Acute severe asthma
|Acute severe asthma|
|Classification and external resources|
Acute severe asthma (also 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 respiratory muscles, labored breathing, and extreme wheezing. It is a life-threatening episode of airway obstruction and is considered a medical emergency. Complications include cardiac and/or respiratory arrest.
It is characterized histologically by smooth muscle hypertrophy and basement membrane thickening.
Signs and symptoms
An exacerbation (attack) of asthma is experienced as a worsening of asthma symptoms with breathlessness and cough (often worse at night). In acute severe asthma, breathlessness may be so severe that it is impossible to speak more than a few words (inability to complete sentences).
On examination, the respiratory rate may be elevated (more than 25 breaths per minute), and the heart rate may be rapid (110 beats per minute or faster). Reduced oxygen saturation levels (but above 92%) are often encountered. Examination of the lungs with a stethoscope may reveal reduced air entry and/or widespread wheeze. The peak expiratory flow can be measured at the bedside; in acute severe asthma the flow is less than 50% a person's normal or predicted flow.
Very severe acute asthma (termed "near-fatal" as there is an immediate risk to life) is characterised by a peak flow of less than 33% predicted, oxygen saturations below 92% or cyanosis (blue discoloration, usually of the lips), absence of audible breath sounds over the chest ("silent chest"), reduced respiratory effort and visible exhaustion or drowsiness. Irregularities in the heart beat and abnormal lowering of the blood pressure may be observed.
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.
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.
- Shah, R; Saltoun, CA (May–Jun 2012). "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. doi:10.2500/aap.2012.33.3547. PMID 22794687.
- Clinical guideline: asthma (October 2014). "SIGN 141 • British guideline on the management of asthma". London: British Thoracic Society and Scottish Intercollegiate Guidelines Network. Retrieved 19 October 2014.
- 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.
- Moore PE, Ryckman KK, Williams SM, Patel N, Summar ML, Sheller JR (9 July 2009). "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.