No abstract

No abstract

Background: Lactate is a well-known marker to estimate prognosis after cardiac surgery and critically ill patients. The liver and kidney have a major role in lactate metabolism; however, there was less characterized about the change of lactate and threshold to predict in-hospital mortality in dialysis-dependent patients undertaking cardiac surgery. We conducted this retrospective observational study to characterize when and how lactate values after cardiac surgery affected in-hospital mortality. Methods: This two-center retrospective study included dialysis-dependent patients who underwent cardiac surgery with a cardiopulmonary bypass from January 2014 to December 2018. Lactate values were collected at three points: at ICU admission (T1), the maximum level of lactate within 24 h postoperatively (T2), and 24 h after ICU admission (T3). We determined hyperlactatemia as more than 2 mmol/L following previous studies. Results: We enrolled 122 dialysis-dependent patients. The mean age was 73 ± 8 years and hyperlactatemia was observed in 100 patients (81.9%). In-hospital mortality was 11.4%. Univariate analysis and area under curve in ROC suggested that T2 lactate was the most significantly associated with in-hospital mortality (AUC = 0.845). Multivariate logistic analysis showed a significant association between in-hospital mortality when patients showed early peak lactate levels of > 4.5 mmol/L after ICU admission (adjusted OR 8.35; 95% CI: 1.44-57.13). Conclusions: In dialysis-dependent patients after cardiac surgery, the early-onset of a maximum arterial lactate concentration of > 4.5 mmol/L was significantly associated with in-hospital mortality.

Background and Objectives: Carbon monoxide (CO) poisoning is responsible for nearly 50,000 emergency department visits and 1200 deaths per year. Compared to oxygen, CO has a 250-fold higher affinity for hemoglobin (Hb), resulting in the displacement of oxygen from Hb and impaired oxygen delivery to tissues. Optimal treatment of CO-poisoned patients involves the administration of hyperbaric 100% oxygen to remove CO from Hb and to restore oxygen delivery. However, hyperbaric chambers are not widely available and this treatment requires transporting a CO-poisoned patient to a specialized center, which can result in delayed treatment. Visible light is known to dissociate CO from carboxyhemoglobin (COHb). In a previous study, we showed that a system composed of six photo-extracorporeal membrane oxygenation (ECMO) devices efficiently removes CO from a large animal with CO poisoning. In this study, we tested the hypothesis that the application of hyperbaric oxygen to the photo-ECMO device would further increase the rate of CO elimination. Study Design/Material and Methods: We developed a hyperbaric photo-ECMO device and assessed the ability of the device to remove CO from CO-poisoned human blood. We combined four devices into a "hyperbaric photo-ECMO system" and compared its ability to remove CO to our previously described photo-ECMO system, which was composed of six devices ventilated with normobaric oxygen. Results: Under normobaric conditions, an increase in oxygen concentration from 21% to 100% significantly increased CO elimination from CO-poisoned blood after a single pass through the device. Increased oxygen pressure within the photo-ECMO device was associated with higher exiting blood PO 2 levels and increased CO elimination. The system of four hyperbaric photo-ECMO devices removed CO from 1 L of CO-poisoned blood as quickly as the original, normobaric photo-ECMO system composed of six devices. Conclusion: This study demonstrates the feasibility and efficacy of using a hyperbaric photo-ECMO system to increase the rate of CO elimination from CO-poisoned blood. This technology could provide a simple portable emergency device and facilitate immediate treatment of CO-poisoned patients at or near the site of injury.