Toxicology laboratory analysis and human exposure to p-chloroaniline.

INTRODUCTION: p-Chloroaniline is more potent at producing methemoglobin than aniline in animal models. This case highlights the clinical presentation of an inhalation exposure to p-chloroaniline and associated laboratory analysis. An in-vitro study evaluating the metabolism of p-chloroaniline in human hepatocytes was undertaken to evaluate the metabolic fate more closely. CASE PRESENTATION: A 20 year-old man was working at a chemical waste plant when he developed dizziness, abdominal pain, and nausea. The exam was remarkable for coma, tachycardia, cyanosis, and pulse oximetry of 75%. Arterial blood gases showed a pH 7.38, pCO(2) 41 mmHg, pO(2) 497 mmHg, bicarbonate 24 mEq/L and methemoglobin 69%. Methylene blue administration led to complete recovery without sequelae. p-Chloroaniline was later identified as the chemical involved. He denied direct contact with the chemical, but was not wearing a dust mask or respirator. GC/MS confirmed p-chloroaniline and metabolites in the patient's urine. METHODS: Human hepatocytes were incubated with 100 microM p-chloroaniline for 24 hours, in both rifampicin- and vehicle only-treated cells. The cell culture medium was collected for GC/MS analysis for p-chloroaniline metabolites. RESULTS: Similar to the patient sample, both p-chloroaniline and p-chloroacetanilide were identified by GC/MS in hepatocytes incubated with p-chloroaniline. Neither p-chloroaniline incubated in empty cell culture nor direct GC/MS injection of p-chloroaniline generated any p-chloroacetanilide via non-enzymatic degradation. DISCUSSION/CONCLUSION: The seemingly innocuous dermal and inhalation exposure to p-chloroaniline dust can lead to life-threatening methemoglobinemia. The diagnosis can be confirmed with GC/MS analysis of the patient's urine, searching for p-chloroaniline and its primary metabolite p-chloroacetanilide.

Dextromethorphan-induced serotonin syndrome.

INTRODUCTION: The ability of dextromethorphan to potentiate serotonin levels and lead to serotonin syndrome is well known but few case reports are published. The lack of published cases suggests therapeutic doses of these drugs are not enough to cause serotonin syndrome. We present two cases of serotonin syndrome associated with supra-therapeutic doses of dextromethorphan and therapeutic levels of a selective serotonin reuptake inhibitors (SSRI). CASE SERIES: In case one, serum drug levels from admission revealed a dextromethorphan level of 950 ng/mL (normal < 5), escitalopram of 23 ng/mL (normal < 200), chlorpheniramine of 430 ng/mL (normal < 20) and undetectable levels of aripiprazole and benztropine. In case two, serum drug levels from admission revealed a dextromethorphan level of 2820 ng/mL, sertraline of 12.5 ng/mL (normal < 200), and caffeine of 1.4 microg/mL (normal < or = 9 microg/mL). DISCUSSION: To our knowledge, these are the first cases to use serum levels of dextromethorphan and a SSRI to confirm dextromethorphan-induced serotonin syndrome. CONCLUSION: Our cases suggest supra-therapeutic dextromethorphan doses with a therapeutic amount of a SSRI are required for serotonin syndrome. More work is needed to answer this question more completely.

Lack of utility of telemetry monitoring during transport to inpatient beds for identification of dysrhythmias for emergency department patients with potential and known acute coronary syndromes.

Patients admitted with acute and potential acute coronary syndromes (ACS) frequently required accompaniment by a registered nurse from the emergency department (ED) to inpatient telemetry beds. We tested the hypothesis that telemetry transport monitoring for patients with acute and potential ACS is of limited utility. We conducted a prospective cohort study of patients who were admitted from the ED with acute and potential ACS. Endpoints were life threatening ventricular dysrhythmias requiring intervention and duration of transport time. The setting was an urban tertiary-care emergency department with 55,000 annual visits, and the subjects were adult patients admitted from the ED to inpatient beds (intensive care unit or floor telemetry) with ACS and potential ("rule-out") ACS. Main outcome measures were the development of a life threatening ventricular dysrhythmias during transport, any intervention by the transporting nurse, and the total transport time. Of 315 total admissions involving 310 patients, there were no life threatening ventricular dysrhythmias and interventions during transport [0%; 95% confidence interval 0-0.95%]. The total nurse time out of the ED spent transporting was 13.6 minutes (SD 5.2, range 4-40). The routine use of nurses accompanying patients admitted with acute and potential acute coronary syndromes is of limited utility. Patient transportation without nurses may help alleviate ED overcrowding by saving almost 15 minutes of nursing time currently being used for transport without measurable benefit.