COPD
COPD
Pathophysiology
Ahmed Kareem
Emphysema ->
Clinical Features
-COPD should be suspected in any patient over the age of 40 years who presents with symptoms of
chronic bronchitis and/or breathlessness.
-First symptoms are chronic cough and sputum production “smoker’s cough”
-Morning headache suggests CO2 retention
-Breath sound typically quiet ( wheezes and crackles may occur )
-Finger clubbing is not a feature of COPD and should trigger further investigation for lung cancer or
fibrosis.
-Pitting edema is due to failure of salt and water excretion by the hypoxic hypercapnic kidney.
DDx
-chronic asthma
-Tb
-bronchiectasis
-congestive cardiac failure
Investigations
-CXR -> to identify alternative diagnoses ( lung cancer , congestive cardiac failure )
, and the presence of bullae
-Blood count -> to exclude anemia and polycythemia and “a1-aniproteinase” in
younger patients
-spirometry -> obstructive pattern ( FEV1/FVC < 70% )
-lung volumes -> assessment of hyperinflation
-HRCT -> detection, c tion and quantification of emphysema and is more sensitive
than a chest X-ray for detecting bullae.
Management
-Reducing exposure to noxious particles and gases
-Bronchodilators
> Short-acting bronchodilators, such as the β 2 -agonists salbutamol and terbutaline, or the
anticholinergic ipratropium bromide for mild cases.
> longer-acting bronchodilators, such as the β 2 -agonists salmeterol, formoterol and
indacaterol, or the anticholinergic tiotropium bromide in moderate and severe cases.
> Oral bronchodilator therapy may be used in patients who cannot use inhaled devices
efficiently.
Management
-Corticosteroids
>ICS reduce the frequency and severity of exacerbations, and 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 and a LABA.
> Oral corticosteroids are useful during exacerbations but maintenance therapy
contributes to osteoporosis and impaired skeletal muscle function and should be avoided.
-Pulmonary rehabilitation
> Multidisciplinary programmes that incorporate physical training, disease education and
nutritional counselling reduce symptoms, improve health status and enhance confidence.
-Oxygen therapy
> The aim of therapy is to increase the PaO 2 to at least 8 kPa (60 mmHg) or SaO 2 to at
least 90%
Management
-Surgical intervention
>bullectomy , if there is large bullae compressing the normal lung tissue with minimal
airflow limitation and no generalized emphysema
> lung volume reduction surgery (LVRS) , for predominant upper lobe emphysema with
preserved gas transfer and no evidence of P.hypertension.
Resection of the emphysematous tissue in aim to reduce hyper inflation and decrease
the work of breathing
>lung transplant may benefit carefully selected patients with advanced disease
-Other measures
> annual influenza vaccination and, as appropriate, pneumococcal
vaccination.
> Obesity, poor nutrition, depression and social isolation should be
addressed as far as possible.
> Mucolytic therapy or antioxidant agents are occasionally used but with
limited evidence.
Prognosis
-The prognosis is inversely related to age and directly related to the post-bronchodilator
FEV 1
-Weight loss and p monary hypertension are poor prognostic indicators.
Acute exacerbations of COPD
-characterised by an increase in symptoms ( beyond normal day-to-day variation ) and deterioration
in lung function and health status.
-usually triggered by bacteria, viruses or a change in air quality.
-may be accompanied by the development of respiratory failure and/ or fluid retention.
Management
-controlled oxygen therapy -> 24%-28% with the aim of m ing a PaO 2 above 8 kPa (60 mmHg) (or an
SaO 2 between 88% and 92%) without worsening acidosis.
-Nebulised short-acting β 2 -agonists, combined with an anticholinergic agent (e.g. salbutamol and
ipratropium), should be administered.
-antibiotics -> in patients with increase in sputum purulence, sputum volume or breathlessness , simple
regimens are advised, such as an aminopenicillin or a macrolide.
Co-amoxiclav is only required in regions where β-lactamase-producing organisms are known to be
common.
-NIV -> If, despite the above measures, the patient remains tachypnoeic, hypercapnic and acidotic
-Mechanical ventilation -> for reversible cause of exacerbation ( e.g. pneumonia ) or no prior history of
respiratory failure