eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Critical Care

Status Asthmaticus

Author: Adam J Schwarz, MD, Consulting Staff, Critical Care Division, Pediatric Subspecialty Faculty, Children's Hospital of Orange County
Contributor Information and Disclosures

Updated: Apr 8, 2009

Introduction

Background

Asthma is the most common chronic disease of childhood, affecting 5-10% of children and resulting in approximately 400,000 hospitalizations annually. In 1997, the National Heart, Lung, and Blood Institute defined asthma as a chronic inflammatory disorder of the airways that involves many different cells, including mast cells, eosinophils, and T lymphocytes. This inflammation causes recurrent episodes of wheezing, dyspnea, and cough. Episodes are associated with obstruction that occurs in predominantly small-to-medium airways and that reverses partially or completely, either spontaneously or with treatment. Asthma is also associated with increased airway hyperresponsiveness to various stimuli.

Status asthmaticus is an acute exacerbation of asthma that remains unresponsive to initial treatment with bronchodilators. Status asthmaticus can vary from a mild form to a severe form with bronchospasm, airway inflammation, and mucus plugging that can cause difficulty breathing; carbon dioxide retention; hypoxemia; and respiratory failure. The typical clinical presentation involves persistent wheezing with retractions. However, not all children with severe asthma wheeze; some may present with cough, dyspnea, or emesis. Alternatively, not all patients who present with wheezing have asthma; some may have one of various other causes of obstructed airways.

Pathophysiology

Exposure to an allergen or trigger causes a characteristic form of airway inflammation in susceptible individuals, exemplified by mast cell degranulation, release of inflammatory mediators, infiltration by eosinophils, and activated T lymphocytes. Multiple inflammatory mediators may be involved, including interleukin (IL)–3, IL-4, IL-5, IL-6, IL-8, IL-10, and IL-13; leukotrienes; and granulocyte-macrophage colony-stimulating factors (GM-CSFs). These, in turn, incite involvement of mast cells, neutrophils, and eosinophils.

Early bronchospastic response

Within minutes of exposure to an allergen, mast cell degranulation is observed along with the release of inflammatory mediators, including histamine, prostaglandin D2, and leukotriene C4. These substances cause airway smooth muscle contraction, increased capillary permeability, mucus secretion, and activation of neuronal reflexes. Early asthmatic response is characterized by bronchoconstriction that is generally responsive to bronchodilators, such as beta2-agonist agents.

Later inflammatory response

Release of inflammatory mediators prime adhesion molecules in the airway epithelium and capillary endothelium, which then allows inflammatory cells, such as eosinophils, neutrophils, and basophils, to attach to the epithelium and endothelium and subsequently migrate into the tissues of the airway. Eosinophils release eosinophilic cationic protein (ECP) and major basic protein (MBP). Both ECP and MBP induce desquamation of the airway epithelium and expose nerve endings. This interaction promotes further airway hyperresponsiveness in asthma. This inflammatory component may even occur in individuals with mild asthma exacerbation.

Bronchospasm, mucus plugging, and edema in the peripheral airways result in increased airway resistance and obstruction. Air trapping results in lung hyperinflation, ventilation/perfusion (V/Q) mismatch, and increased dead space ventilation. The lung becomes inflated near the end-inspiratory end of the pulmonary compliance curve, with decreased compliance and increased work of breathing. The increased pleural and intra-alveolar pressures that result from obstruction and hyperinflation, together with the mechanical forces of the distended alveoli, eventually lead to a decrease in alveolar perfusion. The combination of atelectasis and decreased perfusion leads to V/Q mismatch within lung units. The V/Q mismatch and resultant hypoxemia trigger an increase in minute ventilation.

In the early stages of acute asthma, hyperventilation may result in respiratory alkalosis. This is because obstructed lung units (slow compartment) are relatively less numerous than unobstructed lung units (fast compartment). Hyperventilation allows carbon dioxide removal via the fast compartment. However, as the disease progresses and more lung units become obstructed, an increase in the slow compartments occurs with decreased ability for carbon dioxide removal, eventually resulting in hypercarbia.

Frequency

United States

Asthma affects up to 10% of the US population. Prevalence has increased by 60% in all ages in the past 2 decades, with an approximate 40% increase in children. A significant rise in hospitalization and asthma mortality rates, especially in children aged 0-4 and 9-16 years, has accompanied the increased incidence. Asthma, including status asthmaticus that requires hospitalization,¹ is the leading cause of school absenteeism among children with chronic illness. Factors associated with the increase in asthma include indoor pollution, overcrowding, increased incidence of viral infections, allergens, cockroach allergy, and, possibly, a decrease in breastfeeding.

In addition, some researchers have described the hygiene hypothesis, which suggests that the public health success in reducing early childhood infections through vaccination and hygiene reduces early autoimmunization and increases the likelihood of allergies and asthma. This hypothesis remains controversial.

International

Worldwide incidence is unclear but is estimated to be about 20 million cases, 15% of which occur in children. The dramatic rise in the worldwide incidence of asthma has been attributed, in part, to pollution and industrialization. Under the hygiene hypothesis, improved immunization and public health measures would contribute to the increase in asthma.

Mortality/Morbidity

The mortality rate from asthma has increased at an alarming rate. From 1993-1995, the overall annual age-adjusted death rate for asthma increased 40%. The rise in the mortality rate is even higher among blacks, among people living in poverty, and among children aged 0-4 and 9-16 years.

Race

Although asthma affects people of all races, in the United States, Hispanic children seem to have a higher incidence. The mortality rate in the United States is highest among blacks.

Sex

In infants, males generally have more severe disease than females. In older children, males and females are equally affected. Asthma has a higher incidence among adult females.

Age

Asthma is well distributed among people of all age groups. Children who have asthma in the first year of life and those aged 9-16 years tend to have much more severe disease.

Clinical

History

When obtaining the history from a child 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)
  • Severe previous respiratory syncytial virus (RSV) disease
  • 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, the timing and dosage of medications)
• Risk factors for developing severe or persistent status asthmaticus
  • History of increased use of home bronchodilator treatment without improvement or effect
  • History of previous ICU admissions, with or without intubation
  • Asthma exacerbation despite recent or current use of corticosteroids
  • Frequent emergency department (ED) 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
  • Whether the patient has a severe asthma exacerbation without wheezing (ie, the silent chest): Such patients may have such severe airway obstruction or be fatigued so that he or she is unable to generate enough airflow to wheeze. This is an ominous sign of impending respiratory failure.

Physical

Immediately determine patient's condition and risk for respiratory failure at initial assessment. The acute episode of asthma may begin with mild symptoms of dyspnea. As the degree of airway obstruction worsens, respiratory distress, including retractions, use of abdominal muscles in exhalation, and inability to speak more than one or two words at a time, may all be observed. V/Q 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 children who are able to cooperate and who are able to tolerate the peak flow maneuver without significant distress. Level of consciousness may progress from lethargy to agitation from air hunger and even syncope and seizures. If untreated, prolonged airway obstruction and marked increase in work of breathing may eventually lead to bradycardia, hypoventilation, and even cardiorespiratory arrest.

• General examination
  • In the early stage of acute asthma exacerbation, slight tachycardia and tachypnea may be observed. As the episode progresses, tachycardia and tachypnea may worsen. Blood pressure may be elevated. 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. Use of accessory muscles has been shown to correlate with severity of airflow obstruction. An abnormally prolonged expiratory phase with audible wheezing can be observed.
  • Children with status asthmaticus may appear dehydrated as a result of poor intake, vomiting, and increased work of breathing.
  • Retractions (ie, intercostal, subcostal, use of abdominal muscles) may be observed.
  • The use of accessory muscles correlates to severity of disease.
  • Patients with moderate-to-severe asthma are often unable to speak in full sentences.
  • Cardiovascular symptoms may include tachycardia or hypertension in mild-to-moderate asthma. With worsening hypoxemia, hypercarbia, marked air trapping, and hyperinflation, stroke volume is compromised and hypotension and bradycardia may be observed.
  • CNS status ranges from wide-awake to lethargic, 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. This 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. Other causes of wheezing may include the following:
    • Viral infections/bronchiolitis: Common respiratory viral infections, such as RSV, may cause airway swelling and narrowing in infants and children, causing inflammation and swelling of the bronchioles and resulting in bronchiolitis. Although viral infections may clearly trigger asthma, typical bronchiolitis results from airway swelling and edema, not from bronchospasm, and is generally unresponsive to treatment with bronchodilators.
    • Foreign body: Aspiration of a foreign body is a particularly important consideration in toddlers. These episodes are generally unwitnessed. When the foreign body lodges in the right or left mainstem bronchus or beyond, the child may present with a cough and wheezing, often unilaterally. When suspected, a chest radiograph should be obtained.
    • Cystic fibrosis: Airways are obstructed with thick inspissated secretions.
    • Extrinsic compression: Airways can be compressed from vascular structures, such as vascular rings, lymphadenopathy, or tumors.
    • Congestive heart failure (CHF): Airway edema may cause wheezing in CHF. In addition, vascular compression may compress the airways during systole with cardiac ejection, resulting in a pulsatile wheeze that corresponds to the heart rate. This is sometimes erroneously referred to as cardiac asthma.
    • Tracheomalacia: Although the airway sounds are slightly different from those of asthma, they are often referred to as wheezes.
  • 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 include pneumomediastinum and subcutaneous emphysema.
  • In moderate-to-severe status asthmaticus, abdominal muscle use can cause symptoms of abdominal pain.
  • Pulsus paradoxus is a decrease in the systolic blood pressure during inspiration. It results from a decrease in cardiac stroke volume with inspiration due to greatly increased left-ventricular afterload generated by the dramatic increase in negative intrapleural and transmural pressure in a patient struggling to breathe against significant airways obstruction. Pulsus paradoxus greater than 20 mm Hg correlates well with the presence of severe airways obstruction (ie, forced expiratory volume in 1 second [FEV ₁ ] <60% predicted).

Causes

Asthma results from a number of factors, including genetic predisposition and environmental factors.

• Inhaled allergens
  • Patients often have a history of atopy.
  • The severity of asthma has been correlated with the number of positive skin test results.
• Viral infections
• Air pollutants (eg, dust, cigarette smoke, industrial pollutants)
• Medications, such as beta-blockers, aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs)
• Gastroesophageal reflux disease
  • Studies indicate that reflux of gastric contents with or without aspiration can trigger asthma in susceptible children and adults.
  • Animal studies have shown that the instillation of even minute amounts of acid into the distal esophagus can result in marked increases in intrathoracic pressure and airway resistance. This response is thought to be due to vagal and sympathetic neural responses.
• Cold temperature
• Exercise

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