Disseminated intravascular coagulation pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omer Kamal, M.D.[2]

Overview

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 consequences 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.

Pathophysiology

DIC is an acquired syndrome characterized by the intravascular activation of coagulation due to sepsis, trauma, malignancy, liver disease, obstetric disorders, envenomation, vascular anomalies and major transfusion reactions. It can originate from and cause damage to the microvasculature, which may eventually lead to organ dysfunction. Under homeostatic conditions, the body is maintained in a state of hematological equilibrium of coagulation and fibrinolysis termed as hemostasis. The activation of the coagulation cascade yields thrombin that converts fibrinogen to fibrin; the stable fibrin clot being the final product of coagulation cascade. 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).

DIC as a disease process

  • DIC occurs secondary to a clinical disorder. The clinical spectrum includes sepsis, trauma, malignancy, liver disease, obstetric disorders, envenomation, vascular anomalies and major transfusion reactions.
  • Ocurrence of DIC in a patient should always be seen as an indicator of another life-threatening condition and warrants thorough diagnostic evaluation.

Mediators of induction of DIC

  • DIC may be induced by either or both of the following mechanisms:
    • As a consequence of systemic inflammatory response, there is activation of cytokine network and thereby coagulation system as in sepsis or polytrauma and/or
    • Release of pro-coagulant products into the blood stream such as in malignancies or obstetrical cases.

Activation of coagulation cascade

Consumptive coagulopathy and bleeding sequelae

Summary

As a summary:[8][9][10]

References

  1. Martinod K, Wagner DD (May 2014). "Thrombosis: tangled up in NETs". Blood. 123 (18): 2768–76. doi:10.1182/blood-2013-10-463646. PMC 4007606. PMID 24366358.
  2. Hellum M, Øvstebø R, Brusletto BS, Berg JP, Brandtzaeg P, Henriksson CE (March 2014). "Microparticle-associated tissue factor activity correlates with plasma levels of bacterial lipopolysaccharides in meningococcal septic shock". Thromb. Res. 133 (3): 507–14. doi:10.1016/j.thromres.2013.12.031. PMID 24423888.
  3. Gordon SG, Franks JJ, Lewis B (February 1975). "Cancer procoagulant A: a factor X activating procoagulant from malignant tissue". Thromb. Res. 6 (2): 127–37. PMID 234638.
  4. Martinod K, Demers M, Fuchs TA, Wong SL, Brill A, Gallant M, Hu J, Wang Y, Wagner DD (May 2013). "Neutrophil histone modification by peptidylarginine deiminase 4 is critical for deep vein thrombosis in mice". Proc. Natl. Acad. Sci. U.S.A. 110 (21): 8674–9. doi:10.1073/pnas.1301059110. PMC 3666755. PMID 23650392.
  5. Sack GH, Levin J, Bell WR (January 1977). "Trousseau's syndrome and other manifestations of chronic disseminated coagulopathy in patients with neoplasms: clinical, pathophysiologic, and therapeutic features". Medicine (Baltimore). 56 (1): 1–37. PMID 834136.
  6. Gordon SG, Mielicki WP (March 1997). "Cancer procoagulant: a factor X activator, tumor marker and growth factor from malignant tissue". Blood Coagul. Fibrinolysis. 8 (2): 73–86. PMID 9518049.
  7. Xu J, Zhang X, Pelayo R, Monestier M, Ammollo CT, Semeraro F, Taylor FB, Esmon NL, Lupu F, Esmon CT (November 2009). "Extracellular histones are major mediators of death in sepsis". Nat. Med. 15 (11): 1318–21. doi:10.1038/nm.2053. PMC 2783754. PMID 19855397.
  8. Capon SM, Goldfinger D (June 1995). "Acute hemolytic transfusion reaction, a paradigm of the systemic inflammatory response: new insights into pathophysiology and treatment". Transfusion. 35 (6): 513–20. PMID 7770905.
  9. Levi M, Toh CH, Thachil J, Watson HG (April 2009). "Guidelines for the diagnosis and management of disseminated intravascular coagulation. British Committee for Standards in Haematology". Br. J. Haematol. 145 (1): 24–33. doi:10.1111/j.1365-2141.2009.07600.x. PMID 19222477.
  10. Kim JE, Lee N, Gu JY, Yoo HJ, Kim HK (June 2015). "Circulating levels of DNA-histone complex and dsDNA are independent prognostic factors of disseminated intravascular coagulation". Thromb. Res. 135 (6): 1064–9. doi:10.1016/j.thromres.2015.03.014. PMID 25843168.


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