BACKGROUND Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the ongoing coronavirus disease 2019 (COVID-19) pandemic. Understanding the physiological and immunological processes underlying the clinical manifestations of COVID-19 is vital for the identification and rational design of effective therapies. AIM To describe the interaction of SARS-CoV-2 with the immune system and the subsequent contribution of hyperinflammation and abnormal immune responses to disease progression together with a complete narrative review of the different immunoadjuvant treatments used so far in COVID-19 and their indication in severe and life-threatening subsets. METHODS A comprehensive literature search was developed. Authors reviewed the selected manuscripts following the PRISMA recommendations for systematic review and meta-analysis documents and selected the most appropriate. Finally, a recommendation of the use of each treatment was established based on the level of evidence of the articles and documents reviewed. This recommendation was made based on the consensus of all the authors. RESULTS A brief rationale on the SARS-CoV-2 pathogenesis, immune response, and inflammation was developed. The usefulness of 10 different families of treatments related to inflammation and immunopathogenesis of COVID-19 was reviewed and discussed. Finally, based on the level of scientific evidence, a recommendation was established for each of them. CONCLUSION Although several promising therapies exist, only the use of corticosteroids and tocilizumab (or sarilumab in absence of this) have demonstrated evidence enough to recommend its use in critically ill patients with COVID-19. Endotypes including both, clinical and biological characteristics can constitute specific targets for better select certain therapies based on an individualized approach to treatment.

Background (1): Headache is a prevalent symptom experienced during ongoing SARS-CoV-2 infection, but also weeks after recovery. Whether cardio-pulmonary dysfunction contributes causally to headache persistence is unknown. Methods (2): We conducted a case-control analysis nested in a prospective cohort study. Individuals were recruited from August 2020 to December 2020. Patients were grouped according to the presence or absence of long-COVID headache for three months after COVID-19 resolution. We compared demographic data, clinical variables, cardio-pulmonary laboratory biomarkers, quality of life, and cardio-pulmonary function between groups. Results (3): A cohort of 70 COVID-19 patients was evaluated. Patients with headaches (n = 10; 14.3%) were more frequently female (100% vs. 58.4%; p = 0.011) and younger (46.9 ± 8.45 vs. 56.13 ± 12 years; p = 0.023). No between-group differences in laboratory analysis, resting echocardiography, cardio-pulmonary exercise test, or pulmonary function tests were observed. Conclusion (4): In this exploratory study, no significant differences in cardio-pulmonary dysfunction were observed between patients with and without long-COVID headache during mid-term follow-up.

Aims The aim of this study was to identify the main medication errors, their causality and the highest risk areas in critical care. Design A descriptive, longitudinal and retrospective study. Methods We performed a systematic analysis of the prescription, transcription and administration records of 2,634 dose units of medications that were administered to a total of 87 critically ill patients during 2018. Results Final results have shown important medication errors and a high number of significant drug interactions; prescription phase had the highest mistake rate (71%) and cause of errors (68%); transcription stage had a more variable error typology. A significant correlation was observed between the presence of causes and contributing factors to error during the prescription and the commission of errors during the nurse transcription, being the main risk areas the time of antibiotic administration, dilution errors, concentration and speed of administration of high‐risk medications and the technique used for nasogastric tube drug administration. Conclusion In critical care, an intolerable number of medication errors are still committed, placing the origin of many of them in the causality and contributing factors identified in the prescription stage. Impact The origin of many of the medication errors and most interactions is in the prescription stage, being the nurse transcription (nurse intervention) in an important filter that prevents a considerable number of errors from finally reaching the patient. The schedule of administration of time‐dependent antibiotics, high‐risk medications and the technique of administering medications through a nasogastric tube are important risk areas for the commission of medication errors.

Funding Acknowledgements Type of funding sources: None. Background   The high flow nasal cannula oxygen (HFNC) may offer an alternative to invasive and noninvasive positive pressure ventilation (NIPPV) in patients with acute pulmonary edema (APE) with theoretical advantages related with patient adaptation, comfort and lower need of staff training to achieve optimal therapy. However, clinical efficacy and safety of HFNC is not well established. We aimed to compare the in-hospital clinical outcomes between NIPPV and HFNC in patients without hypercapnia as initial treatment of acute pulmonary edema (APE). Methods In a prospective, observational study, 47 patients treated with HFNC or NIPPV as initial treatment of no-hypercapnic APE were included. Primary endpoint was the composite of death or need for orotracheal intubation within 30 days after admission. Results 47 patients (mean [±SD] age 68.8± 13.1 years, 83% man) were included. 28 (59.6%) patients received HFNC and 19 (40.4%) NIPPV- CPAP as initial treatment to APE. De novo acute heart failure was the initial presentation in 76,6% and 61,7% was secondary to acute coronary syndrome. There was no significant difference in 30-days mortality rates or composite objective of death/intubation in HFNC vs NIPPV (21.5 vs 15.8 p = 0.72) and (37.0 vs 21.1% p= 0.24). However the failure of therapy defined as the combined objective of intubation or change of therapy due to respiratory worsening was more frequent (40.7 vs 15.8 p = 0.07) in HFNC group. Conclusion The HFNC was not associated with increased 30-day mortality in patients with no-hypercapnic EAP, but was associated with no-significant increase of treatment failure secondary to respiratory worsening, despite comparable disease severity and initial treatment. Randomized studies are needed Ends points comparing NIPPV and HFNCVariableOverall (n = 47)CPAP/NIPPVN = 19HFNCn = 28P valueDeath at 30 days (%)19.115.821.50.72Respiratory infection after 48 hours of admission (%)15.226.37.40.107Intubation at 30 days (%)23.915.829.60.32Death or intubation 30 days (%)30.421.137.00.24Intubation or change therapy for worsening RD (%)30.440.715.80.07Length hospital stay (days)11.8 ± 10.912.06 ± 9.611.7 ± 11.80.65Length critical care unit stay(days)5.87 ± 6.86.9 ± 7.25.1 ± 6.50.24RD Respiratory distress

Recent works have demonstrated a significant reduction in cholesterol levels and increased oxidative stress in patients with coronavirus disease 2019 (COVID-19). The cause of this alteration is not well known. This study aimed to comprehensively evaluate their possible association during the evolution of COVID-19. This is an observational prospective study. The primary endpoint was to analyze the association between lipid peroxidation, lipid, and inflammatory profiles in COVID-19 patients. A multivariate regression analysis was employed. The secondary endpoint included the long-term follow-up of lipid profiles. COVID-19 patients presented significantly lower values in their lipid profile (total, low, and high-density lipoprotein cholesterol) with greater oxidative stress and inflammatory response compared to the healthy controls. Lipid peroxidation was the unique oxidative parameter with a significant association with the total cholesterol (OR: 0.982; 95% CI: 0.969–0.996; p = 0.012), IL1-RA (OR: 0.999; 95% CI: 0.998–0.999; p = 0.021) IL-6 (OR: 1.062; 95% CI: 1.017–1.110; p = 0.007), IL-7 (OR: 0.653; 95% CI: 0.433–0.986; p = 0.042) and IL-17 (OR: 1.098; 95% CI: 1.010–1.193; p = 0.028). Lipid abnormalities recovered after the initial insult during long-term follow-up (IQR 514 days); however, those with high LPO levels at hospital admission had, during long-term follow-up, an atherogenic lipid profile. Our study suggests that oxidative stress in COVID-19 is associated with derangements of the lipid profile and inflammation. Survivors experienced a recovery in their lipid profiles during long-term follow-up, but those with stronger oxidative responses had an atherogenic lipid profile.