Asthma is a heterogeneous disease of bronchial inflammation and bronchospasm. Status asthmaticus is a state of respiratory compromise characterized by bronchial inflammation and bronchospasm secondary to asthma with resultant prolonged expiratory phase, tachypnea, dyspnea, and work of breathing; it does not respond to conventional therapy and may lead to respiratory failure.^1,2

Asthma affects 8.7 million children in the United States with the highest prevalence in children 5 to 17 years of age.³

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  Blacks are disproportionately affected, and there is no gender predilection.

  
  
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  Seventy to eighty percent of children have allergic symptoms.

  
  
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  There are familial links, but asthma is more likely to develop if the mother has allergies or asthma rather than the father.³

Asthma and status asthmaticus are due to increased inflammation of the lower airway leading to:

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  Airway irritability and bronchospasm

  
  
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  Overproduction of mucus

  
  
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  Mucosal edema

Combined, these lead to airway obstruction via bronchoconstriction and mechanical obstruction.¹

PULMONARY CHARACTERISTICS OF ASTHMA

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  Hyperinflation and increased functional residual capacity

  
  
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  Heterogeneous lung parenchyma

  
  
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  Airways can be affected in multiple ways²:

  
  
  
  
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    Complete obstruction of the airway (i.e., mucus plugging)

    
    
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    Partial obstruction present throughout the respiratory cycle

    
    
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    Partial obstruction present throughout expiration → prone to air trapping

    
    
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    No bronchial obstruction → prone to overdistention during an asthma exacerbation

    
    
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    V/Q mismatch occurs due to shunt physiology and increased dead space ventilation¹

    
    
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    Areas of atelectasis secondary to mucus plugging lead to intrapulmonary shunt physiology

    
    
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    Areas of hyperinflation can lead to pulmonary blood flow obstruction and increased dead space ventilation

  
  

CARDIOPULMONARY INTERACTIONS

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  Extreme fluctuations in intrathoracic pressures during an acute asthma exacerbation can affect both the preload and the afterload on the heart.

  
  
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  High lung volumes and intrathoracic pressures increase the pulmonary vascular resistance.

  
  
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  High intrathoracic pressures decrease blood return to the right atrium (i.e., preload).

  
  
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  Negative inspiratory pressures increase afterload on the left ventricle.

  
  
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  These changes lead to pulsus paradoxus.

  
  
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  Changes in systolic blood pressure of more than 10 to 15 mmHg between inhalation and exhalation may be an indicator of impending respiratory failure.¹

DIFFERENTIAL DIAGNOSIS^1,3

Pneumonia – viral or bacterial, allergic bronchopulmonary aspergillosis, foreign body aspiration, cardiogenic pulmonary edema, anatomic lesions that may be fixed (e.g., airway web or hemangioma) or dynamic (tracheomalacia), immunodeficiency, bronchopulmonary dysplasia, vocal cord paralysis

HISTORY AND PHYSICAL

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  History

  
  
  
  
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    Acuity of symptoms, presence of fever, upper respiratory symptoms, exposures to allergens, personal or family history of asthma, allergies, eczema

    
    
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    Red flags: intensive care unit (ICU) admissions for asthma, history of mechanical ventilation, frequent emergency room visits¹

  
  
  
  
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  Physical exam

  
  
  
  
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    Respiratory effort (i.e., accessory muscle use), dyspnea, breath sounds

    
    
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    Mental status, perfusion (e.g., capillary refill), liver edge

    
    
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    Ominous signs:

    
    
    
    
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      Lethargy, altered mental status

      
      
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      The silent chest – severe airway obstruction vs. pneumothorax

      
      
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      Paradoxical thorcoabdominal breathing

      
      
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      Severe dyspnea or inability to phonate¹

      
      
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      Altered mental status, poor perfusion, and tachycardia can be signs of hypercarbia

    
    

  
  
  
  
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  Laboratory workup

  
  
  
  
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    Complete blood count: an elevated white blood cell count may raise suspicion for infection; however, could also be secondary to stress response or administration of steroids¹

    
    
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    Electrolytes and metabolic profile:

    
    
    
    
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      Elevated blood urea nitrogen (BUN) and creatinine may indicate level of dehydration

      
      
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      Prolonged β-agonist therapy can decrease extracellular potassium concentration

    
    

  
  
  
  
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  Arterial blood gas

  
  
  
  
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    Initial – hypoxemia and hypocarbia can be seen due to V/Q mismatch and hyperventilation.

    
    
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    Normal or high PCO₂ in a tachypneic patient is a concerning finding and may indicate impending respiratory failure.¹

    
    
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    Lactatemia or lactic acidosis is a common finding in status asthmaticus

    
    
    
    
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      Mostly type B acidosis – not associated with tissue dysoxia but rather secondary to β-adrenergic therapy, leading to derangements in glucose metabolism

      
      
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      Can lead to tachypnea to achieve a compensatory respiratory alkalosis and can lead to a confounding picture for the clinician treating status asthmaticus^4,5

      
      
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      Type A acidosis can be due to impaired oxygen delivery in a setting of shock, overloaded respiratory muscles, or poor clearance⁵

    
    

  
  
  
  
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  Chest x-ray

  
  
  
  
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    Recommended for initial presentations and all ICU admissions

    
    
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    Typically hyperinflated with flattened diaphragms

    
    
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    Look for pneumothorax, foreign body (could manifest as asymmetry), cardiomegaly, pulmonary edema, chest mass, and infectious infiltrate¹