Acute severe asthma

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Acute severe asthma
Other namesStatus asthmaticus, asthmatic status
Specialty Respirology
Symptoms Anxiety, 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. [3] 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. [4]

Contents

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). [5] [6]

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. [6] The peak expiratory flow can be measured at the bedside; in acute severe asthma, the flow is less than 50% of a person's normal or predicted flow. [6]

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" : wheezing is not heard because there is not enough air movement to generate it), reduced respiratory effort and visible exhaustion or drowsiness. Irregularities in the heartbeat and abnormal lowering of the blood pressure may be observed. [6]

Severe asthma attack can cause symptoms such as: [7]

Cause

The cause for acute severe asthma attacks is still unknown and experts are also unsure of why it developed and why it does not respond to typical asthma treatments. [7] [ medical citation needed ]

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-lymphocyte elaboration of immunoglobulin E (IgE) antibodies specific to that allergen. The IgE antibody attaches to surface receptors on the 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 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 experienced 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 [8] 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 ketamine and aminophylline are also effective in children with acute asthma who responds poorly to standard therapy. [9]

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. [10] 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. [4] The study found that a Novell PMN-cDc interaction in the lung is necessary for a 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. [11]

See also

Related Research Articles

<span class="mw-page-title-main">Asthma</span> Long-term inflammatory disease of the airways of the lungs

Asthma is a long-term inflammatory disease of the airways of the lungs. It is characterized by variable and recurring symptoms, reversible airflow obstruction, and easily triggered bronchospasms. Symptoms include episodes of wheezing, coughing, chest tightness, and shortness of breath. These may occur a few times a day or a few times per week. Depending on the person, asthma symptoms may become worse at night or with exercise.

<span class="mw-page-title-main">Shortness of breath</span> Feeling of difficulty breathing

Shortness of breath (SOB), known as dyspnea or dyspnoea, is an uncomfortable feeling of not being able to breathe well enough. The American Thoracic Society defines it as "a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity", and recommends evaluating dyspnea by assessing the intensity of its distinct sensations, the degree of distress and discomfort involved, and its burden or impact on the patient's activities of daily living. Distinct sensations include effort/work to breathe, chest tightness or pain, and "air hunger". The tripod position is often assumed to be a sign.

<span class="mw-page-title-main">Bronchospasm</span> Lower respiratory tract disease that affects the airways leading into the lungs

Bronchospasm or a bronchial spasm is a sudden constriction of the muscles in the walls of the bronchioles. It is caused by the release (degranulation) of substances from mast cells or basophils under the influence of anaphylatoxins. It causes difficulty in breathing which ranges from mild to severe.

<span class="mw-page-title-main">Bronchoconstriction</span> Constriction of the terminal airways in the lungs

Bronchoconstriction is the constriction of the airways in the lungs due to the tightening of surrounding smooth muscle, with consequent coughing, wheezing, and shortness of breath.

Cardiac asthma is the medical condition of intermittent wheezing, coughing, and shortness of breath that is associated with underlying congestive heart failure (CHF). Symptoms of cardiac asthma are related to the heart's inability to effectively and efficiently pump blood in a CHF patient. This can lead to accumulation of fluid in and around the lungs, disrupting the lung's ability to oxygenate blood.

Exercise-induced bronchoconstriction (EIB) occurs when the airways narrow as a result of exercise. This condition has been referred to as exercise-induced asthma (EIA); however, this term is no longer preferred. While exercise does not cause asthma, it is frequently an asthma trigger.

<span class="mw-page-title-main">Allergic bronchopulmonary aspergillosis</span> Medical condition

Allergic bronchopulmonary aspergillosis (ABPA) is a condition characterised by an exaggerated response of the immune system to the fungus Aspergillus. It occurs most often in people with asthma or cystic fibrosis. Aspergillus spores are ubiquitous in soil and are commonly found in the sputum of healthy individuals. A. fumigatus is responsible for a spectrum of lung diseases known as aspergilloses.

Recurrent airway obstruction, also known as broken wind, heaves, wind-broke horse, or sometimes by the term usually reserved for humans, chronic obstructive pulmonary disease or disorder (COPD) – it is a respiratory disease or chronic condition of horses involving an allergic bronchitis characterised by wheezing, coughing and laboured breathing.

<span class="mw-page-title-main">Bird fancier's lung</span> Type of hypersensitivity pneumonitis

Bird fancier's lung (BFL), also known as bird breeder's lung, is a type of hypersensitivity pneumonitis. It can cause shortness of breath, fever, dry cough, chest pain, anorexia and weight loss, fatigue, and progressive pulmonary fibrosis. It is triggered by exposure to avian proteins present in the dry dust of droppings or feathers of a variety of birds. The lungs become inflamed, with granuloma formation. It mostly affects people who work with birds or own many birds.

<span class="mw-page-title-main">Obstructive lung disease</span> Category of respiratory disease characterized by airway obstruction

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Pitrakinra is a 15-kDa human recombinant protein of wild-type human interleukin-4 (IL-4). It is an IL-4 and IL-13 antagonist that has been studied in a phase IIb clinical trial for the treatment of asthma. Two point mutations on pitrakinra confer its ability to block signaling of IL-4 and interleukin-13 (IL-13) by preventing assembly of IL-4 receptor alpha (IL-4Rα) with either IL-2Rγ or IL-13Rα. Upregulation of Th2 cytokines, including IL-4 and IL-13, is thought to be critical for the allergic inflammation associated with atopic diseases such as asthma and eczema. The targets of pitrakinra action are inflammatory cells and structural cells that express IL-4Rα. The drug has been applied both as a subcutaneous injection and as an inhalation, but the latter formulation proved to be more effective.

Vocal cord dysfunction (VCD) is a pathology affecting the vocal folds characterized by full or partial vocal fold closure causing difficulty and distress during respiration, especially during inhalation.

<span class="mw-page-title-main">Acute exacerbation of chronic obstructive pulmonary disease</span> Medical condition

An acute exacerbation of chronic obstructive pulmonary disease, or acute exacerbations of chronic bronchitis (AECB), is a sudden worsening of chronic obstructive pulmonary disease (COPD) symptoms including shortness of breath, quantity and color of phlegm that typically lasts for several days.

<span class="mw-page-title-main">Chronic obstructive pulmonary disease</span> Lung disease involving long-term poor airflow

Chronic obstructive pulmonary disease (COPD) is a type of progressive lung disease characterized by long-term respiratory symptoms and airflow limitation. GOLD 2024 defined COPD as a heterogeneous lung condition characterized by chronic respiratory symptoms due to abnormalities of the airways and/or alveoli (emphysema) that cause persistent, often progressive, airflow obstruction.

<span class="mw-page-title-main">Tracheobronchomalacia</span> Medical condition

Tracheobronchomalacia (TBM) is a condition characterized by flaccidity of the tracheal support cartilage which leads to tracheal collapse. This condition can also affect the bronchi. There are two forms of this condition: primary TBM and secondary TBM. Primary TBM is congenital and starts as early as birth. It is mainly linked to genetic causes. Secondary TBM is acquired and starts in adulthood. It is mainly developed after an accident or chronic inflammation.

<span class="mw-page-title-main">Asthma trigger</span> Factor that provokes symptoms of asthma

Asthma triggers are factors or stimuli that provoke the exacerbation of asthma symptoms or increase the degree of airflow disruption, which can lead to an asthma attack. An asthma attack is characterized by an obstruction of the airway, hypersecretion of mucus and bronchoconstriction due to the contraction of smooth muscles around the respiratory tract. Its symptoms include a wide range of manifestations such as breathlessness, coughing, a tight chest and wheezing.

Asthma-Chronic Obstructive Pulmonary Disease (COPD) Overlap (ACO), also known as Asthma-COPD Overlap Syndrome (ACOS), is a chronic inflammatory, obstructive airway disease in which features of both asthma and COPD predominate. Asthma and COPD were once thought of as distinct entities; however, in some, there are clinical features of both asthma and COPD with significant overlap in pathophysiology and symptom profile. It is unclear whether ACO is a separate disease entity or a clinical subtype of asthma and COPD. The pathogenesis of ACO is poorly understood, but it is thought to involve both type 2 inflammation as well as type 1 inflammation. The incidence and prevalence of ACO are not well known. The risk factors for ACO are also incompletely understood, but tobacco smoke is known to be a major risk factor.

Asthma phenotyping and endotyping is a novel approach to asthma classification inspired by precision medicine. It seeks to separate the clinical presentations or clusters of signs and symptoms of asthma, known as asthma phenotypes, from their underlying etiologies or causes, known as asthma endotypes.

Anti-asthmatic agents refer to drugs that can aid in airway smooth muscle dilation to allow normal breathing during an asthma attack or reduce inflammation on the airway to decrease airway resistance for asthmatic patients, or both. The goal of asthmatic agents is to reduce asthma exacerbation frequencies and related hospital visits.

Anti-allergic agents are medications used to treat allergic reactions. Anti-allergic agents have existed since 3000 B.C in countries such as China and Egypt. It was not until 1933 when antihistamines, the first type of anti-allergic agents, were developed. Common allergic diseases include allergic rhinitis, allergic asthma and atopic dermatitis with varying symptoms, including runny nose, watery eyes, itchiness, coughing, and shortness of breath. More than one-third of the world's population is currently being affected by one or more allergic conditions.

References

  1. 1 2 "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)". Allergy and Asthma Proceedings. 33 Suppl 1 (3): 47–50. doi:10.2500/aap.2012.33.3547. PMID   22794687 . Retrieved 2019-11-06.
  3. ↑ "Asthma". The Lecturio Medical Concept Library. 25 November 2020. Retrieved 1 July 2021.
  4. 1 2 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.
  5. ↑ Kumar, Varun (2020-10-15). "Asthma". Bibo. Retrieved 2020-11-04.
  6. 1 2 3 4 "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.
  7. 1 2 "Status Asthmaticus (Severe Acute Asthma)". WebMD. Retrieved 2019-11-06.
  8. ↑ 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. PMID   3385910.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ 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. S2CID   30530302.
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