Subarachnoid Hemorrhage

• Aneurysm formation is typically located at bifurcations of intracranial arteries 

• Approx 80% of spontaneous non-traumatic SAH are the result of aneurysm rupture 

Causes of non-aneurysmal SAH:

• reversible vasoconstriction syndrome

• perimesencephalic hemorrhage (2/2 venous process) 

• rupture of arterial dissections, blisters, or ulcerations

• trauma

Uncommon causes of SAH:

• coagulopathy

• sympathomimetic drugs

• vasculitis, moyamoya, CAA, AVM rupture 

Risk Factors for Aneurysm Development:

Behavioral influences (modifiable):

• • HTN, smoking, etoh abuse, sympathomimetic drug use

Race & Gender:

• • predilection for african americans and females

Family Hx

Genetic Syndromes:

• • autosomal dominant polycystic kidney disease

  • type IV ehler's danlos syndrome

The onset of a the "worst headache of life (WHOL)" or "thunderclap" is present in up to 97% of those with SAH. Other common symptoms associated with SAH include nausea, vomiting, meningismus, photophobia, and reduced or loss of consciousness 

Sentinel Headache: 

Common complaint of patient's preceding aneurysm rupture likely attributed to "aneurysmal leaking" or microhemorrhage irritating the meninges. Consists of typical sudden onset of severe headache / WHOL that clears. Also0 coinsidered "warning headache". Occurring in approx. 30-60% of aSAH patients. 

Focal Deficits:

Cranial nerve palsies are a common occurrence and are caused by direct compression by the aneurysm or secondary to compression from hematoma / blood products after aneurysm rupture 

Examples of Deficits encountered:

• Pcomm artery aneurysms typically cause ipsilateral CNIII defects

• Abducens (CN VI) nerve palsies can be "falsely localizing" signs caused by abrupt changes in elevated intracranial pressure due to the the long intracranial course of CN VI fibers. Abducens nerve palsies may also be the result of compression / mass effect form the aneurysm or rupture itself, most commonly due to vertebral artery pathology. 

• MCA aneurysms can cause focal deficits corresponding with the MCA territory, with symptoms ranging from hemiparesis to hemiplegia, and varying degrees of aphasia

• ACA aneurysms can cause frontal lobe appearing pathologies and bilateral leg paresis / plegia

• Basilar tip aneurysms can cause profound changes in LOC, even coma, and usually have a significant degree of CN and motor impairment 

Seizures:

The reported incidence of seizures after aSAH rupture is broad, ranging from 5 - 30 %. Seizures occurring after SAH have been associated with clinical and radiographic markers of hemorrhage severity (higher SAH grade/extent of SAH blood burden, lower Glasgow Coma Scale score at presentation, etc), as well as rebleeding. More recent data has com to light suggesting that the true presence of seizures is likely closer to 1 - 10% (AHA / ASA 2016).  

Nevertheless, seizures represent a potentially devastating consequence of aneurysmal rupture, associated with unwanted secondary neurological injury related to changes in cerebral blood flow and / or increased intracranial pressure. 

Use of prophylactic antiseizure medication is controversial. At our institution, we initiate seizure prophylaxis on ALL aSAH patients given concern over secondary injury and neurologic decline if a seizure were to occur prior to the aneurysm being secured. However, after the aneurysm has been effectively treated, we discontinue anti-seizure meds and monitor clinically, unless hematoma associated with aneurysm rupture and location is in area of exquisite cortex (ie mesial temporal lobe) 

CT Scan

> 95 % sensitivity if patient scanned within first 48hrs of aneurysm rupture. Blood appears as "high density" (bright) within subarachnoid space. Particular areas of interest when reviewing a CT scan for SAH are the ventricles, especially the temporal and occipital horns - assessing for the presence of blood within the ventricles, as well as early signs of hydrocephalus.

MRI

Not best imaging modality within 24 - 48hrs of aneurysm rupture due to characteristics of acute blood ( little met-Hb). Better for subacute to remote assessment of SAH (within 4-7 day time window). FLAIR sequences are the most sensitive for detecting blood within the subarachnoid space on MRI.

Cerebral Angiogram 

Also referred to as "DSA" or Digital Subtraction Angiography. The gold standard for evaluation of cerebral aneurysms. Demonstrates source in up to 85% on patients and allows for acute intervention / securing of the ruptured aneurysm. Also allows for assessment of feeding arteries, drainage and collateral flow characteristics. 

Lumbar Puncture

Classically the most sensitive in assessing subarachnoid blood products however has fallen out of favor with advancement in imaging modalities. The opening pressure will be elevated, the csf with have non-clotting bloody fluid that does not clear with sequential tubes. The presence of xanthochromia is the most reliable means of differentiating between subarachnoid blood due to aneurysm rupture and traumatic tap, and is the results of the breakdown of RBCs releasing heme pigments. Usually not apparent until 2-4 hrs after aneurysm rupture and virtually 100% present by 12hrs of SAH. 

Management of aneurysmal subarachnoid hemorrhage requires diagnosis first and foremost. Once this is made we delineate the care into 3 distinct phases of care; resuscitation and monitoring for early complications, aneurysm securement, and then monitoring for DCI and care within the ICU

Resuscitation and Early Complications