Diagnosis & Initial Assessment of SAH
Subarachnoid hemorrhage (SAH) accounts for approximately 5% of all strokes but is disproportionately devastating — carrying a case fatality rate of 25–50% and causing neurological disability in up to 50% of survivors. The median age at presentation is ~55 years, decades younger than ischemic stroke, which means SAH has an outsized impact on productive life-years lost. Misdiagnosis at initial presentation occurs in an estimated 5–12% of cases, most commonly when SAH presents as an isolated headache without focal deficits, and delayed diagnosis is independently associated with worse outcomes. A systematic approach to the evaluation of acute headache is essential: when to image, when to perform lumbar puncture, how to interpret CSF results, and how to identify the causative lesion.
Bottom Line: SAH Diagnosis
- CT within 6 hours is ~100% sensitive: In neurologically intact patients presenting within 6 hours of headache onset, a negative noncontrast CT on a modern scanner, read by an expert, is sufficient to exclude aSAH (AHA 2023 Class 1, LOE B-NR). Lumbar puncture is not routinely required in this scenario.
- After 6 hours, the next test is risk-stratified: CT sensitivity declines to ~93% at 24 hours and keeps falling. If CT is negative and suspicion remains — LP (with xanthochromia) for high pretest probability, and MRI (FLAIR + susceptibility/GRE) as a non-invasive alternative for moderate-to-low suspicion, which also screens for mimics. AHA 2023 still endorses LP after a negative CT >6 h (Class 1); MRI is a reasonable substitute when LP is declined or contraindicated.
- Ottawa SAH Rule: 100% sensitivity for identifying headache patients who need imaging. If none of the 6 criteria are present, SAH workup is not needed.
- CTA for aneurysm detection: Once SAH is confirmed, CTA is first-line for identifying the source. Sensitivity >97% for aneurysms ≥3 mm. DSA remains gold standard for equivocal cases or when endovascular treatment is planned.
- Grading matters: Hunt-Hess and WFNS classify clinical severity; modified Fisher scale predicts vasospasm risk. These guide treatment urgency and prognosis.
- Not all SAH is aneurysmal: Perimesencephalic SAH (~10%) has an excellent prognosis. Other causes include AVMs, dural fistulas, vasculitis, RCVS, and coagulopathy.
1. Clinical Presentation
1.1 The Thunderclap Headache
The hallmark of aSAH is sudden-onset severe headache reaching maximum intensity within seconds to minutes — the classic "thunderclap headache" or "worst headache of my life." However, relying solely on patient-reported severity is insufficient. Key clinical features that raise suspicion:
- Onset pattern: Instantaneous or within seconds to maximum intensity (not a headache that builds over hours). Onset during exertion (Valsalva, coitus, straining) increases probability but is not required.
- Associated symptoms: Neck stiffness/pain (meningismus, develops over hours as blood irritates meninges), nausea/vomiting (75%), transient or sustained loss of consciousness (50% in severe cases), photophobia, seizure at onset (6–16%).
- Neurological findings: May be entirely normal (especially in good-grade SAH). Third nerve palsy with pupil involvement suggests posterior communicating artery (PComA) aneurysm. Focal deficits suggest parenchymal extension or early vasospasm. Altered consciousness indicates high-grade SAH, hydrocephalus, or elevated ICP.
1.2 Sentinel Headache (Warning Leak)
An estimated 10–40% of patients report a sudden severe headache days to weeks before the major hemorrhage — the "sentinel headache" or "warning leak." This represents a minor hemorrhage or aneurysm expansion that precedes catastrophic rupture. Sentinel headaches are frequently misdiagnosed as tension headache or migraine. Recognition and investigation of sentinel headache can be lifesaving, as treatment before major rupture dramatically improves outcomes.
🔴 Red Flags: When Headache May Be SAH
- First or "worst" headache: Any patient presenting with "the worst headache of my life" or a headache distinctly different from any previous headache warrants SAH evaluation.
- Sudden onset: Maximum intensity within 1 hour (Ottawa SAH rule threshold) — but most aSAH headaches peak within seconds.
- Exertional onset: Onset during lifting, straining, sexual activity, or Valsalva maneuver.
- Associated syncope or LOC: Brief loss of consciousness at headache onset is highly concerning.
- Neck stiffness/pain: Particularly if it develops hours after headache onset (meningeal irritation from subarachnoid blood).
- Age ≥40: SAH incidence increases with age. Peak incidence 40–60 years.
- Risk factors: Smoking, hypertension, family history of aneurysm or SAH, known unruptured aneurysm, autosomal dominant polycystic kidney disease, connective tissue disorders (Ehlers-Danlos type IV).
2. The Ottawa SAH Rule
The Ottawa SAH Rule is a validated clinical decision rule that identifies patients with acute headache who require investigation for SAH. It was derived in 1,999 patients, validated in 2,131 patients, and prospectively implemented in 3,672 patients across 6 tertiary-care Canadian emergency departments. It has 100% sensitivity (95% CI 98.1–100%) for SAH and a specificity of ~15%.
2.1 Rule Criteria
The rule applies to alert patients ≥15 years presenting with a new, severe, nontraumatic headache reaching maximum intensity within 1 hour. Investigate for SAH if any ONE of the following is present:
| # | Criterion | Rationale |
|---|---|---|
| 1 | Age ≥40 years | SAH incidence increases with age |
| 2 | Neck pain or stiffness | Meningeal irritation from subarachnoid blood |
| 3 | Witnessed loss of consciousness | Suggests acute ICP elevation from hemorrhage |
| 4 | Onset during exertion | Valsalva-related transmural pressure increase |
| 5 | Thunderclap headache (instant peak) | Most specific clinical feature of SAH |
| 6 | Limited neck flexion on examination | Physical sign of meningismus |
2.2 Exclusions
The Ottawa SAH Rule should not be applied in patients with: new neurological deficits, prior aneurysm or SAH, known brain tumor, chronic recurrent headaches of the same character (≥3 episodes over ≥6 months), or papilledema. These patients require investigation regardless of the rule.
Clinical Relevance: Using the Ottawa SAH Rule
- If all 6 criteria are absent: SAH is effectively ruled out. No imaging or LP is needed. The negative predictive value approaches 100%.
- If any criterion is present: The rule is positive → proceed with noncontrast CT head. The low specificity (~15%) means most positive screens will not be SAH — this is by design (high sensitivity rule-out tool).
- The rule does NOT diagnose SAH. It identifies patients who require further testing. A positive rule is not equivalent to SAH diagnosis.
- Implementation: Prospective implementation reduced LP rates by 34% (from 38.9% to 25.9%) and hospital admissions by 25% without missing any SAH cases.
3. Noncontrast CT Head
Noncontrast CT is the first-line diagnostic study for suspected SAH. Its sensitivity is time-dependent — highest in the first hours after hemorrhage and declining as blood is reabsorbed from the subarachnoid space.
3.1 CT Sensitivity by Time
| Time From Onset | CT Sensitivity | Clinical Implication |
|---|---|---|
| <6 hours | ~98.7–100% | Negative CT effectively rules out aSAH (if read by expert on modern multidetector scanner). LP generally not required. (AHA 2023, Class 1, LOE B-NR) |
| 6–12 hours | ~95–98% | LP should be performed if CT is negative and clinical suspicion remains. |
| 12–24 hours | ~93% | LP required if negative CT. Xanthochromia most reliable at 12+ hours. |
| 24–72 hours | ~85–90% | LP essential. CT alone insufficient. |
| >72 hours | <80% (declining) | CT often normal. LP with spectrophotometry is the primary diagnostic tool. |
| 1 week | ~50% | CT unreliable. MRI FLAIR may be more sensitive than CT at this stage. |
3.2 The "6-Hour CT Rule"
The 6-hour CT rule states that in neurologically intact patients presenting within 6 hours of headache onset, a negative noncontrast CT (on a modern multidetector scanner, interpreted by an expert neuroradiologist) is sufficient to exclude aSAH without the need for lumbar puncture. This was validated prospectively in 3,672 patients with a sensitivity of 95.5% (95% CI 89.8–98.5%) — the 5 missed cases included 1 radiology misread, 2 incidental unruptured aneurysms (without SAH), 1 nonaneurysmal cause, and 1 profoundly anemic patient.
This rule has been adopted by the 2023 AHA/ASA guidelines, the ACEP clinical policy on headache, and NICE 2022 guidelines. Critical caveats:
- The CT must be performed on a modern multidetector scanner (≥16-slice) with thin cuts (≤3 mm) through the posterior fossa.
- The CT must be interpreted by a qualified radiologist or neuroradiologist. Resident-only reads are insufficient for this rule.
- The patient must be neurologically intact (alert, oriented, no focal deficits). Patients with neurological deficits require full evaluation regardless.
- Moderate-to-severe anemia can reduce CT sensitivity (blood appears less hyperdense when hemoglobin is low).
Clinical Relevance: Interpreting CT in SAH
- Distribution patterns on CT predict the source: Diffuse thick basal cistern blood → aneurysmal. Sylvian fissure predominant → MCA aneurysm. Interhemispheric fissure → AComA aneurysm. Blood centered anterior to midbrain only → perimesencephalic (usually benign).
- Look for associated findings: Intraventricular hemorrhage (especially in third/fourth ventricles — raises hydrocephalus risk), intracerebral hematoma (may indicate the aneurysm location and require surgical evacuation), acute hydrocephalus (dilated ventricles), global cerebral edema (poor prognosis).
- Subtle SAH: Small amounts of blood in the dependent portions of the occipital horns, Sylvian fissures, or interpeduncular cistern can be easily missed. Thin-slice reconstructions and careful review of the posterior fossa are essential.
4. Lumbar Puncture
LP remains the most sensitive test after a negative CT and is the recommended next step in patients presenting >6 hours after onset, particularly when clinical suspicion is high — it detects xanthochromia, measures opening pressure, and is the only study that simultaneously screens the CSF for mimics such as meningitis. The primary purpose is to detect blood breakdown products in the CSF that indicate prior subarachnoid hemorrhage.
4.0 Choosing the Next Test: LP vs. MRI by Pretest Probability
In CT-negative patients, many centers now risk-stratify the next study rather than performing LP reflexively on everyone:
- High suspicion (instant-onset thunderclap, exertional onset, syncope at onset, age >40 with risk factors): proceed to LP. It is the most sensitive test for blood breakdown products and the only one that also evaluates CSF for infectious/inflammatory mimics. (Some institutions instead obtain MRI ± CTA to avoid LP even in high-suspicion patients — an acceptable but slightly less sensitive pathway.)
- Moderate-to-low suspicion (atypical features, headache not perfectly thunderclap, low-risk demographics) — or when LP is declined/contraindicated: a non-invasive MRI with FLAIR + susceptibility-weighted (SWI/GRE/T2*) sequences is a reasonable alternative. These sequences are sensitive for subarachnoid and parenchymal blood (and become more sensitive than CT in the subacute phase, >3–4 days) while also detecting common SAH mimics (RCVS, CVT, cervical/intracranial dissection, posterior-fossa lesions). It avoids post-LP headache and the traumatic-tap dilemma.
AHA 2023 continues to recommend LP after a negative CT beyond 6 hours (Class 1, LOE B-NR); MRI is best viewed as a complementary or substitute non-invasive option rather than a formal guideline-endorsed replacement.
4.1 Timing
Xanthochromia (the yellow discoloration of CSF from bilirubin, produced by in vivo hemoglobin degradation) takes at least 2–4 hours to develop after hemorrhage. It is present in nearly all SAH patients by 12 hours and can persist for 2–4 weeks. Therefore, LP performed within 2 hours of symptom onset may yield false-negative results for xanthochromia. Ideally, LP should be performed ≥12 hours after headache onset for optimal sensitivity.
4.2 Interpreting CSF Results
| CSF Finding | Interpretation | Key Points |
|---|---|---|
| Xanthochromia (visual) | Yellow discoloration of centrifuged supernatant | Most specific bedside finding for SAH. Sensitivity ~93% by visual inspection. Compare against water in a white tube under good lighting. Can be present with severe jaundice (bilirubin >10 mg/dL) or very high CSF protein. |
| Xanthochromia (spectrophotometry) | Detects bilirubin and oxyhemoglobin peaks in CSF | Gold standard for xanthochromia detection. More sensitive and specific than visual inspection. Standard in UK/European practice. Not universally available in US EDs. Distinguishes bilirubin (SAH) from oxyhemoglobin (traumatic tap). |
| RBC count | Elevated in SAH (can range from hundreds to >1 million/mm³) | Classically does NOT decrease between tube 1 and tube 4 in SAH (vs. traumatic tap where RBCs "clear"). However, this distinction is unreliable — RBCs from SAH can also decrease across tubes. Do not rely on RBC clearance alone. |
| Tube 4 RBC <2,000 × 10⁶/L + no xanthochromia | SAH ruled out | Per Perry et al. (2015), this combination has ~100% sensitivity for excluding aSAH. Considered a "low-risk tap." |
| Opening pressure | Often elevated in SAH (>20 cmH₂O) | Supportive but not diagnostic. Not always reliably elevated. Do not rely on opening pressure alone. |
🔴 Traumatic Tap vs. SAH: The Clinical Dilemma
- Up to 20% of LPs are "traumatic" (blood introduced by needle trauma). Distinguishing traumatic tap from true SAH is one of the most difficult problems in emergency neurology.
- Do NOT rely on the "tube 1 to tube 4 clearance" rule alone. RBCs from SAH can decrease across tubes, and traumatic taps can produce persistent RBCs.
- Xanthochromia is the key differentiator: Present in SAH (blood has been in the CSF for hours, undergoing hemolysis), absent in fresh traumatic tap (blood was just introduced). However, a severely traumatic tap (>100,000 RBCs) can produce in vitro xanthochromia, creating a false positive.
- If diagnostic uncertainty persists: CTA is the next step. A negative CTA in the setting of an equivocal LP has a negative predictive value approaching 99% for aSAH.
5. Diagnostic Algorithm: CT → LP / MRI → CTA
| Step | Action | Next Step |
|---|---|---|
| 1 | Apply Ottawa SAH Rule. If all criteria absent → SAH ruled out. | If any criterion present → proceed to CT. |
| 2 | Noncontrast CT head | If CT positive for SAH → proceed directly to CTA (step 5). If CT negative → see step 3. |
| 3 | CT negative, onset <6 hours, neurologically intact, modern scanner, expert read | aSAH effectively excluded. No LP required (AHA 2023). Consider CTA only if clinical suspicion is extremely high (instant onset + age >40 + family history). |
| 4 | CT negative, onset >6 hours or suboptimal CT — high clinical suspicion | Lumbar puncture (most sensitive; also screens CSF for mimics). Wait ≥12 hours from onset if possible. Assess xanthochromia + tube-4 RBC count. (Some centers use MRI ± CTA instead to avoid LP.) |
| 4′ | CT negative — moderate-to-low suspicion, or LP declined/contraindicated | MRI (FLAIR + SWI/GRE) as a non-invasive alternative — sensitive for subarachnoid/parenchymal blood and for mimics (RCVS, CVT, dissection). Positive → CTA (step 5). Negative with persisting concern → LP. |
| 4a | LP: No xanthochromia + tube 4 RBC <2,000 | SAH ruled out. |
| 4b | LP: Xanthochromia present OR persistently elevated RBCs | SAH confirmed or highly suspected → proceed to CTA. |
| 4c | LP: Equivocal (borderline RBC, no clear xanthochromia) | CTA to evaluate for aneurysm. Clinical correlation and shared decision-making. |
| 5 | CTA: Identify causative aneurysm | If aneurysm found → neurosurgical/neurointerventional consultation → treatment planning. If CTA negative → DSA (step 6). |
| 6 | DSA (digital subtraction angiography): Gold standard | If DSA negative → repeat DSA in 7–14 days (10–20% of aneurysms are missed on initial study). Consider MRI for non-aneurysmal causes. |
Clinical Relevance: How the Workup Has Evolved
- The old "CTA vs. LP" debate is largely settled. Modern multidetector CTA is fast, non-invasive, and >97% sensitive for aneurysms ≥3 mm, so it is now routinely obtained the moment SAH is confirmed and freely added in equivocal cases — it is no longer weighed against LP as an either/or controversy.
- The live decision today is LP vs. MRI for the CT-negative patient. High pretest probability → LP (most sensitive, plus CSF analysis for mimics). Moderate-to-low probability, or when LP is declined/contraindicated → MRI with FLAIR + susceptibility-weighted sequences as a non-invasive rule-out that also catches RCVS, CVT, and dissection.
- Caveats of a non-invasive (CTA/MRI-only) pathway: incidental unruptured aneurysms (~2–3% of adults) create management dilemmas, and small <3 mm aneurysms or a subtle fresh hemorrhage can still be missed — LP remains the single most sensitive test for blood breakdown products.
- AHA 2023 position: LP remains the recommended next step after a negative CT in patients presenting >6 hours (Class 1, LOE B-NR); CTA is recommended to identify the source once SAH is confirmed. MRI is a reasonable non-invasive adjunct/alternative but is not a formal guideline replacement for LP.
6. Aneurysm Identification
6.1 CT Angiography (CTA)
CTA is the first-line study for identifying the source of hemorrhage once SAH is confirmed. Modern multidetector CTA has sensitivity >97% and specificity >99% for aneurysms ≥3 mm. It provides rapid, noninvasive assessment of aneurysm location, size, morphology (neck width, dome-to-neck ratio), and relationship to branch vessels — all critical for treatment planning.
6.2 Digital Subtraction Angiography (DSA)
DSA remains the gold standard for cerebral vascular imaging. It is indicated when: CTA is negative despite confirmed SAH, CTA findings are equivocal, endovascular treatment is planned (diagnostic + therapeutic in one session), or detailed hemodynamic assessment is needed. The procedure carries a small but real risk of complications (~0.5% transient neurological deficit, ~0.1% permanent deficit).
6.3 Negative Angiography
In approximately 15–20% of confirmed SAH cases, initial CTA and DSA fail to identify a causative lesion. Approximately half of these are perimesencephalic SAH (see Section 7). For the remaining cases, repeat DSA at 7–14 days is recommended, as aneurysm detection rates increase by 5–10% on repeat study. If repeat DSA is negative, MRI with MRA should be performed to evaluate for rare causes (dural AV fistula, spinal vascular malformation, occult AVM). If all imaging remains negative, the prognosis is generally favorable.
7. Clinical & Radiographic Grading Scales
Grading scales serve two purposes: classifying clinical severity (Hunt-Hess, WFNS) to guide treatment urgency and prognostication, and predicting vasospasm risk (modified Fisher) to guide monitoring intensity.
7.1 Hunt-Hess Scale
| Grade | Clinical Description | Approximate Mortality |
|---|---|---|
| I | Asymptomatic or mild headache, slight nuchal rigidity | ~1–5% |
| II | Moderate to severe headache, nuchal rigidity, no neurological deficit other than cranial nerve palsy | ~5–10% |
| III | Drowsy, confused, or mild focal deficit | ~15–20% |
| IV | Stuporous, moderate to severe hemiparesis, possible early decerebrate rigidity | ~30–40% |
| V | Deep coma, decerebrate rigidity, moribund appearance | ~50–70% |
7.2 World Federation of Neurological Surgeons (WFNS) Scale
| Grade | GCS | Motor Deficit |
|---|---|---|
| I | 15 | Absent |
| II | 13–14 | Absent |
| III | 13–14 | Present |
| IV | 7–12 | Present or absent |
| V | 3–6 | Present or absent |
The WFNS scale is preferred over Hunt-Hess in clinical trials and guidelines because it uses the more objective and reproducible GCS rather than subjective descriptions. Grades I–III are considered "good grade" and grades IV–V "poor grade." The AHA 2023 guidelines recommend using WFNS for standardized grading.
7.3 Modified Fisher Scale
| Grade | CT Appearance | Vasospasm Risk |
|---|---|---|
| 0 | No SAH or IVH | ~0% |
| 1 | Thin SAH, no IVH | ~24% |
| 2 | Thin SAH with IVH | ~33% |
| 3 | Thick SAH, no IVH | ~33% |
| 4 | Thick SAH with IVH | ~40% |
"Thick" SAH is defined as a clot ≥1 mm filling a cistern or fissure. The modified Fisher scale is the standard tool for predicting symptomatic vasospasm and guides the intensity of monitoring during the DCI risk window (days 4–14). Patients with modified Fisher 3–4 require the most aggressive surveillance.
Clinical Relevance: Grading in Practice
- Document both clinical and radiographic grades on admission: WFNS grade (for clinical severity) + modified Fisher grade (for vasospasm risk). Both are required for prognostication and treatment planning.
- Grade before sedation: Clinical grade should be assessed before administration of sedatives or paralytics whenever possible. If the patient is intubated and sedated, WFNS grade should be reassessed after sedation is reduced.
- Grade can improve: Poor-grade patients may improve significantly after EVD placement (hydrocephalus treatment), seizure treatment, or correction of metabolic derangements. Always reassess clinical grade after treating reversible confounders.
8. Perimesencephalic & Non-Aneurysmal SAH
8.1 Perimesencephalic SAH
Perimesencephalic SAH (pmSAH) accounts for approximately 10% of all spontaneous SAH and 50–65% of SAH cases with negative angiography. It has a characteristically benign course — rebleeding is exceedingly rare, symptomatic vasospasm occurs in <5%, and long-term outcomes are excellent. The presumed etiology is venous or perforator hemorrhage rather than arterial rupture.
Diagnostic criteria (all must be present):
- Blood centered immediately anterior to the midbrain (prepontine/interpeduncular cistern)
- No extension to the lateral Sylvian fissures (mild basal Sylvian extension is acceptable)
- No complete filling of the anterior interhemispheric fissure
- No frank intraventricular hemorrhage (though trace blood layering in third/fourth ventricles is acceptable)
- Negative CTA and/or DSA for aneurysm
If all radiologic criteria are met and CTA is negative, the AHA 2023 guidelines note there is equipoise regarding whether DSA is additionally needed. Many experts consider high-quality CTA sufficient to exclude aneurysm in classic perimesencephalic patterns. If the CT pattern does NOT meet the strict perimesencephalic criteria, DSA is recommended even if CTA is negative.
8.2 Other Non-Aneurysmal Causes
| Cause | Key Features | Diagnostic Clue |
|---|---|---|
| Arteriovenous malformation (AVM) | Parenchymal + subarachnoid blood. Younger patients. May present with seizures. | CTA/MRA shows nidus with feeding arteries and draining veins. DSA defines angioarchitecture. |
| Dural arteriovenous fistula (dAVF) | Cortical SAH pattern (convexity). May cause pulsatile tinnitus, proptosis, or cranial nerve palsies. | DSA is required — CTA often misses dAVFs. Look for early-draining cortical veins. |
| Reversible cerebral vasoconstriction syndrome (RCVS) | Convexity SAH. Thunderclap headache (often recurrent). Triggers: postpartum, serotonergics, cannabis, sympathomimetics. | "Sausaging" of cerebral arteries on CTA/MRA. Resolves over 1–3 months. May be complicated by ischemic stroke or hemorrhage. |
| Cerebral venous thrombosis (CVT) | Convexity or parasagittal SAH. Headache, seizures, papilledema. Risk factors: OCP, pregnancy, thrombophilia. | CT/MR venography shows thrombus in dural sinuses. "Empty delta sign" on contrast CT. |
| Spinal vascular malformation | Superficial siderosis, myelopathy, or radiculopathy. Recurrent SAH with negative intracranial imaging. | Spinal MRI with contrast. Spinal DSA for definitive diagnosis. |
| Mycotic aneurysm (infectious) | Distal branch aneurysms. History of endocarditis, IV drug use, or dental procedures. | Distal MCA or PCA branch aneurysms on CTA/DSA. Blood cultures positive. Echocardiography shows vegetations. |
| Coagulopathy/anticoagulant-related | Variable SAH patterns. History of anticoagulant or antiplatelet use. Thrombocytopenia. | INR, PT/aPTT, platelet count. Correct coagulopathy. Often no identifiable structural lesion. |
| Cerebral amyloid angiopathy (CAA) | Convexity SAH in elderly. Associated with lobar ICH and superficial siderosis. | MRI shows cortical superficial siderosis, lobar microbleeds. No aneurysm on CTA/DSA. |
| Cocaine/sympathomimetic-related | SAH in younger patients with recent drug use. May cause vasospasm independent of SAH. | Urine toxicology. CTA may show vasospasm without structural lesion. Aneurysm must still be excluded. |
9. Immediate Post-Diagnosis Management
Once SAH is diagnosed, the following actions should occur simultaneously or in rapid sequence:
| Priority | Action | AHA 2023 |
|---|---|---|
| 1. Secure airway | Intubate if GCS ≤8 or unable to protect airway. Use rapid sequence induction to blunt ICP rise. Avoid succinylcholine if hyperkalemia suspected. | Class 1 |
| 2. Blood pressure | SBP <160 mmHg before aneurysm securing. IV nicardipine, clevidipine, or labetalol. Avoid nitroprusside (increases ICP). | Class 2a, LOE B-NR |
| 3. Identify source | CTA immediately (can be performed with initial CT). If positive, consult neurosurgery/neurointerventional for treatment planning. | Class 1, LOE B-NR |
| 4. Treat hydrocephalus | If acute hydrocephalus with clinical deterioration → EVD placement. Do not delay. | Class 1, LOE B-NR |
| 5. Prevent rebleeding | Short-course TXA (≤72h) if aneurysm securing will be delayed. Start nimodipine 60 mg PO q4h × 21 days. | TXA: Class 2a. Nimodipine: Class 1. |
| 6. Transfer if needed | If at non-CSC, arrange emergent transfer to high-volume center (≥35 aSAH cases/year). Initiate BP control and TXA before transfer. | Class 1, LOE B-NR |
| 7. Grade & document | WFNS grade + modified Fisher grade. Reassess after EVD if placed. | Recommended |
| 8. Admit to neuro-ICU | ICU-level monitoring. Telemetry, arterial line, serial neurological assessments. | Class 1, LOE B-NR |
References
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- Perry JJ, et al. Clinical decision rules to rule out subarachnoid hemorrhage for acute headache. JAMA. 2013;310(12):1248–1255.
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- Treggiari MM, et al. Guidelines for the Neurocritical Care Management of Aneurysmal Subarachnoid Hemorrhage. Neurocrit Care. 2023;39(1):1–28.
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