Disseminated intravascular coagulation (DIC) is a syndrome that can be initiated by a myriad of medical, surgical, and obstetric disorders. Also known as consumptive coagulopathy, DIC is a common contributor to maternal morbidity and mortality and is associated with up to 25% of maternal deaths. The etiopathogenesis of DIC is complex and currently thought to be initiated by tissue factor or thromboplastin, which is released from trophoblastic or fetal tissue, or maternal decidua or endothelium. Tissue factor activates the coagulation sequence to cause fibrin clotting and its dissolution by the fibrinolysin system. The result of this process can range from mild, clinically insignificant laboratory derangements to marked coagulopathy with bleeding at sites of minimal trauma. Although clinical recognition varies by disease severity, several organizations have attempted to standardize the diagnosis through development of scoring systems. Several important—albeit not necessarily common—obstetric disorders associated with DIC include placental abruption, amniotic fluid embolism, sepsis syndrome, and acute fatty liver of pregnancy. More common disorders include severe preeclampsia, hemolysis, elevated liver enzymes, and low platelet count syndrome, and massive obstetric hemorrhage. Importantly, many of these disorders either cause or are associated with substantive obstetric hemorrhage. Treatment of DIC is centered on two principles. The first is identification and treatment of the underlying disorder. Because many women with consumptive coagulopathy also have massive hemorrhage, the second tenet of treatment is that obstetric complications such as uterine atony or lacerations must be controlled simultaneously with prompt blood and component replacement for a salutary outcome.
For the obstetric conditions associated with disseminated intravascular coagulation, management demands prompt recognition and treatment of the underlying disorder and associated hemorrhage.
Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas.
Corresponding author: David B. Nelson, MD, Dedman Scholar in Clinical Care, Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-9032; email: email@example.com.
Financial Disclosure The authors did not report any potential conflicts of interest.
Continuing medical education for this article is available at http://links.lww.com/AOG/A704.