Subarachnoid hemorrhage pathophysiology: Difference between revisions
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*[[Cigarette smoking]] | *[[Cigarette smoking]] | ||
*[[Connective tissue disease]] | *[[Connective tissue disease]] | ||
**Ehlers-Danlos syndrome | **[[Ehlers-Danlos syndrome]] | ||
**Pseudoxanthoma elasticum | **[[Pseudoxanthoma elasticum]] | ||
The role for '''genetic factors''' in pathogenesis of aneurysmal formation has been approved. However, the exact pathogenesis remains unknown. It is thought that some connective tissue disease may result in arterial wall weakness and non-laminar flow pattern of blood, which is then progress to tear and breakdown of the wall.<ref name="pmid10706896">{{cite journal| author=Pepin M, Schwarze U, Superti-Furga A, Byers PH| title=Clinical and genetic features of Ehlers-Danlos syndrome type IV, the vascular type. | journal=N Engl J Med | year= 2000 | volume= 342 | issue= 10 | pages= 673-80 | pmid=10706896 | doi=10.1056/NEJM200003093421001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10706896 }} </ref><ref name="pmid6864273">{{cite journal| author=Neil-Dwyer G, Bartlett JR, Nicholls AC, Narcisi P, Pope FM| title=Collagen deficiency and ruptured cerebral aneurysms. A clinical and biochemical study. | journal=J Neurosurg | year= 1983 | volume= 59 | issue= 1 | pages= 16-20 | pmid=6864273 | doi=10.3171/jns.1983.59.1.0016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6864273 }} </ref> | *[[Hyperaldosteronism|Familial aldosteronism type I]] | ||
The role for '''genetic factors''' in pathogenesis of aneurysmal formation has been approved. However, the exact pathogenesis remains unknown. It is thought that some connective tissue disease may result in arterial wall weakness and non-laminar flow pattern of blood, which is then progress to tear and breakdown of the wall.<ref name="pmid10706896">{{cite journal| author=Pepin M, Schwarze U, Superti-Furga A, Byers PH| title=Clinical and genetic features of Ehlers-Danlos syndrome type IV, the vascular type. | journal=N Engl J Med | year= 2000 | volume= 342 | issue= 10 | pages= 673-80 | pmid=10706896 | doi=10.1056/NEJM200003093421001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10706896 }} </ref><ref name="pmid6864273">{{cite journal| author=Neil-Dwyer G, Bartlett JR, Nicholls AC, Narcisi P, Pope FM| title=Collagen deficiency and ruptured cerebral aneurysms. A clinical and biochemical study. | journal=J Neurosurg | year= 1983 | volume= 59 | issue= 1 | pages= 16-20 | pmid=6864273 | doi=10.3171/jns.1983.59.1.0016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6864273 }} </ref> Additionally, it is thought concurrent [[hypertension]] may play a role in patient with [[Autosomal dominant polycystic kidney disease|autosomal dominant polycystic kidney disease (PKD)]].<ref name="pmid21641282">{{cite journal| author=Vlak MH, Algra A, Brandenburg R, Rinkel GJ| title=Prevalence of unruptured intracranial aneurysms, with emphasis on sex, age, comorbidity, country, and time period: a systematic review and meta-analysis. | journal=Lancet Neurol | year= 2011 | volume= 10 | issue= 7 | pages= 626-36 | pmid=21641282 | doi=10.1016/S1474-4422(11)70109-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21641282 }}</ref> | |||
======Histopathologic findings====== | ======Histopathologic findings====== | ||
Unruptured aneurysms wall may present with complete absence of endothelial lining. | Unruptured aneurysms wall may present with complete absence of endothelial lining. | ||
Revision as of 21:57, 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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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][4][5]
The role for genetic factors in pathogenesis of aneurysmal formation has been approved. However, the exact pathogenesis remains unknown. It is thought that some connective tissue disease may result in arterial wall weakness and non-laminar flow pattern of blood, which is then progress to tear and breakdown of the wall.[4][5] Additionally, it is thought concurrent hypertension may play a role in patient with autosomal dominant polycystic kidney disease (PKD).[6]
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:[7]
| Histological types | Consecutive stages of aneurysm walls | Chance of aneurysmal rupture |
|---|---|---|
| Type A |
|
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| Type B |
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| Type C |
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| Type D |
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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.
- ↑ 4.0 4.1 Pepin M, Schwarze U, Superti-Furga A, Byers PH (2000). "Clinical and genetic features of Ehlers-Danlos syndrome type IV, the vascular type". N Engl J Med. 342 (10): 673–80. doi:10.1056/NEJM200003093421001. PMID 10706896.
- ↑ 5.0 5.1 Neil-Dwyer G, Bartlett JR, Nicholls AC, Narcisi P, Pope FM (1983). "Collagen deficiency and ruptured cerebral aneurysms. A clinical and biochemical study". J Neurosurg. 59 (1): 16–20. doi:10.3171/jns.1983.59.1.0016. PMID 6864273.
- ↑ Vlak MH, Algra A, Brandenburg R, Rinkel GJ (2011). "Prevalence of unruptured intracranial aneurysms, with emphasis on sex, age, comorbidity, country, and time period: a systematic review and meta-analysis". Lancet Neurol. 10 (7): 626–36. doi:10.1016/S1474-4422(11)70109-0. PMID 21641282.
- ↑ 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.