Disseminated intravascular coagulation


Disseminated intravascular coagulation (DIC) is a life-threatening syndrome characterized by disseminated and often uncontrolled activation of coagulation. This syndrome is associated with a high risk of macro- and microvascular thrombosis and progressive consumption coagulopathy, which leads to an increased bleeding risk. Several pathological conditions may trigger DIC, the risk of DIC is particularly high in patients with sepsis. Indeed, DIC occurs in 30% to 50% of them, whereas the frequency of DIC is approximately 10% in patients with solid tumors, trauma, or obstetric calamities. The overall prevalence of DIC in hospitalized patients is unknown because the established clinical scoring systems for DIC are not systematically employed in clinical practice. Furthermore, the prevalence of DIC depends on the context of hospitalization and is higher in critically ill patients hospitalized in intensive care units (ICUs). In this subset of patients, the prevalence of DIC ranges from 8.5% to 34% depending on the underlying diagnoses and the diagnostic scoring system used (Papageorgiou et al., 2018).

It is a complex coagulopathic state that can present as a thromboinflammatory response to diverse causes that include septic shock, traumatic injury, pregnancy, and cancer.1 The International Society on Thrombosis and Hemostasis defines DIC as “an acquired syndrome characterized by the intravascular activation of coagulation with loss of localization arising from different causes that can originate from and cause damage to the microvasculature, which if sufficiently severe, can produce organ dysfunction.” In DIC, endothelial injury and microcirculatory abnormalities produced by hemostatic abnormalities cause multiorgan failure. Of note is that DIC is not a primary disease state rather a pathophysiologic response to an underlying disease process and is based on laboratory diagnosis. The clinical (phenotypic) manifestations can range as a spectrum of either bleeding or thrombotic manifestation due to causes that include the underlying disease process (e.g., cancer induced DIC), or the time course of diagnosis and therapy. The basis of therapy for DIC is to treat the underlying disease but also provide temporary support of the coagulation disorder and coagulopathy that depends on whether the patients present with a bleeding or thrombotic phenotype. The complexity of managing DIC is to balance both the bleeding and thrombotic complications that occur (Brown & Levy, 2019).

No single history, physical exam, or laboratory component can lead to a diagnosis of or rule out DIC; therefore, a combination of both subjective, objective, and laboratory findings should be utilized to make a diagnosis of DIC. Laboratory findings suggestive of DIC include both an increased prothrombin time (PT) and an increased partial thromboplastin time (PTT), as well as a decreased fibrinogen level as widespread activation and consumption of the clotting cascade occurs. The overall platelet count and hematocrit level may be reduced as well. Schistocytes or fragmented erythrocytes are also commonly seen on a peripheral blood smear. The presence of fibrin split products additionally has a high sensitivity but low specificity for the presence of DIC. A specific scoring system to assess for the presence of DIC was established in 2007. This score includes platelet count, fibrin markers such as D-dimer, prolonged PT, and fibrinogen level with a score over five indicating a high likelihood for overt DIC (Papageorgiou et al., 2018).

The treatment for DIC centers on addressing the underlying disorder, which ultimately led to this condition. Consequently, therapies such as antibiotics for severe sepsis, possible delivery for placental abruption, and possible exploratory surgical intervention for trauma represent the mainstays of treatment for DIC. Platelet and plasma transfusions should only be considered in patients with active bleeding or a high risk of bleeding or those patients requiring an invasive procedure. A common threshold utilized for platelet transfusions in this patient population is less than 50 x 10^9 platelets per liter for actively hemorrhaging patients and 10-20 x 10^9 platelets per liter for those not actively bleeding but at high risk of future bleeding. Likewise, fresh frozen plasma, typically at a dose of 15 mL/kg to 30 mL/kg, and cryoprecipitate can be transfused to replenish coagulation factors. Prothrombin complex concentrate may also be considered; however, this formulation only contains s

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