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Diseases » DIC » Causes
 

Causes of DIC

Causes of DIC (Diseases Database):

The follow list shows some of the possible medical causes of DIC that are listed by the Diseases Database:

Source: Diseases Database

DIC Causes: Book Excerpts

DIC as a complication of other conditions:

Other conditions that might have DIC as a complication may, potentially, be an underlying cause of DIC. Our database lists the following as having DIC as a complication of that condition:

DIC as a symptom:

Conditions listing DIC as a symptom may also be potential underlying causes of DIC. Our database lists the following as having DIC as a symptom of that condition:

Medical news summaries relating to DIC:

The following medical news items are relevant to causes of DIC:

Related information on causes of DIC:

As with all medical conditions, there may be many causal factors. Further relevant information on causes of DIC may be found in:

Causes of DIC: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of DIC.

Disseminated intravascular coagulation: Causes
(Handbook of Diseases)

DIC may result from:

infection (the most common cause of DIC), including gram-negative or gram-positive septicemia; viral, fungal, or rickettsial infection; and protozoal infection (falciparum malaria)

obstetric complications, such as abruptio placentae, amniotic fluid embolism, and retained dead fetus

neoplastic disease, including acute leukemia and metastatic carcinoma

disorders that produce necrosis, such as extensive burns and trauma, brain tissue destruction, transplant rejection, and hepatic necrosis.

Other causes include heatstroke, shock, poisonous snakebite, cirrhosis, fat embolism, incompatible blood transfusion, cardiac arrest, surgery necessitating cardiopulmonary bypass, giant hemangioma, severe venous thrombosis, and purpura fulminans.

It isn’t clear why such disorders lead to DIC; nor is it certain that they lead to it through a common mechanism. In many patients, the triggering mechanisms may be the entrance of foreign protein into the circulation and vascular endothelial injury.

Results of accelerated clotting

Regardless of how DIC begins, the typical accelerated clotting results in generalized activation of prothrombin and a consequent excess of thrombin. Excess thrombin converts fibrinogen to fibrin, producing fibrin clots in the microcirculation.

This process consumes exorbitant amounts of coagulation factors (especially fibrinogen, prothrombin, platelets, and factor V and factor VIII), causing hypofibrinogenemia, hypoprothrombinemia, thrombocytopenia, and deficiencies in factor V and factor VIII. Circulating thrombin activates the fibrinolytic system, which lyses fibrin clots into fibrin degradation products.

The hemorrhage that occurs may largely be the result of the anticoagulant activity of fibrin degradation products as well as depletion of plasma coagulation factors.

» READ BOOK EXCERPT ONLINE »

Source: Handbook of Diseases, 2003

Disseminated Intravascular Coagulation: Disseminated Intravascular Coagulation - pathophysiology
(The 5-Minute Pediatric Consult)

  • Not a disorder in itself; occurs as a result of various initiating events
  • Characterized by microvascular hemorrhage and thrombosis
  • May be acute (e.g., meningococcemia) or chronic (e.g., malignancy/leukemia)
  • There is a systemic formation of fibrin as a result of increased thrombin generation, suppression of anticoagulant pathways, impaired fibrinolysis, and activation of inflammatory pathways.
  • Thrombin formation is primarily through the extrinsic pathway, factor VIIa. This pathway is activated via tissue factor expression from damaged endothelial cells.
  • Anticoagulant pathways are diminished because of a decrease in the plasma levels of antithrombin and the protein C system through impaired production and increased destruction.
  • The increase in fibrinolytic activity is likely secondary to the release of plasminogen activators from damaged endothelial cells.
  • The inflammatory cascade is activated via the activated coagulation proteins.

Disseminated Intravascular Coagulation - etiology

Most common causes are sepsis (particularly Gram-negative), hypotensive shock, and trauma (particularly head trauma).

  • Infections:
    • Bacterial Gram-negative and -positive sepsis (e.g., group B streptococcus)
    • Meningococcemia
    • Malaria
    • Fungal: Aspergillus
    • Rickettsial: Rocky Mountain spotted fever
    • Viral
  • Tissue injury
  • Massive head trauma
  • Multiple fractures with fat emboli
  • Crush injuries
  • Profound shock or asphyxia
  • Hypothermia or hyperthermia
  • Massive burns
  • Malignancies:
    • Acute promyelocytic leukemia
    • Acute monoblastic or monocytic leukemia
    • Metastatic carcinomas or other widespread malignancies (e.g., neuroblastoma)
  • Obstetric:
    • Retained intrauterine fetal death
    • Amniotic fluid embolism
    • Abruptio placentae
    • Placenta previa
  • GI:
    • Fulminant hepatitis/hepatic failure
    • Severe pancreatitis
    • Reye syndrome
    • Severe inflammatory bowel disease
  • Neonatal:
    • Necrotizing enterocolitis
    • Congenital viral infections
    • Group B streptococcus infection
    • Erythroblastosis fetalis
    • Small for gestational age
  • Miscellaneous:
    • Acute hemolytic transfusion reaction
    • Kasabach-Merritt syndrome
    • Snake bite
    • Severe thrombotic thrombocytopenic purpura
    • Hemolytic uremic syndrome
    • Homozygous protein C deficiency (purpura fulminans)
    • Severe graft rejection
    • Severe collagen vascular disease
    • Heparin-induced thrombosis
    • Infusion of activated prothrombin complex concentrate
    • Ventriculoperitoneal shunt
    • Kawasaki disease
    • Recreational drugs
    • Hemophagocytic lymphohistiocytosis (HLH)

» READ BOOK EXCERPT ONLINE »

Source: The 5-Minute Pediatric Consult, 2008


 » Next page: Symptoms of DIC

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