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This article presents two years of billing and collection data for a bedside toxicology consultation service. The collections rate was 34% or dollars 26.19 per hour of consultative time. There was an inverse correlation between collection rates and patient acuity.

Introduction. No study has focused on the nationwide epidemiology of severe and fatal rattlesnake bites during the last 25 years. We examined rates and temporal trends of severe and fatal rattlesnake bites across the United States. Our hypothesis was that nationwide annual rates of both severe and fatal outcomes from rattlesnake bites have remained unchanged over time. Methods. This study retrospectively analyzed all human rattlesnake bites published in the Annual Reports of the American Association of Poison Control Centers from 1983 through 2007. Annual rates of severe (major) and fatal rattlesnake bites were calculated using the annual number of major outcomes and fatalities as respective numerators and the total annual number of single rattlesnake bites (exposures) as denominators. Negative binomial and Poisson regressions were used to examine trends of severe and fatal rattlesnake bites over time. Results. Annually, from 1985 to 2007, the incidence rate of major outcomes decreased by 2% per year (incidence rate ratio = 0.980; CI = 0.967–0.993), corresponding to an absolute annual rate decrease of two major outcomes per 1,000 bites per year. Annual rates of fatalities showed no statistically significant change from 1983 through 2007. Conclusion. This is the first study to examine rates and trends of published severe and fatal rattlesnake bites across the United States over the past 25 years. Annual rates of severe rattlesnake bites, derived from the published Annual Reports of the American Association of Poison Control Centers, have significantly decreased over time, whereas rates of fatal rattlesnake bites have remained unchanged. [ABSTRACT FROM AUTHOR]

Background: We recently reported on a breastfed infant who succumbed to opioid toxicity following exposure to morphine, the active metabolite of codeine, which was prescribed to his mother who was a cytochrome P450 2D6 (CYP2D6) ultrarapid metabolizer. This report is believed to be the first case of neonatal fatality as a direct result of matemal drug excretion into breast milk and, therefore, it is critical to corroborate the causative relationship between matemal codeine use during breastfeeding and neonatal opioid toxicity with other existing evidence. Objective: To establish whether matemal use of codeine can be a cause of CNS depression in breastfed infants. Study design: A systematic review of the medical literature using several databases was conducted. The Naranjo Adverse Drug Reaction Probability Scale (NADRPS) was used to examine causality. Results: In addition to our case report, three abstracts and two full-length studies reported adverse drug reactions (ADRs) in infants exposed to codeine in breast milk. In total, 35 infants were identified. Specifically, ADRs were described as unexplained episodes of drowsiness, apnea, bradycardia, and cyanosis in suckling infants. Using the NADRPS, codeine was found to be a definite cause of CNS depression in breastfed infants. Conclusion: The use of codeine by breastfeeding mothers can cause adverse CNS events in breastfed infants. Physicians should recognize codeine use during breastfeeding as a cause of CNS depression in infants, and breastfeeding mothers should be educated on these adverse events before receiving codeine. [ABSTRACT FROM AUTHOR]

Antidotal therapy for acetaminophen poisoning is routinely based on a single acetaminophen level obtained four or more hours after ingestion. Some experts recommend additional acetaminophen levels if there are coingestants. This case report describes a 20-year-old woman who ingested acetaminophen 13 g, propoxyphene napsylate 2 g and naproxen sodium 3.75 g. A 4.5 h acetaminophen level was 83.5 mg/L (nontoxic). A 6.75 h acetaminophen level was 124.6 mg/L (toxic). The patient was treated with N-acetylcysteine and recovered without sequelae. This is the first published report of a delayed toxic acetaminophen level occurring after an initial nontoxic level. Although rare, the possibility of a delayed peak acetaminophen level merits consideration, particularly with coingestions that delay gastric emptying. [ABSTRACT FROM AUTHOR]