17.3 Acute Ischemic Stroke & Intracranial Hemorrhage

ABIM Critical Care Medicine Study Guide Exam

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1 Chapter 1: Exam Orientation: Format, Blueprint & Study Strategy

1.1 ABIM Critical Care Medicine Exam: Format, Blueprint & Study Strategy

2 Chapter 2: Acute Respiratory Failure & ARDS

2.1 ARDS Definition, Pathophysiology & Phenotypes 2.2 Lung-Protective Mechanical Ventilation 2.3 Refractory ARDS: Prone Positioning, Neuromuscular Blockade & VV-ECMO

3 Chapter 3: Obstructive Airways, Pulmonary Vascular & Pleural Emergencies

3.1 Severe Asthma & COPD Exacerbations in the ICU 3.2 Massive & Submassive Pulmonary Embolism 3.3 Pulmonary Hypertension & Right Ventricular Failure in the ICU 3.4 Massive Hemoptysis, Complex Pleural Effusions & Thoracic Drainage

4 Chapter 4: Airway, Parenchymal & Nonthrombotic Pulmonary Emergencies

4.1 Airway Management, Upper-Airway Obstruction & Artificial-Airway Complications 4.2 Diffuse Alveolar Hemorrhage, Interstitial Lung Disease, Pulmonary Vasculitis & Noncardiogenic Edema 4.3 Severe Community-Acquired & Viral Pneumonia 4.4 Nonthrombotic Embolism (Air, Fat, Amniotic Fluid, Tumor, Septic) & Acute Chest Syndrome

5 Chapter 5: Mechanical Ventilation Modes, Dyssynchrony & Liberation

5.1 Mechanical Ventilator Modes & Advanced Breath Delivery 5.2 Patient-Ventilator Dyssynchrony & Waveform Analysis 5.3 Ventilator Liberation, Spontaneous Breathing Trials & Post-Extubation Support

6 Chapter 6: Shock Syndromes & Hemodynamic Principles

6.1 Shock Classification, Cellular Pathophysiology & Biomarkers 6.2 Hemodynamic Monitoring: Arterial Lines, CVP & Pulmonary Artery Catheter 6.3 Dynamic Assessment of Fluid Responsiveness & Resuscitation Targets

7 Chapter 7: Vasoactive Therapies & Mechanical Circulatory Support

7.1 Vasopressors & Inotropes: Pharmacology & Clinical Titration 7.2 Temporary Mechanical Circulatory Support: IABP, Impella & TandemHeart 7.3 Venoarterial ECMO (VA-ECMO) & Differential Hypoxemia 7.4 Post-Cardiac Arrest Care, Targeted Temperature Management & Neuroprognostication

8 Chapter 8: Acute Kidney Injury & Renal Replacement Therapy

8.1 KDIGO AKI Classification, Etiologies & Diagnostic Evaluation 8.2 Continuous Renal Replacement Therapy (CRRT) vs Intermittent Hemodialysis 8.3 Indications & Timing for RRT in Critical Illness: AKIKI & STARRT-AKI

9 Chapter 9: Electrolyte, Acid-Base & Endocrine Emergencies

9.1 Severe Dysnatremias: Hyponatremia, Hypernatremia & Osmotic Demyelination 9.2 Potassium, Calcium, Magnesium & Phosphate Disorders 9.3 Complex & Mixed Acid-Base Disorders: Boston vs Copenhagen vs Stewart 9.4 Endocrine Crises: DKA, HHS, Thyroid Storm, Myxedema Coma & Adrenal Crisis

10 Chapter 10: Glycemic Control, Hyperammonemia, Pituitary & Adrenal Disorders

10.1 ICU Glycemic Control & Severe Hypoglycemia 10.2 Non-Hepatic Hyperammonemia & Metabolic Encephalopathy 10.3 Pituitary Emergencies, Adrenal Excess & Critical Illness-Related Corticosteroid Insufficiency

11 Chapter 11: Acute Coronary Syndromes & Cardiac Arrhythmias

11.1 Acute Coronary Syndromes & Mechanical Complications of Myocardial Infarction 11.2 Critical Tachyarrhythmias: Atrial Fibrillation with RVR, VT & VF 11.3 Critical Bradyarrhythmias, Conduction Blocks & Temporary Cardiac Pacing

12 Chapter 12: Acute Heart Failure, Valvular & Pericardial Emergencies

12.1 Acute Decompensated Heart Failure & Cardiogenic Pulmonary Edema 12.2 Acute Valvular Regurgitation & Prosthetic Valve Emergencies 12.3 Pericardial Tamponade & Acute Aortic Syndromes

13 Chapter 13: Myocardial Disease, Hypertensive & Cardiac Device Emergencies

13.1 Fulminant Myocarditis, Stress & Peripartum Cardiomyopathy, and Hypertrophic Cardiomyopathy 13.2 Hypertensive Emergencies & Ruptured Abdominal Aortic Aneurysm 13.3 Implanted Cardiac Devices, LVAD Emergencies & Electrical Storm

14 Chapter 14: Sepsis & Systemic Infectious Diseases

14.1 Sepsis-3 Definitions & Surviving Sepsis Campaign 2026 Guidelines 14.2 Refractory Septic Shock & Adjunctive Therapies 14.3 Multidrug-Resistant Pathogens & Antimicrobial Stewardship in the ICU

15 Chapter 15: ICU-Acquired & Severe Focal Infections

15.1 Hospital-Acquired & Ventilator-Associated Pneumonia 15.2 Central Line-Associated Bloodstream Infections & Catheter-Associated UTIs 15.3 Intra-Abdominal Sepsis, Necrotizing Soft Tissue Infections & CNS Infections

16 Chapter 16: Focal, Special-Host & Systemic Infections

16.1 CNS Infections Beyond Bacterial Meningitis: Encephalitis, Brain Abscess & Epidural Abscess 16.2 Infections in the Immunocompromised Host, Tropical & Bioterror Infections 16.3 Infective Endocarditis, Device Infections & Other Focal Cardiovascular Infections 16.4 Antimicrobial Pharmacokinetics, Allergy, Toxicity & Infection Prevention 16.5 Gastrointestinal & Hepatobiliary Infections: Fulminant C. difficile, Typhlitis, CMV Colitis & Abscesses

17 Chapter 17: Neurocritical Care & Coma

17.1 Coma, Altered Mental Status & Acute Delirium in the ICU 17.2 Status Epilepticus & Non-Convulsive Status Epilepticus 17.3 Acute Ischemic Stroke & Intracranial Hemorrhage

18 Chapter 18: Cerebrovascular Syndromes, Encephalopathy & Withdrawal States

18.1 Cerebral Venous Sinus Thrombosis, PRES & Reversible Cerebral Vasoconstriction Syndrome 18.2 Alcohol & Sedative Withdrawal, Wernicke Encephalopathy & Drug-Induced Encephalopathy

19 Chapter 19: Intracranial Hypertension & Neuromuscular Weakness

19.1 Intracranial Pressure Monitoring, Cerebral Perfusion & Tiered ICP Management 19.2 Acute Neuromuscular Respiratory Failure, ICU-Acquired Weakness & Brain Death Determination

20 Chapter 20: Traumatic Brain Injury, Spinal Cord Injury & Toxin-Mediated Paralysis

20.1 Traumatic Brain Injury Management & Paroxysmal Sympathetic Hyperactivity 20.2 Acute Spinal Cord Injury, Neurogenic Shock & Autonomic Dysreflexia 20.3 Toxin-Mediated Paralysis & Neuromuscular Crises: Botulism, Tetanus, Tick Paralysis & Myasthenic Crisis

21 Chapter 21: Gastrointestinal, Hepatic & Abdominal Emergencies

21.1 Acute Upper & Lower Gastrointestinal Bleeding in the ICU 21.2 Acute Liver Failure & Severe Acute Pancreatitis 21.3 Abdominal Compartment Syndrome & Acute Mesenteric Ischemia

22 Chapter 22: Luminal GI Emergencies & Complications of Cirrhosis

22.1 Esophageal, Gastric & Bowel Emergencies: Perforation, Obstruction, Ogilvie Syndrome & Colonic Ischemia 22.2 Complications of Cirrhosis: Alcohol-Associated Hepatitis, Hepatorenal Syndrome & Pulmonary Vascular Syndromes

23 Chapter 23: Trauma, Burns & Perioperative Critical Care

23.1 Polytrauma Resuscitation, Damage Control & Massive Transfusion 23.2 Severe Burn Injury, Inhalation Injury & Environmental Emergencies 23.3 Perioperative Critical Care for High-Risk Surgical Patients

24 Chapter 24: Thoracic Trauma, Environmental Injury & Obstetric Critical Care

24.1 Thoracic Trauma: Flail Chest, Pulmonary Contusion, Great Vessel & Tracheobronchial Injury 24.2 Environmental Injury: Drowning, Diving, Altitude, Heat, Cold, Electrical & Radiation 24.3 Obstetric & Genitourinary Emergencies and the Physiology of Pregnancy

25 Chapter 25: Transplantation, Donor Management & Post-Cardiac Surgery Care

25.1 Solid Organ Transplant Recipients & Deceased Donor Management 25.2 Post-Cardiac Surgery Critical Care: Bleeding, Tamponade, Low Output & Vasoplegia

26 Chapter 26: Hematologic Emergencies, Toxicology, Critical Ultrasound & ICU Liberation

26.1 Hematologic Emergencies in the ICU: HIT, DIC, TMA & Anticoagulant Reversal 26.2 Critical Care Toxicology, Toxidromes & Specific Antidotes 26.3 Critical Care Point-of-Care Ultrasound (POCUS) 26.4 ICU Liberation, Analgosedation, Goals of Care & Critical Care Ethics

27 Chapter 27: Transfusion Medicine, Hematologic & Oncologic Disorders

27.1 Transfusion Medicine: Products, Thresholds, Reactions & Apheresis 27.2 Red and White Cell Disorders, Hemoglobinopathies, Factor Deficiencies & Hypercoagulable States 27.3 Oncologic Emergencies, Hematopoietic Cell Transplant Complications & Cellular Therapy Toxicity

28 Chapter 28: Clinical Pharmacology, Adverse Drug Reactions & Specific Poisonings

28.1 Pharmacokinetic Principles, Dose Adjustment & Drug Interactions in Critical Illness 28.2 Adverse Drug Reactions: Anaphylaxis, Severe Cutaneous Reactions & Hyperthermic Syndromes 28.3 Specific Poisonings: Sodium-Channel Blockers, Lithium, Valproate, Theophylline, Iron, Sulfonylureas & Methemoglobinemia

29 Chapter 29: Ethics, Research Methods, Administration & Abdominal Ultrasound

29.1 Advance Care Planning, Nonbeneficial Treatment, Informed Consent & Confidentiality 29.2 Critical Care Research Methods, Statistics, IRB Oversight & Quality Improvement 29.3 Abdominal, Vascular & Procedural Point-of-Care Ultrasound

17.3 Acute Ischemic Stroke & Intracranial Hemorrhage

Key Takeaways Explain This Topic AI

In acute ischemic stroke (AIS), intravenous thrombolysis with tenecteplase (0.25 mg/kg, max 25 mg) or alteplase (0.9 mg/kg, max 90 mg) is indicated within 4.5 hours of last known normal; blood pressure must be reduced to <185/110 mmHg prior to thrombolysis and maintained <180/105 mmHg for 24 hours post-infusion.

Endovascular thrombectomy (EVT) provides dramatic functional benefit up to 24 hours from symptom onset in anterior circulation large vessel occlusion (LVO) meeting clinical-imaging mismatch criteria established in the DAWN and DEFUSE-3 trials.

In non-reperfused ischemic stroke, permissive hypertension (<220/120 mmHg) is maintained to preserve penumbral perfusion; for malignant MCA infarction in patients <= 60 years, early decompressive hemicraniectomy (<= 48 hours) reduces mortality from about 71% to 22% (pooled DECIMAL, DESTINY, HAMLET analysis).

Spontaneous intracerebral hemorrhage (ICH) requires rapid, smooth blood pressure reduction targeting systolic BP 130-150 mmHg (INTERACT-2, ATACH-2) using titratable IV agents (nicardipine); coagulopathy must be reversed immediately with 4F-PCC plus IV vitamin K for warfarin, idarucizumab for dabigatran, and 4F-PCC for factor Xa inhibitors (andexanet alfa was withdrawn from the US market in December 2025).

Aneurysmal subarachnoid hemorrhage (aSAH) requires securing the aneurysm as early as feasible, preferably within 24 hours (2023 AHA/ASA); delayed cerebral ischemia (DCI, peak days 4 to 14) is reduced with enteral nimodipine (60 mg q4h for 21 days; NEVER IV) and managed with euvolemia and blood pressure augmentation.

Last updated: October 2026

Acute Ischemic Stroke: Reperfusion Therapies and Hemodynamics

Acute ischemic stroke (AIS) results from sudden focal vascular occlusion, producing an ischemic core of irreversibly infarcted tissue (cerebral blood flow [ C B F ] < 10 − 12 mL/100g/min [CBF] < 10-12\text{ mL/100g/min} [ CBF ] < 10 − 12 mL/100g/min ) surrounded by a dynamic, hypoperfused ischemic penumbra ( C B F 12 − 22 mL/100g/min CBF\ 12-22\text{ mL/100g/min} CBF 12 − 22 mL/100g/min ). The penumbra is functionally silent but metabolically viable, preserved temporarily by leptomeningeal collateral circulation. Time is brain: approximately 1.9 million 1.9\text{ million} 1.9 million neurons undergo apoptotic and necrotic destruction for every minute an acute proximal large vessel occlusion remains untreated.

1. Intravenous Thrombolysis: Tenecteplase vs. Alteplase

Intravenous thrombolysis remains standard care for eligible patients presenting within 4.5 hours 4.5\text{ hours} 4.5 hours of symptom onset (or last known well):

Alteplase (rtPA) : Dosed at 0.9 mg/kg 0.9\text{ mg/kg} 0.9 mg/kg (maximum 90 mg 90\text{ mg} 90 mg ); 10 % 10\% 10% administered as an initial IV bolus over 1 minute, with the remaining 90 % 90\% 90% infused over 60 minutes.

Tenecteplase (TNK) : A genetically engineered tissue plasminogen activator with higher fibrin specificity, greater resistance to plasminogen activator inhibitor-1, and a longer half-life that allows single-bolus dosing. Dosed as a single 0.25 mg/kg 0.25\text{ mg/kg} 0.25 mg/kg IV bolus (maximum 25 mg 25\text{ mg} 25 mg ) over 5 seconds. Contemporary trials (EXTEND-IA TNK, AcT) demonstrate non-inferiority to alteplase with superior early recanalization rates in large vessel occlusions and substantial operational advantages (eliminates pump setup and simplifies inter-facility transport).

2026 AHA/ASA guideline updates : tenecteplase or alteplase is recommended within 4.5 hours for disabling deficits regardless of NIHSS score; for mild non-disabling deficits, dual antiplatelet therapy is preferred to thrombolysis. Thrombolysis can extend to 4.5 to 9 hours or unknown onset when imaging shows a DWI-FLAIR mismatch or salvageable penumbra on perfusion imaging. Adjunctive IV argatroban or eptifibatide is not recommended. Keep glucose at 140 to 180 mg/dL ; tighter targets (80 to 130 mg/dL) are not recommended.

Blood Pressure Thresholds for Thrombolysis

Uncontrolled hypertension during thrombolytic administration dramatically amplifies the risk of catastrophic symptomatic intracranial hemorrhage (sICH):

Pre-Thrombolysis Target : Blood pressure must be reduced to SBP < 185 mmHg \text{SBP} < 185\text{ mmHg} SBP < 185 mmHg and DBP < 110 mmHg \text{DBP} < 110\text{ mmHg} DBP < 110 mmHg prior to initiating thrombolytic infusion.

Post-Thrombolysis Maintenance : Maintain SBP < 180 mmHg \text{SBP} < 180\text{ mmHg} SBP < 180 mmHg and DBP < 105 mmHg \text{DBP} < 105\text{ mmHg} DBP < 105 mmHg continuously for at least 24 hours 24\text{ hours} 24 hours post-thrombolysis.

Preferred Antihypertensive Agents : IV Nicardipine infusion ( 5 mg/h 5\text{ mg/h} 5 mg/h , titrate by 2.5 mg/h 2.5\text{ mg/h} 2.5 mg/h every 5-15 minutes to max 15 mg/h 15\text{ mg/h} 15 mg/h ), IV Clevidipine ( 1 − 2 mg/h 1-2\text{ mg/h} 1 − 2 mg/h , titrate by doubling every 90 seconds to max 16 − 32 mg/h 16-32\text{ mg/h} 16 − 32 mg/h ), or IV Labetalol ( 10 − 20 mg 10-20\text{ mg} 10 − 20 mg IV over 1-2 minutes; may repeat or double every 10 minutes to max 300 mg 300\text{ mg} 300 mg ).

Absolute Contraindications to IV Thrombolysis

Acute intracranial hemorrhage on non-contrast head CT.

Severe head trauma or ischemic stroke within the preceding 3 months.

Active internal bleeding or acute bleeding diathesis (platelets < 100 , 000 / μ L <100,000/\mu\text{L} < 100 , 000/ μ L , INR > 1.7 \text{INR} > 1.7 INR > 1.7 , aPTT > 40 seconds \text{aPTT} > 40\text{ seconds} aPTT > 40 seconds , or PT > 15 seconds \text{PT} > 15\text{ seconds} PT > 15 seconds ).

Use of therapeutic doses of direct oral anticoagulants (DOACs; apixaban, rivaroxaban, dabigatran) within the preceding 48 hours unless specific drug activity assays are normal or reversal agents are administered.

Intra-axial intracranial neoplasm. (A small unruptured intracranial aneurysm is not a contraindication; benefit and risk are uncertain with an unruptured arteriovenous malformation.)

Recent intracranial or intraspinal surgery within 3 months.

Persistent SBP ≥ 185 mmHg \ge 185\text{ mmHg} ≥ 185 mmHg or DBP ≥ 110 mmHg \ge 110\text{ mmHg} ≥ 110 mmHg refractory to aggressive IV antihypertensive therapy.

2. Endovascular Thrombectomy (EVT): Early and Extended Windows

Endovascular mechanical thrombectomy (EVT) using stent retrievers and direct aspiration catheters is the standard of care for acute Large Vessel Occlusion (LVO) of the anterior circulation (intracranial internal carotid artery [ICA] or middle cerebral artery [MCA] M1 segment):

Standard Window ( 0 − 6 Hours 0 - 6\text{ Hours} 0 − 6 Hours ) : Indicated for patients with pre-stroke modified Rankin Scale (mRS) 0 to 1, causative occlusion of the internal carotid artery or proximal MCA (M1), age ≥ 18 \ge 18 ≥ 18 , baseline NIHSS ≥ 6 \text{NIHSS} \ge 6 NIHSS ≥ 6 , and non-contrast CT Alberta Stroke Program Early CT Score ( ASPECTS ) ≥ 6 \ge 6 ≥ 6 .

Extended Window ( 6 − 24 Hours 6 - 24\text{ Hours} 6 − 24 Hours ) : Two landmark randomized trials established the safety and profound efficacy of EVT in patients presenting between 6 and 24 hours from last known normal, using automated CT perfusion (CTP) or diffusion-weighted MRI (DWI) to identify salvageable penumbra:

DAWN Trial ( 6 − 24 Hours 6 - 24\text{ Hours} 6 − 24 Hours ) : Enrolled patients with a clinical-imaging mismatch between clinical stroke severity and core infarct volume: NIHSS ≥ 10 \text{NIHSS} \ge 10 NIHSS ≥ 10 and infarct core volume < 21 mL <21\text{ mL} < 21 mL (age ≥ 80 \ge 80 ≥ 80 ), or infarct core volume < 31 mL <31\text{ mL} < 31 mL (age < 80 <80 < 80 with NIHSS ≥ 10 \text{NIHSS} \ge 10 NIHSS ≥ 10 ), or core volume 31 − 51 mL 31-51\text{ mL} 31 − 51 mL (age < 80 <80 < 80 with NIHSS ≥ 20 \text{NIHSS} \ge 20 NIHSS ≥ 20 ). EVT demonstrated dramatic functional independence at 90 days ( 49 % 49\% 49% vs. 13 % 13\% 13% ; NNT = 2.8 \text{NNT} = 2.8 NNT = 2.8 ).

DEFUSE-3 Trial ( 6 − 16 Hours 6 - 16\text{ Hours} 6 − 16 Hours ) : Enrolled patients with an acute anterior circulation LVO exhibiting target mismatch criteria : initial ischemic core volume < 70 mL <70\text{ mL} < 70 mL , mismatch ratio (penumbra to core) ≥ 1.8 \ge 1.8 ≥ 1.8 , and absolute mismatch volume ≥ 15 mL \ge 15\text{ mL} ≥ 15 mL . EVT improved 90-day functional independence ( 45 % 45\% 45% vs. 17 % 17\% 17% ; NNT = 3.6 \text{NNT} = 3.6 NNT = 3.6 ).

Large-core infarcts : randomized trials (SELECT2, ANGEL-ASPECT, RESCUE-Japan LIMIT, TENSION) showed functional benefit from EVT in selected patients with large ischemic cores (for example ASPECTS 3 to 5), now reflected in the 2026 guideline.

Basilar artery occlusion : EVT within 24 hours is strongly recommended for patients with NIHSS of 10 or more (ATTENTION, BAOCHE).

After successful EVT : intensive lowering to SBP below 140 mmHg is not recommended, because trials of intensive targets (ENCHANTED2/MT, OPTIMAL-BP, BP-TARGET) found no benefit or harm. Keep BP at or below 180/105 mmHg.

3. Permissive Hypertension in Non-Reperfused Patients

In AIS patients who do not receive thrombolysis or endovascular thrombectomy, acute blood pressure lowering is strictly avoided. Autoregulation in the ischemic penumbra is completely impaired; blood flow becomes passively dependent on systemic mean arterial pressure. Precipitous blood pressure reduction drops perfusion across leptomeningeal collaterals, rapidly converting the viable penumbra into irreversible infarction.

Guideline Rule : Blood pressure is not treated unless SBP > 220 mmHg \text{SBP} > 220\text{ mmHg} SBP > 220 mmHg or DBP > 120 mmHg \text{DBP} > 120\text{ mmHg} DBP > 120 mmHg .

If blood pressure exceeds 220 / 120 mmHg 220/120\text{ mmHg} 220/120 mmHg , lower BP cautiously by 15 % 15\% 15% over the first 24 hours using IV labetalol or nicardipine.

Exceptions : Concomitant acute myocardial infarction, acute aortic dissection, severe heart failure with pulmonary edema, or hypertensive encephalopathy mandate immediate, controlled blood pressure reduction.

4. Malignant MCA Infarction & Decompressive Hemicraniectomy

Malignant middle cerebral artery infarction occurs in up to 10 % 10\% 10% of ischemic stroke patients, characterized by massive post-ischemic cytotoxic edema, midline shift, and progressive uncal/subfalcine herniation peaking between post-stroke days 2 and 5 . Medical management alone (hyperosmolar therapy with 3 % 3\% 3% hypertonic saline or mannitol, hyperventilation) carries a catastrophic mortality rate of 70 % 70\% 70% to 80 % 80\% 80% .

Landmark Pooled Trials (DECIMAL, DESTINY, HAMLET) : A pooled individual-patient meta-analysis of three European randomized controlled trials demonstrated that early decompressive hemicraniectomy (large bone flap diameter ≥ 12 cm \ge 12\text{ cm} ≥ 12 cm with duraplasty) performed within 48 hours 48\text{ hours} 48 hours of symptom onset in patients aged ≤ 60 years \le 60\text{ years} ≤ 60 years with malignant MCA infarction:

Reduced 12-month mortality from 71 % 71\% 71% to 22 % 22\% 22% (absolute risk reduction about 50 % 50\% 50% ; NNT \text{NNT} NNT about 2).

Doubled the proportion of patients surviving with moderate disability or better ( mRS ≤ 3 \text{mRS} \le 3 mRS ≤ 3 : 43 % 43\% 43% vs. 21 % 21\% 21% ).

Spontaneous Intracerebral Hemorrhage (ICH)

Spontaneous non-traumatic intracerebral hemorrhage (ICH) accounts for 15 − 20 % 15-20\% 15 − 20% of all strokes and carries a 30-day mortality approaching 40 % 40\% 40% . Primary etiologies include chronic hypertensive lipohyalinosis of small penetrating arterioles (deep locations: putamen, caudate, thalamus, pons, cerebellum) and cerebral amyloid angiopathy (lobar locations in elderly patients). Hematoma expansion occurs in 30 − 40 % 30-40\% 30 − 40% of patients within the first 6 hours and is the most potent predictor of neurological deterioration and death.

1. Acute Blood Pressure Lowering: INTERACT-2 & ATACH-2

Acute hypertension in ICH drives active ongoing bleeding and hematoma expansion. However, excessive blood pressure lowering risks renal hypoperfusion and cerebral ischemia.

INTERACT-2 Trial (NEJM 2013) : Randomized 2,839 patients with spontaneous ICH within 6 hours to intensive SBP lowering ( < 140 mmHg <140\text{ mmHg} < 140 mmHg within 1 hour) vs. standard guideline care ( < 180 mmHg <180\text{ mmHg} < 180 mmHg ). Intensive lowering demonstrated a borderline reduction in functional disability (modified Rankin Scale) and confirmed safety without excess adverse events.

ATACH-2 Trial (NEJM 2016) : Evaluated intensive lowering (target SBP 110 − 139 mmHg \text{SBP}\ 110-139\text{ mmHg} SBP 110 − 139 mmHg ) vs. standard lowering (target SBP 140 − 179 mmHg \text{SBP}\ 140-179\text{ mmHg} SBP 140 − 179 mmHg ) using IV nicardipine. ATACH-2 found no improvement in 90-day mortality or severe disability with aggressive reduction to < 130 mmHg <130\text{ mmHg} < 130 mmHg , but observed a statistically significant increase in acute renal adverse events within 7 days ( 9.0 % 9.0\% 9.0% vs. 4.0 % 4.0\% 4.0% ).

Current Guideline Consensus : Rapidly lower blood pressure targeting a systolic BP of 130 − 150 mmHg 130 - 150\text{ mmHg} 130 − 150 mmHg using continuous, smooth intravenous titrations (IV nicardipine or clevidipine), while strictly avoiding large blood pressure variability and avoiding sustained SBP < 130 mmHg <130\text{ mmHg} < 130 mmHg .

2. Emergency Coagulopathy Reversal Protocols

Immediate pharmacological reversal of coagulopathy is the highest-priority intervention in acute ICH to arrest hematoma expansion:

Anticoagulant Agent Mechanism / Laboratory Marker First-Line Reversal Regimen Clinical Notes & Pitfalls

Warfarin (VKA) Vitamin K epoxide reductase inhibitor; INR > 1.4 \text{INR} > 1.4 INR > 1.4 4-Factor PCC ( 25 − 50 units/kg 25-50\text{ units/kg} 25 − 50 units/kg IV); PLUS Vitamin K ( 10 mg 10\text{ mg} 10 mg slow IV push) 4F-PCC (Kcentra) normalizes INR within 15-30 min. Vitamin K sustains factor production. FFP is inferior (causes volume overload, delayed correction).

Dabigatran Direct thrombin (Factor IIa) inhibitor; prolonged aPTT / TT Idarucizumab ( 5 g 5\text{ g} 5 g IV administered as two 2.5 g 2.5\text{ g} 2.5 g boluses 15 min apart) Humanized Fab fragment; neutralizes dabigatran within minutes. If unavailable, give 4F-PCC ( 50 units/kg 50\text{ units/kg} 50 units/kg ) or hemodialysis.

Apixaban / Rivaroxaban / Edoxaban Direct Factor Xa inhibitors; anti-Xa activity 4F-PCC ( 50 units/kg 50\text{ units/kg} 50 units/kg IV) Andexanet alfa was withdrawn from the US market effective December 22, 2025, after ANNEXA-I showed more thrombotic events (14.6% vs. 6.9%); it remains available in some other countries. Activated charcoal helps if the last dose was within about 2 hours.

Unfractionated Heparin (UFH) Antithrombin activator; prolonged aPTT Protamine sulfate ( 1 mg 1\text{ mg} 1 mg per 100 units 100\text{ units} 100 units heparin given in past 2-3h; max 50 mg 50\text{ mg} 50 mg ) Infuse slowly ( < 5 mg/min <5\text{ mg/min} < 5 mg/min ) to avoid severe anaphylactoid hypotension and bradycardia.

Enoxaparin (LMWH) Antithrombin activator (anti-Xa > anti-IIa) Protamine sulfate ( 1 mg 1\text{ mg} 1 mg per 1 mg 1\text{ mg} 1 mg enoxaparin if < 8 h <8\text{ h} < 8 h ; 0.5 mg 0.5\text{ mg} 0.5 mg per 1 mg 1\text{ mg} 1 mg if 8 − 12 h 8-12\text{ h} 8 − 12 h ) Reverses anti-IIa activity completely, but neutralizes only ~60% of anti-Xa activity.

3. Surgical Indications in ICH

Cerebellar Hemorrhage : Cerebellar hemorrhage with neurological deterioration, brainstem compression, or obstructive hydrocephalus, or a volume of at least 15 mL 15\text{ mL} 15 mL (older series used a diameter above 3 cm 3\text{ cm} 3 cm ), warrants urgent suboccipital decompression with hematoma evacuation (2022 AHA/ASA ICH guideline), with or without an external ventricular drain (EVD). An EVD alone, instead of decompression, is not recommended because of the risk of deterioration and upward herniation.

Supratentorial Lobar / Deep ICH : The STICH I and STICH II trials demonstrated no benefit for routine early open craniotomy in supratentorial deep ganglionic or lobar hemorrhages. However, minimally invasive surgery (MIS) utilizing stereotactic catheter or endoscopic evacuation (the ENRICH trial , 2024: minimally invasive parafascicular evacuation of 30 to 80 mL lobar or anterior basal ganglia hemorrhages within 24 hours) improved 180-day utility-weighted functional outcome, with the benefit driven by lobar hemorrhages.

Aneurysmal Subarachnoid Hemorrhage (aSAH)

Aneurysmal subarachnoid hemorrhage (aSAH) accounts for 5 − 10 % 5-10\% 5 − 10% of all strokes, characteristically presenting as the sudden onset of the "worst headache of life" ( thunderclap headache ), accompanied by transient loss of consciousness, nausea, vomiting, photophobia, and meningismus.

1. Diagnostic Algorithm and Early Securing

Non-Contrast Head CT : Exhibits > 99 % >99\% > 99% sensitivity within the first 6 hours of headache onset. Sensitivity progressively declines to ∼ 85 % \sim 85\% ∼ 85% at 48 hours and ∼ 50 % \sim 50\% ∼ 50% at 1 week as blood mixes with cerebrospinal fluid.

Lumbar Puncture (LP) : Mandatory if non-contrast head CT is negative or equivocal but high clinical suspicion persists. Diagnostic hallmark is xanthochromia (pink or yellow supernatant coloration resulting from enzymatic breakdown of hemoglobin to oxyhemoglobin and bilirubin), confirmed by spectrophotometry. Differentiated from a traumatic tap by absence of clearing between tubes 1 and 4 and presence of xanthochromia after centrifugation.

Early Aneurysm Securing : The ruptured aneurysm must be secured via endovascular coiling or microsurgical clipping as early as feasible, preferably within 24 hours 24\text{ hours} 24 hours (2023 AHA/ASA, Class 1). Catastrophic rebleeding occurs in up to 15 % 15\% 15% of patients within the first 24 hours and carries a mortality rate exceeding 70 % 70\% 70% . Before securing, control blood pressure with short-acting titratable IV agents, avoiding hypotension, severe hypertension, and large swings; the 2023 guideline found insufficient evidence for a specific target (SBP below 160 mmHg 160\text{ mmHg} 160 mmHg is a common pragmatic choice). Antifibrinolytic therapy (tranexamic acid) is not useful for improving outcome (ULTRA trial).

2. Delayed Cerebral Ischemia (DCI) and Vasospasm

Delayed Cerebral Ischemia (DCI) —defined as new focal neurological deficits (hemiparesis, aphasia, neglect) or a sustained decrease in GCS score ≥ 2 \ge 2 ≥ 2 points lasting > 1 hour >1\text{ hour} > 1 hour not explained by hydrocephalus, rebleeding, or metabolic derangement—represents the leading cause of late morbidity and mortality following aSAH.

Temporal Profile : Arterial narrowing (angiographic vasospasm) typically commences on post-bleed day 3 to 4 , reaches peak incidence between days 4 and 14 , and gradually resolves by day 21 .

Enteral Nimodipine : Every patient with aSAH must receive oral/nasogastric Nimodipine 60 mg 60\text{ mg} 60 mg enterally every 4 hours for 21 consecutive days . Nimodipine is a dihydropyridine calcium channel blocker that prevents DCI and dramatically improves functional neurological outcomes.

Caution

FDA Boxed Warning: Nimodipine must NEVER be administered intravenously. Accidental intravenous administration of enteral nimodipine capsules causes profound systemic vasodilation, refractory shock, cardiovascular collapse, and death.

Euvolemia over Prophylactic Hypervolemia : The outdated "triple-H therapy" (hypervolemia, hemodilution, hypertension) has been definitively abandoned. Prophylactic hypervolemia does not prevent DCI and precipitates iatrogenic pulmonary edema, myocardial strain, hyponatremia, and cerebral edema. Patients must be maintained in strict euvolemia utilizing isotonic crystalloids ( 0.9 % 0.9\% 0.9% normal saline).

Management of Clinical DCI :

Induced Hypertension : First-line rescue intervention for secured aneurysms. Titrate continuous IV vasopressors ( norepinephrine or phenylephrine ) to raise blood pressure stepwise while reassessing the neurological examination. The 2023 guideline states that elevating blood pressure in symptomatic vasospasm can reduce progression and severity of DCI; protocols vary and no single target is established. Prophylactic hemodynamic augmentation is not recommended.

Endovascular Rescue Therapy : If clinical DCI fails to improve promptly with induced hypertension, emergent catheter angiography is performed. Endovascular intra-arterial infusion of microvascular vasodilators ( nicardipine, verapamil, milrinone ) or transluminal balloon angioplasty (for proximal, focal vessel spasm) rapidly restores cerebral perfusion.

Clinical Entity Primary Diagnostic Modality Acute Blood Pressure Target Key Acute Reperfusion / Decompression Strategy

Acute Ischemic Stroke (AIS) NCCT + CTA (CTP / DWI if extended window) < 185 / 110 mmHg <185/110\text{ mmHg} < 185/110 mmHg pre-lytic; < 180 / 105 mmHg <180/105\text{ mmHg} < 180/105 mmHg post-lytic; < 220 / 120 mmHg <220/120\text{ mmHg} < 220/120 mmHg if non-reperfused IV Tenecteplase/Alteplase ≤ 4.5 h \le 4.5\text{ h} ≤ 4.5 h ; EVT ≤ 24 h \le 24\text{ h} ≤ 24 h (DAWN/DEFUSE-3); Decompressive hemicraniectomy ≤ 48 h \le 48\text{ h} ≤ 48 h for malignant MCA

Intracerebral Hemorrhage (ICH) Non-contrast head CT SBP 130 − 150 mmHg 130 - 150\text{ mmHg} 130 − 150 mmHg (INTERACT-2 / ATACH-2) Immediate coagulopathy reversal (4F-PCC + Vit K, idarucizumab, 4F-PCC for FXa inhibitors); suboccipital decompression for deteriorating or ≥ 15 mL \ge 15\text{ mL} ≥ 15 mL cerebellar ICH

Aneurysmal SAH (aSAH) NCCT ≤ 6 h \le 6\text{ h} ≤ 6 h ; LP for xanthochromia if CT negative Avoid hypotension and severe hypertension before securing (no proven target); BP augmentation for DCI Aneurysm coiling/clipping, preferably ≤ 24 h \le 24\text{ h} ≤ 24 h ; Enteral Nimodipine 60 mg 60\text{ mg} 60 mg q4h × 21 d \times 21\text{ d} × 21 d (NEVER IV); Euvolemia; Induced hypertension for DCI