Survival of formalin intoxication in a 13-year-old Thoroughbred gelding.

BACKGROUND: Formalin intoxication via the gastrointestinal route has not been previously reported in the horse. Whereas ingestion of formalin in humans, although rare, is well documented. Majority of human cases are either accidental, suicidal or homicidal and often lead to fatality, with a reported lethal formaldehyde dose equating to 0.12 - 0.16 g/kg bwt. OBJECTIVES: To describe a single case report of the clinical management of an adult horse referred to a veterinary teaching hospital following accidental administration of 10% formalin via nasogastric tube. METHODS: A 13-year-old Thoroughbred gelding originally presented to the referring veterinarian for colic where 1.8 L of 10% formalin was accidentally administered instead of mineral oil via nasogastric intubation, a potentially lethal dose of formaldehyde (0.12 g/kg bwt). Approximately 20-hours following 10% formalin administration the horse was admitted to the referral hospital with moderate tachycardia, occasional ectopic beats, tacky and hyperaemic mucous membranes, delayed capillary refill time, reduced borborygmi, and pronounced digital pulses. Diagnostic investigations included laboratory blood analysis, urinalysis, electrocardiogram, abdominal ultrasound, palpation per rectum and gastroscopy. RESULTS: Patient assessment found evidence of toxicity to the gastrointestinal tract, hypovolaemia and risk for laminitis. Intensive care included fluid and electrolyte therapy, anti-inflammatories and analgesia, continuous digital cryotherapy, gastro-protectants and other methods of gastrointestinal support. The horse was discharged from hospital on day 14 with no long-term complications and the client-veterinarian relationship was preserved. DISCUSSION: In human cases of ingestion, gastrointestinal injury is typically accompanied by severe metabolic acidosis and multiple organ dysfunction syndrome due to toxicity of other body systems that can contribute to non-survival. Formaldehyde toxicity in the present case predominantly affected the gastrointestinal tract, most likely a direct result of the route of administration. Aside from gastrointestinal injury, primary toxicity of other body systems was not confirmed. To prevent this medical error recurring, the referring veterinary clinic revised their labelling and storage of 10% formalin. CONCLUSION: This is the first report of systemic formalin intoxication in the horse. Following a high dose of 10% formalin (0.12 g/kg bwt formaldehyde) enterally, the horse survived having received intensive supportive care based on human guidelines for ingested formalin.

Evaluation of the effects of medium-term (57-day) omeprazole administration and of omeprazole discontinuation on serum gastrin and serum chromogranin A concentrations in the horse.

BACKGROUND: Rebound gastric hyperacidity (RGH) secondary to hypergastrinemia has been suggested to contribute to the rapid recurrence of equine squamous gastric disease (ESGD) in horses after discontinuation of omeprazole. HYPOTHESIS/OBJECTIVES: To evaluate changes in serum gastrin and chromogranin A (CgA) concentrations in response to medium-term (57-day) omeprazole treatment and after omeprazole discontinuation. ANIMALS: Fourteen mature Thoroughbred racehorses in simulated race training. METHODS: Horses received 2.28 g of oral omeprazole PO q24h for 57 days within a 61-day period, excluding a withholding period applied mid-protocol during which treatment was stopped as part of a concurrent study. Serum samples were collected on day 0 before omeprazole treatment, on day 1 of each week of the treatment period, and for an additional 5 weeks after discontinuation of treatment. Serum gastrin and CgA concentrations were analyzed using radioimmunoassay (RIA) and ELISA, respectively. RESULTS: Median serum gastrin concentrations increased 2.5-fold from baseline to day 7 (P < .001) but did not increase further during the omeprazole treatment period. Median serum gastrin concentrations returned to baseline within 2 to 4 days after administration of the last dose of omeprazole. No effect of treatment or discontinuation was seen in serum CgA concentrations. CONCLUSIONS AND CLINICAL IMPORTANCE: Serum gastrin concentrations increased in response to omeprazole treatment but returned to baseline within 2 to 4 days after the last dose of omeprazole. No effect of treatment or discontinuation was seen in serum CgA concentrations. Our results do not support the use of tapering protocols in horses.

Equine Gastric Ulcer Syndrome: An Update on Current Knowledge.

Equine Gastric Ulcer Syndrome (EGUS) is a term that has been used since 1999, initially being used to describe all gastric mucosal disease in horses. Since this time, the identification of two distinct main disease entities of the equine gastric mucosa have been described under the umbrella of EGUS; these are Equine Squamous Gastric Disease (ESGD) and Equine Glandular Gastric Disease (EGGD). In 2015 the European College of Equine Internal Medicine (ECEIM) released a consensus statement defining these disease entities. This document highlighted the lack of evidence surrounding EGGD compared to ESGD, and identified knowledge gaps for further research to be directed. Subsequently, many studies on EGGD have been published, especially on pathophysiology, diagnosis, and treatment. This article updates current knowledge on both ESGD and EGGD as understanding has evolved since the last large-scale review.