Pulmonary Board Review

Pulmonary Board Review
2009

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

Respiratory symptoms: cough
Chronic cough = duration > 3 weeks 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

Respiratory symptoms: dyspnea
Chronic dyspnea: lasting > 1 month 2/3 of patients with one of the following COPD Asthma ILD Cardiomyopathy Others: neuromuscular disease, hyperventilation syndrome, GERD, pulmonary vascular disease Work-up: History, PFTs, chest Xray Cardiopulmonary exercise testing

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

Lung volumes

Lung Volumes

PFTs: DLCO Decreased in:
Diseases that obliterate the alveolar-capillary interface: Emphysema Fibrotic lung disease Pulmonary vascular diseases 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

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

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 FEV % 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 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 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

COPD 6th leading cause of death worldwide Underdiagnosed
GOLD: stages of severity Based of spirometry Stage 0: normal spirometry but symptoms present Stage I: Mild ratio < 70% but FEV1 > 80% Stage II: Moderate IIa FEV % IIb FEV % Stage III: Severe

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:

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

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

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.

Interstitial lung diseases or Diffuse parenchymal lung disease
DPLD of known cause: Drugs Connective tissue disease Occupational lung disease Granulomatous disease Sarcoidosis Hypersensitivity pneumonitis Idiopathic interstitial pneumonia (IIP) Idiopathic pulmonary fibrosis (i.e., usual interstitial pneumonia) Others Non-specific interstitial pneumonia Desquamative interstitial pneumonia Respiratory bronchiolitis interstitial lung disease Cryptogenic organizing pneumonia Acute interstitial pneumonia (Hamman Rich syndrome) Lymphocytic interstitial pneumonia Misc Lymphangioleiomyomatosis Histiocyotsis X Pulmonary alveolar proteinosis

DPLD 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

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

DPLD General approach: Timeline Smoking history Occupational history
Environmental and toxin exposures Drug history Extrapulmonary symptoms and manifestations Sarcoidosis CTD Testing PFTs HRCT CTD serologies Assess for exertional hypoxemia

Diagnosis PFTs Bronchoscopy BAL limited utility Biopsy limited utility
Looks 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 Older age, M > F Histopath: UIP
Fibroblastic foci Temporally heterogeneous Minimal inflammation Lots of collagen deposition Predominantly subpleural and basilar Similar findings in abestosis, rheumatoid lung disease Progressive disease with a median survival 2-3 years from diagnosis

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

DIP/RBILD Path: Rad: 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
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
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

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

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%

Pneumoconioses Silicosis CWP Asbestosis Talcosis Berylliosis

Silicosis: Exposure Mining Quarrying Enameling 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

As disease progresses, nodules increase in number and coalesce to form larger lesions

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: Simple Chronic PMF

Asbestos-related lung diseases
Pleural plaques 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% Anterolateral or posterolat surface of parietal pleua Gray white in color Central tendon when diaphgram involved

Asbestos: Pleural plaques

Benign asbestos pleural effusion
Most common pleuropulmonary 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 years after exposure

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

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.

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 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 > 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.

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 or s/p CABG Mesothelial cells: Uncommon in tuberculous effusions. Major exception: AIDS

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%

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: LDH
Serial LDHs can be helpful: Increasing levels: worsening process Decreasing levels: resolving process LDH isoenzymes: Mostly LDH-4 and LDH-5 If predominance LDH-1, the increase is due to blood

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 anaerobically in a heparinized syringe Lidocaine may falsely lower the pH

Pleural fluid analysis: other
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

Pleural fluid analysis: lipid studies
Triglycerides > 110 mg/dL  diagnostic of chylothorax Triglycerides mg/dL  equivocal Triglycerides < 50: not a chylothorax

Parapneumonic effusions and empyemas
Pleural fluid characteristics associated with need for pleural fluid drainage Pus in the pleural space Positive gram stain or culture Glucose < 40 pH < 7.0 LDH > 3 x the ULN Loculated pleural fluid

ACCP recommendations 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

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

Obesity hypoventilation
Treatment OSA present: Trial of CPAP is appropriate Transition to BiPap if volume cycled positive airway pressure if symptoms persist or persistent daytime hypercapnia Treatment of acute respiratory failure: BiPAP or VCPAP

Pulmonary embolism Mortality 30% without apporpriate treatment
Mortality decreases to 2-8% with appropriate diagnosis and treatement Increased risk of death RV dysfunction Elevated BNP Elevated troponin

Clinical Decision Rule*
Writing Group for the Christopher Study Investigators, JAMA 2006;295: Copyright restrictions may apply.

Treatment Anticoagulation IVC filter Thrombolysis

Mechanical ventilation
Complications of invasive mechanical ventilation Recognize PEEP related hypotension Appropriate ventilator management for ARDS

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