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105 Cards in this Set

  • Front
  • Back
1. What are radiographic findings associated with a subpulmonic pneumothorax on a supine radiograph?
2. What is the most common location of a pneumothorax on a supine radiograph?
- Hyperlucent upper abdominal quadrant
- Deep sulcus sign
- Sharp diaphragmatic contour
- Double diaphragm sign (this sign refers to visualization of the anterior and posterior surfaces of the diaphragm).
2. Anteromedial. Look for a sharp outline of the right cardiac and mediastinal contour.
Chronic air-space disease
- Cryptogenic organizing PNA
- Bronchoalveolar cell carcinoma: most commonly presents as nodule of GGO but ~40% of cases present as diffuse or patchy consolidations/GGO.
- Pulmponary alveolar proteinosis
- Lipoid pneumonia
- Lymphoma
- "Alveolar" form of sarcoid
- Churg-Strauss syndrome
1. At what time point following completion of radiation therapy is radiation pneumonitis usually detectable by chest radiography?
2. When does fibrosis develop?
1. 6-8 weeks by radiographs. However, CT may detect subtle abnormalities earlier than radiography. Radiation pnemonitis presents as ground-glass opacities and consolidation. Such opacities are characteristically sharply demarcated and are not limited by anatomic boundaries such as fissures.
2. Fibrosis usually develops within 6 to 12 months following radiation therapy. Look for parenchymal opacity with linear configuration, traction bronchiectasis, and volume loss.
3. Incorrect: Radiation fibrosis is found in patients undergoing treatment for Hodgkin disease (mantle), breast cancer (supraclavicular nodes), and head and neck cancers. There is no history in this example to suggest this diagnosis, and the bony destruction would not be consistent.
1. What is ARDS?
2. What are some of the causes of ARDS?
3. How do you differentiate ARDS from cardiogenic pulmonary edema?
1. ARDS is a form of noncardiogenic pulmonary edema
caused by increased capillary permeability.
2. Trauma, sepsis, severe pneumonia, circulatory shock, aspiration, inhaled toxins, drug overdose, and multiple transfusions.
- Heart size and vascular pedicle width of patients with ARDS are usually normal.
- Common features of hydrostatic edema such as pleural effusions, Kerley (septal) lines, and peribronchial cuffing are not usually evident in patients with ARDS.
- Opacities in ARDS are often patchy and somewhat peripheral in distribution. In contrast, patients with hydrostatic edema more often
demonstrate confluent opacities with a central, perihilar predominance.
- Air bronchograms are visible more frequently in patients with ARDS than in those with hydrostatic edema.
- As ARDS progresses, areas of consolidation are frequently replaced by fibrosis and cyst formation.
- ARDS is more commonly complicated by barotrauma.
1. Which thymic neoplasms demonstrate ill defined margins?
2. What is an invasive thymoma?
3. How do the metastatic patterns of invasive thymoma and thymic carcinoma differ?
1. Most thymic neoplasms demonstrate well-defined margins on imaging studies. Two notable exceptions are invasive thymoma and thymic carcinoma.
2. Invasive thymoma refers to a thymoma that has invaded its fibrous capsule.
4. Invasive thymoma tends to spread locally, with invasion of adjacent mediastinal structures, chest wall invasion, and contiguous spread along the pleural surface (usually unilaterally). Thymic carcinoma is a rare thymic neoplasm that may be indistinguishable from an invasive thymoma on imaging studies unless distant metastases are present. Unlike invasive thymoma, a thymic carcinoma tends to metastasize hematogenously.
4. Thymic neoplasms with well defined margins:
- thymoma (elicit history of myasthenia gravis)
- thymic carcinoid
- thymic lymphoma
- thymolipoma
- benign thymic hyperplasia (rebound hyperplasia): seen in kids following chemotherapy.
1. What are the imaging findings of simple chronic silicosis?
2. What are the imaging findings of complicated chronic silicosis (AKA progressive massive fibrosis)?
3. What is silicoproteinosis and what are its imaging findings?
- Patients are typically asymptomatic.
- Innumerable small nodules with upper lung zone predominance that frequently calcify.
- Enlarged nodes with peripheral eggshell calcification.
- Pts are typically symptomatic with reduced pulmonary function.
- Characterized by one or more areas in which silicotic nodules have become confluent, measuring more than 1 cm in size.
3. Silicoproteinosis is a variant of silicosis that presents acutely within weeks after heavy dust exposure.
- Looks like alveolar proteinosis with ground-glass opacities and septal thickening.
- Hilar/mediastinal LAD is common.
- Progresses rapidly over months evolving into fibrosis with severe architectural distortion, bullae, and pneumothorax.
Whcau diseases have a UIP pattern?
- Idiopathic pulmonary fibrosis
- Asbestosis
- Connective tissue disorders (scleroderma)
- Drug toxicity (bleomycin)
1. What is the stage of lung cancer that causes partial atelectasis?
2. What is the stage of lung cancer that causes complete atelectasis of an entire lung?
3. Malignant pleural effusion?
1. Centrally obstructing neoplasm with associated post-obstructive atelectasis or pneumonia involving less than an entire lung is classified as T2.
2. If the entire lung is involved, then the primary tumor is classified as T3.
3. Malignant pleural effusion is classified as T4,
1. What are the types of wegener's Granulomatous?
2. What is the most common presentation in the lungs?
3. What is a less common presentation in the lungs?
4. What lab test is positive in pts with wegener's granulomatosis?
1. Diffuse and limited.
- Diffuse form presents with involvement of the lungs, kidneys, and upper respiratory tract.
- Limite form presents with pulmonary involvement only.
2. Multiple lung nodules or masses with well-defined margins. Cavitation is evident in up to one half of cases. On CT scans, the nodules frequently demonstrate angiocentric features, such as the presence of feeding vessels and a peripheral distribution.
3. The second most common pattern is focal or diffuse alveolar consolidation, which corresponds to the presence of pulmonary hemorrhage.
4. C-anca.
1. Can aspergillus infection result in pulmonary infarction?
2. What is the cause of the halo seen adjacent to the nodules?
3. What is the signifance of cavitation within the nodules?
1. Yes. Aspergillus organisms invade blood vessels resulting in areas of pulmonary infarction.
2. When imaged with CT scanning early in the course of infection, the nodules typically demonstrate a halo of ground-glass attenuation, which corresponds to the presence of hemorrhage. However, the halo sign is not specific for Aspergillus because it may also be seen with other infections (mucormycosis), vasculitides, and hemorrhagic metastases.
3. Later in the course of infection, the nodules may undergo cavitation (the "air crescent sign"). Such cavitation occurs after granulocyte
recovery and usually indicates a good prognosis.
What is the ddx of low attenuation lymphadenopathy?
1. TB
2. Other mycobacterial infections
3. Fungal infections
4. Metastatic disease (seminoma)
1. What are the radiographic features of PCP?
2. What are the CT findings of PCP?
1. Bilateral perihilar or diffuse symmetric interstitial pattern, which may be finely granular, reticular, or ground glass in appearance. Importantly, the chest radiograph
may be normal at the time of presentation in a significant minority of cases.
- extensive ground-glass attenuation often distributed in a patchy or geographic fashion.
- Predilection for the central, perihilar regions of the lungs.
- Ground-glass attenuation is occasionally accompanied by thickened septal lines.
- Foci of consolidation may also be evident in severe cases.
- In up to a third of cases of PCP, ground-glass opacities are accompanied by cystic lung disease. Such cysts have an upper lobe predominance and demonstrate varying sizes and wall thicknesses.
1. What are the imaging findings in a bronchopleural fistula?
2. How can you confirm the diagnosis of bronchopleural fistula?
3. What are the etiologies of a bronchopleural fistula?
- Pneumonectomy space fails to fill with fluid.
- Abrupt decrease in the air-fluid level in the pneumonectomy space.
- New collection of air in a previously opacified pneumonectomy space.
- Contralateral shift of the mediastinum.
2. The diagnosis can be confirmed with a xenon ventilation study, which will demonstrate xenon activity in the pneumonectomy space.
3. Long bronchial stump, too proximal a ligation of the bronchial arteries, and disruption of bronchial blood supply from extensive lymph node dissection.
Neoplastic involvement of which three structures precludes resection of a superior sulcus tumor?
Vertebral body, brachial plexus, and subclavian artery.
What is the ddx of nodular pleural or septal thickening or nodular thickening along the peribronchovascular structures?
1. Lymphangitic carcinomatosis
2. Lymphoma
3. Sarcoidosis
4. Kaposi sarcoma
What findings are associated with reactivation TB?
1. Apical lung cavity
2. Satellite nodules (favor an infection over malignancy).
3. Tree-in-bud pattern: This pattern is often associated with endobronchial spread of TB, a type of dissemination that occurs when a cavity erodes into an adjacent airway.
4. Large airway stenosis.
What are the imaging findings of carcinoid tumors?
- Central, hilar, or perihilar mass that may be associated with postobstructive atelectasis, pneumonia, mucoid impaction, or bronchiectasis.
- On CT, carcinoids typically demonstrate well-defined margins and slightly lobulated borders.
- Carcinoids are usually located close to the central bronchi, usually near airway bifurcations.
- Calification is observed in approximately 30% of cases on CT but is not usually evident on conventional radiographs.
- Most lesions demonstrate intense contrast enhancement.
- Minority of carcinoids present as a solitary pulmonary nodule in the periphery of the lung.
1. Where does Kaposi sarcoma arise from?
2. What virus is associated with Kaposi sarcoma?
3. What are the imaging findings?
4. Is Kaposi sarcoma gallium avid?
1. Kaposi sarcoma arises from endothelial cells. It may involve multiple organ systems, including the skin, lymphatics, lungs, and gastrointestinal system.
2. HHV-8
3. Peribronchovascular distribution of consolidation and poorly defined lung nodules. Pleural effusions and thoracic lymph node enlargement are relatively common thoracic manifestations. Less commonly, Kaposi sarcoma can present as diffuse GGO and interlobular septal thickening.
4. Kaposi sarcoma is not gallium avid and thus it can be differentiated from lymphoma and PCP.
1. What are the radiographic findings of varicella PNA?
2. Wha pt population is at risk for developing varicella PNA?
3. What is the appearance of healed varicella PNA?
1. Diffuse distribution of poorly defined small lung nodules, some of which have coalesced to form areas of consolidation.
2. The overall incidence of pneumonia in patients with chickenpox is approximately 15%. Predisposing factors include leukemia, lymphoma, immunodeficiency, and pregnancy. Both the incidence and severity of varicella pneumonia are significantly higher in pregnant women than in the general population.
3. healed varicella pneumonia is the presence of diffuse discrete pulmonary calcifications
What is the epicardial fat pad sign?
Positive epicardial fat pad sign (EFPS):
- AKA double-lucency sign that indicates presence of a pericardial effusion.
- refers to widening (>4 mm) of the soft tissue opacity of the pericardium between lucent stripes that represent fat located anterior and posterior (epicardial) to the pericardium.
What are congenital causes of bronchiectasis?
- Williams-Campbell syndrome
- Cystic fibrosis
- Primary hypogammaglobulinemia, - "Yellow nail" syndrome
- Immotile cilia syndrome (Kartagener's syndrome)
- Young's syndrome
- Mounier-Kuhn syndrome
How do you distinguish bronchiectasis from cystic lung disease?
1. When dilated bronchi course perpendicular to the scanning plane, you will always see a pulmonary artery running adjacent to it (signet-ring sign). In contrast, true lung
cysts, such as those associated with LAM, are located randomly in the lung parenchyma.
2. When dilated bronchi course parallel to the scanning plane, you will observe that the cystic spaces connect with one another.
3. Cystic bronchiectasis is often associated with fluid levels, a finding that is not generally observed in
cystic lung disease.
1. What produces the azygoesophageal interface?
2. What is the normal course of the azygoesophageal interface?
1. Produced by the juxtaposition of aerated lung in the right lower lobe and the azygos vein and/or esophagus in the right mediastinum.
2. It starts at the level of the azygous arch and extend inferiorly to the level of the diaphragm. It produces a concave slope as it curves slightly toward the left. Abnormalities of either the azygos vein (e.g.,azygos continuation of the inferior vena cava) or esophagus (e.g., achalasia) may result in rightward displacement of this interface. Subcarinal masses such as bronchogenic cysts and lymph node enlargement may also result in focal rightward displacement of the azygoesophageal interface, usually producing a rightward convexity in the subcarinal region.
1. What are the imaging findings in acute coccidioidomycosis infection?
2. What are the imaging findings in chronic coccidioidomycosis infection?
1. Airspace infection usually located in the lower lobes.
2. Solitary or multiple pulmonary nodules and cavities. Such cavities, may have variable wall thickness. In a minority (10% to 15%) of cases, coccidioidomycosis is associated with characteristic thin-walled ("grapeskin") cavities. Disseminated coccidioidomycosis has a miliary pattern similar to miliary TB.
1. What is ddx of lobulated opacity in the retrosternal region closely associated with the sternm?
1. Intenal mammary Lymphadenopathy: breast cancer and lymphoma
2. Enlarged internal mammary artery: seen with aortic coarctation.
3. Enlarged internal mammary vein: seen with SVC obstruction.
Peripheral lung opacities
1. Chronic eosinophilic PNA: described as photograhic negative of pulmonary edema. Upper lobe predominant
2. Pulmonary infarction (Hampton hump): heart failure (poor flow through bronchial arteries) is a risk factor.
3. Cryptogenic organizing PNA: usually lower lobe predominant.
4. Pulmonary contusion: resolves rapidly unless complicated by infection, laceration, pneumatocele.
5. Churg-Strauss syndrome
5. Alveolar sarcoidosis
1. What are the findings in mediastinitis?
2. At what time period do the findings become specific for mediastinitis?
1. Localized mediastinal fluid and pneumomediastinum are highly sensitive (100%) for mediastinitis.
2. The specificity of these findings is quite low (33%) within the first 14 days following surgery but increases significantly (100%) after postoperative day 14. Thus, when evaluating the CT scan of a postoperative patient with suspected mediastinitis, you must correlate CT findings with the time interval since surgery.
What processes result in lower lung zone emphysema?
Panlobular emphysema
Intravenous drug abuse (methylphenidate)
1. Wha is the cause of mosaic attenuation of the lungs?
2. How can you tell them apart?
3. What are the findings in bronchiolotis obliterans?
4. Name diseases or conditions that may be associated with BO.
1. Small airways disease and pulmonary vascular abnormalities such as chronic pulmonary embolism.
2. The expiratory CT demonstrates
extensive air trapping, a finding that distinguishes small airways disease from pulmonary vascular disease.
3. In BO, there is concentric narrowing of the bronchioles by submucosal and peribronchiolar fibrosis resulting in mosaic perfusion, bronchial dilation (represents dilated bronchi proximal the bronchiolar narrowing), and air trapping.
- Bone marrow transplantation
- Viral infections
- Toxic fume inhalation
- Rheumatoid arthritis
- Lung transplantation
- Inflammatory bowel disease
1. What are the slow growing pulmonary metastases?
2. What pulmonary mets grow rapidly?
1. Metastasizing leiomyoma (histology varies from benign lesion to a low-grade sarcoma) and thyroid mets.
2. Sarcomas, melanomas, and germ cell neoplasms.
What are the HRCT findings of asbestosis?
1. Curvilinear subpleural lines that parallel the pleural surface.
2. Thickened septal lines (the most common finding)
3. Parenchymal bands (linear opacities that are perpendicular to the pleural surface)
4. Honeycombing
5. Rounded atelectasis adjacent to visceral pleural thickening
1. What is post-pneumonectomy syndrome?
2. How is it treated?
- Rare, delayed complication following pneumonectomy that is more common following right pneumonectomy than left pneumonectomy.
- results in compression of the airway secondary to marked mediastinal shift, rotation of the heart and great vessels, and herniation of the remaining lung into the contralateral side of the chest.
2. Treated with surgical repositioning.
1. What is Mounier-Kuhn Syndrome?
2. What is the etiology?
3. What are the complications?
4. Where are tracheal diverticula seen?
1. Congenital tracheobronchomegaly (coronal diameter greater than 2.5 cm measured 2 cm above the aortic arch) and recurrent respiratory
2. Atrophy or absence of elastic fibers and thinning of the muscular mucosa of the trachea and main bronchi. This results in a flaccid airway that abnormally dilates during inspiration and excessively collapses on expiration (like tracheomalacia).
3. Bronchiectasis, emphysema, and pulmonary fibrosis.
4. Posterolateral wall of the trachea is the most common location for a tracheal diverticulum as it represents the junction of the posterior membranous and the anterior cartilaginous portions of the trachea.
1. What are the imaging findings in ABPA?
2. What is the etiology of ABPA?
-**Central bronchiectasis in an asthmatic or pt with CF.
- Affects the upper lobes.
- Mucoid impaction (finger in glove) with hyperattenuating secretions due to presence of calcium oxalate.
2. Hypersensitivity reaction that occurs when aspergillus organisms are inhaled by an atopic individual. The inhaled fungus grows in a noninvasive manner within the bronchi and incites an allergic response. The bronchi become dilated and filled with mucus that contains abundant eosinophils and fragmented fungal hyphae.
Infections associated with Pulmonary Alveolar Proteinosis
Nocardia, Aspergillus, and

1. What is the cause of tracheomalacia?
2. What is considered abnormal collapse of trachea?
1. A primary cause of tracheobronchomalacia is congen

ital deficiency of cartilage. Acquired causes include intu

bation, chronic obstructive pulmonary disease, trauma,

infection, relapsing polychondritis, and extrinsic compression (e.g., from a thyroid goiter).
2. Normally, the airway lumen

shows a decrease of approximately 10% to 30% with

expiration or coughing. A decrease of greater than 50%

is generally considered abnormal.
1. What are the common tracheal neoplasms?
- Squamous cell ca: associated with smoking. Worse prognosis.
- Adenoid cystic ca: better prognosis.

Synchronous or metachronous 2nd primaries are common (up to 40%).
1 what is the ddx of branching tubular opacities?
2. What entities present with mucous impaction?
1. Mucoid impaction and Arteriovenous malformation.
2. Cystic fibrosis, ABPA, bronchial atresia. mucoid im

paction can also occur distal to a bronchial obstruction

from both malignant (e.g., bronchogenic carcinoma,

bronchial carcinoid) and benign (e.g., tuberculosis [TB]

bronchostenosis) etiologies.
1. Are most fibrous tumors of the pleura benign or malignant?
2. What extrapulmoanry symptoms are they associated with?
3. What are the imaging findings?
1. approxi

mately 60% are benign and 40% are malignant. However,

all lesions are associated with a good prognosis, and the

majority are curable by surgical resection.
2. hypertrophic

osteoarthropathy and episodic hypoglycemia.
- round or lobulated masses.
- Lesions that are attached to the

visceral pleura by a pedicle demonstrate mobility in

response to changes in respiration and alterations in

patient positioning.
- intense and homogeneous

contrast enhancement (as shown in the second figure),

reflecting the rich vascularization of these tumors. On

MRI, these lesions typically demonstrate low signal in

tensity on all sequences, reflecting the fibrous content

within the stroma of the tumor.
1. What is the ddx of single or multiple lung nodules or

masses in a patient -who is status post heart transplanta

2. How do you differentiate among the possibilities?
- infection: Aspergillus and Nocardia.
2. mediastinal and/or

hilar lymph node enlargement is seen with PTLD and not

typically associated with Aspergillus and Nocardia in

Calcified pulmonary nodules
- healed histoplasmosis
- healed varicella
- silicosis
- osteosarcoma and chondrosarcoma
- thyroid cancer
- treated mets
- RARELY, a variety of mucinous and papillary neoplasms may result in calcined metastases.
1. What is the ddx of markedly hypervascular lad?
2. What is castleman's disease?
3. What are the features of hyaline vascular type?
4. What are the features of the plasma cell type variant?
1. enhancing nodes are due to

metastatic disease from hypervascular neoplasms such

as renal cell or thyroid carcinoma. The most common

benign etiology is Castleman's disease.
2. benign lymph

node hyperplasia, is an uncommon benign lymphoproli-

ferative disorder. This disorder has been divided into

two histologic subtypes: hyaline vascular and plasma

3. solitary

hilar or mediastinal enhancing nodal mass in asympto

matic patients.
4. bilateral hilar and

multifocal mediastinal lymph node enlargement is com

monly observed. Another differentiating feature is the

relatively low level of enhancement of nodes observed

in the plasma cell subtype compared with the marked

enhancement of nodes in the hyaline vascular subtype. Clinically, this subtype is associated with systemic sx including fever, fatigue, anemia. may also be

associated with lymphocytic interstitial pneumonitis

5. If possible, Castleman disease is usually treated with surgical excision; chemotherapy and radiation has limited success. A progression to lymphoma can occur in Castleman disease.
6. Kaposi sarcoma overlaps with multicentric Castleman disease. Both diagnoses are associated with herpes virus 8. Kaposi and Castleman may be concurrently present in human immunodeficiency virus (HIV) patients. Kaposi sarcoma usually has coexistent lung disease.
1. What organisms are responsible for non-TB mycobacterial infections?
2. What two groups of pts are affected?
3. What is the radiologic appearance in the elderly men with COPD?
4. What is the radiologic appearance in elderly immunocompetent women?
1. Nontuberculous mycobacterial (NTMB) infection is usu

ally caused by MAC and Mycobacterium kansasii.

These organisms are found in soil and water and demon

strate similar features.
- Eldrely men with COPD
- Elderly women who are immunocompetemt
3. The imaging features are almost identical to

reactivation TB and are characterized by slowly progres

sive nbronodular opacities that are often associated with

cavitation. The apical and posterior segments of the

upper lobes and the superior segments of the lower

lobes are most commonly involved.
4. cylindrical bronchiectasis

and multiple small (usually <5-mm diameter) lung nod

ules. In contrast

with the classic form, cavitation is uncommon in this

subgroup. Although the distribution may be diffuse, the

middle lobe and lingula are most commonly involved.
1. Wha is a cardiac bronchus?
2. What is its clinical signifance?
1. an anomalous

blind-ending diverticulum (arrows) arising from the me

dial wall of the bronchus intermedius. It extends medically and caudally towards the mediast um. Its length varies from a small, blind-ending pouch

(such as in this case) to a longer branching structure.

The longer configuration may be associated with rudi

mentary alveolar tissue in some cases.
2. may serve as a reservoir for infectious mate

rial, affected patients may present with recurrent respi

ratory infections
What are the early complications of lung transplantation?
Early pulmonary postoperative complications of lung

transplantation include reperfusion edema, acute rejec

tion, and infection. Reperfusion edema, also referred

to as reimplantation response, is caused by increased

capillary permeability and occurs in the vast majority of

transplanted lungs. It has a characteristic time course,

usually beginning in the first 24 hours, peaking between

1 and 5 days, and resolving within approximately 10

days following transplantation. Acute rejection is a com

mon complication within the first 3 months following

transplantation. The first episode usually occurs in the

first 5 to 10 days following surgery. Note that reperfu

sion edema begins earlier and peaks before this time.

Infection is the most common pulmonary complication

following transplantation.
1. What is the mechanism of airwa involvement fromTB?
2. What are the stages of tb involvement of the airways?
1. Airway involvement in patients with TB may result from

several mechanisms: (1) direct contact of the airway

mucosa with infected secretions; (2) submucosal spread

of infection through the lymphatics from infected lymph

nodes or lung; and (3) direct invasion of the airway by

adjacent lymph nodes.
2. Hperplastic and fibrostenotic
3. The first stage is characterized by hyper

plastic changes.The affected airway

walls appear irregularly thickened with variable degrees

of luminal narrowing. Hilar and mediastinal lymph node

enlargement are commonly observed and frequently

demonstrate peripheral enhancement with central low

attenuation. frequently

reversible with medical therapy.
4. patients

with fibrotic disease generally demonstrated smooth

narrowing of the airways and minimal wall thickening,

a pattern not reversible with medical therapy.
F dings of cop

bilateral airspace consolidation with a peripheral, sub-

pleural distribution. More recently, a peribronchovascu

lar distribution has been described as a relatively fre

quent manifestation, often in association with foci of

peripheral consolidation.
Wha are imaging findings of amiodarone toxicity?
There are two distinct clinical presentations of amio

darone toxicity. The most common presentation is a

subacute onset of dyspnea, nonproductive cough, and

weight loss. Radiographs typically reveal a diffuse linear

pattern. A less common presentation (observed in ap

proximately one third of patients) is characterized by

an acute onset of symptoms that mimic an infectious

pneumonitis. Radiographs of these patients typically

demonstrate patchy alveolar opacities with a peripheral

distribution. CT scans in these patients typically reveal

high-attenuation foci of parenchymal opacification, with

attenuation values ranging from approximately 80 to

175 Hounsfield units. This appearance reflects the high

concentration of amiodarone, a triiodinated agent,

within these regions of lung parenchyma.
Anterior mediastinal mass
- MC = thymoma (associated with myasthenia gravis)
- NOTE: in a child s/p chemotherapy, thymus undergoes hyperplasia
- HL vs NHL
- most are benign
- MC = teratoma
- usually cotiguous with the thyroid gland in neck
- look for mass effect on trachea
- look for evidence of median sternotomy
- rare but serious complication of CABG.
- false aneurysms more common than true aneurysms. m
- Most false aneurysms are located at the anastomotic sites. In contrast, true aneurysms are identified most commonly within the body of the graft.
- COMPLICATIONS = infarction, fistula formation with a cardiac chamber, and rupture.
What nfections are associated with tree in bud opacities?
Bacterial and mycobacterial
1. What is the most common viral pneumonia to occur in solid organ

transplant recipients?
2. What kind of infections are seen pts 1 month after transplant?
1. CMV
2. During the first month following transplantation, the

immunosuppressive agents have not yet had a profound

effect on the patient's immune system. Opportunistic

infections are unusual during this period. Infections are

usually caused by organisms that are typically encountered

in patients with normal immunity after surgery, particu

larly gram-negative organisms, and commonly occur due

to aspiration or wound catheter-related infections.
3. Immunosuppression is usually most severe during

the second, third, and fourth months following renal

transplantation. T-cell mediated immunity is most se

verely depressed, placing patients at highest risk for viral

and fungal infections. CMV is the most common viral

agent to affect these patients. Radiographs may show a

reticular or nodular pattern and, less commonly, consoli

dation and discrete lung nodules and masses.
4. After the fourth month, the immunosuppression regi

men is gradually tapered. As the patient's immune sys

tem recovers, the organisms that most commonly pro

duce pneumonia in this period are those responsible

for most community-acquired pneumonias, such as

Streptococcus pneumoniae. Because immunosuppres

sive agents are tapered but not discontinued, patients

continue to remain at risk for opportunistic infections,

particularly fungal organisms.
1. What is pulmonary veno-occlusive disease?
2. What is the classic triad seen with this disease?
1. rare disorder that

is characterized by obstruction of the pulmonary veins

and venules by intimal fibrosis.
- severe pulmonary artery hypertension: manifested by enlarged pulmonary arteries.
- pulmonary edema: manifested by thickening of the septal lines, groung glass opacities, and pleural effusions.
- normal "wedge pressure.
1. What two conditions are most likely to present with multiple tracheal masses?
2. How can MRI help distinguish amyloid from other causes of tracheal masses?

3. This patient also had laryngeal lesions (not shown). Which diagnosis is most likely?

4. What virus is associated with this condition?
1. Papillomatosis and amyloid.

2. Amyloid demonstrates characteristic low signal

intensity on both T1W and T2W sequences.

3. The

presence of laryngeal and tracheal lesions is most sug

gestive of papillomatosis.

4. Human papillomavirus.
5. Laryngeal papillomatosis is an uncommon condition

characterized by the presence of multiple squamous

papillomas within the larynx. This disorder is seen pri

marily in children. Extension of the disease into the

trachea and bronchi is referred to as tracheobronchial

papillomatosis and occurs in roughly 5% of cases. Iso

lated tracheobronchial disease is seen more frequently

in adults than in children. Rarely, there is dissemination

into the lung parenchyma. When the lung paren

chyma is involved, you may observe centrilobular opaci

ties, nodules, and cavities.
1. What are the imaging findings of bronchiolitis?
2. What are the causes of bronchiolitis?
1. Tree in bud opacities and air trapping.
- Infection is the most common. Classically described for mycobacterium infections, however,it can also be seen with respiratory synctial virus, adenovirus, and Mycoplasma

pneumonia. Other important infectious etiologies in

clude mycobacterial and fungal organisms.
- asthma
- aspiration
- diffuse panbronchiolitis
1. How do you differentiate if the ground glass portions of the Lu vs are normal or abnormal?
When the caliber and number

of vessels are similar, the areas of relative increased

attenuation are abnormal. This appearance is seen in a

variety of entities that are characterized by the presence

of ground-glass opacities, including acute interstitial in

fections such as PCP and chronic infiltrative lung dis

eases. In contrast, a reduction in size and number of

vessels within the low attenuation area implies that the

low-attenuation foci are abnormal. Such an appearance

can be seen in pulmonary vascular disorders, such as

chronic pulmonary embolic disease, and small airways

disease, such as obliterative bronchiolitis. In cases of

small airways disease, the diminished vasculature occurs

secondary to reflex vasoconstriction. You can distin

guish vascular and small airways etiologies by per

forming additional expiratory CT scans. Only small air

ways disease is associated with air trapping on

expiratory scans.
1. What are the imaging findings of tracheobronchial injury?
Early findings:
- pneumothorax (typically severe and refractory to chest tube drain)
- pneumomediastinum (2/2 rupture of extrapleural portion of the airway)
- subcutaneous emphysema

Late findings:
Late imaging findings are related to the develop

ment of granulation tissue and stricture within the in

jured bronchus, a process that occurs within 1 to 4

weeks of injury. Late imaging findings include postob-

structive atelectasis, pneumonia, abscess, and empyema.
1. What is the ddx of upper lung zone mass?
2. What associated findings are seen with PMF?
- Malignancy: primary or metastatic
- Infection: TB/fungal
- Progressive massive fibrosis: Silicosis/coal worker's pneumoconiosis, sarcoidosis, talcosis, berylliosis.
- Upper lobe volume loss with superior retraction of the hila.
- Architectural distortion/bronchiectasis
- Paracicatricial emphysema peripheral to the conglomerate mass.
- Eggshell calcifications of lymph nodes
- Increased risk of lung carcinoma.
3. Pts with pneumoconiosis are at increased risk of TB.
What is plombage?
Old therapy for TB where lucent balls were placed in the extrapleural space resulting in compression of the lung.
Look for cluster of similar sized radiolucencies that project over the lung apices.
Ddx of hyper expanded lungs with interstitial abnormality
Emphysema with Superimposed Process
Viral or Atypical Pneumonia

Cystic Fibrosis (Mimic)

Pulmonary Langerhans Cell Histiocytosis
Ddx of multiple pleural based nodules
Fibrous tumor of pleura
Pleural metastases
Malignant mesothelioma
Invasive thymoma
Askin tumor
Askin tumors are a form of primitive neuroectodermal tumor (PNET). It arises in the soft tissues of the thorax. Children and young adults will present with chest wall pain. Radiographs show a heterogeneous mass with or without rib destruction. Rib destruction is less common in this diagnosis than in Ewing sarcoma. An Askin tumor may or may not have a pleural effusion. Askin tumors that metastasizes to the lung and bone are common.
Empyema neceesitans
Reasonable Alternative: Empyema necessitans is empyema that subsequently invades through the chest wall. This is the most common related bony abnormality. Rib sclerosis or periosteal reaction is secondary to chronic osteomyelitis. The organisms that can cause empyema necessitans can be remembered by the “BATMAN” acronym, as the superhero Batman breaks through barriers: Blastomyces; Actinomyces; Tuberculosis (75% of cases); Mucor; Aspergillus; Nocardia.
Ewing sarcoma chest wall
Reasonable Alternative: Ewing sarcoma is an aggressive lytic lesion, has cortical breakthrough, is a large soft tissue mass, and causes rib lesions that often elicit a large pleural effusion. Proximal and flat bones, such as the ribs, pelvis, and scapula, are generally involved in the older age group; tubular bones in younger children. Late teenage and young adults are the prime age group for Ewing of the rib. It may appear polyostotic since osseous metastases are common.
1. What are the imaging findings of NSIP?
2. What collagen vascular diseases are associated with NSIP?
- Lower lobe predominant ground-glass and reticular interstitial opacities.
- Subpleural sparing
- Scleroderma
- Polymyositis or dermatomyositis
- Sjögren syndrome
- Rheumatoid arthritis
strongly associated with cigarette smoking and is considered to represent the end of a spectrum of respiratory bronchiolitis, associated interstitial lung disease (RB-ILD). DIP is best characterized by diffuse and uniform ground-glass opacities in patients who are current or past smokers.
1. What is the etiology of hypersensitivity pneumonitis?
2. What are the findings of hypersensitivity pneumonitis?
- Allergic lung disease caused by inhalation of antigens (i.e. farmer's lung).
- Classified into acute, subacute, and chronic stages.
- HRCT is typically performed in the subacute stage of HP, weeks to months following the 1st exposure to the antigen or in the chronic phase.
- centrilobular ground-glass nodules (80% of cases)
- mosaic lung pattern caused by bronchiolitis with air-trapping.
- "Head cheese" sign = geographic region of air-trapping, ground-glass opacities, and normal lung
- Upper lung zone distribution is especially common in those with intermittent exposure like farmer's lung.
- Mid-lung predominance is seen in many other antigen exposures that occur continuously, such as bird breeder's lung.
- Can evolve into peribronchial fibrosis mimicking UIP and NSIP.
Air fluid level in the pleural space
- Broncho-pleural fistula (BPF) is an abnormal connection between the pleura and an airway. True BPF involves an abnormal connection between a central airway and pleural space. In the setting of a lobectomy, an interval decrease in accumulation of pleural fluid should raise the concern for a bronchopleural fistula. Also, when a hydropneumothorax develops without intervening pleural intervention or procedure, a BPF should be a diagnostic consideration. Most hydropneumothoraces are related to pleural tubes or thoracentesis. Adequate drainage of pleural fluid collections and antibiotic therapy are essential for treatment.

- connection between the airway and pleura will not be seen with a hydropneumothorax. However, often with the correct diagnosis in this case, depending on the cycle of ventilation, the connection between the airway and pleura may also not be seen. Hydropneumothorax most commonly occurs spontaneously due to a pneumothorax with bleeding. However, it may be iatrogenic in etiology, due to line placement or attempted thoracentesis with bleeding. Hydropneumothorax can also be traumatic in etiology, due to a deceleration injury with rupture of the airway into the pleural space.

- Incorrect: Gas-forming infections in the pleural space are rare. Most gas-forming infections in the pleural space occur due to instrumentation or fistula formation. The most common organisms related to a gas-forming infection in the pleural space are Clostridium perfringens and Bacteroides fragilis. The clinical history in this case suggests an alternative diagnosis
Pneumocystis pneumonia typically shows perihilar or diffuse distribution. It is more severe in upper lung zones of patients on pentamidine aerosol prophylaxis. Patients may have pneumatoceles that typically develop in the periphery of upper lobes. Curiously, pneumatoceles are only seen in those with human immunodeficiency virus (HIV) infection.
Radiation induced pneumonitis
Pulmonary ground-glass opacities and consolidation (radiation pneumonitis) are seen 6-8 weeks after initial treatment. Radiation pneumonitis peaks 3 months after the end of treatment. The evolution of pulmonary opacities into lung fibrosis occurs 3-18 months after the end of treatment. From 18 months after the end of treatment and onward will show stable lung fibrosis.
Alveolar microlithiasis
- Rare idiopathic disorder characterized by diffuse bilateral deposition of intra-alveolar microliths.
- Often, patients will be asymptomatic (70%) in spite of the gross radiographic abnormalities -- Lungs extremely dense, obscuring heart borders and diaphragm.
- Diffuse calcifications with posterior predominance.
- Sparing of subpleural lung
- No known treatment; lung transplant is considered for end stage disease.
Metastatic pulmonary calcifications
Metastatic pulmonary calcification is defined as a deposition of calcium in otherwise normal tissue in hypercalcemic states, such as renal failure. There will be a high pH in the upper lung zones; calcium is less soluble in an alkaline environment. Calcium also tends to deposit in the gastric wall and renal medulla, regions with relative alkaline pH. The high-attenuation centrilobular ground-glass nodules clustered into rosettes resemble mulberries.
- History of IV drug abuse (crushed pills are injected intravenously)
- Mimics sarcoidosis/silicosis/CWP
- Look for perilymphatic distribution of micronodules, upper lung predominant, progressive massive fibrosis when nodules coalesce)
- NOTE: IV ritalin abuse also leads to basilar panlobular emphysema.
Pattern of drug toxicity
Wide array of injury patterns including
- Pulmonary edema
- Pulmonary hemorrhage
- Hypersensitivity pneumonitis
- UIP (usually after long-term therapy)
Churg-Strauss syndrome
- Granulomatous small vessel vasculitis
- 100% have asthma
- Triad of allergic history, peripheral blood eosinophilia, and systemic vasculitis
- Looks similar to chronic eosinophilic pneumonia = peripheral consolidation and ground-glass opacities. Pleural effusions are seen in 25% of cases (extremely rare in eosinophilic pneumonia)
intraluminal broncholith is typically a round calcified structure representing a calcified lymph node that erodes into the bronchial lumen. Additional calcified regional intrapulmonary lymph nodes are typically present in the ipsilateral &/or contralateral lung.
Myasthenia gravis
A thymoma is the most common anterior mediastinal mass in patients greater than 40 years old. The most common thymic abnormality associated with myasthenia gravis is follicular thymic hyperplasia, not thymoma. Treatment is usually surgical excision.
Alpha 1 anti trypsin def
Lower lung zone predominant emphysema.
There is decreased caliber of the vessels straight arrow at the lung bases compared to the vessels at the upper lungs.
What are the imaging findings of Langerhan cell histiocytosis?
- Centrilobular nodules that evolve into cavitary nodules and then thin-walled cysts.
- Cysts may aggregate into bizarre shapes.
- Nodules and cysts are more profuse in upper lung zones.
Lymphocytic interstitial pneumonitis (LIP)
- Hyperplasia of bronchus associated lymphoid tissue resulting in centrilobular nodules of GGO.
- There is lymphocytic infiltration of alveolar septa as well which results in a reticulonodular interstitial pattern on radiographs.
- On CT, look for centrilobular nodules. Some nodules are cavitary with thin walls and appear as cysts (mimicking LCH and LAM). Cysts are basilar in distribution. GGO may also be seen.
- Seen in the setting of Sjogren syndrome in adults and AIDS in children.
posterior and basal subpleural lung. Subpleural reticular or dot-like opacities indicates early fibrosis. Subpleural lines parallel the pleural surface in asbestosis. Short or long parenchymal bands extend inward from abnormal pleural surfaces. Pleural plaques are common (not seen in this case). Late fibrosis shows honeycombing and thickening of interlobular septa.
Ddx of airway related tumors
1. Carcinoid tumors:
2. Lung cancer: squamous cell CA or small cell lung cancer.
3. Mucoepidermoid
4. Adenoid cystic: usually originates from the posterolateral wall.
What is a complication of fibrosing mediastinitis?
- Fibrosis may obstruct a vessel and lead to asymmetric pulmonary edema.
- At times, stents may have to be placed in the vasculature or airway.
1. What are the findings of aortic transection?
2. How is this different than aortic dissection?
3. What is the ductus bump?
- Irregular bulge along the anterior undersurface of the aortic isthmus. (portion of the aorta between the origin of the left subclavian artery and the aortic side of the ligamentum arteriosum).
- Presence of an intimomedial injury (looks like a dissection).
- Contiguous mediastinal hematoma
2. Aortic dissection is reserved for a communicating dissection with formation of true and false lumina separated by an intimomedial flap. The flap typically spirals down the involved portion of the aorta. Blunt chest trauma is a rare cause of this form of acute aortic syndrome.
- Ductus bump represents a focal anteromedial luminal bulge at the origin of the fetal ductus arterious.
- Not associated with an intimomedial injury.
- smooth, non-abrupt continuity (gently sloping "shoulders") with the adjacent proximal and distal aorta.
Which vasculitides produce pulmonary hemorrhage?
- Wegener's granulomatosis
- Churg Straus
- Microscopic polyangiitis
Rounded atelectasis
Correct: Definitive diagnosis of round atelectasis (RA) on CT requires 4 findings. A pleural abnormality is 1 of the 4 definitive findings and may include pleural thickening (seen in this case), a pleural plaque (seen in this case), or pleural effusion. Also, a broad-based attachment of mass-like consolidation to a pleural abnormality, as seen here, is also definitive of this diagnosis. Volume loss with swirling of bronchovasculature into mass-like consolidation, or the "comet-tail" sign, is also diagnostic of round atelectasis and is seen in this case. Lastly, round atelectasis should have acute angles with the pleura, which are also seen here.
- Pulmonary edema
- Pulmonary alveolar proteinosis
- Drug reaction
- Diffuse alveolar hemorrhage
- Radiation pneumonitis
- Lipoid PNA
Silo filler'slung disease
- occupational disease that results from pulmonary exposure to toxic fumes (oxides of nitrogen).
- Diffuse pulmonary edema can occur within hours of toxic fume inhalation. It usually resolves after 3-5 days. Initial chest radiograph may be normal.
- Bronchiolitis obliterans can be a late manifestation
Smoke inhalation
Incorrect: Acutely, bronchial wall thickening and subglottic edema occur in this condition. Perihilar and upper lung zone pulmonary edema is present in this condition. Subsegmental atelectasis is also seen. Skin burns are common.
Rheumatoid arthritis
Incorrect: Rheumatoid arthritis may cause a UIP (usual interstitial pneumonitis) pattern of fibrosis but would not be associated with esophageal dilation. There may be unilateral pleural effusion or pleural thickening, bronchiectasis (30%), and/or rheumatoid nodules (≤ 5%). Look for distal clavicular erosions or a high riding humeral head as secondary clues to clinch this diagnosis.
Calcifications of the pleura
Asbestos related pleural disease
Metastatic adenocarcinoma
Previous empyema
Previous hemothorax
Repeated pneumothorax
Patients with a mediastinal abscess will have a recent history of median sternotomy, esophageal perforation, or a head and neck infection. A mediastinal abscess presents as a typical rim-enhancing lesion with central low density. They may demonstrate air bubbles with communication to adjacent infection. It is difficult to differentiate from postoperative hematomas/seromas. They may require needle aspiration. A postoperative hematoma/seroma should resolve after 2-3 weeks.
Tuberous sclerosis
mimics LAM with mutiple cyst
Centrilobular nodules
- AKA extrinsic allergic alveolitis
- 2/2 exposure to environmental antigens.
- Centrilobular nodules with GGO
- Chronic exposure leads to end stage lung disease with fibrosis.
- look for tree-in-bud
- most commonly seen with tuberculous and non-tuberculous infections.
- diffuse centrilobular nodules (usually upper lobe predominant) and patchy areas of GGO
- looks like subacute hypersensitivity pneumonitis.
- Churg-Strauss = look for centrilobular nodules + peripheral GGO.
Cystic lung disease
- may have cyst like appearance in the setting of pulmonary edema
- diffuse thin walled cysts
- chylous pleural effusion
- associated with HIV in kids and Sjogren syndrome in adults
- look for AML, cysts, and other abnormalities
- cyst and nodules. Cysts have bizzare shapes
- upper lobe predominant with sparing of costophrenic angles.
- GGO and interlobular septal thickening
Cavitary lung nodules
- Wegener's granulomatosis
- Rheumatoid nodules
- Septic emboli
- Fungal infection
- Metastatic disease (especially treated)
Cavitary lung mass
- Secondary TB (upper lobe predominant)
- Fungal infections
- Bacterial PNA with abscess formation
- Primary SCC or metastatic SCC (H/N cancer, cervical cancer)
- Wegener's
- Rheumatoid nodule
Multiple lung nodules
- Septic emobli
- Miliary spread of TB/Fungal disease
- Thyroid, renal, melanoma
- Wegener's
- Rheumatoid arthritis
Lower lobe interstitial lung disease
- Scleroderma: affects the lungs (subpleural reticular opacities, honeycombing, traction bronchiectais); esophagus (dilated, patulous esophagus); MSK
- RA: affects articular surfaces; Chest: pleural and pericardial effusions, ILD affecting the anterior lungs, rheumatoid nodules; Caplan syndrome = coal worker's pneumoconiosis + RA
- SLE = pleural and pericardial effusions are most common.
- pleural effusion
- pleural thickening and calcifications
- rounded atelectasis.
- Subpleural lines and parenchymal bands.
- Bleomycin and busulfan = most common chemotherapeutic agents that cause lower lobe ILD.
- Amiodarone also results in lower lobe ILD along with dense opacities.
Upper lobe interstitial lung disease
- characterzied by scarring and cavitation.
- perilymphatic distribution of nodules
- bronchiectasis, mucus plugging, air trapping, bronchial wall thickening.
Imaging manifestations of TB
- lobar consolidation
- mediastinal and lobar LAD (often low attenuation)
- upper lung zone fibrosis and scarring.
- no LAD
- may be c/b aspergilloma
- seen in children and immunocompromised
- tree in bud opacities
Hyperlucent lung
- s/p mastectomy
- Poland syndrome: absence of pectoralis muscles.
- endobronchial lesion = foreign body, mucus plug, neoplasm
- 2/2 bronchiolitis obliterans
- small lung volumes with diminished blood flow
- air trapping on expiratory phase CT.
Middle mediastinal mass
- Low attenuation = TB, fungal infxn, necrotic post treatment
- Enhancing = Castleman, hypervascular mets, TB, and sarcoid
- Calcification pattern = eggshell (sarcoid, pneumoconiosis)
- Aortic aneurysm/pseudoaneurysm
- foregut duplication cyst
- pericardial cyst
- look for a gas-fluid level (which can also be seen with achalasia/pseudoachalasia)
Bilateral opacification
- Pulmonary edema
- Atypical infection (PCP)
- Pulmonary hemorrhage (Wegener's granulomatosis, Goodpasture)
- Diffuse PNA
- Drug reaction
- Acute eosinophilic PNA
- Pulmonary alveolar proteinosis
- Lipoid PNA
Cryptogenic organizing pneumonia (COP)
- non-specific inflammatory response that results in alveolar fibrosis.
- presents as chronic consolidation in the lower lobes.
- reverse halo sign (foci of ground-glass opacification surrounded by halo of consolidation)
- Can occasionally be migratory (similar to Loffler pneumonia)
- uncommonly presents as crazy-paving pattern.
Eosinophilic PNA
Seen in asthmatic pts with peripheral eosinophilia.
- looks similar to pulmonary edema
- Peripheral pattern of consolidation - often with an apical or axillary distribution with sparing of lung bases.
- Eosinophilia + transient, migratory calcifications.