Subarachnoid hemorrhage pathophysiology: Difference between revisions
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{{Subarachnoid hemorrhage}} | {{Subarachnoid hemorrhage}} | ||
{{CMG}}; {{AE}} {{SaraM}} | |||
==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 the 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 and | |||
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=== | |||
{| style="border: 0px; font-size: 90%; margin: 3px;" align=center | |||
|+ | |||
! style="background: #4479BA; width: 220px;" | {{fontcolor|#FFF|Histological types}} | |||
! style="background: #4479BA; width: 550px;" | {{fontcolor|#FFF|Consecutive stages of aneurysm walls}} | |||
! style="background: #4479BA; width: 550px;" | {{fontcolor|#FFF|Chance of aneurysmal rupture}} | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" |'''Type A | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*Endothelialized wall | |||
*Linearly organized smooth muscle cell | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*41% | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" |'''Type B | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*Thickened wall | |||
*Disorganized smooth muscle cells | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*55% | |||
|- | |||
| style="padding: 5px 5px; background: #F5F5F5;" | '''Type C | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*Hypocellular wall | |||
*Either [[intimal hyperplasia]] or organizing luminal thrombosis | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*64% | |||
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| style="padding: 5px 5px; background: #F5F5F5;" |'''Type D | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*Extremely thin thrombosis-lined hypocellular wall | |||
| style="padding: 5px 5px; background: #F5F5F5;" | | |||
*100% | |||
|} | |||
===Nonaneurysmal subarachnoid hemorrhage=== | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} |
Revision as of 20:05, 5 December 2016
Subarachnoid Hemorrhage Microchapters |
Diagnosis |
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Treatment |
AHA/ASA Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage (2012)
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Case Studies |
Subarachnoid hemorrhage pathophysiology On the Web |
American Roentgen Ray Society Images of Subarachnoid hemorrhage pathophysiology |
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 the 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 and
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
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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