ANTU causes local gastric irritation; when absorbed, it increases permeability of the lung capillaries in all animals, although species variability in dose response is marked. Properties of ANTU, when compared with those of warfarin, have led to near abandonment of its use. Dogs and pigs are occasionally poisoned; ruminants are resistant. Animals with an empty stomach readily vomit after ingestion of ANTU; however, food in the stomach decreases the stimulation to vomit, and fatal quantities may be absorbed. Signs include vomiting, hypersalivation, coughing, and dyspnea. Animals prefer to sit. Severe pulmonary edema, moist rales, and cyanosis are present. Dependent signs include weakness; ataxia; rapid, weak pulse; and subnormal temperature. Death from hypoxia may occur within 2–4 hr of ingestion, while animals that survive 12 hr may recover.

The lesions are suggestive. The most striking findings are pulmonary edema and hydrothorax. Hyperemia of the tracheal mucosa; mild to moderate gastroenteritis; marked hyperemia of the kidneys; and a pale, mottled liver are found in most cases. Tissue for chemical analysis must be obtained within 24 hr.

Emetics should be used only if respiratory distress is not evident. Prognosis is grave when severe respiratory signs occur. Agents providing sulfhydryl groups, eg, n-amyl mercaptan, sodium thiosulfate (10% solution), or n-acetylcysteine are beneficial. Positive-pressure oxygen therapy, an osmotic diuretic (eg, mannitol), and atropine (0.02–0.25 mg/kg) may relieve the pulmonary edema.

Last full review/revision March 2012 by Frederick W. Oehme, DVM, PhD