Influenza A (H1N1)pdm09 infection acquired in the hospital is an independent factor for death in critically ill patients admitted to the ICU.

BackgroundPatients infected with influenza A (H1N1)pdm09 virus requiring admission to the ICU remain an important source of mortality during the influenza season. The objective of the study was to assess the impact of a delay in diagnosis of community-acquired influenza A (H1N1)pdm09 virus infection on clinical outcome in critically ill patients admitted to the ICU.MethodsA prospective multicenter observational cohort study was based on data from the GETGAG/SEMICYUC registry (2009–2015) collected by 148 Spanish ICUs. All patients admitted to the ICU in which diagnosis of influenza A (H1N1)pdm09 virus infection had been established within the first week of hospitalization were included. Patients were classified into two groups according to the time at which the diagnosis was made: early (within the first 2 days of hospital admission) and late (between the 3rd and 7th day of hospital admission). Factors associated with a delay in diagnosis were assessed by logistic regression analysis.ResultsIn 2059 ICU patients diagnosed with influenza A (H1N1)pdm09 virus infection within the first 7 days of hospitalization, the diagnosis was established early in 1314 (63.8 %) patients and late in the remaining 745 (36.2 %). Independent variables related to a late diagnosis were: age (odds ratio (OR) = 1.02, 95 % confidence interval (CI) 1.01–1.03, P < 0.001); first seasonal period (2009–2012) (OR = 2.08, 95 % CI 1.64–2.63, P < 0.001); days of hospital stay before ICU admission (OR = 1.26, 95 % CI 1.17–1.35, P < 0.001); mechanical ventilation (OR = 1.58, 95 % CI 1.17–2.13, P = 0.002); and continuous venovenous hemofiltration (OR = 1.54, 95 % CI 1.08–2.18, P = 0.016). The intra-ICU mortality was significantly higher among patients with late diagnosis as compared with early diagnosis (26.9 % vs 17.1 %, P < 0.001). Diagnostic delay was one independent risk factor for mortality (OR = 1.36, 95 % CI 1.03–1.81, P < 0.001).ConclusionsLate diagnosis of community-acquired influenza A (H1N1)pdm09 virus infection is associated with a delay in ICU admission, greater possibilities of respiratory and renal failure, and higher mortality rate. Delay in diagnosis of flu is an independent variable related to death.

Infection by influenza virus has to be considered as a possible cause of nosocomial infection in the neonatal period. Control measures and prevention are important.

WORD COUNT: 286 1 AbstractPurpose: Ventilator-induced diaphragm dysfunction or damage (VIDD) is highly prevalent in patients under mechanical ventilation (MV), but its analysis is limited by the difficulty of obtaining histological samples. In this study we compared diaphragm histological characteristics in Maastricht III (MSIII) and brain-dead (BD) organ donors and in control subjects undergoing thoracic surgery (CTL) after a period of either controlled or spontaneous MV (CMV or SMV).Methods: In this prospective study, biopsies were obtained from diaphragm and quadriceps.Demographic variables, comorbidities, severity on admission, treatment and ventilatory variables were evaluated. Immunohistochemical analysis (fiber size and type percentages) and quantification of abnormal fibers (a surrogate of muscle damage) were performed.Results: Muscle samples were obtained from 35 patients. MSIII (n=16) had more hours on MV (either CMV or SMV) than BD (n=14) and also spent more hours, and a greater percentage of time with diaphragm stimuli (time in assisted and spontaneous modalities). Cross sectional area (CSA) was significantly reduced in the diaphragm and quadriceps in both groups in comparison with CTL (n=5).Quadriceps CSA was significantly decreased in MSIII compared to BD but there were no differences in the diaphragm CSA between the two groups. Those MSIII who spent 100 or more hours without diaphragm stimuli presented reduced diaphragm CSA without changes in their quadriceps CSA.Proportion of internal nuclei in diaphragms of MSIII tended to be higher than BD, and their proportion of lipofuscin deposits tended to be lower, though there were no differences in the quadriceps fiber evaluation. Conclusions:This study provides the first evidence in humans about the effects of different modalities of MV (controlled, assisted and spontaneous) on diaphragm myofiber damage showing that diaphragm inactivity during mechanical ventilation is associated with the development of VIDD. KeywordsVentilator-induced Diaphragm Dysfunction or damage (VIDD), Atrophy, Mechanical Ventilation, Brain Death, Maastricht III, Muscle dysfunction.Most critically ill patients admitted to the Intensive Care Unit (ICU) require mechanical ventilation (MV) due to respiratory failure. MV may be associated with adverse effects on respiratory muscles, and disuse atrophy may be the most important mechanism in patients under controlled mechanical ventilation (CMV) [1]. During CMV, the electromyographic activity of the respiratory muscle fibers is diminished or may even stop [2], resulting in a rapid development of respiratory muscle dysfunction, especially diaphragm weakness. Ventilator-induced diaphragm dysfunction (VIDD) is defined as the loss of the diaphragm's capacity to generate force, together with muscle injury and fiber atrophy, and the same acronym has been used before to describe ventilator-induced diaphragm damage [3]. Both VIDD are associated particularly with the use of MV, typically after periods of CMV [4,5,6].VIDD may play a key role in th...