Suspected intermediate syndrome in a dog after organophosphate poisoning.

OBJECTIVE: To discuss the clinical presentation and successful treatment of a suspected case of intermediate syndrome due to organophosphate (OP) poisoning in a dog. CASE SUMMARY: Two dogs presented with acute cholinergic signs after ingesting an OP insecticide containing 50% acephate. Clinical signs consistent with acute cholinergic crisis resolved in both dogs within 24 hours postingestion. One dog developed an onset of neurological signs consistent with intermediate syndrome approximately 24 hours postingestion. This patient's clinical signs resolved with the use of pralidoxime chloride. NEW OR UNIQUE INFORMATION PROVIDED: OP poisoning most commonly presents as an acute cholinergic crisis, with rare instances of animals developing intermediate syndrome. Few reports of successful treatment and recovery from intermediate syndrome exist in the veterinary literature, particularly with instances in which 2 dogs within the same exposure setting were treated for acute cholinergic signs and only 1 progressed to an intermediate syndrome. This report also highlights the importance of early intervention with pralidoxime chloride prior to the onset of aging.

Mirabegron Toxicosis in Dogs: a Retrospective Study.

Mirabegron is a selective beta (B)3 adrenoreceptor agonist marketed for human treatment of an overactive bladder (OAB). It has a wide margin of safety in humans, but in dogs, severe adverse effects have occurred. We sought to determine the effects and outcome of mirabegron toxicosis in dogs. A retrospective review of all calls within the Pet Poison Helpline (PPH), an international animal poison control center, database was performed for mirabegron exposures between 2013 and 2015. Potential ingested doses ranging from 1.31 to 8.3 mg/kg. Many dogs remained asymptomatic and no fatalities occurred in any dogs. The most commonly reported signs were tachycardia and erythema. While mirabegron was found to have a very narrow margin of safety and high toxicity risk to dogs during preclinical trials, effects appear to differ greatly in the nonclinical field environment and further study is needed.

Acute Hepatic Failure in a Dog after Xylitol Ingestion.

Xylitol is a five-carbon sugar alcohol produced from natural resources frequently used as a sugar substitute for humans. We report the development and successful treatment of acute hepatic failure and coagulopathy in a dog after xylitol ingestion. A 9-year-old 4.95 kg (10.9 lb) neutered male Chihuahua was evaluated at a veterinary clinic for vomiting after ingesting 224 g (45 g/kg, 20.5 g/lb) of granulated xylitol. Hypoglycemia developed within 1-2 h, elevated liver values, suggesting the development of acute hepatic failure, within 12 h and coagulopathy less than 24 h after ingestion. Treatment included maropitant, intravenous dextrose, phytonadione, metronidazole, and fresh frozen plasma. N-acetylcysteine (NAC) and S-adensoyl-L-methionine (SAMe) provided hepatic detoxification and support. The dog survived and liver values returned to normal within 1 month post ingestion. No adverse effects to hepatic function have been identified 2 years after acute xylitol toxicity. This paper is one of the few reports of successful management of a dog with hypoglycemia, hepatic failure, and coagulopathy caused by xylitol toxicity. To date, this is the highest published xylitol dose survived by a dog, as well as the only reported case that documents laboratory changes throughout the course of toxicity and includes normal hepatic indices for 7 months following xylitol toxicity. The rapidly expanding use of xylitol in a variety of products intended for human consumption has led to a rise in xylitol toxicity cases reported in dogs, and clinicians should be aware that more dogs may potentially be exposed and develop similar manifestations.

Comparison of anesthetic induction in cats by use of isoflurane in an anesthetic chamber with a conventional vapor or liquid injection technique.

OBJECTIVE: To compare 2 techniques for induction of cats by use of isoflurane in an anesthetic chamber. DESIGN: Prospective, randomized study. ANIMALS: 51 healthy cats. PROCEDURES: Cats were randomly allocated to 2 induction techniques. Cats were premedicated with acepromazine (0.1 mg/kg [0.045 mg/lb], SC) and buprenorphine (0.01 mg/kg [0.0045 mg/lb], SC) 30 minutes before induction. Cats were then placed into an induction chamber, and anesthetic induction was initiated. One technique involved a conventional flow-through system that used an oxygen flowmeter and an isoflurane vaporizer to flow vapors into the induction chamber. Alternatively, liquid isoflurane was injected into a vaporization tray that was mounted to the interior surface of the chamber lid. Inductions were videotaped for analysis. Five variables (head bobbing, head swinging side to side, paddling, rotating 180 degrees to 360 degrees, and rolling over or flipping) were scored to assess induction quality. Time variables recorded during induction corresponded to the interval until onset of excitatory motion, duration of excitatory motion, interval until recumbency, and interval until complete induction. RESULTS: Compared with cats anesthetized by use of a conventional vapor chamber technique, cats anesthetized by use of the liquid injection technique had a significantly shorter interval until recumbency and interval until complete induction and lower scores for quality of induction, indicating a smoother induction. CONCLUSIONS AND CLINICAL RELEVANCE: Anesthetic induction in cats by use of a liquid injection technique was more rapid and provided a better quality of induction, compared with results for cats induced by use of a conventional vapor technique.