Chronic obstructive pulmonary disease (COPD)
Chronic obstructive pulmonary disease (COPD)
D E FI N I T ION
Chronic, progressive lung disorder characterized by airflow obstruction, with
the following.
Chronic bronchitis: Chronic cough and sputum production on most days for at least 3
months per year over 2 consecutive years; and/or
Emphysema: Pathological diagnosis of permanent destructive enlargement of air spaces
distal to the terminal bronchioles.
AE T IOLOGY
Bronchial and alveolar damage as a result of environmental toxins (e.g.
cigarette smoke). A rare cause is a1-antitrypsin deficiency (<1%) but should be considered
in young patients or in those who have never smoked. Overlaps and may co-present
with asthma.
Chronic bronchitis: Narrowing of the airways resulting from bronchiole inflammation
(bronchiolitis) and bronchi with mucosal oedema, mucous hypersecretion and squamous
metaplasia.
Emphysema: Destruction and enlargement of the alveoli. This results in loss of the elastic
traction that keeps small airways open in expiration. Progressively larger spaces develop,
termed bullae (diameter is >1 cm).
E P IDEMIOLOGY
Very common (prevalence up to 8%). Presents in middle age or later.
More common in males, but likely to change with " female smokers.
H ISTORY
Chronic cough and sputum production (see Definition).
Breathlessness, wheeze, # exercise tolerance.
EXAMINA T I ON
Inspection: May have respiratory distress, use of accessory muscles, barrel-shaped overinflated
chest, # cricosternal distance, cyanosis.
Percussion: Hyper-resonant chest, loss of liver and cardiac dullness.
Auscultation: Quiet breath sounds, prolonged expiration, wheeze, rhonchi and crepitations
sometimes present.
Signs of CO2retention: Bounding pulse, warm peripheries, flapping tremor of the hands
(asterixis). In late stages, signs of right heart failure (e.g. right ventricular heave, raised JVP,
ankle oedema).
INVE S T I G A T IONS
Spirometry and pulmonary function tests: Obstructive picture as reflected by # PEFR, #
FEV1: FVC ratio (mild, 60–80%; moderate, 40–60%; severe, <40%), " lung volumes and
carbon monoxide gas transfer coefficient # when significant alveolar destruction.
CXR: May appear normal or show hyperinflation (>6 ribs visible anteriorly, flat hemidiaphragms),
# peripheral lung markings, elongated cardiac silhouette.
Blood: FBC (" Hb and PCV as a result of secondary polycythemia).
ABG: May show hypoxia (# PaO2), normal or " PaCO2.
ECG and echocardiogram: For cor pulmonale (see Cardiac failure).
Sputum and blood cultures: In acute exacerbations for treatment.
Consider a1-antitrypsin levels in young patients or minimal smoking history.
MANAGEMENT1
Stop smoking.
Bronchodilators: Short-acting b2-agonists (e.g. salbutamol) and anticholinergics (e.g. ipratropium),
delivered by inhalers or nebulizers. Long-acting bronchodilators should be used
if >2 exacerbations per year.
Steroids: Inhaled beclometasone should be considered for all with FEV1 <50% predicted or
those with >2 exacerbations per year. Regular oral steroids should be avoided but may be
necessary for maintenance.
1Refer to http://www.nice.org.uk/nicemedia/pdf/CG012_niceguideline.pdf (NICE 2004 guidelines) for
complete information.
Chronic obstructive pulmonary disease (COPD) (continued)
Pulmonary rehabilitation.
Oxygen therapy (only for those who stop smoking): Long-term home oxygen therapy has
been shown to improve mortality. Indications are:
. PaO2 < 7.3 kPa on air during a period of clinical stability.
. PaO2 7.3–8.0 kPa and signs of secondary polycythaemia, nocturnal hypoxaemia, peripheral
oedema or pulmonary hypertension.
Oxygen concentrators are more economical if being used for >8 h/day.
Treatment of acute infective exacerbations:
Provide 24% O2 via non-variable flow Venturi mask.
Increase slowly if no hypercapnia and still hypoxic (measured by ABG).
Corticosteroids (oral or inhaled) are of proven benefit.
Start empirical antibiotic therapy (follow local policy) if evidence of infection.
Respiratory physiotherapy is essential to clear sputum.
Consider non-invasive ventilation in severe cases.
Prevention of infective exacerbations: Pneumococcal and influenza vaccination.
COMPL I C A T IONS
Acute respiratory failure, infections (particularly Streptococcus pneumoniae,
Haemophilus influenzae), pulmonary hypertension and right heart failure, pneumothorax
(resulting from bullae rupture), secondary polycythaemia.
P ROGNOS I S
High level of morbidity. Three-year survival rate of 90% if age <60 years and
FEV1 >50% predicted; 75% if >60 years and FEV1 40–49% predicted.
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