Severe Rhabdomyolysis Associated with Acute Amphetamine Toxicosis in a Dog

Smith, Margaret F.; Wurlod, Virginie

doi:10.1155/2020/2816373

Cited by 5 publications

(12 citation statements)

References 20 publications

(37 reference statements)

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“…Hyperlipidemia is an unavoidable consequence of IVLE use and there is concern for precipitating pancreatitis in animals, even though it is yet to be proven in the acute setting with IVLE therapy. Numerous veterinary reports of successful treatment with IVLE for lidocaine, naproxen, carprofen, ibuprofen, vitamin D, bromethalin, and several other toxicoses have been published (11)(12)(13)(14)(15)(16)(17)(18).…”

Section: Discussionmentioning

confidence: 99%

Case Report: Successful Intravenous Lipid Emulsion Therapy for Canine Amphetamine Toxicosis

et al. 2022

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A 4-year-old, female-spayed, mixed breed dog, weighing 24.2 kg, was presented for acute ingestion of ~12.3 mg/kg of Adderall XRⓇ, an extended-release amphetamine medication. In dogs, the oral median lethal dose for amphetamines ranges anywhere from 9–11 mg/kg to 20–27 mg/kg. On presentation, the patient was agitated, tachycardic and hypertensive. Initial treatment was instituted with intravenous lipid emulsion (IVLE) therapy, and baseline and post-treatment amphetamine concentrations were quantified in serum and plasma. In both serum and plasma, post-IVLE concentrations of amphetamine were lower 1 h after treatment and IVLE was the only treatment instituted during this time. The dog improved significantly while in hospital and was discharged <24 h after presentation. This is the first known reported use of IVLE for treatment of amphetamine toxicosis with documented decreases in both serum and plasma amphetamine levels shortly after administration of IVLE.

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Section: Discussionmentioning

confidence: 99%

Case Report: Successful Intravenous Lipid Emulsion Therapy for Canine Amphetamine Toxicosis

et al. 2022

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“…14 In the veterinary literature, acute kidney injury associated with rhabdomyolysis has been described as multifactorial. 13,15 Myoglobin can cause renal toxicity due renal vasoconstriction, intratubular cast formation and direct toxicity to renal tubular cells. 12 The mechanisms that myoglobinuria induces cause vasoconstriction due to a rapid reduction in renal blood flow, shock, secondary renin-angiotensinaldosterone system activation and activation of several vasoactive mediators.…”

Section: Discussionmentioning

confidence: 99%

Monensin toxicosis in a dog with initial apparent recovery followed by severe relapse

Vitello,

Good

2023

Vet Record Case Reports

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This case report describes successful intensive care management of a toxic myopathy in a 7‐month‐old, female, entire springer spaniel secondary to presumed monensin intoxication. The dog was seen chewing a monensin capsule, and was subsequently presented to the local veterinary practice with generalised weakness, ataxia, hypersalivation and pyrexia. Intravenous lipid emulsion‐activated charcoal and intensive fluid therapy were administered. Bloodwork identified a marked increase in serum creatine kinase activity (226,554 iu/L; reference range: 0–400 iu/L). The patient was discharged the following day after initial hospitalisation, with a complete resolution of clinical signs. Five days after exposure, a rapid deterioration required veterinary assessment at the referral hospital. The patient recovered and was discharged after 9 days of hospitalisation. This case report describes recurrence of clinical signs of monensin toxicosis after initial improvement. However, with aggressive emergency care, symptomatic therapy and intense monitoring, a positive outcome was achieved.

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“…Rhabdomyolysis secondary to amphetamine intoxication is reported in people and dogs. 9,13,14 In human medicine, 80% of rhabdomyolysis is drug induced, with amphetamines being implicated frequently. 14 All cats in this series were suspected to have rhabdomyolysis.…”

Section: Discussionmentioning

confidence: 99%

“…Hypoglycemia secondary to amphetamine intoxication (both immediate and extended-release formulations) has been documented in case reports in dogs, typically evident at hospital presentation. 8,9,20 Multiple factors are postulated to contribute to this hematologic change including increased glucose utilization from seizures, increased muscle activity, elevated temperature, or catecholamine release. 8 Decreased glucose production due to concurrent hepatic dysfunction induced by a combination of hypoxic injury, increased metabolism, and a universal increase in ATP demand are other possible contributing factors.…”

Section: Discussionmentioning

confidence: 99%

“…2 Rarely, development of hypoglycemia or rhabdomyolysis has been reported in dogs, experimental rodent models, and people. [6][7][8][9] There is no antidote for amphetamine toxicosis, and standard interventions include symptomatic therapy with IV fluids, anxiolytics, and antihypertensives/antiarrhythmic drugs as indicated. 8 Sedation and provision of an unstimulating environment, repeated doses of activated charcoal if possible, control of muscle fasciculations and seizures, and active cooling are additional supportive measures.…”

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confidence: 99%

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Hypoglycemia and presumptive rhabdomyolysis secondary to lisdexamfetamine toxicosis in 3 cats

Crecraft

Prittie

Mastrocco

2021

J Vet Emergen Crit Care

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Objective: To describe the clinical course and novel biochemical changes in 3 cats with lisdexamfetamine (LDX) toxicosis.Series Summary: Three cats presented with LDX exposure and initially displayed typical clinical signs of amphetamine toxicosis. However, over the course of hospitalization, hypoglycemia and markedly elevated creatine kinase levels consistent with rhabdomyolysis ensued. All cats were treated with sedatives including phenothiazines and dexmedetomidine. Two cats were hospitalized for 4 days and 1 for 5 days. All cats survived. New or Unique InformationProvided: This is the first case series in cats that reports the novel biochemical changes of delayed hypoglycemia and elevated creatine kinase several days into hospitalization for the treatment of LDX toxicity. The development of delayed clinical signs suggests reconsideration of established hospitalization guidelines for amphetamine ingestion in cats. 1 INTRODUCTION Lisdexamfetamine (LDX) dimesylate (Vyvanse) a is an extended-release amphetamine class drug that is a first-line medication for human attention-deficit/hyperactivity disorder. 1 The recognition of this disorder in people is increasing annually, as has inadvertent medication exposure to small animals. Data published by the American Society for the Prevention of Cruelty to Animals' Animal Poison Control Center (ASPCA APCC) reported 5033 exposures to amphetamines in dogs and cats between 2010 and 2018. 2LDX's a main mechanism of action is to prevent reuptake of catecholamines and to prevent their breakdown via inhibition of monoamine oxidase. 3 This results in a surplus of extraneuronal dopamine, norepinephrine, and serotonin. 3,4 Clinical signs of toxicosis in cats are referable to the drug's sympathomimetic effects in the CNS Abbreviations: AKI, acute kidney injury; ALT, alanine aminotransferase; ASPCA APCC,

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Severe Rhabdomyolysis Associated with Acute Amphetamine Toxicosis in a Dog

Cited by 5 publications

References 20 publications

Case Report: Successful Intravenous Lipid Emulsion Therapy for Canine Amphetamine Toxicosis

Case Report: Successful Intravenous Lipid Emulsion Therapy for Canine Amphetamine Toxicosis

Monensin toxicosis in a dog with initial apparent recovery followed by severe relapse

Hypoglycemia and presumptive rhabdomyolysis secondary to lisdexamfetamine toxicosis in 3 cats

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