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Shah D, Dave B, Chorawala MR, Prajapati BG, Singh S, M. Elossaily G, Ansari MN, Ali N. An Insight on Microfluidic Organ-on-a-Chip Models for PM 2.5-Induced Pulmonary Complications. ACS OMEGA 2024; 9:13534-13555. [PMID: 38559954 PMCID: PMC10976395 DOI: 10.1021/acsomega.3c10271] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Figures] [Subscribe] [Scholar Register] [Received: 12/22/2023] [Revised: 02/21/2024] [Accepted: 02/26/2024] [Indexed: 04/04/2024]
Abstract
Pulmonary diseases like asthma, chronic obstructive pulmonary disorder, lung fibrosis, and lung cancer pose a significant burden to global human health. Many of these complications arise as a result of exposure to particulate matter (PM), which has been examined in several preclinical and clinical trials for its effect on several respiratory diseases. Particulate matter of size less than 2.5 μm (PM2.5) has been known to inflict unforeseen repercussions, although data from epidemiological studies to back this are pending. Conventionally utilized two-dimensional (2D) cell culture and preclinical animal models have provided insufficient benefits in emulating the in vivo physiological and pathological pulmonary conditions. Three-dimensional (3D) structural models, including organ-on-a-chip models, have experienced a developmental upsurge in recent times. Lung-on-a-chip models have the potential to simulate the specific features of the lungs. With the advancement of technology, an emerging and advanced technique termed microfluidic organ-on-a-chip has been developed with the aim of identifying the complexity of the respiratory cellular microenvironment of the body. In the present Review, the role of lung-on-a-chip modeling in reproducing pulmonary complications has been explored, with a specific emphasis on PM2.5-induced pulmonary complications.
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Affiliation(s)
- Disha Shah
- Department
of Pharmacology and Pharmacy Practice, L.
M. College of Pharmacy Navrangpura, Ahmedabad, Gujarat 380009, India
| | - Bhavarth Dave
- Department
of Pharmacology and Pharmacy Practice, L.
M. College of Pharmacy Navrangpura, Ahmedabad, Gujarat 380009, India
| | - Mehul R. Chorawala
- Department
of Pharmacology and Pharmacy Practice, L.
M. College of Pharmacy Navrangpura, Ahmedabad, Gujarat 380009, India
| | - Bhupendra G. Prajapati
- Department
of Pharmaceutics and Pharmaceutical Technology, Shree S. K. Patel College of Pharmaceutical Education and Research,
Ganpat University, Mehsana, Gujarat 384012, India
| | - Sudarshan Singh
- Office
of Research Administration, Chiang Mai University, Chiang Mai 50200, Thailand
- Department
of Pharmaceutical Sciences, Faculty of Pharmacy, Chiang Mai University, Chiang
Mai 50200, Thailand
| | - Gehan M. Elossaily
- Department
of Basic Medical Sciences, College of Medicine, AlMaarefa University, P.O. Box 71666, Riyadh 11597, Saudi Arabia
| | - Mohd Nazam Ansari
- Department
of Pharmacology and Toxicology, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Alkharj 11942, Saudi Arabia
| | - Nemat Ali
- Department
of Pharmacology and Toxicology, College of Pharmacy, King Saud University, P.O. Box 2457, Riyadh 11451, Saudi Arabia
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Piriyapatsom A, Trisukhonth A, Chintabanyat O, Chaiwat O, Kongsayreepong S, Thanakiattiwibun C. Adherence to lung protective mechanical ventilation in patients admitted to a surgical intensive care unit and the associated increased mortality. Heliyon 2024; 10:e26220. [PMID: 38404779 PMCID: PMC10884462 DOI: 10.1016/j.heliyon.2024.e26220] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/08/2023] [Revised: 02/05/2024] [Accepted: 02/08/2024] [Indexed: 02/27/2024] Open
Abstract
Background The adherence rate to the lung protective ventilation (LPV) strategy, which is generally accepted as a standard practice in mechanically ventilated patients, reported in the literature is approximately 40%. This study aimed to determine the adherence rate to the LPV strategy, factors associated with this adherence, and related clinical outcomes in mechanically ventilated patients admitted to the surgical intensive care unit (SICU). Methods This prospective observational study was conducted in the SICU of a tertiary university-based hospital between April 2018 and February 2019. Three hundred and six adult patients admitted to the SICU who required mechanical ventilation support for more than 12 h were included. Ventilator parameters at the initiation of mechanical ventilation support in the SICU were recorded. The LPV strategy was defined as ventilation with a tidal volume of equal or less than 8 ml/kg of predicted body weight plus positive end-expiratory pressure of at least 5 cm H2O. Demographic and clinical data were recorded and analyzed. Results There were 306 patients included in this study. The adherence rate to the LPV strategy was 36.9%. Height was the only factor associated with adherence to the LPV strategy (odds ratio for each cm, 1.10; 95% confidence interval (CI), 1.06-1.15). Cox regression analysis showed that the LPV strategy was associated with increased 90-day mortality (hazard ratio, 1.73; 95% CI, 1.02-2.94). Conclusion The adherence rate to the LPV strategy among patients admitted to the SICU was modest. Further studies are warranted to explore whether the application of the LPV strategy is simply a marker of disease severity or a causative factor for increased mortality.
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Affiliation(s)
- Annop Piriyapatsom
- Department of Anesthesiology, Faculty of Medicine Siriraj Hospital, Mahidol University, 10700, Thailand
| | - Ajana Trisukhonth
- Department of Anesthesiology, Faculty of Medicine Siriraj Hospital, Mahidol University, 10700, Thailand
| | - Ornin Chintabanyat
- Department of Anesthesiology, Faculty of Medicine Siriraj Hospital, Mahidol University, 10700, Thailand
| | - Onuma Chaiwat
- Department of Anesthesiology, Faculty of Medicine Siriraj Hospital, Mahidol University, 10700, Thailand
| | - Suneerat Kongsayreepong
- Department of Anesthesiology, Faculty of Medicine Siriraj Hospital, Mahidol University, 10700, Thailand
| | - Chayanan Thanakiattiwibun
- Department of Anesthesiology, Faculty of Medicine Siriraj Hospital, Mahidol University, 10700, Thailand
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Sochet AA, Jaffray J, Branchford BR, Havlicek EE, Mosha M, Amankwah EK, Ignjatovic V, Faustino EVS, Goldenberg NA. Hospital-Acquired Venous Thromboembolism and Invasive Mechanical Ventilation: A Report From the Children's Hospital Acquired Thrombosis Consortium. Pediatr Crit Care Med 2024; 25:e82-e90. [PMID: 37882641 PMCID: PMC10843146 DOI: 10.1097/pcc.0000000000003383] [Citation(s) in RCA: 3] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 10/27/2023]
Abstract
OBJECTIVES To determine if the duration of invasive mechanical ventilation (IMV) was associated with hospital-acquired venous thromboembolism (HA-VTE) among critically ill children. DESIGN A multicenter, matched case-control study as a secondary analysis of Children's Hospital Acquired Thrombosis (CHAT) Consortium registry. SETTING PICUs within U.S. CHAT Consortium participating centers. PATIENTS Children younger than 21 years old admitted to a PICU receiving IMV for greater than or equal to 1 day duration from January 2012 to March 2022 were included for study. Cases with HA-VTE were matched 1:2 to controls without HA-VTE by patient age groups: younger than 1, 1-12, and older than 12 years. INTERVENTIONS None. MEASUREMENTS AND MAIN RESULTS The primary outcome was IMV duration in days. Descriptive data included demographics, anthropometrics, HA-VTE characteristics (i.e., type, location, and timing), central venous catheterization data, thromboprophylaxis practices, and Braden Q mobility scores. Descriptive, comparative, and associative (multivariate conditional logistic regression for HA-VTE) statistics were employed. A total of 152 cases were matched to 304 controls. Cases with HA-VTE were diagnosed at a median of 7 days (interquartile range [IQR], 3-16 d) after IMV. The HA-VTE were limb deep venous thromboses in 130 of 152 (85.5%) and frequently central venous catheterization-related (111/152, 73%). Cases with HA-VTE experienced a longer length of stay (median, 34 d [IQR, 18-62 d] vs. 11.5 d [IQR, 6-21 d]; p < 0.001) and IMV duration (median, 7 d [IQR, 4-15 d] vs. 4 d [IQR, 1-7 d]; p < 0.001) as compared with controls. In a multivariate logistic model, greater IMV duration (adjusted odds ratio, 1.09; 95% CI, 1.01-1.17; p = 0.023) was independently associated with HA-VTE. CONCLUSIONS Among critically ill children undergoing IMV, HA-VTE was associated with greater IMV duration. If prospectively validated, IMV duration should be included as part of prothrombotic risk stratification and future pediatric thromboprophylaxis trials.
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Affiliation(s)
- Anthony A. Sochet
- Department of Medicine, Divisions of Critical Care Medicine , Johns Hopkins All Children’s Hospital, St. Petersburg, FL
- Institute for Clinical and Translational Research, Johns Hopkins All Children’s Hospital, St. Petersburg, FL
- Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD
| | - Julie Jaffray
- Department of Pediatrics, Division of Hematology/Oncology, Rady Children’s Hospital, San Diego, CA
| | - Brian R. Branchford
- Division of Hematology, Oncology, and Bone Marrow Transplant, Medical College of Wisconsin, Milwaukee, WI and Versiti Medical Sciences Institute, Milwaukee, WI
| | - Elizabeth E. Havlicek
- Department of Pediatrics, University of South Florida Morsani College of Medicine, Tampa, FL
| | - Maua Mosha
- Institute for Clinical and Translational Research, Johns Hopkins All Children’s Hospital, St. Petersburg, FL
| | - Ernest K. Amankwah
- Institute for Clinical and Translational Research, Johns Hopkins All Children’s Hospital, St. Petersburg, FL
- Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD
- Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD
| | - Vera Ignjatovic
- Institute for Clinical and Translational Research, Johns Hopkins All Children’s Hospital, St. Petersburg, FL
- Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD
| | | | - Neil A. Goldenberg
- Cancer and Blood Disorders Institute, Division of Hematology, Johns Hopkins All Children’s Hospital, St. Petersburg, FL
- Institute for Clinical and Translational Research, Johns Hopkins All Children’s Hospital, St. Petersburg, FL
- Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD
- Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD
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Liu Y, Cai X, Fang R, Peng S, Luo W, Du X. Future directions in ventilator-induced lung injury associated cognitive impairment: a new sight. Front Physiol 2023; 14:1308252. [PMID: 38164198 PMCID: PMC10757930 DOI: 10.3389/fphys.2023.1308252] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/06/2023] [Accepted: 12/08/2023] [Indexed: 01/03/2024] Open
Abstract
Mechanical ventilation is a widely used short-term life support technique, but an accompanying adverse consequence can be pulmonary damage which is called ventilator-induced lung injury (VILI). Mechanical ventilation can potentially affect the central nervous system and lead to long-term cognitive impairment. In recent years, many studies revealed that VILI, as a common lung injury, may be involved in the central pathogenesis of cognitive impairment by inducing hypoxia, inflammation, and changes in neural pathways. In addition, VILI has received attention in affecting the treatment of cognitive impairment and provides new insights into individualized therapy. The combination of lung protective ventilation and drug therapy can overcome the inevitable problems of poor prognosis from a new perspective. In this review, we summarized VILI and non-VILI factors as risk factors for cognitive impairment and concluded the latest mechanisms. Moreover, we retrospectively explored the role of improving VILI in cognitive impairment treatment. This work contributes to a better understanding of the pathogenesis of VILI-induced cognitive impairment and may provide future direction for the treatment and prognosis of cognitive impairment.
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Affiliation(s)
- Yinuo Liu
- Department of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, China
- The Clinical Medical College of Nanchang University, Nanchang, China
| | - Xintong Cai
- Department of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, China
- The Clinical Medical College of Nanchang University, Nanchang, China
| | - Ruiying Fang
- The Clinical Medical College of Nanchang University, Nanchang, China
| | - Shengliang Peng
- Department of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, China
| | - Wei Luo
- Department of Sports Medicine, Huashan Hospital, Fudan University, Shanghai, China
| | - Xiaohong Du
- Department of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, China
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Jiang W, Liu J, Cui J, Su J, Xu W, Zhang F, Ding Y. Ferroptosis plays a crucial role in lung cell damage caused by ventilation stretch. Free Radic Biol Med 2023; 209:84-95. [PMID: 37827457 DOI: 10.1016/j.freeradbiomed.2023.10.381] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/04/2023] [Revised: 10/07/2023] [Accepted: 10/09/2023] [Indexed: 10/14/2023]
Abstract
Mechanical ventilation is an essential respiratory support in acute respiratory distress syndrome and intensive care cases. However, it is possible to cause ventilator-induced lung damage (VILI). In this work, we used a microfluidic device to provide a mechanical ventilation with cyclic stretch (30% total area change rate and 15 cycles per min) and oxygen (air) flux applied by a controlled pressured airflow. Compared to static control, the ventilation stretch resulted in significant death of A549 cells accompanied by increased lipid peroxidation, mitochondrial reactive oxygen species (ROS) production, and ferrous ion accumulation, while by decreased protein expression of solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4) proteins, as well as ratio of reduced-to-oxidized glutathione. The resulted A549 cell death could be alleviated by two ferroptosis inhibitors, deferoxamine and ferrostatin-1. These similar phenomena also occurred in other three types of human lung cells, such as primary alveolar type II epithelial cells, primary alveolar microvascular endothelial cells, and bronchial epithelial cell line. From the A549 RNA sequence analysis, the gene ontology (GO) based on 85 ferroptosis-related genes (FRGs) indicated that several iron homeostasis-related biological processes and molecular functions were involved in the ventilation-stretch-induced cell death, while the gene set enrichment analysis (GSEA) based on 2901 differentially expressed genes (DEGs) showed that glutathione metabolism was significantly suppressed. Finally, solute carrier family 39 member 14 (SLC39A14), a transporter of uptake extracellular divalent metal ion, was selected to be knocked down to verify its role in the ventilation-stretch-induced death of A549. Our results suggest that ferroptosis may be an alternative pathway for VILI, but it needs to be confirmed by further animal experiments and clinical data.
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Affiliation(s)
- Wei Jiang
- College of Life Sciences, University of Chinese Academy of Sciences, Beijing, 100049, China
| | - Jing Liu
- College of Life Sciences, University of Chinese Academy of Sciences, Beijing, 100049, China
| | - Jingang Cui
- College of Life Sciences, University of Chinese Academy of Sciences, Beijing, 100049, China
| | - Jilei Su
- College of Life Sciences, University of Chinese Academy of Sciences, Beijing, 100049, China
| | - Wei Xu
- College of Life Sciences, University of Chinese Academy of Sciences, Beijing, 100049, China
| | - Fang Zhang
- College of Life Sciences, University of Chinese Academy of Sciences, Beijing, 100049, China
| | - Yongsheng Ding
- College of Life Sciences, University of Chinese Academy of Sciences, Beijing, 100049, China.
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6
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Havlicek EE, Goldman ZA, Faustino EVS, Ignjatovic V, Goldenberg NA, Sochet AA. Hospital-acquired venous thromboembolism during invasive mechanical ventilation in children: a single-center, retrospective cohort study. J Thromb Haemost 2023; 21:3145-3152. [PMID: 37423387 DOI: 10.1016/j.jtha.2023.06.035] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/25/2023] [Revised: 06/01/2023] [Accepted: 06/29/2023] [Indexed: 07/11/2023]
Abstract
BACKGROUND Invasive mechanical ventilation (IMV) has been independently associated with hospital-acquired venous thromboembolism (HA-VTE) among critically ill children, including extremity deep venous thrombosis and pulmonary embolism. OBJECTIVES We aimed to characterize the frequency and timing of HA-VTE following IMV exposure. METHODS This was a single-center, retrospective cohort study including children aged <18 years, hospitalized in a pediatric intensive care unit, undergoing mechanical ventilation for >24 hours from October 2020 through April 2022. Encounters with an existing tracheostomy or receiving treatment for HA-VTE prior to endotracheal intubation were excluded. The primary outcomes characterized clinically-relevant HA-VTE, including timing after intubation, location, and the presence of known hypercoagulability risk factors. Secondary outcomes were IMV exposure magnitude, defined by IMV duration and ventilator parameters (ie, volumetric, barometric, and oxygenation indices). RESULTS Of 170 consecutive, eligible encounters, 18 (10.6%) experienced HA-VTE at a median of 4 days (IQR, 1.4-6.4) following endotracheal intubation. Those with HA-VTE had an increased frequency of a prior venous thromboembolism (27.8% vs 8.6%, P = .027). No differences in frequency of other HA-VTE risk factors (ie, acute immobility, hematologic malignancy, sepsis, and COVID-19-related illness), presence of a concurrent central venous catheter, or the magnitude of IMV exposure were noted. CONCLUSION Children undergoing IMV experience HA-VTE at markedly higher rates than previously estimated in the general pediatric intensive care unit population after endotracheal intubation. While prospective validation is needed, these findings are an important step toward informing the development of risk-stratified thromboprophylaxis trials in critically ill children.
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Affiliation(s)
- Elizabeth E Havlicek
- Department of Pediatrics, University of South Florida Morsani College of Medicine, Tampa, Florida, USA; Institute for Clinical and Translational Research, Johns Hopkins All Children's Hospital, St. Petersburg, Florida, USA.
| | - Zachary A Goldman
- Institute for Clinical and Translational Research, Johns Hopkins All Children's Hospital, St. Petersburg, Florida, USA
| | | | - Vera Ignjatovic
- Institute for Clinical and Translational Research, Johns Hopkins All Children's Hospital, St. Petersburg, Florida, USA; Cancer and Blood Disorders Institute, Johns Hopkins All Children's Hospital, St. Petersburg, Florida, USA
| | - Neil A Goldenberg
- Institute for Clinical and Translational Research, Johns Hopkins All Children's Hospital, St. Petersburg, Florida, USA; Cancer and Blood Disorders Institute, Johns Hopkins All Children's Hospital, St. Petersburg, Florida, USA; Department of Medicine and Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
| | - Anthony A Sochet
- Institute for Clinical and Translational Research, Johns Hopkins All Children's Hospital, St. Petersburg, Florida, USA; Department of Medicine and Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Medicine, Division of Critical Care Medicine, Institute for Clinical and Translational Research, Johns Hopkins All Children's Hospital, St. Petersburg, Florida, USA; Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
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Choi C, Lemmink G, Humanez J. Postoperative Respiratory Failure and Advanced Ventilator Settings. Anesthesiol Clin 2023; 41:141-159. [PMID: 36871996 DOI: 10.1016/j.anclin.2022.11.005] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 03/07/2023]
Abstract
Postoperative respiratory failure has a multifactorial etiology, of which atelectasis is the most common mechanism. Its injurious effects are magnified by surgical inflammation, high driving pressures, and postoperative pain. Chest physiotherapy and noninvasive ventilation are good options to prevent progression of respiratory failure. Acute respiratory disease syndrome is a late and severe finding, which is associated with high morbidity and mortality. If present, proning is a safe, effective, and underutilized therapy. Extracorporeal membrane oxygenation is an option only when traditional supportive measures have failed.
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Affiliation(s)
- Christopher Choi
- Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9068, USA.
| | - Gretchen Lemmink
- Department of Anesthesiology, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267-0531, USA
| | - Jose Humanez
- Department of Anesthesiology, University of Florida College of Medicine - Jacksonville, 655 West 8th Street, C72, Jacksonville, FL 32209, USA
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Sochet AA, Havlicek EE, Faustino EVS, Goldenberg NA. Mechanical Ventilation and Hospital-Acquired Venous Thromboembolism Among Critically Ill Children. Hosp Pediatr 2022; 12:1099-1109. [PMID: 36349533 DOI: 10.1542/hpeds.2022-006697] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/11/2022]
Abstract
OBJECTIVES To estimate the occurrence of, and evaluate associations between, hospital-acquired venous thromboembolism (HA-VTE) and invasive mechanical ventilation (MV) among children hospitalized in the PICU. METHODS We performed a multicenter, retrospective cohort study comparing HA-VTE frequencies among subjects <18 years of age hospitalized in the PICU from January 2018 through December 2019 among 47 participating centers, via the Pediatric Health Information Systems registry. We excluded perinatal encounters, those with VTE present at admission, and those with observational status. The primary outcome was the proportion of HA-VTE events before hospital discharge, including extremity deep venous thrombosis, pulmonary embolism, and organ-specific deep venous thrombosis. The HA-VTE frequencies were compared using χ2 tests. The association between HA-VTE and MV was investigated via multivariable logistic regression, adjusting for previously described VTE risk factors. RESULTS Of the 205 231 PICU encounters identified for study, 70 829 (34.5%) underwent MV. The occurrence of HA-VTE was 2.2% and was greater among children who received, versus did not receive, MV (4.4% versus 1.1%, P < .001). Multivariable logistic regression revealed significant association between MV and HA-VTE (odds ratio 2.51, 95% confidence interval 2.33-2.69; P < .001). CONCLUSIONS In this multicenter, retrospective, registry-based cohort study, HA-VTE were diagnosed in 2.2% of critically-ill children, and after adjustment for central venous catheterization, MV independently increased the risk of HA-VTE 2.5-fold. These findings warrant prospective validation to inform the design of future risk-stratified clinical trials of thromboprophylaxis in critically-ill children.
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Affiliation(s)
- Anthony Alexander Sochet
- Divisions of Critical Care Medicine.,Department of Pediatrics, University of South Florida College of Medicine, Tampa, Florida.,Departments of Anesthesiology.,Critical Care Medicine, Institute for Clinical and Translational Research, Johns Hopkins All Children's Hospital, St. Petersburg, Florida
| | | | | | - Neil Andrew Goldenberg
- Hematology, Department of Medicine, Cancer and Blood Disorders Institute, Johns Hopkins All Children's Hospital, St. Petersburg, Florida.,Critical Care Medicine, Institute for Clinical and Translational Research, Johns Hopkins All Children's Hospital, St. Petersburg, Florida.,Departments of Medicine.,Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland
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Zhang JB, Li LH, Zhu JQ, Zhou SF, Ma JH, Li ZQ, Jin XH, Lin XQ. Application of improved Glasgow coma scale score as switching point for sequential invasive-noninvasive mechanical ventilation on chronic obstructive pulmonary disease (COPD) with respiratory failure. Medicine (Baltimore) 2022; 101:e31857. [PMID: 36401492 PMCID: PMC9678540 DOI: 10.1097/md.0000000000031857] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/05/2022] Open
Abstract
BACKGROUND To compare the efficacy and feasibility of using a modified Glasgow coma scale (GCS) score of 13 or 15 as the criterion for switching chronic obstructive pulmonary disease (COPD) patients with respiratory failure to sequential invasive-noninvasive ventilation. METHODS COPD patients with respiratory failure who had undergone endotracheal intubation and invasive mechanical ventilation (IMV) between June 2017 and June 2020 at 4 different hospitals in China were included. A total of 296 patients were randomly divided into 2 groups. In group A, the patients were extubated and immediately placed on noninvasive ventilation (NIV) when the modified GCS score reached 13. In group B, the same was done when the modified GCS score reached 15. RESULTS No significant differences in the mean blood pressure, oxygenation index, arterial partial pressure of oxygen, and arterial partial pressure of carbon dioxide were seen between groups A and B before extubation and 3 hours after NIV. The re-intubation times were also similar in the 2 groups. Compared to group B, the length of hospital stay, incidence of ventilator associated pneumonia, and time of invasive ventilation were all significantly lower in group A (P = .041, .001, <.001). CONCLUSION Using a modified GCS score of 13 as the criterion for switching from IMV to NIV can significantly reduce the duration of IMV, length of hospital stay, and incidence of ventilator associated pneumonia in COPD patients with respiratory failure.
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Affiliation(s)
- Jin-Bo Zhang
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People’s Hospital of Wenling, Wenling, Zhejiang, China
| | - Li-Hong Li
- Infection Division, Wenling Hospital Affiliated to Wenzhou Medical University, The First People’s Hospital of Wenling, Wenling, Zhejiang, China
| | - Jin-Qiang Zhu
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People’s Hospital of Wenling, Wenling, Zhejiang, China
| | - Shi-Fang Zhou
- Department of Emergency Care, Changsha Central Hospital, Changsha, Hunan, China
| | - Ji-Hong Ma
- Intensive Care Unit, First Affiliated Hospital of Wenzhou Medical University, Wenling, Zhejiang, China
| | - Zhi-Qiang Li
- Intensive Care Unit, The First People’s Hospital of Jingmen, Jingmen, Hubei, China
| | - Xiao-Hong Jin
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People’s Hospital of Wenling, Wenling, Zhejiang, China
| | - Xiao-Qin Lin
- Department of Hepatopancreatobiliary Surgery, Wenling Hospital Affiliated to Wenzhou Medical University, The First People’s Hospital of Wenling, Wenling, Zhejiang, China
- * Correspondence: Xiao-Qin Lin, Department of Hepatopancreatobiliary Surgery, Wenling Hospital Affiliated to Wenzhou Medical University, The First People’s Hospital of Wenling, No. 333 Chuan an south Road, Wenling, Zhejiang 317500, China (e-mail: )
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Fan ML, Tong HQ, Sun T, Zhang HW, Han J, Cheng SY, Lu SF, Han X, Zhang Q, Sun WX, Chen JD, Chen XH. Animal model of coronary microembolization under transthoracic echocardiographic guidance in rats. Biochem Biophys Res Commun 2021; 568:174-179. [PMID: 34246051 DOI: 10.1016/j.bbrc.2021.05.045] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/15/2021] [Accepted: 05/14/2021] [Indexed: 11/20/2022]
Abstract
The aim of the study was to develop a model of coronary microembolization (CME) in rats at a lower cost. We developed a novel rat model without thoracotomy and ventilation under the guidance of echocardiography. Rats were sacrificed at 3 h, 24 h and 1 month postoperatively in both the Echo-CME and Open-chest CME groups for the comparison of the modeling accuracy, mortality, cardiopulmonary circulation, pleural adhesion and ventilation-induced lung injury (VILI). Results showed that the coronary microthrombus formed at 3 h and reached its peak at 24 h postoperatively, which included platelet aggregation and fibrin web. The Echo-group increases success rates, decreased mortality, postoperative complications including pleural adhesion, cardiopulmonary dysfunction and VILI postoperatively than the Open-chest group at 1month postoperatively. The ejection fraction of the CME group decreased to 50% and obvious cardiac fibrosis formed at 3 months postoperatively. Our unique surgical method provided a platform to study molecular mechanisms and potential new pathways for CME treatment.
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Affiliation(s)
- Man-Lu Fan
- First College of Clinical Medicine, Biological Technology Center for Innovation in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China; Department of Cardiology, Jiangsu Provincial Hospital of Chinese Medicine, Nanjing, 210029, China
| | - Hua-Qin Tong
- First College of Clinical Medicine, Biological Technology Center for Innovation in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China; Department of Cardiology, Jiangsu Provincial Hospital of Chinese Medicine, Nanjing, 210029, China
| | - Tong Sun
- First College of Clinical Medicine, Biological Technology Center for Innovation in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China; Department of Cardiology, Jiangsu Provincial Hospital of Chinese Medicine, Nanjing, 210029, China
| | - Hao-Wen Zhang
- School of Health Preservation and Rehabilitation, Key Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, 210023, China
| | - Jie Han
- Department of Cardiology, Jiangsu Provincial Hospital of Chinese Medicine, Nanjing, 210029, China
| | - Song-Yi Cheng
- Department of Cardiology, Nanjing Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210001, China
| | - Sheng-Feng Lu
- Acupuncture and Tuina College, Nanjing University of Chinese Medicine, Key Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210023, China
| | - Xuan Han
- First College of Clinical Medicine, Biological Technology Center for Innovation in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China
| | - Qian Zhang
- First College of Clinical Medicine, Biological Technology Center for Innovation in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China
| | - Wei-Xin Sun
- First College of Clinical Medicine, Biological Technology Center for Innovation in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China; Department of Cardiology, Jiangsu Provincial Hospital of Chinese Medicine, Nanjing, 210029, China
| | - Jian-Dong Chen
- Department of Cardiology, Jiangsu Provincial Hospital of Chinese Medicine, Nanjing, 210029, China.
| | - Xiao-Hu Chen
- Department of Cardiology, Jiangsu Provincial Hospital of Chinese Medicine, Nanjing, 210029, China.
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Enhancing Resident Skills in Mechanical Ventilation. What Do Residents Learn during Intensive Care Unit Rotations? ATS Sch 2021; 2:1-4. [PMID: 33871485 PMCID: PMC8043281 DOI: 10.34197/ats-scholar.2021-0012ed] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/10/2023] Open
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12
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Shurbaji S, El-Sherbiny IM, Alser M, Ali IH, Kordi H, Al-Sadi A, Popelka A, Benslimane F, Yacoub M, Yalcin HC. Nitric Oxide Releasing Hydrogel Nanoparticles Decreases Epithelial Cell Injuries Associated With Airway Reopening. Front Bioeng Biotechnol 2021; 8:579788. [PMID: 33469529 PMCID: PMC7813943 DOI: 10.3389/fbioe.2020.579788] [Citation(s) in RCA: 9] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/03/2020] [Accepted: 11/16/2020] [Indexed: 01/08/2023] Open
Abstract
Acute respiratory distress syndrome (ARDS) is an acute inflammatory lung condition. It is characterized by disruption of gas exchange inside the alveoli, accumulation of protein edema, and an increase in lung stiffness. One major cause of ARDS is a lung infection, such as SARS-COV-2 infection. Lungs of ARDS patients need to be mechanically ventilated for airway reopening. Consequently, ventilation might damage delicate lung tissue leading to excess edema, known as ventilator-induced lung injury (VILI). Mortality of COVID-19 patients under VILI seems to be higher than non-COVID patients, necessitating effective preventative therapies. VILI occurs when small air bubbles form in the alveoli, injuring epithelial cells (EPC) due to shear stress. Nitric oxide (NO) inhalation was suggested as a therapy for ARDS, however, it was shown that it is not effective because of the extremely short half-life of NO. In this study, NO-releasing nanoparticles were produced and tested in an in vitro model, representing airways in the deep lung. Cellular injuries were quantified via fluorescent live/dead assay. Atomic force microscopy (AFM) was used to assess cell morphology. qRT-PCR was performed to assess the expression of inflammatory markers, specifically IL6 and CCL2. ELISA was performed to assess IL6 and confirm qRT-PCR results at the protein level. Finally, ROS levels were assessed in all groups. Here, we show that NO delivery via nanoparticles enhanced EPC survival and recovery, AFM measurements revealed that NO exposure affect cell morphology, while qRT-PCR demonstrated a significant downregulation in IL6 and CCL2 expression when treating the cells to NO both before and after shear exposure. ELISA results for IL6 confirmed qRT-PCR data. ROS experiment results support our findings from previous experiments. These findings demonstrate that NO-releasing nanoparticles can be used as an effective delivery approach of NO to deep lung to prevent/reduce ARDS associated inflammation and cell injuries. This information is particularly useful to treat severe ARDS due to COVID-19 infection. These nanoparticles will be useful when clinically administrated to COVID-19 patients to reduce the symptoms originating from lung distress.
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Affiliation(s)
- Samar Shurbaji
- Biomedical Research Center, Qatar University, Doha, Qatar
| | - Ibrahim M. El-Sherbiny
- Nanomedicine Lab, Center of Materials Sciences, Zewail City of Science and Technology, Giza, Egypt
| | - Maha Alser
- Biomedical Research Center, Qatar University, Doha, Qatar
| | - Isra H. Ali
- Nanomedicine Lab, Center of Materials Sciences, Zewail City of Science and Technology, Giza, Egypt
| | - Haya Kordi
- Biomedical Research Center, Qatar University, Doha, Qatar
- Department of Biomedical Sciences, College of Health Science-QU Health, Qatar University, Doha, Qatar
| | - Ameena Al-Sadi
- Biomedical Research Center, Qatar University, Doha, Qatar
- Department of Biomedical Sciences, College of Health Science-QU Health, Qatar University, Doha, Qatar
| | - Anton Popelka
- Center for Advanced Materials, Qatar University, Doha, Qatar
| | | | - Magdi Yacoub
- Heart Science Centre, Imperial College, National Heart and Lung Institute, London, United Kingdom
| | - Huseyin C. Yalcin
- Biomedical Research Center, Qatar University, Doha, Qatar
- Department of Biomedical Sciences, College of Health Science-QU Health, Qatar University, Doha, Qatar
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13
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Zhu CH, Yu J, Wang BQ, Nie Y, Wang L, Shan SQ. Dexmedetomidine reduces ventilator-induced lung injury via ERK1/2 pathway activation. Mol Med Rep 2020; 22:5378-5384. [PMID: 33173983 PMCID: PMC7647005 DOI: 10.3892/mmr.2020.11612] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/22/2020] [Accepted: 09/15/2020] [Indexed: 02/07/2023] Open
Abstract
Mechanical ventilation (MV) can contribute to ventilator-induced lung injury (VILI); dexmedetomidine (Dex) treatment attenuates MV-related pulmonary inflammation, but the mechanisms remain unclear. Therefore, the present study aimed to explore the protective effect and the possible molecular mechanisms of Dex in a VILI rodent model. Adult male Sprague-Dawley rats were randomly assigned to one of seven groups (n=24 rats/group). Rats were euthanized after 4 h of continuous MV, and pathological changes, lung wet/dry (W/D) weight ratio, the levels of inflammatory cytokines (IL-1β, TNF-α and IL-6) in the bronchoalveolar lavage fluid (BALF), and the expression levels of Bcl-2 homologous antagonist/killer (Bak), Bcl-2, pro-caspase-3, cleaved caspase-3 and the phosphorylation of ERK1/2 in the lung tissues were measured. Propidium iodide uptake and TUNEL staining were used to detect epithelial cell death. The Dex pretreatment group exhibited fewer pathological changes, lower W/D ratios and lower expression levels of inflammatory cytokines in BALF compared with the VILI group. Dex significantly attenuated the ratio of Bak/Bcl-2, cleaved caspase-3 expression levels and epithelial cell death, and increased the expression of phosphorylated ERK1/2. The protective effects of Dex could be partially reversed by PD98059, which is a mitogen-activated protein kinase (upstream of ERK1/2) inhibitor. Overall, dexmedetomidine was found to reduce the inflammatory response and epithelial cell death caused by VILI, via the activation of the ERK1/2 signaling pathway.
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Affiliation(s)
- Chun-Hua Zhu
- Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, Hebei 061000, P.R. China
| | - Jian Yu
- Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, Hebei 061000, P.R. China
| | - Ben-Qing Wang
- Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, Hebei 061000, P.R. China
| | - Yu Nie
- Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, Hebei 061000, P.R. China
| | - Lei Wang
- Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, Hebei 061000, P.R. China
| | - Shi-Qiang Shan
- Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, Hebei 061000, P.R. China
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14
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Shurbaji S, Al-Ruweidi MKAA, Ali FH, Benslimane FM, Yalcin HC. Application of a Flow-Induced Stress Wave and Investigation of Associated Injuries on Cell Monolayers Using a Parallel Plate Flow Chamber. Methods Protoc 2020; 3:mps3040065. [PMID: 32987681 PMCID: PMC7712398 DOI: 10.3390/mps3040065] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/14/2020] [Revised: 09/12/2020] [Accepted: 09/15/2020] [Indexed: 01/08/2023] Open
Abstract
Parallel plate flow chambers are widely used to expose cultured cells to physiological flows for the investigation of a variety of diseases. These applications usually involve the generation of continuous and steady fluid flow over cell monolayers for extended durations, usually a few days. Another technique is to generate a fast high-stress wave over the cells to see the immediate effect of flow-induced stresses. This can be achieved by propagating an air/liquid interface, in other words, a bubble, over cell monolayers. The approach is relevant to the reopening event of fluid-filled lung bronchioles and alveoli during mechanical ventilation therapy of Acute Respiratory Distress Syndrome. This article explains how we generate a stress wave using a parallel plate flow chamber and presents representative results of this wave on cultured lung epithelial cells.
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15
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Zhang JB, Zhu JQ, Cao LX, Jin XH, Chen LL, Song YK, Zhou SF, Ma JH, Fu H, Xu JZ, Dong MP, Yan LC, Wu XD, Wang HP, Zhou JY, Wang YQ. Use of the modified Glasgow Coma Scale score to guide sequential invasive-noninvasive mechanical ventilation weaning in patients with AECOPD and respiratory failure. Exp Ther Med 2020; 20:1441-1446. [PMID: 32742377 PMCID: PMC7388266 DOI: 10.3892/etm.2020.8884] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/16/2019] [Accepted: 05/07/2020] [Indexed: 12/16/2022] Open
Abstract
Sequential invasive-noninvasive ventilation (NIV) improves the outcomes of patients with respiratory failure caused by acute exacerbation of chronic obstructive pulmonary disease (AECOPD); however, there is no clear consensus on the optimal timing of the switch to sequential invasive-NIV in these patients. In the present study, a potential role for the modified Glasgow Coma Scale (GCS) score to guide sequential weaning was investigated. Patients with AECOPD and respiratory failure were prospectively recruited from three study centers (Wenling Hospital Affiliated to Wenzhou Medical University, the First Affiliated Hospital of Wenzhou Medical University and Changsha Central Hospital) between January 1st 2016 and December 31st 2018. Patients were randomly assigned to group A and B, with the switching point for sequential weaning strategy in the two groups being a modified GCS score ≥13 and 10 points, respectively. Each group included 240 patients. Baseline demographic characteristics were comparable in the two groups. The duration of invasive mechanical ventilation (IMV) in group A was significantly shorter than that in group B. However, there were no significant between-group differences with respect to the incidence of re-intubation, ventilator-associated pneumonia, in-hospital mortality or the length of hospital stay. Use of a modified GCS score ≥13 as the switching point for sequential invasive-NIV may help decrease the duration of IMV in patients with AECOPD and respiratory failure.
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Affiliation(s)
- Jin-Bo Zhang
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
| | - Jin-Qiang Zhu
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
| | - Lie-Xiang Cao
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
| | - Xiao-Hong Jin
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
| | - Li-Li Chen
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
| | - Yu-Kang Song
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
| | - Shi-Fang Zhou
- Department of Emergency Care, Changsha Central Hospital, Changsha, Hunan 410004, P.R. China
| | - Ji-Hong Ma
- Intensive Care Unit, First Affiliated Hospital of Wenzhou Medical University, Wenling, Zhejiang 325000, P.R. China
| | - Hui Fu
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
| | - Jin-Zhong Xu
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
| | - Mei-Ping Dong
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
| | - Lai-Chao Yan
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
| | - Xian-Dan Wu
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
| | - Hui-Ping Wang
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
| | - Jun-Yang Zhou
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
| | - Yan-Qiu Wang
- Emergency Intensive Care Unit, Wenling Hospital Affiliated to Wenzhou Medical University, The First People's Hospital of Wenling, Wenling, Zhejiang 317500, P.R. China
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16
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Takahashi N, Nakada TA, Sakai T, Kato Y, Moriyama K, Nishida O, Oda S. A CO 2 removal system using extracorporeal lung and renal assist device with an acid and alkaline infusion. J Artif Organs 2019; 23:54-61. [PMID: 31584110 DOI: 10.1007/s10047-019-01136-0] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/03/2019] [Accepted: 09/22/2019] [Indexed: 01/04/2023]
Abstract
The patients with respiratory failure need high tidal volume by mechanical ventilation, which lead to the ventilator-induced lung injury. We developed an extracorporeal lung and renal assist device (ELRAD), comprising acid infusion, membrane lung, continuous hemodiafiltration and alkaline infusion. To evaluate this system, we conducted in vivo studies using experimental swine which were connected to the new system. In vivo experiments consist of four protocols; baseline = hemodiafiltration only (no O2 gas flow to membrane lung); membrane lung = "Baseline" plus O2 gas flow to membrane lung; "Acid infusion" = "Membrane lung" plus continuous acid infusion; ELRAD = "Acid infusion" plus continuous alkaline infusion. We changed the ventilatory rate of the mechanical ventilation to maintain PCO2 at 50-55 mmHg during the four protocols. The results showed that there was statistically no significant difference in the levels of pH, HCO3-, and base excess when each study protocol was initiated. The amount of CO2 eliminated by the membrane lung significantly increased by 1.6 times in the acid infusion protocol and the ELRAD protocol compared to the conventional membrane lung protocol. Minute ventilation in the ELRAD protocol significantly decreased by 0.5 times compared with the hemodiafiltration only protocol (P < 0.0001), the membrane lung (P = 0.0006) and acid infusion protocol (P = 0.0017), respectively. In conclusion, a developed CO2 removal system efficiently removed CO2 at low blood flow and reduced minute ventilation, while maintaining acid-base balance within the normal range.
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Affiliation(s)
- Nozomi Takahashi
- Department of Emergency and Critical Care Medicine, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo, Chiba, 260-8677, Japan
| | - Taka-Aki Nakada
- Department of Emergency and Critical Care Medicine, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo, Chiba, 260-8677, Japan.
| | - Toshikazu Sakai
- Department of Anesthesiology and Critical Care Medicine, Fujita Health University School of Medicine, 1-98 Dengakugakubo, Kutsukake, Toyoake, Aichi, 470-1192, Japan
| | - Yu Kato
- Department of Anesthesiology and Critical Care Medicine, Fujita Health University School of Medicine, 1-98 Dengakugakubo, Kutsukake, Toyoake, Aichi, 470-1192, Japan
| | - Kazuhiro Moriyama
- Laboratory for Immune Response and Regulatory Medicine, Fujita Health University School of Medicine, 1-98 Dengakugakubo, Kutsukake, Toyoake, Aichi, 470-1192, Japan
| | - Osamu Nishida
- Department of Anesthesiology and Critical Care Medicine, Fujita Health University School of Medicine, 1-98 Dengakugakubo, Kutsukake, Toyoake, Aichi, 470-1192, Japan
| | - Shigeto Oda
- Department of Emergency and Critical Care Medicine, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo, Chiba, 260-8677, Japan
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17
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Wang D, Chai XQ, Magnussen CG, Zosky GR, Shu SH, Wei X, Hu SS. Renin-angiotensin-system, a potential pharmacological candidate, in acute respiratory distress syndrome during mechanical ventilation. Pulm Pharmacol Ther 2019; 58:101833. [PMID: 31376462 PMCID: PMC7110665 DOI: 10.1016/j.pupt.2019.101833] [Citation(s) in RCA: 53] [Impact Index Per Article: 8.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/20/2019] [Revised: 06/24/2019] [Accepted: 07/31/2019] [Indexed: 02/06/2023]
Abstract
While effective treatments for acute respiratory distress syndrome (ARDS) are lacking, mechanical lung ventilation can sustain adequate gas exchange in critically ill patients with respiratory failure due to ARDS. However, as a result of the phenomenon of ventilator-induced lung injury (VILI), there is an increasing need to seek beneficial pharmacological therapies for ARDS. Recent studies have suggested the renin-angiotensin system (RAS), which consists of the ACE/Ang-II/AT1R axis and ACE2/Ang-(1-7)/MasR axis, plays a dual role in the pathogenesis of ARDS and VILI. This review highlights the deleterious action of ACE/Ang-II/AT1R axis and the beneficial role of ACE2/Ang-(1-7)/MasR axis, as well as AT2R, in VILI and ARDS, and also discusses the possibility of targeting RAS components with pharmacological interventions to improve outcomes in ARDS.
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Affiliation(s)
- Di Wang
- Department of Anesthesiology and Pain Medicine, Anhui Provincial Hospital, First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China (USTC), Hefei, 230001, Anhui, China
| | - Xiao-Qing Chai
- Department of Anesthesiology and Pain Medicine, Anhui Provincial Hospital, First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China (USTC), Hefei, 230001, Anhui, China.
| | - Costan G Magnussen
- Menzies Institute for Medical Research, College of Health and Medicine, University of Tasmania, Hobart, 7001, Tasmania, Australia; Research Centre of Applied and Preventive Cardiovascular Research, University of Turku, Turku, 20520, Finland
| | - Graeme R Zosky
- Menzies Institute for Medical Research, College of Health and Medicine, University of Tasmania, Hobart, 7001, Tasmania, Australia; School of Medicine, College of Health and Medicine, University of Tasmania, Hobart, 7001, Tasmania, Australia
| | - Shu-Hua Shu
- Department of Anesthesiology and Pain Medicine, Anhui Provincial Hospital, First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China (USTC), Hefei, 230001, Anhui, China
| | - Xin Wei
- Department of Anesthesiology and Pain Medicine, Anhui Provincial Hospital, First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China (USTC), Hefei, 230001, Anhui, China
| | - Shan-Shan Hu
- Institute of Clinical Pharmacology, Anhui Medical University, Hefei, 230032, Anhui, China
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Peña-López Y, Ramirez-Estrada S, Eshwara VK, Rello J. Limiting ventilator-associated complications in ICU intubated subjects: strategies to prevent ventilator-associated events and improve outcomes. Expert Rev Respir Med 2018; 12:1037-1050. [PMID: 30460868 DOI: 10.1080/17476348.2018.1549492] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
Introduction: Intubation is required to maintain the airways in comatose patients and enhance oxygenation in hypoxemic or ventilation in hypercapnic subjects. Recently, the Centers of Disease Control (CDC) created new surveillance definitions designed to identify complications associated with poor outcomes. Areas covered: The new framework proposed by CDC, Ventilator-Associated Events (VAE), has a range of definitions encompassing Ventilator-Associated Conditions (VAC), Infection-related Ventilator-Associated Complications (IVAC), or Possible Ventilator-Associated Pneumonia - suggesting replacing the traditional definitions of Ventilator-Associated Tracheobronchitis (VAT) and Ventilator-Associated Pneumonia (VAP). They focused more on oxygenation variations than on Chest-X rays or inflammatory biomarkers. This article will review the spectrum of infectious (VAP & VAT) complications, as well as the main non-infectious complications, namely pulmonary edema, acute respiratory distress syndrome (ARDS) and atelectasis. Strategies to limit these complications and improve outcomes will be presented. Expert commentary: Improving outcomes should be the objective of implementing bundles of prevention, based on risk factors amenable of intervention. Promotion of measures that reduce the exposition or duration of intubation should be a priority.
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Affiliation(s)
- Yolanda Peña-López
- a Pediatric Critical Care Department , Vall d'Hebron Barcelona Hospital Campus , Barcelona , Spain
| | | | - Vandana Kalwaje Eshwara
- c Department of Microbiology, Kasturba Medical College, Manipal Academy of Higher Education , Manipal University , Manipal , India
| | - Jordi Rello
- d Clinical Research/epidemiology In Pneumonia & Sepsis , Vall d'Hebron Institut of Research & Centro de Investigacion Biomedica en Red (CIBERES) , Barcelona , Spain
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Ramirez-Estrada S, Peña-Lopez Y, Kalwaje Eshwara V, Rello J. Ventilator-associated events versus ventilator-associated respiratory infections-moving into a new paradigm or merging both concepts, instead? ANNALS OF TRANSLATIONAL MEDICINE 2018; 6:425. [PMID: 30581833 PMCID: PMC6275412 DOI: 10.21037/atm.2018.10.54] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Received: 09/15/2018] [Accepted: 10/21/2018] [Indexed: 01/06/2023]
Abstract
Despite ventilator-associated respiratory infections (VARI) are reported as the most common and fatal complications related to mechanical ventilation (MV), they are not the unique occurrences. The new classification of ventilator-associated events (VAE) proposed by the centers for disease control and prevention (CDC) enhance the spectra of complications due to MV including both infection-related and non-infectious events. Both VAEs and VARIs are associated with prolonged duration of MV, longer stay in hospital and in the intensive care unit (ICU) and more antibiotic consumption, nonetheless patients with VAEs have worst outcomes. The VARI and VAE algorithms are focused on different targets and the correlation between both classifications is shown to be poor. The diagnostic criteria of the traditional classification have limited accuracy and the non-infectious complications may be misinterpreted as VARI. While the VAE surveillance enhances the spectra of MV complications but excludes less severe VARIs. Noninfective events explain up to 30% of VAEs, the main causes being atelectasis, acute respiratory distress syndrome, pulmonary edema and pulmonary embolism. The bundles assessing VAE are associated with less incidence of VAP and improved outcomes but they fail to reduce the rates of VAE. Automated VAE surveillance is efficient and useful as a quality indicator in the ICU while the differences in the interpretation of VARI criteria limit its role in the design of global protocols and preventive strategies. We suggest that a more comprehensive strategy should combine both algorithms with emphasis on clinical outcomes.
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Affiliation(s)
- Sergio Ramirez-Estrada
- Critical Care Department, Clínica Corachan, Barcelona, Spain
- Medicine Department, Universitat Autónoma de Barcelona, (UAB), Barcelona, Spain
| | | | - Vandana Kalwaje Eshwara
- Department of Microbiology, Kasturba Medical College, Manipal Academy of Higher Education, Manipal, India
| | - Jordi Rello
- Vall d'Hebron Institut of Research, Barcelona, Spain
- Centro de Investigación Biomédica en Red (CIBERES), Instituto Salud Carlos III, Madrid, Spain
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20
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Clinical Pearls in Venovenous Extracorporeal Life Support for Adult Respiratory Failure. ASAIO J 2018; 64:1-9. [DOI: 10.1097/mat.0000000000000657] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/21/2022] Open
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Huang C, Pan L, Lin F, Dai H, Fu R. Monoclonal antibody against Toll-like receptor 4 attenuates ventilator-induced lung injury in rats by inhibiting MyD88- and NF-κB-dependent signaling. Int J Mol Med 2017; 39:693-700. [PMID: 28204830 DOI: 10.3892/ijmm.2017.2873] [Citation(s) in RCA: 29] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/01/2015] [Accepted: 01/04/2017] [Indexed: 11/06/2022] Open
Abstract
The mechanisms through which mechanical ventilation causes non-infectious inflammatory diseases and lung injury are poorly understood. Animals models of this type of injury suggest that it involves signaling mediated by Toll‑like receptor (TLR)4 and 9. In this study, in order to gain further insight into the involvement of TLR4 in this type of injury, we performed in vivo and in vitro experiments to determine the mechanisms through which TLR4 triggers inflammation. We also examined whether the use of TLR4 monoclonal antibody (mAb) can alleviate this type of injury. For this purpose, rats were tracheotomized and administered intratracheal injections of anti‑TLR4 mAb or saline, and then ventilated for 4 h at a high tidal volume (HTV) of 40 ml/ kg or allowed to breathe spontaneously for the same period of time (controls). Alveolar macrophages (AMs) were isolated from the bronchoalveolar lavage fluid (BALF) of the rats and stimulated for 16 h with tumor necrosis factor (TNF)‑α in the presence or absence of anti‑TLR4 mAb. Lung injury was assessed by examining lung histopathology, lung wet/dry weight ratio, BALF total protein and cytokine levels in BALF and plasma. The mRNA and protein expression levels of TLR4, TLR9, myeloid differentiation factor 88 (Myd88) and nuclear factor (NF)‑κB were measured in cultured macrophages. Compared to the controls (spontaneous breathing), the ventilated rats exhibited greater pulmonary permeability, more severe inflammatory cell infiltration/lung edema, and higher levels of interleukin (IL)‑1β, IL‑6 and TNF‑α in BALF and plasma. The AMs from the ventilated rats expressed higher mRNA and protein levels of TLR4, TLR9, Myd88 and NF‑κB compared with the macrophages from the spontaneously breathing rats. The ventilated rats pre‑treated with anti‑TLR4 mAb exhibited markedly attenuated signs of ventilation‑induced injury, such as less lung inflammation and pulmonary edema, fewer cells in BALF, and lower levels of ILs and TNF‑α in BALF and plasma. Similarly, the TNF‑α‑dependent increases in the mRNA and protein expression of TLR4, Myd88 and NF‑κB in AMs were attenuated when TNF‑α was co‑administered with anti‑TLR4 mAb than when TNF-α was administered alone. Co‑administering anti-TLR4 mAb also reduced the TNF‑α‑dependent secretion of ILs. On the whole, our data demonstrate that TLR4 contributes significantly to ventilation‑induced lung injury by activating the Myd88/NF‑κB pathway, and pre‑treating rats with anti‑TLR4 mAb partially protects them against this type of injury by inhibiting Myd88/NF-κB signaling.
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Affiliation(s)
- Cuiyuan Huang
- Department of Anesthesiology, The Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China
| | - Linghui Pan
- Department of Anesthesiology, The Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China
| | - Fei Lin
- Department of Anesthesiology, The Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China
| | - Huijun Dai
- Department of Anesthesiology, The Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China
| | - Ruili Fu
- Department of Anesthesiology, The Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China
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22
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Dose-Dependent Protective Effect of Inhalational Anesthetics Against Postoperative Respiratory Complications. Crit Care Med 2017; 45:e30-e39. [DOI: 10.1097/ccm.0000000000002015] [Citation(s) in RCA: 31] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/21/2022]
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Wang T, Gross C, Desai AA, Zemskov E, Wu X, Garcia AN, Jacobson JR, Yuan JXJ, Garcia JGN, Black SM. Endothelial cell signaling and ventilator-induced lung injury: molecular mechanisms, genomic analyses, and therapeutic targets. Am J Physiol Lung Cell Mol Physiol 2016; 312:L452-L476. [PMID: 27979857 DOI: 10.1152/ajplung.00231.2016] [Citation(s) in RCA: 65] [Impact Index Per Article: 7.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/08/2016] [Revised: 12/08/2016] [Accepted: 12/11/2016] [Indexed: 12/13/2022] Open
Abstract
Mechanical ventilation is a life-saving intervention in critically ill patients with respiratory failure due to acute respiratory distress syndrome (ARDS). Paradoxically, mechanical ventilation also creates excessive mechanical stress that directly augments lung injury, a syndrome known as ventilator-induced lung injury (VILI). The pathobiology of VILI and ARDS shares many inflammatory features including increases in lung vascular permeability due to loss of endothelial cell barrier integrity resulting in alveolar flooding. While there have been advances in the understanding of certain elements of VILI and ARDS pathobiology, such as defining the importance of lung inflammatory leukocyte infiltration and highly induced cytokine expression, a deep understanding of the initiating and regulatory pathways involved in these inflammatory responses remains poorly understood. Prevailing evidence indicates that loss of endothelial barrier function plays a primary role in the development of VILI and ARDS. Thus this review will focus on the latest knowledge related to 1) the key role of the endothelium in the pathogenesis of VILI; 2) the transcription factors that relay the effects of excessive mechanical stress in the endothelium; 3) the mechanical stress-induced posttranslational modifications that influence key signaling pathways involved in VILI responses in the endothelium; 4) the genetic and epigenetic regulation of key target genes in the endothelium that are involved in VILI responses; and 5) the need for novel therapeutic strategies for VILI that can preserve endothelial barrier function.
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Affiliation(s)
- Ting Wang
- Department of Medicine, The University of Arizona Health Sciences, Tucson, Arizona
| | - Christine Gross
- Vascular Biology Center, Augusta University, Augusta, Georgia
| | - Ankit A Desai
- Department of Medicine, The University of Arizona Health Sciences, Tucson, Arizona
| | - Evgeny Zemskov
- Department of Medicine, The University of Arizona Health Sciences, Tucson, Arizona
| | - Xiaomin Wu
- Department of Medicine, The University of Arizona Health Sciences, Tucson, Arizona
| | - Alexander N Garcia
- Department of Pharmacology University of Illinois at Chicago, Chicago, Illinois; and
| | - Jeffrey R Jacobson
- Department of Medicine, University of Illinois at Chicago, Chicago, Illinois
| | - Jason X-J Yuan
- Department of Medicine, The University of Arizona Health Sciences, Tucson, Arizona
| | - Joe G N Garcia
- Department of Medicine, The University of Arizona Health Sciences, Tucson, Arizona
| | - Stephen M Black
- Department of Medicine, The University of Arizona Health Sciences, Tucson, Arizona;
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24
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Bos LD, Schouten LR, Schultz MJ. Promising but still uncertain steps towards better prediction of functional outcome in ICU patients. J Thorac Dis 2016; 8:E838-40. [PMID: 27619335 DOI: 10.21037/jtd.2016.07.08] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/06/2022]
Affiliation(s)
- Lieuwe D Bos
- Department of Intensive Care, University of Amsterdam, The Netherlands; Department of Respiratory Medicine, University of Amsterdam, The Netherlands; Laboratory for Experimental Intensive Care and Anesthesiology (L·E·I·C·A), University of Amsterdam, The Netherlands
| | - Laura R Schouten
- Department of Intensive Care, University of Amsterdam, The Netherlands; Laboratory for Experimental Intensive Care and Anesthesiology (L·E·I·C·A), University of Amsterdam, The Netherlands; Department of Pediatrics, Academic medical Center, University of Amsterdam, The Netherlands
| | - Marcus J Schultz
- Department of Intensive Care, University of Amsterdam, The Netherlands; Laboratory for Experimental Intensive Care and Anesthesiology (L·E·I·C·A), University of Amsterdam, The Netherlands
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25
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Herbert JA, Valentine MS, Saravanan N, Schneck MB, Pidaparti R, Fowler AA, Reynolds AM, Heise RL. Conservative fluid management prevents age-associated ventilator induced mortality. Exp Gerontol 2016; 81:101-9. [PMID: 27188767 DOI: 10.1016/j.exger.2016.05.005] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/09/2015] [Revised: 05/09/2016] [Accepted: 05/13/2016] [Indexed: 11/19/2022]
Abstract
BACKGROUND Approximately 800 thousand patients require mechanical ventilation in the United States annually with an in-hospital mortality rate of over 30%. The majority of patients requiring mechanical ventilation are over the age of 65 and advanced age is known to increase the severity of ventilator-induced lung injury (VILI) and in-hospital mortality rates. However, the mechanisms which predispose aging ventilator patients to increased mortality rates are not fully understood. Ventilation with conservative fluid management decreases mortality rates in acute respiratory distress patients, but to date there has been no investigation of the effect of conservative fluid management on VILI and ventilator associated mortality rates. We hypothesized that age-associated increases in susceptibility and incidence of pulmonary edema strongly promote age-related increases in ventilator associated mortality. METHODS 2month old and 20month old male C57BL6 mice were mechanically ventilated with either high tidal volume (HVT) or low tidal volume (LVT) for up to 4h with either liberal or conservative fluid support. During ventilation, lung compliance, total lung capacity, and hysteresis curves were quantified. Following ventilation, bronchoalveolar lavage fluid was analyzed for total protein content and inflammatory cell infiltration. Wet to dry ratios were used to directly measure edema in excised lungs. Lung histology was performed to quantify alveolar barrier damage/destruction. Age matched non-ventilated mice were used as controls. RESULTS At 4h, both advanced age and HVT ventilation significantly increased markers of inflammation and injury, degraded pulmonary mechanics, and decreased survival rates. Conservative fluid support significantly diminished pulmonary edema and improved pulmonary mechanics by 1h in advanced age HVT subjects. In 4h ventilations, conservative fluid support significantly diminished pulmonary edema, improved lung mechanics, and resulted in significantly lower mortality rates in older subjects. CONCLUSION Our study demonstrates that conservative fluid alone can attenuate the age associated increase in ventilator associated mortality.
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Affiliation(s)
- Joseph A Herbert
- Department of Biomedical Engineering, Virginia Commonwealth University, 401 W Main St, PO Box 843067, Richmond, VA 23284, United States
| | - Michael S Valentine
- Department of Biomedical Engineering, Virginia Commonwealth University, 401 W Main St, PO Box 843067, Richmond, VA 23284, United States
| | - Nivi Saravanan
- Department of Biomedical Engineering, Virginia Commonwealth University, 401 W Main St, PO Box 843067, Richmond, VA 23284, United States
| | - Matthew B Schneck
- Department of Biomedical Engineering, Virginia Commonwealth University, 401 W Main St, PO Box 843067, Richmond, VA 23284, United States
| | | | - Alpha A Fowler
- Division of Pulmonary Disease and Critical Care Medicine, Department of Internal Medicine, Virginia Commonwealth University School of Medicine, United States
| | - Angela M Reynolds
- Department of Mathematics and Applies Mathematics 1015 Floyd Avenue P.O. Box 842014 Richmond, VA 23284-2014, United States
| | - Rebecca L Heise
- Department of Biomedical Engineering, Virginia Commonwealth University, 401 W Main St, PO Box 843067, Richmond, VA 23284, United States; Department of Physiology and Biophysics VCU School of Medicine 1101 East Marshall Street P.O. Box 980551 Richmond, VA 23298-0551, United States.
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26
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Sadowitz B, Jain S, Kollisch-Singule M, Satalin J, Andrews P, Habashi N, Gatto LA, Nieman G. Preemptive mechanical ventilation can block progressive acute lung injury. World J Crit Care Med 2016; 5:74-82. [PMID: 26855896 PMCID: PMC4733459 DOI: 10.5492/wjccm.v5.i1.74] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/10/2015] [Revised: 10/15/2015] [Accepted: 01/04/2016] [Indexed: 02/06/2023] Open
Abstract
Mortality from acute respiratory distress syndrome (ARDS) remains unacceptable, approaching 45% in certain high-risk patient populations. Treating fulminant ARDS is currently relegated to supportive care measures only. Thus, the best treatment for ARDS may lie with preventing this syndrome from ever occurring. Clinical studies were examined to determine why ARDS has remained resistant to treatment over the past several decades. In addition, both basic science and clinical studies were examined to determine the impact that early, protective mechanical ventilation may have on preventing the development of ARDS in at-risk patients. Fulminant ARDS is highly resistant to both pharmacologic treatment and methods of mechanical ventilation. However, ARDS is a progressive disease with an early treatment window that can be exploited. In particular, protective mechanical ventilation initiated before the onset of lung injury can prevent the progression to ARDS. Airway pressure release ventilation (APRV) is a novel mechanical ventilation strategy for delivering a protective breath that has been shown to block progressive acute lung injury (ALI) and prevent ALI from progressing to ARDS. ARDS mortality currently remains as high as 45% in some studies. As ARDS is a progressive disease, the key to treatment lies with preventing the disease from ever occurring while it remains subclinical. Early protective mechanical ventilation with APRV appears to offer substantial benefit in this regard and may be the prophylactic treatment of choice for preventing ARDS.
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27
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Nieman GF, Gatto LA, Habashi NM. Impact of mechanical ventilation on the pathophysiology of progressive acute lung injury. J Appl Physiol (1985) 2015; 119:1245-61. [PMID: 26472873 DOI: 10.1152/japplphysiol.00659.2015] [Citation(s) in RCA: 50] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/04/2015] [Accepted: 10/01/2015] [Indexed: 02/08/2023] Open
Abstract
The earliest description of what is now known as the acute respiratory distress syndrome (ARDS) was a highly lethal double pneumonia. Ashbaugh and colleagues (Ashbaugh DG, Bigelow DB, Petty TL, Levine BE Lancet 2: 319-323, 1967) correctly identified the disease as ARDS in 1967. Their initial study showing the positive effect of mechanical ventilation with positive end-expiratory pressure (PEEP) on ARDS mortality was dampened when it was discovered that improperly used mechanical ventilation can cause a secondary ventilator-induced lung injury (VILI), thereby greatly exacerbating ARDS mortality. This Synthesis Report will review the pathophysiology of ARDS and VILI from a mechanical stress-strain perspective. Although inflammation is also an important component of VILI pathology, it is secondary to the mechanical damage caused by excessive strain. The mechanical breath will be deconstructed to show that multiple parameters that comprise the breath-airway pressure, flows, volumes, and the duration during which they are applied to each breath-are critical to lung injury and protection. Specifically, the mechanisms by which a properly set mechanical breath can reduce the development of excessive fluid flux and pulmonary edema, which are a hallmark of ARDS pathology, are reviewed. Using our knowledge of how multiple parameters in the mechanical breath affect lung physiology, the optimal combination of pressures, volumes, flows, and durations that should offer maximum lung protection are postulated.
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Affiliation(s)
- Gary F Nieman
- Department of Surgery, Upstate Medical University, Syracuse, New York;
| | - Louis A Gatto
- Biological Sciences Department, State University of New York, Cortland, New York; and
| | - Nader M Habashi
- R Adams Cowley Shock/Trauma Center, University of Maryland Medical Center, Baltimore, Maryland
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28
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Weirich PP, Tozo TC, Wandeur V, Duarte PAD. Moderate/severe acute respiratory distress syndrome in patients with or without traumatic brain injury. TRAUMA-ENGLAND 2015. [DOI: 10.1177/1460408615589431] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022]
Abstract
Introduction Patients with traumatic brain injury are at risk of developing acute respiratory distress syndrome, which significantly increases morbidity. This study aimed to assess functional difference (respiratory mechanics) and morbidity and mortality of moderate/severe acute respiratory distress syndrome among patients with traumatic brain injury compared with those with other non-traumatic aetiologies, besides assessing the outcomes of patients with severe traumatic brain injury with or without moderate/severe acute respiratory distress syndrome. Methods A prospective cohort study analysed consecutive patients with moderate/severe acute respiratory distress syndrome (PaO2/FiO2 < 200) and consecutive patients with traumatic brain injury during a 14-month period in the general intensive care unit of a teaching hospital in Cascavel, southern Brazil. Results Overall, 85 patients were assessed: 30 with traumatic brain injury without acute respiratory distress syndrome, 17 with traumatic brain injury and acute respiratory distress syndrome and 38 with non-traumatic brain injury (other aetiologies) acute respiratory distress syndrome. Acute respiratory distress syndrome in patients with traumatic brain injury resulted in a longer intensive care unit length of stay and slightly higher mortality. When acute respiratory distress syndrome patients with and without traumatic brain injury are compared, the latter required higher values of positive end expiratory pressure and showed a trend to lower lung static compliance, with slightly higher mortality. Conclusions In patients with traumatic brain injury, the presence of acute respiratory distress syndrome increased hospitalisation time. Patients with non-traumatic brain injury acute respiratory distress syndrome showed lower respiratory compliance and required higher values of positive end expiratory pressure than those with traumatic brain injury – acute respiratory distress syndrome, with higher mortality.
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Affiliation(s)
- Priscila P Weirich
- General Intensive Care Unit, Hospital São Lucas-FAG, Cascavel/PR, Brazil
| | - Tatiane C Tozo
- General Intensive Care Unit, Hospital São Lucas-FAG, Cascavel/PR, Brazil
| | - Vanessa Wandeur
- General Intensive Care Unit, Hospital São Lucas-FAG, Cascavel/PR, Brazil
| | - Péricles AD Duarte
- General Intensive Care Unit, Hospital São Lucas-FAG, Cascavel/PR, Brazil
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29
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Membrane translocation of IL-33 receptor in ventilator induced lung injury. PLoS One 2015; 10:e0121391. [PMID: 25815839 PMCID: PMC4376768 DOI: 10.1371/journal.pone.0121391] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/12/2014] [Accepted: 01/31/2015] [Indexed: 01/24/2023] Open
Abstract
Ventilator-induced lung injury is associated with inflammatory mechanism and causes high mortality. The objective of this study was to discover the role of IL-33 and its ST2 receptor in acute lung injury induced by mechanical ventilator (ventilator-induced lung injury; VILI). Male Wistar rats were intubated after tracheostomy and received ventilation at 10 cm H2O of inspiratory pressure (PC10) by a G5 ventilator for 4 hours. The hemodynamic and respiratory parameters were collected and analyzed. The morphological changes of lung injury were also assessed by histological H&E stain. The dynamic changes of lung injury markers such as TNF-α and IL-1β were measured in serum, bronchoalveolar lavage fluid (BALF), and lung tissue homogenization by ELISA assay. During VILI, the IL-33 profile change was detected in BALF, peripheral serum, and lung tissue by ELISA analysis. The Il-33 and ST2 expression were analyzed by immunohistochemistry staining and western blot analysis. The consequence of VILI by H&E stain showed inducing lung congestion and increasing the expression of pro-inflammatory cytokines such as TNF-α and IL-1β in the lung tissue homogenization, serum, and BALF, respectively. In addition, rats with VILI also exhibited high expression of IL-33 in lung tissues. Interestingly, the data showed that ST2L (membrane form) was highly accumulated in the membrane fraction of lung tissue in the PC10 group, but the ST2L in cytosol was dramatically decreased in the PC10 group. Conversely, the sST2 (soluble form) was slightly decreased both in the membrane and cytosol fractions in the PC10 group compared to the control group. In conclusion, these results demonstrated that ST2L translocation from the cytosol to the cell membranes of lung tissue and the down-expression of sST2 in both fractions can function as new biomarkers of VILI. Moreover, IL-33/ST2 signaling activated by mechanically responsive lung injury may potentially serve as a new therapy target.
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30
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Sutherasan Y, D'Antini D, Pelosi P. Advances in ventilator-associated lung injury: prevention is the target. Expert Rev Respir Med 2014; 8:233-48. [PMID: 24601663 DOI: 10.1586/17476348.2014.890519] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/05/2023]
Abstract
Mechanical ventilation (MV) is the main supportive treatment in respiratory failure due to different etiologies. However, MV might aggravate ventilator-associated lung injury (VALI). Four main mechanisms leading to VALI are: 1) increased stress and strain, induced by high tidal volume (VT); 2) increased shear stress, i.e. opening and closing, of previously atelectatic alveolar units; 3) distribution of perfusion and 4) biotrauma. In severe acute respiratory distress syndrome patients, low VT, higher levels of positive end expiratory pressure, long duration prone position and neuromuscular blockade within the first 48 hours are associated to a better outcome. VALI can also occur by using high VT in previously non injured lungs. We believe that prevention is the target to minimize injurious effects of MV. This review aims to describe pathophysiology of VALI, the possible prevention and treatment as well as monitoring MV to minimize VALI.
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Affiliation(s)
- Yuda Sutherasan
- Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, IRCCS San Martino - IST, Genoa, Italy
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31
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Abstract
PURPOSE OF REVIEW This review discusses our present understanding of postoperative respiratory failure (PRF) pathogenesis, risk factors, and perioperative-risk reduction strategies. RECENT FINDINGS PRF, the most frequent postoperative pulmonary complication, is defined by impaired blood gas exchange appearing after surgery. PRF leads to longer hospital stays and higher mortality. The time frame for recognizing when respiratory failure is related to the surgical-anesthetic insult remains imprecise, however, and researchers have used different clinical events instead of blood gas measures to define the outcome. Still, studies in specific surgical populations or large patient samples have identified a range of predictors of PRF risk: type of surgery and comorbidity, mechanical ventilation, and multiple hits to the lung have been found to be relevant in most of these studies. Recently, risk-scoring systems for PRF have been developed and are being applied in new controlled trials of PRF-risk reduction measures. Current evidence favors carefully managing intraoperative ventilator use and fluids, reducing surgical aggression, and preventing wound infection and pain. SUMMARY PRF is a life-threatening event that is challenging for the surgical team. Risk prediction scales based on large population studies are being developed and validated. We need high-quality trials of preventive measures, particularly those related to ventilator use in both high risk and general populations.
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Aissaoui Y, En-Nafaa I, Chkoura K, Boughalem M, Kamili ND. [Pneumomediastinum: an aspect of pulmonary barotrauma during mechanical ventilation of acute respiratory distress syndrome]. REVUE DE PNEUMOLOGIE CLINIQUE 2014; 70:177-180. [PMID: 24646783 DOI: 10.1016/j.pneumo.2013.09.010] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 06/08/2013] [Revised: 09/24/2013] [Accepted: 09/29/2013] [Indexed: 06/03/2023]
Abstract
Mechanical ventilation is a fundamental treatment of acute respiratory distress syndrome (ARDS). Despite compliance with the recommendations of protective mechanical ventilation, it can results in serious complications including the pulmonary barotrauma. This is often manifested by a pneumothorax. This observation describes an unusual aspect of barotrauma which is pneumomediastinum. The authors also point out the role of chest imaging in the management of mechanical ventilation during ARDS.
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Affiliation(s)
- Y Aissaoui
- Pôle anesthésie réanimation, hôpital militaire Avicenne, université Cadi Ayyad, faculté de médecine et de pharmacie, 40010 Marrakech, Maroc.
| | - I En-Nafaa
- Service d'imagerie médicale, hôpital militaire d'instruction Mohammed V, université Mohammed V-Souissi, faculté de médecine et de pharmacie, 10045 Rabat, Maroc
| | - K Chkoura
- Pôle anesthésie réanimation, hôpital militaire d'instruction Mohammed V, université Mohammed V-Souissi, faculté de médecine et de pharmacie, 10045 Rabat, Maroc
| | - M Boughalem
- Pôle anesthésie réanimation, hôpital militaire Avicenne, université Cadi Ayyad, faculté de médecine et de pharmacie, 40010 Marrakech, Maroc
| | - N Drissi Kamili
- Pôle anesthésie réanimation, hôpital militaire d'instruction Mohammed V, université Mohammed V-Souissi, faculté de médecine et de pharmacie, 10045 Rabat, Maroc
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Duru J, Menges T, Bodner J, Degen M, Greifenberg D, Gehron J, Weigand M, Henrich M. Wach-ECMO-Therapie bei Atemwegsstenose. Anaesthesist 2014; 63:401-5. [DOI: 10.1007/s00101-014-2308-9] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/01/2013] [Revised: 01/10/2014] [Accepted: 01/31/2014] [Indexed: 11/28/2022]
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Whitehouse T, Wendon J. Acute liver failure. Best Pract Res Clin Gastroenterol 2013; 27:757-69. [PMID: 24160932 DOI: 10.1016/j.bpg.2013.08.010] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/16/2013] [Revised: 08/01/2013] [Accepted: 08/11/2013] [Indexed: 01/31/2023]
Abstract
Untreated acute liver failure (ALF) has a poor outcome and so rapid diagnosis and management is vital if the patient is to survive. ALF has such profound and widespread physiological consequences that whenever possible, patients with ALF should be managed in an intensive care unit. Management is to support the physiology and treat the underlying cause. Advice should be sought from a centre capable of performing liver transplantation. Should recovery seem unlikely, liver transplantation is a viable treatment option in some cases.
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Affiliation(s)
- Tony Whitehouse
- University Hospital Birmingham, Edgbaston, Birmingham B15 2WB, UK.
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