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Asthma56
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Difficult asthma
•
• Defined as persistent symptoms and/or frequent exacerbations despite
treatment at step 4/5 of the stepwise approach (above).
• Patients should be systematically evaluated for:
– Confirmation of the asthma diagnosis.
– Identification of the mechanism of the exacerbations/persisting
symptoms.
– Assessment of adherence to therapy.
– Associated co-morbidities.
• Contributing factors:
– Poor adherence
– Psychosocial factors
– Smoking.
• Management should facilitated by a multidisciplinary difficult asthma
service.
• Systemic monoclonal antibody therapy may be appropriate for patients
with high corticosteroid use such as:
– Anti-IgE treatment for atopic patients with perennial allergen
exposure.
– Anti-interleukin-5 treatment for eosinophilic disease.
• Possible role for bronchial thermoplasty (thermoelectric current altering
smooth muscle within endobronchial tree).
9. PROGNOSIS
Persistent airway inflammation and remodelling can result in:
•
• Fixed airway obstruction (becoming more like COPD).
• Worsening lung function.
• An acceleration in lung function decline occurs with frequent and
severe exacerbations.
Life expectancy is similar to the general population:
•
• Approximately 1, 300 people died from asthma in the UK in 2005.
• Mortality is often associated with failure of the patient or staff to recog-
nise the severity of the attack.
• Asthma deaths are associated with 90% of preventable contributing fac-
tors e.g. non-adherence, poor inhaler technique and smoking.
Respiratory Medicine
3.1 Acute Exacerbations of Asthma
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3.1 ACUTE EXACERBATIONS OF ASTHMA
1. RECOGNITION OF ACUTE ASTHMA
Severity of an acute exacerbation of asthma should be assessed using the
•
criteria set out in Table 3.3.
Table 3.3 Recognition of moderate severe and life-threatening asthma.
MODERATE ACUTE SEVERE LIFE-THREATENING
EXACERBATION ASTHMA ASTHMA
PEFR • 50–75% • 33–50% • <33% predicted/best
predicted/best predicted/best
Clinical • Increasing • Resp. rate >25 • SaO
features symptoms • Heart rate >110 • PaO2 <8kPa
• No features of • SaO2 ≥92% • Normal or raised pCO
acute severe • Inability to • Silent chest
asthma complete • Cyanosis
sentence in one • Poor respiratory effort
breath • Bradycardia/
<92%
2
arrhythmia/
hypotension
• Exhaustion
• Confusion
• Coma
57
2
2. MANAGEMENT OF ACUTE ASTHMA EXACERBATIONS
Initial management is carried out according to Figure 3.3:
•
Monitoring of the following should be carried out throughout:
•
• Peak expiratory flow rate:
• Repeat 15 - 30 minutes after starting treatment.
• Pulse oximetry
• Arterial blood gases:
• If SpO29< 2% initially.
• Within 1 hour of starting treatment if initial PaO
normal/raised or patient deteriorates.
Respiratory Medicine
< 8kPaP, aCO
22
Asthma58
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Respiratory Medicine
Figure 3.3 Management of an acute asthma exacerbation.
3.1 Acute Exacerbations of Asthma
https://t.me/med1917
At discharge:
•
• Patients should have been on discharge medication for 12–24 hours.
• Should be off nebulised therapy for minimum 24 hours.
• Inhaler technique should have been checked.
• PEFR > 75% in most cases with diurnal variation < 25%.
• Issue with oral/inhaled steroids.
• Provide written asthma action plan.
• Address concomitant smoking.
• Arrange follow-up:
– With GP within 2 days.
– At respiratory clinic within 4 weeks.
MICRO-case
You are an SHO working nights in A&E when a 20-year-old male student
is brought in acutely short of breath. Initial examination and investigations reveal a respiratory rate of 33 with a heart rate of
SaO
is maintained at 94% . He tells you that he suffers with asthma and
2
you begin management with oxygen, nebulised salbutamol, ipratropium,
and oral prednisolone. His condition improves with this treatment and
he is admitted to the ward where nebulised medication is administered
every 4–6hours until he is stabilised. After a further 24hours without
nebulised medication, he is stable on discharge medication and ready
to go home. His inhaler technique is checked and found to be perfect,
but further history taking reveals a worsening of his asthma over the last
year or so: he is frequently woken by his symptoms and has struggled
when playing football for the university team. Areview of his prescription
reveals that he is prescribed inhaled corticosteroids, LABA and SABA.
He confesses that since starting university, he often forgets to take his
medication, especially after a heavy night on the town. In addition, he is
yet to register with the university GP so has missed several asthma review
appointments.
Key Points
Severe asthma is suggested by:
PEFR of 33- 50% of predicted/best, inability to complete sentences,
•
respiratory rate >25, heart rate >
tion at
> 92%.
Life-threatening asthma is associated with:
•
Signs of exhaustion, such as a decreased respiratory effort, bra-
•
dycardia, silent chest and decrease in
When managing difficult asthma, it is important to consider psychosocial factors and adherence to medication. Inhaler technique should
be checked and an asthma action plan provided upon discharge from
hospital.
110 but maintenance of O
O
117; however,
saturations.
2
satura-
2
59
Respiratory Medicine
4
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Chronic Obstructive
Pulmonary Disease
1. DEFINITION
Chronic obstructive pulmonary disease (COPD) is defined by non-reversible
•
airflow limitation with variable combination of airway inflammation and
parenchymal lung destruction.
2. EPIDEMIOLOGY
It’s estimated that there are ~1 million patients in England and Wales with
•
diagnosed COPD.
COPD is the fifth commonest cause of death in the UK.
•
Diagnosis is usually in the seventh decade of life, and prevalence increases
•
with age.
3. AETIOLOGY AND RISK FACTORS
Cigarette smoking.
•
• Most important risk factor.
α1-Antitrypsin deficiency (see MICRO-Print).
•
Air pollution.
•
Occupational exposures:
•
• Coal mining, concrete manufacturing, construction, foundry work,
manufacturing, farming, transportation.
Neonatal chronic lung disease (due to preterm birth) can result in
•
emphysema.
Repeated lower respiratory tract infections.
•
History of pulmonary TB.
•
MICRO-print
a
Antitrypsin Deficiency
1-
Autosomal recessive gene mutation in SERPINA gene on chromosome
14. Deficiency in a
tease activity, especially neutrophil-derived elastases.
DOI: 10.1201/9781315113937-5
antitrypsin leads to unopposed pro-
1-
continued…
Chronic Obstructive Pulmonary Disease
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61
continued…
the absolute level of α1-antitrypsin, but will also assess the phenotype/
genotype by isoelectric focussing where the protein migrates in a gel
according to its isoelectric point or charge in a pH gradient. Normal
A1AT is termed M, as it migrates toward the centre of the gel. Other
variants are less functional and are termed A–L and N–Z, dependent on
whether they run proximal or distal to the M band. Individuals inherit 2
copies of the gene and so the most common genotypes are:
PiMM: 100% (normal).
•
PiMS:
•
•
•
•
•
Individuals with one normal gene (M) are not at increased risk of disease
but might need counselling on transmission to children. Those with two
abnormal genes are at increased risk of:
•
•
An IV replacement therapy has been developed but is not licensed in
the UK.
4. PATHOPHYSIOLOGY
80%
PiSS
:% 60
PiMZ
:% 60
PiSZ: 40% of normal serum level of A1AT.
PiZZ:
10- 15%
Lung disease: COPD.
Liver disease: neonatal jaundice, hepatitis, cirrhosis, liver failure.
Diagnosed through a blood test – the lab will measure
of normal serum level of A1AT.
of normal serum level of A1AT.
of normal serum level of A1AT.
(severe alpha-1 antitrypsin deficiency).
Prolonged repeated exposure to noxious chemicals leads to increase in oxida-
•
tive stress and results in adaptive changes within the lung.
An exaggerated response to noxious substances may result in pathological
•
changes, described below.
Inflammation in COPD is mediated by neutrophils, macrophages, T-lym-
•
phocytes (particularly CD8 cells) and dendritic cells.
Imbalance present between the action of proteases and anti-proteases (such as
•
α1-antitrypsin).
• Oxidative stress causes release of proteases from inflammatory cells
promoting inactivation of antiproteases.
Oxidative stress is pro-inflammatory and promotes mucus secretion.
•
Chronic inflammation of the small airways, resulting in:
•
• Fibrosis and remodelling.
• Mucous cell hypertrophy.
• Ciliary dysfunction and squamous metaplasia.
– Difficulty expectorating inhaled pathogens, due to failure of the
mucociliary escalator.
Respiratory Medicine
Chronic Obstructive Pulmonary Disease62
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• Long-term airflow limitation:
– In part due to the chronic inflammatory process in the conducting
airways.
Loss of elastic recoil in the airways results in airway collapse on expiration:
•
• Results in air trapping and hyperinflation of the lungs.
• Hyperinflation reduces the inspiratory capacity and functional residual
capacity.
• is causes shortness of breath on exertion.
Ventilation-perfusion mismatch:
•
• Causes hypoxaemia with or without hypercapnia.
5. CLINICAL FEATURES
Symptoms
•
• Productive cough.
• Wheeze.
• Breathlessness, particularly on exertion (see MICRO-Facts mMRC
dyspnoea score).
• Frequent exacerbations, often caused by respiratory infection.
Signs
•
• Mild disease:
– May be none.
– Wheeze.
• In severe disease:
– Tachypnoea.
– Prolonged expiratory phase.
– Use of accessory muscles of respiration.
– Pursing of lips.
– Intercostal indrawing.
– Hyperinflated chest and decreased chest expansion.
– Signs of cor pulmonale in late disease.
– Low BMI.
MICRO-facts
The mMRC (Modified Medical Research Council) Dyspnoea Scale is used
to assess the degree of baseline functional disability due to dyspnoea.
Respiratory Medicine
Chronic Obstructive Pulmonary Disease
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SCORE SYMPTOMS
0 Breathless only with strenuous exercise.
1 Short of breath when hurrying or walking up a hill.
2 Slower than most people of same age on level because of
breathlessness, or have to stop for breath when walking at
own pace on the level.
3 Stop for breath after walking ~100 m or after a few minutes at
own pace on the level.
4 Too breathless to leave house/breathless when dressing.
MICRO-references
British Thoracic Society (BTS) NICE guideline for COPD (updated 2019),
available at:
www.nice.org.uk/guidance/ng115
6. INVESTIGATIONS
Spirometry:
•
• Spirometry should be performed for diagnosis in all patients with sus-
pected COPD.
• A diagnosis of airflow obstruction can be made if the FEV
/FVC ratio
1
is less than 0.7 (70% ). See Chapter 1: Clinical assessment.
• If FEV
> 80% , appropriate symptoms are required to confirm the
1
diagnosis.
• Severity of airflow obstruction is classified as in Table 4.1.
63
Table 4.1 Severity of COPD.
STAGE SEVERITY FEV
1 Mild <0.7 ≥80
2 Moderate <0.7 50–79
3 Severe <0.7 30–49
4 Very Severe <0.7 <30 or <50 with respiratory
POST
BRONCHODILATOR POST BRONCHODILATOR
/FVC FEV1 (% OF PREDICTED)
1
failure
Respiratory Medicine
Chronic Obstructive Pulmonary Disease64
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• Unlike asthma, COPD does not usually demonstrate much reversibility.
– A diagnosis of COPD should be reconsidered if there is a large
(>400 mL) response to inhaled therapy and/or oral prednisolone
(See Table 4.2).
Imaging:
•
• Chest X-ray
– To exclude other lung diseases.
– Often normal in early stages of the disease.
– Advanced COPD may have the following features on chest X-ray
(see Figure 4.1):
◯
Hyperinflated lungs
◯
Flattened diaphragm
◯
Hyperlucent lungs
◯
Central pulmonary artery dilatation
◯
Bullae.
Figure 4.1 Chest X-ray of a patient with COPD. The X-ray shows that the lungs are
Respiratory Medicine
hyperinflated and the diaphragms are flattened.
Chronic Obstructive Pulmonary Disease
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• CT scan:
• is is more effective for detecting pathological changes such as
emphysema but is not routinely performed (See Figure 4.2).
65
Respiratory Medicine
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