Today's Veterinary Practice

SEP-OCT 2018

Today's Veterinary Practice provides comprehensive information to keep every small animal practitioner up to date on companion animal medicine and surgery as well as practice building and management.

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PEER REVIEWED 68 SEPTEMBER/OCTOBER 2018 Clinical signs: Sago palm toxicosis can cause vomiting and diarrhea (with or without blood), lethargy, depression, dehydration, anorexia, ascites, abdominal pain, icterus, tremors, ataxia, seizures, coma, and death. 7 Liver failure, coagulopathies, and thrombocytopenia may also be seen, but their onset may be delayed by 2 to 3 days. 7 Margin of safety: Narrow. All parts of the plant are toxic, but the most toxic parts are the seeds. Any exposure is a concern. Mechanism for hypoglycemia: Direct and indirect. The toxins decrease the activity of mitochondria, adenosine triphosphate, and glucose- 6-phosphatase, thereby decreasing gluconeogenesis and glycogenolysis. 8 Hypoglycemia may also be associated with liver failure and/or sepsis. 9 Treatment Tip The key action to take is aggressive decontamination. For dogs brought to you early, while still asymptomatic, the best course of action is inducing emesis, followed by giving multiple doses of activated charcoal. Cholestyramine may also be used in some cases to decrease enterohepatic recirculation. Cholestyramine is a powdered bile acid sequestrant that is widely available at human pharmacies. It binds bile and, by default, the toxins already bound to the bile. Cholestyramine should be given with food and also aids in elimination of cholecalciferol, amatoxin, and some nonsteroidal anti-inflammatory drugs (NSAIDs) (see numbers 3 and 4 below). 6. ZINC AND ALUMINUM PHOSPHIDE Description: Zinc phosphide is an agent commonly used for mole and gopher control; aluminum phosphide is used to fumigate grain stores for insect and rodent control. Clinical signs can develop from inhalation of aluminum phosphide. After ingestion of zinc phosphide bait, phosphine gas is released when the product is exposed to the acidic environment of the stomach. The phosphine gas is rapidly absorbed via inhalation during eructation or across the gastric mucosa. The hydrolyzed phosphine causes significant oxidative damage throughout the body. Zinc toxicosis is not expected. 10 Clinical signs: Zinc or aluminum phosphide exposures cause vomiting, hypersalivation, tremors, respiratory distress, ataxia, weakness, hyperesthesia, and seizures and, in some cases, may progress quickly to death. It is common for patients to have a strong odor to their breath, often described as a pungent garlic smell. Neurologic signs can develop soon after ingestion. Liver and kidney damage may occur days to weeks after ingestion. 2 Margin of safety: Narrow. Any exposure has the potential to cause clinical signs. Mechanism for hypoglycemia: Direct and indirect. Impairment of glycogenolysis and gluconeogenesis 11 can lead to hypoglycemia. Adrenal gland injury and low levels of cortisol may also play a role. 12 Animals experiencing severe seizure activity may become hypoglycemic because of increased metabolic use of glucose. Treatment Tips ■ As soon as possible, administer 1 tablespoon of aluminum hydroxide or magnesium hydroxide per 20 pounds of body weight. Doing so will increase the pH of the stomach and decrease the amount of phosphine gas released. If possible, avoid inducing emesis with hydrogen peroxide; ideally, emesis should be induced with apomorphine while the animal is outdoors. ■ Phosphine gas is toxic to all living creatures. Clients should drive to the clinic with the windows down, in case the dog vomits in the car. Any questions regarding humans (clients and/or veterinary hospital employees) who may have been exposed to phosphine gas should be immediately directed to Human Poison Control (1-800-222-1222). 5. SYMPATHOMIMETICS Description: Sympathomimetics directly or indirectly cause an increase in catecholamines at the neuronal junction. 13 Examples of sympathomimetics include amphetamines, prescription medications for attention-deficit/hyperactivity disorder or attention-deficit disorder, phenylpropanolamine, decongestants (e.g., pseudoephedrine), and illicit drugs (e.g., cocaine, crystal methamphetamine, and 3, 4-methylenedioxymethamphetamine [MDMA, ecstasy]). Clinical signs: Sympathomimetics can cause agitation, aggression, ataxia, tachycardia or bradycardia, hypertension, hyperthermia, vocalization, mydriasis, tremors, and seizures.

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