I. Epidemiology and Incidence

Aneurysmal subarachnoid hemorrhage (SAH) occurs worldwide at approximately 6–10 per 100,000 person-years with high early mortality. Incidence and outcomes vary by region, age, and sex, impacting critical care resource needs.

• Incidence: 6–10 per 100,000 person-years globally; highest in Japan and Finland, lowest in North America and Western Europe.
• Prehospital mortality: 22–26%; inpatient mortality: 13–20%.
• Demographics: Female to male ratio is approximately 1.6:1; peak age is 40–60 years; older age predicts worse outcome.
• Resource impact: Requires rapid imaging, ICU monitoring, and specialized neurocritical care teams.

II. Risk Factors

SAH risk is driven by modifiable (hypertension, smoking, substances), nonmodifiable (age, sex, genetics), and aneurysm-specific factors (size, location, morphology).

Modifiable Risk Factors

• Hypertension: Dose-dependent risk for aneurysm formation, growth, and rupture.
• Tobacco use: Current and former smokers; risk is synergistic with hypertension.
• Alcohol and cocaine: Acute hypertensive surges increase rupture risk.

Nonmodifiable Risk Factors

• Age and female sex: Post-menopausal risk increases.
• Family history: ≥2 first-degree relatives leads to approximately 12% aneurysm prevalence.
• Genetic syndromes: Autosomal Dominant Polycystic Kidney Disease (ADPKD), Ehlers-Danlos syndrome, Marfan syndrome.

Aneurysm-Specific Risk Factors

• Size: Greater than 7 mm (posterior circulation lesions carry higher risk).
• Morphology: Irregular dome, daughter sacs, multiplicity of aneurysms.

III. Pathophysiology of Aneurysm Formation and Rupture

Aneurysms develop at arterial bifurcations under chronic hemodynamic stress, weakened by endothelial dysfunction and extracellular matrix degradation. Rupture triggers abrupt intracranial pressure (ICP) rise and secondary injury cascades.

• Hemodynamic stress and wall shear forces at Circle of Willis bifurcations lead to endothelial injury.
• Endothelial dysfunction promotes Matrix Metalloproteinase (MMP) activation, extracellular matrix breakdown, and vessel wall weakening.
• Rupture: Blood enters the subarachnoid space, causing a rapid increase in ICP and a decrease in Cerebral Perfusion Pressure (CPP).
• Monro–Kellie dynamics: Compensatory displacement of cerebrospinal fluid (CSF) and venous blood fails, leading to critical ICP elevation.
• Secondary injury mechanisms include excitotoxicity (glutamate-mediated), neuroinflammation, oxidative stress, and microthrombosis.

IV. Clinical Presentation

SAH classically presents with a sudden “thunderclap” headache, meningeal irritation, variable focal deficits, and altered mental status. A systemic catecholamine surge may mimic cardiac or pulmonary events.

• Thunderclap headache: Reaches peak intensity within seconds; often described as the “worst headache of life.” Differential diagnoses include other headache syndromes, meningitis, and intracerebral hemorrhage.
• Meningeal signs: Nuchal rigidity, photophobia, and vomiting. These may be absent in comatose or elderly patients.
• Focal deficits: Hemiparesis, aphasia, cranial nerve palsies (e.g., oculomotor nerve palsy in posterior communicating artery aneurysm).
• Altered consciousness: Ranges from mild confusion to coma; correlates with Hunt–Hess and World Federation of Neurosurgical Societies (WFNS) grades.
• Systemic manifestations: Catecholamine surge can lead to arrhythmias, neurogenic stunned myocardium (Takotsubo cardiomyopathy), and pulmonary edema.

V. Common Complications

Early and delayed complications—including rebleeding, vasospasm/Delayed Cerebral Ischemia (DCI), hydrocephalus, seizures, and hyponatremia—drive morbidity. Timely recognition and intervention optimize outcomes.

• Early rebleeding: Highest risk in the first 6–12 hours. Prevention includes systolic blood pressure (SBP) control (target <160 mmHg) and securing the aneurysm (coiling or clipping) within 24 hours.
• Cerebral vasospasm/DCI: Onset typically between days 3–14 post-SAH. Caused by blood breakdown products, impaired autoregulation, and microthrombosis. Monitored with Transcranial Doppler (TCD) ultrasound or angiography.
• Hydrocephalus: Acute hydrocephalus (developing >48 hours post-SAH) results from CSF flow obstruction and requires an external ventricular drain (EVD). Chronic hydrocephalus may necessitate a permanent shunt.
• Seizures: Occur in approximately 5–10% of patients. Prophylaxis is typically reserved for high-risk cases (e.g., large hemorrhage, focal deficits). Routine long-term antiepileptic drugs (AEDs) are generally avoided.
• Electrolyte disturbances: Hyponatremia is common, often due to Cerebral Salt Wasting (CSW) or Syndrome of Inappropriate Antidiuretic Hormone (SIADH) secretion. Distinguish by volume status and manage with isotonic fluids or fludrocortisone as appropriate.