ACUTE ORGANOPHOSPHATE POISONING IN TWO GORDON SETTERS

Two Gordon Setters, a 2-year-old neutered male (patient A) and an 11-year-old spayed female (patient B), were presented to the Veterinary Teaching Hospital at University of Parma following an acute onset of severe clinical signs. The dogs, which lived indoors and outdoors, were found in lateral recumbency displaying profuse hypersalivation. Upon admission, patient A was stuporous but hemodynamically stable with rhythmic pulses and normotensive blood pressure. Patient B was comatose, experienced two episodes of respiratory arrest, and required intubation and mechanical ventilation. Both dogs had large bowel diarrhea, and patient B showed muscle fasciculations indicating neuromuscular involvement. An acute toxicologic insult with multiorgan damage was suspected, and both patients were hospitalized in the intensive care unit for stabilization and close monitoring. Initial blood work revealed hyperchloremic metabolic acidosis with hypernatremia and hemoconcentration. Patient B also showed marked hypercapnia. CBCs were unremarkable aside from transient band neutrophilia. Serum biochemistry showed evidence of hepatomuscular injury, elevated DGGR lipase, and increased C-reactive protein. Coagulation profiles were normal. Urinalysis in patient A revealed active sediment, borderline proteinuria, and bacteriuria. Supportive therapy was promptly initiated. Fluid resuscitation with lactated Ringer’s solution was performed (10 mL/kg boluses, followed by 3 mL/kg/h maintenance and tapering). Lipid emulsion therapy (Intralipid®) was administered as a bolus and continuous rate infusion. Antiemetics included maropitant (1 mg/kg IV SID) and metoclopramide (1 mg/kg/day). Atropine was given IV at 0.3 mg/kg on admission and 0.1 mg/kg on subsequent days. Ampicillin/sulbactam (25 mg/kg IV TID) was used for antibiotic coverage. Nutritional support was provided via nasogastric tube. Mannitol (0.5 g/kg IV TID for 48h) was administered to manage suspected cerebral edema. Neurological signs including ventroflexion of the neck, weakness of epaxial muscles, and "flying scapula" were observed, and an electromyographic study was also performed. Environmental investigation revealed that the dogs had access to fields treated with Direx 7.5 GR containing chlorpyrifos, confirming acute organophosphate poisoning. Due to the delayed identification of the toxicant, pralidoxime was administered approximately 36 hours post-admission, starting with a loading dose of 50 mg/kg followed by 25 mg/kg BID for 48 hours. This delay likely influenced clinical outcomes, particularly for patient B, who, despite some laboratory and neurological improvement, could not be weaned from mechanical ventilation due to persistent nicotinic effects on respiratory muscles. Compassionate euthanasia was elected on day 4. Patient A showed signs of intermediate syndrome but progressively improved and was discharged on day 6. This case underscores the importance of considering environmental toxicants in the differential diagnosis of acute neurological and gastrointestinal syndromes in companion animals, emphasizing the importance of comprehensive anamnesis and increased community awareness to prevent such intoxications. Early supportive therapy and targeted antidotal treatment are critical in managing organophosphate intoxication. Limitations of this report include the absence of confirmatory diagnostic tests, such as measurement of acetylcholinesterase activity or identification of chlorpyrifos residues in biological samples.