Membraneous edema

Edema in the defeat of capillary walls do not have the characteristic clinical signs and until now reliable clinical methods of investigation are not being captured (Hagglin R. 1993).

The increase in capillary permeability along withthe release of protein from the vessels into the interstitial fluid, lowers the COD, and worsens the ability of capillaries to retain fluid. Mechanisms responsible for the development of edema due to increased vascular permeability are associated with the action of various mediators and other biologically active substances released from cells and formed in them de novo for allergic reactions of immediate type. Such factors include histamine, serotonin, kinin (bradykinin), platelet aggregation factor (FAT), prostaglandins (Pg E2 ) and leukotrienes (Lt B4 ), the complement system, etc. Of great importance are the lysosomal enzymes released during the destruction of tissues, as well as concomitant disorders of the acid-base state.

Edema in certain lesions of the nervous system (state after apoplexy) is probably also caused by an increased permeability of the capillary wall on the ground of disturbance of innervation (Hagglin R. 1993).

In rare cases membranogenous edema can be hereditary in nature. as, for example, angioedema.

A characteristic feature is the dependence on the position of the body exhibiting venous congestion in the corresponding region.

These edemas are associated, mainly, with an increasehydrostatic pressure in the capillaries, which, as follows from Table. can develop with the participation of two mechanisms. With the first of these, the expansion of arterioles and precapillary sphincters leads to an increased transfer of pressure to the capillaries. The second mechanism that determines this form of edema is the increase in resistance to venous outflow, resulting in increased venous pressure. This increase can be local (vein thrombosis) and generalized nature.

The most common cause increase in total venous pressure is an heart failure (Fig.). Persistent heart failure leads to a general edema in the event that increased venous pressure causes an increase in central venous pressure and is transmitted to the venous return system and capillaries. This mechanism is called retrograde component of heart failure. When it is implemented, it is not only difficultresorption of the fluid with its continued filtration in the arterial region, but also the vessels are stretched (as a result of their overflow). Developing hypoxia and metabolic disorders in the tissue (due to the restriction of blood flow in them) cause an increase in the permeability of the vascular wall, as an additional factor aggravating the development of edema (Chereshnev VA Yushkov BG 2001).

The second mechanism for the development of edema in this pathology is cardiac output limitation. It is designated as systolic component of heart failure. The implementation of this mechanism limitsrenal perfusion, which contributes to the retention of sodium and water in the body. Importance is attached to the hyperproduction of aldosterone, which occurs as a secondary phenomenon and supports the formation of edema through reduced sodium excretion. In far-reaching cases, accompanied by congestion in the liver, when hepatic insufficiency develops with hypoproteinemia, a certain role is played by the decrease in oncotic pressure.