| Abstrakt: |
Hemostasis dysfunction plays an important role in the pathogenesis of pancreonecrosis. Platelet and clotting factor activation in the presence of hyperfibrinogenemia and suppressed fibrinolysis develop during the stage of pyonecrotic complications, which provokes microcirculatory disorders, the main cause of pancreonecrosis progress. Treatment with nonfractionated heparin (NFH) for prevention of blood clotting does not prevent the development of the DIC syndrome, as, despite its anticoagulation activity, the drug possesses proaggregation effects and is devoid of the profibrinolytic effect. Laboratory signs of the DIC syndrome were detected in the majority of patients treated with NFH (decreased level of antithrombin III, prothrombin index, and fibrinolysis suppression). Blood clotting prevention with clexane (enoxaparin) was effective, as this drug did not stimulate platelet aggregation and promoted the maximum realization of fibrinolysis, the defense function of the hemostasis system. The absence of microclots in capillaries of patients treated with clexane manifested by intensification of tissue perfusion and hence, more effective draining of destruction zone. Increase of tissue perfusion outside the destruction zone prevented the dissemination of necrosis and disease progress, i.e. promoted the elimination of one of the most important mechanisms of pancreonecrosis pathogenesis. |
