Status Asthmaticus Clinical Presentation

Updated: Mar 03, 2017
  • Author: Constantine K Saadeh, MD; Chief Editor: John J Oppenheimer, MD  more...
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Presentation

History

Patients with status asthmaticus have severe dyspnea that has developed over hours to days. In most cases, there is a lead time of several days. [7] Frequently, these individuals have a previous history of endotracheal intubation and mechanical ventilation, frequent emergency department visits, and previous use of systemic corticosteroids.

If the physician does not obtain a thorough history for a patient with asthma, he or she may not recognize a person with high risk factors for acute and severe decompensation. This failure may prevent the aggressive use of bronchodilators, corticosteroids, and monitoring. When obtaining the history from a patient presenting with an acute exacerbation of asthma, the following should be determined:

  • Presence of current illness, such as upper respiratory tract infection or pneumonia
  • History of chronic respiratory diseases (eg, bronchopulmonary dysplasia, chronic lung disease of infancy)
  • History of atopy
  • History of allergies
  • Family history of asthma
  • Presence of pets or smokers in the home
  • Known triggering factors
  • Home medications - Obtain a detailed list of medications being taken at home and, if possible, their timing and dosage

Risk factors for developing severe or persistent status asthmaticus include the following:

  • History of increased use of home bronchodilator treatment without improvement or effect
  • History of previous intensive care unit (ICU) admissions, with or without intubation and mechanical ventilatory support
  • Asthma exacerbation despite recent or current use of corticosteroids
  • Frequent emergency department visits and/or hospitalization (implies poor control)
  • Less than 10% improvement in peak expiratory flow rate (PEFR) from baseline despite treatment
  • History of syncope or seizures during acute exacerbation
  • Oxygen saturation below 92% despite supplemental oxygen
  • Subgroup of asthma patients who are poor perceivers of dyspnea are a greater risk of intubation and death [8]

Determine whether the patient has a severe asthma exacerbation without wheezing (ie, the silent chest). Such patients may have such severe airway obstruction or be so fatigued that they are unable to generate enough airflow to wheeze. This is an ominous sign of impending respiratory failure.

Next:

Physical Examination

Patients are usually tachypneic upon examination and, in the early stages of status asthmaticus, may have significant wheezing. Initially, wheezing is heard only during expiration, but wheezing later occurs during expiration and inspiration.

The chest is hyperexpanded, and accessory muscles, particularly the sternocleidomastoid, scalene, and intercostal muscles, are used. Later, as bronchoconstriction worsens, the wheezing may disappear, which may indicate severe airflow obstruction.

Normally, the difference in systolic blood pressure between inspiration and expiration does not exceed 15 mm Hg. In patients with severe asthma, a difference of greater than 25 mm Hg usually indicates severe airway obstruction.

An inability to speak more than one or two words at a time may also be observed in the later stages of an acute asthma episode. Ventilation/perfusion mismatch results in decreased oxygen saturation and hypoxia. Vital signs may show tachycardia and hypertension. The peak flow rate should be included in the vital signs in patients who are able to cooperate and who are able to tolerate the peak flow maneuver without significant distress.

The patient’s level of consciousness may progress from lethargy to agitation, air hunger, and even syncope and seizures. If untreated, prolonged airway obstruction and marked increase in the work of breathing may eventually lead to bradycardia, hypoventilation, and even cardiorespiratory arrest.

General examination

The peak flow rate is a standard measure of airflow obstruction and is relatively simple to perform. Most patients with more than a mild exacerbation of asthma have hypoxia and decreased oxygen saturation due to V/Q mismatch. Some patients prefer to remain seated and leaning forward, rather than assuming a supine position.

Retractions (ie, intercostal and subcostal) and the use of abdominal muscles may be observed in patients with status asthmaticus. The use of accessory muscles has been shown to correlate with the severity of airflow obstruction. An abnormally prolonged expiratory phase with audible wheezing can be observed. Patients with moderate to severe asthma are often unable to speak in full sentences.

Dehydration can occur in adults, but is observed less frequently than in children.

Cardiovascular symptoms may include tachycardia or hypertension in mild to moderate asthma. With worsening hypoxemia, hypercarbia, marked air trapping, and hyperinflation, the ventricular stroke volume is compromised and hypotension and bradycardia may be observed.

CNS status ranges from wide awake to lethargic and from agitated to comatose. As hypoxemia progresses, lethargy progresses to agitation caused by air hunger. As more lung units become obstructed, hypoxemia worsens and hypercarbia develops. Both hypoxemia and hypercarbia can lead to seizures and coma and are late signs of respiratory compromise.

Examination of the respiratory system

Wheezing occurs from air moving through narrowed, obstructed airways. Thus exhalation results in turbulent airflow and produces wheezes. Although asthma is the most common cause of wheezing, anything that causes airway obstruction and narrowing that results in turbulent airflow may generate wheezes. Therefore, not all wheezing is asthma.

Auscultation often reveals bilateral expiratory and possibly inspiratory wheezes and crackles. Air entry may or may not be diminished or absent, depending on severity. Remember, the silent chest may herald impending respiratory failure in a patient too obstructed or fatigued to generate wheezing.

If tension pneumothorax develops, signs of tracheal deviation to the opposite side, decreased or absent air entry on the affected side, shift of the location of heart sounds, and hypotension may be evident. Air leaks may also result in pneumomediastinum and subcutaneous emphysema.

In moderate to severe status asthmaticus, abdominal muscle use can cause symptoms of abdominal pain.

Pulsus paradoxus (a decrease in the systolic blood pressure during inspiration) results from a decrease in cardiac stroke volume with inspiration due to greatly increased left-ventricular afterload. This increase is generated by the dramatic increase in negative intrapleural and transmural pressure in a patient struggling to breathe against significant airways obstruction. Pulsus paradoxus of greater than 20 mm Hg correlates well with the presence of severe airways obstruction (ie, forced expiratory volume in 1 second [FEV1] < 60% predicted).

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