ABC of COPD E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Serie: ABC Series
• Sprache: Englisch

Seitenzahl: 356

Veröffentlichungsjahr: 2017

Beschreibung

The third edition of the ABC of COPD provides the entire multidisciplinary team across both primary and secondary care with an up-to-date, easy to read and accessible account of this common lung disorder. Thoroughly updated by experienced clinicians dealing with patients with COPD on a regular basis, it discusses the entire breadth of the condition from epidemiology, causes, diagnosis, treatment and end of life care.   

This practical and highly visual guide contains new and extensively updated chapters on diagnosis, smoking cessation and interventional approaches as well as expanded content on non-pharmacological and pharmacological management taking into account the most recent national and international guidelines. It also explores practical issues relating to COPD in terms of pulmonary rehabilitation, oxygen use, air travel, and end of life care.

The ABC of COPD is an authoritative and essential guide for specialist nurses, general practitioners, physiotherapists, junior doctors, front line staff working in emergency departments, paramedics, physician associates and students of medicine and its allied disciplines.

Leseprobe

Table of Contents

Cover

Title Page

Contributors

Foreword

CHAPTER 1: Definition, Epidemiology and Risk Factors

Definition

Epidemiology

Risk factors

Further reading

CHAPTER 2: Pathology and Pathogenesis

Introduction

Pathology

Pathogenesis

Pathophysiology

Pathology, pathogenesis and pathophysiology of exacerbations

Further reading

CHAPTER 3: Diagnosis

Clinical features

Investigations

Further reading

CHAPTER 4: Spirometry

Introduction

What is spirometry?

Why perform spirometry?

Types of spirometer

How to perform spirometry

Spirometric indices

Other measurements

Interpretation and classification of spirograms

Bronchodilator reversibility testing

Severity of airflow obstruction in COPD

Accuracy and quality of traces

Contraindications to spirometry

Infection control

Further reading

CHAPTER 5: Smoking Cessation

Who smokes and effects of cigarette smoking

The psychology of addiction

Smoking cessation as a treatment for COPD

Helping people to quit smoking

Harm reduction

Electronic cigarettes

Further reading

CHAPTER 6: Non‐pharmacological Management

Aims of management

Smoking cessation

Pulmonary rehabilitation

Nutrition

Immunisation

Anxiety and depression

Acknowledgment

Further reading

CHAPTER 7: Pharmacological Management I –Inhaled Treatment

Physiological effects of inhaled bronchodilators

Short‐acting bronchodilators

Long‐acting bronchodilators

Long‐acting muscarinic antagonists

Long‐acting β2‐agonists

Long‐acting bronchodilator combination inhalers

Inhaled corticosteroids

Adverse effects of inhaled corticosteroids

Combined inhaled corticosteroid plus long‐acting β2‐agonist inhalers

Triple therapy

Practical considerations

Summary of inhaled treatment

References

CHAPTER 8: Pharmacological Management II – Oral Treatment

Theophylline

Phosphodiesterase inhibitors

Oral corticosteroids

Mucolytics

Long‐term antibiotics

β‐Blockers

Other drugs

Acknowledgment

References

CHAPTER 9: Drug Delivery Devices

Choosing the correct inhaler

Errors in patient inhaler technique

Teaching and checking patient inhaler technique

Different types of inhalers

Nebulisers

Further reading

CHAPTER 10: Surgical and Interventional Strategies

Lung volume reduction strategies

Surgical lung volume reduction approaches

Bronchoscopic lung volume reduction strategies

Biological lung volume reduction

Endobronchial and extrapulmonary bypass procedures

Lung transplantation

Summary

Further reading

CHAPTER 11: Oxygen

Oxygen physiology

Pulse oximetry

Oxygen during exacerbations of COPD

Prehospital oxygen

Hospital oxygen

Long‐term oxygen therapy

Ambulatory oxygen

Short‐burst oxygen

Air travel and oxygen

Further reading

CHAPTER 12: Exacerbations

Definition

Mechanism

Clinical features

Aetiology

Impact

Investigations

Management

Aminophylline

General hospital care

Frequent exacerbations

Prevention of exacerbations

Further reading

CHAPTER 13: Ventilatory Support

Why is non‐invasive ventilation useful?

Which patients with COPD should receive non‐invasive ventilation?

How non‐invasive ventilation works

Outcomes of non‐invasive ventilation

Setting

How to use non‐invasive ventilation

Monitoring non‐invasive ventilation

Other measures

Problems with non‐invasive ventilation

Domiciliary non‐invasive ventilation

Invasive mechanical ventilation

Ventilator strategies

Further reading

CHAPTER 14: Primary Care

Quality Outcomes Framework

Identification of patients

Spirometry

Follow‐up of stable COPD in the community

Organisation of care at a practice level

National strategy

Smoking cessation

Referral for specialist opinion

Management of stable disease

Management of acute exacerbations

Further reading

CHAPTER 15: Death, Dying and End‐of‐Life Issues

When do patients enter a palliative phase?

Maintaining quality of life

Symptom control

Breathlessness

Non‐drug approaches

Fatigue

Depression and anxiety

Pain

Advance care planning

Advance refusal of treatment

Do not attempt cardiopulmonary resuscitation decisions

Ways to engage patients in end‐of‐life discussions

End‐of‐life care

Further reading

CHAPTER 16: Future Treatments

The continuing challenge of drug development

New bronchodilators

More effective smoking cessation strategies

Treating pulmonary inflammation

Mediator antagonists

Protease inhibitors

New anti‐inflammatory treatments

Lung repair

Route of delivery

Targeted lung denervation

Further reading

Index

End User License Agreement

List of Tables

Chapter 03

Table 3.1 Modified Medical Research Council breathlessness scale.

Table 3.2 Causes of a chronic (lasting >8 weeks) cough.

Table 3.3 World Health Organization classification of body mass index (BMI) and nutritional status.

Table 3.4 Calculation of the BODE index.

Table 3.5 Conditions in the differential diagnosis of COPD.

Table 3.6 Clinical differences between COPD and asthma.

Table 3.7 Secondary polycythaemia in a male with advanced hypoxic chronic obstructive pulmonary disease. Typically, blood parameters demonstrate an increase in haemoglobin concentration accompanied by an elevated red cell count and haematocrit. This patient had an elevated white cell count (neutrophilia) due to high‐dose oral corticosteroids.

Chapter 04

Table 4.1 Causes of obstructive and restrictive spirometry.

Table 4.2 Typical features of normal, obstructive, restrictive and mixed obstructive/restrictive spirometry.

Table 4.3 Classification of the severity of airway obstruction according to the National Institute for Health and Care Excellence, American Thoracic Society/European Respiratory Society and Global Initiative for Chronic Obstructive Lung Disease.

Table 4.4 Summary of contraindications and the main reasons to avoid testing.

Chapter 05

Table 5.1 Cancers, chronic diseases and miscellaneous conditions caused or adversely influenced by cigarette smoking.

Table 5.2 Possible advantages and disadvantages of e‐cigarettes.

Chapter 06

Table 6.1 Different techniques which may reduce breathlessness and allow more efficient ventilation.

Chapter 07

Table 7.1 Properties of short acting β

2

‐agonists.

Table 7.2 Characteristics of long‐acting bronchodilator monotherapy inhalers.

Table 7.3 Characteristics of long‐acting bronchodilator combination inhalers.

Table 7.4 Characteristics of inhaled corticosteroid and long‐acting β

2

‐agonist combination inhalers.

Table 7.5 Relative effects of the main classes of inhaled drugs on important endpoints, both individually and combined, when used in chronic obstructive pulmonary disease.

Chapter 09

Table 9.1 Common errors with pMDIs and DPIs.

Table 9.2 Advantages and disadvantages of different types of inhaler devices.

Table 9.3 Features of different inhaler devices available for COPD patients.

Chapter 10

Table 10.1 Characteristic of patients likely to benefit and not benefit from surgical lung volume reduction surgery.

Table 10.2 Bronchoscopic lung volume reduction methods, indications and mechanisms of action.

Table 10.3 Early and late complications following lung transplantation.

Chapter 11

Table 11.1 Situations where measurement of SpO

2

with a pulse oximeter can lead to erroneous readings.

Table 11.2 Advice regarding necessity of in‐flight oxygen in commercial aircraft.

Chapter 12

Table 12.1 Arterial blood gas features of type 1 and type 2 respiratory failure.

Chapter 13

Table 13.1 Problems associated with NIV and potential solutions.

Table 13.2 Complications of invasive mechanical ventilation.

Chapter 14

Table 14.1 Factors to consider when deciding where to most suitably manage a patient with an acute exacerbation of COPD.

Chapter 15

Table 15.1 Predictors of poor prognosis.

Table 15.2 Some of the factors which influence quality of life.

Chapter 16

Table 16.1 Mediator antagonists for potential use in COPD.

Table 16.2 Protease inhibitors for potential use in COPD.

List of Illustrations

Chapter 01

Figure 1.1 Known cases of COPD may represent only the ‘tip of the iceberg’ with many cases currently undiagnosed.

Figure 1.2 Lifetime prevalence of diagnosed COPD in males and females (per 1000) resident in England 2001–2005.

Figure 1.3 Prevalence (per 1000) of diagnosed COPD in UK men (▪) and women (●) grouped by age, between 1990 and 1997.

Figure 1.4 Prevalence of COPD confirmed by spirometry in a Finnish National Survey: association with metrics of socioeconomic status.

Figure 1.5 Prevalence of diagnosed COPD in UK men and women (per 1000) between 1990 and 1997.

Figure 1.6 UK death rates from COPD since 1971. Mortality age‐standardised rates per million. based on the European Standard Population.

Figure 1.7 UK deaths from COPD (per 1000 person‐years) by age and severity of COPD.

Figure 1.8 COPD mortality in the United States of America, 1999–2010, expressed as standardised mortality per million.

Figure 1.9 An analysis of the direct costs of COPD to the NHS. A&E, accident and emergency; GP, general practitioner.

Figure 1.10 This patient (with minimal smoking history) was found to have chronic obstructive pulmonary disease, with his occupation (coal miner) being the main risk factor. The image shows coal dust tattoos on his back.

Chapter 02

Figure 2.1 (a) A central bronchus from a cigarette smoker with normal lung function. Very small amounts of muscle and small epithelial glands are shown. (b) Bronchial wall from a patient with chronic bronchitis showing a thick bundle of muscle and enlarged glands. (c) A higher magnification of the enlarged glands from (b) showing chronic inflammation involving polymorphonuclear (

arrowhead

) and mononuclear cells, including plasma cells (

arrow

). Printed with kind permission from J.C. Hogg and S. Green. (d) Scanning electron micrograph of airway from a normal individual showing flakes of mucus overlying the cilia. (e) Scanning electron micrograph of a bronchial wall in a patient with chronic bronchitis. Cilia are covered with a blanket of mucus.

Figure 2.2 (a) Paper‐mounted whole lung section of a normal lung. (b) Paper‐mounted whole lung section from a lung with severe centrilobular emphysema. Note that the centrilobular form is more extensive in the upper regions of the lung. (c) Histological section of a normal small airway and surrounding alveoli connecting with attached alveolar walls. (d) Histological section showing emphysema with enlarged alveolar spaces, loss of alveolar walls and alveolar attachments and collapsed airway.

Figure 2.3 Histological sections of peripheral airways. (a) Section from a cigarette smoker with normal lung function showing a nearly normal airway with small numbers of inflammatory cells. (b) Section from a patient with small airway disease showing inflammatory exudate in the wall and lumen of the airway. (c) Section showing more advanced small airway disease, with reduced lumen causing structural reorganisation of the airway wall, increased smooth muscle and deposition of peribronchial connective tissue.

Figure 2.4 Overview of the pathogenesis of COPD. Cigarette smoke activates macrophages in epithelial cells to produce chemotactic factors that recruit neutrophils and CD8 cells from the circulation. These cells release factors which activate fibroblasts, resulting in abnormal repair processes and bronchiolar fibrosis. An imbalance between proteases released from neutrophils and macrophages and antiproteases leads to alveolar wall destruction (emphysema). Proteases also stimulate the release of mucus. An increased oxidant burden resulting from smoke inhalation or release of oxidants from inflammatory leucocytes causes epithelial and other cells to release chemotactic factors, inactivates antiproteases and directly injures alveolar walls and causes mucus secretion. Several processes are involved in amplifying the inflammatory responses in COPD. TGF‐β, transforming growth factor‐β; CTG, connective tissue growth factor.

Figure 2.5 The development of pulmonary hypertension in COPD.

Chapter 03

Figure 3.1 A patient with advanced hypoxic chronic obstructive pulmonary disease with central cyanosis.

Figure 3.2 Pitting ankle oedema is a feature of cor pulmonale; consider other causes or contributory factors such as oral corticosteroids, calcium channel antagonists, excessive intravenous fluid administration, hypoalbumenaemia or dependant oedema.

Figure 3.3 A patient with tar staining and finger clubbing; chronic obstructive pulmonary disease and non‐small cell lung cancer were both diagnosed in this patient.

Figure 3.4 A right‐handed patient with gross tar staining of the fingers due to chronic cigarette smoking.

Figure 3.5 Whole‐body plethysmography, performed in a rigid chamber of comparable size and shape to a telephone booth, can be used to measure lung volumes.

Figure 3.6 Chest radiograph showing typical changes of advanced COPD (>6 ends of anterior rib visible, flat diaphragms, increased translucency of lung fields and ‘squared‐off’ lung apices).

Figure 3.7 High‐resolution computed tomogram of the chest showing widespread upper lobe emphysematous bullae in a patient with advanced COPD.

Figure 3.8 Electrocardiogram showing typical changes in a patient with cor pulmonale (p‐pulmonale, right axis deviation, partial right bundle branch block).

Chapter 04

Figure 4.1 A wedge bellows spirometer being calibrated.

Figure 4.2 A desktop spirometer.

Figure 4.3 A hand‐held spirometer.

Figure 4.4 Some hand‐held spirometers can deliver results directly to computers.

Figure 4.5 (a) A normal volume/time curve should rise rapidly and smoothly, and in healthy individuals, plateau within 3–4 seconds. A normal flow/volume curve will have a rapid rise to maximal expiratory flow (peak flow) followed by an almost linear uniform decline in flow until all air is exhaled, giving a triangular appearance. (b) Typical volume/time and flow/volume curves in airflow obstruction. Note the reduced forced expiratory volume in 1 second (FEV

1

) and reduced forced vital capacity (FVC) (indicated in green) in the patient compared to the normal curve. FVC is only recorded for 6 seconds; a longer duration may be required to reach plateau in volume in a patient such as this. A concave dip in the flow/volume curve is evident, which becomes more marked with increasing obstruction. (c) Typical volume/time and flow/volume curves in more severe airflow obstruction. Note that both the FEV

1

and FVC are reduced below normal curve (although the former more than the latter). FEV

1

(shown in green) is less than in (b). Due to loss of airway elasticity, airways collapse during forced exhalation and a characteristic sudden fall in flow occurs after maximal expiratory flow is reached – a so‐called steeple curve. With increasing degrees of airflow obstruction, it takes longer to completely exhale (i.e. reach residual volume) – sometimes up to 15 seconds – and the upward slope (gradient) of the volume/time curve is less and a longer time is taken to reach plateau. (d) Typical volume/time and flow/volume curves with a restrictive ventilatory defect. The shape of the flow/volume curve is normal but a reduction in lung volume is apparent which shifts the FVC point to the left compared with the predicted curve. Note that both the FEV

1

and FVC can be proportionally reduced or the FEV

1

can be affected to a lesser extent, leading the FEVR to be normal or above normal. (e) Typical volume/time and flow/volume curves with a mixed obstructive and restrictive ventilatory defect. Note that both the FEV

1

and FVC are disproportionately reduced.

Figure 4.6 (a)

Problem:

Poor spirometry trace due to a ‘slow’ start. An adequate duration (6 seconds) is evident and a plateau reached, meaning that VC is probably accurate but FEV

1

and peak flow are likely to be underestimated.

Solution:

Repeat the test and encourage a maximal effort at the initial ‘blast’. Ensure patient has taken a maximal inspiration prior to the start of the FVC manoeuvre. (b)

Problem:

Poor spirometry trace due to inconsistent/suboptimal effort and a slow start; expiratory flow is interrupted (usually by cough or inhaling then continuing to breathe out).

Solution:

Repeat test and advise the patient to continue to ‘breathe out’ in one continuous breath. (c)

Problem:

Poor spirometry trace due to an ‘early finish’; patient has stopped exhaling after about 2 seconds, before RV is reached: a good effort initially occurs but a plateau is not reached, duration is less than 6 seconds and FVC will be underestimated.

Solution:

Advise the patient to ‘blow out’ until ‘lungs are empty’. (d)

Problem:

Cough interrupting expiratory flow.

Solution:

Repeat the test once cough has settled. (e)

Problem:

No plateau. If no plateau is reached in 6 seconds, as in (i) repeat the test and advise patient to continue to ‘breathe out’ for 12 seconds (or as long as possible). If plateau still not achieved (as in ii), this should be noted when presenting the FVC value. In spirometers that only measure 6 seconds, this can be termed FEV

6

(forced expiratory value in 6 seconds).

Chapter 05

Figure 5.1 King James I of England.

Figure 5.2 Proportion of population who smoke cigarettes, by sex, Great Britain 1974–2013.

Figure 5.3 Proportion who smoke cigarettes, by income band, Great Britain, 2013.

Figure 5.4 Proportion who smoke cigarettes, by age, Great Britain, 1974–2013.

Figure 5.5 Differences in rates of smoking within Great Britain.

Figure 5.6 Cigarette smokers as a proportion of the population fell by over 50% between 1974 and 2013.

Figure 5.7 Beneficial effects of smoking cessation occur at any age. FEV

1

, forced expiratory volume in 1 second.

Figure 5.8 Triggers reported as prompting the most recent quit attempt. HP, health professional.

Figure 5.9 Illustration of the typical components of a ‘first‐generation’ e‐cigarette.

Figure 5.10 Key moments in the growth of the e‐cigarette market. Source: Office for National Statistics licensed under Open Government Licence v.3.0.

Figure 5.11 Proportion of individuals who use e‐cigarettes, by cigarette smoking status. Source: Office for National Statistics licensed under Open Government Licence v.3.0.

Chapter 06

Figure 6.1 Multidisciplinary team input is required for most patients with COPD.

Figure 6.2 An individualised approach to treatment should be explored when encountering patients with chronic obstructive pulmonary disease of any severity.

Figure 6.3 A determined attempt should be made to break the vicious circle of worsening breathlessness, reduced physical activity and deconditioning.

Figure 6.4 Encourage patients to adopt different positions which use less energy and may help reduce work of breathing.

Figure 6.5 Different walking aids may help patients conserve energy and promote safer movement.

Figure 6.6 Electron micrograph showing influenza viruses (

red

) budding from a host cell.

Figure 6.7 Trends in vaccination rates against influenza in patients aged >40 years with chronic obstructive pulmonary disease.

Figure 6.8 Trends in vaccination rates against pneumonia in patients aged >40 years with chronic obstructive pulmonary disease.

Chapter 07

Figure 7.1 Patients with COPD often have pulmonary hyperinflation with an increased functional residual capacity (

purple

) and decreased inspiratory capacity (

white

). This increases the volume at which tidal breathing (

oscillating line

) occurs and places the muscles of respiration at mechanical disadvantage. Hyperinflation worsens with exercise and therefore reduces exercise tolerance (dynamic hyperinflation). Inhaled bronchodilators reduce dynamic hyperinflation, in addition to hyperinflation at rest, thereby reducing the work of breathing and increasing exercise tolerance.

Figure 7.2 Effects of add‐on tiotropium on mean pre‐ and postbronchodilator forced expiratory volume in 1 second (FEV

1

) (a) and forced vital capacity (FVC) (b) in patients with less advanced COPD.

Figure 7.3 Inhaled corticosteroids have not been shown to influence the rate of decline in lung function in COPD. In this study of patients with mild COPD, no difference in mean change in baseline forced expiratory volume in 1 second (FEV

1

) between placebo and budesonide was observed over 36 months.

Figure 7.4 Extensive skin bruising in a patient with COPD using long‐term high‐dose inhaled corticosteroids.

Figure 7.5 Trough forced expiratory volume in 1 second (FEV

1

) at weeks 4, 8 and 12 (full analysis set). Comparable outcomes for glycopyrronium versus tiotropium (i.e. non‐inferiority) were also demonstrated for all other outcome measures (health status, rescue medication use, nocturnal symptoms and activity performance). FP, fluticasone propionate; SAL, salmeterol.

Figure 7.6 The main pharmacological prescribing steps for inhaled treatment in patients with chronic obstructive pulmonary disease.

Chapter 08

Figure 8.1 Chemical structures of (a) caffeine and (b) theophylline are similar.

Figure 8.2 A variety of long‐acting theophylline preparations are available and are usually given to patients in modified‐release preparations.

Figure 8.3 Adverse effects of oral corticosteroids.

Figure 8.4 Patients receiving frequent courses of, or maintained on, long‐term oral corticosteroids should be aware of the risks of osteoporosis. Such patients should ensure an adequate intake of dietary calcium and be encouraged to exercise. Postmenopausal women should consider using hormone replacement therapy.

Figure 8.5 Lateral thoracic spine X‐ray showing osteopenia and an osteoporotic vertebral collapse in a patient using long‐term oral corticosteroids; this elderly patient was not using a bisphosphonate.

Figure 8.6 All patients receiving oral corticosteroids should carry a treatment card at all times.

Figure 8.7 Kaplan–Meier estimate of probability of survival among patients with COPD by use of β‐blockers.

Chapter 09

Figure 9.1 Only a small amount of the drug leaving a metered dose inhaler reaches the lungs.

Figure 9.2 A pressurised metered dose inhaler.

Figure 9.3 A Haleraid.

Figure 9.4 A metered dose inhaler with spacer.

Figure 9.5 Oropharyngeal candidiasis in a patient incorrectly using a pMDI containing high‐dose inhaled corticosteroids.

Figure 9.6 An Easibreathe inhaler.

Figure 9.7 An Autohaler.

Figure 9.8 Respimat soft mist inhalers.

Figure 9.9 An Accuhaler.

Figure 9.10 A Turbohaler.

Figure 9.11 A Handihaler.

Figure 9.12 A Breezhaler.

Figure 9.13 An Ellipta.

Figure 9.14 A Genuair.

Figure 9.15 A Spiromax.

Figure 9.16 A Nexthaler.

Chapter 10

Figure 10.1 A large right‐sided lung bulla in a patient with chronic obstructive pulmonary disease.

Figure 10.2 An endobronchial valve.

Figure 10.3 Illustration of the functional properties of an endobronchial valve

in situ

on expiration and inspiration.

Figure 10.4 An endobronchial coil.

Figure 10.5 Number of transplants according to transplant year for different indications. Abbreviations: CF: cystic fibrosis, IPF: idiopathic pulmonary fibrosis, COPD: chronic obstructive pulmonary disease, Alpha‐1: Alpha‐1 antitrypsin deficiency, IPAH: idiopathic pulmonary arterial hypertension, Retx: retransplantation.

Figure 10.6 Increasing trend for bilateral lung transplantation, compared to single lung transplantion for different indications including α1‐antitrypsin deficiency (a‐ATDef COPD), chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF) and idiopathic pulmonary arterial hypertension (iPAH).

Figure 10.7 Life expectancy post transplant for different indications. Abbreviations: Alpha‐1: Alpha‐1 antitrypsin deficiency, CF: cystic fibrosis, COPD: chronic obstructive pulmonary disease, IPF: idiopathic pulmonary fibrosis, IPAH: idiopathic pulmonary arterial hypertension.

Chapter 11

Figure 11.1 The oxygen dissociation curve.

Figure 11.2 A pulse oximeter.

Figure 11.3 An example of an oxygen alert card.

Figure 11.4 A range of Venturi valves are available to deliver specific concentrations of oxygen at a given flow rate (24%, 28%, 35% and 40% are shown).

Figure 11.5 A Venturi valve plus mask mixes 100% oxygen at a given flow rate with room air (determined by the size of the ports in the valve). This produces a predictable concentration of oxygen in the facemask which is then delivered to the patient.

Figure 11.6 Delivering oxygen through nasal cannulae enables patients to eat, drink and communicate more easily than with a full facemask.

Figure 11.7 A concentrator is the most convenient way to supply long‐term oxygen to patients at home. A contractor supplies all oxygen in the UK. A prescription is sent from the specialist home oxygen assessment team requesting installation of appropriate equipment.

Figure 11.8 Most patients prescribed LTOT can perform daily living activities within their home providing they have sufficiently long oxygen tubing and use nasal cannulae.

Figure 11.9 An example of a homefill cylinder and compressor.

Figure 11.10 Liquid oxygen is provided in a smaller container compared to conventional oxygen cylinders; a range of differently sized flasks are available.

Figure 11.11 Factsheets along with other sources of information (such as https://www.caa.co.uk/Passengers/Before‐you‐fly/Am‐I‐fit‐to‐fly‐/) can be accessed which provide support and practical help for individuals with respiratory‐related (and other) disabilities planning to travel by aircraft.

Chapter 12

Figure 12.1 Mechanism for acute exacerbations in COPD. Triggers of COPD exacerbations include infectious agents such as bacteria and viruses and non‐infectious agents such as air pollution. These stimuli activate airway epithelial cells and macrophages to release inflammatory cytokines including tumor necrosis factor‐α (TNF‐α), interleukin (IL)‐8 and IL‐6. These cytokines lead to neutrophil recruitment and the release of reactive oxidant species and proteases from activated neutrophils, which magnify the inflammatory process.

Figure 12.2 The non‐normal distribution of exacerbations of COPD within a population.

Figure 12.3 Nebulised bronchodilators are frequently given during an exacerbation of COPD.

Figure 12.4 Difference in forced expiratory volume in 1 second (FEV

1

) with oral corticosteroids compared to placebo in patients admitted with an exacerbation of COPD.

Figure 12.5 Antibiotics are generally most effective when patients have increased breathlessness along with greater sputum volume and purulence.

Chapter 13

Figure 13.1 A typical non‐invasive ventilation (NIV) machine can be easily used at the patient’s bedside.

Figure 13.2 An NIV hood can be used in patients intolerant of either a full face or nasal mask.

Figure 13.3 Frequent monitoring of arterial blood gases is required in patients using NIV. This should be performed prior to starting NIV and 1 and 4–6 hours afterwards; it should also be checked within an hour of changing settings. An arterial line is often a more convenient way by which to obtain regular blood gas measurements, especially if it is felt likely that NIV will be required for a prolonged period of time.

Figure 13.4 Patients being treated with NIV can easily become dehydrated and undernourished; adequate hydration and nutrition should not be forgotten in overall management.

Figure 13.5 Severe nasal bridge ulceration in a patient who required NIV for a prolonged period of time. As this problem may arise in up to 10% of patients receiving NIV, facemasks should not be tightened excessively.

Figure 13.6 Fashioning of a tracheostomy can help the weaning process; it can be left

in situ

for days, weeks or even months. It is usually well tolerated, although complications such as bleeding, infection, blockage, displacement or, less commonly, dysphagia, laryngeal damage, pneumothorax, tracheal stenosis, tracheomalacia or tracheo‐oesophageal fistula may occur.

Chapter 14

Figure 14.1 Good‐quality spirometry recordings and their interpretation can only be obtained by regular training and updates, delivered by suitably trained professional staff.

Figure 14.2 All patients should receive written education about COPD and the management strategies involved.

Figure 14.3 Estimated number of patients in Scotland consulting a GP or practice nurse for COPD at least once in the financial year 2012–2013 per 1000 patients registered, by gender and age.

Figure 14.4 Estimated number of consultations with a GP or practice‐employed nurse for COPD in Scotland in the financial years 2003–2004 to 2012–2013, by staff discipline.

Figure 14.5 Simple structured plan for assessing readiness for an attempt to stop smoking.

Chapter 15

Figure 15.1 Typical disease trajectories in patients with COPD, lung cancer and dementia/general frailty.

Figure 15.2 Limbic and higher cognitive factors interact to influence the perception of breathlessness.

Figure 15.3 Distractions, pleasurable and stimulating activities and a calm, relaxing environment can improve quality of life in those with advanced COPD.

Figure 15.4 An open window or bedside fan can help reduce the sensation of breathlessness; a fan blowing air across the face may be of even greater benefit.

Figure 15.5 Focusing on longer ‘outbreaths’ can reduce breathlessness and panic.

Figure 15.6 Opioids and benzodiazepines can influence the limbic and higher cognitive factors that contribute to the perception of breathlessness.

Figure 15.7 Hot/cold pads and TENS machines are useful adjuvants for pain control.

Figure 15.8 World Health Organization three‐step analgesic ladder. Examples of non‐opioids include paracetamol and non‐steroidal anti‐inflammatory drugs, weak opioids include codeine and tramadol, strong opioids include morphine, oxycodone and fentanyl. Adjuvants include other drugs to help with pain management such as those used for neuropathic pain and those used to counteract adverse effects.

Chapter 16

Figure 16.1 Postbronchodilator FEV

1

in patients treated with roflumilast versus placebo over 52 weeks.

Figure 16.2 Mean rate of severe exacerbations or exacerbations leading to hospital admission per patient per year. Rate ratios, 95% confidence intervals (CIs) and p values are based on a negative binomial regression model excluding a correction for overdispersion.

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ABC of COPD

Third Edition

EDITED BY

Graeme P. Currie

Aberdeen Royal InfirmaryAberdeen, UK

This third edition first published 2017 © 2017 by John Wiley & Sons Ltd

Edition HistoryJohn Wiley & Sons Ltd (2e, 2010)

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Library of Congress Cataloging‐in‐Publication Data

Name: Currie, Graeme P., editor.Title: ABC of COPD / [edited] by Dr Graeme P. Currie.Description: Third edition. | Hoboken, NJ : Wiley, 2017. | Series: ABC series | Includes index. |Identifiers: LCCN 2017014503 (print) | LCCN 2017015850 (ebook) | ISBN 9781119212805 (pdf) | ISBN 9781119212812 (epub) | ISBN 9781119212850 (pbk.)Subjects: | MESH: Pulmonary Disease, Chronic ObstructiveClassification: LCC RC776.O3 (ebook) | LCC RC776.O3 (print) | NLM WF 600 | DDC 616.2/4–dc23LC record available at https://lccn.loc.gov/2017014503

Cover design: WileyCover image: © gmutlu/Gettyimages

Contributors

Sanjay AgrawalConsultant in Respiratory and Intensive Care MedicineRespiratory Biomedical Research UnitInstitute of Lung HealthGlenfield Hospital, Leicester, UK

Peter J. BarnesMargaret Turner‐Warwick Professor of MedicineHead of Respiratory MedicineAirway Disease SectionNational Heart and Lung InstituteImperial CollegeLondon, UK

John R. BrittonProfessor of EpidemiologyUK Centre for Tobacco Control StudiesUniversity of Nottingham;Consultant in RespiratoryMedicineCity HospitalNottingham, UK

Mahendran ChettyConsultant in Respiratory MedicineChest Clinic C, Aberdeen Royal InfirmaryAberdeen, Scotland, UK

Graeme P. CurrieConsultant in Respiratory MedicineChest Clinic C, Aberdeen Royal InfirmaryAberdeen, Scotland, UK

Graham S. DevereuxConsultant in Respiratory MedicineChest Clinic C, Aberdeen Royal InfirmaryAberdeen, Scotland, UK

Graham DouglasRetired Consultant in Respiratory MedicineChest Clinic C, Aberdeen Royal InfirmaryAberdeen, Scotland, UK

Claire FotheringhamPrincipal Clinical Respiratory PhysiologistPulmonary Function DepartmentAberdeen Royal InfirmaryAberdeen, Scotland, UK

Cathy JacksonHead of SchoolSchool of MedicineUniversity of Central LancashirePreston, UK

Gordon LinklaterConsultant in Palliative MedicineHighland HospiceInverness, Scotland, UK

Brian J. LipworthConsultant in Respiratory MedicineScottish Centre for Respiratory ResearchNinewells Hospital and Medical SchoolDundee, Scotland, UK

James L. LordanConsultant Respiratory and Lung Transplant PhysicianFreeman HospitalUniversity of Newcastle‐upon‐TyneNewcastle‐upon‐Tyne, UK

Margaret MacleodSenior Respiratory PhysiotherapistChest Clinic C, Aberdeen Royal InfirmaryAberdeen, Scotland, UK

William MacNeeProfessor of Respiratory and Environmental MedicineMRC Centre for Inflammation ResearchQueen’s Medical Research InstituteUniversity of EdinburghEdinburgh, Scotland, UK

David R. MillerConsultant in Respiratory MedicineChest Clinic C, Aberdeen Royal InfirmaryAberdeen, Scotland, UK

Paul K. PlantConsultant Chest Physician and Clinical Director for Respiratory ServicesNorth Cumbria University Hospitals NHS TrustCarlisle, UK

Roberto A. RabinovichSenior Clinical Research FellowMRC Centre for Inflammation ResearchQueen’s Medical Research InstituteUniversity of EdinburghEdinburgh, Scotland, UK

Morag ReillyPrimary Care Respiratory NurseAberdeen City Health and Social Care Community PartnershipAberdeen, Scotland, UK

Waleed SalihSpecialist Registrar in Respiratory MedicineNinewells Hospital and Medical SchoolDundee, Scotland, UK

Stuart SchembriConsultant in Respiratory MedicineNinewells Hospital and Medical SchoolDundee, Scotland, UK

Stephen StottConsultant IntensivistAberdeen Royal InfirmaryAberdeen, Scotland, UK

Foreword

Chronic obstructive pulmonary disease (COPD) continues to be a major global health problem. It is the fourth most common cause of death globally, and in industrialised countries like the UK, has now risen to the third most common cause of death. In the UK, the mortality from COPD in women now well exceeds that of breast cancer. COPD is also the fifth most common cause of chronic disability, increasing because of more prevalent cigarette smoking in developing countries and, most importantly, because of a rapidly ageing population. COPD now affects approximately 10% of individuals over 40 years and is equally common in women, reflecting the lack of gender difference in smoking. Acute exacerbations of COPD remain one of the most common causes of hospital admission. Because of this, COPD has an increasing economic impact, and healthcare costs now exceed those of asthma many times.

Despite these startling statistics, COPD has been relatively neglected and is still greatly underdiagnosed in general practice, where spirometry, needed to establish the diagnosis, is still very underused. This is in marked contrast to asthma which is now recognised and well managed in the community.

There are highly effective medications available for asthma which have transformed patients’ lives. Sadly, this is not the case in COPD where treatments are less effective while no treatment has so far been shown to slow the relentless progression of the disease. However, important advances have been made in understanding the underlying disease and in managing patients with COPD. Of particular importance has been the introduction of several new long‐acting bronchodilators (β‐agonists and muscarinic antagonists) and their combinations, which have been found to be the most effective way to reduce symptoms and prevent exacerbations, particularly in those with severe disease.

In this new edition of the ABC series on COPD, Graeme Currie and colleagues provide an update on diagnosis, pathophysiology and modern management of COPD. There have been important advances since the first edition of the book over 10 years ago. Once the disease is recognised, pharmacological and non‐pharmacological treatments are able to greatly improve the quality of life of patients with COPD. It is important that COPD is recognised and treated appropriately in general practice where most of these patients are managed and this book provides an easy‐to‐read overview of the key issues in this important disease.

Peter J. Barnes FRS, FMedSci

CHAPTER 1Definition, Epidemiology and Risk Factors

Graham S. Devereux

Division of Applied Health Sciences, University of Aberdeen, Aberdeen, UK

Aberdeen Royal Infirmary, Aberdeen, UK

OVERVIEW

Chronic obstructive pulmonary disease (COPD) is defined by relatively fixed airflow obstruction.

The number of individuals diagnosed with COPD is far less than the actual number thought to be affected. Prevalence increases with age and socioeconomic deprivation.

Globally, COPD is projected to be the third leading cause of death by 2030 with the majority of deaths likely to be in low‐/middle‐income countries.

The impact of COPD, particularly exacerbations, on health service resource is considerable.

Risk factors for COPD include cigarette smoking, indoor air pollution (particularly close and regular exposure to combustion of biomass fuels), outdoor air pollution, occupational exposure to some dusts, vapours, irritants and fumes and α1‐antitrypsin deficiency.

Definition

Chronic obstructive pulmonary disease (COPD) is a progressive lung disease characterised by airflow destruction and destruction of the lung parenchyma. The widely used definition put forward by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) is that COPD is ‘a common preventable and treatable disease characterised by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lungs to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients’.

COPD is the preferred name for the airflow obstruction associated with the diseases of chronic bronchitis and emphysema (Box 1.1). A number of other conditions are associated with poorly reversible airflow obstruction, for example bronchiectasis and obliterative bronchiolitis. Although these conditions need to be considered in the differential diagnosis of obstructive airways disease, they are not conventionally covered by the definition of COPD. Although asthma is defined by variable airflow obstruction, there is evidence suggesting that the airway remodelling processes associated with asthma can result in irreversible progressive airflow obstruction that fulfils the definition for COPD. Because of the high prevalence of asthma and COPD, these conditions co‐exist in a sizeable proportion of individuals and can raise diagnostic uncertainty.

Box 1.1 Definitions of conditions associated with airflow obstruction.

COPD is a common preventable and treatable disease characterised by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Exacerbations and co‐morbidities contribute to the overall severity in individual patients.

Chronic bronchitis is defined as the presence of chronic productive cough on most days for 3 months, in each of 2 consecutive years, in a patient whom other causes of productive cough have been excluded.

Emphysema is defined as abnormal, permanent enlargement of the distal airspaces, distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis.

Asthma is characterised by widespread narrowing of the bronchial airways which changes in severity over short periods of time, either spontaneously or following treatment.

Epidemiology

Prevalence

The prevalence of COPD varies considerably between epidemiological surveys. While this reflects the variation between and within countries, differences in methodology, diagnostic criteria and analytical techniques undoubtedly contribute to disparities among studies. There is no consensus as to the optimal metric of COPD prevalence. The lower estimates of prevalence are usually based on self‐reported or ‘doctor‐confirmed’ COPD and are typically 40–50% of the rates derived when spirometry is used. The underdiagnosis of COPD probably arises because many individuals fail to recognise the significance of symptoms and present relatively late with moderate or severe airflow obstruction (Figures 1.1–1.3).

Figure 1.1 Known cases of COPD may represent only the ‘tip of the iceberg’ with many cases currently undiagnosed.

Figure 1.2 Lifetime prevalence of diagnosed COPD in males and females (per 1000) resident in England 2001–2005.

Figure adapted from Simpson CR, Hippisley‐Cox J, Sheikh A. Trends in the epidemiology of chronic obstructive pulmonary disease in England: a national study of 51 804 patients. British Journal of General Practice 2010; 60(576): 277–284.

Figure 1.3