ABSTRACT
Considering the paucity of data on long-term Health-Related Quality of Life (HRQoL) in coronavirus disease 2019 (COVID-19) intensive care unit (ICU) survivors, we present one-year follow-up results on patients' HRQoL and compare them with those of the already reported 6-month follow-up. We conducted a prospective cohort study of patients in COVID-19 ICU between March and June 2020. A HRQoL analysis was performed six months and 1 year after discharge by means of a short-form-36 (SF-36) questionnaire. Hospital mortality in 403 ICU COVID-19 patients was 44.9%;further 4.0% died between hospital discharge and 6-month follow-up and only 0.5% died in the next six months. The median physical component of HRQoL increased from 43.7 (interquartile range (IQR): 31.7-52.7) at 6 months to 46.0 (IQR: 38.0-53.0) 1 year after hospital discharge (p = 0.007). In multivariable regression analysis, age >50 (odds ratio (OR) 0.270) and female sex (OR 0.144) were independently associated with reduced physical HRQoL 1 year after discharge. The median mental component of HRQoL increased from 50.6 (IQR: 42.0-55.8) at 6 months to 53.0 (IQR: 47.0-56.0) 1 year after discharge (p = 0.035), with no significant predictors. Increased HRQoL was associated with an improvement in patients' physical status, role functioning, emotional well-being (all p < 0.001) and social functioning (p = 0.007). ICU COVID-19 patients' HRQoL slightly improved 1 year after discharge, when compared to results of the 6-month follow-up. Medications received during ICU stay had no effect on physical or mental HRQoL.Copyright © 2023 The Author(s). Published by MRE Press.
ABSTRACT
When treating patients with COVID-19, prognostic and diagnostic tests to assess the risk of severe disease and adverse outcome are particularly important. The analysis of demographic, clinical, laboratory and instrumental data obtained on ICU admission was performed on a sample of 109 patients to determine potential predictors of lethal outcome. The factors increasing the risk of adverse outcome included age =57 years (AUC = 0.777, P < 0.001), hypertension (RR = 3.073, P = 0.033), ARDS (RR = 17.455, P < 0.001), advanced chest CT severity score (HR = 1.569, P = 0.039), severe and critical COVID-19 (RR = 6.964, P = 0.016), neutrophilia (AUC = 0.729, P = 0.005), lymphopenia (AUC = 0.705, P = 0.023), thrombocytopenia (AUC = 0.713, P = 0.018), reduced MCHC (AUC = 0.700, P = 0.026), elevated RDW (AUC = 0.718, P = 0.007), LDH (AUC = 0.891, P = 0.005) and D-dimer (AUC = 0.806, P = 0.029).
ABSTRACT
Introduction: COVID-19 patients with acute respiratory distress syndrome (ARDS) have an immune imbalance when systemic inflammation and dysfunction of circulating T and B cells lead to a more severe disease. TREC (T cell receptor excision circle) formed during maturation of naive T cells in the thymus and KREC (kappa-deletion recombination excision circle) developed during maturation of naive B cells in bone marrow. Using TREC/KREC analysis, we studied the level of naive T and B cells in peripheral blood of COVID-19 patients. Methods: TREC/KREC analysis was performed by multiplex real-time quantitative PCR on a DNA samples of peripheral blood. The total sample size was 36 patients from 18 to 45 years old;10 (27.78%) patients had ARDS, and 4 (11.11%) of them did not survive. Results: Patients with ARDS differed from the non-ARDS group ones in reduced lymphocyte count (p = 0.014), increased neutrophil count (p = 0.049), and neutrophil-to-lymphocyte ratio (NLR) (p = 0.002). During days 6 to 20 of hospitalization, a higher NLR was detected in ARDS patients compared with non-ARDS patients (Fig. 1A). Analysis of TREC/KREC levels both per 100,000 cells revealed significant differences: TREC/KREC values were lower in the group of ARDS patients;these differences persisted after adjustment for multiple comparisons (Fig. 1B). The TREC/KREC levels were also lower in non-survivors than in survivors. TREC/KREC negatively correlated with NLR;the highest correlation was recorded for TREC per 100,000 cells (Spearman's rho = - 0.726, p = 1.0 × 10E-06, coefficient of determination R2 = 0.527). Conclusions: Thus, TREC/KREC analysis is a potential prognostic marker for assessing the severity and outcome in COVID-19. (Table Presented).
ABSTRACT
There are various data on negative impact of comorbidities on treatment outcomes in patients with novel coronavirus infection (COVID-19). However, the impact of cardiovascular diseases and especially their therapy on the course of infectious process and unfavorable outcomes in COVID-19patients has not been sufficiently studied. Objective. To assess the impact of concomitant cardiovascular diseases and chronic drug intake for their treatment on in-hospi-tal mortality in ICU patients with COVID-19. Material and methods. A single-center retrospective cohort study of ICU patients with COVID-19 was carried out between March 6, 2020 and June 3, 2020 at the Demikhov Moscow City Clinical Hospital. We analyzed the following data: age, gender, previous comorbidities, Charlson comorbidity index, therapy of chronic cardiovascular diseases, severity of COVID-19, NEWS and SOFA scores. Univariate analysis included assessment of relative risk (RR). Multivariate analysis was carried out using regression model. Results. We analyzed medical records of 403 patients (231 (57.3%) men). Mean age of patients was 62.4±15.3 years. Over-all 30-day mortality rate was 44.9% (n=181). Multivariate analysis showed that coronary artery disease (adj. OR 2.459, 95% CI 1.589—3.806, p<0.001) and hypertension (adj. OR 2.893, 95% CI 1.667—5.019, p<0.001) were independent predictors of mortality in ICU patients with COVID-19. Conclusion. Coronary artery disease and hypertension are independent predictors of poor outcomes. Long-term use of angioten-sin-converting enzyme inhibitors, β-blockers, acetylsalicylic acid or statins for cardiovascular diseases does not significantly affect clinical outcomes in ICU patients with COVID-19. © 2022, Media Sphera Publishing Group. All rights reserved.
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Introduction. Even now — a year after the pandemic announcement by WHO, there is lack of clinical evidence to confirm the efficacy of the majority of anti-COVID drugs, evenly for general and critically ill patients. Objective. To estimate the efficacy and safety of some anti-COVID-19 drugs as well as the impact of the demographic data and comorbidity on clinical outcomes of critically ill patients. Materials and methods. The single-center retrospective cohort study was performed on critically ill patients admitted to the ICU of Moscow Municipal Hospital No. 68 from March 6 to June 3, 2020. Anthropometric parameters, severity of the condition and comorbidities, as well as CT data, treatment in the ICU, duration of mechanical ventilation and the patients’ length of staying the ICU were taken into account and analyzed. Results. Overall, 403 patients (231 male, average age: 62.4 ± 15.3 years, range from 21 to 97 years) were enrolled into the study. In hospital mortality rate appeared to be 44.9 % (181/403) and was equal for men and for women (p = 1,000). The application of low molecular weight heparin was the single one significant predictor of mortality reduction according to the results of multivariate analysis — HR = 0.742 (0.545–0.991), p = 0.045. The main unmodifiable predictors for mortality elevation in the ICU were: age 65+ (RR 2.116 [1.680–2.664], p < 0.001) and Charlson’s comorbidity index (HR 1.136 [1.087–1.188], p < 0.001). The group of patients with a fatal outcome had a higher comorbidity index, the number of points on the SOFA scale (p < 0.001), as well as a larger median number of days in the ICU (p = 0.012). Conclusions. Current study has convincingly proved that low molecular weight heparin to be used for while treating severe acute respiratory syndrome coronavirus 2 patients in intensive care settings. © 2021, Practical Medicine Publishing House LLC. All rights reserved.
ABSTRACT
The search for sensitive and specific markers enabling timely identification of patients with a life-threat-ening novel coronavirus infection (COVID-19) is important for a successful treatment. The aim of the study was to examine the association of molecular biomarkers of air-blood barrier damage, surfactant proteins SP-A and SP-D and Club cell protein CC16, with the outcome of patients with COVID-19. Materials and methods. A cohort of 109 patients diagnosed with COVID-19 was retrospectively divided into two groups. Group 1 comprised survivor patients discharged from the ICU (n=90). Group 2 included the patients who did not survive (n=19). Association of disease outcome and SP-A, SP-D, and CC16 levels in blood serum, clinical, and laboratory data were examined taking into account the day of illness at the time of bio-material collection. Results. The non-survivors had higher SP-A (from days 1 to 10 of symptoms onset) and lower CC16 (from days 11 to 20 of symptoms onset) levels vs survivors discharged from ICU. No significant differences in SP-D levels between the groups were found. Conclusion. According to the study results, the surfactant protein SP-A and Club cell protein CC16 are associated with increased COVID-19 mortality.
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The aim of the study was to identify the pathomorphology of brain damage in patients who died of COVID-19. Material and methods. Autopsy reports and autopsy brain material of 17 deceased patients with pre-mortem confirmed COVID-19 infection were analyzed. Fatal cases in which COVID-19 was the major cause of death were included in the study. Five people were diagnosed with cerebral infarction. Organ samples were taken for histological examination during autopsy. Sections were stained with hematoxylin and eosin and by Nissl to assess brain histopathology. To study the vascular basal membranes the PAS reaction was used, to detect fibrin in vessels phosphotungstic acid-hematoxylin (PTAH) staining was used, to determine DNA in nuclei sections were stained according to Feulgen, to detect RNA in neuronal nuclei and cytoplasm sections were stained with methyl green-pyronin. Immunohistochemical study of a neuronal marker, nuclear protein NeuN, was performed to assess neuronal damage. Results. The signs of neuronal damage found in patients who died of COVID-19 included nonspecific changes of nerve cells (acute swelling, retrograde degeneration, karyolysis and cytolysis, ‘ghost' cells, neuronophagia and satellitosis) and signs of circulatory disorders (perivascular and pericellular edema, diapedesis, congested and engorged microvasculature). Conclusion. Brain histopathological data indicate damage to the central nervous system in COVID-19 patients. Ischemic stroke in patients with COVID-19 is mostly caused by a combination of hypoxia resulting from respiratory failure and individual risk factors, including cerebrovascular atherosclerosis and hypertension.
ABSTRACT
In November-December 2020, the Federation of Anesthesiologists and Reanimatologists has conducted a survey of intensive care units (ICU) in 100 hospitals re-profiled for the treatment of COVID-19. There were regional (n=44), city (n=31), district (n=13), inter-district (n=8) and federal (n=4) hospitals from 27 constituent entities of the Russian Federation. Capacity of 59 hospitals was less than 300 beds, 23 hospitals — over 500 beds, 18 hospitals — 300—500 beds. The number of ICU beds exceeded 10% of repurposed beds in 35 hospitals, 5—10% of ICU beds — in 51 hospitals, less than 5% — in 14 hospitals. There were 6—12 patients per one physician in 68 ICUs, less than 6 patients — in 12 ICUs, over 12 patients — in 20 ICUs. Also, there were 3-6 patients per a nurse in 69 ICUs, less than 3 patients — in 2 ICUs, over 6 patients — in 29 ICUs. Over 70% of the repurposed beds were provided with a networked oxygen supply in 61 hospitals, 50—70% — in 25 hospitals, less than 50% — in 14 hospitals. Oxygen flow rate over 10 l/min was provided in 70 hospitals, 5—10 l/min — in 28 hospitals, less than 5 l/min — in 2 hospitals. Over 80% of ICU beds are equipped with ventilators in 78 hospitals, 50—80% — in 15 hospitals, less than 50% — in 7 hospitals. Less than 5% of ventilators have been out of order throughout the pandemic in 62 ICUs, 5—10% — in 20 departments, over 10% — in 18 ICUs. High-flow oxygen therapy was not available in 48 ICUs, ultrasound — in 10 ICUs. ECMO was available only in 17 ICUs. If we consider the pandemic as a model of health system response to non-standard global challenges, these data are essential for critical analysis despite small sample size. © 2021, Media Sphera Publishing Group. All rights reserved.
ABSTRACT
The aim of the study was to evaluate the histopathological changes in the lungs of patients who died of a new coronavirus infection (COVID-19) in relation to the length of hospital stay. We evaluated lung autopsy material, autopsy reports, and death summaries of 39 patients who died of COVID-19. The length of hospital stay ranged from a few hours to 25 days. At all stages of the disease, lung alterations (desquamation of bronchial and alveolar epithelium), circulatory disorders (alveolar edema and hemorrhages, congestion in small blood vessels, thrombosis), compensatory response (fibrosis) were identified. The patients who died during the first week of hospitalization demonstrated predominant signs of circulatory disorders (alveolar edema, hyaline membranes, alveolar hemorrhages, congestion in small blood vessels). Fibrosis, usually not typical for the first week of acute respiratory distress syndrome, was detected in 46% of the deceased during the first week of hospitalization, which may be due to late hospitalization or patterns of fibrosis development in COVID-19. For those who died in the 2nd and 3rd weeks of hospitalization, the compensatory response and progression of fibrosis were noted. By the 3rd week, pulmonary fibrosis was detected in 91% of patients. Thrombotic complications (thrombosis, pulmonary artery thromboembolism) were observed in almost half of fatalities occurring during weeks 2-3. Hemorrhagic infarction was found in 43% (6 patients) who died during week 2 of hospitalization, three of them were diagnosed with pulmonary embolism, indicating progression of pulmonary vascular damage.
ABSTRACT
Currently, a certain amount of clinical data has been accumulated about the basics of lung ultrasound examination in the patients with pneumonia caused by COVID-19. The use of ultrasound can be informative for assessing the state at the pre-hospital stage and triage, identifying patients with minor forms of the disease and their consequent routing. This review of literature has focused on the principles of the diagnosis of pneumonia using ultrasound in the context of the COVID-19 pandemic. © 2020 Messenger of Anesthesiology and Resuscitation. All rights reserved.
ABSTRACT
Currently, there is a lot of clinical data on the basics of lung ultrasound (US) examina-tion in patients with COVID-19. This article is focused on the principles of pneumonia diagnosis. It is established that the use of ultrasound can be informative at the prehospital stage and triage of patients and also detection of mild forms of the course of the disease.
ABSTRACT
The novel coronavirus infection COVID-19 is associated with increased release of inflammatory cytokines (cytokine storm) and reactive oxygen species. These processes result a damage to the endothelium, pulmonary alveolar epithelium and their basal membranes (including the structures of blood-air barrier), increased vascular permeability and non-cardiogenic pulmonary edema. These mechanisms underlie the pathogenesis of acute respiratory distress syndrome in patients with coronavirus infection COVID-19. In this review, we have analyzed the data on the effect of lithium chloride on cytokine storm, increased vascular endothelial permeabili-ty, apoptosis of endotheliocyte and advanced activation of innate immune cells in patients with coronavirus infection COVID-19. © 2020, Media Sphera. All rights reserved.