Brain edema – the pathological condition, described accumulation of a liquid in a fabric of a brain and intracranial hypertensia clinically shown by a syndrome.
There are 4 basic kinds of brain edema:
They differ by etiology, time of development, localization and methods of preventive maintenance and treatment
Cellulotoxic edema appears because of swelling glia, neurocyte and endotheliocyte and begins in some minutes after damage of a brain, for example hypoxia. As a result of decrease in a metabolism activity Na+, K+-AT phases a cellular membrane is broken. Sodium collects in a cell, and on a gradient of osmotic pressure in a cell water starts to act. Cellulotoxic edema is localized basically in grey substance of a brain.
Vasogenic edema is the most frequent version of a hypostasis of a brain. It develops because of increase of permeability of capillaries. Through a wall of capillaries in extracellular space there are fibers, and after them – water. vasogenic edema is localized basically in white substance of a brain.
Interstitial edema develops at a hydrocephaly because of difficulty of outflow pressure inside ventricle of a brain raises. Under the action of this pressure there is a strengthened filtration of water and low-molecular substances in the fabric of a brain surrounding ventricles.
The ischemia of a brain leads all over again to cellulotoxic, and then – to vasogenic edema. Thus, the pathophysiological picture is so usual that some people suggest to use the term “an ischemic edema”. In the first minutes of an ischemia develops cellulotoxic edema mentioning mainly astrocytes which are located around of capillaries. If blood supply is quickly restored, these changes happen to be backwards. Otherwise because of swelling of astrocytes and endothelial cells the gleam of capillaries is narrowed so, even after restoration of blood supply blood can not act in capillaries. It aggravates an ischemia and necrosis.
In a phase vasogenic edema permeability of a wall of capillaries raises. It is shown, that it occurs cause of pinocytosis increases and as a result of infringement of dense contacts between cells of endothelium. After restoration of a blood-groove permeability of blood-brain barrier increases even more. As well as at other forms of vasogenic edema.
Simultaneously with cellulotoxic and vasogenic edema necrosis develops. Glia and neurocyte in a greater degree are subject of necrosis in comparison with endothelium. In process of their destruction in intercellular substance of a brain osmotically active substances that leads to an even greater output of water from capillaries collect.
The ischemic hypostasis reaches a maximum on 2-4-? day after a heart attack and decreases by the end of the second week. Further in the field of necrosis inflammatory reaction, including phagocytosis develops. Within several day or weeks necrotic weights resolve, and the hypostasis disappears. Believe, that the hypostasis can cause an ischemia and by that to increase a zone of a heart attack.