BLOOD COAGULOPATHY IN DOGS WITH SHOCK-INDUCED BY INJECTION OF HEARTWORM EXTRACT

A crude, whole-body extract of female heartworms was administered IV t o 10 dogs with and 13 dogs without heartworm (HW) infection. Shock dev eloped in 8 of 10 infected dogs and II of 13 noninfected dogs, and blo od coagulopathy was observed in 12 of 19 dogs with shock. Prevalence a nd severity of blood coagulopathy were proportionate to prevalence and severity of shock. Platelet count decreased in all dogs with shock wi th or without blood coagulopathy; thus, the decrease in platelet count might be related to shock. In 4 dogs, activated partial thromboplasti n time (APTT) was prolonged-192.0 seconds at 30 minutes after HW injec tion-and prothrombin time (PT) was increased-13.8 seconds at initial c ollapse. In 8 dogs, APTT was increased-200 seconds for 2 hours after H W injection-and PT was increased-200 seconds at 30 minutes after the i njection. The APTT prolongation might have been caused mainly by decre ases in activities of factors VIII, IX, XI, and XII of the intrinsic b lood coagulation pathway. In dogs with severely prolonged PT, plasma f ibrinogen concentration and factor II activity decreased slightly. Pro longed PT was corrected in vitro by addition of normal plasma at high concentration (> 80%), but prolonged APTT could not be corrected in vi tro by addition of 80% normal plasma. Serum fibrin degradation product s concentration was < 10 mu g/ml, and soluble fibrin monomer complex w as negative in all dogs. Thrombi were not found in blood vessels of an y organ at necropsy and after histologic study. Therefore, it was sugg ested that: blood coagulopathy resulting from inhibition of coagulatio n factor activities might develop in shock induced by HW extract.