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Chronic Obstructive Pulmonary Disease66
https://t.me/med1917
Figure 4.2 CT of a patient with COPD; the CT shows widespread emphysema.
Blood tests:
•
• FBC: May show polycythaemia secondary to persistent hypoxaemia in
severe disease.
ECG and echocardiogram:
•
• Used to determine presence of cor pulmonale.
Carbon monoxide transfer factor (T
•
• is measures the diffusion capacity of gases from the alveoli to the
capillaries.
• A reduced diffusion capacity is a feature of emphysema but can be seen
in other conditions.
Sputum culture:
•
• is can be considered if the patient presents with an infective episode.
Respiratory Medicine
Pulse oximetry:
•
• Pulse oximetry can be performed to screen patients for oxygen therapy
(see below).
lco
):
Chronic Obstructive Pulmonary Disease
https://t.me/med1917
7. DIFFERENTIAL DIAGNOSIS
Asthma (see Table 4.2)
•
Bronchiectasis
•
Lung cancer
•
Congestive cardiac failure
•
Tuberculosis
•
Interstitial lung disease.
•
Table 4.2 Differentiating between COPD and Asthma.
COPD ASTHMA
Age >35 Any age, often younger
Cough Productive, persistent Non-productive, variable
Smoking Nearly always Possible
Breathlessness Progressive Variable
Diurnal Not usual Worse at night/early in the
variability morning
Reversibility Not reversible with Reversible with inhaled
inhaled bronchodilators bronchodilators
Eczema/allergic Possible Common
rhinitis
Family history Not usual Common, as is a family history
of eczema/allergic rhinitis
67
8. MANAGEMENT
Smoking cessation:
•
• is is one of the most important components of COPD management
and should be encouraged at every opportunity (see chapter on smoking
and the lung).
Pharmacological management:
•
• Inhaled therapy (see Figure 4.1):
• Short-acting beta agonists: e.g. salbutamol, terbutaline.
• Short-acting muscarinic antagonists: e.g. ipratropium bromide (rarely
used now as long-acting drugs more effective).
• Long-acting beta agonists: e.g. salmeterol, formoterol.
• Long-acting muscarinic antagonists: e.g. tiotropium, aclidinium.
• Combination long-acting beta agonist and long-acting muscarinic
antagonists: e.g. Spioloto (tiotriopium and olodaterol), Duaklir (formoterol and aclidinium). Can improve symptoms and reduce exacerbations. Currently in use but not within present NICE algorithm.
Respiratory Medicine
Chronic Obstructive Pulmonary Disease68
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• Combination long-acting beta agonist and corticosteroid inhalers:
e.g. Seretide (salmeterol and beclamethasone) and Symbicort (formoterol and budesonide), primarily reserved for patients with increased
exacerbation frequency and reduced lung function.
• Inhaled corticosteroids are not licensed in monotherapy: use of cor-
ticosteroids are linked with increased risk of pneumonia, skin bruising,
reduced bone mineral density, oral candidiasis.
• Oral therapy:
• eophylline: a non-specific phosphodiesterase inhibitor which acts as
a bronchodilator.
– It also has an anti-inflammatory effect and increases mucociliary
clearance.
– A narrow therapeutic index, drug interactions and adverse effects
limit its use, e.g. nausea, palpitations, arrhythmias.
• Oral corticosteroids: Used for their anti-inflammatory effects.
– Little evidence to support their role in long-term use.
– Long-term steroid therapy is associated with systemic adverse effects.
• Mucolytics: Reduce the viscosity of secretions and facilitate
expectoration.
– Carbocysteine and mecysteine hydrochloride are licensed for this
use.
– For use if patients find symptomatic benefit after fixed period trial.
Pulmonary rehabilitation:
•
• Includes physical training, disease education, nutritional, psychological
and behavioural interventions.
• It should be offered to all appropriate patients.
• Not suitable for patients with recent myocardial infarction or unstable
angina, or who have locomotor difficulties that preclude exercise.
Nutrition:
•
• Patients with abnormal BMIs should be referred for dietetic advice.
• Nutritional supplementation may be required.
Long-term oxygen therapy (LTOT):
•
• Offered to patients with respiratory failure. In general decisions about
LTOT should not be made in a stable state and not immediately after
an exacerbation).
– PO
– PO
< 73. kPa
a 2
< 8 kPa and one of the following features:
a 2
◯
Secondary polycythaemia
◯
Peripheral oedema
◯
Nocturnal hypoxaemia
◯
Pulmonary hypertension.
Respiratory Medicine
Chronic Obstructive Pulmonary Disease
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Ambulatory oxygen:
•
• Offered to patients who desaturate on exertion if they are slow to
recover to baseline and if it can be shown to improve their exercise
tolerance.
Lung volume reduction (LVR):
•
• Patients with significant emphysema and hyperinflation on lung
function testing may gain improvement in breathlessness and exercise
tolerance from reducing the volume of lung tissue by “removing” the
most diseased areas of the lung. LVR can be done by surgical resection,
or by collapsing segments/lobes by occluding airways through insertion
of one way valves. Patients must have stopped smoking and completed
pulmonary rehabilitation. Specialist assessment by an LVR MDT is
required.
Non-invasive ventilation (NIV):
•
• Some patients with persistent stable hypercapnic (type 2) respiratory
failure may benefit from domiciliary NIV, which has not been shown to
reduce mortality but does appear to reduce frequency of hospital admission. It can also be used to support delivery of LTOT in such patients.
Lung transplantation:
•
• An option for younger patients who have no other major
co-morbidities.
9. COMPLICATIONS
69
Pulmonary hypertension with signs of cor pulmonale.
•
Respiratory failure.
•
10. PROGNOSIS
COPD has a variable prognosis.
•
Over time, dyspnoea and frequency of infective exacerbations increase.
•
Patients may become oxygen dependant.
•
e BODE Index (see MICRO-Facts box) is used as a measure of disease
•
severity and therefore prognosis.
MICRO-facts
The BODE Index Is a Prognostic Indicator
BMI
•
(Airflow) Obstruction
•
Dyspnoea (see Table4.2)
•
Exercise capacity
•
Respiratory Medicine
continued…
Chronic Obstructive Pulmonary Disease70
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continued…
VARIABLE POINTS
0 1 2 3
Body Mass Index >21 ≤21
Obstruction: ≥65 50–64 36–49 ≤35
(% Predicted)
FEV
1
Dyspnoea: 0–1 2 3 4
mMRC Dyspnoea Scale (see below)
Exercise Tolerance: ≥350 250–349 150–249 ≤149
6-minute walk test in metres
Negative prognostic factors:
•
• Very low weight.
• Low exercise tolerance.
• Increased breathlessness with activity.
• Frequent exacerbations.
• Requiring multiple episodes of intubation and mechanical ventilation.
Factors that improve survival:
•
• Smoking cessation.
• Oxygen supplementation.
4.1 ACUTE EXACERBATIONS OF COPD
1. RECOGNITION
Worsening dyspnoea.
•
Increased cough.
•
Increased sputum volume.
•
Change in sputum colour.
•
Increased wheeze or chest tightness.
•
Reduced exercise tolerance.
•
Increased fatigue.
•
Marked respiratory distress: tachypnoea, cyanosis, confusion, peripheral
•
oedema.
2. PATHOPHYSIOLOGY
Most often caused by acute respiratory viral/bacterial infection.
•
Similar presentation can be seen with pulmonary embolism, heart failure or
•
lung cancer.
Respiratory Medicine
4.1 Acute Exacerbations of COPD
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3. INVESTIGATIONS
FBC, U&E.
•
Pulse oximetry, and consider ABG if hypoxic.
•
Blood cultures if pyrexial.
•
CXR.
•
ECG.
•
MICRO-case
You are working in a respiratory outpatient clinic when a 64-year-old exminer comes to see you after a GP referral. As he walks into the consultation room, you notice that he’s markedly out of breath. He tells you that
for the last few years he’s been becoming gradually more out of breath
and now struggles to do his own cleaning and shopping. He cannot keep
up with friends of the same age and often stops to catch his breath when
walking alone. In addition, he has a persistent cough which brings up yellowy phlegm. In the last few years he’s had a number of chest infections
which he’s struggled to shake off. He has smoked since he was 14, which
you calculate as 50 pack-years. Spirometry reveals an FEV
0.65 and an FEV
and determine that his BMI is 19.5. You emphasise the importance of giving up smoking and commence him on inhaled therapy and recommend
that he book a GP appointment for his annual influenza vaccination. You
refer him for pulmonary rehabilitation, where he is found to be able to
walk 200m in 6 minutes. From the information you have obtained, you
calculate that his BODE index is 5.
Key Points
The BODE index is an important prognostic indicator.
•
It is scored out of 10, with a higher score associated with increased
•
mortality.
The four components are BMI, (Airflow) Obstruction, Dyspnoea and
•
Exercise capacity.
A history of smoking is the most important risk factor and one of the
•
first elements which should be addressed in managing the condition.
Influenza vaccine should be offered to those with COPD (see also
•
Chapter2: Respiratory Infections).
which is 50% of predicted. You weigh and measure him
1
/FVC ratio of
1
71
Respiratory Medicine
4. MANAGEMENT
Assess whether admission to hospital is necessary:
•
• Severe respiratory distress or poor condition.
• Unable to cope at home.
• Already on LTOT.
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• Changes on CXR.
• Impaired consciousness/confusion.
• Associated co-morbidity.
• SaOP
High-dose short-acting bronchodilators: salbutamol or ipratropium
•
bromide.
Oral steroids: prednisolone for 5–7 days.
•
Antibiotic therapy: with sputum colour change and increase in volume, or
•
signs of consolidation.
Nicotine replacement therapy: if an active smoker.
•
Oxygen therapy: in the absence of ABG results, titrate SpO2 to 88- 92%
•
initially.
Physiotherapy: helpful in some cases to aid sputum clearance; used in con-
•
junction with mucolytics such as carbocisteine or nebulised saline.
Non-invasive ventilation (NIV): if persistent hypercapnic respiratory failure
•
with acidosis.
Pulmonary rehabilitation: following recovery from the acute episode.
•
<<90%,
22
Ok77Pa,.pH < 35 .
a
Respiratory Medicine
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Lung Malignancy
5.1 PRIMARY LUNG MALIGNANCY
1. EPIDEMIOLOGY
e rate of lung cancer in men and women is 87 and 67, respectively, per
•
100, 000 per year.
It is the commonest cause of cancer related death in both men and women
•
worldwide.
• ird commonest cause of death in the UK.
• Five-year survival rate is dependent upon histology and stage of disease
but is generally poor.
e incidence of lung cancer in the UK has been declining in both men and
•
women and has been attributed to decreased rates of smoking.
Further epidemiological statistics are available at the Cancer Research UK
•
website: www.cancerresearchuk.org/health-professional/cancer-statistics/
statistics-by-cancer-type/lung-cancer
2. AETIOLOGY AND RISK FACTORS
Cigarette smoking (including passive smoking) accounts for around 70% of
•
lung cancers.
Risk factors:
•
• Tobacco smoking.
• Environmental tobacco exposure.
• Air pollution.
• Radon exposure and other forms of ionising radiation.
• Asbestos exposure.
• Occupational exposure: arsenic, nickel, chromium or petroleum
products.
• Pulmonary fibrosis.
• Chronic obstructive pulmonary disease (COPD).
• Human immunodeficiency virus (HIV)/acquired immunodeficiency
syndrome (AIDS).
DOI: 10.1201/9781315113937-6
Lung Malignancy74
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MICRO-print
Most tumours arise from the bronchi close to the hilum. As a result,
most malignancies of the lung will involve the upper lobe or main
bronchus.
3. PATHOPHYSIOLOGY
Lung cancers are usually divided histologically, into small cell lung cancer
•
(SCLC) and non-small cell lung cancer (NSCLC), and the latter can be
further subdivided. A precise histopathological diagnosis is important due to
general differences in principles of management and prognosis.
NSCLC:
•
• NSCLC accounts for 85% of primary lung malignancy and is further
divided into a number of subtypes, dependent on histological appearance and the cells of origin (Table 5.1).
• Sometimes the NSCLC subtype is well differentiated, and it is easy for
the pathologist to recognise, but often an immunohistochemical panel
will be needed to classify.
Table 5.1 Subtypes of NSCLC.
CLINICAL
TYPES % NSCLC PATHOLOGY FEATURES
Adenocarcinoma Originates from Arises peripherally.
38
Squamous cell Originates from Lesions involve the
carcinoma
(large cell lining of the bronchi. ey tend to grow
neuroendocrine Subset of neuroendo- quickly and are
carcinoma) crine lung tumours. locally invasive but
20
mucous cells in Early metastatic
bronchial epithelium. spread to bone and
Associated with brain.
asbestos exposure and
more common in
non-smokers.
squamous epithelial central airways.
Lesions are cavitating. metastasise late in
the disease course.
(Continued)
Respiratory Medicine
5.1 Primary Lung Malignancy
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Table 5.1 (continued) Subtypes of NSCLC.
CLINICAL
TYPES % NSCLC PATHOLOGY FEATURES
Carcinoid Originating from Can cause carcinoid
tumours
7
neuroendocrine syndrome. e
tissue. Often includes tumour is usually
Kulchitsky cells. extremely vascular and
prone to bleeding.
Large cell Poorly differentiated Often presents as a
5
cell, of uncertain large peripheral
histological origin, mass. High risk for
named for their excess early metastatic
cytoplasm and large spread.
nuclei. Almost a
diagnosis of exclusion
as no features of other
types of NSCLC.
Minimally Can be considered Non-invasive lesion,
invasive
<4
adenocarcinoma-in- completely curable
adenocarci- situ, re-classified in by adequate surgical
noma 2011: resection.
• Pre-invasive atypical Lesion can progress
adenomatous to a sub-type of
hyperplasia adenocarcinoma if
(pre-malignant). left untreated.
• Adenocarcinoma in
situ (AIS) <3 cm,
lacks invasion and
distribution is restricted
to alveolar structures
(so-called lepidic
growth pattern).
• Minimally invasive
AIS, displays
invasion ≤5 mm.
75
Respiratory Medicine
• ere are a small proportion of NSCLC that are unable to be identified
and classified into these main subtypes.
• Immunohistochemistry can also be used to determine if an adeno-
carcinoma has originated in the lung or metastasised from elsewhere
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