Case Description—A 5-year-old castrated male Toy Poodle cross was evaluated because of lethargy, inappetence, and suspected abdominal hemorrhage. The dog had been evaluated on 4 other occasions for episodes of excessive bleeding associated with trauma or surgical procedures.
Clinical Findings—At previous evaluations, results of repeated measurements of prothrombin time, partial thromboplastin time, and buccal mucosal bleeding time were unremarkable; activated clotting time, plasma von Willebrand factor concentration, results of platelet function testing, and plasma factor VII, VIII, IX, X, XI, and XII concentrations were considered normal. At this evaluation, clinicopathologic analyses revealed mild regenerative anemia that progressed over a 4-day period to moderate regenerative anemia and acute inflammation with panhypoproteinemia. Abdominal ultrasonography revealed a large mass (suspected to be a hematoma) near the urinary bladder. Rotational thromboelastometry revealed that clotting times were within reference limits, with abnormal clot formation times and clot firmness. The result of a factor XIII (FXIII) clot solubility assay confirmed FXIII deficiency.
Treatment and Outcome—The dog's bleeding diathesis resolved with inpatient care and IV fluid therapy, although plasma transfusions had been required at previous evaluations. Seven months after discharge from the hospital, the dog continued to do well clinically, although it had several additional episodes of excessive bleeding.
Clinical Relevance—To the authors’ knowledge, this is the first reported case of congenital FXIII deficiency in a dog. In addition to more common inherited coagulopathies, FXIII deficiency should be a differential diagnosis for dogs with episodes of excessive bleeding and apparently normal results of standard coagulation tests.
CASE DESCRIPTION Three 21-week-old sexually intact female sibling domestic shorthair cats were brought to an emergency clinic because of signs of sudden respiratory distress that were noted by the owner after the cats had been confined for approximately 10 hours in a room with an operating ozone-generating air purifier. No other potential toxicant exposures were reported.
CLINICAL FINDINGS On initial examination, the 3 cats were severely dyspneic and tachypneic. Pulmonary crackles were audible on thoracic auscultation. Thoracic radiography revealed a marked peribronchial, unstructured interstitial pulmonary pattern that coalesced to a patchy alveolar pattern, consistent with noncardiogenic pulmonary edema.
TREATMENT AND OUTCOME A diuretic (furosemide, 2 mg/kg [0.9 mg/lb], IV) and bronchodilator (terbutaline sulfate, 0.01 mg/kg [0.005 mg/lb], IM) were administered, and supplemental oxygen was provided by placing the cats in an oxygen cage at 80% oxygen saturation. By 24 hours after placement in the oxygen cage, all cats had unremarkable respiratory rates and thoracic auscultation findings. Complete resolution of the respiratory signs and radiographic pulmonary lesions was achieved within 48 to 72 hours after initial evaluation. At a recheck examination performed 3 months after initial evaluation, the cats remained free of respiratory signs, and no radiographic pulmonary lesions were detected.
CLINICAL RELEVANCE To the authors’ knowledge, this was the first reported case of pulmonary toxicosis believed to have been caused by ozone exposure in cats. Associated respiratory signs were successfully and rapidly reversed following oxygen supplementation and medical treatment.