Abstract Background Disseminated intravascular coagulation (DIC) is a condition characterized by widespread thrombosis and bleeding due to activation of coagulation pathways and consumption of platelets and clotting factors. It is most commonly caused by sepsis, trauma, malignancy, or obstetric complications, though its underlying etiology can be challenging to identify. The management of DIC focuses on addressing the underlying cause and providing supportive blood product transfusions. While anticoagulation with heparin has been suggested in some cases, its efficacy and safety for DIC has not yet been definitively proven. This case of prolonged DIC demonstrated improvement following the administration of heparin and, thus, supports the potential therapeutic role in select cases. Case Summary A 77-year-old woman was admitted with a one-month history of recurrent epistaxis, retrobulbar hematoma, hematuria, and a left-sided pulmonary embolism, with laboratory studies confirming DIC. She had no history of trauma, recent infection, bleeding disorders, or malignancy. Hematologic evaluation revealed a low alpha-2 antiplasmin level, mildly decreased Factors V, VII, and X, and a prolonged prothrombin time (PT) mixing study with mildly elevated partial thromboplastin time (PTT). A rheumatologic workup was negative, and PET/CT imaging for malignancy surveillance was unremarkable. Serum protein electrophoresis (SPEP) identified an M spike, and thromboelastography (TEG) suggested low fibrinogen levels. Despite multiple transfusions followed by steroids and IVIG, her coagulopathy persisted. Heparin initiation led to significant improvements in fibrinogen, D-dimer, INR, and platelet counts. However, heparin was held for surgical repair of a radial artery pseudoaneurysm, after which her coagulation parameters deteriorated. She remains under treatment for DIC and evaluation for monoclonal gammopathy driving an autoimmune process resulting in alpha-2 antiplasmin and fibrinogen deficiencies, and cytotoxic chemotherapy is being considered should her coagulopathy persist. Conclusion This case supports the potential role of anticoagulation in selected DIC patients, particularly when conventional supportive treatments fail and an underlying cause remains unclear. While causality cannot be definitively established, the rapid correction of coagulopathy with heparin suggests it influenced the course of DIC. Heparin may regulate coagulopathy and fibrinolysis through its interaction with antithrombin III, inhibition of factors Xa and IIa, and anti-inflammatory effects6,8,9. While the therapeutic contribution of anticoagulation for DIC has not been definitively established with large-scale randomized controlled trials and has only been suggested by a few studies7, the observed improvement along with tolerable safety in this case support its potential clinical relevance. Further research is needed to define patient profiles and underlying causes of DIC that may respond to anticoagulation. This abstract is funded by: None
Chukwuma et al. (Fri,) studied this question.