1

PulmonaryABIM Certification Exam Review Course

Leslie Zimmerman, MDProfessor of Clinical Medicine, UCSF

ICU Director, SFVAMC

Relative Value? Medical Content

• CV 14%

• Pulmonary 10%

• ID 9%

• GI 9%

Cross Content• Critical Care 10%

• Geriatrics 10%

• Prevention 6%

• Women’s Health 6%

Relative Value?

Pulmonary:• Obstructive disease: 24%

• Pleural Disease: 13%

• Restrictive & Interstitial: 11%

• Pulmonary vascular disease: 11%

• All the other stuff….

2

Lecture Outline Sleep COPD/Asthma ILDs PVD TB Solitary Pulmonary Nodule Etc.

Question 1A 65 year-old man with daytime sleepiness is evaluated for sleep apnea with polysomnography. His Epworth sleepiness scale is 11/24.

The polysomnogram reveals obstructive sleep apnea with an apnea-hyponea index (AHI) of 12 events/hour. Lowest oxygen saturation was 86%. Treatment with continuous positive airway pressure (CPAP):

Question 165 year-old man with 11/24 Epworth & AHI 12. O2 sat’n nadir 86%. CPAP treatment:

A. Will be reimbursed by MedicareB. Will decrease cardiovascular mortalityC. Will likely need to be supplemented

with oxygenD. Should be offered only if “mission

critical job” (airline pilot, bus and truck drivers)

3

Sleep Disorders: Office Visits

www.nhlbi.nih.gov/about/factbook-05/chapter4.htm

Classic patient with OSA

Obesity = #1 risk factor

GeneticsUpper airway/facial abnormalitiesPost-menopauseHypothyroidism/ Acromegaly

Deeper stages of sleep, neural input to upper airway declines, decreased airway tone, tongue falls back. The vibrations from snoring may actually cause a myopathy!

en.wikipedia.org

OSADisruption in sleep

causes daytime sleepiness

Epworth Scale can estimate “sleepiness”

10 = Sleepy

18 = Very sleepyhttp//:epworthsleepinessscale.com

4

OSA

Air flow

Apneas + Hyponeas = AHI

10 seconds 10 seconds

“Hyponea” has 4% desaturation

OSA

Severity

Mild: AHI 5-15

Moderate: AHI 15-30

Severe: > 30

AHI > 15 in everyone or

AHI > 5 if symptoms (sleepiness, fatigue, inattention) or signs of disturbed sleep (snoring, restless sleep, respiratory pauses), or HTN/CAD/CVA

So can have AHI of 6-15 and if asymptomatic, low Epworth, no HTN/CAD/CVA, not “mission critical” many would not treat.

Medicare reimbursement

OSA and Death

Patients with untreated mild OSA may not be at increased risk for mortality compared to individuals without OSA.

IN CONTRAST: Untreated severe OSA (AHI > 30/hour) 3-6 fold increased risk of all-cause mortality compared to individuals without OSA.

Marin JM et al. Lancet 2005;365(9464):1046.

5

Punjabi et al. PLoS Med. 2009 August; 6(8): e1000132

OSA and Mortality

6,441 people with untreated OSAHigher CV mortality in:• Men with severe OSA (AHI > 30) who were < 70 years old • Not enough women enrolled to estimate risk

Martinez-Garcia MA et a;. AJRCCM 2012;186:909

Observational, smaller (939 people) mean age 71. Even in older, untreated OSA 2x CV death if severe (AHI > 30)

Question 165 year-old man with 11/24 Epworth & AHI 12. O2 sat’n nadir 86%. CPAP therapy:

A. Will be reimbursed by MedicareB. Will decrease cardiovascular mortality

C. Likely need to be supplemented with oxygen

D. Should be offered only if “mission critical job” (airline pilot, bus and truck drivers)

If AHI > 30

O2 alone can worsen OSA; with mild–moderate OSA & no sign’t heart/lung disease, CPAP alone typically enough

AHI > 5 & symptoms treat

Sleep Apnea – Cutting Edge

Sharma SK et al. “CPAP for the metabolic syndrome in patients with obstructive sleep apnea” NEJM 2011; 365:2277-86.

• Cross-over of sham CPAP vs. CPAP in obese patients (80% with Metabolic syndrome) with mod to severe OSA

• CPAP decreased:Systolic BP

Diastolic BP

LDL

Hgb A1c

3 mmHg

2.8 mmHg

5 mg/dL

.03%

6

Sleep Apnea – Cutting EdgeKarkow B,et al. “Prospective Assessment of Nocturnal Awakenings in a Case series of Treatment Seeking Chronic Insomnia patients: A Pilot Study of Subjective and Objective Causes” Sleep 2012; 35:1685-92.

• Small study of insomnia patients

• Most night awakenings actually caused by sleep disordered breathing

What were those OSA numbers?

AHI > 5 & symptoms or HTN/CAD/CVA or “mission critical” job CPAP

AHI > 15 CPAP

AHI > 30 and if < 70 years old, clearly at increased CV mortality if not treated (so we really encourage use!)

Question 2A 60 year-old smoker complains of an insidious onset

of dyspnea on exertion. PFTS reveal COPD. The severity of the disease is determined by the:

A. Air-trappingB. Diffusion capacity for carbon monoxide C. FEV1D. FEV1/FVCE. Lack of response to bronchodilators

7

http://www.who.int/mediacentre/factsheets/fs310_2008.pdf

2004: Worldwide Leading Causes of Death

Mill

ions

Affects 9% of World

PopulationBy 2020, will move to 3rd

leading cause of

death

In US, only common disease with RISING mortality

In US, in COPD deaths is driven by very large in women. In 2000, for 1st

time, more women died of COPD than men in US.

Percent Change in Age-Adjusted Death Rates, US, 1965-1998 (proportion of 1965)

3.0

2.5

2.0

1.5

1.0

0.5

0

CAD CVA Other COPD All CVD Other

- 59% - 64% - 35% - 7%+163%

http://www.goldcopd.org

COPD Pathogenesis: Aging + Genes + Noxious Stimuli

Chest 2009;135:173.

In US, 15-20% of COPD caused in part by occupational exposures (esp. dusts)

Lung Mature 18-25 years

Total dysfunction130-140 years

Lung Aging

Healthy

COPD

Lung

func

tion

(FE

V1;

alv

eoli)

8

In non‐smokers, environmental exposure is primary risk factor

Indoor smoke from biomass solid fuels Contribute up to 35% of COPD in above countries

World Health Organization

http://www.who.int/heli/risks/indoorair/en/webiapmap.jpg

Spirometry

TLC

RV

Time

Obstructive disease

Restrictive disease

FVC

FEV1

TLC – elevated reflecting hyperinflation

9

Diffusion Capacity for CO

DCO: integrity of the alveolar–capillary membrane

CO

CO

CO

Destroy alveoli orcapillaries Low DCO

DCO: integrity of the alveolar–capillary membrane

CO

CO

CO

Just narrow airways Normal DCO

Diffusion Capacity for CO

Diffusion Capacity for CONormal

Asthma

Low

Emphysema

Fibrosis

Pneumocystis jiroveci pneumonia

PE

ELEVATED?

Diffuse alveolarhemorrhage

Falling HctElevated DCO

CO

10

Sample PFTs in emphysema

FVC (L) 2.4 (52%)

FEV1 (L) 1.02 (38%)

FEV1/FVC 41%

TLC (L) 6.2 (103%)

RV (L) 3.8 (150%)

DCO 12 (48%)

< 70% diagnoses obstruction

Severity

Suggests emphysema more likely than asthma or chronic bronchitis

Air trapping

Question 2A 60 year-old smoker complains of an insidious onset

of dyspnea on exertion. PFTS reveal COPD. The severity of the disease is determined by the:

A. Air-trappingB. Diffusion capacity for carbon monoxide C. FEV1D. FEV1/FVCE. Lack of response to bronchodilators

Consistent with emphysema; don’t stop BDs.BIG reversibility Asthma component ?

COPD‐ a different GOLD severity scale?

GOLD = Global Initiative for Chronic Obstructive Lung Disease 2013

Spirometry

Breathlessness

Exacerbation number

A = Few symptoms, OK numbersB = Lots of symptoms, OK numbersC = Few symptoms, Bad numbersD = Lots of symptoms, Bad numbers

Why?

Why?

Search for biomarkers

11

Question 3A 45 year-old ex-smoker with 5 years of

progressive DOE has the following CXR

And CT scan of Lung Bases

Question 3

Testing reveals that he has very low levels of alpha-1-antitrypsin (PiZZ variant). Treatment with replacement therapy has been shown to:

A. Prevent liver diseaseB. Decrease risk of lung cancerC. Slow decline of FEV1D. Decrease number of exacerbations/year

12

Alpha 1 Anti‐trypsin Deficiency

Normal: PiMM

Heterozygotes make enough to be protective

Homozygous PiZZ, PiZnull, PiNullNull elastase unchecked early emphysema in smokers, though RARE that lifetime non-smokers get emphysema

A1ATNeutrophil Elastase

Panacinar

Liver Disease?

A1AT made in the liver ZZ variant, it is made but can’t get out of the ER of the hepatocyte liver damage cirrhosis

PiNullNull – makes NO A1AT – they do not get the liver disease

IV Augmentation doesn’t help liver

Augmentation with A1AT

Cost is $60,000 to $150,000/ year

Approved by the FDA if level below the protective level (PiZZ, PiZnull) & COPD

Not in heterozygotes

Not if still smoking

Not if asymptomatic

NIH registry: augmentation decreases rate of decline of lung function & mortality (NOT A RANDOMIZED TRIAL)

13

Question 3

Testing reveals that he has very low levels of alpha-1-antitrypsin (PiZZ variant). Treatment with replacement therapy has been shown to:

A. Prevent liver diseaseB. Decrease risk of lung cancerC. Slow decline of FEV1D. Decrease number of exacerbations/year

Adding normal A1AT won’t hurt; but won’t help

“Air sac” disease, not airway disease

Increased risk, but no improvement with Rx

Other COPD stuff

Recurrent exacerbations are bad

Lung function over lifetime with COPD

Lu

ng

Fu

nct

ion

Question 4

All of the following are risk factors for COPD exacerbations EXCEPT?

A. Prior exacerbations

B. Lower FEV1

C. Male sex

D. History of asthma

14

COPD: Lots of variability in courseExacerbations are bad – more inflammation,

more airway remodeling more rapid decline in FEV1

But who gets exacerbations?

Prior exacerbations

Lower FEV1 ( or ?)

Women

History of asthma

NEJM 2010;363:1128.

Phenotypes of frequent and infrequent “exacebators”

Decrease exacerbations?

Tiotropium (UPLIFT trial: Lancet 2009:374:1171.) But patients not allowed Atrovent or Combivent

Inhaled corticosteroids + LABA (TORCH trial NEJM 2007;356:775).

Roflumilast: phosphodiesterase-4 inhbitor (Lancet

2009 374(9691):685.) But patients not allowed inhaled corticosteroids. Will effect be additive?

Inhaled corticosteroids decrease exacerbations but may increase risk of CAP (Arch Intern Med. 2009;169:219)

Can Azithromycin Help?Albert RK et al. “Azithromycin for Prevention of Exacerbations of COPD” NEJM 2011; 365:689.

570: azithromycin (250 mg daily) vs. 572: placebo x 1 year.

Pro

po

rtio

n f

ree

of

Ex

ac

erb

ati

on

s

da

ys

Macrolides have immunomodulatory, anti-inflammatory, and anti-bacterial effects

Fewer exacerbations

5% more hearing decrement

15

COPD Azithro Saga….Albert RK et al. “Azithromycin for Prevention of Exacerbations of COPD” NEJM 2011; 365:689.

Excluded if Long QTc, other meds that can prolong QT or associated with torsades. NNH for hearing loss = 20

Vs.

Wayne RA, et al “Azithromycin and the Risk of Cardiovascular Death” NEJM 2012; 366:1881

Prescriptions for azithromycin in Tennessee Medicaid registry & sudden death within 10 days – slight increase in sudden death (compared to amoxicillin prescriptions)

Vs.

Svanström H, et al. Use of azithromycin and death from cardiovascular causes. N Engl J Med 2013; 368:1704-1712.

Mostly young/middle aged adults no increased risk

COPD Azithro Saga….RESERVE for:

“Carefully selected patients, such as those who continue to have frequent exacerbations in spite of optimal therapy for their COPD with bronchodilators and anti-inflammatory agents.”

COPD and Pulmonary HTN

Sildenafil? a dud!

Worsens exercise oxygenation

Worsens 6 minute walk distance

PLoS One. 2012;7(12):e52248

COPD. 2012 Jun;9(3):268-75

16

Question 5

Which of the following BEST distinguishes asthma from COPD?

A. Reversibility after bronchodilators

B. Exhaled NO (nitric oxide)

C. Methacholine testing

D. Sputum eosinophilia

Exhaled NO

Arginine ----- NO

NOSNO causes

bronchodilation and vasodilation

Inducible form of NOS (iNOS) up regulated with inflammation so exhaled NO is a marker of airway inflammation.

Studies good but not great that increasing levels can help tailor asthma management and control

Approved by FDA

Vs.

Peak flow meter

COPD & Asthma

COPD• Older, esp. smokers• Slowly progressive• Neutrophils• Partially reversible• Airway remodeling &

Lung destruction

ASTHMA• Any age, esp. children• Episodic• Eosinophils• May be fully reversible• Airway remodeling

10% overlap

Manage similar to asthma

17

Question 5

Which of the following BEST distinguishes asthma from COPD?

A. Reversibility after bronchodilators

B. Exhaled NO (nitric oxide)

C. Methacholine testing

D. Sputum eosinophilia Lots of overlap

Question 6A 27 year-old woman has intermittent SOB &wheezing. She has a history of asthma & is on beta-agonists, high dose ICS, and leukotriene modifiers. 2prior hospitalizations; 1 prior intubation for respiratorydistress. On exam, she is comfortable but anxious.O2 saturation on room air is 99%. Her lungs have afaint inspiratory wheeze throughout.

You send her for pulmonary function testing with flowvolume loop and a chest x-ray. The chest x-ray isnormal.

Question 6

Volume

Flo

w

Normal

Exh

alat

ion

Inha

latio

n

18

Question 6

The clinical picture most likely represents:

A. Allergic pulmonary aspergillosisB. Poor adherence to medicationsC. Tracheal stenosisD. Worsening of her underlying asthmaE. Vocal cord dysfunction

Volume

Flo

w

Normal

Exh

ala

tion

Inh

ala

tion

Flow‐volume Loops

Normal

Restriction

Obstruction

Severe Obstruction

Volume

Flo

w

Volume

Flo

w

Normal

Volume

Flo

w

Normal

Volume

Flo

w

Normal

Exh

ala

tion

Inh

ala

tion

Flow‐volume LoopsUpper Airway Obstruction

VariableExtrathoracic

FixedLarge Airway

+ -

Variable Intrathoracic

+ -

Volume

Flo

wE

xha

latio

nIn

ha

latio

n

Volume

Flo

wE

xha

latio

nIn

ha

latio

n

Volume

Flo

wE

xha

latio

nIn

ha

latio

n

19

Flow‐volume LoopsVariable Extrathoracic Obstruction

from Vocal Cord Dysfunction

• Psychogenic• Most commonly in women, ages

20 - 40• May present with respiratory distress

and dramatic inspiratory stridor• Loudest noise at throat• Normal ABGs and A-a gradient• Resolves when asleep• Minimal response to aggressive

asthma treatment• Really hard when co-exists with

asthma • Diagnosis by endoscopy

Volume

Flo

w

Normal

Exh

ala

tion

Inh

ala

tion

Question 6

The clinical picture most likely represents:

A. Allergic pulmonary aspergillosisB. Poor adherence to medicationsC. Tracheal stenosisD. Worsening of her underlying asthmaE. Vocal cord dysfunction

FV loopFV loop

Question 7A 23 year-old woman is seen for increasingly frequent asthma exacerbations. She has asthma symptoms approximately 3x a week and is awakened at night about 3x a month. The patient is taking a short-acting inhaled beta 2-agonist for symptomatic relief.

Afebrile, BP 120/75, RR 16/min. Lungs: no wheezes.

Her peak flow is 400 liters per minute (her best value is 450 LPM).

20

Question 7Which of the following asthma medications would be the most appropriate addition to the treatment regimen at this time?

A. Oral corticosteroidsB. Oral theophylline C. Low-dose inhaled corticosteroid D. Long-acting beta 2-agonistE. Leukotriene modifier

STEP 3Moderate Persistent

STEP 2Mild PersistentSTEP 1

Mild Intermittent

STEP 4Severe Persistent

STEPS 5 & 6

Management of AsthmaInitial Assessment

Management of AsthmaA Step‐Wise Approach

Symptoms NocturnalSTEP 4, 5, 6 Continual symptoms FrequentSevere persistent Limited physical activity

Frequent exacerbationsSTEP 3 Daily symptoms > one/wkModerate persistent Daily use of inhaler

Exacerbations affect activityExacerbations ≥ 2 times/wk

STEP 2 Symptoms >2 times/wk,<1/day >2/moMild persistent Exacerbations may affect activitySTEP 1 Symptoms ≤ 2 times/wk ≤2/moMild intermittent Asymptomatic between exacerbations

Exacerbations brief

21

Management of AsthmaInitial Assessment

STEP 3Moderate Persistent

STEP 2Mild Persistent

STEP 1Mild Intermittent

STEP 4Severe Persist.

Long-termQuick-relief

Short-actingbeta-2 agonist

Low-dose*inhaled steroids

Long-actingbeta-2 agonist

Low-med dose*inhaled steroids

Med-doseinhaled steroids

ConsiderAnti -IgE

* Alternatives: leukotriene modifiers, cromolyn, nedocromil, theophylline

High-doseInhaled steroids

STEP 5 & 6

Patient education & environmental control at each step

Management of AsthmaInitial Assessment

STEP 3Moderate Persistent

STEP 2Mild Persistent

STEP 1Mild Intermittent

STEP 4Severe Persist.

Long-termQuick-relief

Short-actingbeta-2 agonist

Low-dose*inhaled steroids

Long-actingbeta-2 agonist

Low-med dose*inhaled steroids

Med-doseinhaled steroids

ConsiderAnti -IgE

* Alternatives: leukotriene modifiers, cromolyn, nedocromil, theophylline

High-doseInhaled steroids

STEP 5 & 6

Patient education & environmental control at each step

Tiotropium

Asthma‐ Tiotropiumin moderate to severe asthma

NEJM 2012;367:1198

In asthma patients poorly controlled with standard therapy. Tiotropium vs. placebo• Improved lung function• Decreased time to exacerbation• Decreased # of severe exacerbations• No increase in adverse events

22

Take home points If patient moves from intermittent mild

persistent, add controller medication (best for most = an inhaled corticosteroid)

If poor control on ICS: increase ICS or add long acting b-agonist (deals with concerns about safety of LABA)

Long acting b-agonist without a controllermedication is always the wrong answer

For emergency rescue, b-agonist always the right answer

LABA Pharmacokinetics

• Salmeterol & Formoterol

Effect lasts 12 hours

Formoterol – quick onset

Combo of ICS + Formoterol used for exacerbations (plus action plan!)

Concerns @ safety of LABAs?• Genetic polymorphisms of beta-receptor

LABA

“SMART Trial” Chest. 2006;129:15-26. Usual care +/- SalmeterolAsthma related deaths 4.4 x more likely in

salmeterol group Black Box warning by FDA

Related to LABA, subset with genetic polymorphisms of beta receptor, or non-compliance with ICS?

THIS IS NOT AN ISSUE WITH COPD

23

Question 7Which of the following asthma medications would be the most appropriate addition to regimen at this time (only on short acting b-agonists)?

A. Oral corticosteroidsB. Oral theophylline C. Low-dose inhaled corticosteroid D. Long-acting beta 2-agonistE. Leukotriene modifier

Works, but too big a gun

All acceptable by guidelines, in practice like ICS;Caveat: some young people w/ exercise induced asthma do well on LT agents. Smokers have blunted response to ICS.

Question 8A 32 year old patient has poorly controlled asthma

despite inhaled steroids, LABA, LTR-Blocker. Which of the following would predict a good response to Anti-IgE therapy?

A. Eosinophilia

B. Extremely high IgE levels (>2000 IU)

C. Latex allergy

D. Sensitization to dust mites

Anti‐IgE (Omalizumab)

Consider for Steps 5 & 6 (difficult to control asthma)

Binds IgE complex cleared

Rx: fewer exacerbations & less steroid needed; no change in baseline FEV1

24

Anti‐IgE (Omalizumab) Need to get IgE to extremely low levels for

it to work (very low levels trigger mast cell degranulation)

Baseline serum IgE should be between 30 - 700 IU/mL

+ Skin test or RAST to a perennial aeroallergen (e.g., dust mite, animal danders, cockroach, molds)

Sq each 2-4 weeks Anaphylaxis 1:1,000 Minimum dose $12,000/year

High, but not TOO HIGH

Question 8A 32 year old patient has poorly controlled asthma

despite inhaled steroids, LABA, LTR-Blocker. Which of the following would predict a good response to Anti-IgE therapy?

A. Eosinophilia

B. Extremely high IgE levels (>2000 IU)

C. Latex allergy

D. Sensitization to dust mites

Though usually a partner

TOO high

Best with aeroallergen

Question 930 year-old woman was exposed to chlorine gas 2 months ago at work & now has a persistent cough & mild SOB. At exposure, she noted irritation of her eyes and mucus membranes. Immediately after the exposure, she developed a cough. A chest x-ray was normal. No treatment was given. The patient has no history of asthma, but since this, has been wheezing at night.

Exam is unremarkable with clear lungs. Spirometry: FVC of 89% of predicted

FEV1 of 84% of predicted FEV1/FVC 73%

Methacholine challenge + for bronchial hyperresponsiveness

25

Question 9

Which of the following is the most likely diagnosis?

A. Bronchiolitis obliteransB. Hypersensitivity pneumonitisC.Post nasal dripD.Reactive airways dysfunction

syndrome

Occupational Asthma

Occupational asthma

Irritant-inducedasthma

Reactive airways

dysfunction

Acquired sensitization in the workplace

Multiple exposures to irritant

Single big exposure to irritant

Non-immunologic

20-30% of new onset adult asthma = occupational!

Reactive Airways DysfunctionDiagnostic Criteria

Exposure to irritant in high concentration Onset of symptoms after single exposure

within 24 hrs; persist for at least 3 months and sometimes years!

Symptoms of asthma PFTs +/- airflow obstruction, but

Methacholine test positive

Brooks SM et al. Chest 1985;88:376

26

RADS

Take home points “Big Bang” big exposure, symptoms

right away

+ methacholine challenge

Rx like asthma, though typically harder to control

CHLORINE! (Including mixing household cleaners)

Gulf War sulfur mustard gas

Question 9

Which of the following is the most likely diagnosis?

A. Bronchiolitis obliteransB. Hypersensitivity pneumonitisC. Post nasal dripD. Reactive airways dysfunction

syndrome

Typically slower onset; HRCT scan +

Can exacerbate asthma, but doesn’t CAUSE airway hypereactivity

Asthma – Cutting Edge

High fat meal increases airway inflammation in obese and non-obese asthmatics. J Allergy Clin Immunol 2011;127:1133

ICS non adherence predicts asthma exacerbation. Threshold of 75% adherence significantly fewer exacerbations. J Allergy Clin Immunol 2011;1278:1185

27

Asthma – Cutting Edge

Lebrikizumab (binds IL-13) monthly, sq, improved FEV1 (5.5%) but did not decrease exacerbation or overall control in Phase II trial. NEJM 2011;365:1088.

Mepolizumab (binds IL-5) halved exacerbations in asthma patients with high blood eosinophilia. No change FEV1. Lancet 2012;380:651.

Azithromycin a dud overall (Some benefit in non-eosinophilic asthma?). Thorax 2013;68:322.

Question 1034 year old man has DOE x 6 months and cough

productive of yellow sputum. No fever, chills, or hemoptysis. HIV negative. Exam is normal. Sputum smears are negative for AFB. He has had a pet pigeon for the past 2 years.

Pulmonary function tests:

FEV1/FVC 83% predicted ABG 7.49/30/60

TLC 68% predicted DLCO 50% predicted

Chest X‐ray

28

Chest CT Scan

Lung Biopsy

Question 10Which of the following is the most likely

diagnosis?

A. Idiopathic pulmonary fibrosis

B. Lymphangioleiomyomatosis

C. Mycobacterium Avium Complex (MAC) infection

D. Hypersensitivity pneumonitis

29

Interstitial Lung Diseases

Characterized by restriction on PFTs with low diffusion capacity and desaturation with exercise (or if bad hypoxemia at rest)

High resolution Chest CT scan is almost always the right answer to “what to do next” if hasn’t been ordered• Some ILDs have classic findings• Shows where to biopsy

ILD: HPHypersensitivity pneumonitis: centrilobular

nodules, ground glass opacities, and air trapping on expiratory views

Ground Glass = active alveolitis

30

Air‐trapping?Inspiration Expiration

If small airways inflamed, air can’t exit well with exhalation. On CT scan, involved lung areas remain black. Splotchy pattern suggestive of small airway disease. Can be emphysema or any disease of small airways: HP, sarcoidosis. BUT SOMETHING WRONG!

HRCT What to order? Get inspiratory and expiratory views (small

airway disease)

Plus prone & supine images. Can open up atelectasis that can be confused with an ILD

Hypersensitivity Pneumonitis

Chronic granulomatous inflammation after repeated inhalation of environmental antigens

Can present as acute, subacute or chronic dz

No single test is diagnostic: + serology just tells exposure

Suspect when there is a • History of recurrent “pneumonias”

• Symptoms develop after moving to a new job or home or birds or water damage/visible mold in work/home

• Improvement in symptoms when away from work/home

• No eosinophilia

31

Lung Biopsy

Granulomas a bit less well formed than sarcoidBut will not ask for diagnosis based just on biopsy

How many of these ILDs do you need to know?  My Picks are:

Hypersensitivty pneumonitis• Because non-drug intervention can cure (i.e.,

removing the antigen)

Sarcoid• Common and distinguishing HRCT

IPF• Common and distinguishing HRCT

Sarcoid

32

Sarcoid on HRCTSarcoid: adenopathy and nodular thickening

of bronchovascular bundles (lumpy-bumpy), centrilobular nodules.

ILD: SarcoidDisease @ bronchovascular bundles

LAMProliferation of atypical pulmonary interstitial smooth muscle with cyst formation

Classic LAM story: 35 year old woman with dyspnea and pneumothorax or chylothorax

33

MAC infection

“Tree-in-bud” = infection

Clear increase in prevalence in past few decades

MAC Infection Spectrum

HIV

COPD – older men, upper lobe, cavitary

In prior bronchiectasis (CF patients)

Healthy women in 50s: diffuse infiltrates cause bronchiectasis• This subgroup some have hypersensitivity

reaction to MAC; removal from exposure may help. Biofilm in Hot Tubs

and shower heads.Want hot water > 130oF

Mycobacterium avium Lung Disease

Diagnostic criteria:Symptoms + nodules, cavities, or bronchiectasis

with: Positive cultures from at least 2 separate

sputum samplesOR

Positive culture from at least 1 bronchial washOR

Transbronchial or other lung biopsy with characteristic histology and positive culture on either biopsy or sputum

Am J Resp Crit Care Med 2007;175:367

If smear + or 3-4 + cultures more likely to progress

34

Treatment of Mycobacterium avium Lung Disease

For nodular/bronchiectasis, therapy consists of a macrolide (clari or azithro), ethambutol, and rifamycin (rifampin or rifabutin) 3 times weekly

For cavitary disease, therapy consists of the same drugs given daily +/- streptomycin or amikacin

The goal of therapy is 12 months of negative sputum cultures while on therapy--total duration is often 14-18 months

Am J Resp Crit Care Med 2007;175:367

IPF

Honeycombing

Older man with gradual dyspnea

IPFTraction

bronchiectasis

Bilateral, lower lobe “subpleural” honeycombing

35

Question 1034 yo man with a bird.

Which of the following is the most likely diagnosis?

A. Idiopathic pulmonary fibrosis

B. Lymphangioleiomyomatosis

C. Mycobacterium Avium Complex (MAC) infection

D. Hypersensitivity pneumonitis

Too young Young women; obstruction not restriction on

PFTs

Should have Tree-in bud on CT scan; productive cough

Typical HRCT, bird exposure favor HPDiagnosis important – need to remove antigen (bird)!

Question 1177 year old man has progressive dyspnea x 2 years.

No sputum, hemoptysis, weight loss, or sweats. He previously smoked 1 ppd for 40 years, quit 15 years ago. PMH: HTN and peptic ulcer disease.

Meds: omeprazole and lisinopril

Exam: afebrile, RR 16, SaO2 92% RA

Crackles bilaterally at bases

+ Clubbing

Labs: nl CBC, Chem-20, PFTs: low TLC & DCO

ABG: 7.42/28/58

Chest X‐ray

36

HRCT

Question 1177 yo former smoker with dyspnea and

restriction on PFTs. Which of the following is the most appropriate intervention at this time?

A. Prednisone 1 mg/kg/day

B. Sildenafil to lower pulmonary artery pressures

C. Listing for single lung transplant

D. Assessment for desaturation with exertion

E. Schedule open lung biopsy

Go for the simplest

IPF – Cutting EdgeNoble PW et al. “Pirfenidone in patients with idiopathic pulmonary fibrosis (CAPACITY): two randomised trials.” Lancet 2011 May 21;377(9779):1760.

Slowed rate of FVC decline a bit

FDA approval pending; they want another trial

“A Controlled Trial of Sildenafil in Advanced Idiopathic Pulmonary Fibrosis” NEJM 2010; 363: 620

Slight improvement in QOL and dyspnea, not 1o

outcome of 6 minute walk test

“A Placebo-Controlled Randomized Trial of Warfarin in Idiopathic Pulmonary Fibrosis” AJRCCM 2012;186:88.

A dud

37

IPF – Cutting Edge“Prednisone, azathioprine, and N-acetylcysteine for pulmonary fibrosis” NEJM 2012;366:1968.

Stopped early because of INCREASED death in steroid patients!

NAC vs. placebo arm ongoing 2014

2012 Stable IPF:Enroll in trial vs. NAC vs. pirfenidone (if in Japan, Canada, Europe) vs. supportive care

IPF ‐Summary

No clear BEST option for therapy

Some bad options Move away from steroids!!!

We enroll patients with new diagnosis of IPF in trials or offer NAC

Common reason for Tx evaluation, but many age is an issue – but check with center. Strict age cut-off less common….

IPF – Exacerbation2013 IPF exacerbation:

Think about CHF exacerbation

Think about PE

HRCT to look for classic GGO

BAL (if you can) to look for infection

Antibiotics unless confident no infection

Prednisone 1 mg/kg per day orally or methylprdnisolone 1 to 2 g per day intravenously

75% mortality

38

Question 1177 yo former smoker with dyspnea and

restriction on PFTs. Which of the following is the most appropriate intervention at this time?

A. Prednisone 1 mg/kg/day

B. Sildenafil to lower pulmonary artery pressures

C. Listing for single lung transplant

D. Assessment for desaturation with exertion

E. Schedule open lung biopsy

Biopsy for confusing cases, but IPF flare can be triggered by lung and non lung surgery

Question 1233 year-old woman presents with intermittent fever, night sweats, migratory joint pain, and red, painful nodules on her shins. She has no pulmonary symptoms.

Chest x-ray:

Question 12Bronchoscopy with transbronchial biopsy: non-

caseating granulomas. Stains and cultures for fungi and mycobacteria were negative.

39

Which best describes the status of her lung disease in 2 years?

A. Progression to advanced obstructive lung disease

B. Progression to advanced interstitial lung disease with fibrosis

C. Progression to pulmonary hypertension

D. Normal lung function

Question 12

Overview of Sarcoidosis Multisystem granulomatous disorder of unknown

etiology characterized by non-caseating granulomas in involved organs

Incidence varies geographically; much more common in African-Americans (lifetime risk of 2.4%)

Usually presents ages 10 - 40, half detected by CXR without symptoms

Any organ can be involved, lungs most frequent (90%)

Should you bx asymptomatic pts with hilar adenopathy?Won’t ask

Sarcoidosis‐Staging

Stage I Bilateral hilar adenopathy

Stage II Above + interstitial infiltrates (upper>lower lung zones)

Stage III Interstitial disease with shrinking hilarnodes

Stage IV Advanced fibrosis

Extra-pulmonary disease-skin (E. nodosum, lupus pernio), eyes, liver, lymph nodes most frequent

40

Sarcoidosis: Dx & Rx Histology = granulomas, must exclude infection!

Usual indications for treatment are: worsening pulmonary symptoms, lung function, progressive radiographic changes, cardiac, eye, neuro, disfiguring skin lesions, high calcium

Therapy is NOT indicated in

• Asymptomatic stage I disease patients

• Asymptomatic patients with stage II and mildly abnormal lung function

Follow first for 3-6 months (some say 6-12, even with mild-moderate) and document impairment of lung function

Sarcoidosis No drug has been shown to change the course

Steroids treat granulomatous disease which can cause symptoms but won’t change fibrotic disease• EXAMPLE: hypercalcemia very responsive!

Inhaled corticosteroids ? Most experts don’t give

Lupus pernio skin changes= rare

to have remission, but seems to

be better with infliximab

If severe lung disease by PFTs or need for Oxygen get Echo to check for pulm HTN

Her lung disease in 2 years? She has Stage I CXR, but lots of symptoms.

She had Lofgren's syndrome: “Acute” sarcoid with abrupt onset with erythema nodosum, hilar adenopathy, migratory polyarthralgias, and fever seen primarily in women.

• Strongly associated with HLA-DQB1*0201

• Good prognosis and spontaneous remission in 85-95%. Rx only if painful arthritis.

Question 12

41

Question 1346 year old woman has 4 weeks of fever, night sweats, cough, and 10 lb weight loss. She also has arthralgias, epistaxis, nasal congestion. 2 weeks of clarithromycin did not relieve her symptoms. Now has hemoptysis.Exam: 99.7, RR 24/min, crackles right chest, 1+ edemaWBC 6800/mm3 Hgb 10.3 Platelets 568,000/mm3

Creatinine 1.3 mg/dL Urinalysis: 2+ protein, 0 WBCs, rare RBC casts

X‐ray

American Journal of Roentgenology. 2009;192:676-682

Question 13Which of the following is the best

diagnostic step?

A. Serum angiotensin-converting enzyme

B. Rheumatoid factor

C. Antineutrophil cytoplasmic antibodies

D. Culture of bronchoalveolar lavage fluid

E. Percutaneous needle biopsy of the lung

42

Pulmonary‐Renal Syndromes

Systemic vasculitisWegener’s granulomatosisMicroscopic polyangiitis Pauci-immune GNChurg-Strauss (allergic angiitis and granulomatosis)Goodpastures syndrome Systemic lupus erythematosus Henoch-Schonlein purpura

InfectionPost-streptococcal glomerulonephritis, endocarditis

ANCA?C-ANCA 80% P-ANCA 10%P-ANCA 70%Most P-ANCA½ ANCA

P-ANCA 10-40%Some +

Any + ANCA= bad news. You may not know which vasculitis it is…., but always abnormal.

Approach to Pulmonary‐Renal Syndromes

Serologic tests: ORDER• Anti-GBM Abs, anti-neutrophil cytoplasmic Abs

(ANCA), ANA

ANCAs are positive in 90% of those with generalized Wegener’s (PR3-ANCA or “C-ANCA”)

Tissue should be obtained to provide evidence of vasculitis• Skin (easy), Kidney, or lung (surgical biopsy)

• If Anti-GBM possible, kidney better to bx than lung

Question 13Which of the following is the best diagnostic

step?

A. Serum angiotensin-converting enzyme

B. Measure rheumatoid factor

C. Antineutrophil cytoplasmic antibodies

D. Culture of bronchoalveolar lavage fluid

E. Percutaneous needle biopsy of the lung

Sarcoid is not pulm-renal syndrome

Reasonable, but fungi, TB can not explain GN

Not enough tissue to see vessel

Lupus not RA

43

Question 1430 year old man has increasing dyspnea with

exercise and chronic daily productive cough since adolescence. He also reports frequent bronchial and sinus infections, treated with multiple courses of antibiotics. Twice he was admitted for pneumonia. He has a 20-pack year history of smoking. No other medical problems or prior surgeries. He works in an office.

Exam: SaO2 86%, diffuse crackles, and digital clubbing.

Chest X‐ray

Chest CT Scan

44

Question 14Which of the following should be ordered

to establish the most likely diagnosis?

A. Serum IgG and IgE for Aspergillus

B. Serum IgA and IgG levels

C. Sweat chloride measurement

D. Nasal mucosal biopsy

E. Serum 1-antitrypsin level

Bronchiectasis: Causes

• Bronchopulmonary infections– Bacterial, fungal, mycobacterial

• Bronchial obstruction– Foreign-body, tumors, lymph nodes

• Immunodeficiency states– IgA, IgG deficiency

• Hereditary abnormalities– Cystic fibrosis, ciliary dyskinesia, -1 antitrypsin

deficiency

• Miscellaneous: Rheumatoid, Sjogren’s

Bronchiectasis work‐up in adults

Blood Imaging Other

CBC HRCT Spirometry

IgA, IgE, RF Sinus CT Sputum - Aspergillus- MAC

IgG Sweat chloride

subclasses Nasal mucosal bx

Bronchoscopy

45

Primary Ciliary Dyskinesia

Chronic cough, rhinitis, and sinusitis

Cilia do not beat normally

Triad of situs inversus, chronic sinusitis, and bronchiectasis = Kartagener’s syndrome

Situs inversus is present in 50% of patients with primary ciliary dyskinesia

Question 14Which of the following should be ordered to

establish the most likely diagnosis?

A. Serum IgG and IgE for Aspergillus

B. Serum IgA and IgG levels

C. Sweat chloride measurement

D. Nasal mucosal biopsy

E. Serum 1-antitrypsin level

ABPA

All can cause bronchiectasis with purulent sputum and all part of an adult work-up, but with situs inversus, start with evaluation of cilia

Question 15

65 year old man with a history of TB has intermittent hemoptysis but no fevers/chills/ weight loss.

Recent spirometry: FEV1 1.0L (40%), FVC 1.5L. Today he coughs up 200 mL of bright red blood.

Exam: afebrile, BP 145/82, pulse 104, RR 18, SaO2 93% on air.

Bronchoscopy: blood coming from the left upper lobe bronchus.

46

Chest X‐ray

Chest CT Scan

Question 15

What is the best management option for this patient at the present time?

A. Bronchial arteriography with embolization

B. Four first-line drugs for tuberculosis

C. Intravenous Amphotericin B

D. Left upper lobe resection

47

Causes and Management of Massive Hemoptysis

Massive usually means > 200 mL in 24hrs Most common causes include:

1) TB (active or inactive disease)2) Bronchiectasis 3) Lung cancer4) Mycetoma 5) Immunologic diseases (ANCA-associated vasculitis, Goodpasture’s, SLE)

More commonly chronic mild

hemoptysis

Management of Massive Hemoptysis

First, protect the airway Bronchoscopy can localize; make some diagnoses Majority of massive bleeds have bronchial

circulation Bronchial arteriography with embolization next step. 85% successful especially with bronchiectasis and mycetomas. Less so with cancer

Surgery is definitive, but high M&M if done urgently

Our patient has a mycetoma, and actively bleedingarteriography and embolization successful

Question 15

What is the best management option for this patient at the present time?

A Bronchial arteriography with embolization

B. Four first-line drugs for tuberculosis

C. Intravenous Amphotericin B

D. Left upper lobe resection Old cavity; looks like a classic fungal mycetoma

Doesn’t penetrate fungus ball well;Itraconazole may

48

Question 16

Which of the following are used in the routine treatment of patients with idiopathic pulmonary arterial hypertension?

A. Calcium channel blocker

B. Digoxin

C. Epoprostenol

D. Nitric oxide

E. Warfarin

Pulmonary Hypertension

Smooth Muscle

Cell

Endothelial CellNO

ProstacyclinEndothelin

Smooth muscle relaxation

Smooth muscle contraction

ET-R

Endothelin is also smooth muscle mitogen

Pulmonary Hypertension‐ RX

Prostanoids:Prostacyclin =Epoprostenol

(Flolan) continuous IV

Endothelin receptor-blockersBosentan (Oral)

• Hepatotoxicity

Smooth muscle relaxation

Calcium Channel Blockers

Only 5-10% respond

Iloprost (Inhaled)Treprostinil (IV or sq)

Phosphodiesterase inhibitors:Prolong NO action:Sildenafil & Vardenifil

49

Pulmonary Hypertension‐ RX

Epoprostenol

Bosentan

Calcium Channel BlockersOnly 5-10% respond

Iloprost (Inhaled)Treprostinil (IV or sq)

CheapEven worth a trial?

If severe, most start here

Sildenafil Oral, well tolerated

NOT if hepatopulmonary HTN

Combos with otherdrug classes work

Question 16Which of the following are used in

the routine treatment of patients with IPAH?

A. Calcium channel blocker

B. Digoxin

C. Epoprostenol

D. Nitric oxide

E. Warfarin

Only 5% with sustained benefit, never do without R heart cath to prove efficacy

No portable system yet

Endothelial disruption:in-situ clotting, even small clots can tip a patient over

OK if LV failure

If severe

Don’t forget to correct Hypoxemia!

pH 7.38/ pCO2 44/ pO2 58/ sat’n 89%

Prescribe oxygen!

50

Question 17

52 year old man with alcoholic cirrhosis with prior variceal bleeding has progressive dyspnea on exertion for 3 months. Denies chest pain, fever, or sputum production. Has gained 5 pounds over the past month.

Meds: propranolol.

Chest X‐ray

Lateral Decubitus

Right side

51

Question 17

What is the optimal management in this case?

A. Large volume thoracentesis

B. Chest tube insertion

C. Pleurodesis

D. Medical management with diuretics

Pleural Effusions in Patients with Liver Disease

Hepatohydrothorax: Effusions usually when ascitic fluid is present, but not always

Fluid passes from peritoneum to pleural space via diaphragmatic pores & possibly lymphatic channels. Negative pleural pressure draws fluid up.

Fluid is transudative with very low protein

Typically free-flowing

Pleural Effusions in Patients with Liver Disease

Management: decrease ascites formation • Low salt diet

• Diuretics

• TIPS if refractory

52

Question 17What is the optimal management in this

case?

A. Large volume thoracentesis

B. Chest tube insertion

C. Pleurodesis

D. Medical management

with diuretics

Just keeps draining; reserve large volume thoracentesis for acute dyspnea relief

Can’t get pleural surfaces to meet

Question 18

32 year old woman from China with a known positive PPD has a chronic cough and night sweats for 2 months. Chest radiograph shows a right upper lobe cavity. Two of three smears are positive for acid-fast organisms. She is currently 32 weeks pregnant.

Question 18What is the most appropriate next step?A. Await final sputum culture resultsB. Begin treatment with isoniazid, rifampin,

ethambutol, and pyrazinamideC. Begin treatment with isoniazid, rifampin,

and ethambutolD. Begin treatment with isoniazid, rifampin,

and pyrazinamideE. Call the CDC and transfer her to

National Jewish Hospital

53

TB and Pregnancy Pregnancy per se does not increase the

risk of developing active TB

This is different than simply a positive tuberculin test during pregnancy, when treatment of latent TB infection can usually be deferred until after delivery

TB and Pregnancy Standard initial TB treatment is 4 drugs

(isoniazid/rifampin/ethambutol/ pyrazinamide)

During pregnancy, it is recommended that pyrazinamide be avoided although teratogenicity has not been proven

Mnemonic: P = No PZA in pregnancy! This means that treatment duration will be

prolonged to 9 months!

TB and Drug Resistance

Zhao Y et al. National Survey of Drug Resistant Tuberculosis in China. NEJM 2012;12:2161.

34% some drug resistance

5.7% MDR

.5% XDR

54

Question 1965-year-old man who has recently moved to the United States from Mexico has a tuberculin skin test placed. He denies previous exposure to tuberculosis. Four days later he returns to the clinic and his skin test is read as being 16 mm in induration. A chest radiograph shows apical pleural thickening but no evidence of parenchymal lung disease. He is HIV negative.

Question 19What would be the most appropriate intervention? A. Repeat the tuberculin skin testB. Give 2 months of rifampin for treatment of

latent tuberculosis infectionC. Give 9 months of isoniazid for treatment of

latent tuberculosis infectionD. Collect three sputum specimens and start 4-

drug antituberculosis therapyE. Ignore +PPD if prior BCG vaccination

Who to test for Latent TB?

Contacts to infectious cases

Health care workers

Other workers (prison guards, workers in shelters) who are exposed to TB cases

Risk for New Infection

ATS/CDC AJRCCM 2000;161:S221

55

Who to test for Latent TB?

HIV infection (any stage) Transplant, chemo, or other major

immunocompromise Lymphoma, leukemia, head & neck cancer Abnormal chest x-ray with apical fibronodular

changes typical of healed TB (not granuloma) Silicosis End stage renal disease (dialysis) Treatment with TNF-alpha inhibitors

HIGHEST Risk of Reactivation

ATS/CDC AJRCCM 2000;161:S221

Rx of LTBI: Adult Drug Regimens

Regimen Duration Interval Comments (months)

Isoniazid 9 Daily Preferred300 mg

Isoniazid 9 2/wk DOT900 mg

Rifampin 4 Daily For patients 600 mg exposed to known

INH-R, rifampin-S MTB

JAMA 2005; 293:2776.

Pyridoxine supplementation if on INH especially if predisposed to neuropathy (diabetes, uremia, alcohol, malnutrition & HIV infection) plus pregnancy & seizure disorders.

Question 19What would be the most appropriate intervention? A. Repeat the tuberculin skin testB. Give 2 months of rifampin for treatment of

latent tuberculosis infectionC. Give 9 months of isoniazid for treatment of

latent tuberculosis infectionD. Collect three sputum specimens and start 4-

drug antituberculosis therapyE. Ignore +PPD if prior BCG vaccination

Too short, INH preferred

Apical scarring or calcified granuloma = abnormal but stable

In adults, ignore the BCG

56

Question 20

50 year old man presents for evaluation of a nonproductive cough and chest pain increasing for the past 3 months. He denies weight loss but notes weakness. Exam reveals a mild bilateral ptosis and is otherwise normal. Labs: mild normocytic anemia.

Chest X‐ray

Lateral Chest X‐ray

57

Chest CT Scan

Question 20

What is the most likely diagnosis?

A. Bronchogenic cyst

B. Intrathoracic thyroid

C. Lymphoma

D. Teratoma

E. Thymoma

Mediastinal MassesDifferential Diagnosis

First, localize to anterior, middle, or posterior mediastinum

Anterior Mediastinum Middle Posterior

“The 4 Ts” Bronchogenic cyst Neurogenic cyst

Thymoma Pericardial cyst Esophagus

Thyroid Lymph nodes

Teratoma

“Terrible” lymphoma

58

Thymomas

Pearl: Disease of “35s”

#1 anterior mediastinal mass in those > 35

35% are malignant

35% are associated with myasthenia

35% have a paraneoplastic syndrome

-Pure red blood cell aplasia

-Hypogammaglobulinemia

-Cushing’s syndrome

Question 20

What is the most likely diagnosis?

A. Bronchogenic cyst

B. Intrathoracic thyroid

C. Lymphoma

D. Teratoma

E. ThymomaAsymptomatic until infected

All anterior mediastinal, but most have CT scan characteristics; clue here was anemia, myasthenia symptoms

Question 21A 62 year old patient with COPD complains of SOB

and has a negative CTA for PE, but the CT scan shows

Nodule is not visible on Chest x-ray and there are no prior CT scans. PFTs with FEV1 of 65%.

5 mm

59

Question 21

You recommend:

A. Bronchoscopy

B. PET scan

C. Repeat Chest CT in 6 months

D. Transthoracic needle aspirate

E. Surgical resection

Solitary Pulmonary NoduleFLEISCHNER SOCIETY 2005 Recommendations F/U & Management of Incidental Nodules Detected at Nonscreening CTNodule Size Low-Risk Patient High-risk Patient (Smoker, radon

(mm) asbestos, uranium, 1st degree relative or spiculated nodules)

< or = 4 mm No f/u needed F/u CT 12 mo; if (risk < 1 %) unchanged, no further f/u

>4-6 mm F/u CT 12 mo; F/u CT 6-12 mo thenif unchanged, no f/u 18-24 mo if no change

>6-8 mm F/u CT 6-12 mo, then F/u CT 3-6 mos, then 9-12 18-24 mo if no change and 24 mo if no change

>8 mm F/u CT 3, 9, and 24 mo F/u CT 3, 9, and 24 moif NOT changing if NOT changing vs. PET, FNA, resection vs. PET, FNA, resection

Solitary Pulmonary NoduleFLEISCHNER SOCIETY 2005 Recommendations F/U & Management of Incidental Nodules Detected at Nonscreening CTNodule Size Low-Risk Patient High-risk Patient

(mm)

Translation: Bigger nodules more worrisomeF/u CT at “3, 9, 24 months” means from the 1st CT (not 9 months after the 3 month CT)> 8 mm, we tend to work up now rather than watch CT scans unless other significant morbidities 2 year stability works for most solid nodulesFor “ground glass” nodules, don’t know – we use 3 years of stability

60

Question 21

You recommend:

A. Bronchoscopy

B. PET scan

C. Repeat Chest CT in 6 months

D. Transthoracic needle aspirate

E. Surgical resection

Unless central mass – yield of bronch low.

Yield of FNA high (80% but with 20% risk of PTX)

Too small (1 cm is quoted size cut-off, we see + at 8mm), though if < 1 cm and neg, more false neg, still need to follow

Solitary persistent GGO “Sub‐Solid Nodulesis often BAC (“adenocarcinoma in situ”)

Naidich DP et al. Recommendations for the Mangement of Subsolid Pulmonary Nodules Detected at CT: A Statement from the Fleischner Society”. Radiology 2013;266:304.

PURE GGO < 5 mm no f/u > 5 mm, CT scan at 3 months (many disappear), then if no change CT scan q 1 year x 3 yearsMIXED GGO & solid CT scan 3 months, if persistent esp. if solid component is > 5 mm: think cancer!

Smoking history less important

The End!