Stasis (a2845)

By I. Davydovsky · Pathology, Internal Medicine, History of Medicine

Also known as: Blood Stasis, Venous Stasis

Historical document, translated for reference. It reflects medical knowledge of the 1920s–30s and is not medical advice.

Summary

Stasis refers to the cessation of physiological contents within tubular organs, primarily blood stasis. This article explains the mechanisms of stasis according to Ricker's theory, involving paralysis of blood vessels, and discusses alternative views by Fischer-Wasels and Tannenberg focusing on physicochemical processes.

Encyclopedia article (1928–1936)

STASIS (from Greek stasis - standing), cessation in the lumen of this or that tubular organ of its physiological contents: S., blood S., S., fecal (coprostasis). In practice, it mainly refers to blood stasis. It is necessary first of all to establish that true blood S. is not simply the : cessation of blood flow in the vessel lumen. The essential factor that determines the phenomenon of true S. is the very mechanism of its development, and according to other authors - the colloidal-chemical disturbances that arise in the blood, in the vascular wall, and in the surrounding tissues. According to Ricker's doctrine, blood S. is the highest and final degree of circulatory disturbance, arising under conditions of complete paralysis of both dilators and constrictors (see Ricker's law). The entire phenomenon of S. plays out in the capillary system and from the morphological side is characterized primarily by the occurrence of sharp dilation of capillaries, as if by artificial injection of them. More rarely, vessels in S. are found to be weakly or not dilated at all. The blood column in S. becomes immobile or oscillatory movements forward and backward are discovered in it. It is very characteristic that the differentiation of the blood column itself disappears: the individual formed elements become indistinguishable, forming a homogeneous hyaline-like mass. It is essentially important that when circulation is restored, this homogeneous blood column can again break down into its constituent elements. Thus S. is to a certain extent a reversible phenomenon; on the other hand, the only adequate criterion for the phenomenon of S. can be its observation during life: on histological preparations S. can easily be mistaken for a hyaline thrombus, i.e., for a phenomenon following S. and already irreversible in the indicated sense. Ricker points out that against the background of sharp dilation of capillaries, sharp narrowing and even closure of the feeding artery is distinguished, and this phenomenon is considered by him as preceding the paralytic phenomena in the capillary area. According to Tannenberg's data, the indicated spasm occurs only subsequently as a reaction of the smooth muscle of the wall to its overstretching by blood. While emphasizing the neurogenic factor as the main mechanism in the development of true S., Ricker at the same time points to the stages of development of the entire phenomenon, introducing the concepts of peristatic and pre-static hyperemia. By the first he means the degree of hyperemia characterized by sharp slowing of blood flow and some thickening of the blood itself due to its giving up part of the plasma. Such peristatic hyperemia is also called irritative, neuro-paralytic; examples of it can serve as the inflammatory process, hyperemia in nervous diseases (in trigeminal and sciatic neuralgia, in herpes zoster, etc.), in injuries of sympathetic trunks, under the influence of certain poisons, etc. The sensitivity of the corresponding tissues to this or that agent is of enormous importance in this. By pre-static state should be understood that hyperemia which in the degree of vessel dilation and slowing of blood flow as if directly adjoins S. The blood column in this case makes disorderly movements back and forth (ataxia), phenomena of agglutination of erythrocytes can occur in the column itself. Since the pre-static state is still accompanied by minimal circulation, while at the same time the capillaries undergo significant physical-chemical changes, the frequency of diapedetic hemorrhages in these cases, sometimes very large in volume, becomes understandable. The same danger of hemorrhages is also carried by the so-called post-static hyperemia, arising after the resolution of S. The S. itself, and even more so its transition to thrombosis, excludes hemorrhage. However, usually along the periphery of S. there are also areas of pre-static state with a tendency to diapedesis, to marginal standing of leukocytes, to their emigration, etc.: Emigration-infiltrative processes, characteristic of inflammation, especially manifest in the post-static period. According to Ricker's doctrine, peri-, pre-, and post-static processes in the vascular bed, not to speak of S. as such, play the most important role in the mechanism of development of the most various pathological processes (nephritis, tumors, appendicitis, etc.). Being essentially neurogenic, these processes lead to this or that violations of tissue metabolism, and following them to those morphological reactions which characterize the process from the patho-anatomical side. A significant number of pathologists have joined Ricker's teaching. On the other hand, this teaching is not generally accepted, and is completely denied by a number of authors, especially as to the neurogenicity of everything that happens (Fischer-Wasels, Tannenberg). According to the data of Fischer-Wasels and Tannenberg, the dynamics of S. is headed by physicochemical processes. They point out that significant changes in the tissues themselves precede S., leading to an increase in their hydrophilicity; the liquid parts of the blood, in their opinion, do not leave the stasized vessels because they are squeezed through the violated wall, but primarily because the products of disturbance of tissue metabolism, shifts in the reaction of tissues in the sense of acidosis lead to the binding of water by the tissues. The same factors also lead to an increase in the permeability of vascular walls for high-molecular plasma proteins. In the basis of the stasis of blood itself, in their opinion, lie also physicochemical changes in the blood composition, amounting to a decrease in the colloidal stability of plasma. On the other hand, these changes in the blood are secondary, since they are caused by disturbances of metabolism in the tissue itself in the first place. The data of Fischer-Wasels and Tannenberg essentially supplement the teaching on S. On the other hand, these data are hardly incompatible with the data of Ricker, since the latter's interpretation of the phenomena of S. does not exclude, but assumes a physicochemical complex of phenomena, but as a consequence of disturbance of primary-vascular regulations. The cause of S. can be the most diverse factors of exogenous order: action of high and low t°, acids, alkalis, caustic and volatile substances (some OV, chloroform, ether), glycerin, urea, etc. Under experimental conditions these substances apparently act not only directly on the tissues, vessels, but also on the blood, causing in it changes leading to S. (decrease of surface tension of colloids of the wall and erythrocytes, acceleration of sedimentation of the latter due to change in the ratio of protein fractions, increase of viscosity, etc.). The endogenous factors also have great importance. This significance can be understood in two ways. In some cases S. and pre-static states arise in the order of this or that angioneurotic and psychic disorders, e.g., in infectious diseases, intoxications, in other cases the substances affecting S. can be the body's own substances (of the histamine type), arising in the course of this or that pathological processes and especially those accompanied by necrobiosis, histolysis. This probably includes S. and pre-static hemorrhages in the late periods of trauma, similar phenomena in disintegrating tumors, around infarcts, etc.--To true S. is opposed the occlusive S., arising with complete closure of venous outflow; the existence of such a mechanism of stasis remains however controversial. It is very probable that here also the above-mentioned nervous and humoral factor comes into action. The outcomes and significance of S. are dictated by the volume, duration and place of development of the phenomenon itself. Rapidly passing S. may not leave special changes or give fleeting functional disorders. With greater duration and considerable sensitivity of tissues (for example in the nervous system) they can lead to necrotic changes of irreversible order. Gangrenous processes on the skin, extremities in acute infections probably also have in their basis blood S. and subsequent thrombosis of vessels. As has been pointed out, certain dangers are carried by pre- and post-static states mainly in the sense of hemorrhages, edema, infiltrative-inflammatory processes, etc.

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“Stasis (a2845).” Soviet Medical Encyclopedia. English translation of Bolshaya Meditsinskaya Entsiklopediya, 1st ed. (Moscow, 1928–1936), ed. N. A. Semashko. https://sovietmedicalencyclopedia.pages.dev/article/stasis/