Journal of toxicology. Clinical toxicology最新文献

Background: Amatoxin-containing species are responsible for the most severe cases of mushroom poisoning, with high mortality rate. Therefore, this poisoning should be ruled out in all patients presenting gastrointestinal symptoms after wild mushroom ingestion.

Objective: To determine sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic efficacy (DE) of urinary amanitin analysis in cases of suspected mushroom poisoning.

Methods: All cases of mushroom ingestion referred to a Poison Center during a one-month period were analyzed. Amanitin measurements were performed by ELISA method (functional least detectable dose 1.5 ng/ml; cut-off value not clearly established). Gastrointestinal symptoms latency and initial clinical assessment were considered alternative diagnostic tools. Definitive diagnosis was used as the reference standard.

Results: Among 61 patients included in the study, amatoxin poisoning was diagnosed in 10 cases. Urine samples were collected 5.5 to 92 hours after mushroom ingestion. Urinary amanitin DE was 91.8%, 93.4%, and 80.3%, based on the cut-off value considered (1.5, 5.0, and 10.0 ng/ml, respectively). Symptoms latency longer than 6 hours and initial clinical assessment DE were 70.5% and 67.2%, respectively. To identify amatoxin poisoning, initial clinical assessment resulted more sensitive and urinary amanitin analysis more specific.

Conclusions: Urinary amanitin analysis is a valuable diagnostic tool and may significantly contribute to the management of suspected mushroom poisoning. At present, the best diagnostic accuracy can be obtained taking advantage of both the high sensitivity and negative predictive value of the clinical assessment performed by an experienced toxicologist, and the high specificity and positive predictive value that characterize urinary amanitin analysis.

Objective: This study was undertaken to examine the association of hydrogen cyanide and carboxyhaemoglobin in victims of fire related deaths in Australia. The secondary aim was to document demographic data about Australian fire related deaths.

Methods: An observational retrospective study was undertaken of autopsy reports from the Victorian Institute of Forensic Medicine. Reports of fire related deaths were electronically searched using the terms burns, "smoke" or "fire" as a cause of death in the calender years 1992 to 1998. Data on the circumstances of the fire and results of toxicological screening were obtained on 178 persons. Additional whole blood cyanide levels were determined if blood samples were available in storage. Demographics of the victims were analysed, as well as the relationship between carboxyhaemoglobin and whole blood cyanide levels.

Results: Most (82%) of the victims died at the scene, whilst 32 victims died after a period of hospitalisation (hours to weeks). Suicide as a result of self-immolation was the reported cause of death in 32 cases. Most of the fires were in houses (114) and cars (29). The blood ethanol level was zero in 112 cases; the remaining cases (53) had a mean level of 0.17%. Other central nervous system (CNS) depressants were recorded in 49 of the 134 cases that received a complete toxicological screen. Carboxyhaemoglobin levels were measured in only 154 of 178 cases. The carboxyhaemoglobin level was zero in 43 cases. The remaining cases (111) had a mean level of 40%; with 44 cases having a level greater than 50%, a level considered to be potentially lethal. Whole blood hydrogen cyanide levels were measured in only 138 of 178 cases. The hydrogen cyanide level was zero in 52 cases. The remaining cases (86) had a mean level of 1.65 mg/L; with 11 cases having a level greater than 3.0 mg/L (potentially fatal). Blood ethanol levels were significantly correlated with both carboxyhaemoglobin (R = 0.22, P < 0.01) and cyanide (R = 0.36, P < 0.001). In addition, a significant correlation (r = 0.34) between carboxyhaemoglobin and hydrogen cyanide levels was noted.

Conclusions: This study showed a correlation between elevated blood ethanol and whole blood cyanide levels (r = 0.36, p < 0.001) and between elevated carboxyhaemoglobin and hydrogen cyanide levels (r = 0.34). Although the mean cyanide level was 1.3 mg/L (above the level some consider potentially toxic) in those cases with a carboxyhaemoglobin level of greater than 10%, there is insufficient data to permit recommendations for clinical care. Further studies are required on those victims that reach hospital alive.

Background: Emamectin benzoate is the 4'-deoxy-4'-epi-methyl-amino benzoate salt of avermectin B1 (abamectin), which is similar structurally to natural fermentation products of Streptomyces avermitilis. Emamectin benzoate is being developed as a newer broad-spectrum insecticide for vegetables and has a very low application rate. The mechanism of action involves stimulation of high-affinity GABA receptors and a consequent increase in membrane chloride ion permeability. Animal studies indicate a wide margin of safety because mammalian species are much less sensitive due to lower GABA receptor affinities and relative impermeability of the blood-brain barrier. Notably, the literature has not reported human exposure resulting in toxicity.

Case report: This paper describes a case of acute poisoning with Proclaim insecticide (Syngenta, Taiwan), consisting of 2.15% w/w emamectin benzoate in 2, 6-bis (1, 1-dimethylethyl)-4-methyl-phenol and 1-hexanol. The clinical manifestation was transient gastrointestinal upset with endoscopy-proven gastric erosion and superficial gastritis, mild central nervous system depression, and aspiration pneumonia. No specific antidote exists for emamectin benzoate intoxication; this patient was treated successfully with gastric lavage, administration of activated charcoal, and empiric antibiotics. Drugs that enhance GABA activity such as barbiturates and benzodiazepines were avoided.

Background: There is limited experience treating severe ethylene glycol poisoning in children without hemodialysis. The objective of this study was to describe the clinical course and outcome of severe pediatric ethylene glycol poisoning treated without hemodialysis.

Methods: Patient records were identified retrospectively by hospital discharge diagnosis (ICD-9 code) of ethylene glycol poisoning from 1999 through 2002 at a pediatric medial center. Patients with initial serum ethylene glycol concentrations less than 50 mg/dL or those who received hemodialysis were excluded.

Results: Six patients with an age range of 22 months to 14 years were admitted for treatment of ethylene glycol poisoning over a four-year period. Initial serum ethylene glycol concentrations ranged from 62 to 304 mg/dL (mean 174.0 mg/dL). The lowest-measured individual serum bicarbonates ranged from 4 to 17 mEq/L. All patients were initially admitted to intensive care. One patient received ethanol only, two patients received fomepizole only, and three patients received a loading dose of ethanol and then were converted to fomepizole therapy. None of the patients received hemodialysis. Treatment was continued until the serum ethylene glycol was less than 10 mg/dL. Metabolic acidosis resolved with intravenous fluid and supplemental bicarbonate within 24h. All patients had a normal creatinine upon presentation and at discharge. The mean length of stay in intensive care was 21h and on the ward was 33.7h. One episode of hypoglycemia occurred in a 22-month-old. All patients recovered without evidence of renal insufficiency or other major complications at discharge.

Conclusion: Six pediatric patients with severe ethylene glycol intoxication and normal renal function were successfully treated without hemodialysis.

Background: Sumatriptan has been used in the treatment of migraine and other vascular headaches since 1993 in the United States. Its side effects include chest pains in 3% to 8% of patients who have known cardiac risk factors. This is a case report of a 45-year-old woman with no history of cardiac risk factors who had a myocardial infarction after her monthly dose of oral sumatriptan.

Methods: The patient was examined in the emergency room, evaluated by electrocardiography, and serial evaluations of cardiac enzymes over the next 24 h. She was admitted to the cardiology ward. A cardiac catherization and additional laboratory studies were performed the following day.

Results: The catherization revealed normal heart function, but a 60% to 70% non-flowing stenosis within the first septal perforator. Laboratory indices for cardiac risk were within normal ranges.

Conclusions: Patients without cardiac risk factors may experience myocardial infarction following an oral dose of sumatriptan.

Neuroleptic malignant syndrome (NMS) is an uncommon potentially fatal side effect of neuroleptic drugs, characterized by movement disorder, altered mental status and autonomic instability. A single dose of clotiapine was administered to an 11-year old male with acute psychosis. The previously healthy child had signs consistent with NMS including hyperthermia, hypertension, motor and mental changes. Repeat examination performed two weeks later, demonstrated that while his hyperthermia subsided, his mental status deteriorated. Olanzapine was administered, after which the child had hyperthermia, dystonia and more pronounced restlessness, once again consistent with NMS. He developed respiratory failure and was intubated and mechanically ventilated. Lorazepam, dantrolene and bromocriptine were administered as treatment of possible NMS. His mental condition, movement disorder and autonomic dysfunction improved significantly. Two weeks later, the patient was discharged in good general condition without the need for any ongoing medical treatment. There are only few case reports of NMS in children treated with olanzapine, an atypical antipsychotic. In children, caution must be exercised when prescribing antipsychotics, particularly atypical antipsychotics as these drugs may cause NMS. Because of the low incidence of NMS, a high index of suspicion is needed to identify cases so prompt treatment can be undertaken.

Purpose: To examine the efficacy and safety of administration of calcium and magnesium orally and intraperitoneally to treat severe sodium fluoride intoxication.

Materials and methods: Mice were initially gavaged a lethal dose of sodium fluoride (NaF) or water. Then, mice were treated with water or varying concentrations of calcium chloride (CaCl2) or magnesium sulfate (MgSO4) via intraperitoneal (IP) route or via oral route. Mice were monitored for 24 h, and the time of death was recorded.

Results: IP injections of large amounts of CaCl2 or MgSO4 were dangerous. All mice gavaged with water and then treated with oral CaCl2 or MgSO4 survived and displayed normal activity during the experiment. The survival rate of mice gavaged with a lethal dose of NaF and then treated with a high dose of oral CaCl2 or MgSO4 was significantly higher than those of using low dose.

Conclusion: Oral administration of a high dose of CaCl2 or MgSO4 is a simple, safe, and effective adjunctive method for treating severe oral fluoride poisoning.