Z
Yew Toxicosis
BASIC INFORMATION
EPIDEMIOLOGY
RISK FACTORS
• All parts of the yew are toxic except for the red, fleshy fruit surrounding the hard seed. The hard seed coat is resistant to digestive enzymes. Clinical signs are unlikely if the seed is swallowed whole, but absorption from a cracked or partly chewed seed is possible.
CLINICAL PRESENTATION
HISTORY, CHIEF COMPLAINT
• The onset of systemic clinical signs is extremely rapid (within 30 minutes to 3 hours post ingestion), and progression to death may happen within a few hours.
DIAGNOSIS
INITIAL DATABASE
• Electrocardiogram (ECG; see p. 1253): a wide variety of arrhythmias is possible and fairly common, most commonly atrioventricular (AV) block, ventricular tachycardia, and (ultimately with severe intoxications) ventricular fibrillation/cardiac arrest.
ADVANCED OR CONFIRMATORY TESTING
• Taxines (or metabolites) can be identified in vomitus and stomach contents by gas chromatography, mass spectrometry, and silica gel thin-layer chromatography, although the lengthy turnaround time of such advanced testing usually precludes its use clinically.
• Necropsy: the diagnosis of yew poisoning is generally based on the presence of yew plant in the gut. Taxine affects electrical activity of the heart, so no significant lesions are typically found on necropsy. Fatty degeneration of the kidney, congestion of lungs, and inflammation of the gastrointestinal (GI) tract are possible.
TREATMENT
ACUTE GENERAL TREATMENT
• Evacuation of ingested plant material: in animals not showing clinical signs:
○ Apomorphine, 0.03-0.04 mg/kg IV or IM, or crush tablet portion with water and instill into conjunctival sac and rinse following emesis; or hydrogen peroxide 3%, 2 mL/kg PO (max 45 mL [in large dogs]), repeat in 10 to 15 minutes if no vomiting. Emesis may not remove all plant material from the GI tract. If the ingestion was small and/or the patient has not eaten anything else, some clinicians feed a tasty meal immediately prior to inducing vomiting, to allow mixing and agglutination of plant material with food that is then vomited.
• Treat cardiac arrhythmias as needed:
○ Ventricular tachyarrhythmias (see p. 1165): correct hypokalemia if present and consider lidocaine (dogs: 2 mg/kg IV; cats: use with caution), procainamide (dogs: 6-8 mg/kg IV; cats: 1-2 mg/kg IV), propranolol 0.1 mg/kg slow IV, or esmolol 0.2-0.5 mg/kg slow IV to effect.
• Control seizures (see pp. 353 and 1009): diazepam (dogs/cats: 0.25-0.5 mg/kg IV) or phenobarbital (dogs/cats: 25 mg/kg IV, higher doses often used in dogs)
DRUG INTERACTIONS
Sodium channel blockers (proarrhythmia), calcium channel blockers may potentiate arrhythmias.
Zinc Oxide Toxicosis
BASIC INFORMATION
EPIDEMIOLOGY
SPECIES, AGE, SEX: All animals susceptible; cases commonly involve dogs.
RISK FACTORS: Younger, unsupervised pets are most likely to ingest products containing zinc oxide.
CLINICAL PRESENTATION
ETIOLOGY AND PATHOPHYSIOLOGY
• Zinc oxide–containing ointments or creams are used as topical skin protectants, astringents, and bactericidal agents.
• Some commercial zinc ointment preparations may also contain varying concentrations of vitamin A or D or local anesthetics (benzocaine), cod liver oil, beeswax, petrolatum, or mineral oil.
• Vomiting is self-limiting but may be exacerbated if unlimited water ingestion is allowed before resolution.
TREATMENT
ACUTE GENERAL TREATMENT
• Consider using antiemetics (rarely needed) such as maropitant, 1 mg/kg SQ q 24 h in dogs; or metoclopramide, 0.2-0.5 mg/kg SQ q 6-12 h in dogs, if vomiting is severe and no longer productive (zinc oxide-containing product has been expelled), and gastrointestinal tract obstruction (e.g., with the container as a foreign body) has been ruled out.
• Most cases do not require IV fluids, because clinical signs resolve within 12 hours. Allergic reactions may persist longer (24 hours).
PEARLS & CONSIDERATIONS
COMMENTS
• Single acute ingestion of zinc oxide–containing ointments or creams is not likely to result in zinc toxicosis.
• Repeated use of concentrated zinc oxide–containing products can result in zinc toxicosis, however. Zinc toxicosis has been reported in a dog when 40% zinc oxide ointment was applied dermally for 4 days and dog licked most of the ointment after application.
National Library of Medicine, Medline Plus (human toxicology summary). http://www.nlm.nih.gov/medlineplus/ency/article/002571.htm.
Welch SL. Oral toxicity of topical preparations. Vet Clin North Am Small Anim Pract. 2002;32(2):443-453.
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