Acute severe asthma
|Acute severe asthma|
|Classification and external resources|
Acute severe asthma previously referred to as status asthmaticus is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators(inhalers) and steroids. Symptoms include chest tightness, rapidly progressive dyspnea (shortness of breath), dry cough, use of accessory muscles, labored breathing and extreme wheezing. It is a life-threatening episode of airway obstruction considered a medical emergency. Complications include cardiac and/or respiratory arrest.
It is characterized histologically by smooth muscle hypertrophy and basement membrane thickening.
Status asthmaticus is slightly more common in males and is more common among African Americans and Hispanics. The gene locus glutathione dependent S-nitrosoglutathione (GSNOR) has been suggested as one possible correlation to development of status asthmaticus.
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 (e.g., 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.
Interventions include intravenous (IV) medications, aerosolized medications, and positive-pressure therapy, including mechanical ventilation. Often multiple therapies are used to reverse the effects of status asthmaticus as rapidly as possible; though typically only one or two therapies are ultimately necessary, the permanent or generally long-term damage done by the airway restriction is a concern of clinicians. Intravenous and aerosolized treatments such as corticosteroids,  and methylxanthines are often given. Magnesium sulfate is also commonly administered.
- Shah, R; Saltoun, CA (2012 May-Jun). "Chapter 14: Acute severe asthma (status asthmaticus).". Allergy and asthma proceedings : the official journal of regional and state allergy societies. 33 Suppl 1: S47–50. PMID 22794687.
- Moore PE, Ryckman KK, Williams SM, Patel N, Summar ML, Sheller JR (9). "Genetic variants of GSNOR and ADRB2 influence response to albuterol in African-American children with severe asthma.". Pediatric Pulmonology 44 (7): 649–654. doi:10.1002/ppul.21033. PMID 19514054.
- Ratto D, Alfaro C, Sipsey J, Glovsky MM, Sharma OP (1988). "Are intravenous corticosteroids required in status asthmaticus?". JAMA 260 (4): 527–9. doi:10.1001/jama.1988.03410040099036. PMID 3385910.