Introduction

• Most common acquired primary hemostatic defect in dogs.
• Cause: characterized by immune-mediated destruction of antibody coated platelets.
• Most often occurs as primary autoimmune disease but may occur secondary to infections, neoplasia or as an adverse reaction to medication.
• Treatment: glucocorticoids, immunosuppressive therapy. Platelet transfusions can provide transient improvement, but do not substantially increase platelet counts and as such, are reserved for life threatening hemorrhage.
• Prognosis: good, rarely fatal.
  Print off the owner factsheet on Immune-mediated thrombocytopenia Immune-mediated thrombocytopenia to give to your client.

Pathogenesis

Etiology

• Most often occurs as a primary auto-immune disease.
• Antibody-mediated platelet destruction may occur secondary to other disease processes or as a side-effect of medication.

Predisposing factors

Secondary causes

• Inflammatory and infectious disorders, eg Ehrlichia, Anaplasma platys, Babesia, Leishmania, Leptospirosis, Angiostrongylus vasorum.
• Other immune-mediated diseases, eg immune-mediated hemolytic anemia Anemia: immune mediated hemolytic.
• Neoplasia especially hematopoietic neoplasia and lymphoma.

• Following medication with:
  • Sulfonamides.
  • Cephalosporins.
  • Penicillins.
  • Phenylbutazone.
  • Aspirin.
  • Gold salts.
  • Estrogens.
  • Possible response following live-virus vaccination.

Pathophysiology

• Accelerated destruction of antibody coated platelets → decreased circulating platelet lifespan.
• Thrombocytopenia develops when destruction is greater than production.
• Platelet production in bone marrow normally stimulated though in some cases anti-platelet antibodies cross react with megakaryocytes impairing production.
• Bleeding only occurs when platelet count is markedly reduced (<50 x 10⁹/l).

• Thrombocytopenia -> defective primary hemostasis leading to petechial and ecchymotic hemorrhage.
• Secondary hemostasis is unaffected.

Timecourse

• Development of thrombocytopenia is usually acute or sub-acute.
• Clinical signs invariably acute once severe thrombocytopenia has developed.

Diagnosis

Treatment

Prevention

Outcomes