acute exacerbation of asthma
Written by Sarah Lee
Last Reviewed: April 2019
Review Due: April 2020
DEFINITION
'an acute or subacute episode of progressive worsening of symptoms of asthma, including shortness of breath, wheezing, cough, and chest tightness'
severity
The management of an acute asthma exacerbation is guided by the severity of the attack, as defined below.
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Moderate:
Increasing symptoms
PEF >50-75% of best/predicted
No signs of severe asthma
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Severe (any one of the following):
Peak flow 33-50% best or predicted
Respiratory Rate ≥ 25/min
Heart Rate ≥ 110/min
Inability to complete sentences in one breath
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Life-Threatening (any one of the following):
Peak flow < 33% best or predicted
Arterial oxygen saturation (SpO2) < 92%
Partial arterial pressure of oxygen (PaO2) < 8 kPa
Normal partial arterial pressure of carbon dioxide (PaCO2) (4.6–6.0 kPa)
Silent chest
Cyanosis
Poor respiratory effort
Arrhythmia
Exhaustion
Altered conscious level
Hypotension
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Near-Fatal (any one of the following):
Raised PaCO2
Requiring mechanical ventilation with raised inflation pressures
AETIOLOGY
Multiple factors may contribute to the onset of an acute exacerbation of asthma, including infection or exposure to allergens/precipitants.
SIGNS AND SYMPTOMS
Symptoms
Intermittent Dyspnoea
Cough (often nocturnal)
Wheeze
Sputum Production (yellow)
Chest Tightness
Exercise Intolerance
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Signs
Tachypnoea
Widespread wheeze on auscultation
Hyper-resonant percussion
PATHOPHYSIOLOGY
1. Airway Inflammation
Exposure to allergen triggers an IgE-mediated Type 1 hypersensitivity reaction within the lungs.
Mast cell degranulation and production of inflammatory mediators (eg histamine, leukotrines) and cytokines (eg Il-4, IL-5) occurs.
Inflammatory cells including eosinophils migrate to airways produce more mediators, propagating the inflammatory response.
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2. Airway Obstruction
Inflammation causes bronchospasm, mucosal oedema and increased mucus secretion within airways.
Chronic inflammation may cause bronchial smooth muscle hypertrophy and airway remodelling over time which may cause airflow limitations to be only partially reversible.
3. Bronchial Hyperresponsiveness
Eosinophil products increase resting tone of bronchial smooth muscle.
Bronchi become hyperresponsive and produce a larger response, more quickly to the allergen on the next exposure.
Investigations
Peak Expiratory Flow (PEF)
With comparison to baseline
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FBC
For evidence of infection
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U&Es
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Arterial Blood Gas
To assess oxygenation and determine severity
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CXR
For evidence of infection/pneumothorax
TREATMENT
Oxygen to maintain saturations of 94-98%
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Salbutamol/Terbutaline via oxygen driven nebuliser (can be given multiple times)
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Ipratropium Bromide via oxygen driven nebuliser
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IV Hydrocortisone or PO Prednisolone
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If life-threatening features, consider infusion of IV Magnesium Sulphate
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Ensure patient is monitored for signs of detioration, and consider prompt referral to HDU/ITU if severe or life-threatening features present
DISCHARGE PLANNING
Before discharge from hospital, patients should:
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Have been on discharge medication for 12-24 hours
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Have inhaler technique checked
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Be referred to the respiratory specialist nurse (for new diagnoses)
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Have treatment with oral and inhaled steroids
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Have their own peak flow meter
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Arrange an appointment with their GP within 2 working days
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Have a follow up appointment at the respiratory clinic within 4 weeks
REFERENCES
Oxford Handbook of Clinical Medicine