Acute severe asthma in adults: quick reference

Immediate management

The most dangerous asthma attack is the silent one. A patient who has become calm, quiet in the chest and stopped struggling may be about to stop breathing. Diminishing wheeze means improvement only if air entry, speech, work of breathing, level of consciousness and PEF improve at the same time.

Acute severe asthma is characterised by bronchospasm, mucosal oedema and mucus plugging. Expiratory flow limitation causes air trapping and dynamic hyperinflation. The consequences are increased work of breathing, exhaustion and, in the most severe cases, hypotension, pneumothorax and respiratory arrest [1].

The first few minutes

1. Sit the patient up and minimise physical exertion.
2. Attach continuous pulse oximetry and an ECG.
3. Give oxygen in hypoxaemia.
4. Start an inhaled short-acting β2 agonist immediately.
5. Add ipratropium in a severe or life-threatening attack.
6. Give a systemic steroid early.
7. Insert intravenous access, but do not let blood sampling or cannulation delay inhaled treatment.
8. Reassess speech, work of breathing, level of consciousness and air entry repeatedly.
9. Measure PEF or FEV1 if the patient can manage it without delaying treatment.
10. Call anaesthetics and intensive care early with life-threatening features or an inadequate response.

First-line treatment is oxygen in hypoxaemia, repeated doses of an inhaled short-acting β2 agonist, ipratropium in more severe attacks, and a systemic steroid given early [2,3].

Grading

Grade the severity by the most serious finding. A patient does not have to meet every criterion in a column. Clinical deterioration or a poor response to treatment carries more weight than a single apparently reassuring measurement.

The classification is based on a combination of clinical findings, oxygenation and objective measurement of airflow. International thresholds vary somewhat, but a PEF of 50 percent or less together with marked symptoms indicates a severe attack, while a PEF below 33 percent or signs of ventilatory failure means life-threatening illness [1,2].

Important interpretation of the blood gas

A normal or rising pCO₂ during an ongoing severe asthma attack is an alarm sign.

Early in a severe attack the patient usually hyperventilates and the pCO₂ is low. A normal pCO₂ may therefore mean that alveolar ventilation is already failing. A raised pCO₂, respiratory acidosis, a falling pH or a rising trend indicate exhaustion and impending respiratory arrest.

A venous blood gas can give useful information about pH and the trend in carbon dioxide, but in critical illness, marked hypoxaemia, or when an accurate PaCO₂ is needed, an arterial blood gas should be considered. Do not wait for the blood gas result before starting treatment.

Clinical assessment

History that affects the level of risk

Ask briefly and to the point:

• When did the deterioration begin, suddenly or over several days?
• Which drugs, and how many doses, has the patient taken?
• Is the patient on an inhaled corticosteroid or other anti-inflammatory treatment?
• Previous intensive care, intubation or a near-fatal attack?
• Hospital care or a course of steroids in the past year?
• Triggers such as infection, allergen, smoke, NSAIDs or beta blockers?
• Possible anaphylaxis?
• Chest pain, unilaterally reduced breath sounds or thromboembolic risk?
• Adherence, inhaler technique and access to medication?
• Pregnancy and comorbidity?

People with previously mild or moderate asthma can also have a life-threatening attack. A recent severe exacerbation is a strong risk marker for further exacerbations [1].

Examination

Assess in particular:

• level of consciousness and ability to cooperate
• speech
• respiratory rate and pattern of breathing
• use of accessory muscles
• air entry, symmetry and the presence of a silent chest
• pulse, blood pressure and signs of pulsus paradoxus
• saturation on air and on oxygen
• urticaria, angioedema or circulatory compromise
• signs of pneumothorax, pneumonia or heart failure

Dynamic hyperinflation raises intrathoracic pressure, affects venous return and the load on the right ventricle, and can reduce cardiac output. Pulsus paradoxus and hypotension may therefore be signs of very marked obstruction [4].

PEF or FEV1

Objective measurement of airflow improves the assessment of severity and of the response to treatment [3].

• Measure the PEF before treatment if this can be done without delay.
• Repeat it after the initial intensive treatment and before deciding on the level of care or discharge.
• Use the personal best value where it is known, otherwise the predicted value.
• Do not force an exhausted, confused or peri-arrest patient to perform a PEF.
• A normal or relatively good PEF does not exclude another serious diagnosis.

A single PEF measurement must not outweigh clinical deterioration. Inability to blow can in itself be a serious sign.

Treatment of a severe attack

Exact doses and choice of agent should follow the current local emergency protocol and Swedish drug recommendations. International guidelines may use different steroid preparations and dose conversions from Swedish practice.

Oxygen

Give oxygen in hypoxaemia and titrate the treatment. The target is usually a saturation of 94 to 98 percent. The saturation must be monitored continuously in a severe attack.

Hypoxaemia is due above all to ventilation–perfusion mismatch. Oxygen treats the hypoxaemia but not the bronchospasm, the inflammation or the dynamic hyperinflation. An improved saturation is therefore not sufficient to conclude that the attack has turned.

Short-acting β2 agonist

An inhaled short-acting β2 agonist is the most important immediate bronchodilator treatment. The dose is titrated according to the clinical response, the PEF where this is feasible, and adverse effects.

A metered-dose inhaler with a large spacer is an effective alternative to a nebuliser in a patient who can cooperate. In studies of adults the two routes have given similar lung function and admission rates, but people with life-threatening asthma were poorly represented [5]. A nebuliser is therefore practical in very marked dyspnoea, poor ability to cooperate, concurrent oxygen therapy, or when repeated high doses are needed.

Watch for:

• tachycardia and palpitations
• tremor and agitation
• hypokalaemia
• hyperglycaemia
• a rise in lactate
• chest pain and arrhythmia

High doses of a β2 agonist can cause type B lactic acidosis. The patient may then continue to hyperventilate despite improved airflow. Do not automatically interpret persisting tachypnoea as continuing bronchospasm, and do not escalate the β2 agonist uncritically. First exclude tissue hypoperfusion, sepsis and other dangerous causes of the raised lactate [6].

Ipratropium

In a severe attack, ipratropium should be given in addition to the short-acting β2 agonist. The combination reduces the risk of admission compared with a β2 agonist alone, particularly in severe exacerbations. In a Cochrane review the relative risk of hospital admission was 0.72, with a 95 percent confidence interval of 0.59 to 0.87 [7].

The greatest benefit is during the initial emergency treatment. Continued routine ipratropium after stabilisation or throughout the admission has weaker evidence.

Systemic steroid

The clinical effect of the steroid comes after several hours. Give it early, therefore, not as a last measure.

An oral steroid is as a rule as effective as intravenous treatment. Intravenous administration is reserved mainly for the patient who is vomiting, cannot swallow, has reduced consciousness or is to be intubated. Steroid doses higher than the standard dose have not been shown to give a better effect in patients not on mechanical ventilation [8].

A short oral course after the emergency attendance reduces relapse, further hospital care and the need for extra β2 agonist. In a Cochrane review, relapse during the first week fell with a relative risk of 0.38, with a 95 percent confidence interval of 0.20 to 0.74 [9]. Tapering is not normally needed after a short course, unless the patient is already on long-term systemic steroid.

Intravenous magnesium sulfate

Magnesium sulfate is not routine treatment in mild or moderate exacerbations. Consider it in:

• a life-threatening or near life-threatening attack
• a PEF below about 50 percent with a poor initial response
• persisting marked work of breathing after repeated inhalations
• planned or imminent intensive care

Studies suggest better lung function and reduced admission above all in the subgroup with acute severe asthma. In a systematic review the PEF in this group improved by an average of 52 litres per minute, and the risk of admission fell [10]. A commonly studied adult dose is 2 g intravenously, but dosing, infusion time, contraindications and monitoring should follow the local protocol.

Bear in mind hypotension, reduced tendon reflexes and accumulation in marked renal failure.

Nebulised magnesium must not replace intravenous magnesium. The evidence for a clinically meaningful benefit of nebulised magnesium is uncertain [11].

Intravenous β2 agonist, aminophylline and other rescue treatments

An intravenous β2 agonist should not be used routinely in addition to adequate inhaled treatment. The evidence in adults is very limited and has not shown a definite reduction in admissions, while the risk of hypokalaemia, arrhythmia and myocardial ischaemia increases [12].

Aminophylline has a narrow therapeutic range and can cause nausea, vomiting, tachycardia, arrhythmia and seizures. It should not be given routinely during the initial treatment. If intravenous bronchodilator rescue treatment is considered, it should be done together with anaesthetics, intensive care or respiratory medicine [2,13].

Heliox, ketamine, inhalational anaesthetics, bronchoscopy and extracorporeal life support are specialist treatments for selected refractory cases. They must not delay established drug treatment or necessary intubation.

Antibiotics

A virus is a common trigger of an asthma exacerbation, but that is not an indication for antibiotics. Give antibiotics only where there is clear evidence of bacterial infection, above all radiologically or clinically suspected pneumonia.

Studies of routine antibiotic treatment in asthma exacerbations are small and heterogeneous and give no reliable support for a reduction in admission or relapse [14]. Purulent sputum alone is not sufficient for antibiotics.

Fluids

Many patients are dehydrated because of hyperventilation, sweating and reduced intake. Correct clinical hypovolaemia, particularly in hypotension or before intubation.

At the same time, avoid uncritical large-volume fluid administration. Hypotension may be due to dynamic hyperinflation and reduced venous return, not solely to fluid depletion [4].

Monitoring and investigations

Continuous monitoring

In a severe attack:

• continuous saturation
• continuous ECG
• frequent blood pressure measurement
• repeated assessment of the level of consciousness
• repeated assessment of speech, respiratory rate and work of breathing
• repeated auscultation
• PEF or FEV1 when the patient can perform the measurement

Document the time of every treatment and the patient's response. A severe attack can deteriorate rapidly even after a temporary improvement.

Tests

Consider:

• a blood gas in a severe or life-threatening attack, a saturation below 92 percent, exhaustion or deterioration
• potassium with repeated high doses of β2 agonist
• glucose
• lactate with persisting tachypnoea, acidosis or circulatory compromise
• creatinine before or after magnesium in impaired renal function
• full blood count and inflammatory markers only if infection or another differential diagnosis is suspected
• troponin with chest pain, ischaemic ECG changes or significant cardiovascular risk

A rise in lactate after intensive β2 stimulation can occur without shock. Always interpret the value together with perfusion, blood pressure, clinical airflow and the rest of the acid-base status [6].

Imaging

A chest radiograph is not needed routinely in a typical uncomplicated asthma exacerbation. Request one where there is suspicion of:

• pneumothorax or pneumomediastinum
• pneumonia
• heart failure
• a foreign body
• unilateral findings
• unexplained hypoxaemia
• a poor response to correct treatment
• a need for intensive care or intubation

Lung ultrasound can rapidly support the diagnosis of pneumothorax or pulmonary oedema, but does not replace clinical assessment.

Signs of impending respiratory arrest

Call anaesthetics and intensive care immediately with any of the following:

• a silent or nearly silent chest
• falling level of consciousness or confusion
• exhaustion, or decreasing work of breathing despite persisting obstruction
• bradypnoea, irregular breathing or apnoea
• cyanosis or hypoxaemia despite oxygen
• a normal or rising pCO₂
• respiratory acidosis
• bradycardia or serious arrhythmia
• hypotension or circulatory collapse
• a PEF below 33 percent or an unmeasurable value
• an inadequate response to intensive initial drug treatment
• clinical deterioration even as the wheeze diminishes

Previous mechanical ventilation for asthma is a strong risk marker. In a systematic review, previous intensive care was associated with about a fivefold higher odds of near-fatal or fatal asthma, and previous mechanical ventilation with an even higher risk [15].

NIV and intubation

NIV

NIV has a less established role in acute asthma than in COPD exacerbation. Older randomised trials were small and gave no reliable answer on intubation or mortality [16]. A more recent systematic review found possible reductions in intubation and admission, but the evidence was judged to be of low or very low quality [17].

A brief trial of NIV can be considered if the patient:

• is alert and fully cooperative
• can protect their airway
• has marked work of breathing but is not exhausted
• is haemodynamically stable
• can be monitored somewhere immediate intubation is possible

NIV must not be used to postpone intubation in reduced consciousness, vomiting or a risk of aspiration, haemodynamic instability, increasing hypercapnia, marked exhaustion or peri-arrest.

A high-flow nasal cannula can improve comfort and oxygenation but has no established evidence as ventilatory rescue treatment in life-threatening asthma.

Intubation

The indications are above all:

• respiratory arrest
• severe exhaustion
• reduced consciousness or inability to protect the airway
• progressive respiratory acidosis
• refractory hypoxaemia
• circulatory collapse
• failed NIV in a carefully selected patient

Intubating a severely obstructed patient is hazardous. Arrange experienced airway expertise, haemodynamic support and a plan for immediate treatment of pneumothorax. Peri-intubation collapse may be due to hypovolaemia, drug effects and a sudden worsening of dynamic hyperinflation.

Principles of invasive ventilation

Ventilation must limit dynamic hyperinflation:

• a low respiratory rate
• a sufficiently low minute ventilation
• a long expiratory time
• a high inspiratory flow and a short inspiratory time
• a moderate tidal volume
• monitoring of auto-PEEP and plateau pressure
• acceptance of permissive hypercapnia where this is haemodynamically and neurologically tolerable

Attempting to normalise the pCO₂ rapidly by means of a high minute ventilation can increase air trapping, cause hypotension and precipitate barotrauma. Pneumothorax occurs in approximately 3 to 6 percent of mechanically ventilated patients with severe asthma [6].

With sudden hypotension after intubation, dynamic hyperinflation and ventilator-induced obstructive shock must be considered immediately, while pneumothorax, drug effects and other causes are assessed. Disconnection from the ventilator for a short, controlled period may be needed to allow exhalation, but should be led by anaesthetics or intensive care [6].

Differential diagnoses

The absence of wheeze does not exclude asthma. It can mean either normal airflow or almost no airflow.

Red flags

• Previous intensive care or intubation for asthma.
• Recent hospital care, an emergency attendance or a course of systemic steroids.
• Rapid deterioration over minutes to a few hours.
• Poor perception of airway obstruction.
• Overuse of a short-acting β2 agonist.
• No inhaled corticosteroid, or poor adherence to one.
• Psychosocial problems, substance use or difficulty accessing care and medication.
• NSAIDs in a patient with NSAID-exacerbated respiratory disease.
• A non-selective beta blocker, including as eye drops.
• Smoking and exposure to irritants.
• Sending the patient home before the improvement is stable.

Overuse was defined in a recent meta-analysis as at least three canisters of short-acting β2 agonist per year. This was associated with higher mortality, relative risk 2.04, and more exacerbations, relative risk 1.93. The results rest largely on observational studies and are probably influenced by the fact that high use also marks poor asthma control and inadequate anti-inflammatory treatment [18].

No patient with asthma should leave the emergency department with a short-acting bronchodilator alone as their long-term treatment strategy.

Level of care and observation

Consider admission

Admit, or discuss with respiratory medicine or the on-call medical team, in:

• persisting symptoms after initial treatment
• a PEF or FEV1 below 50 percent after treatment
• a saturation below 92 percent on air
• a need for frequent inhalations
• previous near-fatal asthma
• presentation at night with a severe exacerbation
• pregnancy, significant comorbidity or diagnostic uncertainty
• pneumonia, pneumothorax or another complication
• an inability to follow treatment or to seek help again
• a significant risk of relapse despite improved lung function

Intensive care is indicated with life-threatening findings, a rising pCO₂, respiratory acidosis, exhaustion, impaired consciousness, haemodynamic instability or an inadequate response to maximal initial treatment.

Conditions for discharge

Discharge can be considered when:

• symptoms and work of breathing have clearly improved
• the patient can speak and walk without marked dyspnoea
• the saturation is stable on air
• the PEF has improved and is stable after a period of observation
• the effect persists after the last intensive round of inhalations
• the patient has working inhalers and can use them correctly
• continued anti-inflammatory treatment has been prescribed
• the patient understands when to seek emergency help

The decision must be based on both objective lung function and individual risk factors, not merely on the patient feeling better [19].

Before discharge

• Prescribe a course of oral steroid according to the current local protocol.
• Ensure an inhaled corticosteroid as part of continued treatment.
• Do not prescribe a short-acting β2 agonist alone.
• Check inhaler technique in practice.
• Check that the patient actually has access to the medication.
• Provide a written treatment plan with clear thresholds for stepping up treatment and for seeking emergency care.
• Review the likely trigger and address modifiable risk factors.
• Advise the patient to seek help immediately with impaired speech, deterioration at night, a poor response to bronchodilation, a rising need for medication or a falling PEF.
• Plan follow-up within 1 to 2 weeks, sooner after a life-threatening attack or with persisting symptoms.
• After intensive care or repeated exacerbations, the patient should be assessed by a specialist experienced in asthma.

A short course of steroid reduces the risk of relapse. Intramuscular and oral steroid appear to give equivalent protection against relapse, but oral treatment is normally simpler and more flexible. Intramuscular treatment can be considered if adherence to tablets is likely to be very poor [20].

An inhaled corticosteroid should be continued or started as long-term anti-inflammatory treatment. It does not reliably replace the systemic course of steroid after a severe attack. Studies have not shown any definite additional short-term benefit of adding a high-dose inhaled corticosteroid on top of a systemic steroid merely to treat the current exacerbation, but the patient's usual inhaled corticosteroid must not be stopped [21].

References

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