Obstructive Lung Disease (COPD).pdf

Chronic Obstructive Pulmonary Diseases (COPD) ILOs At the end of this session, the student will be able to: ▪ Define COPD and mention their different etiologies. ▪ Identify the clinical picture of COPD. ▪ Describe the classification of COPD patients. ▪ Describe the treat...

Chronic Obstructive Pulmonary Diseases (COPD) ILOs At the end of this session, the student will be able to: ▪ Define COPD and mention their different etiologies. ▪ Identify the clinical picture of COPD. ▪ Describe the classification of COPD patients. ▪ Describe the treatment plan of COPD. Emphysema and chronic bronchitis are two conditions that make up COPD. Prevalence and Burden of COPD COPD has been and still a major public health problem. Globally, 210 million people are affected, and most of them aged 40-65 COPD causes the death of at least 2.9 million people annually. It is associated with a significant economic burden. Definition a common preventable and treatable disease, is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients. Page 1 of 28 Chronic bronchitis A condition characterized by excessive mucous secretion from the bronchial tree, in which there is productive cough every day, or most days, for at least 3 months of the year, for at least 2 successive years when other causes as bronchiectasis and are excluded. Pathology excessive mucus secretion in chronic bronchitis is the result of increase in the size and number of mucus secreting glands. There is increased ratio of mucus glands to wall thickness (Reid index). Normal 40%, but in COPD, up to 70%. Emphysema Definition: A pathologic term indicating enlargement of the air spaces distal to the terminal bronchioles due to dilatation and/or destruction of the alveolar walls. Page 2 of 28  When the expansion of the air spaces is due to dilatation only, the condition was termed " false emphysema" & it usually does not cause significant respiratory dysfunction. On the other hand, when destruction of the alveolar walls is the main pathology, the condition was termed " true emphysema ". Risk factors: © 2022 Global Initiative for Chronic Obstructive Lung Disease Page 3 of 28 1) Smoking (it is the most important risk factor): Role of smoking in development of COPD: a) Mucosal gland hypertrophy with increased mucus secretion b) inhibitory effect of cigarette smoke on bronchial ciliary blanket predisposing to mucus accumulation. c) respiratory infections are more frequent and severe in smokers than among non-smokers. Infections are associated with mucosal edema and inflammatory cells infiltration both will increase airway obstruction. d) protease-antiprotease imbalance e) Cigarette smoke recruits inflammatory cells to the lungs. Smoke stimulates release of neutrophil elastases and chemo-attractants (increased proteases) cigarette smoke interferes with the efficacy of ά 1 antitrypsin, so balance is shifted towards excess of proteolysis. f) Oxidant-antioxidant theory: g) Cigarettes contain many free oxygen radicals resulting in oxidative stress to the lungs. Also, serum concentration of antioxidants is less in cigarette smokers. 2) Dusty environmental air pollution by burning of biomass fuels or occupational exposure: coal mines, cotton industries. 3) Males are affected more than females (due to smoking). Not anymore. 4) Genetic factors: COPD is a polygenetic disease, homozygous α 1- antitrypsin deficiency is the most common genetic factor. 5) Recurrent bronchopulmonary infections in early childhood Pathology: Patients with COPD have an enhanced or abnormal response to inhaling toxic agents. This amplified response may result in: Page 4 of 28  Large airway inflammation → Chronic bronchitis and mucous hypersecretion Small airway inflammation → Bronchiolitis Lung parenchyma destruction → Emphysema Page 5 of 28 Mechanisms underlying airflow limitation in COPD: Classification of Chronic Obstructive Pulmonary Disease The site of destruction within the acinus (terminal respiratory unit) is the basis for classification of COPD. Page 6 of 28  1) Chronic bronchitis: involves large airways which occur above the 7th or 8th generation of the bronchioles and bronchi. 2) Centriacinar or centrilobular COPD: This type involves the central part of the acinus and is associated with cigarette smoke and chronic bronchitis. 3) Panacinar or panlobular COPD: Involves all the acinus uniformly and is seen in patients with alpha 1-antitrypsin (AAT) deficiency. Clinical Features: 3 extremes of the clinical spectrum of COPD are described: 1) chronic bronchitis which may progress to centriacinar emphysema. 2) centriacinar emphysema or type B-COPD or the bronchitic type of COPD or Blue Bloaters. 3) Panacinar emphysema or type A-COPD or the emphysematous type of COPD or Pink Puffers Sometimes, the term emphysema is used to describe type A COPD and the term chronic bronchitis to describe type B COPD. Despite this, the mixed type of COPD which has combined features of both is the most common. Page 7 of 28  Cardiovascular abnormalities : I. Pulmonary hypertension: due to a) Hypoxia: resulting in Page 8 of 28  Direct vasoconstriction of pulmonary arterioles→ Pulmonary hypertension Peripheral vasodilation leads to hyperdynamic circulation which increases pulmonary blood flow → Pulmonary hypertension. Increased blood viscosity due to erythrocytosis → Pulmonary hypertension b) Reduction of the pulmonary vascular bed: due to Destruction of alveolar septa. Increased intra-alveolar pressure which causes compression of pulmonary capillaries. II. Hypoxic cor-pulmonale: Pulmonary hypertension will lead to right ventricular hypertrophy which may be followed by right ventricular failure. COPD Phenotypes Chronic Bronchitis Emphysematous Asthma-COPD-Overlap Frequent Exacerbator Rare Exacerbator Page 9 of 28 Diagnosis of COPD: Clinical picture : The patient is usually a male, chronic heavy cigarette smoker & above 50 years of age. I. Symptoms: 1) Prolonged history of chronic cough with mucoid or mucopurulent expectoration. Cough often presents only on walking up at first, later cough occurs throughout the day (may be attributed by the patient to smoking "smoker's cough". Page 10 of 28  2) Dyspnea with wheezing. Dyspnea is gradual, slowly progressive over years occurring initially on exertion but later at rest. Wheezing is usually persistent or continuous (not in attacks as bronchial asthma). 3) Chest pain may occur due to: Chronic cough causing strain of intercostal muscles. Rupture of emphysematous bullae causing pneumothorax. Complicating pneumonia causing pleurisy. 4) Manifestations of respiratory failure occur in advanced conditions (See manifestations of hypoxemia & hypercapnia). 5) Oedema of lower limbs may occur due to cor pulmonale, or less commonly due to salt and water retention or DVT. 6) Symptoms of complications as weight loss, muscle wasting. II. Signs: 1) General examination: a. Vital signs: Pulse: - Tachycardia & big pulse volume may be present due to the vasodilator effect of hypercapnia & hypoxemia. - Small pulse volume may be present in severe pulmonary hypertension & heart failure. - Pulsus paradoxus may be present in severe cases. Respiratory rate: tachypnea with working accessory respiratory muscles b. Head examination: - Central cyanosis may be present. - Puffiness of eyelids due to chronic cough. - Expiratory pursed lip breathing. c. Neck examination: The neck veins are usually congested due to: Page 11 of 28  - increased intrathoracic pressure, or occurrence of cor pulmonale & right-sided heart failure. - Prominent accessory respiratory muscles in neck. d. Upper limb examination: Clubbing of fingers occurs if there is associated bronchiectasis or bronchial carcinoma. e. Lower limb examination: Oedema of the lower limbs may occur due to cor pulmonale or less commonly due to salt & water retention or DVT. Generalized oedema may occur due to right-sided heart failure. Generalized muscle wasting in advanced cases. 2) Chest examination: A) Manifestations of airway obstruction: due to chronic obstructive bronchitis vesicular breath sounds with prolonged expiration. generalized wheezes (rhonchi). crepitations may occur, are mainly expiratory & changing with cough. prolongation of forced expiratory time (normally < 5 sec). Suction of supraclavicular, suprasternal & lower intercostal spaces during inspiration & fullness during expiration. B) Manifestations of hyperinflation: due to emphysema 1- Inspection: increased antero-posterior diameter. Barrel chest if: horizontal ribs. wide intercostal spaces. wide subcostal angle. Bilateral limitation of chest expansion. Costal margin retraction on inspiration (Hoover's sign). Weak or absent cardiac pulsations. Page 12 of 28  epigastric pulsations (also may be present due to right ventricular enlargement). Decrease length of extra thoracic trachea: The distance between the suprasternal notch and the cricoid cartilage (normally three finger breadths) may be reduced. 2- Palpation Trachea is central. TVF is decreased bilaterally. 3- Percussion: hyperresonance with encroachment on cardiac & hepatic dullness. 4- Auscultation: Diminished vesicular breath sounds with prolonged expiration (harsh vesicular). Distant heart sounds Generalized wheezes (rhonchi). Early inspiratory crepitations. 3) Abdominal examination: A- The lower border of the liver may be displaced downwards due to: Depression of the liver by flat diaphragm (the liver is not tender). Enlargement of the liver due to cor pulmonale (the liver is tender). B- Ascites may be present: due to right-sided heart failure. 4) Signs of respiratory failure: e.g. Central cyanosis. Drowsiness & hypersomnia (CO2 narcosis). Asterixis (flapping tremors). Increased intracranial tension & papilledema. Coma occurs terminally. Page 13 of 28  Complications of COPD: Acute exacerbations. Acute Respiratory failure. Pneumonia Cor pulmonale & right-sided heart failure. Pneumothorax. Bronchial obstruction & collapse. Erythrocytosis. Thromboembolism. Salt & fluid retention. Complications of chronic cough N.B. Left-sided heart failure may occur in cases of COPD due to: Associated disease affecting the left side of heart especially coronary heart disease. Hypoxia leading to myocardial ischemia. Acidosis leading to myocardial depression. The two ventricles act as a one unit & failure of one ventricle predisposes to failure of the other. Volume overload due to: - hyperdynamic circulation. Hypervolemia. Increased blood viscosity due to erythrocytosis. Investigations: 1. Chest X-ray: Signs of hyperinflation: Hyper translucency of the lungs. Page 14 of 28  Transverse ribs. Wide intercostal spaces. Low flat diaphragm. Heart shadow is elongated “ribbon-shaped heart". Tenting or cupping of the diaphragm (sure sign of hyperinflation). Increased retrosternal air in lateral view (sure sign) May be emphysematous bullae (sure sign) Accentuation of the pulmonary artery near the hilum. (sure sign). 2. Respiratory function tests: A. Ventilation tests: FEV1 & PEFR are decreased. Forced vital capacity (FVC) is decreased. Decreased FEV1/FVC ratio Residual volume (RV) and total lung capacity TLC are increased Maximum breathing capacity (MBC) is markedly reduced. Page 15 of 28 B. Diffusion test: CO transfer factor is decreased in panacinar emphysema. C. Arterial blood gases: decreased PO2, increased PCO2 & increased bicarbonate. Page 16 of 28 3. Sputum culture & sensitivity: may detect organisms especially pneumococci & H. influenzae. 4. Blood picture: may show erythrocytosis. 5. Estimation of serum αl-antitrypsin: decreased in cases of primary emphysema, 6. CT chest: the best method to detect severity of emphysema. Differential diagnosis of COPD: Congestive heart failure: Fine basilar crackles on auscultation Chest x-ray shows dilated heart, pulmonary edema. Pulmonary function indicates restrictive, not obstructive. Bronchiectasis: Large volumes of purulent sputum. Clubbing of fingers. Coarse crackles on auscultation. Page 17 of 28  Chest x-ray/ CT shows bronchial dilation. Tuberculosis: Onset all ages History of contact Microbiological confirmation. High local prevalence of tuberculosis Chest x- ray shows lung infiltrate or nodular lesions. Management of COPD: A. For stable patients I. Prevention: a. Smoking cessation and/or nicotine replacement by patches or gums. b. Reduce or prevent air pollution. c. Pneumococcal or influenza vaccination II. Pulmonary rehabilitation: education, exercise and physiotherapy III. Oxygen therapy IV. Pharmacological treatment of COPD: B2 agonists, anticholinergics, inhaled steroids, oral theophylline. V. Alpha 1-antitrypsin replacement. VI. Surgical treatment Nonpharmacological treatment: Smoking cessation Avoid air pollutants exposure. Long-term oxygen therapy: Long-term oxygen therapy (LTOT) increases survival and improves the quality of life of hypoxemic patients with chronic obstructive pulmonary disease (COPD) and is often prescribed for patients with other hypoxemic chronic lung disease. Page 18 of 28  Avoidance of recurrent infection by regular vaccination: vaccination includes anti-pneumococcal vaccine and influenza vaccine. Pulmonary rehabilitation: Pulmonary rehabilitation is a program of education and exercise to increase awareness about lungs and disease. The patient will learn to achieve exercise with less shortness of breath. The classes are offered in a group setting so patients get the chance to meet others with similar conditions, which provides an opportunity to give and receive peer support. Oxygen therapy: It is the long-term continuous administration of low flow O2 at home. It is indicated in cases of severe hypoxia: PaO2 2 (Exacerbation 3 history) Risk Risk 2 1 (A) (B) 1 0 mMRC 0-1 mMRC > 2 CAT < 10 CAT > 10 Symptoms (mMRC or CAT score) Page 27 of 28  Manage Stable COPD: Pharmacologic Therapy RECOMMENDED FIRST CHOICE C D Exacerbations per year GOLD 4 ICS + LABA ICS + LABA >2 or and/or GOLD 3 LAMA LAMA A B GOLD 2 SAMA prn LABA 1 or or GOLD 1 SABA prn LAMA 0 mMRC 0-1 mMRC > 2 CAT < 10 CAT > 10 Page 28 of 28