The use of neuromuscular blocking agents (NMBAs) is common in the intensive care unit (ICU). NMBAs have been used in critically ill patients with lung diseases to optimize mechanical ventilation, prevent spontaneous respiratory efforts, reduce the work of breathing and oxygen consumption, and avoid patient–ventilator asynchrony. In patients with acute respiratory distress syndrome (ARDS), NMBAs reduce the risk of barotrauma and improve oxygenation. Nevertheless, current guidelines and evidence are contrasting regarding the routine use of NMBAs. In status asthmaticus and acute exacerbation of chronic obstructive pulmonary disease, NMBAs are used in specific conditions to ameliorate patient–ventilator synchronism and oxygenation, although their routine use is controversial. Indeed, the use of NMBAs has decreased over the last decade due to potential adverse effects, such as immobilization, venous thrombosis, patient awareness during paralysis, development of critical illness myopathy, autonomic interactions, ICU-acquired weakness, and residual paralysis after cessation of NMBAs use. The aim of this review is to highlight current knowledge and synthesize the evidence for the effects of NMBAs for critically ill patients with lung diseases, focusing on patient–ventilator asynchrony, ARDS, status asthmaticus, and chronic obstructive pulmonary disease.

Since its molecular isolation on January 7, 2020, the new SARS-CoV-2 coronavirus has spread rapidly, affecting regions such as Latin America. Ecuador received the worst outbreak globally if we count excess mortality per capita. This study describes the clinical, epidemiological and therapeutic characteristics of 89 patients admitted to an intensive care unit (ICU) in a second-level hospital in Quito, Ecuador. Methods: We conducted a retrospective cohort study. We collected data from health records of adult patients with severe COVID-19 admitted to an ICU in Quito, Ecuador, during the first five months of the SARS-CoV-2 outbreak. We used the Chi-square test or Fisher's exact statistics to analyze risk and associations between survivors and non-survivors. We used ROC curve analysis to predict mortality and determine cut-off points for mechanical, analytical, and cytometric ventilation parameters. We used the Wald test to evaluate the categorical predictors of the model at the multivariate level during the regression analysis. Results: 89 patients were recruited. The mean age of the patients was 54.72 years. Men represented 68.54% (n=61) and women 31.46% (n=28). Significant differences in mortality were observed (men 40.98% vs. women 17.76%). LDH and IL-6 at 24 hours after hospital admission were higher among non-survivors than survivors. Persistent hypercapnia (PaCO2 >45 mmHg), a PaFiO2 ratio of less than 140 mmHg, and positive end-expiratory pressure (PEEP) titration >9 mmHg were also associated with increased mortality. Conclusions: Elevated levels of LDH at 24 hours, IL-6 at 24 hours, lymphocyte and platelet count at 48 hours, neutrophil count at 48 hours and NLR are factors associated with higher motility, higher risk of failed extubation and reintubation in patients with acute respiratory distress syndrome due to COVID-19.

El glicocálix endotelial es una estructura sin forma definida que recubre la capa luminal del endotelio vascular y que está constituido, principalmente, por tres elementos: proteoglicanos, glucosaminoglicanos y glicoproteínas. Cumple distintas funciones, como regular la permeabilidad vascular a las moléculas y líquidos, la transducción de las fuerzas mecánicas de tensión y las cascadas de fibrinólisis y coagulación vascular; además, protege de la adhesión leucocitaria, plaquetaria y de patógenos. Los determinantes de lesión del glicocálix pueden ser de varios tipos, por ejemplo, incremento las fuerzas de tensión, especies reactivas de oxígeno (O ), aumento, a nivel plasmático, de sustancias como el sodio (hipernatremia), glucosa (hiperglicemia) y colesterol (hipercolesterolemia), y las moléculas proinflamatorias. Cualquiera de las noxas citadas, individualmente o combinadas, lesionan el glicocálix y la disfunción resultante se expresará clínicamente como disfunción endotelial, aumento de la permeabilidad vascular, paso de lipoproteínas al subendotelio, activación de la coagulación o aumento de la adhesión de plaquetas y leucocitos al endotelio.

Background: There is not much evidence on the prognostic utility of different biological markers in patients with severe COVID-19 living at high altitude. The objective of this study was to determine the predictive value of inflammatory and hematological markers for the risk of mortality at 28 days in patients with severe COVID-19 under invasive mechanical ventilation, living at high altitude and in a low-resource setting. Methods: We performed a retrospective observational study including patients with severe COVID-19, under mechanical ventilation and admitted to the intensive care unit (ICU) located at 2850 m above sea level, between 1 April 2020 and 1 August 2021. Inflammatory (interleukin-6 (IL-6), ferritin, D-dimer, lactate dehydrogenase (LDH)) and hematologic (mean platelet volume (MPV), neutrophil/lymphocyte ratio (NLR), MPV/platelet ratio) markers were evaluated at 24 h and in subsequent controls, and when available at 48 h and 72 h after admission to the ICU. The primary outcome was the association of inflammatory and hematological markers with the risk of mortality at 28 days. Results: We analyzed 223 patients (median age (1st quartile [Q1]–3rd quartile [Q3]) 51 (26–75) years and 70.4% male). Patients with severe COVID-19 and with IL-6 values at 24 h ≥ 11, NLR values at 24 h ≥ 22, and NLR values at 72 h ≥ 14 were 8.3, 3.8, and 3.8 times more likely to die at 28 days, respectively. The SOFA and APACHE-II scores were not able to independently predict mortality. Conclusions: In mechanically ventilated patients with severe COVID-19 and living at high altitude, low-cost and immediately available blood markers such as IL-6 and NLR may predict the severity of the disease in low-resource settings.

Obesity is a common chronic comorbidity of patients with COVID-19, that has been associated with disease severity and mortality. COVID-19 at high altitude seems to be associated with increased rate of ICU discharge and hospital survival than at sea-level, despite higher immune levels and inflammation. The primary aim of this study was to investigate the survival rate of critically ill obese patients with COVID-19 at altitude in comparison with overweight and normal patients. Secondary aims were to assess the predictive factors for mortality, characteristics of mechanical ventilation setting, extubation rates, and analytical parameters. This is a retrospective cohort study in critically ill patients with COVID-19 admitted to a hospital in Quito-Ecuador (2,850 m) from Apr 1, 2020, to Nov 1, 2021. Patients were cathegorized as normal weight, overweight, and obese, according to body mass index [BMI]). In the final analysis 340 patients were included, of whom 154 (45%) were obese, of these 35 (22.7%) were hypertensive and 25 (16.2%) were diabetic. Mortality in obese patients (31%) was lower than in the normal weight (48%) and overweight (40%) groups, but not statistically significant (p = 0.076). At multivariable analysis, in the overall population, older age (> 50 years) was independent risk factor for mortality (B = 0.93, Wald = 14.94, OR = 2.54 95%CI = 1.58–4.07, p < 0.001). Ferritin and the neutrophil/lymphocyte ratio were independent predictors of mortality in obese patients. Overweight and obese patients required more positive and-expiratory pressure compared to normal-weight patients. In obese patients, plateau pressure and mechanical power were significantly higher, whereas extubation failure was lower as compared to overweight and normal weight. This preliminary study suggests that BMI was not associated with mortality in critically ill patients at high altitude. Age was associated with an increase in mortality independent of the BMI. Biomarkers such as ferritin and neutrophils/lymphocytes ratio were independent predictors of mortality in obese patients with COVID-19 at high altitude.

Sepsis is defined as "an organic dysfunction secondary to the dysregulated response of the patient to an infection." This concept only reveals the tip of the iceberg, the clinical expression of organic failures, without understanding their basis, which is currently explained by cellular and molecular phenomena. Neutrophils are crucial pillars of early innate immune responses, and their fundamental function is phagocytosis. Additionally, neutrophils can degranulate upon activation, releasing various antimicrobial enzymes and pro-inflammatory cytokines, and form neutrophil extracellular traps (NETs), whose purpose is to trap pathogens by releasing their "sticky" nuclear content; the presence of activated platelets amplifies this phenomenon. NETosis is a beneficial process; however, deregulated, it can be detrimental, inducing "immunothrombosis" and compromising the microcirculation, thereby increasing the clinical severity of sepsis. The purpose of this review is to clearly describe the pathophysiological role therapeutic target of NETs, their interaction with platelets in sepsis, and their potential as therapeutic targets, since it has been shown that a therapeutic approach aimed at curbing NETs would be beneficial.