Evaluation of oxaliplatin exposure of healthcare workers during heated intraperitoneal perioperative chemotherapy (HIPEC).

The aim of this study was to evaluate air and surface contaminations, and internal contamination of healthcare workers during open-abdomen HIPEC using oxaliplatin. Platinum (Pt) was measured in urine of exposed workers and in multiple air and surface samples. Three successive HIPEC procedures were investigated in each of the two hospitals participating in the study. Analysis of air samples did not detect any oxaliplatin contamination. Heavy contamination of the operating table, the floor at the surgeon's feet, and the surgeon's overshoes were observed. Hand contamination was observed in surgeons using double gloves for intra-abdominal chemotherapy administration, but not in those using three sets of gloves. Pt was not detected in urine samples obtained after HIPEC (<5 ng/L). The main risk of HIPEC is related to direct or indirect skin exposure and can be prevented by correct use of adapted protective equipment.

Acute indoramin poisoning: a review of 55 cases reported to the Paris Poison Centre from 1986 t o 2010.

Authors report a retrospective study of all cases of indoramin-only poisoning notified to the Paris poison Centre from 1986 to 2010. Fifty five cases of indoramin self-poisoning were included: 40 adults and 15 children. The mean supposed ingested dose was about 701 mg±464 mg. ECG showed a prolonged QTc interval (equal to or greater than 0.50 s) in 30% of patients. The lowest observed dose for prolonged QTc was 625 mg. This series includes two cases of seizures occurring around two hours after ingestion of 900 and 2 250 mg of indoramin. A review of the literature showed cardiac disorders, with a delayed mechanism of action up until 18 hours after ingestion. Therefore, rapid medical resuscitation and prolonged cardiac monitoring for at least 24 hours after ingestion of 625 mg are recommended.

Occupational rhinitis and asthma due to EDTA-containing detergents or disinfectants.

BACKGROUND: Detergents and disinfectants are an emerging cause of work-related rhinitis and asthma. These products may contain ethylenediamine tetraacetic acid (EDTA). The authors report 10 cases of EDTA-related asthma and/or rhinitis. METHODS: Review of the medical charts of patients who presented with work-related rhinitis (alone or with asthma), with a history of exposure to aerosols of EDTA-containing products and who underwent a nasal provocation test (NPT) with tetrasodium EDTA (1-4%) in our occupational health unit. RESULTS: Twenty-eight patients underwent a NPT with EDTA, which was positive in 10 cases. These patients, mostly cleaners or healthcare workers, used spray formulations of cleaning products. CONCLUSIONS: This case series is the first report of EDTA-related respiratory disease, documented by a specific test. An irritant mechanism is unlikely. Further studies are required to distinguish between an immunoallergic response and a pharmacological mechanism possibly resulting from calcium chelation, as suggested by animal experiments. A ban of spray preparations would be sufficient to prevent respiratory disease induced by EDTA inhalation, regardless of its mechanism.

[Not Available]. / Acute Indoramin Poisoning: a Review of 55 Cases Reported to the Paris Poison Centre from 1986 to 2010.

Authors report a retrospective study of all cases of indoramin-only poisoning notified to the Paris poison Centre from 1986 to 2010. Fifty five cases of indoramin self-poisoning were included: 40 adults and 15 children. The mean supposed ingested dose was about 701mg±464mg. ECG showed a prolonged QTc interval (equal to or greater than 0.50s) in 30% of patients. The lowest observed dose for prolonged QTc was 625mg. This series includes two cases of seizures occurring around two hours after ingestion of 900 and 2 250mg of indoramin. A review of the literature showed cardiac disorders, with a delayed mechanism of action up until 18hours after ingestion. Therefore, rapid medical resuscitation and prolonged cardiac monitoring for at least 24hours after ingestion of 625mg are recommended.

Toxic doses of paraoxon alter the respiratory pattern without causing respiratory failure in rats.

Respiratory failure, through a combination of muscarinic, nicotinic, and central effects, is the primary cause of death in acute organophosphate poisoning. However, the mechanisms inducing respiratory failure remain unclear. In rats poisoned subcutaneously with paraoxon at doses near the LD(50), we studied the pattern of respiration using whole body plethysmography and the occurrence of respiratory failure using arterial blood gases. Subsequently, we studied the effects of atropine on paraoxon-induced modification of ventilation and arterial blood gases. Fifty and 75%, but not 10% of the subcutaneous LD(50) of paraoxon induced marked and sustained signs and symptoms. At 30min post-injection and throughout the study, there was a significant decrease in the respiratory frequency (34% (50% versus solvent), and 29% (75% versus solvent)) and a significant increase in the expiratory time (72% (50% versus solvent) and 60% (75% versus solvent)) with no modifications of the inspiratory time. The tidal volume was significantly increased for the 75% but not for the 50% dose. Apnea was never detected. Even at the 75% dose, paraoxon had no effects on PaO(2), PaCO(2) or HCO(3)(-); however, a significant decrease in arterial pH was observed at 30min (7.34+/-0.07 versus 7.51+/-0.01, p=0.03). Atropine completely reversed the paraoxon-induced respiratory alterations. We conclude that paraoxon, at doses equal to 50 and 75% of the LD(50), alters ventilation at rest without inducing respiratory failure during the study period.