How we manage haemostasis during sepsis

Abstract

Summary Sepsis may be associated with activation of the coagulation system and, in its most severe form, may result in disseminated intravascular coagulation (DIC). Initially, there is thrombosis primarily affecting small and medium sized vessels and contributing to organ dysfunction, but continued activation results in consumption of coagulation factors. This results in prolongation of global coagulation parameters. Often thrombocytopenia is the initial feature in sepsis, which may be followed by prolongation of global coagulation assays, and in severe cases, associated with hypofibrinogenaemia, with overactivation of the fibrinolytic path. The end result is a bleeding phenotype. Scoring systems can be used to help identify patients at risk of DIC and aid in confirming a diagnosis of DIC utilising routine laboratory parameters. Discussion includes medical and blood product support of haemostasis, from thrombotic to bleeding states, in relation to sepsis trigger.

Sepsis-induced Coagulopathy and Disseminated Intravascular Coagulation

“…Thus, identifying patients earlier in the course of their hemostatic dysfunction would be important for potential management, especially in the intensive care unit. 17 Coagulopathy in patients with sepsis continues from an initial compensatory phase to the decompensated stage of DIC. Although there is still debate regarding the definition of coagulopathy, it is generally suggested as "a condition in which the ability of the blood to clot is impaired," 18 and conventionally, the term coagulopathy predominantly had represented a hemorrhagic state.…”

Head, Neck, and Abdominopelvic Septic Thrombophlebitis: Current Evidence and Challenges in Diagnosis and Treatment

“…Coagulation plays a defensive role during infections by limiting the dissemination of pathogens and contributing to their destruction. 10 The systemic inflammatory response during sepsis includes the increased expression of procoagulant cytokines such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor-α, 11 which also activate platelets. 12 Locally, bacteria and viruses elicit a prothrombotic environment both indirectly, through endothelial damage and inflammation, 13 and directly, by inducing the expression of tissue factor on monocytes and endothelial cells, 14 activating the intrinsic coagulation pathway, 10 inhibiting the physiologic anticoagulation mechanisms, 15 and promoting platelet aggregation, 16 particularly via complement activation.…”

Expert consensus on the diagnosis and treatment of thrombocytopenia in adult critical care patients in China

“…For sepsis patients, anticoagulation therapy should be administered in cases of persistent decline in platelet count, persistent elongation of coagulation time, organ dysfunction due to microthrombosis, and when required to manage thrombotic events duringthe hypercoagulable stage of DIC [107]. If the patient is in a hypocoagulable state and at risk for bleeding, anticoagulation therapy may be providedwhile replenishing the patient's coagulation substrates [108]. Randomized controlled trials (RCTs) have shown that recombinant activated protein C, tissue factor pathway inhibitor (TFPI), and thrombomodulin (TM) have no effect in improving the prognosis of sepsis [109][110][111].…”