Last reviewed: March 2026
Contents
MDM Templates
SAH — Confirmed
Patient presents with acute onset severe headache reaching maximal intensity within seconds to minutes. CT head demonstrates subarachnoid hemorrhage. This is a neurosurgical emergency.
Priorities are blood pressure control, prevention of rebleeding, and identification of the bleeding source. Aneurysmal rupture is the most common nontraumatic cause and carries high mortality if it rebleeds. Not consistent with primary intracerebral hemorrhage (blood in subarachnoid space, not parenchyma), migraine (acute thunderclap onset with blood on imaging), or hypertensive emergency without end-organ damage.
If neurosurgery consulted: Neurosurgery consulted regarding CTA findings, Hunt-Hess grade, and disposition for definitive management (clipping vs coiling).
Plan: Blood pressure controlled (SBP <160). Nimodipine 60 mg PO every 4 hours initiated for vasospasm prevention. Neurosurgery consulted. Admit to ICU.
Thunderclap Headache — SAH Workup
Patient presents with acute onset severe headache reaching maximal intensity within seconds to minutes. This is a thunderclap headache pattern requiring evaluation for subarachnoid hemorrhage. Patient is neurologically intact with no focal deficits.
Thunderclap headache has a broad differential but the priority is excluding SAH given its mortality if missed. Also considered are cerebral venous sinus thrombosis, reversible cerebral vasoconstriction syndrome (RCVS), pituitary apoplexy, and cervical artery dissection. Migraine and tension headache do not present with thunderclap onset.
If CT negative and LP performed: CT head negative for hemorrhage. LP performed — CSF clear, no xanthochromia, no RBCs or RBCs clearing across tubes consistent with traumatic tap. SAH effectively excluded.
If CT negative and CTA performed instead of LP: CT head negative for hemorrhage. CTA negative for aneurysm. Given negative CT within 6 hours of onset and negative CTA, SAH effectively excluded per Ottawa SAH rule validation data.
Plan: Discharge with close follow-up. Return immediately for recurrent thunderclap headache, worst headache of life, neck stiffness, vision changes, or focal weakness.
Clinical Education
Approach to Suspected SAH
The question is always: does this headache need a SAH workup? The classic teaching is “worst headache of my life,” but many patients with SAH describe it as severe, not necessarily the worst ever. The key feature is thunderclap onset — reaching maximal intensity within seconds to minutes. A headache that builds gradually over hours is not thunderclap.[1]
The Ottawa SAH Rule helps identify which patients with acute headache need investigation: age ≥40, neck pain or stiffness, witnessed LOC, onset during exertion, thunderclap onset (peak intensity within 1 second), or limited neck flexion on exam. If none are present, SAH is effectively ruled out clinically. Sensitivity is 100% (95% CI 97–100%) for SAH.[2]
CT Sensitivity and the LP Question
CT within 6 hours of onset is extremely sensitive. Perry et al. (2011) demonstrated 100% sensitivity (95% CI 97–100%) for CT performed within 6 hours on a third-generation scanner, interpreted by an attending radiologist. After 6 hours, sensitivity drops — approximately 98% at 6–12 hours, falling further with time as blood is reabsorbed.[3]
The CT-alone vs CT+LP debate: If CT is negative within 6 hours on a modern scanner with quality radiology reads, many centers now accept CT + CTA as sufficient to rule out SAH without LP. The argument is that the few cases CT misses at 6 hours would be perimesencephalic bleeds with benign prognosis, and CTA would catch any aneurysm. This is increasingly accepted practice but not yet universal — know your institution’s protocol.[4]
If CT is beyond 6 hours or equivocal, LP is still indicated. Don’t skip it because the patient doesn’t want one.
LP Interpretation
Xanthochromia is the key finding. It takes approximately 12 hours for RBCs in the CSF to lyse and produce xanthochromia. An LP performed <12 hours after symptom onset may be negative for xanthochromia even in true SAH — in this window you’re relying on RBC count and tube-to-tube clearance.
Traumatic tap vs SAH: Classic teaching is that RBCs clear from tube 1 to tube 4 in a traumatic tap but remain constant in SAH. In practice, this is unreliable. A cell count ratio (tube 4 / tube 1) <0.25 suggests traumatic tap. If there’s any ambiguity, send for xanthochromia (visual inspection or spectrophotometry depending on your lab) and manage conservatively until results return.
Negative LP effectively rules out SAH when performed >12 hours after onset (allowing time for xanthochromia to develop). Clear CSF with no xanthochromia and no RBCs is as definitive as it gets.
Hunt-Hess and Fisher Grading
| Hunt-Hess Grade | Clinical Presentation |
| 1 | Asymptomatic or mild headache, slight nuchal rigidity |
| 2 | Moderate to severe headache, nuchal rigidity, no neurologic deficit (other than cranial nerve palsy) |
| 3 | Drowsy, confused, mild focal deficit |
| 4 | Stupor, moderate to severe hemiparesis |
| 5 | Deep coma, decerebrate posturing, moribund |
Modified Fisher Scale predicts vasospasm risk based on CT: Grade 0 (no SAH or IVH) → low risk. Grade 1 (thin SAH, no IVH) → low. Grade 2 (thin SAH with IVH) → moderate. Grade 3 (thick SAH, no IVH) → high. Grade 4 (thick SAH with IVH) → highest risk. “Thick” is ≥1 mm in vertical plane.[5]
Complications
Rebleeding is the most feared early complication — 4% in the first 24 hours, mortality >70%. Prevention: keep SBP <160 until the aneurysm is secured. Definitive treatment (clipping or coiling) should happen as early as possible, ideally within 24 hours.
Vasospasm peaks at days 4–14 after hemorrhage. Nimodipine 60 mg PO (or via NGT) every 4 hours is the standard prophylaxis — start within 48 hours of symptom onset and continue for 21 days. Never give nimodipine IV (can cause fatal hypotension). Nimodipine improves outcomes but does not actually prevent angiographic vasospasm — its benefit is likely neuroprotective.[6]
Hydrocephalus can be acute (obstructive, from intraventricular blood) or delayed (communicating, from impaired CSF absorption). Acute hydrocephalus with declining GCS requires emergent EVD placement.
Seizures occur in ~10% of SAH patients. Prophylactic AEDs are controversial — some centers give a brief course (levetiracetam for 3–7 days), others treat only if seizures occur.
Hyponatremia is common after SAH, usually from cerebral salt wasting (not SIADH). The distinction matters: cerebral salt wasting causes volume depletion and is treated with isotonic or hypertonic saline. SIADH causes euvolemia and is treated with fluid restriction — which is dangerous in SAH because hypovolemia worsens vasospasm.
Disposition
All confirmed SAH patients are admitted to the ICU. They need continuous monitoring, frequent neuro checks, and neurosurgical management for aneurysm securing. There is no outpatient management for confirmed aneurysmal SAH.
Transfer if no neurosurgery or interventional neuroradiology available. Start nimodipine and control BP before transfer. Ensure the patient has 2 IV access sites and intubation meds available for the transport.
SAH ruled out (negative CT + negative LP, or negative CT within 6 hours + negative CTA): Discharge with close follow-up. Consider outpatient MRA if there is strong clinical suspicion despite negative workup, or if there is a family history of aneurysmal disease.
References
- Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med. 2000;342(1):29-36. PubMed
- Perry JJ, Stiell IG, Sivilotti ML, et al. Clinical decision rules to rule out subarachnoid hemorrhage for acute headache. JAMA. 2013;310(12):1248-1255. PubMed
- Perry JJ, Stiell IG, Sivilotti ML, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage. BMJ. 2011;343:d4277. PubMed
- American College of Emergency Physicians. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute headache. Ann Emerg Med. 2019;74(4):e41-e74. PubMed
- Frontera JA, Claassen J, Schmidt JM, et al. Prediction of symptomatic vasospasm after subarachnoid hemorrhage: the modified Fisher scale. Neurosurgery. 2006;59(1):21-27. PubMed
- Dorhout Mees SM, Rinkel GJ, Feigin VL, et al. Calcium antagonists for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev. 2007;(3):CD000277. PubMed
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