This lady has presented with clinical features of placental abruption; this diagnosis is confirmed by the ultrasound scan. There is cardiotocographic evidence of fetal distress; but even more importantly, there is obvious maternal distress, with her vital signs indicating the presence of grade III hypovolemic shock. She needs immediate resuscitation, including administration of high flow oxygen to maintain an oxygen saturation of over 95%, and a blood transfusion. This should be followed by urgent delivery via cesarean section (as the cervix is unfavorable). A full blood count and coagulation profile should be ordered in parallel, and corticosteroids administered to promote fetal lung maturity (these may confer some benefit, even during such a short time period). However, the test results reveal a deranged coagulation profile; in the context of an obstetric emergency, this is suggestive of disseminated intravascular coagulation (DIC); this is confirmed by the presence of elevated D-Dimers (which are a form of fibrin degradation products). The DIC will most likely correct itself spontaneously following delivery; thus, her coagulation abnormalities should be corrected urgently, so that surgery can proceed. Note that recombinant human activated protein C is not indicated in the management of DIC anymore, as there is very little evidence to indicate benefit, while several studies have showed potential harm.
Disseminated intravascular coagulation (DIC) is an acquired coagulation disorder characterized by disruption of the finely controlled mechanisms of hemostasis, resulting in bleeding manifestations and impaired organ perfusion. DIC is a sequela of an underlying disorder, rather than a separate clinical entity; known causative entities include sepsis, burns, severe trauma, severe hemorrhage, malignancies, and certain obstetric conditions and vascular disorders. Note that due to the numerosity of the underlying etiologies, the overall incidence of the condition is difficult to estimate. The pathophysiology of DIC is complex, with certain aspects unclear even today; however, it is believed that pro-inflammatory cytokines play a key role in the process, causing systemic activation of the coagulation cascades and uncontrolled fibrin and thrombin generation. Uncontrolled thrombin generation results in widespread microvascular thrombosis, with subsequent tissue necrosis and organ hypoperfusion; to counteract this, fibrinolytic systems are activated resulting in generation of fibrin and fibrinogen degradation products (FDP). The FDPs impair platelet function and polymerization of fibrin, resulting in a hypocoagulable state with excessive bleeding; exhaustion of platelets and coagulation factors also contributes to bleeding. The clinical presentation of DIC ranges from asymptomaticity to overt bleeding; this variance is believed to be because the underlying etiology affects the clinical signs and symptoms; Thus, when hypercoagulability outstrips activation of the fibrinolytic system, patients tend to have a form of DIC with fewer symptoms and a more protracted course; this is referred to as 'chronic' (or non-overt) DIC. In contrast, when activation of the fibrinolytic system overrules hypercoagulation, patients present with excessive bleeding; this known as 'acute' (or overt) DIC. Note that despite the above arbitrary classification, it is not uncommon for thrombosis and bleeding to coexist. Thus, patients may demonstrate ischemic manifestations involving the kidneys, liver, lungs and bowel; they may also show bleeding tendencies such as prolonged bleeding from venipuncture sites, epistaxis, petechiae or ecchymoses, hematoma formation, mucosal bleeding and intracavitary hemorrhage. Note that the assemblage of hypercoagulation, widespread thrombosis and organ dysfunction is usually more common, and may precede frank bleeding; furthermore, while identification of DIC in the early, hypercoagulable state is demanding, this is much more likely to result in a favorable outcome. There is no single, gold-standard test to diagnose DIC; the diagnosis results on a combination of clinical findings and laboratory results. In patients in whom the condition is suspected, key investigations include a full blood count (FBC); tests of hemostatic function including prothrombin time (PT), activated partial thromboplastin time (aPTT) and serum fibrinogen levels; fibrin-related markers such as fibrinogen degradation products FDP), D-dimers, or soluble fibrin (SF); and natural anticoagulant levels such as antithrombin (AT) and protein C. Prolongation of PT and aPTT, with or without a low platelet count reflects uncontrolled activation and consumption of coagulation factors; low fibrinogen and natural anticoagulant levels and/or elevated fibrin-related markers confirm the presence of widespread thrombosis, indicating the body's losing battle to lyse the excessive clots and maintain hemostasis. It is important to appreciate that none of the above tests are specific for DIC when performed alone; they may be used in conjunction with a scoring system, such as that put forward by the International Society for Thrombosis and Haemostasis (ISTH) for further accuracy. However, use of a scoring system is not mandatory for the diagnosis - a suggestive clinical picture in combination with most of the aforementioned hematological abnormalities (but not necessarily all) is sufficient. Note also that the hepatic and renal functions should also be assessed via investigations, as these patients are at high risk of multiple organ failure. The cornerstone of DIC management is aggressive treatment of the underlying cause, i.e. administration of antibiotics in sepsis, transfusion of blood and/or blood components in severe hemorrhage and anticancer treatment in malignancy. Supportive management measures are also essential to alleviate the disastrous consequences of DIC. Appropriate fluid resuscitation is vital to maintain optimal organ perfusion while timely adjustments in fluid therapy are important to prevent deterioration of renal functions due to fluid overload. Oxygen supplementation and even mechanical ventilation may be necessary to rectify hypoxia and associated sequelae, due to pulmonary compromise. Antacid therapy is also important, while enteral nutrition may be necessary to help maintain gastrointestinal mucosal integrity and to prevent bacterial translocation. In many cases, prompt and proper management of the underlying cause and the correct supportive management results in spontaneous resolution of DIC. While specific management of the hematological derangements may be required occasionally; it is important to appreciate that the treatment should be guided by the patient's clinical picture, and not by laboratory reports alone.