Definition - Progressive disease state characterised by airflow limitation that is not fully reversible.
- Suspected in patients with a history of smoking,
occupational and environmental risk factors, or a personal or family
history of chronic lung disease.
- Presents with progressive shortness of breath, wheeze, cough, and sputum production, including haemoptysis.
- Diagnostic tests include PFTs, CXR, chest CT scan, oximetry, and ABG analysis.
- Patients should be encouraged to stop smoking and be vaccinated against viral influenza and Streptococcus pneumoniae.
- Treatment options include bronchodilators, inhaled corticosteroids, and systemic corticosteroids.
- Long-term oxygen therapy improves survival in severe COPD.
Risk Factors - Cigarette smoking
- Most important risk factor. It causes 90% of cases of COPD
- Elicits an inflammatory response and causes cilia dysfunction and oxidative injury
- Advanced age
- May be related to a longer period of cigarette smoking as well as the normal age-related loss of FEV1
- Genetic factors
- Airway responsiveness to inhaled insults depends on genetic factors.
- Alpha-1 antitrypsin deficiency causes panacinar emphysema in lower lobes in young people
- White ancestry
- COPD is more common in white people
- Exposure to air pollution or occupational exposure
- Chronic exposure to dust, traffic exhaust fumes, and sulphur dioxide increases risk of COPD.
- Developmentally abnormal lung
- Frequent childhood infection may cause scarring of lungs, decrease elasticity, and increase risk for COPD
- Male gender
- COPD is more common in men, but that is probably secondary to more smokers being male
- But there is a suggestion that women may be more susceptible than men to the effects of tobacco smoke
- Low socio-economic status
- The risk for developing COPD is increased in people with lower socio-economic status
- However, this may reflect exposure to cigarette smoke, pollutants, or other factors.
Differential diagnosis Epidemiology - COPD is more common in older people, especially those >65 years
- In 2002, the WHO stated that COPD had become the fifth leading cause of death and disability worldwide
- Predicted that it would be the third most common by 2030. [4]
- Worldwide population prevalence of COPD for stages II or higher as equivalent to 10.1 ± 4.8% overall
- 11.8 ± 7.9% for men and 8.5 ± 5.8% for women. [5]
- It is the fourth leading cause of death in the US
- COPD affects 1% to 3% of white women and 4% to 6% of white men in the US
- COPD prevalence estimated to be 2% in men and 1% in women in the UK in the 1990s. [7]
Aetiology - Tobacco smoking is by far the main risk factor for COPD
- It is responsible for 90% of COPD cases
- Exerts its effect by causing an inflammatory response, cilia dysfunction, and oxidative injury
- Air pollution and occupational exposure are other common aetiologies
- Oxidative stress and an imbalance in proteinases and antiproteinases are also important factors
- Especially in patients with alpha-1 antitrypsin deficiency
Clinical features - Key features
- Presence of risk factors (e.g., smoking)
- Cough
- Shortness of breath
- Other diagnostic factors
- Barrel chest (common)
- Hyper-resonance (common)
- Distant breath sounds (common)
- Poor air movement (common)
- Wheezing (common)
- Coarse crackles (common)
- Hypoxia (common)
- Tachypnoea (uncommon)
- Asterixis (uncommon)
- Distended neck veins (uncommon)
- Lower-extremity swelling (uncommon)
- Fatigue (uncommon)
- Headache (uncommon)
- Cyanosis (uncommon)
- Loud P2 (uncommon)
- Hepatojugular reflux (uncommon)
- Hepatosplenomegaly (uncommon)
- Clubbing (uncommon)
Pathophysiology - The hallmark of COPD is chronic inflammation
- Affects central airways, peripheral airways, lung parenchyma and alveoli, and pulmonary vasculature.
- The main components of these changes are:
- narrowing and remodelling of airways
- increased number of goblet cells
- enlargement of mucus-secreting glands of the central airways
- subsequent vascular bed changes leading to pulmonary hypertension
- This is thought to lead to the pathological changes that define the clinical presentation.
- Activated macrophages, neutrophils, and leukocytes are the core cells in this process
- In contrast to asthma, eosinophils play no role in COPD, except for occasional acute exacerbations.
- In emphysema, the final outcome is elastin breakdown and subsequent loss of alveolar integrity. [8]
- In chronic bronchitis changes lead to ciliary dysfunction and increased goblet cell size and number
- Leads to the excessive mucus secretion
- Responsible for decreased airflow, hypersecretion, and chronic cough
- Increased airway resistance is the physiological definition of COPD
- Decreased elastic recoil, fibrotic changes in lung parenchyma, and luminal obstruction of airways by secretions all contribute to increased airways resistance
- Expiratory flow limitation promotes hyperinflation.
- This finding, in addition to destruction of lung parenchyma, predisposes COPD patients to hypoxia
- Progressive hypoxia causes vascular smooth muscle thickening with subsequent pulmonary hypertension
- Late development conveying a poor prognosis. [9] [10] [11]
Investigations- Spirometry
- FEV1/FVC ratio <70% with no evidence of reversibility with bronchodilator
- Total absence of reversibility is neither required nor the most typical result
- Pulse oximetry
- ABG
- PaCO2 >50 mmHg and/or PaO2 of <60 mmHg suggests respiratory insufficiency
- CXR
- FBC
- Raised haematocrit
- Possible increased WBC count
- ECG
- Signs of right ventricular hypertrophy, arrhythmia, ischaemia
- Sputum culture
- PFTs
- Obstructive pattern
- Decreased DLCO
- Chest CT scan
- Aalpha-1 antitrypsin
- Level should be normal in patients with COPD
- Exercise testing
- Poor exercise performance or exertional hypoxaemia is suggestive of advanced disease
- Ssleep study
- Elevated apnoea-hypopnoea index and/or nocturnal hypoxaemia
- Respiratory muscle function
- Reduced maximal inspiratory pressure
Management- Stage I disease
- Short-acting bronchodilator as required
- Patient education and vaccination
- Smoking cessation
- Stage II disease
- Long-acting bronchodilator
- Short-acting bronchodilator as required
- Patient education and vaccination
- Smoking cessation
- Pulmonary rehabilitation
- Stage III disease
- Long-acting bronchodilator
- Short-acting bronchodilator as required
- Patient education and vaccination
- Smoking cessation
- Inhaled corticosteroid
- Theophylline
- Pulmonary rehabilitation
- Stage IV disease
- Long-acting bronchodilator
- Short-acting bronchodilator as required
- Patient education and vaccination
- Smoking cessation
- Inhaled corticosteroid
- Theophylline
- Supplemental oxygen
- Pulmonary rehabilitation
- Surgical interventions
Prognosis- COPD is a disease with an indeterminate course and variable prognosis
- Prognosis depends on a number of factors
- Genetic predisposition
- Environmental exposures
- Comorbidities
- Acute exacerbations.
- Long-term survival is primarily influenced by the severity of COPD and the presence of comorbid conditions
- An FEV1 of less than 35% of predicted means very severe disease
- More than half of patients with very severe disease may not be expected to survive for 4 years. [1]
- In addition to the FEV1, other factors that predict prognosis are:
- Weight (very low weight is a negative prognostic factor)
- Distance walked in 6 minutes
- Degree of shortness of breath with activities
- These factors, known as the BODE index, provide information on prognosis for 1-year, 2-year, and 4-year survival. [77]
- Among different therapeutic modalities in COPD, the only 2 factors that improve survival are smoking cessation and oxygen supplementation.
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