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Acute severe asthma

acute severe asthma, acute severe asthma management guidelines
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 steroids1 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


  • 1 Signs and symptoms
  • 2 Pathophysiology
  • 3 Treatment
  • 4 Epidemiology
  • 5 References

Signs and symptomsedit

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 sentences2

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 wheeze2 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 flow2

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 observed2


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


Interventions include intravenous IV medications eg magnesium sulfate, aerosolized medications, and positive-pressure therapy, including mechanical ventilation Multiple therapies may be used simultaneously to rapidly reverse the effects of status asthmaticus and reduce permanent damage of the airways Intravenous and aerosolized treatments such as corticosteroids3 and methylxanthines are often given According to a new randomized control trial ketamine and aminophylline are also effective in children with acute asthma who responds poorly to standard therapy4


Status asthmaticus is slightly more common in males and is more common among people of African and Hispanic origin The gene locus glutathione dependent S-nitrosoglutathione GSNOR has been suggested as one possible correlation to development of status asthmaticus5


  1. ^ Shah, R; Saltoun, CA May–Jun 2012 "Chapter 14: Acute severe asthma status asthmaticus" Allergy and Asthma Proceedings 33 Suppl 1: S47–50 PMID 22794687 doi:102500/aap2012333547 
  2. ^ a b c d "SIGN 141 British guideline on the management of asthma" Clinical guideline: asthma London: British Thoracic Society and Scottish Intercollegiate Guidelines Network BTS/SIGN October 2014 Retrieved 19 October 2014 
  3. ^ Ratto D, Alfaro C, Sipsey J, Glovsky MM, Sharma OP 1988 "Are intravenous corticosteroids required in status asthmaticus" JAMA 260 4: 527–9 PMID 3385910 doi:101001/jama198803410040099036 
  4. ^ Tiwari Abhimanyu, Vishal Guglani, and Kana Ram Jat "Ketamine versus aminophylline for status asthmatic in children: A randomized, controlled trial" European respiratory journal 44Suppl 58 2014: 281
  5. ^ 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 PMID 19514054 doi:101002/ppul21033 

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