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Acute severe asthma (also referred to in, latin as status asthmaticus, or asthmatic status ) is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators (inhalers) and steroids. 1, 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.
Contents, signs and symptoms edit.
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). 2, 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. 2, 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.
2, 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.
Irregularities in the heart beat and abnormal lowering of the blood pressure may be observed.
2, pathophysiology edit, 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 lymphocytedriven, as opposed to helper T1 lymphocytedriven, 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 asthma 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.