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COPD with acute exacerbation

COPD with acute exacerbation. What is COPD?. COPD is a chronic slowly progressive disorder characterized by airflow obstruction (FEV1 < 80% predicted and FEV1/FVC ratio < 70%) which does not change markedly over several months. It encompasses three clinical entities : EMPHYSEMA

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COPD with acute exacerbation

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  1. COPD with acute exacerbation

  2. What is COPD? • COPD is a chronic slowly progressive disorder characterized by airflow obstruction (FEV1 < 80% predicted and FEV1/FVC ratio < 70%) which does not change markedly over several months. • It encompasses three clinical entities : • EMPHYSEMA • CHRONIC BRONCHITIS • SMALL AIRWAYS DISEAES

  3. DEFINITIONS • CHRONIC BRONCHITIS : It is defined as cough with sputum on most days for at least three consecutive months for more than two successive years. • EMPHYSEMA : It is defined as permanent destructive enlargement of the air spaces distal to the terminal bronchioles. • SMALL AIRWAYS DISEASE : A condition in which small bronchioles are narrowed.

  4. RISK FACTORS • SMOKING: studies have shown accelerated decline in FEV1 in a dose response relationship to the intensity of cigarette smoking which is expressed as pack years. • AIR WAY RESPONSIVENESS: Increased air way responsiveness is a significant predictor of subsequent decline in pulmonary function. • RESPIRATORY INFECTIONS: Though respiratory infections are an important cause of exacerbation of COPD , their association to the development and progression of COPD remains to be proven.

  5. RISK FACTORS contd.. • OCCUPATIONAL EXPOSURE: Including coal mine , gold mining and cotton textile dust have been suggested as risk factors. • AMBIENT AIR POLLUTION: with high rates of COPD in non smoking women in developing countries indoor air pollution associated with cooking has been suggested as potential contributor. • ALPHA 1 ANTI TRYPSIN DEFICIENCY: Cigarette smokers with alpha 1 anti-trypsin deficiency are more likely to develop COPD at early ages.

  6. CLINICAL PRESENTATION • HISTORY: three most common symptoms of COPD are cough, sputum production and exertional dyspnea. • As disease progresses dyspnea occurs with mild activity and in severe cases at rest. • Hallmark of COPD is frequent exacerbation of illness. • Pneumonia , pulmonary HTN , cor pulmonale and chronic respiratory failure characterize the late stages of the disease.

  7. SIGNS OF COPD • Nicotine staining of finger nails. • Pursed lip breathing. • Characteristic tripod position. • Use of accessory muscles. • Barrel shaped chest. • Excavation of suprasternal and supraclavicular fossae during respiration. • Cyanosis. • Weight loss , bitemporal wasting. • Hoover’s sign : paradoxical inward movement of rib cage during inspiration.

  8. SIGNS OF COPD contd.. • Tracheal tug • Loss of cardiac dullness • Prolonged expiratory phase with wheezing • Signs of hypercapnia i.e bounding pulse, warm extremities and flapping tremors • Signs of cor pulmonale namely elevated JVP , right ventricular heave , loud P2 , S3 , hepatic congestion , ascities . Peripheral edema • Clubbing is not a sign of COPD ; CA lung is the most likely explanation for clubbing in COPD.

  9. INVESTIGATIONS • PFTs: Reduction in FEV1 and FEV1/FVC ratio. • ABGs: Indicated if • Hypoxemia or hypercapnia is suspected. • FEV1 is less than 40% of predicted. • Clinical signs of heart failure. • SPUTUM EXAMINATION for micro organisms in acute exacerbation • ECG may show sinus tachycardia , signs of RVH and Supraventricular arrythmias. • HAEMATOLOGY may show polycythemia.

  10. INVESTIGATIONS contd.. • CXR may show hyperinflation with flattening of diaphragm or peripheral arterial deficiency , parenchymal bullae and enlargement of central pulmonary arteries. • CT SCAN is the current definitive test for the establishing the presence or absence of emphysema. • ALPHA 1 ANTI TRYPSIN LEVEL in patients presenting with age < 50 yrs, strong family history , predominant basilar disease or with minimal smoking history. • ECHO for suspected pulmonary HTN,

  11. GOLD CRITERIA FOR COPD SEVERITY

  12. TREATMENT • STABLE PHASE COPD: • Smoking cessation is one of the two interventions that influence the natural history of patients with COPD. Nicotine transdermal patch, nicotine gum and bupropion increase cessation rates in motivated smokers. • Oxygen therapy also influence natural history of disease in patients with resting hypoxemia. Survival in hypoxemic patients with COPD is directly proportionate to the no. of hrs / day oxygen is administered. ABG analysis is prefered over oximetry to guide initial oxygen therapy. Oxygen by nasal prongs must be given for at least 15 hrs a day.Transtracheal oxygen is alternative method of delivery in pts. who require high flows of oxygen than can be deliverd by nasal prongs.

  13. BRONCHODILATORS • Anticholinergic agents like ipratropium bromide is first line agent because of its longer duration of action and absence of sympathomimetic side effects. Dose 2 puffs every 6 hrs. • Beta agonists • Short acting: like salbutamol are less expensive, have rapid duration of action and have bronchodilator effect equal to ipratropium bromide but may cause tachycardia, tremor and hypokalemia. • Long acting: like salmeterol appear to achieve bronchodilation that is equivalent or superior to ipratropium but their role in stable COPD is under research.

  14. THEOPHYLLINE • Theophylline is third line agents in COPD patients who fail to achieve adequate symptoms with anticholinergics and beta 2 agonists. • SR theophylline improve arterial oxygen Hb saturation during sleep in COPD pts and is a first line agent for those with sleep related breathing disorders. • Its benefits may result from anti inflammatory properties and extra pulmonary effects on diaphragm strength , myocardial activity and renal function.

  15. CORTICOSTEROIDS • Apart from acute exacerbation , COPD is not generally steroid responsive disease. • A trial of inhaled glucocorticoids should be considered in pts with frequent exacerbations defined as 2 or more per year, and in pts who demonstrate a significant amount of acute reversibility in response to inhaled bronchodilators. • Chronic use of oral glucocorticoids for treatment of COPD is not recommended.

  16. OTHER AGENTS • N ACETYL CYSTEINE: has been used in pts of COPD for its mucolytic and anti oxidant properties. • ALPHA 1 ANTI TRYPSIN THERAPY for severe anti trypsin deficiency. • Pts over 18 years of age with air flow obstruction on spirometry and level less than 11 umol/l are candidates for replacement therapy.

  17. NON PHARMACOLOGICAL THERAPIES • General medical care : influenza vaccine annually. Pneumococcal vaccine is also recommended. • Pulmonary rehabilitation: graded aerobic physical exercise programs • walking 20 mins at least thrice weekly, • bicycling are helpful for preventing deterioration of physical condition and to improve patient’s ability to carry out daily activities. • Pursed lip respiration to slow the rate of breathing and abdominal breathing exercises to relieve fatigue of accessory muscles of respiration may reduce dyspnea in some pts. • Adequate systemic hydration and cough training methods for mobilization of secretions in pts with ch bronchitis.

  18. SURGICAL TREATMENT • LUNG TRANSPLANTATION: for pts with FEV1 less than 25% and severe limitation in quality of life esp with hypercapnia and hypoxemia.It is not an option for elderly pts. • BULLECTOMY: Is considered in pts with COPD and dyspnea in whom a bulla or bullae occupy 50% of hemithorax. • LUNG VOLUME REDUCTION SURGERY: In highly selected pts with severe COPD due to emphysema.

  19. ACUTE EXACERBATION • Exacerbations are commonly considered to be episodes of increased dyspnea and cough and change in amount and character of sputum. • It may or may not be accompanied by fever, myalgias and sore throat. • Approach to the pt includes assesment of severity , identification of the precipitating factor and institution of therapy.

  20. PRECIPITATING CAUSES • Bacterial infections play a role in many episodes. (H.influenzae,S.pneomoniae,M.catarrhalis and Mycoplasma) • Viral infections are involved in 1/3 rd of cases. (Influenza and Adenovirus) • In 20 – 35% no specific precipitant can be identified.

  21. PATIENT ASSESMENT • History include degree of dyspnea , by asking about breathlessness during activities , ask about fever , change in character of sputum and associated symptoms as nausea , vomiting , diarrhea , myalgias and chills. • Inquire about frequency and severity of previous exacerbations. • Physical examination : process degree of distress. • CXR and ABGs

  22. INSTITUTION OF THERAPY • OXYGEN to achieve and maintain PaO2 > 55-60 mm Hg and to keep arterial saturation > 90%. Hypoxic respiratory drive plays a small role in pts of COPD. • INHALED BRONCHODILATORS • Short acting beta agonists are first line agents as albuterol has reduced duration of action in acute exacerbation allowing a treatment frequency of every 30 – 60 mins as tolerated. Subsequent treatment can be reduced to 2- 4 puffs every 4 hrs. • Anticholinergic agents are equally effective to short acting beta 2 agonists. Dose : 2 puffs QID can be increased to 4-6 puffs every 4-6 hrs. • Combination therapy has synergistic bronchodilation , rapid onset of action and fewer S/E.

  23. Contd.. • GLUCOCORTICOIDS: GOLD guidelines recommend 30 – 40 mg of oral prednisolone over 10 – 14 days. They reduce hospital stay , hasten recovery and reduce the chance of subsequent exacerbation or relapse for a period upto 6 mths. • ANTIBIOTICS: First line antibiotic regimes are Septran (160/800 mg every 12 hrs) , Amoxycillin ( 500mg tds) Doxycycline (100mg bd) for 7-10 days. • For severe exacerbation recommended antibiotics include Azithromycin , Clarithromycin , Levofloxacin and Gatifloxacin.

  24. Contd.. • PSYCHOACTIVE DRUGS :low dose anxiolytics may reduce anxiety . Buspirone 5-10 mg tds is usually tolerated well.

  25. INDICATIONS FOR ICU ADMISSION • SEVER DYSPNEA • MENTAL STATUS CHANGES • PERSISTENT WORSENING HYPOXEMIA • HYPERCAPNIA • RESPIRATORY ACIDOSIS ALL DESPITE MEDICAL THERAPY.

  26. MECHANICAL VENTILATORY SUPPORT • Non Invasive positive pressure pressure ventilation (NIPPV) in pts with respiratory failure , defined as Pco2 > 45 mm Hg results in significant reduction in mortality, need for intubation , complication of therapy and duration of hospital stay. • IPPV with ETT is indicated for pts with severe respiratory distress despite initial therapy , life threatening hypoxemia , severe hypercapnia and/or acidosis , impaired mental status , respiratory arrest and hemodynamic instability.

  27. DISCHARGE CRITERIA • Use of inhaled bronchodilators less frequently than every 4 hrs. • Clinical and ABG stability for at least 12 – 24 hrs and • Acceptable ability to eat , sleep and ambulate.

  28. THANK YOU !

  29. SCENARIO • 50 years oil male presented in emergency department with history of severe shortness of breath associated with productive cough with yellow color sputum and fever. • He has past history of cigarette smoking 2 pack year for last 35 years. • What physical signs you can suspect in this case ?

  30. SCENARIO • BP 100/60mmHg • Pulse 110 beats/min • R/R 34/min • Temp 101 F Pt is cyanosed a

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