Study guide
20.1 Intracerebral Hematoma (03.D.1)
ABIM Neurocritical Care Subspecialty Certification Exam
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1 Introduction & Exam Overview
1.1 Current Exam Facts 1.2 Eligibility, Practice Pathway, and the IM Training Route 1.3 Format, Scoring, Pearson VUE, and Score Reports 1.4 How to Use This Independent Study Guide
2 ICU Neurologic Exam, Cerebral Physiology, and CSF
2.1 Neurological Examination in the ICU 2.2 Cerebral Physiology, ICP, CBF, and Autoregulation 2.3 CSF Physiology
3 Core Neuropharmacology
3.1 Osmotic Agents 3.2 Anti-Seizure Drugs 3.3 Anesthetics, Sedatives, Analgesia, and Paralytics 3.4 Antihypertensives, Vasopressors, and Inotropes
4 Reperfusion Drugs, Airway, and Ventilation
4.1 Thrombolytics, Anticoagulants, and Antiplatelets 4.2 Reversal of Anticoagulation After Acute Hemorrhage 4.3 Airway Management and Tracheostomy 4.4 Mechanical Ventilation
5 Hemodynamics and Shock
5.1 Hemodynamic Monitoring 5.2 IABP, Temporary VADs, LVAD, and ECMO 5.3 Diagnosis and Management of Shock
6 Nutrition, Temperature, and ICU Prophylaxis
6.1 Nutrition (01.J) 6.2 Temperature Control (01.K) 6.3 ICU Prophylaxis, Delirium, and Early Mobility (01.L)
7 General Trauma
7.1 Emergency Evaluation of Polytrauma, Chest, and Abdominal Trauma 7.2 Long-Bone Fractures and Fat Embolism 7.3 Burns, Electrical Injury, and Hanging/Strangulation
8 Pulmonary Critical Care
8.1 Pulmonary Physiology and ARDS (01.N.1–2) 8.2 PE, Pneumonia, and Pulmonary Edema (01.N.3, 7–8) 8.3 COPD, Asthma, PAH, and Bronchoscopy Basics (01.N.4–6, 9)
9 Cardiovascular Critical Care
9.1 Cardiovascular Physiology, Stress Cardiomyopathy, ACS, and Valves 9.2 Arrhythmias and Pacing 9.3 Acute Aortic Dissection and Cardiac Ultrasound
10 Renal and Infectious Disease
10.1 AKI, RRT, and Renal Drug Dosing 10.2 Acid-Base and Electrolyte Disorders 10.3 Severe Sepsis, Septic Shock, and Infective Endocarditis 10.4 Antimicrobial Use and Infection in the Immunosuppressed
11 Endocrine and Salt-Water Disorders
11.1 Pituitary Apoplexy, DI, and Panhypopituitarism (01.R.1–4) 11.2 SIADH and Cerebral Salt Wasting (01.R.5–6) 11.3 Thyrotoxicosis, Myxedema, Adrenal Crisis, and Dysglycemia (01.R.7–9)
12 Gastrointestinal Critical Care
12.1 GI Physiology, Acute Abdomen, Bleed, Ileus, and Perforation (01.S.1–5) 12.2 Mesenteric Ischemia and Abdominal Compartment Syndrome (01.S.6–7) 12.3 Fulminant Liver Failure, Cirrhosis Decompensation, and Hepatic Dosing (01.S.8–10)
13 Hematologic Disorders
13.1 Anemia, Transfusion, Thrombocytopenia, Coagulopathy, and DIC (01.T.1–4) 13.2 VTE in the Neuro ICU (01.T.5) 13.3 Chemo/Immune, SCT, CAR-T, Sickle Cell, and TMA (01.T.6–10)
14 Neuroimaging
14.1 CT of Brain and Spine 14.2 MRI and CT/MR Perfusion 14.3 Noninvasive Angiography and Catheter Angiography
15 EEG, EMG, and CSF Analysis
15.1 EEG, Standard and Processed (02.B) 15.2 Basic EMG Interpretation (02.G) 15.3 CSF Analysis (02.H)
16 ICP, TCD, and Multimodality Monitoring
16.1 ICP Monitoring (02.C) 16.2 Transcranial Doppler (02.D) 16.3 Brain-Tissue Oxygen and Multimodality Monitoring (02.E–F)
17 Brain Death and Bedside Procedures
17.1 Brain Death Prerequisites and Clinical Exam (02.I) 17.2 Apnea Testing and Ancillary Studies (02.I) 17.3 Vascular Access, Thoracic Echo, and Lung Ultrasound (02.J–L)
18 Coma, Anoxia, and Intracranial Hypertension
18.1 Coma and Other States of Altered Consciousness (03.A) 18.2 Global Anoxia-Ischemia and Post-Resuscitation Encephalopathy (03.A.1) 18.3 Toxidromes, ICU Delirium, and Hypertensive Encephalopathy (03.A.2–4) 18.4 Intracranial Hypertension as a Disease State (03.B)
19 Acute Ischemic Stroke
19.1 IV Reperfusion Therapy (03.C.3) 19.2 Mechanical Thrombectomy Windows and Imaging Selection (03.C.3) 19.3 Malignant Hemispheric Infarction and Basilar Artery Occlusion (03.C.1–2)
20 Intraparenchymal Hemorrhage
20.1 Intracerebral Hematoma (03.D.1) 20.2 Cerebellar Hematoma (03.D.2) 20.3 Intraventricular Hemorrhage (03.D.3)
21 SAH, CVST, and Spinal Cord Infarction
21.1 Aneurysmal Subarachnoid Hemorrhage (03.E.1) 21.2 Non-Aneurysmal SAH (03.E.2) 21.3 Cerebral Venous Sinus Thrombosis (03.F) 21.4 Spinal Cord Infarction (03.G)
22 Vascular Anomalies and Traumatic Brain Injury
22.1 Unruptured Aneurysm, Cavernoma, AVM, and Dural AVF (03.H) 22.2 Diffuse Axonal Injury and Cerebral Contusions (03.I.1–2) 22.3 Epidural Hematoma, Subdural Hematoma, and Penetrating Injury (03.I.3–4, 7) 22.4 Arterial Dissection and Carotid-Cavernous Fistula (03.I.5–6)
23 Spine, Hydrocephalus, and CNS Infection
23.1 Spinal Cord Injury, Central Cord, and Neurogenic Shock (03.J) 23.2 Unstable Spine Fractures (03.K) 23.3 Hydrocephalus and CSF Diversion (03.L) 23.4 Acute CNS Infections (03.M)
24 Seizures and Neuromuscular Emergencies
24.1 Status Epilepticus and Seizures (03.N) 24.2 Guillain-Barré Syndrome (03.O.1) 24.3 Myasthenic Crisis (03.O.2) 24.4 Motor Neuron Disease, Acute Myopathies, Rhabdomyolysis, and CINM (03.O.3–6)
25 Inflammatory Disease, Neuro-Oncology, and Special Populations
25.1 Fulminant Demyelinating Diseases (03.P) 25.2 Autoimmune Encephalitis and Acute Autonomic Hyperactivity (03.Q–R) 25.3 Neuro-Oncology and Treatment Complications (03.S) 25.4 Pregnancy/Post-Partum, Post-Transplant, and Pediatric Patients (03.T–U)
26 Neurosurgical and Perioperative Complications
26.1 Postoperative Seizures, Hemorrhage, Ischemia, and Hyperperfusion (04.A, C, D, H) 26.2 Infection, CSF Leak, and Pneumocephalus (04.B, E, F) 26.3 Complications of EVD and Lumbar Drain (04.G, I)
27 Ethics, Prognostication, and Organ Donation
27.1 Communication, Decision-Makers, Advance Directives, and DNR (05.A, B, G) 27.2 Uncertainties of Prognostication and the Self-Fulfilling Prophecy (05.C) 27.3 Palliative Care, Withdrawal, Withholding, and Futility (05.D–F) 27.4 Donation After Cardiac Death and Care of the Organ Donor (05.H–I)
20.1 Intracerebral Hematoma (03.D.1)
Key Takeaways Explain This Topic AI
The ICH score (Glasgow Coma Scale, hematoma volume of 30 mL or more, intraventricular blood, infratentorial origin, age 80 years or older) estimates 30-day mortality and must not be used as a reason to withhold reversible care.
For typical mild-to-moderate ICH with systolic pressure 150–220 mm Hg, the 2022 AHA/ASA spontaneous ICH guideline supports lowering toward 140 mm Hg (about 130–140) while avoiding overshoot into the 110–120 mm Hg range used in ATACH-2.
INTERACT3’s 7-day care bundle—systolic pressure under 140 mm Hg, protocolized glucose and fever control, and anticoagulation reversal—improved ordinal modified Rankin Scale outcome versus usual care.
Warfarin ICH is reversed with 4-factor prothrombin complex concentrate plus intravenous vitamin K; dabigatran with idarucizumab; factor Xa inhibitors with andexanet, which in ANNEXA-I (NEJM 2024) improved hematoma control at the cost of more thrombosis.
STICH and STICH II do not support routine early open evacuation of lobar ICH; ENRICH supports early minimally invasive evacuation in selected lobar hematomas of 30–80 mL.
Last updated: September 2026
Spontaneous intracerebral hemorrhage (ICH) —bleeding into brain parenchyma—causes about 10–15% of strokes and a much larger share of stroke deaths. Thirty-day case fatality is often near 40%, and only about one in five survivors is independent at six months. Blueprint item 03.D.1 asks you to localize the clot, estimate volume, apply the ICH score conceptually, stop hematoma expansion, reverse coagulopathy, and know when hemispheric surgery helps—and when trial evidence says it does not.
Deep hypertensive versus lobar disease
Classic hypertensive ICH ruptures small penetrating arteries damaged by lipohyalinosis in deep gray matter: putamen, caudate, thalamus, pons, and the cerebellar dentate nucleus. Cerebral amyloid angiopathy (CAA) produces lobar, often cortical–subcortical, hematomas in older adults and may be accompanied by convexity subarachnoid blood or cortical superficial siderosis. Younger patients, isolated lobar bleeds without chronic hypertension, or atypical locations need a vascular search (CTA or MRA, then catheter angiography when noninvasive studies are inconclusive) because arteriovenous malformation, aneurysm, dural fistula, or cerebral venous thrombosis changes both the operation and the reversal plan. Anticoagulant-associated ICH can occupy any territory and expands more often than hypertensive deep bleeds of the same size.
Noncontrast head CT is the first test. Volume is estimated with the ABC/2 ellipsoid method: A is the largest axial diameter, B the perpendicular diameter on the same slice, and C the number of slices that contain hematoma multiplied by slice thickness in centimeters. ABC/2 is accurate enough for triage and ICH scoring; it can overestimate irregular or anticoagulant clots. Most hematoma expansion occurs in the first 3–6 hours and becomes uncommon after 24 hours, which is why the first hours of blood-pressure control and reversal actually change anatomy.
ICH score, used conceptually
The original ICH score (Hemphill and colleagues, Stroke 2001) is a 0–6 integer built from five admission findings. It estimates 30-day mortality in the derivation cohort. It is not a mandate to withdraw care. Early do-not-resuscitate orders create a self-fulfilling prophecy that inflates predicted death, especially at intermediate scores.
- Component 0 points 1 point 2 points
- Glasgow Coma Scale 13–15 5–12 3–4
- Hematoma volume <30 mL ≥30 mL —
- Intraventricular blood Absent Present —
- Origin Supratentorial Infratentorial —
- Age <80 years ≥80 years —
In the original cohort, 30-day mortality rose from 0% at score 0 to 13%, 26%, 72%, and 97% at scores 1–4, with scores 5–6 near 100%. Later series often show lower mortality at scores 3–4 because intensive care improved. Use the integer to communicate severity and to risk-stratify, not to skip a reversible coagulopathy or a cerebellar decompression.
Worked example: an 82-year-old with GCS 10, a 40 mL putaminal hematoma, and IVH scores 1 (age) + 1 (GCS 5–12) + 1 (volume) + 1 (IVH) + 0 (supratentorial) = 4 . That is a high predicted mortality—and still not a reason to withhold nicardipine or 4-factor PCC.
CTA spot sign
The spot sign is one or more punctate foci of contrast within the hematoma on CTA, representing active extravasation. Pooled series show moderate sensitivity (about 62%) and high specificity (about 88%) for later growth, with expansion in more than half of spot-positive scans versus about 10% of spot-negative scans. A positive spot sign should speed reversal, tighten blood-pressure control, and prompt an early stability CT. It is not , by itself, an indication for craniotomy.
Blood pressure: INTERACT2, ATACH-2, and the 2022 AHA/ASA ICH guideline
Higher presenting systolic pressure tracks with expansion. INTERACT2 (Anderson et al., NEJM 2013; 2,839 patients within 6 hours) compared intensive lowering to systolic <140 mm Hg within 1 hour versus a then-usual target <180 mm Hg . Death or major disability (modified Rankin Scale 3–6) at 90 days was 52.0% versus 55.6% (odds ratio 0.87, 95% CI 0.75–1.01, p = 0.06 )—not significant on the primary endpoint. An ordinal analysis of the full Rankin scale suggested a modest shift toward better function (p = 0.04). Achieved minima in the intensive arm clustered near 150 mm Hg , not 120.
ATACH-2 (Qureshi et al., NEJM 2016; 1,000 patients) pushed further with intravenous nicardipine to 110–139 mm Hg versus 140–179 mm Hg . Death or disability (mRS 4–6) at 3 months was 38.7% versus 37.7% (no benefit). Renal adverse events within 7 days were 9.0% versus 4.0% . Mean minimum systolic pressure in the intensive arm was about 129 mm Hg. The practical harm is overshoot : driving systolic pressure into the 110–120 mm Hg band (ATACH-2’s intensive floor) trades expansion risk for hypoperfusion and kidney injury without improving disability.
The 2022 AHA/ASA spontaneous ICH guideline (Greenberg et al., Stroke 2022) synthesizes those trials for typical mild-to-moderate ICH with presenting systolic pressure 150–220 mm Hg: start treatment promptly (ideally within 2 hours), lower toward 140 mm Hg , keep systolic pressure about 130–140 mm Hg with smooth, low-variability control, and treat lowering <130 mm Hg as potentially harmful. For presenting systolic pressure >220 mm Hg , more gradual reduction is reasonable; those patients were under-represented in INTERACT2. Use a titratable intravenous agent (nicardipine or clevidipine are common) rather than intermittent boluses that sawtooth the tracing.
INTERACT3 care bundle
INTERACT3 (Ma et al., Lancet 2023; 7,036 patients, stepped-wedge cluster design) tested a 7-day care bundle , not blood pressure in isolation:
Systolic <140 mm Hg within 1 hour of starting treatment, with 130 mm Hg as the stop threshold.
Glucose 6.1–7.8 mmol/L (110–140 mg/dL) without diabetes and 7.8–10.0 mmol/L (140–180 mg/dL) with diabetes.
Temperature <37.5 °C within 1 hour.
Warfarin reversal to INR <1.5 within 1 hour using prothrombin complex concentrate or plasma.
The bundle produced a favorable ordinal mRS shift (odds ratio 0.86, p = 0.015) versus usual care. Teach it as coordinated ICU hygiene plus blood pressure—not as a license to overshoot systolic pressure below 130 mm Hg.
Reverse anticoagulants at the ICH bedside
Reversal pharmacology is covered in depth in Chapter 4 (Reversal of Anticoagulation After Acute Hemorrhage). The hematoma exam still requires you to pick the correct agent immediately, without waiting for every laboratory result when the exposure is known.
Exposure Immediate reversal Exam-relevant detail
Warfarin 4-factor PCC plus intravenous vitamin K (typically 10 mg) Do not wait for a repeat INR to start. Typical labeled 4F-PCC dosing is about 25 IU/kg for INR 2–<4, 35 IU/kg for INR 4–6, and 50 IU/kg for INR >6, with product-specific caps. PCC is preferred over plasma for speed and volume.
Dabigatran Idarucizumab 5 g IV (two 2.5 g vials) Specific monoclonal fragment (RE-VERSE AD). PCC is a fallback only if idarucizumab is unavailable.
Apixaban, rivaroxaban, edoxaban Andexanet alfa (low versus high dose by last factor Xa amount and timing) ANNEXA-I (Connolly et al., NEJM 2024; 390:1745–1755): hemostatic efficacy 67.0% versus 53.1% usual care (mostly PCC), adjusted difference 13.4 points, p = 0.003. Thrombotic events 10.3% versus 5.6%, including ischemic stroke 6.5% versus 1.5%. Hematoma control improved; 30-day function was not clearly better.
Unfractionated heparin Protamine Dose to heparin still circulating.
PATCH showed that platelet transfusion worsens outcome in antiplatelet-associated ICH outside emergency surgery or severe thrombocytopenia—do not “cover” aspirin with a unit of platelets. Tranexamic acid ( TICH-2 ) reduced expansion slightly without a functional-outcome win and is not standard ICH rescue.
Surgery for hemispheric ICH: STICH, STICH II, and ENRICH
STICH (Mendelow et al., Lancet 2005; 1,033 patients) compared early surgery with initial conservative care for spontaneous supratentorial ICH when the surgeon was uncertain. Favorable 6-month outcome was 26% versus 24% (odds ratio 0.89, p = 0.414). STICH II ( Lancet 2013; 601 patients) restricted enrollment to lobar clots 10–100 mL within 1 cm of the cortex and without IVH . Early evacuation within 12 hours of randomization produced a favorable outcome in 41% versus 38% (odds ratio 0.86, p = 0.367)—still not a significant primary-endpoint win. Mortality trended lower (18% versus 24%). Exam translation: routine early open evacuation of lobar ICH is not generally beneficial.
MISTIE III used stereotactic catheter drainage plus alteplase for large intraparenchymal clots; the primary functional endpoint was not met, although residual volume of 15 mL or less associated with better outcomes in secondary analyses. That catheter-plus-thrombolytic approach is not the same operation as ENRICH.
ENRICH (Pradilla et al., NEJM 2024) tested early minimally invasive parafascicular surgery (imaging-guided trans-sulcal corridor with a tubular retractor and automated resection device) within 24 hours plus medical care versus medical care alone in 300 patients with 30–80 mL spontaneous ICH. Mean utility-weighted mRS at 180 days was 0.458 versus 0.374 (posterior probability of superiority 0.981). The benefit was in lobar hemorrhage (between-group difference 0.127). Enrollment of anterior basal ganglia hemorrhages was stopped for futility (difference −0.013). Thirty-day death was 9.3% versus 18.0%. Mention ENRICH for selected lobar ICH in that volume window at centers that perform the procedure. Do not generalize it to routine craniotomy for deep ICH, and do not treat it as a reversal of STICH/STICH II for open surgery.
Glucose, VTE, and seizures—what is not routine
Treat hyperglycemia and avoid insulin-induced hypoglycemia; INTERACT3’s stratified glucose targets are a practical bundle rather than a license for intensive insulin. For venous thromboembolism , start intermittent pneumatic compression on admission in non-ambulatory patients (CLOTS 3 logic; 2022 AHA/ASA Class 1). Pharmacologic prophylaxis with low-molecular-weight or unfractionated heparin is reasonable 24–48 hours after onset once a stability scan shows no important expansion. Graduated compression stockings alone do not prevent DVT. Seizure prophylaxis is not routine , including for lobar ICH without a clinical or electrographic seizure. Treat witnessed seizures. Continuous EEG is reasonable when consciousness is unexplained or events might be nonconvulsive. Prophylactic corticosteroids and standing hyperosmolar therapy do not improve ICH outcome.
Exam traps: mixing the ischemic-stroke lytic ceiling (185/110 mm Hg) with ICH targets; treating ATACH-2’s 110–139 mm Hg arm as “more is better”; quoting STICH II as a positive surgical trial; transfusing platelets for aspirin-associated ICH; starting levetiracetam on every lobar bleed “because CAA seizes.”