| ethylene dibromide (1,2-dibromoethane) is widely used to fumigate grain and fruit in india. However, acute poisoning due to it has rarely been reported in the literature and most of these patients had an fatal outcome. We describe the suicide attempt of a young male who ingested an ampoule (3 ml) of it, developed acute hepatic and renal failure, metabolic acidosis and coagulopathy but survived following supportive measures. ( info) |
32/449. 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. ( info) |
33/449. Deliberate sulphonylurea poisoning mimicking hyperinsulinaemia of infancy. A 6 month old child presenting with seizures was found to be hypoglycaemic secondary to hyperinsulinism. A family history of type II diabetes prompted estimation of sulphonylurea in the baby's blood, which was found to be high. A multidisciplinary case conference concluded that the sulphonylurea ingestion was likely to be the result of munchausen syndrome by proxy. When investigating hypoglycaemia of infancy this possibility should be considered. ( info) |
| Ingestion of paraquat is the most common cause of fatal pesticide poisoning. liver involvement in acute paraquat poisoning is self-limited and usually consists of cholestasis. However, long-term hepatic effects after paraquat exposition have not been described up to now, probably because of the high mortality rate of this acute poisoning. We report the case of an agricultural worker who developed persistent cholestasis after an episode of acute paraquat poisoning through skin absorption. ( info) |
| cantharidin, the active ingredient of "Spanish Fly", is contained in a number of insects collectively called blister beetles and is a well known toxin and vesicant. We report on a case of ingestion of Mylabris dicincta ("blister beetle") in zimbabwe by a 4 year old girl. The ingested beetles were probably mistaken for the edible Eulepida mashona. She presented with many of the classic signs and symptoms of cantharidin poisoning including haematuria and abdominal pains. This was recognised only after consultation with the drug information centre. She was managed conservatively, recovered and was discharged after 9 days. A overview of the clinical effects of cantharidin toxicity and its treatment is presented. ( info) |
36/449. Heavy metal poisoning in glass worker characterised by severe. The paper presents the clinical description of the masticatory organ and biochemical assessment of dental tissue in a patient employed in a glassworks for 20 years. During 12 years the patient has suffered baldness ("alopecia areata") and atypical extensive and non-healing cutaneous lesions. Dental examination revealed changes typical of chronic poisoning by cadmium and bismuth compounds. ( info) |
37/449. 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). ( info) |
38/449. Unusual cases of suicide among health care workers. We describe three unusual cases of suicide committed by health care workers. The aim of this paper was to analyze and evaluate the evidence of general diagnostic elements of poisoning in these cases. ( info) |
| 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. ( info) |
| verapamil intoxications are life-threatening conditions with a far too often fatal outcome. In 2 patients, severe suicidal intoxication by 2.4 g and 9.6 g of verapamil orally resulted in life threatening hypotension and bradycardia with the need of heart-pacing and resuscitation. plasmapheresis was started within less then 4 hours after intoxication and seemed to reduce the verapamil plasma concentration to less then 40%. A dramatic improvement of cardiovascular stability was already observed during plasmapheresis. In-vitro plasmapheresis was performed to verify the effectiveness of the extracorporeal detoxification. verapamil was removed out of the blood by a clearance of 29.2 ml/min at blood flow of 200 ml/min.In conclusion, severe verapamil poisoning should be treated by early aggressive gut decontamination and an appropriate management of the haemodynamic complications. In case of lack of effectiveness for stabilisation, plasmapheresis can reduce verapamil related life threatening symptoms and bridge the time for the hepatic detoxification. ( info) |