Background: This study aimed to describe the clinical course, outcomes, and prognostic factors of chronic obstructive pulmonary disease (COPD) patients with acute hypercapnic respiratory failure.Methods: This retrospective study involved patients with acute hypercapnic respiratory failure due to COPD of any cause admitted to the intensive care unit (ICU) for non-invasive or invasive mechanical ventilation (IMV) support between December 2015 and February 2020. Results: One hundred patients were evaluated. The main causes of acute hypercapnic respiratory failure were bronchitis, pneumonia, and heart failure. The patients’ mean Acute Physiology and Chronic Health Evaluation (APACHE) II score was 23.0±7.2, and their IMV rate was 43%. ICU, in-hospital, and 90-day mortality rates were 21%, 29%, and 39%, respectively. Non-survivors had greater pneumonia, shock within the first 24 hours of admission, IMV, vasopressor use, and renal replacement therapy, along with higher APACHE II scores, lower admission albumin levels and PaO2/FiO2 ratios, and longer ICU and hospital stays than survivors. Logistic regression analysis identified APACHE II score (odds ratio [OR], 1.157; 95% confidence interval [CI], 1.017–1.317; P=0.026), admission PaO2/FiO2 ratio (OR, 0.989; 95% CI, 0.978–0.999; P=0.046), and vasopressor use (OR, 8.827; 95% CI, 1.650–47.215; P=0.011) as predictors of ICU mortality. APACHE II score (OR, 1.099; 95% CI, 1.021–1.182; P=0.011) and admission albumin levels (OR, 0.169; 95% CI, 0.056–0.514; P=0.002) emerged as predictors of 90-day mortality.Conclusions: APACHE II scores, the PaO2/FiO2 ratio, vasopressor use, and albumin levels are significant short-term mortality predictors in severely ill COPD patients with acute hypercapnic respiratory failure.

Background: Alterations in the neuroendocrine system occur during critical illness. Chronic obstructive pulmonary disease (COPD) itself causes hormonal changes. The aim of this study was to determine neu roendocrine hormones of COPD patients with acute respiratory failure and to investigate the relationship between hormonal changes, mortality, and morbidity.Methods: We enrolled 21 patients (13 F/8 M) with COPD exacerbation requiring artificial airway support. Blood samples were collected on admission to the ICU, and on the day of hospital discharge. Eighteen healthy people were included as controls. Results: Female patients had lower luteinizing hormone (LH), follicle stimulating hormone (FSH), and free triiodothyronine (fT3), and higher prolactin (PRL) levels than controls on admission to the ICU (FSH: 70.3 vs. 29.3 mlU/mL; LH: 26.6 vs. 6.8 mlU/mL; fT3: 2.9 vs. 2.0 pg/mL; PRL: 12.4 vs. 21.3 ng/mL). Male patients had low testosterone and TSH and high PRL but only changes in TSH and PRL reached statistical significance (testosterone: 3.5 vs. 1.5 ng/mL, TSH: 1.1 vs. 0.5 ulU/mL, PRL: 9.7 vs. 14.2 ng/mL). Female patients had lower fT3 than males (fT3_female: 2.7 vs. fT3_male: 2.0 pg/mL). On follow-up, significantly elevated FSH and fT3 and decreased estradiol concentrations were documented among recovered women (FSH: 28.4 vs. 46.6 mlU/mL, fT3,: 2.0 vs. 2.6 pg/mL, E₂: 27.7 vs. 19.0 pg/mL). Patients had high C-reactive protein levels and acute physiologic and chronic health evaluation II scores. Mortality rate was 9.5% and a negative correlation between E₂ and duration of noninvasive mechanical ventilation and length of hospital stay was found in male patients. Conclusion: Men and women with acute respiratory failure in the presence of COPD develop significant changes in the neuroendocrine axis. Hormonal suppression vanishes with disease improvement.

Objective: This study aimed to evaluate epidemiology and outcome among critically ill patients under a restrictive transfusion practice. Methods: One hundred sixty-nine patients who were admitted to the intensive care unit (ICU) between March 2016 to December 2017 and remained in the ICU > 24 hours were retrospectively included. Results: Hemoglobin levels on admission were <12 g/dL in 85% and <9 g/dL in 37.9% of patients. The median admission hemoglobin level was decreased on the last day of the ICU stay. Erythrocyte transfusion was required for 34% of patients. Transfused patients had high Acute Physiology and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores, more requirement for invasive mechanical ventilation, vasopressors, and dialysis, long ICU and hospital stays, low hemoglobin levels, and high hospital and ICU mortality rates. Multivariate analysis showed that the likelihood of transfusion increased from 6.6 to 25.8 fold when the ICU stay extended from ≥7 to ≥15 days. Age, vasopressor use, dialysis, and erythrocyte transfusion ≥5 units were predictors of mortality. Conclusion: Patients receiving transfusion are severely ill and have more life support therapies. The number of erythrocyte units transfused, age, and organ support therapies are independent predictors of mortality.

There are limited data on the long-term outcomes of COVID-19 from different parts of the world. To determine risk factors of 90-day mortality in critically ill patients in Turkish intensive care units (ICUs), with respiratory failure. Retrospective, observational cohort. Patients with laboratory-confirmed COVID-19 and who had been followed up in the ICUs with respiratory failure for more than 24 hours were included in the study. Their demographics, clinical characteristics, laboratory variables, treatment protocols, and survival data were recorded. A total of 421 patients were included. The median age was 67 (IQR: 57-76) years, and 251 patients (59.6%) were men. The 90-day mortality rate was 55.1%. The factors independently associated with 90-day mortality were invasive mechanical ventilation (IMV) (HR 4.09 [95% CI: [2.20-7.63], P < .001), lactate level >2 mmol/L (2.78 [1.93-4.01], P < .001), age ≥60 years (2.45 [1.48-4.06)], P < .001), cardiac arrhythmia during ICU stay (2.01 [1.27-3.20], P = .003), vasopressor treatment (1.94 [1.32-2.84], P = .001), positive fluid balance of ≥600 mL/day (1.68 [1.21-2.34], P = .002), PaO₂/FiO₂ ratio of ≤150 mmHg (1.66 [1.18-2.32], P = .003), and ECOG score ≥1 (1.42 [1.00-2.02], P = .050). Long-term mortality was high in critically ill patients with COVID-19 hospitalized in intensive care units in Turkey. Invasive mechanical ventilation, lactate level, age, cardiac arrhythmia, vasopressor therapy, positive fluid balance, severe hypoxemia and ECOG score were the independent risk factors for 90-day mortality.

Background: Cardiac troponin I (TnI) is a specific marker of myocardial damage used in the diagnosis of acute coronary syndrome (ACS). TnI levels can also be elevated in patients without ACS, which is linked to a worse prognosis and mortality. We evaluated the clinical implications and prognostic significance of serum TnI levels in critically ill non-cardiac patients admitted to the intensive care unit (ICU) at a tertiary-level hospital. Materials and Methods: A three-year retrospective study including the years 2017–2020 was conducted to evaluate in-hospital mortality during ICU stay and mortality rates at 28 and 90 days, as well as one and two years after admission, in 557 patients admitted to the medical ICU for non-cardiac causes. Results: TnI levels were elevated in 206 (36.9%) patients. Patients with elevated TnI levels were significantly older and had higher rates of comorbidities, including chronic heart failure, coronary heart disease, and chronic kidney disease (p < 0.05 for all). Patients with elevated TnI levels required more invasive mechanical ventilation, vasopressor infusion, and dialysis in the ICU and experienced more shock within the first 72 h (p = 0.001 for all). High TnI levels were associated with higher Acute Physiological and Chronic Health Evaluation (APACHE) II (27.6 vs. 20.3, p = 0.001) and Sequential Organ Failure assessment (8.8 vs. 5.26, p = 0.001) scores. Elevated TnI levels were associated with higher mortality rates at 28 days (58.3% vs. 19.4%), 90 days (69.9% vs. 35.0%), one year (78.6% vs. 46.2%), and two years (82.5% vs. 55.6%) (p < 0.001 for all). Univariate logistic regression analysis revealed that high TnI levels were a strong independent predictor of mortality at all time points: 28 days (OR = 1.2, 95% CI: 1.108–1.3, p < 0.001), 90 days (OR = 1.207, 95% CI: 1.095–1.33, p = 0.001), one year (OR = 1.164, 95% CI: 1.059–1.28, p = 0.002), and two year (OR = 1.119, 95% CI: 1.026–1.22, p = 0.011). Multivariate analysis revealed that age, albumin level, APACHE II score, and requirements for dialysis and vasopressor use in the ICU were important predictors of mortality across all timeframes, but elevated TnI levels were not. Conclusions: Elevated TnI levels in critically ill non-cardiac patients are markers of disease severity. While elevated TnI levels were significant predictors of mortality in the univariate analysis, they lost significance in the multivariate model when adjusted for other factors. Patients with elevated TnI levels had higher mortality rates across all timeframes, from 28 days to two years.