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98 Cards in this Set

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Mosaic attenuation on lung CT
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.
Common cause of small vessel disease
Chronic pulmonary emboli
Common cause of small airways disease
Obliterative bronchiolitis post infectious (i.e. Swyer-James, but localized to just a segment)
Cystic lung space with air-fluid level and another cyst on top of the air-fluid level
CYST WITHIN A CYST APPEARANCE, or WATER LILY SIGN

= HYDATID DISEASE OF THE LUNG
Hydatid disease
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.
Small airways disease
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
Tree in bud
Infectious bronchiolitis, with causes such as RSV, adenovirus and Mycoplasma


TB


Fungal pneumonia
Small fine nodules in lung
LOOK FOR THE PATTERN IMMEDIATELY
Septal thickening, ground glass opacity, and mildly enlarged pulmonary arteries
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.
Multiple tracheal masses
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.
Is papillomatosis more common in adults or peds?
ADULTS -- one needs time to acquire the virus, and then time for it to work its magic
Tree in bud in patient with history of HIV
TB


Fungal


Bacterial
Hazy ground glass opacity limited to a lung zone
Can be viral pneumonia
Same appearance in patient who is s/p renal or other solid organ transplant
CMV Pneumonia


PCP IS NOT COMMON POST TRANSPLANT DUE TO PROPHYLAXIS
Anterior mediastinal mass in patient with CABG clips
THINK SAPHENOUS GRAFT PSEUDOANEURYSM or ANEURYSM


Confirm finding with CT


TYPICALLY HAVE A LOT OF CLOT PERIPHERALLY WITHIN THE GRAFT
Difference between saphenous graft aneurysm and pseudoaneurysm?
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
DDx perilymphatic nodules
Sarcoidosis


Lymphangitic carcinomatosis


Lymphoma


Kaposi sarcoma
Perilymphatic nodule distribution
All the places lymphatics like to be


Pleural surfaces


Along bronchovascular bundles
Where do sarcoid nodules predominate
Along bronchovascular bundles, less so along pleural surfaces
Characteristic finding in sarcoid
AIR TRAPPING on expiratory CT examinations, looking like mosaic attenuation pattern
Appearance of pulmonary findings in amiodarone toxicity
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
Cystic thymic mass
THYMIC CYST -- can be congenital or acquired based on HIV or radiation treatment for Hodgkin's
Cystic and solid thymic mass
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
Tracheal bronchus
SERVES THE RIGHT UPPER LOBE


Complication usually only occurs with intubation, resulting in atelectasis
DDx peripheral consolidations
Pulmonary infarcts


Vasculitis


Chronic eosinophilic pneumonia


Lofflers


BOOP
Which one of these is special?
BOOP -- it has BOTH peripheral AND peribronchovascular involvement -- SO, think of BOOP as the consolidation equivalent of perilymphatic nodular distribution (minus the fissural involvement)
Unresectable tracheal mass
RECOMMEND STENTING
Indications for tracheal stent
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
How does tracheobronchial stent work?
Become epithelialized, so they do not limit ciliary motility.


BUT they become incorporated into the wall, so removal is not simple
Complications of tracheobronchial stent
Migration


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


Collapse


Erosion through airway
Placement of stent
1) CT with multiplanar reformats to determine location, severity, length, and number of stenoses


2) Place it fluoroscopically


3) Follow it up with imaging
Beaking of a pulmonary artery
FIRST THOUGHT IS ACUTE PE


Pulmonary artery sarcoma


Hilar or mediastinal mass with compression
V/Q scan with perfusion absent in one lung
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
Thinner and fewer pulmonary vessels
ALPHA-1 ANTITRYPSIN

causes appearance of:

SIMPLIFICATION OF LUNG ARCHITECTURE



BASILAR PREDOMINANT
What is it associated with
Mild bronchiectasis


CIRRHOSIS
What is the pathophysiology
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.
cases 124-131 not
represented
Soft tissue separating left and right atria
Is it fatty?


LIPOMAOUS HYPERTROPHY of the INTERATRIAL SEPTUM
CXR with smaller vessels in one lung
SWYER JAMES -- unilateral hyperlucent lung of obliterative bronchiolitis
What is cause of Swyer James
VIRAL PNEUMONIA in infancy or early childhood resulting in obliterative bronchiolitis and abnormal lung development.
What are the findings in Swyer James?
Slightly smaller ipsilateral hemithorax


Decreased vessel size


Mild bronchiectasis evident on CT


Areas of air trapping evident on CT, accentuated in expiration scanning.
Cylindrical bronchiectasis with few nodules, mainly affecting mid to lower lungfields.
THINK MAI IN IMMUNOCOMPETENT ELDERLY FEMALE
MAI
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.
Mass lateral to aortic arch
SACCULAR AORTIC ANEURYSM



Vertical vein of TAPVR


Left sided SVC
Black blood imaging
SPIN ECHO
White blood imaging
GRADIENT ECHO

or

Gadolinium enhanced MRA
Diffuse tracheobronchial narrowing with auricular abnormalities
Relapsing polychondritis
Diffuse tracheobronchial narrowing
Relapsing polychondritis


Tracheopathia osteochondroplastica


Wegeners


Amyloid


Sarcoid


Infection (TB, HPV = papillomatosis)
Multiple tracheal masses
Again . . .


Papillomatosis and Amyloid


Therefore, these 2 are causes of both multiple tracheal masses, AND of diffuse tracheobronchial narrowing
Solitary enhancing mediastinal or hilar lymph node
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
Castleman's disease
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.
Miliary nodules
TB


Thyroid CA


Renal Cell CA


Melanoma


Silicosis
Calcified nodules
Silicosis


Healed varicella


Healed histoplasmosis


Alveolar microlithiasis


Osteosarcoma mets


Thyroid Ca mets


Colon or other adenoCa mets
Pulmonary hypertension
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
Dilated pulmonary arteries with differing areas of attenuation
PROBABLY MURAL THROMBUS


Chronic pulmonary emboli
Calcified pulmonary artery walls
Calcification in mural thrombus is common in chronic PE
Atelectasis of entire lung
Hilar mass


Foreign body


Mucus plug


Endobronchial lesion
Endobronchial lesion ddx
Carcinoid


Mucoepidermoid


Lung CA


Lymphoma


Mets -- breast CA common
critera for T1 lung nodule
less than 3 cm

completely surrounded by lung or visceral pleura
overinflation with poor vascularity
EMPHYSEMA
How is overinflation diagnosed
Flattening of hemidiaphragms and increase in the retrosternal clear space
Miliary pattern
TB


Fungal infection


Mets (thyroid, melanoma)


sarcoid


E gran


Silicosis
bilateral hilar adenopathy on CXR
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.
Tracheal stenosis
short or long segment?
Tracheal stenosis, short segment
incubation/tracheostomy, Wegener's, extrinsic compression mass, TB (especially after erosion into airway by broncholith), sarcoidosis.
Tracheal stenosis with thickening of cartilage rings
Wegener's (short segment), relapsing polychondritis (long segment)
tracheal stenosis with wall irregularity
Wegener's, sarcoidosis, TB, amyloidosis
subglottic stenosis
Post intubation or tracheostomy, sarcoidosis
tracheal wall calcification
TB, amyloidosis, tracheobronchopathia osteochochondroplastica (TBO)
tracheal or bronchial collapse on inspiration
relapsing polychondritis, tracheobronchomegaly (large trachea, though)
tracheal wall with dense calcifications in cartilagenous ring
TBO
diffuse tracheal and bronchial enlargement
tracheobronchomegaly (Mournier Kuhn), collagen vascular diseases (scleroderma, lupus)
widening of trachea on AP view, but narrowed on lateral
saber sheath trachea
cause of the saber sheath trachea
COPD, most commonly emphysema
focal diverticulum coming off of trachea
tracheocele
intrinsic tracheal mass
primary tracheal tumor versus metastasis
solitary intrinsic tracheal mass
90% are malignant
primary intrinsic tracheal tumors
common -- Mucoepidermoid and adenoid cystic. Less common -- squamous cell carcinoma and carcinoid.
Tracheal metastasis
melanoma, RCCA, breast
multiple noncalcified tracheal nodules
laryngeal papillomatosis -- 5% of laryngeal papillomatosis involves endobronchial trachea as well
endobronchial mass
bronchogenic carcinoma and all of the tumors affecting trachea (adenoid cystic, Muco Epidermoid, metastases, squamous cell, carcinoid)
extrinsic tumor invasion into trachea or large bronchus
bronchogenic lung cancers, thyroid
cystic bronchiectasis
cystic fibrosis
other forms of bronchiectasis
varicose and cylindrical
Mosaic perfusion
must see different levels of attenuation as well as smaller vessels within the dark poorly perfused areas.
Mosaic perfusion differential
differential is small airways disease versus small vessel disease.
Differentiate between them
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.
No air trapping is present on end-expiratory C. T.
small vessel disease. Usually chronic PE.
Air trapping is present on end-expiratory C. T.
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.
Terminology on inspiratory versus excretory CT
Mosaic perfusion on inspiratory, air trapping on expiratory.
Plain film with numerous cystic lesions best seen centrally, lung expansion, with large anterior clear space on lateral view
cystic fibrosis
What should you expect to see on chest section
cystic fibrosis.
Thick walled cysts with Mosaic perfusion
cystic fibrosis
C. T. with numerous lung cysts
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.
History of eosinophilia
think ABPA. Also if there is history of chronic asthma or reactivity to Aspergillus antigen.
Central bronchiectasis
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.
High attenuation tubular structure
think mucoid impaction
nodular lung disease on C. T.
immediately define pattern of distribution.