Status Asthmaticus

Updated: Nov 18, 2024
  • Author: Wael Azzam, MD; Chief Editor: John J Oppenheimer, MD  more...
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Overview

Practice Essentials

Status asthmaticus is an acute exacerbation of asthma that remains unresponsive to initial treatment with bronchodilators. Status asthmaticus can range 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. (See Prognosis and Presentation.) It is considered a medical emergency, requiring immediate recognition and treatment to prevent progression to respiratory failure.

Typically, patients present a few days after the onset of a viral respiratory illness, after exposure to a potent allergen or irritant, or after exercise in a cold environment. Frequently, patients have underused or been nonadherent to anti-inflammatory therapy, or such therapy has been underprescribed. Illicit drug use not only plays a role in poor adherence to anti-inflammatory therapy but also can be a precipitant for severe asthma exacerbations. [1, 2, 3]  (See Etiology.)

A study published in 2004 noted that the number of patients with status asthmaticus requiring intensive care admissions had declined over 10 years. [4] The trend was toward less advanced presentations. This may reflect improvements in medication compliance, education, or access to medical care. Nonetheless, concerns have been raised about an increase that has since been observed in the severity of asthma symptoms and the need for more intensive care management. [5]  (See PrognosisWorkupTreatment, and Medication.)

Patients report chest tightness, rapidly progressive shortness of breath, dry cough, and wheezing and may have increased the frequency of their beta-agonist intake (either inhaled or nebulized) to as often as every few minutes. (See Presentation.)

Optimal management of status asthmaticus involves prevention (eg, through enhancing patient compliance with controller medications such as steroid inhalers in an outpatient setting). Once a severe exacerbation has developed, management goals are (1) to reverse airway obstruction rapidly through the aggressive use of beta2-agonist agents and early use of corticosteroids, (2) to correct hypoxemia by monitoring and administering supplemental oxygen, and (3) to prevent or treat complications such as pneumothorax and respiratory arrest. (See Treatment and Medication).

Patient education plays a crucial role in preventing recurrent attacks of status asthmaticus. In a study by Rice et al, inpatient asthma education was studied in children and adolescents following status asthmaticus. [6] Subjects were enrolled in two groups. One group received the usual posthospitalization instructions and the other group received additional education by lay asthma education volunteers. The group that received the additional education had better compliance in the outpatient setting.

Pathophysiology

The pathophysiology of status asthmaticus can be attributed to multiple key mechanisms that collectively result in severe airflow obstruction, impaired gas exchange, and respiratory failure, necessitating aggressive and prompt medical intervention. Those mechanisms are airway inflammation and edema, mucus plugging, bronchoconstriction, ultimately leading to V/Q mismatch resulting in severe hypoxemia.

Etiology

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, as well as leukotrienes and granulocyte-macrophage colony-stimulating factors (GM-CSFs). These, in turn, incite involvement of mast cells, neutrophils, and eosinophils. (See the image below.)

Antigen presentation by  dendritic cell, with lympAntigen presentation by dendritic cell, with lymphocyte and cytokine response leading to airway inflammation and asthma symptoms.

Physiologically, acute asthma has two components: an early, acute bronchospastic aspect marked by smooth-muscle bronchoconstriction and a later inflammatory component resulting in airway swelling and edema.

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. The early asthmatic response is characterized by bronchoconstriction that is generally responsive to bronchodilators (eg, beta2-agonist agents).

Later inflammatory response

The release of inflammatory mediators primes adhesion molecules in the airway epithelium and capillary endothelium, and this priming then allows inflammatory cells (eg, 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 occur even 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.

Risk factors

Asthma results from a number of factors, including genetic predisposition and environmental factors. Patients often have a history of atopy. The severity of asthma has been correlated with the number of positive skin test results.

Gastroesophageal reflux disease (GERD) is another risk factor for asthma, with studies indicating that the 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.

Risk factors for asthma exacerbation include the following: 

  • Viral infections
  • Air pollutants (eg, dust, cigarette smoke, and industrial pollutants)
  • Medications (eg, beta blockers, aspirin, and nonsteroidal anti-inflammatory drugs [NSAIDs])
  • Cold temperature
  • Exercise
  • Illicit drug use

Epidemiology

United States and international statistics

According to the US Centers for Disease Control and Prevention (CDC), asthma affects 7.7% of the US population, or an estimated 25 million persons, including 5 million children. [7] Prevalence has increased by 60% in all ages in the past two decades. A significant rise in hospitalization and asthma mortality has accompanied the increased incidence.

Status asthmaticus is usually more common among persons in low socioeconomic groups, regardless of race, because they have less access to regular specialist medical care. [8] People who live alone are particularly affected. In the United States, more than 11 million people with asthma (~44% of the total) live at or below the poverty level. [7]

The worldwide incidence of asthma is unclear but has been estimated at about 20 million cases. The dramatic rise in incidence has been attributed, in part, to pollution and industrialization.

Age-, sex-, and race-related demographics

In the United States, asthma prevalence is higher among adults, women, Blacks, and persons with reported income below the federal poverty level. [9]

COVID-19 effect

During the COVID-19 pandemic, there was a significant decline in new diagnoses of childhood asthma, with a 52% reduction in incident diagnosis rates as compared with the 3 years preceding the pandemic. Additionally, emergency department visits for asthma also declined significantly during the pandemic, particularly among children. [10, 11]

Prognosis

In general, unless a complicating illness such as congestive heart failure (CHF) or chronic obstructive pulmonary disease (COPD) is present, status asthmaticus has a good prognosis if appropriate therapy is administered early. A delay in initiating treatment is probably the worst prognostic factor. Delays can result from poor access to healthcare on the part of the patient or even delays in using corticosteroids. Patients with acute asthma should use corticosteroids early and aggressively.

Mortality

Asthma death rates decreased overall from 2001 to 2021, but significant disparities remain, particularly affecting older adults, females, and non-Hispanic Black individuals. The COVID-19 pandemic likely contributed to the increase in asthma deaths observed in 2020. [9]  

Data for 2022 cited 3602 deaths in the United States that were attributable to asthma, for an incidence of 1.1 per 100,000 population. [12]

Mortality risk is also particularly high in patients who delay medical treatment, especially treatment with systemic corticosteroids. Patients with other preexisting conditions (eg, restrictive lung disease, CHF, or chest deformities) are at particular risk for death from status asthmaticus. In addition, patients who smoke regularly have chronic small-airway inflammation and are at greater risk for death from status asthmaticus. Data also suggest higher mortality in persons of lower socioeconomic status, those with psychiatric illness, those with recent poorly controlled asthma, and those with a history of prior intubation. One study linked exposure to the common mold Alternaria alternata with mortality in asthma. [13]

Patient Education

Asthma is a chronic illness. Patients and their families must be provided with a team that can offer education and follow-up care. Before discharge, the team that provides asthma education should meet with the family and the patient to impart information regarding maintenance, monitoring, and measures for environmental control. Identifying exacerbations as early as possible and stressing the importance of adherence with therapy are paramount considerations.

Studies have also demonstrated the importance of an asthma education plan. Guidelines regarding this literature have been published. [14]  

Patients require instruction to use inhalers appropriately, to be compliant with therapy, and to practice stress-avoidance measures. Stress factors (ie, triggers of asthma attacks) include pet dander, house dust, and mold. Patients should be strongly discouraged from smoking; this habit should be avoided at all costs.

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