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1.
Am J Case Rep ; 23: e937147, 2022 Oct 25.
Article in English | MEDLINE | ID: covidwho-2090898

ABSTRACT

BACKGROUND Inhaled nitric oxide (iNO) is used as a treatment for pulmonary arterial hypertension (PAH). Severe hypoxia with hypoxic vasoconstriction caused by severe acute respiratory distress syndrome (ARDS) can induce pulmonary hypertension with hemodynamic implications, mainly secondary to right ventricle (RV) systolic function impairment. We report the case of the use of iNO in a critically ill patient with bilateral SARS-CoV-2 pneumonia and severe ARDS and hypoxemia leading to acute severe PAH, causing a ventilation/perfusion mismatch, RV pressure overload, and RV systolic dysfunction. CASE REPORT A 36-year-old woman was admitted to the Intensive Care Unit with a severe ARDS associated with SARS-CoV-2 pneumonia requiring invasive mechanical ventilation. Severe hypoxia and hypoxic vasoconstriction developed, leading to an acute increase in pulmonary vascular resistance, severe to moderate tricuspid regurgitation, RV pressure overload, RV systolic function impairment, and RV dilatation. Following 24 h of treatment with iNO at 15 ppm, significant oxygenation and hemodynamic improvement were noted, allowing vasopressors to be stopped. After 24 h of iNO treatment, echocardiography showed very mild tricuspid regurgitation, a non-dilated RV, no impairment of transverse free wall contractility, and no paradoxical septal motion. iNO was maintained for 7 days. The dose of iNO was progressively decreased with no adverse effects and maintaining an improvement of oxygenation and hemodynamic status, allowing respiratory weaning. CONCLUSIONS Sustained acute hypoxia in ARDS secondary to SARS-CoV-2 pneumonia can lead to PAH, causing a ventilation/perfusion mismatch and RV systolic impairment. iNO can be considered in patients with significant PAH causing hypoxemia and RV dysfunction.


Subject(s)
COVID-19 , Hypertension, Pulmonary , Respiratory Distress Syndrome , Tricuspid Valve Insufficiency , Female , Humans , Adult , Nitric Oxide/therapeutic use , Hypertension, Pulmonary/drug therapy , Hypertension, Pulmonary/etiology , COVID-19/complications , Administration, Inhalation , SARS-CoV-2 , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/therapy , Hypoxia/etiology
3.
Medicine (Baltimore) ; 101(41): e31077, 2022 Oct 14.
Article in English | MEDLINE | ID: covidwho-2077960

ABSTRACT

Acute respiratory distress syndrome (ARDS) with (COVID-19 often result in mortality. Treatment outcomes among puerperant, when compared with non-pregnant women (NPW) with the same syndrome. Physiological changes underwent within the gestation period have a considerable impact on the immune system, respiratory system, cardiovascular function, and coagulation. Through this research, it was aimed to compare intensive care unit (ICU) follow-up and treatment results of postpartum-period patients with those of non-pregnant ones. During the first week of ICU, 23 puerperant COVID-19 patients with ARDS and 34 non-pregnant COVID-19 patients took part in the study. Age, height, and predictive body weight (PBW) at admission to the ICU were compared with the clinical parameters of disease severity, such as FiO2 (fraction of inspired oxygen), PaO2 (arterial oxygen partial pressure), Horowitz index (PaO2/FiO2), procalcitonin (PCT), and C-reactive protein (CRP). Respiration parameters were recorded a meta-vision back server. Demographic data, FiO2, PaO2, Horowitz index, PCT, CRP and respiration parameters values were similar in both groups. The duration of non-mechanical ventilation and number of patients were seen to be significantly greater among the puerperant group than control group (P; .04 and .002, respectively). The duration of mechanical ventilation was similar in both groups (P; .07), while the mortality rate was lower in the puerperant group (P; .004). The postpartum women with COVID-19 induced ARDS were observed to have better ICU follow-up results and lower mortality. However, it is considered that the present results need to be supported greater number of participants.


Subject(s)
COVID-19 , Respiratory Distress Syndrome , C-Reactive Protein , COVID-19/complications , COVID-19/therapy , Critical Care , Female , Humans , Intensive Care Units , Oxygen , Postpartum Period , Procalcitonin , Respiration, Artificial , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/therapy
4.
Crit Care Med ; 50(11): 1638-1643, 2022 Nov 01.
Article in English | MEDLINE | ID: covidwho-2077907

ABSTRACT

OBJECTIVES: Cerebrovascular injury associated with COVID-19 has been recognized, but the mechanisms remain uncertain. Acute respiratory distress syndrome (ARDS) is a severe pulmonary injury, which is associated with both ischemic and hemorrhagic stroke. It remains unclear if cerebrovascular injuries associated with severe COVID-19 are unique to COVID-19 or a consequence of severe respiratory disease or its treatment. The frequency and patterns of cerebrovascular injury on brain MRI were compared among patients with COVID-19 ARDS and non-COVID-19 ARDS. DESIGN: A case-control study. SETTING: A tertiary academic hospital system. PATIENTS: Adult patients (>18 yr) with COVID-19 ARDS (March 2020 to July 2021) and non-COVID-19 ARDS (January 2010-October 2018) who underwent brain MRI during their index hospitalization. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Cerebrovascular injury on MRI included cerebral ischemia (ischemic infarct or hypoxic ischemic brain injury) and intracranial hemorrhage (intraparenchymal, subarachnoid, or subdural, and cerebral microbleed [CMB]).Twenty-six patients with COVID-19 ARDS and sixty-six patients with non-COVID ARDS underwent brain MRI during the index hospitalization, resulting in 23 age- and sex-matched pairs. The frequency of overall cerebrovascular injury (57% vs 61%), cerebral ischemia (35% vs 43%), intracranial hemorrhage (43% vs 48%), and CMB (52% vs 41%) between COVID-19 ARDS and non-COVID-19 ARDS patients was similar (all p values >0.05). However, four of 26 patients (15%) with COVID-19 and no patients with non-COVID-19 ARDS had disseminated leukoencephalopathy with underlying CMBs, an imaging pattern that has previously been reported in patients with COVID-19. CONCLUSIONS: In a case-control study of selected ARDS patients with brain MRI, the frequencies of ischemic and hemorrhagic cerebrovascular injuries were similar between COVID-19 versus non-COVID-19 ARDS patients. However, the MRI pattern of disseminated hemorrhagic leukoencephalopathy was unique to the COVID-19 ARDS patients in this cohort.


Subject(s)
Brain Ischemia , COVID-19 , Leukoencephalopathies , Respiratory Distress Syndrome , Adult , Brain Ischemia/diagnostic imaging , Brain Ischemia/epidemiology , COVID-19/complications , Case-Control Studies , Humans , Intracranial Hemorrhages , Magnetic Resonance Imaging , Respiratory Distress Syndrome/diagnostic imaging , Respiratory Distress Syndrome/epidemiology , Respiratory Distress Syndrome/etiology
5.
BMC Anesthesiol ; 22(1): 307, 2022 10 01.
Article in English | MEDLINE | ID: covidwho-2053860

ABSTRACT

BACKGROUND: Data on the efficacy of non-invasive ventilation (NIV) after progression of respiratory failure in patients who have already received oxygen therapy, or CPAP outside ICU is limited. The study aimed to find predictors of NIV failure based on breathing pattern, gas exchange, and accessory respiratory muscles evaluation in patients who progressed to moderate-to-severe COVID-19 ARDS. METHODS: This was a prospective observational study in patients with moderate-to-severe COVID-19-ARDS on NIV (n = 80) admitted to COVID-ICU of Sechenov University. The combined success rate for conventional oxygen and CPAP outside ICU was 78.6% (440 of 560 patients). The primary endpoints were intubation rate and mortality. We measured respiratory rate, exhaled tidal volume (Vte), mean peak inspiratory flow (PIF), inspiratory time (Ti), PaO2, SpO2, end-tidal carbon dioxide (PETCO2), and Patrick score, and calculated ROX index, PaO2/FiO2, ventilatory ratio, and alveolar dead space (Vdalv/Vt) on Days 1, 3, 5, 7, 10, and 14. For all significant differences between NIV success and failure groups in measured data, we performed ROC analysis. RESULTS: NIV failure rate in ICU after deterioration of respiratory failure outside ICU was 71.3% (n = 57). Patients with the subsequent NIV failure were older at inclusion, more frail, had longer duration of disease before ICU admission, and higher rate of CPAP use outside ICU. ROC-analysis revealed that the following respiratory parameters after 48 h of NIV can serve as a predictors for NIV failure in moderate-to-severe COVID-19-associated ARDS: PaO2/FiO2 < 112 mmHg (AUROC 0.90 (0.93-0.97), p < 0.0001); PETCO2 < 19.5 mmHg (AUROC 0.84 (0.73-0.94), p < 0.0001); VDalv/VT > 0.43 (AUROC 0.78 (0.68-0.90), p < 0.0001); ROX-index < 5.02 (AUROC 0.89 (0.81-0.97), p < 0.0001); Patrick score > 2 points (AUROC 0.87 (0.78-0.96), p = 0.006). CONCLUSION: In patients who progressed to moderate-to-severe COVID-19-ARDS probability of NIV success rate was about 1/3. Prediction of the NIV failure can be made after 48 h based on ROX index < 5.02, PaO2/FiO2 < 112 mmHg, PETCO2 < 19.5 mmHg, and Patrick score > = 2. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT04667923 , registered on 16/12/2020.


Subject(s)
COVID-19 , Noninvasive Ventilation , Respiratory Distress Syndrome , Respiratory Insufficiency , COVID-19/complications , COVID-19/therapy , Carbon Dioxide , Humans , Intensive Care Units , Oxygen , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/therapy , Respiratory Insufficiency/etiology , Respiratory Insufficiency/therapy , Respiratory Muscles , Respiratory Rate
7.
Am J Respir Crit Care Med ; 206(7): 857-873, 2022 10 01.
Article in English | MEDLINE | ID: covidwho-2053494

ABSTRACT

Rationale: The leading cause of death in coronavirus disease 2019 (COVID-19) is severe pneumonia, with many patients developing acute respiratory distress syndrome (ARDS) and diffuse alveolar damage (DAD). Whether DAD in fatal COVID-19 is distinct from other causes of DAD remains unknown. Objective: To compare lung parenchymal and vascular alterations between patients with fatal COVID-19 pneumonia and other DAD-causing etiologies using a multidimensional approach. Methods: This autopsy cohort consisted of consecutive patients with COVID-19 pneumonia (n = 20) and with respiratory failure and histologic DAD (n = 21; non-COVID-19 viral and nonviral etiologies). Premortem chest computed tomography (CT) scans were evaluated for vascular changes. Postmortem lung tissues were compared using histopathological and computational analyses. Machine-learning-derived morphometric analysis of the microvasculature was performed, with a random forest classifier quantifying vascular congestion (CVasc) in different microscopic compartments. Respiratory mechanics and gas-exchange parameters were evaluated longitudinally in patients with ARDS. Measurements and Main Results: In premortem CT, patients with COVID-19 showed more dilated vasculature when all lung segments were evaluated (P = 0.001) compared with controls with DAD. Histopathology revealed vasculopathic changes, including hemangiomatosis-like changes (P = 0.043), thromboemboli (P = 0.0038), pulmonary infarcts (P = 0.047), and perivascular inflammation (P < 0.001). Generalized estimating equations revealed significant regional differences in the lung microarchitecture among all DAD-causing entities. COVID-19 showed a larger overall CVasc range (P = 0.002). Alveolar-septal congestion was associated with a significantly shorter time to death from symptom onset (P = 0.03), length of hospital stay (P = 0.02), and increased ventilatory ratio [an estimate for pulmonary dead space fraction (Vd); p = 0.043] in all cases of ARDS. Conclusions: Severe COVID-19 pneumonia is characterized by significant vasculopathy and aberrant alveolar-septal congestion. Our findings also highlight the role that vascular alterations may play in Vd and clinical outcomes in ARDS in general.


Subject(s)
COVID-19 , Pneumonia , Respiratory Distress Syndrome , Vascular Diseases , COVID-19/complications , Humans , Lung/diagnostic imaging , Lung/pathology , Pulmonary Alveoli/pathology , Respiratory Distress Syndrome/etiology
9.
Lancet ; 400(10358): 1145-1156, 2022 10 01.
Article in English | MEDLINE | ID: covidwho-2050101

ABSTRACT

Acute respiratory distress syndrome (ARDS) is a common clinical syndrome of acute respiratory failure as a result of diffuse lung inflammation and oedema. ARDS can be precipitated by a variety of causes. The pathophysiology of ARDS is complex and involves the activation and dysregulation of multiple overlapping and interacting pathways of injury, inflammation, and coagulation, both in the lung and systemically. Mechanical ventilation can contribute to a cycle of lung injury and inflammation. Resolution of inflammation is a coordinated process that requires downregulation of proinflammatory pathways and upregulation of anti-inflammatory pathways. The heterogeneity of the clinical syndrome, along with its biology, physiology, and radiology, has increasingly been recognised and incorporated into identification of phenotypes. A precision-medicine approach that improves the identification of more homogeneous ARDS phenotypes should lead to an improved understanding of its pathophysiological mechanisms and how they differ from patient to patient.


Subject(s)
Respiratory Distress Syndrome , Anti-Inflammatory Agents , Humans , Inflammation , Phenotype , Respiration, Artificial , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/therapy
10.
Lancet ; 400(10358): 1157-1170, 2022 10 01.
Article in English | MEDLINE | ID: covidwho-2050100

ABSTRACT

Acute respiratory distress syndrome (ARDS) is characterised by acute hypoxaemic respiratory failure with bilateral infiltrates on chest imaging, which is not fully explained by cardiac failure or fluid overload. ARDS is defined by the Berlin criteria. In this Series paper the diagnosis, management, outcomes, and long-term sequelae of ARDS are reviewed. Potential limitations of the ARDS definition and evidence that could inform future revisions are considered. Guideline recommendations, evidence, and uncertainties in relation to ARDS management are discussed. The future of ARDS strives towards a precision medicine approach, and the framework of treatable traits in ARDS diagnosis and management is explored.


Subject(s)
Respiratory Distress Syndrome , Respiratory Insufficiency , Adult , Diagnostic Imaging , Humans , Phenotype , Respiratory Distress Syndrome/diagnosis , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/therapy
11.
Sci Rep ; 12(1): 16528, 2022 Oct 03.
Article in English | MEDLINE | ID: covidwho-2050546

ABSTRACT

Real-time effects of changing body position and positive end-expiratory pressure (PEEP) on regional lung overdistension and collapse in individual patients remain largely unknown and not timely monitored. The aim of this study was to individualize PEEP in supine and prone body positions seeking to reduce lung collapse and overdistension in mechanically ventilated patients with coronavirus disease (COVID-19)-induced acute respiratory distress syndrome (ARDS). We hypothesized that prone positioning with bedside titrated PEEP would provide attenuation of both overdistension and collapse. In this prospective observational study, patients with COVID-19-induced ARDS under mechanical ventilation were included. We used electrical impedance tomography (EIT) with decremental PEEP titration algorithm (PEEPEIT-titration), which provides information on regional lung overdistension and collapse, along with global respiratory system compliance, to individualize PEEP and body position. PEEPEIT-titration in supine position followed by PEEPEIT-titration in prone position were performed. Immediately before each PEEPEIT-titration, the same lung recruitment maneuver was performed: 2 min of PEEP 24 cmH2O and driving pressure of 15 cmH2O. Forty-two PEEPEIT-titration were performed in ten patients (21 pairs supine and prone positions). We have found larger % of overdistension along the PEEP titration in prone than supine position (P = 0.042). A larger % of collapse along the PEEP titration was found in supine than prone position (P = 0.037). A smaller respiratory system compliance was found in prone than supine position (P < 0.0005). In patients with COVID-19-induced ARDS, prone body position, when compared with supine body position, decreased lung collapse at low PEEP levels, but increased lung overdistension at PEEP levels greater than 10 cm H2O.Trial registration number: NCT04460859.


Subject(s)
COVID-19 , Positive-Pressure Respiration , Pulmonary Atelectasis , Respiratory Distress Syndrome , COVID-19/complications , COVID-19/therapy , Humans , Lung/pathology , Prone Position , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/therapy
12.
Acta Med Indones ; 54(3): 444-450, 2022 Jul.
Article in English | MEDLINE | ID: covidwho-2047003

ABSTRACT

Mortality rate among maintenance hemodialysis (HD) patients with COVID-19 is alarmingly high. In Fatmawati General Hospital, most of HD patients with COVID-19 presented with acute respiratory distress syndrome (ARDS). Hemoperfusion (HP) is a blood purification therapy used to remove cytokines and inflammatory mediators to prevent ARDS worsening and organ failure. We report 6 cases of COVID-19 in maintenance HD patients. HP and HD were performed in two consecutive days when patient developed early ARDS as indicated by inflammatory markers elevation. HP and HD were conducted by using resin-containing cartridge and high-flux dialyzer, respectively, for 4 hours. Improvements in CRP levels, PaO2/FiO2 ratios, and chest X-rays were observed after 2 sessions of HP in most of our patients. Based on our clinical experience, the timing of HP delivery is critical and should be undertaken in the early phase of ARDS, but larger studies are still needed.


Subject(s)
COVID-19 , Hemoperfusion , Respiratory Distress Syndrome , COVID-19/complications , COVID-19/therapy , Cytokines , Humans , Inflammation Mediators , Renal Dialysis , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/therapy
13.
Medicine (Baltimore) ; 101(38): e30759, 2022 Sep 23.
Article in English | MEDLINE | ID: covidwho-2042660

ABSTRACT

BACKGROUND: Patients with severe acute respiratory distress syndrome (ARDS) have high mortality rates; therefore, new biomarkers are necessary to predict the prognosis in the early stages. Serum lactate dehydrogenase (LDH) level is a specific marker of lung damage, but it is not sensitive because it is affected by several factors. This study aimed to determine whether the LDH/albumin ratio could be used as a prognostic biomarker in patients with severe ARDS due to COVID 19. METHODS: Tertiary intensive care unit (ICU) patients with severe ARDS and confirmed COVID-19 diagnosis between August 1, 2020, and October 31, 2021, were included. The demographic and clinical characteristics of the patients were recorded from the hospital databases, together with laboratory results on the day of admission to the ICU and the length of stay in the ICU and hospital. LDH/albumin, lactate/albumin, C-reactive protein (CRP)/albumin, and BUN/albumin ratios were calculated. Logistic regression analysis was performed to determine independent risk factors affecting mortality. RESULTS: Nine hundred and five patients hospitalized in a tertiary ICU were evaluated. Three hundred fifty-one patients with severe ARDS were included in this study. The mortality rate of the included patients was 61.8% (of 217/351). LDH/albumin, lactate/albumin, and BUN/albumin ratios were higher in the nonsurvivor group (P < .001). The area under the curve (AUC) from the receiver operating characteristic analysis that predicted in-hospital mortality was 0.627 (95% confidence intervals (CI): 0.574-0.678, P < .001) for the LDH/albumin ratio, 0.605 (95% CI: 0.551-0.656, P < .001) for lactate/albumin, and 0.638 (95% CI: 0.585-0.688, P < .001) for BUN/albumin. However, LDH/albumin ratio was independently associated with mortality in multivariate logistic regression analysis. CONCLUSION: LDH/albumin ratio can be used as an independent prognostic factor for mortality in patients with severe ARDS caused by COVID-19.


Subject(s)
COVID-19 , Respiratory Distress Syndrome , Biomarkers , C-Reactive Protein , COVID-19/complications , COVID-19/diagnosis , COVID-19 Testing , Humans , Intensive Care Units , L-Lactate Dehydrogenase , Lactates , Prognosis , ROC Curve , Respiratory Distress Syndrome/diagnosis , Respiratory Distress Syndrome/etiology , Retrospective Studies
14.
PLoS Pathog ; 18(9): e1010819, 2022 09.
Article in English | MEDLINE | ID: covidwho-2039445

ABSTRACT

BACKGROUND: Acute respiratory distress syndrome (ARDS), a life-threatening condition characterized by hypoxemia and poor lung compliance, is associated with high mortality. ARDS induced by COVID-19 has similar clinical presentations and pathological manifestations as non-COVID-19 ARDS. However, COVID-19 ARDS is associated with a more protracted inflammatory respiratory failure compared to traditional ARDS. Therefore, a comprehensive molecular comparison of ARDS of different etiologies groups may pave the way for more specific clinical interventions. METHODS AND FINDINGS: In this study, we compared COVID-19 ARDS (n = 43) and bacterial sepsis-induced (non-COVID-19) ARDS (n = 24) using multi-omic plasma profiles covering 663 metabolites, 1,051 lipids, and 266 proteins. To address both between- and within- ARDS group variabilities we followed two approaches. First, we identified 706 molecules differently abundant between the two ARDS etiologies, revealing more than 40 biological processes differently regulated between the two groups. From these processes, we assembled a cascade of therapeutically relevant pathways downstream of sphingosine metabolism. The analysis suggests a possible overactivation of arginine metabolism involved in long-term sequelae of ARDS and highlights the potential of JAK inhibitors to improve outcomes in bacterial sepsis-induced ARDS. The second part of our study involved the comparison of the two ARDS groups with respect to clinical manifestations. Using a data-driven multi-omic network, we identified signatures of acute kidney injury (AKI) and thrombocytosis within each ARDS group. The AKI-associated network implicated mitochondrial dysregulation which might lead to post-ARDS renal-sequalae. The thrombocytosis-associated network hinted at a synergy between prothrombotic processes, namely IL-17, MAPK, TNF signaling pathways, and cell adhesion molecules. Thus, we speculate that combination therapy targeting two or more of these processes may ameliorate thrombocytosis-mediated hypercoagulation. CONCLUSION: We present a first comprehensive molecular characterization of differences between two ARDS etiologies-COVID-19 and bacterial sepsis. Further investigation into the identified pathways will lead to a better understanding of the pathophysiological processes, potentially enabling novel therapeutic interventions.


Subject(s)
Acute Kidney Injury , COVID-19 , Janus Kinase Inhibitors , Respiratory Distress Syndrome , Sepsis , Thrombocytosis , Arginine , COVID-19/complications , Humans , Interleukin-17 , Lipids , Respiratory Distress Syndrome/etiology , Sepsis/complications , Sphingosine
16.
Neurology ; 99(20): e2326-e2335, 2022 Nov 15.
Article in English | MEDLINE | ID: covidwho-2021404

ABSTRACT

BACKGROUND AND OBJECTIVES: Neurologic complications have been associated with COVID-19, including delirium. Such complications have been reported to be frequent among intensive care unit (ICU)-admitted patients. We hypothesized that the rate of neurologic complications would be higher in COVID-19 associated acute respiratory distress syndrome (ARDS) than those who develop ARDS from a different cause. METHODS: We conducted a retrospective cohort study in the adult ICU of Lausanne University Hospital, including all consecutive patients fulfilling the Berlin criteria for ARDS hospitalized between December 2017 and June 2021, stratifying exposure between COVID-19 or not. The primary outcome was delirium onset during ICU stay, defined by the confusion assessment method (CAM-ICU). Exploratory outcomes included development of neurologic complications of the central nervous system (stroke, hemorrhage, and vasculitis), critical illness weakness, and 30- and 180-day all-cause mortality. RESULTS: Three hundred eleven patients were included in the study (253 with COVID-19 and 58 with other causes) and CAM-ICU could be assessed in 231 (74.3% in COVID-19 vs 74.1% in non-COVID-19). The proportion of patients developing delirium was similar in patients with COVID-19 and controls in univariate comparison (69.1% vs 60.5%, p = 0.246). Yet, patients with COVID-19 had a higher body mass index, lower ICU severity, longer mechanical ventilation, and higher sedation doses (propofol and dexmedetomidine). After adjusting for these factors in a multivariable analysis, the risk of delirium remained comparable across groups (adjusted OR [95% CI]: 0.86 [0.35-2.1]). Similarly, COVID-19-related ARDS had no effect on all-cause mortality at 30 days (adjusted OR: 0.87 [0.39-1.92]) and 180 days (adjusted OR: 0.67 [0.33-1.35]). Finally, neurologic complications affecting the CNS (adjusted OR: 1.15 [0.25-5.29]) and critical illness weakness (adjusted OR: 2.99 [0.97-9.1]) were not higher in the COVID-19 group. DISCUSSION: Compared with other etiologies, patients with COVID-19 did not have higher incidence of delirium and other neurologic complications, after accounting for underlying disease severity in patients with ARDS. Management of COVID-19-associated ARDS needed longer invasive ventilation and higher sedation, which could explain higher rates of delirium in uncontrolled studies.


Subject(s)
COVID-19 , Delirium , Respiratory Distress Syndrome , Humans , Adult , Critical Illness , Retrospective Studies , COVID-19/complications , Respiratory Distress Syndrome/epidemiology , Respiratory Distress Syndrome/etiology , Intensive Care Units , Respiration, Artificial , Delirium/epidemiology , Delirium/etiology
17.
J Card Surg ; 37(11): 3609-3618, 2022 Nov.
Article in English | MEDLINE | ID: covidwho-2019481

ABSTRACT

BACKGROUND: Although several studies have characterized the risk of coinfection in COVID pneumonia, the risk of the bloodstream and respiratory coinfection in patients with COVID-19 pneumonia on extracorporeal membrane oxygenation (ECMO) supports severe acute respiratory distress syndrome (ARDS) is poorly understood. METHODS: This is a retrospective analysis of patients with COVID-19 ARDS on ECMO at a single center between January 2020 and December 2021. Patient characteristics and clinical outcomes were compared. RESULTS: Of 44 patients placed on ECMO support for COVID-19 ARDS, 30 (68.2%) patients developed a coinfection, and 14 (31.8%) patients did not. Most patients underwent venovenous ECMO (98%; 43/44) cannulation in the right internal jugular vein (98%; 43/44). Patients with coinfection had a longer duration of ECMO (34 [interquartile range, IQR: 19.5, 65] vs. 15.5 [IQR 11, 27.3] days; p = .02), intensive care unit (ICU; 44 [IQR: 27,75.5] vs 31 [IQR 20-39.5] days; p = .03), and hospital (56.5 [IQR 27,75.5] vs 37.5 [IQR: 20.5-43.3]; p = .02) length of stay. When stratified by the presence of a coinfection, there was no difference in hospital mortality (37% vs. 29%; p = .46) or Kaplan-Meier survival (logrank p = .82). Time from ECMO to first positive blood and respiratory culture were 12 [IQR: 3, 28] and 10 [IQR: 1, 15] days, respectively. Freedom from any coinfection was 50 (95% confidence interval: 37.2-67.2)% at 15 days from ECMO initiation. CONCLUSIONS: There is a high rate of co-infections in patients placed on ECMO for COVID-19 ARDS. Although patients with coinfections had a longer duration of extracorporeal life support, and longer length of stays in the ICU and hospital, survival was not inferior.


Subject(s)
COVID-19 , Coinfection , Extracorporeal Membrane Oxygenation , Respiratory Distress Syndrome , COVID-19/complications , COVID-19/epidemiology , COVID-19/therapy , Coinfection/epidemiology , Humans , Respiratory Distress Syndrome/epidemiology , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/therapy , Retrospective Studies
19.
Eur J Med Res ; 27(1): 150, 2022 Aug 13.
Article in English | MEDLINE | ID: covidwho-2002233

ABSTRACT

A complex interrelation between lung and brain in patients with acute lung injury (ALI) has been established by experimental and clinical studies during the last decades. Although, acute brain injury represents one of the most common insufficiencies in patients with ALI and acute respiratory distress syndrome (ARDS), the underlying pathophysiology of the observed crosstalk remains poorly understood due to its complexity. Specifically, it involves numerous pathophysiological parameters such as hypoxemia, neurological adverse events of lung protective ventilation, hypotension, disruption of the BBB, and neuroinflammation in such a manner that the brain of ARDS patients-especially hippocampus-becomes very vulnerable to develop secondary lung-mediated acute brain injury. A protective ventilator strategy could reduce or even minimize further systemic release of inflammatory mediators and thus maintain brain homeostasis. On the other hand, mechanical ventilation with low tidal volumes may lead to self-inflicted lung injury, hypercapnia and subsequent cerebral vasodilatation, increased cerebral blood flow, and intracranial hypertension. Therefore, by describing the pathophysiology of ARDS-associated acute brain injury we aim to highlight and discuss the possible influence of mechanical ventilation on ALI-associated acute brain injury.


Subject(s)
Acute Lung Injury , Brain Injuries , Respiratory Distress Syndrome , Acute Lung Injury/etiology , Brain , Brain Injuries/complications , Humans , Lung , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/therapy , Tidal Volume
20.
Front Immunol ; 13: 942443, 2022.
Article in English | MEDLINE | ID: covidwho-1993790

ABSTRACT

Introduction: Bronchial aspirates (BAS) obtained during invasive mechanical ventilation (IMV) constitutes a useful tool for molecular phenotyping and decision making. Aim: To identify the proteomic determinants associated with disease pathogenesis, all-cause mortality and respiratory sequelae in BAS samples from critically ill patients with SARS-CoV-2-induced ARDS. Methods: Multicenter study including 74 critically ill patients with COVID-19 and non-COVID-19 ARDS. BAS were obtained by bronchoaspiration after IMV initiation. Three hundred sixty-four proteins were quantified using proximity extension assay (PEA) technology. Random forest models were used to assess predictor importance. Results: After adjusting for confounding factors, CST5, NADK, SRPK2 and TGF-α were differentially detected in COVID-19 and non-COVID-19 patients. In random forest models for COVID-19, CST5, DPP7, NADK, KYAT1 and TYMP showed the highest variable importance. In COVID-19 patients, reduced levels of ENTPD2 and PTN were observed in nonsurvivors of ICU stay, even after adjustment. AGR2, NQO2, IL-1α, OSM and TRAIL showed the strongest associations with in-ICU mortality and were used to construct a protein-based prediction model. Kaplan-Meier curves revealed a clear separation in mortality risk between subgroups of PTN, ENTPD2 and the prediction model. Cox regression models supported these findings. In survivors, the levels of FCRL1, NTF4 and THOP1 in BAS samples obtained during the ICU stay correlated with lung function (i.e., DLCO levels) 3 months after hospital discharge. Similarly, Flt3L and THOP1 levels were correlated with radiological features (i.e., TSS). These proteins are expressed in immune and nonimmune lung cells. Poor host response to viral infectivity and an inappropriate reparative mechanism seem to be linked with the pathogenesis of the disease and fatal outcomes, respectively. Conclusion: BAS proteomics identified novel factors associated with the pathology of SARS-CoV-2-induced ARDS and its adverse outcomes. BAS-based protein testing emerges as a novel tool for risk assessment in the ICU.


Subject(s)
COVID-19 , Respiratory Distress Syndrome , COVID-19/complications , Critical Illness , Humans , Mucoproteins , Oncogene Proteins , Protein Serine-Threonine Kinases , Proteomics , Respiratory Distress Syndrome/etiology , SARS-CoV-2
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