Thrombocytopenia and thrombosis in disseminated intravascular coagulation (DIC)

Abstract

Disseminated intravascular coagulation (DIC) is the physiologic result of pathologic overstimulation of the coagulation system. Despite multiple triggers, a myriad of laboratory abnormalities, and a clinical presentation ranging from gross hemostatic failure to life-threatening thrombosis, or even both simultaneously, a simplified clinical approach augmented by a few readily available tests allows prompt identification of the process and elucidation of treatment opportunities. Platelet counts in DIC may be low, especially in acute sepsis-associated DIC, yet increased in malignancy-associated chronic DIC. Thrombotic risk is not a function of the platelet count, and thrombocytopenia does not protect the patient from thrombosis. The stratification of both thrombotic risk and hemorrhagic risk will be addressed.

Increased Von Willebrand factor, decreased ADAMTS13 and thrombocytopenia in melioidosis

“…We note, incidentally, that other additional mechanisms may contribute to the accumulation of VWF during sepsis: for example, oxidative modification of VWF in sepsis has been shown to prevent cleavage of VWF by ADAMST13 [45, 46]. Another potential driver of thrombocytopenia includes diffuse intravascular coagulation (DIC) [47]. Activation of the coagulation pathway may be deleterious when the triggered blood coagulation is insufficiently controlled.…”

Serum Amyloid A and Its Potential Physiological / Pathological Functions - an Overview of Patents

“…It would be necessary to identify early DIC in order to facilitate immediate and appropriate intervention, since therapy is aggressive when directed at forestalling or eradicating the primary pathology. Relying on acute DIC diagnosis is now based upon traditional screening tests such as prothrombin time, activated partial thromboplastin time, platelet count and others [82]. These tests are often performed too late, lack specificity on an individual basis and are only useful in DIC if they lead on to further determinations of fibrinogen.…”

Safety of plasma‐derived protein C for treating disseminated intravascular coagulation in adult patients with active cancer

“…Many factors can contribute to coagulopathy in tumors. Cancer cells express different procoagulant molecules as well as fibrinolytic proteins [10][11][12][13], and chemotherapy may enhance the risk of thrombosis due to its damaging effect on the endothelium [11]. Some clinical differences exist between the coagulopathy that occurs in sepsis in comparison to the one occurring in cancer.…”

“…In general, a less severe picture occurs in cancer patients where chronic activation of coagulation can proceed with few clinical events. This process usually leads to exhaustion of platelets and coagulation factors, thus making bleeding (e.g., at the site of the tumour) the first clinical symptom of DIC, while in other cases, cancerrelated coagulopathy occurs in the form of thrombotic microangiopathies [10][11][12][13]. In cancer-related DIC, conventional treatment is related to high mortality also due to the difficulty in properly treating the underlying neoplasm [10].…”

“…Less is known regarding the correlation between active cancer and coagulation consumption leading to DIC in patients without signs or symptom of sepsis [10][11][12][13]. As the presenting condition, DIC occurs in 2-5% of patients suffering from solid neoplasm [10].…”