COPD
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
Upper airway dysfunction
Gastro-oesophageal reflux disease (GORD)
ACE inhibitor cough
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
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
Low oxygen saturation
ABG
PaCO2 >50 mmHg and/or PaO2 of <60 mmHg suggests respiratory insufficiency
CXR
Hyperinflation
FBC
Raised haematocrit
Possible increased WBC count
ECG
Signs of right ventricular hypertrophy, arrhythmia, ischaemia
Sputum culture
Infecting organism
PFTs
Obstructive pattern
Decreased DLCO
Chest CT scan
Hyperinflation
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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