Diabetes and Hypercoagulability

QUESTION: 

Can a diagnosis of  secondary hypercoagulable state, (D68.69) be assigned for an uncontrolled diabetic patient who is treated with 81 mg ASA QD?

ANSWER:

Yes, as long as the documentation links the diabetes to the hypercoagulable state.

The coagulability of the blood is crucially important in ischemic cardiovascular events because the majority of MI and stroke events are caused by the rupture of atherosclerotic plaque and the resulting occlusion of a major artery by a blood clot (thrombus).

Up to 80% of patients with diabetes die a thrombotic death. Seventy-five percent of these deaths are the result of an MI, and the remainder are the result of cerebrovascular events and complications related to PVD.

The first defense against a thrombotic event is the vascular endothelium. Diabetes contributes to widespread endothelial dysfunction. The endothelium and the components of the blood are intricately linked, such that clotting signals initiated in the endothelial cell can activate platelets and other blood components, and vice versa.

Patients with diabetes exhibit enhanced activation of platelets and clotting factors in the blood. Increased circulating platelet aggregates, increased platelet aggregation in response to platelet agonists, and the presence of higher plasma levels of platelet coagulation products, such as beta-thromboglobulin, platelet factor 4, and thromboxane B2, demonstrate platelet hyperactivity in diabetes. Coagulation activation markers, such as prothrombin activation fragment 1+2 and thrombin–anti-thrombin complexes, are also elevated in diabetes. In addition, patients with diabetes have elevated levels of many clotting factors including fibrinogen, factor VII, factor VIII, factor XI, factor XII, kallikrein, and von Willebrand factor.

Conversely, anticoagulant mechanisms are diminished in diabetes. The fibrinolytic system, the primary means of removing clots, is relatively inhibited in diabetes because of abnormal clot structures that are more resistant to degradation, and also because of an increase in PAI-1.47

Clinicians attempt to reverse this hypercoagulable state with aspirin therapy, widely recommended for use as primary prevention against thrombotic events in patients with diabetes. However, numerous studies have suggested that aspirin in recommended doses does not adequately inhibit platelet activity in patients with diabetes.

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