Cases reported "Poisoning"

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1/16. adult respiratory distress syndrome and renal failure associated with citalopram overdose.

    A 45-year-old man ingested 3000 mg of citalopram hydrobromide (2400 mg citalopram). He presented to the Emergency Department 2 hours post-ingestion with a pulse of 100 beats/min and blood pressure of 120/80 mmHg. His electrocardiogram (ECG) was normal. Chest X-ray showed bilateral shadowing, with no evidence of aspiration of gastric contents. Shortly after, he had three tonic-clonic seizures, requiring intravenous diazepam. Eight hours post-ingestion he became oliguric with deteriorating renal function, despite normal arterial and central venous pressures. He became increasingly hypoxic, with chest X-ray changes compatible with adult respiratory distress syndrome (ARDS). Despite treatment with 100% oxygen and continuous positive airway pressure, his gas exchange continued to deteriorate, requiring intubation and ventilation. His renal function also deteriorated with a peak creatinine of 492 micromol/L on day 4 in the absence of rhabdomyolysis. There was complete spontaneous recovery of renal function after 2 weeks. A peak plasma total citalopram (R S enantiomers) concentration of 1.92 mg/L was recorded 2 hours post-ingestion. Total norcitalopram concentrations continued to rise up to 24 hours post-ingestion. citalopram has been associated with seizures, ECG abnormalities, rhabdomyolysis and coma after overdose. The renal and respiratory complications seen in this patient have not been reported previously.
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2/16. A case of percutaneous industrial methanol toxicity.

    methanol (CH3OH) is a chemical feedstock of increasing importance as well as a commonly used solvent. In the early 1980s methanol production was introduced at a new petrochemical complex in the Saudi port of Jubail. A case is presented of a consultant supervising tank cleaning prior to methanol loading. He wore positive pressure breathing apparatus but no protective clothing. After 2-3 hours working in the confined space of the tank, he worked on deck and continued to wear his methanol-soaked clothing which eventually dried out. Visual symptoms of acute methanol toxicity presented some 8 hours after exposure. The appropriate treatment (with ethanol provided by the ship bond) was carried out in hospital and the individual recovered completely. Most reported cases of methanol toxicity are social in origin, arising from ingestion. This particular case, though unusual, does present some interesting lessons.
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3/16. A case of acute strychnine poisoning.

    In most severe cases of strychnine poisoning, the patient dies before reaching the hospital. This report describes the treatment and successful outcome of a patient who had taken a dose of strychnine that would normally be fatal. A 28-y-old man was admitted 2 h after ingestion of 1 to 1.5 g of strychnine. He had a Glasgow coma Score of 14/15 and was severely agitated and in mild respiratory distress; blood pressure was 90/60 mmHg, pulse 110/min, and peripheral pulses weak. He had generalized hyperactive reflexes and had several generalized tonic-clonic convulsions in the emergency department. Treatment consisted of gastric lavage with water, oral administration of activated charcoal and sorbitol solution, continuous intravenous administration of midazolam and then sodium thiopental, furosemide, sodium bicarbonate and hemodialysis for acute renal failure. His clinical course included respiratory distress, agitation, generalized tonic-clonic convulsions, hyperactivity, oliguria and acute tubular necrosis prior to recovery in 23 days. This patient ingested what would normally be a fatal amount of strychnine, had signs and symptoms of severe toxicity and recovered, suggesting that with aggressive supportive care patients may have favorable outcomes.
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4/16. The electrocardiographic toxidrome: the ECG presentation of hydrofluoric acid ingestion.

    The clinician can approach the poisoned patient using the toxidrome system of toxin identification; this approach makes use of findings noted on the physical examination, highlighting the importance of abnormalities in blood pressure, heart rate, respiratory effort, body temperature, mental status, pupillary size, skin color, diaphoresis, and gastrointestinal sounds. Such a method provides structure and guidance to the clinical evaluation, providing the clinician with rapid diagnostic information and suggesting urgent management issues. A case of hydrofluoric acid poisoning is used as an example of this diagnostic approach. The patient demonstrated systemic toxicity accompanied by oral irritation and electrocardiographic abnormality (QRS complex widening and QT interval prolongation). The constellation of these findings suggested the possibility of a caustic agent (history and examination) with potential effect on potassium and calcium metabolism (electrocardiographic abnormalities). Such a constellation strongly suggested hydrofluoric acid as the culprit toxin.
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5/16. ARDS following acute lithium carbonate intoxication.

    Lithium is a two-edged sword; it is on the one hand a unique drug with invaluable psychoactive potential and on the other a drug which can cause multisystem toxicity and even death. We present a case of severe lithium intoxication with multiple organ involvement. Our patient developed the adult respiratory distress syndrome (ARDS), nephrogenic diabetes insipidus (DI), distinctive neurological abnormalities, and hyperglycemia. We believe that this is a case of ARDS due to lithium toxicity in which elevated left atrial pressures were excluded by right heart catheterization and suggest a causal relationship between lithium and ARDS.
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6/16. adult respiratory distress syndrome from organophosphate poisoning.

    A 46-year-old man after an accidental exposure to organophosphates developed florid adult respiratory distress syndrome (ARDS). A markedly suppressed level of pseudocholinesterase and red blood cell cholinesterase with profuse salivation and sweating confirmed the diagnosis of organophosphate poisoning. Within 48 hours, patient developed respiratory distress needing intubation. Despite maximum ventilatory support and positive end-expiratory pressure, hypoxia persisted, Swan Ganz (Baxter Healthcare Inc, Irvine, CA) pressures showed low pulmonary capillary wedge pressure and patient died on the third hospital day. An autopsy confirmed the picture of ARDS. Other potential causes of ARDS were excluded. Although rare, organophosphate poisoning should be added to the list of toxins causing ARDS.
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7/16. Clinical experience with the benzodiazepine antagonist flumazenil in suspected benzodiazepine or ethanol poisoning.

    The clinical efficacy of different doses of the specific benzodiazepine antagonist flumazenil was studied in a total of 72 patients with benzodiazepine or ethanol overdose. In a randomized double-blind study, 18 patients (group 1) and eight patients (group 2) with suspected benzodiazepine overdose received 5 mg (group 1) or 1 mg (group 2) flumazenil or placebo, respectively. The stage of coma, heart rate, blood pressure and respiratory rate were monitored within the following 15 min. If no change in the stage of coma was observed, 5 mg (group 1) or 1 mg (group 2) flumazenil were given, and the stage of coma, heart rate and blood pressure were again monitored. In a similar way, the effect of 5 and 1 mg flumazenil was investigated in 13 patients (group 3) and four patients (group 4) with ethanol intoxication. In an open trial, the clinical efficacy of flumazenil for the diagnosis of benzodiazepine or ethanol overdose was studied in 29 patients (group 5). In all patients, a toxicological screening confirmed benzodiazepine or ethanol overdose. None of the patients receiving placebo showed effects on stage of coma, heart rate, blood pressure or respiratory rate. patients with benzodiazepine overdose who received 5 mg flumazenil regained consciousness about 1-2 min after the end of injection. The effect of 1 mg flumazenil (group 2) on benzodiazepine-induced coma was less pronounced. In patients with ethanol overdose (group 3), ethanol-induced coma was reversed after 5 mg flumazenil more slowly than in patients of group 1. No effect of flumazenil on ethanol-induced coma was observed in group 4. In group 5, flumazenil proved to be useful for diagnosing benzodiazepine or ethanol intoxication. In one patient with coma due to carbamazepine overdose, flumazenil was also found to be effective. Additionally, a possible analytical interference of flumazenil and its metabolites with the identification of other benzodiazepines by a toxicological screening procedure was studied. Even after an oral dose of 200 mg flumazenil, no interference with immunological benzodiazepine assays (EMIT, TDX, and RIA) was found. A metabolite and an artifact of flumazenil could be identified in urine by gas chromatography/mass spectrometry.
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8/16. propranolol-induced hypertension in treatment of cocaine intoxication.

    The case of a patient with apparent cocaine toxicity and drug-mediated hypertension and tachycardia is presented. IV propranolol was used as the initial treatment for his hyperadrenergic state, resulting in a decrease in heart rate but a paroxsymal increase in blood pressure. The patient required nitroprusside for control of elevated blood pressure. A mechanism of unopposed alpha stimulation as a result of beta-2 receptor blockade is proposed, and a cautious approach to the use of propranolol in these patients is suggested.
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9/16. Management of a child with acute thyroxine ingestion.

    We report a case of thyroxine overdose in a child. Despite extremely high thyroxine (T4RIA) levels on admission, the patient's only symptoms were mild hypertension and tachycardia. Both symptoms responded to propranolol, with a drop in pulse rate and a decrease in blood pressure to normal levels. After four days of cardiac monitoring, the patient was released and received propranolol for five additional days as an outpatient.
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10/16. caffeine fatality: a case report.

    A case of fatal caffeine toxicity due to suicidal ingestion of a "look-alike" illicit drug is reported. caffeine concentrations were determined by high pressure liquid chromatography (HPLC) with the brain having the highest level reported in the literature to date. Also, the blood concentration of caffeine was one of the highest among the cases reported. A literature review of caffeine fatalities is presented.
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