Subarachnoid hemorrhage pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Aneurysmal subarachnoid hemorrhage=== | ===Aneurysmal subarachnoid hemorrhage=== | ||
Saccular aneurysms | Aneurysmal subarachnoid hemorrhage is a result of : | ||
* Saccular aneurysms (responsible for most SAHs) | |||
* Fusiform aneurysms (dilatation of the entire circumference of the vessel that may in part be formed due to atherosclerosis) | |||
* Mycotic aneurysms (infected emboli due to infective endocarditis) | |||
==== Saccular aneurysms ==== | |||
Saccular (berry) aneurysms are responsible for most cases of subarachnoid hemorrhage (SAH). | |||
Multiple factors play a role in formation of a saccular aneurysms. Saccular aneurysms usually results from degenerative change in the vessel wall following:<ref name="pmid7681275">{{cite journal| author=Austin G, Fisher S, Dickson D, Anderson D, Richardson S| title=The significance of the extracellular matrix in intracranial aneurysms. | journal=Ann Clin Lab Sci | year= 1993 | volume= 23 | issue= 2 | pages= 97-105 | pmid=7681275 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7681275 }}</ref> | |||
*Hemodynamic stress (turbulent blood flow) which it may result in excessive tear and breakdown of the [[internal elastic lamina]] which it progress to lack of elastic lamina. | *Hemodynamic stress (turbulent blood flow) which it may result in excessive tear and breakdown of the [[internal elastic lamina]] which it progress to lack of elastic lamina. | ||
Common associated conditions may include: | It is also thought that inflammatory process is also play a role in pathogenesis of aneurysms.<ref name="pmid20128708">{{cite journal| author=Aoki T, Nishimura M| title=Targeting chronic inflammation in cerebral aneurysms: focusing on NF-kappaB as a putative target of medical therapy. | journal=Expert Opin Ther Targets | year= 2010 | volume= 14 | issue= 3 | pages= 265-73 | pmid=20128708 | doi=10.1517/14728221003586836 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20128708 }}</ref> | ||
*Hypertension | |||
*Cigarette smoking | Common associated conditions may include:<ref name="pmid23713738">{{cite journal| author=Starke RM, Chalouhi N, Ali MS, Jabbour PM, Tjoumakaris SI, Gonzalez LF et al.| title=The role of oxidative stress in cerebral aneurysm formation and rupture. | journal=Curr Neurovasc Res | year= 2013 | volume= 10 | issue= 3 | pages= 247-55 | pmid=23713738 | doi= | pmc=3845363 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23713738 }}</ref> | ||
*Connective tissue disease | *[[Hypertension]] | ||
*[[Cigarette smoking]] | |||
=====Histopathologic findings===== | *[[Connective tissue disease]] | ||
======Histopathologic findings====== | |||
Unruptured aneurysms wall may present with complete absence of endothelial lining. | Unruptured aneurysms wall may present with complete absence of endothelial lining. | ||
However, ruptured aneurysm walls may present with | However, ruptured aneurysm walls may present with [[Inflammatory process|Inflammatory cells]] ([[T cell proliferation|T cell]] and [[Macrophage|macrophage infiltration]]) in addition to complete absence of endothelial lining. | ||
Histological types of aneurysm walls may be identified as follow:<ref name="pmid15322297">{{cite journal| author=Frösen J, Piippo A, Paetau A, Kangasniemi M, Niemelä M, Hernesniemi J et al.| title=Remodeling of saccular cerebral artery aneurysm wall is associated with rupture: histological analysis of 24 unruptured and 42 ruptured cases. | journal=Stroke | year= 2004 | volume= 35 | issue= 10 | pages= 2287-93 | pmid=15322297 | doi=10.1161/01.STR.0000140636.30204.da | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15322297 }}</ref> | |||
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Revision as of 21:13, 5 December 2016
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Subarachnoid Hemorrhage Microchapters |
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Diagnosis |
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Treatment |
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AHA/ASA Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage (2012)
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Case Studies |
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Subarachnoid hemorrhage pathophysiology On the Web |
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American Roentgen Ray Society Images of Subarachnoid hemorrhage pathophysiology |
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Risk calculators and risk factors for Subarachnoid hemorrhage pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Mehrsefat, M.D. [2]
Overview
Pathophysiology
Aneurysmal subarachnoid hemorrhage
Aneurysmal subarachnoid hemorrhage is a result of :
- Saccular aneurysms (responsible for most SAHs)
- Fusiform aneurysms (dilatation of the entire circumference of the vessel that may in part be formed due to atherosclerosis)
- Mycotic aneurysms (infected emboli due to infective endocarditis)
Saccular aneurysms
Saccular (berry) aneurysms are responsible for most cases of subarachnoid hemorrhage (SAH). Multiple factors play a role in formation of a saccular aneurysms. Saccular aneurysms usually results from degenerative change in the vessel wall following:[1]
- Hemodynamic stress (turbulent blood flow) which it may result in excessive tear and breakdown of the internal elastic lamina which it progress to lack of elastic lamina.
It is also thought that inflammatory process is also play a role in pathogenesis of aneurysms.[2]
Common associated conditions may include:[3]
Histopathologic findings
Unruptured aneurysms wall may present with complete absence of endothelial lining.
However, ruptured aneurysm walls may present with Inflammatory cells (T cell and macrophage infiltration) in addition to complete absence of endothelial lining.
Histological types of aneurysm walls may be identified as follow:[4]
| Histological types | Consecutive stages of aneurysm walls | Chance of aneurysmal rupture |
|---|---|---|
| Type A |
|
|
| Type B |
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|
| Type C |
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| Type D |
|
|
Nonaneurysmal subarachnoid hemorrhage
References
- ↑ Austin G, Fisher S, Dickson D, Anderson D, Richardson S (1993). "The significance of the extracellular matrix in intracranial aneurysms". Ann Clin Lab Sci. 23 (2): 97–105. PMID 7681275.
- ↑ Aoki T, Nishimura M (2010). "Targeting chronic inflammation in cerebral aneurysms: focusing on NF-kappaB as a putative target of medical therapy". Expert Opin Ther Targets. 14 (3): 265–73. doi:10.1517/14728221003586836. PMID 20128708.
- ↑ Starke RM, Chalouhi N, Ali MS, Jabbour PM, Tjoumakaris SI, Gonzalez LF; et al. (2013). "The role of oxidative stress in cerebral aneurysm formation and rupture". Curr Neurovasc Res. 10 (3): 247–55. PMC 3845363. PMID 23713738.
- ↑ Frösen J, Piippo A, Paetau A, Kangasniemi M, Niemelä M, Hernesniemi J; et al. (2004). "Remodeling of saccular cerebral artery aneurysm wall is associated with rupture: histological analysis of 24 unruptured and 42 ruptured cases". Stroke. 35 (10): 2287–93. doi:10.1161/01.STR.0000140636.30204.da. PMID 15322297.