Disseminated intravascular coagulation in Horses (Equis) | Vetlexicon
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Disseminated intravascular coagulation

ISSN 2398-2977


Synonym(s): DIC, endotoxemia

Introduction

  • A coagulopathy triggered by a primary disease; presents as low grade thrombosis or hemorrhagic diathesis and possibly shock.
  • Cause: systemic inflammatory response syndrome is the most common cause.
  • Signs: petechiae, ecchymoses of mucous membranes; thrombosis or hematoma following venipuncture; epistaxis, melena; associated primary cause.
  • Diagnosis: clinical signs of SIRS and DIC, assessment of hemostatic system.
  • Treatment: as for primary disease; fluid therapy   Fluid therapy: overview  +/- anticoagulants, eg heparin or aspirin; as for sequelae.
  • Prognosis: depends on severity and management of primary disorder; potentially catastrophic and can result in multi-organ dysfunction/failure characterized by laminitis   Foot: laminitis   or respiratory distress, neurological signs or colic.

Presenting signs

Acute presentation

  • DIC always presents acutely secondary to a primary disease which results in SIRS.
  • DIC will not present alone so clinical signs usually reflect the primary underlying disease..

Age predisposition

  • Foals in septic shock are susceptible to DIC but it can occur at any age.

Cost considerations

  • Once a horse/foal has gone into DIC the prognosis is extremely poor and considerable intensive treatment is required to treat them.
  • The treatments are often very expensive.

Special risks

  • It is not recommended to anesthetize a horse in DIC as they can become profoundly hypotensive.

Pathogenesis

Etiology

Pathophysiology

  • Primary disease results in SIRS with an overwhelming inflammatory response.
  • The inflammatory response (in particular TNF-alpha, IL1 and IL6)    →   activation of intrinsic coagulation, reduction in fibrinolysis and increased fibrin formation.
  • Fibrin deposits in microvasculature = general and visceral microthrombi.
  • Primary disease   →   increase of systemic procoagulant substance(s) or endothelium dysfunction that allows exposure of collagen to platelets
  • Decreased perfusion   →   vascular ischemia (eg digital ischemia   →   laminitis)   →   fibrinolysis.
  • Fibrin degradation products (anticoagulants)   →   into circulation   →   hemorrhage.

Timecourse

  • Usually low grade or fulminant.
  • Most commonly detected when fulminant.

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.
  • Cesarini C et al (2010) Association of admission plasma D-dimer concentration with diagnosis and outcome in horses with colic. J Vet Intern Med 24 (6), 1490-1497 PubMed.
  • Dunkel B et al (2010) Association between hypercoagulability and decreased survival in horses with ischemic or inflammatory gastrointestinal disease. J Vet Intern Med 24 (6), 1467-1474 PubMed.
  • Monreal L & Cesarini C (2009) Coagulopathies in horses with colic. Vet Clin North Am Eq Pract 25 (2), 247-258 PubMed.
  • Dallap B L (2004) Coagulopathy in the equine critical care patient. Vet Clin North Am Eq Pract 20 (1), 231-251 PubMed.
  • Jarvis G E & Evans R J (1994) Endotoxin-induced platelet aggregation in heparinised equine whole blood in vitro. Res Vet Sci 57 (3), 317-324 PubMed.
  • Welch R D et al (1992) Disseminated intravascular coagulation associated with colic in 23 horses (1984-1989). J Vet Intern Med  (1), 29-35 PubMed.
  • Morris D D (1988) Recognition and management of disseminated intravascular coagulation in horses. Vet Clin North Am Equine Pract 4, 115-143 PubMed.