Hemorrhagic stroke

Associated with a higher risk of fatality then ischemic stroke.

Accounts for 6.5-19.6% of cases of stroke, but is associated with the greatest rate of mortality: one year survival from a spontaneous intraparenchymal hemorrhage is approximately 40%, and 10 years survival is 24%.

In a meta-analysis of 36 studies the incidence of intracranial parenchymal hemorrhage was 24.6 per hundred thousand person-years and was significantly higher in Asian and older populations.

Approximately one third of patients die within 30 days after a hemorrhagic stroke.

Categorized by the location of the hemorrhage as either intracerebral for subarachnoid with the former being more common.

Approximately 88% of cases are due to intracerebral hemorrhage, which is characterized by bleeding directly into the brain parenchyma.

Primary intraparenchymal hemorrhage, accounts for 78-88% of cases of hemorrhagic stroke, and refers to rupture of damaged small arteries or arterioles,most common secondary to either hypertension or cerebral amyloid angiopathy.

E2 and E4 alleles of apolipoprotein E are associated with increased deposition of beta-amyloid in the vessel wall and consequently, hemorrhagic risk.

Distinguishing cerebral amyloid angiopathy from hypertensive intracranial parenchymal hemorrhage is relevant because the rebleed and dementia risks were significantly higher after a cerebral amyloid angiopathy related bleed.

Secondary intraparenchymal hemorrhage can occur secondary to coagulopathy, cerebral venous thrombosis, vasculitis, tumor, hemorrhagic conversion of ischemic stroke or rupture of a mycotic aneurysm or vascular of malformation, such as an AV malformation, arteriovenous fistula, or cavernous malformation.

Secondary intraparenchymal hemorrhage can result result from coagulopathy, vascular malformation rupture, cerebral venous thrombosis, mycotic aneurysm rupture, moyamoya, tumor, hemorrhagic conversion of ischemic stroke or a vasculitis.

Vascular malformations that can lead to rupture include AVMs and cavernous malformations.

Additional significant risk factors for hemorrhagic stroke include: smoking and alcohol intake.

Increased alcohol intake is suggested to increase the risk of hemorrhagic stroke by inducing platelet dysfunction/coagulation problems and endothelial damage.

Increased HDL cholesterol, low total cholesterol, and low non-high density lipoprotein cholesterol are associated with intraparenchymal hemorrhage.

Cerebral amyloid angiopathy results from beta-amyloid deposition in cortical blood vessels that are subsequently weakened and have an increased tendency to rupture, making cerebral amyloid an independent risk factor for lobar intraparenchymal hemorrhage.

Intraventricular hemorrhage describes bleeding that extends into the ventricles.

Hypertension is the primary risk factor for intra-parenchymal hemorrhage as it induces degenerative changes in small arterial perforators which increase the likelihood of rupture, and hypertensive hemorrhage has a proclivity to occur in the deep brain structures supplied by such vessels.

Such deep brain structures include: the basal ganglia, thalamus, brainstem, and deep cerebellum.

Non traumatic intracranial hemorrhage is characterized as primary, being unrelated to congenital or acquired lesions, or secondary, caused by congenital or acquired conditions, or spontaneous unrelated either to trauma or surgery.


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