Venous infarction

Venous infarction (outdated, i.venosus) is an acute disorder of blood circulation and metabolism in the brain that occurs when large cerebral arteries are blocked by a thrombus. This term is outdated and is not used in modern medicine.

Venous type infarctions are characterized by

Venous infarction

Venous infarction is a pathological condition in which hemorrhage, or organized thrombosis or embolism occurs in the deep venous system of various parts of the organ, accompanied by the effusion of hemorrhagic extravasate into the paravascular space. The clinical picture of venous infarction is similar to other venous diseases. The diagnosis is verified using Doppler sonography and contrast angiography. The main method of therapy is surgery, which is accompanied by a lower frequency of relapses.

The term “venous infarction” was introduced into clinical practice at the beginning of the 20th century and was accepted, but never received an official explanation. The term "i. venosus" described a clinical and morphological syndrome characterized by a certain similarity of vascular changes in the deep veins of the extremities and lungs. A true infarction, i.e., a functionally and morphologically self-sufficient state of tissue edema due to blockage of the main arterial vessel, exists only in a matter of minutes, and the development of the subsequent clinical picture is associated both with the rate of spread of thrombosis in the arteries and with the duration of the period of hypoperfusion. The tissues of the human body contain a sufficient number of small-diameter vessels (precapillary and capillary), which makes it possible to maintain tissue perfusion through microcirculation in the first minutes after disruption of blood flow. When pressure exists in the main artery, first of all, the areology of the muscles of the leg and thigh is absent, and a gradient is created in the deep vein system. Centrifugal blood from the arteries enters sequentially into all deep-lying muscle groups and is deposited in the anastomosing central venous bed of the leg and pelvis. It is hemodynamically acceptable to call this condition “peripheral ischemia.” Later, depending on the degree of stenosis or occlusion of the main arteries, a staged clinical symptom complex of damage to each of the muscle groups is formed. While remaining at a biologically adequate level, perfusion is of a turbulent transient nature. A deficiency of erythema in all cases clearly indicates the rapid stealing of the arterial bed. If within an hour it covers 40%, then we can say