Disseminated Intravascular Coagulation in Diabetes Mellitus, with Reference to the Role of Increased Platelet Aggregation

A state of hypercoagulability associated with changes in the clotting factors and platelet function has been postulated to be important in the increased thrombotic complications in diabetes mellitus. A fifty-nine-year-old man was admitted with severe diabetic ketoacidosis and shock. Shortly after restoration of his gross fluid and electrolyte imbalance, he developed extensive bleeding into his lungs and gastrointestinal tract. His serum was grossly lactescent. His blood was incoagulable. The existence of disseminated intravascular coagulation was indicated by a decrease in the platelet count and in the levels of fibrinogen, plasminogen, and Factors V and VIII. Plasminogen activator, plasmin, and fibrinogen degradation products all were increased in the plasma, as were cholesterol, triglycerides, phospholipids, total lipids, and free fatty acid concentrations. Postmortem examination revealed widespread hemorrhages. Microthrombi characteristic of platelet aggregates were present in his lungs and kidneys. Serial dilutions of his lipidemic plasma up to 1:150 resulted in increased ADP-induced aggregation of normal platelets. We postulate that the strong influence of the patient's plasma on platelet aggregation was the initial event leading to his disseminated intravascular coagulation. The finding of a platelet aggregation-enhancing factor in other diabetic subjects may shed light on the mechanism of thrombogenesis in diabetes.