Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition caused by injury to the lungs. The document discusses the history, definition, risk factors, stages, pathophysiology, management, and treatment of ARDS. Key points include: ARDS was first described in 1967 and involves diffuse lung inflammation and fluid buildup in the lungs. The mortality rate is 40-60% despite advances in ventilation strategies and treatment. Current research focuses on optimizing oxygen delivery and utilization through various ventilation techniques while minimizing lung injury.
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.
CXR-2 is most likely to belong to this patient based on the clinical scenario provided. The patient presents with shortness of breath, fever, and crackles on lung exam suggestive of pneumonia. CXR-2 shows bilateral infiltrates consistent with pneumonia.
The document discusses Coronaviruses and COVID-19. It defines Coronaviruses as large, spherical RNA viruses with crown-like spikes that give them their name. COVID-19 is caused by SARS-CoV-2, which binds better than SARS to the ACE2 receptor in humans, causing symptoms ranging from mild to critical illness. The pathogenesis involves viral entry, replication, avoidance of the immune system, and cytokine storm. Diagnosis is via PCR or antigen tests of respiratory or stool samples. Treatment is supportive care, with some antivirals under investigation but none yet approved. Prevention emphasizes social distancing, PPE, sanitization and vaccination research.
This document provides an overview of interstitial lung disease (ILD). It discusses the pulmonary interstitium and pathogenesis of ILD. It reviews the classification of ILD and differentiates between known and idiopathic causes. Common ILDs include idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, desquamative interstitial pneumonia, and cryptogenic organizing pneumonia. A thorough clinical assessment involves obtaining a detailed history, physical exam, radiographs, pulmonary function tests, and potentially tissue sampling.
This document provides a summary of an presentation on approaches to interstitial lung disease (ILD) and updates in idiopathic pulmonary fibrosis (IPF) management. It begins with an introduction to ILDs and the pulmonary interstitium. It then covers the pathogenesis, classification, epidemiology, clinical assessment including history, exams, tests and tissue sampling, and radiological and pathological findings of ILDs. A significant portion discusses IPF specifically, including prognosis, guidelines for diagnosis, and medical therapies including pirfenidone and nintedanib which have been shown to reduce lung function decline in clinical trials. It concludes with experience using pirfenidone in Saudi Arabia.
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.
1. A 24-year-old woman presents with fever and enlarged hilar lymph nodes on chest X-ray. Her calcium level is elevated, suggesting the probable diagnosis of sarcoidosis.
2. A 37-year-old woman develops acute pneumonia symptoms and chest X-ray shows consolidation of her right lower lobe. Histology shows neutrophilic exudates in bronchioles and alveoli, consistent with bacterial pneumonia.
3. Bacterial pneumonia is usually caused by pathogens like Streptococcus pneumoniae and Haemophilus influenzae spreading via inhalation or aspiration due to impaired defenses. The patient's symptoms and radiological findings are consistent with a diagnosis of bacterial pneumonia.
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.
CXR-2 is most likely to belong to this patient based on the clinical scenario provided. The patient presents with shortness of breath, fever, and crackles on lung exam suggestive of pneumonia. CXR-2 shows bilateral infiltrates consistent with pneumonia.
The document discusses Coronaviruses and COVID-19. It defines Coronaviruses as large, spherical RNA viruses with crown-like spikes that give them their name. COVID-19 is caused by SARS-CoV-2, which binds better than SARS to the ACE2 receptor in humans, causing symptoms ranging from mild to critical illness. The pathogenesis involves viral entry, replication, avoidance of the immune system, and cytokine storm. Diagnosis is via PCR or antigen tests of respiratory or stool samples. Treatment is supportive care, with some antivirals under investigation but none yet approved. Prevention emphasizes social distancing, PPE, sanitization and vaccination research.
This document provides an overview of interstitial lung disease (ILD). It discusses the pulmonary interstitium and pathogenesis of ILD. It reviews the classification of ILD and differentiates between known and idiopathic causes. Common ILDs include idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia, desquamative interstitial pneumonia, and cryptogenic organizing pneumonia. A thorough clinical assessment involves obtaining a detailed history, physical exam, radiographs, pulmonary function tests, and potentially tissue sampling.
This document provides a summary of an presentation on approaches to interstitial lung disease (ILD) and updates in idiopathic pulmonary fibrosis (IPF) management. It begins with an introduction to ILDs and the pulmonary interstitium. It then covers the pathogenesis, classification, epidemiology, clinical assessment including history, exams, tests and tissue sampling, and radiological and pathological findings of ILDs. A significant portion discusses IPF specifically, including prognosis, guidelines for diagnosis, and medical therapies including pirfenidone and nintedanib which have been shown to reduce lung function decline in clinical trials. It concludes with experience using pirfenidone in Saudi Arabia.
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.
1. A 24-year-old woman presents with fever and enlarged hilar lymph nodes on chest X-ray. Her calcium level is elevated, suggesting the probable diagnosis of sarcoidosis.
2. A 37-year-old woman develops acute pneumonia symptoms and chest X-ray shows consolidation of her right lower lobe. Histology shows neutrophilic exudates in bronchioles and alveoli, consistent with bacterial pneumonia.
3. Bacterial pneumonia is usually caused by pathogens like Streptococcus pneumoniae and Haemophilus influenzae spreading via inhalation or aspiration due to impaired defenses. The patient's symptoms and radiological findings are consistent with a diagnosis of bacterial pneumonia.
This document discusses acute respiratory distress syndrome (ARDS). It begins by defining ARDS and describing its signs and symptoms. It then discusses the history of ARDS definitions and criteria. It outlines the pathophysiology and three phases of ARDS. Treatment strategies covered include mechanical ventilation, monitoring, infection control, and specific therapies. Prognosis and risk factors are also summarized.
1) The document discusses various lung infections (infecciones pulmonares) including bacterial, viral, and fungal pneumonias.
2) It provides details on the typical radiographic manifestations of different pathogen types, such as lobar or lobular opacities for streptococcal pneumonia and cavitating nodules for staphylococcal infections.
3) CT findings are also summarized, like the centrilobular nodules and ground-glass opacities seen with influenza virus pneumonia.
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%.
1. The document discusses several cases of interstitial lung disease and pulmonary infection. Case 1 describes a man with nodularity and calcification found on chest x-ray, with biopsy revealing birefringent particles.
2. Case 2 involves a retired shipyard worker with shortness of breath and pleural plaques on CT, with dumbbell-shaped structures staining blue.
3. The document then reviews the etiology, pathogenesis, clinical features, patterns on imaging, and pathology of various forms of interstitial lung disease and pulmonary infections like bacterial pneumonia.
This article discusses diffuse alveolar hemorrhage, which occurs when blood floods the alveoli in the lungs. Diffuse alveolar hemorrhage can be caused by many conditions including vasculitis, connective tissue disorders, infections, drugs, and other medical problems. The most common causes are Wegener's granulomatosis, Goodpasture's syndrome, and microscopic polyangiitis. Diffuse alveolar hemorrhage presents with symptoms like dyspnea, cough, and hemoptysis. Early bronchoscopy with bronchoalveolar lavage is generally required to diagnose it by identifying blood and erythrocytes in the lavage fluid. Treatment focuses on addressing the underlying cause with cort
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-
Pulmonary alveolar proteinosis (PAP) is a disease characterized by accumulation of surfactant in alveoli due to defects in surfactant clearance. The accumulation impairs gas exchange and can cause respiratory failure. Whole lung lavage is the primary treatment and improves symptoms in most patients by removing surfactant from the lungs. Exogenous GM-CSF may also be used but does not provide a cure. The document provides details on the pathophysiology, clinical presentation, diagnosis, and management of PAP.
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.
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.
1. Interstitial lung disease (ILD) refers to a group of lung disorders that involve the interstitium and can have various causes including connective tissue diseases, drugs, occupational exposures, and idiopathic fibrosis.
2. Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive form of ILD of unknown cause with poor prognosis. Diagnosis requires exclusion of other causes and evidence of fibrosis on radiology and lung biopsy.
3. Treatment options for IPF are limited but include steroids, immunosuppressants, pirfenidone, and n-acetylcysteine with mixed results reported. Research into new treatments is ongoing.
This document provides information on diffuse parenchymal lung disease (DPLD) and idiopathic interstitial pneumonias (IIPs). It begins with an overview of common IIPs including idiopathic pulmonary fibrosis (IPF), other IIPs, familial IIP, IIP with autoimmune features, and smoking-related ILDs. It then discusses diagnosing other ILDs through clinical, radiological findings and management approaches. Specific ILDs covered include CTD-associated ILDs, diffuse cystic lung diseases like lymphangioleiomyomatosis, pulmonary Langerhans cell histiocytosis, pulmonary alveolar proteinosis, and diffuse alveolar damage
Legionellosis is a respiratory disease caused by Legionella bacteria.
The term“legionellosis” may be used to refer to either Legionnaires’ disease or Pontiac fever.
https://www.cdc.gov/legionella/index.html
This document provides an overview of diffuse parenchymal lung disease (DPLD) and idiopathic interstitial pneumonias (IIPs). It discusses the classification of IIPs including idiopathic pulmonary fibrosis (IPF), nonspecific interstitial pneumonia (NSIP), respiratory bronchiolitis-associated interstitial lung disease (RB-ILD), and others. It also covers the clinical presentation, diagnostic approach involving history, physical exam, pulmonary function tests, radiological findings on high-resolution CT, and role of bronchoscopy with bronchoalveolar lavage in evaluating these conditions. Key points like reduced diffusing capacity on pulmonary function tests and honeycombing on imaging in IPF
The CT scan shows bilateral, basal-predominant reticular opacities and honeycombing. Given the patient's history of asbestos exposure, though brief, the radiological findings are most consistent with a diagnosis of asbestosis. Asbestosis is the correct answer.
ACUTE RESPIRATORY FAILURE MAGDI SASI 2015cardilogy
1. Acute respiratory failure is defined as a severe form of respiratory insufficiency resulting in a PaO2 of less than 60 mmHg or a PaCO2 of more than 50 mmHg.
2. There are two main types - type 1 with low PaO2 and normal or low PaCO2, and type 2 with low PaO2 and high PaCO2.
3. Major causes include diffuse airway obstruction, central airway obstruction, restrictive lung disease, pulmonary vascular disease, pleural and chest wall diseases, and neuromuscular diseases.
The document discusses diffuse parenchymal lung disease (DPLD), also known as interstitial lung disease. It describes that DPLD encompasses hundreds of diseases that can be classified based on known versus unknown causes. Key points include that DPLD involves the lung interstitium and alveoli, and common patterns include reticulation, ground glass opacities, and nodules. Diagnosis involves considering clinical presentation, disease progression, radiological findings such as high-resolution CT, and histopathology from procedures like bronchoscopy. Common etiologies include connective tissue disease, hypersensitivity pneumonitis, drugs, radiation, and idiopathic interstitial pneumonias.
The document discusses diffuse parenchymal lung diseases (DPLDs), a heterogeneous group of conditions that affect the lungs. Key points:
- DPLDs include idiopathic pulmonary fibrosis, which has characteristic radiologic and histologic patterns. It typically presents with progressive breathlessness.
- Sarcoidosis is a multisystem granulomatous disorder characterized by non-caseating granulomas. It commonly causes bilateral hilar lymphadenopathy and lung infiltrates.
- Pulmonary eosinophilia refers to lung abnormalities and blood eosinophilia. It includes conditions like Churg-Strauss syndrome and acute eosinophilic pneumonia.
This document discusses updates in interstitial lung disease (ILD). ILD encompasses over 200 diseases involving fibrosis and inflammation of the lung parenchyma. While traditionally considered rare, ILD now constitutes 10-15% of respiratory patients due to increased recognition through advanced imaging techniques. A clinical diagnosis is possible for some forms but lung biopsy is often needed. Common symptoms include dyspnea. Physical exam may reveal crackles. Imaging like HRCT is useful for diagnosis and monitoring. Pulmonary function tests typically show a restrictive pattern.
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 provides an overview of interstitial lung disease and CT diagnosis techniques. It begins with disclosures from the author and an outline of topics to be covered, including CT protocols, patterns seen in ILD, and integrating imaging findings with patient history. Specific ILD patterns like ground glass opacity, reticulation, honeycombing, and others are defined. Case examples are presented and classified by predominant pattern. The classification of interstitial pneumonias including UIP, NSIP, and others is discussed. Etiologies, features and prognosis of conditions like IPF and NSIP are also summarized.
This document discusses acute respiratory distress syndrome (ARDS). It begins by defining ARDS and describing its signs and symptoms. It then discusses the history of ARDS definitions and criteria. It outlines the pathophysiology and three phases of ARDS. Treatment strategies covered include mechanical ventilation, monitoring, infection control, and specific therapies. Prognosis and risk factors are also summarized.
1) The document discusses various lung infections (infecciones pulmonares) including bacterial, viral, and fungal pneumonias.
2) It provides details on the typical radiographic manifestations of different pathogen types, such as lobar or lobular opacities for streptococcal pneumonia and cavitating nodules for staphylococcal infections.
3) CT findings are also summarized, like the centrilobular nodules and ground-glass opacities seen with influenza virus pneumonia.
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%.
1. The document discusses several cases of interstitial lung disease and pulmonary infection. Case 1 describes a man with nodularity and calcification found on chest x-ray, with biopsy revealing birefringent particles.
2. Case 2 involves a retired shipyard worker with shortness of breath and pleural plaques on CT, with dumbbell-shaped structures staining blue.
3. The document then reviews the etiology, pathogenesis, clinical features, patterns on imaging, and pathology of various forms of interstitial lung disease and pulmonary infections like bacterial pneumonia.
This article discusses diffuse alveolar hemorrhage, which occurs when blood floods the alveoli in the lungs. Diffuse alveolar hemorrhage can be caused by many conditions including vasculitis, connective tissue disorders, infections, drugs, and other medical problems. The most common causes are Wegener's granulomatosis, Goodpasture's syndrome, and microscopic polyangiitis. Diffuse alveolar hemorrhage presents with symptoms like dyspnea, cough, and hemoptysis. Early bronchoscopy with bronchoalveolar lavage is generally required to diagnose it by identifying blood and erythrocytes in the lavage fluid. Treatment focuses on addressing the underlying cause with cort
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-
Pulmonary alveolar proteinosis (PAP) is a disease characterized by accumulation of surfactant in alveoli due to defects in surfactant clearance. The accumulation impairs gas exchange and can cause respiratory failure. Whole lung lavage is the primary treatment and improves symptoms in most patients by removing surfactant from the lungs. Exogenous GM-CSF may also be used but does not provide a cure. The document provides details on the pathophysiology, clinical presentation, diagnosis, and management of PAP.
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.
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.
1. Interstitial lung disease (ILD) refers to a group of lung disorders that involve the interstitium and can have various causes including connective tissue diseases, drugs, occupational exposures, and idiopathic fibrosis.
2. Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive form of ILD of unknown cause with poor prognosis. Diagnosis requires exclusion of other causes and evidence of fibrosis on radiology and lung biopsy.
3. Treatment options for IPF are limited but include steroids, immunosuppressants, pirfenidone, and n-acetylcysteine with mixed results reported. Research into new treatments is ongoing.
This document provides information on diffuse parenchymal lung disease (DPLD) and idiopathic interstitial pneumonias (IIPs). It begins with an overview of common IIPs including idiopathic pulmonary fibrosis (IPF), other IIPs, familial IIP, IIP with autoimmune features, and smoking-related ILDs. It then discusses diagnosing other ILDs through clinical, radiological findings and management approaches. Specific ILDs covered include CTD-associated ILDs, diffuse cystic lung diseases like lymphangioleiomyomatosis, pulmonary Langerhans cell histiocytosis, pulmonary alveolar proteinosis, and diffuse alveolar damage
Legionellosis is a respiratory disease caused by Legionella bacteria.
The term“legionellosis” may be used to refer to either Legionnaires’ disease or Pontiac fever.
https://www.cdc.gov/legionella/index.html
This document provides an overview of diffuse parenchymal lung disease (DPLD) and idiopathic interstitial pneumonias (IIPs). It discusses the classification of IIPs including idiopathic pulmonary fibrosis (IPF), nonspecific interstitial pneumonia (NSIP), respiratory bronchiolitis-associated interstitial lung disease (RB-ILD), and others. It also covers the clinical presentation, diagnostic approach involving history, physical exam, pulmonary function tests, radiological findings on high-resolution CT, and role of bronchoscopy with bronchoalveolar lavage in evaluating these conditions. Key points like reduced diffusing capacity on pulmonary function tests and honeycombing on imaging in IPF
The CT scan shows bilateral, basal-predominant reticular opacities and honeycombing. Given the patient's history of asbestos exposure, though brief, the radiological findings are most consistent with a diagnosis of asbestosis. Asbestosis is the correct answer.
ACUTE RESPIRATORY FAILURE MAGDI SASI 2015cardilogy
1. Acute respiratory failure is defined as a severe form of respiratory insufficiency resulting in a PaO2 of less than 60 mmHg or a PaCO2 of more than 50 mmHg.
2. There are two main types - type 1 with low PaO2 and normal or low PaCO2, and type 2 with low PaO2 and high PaCO2.
3. Major causes include diffuse airway obstruction, central airway obstruction, restrictive lung disease, pulmonary vascular disease, pleural and chest wall diseases, and neuromuscular diseases.
The document discusses diffuse parenchymal lung disease (DPLD), also known as interstitial lung disease. It describes that DPLD encompasses hundreds of diseases that can be classified based on known versus unknown causes. Key points include that DPLD involves the lung interstitium and alveoli, and common patterns include reticulation, ground glass opacities, and nodules. Diagnosis involves considering clinical presentation, disease progression, radiological findings such as high-resolution CT, and histopathology from procedures like bronchoscopy. Common etiologies include connective tissue disease, hypersensitivity pneumonitis, drugs, radiation, and idiopathic interstitial pneumonias.
The document discusses diffuse parenchymal lung diseases (DPLDs), a heterogeneous group of conditions that affect the lungs. Key points:
- DPLDs include idiopathic pulmonary fibrosis, which has characteristic radiologic and histologic patterns. It typically presents with progressive breathlessness.
- Sarcoidosis is a multisystem granulomatous disorder characterized by non-caseating granulomas. It commonly causes bilateral hilar lymphadenopathy and lung infiltrates.
- Pulmonary eosinophilia refers to lung abnormalities and blood eosinophilia. It includes conditions like Churg-Strauss syndrome and acute eosinophilic pneumonia.
This document discusses updates in interstitial lung disease (ILD). ILD encompasses over 200 diseases involving fibrosis and inflammation of the lung parenchyma. While traditionally considered rare, ILD now constitutes 10-15% of respiratory patients due to increased recognition through advanced imaging techniques. A clinical diagnosis is possible for some forms but lung biopsy is often needed. Common symptoms include dyspnea. Physical exam may reveal crackles. Imaging like HRCT is useful for diagnosis and monitoring. Pulmonary function tests typically show a restrictive pattern.
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 provides an overview of interstitial lung disease and CT diagnosis techniques. It begins with disclosures from the author and an outline of topics to be covered, including CT protocols, patterns seen in ILD, and integrating imaging findings with patient history. Specific ILD patterns like ground glass opacity, reticulation, honeycombing, and others are defined. Case examples are presented and classified by predominant pattern. The classification of interstitial pneumonias including UIP, NSIP, and others is discussed. Etiologies, features and prognosis of conditions like IPF and NSIP are also summarized.
The simplified electron and muon model, Oscillating Spacetime: The Foundation...RitikBhardwaj56
Discover the Simplified Electron and Muon Model: A New Wave-Based Approach to Understanding Particles delves into a groundbreaking theory that presents electrons and muons as rotating soliton waves within oscillating spacetime. Geared towards students, researchers, and science buffs, this book breaks down complex ideas into simple explanations. It covers topics such as electron waves, temporal dynamics, and the implications of this model on particle physics. With clear illustrations and easy-to-follow explanations, readers will gain a new outlook on the universe's fundamental nature.
A workshop hosted by the South African Journal of Science aimed at postgraduate students and early career researchers with little or no experience in writing and publishing journal articles.
Walmart Business+ and Spark Good for Nonprofits.pdfTechSoup
"Learn about all the ways Walmart supports nonprofit organizations.
You will hear from Liz Willett, the Head of Nonprofits, and hear about what Walmart is doing to help nonprofits, including Walmart Business and Spark Good. Walmart Business+ is a new offer for nonprofits that offers discounts and also streamlines nonprofits order and expense tracking, saving time and money.
The webinar may also give some examples on how nonprofits can best leverage Walmart Business+.
The event will cover the following::
Walmart Business + (https://business.walmart.com/plus) is a new shopping experience for nonprofits, schools, and local business customers that connects an exclusive online shopping experience to stores. Benefits include free delivery and shipping, a 'Spend Analytics” feature, special discounts, deals and tax-exempt shopping.
Special TechSoup offer for a free 180 days membership, and up to $150 in discounts on eligible orders.
Spark Good (walmart.com/sparkgood) is a charitable platform that enables nonprofits to receive donations directly from customers and associates.
Answers about how you can do more with Walmart!"
Strategies for Effective Upskilling is a presentation by Chinwendu Peace in a Your Skill Boost Masterclass organisation by the Excellence Foundation for South Sudan on 08th and 09th June 2024 from 1 PM to 3 PM on each day.
How to Setup Warehouse & Location in Odoo 17 InventoryCeline George
In this slide, we'll explore how to set up warehouses and locations in Odoo 17 Inventory. This will help us manage our stock effectively, track inventory levels, and streamline warehouse operations.
Main Java[All of the Base Concepts}.docxadhitya5119
This is part 1 of my Java Learning Journey. This Contains Custom methods, classes, constructors, packages, multithreading , try- catch block, finally block and more.
How to Build a Module in Odoo 17 Using the Scaffold MethodCeline George
Odoo provides an option for creating a module by using a single line command. By using this command the user can make a whole structure of a module. It is very easy for a beginner to make a module. There is no need to make each file manually. This slide will show how to create a module using the scaffold method.
A review of the growth of the Israel Genealogy Research Association Database Collection for the last 12 months. Our collection is now passed the 3 million mark and still growing. See which archives have contributed the most. See the different types of records we have, and which years have had records added. You can also see what we have for the future.
Azure Interview Questions and Answers PDF By ScholarHat
ARDS
1. ACUTE RESPIRATORY DISTRESS
SYNDROME
Michael L. Fiore, MD – Fellow in Critical Care Medicine
Mary W. Lieh-Lai, MD, Director, ICU and Fellowship Program
Division of Critical Care Medicine
Children’s Hospital of Michigan/Wayne State University
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2. A.K.A.
Adult Respiratory
Distress Syndrome
Da Nang Lung
Transfusion Lung
Post Perfusion Lung
Shock Lung
Traumatic Wet Lung
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3. HISTORICAL PERSPECTIVES
Described by William Osler in the 1800’s
Ashbaugh, Bigelow and Petty, Lancet – 1967
12 patients
pathology similar to hyaline membrane
disease in neonates
ARDS is also observed in children
New criteria and definition
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4. ORIGINAL DEFINITION
Acute respiratory distress
Cyanosis refractory to oxygen therapy
Decreased lung compliance
Diffuse infiltrates on chest radiograph
Difficulties:
lacks specific criteria
controversy over incidence and mortality
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5. REVISION OF DEFINITIONS
1988: four-point lung injury score
Level of PEEP
PaO2 / FiO2 ratio
Static lung compliance
Degree of chest infiltrates
1994: consensus conference
simplified the definition
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6. 1994 CONSENSUS
Acute onset
may follow catastrophic event
Bilateral infiltrates on chest radiograph
PAWP < 18 mm Hg
Two categories:
Acute Lung Injury - PaO /FiO ratio < 300
2 2
ARDS - PaO2/FiO2 ratio < 200
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7. EPIDEMIOLOGY
Earlier numbers inadequate (vague definition)
Using 1994 criteria:
17.9/100,000 for acute lung injury
13.5/100,000 for ARDS
Current epidemiologic study underway
In children: approximately 1% of all PICU admissions
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8. INCITING FACTORS
Shock
Aspiration of gastric contents
Trauma
Infections
Inhalation of toxic gases and fumes
Drugs and poisons
Miscellaneous
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9. STAGES
Acute, exudative phase
rapid onset of respiratory failure after trigger
diffuse alveolar damage with inflammatory cell
infiltration
hyaline membrane formation
capillary injury
protein-rich edema fluid in alveoli
disruption of alveolar epithelium
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10. STAGES
Subacute, Proliferative phase:
persistent hypoxemia
development of hypercarbia
fibrosing alveolitis
further decrease in pulmonary
compliance
pulmonary hypertension
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11. STAGES
Chronic phase
obliteration of alveolar and bronchiolar
spaces and pulmonary capillaries
Recovery phase
gradual resolution of hypoxemia
improved lung compliance
resolution of radiographic
abnormalities
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12. MORTALITY
40-60%
Deaths due to:
multi-organ failure
sepsis
Mortality may be decreasing in recent years
better ventilatory strategies
earlier diagnosis and treatment
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13. PATHOGENESIS
Inciting event
Inflammatory mediators
Damage to microvascular endothelium
Damage to alveolar epithelium
Increased alveolar permeability results
in alveolar edema fluid accumulation
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14. NORMAL ALVEOLUS
Type I cell
Alveolar
macrophage
Endothelial
Cell
RBC’s Type II
cell
Capillary
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15. ACUTE PHASE OF ARDS
Type I cell
Alveolar
macrophage
Endothelial
Cell
RBC’s Type II
cell
Capillary
Neutrophils
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16. PATHOGENESIS
Target organ injury from host’s inflammatory response and
uncontrolled liberation of inflammatory mediators
Localized manifestation of SIRS
Neutrophils and macrophages play major roles
Complement activation
Cytokines: TNF-α, IL-1β, IL-6
Platelet activation factor
Eicosanoids: prostacyclin, leukotrienes, thromboxane
Free radicals
Nitric oxide
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17. PATHOPHYSIOLOGY
Abnormalities of gas exchange
Oxygen delivery and consumption
Cardiopulmonary interactions
Multiple organ involvement
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18. ABNORMALITIES OF GAS EXCHANGE
Hypoxemia: HALLMARK of ARDS
Increased capillary permeability
Interstitial and alveolar exudate
Surfactant damage
Decreased FRC
Diffusion defect and right to left shunt
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19. OXYGEN EXTRACTION
Cell
O2
Arterial O2 O2
Venous
O2
Inflow Outflow
O2 O2 O2 O2
(Q) capillary (Q)
VO2 = Q x Hb X 13.4 X (SaO2 - SvO2)
(Adapted from the ICU Book by P. Marino)
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20. OXYGEN DELIVERY
DO2 = Q X CaO2
DO2 = Q X (1.34 X Hb X SaO2) X 10
Q = cardiac output
CaO2 = arterial oxygen content
Normal DO2: 520-570 ml/min/m2
Oxygen extraction ratio = (SaO2-SvO2/SaO2) X 100
Normal O2ER = 20-30%
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21. HEMODYNAMIC SUPPORT
Max O2 Max O2
extraction extraction
VO2 VO2
Critical DO2 Critical DO2
DO2 DO2
Normal Septic Shock/ARDS
VO2 = DO2 X O2ER Abnormal Flow Dependency
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22. OXYGEN DELIVERY & CONSUMPTION
Pathologic flow dependency
Uncoupling of oxidative dependency
Oxygen utilization by non-ATP producing
oxidase systems
Increased diffusion distance for O2 between
capillary and alveolus
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23. CARDIOPULMONARY INTERACTIONS
A = Pulmonary hypertension resulting in
increased RV afterload
B = Application of high PEEP resulting
in decreased preload
A+B = Decreased cardiac output
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24. RESPIRATORY SUPPORT
Conventional mechanical ventilation
Newer modalities:
High frequency ventilation
ECMO
Innovative strategies
Nitric oxide
Liquid ventilation
Exogenous surfactant
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25. MANAGEMENT
Monitoring:
Respiratory
Hemodynamic
Metabolic
Infections
Fluids/electrolytes
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26. MANAGEMENT
Optimize VO2/DO2 relationship
DO2
hemoglobin
mechanical ventilation
oxygen/PEEP
VO2
preload
afterload
contractility
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27. CONVENTIONAL VENTILATION
Oxygen
PEEP
Inverse I:E ratio
Lower tidal volume
Ventilation in prone position
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28. RESPIRATORY SUPPORT
Goal: maintain sufficient oxygenation
and ventilation, minimize complications
of ventilatory management
Improve oxygenation: PEEP, MAP,
Ti, O2
Improve ventilation: change in
pressure
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29. Mechanical Ventilation Guidelines
American College of Chest Physicians’ Consensus
Conference 1993
Guidelines for Mechanical Ventilation in ARDS
When possible, plateau pressures < 35 cm H O
2
Tidal volume should be decreased if necessary to
achieve this, permitting increased pCO2
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30. PEEP - Benefits
Increases transpulmonary distending pressure
Displaces edema fluid into interstitium
Decreases atelectasis
Decrease in right to left shunt
Improved compliance
Improved oxygenation
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31. No Benefit to Early Application of
PEEP
Pepe PE et al. NEJM 1984;311:281-6.
Prospective randomization of intubated patients at
risk for ARDS
Ventilated with no PEEP vs. PEEP 8+ for 72 hours
No differences in development of ARDS,
complications, duration of ventilation, time in
hospital, duration of ICU stay, morbidity or mortality
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32. Everything hinges
on the matter of
evidence
Carl Sagan
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33. Pressure-controlled Ventilation
(PCV)
Time-cycled mode
Approximate square waves of a preset pressure are
applied and released by means of a decelerating flow
More laminar flow at the end of inspiration
More even distribution of ventilation in patients with
marked different resistance values from one region of
the lung to another
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34. Pressure-controlled Inverse-ratio
Ventilation
Conventional inspiratory-expiratory ratio is reversed
(I:E 2:1 to 3:1)
Longer time constant
Breath starts before expiratory flow from prior breath
reaches baseline → auto-PEEP with recruitment of
alveoli
Lower inflating pressures
Potential for decrease in cardiac output due to increase
in MAP
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35. Extracorporeal Membrane Oxygenation
(ECMO)
Zapol WM et al. JAMA 1979;242(20):2193-6
Prospectively randomized 90 adult patients
Multicenter trial
– Conventional mechanical ventilation vs.
mechanical ventilation supplemented with partial
venoarterial bypass
– No benefit
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36. Partial Liquid Ventilation (PLV)
Ventilating the lung with conventional ventilation after
filling with perfluorocarbon
Perflubron
20 times O and 3 times the CO solubility
2 2
Heavier than water
Higher spreading coefficient
Studies in animal models suggest improved
compliance and gas exchange
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37. Partial Liquid Ventilation (PLV)
CL Leach, et al. NEJM 1996;335:761-7. The LiquiVent
Study Group
13 premature infants with severe RDS refractory to
conventional treatment
No adverse events
Increased oxygenation and improved pulmonary
compliance
8 of 10 survivors
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38. Partial Liquid Ventilation (PLV)
Hirschl et al
JAMA 1996;275:383-389
• 10 adult patients on ECMO with ARDS
Ann Surg 1998;228(5):692-700
• 9 adult patients with ARDS on conventional
mechanical ventilation
Improvements in gas exchange with few
complications
No randomized or case controlled trials
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39. High-Frequency Jet Ventilation
Carlon GC et al. Chest 1983;84:551-59
Prospective randomization of 309 adult patients with
ARDS to receive HFJV vs. Volume Cycled
Ventilation
VCV provided a higher PaO
2
HFJV had slightly improved alveolar ventilation
No difference in survival, ICU stay, or complications
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40. High Frequency Oscillating Ventilator
(HFOV)
Raise MAP
Recruit lung volume
Small changes in tidal volume
Impedes venous return necessitating intravascular
volume expansion and/or pressors
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41. Predicting outcome in children with severe acute
respiratory failure treated with high-frequency
ventilation
Sarnaik AP, Meert KL, Pappas MD, Simpson PM, Lieh-Lai
MW, Heidemann SM
Crit Care Med 1996; 24:1396-1402
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42. SUMMARY OF RESULTS
Significant improvement in pH, PaCO2, PaO2 and PaO2/FiO2
occurred within 6 hours after institution of HFV
The improvement in gas exchange was sustained
Survivors showed a decrease in OI and increase in PaO2/FiO2
twenty four hours after instituting HFV while non-survivors did not
Pre-HFV OI > 20 and failure to decrease OI by > 20% at six hours
predicted death with 88% (7/8) sensitivity and 83% (19/23)
specificity, with an odds ratio of 33 (p= .0036, 95% confidence
interval 3-365)
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43. STUDY CONCLUSIONS
In patients with potentially reversible underlying
diseases resulting in severe acute respiratory failure
that is unresponsive to conventional ventilation, high
frequency ventilation improves gas exchange in a rapid
and sustained fashion.
The magnitude of impaired oxygenation and its
improvement after high frequency ventilation can predict
outcome within 6 hours.
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44. High Frequency Oscillating Ventilation
(HFOV) – Pediatric ARDS
Arnold JH et al. Crit Care Med 1994; 22:1530-1539.
Prospective, randomized clinical study with
crossover of 70 patients
HFOV had fewer patients requiring O at 30 days
2
HFOV patients had increase survivor
Survivors had less chronic lung disease
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45. New England Journal of Medicine
2000;342:1301-8
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46. STUDY CONCLUSION
In patients with acute lung injury and the acute
respiratory distress syndrome, mechanical ventilation
with a lower tidal volume than is traditionally used
results in decreased mortality and increases the number
of days without ventilator use
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47. Prone Position
Improved gas exchange
More uniform alveolar ventilation
Recruitment of atelectasis in dorsal regions
Improved postural drainage
Redistribution of perfusion away from edematous,
dependent regions
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48. Prone Position
Nakos G et al. Am J Respir Crit Care Med
2000;161:360-68
Observational study of 39 patients with ARDS in
different stages
Improved oxygenation in prone (PaO /FiO 189±34
2 2
prone vs. 83±14 supine) after 6 hours
No improvement in patients with late ARDS or
pulmonary fibrosis
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49. Prone Position
NEJM 2001;345:568-73
Prone-Supine Study Group
Multicenter randomized clinical trial
304 adult patients prospectively randomized to 10
days of supine vs. prone ventilation 6 hours/day
Improved oxygenation in prone position
No improvement in survival
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50. Exogenous Surfactant
Success with infants with neonatal RDS
Exosurf ARDS Sepsis Study. Anzueto et al. NEJM
1996;334:1417-21
Randomized control trial
Multicenter study of 725 patients with sepsis induced
ARDS
No significant difference in oxygenation, duration of
mechanical ventilation, hospital stay, or survival
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51. Exogenous Surfactant
Aerosol delivery system – only 4.5% of radiolabeled
surfactant reached lungs
Only reaches well ventilated, less severe areas
New approaches to delivery are under study, including
tracheal instillation and bronchoalveolar lavage
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52. Inhaled Nitric Oxide (iNO)
Pulmonary vasodilator
Selectively improves perfusion of ventilated areas
Reduces intrapulmonary shunting
Improves arterial oxygenation
T1/2 111 to 130 msec
No systemic hemodynamic effects
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53. Inhaled Nitric Oxide (iNO)
Inhaled Nitric Oxide Study Group
Dellinger RP et al. Crit Care Med 1998; 26:15-23
Prospective, randomized, placebo controlled, double
blinded, multi-center study
177 adults with ARDS
Improvement in oxygenation index
No significant differences in mortality or days off
ventilator
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54. Inhaled Aerosolized Prostacyclin
(IAP)
Potent selective pulmonary vasodilator
Effective for pulmonary hypertension
Short half-life (2-3 min) with rapid clearance
Little or no hemodynamic effect
Randomized clinical trials have not been done
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55. Corticosteroids
Acute Phase Trials
Bernard GR et al. NEJM 1987;317:1565-70
99 patients prospectively randomized
Methylprednisolone (30mg/kg q6h x 4) vs. placebo
No differences in oxygenation, chest radiograph,
infectious complications, or mortality
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56. Corticosteroids
Fibroproliferative Stage
Meduri GU et al. JAMA 1998;280:159-65
24 patients with severe ARDS and failure to improve
by day 7 of treatment
Placebo vs. methylprednisolone 2mg/kg/day for 32
days
Steroid group showed improvement in lung injury
score, improved oxygenation, reduced mortality
No significant difference in infection rate
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57. PROGNOSIS
Underlying medical condition
Presence of multiorgan failure
Severity of illness
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58. We are constantly misled
by the ease with which our
minds fall into the ruts of
one or two experiences.
Sir William Osler
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