Journal of toxicology. Clinical toxicology最新文献

Syrup of ipecac should not be administered routinely in the management of poisoned patients. In experimental studies the amount of marker removed by ipecac was highly variable and diminished with time. There is no evidence from clinical studies that ipecac improves the outcome of poisoned patients and its routine administration in the emergency department should be abandoned. There are insufficient data to support or exclude ipecac administration soon after poison ingestion. Ipecac may delay the administration or reduce the effectiveness of activated charcoal, oral antidotes, and whole bowel irrigation. Ipecac should not be administered to a patient who has a decreased level or impending loss of consciousness or who has ingested a corrosive substance or hydrocarbon with high aspiration potential. A review of the literature since the preparation of the 1997 Ipecac Syrup Position Statement revealed no new evidence that would require a revision of the conclusions of that Statement.

Background: The administration of intravenous (IV) calcium to treat hyperkalemia resulting from digoxin poisoning is considered potentially dangerous, based on a body of older literature which, in sum, reported increased cardiac glycoside toxicity with calcium administration (increased arrhythmias, higher rate of death).

Objective: This pilot study sought to determine if the administration of calcium chloride when compared to normal saline would affect time to death when given to hyperkalemic, digoxin toxic swine.

Methods: Digoxin IV at 0.25 mg/kg was determined to be appropriately toxic for this study. When arrhythmias consistent with hyperkalemia developed, animals were given either IV calcium chloride (CaCl) bolus (10 mg/kg, Group 1, n=6) or normal saline volume equivalent (Group 2, n=6). Three intervals were observed: Interval 1: time interval from digoxin administration (T0) to when ECG changes consistent with hyperkalemia developed (at which point calcium chloride or normal saline was administered); Interval 2: time interval from the development of ECG changes consistent with hyperkalemia to asystole; Interval 3: time interval from digoxin administration to asystole. Both groups were monitored for changes in heart rhythms, serum potassium levels, and time to asystole.

Results: The intravenous digoxin dose of 0.25 mg/kg induced hyperkalemia, arrhythmias, and death approximately 1 h after administration in all animals studied. Group 1: Interval 1 averaged 18.75 (S.D. +/-7.96) min, Interval 2 averaged 16.75 (S.D. +/-17.17) min, and Interval 3 averaged 35.5 (S.D. +/-14.49) min range; Group 2: average Interval 1 24.8 (S.D. +/-4.71) min, Interval 2 averaged 19.5 (S.D.+/-15.92), Interval 3 averaged 44.3 (S.D. +/-13.80) minutes. There was no statistically significant difference between the groups at any time interval, Interval 1 (p=0.43), Interval 2 (p=0.65), Interval 3 (p=0.40). There was no difference in serum potassium throughout the study period.

Conclusion: The administration of intravenous CaCl in the setting of hyperkalemia from acute digoxin toxicity did not affect mortality or time to death at the dose administered.

Background: Methanol poisoning during human pregnancy rarely has been described. We report the first human newborn with a documented methanol concentration resulting from maternal exposure.

Case report: A 28-year-old pregnant woman EGA 30 weeks with HIV infection and asthma presented to the emergency department in respiratory distress. She was acidotic (pH 7.17) with an anion gap of 26, and fetal bradycardia was noted. Her son was delivered by emergent C-section (birthweight 950 g, Apgars 1 and 3) and required aggressive resuscitation. During his hospital course, acidosis (initial pH 6.9) persisted despite fluid, blood, and bicarbonate administration. His mother also had persistent metabolic acidosis despite fluids, bicarbonate, and dopamine. Results of other laboratory tests on the mother included undetectable ethanol and salicylates and an osmolar gap of 41. An ethanol drip was initiated for the mother 36 h after admission when a methanol level of 54 mg/dL was reported. When consulted on hospital day 3, our regional poison center recommended hemodialysis for the mother and administering fomepizole and testing the methanol level of the newborn (61.6 mg/dL). Because the infant developed a grade 4 intraventricular bleed, no further therapy was offered, and he died on day 4. His mother died on day 10.

Conclusion: Fatal neonatal methanol toxicity can result from transplacental exposure.

Purpose: To investigate regional variations in public awareness and utilization of the services of Poison Control Centers (PCC) before and after an intervention.

Methods: This study examines call rates of different California regions based on the final five regional PCCs prior to the consolidation of these services under a single statewide California Poison Control System (CPCS) and interventions to increase utilization. Awareness surveys were performed before and after a media campaign that was directed primarily to the Los Angeles basin and to a lesser extent other high Hispanic concentration areas. Focus groups were also utilized to better define specific areas of poison knowledge and awareness of CPCS services.

Findings: Large differences in regional California call rates were seen, with the Los Angeles basin showing the lowest utilization of CPCS services compared with the rest of California. Significant seasonal variation in utilization was also found, with the highest average call rates observed in August and the lowest in February. Focus groups demonstrated that urban awareness of PCC was lower than suburban awareness, particularly in monolingual Hispanic households. An improvement was seen after the institution of a media education campaign that included use of Spanish language material and radio spots. Similar increases in call rates were also seen in Fresno county category, with a higher percentage of Hispanic population that was not as aggressively targeted by the awareness campaign.

Conclusions: Significant regional variations in CPCS call rates were found and an increased awareness and utilization was seen in the Los Angeles basin after a directed media campaign compared with most areas of California. Further efforts to increase CPCS utilization in the Los Angeles region, primarily among urban monolingual Hispanics, are needed.

Background: Sources of cyanide exposure are many, including combustion of plastic and vinyl, such as in a house fire, laboratory or industrial exposures including exposure in the electroplating industry both of printed circuit boards and in jewelry work. Rapid and definitive diagnosis of cyanide poisoning is unavailable in the emergency department setting. It is desirable to make a definitive diagnosis in order to prevent potential complications of empiric treatment of presumptive cyanide poisoning from the cyanide antidote kit currently approved by the US Food and Drug Administration (FDA). We investigated a technique to detect cyanide currently utilized by water treatment facilities to determine if it can be applied to rapidly detect concentrations of cyanide in the clinically important range.

Methods: Varying standardized dilutions of KCN ranging from 0.25 microg/mL to 30 microg/mL were acidified with a drop of sulphuric acid in a closed system under a ventilation hood. Cyantesmo test strips were placed into the test tubes above the fluid level where liberated HCN gas interacted with the test strip to effect a color change. Color changes were compared to negative controls and to each other.

Results: The test strips demonstrated an incrementally increasing deep blue color change over a progressively longer portion of the test strip in less than 5 minutes for each concentration of KCN including 1, 3, 10, and 30 microg/mL. The concentrations of 0.25, 0.5, and 0.75 required more than 2 hours to begin demonstration of any color change.

Conclusion: The Cyantesmo test strips accurately and rapidly detected, in a semi-quantifiable manner, concentrations of CN greater than 1 microg/mL contained in each test sample. Future work to validate this test in blood and in clinical specimens is planned.

Gastric lavage should not be employed routinely, if ever, in the management of poisoned patients. In experimental studies, the amount of marker removed by gastric lavage was highly variable and diminished with time. The results of clinical outcome studies in overdose patients are weighed heavily on the side of showing a lack of beneficial effect. Serious risks of the procedure include hypoxia, dysrhythmias, laryngospasm, perforation of the GI tract or pharynx, fluid and electrolyte abnormalities, and aspiration pneumonitis. Contraindications include loss of protective airway reflexes (unless the patient is first intubated tracheally), ingestion of a strong acid or alkali, ingestion of a hydrocarbon with a high aspiration potential, or risk of GI hemorrhage due to an underlying medical or surgical condition. A review of the 1997 Gastric Lavage Position Statement revealed no new evidence that would require a revision of the conclusions of the Statement.