Extensive studies performed over the past 6 years have shown that a degradation product of hematin produces a unique coagulopathy, characterized by thrombocytopenia with platelet degranulation, alteration in the function of numerous clotting and fibrinolytic proteins, and reversible changes in endothelial cells. With the use of degraded hematin, it can be demonstrated that platelet aggregation is stimulated, that platelet adhesion to endothelial cells is enhanced, that the dissociation of factor VIII: C from von Willebrand factor is inhibited, and that the binding of the factor VII/von Willebrand factor complex to platelets is impaired. Even freshly reconstituted solutions of sorbitol-stabilized hematin affect hemostasis and induce thrombophlebitis, presumably because of in vivo degradation of the hematin. Recently, a new formulation of hematin, heme arginate, has been shown to be extraordinarily stable and to have virtually no effects on coagulation. This review compares and summarizes the effects of these various hematin compounds on hemostasis.