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OBJECTIVE: To describe the clinical features, clinicopathological features, treatment, and outcome of dogs presented for albuterol exposure. DESIGN: Retrospective case series from January 2007 to December 2017. SETTING: Tertiary veterinary facility. ANIMALS: Thirty-six client-owned dogs presenting for known or suspected albuterol exposure secondary to chewing on albuterol metered-dose inhalers (MDIs). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: All dogs presented with clinical signs attributable to albuterol exposure. The most common physical examination abnormality was sinus tachycardia, noted in 34 of 36 (94%) dogs. Twenty-seven patients (75%) were admitted to the hospital for therapy, with a median length of hospitalization of 20.5 hours (16.75-24.5). Thirty-two of 36 dogs had serum electrolytes evaluated at admission, with 22 of 32 (69%) presenting with hypokalemia ([K+] < 3.62 mmol/L]). Hyperlactatemia ([lactate] > 2.80 mmol/L) was noted in 23 of 28 (82%) dogs. A negative correlation was found between serum lactate and potassium (r = -0.64, r2  = 0.40, P = 0.0003). Hyperglycemia ([glucose] > 6.44 mmol/L) was noted in 20 of 30 (67%) dogs. Beta antagonist therapy was utilized in 20 of 36 (56%) of dogs. CONCLUSIONS: Although uncommon, albuterol intoxication can lead to significant clinical and electrolyte abnormalities. Albuterol-induced hypokalemia and associated tachyarrhythmias can be successfully managed, and albuterol intoxication has an excellent prognosis for survival to discharge. A minimum database should be evaluated in all dogs presenting for suspected albuterol exposure, with lactate and glucose monitored carefully in dogs with moderate or severe hypokalemia given the correlation found.

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INTRODUCTION: Ractopamine is a leanness-enhancing agent approved in the United States and 26 other countries to reduce body fat content, increase muscle mass, and improve growth rate of certain food-producing animals. Other ß-agonists with stronger pharmacologic effects, especially clenbuterol, had been illegally used as leanness-enhancing agents in the United States, China, and the European Union, and foodborne poisonings related to clenbuterol residue in meat or liver were rarely reported in the European Union and China. We describe an unusual outbreak of leanness-enhancing agent-related food poisoning in Taiwan and its associated diagnostic challenge. REPORT OF THE OUTBREAK: Twelve patients presented to the emergency department of a regional hospital after having dinner together. Their clinical manifestations included nausea, vomiting, palpitation, facial flush, trunk or limb numbness, tremor, headache, weakness, chill, and dyspnea. Laboratory workup revealed the presence of hypokalemia, leukocytosis, and hyperglycemia. Poisoning attributable to ß-agonists was suspected; however, the diagnosis of leanness-enhancing agent poisoning was delayed because there was no leftover meat for analysis and because the veterinary medicine was illegal in Taiwan. Clenbuterol and salbutamol were eventually detected in 10 patients' urine sample by using liquid chromatography-tandem mass spectrometry, and the concentrations ranged from 54 to 806 µg/L and from 0 to 4052 µg/L, respectively. CONCLUSION: ß-Agonist leanness-enhancing agent-related food poisonings are rarely encountered, especially in those countries where relevant veterinary medicines are banned, and may thus pose diagnostic challenge to both emergency physicians and clinical toxicologists.

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An 18-month-old male infant with oral albuterol intoxication was admitted to our pediatric emergency medicine unit with agitation, moderate hypokalemia (2.36 mEq/L), and hyperglycemia (180 mg/dL). His initial electrocardiogram showed sinus tachycardia with a low-amplitude T waves. He was admitted for observation, intravenous hydration was started with added potassium, blood glucose levels were closely monitored along with serum potassium and magnesium, and serial electrocardiography was performed. It should be stressed that as an oral bronchodilator, albuterol does not improve symptoms of asthma, and it can lead to severe complications, which can be avoided when this drug is delivered by inhalation or by a metered dose inhaler.

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Intoxication with the beta2-agonist Albuterol may lead to immediate signs of beta-adrenergic stimulation like excitation, tachypnea and tachycardia. Furthermore, it typically causes severe hypokalemia, which then leads to muscle weakness and which predisposes to ventricular arrhythmias. We describe a dog where albuterol intoxication caused runs of fast paroxysmal ventricular tachycardia that persisted after normalization of the hypokalemia. Based on a markedly elevated serum troponin I level acute myocardial damage was identified as cause of the tachyarrhythmia. Repeated Troponin I measurements and Holter-ECGs were the means to document complete cure.

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Salbutamol is a short-acting agonist of the ß(2) adrenergic receptors sometimes misused or abused, which can result in various cardiovascular adverse effects. We report one case of fatal salbutamol misuse or abuse in a 36-year-old poorly controlled female asthmatic patient with a past medical history of alcoholism and a recent smoking cessation. She died shortly after hospital admission following acute dyspnea and sudden collapse at home. Toxicological analyses evidenced salbutamol overdose, and necropsy showed acute lung edema and marked dysplasia of the right ventricle and revealed the patient was pregnant. The involvement of an initial disorder of the ventricular rhythm leading to cardiac failure is suggested by the presence of several combined pro-arrhythmogenic factors, such as arrhythmogenic right ventricle dysplasia, hypoxemia related to bronchospasm and salbutamol overdose.

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Se presenta el caso de una mujer de 33 años que ingirió una sobredosis de salbutamol con fines suicidas. Presentó taquicadia, hipokalemia severa, hiperglicemia y acidosis láctica. Recibió fluidoterapia, infusión de potasio y propranolol. Se estabilizó doce horas después del tratamiento.

It is presented a 33 year old woman who ingested an over dose of salbutamol trying to commit suicide. She showed tachycardia, severe hypokalemia, hyperglycemia and lactic acidosis. Hydration, potassium replacement and propranol of were administered. The patient was recovered after 12 hours of treatment.

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Pediatricians examine increasing numbers of children with bronchial asthma every year. In Japan, medical institutions can provide standardized therapies according to the Japanese Pediatric Guideline for the Treatment and Management of Asthma 2005. Inhalation therapy is highly beneficial, and a substantial proportion of patients choose to purchase inhalators and practice inhalation therapy at home. Recently, we experienced a case of accidental ingestion of a salbutamol sulfate inhalant by a non-asthmatic child, which reminded us anew of the importance of managing the medicines for asthma. We also recognized the need to educate patients and their families on the knowledge of these medicines. In this report, we analyze the case and discuss measures that pediatricians can implement to avoid accidental inhalant ingestion by children.

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CASE DESCRIPTION: A 6-year-old male castrated Shetland Sheepdog was evaluated because of severe hypokalemia and progressive paresis. CLINICAL FINDINGS: Physical examination revealed fever, tachypnea, mydriasis, hyperemic mucous membranes, severe forelimb paresis, and hind limb paraplegia. The dog had superficial and deep pain sensation in all 4 limbs. Forelimb spinal reflexes were considered normal, but hind limb reflexes were normal to slightly hyperreflexive. The panniculus reflex was considered to be normal, and cranial nerve reflexes were intact. A CBC revealed mild leukocytosis and erythrocytosis, and serum biochemical analysis revealed severe hypokalemia. Thoracic and abdominal imaging did not reveal relevant findings. Blood pressure and ECG findings were within reference limits. Questioning of the owner revealed possible exposure to albuterol via ingestion of medication intended for the owner's horse. Results of serum testing via immunoassay were suggestive of albuterol toxicosis. TREATMENT AND OUTCOME: Treatment included IV administration of an electrolyte solution and supplemental potassium chloride. The rate of potassium chloride supplementation was slowly decreased as serum potassium concentration increased. No other medical intervention was required, and the dog made a rapid and complete recovery. CLINICAL RELEVANCE: Ingestion of albuterol can lead to profound physical and serum biochemical abnormalities. Appropriate historical information should be obtained to identify possible sources and routes of exposure to intoxicants. Albuterol-induced hypokalemia can be successfully managed medically.

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A four-year-old female with salbutamol intoxication was referred to our paediatric emergency medicine unit, due to agitation, tremulousness, sinus tachycardia, mild hypokalaemia and hyperglycaemia. On admission the child was agitated and had a noticeable tremor, an axillary temperature of 38 degrees C and a pulse rate of 185 beats/min. She had no identifiable focus of infection on physical examination to explain her fever. Gastric lavage, activated charcoal, intravenous hydration and electrocardiogram (ECG) monitoring were performed. Her plasma potassium level, blood sugar and QT interval were closely monitored during her hospital stay. Her fever, tachycardia and serum potassium and glucose levels returned to normal and she was discharged in good condition 24 h after admission. The difference of this case from prior cases of salbutamol intoxication was the observation of fever in the absence of evidence of infection. Since the cause of fever was not a reaction to the medication used in the treatment or related to environmental factors, it is assumed that salbutamol is a fever-inducing drug.

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A 20-year-old asthmatic woman who ingested 300 mg of salbutamol (Albuterol) and 30 g of paracetamol is presented. She had sinus tachycardia up to 160/min, hypotension (80/50 mmHg), tremor, hypokalemia (2.1 mEq/l) and hyperglycemia (12.1 mEq/l). Treatment was by gastric lavage, fluids, potassium and N-acetylcysteine. Symptoms resolved in 24 hours.

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This study was designed to determine the threshold dose for toxicity, the potential for serious medical complications, and the medical care required after unintentional albuterol ingestion in children. This study was prospective and descriptive. Data were obtained on pediatric albuterol ingestions evaluated emergently as reported to three regional poison control centers. Data elements included dose ingested, physical findings, medical treatment, and outcome. During 18 months, 78 patients who ingested albuterol and who received urgent medical evaluation were identified. Mean age was 2.8 years. The amount ingested ranged from 0.2 to 8.8 mg/kg. The most commonly reported signs of toxicity were tachycardia (57%, 44/78), widened pulse pressure (50%, 27/54), hyperglycemia (50%, 12/24), agitation (45%, 35/78), low serum carbon dioxide (42%, 10/24), vomiting (26%, 20/78), and hypokalemia (26%, 9/35). We found a threshold dose o 1 mg/kg for three or more signs of toxicity (P < 0.01). No patient required any specific treatment for toxicity. Seventy-two percent of patients were discharged from medical care within six hours of ingestion. Albuterol overdose in children causes a variety of cardiovascular, neuromuscular, and metabolic effects that are usually benign. The threshold dose for the development of three or more signs of toxicity is 1 mg/kg or three to 10 times the recommended daily dose. Toxicity is short-lived and does not require specific therapy or hospital admission in most cases.

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Occupational asthma after exposure to salbutamol in the pharmaceutical industry has not been previously reported. The occurrence of occupational asthma is described in two pharmaceutical process workers who were likely to have inhaled doses appreciably in excess of the therapeutic dose range. The findings do not lead to an unequivocal conclusion on the mechanism of the asthma but it was probably a pharmacological consequence of high exposure.

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Sympathomimetic use results in a triad of hypokalemia, hyperglycemia, and elevated white blood cell count. Transient hypokalemia results from activation of the Na+/K+ pump and transport of potassium intracellularly. Increased serum glucose and insulin may also contribute to the intracellular shift of potassium after sympathomimetic use. Four cases of accidental pediatric albuterol ingestion with significant hypokalemia are reported. Four children between 1 and 6 years of age presented to the emergency department within 5 hours of ingesting 3.0, 1.1, 3.7, and 1.7 mg/kg albuterol, respectively. All four presented alert and oriented in no apparent distress. The most common findings were vomiting, sinus tachycardia, and hypokalemia (2.3, 2.5, 2.8, and 2.5 mmol/L, respectively). Each child received a single dose of activated charcoal and intravenous potassium replacement. All patients recovered uneventfully within 12 to 24 hours with supportive care only. These cases demonstrated that significant depressions in serum potassium can occur after pediatric albuterol overdose. Although transient, the dose-response relationship and duration of effect is unknown. Although significant hypokalemia can occur after ingestion of oral sympathomimetics, replacement should be managed on an individual basis until further studies are completed.

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A two-year retrospective review of accidental albuterol ingestions in children less than 12 years old was performed to assess overdose toxicity and to investigate a dose-effect relationship. One hundred twelve exposures were located. Seventeen cases were excluded owing to coingestants, leaving 95 cases for evaluation. Twenty-nine children (30%) remained at home without intervention or telephone followup because of an ingestion of less than 0.6 mg/kg. Twenty-eight patients (30%) were followed at home by telephone (12 of whom received ipecac). Dosages ranged from 1 to 27 mg, with dose/weight ratios of 0.1 to 1.9 mg/kg. Two children experienced transient mild symptoms (irritability, brief nausea, and vomiting). The remaining 26 children were asymptomatic. Thirty eight cases (40%) were treated in an emergency department. Ingestions ranged from 2 to 96 mg, with dose/weight ratios of 0.3 to 6.3 mg/kg. Ages ranged from one to 11 years. Transient restlessness or irritability was observed in 16 patients, tachycardia in 15, tremors in six, and a widened pulse pressure in one. No serious events occurred in this series, and no patient required treatment beyond gastrointestinal decontamination. For ingestions of 0.6 mg/kg or less, treatment at home with observation may be sufficient. For larger ingestions, eg, greater than 0.6 mg/kg, consideration should be given to direct medical evaluation and gastrointestinal decontamination.

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The cases of two asthmatic adolescents who overdosed on albuterol are presented. Both patients were tremulous, tachycardic, and hypokalemic. Both were treated successfully with IV propranolol. Neither patient developed bronchospasm. The toxicity of albuterol overdoses and its treatment are discussed.

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