Copdchronic obstructive pulmonary disease Objectives Definition Risk factors

Copd(chronic obstructive pulmonary disease)

Objectives: � Definition � Risk factors � Pathophysiology � Clinical features � Investigations � Management � prognosis

copd: definition COPD is defined as a preventable and treatable lung disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. The pulmonary component is characterised by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.

Copd: Related diagnoses include • chronic bronchitis (cough with sputum on most days for at least 3 consecutive months for at least 2 successive years) and • emphysema (abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and with-out obvious fibrosis). Extrapulmonary manifestations include impaired nutrition, weight loss and skeletal muscle dysfunction.

copd: epidemiology Prevalence is directly related to the prevalence of tobacco smoking and, in low- and middle-income countries, the use of biomass fuels. Current estimates suggest that 80 million people world -wide suffer from moderate to severe disease. In 2005, COPD contributed to more than 3 million deaths (5% of deaths globally), but by 2020 it is forecast to represent the third most important cause of death world-wide.

copd: risk factors Tobacco smoke � Biomass solid fuel fires � Occupation: coal miners and those who work with cadmium. � Outdoor and indoor air pollution � Low birth weight � Infections: recurrent infection may accelerate decline in FEV 1 ; persistence of adenovirus in lung tissue may alter local inflammatory response predisposing to lung damage; HIV infection is associated with emphysema. �

copd: risk factors � Low socioeconomic status � Nutrition � Cannabis smoking � Genetic factors: α 1 -antiproteinase deficiency; other COPD susceptibility genes are likely to be identified. � Airway hyper-reactivity.

copd: pathophysiology The changes in pulmonary and chest wall compliance mean that collapse of intrathoracic airways during expiration is exacerbated, during exercise as the time available for expiration shortens, resulting in dynamic hyperinflation. The work of breathing is therefore markedly increased, first on exercise but, as the disease advances, at rest too. Emphysema may be classified by the pattern of the enlarged airspaces: � centriacinar, � panacinar � periacinar. Bullae form in some individuals. This results in impaired gas exchange and respiratory failure.

Copd: pathophysiology

copd: clinical features Depending on the presentation, important differential diagnoses include § chronic asthma, § tuberculosis, § bronchiectasis and § congestive cardiac failure. Cough and associated sputum production are usually the first symptoms, often referred to as a ‘smoker’s cough’. Breathlessness usually brings about the first presentation to medical attention.

Copd: MRC dyspnea scale 0 : No breathlessness except with strenuous exercise. 1 : Breathlessness when hurrying on the level or walkingup 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 100 m or after a few minutes on level ground. 4 : Too breathless to leave the house, or breathless when dressing or undressingy also be useful.

Copd: clinical features In advanced disease, the presence of oedema (which may be seen for the first time during an exacerbation) and morning headaches, which may suggest hypercapnia. Physical signs are non-specific, correlate poorly with lung function, and are seldom obvious until the disease is advanced. Breath sounds are typically quiet; crackles may accompany infection but if persistent raise the possibility of bronchiectasis. Finger clubbing is not a feature of COPD and should trigger further investigation for lung cancer, bronchiectasis or fibrosis.

Copd: clinical features The presence of pitting oedema should be documented but the frequently used term ‘cor pulmonale’ is actually a misnomer, as the right heart seldom ‘fails’ in COPD and the occurrence of oedema usually relates to failure of salt and water excretion by the hypoxic, hypercapnic kidney. The body mass index (BMI) is of prognostic significance and should be recorded. Two classical phenotypes have been described: ‘pink puffers’ and ‘blue bloaters’. The former are typically thin and breathless, and maintain a normal Pa. CO 2 until the late stage of disease. The latter develop (or tolerate) hypercapnia earlier and may develop oedema and secondary polycythaemia.

Copd: investigations chest X-ray is essential to identify alternative diagnoses such as cardiac failure, oher complications of smoking such as lung cancer, and the presence of bullae. § A full blood count is useful to exclude anaemia or document polycythaemia. § in younger patients with predominantly basal emphysema, α 1 -antiproteinase should be assayed. § spirometry and is established when the postbronchodilator FEV 1 is less than 80% of the predicted value and accompanied by FEV 1 /FVC < 70%. §

copd; : investgations § § Measurement of lung volumes provides an assessment of hyperinflation. performed by using the helium dilution technique , however, in patients with severe COPD, and in particular large bullae, body plethysmography is preferred. Exercise tests provide an objective assessment of exercise tolerance and may also be valuable when assessing prognosis. Pulse oximetry may prompt referral for a domiciliary oxygen assessment if less than 93%. HRCT as it allows the detection, characterisation and quantification of emphysema and is more sensitive than a chest X-ray at detecting bullae.

Copd:

Copd: management � Smoking cessation : Reducing the number of cigarettes smoked each day has little impact on the course and prognosis of COPD, but complete cessation is accompanied by an improvement in lung function and deceleration in the rate of FEV 1 decline. In regions where the indoor burning of biomass fuels is important, the introduction of non-smoking cooking devices or the use of alternative fuels should be encouraged.

Copd: management

Copd: management � � � Bronchodilators: Bronchodilator therapy is central to the management of breathlessness. The inhaled route is preferred and a number of different agents delivered by a variety of devices are available. Short-acting bronchodilators, such as the β 2 -agonists salbutamol and terbutaline, or the anticholinergic, ipratropium bromide, may be used for patients with mild disease. Longeracting bronchodilators, such as the β 2 -agonists salmeterol and formoterol, or the anticholinergic tiotropium bromide, are more appropriate for patients with moderate to severe disease. Oral bronchodilator therapy in patients who cannot use inhaled devices efficiently. Theophylline preparations improve breathlessness and quality of life, but their use has been limited by sideeffects, unpredictable metabolism and drug interactions. Bambuterol, a pro-drug of terbutaline, is used on occasion. Orally active highly selective phosphodiesterase inhibitors are currently under development

Copd: management � Corticosteroids Inhaled corticosteroids (ICS) reduce the frequency and severity of exacerbations; they are currently recommended in patients with severe disease (FEV 1 < 50%) who report two or more exacerbations requiring antibiotics or oral steroids per year. It is more usual to prescribe a fixed combination of an ICS with a LABA. � Oral corticosteroids are useful during exacerbations but maintenance therapy contributes to osteoporosis and impaired skeletal muscle function and should be avoided.

Copd: management Pulmonary rehabilitation: Multidisciplinary programmes that incorporate physical training, disease education and nutritional counselling reduce symptoms, improve health status and enhance confidence. � Long-term domiciliary oxygen therapy (LTOT) Arterial blood gases measured in clinically stable patients on optimal medical therapy on at least two occasions 3 weeks apart: • Pa. O 2 < 7. 3 k. Pa (55 mm. Hg) irrespective of Pa. CO 2 and FEV 1 < 1. 5 L • Pa. O 2 7. 3– 8 k. Pa (55– 60 mm. Hg) plus pulmonary hypertension, peripheral oedema or nocturnal hypoxaemia • patient stopped smoking. Use at least 15 hours/day at 2– 4 L/min to achieve a Pa. O 2 > 8 k. Pa (60 mm. Hg) without unacceptable rise in Pa. CO 2. �

Copd: management � § § § Ø Surgical intervention: Bullectomy lung volume reduction surgery (LVRS) Lung transplantation may benefit carefully selected patients with advanced disease but is limited by shortage of donor Other measures : annual influenza vaccination and, as appropriate, pneumococcal vaccination. Obesity, poor nutrition, depression and social isolation should be identified and, if possible, improved. Mucolytic therapy such as acetylcysteine, or antioxidant agents are occasionally used but with limited evidence. Palliative care: Morphine preparations may be used for palliation of breathlessness in advanced disease and benzodiazepines in low dose may reduce anxiety. Decisions regarding resuscitation should be addressed in advance of critical illness. organs.

� COPD has a variable natural history but is usually progressive. The prognosis is inversely related to age and directly related to the post-bronchodilator FEV 1. Additional poor prognostic indicators include weight loss and pulmonary hypertension. Respiratory failure, cardiac disease and lung cancer represent common modes of death.

Copd: prognosis