Disseminated intravascular coagulation: Difference between revisions

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Usually in the context of [[critical care | critical care medicine]], '''disseminated intravascular coagulation (DIC)''' is a syndrome, always produced by underlying cause(s) and not a diagnosis in itself, which has two seemingly opposite and potentially life-threatening manifestations: simultaneous disorders of clotting and hemorrhage. First, the body-wide [[coagulation]] system activates, and produces widepread but small clots (i.e., [[thrombus|thrombi]]).  These thrombi interfere with the ability of the blood to reach cells and deliver oxygen, and may lead to failure of multiple organs.
In the second stage, the intense coagulation can exhaust the precursors of thrombi, and produce extensive and diffuse bleeding. The bleeding can also be due to a derangement of the mechanisms of [[fibrinolysis]], perhaps due to comsumption of a regulatory factor such as [[alpha2-antiplasmin]].
It is usually an acute and life-threatening presentation, but also can appear in subacute or chronic disease, as a generalized thromboembolic disorder. Warnings during patient evaluation include extensive bruising around the sites of routine venepunctures.
==Pathways==
The main pathways leading to fibrin deposition are:<ref name=eMed-Over>{{citation
| journal = eMedicine Specialties > Hematology > Coagulation, Hemostasis, and Disorders
| title = Disseminated Intravascular Coagulation
| author = Marcel M Levi, Alvin H Schmaier
| date = 4 October 2009
| url = http://emedicine.medscape.com/article/199627-overview
}}</ref>
#tissue factor-mediated thrombin generation
#dysfunctional physiologic anticoagulant mechanisms, such as the antithrombin system and the protein C system, which insufficiently balance this thrombin generation.
#impaired fibrin removal due to depression of the fibrinolytic system. This impairment of endogenous thrombolysis is mainly caused by high circulating levels of the fibrinolytic inhibitor PAI-1. 
==Etiologies==
A wide range of causes need to be considered. <ref name=FP>{{citation
| url  = http://www.fpnotebook.com/Hemeonc/Coags/DsmntdIntrvsclrCgltn.htm
| journal = Family Practice Notebook
| title = Disseminated Intravascular Coagulation
}}</ref>
*Infection, such as:
**Gram Negative Sepsis
**[[Neisseria meningitidis]] Meningococcemia
**Rocky Mountain Spotted Fever
*Neoplastic disease
**Mucin-Secreting [[adenocarcinoma]]
**Promyelocytic Leukemia
**Prostate Cancer
**Lung Cancer
*Tissue Damage
**Mechanical [trauma]]
**Surgery (e.g. Prostate Surgery)
**Heat Stroke
**Burn injury
**Dissecting aneurysm
*Obstetrical Complication
**[[Abruptio placentae]]
**Amniotic fluid embolism
**Retained fetal products on intrauterine fetal death
**Severe [[preeclampsia]]
**HELLP Syndrome
**Acute Fatty Liver of Pregnancy
*Hemolytic disease
**[[Thrombotic thrombocytopenic purpura]] (TTP)
**[[Hemolytic uremic syndrome]] (HUS)
*Immunologic Disorders
**Immune complex disorders
**Allograft rejection
**Incompatible blood transfusion
**[[Anaphylaxis ]]
*Metabolic
**[[Diabetic ketoacidosis ]]
*Miscellaneous
**[[Shock]]
**[[Snake (animal)bite]]
**Cyanotic Congenital Heart Disease
**Fat embolism
**Severe liver disease
**Cavernous Hemangioma
==References==
{{Reflist|2}}[[Category:Suggestion Bot Tag]]

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Usually in the context of critical care medicine, disseminated intravascular coagulation (DIC) is a syndrome, always produced by underlying cause(s) and not a diagnosis in itself, which has two seemingly opposite and potentially life-threatening manifestations: simultaneous disorders of clotting and hemorrhage. First, the body-wide coagulation system activates, and produces widepread but small clots (i.e., thrombi). These thrombi interfere with the ability of the blood to reach cells and deliver oxygen, and may lead to failure of multiple organs.

In the second stage, the intense coagulation can exhaust the precursors of thrombi, and produce extensive and diffuse bleeding. The bleeding can also be due to a derangement of the mechanisms of fibrinolysis, perhaps due to comsumption of a regulatory factor such as alpha2-antiplasmin.

It is usually an acute and life-threatening presentation, but also can appear in subacute or chronic disease, as a generalized thromboembolic disorder. Warnings during patient evaluation include extensive bruising around the sites of routine venepunctures.

Pathways

The main pathways leading to fibrin deposition are:[1]

  1. tissue factor-mediated thrombin generation
  2. dysfunctional physiologic anticoagulant mechanisms, such as the antithrombin system and the protein C system, which insufficiently balance this thrombin generation.
  3. impaired fibrin removal due to depression of the fibrinolytic system. This impairment of endogenous thrombolysis is mainly caused by high circulating levels of the fibrinolytic inhibitor PAI-1.

Etiologies

A wide range of causes need to be considered. [2]

References

  1. ↑ Marcel M Levi, Alvin H Schmaier (4 October 2009), "Disseminated Intravascular Coagulation", eMedicine Specialties > Hematology > Coagulation, Hemostasis, and Disorders
  2. ↑ "Disseminated Intravascular Coagulation", Family Practice Notebook
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