scholarly journals Barotrauma in COVID-19 Patients

2022 ◽  
Author(s):  
Farahnaz Fallahian ◽  
Atabak Najafi ◽  
Arezoo Ahmadi
Keyword(s):  
Retrospective Study ◽  
Lung Injury ◽  
Host Response ◽  
Clinical Manifestations ◽  
Chest Imaging ◽  
Common Complication ◽  
Invasive Ventilation ◽  
Pulmonary Barotrauma ◽  
Ventilation Induced Lung Injury

Clinical manifestations of COVID 19 is still unknown. We performed this study to determine the occurrence of pulmonary barotrauma as a complication of this disease. In this retrospective study, a total of 955 COVID 19 patients with respiratory insufficiency requiring oxygen support or invasive ventilation admitted to ICU of Sina Hospital from 20 March 2020 to 9 June 2021, were included and their chest imaging reviewed. Here, we report results of chest imaging of first 92 patients of this group. Barotrauma (pneumothorax, pneumomediastinum, pneumopericardium) occurred in 11 (11.9%) of 92 patients with coronavirus disease 2019 (COVID-19) infection requiring ICU admission for respiratory support and monitoring. It seems barotrauma is a common complication of COVID 19 disease. The role of increased respiratory efforts, patient or ventilation induced lung injury, viral and host response should be assessed. It needs to consider the occurrence of barotrauma in Patients with COVID-19, before expansion of dead space for treatment and limiting the ventilation effects.

scholarly journals Emerging concepts in ventilation-induced lung injury

F1000Research ◽  
2020 ◽  
Vol 9 ◽  
pp. 222 ◽  
Author(s):  
Purnema Madahar ◽  
Jeremy R Beitler
Keyword(s):  
Lung Injury ◽  
Positive Pressure Ventilation ◽  
Clinical Importance ◽  
Positive Pressure ◽  
Mechanical Heterogeneity ◽  
Organ Failures ◽  
Clinically Significant ◽  
High Degree ◽  
Ventilation Induced Lung Injury

Ventilation-induced lung injury results from mechanical stress and strain that occur during tidal ventilation in the susceptible lung. Classical descriptions of ventilation-induced lung injury have focused on harm from positive pressure ventilation. However, injurious forces also can be generated by patient effort and patient–ventilator interactions. While the role of global mechanics has long been recognized, regional mechanical heterogeneity within the lungs also appears to be an important factor propagating clinically significant lung injury. The resulting clinical phenotype includes worsening lung injury and a systemic inflammatory response that drives extrapulmonary organ failures. Bedside recognition of ventilation-induced lung injury requires a high degree of clinical acuity given its indistinct presentation and lack of definitive diagnostics. Yet the clinical importance of ventilation-induced lung injury is clear. Preventing such biophysical injury remains the most effective management strategy to decrease morbidity and mortality in patients with acute respiratory distress syndrome and likely benefits others at risk.

Role of Cardiorespiratory Abnormalities, Smoking and Dive Characteristics in the Manifestations of Neurological Decompression Illness

1994 ◽  
Vol 86 (3) ◽  
pp. 297-303 ◽  
Author(s):  
Dr Peter Wilmshurst ◽  
Craig Davidson ◽  
Geraldine O'Connell ◽  
Christopher Byrne
Keyword(s):  
Clinical Manifestations ◽  
Paradoxical Embolism ◽  
Neurological Symptoms ◽  
Smoking History ◽  
Small Airways ◽  
Pulmonary Barotrauma ◽  
Nitrogen Loads ◽  
Significance Levels ◽  
Tissue Nitrogen

1. Blind analysis of contrast echocardiograms to detect intracardiac shunts, blind analysis of lung function tests for evidence of small airways disease, smoking history and dive characteristics were examined in an attempt to explain neurological symptoms that occurred within 5 min of surfacing from unprovocative dives. 2. Pulmonary abnormalities were significantly more frequent in those divers without intracardiac shunts (50%) than in those with shunts (0%). Smoking was more common in those divers without shunts (55% versus 15%), although this just failed to reach conventional significance levels. Divers without shunts experienced cerebral rather than spinal symptoms after significantly shallower dives with lower tissue nitrogen loads. Depths of dives, tissue nitrogen loads and clinical manifestations in those divers without shunts were similar to the findings in divers who had symptoms after rapid ascents. Despite conservative dive profiles, clinical manifestations in divers with shunts resembled those observed after missed decompression stops. 3. The findings suggest that occult lung disease, and probably smoking, increase the risk of neurological symptoms, even after unprovocative dives, and the similarity of the dive profiles and clinical manifestations to cases with rapid ascents suggest that pulmonary barotrauma and arterial gas embolism are responsible. In divers with intracardiac shunts the different dive profiles and clinical manifestations imply that there is another mechanism, involving different tissue and bubble nitrogen kinetics resulting in venous gas liberation and peripheral amplification in embolized tissues, rather than paradoxical embolism per se.

Aktuelle Konzepte zur Entstehung und Behandlung eines beatmungsinduzierten Lungenschadens

2020 ◽  
Vol 8 (4) ◽  
pp. 212-214
Author(s):  
Wolfgang Galetke
Keyword(s):  
Lung Injury ◽  
Positive Pressure Ventilation ◽  
Clinical Importance ◽  
Positive Pressure ◽  
Mechanical Heterogeneity ◽  
Organ Failures ◽  
Clinically Significant ◽  
High Degree ◽  
Ventilation Induced Lung Injury

Ventilation-induced lung injury results from mechanical stress and strain that occur during tidal ventilation in the susceptible lung. Classical descriptions of ventilation-induced lung injury have focused on harm from positive pressure ventilation. However, injurious forces also can be generated by patient effort and patient–ventilator interactions. While the role of global mechanics has long been recognized, regional mechanical heterogeneity within the lungs also appears to be an important factor propagating clinically significant lung injury. The resulting clinical phenotype includes worsening lung injury and a systemic inflammatory response that drives extrapulmonary organ failures. Bedside recognition of ventilation-induced lung injury requires a high degree of clinical acuity given its indistinct presentation and lack of definitive diagnostics. Yet the clinical importance of ventilation-induced lung injury is clear. Preventing such biophysical injury remains the most effective management strategy to decrease morbidity and mortality in patients with acute respiratory distress syndrome and likely benefits others at risk.

scholarly journals The Role of Cyclooxygenase-2 in Mechanical Ventilation–Induced Lung Injury

2012 ◽  
Vol 47 (3) ◽  
pp. 387-394 ◽  
Author(s):  
Joshua A. Robertson ◽  
David Sauer ◽  
Jeffrey A. Gold ◽  
Stephanie A. Nonas
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Cyclooxygenase 2 ◽  
Ventilation Induced Lung Injury

scholarly journals Citrullinated Histone H3 Mediates Sepsis-Induced Lung Injury Through Activating Caspase-1 Dependent Inflammasome Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Yuzi Tian ◽  
Patrick Li ◽  
Zhenyu Wu ◽  
Qiufang Deng ◽  
Baihong Pan ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Lung Injury ◽  
Host Response ◽  
Distress Syndrome ◽  
Histone H3 ◽  
Caspase 1 ◽  
Sepsis Model ◽  
Important Mediator ◽  
Life Threatening

Sepsis is a life-threatening organ dysfunction caused by dysregulated host response to infection that often results in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). An emerging mechanism of sepsis-induced ARDS involves neutrophils/macrophages undergoing cell death, releasing nuclear histones to cause tissue damage that exacerbates pulmonary injury. While published studies focus on unmodified histones, little is known about the role of citrullinated histone H3 (CitH3) in the pathogenesis of sepsis and ALI. In this study, we found that levels of CitH3 were elevated in the patients with sepsis-induced ARDS and correlated to PaO2/FiO2 in septic patients. Systematic administration of CitH3 peptide in mice provoked Caspase-1 activation in the lung tissue and caused ALI. Neutralization of CitH3 with monoclonal antibody improved survival and attenuated ALI in a mouse sepsis model. Furthermore, we demonstrated that CitH3 induces ALI through activating Caspase-1 dependent inflammasome in bone marrow derived macrophages and bone marrow derived dendritic cells. Our study suggests that CitH3 is an important mediator of inflammation and mortality during sepsis-induced ALI.

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