| ID | 88 |
|---|---|
| Name | CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) |
| Cause | |
| Signs Symptoms | |
| Diagnosis | |
| Investigations | Investigations: 1. Chest X-ray- may be normal; but in typical cases, there may be presence of bullae, severe overinflation of the lungs with low, flattened diaphragm, and a large retrosternal air space on the lateral film. Peripheral vessels of the lung fields are relatively invisible, whereas proximal vessels are easily visible3. 2. Blood haematocrit- haemoglobin level & PCV usually elevated due to secondary polycythemia (in advanced COPD as a result of persistent hypoxaemia). 3. Sputum for gram-stain & C/S- may reveal bacterial infection. 4. Arterial blood gas analysis- it is usually unnecess-ary unless hypoxia or hypercapnia is suspected. 5. Pulmonary function tests- findings of airflow limitation. 6. ECG- findings may correlate with cardiac changes. 7. Echocardiogram- may be done to assess cardiac function. 8. al-Antitrypsin- in case of emphysema, it may be a cause; the normal range is 2-4gIA |
| Management | Management: 1. Oxygen therapy- should immediately be started & monitored by blood gas analysis (controlled oxygen at 24-28% or maintaining a PaO2 > 8 kPa or 60 mmHg). (Excess oxygen may cause respiratory depression and worsening acidosis). 2. Bronchodilator therapy: Nebulised a short-acting p2-adrenoceptor agonist bronchodilator e.g salbutamol 5mg or terbutaline 10mg in combination with an anticholinergic bronchodilator agent e.g ipratropium bromide 0.5mg 6 hourly. It is safe to drive nebuliser with supplemental oxygen. Theophylline should not be given in acute exacervations of COPD. It is better to advise as maintenance therapy in stable COPD. 3. Antibiotic treatment- like above (parenteral can be used). 4. Diuretic therapy- Frusemide 40-120mg daily orally or i.v according to the extent of oedema. 5. Corticosteroid therapy: In most cases of acute exacervations, oral prednisolone 30mg or 0.5mg/kg daily for 10 days or for shorter period reduces symptoms and improves lungs functions. If there is an appreciable improvement in bronchial airflow in spirometric measure i.e FEV1 >20%, oral prednisolone should be gradually reduced & replaced by inhaled steroid e.g beclomethasone 100-500mg thrice daily. 6. Respiratory stimulant- by doxapram hydrochloride 1.5-4mg/min by i.v infusion can be given in profound respiratory acidosis. 7. Chest physiotherapy in selected cases. 8. Mechanical ventilation- when requird. 9. Other measures- i. bed rest ii. correction of acidaemia if any, iii. salt restriction. |
| Introduction | Chronic obstructive pulmonary diseases (COPD) are ‘chronic, slowly progressive disorders characterized by airflow obstruction (FEV1< 80% predicted, & FEV1/VC ratio < 70%) which don’t change markedly over several months & may be partially reversible by bronchodilator therapy. By definition COPDs include- chronic bronchitis, emphysema & some cases of chronic asthma. Most patients with COPD have features of both chronic bronchitis & emphysema. The difference between COPD & asthma is virtually blurred, because most patients with COPD have some reversible airflow obstruction like asthma. |
| History | |
| Etiology | Etiology: 1. Cigarette smoking- single most important cause. 2. Contributory causes- i. dusty or air-polluted environments ii. alphal-antitrypsin deficiency can cause emphysema. 3. Co-existing factors- such as low birth weight, & bronchial hyper-responsiveness have some association with the development of COPD. |
| Clinical Features | Clinical feature: 1. Usual age period of presenting features of COPD, 5th to 6th decade. 2. Patients usually come & present complaints with long history of suffering. 3. History of cigarette smoking in most cases. 4. Presenting features are- chronic cough with sputum production (in chronic bronchitis) and dyspnoea (in emphysema) 5. On examination- rhonchi, decreased intensity of breath sounds and prolonged expiration. 6. In late or severe stage of COPD, there may be- dyspnea at rest, absence from work due to disability; pulmonary hypertension, cor-pulmonale and chronic respiratory failure; occasional haemoptysis. 7. May be sign of secondary infection or pneumonia. Acute exacervation of COPD:1-2 Features of acute exacervation: Acute exacervations of COPD are characterised by: 1. Intense presentation of symptoms. 2. Deterioration of lung functions, may be accompanied by the development of respiratory failure and/or fluid retention (presence of cyanosis, peripheral oedema or an alteration in consciousness). 3. Signs of infections. Indications for immediate hospitalization: 1. Patient with acute exacervation of COPD which fails to respond to ambulatory measure. 2. Complications, such as acute respiratory failure, corpulmonale or pneumothorax. |
| Preventions | Prevention: Chronic obstructive pulmonary disease (COPD) may be a preventable disease. Removal of primary causes and early diagnosis and treatment can prevent relentless progression of the disease, such as- 1. Cessation of smoking. 2. Early treatment of airway infections. 3. Vaccination against influenza & pneumococcal infection disease. |
| Treatment | Treatment: 1. Avoidance of causative factors: Causes of bronchial irritation must be avoided or reduced, e.g by avoiding smoking, dusty & air-polluted environment. 2. Oxygen therapy: Supplimental oxygen therapy is most effective and useful in COPD patients with resting hypoxaemia, or other severe lung diseases who have significant hypoxaemia. Oxygen may be given for continuous use, only at night or with exercise. Home oxygen therapy- hypoxaemic patients with pulmonary hypertension, chronic cor-pulmonale, erythrocytosis, impaired cognitive function, exercise intolerance, nocturnal restlessness, or morning headache are particularly likely to benefit from home oxygen therapy. 2. Bronchodilator therapy: Bronchodilator therapy should be given to all patients with reversible air flow obstruction. Two groups of bronchodilators-anticholinergic (antimuscarinic) bronchodilator agents with more prolonged action, such as ipratropium or oxitropium bromide & short-acting (b2-adrenoceptor agonists, such as salbutamol, albuterol, metaproterenol, are the mainstay of COPD therapy. But, recent studies prefered ipratropium bromide as the first line agent in the treatment of COPD over the short-acting b2-agonists, because of its longer duration of action, superior bronchodilation and absence of sympathomimetic side effects. However, in case of mild COPD, for symptomatic relief or prior to exercise short-acting sympathomimetic agents e.g salbutamol may be given 200mgm (2 puff) 4-6 hourly, or ipratropium bromide 2 to 4 inhalations (18mgm each) every 6 hours may be given alone. In moderate to severe COPD, the above two agents should be used regularly and in combination (doage, as above). Ipratropium bromide may be given by using nebulizer (0.02%) 1 unit dose (500mgm) in every 6-8 hours. Use of long-acting P2-adrenoceptor agonists (e.g formoterol, salmeterol) are of limited value in COPD treatment. Oral theophylline (with sustained-release preparation) improves hemoglobin saturation during sleep in COPD patients and that is why it is considered as a first-line agent for those with sleep-related breathing disorders. Theophylline also improves dyspnea, exercise performance, and pulmonary function in many patients with stable COPD. Therefore, oral theohylline is advised as maintenance therapy once-daily dose, preferably at night. 4. Corticosteroid therapy: Generally steroids are not effective in the treatment of COPD. Apart from acute exacerbations, only 10-20% of stable outpatients of COPD treated with oral steroid respond and have an increased bronchial airflow, i.e FEV1 is greater than 20%. Currently, inhaled corticosteroids alone are also not considered as first-line therapy in stable COPD patients; combination therapy with an inhaled corticosteroid and a long-acting (b2-agonist reduces the frequency of COPD exacerbations and improves self-reported functional status in COPD patients. But, which patient will respond to steroid therapy can’t be predicted. Therefore, most cases of severe COPD are treated with steroids such as, prednisolone 30mg or 0.5mg/kg daily for 2 to 3 weeks in addition to bronchodilators (long-acting b2-agonist). If there is an appreciable improvement in bronchial airflow in spirometric measure i.e FEV1 >20%, oral prednisolone should be gradually reduced & replaced by inhaled steroid e.g beclomethasone 100-500mg thrice daily. Following steroid therapy, if there is no airflow improvement, it should be discontinued after 2-3 weeks. 5. Antibiotic therapy in COPD: There is no need of use of prophylactic antibiotics in COPD. Antibiotic therapy should only be given, when it is clearly indicated, such as, COPD patients associated with increased dyspnea and a change in the quantity and/or character of sputum as in acute exacerbation. Antibiotics recommended are- Amoxycillin 250-500mg every 8 hours (or Co-amoxiclav 375-625mg in cases of b-lactamase-producing organisms), or Cotrimoxazole 960mg every 12 hours may be given orally for 7-10 days. Cefaclor 500mg 8-hourly or Cefixime 400mg once daily also considered as the antibiotics of choice, as there is very less chance of resistance. In severe COPD exacerbations, parenteral antibiotics may be preferred for prompt administration & action. 6. Symptomatic measures: a. Cough suppressant at night. b. Bed room should be warmed. c. A hot drink 6r inhalation of steam to liquefy the sputum. d. Oxygen if needed. e. If there is bronchospasm- aminophylline should be given. 7. Physiotherapy- with emphasis on coughing and relaxation. 8. Polycythaemia- managed by venesection, if Hb% 20gm/dl or more. |
| Complications | Complications: Acute bronchitis, pneumonia, pulmonary hypertension, corpulmonale, chronic respiratory failure etc. |
| Prognosis | |
| Types | Chronic Bronchitis Definition: A patient can be considered to be suffering from chronic bronchitis if excessive sputum (due to increased bronchial mucus secretion) has been coughed up on most days on atleast three consecutive months for more than two successive years, providing other causes of productive cough such as bronchiectasis and untreated chronic asthma have been excluded. Pulmonary Emphysema Definition: According to American thoracic society ‘emphysema’ can be defined as ‘abnormal permanent enlargement of ah- spaces distal to the terminal bronchioles with destruction of their walls & without obvious fibrosis’. Emphysema can be classified into 3 categories according to the site of involvement- i. Centri-acinar emphysema, ii. Pan-acinar emphysema, iii. Irregular emphysema. |
| Classification | |
| Observation | |
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