disseminated intravascular coagulation (DIC)
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Introduction
DIC results from activation of the coagulation & fibrinolytic systems. It occurs in conditions which promote tissue factor release. DIC may be acute or chronic. Patients with chronic DIC present with bleeding such as epistaxis or gingival bleeding; the condition is problematic, but not life threatening as is acute DIC.
Etiology
- obstetric
- amniotic fluid embolism
- abruptio placentae
- eclampsia
- uterine rupture
- retained placental products
- dead fetus
- septic or missed abortion
- tissue injury
- trauma (head injury or crush injury)
- severe burns
- surgery
- hypothermia
- hyperthermia
- anoxia or asphyxia
- ischemia or infarction
- immunologic
- pulmonary
- infection
- malignancy
- acute leukemia, especially acute promyelocytic leukemia
- solid tumors, especially adenocarcinomas
- chronic DIC is generally associated with malignancy
- cardiovascular
- miscellaneous
- liver disease, acute & chronic
- envenomation
- embolism
- amyloidosis
- SGLT2 inhibitors (serum glucose may be normal)
Pathology
- initiation
- release of tissue factor or generation of tissue factor on the surface of endothelial cells & monocytes
- release of tumor necrosis factor
- IL-1 release
- endotoxin release
- placental tissue substances
- activation of extrinsic pathway of coagulation
- excessive formation of thrombin & plasmin
- formation & breakdown of fibrin
- clot formation & breakdown
- depletion of coagulation factors & platelets
- microvascular fibrin deposition
- microangiopathic hemolysis
Clinical manifestations
- bleeding
- bleeding at site of wound
- gingival bleeding
- vascular access site oozing
- epistaxis
- petechiae
- echymosis
- hemorrhagic bullae
- gangrene
- purpura: purpura fulminans
- acral cyanosis
- hematuria
- thromboses (chronic), venous or arterial
- skin infarction
Laboratory
- platelets in plasma < 60,000/mm3 (thrombocytopenia)
- PT & aPTT may be prolonged or normal, INR may be elevated
- increased fibrin degradation products
- elevated D-dimer
- diminished plasma fibrinogen
- may be elevated with inflammatory process
- progressively diminishes with DIC
- microangiopathic anemia
- schistocytosis in peripheral smear (30-50%)[2]
- elevated factor VIII activity rules out DIC[2]
- see ARUP consult[2]
Differential diagnosis
- vitamin K deficiency
- renal failure
- dysfibrinogenemia
- systemic lupus erythematosus
- thrombotic thrombocytopenic purpura (TTP)
- liver disease
- normal or elevated factor VIII activity suggests liver failure[2]
- factor V not consumed during DIC
- DIC often co-eixsts with liver disease[2]
- sickle cell crisis
- sepsis
Management
- acute DIC
- treatment of underlying pathology
- fresh frozen plasma
- cryoprecipitate:
- indicated for hypofibrinogenemia
- 0.2 bags/kg, 1-12 bags for 70 kg person
- platelet transfusion
- heparin
- indications:
- contraindications
- administration
- chronic DIC
- treatment of underlying pathology
- low dose subcutaneous heparin
- combination antiplatelet agents
- aspirin 600 mg BID with 30 mL of liquid antacid plus dipyridamole 50 mg QID
- sulfinpyrazone 200 mg BID with 30 mL of liquid antacid plus dipyridamole 50 mg QID
More general terms
Additional terms
- localized intravascular coagulation
- Trousseau's syndrome; Trousseau's sign of malignancy; thrombophlebitis migrans
References
- ↑ Saunders Manual of Medical Practice, Rakel (ed), WB Saunders, Philadelphia, 1996, pg 617-618
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Medical Knowledge Self Assessment Program (MKSAP) 11, 16, 17, 18. American College of Physicians, Philadelphia 1998, 2012, 2015, 2018.
- ↑ Schiller G, in: UCLA Intensive Course in Geriatric Medicine & Board Review, Marina Del Ray, CA, Sept 12-15, 2001
- ↑ ARUP Consult: Disseminated Intravascular Coagulation - DIC The Physician's Guide to Laboratory Test Selection & Interpretation https://www.arupconsult.com/content/disseminated-intravascular-coagulation