Case Review Chest

Front 1

Mosaic attenuation on lung CT

Back 1

LOOK AT THE RELATIVE SIZE AND NUMBER OF VESSELS IN THE AREAS


If the number and size of vessels is the same in both the normal lung and the mosaic areas, then it is the more dense areas that are abnormal, and you are dealing with ground glass opacities, such as that caused by PCP and chronic IPs.


If the number and size of the vessels is diminished in the area of mosaic attenuation, then it is that area which is abnormal, and that area will always be hypoattenuated versus the rest of the lung. This is caused either by small airways disease or small vessel disease. Then, to differentiate definitively between these, perform EXPIRATORY CT. ONLY SMALL AIRWAYS DISEASE WILL CAUSE AIR TRAPPING.

Front 2

Common cause of small vessel disease

Back 2

Chronic pulmonary emboli

Front 3

Common cause of small airways disease

Back 3

Obliterative bronchiolitis post infectious (i.e. Swyer-James, but localized to just a segment)

Front 4

Cystic lung space with air-fluid level and another cyst on top of the air-fluid level

Back 4

CYST WITHIN A CYST APPEARANCE, or WATER LILY SIGN

= HYDATID DISEASE OF THE LUNG

Front 5

Hydatid disease

Back 5

ECHINOCOCCUS


Forms cysts wherever it occurs


Cysts have two components: Exocyst, which houses the whole complex, and an endocyst, which can contain multiple smaller cysts.


If the exocyst gains communication with the bronchial tree, a crescent sign between the intact fluid filled endocyst and the air filled exocyst will form.

If the endocyst gains direct communication with the bronchial tree, the contents are expectorated, inciting a coughing reaction of rapid onset, as the contents come out into the large airways. If the patient is imaged at this stage, there will be seen an outer cyst with dependent fluid leaked out of the endocyst, and the endocyst itself will be seen floating on top of the fluid = Cyst within a cyst.

Front 6

Small airways disease

Back 6

Disease involving peripheral bronchioles. If infectious, can cause tree-in-bud appearance. Will be a CENTRILOBULAR pattern, because the bronchiole is located in the center of the secondary pulmonary lobule

Front 7

Tree in bud

Back 7

Infectious bronchiolitis, with causes such as RSV, adenovirus and Mycoplasma


TB


Fungal pneumonia

Front 8

Small fine nodules in lung

Back 8

LOOK FOR THE PATTERN IMMEDIATELY

Front 9

Septal thickening, ground glass opacity, and mildly enlarged pulmonary arteries

Back 9

PULMONARY EDEMA is what you should say, but, if you notice that the pulmonary veins are normal in size, something is wrong, as it cannot be cardiogenic pulmonary edema. It also cannot be normal noncardiogenic causes because they would not have enlarged pulmonary arteries, because they are due to increased capillary permeability, not increased pressures. Therefore, the only thing left is abnormality of the pulmonary veins = PULMONARY VENOOCCLUSIVE DISEASE.


Triad of severe pulmonary artery hypertension, pulmonary edema, and normal wedge pressure.


Caused by intimal hyperplasia of the pulmonary veins.


Causes are viral infections, toxins, chemo, radiation, intracardiac shunts (cause of Eisenmengers's?), and contraceptives.


Poor prognosis. Lung transplantation required.

Front 10

Multiple tracheal masses

Back 10

PAPILLOMATOSIS versus AMYLOIDOSIS


Tell them apart because amyloid nodules have characteristic low signal on both T1 and T2


AND


Because PAPILLOMATOSIS IS ALSO ASSOCIATED WITH LARYNGEAL LESIONS -- In fact papillomatosis IS A LARYNGEAL DISEASE = Laryngeal papillomatosis, an already rare entity, which EXTENDS inferiorly to involve the trachea in just 5% of cases. When it does, it is called TRACHEOBRONCHIAL PAPILLOMATOSIS.

Front 11

Is papillomatosis more common in adults or peds?

Back 11

ADULTS -- one needs time to acquire the virus, and then time for it to work its magic

Front 12

Tree in bud in patient with history of HIV

Back 12

TB


Fungal


Bacterial

Front 13

Hazy ground glass opacity limited to a lung zone

Back 13

Can be viral pneumonia

Front 14

Same appearance in patient who is s/p renal or other solid organ transplant

Back 14

CMV Pneumonia


PCP IS NOT COMMON POST TRANSPLANT DUE TO PROPHYLAXIS

Front 15

Anterior mediastinal mass in patient with CABG clips

Back 15

THINK SAPHENOUS GRAFT PSEUDOANEURYSM or ANEURYSM


Confirm finding with CT


TYPICALLY HAVE A LOT OF CLOT PERIPHERALLY WITHIN THE GRAFT

Front 16

Difference between saphenous graft aneurysm and pseudoaneurysm?

Back 16

PSEUDOANEURYM is more common, occurs at the anastomotic site, and occurs weeks to months post op


ANEURYSM occurs later, usually 5 years or more post op

Front 17

DDx perilymphatic nodules

Back 17

Sarcoidosis


Lymphangitic carcinomatosis


Lymphoma


Kaposi sarcoma

Front 18

Perilymphatic nodule distribution

Back 18

All the places lymphatics like to be


Pleural surfaces


Along bronchovascular bundles

Front 19

Where do sarcoid nodules predominate

Back 19

Along bronchovascular bundles, less so along pleural surfaces

Front 20

Characteristic finding in sarcoid

Back 20

AIR TRAPPING on expiratory CT examinations, looking like mosaic attenuation pattern

Front 21

Appearance of pulmonary findings in amiodarone toxicity

Back 21

2 DISTINCT PATTERNS


1) Diffuse interstitial disease

or


2) Hyperdense subpleural nodules


BUT BOTH WILL BE ASSOCIATED WITH HYPERDENSE LIVER, SO ASK TO SEE CT IMAGE THROUGH LIVER

Front 22

Cystic thymic mass

Back 22

THYMIC CYST -- can be congenital or acquired based on HIV or radiation treatment for Hodgkin's

Front 23

Cystic and solid thymic mass

Back 23

Thymoma and Hodgkins can both contain cystic areas


of course germ cell tumors (Teratoma) do too -- but they should also have fat and calcium to clinch the diagnosis

Front 24

Tracheal bronchus

Back 24

SERVES THE RIGHT UPPER LOBE


Complication usually only occurs with intubation, resulting in atelectasis

Front 25

DDx peripheral consolidations

Back 25

Pulmonary infarcts


Vasculitis


Chronic eosinophilic pneumonia


Lofflers


BOOP

Front 26

Which one of these is special?

Back 26

BOOP -- it has BOTH peripheral AND peribronchovascular involvement -- SO, think of BOOP as the consolidation equivalent of perilymphatic nodular distribution (minus the fissural involvement)

Front 27

Unresectable tracheal mass

Back 27

RECOMMEND STENTING

Front 28

Indications for tracheal stent

Back 28

Palliative treatment of malignancy


External tracheal compression


Congenital tracheal stenosis


Tracheobronchomalacia


Tracheal stricture or narrowing post-intubation or from other inflammatory/infectious process


Anastomotic narrowing post lung transplantation

Front 29

How does tracheobronchial stent work?

Back 29

Become epithelialized, so they do not limit ciliary motility.


BUT they become incorporated into the wall, so removal is not simple

Front 30

Complications of tracheobronchial stent

Back 30

Migration


Fracture or fragmentation (patient presents with wire fragments in sputum)


Collapse


Erosion through airway

Front 31

Placement of stent

Back 31

1) CT with multiplanar reformats to determine location, severity, length, and number of stenoses


2) Place it fluoroscopically


3) Follow it up with imaging

Front 32

Beaking of a pulmonary artery

Back 32

FIRST THOUGHT IS ACUTE PE


Pulmonary artery sarcoma


Hilar or mediastinal mass with compression

Front 33

V/Q scan with perfusion absent in one lung

Back 33

DO NOT THINK ACUTE PE FIRST, as it is uncommon to have acute PE present as a single large unilateral main PA obstruction


THINK -- Mediastinal or hilar mass causing vascular obstruction, but not yet compressing the airway, so that ventilation scan still shows exchange.


Aneurysm or dissection of ascending aorta


Pulmonary artery hypoplasia or agenesis


Pulmonary artery sarcoma


If both V and Q gone, then pneumonectomy

Front 34

Thinner and fewer pulmonary vessels

Back 34

ALPHA-1 ANTITRYPSIN

causes appearance of:

SIMPLIFICATION OF LUNG ARCHITECTURE



BASILAR PREDOMINANT

Front 35

What is it associated with

Back 35

Mild bronchiectasis


CIRRHOSIS

Front 36

What is the pathophysiology

Back 36

Alpha 1 antitrypsin is an inhibitor of proteases. When deficient because a patient is homozygous for this disorder, the proteases go unchecked, eating away at lung. Smoking makes things even worse.

Front 37

cases 124-131 not

Back 37

represented

Front 38

Soft tissue separating left and right atria

Back 38

Is it fatty?


LIPOMAOUS HYPERTROPHY of the INTERATRIAL SEPTUM

Front 39

CXR with smaller vessels in one lung

Back 39

SWYER JAMES -- unilateral hyperlucent lung of obliterative bronchiolitis

Front 40

What is cause of Swyer James

Back 40

VIRAL PNEUMONIA in infancy or early childhood resulting in obliterative bronchiolitis and abnormal lung development.

Front 41

What are the findings in Swyer James?

Back 41

Slightly smaller ipsilateral hemithorax


Decreased vessel size


Mild bronchiectasis evident on CT


Areas of air trapping evident on CT, accentuated in expiration scanning.

Front 42

Cylindrical bronchiectasis with few nodules, mainly affecting mid to lower lungfields.

Back 42

THINK MAI IN IMMUNOCOMPETENT ELDERLY FEMALE

Front 43

MAI

Back 43

May affect immunocompromised hosts, like severely compromised AIDS patients, BUT, classically affects the elderly.


The classic form of the disease affects elderly men who are mildly immunocompromised due to COPD. They present radiographically with changes identical to progressive reactivation TB, with cavitation and fibrosis predominantly affecting the apical and posterior segments of the upper lobe, and superior segment of lower lobe.


The other group commonly affected by MAI is elderly women. They are immunocompetent, with no history of COPD. Their imaging findings are different than in the men, simply developing centrilobular nodules and cylindrical bronchectasis. Their disease affects the lingula and right middle lobe.

Front 44

Mass lateral to aortic arch

Back 44

SACCULAR AORTIC ANEURYSM



Vertical vein of TAPVR


Left sided SVC

Front 45

Black blood imaging

Back 45

SPIN ECHO

Front 46

White blood imaging

Back 46

GRADIENT ECHO

or

Gadolinium enhanced MRA

Front 47

Diffuse tracheobronchial narrowing with auricular abnormalities

Back 47

Relapsing polychondritis

Front 48

Diffuse tracheobronchial narrowing

Back 48

Relapsing polychondritis


Tracheopathia osteochondroplastica


Wegeners


Amyloid


Sarcoid


Infection (TB, HPV = papillomatosis)

Front 49

Multiple tracheal masses

Back 49

Again . . .


Papillomatosis and Amyloid


Therefore, these 2 are causes of both multiple tracheal masses, AND of diffuse tracheobronchial narrowing

Front 50

Solitary enhancing mediastinal or hilar lymph node

Back 50

LIMITED DIFFERENTIAL versus nodes which do not significantly enhance


Most common cause is hypervascular metastatic disease (RCCA, thyroid, small cell lung CA)


The most common benign cause is CASTLEMAN's DISEASE

Front 51

Castleman's disease

Back 51

Benign lymphoproliferative disease


2 types: Hyaline vascular and plasma cell


Hyaline vascular (90%) -- Presents as solitary MARKEDLY ENHANCING (as suggested by the subtype name, hyaline VASCULAR) hilar or mediastinal lymphadenopathy



Plasma cell variety is less common, but has more diffuse involvement of nodes, more constitutional symptoms. Enhances, but not markedly like hyaline vascular variety.

Front 52

Miliary nodules

Back 52

TB


Thyroid CA


Renal Cell CA


Melanoma


Silicosis

Front 53

Calcified nodules

Back 53

Silicosis


Healed varicella


Healed histoplasmosis


Alveolar microlithiasis


Osteosarcoma mets


Thyroid Ca mets


Colon or other adenoCa mets

Front 54

Pulmonary hypertension

Back 54

Idiopathic pulmonary hypertension -- young to middle age women.



Chronic pulmonary embolism



Eisenmenger's -- chronic high flow resulting in intimal hyperplasia and eventual narrowing and increased resistance in the pulmonary circuit



Left heart failure, mitral regurg, mitral stenosis

Front 55

Dilated pulmonary arteries with differing areas of attenuation

Back 55

PROBABLY MURAL THROMBUS


Chronic pulmonary emboli

Front 56

Calcified pulmonary artery walls

Back 56

Calcification in mural thrombus is common in chronic PE

Front 57

Atelectasis of entire lung

Back 57

Hilar mass


Foreign body


Mucus plug


Endobronchial lesion

Front 58

Endobronchial lesion ddx

Back 58

Carcinoid


Mucoepidermoid


Lung CA


Lymphoma


Mets -- breast CA common

Front 59

critera for T1 lung nodule

Back 59

less than 3 cm

completely surrounded by lung or visceral pleura

Front 60

overinflation with poor vascularity

Back 60

EMPHYSEMA

Front 61

How is overinflation diagnosed

Back 61

Flattening of hemidiaphragms and increase in the retrosternal clear space

Front 62

Miliary pattern

Back 62

TB


Fungal infection


Mets (thyroid, melanoma)


sarcoid


E gran


Silicosis

Front 63

bilateral hilar adenopathy on CXR

Back 63

Lymphoma vs sarcoid.


How do you tell them apart? Go to CT. Look for mediastinal adenopathy. If mediastinal adenopathy is prominent, then it is probably lymphoma, not sarcoid.

Front 64

Tracheal stenosis

Back 64

short or long segment?

Front 65

Tracheal stenosis, short segment

Back 65

incubation/tracheostomy, Wegener's, extrinsic compression mass, TB (especially after erosion into airway by broncholith), sarcoidosis.

Front 66

Tracheal stenosis with thickening of cartilage rings

Back 66

Wegener's (short segment), relapsing polychondritis (long segment)

Front 67

tracheal stenosis with wall irregularity

Back 67

Wegener's, sarcoidosis, TB, amyloidosis

Front 68

subglottic stenosis

Back 68

Post intubation or tracheostomy, sarcoidosis

Front 69

tracheal wall calcification

Back 69

TB, amyloidosis, tracheobronchopathia osteochochondroplastica (TBO)

Front 70

tracheal or bronchial collapse on inspiration

Back 70

relapsing polychondritis, tracheobronchomegaly (large trachea, though)

Front 71

tracheal wall with dense calcifications in cartilagenous ring

Back 71

TBO

Front 72

diffuse tracheal and bronchial enlargement

Back 72

tracheobronchomegaly (Mournier Kuhn), collagen vascular diseases (scleroderma, lupus)

Front 73

widening of trachea on AP view, but narrowed on lateral

Back 73

saber sheath trachea

Front 74

cause of the saber sheath trachea

Back 74

COPD, most commonly emphysema

Front 75

focal diverticulum coming off of trachea

Back 75

tracheocele

Front 76

intrinsic tracheal mass

Back 76

primary tracheal tumor versus metastasis

Front 77

solitary intrinsic tracheal mass

Back 77

90% are malignant

Front 78

primary intrinsic tracheal tumors

Back 78

common -- Mucoepidermoid and adenoid cystic. Less common -- squamous cell carcinoma and carcinoid.

Front 79

Tracheal metastasis

Back 79

melanoma, RCCA, breast

Front 80

multiple noncalcified tracheal nodules

Back 80

laryngeal papillomatosis -- 5% of laryngeal papillomatosis involves endobronchial trachea as well

Front 81

endobronchial mass

Back 81

bronchogenic carcinoma and all of the tumors affecting trachea (adenoid cystic, Muco Epidermoid, metastases, squamous cell, carcinoid)

Front 82

extrinsic tumor invasion into trachea or large bronchus

Back 82

bronchogenic lung cancers, thyroid

Front 83

cystic bronchiectasis

Back 83

cystic fibrosis

Front 84

other forms of bronchiectasis

Back 84

varicose and cylindrical

Front 85

Mosaic perfusion

Back 85

must see different levels of attenuation as well as smaller vessels within the dark poorly perfused areas.

Front 86

Mosaic perfusion differential

Back 86

differential is small airways disease versus small vessel disease.

Front 87

Differentiate between them

Back 87

perform end-expiratory high-resolution C. T. to look for geographic areas of air trapping. If air trapping is present it is small airways disease. If air trapping is not present, it is small vessel disease.

Front 88

No air trapping is present on end-expiratory C. T.

Back 88

small vessel disease. Usually chronic PE.

Front 89

Air trapping is present on end-expiratory C. T.

Back 89

small airways disease. Differential for air trapping is asthma, bronchiolitis obliterans, and hypersensitivity pneumonitis. Can also be due to cystic fibrosis or small airways infection, however, other findings suggesting these entities would be present.

Front 90

Terminology on inspiratory versus excretory CT

Back 90

Mosaic perfusion on inspiratory, air trapping on expiratory.

Front 91

Plain film with numerous cystic lesions best seen centrally, lung expansion, with large anterior clear space on lateral view

Back 91

cystic fibrosis

Front 92

What should you expect to see on chest section

Back 92

cystic fibrosis.

Front 93

Thick walled cysts with Mosaic perfusion

Back 93

cystic fibrosis

Front 94

C. T. with numerous lung cysts

Back 94

immediately check to see if you can find any of the structures branching so you know it's not cystic lung disease. Also look at the general thickness of the walls. Wall thickness should not be so great in cystic lung disease but can be very great and cystic fibrosis. Often you can follow the tubular structures image to image.

Front 95

History of eosinophilia

Back 95

think ABPA. Also if there is history of chronic asthma or reactivity to Aspergillus antigen.

Front 96

Central bronchiectasis

Back 96

think ABPA. Bronchiectasis and cystic fibrosis goes close to the periphery whereas in ABPA it stays much more central the walls are thinner and there'll be evidence of mucoid impaction.

Front 97

High attenuation tubular structure

Back 97

think mucoid impaction

Front 98

nodular lung disease on C. T.

Back 98

immediately define pattern of distribution.