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Pulmonary Board
Review
2010
What we’re going to speed through
1.
2.
3.
4.
5.
6.
7.
8.
Evaluation of symptoms: cough and dyspnea
PFTs
Asthma
COPD
Interstitial lung diseases
Pneumoconioses
Pleural disease
Sleep
Chronic cough

Definition: cough lasting more than:
1.
2.
3.
4.
3 weeks
1 month
3 months
1 year
Chronic cough

Definition: cough lasting more than:
1.
2.
3.
4.
3 weeks
1 month
3 months
1 year
Chronic Cough- Etiology

In non-smoking adults with a normal CXR
who are not taking ACE inhibitors, chronic
cough is almost always due to which of
the following 3 conditions?
a)
b)
c)
d)
e)
Congestive Heart Failure
Post-nasal drip syndrome (PNDS)
Asthma
Gastroesophageal reflux disease (GERD)
Chronic Bronchitis
Chronic Cough- Etiology

In non-smoking adults with a normal CXR
who are not taking ACE inhibitors, chronic
cough is almost always due to which of
the following 3 conditions?
a)
b)
c)
d)
e)
Congestive Heart Failure
Post-nasal drip syndrome (PNDS)
Asthma
Gastroesophageal reflux disease (GERD)
Chronic Bronchitis
Respiratory symptoms: cough

Chronic Cough


First: Make sure the patient is not on an ACE inhibitor
Most common etiologies




Postnasal drip syndrome
Asthma
GERD
Others:






Chronic bronchitis
Bronchiectasis
ACE inhibitor
Post-infectious
Eosinophilic bronchitis
Endobronchial lesion
Respiratory symptoms: dyspnea

The 4 most common etiologies of
chronic dyspnea ( dyspnea lasting > 1
month) are:
1.
2.
3.
4.
5.
Cardiomyopathy
Deconditioning
Interstitial lung disease
COPD
Asthma
Respiratory symptoms: dyspnea

The 4 most common etiologies of
chronic dyspnea ( dyspnea lasting > 1
month) are:
1.
2.
3.
4.
5.
Cardiomyopathy
Deconditioning
Interstitial lung disease
COPD
Asthmma
These four etiologies account for 2/3 of all cases of chronic dyspnea
Dyspnea - Assessment

Pratter MR, et al. Cause and evaluation of chronic dyspnea
in a pulmonary disease clinic. Arch of Intern Med.
1989;149:2277-82.









Asthma (29%)
COPD (14%)
ILD (14%)
Cardiomyopathy (11%)
Upper airway (8%)
Psychogenic (5%)
Deconditioning (5%)
GE reflux (4%)
Extrapulmonary (4%)
Dyspnea - Assessment

PFTs, spirometry with bronchodilator, lung volumes, flow-volume loop,
DLCO, ABG, muscle pressures (inspiratory and expiratory)
methacholine
CXR, CT scan of the chest, PE protocol CT, fluoroscopy of the
diaphragm
6 minute walk
Cardiac echo, right heart cath
Chemistries and CBC, proBNP, Mg, CPK, aldolase, serologies, TFT
EMGs, MRI of the brain

Exercise ergotomy






PFTs
Inhalation to
Total lung
capacity
Normal tidal
breathing
Beginning of
Forced
Expiratory
maneuver
Volume of air
Exhaled 1 sec
Into forced expiration
Exhalation to
Residual volume
PFTs: Spirometry

Approach

Is it a good test?






reproducible,
adequate exhalation time (at least 6 seconds),
technician comments regarding patient effort and compliance
Is there obstruction? FEV1/FVC < 70% indicates obstructive disease.
Severity of obstruction as follows:



I: Mild
II: Moderate
III: Severe
FEV1 > 80% predicted
FEV1 < 50-80% predicted
FEV1 < 30- 50% predicted

IV: Very Severe
FEV1 < 30% predicted
Is there restriction? FVC < 80% predicted indicates possible restrictive
disease
Is there airway reactivity? Response to bronchodilator testing: > 12% or >
200mL
Lung volumes
Lung Volumes
120
100
80
RV
FRC
TLC
60
40
20
0
nl
COPD
rest
n-m
obese

Which of the following can cause a
reduced vital capacity?
1.
2.
3.
4.
5.
Asthma
Kyphoscoliosis
Pulmonary fibrosis
Obesity
Myasthenia gravis

Which of the following can caused a
reduced vital capacity?
1.
2.
3.
4.
5.
Asthma
Kyphoscoliosis
Pulmonary fibrosis
Obesity
Myasthenia gravis
DLCO
The blood gas barrier

Gas exchange
surface



50-100 sq meters
0.3 microns
Each alveolus is
enveloped by
pulmonary
capillaries
 There are
about 500 to
1000
capillaries per
alveolus!
Diffusion: Fick’s law

The amount of gas
transferred through a
membrane is
proportional to


A: area of the
membrane
D: diffusion constant
which is determined by




Solubiility of the gas
Inversely proportional
to the square root of
the moelcular weight
Difference in partial
pressure
Inversely proportional
to the thickness of the
membrane
PFTs: DLCO

Decreased in:

Diseases that obliterate the alveolar-capillary interface:




Diseases that increase the thickness of the interface:



Emphysema
Fibrotic lung disease
Pulmonary vascular diseases: pulmonary emboli, PAH
Fibrotic lung diseases
Interstitial edema/alveolar edema
Anemia
PFTs: flow volume loops

Useful in looking for
central airway
obstruction
Flow volume volumes
Obstructive airway
diseases
4-8 questions
Asthma

22 millions pts per year in U.S.



Overall increasing disease prevalence
Decreasing number of asthma deaths
Significant racial disparities in disease burden


Puerto Ricans
African Americans
Asthma categories of severity 2007
NAEPP report





Intermittent
Mild persistent
Moderate persistent
Severe persistent
Treatment recommendations based upon
severity
Classification of severity in treatment naïve
Persistent
patient
Components of severity
Impairment
Mild
Moderate
Severe
Symptoms
≤ 2 x/week
≥ 2 days per
week
Daily
Throughout
the day
Nocturnal
awakenings
≤ 2x/month
3-4 x/month
> 1/week
Near nightly
SABA use
≤ 2x/ week
> 2x/week
Daily
Several times
per day
Interference
with normal
activity
None
Minor
Some
Significant
Normal
between
exacerbations
FEV1 >80%
FEV1 > 60%
FEV1 < 60%
FEV1/FVC
normal
FEV1/FVC
reduced 5%
FEV1/FVC
reduced>5%
≤ 1 per year
≥ 2 per year
Lung function
Risk
Intermittent
Exacerbations
requiring
systemic
steroids
Level of severity assigned based upon the single feature of the highest severity category

22 year old man presents because he gets out of breath
playing basketball after being on the court of 30 minutes.
He otherwise has no symptoms. His pulmonary function
testing demonstrates FEV 86% FVC 102% and
FEV1/FVC of 64%. Which severity category does he fall
into?
1.
2.
3.
4.
Intermittent
Mild persistent
Moderate persistent
Severe persistent
Classification of severity based upon lowest
level treatment required to maintain control
Classification of asthma severity
Intermittent
Persistent
Mild
Moderate
Severe
PRN shortacting
bronchodilator
Low dose ICS
OR
Alternative
Cromolyn
LTRA
Step 2
Step 1
Low dose ICS +
LABA
OR
Medium dose
ICS
OR
Medium dose
ICS + LABA
High dose ICS +
LABA
AND
Omalizumab,
oral
corticosteroid
Step 3 or 4
Step 5

Intermittent asthma:

Symptoms ≤ 2 days per week
Requirement for rescue albuterol ≤ 2 days per
week
Nocturnal awakenings ≤ 2 times per month
No limitations in ADLs
Normal PFTs

RX: Intermittent albuterol





Mild persistent asthma
Symptoms > 2 days per week or
 3-4 nocturnal awakenings a month or
 Minor limitation in ADLs
AND
 Normal PFTs


RX: Step 2 low dose inhaled corticosteroids

Moderate persistent asthma





Daily symptoms or
> 1 nocturnal awakening per week or
Moderate limitation in ADLs or
Decreased FEV1 but > 60% and FEV/FVC ratio reduced
< 5%
Rx: step 3 in asthma treatment protocol


Low dose inhaled corticosteroids + LABA
Medium dose inhaled corticosteroid

Severe persistent symptoms

Ongoing daily symptoms with significant exercise
limitation and frequent nocturnal awakenings
FEV1 < 60% or FEV1/FVC reduced by > 5%

Rx:




Step 4: High dose ICS + LABA
Step 5: High dose ICS + LABA + systemic corticosteroid
therapy
AND consider omalizumab
Asthma syndromes





Cough variant asthma
Aspirin-induced asthma or triad asthma
Exercise induced asthma
Occupational asthma
Allergic bronchopulmonary aspergillosis
Occupational asthma



5 – 15% of all asthmatics
Over 300 agents have been reported to cause OA
Different prevalence for specific populations




OA may develop in 2.5% for hospital workers exposed to
latex
2-40% millers and bakers
20% exposed to acid anhydrides
5% exposed to toluene diisocyanate (TDI)

OA with a latency period: specific antigens
identified, mostly HMW antigens although some
LMW antigens as well



IgE mediated: usually HMV antigen with a median latency
period of ~ 5 years. Atopy is a risk factor
Non-IgE mediated: usually LMW antigens with a median
latency period of 2 years. Atopy is not a risk factor
OA without a latency period:


1) nonspecific irritant-induced asthma or
2) reactive airways dysfunction syndrome
COPD: The Burden

Affects up to 30 million Americans (~5% of adult population)1

Annual cost more than $30 billion2
 70% with COPD are younger than age 65
 Direct health care costs of $14.7 billion
 Indirect costs of $15.7 billion

Between 1985 and 1995, the number of physician visits for COPD
increased from 9.3 to 16 million.

The number of hospitalizations for COPD in 2000 was estimated to be
726,000.

2nd leading cause of disability (behind heart disease)
1 Petty
TL. J Resp Dis. 1997;18:365–369.
Lung Association. COPD Fact Sheet. August 1999.
2 American
COPD risk factors

Tobacco:








15-20% 1ppd smokers develop COPD
25% 2ppf smokers develop COPD
Genetic factors: Alpha1-antitrypsin deficiency
Gender: Males more at risk than females
Bronchial hyperresponsiveness
Atopy and asthma
Childhood illnesses
Prematurity
Exercise Performance Over Time
FEV1 (%) Relative to Age 25
100
Healthy
80
COPD
Symptoms
60
40
Disability
20
Death
Rehabilitation
at 45 (mild COPD)
Rehabilitation
at 65 (severe
COPD)
0
0
25
50
Age (years)
Adapted from Fletcher et al. BMJ. 1977;1:1645-1648.
75
GOLD Classification of Severity of COPD
Stage
Characteristics
0: At Risk
Normal spirometry
Chronic symptoms (cough, sputum
production)
I: Mild COPD
FEV1/FVC <70 percent
FEV1 ≥80 percent predicted
II: Moderate COPD
FEV1/FVC <70 percent
FEV1 50-80 percent predicted
III: Severe COPD
FEV1/FVC <70 percent
FEV1 30-50 percent predicted
IV: Very Severe COPD
FEV1/FVC <70 percent
FEV1 <30 percent predicted
or
FEV1 <50 percent predicted
plus respiratory failure
COPD

Treatment:

Smoking cessation
Oxygen therapy
Medical therapy
Pulmonary rehabilitation
LVRS

Transplantation




Clinical Algorithm for the Treatment of COPD
Clinical
stage
GOLD Stage
(approximate)
At risk
0
Intermittent
symptoms
I
Persistent
symptoms‡
Inhaled Therapy
Smoking cessation
Avoidance of exposure
*Short-acting bronchodilator as needed
(for example, ipratropium, salbutamol, or combination)
†
II
Frequent
exacerbations¶
III
Respiratory failure
IV
Nonpharmacologic
Therapy
*Tiotropium +
albuterol
Salmeterol or formoterol +
ipratropium, salbutamol,
or combination
*Tiotropium +
salmeterol or formoterol§
Salmeterol or Formoterol +
Tiotropium§
Vaccination
(influenza, pneumococcal)
Pulmonary rehabilitation
(Exercise prescription)
*Tiotropium + salmeterol or formoterol
+ inhaled corticosteroid§
Supplemental oxygen
Lung volume reduction surgery
Lung transplantation
*Four-step algorithm for the implementation of inhaled treatment; †Pathway on left is recommended; pathway on right side is a
valid alternative; ‡Defined as need for rescue medication on more than 2 occasions per week; §A short-acting bronchodilator
can be used for rescue. Low-dose methylxanthines can be prescribed if the response to inhaled bronchodilator therapy is
insufficient;
¶ Defined as 2 or more exacerbations per year.
Restrictive lung
disease/ Interstitial
lung disease/DPLD
Up to 5 questions
Restrictive lung disease

Definition:

Any disease process that results in a decrease in
total lung capacity






Interstitial lung disease
CHF
Obesity
Neuromuscular disease
Thoracic cage disease
Pleural disease
Classification
ATS/ERS International Multidisciplinary Consensus Classification of IIP. AJRCCM 2002
Normal CXR
Patient 1 CXR
Workup of ILD: Hx & PE








Occupation
Travel
Drugs
Pets
Hobbies
Systemic symptoms
Smoking
Family Hx







Clubbing
Bibasilar rales
Signs of cor
pulmonale
Lymphadenopathy
Rash
Arthritis
Fever
ATS/ERS International Multidisciplinary Consensus Classification of IIP. AJRCCM 2002
Studies







CBC with diff
ESR
Renal & liver function
Urinalysis
ANA/ ANCA/RF
EKG
Chest Xray






ABG
6 min. walk
PFTs
DLCO
HRCT
Bronchoscopy with
BAL & TBBX if you are
thinking of specific
disease entities

Which is the earliest PFT abnormality
seen in interstitial lung disease?
1.
2.
3.
4.
5.
Decreased vital capacity
Decreased total lung capacity
Decreased residual volume
Increase in mid flows (FEF 25-75)
Decrease in DLCO

Which is the earliest PFT abnormality
seen in interstitial lung disease?
1.
2.
3.
4.
5.
Decreased vital capacity
Decreased total lung capacity
Decreased residual volume
Increase in mid flows (FEF 25-75)
Decrease in DLCO
PFTs in ILD





Earliest sign is a widened A-a gradient or
desaturation with exercise
Decreased DLCO precedes restrictive FVC,
FEV1, TLC and RV
Flows as seen by FEV1/FVC ratio are
supernormal due to increased elastic recoil in
pure restrictive disease
However, in specific diseases or mixed disease,
you can see a mixed obstructive/restrictive picture
Hypercarbia is a late, preterminal finding
DPLD radiologgy

Chest Xray can be normal in




10-15% patients with diffuse lung disease
30% patients with bronchiectasis
60% patients with emphysema
High resolution chest CT



Sensitivity of 90% and specificity approaching 100%
Can provide a confident diagnosis in ~50% cases; ~93% of these cases
are ultimately proven correct
Findings usually seen in DPLD


Ground glass opacity
Findings consistent with fibrosis
 Interlobular and intralobular septal thickening
 Honeycombing
HRCT findings: linear and reticular
opacities

Intralobular interstitial thickening




“fine reticular pattern” with lines of opacity separated by a few mmm
Fine lacy or netlike appearance
When seen in fibrosis, often seen in conjunction with dilated bronchioles
(“bronchiolectasis”)
DDX:









IPF
Chronic hypersensitivity pneumonitis
Pneumoconioses
ILD: NSIP, DIP
Lymphangitis carcinomatosis
Pulmonary edema
Pulmonary hemorrhage
Pneumonia
Alveolar proteinosis
Figure 3-24
IIPs and HRCT rules of thumb
Diagnosis
Typical distribution
Typical radiographic features
IPF (UIP)
Peripheral & subpleural
Basilar
Reticular,
NSIP
Peripheral & subpleural
Basilar
Ground
COP
Subpleural and peribronchial
Patchy
AIP
Diffuse
Consolidation
DIP
Lower lung zone
Peripheral predominance
(mostly)
Ground
RBILD
Diffuse and can be upper
Bronchial
LIP
Diffuse
Centrilobular
honeycombing
Traction bronchiectasis and bronchiolectasis
Architectural distortion, modest ground glass
glass opacities predominent
Reticular opacities present
bilateral consolidation
and ground
Traction bronchiectasis occurs later
glass
Reticular lines
wall thickening
Centrilobular nodules
Patchy ground glass
nodules, ground glass, septal and
bronchovascular thickening. Thin-walled cysts
Diagnosis

Bronchoscopy

BAL limited utility




Look for eosinophilia (> 10%)
Lymphocytosis
Mast cells
Biopsy limited utility


Helps if high pre-test probability of sarcoidosis, HP, LIP,
lymphangitic carcinomatosis
Dismal if you are thinking UIP or NSIP
IPF or Usual Interstitial Pneumonitis





> 60% of all cases of IPF
age > 50 with 2/3 > 60 M>F
prevalence 10-20 cases per 100,000 pop.
Risk factors: smoking, chronic aspiration,
metal & wood dust, viruses, genetic autosomal dominant with variable
penetrance
Median survival after Dx 2.8 years.
ATS/ERS International Multidisciplinary Consensus Classification of IIP. AJRCCM 2002
ATS/ERS International Multidisciplinary Consensus Classification of IIP. AJRCCM 2002
Example of disease progression over time
ATS/ERS International Multidisciplinary Consensus Classification of IIP. AJRCCM 2002
UIP Continued

Histopathology



Temporally heterogeneous
Fibroblastic foci
Interstitial inflammation is only mild to moderate
with infiltration by




Lymphocyte
Plasma cells
Histiocytes
Full spectrum of fibrosis
Nonspecific Interstitial
Pneumonitis


Second most common IIP
Clinical presentation






DOE & cough for months to years
Flu-like symptoms may precede or co-exist
Median age of onset 40 to 50
W>M
No association with smoking
Examination



10-35% patients have clubbing
Most have crackles
Chest Xray - lower zone reticular opacities
NSIP CT scan
ATS/ERS International Multidisciplinary Consensus Classification of IIP. AJRCCM 2002
NSIP



Path: temporally uniform with interstital
inflammation
Rad: ground glass with areas of fibrosis
Often also seen with CTD such as
scleroderma
Cryptogenic organizing pneumonia


First described 1983
Clinical presentation





M=F
Mean age 55 years
Mean symptom duration 3months: cough, dyspnea,
weight, seats, chills, fevers and myalgias
Labs: Elevated ESR, CRP, and ANC
BAL


Lymphocytosis (can be > 40%)
CD4:CD8 decreased
COP: radiographic findings

>90% with areas of consolidation on CT





~60% with ground glass attenuation usually seen
associated with the areas of consolidation
10-50% cases with small nodular opacities
15% cases with large nodular opacities (> 1cm)


Tends to be patchy
Subpleural or peribronchial distribution in up to 50% cases
Tend to have an irregular margin with air bronchograms
+/- pleural tags, spicules, pleural thickening, and
parenchymal bands
Minority with a reticulonodular pattern
Histopath “Organizing pneumonia”

Histopathologic correlate: Organizing pneumonia within the alveolar ducts
and alveoli +/- organization within the bronchioles




Intraluminal organizing fibrosis
Patchy distribution with preservation of the lung architecture and associated mild interstitial
chronic inflammation
You do NOT see: interstitial fibrosis, granulomas, neurophils, necrosis, airspace fibrin
Non-specific and seen with a multitude of clinical conditions!










COP
Organizing DAD
Organizing infection
Organizing aspiration pneumonia
Organizing drug reactions, inhalational injuries
Collagen vascular disease
HP
Eosinophilic lung disease
IBD
Reparative reaction around abscesses, neoplasms, Wegeners’s, etc……..
AIP


Rapidly progressive form of ILD histopathologically
indistinguishable from ARDS
Clinical presentation







Wide age range although mean age 50
No gender predominance and no association with tob
Typically prior illness consistent with viral URI
Median time from first symptoms to presentation < 3 weeks
No proven treatment
Mortality rate 50% + with most deaths occurring within 1 to
2 months of illness onset
Most survivors experience recurrence and chronic
progressive ILD
DIP/RBILD “smoking related ILD”

RBILD

Clinical presentation









Current smokers usually 40 to 50 years
old
Average > 30 pack years; when it
occurs in younger smokers, typically
seen with heavier tobacco use
M>W
PFTS: Usually primarily obstructive
physiology with a decrease in transfer
factor
Radiology



Centrilobular nodules
Patchy ground glass
Thicekning of bronchial walls
Mosaic pattern due to air trapping
BAL fluid contains pigmented
macrophages +/- modest increase in
neutrophils
Histopath: Pigmented intraluminal
macrophages within the first and
second order respiratory bronchioles
DIP



Considered to represent the end of a
spectrum of RBILD
Rare < 3% of all ILDs
Clinical manifestations






90% are smokers, M>F
age - 40s,
Clubbing in ~ 50%
Subacute illness with dyspnea &
cough, fatigue, weight loss, weakness,
chest pain
Chest Xray is normal in 20%
Survival : 70% 10 yrs., steroids help
60%
DIP/RBILD

Path:



Pigmented macrophages
Peribronchiolar inflammation
Rad:



Patchy ground glass
Intralobular septal thickening
Mosaic pattern
DPLD: Hypersensitivity pneumonitis


Disease of varying intensity and manifestation caused by the
immunologic response to inhaled antigen, usually organic
Hundreds of antigens have been described. Occupations
with highest frequency of HP:







Farmers “Farmer’s lung”
Poultry workers “Poultry worker’s lung,” “Bird breeder’s lung,”
“Bird fancier’s lung”
Animal workers
Grain processing “Grain handler’s lung”
Textiles
Lumber
Also described with inhalation of contaminated water

“Humidifier lung,” “Air conditioner lung,” “Hot tub lung”
Subacute HP
Mostly mid to upper lung zones
Chronic HP
HP: Treatment and prognosis

Treatment



Remove the inciting antigen from the environment
or remove the patient from the environment
Corticosteroids for severe cases
Prognosis


Acute and subacute disease have excellent
outlooks
Chronic can progress to end stage fibrosis
Y. Rosen, M.D. Atlas of Granulomatous Diseases
Sarcoidosis: Four stages
Sarcoidosis in the lungs: Stage I



Only the lymph nodes
are enlarged
Pulmonary function is
intact
55-90% pts with Stage
I sarcoidosis resolve
spontaneously
Sarcoidosis: Stage II




Lymph nodes
enlarged
Inflammation in
the lung
Lung function is
impaired
40-70% pts
resolve
spontaneously
Sarcoidosis: Stage III


Lymph nodes are not
enlarged
Only 10-20% resolve
spontaneously
Sarcoidosis








90% with lung
involvement
75% liver
20% skin
20% eyes
25% spleen
10% MSK
5% heart
5%
Occupational lung
diseases
Up to 4 questions
Occupational and environmental lung
diseases



Occupational asthma
Hypersensitivity pneumonitis
Pneumoconioses
Pneumoconioses





Silicosis
CWP
Asbestosis
Talcosis
Berylliosis
Silicosis: Exposure







Mining
Quarrying
Tunneling
Stone cutters
Sandblasting
Glass manufacturing
Foundry work



Enameling
Quartz crystal
manufacturing
Rubber industry
Silicosis: clinical presentations




Chronic silicosis
Accelerated silicosis
Progressive massive fibrosis
Acute silicosis
Chronic silicosis



Usually 10-30 years after initial exposure.
Can become radiographically apparent
even after removal of exposure
Ranges from asymptomatic with normal
PFTs to very very symptomatic with
restrictive spirometry and low DLCO
Chronic silicosis: CXR findings


Simple silicosis is the
earliest finding of
chronic silicosis
Nodules usually 1-3
mm
Chronic silicosis: CXR findings

As disease
progresses, nodules
increase in number
and coalesce to form
larger lesions
Chronic silicosis: CXR findings

Eggshell calcification
Progressive massive fibrosis (PMF)



Occurs in a minority of pts with chronic
silicosis
More likely to occur in pts with accelerated
silicosis
PFTs abnormalities: mixed
obstructive/restriction, air trapping
PMF: CXR findings


The nodules coalesce
into conglomerate
masses
Calcified lymph nodes
“eggshell calcification”
Coal worker’s pneumoconiosis



AKA, black lung disease or anthrasilicosis
Rate and quantity of dust accumulation
most important factor in pathogenesis of
CWP
Clinical presentations similar to silicosis:
1.
2.
3.
Simple
Chronic
PMF
Asbestos-related lung diseases





Pleural plaques
Pleural fibrosis
Benign asbestos related pleural effusion
Asbestosis
Mesothelioma
Asbestos: Pleural plaques




Usually first identified > 20 years after initial
exposure
Occur in 50% persons exposed to asbestos
Parietal pleura adjacent to ribs, particularly
along 6th-9th ribs and along diaphragm
Calcifications on CXR in 20% and on chest
CT in 50%
Asbestos: Pleural plaques
Pleural fibrosis


Very rare, progressive process
characterized by diffuse pleural fibrosis
Can be exacerbated with concurrent
administration of medications such as
bromocriptine
Benign asbestos pleural effusion





Most common pulmonary manifestation within the
first 20 years of exposure… but can present <1
post-exposure to >50 years after first exposure
Typical presentation: acute pleuritic CP, fever,
other systemic sx but can be insidious
Can resolve spontaneously
Pleural fluid analysis: exudative, serosanguinous,
predominance of eosinophils, cytology with
atypical macs, occasionally positive for RF
Rounded atelectasis and/or diffuse pleural
thickening may be sequelae
Rounded atelectasis
Asbestos: Mesothelioma




Annual incidence 1:1,000,000/year
Incidence peaking now b/c of inadequate
control measures in 60s and 70s
Any level of exposure may be a risk factor
Usually presents 20-40 years after
exposure
Asbestosis



Presents > 30 years after initial exposure
Requires long term, heavy exposure
Criteria for diagnosis:
1.
2.
3.
4.
5.
History of asbestos exposure
Dyspnea
Basilar crackles in two or more locations
Reduced lung volumes
Radiographic abnormalities
Talc related diseases




Talcosilicosis: caused talc mined with a high
silica content
Talcoasbestosis: crystalline talc contaminated by
asbestos fibers
Talcosis: inhalated of pure talc leading to
bronchitis
IV talc injection: from cutting heroin with talc 
formation of granulomas within the pulmonary
vasculature  pulmonary hypertension
Berylliosis


Think aerospace, automotive, computer,
ceramics, and nuclear industries
Clinical manifestations:


Acute disease due to direct irritant effects:
rhinitis, pharyngitis, tracheobronchitis, chemical
pneumonitis
Chronic disease: Think sarcoidosis except we
have an etiology. Dx: finding beryllium
somewhere or lymphocyte transformation test.
Pleural disease
Up to 4 questions
Diagnostic evaluation of pleural
effusion

Thoracentesis



Helpful in 75% cases
Can be therapeutic as well
Routine labs:


LDH, total protein, glucose, pH, gram stain and
culture, cytology, cell count and differential
Additional labs that may also be helpful

Albumin, cholesterol, triglycerides, amylase,
adenosine deaminase, AFB
Pleural fluid analysis: Light’s criteria



Pleural fluid protein/serum protein > 0.5
Pleural fluid LDH / serum LDH > 0.6
Pleural fluid LDH > 2/3 upper limits of
normal for serum LDH
*Very accurate at identifying exudates
(~98%) but less accurate with transudates
Pleural fluid analysis: Other pleural
chemistries to help differentiate exudate
from transudate

Cholesterol



Absolute pleural fluid cholesterol > 45- 60mg/dL
Pleural fluid albumin gradient < 1.2 g/dL
Bilirubin: pleural fluid bilirubin/serum
bilirubin > 0.6
Pleural fluid analysis: cell count

Red blood cells


Blood-tinged fluid typically 5000 to 10000
RBC/mm3
Grossly bloody: 100000 RBC mm3





Trauma
Malignancy
Pulmonary embolism
Infection
Hemothorax: pleural fluid hct to blood hct > 50%
Pleural fluid analysis: Cell count and
differential

Neutrophils


Typical of acute inflammatory process
Eosinophils > 10%


air, blood most common etiologies.
Other:



Lymphocytes > 50%


Parapneumonic #1,
malignancy, tuberculosis, BAPE, drugs (dantrolene, bromocriptine,
nitrofurantoin), parasites, Churg-Strauss
malignancy, tuberculosis (sarcoidosis, s/p CABG)
Mesothelial cells:

Uncommon in tuberculous effusions. Major exception: AIDS
Pleural fluid analysis: Glucose

Glucose < 60mg/dL suggestive of the following
disorders

Parapneumonic effusion:


Malignant effusion:



15-25% pts with malignant effusion have low pleural glucose
levels. The lower the glucose, the higher the tumor burden
Rheumatoid disease:


the lower the glucose, the more complicated the effusion
majority of pts with rheumatoid effusion (78%) have pleural
glucose < 30mg/dL
Tuberculous effusion
Rare: Paragonimiasis, hemothorax, Churg-Strauss, lupus
Pleural fluid analysis: amylase

Elevated levels suggestive of 1 of 3 dx

Pancreatitis: often higher than serum levels
**Pseudocyst communication: amylase > 1000U/L


Esophageal rupture
Malignant effusions: amylase level elevated in
10%
Pleural fluid analysis: pH

pH < 7.2:










Parapneuymonic effusion
Esophageal rupture
Rheumatoid pleuritis
Tuberculous pleuritis
Malignant pleural disease
Hemothorax
Systemic acidosis
Paragonimiasis
Lupus pleuritis
Urinothorax

Reasons for caution



Often not measured
correctly: must be
measured using a blood
gas machine
Must be collected in a
heparinized syringe
Lidocaine may falsely
lower the pH
Pleural fluid analysis: some
pathognomic findings






ADA level > 50 U/L in pts without empyema or
rheumatoid arthritis is virtually diagnostic of a
tuberculous effsuion
Interferon-gamma level > 3.7 U/mL also quite good at
distinguishing tuberculous effusions
RF: Pleural fluid titer > 1:320 strongly suggestive of
rheumatoid effusion
ANA: tends to correlate with serum ANA
Triglycerides > 110 mg/dL  diagnostic of chylothorax
Pus or positive culture  empyema
Parapneumonic effusions
ACCP recommedations

Class I: Small < 10mm on decubitus film


No thoracentesis needed
Class II: Typical parapneumonic effusion


More than 10mm on decubitus film  needs sampling
Pleural fluid characteristics:





Treatment: antibiotics alone
Class III: Borderline complicated





Glucose > 40
pH > 7.2
LDH < 3x ULN
pH 7.0 -7.2 or LDH > 3x ULN
Normal glucose
Negative pleural micro
Treatment: Antibiotics plus serial thoracenteses
Class IV through VII: Complicated

pH < 7.0 or glucose < 40 or pleural fluid micro positive  tube thoracostomy
Sleep disordered breathing

Obstructive sleep apnea

RFs






Mild




AHI 5-15
Sedentary daytime sleepiness
Sats > 90% more than 95% of time during sleep
Moderate:



Obesity
Facial soft tissue abnormalities
Smoking!
Nasal congestion
DM
AHI 15-30
Daytime sleepiness requiring behavioral changes
Severe:



> 30
disabling daytime sleepiness and signs of cardiopulmonary failure
Nocturnal sats < 90% more than 20% of the time
Sleep disordered breathing

Outcomes:




3-6x risk of all cause mortality
Associated with: HTN, PH, MI, CVA, arrythrmias
Treatment is associated with decreased mortality
Treatment:



Weight
Alcohol and drug avoidance
NIPPV for




AHI > 5 and clinical sequelae (sleepiness, mood disorder,
cardiovascular disease)
AHI > 15 without symptoms
Oral appliances
Surgery (UPPP)
Obesity hypoventilation syndrome

Definition




Usually seen with



Awake alveolar hypoventilation (pCO2 > 45)
Obesity (BMI > 35)
No other cause of hypoventilation
OSA
Cor pulmonale
Outcomes:

High mortality
Whew!
Thanks for your attention