Chronic Obstructive Pulmonary Disease (COPD)
COPD is a term to describe a spectrum of pathological changes in the lung that cause obstruction of the airflow that is not reversible and is most often caused by smoking.
Pathophysiology
In some people an extrinsic trigger, most commonly smoking, causes over time a pathological change in the alveoli and in the bronchi. The changes in the alveoli are described as emphysema and the changes in the bronchi are called 'chronic bronchitis'.
There is a chronic inflammation in the lungs of people with COPD. Active Macrophages, Neutrophils and CD8+ T-cells are found in abundance around the bronchi, alveoli and in the pulmonary vasculature in such people. It is believed that the neutrophils secrete proteases as part of the inflammatory response. Normally these proteases are buffered by the production of anti-proteases. In COPD this process fails and proteases predominate. These enzymes then go on to destroy the walls of alveoli, causing adjacent alveoli to merge into each other creating giant airspaces and reducing the total surface area of the lung available for gas exchange. This leaves people with COPD prone to becoming breathless, especially when they increase their level of activity (exertional breathlessness).
One of the predominate enzymes secreted by the inflammatory cells is called elastase. Elastase breaks down the elastin within the lungs causing the lungs to lose their elastic recoil. In normal people during inspiration as the lungs expand the elastic tissue gets stretched like a rubber band, when the negative pressure of inspiration stops and a positive pressure of expiration begins, the elastic tissue snaps back to it's normal length helping to drive air out of the lungs. As this elastic recoil is lost in COPD there is less force driving air out during expiration in such patients and as such expiration becomes prolonged.
In the presence of an extrinsic irritant, usually tobacco smoke, the airways begin to hypersecrete mucus. With chronic exposure the apparatus behind mucus production (goblet cells and submucosal glands) begin to proliferate and hypertrophy. These changes occur through out the tracheobronchi tree and into the bronchiolos. The increased production of mucus into the airways reduces the size of the lumen causing obstruction of airflow. To clear the mucus the patient develops a productive cough. In a normal lung the mucus serves to trap infectious agents and irritants and move them out of the lungs via the mucociliary escalator. As ciliary function is severely impaired in smokers and the production of mucus is so overwhelming it instead acts as a breeding ground for infectious agents in COPD, it can also help to trap infectious agents in the lungs. This is why patients with COPD are prone to respiratory infections. The airways are also inflammed, the subsequent oedema and infiltration with inflammatory cells contributes to the obstruction of the airways which causes turbulent airflow which may be heard as a wheeze.
A person with COPD has giant sacs of air supported by thin, broken down walls and narrowed airways in which to pass that air through. COPD lungs find it difficult to shift all this air out during expiration due to the aforementioned lack of elasic recoil and narrowing of the airways. This air becomes trapped. The patient may becomes hypoxic and feel short of breath chronically. They may become barrel chested as their lungs become filled with air that they find difficult to expel.
Patients with COPD can also lose a lot of weight, so much so that a cancerous process is suspected at first in some patients.
Acute Exacerbation of COPD
Acute exacerbations in COPD are most often due to infections
Patients with COPD should be taught how to self-manage their exacerbation at an early stage.
- they should adjust their bronchodilator therapy for symptom relief
- be given corticosteroids to keep at home and to take only if their breathlessness begins to increase
- be given antibiotics to keep at home and take only if their sputum becomes purulent
Not all exacerbations can be self-managed though, and patients should be taught to seek medical attention if so.
Assessment
You should first illicit a Hx to judge if this is likely to be an exacerbation of their COPD. Unless the patient is severely unwell in which case proceed to ABC as always and call for help.
In the community
Hx
- Worsening of the patients breathlessness/ cough/ wheeze
- Increased production of purulent sputum
- confusion/ impaired consciousness
- Normal medications not helping with symptom relief
- If the patients level of activity has been effected
Ex
- Signs of infection (fever, sputum production)
- Signs of Respiratory Distress (cyanosis, severe breathlessness)
Investigations
- Pulse oximetry if exacerbation is severe
- Sputum culture isn't usually required in the community, nor is x-ray unless diagnosis uncertain or if the patient isn't improving on antibiotics
Management
- Increase the frequency of bronchodilator use by the patient, consider giving it via a nebuliser.
- If suspected pneumonia give antibiotics (usually amoxicillin/ macrolide/ tetracycline)
- 7-14 day oral course of 30mg prednisolone
In hospital
Hx
- Worsening of the patients breathlessness/ cough/ wheeze
- Increased production of purulent sputum
- confusion/ impaired consciousness
- Normal medications not helping with symptom relief
- If the patients level of activity has been effected
COPD
Initial assessment
Hx
COPD, like asthma, is a obstructive lung disease. As such the two disease often share features and can sometimes be difficult to distinguish.
Symptoms to ask for in the Hx to help differentiate COPD v Asthma
- Diurnal +/ day to day variability of symptoms is more common in asthma
- Night time waking with breathlessness +/ wheeze is more suggestive of asthma
- Breathlessness in COPD is persistent and progressive, in asthma it is episodic and variable
- COPD is rare <35yrs of age, asthma isn't.
Smoking should be asked about, and patients should be encouraged to stop smoking and offered access to a support programme and varenicline / bupropion / nicotine replacement therapy.
Ex
- Clubbing of the fingers
- Bounding Pulse (retained CO2)
- Co2 flap
- Breathing through pursed lips
- Use of accessory respiratory muscles
- Expiration > Inspiration
- Barrel Chested
It's also important to look for signs of cor-pulmonae. As the lung parenchyma is destroyed and more air is retained and trapped within the destroyed alveoli spaces the pressure around the pulmonary vasculature may increase causing Right Sided Heart Failure.
Ex (cor pulmonae)
- Raised JVP
- Parasternal Heave (due to RV hypertrophy)
- Hepatomegaly
- Peripheral Oedema
The patient with cor pulmonae will need further invesitgation with ECG/ pulse oximetry/ Echocardiogram. If the patient has cor pulmonae consider giving Diuretics, the need for Oxygen therapy and possible referral if severe.
Investigations
- Post-bronchodilator Spirometry. To assess the degree of airway obstruction
moderate = FEV1 50-79%
severe = FEV1 30-49%
very severe = FEV1 <30%
- CXR to exclude other diagnoses
- BMI
- MRC dyspnoea scale
1. Not troubled by breathless except on strenuous exercise
2. Short of breathe when hurrying or walking up a slight hill
3. Walks slower than contemporaries on level ground because of
breathlessness OR has to stop for breath when walking at own pace
4. Stops for breath after walking about 100m or after a few minutes
on level ground
5. Too breathless to leave the house OR
breathless while dressing/ undressing
- FBC - looking for anaemia and polycythaemia
- ABG
- Pulse Oximetry
- Carbon Monoxide Lung Transfer factor
Treatment
Breathlessness
If SABA and SAMA therapies are not reducing breathlessness to a satisfactory level consider adding a theophylline. The therapeutic dose of theophylline is close to it's toxic dose it also interacts with many drugs so it should be used with care, especially in elderly patients. The drugs it interacts with include macrolides and fluroquinolone antibiotics.
Consider Pulmonary Rehabilitation in all patients with a MRC > 3, or who consider
themselves disabled.
Chronic Productive Cough can be treated with mucolytic drugs (such as Carbocisteine / Mecysteine)
Home Oxygen Therapy
Patients with any of the following:
+ very severe airflow obstruction
+ cyanosis
+ polycythaemia
+ peripheral oedema
+ raised JVP
+ SpO2 <92% on air
should be assessed for Long Term Oxygen Therapy (LTOT). This is done by taking ABGs on two occasions three weeks apart from each other in a patient who is receiving optimal medical therapy. This is to assess their need for LTOT.
LTOT is indicated for patients have a PaO2 of <7.3kPa when stable or 7.3-8kPa when stable and they have one of the following:
+ Polycythaemia
+ Nocturnal Hypoxaemia
+ Peripheral Oedema
+ Pulmonary Hypertension
Patients on LTOT should be breathing supplemental O2 for at least 15 hours/day
There are also options to offer patients ambulatory oxygen therapy and short-burst oxygen therapies
Managing COPD is not just about treating symptoms you should also be aiming to prevent exacerbation. This can be done by
- ensuring patients get a pneumoccal vaccination and their annual flu vaccination
- optimising bronchodilator therapy
- giving advice on self-management of mild exacerbation (including providing antibiotics and steroids to keep at home in case of such exacerbations)
Patients with severe COPD should be screened for depression if appropriate.
Surgical Management
Consider referral for bullectomy when:
1. Patient is breathless
2. Single large bulla on CT scan
3. FEV1 <50% of predicted
Consider referral for lung reduction surgery when:
1. On maximum medical therapy
2. But remain breathless and the
breathless restricts
activities of daily living
3. FEV1 >20% of predicted
4. PaCO2 < 7.3kPa
5. Upperlobe predominant
emphysema
6. TlCO >20% of predicted
Some patients may also be appropriate for lung transplantation
