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contr I butors

Juan carlos baez, MD

Resident in Radiology, Brigham and Women’s Hospital

beryl r. benacerraf, MD

Clinical Professor of Radiology and obstetrics and Gynecology, Harvard Medical School

scott britz-cunningham, MD, PhD

Staff Radiologist, department of Nuclear medicine, Brigham and Women’s Hospital

Assistant Professor of Radiology, Harvard Medical School

Paul M. bunch, MD

Resident in Radiology, Brigham and Women’s Hospital

Michael J. callahan, MD

director, Computed Tomography

division Chief, Abdominal Imaging department of Radiology, Boston Children’s Hospital

Assistant Professor of Radiology, Harvard Medical School

Jeffrey Forris beecham chick, MD

Resident in Radiology, Brigham and Women’s Hospital

sona A. chikarmane, MD

Resident in Radiology, Brigham and Women’s Hospital

Mary Elizabeth cunnane, MD

Staff Radiologist, massachusetts Eye and Ear Infirmary Instructor of Radiology, Harvard Medical School

Pamela Deaver Ketwaroo, MD

Resident in Radiology, Brigham and Women’s Hospital

christine M. Denison, MD

Staff Radiologist, division of Breast Imaging, Brigham and Women’s Hospital

Assistant Professor of Radiology, Harvard Medical School

naman s. Desai, MD

Resident in Radiology, Brigham and Women’s Hospital

Alexandra Fairchild, MD

Resident in Radiology, Brigham and Women’s Hospital

ritu r. Gill, MD, MPH

Staff Radiologist, division of Thoracic Imaging, Brigham and Women’s Hospital

Assistant Professor of Radiology, Harvard Medical School

Alisa suzuki Han, MD

Staff Radiologist, division of Angiography and Interventional Radiology, Brigham and Women’s Hospital

Instructor of Radiology, Harvard Medical School

Michael Hanley, MD

Staff Radiologist, division of Thoraco-Abdominal Imaging, University of virginia Health System

Assistant Professor of Radiology, University of virginia School of medicine

timothy P. Killoran, MD

Staff Radiologist, division of Angiography and Interventional Radiology, Brigham and Women’s Hospital

Instructor of Radiology, Harvard Medical School

Meaghan M. Mackesy, MD

Resident in Radiology, Brigham and Women’s Hospital

Jonathan opraseuth, MD

Resident in Radiology, Brigham and Women’s Hospital

sanjay Prabhu, Mbbs, DcH, MrcPcH, Frcr

director, Radiology Advanced Image Analysis Lab, Staff Radiologist, Boston Children’s Hospital

Instructor in Radiology, Harvard Medical School

sughra raza, MD

Associate director of Breast Imaging, Brigham and Women’s Hospital

Associate Professor of Radiology, Harvard Medical School

Julie A. ritner, MD

Staff Radiologist, divisions of Ultrasound and Breast Imaging, Brigham and Women’s Hospital

Instructor in Radiology, Harvard Medical School

Justin r. routhier, MD

Resident in Radiology, Brigham and Women’s Hospital

Ari sacks, MD

Resident in Radiology, Brigham and Women’s Hospital

cheryl A. sadow, MD

Staff Radiologist, division of Abdominal Imaging and Intervention, Brigham and Women’s Hospital

Assistant Professor of Radiology, Harvard Medical School

Asha sarma, MD

Resident in Radiology, Brigham and Women’s Hospital

nehal shah, MD

Staff Radiologist, division of musculoskeletal

Imaging and Intervention, Brigham and Women’s Hospital

Instructor in Radiology, Harvard Medical School

Jeffrey Y. shyu, MD

Resident in Radiology, Brigham and Women’s Hospital

Kirstin M. small, MD

Staff Radiologist, division of musculoskeletal Imaging and Intervention, Brigham and Women’s Hospital

Instructor in Radiology, Harvard Medical School

stacy E. smith, MD

Section Head and Barbara N. Weissman

distinguished Chair of musculoskeletal Imaging and Intervention

Associate director, Radiology Residency Program, Brigham and Women’s Hospital

Assistant Professor of Radiology, Harvard Medical School

Darryl b. sneag, MD

Resident in Radiology, Brigham and Women’s Hospital

shreya sood, MD

Resident in Radiology, Brigham and Women’s Hospital

Michael steigner, MD

Staff Radiologist, division of Non-invasive Cardiovascular Imaging, Brigham and Women’s Hospital Instructor in Radiology, Harvard Medical School

barbara n. Weissman, MD

vice Chair, department of Radiology, Section Head Emeritus, musculoskeletal Imaging director, Radiology Residency Program

Brigham and Women’s Hospital Professor of Radiology, Harvard Medical School

Ged Wieschhoff, MD

Resident in Radiology, Brigham and Women’s Hospital

Jeremy r. Wortman, MD

Resident in Radiology, Brigham and Women’s Hospital

Gregory L. Wrubel, MD

Clinical Fellow in diagnostic Neuroradiology, Brigham and Women’s Hospital

1 Thoracic Imaging

Contents

Introductory concepts 2

Patterns of lung disease 8

Pulmonary infection 20

Infections in the immunocompromised 27

Pulmonary edema and ICU imaging 31

Lung cancer 34

Pulmonary vascular disease 43

Diffuse lung disease 48

Mediastinum 65

Airways 75

Pleura 83

Introductory concepts

Anatomy

Lobar and segmental anatomy

Interlobar fissures

Some references fuse the medial basal and anterior basal segments of the left lower lobe

• The minor fissure separates the right upper lobe (RUL) from the right middle lobe (RML) and is seen on both the frontal and lateral views as a fine horizontal line.

• The major (oblique) fissures are seen only on the lateral radiograph as oblique lines.

On the right, the major fissure separates the RUL and RML from the right lower lobe.

On the left, the major fissure separates the left upper lobe from the left lower lobe.

• The azygos fissure is an accessory fissure present in less than 1% of patients, seen in the presence of an azygos lobe. An azygos lobe is an anatomic variant where the right upper lobe apical or posterior segments are encased in their own parietal and visceral pleura.

Overview of atelectasis

• Atelectasis is loss of lung volume due to decreased aeration. Atelectasis is synonymous with collapse.

• Direct signs of atelectasis are from lobar volume loss and include:

Displacement of the fissures. Vascular crowding.

• Indirect signs of atelectasis are due to the effect of volume loss on adjacent structures and 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.

• Subsegmental atelectasis and mild fever are both commonly encountered in postsurgical patients, although it has been proposed that there is no causative relationship between atelectasis and postoperative fever.

Mechanisms of atelectasis

• 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.

Obstructive atelectasis can cause lobar atelectasis, which is complete collapse of a lobe, discussed on the following page.

Obstructive atelectasis occurs more quickly when the patient is breathing supplemental oxygen since oxygen is absorbed from the alveoli more rapidly than nitrogen.

In general, obstructive atelectasis 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.

• Relaxation (passive) atelectasis is caused by relaxation of lung adjacent to an intrathoracic lesion causing mass effect, such as a pleural effusion, pneumothorax, or pulmonary mass.

• Adhesive atelectasis is due to surfactant deficiency.

Adhesive atelectasis is seen most commonly in neonatal respiratory distress syndrome, but can also be seen in acute respiratory distress syndrome (ARDS).

• Cicatricial atelectasis is volume loss from architectural distortion of lung parenchyma by fibrosis.

Lobar atelectasis

• Lobar atelectasis is usually caused by central bronchial 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 is seen in an 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.

frontal schematic

lateral schematic

• Each of the five lobes tends to collapse in a predictable direction, as shown above.

right lung
right lung left lung left lung

Left

Left upper lobe collapse and luftsichel sign: Frontal radiograph (left image) shows a veil-like left upper lung opacity representing the collapsed left upper lobe (red arrow). A crescent of air lateral to the aortic arch is the luftsichel (yellow arrows). The lateral view (right image) shows the anterior wedge-shaped collapsed left upper lobe (red arrows). Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital.

• The luftsichel (air-sickle in German) sign of left upper lobe collapse is a crescent of air seen on the frontal radiograph, which represents the interface between the aorta and the hyperexpanded superior segment of the left lower lobe.

• It is important to recognize left upper lobe collapse and not mistake the left lung opacity for pneumonia, since a mass obstructing the airway may be the cause of the lobar atelectasis.

Right upper lobe atelectasis

Right upper lobe collapse and Golden’s S sign: Frontal radiograph (left image) shows a right upper lobe opacity with superior displacement of the minor fissure (red arrow) and a convex mass (yellow arrow). Lateral radiograph (right image) shows the wedge-shaped collapsed RUL projecting superiorly (red arrows).

• The reverse S sign of Golden is seen in right upper lobe collapse caused by an obstructing mass. The central convex margins of the mass form a reverse S. Although the sign describes a reverse S, it is also commonly known as Golden’s S sign. Similar to left upper lobe collapse, a right upper lobe collapse should raise concern for an underlying malignancy, especially with a Golden’s S sign present.

• 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 collapse: Frontal and lateral radiographs demonstrate a triangular retrocardiac opacity representing the collapsed left lower lobe (red arrows). There is loss of concavity of the left heart border (the flat waist sign; yellow arrow).

Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital.

• In left lower lobe collapse, the heart slightly rotates and the left hilum is pulled down.

• The flat waist sign describes the flattening of the left heart border as a result of downward shift of hilar structures and resultant cardiac rotation.

Right lower lobe atelectasis

Right lower lobe collapse: Frontal radiograph shows an abnormal vertically oriented interface medial to the right heart border (red arrow), which corresponds to a wedge-shaped opacity projecting over the heart on the lateral view (red arrow) and represents the collapsed right lower lobe. On the frontal radiograph, there is subtle crowding of the ribs (yellow arrows) in the right hemithorax due to volume loss.

• Right lower lobe atelectasis is the mirror-image of left lower lobe atelectasis.

• The collapsed lower lobe appears as a wedge-shaped retrocardiac opacity.

Right middle lobe atelectasis: Frontal chest radiograph shows an indistinct opacity in the right lung with focal silhouetting of the right heart border (arrow). There is elevation of the right hemidiaphragm due to volume loss. The lateral radiograph shows a wedge-shaped opacity (arrow) projecting over the midheart representing the collapsed right middle lobe.

Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital.

• The findings of right middle lobe atelectasis can be subtle on the frontal radiograph. Silhouetting 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

• Round atelectasis is 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 present 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.

Round atelectasis: Noncontrast CT shows a rounded opacity in the medial right lower lobe (red arrows). This example meets all five criteria for round atelectasis including adjacent pleural abnormality (effusion), opacity in contact with the pleura, round shape, volume loss in the affected lobe, and the comet tail sign (yellow arrows) representing curved vessels and bronchi leading to the focus of round atelectasis.

Patterns of lung disease

Essential anatomy

Secondary pulmonary lobule (SPL)

acinus, not visible on CT (approximately 12 per secondary lobule)

acinar artery and respiratory bronchiole

centrilobular bronchus and artery

pulmonary veins (and lymphatics, not pictured) run in the interlobular septa 1

• The secondary pulmonary lobule (SPL) 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, encases each SPL.

Thickening of the interlobular septa can be seen on CT and suggests pathologic enlargement of either the venous or lymphatic spaces, as discussed on subsequent pages.

• Each SPL is between 1 and 2.5 cm in diameter.

Abnormalities of the secondary pulmonary lobule

Consolidation and ground glass

• Consolidation and 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.

• C onsolidation can be described on either a chest radiograph or CT, while ground glass is generally reserved for CT.

• Although consolidation often implies pneumonia, both consolidation and ground glass are nonspecific findings with a broad differential depending on chronicity (acute versus chronic) and distribution (focal versus patchy or diffuse).

Consolidation

Schematic demonstrates complete filling of the alveolus with obscuration of the pulmonary vessels. The bronchus is visible as an air bronchogram.

Consolidation: Contrast-enhanced CT shows bilateral consolidative opacities, more densely consolidated on the left. There are bilateral air bronchograms (arrows). Although these imaging findings are nonspecific, this was a case of multifocal bronchioloalveolar carcinoma.

• Consolidation is histologically due to complete filling of affected alveoli with a liquidlike 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).

Acute respiratory distress syndrome (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 diagnosis of chronic consolidation includes:

Bronchioloalveolar carcinoma mucinous subtype, a form of adenocarcinoma.

Organizing pneumonia, which is a 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.

Ground glass opacification (GGO)

Schematic demonstrates complete hazy filling of the alveolus. The pulmonary vessels are still visible.

Ground glass opacification: Noncontrast CT shows diffuse ground glass opacification (GGO). The pulmonary architecture, including vasculature and bronchi, can be still seen, which is characteristic for GGO. Although these imaging findings are nonspecific, this was a case of acute respiratory distress syndrome (ARDS).

• Ground glass opacification is histologically due to either partial filling of the alveoli (by blood, pus, water, or cells), alveolar wall thickening, or reduced aeration of alveoli (atelectasis).

• Ground glass is usually a term reserved for CT. CT shows a hazy, gauze-like opacity, through which pulmonary vessels are still visible.

The term ground glass was originally described for unenhanced CT as enhanced vessels are visible in consolidation as well; however, in common practice ground glass is used for any type of CT.

• As with consolidation, air bronchograms may be present.

• Acute ground glass opacification has a similar differential to acute consolidation, since many of the entities that initially cause partial airspace filling can progress to completely fill the airspaces later in the disease. The differential of acute ground glass includes:

Pulmonary edema, which is usually dependent.

Pneumonia. Unlike consolidation, ground glass is more commonly seen in atypical pneumonia such as viral or Pneumocystis jiroveci pneumonia.

Pulmonary hemorrhage

Acute respiratory distress syndrome (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:

Bronchioloalveolar 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.

Diffuse but central-predominant ground glass

Coronal schematic shows central-predominant ground glass attenuation.

Coronal CT demonstrates central-predominant ground glass and associated septal thickening (the crazy paving pattern) in a case of alveolar proteinosis.

• The differential diagnosis for ground glass in a central distribution includes:

Pulmonary edema.

Alveolar hemorrhage.

Pneumocystis jiroveci pneumonia.

Alveolar proteinosis.

Peripheral ground glass or consolidation

Coronal schematic demonstrates peripheral ground glass.

Axial CT shows peripheral and subpleural ground glass attenuation. This was a case of organizing pneumonia.

• The differential diagnosis for peripheral consolidation or ground glass includes:

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 drug reaction. Peripheral consolidation/ground glass is unusual for cardiogenic pulmonary edema.

Interlobular septal thickening – smooth

Schematic demonstrates smooth interlobular septal thickening. Smooth interlobular septal thickening: CT demonstrates smooth thickening of the interlobular septa (arrows) in pulmonary edema.

Courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital.

• 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 (by far the most common cause of smooth interlobular septal thickening).

Pulmonary alveolar proteinosis

Pulmonary hemorrhage

Atypical pneumonia, especially Pneumocystis jiroveci pneumonia.

Interlobular septal thickening – nodular, irregular, or asymmetric

Schematic demonstrates irregular and nodular interlobular septal thickening.

Nodular septal thickening: CT shows a dominant mass in the right lung (yellow arrows) with peripheral nodularity and septal thickening. This was a case of lymphangitic carcinomatosis.

• Nodular, irregular, or asymmetric 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.

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Majuri. Asuitte luultavasti vastatusten?

Molemmat. Niin — minä — te — hän.

Majuri. Ha, ha, ha! Hupaista pakinaa! Lapset, te olette narrinparisia! Herra pastori! Viisi vuotta takaperin mahdoitte kyllä useasti toivoa saadaksenne tunnustaa rakkauttanne tälle kauniille naiselle, mutta sitä ette silloin saanut, nyt sen saatte ja vaikenette —

Wahl. Tälle naiselle —

Majuri. Joka on juuri se leski, josta puhuin. Kätenne tänne, tyttäreni! Ette ole tämän miehen kanssa vaihtanut vielä sanaakaan — ensimmäinen sananne olkoon: »Jaa».

Amalia. Uneksinko?

Wahl. Oi, mikä kaunis unelma!

Majuri. Uneksikaa sitten ikuisesti!

KAHDEKSASTOISTA KOHTAUS.

Rouva Äyriäinen (hyvin siististi puettuna). Heti jälestä Krumm. Edelliset.

RouvaÄyriäinen. Tässä olen. Ja herra vaalipappi Krummkin jo tulla häälyy yli pihan.

Majuri. Jahah! Tässä on kahdet naimiset tekeillä.

RouvaÄyriäinen. Kahdet? Heh! Mitenkä niin?

Krumm(käyden sisään). Korkealla suosiollanne olen alhaisuudessa taasen rohjennut astua sisään, toivoen kaikki esteet sillä poistaneeni, kun juhlallisesti julistan päättäneeni viedä tämän kunnioitettavan leskirouvan aviopuolisonani kotiani.

RouvaÄyriäinen. Minäkin olen asiaa miettinyt ja olen päättänyt —

Majuri. Malttakaa! malttakaa! Ensin on pieni erehdys selitettävä. Te luulette tuon rouvan olevan pastorivainajan lesken?

Krumm. Kuinkas sitten?

Majuri. Se hän kumminkaan ei ole, vaan tämä tässä.

Krumm. Tämäkö? No sitä parempi.

RouvaÄyriäinen(kiivastuneena). Mitä parempi.

Majuri. Te luulette myöskin olevanne uusi pastori?

Krumm. Minä toivon —

Majuri. Se ette kumminkaan ole, vaan tämä tässä!

Krumm. Kuinka, herra majuri?

Majuri. Herra pastori, te kulitte mutkateitä, mutta tämä herra tässä tuli suoraan, ja tästä huomatkaa, että »suorin tie on paras».

(Esirippu alas.)

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