Subarachnoid hemorrhage pathophysiology

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Subarachnoid Hemorrhage Microchapters

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Differentiating Subarachnoid Hemorrhage from other Diseases

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AHA/ASA Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage (2012)

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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

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.

Histological types Consecutive stages of aneurysm walls Chance of aneurysmal rupture
Type A
  • Endothelialized wall
  • Linearly organized smooth muscle cell
  • 41%
Type B
  • Thickened wall
  • Disorganized smooth muscle cells
  • 55%
Type C
  • 64%
Type D
  • Extremely thin thrombosis-lined hypocellular wall
  • 100%


Nonaneurysmal subarachnoid hemorrhage

References

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