Subarachnoid Hemorrhage & Cerebral Aneurysms
Catch the thunderclap, secure the aneurysm, then outlast the complication clock
Overview and Presentation
Causes. Trauma is the most common cause of subarachnoid blood overall, but about 85% of nontraumatic subarachnoid hemorrhage (SAH) comes from a ruptured saccular ("berry") aneurysm. These aneurysms form at arterial branch points of the circle of Willis, where the media is deficient, and most lie in the anterior circulation: the anterior communicating artery (most common), the posterior communicating artery (PComm), and the MCA bifurcation.
Thunderclap headache. Rupture produces a sudden, severe headache that peaks within about a minute, typically described as the worst of the patient's life, often with brief loss of consciousness, vomiting, and photophobia. Meningismus develops over hours as blood irritates the meninges, so a supple neck early does not exclude SAH. Focal signs, seizures, or coma may follow.
Warning signs before rupture. A smaller sentinel headache from a minor leak often precedes rupture by days to weeks. An enlarging PComm aneurysm can compress CN III and dilate the pupil, and an anterior communicating artery aneurysm can press on the optic chiasm and cause a bitemporal field defect.
Diagnosis
- Noncontrast head CThyperdense blood in the basal cisterns and sylvian fissures; nearly 100% sensitive within 6 hours of onset, with sensitivity falling over the following days
- Lumbar puncture if CT is negative and suspicion persistsespecially beyond 6 hours: xanthochromia and RBC counts that do not fall from the first to the last tube, usually with a raised opening pressure
- CT angiography once SAH is confirmedlocalizes the aneurysm and plans treatment
- Catheter digital subtraction angiographythe gold standard when CTA is negative or more anatomic detail is needed
Reading the CSF. Xanthochromia is the yellow tint of bilirubin produced as red cells lyse within the CSF; it becomes detectable about 12 hours after the bleed and persists for up to about 2 weeks. A traumatic tap instead shows red cells that clear across successive tubes and no xanthochromia when the sample is processed promptly.
Acute Management
Secure the aneurysm early. Patients are admitted to a neurocritical care unit, and the ruptured aneurysm is treated as early as feasible, ideally within 24 hours, because early securing is the main defense against rebleeding. Endovascular coiling is used when anatomy allows; in the ISAT trial it gave better 1-year functional outcomes than clipping for aneurysms suitable for either approach. Microsurgical clipping is chosen for some MCA aneurysms and when a large hematoma needs evacuation.
Before the aneurysm is secured. Lower systolic blood pressure to below 160 mm Hg with a titratable agent (nicardipine, clevidipine, or labetalol) and treat pain. Reverse anticoagulation immediately: 4-factor prothrombin complex concentrate plus IV vitamin K for warfarin, idarucizumab for dabigatran, and 4-factor PCC for factor Xa inhibitors (andexanet alfa was withdrawn from the US market in December 2025).
Nimodipine and supportive care. Oral nimodipine 60 mg every 4 hours for 21 days improves neurologic outcome, although it does not reliably prevent angiographic vasospasm; the main side effect is hypotension. Maintain euvolemia: prophylactic hypervolemia is no longer used, and hypovolemia must be avoided. Treat seizures promptly; if prophylaxis is used it is brief, and phenytoin is avoided because it has been linked to worse outcomes.
Complications by Timing
| Complication | Timing | Clues | Management |
|---|---|---|---|
| Rebleeding | Highest in the first 24 hours | Abrupt worsening of headache and consciousness; high mortality | Early securing, blood pressure control |
| Acute hydrocephalus | Hours to days | Declining consciousness; enlarging ventricles on CT | External ventricular drain; shunt if chronic |
| Vasospasm and delayed cerebral ischemia | Days 3–14, peak around days 7–10 | New focal deficit or confusion; rising transcranial Doppler velocities | Induced hypertension, then intra-arterial vasodilators or angioplasty |
| Hyponatremia | First 2 weeks | Cerebral salt wasting or SIADH | Saline; avoid fluid restriction |
| Neurogenic stunned myocardium | Early | Troponin leak, deep T-wave inversions, QT prolongation, arrhythmias, takotsubo-like wall motion, neurogenic pulmonary edema | Supportive; usually reversible |
Hydrocephalus. Blood obstructs CSF outflow and resorption. An external ventricular drain relieves pressure and monitors ICP; lumbar drainage is avoided when flow is obstructed because it risks herniation. Chronic communicating hydrocephalus may later require a ventriculoperitoneal shunt.
Delayed cerebral ischemia. Vasospasm of large intracranial arteries is monitored with daily transcranial Doppler; CTA with perfusion imaging or angiography confirms it. In a euvolemic patient, blood pressure is raised with vasopressors, and refractory cases receive intra-arterial vasodilators or balloon angioplasty. Thrombolysis is contraindicated.
Hyponatremia. Both disorders show low serum osmolality, concentrated urine, and high urine sodium; volume status separates them.
| Feature | Cerebral salt wasting | SIADH |
|---|---|---|
| Mechanism | Renal salt loss (natriuresis) | Excess ADH, water retention |
| Volume status | Hypovolemic: orthostasis, rising hematocrit and BUN | Euvolemic |
| Urine output | High | Low to normal |
| Treatment after SAH | Isotonic or hypertonic saline, with or without fludrocortisone | Saline as needed; fluid restriction avoided |
Fluid restriction or vaptans after SAH deepen hypovolemia and worsen delayed cerebral ischemia; replace salt and volume instead.
Neurogenic stunned myocardium can mimic an acute coronary syndrome, but anticoagulation, antiplatelet loading, and thrombolysis are dangerous with an unsecured aneurysm.
Unruptured Aneurysms and Screening
Risk factors. Smoking and hypertension are the key modifiable risk factors for aneurysm formation, growth, and rupture. Others include ADPKD, vascular Ehlers-Danlos syndrome, coarctation of the aorta, fibromuscular dysplasia, and a family history of aneurysm or SAH.
Who to screen. Noninvasive screening with MRA (or CTA) is offered to patients with ADPKD who have a family history of aneurysm or SAH and to people with two or more affected first-degree relatives. Noncontrast CT and LP detect blood, not unruptured aneurysms.
Management. All patients should stop smoking and control blood pressure. The decision to coil or clip an unruptured aneurysm weighs its size and growth, posterior circulation location, symptoms such as a new CN III palsy (which calls for urgent treatment), and patient age and comorbidity.