Nervous System & Special Senses

Subarachnoid hemorrhage: diagnosis and management

Clinical Overview and When to Suspect Subarachnoid Hemorrhage

— "Thunderclap" headache: maximal intensity within seconds to a minute ("worst headache of life")

— Sudden headache during exertion, Valsalva, sex, or defecation

— Headache + transient LOC, seizure, vomiting, or neck stiffness

— Sentinel headache: a severe headache days to weeks earlier (warning leak in 10–40%)

— Sudden death or coma without obvious cause

Definition: Bleeding into the subarachnoid space, most often from rupture of a saccular ("berry") aneurysm at the circle of Willis (~80% of non-traumatic SAH). Other causes: perimesencephalic (venous, benign), AVM, mycotic aneurysm, vasculitis, RCVS, dural fistula, cocaine/sympathomimetic use.

Epidemiology: Peak age 40–60, F>M, mortality ~25–50% including pre-hospital deaths. ~10–15% die before reaching care.

Modifiable risks: Hypertension, smoking, heavy alcohol use, sympathomimetics. Non-modifiable: ADPKD, Ehlers-Danlos IV, fibromuscular dysplasia, first-degree relative with SAH (screen with MRA if ≥2 affected first-degree relatives), coarctation of aorta.

When to suspect — the trigger phrases:

Step 3 management: A patient calling the clinic with new "worst headache of life" or thunderclap onset → send to ED immediately for non-contrast CT head; do not order outpatient MRI or "wait and see." This is a time-critical diagnosis where delay costs lives via rebleed.

Why Step 3 cares: SAH is a low-prevalence, high-stakes diagnosis where the test-question stem rewards aggressive workup despite normal exam. The classic trap is the patient with a normal neuro exam, resolved headache, and "ibuprofen helped" — they still need imaging.

Board pearl: Up to 50% of SAH patients give a sentinel headache history in the days–weeks before catastrophic rupture. Always ask, "Have you had any other unusual severe headaches recently?" — a missed sentinel bleed is a classic malpractice and exam vignette.

Presentation Patterns and Key History

— Loss of consciousness at onset (~50%) — strongly suggests SAH over migraine

— Seizure at onset (~10%) — also raises SAH probability

— Nausea/vomiting (~75%), photophobia, neck pain/stiffness (often delayed 3–12 hr as blood irritates meninges)

— Transient focal deficits, diplopia (CN III palsy from posterior communicating artery aneurysm)

— Visual loss (Terson syndrome — vitreous hemorrhage)

— ADPKD (10% have aneurysms), connective tissue disease, prior SAH

— Hypertension control, tobacco, stimulant use

— Anticoagulant or antiplatelet use (changes management urgency)

Classic stem: Sudden, severe headache reaching peak intensity in <1 minute, often described as "thunderclap" or "like being hit in the head." Frequently occipital or holocephalic.

Associated features to elicit:

Trigger context: Exertion, sexual activity, straining, cocaine/methamphetamine use, Valsalva. Many occur at rest, so absence of trigger does not exclude.

Sentinel ("warning") leak history: Ask specifically about prior severe, atypical headaches in past 2–8 weeks. Often misdiagnosed as migraine, sinusitis, or tension headache.

Family and personal history:

Ottawa SAH Rule (age ≥15, new severe non-traumatic headache peaking within 1 hr, normal neuro exam) — investigate if any of: age ≥40, neck pain/stiffness, witnessed LOC, onset during exertion, thunderclap, limited neck flexion on exam. Sensitivity ~100%, but specificity low (~15%) — use to rule OUT, not in.

Key distinction: Migraine builds over minutes to an hour and typically has prior similar episodes; SAH peaks in seconds. A patient with a new, instantaneously maximal headache, even if it "feels like my migraines," needs imaging.

Board pearl: Document onset characteristics in patient's own words — "peak intensity in seconds" is the single highest-yield historical feature. A headache that "got worse over an hour" is much less suspicious for SAH than one "like a thunderclap." Always ask: "How long from nothing to maximum pain?"

Physical Exam Findings and Hemodynamic Assessment

— Hypertension is common — both reactive (pain, catecholamine surge) and a risk factor. SBP often >160.

— Bradycardia + hypertension = Cushing response → suggests elevated ICP from hydrocephalus or rebleed

— Fever may develop within 72 hr (chemical meningitis from blood)

— Cardiac: arrhythmias, ST/T-wave changes mimicking ischemia ("neurogenic stunned myocardium," takotsubo)

— Level of consciousness — basis of Hunt-Hess and WFNS grading

— Meningismus: nuchal rigidity, Kernig/Brudzinski (delayed 6–24 hr)

— Cranial nerves: CN III palsy (down-and-out eye, dilated pupil) → posterior communicating artery aneurysm until proven otherwise; CN VI palsy nonspecific (raised ICP)

— Focal motor deficits suggest parenchymal extension, vasospasm, or ICH

— Fundoscopy: subhyaloid/preretinal hemorrhages (Terson syndrome) — pathognomonic clue

— Hunt-Hess: I asymptomatic/mild HA; II moderate-severe HA, no deficit except CN palsy; III drowsy/mild deficit; IV stupor, hemiparesis; V coma, decerebrate

— WFNS: GCS-based; grade I (GCS 15) to V (GCS 3–6)

— Modified Fisher (CT-based, predicts vasospasm risk)

— Keep SBP <140–160 mmHg to reduce rebleed risk (AHA: <160; many centers target <140)

— Use titratable IV agents: nicardipine, clevidipine, labetalol — avoid nitroprusside (raises ICP)

— Maintain euvolemia; avoid hypotension (risk of ischemia)

General appearance: Patient often appears acutely distressed, may be obtunded, agitated, or comatose. Vomiting common.

Vital signs:

Neurologic exam:

Grading scales (memorize for triage):

Hemodynamic targets pre-securing aneurysm:

CCS pearl: On the CCS case, on arrival order continuous cardiac monitoring, pulse ox, two large-bore IVs, NPO, head of bed 30°, IV nicardipine drip with arterial line, plus emergent non-contrast CT head — all within the first simulated minutes.

Board pearl: Isolated CN III palsy with pupil involvement in an adult = PCom aneurysm — emergent CTA, even without headache.

Diagnostic Workup — Initial Labs and Imaging

— Sensitivity ~100% within 6 hours of headache onset on modern multidetector CT read by an experienced reader (in awake, neurologically intact patients with Hct >30%)

— Sensitivity drops to ~85–90% at 24 hr, ~50% at 1 week as blood becomes isodense

— Hyperdense blood in basal cisterns, sylvian fissures, interhemispheric fissure, sulci, ventricles

— Pattern clues: perimesencephalic blood (around brainstem, no aneurysm in 95%) — benign prognosis; diffuse cisternal/sylvian → aneurysmal

— Elevated opening pressure

— RBCs in tube 1 that do not clear by tube 4 (vs. traumatic tap, which clears)

— Xanthochromia — yellow CSF supernatant from RBC breakdown (oxyhemoglobin → bilirubin); develops 6–12 hr after bleed, persists 2 weeks. Spectrophotometry > visual inspection where available.

— Elevated CSF protein

— CBC, CMP (sodium baseline — SIADH/CSW), coags (PT/INR, aPTT), type & screen, troponin, BNP

— Toxicology screen (cocaine, methamphetamine) — alters etiology and counseling

— Beta-hCG in reproductive-age women (contrast/angiography planning)

— ECG — look for prolonged QT, deep T-wave inversions ("cerebral T waves"), arrhythmia

— CXR — neurogenic pulmonary edema, aspiration

Non-contrast CT head — the first test, no exceptions:

If CT negative and <6 hr from onset with classic story + low-risk patient: Many guidelines now accept CT alone to rule out, but this remains controversial. Shared decision-making essential.

If CT negative and >6 hr OR high clinical suspicion: Proceed to lumbar puncture OR CT angiography (institution-dependent).

Lumbar puncture findings:

Initial labs to order in parallel:

Step 3 management: Order non-contrast CT head STAT; do not wait for labs. If CT is negative and clinical suspicion remains, LP next — do not discharge on the basis of a negative CT alone if presentation is >6 hr old.

Board pearl: A "traumatic tap" clears across tubes 1→4 and lacks xanthochromia. True SAH shows persistent RBCs + xanthochromia — the latter is the discriminator.

Diagnostic Workup — Advanced and Confirmatory Studies

— Performed immediately after SAH is confirmed to localize the bleeding source (aneurysm, AVM, dissection)

— Sensitivity ~95–98% for aneurysms ≥3 mm; less sensitive for tiny aneurysms or vasculitis

— Guides surgical vs. endovascular planning

— Indicated if CTA negative but high suspicion remains, or for treatment planning/coiling

— Repeat DSA in 1–2 weeks if initial negative and bleed pattern is non-perimesencephalic (vasospasm or thrombosed aneurysm may obscure initial study)

— Perimesencephalic SAH with negative initial CTA/DSA: repeat imaging often unnecessary if pattern classic

— Useful in subacute presentations (>1 week) when CT sensitivity drops — FLAIR and GRE/SWI sequences detect subacute blood

— MRA an alternative for screening at-risk patients (ADPKD, family history) but not preferred acutely

— Daily monitoring days 3–14 post-SAH to detect vasospasm (elevated MCA velocities >120 cm/s, Lindegaard ratio >3)

— Non-invasive surveillance; complements clinical exam

— Grade 1: focal/diffuse thin SAH, no IVH

— Grade 2: thin SAH + IVH

— Grade 3: thick SAH, no IVH

— Grade 4: thick SAH + IVH — highest vasospasm risk

CT angiography (CTA) head and neck:

Digital subtraction angiography (DSA) — gold standard:

MRI/MRA:

Transcranial Doppler (TCD):

EEG: If unexplained altered mental status, consider non-convulsive seizures (occur in 10–20%).

Modified Fisher Scale (predicts vasospasm/DCI risk):

Family screening: First-degree relatives of SAH patients with ≥2 affected relatives → MRA screening every 5 years. Single affected relative — routine screening not recommended.

CCS pearl: Sequence on CCS: non-contrast CT → if positive, CTA head/neck → neurosurgery/neuro-IR consult simultaneously → transfer to neuro-ICU. Do not delay consult waiting for CTA results.

Board pearl: Perimesencephalic SAH (blood confined to prepontine/interpeduncular cisterns) with negative angiography = venous origin, excellent prognosis, minimal vasospasm risk. Recognize the pattern.

Risk Stratification and First-Line Management Logic

— Hunt-Hess I–II / WFNS I–II: good-grade SAH, mortality 5–15%, candidates for early aneurysm securing

— Hunt-Hess III: intermediate

— Hunt-Hess IV–V / WFNS IV–V: poor-grade, mortality 50–80%, ICU stabilization first

1. ABCs — intubate if GCS ≤8 or unable to protect airway

2. BP control — SBP <140–160 mmHg pre-securing aneurysm (rebleed risk ~4% in first 24 hr, peaks early)

3. Reverse anticoagulation — vitamin K + 4-factor PCC for warfarin; idarucizumab for dabigatran; andexanet alfa or PCC for factor Xa inhibitors; platelets for antiplatelet only if neurosurgery/active bleeding

4. Analgesia/antiemetics — fentanyl preferred (short-acting, allows neuro exam); ondansetron

5. Seizure prophylaxis — short course (3–7 days) of levetiracetam in some centers; not all guidelines endorse routine use

6. Nimodipine 60 mg PO/NG q4h × 21 days — start within 96 hr; reduces delayed cerebral ischemia

7. Glucose control (140–180), normothermia, DVT prophylaxis (mechanical only until aneurysm secured, then add pharmacologic)

— Antiplatelet/anticoagulant administration

— Hypotonic fluids (worsen cerebral edema) — use isotonic saline

— Aggressive overhydration ("triple-H" therapy no longer standard)

— Hyperventilation except as bridge for impending herniation

Grading drives prognosis and triage:

Immediate priorities (first hour):

Avoid:

Disposition: ALL aneurysmal SAH patients → neuro-ICU at a high-volume aneurysm center (>35 cases/year improves outcomes). Transfer early.

Step 3 management: Within first 60 minutes: CT confirms SAH → start nicardipine drip for SBP <160, call neurosurgery and neuro-IR, give nimodipine, reverse anticoagulants, NPO, HOB 30°, transfer to neuro-ICU, CTA for surgical planning.

Board pearl: Nimodipine is the only drug proven to improve neurologic outcome in SAH — by reducing delayed cerebral ischemia, not by preventing angiographic vasospasm. Give enterally, not IV (causes hypotension).

Pharmacotherapy — First-Line Drug Regimen

— Mechanism: L-type calcium channel blocker, neuroprotective effect (mechanism not fully understood; not via large-vessel dilation)

— Reduces delayed cerebral ischemia and improves functional outcome (number needed to treat ~13)

— If hypotensive, split dose to 30 mg q2h rather than discontinue

— Never give IV in the US (associated with cardiac arrest)

— Nicardipine drip 5 mg/hr, titrate by 2.5 mg/hr q5–15 min, max 15 mg/hr — preferred; smooth control

— Clevidipine — short half-life, useful in volume overload

— Labetalol boluses 10–20 mg or drip — bradycardia limits

— Avoid nitroprusside and nitroglycerin — increase ICP via cerebral vasodilation

— Warfarin: 4-factor PCC + vitamin K 10 mg IV

— Dabigatran: idarucizumab 5 g IV

— Apixaban/rivaroxaban: andexanet alfa (or 4-factor PCC if unavailable)

— Heparin: protamine

— Antiplatelets: platelet transfusion only if active neurosurgery planned (recent data discourage routine use in spontaneous ICH)

Nimodipine 60 mg PO/NG every 4 hours × 21 days:

Antihypertensives (pre-aneurysm securing, target SBP <140–160):

Anticoagulation reversal:

Analgesia: Acetaminophen scheduled; fentanyl IV for breakthrough (short half-life preserves serial neuro exams). Avoid NSAIDs (platelet inhibition, bleed risk) and long-acting opioids early.

Antiemetics: Ondansetron (monitor QTc).

Seizure prophylaxis: Levetiracetam 1000 mg BID × 3–7 days in select patients (cortical blood, prior seizure). Avoid phenytoin (worse cognitive outcomes in SAH).

DVT prophylaxis: Sequential compression devices from admission; add enoxaparin or UFH 24 hours after aneurysm secured.

Stress ulcer prophylaxis: PPI or H2 blocker if intubated/coagulopathic.

Fluids: Isotonic saline at maintenance for euvolemia. Treat hyponatremia (often cerebral salt wasting) with hypertonic saline or fludrocortisone — avoid fluid restriction (worsens DCI).

Board pearl: In SAH-related hyponatremia, distinguish CSW (hypovolemic, treat with salt/volume) from SIADH (euvolemic, restrict fluids) — but in SAH, fluid restriction is dangerous, so when in doubt, give salt.

Procedures — Aneurysm Securing and Adjunctive Interventions

— Platinum coils placed via femoral/radial catheter to thrombose aneurysm

— ISAT trial: coiling → better 1-year independent survival vs. clipping for ruptured aneurysms amenable to both

— Preferred for posterior circulation, elderly, poor-grade, deep-seated aneurysms

— Disadvantage: higher rate of recurrence/retreatment; requires follow-up imaging

— Craniotomy with metal clip across aneurysm neck

— Preferred for MCA bifurcation aneurysms, large hematomas requiring evacuation, wide-necked aneurysms

— More durable; lower retreatment rate

— Indication: acute hydrocephalus (20–30% of SAH) → declining mental status, ventriculomegaly on CT

— Therapeutic (drains CSF, controls ICP) and diagnostic (ICP monitoring)

— Risk: rebleed if pressure dropped too rapidly; ventriculitis

— First-line: induced hypertension (raise SBP 20–30% above baseline with norepinephrine) once aneurysm secured

— Endovascular rescue: intra-arterial verapamil/nicardipine infusion or balloon angioplasty for refractory symptomatic vasospasm

— Maintain euvolemia (triple-H abandoned)

Goal: secure ruptured aneurysm within 24–72 hours to prevent rebleed (highest risk in first 24 hr, ~4–15%; cumulative 20% in first 2 weeks if untreated).

Endovascular coiling (preferred when feasible):

Surgical clipping:

Flow diverters / stent-assisted coiling: For complex, wide-neck, or giant aneurysms; require dual antiplatelet therapy (relative contraindication in acute SAH).

External ventricular drain (EVD):

Lumbar drain: Alternative if no hydrocephalus, communicating only; some evidence for reducing vasospasm.

Management of vasospasm / delayed cerebral ischemia (peak days 4–14):

Decompressive craniectomy: For malignant cerebral edema or large parenchymal hematoma with mass effect.

Tracheostomy/PEG: Day 7–14 for prolonged dependency.

CCS pearl: Order neurosurgery AND neuro-interventional consults simultaneously on CCS — the choice between coil and clip is institution- and aneurysm-specific. Document discussion with family regarding both options.

Board pearl: ISAT favored coiling for outcomes, but the modality must match aneurysm anatomy. MCA aneurysms with intraparenchymal hematoma → clip. Basilar tip → coil.

Special Populations — Elderly and Renal/Hepatic Impairment

— Worse functional outcomes; higher rates of medical complications (pneumonia, cardiac events, delirium)

— Coiling generally preferred over clipping — less surgical morbidity

— Pre-existing cognitive impairment, frailty, advanced dementia → discuss goals of care early; aggressive intervention may not align with values

— Higher rebleed mortality; lower threshold for early aneurysm securing

— Watch for delirium — minimize benzodiazepines, anticholinergics; promote sleep-wake cycle

— Contrast for CTA/DSA: balance against urgent diagnostic need; iso-osmolar contrast + IV isotonic saline pre/post — do not withhold imaging for SAH workup

— Nimodipine: no dose adjustment, but monitor for hypotension

— Nicardipine: hepatic clearance, safe in renal disease

— Levetiracetam: renal clearance — reduce dose in CrCl <50

— Enoxaparin: switch to UFH if CrCl <30

— Apixaban/rivaroxaban reversal: dose andexanet by time since last dose

— Coagulopathy from synthetic dysfunction — give FFP/PCC pre-procedure

— Acetaminophen: limit to 2 g/day in cirrhosis

— Nicardipine, labetalol: caution, hepatic metabolism — titrate carefully

— Avoid hepatotoxic seizure prophylaxis (phenytoin, valproate)

— Reverse immediately (see Chunk 7)

— Restart anticoagulation: depends on indication; for AFib without mechanical valve, typical delay 4–8 weeks after bleeding control; individualize with neurology/cardiology input

Elderly (age >70):

Renal impairment:

Hepatic impairment:

Anticoagulant-associated SAH:

Step 3 management: For an 82-year-old with poor-grade SAH and advanced dementia, the right next step on a vignette may be family meeting and palliative care consult, not transfer to a quaternary center — recognize when the test is asking about goals of care.

Board pearl: Age alone is not a contraindication to aneurysm securing. Functional status, baseline cognition, and patient/family goals drive decisions — frailty score > chronological age.

Special Populations — Pregnancy and Other Subgroups

— SAH risk increases in third trimester and peripartum; pregnancy itself is not a major aneurysm rupture risk factor but rupture during pregnancy carries high maternal/fetal mortality (~30%/25%)

— Differential expands: eclampsia, PRES, cerebral venous thrombosis, RCVS, postpartum angiopathy, pituitary apoplexy

— Imaging: non-contrast CT head is safe (low fetal dose with abdominal shielding); CTA acceptable for life-threatening indication; MRI/MRA without gadolinium preferred when feasible

— Treatment: secure aneurysm regardless of pregnancy; coiling preferred (less physiologic disruption)

— Delivery: vaginal delivery acceptable after aneurysm secured; cesarean for unsecured aneurysm near term or obstetric indications

— Labetalol and nicardipine are pregnancy-compatible for BP control

— Rare; usually AVM, mycotic aneurysm, or trauma rather than berry aneurysm

— Sickle cell disease → moyamoya → SAH risk

— Lower threshold to seek underlying vascular malformation

— 10% prevalence of intracranial aneurysms; family clustering

— Screen with MRA at diagnosis or age 30 in patients with family history of SAH/aneurysm, high-risk occupations (pilots), or pre-transplant evaluation

— Rescreen every 5–10 years if initial negative

Pregnancy:

Pediatrics:

Polycystic kidney disease (ADPKD):

Sickle cell disease: SAH often from moyamoya-like vasculopathy; transfusion to lower HbS, neurosurgical evaluation.

Cocaine/methamphetamine users: Counsel cessation; rupture risk persists; screen for additional aneurysms.

Connective tissue disease (EDS IV, Marfan, Loeys-Dietz): Higher aneurysm and dissection risk; coiling preferred (fragile tissues).

Key distinction: Postpartum thunderclap headache with normal CT/LP → think RCVS or cerebral venous sinus thrombosis, not SAH. Get MRV and consider repeat MRA in 1–3 months (RCVS shows reversible segmental vasoconstriction).

Board pearl: In ADPKD with family history of SAH, screen at diagnosis — do not wait for symptoms. Unruptured aneurysms ≥7 mm or symptomatic merit intervention discussion.

Complications and Adverse Outcomes

— Mortality of rebleed ~70%

— Prevention: aggressive BP control + early aneurysm securing within 24–72 hr

— Presents as sudden neurologic decline, new hyperdensity on CT

— Blood blocks arachnoid villi or aqueduct → obstructive or communicating

— Presents within hours: declining LOC, upgaze palsy

— Treatment: EVD; some require permanent VP shunt (10–20% chronically)

— Angiographic vasospasm in 60–70%; symptomatic DCI in 20–30%

— Presents as new focal deficit or declining LOC

— Risk: modified Fisher 3–4

— Detected by daily exam, TCDs, CT perfusion

— Treat with induced hypertension + endovascular rescue

— Cerebral salt wasting (hypovolemic, treat with salt/volume) — more common in SAH

— SIADH (euvolemic, treat with fluid restriction — but cautiously in SAH due to DCI risk)

— Hypertonic saline is the safer bet

— Neurogenic stunned myocardium / takotsubo — apical ballooning, elevated troponin, transient

— Neurogenic pulmonary edema — non-cardiogenic, catecholamine surge

— Arrhythmias, prolonged QT

Rebleeding (peak first 24 hr, 4–15%):

Acute hydrocephalus (15–30%):

Vasospasm / Delayed Cerebral Ischemia (DCI), peak days 4–14:

Hyponatremia (30–50%):

Cardiopulmonary:

Seizures (5–15%): Acute or delayed; treat clinically apparent or electrographic seizures, but routine long-term prophylaxis not indicated.

Fever: Often non-infectious ("central fever"); workup for infection; aggressive normothermia improves outcomes.

VTE: Risk elevated; start pharmacologic prophylaxis 24 hr after aneurysm secured.

Cognitive and psychiatric: Depression, anxiety, PTSD, executive dysfunction — even in "good outcome" survivors. Up to 50% don't return to prior occupational level.

CCS pearl: On day 5–10 of a CCS SAH case, expect a new focal deficit → recognize DCI, order CT (rule out rebleed/hydrocephalus), then induce hypertension and arrange angiography for intra-arterial vasodilator/angioplasty.

Board pearl: New focal deficit + day 7 + treated SAH = vasospasm/DCI until proven otherwise.

When to Escalate Care — ICU, Consult, and Transfer

— Centers performing >35 aneurysm cases/year have better outcomes (volume-outcome relationship)

— If at a community ED: stabilize, control BP, reverse anticoagulation, start nimodipine, and transfer immediately by critical care transport

— Neurosurgery — for clipping, EVD placement, decompression

— Neuro-interventional radiology / endovascular neurosurgery — for coiling, intra-arterial therapy

— Neurocritical care — primary ICU team

— Anesthesia — pre-procedural

— Palliative care — for poor-grade SAH with goals-of-care discussions

— Rehabilitation medicine — early consult for disposition planning

— GCS decline by ≥2 points → CT, evaluate for rebleed/hydrocephalus

— New focal deficit → DCI workup

— Cushing response → impending herniation, may need decompression

— Refractory ICP elevation → osmotherapy (hypertonic saline preferred over mannitol in hyponatremic SAH), hyperventilation as bridge, surgical decompression

— Hunt-Hess V with bilateral fixed pupils, severe comorbidities, advanced age, prior poor functional status — comfort-focused care is appropriate; document goals and offer organ donation discussion via OPO

All confirmed SAH → admit to neuro-ICU at a comprehensive stroke / aneurysm center.

Consults required:

Triggers for emergent intervention:

Intubation criteria: GCS ≤8, loss of airway reflexes, refractory hypoxemia, agitation precluding management. Use RSI with hemodynamic stability — etomidate or ketamine; rocuronium. Avoid coughing/bucking — surge can rupture aneurysm.

Family communication: Frequent updates, prognosis discussion using Hunt-Hess/WFNS grade; involve them in clip-vs-coil decision.

When palliative care is the right escalation:

Step 3 management: A community ED with confirmed aneurysmal SAH: do not delay for "stabilization perfection." Stabilize → call referral center → transfer by air/critical care ground while continuing BP control. Time-to-aneurysm-securing matters more than transfer optimization.

Board pearl: Volume-outcome relationship is real — Step 3 may test transfer decisions. Always transfer to a comprehensive center capable of both clipping and endovascular options.

Key Differentials — Same-Category (Sudden Severe Headache) Causes

— Recurrent thunderclap headaches over days–weeks, often triggered by sex, exertion, vasoactive drugs (SSRIs, triptans, cocaine, postpartum state)

— Normal CT/LP initially; convexity (sulcal) SAH possible

— Angiography: "sausage on a string" multifocal vasoconstriction; reverses within 3 months

— Treat with calcium channel blockers, remove triggers

— Subacute or thunderclap headache; risk factors: OCPs, pregnancy/postpartum, hypercoagulability, dehydration, infection

— Imaging: empty delta sign on contrast CT; MRV is diagnostic

— Treat with anticoagulation (yes, even with hemorrhagic infarct)

— Unilateral neck/head pain ± Horner syndrome ± stroke

— CTA neck diagnostic; antiplatelet or anticoagulation per guidelines

— Sudden headache + visual field defect (bitemporal hemianopia) + ophthalmoplegia + hormonal collapse

— MRI pituitary; urgent stress-dose hydrocortisone + neurosurgery

— Headache, visual changes, seizures, very high BP

— Posterior white matter edema on MRI

— Positional thunderclap headache, "drop attacks," hydrocephalus

— MRI diagnostic; neurosurgical resection

— Orthostatic headache (worse standing, better recumbent) from CSF leak

— MRI: pachymeningeal enhancement, sagging brain

— Treat with epidural blood patch

Reversible Cerebral Vasoconstriction Syndrome (RCVS):

Cerebral venous sinus thrombosis (CVST):

Primary thunderclap headache: Diagnosis of exclusion; only after full SAH workup negative.

Cervical artery dissection:

Pituitary apoplexy:

Acute hypertensive crisis / PRES:

Colloid cyst of third ventricle:

Spontaneous intracranial hypotension:

Migraine with thunderclap onset: Possible but diagnosis of exclusion — first thunderclap always warrants imaging.

Key distinction: All thunderclap headaches deserve non-contrast CT + LP (if CT negative and >6 hr) before being attributed to migraine, RCVS, or "primary" causes. The exam rewards the workup, not the gestalt.

Board pearl: Postpartum thunderclap headache: think RCVS, CVST, eclampsia, PRES, pituitary apoplexy alongside SAH — broader differential than the general population.

Key Differentials — Other-Category Causes

— Fever, headache, neck stiffness, altered mental status

— Onset over hours to a day (not seconds), often preceded by infectious prodrome

— LP: high WBC (neutrophilic), low glucose, high protein, positive Gram stain/culture

— Empiric ceftriaxone + vancomycin + dexamethasone (+ ampicillin if age >50/immunocompromised) immediately; do not delay for CT

— Fever, headache, altered mentation, seizures, temporal lobe findings

— MRI: temporal lobe edema; CSF lymphocytic pleocytosis, HSV PCR

— Empiric IV acyclovir

— Sudden severe headache + eye pain + halos around lights + red eye + fixed mid-dilated pupil

— Tonometry shows elevated IOP; ophthalmology emergency

— Headache, nausea, confusion in multiple household members; check carboxyhemoglobin

— Severe BP elevation + headache + altered mentation + papilledema

— Lower BP gradually (25% in first hour)

— Rare but documented: posterior MI/aortic dissection presenting as thunderclap headache via vagal/sympathetic pathways — always check ECG

— Chest/back pain radiating to neck + neuro deficit + pulse asymmetry; CT angiogram chest

— Hyponatremia, hypoglycemia — headache with altered mentation; basic labs catch

— Nitrates, PDE-5 inhibitors, MAOIs + tyramine, cocaine — headache and hypertensive surge

Bacterial meningitis:

Viral encephalitis (HSV):

Acute angle-closure glaucoma:

Carbon monoxide poisoning:

Acute glaucomatous, sinus, or dental sources: Usually subacute, focal pain.

Hypertensive encephalopathy:

Cardiac referred:

Aortic dissection with carotid involvement:

Toxic-metabolic:

Medication-related:

Psychogenic/functional: Diagnosis of exclusion — never the first answer for thunderclap headache on Step 3.

Key distinction: Fever + neck stiffness + headache: SAH typically has delayed meningismus (6–24 hr) with abrupt onset; meningitis has progressive onset over hours with early fever and prodrome. Both still need LP — but the imaging-first sequence differs (SAH needs CT first; meningitis empiric antibiotics first).

Board pearl: In a thunderclap headache vignette with negative CT and negative LP, the next test is often MRI/MRV or CTA to catch RCVS, CVST, or dissection — don't stop the workup at "negative SAH."

Secondary Prevention and Discharge Plan

— After coiling, follow-up DSA or MRA at 6 months, 1 year, then periodically — retreatment rate ~10–20%

— After clipping, surveillance imaging less intensive; consider MRA every 5 years

— De novo aneurysm risk ~1–2% per year — counsel on long-term follow-up

— Hypertension: Target <130/80 (ACC/AHA); lifelong antihypertensives (ACEi/ARB, thiazide, CCB combinations as needed); home BP monitoring

— Smoking cessation: Most important modifiable factor; offer varenicline or combination NRT + behavioral counseling; document at every visit

— Alcohol: Limit to ≤1 drink/day women, ≤2 men; screen for AUD

— Stimulant cessation: Cocaine, methamphetamine, ecstasy — referral to addiction services

— Sympathomimetic medication review: Decongestants, ADHD stimulants — individualize risk

— If AFib or mechanical valve: resume anticoagulation after aneurysm secured and bleeding stable, typically 1–4 weeks; involve neurology

— Avoid aspirin unless cardiovascular indication outweighs bleed risk

— Complete 21-day course of nimodipine even after discharge

— Antihypertensive regimen

— Stool softener (avoid Valsalva)

— Analgesic (acetaminophen-based; avoid NSAIDs early)

— Antiepileptic only if had documented seizure

— DVT prophylaxis until ambulating well

— ≥2 first-degree relatives with SAH → MRA screening for first-degree relatives every 5 years

Aneurysm recurrence and de novo formation:

Modifiable risk factor control:

Anticoagulation/antiplatelet decisions:

Discharge medications (typical good-outcome SAH patient):

Family screening:

Vaccinations: Influenza, pneumococcal, COVID — standard preventive care; immobility ↑ infection risk

Step 3 management: At discharge, ensure: BP medications reconciled, smoking cessation prescription written, follow-up appointments scheduled (neurosurgery 2–4 weeks, neurology/PCP 1–2 weeks, surveillance angiography per protocol), family screening offer discussed and documented.

Board pearl: Smoking cessation alone reduces rebleed and de novo aneurysm risk substantially — it is the single highest-impact secondary prevention intervention. Step 3 loves the "what's the most effective long-term intervention?" question.

Follow-Up, Monitoring, and Rehabilitation

— PCP / neurology: 1–2 weeks post-discharge for medication reconciliation, BP check, mood screen

— Neurosurgery / neuro-IR: 2–4 weeks for wound check; vascular follow-up imaging at 6 months and 1 year

— Rehabilitation: ongoing PT/OT/speech therapy as needed

— Mental health: screen at every visit (PHQ-9, GAD-7); 30–50% of survivors develop depression/anxiety/PTSD

— Coiled aneurysms: DSA or MRA at 6 months, 1 year, then every 1–5 years depending on stability; recanalization requires re-treatment

— Clipped aneurysms: less frequent (every 5 years MRA)

— De novo aneurysm screening every 5 years

— Home BP cuff, target <130/80

— Office check 2 weeks, 1 month, then every 3 months until stable

— Neuropsychological testing at 3–6 months to characterize deficits (executive function, memory, attention)

— Cognitive rehabilitation, occupational therapy for return-to-work

— Driving evaluation before resuming driving — formal assessment recommended, especially for poor-grade survivors or those with visual field defects

— Return to work: graduated, often delayed 3–6 months

— Avoid Valsalva (heavy lifting, straining) for ~6 weeks post-procedure

— Sexual activity: typically resume when able to tolerate moderate exertion (~2–6 weeks)

— Air travel: usually safe 2 weeks post-procedure

— Pregnancy planning: if previously ruptured aneurysm now secured, generally safe; discuss with neurosurgery

Outpatient follow-up cadence:

Surveillance imaging:

BP monitoring:

Cognitive and functional rehabilitation:

Counseling topics:

Fatigue and recovery: Persistent fatigue is the most common long-term symptom (up to 80%); validate it, encourage gradual reconditioning, screen for depression/sleep apnea

Step 3 management: Always pair return-to-work and driving questions with formal evaluation — neuropsych testing and driving rehab — rather than self-assessment. This protects patient and public.

Board pearl: Persistent fatigue and cognitive complaints in a "good outcome" SAH survivor are real, not malingering. Refer for neuropsych testing and rehab; don't dismiss.

Ethical, Legal, and Patient Safety Considerations

— Ruptured aneurysm patient may be obtunded or intubated → use surrogate decision-makers per state hierarchy (spouse, adult children, parent, sibling)

— If life-threatening and no surrogate available, emergency exception allows treatment under implied consent

— Document discussion of clip vs. coil with surrogate, including ISAT data and aneurysm-specific factors

— Hunt-Hess V with poor prognostic features (age, comorbidities, bilateral fixed pupils, large hematoma): palliative care consult early

— Avoid premature withdrawal — early prognostication is unreliable; many guidelines recommend waiting 72 hr before formal prognosis discussions

— Document advance directives, POLST, and prior expressed wishes

— SAH is a leading cause of brain death and donation eligibility

— Required referral to organ procurement organization (OPO) for all imminent deaths — federal law (CMS)

— The treating team should not raise donation directly; OPO handles family approach

— Strict clinical criteria: coma, absent brainstem reflexes, apnea test

— Confirmatory tests (EEG, nuclear flow) if exam unreliable

— Two qualified examinations per institutional/state policy

— Handoff from ED to ICU: explicit communication of aneurysm status (secured vs. unsecured), BP targets, anticoagulation reversal status, nimodipine started — use a structured handoff (I-PASS, SBAR)

— Discharge from ICU to ward: ongoing nimodipine, BP medications, DVT prophylaxis, follow-up imaging schedule

— Hospital to home: written instructions, medication reconciliation, family screening discussion documented, follow-up appointments scheduled before discharge

— Failure to image a thunderclap headache is a leading neuro-malpractice scenario

— Document onset characteristics, exam, decision-making rationale

— Use clinical decision rules (Ottawa) to standardize approach

— Mandatory reporting of seizure history to DMV varies by state; know local rules

— Pilots, commercial drivers, surgeons → specialized fitness-for-duty evaluation

Informed consent for emergent intervention:

Goals of care in poor-grade SAH:

Organ donation:

Brain death determination:

Transition-of-care risks (high-yield Step 3 safety):

Missed sentinel headache — malpractice landscape:

Driving and occupational safety:

Step 3 management: A patient with thunderclap headache, normal CT at 8 hours post-onset, who refuses LP: document shared decision-making, capacity assessment, risks of missed SAH, and offer CTA as alternative. Never let the patient leave without a documented informed refusal.

Board pearl: The single highest-yield safety pearl is: never attribute a first thunderclap headache to migraine without imaging — even in known migraineurs.

High-Yield Associations and Rapid-Fire Clinical Facts

— Anterior communicating artery (~35%)

— Posterior communicating artery (~30%) — CN III palsy

— Middle cerebral artery bifurcation (~20%)

— Basilar tip / posterior circulation (~5–10%)

Berry aneurysm associations: ADPKD, Ehlers-Danlos type IV, fibromuscular dysplasia, coarctation of aorta, alpha-1 antitrypsin deficiency, neurofibromatosis type 1.

Most common aneurysm locations:

CN III palsy with pupil involvement = PCom aneurysm until proven otherwise (parasympathetic fibers on outside of nerve, compressed first).

Terson syndrome: Vitreous/preretinal hemorrhage from acute ICP spike → fundoscopic clue; associated with worse prognosis.

Nimodipine 60 mg PO q4h × 21 days — the only drug proven to improve neuro outcome.

ISAT: Coiling beat clipping for 1-year independent survival in eligible aneurysms.

Modified Fisher 3–4 predicts highest vasospasm/DCI risk.

Vasospasm window: Days 4–14 (peak 7–10).

Rebleed window: First 24–72 hours (highest in first 24 hr).

Hydrocephalus window: Acute (hours), can recur subacutely or chronically.

Hyponatremia in SAH: Usually cerebral salt wasting — treat with salt and volume, NOT fluid restriction.

ECG changes in SAH: Deep symmetric T-wave inversions ("cerebral T waves"), prolonged QT, U waves; troponin can be elevated from neurogenic stunned myocardium.

Perimesencephalic SAH: Benign venous bleed pattern; rarely re-bleeds; negative angiography typical.

Family screening: ≥2 first-degree relatives with SAH → MRA at age 30 or diagnosis, every 5 years.

Unruptured aneurysm intervention threshold: ≥7 mm (anterior circulation) or any symptomatic/posterior circulation aneurysm — individualize using ISUIA/PHASES score.

Avoid in SAH: Nitroprusside (↑ICP), aggressive hyperventilation (cerebral ischemia), fluid restriction (DCI), NSAIDs/aspirin (bleed), phenytoin (cognitive harm).

Xanthochromia: Detectable 6–12 hr after bleed; persists 2 weeks; spectrophotometry > visual.

Ottawa SAH Rule: ~100% sensitive, low specificity — rules out, doesn't rule in.

CCS pearl: On a CCS case, by simulated hour 1 you should have: CT confirming SAH, nicardipine drip, nimodipine, neurosurgery + neuro-IR consults, neuro-ICU admission orders, anticoagulation reversal if applicable, and CTA ordered.

Board pearl: The "worst headache of life" + transient LOC + normal exam = SAH workup regardless of how good the patient looks now. Sentinel bleeds reabsorb; aneurysms don't.

Board Question Stem Patterns

Stem 1 — Classic thunderclap: 47F with "worst headache of life" peaking in seconds during sex, vomited once, now neuro intact. Next step? Non-contrast CT head. If CT negative >6 hr post-onset → LP.

Stem 2 — Sentinel headache miss: 52M presents with severe headache and stiff neck 10 days after a "bad headache" he attributed to migraine 2 weeks ago that resolved with rest. Diagnosis? SAH with sentinel bleed. Next step? Non-contrast CT → likely diagnostic; if negative LP for xanthochromia.

Stem 3 — CN III palsy: Patient with new headache + diplopia + dilated pupil on one side. Next step? CTA head — concern for PCom aneurysm; even without rupture, this is a surgical emergency.

Stem 4 — Negative CT, high suspicion: 8 hours post thunderclap, CT normal. Next step? LP looking for xanthochromia and persistent RBCs in tubes 1 and 4.

Stem 5 — Vasospasm: Day 7 post-SAH patient develops new left hemiparesis. Next step? Non-contrast CT (rule out rebleed/hydrocephalus), then induced hypertension + angiography for intra-arterial vasodilator or angioplasty.

Stem 6 — Hyponatremia: Day 5 post-SAH patient with Na 128, BP 100/60, dry mucous membranes. Diagnosis? Cerebral salt wasting. Treatment? Hypertonic saline + isotonic fluids; NOT fluid restriction.

Stem 7 — ECG abnormality: SAH patient has new deep T-wave inversions and troponin 0.4. Best next step? Continue SAH management, get echo (likely takotsubo / neurogenic stunned myocardium); avoid catheterization unless clear coronary indication.

Stem 8 — Pre-securing BP: SAH confirmed, BP 195/110. Best agent? Nicardipine drip (target <140–160 SBP). Avoid nitroprusside.

Stem 9 — Anticoagulation reversal: SAH on warfarin INR 3.5. Treatment? 4-factor PCC + IV vitamin K immediately.

Stem 10 — Best long-term prevention: Recovered SAH survivor asks what reduces future risk most. Answer: Smoking cessation + BP control.

Stem 11 — ADPKD screening: ADPKD patient with father who died of SAH asks about screening. Answer: MRA of brain; repeat every 5 years.

Stem 12 — Pregnancy: 28F at 32 weeks with thunderclap headache. Next step? Non-contrast CT head (with abdominal shielding) — diagnostic priority outweighs minimal fetal radiation risk.

Stem 13 — Perimesencephalic: Thunderclap with CT showing blood only in prepontine cistern; CTA negative. Prognosis? Excellent; minimal vasospasm risk; no repeat DSA needed if pattern classic.

Board pearl: When stuck, default to: CT first, LP if negative and >6 hr, CTA after confirmation, neurosurgery + neuro-IR consults, neuro-ICU, nimodipine, BP control, anticoagulation reversal. This algorithm answers ~80% of SAH stems.

One-Line Recap

Subarachnoid hemorrhage is a time-critical diagnosis driven by thunderclap headache — confirm with non-contrast CT (LP if >6 hr and CT negative), control SBP to <140–160 with nicardipine, give nimodipine 60 mg q4h × 21 days, reverse anticoagulation, secure the aneurysm within 24–72 hours via coiling or clipping at a high-volume center, and monitor for rebleed, hydrocephalus, and vasospasm/DCI.

Diagnose fast: Non-contrast CT head is ~100% sensitive within 6 hours; beyond that, LP for xanthochromia. CTA localizes the aneurysm. Never attribute a first thunderclap headache to migraine without imaging.

Stabilize early: SBP <140–160 with nicardipine (not nitroprusside), reverse anticoagulation immediately (PCC + vitamin K for warfarin; idarucizumab for dabigatran; andexanet/PCC for Xa inhibitors), start nimodipine within 96 hours, admit to neuro-ICU at a comprehensive center.

Secure the aneurysm: Within 24–72 hours — coiling preferred per ISAT for most eligible aneurysms; clipping for MCA bifurcation, large hematomas, or unfavorable anatomy. Simultaneous neurosurgery + neuro-IR consults.

Anticipate complications: Rebleed (first 24 hr), hydrocephalus (acute), vasospasm/DCI (days 4–14, treat with induced hypertension + endovascular rescue), hyponatremia from cerebral salt wasting (give salt, don't restrict), neurogenic stunned myocardium, seizures.

Long-term: Smoking cessation (highest-impact intervention), BP <130/80, surveillance imaging, family screening if ≥2 first-degree relatives affected, neuropsych testing and rehab for cognitive/fatigue sequelae.

Board pearl: The two highest-yield single facts — nimodipine is the only outcome-improving drug and smoking cessation is the most powerful long-term prevention — answer a disproportionate share of SAH questions on Step 3.