pulmonary board review

Pulmonary Board Review

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

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 >

Lung volumes

Lung Volumes

nl COPD rest n-m obese

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

Alternative

Cromolyn

Step 2

Low dose ICS + LABA

Medium dose ICS

Medium dose ICS + LABA

Step 3 or 4

High dose ICS + LABA

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 <

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.

Disability

Age (years)5050 7575252500

Symptoms

100100

Healthy

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

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

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

IIIIIIIIIIII

Salmeterol or Formoterol +Salmeterol or Formoterol +Tiotropium§Tiotropium§

*Tiotropium +*Tiotropium +salmeterol or formoterol§salmeterol or formoterol§

IVIVIVIV

*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

VaccinationVaccination(influenza, pneumococcal)(influenza, pneumococcal)

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)

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

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.

Example of disease progression over time

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

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……..

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

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

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

Whew!Thanks for your attention

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pulmonary hypertension “out of proportion” in patients...

ccrn review pulmonary - adult critical care nursing ... ·...

radiographic analysis of pulmonary vascular distribution: a...

pulmonary circulation- this is a review!!!! ______________...

basic pulmonary physiology - m5 board review

unsom ite review: pulmonary