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Disease Summaries

Acute Asthma

Posted: September 2004

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Michael A. Kaliner, MD FAAAAI
Medical Director, Institute for Asthma and Allergy
Chevy Chase and Wheaton, Maryland
Professor of Medicine, George Washington University School of Medicine
Washington, DC
Richard F. Lockey, MD
Professor of Medicine, Pediatrics and Public Health
Director of the Division of Allergy and Immunology
Joy McCann Culverhouse Chair of Allergy and Immunology
University of South Florida College of Medicine and the James A. Haley Veterans' Hospital
Tampa, FL


Asthma exacerbations are avoidable with appropriate, regular therapy backed up by patient education, but in spite of this, in the USA alone, each year approximately 2 million people require emergency treatment, of which a quarter require hospitalization.

To prevent severe exacerbations of asthma, the goals for the physician managing patients with asthma are:

  1. recognition of patients who are at a greater risk for near-fatal or fatal asthma
  2. education of the patient to recognize a deterioration in their disease
  3. provision of an individual action plan for the patient to manage the exacerbation, ie, to know when to seek professional help
  4. management of co-morbidities such as rhinitis, sinusitis, obesity and gastro-esophageal reflux disease (GERD)


Asthma Exacerbations are staged according to severity.

Stage 1

  • Cannot perform full physical activities without shortness of breath


  • Some wheezes on examination
  • Respiratory rate, 15 (normal <12)
  • Pulse 100
  • Peak flows and spirometry reduced by 10%

Stage 2

  • Less able to do physical activity due to shortness of breath
  • Dyspnea on walking stairs
  • May wake up at night short of breath
  • Uncomfortable on lying down
  • Some use of accessory muscles of respiration


  • Wheezing
  • Respiratory rate 18
  • Pulse 111
  • Peak flows and spirometry reduced by 20+%

Stage 3

  • Unable to perform physical activity without shortness of breath
  • Cannot lie down without dyspnea
  • Speaks in short sentences
  • Using accessory muscles


  • Wheezing
  • Respiratory rate 19-20
  • Pulse 120
  • Peak flows and spirometry reduced by 30+%

Stage 4

  • Sitting bent forward
  • Unable to ambulate without shortness of breath
  • Single word sentences (monosyllabic)
  • Mentally-oriented and alert
  • Use of accessory muscles


  • Wheezing less pronounced than anticipated
  • Respiratory rate 20-25
  • Pulse 125+
  • Peak flows and spirometry reduced by 40+%
  • SaO2 91-92%

Stage 5

  • Reduced consciousness/altered mental status
  • Dyspnea
  • Silent chest – no wheezing


  • Fast, superficial respiration
  • Respiratory rate >25
  • Unable to perform peak flows or spirometry
  • Pulse 130-150+
  • SAO2 <90 


Clinical estimates of severity based on interview and examination can result in inaccurate estimation of disease severity; audible wheezing is usually a sign of moderate asthma, whereas no wheezing can be a sign of severe airflow obstruction. Symptoms of severe asthma include severe chest tightness, cough (with or without sputum), sensation of air hunger, inability to lie flat, insomnia and severe fatigue. The signs of severe asthma include use of accessory muscles of respiration, hyperinflation of the chest, tachypnea, tachycardia, sweating, diaphoresis, obtundation, apprehensive appearance, wheezing, inability to complete sentences and difficulty in lying down. Altered mental status, with or without cyanosis, is an ominous sign and immediate emergency care and hospitalization is required. Detailed examination should include looking for signs and symptoms of pneumonia, pneumothorax or a pneumomediastinum, the latter can be investigated by palpation for subcutaneous crepitations, particularly in the supraclavicular areas of the chest wall. Special attention should be paid to the patient's blood pressure, pulse and respiratory rate. Clinical parameters indicating a severe attack are:

  • Pulsus paradoxicus >25 mm Hg
  • Pulse > 110 BPM
  • Respiratory rate >25-30 breaths/min
  • PEFR or FEV1 < 50% predicted
  • SaO2 <91-92%

Differential Diagnosis of Acute Asthma

The differential diagnosis of acute asthma includes chronic obstructive pulmonary disease (COPD), bronchitis, bronchiectasis, endobronchial diseases, foreign body, extra-or intra-thoracic tracheal obstruction, cardiogenic pulmonary oedema, non-cardiogenic pulmonary oedema, pneumonia, pulmonary emboli, chemical pneumonitis, hyperventilation syndrome, pulmonary embolus and carcinoid syndrome.

Risk Factors for Asthma Exacerbations

Particular risk factors for asthma exacerbations can be identified from the clinical history. Patient interview should include questions about recent events including:

  • Lower or upper respiratory tract infections
  • Cessation or reduction of medication
  • Concomitant medication, e.g. ß-blockers
  • Allergen or pollutant exposure 

Predictors of fatal or near fatal asthma

Major risk factors for near-fatal and fatal asthma are recognised, and their presence makes early recognition and treatment of an asthma exacerbation essential. History should include a review of previous episodes of near-fatal asthma and whether the patient has experienced multiple ER visits or hospitalizations, particularly those requiring admission to an intensive care unit, involving respiratory failure, intubation and mechanical ventilation. A history of allergic asthma and other known or suspected allergic symptoms should be obtained; a recognized trigger for severe asthma is allergy to the mold Alternaria.

Compliance with medical treatments should be reviewed; poor compliance with prescribed therapies is a major risk factor. Inadequate therapy may include excessive use of ß2-agonists, concomitant use of ß-blockers, and failure to prescribe or use inhaled corticosteroids as a primary therapy. Recent withdrawal of oral corticosteroids suggests that the patient is at greater risk for a severe exacerbation. Limited access of the patient to appropriate health care and lack of education about appropriate management strategies are additional risk factors.

Socio-economic factors associated with severe asthma exacerbations include the non-compliant adolescent or old age and asthmatics living in inner city environments. Certain ethnic groups within a population may have a higher incidence of severe asthma.

Physiological and Laboratory Parameters

Serial measurements of lung function facilitate quantification of the severity of airflow obstruction and response to therapy. Peak expiratory flow measurement provides a simple, quick, and cost effective assessment of the severity of airflow obstruction. The patient takes a deep breath to maximum inspiration, holds the breath, and with lips sealed around a mouthpiece blows out as hard and fast as possible. The best of three recordings is logged as the peak expiratory flow rate (PEFR) and compared to predicted normal values based on gender, age and height.

Patients can be supplied with an inexpensive peak expiratory flow meter and taught to perform PEFR measurements at home to detect deterioration of their asthma. An individual management plan will be based upon the personal best PEFR value, and pre-determined PEFR values can be set at which time the patient is alerted to the degree of severity of symptoms and can institute appropriate therapy and consult their physician.

The forced expiratory volume in one second (FEV1) is measured by spirometry to assess the volume of air exhaled over time and is the most sensitive test for airflow obstruction. FEV1 is much less variable than PEFR and is independent of effort once a moderate effort has been made by the patient. The patient is asked to forcibly exhale from the point of maximal inhalation into the spirometer, ideally over 6 seconds. Three determinations should be obtained, if possible, with the best being recorded, and severity of assessment is made by comparison to predicted normal values for the gender, height and age of the patient.

FEV% predicted Severity
< 35


Moderately severe
Very severe (life-threatening)

In non-acute settings, assessment of PEFR and spirometry before and after administration of a bronchodilator can indicate the likely degree of improvement in lung function which can be achieved by adequate therapy.

Chest radiographs are not usually necessary for the diagnosis of acute asthma if the examination of the chest reveals no abnormal findings, but if a complication is suspected, such as pneumonia, pneumothorax, pneumomediastinum, or atlectasis secondary to mucous plugging, a chest X-ray should be obtained.


Treatment is based not only on assessment of lung function parameters but on clinical findings and the efficacy of previous treatment. A seasonal exacerbation of asthma in a pollen-sensitive patient is more easily treatable than an exacerbation triggered by a viral infection. Allergic asthma is more likely to respond immediately to inhaled ß2-agonist therapy and to an adjustment in inhaled corticosteroids, whereas the infected patient is more likely to require a systemic corticosteroid. A patient who is over-using short-acting ß2-agonists may be refractory to nebulized ß2-agonists and will usually require systemic corticosteroids. Physician knowledge of an individual patient will suggest whether systemic corticosteroids are required or whether an exacerbation can be managed on very high doses of inhaled corticosteroids.

Recommended treatment choices in order of introduction in the acute setting are:

  1. ß2-agonists; inhaled by MDI or by nebulizer, or systemic (injected)
  2. Anticholinergics; inhaled by MDI or nebulizer
  3. Corticosteroids; parenteral, oral or inhaled

Secondary treatment choices may include:

Theophylline; oral, parenteral
Leukotriene receptor antagonists; oral
Magnesium sulfate


Treatment should begin with albuterol, either administered by a metered dose inhaler with a spacer device, 4 to 8 puffs, or nebulized at 2.5 to 5.0 mg in normal saline, 2.5 to 3.0 cc, and repeated as necessary every 20 minutes until the patient has stabilized or a decision to hospitalize has been made.

Levalbuterol HCl nebulizer solution (0.63 mg) can be given in a similar fashion and increased to 1.25 mg for those with more severe symptoms not responding to the lower dose or those who have over-used albuterol prior to emergency care.

For patients with severe asthma or those unable or unwilling to use an MDI/spacer or nebulizer, this can be substituted by epinephrine injected subcutaneously in the arm, 0.3 to 0.5ml (0.01 ml/kg children), every 20 minutes for several doses, as long as the patient is carefully monitored for signs of adrenergic toxicity. If there is no immediate response to epinephrine it should be discontinued and the patient hospitalized.


Ipratropium bromide is a quaternary derivative of atropine available as a nebulizer solution. It provides competitive inhibition of acetylcholine at the muscarinic cholinergic receptor, thus relaxing smooth muscle in large central airways. It is not a first line therapy, but can be added in severe asthma particularly when albuterol is not optimally beneficial. It can be given simultaneously with albuterol or levalbuterol.

Ipratropium bromide is given by nebulizer 0.5 mg every 30 minutes for three doses then every 2-4 hours as needed. MDI administration,18 µg/puff can be administered every 30 minutes for three doses then every 2-4 hours as required.


There is no substantial data for the immediate usefulness of corticosteroids in the acute setting because effectiveness of action is not seen for hours after administration. However, oral corticosteroids are the most powerful medications available to reduce airway inflammation and should be used immediately and until the attack has abated as evidenced by the PEFR and FEV1 returning to near baseline levels and the patient becoming asymptomatic.

Patients with mild, moderate or severe exacerbations can be successfully treated using a higher than recommended dose of inhaled corticosteroids, even if they are already on inhaled corticosteroid therapy. For example, a top recommended maintenance dose of fluticasone may be increased from 440 µg 2x/day to 440 µg 4x/day, or even to 660 µg 4x/day for an asthma exacerbation. Any inhaled corticosteroid can be used in this way by doubling or tripling the highest recommended dose. Treatment should be started before the patient becomes too ill to manage their disease at home. Inhaled therapy reduces the risk of unwanted effects associated with oral corticosteroids (eg, insomnia, increased appetite, hyperactivity, and effects on bone metabolism and other organ systems). Inhaled corticosteroids are less likely to be effective in patients with upper respiratory tract infections exacerbating their asthma or those who are over-using ß2-agonists.

Short courses of systemic corticosteroids are effective for establishing control in flare-ups of asthma or during a period of gradual deterioration which is not responding to increased doses of inhaled corticosteroid. Prednisolone or its equivalent, 45 to 60 mg/day, in three divided doses, is recommended. Higher doses result in increased side effects and no appreciable increased therapeutic benefit.

Treatment should be continued until the patient is well or achieves a PEFR of 80% of personal predicted best. Improvement may be seen between 5 to 14 days, although patients whose asthma is corticosteroid-resistant may take weeks to show a response. It is not necessary to taper the dose of systemic corticosteroids after a course of less than one week, but after use for longer than 10 to 14 days, it is advisable to taper the medication over a few days or one to two weeks to lessen post-corticosteroid side effects such as depression, fatigue, arthralgias, or myalgias.

IM corticosteroids may be used in the initial treatment of acute asthma, but there is no evidence that giving corticosteroids intravenously or by injection results in a more rapid onset of action than oral administration. The recommended dose for intravenous methylprednisolone is 1 to 2 mg/kg for 24 hours in divided doses.

Methylxanthines (aminopohylline and theophylline)

There are conflicting reports on whether methylxanthines are effective for the treatment of acute asthma, but intravenous aminophylline may be useful when the patient is refractory to more conventional therapy. The treating physician must be aware of drug interactions, clinical situations that warrant dose adjustment, and the importance of monitoring therapy. For adult non-smokers the aminophylline dose is 5 to 6 mg/kg given slowly intravenously over 20 to 30 minutes followed by a maintenance dose of 0.4 mg/kg/hr. The dose should be adjusted to 0.6 mg/kg/hr for smokers and to 0.2 mg/kg/hr for patients in congestive heart failure or with liver disease. Serum concentration should be determined every 4 to 6 hours after commencing therapy and should be maintained at 5 to 15 µg/ml. Serum concentrations above 20 µg/ml are considered toxic and can result in nausea, vomiting, headache and cardiac effects. Doses for theophylline are slightly less than for aminophylline.

Magnesium Sulfate

The use of magnesium sulfate is controversial and inconsistent data exists on its efficacy. It is used in very severe asthma in emergency settings, when FEV1 < 25% predicted, or there are other signs of severe disease. 1.2 – 2 gm is administered intravenously over 10-20 min in 50 ml saline. Minor side effects can occur.

Leukotriene Modifiers

Leukotrienes are pro-inflammatory mediators involved in the pathogenesis of asthma. They have a rapid onset of action and improve the FEV1 within one to two hours. There are few studies on the role of leukotriene modifiers in the acute setting.


Failure to respond to treatment necessitates hospitalization. The patient should be hydrated, orally if possible, or with IV fluids, administered oxygen 2 to 4 L/min via a nasal cannula and followed with telemetry and pulse oximetry. Blood gases are determined until the patient is stable. The patient should be treated with continuous nebulized albuterol or levalbuterol, with or without ipratropium bromide, and high-dose corticosteroids, eg, methylprednisolone or its equivalent 1-2 mg/kg in divided doses every 24 hours. If the patient is not responding and is deteriorating a decision should be made to assist ventilation before the patient has a respiratory arrest.

Follow-up of a severe exacerbation of asthma

The patient should be placed on high dose inhaled corticosteroids, eg, fluticasone, 880-1760 µg or budesonide, 800-1600 µg daily. Once oral corticosteroids are withdrawn, the inhaled dose can be reduced incrementally while maintaining the PEFR at personal best level. A combination of long acting β2-agonist and inhaled corticosteroid can be considered in order to achieve the lowest dose of corticosteroid possible.

The patient should be evaluated for allergy with skin prick/puncture tests or serum testing for IgE-sensitization and allergen avoidance strategies discussed if the clinical history suggests that allergen contact may have precipitated the asthma exacerbation. Compliance with prescribed therapy should be reviewed, and the patient's technique in using metered dose inhalers should be checked. The patient should be questioned regarding inappropriate concomitant medications which may have been prescribed for other conditions. Contact with tobacco, drugs, irritants and fumes which may have precipitated an attack should be considered and the patient advised how to avoid contact with such agents. Social factors which may be risk factors for a severe exacerbation and psychiatric disorders should be recorded.

Patient education is important to ensure that patients understand that asthma is a chronic disease and necessitates the avoidance of allergens and prevention of infections. The importance of taking anti-inflammatory therapy on a regular basis and limiting bronchodilator usage should be discussed. An individual management plan should include how to recognize an impending exacerbation and provide an incremental therapy regime to be implemented according to the degree of severity, based upon home monitoring of PEFR.


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Ramirez NC, Lockey, RF. Management of Acute Asthma in the Office Setting. In: Asthma. Eds. Slavin, R G, Reisman RE, American College of Physicians, Philadelphia, 2002. pp. 51-70

Brenner BE, Tyndall JA, Crain EF. The clinical presentation of acute asthma in adults and children. In: Emergency Asthma. Marcel Dekker, New York, 1999

Kaliner MA. Asthma Pearls. In: Current Review of Asthma. Current Medicine, Philadelphia, 2003. pp. 223-231