Community-acquired pneumonia is an acute infection of the lung parenchyma acquired outside of a hospital setting. Risk factors include older age, smoking, and underlying medical conditions. Common causes are Streptococcus pneumoniae, Haemophilus influenzae, and respiratory viruses. Clinical presentation varies from mild to severe, with symptoms like cough, fever, and shortness of breath. Chest imaging typically shows infiltrates. Subtypes include bronchopneumonia, atypical pneumonia, and viral pneumonia, which have characteristic imaging patterns of involvement.
This document discusses 5 cases of pulmonary tuberculosis presenting with various symptoms and radiographic findings. It provides details on the chest x-ray and CT scan images for each case. It also includes background information on the types of tuberculosis infection including primary TB, reactivation TB, and miliary TB. Common radiologic signs seen in TB are described, such as the tree-in-bud sign, lung nodules, and cavitations. Differential diagnoses and diagnostic criteria for pulmonary TB are also outlined.
The chest x-ray shows a wedge-shaped opacity in the right middle lobe of the lung with a thick-walled irregular cavity and associated collapse. This could indicate sequelae from a previous infection, malignancy, or other conditions. Cavities in the lung can be caused by infections like tuberculosis, fungi, and parasites; immune-mediated diseases like Wegener's granulomatosis and sarcoidosis; neoplasms; blood clots; or airway diseases such as bullae and cystic bronchiectasis. Further evaluation is needed to determine the underlying etiology.
Updates on Acute respiratory distress syndromeHamdi Turkey
The document provides an overview of acute respiratory distress syndrome (ARDS). It begins with a case presentation of a patient exhibiting symptoms of ARDS and then outlines the learning objectives which include understanding the definition, pathology, ventilation strategies, and adjunct therapies for ARDS. It reviews the history and evolving definitions of ARDS from 1967 to the current Berlin Definition from 2012. Key aspects of the Berlin Definition are described. The document discusses the incidence, outcomes, risk factors, pathophysiology involving different phases, clinical features, investigations, management goals and therapies for ARDS. Images are included showing histology, chest x-rays and CT scans of ARDS patients.
The document summarizes various pulmonary manifestations that can occur in patients with systemic lupus erythematosus (SLE). The most common manifestations are pleuritis and pleural effusions, as well as upper respiratory tract infections. Other potential manifestations include acute lupus pneumonitis, interstitial lung disease, pulmonary hypertension, shrinking lung syndrome, pulmonary hemorrhage, and cryptogenic organizing pneumonia. Diagnosis involves imaging tests, pulmonary function tests, biopsy, and ruling out other causes. Treatment depends on the specific manifestation but often involves corticosteroids, immunosuppressants, and other medications.
The document discusses interstitial lung disease (ILD), including its common features, types, causes, diagnostic approach and treatment. It describes various ILD types such as idiopathic pulmonary fibrosis and sarcoidosis. Imaging and biopsy are used to diagnose ILD and determine prognosis. Treatment involves identifying and removing environmental causes, suppressing inflammation, and managing complications like right heart failure.
This document discusses pulmonary manifestations in HIV patients. It begins with an introduction to HIV transmission and risk groups. It then discusses how HIV affects the lungs, causing direct infection and immune dysfunction. Common pulmonary conditions in HIV patients are described, including opportunistic infections like Pneumocystis pneumonia and tuberculosis, which present differently based on CD4 count. Imaging findings for various lung diseases seen in HIV are provided, with examples of abnormalities seen on chest x-ray and CT for conditions like Pneumocystis pneumonia and bacterial/mycobacterial infections. Risk factors, diagnosis and treatment approaches are also summarized.
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 discusses 5 cases of pulmonary tuberculosis presenting with various symptoms and radiographic findings. It provides details on the chest x-ray and CT scan images for each case. It also includes background information on the types of tuberculosis infection including primary TB, reactivation TB, and miliary TB. Common radiologic signs seen in TB are described, such as the tree-in-bud sign, lung nodules, and cavitations. Differential diagnoses and diagnostic criteria for pulmonary TB are also outlined.
The chest x-ray shows a wedge-shaped opacity in the right middle lobe of the lung with a thick-walled irregular cavity and associated collapse. This could indicate sequelae from a previous infection, malignancy, or other conditions. Cavities in the lung can be caused by infections like tuberculosis, fungi, and parasites; immune-mediated diseases like Wegener's granulomatosis and sarcoidosis; neoplasms; blood clots; or airway diseases such as bullae and cystic bronchiectasis. Further evaluation is needed to determine the underlying etiology.
Updates on Acute respiratory distress syndromeHamdi Turkey
The document provides an overview of acute respiratory distress syndrome (ARDS). It begins with a case presentation of a patient exhibiting symptoms of ARDS and then outlines the learning objectives which include understanding the definition, pathology, ventilation strategies, and adjunct therapies for ARDS. It reviews the history and evolving definitions of ARDS from 1967 to the current Berlin Definition from 2012. Key aspects of the Berlin Definition are described. The document discusses the incidence, outcomes, risk factors, pathophysiology involving different phases, clinical features, investigations, management goals and therapies for ARDS. Images are included showing histology, chest x-rays and CT scans of ARDS patients.
The document summarizes various pulmonary manifestations that can occur in patients with systemic lupus erythematosus (SLE). The most common manifestations are pleuritis and pleural effusions, as well as upper respiratory tract infections. Other potential manifestations include acute lupus pneumonitis, interstitial lung disease, pulmonary hypertension, shrinking lung syndrome, pulmonary hemorrhage, and cryptogenic organizing pneumonia. Diagnosis involves imaging tests, pulmonary function tests, biopsy, and ruling out other causes. Treatment depends on the specific manifestation but often involves corticosteroids, immunosuppressants, and other medications.
The document discusses interstitial lung disease (ILD), including its common features, types, causes, diagnostic approach and treatment. It describes various ILD types such as idiopathic pulmonary fibrosis and sarcoidosis. Imaging and biopsy are used to diagnose ILD and determine prognosis. Treatment involves identifying and removing environmental causes, suppressing inflammation, and managing complications like right heart failure.
This document discusses pulmonary manifestations in HIV patients. It begins with an introduction to HIV transmission and risk groups. It then discusses how HIV affects the lungs, causing direct infection and immune dysfunction. Common pulmonary conditions in HIV patients are described, including opportunistic infections like Pneumocystis pneumonia and tuberculosis, which present differently based on CD4 count. Imaging findings for various lung diseases seen in HIV are provided, with examples of abnormalities seen on chest x-ray and CT for conditions like Pneumocystis pneumonia and bacterial/mycobacterial infections. Risk factors, diagnosis and treatment approaches are also summarized.
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.
Non-resolving pneumonia can have several causes, including misdiagnosis of the pathogen, host factors like comorbidities or immune deficiencies, or development of complications from the initial infection. Normal resolution of pneumonia involves improvement within 3-5 days, while slow resolution may take over a month. Factors like age, severity of illness, and the infectious agent can impact the rate of resolution. Evaluation of non-resolving cases should consider multidrug-resistant bacteria, non-bacterial pathogens, underlying host conditions, or non-infectious mimickers of pneumonia.
This document discusses pulmonary hypertension (PH), defining it as a mean pulmonary artery pressure over 22 mmHg. PH is classified into 5 groups, with Group 1 being pulmonary arterial hypertension (PAH). PAH is defined by a mPAP over 25 mmHg and PCWP under 15 mmHg on right heart catheterization. Symptoms are nonspecific but include dyspnea and fatigue. Diagnosis involves echocardiogram, right heart catheterization, and tests like CT, V/Q scan, and PFTs. Treatments include diuretics, anticoagulants, oxygen, PAH-specific therapies like prostanoids, ERAs, PDE5is, and transplant for severe cases.
This document discusses idiopathic pulmonary fibrosis (IPF), a chronic, progressive fibrosing interstitial pneumonia of unknown cause associated with a histopathologic pattern of usual interstitial pneumonia (UIP). It defines IPF and outlines the diagnostic criteria, which involves ruling out known causes, abnormal pulmonary function tests, characteristic radiologic findings on high-resolution computed tomography (HRCT), and surgical lung biopsy showing UIP pattern. HRCT features that are consistent and inconsistent with UIP are described. Guidelines for management of IPF are provided, including recommendations for pirfenidone and nintedanib based on recent clinical trials. Lung transplantation is the only treatment that increases long-term survival for patients with IPF.
The pulmonary vascular circuit has low resistance and carries 70ml of blood normally. Blood flow is normally higher in the lung bases than apices due to gravity. The pulmonary arteries have a small diameter of 3mm or less in the upper intercostal spaces. Pulmonary hypertension is defined as a sustained elevation of pulmonary arterial pressure over 25mmHg at rest or 30mmHg during exercise, with normal pulmonary capillary wedge pressure and left ventricular end-diastolic pressure. Signs on chest X-ray include enlarged pulmonary arteries, loss of peripheral vessel markings, and enlargement of the right side of the heart in advanced disease.
An approach to Interstitial Lung Disease / Diffuse Parenchymal Lung DiseaseThomas Kurian
YouTube link: https://youtu.be/gPr31qrivUc
An approach to Diffuse Parenchymal Lung disease / Interstitial Lung disease with emphasis on the idiopathic causes.
This document provides information on community-acquired pneumonia (CAP). It defines CAP and distinguishes it from other types of pneumonia. It then discusses the epidemiology, clinical presentation, etiology, symptoms, diagnosis, treatment, and antibiotic resistance patterns associated with CAP. Key points include that CAP affects millions annually in the US with high costs, accurate diagnosis and treatment is important to reduce mortality, and resistance to commonly used antibiotics is a concern.
1. Dr. Rajkoti discusses the approach to evaluating and managing non-resolving pneumonia. Key factors that can delay resolution are host factors like age, comorbidities, and smoking as well as drug-resistant or unusual pathogens.
2. Three case studies are presented. The first involves a teenage boy with empyema that required drainage. The second is a middle-aged man with hypersensitivity pneumonitis related to his job that responded to steroids. The third involves further evaluation of a woman's non-productive cough to identify potential non-infectious causes.
3. For non-resolving pneumonia, re-emphasis is placed on thorough history, microbiology testing, imaging,
This document discusses the approach to interstitial lung diseases (ILD) and diffuse parenchymal lung diseases (DPLD). It begins by reviewing the spectrum of ILD and DPLD, identifying clues from clinical presentation to make a diagnosis, and reviewing common radiographic findings. Key points include that ILD involves the pulmonary interstitium located between the epithelial and endothelial basement membranes. Clinical presentation of DPLD/ILD often involves dyspnea, cough, and abnormal chest imaging. Diagnosis involves considering history, physical exam, pulmonary function tests, imaging like chest radiographs and CT, and tissue sampling. Management depends on the specific diagnosis but may include treatments like corticosteroids, immunosuppressants, anti
PowerPoint presentation describing various aspects of Pulmonary Hypertension. Please mail me your feedback on this presentation to following Email ID: tinkujoseph2010@gmail.com.
Cor pulmonale, or right heart failure caused by pulmonary or thoracic disease, can result from pulmonary arterial hypertension (PAH) due to conditions that obstruct the pulmonary vasculature. Common causes of PAH include heartworm disease, pulmonary thromboembolism from conditions causing blood stasis or hypercoagulability, and chronic lung diseases. Physical exam may reveal murmurs, respiratory distress, and signs of congestion. Diagnosis involves detecting abnormal gas exchange on bloodwork, radiographic evidence of lung disease or right heart enlargement, and ECG changes reflective of right heart strain. However, diagnosing the underlying cause like pulmonary thromboembolism can be challenging as exams and tests may be normal in some
This document provides information on eosinophils and pulmonary eosinophilic syndromes. It discusses the classification of pulmonary eosinophilic syndromes including Loeffler's syndrome, drug-induced pulmonary eosinophilia, idiopathic acute eosinophilic pneumonia, tropical pulmonary eosinophilia, and chronic eosinophilic pneumonia. For each condition, it describes the clinical features, investigations, treatment, and prognosis. Radiographic and microscopic images are also included to illustrate common findings.
Pulmonary Langerhans cell histiocytosis (PLCH) is an uncommon lung disease that typically affects young adult smokers. It is characterized by inflammatory lesions surrounding small airways and blood vessels that can progress to interstitial fibrosis. Common symptoms include cough, dyspnea, and weight loss. Diagnosis involves imaging showing nodules and cysts predominantly in the mid and upper lung zones. Transbronchial biopsy can confirm the presence of Langerhans cells. Cessation of smoking is the primary treatment and can lead to remission of symptoms.
This document defines and outlines Churg-Strauss Syndrome (CSS), a rare eosinophilic vasculitis disease. It provides details on the epidemiology, pathogenesis, clinical manifestations, diagnosis, treatment, and prognosis of CSS. CSS is characterized by eosinophil-rich inflammation involving small to medium blood vessels and is associated with asthma, allergies, and eosinophilia. Treatment involves high doses of corticosteroids, with immunosuppressants used for resistant cases. Prognosis is generally better than other vasculitis diseases but mortality can occur from cardiac or neurological involvement.
Small airways disease refers to pathologies that affect the small conducting airways less than 3mm in diameter. CT scanning is the imaging modality of choice for evaluating small airways disease. On HRCT, direct signs of small airways disease include thickened airway walls, dilated or obliterated airways, and nodules. Indirect signs include air trapping, subsegmental atelectasis, centrilobular emphysema, and centrilobular nodules. Common patterns seen on HRCT include tree-in-bud, poorly defined centrilobular nodules, decreased lung attenuation, and ground glass opacities with consolidation.
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.
Sarcoidosis is a systemic granulomatous disease of unknown origin characterized by non-caseating granulomas that commonly affect the lungs. Pulmonary manifestations are present in 90% of patients and include bilateral hilar lymphadenopathy and pulmonary infiltrates. While two thirds of patients experience remission within ten years, one third have progressive disease that can lead to pulmonary fibrosis and, in rare cases, death. Computed tomography is more sensitive than chest x-rays in detecting lymph node enlargement and lung abnormalities associated with sarcoidosis.
This document discusses radiation pneumonitis, which is an inflammation of the lungs caused by radiation therapy. It can occur in 5-15% of people receiving radiation to the chest. Symptoms include dyspnea, cough, and fever and typically appear 1-6 months after radiation. Diagnosis is based on chest imaging showing changes corresponding to the radiation site. Treatment involves corticosteroids to reduce inflammation. Radiation pneumonitis can progress to pulmonary fibrosis with permanent lung damage if left untreated.
Chest pain has many potential causes, both cardiac and non-cardiac. A thorough history and physical exam are important to establish a pre-test probability of different diseases. Clinical decision rules can help quantify the likelihood of conditions like myocardial infarction, pneumonia, and pulmonary embolism. No single diagnostic test is perfect, so likelihood ratios provide a framework for interpreting test results in the context of the pre-test probability. An evidence-based approach uses all available information to guide appropriate testing and diagnosis.
This document provides an outline and summary of various pulmonary imaging findings. It begins with an introduction by Dr. Mazen Qusaibaty and provides sections on CT halo sign (part 2), Hampton hump sign, and Westermark sign. Specific cases and images are presented to demonstrate findings of bronchiolitis obliterans with organizing pneumonia (BOOP), pulmonary endometriosis, focal traumatic lung injury, and pseudonodules. Radiographic signs of pulmonary embolism on chest x-ray and CT findings of acute pulmonary embolism on helical CT are also summarized.
Obesity hypoventilation syndrome is characterized by obesity (BMI > 40), sleep disordered breathing (90% have obstructive sleep apnea), and hypercapnia and hypoxemia. It is caused by changes in respiratory mechanics and central drive due to obesity, as well as sleep disordered breathing and leptin resistance. Treatment involves a multidisciplinary approach including positive airway pressure therapy, weight loss, supplemental oxygen, and pharmacological therapy to normalize ventilation and prevent oxygen desaturation. Early diagnosis and treatment are important to improve outcomes.
Community acquired pneumonia (CAP) is an acute lung infection that develops outside of a hospital setting. It is caused by bacteria, viruses, fungi or protozoa. The most common bacteria that cause CAP include Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Moraxella catarrhalis. Risk factors for CAP include chronic health conditions, smoking, HIV, and medications that suppress the immune system. Symptoms typically include fever, cough, shortness of breath, and chest pain. Diagnosis involves chest x-ray and testing sputum or blood samples. Complications can include respiratory failure, organ damage,
Pneumonia is an acute lung infection that can affect the alveoli and interstitial tissue in different patterns. It is commonly caused by bacteria like Streptococcus pneumoniae and viruses. Risk factors include smoking, age, diseases like COPD, and immunosuppression. Symptoms include fever, cough, difficulty breathing. Diagnosis involves tests like CXR, sputum culture, blood tests. Treatment depends on severity and includes oxygen, fluids, and antibiotics chosen based on location and patient factors. Complications can include empyema, abscesses, and respiratory failure.
Non-resolving pneumonia can have several causes, including misdiagnosis of the pathogen, host factors like comorbidities or immune deficiencies, or development of complications from the initial infection. Normal resolution of pneumonia involves improvement within 3-5 days, while slow resolution may take over a month. Factors like age, severity of illness, and the infectious agent can impact the rate of resolution. Evaluation of non-resolving cases should consider multidrug-resistant bacteria, non-bacterial pathogens, underlying host conditions, or non-infectious mimickers of pneumonia.
This document discusses pulmonary hypertension (PH), defining it as a mean pulmonary artery pressure over 22 mmHg. PH is classified into 5 groups, with Group 1 being pulmonary arterial hypertension (PAH). PAH is defined by a mPAP over 25 mmHg and PCWP under 15 mmHg on right heart catheterization. Symptoms are nonspecific but include dyspnea and fatigue. Diagnosis involves echocardiogram, right heart catheterization, and tests like CT, V/Q scan, and PFTs. Treatments include diuretics, anticoagulants, oxygen, PAH-specific therapies like prostanoids, ERAs, PDE5is, and transplant for severe cases.
This document discusses idiopathic pulmonary fibrosis (IPF), a chronic, progressive fibrosing interstitial pneumonia of unknown cause associated with a histopathologic pattern of usual interstitial pneumonia (UIP). It defines IPF and outlines the diagnostic criteria, which involves ruling out known causes, abnormal pulmonary function tests, characteristic radiologic findings on high-resolution computed tomography (HRCT), and surgical lung biopsy showing UIP pattern. HRCT features that are consistent and inconsistent with UIP are described. Guidelines for management of IPF are provided, including recommendations for pirfenidone and nintedanib based on recent clinical trials. Lung transplantation is the only treatment that increases long-term survival for patients with IPF.
The pulmonary vascular circuit has low resistance and carries 70ml of blood normally. Blood flow is normally higher in the lung bases than apices due to gravity. The pulmonary arteries have a small diameter of 3mm or less in the upper intercostal spaces. Pulmonary hypertension is defined as a sustained elevation of pulmonary arterial pressure over 25mmHg at rest or 30mmHg during exercise, with normal pulmonary capillary wedge pressure and left ventricular end-diastolic pressure. Signs on chest X-ray include enlarged pulmonary arteries, loss of peripheral vessel markings, and enlargement of the right side of the heart in advanced disease.
An approach to Interstitial Lung Disease / Diffuse Parenchymal Lung DiseaseThomas Kurian
YouTube link: https://youtu.be/gPr31qrivUc
An approach to Diffuse Parenchymal Lung disease / Interstitial Lung disease with emphasis on the idiopathic causes.
This document provides information on community-acquired pneumonia (CAP). It defines CAP and distinguishes it from other types of pneumonia. It then discusses the epidemiology, clinical presentation, etiology, symptoms, diagnosis, treatment, and antibiotic resistance patterns associated with CAP. Key points include that CAP affects millions annually in the US with high costs, accurate diagnosis and treatment is important to reduce mortality, and resistance to commonly used antibiotics is a concern.
1. Dr. Rajkoti discusses the approach to evaluating and managing non-resolving pneumonia. Key factors that can delay resolution are host factors like age, comorbidities, and smoking as well as drug-resistant or unusual pathogens.
2. Three case studies are presented. The first involves a teenage boy with empyema that required drainage. The second is a middle-aged man with hypersensitivity pneumonitis related to his job that responded to steroids. The third involves further evaluation of a woman's non-productive cough to identify potential non-infectious causes.
3. For non-resolving pneumonia, re-emphasis is placed on thorough history, microbiology testing, imaging,
This document discusses the approach to interstitial lung diseases (ILD) and diffuse parenchymal lung diseases (DPLD). It begins by reviewing the spectrum of ILD and DPLD, identifying clues from clinical presentation to make a diagnosis, and reviewing common radiographic findings. Key points include that ILD involves the pulmonary interstitium located between the epithelial and endothelial basement membranes. Clinical presentation of DPLD/ILD often involves dyspnea, cough, and abnormal chest imaging. Diagnosis involves considering history, physical exam, pulmonary function tests, imaging like chest radiographs and CT, and tissue sampling. Management depends on the specific diagnosis but may include treatments like corticosteroids, immunosuppressants, anti
PowerPoint presentation describing various aspects of Pulmonary Hypertension. Please mail me your feedback on this presentation to following Email ID: tinkujoseph2010@gmail.com.
Cor pulmonale, or right heart failure caused by pulmonary or thoracic disease, can result from pulmonary arterial hypertension (PAH) due to conditions that obstruct the pulmonary vasculature. Common causes of PAH include heartworm disease, pulmonary thromboembolism from conditions causing blood stasis or hypercoagulability, and chronic lung diseases. Physical exam may reveal murmurs, respiratory distress, and signs of congestion. Diagnosis involves detecting abnormal gas exchange on bloodwork, radiographic evidence of lung disease or right heart enlargement, and ECG changes reflective of right heart strain. However, diagnosing the underlying cause like pulmonary thromboembolism can be challenging as exams and tests may be normal in some
This document provides information on eosinophils and pulmonary eosinophilic syndromes. It discusses the classification of pulmonary eosinophilic syndromes including Loeffler's syndrome, drug-induced pulmonary eosinophilia, idiopathic acute eosinophilic pneumonia, tropical pulmonary eosinophilia, and chronic eosinophilic pneumonia. For each condition, it describes the clinical features, investigations, treatment, and prognosis. Radiographic and microscopic images are also included to illustrate common findings.
Pulmonary Langerhans cell histiocytosis (PLCH) is an uncommon lung disease that typically affects young adult smokers. It is characterized by inflammatory lesions surrounding small airways and blood vessels that can progress to interstitial fibrosis. Common symptoms include cough, dyspnea, and weight loss. Diagnosis involves imaging showing nodules and cysts predominantly in the mid and upper lung zones. Transbronchial biopsy can confirm the presence of Langerhans cells. Cessation of smoking is the primary treatment and can lead to remission of symptoms.
This document defines and outlines Churg-Strauss Syndrome (CSS), a rare eosinophilic vasculitis disease. It provides details on the epidemiology, pathogenesis, clinical manifestations, diagnosis, treatment, and prognosis of CSS. CSS is characterized by eosinophil-rich inflammation involving small to medium blood vessels and is associated with asthma, allergies, and eosinophilia. Treatment involves high doses of corticosteroids, with immunosuppressants used for resistant cases. Prognosis is generally better than other vasculitis diseases but mortality can occur from cardiac or neurological involvement.
Small airways disease refers to pathologies that affect the small conducting airways less than 3mm in diameter. CT scanning is the imaging modality of choice for evaluating small airways disease. On HRCT, direct signs of small airways disease include thickened airway walls, dilated or obliterated airways, and nodules. Indirect signs include air trapping, subsegmental atelectasis, centrilobular emphysema, and centrilobular nodules. Common patterns seen on HRCT include tree-in-bud, poorly defined centrilobular nodules, decreased lung attenuation, and ground glass opacities with consolidation.
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.
Sarcoidosis is a systemic granulomatous disease of unknown origin characterized by non-caseating granulomas that commonly affect the lungs. Pulmonary manifestations are present in 90% of patients and include bilateral hilar lymphadenopathy and pulmonary infiltrates. While two thirds of patients experience remission within ten years, one third have progressive disease that can lead to pulmonary fibrosis and, in rare cases, death. Computed tomography is more sensitive than chest x-rays in detecting lymph node enlargement and lung abnormalities associated with sarcoidosis.
This document discusses radiation pneumonitis, which is an inflammation of the lungs caused by radiation therapy. It can occur in 5-15% of people receiving radiation to the chest. Symptoms include dyspnea, cough, and fever and typically appear 1-6 months after radiation. Diagnosis is based on chest imaging showing changes corresponding to the radiation site. Treatment involves corticosteroids to reduce inflammation. Radiation pneumonitis can progress to pulmonary fibrosis with permanent lung damage if left untreated.
Chest pain has many potential causes, both cardiac and non-cardiac. A thorough history and physical exam are important to establish a pre-test probability of different diseases. Clinical decision rules can help quantify the likelihood of conditions like myocardial infarction, pneumonia, and pulmonary embolism. No single diagnostic test is perfect, so likelihood ratios provide a framework for interpreting test results in the context of the pre-test probability. An evidence-based approach uses all available information to guide appropriate testing and diagnosis.
This document provides an outline and summary of various pulmonary imaging findings. It begins with an introduction by Dr. Mazen Qusaibaty and provides sections on CT halo sign (part 2), Hampton hump sign, and Westermark sign. Specific cases and images are presented to demonstrate findings of bronchiolitis obliterans with organizing pneumonia (BOOP), pulmonary endometriosis, focal traumatic lung injury, and pseudonodules. Radiographic signs of pulmonary embolism on chest x-ray and CT findings of acute pulmonary embolism on helical CT are also summarized.
Obesity hypoventilation syndrome is characterized by obesity (BMI > 40), sleep disordered breathing (90% have obstructive sleep apnea), and hypercapnia and hypoxemia. It is caused by changes in respiratory mechanics and central drive due to obesity, as well as sleep disordered breathing and leptin resistance. Treatment involves a multidisciplinary approach including positive airway pressure therapy, weight loss, supplemental oxygen, and pharmacological therapy to normalize ventilation and prevent oxygen desaturation. Early diagnosis and treatment are important to improve outcomes.
Community acquired pneumonia (CAP) is an acute lung infection that develops outside of a hospital setting. It is caused by bacteria, viruses, fungi or protozoa. The most common bacteria that cause CAP include Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Moraxella catarrhalis. Risk factors for CAP include chronic health conditions, smoking, HIV, and medications that suppress the immune system. Symptoms typically include fever, cough, shortness of breath, and chest pain. Diagnosis involves chest x-ray and testing sputum or blood samples. Complications can include respiratory failure, organ damage,
Pneumonia is an acute lung infection that can affect the alveoli and interstitial tissue in different patterns. It is commonly caused by bacteria like Streptococcus pneumoniae and viruses. Risk factors include smoking, age, diseases like COPD, and immunosuppression. Symptoms include fever, cough, difficulty breathing. Diagnosis involves tests like CXR, sputum culture, blood tests. Treatment depends on severity and includes oxygen, fluids, and antibiotics chosen based on location and patient factors. Complications can include empyema, abscesses, and respiratory failure.
Bronchopneumonia is a type of pneumonia characterized by patchy lung inflammation and infection. It is often caused by aspiration of oropharyngeal bacteria. Community-acquired pneumonia is commonly seen in children and the elderly. Hospital-acquired pneumonia is a major complication for hospitalized patients, especially those on ventilators. Diagnosis involves clinical features, imaging, and microbiological testing of sputum or bronchial samples. Treatment focuses on oxygenation, fluid balance, and antibiotics tailored to likely causative organisms. Immunocompromised patients are at higher risk for opportunistic pathogens.
Pneumonia and case studies for medical studentsGokulnathMbbs
This document discusses pneumonia, including its pathophysiology, types (community-acquired, hospital-acquired), clinical manifestations, diagnosis, and common causes. Pneumonia results from microbial infection and host inflammatory response in the lungs. It can range from mild to life-threatening. Diagnosis involves clinical assessment, chest imaging, and tests to determine the causative pathogen, though a cause is often not identified. Common causes of community-acquired pneumonia include Streptococcus pneumoniae, Haemophilus influenzae, and atypical bacteria.
Dr. Md. Khairul Hassan Jessy
Associate Professor, Respiratory Medicine
National Institute of Diseases of the Chest and Hospital (NIDCH), Mohakhali, Dhaka.
Acknowledment:
Davidson’s Principles and Practice of Medicine
This document provides an overview of pneumonia, including its definition, classification, pathophysiology, clinical manifestations, diagnosis, treatment and antibiotic resistance. Pneumonia is an infection of the lungs that can be caused by bacteria, viruses or other pathogens. It is commonly classified as community-acquired or healthcare-associated pneumonia. Clinical diagnosis involves assessing symptoms and chest imaging, while etiologic diagnosis may involve sputum/blood cultures, antigen tests and PCR. Treatment depends on pneumonia severity and risk factors. Antibiotic resistance among pathogens like Streptococcus pneumoniae and gram-negative bacilli is an ongoing concern.
1. Community acquired pneumonia (CAP) is pneumonia that develops outside of the hospital. It is commonly caused by bacteria like Streptococcus pneumoniae or viruses.
2. There are several classifications of pneumonia including by causative agent (bacterial, viral, fungal), by location in the lungs (lobar, bronchopneumonia), and by how it is acquired (nosocomial, community acquired).
3. Diagnosis involves assessing symptoms, signs on physical exam, chest x-ray findings, and tests like sputum culture. Severity is evaluated using scoring systems like CURB-65 to determine treatment setting and antibiotic selection.
Pneumonia is an infection of the lungs caused by bacteria, viruses or other pathogens. It is commonly transmitted when germs are inhaled into the lungs. Risk factors include impaired immunity, smoking, neurological conditions that impact swallowing, and chronic lung diseases. Diagnosis involves chest x-ray, sputum culture, blood tests and assessment of severity using CURB65 score. Treatment focuses on antibiotics, oxygen supplementation, hydration and symptom relief. Complications can include respiratory failure and sepsis.
Pneumonia is an infection of the lungs caused by bacteria, viruses or other pathogens. It is commonly transmitted when germs are inhaled into the lungs. Risk factors include impaired immunity, smoking, neurological conditions that impact swallowing, and chronic lung diseases. Diagnosis involves chest x-ray, sputum culture, blood tests and assessment of severity using CURB65 score. Treatment focuses on antibiotics, oxygen supplementation, hydration and symptom relief. Complications can include respiratory failure and sepsis.
Community acquired pneumonia by dr md abdullah saleemsaleem051
This document provides information on community-acquired pneumonia (CAP), including epidemiology, risk factors, presentation, diagnosis, treatment recommendations, and prevention strategies. It notes that CAP is one of the most common infectious diseases worldwide, with higher rates among the elderly. Common bacterial causes are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Clinical assessment and chest imaging are important for diagnosis and management. Antibiotic treatment should be based on likely pathogens and severity of illness. Immunization can help prevent CAP in high-risk groups.
This document discusses the etiology, pathophysiology, clinical manifestations, and complications of pneumonia acquired in community, hospital, and ventilator settings. It describes the typical and atypical bacterial, viral, and fungal pathogens that can cause community-acquired pneumonia and notes increasing cases of Mycoplasma and Chlamydophila pneumonia. For hospital-acquired and ventilator-associated pneumonia, it outlines the risk of multi-drug resistant pathogens and worse clinical outcomes compared to community-acquired cases. The pathophysiology section overviews the host immune response and factors influencing the lung microbiota and pneumonia development. Clinical features ranging from mild to life-threatening are outlined for the different settings. Potential complications include respiratory
Pneumonia is an inflammation of the lungs that can have multiple causes. It is typically caused by bacterial, viral or fungal infections. Pneumonia can be classified based on location in the lungs, cause, or clinical setting. Common symptoms include cough, fever, chest pain and difficulty breathing. Diagnosis involves physical exam, chest x-ray, blood tests and sputum/fluid cultures. Treatment focuses on antibiotics, oxygen therapy and treatment of complications. Hospital-acquired pneumonia requires broader-spectrum antibiotics due to more drug-resistant organisms. Prevention emphasizes hand hygiene, limiting aspiration and prudent antibiotic use.
This document discusses non-resolving pneumonia, defined as persisting symptoms or deterioration after at least 72 hours of antimicrobial treatment. Infectious causes are responsible for 40% of non-resolving cases, with common organisms including S. pneumoniae, Legionella, P. aeruginosa, and S. aureus. Non-infectious causes like cancer, connective tissue diseases, and drug reactions must also be considered. Evaluation involves history, physical exam, labs, imaging like chest X-ray and CT, and bronchoscopy with samples for microbiology. Treatment requires correcting any host abnormalities, adjusting antimicrobial therapy to expand coverage of possible resistant organisms, and draining any abscesses.
This document discusses different types of pneumonia including definitions, classifications, symptoms, investigations, management, and complications. It covers community acquired pneumonia, hospital acquired pneumonia, pneumonia in immunocompromised patients, and specific types like lobar pneumonia, bronchopneumonia, suppurative pneumonia, and aspiration pneumonia. Pneumonia is defined as acute lung inflammation seen on imaging and is classified by location and cause of acquisition. Signs, testing, treatment, and prognosis vary depending on the type and severity of pneumonia.
1. Pneumonia is an inflammatory lung condition caused by infection, usually bacterial, that is characterized by consolidation of the lung tissue.
2. Community-acquired pneumonia is defined as pneumonia acquired outside of a hospital setting, within 14 days of symptoms. Healthcare-associated pneumonia refers to pneumonia acquired in other healthcare settings such as nursing homes.
3. Hospital-acquired pneumonia refers to pneumonia that develops 48 hours or more after admission to the hospital. Risk factors include mechanical ventilation, underlying diseases, and antibiotic resistance of hospital-acquired pathogens.
This document provides information on pneumonia, including its definition, classification, infectious agents, host defenses in the lungs, routes of infection, community-acquired pneumonia, symptoms, diagnosis, treatment, and complications. It defines pneumonia as an infection of the lungs that causes consolidation and filling of alveoli. Community-acquired pneumonia is most often caused by Streptococcus pneumoniae, Haemophilus influenzae, or Mycoplasma pneumoniae. Diagnosis involves assessment of severity, consideration of possible causes, chest imaging, and microbiological testing of sputum or blood. Empiric antibiotic therapy depends on location of treatment and severity of illness. Duration of treatment typically ranges from 7 to 14 days depending on the causative
Pneumonia is an infection of the lungs that is commonly caused by bacteria or viruses. It presents with symptoms like cough, fever, and chest pain. Pneumonia can be classified based on location in the lungs (lobar vs. bronchopneumonia) or cause (typical bacterial vs. atypical vs. viral). Common types include pneumococcal, mycoplasma, and viral pneumonia. Diagnosis involves chest x-ray, sputum culture, and clinical assessment. Treatment depends on severity but generally involves antibiotics and symptom relief. Complications can include lung abscesses or empyema if the infection spreads to the pleural space.
Pneumonia is a form of acute respiratory infection that affects the lungs. The lungs are made up of small sacs called alveoli, which fill with air when a healthy person breathes. When an individual has pneumonia, the alveoli are filled with pus and fluid, which makes breathing painful and limits oxygen intake.
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Overview of community-acquired pneumonia in adults.pdf
1. Overview of community-acquired
pneumonia in adults
July 2023 Dr. Emad Efat
MD (chest)- Cairo University
Consultant of chest diseases-
El-Bagour specialized hospital
2. DEFINITIONS
Pneumonia is frequently categorized based on site of acquisition:
❑ Community-acquired pneumonia (CAP):
Refers to an acute infection of the pulmonary parenchyma acquired outside of
the hospital.
❑ Nosocomial pneumonia:
Refers to an acute infection of the pulmonary parenchyma acquired in hospital
settings and encompasses both hospital-acquired pneumonia (HAP) and
ventilator associated pneumonia (VAP).
❑ HAP refers to pneumonia acquired ≥48 hours after hospital admission.
❑ VAP refers to pneumonia acquired ≥48 hours after endotracheal
intubation.
❑ Health care-associated pneumonia (HCAP; no longer used) .
3. Risk factors
❑ Older age
❑ Chronic comorbidities – chronic obstructive pulmonary disease (COPD),
chronic lung disease (eg, bronchiectasis, asthma), chronic heart disease
(particularly congestive heart failure), stroke, diabetes mellitus, malnutrition,
and immunocompromising conditions.
❑ Viral respiratory tract infection – Viral respiratory tract infections can lead to
primary viral pneumonias and also predispose to secondary bacterial
pneumonia. This is most pronounced for influenza virus infection.
❑ Impaired airway protection – Conditions that increase risk of macroaspiration
of stomach contents and/or microaspiration of upper airway secretions, such
as alteration in consciousness (eg, due to stroke, seizure, anesthesia, drug or
alcohol use) or dysphagia due to esophageal lesions or dysmotility.
❑ Smoking and alcohol overuse
❑ Other lifestyle factors – crowded living conditions (eg, prisons, homeless
shelters), residence in low-income settings, and exposure to environmental
toxins (eg, solvents, paints, or gasoline).
4. MICROBIOLOGY
Common causes — Streptococcus pneumoniae (pneumococcus) and respiratory
viruses are the most frequently detected pathogens in patients with CAP.
However, in a large proportion of cases (up to 62 percent in some studies
performed in hospital settings), no pathogen is detected despite extensive
microbiologic evaluation.
The most commonly identified causes of CAP can be grouped into three
categories:
❑ Typical bacteria
❑ S. pneumoniae (most common bacterial cause)
❑ Haemophilus influenzae
❑ Moraxella catarrhalis
❑ Staphylococcus aureus
❑ Group A streptococci
❑ Aerobic gram-negative bacteria (eg, Enterobacteriaceae such as Klebsiella
spp or Escherichia coli)
❑ Microaerophilic bacteria and anaerobes (associated with aspiration)
5. MICROBIOLOGY
❑ Atypical bacteria ("atypical" refers to the intrinsic resistance of these
organisms to beta-lactams and their inability to be visualized on Gram stain or
cultured using traditional techniques)
❑ Legionella spp
❑ Mycoplasma pneumoniae
❑ Chlamydia pneumoniae
❑ Chlamydia psittaci
❑ Coxiella burnetii
❑ Respiratory viruses
❑ Influenza A and B viruses
❑ Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
❑ Other coronaviruses (eg, CoV-229E, CoV-NL63, CoV-OC43, CoV-HKU1)
❑ Rhinoviruses and Parainfluenza viruses
❑ Adenoviruses
❑ Respiratory syncytial virus
❑ Human metapneumovirus
❑ Human bocaviruses
6. MICROBIOLOGY
Certain epidemiologic exposures also raise the likelihood of infection with a
particular pathogen.
As examples:
❑ exposure to contaminated water is a risk factor for Legionella infection
❑ exposure to birds raises the possibility of C. psittaci infection
❑ travel or residence in the southwestern United States should raise
suspicion for coccidioidomycosis
❑ poor dental hygiene may predispose patients with pneumonia caused by
oral flora or anaerobes
❑ In immunocompromised patients, the spectrum of possible pathogens also
broadens to include fungi and parasites as well as less common bacterial
and viral pathogens.
7. PATHOGENESIS
❑ Respiratory pathogens are transmitted from person to person via droplets or,
less commonly, via aerosol inhalation (eg, as with Legionella or Coxiella).
❑ Following inhalation, the pathogen colonizes the nasopharynx and then
reaches the lung alveoli via microaspiration
❑ Replication of the pathogen, the production of virulence factors, and the host
immune response lead to inflammation and damage of the lung parenchyma,
resulting in pneumonia.
❑ The alveolar microbiome is similar to oral flora and is primarily comprised of
anaerobic bacteria (eg, Prevotella and Veillonella) and microaerophilic
streptococci
❑ The host immune response to microbial replication within the alveoli plays an
important role in determining disease severity:
❑ For some patients, a local inflammatory response within the lung
predominates and may be sufficient for controlling infection.
❑ In others, a systemic response is necessary to control infection and to prevent
spread or complications, such as bacteremia.
❑ In a minority, the dysregulated systemic response can become, leading to
tissue injury, sepsis, acute respiratory distress syndrome, and/or multiorgan
dysfunction.
8. CLINICAL PRESENTATION
The clinical presentation of CAP varies widely, ranging from
❑ mild pneumonia characterized by fever, cough, and shortness of breath
❑ severe pneumonia characterized by sepsis and respiratory distress.
Symptom severity is directly related to the intensity of the local and
systemic immune response in each patient
❑ Pulmonary signs and symptoms :
❑ Cough (with or without sputum production), dyspnea, and pleuritic chest
pain are among the most common symptoms associated with CAP.
❑ Signs of pneumonia on physical examination include Hypoxemia,
tachypnea, increased work of breathing, and adventitious breath sounds,
including rales/crackles and rhonchi. Tactile fremitus, egophony, and
dullness to percussion also suggest pneumonia.
❑ Systemic signs and symptoms – The great majority of patients with CAP
present with fever. Other systemic symptoms such as chills, fatigue, malaise,
chest pain (which may be pleuritic), Tachycardia and anorexia are also
common. CAP is also the leading cause of sepsis; thus, the initial presentation
may be characterized by hypotension, altered mental status, and other signs of
organ dysfunction such as renal dysfunction, liver dysfunction, and/or
thrombocytopenia.
9. CLINICAL PRESENTATION
❑ leukocytosis with a leftward shift, or leukopenia are also findings that are
mediated by the systemic inflammatory response. Inflammatory markers, such
as the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and
procalcitonin may rise, though the latter is largely specific to bacterial
infections
❑ Signs and symptoms of pneumonia can also be subtle in patients with
advanced age and/or impaired immune systems, and a higher degree of
suspicion may be needed to make the diagnosis. As examples, older patients
may present with mental status changes but lack fever or leukocytosis. In
immunocompromised patients, pulmonary infiltrates may not be detectable
on chest radiographs but can be visualized with computed tomography.
10. DIAGNOSIS
❑ The diagnosis of CAP generally requires the demonstration of an infiltrate on
chest imaging in a patient with a clinically compatible syndrome (eg, fever,
dyspnea, cough, and sputum production)
❑ For most patients with suspected CAP, we obtain posteroanterior and lateral
chest radiographs. Radiographic findings consistent with the diagnosis of CAP
include lobar consolidations, interstitial infiltrates, and/or cavitations.
❑ For selected patients in whom CAP is suspected based on clinical features
despite a negative chest radiograph, we obtain computed tomography (CT) of
the chest. These patients include immunocompromised patients, who may not
mount strong inflammatory responses and thus have negative chest
radiographs, as well as patients with known exposures to epidemic pathogens
that cause pneumonia (eg, Legionella). Because there is no direct evidence to
suggest that CT scanning improves outcomes for most patients and cost is
high, we do not routinely obtain CT scans when evaluating patients for CAP
11. lung field abnormalities - Consolidation
Aspiration Pneumonitis and Pneumonia: Imaging Findings:
❑ Chest x-ray shows an
infiltrate, frequently in the
superior or posterior basal
segments of a lower lobe or
the posterior segment of an
upper lobe (The right lower
lobe is the most frequent
location).
❑ Aspiration-related lung
abscess
❑ Interstitial or nodular
infiltrates, pleural effusion,
and other changes may be
slowly progressive.
Typically localized pneumonia in
the right lower lobe.
12. lung field abnormalities - Consolidation
Aspiration Pneumonitis and Pneumonia: Imaging Findings:
❑ An infiltrate, frequently in
the posterior segment of an
upper lobe and the superior
or posterior basal segments
of a lower lobe (The right
lower lobe is the most
frequent location).
❑ Aspiration-related lung
abscess
❑ Interstitial or nodular
infiltrates, pleural effusion,
and other changes may be
slowly progressive.
❑ Aspirated material can be
demonstrated on CT scans
Ct shows centrilobular nodules with
surrounding ground-glass opacities and
subpleural non-segmental
consolidations (yellow arrow) at the
dorsal portions of the right lung. Note
that the lumens of segmental bronchi
are filled with aspirated materials (red
arrow).
13. lung field abnormalities - Consolidation
Klebsiella pneumonia (Friedländer’s pneumonia):
Imaging Findings:
❑ Usually involves one of
the upper lobes
❑ Homogeneous,
nonsegmental, lobar
consolidation
❑ Bulging Fissure Sign:
bulging of usually minor
fissure from heavy,
exudate ( arrow)
❑ Lung abscess (es)
❑ Pleural effusion (70%)
and/or empyema
14. lung field abnormalities - Consolidation
Klebsiella pneumonia (aka Friedländer’s pneumonia):
Imaging Findings:
❑ usually involves one of the
upper lobes
❑ ground glass opacities
❑ consolidation
➢ intralobular reticular opacities
➢ interlobular septal thickening
➢ centrilobular nodules
✓ cavitation
✓ necrotising pneumonia
✓ Pleural effusion and/or
empyema
✓ Bulging fissure sign
Transverse thin-section CT of right lower
lobe showing consolidation (arrowhead)
and intralobular reticular opacity
(arrows) with peripheral distribution.
Pleural effusion was also present
15. lung field abnormalities - Consolidation
Necrotising pneumonia (NP): refers to a pneumonia characterised by
the development of the necrosis within infected lung tissue.
❑ Causative pathogens include ( Staphylococcus aureus, Klebsiella
pneumonia, Enterobacter, Nocardai, Actinomyces, Pseudomonas,
Pneumococcus, Haemophilus influenza)
❑ CT with may be better as it allows appreciation of low attenuation
and non enhancement within the necrosed portions (representing
liquifaction) of the affected area of infection (consolidation).
Necrotizing
pneumonia.
heterogeneous
enhancing
consolidation with
smooth air
bronchograms and
cavities in the right
upper lobe
16. lung field abnormalities - Consolidation
Adult Respiratory Distress Syndrome ( ARDS )
ARDS versus Congestive Heart Failure:
❑Diffuse bilateral
patchy infiltrates
❑More uniform
opacification
❑Homogenously
distributed
❑No cardiomegaly
❑No cephalization
❑Usually no pleural
effusion or Kerley
B lines
18. lung field abnormalities - Consolidation
Bronchopneumonia characterised by:
❑ Multiple small nodular or reticulonodular opacities which
tend to be patchy and/or confluent.
❑ The distribution is often bilateral and asymmetric, and
predominantly involves the lung bases
19. lung field abnormalities - Consolidation
Bronchopneumonia: bilateral and predominantly in the lung bases
late stages
Early stages
❑ Extends peripherally along the bronchus to involve
the entire pulmonary lobule
❑ Multifocal heterogeneous confluent consolidation
= patchwork quilt; eventually coalesce.
❑ Exudates fill airways = no air bronchograms
❑ 25-75% form abscess
❑ Empyema and parapneumonic effusion common
❑ Multiple foci of opacity
❑ Begins centrally in and
around lobular bronchi
❑ Peribronchial thickening
and poorly defined
bronchovascular nodules
❑ May result in a tree-in-bud
appearance
20. lung field abnormalities - Consolidation
Atypical pneumonia (AP) characterised by:
❑ Focal ground-glass opacity in a lobular distribution (Diffuse and
bilateral)
❑ Diffuse ground glass nodules in a centrilobular pattern
❑ Bronchial wall thickening
❑ pleural effusion may present
30-year-old woman with
Mycoplasma pneumoniae
pneumonia. CT shows
bronchial wall thickening
(arrows). Lobular areas of
consolidation and ground-
glass attenuation are also
seen.
21. lung field abnormalities - Consolidation
(AP) Legionella pneumonia:
➢ Multifocal and bilateral patchy infiltrate (ground glass and/or
consolidation), Middle and lower zone predominance
➢ Pleural effusions can be common
➢ Associated hilar adenopathy
may be present
➢ Cavitation and a masslike
appearance
Legionella pneumonia. (A) Typical non-
segmental lesion in the right middle
lobe and the right lower lobe. (B) sharp-
bordered fissures (arrow), which is a
characteristic feature of non-segmental
distribution. (C) Segmental lesions in
the right lower lobe. (D) consolidation
and ground-glass opacity
22. lung field abnormalities - Consolidation
(AP) Mycoplasma pneumonia characterised by:
❑ Areas of ground-glass attenuation and air-space consolidation
Mycoplasma pneumoniae pneumonia.
HRCT shows bilateral lobular areas of
consolidation, patchy ground-glass
opacities, interlobular septal thickening
❑ lobular distribution
❑ Centrilobular nodules
❑ Thickening of the
peribronchovascular
interstitium
❑ Interlobular septal
thickening
❑ Mosaic perfusion
❑ lower lobe
predominance
23. lung field abnormalities - Consolidation
(AP) Chlamydia pneumonia characterised by:
❑ Areas of ground-glass attenuation and air-space consolidation
❑ lobular distribution
❑ Findings are often limited to a single lobe.
Chlamydia pneumonia. an
acinar pattern on a
background of ground-glass
attenuation. Right pleural
effusion is also present.
❑ lower lobe involvement occurring more frequently
❑ bronchovascular bundle thickening.
❑ Centrilobular nodules
❑ Up to 25% of patients may have a small to moderate-sized pleural
effusion
❑ lymphadenopathy: uncommon
24. lung field abnormalities - Consolidation
Respiratory syncytial
pneumonia. bilateral ill-
defined centrilobular nodules
(arrows) and bronchial wall
thickening (arrowhead).
(AP) Viral pneumonia characterised by:
❑ Patchy, unilateral, or bilateral consolidations and ground-glass
opacity or poorly defined centrilobular nodules.
❑ Peribronchial thickening
❑ Thickened interlobular septa
❑ Areas of atelectasis or air trapping
❑ Pleural effusion, hilar
lymphadenopathy and
pneumothorax are
uncommon findings.
25. lung field abnormalities - Consolidation
(AP) Covid-19 pneumonia: The primary findings of
COVID-19 on chest radiograph and CT are those of
atypical pneumonia or organizing pneumonia.
❑ Normal in up to 63% in the early stages
❑ Ground glass (68.5%), coarse horizontal linear
opacities, and consolidation.
❑ Crazy paving
❑ These are more likely to be multifocal, bilateral,
peripheral and in the lower zones
❑ Vascular dilatation and bronchovascular
thickening
❑ Traction Bronchiectasis
❑ Atypical CT findings
(mediastinal lymphadenopathy,
pleural effusion, multiple tiny
pulmonary nodules, tree-in-bud,
pneumothorax, cavitation)
(COVID-19).
A, ground-glass
opacity (GGO),
B, crazy-paving
pattern, and,
C, consolidation
26. Defining severity and site of care
❑ The most commonly used severity scores are the Pneumonia Severity Index
(PSI) and CURB-65. the PSI is the most accurate. However, the CURB-65 score is
preferred by many clinicians because it is easier to use
The three levels of severity (mild, moderate, and severe) generally correspond to
three levels of care:
❑ Ambulatory care – Most patients who are otherwise healthy with normal vital
signs (apart from fever) and no concern for complication are considered to
have mild pneumonia. These patients typically have PSI scores of I to II and
CURB-65 scores of 0 (or a CURB-65 score of 1 if age >65 years)
❑ Hospital admission – Patients who have peripheral oxygen saturations <92
percent on room air (and a significant change from baseline) should be
hospitalized. In addition, patients with PSI scores of ≥III and CURB-65 scores ≥1
(or CURB-65 score ≥2 if age >65 years) should also generally be hospitalized.
❑ Because patients with early signs of sepsis, rapidly progressive illness, or
suspected infections with aggressive pathogens are not well represented in
severity scoring systems, these patients may also warrant hospitalization in
order to closely monitor the response to treatment
27. Defining severity and site of care
❑ Practical concerns that may warrant hospital admission include an inability to
take oral medications, cognitive or functional impairment, or other social
issues that could impair medication adherence or ability to return to care for
clinical worsening (eg, substance abuse, homelessness, or residence far from a
medical facility)
❑ Intensive care unit (ICU) admission – Patients who meet either of the following
major criteria have severe CAP and should be admitted to the ICU :
❑ Respiratory failure requiring mechanical ventilation
❑ Sepsis requiring vasopressor support
❑ To help identify patients with severe CAP before development of organ failure,
the American Thoracic Society (ATS) and the Infectious Diseases Society of
America (IDSA) suggest minor criteria. The presence of three of these criteria
warrants ICU admission:
❑ Altered mental status
❑ Hypotension requiring fluid support
❑ Temperature <36°C (96.8°F)
❑ Respiratory rate ≥30 breaths/minute
❑ Arterial oxygen tension to fraction of inspired oxygen (PaO2 /FiO2 ) ratio ≤250
28. Defining severity and site of care
❑ Blood urea nitrogen (BUN) ≥20 mg/dL (7 mmol/L)
❑ Leukocyte count <4000 cells/microL
❑ Platelet count <100,000/mL
❑ Multilobar infiltrates
29. Microbiologic testing
❑ Outpatients − microbiologic testing is not needed (apart from testing for SARS-
CoV-2 during the pandemic)
❑ Patients with moderate CAP admitted to the general medicine ward − we
obtain the following:
❑ Blood cultures
❑ Sputum Gram stain and culture
❑ Urinary antigen testing for S. pneumoniae
❑ Testing for Legionella spp (polymerase chain reaction [PCR] when available,
urinary antigen test as an alternate)
❑ SARS-CoV-2 testing
❑ Patients with severe CAP (including ICU admission) −, we send blood cultures,
sputum cultures, urinary streptococcal antigen, and Legionella testing. In
addition, we obtain bronchoscopic specimens for microbiologic testing (for
aerobic culture, Legionella culture, fungal stain and culture, and testing for
respiratory viruses) when feasible, weighing the benefits of obtaining a
microbiologic diagnosis against the risks of the procedure (eg, need for
intubation, bleeding, bronchospasm, pneumothorax) on a case-by-case basis
30. Microbiologic testing
❑ In all cases, we modify this approach based on epidemiologic exposures,
patient risk factors, and clinical features regardless of CAP severity or
treatment setting. As examples:
❑ For patients with known or probable exposures to epidemic pathogens such as
Legionella or epidemic coronaviruses, we broaden our evaluation to include
tests for these pathogens
❑ For patients with cavitary pneumonia, we may include testing for tuberculosis,
fungal pathogens, and Nocardia
❑ For immunocompromised patients, we broaden our differential to include
opportunistic pathogens such as Pneumocystis jirovecii, fungal pathogens,
parasites, and less common viral pathogens such as cytomegalovirus
31. DIFFERENTIAL DIAGNOSIS
❑ Non-infectious illnesses that mimic CAP or co-occur with CAP and present with
pulmonary infiltrate and cough include:
❑ Congestive heart failure with pulmonary edema
❑ Pulmonary embolism
❑ Pulmonary hemorrhage
❑ Atelectasis
❑ Aspiration or chemical pneumonitis
❑ Drug reactions
❑ Lung cancer
❑ Collagen vascular diseases
❑ Vasculitis
❑ Acute exacerbation of bronchiectasis
❑ Interstitial lung diseases (eg, sarcoidosis, asbestosis, hypersensitivity
pneumonitis, cryptogenic organizing pneumonia)
❑ Respiratory illnesses that mimic CAP or co-occur with CAP include:
❑ Acute exacerbations of chronic obstructive pulmonary disease or asthma
Influenza and other respiratory viral infections
❑ Acute bronchitis
32. DIFFERENTIAL DIAGNOSIS
❑ For patients with an initial clinical diagnosis of CAP who have rapidly resolving
pulmonary infiltrates, alternate diagnoses should be investigated.. A
pulmonary infiltrate that resolves in one or two days may be caused by
accumulation of fluid in the alveoli (ie, pulmonary edema) or a collapse of the
alveoli (ie, atelectasis) but not due to accumulation of WBCs
33. TREATMENT
❑ For most patients with CAP and excluding COVID-19, the aetiology is not
known at the time of diagnosis, and antibiotic treatment is empiric, targeting
the most likely pathogens. The pathogens most likely to cause CAP vary with
severity of illness, local epidemiology, and patient risk factors for infection
with drug-resistant organisms
❑ As an example, for most patients with mild CAP who are otherwise healthy
and treated in the ambulatory setting, the range of potential pathogens is
limited. By contrast, for patients with CAP severe enough to require
hospitalization, potential pathogens are more diverse, and the initial
treatment regimens are often broader
❑ Outpatient antibiotic therapy — For all patients with CAP, empiric regimens
are designed to target S. pneumoniae (the most common and virulent
bacterial CAP pathogen) and atypical pathogens
❑ Coverage is expanded for outpatients with comorbidities, smoking, and recent
antibiotic use to include or better treat beta-lactamase-producing H.
influenzae, M. catarrhalis, and methicillin-susceptible S. aureus
❑ For those with structural lung disease, we further expand coverage to include
Enterobacteriaceae, such as E. coli and Klebsiella spp
34. TREATMENT
❑ Selection of the initial regimen depends on the adverse effect profiles of
available agents, potential drug interactions, patient allergies, and other
patient-specific factors:
❑ For most patients aged <65 years who are otherwise healthy and have not
recently used antibiotics, the American Thoracic Society (ATS)/Infectious
Diseases Society of America (IDSA), recommend monotherapy with amoxicillin
as first line and monotherapy with either doxycycline or a macrolide
❑ For patients who have major comorbidities (eg, chronic heart, lung, kidney, or
liver disease, diabetes mellitus, alcohol dependence, or immunosuppression),
who are smokers, and/or who have used antibiotics within the past three
months, we suggest oral amoxicillin-clavulanate (875 mg twice daily or
extended release 2 g twice daily) plus either a macrolide (preferred) or
doxycycline
❑ For patients who can use cephalosporins, we use a third-generation
cephalosporin (eg, cefpodoxime) plus either a macrolide or doxycycline
❑ For patients who cannot use any beta-lactam, we select a respiratory
fluoroquinolone (eg, levofloxacin, moxifloxacin, gemifloxacin)
❑ For those with structural lung disease, we prefer a respiratory fluoroquinolone
because its spectrum of activity includes Enterobacteriaceae
35. TREATMENT
❑ Modifications to these regimens may be needed for antibiotic allergy, drug
interactions, specific exposures, and other patient-specific factors. In
particular, during influenza season, patients at high risk for poor outcomes
from influenza may warrant antiviral therapy.
❑ We treat most patients for five days. However, we generally ensure that all
patients are improving on therapy and are afebrile for at least 48 hours before
stopping antibiotics. In general, extending the treatment course beyond seven
days does not add benefit.
❑ Inpatient antibiotic therapy:
❑ General medical ward — empiric antibiotic regimens are designed to treat S.
aureus, gram-negative enteric bacilli (eg, Klebsiella pneumoniae) in addition to
typical pathogens (eg, S. pneumoniae, H. influenzae, and M. catarrhalis) and
atypical pathogens (eg, Legionella, M. pneumoniae, and C. pneumoniae)
❑ For patients without suspicion for MRSA or Pseudomonas, use one of two
regimens: combination therapy with a beta-lactam plus a macrolide or
monotherapy with a respiratory fluoroquinolone . Because these two
regimens have similar clinical efficacy, we select among them based on other
factors (eg, antibiotic allergy, drug interactions). For patients who are unable
to use either a macrolide or a fluoroquinolone, we use a beta-lactam plus
doxycycline
36. TREATMENT
❑ For patients with known colonization or prior infection with Pseudomonas,
recent hospitalization with IV antibiotic use, or other strong suspicion for
pseudomonal infection, we typically use combination therapy with both an
antipseudomonal beta-lactam (eg, piperacillintazobactam, cefepime,
ceftazidime, meropenem, or imipenem) plus an antipseudomonal
fluoroquinolone (eg, ciprofloxacin or levofloxacin).
❑ For patients with known colonization or prior infection with MRSA or other
strong suspicion for MRSA infection, we add an agent with anti-MRSA activity,
such as vancomycin or linezolid, to either of the above regimens. Antiviral
treatment (eg, oseltamivir) should be given as soon as possible for any
hospitalized patient with known or suspected influenza.
❑ ICU admission:
❑ For most patients without suspicion for MRSA or Pseudomonas, we treat with
a beta-lactam (eg, ceftriaxone, cefotaxime, ceftaroline, ampicillin-sulbactam,
ertapenem) plus a macrolide (eg, azithromycin or clarithromycin) or a beta-
lactam plus a respiratory fluoroquinolone (eg, levofloxacin or moxifloxacin)
37. TREATMENT
❑ For patients with known colonization or prior infection with MRSA, recent
hospitalization with IV antibiotic use, or other strong suspicion for MRSA
infection, we add an agent with anti-MRSA activity, such as vancomycin or
linezolid, to either of the above regimens .
❑ For patients with known colonization or prior infection with Pseudomonas,
recent hospitalization with IV antibiotic use, or other strong suspicion for
pseudomonal infection, we typically use combination therapy with both an
antipseudomonal beta-lactam (eg, piperacillin-tazobactam, cefepime,
ceftazidime, meropenem, or imipenem) plus an antipseudomonal
fluoroquinolone (eg, ciprofloxacin or levofloxacin) for empiric treatment .
❑ antiviral treatment (eg, oseltamivir) should be given as soon as possible for
any hospitalized patient with known or suspected influenza
❑ Adjunctive glucocorticoids — The use of glucocorticoids as an adjunctive
treatment for CAP is controversial, and the American Thoracic Society
(ATS)/Infectious Diseases Society of America (IDSA), do not advise routine use.
Indicated for refractory septic shock, acute exacerbations of COPD, COVID-19
pneumonia
38. TREATMENT
❑ Disposition —Clinical response should be assessed during daily rounds. While
various criteria have been proposed to assess clinical response , we generally
look for subjective improvement in cough, sputum production, dyspnea, and
chest pain. Objectively, we assess for resolution of fever and normalization of
heart rate, respiratory rate, oxygenation, and white blood cell count.
Generally, patients demonstrate some clinical improvement within 48 to 72
hours.
❑ Antibiotic de-escalation —we continue empiric treatment for the duration of
therapy, provided that the patient is improving. Intravenous antibiotic
regimens can be transitioned to oral regimens with a similar spectrum activity
as the patient improves.
❑ Duration of therapy — We generally determine the duration of therapy based
on the patient's clinical response to therapy.
❑ For all patients, we treat until the patient has been afebrile and clinically
stable for at least 48 hours and for a minimum of five days. Patients with mild
infection generally require five to seven days of therapy.
39. TREATMENT
❑ Patients with severe infection or chronic comorbidities generally require 7 to
10 days of therapy. Extended courses may be needed for
immunocompromised patients, patients with infections caused by certain
pathogens (eg, P. aeruginosa), or those with complications.
❑ Procalcitonin levels — We generally obtain a level at the time of diagnosis and
repeat the level every one to two days in patients who are clinically stable. We
determine the need for continued antibiotic therapy based on clinical
improvement and serial procalcitonin levels
❑ Discharge — Hospital discharge is appropriate when the patient is clinically
stable, can take oral medication, has no other active medical problems, and
has a safe environment for continued care.
❑ Immunocompromised patients — The spectrum of potential pathogens
expands considerably in immunocompromised patients to include invasive
fungal infections, less common viral infections (eg, cytomegalovirus), and
parasitic infections (eg, toxoplasmosis).
❑ Prolonged neutropenia, T cell immunosuppression, and use of tumor necrosis
factor-alpha inhibitors predispose to invasive fungal infections (eg,
aspergillosis, mucormycosis) as well as mycobacterial infections.
40. TREATMENT
❑ Advanced human immunodeficiency virus (HIV) infection (eg, CD4 cell count
<200 cells/microL), prolonged glucocorticoid use (particularly when used with
certain chemotherapeutics), and lymphopenia each should raise suspicion for
pneumocystis pneumonia.
❑ FOLLOW-UP IMAGING:
❑ The ATS/IDSA recommend not obtaining a follow-up chest radiograph in
patients whose symptoms have resolved within five to seven days
41. COMPLICATIONS AND PROGNOSIS
❑ Clinical failure — Clear indicators of clinical failure include progression to
sepsis and/or respiratory failure despite appropriate antibiotic treatment and
respiratory support.
❑ Non-resolving CAP — For some patients, initial symptoms will neither progress
nor improve with at least seven days of appropriate empiric antibiotic
treatment. Potential causes of non-resolving CAP include:
❑ Delayed clinical response – For some patients, particularly those with multiple
comorbidities, severe pneumonia, bacteremia, and infection with certain
pathogens (eg, S. pneumoniae), treatment response may be slow.
❑ Loculated infection – Patients with complications such as lung abscess,
empyema, or other closed space infections. Such infections may require
drainage and/or prolonged antibiotic treatment.
❑ Bronchial obstruction – Bronchial obstruction (eg, by a tumor) can cause a
post-obstructive pneumonia that may fail to respond or slowly respond to
standard empiric antibiotic regimens for CAP.
❑ Pathogens that cause subacute/chronic CAP – Mycobacterium tuberculosis,
nontuberculous mycobacteria (eg, Mycobacterium kansasii), fungi (eg,
Histoplasma capsulatum, Blastomyces dermatitidis), or less common bacteria
(eg, Nocardia spp, Actinomyces israelii).
42. COMPLICATIONS AND PROGNOSIS
❑ Incorrect initial diagnosis – Failure to improve despite seven days of treatment
also raises the possibility of an alternate diagnosis (eg, malignancy or
inflammatory lung disease).
❑ Once a patient is characterized as having non-resolving CAP, a complete new
physical examination, laboratory evaluation, imaging studies, and
microbiologic workup will be necessary to define the etiology of non-resolving
CAP.
43. PREVENTION
❑ The three primary pillars for the prevention of CAP are:
❑ Smoking cessation (when appropriate)
❑ Influenza vaccination for all patients
❑ Pneumococcal vaccination for at-risk patients