Morphologic Diagnosis of Disseminated Intravascular Coagulation: Histologic, Histochemical and Electronmicroscopic Studies

Abstract

The syndrome "disseminated intravascular coagulation" (DIC) is an "inter mediary mechanism of disease" [57] initiated by a local or generalized activation of coagulation and characterized by the dynamics of an enhanced consumption of procoagulant as well as anticoagulant coagulation factors ["consumption coagulo pathy," 42, 43]. The consumption involves not only the plasmatic but also the thrombocytic coagulation factors.The consumption of platelets and platelet factors already occurs during the initial phase of DIC and is characterized by the formation of platelet-rich microthrombi in the peripheral circulation and by the embolization of these microthrombi. In contrast, the consumption proper of the procoagulant and anticoagulant plasmatic coagulation factors, except the tissue plasminogen acti vator [5,21,31], cannot be histomorphologically visualized. Thus the decisive histomorphologic symptom of a preceding plasmatic consumption is provided by characteristic morphologic changes that only concern fibrinogen and its high molecular weight derivatives during the final phase of DIC. PLATELET-RICH MICROTHROMBIIn the initial stages of DIC, platelet-rich microthrombi are particularly observed in the capillaries of the lungs [4,33,44,52]. The lungs can be considered as a filter for all platelet aggregates which are generated in the microcirculation or in the venous blood (Fig. 1). The pulmonary clearance of platelets has been termed "trapping of the platelets by the lungs."Three pathophysiologic phases can normally be distinguished: In the course of the first phase, platelets aggregate reversibly or adhere to the surface of endothelial cells. In a second phase, these platelets can either disaggregate or form irreversible accumulations with consecutive viscous metamorphosis. It is only during this second phase that vasoactive substances and procoagulative material are released into the surrounding medium [4,35,61,63,67,81]. In the third phase, platelet-rich microthrombi can convert to fibrin-rich microthrombi after destruc tion of platelets and inhibition of platelet aggregates by plasma factors [41,69,70].

Thrombotic Thrombocytopenic Purpura: An Extended Editorial

“…The Sanarelli-Shwartzman reaction is excluded from a pathogenetic function in TTP because it is thrombin-mediated. It cannot have a primary causal role as some have suggested [18,20,62,99,123,125,155,159,162] if the Kwaan hypothesis is correct. A DIC syndrome may develop in the course of a case of TTP, but such an independent event constitutes a complication and not the true course of the disease.…”