Subarachnoid Hemorrhage

Etiology and Epidemiology

Intracranial aneurysm ruptures are responsible for approximately 80% of nontraumatic subarachnoid hemorrhage (SAH). Saccular aneurysms are the most common type and occur in regions of high mechanical wall shear stress like branch points (circle of Willis, etc.). Fifteen to 20% of patients with SAH have no aneurysm and typically have a perimesencephalic distribution of the clot. The source of hemorrhage is venous in these patients. Other causes of SAH include trauma (most common cause), intracranial and spinal arteriovenous malformation (AVM), hemorrhagic tumor, blood dyscrasias, amyloid angiopathy, moyamoya disease, and secondary leakage of blood from primary intraparenchymal hemorrhage.

Approximately 15-30% of patients die from their aneurysm rupture before reaching the hospital. Up to 25% of patients with an aneurysm have a second aneurysm. Between 0.5 and 1% of patients undergoing cerebral angiography for other reasons are incidentally found to have an aneurysm. The risk of aneurysm rupture in a person with no history of aneurysm rupture varies from 0.05-2% per year depending on the size and site of the aneurysm.

Risk factors for intracranial aneurysm include increasing age, female gender, hypertension, alcohol, smoking, and family history. Intracranial aneurysms are associated with fibromuscular dysplasia, autosomal dominant polycystic kidney disease, connective tissue disorders, congenitally anomalous vessels, AVMs, tumors, vasculitis, and infections.

Symptoms and Signs

Classically, the symptoms of an intracranial aneurysm rupture include “worst headache of life,” loss of consciousness, photophobia, meningismus, nausea, and vomiting. Only 10-15% of patients who complain of “worst headache of life” will have SAH. Sentinel headaches occur in approximately one half of patients before rupture, presumably caused by transient small leak of the aneurysm. Localized headache may occur from expansion of an aneurysm before rupture, requiring imaging to exclude this diagnosis even in the absence of blood in the cerebrospinal fluid. Expanding aneurysms can also cause focal neurologic deficits including visual field cuts, oculomotor paresis, and focal weakness. Classically, an aneurysm of the posterior communicating artery can cause third cranial nerve palsy with a dilated and relative fixed pupil. Differential diagnosis includes stroke, migraine, meningitis, and sinusitis.


  • Hydrocephalus can be either acute (20% of patients) or delayed. Acute hydrocephalus is related to amount of ventricular blood and usually appears within 3 days of the SAH, requiring immediate treatment. Delayed hydrocephalus occurs after 10 days and is related to amount of SAH.
  • Seizures occur acutely in 3-5% of patients. Fifteen percent of patients can develop epilepsy following an SAH, usually within the first 18 months.
  • Rebleeding occurs in up to 4-20% of patients with aneurysms.
  • Delayed cerebral ischemia is caused by vasospasm and usually occurs 5 days from the initial hemorrhage. Vasospasm can affect any or all of the major branches of the circle of Willis. Ischemic complications have been reported to occur in up to one third of patients, with the amount of blood on the initial head computed tomography (CT) correlating to the severity of the vasospasm.
  • Neurogenic pulmonary edema and syndrome of inappropriate secretion of antidiuretic hormone (SIADH) are potential systemic complications of SAH.
  • Overall mortality is high (one third to two thirds of cases). Most survivors have significant permanent disability.

Computed Tomography

A noncontrast head CT is the study of choice in the evaluation of a patient presenting with a severe headache in the emergency room setting. A noncontrast head CT is the fastest, easiest and most accurate test for detection of SAH. It has very high sensitivity (>96%) for the detection of SAH occurring within the last 24 hours. The sensitivity falls to 80% at 72 hours. Head CT is important for risk stratification (more blood = more complications), identification of the potential location of the aneurysm (where most blood is located), and detection of complications which can include hydrocephalus, mass, ischemia, and herniation. Occasionally, a noncontrast CT can identify a calcified aneurysm. The use of computed tomographic angiography (CTA) in the setting of acute SAH is evolving. CTA has a comparable sensitivity to digital subtraction angiography (DSA) for aneurysm detection, but a negative CTA requires follow-up DSA. Many surgeons will request DSA for preoperative assessment, limiting the practicality of CTA in the setting of acute SAH.

Possible Findings

  • Noncontrast CT
    • High attenuation (blood) within the cisterns, subarachnoid spaces, and ventricles can be subtle!
    • Look for predisposing causes: masses, trauma, and so on.
    • Complications including hydrocephalus, herniation, and infarction.
  • CTA
    • Abnormal outpouching of vessel representing aneurysm. Occasional calcified aneurysm.

Magnetic Resonance Imaging

The sensitivity of T1-weighted imaging(T1-WI) and T2-weighted imaging (T2-WI) sequences for acute SAH is low. Fluid attenuation inversion recovery (FLAIR) sequence imaging is critical for detection of subarachnoid blood. Magnetic resonance imaging (MRI) is more sensitive than CT to subacute SAH. MRI can also help identify the culprit aneurysm in a patient with multiple aneurysms by localizing blood by-products. Magnetic resonance angiography (MRA) can be useful for the detection of intracranial aneurysms; however, it is inferior to CTA and DSA.

Possible Findings

  • MRI
    • FLAIR: acute and subacute blood appears bright in the subarachnoid space.
    • Potential causes for SAH (other than aneurysm): tumors, AVMs, vasculitis, and infection.
    • Complications including hydrocephalus, herniation, and infarction.
  • MRA
    • Abnormal outpouching of vessel representing aneurysm.

Digital Subtraction Angiograohy

Four-vessel DSA is the gold standard in the evaluation of SAH. If the initial angiogram is negative, a repeat angiogram is performed to exclude the possibility of vasospasm that may have prevented the filling of the aneurysm.

Possible Challenges in Interpretation

  • Vascular loop versus aneurysm: a vascular loop has the same wash-in and wash-out as the parent vessel compared to the aneurysm which has different flow dynamics.
  • Infundibular dilatation versus aneurysm: typically occurs at the origin of the posterior communicating artery. Infundibular dilatation lacks an aneurysmal neck or irregularity. Infundibulum is tentlike or cone-shaped rather than saccular. Size of an infundibulum is less than 3 mm.
  • Multiple aneurysms found: correlate with prior head CT for localization of blood products. Look for adjacent vasospasm, most irregular aneurysm, largest aneurysm, and demonstration of contrast extravasation (rare).
  • Patients with a negative angiogram and blood localized anterior to the brainstem and adjacent areas such as the interpeduncular fossa and ambient cistern are thought to have a perimesencephalic hemorrhage, caused by venous bleeding. There should not be significant extension of blood into the Sylvian fissure or interhemispheric fissure. These patients tend to have a more benign course.