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Acute severe asthma

Acute severe asthma
Other namesStatus asthmaticus, asthmatic status
SpecialtyRespirology
SymptomsAnxiety, panic, laboring to breath, tightened neck and chest muscles, difficulty performing normal daily activities[1]
Usual onsetSilent chest, worsening symptoms despite use of medication.[1]

Acute severe asthma, also known as status asthmaticus, is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators (inhalers) and corticosteroids. [2] Asthma is caused by multiple genes, some having protective effect, with each gene having its own tendency to be influenced by the environment although a genetic link leading to acute severe asthma is still unknown.[citation needed] Symptoms include chest tightness, rapidly progressive dyspnea(shortness of breath), dry cough, use of accessory respiratory muscles, fast and/or 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. The increasing prevalence of atopy and asthma remains unexplained but may be due to infection with respiratory viruses. [3]

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).[4]

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.[4] 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.[4]

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.[4] Severe asthma attack can cause symptoms such as: [5]

Cause

The cause for Acute Severe Asthma attacks is still unknown and experts are also unsure of why its developed and why it doesn't respond to typical asthma treatments,[6] although there are some speculations: [5]

  • Not seeing a doctor regularly, therefore asthma is not under good control
  • Coming in contact with asthma triggers
  • Allergies or severe allergic reactions
  • Not using the peak flow meter and not taking asthma medication as directed by a primary care physician (PCP) correctly
  • Not following an asthma action plan correctly
  • respiratory infections[6]
  • severe stress
  • cold weather
  • air pollution
  • exposure to chemicals and other irritants
  • smoking

Mechanism

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 Th2 helper T cells leads to B-lymphocyteelaboration 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 low levels of oxygen in the blood.

Diagnosis

Severe Acute Asthma can be diagnosed by a primary care physician (PCP). A PCP will ask questions in regards to symptoms and breathing; they will also ask if fatigue or wheezing has been experience when breathing in or out; and also test using a peak expiratory flow and an oxygen saturation.

Status asthmaticus can be misdiagnosed when wheezing occurs from an acute cause other than asthma. Some of these alternative causes of wheezing are discussed below.

Extrinsic compression

Airways can be compressed from vascular structures, such as vascular rings, lymphadenopathy, or tumors.

Congestive heart failure

Airway edema may cause wheezing in CHF. In addition, vascular compression may compress the airways during systole with cardiac ejection, resulting in a pulsatile wheeze that corresponds to the heart rate. This is sometimes erroneously referred to as cardiac asthma.

Differential diagnoses

Treatment

Interventions include intravenous (IV) medications (e.g. magnesium sulfate), aerosolized medications to dilate the airways (bronchodilation) (e.g., albuterol or ipratropium bromide/salbutamol), 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 corticosteroids[7] and methylxanthines are often given. If the person with a severe asthma exacerbation is on a mechanical ventilator, certain sedating medications such as ketamine or propofol, have bronchodilating properties. According to a new randomized control trial ketamineand aminophylline are also effective in children with acute asthma who responds poorly to standard therapy.[8]

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 the development of status asthmaticus.

Recent Research

A recent study proposed that the interaction between host airway epithelial cells and respiratory viruses is another aspect of innate immunity that is also a critical determination of asthma.[9] It was also proposed that a rationale for how antiviral performance at the epithelial cell level might be improved to prevent acute infectious illness and chronic inflammatory disease caused by respiratory viruses.

Another study aimed to show that experimental asthma after viral infection inmate depended on Type I IFN-driven up-regulation of the high-affinity receptor for IgE (FcεRI) on conventional dendritic cells (cDCs) in the lungs.[3] The study found that a Novell PMN-cDc interaction in the lung that is necessary of viral infection to induce atopic disease.

Epidemiology

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 asthmaticus.[10]

References

  1. ^ a b "What Is an Asthma Attack?". WebMD. 2019-01-30. Retrieved 2020-03-24.
  2. ^ Shah, Rachna; Saltoun, Carol A. (May–June 2012). "Chapter 14: Acute severe asthma (status asthmaticus)". www.ingentaconnect.com. PMID 22794687. Retrieved 2019-11-06.
  3. ^ a b Cheung, Dorothy S.; Ehlenbach, Sarah J.; Kitchens, Robert T.; Riley, Desiré A.; Thomas, Larry L.; Holtzman, Michael J.; Grayson, Mitchell H. (2010-11-01). "CD49d+ neutrophils induce FcεRI expression on lung dendritic cells in a mouse model of postviral asthma". Journal of Immunology. 185 (9): 4983–4987. doi:10.4049/jimmunol.1002456. ISSN 0022-1767. PMC 2959147. PMID 20876348.
  4. ^ 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. Archived from the original on 12 September 2017. Retrieved 19 October 2014.
  5. ^ a b "Status Asthmaticus (Severe Acute Asthma)". WebMD. Retrieved 2019-11-06.
  6. ^ a b c "Status Asthmaticus: Symptoms, Causes, Diagnosis, and Treatment". Healthline. Retrieved 2019-11-06.
  7. ^ Ratto, David; Alfaro, Carlos; Sipsey, Jeff; Glovsky, M. Michael; Sharma, Om P. (1988-07-22). "Are Intravenous Corticosteroids Required in Status Asthmaticus?". JAMA. 260 (4): 527–529. doi:10.1001/jama.1988.03410040099036. ISSN 0098-7484.
  8. ^ Jat, KanaRam; Tiwari, Abhimanyu; Guglani, Vishal (2016). "Ketamine versus aminophylline for acute asthma in children: A randomized, controlled trial". Annals of Thoracic Medicine. 11 (4): 283–288. doi:10.4103/1817-1737.191874. ISSN 1817-1737. PMC 5070438. PMID 27803755.
  9. ^ Holtzman, Michael J.; Patel, Dhara; Zhang, Yong; Patel, Anand C. (August 2011). "Host epithelial-viral interactions as cause and cure for asthma". Current Opinion in Immunology. 23 (4): 487–494. doi:10.1016/j.coi.2011.05.010. ISSN 0952-7915. PMC 3163712. PMID 21703838.
  10. ^ 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.

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