Felis ISSN 2398-2950

Disseminated intravascular coagulation

Synonym(s): DIC, Consumption coagulopathy

Contributor(s): Clare Knottenbelt

Introduction

  • Intravascular activation of blood coagulation system concurrently with activation of fibrinolytic system.
  • Cause: variety of diseases, eg infections, neoplasia.
  • Signs: bleeding, coagulopathy, hypovolemic shock.
  • Intravascular coagulation results in thrombosis of vessels in many organs   →   organ failure = consumptive coagulopathy.
  • Depleted supply of platelets and coagulation factors results in bleeding disorder/coagulopathy.
  • Treatment: removal of underlying cause, heparin, fluid therapy.
  • Prognosis: very poor, frequently fatal. ('DIC = Death Is Coming.)'

Pathogenesis

Etiology

Pathophysiology

  • Platelets and coagulation cascades activated by various inflammatory, neoplastic and other conditions which result in cell damage and release of tissue thromboplastin or endothelial damage with exposure of collagen.
  • Thrombi form in many organs   →   organ dysfunction/failure.
  • Fibrinolytic system activated   →   increased fibrinogen degradation products (FDPs) in blood. FDPs = potent anticoagulants (by inhibiting platelet function + various factors within clotting cascade).
  • Consumption of clotting proteins and platelets   →   bleeding tendency.
  • Concurrent coagulopathy and thrombotic disease.
  • Damage to endothelial surfaces or antigen-antibody complexes: damaged necrotic cells   →   release tissue thromboplastin   →   activate extrinsic pathway   →   platelet aggregation and activation of intrinsic pathway.
  • Inflammatory/infectious/neoplastic disease   →   create areas of necrosis and exposed collagen   →   stimulates clotting.
  • Clotting   →   formation of thrombi in capillaries, arterioles and venules in many organs   →   severe circulatory and respiratory insufficiency, neurological disturbances, renal failure, gastrointestinal problems, liver damage.
  • Activated fibrinolytic system   →   fibrin dissolved   →   fibrin degradation products released into blood.
  • Activated clotting and fibrinolytic systems   →   interact with kallikrein-kinin system   →   vasomotor disturbance   →  shock.
  • Consumption of platelets and clotting factors   →  bleeding tendency.

Timecourse

  • Acute form: 1-5 days.
  • Chronic form: days to weeks.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Estrin M A, Wehausen C E, Jessen C R et al (2006) Disseminated intravascular coagulation in cats. J Vet Intern Med 20 (6), 1334-1339 PubMed.
  • O'Keefe D A & Couto C G (1988) Coagulation abnormalities associated with neoplasia. Vet Clin North Am Small Anim Pract 18 (1), 157-168 PubMed.
  • Slappendel R J (1988) Disseminated intravascular coagulation. Vet Clin North Am Small Anim Prac 18 (1), 169-184 PubMed.
  • Thomas J S & Green R A (1988) Clotting times and antithrombin III activity in cats with naturally developing diseases: 85 cases (1984-1994). JAVMA 213 (9), 1290-1295 PubMed.

Other sources of information

  • Rudloff E & Kirby R (2009) Disseminated Intravascular Coagulation: Diagnosis and Management. In: Kirks' Current Veterinary Therapy XIV. Bonagura J C & Twedt D C (eds), Philadelphia: W B Saunders. pp 287-291.
  • Feldman B F, Kirby R & Caldin M (1999) Recognition and Treatment of Intravascular Coagulation. In: Kirks' Current Veterinary Therapy XIII. Bonagura J C (ed), Philadelphia: W B Saunders. pp 190-199.


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