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DASPITE is an educational resource for healthcare professionals in training. DASPITE should not be used for diagnostic purposes. Always consult local guidelines for treatment decisions. Should you have concerns about your health, please visit your doctor. 

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DASPITE Limited is a company registered in Scotland (No. SC627155)

DASPITE © 2019

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.

Moderate:

Increasing symptoms

PEF >50-75% of best/predicted

No signs of severe asthma

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

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

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

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.

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

FBC

For evidence of infection

U&Es

Arterial Blood Gas

To assess oxygenation and determine severity

CXR

For evidence of infection/pneumothorax

 

TREATMENT

Oxygen to maintain saturations of 94-98%

Salbutamol/Terbutaline via oxygen driven nebuliser (can be given multiple times)

Ipratropium Bromide via oxygen driven nebuliser

IV Hydrocortisone or PO Prednisolone

If life-threatening features, consider infusion of IV Magnesium Sulphate

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:

  • Have been on discharge medication for 12-24 hours

  • Have inhaler technique checked

  • Be referred to the respiratory specialist nurse (for new diagnoses)

  • Have treatment with oral and inhaled steroids

  • Have their own peak flow meter

  • Arrange an appointment with their GP within 2 working days

  • Have a follow up appointment at the respiratory clinic within 4 weeks

REFERENCES