Disseminated intravascular coagulation medical therapy
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2]; Associate Editor(s)-in-Chief: Omer Kamal, M.D.[3]
Overview
The underlying cause must be treated initially. Anticoagulants are only given when indicated (development of thrombotic renal complications) as patients with DIC are prone to bleeding. Platelets may be transfused if counts are very low, and fresh frozen plasma may be administered. DIC results in lower fibrinogen (as it has all been converted to fibrin), and this can be tested for in the hospital lab. A more specific test is for "fibrin split products" (FSPs) or "fibrin degradation products" (FDPs) which are produced when fibrin undergoes degradation when blood clots are dissolved by fibrinolysis. In some situations, infusion with antithrombin may be necessary. A new development is drotrecogin alfa (Xigris®), a recombinant activated protein C product. Activated Protein C (APC) deactivates clotting factors V and VIII, and the presumed mechanism of action of drotrecogin is the cessation of the intravascular coagulation. Due to its high cost, it is only used strictly on indication in intensive care patients. The prognosis for those with DIC, depending on its cause, is often grim, leading the initials to be known colloquially as "death is coming"
Medical therapy
The gold standard and central principle of treatment of DIC is to treat the underlying cause. If the major clinical feature of DIC involved bleeding, treatment should focus on correcting the bleeding. If the major clinical feature of DIC involved clotting, treatment should focus on correcting the clotting (via anticoagulation). The underlying cause must be treated initially. Anticoagulants are only given when indicated (development of thrombotic renal complications) as patients with DIC are prone to bleeding. Platelets may be transfused if counts are very low, and fresh frozen plasma may be administered.
DIC results in lower fibrinogen (as it has all been converted to fibrin), and this can be tested for in the hospital lab. A more specific test is for "fibrin split products" (FSPs) or "fibrin degradation products" (FDPs) which are produced when fibrin undergoes degradation when blood clots are dissolved by fibrinolysis.
In some situations, infusion with antithrombin may be necessary. A new development is drotrecogin alfa (Xigris®), a recombinant activated protein C product. Activated Protein C (APC) deactivates clotting factors V and VIII, and the presumed mechanism of action of drotrecogin is the cessation of the intravascular coagulation. Due to its high cost, it is only used strictly on indication in intensive care patients.[1]
The prognosis for those with DIC, depending on its cause, is often grim, leading the initials to be known colloquially as "death is coming".[2]
Essentials of DIC Therapy
- The heterogeneity of DIC has been a major obstacle in the development of controlled prospective trials of therapy.
- The overall goal of therapy should be to reverse the inciting event, and control the major suspected pathophysiologic process in addition to providing overall supportive care.
- As micro and macrovascular thrombi are thought to be major contributors to morbidity and mortality, a great deal of attention has focused on anticoagulation, and even thrombolysis.
- In cases where bleeding is the predominant manifestation, however, inhibition of plasmin may be crucial.
- Transfusion: FFP (fresh frozen plasma), cryoprecipitate and platelets can be used in patients with severe hemorrhage and hemodynamic compromise as long as ‘the accelerated consumption process is under control’.
- The feared ‘adding fuel to the fire’ has never been unequivocally proved.
Pharmacotherapy
Acute Pharmacotherapies
- Heparin is an active inhibitor of thrombin formation and its effects.
- However, heparin requires AT III in order to produce anticoagulation, and AT III levels are often low in DIC.
- Additionally platelet factor 4 levels are often elevated in DIC and serve to neutralize heparin.
- As heparin can induce thrombocytopenia and activate leukocytes and complement, it may not only aggravate bleeding, but possibly induce thrombosis as well.
- Thus, there is no consensus on its use, though many hematologists would recommend its use as long as there is not excessive clinical bleeding.
- AT III irreversibly inhibits thrombin and factor Xa.
- As AT III is reduced in DIC, some authors have suggested that AT III repletion can neutralize excess thrombin and minimize DIC.
- Recent RTCs in humans have shown a 44% reduction in mortality in patients with DIC who were treated (early) with AT III (this did not reach statistical significance, however).
- Riewald and Riess recommend that until larger studies are out, AT III should be considered in all patients with DIC and AT III deficiency.
- Hirudin is a direct thrombin inhibitor that does not require AT III for its anticoagulant activity.
- It may therefore be even more useful than AT III infusions (studies underway).
Contraindicated medications
Disseminated intravascular coagulation（DIC） is considered an absolute contraindication to the use of the following medications:
References
- ↑ Dhainaut J, Yan S, Joyce D, Pettilä V, Basson B, Brandt J, Sundin D, Levi M (2004). "Treatment effects of drotrecogin alfa (activated) in patients with severe sepsis with or without overt disseminated intravascular coagulation". J Thromb Haemost. 2 (11): 1924–33. PMID 15550023.
- ↑ Norman K (2004). "Alternative treatments for disseminated intravascular coagulation". Drug News Perspect. 17 (4): 243–50. PMID 15334173.