ISSN 2398-2969      

Disseminated intravascular coagulation

Clapis

Synonym(s): DIC, Hemorrhagic diathesis


Introduction

  • A clinical syndrome arising secondary to a systemic disease resulting in a hypercoagulable state and exhaustion of the clotting cascade.
  • Cause: viral (RHD), sepsis, heat stroke, neoplasia, immune-mediated disorders and severe injury.
  • Signs: ongoing hemorrhage due to coagulopathy, hypovolemic shock.
  • Diagnosis: hematology and biochemistry, diagnostic imaging, PCR.
  • Treatment: removal or management of inciting cause, fluid therapy, plasma blood products, intensive supportive care.
  • Prognosis: guarded to very poor. Some affected animals present deceased with no prior clinical signs.

Pathogenesis

Etiology

Predisposing factors

General

  • Extensive tissue damage or trauma.

Specific

  • Cellular apoptosis or necrosis and release of thromboplastin (phospholipid from cell membranes) into the blood.

Pathophysiology

  • Exposure of collagen from damaged tissues and vasculature → stimulates thrombocyte aggregation (intrinsic pathway).
  • Thromboplastin released by damaged cells into the bloodstream activates the clotting cascade → cleaves prothrombin into active thrombin → Fibrinogen is cleaved to form fibrin mesh → Part of clot with thrombocytes (extrinsic pathway).
  • Intravascular clot formation is exacerbated, and thrombi form in many vessels and organs → impeded oxygen and nutrient supply, infarcts → Multiorgan failure.
  • Depleted supply of coagulation factors and thrombocytes results in consumptive coagulopathy → bleeding disorders Thrombocytopenia.
  • Excessive fibrin deposition activates fibrinolytic system → fibrinogen degradation products (FDPs) in blood → anticoagulant effect → fibrin dissolved and released into bloodstream.
  • Ongoing tissue damage further stimulates the clotting cascade and fibrinolytic pathways leading to more extensive depletion of components → risk of bleeding increases.
  • Bleeding is exacerbated by loss of anticoagulant factors, eg antithrombin III, via damaged renal tubules and decreased production by damaged liver tissue.
  • Concurrent coagulopathy and thrombotic disease → kallikrein-kinin system → vasomotor abnormalities → Shock.

Timecourse

  • Presents as an acute syndrome (1-5 days) in many cases even though the underlying cause may have been present for longer.
  • DIC can be chronic and progress slowly over several days if the underlying cause is not addressed → it is not clear how common this may be in rabbits.
  • In some cases, the disease may be self-limiting and resolve without progression to the overt hypocoagulable bleeding phase.

Epidemiology

  • Outbreaks often occur in unvaccinated groups of rabbits where the underlying cause is RHD1/2 infection.

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.
  • Semerjyan A B et al (2019) Immune cell pathology in rabbit hemorrhagic disease. Vet World 12 (8), 1332-1340 PubMed.
  • Alonso C et al (2014) Programmed cell death in the pathogenesis of rabbit hemorrhagic disease. Arch Virol 143 (1), 321-332 PubMed.
  • Hermida J, Montes R, Paramo J A & Rocha E (1998) Endotoxin-induced disseminated intravascular coagulation in rabbits: Effect of recombinant hirudin on hemostatic parameters, fibrin deposits, and mortality. J Lab Clin Med 131 (1), 77-83 PubMed.
  • Ueda K, Park J-H, Ochiai K & Itakura C (1992) Disseminated intravascular coagulation (DIC) in Rabbit Haemorrhagic Disease. Jpn J Vet Res 40 (1) 133-141 PubMed.

Other sources of information

  • Meredith A & Lord B (2014) Chapter 9 – Clinical Pathology. In: BSAVA Manual of Rabbit Medicine. BSAVA, UK. pp 124-137.
  • Rudloff E & Kirby R (2009) Disseminated Intravascular Coagulation: Diagnosis and Mangement. In: Kirks' Current Veterinary Therapy XIV. Eds: Bonagura J C & Twedt D C. W B Saunders, USA. pp 287-291.

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