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CHAPTER10 Respiratorymedicine
Pneumonia inadults
Acute infection of lung parenchyma. Common condition, aecting 0.5– 1%
adults annually in the UK. Incidence i with age and peaks in the winter.
Mortality rate <1% in those managed in primary care. 22– 42% require hospital admission, where mortality rate is 5– 14%.
Presentation Acute illness is characterized by:
• Symptoms of an acute lower respiratory tract illness (cough + ≥1 other
lower respiratory tract symptom, e.g. purulent sputum, pleurisy, wheeze,
pleuritic pain)
• New focal chest signs on examination (consolidation or d air entry,
coarse crackles and/ or pleural rub)
• ≥1 systemic feature:sweating, fevers, shivers, aches and pains, and/ or
temperature ≥38°C
• No other explanation for the illness
0 The elderly may present atypically, e.g. ‘o legs’ or acute confusion.
Common causative organisms:Usually bacterial
• S.pneumoniae (36%)— E p. 630
• H.inuenzae (10%)— more common among the elderly— E p. 632
• Inuenza Aand B (8%)— annual epidemics during the winter months;
~3% develop pneumonia— E p. 292
• Mycoplasma pneumoniae (1.3%)— less common in the elderly. Epidemics
occur every 4y in the UK— E p. 298
• Gram −ve enteric bacteria (1.3%)
• C.psittaci (1.3%)— ~20% have history of bird contact— E p. 298
• S.aureus (0.8%)— more common in the winter months; may be
associated with viral infection, e.g. u— E p. 630
• Legionella spp. (0.4%)— most common in September/ October— >50%
related to travel
• No cause identied (45%)
TB E p. 296
Immunocompromised patients E p. 626
Vaccination forprevention
• Inuenza E p. 293 • Pneumococcal E p. 630
Dierential diagnosis Pneumonitis, e.g. secondary to radiotherapy;
malignancy; pulmonary oedema; PE; asthma/ COPD exacerbation; TB.
Investigations Often unnecessary in general practice. Consider:
• Pulse oximetry Use to assess severity. If oxygen saturation is <94% in
air, the patient is hypoxic and requires admission
• CXR If diagnostic uncertainty, symptoms not resolving, or risk of lung
cancer. CXR changes may lag behind clinical signs, but should return to
normal <6wk after recovery. Persistent changes on CXR >6wk after
recovery require further investigation
• Sputum culture If not responding to treatment. If weight d, malaise,
night sweats, or risk factors for TB (ethnic origin, history of TB
exposure, social deprivation or elderly), request mycobacterium culture
• Blood FBC— i WCC; i ESR; acute and convalescent titres to conrm
‘atypical’ pneumonia (Legionella, C.psittaci, M.pneumoniae)
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PNEUMONIA INADULTS
Table10.11 Assessment ofseverity ofpneumonia
H Red ag features Intermediate features
• Objective evidence of new altered
mental state
• i respiratory rate:≥25 breaths/ min
• New need for O
saturation >92% (or >88% if COPD)
• Systolic BP:≤90mmHg or
>40mmHg below normal
to maintain
2
• i heart rate:>130bpm
• Not passed urine in ≥18h (if
catheterized, passed <0.5mL/ kg/ h
of urine)
• Mottled or ashen appearance
• Cyanosis of skin, lips, or tongue
• Non- blanching skin rash
• History from patient, friend, or relative
of new onset of altered behaviour or
mental state
• History of acute deterioration of
functional ability
• i respiratory rate:21– 24 breaths/ min
• Systolic BP:91– 100mmHg
• i heart rate:91– 130bpm (pregnant
♀:100– 130bpm) or new onset
arrhythmia
• Not passed urine in 12– 18h (if
catheterized, passed 0.5– 1mL/ kg/ h
of urine)
• Tympanic temperature <36°C
Management
Consider theneed foradmission Table 10.11
• Admit as a blue light emergency— if any ‘red ag’ features. If
life- threatening infection or considerable delay (>2h), consider
administering antibiotics before admission
• Consider admission— if any ‘intermediate features’. Have a low
threshold if:≥65y, poor social situation, concomitant illness (e.g. heart
failure, chronic lung, renal or liver disease, DM, cancer), impairment
in immune function (immunosuppressant drugs, steroids), or trauma,
surgery, or invasive procedure in the last 6wk
If a decision is made totreat athome
• Advise not to smoke Take analgesia, rest, and drink plenty of uids
• If no intermediate features Give antibiotics for 5d, e.g. amoxicillin
500mg tds or doxycycline 200mg on day 1 then 100mg od, or
clarithromycin 500mg bd. Review after 3d:if poor response, extend
treatment to 7– 10d
• If any intermediate features Consider dual therapy with amoxicillin
500mg tds + clarithromycin 500mg bd for 7– 10d, or monotherapy with
doxycycline for 7– 10d. Review within 3d:if poor response, admit
Complications Require specialist management— refer.
• Pleural eusion (may be reactive or empyema— pus in the lung cavity)
• Lung abscess (presents with swinging fever and worsening pneumonia)
• Septicaemia— E p. 1056 • Respiratory failure
• Metastatic infections • Jaundice
Further information
NICE (2014) Pneumonia in adults:diagnosis and management. M www.
nice.org.uk/ guidance/ cg191
NICE (2016, updated 2017)Sepsis:recognition, diagnosis and early management. M www.nice.org.uk/ guidance/ ng51
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CHAPTER10 Respiratorymedicine
Tuberculosis
Caused by bacteria of the Mycobacterium tuberculosis complex. In 2015,
there were 10.4million new cases worldwide and 1.8 million deaths. In
the UK, 6240 cases were notied in 2015 and accounted for ~300 deaths.
ND
Risk factors In the UK:
• Born in high- prevalence areas, e.g. India, Pakistan, Nigeria
• Active TB contact in same household; close contacts at school/ work
• Previous (especially incomplete) TB treatment— in 2013, 7% of
reported TB cases had a diagnosis of TB >12mo previously
• Immunosuppression, e.g. by medications (steroids, chemotherapy) or
co- morbidities (HIV, diabetes). People living with HIV accounted for
1.2million (11%) new cases in 2015 worldwide
• Smoking, alcohol, and drug misuse
• Social factors ~70% of all patients with TB in the UK were resident in the
40% most deprived areas. At particular risk are the homeless, institutionalized
people, and people living in overcrowded conditions or prisons
Prevention Bacille Calmette– Guérin (BCG) is a live attenuated strain of
bacteria derived from M.bovis. BCG vaccination provides immunity lasting
≤15y to 70– 80% of recipients. It is given by intradermal injection into the
left upper arm. Target groups:
• All infants living in areas where incidence of TB is ≥40/ 100,000 and
infants whose parents or grandparents were born in a country with TB
incidence of ≥40/ 100,000
• Previously unvaccinated new immigrants from countries where there is
a high prevalence of TB
• Occupational risk, e.g. healthcare workers, veterinary sta, prison sta
• Contacts of known cases or those living or working in high- prevalence
countries for extended periods (generally ≥3mo)
• Do not give other immunizations into the same arm for 3mo.
Screening TB is a notiable disease. After notication, contact tracing is
initiated, usually through chest clinics. Screening may be done with tuberculin test or interferon gamma release assay, depending on the scenario.
Tuberculin skin test Standard in the UK is the Mantoux test. Useful
to detect previous exposure to organism (or BCG vaccination) by provoking an immune reaction. Apuried protein derivative of M.tuberculosis
is injected intradermally in the forearm. Response is read after 48– 72h
(Table10.12). Test can be suppressed by:
• Hodgkin’s disease
• Glandular fever
• Live viral vaccines— do not do a tuberculin test <4wk after vaccination
• Immunosuppressant treatment or diseases, including HIV
• Viral infections
• Corticosteroid therapy
• Sarcoidosis
• If a patient has a +ve tuberculin test— DO NOT give BCG vaccination.
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TUBERCULOSIS
ND
Primary TB Initial infection. Transmitted by droplet infection. Alesion
forms (usually pulmonary) which drains to local LNs. Immunity develops
and the infection becomes quiescent. May be asymptomatic or include:
• Fever
• Night sweats
• Persistent cough ± sputum
• Haemoptysis
• Pneumonia
• Pleural eusion
• Anorexia
• Weight d
• Erythema nodosum
Table10.12 Tuberculin testing and interpretation ofresults
Diameter of
induration
<6mm Negative Suggests no TB infection— beware false negatives.
6– 14mm Positive Should not be given BCG. May be due to
≥15mm Strongl y positive Suggests TB infection or disease. Refer for
Positivity Interpretation
Previously unvaccinated people may be given
BCG provided there are no contraindications
previous TB infection or BCG or exposure to
non- tuberculous mycobacteria
investigation
Investigations andmanagement
• CXR
• 3× sputum samples for culture and microscopy for acid- fast bacilli
• Refer to a TB specialist service for diagnosis and ongoing management
Post- primary TB Reactivation of a primary infection. Initial lesions
(usually in the upper lobes of the lung) progress and brose. Other sites
may develop disease. Multiple small lesions throughout the body results in
miliary TB and is common in immunocompromised patients. Symptoms and
signs relate to the organs infected. In all cases, refer for specialist treatment.
Extra- pulmonary disease sites:
• CNS
• Lymph nodes
Treatment
• Spine (rarely other bones/ joints)
• Peripheral cold abscess
N
0 Always refer to the chest clinic; 10% are resistant to
• Pericardium
• Miliary
rst- line antibiotics. Specialist management will involve:
• Antibiotic drug treatment with combination regimens— usually 6months
of isoniazid + rifampicin, with pyrazinamide + ethambutol for the rst
2months. All have potentially serious side eects and need monitoring
• Risk assessment for drug- resistant TB and HIV infection. Care
coordination and allocation of key worker to monitor treatment
concordance, side eects, and clinical response. ‘Directly observed
therapy’ (DOT) is used in high- risk groups (e.g. homeless patients) to
ensure concordance. Medications are taken under observation
• Contact tracing
Further information
DH The Green Book. Chapter32:Tuberculosis. M www.gov.uk/ govern-
ment/ publications/ tuberculosis- the- green- book- chapter- 32
NICE (2016) Tuberculosis. M www.nice.org.uk/ guidance/ ng33
World Health Organization Tuberculosis. M http:// www.who.int/ tb/ en/
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CHAPTER10 Respiratorymedicine
Other respiratoryinfections
Mycoplasma Mycoplasma pneumoniae causes epidemics of lower re-
spiratory tract infection every 3– 4y. Spread by droplet infection.
• Incubation 12– 14d
• Presentation Dry, persistent cough ± arthralgia. CXR shows bilateral,
patchy consolidation. Infection is conrmed with serology
• Management Clarithromycin 500mg bd for 2wk or doxycycline 100–
200mg daily for 2wk. Relapse is common. Severe infections may require
hospital admission
Respiratory chlamydialinfection
• C.pneumoniae Accounts for 6– 19% of community- acquired
pneumonia— especially in children/ young adults. Clinically
indistinguishable from Mycoplasma pneumoniae. Treat with doxycycline
100– 200mg/ d or clarithromycin 500mg bd for 2wk, or azithromycin
500mg od for 3d
• C.psittaci Infects many animals, but human infection is closely related to
contact with birds. Treat as for C.pneumoniae
Pertussis (whooping cough)
• Presentation Incubation:7– 10d; Symptoms:
• Catarrhal stage Symptoms and signs of URTI— lasts 1– 2wk
• Coughing stage Increasingly severe, paroxysmal cough with spasms of
coughing followed by a ‘whoop’— associated with vomiting, cyanosis
during coughing spasms ± exhaustion. Lasts 4– 6wk, then cough
improves over 2– 3wk. Chest is clear between coughing bouts
• Investigation Microscopy and culture of nasal swabs (special swab and
culture medium available from the laboratory); FBC— lymphocytosis
• Management Macrolide antibiotics (clarithromycin, erythromycin, or
azithromycin) are recommended if onset of cough was in the last 21d
• Complications Pneumonia, bronchiectasis, convulsions, subconjunctival
haemorrhages, and facial petechiae
Prevention
• Proven contacts Treat with clarithromycin or erythromycin
• Childhood vaccination E p. 619. Personal or FH of febrile convulsion,
FH of epilepsy and well- controlled epilepsy are not contraindications—
give advice on fever prevention. Defer vaccination if any undiagnosed/
evolving neurological condition or poorly controlled epilepsy until the
condition is stable— if in doubt, seek specialist paediatric advice
• Vaccination in pregnancy Oered from 16– 32wk gestation in the UK to
i passive immunity in newborn babies. Combination vaccine containing
inactivated polio, tetanus, and diphtheria vaccine as well as pertussis is
recommended. If missed, can be given until the ♀ goes into labour
0 Pertussis immunity wanes after vaccination— do not rule out the possibility of pertussis because a person has been vaccinated.
Further information
DH The Green Book. Chapter24:Pertussis M www.gov.uk/ government/
publications/ pertussis- the- green- book- chapter- 24
ND
Caused by Bordetella pertussis.
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OTHER RESPIRATORYINFECTIONS
Aspergillosis Spores ofAspergillus fungus present in the soil and decaying
vegetation can be inhaled any time of the year, but reach peak levels in autumn/winter. Inhaled spores colonize bronchial mucosa and nasal sinuses.
Presentations
• Asthma E p. 278
• Allergic bronchopulmonary aspergillosis Presents with episodes of
eosinophilic pneumonia (characterized by wheeze, cough, fever, and
malaise) throughout the year, but worse in late autumn. CXR shows
eeting lung shadows (cleared by expectorating rm, brown plugs of
mucus). Untreated l upper lobe brosis and ‘proximal’ bronchiectasis
• Invasive aspergillosis Only occurs in the immunocompromised.
Aspergillus disseminates from the lung l brain, kidneys, and other
organs. Carries very poor prognosis
• Aspergillus sinusitis Nasal congestion, headache, and facial pain
• Aspergilloma Growth within existing lung cavities (e.g. from previous TB
or sarcoidosis). Aball of fungus forms. CXR shows a round lesion with
air halo above it. Occasionally results in haemoptysis
Management Refer for specialist management.
Pneumocystis jiroveci (PCP) May be classied as a protozoan or
fungus. Causes pneumonia in immunocompromised patients.
• Presentation Fever, breathlessness, tachypnoea, dry cough, respiratory
failure (± cyanosis)
• Investigation CXR normal or ‘ground- glass’ appearance; sputum culture
may be diagnostic
• Management If suspected, refer for specialist care. Treatment is with co-
trimoxazole or dapsone
• Prevention Prophylactic antibiotics (usually co- trimoxazole) are given to
AIDS patients with CD4 counts <200 cells/ mm
Novel corona virus infections
ND
Include: SARS (sudden acute respira-
3
tory syndrome), MERS (Middle East respiratory syndrome) and COVID-19
(corona virus disease 2019). Spread: direct contact with infected individual/
contaminated surface or aerosol. Incubation: 2–14d (mean 5.5d).
Twostages:
• Prodrome Fever (>37.8oC), malaise, headache, myalgia
• Respiratory phase Develops after 3– 7d— dry cough and breathlessness.
Other symptoms Watery diarrhoea, conjunctivitis, URTI symptoms, e.g.
rhinitis, sore throat. Asymptomatic patients may still spread the virus.
>95% recover after 7–10d but 1–2% progress to respiratory failure and/or
2° complications, e.g. pneumonia. If mild symptoms, manage at home—
patients must self-isolate for ≥7d or until full recovery. If breathless at rest,
peripheral oxygen saturation <92% on air, circulatory compromise, or persistent fever >7d, admit as an acute medical emergency. Personal contacts
of patients with suspected/conrmed infections must self-isolate for 14d.
ACOVID-19 vaccine is likely to be available by 2020/2021.
• Always wear personal protective equipment (PPE) when assessing/
managing patients with suspected corona virus infection and pre-warn
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CHAPTER10 Respiratorymedicine
Cystic fibrosis and Kartagenersyndrome
Cystic brosis (CF) The most common inherited disorder in the UK
(prevalence:1 in 2500). Around 10,800 people in the UK have CF. Median
survival has i dramatically and is now >40y, but of the 7500 CF patients in
the UK, 6000 are <25y old.
Genetics Results from mutation of a single gene on chromosome 7 (cystic
brosis transmembrane conductance regulator) essential for salt and water
movement across cell membranes. This causes thickened secretions. >2000
dierent mutations have been described. Autosomal recessive inheritance
results in a 1 in 4 chance of having a child with CF if both parents are carriers. ~1 in 25 adults in the UK carries the CF gene. Most common in
Caucasians— rare in people of Afro- Caribbean origin.
Screening Several possibilities:
• Pre- conceptual screening Buccal smears to karyotype prospective
parents
• Antenatal screening Chorionic villous sampling at ~10wk— for parents
with an aected child already or where both parents are +ve on
karyotyping
• Neonatal screening E p. 830
Common problems associated withCF Figure 10.4
Diagnosis
• Screening
• If clinical suspicion of CF, refer to paediatrics. A+ve sweat test
(>60mmol/ L on 2 occasions) is diagnostic as is i potential dierence
across the nasal respiratory epithelium. An elevated sodium level may
be found on the sweat test, as well as i chloride:sodium ratio (>1)
Management CF is a multisystem disease requiring a holistic approach to
care, which aims to maintain patients’ independence, improve quality of
life, and extend life expectancy. Amultidisciplinary team in a specialist CF
centre is best placed to achieve this. Patients usually have direct access.
Management involves:
• Treatment of lung disease, e.g. with exercise, physiotherapy, antibiotics,
and mucolytics
• Maintaining good nutritional state, e.g. pre- meal oral pancreatic
enzymes, high- calorie diet, and fat- soluble vitamin supplements (A,
D, and E)
• Treatment of complications, e.g. DM, osteoporosis
Further information forpatients and professionals
CF Trust F 0300 373 1000 M www.cysticbrosis.org.uk
Kartagener syndrome (immotile cilia syndrome) Autosomal
recessive inherited condition results in abnormal structure and function of
cilia. Consists of a combination of bronchiectasis, chronic sinusitis, and male
infertility plus situs inversus (transposed heart and abdominal organs). Otitis
media and salpingitis are frequent. Specialist treatment is supportive.
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CYSTIC FIBROSIS AND KARTAGENERSYNDROME
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Figure10.4 Features of cystic brosis
Modied from the MSD Manual Consumer Version (Known as the Merck Manual in the US and
Canada and the MSD Manual in the rest of the world), edited by Robert Porter. Copyright 2019
by Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc., Kenilworth, NJ. Available at
http:// www.msdmanuals.com/ consumer. Accessed 20 May 2019.
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CHAPTER10 Respiratorymedicine
Interstitial lungdisease
Also known as diuse parenchymal lung disease. Comprises >200 dierent
diseases (many rare) in which inammation aects the alveolar wall, leading
to uid in the alveolar air spaces.
Presentation Increasing dyspnoea ± cough. More rarely wheeze, pleurisy,
and/ or haemoptysis. May present incidentally with changes on CXR.
Furtherassessment
• History of the condition— acute, episodic, chronic?
• Severity— exercise tolerance
• Possible causes:
• Smoking
• Hobbies and occupation
• Usual environment (e.g. lives on a farm) and travel
• Past medical history (particularly rheumatological symptoms and
immunosuppression e.g. HIV) and family history
• Drugs
• Examine looking for ne inspiratory crackles in the chest, and evidence
of systemic disease, e.g. fever, rashes, or other skin changes, eye signs
(particularly red eye), hepatomegaly, and/ or splenomegaly, arthritis
• Pulse oximetry— d peripheral oxygen saturations
Investigations
• CXR— diuse shadowing
• Urine dipstick— for protein and blood
• Blood— FBC, ESR, liver and kidney function tests, thyroid function tests,
autoimmune prole
• Lung function tests— usually show restrictive picture— rarely no
abnormalities or obstructive picture
Classication Table10.13
Hypersensitivity pneumonitis Also known as extrinsic allergic alveol-
itis, farmer’s lung, and bird fancier’s lung. Inhaled particles (e.g. fungal spores,
avian proteins) cause an allergic reaction in lungs of hypersensitive individuals.
May present as an acute or chronic reaction, or both may occur together.
• Acute reaction 2– 4h post exposure. Fever, malaise, dry cough,
shortness of breath
• Chronic reaction Malaise, weight d, exertional dyspnoea, ne
crepitations in both lung elds
Investigations
• Blood FBC:i neutrophils (acute reaction); ESR i (acute reaction)
• CXR May be normal or show typical changes (shadowing, widespread
small nodules or ground glass appearance)
• Diagnosis Based on history and high- resolution CT scan ndings. Serum
precipitins to the provoking factor are found in ≥90%
Management If possible prevent further exposure to the allergen. In all
cases refer for specialist advice. Treatment is usually with corticosteroids. If
occupational exposure, may qualify as industrial disease and be eligible for
compensation— E p. 90.
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INTERSTITIAL LUNGDISEASE
Table10.13 Classication ofinterstitial lung disease
Classication Causes
Acute Infective:
Episodic Eosinophilic pneumonia, e.g. allergic bronchopulmonary
Chronic due to
occupational or
environmental
exposure
Chronic with
evidence of
systemic disease
Chronic without
evidence of
systemic disease
•
Bacterial (TB)
•
Viral (chicken pox, measles)
•
Fungal
Allergy— drugs, fungi, helminths
Toxins— drugs, gases
Haemodynamic— LVF, uid overload, renal failure
Vasculitis
Adult respiratory distress syndrome
aspergillosis
Vasculitis, e.g. eosinophilic granulomatosis with polyangiitis
(formerly Churg– Strauss syndrome)
Hypersensitivity pneumonitis
Cryptogenic organizing pneumonia
Dust- induced (E p. 306)— asbestosis, silicosis, coal worker’s
pneumoconiosis, siderosis (iron)
Farmer’s lung
Bird fancier’s lung
Radiation
Drugs, e.g. nitrofurantoin, sulfasalazine, gold, penicillamine,
aspirin, amiodarone, bleomycin, methotrexate, hydralazine,
heroin, methadone, oxygen
Connective tissue disease, e.g. RA, Sjögren’s syndrome, SLE
Neoplastic, e.g. lymphoma
Vasculitis, e.g. granulomatosis with polyangiitis (formerly
Wegener’s granulomatosis), Goodpasture’s syndrome
Sarcoidosis
Inherited disorders, e.g. tuberous sclerosis, neurobromatosis
Miscellaneous, e.g. HIV, inammatory bowel disease, post
bone marrow transplant, amyloidosis
Idiopathic pulmonary brosis
Chronic aspiration
303
• Advise all patients with interstitial lung disease to stop smoking. This
results in better prognosis for their interstitial lung disease. Furthermore,
patients with chronic interstitial lung disease are at substantially i risk of
lung cancer.
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