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">Cough</span> Sudden expulsion of air from the lungs as a reflex to clear irritants

A cough is a sudden expulsion of air through the large breathing passages which can help clear them of fluids, irritants, foreign particles and microbes. As a protective reflex, coughing can be repetitive with the cough reflex following three phases: an inhalation, a forced exhalation against a closed glottis, and a violent release of air from the lungs following opening of the glottis, usually accompanied by a distinctive sound.

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

Shortness of breath (SOB), also medically 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">Pulmonary heart disease</span> Medical condition

Pulmonary heart disease, also known as cor pulmonale, is the enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance or high blood pressure in the lungs.

<span class="mw-page-title-main">Bronchiolitis</span> Blockage of the small airways in the lungs due to a viral infection

Bronchiolitis is inflammation of the small airways in the lungs. Acute bronchiolitis is due to a viral infection usually affecting children younger than two years of age. Symptoms may include fever, cough, runny nose, wheezing, and breathing problems. More severe cases may be associated with nasal flaring, grunting, or the skin between the ribs pulling in with breathing. If the child has not been able to feed properly, signs of dehydration may be present.

<span class="mw-page-title-main">Immunoglobulin E</span> Immunoglobulin E (IgE) Antibody

Immunoglobulin E (IgE) is a type of antibody that has been found only in mammals. IgE is synthesised by plasma cells. Monomers of IgE consist of two heavy chains and two light chains, with the ε chain containing four Ig-like constant domains (Cε1–Cε4). IgE is thought to be an important part of the immune response against infection by certain parasitic worms, including Schistosoma mansoni, Trichinella spiralis, and Fasciola hepatica. IgE is also utilized during immune defense against certain protozoan parasites such as Plasmodium falciparum. IgE may have evolved as a defense to protect against venoms.

<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.

<span class="mw-page-title-main">Pneumonitis</span> General inflammation of lung tissue

Pneumonitis describes general inflammation of lung tissue. Possible causative agents include radiation therapy of the chest, exposure to medications used during chemo-therapy, the inhalation of debris, aspiration, herbicides or fluorocarbons and some systemic diseases. If unresolved, continued inflammation can result in irreparable damage such as pulmonary fibrosis.

Eosinophilic pneumonia is a disease in which an eosinophil, a type of white blood cell, accumulates in the lungs. These cells cause disruption of the normal air spaces (alveoli) where oxygen is extracted from the atmosphere. Several different kinds of eosinophilic pneumonia exist and can occur in any age group. The most common symptoms include cough, fever, difficulty breathing, and sweating at night. Eosinophilic pneumonia is diagnosed by a combination of characteristic symptoms, findings on a physical examination by a health provider, and the results of blood tests and X-rays. Prognosis is excellent once most eosinophilic pneumonia is recognized and treatment with corticosteroids is begun.

Exercise-induced asthma (EIA) occurs when the airways narrow as a result of exercise. The preferred term for this condition is exercise-induced bronchoconstriction (EIB). While exercise does not cause asthma, it is frequently an asthma trigger.

Feline asthma is a common allergic respiratory disease in cats, affecting at least one percent of all adult cats worldwide. It is a chronic progressive disease for which there is no cure. Common symptoms include wheezing, coughing, labored breathing and potentially life-threatening bronchoconstriction. There is conjecture that the disease has become more common due to increased exposure to industrial pollutants. Feline asthma can also be attributed to lung damage caused by long-term exposure to second-hand smoke.

<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">Obstructive lung disease</span> Category of respiratory disease characterized by airway obstruction

Obstructive lung disease is a category of respiratory disease characterized by airway obstruction. Many obstructive diseases of the lung result from narrowing (obstruction) of the smaller bronchi and larger bronchioles, often because of excessive contraction of the smooth muscle itself. It is generally characterized by inflamed and easily collapsible airways, obstruction to airflow, problems exhaling, and frequent medical clinic visits and hospitalizations. Types of obstructive lung disease include; asthma, bronchiectasis, bronchitis and chronic obstructive pulmonary disease (COPD). Although COPD shares similar characteristics with all other obstructive lung diseases, such as the signs of coughing and wheezing, they are distinct conditions in terms of disease onset, frequency of symptoms, and reversibility of airway obstruction. Cystic fibrosis is also sometimes included in obstructive pulmonary disease.

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. The main symptoms of COPD include shortness of breath and a cough, which may or may not produce mucus. COPD progressively worsens, with everyday activities such as walking or dressing becoming difficult. While COPD is incurable, it is preventable and treatable. The two most common types of COPD are emphysema and chronic bronchitis and have been the two classic COPD phenotypes. Emphysema is defined as enlarged airspaces (alveoli) whose walls have broken down resulting in permanent damage to the lung tissue. Chronic bronchitis is defined as a productive cough that is present for at least three months each year for two years. Both of these conditions can exist without airflow limitation when they are not classed as COPD. Emphysema is just one of the structural abnormalities that can limit airflow and can exist without airflow limitation in a significant number of people. Chronic bronchitis does not always result in airflow limitation but in young adults who smoke the risk of developing COPD is high. Many definitions of COPD in the past included emphysema and chronic bronchitis, but these have never been included in GOLD report definitions. Emphysema and chronic bronchitis remain the predominant phenotypes of COPD but there is often overlap between them and a number of other phenotypes have also been described. COPD and asthma may coexist and converge in some individuals. COPD is associated with low-grade systemic inflammation.

<span class="mw-page-title-main">Asthma trigger</span>

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.

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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