Study guide
21.1 Aneurysmal Subarachnoid Hemorrhage (03.E.1)
ABIM Neurocritical Care Subspecialty Certification Exam
Track your progress as you read
Finished sections get a check mark.
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)
21.1 Aneurysmal Subarachnoid Hemorrhage (03.E.1)
Key Takeaways Explain This Topic AI
The 2023 AHA/ASA aSAH guideline recommends early enteral nimodipine for all aneurysmal SAH; the practical regimen remains 60 mg by mouth or feeding tube every 4 hours for 21 days, split to 30 mg every 2 hours if hypotension appears.
Secure the ruptured aneurysm as early as feasible, preferably within 24 hours. For good-grade anterior-circulation aneurysms equally suitable for coiling and clipping, ISAT and AHA/ASA 2023 prefer primary coiling to improve 1-year functional outcome.
Maintain euvolemia. Induced hypertension is for symptomatic delayed cerebral ischemia; prophylactic hypervolemia and classic triple-H therapy are not used.
Hunt-Hess and WFNS grade clinical severity; the modified Fisher scale grades cisternal blood and IVH to estimate vasospasm risk. DCI typically appears on days 4–14.
Urgent EVD (or lumbar drainage when anatomy allows) treats acute symptomatic hydrocephalus. Hyponatremia is often cerebral salt wasting; do not fluid-restrict an aSAH patient the way textbook SIADH is treated.
Last updated: September 2026
Aneurysmal subarachnoid hemorrhage ( aSAH ) is the classic thunderclap catastrophe of the neuro ICU: a saccular aneurysm ruptures into the basal cisterns, intracranial pressure spikes, and the patient either dies before arrival or enters a two-week window of rebleeding, hydrocephalus, and delayed ischemia. This topic is heavily tested because the decisions are time-stamped and easy to mix up with older dogma. Independent ExamFinch material for ABIM Neurocritical Care candidates should treat aSAH as a sequence: confirm blood, grade the patient, find and secure the aneurysm, start nimodipine, keep the patient euvolemic, drain symptomatic hydrocephalus, then hunt for delayed cerebral ischemia ( DCI ) from day 4 through day 14.
The 2023 American Heart Association/American Stroke Association (AHA/ASA) guideline (Hoh BL et al., Stroke 2023;54:e314–e370) replaced the 2012 document. It does not invent a new disease, but it does retire several habits still lingering on boards: routine antifibrinolytics, prophylactic hypervolemia, routine statins, and intravenous magnesium as DCI prophylaxis. Cite the guideline as a source of recommendations. This is independent ExamFinch teaching, not an official AHA or ABIM product.
Why the first 24 hours decide survival
Rebleeding is the early killer. Risk is highest in the first 24 hours after the sentinel bleed. The 2023 guideline states that surgical or endovascular treatment of the ruptured aneurysm should be performed as early as feasible, preferably within 24 hours of onset , with the goal of complete obliteration whenever that is technically possible. Partial coiling of the rupture site is a temporizing option only when complete obliteration cannot be achieved acutely in a salvageable patient.
Until the aneurysm is secured, avoid wild blood-pressure swings. AHA/ASA 2023 does not lock a single systolic target as a Class 1 number. Supportive text recommends gradual reduction when patients are severely hypertensive (systolic values in the 180–200 mm Hg range), strict avoidance of hypotension ( mean arterial pressure below 65 mm Hg ), and short-acting intravenous agents so you can reverse overshoot. Observational series still associate rebleeding with systolic pressure above 160 mm Hg , which is why many ICUs continue to use an unsecured-aneurysm systolic ceiling near 160 mm Hg while watching the neurologic exam. After the aneurysm is secured, that ceiling comes off so you can raise pressure if DCI appears.
Routine antifibrinolytic therapy (tranexamic acid or aminocaproic acid) is not useful for improving functional outcome (Class 3: No Benefit, Level A in the 2023 document). Reverse anticoagulants immediately. Nicardipine or labetalol infusions are typical pre-secure antihypertensives; avoid long-acting agents that will trap you when vasospasm later demands hypertension.
Clinical grading: Hunt-Hess and WFNS
AHA/ASA 2023 recommends a clinical scale at presentation to describe severity and frame prognosis. Two scales dominate test questions. Hunt-Hess is a bedside clinical grade. World Federation of Neurosurgical Societies (WFNS) grade is built from the Glasgow Coma Scale (GCS) plus the presence or absence of a motor deficit. High-grade aSAH (Hunt-Hess 4–5 or WFNS 4–5) does not automatically mean comfort care: aneurysm treatment is still reasonable after a frank discussion of likely outcome, including in older adults.
- Hunt-Hess grade Typical bedside picture
- 1 Asymptomatic, mild headache, or slight nuchal rigidity
- 2 Moderate-to-severe headache, nuchal rigidity; cranial-nerve palsy allowed, no other deficit
- 3 Drowsiness, confusion, or a mild focal deficit
- 4 Stupor, moderate-to-severe hemiparesis, early decerebrate posturing
- 5 Deep coma, decerebrate rigidity, moribund appearance
- WFNS grade GCS Motor deficit
- I 15 None
- II 13–14 None
- III 13–14 Present
- IV 7–12 With or without
- V 3–6 With or without
A patient who is GCS 14 with a hemiparesis is WFNS III, not II. A patient who is GCS 15 with an isolated third-nerve palsy from a posterior communicating artery aneurysm is still Hunt-Hess 2 and WFNS I. Those distinctions show up as one-best-answer traps.
Modified Fisher: blood burden and vasospasm risk
Clinical grade predicts death and disability. Modified Fisher (mFS) grade predicts radiographic vasospasm and, imperfectly, DCI. Thick cisternal clot and intraventricular hemorrhage ( IVH ) raise risk. The scale used at the bedside (Frontera and colleagues, building on Claassen) is:
- Modified Fisher CT pattern Approximate symptomatic vasospasm rate
- 0 No SAH or IVH Negligible
- 1 Thin SAH, no IVH ~24%
- 2 Thin SAH plus IVH ~33%
- 3 Thick SAH, no IVH ~33%
- 4 Thick SAH plus IVH ~40%
Thick is generally clot filling a cistern or fissure (historically >1 mm). Thin is a film that does not fill the cistern. Original Fisher grade 4 (ICH or IVH without thick cisternal blood) was paradoxically lower-risk than Fisher 3; modified Fisher fixes that by giving thick blood plus IVH its own high-risk bin. Do not confuse mFS with Hunt-Hess: a wide-awake patient can still be mFS 4 and needs aggressive DCI surveillance.
Securing the aneurysm: ISAT and anatomy
The International Subarachnoid Aneurysm Trial ( ISAT , Lancet 2002) randomized 2,143 patients whose ruptured aneurysms were judged suitable for both coiling and clipping. Death or dependence at 1 year was 23.7% after coiling versus 30.6% after clipping (absolute risk reduction about 7 percentage points). The ISAT population was mostly good-grade, small, anterior-circulation aneurysms. That is the evidence AHA/ASA 2023 uses when it gives Class 1, Level A preference to primary coiling for good-grade anterior-circulation aneurysms equally suitable for both treatments.
Other 2023 modality rules worth memorizing:
Posterior-circulation aneurysms amenable to coiling: coiling in preference to clipping (Class 1).
Large intraparenchymal hematoma with a depressed exam in a salvageable patient: emergency clot evacuation (Class 1).
Age under 40 years: clipping might be considered for durability (Class 2b).
Age over 70 years: superiority of coiling versus clipping is not well established (Class 2b).
Specialists with both endovascular and open expertise should choose the modality from patient and aneurysm features (wide neck, MCA bifurcation with branches, hematoma needing decompression, blister aneurysm).
The Barrow Ruptured Aneurysm Trial (BRAT) was not a true randomized ISAT replica; it showed an early coiling advantage that attenuated with long follow-up and more incomplete occlusions after coiling. Boards still want ISAT numbers plus the caveat: suitable anatomy . A wide-necked middle-cerebral-artery aneurysm with an associated temporal hematoma is not an ISAT aneurysm.
Nimodipine: the one drug every aSAH patient receives
Nimodipine is a dihydropyridine calcium-channel blocker. It does not reliably angiographically reverse large-vessel vasospasm. It does improve functional outcome, which is why it is given to all aSAH patients, not only those with documented spasm.
AHA/ASA 2023 Class 1, Level A: early initiation of enteral nimodipine is beneficial in preventing DCI and improving functional outcomes. Supportive text specifies continued enteral administration at 60 mg six times a day . That is 60 mg by mouth or feeding tube every 4 hours for 21 days , the British aneurysm nimodipine trial regimen, started as soon as the diagnosis is made (FDA labeling: within 96 hours of onset).
If systolic pressure collapses after a dose, do not simply abandon the drug. Split to 30 mg every 2 hours so the 24-hour exposure stays near 360 mg while the peak hypotensive hit is smaller. If hypotension persists and threatens perfusion, hold a dose, restore volume, and add a vasopressor rather than leaving the patient both dry and nimodipine-naive. Never inject the oral liquid or capsule contents intravenously — that error has caused cardiovascular collapse and death and carries a boxed warning.
Routine statins and intravenous magnesium are not recommended for DCI prevention in the 2023 guideline.
Volume, blood pressure, and delayed cerebral ischemia — not triple-H
DCI is a clinical syndrome: a new focal deficit or a drop in consciousness lasting more than an hour, not explained by hydrocephalus, rebleeding, seizure, fever, or metabolic derangement, typically between days 4 and 14 (peak around days 7–10). Angiographic vasospasm is common; not all spasm causes DCI, and DCI can occur with only distal or microcirculatory disease.
Classic triple-H therapy (hypertension, hypervolemia, hemodilution) is retired as a prophylactic bundle:
- Component Prophylaxis Established symptomatic DCI
- Hypertension Do not induce Reasonable: raise systolic pressure (Class 2b)
- Hypervolemia Harmful; avoid Not the goal
- Hemodilution Not used Not used
- Euvolemia Beneficial (Class 2a) Maintain while raising pressure
AHA/ASA 2023: maintaining euvolemia can be beneficial (Class 2a). Elevating systolic pressure in symptomatic vasospasm may be reasonable (Class 2b). Prophylactic hemodynamic augmentation and hypervolemia should not be performed. For severe spasm with progressing deficits, intra-arterial vasodilators and balloon angioplasty may be reasonable (Class 2b).
Practical ICU translation: pick a euvolemic target (neutral daily fluid balance, clinical exam, maybe pulse-pressure variation or bedside ultrasound — not a standing order for 200 mL/h of albumin). When the patient develops a new arm drift on day 7, raise MAP with norepinephrine or phenylephrine after the aneurysm is secured, obtain CTA/CTP or catheter angiography, and call the endovascular team if deficits persist.
Hydrocephalus, EVD, and seizures
Acute hydrocephalus — enlarging ventricles, declining GCS, upward-gaze palsy, or a small fourth ventricle with a tight third — is treated with urgent CSF diversion . AHA/ASA 2023 Class 1: external ventricular drain ( EVD ) and/or lumbar drainage for acute symptomatic hydrocephalus. EVD is the default when the exam is poor, there is obstructive blood, or you need ICP data. Lumbar drainage requires communicating cisterns and a secured (or at least not actively rebleeding) aneurysm in most protocols; it is not the first move in a comatose patient with a casted fourth ventricle. Use an EVD insertion bundle to cut infection. Chronic symptomatic hydrocephalus later gets a shunt (Class 1).
New-onset seizures after aSAH: treat with an antiseizure medication for 7 days . Do not use routine prophylaxis in every patient; it can be considered in high-risk anatomy (ruptured MCA aneurysm, intraparenchymal hematoma, high clinical grade, hydrocephalus, cortical infarction). Avoid phenytoin because of excess morbidity in this population. Continuous EEG is useful when the exam is poor or fluctuating.
TCD and other DCI surveillance
AHA/ASA 2023: trained nursing detection of exam change is the core monitor. Transcranial Doppler (TCD) , CTA, and CT perfusion, interpreted by people who do this work, can detect vasospasm and help predict DCI. Continuous EEG and invasive monitors may help in high-grade patients with no exam.
TCD numbers that still appear on exams (middle cerebral artery, adult):
- Finding Typical threshold
- Mean flow velocity >120 cm/s raises concern; ≥200 cm/s suggests severe spasm
- Lindegaard ratio (MCA / extracranial ICA) >3 favors spasm over hyperemia; >6 severe
- Hyperemia High MCA velocity with Lindegaard ratio <3
TCD is a trend tool, not a diagnosis of DCI. Pair a velocity jump with the exam and, when needed, CTA/CTP.
Hyponatremia: cerebral salt wasting versus SIADH
Hyponatremia after aSAH is common and dangerous because it tracks with volume loss and DCI. Two mechanisms dominate, and the treatment is not the internist's default fluid restriction.
- Feature Cerebral salt wasting (CSW) SIADH
- Volume Hypovolemic (high urine output, falling weight, rising hematocrit) Euvolemic
- Urine sodium High High
- Urine osmolality High High
- Driver Renal sodium wasting, often with high BNP Inappropriate ADH
Treatment in aSAH Volume and sodium replacement; hypertonic saline; fludrocortisone Do not fluid-restrict; use hypertonic saline or urea if needed
If you cannot tell them apart at 3 a.m., treat as CSW: replace volume and sodium. Fluid restriction in aSAH is a classic harm pathway.
Neurogenic stunned myocardium and neurogenic pulmonary edema
Catecholamine surge at rupture injures heart and lung. Neurogenic stunned myocardium (neurogenic stress cardiomyopathy) produces troponin rise, deep T-wave inversion or QT prolongation, and wall-motion abnormalities that often cross a single coronary territory or resemble apical ballooning. Coronary occlusion is the alternative, so ECG plus echocardiography (and catheterization when the story is ambiguous) still matter — but do not delay aneurysm treatment for an expected-to-recover neurogenic cardiomyopathy in an otherwise typical aSAH patient. The ventricle usually improves over days to weeks.
Neurogenic pulmonary edema (NPE) is acute, protein-rich alveolar flooding from sympathetic pulmonary vasoconstriction and capillary leak. It can look like aspiration or cardiogenic edema. Treat the airway, use lung-protective ventilation if intubated, and treat the brain (secure the aneurysm, control ICP). Distinguishing NPE from volume overload matters because the aSAH patient still needs euvolemia, not days of furosemide-driven hypovolemia.
Venous thromboembolism prophylaxis is part of the ICU bundle once the aneurysm is secured. Standard ventilator bundles apply. Glucose targets follow ordinary critical-care practice (avoid both hypoglycemia and uncontrolled hyperglycemia).
A worked ICU timeline
A 52-year-old with a thunderclap headache is Hunt-Hess 2, WFNS I. CT shows thick cisternal blood and IVH (modified Fisher 4). CTA shows a 6-mm anterior communicating artery aneurysm suitable for coiling. SBP is 188 mm Hg. You start a nicardipine infusion, give nimodipine 60 mg enterally, reverse nothing because the patient is not anticoagulated, and take the patient for coiling within hours. An EVD is placed for a declining GCS from hydrocephalus. Day 7: new right-arm drift, TCD MCA mean velocity 190 cm/s, Lindegaard ratio 4.8. The aneurysm is secured, so you raise MAP, keep the patient euvolemic, and obtain CTA. That sequence — early securement, nimodipine, EVD, then induced hypertension for DCI rather than prophylactic triple-H — is the chapter in one patient.