Cases reported "Poisoning"

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1/17. 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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2/17. An adolescent case of sulfhemoglobinemia associated with high-dose metoclopramide and N-acetylcysteine.

    We describe the case of an adolescent girl who received high-dose metoclopramide in combination with oral N-acetylcysteine therapy for acute acetaminophen toxicity. Whole blood-sample analysis for abnormal hemoglobin pigments established the diagnosis of sulfhemoglobinemia. metoclopramide has been shown to cause sulfhemoglobinemia, particularly when used in repeated high doses. Although N-acetylcysteine alone has not been associated as the cause, we suggest that sulfhemoglobine-mia is a potential complication in patients treated with metoclopramide for the nausea that often accompanies oral N-acetylcysteine therapy for acetaminophen toxicity. cyanosis without respiratory distress should suggest this diagnosis.
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3/17. hemoperfusion is ineffectual in severe chloroquine poisoning.

    OBJECTIVES: To study the toxicokinetics in severe chloroquine poisoning, and to evaluate the efficacy of hemoperfusion. DESIGN: Case report on one observation. SETTING: Medical intensive care unit (ICU) of the University Medical Center Utrecht, The netherlands. PATIENT history: A previously healthy, 52-yr-old woman ingested 100 tablets containing 100 mg chloroquine base 1 hr before admission. At admission, she was drowsy, agitated, hypotensive, and in respiratory distress. Shortly thereafter, she was resuscitated from cardiac arrest. After hemodynamic and respiratory stabilization, the patient was transferred to the medical ICU. TOXICOKINETICS EVALUATION: During the course of her stay at the ICU, blood samples were taken for the determination of chloroquine and the metabolite desethylchloroquine concentration. hemoperfusion was started 3.5 hrs after ingestion of the chloroquine tablets. MEASUREMENTS AND MAIN RESULTS: The following toxicokinetics data during this severe chloroquine poisoning were calculated: apparent volume of the central compartment 181 L, apparent volume of distribution 1137 L, half-life in the distribution phase 6.4 hrs, half-life in the elimination phase 392.8 hrs, and total body clearance 2.01 L/hour. The average extraction ratio during hemoperfusion was 0.07, 0.28, and 0.25, in plasma, erythrocytes and whole blood, respectively. The total amount of chloroquine removed by hemoperfusion was only 480 mg (5.3% of the amount ingested). Simulation of a hemoperfusion session over 5 hrs by using a column with an optimal extraction ratio of 1.0 would have removed 1,816 mg chloroquine, only 18.2% of the amount ingested. This limited contribution of hemoperfusion to the total clearance makes it ineffective. CONCLUSION: hemoperfusion is not effective in severe chloroquine poisoning, even when started (relatively) early in the course of the intoxication. Toxicokinetic evaluation of a chloroquine poisoning should be based on the evaluation of plasma and whole blood concentrations.
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4/17. Analysis of single hair by XRF discloses mercury intake.

    Utilizing information obtained from the X-ray fluorescence linear scanning along a single strand of hair in a recent fatal exposure to dimethylmercury, it was possible to determine the circumstances leading to the fatal result. When the Dartmouth chemistry professor displayed symptoms of mercury toxicity, samples of her urine and blood were found to have considerable amounts of mercury by a commercial laboratory. The Dartmouth medical people immediately started treatment with a chelator on January 29, 1997 to remove the mercury, and sent the first samples of blood, urine and hair taken on January 31, 1997 to our laboratory. Our X-ray fluorescence analysis of a single strand of hair shown in Figure 1 shows a single large peak of intake of mercury confirming the information revealed by examination of her laboratory notebook that she had spilled some dimethylmercury about 5 months previous to the date the hair sample was taken. Figure 2 shows two peaks, the peak closest to the scalp end of the hair shows the effect of the large amount of mercury released by the chelator, part of which appeared in the blood. Utilizing the start of the first increase in the blood level as August 14, 1996, and the second as caused by the chelator on January 29, 1997, a count of the number of 2-mm points measured between the two dates gives an accurate growth of the hair during that time. A close examination of Figure 1 indicates that it required five points, each of 2 mm, along the hair to reach the maximum. This indicates a time period of 10 mm of growth equal to 23 days during which a large concentration of methylmercury was entering the blood as evidenced by the hair concentration. The professor died on June 11, 1997.
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5/17. Repeated measurements of aldicarb in blood and urine in a case of nonfatal poisoning.

    A nonfatal case of poisoning involving aldicarb, an extremely toxic carbamate pesticide, is presented. A 39-year-old female ingested an unknown amount of aldicarb, together with alprazolam and sertraline. On admission to ICU (T0), she displayed marked cholinergic symptoms and a deep coma. The patient was given pralidoxime and atropine. Her condition gradually improved on days 2 and 3 and she was discharged at T0 80 h. aldicarb was assayed by high-performance liquid chromatography on 21 blood and 8 urine samples successively taken during hospitalization. At the same time, serum pseudocholinesterase activity was followed on 21 successive samples. Blood aldicarb level was 3.11 microg/mL at T0 and peaked at T0 3.5 h (3.22 microg/mL), then followed a two-slope decay with a terminal half-life of ca. 20 h. aldicarb was detected in all urine samples (peak level: 6.95 microg/mL at T0 31.5 h) and was still present at the time of discharge. serum pseudo-cholinesterase activity remained low (< or = 10% of normal) until the 30th hour then rapidly increased and returned to normal after the 60th hour. The patient's clinical picture closely followed blood aldicarb levels and serum pseudo-cholinesterase activities. To our knowledge, this is the first report of an aldicarb poisoning documented by repeated measurements of the drug in the intoxicated person.
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6/17. Case report: survival after deliberate strychnine self-poisoning, with toxicokinetic data.

    INTRODUCTION: strychnine poisoning is uncommon, and in most severe cases, the patient dies before reaching hospital. The management of strychnine poisoning is well documented, although there are few data on the kinetics of elimination of strychnine after overdose. CASE REPORT: A 42-year-old man presented shortly after ingestion of an unknown quantity of strychnine powder. After a respiratory arrest, with intensive supportive management requiring admission to an intensive care unit, he survived. Eight serum samples were taken over the first 5 days and analysed subsequently for strychnine concentrations. RESULTS: The initial concentration at 1.5 hours after ingestion was 4.73 mg/l, falling to 0.38 mg/l at 74 hours postingestion. serum concentrations followed a monoexponential elimination curve with a calculated elimination half-life of 12 hours. DISCUSSION AND CONCLUSION: strychnine poisoning presents with classical features, and with early diagnosis and supportive management, the patient can survive. The initial serum concentration of 4.73 mg/l is the highest reported concentration in a patient who has survived. Previous reports of the elimination half-life have suggested it is between 10 and 16 hours, which conforms to the elimination data in our case.
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7/17. Treatment of a patient with severe digitoxin intoxication by Fab fragments of anti-digitalis antibodies.

    A massive digitoxin (DGTX) intoxication in a 36-year-old man (35 mg DGTX) was treated by prolonged and repeated i.v.-infusions of Fab fragments of anti-digitalis antibodies (FAB). Blood and urine samples were collected over a 98 h period for monitoring the efficacy and adequacy of FAB treatment. DGTX concentrations were determined after protein precipitation (release of FAB-bound and protein-bound DGTX) in unprocessed serum and urine samples, and after aliquots of these samples had been dialysed in vitro against DGTX-free buffer (elimination of DGTX not bound to FAB). The difference in DGTX concentration between the unprocessed and dialysed samples was the amount of DGTX bound to plasma proteins and the small fraction of unbound DGTX being relevant for the therapeutic and toxic effects of the drug. Before FAB therapy was started, the total serum DGTX concentration was 535 nmol/l. The first FAB infusion (320 mg) was started 11 h after drug ingestion. Since this amount of FAB was insufficient to bind all DGTX present in the serum, cardiac DGTX toxicity (total AV-block) persisted. During a second FAB infusion (400 mg) the patient reverted to regular AV-conduction. At this time most of the DGTX in serum was FAB-bound. Toxic symptoms (sinus arrest) reappeared twice and were accompanied by increasing amounts of non-antibody-bound DGTX in the serum. Additional application of FAB (2 x 80 mg) resulted in the immediate disappearance of arrhythmia. During FAB-treatment total DGTX serum concentrations and renal DGTX clearance rose, indicating redistribution of drug from tissue to serum and urinary elimination of FAB-bound DGTX, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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8/17. role of laboratory in the management of phenylbutazone poisoning.

    We report a rare case of intentional overdose of phenylbutazone in a 15-yr-old female. The patient exhibited symptoms of phenylbutazone toxicity and the presence of the drug was confirmed by gas chromatography mass-spectrometry (GC-MS) analysis of the initial urine sample. The patient underwent plasmapheresis to remove the drug from the circulation. Semiquantitation of sequential serum samples by GC-MS revealed elimination of phenylbutazone by day 5 of admission at which time the plasmapheresis was discontinued. Elevated blood urea nitrogen (BUN) and creatinine returned to normal. Analysis of biomarkers for liver necrosis and regeneration in sequential serum samples revealed the restoration of normal liver function by day 5. This case further confirms our previous observations that biomarkers for liver necrosis and regeneration can predict the outcome of patients with liver damage due to toxins.
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9/17. The nail and hair in forensic science.

    Drugs, chemicals, and biological substances accumulate and are stored in hair and nails where they can be detected and measured. Advantages of analyzing hair and nail samples also include their easy and non-invasive collection, the small sample size required for analysis, and their easy storage at room temperature. We report 3 examples of heavy metal poisoning diagnosed because of the hair or nail symptoms. Drugs and toxins that can be detected in hair and nails are reviewed and the application of hair/nail analysis in general and in forensic medicine is discussed.
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10/17. Usefulness of multi-parameter opiate analysis in hair of drug users and victims of fatal poisonings.

    The results of a multi-parameter analysis of opiates in the hair of drug users and victims of fatal poisonings with these xenobiotics have been presented. The analysis was carried out with the use of liquid chromatography coupled with mass spectrometry (LC-MS). The article discusses the monitoring of the drug users' adherence to pharmacotherapy and the usefulness of hair analysis for medico-legal purposes. The authors evaluate the differences in the contents of particular opiates in the hair as related to the origin of a sample (untreated drug user, drug user in the course of treatment, victim of fatal poisoning). The report presents differences between the Polish and American profiles of abuse, providing confirmation that a great part of drug users undergoing methadone treatment do not abstain from opiates and/or amphetamine, the latter as a rule being very often taken with opiates.
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