ISSN 2398-2969      

Disseminated intravascular coagulation

icanis

Synonym(s): DIC, Consumption coagulopathy


Introduction

  • Intravascular activation of blood coagulation system concurrently with activation of fibrinolytic system.
  • Cause: variety of diseases, eg infections, neoplasia, immune-mediated hemolytic anemia, pancreatitis, severe trauma.
  • 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, low molecular weight heparin, fluid therapy, plasma blood products.
  • Prognosis: very poor, frequently fatal, ('DIC = Death Is Coming').

Pathogenesis

Etiology

Predisposing factors

General
  • Tissue damage.

Specific

  • Release of tissue thromboplastin (phospholipid from cell membranes and organelle membranes), into vasculature.

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, fibrin polymerization and 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 Shock.
  • Consumption of platelets and clotting factors →bleeding tendency.

Timecourse

  • Acute form: 1-5 days.
  • Chronic form has not been proven in veterinary medicine in dogs.

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.
  • Ruiz de Gopegui R, Suliman H B & Feldman B F (1995) Disseminated intravascular coagulation - present and future perspective. Comp Haem Int 5 (4), 213-226 SpringerLink.
  • O'Keefe D A, Couto C G (1988) Coagulation abnormalities associated with neoplasia. Vet Clin North Am Small Anim Pract 18, 157-168 PubMed.
  • Shappendel R J (1988) Disseminated intravascular coagulation. Vet Clin N Am Small Anim Pract 18 (1), 169-184 PubMed.

Other sources of information

  • Rudloff E & Kirby R (2009)Disseminated Intravascular Coagulation: Diagnosis and Mangement.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 XIV.Bonagura J C (ed) Philadelphia: W B Saunders. pp 190-199.

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