Last updated date: 23-May-2023
Originally Written in English
Asthma is a common chronic disease that affects roughly 26 million people in the United States. It is the most common chronic childhood disease, affecting an estimated 7 million children. Asthma has a complicated pathophysiology that includes airway inflammation, intermittent airflow obstruction, and bronchial hyperresponsiveness.
Asthma is a common disease with varying degrees of severity, ranging from a very mild, infrequent wheeze to an acute, life-threatening airway closure. It typically manifests in childhood and is associated with other atopy symptoms such as eczema and hay fever.
Asthma is a common childhood illness that results in multiple hospitalizations and increased healthcare costs. The main feature is airway hyperresponsiveness, which can be caused by a variety of factors. Asthma has a high mortality rate if not treated promptly.
The lungs' airways are made up of cartilaginous bronchi, membranous bronchi, and gas-exchanging bronchi known as respiratory bronchioles and alveolar ducts. While the first two types primarily serve as anatomic dead space, they also contribute to airway resistance. The terminal bronchioles are the smallest non-gas-exchanging airways, measuring about 0.5 mm in diameter; airways are considered small if they are less than 2 mm in diameter.
Airway structure consists of the following:
- Mucosa, which is composed of epithelial cells that are capable of specialized mucous production and a transport apparatus
- Basement membrane
- A smooth-muscle matrix extending to the alveolar entrances
- Predominantly fibrocartilaginous or fibroelastic-supporting connective tissue.
Mast cells are cellular elements that play a complex role in the release of histamine and other mediators. In the early and late stages of bronchial asthma, basophils, eosinophils, neutrophils, and macrophages are also responsible for extensive mediator release.
Stretch and irritant receptors, as well as cholinergic motor nerves that innervate smooth muscle and glandular units, are found in the airways. Smooth muscle contraction in an airway is greater than would be expected for its size if it were functioning normally in bronchial asthma, and the distribution of this contraction varies.
Asthma is a common pathology, affecting approximately 15% to 20% of people in developed countries and 2% to 4% in less developed countries. It is far more prevalent in children. Regardless of lung function tests, up to 40% of children will experience wheezing at some point, which, if reversible with beta-2 agonists, is classified as asthma. Asthma is linked to tobacco smoke and inhaled particulates, and it is thus more common in people who are exposed to these pollutants.
Asthma is more frequent in boys during childhood, with a male to female ratio of 2:1 until adolescence, when the ratio changes to 1:1. Females have a higher frequency of asthma after puberty, and adult-onset cases after the age of 40 are primarily females. Asthma prevalence increases with age due to decreased airway responsiveness and reduced levels of lung function.
Approximately 66 percent of all asthma cases are diagnosed before the age of 18 years. During early adulthood, about half of all children with asthma see a reduction in intensity or cessation of symptoms.
Asthma is a group of disorders that have a wide range of characteristics. A genetic predisposition, especially a personal or family history of atopy, is one of the established risk factors for asthma (propensity to allergy, usually seen as eczema, hay fever, and asthma). Exposure to cigarette smoke and other inflammatory chemicals or particulate matter has also been linked to asthma.
The overall etiology is complex and still not fully understood, particularly when it comes to predicting which children with pediatric asthma will develop asthma as adults (up to 40% of children have a wheeze, whereas only 1% of adults have asthma), but it is agreed that it is a multifactorial pathology influenced by both genetics and environmental exposure.
Triggers for asthma include:
- Viral respiratory tract infections
- Gastroesophageal reflux disease
- Chronic sinusitis
- Environmental allergens
- Use of aspirin, beta-blockers
- Tobacco smoke
- Insects, plants, chemical fumes
- Emotional factors or stress
Asthma is a disorder characterized by acute, entirely reversible airway inflammation, which frequently occurs in response to an environmental stimulus. The pathogenic process begins with the intake of an irritant (e.g., cold air) or allergen (e.g., pollen), which causes airway inflammation and an increase in mucus production owing to bronchial hypersensitivity. This results in a considerable increase in airway resistance, which is most noticeable during expiration.
Airway obstruction occurs due to the combination of:
- Inflammatory cell infiltration.
- Mucus hypersecretion with mucus plug formation.
- Smooth muscle contraction.
These irreversible changes may become irreversible over time due to
- Basement membrane thickening, collagen deposition, and epithelial desquamation.
- Airway remodeling occurs in chronic disease with smooth muscle hypertrophy and hyperplasia.
Asthma may become more difficult to treat if not treated promptly because mucus development inhibits inhaled medicine from reaching the mucosa. The inflammation gets more edematous as well. This process is resolved (in theory, complete resolution is required in asthma, but this is not checked or tested) with beta-2 agonists (e.g., salbutamol, salmeterol, albuterol) and can be aided by muscarinic receptor antagonists (e.g., ipratropium bromide), which act to reduce inflammation and relax the bronchial musculature, as well as mucus production.
When the tidal volume approaches the volume of the pulmonary dead space, hyperinflation compensates for the airflow blockage, but this compensation is limited, resulting in alveolar hypoventilation.
Uneven variations in airflow resistance, the accompanying uneven distribution of air, and changes in circulation caused by hyperinflation's increased intra-alveolar pressure all contribute to ventilation-perfusion mismatch. This mismatch is exacerbated by vasoconstriction caused by alveolar hypoxia. Vasoconstriction is also thought to be an adaptive response to a mismatch in ventilation/perfusion.
When the ventilation-perfusion mismatch causes hypoxia, the easy passage of carbon dioxide through alveolar capillary membranes prevents hypercarbia. In the absence of carbon dioxide retention, individuals with asthma in the early stages of an acute episode develop hypoxemia. The hypoxic drive produces hyperventilation, which causes a reduction in PaCO2. Hypercarbia is avoided by increasing alveolar ventilation in the early stages of an acute exacerbation.
Carbon dioxide retention develops when the blockage worsens and the ventilation-perfusion mismatch increases. Respiratory alkalosis is caused by hyperventilation in the early stages of an acute episode. Later, metabolic acidosis is caused by increased labor of breathing, increased oxygen demand, and increased cardiac output. Respiratory failure causes respiratory acidosis owing to carbon dioxide retention when alveolar ventilation declines.
Bronchial asthma symptoms
Patients will typically describe a wheeze or cough that has been aggravated by allergies, exertion, or a cold. There is frequently diurnal fluctuation, with symptoms stronger at night. Other types of atopy, such as eczema and hay fever, may be mentioned by the patient. With acute exacerbations, there may be some modest chest discomfort. Many asthmatics experience nighttime coughing bouts yet seem fine during the day.
A slight tremor in the hands and modest tachycardia may occur during an acute exacerbation due to salbutamol administration. Patients will exhibit some breathing difficulty and will frequently sit forward to splint expand their airways. A bilateral, expiratory wheeze will be noted on auscultation. The chest may be quiet in life-threatening asthma because air cannot enter or exit the lungs, and there may be indicators of systemic hypoxia.
Children who are about to be arrested may look sleepy, unresponsive, cyanotic, and disoriented. There may be no wheezing and bradycardia, suggesting significant respiratory muscle tiredness.
A kind of asthma that is life-threatening does not respond to systemic steroids or beta 2 agonist nebulization. It is critical to detect it early since it might result in a high mortality rate. On investigation, it reveals the following characteristics:
- Peak expiratory flow less than 33% of personal best
- Oxygen saturation less than 92%
- The normal partial pressure of carbon dioxide
- Silent chest
- Feeble respiratory effort
- Confusion, coma
In near-fatal asthma, the partial pressure of carbon dioxide is increased, or mechanical ventilation with increased inflation pressures is necessary.
Pulse oximetry can be used to determine the intensity of an asthma episode or to monitor for worsening. Because of the physiological reserve of many patients, a declining pO2 on pulse oximetry is a late discovery, suggesting a critically ill or peri-arrest patient.
Peak flow measurements may also be used to evaluate asthma and should always be compared to a nomogram as well as the particular patient's normal baseline function. The severity of acute asthma episodes is connected with a peak flow measurement, which is reported as a percentage of projected peak flow.
If the patient receives a large dosage or repeat salbutamol, urea and electrolytes (kidney function) should be taken, since one of the adverse effects of salbutamol is that it causes potassium to transfer into the intracellular space transiently, which can produce transient, iatrogenic hypokalaemia. Eosinophilia is widespread, however it is not associated with asthma. Recent research suggests that sputum eosinophil levels may help guide treatment. Furthermore, some individuals may have an increase in serum IgE.
Hypoxemia and respiratory acidosis may be revealed by arterial blood gas analysis. Periostin may be a marker for asthma, according to research, although its clinical relevance is unknown. An ECG will show sinus tachycardia, which might be caused by asthma, albuterol, or theophylline.
A chest x-ray is an useful exam, especially if the patient has a history of foreign body or infection risk. Patients with persistent symptoms who do not respond to treatment are given a chest CT scan.
Spirometry is the preferred diagnostic approach, revealing an obstructive pattern that is partially or totally relieved by salbutamol. To establish the severity of the disease, spirometry should be performed prior to therapy. A lower FEV1 to FVC ratio indicates airway blockage, which can be reversed with therapy. Reversibility testing is performed by administering inhaled short-acting beta 2 agonists to the patient, followed by a repeat spirometry test.
If FEV1 improves by 12% or 200ml from the prior figure, it indicates reversibility and is diagnostic for bronchial asthma. Peak expiratory flow measurement is now common and allows one to document therapy response. The fact that this test is effort dependent is one of its limitations.
A methacholine/histamine challenge may be necessary in some individuals to evaluate if airway hyper-reactivity exists. Only trained personnel should do this exam. Exercise spirometry may aid in the identification of patients suffering from exercise-induced bronchoconstriction.
Exercise-induced asthma (EIA) or exercise-induced bronchoconstriction (EIB) is an asthma variation defined as a condition in which excessive physical activity causes acute bronchoconstriction in those who already have a high level of airway responsiveness. It is most commonly seen in people with asthma (exercise-induced bronchoconstriction in asthmatic people), although it may also be seen in people with atopy, allergic rhinitis, or cystic fibrosis, as well as in healthy people, many of whom are elite or cold weather athletes
Activity-induced bronchoconstriction is frequently misdiagnosed, and the underlying asthma may be asymptomatic in up to 50% of patients until during exercise.
The pathophysiology of exercise-induced bronchoconstriction remains debatable. Water loss from the airway, heat loss from the airway, or a combination of the two may be responsible for the condition. The upper airway is meant to maintain 100% humidity in the inspired air and a body temperature of 37°C (98.6°F). The nose is unable of conditioning the increased volume of air needed for activity, especially in athletes who breathe through their lips.
Bronchoconstriction occurs within minutes after completing exercise due to aberrant heat and water fluxes in the bronchial tree. Bronchoalveolar lavage investigations have not revealed an increase in inflammatory mediators. In most cases, these individuals have a refractory phase during which a second exercise stimulus does not elicit considerable bronchoconstriction.
Factors that contribute to exercise-induced bronchoconstriction symptoms (in both persons with asthma and athletes) include the following:
- Exposure to cold or dry air
- Environmental pollutants (eg, sulfur, ozone)
- level of bronchial hyperreactivity
- Chronicity of asthma and symptomatic control
- Duration and intensity of exercise
- Allergen exposure in atopic individuals
- Coexisting respiratory infection
Calming the patient to get them to relax, relocating the person outside or away from the likely source of allergen, and cooling the individual are all measures to take. It is occasionally done to remove clothing and wash the face and mouth to eliminate allergies, however this is not supported by research. Environmental management is critical if recurring episodes are to be avoided. Avoiding allergens can dramatically enhance one's quality of life. This includes staying away from cigarettes, dust mites, animals, and pollen.
Obese asthmatics who lose weight have better control. Allergen immunotherapy is still debatable. Large-scale trials have found no substantial effect, and the method is extremely costly. Patients with moderate to severe asthma who have a positive skin test should get monoclonal antibody treatment. The medication can reduce IgE levels, which reduces histamine production. However, the injections are expensive.
Bronchial thermoplasty is a relatively recent procedure for delivering heat energy to the airway wall and reducing airway constriction. Several studies have shown that it can minimize emergency room visits and school days lost.
Bronchodilators such as beta-2 agonists and muscarinic antagonists (salbutamol and ipratropium bromide, respectively) and anti-inflammatories such as inhaled steroids are used in medical therapy (usually beclometasone but steroids via any route will be helpful).
Chronic asthma management consists of five phases; therapy is initiated based on severity and subsequently escalated or de-escalated based on response to treatment.
- Step 1: As needed, a low dosage inhaled corticosteroid and formoterol are used as a controller.
- Step 2: The recommended controls are daily low-dose inhaled corticosteroids combined with short-acting beta 2 agonists as required.
- Step 3: Low-dose inhaled corticosteroids and long-acting beta 2 agonists, as well as as-needed short-acting beta 2 agonists, are the recommended controllers.
- Step 4: The preferred controller is a medium-dose inhaled corticosteroid and long-acting beta 2 agonist, with short-acting beta 2 agonists used as needed.
- Step 5: Inhaled corticosteroid at a high dosage and a long-acting beta 2 agonist, as well as a long-acting muscarinic antagonist/anti-IgE.
Indications for admission
If a patient has had three doses of an inhaled bronchodilator and still does not respond, the following variables should be considered while admitting the patient:
- The severity of airflow obstruction
- Duration of asthma
- Response to medications
- Adequacy of home support
- Any mental illness
High flow oxygen inhalation, systemic steroids, back-to-back nebulizations with short-acting beta 2 agonists and short-acting muscarinic antagonists, and intravenous magnesium sulfate are used to treat patients with life-threatening asthma. The early engagement of the intensive care team consultation aids in the reduction of mortality. Early intubation and mechanical breathing are required in cases with near-fatal asthma.
There is no surgical input into the management of typical asthma.
Weight loss, smoking cessation, occupational change, and self-monitoring are all important in preventing disease progression and reducing the number of acute attacks.
An anaphylactic response is the key differentiator for a life-threatening asthma episode. The patient may also exhibit orofacial edema, a rash, and itching in this scenario. Salbutamol and steroids will have a limited effect on the patient, but injectable adrenaline is the life-saving drug required to handle these individuals.
Other possible diagnoses include voice cord dysfunction, tracheal or bronchial blockage caused by a foreign substance or tumor, heart failure, gastric reflux, chronic sinusitis, and chronic obstructive pulmonary disease.
Chronic asthma is usually classified as follows:
- Mild persistent
- Moderate persistent
- Severe persistent
Acute asthma is classified as below:
- Acute severe asthma
- Life-threatening asthma
- Near-fatal asthma
Asthma mortality has been found to be as high as 0.86 fatalities per 100,000 people in various countries. Asthma mortality rates in the United States were reported to be one per 100,000 people in 2009. Death is mostly connected to lung function, with an 8-fold increase in patients in the lowest quartile, although asthma treatment failure has also been associated to mortality, particularly in young people.
Other risk factors for death include being over 40 years old, smoking more than 20 pack-years, having blood eosinophilia, having a forced expiratory volume in one second (FEV1) of 40-69 percent anticipated, and being more reversible.
Asthma is estimated to cause 100 million days of limited activity at work and in school. Asthma causes approximately 500,000 hospitalizations every year. Every year, an estimated 1.7 million people (47.8 percent of whom are under the age of 18) require emergency room treatment. The yearly expenses for health and lost productivity due to asthma were estimated to reach $20.7 billion in 2010.
By late adolescence or early adulthood, about half of children with asthma will have reduced symptoms and require less therapy. In a trial of 900 children with asthma, 6% required no therapy after a year, while 39% required only sporadic treatment.
Long-term alterations occur in patients with poorly managed asthma (i.e., with airway remodeling). This can result in persistent symptoms as well as a strong irreversible component to their condition. Many people who develop asthma at a later age have persistent symptoms.
Asthma kills one out of every 100,000 people in numerous nations, including the United States. The lower the lung function, the greater the risk of death. Furthermore, mortality has been linked to poor treatment and a lack of drug adherence, particularly in young people. Smoking and the use of illegal substances are two more variables that enhance the chance of mortality.
According to a systematic literature review by Coffman et al, school-based asthma education programs improved knowledge of asthma, self-efficacy, and self-management behaviors in children aged 4-17 years, but the programs had less effect on quality of life, days of symptoms, nights with symptoms, and school absences.
Asthma also causes millions of school and workdays to be missed. Close to 2 million asthmatics require frequent care in the emergency room in the United States alone, which raises healthcare expenses.
Despite the fact that asthma is a curable condition, poor lifestyle choices and a lack of care can result in airway remodeling, which leads to persistent symptoms that are burdensome. Because there is no treatment for the illness, it must be monitored for the rest of one's life. An interdisciplinary approach is recommended for the greatest results.