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[Disseminated intravascular coagulations]
Insights
Disseminated intravascular coagulation (DIC) involves microcirculation fibrin deposits and consumption coagulopathy. Treatment focuses on the underlying cause, with limited use for heparin and supportive transfusions for bleeding.
Area of Science:
- Hematology and Coagulation Disorders
- Pathophysiology of Thrombosis and Hemorrhage
Context:
- Disseminated intravascular coagulation (DIC) is a complex syndrome characterized by widespread fibrin deposition in the microcirculation.
- It presents with a consumption coagulopathy, leading to diverse clinical manifestations from subtle to severe bleeding.
- Understanding DIC pathophysiology has evolved, revealing non-occlusive fibrin deposits cleared by secondary fibrinolysis.
Purpose:
- To define Disseminated intravascular coagulation (DIC) syndromes and their biological counterpart, consumption coagulopathy.
- To review the clinical profiles, diagnostic tests, and pathophysiology of DIC.
- To discuss current treatment strategies and emerging therapeutic approaches for DIC.
Summary:
- DIC involves microcirculation fibrin deposits and consumption coagulopathy, with varied clinical presentations like purpura fulminans.
- Diagnostic tools include standard coagulation tests, D-dimers, Antithrombin-III, protein C, and alpha 2-antiplasmin.
- Treatment primarily addresses the underlying cause, with strict indications for heparin, and supportive measures like FPC and platelet transfusions for hemorrhage.
Impact:
- Advances in understanding DIC pathophysiology clarify the role of fibrinolysis and its limited association with organ failure.
- Prognosis in DIC is not directly correlated with coagulopathy severity, as seen in contrasting mortality rates between abruptio placentae and septic shock.
- Ongoing research explores novel treatments, including antithrombin-III and C1-esterase inhibitors, for specific DIC complications.
Abstract:
Disseminated intravascular coagulation (DIC) syndromes can be defined as the formation of fibrin deposits within the microcirculation, occurring in definite clinical situations. Their biological counterpart is a consumption coagulopathy. The clinical profiles of DIC have been well known for decades, are multiform and range from latency to overwhelming haemorrhagic diatheses, including also characteristic but rare situations, such as purpura fulminans, acral cyanosis and pictures resembling thrombotic thrombocytopenic purpura or haemolytic-uraemic syndrome. Biological tests of DIC show a consumption coagulopathy, displayed on the standard haemostasis sheet; along with signs of paracoagulation and/or of secondary fibrinolysis (FDP). New tests have recently been introduced: D-dimers are specific and sensible; Antithrombin-III, protein C and alpha 2-antiplasmin also can sometimes be useful. The knowledge of the pathophysiology of DIC has made advances with passing years. Fibrin deposits may be non-occlusive, and indeed they are swiftly removed by a secondary fibrinolysis. Except in very rare situations, such as those leading to a cortical renal necrosis, and perhaps in some ARDS, there is little evidence relating DIC to organ failure syndromes. Moreover, there is no clear relationship between the severity of the consumption coagulopathy and the prognosis. For instance, the mortality is much lower in abruptio placentae, where the coagulopathy is very severe, than in septic shock, where it is usually moderate. In septic shock, the disorders of haemostasis were related initially to a platelet activation, then to an activation of the contact system (releasing kinins and triggering complement cascade), and nowadays to the activation of the extrinsic coagulation system. The treatment of DIC is mainly the treatment of its cause. Indications for heparin therapy should be strictly limited to a few exceptional circumstances. When haemorrhagic diathesis threatens, FPC and/or platelet transfusion may be indicated. Aprotinin can be useful in rare cases of overwhelming secondary fibrinolysis. Trials with antithrombin-III or C1-esterase inhibitors are in progress.