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.
