| Acute severe asthma | |
|---|---|
| Other names | Status asthmaticus, asthmatic status |
| Specialty | Respirology |
| Symptoms | Anxiety, panic, laboring to breathe,tightened neck and chest muscles, difficulty performing normal daily activities[1] |
| Usual onset | Silent chest, worsening symptoms despite use of medication.[1] |
Acute severe asthma, also known asstatus asthmaticus, is anacute exacerbation ofasthma that does not respond to standard treatments ofbronchodilators (inhalers) andcorticosteroids.[2] Asthma is caused by multiplegenes, 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 progressivedyspnea (shortness of breath), drycough, use of accessoryrespiratory muscles, fast and/or labored breathing, and extremewheezing. 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 ofatopy and asthma remains unexplained but may be due to infection with respiratory viruses.[4]
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, therespiratory rate may be elevated (more than 25 breaths per minute), and theheart 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] Thepeak 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% orcyanosis (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 andabnormal lowering of the blood pressure may be observed.[6]
Severe asthma attack can cause symptoms such as:[7]
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]
Inflammation in asthma is characterized by an influx ofeosinophils during the early-phase reaction and a mixed cellular infiltrate composed of eosinophils,mast cells,lymphocytes, andneutrophils during the late-phase (or chronic) reaction. The simple explanation for allergic inflammation in asthma begins with the development of a predominantly helper T2lymphocyte–driven, as opposed to helper T1lymphocyte–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 helperTh2 helper T cells leads toB-lymphocyte elaboration ofimmunoglobulin E (IgE) antibodies specific to that allergen. The IgE antibody attaches to surface receptors on the airwaymucosalmast cells. One important question is whetheratopic 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 ofIgE molecules and activation of mast cells, with elaboration and release of a vast array of mediators. These mediators includehistamine;leukotrienes C4, D4, and E4; and a host ofcytokines. 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 thesmooth 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 andlow levels of oxygen in the blood.
Severe acute asthma can be diagnosed by a primary care physician (PCP). APCP 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.
Statusasthmaticus can be misdiagnosed when wheezing occurs from an acute cause other than asthma. Some of these alternative causes of wheezing are discussed below.
Airways can be compressed from vascular structures, such as vascular rings, lymphadenopathy, or tumors.
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 ascardiac asthma.
Interventions includeintravenous (IV) medications (e.g.magnesium sulfate), aerosolized medications to dilate the airways (bronchodilation) (e.g.,albuterol oripratropium bromide/salbutamol), andpositive-pressure therapy, includingmechanical ventilation. Multiple therapies may be used simultaneously to rapidly reverse the effects of status asthmaticus and reduce permanent damage of the airways. Intravenouscorticosteroids[8] andmethylxanthines are often given. If the person with a severe asthma exacerbation is on a mechanical ventilator, certain sedating medications such asketamine orpropofol, have bronchodilating properties. According to a new randomized control trialketamine andaminophylline are also effective in children with acute asthma who responds poorly to standard therapy.[9]
A recent study proposed that the interaction between host airwayepithelial cells and respiratory viruses is another aspect of innate immunity that is also a critical determination ofasthma.[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 experimentalasthma after viral infection inmate depended on Type IIFN-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.
Status asthmaticus is slightly more common in males and is more common among people of African and Hispanic origin. The gene locusglutathione dependent S-nitrosoglutathione (GSNOR) has been suggested as one possible correlation to development of status asthmaticus.[11]
