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)



