Thoracic Imaging Flashcards
Lobar and Segmental Anatomy of the Lung
Right upper lobe - apical, posterior, anterior Right middle lobe - lateral and medial Right lower lobe - Superior, lateral basal, anterior basal, posterior basal, and medial basal Left upper lobe - Apical posterior, anterior, superior lingula, inferior lingula Left lower lobe - Superior, medial basal, posterior basal, anterior basal, and lateral basal
Lung Azygous fissue
Accessory fissure present in less than 1% of patients, seen in the presence of an azygous lobe. An azygous lobe is an anatomic varian where the right upper lobe apical or posterior segments are encased in their own parietal and visceral pleura.
Atelectasis
Loss of lung volume due to decreased aeration. Synonymous with collapse. Direct signs of atelectasis are from lobar volume loss and include: displacement of the fissures and vascular crowding. Indirect signs include elevation of the diaphragm, rib crowding on the side with volume loss, mediastinal shift to the side with volume loss, overinflation of adjacent or contralateral lobes, hilar displacement. Air bronchograms are not seen in atelectasis when the cause of the atelectasis is central bronchial obstruction, but air bronchograms can be seen in subsegmental atelectasis. Subsegmental atelectasis is caused by obstruction of small peripheral bronchi, usually by secretions.
Obstructive Atelectasis
Occurs when alveolar gas is absorbed by blood circulating through alveolar capillaries but is not replaced by inspired air due to bronchial obstruction. Can cause lobar atelectasis, which is complete collapse of a lobe. Occurs more quickly when the patient is breathing supplemental oxygen since oxygen is absorbed from the alveoli more rapidly than nitrogen. In general, is associated with volume loss. In critically ill ICU patients, however, there may be rapid transudation of fluid into the obstructed alveoli, causing superimposed consolidation. In children, airway obstruction is most often due to an aspirated foreign object. In contrast to adults, the affected side becomes hyperexpanded in children due to a ball-valve effect. Subsegmental atelectasis is a subtype of obstructive atelectasis commonly seen after surgery or general illness, due to mucus obstruction of the small airways. Causes: obstructing neoplasms, mucous plugging in asthmatics or critically ill patients, and foreign body aspiration.
Relaxation (passive) Atelectasis
Caused by relaxation of lung adjacent to an intrathoracic lesion causing mass effect, such as a pleural effusion, pneumothorax, or pulmonary mass. Also known as compressive atelectasis. Causes: most classicaly seen adjacent to a pleural effusion. Could also be seen from adjacent compression of lung from a mass, hiatal hernia, or a large bleb - anything directly pushing on the lung.
Adhesive atelectasis
Due to surfactant defiency. Is seen most commonly in neonatal respiratory distress synrome, but can also be seen in acute respiratory distress syndrome (ARDS). Causes: RDS (premature infants), ARDS (more diffuse pattern), and in the setting of pulmonary embolism (loss of blood flow/lack of CO2 disrupts integrity of surfactant).
Cicatricial Atelectasis
Fibrotic atelectasis or cicatricial atelectasis is volume loss from architectural distortion of lung parenchyma by fibrosis. Causes: most classic is TB, but scarring from radiation, other infections, or really any other cause of fibrosis.
Lobar Atelectasis
Usually caused by central broncial obstruction (obstructive atelectasis), which may be secondary to mucus plugging or an obstructing neoplasm. If the lobar atelectasis occurs acutely, mucus plugging is the most likely cause. If lobar atelectasis isseen in outpatient, an obstructing central tumor must be ruled out. Lobar atelectasis, or collapse of an entire lobe, has characteristic appearances depending on which of the five lobes is collapsed.
Left upper Lobe atelectasis
Luftsichel sign: a cresent of air lateral to the aortic arch. Seen with left upper lobe collapse.
Right Upper Lobe atelectasis
The reverse S sign of Golden is seen in right upper lobe collapse.
The juxtaphrenic peak sign is a peridiaphragmatic triangular opacity caused by diaphragmatic traction from an inferior accessory fissure or an inferior pulmonary ligament.
Left lower lobe atelectasis
The heart slightly rotates and the left hilum is pulled down. The flat waist sign describes the flattenin of the left heart border as a result of downward shift of hilar structures and resultant cardiac rotation.
Right lower lobe atelectasis
Mirror image of left lower lobe atelectasis. Collapsed lower lobe appears as a wedge-shaped retrocardiac opacity.
Right middle lobe atelectasis
The findings of right middle lobe atelctasis can be subtle on the frontal radiograph. Silhoutting of the right heart border by the collapsed medial segment of the middle lobe may be the only clue. The lateral radiograph shows a wedge-shaped opacity anteriorly.
Round Atelectasis
Focal atelectasis with a round morphology that is always associated with an adjacent pleural abnormality (e.g. pleural effusion, pleural thickening or plaque, pleural neoplasm, etc). Round atelectasis is most common in the posterior lower lobes. All five of the following findings must be resent to diagnose round atelectasis: 1. Adjacent pleura must be abnormal. 2. Opacity must be peripheral and in contact with the pleura. 3. Opacity must be round or elliptical. 4. Volume loss must be present in the affected lobe. 5. Pulmonary vessels and bronchi leading into the opacity must be curved, this is the comet tail sign.
Secondary Pulmonary lobule
The secondary pulmonary lobule is the elemental unit of lung function. Each SPL contains a central artery (the aptly named centrilobular artery) and a central bronchus, each branching many times to ultimately produce 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. There are generally 12 or fewer acini per secondary lobule. Pulmonary veins and lymphatics collect in the periphery of each SPL. Connective tissue, called interlobular septa, ecases each SPL. Thickening of the interlobular septa can be seen on CT and suggests pathologic enlargement of either the venous or lymphatic spaces. Each SPL is between 1 and 2.5 cm in diameter.
Abnormalities of the secondary pulmonary lobule
Consolidation of the ground glass opacification are two very commonly seen patterns of lung disease caused by abnormal alveoli. The alveolar abnormality may represent either filling of the alveoli with fluid or incomplete alveolar aeration. Consolidation can be described on either a chest radiograph or CT, while ground glass is generally reserved for CT.
Consolidation
Histologically due to complete filling of affected alveoli with a liquid like substance (commonly remembered as blood, pus, water, or cells). Pulmonary vessels are not visible through the consolidation on an unenhanced CT. Air bronchograms are often present if the airway is patent. An air bronchogram represents a lucent air-filled bronchus (or bronchiole) seen within a consolidation. Consolidation causes silhouetting of adjacent structures on conventional radiography.
Acute consolidation is most commonly due to pneumonia but the differential includes: pneumonia (by far the most common cause of acute consolidation), pulmonary hemorrhage (primary pulmonary hemorrhage or aspiration of hemorrhage), ARDS (which is noncardiogenic pulmonary edema seen in critically ill patients and thought to be due to increased capillary permeability), pulmonary edema (may cause consolidation, although this is an uncommon manifestation).
The differential of chronic consolidation includes: Bronchioloalveolar 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 (inflammatory process characterized by eosinophils causing alveolar filling in an upper-lobe distribution).
Ground Glass opacification
Histologically due to either partial filling of the alveoli (by blood, pus, water, or cells), alveolar wall thickening, or reduced aeration of alveoli (atelectasis). CT shows a hazy, gauze-like opacity, through which pulmonary vessels are still visible. As with consolidation, air bronchograms may be present.
Acute ground glass opacification has a similar differential to acute consolidation, since many fo the entities that initially cause partial airspace filling can progress to completley fill the airspaces later in the disease. The differential fo acute ground includes: pulmonary edema (which is usually dependent), pneumonia (more commonly seen in atypical pneumonia such as viral or Pneumocystis jiroveci pneumonia), pulmonary hemorrhage, ARDS.
Chronic ground glass opacification has a similar but broader differential diagnosis compared to chronic consolidation. In addition to all of the entities which may cause chronic consolidation, the differential diagnosis of chronic ground glass also includes: Bronchioalveolar carcinoma (which tends to be focal or multifocal), organizing pneumonia (typically presenting as rounded, peripheral chronic consolidation), chronic eosinophilic pneumonia (usually with an upper-lobe predominance), Idiopathic pneumonias (which are a diverse group of inflammatory responses to pulmonary injury), hypersensitivity pneumonitis (HSP) (Especially the subacute phase, HSP is a type III hypersensitivity reaction to inhaled organic antigens. In the subacute phase there is ground glass, centrilobular nodules, and mosaic attenuation), Alveolar proteinosis (an idiopathic disease characterized by alveolar filling by a proteinaceous substance. The distribution is typically central, with sparing of the periphery)
Ground glass in a central distribution
Pulmonary edema
Alveolarr hemorrhage
Pneumocystis jiroveci pneumonia
Alveolar proteinosis
Peripheral ground glass or consolidation
Organizing pneumonia
Chronic eosinophilic pneumonia (typically with an upper lobe predominance)
Atypical or viral pneumonia
Pulmonary edema (peripheral pulmonary edema tends to be noncardiogenic in etiology, such as edema triggered by a drug reaction. Peripheral consolidation/ground glass is unusual for cardiogenic pulmonary edema)
Interlobular Septal thickening (smooth)
Conditions that dilate the pulmonary veins cause smooth interlobular septal thickening. By far the most common cause of smooth interlobular septal thickening is pulmonary edema; however, the differential diagnosis for smooth interlobular septal thickening is identical to the differential for central ground glass: Pulmonary edema, pulmonary alveolar proteinosis, pulmonary hemorrhage, atypical pneumonia (especially Pneumocystis jiroveci pneumonia)
Interlobular septal thickening (Nodular, irregular, or asymmetric)
Nodular, irregular, or asymmetri septal thickening tends to be caused by processes that infiltrate the peripheral lymphatics, most commonly lymphangitic carcinomatosis and sarcoidosis.
Lymphangitic carcinomatosis is tumor spread through the lymphatics.
Sarcoidosis is an idiopathic, multi-organ disease characterized by noncaseating granulomas, which form nodules and masses primarily in a lymphatic distribution.
Crazy paving
Crazy paving describes interlobular septal thickening with superimposed ground glass opacification, which is though to resemble the appearance of broken pieces of stone. Although nonspecific, this pattern was first described for alveolar proteinosis, where the ground glass opacification is caused by filling of alveoli by proteinaceous material and the interlobular septal thickening is caused by lymphatics taking up the same material.
The differential diagnosis for crazy paving includes: Alveolar proteinosis, Pneumocystis jiroveci pneumonia, organizing pneumonia, bronchoalveolar carcinoma (mucinous subtype), lipoid pneumonia (an inflammatory pneumonia caused by a reaction to aspirated lipids), acute respiratory distress syndrome, pulmonary hemorrhage
Centrilobular Nodules
Represent opacification of the centrilobular bronciole (or less commonly the centrilobular artery) at the center of each secondary pulmonary lobule. On CT, multiple small nodules are seen in the centers of secondary pulmonary lobules. Centrilobular nodules never extend to the pleural surface. The nodules may be solid or of ground glass attenuation, and range in size from tiny up to a centimeter. Centrilobular nodules may be caused by infectious or inflammatory conditions.
Infectious causes of centrilobular nodules include: Endobronchial spread of tuberculosis or atypical mycobacteria (atypical mycobacteria are a diverse spectrum of acid-fast mycobacteria that do not cause tuberculosis. the typical pulmonary manifestation of atypical mycobacteria is a low-grade infection typically seen in elderly women, most commonly caused by Mycobacterium avium intracellulare) Bronchopneumonia (which is a spread of infectious pneumonia via the airways), and atypical pneumonia (especially mycoplasma pneumonia).
The two most common inflammatory causes of centrilobular nodules include hypersensitivity pneumonitis and respiratory bronchiolitis interstitial lung disease (RB-ILD), both exposure-related lung diseases. More prominent centrilobular nodules are suggestive of HSP. Inflammatory causes include: HSP (type III hypersensitivity reaction to an inhaled organic antigen. The subacute phase of HSP is primarily characterized by centrilobular nodules), Hot tub lung (hypersensitivity reaction to inhaled atypical mycobacteria, with similar imaging to HSP), 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. It typically affects patients of Asian descent), Silicosis (inhalation lung disease that develops in response to inhaled silica particles, is characterized by upper lobe predominant centrilobular and perilymphatic nodules)
Perilymphatic Nodules
Perilymphatic nodules follow the anatomic locations of pulmonary lymphatics, which can be seen in three locations in the lung: 1. subpleural 2. Peribronchovascular 3. Septal (within the interlobular septa separating the hexagonal secondary pulmonary lobules).
Sarcoidosis is by far the most common cause of perilymphatic nodules, typically with an upper-lobe distribution. The nodules may become confluent creating the galaxy sign. The differential of perilymphatic nodules includes: Sarcoidosis, pneumoconiosis (silicosis and coal workers pneumoconiosis, are reactions to inorganic dust inhalation, the imaging may look identical to sarcoidosis with perilymphatic nodules, but there is usually a history of exposure (e.g. a sandblaster who develops silicosis)), and Lymphangitic carcinomatosis
Random Nodules
Randomely distributed nodules usually occur via hematogenous spread and have an angiocentric distribution. The differential of random nodules includes: Hematogenous metastases, septic emboli (embolic infection has a propensity to cavitate but early emboli may be irregular or solid), pulmonary langerhans’s cell histiocystosis (PLCH, a smoking-related lung disease that progresses from airway-associated and random nodules to irregular cysts. PLCH is usually distinguishable from other causes of random nodules due to the presence of cysts and non-angiocentric distribution).
Miliary pattern of nodules
A miliary pattern is innumerable tiny random nodules disseminated hematogenously, suggestive of the appearance of millet seeds. The differential of miliary nodules includes: disseminated tuberculosis, disseminated fungal infection, disseminated hematogenous metastases.
Tree-in-bud nodules
Tree-in-bud nodules are multiple small nodules connected to linear branching structures, which resembles a budding tree branch in springtime as seen on CT. The linear branching structures represent the impacted bronchioles, which are normally invisible on CT, and the nodules represent the impacted terminal bronchioles. Tree-in-bud nodules are due to mucs, pus, or fluid impacting bronchioles and terminal bronchioles.
Tree-in-bud nodules are almost always associated with small airways infection, such as endobronchial spread of tuberculosis. The differential of tree-in-bud nodules include: Mycobacteria tuberculosis and aytpical mycobacteria, bacterial pneumonia, aspiration pneumonia, airway-infasive aspergillus (aspergillus is an opportunistic fungus with several patterns of disease. The airway-invasive pattern is seen in immunocompromised patients and may represent either as bronchopneumonia or small airways infection)
Solid Cavitary nodule/mass
A cavitary lesion has a thick, irregular wall, often with a solid mural component. Although the findings of benign and malignant cavitary nodules overlap, a maximum wall thickness of = 4mm is usually benign and a wall thickness of >15 mm is usually malignant. Spiculated margins also suggest malignancy.
A solitary cavitary lesion is most likely cancer or infection.
Primary bronchogenic carcinoma (while both squamous cell and adenocarcinoma can cavitate, squamous cell cavitates more frequently. Small cell carcinoma is never known to cavitate.)
Tuberculosis (classically produces an upper-lobe cavitation).
Multiple Cavitary Nodules
Multiple cavitary lesions are typically vascular or spread through the vascular system: Septic emboli, vasculitis (including Wegener granulomatosis, which is especially prone to cavitate), metastases (of which squamous cell carcinoma and uterine carcinosaroma are known to cavitate).
Cystic lung disease
A cyst is an air-containing lucency with a thin, nearly imperceptible wall. In general, cystic lung disease is usually due to a primary airway abnormality.
Multiple lung cysts
Lymphangiomyomatosis (LAM) - a diffuse cystic lung disease caused by smooth muscle proliferation of the distal airways. LAM causes uniformly distributed, thin-walled cysts in a diffuse distribution. It is classically associated with chylous effusion.
Emphysema - which tends to be upper lobe predominant in a smoker
Pulmonary Langerhans cell histiocytosis - which features irregular cysts and nodules predominantly in the upper lungs.
Diffuse cystic bronchiectasis - Bronchiectasis is dilation of the bronchioles. Although cystic fibrosis is the most common cause of bronchiectasis and has an upper-lobe predominance, congenital or post-infectious causes can have a diffuse or lower-lobe distribution.
Pneumocystis jiroveci pneumonia - which features cysts in late-stage disease.
Lymphoid interstitial pneumonia (LIP) - an exceptionally rare disease usually associated with Sjogren syndrome and characterized by alveolar distortion from lymphocytic infiltrate and multiple cysts.
Single Lung Cyst
The differential for a single lung cyst includes:
Bulla - an air filled cyst measuring >1 cm. A giant bulla occupies at least 30% of the volume of the thorax.
Bleb - air filled cystic structure contiguous with the pleura measuring <1 cm. Rupture of a bleb is the most common cause of spontaneous pneumothorax.
Pneumatocele - air-filled space caused by prior lung trauma or infection.
Lower lobe fibrotic changes
The differential diagnosis of basal-predominant fibrotic change includes:
Idiopathic pulmonary fibrosis (IPF) - clinical syndrome of progressive pulmonary fibrosis of unknown etiology and is most common cause of basilar fibrosis. It almost always features basilar 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 pleaural plaques.
Nonspecific interstitial pneumonia (NSIP), fibrotic form - NSIP is an idiopathic pneumonia. It is a lung response to injury commonly associated with collagen vascular disease and drug reaction. The two histologic subtypes are cellular and fibrotic forms, of which the latter may produce basal-predominant fibrosis. In contrast to IPF, honeycombing is usually absent.
Upper Lobe fibrotic changes
Although IPF is the most common cuase of pulmonary fibrosis, fibrosis primarily affecting the upper lobes should raise concern for an alternative diagnoses, such as: End-stage sarcoidosis (Sarcoidosis is a disease that primarily affects the upper lobes. The late stage of sarcoidosis leads to upper-lobe predominant fibrosis), Chronic hypersensitivity pneumonitis (may cause upper-lobe fibrosis in long-standing disease), end-stage silicosis (the late stage of silicosis may lead to fibrosis with an upper lobe predominance)
Community acquired pneumonia
S. pneumoniae is the most common cause of CAP. Atypical pneumonia, including Mycoplasma, viral, and Chlamydia, typically infects young and otherwise healthy patients (Mycoplasma has a varied appearance and can produce consolidation, areas of ground glass attenuation, centrilobular nodules, and tree-in-bud nodules). Legionella most commonly occurs in elderly smokers. Infections tend to be severe. (Peripheral consolidation often progresses to lobar and multifocal pneumonia) Infection by Klebsiella and other gram-negatives occurs in alcoholics and aspirators. (Klebsiella classically leads to voluminous inflammatory exudates causing the bulging fissure sign)
Hospital acquired pneumonia
HAP occurs in hospitalized patients and is due to aspiration of colonized secretions. HAP is caused by a wide variety of organisms, but the most important pathogens include MRSA and resistant gram-negatives including Pseudomonas.
Health care associated pneumonia
HCAP defined as pneumonia in a nursing home resident or in a patient with a >2 day hospitalization over the past 90 days. Pathogens are similar to HAP.
Ventilator associated pneumonia
Ventilator associated pneumonia is caused by infectious agents not present at the time mechanical ventilation was started. Most infections are polymicrobial and primarily involve gram-negative rods such as Pseudomonas and Actinetobacter.
Pneumonia in the immunocompromised patient
Any of the above pathogens, plus opportunistic infections including Pneumocystis, fungi such as Aspergillus, Nocardia, CMV etc., can be seen in immunocompromised patients.
Lobar Pneumonia
Lobar pneumonia is consolidation of a single lobe. It is usually bacterial in origin and is the most common presentation of community acquried pneumonia. The larger bronchi remain patent, causing air bronchograms.
Lobular pneumonia (bronchopneumonia)
Lobular pneumonia manifests as patchy consolidation with poorly defined airspace opacities, usually involving several lobes, and most commonly due to S. aureus.
Interstitial Pneumonia
Interstitial pneumonia is caused by inflammatory cells located predominately in the interstitial tissue of the alveolar septa causing diffuse or patchy ground glass opacification. It can be caused by viral pneumonia, Mycoplasma, Chlamydia, or Pneumocystis.
Round pneumonia
Round pneumonia is an infectious mass-like opacity seen only in children, most commonly due to Streptococcus pneumoniae. Infection remains somewhat confined due to incomplete formation of pores of Kohn.
Pulmonary abscess
Necrosis of the lung parenchyma typically due to Stayphylococcus aureas, pseudomonas, or anaerobic bacteria. An air-fluid level is almost always present. An abscess is usually sphericl, with equal dimensions on frontal and lateral views.
Pulmonary gangrene
Pulmonary gangrene is a very rare complication of pneumonia where there is extensive necrosis or sloughing of a pulmonary segment of lobe. Pulmonary gangrene is a severe manifestation of pulmonary abscess.
Empyema
Empyema is infection within the pleural space. There are three stages in the development of an empyema: 1. Free-flowing exudative effusion (can be treated with needle aspiration or simple drain) 2. Development of fibrous strands (requires large-bore chest tube and fibrinolytic therapy) 3. Fluid becomes solid and jelly-like (usually requries surgery).
Although pneumonia is often associated with a parapneumonic effusion, most pleural effusions associateed with pneumonia are not empyema, but are instead a sterile effusion caused by increased capillary permeability.
An empyema confomrs to the shape fo the pleural space, causing a longer air-filled level on the lateral radiograph. This is in contrast to an abscess, discussed above, which typically is spherical and has the same dimensions on the frontal and lateral radiographs.
The split pleura sign describes enchancing parietal and visceral pleura of an empyema seen on contrast-enhanced study.
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.
Bronchopleural fistula (BPF)
Bronchopleural fistula is an abnormal communication between the airway and the pleural space. It is caused by rupture of the visceral pleura. By far the most common cause of BPF is surgery; however, other etiologies include lung abscess, empyema, and trauma.
On imaging, new or increasing gas is present in a pleural effusion. A connection between the bronchial tree and the pleura is not always apparent, but is helpful when seen.
The treatment of BPF is controversial and highly individualized.
Empyema necessitans
Extension of an empyema to the chest wall, most commonly secondary to tuberculosis. Other causative organisms include Nocardia and Actinomyces.
Tuberculosis
Tuberculosis cause by Mycobacterium tuberculosis, remains an important disease despite remarkable progress in public health and antituberculous therapy over the past century. Tuberculosis remains a significant problem in developing countries. In the United States, TB is seen primarily in the immigrant population and immunocompromised individuals.
Initial exposure to TB can lead to two clinical outcomes: 1. Contained disease (90%) results in calcified granulomas and/or calcified hilar lymph nodes. In a patient with normal immunity, the tuberculous bacilli are sequestered with a caseating granulomatous response. 2. Primary tuberculosis results when the host cannot contain the organism. Primary tuberculosis is seen more commonly in children and immunocompromised patients.
Reactivation (post-primary) TB is reactivation of a previously latent infection.
Primary tuberculosis
Primary tuberculosis represents infection from the first exposure to TB. Primary TB may inovle the pulmonary parenchyma, the airways, and the pleura. Primary TB often causes adenopathy.
As many as 15% of patients infected with primary TB have no radiographic changes and the imaging appearance of primary tuberculosis is nonspecific.
The four imaging manifestations of primary TB (of which any, non, or all may be present) are ill-defined consolidation, pleural effusion, lymphadenopathy, and miliary disease. Primary TB may occur in any lobe, but the most typical locations are the lower lobes or right middle lobe. It can be difficult to distinguish between primary and post-primary TB, and in clinical practice, the treatment (antituberculous therapy) is the same.
Classic imaging findings are not always seen but include: Ghon focus (initial focus of parenchyal infection, usually located in the upper part of the lower lobe or the upper lobe. Ranke complex (Ghon focus and lymphadenopathy).
Cavitation is rare in primary TB, in contrast to reactivation TB.
Adenopathy is common in primary TB, typically featuring central low-attenuation and peripheral enhancement, especially in children. In contrast, post-primary TB does not feature prominent adenopathy.
Reactivation (post-primary) tuberculosis
Reactivation TB, also called post-primary TB, usually occurs in adolescents and adults and is caused by reactivation of a dormant infection acquried earlier in life. Clinical manifestations of reactivation TB include chronic cough, low-grade fever, hemoptysis, and night sweats.
Reactivation TB most common occurs in the upper lobe apical and posterior segments.
In an immunocompetent patient, the imaging hallmarks of reactivation TB are upper-lobe predominant disease with cavitation and lack of adenopathy. Focal upper lobe consolidation and endobronchial spread are common. Although not specific to TB, tree-in-bud nodules suggest active endobronchial spread.
In an immunosuppressed patient (such as HIV), low-attenuation adenopathy is a typical additional finding, similar to the adenopathy seen in primary TB. Low density lymph nodes may mimic immune reconstitution syndrome in HIV patients.
A tuberculoma is a well-defined rounded opacity usually in the upper lobes.
Healed tuberculosis
Healed TB is evident on radiolgraphy as 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.
Miliary tuberculosis
Miliary tuberculosis is a diffuse random distribution of tiny nodules seen in hematogenously disseminated TB.
Miliary TB can occur in primary or reactivation TB.
Atypical Mycobacteria infection
The classic presentation of atypical mycobacteria is an elderly woman with cough, low-grade fever, and weight-loss, called Lady Windermere syndrome. Mycobacterium avium intracellulare and M. kansasii are the two most ommon organisms.
Classic radiographic findings are bronchiectasis and tree-in-bud nodules, most common in the right middle lobe or lingula.
“Hot-tub” lung
“Hot-tub” lung is a hypersensitivity pneumonitis in response to atypical mycobacteria which are often found in hot tubs. There is no active infection and the typical patient is otherwise healthy. Imaging is similar to other causes of hypersensitivity pneumonitis, featuring centrilobular nodules.
Endemic Fungi
Endemic fungi can cause community acquired pneumonia in normal individuals, wieth each subtype having a specific geographic distribution. Most infected patients are asymptomatic.
Histoplasma capsulatum
Histoplasma capsulatum is localized to the Ohio and Mississippi river valleys, in soil contaminated with bat or bird guano. The most common sequela of infection is a calcified granuloma. A less common radiologic manifestation is a pulmonary nodule (histoplasmoma), which can mimic a neoplasm. Chronic infection can mimic reactivation TB with upper lobe fibrocavitary consolidation. Fibrosisng mediastinitis is a rare complication of Histoplasma infection of mediastinal lymph nodes leading to pulmonary venous obstruction, bronchial stenosis, and pulmonary artery stenosis. Affected lymph nodes tend to calcify.
Coccidiodes immitis and Blastomyces dermatitidis
Coccidioides immitis is found in the southwestern US and has a variety of radiologic appearances, including multifocal consolidation, multiple pulmonary nodules, and miliary nodules. Blastomyces dermatitidis is found in central and southeastern US. Infection is usually asymptomatic, but may present as flu-like illness that can progress to multifocal consolidation, ARDS, or miliary disease.
Lung Infections in the immunocompromised
Immunosuppressed patients are susceptible to the same organisms that infect immunocompetent patients; however, one must be aware of several additional opportunistic organisms that may present in the immunocompromised.
An immunocompromised patient with a focal air space opacity is most likely to have a bacterial pneumonia (most commonly pneumococcus), but TB should also be considered if the CD4 count is low.
In contrast, multifocal opacities have a wider differential diagnosis including Pneumocystis pneumonia and opportunistic fungal infection such as Cryptococcus or Aspergillus.
Pneumocystis jiroveci pneumonia
Pneumocystsis jiroveci (previously called Pneumocystis carinii) is an opportunistic fungus that may cause pneumonia in individuals with CD4 counts <200 cells/cc. The incidence of Pneumocystis pneumonia is decreasing due to routine antibiotic prophylaxis.
Chest radiograph findings can be normal but a classic finding of Pneumocystis pneumonia is bilateral perihilar (central) airspace opacities with peripheral sparing. The classic CT appearance is geometric perihilar ground glass opacification, sometimes with crazy paving (ground glass and thickening of the interlobular septa).
A normal CT rules out Pneumocystis pneumonia; however, the disease can hide in a normal chest radiograph.
Pneumocystis pneumonia has a propensity to cause upper lobe pneumatoceles, which may predispose to pneumothorax or pneumomediastinum.
Cryptoccuss neoformans
Cryptococcus is an opportunisitc organism and ist he most common fungal infection in AIDS patients. Pulmonary infection usually coexists with cryptococcal meningitis (Typically CD4 count is less than 100 cells/cc in affected individuals)
In the immunosuppressed, Cryptococcus can have a wide range of appearances ranging from ground glass attenuation to focal consolidation to cavitating nodules. Cryptococcus can also prsent as miliary disease, often associated with lymphadenopathy or effusions.
Aspergillus
Aspergillus is an ubiquitous soil fungus that manifests as five distinct categories of pulmonary disease. Aspergillus only affects individuals with abnormal immunity or preexisting pulmonary disease. Depending on the manifestation, the predisposing abnormality may include asthma, immunocompromised state, prior infection, or structural/congenital abnormality.
Allergic Bronchopulmonary aspergillosis (ABPA)
Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity reaction to aspergillus seen most commonly in patients with long-standing asthma.
Patients present clinically with recurrent wheezing, low-grade fever, cough, and sputum production. The sputum contains fragments of aspergillus hyphae.
The key finding on CT is upper lobe bronchiectasis and mucoid impaction, which can be high attenuation or even calcified. This combination of mucoid impaction within the bronchiectatic airways represents the finger-in-glove sign (The finger-in-glove sign is not specific to ABPA and can also be seen in segmental bronchial atresia and many other diseases including cystic fibrosis (less commonly seen on a case-by-case basis).
Saprophytic aspergillosis (aspergilloma)
An aspergilloma is a conglomeration of intertwined aspergillus fungal hyphae and cellular debris (a mycetoma or “fungus ball”) in a preexisting pulmonary cavity (The aspergilloma is mobile and will change position when the patient is imaged in a different position)
The most common causes of a preexisting cavity are prior tuberculosis and sarcoidosis (less common causes include congenital anomalies such as bronchogenic cyst or sequestration, and post-infectious/post-traumatic pneumatocele)
If an aspergilloma is symptomatic, hemoptyssi is the most common symptom.
When a crescent of air is seen outlining the mycetoma against the wall of the cavity, the correct term is Monod sign. The air crescent sign is reserved for angioinvasive aspergillus.
Semi-invasive (chronic necrotizing) aspergillosis
Semi-invasive aspergillosis is a necrotizing granulomatous inflammation (analogous in pathology to reactivation TB) in response to chronic aspergillus infection. Semi-invasive aspergillosis is seen in debilitated, diabetic, alcoholic, and COPD patients.
Clinical symptoms include cough, chronic fever, and less commonly hemoptysis.
On CT, there are segmental areas of consolidation, often with cavitation and pleural thickening, which progress slowly over months or years.
Airway-invasive aspergillosis
Airway-invasive aspergillosis is aspergillus infection deep to the airway epithelial cells. It is seen only in the immunocompromised, including neutropenic and AIDS patients. The spectrum of clinical disease ranges from bronchilitis to bronchopneumonia.
The 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.
Angioinvasive aspergillosis
Angioinvasive aspergillosis is an aggressive infection characterized by invasion and occlusion of arteriorles and smaller pulmonary arteries by fungal hyphae. Angioinvasive aspergillosis is seen almost exclusively in the severely immunocompromised, including patients on chemotherapy, stem cell or solid organ transplant recipients, and in AIDS.
The CT halo sign represents a halo of ground glass attenuation surrounding a consolidation. The ground glas is thought to correspond to hemorrhagic infarction of the lung.
Halo sign
Can be seen in viral infection, Wegener granulomatosis, Kaposi sarcoma, hemorrhagic metastasis, angioinvasive aspergillus, and others.
Air crescent sign
Visually similar to Monod sign surrounding a mycetoma, represents a crescent of air from retraction of infarcted lung. It is a good prognostic sign as it indicates taht the patient is in the recovery phase.
Overview of lung cancer staging
The 7th edition fo the TNM system, published 2009, is based on data collected on over 100,000 patients with lung cancer from 1990 to 2000.
Staging of small cell lung cancer was previously simplified to “limited-stage” or “extensive-stage”. The new 7th TNM system, however, recommends that the same TNM staging system be used for both small cell and non-small cell lung cancer.
N (nodes) lung cancer
The color coding of the lymph nodes on the diagram below represents the nodal staging of lung cancer for an example of a left-sided mass:
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.
Idiopathic Interstitial Pneumonia overview
The lung has a limited repertoire of responses to injury. Common responses to injury range from recruiting lymphocytes or macrophages, increasing inflammatory debris, and instigating a fibrotic reaction.
The idiopathic interstitial pneumonias (IIPs) are seven different patterns of injury response. These patterns can be associated with collagen vascular disease, durg reaction, occupational exposure, or they may be idiopathic.
A disease can only be classified as an IIP if there is no other explanation for the pathologic changes.
Each of the seven entities has both a clinical syndrome and a separate pathologic diagnossi. Sometimes the clinical syndrome and the pathologic terms have different names and sometimes they share the same name, but in every case there is an acronym.
In order to understand the histopathological responses to injury, it is important to review the normal alveolar anatomy.
Lines, Stripes, and Interfaces of the Mediastinum
Interfaces between anatomic structures in the lungs, mediastinum, and pleura may be displaced or thickened in the presence of a mediastinal mass or abnormality. With the exception of the right paratracheal stripe, it is generally uncommon to see these interfaces in the absence of pathology.
(a “line” is a thin interface formed by tissue (typically <1 mm in thickness) with air on both sides)
(A “stripe” is a thicker interface formed between air and adjacent soft tissue)
(An “interface” is formed by the contact of two soft tissue structures of different densities)
The anterior junction line is 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)
The posterior junction line is also 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.)
The right and left paratrachearl stripes are formed by two layers of pleura where the medial aspect of each lung abuts the lateral wall fo the trahea 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 fo the right paratracheal stripe is most commonly due to pleural thickening, although a paratracheal or tracheal mass (including adenopathy or thyroid or traheal 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.)
The posterior tracheal stripe is the only interface seen on the lateral radiograph, representing the interface of the posterior wall of the trachea with the two plerual layers of the medial right lung.
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.)
The azygoesophageal recess is 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.)
