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Chronic Obstructive Pulmonary Disease (COPD)

by | 5 Apr, 2021

Introduction

Chronic Obstructive Pulmonary Disorder (COPD) is the name for a group of respiratory diseases, including emphysema and chronic bronchitis. These conditions cause a loss of alveoli and an increase in airway inflammation, leading to a progressive limitation in airflow and shortness of breath which is not fully reversible with medication.

COPD is often seen in older patients with a history of cigarette smoking or of employment in an environment with respiratory irritants, such as dust, fumes or chemicals.

Epidemiology

Approximately 2% of the UK population are diagnosed with COPD, with prevalence rising to 4.5% in those over 40. Overall prevalence within the UK population is rising, but it is predicted that a large proportion of cases remained undiagnosed.  

Causes

The symptoms of COPD are caused by an overall decline in pulmonary function from damage caused by an inflammatory response within the airway to an irritant or noxious chemical. The most common causes of this inflammatory response are:

  • Inhaled cigarette smoke
  • Inhaled dust particles (including paint particles)
  • Inhaled workplace chemicals/fumes

However, there are a number of risk factors which may increase the chances of getting COPD:

  • Older age
  • Geographical location and occupation (increased exposure to particles)
  • Asthma
  • Genetic factors (specifically, a hereditary deficiency of alpha-1 antitrypsin, an inhibitor of serum proteases)
  • History of childhood respiratory infections.

Pathophysiology

The irreversible airflow obstruction seen in COPD occurs due to structural changes within the lungs that prevent air from properly entering or leaving via the airways and inhibiting efficient gas exchange.

These structural changes are caused by an inflammatory reaction, which is triggered by inhaled noxious chemicals/particles such as cigarette smoke. Examples of the structural changes seen within the pulmonary system are listed below.

Structural changes within the airways

  • Increased numbers of immune cells, including macrophages, T lymphocytes and eosinophils – these contribute to the inflammation of the airways seen within COPD and prevent airflow by constricting the airway with inflammatory exudate.
  • Increased numbers of goblet cells – these cells produce mucus, which leads to excessive mucus production and the chronic productive cough experienced by COPD patients (called chronic bronchitis).
  • Hypertrophy of bronchial smooth muscle and connective tissue – this narrows the airways, obstructing airflow.

Structural changes within the bronchioles and alveoli

  • Increased numbers of inflammatory cells
  • Alveolar scarring and wall destruction, and abnormal enlargement of airspaces –  these features are characteristic of emphysema (a part of COPD) and impair gas exchange, leading to decreased levels of oxygen within the blood. The enlargement of airspaces traps gas within the lungs, leading to the hyperinflation visible on chest x-ray of those with COPD.
  • Dilation and destruction of bronchioles – this also impairs gas exchange.

Changes in pulmonary vasculature

  • Early changes: Endothelial cell dysfunction and thickening of vessel walls
  • Later changes: Hypertrophy of smooth muscle within the vascular walls limits blood flow to the capillary beds, which are destroyed. Blood backs up within the pulmonary vasculature due to limited flow, causing pulmonary hypertension and eventual cor pulmonale (right-sided heart failure).

Clinical features

Symptoms

The main symptom of COPD is progressively worsening shortness of breath, particularly when exercising/performing physical tasks. Other symptoms include:

  • A productive cough, often worse in the morning
  • Excessive sputum production (sputum may be green during exacerbations caused by bacterial infections)
  • A wheeze
  • A previous history of many lower respiratory tract infections

Signs

Many signs of COPD can be observed during examination. These include:

  • Tachypnoea
  • Central or peripheral cyanosis (observed as blue lips, or cold/white peripheries)
  • Visible hyperinflation of chest wall
  • Poor chest expansion when breathing
  • Hyper-resonant percussion on chest wall with no dullness in percussion of liver/heart
  • When auscultating: decreased breath sounds and a polyphonic wheeze
  • Advanced diseases can have signs of respiratory distress when breathing normally (tracheal tug, use of accessory muscles)
  • If the condition is severe, a raised JVP may be present (a sign of cor pulmonale, a complication of COPD)

Classification of COPD

COPD airflow limitation is often classified using the GOLD stages. The stages are as follows:

  • GOLD stage 1 (mild): FEV1 over 80% of predicted
  • GOLD stage 2 (moderate): FEV1 is 50-80% of predicted
  • GOLD stage 3 (severe): FEV1 is 30-50% of predicted
  • GOLD stage 4 (very severe): FEV1 is 30% of predicted

However, COPD can also be classified according to a patient’s symptoms. Breathlessness is often classified using the mMRC dyspnoea scale, which is as follows:

  • mMRC grade 0: Only breathless with strenuous exercise
  • mMRC grade 1: Breathlessness when walking fast on flat ground or walking up a hill
  • mMRC grade 2: Breathless causes slower walking on flat ground, or having to stop frequently when walking.
  • mMRC grade 3: Stopping for breath when walking 100m or after a few minutes when on flat ground
  • mMRC grade 4: Too breathless to leave the house or breathless when dressing/undressing.

An 8-item measure called the COPD Assessment Test (CAT) is also used to determine the severity of other symptoms, such as cough, sputum and energy levels.

The overall classification of the severity of COPD takes into account these measures, along with information on a patient’s comorbidities and number of exacerbation or hospitalisations in recent years.

Investigations

Blood tests

As with many investigations, a set of blood tests are carried out to rule out certain differentials, such as asthma and bronchiectasis, and gain an overall picture of a person’s health. In COPD, 2 tests are of particular importance:

  1. FBC: In COPD, the packed cell volume (PCV) is often decreased and the patient is anaemic. If a patient has more severe COPD with complications, polycythaemia (an increase in RBCs) is often observed.
  2. Arterial blood gases (ABGs): These tests show the amount of oxygen and CO2 in a patient’s blood and can be an indicator of poor gas exchange. In COPD, the partial pressure of oxygen (PaO2) in the blood is often decreased and the patients can be hypercapnic (terms ‘CO2 retainers’) due to the poor gas exchange caused by a loss of alveoli in emphysema.

Imaging

Chest x-ray: Hyperinflation of the chest is often seen on chest x-rays of COPD patients, with flattened hemidiaphragms. A decrease in peripheral vascular markings within the lungs may also be seen.

CT: A CT can reveal thickening of the bronchial wall which is an indicator of the airway inflammation caused by COPD. It can also reveal scarring of the lungs and airways, a sign of emphysema.

Spirometry

Spirometry is a series of tests which are used to measure lung volumes. It involves the patient making deep breaths into a machine, which determines certain volumes such as:

  • FEV1: Forced expiratory volume in one second – how much air a patient can expel from the lungs in one second
  • FEV: Forced vital capacity – the amount of air a patient can expel from the lungs in one breath
  • FEV1/FVC ratio: A measure of lung obstruction calculated by dividing the above two measurements.

COPD is an obstructive disorder, which means that there is difficulty in expelling air from the lungs quickly due to airway inflammation. Typical spirometry results for COPD are as follows:

  • FEV1: under 80% of predicted
  • FVC: either normal or decreased
  • FEV1/FVC: under 70% of predicted

Management

Perhaps the most crucial part of COPD management is encouraging the patient to stop smoking completely as this improves symptoms and prognosis.

Management then focuses around controlling the symptoms of COPD and preventing exacerbations. This is done through a mixture of pharmacological and lifestyle interventions, as detailed below.

Many of those with COPD are of older age and therefore may have multiple comorbidities which impact their quality of life. Managing these comorbidities can also help to improve the overall health and prognosis of a patient with COPD.

Smoking cessation

All patients should be strongly advised to stop smoking immediately. Referral to smoking cessation service or advice surrounding coping strategies should be offered, as should nicotine replacement therapy options. Where a patient is unable to stop smoking, a plan should be discussed to reduce the number of cigarettes smoked.

Vaccinations

Influenza and pneumococcal vaccinations should be offered to all patients with COPD, especially those over 65 years of age, to limit exacerbations caused by these infections.

Pulmonary rehabilitation

Pulmonary rehabilitation is a combination of exercise and educational activities which are designed to help a patient with COPD cope better with their symptoms and improve their daily functioning. The sessions are usually run in groups by an MDT, and are focused on different aspects of daily life, such as:

  • Healthy eating
  • Finding the right level of exercise for a patient
  • Breathing techniques for when a patient is feeling breathless
  • How to use inhalers/medication advice
  • Planning for an exacerbation
  • Stress management.

Pharmacological therapy

Pharmacological therapy should only be started in patients who are limited by their symptoms and are still breathless after the interventions mentioned above are implemented.

First line therapy consists of a short-acting bronchodilator, given in inhaler form to use when needed (when a patient is feeling breathless). There are 2 types of bronchodilators offered:

  • A short acting beta-agonist (e.g. salbutamol)
  • A short acting muscarinic antagonist (e.g. ipratropium)

Both of these inhalers act to relax the airway, increasing the amount of air that can pass through.

If first line therapy is unsuccessful, further treatment options depend on whether a patient has asthmatic features: history of asthma/atopy, substantial variation in FEV1, eosinophilia or diurnal variation in peak expiratory flow). Management options are as follows:

  • If patient has no asthmatic features/aren’t responsive to steroids: Offer a long acting beta agonist (LABA) and a long acting ant muscarinic antagonist (LAMA)
    • If unresponsive: Consider LABA + LAMA + an inhaled corticosteroid
  • If a patient has asthmatic features/is sensitive to steroids: Consider a LABA + an ICS
    • If unresponsive: Consider LABA + LAMA + ICS

Further specialist treatment options are available if these are unsuccessful.

Treatment considerations in CO2 retention

Due to obstructive deficits in lung function in COPD, some patients are unable to expel the CO2 within the lungs fully during expiration. As a result, the level of CO2 within the patient’s blood rises and they become ‘CO2 retainers’. These patients have high levels of CO2 in the blood (high PaCO2) and are usually hypoxic (low PaO2) but are usually not breathless as their body has adapted to this level of hypoxia.

Patients with chronic CO2 retention rely heavily on their hypoxic drive to maintain respiration. Therefore, supplemental oxygen should be given with care as giving high flow oxygen may lead to a loss of this hypoxic drive, leading the patient to deteriorate.

After exacerbations of COPD, patients should be monitored with regular arterial blood gas measurements (ABGs) to ensure that the level of CO2 in the blood returns to a safe level.

Complications

COPD exacerbations

Exacerbations are acute worsening of COPD symptoms, such as shortness of breath, which are caused by an abrupt increase in a patient’s airflow limitation. Exacerbations can be triggered by factors such as infections (viral and bacterial) or smoking, and can lead to hospitalisation.

Treatment of exacerbations focuses on increasing bronchodilator frequency, giving short course of corticosteroids (e.g. prednisolone 30mg for 7-14 days) and treating triggers. For example, antibiotics should be given cases of bacterial infections, which is suggested by the presence of purulent sputum.

The commonest bacterial organisms in COPD exacerbation are S. pneumoniae, H. influenzae and Moraxella catarrhalis. First-line empirical antibiotics for acute COPD exacerbations include:

  • Amoxicillin
  • Doxycycline
  • Clarithromycin

If a patient cannot take oral antibiotics or is severely unwell, IV agents may be used. Taking sputum cultures and discovering antibiotic sensitivities is encouraged to limit the chance of resistant infections developing.

In severe exacerbations that do not respond to the above therapies, consider the use of non-invasive ventilation. This should be particularly considered in patients that are hypercapnic, hypoxic and acidotic despite the above therapies.

Other complications

A range of complications can present in patients with severe COPD, particularly if not properly managed. These complications include:

  • Polycythaemia
  • Respiratory failure
  • Cor pulmonale: Enlargement of the right side of the heart due caused by oedema backing up in the venous system as the lungs are inefficient at absorbing fluid due to damage.
  • Lung carcinoma (particularly if the patient has a long history of cigarette smoking).

Prognosis

Prognosis of COPD is complex and is influenced by many factors, including:

  • Smoking status
  • FEV1 score
  • BMI
  • Hypoxia
  • Severity and frequency of exacerbations (including hospitalisations)
  • Severity and impact of symptoms
  • Ability to perform physical exercise
  • Comorbidities
  • Smoking status
  • If a patient is eligible for long term oxygen therapy

These factors should all be considered when determining a patient’s possible prognosis. There are only 2 treatments that can improve prognosis for a patient with COPD, there are smoking cessation and oxygen therapy.

References

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