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CHAPTER10 Respiratorymedicine
Chronic obstructive pulmonarydisease
Chronic obstructive pulmonary disease (COPD) is a slowly progressive disorder characterized by airow obstruction. In the UK, it aects ~3million
people, with two- thirds undiagnosed. ♂ > ♀. Responsible for 1 in 8 emergency hospital admissions and ~5% of deaths in the UKN. Causes:
• Tobacco smoking (90% of cases)
• Occupational exposure, e.g. coal, silica, welding fumes
• Air pollution
• Genetic— bronchial hyper- responsiveness; α1- antitrypsin deciency
• Poor lung growth and development e.g. low birth weight, infections
Incidental CXR/ CT scan abnormalities E p. 272
Diagnosis Suggested by history, signs, and baseline spirometry. Consider
in patients >35y with a risk factor for COPD (generally smoking) and typical
symptoms:
• Shortness of breath on exertion— use an objective measure, e.g. MRC
dyspnoea scale (Table 10.6) to grade breathlessness
• Chronic cough
• Wheeze
Table10.6 MRC Dyspnoea Scale
Grade Degree of breathlessness related to physical activity
1 Not troubled by breathlessness except on strenuous exercise
2 Short of breath 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 100m or after a few minutes on level ground
5 Too breathless to leave the house or breathless on dressing/ undressing.
Used with the permission of the Medical Research Council.
If diagnosis is suspected also ask about Weight d, eort intolerance, waking
at night, ankle swelling, fatigue, and occupational hazards.
• Chest pain or haemoptysis are uncommon in COPD— if present consider an alternative diagnosis.
• Regular sputum production
• Frequent winter ‘bronchitis’
Signs May be none. Possible signs:
• Hyperinated chest ± poor chest
expansion on inspiration
• d crico- sternal distance
• Hyper- resonant chest with d cardiac
dullness on percussion
• Wheeze or quiet breath sounds
• Paradoxical movement of lower ribs
• Use of accessory muscles
Spirometry E p. 272. Predicts severity and prognosis but not disability/
quality of life. Measured post- bronchodilator, e.g. 200mcg salbutamol via
spacer. Diagnose airow obstruction if FEV1/ FVC <0.7 (<70%). Grade severity according to the reduction in FEV1 (Table 10.7).
• Tachypnoea
• Pursing of lips on expiration
(pursed lip breathing)
• Peripheral oedema
• Cyanosis
• i JVP
• Cachexia
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CHRONIC OBSTRUCTIVE PULMONARYDISEASE
Table10.7 Severity ofCOPD and expected clinical picture
Severity Spirometry (FEV1/ FVC <0.7) Clinical picture
Stage 1—
mild
Stage 2—
moderate
Stage 3—
severe
Stage 4—
very severe
FEV1 ≥80% Cough. Little/ no breathlessness. No
FEV1 50– 79% predicted Breathlessness, wheeze on exertion,
FEV1 30– 49% predicted SOBOE. Marked wheeze/ cough. Usually
FEV1 <30% predicted As for stage 3 but more breathless;
abnormal signs. No i use of services
cough ± sputum. Some abnormal signs.
Known to GP— intermittent problems
other signs. Known to GP and specialist
with frequent problems/ admissions
severely restricted activities of daily living
Reversibility testing Can be misleading. Not routinely recommended:
• >400mL i in FEV1 following trial of bronchodilator or prednisolone
(30mg od for 2wk) suggests asthma
• Clinically signicant COPD is not present if FEV1 and FEV1/ FVC return
to normal after drug therapy
PEFR E p. 272. Patients with COPD have little variability in PEFR. Serial
home PEFR measurements can help distinguish between asthma and
COPD. PEFR may underestimate severity of airow limitation and a normal
PEFR does not exclude airow obstruction.
Other investigations organized inprimarycare
• CXR/ CT Indicated to exclude other diagnoses e.g. lung cancer
• FBC To identify secondary polycythaemia or anaemia
• BMI
• α1- antitrypsin If early onset COPD or family history— E p. 398
• ECG/ Echo/ serum natriuretic peptide If cor pulmonale is suspected
• Sputum culture If purulent sputum is persistent
• Pulse oximetry To assess need for oxygen therapy
Dierential diagnosis Asthma (Table 10.8), bronchiectasis, heart
failure, lung cancer, interstitial lung disease, anaemia, tuberculosis. Refer for
specialist review if diagnostic uncertainty.
Table10.8 Comparison ofCOPD and asthma
COPD Asthma
Symptoms <35y Rare Often
Smoking history Nearly all Maybe
Breathlessness Persistent and progressive. Poor
Chronic productive
cough
Waking at night with
cough/ wheeze
response to inhaled therapy— if
good reconsider diagnosis
Common Uncommon
Uncommon Common
Variable throughout the day and
from day to day. Good response
to inhaled therapy is typical
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CHAPTER10 Respiratorymedicine
Management ofCOPD
Develop an individualized management plan for each patient. Review
≥1×/y. Record spirometry results and progression, BMI, current symptoms, problems since last seen, exercise tolerance, and smoking status.
Educate patient/ family about COPD, medication, and self- help.
Non- drugtherapy
• Smoking cessation Most important. Improves outcome (Table 10.9)
• Vaccination All patients with COPD should have inuenza and
pneumococcal vaccination
• Pulmonary rehabilitation Lack of exercise d FEV1. Multidisciplinary
pulmonary rehabilitation is of proven benet— refer for patients who
consider their COPD hinders everyday activities
• Nutrition Weight d in obese patients improves exercise tolerance
• Cognitive behavioural techniques Can help patients who nd the
sensation of being breathless frightening
• Screening for depression E p. 173
Table10.9 Smoking and COPD
FEV1 as % of value aged 25y
Age 60y Age 75y
Non- smoker 85% 80%
Ex- smoker:quit aged 40y 60% 45% (symptoms)
Ex- smoker:quit aged 60y 33% (severe symptoms) 15% (severe disability)
Ongoing smoker 33% (severe symptoms) Dead
Rescue medication and escalation plans E p. 288
Management ofacute exacerbations E p. 288
Long- term drug therapy Document eects of each drug treatment
on symptoms, quality of life, and lung function as tried.
• Step 1 Oer a short- acting β2 agonist (SABA) e.g. salbutamol inhaler
1– 2 pus as needed, or short- acting muscarinic antagonist (SAMA) e.g.
ipratropium 20– 40mcg. Both i FEV1 and d breathlessness
• Step 2 Add:
• If asthma features (i.e. some steroid responsiveness). Long- acting β2
agonist (LABA) + inhaled corticosteroid (e.g. uticasone/ vilanterol)
• If no asthma features Long- acting muscarinic antagonist (LAMA)+
LABA (e.g. vilanterol/ umeclidinium)
• Step 3 If asthma features/ steroid responsiveness, continue short- acting
bronchodilator and change long- acting medication to a LABA + LAMA +
inhaled corticosteroid inhaler (e.g. uticasone/ vilanterol/ umeclidinium)
Spacer devices E p. 277 Nebulizers E p. 277
Add- ontherapy
Oral mucolytic therapy e.g. carbocisteine. Consider if chronic cough +
sputum. Discontinue if no symptomatic improvement.
Oral prophylactic antibioticsN Azithromycin 250mg 3×/ wk. Oer if non-
smoker/ ex- smoker, optimized inhaled therapies, and has undertaken pulmonary rehabilitation but frequent (≥4/ y)/ prolonged exacerbations with
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MANAGEMENT OFCOPD
sputum production, or hospitalizations. Before starting, check sputum for
M,C&S to exclude resistant organisms/ Pseudomonas aeruginosa, baseline
LFTs, and ECG (for prolonged QT interval). Advise small risk of hearing
loss/ tinnitus. Review after 3mo and then every 4– 6mo. Only continue if
benets > risks. Doxycycline 100mg od is an alternative.
Long- term oral steroids Avoid if possible. If unavoidable keep dose as low as
possible and provide bone protection (E p. 484).
Theophylline M/ R Only use if inhaled LABA/ LAMA is ineective or unable
to use inhaled medication. Monitoring of serum drug levels is required. Be
wary of drug interactions— especially with antibiotics.
Roumilast Specialist initiation only. Adjunct to bronchodilators for patients
with severe COPD with a history of frequent exacerbations.
Referral forspecialistcare
• Uncertain diagnosis
• Age <40y
• Severe COPD
• Rapid decline in FEV
• Assessment for:LTOT, withdrawal of long term steroids, long- term
nebulizer therapy, surgery, e.g. lung transplant, bullectomy
• Haemoptysis— urgent referral
• Frequent exacerbations
• Pulmonary hypertension/ cor pulmonale
• α1- antitrypsin deciency
1
Long- term oxygen therapy (LTOT) Only prescribe after evaluation
by a respiratory physician. Refer patients with:
• Severe airow obstruction (FEV1 <30%— consider if 30– 49%)
• Hypoxaemia (oxygen saturation ≤92% breathing air)
• Cyanosis
• Polycythaemia
Treatment for >15h/ d i survival and quality of life. Ambulatory oxygen can
i exercise tolerance in some patients. 0 Always warn patients about the
re risks of having pure oxygen in their homes.
O2 cylinders and associated equipment Arrangements for supply of oxygen
are dier across the UK— see BNF. Specify amount of O2 required (h/ d)
and ow rate. O2 concentrators are more economical for LTOT. Supply
back up cylinders in case of breakdown or power cut.
• Peripheral oedema
• i JVP
Prognosis Poor prognosis is associated with:
• Smoking status (smoker)
• Low BMI
• Severe/ frequent exacerbations ± hospital admissions
• Breathless (MRC4/ 5), high symptom burden ± d exercise capacity
• Low FEV1 and/ or meets criteria for LTOT
• Chronic hypoxia and/ or cor pulmonale
• Multimorbidity/ frailty
Cor pulmonale E p. 236
Palliative care E p. 1011
Further information
NICE (2018) Chronic obstructive pulmonary disease in over 16s:diagnosis
and management. M www.nice.org.uk/ guidance/ ng115
Patient support
British Lung Foundation F 03000 030 555 M www.lunguk.org
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CHAPTER10 Respiratorymedicine
Acute exacerbations ofCOPD
Risk factors forexacerbation
• Exposure to passive smoke
• Viral or bacterial infection
• Continued smoking or relapse for ex- smokers
• Indoor and outdoor air pollution, e.g. nitrous oxide, ozone
Presentation Worsening of previous stable condition. Features:≥1 of
• i dyspnoea— marked dyspnoea,
tachypnoea (>25 breaths/ min), use
of accessory muscles at rest and
pursed lip breathing are signs of severe
exacerbation
• d exercise tolerance— marked d in
activities of daily living is a sign of
severe exacerbation
• i fatigue
• i uid retention— new onset oedema
is a sign of severe exacerbation
0 Fever and chest pain are uncommon presenting features— consider alternative diagnosis.
Dierentialdiagnosis
• Pneumonia
• LVF/ pulmonary oedema
• Lung cancer
• Pleural eusion
Investigations
• Pulse oximetry Can be used to assess severity (saturation ≤92% on air
suggests hypoxaemia— consider admission) and to monitor progress
• CXR Consider if diagnostic doubt and/ or to exclude other causes of
symptoms
• Sputum culture Not recommended routinely in the community
Rescue medication and escalation plans Develop an individual-
ized escalation plan with each patient to manage acute exacerbations, If
able to understand their use, oer patients at risk of exacerbations a short
course of oral steroids and antibiotics to keep at home to enable prompt
treatment of exacerbations.
0 Review if using ≥3 courses of oral steroids and/ or antibiotics per year.
GP management Decide whether to treat at home or admit to
hospital— Table 10.10. If managing in the community:
• Add or i bronchodilators Consider if inhaler device and technique are
appropriate
• Oral corticosteroids Start early in the course of the exacerbation if i
breathlessness which interferes with daily activities. Dosage— 30– 40mg/
d of prednisolone for 1– 2wk. Consider osteoporosis prophylaxis with a
bisphosphonate if frequent courses are required (E p. 484)
• Lack of physical activity
• Seasonal variation (winter and spring)
• i wheeze
• Chest tightness
• i cough
• i sputum purulence
• i sputum volume
• Upper airways symptoms,
e.g.cold, sore throat
• New- onset cyanosis— severe
exacerbation
• Acute confusion— severe
exacerbation
• Recurrent aspiration
• Pneumothorax
• PE
• Upper airway obstruction
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ACUTE EXACERBATIONS OFCOPD
Table10.10 Deciding totreat exacerbations athome or inhospital. The
more features inthe ‘treat inhospital column’, themore likely theneed
foradmission
Treat at home Treat in hospital
Ability to cope at home Ye s No
Breathlessness Mild Severe
General condition Good Poor— deteriorating
Level of activity Good Poor/ conned to bed
Cyanosis No Ye s
Worsening peripheral oedema No Ye s
Level of consciousness Normal Impaired
Already receiving LTOT No Ye s
Social circumstances Good Living alone/ not coping
Acute confusion No Yes
Rapid rate of onset No Ye s
Signicant co- morbidity (e.g. cardiac
disease, DM)
SaO2<90% on air No Ye s
Changes on CXR (if available) No Present
a
Hospital- at- home schemes and assisted discharge schemes are a suitable alternative.
Source:data from Gravil, JH, etal. Home treatment of exacerbations of chronic obstructive pulmonary disease by an acute respiratory assessment service. Lancet 1998; 351(9119):1853– 5.
No Ye s
a
• Start antibiotics Use broad- spectrum antibiotic for 5d (e.g. amoxicillin
500mg tds, erythromycin 500mg qds, clarithromycin 500mg bd, or
doxycycline 200mg on day 1 then 100mg od) if sputum changes colour
or i in volume/ thickness beyond normal day- to- day variation, clinical
signs of pneumonia, or consolidation on CXR
Follow- up
• Reassess as necessary. If the patient deteriorates reconsider the need
for hospital admission. If not fully improved in within 2wk consider CXR
and/ or hospital referral
• Reassess patients who have been admitted 4– 6wk after discharge
Assess their ability to cope at home. ~1 in 3 are readmitted in <3mo
• Reassess inhaler technique and understanding of treatment regimen
• In severe cases, reassess the need for LTOT and/ or home nebulizer
• Check FEV
• Emphasize the potential benet of lifestyle modication— smoking
1
cessation, exercise, weight loss if obese
• Arrange ongoing regular follow- up
Further information
NICE (2018) Chronic obstructive pulmonary disease in over 16s:diagnosis
and management. M https:// www.nice.org.uk/ guidance/ ng115
NICE (2018) Chronic obstructive pulmonary disease (acute exacerbation):antimicrobial prescribing. M https:// www.nice.org.uk/ guidance/ ng114
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CHAPTER10 Respiratorymedicine
Lungcancer
Referral forsuspected lung cancer
Immediate referral/ acuteadmission
• Stridor
• Superior vena cava obstruction (swelling of face/ neck with xed i JVP)
Urgentreferral To a team specializing in management of lung cancer:
• CXR suggestive of lung cancer
• ≥40y with unexplained haemoptysis
Urgent referral forCXR
• If ≥40y + ≥2 of the following unexplained symptoms (≥1 if current/
previous smoker or exposure to asbestos):
• Cough • Chest pain
• Fatigue • Weight d
• Shortness of breath • Appetite d
Consider urgent referral forCXR If
• Persistent or recurrent chest infections
• Finger clubbing
• Supraclavicular lymphadenopathy or persistent cervical lymphadenopathy
• Chest signs consistent with lung cancer
• Thrombocytosis
Lung cancer is the third most common cancer in the UK, but the most
common cause of cancer death (22%). There are more than 39,000 new
cases of lung cancer in the UK each year. Incidence i with age— 48% of
lung cancer deaths each year occur in those aged ≥75y. Historically, more
common in males, though 45% of new diagnoses are now in females.
Types
• Small cell lung cancer 720% all cases. Often disseminated at diagnosis.
Spreads to liver, bones, brain, and adrenals
• Non- small cell lung cancer ~80% all cases. Mainly adenocarcinoma or
squamous cell carcinoma. Not always smoking- related
Screening Current evidence does not support screening for lung cancer
with chest radiography or sputum cytology. Frequent chest X- ray screening
may be harmful. Screening with low- dose CT was found in one trial to d the
number people of who died from lung cancer, but this trial included very highrisk smokers and ex- smokers. However, there were high false +ve rates. More
research is needed about the use of CT screening in lower- risk individuals.
Prevention
• Smoking cessation ~90% of lung cancers are caused by smoking. The
younger a person is when he/ she starts smoking, the greater the risk
of developing lung cancer. Risk also i with amount smoked (duration
of smoking and number of cigarettes smoked/ d). Oer support
and treatments to aid smoking cessation, e.g. e- cigarettes, nicotine
replacement, varenicline, bupropion— E p. 156
N
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LUNGCANCER
• Diet i consumption of fruit, carrots, and green vegetables may
dincidence but there is no evidence that vitamin supplements are
benecial and they might be harmful
C
Presentation >90% have symptoms at the time of diagnosis. Common
presenting features:
• Cough
• Chest/ shoulder pain
• Haemoptysis
• Dyspnoea
• Hoarseness
• Weight d
• Finger clubbing
• General malaise
• Distant metastases
• Incidental nding on CXR
Pancoast syndrome Apical lung cancer + ipsilateral Horner’s syndrome.
Cause:invasion of the cervical sympathetic plexus. Other features: shoulder
and arm pain (brachial plexus invasion C8– T2) ± hoarse voice/ bovine cough
(unilateral recurrent laryngeal nerve palsy and vocal cord paralysis).
Paraneoplastic syndromes e.g. ectopic ACTH production, SIADH,
hypercalcaemia, hypercoagulability. Aect 10– 20% of patients with lung
cancer— particularly small cell. Have a high index of suspicion and refer for
specialist management if suspected.
Management Once the diagnosis has been conrmed, liaise with the
chest physician, specialist lung cancer team, PHCT, and specialist palliative
care services (e.g. Macmillan Nurses). Active treatment options depend
on type and extent of tumour and include surgery, radiotherapy, and/ or
chemotherapy. Follow- up regularly. 70% die in <1y. Long- term survival
(>10y) is currently only ~5.5%.
Palliative radiotherapy Radiotherapy is a key component of symptomatic
treatment for:
• Haemoptysis
• Chest pain
• Breathlessness due to bronchial occlusion
Radiotherapy may be combined with palliative chemotherapy, particularly
for patients with non- small cell lung cancer.
• Pain from bone metastasis
• Symptoms from brain metastasis
Mesothelioma E p. 307
Palliative care E p. 1011
Further information
NICE (2015, updated 2017)Suspected cancer:recognition and referral.
Mwww.nice.org.uk/ guidance/ ng12
NICE (2019) Lung cancer:diagnosis and management. M www.nice.org.
uk/ guidance/ ng122
SIGN (2014) Management of lung cancer. M www.sign.ac.uk/ sign- 137-
management- of- lung- cancer.html
Information and support forpatients
British Lung Foundation F 03000 030 555 M www.blf.org.uk
Cancer Research UK F 0808 800 4040 M www.cancerhelp.org.uk
Macmillan Cancer Support F 0808 808 0000 M www.macmillan.org.uk
Roy Castle Lung Cancer Foundation F 0333 323 7200 M www.roycastle.org
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CHAPTER10 Respiratorymedicine
Colds andinfluenza
The common cold Mild, acute, self- limiting upper respiratory tract in-
fection more frequent in winter. Most common in children. Adults have on
average 2– 3/ y.
• Causes Rhino- (30– 50%), corona- (10– 15%), inuenza (5– 15%) viruses
most commonly. Others include RSV, entero- and adenoviruses. 25% of
colds have no identiable cause. Infection with ≥2 viruses occurs in 5%
of cases
• Spread Direct contact and droplet infection
• Management Advise patients to rest, take plenty of uids, and
paracetamol or ibuprofen for symptom relief. Usually symptoms resolve
in <7d for adults and <14d for younger children. Mild cough may persist
for 3wk
• Complications Exacerbation of asthma/ COPD; secondary infection
(bronchitis, pneumonia, conjunctivitis, OM, sinusitis, tonsillitis)
Acute bronchitis Inammation of major bronchi. Often follows viral
URTI especially in winter months. Symptoms include cough ± sputum,
breathlessness, and wheeze. On examination, wheeze is often heard
without other focal signs. Systemic features may be present, e.g. sweats,
fevers, myalgia.
Management Self- limiting illness (settles in <3wk) in normally healthy
people. Consider: bronchodilators if wheeze is heard; antibiotics— may
shorten symptoms but weigh benets against possible side eects (i in
community antibiotic resistance and ‘medicalizing’ a self- limiting condition).
If recurrent bronchitis, consider a diagnosis of COPD.
Reasons toprescribe antibiotics immediatelyN Investigate further and/ or give
antibiotics (e.g. amoxicillin 500mg tds for 5– 10d) if:
• Systemically very unwell
• Symptoms/ signs of serious illness or complications, e.g. pneumonia
• At high risk of serious complications because of pre- existing co-
morbidity, e.g. signicant heart, lung, renal, liver, or neuromuscular
disease, immunosuppression, CF, or young children born prematurely
• Aged >65y with acute cough and ≥2, or aged >80y with acute cough
and ≥1, of the following:
• Hospitalization in the previous year
• Type 1 or type 2 DM
Inuenza Sporadic respiratory illness in winter months causing ~600
deaths/ y in non- epidemic years. Minor changes in virus proteins cause
annual epidemics. Pandemics occur with major shifts in surface proteins,
resulting in global eects as most people lack immunity. Causes:Inuenza
viruses A, B, or C.Spread:Droplet infection, person- to- person contact, or
contact with contaminated items. Incubation:1– 7d.
Presentation Symptoms include fever, cough, sore throat, myalgia, and
headache. Usually self- limiting, with acute illness lasting 3– 4d. Some symptoms may persist for 1– 2wk. Severity varies from asymptomatic to lifethreatening complications. Most common complications are secondary
bacterial infections, e.g. otitis media, pneumonia, and bronchitis.
• History of CCF
• Current use of oral steroids
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COLDS ANDINFLUENZA
Management Rest, uids, and paracetamol or ibuprofen for fever/ symptom
control. Treat complications, e.g. antibiotics for chest infection; treatment
of exacerbations of COPD or asthma.
Antivirals Oseltamivir and zanamivir are recommended to d complications
in adults and children if all of the following apply:
• National surveillance schemes indicate circulating inuenza
• The person is in an ‘at- risk’ group (Box 10.1)
• The person presents with an inuenza- like illness and can start
treatment within 48h (or within 36h for zanamivir treatment in children)
of the onset of symptoms as per licensed indications
Antiviral drugs may also be used for prophylaxis if:
• National surveillance schemes indicate circulating inuenza
• An ‘at- risk’ person has not been immunized and has had close contact
with a person with inuenza symptoms
• The person can start treatment <48h after contact for oseltamivir
(<36h for zanamivir)
Inuenza vaccination Oered annually in the UK:
• All patients aged ≥65y— adjuvant vaccine to i eectiveness
• Children aged 2– 17y— intranasal live, attenuated vaccine— programme
being phased in across the UK
• All aged ≥6mo in high- risk groups (Box 10.1)— quadrivalent, inactivated
vaccine <2y; intranasal, live attenuated vaccine if 2–18y; non- adjuvant
vaccine aged 18– 65y; adjuvant vaccine aged ≥65y
Box 10.1 Risk factors forsevere disease withinuenza
• Aged ≥65y
• DM
• Immunosuppression
• BMI ≥40kg/ m
2
• Pregnant women or ≤2wk postpartum
• Chronic respiratory/ heart/ renal/ liver/ neurological disease
High- risk groups eligible forinuenzavaccination
• DM
• BMI ≥40kg/ m
2
• Chronic respiratory/ heart/ renal/ liver/ neurological disease
• Immunocompromised or asplenic patients
• Pregnant women
• Long- stay care facility residents, e.g. nursing homes
• Household contacts of immunocompromised people
• Healthcare and social care workers
• Hajj and Umrah pilgrims
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Further information
DH The Green Book. Chapter19:Inuenza. M www.gov.uk/ govern-
ment/ publications/ inuenza- the- green- book- chapter- 19
NICE (2008) Respiratory tract infections (self- limiting):prescribing antibiotics. M www.nice.org.uk/ guidance/ cg69
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