case review chest
Terms
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- Mosaic attenuation on lung CT
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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
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CYST WITHIN A CYST APPEARANCE, or WATER LILY SIGN
= HYDATID DISEASE OF THE LUNG - Hydatid disease
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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
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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
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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
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Again . . .
Papillomatosis and Amyloid
Therefore, these 2 are causes of both multiple tracheal masses, AND of diffuse tracheobronchial narrowing - 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
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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
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CMV Pneumonia
PCP IS NOT COMMON POST TRANSPLANT DUE TO PROPHYLAXIS - Anterior mediastinal mass in patient with CABG clips
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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?
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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
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Sarcoidosis
Lymphangitic carcinomatosis
Lymphoma
Kaposi sarcoma - Perilymphatic nodule distribution
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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
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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
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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
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SERVES THE RIGHT UPPER LOBE
Complication usually only occurs with intubation, resulting in atelectasis - DDx peripheral consolidations
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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
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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?
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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
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Migration
Fracture or fragmentation (patient presents with wire fragments in sputum)
Collapse
Erosion through airway - Placement of stent
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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
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FIRST THOUGHT IS ACUTE PE
Pulmonary artery sarcoma
Hilar or mediastinal mass with compression - V/Q scan with perfusion absent in one lung
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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
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ALPHA-1 ANTITRYPSIN
causes appearance of:
SIMPLIFICATION OF LUNG ARCHITECTURE
BASILAR PREDOMINANT - What is it associated with
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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
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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?
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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
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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
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SACCULAR AORTIC ANEURYSM
Vertical vein of TAPVR
Left sided SVC - Black blood imaging
- SPIN ECHO
- White blood imaging
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GRADIENT ECHO
or
Gadolinium enhanced MRA - Diffuse tracheobronchial narrowing with auricular abnormalities
- Relapsing polychondritis
- Diffuse tracheobronchial narrowing
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Relapsing polychondritis
Tracheopathia osteochondroplastica
Wegeners
Amyloid
Sarcoid
Infection (TB, HPV = papillomatosis) - Solitary enhancing mediastinal or hilar lymph node
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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
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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
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TB
Thyroid CA
Renal Cell CA
Melanoma
Silicosis - Calcified nodules
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Silicosis
Healed varicella
Healed histoplasmosis
Alveolar microlithiasis
Osteosarcoma mets
Thyroid Ca mets
Colon or other adenoCa mets - Pulmonary hypertension
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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
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PROBABLY MURAL THROMBUS
Chronic pulmonary emboli - Calcified pulmonary artery walls
- Calcification in mural thrombus is common in chronic PE
- Atelectasis of entire lung
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Hilar mass
Foreign body
Mucus plug
Endobronchial lesion - Endobronchial lesion ddx
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Carcinoid
Mucoepidermoid
Lung CA
Lymphoma
Mets -- breast CA common - critera for T1 lung nodule
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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
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TB
Fungal infection
Mets (thyroid, melanoma)
sarcoid
E gran
Silicosis - bilateral hilar adenopathy on CXR
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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.