Journal of veterinary emergency and critical care (San Antonio, Tex. : 2001) · 2023
Phenibut toxicosis in a dog.
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Sahagian Michael, Mastrocco Alicia, Prittie Jennifer
Аннотация
OBJECTIVE: To describe the successful treatment of severe neurological and cardiovascular abnormalities in a dog following ingestion of the neuropsychotropic drug, phenibut.
CASE SUMMARY: A 2-year-old neutered male Weimaraner was found unresponsive and laterally recumbent in his urine after ingesting approximately 1600 mg/kg of phenibut. On presentation to an emergency clinic, the dog was neurologically inappropriate, tachycardic, hypertensive, and exhibiting a profoundly decreased respiratory rate. Because of progressive clinical signs, electrolyte abnormalities, increased hepatic enzyme activity and bilirubin concentrations, and the development of pigmenturia, referral to specialist care was sought. On presentation, the dog was intermittently somnolent and then maniacal. Sinus tachycardia persisted, and hyperthermia was documented. Hospitalization for supportive care was undertaken, and the dog was administered IV fluids, flumazenil, antiepileptics, and IV lipid emulsion therapy. The dog developed hypoglycemia and treated with dextrose supplementation. Progressive increases in liver enzyme activities as well as pronounced increase in creatine kinase activity, consistent with rhabdomyolysis, were noted. Over the course of 48 hours, the hypoglycemia resolved, and clinical signs significantly improved. Ultimately, the dog was discharged with improved clinical signs, with the owner reporting that 1 week after discharge, a full recovery had been made, and no residual clinical signs persisted.
NEW INFORMATION PROVIDED: To the authors' knowledge, there are no previous reports of phenibut intoxication in small animals. The growing availability and use of this drug by people in the past several years highlight the need for a greater understanding of its effects in companion animals.
CASE SUMMARY: A 2-year-old neutered male Weimaraner was found unresponsive and laterally recumbent in his urine after ingesting approximately 1600 mg/kg of phenibut. On presentation to an emergency clinic, the dog was neurologically inappropriate, tachycardic, hypertensive, and exhibiting a profoundly decreased respiratory rate. Because of progressive clinical signs, electrolyte abnormalities, increased hepatic enzyme activity and bilirubin concentrations, and the development of pigmenturia, referral to specialist care was sought. On presentation, the dog was intermittently somnolent and then maniacal. Sinus tachycardia persisted, and hyperthermia was documented. Hospitalization for supportive care was undertaken, and the dog was administered IV fluids, flumazenil, antiepileptics, and IV lipid emulsion therapy. The dog developed hypoglycemia and treated with dextrose supplementation. Progressive increases in liver enzyme activities as well as pronounced increase in creatine kinase activity, consistent with rhabdomyolysis, were noted. Over the course of 48 hours, the hypoglycemia resolved, and clinical signs significantly improved. Ultimately, the dog was discharged with improved clinical signs, with the owner reporting that 1 week after discharge, a full recovery had been made, and no residual clinical signs persisted.
NEW INFORMATION PROVIDED: To the authors' knowledge, there are no previous reports of phenibut intoxication in small animals. The growing availability and use of this drug by people in the past several years highlight the need for a greater understanding of its effects in companion animals.