COPD in 2009

1. COPD in 2009 Perspective of Respiratory Physicians Ramesh Kaul, MD M. Surgery FCCP

2. Speaker disclosure • Presently Speaker for Astra Zeneca( Symbicort) • Previous speaker for GlaxoSmithKline (Advair) • Previous speaker for Boeringer Inghelheim (Spiriva , Atrovent) No funding was received from any Organization for this lecture at 36th Annual Western PSRC Seminar in Respiratory Care and Sleep Medicine.  Information presented mostly from reading Chest, GOLD and AJRCCM

3. WHY A NEW NAME COPD • Classical picture is no more seen of Pink Puffer of Emphysema • Blue Bloater Of Chronic Bronchitis • Early awareness by Providers of care • Early Intervention • Smoking Cessation • Avoidance of Precipitating factors

4. Epidemiology of COPD • COPD is the 4th leading cause of death, and the 2nd leading cause of disability in the U.S. And yet, COPD is under-diagnosed and under-treated: • About 24 million U.S. adults have evidence of impaired lung function • 12 million people have been diagnosed with COPD • 5.8 million COPD patients are untreated • The COPD death rate among women is increasing REFERENCES GOLD 2008 and American Thoracic Society

5. Socioeconomic factors in COPD • Poverty • Congested Living space • Lack of Education • Use of Biomass fuels, wood stoves • Inner City population has more prevalence • Stress of environment • Lack of funds for treatment in exacerbations • Malnourishment

6. Pollution in COPD • Second hand tobacco smoke • Wood, leaves and coal burning • Plastic and paper burning • Welding • Spraying of crops • Unclean air ducts with dust • Farming with exposure to animal excreta • Exposure to moldy hay, and gases in silos. • Spray painting • Fireworks fumes. • Animal fur, cat and dog dander • Gas fumes, diesel fumes and the list goes on and on

7. Definition of COPD • COPD: Definition World Health Organization • Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by chronic obstruction of lung airflow that interferes with normal breathing and is not fully reversible. The more familiar terms 'chronic bronchitis' and 'emphysema' are no longer used, but are now included within the COPD diagnosis. COPD is not simply a "smoker's cough" but an under-diagnosed, life-threatening lung disease. • A COPD diagnosis is confirmed by a simple test called Spirometry, which measures how deeply a person can breathe and how fast air can move into and out of the lungs. Such a diagnosis should be considered in any patient who has symptoms of cough, sputum production, or dyspnea (difficult or labored breathing), and/or a history of exposure to risk factors for the disease. Where Spirometry is unavailable, the diagnosis of COPD should be made using all available tools. Clinical symptoms and signs, such as abnormal shortness of breath and increased forced expiratory time, can be used to help with the diagnosis. A low peak flow is consistent with COPD, but may not be specific to COPD because it can be caused by other lung diseases and by poor performance during testing. Chronic cough and sputum production often precede the development of airflow limitation by many years, although not all individuals with cough and sputum production go on to develop COPD.

8. Classification of Severity of COPD • Stage Characteristics • Stage 0: At Risk • normal Spirometry • chronic symptoms (cough, sputum production) • Stage I: Mild COPD • FEV1/FVC < 70%• FEV1 ≥ 80% predicted • with or without chronic symptoms (cough, sputum production) • Stage II: Moderate COPD • FEV1/FVC < 70% • 50% ≤ FEV1 < 80% predicted • with or without chronic symptoms (cough, sputum production) • Stage III: Severe COPD • FEV1/FVC < 70% • 30% ≤ FEV1 < 50% predicted • with or without chronic symptoms(cough, sputum production) • Stage IV: Very Severe COPD • FEV1/FVC < 70%• FEV1 ≤ 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure • Ref GOLD Newletter AUG 8/29/03

9. Differential Diagnosis of COPD • COPD: older patient, smoker, irreversible , Dyspnea and cough. CD8 T Lymphocytes Macrophages and Neutrophils in sputum • Asthma:younger patients , allergic, reversible, IGE and RAST positive CD4 T Lymphocytes Eosinophils in airways and sputum. • Congestive Heart Failure: Dyspnea, Rales , large heart, ECHO and Chest XRAY diagnostic • Pneumoconiosis: Occupational diseases, restriction and diffusion defect • Obliterative Bronchiolitis:young, fumes, Rheumatoid Arthritis, Expiration CT shows hypo dense areas. • Bronciectasis: sputum in excess, crackles and clubbing, HRCT • Diffuse Panbronchiolitis: Chronic sinusitis, non smoker HRCT Chest X ray nodular. • Pulmonary Fibrosis:HRCT diagnostic, Restrictive lungs, Honey combing severe diffusion defect, Increased FEV1/FEV • Tuberculosis: Dyspnea, any age, toxic symptoms, wasted, X Ray and Sputum are positive

10. Medical HX in COPD • Shortness of breath • Cough • Production of sputum, quantity, color, blood in sputum • Fever • Loss of weight • Smoking • Inhalation injury • Occupational exposure • Mood • Appetite • Chest discomfort • Exercise tolerance • Sleep disorder • Palpitations • Pollution • Socioeconomic status

11. Exam in COPD • Skin color, dryness, ecchymosed, increased creases. • Nail beds, clubbing, • Nasal flaring, septum , turbinate, uvula, oral space • Accessory muscle use, AP diameter • Thoracic-abdominal breathing assessment • Auscultation wheeze, rhonchi, Rales, air movement and trapping • palpation and percussion • Tracheal position • Heart sounds with augmented right heart sounds • Jugular veins and distension • Orthopnea • Walk test • Evaluate Tremors , muscle strength

12. Occupational Exposure in COPD • Spray painting • Arc welding • Farming • Miners • Vegetable spraying • Lawn mowing • Furnaces • Barbers/Beauticians • Hospitals

13. Genetics in COPD • Alpha -1 Anti Trypsin deficiency ZZ type require treatment, testing available without charge by squeezing a drop of blood on a paper and mailing to lab. Genetic counseling done • Our office we test every new patient and at least once in established patient We follow levels in below normal patients Once established significantly deficient Home IV therapy is given weekly. Alpha-1 Antitrypsin Deficiency (A1AD) is a hereditary disorder characterized by low levels of a protein called alpha-1 antitrypsin (A1AT) which is found in the blood. This deficiency may predispose an individual to several illnesses but most commonly appears as emphysema, less commonly as liver disease, or more rarely, as a skin condition called panniculitis. A deficiency of A1AT allows substances that break down protein (proteolytic enzymes) to attack various tissues of the body. This results in destructive changes in the lungs (emphysema) and may also affect the liver and skin. Alpha-1 Antitrypsin is ordinarily released by specialized, granular white blood cells (neutrophils) in response to infection or inflammation. A deficiency of Alpha-1 Antitrypsin results in unbalanced (relatively unopposed) rapid breakdown of proteins (protease activity), especially in the supporting elastic structures of the lungs. This destruction over many years leads to emphysema and is accelerated by smoking and some occupational exposures.

14. Testing in COPD • PFT: Pulmonary function tests TLC, FEV1/FVC, Diffusion, MVV. • ABG: Arterial Blood Gas PO2 PCO2 PH • Exercise Test: Goodtest for overall pulmonary efficiency • ECHO: EKG, Right heart Catheterization • CT CHEST: lung and bronchial anatomy • Ventilation perfusion Scan: bulla, mismatch, vascular deficit • Hb and HCO3 in blood: Tests for severity and chronic state • Sputum: Tests for colonization in Bronchitis • MIP MEP: Muscular and Breathing power efficiency • Sleep study: Explains COPD exacerbations in sleep

15. Systemic Effects in COPD • Pulmonary hypertension • Cor Pulmonale • Osteoporosis • Depression • Normochromic normocytic anemia • Skeletal muscle wasting • Increased risk of Coronary artery Disease correlates with increasing CRP

16. PFT in COPD • Spirometry reduced FEV1, FEV1/FVC ratio, Reduced FEF25-75 Helps in classification of severity and disability • Pre and Post B2-Agonist therapy shows reversibility • Lung Volumes hyperinflation, increased air trapping, Reduced Vital capacity, Increased RV • MVV is reduced due to flow obstruction and muscle weakness • DLCO is reduced more frequently in loss of alveolar unit, atelectasis, mucus plugs, air trapping. Less reduction of DLCO in bronchitis

17. Radiology in COPD • HRCTHigh resolution chest CT shows anatomy of airway, lung parenchyma, bulla, atelectasis. • Chest X Rays Pneumothorax, radiological changes of emphysema, hyperinflation, rarification of parenchyma, cardiac silhouette • Ventilation and perfusion scans • Fluoroscopy for procedures, developing countries use as a diagnostic tool in occupational surveillance

18. Smoking in COPD • Smoking is the main culprit in COPD it has noxious gases, heat, CO, SO2 , tar. • Cascade of inflammation CD8, Interleukins, Neutrophils and Macrophages Destructive enzymes released by inflammatory cells • Cessation the first line in COPD management. • Welbutrin works better with women • Nicotine patch, gum, inhaler • Chantix • Hypnosis

19. Counseling in COPD • Quit smoking • Vaccination influenza • Pneumococcal vaccine not as important • Use of inhalers • Mouth rinsing after inhaler use • Over use of certain inhalers • While with Pets and children • Washing hands

20. Medications in COPD • Short acting Anticholinergics • Long acting Anticholinergic • Short acting B2-agonists • Long acting B2-agonists • Inhaled glucocorticosteroids • Systemic glucocorticosteroids • Combined long acting B2-agonists plus glucocorticosteroids in one inhaler • Combined short acting B2-agonists plus Anticholinergic in one inhaler • Methylxanthines • Systemic glucocorticosteroids

21. Beta2-Agonists in COPD • Short acting B2-Agonists: Salbutamol ( albuterol )(4-6hrs) , fenoterol (4-6hrs), levalbuterol (6-8hrs), terbutaline94-6hrs) • Excellent bronchodilator and quick effect. Therapy for All stages, mostly rescue and as needed dosing every 4 to 6 hours for shortness of breath. • Relax airway smooth muscles by stimulation of B2- adrenergic receptors which increases cyclic AMP and produce antagonist effect to bronchoconstriction. • Excess doses cause tremors, anxiety, tachycardia, arrhythmias, hypokalemia • Long acting B2-Agonists (LABA ) salmetrol(12+ hrs), formoterol(12+hrs) ,Arformoterol(12+hrs) Therapy for Stage 2 ,3 and stages 4 of COPD.

22. Anticholinergics in COPD • Short acting Anticholinergics started with historical Atropine atomizers and smoking atropa plant • Research brought quaternary compound of atropine called iprotropium bromide(6-8 hrs) now nebulised and inhaler. and oxitropium bromide (7-9hrs) in solution and inhaler. • Long acting Tiotropium inhaled(24+hrs) aerolised powder. • ipratropium bromide/salbutamol (Combivent) • fenoterol/ipratropium bromide (Berodual) • Mechanism: Blockage of acetycholine on M3 receptors. • It is believed COPD the cholinergic tone is very high and mediates in bronchoconstriction Side Effects Relatively safe Dryness of mouth, Blurring of vision, Prostatic symptoms reported,

23. Methylxanthines and steroids in COPD • Theophyllin PO or IV and Aminophyllin IV non specific inhibitors of all subsets of phospho-diesterase enzyme. Cytochrome P450 metabolism drug interactions are many. • Theophyllin side effects are large, as drugs of this class have low therapeutic index. • Methylxanthines may trigger atrial fibrillation, ventricular arrhythmias, Insomnia, anxiety, seizures • Methyl prednisone IV or PO Prednisone or Methyl prednisolone for short term benefit in exacerbation • Steroid Side effects are steroid psychosis, thrush, hyperglycemia, elevated blood pressures, gastritis • Chronic treatment with systemic corticosteroids should be avoided as benefit-risk ratio is poor • Steroid side effects are osteoporosis, fractures, steroid myopathy, weight gain, hirsutism , steroid acne, cushingoid moon facies

24. Inhaled Steroids in COPD • Front line therapy for COPD stages 3 and 4 • Budenoside Nebulizer • Inhaled fluticasone • Inhaled triamcinolone • Inhaled beclomethasone • Inhaled budenoside • LABA and budenoside mixed in inhaler

25. Other Treatments in COPD • Oxygen Therapy Benefit For all stage 4 COPD • Mucolytics Benefit some with thick mucus • Antioxidants No proven benefit N-Acetyl Cystiene • Anabolic steroids no benefit • Immunoregulators : still in research these may help • Antitussives no benefit for regular use • Narcotics no benefit except palliative care and symptoms of dyspnea relief in some. • Nedocromil not tested adequately • Leukotriene modifiers not tested adequately • Herbal treatments no benefit • Acupuncture or hypnosis no benefit on disease may help in smoking cessation in rare subjects.

26. Surgery in COPD • Bullectomy makes space for normal collapsed segments of lung, increases breathing space • Lung Volume reduction surgery improves compliance and diaphragm function. • Lung transplant for end stage COPD. • Enroll patients with End stage COPD in transplant programs ahead of time. • Pulmonary rehab prior to surgery • Chest tubes if spontaneous Pneumothorax

27. Bronchoscopy in COPD • Bronchial toilet • Removal of mucus plugs • Resistant Pneumonia may need cultures • Different approaches of bronchoscopic lung volume reduction have been described • radiofrequency fenestration of the bronchial wall with stent placement • umbrella blockers • injection of fibrin glue. • Endo-bronchial valve (EBV)

28. Mechanical Ventilation • BIPAP in COPD • Non-Invasive MechanicalVentilation for Acute COPD • Transtracheal Augmented Ventilation (TTAV) is the only technology that augments ventilation during SBT in weaning trials in tracheotomised COPD. • Mechanical Ventilation in AECOPD

29. Pulmonary Rehab in COPD • Effective tool in improving ADLs (activities of daily living ) • Builds Self esteem and decreases social stigma in group therapy. • Cost can be from thousands of dollars to $50 per month at subsidized institutions. • No improvement in lung function, helps only in performance and quality of life. • Improves adherence to use of Inhalers and lesser exacerbations due to compliance. • Pulmonary rehab RT and RN help in early evaluation and prevention of exacerbations • Better use of various gadgets like spacers, Flutter valve, BIPAP, CPAP oxygen in judicious fashion

30. Acapella and Flutter valve • Flutter valve mucus clearing device • Mechanism of action probably by counteracting auto PEEP reducing hyperinflation and vibrations causing mobilization of mucus Acapella (Oscillating PEP) available in market and help clear mucus.

31. Diet in COPD • Good nourishment is the key in management of disease state • Anorexic and bulimic individuals may develop emphysema without smoking and without inhalation injury. • Postmortem studies of patients who died in the Warsaw Ghetto during World War II suggested that death from starvation was associated with pulmonary emphysema • The CT measurements of lung density, emphysema, and surface area-to-volume ratio were obtained using the X ray attenuation values found changes of early emphysema.( 21 subjects vs. 16 controls) Harvey O. Coxson et al American Journal of Respiratory and Critical Care Medicine Vol 170. pp. 748-752, (2004) • Nutritional Support for Individuals With COPD A Meta-analysis • Conclusion: Nutritional support had no effect on improving anthropometric measures, lung function, or functional exercise capacity among patients with stable COPD Ivone M. Ferreira, MD, PhD Et al10.1378/chest.117.3.672 CHEST March 2000 vol. 117 no. 3 672-678

32. Infections in COPD • Viral Influenza, Coxsackie, RSV, Rhino, Picorna, Adenovirus • Bacterial Stenotrophomonas maltophilia. Burkholderia cepacia. Streptococcus pneumoniae, Haemophilus influenzae. Haemophilus parainfluenzae,Methicillin-Resistant Staphylococcus aureus (MRSA), E. coli and Klebsiella pneumoniae,Citrobacter, Serratia, and Pseudomonas. • Fungal Candida oropharynx trachea, Aspergillum colonized and Aspergilomas in cavities • Mycobacterium M. avium and rarely M. szulgai • Atypical InfectionsChlamydia pneumoniae, Mycoplasma pneumoniae and Legionella pneumophila • Mixed Infections of all above possible.

33. Long term Antibiotics in COPD • Long Term Erythromycin Therapy is Associated with Decreased COPD Exacerbations Terence AR Seemungal et alAm. J. Respir. Crit. Care Med., Volume 178, Number 11, December 2008, 1139-1147 • Investigational A lot of claims that macrolides like drugs may decrease exacerbations government trials are enrolling patients. • Serum levels of procalcitonin increase rapidly in the presence of infection Antibiotic Treatment of Exacerbations of COPD* A Randomized, Controlled Trial Comparing Procalcitonin-Guidance With Standard Therapy Daiana Stolz, MD et al 10.1378/chest.06-1500 CHEST January 2007 vol. 131 no. 1 9-19

34. Risk Assessment in COPD • Preoperative risk assessment is always done for surgery • Thoracic, abdominal, surgery effects the diaphragm thoracic cage effects abdominal breathing • Neurosurgery CNS drive is suppressed and more central apneas, less rate and volume, decreases sensing of CO2 and oxygen • Orthopedic effect and clearance of anesthetics, pain medications suppress respiration drive and depth. • Pre and postoperative CXR,ABG, PFT, Exercise oximetry, Stair stepper, use of Incentives, life style modification

35. Take home messagesCOPD In 2009 • Smoking and inhalant injury needs to be eliminated from our environment. • Early intervention, counseling , good diet, should be frontline. • Vaccinations, inhalers and Rehab are main management. • Anticholinergics and Long acting are beneficial in Stage one to Four. • Inhaled steroids are beneficial for stages three and Four • LAB2A are beneficial for stages two onwards. • Long term oxygen therapy and sleep studies help in maintenance of advanced disease • Surgical options for End Stage COPD with LVRS and transplant are available. • Genetic research to find the sensitive population and prevention of COPD • THANK YOU • These slides are available at www.thorax.us at specials