Toxicology Brief: Phenylpropanolamine toxicosis in dogs and cats
Adverse effects can potentially be seen at therapeutic doses and include restlessness, urine retention, anorexia, tachycardia, and hypertension. Stroke-like clinical signs have been reported rarely in dogs at therapeutic doses of PPA.1
The most common clinical finding of PPA toxicosis is hypertension secondary to peripheral vasoconstriction. A reflex bradycardia can be seen.4 Other clinical manifestations of toxicosis may include piloerection, vomiting, tachypnea, anxiety or agitation, hyperthermia, tachycardia, tremors, and potential seizures.1In one case report, a 5-year-old dog developed tachypnea, tachycardia, and ataxia after ingesting about 48 mg/kg of PPA.8 Diagnostic test results (electrocardiography, echocardiography, creatine kinase activity, and cardiac troponin concentration) revealed areas of focal myocardial necrosis and multiform ventricular tachycardia consistent with myocardial damage from infarction or direct catecholamine-induced myocardial toxicity. During hospitalization, the dog developed ventricular tachycardia that was successfully treated with lidocaine. Enalapril and atenolol were also administered and continued after discharge. The owners were instructed on discharge to restrict the dog's activity. All abnormalities resolved within six months.8
ASPCA APCC DATA
From 2003 to 2011, the ASPCA Animal Poison Control Center (APCC) database contains 823 cases of PPA exposures; 97% of the cases involved dogs, 3% cats, and < 1% birds.4
Only single-exposure cases were included. One cat receiving 2.8 mg/kg of PPA developed no signs.4 Another cat that ingested 9.1 mg/kg presented with vomiting and mild hypertension, and a third cat that ingested 13.8 mg/kg developed moderate hypertension and tachypnea.4
In dogs, doses of 2.8 and 6.8 mg/kg resulted in mild hypertension and bradycardia.4 Ingestion of > 15 mg/kg often resulted in significant cardiovascular signs.4 At 16.6 mg/kg, a dog developed agitation, moderate hypertension, and ventricular tachycardia.4 Ingestion of a similar dose at 16.7 mg/kg resulted in severe hypertension that responded to administration of acepromazine.4 After ingestion of 43 mg/kg, one dog developed anxiety, severe hypertension, and bradycardia.4 Both acepromazine and nitroprusside were administered to control the hypertension. Final outcomes were not obtained in these cases.
Because of the rapid onset of action, emesis, using 3% hydrogen peroxide (2 ml/kg orally with a maximum of 50 ml) or apomorphine (0.03 mg/kg intravenously; or, in the conjunctival sac, 0.25 mg/kg after dissolving the tablet in saline solution), may be attempted within the first 10 to 15 minutes of exposure in animals not exhibiting clinical signs.1 After, or in lieu of, emesis, activated charcoal (1 to 2 g/kg orally) with a cathartic such as sorbitol may be given.9 The decision to give charcoal should be based on the dose of PPA ingested, weighing the benefit of activated charcoal with the potential risks for aspiration and the development of hypernatremia.