Is an increased PaO2 in a normobaric state safe in acute CO poisoning?

Our objective was to determine how much PaO2 levels increase after normobaric oxygen (NBO) therapy and whether NBO therapy exerts therapeutic effects regardless of the PaO2 level. We suggest the optimal PaO2 level to use during NBO therapy for the acute treatment of carbon monoxide (CO) poisoning. This retrospective study included 311 patients who received oxygen administration after CO poisoning and had a measurable PaO2 level upon arrival. Baseline characteristics, clinical courses and long-term neurological outcome were collected and compared. The PaO2 level upon arrival was 192 (161-225) mm Hg, and 272 (87.5%) of the patients presented with hyperoxia. The incidence of poor long-term neurological outcome was 11.3% at a median follow-up period of 35 months. PaO2 levels upon arrival were higher in patients with good long-term neurological outcome than in those with poor outcome. The incidence of poor long-term neurological outcome was significantly dependent on the PaO2 level when patients were stratified at 100-mm Hg increments. A multivariate regression analysis showed that PaO2 levels, when considered a continuous, interval or ordinal variable, were associated with long-term neurological outcome in separate models. According to the three models, a PaO2 level of 200-300 mm Hg has the lowest risk of poor long-term neurological outcome. The results of the analysis of the predicted probability of poor long-term outcome according to the PaO2 level exhibited a U-shaped curve. Further large-scale studies are needed to confirm the association between 200-300 mm Hg of PaO2 and long-term neurological outcome and evaluate the impact of PaO2 levels above 300 mm Hg on acute CO poisoning outcome.

Quantitative analysis of aconitine in body fluids in a case of aconitine poisoning.

Aconitine belongs to the Aconitum alkaloids and is a natural toxic substance. Aconitine has been used as a traditional medicine in East Asian culture. Today, aconitine is still in use with or without a prescription, in the Republic of Korea. Here we present a case report of accidental death due to acute aconitine poisoning. An 81-year-old woman ingested liquid that had been heat extracted from the root of the Aconitum plant; she presented to the emergency room 1 h after ingestion. Her electrocardiogram showed irregular ventricular arrhythmias including ventricular tachycardia; she progressed to cardiac arrest. Cardiopulmonary resuscitation and anti-arrhythmic drugs were administered, but the patient did not survive. An autopsy was performed 2 days postmortem. Toxicological analysis was performed, and aconitine was detected by liquid chromatography tandem mass spectrometry. The antemortem blood concentration of aconitine was 39.1 ng/ml and the concentrations of aconitine in the postmortem cardiac blood, peripheral blood, cerebrospinal fluid (CSF), pericardial fluid, and urine were 21.1 ng/ml, 28.6 ng/ml, 6.8 ng/ml, 24.1 ng/ml, and 67.4 ng/ml, respectively. This is the first forensic case report of an aconitine poisoning death in the Republic of Korea with quantitative measurement of aconitine in the antemortem blood and various postmortem body fluids. To the best of our knowledge, this is the first report of the detection of aconitine in the CSF. These data about the distribution of aconitine in the antemortem blood and various postmortem body fluids is helpful for future aconitine poisoning death cases.

The efficacy of high doses of vitamin C in patients with paraquat poisoning.

Paraquat (PQ) poisoning is an extremely difficult condition to manage clinically because of the lack of effective treatments. The purpose of this study was to assess the effect of high doses of vitamin C in combination with anti-inflammatory and immunosuppressant therapy in patients with PQ poisoning. The medical records of 134 patients who presented to the emergency department within 24 hours after PQ poisoning were reviewed retrospectively. The 57 patients presented between January 2004 and September 2005 were group 1; they received pulse therapy, which included cyclophosphamide and methylprednisolone, followed by the administration of dexamethasone over 2 weeks. The 77 patients that presented between October 2005 and January 2008 were group 2; they received the above-mentioned therapy and high-dose vitamin C for 2 weeks. There was no difference in the distribution of baseline variables between the 2 groups. However, group 2 showed a significant reduction in acute kidney injury related to PQ. Furthermore, a multivariate logistic regression analysis showed that the addition of vitamin C to the treatment was significantly associated with an increased survival of the patients. Larger trials will be needed to verify the effect of high-dose vitamin C on survival in patients with PQ poisoning.