ISSN 2398-2977      

Blood: coagulation defects - acquired/inherited


Synonym(s): Acquired and inherited coagulation defects


  • Coagulation defects are rare but important.
  • There are 2 stages to coagulation - primary and secondary hemostasis.
  • Primary hemostasis is the initial reaction to disruption of the vascular endothelium.
  • Secondary hemostasis stabilizes the clot formed by primary hemostasis.
  • Defects can occur in either the primary or secondary hemostatic mechanisms.
  • Cause: acquired forms such as immune-mediated thrombocytopenia, congenital abnormalities, secondary effects to major organ disease and systemic inflammatory response syndrome, iatrogenic forms, poisonings, infections resulting in platelet destruction.
  • Signs: hemorrhage.
  • Diagnosis: clotting tests, platelet count, fibrinogen estimation.
  • Treatment: blood/plasma transfusion, vitamin K1, protamine.
  • Prognosis: guarded to poor.



  • Primary hemostasis disorders:
    • Platelet destruction: immune-mediated - primary autoimmune, eg foal thrombocytopenia and dermatitis syndrome, or secondary or neonatal alloimmune disease, drug induced, infectious diseases, eg EIA   Equine infectious anemia (EIA)   andAnaplasma phagocytophilum  Anaplasma phagocytophilum  .
    • Platelet dysfunction: genetic platelet dysfunction, eg glanzmann thrombasthenia or acquired dysfunction, eg secondary to uremia, or drug induced, eg aspirin irreversibly binds Cox and therefore prevents aggregation.
    • Insufficient platelet production: myelophthsis/myelodysplasia or drug induced - phenylbutazone   Phenylbutazone  , chloramphenicol   Chloramphenicol  .
  • Secondary hemostasis disorders:
    • Genetic clotting factor deficiency: vWF deficiency, VIII deficiency (Hemophilia A), prekallikrein deficiency.
    • Vitamin K deficiency: liver disease, warfarin poisoning or other dicumarol derivatives, moldy sweet clover toxicity.
    • Liver disease can result in decreased bile secretion and thus decreased vitamin K absorption (fat soluble).
    • Abnormal consumption of clotting factors: DIC, hemorrhage, thrombosis.
    • Iatrogenic forms also occur: overdose of warfarin   Warfarin sodium   in treatment of navicular disease   Navicular bone: syndrome   (no longer used). Heparin   Heparin   overdose (antidote protamine   Protamine sulfate  ).
  • Poisonings:

Predisposing factors

  • Any condition that affects coagulation cascades either directly or secondarily.


  • Toxins/drugs that target clotting directly, eg warfarin   Warfarin sodium  , used therapeutically and as accidental ingestion of rat poison.
  • Acquired forms affect each component of the clotting cascades:
    • Cells, especially platelets.
    • Specific factor deficits.
    • Fibrinogen deficits.
  • Common secondary effects to other major organ disease, including:
    • Liver failure:
      • Fibrinogens deficits.
      • Clotting factor deficits.
    • Disseminated intravascular coagulopathy   Disseminated intravascular coagulation  :
      • Consumptive coagulopathy with preliminary hypercoagulable state.
      • Removes all clotting factors and releases anticoagulant fibrin degradation products (FDP).
  • Iatrogenic forms also occur:
  • Poisonings:
    • Coumarin from moldy hay Link: Toxicity: mycotoxic leukoencephalomalacia (NEW).
    • Rat poison (warfarin   Warfarin sodium  ) ingestion.
    • Aspirin   Acetylsalicylic acid  medication - blocks platelet adhesion.
  • Immune-mediate thrombocytopenia   Blood: thrombocytopenia  :
    • Alloimmune thrombocytopenia probably due to sensitization to thrombocyte antigens during previous pregnancy or transfusion.


  • Disorders of the primary or secondary hemostasis result in excessive bleeding.


  • Slow onset usually associated with progressive consumption (possibly without regeneration) of clotting factors.
  • Alloimmune thrombocytopenia   Thrombocytopenia: overview  presents with profound signs in first days of life.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Epstein K L, Brainard B M et al (2011) Thrombelastography in horses with acute gastrointestinal disease. J Vet Intern Med 25 (2), 307-314 PubMed.
  • Bentz A I, Palmer J E et al (2009) Prospective evaluation of coagulation in critically ill neonatal foals. J Vet Intern Med 23 (1), 161-167 PubMed.
  • Johns I C & Sweeney R C (2008) Coagulation abnormalities and complications after percutaneous liver biopsy in horses. J Vet Intern Med 22 (1), 185-189 PubMed.
  • Pusterla N, Luff J A et al (2007) Disseminated intravascular coagulation in a horse withStreptococcus equi subspecies zooepidemicus meningoencephalitis and interstitial pneumonia. J Vet Intern Med 21 (2), 344-347 PubMed.
  • Lechner K (2001) Management of an adult immune thrombocytopaenia. Rev Clin Exp Haem (3), 222-235 PubMed.
  • Brooks M, Leith G S, Allen A K et al (1991) Bleeding disorder (von Willebrands Disease) in a Quarter horse.  JAVMA 198, 114-116 PubMed.
  • Littlewood J D, Bevan  S A & Corke M J (1991) Haemophilia A (classic haemophilia factor VIII deficiency) in a thoroughbred colt foal. Equine Vet J 23, 70-72 PubMed.
  • Johnstone I B & Crane S (1986) Haemostatic abnormalities in horses with colic: their prognotic value. Equine Vet J 18, 271-273 PubMed.
  • Scott E A, Byars T D & Lamar A M (1980) Warfarin anticoagulation in the horse. JAVMA 177, 1146 PubMed.
  • Scott E A, Sandler G A & Byars T D (1978) Warfarin: effects of intravenous loading doses and vitamin K on warfarin anticoagulation in the pony. Am J Vet Res 39, 1888-1889 PubMed.

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