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COPD QA 60 year old patient presents with cough and yellowish sputum and SOB for three days .He has chronic cough and SOB for five years . Mention the DD. Asthma/COPD PTB Ca lung Interstitial fibrosis Bronchiectasis Shortness of breath was associated with wheezing. Diagnosis? COPD/asthma COPD ...
COPD QA 60 year old patient presents with cough and yellowish sputum and SOB for three days .He has chronic cough and SOB for five years . Mention the DD. Asthma/COPD PTB Ca lung Interstitial fibrosis Bronchiectasis Shortness of breath was associated with wheezing. Diagnosis? COPD/asthma COPD is a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases Chronic bronchitis cough and sputum on most days for at least 3 months, in each of 2 consecutive years Emphysema abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis Risk factors for development of COPD Environmental Tobacco smoke accounts for 95% of cases in UK Indoor air pollution; cooking with biomass fuels in confined areas in developing countries Occupational exposures, such as coal dust, silica and cadmium; construction worker Risk factors (Cont..) Infections: recurrent infection may accelerate decline in FEV1; persistence of adenovirus in lung tissue may alter local inflammatory response, predisposing to lung damage; HIV infection is associated with emphysema Cannabis smoking Host factors Genetic factors: α1-antiproteinase deficiency; other COPD susceptibility genes are likely to be identified Airway hyper-reactivity Clinical Features Symptoms Cough and associated sputum production (first symptoms) (smoker’s cough) Breathlessness usually precipitates the presentation (Modified MRC dyspnoea scale) wheeze Morning headaches ( hypercapnia) Other systemic effects on cardiovascular function e.g. hypertension, osteoporosis, depression, metabolic problems leading to weight loss and loss of muscle mass with weakness History taking COPD Dyspnoea: initially exertional, but can progress to resting dyspnoea /wheezing over the course of the condition (months to years). Dyspnoea is graded using the Medical Research Council (MRC) dyspnoea scale Inhalers used; no of puffs Chronic productive cough: usually colourless sputum, which may become green during lower respiratory tract infections (LRTIs) Recurrent LRTIs/past admissions Fatigue Headache/confusion (due to CO2 retention) Smoking /occupation TRO other causes of chronic cough- eg Ca lung/TB etc Signs no signs or nothing more than quiet wheezes throughout the chest (mild disease) In severe disease, tachypnoeic, with prolonged expiration accessory muscles of respiration are used intercostal indrawing on inspiration and pursing of the lips on expiration chest expansion is poor Hyperinflated lungs/barrel shaped lungs (loss of the normal cardiac and liver dullness) Signs of hypercapnia (RF)- (e,g.,peripheral vasodilatation, a bounding pulse, a coarse flapping tremor) Cor pulmonale signs of pulmonary hypertension, right ventricular hypertrophy, and right heart failure Two classical phenotypes pink puffers (emphysema) - typically thin and breathless, and maintain a normal PaCO2 until the late stage of disease blue bloaters(chronic bronchitis) - develop (or tolerate) hypercapnia earlier and may develop oedema and secondary polycythaemia Complications Pneumonia Acute type II respiratory failure Pulmonary hypertension with Corpulmonale Tension pneumothorax (rupture bullae) Secondary polycythemia INVESTIGATIONS CXR FBC ABG Sputum c&S ECG Spirometry Hypertranslucent lung fields Tubular heart Lowset diaphragm (4)Haemoglobin level and PCV can be elevated as a result of persistent hypoxaemia (secondary polycythaemia) CRP- increased (5) Blood Gases (ABG) Normal at rest Advanced- hypoxaemia, hypercapnia (6)Sputum examination Strep. pneumoniae and H. influenzae -common organisms to produce acute exacerbations Occasionally Moraxella catarrhalis may cause infective exacerbations (7) ECG cor pulmonale - P wave is taller (P pulmonale) and there may be right bundle branch block (RSR′ complex) and the changes of right ventricular hypertrophy Investigations (1)Lung function tests show evidence of airflow limitation FEV1 : FVC ratio - reduced <80 % PEFR – low (3)High resolution CT scans To show emphysematous bullae Centrilobular lesions (8)Echocardiogram useful to assess cardiac function where there is disproportionate dyspnoea (9) α1-Antitrypsin levels and genotype especially in premature disease or non-smokers Management of Acute exacerbation Of COPD • Oxygen Check arterial blood gas and pulse oximetry on presentation and then after 30 to 60 minutes to ensure satisfactory oxygenation and monitor for carbon dioxide retention and acidosis. Administer the oxygen in a controlled fashion via a Venturi mask to deliver 24% to 28% oxygen. •Short-acting beta-2 agonists are typically favoured as a first-line option as they tend to have a more rapid effect than antimuscarinics. Give ipratropium alone if the patient experiences adverse effects due to salbutamol (e.g., tremor, palpitations, headache, nausea, dizziness). • Intravenous hydrocortisone 100 to 200mg 6 hrly IV • .Give antibiotics to any patient who needs ventilation (invasive or non-invasive) or patients experiencing exacerbations with:[Increase in sputum purulence, plusIncrease in sputum volume, and/or Increased dyspnoea • IV aminophylline • Start non-invasive ventilation (NIV) for patients who have acute hypercapnic respiratory failure (pH <7.35, PaCO 2 >6.5 kPa), despite optimal medical therapy, [100] and have no contraindications BiPap machine can help push air into your lungs. You wear a mask or nasal plugs that are connected to the ventilator. The machine supplies pressurized air into your airways. It is called “positive pressure ventilation” because the device helps open your lungs with this air pressure. (1) Oxygen Therapy (iii) Antibiotics To shortens exacerbations and acute episodes To prevent hospital admission and further lung damage Amoxicillin Cefaclor (500 mg 8-hourly) or Cefixime (400 mg once daily) Co-amoxiclav is a useful alternative (iv) Antimucolytic agents reduce sputum viscosity and can reduce the number of acute exacerbations (v) Diuretic therapy necessary for all oedematous patients daily weights should be recorded during acute inpatient episodes (2) Removal of retained secretions encouraged to cough Physiotherapy bronchoscopy and/or aspiration via an endotracheal tube tracheostomy (rare) Management of chronic COPD (1)Smoking cessation Reducing the number of cigarettes smoked each day has little impact on the course and prognosis of COPD complete cessation is accompanied by an improvement in lung function and deceleration in the rate of FEV1 decline Medical management of COPD (2)Drug therapy (i)Bronchodilators Mild COPD Short-acting bronchodilators, such as the β2-agonists Salbutamol and Terbutaline (SABA) or the anticholinergic Ipratropium bromide Salbutamol (200 μg every 4–6 hours) Moderate or Severe COPD Longer acting bronchodilators, such as the β2-agonists Salmeterol, Formoterol and Indacaterol (LABA) or the anticholinergic Tiotropium bromide Formoterol 12 μg powder inhaled twice daily or Salmeterol 50 μg twice daily More prolonged and greater bronchodilatation Antimuscarinic agents: Tiotropium (long-acting) (18 μg daily), Ipratropium (40 μg four times daily) or Oxitropium (200 μg twice daily) *Long-acting preparations of Theophylline are of little benefit *Orally active, highly selective phosphodiesterase inhibitors are currently under appraisal (3) Oxygen Therapy • fall in pulmonary artery pressure was achieved if oxygen was given for 15 hours daily • but substantial improvement in mortality was only achieved by the administration of oxygen for 19 hours daily • 19 hours of oxygen daily at a flow rate of 1–3 L/min using a 28% oxygen mask is best achieved using an oxygen concentrator (4) Pulmonary rehabilitation modest increase in exercise capacity- diminution in the sense of breathlessness and improved general well-being nutritional advice, psychological, social and behavioural intervention is helpful most programmes include 2–3 sessions per week for 6 and 12 weeks (5) Additional measures (i)Vaccines yearly influenza vaccine one dose of the polyvalent pneumococcal polysaccharide vaccine (a single dose usually provides lifelong immunity) (ii) α1-Antitrypsin replacement weekly or monthly infusions patients with serum levels of this compound < 310 mg/L and abnormal lung function (vii) Air travel patients whose saturation drops below 85% within 15 minutes should be advised to contact their airline to request supplemental oxygen during flight (viii) Surgery large emphysematous bullae – bullectomy severe COPD (FEV1 < 1 L) - lung volume reduction surgery end-stage emphysema - Single lung transplantation (iii) Treat Heart failure (iv) Secondary polycythaemia venesection is recommended if the PCV is > 55% Complications • Hypercapnic respiratory failure (PaO2 < 8.0 and PaCO2 > 6.0) • Secondary polycythaemia (raised haemoglobin): due to chronic hypoxaemia • Cor pulmonale: right heart failure, caused by pulmonary hypertension as a result of chronic hypoxic pulmonary vasoconstriction • Bronchiectasis: due to chronic and repeated infections • Anxiety and depression • Osteoporosis: due to chronic steroid use, smoking, lack of bone-strength exercise and vitamin D deficiency • Sleep disturbance Key points • COPD is a triad of emphysema, chronic bronchitis and small airway fibrosis. • The main risk factors are tobacco smoking and inhaled pollutants. • COPD presents with progressive dyspnoea and productive cough. • Diagnosis is based on clinical features + spirometry (FEV1/FVC <70%). • Management consists of conservative measures (such as smoking cessation) and inhaled bronchodilators. • Complications include respiratory failure and cor pulmonale.