Chest Flashcards
The Lateral CXR
Right Ribs vs Left Ribs
By convention, lateral CXRs are taken in the left lateral position (left side against the x-ray film/cassette). Therefore, the left ribs will not be magnified (right ribs will be magnified). Right ribs also project more posteriorly. Another strategy is to follow the diaphragm over the stomach bubble (usually left sided).
The Lateral CXR
Normal Hilum on Lateral
If you put your finger in the “Dark Hole ” - which is the left upper lobe b ro n c h u s , in front of it will be the right PA, and overtop o f it w ill be the left PA. The posterior wall o f the bronchus intermedius runs through the black hole, and can be thickened by edema.
Normal Hilum on Frontal:
right side
Top to bottom
Truncus anteior
superior pulmonary vein
hilar angle or hila point (where the vein and artery cross) (also at the same level of the upper lobe)
Right interlobar artery (runs parallel to the bronchus intermedius, less than 15-16 mm away)
Normal Hilum on Frontal:
left side
The left hilar point should always be
around 1cm higher than the right
Retrotracheal Triangle
Raider Triangle
This is a triangle which sits on the aortic arch and is bordered anteriorly by the back wall of the trachea, and posteriorly by the upper thoracic vertebral bodies. Many things can obliterate this, but for the purpose of multiple choice tests an opacity in the Raider Triangle is an Aberrant right subclavian artery.
The Lateral CXR, heart valves
pulmonary is on the top center
aorta middle middle
tricuspid anterior low
mitral posterior low
frontal CXR, heart valves
pulmonary top left
aorta middle middle
tricuspid lower right
mistral lower left
what heart valve is the most superior
pulmonic
what heart valve is most anterior
tricuspid
is the aorta anterior or posterior to the mitral on the lateral
anterior
pointy part of mechanical valves points towards or away of blood flow
towards
mitral valve is smaller or larger than the aortic
larger
Azygos Lobe Fissure
This is considered variant anatomy. These things happen when the azygos vein is displaced laterally during development. The result is a deep fissure in the right upper lobe. It’s not actually an accessory lobe but rather a variant of the right upper lobe. If they show you one, I suspect the question will revolve around the pleura. Something like “how many layers of pleura? ” The answer is 4.
Segments on the right
10 segments (3 upper, 2 middle, and 5 lower).
segments on the left
8 (4 upper lobe / lingula, and 4 lower lobe).
Right lung upper segments
apical
anterior
posterior
right lung middle segments
medial and lateral
right lung lower segments
superior posterior lateral anterior basal medial basal
Left lung upper segments
anterior
apical-posterior
left lung lingular segments
superior
inferior
left lung lower segments
superior
anterior-medial -basal
lateral
posterior
Pig Bronchus
Tracheal Bronchus
Bronchus that comes right o ff the trachea (prior to bifurcation into right and left mainstem).
Means nothing clinically, but occasionally people can get some air trapping or recurrent infections from impaired ventilation.
Trigger: Recurrent RUL Pneumonia in kid.
Cardiac Bronchus
Bronchus that comes o ff bronchus intermedius, opposite to the origin o f the right upper lobe bronchus In, contrast to the Pig Bronchus this thing is often blind ending - and supposedly represents the only true supernumerary bronchus
Similar to the pig bronchus, it means nothing clinically, but occasionally people can get recurrent infections
Superior mediastinal border
The inferior border is the oblique plane from the stemal-manubrial junction.
Anterior mediastinal border
The posterior border is the pericardium
Middle mediastinal border
The heart, pericardium, and bifurcation o f the trachea are all included. On lateral CXR, people sometimes say posterior to the trachea, and anterior to the vertebral bodies (or 1cm posterior to the vertebral bodies).
Posterior mediastinal border
From the back o f the heart to the spine. Contains the esophagus, thoracic duct, and descending aorta.
Mediastinal Variant Anatamy
pulmonary veins
Pulmonary vein anatomy is highly variable. You typically have 4 total (2 right - upper and lower, 2 left - upper and lower). The most common anatomic variation is a separate vein draining the right middle lobe (seen 30% o f the time). Who cares??? Two people (1) People who write multiple choice tests, (2) Electrophysiologists prior to ablations.
Mediastinal Variant Anatamy
Proximal Interruption of the Pulmonary Artery:
Basically you have congenital absence o f the right (or left) PA with the more distal pulmonary vasculature present. It’s also called unilateral absence o f the PA, but that is confusing because the distal pulmonary vasculature is present.
Mediastinal Variant Anatamy
Proximal Interruption of the Pulmonary Artery:
how it could be shown
Classically with volume loss o f one hemi-thorax (could be on CXR or CT), then a contrast CT shot through the heart with only one PA. Normally, you might think one PA is just volume averaging - but once you’ve been shown volume loss on one side your suspicion for this should be raised.
Mediastinal Variant Anatomy
Proximal Interruption of the Pulmonary Artery:
trivia
- It’s seen on the opposite side o f the aortic arch (Absent right PA with left-sided aortic arch, Absent left PA with right-sided aortic arch).
- Associated with PDA
- Interrupted left PA is associated with TOF and Truncus
Atelectasis (incomplete lung expansion) exists on a scale of
tiny horizontal “plate-like” / “discoid” subsegmental to complete collapse of the lung (lobar).
the degree of collapse depends on the location of obstuction (peripheral vs central)
Atelectasis
Obstructive
Absorptive
- Result o f complete obstruction o f an airway
- No new air can enter and any air that is already there is eventually absorbed leaving a collapsed section o f lung
- Causes: Obstructing neoplasms, mucous plugging in asthmatics or critically ill patients, and foreign body aspiration.
Atelectasis
Compressive
Relaxation / Passive
- Results from direct mass • effect on the lung
- Causes: Most classically seen adjacent to a pleural effusion. Could also be seen from adjacent compression o f lung from a mass, hiatal hernia, or a large bleb - anything directly pushing on the lung.
Atelectasis
Fibrotic
Cicatrization
Results from scarring / fibrosis which fails to allow the lung to collapse completely.
Causes: Most classic is TB , but scarring from radiation, other infections, or really any other cause o f fibrosis can do this.
Atelectasis
Adhesive
- Results from loss o f surface tension / inadequate pleural adherence o f the alveolar walls - from a surfactant deficiency.
- Alveoli become unstable and collapse.
- Causes: RDS (premature infants), ARDS (more diffuse pattern), and in the setting o f pulmonary embolism (loss o f blood flow / lack o f CO2 disrupts integrity o f surfactant).
Atelectasis
Primary and secondary signs
Another easily testable topic related to atelectasis are the primary and secondary signs. The big 3 ones being shadow, silhouette, and shift. Just like any normal person would, when I think of the word “shadow,” I immediately think of either Lamont Cranston (hypnotist and master detective), or Carl Jung’s “Phenomenology of the Self.” I’m sure you do too. However, in the case of atelectasis “shadow” refers to the shadow made by the opacified (collapsed lung). This is the direct sign, The silhouette refers to the loss of interface between this opacity and the adjacent normal structures. This is useful in localization. The shift refers to the movement of structures as they are “pulled” towards the site of volume loss. Remember, space occupying things (tumors, pneumonia, pleural effusion, cavitary lesions, etc…) push things away. Atelectasis is a volume losing process - so it pulls (examples - pulling the right hilar point above the left, pulling the left hilar point below the right, shifting the mediastinum, etc…).
Atelectasis
Right middle lobe
- Classic look is increased density at the right heart border with loss of that border (shadow and silhouette)
- The lateral will show anterior density over the heart (as the RML is anterior)
Atelectasis
Right Middle Lobe Syndrome:
Chronic collapse of the RML is classically
described with MAI infection in an elderly women who is too proper too cough (Lady Windermere syndrome). On CT you’d see additional findings of small nodules and bronchiectasis - with additional involvement of the Lingula.
Atelectasis
Right Lower Lobe:
- Classic look is increased density at the right heart border similar to collapse of the RML.
- The critical distinction is the right heart border. You should NOT lose the border of the right heart with RLL collapse. In fact it should be easier to see from compensatory hyper-expansion of the
RML.
Atelectasis
Right lower lobe superior triangle sign
In some cases, the mediastinal vessels are pulled to the right creating a triangle of opacity to the right of the trachea (Superior Triangle Sign)
Atelectasis
Right Lower Lobe + Right Middle Lobe:
- Uncommon Combination and a Sneaky Move
- The trick is a loss of visualization of the right hemidiaphragm and right heart border
Atelectasis
Right upper lobe
- Closes like a fan attached at the Hilum
- Horizontal Fissure may bow upward
- Hilum may elevate
- The lateral will again show this hilar attachment with the lobe collapsing from both the anterior
and posterior directions. - The top half of the oblique fissure will be pulled anterior.
Atelectasis
S Sign of Golden
Refers to a reverse “S” shape that the minor fissure in cases of RUL collapse resulting from a central obstructing mass.
Atelectasis
Left Upper Lobe
- This is different than the right upper lobe (which collapsed like a fan making a dense wedge shaped opacity.
- The LUL tends to be more subtle with a subtle increased density medially. There won’t be any well defined borders
- A hint may be non-visualization of the aortic knob.
- Sometimes (if you are lucky) you can get some nonspecific peaking of the diaphragm from upward traction
Atelectasis
luftsichel sign
“Air Sickle” - appearance from the lucent stripe appearance of the hyper inflated superior (apical) segment of the lower lobe pinned between the medial edge of the collapsed segment and the aortic arch
Atelectasis
Left Lower Lobe
- Can Be sneaky on a frontal only (opacity is hidden behind the heart)
- The lateral makes it more obvious with a posteriorly directed triangular opacity
Atelectasis
left lower lobe flat waist
The Flat Waist Sign - has been used as a description of the flattened appearance of the contours of the hilum and heart border.
Posterior junction line
above the clavicles
Cervicothoracic sign
This takes advantage of the posterior
junction line, which demonstrates that
things above the clavicles are in the
posterior mediastinum.
Hilum Overlay Sign
Mass at the level o f the hilum arising from the hilum will obliterate the silhouette o f the pulmonary vessels. If you can see the edge o f the vessels through the mass, then the mass is not in the hilum (so it is either anterior or posterior).
Pulmonary vs Mediastinal Origin
The easiest trick is if they show you air bronchograms. Only a pulmonary mass will have air bronchograms. The harder trick is the angle with the lung. The mass will make an acute angle with the lung if it’s within the lung. The mass will make an obtuse margin with the lung if it’s in the mediastinum.
Pulmonary origin
-makes an acute angle with the lung
Mediastinal origin
-makes an obtuse angle with the lung
Strep Pneumo
Lobar Consolidation
Favors lower lobes. Can be severe in sickle cell
patients post splenectomy. The most common
cause of pneumonia in AIDS patient.
Staph A.
Bronchopneumonia -
patchy opacities
Often bilateral, and can make abscess. Can be
spread via the blood in endocarditis patients
Anthrax
Hemorrhagic lymphadenitis,
mediastinitis, and
hemothorax
Classic Look: Mediastinal widening with pleural
effusion in the setting of bio-terrorism
Klebsiella
Buzzword: “Bulging Fissure” from exuberant inflammation. More likely to have pleural effusions, empyema, and cavity than conventional pneumonia.
Alcoholic and Nursing Home Patients.
Step 1 Buzzword was “currant jelly sputum”
H Flu
Usually bronchitis,
sometimes bilateral lower
lobe bronchopneumonia
Seen in COPDers, and people without a spleen
Pseudomonas
Patchy opacities, with abscess
formation
ICUers on a ventilator (also CF and Primary
Ciliary Dyskinesia). Pleural effusions are
common, but usually small
Legionella
Peripheral and sublobar
airspace opacity
Seen in COPDers, and around crappy air
conditioners. Only cavitates in immunosuppressed
patients. X-ray tends to lag behind resolution of
symptoms.
Aspiration
Anaerobes, with airspace
opacities. They can cavitate,
and abscess is not uncommon
Posterior lobes if supine when aspirating, Basal
Lower lobes in upright aspiration May favor the
right side, just like an ET tube. The most common
complication is empyema (which can get a
bronchopleural fistula).
Actinomycosis
Airspace in peripheral lower
lobes. Can be aggressive and
cause rib osteomyelitis/
invade adjacent chest wall.
Classic story is dental procedure gone bad, leading
to mandible osteo, leading to aspiration.
Mycoplasma
Fine reticular pattern on
CXR, Patchy airspace opacity
with tree-in-bud
Post Bone Marrow Transplant
overview
You see pulmonary infections in nearly 50% of people
after bone marrow transplant, and this is often listed as the most common cause of death in this
population. Findings are segregated into: early neutropenic, early, and late - and often tested as such.
Post Bone Marrow Transplant Graft vs Host
acute
Acute (20-100 Days)
Favors extrapulmonary systems (skin, liver, GI tract)
Post Bone Marrow Transplant Graft vs Host
chronic
Chronic (> 100 days)
Lymphocytic Infiltration of the airways and obliterative bronchiolitis.
Post Bone Marrow Transplant (Pulmonary Findings)
early neutropenic
(0-30 days
Pulmonary Edema, Flemorrhage,
Drug Induced Lung Injury
Fungal Pneumonia (invasive aspergillosis)
Post Bone Marrow Transplant (Pulmonary Findings)
early
Early (30-90)
PCP, CMV
Post Bone Marrow Transplant (Pulmonary Findings)
late
Late > 90
Bronchiolitis Obliterans, Cryptogenic
Organizing Pneumonia
AIDS Related Pulmonary Infection
Questions related to AIDS and pulmonary infection are typically written in one of two ways (1) with
regard to the CD4 count, and (2) by showing you a very characteristic infection.
PCP
overview
This is the most classic AIDS infection. This is the one they are most likely to show you.
Ground glass opacity is the dominant finding, and is seen bilaterally in the perihilar regions with
sparing of the lung periphery. Cysts, which are usually thin-walled, can occur in the ground glass
opacities about 30% of the time.
AIDS
Buzzwords
*Most common airspace opacity = Strep Pneumonia
*If they show you a CT with ground glass = PCP
•“Flame-Shaped” Perihilar opacity = Kaposi Sarcoma
’Persistent Opacities = Lymphoma
’Lung Cysts = LIP
‘Lungs Cysts + Ground Glass + Pneumothorax = PCP
‘Hypervascular Lymph Nodes = Castleman or Kaposi
Infections in
AIDS by CD4
> 200
Bacterial, TB
Infections in
AIDS by CD4
<200
PCP, Atypical Mycobacterial
Infections in
AIDS by CD4
<100
CMV, Disseminated Fungal, Mycobacterial
CT Pattern - With AIDS
focal airspace opacity
Bacterial Infection (Strep Pneumonia) is
the most common. DDx should include
TB if low CD4. If it’s a chronic opacity
think Lymphoma or Kaposi.
CT Pa tte rn - With AIDS
multi-focal airspace opacity
Bacterial, or Fungal
CT Pa tte rn - With AIDS
ground glass
PCP (if that’s not a choice it could be
CMV if CD4 is < 100).
You can think about TB as either
(a) Primary, (b) Primary Progressive, (c) Latent or (d) Post Primary / Reactivation.
Primary TB
Essentially you inhaled the bug, and it causes necrosis. Your body attacks and forms a
granuloma (Ghon Focus). You can end up with nodal expansion (which is bulky in kids, and less
common in adults), this can calcify and you get a “Ranke Complex. ” The bulky nodes can
actually cause compression leading to atelectasis (which is often lobar). If the node ruptures you
can end up with either (a) endobronchial spread or (b) hematogenous spread - depending on if the
rupture is into the bronchus or a vessel. This hematogenous spread manifests as a miliary pattern.
Cavitation in the primary setting is NOT common. Effusions can be seen but are more
common in adults (uncommon in kids).
Primary progressive TB
This term refers to local progression of parenchymal disease with the
development of cavitation (at the initial site of infection / or hematogenous spread). This primary
progression is uncommon - with the main risk factor being HIV. Other risk factors are all the
things that make you immunosuppressed - transplant patients, people on steroids. The ones you
might not think about is jejunoileal bypass, subtotal gastrectomy, and silicosis. This form is
similar in course to post primary disease.
Latent TB
This is a positive PPD, with a negative CXR, and no symptoms. If you got the TB
vaccine, you are considered latent by the US health care system/industry if your PPD converts.
This scenario buys you 9 months of INH and maybe some nice drug induced hepatitis.
Post Primary (reactivation) TB
This happens about 5% of
the time, and describes an endogenous reactivation of a
latent infection. The classic location is in the apical and
posterior upper lobe and superior lower lobe (more
oxygen, less lymphatics). In primary infection you tend
to have healing. In post primary infection you tend to
have progression. The development of a cavity is the
thing to look for when you want to call this. Arteries near
the cavity can get all pseudoaneursym’d up - “Rasmussen
Aneurysm” they call it - in the setting of a TB cavity.
Immune Reconstitution
Inflammatory Syndrome:
The story will be a patient with TB and AIDS started on highly active anti-retroviral therapy (HAART) and now doing worse. The therapy is steroids.
Pleural Involvement with TB
This can occur at any time after initial infection. In primary TB
development of a pleural effusion can be seen around 3-6 months after infection - hypersensitivity
response. This pleural fluid is usually culture negative (usually in this case is like 60%). You have
to actually biopsy the pleura to increase your diagnostic yield. You don’t see pleural effusions as
much with post primary disease, but when you do, the fluid is usually culture positive.
Latent TB
This is a positive PPD, with a negative CXR, and no symptoms. If you got the TB
vaccine, you are considered latent by the US health care system/industry if your PPD converts.
This scenario buys you 9 months of INH and maybe some nice drug induced hepatitis.
High Yield Factoids Regarding TB
High Yield Factoids Regarding TB:
* Primary = No Cavity, Post Primary / Primary Progressive = Cavity
* Ghon Lesion = Calcified TB Granuloma ; sequela of primary TB
* Ranke Complex = Calcified TB Granuloma + Calcified Hilar Node ; Healed primary TB
* Bulky Hilar and Paratracheal Adenopathy = Kids
* Location for Reactivation TB = Posterior / Apical upper lobes, Superior Lower Lobes
* Miliary Spread when? - Hematogenous dissemination (usually in the setting of reactivation), but
can be in primary progressive TB as well
* Reactive TB Pattern (Cavitation) seen in HIV patient when the CD4 is > 200
* Primary Progressive Pattern (Adenopathy, Consolidation, Miliary Spread) in HIV is CD4 < 200
* TB does NOT usually cause a lobar pattern in HIV
Non Tuberculous Mycobacteria
Cavitary
(“Classic”) - This one is usually caused by MAC. It favors an old white man with COPD (or other chronic lung disease), and it looks like reactivation TB. So you have an upper lobe cavitary lesion with adjacent nodules (suggesting endobronchial spread).
Non Tuberculous Mycobacteria
bronchiectatic
(“Non-Classic”) - This is the so-called “Lady Windermere” disease (everyone
knows it’s just not lady-like to
cough). They often do not cough, and are asymptomatic. This favors an old white lady. You see tree-in-bud opacities and cylindric bronchiectasis in the right middle lobe and lingula.
Non Tuberculous Mycobacteria
HIV
You see this with low CD4s (< 100). The idea is that it’s a GI infection disseminated in the blood. You get a big spleen and liver. It frequently is mixed with other pulmonary infections (PCP, e tc …) given the low CD4 - so the lungs can look like anything. Mediastinal lymphadenopathy is the most common manifestation.
Non Tuberculous Mycobacteria
Hypersensitivity Pneumonitis
This is the so-called “hot-tub lung.” Where you get aerosolized bugs (which exist in natural sea water and in fresh water). The lungs look like ill-defined, ground glass centrilobular nodules.
Non Tuberculous Mycobacteria
rapid cavitary
O ld W h ite M a le Sm o k e r
L o o k s lik e re a c tiv a tio n TB
Non Tuberculous Mycobacteria
rapid non-classic (lady windermere)
O ld L ady
M id d le Lobe an d L in g u la ,
b ro n c h ie c ta s is a n d tre e in bud.
Non Tuberculous Mycobacteria
rapid HIV
Low CD 4 (< 100)
M e d ia s tin a l L ym p h a d en o p a th y
Non Tuberculous Mycobacteria
Rapid Hypersensitiviy (hot tub lung)
H isto ry o f h o t tub use
G ro u n d g la ss c e n trilo b u la r n o d u le s
Non Tuberculous Mycobacteria
Rapid Hypersensitiviy (hot tub lung)
H isto ry o f h o t tub use
G ro u n d g la ss c e n trilo b u la r n o d u le s
Fungal infection - 3 flavors
(1) Normal Immune, (2) Suppressed Immune, or (3) Hyper-Immune.
Fungal
normal immune
Aspergillus makes a fungus ball “Aspergilloma” in a pre-existing cavity. The fungus didn’t make the cavity - it
found the cavity. It is squatting in an abandoned cavity -
Fungus balls can occur normal people who have a cavity from trauma, or prior infection ec t… like a hobo.
Fungal
normal immune gamesmanship
You could be shown a fungus ball, and they want you to call it invasive. Don’t fall for that. This is not invasive.
Fungal
Suppressed Immune
Aspergillus is NOT getting held in check by a normal immune system, invasive Aspergillus” they call it.
You are gonna see this in your AIDS, or Transplant Patients.
Fungal
Suppressed Immune halo sign
(1) Halo Sign - consolidative nodule/mass with a ground glass halo. The halo o f ground glass is actually the invasive component.
Fungal
Suppressed Immune air crescent sign
a thin crescent o f air within the consolidative mass. This actually represents healing, as the necrotic lung separates from the parenchyma. The timing is usually about 2-3 weeks after treatment. Lastly, they could show you some peripheral wedge shaped infarcts in the setting o f some halo signs.
Fungal
;hyperimmune
Aspergillus behaves differently in the setting o f a hyper-acute immune system. Allergic Broncho- Eulmonary Aspergillosis (A BPA I they call it.
Fungal
;hyperimmune gamesmanship
This is “Always” seen in patients with long standing Asthma (sometimes CF). You classically have upper lobe central saccular bronchiectasis with mucoid impaction (finger-in-glove). Central Bronchiectasis + Asthma (or CF) = ABPA
Diagnosis o f ABPA requires
BOTH:
• Elevated Serum Immunoglobulin E levels OR a positive skin hypersensitive test against the asshole fungus • Elevated Total IgE levels > 1000
Aspergilloma - Fungus Ball
rapid
■ Normal immune system
**That ball will move
with positional change
Invasive aspergillus
rapid
• Air Crescent Sign
~ Dude has AIDS
ABPA rapid
- Finger in Glove; think asthma
CMV
h is can be seen in two classic scenarios: (1) Reactivation o f the latent virus after
prolonged immunosuppression (post bone marrow transplant), and (2) Infusing o f CMV
positive marrow or in other blood products. The timing for bone marrow patients is “early”
between 30-90 days. The radiographic appearance is multiple nodules, ground glass or
consolidative.
Random V ira l Trivia
measles
Multifocal ground glass
opacities with small nodular
opacities
Pneumonia can be before or after the skin lesions. Complications higher in pregnant and immunocompromised
Random V ira l Trivia
ingluenza
Coalescent lower lobe
opacity. Pleural effusion is
rare.
Random V ira l Trivia
SARS
Lower lobe predominant
ground glass opacities
Random V ira l Trivia
Varicella
Multiple peripheral nodular
opacities. They form small
round calcific lung nodules
in the healed version.
Most commonly causes Chickenpox in kids. The pneumonia more commonly occurs in immunocompromised adults (with AIDS or lymphoma).
Random V ira l Trivia
EBstein Barr
Uncommonly affects the
lung. Can cause lymph node
enlargement
Most common radiographic
abnormality is a big spleen
Septic Emboli Trivia
- It’s lower lobe predominant (more blood flow)
- You get peripheral nodular densities and wedge shaped densities (can infarct).
- They can cavitate, and likely will be cavitated if they show you a CT image.
- The feeding vessel sign - nodule with a big vessel going into it can be shown (also seen with hematogenous mets).
- Empyema and pneumothorax are both known complications.
Lemierre Syndrome
This is an eponym referring to jugular vein thrombosis with septic emboli classically seen
after an oropharyngeal infection or recent ENT surgery.
Lemierre Syndrome
high yield trivia
Q: What is the bacterial agent responsible in the majority o f cases?
ACFusobacterium Necrophorum.”
CAVITY Mnemonic For Lung Cavity
Cancer (usually squamous cell)
Auto-immune (Wegeners, Rheumatoid / Caplan Syndrome)
Vascular - Septic Emboli / Bland Emboli
Infection - TB
Trauma - Pneumatoceles
Young - “Congenital” - CCAMs, Sequestrations
Lung Cancer Risk Factors:
being over 30 (under 30 is super rare), exposures
to bad stuff (arsenic, nickel, uranium, asbestos, chromium, beryllium, radon), having lung
fibrosis, COPD (even if you didn’t smoke), and family history. Diffuse fibrosis supposedly
gives you 1 Ox the risk. Having said all o f that, smoking is still the big one - supposedly a
factor in 90% o f cases.
Lung cancer screening
Recently, the US preventive services task force has
approved lung cancer screening with low dose CT for
asymptomatic adults aged 55-80 who have a 30 packyear
history and currently smoke (or have quit within
the past 15 years).
Pack years
Number of packs of cigarettes smoked per day multiplied by number of years the person has smoked = “Pack Years” 30 pack years will qualify you for screening
Lung cancer screening trivia
• Shockingly, it is backed up by evidence (which is extremely rare in medical screening programs), and legit improves outcomes (also rare in medicine).
• The follow up recommendations are NOT the same as the Fleischner Society
Recommendations. So nodules found on a CT done for any reason other than official lung cancer screening will follow Fleischner and not the LUNG RADS recommendations used with the screening program.
• Dose on the screening CTs is supposed to be low - recommended below CTDIvoi 3 mGy
• “Growth” is considered 1,5mm or more in one year
• LUNG RADS scoring is based off the most suspicious nodule. You don’t give multiple ratings for multiple nodules.
• Endobronchial “lesions” (mucus) are treated as 4a - and given a 3 month follow up.
• A treated remote (> 5 years) lung cancer patient must still meet the normal screening criteria toenrolled in the lung cancer screening program
Lung Rads category 0
Scan is a piece of shit and you can’t read, or you need priors
Repeat or get priors
Lung Rads category 1
Negative, < 1 % chance of cancer. Either no nodules or granulomas.
1 year follow up
Lung Rads category 2
Benign < 1 % chance of cancer. Baseline exam - nodules smaller
than 6mm. Subsequent exam - no new nodules larger than 4mm.
Ground glass nodule smaller than 20mm.
1 year follow up
Lung Rads category 3
Probably Benign, 1-2% chance of cancer. Baseline nodule 6-8mm.
Subsequent exam new nodule > 4mm. Ground glass > 20mm.
6 month follow up
Lung Rads category 4a
Suspicious, 5-15% chance of cancer, Baseline 8-15mm. New
nodule 6-8mm
3 month follow up
vs PET
Lung Rads category 4b
Suspicious, > 15% chance of cancer, > 15mm at baseline
New nodule > 8mm
PET vs Tissue
Sampling
Lung Rads category 4x
> 1 5% chance of cancer
Worsening of category 3 or 4 nodules (growth or new spiculation)
PET vs Tissue
Sampling
Nodules (incidental discover):
As discussed on the prior page, nodules discovered incidentally on non-screening scans are treated different for followup. These nodules are the captives of the dreaded Fleischner Society recommendations.
Fleischner pearls
- Fleischner guidelines only apply for patients older than 35
- They do NOT apply to patients with known or suspected cancer
- They do NOT apply to patients who are immunocompromised
- Measurements are reported as the average diameter (short + long / 2) obtained in the same plane.
- Risk stratification for followup (low, intermediate, high) is based on multiple risk factors (smoking, cancer history, family history, age, uranium / random / asbestos exposure and nodules characteristics / size).
- Follow up is based off the arbitrary guess of a cancer risk > 1%
- Perifissural nodules (discussed later) - do not need a follow up, even if they are > 6mm in size.
- Nodule characterization should be performed on thin-slice CT images <1.5 mm. This is done to look for a small solid component hiding behind partial volume effect in a ground glass nodule.
- Multiple nodules (> 5) makes malignancy statistically less likely.
Fleischner Society Overview for SOLID nodules
<6 mm, single, low risk
no follow up
Fleischner Society Overview for SOLID nodules
<6 mm, single, high risk
12 month repeat
Fleischner Society Overview for SOLID nodules
<6 mm, multiple, low risk
no follow up
Fleischner Society Overview for SOLID nodules
<6 mm, multiple, high risk
12 month repeat
Fleischner Society Overview for SOLID nodules
6-8 mm, single, low risk
6-12 month follow up
Fleischner Society Overview for SOLID nodules
6-8 mm, single, high risk
6-12 month follow up
Fleischner Society Overview for SOLID nodules
6-8 mm, multiple, low risk
3-6 month rollow up
Fleischner Society Overview for SOLID nodules
6-8 mm, multiple, high risk
3-6 month follow up
Fleischner Society Overview for SOLID nodules
> 8 mm, single, low and high
PET or biopsy
Fleischner Society Overview for SOLID nodules
> 8 mm, multiple, low and high risk
3-6 month followup
Fleishner
Ground glass nodule
follow up recommendations are variable. Most people will not follow up
nodules smaller than 6mm. If they are greater than 6mm people will either do 6 month or 1 year
(depends on who you ask). Follow up is persistent for 5 years, because of the slow growth of the
potential adenocarcinoma in situ.
Fleischner part solid nodules
maller than 6mm still gets ignored. However, the ones
larger than 6mm get a 3 month follow up - with interval widening but persisting up to 5 years.
Regular solid nodules typically get set free after 2 years of stability.
Solitary Pulmonary Nodule
A SPN is defined as a round or oval lesion measuring less than
3cm in diameter (more than 3cm = mass). Technically to be “solitary” it needs to be surrounded by
lung parenchyma, with no associated adenopathy, or pleural effusion. So, you can have numerous
“solitary” nodules in the lungs.
Solitary Pulmonary Nodule
calcification patterns
solid/diffuse laminated central popcorn ?eccentric (suspicious)
SPN
makes you think B9
Presence of Fat
Rapid Doubling Time (less than 1 month)
Slow Doubling Time (longer than 16 months) *Stable at two years = B9
SPN makes you think cancer
Spiculated Margins “Corona Radiata Sign”
Air Bronchogram through the nodules (usually Adenocarcinoma in situ)
Partially solid lesions with ground glass component
Solid and Ground Glass Components:
A part solid lesion with a ground glass component is the most suspicious morphology you can have. Non-solids (only ground glass) is intermediate.
Totally solid is actually the least likely morphology to be cancer.
PET for SPN:
overview
You can use PET for SPNs larger than 1 cm. Lung Cancer is supposed to be HOT (SUV > 2.5). Having said that, infectious and granulomatous nodules can also be hot.
PET for SPN:
Solid Nodule ( > 1cm in size):
HOT = Cancer, COLD = Not Cancer
PET for SPN:
Ground Glass Nodules:
HOT = Infection , COLD = Cancer
SPN / Cancer Trivia:
• Lung Cancer is 1.5 x more likely in the Right Lung
• 70% of Lung Cancer is in the Upper Lobes
• Exception to the rule is pulmonary fibrosis - where peripheral basilar cancer is more common.
• SPN in the setting of head and neck CA is more likely to be a primary bronchogenic carcinoma
rather than a metastasis (they have similar risk factors).
• Lung Cancer is very rare under 40 (unless the patient has AIDS)
• Air Bronchograms are 5x more common in malignant SPN
• Air Bronchograms are found in 50% of BACs
• Just because a nodule gets smaller doesn’t mean it is benign. Especially if the nodule increases
Nodule Volume / Size Change
Most people will call nodule “growth” at 1.5 mm per year. Anything smaller than that can easily be
attributed to technical factors. Anyone who describes 0.1mm differences in stuff sucks at Radiology.
This growth, in particular the concept of “doubling time ” makes up the basis of differentiated benign
vs malignant. With out this concept you would be forced into follow nodules forever. The trivia
worth knowing is that lung cancers doubling times range from 20 days to 400 days.
Any nodule that doubles in size in less than 20 days is almost certainly benign (statistically
infectious or inflammatory). The same is true with doubling times greater than 400 days.
The notable difference is the ground glass or part solid nodule vs the solid nodule. Ground glass and
part solid nodules are more characteristic of the adenocarcinoma in situ (formerly BAC) and they
tend to grow slower. This is why the follow up term for GGN and part solid nodules in 5 years, vs 2
years for a pure solid nodule.
Perifissurai Nodule (PFNs)/Intrapulmonary Lymph Node
Typical morphological features would
include well circumscribed, smoothly
marginated, triangular, oval, or polygonal
nodules which either contact the fissure or
pleural surface directly.
They technically don’t have to contact a pleural surface, as long as they are within 15 mm (some people say 20mm).
Spiculated or Round nodules are not typical for PFNs. These two guys should be treated like “regular” nodules.
Perifissurai Nodule (PFNs)/Intrapulmonary Lymph Node
Trivia
PFNs are probably lymph nodes
• They are almost certainly benign and treated as such by the Fleischner society
• LUNG-RADS v l.l says mean diameter less than 10mm = category 2 (benign), larger than
10mm means you treat than like any other nodule
• Interval growth does NOT mean they are full of cancer - lymph nodes normally fluctuate in size.
• Size greater than 6mm still doesn’t justify follow up per Fleischner.
Non Small Cell Squamous
location
Central
Non Small Cell Squamous
features
Strong Association with Smoking
Cavitation is Classic
Does NOT express the tissue maker thyroid transcription factor 1 “TTF-1” (other
subtypes can).
Non Small Cell Squamous
paraneoplastic
Paraneoplastic Syndromes can be associated with ectopic Parathyroid Hormone
Non Small Cell Large Cell
location
Peripheral
Non Small Cell Large Cell
Features
Least common subtype (15%)
Usually large (> 4cm)
Prognosis Suck — this is the subtype of Cancer that killed comedy legend Andy Kaufman in his 30s.
Non Small Cell
Adenocarcinoma
Location
peripheral
Non Small Cell
Adenocarcinoma
Features
Most Common subtype (35%)
Favors the upper lobe
Most Common subtype to present as a solitary pulmonary nodule
Most Common subtype in a non smoker (although also common in smokers)
Known association with pulmonary fibrosis
Non Small Cell
Adenocarcinoma
trivia
Strong Association with
Smoking (nearly every case is
a smoker)
Small Cell
location
Central
Small Cell
features
May only present with central lymphadenopathy
Most Common primary lung CA to cause SVC obstruction and paraneoplastic syndromes
Terrible Horrible Incredibly Shitty Prognosis (metastasizes early)
Paraneoplastic Syndromes can be associated with SIADH and ACTH
Small Cell
trivia
Lambert Eaton. They get proximal weakness from abnormal release of acetylcholine at the neuromuscular junction. The clinical presentation often comes before the cancer diagnosis.
LA is on the Coast
Large and Adeno favor peripheral locations
Lung cancer gamesmanship
Location o f the tumor can sometimes be predicted based on symptoms.
Central tumors = hemoptysis. Peripheral tumors = pleuritic chest pain.
AIS
Pre-invasive lesions AAH
Atypical Adenomatous Hyperplasia of Lung (AAH):
The smaller (< 5mm) and more mild pre invasive subtype. Usually a pure ground glass nodule.
AIS
Pre-invasive lesion ACIS
Adenocarcinoma in situ (ACIS):
Typically larger than AAH but < 3 cm. Although features
overlap with AAH, they tend to be more part-solid (rather
than pure ground glass)
AIS
Minimally Invasive Adenocarcinoma (MIA)
These are also < 3 cm. The distinction is that there is < 5
mm of stromal invasion ( > 5 mm will be called a lepidic
predominant adenocarcinoma).
AIS
Invasive Mucinous Adenocarcinoma
This is what most people used to call BAC
bronchoalveolar carcinoma
AIS subtypes
Key concetp
The larger the solid component of the “part solid” nodule gets the more likely it is to be malignant. Partially solid nodules are more likely to be cancer than ground glass nodules.
AIS subtypes on PET
cold
Superior Sulcus I Pancoast Tumors
overview
Some people make a big deal about only using the
word “pancoast” when the tumor causes the associated syndrome (shoulder pain, C8-T2
radiculopathy, and Homer Syndrome). In my experience most everyone just calls apical tumors
“pancoast” with no regard to symptoms. Having said that, I would remember “shoulder pain” as a
possible hint in the question header. These things are typically non-small cell cancers.
Superior Sulcus I Pancoast Tumors
staging
MRI is the tool of choice (you need to look at that brachial plexus).
Superior Sulcus I Pancoast Tumors
general contraindication to surgical resection
invasion of the
vertebral body (> 50%), invasion of the spinal canal, involvement in the upper brachial plexus (C8 or
higher), diaphragm paralysis (infers phrenic nerve C3-5 involvement), distal mets.
Lung cancer staging overview
Lung cancer staging used to be different for small cell vs non-small cell (NSCLC). In 2013 the 7thedition of the TNM made them the same. Below is a chart describing the staging based on tumor
size. For a solid lesion, the size is defined as maximum diameter in any of the three orthogonal planes
- measured on lung window. If the lesion is subsolid, then you define the T classification by the
diameter of the solid component only (NOT the ground glass part).
Lung Cancer Staging (8th edition)
T1
Tumor is < 3cm
Lung Cancer Staging (8th edition)
T2
Tumor is 3-5 cm
Irregardless of size the tumor
• Invades the visceral pleura
• Invades the main bronchus
• Causes obstruction (atelectasis or pneumonia) that extends to the hilum
Lung Cancer Staging (8th edition)
T3
Tumor is 5-7 cm
Irregardless of size the tumor
• Invades the chest wall
• Invades the pericardium
• Invades the phrenic nerve (diaphragm paralysis)
• Has one or more satellite nodule in the same lung lobe
Pancoast (Superior Sulcus) Tumor that is
limited to involvement o f Tl and T2 nerve roots
Lung Cancer Staging (8th edition)
T4
Tumor > 7cm
Irregardless of size the tumor
• Invades the mediastinal fat or great vessels
• Invades the diaphragm
• Involves the carina
• Has one or more satellite nodule in another lobe in the same
long
Pancoast (Superior Sulcus) Tumor that involves level C8 or higher
Lung cancer
Multiple Lesions
The handling of multiple lung lesion is complicated. Deciding if
lesions are going to be treated as synchronous primaries or a
single lung cancer with metastatic disease often requires a
discussion at tumor board (after imaging, and path results).
If the lesions are decided to be separate primaries each cancer
will be staged separately within the TNM system and given an
overall stage. If the lesions arc decided to be metastatic their
distribution will alter the stage.
Synchronous
Two or more
primary carcinomas which
coexist at the time of
diagnosis.
Metachronous
A cancer
that develops consequently
(some time interval) after the
first primary.
Lung cancer staging nodal disease
N1
Ipsilateral within the lung
up to the hilar nodes.
Nl is a worse prognosis than NO (no nodes) but the management is not changed.
Lung cancer staging nodal disease
N2
Ipsilateral mediastinal or subcarinal nodes
In many cases NOT Resectable
Only those with microscopic disease (negative
mediastinoscopy) will benefit from resection
Lung cancer staging nodal disease
N3
Contralateral mediastinal
or contralateral hilum. or scalene or supraclavicular nodes
not resectable (probablyl)
Lung cancer staging nodal disease
overview
First it is important to point out that CT is unreliable for nodal staging. PET-CT is far superior, regardless of the size threshold that is chosen. This is why PET is pretty much always done on lung cancer patients prior to surgical evaluation.
For the purpose o f multiple choice (and real life) the most important anatomy boundary to consider is the distinction between level l nodes (which at N3) and level 2 nodes (which are N2).
In some cases, this can literally make
the difference between resectable disease or not. The border is the lower
level of the clavicles / upper border of the manubrium (above this is level I).
Typical Contraindications to Lobectomy / Resection
- G row th o f the tum o r th ro u g h a fissure
- In v asio n o f the P u lm o n a ry V asculature
- In v a sio n o f the m a in b ro n ch u s
- In v a sio n o f bo th th e u p p e r an d low e r lobe bro n ch i.
- N 2 * (if th e tum o r is > 5cm ) o r N3 N o d a l D ise a se — co rre sp o n d in g to a Sti
- M u lti-lo b a r Disease
- M a lig n an t P leu ral Effusion
Staoe 3B implies
N3 o r T 4 d ise a se
For the purpose o f multiple choice, the distinction between 3a vs 3b is the critical staee
3b is surgically unresectable (technically this varies widely by institution and depends on lots o f factors).
Wedge Resection V S Lobectomy
This is on the fringe of what should be considered fair game, and I’m certain the decision varies by institution and the size and composition (percentage
of brass) of the surgeon’s testicles. In general, if a stage 1A or IB cancer is peripheral and less than
2cm they can consider a wedge resection. The advantage to doing this over a lobectomy is preserving
pulmonary reserve. If the tumor is larger than 3cm then lobectomy seems to (in general) be a better
option.
Bronchopleural Fistula
This is an uncommon complication of
pneumonectomy, that has a characteristic look and
therefore easy to test.
So normally after a pneumonectomy the space will
fill with fluid. If you see it filling with air than this
is the dead give away.
If you are a weirdo, you could confirm the
diagnosis with a xenon nuclear medicine
ventilation study, which will show xenon in the
pneumonectomy space. The major risk factor is
ischemia to the bronchi (disrupted blood supply
from aggressive lymph node dissection, or using a
long bronchial stump).
Normal postsurgical lungs
become more fluid filled
bronchopleura fistula postsurgical lungs
become more air filled
Radiation Changes
ovverivew
The appearance of radiation
pneumonitis is variable and based on the volume of
lung involved, how much/long radiation was given, and
if chemotherapy was administered as well.
Radiation Changes
rib fx
Ribs within the treatment field are
susceptible to degradation and fracture.
Radiation Changes
rfa/mwa pearl
It is normal to see bubbles in the
lesion immediately after treatment.
Radiation Changes
early
Homogenous or
patchy ground
glass opacities.
Radiation Changes
late
Dense consolidation, traction bronchiectasis, and volume loss.
Recurrent Disease (lung cancer)
Recurrence rates are relatively high (especially in the first 2 years). From
a practical stand point, I always focus my attention towards the periphery of the radiation bed,
regional nodes, and/or the bronchial stump. A useful concept is to focus on morphology - radiation
scarring is usually not round. If you see something with a round morphology - especially if it is
growing over time, that is highly suspicious.
Other findings concerning for recurrence
- Enhancing solid tissue along the resection line (or bronchial stump) which is enlarging over time.
- New enlarged mediastinal nodes with a short axis greater than 1 cm
- New pleural effusion (that persists on follow ups)
Pulmonary Hamartoma
This is not a cancer, but to
the uninitiated can look scary. It is usually described as is an
Aunt Minnie because it will have macroscopic fat and
“■popcorn” calcifications. It is the most common benign
lung mass. It’s usually incidental, but can cause symptoms if
it’s endobronchial (rare - like 2%).
Technically the fat is only seen in 60%, but for sure if the
exam shows it, it will have fat. These can be hot on PET,
they are still benign.
Pulm hamartoma quick
popcorn calcs
fat density
Lung mets
overview
Metastatic disease to the lungs can be thought of in 3 categories; direct invasion,
hematogenous, lymphangitic:
Lung mets
direct invations
This is seen with cancer of the mediastinum, pleura, or chest wall. The most
common situation is an esophageal carcinoma, lymphoma, or malignant germ cell tumor. More rarely
you are going to have mets to the pleura then invading the lung. Even more rarely you can have
malignant mesothelioma, which can invade the lung. It should be obvious.
Lung mets
hematogenous
The most common manifestation of
hematogenous mets to the lung is the pulmonary nodule
(usually multiple, in a random distribution, and favoring the
lower lobes which have greater blood volume). The nodules
tend to be smoother than the primary neoplasm. The main
culprits are breast, kidney, thyroid, colon, and head & neck
squamous cells. Obviously the squamous mets can cavitate.
“Cannonball Mets” are classically from renal cell or
choriocarcinoma (testicle).
Lung mets
lymphangitic carcinomatosis
The most common cause of unilateral LC is actually
bronchogenic carcinoma lung cancer invading the lymphatics. The most common extrathoracic
culprits are breast, stomach, pancreas, and prostate. The finding is nodular thickening of the
interlobular septa and subpleural interstitium. Unlike interstitial fibrosis, this thickening classically
does NOT distort the pulmonary lobule.
Lung mets
feeding vessel sign
A prominent pulmonary vessel heading into a nodule. This supposedly means it’s from a hematogenous origin. It’s nonspecific - but if you see it the answer is (1) mets , or (2) septic emboli.
Kaposi Sarcoma
key points
’ Most common lung tumor in AIDS (requires CD4 < 200)
‘Most common hepatic neoplasm in AIDS
‘Buzzword = Flame Shaped Opacities
‘Slow Growth, with asymptomatic patients (despite lungs
looking terrible)
‘Thallium Positive, Gallium Negative
Kaposi Sarcoma
overview
This is the most common lung tumor is
AIDS patients (Lymphoma is number two). The tracheobronchial
mucosa and perihilar lung are favored. The buzzword is “flame
shaped.” A bloody pleural effusion is common (50%).
Lymphoma
overview
There are basically 4 flavors of pulmonary lymphoma; primary, secondary, AIDS
related, or PTLD. Radiographic patterns are variable and can be lymphangitic spread (uncommon),
parahilar airspace opacities, and/or mediastinal adenopathy.
Lymphoma
primary
This is rare, and usually non- Hodgkin in subtype. You define it as the lack of extrathoracic involvement for 3 months. Almost always (80%) we are talking about a low grade MALToma.
Lymphoma
secondary
Here we are talking about pulmonary involvement of a systemic lymphoma. This is much much much more common than primary lung lymphoma. The thing to see is that NHL is much more common, but if you have HL it is more likely to involve the lungs. With HL you gets nodes and parenchyma, in NHL you might just get parenchyma.
Lymphoma
PTLD
This is seen after solid organ or stem cell transplant. This usually occurs within a year of transplant (late presentations > 1 year have a more aggressive course). This is a B-Cell lymphoma,
with a relationship with EB Virus. You can have both nodal and extra nodal disease. The typical look
is well-defined pulmonary nodules / mass, patchy airspace consolidation, halo sign, and interlobular
septal thickening.
Lymphoma
AIDS related pulmonary lymphoma
This is the second most common lung tumor in
AIDS patients (Kaposi’s is first). Almost exclusively a high grade NHL. There is a relationship with
EBV. It is seen in patients with a CD4 < 100. The presentation is still variable with multiple
peripheral nodules ranging from 1 cm-5 cm being considered the most common manifestation.
Extranodal locations (CNS, bone marrow, lung, liver, bowel) is common. AIDS patient with lung
nodules, pleural effusion, and lymphadenopathy = Lymphoma.
Secondary NHL overview
80-90% of lymphoma
cases
45% have intrathoracic
disease at presentation
25% have pulmonary
parenchymal disease
Pulmonary involvement
frequently occurs in the
absence of mediastinal
disease
Secondary HL overview
10-20% of lymphoma
cases
85% have intrathoracic
disease at presentation
40% have pulmonary
parenchymal disease
Lung involvement
almost always associated
with intrathoracic lymph
node enlargement
Thallium is a potassium analog
Things with afunctional Na/K/ATP pump tend to be alive, Hence anything htat is alive will be positive.
Gallium is an Iron analog
Iron is an
inflammatory marker (acute phase
reactant) hence things that are
“smoldering” tend to be gallium negative,
and things that are inflamed - infection,
active sarcoid, most cancers - tend to be
Gallium hot.
In general, it is safe to say “Lymphoma is
HOT on Gallium.” Where things can get sneaky is
the subtype. Hodgkin is nearly always Gallium Avid. Certain Non-Hodgkin subtypes can be
Gallium cold. As such (and because it’s not 1970) PET is usually used for staging and not Gallium.
Kaposi Sarcoma
nucs
Thallium 201 Positive
Gallium67 Negative
Lymphoma
nucs
Thallium 201 Positive
Gallium67 Positive
Poland Syndrome
Unilateral absence of a pectoral
muscle (white arrow). Can cause a unilateral hyper-lucent chest. Can have limb issues (small weird arms / hands).
Bronchial Atresia
overview
This is a congenital obliteration of a short segment of a lobar, segmental,
or subsegmental bronchus near its origin (most commonly involves the apical-posterior segment of
the left upper lobe). Like many atresias a vascular insult in utero is the probable etiology.
Bronchial Atresia
imaging
On CT, you will see a hyper lucent region with decreased
vascularity. It is somewhat counterintuitive that loss of the
bronchus would make the lung trap air (hyper lucent). The
explanation is collateral flow through the varies pores of
Kohn and canals of Lambert. You will often see a large
“nodule” (sometimes with a branching or “finger in the
glove” morphology) nearby in the hilum — which represents
mucoid impaction in the blind ended bronchus.
Bronchial Atresia
ddx
The primary differential would be an endobronchial tumor.
If you can measure (or they show you) a low density focus
(< 25 HU) in the mucus plug then you are safe to call it
mucoid impaction. If you can’t make the distinction the next
step should be bronchoscopy to be certain.
Bronchial Atresia
symptoms
Bronchial atresia is usually
asymptomatic, although they can
presentation
Bronchial Atresia findings brief
Hyperinflated lobe is the most
common radiographic appearance
(sometimes with a hilar nodule
visible).
CT will show a blind ending
bronchus, filled with mucus and
the distal lung Hvper-lnflated
(lucent).
AVM
They can occur sporadically. For the putpose of multiple choice when you see them think
about HHT (Hereditary Hemorrhagic Telangiectasia / Osier Weber Rendu). Pulmonary AVMs are
most commonly found in the lower lobes (more blood flow), and can be a source of right to left shunt
(worry about stroke and brain abscess). The rule of treating once the afferent vessel is 3 mm is
based on some tiny little abstract and not powered at all. Having said that, it’s quoted all the time,
and a frequent source of trivia that is easily tested.
Persistent Left SVC
This is the most common congenital venous anomaly of the chest. It
usually only matters when the medicine guys drop a line in it on the floor and it causes a confusing
post CXR (line is in a left paramedian location). It usually drains into the coronary sinus. In a
minority of cases (like 5%) it will drain into the left atrium, and cause right to left shunt physiology
(very mild though). This is typically shown on an axial CT at the level of the AP window, or with a
pacemaker (or line) going into the right heart from the left.
Swyer-James
This is the classic unilateral lucent lung. It typically occurs after a viral lung
infection in childhood resulting in post infectious obliterative bronchiolitis (from constrictive
bronchiolitis). The size o f the affected lobe is smaller than a normal lobe (it’s not hyper-expanded).
Horseshoe Lung
Defined by fusion of the posterior basilar
segments of the lower lobes behind the heart.
The most likely testable points are:
(1) What is it ? and
(2) What is the association ? Scimitar syndrome
Cystic lung disease
ddx
lch lam birt hogg dube LIP PCP
Birt hogg dube
This is a total zebra. This cystic lung disease has thin walled “oval” shaped cysts. There is an association with renal findings (bilateral oncocytomas, and chromophobe RCCs). They also have a bunch of gross skin stuff.
Lymphangiomyomatosis (LAM)
This cystic lung disease can occur in child bearing aged
women or in association with Tuberous Sclerosis (a trick
is to show the kidneys with multiple AMLs first). The
cysts are thin walled with a uniform distribution. There is
an association with chylothorax (which is HIGH YIELD
Trivia). The pathophysiology is that it is estrogen
dependent (why it strongly favors women). This is usually
progressive despite attempts at hormonal therapy
(tamoxifen).
Alternate way to suggest TS
ould be the step 1 “clinical triad” — even though < 50% o f TS patients have the complete triad. 1 - Seizures, 2- Mental Retardation, 3 - Adenoma Sebaceum SSS: Seizures, Sebaceum, & Stupid
Pulmonary Langerhans Cell Histiocytosis (LCH) -
This cystic lung disease classically effects smokers, who are young
(20s-30s). The disease starts out with centrilobular nodules with an
upper lobe predominance. These nodules eventually cavitate into cysts
which are thin walled to start, and then some become more thick
walled. Late in the disease you are primarily seeing cysts. The
buzzword is bizarre shaped, which occurs when 2 or more cysts merge
together. In about half the cases this spontaneously resolves (especially
if you stop smoking). Another piece of trivia is that LCH spares the
costophrenic angles.
what spares the costophrenic angle
(1) LCH and
(2) Hypersensitivity
Pneumonitis
LCH Vs LAM
Cysts and Nodules Cysts (no nodules)
Smoker Women, Pts with Tuberous Sclerosis
Upper and Mid Lungs Diffuse
Thicker Cysts (Bizarre) Thin Round Cysts
LCH
LAM
BHD
Bizarre Shape, ThickWall
Round, thin wall
oval, thin wall
Lymphocytic Interstitial Pneumonitis (LIP)
This is a benign
lymphoproliferative disorder, with infiltration of the lungs. It has an association with
autoimmune diseases (SLE, RA, Sjogrens). The big one to know is Sjogrens which is
concomitant in 25% of LIP cases. The other one to know is HIV - which is the LIP in a
younger patient (children, - LIP in HIV positive adults is rare). There is also an association
with Castlemans. The appearance of LIP varies depending on the underlying cause. The
cystic lung disease is usually thin walled, “deep within the lung parenchyma,” and seen
predominantly with Sjogrens. The dominant feature described as ground glass or nodules is
seen more in the other causes and is far beyond the scope o f the exam.
When i say LIP
you say sjogrrens and HIV
When i say LIP in a kid
you say HIV
Pneumocystis Pneumonia (PCP)
This is the most common opportunistic
infection in AIDS.
The typical buzzword is ground glass appearance, predominantly in the hilar and mid
lung zones.
Pneumatoceles are present in 30% of cases. In patients receiving aerosolized prophylaxis, a
cystic form is more common, which may have bilateral thin walled upper lung
predominant cysts. Gallium 67 scan will show diffuse uptake (Thallium will be negative).
When I say aids and ground glass lungs you say
PCP
Emphysema
overview
The textbook definition is “permanent enlargement o f the airspaces distal to the terminal
bronchioles accompanied by destruction o f the alveolar wall without clear fibrosis.” What
you need to know are (1) the CXR findings and (2) the different types.
Emphysema
CXR
Until it’s really really bad, CXR doesn’t have direct signs, but instead has
indirect signs. Flattening of the hemidiaphrams is regarded as the most reliable sign. The
AP diameter increases. The retrosternal clear space becomes larger. There is a paucity of, or
pruning o f the blood vessels.
Emphysema
centrilobular
By far the most common type. Common in asymptomatic elderly patients.
It has an apical to basal gradient - favoring the upper zones of each lobe. It appears as
focal lucencies, located centrally within the secondary pulmonary lobule, often with a
central dot representing the central bronchovascular bundle. This central dot sign is a
buzzword. This is the type of emphysema dominant in smokers.
Emphysema
perilobular
In contradistinction to centrilobular this one favors the lower lobes. It also
has a more uniform distribution across parts o f the secondary pulmonary lobule. The
association is with alpha 1 antitrypsin. A piece o f trivia is the “’Ritalin Lung” from IV
Ritalin use can also cause a pan-lobular appearance (“Ritalin keeps you from ‘trypsn’
out”). I f they show this it will be in the coronal view on CT to demonstrate the lower lobe
predominance. Patient’s will present in their 60s and 70s (unless they smoke - then they
present in their 30s). Smoking accelerates the process.
Emphysema
paraseptal
This one is found adjacent to the pleura and septal lines with a peripheral
distribution within the secondary pulmonary lobule. The affected lung is almost always
sub-pleural, and demonstrates small focal lucencies up to 10 mm in size. This looks like
honeycombing but is less than 3 bubbles thick.
Emphysema
trivia
• Saber Sheath Trachea - Diffuse coronal narrowing o f the trachea, sparing the extrathroacic
portion. This is said to be pathognomonic for COPD.
• If the Main PA is larger than the Aorta COPD patients have a worse outcome (pulmonary
HTN can be caused by emphysema).
• Surgery to remove bad lung “volume reduction” is sometimes done
Vanishing Lung Syndrome
This is an
idiopathic cause of giant bullous emphysema,
resulting from avascular necrosis of the lung
parenchyma and hyperinflation. It favors the
bilateral upper lobes, and is defined as bullous
disease occupying at least one-third of a
hemithorax. The most common demographic is a
young man. About 20% of these guys have alpha-1
antitrypsin deficiency. Tension pneumothorax is a
described complication.
Vanishing Lung Risk Factors
• Smoking (tobacco) • Alpha-1 antitrypsin deficiency • Male • Smoking Marijuana is also a described risk factor (although it is probably bullshit propaganda from the pharmaceutical industry)
Compensatory Emphysema (Postpneumonectomy Syndrome):
There is no obstructive process here. Instead you have hyper-expansion of one lung to compensate
for the absence o f the other one.
Honeycomb Lung
When I say honeycombing you should say UIP. However, this is
seen with a variety of causes o f end stage fibrotic lung processes. The cysts are tightly
clustered (2-3 rows thick) and subpleural. The walls are often thick.
p NEUMOc o n io s i s
overivew
As a general rule, these are inhaled so they tend to be upper lobe predominant. You can have
centrilobular nodules (which makes sense for inhalation), or often perilymphatic nodules -
which makes a little less sense, but is critical to remember * especially with silicosis and
CWP.
p NEUMOc o n io s i s
dz
asbestosis silicosis silicotuberculosis coal workers lung talcosis silo fillers dz berylliosis
Asbestos Exposure
The term “Asbestosis” refers to the changes o f pulmonary
fibrosis - NOT actual exposure to the disease. The look is very similar to UIP, with the
presence of parietal pleural thickening being the “most important feature” to distinguish
between IPF and Asbestosis. Obviously, the history o f working in a ship yard or finding
asbestos bodies in a bronchoalveolar lavage is helpful.
Things to know about Asbestos
“Asbestosis” = the lung fibrosis associated with exposure, NOT actual exposure
• Interstitial pattern looks like UIP + parietal pleural thickening
* There is a 20 year latency between initial exposure and development of lung cancer or
pleural mesothelioma
* There is an association with extrapulmonary cancer including: Peritoneal mesothelioma,
GI cancer, Renal Cancer, Laryngeal Cancer, and Leukemia
# Benign pleural effusions are the “earliest pleural-based phenomenon” associated with
exposure - still with a lag time of around 5 years
Benign Asbestosis Related Changes
Pleural effusion is the earliest and most common. Pleural plaques may develop around 20-30
years, with calcifications occurring around 40 years. These plaques tend to spare the apices and
Costophrcnic angles. Round atelectasis - which is associated with pleural findings is sometimes
called the “asbestos pseudotumor. “
Malignant Mesothelioma
overview
The most common cancer of the pleura. About 80% of them have had asbestos exposure, and
development is NOT dose-dependent. The lag time is around 30-40 years from exposure.
Malignant Mesothelioma
key features
• Circumferential Pleural Thickening extending to
the medial surface of the pleura (near the heart)
• Pleural Thickness > 1 cm
• Extension into the fissure = highly suggestive
Malignant Mesothelioma
evaluating direct invasion and mets
Mesothelioma believes in nothing
Lebowski with a known tendency for
direct invasion.
MRI with Contrast = For evaluating
local chest wall, diaphragm and
pericardial invasion
PET CT = Good for mets. Useful for
evaluating treatment response.
Malignant Mesothelioma
buzzword
pleural rind
thick lateral pleura
Common
**think old rib fx
thick medial pleura
NOT Common
**think mesothelioma.
Silicosis
This is seen in miners, and quarry workers. You can have simple silicosis, which is going to be multiple nodular opacities favoring the upper lobes, with egg shell calcifications o f the hilar nodes. You also get perilymphatic nodules. The complicated type is called progressive massive fibrosis (PMF). This is the formation of large masses in the upper lobes with radiating strands. You can see this with both silicosis and coal workers pneumoconiosis (something similar also can happen with Talcosis). These masses can sometimes cavitate - but you should always raise the suspicion o f TB when you see this (especially in the setting o f silicosis).
progressive massive fibrosis
lare paical masses with radiating strands
silicosis
Silicotuberculosis:
Silicosis actually raises your
risk of TB by about 3 fold. If you see cavitation in the
setting o f silicosis you have to think about TB.
MRI : Cancer vs PMF
Cancer = T2 Bright PMF = T2 Dark
Coal Workers Pneumoconiosis
This is the result o f exposure to “washed coal.”
Just like silicosis there are simple and complicated forms. There is also an increased risk of
TB (just like silicosis). The simple form was multiple nodular opacities, with calcifications
showing a central nodular dot. The small nodule pattern tends to have a perilymphatic
distribution. The complicated form gives you a progressive massive fibrosis that is
similar to that seen in silicosis.
Berylliosis
Metal used in aircraft and
space industries
Generalized granulomatous disease
with hilar adenopathy and upper lobe
predominant reticular opacities.
Silo Filler’s Disease
Nitrogen Dioxide
Pulmonary Edema Pattern. Recovery
is typically within 5 weeks.
Talcosis
Filler in tablets, sometimes
injected (along with drugs)
in IV drug users.
Hyperdense micronodules, with
conglomerate masses (similar to PMF).
Ground glass opacities
Consolidation
Density that obscures underlying vessels
Ground Glass Opacity
Density that does NOT obscure underlying vessels
Secondary Pulmonary Lobule
The basic unit o f pulmonary structure and function. It is the smallest part of the lung that is surrounded by connective tissue. In the middle
runs a terminal bronchial with an accompanying artery. Around the periphery runs the
vein and lymphatics
Telling them apart can he done by firs t asking i f they abut the pleura?
If the answer is no they are
centrilobular
Telling them apart can he done by firs t asking i f they abut the pleura?
If the answer is yes then ask if they follow a peribronchovascular pattern
yes then perilymphatic
no then random
Perilymphatic ddx
- S a rco id (9 0% ),
- L ym p h an g itic S p re ad o f CA
- S ilico sis
Random ddx
- M ilia ry TB
- M e ts
- Funga l
Centrilobular ddx
- In fec tio n
- R B -ILD
- H y p e rs en s itiv ity P n eum o n itis ( i f g rou n d g la ss )
Interlobular Septal Thickening
Reticular abnormality, that outlines the lobules’
characteristic shape and size (about 2 cm). It’s usually from pulmonary edema (usually
symmetric and smooth), or lymphangitic spread of neoplasm (often asymmetric and
nodular). Kerley B Lines are the plain film equivalent.
Honeycombing
Cystic areas of lung
destruction in a subpleural location. This is a
hallmark o f U1R Paraseptal emphysema is a
mimic, but the distinction is made by how
many rows o f bubbles.
One Row o f Bubbles =
paraseptal emphysema
Two-Three Rows o f Bubbles =
honeycombing
Idiopathic Interstitial Pneumonias
These are NOT diseases, but instead lung reactions to
lung injury. They occur in a variety o f patterns and variable degrees o f inflammation and
fibrosis. The causes include: idiopathic, collage vascular disease, medications, and inhalation.
For practical purposes the answer is either (a) UIP or (b) Not U1P. Not U1P will get better
with steroids. UIP will not. UIP has a dismal prognosis (similar to lung cancer). Not UIP
often does ok. The exam will likely not make it this simple, and will instead focus on
buzzwords, patterns, and associations (which I will now discuss).
UIP (Usual Interstitial Pneumonia)
overview
The most common ILD. When the cause is
idiopathic it is called 1PF. On CXR the lung volume is reduced (duh, it’s fibrosis). Reticular
pattern in the posterior costophrenic angle is supposedly the first finding on CXR.
UIP (Usual Interstitial Pneumonia)
buzzwords
Apical to basal gradient (it’s worse in the lower lobes)
Traction bronchiectasis, and honeycombing
Honeycombing is found 70% of the time,
and people expect you to knee jerk UIP when that term is uttered
Histologic Buzzword = Heterogeneous.
“Histology was heterogeneous” = UIP
UIP
end stage
It’s important to know that basically any end
stage lung disease (be it from sarcoid, RA,
Scleroderma, or other collagen vascular disease)
has a similar look once the disease has ruined the
lungs. *Technically honeycombing is uncommon
in end stage sarcoid - but the rest o f the lung
looks jacked up.
The prognosis is terrible (similar to lung cancer).
This vs That: Chronic Hypersensitivity
Pneumonitis (HP) vs UIP.
Features that favor Chronic HP over UIP:
• Air Trapping involving 3 more lobes
• Mid-Upper lobe predominant fibrosis
Definite UIP Criteria
• Honeycombing (must be present)
• +/- traction bronchiectasis
• Reticular abnormalities
• Subpleural basal predominant distribution
• Absence o f inconsistent features: upper lobe
predominance, ground glass > reticulations,
air trapping involving 3 or more lobes
Definite UIP Pattern =
Don’t Need to Biopsy to Prove Diagnosis
Fibrosis and Cancer Go Together Like Tacos and Tuesdays
Pulmonary fibrosis is a risk factor for lung cancer
especially if these patients are dumb enough to also smoke
Cancer in the Fibrotic Lung Trivia:
Cancer in the Fibrotic Lung Trivia:
• Favors the lower lobes
• Favors the interface between the fibrotic cvsts and normal lung
• Progressive wall thickening or a developing nodule within a cyst is suspicious for cancer
(enlarging pericystic nodules are dodgy as fuck - hide your kids / hide your wife)
• NELSON Lung Cancer Screening Trial showed cancers associated with cystic lesions were
commonly missed (people thought they were just areas of focal thickening within a bulla).
— Then I said “Come on Judge… let him go, h e ’s doing his best. ’’
NSIP (Nonspecific Interstitial Pneumonia)
overview
Less Common than UIP. Even though the name infers that its non-specific, it’s actually is
a specific entity. Histologically it is homogenous inflammation or fibrosis (UIP was
heterogeneous). It is a common pattern in collagen vascular disease, and drug reactions.
NSIP (Nonspecific Interstitial Pneumonia)
flavors
It comes in 2 flavors (cellular or fibrotic):
■ Ground Glass Alone = Cellular
■ Ground Glass + Reticulation = Cellular or Fibrotic
■ Reticulation + Traction Bronchiectasis = Fibrotic NSIP
■ Honeycombing - uncommon and usually minimal in extent
NSIP (Nonspecific Interstitial Pneumonia)
trivia
NSIP is the most common Interstitial Lung Disease in Scleroderma
NSIP (Nonspecific Interstitial Pneumonia)
findings
The disease has a lower lobe, posterior, peripheral predominance with sparing of the
immediate subpleural lung seen in up to 50% o f cases. This finding of immediate
subpleural sparing is said to be highly suggestive. Ground glass is the NSIP equivalent
o f honeycombing.
NSIP findings quick
P e rip h e ra l G ro un d Glass with S u b p le u ra l Sparing
UIP quick overview
Apical to Basal Gradient
Heterogeneous Histology
Honeycombing Ground Glass
Traction Bronchiectasis
.
NSIP quick overview
Gradient is less obvious
(but still more in lower lobes)
Homogenous Histology
Ground Glass
Micronodules
.
RB-ILD and DIP
overview
I’m going to discuss these two together because some people feel they are a spectrum. For sure they are both smoking related diseases.
• RB-ILD - Apical Centrilobular ground glass nodules
• DIP - More diffuse GGO, with patchy or subpleural distribution
RB-ILD
overview
This tends to be more upper lobe predominant (note that DIP tends to be more lower lobe predominant). Localized centrilobular ground glass nodules. The pathology tends to involve the entire cross section of lung.
Respiratory Brochiolitis +
Symptoms =
RB-ILD
RB-ILD-
Apical Centrilobular ground glass nodules + Smoking History
DIP
overview
Desquamative interstitial pneumonia is
thought o f as the end spectrum of RB-ILD,
and generally seen in 50 year old heavy
smokers. Extras from 1984 comedy classic
“Revenge o f the Nerds” seem to enjoy going
to radiology conferences to voice their
disapproval o f the term “DIP” because the
pathology is not desquamation of alveolar
epithelium but instead represents a filling of
alveolar spaces with macrophages. Could
these same weirdos be writing the questions ?
The dark side clouds everything. Impossible to
see the future is.
DIP…..just think
peripheral lower lobe predominant ground glass, with small cystic spaces
You can see consolidations - but they are usually associated with cryptogenic pneumonia.
You can see fibrosis - but it is rare (like 5-10%) - I would not expect that on the exam.
DIP-
B ila te ra l F airly S ym m e tric B a sila r
P re d om in a n t G ro u n d G lass
Sarcoid:
overivew
This is a multi-system disease that creates “non-caseating granulomas.” The classic age is between 20-40. Along those lines, if the header to the question describes an African American female in her 20s-30s the answer is probably sarcoid. The lungs are by far the most common organ affected (90%).
Sarcoid:
thingks to know
Elevated angiotensin-converting enzyme (ACE)
Hypercalcemia
Sarcoid:
lymph nodes
Mediastinal lymph nodes are seen in 60-90% o f patients (classically in a 1-2-3 pattern of
bilateral hila and right paratracheal). They have perilymphatic nodules, with an upper
lobe predominance. Late changes include, upper lobe fibrosis, and traction bronchiectasis
(honeycombing is rare). Aspergillomas are common in the cavities o f patients with end
stage sarcoid.
Sarcoid:
CXR for staging
Stage 0 = Normal Stage 1 = Hilar / Mediastinal Nodes Only Stage 2 = Nodes + Parenchyma Disease Stage 3 = Parenchymal Disease Stage 4 = End Stage (Fibrosis)
Sarcoid:
signs
- 1-2-3 Sign - bilateral hila and right paratracheal
- Lambda Sign - same as 1-2-3, but on Gallium Scan
- CT Galaxy Sign - upper lobe masses (conglomerate o f nodules) with satellite
nodules
CHF
overview
CHF is obviously not an ILD. However, it can sorta look like one on Chest X-Ray so I
opted to lump it in here. Congestive heart failure occurs because of cardiac failure, fluid
overload, high resistance in the circulation, or some combination o f the three. There are
three phases o f CHF, and these lend themselves to testable trivia.
CHF
stage 1
Stage 1 “ Redistribution”
Wedge Pressure
13-18
Cephalization o f vessels, Big
heart, Big Vascular Pedicle
CHF
stage 2
Stage 2 “ Interstitial Edema”
Wedge Pressure
18-25
Kerley Lines, Peribronchial
Cuffing, Less distinct contour of
Central Vessels
CHF
stage 3
Stage 3 “Alveolar Edema”
Wedge Pressure
> 2 5
Airspace “fluffy” opacity,
Pleural effusion
*Swan Ganz Pulmonary Wedge Pressures
Swan Ganz Pulmonary Wedge Pressures are an indirect measurement o f left atrial
pressure. They can help prove a cardiogenic etiology> to pulmonary edema.
Right Heart Failure
This is less common than left heart failure, which ironically is the most common cause. Left
heart failure causes pulmonary venous HTN which causes pulmonary arterial HTN, which
causes right heart failure. Some other less common causes o f right heart failure include
chronic PE and right-sided valve issues (tricuspid regurg). The imaging features of right
heart failure include dilation of the azygos vein, dilation o f the right atrium, dilation of the
SVC, ascites, big liver, and contrast reflux into the hepatic veins on CTPA.
Lung Transplant
Immediate Complications (< 24 hours)
Donor-Recipient Size Mismatch
Mismatch up to 25% is ok. You can have a
compressed lung (by the hyperexpanded
emphysematous lung). Imaging is usually
atelectasis.
Lung Transplant
Immediate Complications (< 24 hours
Hyperacute Rejection
Secondary to HLA and ABO antigens. It’s
rapid and often fatal. Imaging shows massive
homogenous infiltration
Lung Transplant
Early Complications (24 hours - 1 week)
Reperfusion Injury
Peaks at day 4 as a non-cardiogenic edema
related to ischemia-reperfusion. Typically
improves by day 7.
Lung Transplant
Early Complications (24 hours - 1 week)
air leak/peristant pneumothorax
Defined as a continuous leak for more than 7
days.
Lung Transplant
Intermediate Complication (8 days - 2 months)
Acute Rejection
Ground Glass opacities and intralobular septal
thickening. (No ground glass = no rejection).
Improves with steroids.
Lung Transplant
Intermediate Complication (8 days - 2 months)
Bronchial Anastomotic Complications
Leaks occur in the first month, stenosis can develop later (2-4 months).
Lung Transplant
Late Complications (2-4 months)
CMV Infection
The most common opportunistic infection.
Ground glass, tree-in-bud. Rare before 2 weeks.
Lung Transplant
Later Complications (> 4 months)
Chronic Rejection
Bronchiolitis Obliterans; Affects 50% at 5 years. Brochiectasis, bronchial wall thickening, air
trapping.
Lung Transplant
Later Complications (> 4 months)
Cryptogenic Organizing Pneumonia
Occurs with chronic rejection (but more
commonly with acute rejection). Responds to steroids.
Lung Transplant
Later Complications (> 4 months)
PTLD
Typically seen within the first year. EBV in 90%.
Lung Transplant
Later Complications (> 4 months)
Upper Lobe Fibrosis
Associated with chronic rejection
Chronic Rejection I Bronchiolitis Obliterans Syndrome
This is the
major late complication, that affects at least half o f the transplants at 5 years (most
commonly at 6 months). The term bronchiolitis obliterans is often used interchangeably
with chronic rejection. The findings on CT include bronchiectasis, bronchial wall
thickening, air trapping, and interlobular septal thickening. Just think air trapping on
expiration seen at or after 6 months = chronic rejection.
Recurrence of Primary Disease a fte r Transplant
For the purpose of
multiple choice tests know that sarcoidosis is the most common recurrent primary
disease (around 35%). Lots o f other things can recur.
Lung Cancer a fte r Transplant
Just remember that the native lung is still
diseased, and can get cancer. The highest rate is with pulmonary fibrosis, and the most
common risk factor is heavy tobacco use.
Pulmonary Alveolar Proteinosis (PAP):
overview
For the purpose o f multiple
choice, this is an Aunt Minnie - always shown as crazy paving lung (interlobular septal
thickening with ground glass). This can be primary (90%), or secondary (10%). The
secondary causes worth knowing are cancer or inhalation (silico-proteinosis).
Pulmonary Alveolar Proteinosis (PAP):
trivia
• They are at increased risk o f Nocardia infections, and can have nocardia brain
abscesses.
• Smoking is strongly associated with the disease.
• When seen in children (presenting before age 1) there is a known association with alymphoplasia.
• Can progress to pulmonary fibrosis (30%).
• Treatment is bronchoalveolar lavage
Crazy Paving
Interlobular septal thickening and ground glass. This isn’t always PAP, in fact in real life that it is usually NOT PAP. There is a differential that includes common things like edema, hemorrhage, BAC, Acute Interstitial Pneumonia.
always pap on test
Lipoid Pneumonia
types
There are actually two types; endogenous and exogenous.
Lipoid Pneumonia
exogenous
A certain percentage o f elderly people become absolutely obsessed with
their bowel movements. If you did Family Medicine addressing this psychopathology
would steal a certain amount of hours out o f your life per week. Lipoid pneumonia is
seen in old people who like to drink/aspirate mineral oil (as a laxative). It can also be
seen with the aspiration o f vegetable oil or other animal oils. The look on plain film is an
area o f lung opacification that is chronic or slowly increases with time. The look on CT
is a dead give away and the most likely way this will be shown is with low attenuation /
fat density in the consolidation. Having said that this is also in the crazy paving
differential.
Lipoid Pneumonia
acute exogenous
This is seen in children who accidentally poison
themselves with hydrocarbons, or idiots trying to perform fire-eating or flame blowing
Lipoid Pneumonia
endogenous
This is actually more common than the exogenous type, and results from
post obstructive processes (cancer) causing build up o f lipid laden macrophages
Lipoid Pneumonia
findings
Fat Density in the Consolidation
Lipoid Pneumonia
gamesmanship
“Why a re you showing me th e lung on that window?”
O b v io u sly p u lm o n a ry p a th o lo g y is b e s t sh ow n on a lu n g window. So an y tim e the te s t w rite r is sh ow in g y o u a p u lm o n a ry p a th o lo g y on a n o n -lu n g window, that
™ y sh o u ld cu e you to th in k ab o u t som e d iffe ren t things.
(1): Is th e fin d in g in the m e d ia s tin um or ribs?
(2): I f it’s c le a rly a lung fin d in g then w h a t w in d ow are th ey u sin g ?
• S o ft tis su e w in d ow is c la s s ic a lly u se d to sh ow fa t in a le sio n - th in k h am a rtom a o r lip o id p n eum o n ia.
• B o n e w in d ow might be u sed to sh ow a d iffu s e p ro c e s s su ch a s p u lm o n a ry m ic ro lith ia sis.
Organizing Pneumonia
overview
This used to be called BOOP, which was a lot more fun to say. It’s not an active infection (as the name would suggest) but instead granulation tissue deposition within the alveolar spaces secondary to fibroblast proliferation. Because it is not an active infection antibiotics won’t help. However, it does respond well to steroids, and has an excellent prognosis.
Organizing Pneumonia
causes
There are lots o f different causes; idiopathic, prior infection, drugs (amiodarone), collagen vascular disease, fumes, etc... You will see the word “cryptogenic” used when there is no specific cause known. Then it is COP instead of OP.
Organizing Pneumonia
findings
Patchy air space consolidation or GGO (90%), in a peripheral or peri-bronchial distribution.
Opacities tend to be irregular in shape. Both OP and Chronic Eosinophilic Pneumonia can
present as peripheral consolidations. Findings of fibrosis are typically absent.
Organizing Pneumonia
hx
The history o f “persistent symptoms following treatment for pneumonia” could be a clue to
think OP. The most common “persistent symptoms” are a cough lasting several months, low
grade fever, SOB, and just generally feeling like shit.
Reverse Halo (Atoll) Sign
COP
the classic sign - seen in around 30% of cases:
Consolidation around a ground glass center.
Chronic Eosinophilic Pneumonia
overview
Can be idiopathic or associated with a known antigen. Peripheral eosinophilia (blood test) is
usually present. An asthma history is found in about 50% o f cases. It looks exactly look COP
(both can present as peripheral consolidations). When you say COP you should say this one too
(some people think it’s the same disease as COP).
Chronic Eosinophilic Pneumonia
CT Findins
Peripheral GGO or consolidation. Upper lobes tend to be favored.
Halo sign overview
- Nodule with ground glass around it
- Represents hemorrhage / invasion into surrounding tissues
- Invasive Aspergillosis (Classic)
- Other Fungus
- Hemorrhagic Mets
- Adenocarcinoma in Situ (BAC)
- Wegeners
Reverse (atoll) halo overview
Central ground glass with rim of consolidation - COP (Classic) - TB - Pulmonary Infarct - Invasive Fungal and Wegeners ** these can also be seen with regular Halo
Hypersensitivity Pneumonitis
overview
This is actually common. It’s caused by inhaled organic antigens. It has acute, subacute,
and chronic stages. Most of the time it’s imaged in the subacute stage.
Hypersensitivity Pneumonitis
subacute
Patchy ground glass opacities. Ill-defined Centrilobular ground glass nodules
(80%). Often has mosaic perfusion, and air trapping.
Hypersensitivity Pneumonitis
chronic
Looks like UIP + Air trapping.
You are gonna have traction bronchiectasis
and air trapping.
Hypersensitivity Pneumonitis
buzzword
“headcheese” because it’s a mix o f everything (Ground Glass,
Consolidation, Air-Trapping, and Normal Lung)
This vs That: Chronic Hypersensitivity Pneumonitis (HP) vs UIP.
Features that favor Chronic HP over UIP:
• Air Trapping involving 3 more lobes
• Mid-Upper lobe predominant fibrosis
Airway anatomy
The basic anatomy of the trachea is a bunch of anterior horseshoes of cartilage,
with a posterior floppy membrane. This membrane can bow inward on expiratory CT (and this
is normal). The transverse diameter should be no more than 2.5 cm (same as the transverse
diameter of an adjacent vertebral body).
Tracheal Disease Game Plan:
Three big questions to ask yourself.
(1) Does it involve the posterior membrane ? (2) is it focal or diffuse ? and (3) is there calcification ?
Relapsing Polychondritis
Spares the posterior membrane. Diffuse thickening o f the
trachea. No calcifications. Characterized by recurrent episodes of cartilage inflammation, and
recurrent pneumonia.
Recurrent episodes of cartilage inflammation (ears, nose, joints, laryngeal and thyroid cartilage). Recurrent pneumonia is the most common cause of death.
Post Intubation Stenosis
Focal Subglottic circumferential stenosis, with an hourglass configuration.
Focal Subglottic
Wegener’s airway
Circumferential thickening, which can be focal or long segment. No
calcifications. Subglottic involvement is common.
C-ANCA+, Sub-glottic
trachea is the most
common location.
Tracheobronchopathia Osteochondroplastica (TBO):
Spares the posterior membrane. You have development of cartilaginous and osseous
nodules within the submucosa of the tracheal and bronchial walls.
Development of cartilaginous and osseous nodules. Typically occurs in men older than 50.
Amyloidosis
airway
Irregular focal or short segment thickening, which can involve the posterior membrane. Calcifications are common.
Often confined to the
trachea and main
bronchi. Calcifications
are common.
Spares the Posterior Membrane
Relapsing
Polychondritis
Tracheobronchopathia
Osteochondroplastica
(TBO):
Does NOT Spare the Posterior Membrane
amyloid
post intubation
wegeners
Saber-Sheath Trachea
Coronal diameter of less than two thirds the sagittal diameter.
I say “saber-sheath trachea,” you say COPD.
Trivia: The main bronchi will be normal in size.
The tracheal wall will be normal in thickness.
Pulmonary Neuroendocrine Tumors
in the airway
Typical Carcinoid
-Low-Grade Malignant-
< 3cm
More Likely to Be
Central (tracheal
bifurcation)
More likely to appear to
be within the lumen o f
the airway. More likely
to be calcified (-30%).
Age - 50s
Pulmonary Neuroendocrine Tumors
kindof in the airway
Atypical Carcinoid
-Intermediate Malignant-
> 3cm
More Likely to Be
Peripheral (distal to the
segmental bronchi).
May not show a
bronchial relationship -
or be partially
endobronchial.
Age - 6 0 s
Association with Smoking
Pulmonary Neuroendocrine Tumors
not in the airway
Large Cell (LCNEC)
and Small Cell (SCLC)
-High Grade Malignant-
LCNEC: Peripheral
pulmonary mass -
around 3.5 cm
SCLC: Large central /
mediastinal mass
involving the hilum
Pulmonary Neuroendocrine Tumors
tribia
Bronchial Carcinoid is more likely to Met inside the eyeball (uveal tract). Where as a GI carcinoid is most likely to met to the extra ocular muscles
Tracheal tumors
carcinoid
• Extremely rare in the trachea (< 1%).
• More typically seen Endobronchial
• Carcinoids usually have a central endobronchial location
(although they can rarely be found in the pulmonary parenchymapresented
as a nodule or mass in an older patient).
• Pulmonary carcinoid tends to be slow growing and locally
invasive (only met to nodes about 10% o f the time).
• No surprise they can cause obstructive symptoms. They can also
cause hemoptysis because they are highly vascular.
• For the purpose of multiple choice = No association with smoking
(**there maybe an association with the atypical sub-type)
• An octreotide scan can be used to localize a carcinoid tumor.
• PET can be falselv negative in ~ 25% o f cases (thev can be cold
on PETV
• Rarely they can cause a carcinoid syndrome with flushing etc…
The valvular degradation that occurs tends to be on the left side
(mitral and aortic), as opposed to the GI carcinoid syndrome
which targets the right side (tricuspid and pulmonic).
Tracheal tumors
adenoid cystic
- 2nd Most common tracheal malignancy
- Favors the upper trachea, and prefers the posterior lateral trachea
- 20x more likely to be in the trachea (relative to carcinoid).
- Has a variable look - can be thickening, a mass, or a nodule.
- It is NOT associated with smoking.
- They are usually in the main or lobar bronchus.
Tracheal tumors
squamos cell
• Most Common tracheal malignancy.
• Associated with smoking,
• Often multifocal (10%), favors the lower trachea / proximal
bronchus
Tracheal tumors
mets
Usually via direct extension (lung, thyroid, esophagus)
squamos cell papilloma
- Most common benign tumor o f the trachea
- When it’s a single papilloma think smoking.
- When it’s multiple papillomas think HPV.
Cystic Fibrosis
things to know
Bronchiectasis (begins as cylindrical and progresses to varicoid)
It has an apical predominance (lower lobes are less affected)
Hyperinflation
Pulmonary Arterial Hypertension-
Mucus plugging (finger in glove)
Primary Ciliary Dyskinesia
Those little hairs in your lungs that clear
secretions don’t work. You end up with bilateral lower lobe bronchiectasis (remember that
CF is mainly upper lobe). Other things these kids get is chronic sinusitis (prominent from an
early age), and impaired fertility (sperm can’t swim, girls get ectopics). They have chronic
mastoid effusions, and conductive hearing loss is common (those little ear nerve hair things
are fucked up too). An important testable fact is that only 50% of the primary ciliary
dyskinesia patients have Kartagener’s Syndrome.
CF quick
Abnormal Mucus, Cilia cannot move it
Normal Sperm, Absent Vas Deferens
Upper lobe bronchiectasis
primary ciliary dyskinesia quick
Normal Mucus, Cilia don’t work
Abnormal Sperm (they can’t swim), Normal Vas Deferens
Lower lobe bronchiectasis
Williams Campbell Syndrome
Huge zebra that manifests as
congenital cystic bronchiectasis from a deficiency of cartilage in the 4,h-6” order bronchi
Mounier-Kuhn
Tracheobronchomegaly
There is a massive dilatation o f the trachea
(> 3cm). It’s not well understood, and really the
only thing that does this.
Mounier-Kuhn=
Big Fucking Trachea
Small Airways Disease
bronchiolitis overview
This is an inflammation o f the small airways. It can be infectious (like
the viral patterns you see in kids) or inflammatory like RB-ILD in smokers, or asthma in kids.
Small Airways Disease
bronchiolitis air trapping
When you see areas o f lung that
are more lucent than others - you are likely
dealing with air trapping. Technically, air
trapping can only be called on an expiratory
study as hypoperfusion in the setting of
pulmonary arterial hypertension can look
similar. Having said that, for the purpose of
multiple choice test taking, I want you to think
(1) bronchiolitis obliterans in the setting o f a
lung transplant, or (2) small airway disease -
asthma / bronchiolitis.
Small Airways Disease
bronchiolitis tree in bud
This is a nonspecific finding that can make you think small airway disease. It’s
caused by dilation and impaction o f the centrilobular airways. Because the centrilobular
airways are centered 5-10 mm from the pleural surface, that’s where they will be. It’s usually
associated with centrilobular nodules.
Small Airways Disease
follicular bronchiolitis
This is an inflammatory process seen in rheumatoid arthritis
or Sjogrens. It’s not well understood and is related to lymphoid hyperplasia. It looks like
centrilobular ground glass nodules with scattered areas o f bronchial dilation.
Small Airways Disease
follicular bronchiolitis
This is an inflammatory process seen in rheumatoid arthritis
or Sjogrens. It’s not well understood and is related to lymphoid hyperplasia. It looks like
centrilobular ground glass nodules with scattered areas o f bronchial dilation.
Small airway disease
constrictive bronchiolitis
This is another inflammatory process that can be seen
in viral illness, transplant patients, drug reactions, or inhalation injury. It is also often
identified in patients with DIPNECH. It occurs secondary to mononuclear cells which form
granulation tissue and plug the airway. You see air trapping on expiratory imaging. This is
supposedly the cause o f Swyer-James hyperlucent lung.
Infectious Bronchiolitis
tree in bud
RBILD
Smokers. Centrilobular ground glass nodules
upper lobe predominant
Sub-Acute Hypersensitivity Pneumonitis
Inhaling dust / other misc garbage.
Centrilobular Ground glass nodules
Follicular Bronchiolitis
RA and Sjogrens. Centrilobular ground glass nodules
Constrictive Bronchiolitis
Viral, Drugs, Transplant, Inhalation.
Air-Trapping. DIPNECH
Aspiration Pneumonia
overview
Stroked-out old people and drunks love to aspirate.
The testable trivia is to know the typical location o f aspiration; posterior segment o f upper
lobes and superior segment o f lower lobes if supine when aspirating, bilateral basal lower
lobes in upright aspiration. May favor the right side, just like an ET tube.
The most common complication is infection which can manifest as an empyema
(which can then get a broncho-pleural fistula).
Aspiration Pneumonia
Aspiration o f Gastric Acid
“Mendelson’s Syndrome”
Gives you an airspace opacity, if massive
can look like pulmonary edema
Aspiration Pneumonia
Aspiration o f water or neutralized gastric
contents
“Fleeting Opacity” that resolves in hours
Aspiration Pneumonia
Aspiration o f Bugs (often mouth bugs)
Gives you a real pneumonia, can get parapneumonic
effusion, empyema, or even
broncho-pleural fistula.
Aspiration Pneumonia
Aspiration o f Oil (often mineral oil)
Lipoid Pneumonia. Will be low density
Collagen vascular disease
Interstitial lung diseases are common in patients with
collagen vascular diseases. The association are easily tested, so I made you this chart. I tried
to hit the high points of testable trivia.
Collagen Vascular Disease Pulmonary Manifestations
lupus
More pleural effusions and
pericardial effusions than with
other connective tissue disease
Fibrosis is uncommon. Can
get a “shrinking lung.”
Collagen Vascular Disease Pulmonary Manifestations
RA
Looks like UIP and COP. Lower
lobes are favored.
Reticulations with or without
honeycombing, and
consolidative opacities which
are organizing pneumonia
Collagen Vascular Disease Pulmonary Manifestations
Scleroderma
NSIP> UIP; lower lobe
predominant findings.
Look for the dilated fluid
filled esophagus.
Collagen Vascular Disease Pulmonary Manifestations
Sjogrens
LIP
Extensive ground glass
attenuation with scattered thin
walled cysts.
Collagen Vascular Disease Pulmonary Manifestations
AS
Unoer lobe fibrobullous disease
Usually unilateral first, then
progresses to bilateral.
Caplan Syndrome
Rheumatoid Arthritis + Upper Lobe Predominant Lung Nodules.
These nodules can cavitate, and there may also be a pleural effusion.
“Shrinking Lung”
This is a progressive loss of lung volume in both lungs seen in
patients with Lupus ( “S” hrinking “L” ung for “SLe”). The etiology is either diaphragm
dysfunction or pleuritic chest pain.
Shrinking lung trivia
Most common manifestation of SLE in Chest = Pleuritis with/without pleural effusion.
Hepatopulmonary syndrome
This is seen in liver patients with the classic history of
“shortness o f breath when sitting up.” The opposite of what you think about with a CHF
patient. The reason it happens is that they develop distal vascular dilation in the lung bases
(subpleural telangiectasia), with dilated subpleural vessels that don’t taper and instead extend
to the pleural surface. When the dude sits up, these things engorge and shunt blood - making
him/her short of breath. A Tc MAA scan will show shunting with tracer in the brain (outside the
lungs). They have to either tell you the patient is cirrhotic, show you a cirrhotic liver, or give
you that classic history if they want you to get this.
Wegener Granulomatosis
overview
The classic triad is upper tract, lung, and kidneys
(although this triad is actually rare). The lungs are
actually the most common organ involved (95%).
There is a highly variable look.
Wegeners
findings
The most common presentation is also probably the
most likely to be tested; nodules with cavitation.
The nodules tend to be random in distribution with
about half o f them cavitating. They can also show you
ground glass changes which may represent
hemorrhage.
wegenrs new name
“Granulomatosis with Polyangiitis ” because Wegener was a member of the Nazi party. It is also possible that he worked with the deep science unit Hydra which plagued the world with schemes of global domination and genocide. Seriously, I’ve heard the guy was a real asshole. Not just a Nazi, but a bad tipper, and a habitual line stepper (deliberately didn’t wash his hands after he took a shit).
Goodpasture Syndrome
Another autoimmune pulmonary renal syndrome. It favors young men. It’s a super
nonspecific look with bilateral coalescent airspace opacities that look a lot like edema (but
are hemorrhage). They resolve quickly (within 2 weeks). If they are having recurrent
bleeding episodes then they can get fibrosis. Pulmonary hemosiderosis can occur from
recurrent episodes o f bleeding as well, with iron deposition manifesting as small, ill-defined
nodules.
Pleural plaque
If they show you a pleural plaque they probably want you to say
asbestos-related disease. Remember the plaque doesn’t show up for
like 20-30 years after exposure.
Remember that the pleural plaque of asbestosis typically spares the
Costophrenic angles.
Pleural Calcifications
other than asbestos
- Old Hemothorax
- Old Infection
- TB
- Extraskeletal
Osteosarcoma
Mesothelioma
rapid review
• Most common cancer of the pleura.
• About 80% of them have had asbestos exposure
(NOT dose-dependent).
• Lag time is around 30-40 years from exposure.
• “Pleural rind” - thickening that wraps all the way around
the lung - including the medial surface of the pleura (near
the heart)
• Extension into the fissure is highly suggestive.
Solitary Fibrous Tumor of the Pleura (SFTP)
overivew
This is a solitary (usually) tumor
arising from the visceral pleura. The key is to know that they are NOT associated with asbestos,
smoking, or other environmental pollutants. They can get very large, and be a source of chest pain
(although 50% are incidentally found).
Solitary Fibrous Tumor of the Pleura (SFTP)
trivia
- Not associated with asbestos, smoking, or other environmental pollutants
- Even when they are big, they are usually benign
- Doege-Potter syndrome occurs in like 5% of cases. This is an episodic hypoglycemia (tumor
can secrete an insulin like growth factor) - Hypertrophic osteoarthropathy occurs in like 30% of the cases.
Pleural mets
Here is the high yield trivia on this. As a general rule the subtype of
adenocarcinoma is the most likely to met to the pleura. Lung cancer is the most common primary,
with breast and lymphoma at 2nd and 3rd. Remember that a pleural effusion is the most common
manifestation of mets to the pleura
Pleural lipoma
This is the most common benign soft tissue tumor of the pleura. The patients
sometimes feel the “urge to cough.” They will not cause rib erosion. They “never” turn into a
sarcoma. The differential consideration is extra-pleural fat, but it is usually bilateral and
symmetric.
Pleural Effusion:
Some random factoids on pleural effusions that could be potentially testable.
There has to be around 175 cc of fluid to be seen on the frontal view (around 75cc can be seen on the
lateral). Remember that medicine docs group these into transudative and exudative based on protein
Pleural Effusion:
subpulmonic effusion
A pleural effusion can accumulate between the lung base and the diaphragm.
These are more common on the right, with “ski-slopping” or lateralization of the diaphragmatic
peak. A lateral decubitus will sort it out in the real world.
Right sided subpulmonic effusion
Notice
the high point o f the
diaphragm is shifted
laterally
left sided subpulmonic effusion
The key here is the increased space between the stomach bubble and lung base.
Encysted Pleural Effusion
It is possible to have pleural fluid
collect between the layers o f the
pleura creating a oval / round
appearance mimicking a Cancer.
Empyema
Basically this is an infected pleural
effusion. It can occur with a simple pneumonia but
is seen more in people with AIDS. Usually these
are more asymmetric than a normal pleural
effusion. Other features include enhancement of the
pleura, obvious septations, or gas
Empyema Necessitans
This is the fancy
Latin word for when the empyema eats through the
chest wall and into the soft tissues. It’s classically
seen with TB (70%), with the second most common
cause being actinomyces.
empyema signs
lentiform
Split Pleural Sign (thickening and separation o f the visceral and parietal pleura)
Treated with chest
tube
Pulmonary abscess signs
round
claw sign (acute angle with pleura
NOT treated with chest
tube (risk o f
bronchopleural fistula).
Diaphragmatic Hernia
These can be acquired via trauma, or congenital. The congenital
ones are most common in the back left (Bochdalek), with anterior small and right being less
common (Morgagni). The traumatic ones are also more common on the left (liver is a buffer).
Paralysis
This is a high yield topic because you can use fluoro to help make the diagnosis.
Obviously the dinosaurs that write these tests love to ask about fluoro (since that was the only thing
they did in residency). Diaphragmatic paralysis is actually idiopathic 70% of the time, although
when you see it on multiple choice tests they want you to think about phrenic nerve compression
from a lung cancer. Normally the right diaphragm is higher, so if you see an elevated left
diaphragm this should be a consideration.
sniff test
On a fluoroscopic sniff test you are looking for paradoxical movement (going up on inspiration -
instead of down).
Anterior mediastinal masses
thymus thyroid thoracic aorta teratoma (germ cell tumors) terrible lymphoma
Thymus
overview
The thymus can do a bunch of sneaky things.
It can rebound from stress or chemotherapy and look huge.
It can get cysts, cancer, carcinoid, etc…
Thymus
rebound
Discussed in detail in the Peds chapter.
After stress or chemotherapy the thing can blow up 1.5
times the normal size and simulate a mass. Can be hot
on PET.
thymus cyst
Can be congenital or acquired.
Acquired is classic after thoracotomy, chemotherapy,
or HIV. They can be unilocular or multilocular. T2
bright is gonna seal the deal for you.
thymoma
So this is kind of a spectrum ranging from non-invasive thymoma, to invasive
thymoma, to thymic carcinoma. Calcification makes you think it’s more aggressive. The
thymic carcinomas tend to eat up the mediastinal fat and adjacent structures. The average
age is around 50, and they are rare under 20. These guys can “drop met” into the pleural and
retroperitoneum, so you have to image the abdomen.
Thymus
assocations
Myasthenia Gravis, Pure Red Cell Aplasia, Hypogammaglobinemia.
thymolipoma
1 only mention this zebra because it has a characteristic look. It’s got a
bunch of fat in it. Think “fatty mass with interspersed soft tissue.”
thymus rebound vs residual lymphoma
• PET might help - both arc hot, but lymphoma is hotter. • MRI - Thymic Rebound should drop out on in-out of phase imaging (it has fat in it). Lymphoma will not drop out.
Germ cell tumor
Almost always Teratoma (75%). Mediastinal Teratoma - This is
the most common extragonadal germ cell tumor. They occur in kids (below age 1) and adults
(20s-30s). They are benign, but carry a small malignant transformation risk. Mature subtypes
arc equal in Men and Women, but immature subtypes are exclusively seen in men (which should
be easy to remember). There is an association with mature teratomas and Klinefelter
Syndrome. The imaging features include a cystic appearance (90%), and fat. They can have
calcifications including teeth - which is a dead give away
Pericardial Cyst
This is uncommon and benign. The classic location
is the right anterior cardiophrenic angle. This
classic location is the most likely question.
Fibrosing Mediastinitis (Sclerosing Mediastinitis) -
OVERVIEW
This is a proliferation o f fibrous tissue that occurs within the mediastinum.
Fibrosing Mediastinitis (Sclerosing Mediastinitis) -
granulomatous
(the one everyone thinks
about) classically caused by histoplasmosis).
Other causes include TB, and Sarcoid.
This will look like a soft tissue mass with
calcifications that infiltrates the normal fat planes
of the mediastinum.
Fibrosing Mediastinitis (Sclerosing Mediastinitis) -
non-granulomatous
is the more rare subtype that people read about once and then
forget. Some people will call this form “idiopathic” although the subtype is better thought
o f as a response to an autoimmune disease (SLE, RA, Behcet, etc…) or a complication to
radiation therapy. There is also a testable association with the headache medication
methysergide. It’s associated with retroperitoneal fibrosis when idiopathic.
This subtype also looks like a soft tissue mass but tends to be more infiltrative, lack
calcifications, and can enhance post contrast.
Fibrosing Mediastinitis (Sclerosing Mediastinitis) -
both types cause
superior vena cava syndrome.
Bronchogenic Cyst
These congenital lesions are usually within the mediastinum
(most commonly found in the subcarinal space) or less commonly intraparenchymal. For the
purpose of the exam, they are going to be in the subcarinal region, causing obliteration of the
azygoesophageal line on a CXR, and being waterish density on CT.
Lymphadenopathy -
in the anterior mediastium
Could be mets, could be infection, could be reactive. It is
generally abnormal to be larger than 2cm in short axis (makes you suspect cancer).
Mediastinal Lipomatosis
Excess unencapsulated fat seen in patients with iatrogenic
steroid use, Cushings, and just plain old obesity.
Posterior Mediastinal Masses
neurogenic
The most common posterior mediastinal mass is one of neurogenic origin.
This includes schwannomas, neurofibromas, and malignant peripheral nerve sheath tumors.
Posterior Mediastinal Masses
bone marrow
Extramedullary hematopoiesis (EMH) is a response to failure of the bone
marrow to respond to EPO. Classic conditions include CML, Polycythemia vera, myelofibrosis,
sickle cell, and thalassemia.
Pulmonary Embolism
This is a significant cause of mortality in
hospitalized patients. The gold standard is
catheter angiography, although this is invasive and
carries risks. As a result tests like the D-Dimer
(which has an almost 100% negative predictive
value), and the DVT lower extremity ultrasound
were developed. Now, the CTPA is the primary
tool.
Historical Signs of PE on a CXR
Westermark Sign Regional Oligemia
Fleischner Sign Enlarged Pulmonary Artery
Hampton’s Hump Peripheral Wedge Shaped opacity
Pleural Effusion
Obviously not specific, but seen in 30% of PEs.
Acute PE
Clot is Central
Venous Dilation
Perivenous soft tissue edema
Pleural Effusion is common
Acute PE can cause sudden
death from arrhythmia or acute
right heart failure
CTPA is the exam of choice.
Chronic PE
Clot (if seen) is more Peripheral. May be “web like”
Shrunken Veins with collateral vessels
Calcifications within the thrombi and within the venous walls
Lungs may show a mosaic attenuation pattern
Chronic PE is a well described cause of pulmonary
hypertension (obstruction in the vascular bed causes an increase
in vascular resistance)
VQ Scan (believe it or not) is probably superior to CT.
Massive PE
Hypotension (SBP < 90)
Sub-massive PE
Stable BP, but RV dysfunction or positive cardiac enzymes (myocardial
necrosis).
Right Heart Strain
RV Dilated Larger Than LV
- Probably the best sign
- Leftward bowing of the ventricular septum is also helpful
Contrast Reflux into the Hepatic Veins
-Less Reliable.
Pulmonary Infarct Mimics:
A pulmonary infarct is a wedge-shaped opacity that is going to
“melt” (resolve slowly), and sometimes can cavitate. Obviously a cavitary lesion throws up lots of
flags and makes people say TB, or cancer. When it’s an opacity in the lung and the patient doesn’t
have a fever, sometimes people think cancer - plenty of pulmonary infarcts have been biopsied
Pulmonary Veno-Occlusive Disease
Uncommon variant of primary pulmonary
hypertension, that affects the post capillary pulmonary vasculature. For gamesmanship: PAH +
Normal Wedge, you should think this. The normal wedge pressure differentiates it from other post
capillary causes; such as left atrial myxoma, mitral stenosis, and pulmonary vein stenosis.
Pulmonary Artery Aneurysm/Pseudoaneurysm
overview
Think about three things for
multiple choice; (1) Iatrogenic from swan ganz catheter *most common (2) Behcets, (3) Chronic
PE. When they want to lead towards swan ganz they may say something like “patient in the ICU.”
The buzzwords for Behcets are: “Turkish descent” and “mouth and genital ulcers.”
Pulmonary Artery Aneurysm/Pseudoaneurysm
Rasmussen Aneurysm
This has a cool name, which instantly makes it high yield for testing.
This is a pulmonary artery pseudoaneurysm secondary to pulmonary TB. It usually involves
the upper lobes in the setting of reactivation TB.
Pulmonary Artery Aneurysm/Pseudoaneurysm
Hughes-Stovin Syndrome
This is a zebra cause of pulmonary artery aneurysm that is similar
(and maybe the same thing) as Behcets. It is characterized by recurrent thrombophlebitis and
pulmonary artery aneurysm formation and rupture
Pulmonary Artery Aneurysm/Pseudoaneurysm
Tetralogy of Fallot Repair Gone South
So another possible testable scenario is the patch
aneurysm, from the RVOT repair.
Pulmonary Hypertension
overview
Pulmonary arterial pressures over 25 are going to make the
diagnosis. I prefer to use the “outdated” primary and secondary way of thinking about this
Pulmonary Hypertension
primary
Idiopathic type is very uncommon, seen in a small group of young women in their 20s.
Pulmonary Hypertension
secondary
This is by far the majority, and there are a few causes you need to know: Chronic PE ,
Right Heart Failure/ Strain, Lung Parenchymal Problems- (This would include emphysema, and
various causes of fibrosis). COPDers with a pulmonary artery bigger than the aorta (A/PA ratio) have
increased mortality (says the NEJM).
Pulmonary Hypertension
imagins signs
The numbers people use for what is abnonnal are all over the
place - if forced I’d pick 29 mm. A superior strategy is to compare the size of the aorta and
pulmonary artery (a normal PA should not be bigger than the aorta). You can also compare the
segmental artery-to adjacent bronchus (>1:1 is abnonnal). Mural calcifications of central
pulmonary arteries (seen in Eisenmenger phenomenon) have been described. Additional nonspecific
signs include right ventricular dilation / hypertrophy, and centrilobular ground-glass nodules.
Pulmonary Hypertension
banana and egg
visualization of th main pulmonary artery (egg) at the level of the aortic arch (banana)
Pulmonary Hypertension
carina crossover
right pa crosses the carina midline anteriorly. it normally crosses more caudally
Diaphragmatic Injury
- Left side is involved 3 times more than the right (liver is a buffer)
- Most ruptures are “radial”, longer than 10 cm, and occur in the posterior lateral portion
- Collar Sign - This is sometimes called the hour glass sign, is a waist-like appearance o f the herniated organ through the injured diaphragm
- Dependent Viscera Sign - This is an absence o f interposition of the lungs between the chest wall and upper abdominal organs (liver on right, stomach on left).
Tracheo-Bronchial Injury
Airway injury is actually pretty uncommon. When it
does occur it’s usually within 2 cm o f the carina. Injury close to the carina is going to
cause a pneumomediastinum rather than a pneumothorax - that is a testable fact. When
you get a tracheal laceration, it most commonly occurs at the junction o f the cartilaginous
and membranous portions o f the trachea.
Macklin Effect
This is probably the most common cause o f pneumomediastinum in
trauma patients (and most people haven’t heard of it). The idea is that you get alveolar
rupture from blunt trauma, and the air dissects along bronchovascular sheaths into the
mediastinum.
Boerhaave Syndrome
You probably remember this from step 1. The physical exam
buzzword was “Hammonds Crunch.” Basically you have a ruptured esophageal wall from
vomiting, resulting in pneumomediastinum / mediastinitis
Flail Chest
This is 3 or more segmental (more than one fracture in a rib) fractures, or
more than 5 adjacent rib fractures. The physical exam buzzword is “paradoxical motion with breathing.”
Pneumothorax
Obviously you don’t want to miss the tension pneumothorax. The thing
they could ask is “inversion or flattening o f the ipsilateral diaphragm.”
Malpositioned Chest Tubes
Sometimes the ED will ram them into the
parenchyma. This is more likely to occur in the setting o f background lung disease or
pleural adhesions. You’ll see blood around the tube. Bronchopleural fistula may occur as
a sequela. The placement o f a tube in a fissure is sorta controversially bad (might be ok).
Hemothorax
If you see pleural fluid in the setting o f trauma, it’s probably blood.
The only way 1 can see them asking this is a density question; a good density would be 35-70 H.U.
Extrapleural Hematoma
This is a little tricky, and they could show you a picture
o f it. If you have an injury to the chest wall that damages the parietal pleura then you get
a hemothorax. If you have an injury to the chest wall, but your parietal pleural is still
intact, you get an extrapleural hematoma. The classic history is “persistent fluid
collection after pleural drain/tube placement.” The buzzword / sign is displaced
extrapleural fat. There is a paper out there that suggests a biconvex appearance is more
likely arterial and should be watched for rapid expansion. This may be practically useful,
but is unlikely to be asked. Just know the classic history, and displaced extrapleural fat
sign.
Pulmonary Contusion
This is the most common lung injury from blunt trauma.
Basically you are dealing with alveolar hemorrhage without alveolar disruption. The
typical look is non-segmental ill-defined areas of consolidation with sub pleural sparing.
Contusion should appear within 6 hours, and disappear within 72 hours (if it lasts longer
it’s probably aspiration, pneumonia, or a laceration).
Pulmonary Laceration
So a tear in the lung will end up looking like a
pneumatocele. If they show you one it will probably have a gas -fluid (blood) level in it.
These things can be masked by surrounding hemorrhage early on. The major difference
between contusion and laceration is that a laceration resolves much more slowly and can
even produce a nodule or a mass that persists for months.
Aorta
The aorta is injured most commonly at the aortic isthmus (some sources say
90%). The second and third most common locations are the root and at the diaphragm.
Some people say the root is actually the most common, but most o f these people die prior
to making it to the hospital. This is a minority opinion. If asked what is the most common
site o f traumatic aortic injury, the answer is isthmus. It’s usually obvious on a candy cane
CTA. The main mimic would be a “ductus bump,” which is a normal variant. The way to
tell (if it isn’t obvious) is the presence of secondary signs o f trauma (mediastinal
hematoma).
Blunt Cardiac Injury
If you have hemopericardium in the setting o f trauma, you
can suggest this and have the ED correlate with cardiac enzymes and EKG findings.
Fat Embolization Syndrome
This is seen in the setting of a long bone fracture or
Intramedullary rod placement. You get fat embolized to the lungs, brain, and skin (clinical
triad of rash, altered mental status, and shortness o f breath). The timing is 1-2 days after
the femur fracture. The lungs will have a ground glass appearance that makes you think
pulmonary edema. You will not see a filling defect - like a conventional PE. If they don’t
die, it gets better in 1-3 weeks.
Barotrauma
Positive pressure ventilation can cause alveolar injury, with air dissecting
into the mediastinum (causing pneumomediastinum and pneumothorax). Patients with
acute lung injury or COPD have a high risk o f barotrauma from positive pressure
ventilation. Lungs with pulmonary fibrosis are actually protected because they don’t stretch.
Central Lines
The main way to ask questions about central lines is to show them
being malpositioned and asking you where they are. An abrupt bend at the tip of the
catheter near the cavo-atrial junction should make you think azygos. If it’s on the left side
of the heart, it’s either (1) arterial or (b) in a duplicated SVC.
This is a sneaky trick, related to Central Lines. They can show you the pseudo lesion /
hot quadrate sign (seen with SVC syndrome), and then show you a CXR with a central
venous catheter. The idea is that central lines are a risk factor for SVC occlusion.
Endotracheal Tube (ETT) Positioning
The tip o f the ETT should be about 5
cm from the carina (halfway between the clavicles and the carina). The tip will go down with the chin tucked, and up with the chin up (“the hose goes, where the nose goes”). Intubation o f the right main stem is the most common goof (because of the more shallow angle) - this can lead to left lung collapse. You can sometimes purposefully intubate one
lung if you have massive pulmonary hemorrhage (lung biopsy gone bad), to protect the good lung.
Intra-Aortic Balloon Pump (IABP)
overview
This is used in cardiogenic shock to help
with “diastolic augmentation,” - essentially providing some back pressure so the vessels of
the great arch (including the coronaries) enjoy improved perfusion.
Intra-Aortic Balloon Pump (IABP)
what is the function
decrease LV afterload and increase myocardial perfusion,
Intra-Aortic Balloon Pump (IABP)
what is the correct location
the balloon should be located in the proximal descending aorta, just below the origin of the left subclavian artery (balloon terminates just above the splanchnic vessels)
ideal position is in the region of the left main stem
Intra-Aortic Balloon Pump (IABP)
complications
dissection during
insertion, obstruction of
the left subclavian from
malpositioning
Cardiac Conduction Device
types
• Pacemakers
• Implantable Cardiac Defibrillators (ICDs) - the one with “shock coils” - i.e. the thick
bands.
• Mixed (Pacemaker + ICD)
Cardiac Conduction Device
locations
• Leads are placed in the RV, RA, and LV. The LV leads get there via the coronary sinus to
the posterior / lateral cardiac vein.
• “Cardiac resynchronization therapy device” is the vocab word the bi-ventricular
pacemaker (RV + LV and usually RA). Remember vocab words are easily testable.
• Pearls on locations: (1) The RV lead should cross the midline on a frontal view,
(2) The RA and RV leads are anterior on the lateral view, (3) The LV lead should be
posterior on the lateral, (4) the idea location for the RA lead is actually the RA appendage
- so it should course down then back up/anterior.
Cardiac Conduction Device
complications
• Myocardial Perforation - The number is 3 mm. If the lead is 3 mm within the epidcardial fat you should suspect penetration.
• Rib Clavicle Crush - The leads are mostly commonly fractured in the region o f the clavicle, and first rib.
• Twiddler Syndrome - The generator pack gets flipped and twisted in the pocket, leading to lead displacement. This happens because Grandpa just can’t leave the thing alone (gotta put those dementia mittens on him). Can’t have him dying on us… we need those social security checks.
• Acute - All the stuff you get with central line placement: pneumothorax, hemothorax, etc…
Generator Related - Terminal connector pin displacement. This is actually common.
