Subarachnoid hemorrhage pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Aneurysmal subarachnoid hemorrhage=== | ===Aneurysmal subarachnoid hemorrhage=== | ||
Saccular aneurysms are responsible for most SAHs, although fusiform and mycotic aneurysms can also result in suarachnoid hemorrhage | Saccular aneurysms are responsible for most SAHs, although fusiform and mycotic aneurysms can also result in suarachnoid hemorrhage. | ||
It is thought that | It is thought that formation of saccular aneurysm is multifactorial. It usually result from degenerative change in the vessel wall following: | ||
*Hemodynamic stress (turbulent blood flow) 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: | Common associated conditions may include: | ||
*Hypertension | *Hypertension | ||
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*Connective tissue disease | *Connective tissue disease | ||
It is also thought that inflammatory process is also play a role in pathogenesis of aneurysms | It is also thought that inflammatory process is also play a role in pathogenesis of aneurysms | ||
====Histopathologic findings=== | =====Histopathologic findings===== | ||
Unruptured aneurysms wall may present with complete absence of endothelial lining. | |||
However, ruptured aneurysm walls may present with Inflammatory (T cell and macrophage infiltration) in addition to complete absence of endothelial lining. | |||
* Complete absence of endothelial lining | |||
* [[Inflammatory process]] ([[T cell proliferation|T cell]] and [[Macrophage|macrophage infiltration]]) | |||
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Revision as of 20:20, 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
Saccular aneurysms are responsible for most SAHs, although fusiform and mycotic aneurysms can also result in suarachnoid hemorrhage. It is thought that formation of saccular aneurysm is multifactorial. It usually result from degenerative change in the vessel wall following:
- 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:
- Hypertension
- Cigarette smoking
- Connective tissue disease
It is also thought that inflammatory process is also play a role in pathogenesis of aneurysms
Histopathologic findings
Unruptured aneurysms wall may present with complete absence of endothelial lining.
However, ruptured aneurysm walls may present with Inflammatory (T cell and macrophage infiltration) in addition to complete absence of endothelial lining.
- Complete absence of endothelial lining
- Inflammatory process (T cell and macrophage infiltration)
| Histological types | Consecutive stages of aneurysm walls | Chance of aneurysmal rupture |
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| Type A |
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| Type B |
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| Type C |
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| Type D |
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