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1.
Crit Care ; 26(1): 252, 2022 08 22.
Article in English | MEDLINE | ID: mdl-35996150

ABSTRACT

Pulmonary microbial diversity may be influenced by biotic or abiotic conditions (e.g., disease, smoking, invasive mechanical ventilation (MV), etc.). Specially, invasive MV may trigger structural and physiological changes in both tissue and microbiota of lung, due to gastric and oral microaspiration, altered body posture, high O2 inhalation-induced O2 toxicity in hypoxemic patients, impaired airway clearance and ventilator-induced lung injury (VILI), which in turn reduce the diversity of the pulmonary microbiota and may ultimately lead to poor prognosis. Furthermore, changes in (local) O2 concentration can reduce the diversity of the pulmonary microbiota by affecting the local immune microenvironment of lung. In conclusion, systematic literature studies have found that invasive MV reduces pulmonary microbiota diversity, and future rational regulation of pulmonary microbiota diversity by existing or novel clinical tools (e.g., lung probiotics, drugs) may improve the prognosis of invasive MV treatment and lead to more effective treatment of lung diseases with precision.


Subject(s)
Lung , Microbiota , Respiration, Artificial , Humans , Lung/microbiology , Respiration, Artificial/adverse effects , Ventilator-Induced Lung Injury/epidemiology
2.
Crit Care ; 25(1): 44, 2021 02 02.
Article in English | MEDLINE | ID: mdl-33531078

ABSTRACT

BACKGROUND: Ventilator-associated pneumonia (VAP) is the most common hospital-acquired infection (HAI) in intensive care units (ICUs). Ventilator-associated event (VAE), a more objective definition, has replaced traditional VAP surveillance and is now widely used in the USA. However, the adoption outside the USA is limited. This study aims to describe the epidemiology and clinical outcomes of VAEs in China, based on a prospectively maintained registry. METHODS: An observational study was conducted using an ICU-HAI registry in west China. Patients that were admitted to ICUs and underwent mechanical ventilation (MV) between April 1, 2015, and December 31, 2018, were included. The characteristics and outcomes were compared between patients with and without VAEs. The rates of all VAEs dependent on different ICUs were calculated, and the pathogen distribution of patients with possible VAP (PVAP) was described. RESULTS: A total of 20,769 ICU patients received MV, accounting for 21,723 episodes of mechanical ventilators and 112,697 ventilator-days. In all, we identified 1882 episodes of ventilator-associated condition (VAC) events (16.7 per 1000 ventilator-days), 721 episodes of infection-related ventilator-associated complications (IVAC) events (6.4 per 1000 ventilator-days), and 185 episodes of PVAP events (1.64 per 1000 ventilator-days). The rates of VAC varied across ICUs with the highest incidence in surgical ICUs (23.72 per 1000 ventilator-days). The median time from the start of ventilation to the onset of the first VAC, IVAC, and PVAP was 5 (3-8), 5 (3-9), and 6 (4-13) days, respectively. The median length of hospital stays was 28.00 (17.00-43.00), 30.00 (19.00-44.00), and 30.00 (21.00-46.00) days for the three VAE tiers, which were all longer than that of patients without VAEs (16.00 [12.00-23.00]). The hospital mortality among patients with VAEs was more than three times of those with non-VAEs. CONCLUSIONS: VAE was common in ICU patients with ≥ 4 ventilator days. All tiers of VAEs were highly correlated with poor clinical outcomes, including longer ICU and hospital stays and increased risk of mortality. These findings highlight the importance of VAE surveillance and the development of new strategies to prevent VAEs.


Subject(s)
Intensive Care Units/statistics & numerical data , Outcome Assessment, Health Care/statistics & numerical data , Respiration, Artificial/adverse effects , Adolescent , Adult , Aged , Aged, 80 and over , China/epidemiology , Female , Hospital Mortality/trends , Humans , Intensive Care Units/organization & administration , Male , Middle Aged , Pneumonia, Ventilator-Associated/epidemiology , Pneumonia, Ventilator-Associated/mortality , Registries/statistics & numerical data , Respiration, Artificial/methods , Respiration, Artificial/trends , Ventilator-Induced Lung Injury/epidemiology , Ventilator-Induced Lung Injury/mortality
3.
Br J Anaesth ; 127(3): 353-364, 2021 09.
Article in English | MEDLINE | ID: mdl-34217468

ABSTRACT

COVID-19 pneumonia is associated with hypoxaemic respiratory failure, ranging from mild to severe. Because of the worldwide shortage of ICU beds, a relatively high number of patients with respiratory failure are receiving prolonged noninvasive respiratory support, even when their clinical status would have required invasive mechanical ventilation. There are few experimental and clinical data reporting that vigorous breathing effort during spontaneous ventilation can worsen lung injury and cause a phenomenon that has been termed patient self-inflicted lung injury (P-SILI). The aim of this narrative review is to provide an overview of P-SILI pathophysiology and the role of noninvasive respiratory support in COVID-19 pneumonia. Respiratory mechanics, vascular compromise, viscoelastic properties, lung inhomogeneity, work of breathing, and oesophageal pressure swings are discussed. The concept of P-SILI has been widely investigated in recent years, but controversies persist regarding its mechanisms. To minimise the risk of P-SILI, intensivists should better understand its underlying pathophysiology to optimise the type of noninvasive respiratory support provided to patients with COVID-19 pneumonia, and decide on the optimal timing of intubation for these patients.


Subject(s)
Acute Lung Injury/epidemiology , Acute Lung Injury/therapy , Anesthesiologists , COVID-19 , Noninvasive Ventilation , Respiration, Artificial , Ventilator-Induced Lung Injury/epidemiology , Ventilator-Induced Lung Injury/therapy , Humans , Noninvasive Ventilation/adverse effects , Positive-Pressure Respiration/adverse effects , Respiratory Insufficiency , Respiratory Mechanics
4.
Crit Care ; 24(1): 73, 2020 Mar 04.
Article in English | MEDLINE | ID: mdl-32131872

ABSTRACT

INTRODUCTION: Patient safety and critical care quality remain a challenging issue in the ICU. However, the effects of the national quality improvement (QI) program remain unknown in China. METHODS: A national ICU QI program was implemented in a controlled cohort of 586 hospitals from 2016 to 2018. The effects of the QI program on critical care quality were comprehensively investigated. MAIN RESULTS: A total of 81,461,554 patients were enrolled in 586 hospitals, and 1,587,724 patients were admitted to the ICU over 3 years. In 2018, there was a significantly higher number of ICU beds (2016 vs. 2018: 10668 vs. 13,661, P = 0.0132) but a lower doctor-to-bed ratio (2016 vs. 2018: 0.64 (0.50, 0.83) vs. 0.60 (0.45, 0.75), P = 0.0016) and nurse-to-bed ratio (2016 vs. 2018: 2.00 (1.64, 2.50) vs. 2.00 (1.50, 2.40), P = 0.031) than in 2016. Continuous and significant improvements in the ventilator-associated pneumonia (VAP) incidence rate, microbiology detection rate before antibiotic use and deep vein thrombosis (DVT) prophylaxis rate were associated with the implementation of the QI program (VAP incidence rate (per 1000 ventilator-days), 2016 vs. 2017 vs. 2018: 11.06 (4.23, 22.70) vs. 10.20 (4.25, 23.94) vs. 8.05 (3.13, 17.37), P = 0.0002; microbiology detection rate before antibiotic use (%), 2016 vs. 2017 vs. 2018: 83.91 (49.75, 97.87) vs. 84.14 (60.46, 97.24) vs. 90.00 (69.62, 100), P < 0.0001; DVT prophylaxis rate, 2016 vs. 2017 vs. 2018: 74.19 (33.47, 96.16) vs. 71.70 (38.05, 96.28) vs. 83.27 (47.36, 97.77), P = 0.0093). Moreover, the 6-h SSC bundle compliance rates in 2018 were significantly higher than those in 2016 (6-h SSC bundle compliance rate, 2016 vs. 2018: 64.93 (33.55, 93.06) vs. 76.19 (46.88, 96.67)). A significant change trend was not found in the ICU mortality rate from 2016 to 2018 (ICU mortality rate (%), 2016 vs. 2017 vs. 2018: 8.49 (4.42, 14.82) vs. 8.95 (4.89, 15.70) vs. 9.05 (5.12, 15.80), P = 0.1075). CONCLUSIONS: The relationship between medical human resources and ICU overexpansion was mismatched during the past 3 years. The implementation of a national QI program improved ICU performance but did not reduce ICU mortality.


Subject(s)
Intensive Care Units/standards , Quality Improvement/trends , China/epidemiology , Cohort Studies , Cross Infection/epidemiology , Cross Infection/prevention & control , Hospitals/standards , Hospitals/statistics & numerical data , Humans , Intensive Care Units/organization & administration , Intensive Care Units/statistics & numerical data , Quality Indicators, Health Care/statistics & numerical data , Ventilator-Induced Lung Injury/epidemiology , Ventilator-Induced Lung Injury/prevention & control
5.
Anesth Analg ; 129(1): 129-140, 2019 07.
Article in English | MEDLINE | ID: mdl-30222649

ABSTRACT

In patients with uninjured lungs, increasing evidence indicates that tidal volume (VT) reduction improves outcomes in the intensive care unit (ICU) and in the operating room (OR). However, the degree to which this evidence has translated to clinical changes in ventilator settings for patients with uninjured lungs is unknown. To clarify whether ventilator settings have changed, we searched MEDLINE, Cochrane Central Register of Controlled Trials, and Web of Science for publications on invasive ventilation in ICUs or ORs, excluding those on patients <18 years of age or those with >25% of patients with acute respiratory distress syndrome (ARDS). Our primary end point was temporal change in VT over time. Secondary end points were changes in maximum airway pressure, mean airway pressure, positive end-expiratory pressure, inspiratory oxygen fraction, development of ARDS (ICU studies only), and postoperative pulmonary complications (OR studies only) determined using correlation analysis and linear regression. We identified 96 ICU and 96 OR studies comprising 130,316 patients from 1975 to 2014 and observed that in the ICU, VT size decreased annually by 0.16 mL/kg (-0.19 to -0.12 mL/kg) (P < .001), while positive end-expiratory pressure increased by an average of 0.1 mbar/y (0.02-0.17 mbar/y) (P = .017). In the OR, VT size decreased by 0.09 mL/kg per year (-0.14 to -0.04 mL/kg per year) (P < .001). The change in VTs leveled off in 1995. Other intraoperative ventilator settings did not change in the study period. Incidences of ARDS (ICU studies) and postoperative pulmonary complications (OR studies) also did not change over time. We found that, during a 39-year period, from 1975 to 2014, VTs in clinical studies on mechanical ventilation have decreased significantly in the ICU and in the OR.


Subject(s)
Lung/physiology , Respiration, Artificial/instrumentation , Respiratory Distress Syndrome/prevention & control , Tidal Volume , Ventilator-Induced Lung Injury/prevention & control , Ventilators, Mechanical , Humans , Incidence , Respiration, Artificial/adverse effects , Respiration, Artificial/trends , Respiratory Distress Syndrome/epidemiology , Respiratory Distress Syndrome/physiopathology , Risk Factors , Time Factors , Ventilator-Induced Lung Injury/epidemiology , Ventilator-Induced Lung Injury/physiopathology , Ventilators, Mechanical/adverse effects , Ventilators, Mechanical/trends
6.
Br J Anaesth ; 121(4): 909-917, 2018 Oct.
Article in English | MEDLINE | ID: mdl-30236253

ABSTRACT

BACKGROUND: Emergency abdominal surgery is associated with a high risk of postoperative pulmonary complications (PPCs). The primary aim of this study was to determine whether patients undergoing emergency laparotomy are ventilated using a lung-protective ventilation strategy employing tidal volume ≤8 ml kg-1 ideal body weight-1, PEEP >5 cm H2O, and recruitment manoeuvres. The secondary aim was to investigate the association between ventilation factors (lung-protective ventilation strategy, intraoperative FiO2, and peak inspiratory pressure) and the occurrence of PPCs. METHODS: Data were collected prospectively in 28 hospitals across London as part of routine National Emergency Laparotomy Audit (NELA). Patients were followed for 7 days. Complications were defined according to the European Perioperative Clinical Outcome definition. RESULTS: Data were collected from 568 patients. The median [inter-quartile range (IQR)] tidal volume observed was 500 ml (450-540 ml), corresponding to a median tidal volume of 8 ml kg-1 ideal body weight-1 (IQR: 7.2-9.1 ml). A lung-protective ventilation strategy was employed in 4.9% (28/568) of patients, and was not protective against the occurrence of PPCs in the multivariable analysis (hazard ratio=1.06; P=0.69). Peak inspiratory pressure of <30 cm H2O was protective against development of PPCs (hazard ratio=0.46; confidence interval: 0.30-0.72; P=0.001). Median FiO2 was 0.5 (IQR: 0.44-0.53), and an increase in FiO2 by 5% increased the risk of developing a PPC by 8% (2.6-14.1%; P=0.008). CONCLUSIONS: Both intraoperative peak inspiratory pressure and FiO2 are independent factors significantly associated with development of a postoperative pulmonary complication in emergency laparotomy patients. Further studies are required to identify causality and to demonstrate if their manipulation could lead to better clinical outcomes.


Subject(s)
Laparotomy/adverse effects , Postoperative Complications/prevention & control , Respiration, Artificial/methods , Ventilator-Induced Lung Injury/prevention & control , Adult , Aged , Emergency Medical Services , Female , Humans , Inspiratory Capacity , London , Male , Middle Aged , Oxygen/blood , Positive-Pressure Respiration , Postoperative Complications/epidemiology , Prospective Studies , Tidal Volume , Ventilator-Induced Lung Injury/epidemiology
7.
Crit Care Med ; 45(8): e831-e839, 2017 Aug.
Article in English | MEDLINE | ID: mdl-28426531

ABSTRACT

OBJECTIVE: Obesity has a complex impact on acute respiratory distress syndrome patients, being associated with increased likelihood of developing the syndrome but reduced likelihood of dying. We propose that such observations are potentially explained by a model in which obesity influences the iatrogenic injury that occurs subsequent to intensive care admission. This study therefore investigated whether fat feeding protected mice from ventilator-induced lung injury. DESIGN: In vivo study. SETTING: University research laboratory. SUBJECTS: Wild-type C57Bl/6 mice or tumor necrosis factor receptor 2 knockout mice, either fed a high-fat diet for 12-14 weeks, or age-matched lean controls. INTERVENTIONS: Anesthetized mice were ventilated with injurious high tidal volume ventilation for periods up to 180 minutes. MEASUREMENTS AND MAIN RESULTS: Fat-fed mice showed clear attenuation of ventilator-induced lung injury in terms of respiratory mechanics, blood gases, and pulmonary edema. Leukocyte recruitment and activation within the lungs were not significantly attenuated nor were a host of circulating or intra-alveolar inflammatory cytokines. However, intra-alveolar matrix metalloproteinase activity and levels of the matrix metalloproteinase cleavage product soluble receptor for advanced glycation end products were significantly attenuated in fat-fed mice. This was associated with reduced stretch-induced CD147 expression on lung epithelial cells. CONCLUSIONS: Consumption of a high-fat diet protects mice from ventilator-induced lung injury in a manner independent of neutrophil recruitment, which we postulate instead arises through blunted up-regulation of CD147 expression and subsequent activation of intra-alveolar matrix metalloproteinases. These findings may open avenues for therapeutic manipulation in acute respiratory distress syndrome and could have implications for understanding the pathogenesis of lung disease in obese patients.


Subject(s)
Diet, High-Fat , Obesity/physiopathology , Ventilator-Induced Lung Injury/prevention & control , Ventilator-Induced Lung Injury/physiopathology , Animals , Blood Gas Analysis , Cytokines/metabolism , Matrix Metalloproteinases/metabolism , Mice , Mice, Inbred C57BL , Mice, Knockout , Neutrophil Infiltration/physiology , Neutrophils/metabolism , Obesity/epidemiology , Pulmonary Edema/physiopathology , Pulmonary Edema/prevention & control , Respiratory Mechanics , Tidal Volume , Ventilator-Induced Lung Injury/epidemiology
8.
Curr Opin Anaesthesiol ; 30(1): 36-41, 2017 Feb.
Article in English | MEDLINE | ID: mdl-27941354

ABSTRACT

PURPOSE OF REVIEW: Ventilator-induced lung injury is a major contributor to perioperative lung injury. The end-expiratory lung volume, regional lung overdistension, and tidal recruitment are known to be the main factors causing subsequent alveolar damage and inflammation. The alveolar-capillary membrane including the endothelial glycocalyx as an integral part of the vascular endothelium seems to play a major role in different kinds of lung injury. RECENT FINDINGS: Recent studies underline the pivotal importance of the endothelial glycocalyx in lung injury. The glycocalyx regulates and modulates plasma endothelial cell interactions. Several triggers are known to deteriorate the gylcocalyx such as fluid overload, ischemia, and TRALI. The clinical manifestation is inflammation, capillary leak, and edema formation. Breakdown of the endothelial gylcocalyx is of gaining importance in the context of one-lung ventilation, known to be a major risk factor for postoperative lung injury. Studies suggest that volatile anesthetics may have a protective influence on the endothelial glycocalyx of pulmonary capillaries and reduce ischemia-reperfusion injury. This might be of clinical relevance for postoperative outcome. SUMMARY: This review focuses on the involvement of the pulmonary endothelial glycocalyx in the context of perioperative lung injury. The pathophysiological mechanisms and trigger factors of glycocalyx deterioration are discussed, and prevention strategies are taken into consideration.


Subject(s)
Endothelium/injuries , Glycocalyx/pathology , Lung/pathology , Respiration, Artificial/adverse effects , Ventilator-Induced Lung Injury/pathology , Capillary Permeability , Endothelium/blood supply , Endothelium/cytology , Humans , Incidence , Lung/blood supply , Lung/cytology , Perioperative Period , Postoperative Complications/epidemiology , Postoperative Complications/etiology , Postoperative Complications/pathology , Postoperative Complications/prevention & control , Respiration, Artificial/methods , Ventilator-Induced Lung Injury/epidemiology , Ventilator-Induced Lung Injury/etiology , Ventilator-Induced Lung Injury/prevention & control
9.
Crit Care Med ; 44(8): e678-88, 2016 08.
Article in English | MEDLINE | ID: mdl-27002273

ABSTRACT

OBJECTIVES: We recently described how spontaneous effort during mechanical ventilation can cause "pendelluft," that is, displacement of gas from nondependent (more recruited) lung to dependent (less recruited) lung during early inspiration. Such transfer depends on the coexistence of more recruited (source) liquid-like lung regions together with less recruited (target) solid-like lung regions. Pendelluft may improve gas exchange, but because of tidal recruitment, it may also contribute to injury. We hypothesize that higher positive end-expiratory pressure levels decrease the propensity to pendelluft and that with lower positive end-expiratory pressure levels, pendelluft is associated with improved gas exchange but increased tidal recruitment. DESIGN: Crossover design. SETTING: University animal research laboratory. SUBJECTS: Anesthetized landrace pigs. INTERVENTIONS: Surfactant depletion was achieved by saline lavage in anesthetized pigs, and ventilator-induced lung injury was produced by ventilation with high tidal volume and low positive end-expiratory pressure. Ventilation was continued in each of four conditions: positive end-expiratory pressure (low or optimized positive end-expiratory pressure after recruitment) and spontaneous breathing (present or absent). Tidal recruitment was assessed using dynamic CT and regional ventilation/perfusion using electric impedance tomography. Esophageal pressure was measured using an esophageal balloon manometer. MEASUREMENTS AND RESULTS: Among the four conditions, spontaneous breathing at low positive end-expiratory pressure not only caused the largest degree of pendelluft, which was associated with improved ventilation/perfusion matching and oxygenation, but also generated the greatest tidal recruitment. At low positive end-expiratory pressure, paralysis worsened oxygenation but reduced tidal recruitment. Optimized positive end-expiratory pressure decreased the magnitude of spontaneous efforts (measured by esophageal pressure) despite using less sedation, from -5.6 ± 1.3 to -2.0 ± 0.7 cm H2O, while concomitantly reducing pendelluft and tidal recruitment. No pendelluft was observed in the absence of spontaneous effort. CONCLUSIONS: Spontaneous effort at low positive end-expiratory pressure improved oxygenation but promoted tidal recruitment associated with pendelluft. Optimized positive end-expiratory pressure (set after lung recruitment) may reverse the harmful effects of spontaneous breathing by reducing inspiratory effort, pendelluft, and tidal recruitment.


Subject(s)
Respiration, Artificial/adverse effects , Respiration, Artificial/methods , Ventilator-Induced Lung Injury/epidemiology , Animals , Female , Lung/physiopathology , Positive-Pressure Respiration/methods , Pulmonary Gas Exchange/physiology , Pulmonary Surfactants/metabolism , Respiratory Distress Syndrome , Respiratory Mechanics/physiology , Swine , Tidal Volume
10.
Crit Care Med ; 43(5): 937-46, 2015 May.
Article in English | MEDLINE | ID: mdl-25746744

ABSTRACT

OBJECTIVE: Although all definitions of acute respiratory distress syndrome use some measure of hypoxemia, neither the Berlin definition nor recently proposed pediatric-specific definitions proposed by the Pediatric Acute Lung Injury Consensus Conference utilizing oxygenation index specify which PaO2/FIO2 or oxygenation index best categorizes lung injury. We aimed to identify variables associated with mortality and ventilator-free days at 28 days in a large cohort of children with acute respiratory distress syndrome. DESIGN: Prospective, observational, single-center study. SETTING: Tertiary care, university-affiliated PICU. PATIENTS: Two-hundred eighty-three invasively ventilated children with the Berlin-defined acute respiratory distress syndrome. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Between July 1, 2011, and June 30, 2014, 283 children had acute respiratory distress syndrome with 37 deaths (13%) at the Children's Hospital of Philadelphia. Neither initial PaO2/FO2 nor oxygenation index at time of meeting acute respiratory distress syndrome criteria discriminated mortality. However, 24 hours after, both PaO2/FIO2 and oxygenation index discriminated mortality (area under receiver operating characteristic curve, 0.68 [0.59-0.77] and 0.66 [0.57-0.75]; p < 0.001). PaO2/FIO2 at 24 hours categorized severity of lung injury, with increasing mortality rates of 5% (PaO2/FIO2, > 300), 8% (PaO2/FIO2, 201-300), 18% (PaO2/FIO2, 101-200), and 37% (PaO2/FIO2, ≤ 100) across worsening Berlin categories. This trend with 24-hour PaO2/FIO2 was seen for ventilator-free days (22, 19, 14, and 0 ventilator-free days across worsening Berlin categories; p < 0.001) and duration of ventilation in survivors (6, 9, 13, and 24 d across categories; p < 0.001). Similar results were obtained with 24-hour oxygenation index. CONCLUSIONS: PaO2/FIO2 and oxygenation index 24 hours after meeting acute respiratory distress syndrome criteria accurately stratified outcomes in children. Initial values were not helpful for prognostication. Definitions of acute respiratory distress syndrome may benefit from addressing timing of oxygenation metrics to stratify disease severity.


Subject(s)
Intensive Care Units, Pediatric/statistics & numerical data , Respiratory Distress Syndrome/mortality , Respiratory Distress Syndrome/therapy , Ventilator-Induced Lung Injury/epidemiology , Blood Gas Analysis , Child , Child, Preschool , Female , Hospitals, University , Humans , Infant , Male , Predictive Value of Tests , Prognosis , Prospective Studies , Respiratory Function Tests , Risk Factors
11.
Curr Opin Crit Care ; 20(1): 3-9, 2014 Feb.
Article in English | MEDLINE | ID: mdl-24309954

ABSTRACT

PURPOSE OF REVIEW: The purpose of this review is to examine and discuss the incidence and outcome of patients with the acute respiratory distress syndrome (ARDS). This is a challenging task, as there is no specific clinical sign or diagnostic test that accurately identifies and adequately defines this syndrome. RECENT FINDINGS: This review will focus on published epidemiological studies reporting population-based incidence of ARDS, as defined by the American-European Consensus Conference criteria. In addition, the current outcome figures for ARDS patients reported in observational and randomized controlled trials will be reviewed. The focus will be on studies published since 2000, when the ARDSnet study on protective mechanical ventilation was published, although particular emphasis will be on those articles published in the last 24 months. SUMMARY: On the basis of current evidence, and despite the order of magnitude of reported European and USA incidence figures, it seems that the incidence and overall mortality of ARDS has not changed substantially since the original ARDSnet study. The current mortality of adult ARDS is still greater than 40%.


Subject(s)
Critical Care , Respiration, Artificial/methods , Respiratory Distress Syndrome/epidemiology , Ventilator-Induced Lung Injury/epidemiology , Adult , Europe/epidemiology , Female , Humans , Incidence , Male , Outcome Assessment, Health Care , Randomized Controlled Trials as Topic , Respiration, Artificial/adverse effects , Respiratory Distress Syndrome/diagnosis , Respiratory Distress Syndrome/mortality , Respiratory Distress Syndrome/therapy , Sepsis/mortality , United States/epidemiology , Ventilator-Induced Lung Injury/mortality , Ventilator-Induced Lung Injury/prevention & control
12.
Crit Care Med ; 41(11): 2467-75, 2013 Nov.
Article in English | MEDLINE | ID: mdl-24162674

ABSTRACT

OBJECTIVE: To develop and implement an objective, reliable approach to surveillance for ventilator-associated events in adult patients. DESIGN: The Centers for Disease Control and Prevention (CDC) convened a Ventilator-Associated Pneumonia (VAP) Surveillance Definition Working Group in September 2011. Working Group members included representatives of stakeholder societies and organizations and federal partners. MAIN RESULTS: The Working Group finalized a three-tier, adult surveillance definition algorithm for ventilator-associated events. The algorithm uses objective, readily available data elements and can identify a broad range of conditions and complications occurring in mechanically ventilated adult patients, including but not limited to VAP. The first tier definition, ventilator-associated condition (VAC), identifies patients with a period of sustained respiratory deterioration following a sustained period of stability or improvement on the ventilator, defined by changes in the daily minimum fraction of inspired oxygen or positive end-expiratory pressure. The second tier definition, infection-related ventilator-associated complication (IVAC), requires that patients with VAC also have an abnormal temperature or white blood cell count, and be started on a new antimicrobial agent. The third tier definitions, possible and probable VAP, require that patients with IVAC also have laboratory and/or microbiological evidence of respiratory infection. CONCLUSIONS: Ventilator-associated events surveillance was implemented in January 2013 in the CDC's National Healthcare Safety Network. Modifications to improve surveillance may be made as additional data become available and users gain experience with the new definitions.


Subject(s)
Algorithms , Intensive Care Units , Population Surveillance/methods , Respiration, Artificial/adverse effects , Ventilator-Induced Lung Injury/epidemiology , Centers for Disease Control and Prevention, U.S. , Humans , Patient Safety , Pneumonia, Ventilator-Associated/epidemiology , United States
13.
Crit Care ; 15(2): 206, 2011 Mar 11.
Article in English | MEDLINE | ID: mdl-21457528

ABSTRACT

Diaphragmatic function is a major determinant of the ability to successfully wean patients from mechanical ventilation. However, the use of controlled mechanical ventilation in animal models results in a major reduction of diaphragmatic force-generating capacity together with structural injury and atrophy of diaphragm muscle fibers, a condition termed ventilator-induced diaphragmatic dysfunction (VIDD). Increased oxidative stress and exaggerated proteolysis in the diaphragm have been linked to the development of VIDD in animal models, but much less is known about the extent to which these phenomena occur in humans undergoing mechanical ventilation in the ICU. In the present review, we first briefly summarize the large body of evidence demonstrating the existence of VIDD in animal models, and outline the major cellular mechanisms that have been implicated in this process. We then relate these findings to very recently published data in critically ill patients, which have thus far been found to exhibit a remarkable degree of similarity with the animal model data. Hence, the human studies to date have indicated that mechanical ventilation is associated with increased oxidative stress, atrophy, and injury of diaphragmatic muscle fibers along with a rapid loss of diaphragmatic force production. These changes are, to a large extent, directly proportional to the duration of mechanical ventilation. In the context of these human data, we also review the methods that can be used in the clinical setting to diagnose and/or monitor the development of VIDD in critically ill patients. Finally, we discuss the potential for using different mechanical ventilation strategies and pharmacological approaches to prevent and/or to treat VIDD and suggest promising avenues for future research in this area.


Subject(s)
Diaphragm/injuries , Diaphragm/physiopathology , Disease Models, Animal , Respiration, Artificial/adverse effects , Animals , Clinical Trials as Topic/methods , Critical Illness/epidemiology , Critical Illness/therapy , Humans , Intensive Care Units , Ventilator Weaning/adverse effects , Ventilator Weaning/methods , Ventilator-Induced Lung Injury/epidemiology , Ventilator-Induced Lung Injury/physiopathology
14.
Crit Care ; 15(2): 304, 2011 Apr 07.
Article in English | MEDLINE | ID: mdl-21489320

ABSTRACT

Ventilator-induced lung injury (VILI) consists of tissue damage and a biological response resulting from the application of inappropriate mechanical forces to the lung parenchyma. The current paradigm attributes VILI to overstretching due to very high-volume ventilation (volutrauma) and cyclic changes in aeration due to very low-volume ventilation (atelectrauma); however, this model cannot explain some research findings. In the present review, we discuss the relevance of cyclic deformation of lung tissue as the main determinant of VILI. Parenchymal stability resulting from the interplay of respiratory parameters such as tidal volume, positive end-expiratory pressure or respiratory rate can explain the results of different clinical trials and experimental studies that do not fit with the classic volutrauma/atelectrauma model. Focusing on tissue deformation could lead to new bedside monitoring and ventilatory strategies.


Subject(s)
Lung/pathology , Lung/physiology , Respiratory Distress Syndrome/therapy , Ventilator-Induced Lung Injury/physiopathology , Animals , Clinical Trials as Topic/methods , Humans , Positive-Pressure Respiration/adverse effects , Positive-Pressure Respiration/methods , Respiratory Distress Syndrome/epidemiology , Respiratory Distress Syndrome/physiopathology , Tidal Volume/physiology , Ventilator-Induced Lung Injury/diagnosis , Ventilator-Induced Lung Injury/epidemiology
15.
Respir Care ; 56(9): 1298-311; discussion 1311-3, 2011 Sep.
Article in English | MEDLINE | ID: mdl-21944682

ABSTRACT

Although the trend in the neonatal intensive care unit is to use noninvasive ventilation whenever possible, invasive ventilation is still often necessary for supporting pre-term neonates with lung disease. Many different ventilation modes and ventilation strategies are available to assist with the optimization of mechanical ventilation and prevention of ventilator-induced lung injury. Patient-triggered ventilation is favored over machine-triggered forms of invasive ventilation for improving gas exchange and patient-ventilator interaction. However, no studies have shown that patient-triggered ventilation improves mortality or morbidity in premature neonates. A promising new form of patient-triggered ventilation, neurally adjusted ventilatory assist (NAVA), was recently FDA approved for invasive and noninvasive ventilation. Clinical trials are underway to evaluate outcomes in neonates who receive NAVA. New evidence suggests that volume-targeted ventilation modes (ie, volume control or pressure control with adaptive targeting) may provide better lung protection than traditional pressure control modes. Several volume-targeted modes that provide accurate tidal volume delivery in the face of a large endotracheal tube leak were recently introduced to the clinical setting. There is ongoing debate about whether neonates should be managed invasively with high-frequency ventilation or conventional ventilation at birth. The majority of clinical trials performed to date have compared high-frequency ventilation to pressure control modes. Future trials with premature neonates should compare high-frequency ventilation to conventional ventilation with volume-targeted modes. Over the last decade many new promising approaches to lung-protective ventilation have evolved. The key to protecting the neonatal lung during mechanical ventilation is optimizing lung volume and limiting excessive lung expansion, by applying appropriate PEEP and using shorter inspiratory time, smaller tidal volume (4-6 mL/kg), and permissive hypercapnia. This paper reviews new and established neonatal ventilation modes and strategies and evaluates their impact on neonatal outcomes.


Subject(s)
Infant, Premature, Diseases/therapy , Lung Diseases/therapy , Respiration, Artificial , Apnea/therapy , High-Frequency Ventilation , Humans , Infant, Newborn , Infant, Premature , Respiration, Artificial/methods , Respiratory Insufficiency/therapy , Ventilator-Induced Lung Injury/epidemiology , Ventilator-Induced Lung Injury/prevention & control
16.
Br J Hosp Med (Lond) ; 82(6): 1-9, 2021 Jun 02.
Article in English | MEDLINE | ID: mdl-34191558

ABSTRACT

Ventilatory support is vital for the management of severe forms of COVID-19. Non-invasive ventilation is often used in patients who do not meet criteria for intubation or when invasive ventilation is not available, especially in a pandemic when resources are limited. Despite non-invasive ventilation providing effective respiratory support for some forms of acute respiratory failure, data about its effectiveness in patients with viral-related pneumonia are inconclusive. Acute respiratory distress syndrome caused by severe acute respiratory syndrome-coronavirus 2 infection causes life-threatening respiratory failure, weakening the lung parenchyma and increasing the risk of barotrauma. Pulmonary barotrauma results from positive pressure ventilation leading to elevated transalveolar pressure, and in turn to alveolar rupture and leakage of air into the extra-alveolar tissue. This article reviews the literature regarding the use of non-invasive ventilation in patients with acute respiratory failure associated with COVID-19 and other epidemic or pandemic viral infections and the related risk of barotrauma.


Subject(s)
Barotrauma/epidemiology , COVID-19/complications , COVID-19/therapy , Noninvasive Ventilation/adverse effects , Ventilator-Induced Lung Injury/epidemiology , Humans , Risk Assessment
20.
Burns ; 46(4): 762-770, 2020 06.
Article in English | MEDLINE | ID: mdl-31202528

ABSTRACT

OBJECTIVE: Ventilation strategies aiming at prevention of ventilator-induced lung injury (VILI), including low tidal volumes (VT) and use of positive end-expiratory pressures (PEEP) are increasingly used in critically ill patients. It is uncertain whether ventilation practices changed in a similar way in burn patients. Our objective was to describe applied ventilator settings and their relation to development of VILI in burn patients. DATA SOURCES: Systematic search of the literature in PubMed and EMBASE using MeSH, EMTREE terms and keywords referring to burn or inhalation injury and mechanical ventilation. STUDY SELECTION: Studies reporting ventilator settings in adult or pediatric burn or inhalation injury patients receiving mechanical ventilation during the ICU stay. DATA EXTRACTION: Two authors independently screened abstracts of identified studies for eligibility and performed data extraction. DATA SYNTHESIS: The search identified 35 eligible studies. VT declined from 14 ml/kg in studies performed before to around 8 ml/kg predicted body weight in studies performed after 2006. Low-PEEP levels (<10 cmH2O) were reported in 70% of studies, with no changes over time. Peak inspiratory pressure (PIP) values above 35 cmH2O were frequently reported. Nevertheless, 75% of the studies conducted in the last decade used limited maximum airway pressures (≤35 cmH2O) compared to 45% of studies conducted prior to 2006. Occurrence of barotrauma, reported in 45% of the studies, ranged from 0 to 29%, and was more frequent in patients ventilated with higher compared to lower airway pressures. CONCLUSION: This systematic review shows noticeable trends of ventilatory management in burn patients that mirrors those in critically ill non-burn patients. Variability in available ventilator data precluded us from drawing firm conclusions on the association between ventilator settings and the occurrence of VILI in burn patients.


Subject(s)
Burns/therapy , Respiration, Artificial/trends , Ventilator-Induced Lung Injury/prevention & control , Barotrauma , Humans , Positive-Pressure Respiration/methods , Respiration, Artificial/methods , Smoke Inhalation Injury/therapy , Tidal Volume , Ventilator-Induced Lung Injury/epidemiology
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