pulmonary board review
DESCRIPTION
Pulmonary Board Review. 2010. What we’re going to speed through. Evaluation of symptoms: cough and dyspnea PFTs Asthma COPD Interstitial lung diseases Pneumoconioses Pleural disease Sleep. Chronic cough. Definition: cough lasting more than: 3 weeks 1 month 3 months 1 year. - PowerPoint PPT PresentationTRANSCRIPT
Pulmonary Board Review
2010
What we’re going to speed through1. Evaluation of symptoms: cough and dyspnea2. PFTs3. Asthma4. COPD5. Interstitial lung diseases6. Pneumoconioses7. Pleural disease8. Sleep
Chronic cough Definition: cough lasting more than:
1. 3 weeks
2. 1 month
3. 3 months
4. 1 year
Chronic cough Definition: cough lasting more than:
1. 3 weeks
2. 1 month
3. 3 months
4. 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) Congestive Heart Failureb) Post-nasal drip syndrome (PNDS)c) Asthmad) Gastroesophageal reflux disease (GERD)e) 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) Congestive Heart Failureb) Post-nasal drip syndrome (PNDS)c) Asthmad) Gastroesophageal reflux disease (GERD)e) 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. Cardiomyopathy
2. Deconditioning
3. Interstitial lung disease
4. COPD
5. Asthma
Respiratory symptoms: dyspnea The 4 most common etiologies of
chronic dyspnea ( dyspnea lasting > 1 month) are:
1. Cardiomyopathy
2. Deconditioning
3. Interstitial lung disease
4. COPD
5. 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 toTotal lung capacity
Normal tidalbreathing
Beginning of Forced Expiratorymaneuver
Volume of airExhaled 1 secInto forced expiration
Exhalation toResidual 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 FEV1 > 80% predicted
II: Moderate FEV1 < 50-80% predicted III: Severe 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
0
20
40
60
80
100
120
nl COPD rest n-m obese
RV
FRC
TLC
Which of the following can cause a reduced vital capacity?
1. Asthma
2. Kyphoscoliosis
3. Pulmonary fibrosis
4. Obesity
5. Myasthenia gravis
Which of the following can caused a reduced vital capacity?
1. Asthma
2. Kyphoscoliosis
3. Pulmonary fibrosis
4. Obesity
5. Myasthenia gravis
DLCOThe 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: Emphysema Fibrotic lung disease Pulmonary vascular diseases: pulmonary emboli, PAH
Diseases that increase the thickness of the interface: Fibrotic lung diseases Interstitial edema/alveolar edema
Anemia
PFTs: flow volume loops Useful in looking for
central airway obstruction
Flow volume volumes
Obstructive airway diseases4-8 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 patient
Components of severity Intermittent
Persistent
Mild Moderate Severe
Impairment
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
Lung function Normal between exacerbations
FEV1 >80% FEV1 > 60% FEV1 < 60%
FEV1/FVC normal
FEV1/FVC reduced 5%
FEV1/FVC reduced>5%
Risk Exacerbations requiring systemic steroids
≤ 1 per year ≥ 2 per year
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. Intermittent
2. Mild persistent
3. Moderate persistent
4. Severe persistent
Classification of severity based upon lowest level treatment required to maintain control
Classification of asthma severity
Intermittent Persistent
Mild Moderate SeverePRN short-acting bronchodilator
Step 1
Low dose ICS
OR
Alternative
Cromolyn
LTRA
Step 2
Low dose ICS + LABA
OR
Medium dose ICS
OR
Medium dose ICS + LABA
Step 3 or 4
High dose ICS + LABA
AND
Omalizumab, oral corticosteroid
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;18:365–369.2 American Lung Association. COPD Fact Sheet. August 1999.
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
Adapted from Fletcher et al. BMJ. 1977;1:1645-1648.
FE
VF
EV
11 (%
) R
elat
ive
to A
ge
25 (
%)
Rel
ativ
e to
Ag
e 25
Death
Disability
Age (years)5050 7575252500
Symptoms
00
2020
6060
100100
8080
4040
Healthy
COPD
Rehabilitationat 45 (mild COPD)
Exercise Performance Over Time
Rehabilitationat 65 (severe 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
GOLD Classification of Severity of COPD
COPD Treatment:
Smoking cessation Oxygen therapy Medical therapy Pulmonary rehabilitation LVRS
Transplantation
*Four-step algorithm for the implementation of inhaled treatment; *Four-step algorithm for the implementation of inhaled treatment; ††Pathway on left is recommended; pathway on right side is a Pathway on left is recommended; pathway on right side is a valid alternative; valid alternative; ‡‡Defined as need for rescue medication on more than 2 occasions per week; Defined as need for rescue medication on more than 2 occasions per week; §§A short-acting bronchodilator A short-acting bronchodilator can be used for rescue. Low-dose methylxanthines can be prescribed if the response to inhaled bronchodilator therapy is can be used for rescue. Low-dose methylxanthines can be prescribed if the response to inhaled bronchodilator therapy is insufficient; insufficient; ¶¶ Defined as 2 or more exacerbations per year. Defined as 2 or more exacerbations per year.Cooper et al. Cooper et al. BMJBMJ. 2005;330;640-644. (B). 2005;330;640-644. (B)
Inhaled TherapyInhaled Therapy
0000
IIII
IIIIIIII Salmeterol or formoterol +Salmeterol or formoterol +ipratropium, salbutamol, ipratropium, salbutamol,
or combinationor combination
Salmeterol or formoterol +Salmeterol or formoterol +ipratropium, salbutamol, ipratropium, salbutamol,
or combinationor combination
*Tiotropium +*Tiotropium +albuterolalbuterol
*Tiotropium +*Tiotropium +albuterolalbuterol
IIIIIIIIIIII
Salmeterol or Formoterol +Salmeterol or Formoterol +Tiotropium§Tiotropium§
Salmeterol or Formoterol +Salmeterol or Formoterol +Tiotropium§Tiotropium§
*Tiotropium +*Tiotropium +salmeterol or formoterol§salmeterol or formoterol§
*Tiotropium +*Tiotropium +salmeterol or formoterol§salmeterol or formoterol§
IVIVIVIV
*Tiotropium + salmeterol or formoterol *Tiotropium + salmeterol or formoterol + inhaled corticosteroid+ inhaled corticosteroid§§
*Tiotropium + salmeterol or formoterol *Tiotropium + salmeterol or formoterol + inhaled corticosteroid+ inhaled corticosteroid§§
Clinical Algorithm for the Treatment of COPDClinical Algorithm for the Treatment of COPDNonpharmacologic Nonpharmacologic
TherapyTherapy
Smoking cessationSmoking cessationAvoidance of exposureAvoidance of exposure
Smoking cessationSmoking cessationAvoidance of exposureAvoidance of exposure
VaccinationVaccination(influenza, pneumococcal)(influenza, pneumococcal)
VaccinationVaccination(influenza, pneumococcal)(influenza, pneumococcal)
Pulmonary rehabilitationPulmonary rehabilitation(Exercise prescription)(Exercise prescription)
Pulmonary rehabilitationPulmonary rehabilitation(Exercise prescription)(Exercise prescription)
Supplemental oxygenSupplemental oxygenLung volume reduction surgeryLung volume reduction surgery
Lung transplantationLung transplantation
Supplemental oxygenSupplemental oxygenLung volume reduction surgeryLung volume reduction surgery
Lung transplantationLung transplantation
*Short-acting bronchodilator as needed*Short-acting bronchodilator as needed(for example, ipratropium, salbutamol, or combination)(for example, ipratropium, salbutamol, or combination)
*Short-acting bronchodilator as needed*Short-acting bronchodilator as needed(for example, ipratropium, salbutamol, or combination)(for example, ipratropium, salbutamol, or combination)
GOLD StageGOLD Stage(approximate)(approximate)
ClinicalClinicalstagestage
At riskAt risk
IntermittentIntermittentsymptomssymptoms
PersistentPersistentsymptomssymptoms‡‡
FrequentFrequentexacerbationsexacerbations¶¶
Respiratory failureRespiratory failure
††
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. Decreased vital capacity
2. Decreased total lung capacity
3. Decreased residual volume
4. Increase in mid flows (FEF 25-75)
5. Decrease in DLCO
Which is the earliest PFT abnormality seen in interstitial lung disease?
1. Decreased vital capacity
2. Decreased total lung capacity
3. Decreased residual volume
4. Increase in mid flows (FEF 25-75)
5. 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 thumbDiagnosis Typical distribution Typical radiographic features
IPF (UIP) Peripheral & subpleural
Basilar
Reticular, honeycombingTraction bronchiectasis and bronchiolectasisArchitectural distortion, modest ground glass
NSIP Peripheral & subpleural
Basilar
Ground glass opacities predominentReticular opacities present
COP Subpleural and peribronchial Patchy bilateral consolidation
AIP Diffuse Consolidation and groundTraction bronchiectasis occurs later
DIP Lower lung zone
Peripheral predominance (mostly)
Ground glassReticular lines
RBILD Diffuse and can be upper Bronchial wall thickeningCentrilobular nodulesPatchy ground glass
LIP Diffuse Centrilobular 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 Tends to be patchy Subpleural or peribronchial distribution in up to 50% cases
~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)
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. Simple
2. Chronic
3. 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. History of asbestos exposure
2. Dyspnea
3. Basilar crackles in two or more locations
4. Reduced lung volumes
5. 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 diseaseUp 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:
Parapneumonic #1, malignancy, tuberculosis, BAPE, drugs (dantrolene, bromocriptine,
nitrofurantoin), parasites, Churg-Strauss Lymphocytes > 50%
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:
the lower the glucose, the more complicated the 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: 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 effusionsACCP 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:
Glucose > 40 pH > 7.2 LDH < 3x ULN
Treatment: antibiotics alone Class III: Borderline complicated
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 Obesity Facial soft tissue abnormalities Smoking! Nasal congestion DM
Mild AHI 5-15 Sedentary daytime sleepiness Sats > 90% more than 95% of time during sleep
Moderate: 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
Awake alveolar hypoventilation (pCO2 > 45) Obesity (BMI > 35) No other cause of hypoventilation
Usually seen with OSA Cor pulmonale
Outcomes: High mortality
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