Cases reported "Poisoning"

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1/45. Contamination of antibiotics resulting in severe pediatric methadone poisoning.

    OBJECTIVE: To report an accidental contamination of antibiotic suspension by methadone that occurred in a retail Canadian pharmacy, leading to severe poisoning in a young child. CASE SUMMARY: A 4 1/2-year-old healthy Asian boy was prescribed amoxicillin suspension for cough and fever. Shortly after receiving the second dose of 5 mL he became drowsy and less responsive. On admission, he was arousable by deep pain, and pinpoint pupils were noted. A urine sample sent for a toxicology screen revealed the presence of methadone and its metabolite. blood methadone concentrations were 0.23 and 0.14 mg/L, five and nine hours after the second dose of amoxicillin was given, respectively. The amoxicillin suspension was tested for methadone and was found to have a concentration of 2.4 g/L. The child gradually improved and was discharged on day 4 in good condition. The pharmacy in which the antibiotic was dispensed has been a dispensing center for a local methadone maintenance program, and methadone was accidentally mixed with the antibiotics. DISCUSSION: In this case, a near fatal outcome occurred when methadone was inadvertently mixed with antibiotics in a community pharmacy. A literature search revealed two previous reports of opiate toxicity in children following ingestion of oral antibiotic preparations. CONCLUSIONS: Prompt action is needed in Canadian pharmacies that dispense methadone in order to minimize such errors in the future. general practitioners, pediatricians, and emergency department physicians should recognize and suspect this rare cause of opiate toxicity in a child. In a patient presenting with a decreased level of consciousness and miosis, with or without respiratory depression, naloxone administration should be considered, whether or not a history of opioid ingestion is obtained.
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2/45. Medical treatment of the adolescent drug abuser. An opportunity for rehabilitative intervention.

    Illnesses related to both the pharmacologic properties of abused substances and their methods of administration often bring the teenager to medical attention and may provide sufficient motivation for the adolescent to seek help beyond the acute problem. Successful treatment of an overdose reaction, an abstinence syndrome, or any other medical complication of drug abuse may give the physician a unique opportunity to begine further evalution for future care.
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3/45. A case of serious organophosphate poisoning treated by percutaneus cardiopulmonary support.

    We report a case of respiratory arrest, refractory circulatory collapse, and severe hypothermia following ingestion of an organophosphate insecticide. In addition to conventional management, including mechanical ventilation, administration of vasopressors, enteral lavage, charcoal hemoperfusion and administration of antidotes, extracorporeal cardiopulmonary support in the form of percutaneous cardiopulmonary support was successfully employed. Percutaneous cardiopulmonary support may be used for severe but potentially reversible pulmonary or cardiovascular toxicity induced by organophosphates as well as complicated severe hypothermia.
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4/45. A case of transient diabetes insipidus associated with poisoning by a herbicide containing glufosinate.

    BACKGROUND: The herbicide BASTA (AgrEvo, germany), containing glufosinate ammonium (20%) and an anionic surfactant, polyoxyethylene alkylether sulfate (33%), is widely used. In acute oral BASTA poisoning, patients develop a variety of clinical signs, including disturbed consciousness, convulsions, and apnea. These effects are suspected to be due to the effects of glufosinate on the central nervous system. CASE REPORT: A 60-year-old man ingested 500 mL of BASTA herbicide in a suicide attempt. He developed not only unconsciousness, respiratory distress, and convulsions but also an increase in urine output (7885 mL/d), elevated serum sodium (167 mEq/L), elevated plasma osmolality (332 mOsm/kg), and a decrease in both urine osmolality (200 mOsm/kg) and urine specific gravity (1.003), which suggested the development of diabetes insipidus. The plasma level of antidiuretic hormone remained within the normal range (1.3 pg/mL), despite high plasma osmolality. The administration of desmopressin was successful in normalizing urine volume, specific gravity, and osmolality. serum sodium corrected gradually within 48 hours. The possible mechanisms causing the diabetes insipidus are discussed.
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5/45. plasma exchange for the removal of digoxin-specific antibody fragments in renal failure: timing is important for maximizing clearance.

    life-threatening digoxin toxicity may be effectively treated with digoxin-specific antibody fragments (Fab). However, in end-stage renal disease, the digoxin-Fab complexes persist in the circulation and dissociate, potentially resulting in rebounding free digoxin levels and the recurrence of symptomatic toxicity. To prevent this rebound phenomenon, plasma exchange (PE) has been implemented for the removal of the digoxin-Fab complexes in renal failure. However, there is only one case report describing its use in this setting. To better determine the optimal timing of PE after Fab administration, we performed two PE treatments (each preceded by Fab) in a patient with acute renal failure and acute digoxin poisoning. The admission serum digoxin level was 21 ng/mL. The timing of the PE treatments relative to Fab dosing was as follows: the first PE was performed 26 hours post-Fab, and the second PE was performed 2.5 hours post-Fab. The plasma ultrafiltrate digoxin concentration was 2.5-fold greater when PE was performed 2.5 hours versus 26 hours after Fab administration (19.9 versus 8.1 ng/mL). The combined total amount of digoxin removed in the ultrafiltrate plasma was minimal (0.13 mg), less than 1% of the total amount of ingested drug. We conclude that the optimal timing of PE is within the first 3 hours after Fab administration. Although PE is efficacious for removing digoxin-Fab complexes, thus preventing rebound digoxin toxicity, it is not efficacious for improving total digoxin clearance because of the large apparent volume of distribution of digoxin (5 to 8 L/kg).
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6/45. Electrocardiographic manifestations: digitalis toxicity.

    Toxicity from the digitalis family of cardiac glycoside medications remains common. Successful treatment depends on early recognition; however, the diagnosis of potentially life-threatening toxicity remains difficult because the clinical presentation is often nonspecific and subtle. The hallmark of cardiac toxicity is increased automaticity coupled with concomitant conduction delay. Though no single dysrhythmia is always present, certain aberrations such as frequent premature ventricular beats, bradydysrhythmias, paroxysmal atrial tachycardia with block, junctional tachycardia, and bidirectional ventricular tachycardia are common. Treatment depends on the clinical condition rather than serum drug level. Management varies from temporary withdrawal of the medication to administration of digoxin-specific Fab fragments for life-threatening cardiovascular compromise.
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7/45. Childhood poisoning: access and prevention.

    OBJECTIVES: To investigate the circumstances and means of access to six poisoning agents by children under 5 years of age and to make recommendations for countermeasures and strategies for implementation. METHODOLOGY: A case series study of access to six poisoning agents was conducted. Cases were identified prospectively through a poisons information centre and hospital emergency departments. Interviews were conducted with 523 parents and caregivers using a structured questionnaire. RESULTS: The majority of children (94.1%) accessed the agent in their own home or another home and, in 38% of cases (excluding mistakes in administration), the parent or caregiver was present in the immediate area at the time of the incident. In cases in which the child was alone in the room, caregivers were frequently involved in household duties (51%), with only 10% undertaking leisure activities and 8% on the telephone. The span of unsupervised time reported was 5 min or less in 79.5% of these cases. The means of access was generally during periods of use of the agent (75.3%), including just purchased, rather than when agents were in their usual storage place. CONCLUSIONS: There is little scope for improved supervision as a major intervention. Design and regulatory changes such as local safe storage for bench tops and while travelling, improved labelling and packaging, improved child-resistant packaging and its more general application are required. These and agent-specific interventions, including child-resistant bait stations for rodenticides and well covers for vaporizers, are more likely to prevent poisoning. The recent identification of childhood poisoning prevention as a national priority may lead to coordinated action to implement these and other preventive measures.
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8/45. Basic toxicological approach has been effective in two poisoned patients with amitraz ingestion: case reports.

    Amitraz, a formamidine insecticide and acaricide used in veterinary practice, presents side effects in humans related to its pharmacological activity on alpha 2-adrenergic receptors. There is little information available in the literature about the toxicology of the product in man and the treatment of this poisoning. In this report, the clinical and laboratory features of amitraz poisoning in two patients by a veterinary formulation also containing xylene are presented. The major clinical findings were unconsciousness, drowsiness, respiratory failure requiring mechanical ventilation, miosis, hypothermia and bradycardia. The laboratory findings were hyperglycemia, hypertransaminasemia and increased urinary output. Supportive management of this poisoning in humans is suggested in only a few articles and there is no specific antidote for the subsequent possible pharmacological effects of amitraz. In our two cases, we performed supportive treatment such as mechanical ventilation, atropine, gastric lavage, active carbon, oxygen and fluid administration. We concluded that the basic approach to the patient with amitraz poisoning, including initial stabilization to correct immediate life-threatening problems, treatment to reduce absorption and measures to improve elimination of the toxin, is effective.
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9/45. Prolonged apnea following succinylcholine administration in undiagnosed acute organophosphate poisoning.

    organophosphates (OP) are irreversibly bound to cholinesterase, causing deactivation of acetylcholinesterase. As a result of inhibition of plasma cholinesterase, increased sensitivity to drugs hydrolyzed by this enzyme can occur, e.g. succinylcholine and mivacurium. A case of more prolonged succinylcholine-induced paralysis in a child with undiagnosed acute OP insecticide poisoning is presented. A 7-h period of apnea and paralysis after administration of succinylcholine was attributed to the decreased rate of succinylcholine metabolism resulting from inhibition of pseudocholinesterase by the insecticide. In seven previously reported cases of prolonged succinycholine apnea after OP poisoning, exposure to insecticide was in chronic or subacute form without any obvious symptoms, and the duration of apnea did not extend up to 4 h, whereas in our case with acute, severe poisoning, succinylcholine led to more prolonged muscle paralysis. In the anesthetic management of patients with acute OP poisoning, succinylcholine should be avoided.
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10/45. Pulmonary toxic effects of continuous desferrioxamine administration in acute iron poisoning.

    The drug of choice for the treatment of iron poisoning is desferrioxamine, though the best route of administration, dose, and duration of treatment are unclear. We report fatal lung injury in four patients who were treated with continuous intravenous infusions. The patients, aged 19-26 years, had received desferrioxamine infusions of 15 mg/kg per h for 65-92 h. Respiratory distress developed after 32-72 h. The patients met clinical, physiological, and necropsy criteria for the diagnosis of adult respiratory distress syndrome (ARDS); none had any of the known risk factors for the development of this disorder. We reviewed the records of forty-three iron-poisoned patients treated with desferrioxamine infusions. No patient treated for less than 24 h had pulmonary complications; however, of the fourteen treated for longer than 24 h, four were the patients with ARDS and four others had pulmonary oedema of other causes. We suggest that the pulmonary complications are caused by continuous infusion of desferrioxamine and that the ARDS in these patient was a consequence of free-radical generation. We recommend that desferrioxamine infusion should not be administered for longer than 24 h.
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