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What is the differential for SVC obstruction?
1) Tumor (Bronchogenic more commonly than lymphoma)


2) Fibrosing mediastinitis


3) Thrombus


4) Huge goiter
What are the causes of thrombosis of SVC?
Most commonly due to indwelling catheter, especially if there is catheter related infection.


Also occurs in hypercoag state (i.e. cancer, local infection)
What are the two most common causes of fibrosing mediastinitis in USA?
1) Histo



2) Tb
What is another common cause?
Drugs -- Methysergide
What else do those drugs cause?
Retroperitoneal fibrosis
What are systemic associations?
Sarcoidosis


Riedels thyroiditis


Sclerosing cholangitis
What structures are commonly involved?
1) SVC



2) esophagus



3) airways




4) Major pulmonary vessels -- can cause unilateral edema



5) thoracic duct -- chylothorax
What is DDx for left upper mediastinal mass appearing like a second (higher) aortic arch?
1) Pseudocoarctation



2) Coarctation



3) L Subclavian aneurysm



4) Lymphadenopathy



5) Primary mediastinal mass (i.e. duplication cyst)
What is pseudocoarctation?
Basically the aortic arch is bigger than it should be, and therefore extends higher up into chest than it should, and, since it still has attachment to the pulm artery, via ligamentum arteriosum, develops a kink at the place where it is tethered in.
Is there narrowing associated with pseudocoarc?
There can be, but there is no significant pressure differential (less than 10mmHg) across any stenosis that may be present.
When you see such an appearance, what should you immediately look for on the CXR?
Rib notching
Is there ever rib notching in pseudocoarc?
NO, otherwise it is not pseudo.
What is the appearance of pseudocoarc on CXR?
Looks like a 3, but the dent appears to be wider than for actual coarctation, which has a sharp dent.
What is the differential for long segment tracheal or bronchial narrowing?
1) Intubation injury / tracheobronchomalacia




2) Wegeners




3) Relapsing polychondritis




4) Papillomatosis (when extensive / severe)




5) Tracheobronchopathia osteochondroplastica




6) Tracheobronchial amyloidosis






7) Rhinoscleroma (a chronic granulomatous infection caused by Klebsiella rhinoscleromatis)
What is tracheobronchopathia osteochondroplastica?
A Rare, non-neoplastic disorder in which 2 to 5 mm osteocartilaginous nodules form within the trachea > bronchi.
What percent of patients are symptomatic?
Only 10%
What are the nodules?
Enchondroses
Where do they arise from?
Tracheobronchial cartilage rings
Where are the nodules not present?
Posteriorly, because no cartilage back there
As opposed to what?
Tracheobronchal amyloid, where there is no posterior sparing
What does the presence of fluid pockets and air fluid levels in the mediastinum diagnostic of?
Acute mediastinitis
What is the most common etiology?
Recent cardiac surgery
What is the next most common cause?
Esophageal perforation
What is another potential cause?
Extension of abscess from another region
What places?
Retropharyngeal space



Retroperitoneum



Chest wall



Hepatic abscess (traversing diaphragm)
In the most common cause, what additional findings are seen?
Sternotomy wires, usually with dehiscence and evidence of bony destruction.
What else is seen in this most common cause?
Fluid pockets extending both anterior and posterior to sternum
What are causes of proximal airway mass?
* carcinoid


* bronchogenic carcinoma


* adenoid cystic carcinoma


* mucoepidermoid carcinoma


* benign stromal tumor


* foreign body
What is the appearance of carcinoid tumor if more peripheral?
Lung nodule.
What are characteristics of carcinoid?
Enhance



Well circmscribed



20% calcify
What is differential diagnosis of numerous small pulmonary nodules
1) Miliary Tuberculosis



2) Thyroid mets



3) Varicella pneumonia



4) Silicosis



5) Sarcoidosis



6) Disseminated fungal infection (histoplasmosis, coccidioidomycosis)



7) Hypersensitivity Pneumonitis



8) Histiocytosis X



9) Pneumocystis (sometimes)



10) Alveolar Microlithiasis (calcified micronodules)
What is ddx for upper lobe predominant micronodular disease?
1) Silicosis



2) Varicella pneumonia



3) Sarcoidosis


4) Histiocytosis X
What is the appearance of Histiocytosis X?
Initial stage: Upper lobe predominant nodules in a bronchovascular distribution



Later stage: Nodules cavitate, forming cysts of variable wall thickness
What is the main differential for late stage histiocytosis X?
LAM
How do you make the distinction?
LAM does not have nodules associated with it, so if you see nodules, you know its not LAM, and likely Histiocytosis.



LAM has uniform thin-walled cysts.
What are patients who survive an acute PE at risk for?
Recurrent PE and the development of pulmonary hypertension
What are the signs of acute PE on CXR?
Westermark sign


Hamptons hump
What is Westermark sign?
Dilatation of pulmonary vessels proximal to a PE, with sharp cut-off (size diminishment) distal to the obstruction
What is Hampton's hump?
Segmental pleural-based infiltrate with apex of the wedge pointing to the hilum, consistent with pulmonary infarct.
What tracer is perfusion imaging performed with?
Technetium 99m macro-aggregated albumin.
What is the most commonly used ventilation agent?
Xenon 133

Half-life of and energy of
What is its half-life?
5.3 days.


Thus, requires special ventilation system to remove all xenon from room.
What is its energy?
81keV

(so, lower energy)
What do we use at Jacobi for ventilation?
Tc 99m labeled DTPA, performed before perfusion imaging (couldn't do after, because of microembolization, wouldn't be able to see anything), so there is problem of retention of aerosolized tracer in large airways.
What is the first thing you need to do when evaluating a lung scan?
Ask for a CXR
What is definition of normal V/Q scan?
No perfusion defects
What is the negative predictive value of a normal scan?
96%

Thus, 4% of patients with this pattern of scan will have a PE
What are criteria for low probability scan?
1) Nonsegmental defects



2) Any perfusion defect with much larger radiographic abnormality



3) Matched ventilation and perfusion defects with normal CXR



4) Small subsegmental perfusion defects
Basically, what do you need to remember about low probability scans?
1) Matched defects with clear CXR



2) Small (subsegmental) defects
What if the matched defect is large?
Still low probability
What is the definition of a small subsegmental defect?
Less than 25% of a segment
If there are multiple small subsegmental defects, what is special about this situation?
You don't even have to look at the ventilation images as long as all perfusion defects are less than 25% of segment size. It is low probability.
If you have decided that a scan is low probablility, what can you do next?
Then decide if it is also very low probability.
What are criteria for that?
If there are 3 or fewer of the small subsegmental defects.



If the nonsegmental defects can be attributed to heart, vessels, diaphragm, or small pleural effusions
What other findings make very low probability?
Triple match in upper lung zone



Triple match confined to single segment
What else?
Overanticoagulated patient
What is point of stripe sign?
Indicates that there is perfused lung peripheral to the defect, which cannot be due to vascular occlusion
What is a large defect?
> 75% of segment
What is moderate sized defect?
25-75% of segment
What is small defect?
Obvious
What is high probability scan?
2 or more large mismatched defects (or equivalent of 2 large if they add up to such and at least one is moderate or larger)
What is the other appearance that would be characterized as large?
Any perfusion defect substantially larger than radiographic abnormality
What is the most testable intermediate prob scan?
Triple match
What is triple match?
Moderate to large matching segmental defect with matching x-ray.
Why are defects substantially smaller than CXR abnormality considered low prob?
Because infiltrate related to infarct should be same size as perfusion defect. If larger, probably related to another type of pathology, such as pneumonia or contusion or hemorrhage, etc.
What is first step in evaluating V/Q scan?
Examine CXR performed within 24 hours
What do you do with CXR?
1) Look for radiographic signs of PE



2) Look for any alternative causes of symptoms (PTX, pneumonia)
What is done with all abnormalities found on CXR?
Classify as acute or chronic
What are acute abnormalities?
Atelectasis


Infiltrate


Effusions
Why these 3?
Because these are the lesions that could cause a triple match if a perfusion defect was found in same location
What else should you pay attention to?
Anything else that you would expect would cause nonsegmental defect on perfusion scan
Such as?
Cardiomegaly


Elevated diaphragm


Hilar enlargement
What is the next step?
Examine the ventilation scan just in the regions of the perfusion defects to look for matches
What is done after that?
Examine the CXR again just in the regions of the perfusion defects to look for matches
What is true of any moderate or large size perfusion defect without associated ventilation or CXR match?
Candidate for PE
How many moderate defects are equivalent to a large defect?
2
What would be considered high probability?
4 or more moderate equivalent unmatched defects
What would be considered intermediate prob?
1-3 moderate equivalent unmatched defects
What is low prob?
No moderate equivalent unmatched defects (no number of small defects adds up to a moderate defect)
What should you always consider when there is cardiomegaly?
Pericardial effusion must ALWAYS be in the differential!!!!!
What test would be ordered to rule out effusion?
CT or echo
On CT, what is differential for pericardial effusion?
Viral pericarditis


Myocardial rupture



Aortic dissection



Cardiac mass
What can be obscured by pericardial effusion on CT?
Cardiac mass, especially on unenhanced CT
What is the differential diagnosis for a cardiac mass with pericardial effusion?
1) Metastases (the most likely diagnosis)



2) Angiosarcoma




3) Pericardial mesothelioma




4) Lymphoma
What is more common, atrial myxoma or cardiac metastasis?
Metastasis.
How much more common are mets than all primary cardiac tumors combined?
10 to 20 X more common
What is the most common cardiac tumor?
Atrial myxoma
What percent of primary cardiac tumors does myxoma represent?
50%
What is the most common primary malignant cardiac tumor?
Angiosarcoma
What is the second most common primary malignant cardiac tumor?
Rhabdomyosarcoma
When considering thymic disease in the differential for anterior mediastinal masses, what is the array of possibilities that can originate from thymus?
Thymoma, thymic cyst (very rare), thymolipoma (lobulated), thymic hyperplasia (post chemo), thymic carcinoid, thymic carcinoma
What about lymphoma?
Hodgkins is common in the anterior mediastinum.
What about teratoma?
Happens. BUT, so do other germ cell tumors such as seminoma and choriocarcinoma.
What other entities besides the 4 Ts go in the differential?
1) Mesenchymal tumors


2) Mediastinal hematoma
What are the mesenchymal tumors occurring in the anterior mediastinum?
Lipoma


Liposarcoma


Leiomyoma
What is the clinical situation that you commonly think of with mediastinal hematoma?
Trauma
What is the most common primary mediastinal neoplasm in adults?
Lymphoma
What is the second most common mediastinal neoplasm in adults?
Thymoma
What finding that is sometimes seen in thymoma discriminates it from lymphoma?
Calcification
What percent of thymomas calcify?
20%
What is the most common benign anterior mediastinal germ cell tumor? Malignant?
Thymoma



Seminoma
What is the differential diagnosis for multiple cavitating masses/nodules?
Metastasis (esp treated or fast-growing)



Septic emboli



Necrotizing pneumonia / abscesses



Tuberculosis



Wegener’s granulomatosis



Fungal infection:
Aspergillus (tell-tale fungus ball within cavity)
Coccidioidal cavity (thin wall, no air-fluid level, no surrounding infiltrate)
Cryptococcus




Lymphoma (cavitating mass or masses)



Rheumatoid nodules
What is the differential diagnosis for thin walled cavity?
Pneumatocele




Bulla




Bronchogenic cyst



Coccidioides
What is appearance of Wegener's granulomatosis?
Discrete focal opacities that vary from nodular masses to ill-defined areas of consolidation, either of which may cavitate.


Cavities may be unilocular or multilocular.


Outer wall margins irregular.


Typically thick walls.
What other finding is associated with Wegener's?
Can have diffuse pulmonary hemorrage
What other finding is sometimes seen?
Tracheal narrowing
What is Churg Strauss syndrome?
Another ANCA associated vasculitis
In whom does it occur?
Only asthmatics
What is seen serologically?
Marked peripheral eosinophilia
What is lung appearance on CXR?
Peripheral non-fixed pulmonary consolidations
What is this just like?
Eosinophilic pneumonia (makes sense)
What is Loffler's syndrome?
Eosinophilic pneumonia
Is Loffler's chronic or acute?
Acute/subacute
How are Loffler's and chronic eosinophilc pneumonia differentiated?
Just by the duration that it lasts. Longer than one month is chronic EP.
Why is this distinction not useful?
Because they are all treated with steroids now, which limits their course
What is appearance of Loffler's on CXR?
One or more nonsegmental pulmonary consolidations that are transitory and/or migratory
What is NOT seen in Loffler's?
Pleural effusions



Adenopathy



Cavitation
What is the epidemiology of chronic eosinophilic pneumonia?
50% atopic


40% asthmatic
What is the appearance?
Bilateral basilar infiltrates
What is a way to describe it?
Photographic negative of pulmonary edema
If the whole lung is not rind encased, what part will be involved?
Upper zones more than lower zones
What is the most common cause of eosinophilic lung disease?
ABPA
Who gets ABPA?
Same crowd as chronic eosinophilic pneumonia -- atopic and/or asthmatic
What is the disease like clinically?
Relapsing remitting episodes of dyspnea, wheeze, and cough with small amounts of hemoptysis
What does it mimic clinically?
Asthma attack
What are the types of lung changes seen in ABPA?
Acute/transient changes as well as chronic/permanent changes
What are the acute/transient changes?
Consolidations


***Bronchoceles***


Atelectasis
What are the consolidations like?
Differ from eosinophilic pneumonias: Segmental and more central
What are bronchoceles?
Mucoid impaction, but the subtended segment stays open due to collateral air drift, and you get contrast of the mucus filled bronchus with air filled lung
Where do they occur?
Upper lung zones
What are they purported to look like?
Gloved fingers
What is the basic appearance?
Linear, sharply demarcated branched or unbranched bandlike shadows that point to the hilum
What are the permanent changes?
Bronchiectasis
What is the importance of this for boards?
When you see bronchiectasis, ABPA must be in the differential
What is hypersensitivity pneumonitis?
Repeated inhalation of organic antigens causes immunologic response in the air-exchange units of the lung
What is true of the disease appearance on imaging?
Pretty much looks the same regardless of causative agent
What are come causes?
Moldy hay -- farmer's lung



Moldy sugar cane -- Bagassosis



Droppings and feathers -- Bird fancier's lung
Where are the micronodules seen?
Diffusely
What is the appearance of the chronic phase?
Upper lobe scarring
What are the larger ring shadows due to?
(3 b's)



Bullae


Blebs


Bronchiectasis
Is this a serious disease?
YES. Up to 17% die from it.
What happens usually after a single attack?
If patient stays away from offending agent, changes usually resolve. But if chroinically exposed to, will go on to irreversible chronic disease.
What are the common lung findings in Rheumatoid Disease?
Interstitial pneumonia with fibrosis


Intrapulmonary nodules


Pleural thickening +/- effusion
What is the most common finding in rheumatoid?
Pleural thickening
What is the second most common finding?
Pleural effusion
What percent get effusion?
3%
What is the third most common finding?
Interstitial pneumonia
What is the pattern of interstitial pneumonia most commonly seen in patients with rheumatoid disease
UIP
What percent have UIP?
1.5%
What is actually a very rare finding in rheumatoid?
Nodules
When do they occur?
Advanced disease states
What can the nodules do?
Cavitate
What is the most common finding in Lupus?
Pleuritis, resulting in pleural effusion
What percent get it?
50%
What are the common intrapulmonary processes in Lupus?
Lupus pneumonitis



Pulmonary hemorrhage
What is the clinical setting of acute lupus pneumonitis?
Acute onset of life threatening hypoxia, fever, etc.
What is acute lupus pneumonitis an example of?
A more localized version of ARDS. Nevertheless, up to 50% mortality.
What is even more uncommon in lupus?
Clinically significant pulmonary hemorrhage.
What are symptoms/signs of pulm hemorrhage?
Hemoptysis


Drop in HCT
What is the appearance of pulm hemorrage?
Nonspecific bilateral airspace opacity. Can take on many patterns (mult acinar shadows, ill defined coalescent shadows, GGO, segmental/lobar consolidation).
What is a common finding in lupus?
Diaphragm dysfunction: Elevation of one or both hemidiaphragms. == Shrinking lungs.
Why is this thought to occur?
Diaphragmatic weakness due to myopathy
What is another process that occurs
Interstitial lung disease
What are the main causes of diffuse pulmonary hemorrhage?
Goodpastures



Wegeners



Lupus



Idiopathic primary pulmonary hemosiderosis




Coagulopathy
What is stage 0 sarcoid?
Normal CXR
What is the classic pattern of adenopathy in sarcoid?
Symmetric bilateral hilar adenopathy with som form of paratracheal adenopathy
Why is symmetric pattern important?
Because symmetric pattern is unlikely in the other diagnostic considerations for hilar enlargement
Which are?
Lymphoma


Tuberculosis



Metastatic disease
What differentiates hilar adenopathy from pulmonary artery enlargement?
The outer margin of the hila are lobulated in adenopathy.
If a patient is suspected to have sarcoid and CT reveals anterior and subcarinal mediastinal adenopathy, what does that mean?
Still can be sarcoid.


But if there is anterior adenopathy and NO associated symmetric hilar adenopathy, then it is NOT sarcoid, and lymphoma would be most likely dx.
How are the parenchymal changes of sarcoid divided?
Reversible changes and prefibrotic changes
What are the reversible changes of sarcoid?
(Reticulo)nodular opacities



Alveolar opacities



Large nocular disease
What are the most common of these changes?
By far (reticulo)nodular.


The most common appearance is small rounded or irregular opacities.
What percent of sarcoid patients with parenchymal dz have this pattern?
90%, thus essentially all patients with parenchymal disease will have this pattern.
What size are the nodules?
2 to 4 mm
What lung zones are they seen in?
All, with upper and middle zone predominance
What percent of patients with sarcoid get alveolar sarcoid?
15%
What do they look like?
bilateral multifocal opacities
Is there a regional predilection?
Can occur anywhere, but most common in peripheral lung mid lung zone
How common is large nodular disease?
Uncommon. Only 2% of pts. get it.
What is the appearance of large nodular sarcoid dz?
5 mm to 5 cm ill defined nodules, which can coalesce with one another.
Where are they located?
Again, anywhere but more common peripheral midlung zones
What is a special feature of alveolar and large nodular sarcoid?
BOTH FORMS CAN CAVITATE
What are the irreversible changes?
As reversible lesions heal, they can go away completely or heal by fibrosis. The fibrotic changes are permanent.
What is the appearence of fibrotic changes in sarcoid?
Coarse lines radiating from the hilum to the middle and upper lung zones
What is sarcoid called when it gets to this stage?
Stage III to IV (fibrosis)
what is a common benign complication of fibrotic disease of sarcoid?
Mycetoma
What is pathology of langerhans cell histiocytosis (LCH)?
Diffuse destructive disorder of distal airways caused by granulomas

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