Disseminated intravascular coagulation
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| Disseminated intravascular coagulation or Disseminated intravascular coagulopathy | |
| ICD-10 | D65 |
|---|---|
| ICD-9 | 286.6 |
| DiseasesDB | 3765 |
| MedlinePlus | 000573 |
| MeSH | D004211 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Omer Kamal, M.D.[2]
Synonyms and keywords: Disseminated intravascular coagulation, Disseminated intravascular coagulopathy, Consumptive coagulopathy, DIC
Overview
Historical Perspective
Classification
Disseminated intravascular coagulation may be classified according to the degree of fibrinolytic activation into suppressed-fibrinolytic-type DIC (DIC with suppressed fibrinolysis), enhanced-fibrinolytic-type DIC (DIC with enhanced fibrinolysis) and balanced-fibrinolytic-type DIC (DIC with balanced fibrinolysis). Each type differs in clinical features and laboratory findings.
Pathophysiology
DIC is a hemorrhagic syndrome originating in the small blood vessels. DIC is caused by uncontrolled activation of clotting factors and fibrinolytic enzymes. Tissue necrosis and bleeding are results of DIC. Under homeostatic conditions, the body is maintained in a finely tuned balance of coagulation and fibrinolysis. The activation of the coagulation cascade yields thrombin that converts fibrinogen to fibrin; the stable fibrin clot being the final product of hemostasis. The fibrinolytic system then functions to break down fibrinogen and fibrin. Activation of the fibrinolytic system generates plasmin (in the presence of thrombin), which is responsible for the lysis of fibrin clots. The breakdown of fibrinogen and fibrin results in polypeptides called fibrin degradation products (FDPs) or fibrin split products (FSPs). In a state of homeostasis, the presence of thrombin is critical, as it is the central proteolytic enzyme of coagulation and is also necessary for the breakdown of clots, or fibrinolysis.
Causes
There are a variety of causes of DIC, all usually causing the release of chemicals into the blood that instigates the coagulation. Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. Disseminated intravascular coagulation in itself is a life-threatening condition and must be treated as such irrespective of the cause. Common causes include abruptio placentae, amniotic fluid embolism, aortic aneurysm, blood transfusion reaction, drugs (e.g. Amphetamines), beractant eclampsia, giant hemangioma, graft-versus-host disease, HELLP syndrome and hemolytic transfusion reaction.
Differentiating Disseminated intravascular coagulation from other Diseases
Disseminated intravascular coagulation (DIC) must be differentiated from other diseases that cause symptoms of DVT and pulmonary embolism such as: factor V Leiden mutation, protein C deficiency, protein S deficiency, prothrombin gene mutation, antithrombin III deficiency, antiphospholipid antibody syndrome.
Epidemiology and Demographics
The incidence of DIC is different in different diseases as it is almost always related to a life threatening condition. It depends on the cause of DIC such as cancer, infection, trauma and Obstetrical complications. The incidence of DIC is different in different diseases as it is almost always related to a life threatening condition. It depends on the cause of DIC such as cancer, infection, trauma and obstetrical complications. The prevalence of DIC depends on the clinical settings, higher versus low acquity settings. The data sometimes may underestimate the incidence of trasient or mild cases of DIC.
Risk Factors
Common risk factors in the development of DIC include trauma, sepsis, obstetric complications, cancers, and immunologic reactions
Screening
There is insufficient evidence to recommend routine screening for DIC as it does not suggest any changes in mortality except in sepsis
Natural History, Complications and Prognosis
If left untreated, 40-80% patients with DIC may progress to develop organ dysfunction. Common complications of DIC include renal failure, hepatic dysfunction, acute lung injury, neurologic dysfunction and adrenal failure. Low levels of antithrombin at the onset if shock may predict an unfavorable prognosis.
Diagnosis
Diagnostic Study of Choice | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X Ray | Echocardiograph and Ultrasound | CT | MRI | Other Imaging Findings | Other Diagnostic Studies
Treatment
Medical Therapy | Surgery | Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies