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Pulmonary Board Review

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1 Pulmonary Board Review

2 What we’re going to speed through
Evaluation of symptoms: cough and dyspnea PFTs Asthma COPD Interstitial lung diseases Pneumoconioses Pleural disease Sleep

3 Chronic cough Definition: cough lasting more than: 3 weeks 1 month
3 months 1 year

4 Chronic cough Definition: cough lasting more than: 3 weeks 1 month
3 months 1 year

5 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? Congestive Heart Failure Post-nasal drip syndrome (PNDS) Asthma Gastroesophageal reflux disease (GERD) Chronic Bronchitis

6 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? Congestive Heart Failure Post-nasal drip syndrome (PNDS) Asthma Gastroesophageal reflux disease (GERD) Chronic Bronchitis

7 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 PNDS: sinusitis, allergic rhinitis, perennial nonallergic rhinitis, postinefectious rhinitis, vasomotor rhinitis, environmental irritants Rx: first generation antihistamine with decongestant +/- intranasal coritcosteroids, avoidance of allergens, cromolyn sodium Cough variant asthma: up to 57% with asthma; often with normal PFTs thus methacholine challenge. Treatment: inhaled corticosteroid for at least 6-8 weeks to see benefit GERD

8 Respiratory symptoms: dyspnea
The 4 most common etiologies of chronic dyspnea ( dyspnea lasting > 1 month) are: Cardiomyopathy Deconditioning Interstitial lung disease COPD Asthma

9 Respiratory symptoms: dyspnea
The 4 most common etiologies of chronic dyspnea ( dyspnea lasting > 1 month) are: Cardiomyopathy Deconditioning Interstitial lung disease COPD Asthmma These four etiologies account for 2/3 of all cases of chronic dyspnea

10 Dyspnea - Assessment Pratter MR, et al. Cause and evaluation of chronic dyspnea in a pulmonary disease clinic. Arch of Intern Med. 1989;149: Asthma (29%) COPD (14%) ILD (14%) Cardiomyopathy (11%) Upper airway (8%) Psychogenic (5%) Deconditioning (5%) GE reflux (4%) Extrapulmonary (4%)

11 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

12 PFTs

13 Inhalation to Total lung capacity Beginning of Forced Expiratory maneuver Normal tidal breathing Volume of air Exhaled 1 sec Into forced expiration Exhalation to Residual volume

14 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 < % 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

15 Lung volumes

16 Lung Volumes

17 Which of the following can cause a reduced vital capacity?
Asthma Kyphoscoliosis Pulmonary fibrosis Obesity Myasthenia gravis

18 Which of the following can caused a reduced vital capacity?
Asthma Kyphoscoliosis Pulmonary fibrosis Obesity Myasthenia gravis


20 DLCO The blood gas barrier
Gas exchange surface sq meters 0.3 microns Each alveolus is enveloped by pulmonary capillaries There are about 500 to 1000 capillaries per alveolus!

21 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

22 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

23 PFTs: flow volume loops
Useful in looking for central airway obstruction

24 Flow volume volumes

25 Obstructive airway diseases
4-8 questions

26 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

27 Asthma categories of severity 2007 NAEPP report
Intermittent Mild persistent Moderate persistent Severe persistent Treatment recommendations based upon severity

28 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 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 28

29 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? Intermittent Mild persistent Moderate persistent Severe persistent

30 Classification of severity based upon lowest level treatment required to maintain control
Classification of asthma severity Intermittent Persistent Mild Moderate Severe PRN short-acting bronchodilator Step 1 Low dose ICS OR Alternative Cromolyn LTRA Step 2 Low dose ICS + LABA Medium dose ICS Medium dose ICS + LABA Step 3 or 4 High dose ICS + LABA AND Omalizumab, oral corticosteroid Step 5 30

31 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

32 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

33 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

34 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

35 Asthma syndromes Cough variant asthma
Aspirin-induced asthma or triad asthma Exercise induced asthma Occupational asthma Allergic bronchopulmonary aspergillosis

36 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)

37 OA without a latency period:
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

38 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.

39 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

40 Exercise Performance Over Time
100 Healthy 80 COPD Symptoms 60 Rehabilitation at 45 (mild COPD) FEV1 (%) Relative to Age 25 Disability 40 Fletcher and Peto found that over a lifetime, FEV1 falls gradually. However, clinically significant airflow obstruction may never develop in many smokers. In those susceptible to COPD, smoking can cause permanent obstructive changes to air passages. The researchers found that if a susceptible smoker quits smoking, rates of FEV1 loss will revert to normal, but lung function is reduced. It is possible to prevent severe or fatal COPD by screening lung function in middle-aged smokers, who could be urged to stop smoking. Main point: Decline in FEV1 is accelerated in COPD. Quitting smoking has a profound effect on the rate of decline of FEV1. 20 Death Rehabilitation at 65 (severe COPD) 25 50 75 Age (years) Adapted from Fletcher et al. BMJ. 1977;1: Fletcher C, Peto R. The natural history of chronic airflow obstruction. BMJ. 1977;1:

41 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 FEV percent predicted III: Severe COPD FEV percent predicted IV: Very Severe COPD FEV1 <30 percent predicted or FEV1 <50 percent predicted plus respiratory failure

42 COPD Treatment: Smoking cessation Oxygen therapy Medical therapy
Pulmonary rehabilitation LVRS Transplantation

43 Clinical Algorithm for the Treatment of COPD
Clinical stage GOLD Stage (approximate) Nonpharmacologic Therapy Inhaled Therapy Smoking cessation Avoidance of exposure At risk Intermittent symptoms I *Short-acting bronchodilator as needed (for example, ipratropium, salbutamol, or combination) Vaccination (influenza, pneumococcal) Persistent symptoms‡ II *Tiotropium + albuterol Salmeterol or formoterol + ipratropium, salbutamol, or combination Pulmonary rehabilitation (Exercise prescription) *Tiotropium + salmeterol or formoterol§ Salmeterol or Formoterol + Tiotropium§ Frequent exacerbations¶ III *Tiotropium + salmeterol or formoterol + inhaled corticosteroid§ Respiratory failure IV 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. Cooper et al. BMJ. 2005;330; (B) Tashkin DP, Cooper CB. The role of long-acting bronchodilators in the management of stable COPD. Chest. 2004;125: Global Initiative for Chronic Obstructive Lung Disease: Executive Summary Updated Global Strategies for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. Available at: Accessed February 21, 2005.

44 Restrictive lung disease/ Interstitial lung disease/DPLD
Up to 5 questions

45 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

46 Classification ATS/ERS International Multidisciplinary Consensus Classification of IIP. AJRCCM 2002

47 Normal CXR Patient 1 CXR

48 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

49 ATS/ERS International Multidisciplinary Consensus Classification of IIP. AJRCCM 2002

50 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

51 Which is the earliest PFT abnormality seen in interstitial lung disease?
Decreased vital capacity Decreased total lung capacity Decreased residual volume Increase in mid flows (FEF 25-75) Decrease in DLCO

52 Which is the earliest PFT abnormality seen in interstitial lung disease?
Decreased vital capacity Decreased total lung capacity Decreased residual volume Increase in mid flows (FEF 25-75) Decrease in DLCO

53 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

54 DPLD radiologgy Chest Xray can be normal in High resolution chest CT
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


56 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

57 Figure 3-24




61 IIPs and HRCT rules of thumb
Diagnosis Typical distribution Typical radiographic features IPF (UIP) Peripheral & subpleural Basilar Reticular, honeycombing Traction bronchiectasis and bronchiolectasis Architectural distortion, modest ground glass NSIP Ground glass opacities predominent Reticular opacities present COP Subpleural and peribronchial Patchy bilateral consolidation AIP Diffuse Consolidation and ground Traction bronchiectasis occurs later DIP Lower lung zone Peripheral predominance (mostly) Ground glass Reticular lines RBILD Diffuse and can be upper Bronchial wall thickening Centrilobular nodules Patchy ground glass LIP Centrilobular nodules, ground glass, septal and bronchovascular thickening. Thin-walled cysts

62 Diagnosis Bronchoscopy BAL limited utility Biopsy 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

63 IPF or Usual Interstitial Pneumonitis
> 60% of all cases of IPF age > 50 with 2/3 > 60 M>F prevalence 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.

64 ATS/ERS International Multidisciplinary Consensus Classification of IIP. AJRCCM 2002

65 ATS/ERS International Multidisciplinary Consensus Classification of IIP. AJRCCM 2002

66 Example of disease progression over time
ATS/ERS International Multidisciplinary Consensus Classification of IIP. AJRCCM 2002

67 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


69 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

70 NSIP CT scan ATS/ERS International Multidisciplinary Consensus Classification of IIP. AJRCCM 2002

71 NSIP Path: temporally uniform with interstital inflammation
Rad: ground glass with areas of fibrosis Often also seen with CTD such as scleroderma

72 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

73 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


75 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……..


77 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

78 DIP/RBILD “smoking related ILD”
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%

79 DIP/RBILD Path: Rad: Pigmented macrophages
Peribronchiolar inflammation Rad: Patchy ground glass Intralobular septal thickening Mosaic pattern

80 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”

81 Subacute HP Mostly mid to upper lung zones

82 Chronic HP

83 HP: Treatment and prognosis
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

84 Y. Rosen, M.D. Atlas of Granulomatous Diseases
Non-granulomatous interstitial pneumonitis B. Poorly circumscribed collection of macrophages and multinucleate giant cells. Evolving granuloma. C. Later phase of granuloma formation. Lesion becoming more compact and circumscribed D. Fully mature non-necrotizing granuloma. Y. Rosen, M.D. Atlas of Granulomatous Diseases

85 Sarcoidosis: Four stages
Lungs are affected in more than 90% of patients with dyspnea, np cough, and CP occurring in 1/3 to ½ of pts Radiographic stages Stage 4- fibrosis with hilar retraction, honeycomb changs, and large bullae and cysts Surprsingly, on exam lungs are usually clear

86 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

87 Sarcoidosis: Stage II Lymph nodes enlarged Inflammation in the lung
Lung function is impaired 40-70% pts resolve spontaneously

88 Sarcoidosis: Stage III
Lymph nodes are not enlarged Only 10-20% resolve spontaneously

89 Sarcoidosis 90% with lung involvement 75% liver 20% skin 20% eyes
25% spleen 10% MSK 5% heart 5%

90 Occupational lung diseases
Up to 4 questions

91 Occupational and environmental lung diseases
Occupational asthma Hypersensitivity pneumonitis Pneumoconioses

92 Pneumoconioses Silicosis CWP Asbestosis Talcosis Berylliosis

93 Silicosis: Exposure Mining Quarrying Enameling Tunneling
Stone cutters Sandblasting Glass manufacturing Foundry work Enameling Quartz crystal manufacturing Rubber industry

94 Silicosis: clinical presentations
Chronic silicosis Accelerated silicosis Progressive massive fibrosis Acute silicosis

95 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

96 Chronic silicosis: CXR findings
Simple silicosis is the earliest finding of chronic silicosis Nodules usually 1-3 mm

97 Chronic silicosis: CXR findings
As disease progresses, nodules increase in number and coalesce to form larger lesions

98 Chronic silicosis: CXR findings
Eggshell calcification

99 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

100 PMF: CXR findings The nodules coalesce into conglomerate masses
Calcified lymph nodes “eggshell calcification”

101 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: Simple Chronic PMF

102 Asbestos-related lung diseases
Pleural plaques Pleural fibrosis Benign asbestos related pleural effusion Asbestosis Mesothelioma

103 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% Anterolateral or posterolat surface of parietal pleua Gray white in color Central tendon when diaphgram involved

104 Asbestos: Pleural plaques


106 Pleural fibrosis Very rare, progressive process characterized by diffuse pleural fibrosis Can be exacerbated with concurrent administration of medications such as bromocriptine

107 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

108 Rounded atelectasis

109 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 years after exposure

110 Asbestosis Presents > 30 years after initial exposure
Requires long term, heavy exposure Criteria for diagnosis: History of asbestos exposure Dyspnea Basilar crackles in two or more locations Reduced lung volumes Radiographic abnormalities

111 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

112 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.

113 Pleural disease Up to 4 questions

114 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

115 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

116 Pleural fluid analysis: Other pleural chemistries to help differentiate exudate from transudate
Cholesterol Absolute pleural fluid cholesterol > mg/dL Pleural fluid albumin gradient < 1.2 g/dL Bilirubin: pleural fluid bilirubin/serum bilirubin > 0.6 Light’s criteria superior to any of the above in identifying exduates. Howver, less accurate in identifying transudates, Albumin graidnet can be utilized.

117 Pleural fluid analysis: cell count
Red blood cells Blood-tinged fluid typically 5000 to RBC/mm3 Grossly bloody: RBC mm3 Trauma Malignancy Pulmonary embolism Infection Hemothorax: pleural fluid hct to blood hct > 50%

118 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

119 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

120 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%

121 Pleural fluid analysis: pH
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

122 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

123 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: Glucose > 40 pH > 7.2 LDH < 3x ULN Treatment: antibiotics alone Class III: Borderline complicated pH 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

124 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

125 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)

126 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

127 Thanks for your attention
Whew! Thanks for your attention

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