Lavro Z. Y., Lebed H. B., Yastremska O. O., Maksymyuk H. V., Demianchuk N. R., Porokhnavets L. Ye.


About the author:

Lavro Z. Y., Lebed H. B., Yastremska O. O., Maksymyuk H. V., Demianchuk N. R., Porokhnavets L. Ye.



Type of article:

Scentific article


Topicality. Despite the early diagnosis of gastrointestinal bleeding (GI bleed) causes, lethality in these conditions still remains rather high. Integrated conservative therapy using endoscopic hemostasis does not always allow surgical intervention to be avoided, but in some patients after its application occurs repeated bleeding. This is the reason for a more careful choice of the therapeutic tactics, taking into account the criteria for pathogenesis of this pathology, in particular the state of the hemostasis system. The study of hemostasis is an important element of the integrated approach to the assessment of the thrombotic or hemorrhagic complications risk. In this regard, it is relevant not only to clarify the pathophysiological changes in the hemostasis system in the gastrointestinal tract, but also to identify their effect on the dynamics of bleeding, which will further promote adequate patient management. Aim. To find out the features of the state of the hemostasis system reaction in patients of different ages with gastrointestinal bleeding in the dynamics of the disease and with varying severity of its course. The object and methods of research. A hemostasis study was performed in 170 patients (Me age 45 years) with gastrointestinal bleeding on 1st, 3rd and 7th days of the acute period. The hemostasis included: counting platelets, determining the prothrombin time with the calculation of the international normalized ratio (INR), studying the activated partial thromboplastin time (APTT), thrombin time, the content of fibrinogen, soluble fibrin-monomeric complexes (SFMC), antithrombin III, protein C, and determination of Hageman-dependent fibrinolysis. The control group comprised the hemostatic index of 20 practically healthy individuals. Results of the research and their discussion. Analyzing changes in hemostasis at a light degree of severity, the signs of hypercoagulation were observed for only 1 day, which generally indicates the normal response of the body, aimed at the formation of a thrombus and stopping the bleeding when damage to the blood vessels of the mucous membrane of the gastrointestinal tract occurred. With an average degree of hemorrhage, hypercoagulation changes in the blood of the first day were expressed more to a degree compared to bleeding of a mild degree, and were characterized by a decrease in INR, a shortened APTT, an increase in fibrinogen, an increase in SFMC and decrease in platelet counts. But at day 3, these rates returned to the reference values, and the platelet count and the SFMC content were up to the seventh day of observation. In the course of a severe GI bleed, the first day of the disease was dominated by increased hypercoagulability, which could have resulted in rapid depletion of the hemostasis system with the development of the DICs syndrome, and increased ischemia in the area of ulceration or defect with a violation of the reparative processes. Syndrome of hypocoagulation at 3-7 days indicates the inability of the hemostasis system to adequately respond to damage to the vessel and the formation of hemorrhage, with the possible threat of re-bleeding. Conclusions The nature of changes in platelet, procoagulant, anticoagulant and fibrinolytic hemostasis in patients with gastrointestinal bleeding depends on the severity of the pathological process and indicates the pathogenetic significance of violations of adequate blood supply to the gastrointestinal mucosa in the development of bleeding, and therefore may serve as a criterion for evaluation of the effectiveness of the therapy and prognosis of the end of the disease


gastrointestinal bleeding, hemostasis study, hypercoagulation, DICs syndrome


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Publication of the article:

«Bulletin of problems biology and medicine» Issue 3 (152), 2019 year, 138-143 pages, index UDK 616-005.3-08-074/.078:616.33/.34-005.1