INTRODUCTION Chronic obstructive pulmonary disease(COPD) is an irreversible airway obstruction. It is a preventable and treatable disease characterized by persistent airflow limitation that is usually progressive. Associated with an enhanced chronic inflammatory response in the airways and the lungs to noxious particles or gases. Exacerbations and comorbidities contribute to the severity of COPD in patients. Related diagnoses include; Chronic bronchitis; characterized by cough with sputum production on most of the days for at least 3 months in each 2 consecutive years.
Continued… EMPHYSEMA; abnormal permanent enlargement of the airspaces distal to the terminal bronchioles accompanied by destruction of their walls and without obvious fibrosis. Comorbidities associated with COPD include; cardiovascular disease, cerebrovascular disease, metabolic syndrome, osteoporosis, depression and lung cancer. Weight loss and skeletal muscle dysfunction are among the extra-pulmonary effects of COPD.
Epidemiology and risk factors The prevalence of COPD is directly related to the prevalence of risk factors in the community, such as tobacco smoking, coal dust exposure or the use of biomass fuels, and to the age of the population being studied. 80 million people worldwide suffer from COPD. In 2005,3 million people died from COPD. In Uganda, the prevalence of COPD is up to 16.2% from a study done in 2012. Mortality and morbidity from COPD is highest in Asian and African countries where tobacco smoking is much more. Environmental risk factors include; 1)Cigarette smoking is the major risk factor for COPD. However, the risk of developing COPD depends on the amount and duration of smoking. This is because it is unusual to develop COPD with less than 10 pack years . Individual susceptibility factors plays a role as not all smokers develop COPD.
Continued…. biomass fuels occupational exposures such as coal dust, silica and cadmium low birth weight affected lung growth due to maternal smoking, or childhood infections infections especially recurrent infections. low socio-economic status cannabis smoking. Host factors include; 1) genetics e.g. alpha-1 antiproteinase deficiency(antitrypsin deficiency) 2) Airway hyper-reactivity.
pathophysiology The presence of airflow limitation combined with premature airway closure leads to gas trapping and hyperinflation. This leads to reduced pulmonary and chest wall compliance. Pulmonary hyperinflation also flattens the diaphragmatic muscles and leads to an increasingly horizontal alignment of the intercostal muscles placing the respiratory muscles at a mechanical disadvantage. Work of breathing is therefore markedly increased; first on exercise when the time for expiration is further shortened and as the disease advances, even at rest.
Continued… Emphysema may be classified by pattern of the enlarged airspaces as centriacinar,panacinar or paraseptal. Bullae forms in some individuals and this results in impaired gas exchange and respiratory failure.
Clinical features Cough with sputum production Hemoptysis Breathlessness Edema Morning headaches (may suggest hypercapnia) Note that the above are reported by the patient during history taking. On examination; Typically quiet breath sounds Crackles may accompany inf; if persistent, bronchiectasis should be suspected.
Continued… Right heart failure may develop in patients with advanced COPD, particularly if there is coexisting sleep apnea or thromboembolic disease (‘cor pulmonale’). Two classical phenotypes have been described: ‘pink puffers’ and ‘blue bloaters’. The former are typically thin and breathless, and maintain a normal PaCO2 until the late stage of disease. The latter develop (or tolerate) hypercapnia earlier and may develop oedema and secondary polycythemia. In practice, these phenotypes often overlap.
Modified MRC dyspnea scale GRADE DEGREE OF BREATHLESSNESS RELATED TO ACTIVITIES No breathlessness except with strenuous exercise 1 Breathlessness when hurrying on the level or walking up a slight hill 2 Walks slower than contemporaries on level ground because of breathlessness or has to stop for breath when walking at own pace 3 Stops for breath after walking about 100m or after a few minutes on level ground 4 Too breathless to leave the house, or breathless when dressing or undressing.
Continued… Note that; BMI is of prognostic significance. Pink puffers; they are thin and breathless, maintain a normal arterial partial pressure of carbon dioxide until the late stages of the disease. Blue bloaters develop hypercapnia earlier, edema and secondary polycythemia. These phenotypes often overlap in clinical practice.
Diagnosis After taking history from the patient and doing a physical examination, investigations are done to confirm the diagnosis of COPD. chest X-ray; this helps to rule in or rule out other differential diagnoses of COPD e.g. cardiac failure, lung cancer. The presence of a bullae can also be seen on chest X-ray complete blood count to exclude/include anemia or polycythemia spirometry; to detect the rate of airflow using the FEV1/FVC ratio, a ratio of less than 70% indicates obstructive lung disease. helium dilution technique can be used to measure lung volumes which Is used to assess hyperinflation. plethysmography can be done for the same purpose as helium dilution technique and it is more preferred especially in patients with severe COPD and with a large bullae.
Continued… 6) Exercise tests which provide the degree of exercise tolerance. 7) pulse oximetry to detect the oxygen saturation etc. Note that the severity of COPD is classified based on post-bronchodilator FEV1 as follows:
continued…. STAGE SEVERITY FEV1 1 mild FEV1/FVC<0.70 FEV1 greater than or equals to 80% predicted 2 moderate FEV1/FVC<0.70 FEV1 50-79% PREDICTED 3 severe FEV1/FVC<0.70 FEV1 30-49% predicted 4 Very severe FEV1/FVC<0.70 FEV1<30% predicted or FEV1,50% predicted if respiratory failure is present.
Management reducing exposure to noxious particles and gases bronchodilator therapy; such as short acting bronchodilators (salbutamol,terbutaline,ipratropium bromide),long acting bronchodilators (salmeterol,formoterol,indacaterol,tiotropium bromide).Inhalation Is the preferred route but oral drugs can be given to those who cannot use inhaled devices efficiently,Bambuterol is a prodrug of terbutaline and is taken orally. corticosteroids; however a fixed combination of inhaled corticosteroid and a LABA is more useful.
Continued… 4. pulmonary rehabilitation 5. oxygen therapy; patients are advised to use oxygen for a minimum of 15hrs per day, however greater benefits are seen in those who use oxygen for 20hrs per day. The aim is to increase oxygen saturation to at least 90%. 6. surgical intervention; bullectomy is done in patients with a large bullae that is compressing the surrounding normal lung tissue with minimal airflow limitation and a lac of generalized emphysema. Lung volume reduction surgery(LVRS) is done on patients with upper lobe emphysema having preserved gas transfer and no evidence of pulmonary hypertension. Lung transplant is done on those with advanced disease.
others Patients with COPD should receive annual influenza and pneumococcal vaccines. Obesity, poor nutrition, depression and social isolation should be addressed. Mucolytic therapy and antioxidant agents are occasionally used Morphine may be used for palliation of breathlessness in advanced disease Benzodiazepines can be used in low doses to reduce anxiety Resuscitation is done in critical situations however consent should be seek prior to it.
prognosis Prognosis of COPD is inversely related to age and directly related to the post-bronchodilator FEV1. Indicators of poor prognosis include: Weight loss and Pulmonary hypertension The BODE score is used for indicating prognosis of COPD: B-body mass index O-degree of airflow obstruction D-measurement of dyspnea E-exercise capacity
complications 1)respiratory failure 2)cardiac disease 3)lung cancer
Acute exacerbation of COPD Acute exacerbations of COPD are characterized by an increase in symptoms and deterioration in lung function and health status. They become more frequent as the disease progresses and are usually triggered by bacteria, viruses or a change in air quality. They may be accompanied by the development of respiratory failure and/or fluid retention. They are an important cause of death in these patients. Most patients can be managed at home with the use of increased bronchodilator therapy, a short course of oral corticosteroids and if appropriate, antibiotics.
Continued…. However, presence of cyanosis, peripheral edema or alteration in the level of consciousness indicates the need for referral to a hospital. Management: 1)oxygen therapy; high concentration of oxygen causes respiratory depression in these patients thus worsening the acidosis. Thus oxygen should be given in a concentration of 24% or 28%. The aim is to maintain oxygen saturation between 88% and 92% without worsening acidosis. 2)Short acting beta 2 agonists combined with an anticholinergic agent should be administered via a nebulizer i.e. salbutamol and ipratropium bromide.
Continued… 3)oral prednisolone; this reduces symptoms and improve lung function. A dose of 30mg for 10 days is given. Commonest side effect is osteoporosis which can be prevented by co-administering with bisphosphonates. 4)antibiotics where necessary, usually aminopenicillins or macrolides are used. 5)if all the above medications fail to maintain the required oxygen saturation, NIV(non invasive ventilation is used as the last alternative. 6)diuretics can be used for the edema 7)aminophylline can sometimes be used, however it is associated with side effects like inducing arrhythmias, narrow therapeutic window and is susceptible to drug interactions. 8)respiratory stimulant doxapram can also be used especially in patients with low respiratory rate but it has been superseded by NIV.
Continued… Consider discharge from the hospital only when patient is clinically stable on his/her usual maintenance medication. A “nurse-led hospital at home” team that provides short-term nebulizer loan improves discharge rates and additional support for the patients.
Reference Davidson text book of clinical medicine….