This document summarizes reexpansion pulmonary edema (RPE), which occurs when a lung that has been collapsed for more than several days is rapidly reexpanded. It discusses the history, clinical features, morphophysiological features, pathogenesis, and treatment of RPE. RPE is a type of permeability pulmonary edema caused by injury to the pulmonary microvessels from both the histological abnormalities developed during chronic collapse and the mechanical stress of reexpansion. While reducing mechanical stress during reexpansion can help manage symptoms, further research is needed to fully understand and treat the underlying cause of microvascular changes from chronic collapse.
Repeated open endotracheal suctioning (OS) in a rabbit model of acute respiratory distress syndrome (ARDS) caused a gradual decline in oxygen levels over 6 hours compared to closed endotracheal suctioning (CS). However, OS did not appear to exacerbate lung injury more than CS based on lung morphology and levels of inflammatory cytokines after 6 hours, though OS did cause more derecruitment with each suctioning. The study aimed to determine if repeated OS during mechanical ventilation worsened lung injury more than repeated CS in an ARDS rabbit model over a longer period of 6 hours.
Pathology of Acute Lungi Injury- Recent advancesDr Snehal Kosale
1. Diffuse alveolar damage is the most common histologic pattern seen in acute lung injury and acute respiratory distress syndrome. It is characterized by hyaline membranes, edema, and inflammation in two phases - acute/exudative and organizing/proliferative.
2. Other histologic patterns that can present similarly include acute eosinophilic pneumonia, diffuse alveolar hemorrhage with capillaritis, acute fibrinous and organizing pneumonia, and organizing pneumonia. These differ in their inflammatory cell profiles and distributions within the lung.
3. A careful histologic examination coupled with clinical information is needed to distinguish between these patterns and make an accurate diagnosis, which guides further management and prognosis. Transfusion-
This document provides an overview of acute respiratory distress syndrome (ARDS). It defines ARDS and discusses its causes, pathophysiology, diagnosis, incidence, prognosis and long-term outcomes. Treatment focuses on supportive care including mechanical ventilation with low tidal volumes, conservative fluid management, prone positioning and other strategies to improve oxygenation. Corticosteroids are not recommended for treatment due to lack of proven benefit. With treatment, prognosis depends on the underlying cause, but many ARDS survivors can expect to return to normal lifestyles within a year.
This document discusses guidelines for use of noninvasive positive pressure ventilation (NPPV) in patients with COPD exacerbations. It recommends starting NPPV in severe COPD exacerbations to prevent intubation. Factors that may indicate need for intubation include worsening gas exchange, encephalopathy, inability to clear secretions, or hemodynamic instability. Close monitoring is important to assess NPPV effectiveness and make adjustments or intubate if needed to avoid adverse outcomes. The document also reviews NPPV modes, interfaces, humidification and provides tips for troubleshooting issues that may arise with NPPV.
Pulmonary fibrosis is a chronic lung disease that causes scarring and stiffening of lung tissues. It commonly occurs in people ages 50-70 and has no known cause in many cases. Diagnosis involves tests like chest X-rays, lung biopsies, and pulmonary function tests. Symptoms include cough, shortness of breath, fatigue, and weight loss. While there is no cure, treatments aim to reduce inflammation and complications through medications, oxygen therapy, and possibly lung transplantation in severe cases. Research continues on new drugs that may slow scarring of the lungs.
Whole-lung lavage is a large-volume BAL that is performed mainly in the treatment of PAP. In brief, it involves the induction of general anesthesia followed by isolation of the two lungs with a double-lumen endotracheal tube and performance of single-lung ventilation while large volume lavages are performed on the nonventilated lung. Warmed normal saline solution in 1-L aliquots (total volumes up to 20 L) is instilled into the lung, chest physiotherapy is performed, then the proteinaceous effluent is drained with the aid of postural positioning. The sequence of events is repeated until such time as the effluent, which is initially milky and opaque, becomes clear. This procedure results in significant clinical and radiographic improvement secondary to the washing out of the proteinaceous material from the alveoli. The whole-lung lavage video details all aspects of the procedure, including case selection, patient preparation and equipment, a step-by-step review of the procedure, and postoperative considerations.
Practical approach to Idiopathic Pulmonary Fibrosis.Hiba Ashibany
This document provides information on idiopathic pulmonary fibrosis (IPF), including its causes, diagnosis, clinical features, prognosis, and treatment approaches. It summarizes that IPF is a progressive lung disease of unknown cause where scarring develops in the lungs. Diagnosis involves ruling out other conditions, imaging, and sometimes biopsies. Prognosis is generally poor with median survival of 3 years. Treatment includes drugs like pirfenidone and nintedanib that can slow disease progression in mild to moderate IPF.
The document summarizes information about acute respiratory distress syndrome (ARDS). It defines ARDS and provides diagnostic criteria. It discusses the pathophysiology and progression of ARDS. It outlines ventilation strategies for ARDS including low tidal volumes, limiting plateau pressures, use of PEEP, recruitment maneuvers, prone positioning, and extracorporeal membrane oxygenation. It also discusses pharmacologic interventions like steroids and fluid management considerations for ARDS patients.
Repeated open endotracheal suctioning (OS) in a rabbit model of acute respiratory distress syndrome (ARDS) caused a gradual decline in oxygen levels over 6 hours compared to closed endotracheal suctioning (CS). However, OS did not appear to exacerbate lung injury more than CS based on lung morphology and levels of inflammatory cytokines after 6 hours, though OS did cause more derecruitment with each suctioning. The study aimed to determine if repeated OS during mechanical ventilation worsened lung injury more than repeated CS in an ARDS rabbit model over a longer period of 6 hours.
Pathology of Acute Lungi Injury- Recent advancesDr Snehal Kosale
1. Diffuse alveolar damage is the most common histologic pattern seen in acute lung injury and acute respiratory distress syndrome. It is characterized by hyaline membranes, edema, and inflammation in two phases - acute/exudative and organizing/proliferative.
2. Other histologic patterns that can present similarly include acute eosinophilic pneumonia, diffuse alveolar hemorrhage with capillaritis, acute fibrinous and organizing pneumonia, and organizing pneumonia. These differ in their inflammatory cell profiles and distributions within the lung.
3. A careful histologic examination coupled with clinical information is needed to distinguish between these patterns and make an accurate diagnosis, which guides further management and prognosis. Transfusion-
This document provides an overview of acute respiratory distress syndrome (ARDS). It defines ARDS and discusses its causes, pathophysiology, diagnosis, incidence, prognosis and long-term outcomes. Treatment focuses on supportive care including mechanical ventilation with low tidal volumes, conservative fluid management, prone positioning and other strategies to improve oxygenation. Corticosteroids are not recommended for treatment due to lack of proven benefit. With treatment, prognosis depends on the underlying cause, but many ARDS survivors can expect to return to normal lifestyles within a year.
This document discusses guidelines for use of noninvasive positive pressure ventilation (NPPV) in patients with COPD exacerbations. It recommends starting NPPV in severe COPD exacerbations to prevent intubation. Factors that may indicate need for intubation include worsening gas exchange, encephalopathy, inability to clear secretions, or hemodynamic instability. Close monitoring is important to assess NPPV effectiveness and make adjustments or intubate if needed to avoid adverse outcomes. The document also reviews NPPV modes, interfaces, humidification and provides tips for troubleshooting issues that may arise with NPPV.
Pulmonary fibrosis is a chronic lung disease that causes scarring and stiffening of lung tissues. It commonly occurs in people ages 50-70 and has no known cause in many cases. Diagnosis involves tests like chest X-rays, lung biopsies, and pulmonary function tests. Symptoms include cough, shortness of breath, fatigue, and weight loss. While there is no cure, treatments aim to reduce inflammation and complications through medications, oxygen therapy, and possibly lung transplantation in severe cases. Research continues on new drugs that may slow scarring of the lungs.
Whole-lung lavage is a large-volume BAL that is performed mainly in the treatment of PAP. In brief, it involves the induction of general anesthesia followed by isolation of the two lungs with a double-lumen endotracheal tube and performance of single-lung ventilation while large volume lavages are performed on the nonventilated lung. Warmed normal saline solution in 1-L aliquots (total volumes up to 20 L) is instilled into the lung, chest physiotherapy is performed, then the proteinaceous effluent is drained with the aid of postural positioning. The sequence of events is repeated until such time as the effluent, which is initially milky and opaque, becomes clear. This procedure results in significant clinical and radiographic improvement secondary to the washing out of the proteinaceous material from the alveoli. The whole-lung lavage video details all aspects of the procedure, including case selection, patient preparation and equipment, a step-by-step review of the procedure, and postoperative considerations.
Practical approach to Idiopathic Pulmonary Fibrosis.Hiba Ashibany
This document provides information on idiopathic pulmonary fibrosis (IPF), including its causes, diagnosis, clinical features, prognosis, and treatment approaches. It summarizes that IPF is a progressive lung disease of unknown cause where scarring develops in the lungs. Diagnosis involves ruling out other conditions, imaging, and sometimes biopsies. Prognosis is generally poor with median survival of 3 years. Treatment includes drugs like pirfenidone and nintedanib that can slow disease progression in mild to moderate IPF.
The document summarizes information about acute respiratory distress syndrome (ARDS). It defines ARDS and provides diagnostic criteria. It discusses the pathophysiology and progression of ARDS. It outlines ventilation strategies for ARDS including low tidal volumes, limiting plateau pressures, use of PEEP, recruitment maneuvers, prone positioning, and extracorporeal membrane oxygenation. It also discusses pharmacologic interventions like steroids and fluid management considerations for ARDS patients.
1. Tracheobronchomalacia (TBM) and excessive dynamic airway collapse (EDAC) are conditions characterized by weakness and collapse of the trachea and main bronchi.
2. TBM involves weakness of the tracheal cartilage, surrounding muscles, and elastic fibers, leading to tracheal stenosis, increased secretions, coughing, wheezing, and recurrent infections. EDAC involves weakness of the elastic membrane on the dorsal side of the trachea not covered by cartilage, allowing collapse.
3. Diagnosis involves detecting airway collapse on expiratory CT scans or fluoroscopy. A decrease in tracheal cross-sectional area of over 18% in the upper airway or over
This document discusses idiopathic interstitial pneumonias other than idiopathic pulmonary fibrosis. It provides the revised ATS/ERS classification of idiopathic interstitial pneumonias and describes non-specific interstitial pneumonia (NSIP) and cryptogenic organizing pneumonia (COP) in detail. NSIP is characterized by a uniform pattern of interstitial inflammation and fibrosis. It commonly occurs in connective tissue diseases and has a good prognosis with treatment. COP is defined by organizing pneumonia in the absence of an identifiable cause, and presents with patchy consolidations that are typically peripheral and migratory.
The document defines acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) according to criteria from a 1994 consensus conference. It discusses the epidemiology and clinical disorders associated with ALI/ARDS development. Ventilator-based strategies for management include using low tidal volumes (6 ml/kg) and positive end-expiratory pressure (PEEP) of 13-16 cm H2O to reduce ventilator-induced lung injury from overdistension and repetitive opening/closing of alveoli. Recruitment maneuvers involving brief increases in pressure have been used to improve oxygenation by opening collapsed lung regions.
Dr. Melaku Y. will present on acute respiratory distress syndrome (ARDS) and be moderated by Dr. Endashaw and Dr. Dejene. ARDS is a clinical syndrome characterized by rapid onset of severe breathing difficulties, low oxygen levels, and diffuse lung infiltrates leading to respiratory failure. It has multiple underlying causes and stages of severity. Treatment focuses on managing the underlying condition, limiting lung injury from mechanical ventilation, and maintaining optimal fluid levels.
This document discusses idiopathic pulmonary fibrosis (IPF), a chronic and fatal lung disease. It provides definitions and diagnostic criteria for IPF. Historically, IPF was viewed as an inflammatory disease, but anti-inflammatory therapies have proven ineffective. The document argues that persistent epithelial injury and failure of re-epithelialization is critical in the pathogenesis of IPF. Key features seen in IPF lungs are fibroblastic foci containing myofibroblasts that deposit collagen, and a reactive epithelium that is simultaneously dividing and undergoing apoptosis. The epithelium normally inhibits fibrosis, but its damage releases these inhibitions and may contribute to fibrosis through epithelial-mesenchymal transition.
This document discusses diffuse parenchymal lung diseases (DPLD), also known as interstitial lung diseases. It describes the different categories and subtypes of DPLD, including idiopathic interstitial pneumonias (IIP) such as idiopathic pulmonary fibrosis (IPF). IPF is the most important subtype of IIP, with a poor prognosis. The document outlines approaches to diagnosing and treating IPF.
Recruitment Maneuvers in ARDS Dr Chennamchetty Vijay KumarVizae Kumar Chennam
This document discusses recruitment maneuvers for mechanically ventilated patients. It begins with a case study of a patient presenting with respiratory failure. It then provides definitions and the physiological rationale for recruitment maneuvers, including how alveolar collapse occurs in ARDS. Different types of recruitment maneuvers are described, as well as factors that influence their effectiveness. Clinical trials on recruitment maneuvers are summarized, which found no significant reduction in mortality but some improvement in secondary outcomes. Limitations of recruitment maneuvers are discussed, such as potential hemodynamic effects. The document concludes with emphasizing the complexity of lung recruitment and ongoing controversies regarding recruitment maneuvers.
1. ARDS is a respiratory condition characterized by diffuse pulmonary edema and hypoxemia that develops rapidly within one week of a known clinical insult.
2. The Berlin Definition from 2011 revised the diagnostic criteria for ARDS, requiring an onset within 1 week of a known clinical insult, bilateral opacities on chest imaging not fully explained by cardiac failure or fluid overload, and a ratio of arterial oxygen partial pressure to fractional inspired oxygen of ≤300 mm Hg for mild ARDS or ≤200 mm Hg for moderate/severe ARDS.
3. Management of ARDS involves mechanical ventilation with low tidal volumes, conservative fluid management to avoid pulmonary edema, and treating the underlying cause of lung injury while minimizing additional lung injury from
The disease epidemiology covered in the report provides historical as well as forecasted ARDS epidemiology scenario in the 7MM covering the United States, EU5 countries (Germany, Spain, Italy, France, and the United Kingdom), and Japan from 2017 to 2030.
A study that has been conducted to assess incidence and risk factors of postintubation cardiovascular collapse and its impact on ICU length of stay and ICU mortality
1) Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition caused by injury to the lungs. It can result from direct lung injury, such as pneumonia, or indirect injury, like sepsis.
2) ARDS progresses through exudative and proliferative phases characterized by fluid accumulation and scarring in the lungs. This impairs gas exchange and causes respiratory failure.
3) Mechanical ventilation is used to treat respiratory failure but can further damage the lungs if not done carefully. The ARDSNet trial showed using low tidal volumes of 6 ml/kg improved survival compared to larger volumes.
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are considered part of the same spectrum of disease. ARDS was first described in 1967 and involves acute respiratory failure from pulmonary edema without heart failure. In 1994, diagnostic criteria were established for ALI and ARDS based on severity. A landmark 2000 study found that using low tidal volume ventilation (6-8 mL/kg) compared to conventional volumes (10-12 mL/kg) reduced mortality in ARDS patients by 22%. Low tidal volumes are now the standard of care for reducing mortality and improving outcomes in ARDS.
1) ARDS is a common and serious condition in the ICU characterized by diffuse lung inflammation and damage to the lungs' ability to oxygenate blood. It can develop due to direct or indirect injury to the lungs from a variety of causes like pneumonia, sepsis, trauma, etc.
2) Mechanical ventilation can further damage injured lungs if not performed carefully. A lung protective strategy using low tidal volumes has been shown to significantly reduce mortality in ARDS patients.
3) Treatment involves identifying and treating the underlying cause, conservative fluid management, nutritional support, and lung protective ventilation with low tidal volumes and adequate PEEP to prevent lung collapse without overdistension.
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrosing interstitial pneumonia of unknown cause that primarily affects older adults. It is characterized by scarring (fibrosis) of the lungs that gets worse over time. The diagnosis of IPF requires the exclusion of other known causes of lung fibrosis and the presence of a usual interstitial pneumonia pattern on HRCT or lung biopsy. High-resolution CT is an essential tool that typically shows subpleural reticulation and honeycombing. Pulmonary function tests reveal a restrictive ventilatory defect. The cause remains unknown but genetic factors and environmental exposures may play a role.
A presentation by Jon Henrik Laake at the 2017 meeting of the Scandinavian Society of Anaestesiology and Intensive Care Medicine.
All available content from SSAI2017: https://scanfoam.org/ssai2017/
Delivered in collaboration between scanFOAM, SSAI & SFAI.
Adult respiratory distress syndrome (ARDS) involves diffuse damage to the alveolar epithelium and capillaries resulting in progressive respiratory failure unresponsive to oxygen treatment. It has numerous causes including shock, sepsis, trauma, and infections. On x-ray, ARDS appears as bilateral diffuse widespread lung opacity. Respiratory distress syndrome of the newborn (also called hyaline membrane disease) occurs most commonly in preterm infants and those with maternal diabetes or multiple births. It results from a deficiency of surfactant causing atelectasis and hyaline membrane formation. Pulmonary embolism occurs when blood clots most often from the legs travel to the lungs. While most emboli do not cause infarction, large embol
Acute Respiratory Distress Syndrome (ARDS) is an acute hypoxemic respiratory failure following a lung or systemic insult without heart failure. It involves diffuse bilateral lung infiltrates, normal heart functioning, and profound hypoxemia. Common causes include pneumonia, aspiration, and sepsis. Patients experience rapid onset of labored breathing and hypoxemia. Chest imaging shows bilateral infiltrates. Treatment focuses on supportive care, mechanical ventilation with low tidal volumes, and treating the underlying condition. While the mortality rate is high, especially with sepsis, outcomes have improved in recent decades.
This document discusses interstitial lung disease (ILD), focusing on idiopathic pulmonary fibrosis (IPF). ILD describes a group of lung disorders involving scarring of the lungs. IPF is the most common and severe type of ILD. The document defines ILD and its subtypes. It describes the diagnostic challenges of ILD and importance of investigating each case. Causes of ILD include exposures to irritants like asbestos as well as some autoimmune diseases. IPF is characterized by worsening shortness of breath and cough. It involves scarring of the lung tissue and has a poor prognosis. The document provides details on the prevalence, risk factors, diagnosis, and outcomes of IPF.
This document discusses acute respiratory distress syndrome (ARDS). It begins with defining ARDS and reviewing its pathophysiology and risk factors. ARDS involves acute inflammation of the alveolar-capillary membrane causing pulmonary edema. Major risk factors include sepsis, trauma, burns, and pneumonia. The document then covers the clinical presentation of ARDS, including dyspnea, hypoxemia, and decreased lung compliance. It reviews guidelines for managing ARDS, such as using low tidal volume ventilation, conservative fluid strategies, and considering prone positioning for moderate to severe cases. Overall treatments aim to protect the lungs from further injury while supporting other vital organ functions.
- Acute Respiratory Distress Syndrome (ARDS) is characterized by severe respiratory failure caused by diffuse lung injury from medical or surgical disorders. It involves three phases - exudative, proliferative, and fibrotic.
- The management of ARDS focuses on treating the underlying cause, lung-protective ventilation with low tidal volumes, use of PEEP to prevent alveolar collapse, and consideration of prone positioning. Adjunctive therapies like neuromuscular blockade and fluid restriction may help but other proposed therapies like steroids have not proven beneficial. Mortality remains high depending on severity of hypoxemia and presence of other organ failure.
ING reported poor quarterly earnings results across its insurance and banking divisions. The banking results were negatively impacted by bad investments in CDOs, while the insurance results suffered mainly in life insurance which is linked to stock market performance. Overall, ING saw weak results across its European, American, and Asian insurance businesses as well as in its retail, wholesale, and corporate banking lines.
This document summarizes reexpansion pulmonary edema (RPE), which occurs when a lung that has been collapsed for more than several days is rapidly reexpanded. It discusses the history, clinical features, morphophysiological features, and pathogenesis of RPE. The key points are:
1) RPE is a type of permeability pulmonary edema caused by injury to pulmonary microvessels from the histological abnormalities that develop during chronic lung collapse as well as the mechanical stress of reexpansion.
2) RPE typically occurs within 1 hour of reexpansion when the lung has been collapsed for 3 or more days and 2,000mL or more of fluid is evacuated.
3) Treatment aims to reduce mechanical stress during re
1. Tracheobronchomalacia (TBM) and excessive dynamic airway collapse (EDAC) are conditions characterized by weakness and collapse of the trachea and main bronchi.
2. TBM involves weakness of the tracheal cartilage, surrounding muscles, and elastic fibers, leading to tracheal stenosis, increased secretions, coughing, wheezing, and recurrent infections. EDAC involves weakness of the elastic membrane on the dorsal side of the trachea not covered by cartilage, allowing collapse.
3. Diagnosis involves detecting airway collapse on expiratory CT scans or fluoroscopy. A decrease in tracheal cross-sectional area of over 18% in the upper airway or over
This document discusses idiopathic interstitial pneumonias other than idiopathic pulmonary fibrosis. It provides the revised ATS/ERS classification of idiopathic interstitial pneumonias and describes non-specific interstitial pneumonia (NSIP) and cryptogenic organizing pneumonia (COP) in detail. NSIP is characterized by a uniform pattern of interstitial inflammation and fibrosis. It commonly occurs in connective tissue diseases and has a good prognosis with treatment. COP is defined by organizing pneumonia in the absence of an identifiable cause, and presents with patchy consolidations that are typically peripheral and migratory.
The document defines acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) according to criteria from a 1994 consensus conference. It discusses the epidemiology and clinical disorders associated with ALI/ARDS development. Ventilator-based strategies for management include using low tidal volumes (6 ml/kg) and positive end-expiratory pressure (PEEP) of 13-16 cm H2O to reduce ventilator-induced lung injury from overdistension and repetitive opening/closing of alveoli. Recruitment maneuvers involving brief increases in pressure have been used to improve oxygenation by opening collapsed lung regions.
Dr. Melaku Y. will present on acute respiratory distress syndrome (ARDS) and be moderated by Dr. Endashaw and Dr. Dejene. ARDS is a clinical syndrome characterized by rapid onset of severe breathing difficulties, low oxygen levels, and diffuse lung infiltrates leading to respiratory failure. It has multiple underlying causes and stages of severity. Treatment focuses on managing the underlying condition, limiting lung injury from mechanical ventilation, and maintaining optimal fluid levels.
This document discusses idiopathic pulmonary fibrosis (IPF), a chronic and fatal lung disease. It provides definitions and diagnostic criteria for IPF. Historically, IPF was viewed as an inflammatory disease, but anti-inflammatory therapies have proven ineffective. The document argues that persistent epithelial injury and failure of re-epithelialization is critical in the pathogenesis of IPF. Key features seen in IPF lungs are fibroblastic foci containing myofibroblasts that deposit collagen, and a reactive epithelium that is simultaneously dividing and undergoing apoptosis. The epithelium normally inhibits fibrosis, but its damage releases these inhibitions and may contribute to fibrosis through epithelial-mesenchymal transition.
This document discusses diffuse parenchymal lung diseases (DPLD), also known as interstitial lung diseases. It describes the different categories and subtypes of DPLD, including idiopathic interstitial pneumonias (IIP) such as idiopathic pulmonary fibrosis (IPF). IPF is the most important subtype of IIP, with a poor prognosis. The document outlines approaches to diagnosing and treating IPF.
Recruitment Maneuvers in ARDS Dr Chennamchetty Vijay KumarVizae Kumar Chennam
This document discusses recruitment maneuvers for mechanically ventilated patients. It begins with a case study of a patient presenting with respiratory failure. It then provides definitions and the physiological rationale for recruitment maneuvers, including how alveolar collapse occurs in ARDS. Different types of recruitment maneuvers are described, as well as factors that influence their effectiveness. Clinical trials on recruitment maneuvers are summarized, which found no significant reduction in mortality but some improvement in secondary outcomes. Limitations of recruitment maneuvers are discussed, such as potential hemodynamic effects. The document concludes with emphasizing the complexity of lung recruitment and ongoing controversies regarding recruitment maneuvers.
1. ARDS is a respiratory condition characterized by diffuse pulmonary edema and hypoxemia that develops rapidly within one week of a known clinical insult.
2. The Berlin Definition from 2011 revised the diagnostic criteria for ARDS, requiring an onset within 1 week of a known clinical insult, bilateral opacities on chest imaging not fully explained by cardiac failure or fluid overload, and a ratio of arterial oxygen partial pressure to fractional inspired oxygen of ≤300 mm Hg for mild ARDS or ≤200 mm Hg for moderate/severe ARDS.
3. Management of ARDS involves mechanical ventilation with low tidal volumes, conservative fluid management to avoid pulmonary edema, and treating the underlying cause of lung injury while minimizing additional lung injury from
The disease epidemiology covered in the report provides historical as well as forecasted ARDS epidemiology scenario in the 7MM covering the United States, EU5 countries (Germany, Spain, Italy, France, and the United Kingdom), and Japan from 2017 to 2030.
A study that has been conducted to assess incidence and risk factors of postintubation cardiovascular collapse and its impact on ICU length of stay and ICU mortality
1) Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition caused by injury to the lungs. It can result from direct lung injury, such as pneumonia, or indirect injury, like sepsis.
2) ARDS progresses through exudative and proliferative phases characterized by fluid accumulation and scarring in the lungs. This impairs gas exchange and causes respiratory failure.
3) Mechanical ventilation is used to treat respiratory failure but can further damage the lungs if not done carefully. The ARDSNet trial showed using low tidal volumes of 6 ml/kg improved survival compared to larger volumes.
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are considered part of the same spectrum of disease. ARDS was first described in 1967 and involves acute respiratory failure from pulmonary edema without heart failure. In 1994, diagnostic criteria were established for ALI and ARDS based on severity. A landmark 2000 study found that using low tidal volume ventilation (6-8 mL/kg) compared to conventional volumes (10-12 mL/kg) reduced mortality in ARDS patients by 22%. Low tidal volumes are now the standard of care for reducing mortality and improving outcomes in ARDS.
1) ARDS is a common and serious condition in the ICU characterized by diffuse lung inflammation and damage to the lungs' ability to oxygenate blood. It can develop due to direct or indirect injury to the lungs from a variety of causes like pneumonia, sepsis, trauma, etc.
2) Mechanical ventilation can further damage injured lungs if not performed carefully. A lung protective strategy using low tidal volumes has been shown to significantly reduce mortality in ARDS patients.
3) Treatment involves identifying and treating the underlying cause, conservative fluid management, nutritional support, and lung protective ventilation with low tidal volumes and adequate PEEP to prevent lung collapse without overdistension.
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrosing interstitial pneumonia of unknown cause that primarily affects older adults. It is characterized by scarring (fibrosis) of the lungs that gets worse over time. The diagnosis of IPF requires the exclusion of other known causes of lung fibrosis and the presence of a usual interstitial pneumonia pattern on HRCT or lung biopsy. High-resolution CT is an essential tool that typically shows subpleural reticulation and honeycombing. Pulmonary function tests reveal a restrictive ventilatory defect. The cause remains unknown but genetic factors and environmental exposures may play a role.
A presentation by Jon Henrik Laake at the 2017 meeting of the Scandinavian Society of Anaestesiology and Intensive Care Medicine.
All available content from SSAI2017: https://scanfoam.org/ssai2017/
Delivered in collaboration between scanFOAM, SSAI & SFAI.
Adult respiratory distress syndrome (ARDS) involves diffuse damage to the alveolar epithelium and capillaries resulting in progressive respiratory failure unresponsive to oxygen treatment. It has numerous causes including shock, sepsis, trauma, and infections. On x-ray, ARDS appears as bilateral diffuse widespread lung opacity. Respiratory distress syndrome of the newborn (also called hyaline membrane disease) occurs most commonly in preterm infants and those with maternal diabetes or multiple births. It results from a deficiency of surfactant causing atelectasis and hyaline membrane formation. Pulmonary embolism occurs when blood clots most often from the legs travel to the lungs. While most emboli do not cause infarction, large embol
Acute Respiratory Distress Syndrome (ARDS) is an acute hypoxemic respiratory failure following a lung or systemic insult without heart failure. It involves diffuse bilateral lung infiltrates, normal heart functioning, and profound hypoxemia. Common causes include pneumonia, aspiration, and sepsis. Patients experience rapid onset of labored breathing and hypoxemia. Chest imaging shows bilateral infiltrates. Treatment focuses on supportive care, mechanical ventilation with low tidal volumes, and treating the underlying condition. While the mortality rate is high, especially with sepsis, outcomes have improved in recent decades.
This document discusses interstitial lung disease (ILD), focusing on idiopathic pulmonary fibrosis (IPF). ILD describes a group of lung disorders involving scarring of the lungs. IPF is the most common and severe type of ILD. The document defines ILD and its subtypes. It describes the diagnostic challenges of ILD and importance of investigating each case. Causes of ILD include exposures to irritants like asbestos as well as some autoimmune diseases. IPF is characterized by worsening shortness of breath and cough. It involves scarring of the lung tissue and has a poor prognosis. The document provides details on the prevalence, risk factors, diagnosis, and outcomes of IPF.
This document discusses acute respiratory distress syndrome (ARDS). It begins with defining ARDS and reviewing its pathophysiology and risk factors. ARDS involves acute inflammation of the alveolar-capillary membrane causing pulmonary edema. Major risk factors include sepsis, trauma, burns, and pneumonia. The document then covers the clinical presentation of ARDS, including dyspnea, hypoxemia, and decreased lung compliance. It reviews guidelines for managing ARDS, such as using low tidal volume ventilation, conservative fluid strategies, and considering prone positioning for moderate to severe cases. Overall treatments aim to protect the lungs from further injury while supporting other vital organ functions.
- Acute Respiratory Distress Syndrome (ARDS) is characterized by severe respiratory failure caused by diffuse lung injury from medical or surgical disorders. It involves three phases - exudative, proliferative, and fibrotic.
- The management of ARDS focuses on treating the underlying cause, lung-protective ventilation with low tidal volumes, use of PEEP to prevent alveolar collapse, and consideration of prone positioning. Adjunctive therapies like neuromuscular blockade and fluid restriction may help but other proposed therapies like steroids have not proven beneficial. Mortality remains high depending on severity of hypoxemia and presence of other organ failure.
ING reported poor quarterly earnings results across its insurance and banking divisions. The banking results were negatively impacted by bad investments in CDOs, while the insurance results suffered mainly in life insurance which is linked to stock market performance. Overall, ING saw weak results across its European, American, and Asian insurance businesses as well as in its retail, wholesale, and corporate banking lines.
This document summarizes reexpansion pulmonary edema (RPE), which occurs when a lung that has been collapsed for more than several days is rapidly reexpanded. It discusses the history, clinical features, morphophysiological features, and pathogenesis of RPE. The key points are:
1) RPE is a type of permeability pulmonary edema caused by injury to pulmonary microvessels from the histological abnormalities that develop during chronic lung collapse as well as the mechanical stress of reexpansion.
2) RPE typically occurs within 1 hour of reexpansion when the lung has been collapsed for 3 or more days and 2,000mL or more of fluid is evacuated.
3) Treatment aims to reduce mechanical stress during re
Teachers in the Balance is a team that believes individuals can reduce their collective carbon footprint through more purposeful actions. They are seeking help moving from thought to action by joining their efforts to lessen environmental impacts through conferences in 2009 and 2010. Members hope to make resources go further and decrease impacts through cooperation.
It is a presentation about all the aid that is currently available to entrepreneurs to start they own business in Portugal.
This talk was presented at SWITCH Conference in Coimbra, Portugal on May 16th, 2010.
The document summarizes phone conferencing services, including two types of solutions: reservationless operator assisted. It provides highlights of features like 24/7 support, billing options, web conferencing management, and usage reports. Sample commands and a billing code example are also included.
Apresentação na Pós-Graduação em Segurança da Informação:
- Sniffer de senhas em plain text;
- Ataque de brute-force no SSH;
- Proteção: Firewall, IPS e/ou TCP Wrappers;
- Segurança básica no sshd_config;
- Chaves RSA/DSA para acesso remoto;
- SSH buscando chaves no LDAP;
- Porque previnir o acesso: Fork Bomb
The document discusses Portuguese "Hidden Champions", which are companies that are worldwide leaders in their industry segments but are not widely known by the general public. It provides examples of several Portuguese hidden champion companies, including Nelo (kayaks), Vision Box (biometric and border control systems), Yellow Wood Fingerboard (fingerboard products), Petratex (swimwear innovation), WeDo Technologies (revenue assurance software), COBUS (airport buses), Corticeira Amorim (cork derivatives), Fepsa (felt for hats), Sonae Industria (wood panels), and Portucel Soporcel (paper production). It also outlines strategies used by hidden champions, such as differentiation, innovation
The document discusses the evolution of the web from version 1.0 to 3.0. Web 1.0 involved traditional printed media like newspapers that later transitioned online. Web 2.0 saw greater interactivity and user-generated content through sites like blogs and social media. Web 3.0 is proposed to involve semantic web technology that enables machines to understand the meaning, context and intent of information on the web. Some examples of tools and sites for designing different elements of web content are also listed.
Reexpansion pulmonary edema is a serious complication after sudden expansion of collapsed lung.Re-expansion pulmonary edema is an uncommon complication following drainage of a pneumothorax , pleural effusion or removal of any space occupying lesion.
The incidence referred is less than 1%, andmortality can reach up to 20%.
This document discusses acute respiratory distress syndrome (ARDS). It begins by defining ARDS according to the Berlin criteria and describing the pathophysiology involving increased permeability of the lungs. It then discusses diagnosing ARDS using chest imaging and oxygenation levels. The document outlines the exudative, proliferative and fibroproliferative phases of ARDS. It discusses managing ARDS through ventilation strategies, conservative fluid management, limiting sedation and paralysis, and providing nutrition. Key trials on fluids and neuromuscular blockers in ARDS are summarized.
Abstract Lung Abscess is a liquefactive necrosis of the lung tissue and arrangement of cavitation (in excess of 2 cm) containing necrotic debris and liquid brought about by parenchymal infection. It very well may be brought about by yearning, which may happen during changed cognizance and it for the most part causes a discharge filled depression. In addition, liquor addiction is the most widely recognized condition inclining to lung abscesses. Lung abscess is viewed as essential (60%) when it comes about because of existing lung parenchymal process and is named auxiliary when it entangles another procedure, e.g., vascular emboli or follows rupture of extrapulmonary abscess into lung. There are a few imaging strategies which can distinguish the material inside the thorax, for example, electronic tomography (CT) output of the thorax and ultrasound of the thorax. Broad Spectrum anti-biotics to cover blended vegetation is the pillar of treatment. Pneumonic physiotherapy and postural drainage are additionally significant. Surgeries are required in specific patients for pneumonic resection Keywords: Lung abscess, anti-bodies, video-assissted thoracoscopic medical procedure (VATS), thoracoscopy
Reexpansion pulmonary edema (RPE) is a rare but potentially lethal condition that can occur after the rapid expansion of a collapsed lung. The pathophysiology is multifactorial but is believed to involve decreased pulmonary surfactant levels and a pro-inflammatory response due to the lung collapse and reexpansion. Early diagnosis is important as prognosis depends on prompt treatment, but prevention through slow, controlled reexpansion is the best strategy due to the high mortality rates associated with RPE.
Discussion #11. What physical findings might be indicative of a .docxmecklenburgstrelitzh
Discussion #1
1. What physical findings might be indicative of a patient with emphysema? The diagnosis is made on patients that usually are long term smokers, and they complaint of dyspnea, cough, and mucus expectoration. Most patients seek medical attention late in the course of their disease, usually ignoring smoldering symptoms that start gradually and progress over the course of years. The cough typically is worse in the morning with finite production of clear-to-white sputum. Dyspnea, emphysema's most significant symptom, does not generally occur until the sixth decade of life. However, patients with emphysema due to alpha 1 -antitrypsin deficit will exhibit the following characteristics: early presentation (< 45 y), predilection of emphysematous changes in the lung bases, and the panacinar morphological pattern.
Although the sensitivity of the physical evaluation in mild-to-moderate disease is relatively poor, the physical signs are quite sensitive and specific in severe disease. Patients with severe disease may experience tachypnea and dyspnea with mild exertion.
The respiratory rate increases in proportion to disease severity with the use of accessory respiratory muscles and paradoxical contraction of lower intercostal spaces becoming evident during exacerbations.
In end-stage emphysema, cyanosis, elevated jugular venous pressure, atrophy of limb musculature, and peripheral edema due to the development of pulmonary hypertension, right-to-left shunting, and/or right heart failure can easily be observed.
Thoracic examination reveals a 2:1 increase in anterior to posterior diameter (“barrel chest”), diffuse or focal wheezing, diffusely diminished breath sounds, hyperresonance upon percussion, prolonged expiration, and/or hyperinflation on chest radiographs.
2. What is the purpose and interpretations of the pulmonary function test? Pulmonary function tests will test the mechanical function of the lungs, chest wall, and respiratory muscles by measuring the total volume of air exhaled from a full lung (total lung capacity [TLC]) to maximal expiration (residual volume [RV]). This volume, the forced vital capacity (FVC) and the forced expiratory volume in the first second of the forceful exhalation (FEV1), In Emphysema, spirometry may show typical obstructive pattern due to the blockage of the air during expiration. As a result of the air trapping, the spirometry will show decreased in FVC, but less than the FEV 1, and increased FRC and RV.(McCance, & Huether, 2013).
3. What are the pathophysiological findings specifying emphysema? As a result of the cellular apoptosis, and early cellular senescence, the alveolar cells are damaged, and a reduced surface of gas exchanged occurred. The destruction of the alveoli creates bullae, which are large spaces in the lung parenchyma and air spaces adjacent to pleurae(blebs). Both elements bullae, and blebs difficult the air exchange. In addition, areas of the lungs that are bad perfused contributes to w.
1) ARDS is characterized by hypoxemia, bilateral lung infiltrates, and respiratory failure not fully explained by cardiac failure. The Berlin definition classifies ARDS as mild, moderate, or severe based on oxygenation levels.
2) Management of ARDS focuses on treating underlying causes, preventing complications, and using ventilator strategies like low tidal volume ventilation to prevent ventilator-induced lung injury.
3) Other ventilator strategies discussed include prone positioning, neuromuscular blockade, recruitment maneuvers, and extracorporeal membrane oxygenation for severe cases, though evidence on benefits is mixed.
This document presents guidelines for the management of spontaneous pneumothorax from the British Thoracic Society. It defines primary and secondary pneumothorax and discusses their incidence, risk factors like smoking, and pathogenesis involving blebs and bullae. The guidelines emphasize strongly discouraging smoking in patients. Clinical evaluation involves chest x-rays, with lateral views used if primary films are unclear. CT scanning is recommended in some complex cases. A history is unreliable for pneumothorax size. The guidelines provide algorithms for treatment of primary and secondary pneumothorax.
This document discusses the classification and etiology of pneumothorax. It begins with an overview of the historical understanding and definitions of pneumothorax. It then discusses the epidemiology, including incidence and recurrence rates. Pneumothorax is classified based on size (partial, incomplete, complete), pathophysiology (tension vs spontaneous), and etiology (primary spontaneous, secondary spontaneous, traumatic). The exact causes are often unknown but involve an interplay between lung abnormalities and environmental factors in most cases.
This document discusses the approach to bullous lung disease. It defines a bulla as a large air-containing space within the lung larger than 1 cm in diameter. Bullae can occur with emphysema, pulmonary fibrosis, or in otherwise normal lungs. HRCT is useful for evaluating the size, number and relationships of bullae. Pulmonary function testing may show obstructive lung disease, hyperinflation and reduced diffusion capacity. For surgical candidates, bullectomy or lung volume reduction surgery may be considered to treat symptoms or complications like spontaneous pneumothorax.
LVRS involves surgically removing portions of emphysematous lung to allow the remaining lung tissue to expand. The NETT trial found LVRS benefits patients with upper lobe-predominant emphysema and low exercise capacity by improving lung function, exercise ability, and quality of life. Candidates for LVRS have severe emphysema, poor exercise capacity, marked lung hyperinflation, and meet criteria for pulmonary function tests, exercise testing, and cardiac/pulmonary evaluations. The procedure aims to improve ventilation/perfusion matching, reduce airway resistance, and allow the chest wall and diaphragm to resume a more normal position.
1. The document discusses acute respiratory distress syndrome (ARDS), describing its pathophysiology, causes, diagnosis, treatment and prognosis.
2. ARDS is characterized by hypoxemia, reduced lung compliance and diffuse pulmonary infiltrates leading to respiratory failure. Common causes include sepsis, pneumonia and trauma.
3. Treatment involves treating the underlying cause, supportive care including mechanical ventilation with low tidal volumes, and managing fluid levels and oxygenation. Prognosis depends on severity of illness, with reported mortality ranging from 41-65%.
ARDS is a severe lung condition characterized by hypoxemia that cannot be explained by heart failure. It is caused by direct or indirect lung injury and inflammation. Key treatments include low tidal volume ventilation, conservative fluid management, and treating the underlying condition. While in-hospital mortality has decreased, many survivors have long-term functional impairments. Several large clinical trials have helped identify best practices for ventilation and other supportive therapies, though no pharmacologic treatments have proven definitively effective to date.
1) The document describes a study of 40 patients with prolonged pulmonary air leaks treated with endobronchial valves.
2) Ninety-two percent of patients experienced resolution or reduction of their air leak after valve placement. Nearly half saw complete resolution.
3) On average, chest tubes were removed 21 days after valve placement and patients were discharged from the hospital 19 days after the procedure.
This document discusses ARDS (acute respiratory distress syndrome), including its history, definitions, pathophysiology, and evidence-based treatment strategies. ARDS is characterized by diffuse pulmonary inflammation and reduced lung compliance. Traditional ventilator strategies have been shown to cause ventilator-induced lung injury, so current recommendations focus on lung-protective ventilation with low tidal volumes and high PEEP. Additional rescue therapies for refractory hypoxemia include recruitment maneuvers, proning, and ECMO. Proper diagnosis requires consideration of alternative conditions and use of diagnostic tools like echocardiogram, bronchoscopy, and chest CT scan.
Non-cardiogenic pulmonary edema (NPE) can have many causes that result in increased pulmonary capillary permeability and fluid leakage into the lungs. These include conditions like acute respiratory distress syndrome (ARDS), neurogenic pulmonary edema, renal failure, negative pressure pulmonary edema, high altitude pulmonary edema, drug overdoses, chemotherapy, and more. The pathogenesis usually involves elevated pulmonary vascular pressures or a direct injury to the lung tissues. Radiographically, NPE presents as diffuse bilateral infiltrates that resolve more quickly than cardiogenic pulmonary edema, lacking features like Kerley lines or enlarged heart size.
Dr. Sagar Gandhi discusses pneumothorax in this document. Pneumothorax is defined as air in the pleural space between the lungs and chest wall. It can be primary or secondary and spontaneous or traumatic. Diagnosis is made through chest x-ray or CT scan. Treatment depends on size and includes observation, oxygen therapy, needle aspiration, catheter drainage, or chest tube placement. The goal is to promote lung re-expansion and prevent recurrence.
This document summarizes a presentation on Acute Respiratory Distress Syndrome (ARDS). It discusses the history, epidemiology, causes, pathogenesis, clinical features, investigations and management of ARDS. The key points are: ARDS is caused by diffuse lung inflammation from various diseases and injuries and results in hypoxemia resistant to oxygen therapy. It has been recognized since World War I. The incidence is 13.5-78.9 cases per 100,000 people. Common causes include asthma, pneumonia, burns and pancreatitis. Pathogenesis involves neutrophils, macrophages and inflammatory mediators damaging the lungs. Clinical features range from hyperventilation to respiratory failure and multi-organ dysfunction. Diagnosis is based on hypoxemia,
This document provides an overview of chronic obstructive pulmonary disease (COPD). It defines COPD as a progressive lung disease characterized by airflow limitation. The document discusses the causes of COPD, including cigarette smoking which is the primary cause in over 90% of patients. It also examines the pathophysiology of the two main types of COPD - chronic bronchitis and emphysema. The clinical evaluation and diagnostic tests used to diagnose COPD are outlined, including the use of spirometry to confirm airflow limitation. Treatment objectives for COPD and its management are briefly mentioned.
1) The document discusses three lung conditions: atelectasis, ARDS, and interstitial pneumonia. It provides details on the causes, symptoms, diagnosis, and pathogenesis of each condition.
2) ARDS is characterized by diffuse pulmonary edema and hypoxemia. It develops due to acute lung injury from direct or indirect causes like sepsis, trauma, pneumonia, etc. There are three stages: exudative, proliferative, and fibrotic.
3) The pathogenesis of ARDS involves damage to lung endothelial and epithelial cells by cytokines and neutrophils, leading to accumulation of fluid in the lungs and impaired gas exchange. This results in hypoxemia and reduced lung compliance.
Bilateral diaphragm plication prior to transplantationmshihatasite
This document reports a case study of a 58-year-old man with end-stage lung disease who underwent bilateral sequential lung transplantation. He had bilateral elevated diaphragms due to underlying lung fibrosis and left-sided diaphragmatic paralysis. During the transplantation surgery, the surgeons performed bilateral diaphragmatic plication to lower the diaphragms and improve ventilation. The patient had an excellent postoperative outcome with a short hospital stay and no respiratory complications. The case study concludes that bilateral diaphragmatic plication can be a useful surgical technique for lung transplant patients with diaphragmatic paralysis or weakness.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
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1. 205Ann Thorac Cardiovasc Surg Vol. 14, No. 4 (2008)
Review
Reexpansion Pulmonary Edema
Yasunori Sohara, MD
From Department of Surgery, Faculty of Medicine, Jichi
Medical University, Shimotsuke, Japan
Received October 29, 2007; accepted for publication December
20, 2007
Address reprint requests to Yasunori Sohara, MD: Department
of Surgery, Faculty of Medicine, Jichi Medical University,
3311–1 Yakushiji, Shimotsuke, Tochigi 329–0498, Japan.
When a rapidly reexpanding lung has been in a state of collapse for more than several days,
pulmonary edema sometimes occurs in it. This is called reexpansion pulmonary edema
(RPE). In this article, I present my views on the history, clinical features, morphophysiologi-
cal features, pathogenesis, and treatment of RPE. Histological abnormalities of the pulmo-
nary microvessels in a chronically collapsed lung will cause RPE, as well as mechanical
stress exerted during reexpansion. Although the most effective treatment method is to treat
the histological abnormalities of the pulmonary microvessels formed in a chronically col-
lapsed lung, the cause of these abnormalities is not clear, making it difficult to put forward
a precise treatment method. However, reasonably good effects can be expected from a symp-
tomatic therapy that reduces the level of mechanical stress during reexpansion. In the fu-
ture, it is expected that the cause of histological changes of the pulmonary microvessels in a
chronically collapsed lung will be revealed, and appropriate therapies will therefore be de-
veloped according to this cause. (Ann Thorac Cardiovasc Surg 2008; 14: 205–209)
Key words: reexpansion pulmonary edema, permeability pulmonary edema, chronic lung
collapse, pulmonary microvascular injury, oxygen-derived free radical
When a lung that has collapsed for more than several
days is rapidly reexpanded, pulmonary edema some-
times occurs in the reexpanded lung. This is called re-
expansion pulmonary edema (RPE).
Because the protein concentration of sputum is extraor-
dinarily high during the onset of pulmonary edema,
it is believed that RPE belongs to the type of per-
meability pulmonary edema caused by an injury to the
pulmonary microvessels.
RPE is unlikely to occur if the period of lung col-
lapse is less than 3 days, nor does it always occur even
when the collapse lasts for 3 days or more. RPE also
has other remarkably interesting characteristics, such as
the manner in which it occurs, even in regions where
there is no visible collapse, and considerable research
has been conducted to explain its pathogenesis.
1. History of RPE
In 1853, Pinault reported that pulmonary edema oc-
curred in a reexpanded lung after the removal of pleural
effusion. It is believed that this was the first report of
RPE.1)
Since then, there have been many reports regard-
ing the removal of pleural effusion and RPE.2–12)
In
1959, Carlson et al.13)
reported that pulmonary edema
occurred when a lung that had collapsed as a result of
pneumothorax was reexpanded by means of thoracente-
sis. There have since been many reports regarding the
evacuation of pneumothorax and RPE.14–30)
Moreover, there are reports of RPE occurring in re-
expanded lungs when large quantities of cystic fluid are
removed from a giant hepatic cyst,31)
and reports also of
RPE occurrences in reexpanded lungs after the excision
of a giant mediastinal tumor,32–34)
in the contralateral
lung of a reexpanded lung,35–38)
and in a reexpanded
lung after decortication.39)
As evidenced by these reports, it is possible for RPE
to occur in every type of chronically collapsed lung that
2. 206
Sohara
Ann Thorac Cardiovasc Surg Vol. 14, No. 4 (2008)
can be reexpanded.
2. Clinical Features of RPE
The most representative disorder that can cause RPE is
pneumothorax. Mahfood et al. conducted a detailed in-
vestigation using 47 cases of RPE associated with pneu-
mothorax that were reported from 1958 to 1987.21)
Accord-
ing to this report, RPE is more common among men in
a ratio of 38:9, with an average age of 42 (ranging from
18 to 84), and 83% of the cases experienced periods of
lung collapse lasting 3 days or more (39/47 patients). Of
these cases, 64% (30/47 patients) experienced the onset
of RPE within an hour after reexpansion, and in all
cases the onset occurred within 24 h. Regarding the
method of evacuation, 79% (37/47 patients) of cases
underwent suction, and 17% underwent an underwater
seal. RPE occurred in the reexpanded lung of 94%
(44/47 patients) of the cases. Three patients also had
RPE in the contralateral lung, and 2 of these 3 patients
have died. The overall mortality was 19% (9/47
patients), with patients aged 50 and above accounting
for 78% (7/9 patients) of those deaths.
The oldest report regarding RPE is of RPE associated
with the removal of pleural effusion. In 9 reports re-
garding RPE that occurred after the removal of pleural
effusion, among the diseases were mesothelioma, pleu-
risy, carcinomatous pleurisy, pancreatitis, lymphoma,
hepatic hydrothorax, and similar. It is more common
among women by a ratio of 4:5, with an average age of
40 (ranging from 8 to 60). The duration of symptoms
associated with the pleural effusion was 4 days or more
(4 to 120 days) for all cases. The aspired volume aver-
aged 2,483 mL (1,000 to 4,500 mL), and 89% (8/9 pa-
tients) of the cases experienced the onset of RPE within
2 h; all onsets occurred within 24 h. Overall mortality
was 22%.2,4–6,8,9,35,36)
The clinical progressions of RPE caused by disorders
other than pneumothorax and pleural effusion are almost
identical.31–39)
From these facts, the clinical features of RPE are a
lung collapse period of 3 days or more; an evacuation
volume of 2,000 mL or more; a period of less than 1 h
from reexpansion to the onset of RPE; and the type of
pulmonary edema is permeability pulmonary edema.
On the other hand, there are also reports of pulmo-
nary edema occurring in the contralateral lung.35–38)
Of
these reports, 3 cases of edema were caused by pleural
effusion and 1 by tension pneumothorax. In all, the me-
diastinum had shifted to the opposite side resulting
from either effusion or pneumothorax. Although the in-
volvement of aspiration pneumonia, barotrauma, and
cytokine cannot be denied, compression atelectasis of
the contralateral lung associated with the shift of the
mediastinum is believed to be the main cause.
3. Morphophysiological Features of RPE
In 1978, Sewell et al. conducted the first experiment on
RPE. Using the gravimetric method, he confirmed that
when reexpanding the right lung of a goat after using a
chest tube to collapse it for 24, 48, and 72 h, RPE oc-
curred only in the lung that had been collapsed for 72
h.16)
Pavlin et al.40)
and Doerschuk et al.41)
used both the
gravimetric method and radioisotope method on rabbits
to reveal that RPE is a form of permeability pulmonary
edema. Koike et al.42)
conducted a vital measurement of
lung lymph flow using sheep and concluded from the
flow volume and protein concentration that RPE does
not occur in lungs collapsed for 24 h or less. In our vital
observation of pulmonary microcirculation in rats, we
confirmed that plasma albumin leaks from all the pul-
monary microvessels immediately after reexpansion
when reexpanding a lung that had been in a state of col-
lapse for 3 days.43)
In a histological examination of RPE, Doerschuk et
al. noted the presence of alveolar fluid and interstitial
edema and the remarkable increase in the number of al-
veolar macrophages.41)
Sewell et al. used an electron
micrograph to confirm the remarkable thickening of the
basement membrane.16)
We confirmed both the thicken-
ing of pulmonary capillary endothelium in a chronical-
ly collapsed lung and the interruption of endothelium
during reexpansion.43)
Based on these facts, it is believed that RPE is a per-
meability pulmonary edema associated with the injury
of pulmonary microvessels.
4. Pathogenesis of RPE
There are 2 major causes of RPE. One is a histological
abnormality of the pulmonary microvessels caused by
chronic lung collapse, and the other is the mechanical
stress that is added to the pulmonary microvessels by
reexpansion.
A thickening of the pulmonary capillary endotheli-
um and of the basement membrane, both caused by
chronic lung collapse, harden the pulmonary microves-
3. Reexpansion Pulmonary Edema
Ann Thorac Cardiovasc Surg Vol. 14, No. 4 (2008) 207
sels and diminish their flexibility. Therefore these pul-
monary microvessels are quite likely to be destroyed
when they are stretched by the enlargement of the lung.
Through a histological examination of the lung imme-
diately after expansion, we confirmed that the pulmo-
nary microvascular endothelium was destroyed.43)
Why does chronic lung collapse present histological
changes to the pulmonary microvascular endothelium?
Anoxic stress, mechanical stress exerted on the en-
dothelium by blood corpuscles, and changes of lung
lymph flow associated with lung collapse are all be-
lieved to be causes; however, there is no clear evidence
to prove this. Although there are reports of the superox-
ide dismutase (SOD) and cytochrome oxidase of mito-
chondria declining in a collapsed lung, it is unclear how
these factors are involved in the histological abnormali-
ties of the pulmonary microvessels.44)
Sewell et al. points out the decrease of alveolar sur-
factant activity as an effect added by reexpansion to the
pulmonary microvessels.16)
The decrease of alveolar
surfactant activity is said to induce pulmonary edema
by drastically lowering the intrapleural pressure and
further lowering the perivascular pressure of pulmonary
microvessels. However, it is difficult to believe that this
alone can cause RPE.
McCord has pointed out that organ injuries were
caused by the oxygen-derived free radicals produced
during reperfusion.45)
Saito et al. have reported that
xanthine oxidase increased in a reexpanded lung.46)
Jackson et al. have reported the increase of oxygen-
derived free radicals and the increase of activity of its
scavenger, catalase, in a reexpanded lung.47)
As stated
above, because the collapse and reexpansion of lung
produce these oxygen-derived free radicals, it is very
likely that these radicals injure the pulmonary microve-
ssels. However, there are also reports of SOD, a free
radical scavenger, being unable to prevent RPE, so it is
difficult to explain RPE by looking only at the produc-
tion of oxygen-derived free radicals.44)
Nakamura et al. have reported on increases in leuko-
cyte sequestration, as well as increases of interleukin
(IL)-8, leukotriene (LT) B4, and polymorphonuclear
leukocyte (PMN) elastase levels in the sputum in a re-
expanded lung.48)
Sakao et al. have reported a sequestra-
tion of PMN and an increase of IL-8 and mono-
cytechemoattractant protein (MCP)-1.49)
As stated
above, leukocytes migrate to the lung associated with
the reexpansion, so it is most likely that they injure the
pulmonary microvessels. However, there are reports in
which the occurrence of RPE could not be prevented
even in rabbits, whose leukocyte levels had been previ-
ously reduced; so it is difficult to explain RPE by look-
ing only at leukocyte sequestration.50)
Herein I state my theory on the pathogenesis of RPE.
Chronic lung collapse thickens the pulmonary micro-
vascular endothelium to harden it. The reexpansion of
the chronically collapsed lung injures the pulmonary
microvessels by stretching them. Alveolar surfactant
activity decreases in the reexpanded lung; thus perivas-
cular pressure decreases, and injury to the pulmonary
microvessels further increases. Subsequently, when re
perfusion occurs in the injured pulmonary microvessels,
oxygen-derived free radicals are produced. The oxygen-
derived free radicals and pulmonary microvascular in-
jury induce leukocyte sequestration into the lung. Leu-
kocytes that have migrated to the pulmonary microves-
sels further injure them. Biological injuries caused by
oxygen-derived free radicals and leukocytes cause ma-
jor damage to the pulmonary microvessels, and RPE is
established.
When reexpanding a chronically collapsed lung, we
find cases in which RPE occurs and others in which
RPE does not occur. It is believed that the mechanical
stress exerted during reexpansion is small in those
where it does not. In this condition, biological injury is
not induced, and therefore RPE is not established.43)
5. Treatments for RPE
One of the treatments for RPE is of the histological ab-
normalities of the pulmonary microvessels that are
formed in a chronically collapsed lung, and another is a
response to the mechanical stress exerted on the pulmo-
nary microvessels during reexpansion.
Although the treatment for histological changes of
the pulmonary microvessels in a chronically collapsed
lung is most effective, the cause of these abnormalities
is currently unclear, making it difficult to present a pre-
cise treatment method. There have been reports that lo-
doxamide tromethamine inhibits leukocyte sequestra-
tion and plasma leakage in RPE.51)
It is possible that a
steroid could work effectively to stabilize the pulmo-
nary microvessel membrane.
On the other hand, various attempts are being made
to respond to the mechanical stress exerted during reex-
pansion on the pulmonary microvessels. The most real-
istic response is to avoid rapid lung reexpansion. Exten-
sive occurrences of pulmonary microvascular injury
4. 208
Sohara
Ann Thorac Cardiovasc Surg Vol. 14, No. 4 (2008)
can be avoided by expanding the lung at a moderate
pace. The administration of diuretics and hyperosmotic
colloidal solution can diminish the occurrence of pul-
monary edema by raising the osmotic pressure and de-
creasing pulmonary blood flow. The most reliable
method is to prepare for tracheal intubation and nonin-
vasive positive pressure ventilation on the assumption
that RPE will occur when reexpanding a chronically
collapsed lung.
References
1. Riesman D. Albuminous expectoration following
thoracocentesis. Am J Med Sci 1902; 123: 620–30.
2. Trapnell DH, Thurston JG. Unilateral pulmonary
oedema after pleural aspiration. Lancet 1970; 1:
1367–9.
3. Johnstone W. Can you diagnose this? Reexpansion
pulmonary edema. Va Med 1980; 107: 791–2.
4. Sprung CL, Loewenherz JW, Baier H, Hauser MJ.
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