Background: A key role of oxidative stress has been highlighted in the pathogenesis of COVID-19. However, little has been said about oxidative stress status (OSS) of COVID-19 patients hospitalized in intensive care unit (ICU). Material and Methods: Biomarkers of the systemic OSS included antioxidants (9 assays), trace elements (3 assays), inflammation markers (4 assays) and oxidative damage to lipids (3 assays). Results: Blood samples were drawn after 9 (7–11) and 41 (39–43) days of ICU stay, respectively in 3 and 6 patients. Vitamin C, thiol proteins, reduced glutathione, γ-tocopherol, β-carotene and PAOT® score were significantly decreased compared to laboratory reference values. Selenium concentration was at the limit of the lower reference value. By contrast, the copper/zinc ratio (as a source of oxidative stress) was higher than reference values in 55% of patients while copper was significantly correlated with lipid peroxides (r = 0.95, p < 0.001). Inflammatory biomarkers (C-reactive protein and myeloperoxidase) were significantly increased when compared to normals. Conclusions: The systemic OSS was strongly altered in critically ill COVID-19 patients as evidenced by increased lipid peroxidation but also by deficits in some antioxidants (vitamin C, glutathione, thiol proteins) and trace elements (selenium).

OBJECTIVES: To investigate exercise capacity at 3 and 6 months after a prolonged ICU stay. DESIGN: Observational monocentric study. SETTING: A post-ICU follow-up clinic in a tertiary university hospital in Liège, Belgium. PATIENTS: Patients surviving an ICU stay greater than or equal to 7 days for a severe coronavirus disease 2019 pneumonia and attending our post-ICU follow-up clinic. MEASUREMENTS AND MAIN RESULTS: Cardiopulmonary and metabolic variables provided by a cardiopulmonary exercise testing on a cycle ergometer were collected at rest, at peak exercise, and during recovery. Fourteen patients (10 males, 59 yr [52–62 yr], all obese with body mass index > 27 kg/m2) were included after a hospital stay of 40 days (35–53 d). At rest, respiratory quotient was abnormally high at both 3 and 6 months (0.9 [0.83–0.96] and 0.94 [0.86–0.97], respectively). Oxygen uptake was also abnormally increased at 3 months (8.24 mL/min/kg [5.38–10.54 mL/min/kg]) but significantly decreased at 6 months (p = 0.013). At 3 months, at the maximum workload (67% [55–89%] of predicted workload), oxygen uptake peaked at 81% (64–104%) of predicted maximum oxygen uptake, with oxygen pulse and heart rate reaching respectively 110% (76–140%) and 71% (64–81%) of predicted maximum values. Ventilatory equivalent for carbon dioxide remains within normal ranges. The 50% decrease in oxygen uptake after maximum effort was delayed, at 130 seconds (115–142 s). Recovery was incomplete with a persistent anaerobic metabolism. At 6 months, no significant improvement was observed, excepting an increase in heart rate reaching 79% (72–95%) (p = 0.008). CONCLUSIONS: Prolonged reduced exercise capacity was observed up to 6 months in critically ill coronavirus disease 2019 survivors. This disability did not result from residual pulmonary or cardiac dysfunction but rather from a metabolic disorder characterized by a sustained hypermetabolism and an impaired oxygen utilization.

Introduction: Oral nutrition is delivered frequently in intensive care units (ICUs) but rarely studied. The primary objective of this study was to quantify nutrition intakes in patients exclusively orally fed (OF) and in those receiving medical nutrition solutions or both. Methods: Adults who stayed in a mixed ICU for ≥3 days were studied. Nutrition deficits were calculated as the difference between estimated energy or protein targets (determined by weight-based formulas) and actual intakes (recorded on a daily basis by nurses). Total volumes of enteral or parenteral nutrition solutions, propofol, and glucose infused over 24 hours were collected and energy and protein amounts were calculated. In OF patients, food intake at each meal (breakfast, lunch, and dinner) was estimated using the "one-quarter portion" method. Results: Among the 289 included patients aged 67 (57-75.5) years, 253 were fed and received, on average, 14.3 (7.8-19) kcal/kg/d and 0.53 (0.27-0.8) g/kg/d protein. In OF patients (n = 126), intakes were 9.7 (5.8-19) kcal/kg/d and 0.35 (0.17-0.57) g/kg/d protein. In the subset of OF patients with ICU stay ≥ 7 days (n = 37), respectively, 51% and 94% never received ≥80% of their energy and protein targets. Conclusion: Nutrition intakes were lower by oral feeding compared with other exclusive or combined medical nutrition. Compared with the prescribed amounts, the deficit was larger for proteins than for energy.

Background & aims: Hyperuricemia is an independent risk factor for the metabolic syndrome and cardiovascular disease. We hypothesized that asymptomatic carriers for hereditary fructose intolerance (OMIM 22960) would have increased uric acid and altered component of the metabolic syndrome when exposed to fructose overfeeding. Methods: Six heterozygotes for HFI (hHFI) and 6 controls (Ctrl) were studied in a randomized, controlled, crossover trial. Participants ingested two identical test meals containing 0.7 g kg À1 glucose and 0.7 g kg À1 fructose according to a cross-over design, once after a 7-day on a low fructose diet (LoFruD, <10 g/d) and on another occasion after 7 days on a high fructose diet (HiFruD, 1.4 g kg À1 day À1 fructose þ 0.1 g kg À1 day À1 glucose). Uric acid, glucose, and insulin concentrations were monitored in fasting conditions and over 2 h postprandial, and insulin resistance indexes were calculated. Results: HiFruD increased fasting uric acid (p < 0.05) and reduced fasting insulin sensitivity estimated by the homeostasis model assessment (HOMA) for insulin resistance (p < 0.05), in both groups. Postprandial glucose concentrations were not different between hHFI and Ctrl. However HiFruD increased postprandial plasma uric acid, insulin and hepatic insulin resistance index (HIRI) in hHFI only (all p < 0.05). Conclusions: Seven days of HiFruD increased fasting uric acid and slightly reduced fasting HOMA index in both groups. In contrast, HiFruD increased postprandial uric acid, insulin concentration and HIRI in hHFI only, suggesting that heterozygosity for pathogenic Aldolase B variants may confer an increased susceptibility to the effects of dietary fructose on uric acid and hepatic insulin sensitivity. This trial was registered at the U.S. Clinical Trials Registry as NCT03545581.

Malnutrition is associated to poor outcomes in critically ill patients. Oral nutrition is the route of feeding in less than half of the patients during the intensive care unit (ICU) stay and in the majority of ICU survivors. There are growing data indicating that insufficient and/or inadequate intakes in macronutrients and micronutrients are prevalent within these populations. The present narrative review focuses on barriers to food intakes and considers the different points that should be addressed in order to optimize oral intakes, both during and after ICU stay. They are gathered in the SPICES concept, which should help ICU teams improve the quality of nutrition care following 5 themes: swallowing disorders screening and management, patient global status overview, involvement of dieticians and nutritionists, clinical evaluation of nutritional intakes and outcomes, and finally, supplementation in macro-or micronutrients.