Trauma or aneurysm/AVM rupture can lead to bleeding into the subarachnoid space, which exists between the arachnoid membrane and the pia mater.
Trauma is the single most common overall cause of SAH.
The most common cause of non-traumatic SAH is rupture of a cerebral aneurysm. Aneurysms come in all shapes and sizes e.g. fusiform (may have atherosclerotic areas within), saccular/berry (deteriorated tunica media), and mycotic (from infected emboli in patients with infective endocarditis).
Arteriovenous malformations (AVM) can lead to SAH in 5-10% of cases.
Vasospasm occurs days following SAH and is due to blood breakdown products. It is a major cause of morbidity and mortality in patients with SAH. Thus, subarachnoid hemorrhage is treated with nimodipine (a calcium channel blocker) to prevent this.
Patients classically present with the ‘worst headache of my life’. This complaint is almost pathognomonic when paired with a correlating history. Other clinical manifestations include change in the level of consciousness and meningismus from subarachnoid blood irritating the meninges.
Noncontrast head CT is the best initial test to look for bleeding in the subarachnoid space. It allows for diagnosis in >90% of cases within 24 hours of initial bleeding.
If CT is negative but SAH is still suspected, a lumbar puncture could be performed to look for blood in the cerebrospinal fluid (CSF), which manifests as xanthochromia. Xanthochromia is described as a yellow tint to the CSF, which occurs due to bilirubin from blood breakdown products.
Digital Subtraction Angiography (DSA) is performed to determine the exact etiology and location of bleeding (e.g. location of aneurysm). CT angiography (CTA) may be utilized if initial head CT were equivocal/non-confirmatory.
Definitive treatment is neurosurgery with either open surgical clipping or endovascular coiling depending on various patient factors. If hydrocephalus is present, the patient may require an external ventricular drain or ventriculoperitoneal shunt to alleviate the intracranial pressure. Also remember to reverse any anticoagulation therapy the patient may previously have been taking.
After establishing intravenous access for fluid resuscitation and pharmacologic management, the clinician should aim to maintain blood pressure below 160 mm Hg systolic. This helps prevent rebleeding. Beta blockers are usually preferred unless contraindications exist.
The addition of blood into the subarachnoid space causes intracranial pressure (ICP) to increase. Over time, an elevated ICP may lead to cranial nerve palsies or even herniation. Thus methods such as IV mannitol, hyperventilation, 30° elevation of the head of the bed, and stool softeners may be employed to control ICP.
Nimodipine is a calcium channel blocker given orally that helps prevent vasospasm after SAH. Vasospasm is a dangerous complication of SAH that may lead to ischemic stroke. Seizure prophylaxis may also be considered; however, this is not routine.
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