- Clinical science
Subarachnoid hemorrhage (SAH) refers to bleeding into the subarachnoid space. SAH most often results from head trauma, while nontraumatic SAH is most commonly due to the rupture of an aneurysm involving the circle of Willis. SAH typically presents with severe headache, nausea/vomiting, and/or acute loss of consciousness. A fresh intracranial hemorrhage appears hyperdense on a non-contrast CT scan, confirming diagnosis. CT angiography and lumbar puncture may be necessary for further evaluation. Treatment consists of carefully lowering blood pressure and measures to prevent cerebral vasospasm. Clipping or coiling of the bleeding aneurysm may be necessary to prevent potentially fatal rebleeding. SAH is associated with a high mortality as a result of frequent complications such as rebleeding and secondary ischemic strokes due to vasospasm.
- Traumatic: head trauma is the most common cause of SAH
Epidemiological data refers to the US, unless otherwise specified.
- May also lead to traumatic aneurysms
Ruptured aneurysm usually in the circle of Willis
- Berry aneurysm: (80% of cases of nontraumatic SAH)
- Fusiform aneurysm: low risk of bleeding
Mycotic aneurysm: low risk of bleeding
- Shape: mushroom-shaped
- Cause: septic embolisms (mostly due to bacterial endocarditis)
- Site: small, peripheral segments of cerebral vessels
- Ruptured arteriovenous malformation (AVM) (10% of cases of nontraumatic SAH)
- Others: cortical thrombosis, angioma, neoplasm, infection
- Ruptured aneurysm usually in the circle of Willis
- Triggers: most cases unknown, may be triggered by an acute rise in blood pressure (e.g., caffeine consumption, acute anger, physical exertion)
- Risk factors
World Federation of Neurological Surgeons grading
- Grade 1: asymptomatic, mild headache, and/or meningism; (GCS = 15)
- Grade 2: moderate to severe headache, meningism, and/or cranial nerve deficits; consciousness is not impaired (GCS = 14–13)
- Grade 3: somnolence and focal neurological deficit; (GCS = 14–13)
- Grade 4: altered state of consciousness, severe neurological deficits including impairment of the autonomic nervous system (GCS = 12–7)
- Grade 5: coma, ; (GCS = 6–3)
- Bleeding into the subarachnoid space
- → secondary ischemic stroke by one of the two following mechanisms:
- → elevated intracranial pressure → hypertension, bradycardia, and irregular breathing (see )
- Elevated systolic blood pressure also increases SAH from the ruptured aneurysm, initiating a vicious cycle.
- Severe headache (days to weeks prior in > ⅓ of patients) due to a sentinel leak (warning leak); sometimes accompanied with transient diplopia that resolves completely
- Oculomotor nerve palsy: defective vision with an ipsilaterally fixed, dilated pupil
- aneurysm may occur due to the formation of embolisms in the
- Thunderclap headache: sudden, severely painful headache : - spreads over the entire head (holocephalic) and radiates to the neck and back (may present with opisthotonus)
- Meningism: : neck stiffness, photophobia, nausea and vomiting, meningeal stretch signs (e.g., and )
- Impaired consciousness (somnolent to comatose)
- Sweating, hemodynamic instability
- Mass effects
- Nonenhanced CT (best initial test ): shows blood in subarachnoid space
- Lumbar puncture (LP), if CT negative
- Digital subtraction angiography (DSA): determines the site of bleeding/aneurysm (also identifying mycotic aneurysms) preoperatively
- CT angiography (CTA); : if CT does not confirm SAH in clinically suspected or high-risk cases (emergent or unstable patients)
- MRI with or without angiography : consider if no lesion found with other angiography methods
- Additional baseline tests in all patients
- Strict bedrest
- Analgesia (acetaminophen)
- IV fluids for hydration and to avoid hyponatremia
- Reverse anticoagulation
- Control BP ; : maintain BP below 160 mm Hg to prevent rebleeding
- Prevent vasospasm in all patients → administer calcium channel blocker (especially oral nimodipine)
- Control ↑ ICP: 30° head elevation, administer IV mannitol, hyperventilation in intubated patients, stool softeners
- Seizure prophylaxis with anticonvulsants: e.g., phenytoin for select cases
- Control blood glucose levels
- Surgical clipping (treatment of choice) and/or endovascular coiling (increasingly used alternative for poor surgical candidates) should be performed early to prevent rebleeding
- If hydrocephalus is present → ventricular drain, serial LPs, or permanent
Use of nitrates should be avoided since they may raise ICP!
Vasospasm (∼ 30% of cases, often in those with ruptured aneurysms): usually occurs between the 3rd and the 8th day after SAH
- ⅓ of patients suffer ischemic strokes due to vasospasm
- Transcranial doppler study should be performed daily to assess the severity of vasospasms.
Rebleeding (∼ 20% of cases): most often within the first two weeks
- The risk of rebleeding is highest during the first 24 hours after SAH.
- The cumulative risk of recurrent bleeding within the first six months is about 50%.
- Hydrocephalus (∼ 15% of cases)
- much less often, volume depletion and hyponatremia induced by cerebral salt wasting
- Cardiac dysfunction
- Cardiac complications: arrhythmias, myocardial ischemia
- Cerebral edema
- Terson syndrome (20% of cases): preretinal hemorrhage due to SAH
We list the most important complications. The selection is not exhaustive.
- 50% mortality rate within the first 30 days
- Survivors: increased rates of neurologic impairment (e.g., cognitive, mood changes, functional, epilepsy) and increased risk of recurrent SAH
- 10% of patients die before they can be brought to the hospital and another 10% die during the first 24 hours (30-day mortality is approximately 35%).