Intracerebral hemorrhage pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Intraparnchaimal hemorrhage=== | |||
Intracerebral hemorrhage (ICH) is bleeding directly into the brain tissue, forming a gradually enlarging [[hematoma]] (pooling of blood). The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the [[ventricular system]], [[cerebrospinal fluid|CSF]] or the [[pia]]l surface. ICH has a [[mortality rate]] of 44 percent after 30 days, higher than ischemic stroke or even the very deadly subarachnoid hemorrhage.<ref name="caplan">{{cite journal | author= Caplan LR | title= Intracerebral hemorrhage | journal= Lancet | year=1992 | pages=656-8 | volume=339 | issue=8794 | id=PMID 1347346}}</ref> | Intracerebral hemorrhage (ICH) is bleeding directly into the brain tissue, forming a gradually enlarging [[hematoma]] (pooling of blood). The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the [[ventricular system]], [[cerebrospinal fluid|CSF]] or the [[pia]]l surface. ICH has a [[mortality rate]] of 44 percent after 30 days, higher than ischemic stroke or even the very deadly subarachnoid hemorrhage.<ref name="caplan">{{cite journal | author= Caplan LR | title= Intracerebral hemorrhage | journal= Lancet | year=1992 | pages=656-8 | volume=339 | issue=8794 | id=PMID 1347346}}</ref> | ||
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*[[Pons]] | *[[Pons]] | ||
The small arteries in these areas seem more sensitive to hypertension and as a result, it may progress to vascular injury. | The small arteries in these areas seem more sensitive to hypertension and as a result, it may progress to vascular injury. | ||
Breaks in the vessel wall usually occurs following chronic hypertension. Prolonged hypertentsion usually result in [[intimal hyperplasia]] and [[hyalinosis]], which may result in [[focal necrosis]] and cause in vessel wall breaks. massive hemorrhage may occur when the bleeding disorder | |||
The penetrator vessels in patients with chronic hypertension develop intimal hyperplasia with hyalinosis in the vessel wall; this predisposes to focal necrosis, causing breaks in the wall of the vessel. These "pseudoaneurysms" have been associated with small amounts of blood outside their walls. Pseudoaneurysm formation with subclinical leaks of blood may be relatively common; massive hemorrhage can occur when the clotting system is unable to compensate for the disruption in the vessel wall. | |||
If intracerebral hemorrhage (ICH) occurs in other brain areas or in non hypertensive patients, the other causes of [[intracerebral hemorrhage]] should be considered such as: | If intracerebral hemorrhage (ICH) occurs in other brain areas or in non hypertensive patients, the other causes of [[intracerebral hemorrhage]] should be considered such as: |
Revision as of 15:46, 23 November 2016
Intracerebral hemorrhage Microchapters |
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AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage (2015) |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Mehrsefat, M.D. [2]
Overview
Pathophysiology
Intraparnchaimal hemorrhage
Intracerebral hemorrhage (ICH) is bleeding directly into the brain tissue, forming a gradually enlarging hematoma (pooling of blood). The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or the pial surface. ICH has a mortality rate of 44 percent after 30 days, higher than ischemic stroke or even the very deadly subarachnoid hemorrhage.[1]
High blood pressure and aging blood vessels are the most common causes of intracerebral hemorrhage. Hypertensive Intracerebral hemorrhage (ICH) usually results from spontaneous rupture of a small artery deep in the brain. The most common sites include:
- Basal ganglia (especially the putamen)
- Thalamus
- Cerebellum
- Pons
The small arteries in these areas seem more sensitive to hypertension and as a result, it may progress to vascular injury.
Breaks in the vessel wall usually occurs following chronic hypertension. Prolonged hypertentsion usually result in intimal hyperplasia and hyalinosis, which may result in focal necrosis and cause in vessel wall breaks. massive hemorrhage may occur when the bleeding disorder
The penetrator vessels in patients with chronic hypertension develop intimal hyperplasia with hyalinosis in the vessel wall; this predisposes to focal necrosis, causing breaks in the wall of the vessel. These "pseudoaneurysms" have been associated with small amounts of blood outside their walls. Pseudoaneurysm formation with subclinical leaks of blood may be relatively common; massive hemorrhage can occur when the clotting system is unable to compensate for the disruption in the vessel wall.
If intracerebral hemorrhage (ICH) occurs in other brain areas or in non hypertensive patients, the other causes of intracerebral hemorrhage should be considered such as:
- Neoplasms
- Hemorrhagic disorders
- Vascular malformations
- Arteriovenous malformation (AVM) is a genetic condition of abnormal connection between arteries and veins. when AVM occurs in the brain, vessels can break and bleed into the brain and result in intracerebral hemorrhagic stroke.
- Cerebral amyloid angiopathy
- In older people, an abnormal protein called amyloid may accumulate in arteries of the brain. Amyloid angiopathy weakens the arteries and can cause hemorrhage.
Intraventricular hemorrhage
Intraventricular hemorrhage (IVH) can be:[2][3]
- Primary, confined to the ventricles
- Secondary, originating as an extension of an ICH
Most IVH is secondary and related to hypertensive hemorrhages involving the basal ganglia and thalamus.
References
- ↑ Caplan LR (1992). "Intracerebral hemorrhage". Lancet. 339 (8794): 656–8. PMID 1347346.
- ↑ Engelhard HH, Andrews CO, Slavin KV, Charbel FT. Current manage- ment of intraventricular hemorrhage. Surg Neurol. 2003;60:15–21.
- ↑ Huttner HB, Hartmann M, Köhrmann M, Neher M, Stippich C, Hähnel S, Kress B. Repeated digital substraction angiography after perimesencephalic subarachnoid hemorrhage? J Neuroradiol. 2006;33:87–89.