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.
- ARDS is an acute respiratory condition characterized by diffuse lung inflammation and fluid buildup in the lungs, causing hypoxemia. Common causes include sepsis, aspiration, and pneumonia.
- The document discusses the definition, pathogenesis, clinical presentation, diagnosis, and management of ARDS. The primary goals of management are treating the underlying cause, maintaining oxygenation levels through ventilation strategies like low tidal volumes, and preventing further lung injury.
- Low tidal volume ventilation, which aims to limit overexpansion of alveoli, is the best proven strategy to improve survival based on current evidence. Other adjuncts like prone positioning and PEEP may also help optimize oxygenation in some cases.
Pulmonary edema is often caused by congestive heart failure. When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs.
Diffuse alveolar hemorrhage (DAH) is a life-threatening condition characterized by widespread bleeding from the pulmonary microcirculation. It can be caused by capillaritis due to conditions like Wegener's granulomatosis or idiopathic. Diagnosis involves clinical evaluation, chest imaging, hematological and urine tests, and bronchoscopy with BAL. Treatment focuses on controlling bleeding with corticosteroids, immunosuppressants, and supportive care. DAH requires prompt diagnosis and treatment to reduce high morbidity and mortality risks.
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 provides an overview of acute respiratory distress syndrome (ARDS), including:
1) The updated Berlin definition of ARDS which requires a minimum PEEP of 5 cm H2O and specifies diagnostic criteria based on oxygenation levels.
2) The pathophysiology of ARDS involves an initial exudative phase followed by a proliferative phase and sometimes a fibrotic phase.
3) Management focuses on supportive ventilation with low tidal volumes and identification and treatment of precipitating factors, with corticosteroids and prone positioning helping in some cases. Refractory hypoxemia may be addressed through approaches like HFOV, IRV, APRV, inhaled nitric oxide, or ECMO.
The document provides information about Acute Respiratory Distress Syndrome (ARDS) including its definition, pathophysiology, diagnosis, management, and prognosis. ARDS is defined as rapid onset hypoxemia and diffuse pulmonary infiltrates leading to respiratory failure. It is caused by direct lung injury from conditions like pneumonia or indirect injury from sepsis or trauma. Diagnosis involves criteria of acute onset, hypoxemia with PaO2/FiO2 ≤200, and no heart failure. Management focuses on treating the underlying cause and providing ventilator support using low tidal volumes per the ARDSNet protocol to reduce ventilator-induced lung injury. Prognosis depends on risk factors and mortality ranges from 26-44%.
This document provides an overview of the diagnosis and management of Acute Respiratory Distress Syndrome (ARDS). It begins with defining ARDS and discussing the Berlin definition. It then covers risk factors, etiology, clinical course, pathophysiology, differential diagnosis, and management approaches. The management section emphasizes the importance of lung-protective ventilation with low tidal volumes to prevent ventilator-induced lung injury in ARDS patients.
- ARDS is an acute respiratory condition characterized by diffuse lung inflammation and fluid buildup in the lungs, causing hypoxemia. Common causes include sepsis, aspiration, and pneumonia.
- The document discusses the definition, pathogenesis, clinical presentation, diagnosis, and management of ARDS. The primary goals of management are treating the underlying cause, maintaining oxygenation levels through ventilation strategies like low tidal volumes, and preventing further lung injury.
- Low tidal volume ventilation, which aims to limit overexpansion of alveoli, is the best proven strategy to improve survival based on current evidence. Other adjuncts like prone positioning and PEEP may also help optimize oxygenation in some cases.
Pulmonary edema is often caused by congestive heart failure. When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs.
Diffuse alveolar hemorrhage (DAH) is a life-threatening condition characterized by widespread bleeding from the pulmonary microcirculation. It can be caused by capillaritis due to conditions like Wegener's granulomatosis or idiopathic. Diagnosis involves clinical evaluation, chest imaging, hematological and urine tests, and bronchoscopy with BAL. Treatment focuses on controlling bleeding with corticosteroids, immunosuppressants, and supportive care. DAH requires prompt diagnosis and treatment to reduce high morbidity and mortality risks.
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 provides an overview of acute respiratory distress syndrome (ARDS), including:
1) The updated Berlin definition of ARDS which requires a minimum PEEP of 5 cm H2O and specifies diagnostic criteria based on oxygenation levels.
2) The pathophysiology of ARDS involves an initial exudative phase followed by a proliferative phase and sometimes a fibrotic phase.
3) Management focuses on supportive ventilation with low tidal volumes and identification and treatment of precipitating factors, with corticosteroids and prone positioning helping in some cases. Refractory hypoxemia may be addressed through approaches like HFOV, IRV, APRV, inhaled nitric oxide, or ECMO.
The document provides information about Acute Respiratory Distress Syndrome (ARDS) including its definition, pathophysiology, diagnosis, management, and prognosis. ARDS is defined as rapid onset hypoxemia and diffuse pulmonary infiltrates leading to respiratory failure. It is caused by direct lung injury from conditions like pneumonia or indirect injury from sepsis or trauma. Diagnosis involves criteria of acute onset, hypoxemia with PaO2/FiO2 ≤200, and no heart failure. Management focuses on treating the underlying cause and providing ventilator support using low tidal volumes per the ARDSNet protocol to reduce ventilator-induced lung injury. Prognosis depends on risk factors and mortality ranges from 26-44%.
This document provides an overview of the diagnosis and management of Acute Respiratory Distress Syndrome (ARDS). It begins with defining ARDS and discussing the Berlin definition. It then covers risk factors, etiology, clinical course, pathophysiology, differential diagnosis, and management approaches. The management section emphasizes the importance of lung-protective ventilation with low tidal volumes to prevent ventilator-induced lung injury in ARDS patients.
A pulmonary embolism occurs when a blood clot forms in the deep veins of the legs or pelvis and travels through the bloodstream, lodging in the pulmonary arteries of the lungs. It can be difficult to diagnose and is a potentially life-threatening condition. Diagnostic tests may include a d-dimer blood test, CT scan, ventilation-perfusion scan, echocardiogram, and angiogram. Treatment involves anticoagulation medications to prevent further clotting and thrombolysis in some severe cases. Prevention by minimizing risk factors for deep vein thrombosis is important.
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.
This document provides an overview of Acute Respiratory Distress Syndrome (ARDS). It defines ARDS as sudden acute respiratory failure caused by damage to the alveolar capillary membrane, resulting in pulmonary edema. The document outlines the etiology, pathology, clinical presentation, diagnosis, and management of ARDS. It describes the exudative, proliferative, and fibrotic stages of ARDS and emphasizes the importance of supportive care including mechanical ventilation with low tidal volumes to prevent further lung injury. The mortality rate for ARDS is reported to be 40-60% despite advances in understanding its pathogenesis.
This document provides an overview of pulmonary cysts and how to differentiate them from other air-filled lung lesions using computed tomography (CT) imaging. It outlines an algorithmic approach involving 5 steps to identify cystic lung diseases based on CT findings. True cysts are defined as round parenchymal spaces surrounded by a thin wall. Other mimics like cavities and emphysema are also described. Cystic lung diseases can present as solitary cysts, subpleural cysts, or multiple intraparenchymal cysts, with or without associated nodules or ground glass opacities. Major cystic lung diseases and their characteristic CT and pathological features are reviewed. Additional testing beyond CT may be needed to
This document defines acute respiratory distress syndrome (ARDS) and discusses its pathophysiology, risk factors, diagnosis, management, and ventilator strategies. ARDS is defined as acute onset bilateral pulmonary infiltrates, hypoxemia, and no heart failure. It was initially defined in 1971 and revised definitions in 1988 and 1994 established clearer criteria. Common causes are pneumonia, aspiration, and sepsis. Management involves treating the underlying cause, supportive ICU care, and lung protective ventilation with low tidal volumes (6 ml/kg) and moderate PEEP levels. Adjuncts like conservative fluid management, prone positioning, and recruitment maneuvers may provide benefits.
This document provides an overview of pulmonary edema, including its definition, epidemiology, pathophysiology, classifications, causes, clinical manifestations, diagnosis, and treatment. Pulmonary edema is fluid accumulation in the lungs caused by increased fluid filtration from pulmonary capillaries into lung tissue. It can be cardiogenic, caused by left ventricular failure which increases hydrostatic pressure, or non-cardiogenic, caused by altered capillary permeability independent of cardiac issues. Symptoms include shortness of breath, cough, and hypoxemia. Treatment focuses on supporting oxygenation, reducing preload and afterload on the heart, and addressing any underlying conditions.
Pulmonary embolism (PE) is a blockage in the lungs caused by blood clots that travel from deep veins, usually in the legs. It is the third most common cause of death in hospitalized patients, with over 650,000 cases occurring per year in the US. Risk factors include immobilization, hypercoagulability, and recent surgery or trauma. Symptoms can include chest pain, shortness of breath, cough, or fainting. Diagnosis is confirmed through imaging tests like CT angiography or ventilation-perfusion scans. Treatment involves blood thinners like heparin, warfarin, or newer oral anticoagulants to prevent further clotting. Thrombolytic drugs
Pulmonary edema is fluid accumulation in the lungs caused by fluid leaking from blood vessels into the lung tissue and air spaces. It can be caused by issues that increase pressure in the blood vessels of the lungs like heart failure, or by problems that damage the blood vessel walls. Symptoms include shortness of breath, cough, and anxiety. Treatment depends on the underlying cause but aims to reduce fluid buildup and support breathing. Differentiating cardiogenic from non-cardiogenic pulmonary edema involves considering medical history, symptoms, physical exam findings, and chest imaging results.
Pulmonary Oedema is accumulation of fluid in lungs. It can be due to cardiogenic or non-cardiogenic causes. This presentation was a class presentation and discussed its management alongwith diagnosis.
1) Respiratory failure is defined as failure of oxygenation or carbon dioxide elimination and can be acute or chronic. It is classified as type 1 (hypoxemic) or type 2 (hypercapnic).
2) Causes of acute respiratory failure include hypoventilation, V/Q mismatching, intrapulmonary shunting, and diffusion abnormalities. Common causes are pneumonia, pulmonary edema, and ARDS.
3) Diagnosis involves clinical presentation, blood gas analysis, chest imaging, and pulmonary function tests. Management focuses on airway support, oxygen therapy, mechanical ventilation, and treating the underlying cause.
- Pulmonary embolism (PE) is a blockage in the lung's arteries caused by blood clots that travel from deep veins, most often in the legs.
- Risk factors include recent surgery or trauma, cancer, older age, and genetic predispositions. Symptoms can range from mild to life-threatening depending on the size and location of the clots.
- Diagnosis involves blood tests, imaging like CT scans, ventilation-perfusion scans, or angiography. Treatment focuses on anticoagulation with blood thinners to prevent further clotting as well as supporting heart and lung function. For some patients, more aggressive options like thrombolysis or surgery may be considered.
This document discusses the etiopathogenesis and diagnostic approach to pleural effusion. It begins by describing the anatomy of the pleura, formation and absorption of pleural fluid, and factors that influence pleural fluid composition. Transudative pleural effusions are caused by increased hydrostatic pressure or decreased oncotic pressure, while exudative effusions result from infections, malignancies, or inflammatory conditions. A diagnostic approach involves distinguishing transudates from exudates using Light's criteria and considering likely etiologies based on clinical and laboratory findings. Parapneumonic effusions may progress to empyema, which is divided into exudative, fibropurulent, and organization stages based on pathophysiology
1) Aspiration pneumonitis is a chemical injury caused by inhalation of sterile gastric contents, while aspiration pneumonia is an infectious process caused by inhalation of oropharyngeal secretions colonized by bacteria.
2) Risk factors for aspiration pneumonia include neurological dysphagia, gastroesophageal reflux, poor oral hygiene, and silent aspiration which is common in stroke patients.
3) Treatment of aspiration pneumonitis includes suctioning the airway after witnessed aspiration and possible intubation. Antibiotics are not routinely recommended but may be used if infection develops. Corticosteroids are not proven to provide clear benefits.
Pulmonary hypertension is an abnormal elevation in pulmonary artery pressure. It is classified into 5 groups based on underlying causes. Group 1 includes pulmonary arterial hypertension which is characterized by pre-capillary pulmonary hypertension in the absence of other causes. Molecular abnormalities in pulmonary arterial hypertension include decreased prostacyclin and nitric oxide, and increased endothelin-1. Genetic mutations like in the BMPR2 gene are also associated. Idiopathic pulmonary arterial hypertension has no known cause. Symptoms include fatigue, chest pain and syncope with exertion. Signs include increased pulmonary component of heart sound and murmurs.
Pulmonary Complications of Sickle Cell Disease. pptxSarfraz Saleemi
This document summarizes pulmonary complications of sickle cell disease (SCD), including acute chest syndrome (ACS) and pulmonary hypertension (PH). It notes that ACS and PH are the most serious complications, with high morbidity and mortality. The document reviews the definition, risk factors, pathophysiology, diagnosis, and management of ACS. It also discusses the prevalence of PH in SCD populations worldwide and in Saudi Arabia, ranging from 20-38%. The pathophysiology of SCD-related PH involves chronic hypoxemia, endothelial dysfunction, and elevated pulmonary pressures from infarcts and vaso-occlusion. Independent risk factors for PH development in SCD include low hemoglobin, cardiovascular or renal disease, and elevated
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.
Updates in Parapneumonic Effusion and EmpyemaGamal Agmy
The document discusses parapneumonic effusion and empyema. It classifies pneumonias and defines related terms like pleurisy, parapneumonic effusion, and empyema. It describes the pathophysiology of effusions in stages from pleuritis sicca to organization. Clinical presentation and differential diagnosis are also covered. Laboratory studies and imaging studies like chest radiography are important for diagnosing complicated parapneumonic effusions or empyemas to allow for optimal management.
Copd systemic inflammation or systemic manifestationsWaheed Shouman
COPD is associated with systemic inflammation that can lead to several extra-pulmonary effects and comorbidities. Low-grade systemic inflammation in COPD patients is characterized by elevated levels of pro-inflammatory cytokines and acute phase proteins. This systemic inflammation may originate from pulmonary inflammation spilling over into the systemic circulation, or from other sources like smoking, hypoxia, or bacterial products during exacerbations. Systemic inflammation in COPD has been implicated in several systemic effects and comorbidities including weight loss, muscle dysfunction, cardiovascular diseases, osteoporosis, and depression. Treatments like pulmonary rehabilitation, smoking cessation, and some medications can help reduce systemic inflammation and its associated manifestations in COPD.
This document defines non-resolving pneumonia and discusses its causes and diagnostic evaluation. Non-resolving pneumonia is defined as persistence of clinical symptoms and radiographic abnormalities for longer than expected despite adequate antibiotic therapy. Common causes include inappropriate antibiotic therapy, complications of the initial infection, host factors, and presence of resistant or unusual pathogens. A thorough diagnostic evaluation includes assessing treatment response, looking for complications or superinfections, evaluating for unusual organisms, and examining host immune function. Radiological imaging, bronchoscopy with protected specimen brushing or biopsy, and CT-guided biopsies can help identify causative organisms or underlying conditions.
This document discusses the pathophysiology and management of acute respiratory distress syndrome (ARDS). It notes that ARDS is characterized by pulmonary edema due to increased capillary permeability. Conservative fluid strategies aiming for zero balance can improve outcomes in ARDS patients without shock by reducing pulmonary pressures and edema. A biphasic approach starting with liberal fluids then transitioning to conservative is recommended as hemodynamics stabilize. Diuretics, fluid restriction, and potentially beta-2 agonists or albumin with furosemide in hypoproteinemic patients may help resolve edema. Central pressures, weight, fluid balance, and extravascular lung water should be monitored.
The document discusses enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay (RIA). ELISA involves coating an antigen or antibody on a solid surface, detecting it with a specific antibody or antigen linked to an enzyme. The enzyme then catalyzes a reaction producing a detectable color change. ELISA can be used to detect antibodies or antigens in samples. RIA uses a radioactive label instead of an enzyme. Both techniques are quantitative and can detect small amounts of target molecules in samples.
A pulmonary embolism occurs when a blood clot forms in the deep veins of the legs or pelvis and travels through the bloodstream, lodging in the pulmonary arteries of the lungs. It can be difficult to diagnose and is a potentially life-threatening condition. Diagnostic tests may include a d-dimer blood test, CT scan, ventilation-perfusion scan, echocardiogram, and angiogram. Treatment involves anticoagulation medications to prevent further clotting and thrombolysis in some severe cases. Prevention by minimizing risk factors for deep vein thrombosis is important.
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.
This document provides an overview of Acute Respiratory Distress Syndrome (ARDS). It defines ARDS as sudden acute respiratory failure caused by damage to the alveolar capillary membrane, resulting in pulmonary edema. The document outlines the etiology, pathology, clinical presentation, diagnosis, and management of ARDS. It describes the exudative, proliferative, and fibrotic stages of ARDS and emphasizes the importance of supportive care including mechanical ventilation with low tidal volumes to prevent further lung injury. The mortality rate for ARDS is reported to be 40-60% despite advances in understanding its pathogenesis.
This document provides an overview of pulmonary cysts and how to differentiate them from other air-filled lung lesions using computed tomography (CT) imaging. It outlines an algorithmic approach involving 5 steps to identify cystic lung diseases based on CT findings. True cysts are defined as round parenchymal spaces surrounded by a thin wall. Other mimics like cavities and emphysema are also described. Cystic lung diseases can present as solitary cysts, subpleural cysts, or multiple intraparenchymal cysts, with or without associated nodules or ground glass opacities. Major cystic lung diseases and their characteristic CT and pathological features are reviewed. Additional testing beyond CT may be needed to
This document defines acute respiratory distress syndrome (ARDS) and discusses its pathophysiology, risk factors, diagnosis, management, and ventilator strategies. ARDS is defined as acute onset bilateral pulmonary infiltrates, hypoxemia, and no heart failure. It was initially defined in 1971 and revised definitions in 1988 and 1994 established clearer criteria. Common causes are pneumonia, aspiration, and sepsis. Management involves treating the underlying cause, supportive ICU care, and lung protective ventilation with low tidal volumes (6 ml/kg) and moderate PEEP levels. Adjuncts like conservative fluid management, prone positioning, and recruitment maneuvers may provide benefits.
This document provides an overview of pulmonary edema, including its definition, epidemiology, pathophysiology, classifications, causes, clinical manifestations, diagnosis, and treatment. Pulmonary edema is fluid accumulation in the lungs caused by increased fluid filtration from pulmonary capillaries into lung tissue. It can be cardiogenic, caused by left ventricular failure which increases hydrostatic pressure, or non-cardiogenic, caused by altered capillary permeability independent of cardiac issues. Symptoms include shortness of breath, cough, and hypoxemia. Treatment focuses on supporting oxygenation, reducing preload and afterload on the heart, and addressing any underlying conditions.
Pulmonary embolism (PE) is a blockage in the lungs caused by blood clots that travel from deep veins, usually in the legs. It is the third most common cause of death in hospitalized patients, with over 650,000 cases occurring per year in the US. Risk factors include immobilization, hypercoagulability, and recent surgery or trauma. Symptoms can include chest pain, shortness of breath, cough, or fainting. Diagnosis is confirmed through imaging tests like CT angiography or ventilation-perfusion scans. Treatment involves blood thinners like heparin, warfarin, or newer oral anticoagulants to prevent further clotting. Thrombolytic drugs
Pulmonary edema is fluid accumulation in the lungs caused by fluid leaking from blood vessels into the lung tissue and air spaces. It can be caused by issues that increase pressure in the blood vessels of the lungs like heart failure, or by problems that damage the blood vessel walls. Symptoms include shortness of breath, cough, and anxiety. Treatment depends on the underlying cause but aims to reduce fluid buildup and support breathing. Differentiating cardiogenic from non-cardiogenic pulmonary edema involves considering medical history, symptoms, physical exam findings, and chest imaging results.
Pulmonary Oedema is accumulation of fluid in lungs. It can be due to cardiogenic or non-cardiogenic causes. This presentation was a class presentation and discussed its management alongwith diagnosis.
1) Respiratory failure is defined as failure of oxygenation or carbon dioxide elimination and can be acute or chronic. It is classified as type 1 (hypoxemic) or type 2 (hypercapnic).
2) Causes of acute respiratory failure include hypoventilation, V/Q mismatching, intrapulmonary shunting, and diffusion abnormalities. Common causes are pneumonia, pulmonary edema, and ARDS.
3) Diagnosis involves clinical presentation, blood gas analysis, chest imaging, and pulmonary function tests. Management focuses on airway support, oxygen therapy, mechanical ventilation, and treating the underlying cause.
- Pulmonary embolism (PE) is a blockage in the lung's arteries caused by blood clots that travel from deep veins, most often in the legs.
- Risk factors include recent surgery or trauma, cancer, older age, and genetic predispositions. Symptoms can range from mild to life-threatening depending on the size and location of the clots.
- Diagnosis involves blood tests, imaging like CT scans, ventilation-perfusion scans, or angiography. Treatment focuses on anticoagulation with blood thinners to prevent further clotting as well as supporting heart and lung function. For some patients, more aggressive options like thrombolysis or surgery may be considered.
This document discusses the etiopathogenesis and diagnostic approach to pleural effusion. It begins by describing the anatomy of the pleura, formation and absorption of pleural fluid, and factors that influence pleural fluid composition. Transudative pleural effusions are caused by increased hydrostatic pressure or decreased oncotic pressure, while exudative effusions result from infections, malignancies, or inflammatory conditions. A diagnostic approach involves distinguishing transudates from exudates using Light's criteria and considering likely etiologies based on clinical and laboratory findings. Parapneumonic effusions may progress to empyema, which is divided into exudative, fibropurulent, and organization stages based on pathophysiology
1) Aspiration pneumonitis is a chemical injury caused by inhalation of sterile gastric contents, while aspiration pneumonia is an infectious process caused by inhalation of oropharyngeal secretions colonized by bacteria.
2) Risk factors for aspiration pneumonia include neurological dysphagia, gastroesophageal reflux, poor oral hygiene, and silent aspiration which is common in stroke patients.
3) Treatment of aspiration pneumonitis includes suctioning the airway after witnessed aspiration and possible intubation. Antibiotics are not routinely recommended but may be used if infection develops. Corticosteroids are not proven to provide clear benefits.
Pulmonary hypertension is an abnormal elevation in pulmonary artery pressure. It is classified into 5 groups based on underlying causes. Group 1 includes pulmonary arterial hypertension which is characterized by pre-capillary pulmonary hypertension in the absence of other causes. Molecular abnormalities in pulmonary arterial hypertension include decreased prostacyclin and nitric oxide, and increased endothelin-1. Genetic mutations like in the BMPR2 gene are also associated. Idiopathic pulmonary arterial hypertension has no known cause. Symptoms include fatigue, chest pain and syncope with exertion. Signs include increased pulmonary component of heart sound and murmurs.
Pulmonary Complications of Sickle Cell Disease. pptxSarfraz Saleemi
This document summarizes pulmonary complications of sickle cell disease (SCD), including acute chest syndrome (ACS) and pulmonary hypertension (PH). It notes that ACS and PH are the most serious complications, with high morbidity and mortality. The document reviews the definition, risk factors, pathophysiology, diagnosis, and management of ACS. It also discusses the prevalence of PH in SCD populations worldwide and in Saudi Arabia, ranging from 20-38%. The pathophysiology of SCD-related PH involves chronic hypoxemia, endothelial dysfunction, and elevated pulmonary pressures from infarcts and vaso-occlusion. Independent risk factors for PH development in SCD include low hemoglobin, cardiovascular or renal disease, and elevated
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.
Updates in Parapneumonic Effusion and EmpyemaGamal Agmy
The document discusses parapneumonic effusion and empyema. It classifies pneumonias and defines related terms like pleurisy, parapneumonic effusion, and empyema. It describes the pathophysiology of effusions in stages from pleuritis sicca to organization. Clinical presentation and differential diagnosis are also covered. Laboratory studies and imaging studies like chest radiography are important for diagnosing complicated parapneumonic effusions or empyemas to allow for optimal management.
Copd systemic inflammation or systemic manifestationsWaheed Shouman
COPD is associated with systemic inflammation that can lead to several extra-pulmonary effects and comorbidities. Low-grade systemic inflammation in COPD patients is characterized by elevated levels of pro-inflammatory cytokines and acute phase proteins. This systemic inflammation may originate from pulmonary inflammation spilling over into the systemic circulation, or from other sources like smoking, hypoxia, or bacterial products during exacerbations. Systemic inflammation in COPD has been implicated in several systemic effects and comorbidities including weight loss, muscle dysfunction, cardiovascular diseases, osteoporosis, and depression. Treatments like pulmonary rehabilitation, smoking cessation, and some medications can help reduce systemic inflammation and its associated manifestations in COPD.
This document defines non-resolving pneumonia and discusses its causes and diagnostic evaluation. Non-resolving pneumonia is defined as persistence of clinical symptoms and radiographic abnormalities for longer than expected despite adequate antibiotic therapy. Common causes include inappropriate antibiotic therapy, complications of the initial infection, host factors, and presence of resistant or unusual pathogens. A thorough diagnostic evaluation includes assessing treatment response, looking for complications or superinfections, evaluating for unusual organisms, and examining host immune function. Radiological imaging, bronchoscopy with protected specimen brushing or biopsy, and CT-guided biopsies can help identify causative organisms or underlying conditions.
This document discusses the pathophysiology and management of acute respiratory distress syndrome (ARDS). It notes that ARDS is characterized by pulmonary edema due to increased capillary permeability. Conservative fluid strategies aiming for zero balance can improve outcomes in ARDS patients without shock by reducing pulmonary pressures and edema. A biphasic approach starting with liberal fluids then transitioning to conservative is recommended as hemodynamics stabilize. Diuretics, fluid restriction, and potentially beta-2 agonists or albumin with furosemide in hypoproteinemic patients may help resolve edema. Central pressures, weight, fluid balance, and extravascular lung water should be monitored.
The document discusses enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay (RIA). ELISA involves coating an antigen or antibody on a solid surface, detecting it with a specific antibody or antigen linked to an enzyme. The enzyme then catalyzes a reaction producing a detectable color change. ELISA can be used to detect antibodies or antigens in samples. RIA uses a radioactive label instead of an enzyme. Both techniques are quantitative and can detect small amounts of target molecules in samples.
This document provides an overview of acute respiratory distress syndrome (ARDS). It defines ARDS and differentiates it from acute lung injury. The pathophysiology of ARDS involves diffuse lung inflammation from neutrophils and proteinaceous fluid in the alveoli, reducing gas exchange. Management focuses on low tidal volume ventilation to prevent further lung injury while allowing permissive hypercapnia. Diuretics may help lung function if used conservatively. Pulmonary artery catheters are no longer routinely recommended as they do not improve outcomes and carry risk of complications.
Pulmonary edema is the abnormal accumulation of fluid in the interstitial spaces and alveoli of the lungs. There are three main types: cardiogenic, noncardiogenic, and neurogenic. Cardiogenic pulmonary edema is caused by issues like hypertension and heart failure that increase fluid filtration from blood vessels into the lungs. Noncardiogenic pulmonary edema has causes such as drug reactions, pneumonia, and smoke inhalation. Neurogenic pulmonary edema is caused by head injuries. Symptoms include dyspnea, tachycardia, cough with frothy sputum, and crackles heard on auscultation. Treatment focuses on correcting hypoxemia, reducing fluid overload with diuretics and positioning, and
Pulmonary edema is an accumulation of fluid in the lungs that can be either cardiogenic (heart-related) or non-cardiogenic in origin. Cardiogenic pulmonary edema is caused by heart damage or dysfunction leading to inadequate circulation, while non-cardiogenic is caused by toxic inhalation, aspiration, transfusions or infection. Symptoms include cough, difficulty breathing, anxiety and frothy sputum. Treatment involves oxygen, diuretics to reduce fluid, morphine for anxiety, positioning the patient upright, and treating the underlying cause. Nurses monitor vital signs closely, administer treatments, educate the patient, and assess for complications of pulmonary edema and its management.
Dokumen tersebut membahas tentang edema paru, yaitu penumpukan cairan di alveoli paru yang menyebabkan kesulitan bernapas. Edema paru dibedakan menjadi kardiogenik, yang disebabkan gagal jantung, dan non-kardiogenik, yang berkaitan dengan infeksi, cedera, atau kondisi medis lainnya. Gejala utama edema paru adalah sesak napas."
1. Atelektasis adalah kondisi paru atau sebagian paru yang tidak berkembang sempurna sehingga tidak berisi udara.
2. Penyebabnya antara lain penyumbatan bronkus, tekanan luar, dan gangguan pernapasan.
3. Pada radiologi tampak penurunan volume paru, pergeseran mediastinum dan fissura.
Dokumen tersebut membahas tentang edema paru, yaitu penimbunan cairan di jaringan interstisial dan alveolus paru yang disebabkan peningkatan permeabilitas dinding pembuluh darah paru. Edema paru dapat disebabkan oleh ketidakseimbangan tekanan hidrostatik dan onkotik, perubahan permeabilitas membran alveolar-kapiler, atau gangguan sistem limfatik. Gejala klinisnya antara lain sesak napas, batuk, dan hip
This document discusses chronic obstructive pulmonary disease (COPD) and asthma. It defines COPD as a progressive lung disease characterized by airflow limitation caused by damage to the lungs, usually from smoking. Risk factors include smoking, indoor pollution, occupational exposures, and genetic conditions. Symptoms include dyspnea, cough, and sputum production. Diagnosis involves pulmonary function tests showing reduced airflow. Treatment focuses on reducing symptoms and exacerbations through bronchodilators, anti-inflammatories, pulmonary rehabilitation, and managing exacerbations. Asthma is similarly characterized by variable and reversible airflow obstruction caused by inflammation. It has genetic and environmental triggers and is diagnosed through symptoms and pulmonary function testing showing reversibility. Treatment involves controlling triggers and a
Acute pulmonary edema refers to excess fluid in the lungs that can have cardiogenic or non-cardiogenic causes. Cardiogenic pulmonary edema is often due to left ventricular dysfunction that leads to increased pulmonary capillary pressure. Common causes of left ventricular dysfunction include congestive heart failure, myocardial infarction, cardiomyopathy, and valvular diseases. Pulmonary edema progresses through three stages as excess fluid builds up first in small blood vessels then the lung interstitium and alveoli, impairing gas exchange.
The document describes pulmonary edema and congestive heart failure. Pulmonary edema is an abnormal accumulation of fluid in the lungs, causing anxiety, suffocation, pale skin, and noisy breathing. Diagnosis involves lung auscultation and chest x-ray. Treatment includes oxygen, diuretics, morphine, and positioning the patient. Congestive heart failure occurs when the heart cannot supply enough oxygen to tissues, causing hypoxia, low blood pressure, crackles, and decreased urine output. It is diagnosed using a pulmonary artery catheter and treated with vasodilators, diuretics, inotropic medications, and balloon pumps while monitoring the patient's condition.
Pulmonary edema is an abnormal buildup of fluid in the lungs causing shortness of breath. It can be caused by conditions affecting the heart like heart failure, heart attack, or heart valve problems. Symptoms include cough, trouble breathing, and anxiety. Diagnosis involves listening to the lungs, blood tests, chest x-ray, and echocardiogram. Treatment is focused on relieving symptoms like giving oxygen, using diuretics to remove fluid, and treating the underlying cause. Nursing care focuses on monitoring the patient, administering medications, educating on treatment and preventing future episodes.
This document discusses the case of a 62-year-old man presenting with acute dyspnea. On examination, the patient is pale, sweaty, coughing pink sputum, and in respiratory distress. His pulse is 140 BPM, respiratory rate is 30, and oxygen saturation is 85%. The document outlines potential causes of acute dyspnea including pulmonary edema and provides guidance on evaluating, diagnosing, and initially managing such a patient. Key factors to consider include the patient's medical history, signs of heart failure on examination, and portable chest x-ray findings suggestive of pulmonary edema. The goals of treatment are to place the patient in a sitting position, provide high-flow oxygen, administer diuretics and opioids,
Discussion on the 2 kinds of Disperse Systems 1. Suspensions 2. Emulsions. The principles of emulsification, types and examples of emulsifying agents used.
1) Respiratory failure is a condition where the lungs cannot properly oxygenate the blood and remove carbon dioxide, classified as Type I (hypoxemic) or Type II (hypercapnic).
2) It can result from problems affecting gas exchange in the lungs, respiratory control centers in the brain, or the chest wall muscles.
3) Common causes of Type I respiratory failure include pneumonia, ARDS, and severe asthma, while Type II is often due to conditions that decrease breathing, such as COPD.
This document provides an overview of respiratory failure, including its causes, types, symptoms, diagnosis, and management. It begins by defining respiratory failure as the failure of the respiratory system in gas exchange functions of oxygenation and carbon dioxide elimination. Respiratory failure is then classified based on PaO2 and PaCO2 levels into hypoxemic (Type I) and hypercapnic (Type II) types. Common causes, clinical features, investigations, and general management principles are discussed for respiratory failure. Key aspects of managing hypoxemia and hypercapnia are also summarized.
1) Dyspnea, or shortness of breath, is a subjective experience that results from interactions between physiological, psychological, and environmental factors. It can be caused by disorders of the ventilatory pump or sensory receptors in the lungs and muscles.
2) Pulmonary edema occurs when fluid accumulates in the lungs, which can be cardiogenic due to increased hydrostatic pressures from heart problems, or noncardiogenic from direct lung injury or diseases affecting the lung barrier.
3) Differentiating cardiogenic and noncardiogenic pulmonary edema involves examining physical exam findings, chest x-rays, and response to supplemental oxygen, as they have distinct mechanisms and presentations.
1) Cardiogenic pulmonary edema (CPE) occurs when increased hydrostatic pressure in the pulmonary capillaries causes fluid to leak into the lungs due to left ventricular dysfunction or elevated left atrial pressure.
2) Diagnosis is based on history, physical exam findings of tachypnea, tachycardia, crackles on auscultation, and tests like chest x-ray, EKG, BNP, echocardiogram and pulmonary artery catheter.
3) Treatment focuses on reducing preload and afterload through medications like nitrates, ACE inhibitors, diuretics and vasodilators, as well as providing supportive care through oxygen, ventilation if needed, and inotro
Pulmonary hypertension of the newborn (PPHN) is defined as failure of the normal decrease in pulmonary vascular resistance after birth, resulting in right-to-left shunting of blood and hypoxemia. It can occur due to underdevelopment, maldevelopment, or maladaptation of the pulmonary vasculature. Clinically, infants present with respiratory distress and hypoxemia unresponsive to oxygen therapy alone. Diagnosis involves echocardiography demonstrating elevated pulmonary pressures and right-to-left shunting. Management consists of supportive care including ventilation and targeting appropriate oxygen saturations, with vasodilating agents like inhaled nitric oxide or ECMO for severe cases.
The document summarizes acute respiratory distress syndrome (ARDS), including its definition, risk factors, pathophysiology, clinical presentation, management, and treatment. ARDS is characterized by hypoxemia, bilateral lung infiltrates, and respiratory failure caused by various lung injuries. It involves exudative, proliferative and fibrotic phases. Management includes mechanical ventilation with low tidal volumes, positive end-expiratory pressure, fluid restriction and treatment of underlying conditions. However, mortality remains high at 50-60%.
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,
mechanical ventilation in restrictive lung disease.pptxnigatendalamaw2
1. The document discusses mechanical ventilation in restrictive pulmonary diseases. It outlines causes of restrictive diseases including lung parenchyma disorders, pleural disorders, and extra-pulmonary disorders.
2. Lung parenchyma disorders discussed in detail include interstitial lung diseases like sarcoidosis and hypersensitivity pneumonitis, occupational lung diseases, and atelectatic disorders like ARDS.
3. The key characteristics of restrictive diseases are decreased vital capacity, total lung capacity, and gas exchange. Ventilator settings for restrictive diseases aim to use low tidal volumes and pressures to prevent further lung injury.
Acute pulmonary edema can be either cardiogenic or non-cardiogenic in origin. Cardiogenic pulmonary edema is caused by elevated pulmonary capillary hydrostatic pressure due to conditions that increase left atrial pressure like heart failure, myocardial infarction, or valvular disease. It presents with dyspnea, crackles on exam, and chest x-ray findings of vascular congestion and fluid in the lungs. Treatment involves oxygen, diuretics, vasodilators, and inotropes. Non-cardiogenic pulmonary edema is caused by damage to the lung capillaries from conditions like near-drowning or neurogenic injury and presents with hypoxemia that does not resolve with oxygen alone.
Noncardiogenic pulmonary edema, also known as acute respiratory distress syndrome (ARDS), results from increased permeability of the alveolar-capillary membrane and accumulation of fluid in the alveoli. It can develop due to direct lung injury from inhalation or aspiration, or indirectly from systemic processes that release inflammatory mediators. Treatment involves supportive ventilation and oxygenation, as no treatments currently exist to correct the underlying membrane permeability issues. Early use of non-invasive ventilation techniques for mild cases may reduce complications and mortality compared to delayed intubation.
Pulmonary edema is excess fluid in the lungs that can be cardiogenic (heart-related) or non-cardiogenic. Cardiogenic pulmonary edema is caused by high pressures in the lungs from heart issues. Non-cardiogenic pulmonary edema can result from lung injury, infection, or high altitudes. Symptoms include shortness of breath, cough, and crackles in the lungs. Treatment focuses on oxygen, reducing pressures on the heart, and supporting breathing. Outcomes depend on the underlying cause but respiratory failure and death are possible complications if not properly managed.
Sequelae & Complications of Pneumonectomycairo1957
Pneumonectomy, or surgical removal of an entire lung, carries several potential sequelae and complications. Post-pneumonectomy pulmonary edema, which occurs within 72 hours of surgery and has a mortality rate over 50%, may be due to high oxygen levels or reperfusion injury. Over months, the remaining lung expands and the mediastinum shifts to fill the space, potentially leading to post-pneumonectomy syndrome through tracheal compression years later. Pulmonary function generally declines less than 50% with FEV1 and FVC decreasing the least. Mortality risk depends on preoperative lung function tests and cardiopulmonary exercise capacity.
Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition characterized by poor oxygenation, pulmonary infiltrates, and acute onset. It occurs when lung injury from direct or indirect causes results in increased permeability of the lungs and loss of aerated lung tissue. Management involves respiratory support through oxygen therapy, mechanical ventilation with low tidal volumes and PEEP, and prone positioning to improve oxygen levels. Complications can include infections, barotrauma, and multi-organ dysfunction if not properly managed.
This document defines acute respiratory distress syndrome (ARDS) and describes its pathophysiology and clinical presentation. ARDS is characterized by damage to the alveolar-capillary membrane resulting in fluid-filled lungs and severe hypoxemia. It has three phases - injury, proliferation, and fibrosis. The injury phase involves neutrophil infiltration and damage leading to edema, atelectasis, and hypoxemia. The proliferation phase involves repair through fibrosis. The fibrosis phase results in permanent scarring and continued hypoxemia. Clinical features progress from mild dyspnea to severe respiratory distress and hypoxemia unresponsive to oxygen supplementation.
The document provides information on acute respiratory distress syndrome (ARDS), including its definition, etiology, pathophysiology, clinical manifestations, complications, diagnostic findings, and collaborative therapy. ARDS is defined as acute respiratory failure caused by damage to the alveolar-capillary membrane, resulting in fluid-filled alveoli. It has three pathophysiology phases: injury/exudative, reparative/proliferative, and fibrotic. Clinical features include hypoxemia, reduced lung compliance, and diffuse pulmonary infiltrates on chest imaging. Treatment involves mechanical ventilation with low tidal volumes, application of PEEP, and prone positioning to improve oxygenation.
This document discusses bronchiectasis, including its definition, etiology, clinical features, diagnosis, management, and complications. Some key points:
- Bronchiectasis is irreversible dilation of the airways caused by infection or other insults that damages the airways and impairs mucus clearance.
- It has various etiologies including infection, immunodeficiency, genetic disorders, and aspiration. Recurrent infections lead to a vicious cycle of inflammation and further airway damage.
- Symptoms include chronic productive cough and sputum. Investigations include chest CT, which shows characteristic findings like airway dilation.
- Management focuses on airway clearance, antibiotics for infections, and
Persistent Pulmonary Hypertension by Dr. Joshua Petrikin, Neonatology, Direct...CMHRespiratoryCare
This document provides an overview of persistent pulmonary hypertension of the newborn (PPHN). It describes the normal transition from fetal to neonatal circulation at birth. PPHN occurs when there is a failure of the normal decrease in pulmonary vascular resistance after birth. The document discusses the pathophysiology and conditions associated with PPHN, including meconium aspiration syndrome and congenital diaphragmatic hernia. Clinical presentation, diagnosis, and management strategies are outlined, including inhaled nitric oxide and extracorporeal membrane oxygenation. Prognosis and potential follow up issues are also reviewed.
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 life-threatening form of respiratory failure characterized by diffuse lung inflammation and damage leading to hypoxemia. It has multiple causes but is commonly due to sepsis, pneumonia, or trauma. The pathology involves damage to the lung epithelium and endothelium, resulting in fluid accumulation in the alveoli. Treatment focuses on lung-protective ventilation with low tidal volumes, moderate levels of PEEP, and consideration of prone positioning. Other strategies include corticosteroids, neuromuscular blockade, and restrictive fluid management. More severe cases may require advanced support such as ECMO.
Pulmonary edema is the abnormal accumulation of fluid in the lungs, which can be caused by conditions that increase hydrostatic pressure (cardiogenic) or abnormalities that damage the lung tissue and cause fluid leakage (noncardiogenic). Common symptoms include dyspnea, cough, and crackles heard on auscultation. Diagnosis involves chest imaging, blood gases, and echocardiogram. Treatment focuses on correcting hypoxemia with oxygen supplementation and reducing pulmonary hydrostatic pressure through diuretics, afterload reducers, and positioning the patient upright.
Presentation1.pptx, radiological imaging of restrictive lung diseases.Abdellah Nazeer
1. Restrictive lung diseases are characterized by diffuse involvement of the pulmonary connective tissue leading to stiff lungs and reduced expansion.
2. Fibrosis results in the stiffening of the lung tissue, predominantly in the delicate alveolar walls.
3. Common restrictive lung diseases include idiopathic pulmonary fibrosis, hypersensitivity pneumonitis, and pneumoconiosis.
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.
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.
2. PATHOGENESIS changes in permeability of the pulmonary capillary membrane as a result of either a direct or an indirect pathologic insult elevated intravascular pressure and pulmonary capillary leak
3. Blast Theory An initial and rapid increase in pulmonary vascular pressure due to pulmonary vasoconstriction or pulmonary blood flow can lead to pulmonary microvascular injury. An increase in vascular permeability consequently results in edema formation, as suggested by the frequent observation of pulmonary hemorrhage in NPE
4. Causes ARDS Neurogenic pulmonary edema Pulmonary edema in renal failure and/or fluid overload Negative-pressure pulmonary edema Pulmonary edema in marathon runners Decompression sickness Heroin and naloxone overdose NPE associated with cytotoxic chemotherapy Pulmonary complications of pregnancy Drowning NPE induced by a molecular adsorbent recirculating system Transfusion-related pulmonary edema between mother and child NPE after lung transplantation NPE in children with nonaccidental injury
5. Adult respiratory distress syndrome presence of bilateral pulmonary infiltrates on chest radiograph, impaired oxygenation resulting in a PaO2 -to–fraction of inspired oxygen (FIO2) ratio of less than 200, and absence of elevated pulmonary arterial occlusion pressure (PAOP) or left atrial pressure. originates from a number of insults involving damage to the alveolocapillary membrane with subsequent fluid accumulation in the airspaces of the lung.
6. Neurogenic pulmonary edema increased intracranial pressure, stimulate the hypothalamus and the vasomotor centers of the medulla. Pulmonary venoconstriction occurs with sympathetic stimulation dramatic change in Starling forces, govern the movement of fluid between capillaries and the interstitium
7. Pulmonary edema in renal failure/fluid overload Impaired salt and/or water excretion leads to plasma volume expansion. along with decreased plasma oncotic pressure and an increase in capillary permeability
8. Negative-pressure pulmonary edema associated with upper airway obstruction Most cases are croup or epiglottitis in the pediatric and adults requiring emergent airway intervention for laryngospasm or upper airway tumors Negative intrapleural pressure is the primary pathologic event increasing venous return to the right heart and by decreasing the output of the left ventricle, increasing pulmonary blood volume and microvascular pressures.
9. Pulmonary edema in marathon runners Hyponatremia, cerebral edema, and NPE can occur in healthy marathon runners. often associated with hyponatremic encephalopathy
11. High-Altitude Pulmonary Edema prolonged exposure to an environment with a lower partial oxygen atmospheric pressure. occurs most frequently in young males 24–48 hours after they have made a rapid ascent to heights greater than 3,000 meters and have remained in that environment (52-54)
12. Heroin and naloxone overdose Pathogenesis is unknown clinically apparent immediately after or within 2 hours following drug use. Signs include rales; significant hypoxia; pink, frothy sputum; and bilateral, fluffy infiltrates on chest radiography
13. Drug-Related NPE reported following the accidental intra-arterial injection of benzathine penicillin in the gluteal region reported on a patient in whom pulmonary edema was associated with low left ventricular filling pressures and hypotension, which developed soon after the person ingested 12.5 mg of hydrochlorothiazide. life-threatening NPE has been reported following an idiosyncratic reaction after clopidogrel use
14. NPE associated with cytotoxic chemotherapy said to occur in 20% of patients receiving cytotoxic chemotherapy. clinical and imaging findings are similar to those of NPE due to other causes.
15. Pulmonary complications of pregnancy Physiologic changes diaphragm is elevated by as much as 4 cm because of displacement of the abdominal organs by the gravid uterus, decreasing lung volumes. Maternal blood volume and cardiac output increase approximately 45% by midpregnancy. Cardiac output can increase as much as 80% during vaginal delivery and up to 50% with cesarean delivery
16. Drowning extent and severity of the edema depends on the amount of water aspirated and the degree of hypoxia injury of the alveolar septa, increased permeability of the pulmonary vascular endothelium, pulmonary microvascular platelet aggregation, and intra-alveolar edema Whether the water is fresh or salt makes no difference
17. NPE induced by a molecular adsorbent recirculating system related, among others, to blood or blood-product transfusion, intravenous contrast injection, air embolism, and drug ingestion. possibly by means of an immune-mediated mechanism.
18. Transfusion-related pulmonary edema between mother and child(TRALI) underdiagnosed and serious complication of blood transfusion presence of anti–human leukocyte antigen (anti-HLA) and/or antigranulocyte antibodies in the plasma of donors is implicated in the pathogenesis of TRALI. Designated blood transfusion between multiparous mothers and their children might add an additional transfusion-related risk owing to the increased likelihood of the HLA antibody-antigen specificity between mother and child.
19. NPE after lung transplantation Complications of lung transplantation include the reimplantation response, acute rejection, pleural effusion, lymphoproliferative disorders, bronchiolitisobliterans, infection, and airway stenosis or dehiscence. reimplantation response is a form of NPE that begins soon after surgery and resolves in days to weeks.
20. NPE in children with nonaccidental injury NPE in children may occur after head injury, prolonged seizure, acute airway obstruction, or ingestion or inhalation of toxic drugs or chemicals. Rarely, NPE may be associated with child abuse or maltreatment.
21. RADIOLOGICAL FEATURE Heart size may be normal in lung injury and NPE nephrogenic pulmonary edema are classically described as having a bat-wing distribution those in lung injury tend to be more peripherally finding, diffuse variety is seen with equal frequency, presence of air bronchograms ARDS may resemble cardiac pulmonary edema. However, over the course of 24-48 hours following the onset of tachypnea, dyspnea, and hypoxia, ARDS becomes more widespread and uniform
22. characteristic for differentiating cardiac pulmonary edema from NPE, as well as from pneumonia and other widespread exudates, is the amount of time it takes for the edema to develop and to vanish. The reimplantation response (NPE due to ischemia, trauma, denervation, and lymphatic interruption) occurred in 12 patients and usually consisted of bilateral perihilar and basal consolidation
23.
24. ARDS associated with DAD in a 20-year-old man involved in a motor vehicle accident who underwent massive bronchoaspiration during tracheal intubation. bilateral diffuse airspace consolidations with a marked anteroposterior gradient. In addition, bilateral peripheral areas of hyperlucency representing trapped air are seen. Kerley lines are notably absent, and pleural effusions are minor compared with the extent of the airspace lesions.
25. Neurogenic pulmonary edema in a 54-year-old woman who was admitted for intracranial hemorrhage due to arterial hypertension. Chest x-ray shows airspace consolidations predominantly at the apices. There are no pleural effusions or Kerley lines, and heart size is normal.
26. High-altitude pulmonary edema in an experienced 30-year-old female at an altitude of 4,500 meters demonstrate numerous small, confluent airspace consolidations that spare the apices and most of the lung cortex. No Kerley lines or pleural effusions are seen. The heterogeneity of the airspace disease may reflect the heterogeneity of the pulmonary vascular constriction.
27. Heroin-induced pulmonary edema in a 19-year-old male addict with ARDS. Chest radiograph reveals massive diffuse pulmonary edema.
28. Heroin-induced pulmonary edema in a 19-year-old male addict with ARDS obtained 27 hours later reveals substantial resolution of the pulmonary edema, which is only possible in the absence of DAD
29. Heroin-induced pulmonary edema in a 24-year-old male addict who was admitted with a Glasgow coma score of 3. (a) Chest radiograph obtained at the time of admission demonstrates confluent right pulmonary edema due to the right lateral decubitus position the patient had maintained for the previous 24 hours
30. Pulmonary edema following administration of a cytokine in a 37-year-old woman with malignant melanoma. obtained 48 hours after treatment demonstrates bilateral diffuse pulmonary edema with peribronchial cuffing (arrow), enlarged hila, ill-defined vessels, and pleural effusions. Note the absence of alveolar areas of increased opacity. The infiltrates disappeared within 5 days.
31. Pulmonary edema in a 34-year-old man who had undergone bilateral lung transplantation for end-stage cystic fibrosis. radiograph obtained 48 hours after transplantation demonstrates diffuse, confluent alveolar areas of increased opacity.
32. Chest radiograph, before blood transfusion, of a patient with transfusion-related acute lung injury (TRALI)
33. Chest radiograph after blood transfusion, of a patient with transfusion-related acute lung injury (TRALI). Bilateral pulmonary infiltrates consistent with pulmonary oedema are an essential criterion for the clinical diagnosis of TRALI. Radiographs may be patchy in the first hours following transfusion, with progression of the alveolar and interstitial infiltrates such that there can be a ‘whiteout’ of the entire lung.
34. Pulmonary edema in a 34-year-old man who had undergone bilateral lung transplantation for end-stage cystic fibrosis. obtained 2 days later, the areas of increased opacity have decreased markedly. The heart and vascular axes are normal in size.