Chest Flashcards
What are the RUL pulmonary segments?
Apical
Posterior
Anterior
What are the LUL pulmonary segments?
Apical posterior
Anterior
Superior lingula
Inferior lingula
What are the RML pulmonary segments?
Lateral
Medial
What are the RLL pulmonary segments?
Superior Lateral Basal Medial Basal Anterior Basal Posterior Basal
What are the LLL pulmonary segments?
Superior Lateral Basal Medial Basal Anterior Basal Posterior Basal
What are the mechanisms of atelectasis?
Obstructive Relaxation (passive) Adhesive - surfactant deficiency Cicatrical - volume loss from architectural distortion of lung parenchyma by fibrosis
What happens to atelectasis in ICU patients?
Generally causes volume loss. In critically ill ICU patients, however, there may be rapid transudation of fluid into the obstructed alveoli, causing superimposed consolidation.
What is relaxation atelectasis?
Passive atelectasis - caused by relaxation of lung adjacent to an intrathoracic lesion causing mass effect, such as pleural effusion, pneumothorax, or pulmonary mass.
What is adhesive atelectasis?
Due to surfactant deficiency
MC in neonatal respiratory distress syndrome, but can also be seen in acute respiratory distress syndrome (ARDS)
What is Cicatricial atelectasis?
Volume loss from architectural distortion of lung parenchyma by fibrosis.
Sign associated with LUL atelectasis?
Luftsichel - cresent of air seen on the frontal radiograph - interface between the aorta and the hyperexpanded superior segement of the LLL.
Signs associated with RUL atelectasis?
Reverse S sign of Golden - caused by an obstrucgint mass. The central convex margins of the mass form a reverse S.
Justaphrenic peak sign - peridiaphragmatic triangular opacity caused by diaphragmatic traction from an inferior accessory fissure or an inferior pulmonary ligament.
Collapse of which lobe causes silhouetting of the right heart border?
RML collapse.
What things need to be present to diagnose round atelectasis?
Adjacent pleura must be abnormal
Opacity must be peripheral and in contact with the pleura
Opacity must be round or elliptical
Volume loss must be present in the affected lobe
Pulmonary vessels and bronchi leading to the opacity must be curved - comet tail sign
What is the elemental unit of lung function?
Secondary Pulmonary Lobule
What are the contents of a secondary pulmonary lobule?
Central artery (centrilobular artery) and a central bronchus - each branching many times to ultimately produced acinar arteries and respiratory bronchioles.
On CT, the centrilobular artery is often visible as a faint dot. The centrilobular bronchus is not normally visible.
The acinus is the basic unit of gas exchange, containing several generations of branching respiratory bronchioles, alveolar ducts, and alveoli.
Pulmonary veins and lymphatics collect in the periphery of each SPL.
Connective tissue, called interlobular septa, encases each SPL.
Thickening of the interlobular septa can be seen on CT and suggests pathologic enlargement of either the venous or lymphatic spaces.
Where are the pulmonary veins and lymphatics in the secondary pulmonary lobules?
In the periphery.
Connective tissue, called interlobular septa, encases each SPL.
Thickening of the interlobular septa can be seen on CT and suggests pathologic enlargement of either the venous or lymphatic spaces.
What is the DDx of an acute consolidation?
Pneumonia - MC cause
Pulmonary hemorrhage - primary or aspiration
Acute Respiratory Distress Syndrome (ARDS) - Noncardiogenic pulmonary edema seen in critically ill patients and though to be due to increased capillary permeability.
Pulmonary Edema - May cause consolidation, uncommon manifestation.
DDx of chronic consolidation?
Bronchioalveolar Carcinoma - mucinous subtype, a form of adenocarcinoma.
Organizing pneumonia - nonspecific response to injury characterized by granulation polyps which fill the distal airways, producing peripheral rounded and nodular consolidation.
Chronic eosinophilic pneumonia - an inflammatory process characterized by eosinophils causing alveolar filling in an upper-lobe distribution.
What is organizing pneumonia?
Nonspecific response to injury characterized by granulation polyps which fill the distal airways, producing peripheral rounded and nodular consolidation.
Causes chronic consolidation
What is chronic eosinophilic pneumonia?
An inflammatory process characterized by eosinophils causing alveolar filling in an upper-lobe distribution.
Causes chronic consolidation
What is the difference between consolidation and ground glass opacification?
Consolidation - complete filling of affected alveoli with a liquid-like substance (blood, pus, water, or cells). Pulmonary vessels are not visible through the consolidation on an unehanced CT. Air bronchograms are often present if airway is patent.
Ground glass opacification - partial filling of alveoli - pulmonary vessels are still visible.
DDX of acute ground glass opacification?
Similar to acute consolidation.
Pulmonary edema - usually dependent
Pneumonia - more commonly seen in atypical pneumonia such as viral or Pneumocystis jiroveci pneumonia
Pulmonary hemorrhage
Acute respiratory distress syndrome (ARDS)
DDx of chronic ground glass opacification?
Similar but broader DDx compared to chronic consolidation
Bronchioalveolar Carcinoma - tends to be focal or multifocal
Organizing Pneumonia - Rounded, peripheral chronic consolidation
Idiopathic Pneumonias - Inflammatory responses to pulmonary injury.
Hypersensitivity Pneumoitis (HSP), especially in the subacute phase. A type III hypersensitivity reaction to inhaled organic antigens. Subacute there is ground glass, centrilobular nodules, and mosaic attenuation.
Alveolar proteinosis - idiopathic disease characterized by alveolar filling by a proteinaceous substance. Distribution is typically central, with sparing of the periphery.
DDx of ground glass in a central distribution?
Pulmonary edema
Alveolar hemorrhage
Pneumocystis jiroveci pneumonia
Alveolar proteinosis
DDx of peripheral ground glass or consolidation?
Organizing pneumonia
Chronic eosinophilic pneumonia - typically with an upper lobe predominance
Atypical or viral pneumonia
Pulmonary edema - peripheral tends to be noncardiogenic in etiology, such as triggered by drug reaction - peripheral is unusual for cardiogenic pulmonary edema.
DDx of smooth interlobular septal thickening?
Conditions that dilate the pulmonary veins - pulmonary edema is most common. However, the DDx is identical to the differential for central ground glass.
Pulmonary edema
Pulmonary alveolar proteinosis
Pulmonary hemorrhage
Atypical pneumonia - especially Pneumocystis jiroveci pneumonia
DDx of nodular, irregular, or asymmetric septal thickening?
Processes that infiltrate the peripheral lymphatics - MC lymphangitic carcinomatosis and sarcoidosis.
Lymphangitic carcinomatosis - tumor spread through the lymphatics
Sarcoidosis - noncaseating granulomas, which form nodules and masses primarily in a lymphatic distribution.
What is crazy paving?
Interlobular septal thickening with superimposed ground glass opacification.
Nonspecific, but first described for alveolar proteinosis, where the GGO is caused by filling of alveoli by proteinaceous material and the interlobular septal thickening is caused by lymphatics taking up the same material.
DDx of crazy paving?
Alveolar proteinosis
Pneumocystis jiroveci pneumonia
Organizing pneumonia
Bronchioloalveolar carcinoma, mucinous subtype
Lipoid pneumonia - inflammatory pneuonia caused by a reaction to aspirated lipids.
Acute respiratory distress syndrome
Pulmonary hemorrhage
What are centrilobular nodules?
Opacification of the centrilobular bronchiole (or less commonly the centrilobular artery) at the center of each secondary pulmonary lobule
Multiple small nodules seen in the centers of the secondary pulmonary lobule - never extend to the pleural surface.
May be solid or ground glass attenuation - range in size from tiny up to a cm.
May be caused by infectious or inflammatory conditions.
What are the general categories of causes of centrilobular nodules?
Infectious or inflammatory conditions
What are the infectious causes of centrilobular nodules?
Endobronchial spread of TB or atypical mycobacteria.
Bronchopneumonia - spread of infectious pneumonia via the airways.
Atypical pneumonia, especially mycoplasma pneumonia.
What are the inflammatory causes of centrilobular nodules?
Hypersensitivity Pneumonitis- a type III hypersensitivity reaction to an inhaled organic antigen. The subacute phase is primarily characterized by centrilobular nodules.
Hot tube lung - hypersensitivity reaction to inhaled atypical mycobacteria, with similar imaging to HSP.
Respiratory Bronchiolitis Interstitial Lung Disease (RB-ILD) - inflammatory reaction to inhaled cigarette smoke mediated by pigmented macrophages.
Diffuse panbronchiolitis - Chronic inflammatory disorder characterized by lymphoid hyperplasia in the walls of the respiratory bronchioles resulting in bronchiolectasis. Typically affects patients of Asian descent.
Silicosis - Inhalation lung disease that develops in response to inhaled silica particles - upper lobe predominant centrilobular and perilymphatic nodules.
What is Hypersensitivity Pneumonitis?
A type III hypersensitivity reaction to an inhaled organic antigen. The subacute phase is primarily characterized by centrilobular nodules.
What is Hot Tube Lung?
Hypersensitivity reaction to inhaled atypical mycobacteria, with similar imaging to HSP
What is Respiratory Bronchiolitis Interstitial Lung Disease (RB-ILD)?
Inflammatory reaction to inhaled cigarette smoke mediated by pigmented macrophages
What is Diffuse Panbronchiolitis?
Chronic inflammatory disorder characterized by lymphoid hyperplasia in the walls of the respiratory bronchioles resulting in bronchiolectasis. Typically affects patients of Asian descent.
What is Silicosis?
Inhalation lung disease that develops in response to inhaled silica particles - upper lobe predominant centrilobular and perilymphatic nodules.
Where are perilymphatic nodules located?
Follow the anatomic locations of pulmonary lymphatics - 3 locations.
- Subpleural
- Peribronchovascular
- Septal (within the interlobular septa separating the hexagonal secondary pulmonary lobules).
DDx of perilymphatic nodules?
Sarcoidosis - MC by far, typically with an upper lobe distribution.
Pneumoconioses (silicosis and coal workers pneumoconiosis) are reactions to inorganic dust inhalation. Imaging may look identical to sarcoidosis with perilymphatic nodules, but there is usually a history of exposure (e.g. sandblaster who develops silicosis).
Lymphangitic carcinomatosis
What are Pneumoconioses?
Silicosis and Coal Workers Pneumoconiosis - reactions to inorganic dust inhalation.
Imaging may look identical to sarcoidosis with perilymphatic nodules, but there is usually a history of exposure (e.g. sandblaster who develops silicosis).
DDx of randomly distributed nodules?
Hematogenous metastases
Septic emboli - has a propensity to cavitate, but early emboli may be irregular or solid
Pulmonary Langerhan’s Cell Histiocytosis - a smoking-related lung disease that progresses from airway-associated and random nodules to irregular cysts. Usually distinguishable from other causes of random nodules due to the presence of cysts and non-angiocentric distribution.
What is Pulmonary Langerhan’s Cell Histiocytosis?
A smoking-related lung disease that progresses from airway-associated and random nodules to irregular cysts. Usually distinguishable from other causes of random nodules due to the presence of cysts and non-angiocentric distribution.
DDx of miliary nodules?
Disseminated TB
Disseminated fungal infection
Disseminated hematogenous metastases.
What are tree-in-bud nodules?
Multiple small nodules connecting to linear branching structures, which resembles a budding tree branch in springtime as seen on CT.
Linear branching structures represent impacted terminal bronchioles.
Tree-in-bud nodules are due to mucus, pus, or fluid impacting bronchioles and terminal bronchioles.
DDx of tree-in-bud nodules?
Mycobacteria TB and atypical mycobacteria.
Bacterial pneumonia.
Aspiration pneumonia
Airway-invasive aspergillus - opportunistic fungus with several patterns of disease. Seen in immunocompromised patients and may present either as bronchopneumonia or small airways infection.
What is airway-invasive Aspergillus?
Opportunistic fungus with several patterns of disease. Seen in immunocompromised patients and may present either as bronchopneumonia or small airways infection.
What is a solitary cavitary nodule/mass?
Thick, irregular wall, often with a solid mural component.
Overlap between benign and malignant nodules.
Maximum wall thickness <4 mm is usually benign
Wall thickness >15 mm is usually malignant.
Spiculated margins also suggest malignancy.
DDx of solitary cavitary lesion?
Primary bronchogenic carcinoma - SCC and adenocarcinoma can cavitate - SCC more frequently. Small cell never cavitates.
Tuberculosis - classically produces an upper-lobe cavitation.
DDx of multiple cavitary lesions?
Septic emboli
Vasculitis - including Wegener granulomatosis, which is especially prone to cavitate
Metastases - SCC and uterine carcinoma are known to cavitate.
DDx of multiple lung cysts?
Lymphangioleiomyomatosis (LAM) - diffuse cystic lung disease caused by smooth muscle proliferation of the distal airways. LAM causes uniformly distributed, thin-walled cysts in a diffuse distribution. Classically associated with a chylous effusion.
Emphysema - tends to be upper lobe predominant in a smoker.
Pulmonary Langerhans Cell Histiocytosis - irregular cysts and nodules predominately in the upper lungs.
Diffuse Cystic Bronchiectasis - Congenital or post-infectious causes can have a diffuse or lower-lobe distribution. CF is the MC cause of bronchiectasis has an upper lobe predominance.
Pneumocystis Jiroveci Pneumonia - features cysts in late-stage disease.
Lymphoid Interstitial Pneumonia (LIP) - Rare disease usually associated with Sjogren syndrome and characterized by alveolar distortion from lymphotic infiltrate and multiple cysts.
What is Lymphangioleiomyomatosis (LAM)?
Diffuse cystic lung disease caused by smooth muscle proliferation of the distal airways. LAM causes uniformly distributed, thin-walled cysts in a diffuse distribution. Classically associated with a chylous effusion.
What is Pulmonary Langerhans Cell Histiocytosis?
Irregular cysts and nodules predominately in the upper lungs.
What is Lymphoid Interstitial Pneumonia (LIP)?
Rare disease usually associated with Sjogren syndrome and characterized by alveolar distortion from lymphotic infiltrate and multiple cysts
DDx for a single cyst?
Bulla - Air filled cyst >1 cm
Bleb - Air-filled cystic structure continguous with the pleura measuring <1 cm. Rupture of a bleb is the MC cause of spontaneous pneumothorax.
Pneumatocele - Air-filled space caused by prior lung trauma or infection.
DDx of basal-predominant fibrotic change?
Idiopathic Pulmonary Fibrosis (IPF)- clinical syndrome of progresive pulmonary fibrosis of unknown etiology and is MC cause of basilar fibrosis. Almost always features honeycombing.
End-stage asbestosis - Asbestosis is an asbestos-induced inflammatory process ultimately producing pulmonary fibrosis. Usually other signs of asbestos exposure are present, such as pleural plaques.
Nonspecific Interstitial Pneumonia (NSIP), fibrotic form - Idiopathic pneumonia. Lung response to injury commonly associated with collagen vascular disease and drug reaction. Two histiologic subtypes- cellular and fibrotic forms - the latter may produce basal-predominant fibrosis. In contrast to IPF, honeycombing is usually absent.
What is Idiopathic Pulmonary Fibrosis (IPF)?
Clinical syndrome of progresive pulmonary fibrosis of unknown etiology and is MC cause of basilar fibrosis. Almost always features honeycombing.
What is Nonspecific Interstitial Pneumonia (NSIP)- fibrotic form?
Idiopathic pneumonia. Lung response to injury commonly associated with collagen vascular disease and drug reaction. Two histiologic subtypes- cellular and fibrotic forms - the latter may produce basal-predominant fibrosis. In contrast to IPF, honeycombing is usually absent.
MC cause of pulmonary fibrosis?
Idiopathic Pulmonary Fibrosis
DDx of upper lobe fibrotic changes?
End-stage sarcoidosis
Chronic hypersensitivity pneumonitis
End-stage silicosis
MC cause of community-acquired pneumonia?
S. pneumoniae
Pneumonia cause in young and otherwise healthy patients?
Atypical pneumonia, including Mycoplasma, viral, and Chlamydia.
Mycoplasma has a varied appearance and can produce consolidation, areas of ground glass attenuation, centrilobular nodules, and tree-in-bud nodules.
MC cause of pneumonia in elderly smokers?
Legionella - infection tends to be severe.
Peripheral consolidation often progresses to lobar and multifocal pneumonia.
Cause of pneumonia in alcoholics and aspirators?
Klebsiella and other gram-negatives.
Klebsiella classically leads to voluminous inflammatory exudates causing the bulging fissure sign.
What is the Bulging Fissure Sign?
Secondary to voluminous inflammatory exudates due to Klebsiella
What causes Hospital Acquired Pneumonia?
Aspiration of colonized secretions due to aspiration of colonized secretions.
Wide variety of organisms- most important pathogens include MRSA and resistant gram-negatives including Pseudomonas.
What is Health Care Associated Pneumonia (HCAP)?
Pneumonia in a nursing home resident or a patient with a >2 day hospitalization over the past 90 days.
Pathogens are similar to Hospital Acquired Pneumonia- MRSA and gram-negatives including Pseudomonas.
What is Ventilator Associated Pneumonia (VAP)?
Caused by infectious agents not present at the time mechanical ventilation was started.
Most are polymicrobial and primarily involve gram-negative rods such as Pseudomonas and Acinetobacter.
What causes pneumonia in immunocompromised patients?
Any pathogens plus opportunistic infections including Pneumocystis, fungi such as Aspergillus, Nocardia, CMV, etc.
What is Lobar Pneumonia?
Consolidation of a single lobe.
Usually bacterial in origin and is MC presentation of community acquired pneumonia.
What is lobular pneumonia (bronchopneumonia)?
Patchy consolidation with poorly defined airspace opacities, usually involving several lobes, and most commonly due to S. aureus.
Difference between Lobar and Lobular Pneumonia?
Lobular pneumonia = bronchopneumonia
Patchy consolidation with poorly defined airspace opacities, usually involving several lobes, and most commonly due to S. aureus.
Lobar = Consolidation of a single lobe.
What is interstitial pneumonia?
Inflammatory cells located predominantly in the interstitial tissue of the alveolar septa causing diffuse or patchy ground glass opacification.
Can be viral pneumonia, Mycoplasma, Chlamydia, or Pneumocystis.
What is Round Pneumonia?
Infectious mass-like opacification seen only in children, MC due to Streptococcus pneumoniae.
Infection remains somewhat confined due to incomplete formation of pores of Kohn.
Causes of lung abscesses?
Staphylococcus aureus, Pseudomonas, or anaerobic bacteria.
Air-fluid level is almost always present.
An abscess is usually spherical, with equal dimensions on frontal and lateral views.
What is pulmonary gangrene?
Very rare complication of pneumonia - extensive necrosis or sloughing of a pulmonary segment or lobe.
Severe manifestation of pulmonary abscess.
What are the three stages of development of an empyema?
- Free-flowing exudative effusion- can be treated with needle aspiration or simple drain.
- Development of fibrous strands- requires large-bore chest tube and fibrinolytic therapy.
- Fluid becomes solid and jelly-like- usually requires surgery.
What is a pneumatocele?
Thin-walled, gas-filled cyst that may be post-traumatic or develop as a sequela of pneumonia- typically from Staphylococcus aureus or Pneumocystis.
Pneumatoceles almost always resolve.
What is a Bronchopleural Fistula?
Abnormal communication between the airway and the pleural space - caused by rupture of the visceral pleura.
MC cause is surgery, but can get with lung abscess, empyema, and trauma.
What is Empyema Necessitans?
Extension of an empyema to the chest wall - MC secondary to TB.
Other causative organisms include Nocardia and Actinomyces.
What can initial exposure to TB lead to?
- Contained disease (90%)- results in classified granulomas and/or calcified hilar lymph nodes. With normal immunity, the tuberculous bacilli are sequestered with a caseating granulomatous response.
- Primary Tuberculosis - host cannot contain the organism. More common in children and immunocompromised patients.
What is Primary TB?
Infection from the first exposure to TB. May involve the pulmonary parenchyma, airways, and the pleura. Often causes adenopathy.
Up to 15% may have no radiographic changes and the imaging appearance of primary TB is nonspecific.
Four imaging manifestations: ill-defined consolidation, pleural effusion, lymphadenopathy, and miliary disease.
Primary may occur in any lobe, but most typical locations are the lower lobes or RML. Can be difficult to distinguish between primary and post-primary TB - treatment is the same.
Gohn Focus: Initial focus of parenchymal infection, usually located in the upper part of the lower lobe or lower part of the upper lobe.
Ranke Complex: Ghon focus and LAD.
Cavitation is rare in primary TB, in contrast to reactivation TB.
What are the four imaging manifestations of primary TB?
Ill-defined consolidation, pleural effusion, lymphadenopathy, and miliary disease.
Most typical locations of primary TB?
Primary may occur in any lobe, but most typical locations are the lower lobes or RML.
What is a Gohn Focus?
Initial focus of parenchymal infection, usually located in the upper part of the lower lobe or lower part of the upper lobe.
What is a Ranke Complex?
Ghon focus and LAD.
What is reactivation TB?
Post-primary TB
Adolescents and adults- reactivation of dormant infection acquired earlier in life.
Chronic cough, low-grade fever, hemoptysis, and night sweats.
MC occurs in the upper lobe apical and posterior segments.
Immunocompetent- upper-lobe predominant disease with cavitation and lack of adenopathy. Focal upper lobe consolidation and endobronchial spread are common. Tree-in-bud nodules suggest active endobronchial spread.
Immunosuppressed patient (such as HIV), low-attenuation adenopathy is typical additional finding, similar to adenopathy seen in primary TB. Low density lymph nodes may mimic immune reconstitution syndrome in HIV patients.
Tuberculoma is a well-defined rounded opacity usually in the upper lobes.
What does reactivation TB look like in immunocompetent patients?
Upper-lobe predominant disease with cavitation and lack of adenopathy. Focal upper lobe consolidation and endobronchial spread are common. Tree-in-bud nodules suggest active endobronchial spread.
What does reactivation TB look like in immunocuppressed patients?
Low-attenuation adenopathy is typical additional finding, similar to adenopathy seen in primary TB. Low density lymph nodes may mimic immune reconstitution syndrome in HIV patients.
What is a Tuberculoma?
Tuberculoma is a well-defined rounded opacity usually in the upper lobes.
Signs of healed tuberculosis?
Apical scarring, usually with upper lobe volume loss and superior hilar retraction.
Calcified granulomas may be present as well, which indicate containment of the initial infection by a delayed hypersensitivity response.
What form of TB can miliary TB seen?
Primary or reactivation TB.
What is the classic presentation of atypical mycobacteria?
Elderly woman with cough, low-grade fever, and weight loss - Lady Windermere syndrome.
What are the atypical mycobacterial infections?
Mycobacterium avium intracellulare and M. kanasii.
Findings of atypical mycobacteria infection?
Bronchiectasis and tree-in-bud nodules - MC in RML or lingula.
What is Lady Windermere Syndrome?
Elderly woman with cough, low-grade fever, and weight loss - Atypical mycobacteria infection.
What is hot tube lung?
Hypersensitivity pneumonitis in response to atypical mycobacteria which are found in hot tubs.
No active infection and the typical patient is otherwise healthy.
Imaging is similar to other causes of hypersensitivity pneumonitis, featuring centrilobular nodules.
What is Histoplasma Capsulatum found?
Localized to the Ohio and Mississippi river valleys - in soil contaminated with bat or bird guano.
Chronic infection can mimic reactivation TB with upper lobe fibrocavitary consolidation.
What is a rare complication of Histoplasma capsulatum infection?
Fibrosing medastinitis - infection of mediastinal lymph nodes leading to pulmonary venous obstruction, bronchial stenosis, and pulmonary artery stenosis. Affected lymph nodes tend to calcify.
What is Fibrosing Mediastinitis?
Rare complication of Histoplasma capsulatum infection
infection of mediastinal lymph nodes leading to pulmonary venous obstruction, bronchial stenosis, and pulmonary artery stenosis. Affected lymph nodes tend to calcify.
Where is Coccidioides Immitus found and what does it look like on imaging?
SW US and has a variety of radiologic appearances, including multifocal consolidation, multiple pulmonary nodules, and miliary nodules.
Where is Blastomyces Dermatitidis and what does it look like?
Central and SE US.
Infection is usually asymptomatic, but may present with flu-like illness that can progress to multifocal consolidation, ARDS, or miliary disease.
Immunocompromised patient with a focal air space opacity?
Most likely to have a bacterial pneumonia (MC pneumococcus), but TB should also be considered if CD count is low.
Multifocal opacities have a wider DDx including Pneumocystis pneumonia and opportunistic lung fungal infection such as Cryptococcus or Aspergillus.
Immunocompromised patient with mulfifocal opacities?
Multifocal opacities have a wider DDx including Pneumocystis pneumonia and opportunistic lung fungal infection such as Cryptococcus or Aspergillus.
Most likely to have a bacterial pneumonia (MC pneumococcus), but TB should also be considered if CD count is low.
What is Pneumocystis jiroveci pneumonia?
Opportunistic fungus that may cause pneumonia in individuals with CD4 counts <200 cells/cc.
CXR can be normal, but classic finding is bilateral perihilar (central) airspace opacities with peripheral sparing.
CT: geometric perihilar ground glass opacification, sometimes with crazy paving.
Normal CT rules out Pneucystis pneumonia, but can hide in a normal CXR.
Propencity to cause upper lobe pneumatoceles, which may predispose to pneumothorax or pneumomediastinum.
CXR findings of Pneumocystis jiroveci pneumonia?
CXR can be normal, but classic finding is bilateral perihilar (central) airspace opacities with peripheral sparing.
Normal CT rules out Pneucystis pneumonia, but can hide in a normal CXR.
CT findings of Pneumocystis jiroveci pneumonia?
CT: geometric perihilar ground glass opacification, sometimes with crazy paving.
Normal CT rules out Pneucystis pneumonia, but can hide in a normal CXR.
What does Pneumocystis jiroveci pneumonia have a propensity to cause?
Propencity to cause upper lobe pneumatoceles, which may predispose to pneumothorax or pneumomediastinum.
What is Cryptococcus Neoformans pneumonia?
Opportunistic organism and is the MC fungal infection in AIDS patients. Pulmonary infection usually coexists with cryptococcal meningitis. CD4 is usually less than 100 in affected individuals.
Can have a wide range of appearances ranging from GG attenuation to focal consolidation to cavitating nodules.
Can also present as milliary disease, often with LAD or effusions.
Spectrum of pulmonary Aspergillus with Asthma?
Increased/inappropriate immune response
Allergic bronchopulmonary aspergillus
Finger-in-glove sign: mucoid impaction of bronchiectasis.
Spectrum of pulmonary Aspergillus with preexisting cavity (e.g. sarcoid, TB)?
Abnormal lungs or abnormal host
Aspergilloma/Mycetoma
Mobile mycetoma
Monad Sign: Air surrounding mycetoma
Spectrum of pulmonary Aspergillus with debilitated, diabetic, or alcoholic?
Abnormal lungs or abnormal host
Semi-invasive (chronic necrotizing)
Chronic consolidation
Cavitation
Spectrum of pulmonary Aspergillus with neutropenic or immunocompromised?
Invasive disease seen in immunocompromised
Airway invasive (Bronchopneumonia, Centrilobular nodules, Tree-in-bud nodules)
Angioinvasive
Halo sign: acute infection - peripheral ground glass
Air Crescent Sign: resolving - crescentic air in cavity
Who does Aspergillus affect?
Only affects individuals with abnormal immunity or preexisting pulmonary disease.
Asthma, immunocompromised state, prior infection, or structural/congenial abnormality.
What is Allergic Bronchopulmonary aspergillosis (ABPA)?
Hypersensitivity reaction to aspergillus seen most commonly in patients with long-standing asthma.
Present with recurrent wheezing, low-grade fever, cough, and sputum production. Sputum contains fragments of aspergillus hyphae.
Key finding is upper lobe bronchiectasis and mucoid impaction, which can be high attenuating or even calcified. Combination of mucoid impaction within bronchiectatic airways represents the finger-in-glove sign- not specific for ABPA and can also be seen in segmental bronchial atresia and many other diseases including CF.
What is Saprophytic Aspergillosis?
Aspergilloma- conglomeration of intertwined aspergillus fungal hyphae and cellular debris (a mycetoma or “fungus ball”) in preexisting pulmonary cavity - mobile and will change position.
MC is preexisting cavity from TB or sarcoidosis. Less common are congenital abnormalities such as bronchogenic cyst or sequestration, and post-infectious/post-traumatic pneumatocele.
Can cause hemoptysis.
Air outlining the mycetoma = Monad sign
Air crescent sign is reserved for angioinvasive aspergillus.
What is the Monad Sign?
Air outlining the mycetoma in the pulmonary cavity
What is the air crescent sign?
Visually similar to the Monod Sign surrounding a mycetoma- represents a crescent of air from retraction of infarcted lung.
Seen in angioinvasive aspergillus.
Good prognostic sign - indicateds that the patient is in the recovery phase.
What is semi-invasive aspergillosis?
Necrotizing granulomatous inflammation (analogous in pathology to reactivation TB) in response to chronic aspergillus infection.
Seen in debilitated, diabetic, alcoholic, and COPD patients.
Cough, chronic fever, and less commonly hemoptysis.
CT: segmental areas of consolidation, often with cavitation and pleural thickening which progress slowly over months to years.
What is Airway-invasive Aspergillosis?
Aspergillus infection deep to the airway epithelial cells. Seen only in immunocompromised, including neutropenic and AIDS patients.
Clinical disease ranges from bronchiolitis to bronchopneumonia.
Main CT findings of airway-invasive aspergillosis are centrilobular and tree-in-bud nodules. When bronchopneumonia is present, radiograph and CT findings are indistinguishable from other causes of bronchopneumonia, such as staph aureus.
What is Angioinvasive Aspergillosis?
Aggressive infection characterized by invasion and occlusion of arterioles and smaller pulmonary arteries by fungal hyphae.
Almost seen exclusively in the severely immunocompromised- chemotherapy, stem cell or solid organ transplant recipients, and in AIDS.
CT halo sign- halo of ground glass surrounding a consolidation. GG is though to correspond to hemorrhagic infarction of the lung.
Air crescent sign- visually similar to the Monod sign surrounding a mycetoma, represents a crescent of air from retraction of infarcted lung. It a good prognostic sign as it indicates that the patient is in the recovery phase.
What is the CT halo sign?
Seen in angioinvasive aspergillosis
Halo of ground glass surrounding a consolidation. GG is though to correspond to hemorrhagic infarction of the lung.
What is the Air Crescent Sign?
Visually similar to the Monod sign surrounding a mycetoma, represents a crescent of air from retraction of infarcted lung. It a good prognostic sign as it indicates that the patient is in the recovery
What are the three stages of pulmonary edema severity?
Vascular redistribution - first radiographic sign of increased pulmonary venous pressure. Imaging shows increased caliber of the upper lobe vessels compared to the lower lobe vessels.
Interstitial edema - increased fluid within the pulmonary veins, which surround the periphery of each hexagonal secondary pulmonary lobule - increased interstitial markings, indistinctness of the pulmonary vasculature, peribronchial cuffing, and Kerley B (peripheral of lung- represent thickened interlobular septa) and A lines (radiate outward from the hila and represent dilation of lymphatic channels - no thought to be clinically relevant).
Alveolar edema - filling of the alveoli with fluid. On imaging, perihilar (central) opacifications are present. Pleural effusions and cardiomegaly are often present.
Difference betwen Kerly B and A lines
Kerley B (peripheral of lung- represent thickened interlobular septa) and A lines (radiate outward from the hila and represent dilation of lymphatic channels - no thought to be clinically relevant).
Cause of asymmetric isolated RUL pulmonary edema?
Acute mitral regurgitation secondary to MI and papillary muscle rupture.
What is the vascular pedicle on radiograph and what makes it up?
The transverse width of the upper mediastinum.
Right border - interface of the superior vena cava (SVC) and theright mainstem bronchus
Left border - lateral border of the takeoff of the subclavian from the aorta
Normally <58mm
Interval increase in pedicle width (>63 or >70 mm) on sequential supine AP ICU-type CXR generally correlates with increased pulmonary capillary wedge pressure and fluid overload.
Where should the tip of a Swan-Ganz catheter be?
Swan–Ganz pulmonary artery catheter should be in either the main, right, or left pulmonary artery.
If the tip is distal to the proximal interlobar pulmonary artery, there is a risk of pulmonary artery rupture or pseudoaneurysm. Other complications of pulmonary artery catheter placement include intracardiac catheter knot and arrhythmia.
Leading cause of cancer death in the US?
Lung cancer.
Lung cancer type in a lifelong nonsmoker with no history of secondhand exposure
Adenocarcinoma
Is also associated with smoking, but not as much as SCC and small cell.
Any type of lung scarring or fibrosis increases the risk of lung cancer.
Exposures- beryllium, radon, arsenic, etc. Asbestos.
Pulmonary nodule with popcorn calcification
Pulmonary hamartoma - benign
Pulmonary nodule with intra-lesional fat
Suggestive of hamartoma or lipoid granuloma - benign
Single most important risk factor for malignancy of a pulmonary nodule?
Large size
0.8 to 3 cm nodules have 18% risk of being lung cancer and masses >3 cm have a very high chance of being malignant.
Irregular edge or spiculated margin is concerning.
Round shape (as opposed to oblong) is suggestive of malignancy.
Cavitary nodule or nodule containing small cystic spaces is suspicious for malignancy.
MC subtype of lung cancer
Adenocarcinoma
Characteristics of lung adenocarcinoma
Most common subtype of lung cancer. It is related to smoking, but less strongly than squamous cell.
Tends to occur in the peripheral lung.
Typical radiographic appearance of adenocarcinoma is of a pulmonary nodule, which often has a spiculated margin due to reactive fibrosis.
Cavitation can occur but is less commonly seen compared to squamous cell
Pathologic marker is TTF-1 (thyroid transcription factor), which is positive
in primary lung adenocarcinoma and negative in pulmonary metastases from an extrathoracic adenocarcinoma.
What is a useful pathologic marker for lung adenocarcinoma?
TTF-1 (thyroid transcription factor), which is positive in primary lung adenocarcinoma and negative in pulmonary metastases from an extrathoracic adenocarcinoma.
What is Bronchioloalveolar Carcinoma (BAC)?
Spectrum of well-differentiated adenocarcinoma that demonstrates lepidic growth. The hallmark of lepidic growth is a spreading of malignant cells using the alveolar walls as a scaffold.
The opposite of lepidic growth is hilic growth, demonstrated by most other forms of lung cancer, which describes cancer growth by invasion and destruction of lung parenchyma.
Variable spectrum- MC indolent and often negative on PET.
Classification is primarily based on pathology of the lesion - referred to clinically as BAC.
Adenomatous hyperplasia (AAH): A precursor lesion.
Adenocarcinoma in situ: A preinvasive lesion.
Minimally invasive adenocarcinoma.
Adenocarcinoma, predominantly invasive with some nonmucinous lepidic component: Formerly nonmucinous BAC.
Invasive mucinous adenocarcinoma: Formerly mucinous BAC. Nonmucinous and mucinous subtypes of BAC occur with approximately equal prevalence.
Difference between lepidic and hilic growth?
Lepidic growth is a spreading of malignant cells using the alveolar walls as a scaffold- BAC
The opposite of lepidic growth is hilic growth, demonstrated by most other forms of lung cancer, which describes cancer growth by invasion and destruction of lung parenchyma.
What are the two main subtypes of Bronchioloalveolar Carcinoma (BAC)?
Nonmucinous BAC (adenocarcinoma, predominantly invasive with some nonmucinous lepidic component) classically presents as a ground glass or solid nodule with air bronchograms and has a better prognosis compared to the mucinous subtype.
Mucinous BAC (invasive mucinous adenocarcinoma) tends to present with chronic consolidation. It has a worse prognosis compared with non-mucinous BAC.
What is Nonmucinous BAC?
(Adenocarcinoma, predominantly invasive with some nonmucinous lepidic component) classically presents as a ground glass or solid nodule with air bronchograms and has a better prognosis compared to the mucinous subtype.
What is Mucinous BAC?
(Invasive mucinous adenocarcinoma) tends to present with chronic consolidation. It has a worse prognosis compared with non-mucinous BAC.
An important differential consideration for chronic ground glass or consolidation, often with air bronchograms.
What is small cell lung cancer?
Small cell carcinoma is the third most common lung cancer cell type (after adenocarcinoma and squamous cell). Neoplastic cells are of neuroendocrine origin and are associated with various paraneoplastic syndromes.
Small cell carcinoma is strongly associated with smoking.
Small cell tends to occur in central bronchi with invasion through the bronchial wall, typically presenting as a large hilar or parahilar mass.
Involvement of the SVC may cause SVC syndrome. Small cell rarely presents as a solitary pulmonary nodule.
What is Large cell lung cancer?
Large cell carcinoma is a wastebasket pathologic diagnosis for tumors that are not squamous, adenocarcinoma, or small cell. Large cell carcinoma is strongly associated with smoking and has a poor prognosis.
Large cell carcinoma often occurs in the lung periphery, where it presents as a large mass.
What is carcinoid lung cancer?
Neoplastic carcinoid cells originate from neuroendocrine cells in the bronchial walls.
Endobronchial mass distal to the carina, which may cause obstructive atelectasis.
Carcinoid may be typical (low-grade) or the more aggressive atypical variant.
Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) is an extremely uncommon precursor lesion to typical carcinoid tumor, characterized by multiple foci of neuroendocrine hyperplasia or tumorlets (carcinoid foci <5 mm in size) and bronchiolitis obliterans.
What is Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH)?
Extremely uncommon precursor lesion to typical carcinoid tumor, characterized by multiple foci of neuroendocrine hyperplasia or tumorlets (carcinoid foci <5 mm in size) and bronchiolitis obliterans.
What type of lung cancer typically presents as a solitary pulmonary nodule?
Adenocarcinoma, including subtypes formerly called BAC, comprises approximately 50% of cancers presenting as a solitary pulmonary nodule.
Common presentation of SC and small cell lung cancer?
Hilar mass
What is the stage of a superior sulcus tumor?
T3.
T stages of lung cancer?
T1: Tumor ≤3 cm surrounded by lung or visceral pleura.
T1a: Tumor ≤2 cm; 5-year survival rate 77%; T1b: >2 and ≤3 cm; 5-year survival rate 71%.
T2: Tumor >3 cm and ≤7 cm, or local invasion of the visceral pleura, or endobronchial lesions >2 cm from the carina.
T2a: >3 and ≤5 cm; 5-year survival rate 58%; T2b: >5 and ≤7 cm; 5-year survival rate 49%.
T3: Tumor >7 cm, or local invasion of chest wall, diaphragm, pleura, or superior sulcus tumor, or endobronchial lesion <2 cm from carina.
T3: 5-year survival rate 35%.
T3: Separate tumor nodule in the same lobe; 5-year survival rate 28%.
T4: Separate tumor nodule in a different lobe in the ipsilateral lung, or tumor of any size with invasion of mediastinal structures including carina, heart, great vessels, or vertebral bodies.
T4: 5-year survival rate 22%.
N stages of lung cancer?
N0: No lymph node metastases.
N1: Ipsilateral hilar or intrapulmonary lymph nodes.
N2: Ipsilateral mediastinal nodes.
N3: Contralateral lymph nodes or supraclavicular nodes on either side.
M stages of lung cancer?
M0: No metastatic disease.
M1a: Local thoracic metastatic disease.
Separate tumor nodule in contralateral lung; 5-year survival rate 3%.
Malignant pleural or pericardial effusion; 5-year survival rate 2%.
M1b: Distant or extrathoracic metastatic disease.
Median survival 6 months. 1-year survival rate 22%.
Pressures defining pulmonary arterial hypertension?
Pulmonary arterial systolic pressure ≥25 mm Hg at rest or ≥30 mm Hg during exercise.
Pressures defining pulmonary venous hypertension?
Pulmonary capillary wedge pressure (an approximation of pulmonary venous pressure) is ≥18 mm Hg.
What are the classifications of pulmonary HTN?
In precapillary causes of pulmonary hypertension, the primary abnormality is either the pulmonary arterial system or pulmonary arterial blood flow. Abnormalities of the pulmonary parenchyma leading to chronic alveolar hypoxia are also included in this category.
In postcapillary causes of pulmonary hypertension, an abnormality of the pulmonary veins or elevation of pulmonary venous pressure leads to pulmonary arterial hypertension.
WHO classification divides into 5 groups based on etiology. No correlation between pre/postcapillary classification.
What finding is pathognomonic for chronic PA HTN?
PA calcifications.
What is the Hilum Convergence Sign?
Describes the appearance of hilar pulmonary artery branches converging into an enlarged pulmonary artery.
An enlarged pulmonary artery can mimic a mediastinal mass. The hilum convergence sign is helpful to confirm that the apparent “mass” in fact represents the pulmonary artery.
What is the Hilum Overlay Sign?
Visualization of hilar vessels through a mass. It indicates that a mediastinal mass is present, which cannot be in the middle mediastinum. Usually this means the mass is in the anterior mediastinum.
What is primary pulmonary HTN?
The pathologic hallmark of primary pulmonary hypertension (PPH) is the plexiform lesion in the wall of the muscular arteries, which is a focal disruption of the elastic lamina by an obstructing plexus of endothelial channels. There is a relative paucity of prostacyclins and nitric oxide expressed by endothelial cells.
PPH may be idiopathic (females > males) or familial (approximately 10% of cases).
On imaging, there is typically enlargement of the main pulmonary arteries with rapidly tapering peripheral vessels.
What is Pulmonary Veno-occlusive Disease?
Caused by fibrotic obliteration of the pulmonary veins and venules. Pulmonary veno-occlusive disease may be idiopathic but is associated with pregnancy, drugs (especially bleomycin), and bone marrow transplant.
Imaging features pulmonary arterial enlargement. Pulmonary edema and ground glass centrilobular nodules are often present.
What is pulmonary HTN associated with hypoxemic lung disease?
COPD, sleep apnea, and interstitial lung disease can all lead to pulmonary hypertension.
Chronic hypoxic vasoconstriction is thought to invoke vascular remodeling leading to hypertrophy of pulmonary arterial vascular smooth muscle and intimal thickening.
Chronic lung disease can further contribute to obliteration of pulmonary microvasculature through emphysema and the perivascular fibrotic changes of pulmonary fibrosis.
What is Fibrosing Mediastinitis?
Progressive proliferation of fibrous tissue within the mediastinum may lead to encasement and compression of mediastinal structures. The most common causes of fibrosing mediastinitis are histoplasmosis and tuberculosis.
Fibrous encasement of the pulmonary veins leads to permanent histological changes within the endothelial cells.
Fibrosing mediastinitis may also encase the pulmonary arteries, creating a precapillary pulmonary hypertension.
Imaging features of fibrosing mediastinitis include increased mediastinal soft tissue, often with calcified lymph nodes due to prior granulomatous infection.
What is the Fleischner Sign?
Widening of the pulmonary arteries due to clot
What is Hamptom’s Hump?
A peripheral wedge-shaped opacity representing pulmonary infarct.
What is Westermark Sign?
Regional oligemia in the lung distal to the pulmonary artery thrombus.
What are the jobs of the Type I and II pneumocytes and alveolar macrophages in the alveoli?
Type I pneumocytes form alveolar wall and participate in gas exchange.
Type II pneumocytes produce surfactant, which prevents atelectasis.
Alveolar macrophages ingest and process inhaled particulate materials.
What is the most common idiopathic interstitial pneumonia?
IPF
2nd worst prognosis - 2-4 years
Only acute interstitial pneumonitis (AIP) has a worse prognosis
What interstitial pneumonia has the worst prognosis?
Acute Interstitial Pneumonitis
IPF has the 2nd worst.
Interstitial pneumonia with interstitial fibroblastic foci on pathology =
UIP
What is the relationship between UIP and IPF?
IPF is the clinical syndrome of UIP with unknown cause and is the most common cause of UIP.
IPF has a much worse clinical outcome compared to secondary causes of UIP.
What are the secondary causes of UIP?
MC cause is IPF
Collagen vascular disease (rheumatoid arthritis much more commonly than scleroderma).
Drug injury.
Asbestosis. An imaging clue to the presence of asbestosis is calcified plaques indicative of prior asbestos exposure.
What does NSIP look like on pathology?
Thickened alveolar septa from chronic inflammation. In contrast to IPF/UIP, there is less fibrotic change.
Septal thickening (causing ground glass attenuation) due to chronic inflammation and collagen deposition Unlike IPF, there are no interstitial fibroblastic foci
nonpigmented macrophages in alveoli
Causes of NSIP
May be idiopathic or associated with other diseases. NSIP is the most common
pulmonary manifestation in patients with collagen vascular disease.
NSIP may also be caused by drug reaction or occupational exposure.
NSIP may be associated with dermatomyositis
Two forms of NSIP?
An important imaging feature of NSIP, regardless of the form, is the presence of ground glass opacities (GGO), which are nearly always bilateral. A key feature differentiating NSIP from IPF is the presence of ground glass in NSIP.
Fibrotic NSIP predominantly features GGO with fine reticulation and traction bronchiectasis. Honeycombing is usually absent. If honeycombing is present, consider UIP. Worse prognosis compared to cellular NSIP, but a better prognosis compared to UIP.
Cellular NSIP also features GGO, but without significant fibrotic changes. Much less common than fibrotic NSIP and has a better prognosis compared to fibrotic NSIP.
A key imaging finding (not always seen but very specific) is sparing of immediate subpleural lung. This feature is NOT seen in UIP, and can be seen in both cellular and fibrotic NSIP.
What is Cryptogenic Organizing Pneumonia (COP)?
clinical syndrome of organizing
pneumonia (OP) without known cause.
responds to steroids with a good prognosis
pathologic pattern of granulation tissue polyps that fill the distal airways and alveoli. Organizing pneumonia may be a response to infection, drug reaction, or inhalation
myxoid fibroblastic organizing pneumonia completely fills the alveolar spaces unlike in IPF, these fibroblastic foci completely resolve as the disease regresses chronic lymphocytic inflammation thickens alveolar septa
CT of OP shows mixed consolidation and ground glass opacities in a peripheral and peribronchovascular distribution. The reverse halo sign (also known as the atoll sign) is relatively specific for OP and features a central lucency surrounded by a ground glass halo.
Pathology of COP?
pathologic pattern of granulation tissue polyps that fill the distal airways and alveoli. Organizing pneumonia may be a response to infection, drug reaction, or inhalation
myxoid fibroblastic organizing pneumonia completely fills the alveolar spaces unlike in IPF, these fibroblastic foci completely resolve as the disease regresses chronic lymphocytic inflammation thickens alveolar septa
What is the reverse halo sign?
(also known as the atoll sign) is relatively specific for OP and features a central lucency surrounded by a ground glass halo.
What is Respiratory Bronchiolitis-interstitial lung disease (RB-ILD)?
RB-ILD is both the clinical syndrome and the pathologic diagnosis of this smoking related interstitial lung disease.
Respiratory bronchiolitis (RB, without the ILD) is very common in smokers, where pigmented macrophages are found in respiratory bronchioles. RB is usually asymptomatic, but if symptoms are present (usually cough and shortness of breath), the clinical syndrome is called RB-ILD.
Histologically, RB-ILD is characterized by sheets of macrophages filling the terminal airways, with relative sparing of the alveoli.
key imaging features of RB-ILD are centrilobular nodules and patchy ground glass opacities. In contrast to NSIP, the distribution of ground glass in RB-ILD is more random than the peripherally predominant pattern of NSIP.
Imaging features of RB-ILD?
key imaging features of RB-ILD are centrilobular nodules and patchy ground glass opacities. In contrast to NSIP, the distribution of ground glass in RB-ILD is more random than the peripherally predominant pattern of NSIP.
What is Desquamative Interstitial Pneumonia (DIP)?
RB, RB-ILD, and DIP represent a continuous spectrum of smoking-related lung disease.
Like RB, brown-pigmented macrophages are involved in DIP; however, sheets of these abnormal macrophages also extend into the alveoli in DIP.
Imaging of DIP shows diffuse basal-predominant patchy or subpleural ground glass opacification, more extensive than RB-ILD. Although the predominant abnormality is ground glass, a few cysts may also be present.
Difference between RB-ILD and DIP?
Like RB, brown-pigmented macrophages are involved in DIP; however, sheets of these abnormal macrophages also extend into the alveoli in DIP.
Imaging of DIP shows diffuse basal-predominant patchy or subpleural ground glass opacification, more extensive than RB-ILD. Although the predominant abnormality is ground glass, a few cysts may also be present.
What is Lymphoid Interstitial Pneumonia?
LIP is exceptionally rare as an isolated idiopathic disease and is more commonly associated with Sjögren syndrome or HIV.
histologic hallmark of LIP is diffuse infiltration of the interstitium by lymphocytes and other immune cells, with resultant distortion of the alveoli.
lymphocytes expand alveolar septa
forming germinal centers, secondarily
compressing alveoli
Imaging findings of LIP include diffuse or lower-lobe predominant ground glass. Scattered thin-walled perivascular cysts are often present, which are thought to be due to air trapping from peribronchiolar cellular debris. LIP may be complicated by pneumothorax in advanced disease.
Interstitial pneumonia associated with Sjogren syndrome and HIV?
Lymphoid Interstitial Pneumonia
histologic hallmark of LIP is diffuse infiltration of the interstitium by lymphocytes and other immune cells, with resultant distortion of the alveoli.
lymphocytes expand alveolar septa
forming germinal centers, secondarily
compressing alveoli
Imaging findings of LIP include diffuse or lower-lobe predominant ground glass. Scattered thin-walled perivascular cysts are often present, which are thought to be due to air trapping from peribronchiolar cellular debris. LIP may be complicated by pneumothorax in advanced disease.
What is the pathology of LIP?
histologic hallmark of LIP is diffuse infiltration of the interstitium by lymphocytes and other immune cells, with resultant distortion of the alveoli.
lymphocytes expand alveolar septa
forming germinal centers, secondarily
compressing alveoli
Imaging findings of LIP?
Imaging findings of LIP include diffuse or lower-lobe predominant ground glass. Scattered thin-walled perivascular cysts are often present, which are thought to be due to air trapping from peribronchiolar cellular debris. LIP may be complicated by pneumothorax in advanced disease.
What is Acute Interstitial Pneumonia (AIP)?
Acute Interstitial pneumonia (AIP), synonymous with diffuse alveolar damage (DAD), is the pathologic diagnosis seen in the clinical syndrome of acute respiratory distress syndrome (ARDS). Unlike the other IIPs, AIP is the only syndrome with an acute onset and has the worst prognosis.
Primary cause of AIP is surfactant destruction.
Two phases of AIP are recognized: Early (exudative) and chronic (organizing).
The early (exudative) phase features hyaline membranes, diffuse alveolar infiltration by immune cells, and noncardiogenic pulmonary edema.
The chronic (organizing) phase features alveolar wall thickening due to granulation tissue. The chronic phase usually begins one week after the initial injury.
What is the primary cause of AIP?
Primary cause of AIP is surfactant destruction.
What are the two phases of AIP and what causes them?
The early (exudative) phase features hyaline membranes, diffuse alveolar infiltration by immune cells, and noncardiogenic pulmonary edema.
The chronic (organizing) phase features alveolar wall thickening due to granulation tissue. The chronic phase usually begins one week after the initial injury.
What is Hypersensitivity Pneumonitis?
Hypersensitivity pneumonitis (HSP) is a common lung disease caused by a
hypersensitivity reaction to inhaled organic antigens, such as bird proteins or
thermophilic actinomycetes, although a history of antigen exposure is not always elicited.
Acute HSP is characterized by inflammatory exudate filling the alveoli, which manifests on imaging as nonspecific groundglass or consolidation. Small, ill-defined centrilobular nodules may also be present.
The imaging hallmark of subacute HSP is centrilobular ground glass nodules. Mosaic attenuation (geographic areas of relative lucency) and ground glass can also be seen.
Mosaic attenuation can be secondary to mosaic perfusion on inspiration and air trapping on expiration.
The abnormalities of subacute HSP involve the entire axial cross-section of lung.
The head-cheese sign describes the combination of patchy ground glass and areas of lucency due to mosaic perfusion or air trapping.
Chronic HSP, from long-term exposure to the offending antigen, leads to upper-lobe
predominant pulmonary fibrosis. Often the findings of subacute disease, including
centrilobular nodules, ground glass, and mosaic attenuation, may be superimposed.
Unlike IPF, honeycombing is not common in HSP, but when present may involve the upper lobes. If there is relative sparing of the bases, chronic HSP is much more likely than IPF.
What is acute HSP and what does it look like?
Acute HSP is characterized by inflammatory exudate filling the alveoli, which manifests on imaging as nonspecific groundglass or consolidation. Small, ill defined centrilobular nodules may also be present.
What is subacute HSP and what does it look like?
The imaging hallmark of subacute HSP is centrilobular ground glass nodules. Mosaic attenuation (geographic areas of relative lucency) and ground glass can also be seen.
Mosaic attenuation can be secondary to mosaic perfusion on inspiration and air trapping on expiration.
The abnormalities of subacute HSP involve the entire axial cross-section of lung.
The head-cheese sign describes the combination of patchy ground glass and areas of lucency due to mosaic perfusion or air trapping.
What is chronic HSP and what does it look like?
Chronic HSP, from long-term exposure to the offending antigen, leads to upper-lobe
predominant pulmonary fibrosis. Often the findings of subacute disease, including
centrilobular nodules, ground glass, and mosaic attenuation, may be superimposed.
Unlike IPF, honeycombing is not common in HSP, but when present may involve the upper lobes. If there is relative sparing of the bases, chronic HSP is much more likely than IPF.
What is a Pneumoconiosis?
Lung disease secondary to inorganic dust inhalation.
In contrast, hypersensitivity pneumonitis is caused by organic dust inhalation.
Silicosis, Coal Workers Pneumoconiosis, and Asbestosis.
What are the findings of Silicosis and Coal Workers Pneumoconiosis?
Silicosis is due to inhalation of silica dust, which miners may be exposed to.
CWP is caused by inhalation of coal dust, which does not contain any silica.
The most characteristic finding of uncomplicated disease is multiple upper lobe predominant centrilobular and subpleural nodules.
Eggshell lymph node calcifications are commonly seen in silicosis, less commonly in CWP.
Silicosis or CWP can become complicated with large conglomerate masses or progressive massive fibrosis.
Both silicosis and CWP confer an increased risk of TB.
Caplan syndrome is seen in patients with rheumatoid arthritis and either CWP or silicosis (more common in CWP) and represents necrobiotic rheumatoid nodules superimposed on the smaller centrilobular and subpleural nodules of the pneumoconiosis.
What causes eggshell lymph node calcifications?
Eggshell lymph node calcifications are commonly seen in silicosis, less commonly in CWP.
What is a complication of silicosis or CWP?
Can become complicated with large conglomerate masses or progressive massive fibrosis.
Both silicosis and CWP confer an increased risk of TB.
What is Caplan Syndrome?
Caplan syndrome is seen in patients with rheumatoid arthritis and either CWP or silicosis (more common in CWP) and represents necrobiotic rheumatoid nodules superimposed on the smaller centrilobular and subpleural nodules of the pneumoconiosis.
Findings of Asbestosis?
Unlike the other inhalational lung diseases, asbestosis predominantly affects the lower lobes because the asbestos particles are too large to be removed by the alveolar macrophages and lymphatic system.
The radiographic/CT appearance and distribution of advanced asbestosis may be indistinguishable from IPF; however, an important clue seen in asbestosis is evidence of asbestos exposure, such as pleural thickening and plaques.
What is Simple Pulmonary Eosinophilia?
Loffler Syndrome
Transient and migratory areas of focal consolidation, with an elevated eosinophil
count in the peripheral smear.
An identical appearance can be seen as a response to injury, especially with parasitic
disease and drug reactions. The term simple pulmonary eosinophilia is reserved for idiopathic cases.
What is Loffler syndrome?
Simple Pulmonary Eosinophilia
Transient and migratory areas of focal consolidation, with an elevated eosinophil
count in the peripheral smear.
What are the findings of Chronic Eosinophilic Pneumonia?
Important consideration in the differential
diagnosis of chronic consolidation. Chronic eosinophilic pneumonia causes extensive alveolar filling and interstitial infiltration with inflammatory eosinophils.
Consolidation is patchy and peripheral, with an upper lobe predominance. Unlike simple pulmonary eosinophilia, the pattern of consolidation can remain unchanged for months.
Responds rapidly to steroids.
What is Churg-Strauss?
Also called allergic angiitis and granulomatosis, Churg–Strauss is a systemic smallvessel vasculitis associated with asthma and peripheral eosinophilia.
P-ANCA is positive, which is not very specific. P-ANCA can also be positive in collagen vascular disease and microscopic polyangiitis.
Imaging findings of Churg–Strauss are varied. The most common appearance is
peripheral consolidation or ground glass.
What is Microscopic Polyangiitis?
Most common cause of pulmonary hemorrhage with renal failure. P-ANCA is positive.
Imaging shows diffuse central predominant ground glass representing hemorrhage.
What is Wegener Granulomatosis?
systemic small-vessel vasculitis with a classic clinical triad of sinusitis, lung involvement, and renal insufficiency.
C-ANCA is positive, which is very specific for Wegener granulomatosis.
In the upper airways, WG may cause nasopharyngeal and eustachian tube obstruction. Involvement of the larynx and bronchi is common, leading to airway stenosis.
In the lungs, WG may cause multiple cavitary nodules that don’t respond to antibiotic therapy. An intra-cavitary fluid level suggests superimposed infection
Findings and time frame of radiation-induced lung disease?
Radiation pneumonitis is the early stage of radiation injury, which can occur within 1 month of radiotherapy and is most severe 3–4 months after treatment. Radiation pneumonitis features ground glass centered on the radiation port, although extension out of the port is relatively common.
Radiation fibrosis is the late stage of radiation injury. Fibrosis becomes apparent approximately 6–12 months after therapy. The key imaging finding is the distribution of fibrosis and traction bronchiectasis within the radiation port, although fibrosis may extend outside the port in 20%
What does end stage sarcoidosis look like?
Pulmonary sarcoidosis may progress to pulmonary fibrosis with honeycombing. Unlike IPF (the most common cause of pulmonary fibrosis), the fibrotic changes of sarcoid have a mid and upper-lung predominance, similar to end-stage hypersensitivity pneumonitis.
What are the stages of sarcoidosis?
Stage 0: Normal radiograph.
Stage 1: Hilar or mediastinal adenopathy only, without lung changes - nodes may contain stippled or eggshell calcification in up to 50%.
Stage 2: Adenopathy with lung changes.
Stage 3: Diffuse lung disease without adenopathy.
Stage 4: End-stage fibrosis.
MC CT finding of sarcoidosis?
Upper-lobe predominante perilymphatic nodules of variable sizes.
In addition to adenopathy.
Bronchial involvement may cause mosaid perfusion due to air trapping.
What is the Galaxy Sign?
Perilymphatic nodules may coalesce into a mass up to several centimeters in diameter.
Galaxy sign is seen when small nodules are peripheral to a confluent mass.
What is Pulmonary Langerhans Cell Histiocytosis (PLCH)?
Smoking-related lung disease – nearly 100% of adults with PLCH are smokers.
The other smoking-related interstitial lung diseases (aside from emphysema) are RB-ILD and DIP.
Multiple smoking-related lung diseases may be present simultaneously.
PLCH may present as a spontaneous pneumothorax.
Disease is most often isolated to the lungs; however, lucent bone lesions, diabetes insipidus from inflammation of the pituitary stalk (hypophysitis), and skin involvement can occasionally be seen.
The first detectable abnormality is nodules associated with airways. As the disease progresses, the nodules cavitate and resultant irregular cysts predominate.
nodules –> cavitary nodules –> irregular cysts.
Radiographic and CT findings include upper lobe predominant cysts and irregular peribronchovascular nodules, both sparing the costophrenic sulci.
Steroid responsive. Stop smoking.
What are the smoking-related lung diseases?
Besides emphysema
Pulmonary Langerhans Cell Histiocytosis (PLCH)
RB-ILD
DIP
DDx of diseases affecting the lungs and bones?
Pulmonary Langerhans Cell Histiocytosis (PLCH)
Malignancy, tuberculosis, fungal disease (including blastomycosis, histoplasmosis, and coccidiomycosis), sarcoidosis, and Gaucher disease (pulmonary involvement is rare and may resemble DIP).
In what diseases can crazy paving pattern be seen?
Originally described for pulmonary alveolar proteinosis (PAP).
Pneumocystis pneumonia, cryptogenic organizing pneumonia, bronchoalveolar carcinoma, and lipoid pneumonia, among others.
Patients with pulmonary alveolar proteinosis are ssuceptible to what?
Superimposed infection - classically Nocardia - which typically presents with consolidation.
What is Lymphangioleiomyomatosis (LAM)?
A diffuse cystic lung disease caused by bronchiolar obstruction and lung destruction due to proliferation of immature smooth muscle cells in small vessels, lymphatics, and bronchioles.
Approximately 1% of patients with tuberous sclerosis (triad of seizures, mental retardation, and adenoma sebaceum) have a lung disease that is nearly identical to LAM.
Almost all cases of sporadic LAM are in women of childbearing age.
Some cases respond to anti-estrogen therapy.
LAM is associated with pneumothorax and chylous pleural effusion.
CT of LAM shows numerous thin-walled lung cysts. In contrast to LCH, the cysts tend to be round and regular. Also, LAM affects all five lobes while LCH is upper lobe predominant.
Contents of the anterior mediastinum?
Thymus
Lymph nodes
Enlarged thyroid gland - if it extends inferiorly into the mediastinum.
Contents of the middle mediastinum?
Heart and pericardium. Some authors place the heart in the anterior mediastinum. However, for the purpose of differential diagnosis, diseases of the heart and pericardium have more in common with the other vascular structures of the middle mediastinum.
Ascending aorta and aortic arch.
Great vessels including SVC, IVC, pulmonary arteries and veins, and brachiocephalic vessels.
Trachea and bronchi.
Lymph nodes.
Phrenic, vagus, and recurrent laryngeal nerves (all of which pass through the AP window).
Contents of the posterior mediastinum?
Esophagus Descending thoracic aorta Azygos and hemiazygos vein Thoracic duct Vagus nerves Lymph nodes
What is the anterior junctional line?
Formed by four layers of pleura (parietal and visceral
pleura of each lung) at the anterior junction of the right and left lungs.
On a frontal radiograph, the anterior junction line is a vertical line projecting over the superior two thirds
of the sternum.
Abnormal convexity or displacement of this line suggests an anterior mediastinal mass
What is the posterior junctional line?
Formed by four layers of pleura (parietal and visceral
pleura of each lung), but at the posterior junction of the right and left lungs.
On a frontal radiograph, the posterior junction line is a vertical line projecting through the trachea
on the frontal view, more superior than the anterior junction line. Unlike the anterior junction line,
the posterior junction line is seen above the clavicles because the posterior lungs extend more
superiorly than the anterior lungs.
Abnormal convexity or displacement of this line suggests a posterior mediastinal mass or aortic aneurysm.
What are the right and left paratracheal stripes?
Formed by two layers of pleura where the medial
aspect of each lung abuts the lateral wall of the trachea and intervening mediastinal fat.
The right paratracheal stripe is the most commonly seen of these landmarks, seen in up to 97% of
normal PA chest radiographs.
Thickening of the right paratracheal stripe is most commonly due to pleural thickening, although a
paratracheal or tracheal mass (including adenopathy or thyroid or tracheal neoplasm) can also be a cause.
Thickening of the left paratracheal stripe has a similar differential. In addition, however, a mediastinal hematoma should also be considered, especially in trauma.
Which CXR line is commonly seen without pathology?
Right paratracheal stripe.
What is the posterior tracheal stripe?
The only interface seen on the lateral radiograph,
representing the interface of the posterior wall of the trachea with the two pleural
layers of the medial right lung.
What are the right and left paraspinal lines?
Are actually interfaces but appear as lines due to
Mach effect and are formed by 2 layers of pleura abutting the posterior mediastinum.
In contrast to the posterior junction line, the paraspinal lines are located inferiorly in the thorax,
typically from the 8th through 12th ribs.
A paraspinal line abnormality suggests a posterior mediastinal mass lesion, including hematoma, neurogenic tumor, aortic aneurysm, extramedullary hematopoiesis, esophageal mass, and osteophyte.
What is the Azygoesophageal Recess?
An interface formed by the contact of the
posteromedial right lower lobe and the retrocardiac mediastinum.
The azygoesophageal recess extends from the subcarinal region to the diaphragm inferiorly.
Distortion of the azygoesophageal recess may be due to esophageal mass, hiatal hernia, left atrial enlargement, and adenopathy.
What is the Aortopulmonary (AP) window?
A mediastinal space nestled underneath the aortic arch (which forms the superior, anterior, and posterior boundaries) and the top of the pulmonary artery. The medial border of the AP window is formed by the
esophagus, trachea, and left mainstem bronchus.
On a normal frontal radiograph, the AP window is a shallow concave contour below the aortic knob and above the pulmonary artery.
Abnormal convexity (outwards bulging) of the AP window suggests a mass arising from or involving structures that normally live within the AP window, including: Lymph nodes: Adenopathy is the most common cause of an AP window abnormality.
Left phrenic nerve: Injury may cause paralysis of the left hemidiaphragm.
Recurrent laryngeal nerve: The AP window should be carefully evaluated in new-onset hoarseness, especially if associated with diaphragmatic paralysis.
Left vagus nerve.
Ligamentum arteriosum.
Left bronchial arteries.
DDx of convexity of the AP window?
Abnormal convexity (outwards bulging) of the AP window suggests a mass arising from or involving structures that normally live within the AP window, including:
Lymph nodes: Adenopathy is the most common cause of an AP window abnormality.
Left phrenic nerve: Injury may cause paralysis of the left hemidiaphragm.
Recurrent laryngeal nerve: The AP window should be carefully evaluated in new-onset hoarseness, especially if associated with diaphragmatic paralysis.
Left vagus nerve.
Ligamentum arteriosum.
Left bronchial arteries.
DDx of retrosternal space obliteration?
Anterior mediastinal mass, RV dilation, or PA enlargement.
Increase in the retrosternal space can be seen in emphysema.
What is the Left superior intercostal vein?
The left superior intercostal vein (LSIV) is a normal vein that is not often seen on radiography. When visible, the LSIV produces the aortic nipple, appearing as a small round shadow to the left of the aortic knob on the frontal radiograph.
The LSIV may be dilated as a collateral pathway in SVC obstruction
Radiographic signs of an anterior mediastinal mass?
Deformation of the anterior junction line suggests an anterior mediastinal mass. However, since the anterior junction line is not always seen, it is more common to infer the anterior location of a mass by preservation of the posterior lines in the presence of a mass.
The hilum overlay sign is present on the frontal view if hilar vessels are visualized through the mass. It indicates that the mass cannot be in the middle mediastinum. The mass may be in the anterior (most likely) or posterior mediastinum.
Obliteration of the retrosternal clear space on the lateral radiograph is a direct sign of anterior mediastinal location
Radiographic signs of middle mediastinal mass?
Distortion of the paratracheal stripes or convexity of the AP window suggests a middle mediastinal mass
Radiographic signs of a posterior mediastinal mass?
Distortion of the azygoesophageal recess, distortion of the posterior junction line, or displacement of the paraspinal lines suggest paravertebral/posterior mediastinal disease.
DDx of anterior mediastinal mass?
Four T’s: Thymoma, teratoma, thyroid lesion, and terrible lymphoma.
Thymic epithelial neoplasm, such as thymoma if the patient is middle aged or older, or has a history of myasthenia gravis. Less common would be thymic carcinoma.
Germ cell tumor, including teratoma, if the patient is a young adult.
Thyroid lesion, if there is extension of the mass above the thoracic inlet.
Lymphoma.
What is the MC primary tumor of the anterior mediastinum?
Thymoma
What is a Thymoma?
Thymoma is the most common primary tumor of the anterior mediastinum and typically occurs in middle-aged or older individuals, between 45 and 60 years.
Associated with myasthenia gravis (MG).
In addition to MG, thymomas are often associated with other diseases including red cell aplasia, hypogammaglobulinemia, paraneoplastic syndromes, and malignancies such as lymphoma or thyroid cancer.
Thymoma can be pathologically classified as low-risk or high-risk based on histology, and non-invasive or invasive based on whether the capsule is intact.
Approximately 30% of thymomas are invasive. If invasive, the tumor may invade adjacent structures including the airways, chest wall, great vessels, and phrenic nerves.
Elevation of a hemidiaphragm is suggestive of phrenic nerve invasion.
Invasive thymoma may spread along pleural and pericardial surfaces, called drop metastases. However, hematogenous metastases are exceedingly rare.
What is Thymic carcinoma?
Unlike invasive thymoma, thymic carcinoma is histologically malignant, very aggressive, and often metastasizes hematogenously to lungs, liver, brain, and bone. Prognosis is poor.
Distinction between invasive thymoma and thymic carcinoma is difficult on CT, unless there is evidence of distant metastatic disease.
What is Thymic carcinoid?
Thymic carcinoid is of neural crest origin. 50% of thymic carcinoids are hormonally active, often secreting ACTH and causing Cushing syndrome.
Thymic carcinoid is associated with multiple endocrine neoplasia (MEN) I and II.
On imaging, thymic carcinoid is generally indistinguishable from thymoma and thymic carcinoma on CT.
If carcinoid is suspected, a preoperative Indium-111 Octreotide scan can be performed.
What is a Thymic Cyst?
A thymic cyst may be secondary to radiation therapy (e.g., administered to treat Hodgkin disease), may be associated with AIDS (especially when multilocular), or may be congenital. When congenital, thymic cysts arise from remnants of the thymopharyngeal duct. A congenital thymic cyst may occur anywhere along the course of thymic descent from the neck, but most commonly in the anterior mediastinum.
Thymic cyst is typically evident on CT as a simple fluid-attenuation cyst in the anterior mediastinum.
What is a Thymolipoma?
Thymolipoma is a benign fat-containing lesion with interspersed soft tissue. It may become quite
large and drape over the mediastinum.
What types of germ cell tumors can arise from the anterior mediastinum?
Teratoma is the most common anterior mediastinal germ cell tumor, usually encapsulated and predominantly cystic in nature, but fat and calcification are common. A fat/fluid level is specific for teratoma, but is not commonly seen. Teratoma can rarely be malignant, especially if large in size and irregular in shape.
Seminoma is the most common malignant anterior mediastinal germ cell tumor. It occurs almost exclusively in men.
DDx of Low attenuation lymph nodes?
Nonspecific
Active TB
Fungal infection
Lymphoma
Metastatic disease
DDx of avid lymph node enhancement?
Castleman Disease
Sarcoidosis
TB
Vascular metastases - RCC, thyroid, lung, sarcoma, and melanoma.
What is Castleman Disease?
Castleman disease, also known as angiofollicular lymph node hyperplasia, is a cause of highly vascular thoracic lymph node enlargement, of uncertain etiology.
Localized Castleman disease is seen in children or young adults. Surgical resection is usually curative.
Multicentric Castleman disease manifests in older patients or in association with AIDS. Multicentric disease often results in systemic illness including fever, anemia, and lymphoma. It is typically treated with chemotherapy.
The key imaging finding of Castleman disease is avidly enhancing adenopathy.
Where do Morgagni hernias commonly occur?
Anterior right
DDx of middle mediastinal mass?
LAD
Ascending aortic or aortic arch aneurysm
Enlarged PA - Hilum convergence sign - peripheral PAs converging into the “mass”.
Foregut duplication cyst - bronchogenic cysts, esophageal duplication cysts, and neurenteric cysts.
DDx of posterior mediastinal mass?
Neurogenic tumor Hiatal hernia Descending thoracic aneurysm Extramedullary hematopoiesis Lateral meningocele Esophageal neoplasm Foregut duplication cyst Paraspinal abscess
What are neurogenic tumors that can make a posterior mediastinal mass?
May arise from either a peripheral nerve or the sympathetic ganglia. Most adult tumors are peripheral nerve sheath tumors and the vast majority of tumors in children are of sympathetic ganglionic origin. Overall, neurogenic tumors are the most common posterior mediastinal masses.
Peripheral nerve tumors (more common in adults) include:
Schwannoma (most common), neurofibroma, and malignant peripheral nerve sheath tumor.
Sympathetic ganglion tumors (more common in children/young adults) include:
Ganglioneuroma (most common), a benign tumor of sympathetic ganglion cells.
Neuroblastoma, a malignant tumor of ganglion cells seen in early childhood.
Ganglioneuroblastoma, intermediate in histology between ganglioneuroma and neuroblastoma, seen in older children than neuroblastoma.
What are the peripheral nerve tumors that can cause a posterior mediastinal mass?
Schwannoma (most common), neurofibroma, and malignant peripheral nerve sheath tumor.
What are the sympathetic ganglion tumors that can cause a posterior mediastinal mass?
Ganglioneuroma (most common), a benign tumor of sympathetic ganglion cells.
Neuroblastoma, a malignant tumor of ganglion cells seen in early childhood.
Ganglioneuroblastoma, intermediate in histology between ganglioneuroma and neuroblastoma,
seen in older children than neuroblastoma
What is a lateral meningocele?
Can look like a posterior mediastinal mass
A lateral meningocele is lateral herniation of the spinal meninges through either an intervertebral foramen or a defect in the vertebral body. Lateral meningocele is associated with neurofibromatosis.
Multifocal or diffuse non-neoplastic tracheal thickening with sparing of the posterior trachea and cartilage abnormalities of the ear or nose?
Relapsing polychondritis
Multifocal or diffuse non-neoplastic tracheal thickening with sparing of the posterior trachea and nodularly calcified tracheal wall?
Tracheobronchoplasthia osteochondroplastica
Multifocal or diffuse non-neoplastic tracheal thickening with circumferential thickening and smooth concentric thickening? Other signs of endobronchial or parenchymal TB?
Tuberculosis
Multifocal or diffuse non-neoplastic tracheal thickening with circumferential thickening with irregular thickening +/- calcification?
Amyloidosis
Multifocal or diffuse non-neoplastic tracheal thickening with circumferential thickening with subglottic tracheal thickening?
Wegener granulomatosis
Multifocal or diffuse non-neoplastic tracheal thickening with circumferential thickening with hilar or mediastinal adenopathy? Perilymphatic nodules?
Sarcoidosis
What is Relapsing Polychondritis?
Multysystmic disease of unknown etiology characterized by recurrent inflammation of cartilaginous structures.
Nose, ear, joints, larynx, trachea, and bronchi can be affected, with airway involvement seen in 50% of patients - larynx and subglottic trachea are the MC sites of airway involvement.
Usually occurs in middle aged women.
Shows smooth tracheal/bronchial wall thickening, with sparing of the posterior membranous trachea - tracheal cartilage is incomplete - no cartilage in the posterior membranous portion.
Often attenuation of the airway wall, ranging from subtly increased attenuation to frank calcification.
MC sites of airway involvement in Relapsing Polychondritis?
Nose, ear, joints, larynx, trachea, and bronchi can be affected, with airway involvement seen in 50% of patients - larynx and subglottic trachea are the MC sites of airway involvement.
What causes smooth tracheal/bronchial wall thickening, with sparing of the posterior membranous trachea?
Relapsing Polychondritis
What is Tracheobronchopathia osteochondroplastica (TPO)?
Benign condition of multiple submucosal calcified osteocartilaginous nodules along the tracheal walls.
Spares the posterior membranous trachea, similar to relapsing polychondritis.
DDx of nodular irregular thickening of the trachea?
Amyloidosis
Sarcoidosis
Multifocal adenoid cystic carcinoma
Tracheal metastases
What is bronchiectasis?
Progressive, irreversible dilation of cartilage-containing bronchi.
Three etiologies final common pathway of mucus plugging, superimposed bacterial colonization, and inflammatory response:
Bronchial wall injury, typically from infection or inflammation
Bronchial lumen obstruction
Traction from adjacent fibrosis.
What are specific causes of bronchiectasis?
Ineffective clearing of secretion - CF and Kartagener (primary ciliary dyskinesia)
Recurrent pneumonia
Bronchocentric infections- TB and atypical mycobacteria
Exaggerated immune response - ABPA and vasculitis
Impaired immunity- Congenital immunodeficiency, transplant recipients, and aggamaglobulinemia.
Congenital connective tissue disorders- Mounier-Kuhn (causing tracheobronchomegaly leading to recurrent pneumonia) or Williams-Campbell (disorder of distal bronchial cartilage, which may be congenital or acquired as a sequela of viral infection).
What is Mounier-Kuhn Syndrome?
Congenital connective tissue disorder causing tracheobronchomegaly leading to recurrent pneumonia
What is Williams-Campbell Syndrome?
Congenital connective tissue disorder - disorder of the distal bronchial cartilage, which may be congenital or acquired as a sequela of viral infection.
Mnemonic for common causes of bronchiectasis?
CAPTAIn Kangaroo has Mounier-Kuhn
Cystic Fibrosis - one of the MC ABPA Post infectious TB/Atypical mycobacteria Agammaglobulinemia Immunodeficiency Kartagener Mounier-Kuhn
Morphologic classifications of bronchiectasis?
Cylindrical (least severe): mild bronchial dilation
Varicose (moderately severe): bronchi may become beaded and irregular
Cystic (most severe): bronchi are markedly enlarged and ballooned, with formation of multiple cysts that may not connect to the airways.
What is the signet ring sign?
Dilated bronchus adjacent to a normal pulmonary artery branch.
Normally each bronchus should be approximately the same size as the adjacent PA branch.
Other CT findings: lack of bronchial tapering, bronchial wall thickening, and mucus-filled bronchi. Often, adjacent tree-in-bud nodules are present, likely representing associated small-airways infection.
Mechanism of emphysema in smokers?
Elastase is a powerful destructive enzyme which functions in host defense mechanism, but excess elastase is harmful to native tissues - produced by alveolar macrophages and neutrophils - both of which are increased in smokers.
Alpha-1-antitrypsin normally neutralizes elastase - either surplus of elastase (in smoking-related emphysema) or a deficiency of neutralizing emzyme (in alpha-1-antitrypsin) can cause lung destruction and resulting emphysema.
Alpha-1-antitrypsin deficiency is an important cause of panacinar emphysema.
DDx of primary central airway tumors?
SCC and adenoid cystic carcinoma are MC
Carcinoid Mucoepidermoid carcinoma Tracheal lymphoma Endobronchial metastasis Direct invasion of the central airways by adjacent malignancy Benign endobronchial lesions
What is Adenoid Cystic Carcinoma of the trachea?
Low grade malignancy that usually affects patients in their 40s - decade or two younger than typical SCC patient.
Propensity for perineural and submucosal spread. Despite indolent growth, metastatic disease tends to have intense FDG uptake on PET.
CT appearance: submucosal mass that infiltrates the trachea wall and surrounding mediastinal fat. May also present as circumferential tracheal or bronchial thickening causing airway stenosis.
What is bronchial carcinoid?
Spectrum of neuroendocrine neoplasms including low-grade carcinoid, aggressive carcinoid, and small cell carcinoid, featuring a range of biologic behaviors.
Carcinoid tumors rarely secrete hormones such as ACTH.
Endobronchial carcinoid is rare in adults- it is MC bronchial tumor in children.
Almost always occurs distal to the carina.
CT shows endoluminal mass with homogeneous arterial enhancement.
MC endobronchial tumor in children?
Carcinoid
DDx of enhancing endobronchial mass
Carcinoid
Mucoepidermoid carcinoma
Hemangioma
Glomus tumor
What is Mucoepidermoid carcinoma of the trachea?
Rare tumor that originates from tiny salivary glands lining the tracheobronchial tree.
Younger patients than adenoid cystic carcinoma
CT: round or oval endobronchial mass- indistinguishable from carcinoid.
Cancers that metastasize to central airways?
BReTh Lung
Breast
Renal cell
Thyroid
Lung
Melanoma
Sarcoma
What are the benign endobronchial lesions?
Papilloma - benign but potentially pre-malignant that may transform into carcinoma, usually followed.
Single- usually caused by chronic irritation
Multiple (laryngotracheal papillomatosis)- HPV.
Chondroma- benign cartilaginous tumor that rarely may occur in the airways.
Schwannoma, adenoma, hamartoma, hemangioma, lipoma, and leiomyoma
What is a Fibrous Tumor of the Pleura?
Focal pleural mass not related to asbestosis or mesothelioma.
20-30% are malignant - so all excised.
May be associated with hypoglycemia or hypertrophic pulmonary osteoarthropathy.
May be pedunculated - pleural-based mass that changes position is suggestive of FTP- low FDG uptake on PET.
Thoracentesis fluid that determines exudate
Light’s Criteria (if any one present):
Ratio of pleural fluid protein to serum protein >0.5
Ratio of pleural fluid LDH to serum LDH >0.6
Pleural fluid LDH >2/3 upper limits of normal of normal for serum
Causes of exudative pleural effusion?
Implies pleural disease causing increased permeability of pleural capillaries which may be due to:
Pneumonia with parapneumonic effusion, empyema, or TB pleuritis.
Mesothelioma or pleural metastasis
RA or other collagen vascular diseases.
