Status asthmaticus is a medical emergency in which asthma symptoms are refractory to initial bronchodilator therapy in the emergency department. Patients report chest tightness, rapidly progressive shortness of breath, dry cough, and wheezing. Typically, patients present a few days after the onset of a viral respiratory illness, following exposure to a potent allergen or irritant, or after exercise in a cold environment. Frequently, patients have underused or have been underprescribed anti-inflammatory therapy. Illicit drug use may play a role in poor adherence to anti-inflammatory therapy. Patients may have increased their beta-agonist intake (either inhaled or nebulized) to as often as every few minutes.
The Medscape Asthma Resource Center may be of interest.
Inflammation in asthma is characterized by an influx of eosinophils during the early-phase reaction and a mixed cellular infiltrate composed of eosinophils, mast cells, lymphocytes, and neutrophils during the late-phase (or chronic) reaction. The simple explanation for allergic inflammation in asthma begins with the development of a predominantly helper T2 lymphocyte–driven, as opposed to helper T1 lymphocyte–driven, immune milieu, perhaps caused by certain types of immune stimulation early in life. This is followed by allergen exposure in a genetically susceptible individual.
Specific allergen exposure (eg, dust mites) under the influence of helper T2 lymphocytes leads to B-lymphocyte elaboration of immunoglobulin E (IgE) antibodies specific to that allergen. The IgE antibody attaches to surface receptors on airway mucosal mast cells. One important question is whether atopic individuals with asthma, in contrast to atopic persons without asthma, have a defect in mucosal integrity that makes them susceptible to penetration of allergens into the mucosa.
Subsequent specific allergen exposure leads to cross-bridging of IgE molecules and activation of mast cells, with elaboration and release of a vast array of mediators. These mediators include histamine; leukotrienes C4, D4, and E4; and a host of cytokines. Together, these mediators cause bronchial smooth muscle constriction, vascular leakage, inflammatory cell recruitment (with further mediator release), and mucous gland secretion. These processes lead to airway obstruction by constriction of the smooth muscles, edema of the airways, influx of inflammatory cells, and formation of intraluminal mucus. In addition, ongoing airway inflammation is thought to cause the airway hyperreactivity characteristic of asthma. The more severe the airway obstruction, the more likely ventilation-perfusion mismatching will result in impaired gas exchange and hypoxemia.
The prevalence and severity of asthma cases are on the rise (see Asthma). Also increasing are the occurrences of asthma hospitalization and mortality resulting from status asthmaticus. Status asthmaticus is usually more common among persons in low socioeconomic groups, regardless of race, and particularly in people who live alone.
A 2004 study conducted at the Columbia University Medical Center,1 however, noted the number of patients with status asthmaticus requiring intensive care admissions declined over the past 10 years. The trend was toward less advanced presentations. This may reflect improvements in medication compliance, education, or access to medical care.
Similar to the US data, asthma mortality rates are increasing.
Patients who delay medical treatment, particularly treatment with systemic steroids, have a greater chance of dying.
Patients with other preexisting conditions (eg, restrictive lung disease, congestive heart failure, chest deformities) are at particular risk of death from status asthmaticus.
Patients who smoke regularly have chronic inflammation of the small airways and are at particular risk of death from status asthmaticus.
A 1997 study by Hanania et al2 noted that although asthma is more common among African American and Hispanic persons, this prevalence may be the result of socioeconomic factors rather than race.
African American and Hispanic persons in the United States, in association with lower socioeconomic factors, have less access to regular specialist medical care, which leads to an increased risk of status asthmaticus.
In the United States, particularly in large cities, illiteracy and lower educational competence are more prevalent in African American and Hispanic families, and children in these families have increased morbidity from asthma.
Status asthmaticus is slightly more common in males than in females.
Status asthmaticus can occur in persons of any age group, including infants and geriatric patients. Mortality rates are higher in very young children and elderly adults.
Children younger than 2 years, and sometimes those older, may have respiratory syncytial virus (RSV) infections that can result in severe attacks of wheezing that mimic status asthmaticus. Also, RSV infections can predispose patients to asthma later in life.
Patients with status asthmaticus have severe dyspnea that has developed over hours to days.
Frequently, patients have a prior history of endotracheal intubation and mechanical ventilation, frequent emergency department visits, and previous use of systemic corticosteroids.
Patients usually present with audible wheezing.
Patients are usually tachypneic upon examination and, in early stages of status asthmaticus, may have significant wheezing. Initially, wheezing is heard only during expiration, but, later, wheezing occurs during both expiration and inspiration.
The chest is hyperexpanded, and accessory muscles, particularly the sternocleidomastoid, scalene, and intercostal muscles, are used. Later, as bronchoconstriction worsens, patients’ wheezing may disappear, which may indicate severe airflow obstruction.
Normally, the pulsus paradoxus (ie, the difference in systolic blood pressure between inspiration and expiration) does not exceed 15 mm Hg. In patients with severe asthma, a pulsus paradoxus of greater than 25 mm Hg usually indicates severe airway obstruction.
In persons with acute asthma, bronchospasms occur as a result of one or more inciting factors that may include, but are not limited to, a viral upper or lower respiratory tract infection, significant allergic response to an allergen (eg, pollen, mold, animal dander, house dust mites), exposure to an irritant, or vigorous exercise in a cold environment.
Precipitating factors can include infection, allergen or irritant exposure, poor adherence to the medical regimen, strenuous exercise, and a rapid decrease in long-term oral steroid therapy.
Inflammation can be the result of infection; lymphocyte, mast cell, eosinophilic, and neutrophilic responses; and airway epithelial damage. In addition, elevated plasma lactate levels were noted in patients with this condition in the first hours of inhaled beta-agonist treatment.3 The presence of a previous hyperadrenergic state may predispose to the development of this condition. This may also correlate with improvements in lung function.