Subarachnoid Hemorrhage

complete reference · Hunt-Hess/Fisher · secure aneurysm · nimodipine · vasospasm/DCI · Full Card

Symptoms / Associated Sx

• Abrupt, severe thunderclap headache — maximal within seconds to a minute, classically "the worst headache of my life." Often with transient loss of consciousness, vomiting, meningismus (neck stiffness, photophobia developing over hours as blood irritates meninges). A third nerve palsy (down-and-out eye, dilated pupil) suggests a posterior communicating artery aneurysm.

• Sentinel headache — a warning leak in the days-to-weeks before a major rupture; an unusually severe sudden headache should never be dismissed.

• Grade severity with Hunt-Hess (clinical) and the modified Fisher scale (blood burden on CT — predicts vasospasm).

Neg

• Pt denies a gradual crescendo headache building over hours with prior identical episodes — argues against migraine/tension (SAH is instantaneous-onset; "thunderclap" is the discriminator — but image, do not assume)

• No fever or rash preceding — argues against meningitis as the primary process (though chemical meningismus from SAH overlaps; CT/LP separate them)

• No purely positional/cough- or exertion-only headache that resolves when supine — argues against low-pressure/CSF-leak headache (different mechanism, no acute danger)

• Not recurrent stereotyped thunderclaps over days with diffuse vasoconstriction — would suggest RCVS instead (angiography shows beading; management differs)

Social History (SHx)

• Smoking (the strongest modifiable risk), hypertension, heavy alcohol, cocaine/stimulant use.

• Family history of aneurysm or SAH (≥2 first-degree relatives warrants screening); polycystic kidney disease, connective tissue disorders.

Main Etiology

• Ruptured saccular (berry) aneurysm accounts for ~80% of non-traumatic SAH — typically at circle-of-Willis branch points. Perimesencephalic non-aneurysmal hemorrhage (benign, venous, normal angiogram). Arteriovenous malformation. Less common: mycotic aneurysm, vasculitis, reversible cerebral vasoconstriction syndrome, dural fistula. Trauma is the overall most common cause but is a separate clinical context.

RF

• Modifiable: smoking (dominant), hypertension, cocaine/sympathomimetics, heavy alcohol.

• Non-modifiable: family history, autosomal-dominant PCKD, connective tissue disease (Ehlers-Danlos type IV, Marfan), female sex, larger/posterior-circulation aneurysms.

Data

• Non-contrast head CT (sensitivity approaches 100% within 6h of onset; blood in basal cisterns/sulci — sensitivity falls with time as blood clears)

• Lumbar puncture if CT negative but suspicion persists (xanthochromia from RBC breakdown, and RBC count that does not clear tube 1 → tube 4 — distinguishes true SAH from traumatic tap; xanthochromia takes ~6–12h to develop)

• CT angiography (then digital subtraction angiography) (locates and characterizes the aneurysm to guide clipping vs coiling)

• ECG and troponin (neurogenic stress cardiomyopathy/stunned myocardium, ST/T changes, QT prolongation)

• Serial sodium (hyponatremia from cerebral salt wasting or SIADH — common, affects volume management); CBC, coags, glucose

• Transcranial Dopplers (serial — rising velocities flag developing vasospasm during the day 4–14 window)

DDx

Migraine / tension headache (gradual onset, prior identical, no thunderclap) · meningitis (fever, gradual, no instantaneous peak) · RCVS (recurrent thunderclaps, segmental vasoconstriction, often postpartum/drug-triggered) · cervical artery dissection (neck pain, Horner, can cause SAH) · pituitary apoplexy (sudden headache + visual loss + endocrine collapse) · cerebral venous thrombosis (subacute headache, prothrombotic, venous pattern)

Home Meds

• Stop and reverse any anticoagulant/antiplatelet.

• Hold stimulants/sympathomimetics.

• Start nimodipine; continue essential home meds compatible with BP goals.

Plan

Consults

• Neurosurgery and neuro-interventional — emergent, together: the aneurysm must be secured (coil or clip) as early as possible.

• Neurology / neurocritical care — vasospasm and DCI management.

• ICU — SAH is an ICU diagnosis; ward involvement is post-stabilization or for low-grade perimesencephalic bleeds with a normal angiogram.

Secure the aneurysm

• Endovascular coiling or surgical clipping within 24h — rebleeding risk is highest in the first 24–72h and is frequently fatal (ISAT favored coiling where anatomy permits). Until secured, this is the overriding priority.

Neuroprotection / BP

• Nimodipine (Nimotop) 60 mg PO/NG q4h for 21 days — reduces delayed cerebral ischemia and improves outcomes (it does not reduce angiographic vasospasm — the benefit is neuroprotective). Hold/dose-adjust if it drops BP excessively (split to 30 mg q2h).

• Before the aneurysm is secured: keep SBP <140–160 to limit rebleeding (nicardipine/Cardene gtt); analgesia for pain-driven surges. After securing: liberalize BP and maintain euvolemia to prevent DCI.

Vasospasm / DCI (days 4–14)

• Serial neuro exams + transcranial Dopplers; new focal deficit or decline in this window is delayed cerebral ischemia until proven otherwise.

• Treat with induced hypertension (maintain euvolemia, raise BP with vasopressors as needed); endovascular rescue (intra-arterial vasodilators or angioplasty) for refractory cases. Avoid prophylactic hypervolemia ("triple-H" is outdated — euvolemia + induced HTN is current).

Complications / supportive

• Acute hydrocephalus → external ventricular drain. Seizures → treat (levetiracetam/Keppra); no routine prophylaxis. Monitor sodium daily and distinguish cerebral salt wasting (hypovolemic — replace salt/volume) from SIADH (euvolemic — caution with fluid restriction in SAH given DCI risk).

• Analgesia, antiemetics, stool softeners (avoid Valsalva), bed rest until secured, VTE prophylaxis with SCDs (chemical prophylaxis after the aneurysm is secured).

Always

• PT / OT / SLP eval and treat — once stabilized and aneurysm secured.

• Trend: hourly neuro checks; daily transcranial Dopplers through the vasospasm window; daily sodium and volume status; ECG/troponin if cardiac changes.

• Escalation triggers: any sudden re-deterioration before securing → rebleed, emergent angiography/surgery · new deficit days 4–14 → DCI, induced HTN + endovascular rescue · declining LOC + enlarging ventricles → EVD for hydrocephalus · GCS drop/airway → intubate.

• Discharge checklist: complete the 21-day nimodipine (Nimotop) course · BP control · smoking cessation (critical — reduces recurrence and new aneurysm formation) · neurosurgery + neuro-IR follow-up with surveillance imaging · screening discussion for first-degree relatives if familial/PCKD · headache and return precautions (recurrent thunderclap → 911).

Red Flags — ICU / Neurosurgery

• Unsecured aneurysm — rebleeding is the early killer; secure within 24h, keep SBP <140–160 until then.
• Acute hydrocephalus (declining LOC, sluggish pupils, enlarging ventricles) → EVD.
• Delayed cerebral ischemia / vasospasm days 4–14 (new deficit, rising TCD velocities) → induced HTN, endovascular rescue.
• Neurogenic stunned myocardium / pulmonary edema → ICU hemodynamic support.
• Hunt-Hess IV–V / GCS drop → intubation, neurocritical care.

Senior IM Resident Pearls

• CT within 6 hours is near-perfect; after that, do the LP. A negative CT beyond 6h does not exclude SAH — xanthochromia and a non-clearing RBC count on LP are how you avoid missing a sentinel bleed.
• The whole game early is preventing the rebleed: secure the aneurysm fast and keep SBP controlled. Rebleeding in the first days carries very high mortality.
• Nimodipine helps the brain, not the artery. It reduces delayed cerebral ischemia and improves outcomes without changing angiographic vasospasm — give the full 21 days, the benefit is neuroprotective.
• Days 4–14 is the vasospasm/DCI window. Any new deficit in this period is delayed cerebral ischemia until proven otherwise — escalate, don't observe.
• "Triple-H" is dead. Current management is euvolemia plus induced hypertension; prophylactic hypervolemia and hemodilution caused harm.
• Watch the sodium. Cerebral salt wasting (hypovolemic) and SIADH (euvolemic) both cause hyponatremia but need opposite fluid strategies — and over-restricting in SAH worsens DCI.
• The ECG will scare you. Neurogenic stunned myocardium produces ST changes, troponin bumps, and reduced EF that mimic ACS — don't anticoagulate or cath reflexively; it usually recovers.
• Common mistake: labeling a perimesencephalic, angiogram-negative bleed as missed pathology — it's benign with an excellent prognosis, but still requires a quality angiogram to confirm no aneurysm.