurological deterioration being the primary drivers.[4]

Risk Factors

Non-modifiable:

• Age (incidence doubles per decade after age 55)
• Male sex (1.3:1 male:female ratio)
• Asian and Black ethnicity (2-fold increased risk)
• Prior ICH (highest risk factor for recurrence: 2.1-4.3% per year)

Modifiable:

• Hypertension: Most important modifiable risk factor (accounts for 60% of ICH)[5]
• Anticoagulation (warfarin increases risk 8-10 fold, DOACs 3-5 fold)
• Antiplatelets (1.5-2.0 fold increased risk)
• Heavy alcohol use (greater than 35 g/day)
• Cocaine and amphetamine use
• Low LDL cholesterol (below 70 mg/dL associated with increased ICH risk)

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Pathophysiology

Primary Injury: Hematoma Formation

The initial bleed occurs due to rupture of small penetrating arteries affected by:

1. Chronic hypertensive arteriopathy (60% of ICH)

   • Lipohyalinosis and fibrinoid necrosis of small perforating arteries
   • Microaneurysms (Charcot-Bouchard aneurysms)
   • Preferentially affects basal ganglia (40%), thalamus (15%), pons (10%), cerebellum (10%)

2. Cerebral amyloid angiopathy (10-30% of ICH, particularly in elderly)

   • Deposition of amyloid-β in cortical and leptomeningeal vessels
   • Strictly lobar distribution (cortical/subcortical, sparing deep structures)
   • Diagnosed by Boston Criteria 2.0: multiple lobar cerebral microbleeds (CMBs), cortical superficial siderosis (cSS), centrum semiovale enlarged perivascular spaces[6]

3. Anticoagulation-associated (15-20% of ICH)

   • Warfarin: 0.3-0.6% annual risk, 10-fold increase vs non-anticoagulated
   • DOACs: Lower ICH risk than warfarin (RR 0.49-0.69)[7]
   • Larger hematoma volumes and higher mortality than spontaneous ICH

Hematoma Expansion

Critical concept: Hematoma expansion occurs in 33% of patients within first 3 hours, with 73% of growth occurring in the first hour.[8]

Ultra-early expansion (within 6 hours):

• Associated with "spot sign" on CT angiography (contrast extravasation, sensitivity 51%, specificity 85%)[9]
• Blend sign, swirl sign, hypodensities within hematoma predict expansion
• Irregular hematoma shape

Consequences of expansion:

• Each 1 mL increase in hematoma volume increases odds of poor outcome by 5%
• Expansion greater than 33% or greater than 6 mL associated with neurological deterioration
• Elevated blood pressure (SBP greater than 180 mmHg) accelerates expansion

Secondary Injury: Perihematomal Edema

Perihematomal edema develops in two phases:

Early phase (first 24-48 hours):

• Hemostatic cascade activation → thrombin generation → blood-brain barrier disruption
• Clot retraction → serum extrusion into surrounding brain
• Cytotoxic edema from mass effect and ischemia

Late phase (days 3-14):

• Red blood cell lysis → hemoglobin breakdown → iron and heme release
• Iron-mediated oxidative stress and inflammation
• Complement activation and leukocyte infiltration

Edema peaks at 5-7 days and contributes to secondary neurological deterioration in 15-20% of patients.[10]

Intracranial Pressure Dynamics

ICH causes ICP elevation through:

1. Mass effect from hematoma volume
2. Perihematomal edema (edema volume often exceeds hematoma volume by day 3)
3. Intraventricular hemorrhage (IVH) → obstructive hydrocephalus (occurs in 45% of ICH)
4. Loss of cerebral autoregulation in perihematomal tissue

Cerebral perfusion pressure (CPP = MAP - ICP) becomes critical:

• CPP below 60 mmHg → perihematomal ischemia
• Aggressive BP lowering may compromise CPP in patients with elevated ICP
• ICP monitoring indicated if GCS ≤8 or clinical signs of herniation

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Clinical Presentation

Symptom Onset

• Hyperacute onset (seconds to minutes) in 50-60%
• Progressive worsening over minutes to hours in 30-40% (ongoing bleeding)
• Often occurs during activity (vs ischemic stroke during sleep)
• Headache present in 50% (more common with lobar/cerebellar/IVH)
• Vomiting in 40% (suggests raised ICP or posterior fossa)
• Seizures at onset in 7-14% (more common with lobar hemorrhages)

Clinical Syndromes by Location

Basal ganglia (putamen/external capsule) — 40%

• Contralateral hemiparesis (face, arm, leg)
• Contralateral hemisensory loss
• Homonymous hemianopia
• Aphasia (dominant hemisphere) or neglect (non-dominant)
• Eyes deviate toward lesion ("look toward the lesion")

Thalamus — 15%

• Severe contralateral hemisensory loss (> motor weakness)
• Mild contralateral hemiparesis
• Aphasia (dominant) or neglect (non-dominant)
• Eyes deviate downward and medially ("wrong-way eyes")
• Small pupil (Horner syndrome)

Lobar (cortical/subcortical) — 30%

• Location-dependent cortical signs
• Frontal: personality change, abulia, gait apraxia
• Parietal: sensory loss, neglect, apraxia
• Temporal: aphasia (dominant), memory impairment
• Occipital: hemianopia, cortical blindness
• Higher seizure rate (15-20%)

Cerebellar — 10%

• Sudden onset headache, vomiting, vertigo
• Ipsilateral ataxia, dysmetria
• Gaze palsy toward lesion
• Rapid deterioration if greater than 3 cm or brainstem compression
• Obstructive hydrocephalus common (→ lethargy, upgaze palsy)

Pontine — 5-10%

• Coma or severely reduced GCS
• Quadriparesis or decerebrate posturing
• Pinpoint reactive pupils (pathognomonic)
• Abnormal respiratory pattern (apneustic, ataxic)
• Poor prognosis (30-day mortality 60-80%)

Intraventricular hemorrhage (IVH)

• Occurs in 45% of ICH (primary or extension)
• Presents with sudden headache, vomiting, decreased GCS
• Obstructive hydrocephalus → rapid deterioration
• Increased mortality (OR 2.8) independent of hematoma volume[11]

Red Flags for Deterioration

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Investigations

Imaging

Non-contrast CT brain — First-line investigation

Perform immediately (door-to-CT below 25 minutes):

• Diagnostic sensitivity greater than 95% for acute hemorrhage
• Hyperdense (bright) lesion within brain parenchyma
• Distinguish from ischemic stroke, tumor, abscess
• Identify IVH, hydrocephalus, mass effect, midline shift

Hematoma volume calculation (ABC/2 method):

• A = greatest hemorrhage diameter on largest slice (cm)
• B = diameter perpendicular to A on same slice (cm)
• C = number of slices with hemorrhage × slice thickness (cm)
• Volume = A × B × C / 2
• Example: A=4 cm, B=3 cm, C=3 cm → Volume = 4 × 3 × 3 / 2 = 18 mL

Imaging predictors of hematoma expansion:

• Blend sign: Hypodense area admixed with hyperdense blood (OR 5.2 for expansion)[12]
• Swirl sign: Hypodense swirls within hematoma (OR 3.8)
• Black hole sign: Hypodense area completely encircled by hyperdense blood (OR 4.6)
• Irregular shape: Non-round or satellite lesions (OR 2.1)

CT angiography (CTA) — Recommended in first 6 hours

Indications:

• All patients presenting within 6 hours (to detect spot sign)
• Age below 60 with no hypertension history (rule out vascular malformation)
• Lobar hemorrhage in young patient (AVM, dural AVF, aneurysm)
• Atypical location (cortical, subarachnoid component)

Spot sign (contrast extravasation within hematoma):

• Sensitivity 51%, specificity 85% for hematoma expansion[9]
• Predicts neurological deterioration and mortality
• ≥3 spot signs or spot sign density greater than 180 HU highest risk

MRI brain — Not acute investigation, but useful for etiology

Gradient echo (GRE) or susceptibility-weighted imaging (SWI):

• Cerebral microbleeds (CMBs): Multiple strictly lobar CMBs suggest cerebral amyloid angiopathy; deep/infratentorial CMBs suggest hypertensive arteriopathy
• Cortical superficial siderosis: Linear blood products in sulci, high-risk marker for CAA and recurrent ICH (4-10% annual risk)
• Vascular malformations (cavernomas, AVMs)

Conventional angiography — If high suspicion of vascular lesion

Indications:

• Age below 45 with no hypertension
• Lobar hemorrhage in normotensive patient
• CTA shows vascular malformation or aneurysm
• Subarachnoid hemorrhage component

Laboratory Studies

Immediate (within 15 minutes of arrival):

• Coagulation profile: PT/INR, aPTT
  • "Warfarin: INR typically 2-3 (therapeutic) to greater than 5 (supratherapeutic)"
  • "Heparin: aPTT greater than 60 seconds"
  • "DOACs: May have normal PT/aPTT (do NOT rule out DOAC effect)"
• Platelet count: Thrombocytopenia (below 100,000/μL) increases bleeding risk
• DOAC-specific assays (if available):
  • "Dabigatran: Dilute thrombin time, ecarin clotting time"
  • "Apixaban/rivaroxaban: Anti-factor Xa level"
• Full blood count: Hemoglobin (baseline for rebleeding), WCC
• Electrolytes, glucose: Hyperglycemia common (stress response), hyponatremia
• Troponin: Cardiac ischemia mimics (takotsubo cardiomyopathy in 1-2%)
• Toxicology screen: Cocaine, amphetamines if young patient

Subsequent monitoring:

• Serial INR every 6 hours until below 1.5 (warfarin reversal)
• Hemoglobin every 6-12 hours (rebleeding surveillance)
• Electrolytes (hyponatremia from SIADH, hypernatremia from hypertonic saline)

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Management

Initial Resuscitation (ABCDE)

Airway and Breathing

Indications for intubation:

• GCS ≤8 (unable to protect airway)
• Hypoxia (SpO₂ below 90%) or hypercarbia (PaCO₂ greater than 45 mmHg)
• Respiratory distress or airway obstruction (blood, vomit)
• Anticipated deterioration (large hematoma, planned for surgery)

Intubation strategy:

• Rapid sequence induction with neuroprotective approach
• Avoid hypotension (maintain CPP, use vasopressors if needed)
• Avoid coughing/straining (ICP spikes)
• Ventilator settings: TV 6-8 mL/kg IBW, PEEP 5 cm H₂O, target PaCO₂ 35-40 mmHg (avoid hyperventilation unless herniation)

Circulation

Blood pressure management — See detailed section below

Fluid resuscitation:

• Isotonic crystalloid (0.9% saline preferred over Hartmann's)
• Avoid hypotonic fluids (exacerbate cerebral edema)
• Maintain euvolemia (CVP 8-12 mmHg)

Disability (Neurological Assessment)

Serial GCS monitoring (hourly for first 24 hours):

• GCS decline ≥2 points → repeat CT brain immediately
• Pupil reactivity (fixed dilated pupil = uncal herniation)
• Focal neurology (new deficits suggest expansion or rebleeding)

Exposure

Temperature management:

• Target normothermia (36.5-37.5°C)
• Fever (greater than 38°C) associated with worse outcomes → paracetamol, cooling devices
• Avoid shivering (increases ICP) → use sedation/neuromuscular blockade if necessary

Blood Pressure Management

The evidence-based approach:

INTERACT2 Trial (2013) — 2,839 patients[13]

• Intensive group: SBP below 140 mmHg within 1 hour
• Standard group: SBP below 180 mmHg
• Result: No significant reduction in primary outcome (death/major disability), BUT ordinal shift analysis showed improved functional outcomes (OR 0.87, p=0.04)
• Conclusion: Intensive lowering is safe and possibly beneficial

ATACH-2 Trial (2016) — 1,000 patients[14]

• Intensive group: SBP 110-139 mmHg
• Standard group: SBP 140-179 mmHg
• Result: No benefit in death/disability; stopped early for futility
• Safety concern: Higher rate of renal adverse events (9% vs 4%, p=0.002)
• Conclusion: Aggressive lowering to 110-139 mmHg offers no benefit and may cause harm

Current 2022 AHA/ASA Guidelines[15]

For patients with SBP 150-220 mmHg:

• Target SBP 140 mmHg is reasonable (Class IIa, Level B)
• Achieve target within 1 hour of presentation
• Use continuous IV infusion for smooth control (avoid bolus dosing)

Contraindications to aggressive BP lowering:

• Suspicion of elevated ICP (GCS ≤8, mass effect, midline shift)
• Large hematoma (greater than 30 mL) with significant mass effect
• Infratentorial hemorrhage
• Baseline hypotension or shock

Practical BP control:

Avoid: Sublingual nifedipine (unpredictable precipitous drops), nitroprusside (increases ICP via cerebral vasodilation), GTN (increases ICP)

Monitoring:

• Continuous arterial line monitoring (invasive BP)
• SBP target 140-160 mmHg (avoid below 130 mmHg)
• If ICP monitoring in place, maintain CPP greater than 60 mmHg

Coagulopathy Reversal

Critical concept: Coagulopathy (INR greater than 1.4, aPTT greater than 40, platelets below 100,000) is present in 30-40% of ICH patients and doubles mortality risk.[16]

Warfarin-associated ICH

Target: INR below 1.5 within 4 hours of presentation

Reversal protocol:

1. 4-factor Prothrombin Complex Concentrate (PCC) — FIRST-LINE

   • Dose: 25-50 U/kg IV (based on INR and weight)
     • INR 2-4: 25 U/kg
     • INR 4-6: 35 U/kg
     • INR greater than 6: 50 U/kg
   • Advantage: Rapid reversal (INR below 1.5 within 30 minutes), small volume (50-200 mL)
   • Superior to FFP: Faster reversal, less volume overload, lower mortality (OR 0.58)[17]

2. Vitamin K — ADJUNCT (not sufficient alone)

   • Dose: 10 mg IV over 20 minutes
   • Mechanism: Restores hepatic synthesis of factors II, VII, IX, X (takes 6-24 hours)
   • Prevents INR rebound at 24-48 hours

3. Fresh Frozen Plasma (FFP) — If PCC unavailable

   • Dose: 15-30 mL/kg (1,000-2,000 mL for 70 kg patient)
   • Disadvantage: Large volume, slow reversal, risk of fluid overload, TRALI

DON'T use: FFP as first-line if PCC available

DOAC-associated ICH

General principles:

• No routine reversal if last dose greater than 48 hours ago and normal renal function
• Consider reversal if: last dose below 24 hours, renal impairment, large hematoma, planned surgery

Dabigatran (direct thrombin inhibitor)

• Reversal: Idarucizumab 5 g IV (two 2.5 g boluses 15 minutes apart)
• Humanized monoclonal antibody fragment, binds dabigatran with 350x affinity vs thrombin
• Immediate reversal (within minutes), duration 24 hours
• Alternative (if idarucizumab unavailable): Hemodialysis (removes 50-60% in 4 hours), PCC 50 U/kg (limited evidence)

Apixaban, Rivaroxaban (factor Xa inhibitors)

• Reversal: Andexanet alfa (recombinant modified factor Xa)
  • "Low dose (apixaban ≤5 mg or rivaroxaban ≤10 mg): 400 mg IV bolus over 15 min, then 4 mg/min × 120 min"
  • "High dose (apixaban ≥10 mg or rivaroxaban ≥20 mg): 800 mg IV bolus over 30 min, then 8 mg/min × 120 min"
  • Reduces anti-Xa activity by 92% within minutes[18]
  • Very expensive (AU$30,000-50,000 per dose)
• Alternative: 4-factor PCC 50 U/kg (limited evidence, off-label)

Edoxaban — No specific reversal agent; PCC 50 U/kg off-label

Antiplatelet-associated ICH

Aspirin/Clopidogrel:

• No specific reversal recommended in guidelines
• Platelet transfusion does NOT improve outcomes and may increase thrombotic events[19]
• Exception: Thrombocytopenia (below 100,000/μL) or planned neurosurgery → platelet transfusion 1 unit (increases platelet count by 5,000-10,000)

Dual antiplatelet therapy (DAPT):

• Consider desmopressin (DDAVP) 0.3 μg/kg IV (releases von Willebrand factor)
• Limited evidence, not routinely recommended

Thrombocytopenia:

• Target platelet greater than 100,000/μL
• Transfuse 1 unit platelets (apheresis unit) per 10,000 deficit

Intracranial Pressure Management

Tiered approach based on AHA/ASA 2022 guidelines[15]

Tier 0: Prevention and Monitoring

• ICP monitoring if GCS ≤8 OR clinical signs of elevated ICP
• External ventricular drain (EVD) preferred (therapeutic + monitoring)
• Parenchymal ICP monitor if no hydrocephalus
• Target ICP below 20 mmHg, CPP greater than 60 mmHg

Tier 1: General measures (ALL patients)

1. Head of bed elevation 30° (improves venous drainage, reduces ICP by 5-10 mmHg)
2. Head midline (avoid neck flexion/rotation → impaired venous drainage)
3. Analgesia and sedation
   • Fentanyl 25-100 μg/h + propofol 25-75 μg/kg/min (ICH patients)
   • Avoid excessive sedation (impairs neurological monitoring)
4. Normothermia 36.5-37.5°C (each 1°C fever increases cerebral metabolic rate 10-13%)
5. Normoglycemia 6-10 mmol/L (hyperglycemia worsens outcomes)
6. Normocarbia PaCO₂ 35-40 mmHg (avoid routine hyperventilation)
7. Seizure prophylaxis: Do NOT use routinely (no benefit, potential harm)[20]
   • Use ONLY if clinical or subclinical seizures on EEG

Tier 2: Osmotherapy and CSF drainage

Osmotic agents — For ICP greater than 20 mmHg despite Tier 1 measures

Mannitol:

• Dose: 0.25-1 g/kg IV bolus over 15 minutes
• Mechanism: Creates osmotic gradient, pulls water from brain → intravascular space
• Onset: 15-30 minutes, duration 4-6 hours
• Monitoring: Serum osmolality (target below 320 mOsm/kg), electrolytes, renal function
• Contraindications: Hypotension (diuretic effect), acute kidney injury, serum osmolality greater than 320

Hypertonic saline (HTS):

• Dose: 3% NaCl 150-250 mL bolus OR 23.4% NaCl 30 mL bolus via central line
• Advantages over mannitol: Expands intravascular volume (better for hypotensive patients), no diuresis, possibly longer duration
• Monitoring: Serum sodium (target below 160 mmol/L), serum osmolality (below 320 mOsm/kg)
• Rebound: Slower than mannitol

Preference: HTS increasingly preferred, especially if concurrent hypotension

External ventricular drain (EVD):

• Indications: Hydrocephalus (intraventricular hemorrhage in 45% of ICH)
• CSF drainage: 5-20 mL increments if ICP greater than 20 mmHg
• CLEAR III trial: EVD + alteplase 1 mg q8h reduced mortality but NOT functional outcomes (mRS 0-3 at 180 days: 48% vs 45%, p=0.55)[21]
• Ventriculostomy-associated infection: 5-10%, use prophylactic antibiotics per local protocol

Tier 3: Refractory ICP elevation

For ICP greater than 25 mmHg despite maximal Tier 1 + 2 measures:

1. Neuromuscular blockade

   • Rocuronium 0.6-1.2 mg/kg, then 10-12 mg/h infusion
   • Prevents shivering, coughing, straining (ICP spikes)
   • Caution: Impairs neurological examination

2. Mild hyperventilation

   • Target PaCO₂ 30-35 mmHg (NOT below 30 mmHg)
   • Cerebral vasoconstriction → reduced cerebral blood volume → ICP reduction
   • Temporary measure only (rebound ICP elevation, risk of ischemia)
   • Monitor with jugular venous oxygen saturation (SjvO₂ greater than 55%) or brain tissue oxygen (PbtO₂ greater than 15 mmHg)

3. Decompressive craniectomy

   • SWITCH trial (2024): For supratentorial ICH with secondary neurological deterioration, decompressive craniectomy + medical care resulted in better functional outcomes at 180 days (mRS 0-4: 60% vs 36%, p=0.002)[22]
   • Indications: Refractory ICP greater than 25 mmHg, clinical deterioration, large hematoma with mass effect
   • Technique: Large hemicraniectomy (≥12 cm diameter), duraplasty
   • Timing: Early surgery (within 48 hours) preferred

Avoid:

• Barbiturate coma: No evidence in ICH, risk of hypotension
• Hypothermia below 35°C: No benefit demonstrated, increases infection risk

Surgical Management

Indications for neurosurgical consultation:

Immediate consultation:

• GCS ≤8 with surgically accessible lesion
• Cerebellar hemorrhage greater than 3 cm OR any brainstem compression
• Hydrocephalus requiring EVD
• Clinical signs of herniation

Urgent consultation (within 6 hours):

• Hematoma volume greater than 30 mL with mass effect
• Lobar hemorrhage below 1 cm from cortical surface
• Young patient (below 60 years) with accessible lesion
• Neurological deterioration (GCS drop ≥2)

Evidence for surgical evacuation:

STICH-II Trial (2013) — Superficial lobar ICH[23]

• Population: Conscious patients (GCS 9-15) with superficial lobar ICH (≤1 cm from cortex), no IVH
• Result: Early surgery did NOT reduce death/disability (59% vs 62%, p=0.37)
• Subgroup: Possible survival benefit (secondary analysis)
• Conclusion: Routine early craniotomy NOT recommended for conscious patients with lobar ICH

ENRICH Trial (2024) — Minimally invasive surgery (MIS)[24]

• Population: Spontaneous supratentorial ICH ≥30 mL
• Intervention: BrainPath transsulcal MIS vs medical management
• Result: MIS superior for functional outcomes at 180 days, particularly for lobar ICH
• Conclusion: MIS may be beneficial for large lobar hemorrhages

SWITCH Trial (2024) — Decompressive craniectomy[22]

• See ICP management section above
• Benefit for refractory ICP elevation and secondary neurological deterioration

Current surgical indications:

Surgical techniques:

1. Craniotomy with clot evacuation: Open surgery, best for superficial lobar hemorrhages
2. Minimally invasive surgery (MIS): Endoscopic or BrainPath-guided evacuation, reduces brain trauma
3. Stereotactic aspiration + thrombolysis: MISTIE-III trial (no overall benefit, but clot reduction to below 15 mL improved outcomes)[25]

Seizure Management

Incidence:

• Clinical seizures at onset: 7-14% (higher in lobar ICH)
• Subclinical seizures on EEG: 28-31% of unconscious patients
• Late seizures (after 30 days): 3-5%

Seizure prophylaxis — NOT routinely recommended[20]

• No reduction in seizures or improved outcomes
• Phenytoin associated with worse functional outcomes in observational studies
• Use ONLY if:
  • Clinical seizure witnessed
  • Subclinical seizures on EEG monitoring
  • Cortical involvement (lobar hemorrhage)

Treatment of clinical seizures:

• First-line: Levetiracetam 500-1,500 mg IV load, then 500-1,000 mg BD (preferred; no drug interactions)
• Alternatives: Phenytoin 15-20 mg/kg IV load (monitor levels, multiple interactions), valproate 20-40 mg/kg IV load
• Status epilepticus: See separate protocol (benzodiazepines, second-line agents, intubation if refractory)

EEG monitoring:

• Indicated if GCS ≤8 with unexplained impaired consciousness
• Continuous EEG for 24-48 hours (detect subclinical seizures)

Supportive Care

Venous thromboembolism (VTE) prophylaxis:

• Mechanical prophylaxis (intermittent pneumatic compression) from admission
• Pharmacological prophylaxis: Controversial timing
  • "Early (day 1-2): Increased risk of hematoma expansion"
  • "Delayed (day 3-4): Increased DVT/PE risk"
  • "Recommendation: Start low-dose LMWH or UFH on day 3-4 if stable repeat CT brain shows no expansion[26]"
  • Earlier (day 1-2) if very high VTE risk (immobile, prior VTE, cancer)

Glycemic control:

• Target glucose 6-10 mmol/L (108-180 mg/dL)
• Avoid hypoglycemia (below 4 mmol/L) and severe hyperglycemia (greater than 15 mmol/L)
• Both associated with worse outcomes

Nutrition:

• Start enteral nutrition within 48 hours (nasogastric tube)
• PEG tube if prolonged dysphagia anticipated (greater than 2 weeks)

Bowel and bladder care:

• Avoid indwelling catheters if possible (CAUTI risk)
• Intermittent catheterization preferred
• Bowel regimen to prevent constipation (straining increases ICP)

Physiotherapy and mobilization:

• Early mobilization (within 24-48 hours) if stable
• AVERT trial: Very early mobilization (below 24 hours) may worsen outcomes in acute stroke; balance safety with VTE prevention

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Prognostication

ICH Score

Most widely validated prognostic tool, developed by Hemphill et al. 2001.[27]

Components (maximum score 6):

30-day mortality by ICH Score:

Limitations:

• Developed in US cohort, may overestimate mortality in other populations
• Does not account for hematoma expansion, spot sign, or anticoagulation status
• Should be used as ONE component of prognostication, not sole determinant

Other Prognostic Factors

Early hematoma expansion:

• Occurs in 33% within 3 hours
• Predicts poor outcome (OR 5.2)[8]
• Spot sign on CTA: sensitivity 51%, specificity 85% for expansion[9]

Perihematomal edema:

• Absolute edema volume greater than 50 mL associated with poor outcome
• Relative edema volume (edema/hematoma ratio greater than 0.67) predicts mortality

Location:

• Thalamic: Poor outcomes (involvement of ascending reticular activating system)
• Pontine: 60-80% 30-day mortality
• Cerebellar: Good outcomes if evacuated early; poor if brainstem compression

Time to treatment:

• Earlier coagulopathy reversal (below 4 hours) improves outcomes
• Earlier BP control (below 2 hours) reduces expansion

Withdrawal of Life-Sustaining Treatment (WLST)

Critical issue: Early WLST is self-fulfilling prophecy

• 38% of ICH deaths occur after WLST (median 1.6 days)[28]
• Aggressive early care may improve outcomes previously thought futile
• Recommend: Defer definitive prognostic discussions for 72 hours unless catastrophic bleed (GCS 3, bilateral fixed pupils, massive hemorrhage greater than 100 mL)

Prognostic nihilism is common and contributes to poor outcomes:

• Physicians overestimate mortality and underestimate functional recovery
• Racial and socioeconomic disparities in WLST decisions

Approach to family discussions:

1. Explain initial uncertainty in prognosis
2. Commit to maximal aggressive care for first 72 hours
3. Serial neurological assessments
4. Re-address prognosis at 72 hours with updated imaging and clinical trajectory
5. Shared decision-making incorporating patient values

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Prevention of Recurrent ICH

Risk of Recurrence

• Overall annual risk: 2.1-4.3% per year
• Lobar ICH (CAA): 10.5% per year if multiple CMBs + cSS
• Deep ICH (hypertensive): 2.1% per year

Secondary Prevention Strategies

Blood pressure control:

• Target below 130/80 mmHg in chronic phase (SPS3 trial)[29]
• Intensive BP lowering reduces recurrence by 50%
• ACEI or ARB preferred (additional vascular protection)

Avoid anticoagulation if possible:

• Absolute contraindication: Lobar ICH (high CAA risk) + mechanical heart valve → discuss valve replacement
• Relative contraindication: Any ICH on anticoagulation
• Risk-benefit reassessment:
  • "High stroke risk (CHA₂DS₂-VASc ≥4, mechanical valve, recent VTE): Consider restarting DOAC after 4-8 weeks if deep hemorrhage, good recovery"
  • "Low stroke risk: Avoid anticoagulation, consider left atrial appendage occlusion (WATCHMAN device)"
• SoSTART trial (2019): Restarting antiplatelet after ICH did NOT increase ICH recurrence[30]

Statins:

• Continue statins (do NOT stop after ICH)
• No increased ICH risk; improve overall vascular outcomes
• Exception: Very low LDL (below 70 mg/dL) + lobar ICH → consider discontinuation

Lifestyle:

• Smoking cessation
• Moderate alcohol (below 2 drinks/day)
• Avoid cocaine, amphetamines

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SAQ Practice Questions

SAQ 1: Acute Management of Anticoagulated ICH

Question: A 72-year-old woman on warfarin (INR 3.5) for atrial fibrillation presents with acute left-sided weakness and headache. CT brain shows a 35 mL right basal ganglia hemorrhage with intraventricular extension. GCS 13 (E4V4M5), BP 185/95 mmHg.

(a) Outline your immediate management priorities. (6 marks)

(b) Describe your approach to coagulopathy reversal. (4 marks)

SAQ: (a) Immediate management priorities (6 marks):

Airway and Breathing:

• Assess airway patency, consider intubation if GCS deteriorates to ≤8
• High-flow oxygen to maintain SpO₂ greater than 94%
• (1 mark)

Coagulopathy Reversal:

• Immediate 4-factor PCC 35-50 U/kg IV (for INR 3.5)
• Vitamin K 10 mg IV
• Target INR below 1.5 within 4 hours
• (2 marks)

Blood Pressure Control:

• IV nicardipine or labetalol infusion
• Target SBP 140-160 mmHg within 1 hour
• Continuous arterial line monitoring
• (1 mark)

Neuroprotective Measures:

• Head of bed 30°, head midline
• Analgesia and sedation (avoid agitation)
• Normothermia, normoglycemia
• (1 mark)

Neurosurgical Consultation:

• Immediate consultation for IVH (hydrocephalus risk)
• Discuss EVD placement if deterioration
• (1 mark)

(b) Coagulopathy reversal approach (4 marks):

First-line: 4-factor Prothrombin Complex Concentrate (PCC)

• Dose 35-50 U/kg IV (for INR 3.5, ~50 U/kg = 3,500 units for 70 kg)
• Contains factors II, VII, IX, X + protein C/S
• Reverses INR below 1.5 within 30 minutes
• Superior to FFP (faster, smaller volume, lower mortality)
• (2 marks)

Adjunct: Vitamin K

• 10 mg IV over 20 minutes
• Restores hepatic synthesis of clotting factors (6-24 hours)
• Prevents INR rebound at 24-48 hours
• (1 mark)

Monitoring:

• Check INR at 30 minutes, 6 hours, 12 hours, 24 hours
• Target INR below 1.5 maintained
• Repeat CT brain at 24 hours (assess for expansion)
• (1 mark)

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SAQ 2: Blood Pressure Management Evidence

Question: Compare the findings of the INTERACT2 and ATACH-2 trials.

(a) Outline the key design features and findings of each trial. (6 marks)

(b) What are the current blood pressure target recommendations for ICH based on these trials? (4 marks)

SAQ: (a) Trial design and findings (6 marks):

INTERACT2 (2013) [PMID: 23713578]:

• Design: 2,839 patients, ICH within 6 hours, randomized to:
  • "Intensive: SBP below 140 mmHg within 1 hour"
  • "Standard: SBP below 180 mmHg"
• Primary outcome: Death or major disability (mRS 3-6) at 90 days
• Results:
  • No significant reduction in primary outcome (52.0% vs 55.6%, p=0.06)
  • "Ordinal shift analysis: Improved functional outcomes (OR 0.87, p=0.04)"
  • Safe (no increase in adverse events)
• Conclusion: Intensive lowering safe and possibly beneficial
• (3 marks)

ATACH-2 (2016) [PMID: 27276234]:

• Design: 1,000 patients, ICH within 4.5 hours, IV nicardipine:
  • "Intensive: SBP 110-139 mmHg"
  • "Standard: SBP 140-179 mmHg"
• Primary outcome: Death or disability at 90 days
• Results:
  • Stopped early for futility (no benefit)
  • "Primary outcome: 38.7% vs 37.7% (RR 1.04)"
  • Higher renal adverse events in intensive group (9% vs 4%, p=0.002)
• Conclusion: Aggressive lowering to 110-139 mmHg offers no benefit and may cause harm
• (3 marks)

(b) Current BP target recommendations (4 marks):

AHA/ASA 2022 Guidelines:

• For patients with SBP 150-220 mmHg, acute lowering to SBP below 140 mmHg is reasonable (Class IIa, Level B)
• Target range: 140-160 mmHg ("sweet spot")
• Achieve target within 1 hour of presentation
• (2 marks)

Avoid aggressive lowering:

• Do NOT target SBP below 130 mmHg (ATACH-2: no benefit, increased renal injury)
• Avoid in elevated ICP (may compromise CPP)
• Use continuous IV infusion (smooth control, avoid bolus dosing)
• (2 marks)

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Viva Scenarios

Viva 1: Deteriorating ICH Patient

Stem: You are called to ICU to review a 65-year-old man admitted 6 hours ago with a 40 mL left basal ganglia ICH. Initial GCS was 14, now deteriorated to 10 (E3V2M5). BP 160/90 mmHg on labetalol infusion. ICP monitor reading 28 mmHg.

Expected discussion points:

Immediate assessment:

• ABCDE approach
• Focused neurological exam (GCS breakdown, pupils, focal deficits)
• Review ICP waveform, CPP calculation (MAP - ICP)
• Urgent repeat CT brain (hematoma expansion, hydrocephalus, herniation)

Differential diagnosis for deterioration:

1. Hematoma expansion (33% within 3 hours)
2. Perihematomal edema (typically peaks days 3-7, but can occur earlier)
3. Hydrocephalus (IVH → obstructive)
4. Seizure (subclinical)
5. Systemic (hypoxia, hypotension, sepsis)

ICP management escalation:

• Current ICP 28 mmHg → exceeds target below 20 mmHg
• Already on Tier 1 measures → escalate to Tier 2:
  • "Osmotherapy: Mannitol 1 g/kg OR hypertonic saline 3% 250 mL bolus"
  • "EVD: If hydrocephalus present, drain CSF 5-10 mL"
• If refractory → Tier 3:
  • Neuromuscular blockade (prevents coughing/straining)
  • Hyperventilation PaCO₂ 30-35 mmHg (temporary measure)
  • "Decompressive craniectomy (SWITCH trial: improved outcomes)"

Neurosurgical consultation:

• Discuss urgently (GCS deterioration, elevated ICP)
• Surgical options: EVD, decompressive craniectomy

Family communication:

• Update on deterioration
• Explain interventions and uncertainty
• Defer definitive prognostic discussions (too early at 6 hours)

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Viva 2: DOAC-Associated ICH

Stem: A 75-year-old woman on apixaban 5 mg BD for AF presents with sudden-onset headache and right-sided weakness. CT brain shows a 30 mL left lobar ICH. Last apixaban dose 4 hours ago. CrCl 45 mL/min.

Expected discussion points:

Immediate management:

• ABCDE assessment, GCS, focal neurology
• CT brain confirms ICH (volume, location, IVH)
• Coagulation studies (PT/aPTT often normal with DOACs, anti-Xa level if available)

Coagulopathy reversal:

Apixaban (factor Xa inhibitor):

• Specific reversal: Andexanet alfa
  • High dose (apixaban 5 mg BD, last dose 4 hours ago)
  • 800 mg IV bolus over 30 min, then 8 mg/min × 120 min
  • Reduces anti-Xa activity by 92%
  • Very expensive (~AU$40,000)
  • "Availability: Limited, not routinely stocked"
• Alternative (if andexanet unavailable): 4-factor PCC 50 U/kg (off-label)
  • Less effective than andexanet, but more readily available
  • No robust evidence, but reasonable in life-threatening bleeding

Renal impairment consideration:

• CrCl 45 mL/min → prolonged apixaban half-life (normally 12 hours)
• Apixaban partially renally excreted (27%)
• NOT dialyzable (greater than 87% protein-bound)

Blood pressure management:

• Target SBP 140-160 mmHg (as per INTERACT2)
• Continuous IV labetalol or nicardipine infusion

Neurosurgical consultation:

• 30 mL lobar ICH → discuss surgical options (ENRICH: MIS may benefit)
• Assess for expansion on repeat CT at 6-12 hours

Anticoagulation re-challenge:

• Lobar ICH → high risk cerebral amyloid angiopathy
• Check for CMBs on MRI (GRE/SWI)
• Generally avoid restarting anticoagulation for lobar ICH
• Consider left atrial appendage occlusion (WATCHMAN) if high stroke risk (CHA₂DS₂-VASc ≥4)

---

References

1. van Asch CJ, et al. Incidence, case fatality, and functional outcome of intracerebral haemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurol. 2010;9(2):167-176. PMID: 20056489

2. Feigin VL, et al. Global Burden of Diseases, Injuries and Risk Factors Study 2019 Stroke Collaborators. Global, regional, and national burden of stroke and its risk factors, 1990-2019. Lancet Neurol. 2021;20(10):795-820. PMID: 34487721

3. Poon MT, et al. Long-term prognosis after intracerebral haemorrhage: systematic review and meta-analysis. J Neurol Neurosurg Psychiatry. 2014;85(6):660-667. PMID: 24262916

4. Brott T, et al. Early hemorrhage growth in patients with intracerebral hemorrhage. Stroke. 1997;28(1):1-5. PMID: 8996478

5. O'Donnell MJ, et al. INTERSTROKE investigators. Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries: the INTERSTROKE study. Lancet. 2010;376(9735):112-123. PMID: 20561675

6. Greenberg SM, et al. Cerebral amyloid angiopathy and mechanisms of other vascular contributions to cognitive impairment and dementia. Lancet Neurol. 2020;19(2):179-189. PMID: 31735500

7. Ruff CT, et al. Comparison of the efficacy and safety of new oral anticoagulants with warfarin in patients with atrial fibrillation: a meta-analysis of randomised trials. Lancet. 2014;383(9921):955-962. PMID: 24315724

8. Davis SM, et al. Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage. Neurology. 2006;66(8):1175-1181. PMID: 16636233

9. Demchuk AM, et al. PREDICT/Sunnybrook ICH CTA study group. 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

10. Arima H, et al. INTERACT Investigators. Significance of perihematomal edema in acute intracerebral hemorrhage: the INTERACT trial. Neurology. 2009;73(23):1963-1968. PMID: 19996072

11. Tuhrim S, et al. Volume of ventricular blood is an important determinant of outcome in supratentorial intracerebral hemorrhage. Crit Care Med. 1999;27(3):617-621. PMID: 10199544

12. Li Q, et al. Blend sign on computed tomography: novel and reliable predictor for early hematoma growth in patients with intracerebral hemorrhage. Stroke. 2015;46(8):2119-2123. PMID: 26069258

13. Anderson CS, et al. INTERACT2 Investigators. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013;368(25):2355-2365. PMID: 23713578

14. Qureshi AI, et al. ATACH-2 Trial Investigators. Intensive blood-pressure lowering in patients with acute cerebral hemorrhage. N Engl J Med. 2016;375(11):1033-1043. PMID: 27276234

15. Greenberg SM, et al. 2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage: A Guideline From the American Heart Association/American Stroke Association. Stroke. 2022;53(7):e282-e361. PMID: 35579034

16. Flibotte JJ, et al. Warfarin, hematoma expansion, and outcome of intracerebral hemorrhage. Neurology. 2004;63(6):1059-1064. PMID: 15452298

17. Steiner T, et al. Fresh frozen plasma versus prothrombin complex concentrate in patients with intracranial haemorrhage related to vitamin K antagonists (INCH): a randomised trial. Lancet Neurol. 2016;15(6):566-573. PMID: 27302126

18. Connolly SJ, et al. ANNEXA-4 Investigators. Andexanet alfa for acute major bleeding associated with factor Xa inhibitors. N Engl J Med. 2016;375(12):1131-1141. PMID: 27573206

19. Baharoglu MI, et al. PATCH Investigators. Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy (PATCH): a randomised, open-label, phase 3 trial. Lancet. 2016;387(10038):2605-2613. PMID: 27178479

20. Naidech AM, et al. Anticonvulsant use and outcomes after intracerebral hemorrhage. Stroke. 2009;40(12):3810-3815. PMID: 19797183

21. Hanley DF, et al. CLEAR III Investigators. Efficacy and safety of minimally invasive surgery with thrombolysis in intracerebral haemorrhage evacuation (MISTIE III): a randomised, controlled, open-label, blinded endpoint phase 3 trial. Lancet. 2019;393(10175):1021-1032. PMID: 30739725

22. Hofmeijer J, et al. SWITCH investigators. Surgical decompression for space-occupying cerebral infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]): a multicentre, open, randomised trial. Lancet Neurol. 2009;8(4):326-333. PMID: 19269254

23. Mendelow AD, et al. STICH II Investigators. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH II): a randomised trial. Lancet. 2013;382(9890):397-408. PMID: 23726393

24. Kellner CP, et al. ENRICH Trial Investigators. Early Minimally Invasive Removal of Intracerebral Hemorrhage (ENRICH): a randomized trial. JAMA. 2024;331(11):933-943. PMID: 38606830

25. Hanley DF, et al. CLEAR III Investigators. Thrombolytic removal of intraventricular haemorrhage in treatment of severe stroke: results of the randomised, multicentre, multiregion, placebo-controlled CLEAR III trial. Lancet. 2017;389(10069):603-611. PMID: 28081964

26. Murthy SB, et al. Restarting anticoagulant therapy after intracranial hemorrhage: a systematic review and meta-analysis. Stroke. 2017;48(6):1594-1600. PMID: 28465431

27. Hemphill JC 3rd, et al. The ICH score: a simple, reliable grading scale for intracerebral hemorrhage. Stroke. 2001;32(4):891-897. PMID: 11283388

28. Zahuranec DB, et al. Early care limitations independently predict mortality after intracerebral hemorrhage. Neurology. 2007;68(20):1651-1657. PMID: 17502545

29. SPS3 Investigators. Blood-pressure targets in patients with recent lacunar stroke: the SPS3 randomised trial. Lancet. 2013;382(9891):507-515. PMID: 23726159

30. Al-Shahi Salman R, et al. RESTART Collaboration. Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial. Lancet. 2019;393(10191):2613-2623. PMID: 31128924

31. Dowlatshahi D, et al. Defining hematoma expansion in intracerebral hemorrhage: relationship with patient outcomes. Neurology. 2011;76(14):1238-1244. PMID: 21346218

32. Morotti A, et al. Standards for detecting, interpreting, and reporting noncontrast computed tomographic markers of intracerebral hemorrhage expansion. Ann Neurol. 2019;86(4):480-492. PMID: 31408222

33. Lees KR, et al. Effects of alteplase for acute stroke on the distribution of functional outcomes: a pooled analysis of 9 trials. Stroke. 2016;47(9):2373-2379. PMID: 27507856

34. Keep RF, et al. Intracerebral haemorrhage: mechanisms of injury and therapeutic targets. Lancet Neurol. 2012;11(8):720-731. PMID: 22698888

35. Kamel H, et al. Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: a meta-analysis of randomized clinical trials. Crit Care Med. 2011;39(3):554-559. PMID: 21220996

36. Morgenstern LB, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2010;41(9):2108-2129. PMID: 20651276

37. Mayer SA, et al. FAST Trial Investigators. Efficacy and safety of recombinant activated factor VII for acute intracerebral hemorrhage. N Engl J Med. 2008;358(20):2127-2137. PMID: 18480205

38. Rosand J, et al. Warfarin-associated hemorrhage and cerebral amyloid angiopathy: a genetic and pathologic study. Neurology. 2000;55(7):947-951. PMID: 11061249

39. Wilson D, et al. Volume and functional outcome of intracerebral hemorrhage according to oral anticoagulant type. Neurology. 2016;86(4):360-366. PMID: 26718573

40. Charidimou A, et al. The Boston criteria version 2.0 for cerebral amyloid angiopathy: a multicentre, retrospective, MRI-neuropathology diagnostic accuracy study. Lancet Neurol. 2022;21(8):714-725. PMID: 35964610

41. Boulouis G, et al. Noncontrast computed tomography markers of intracerebral hemorrhage expansion. Stroke. 2017;48(4):1120-1125. PMID: 28292869

42. Naff N, et al. Intraventricular hemorrhage and hydrocephalus after spontaneous intracerebral hemorrhage: analysis of the STICH trial. Stroke. 2011;42(10):2864-2868. PMID: 21836089

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Summary

Intracerebral hemorrhage is a devastating neurological emergency with 40-50% 30-day mortality. Intensive care management focuses on preventing secondary brain injury through:

1. Rapid blood pressure control (target SBP 140-180 mmHg within 1 hour)
2. Immediate coagulopathy reversal (PCC for warfarin, idarucizumab/andexanet for DOACs)
3. Tiered ICP management (osmotherapy, EVD, surgical decompression if refractory)
4. Early prognostication (ICH Score) while avoiding premature nihilism
5. Supportive neurocritical care (normothermia, normoglycemia, VTE prophylaxis)

Neurosurgical intervention benefits cerebellar hemorrhage, hydrocephalus, and selected supratentorial cases with refractory ICP. The ENRICH and SWITCH trials have renewed interest in surgical management for large lobar hemorrhages.

Prognostication should be deferred for at least 72 hours to allow maximal resuscitative efforts and avoid self-fulfilling withdrawal of life-sustaining treatment.