Initial assessment
- Clinical features (N.B. none of these singly or together is specific and their absence does not exclude a severe attack)
- Dyspnoea
- Tachypnoea
- Tachycardia
- Wheezing
- Silent chest
- Cyanosis
- Accessory muscle use
- Altered consciousness
- Collapse
- Peak expiratory flow (PEF) or FEV1
- Measurements of airway calibre improve recognition of the degree of severity, the appropriateness or intensity of therapy, and decisions about management in hospital or at home.
- PEF or FEV1 are useful and valid measures of airway calibre. PEF is more convenient in the acute situation.
- PEF expressed as a percentage of the patient’s previous best value is most useful clinically, however PEF as a percentage of predicted (dependent on age, height and sex) gives a rough guide in the absence of a known previous best value.
- Pulse oximetry
- Measurement of oxygen saturations (SpO2) determine the adequacy of oxygen therapy and the need for arterial blood gas measurement.
- SpO2 should be maintained between 94 - 98%.
- Blood gases
- Patients with SpO2 < 92% (regardless of whether the patient is on air or oxygen) or other features of life-threatening asthma require arterial blood gas measurement.
- SpO2 < 92% is associated with a risk of hypercapnia, which is not detected with pulse oximetry (the risk of hypercapnia with SpO2 > 92% is much less).
- Chest x-ray
- Chest x-ray is not routinely recommended in the absence of:
- Suspected pneumomediastinum or pneumothorax
- Suspected consolidation
- Life-threatening asthma
- Failure to respond to treatment satisfactorily
- Requirement for ventilation
Classification
Levels of severity of acute asthma attacks in adults:
| Level of severity |
Criteria |
| Moderate |
- Increasing symptoms
- PEFR > 50 - 75% of best or predicted
- No features of acute severe asthma
|
| Severe |
Any one of:
- PEFR 33 - 50% of best or predicted
- Respiratory rate ≥ 25 breaths/minute
- Heart rate ≥ 110 beats/minute
- Inability to complete sentences in one breath
|
| Life-threatening |
SpO2 <92% plus any one of the following in a patient with severe asthma:
- Clinical signs
- Altered conscious level
- Exhaustion
- Arrhythmia
- Hypotension
- Cyanosis
- Silent chest
- Poor respiratory effort
- Measurements
- PEFR < 33% of best or predicted
- PaO2 < 8 kPa
- 'Normal' PaCO2 (4.6 - 6.0 kPa)
|
| Near-fatal |
Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures |
Management
- Oxygen therapy
- Give controlled supplementary oxygen to all hypoxaemic patients with acute severe asthma titrated to maintain an SpO2 level of 94 - 98%.
- Do not delay oxygen administration in the absence of pulse oximetry but commence monitoring of SpO2 as soon as it becomes available.
- β2-agonist bronchodilators
- Use high-dose inhaled β2 agonists as first-line agents in patients with acute asthma and administer as early as possible.
- In most cases inhaled β2 agonists given in high doses act quickly to relieve bronchospasm with few side effects.
- There is no evidence for any difference in efficacy between salbutamol and terbutaline. Nebulised adrenaline (epinephrine), a non-selective β2 agonist, does not have significant benefit over salbutamol or terbutaline.
- In patients with mild to moderate asthma, β2 agonists can be administered by repeated activations of a pMDI via an appropriate large volume spacer.
- In patients with with acute-severe or life-threatening features, β2 agonists should be administered by wet nebulisation driven by oxygen, if available.
- In patients with severe asthma that is poorly responsive to an initial bolus dose of β2 agonist, repeat doses of β2 agonists at 15 - 30 minute intervals or give continuous nebulisation of salbutamol at 5 - 10 mg/hour (requires the appropriate nebuliser).
- Reserve intravenous β2 agonists for those patients in whom inhaled therapy cannot be used reliably. If intravenous β2 agonists are used, consider monitoring serum lactate to monitor for toxicity.
- Ipratropium bromide
- Combining nebulised ipratropium bromide with a nebulised β2 agonist produces significantly greater bronchodilation than β2 agonist alone, leading to faster recovery and shorter duration of admission.
- Add nebulised ipratropium bromide (0.5 mg 4 – 6 hourly) to β2 agonist treatment for patients with acute severe or life threatening asthma or those with a poor initial response to β2 agonist therapy.
- Steroid therapy
- Steroids reduce mortality, relapses, subsequent hospital admission and requirement for β2 agonist therapy. The earlier they are given in the acute attack the better the outcome.
- Give steroids in adequate doses to all patients with an acute asthma attack.
- Steroid tablets are as effective as injected steroids provided they can be swallowed and retained.
- Oral prednisolone 40 – 50 mg or parenteral hydrocortisone 400 mg daily (100 mg six hourly) are as effective as higher doses.
- Continue prednisolone (40–50 mg daily) for at least five days or until recovery if longer.
- Do not stop inhaled corticosteroids during prescription of oral corticosteroids.
- Other therapies:
- Magnesium sulphate
- Nebulised magnesium sulphate is not recommended for treatment of adults with acute asthma.
- Consider giving a single dose of IV magnesium sulphate to patients with acute severe asthma (PEF < 50% best or predicted) who have not had a good initial response to inhaled bronchodilator therapy.
- Magnesium sulphate (1.2 - 2 g IV infusion over 20 minutes) should only be used following consultation with senior medical staff.
- Aminophylline
- In an acute asthma attack, IV aminophylline is not likely to result in any additional bronchodilation compared to standard care with inhaled bronchodilators and steroids and may cause side effects such as arrhythmias and vomiting.
- Use IV aminophylline only after consultation with senior medical staff.
- Some patients with near-fatal asthma or life-threatening asthma with a poor response to initial therapy may gain additional benefit from IV aminophylline (5 mg/kg loading dose over 20 minutes unless on maintenance oral therapy, then infusion of 0.5–0.7 mg/kg/hr).
- Antibiotics
- Routine prescription of antibiotics is NOT indicated for patients with acute asthma.
Criteria for hospital admission
- Admit patients with any feature of a life-threatening or near-fatal asthma attack
- Admit patients with any feature of a severe asthma attack persisting after initial treatment
- Patients whose peak flow is greater than 75% best or predicted one hour after initial treatment may be discharged from ED unless they meet any of the following criteria, when admission may be appropriate:
- Still have significant symptoms
- Concerns about adherence
- Living alone/socially isolated
- Psychological problems
- Physical disability or learning difficulties
- Previous near-fatal asthma attack
- Asthma attack despite adequate dose of oral corticosteroid prior to presentation
- Presentation at night
- Pregnancy
Criteria for ITU/HDU referral
Indications for admission to intensive care or high-dependency units include patients requiring ventilatory support and those with acute severe or life-threatening asthma who are failing to respond to therapy, as evidenced by:
- Deteriorating PEF
- Persisting or worsening hypoxia
- Hypercapnia
- ABG analysis showing decreased pH or increased H+
- Exhaustion, feeble respiration
- Drowsiness, confusion, altered conscious state
- Respiratory arrest
Further investigation and monitoring
- Measure and record PEF 15–30 minutes after starting treatment, and thereafter according to the response. Measure and record PEF before and after nebulised or inhaled β2 agonist.
- Record oxygen saturation by oximetry and maintain arterial SpO2 at 94–98%.
- Repeat measurements of blood gas tensions within one hour of starting treatment if:
- the initial PaO2 is <8 kPa unless SpO2 is >92%; or
- the initial PaCO2 is normal or raised; or
- the patient’s condition deteriorates.
- Measure them again if the patient’s condition has not improved by 4–6 hours.
- Measure and record the heart rate.
- Measure serum potassium and blood glucose concentrations.
- Measure the serum theophylline concentration if aminophylline is continued for more than 24 hours (aim for a concentration of 10–20 mg/L or 55–110 mol/L).
Follow up
- It is essential that the patient's primary care practice is informed with 24 hours of discharge from the emergency department or hospital following an asthma attack
Cardiac arrest associated with asthma
Patients most at risk of asthma-related cardiac arrest include those with:
- a history of near-fatal asthma requiring intubation and mechanical ventilation
- hospitalisation or emergency care for asthma in the past year
- low or no use of inhaled corticosteroids
- increasing use and dependence on β2-agonists
- anxiety, depressive disorders and/or poor compliance with therapy
- a history of food allergy in addition to asthma
Causes of cardiac arrest associated with asthma include:
- Severe bronchospasm and mucous plugging leading to asphyxia
- Cardiac arrhythmias caused by hypoxia (or by treatment drugs e.g. β2-agonists or electrolyte abnormalities)
- Dynamic hyperinflation (auto positive end-expiratory pressure (auto-PEEP)) in mechanically ventilated patients; air trapping and 'breath-stacking' causes gradual build up of pressure leading to decreased venous return and blood pressure
- Tension pneumothorax (may be bilateral)
Modifications to resuscitation associated with asthma:
- Follow standard BLS and ALS protocols; ventilation will be difficult because of increased airway resistance; try to avoid gastric inflation
- Intubate the trachea early; there is significant risk of gastric inflation and hypoventilation of the lungs when attempting to ventilate a severe asthmatic without a tracheal tube
- Follow the recommended respiratory rate of 10 breaths/min and tidal volume required for a normal chest rise during CPR (to avoid gas trapping and dynamic hyperinflation)
- If dynamic hyperinflation of the lungs is suspected during CPR, compression of the chest wall and/or a period of apnoea (disconnection of tracheal tube) may relieve gas trapping
- Dynamic hyperinflation increases transthoracic impedance but modern defibrillators are no less effective in patients with higher impedance; as with standard ALS protocol, consider increasing defibrillation energy if the first shock is unsuccessful
- Look for reversible causes using the 4Hs and 4Ts
- Tension pneumothorax can be difficult to recognise during cardiac arrest; it may be indicated by unilateral expansion of the chest wall, shifting of the trachea and subcutaneous emphysema; pleural ultrasound in skilled hands is faster and more sensitive than chest x-ray for detection; early needle decompression followed by chest drain insertion is needed; thoracostomy may be quicker and more effective in the ventilated patient; always consider bilateral pneumothoraces in asthma-related cardiac arrest
- Extracorporeal life support (ECLS) can provide both organ perfusion and gas exchange in cases of otherwise refractory respiratory and circulatory failure