Asthma is a disease of diffuse airway inflammation caused by a variety of triggering stimuli resulting in partially or completely reversible bronchoconstriction. Symptoms and signs include dyspnea, chest tightness, cough, and wheezing. The diagnosis is based on history, physical examination, and pulmonary function tests. Treatment involves controlling triggering factors and drug therapy, most commonly with inhaled beta-2 agonists and inhaled corticosteroids. Prognosis is good with treatment. Show More than 25 million people in the US are affected. Asthma is one of the most common chronic diseases of childhood, affecting about 6 million children in the US. It also occurs more frequently in non-Hispanic Blacks and Puerto Ricans.
Development of asthma is multifactorial and depends on the interactions among multiple susceptibility genes and environmental factors. More than 100 asthma susceptibility genes have been reported. Many are thought to involve the broad category of T-helper cells type 2 (TH2) and may play a role in inflammation. Examples include the FCER1B gene, which encodes the beta chain of the high-affinity IgE receptor; the genes encoding certain interleukins (IL) such as IL-4, IL-13, and the IL-4 receptor; genes responsible for innate immunity (HLA-DRB1, HLA-DQB1, CD14); and genes participating in cellular inflammation (eg, genes encoding granulocyte-monocyte colony-stimulating factor [GM-CSF] and tumor necrosis factor-alpha [TNF-α]). Also, the ADAM33 gene may stimulate airway smooth muscle and fibroblast proliferation and remodeling; it was the first asthma risk locus found with whole-genome family linkage studies. More recently, the most replicated is at the chromosome 17q21 locus. This locus contains the ORMDL3 gene, which is an allergen and cytokine (IL-4/IL-13)–inducible gene implicated in epithelial cell remodeling and sphingolipid metabolism to affect bronchial hyperreactivity. Environmental risk factors for asthma may include the following:
Evidence clearly implicates household allergens (eg, dust mite, cockroach, pet) and other environmental allergens in disease development in older children and adults. Diets low in vitamins C and E and in omega–3 fatty acids have been linked to asthma; however, several studies supporting dietary influence are limited by sample size or did not account for differences in socioeconomic, environmental, and demographic factors. Dietary supplementation with these substances does not appear to prevent asthma. Asthma has also been linked to perinatal factors, such as young maternal age, poor maternal nutrition, prematurity, low birthweight, and lack of breastfeeding. On the other hand, endotoxin exposure early in life can induce tolerance and may be protective. Air pollution is not definitively linked to disease development, although it may trigger exacerbations. The role of childhood exposure to cigarette smoke is controversial, with some studies finding a contributory and some a protective effect. Genetic and environmental components may interact. Infants may be born with a predisposition toward proallergic and proinflammatory type 2 (T2) immune responses(immune responses related to T-helper 2 cells). The proinflammatory T2 response is characterized by growth and activation of eosinophils and IgE production. Asthma with this pattern of inflammation has often been referred to as eosinophilic asthma. Early childhood exposure to bacterial and viral infections and endotoxins may shift the body to T-helper cells type 1 (TH1) responses, which suppresses TH2 cells and induce tolerance. Type 1 (T1) responses are characterized by a proliferation of type 1 T-helper cells. Trends toward smaller families with fewer children, cleaner indoor environments, and early use of vaccinations and antibiotics may deprive children of these T2-suppressing, tolerance-inducing exposures and may partly explain the continuous increase in asthma prevalence in higher income countries (the hygiene hypothesis).
Numerous substances have been implicated, including chlorine gas, nitrogen oxide, and volatile organic compounds (eg, from paints, solvents, adhesives). The exposure event is usually obvious to the patient, particularly when symptoms begin almost immediately. Irritant-induced asthma refers to a similar, persistent asthma-like response following multiple or chronic inhalational exposure to high levels of similar irritants. Manifestations are sometimes more insidious, and thus the connection to the inhalational exposure is clear only in retrospect. RADS and chronic irritant-induced asthma have many clinical similarities to asthma (eg, wheezing, dyspnea, cough, presence of airflow limitation, bronchial hyperresponsiveness) and respond significantly to bronchodilators and often corticosteroids. Unlike in asthma, the reaction to the inhaled substance is not thought to be an IgE-mediated allergy; low-level exposures do not cause RADS or irritant-induced asthma. However, repeated exposure to the initiating agent may trigger additional symptoms. Asthma involves
In patients with asthma, TH2 cells and other cell types—notably, eosinophils and mast cells, but also other CD4+ subtypes and neutrophils—form an extensive inflammatory infiltrate in the airway epithelium and smooth muscle, leading to airway remodeling (ie, desquamation, subepithelial fibrosis, angiogenesis, smooth muscle hypertrophy). Hypertrophy of smooth muscle narrows the airways and increases reactivity to allergens, infections, irritants, parasympathetic stimulation (which causes release of proinflammatory neuropeptides, such as substance P, neurokinin A, and calcitonin gene-related peptide), and other triggers of bronchoconstriction. Additional contributors to airway hyperreactivity include loss of inhibitors of bronchoconstriction (epithelium-derived relaxing factor, prostaglandin E2) and loss of other substances called endopeptidases that metabolize endogenous bronchoconstrictors. Mucus plugging and peripheral blood eosinophilia are additional classic findings in asthma and may be epiphenomena of airway inflammation. However, not all patients with asthma have eosinophilia. Common triggers of an asthma exacerbation include
Infectious triggers in young children include respiratory syncytial virus Respiratory Syncytial Virus (RSV) and Human Metapneumovirus Infections Respiratory syncytial virus and human metapneumovirus infections cause seasonal lower respiratory tract disease, particularly in infants and young children. Disease may be asymptomatic, mild... read more , rhinovirus, and parainfluenza virus infection. In older children and adults, upper respiratory infections (particularly with rhinovirus) and pneumonia are common infectious triggers. Exercise can be a trigger, especially in cold or dry environments, and cold air alone can also trigger symptoms. Inhaled irritants, such as air pollution, cigarette smoke, perfumes, and cleaning products can also trigger symptoms in patients with asthma. (Inhaled irritants that trigger asthma exacerbations do so by inducing a T2 response, in contrast to what happens in reactive airways dysfunction syndrome and chronic irritant-induced asthma.) Emotions such as anxiety, anger, and excitement sometimes trigger exacerbations. Aspirin is a trigger in up to 30% of patients with severe asthma and in < 10% of all patients with asthma. Aspirin-sensitive asthma is typically accompanied by nasal polyps with nasal and sinus congestion, which is a condition also known as Samter's triad (asthma, nasal polyps, and sensitivity to aspirin and NSAIDs). GERD is a common trigger among some patients with asthma, possibly via esophageal acid-induced reflex bronchoconstriction or by microaspiration of acid. However, treatment of asymptomatic GERD (eg, with proton pump inhibitors) does not seem to improve asthma control. Allergic rhinitis often coexists with asthma; it is unclear whether the two are different manifestations of the same allergic process or whether rhinitis is a discrete asthma trigger. In the presence of triggers, there is reversible airway narrowing and uneven lung ventilation. In lung regions distal to narrowed airways, relative perfusion exceeds relative ventilation; thus, alveolar oxygen tensions fall and alveolar carbon dioxide tensions rise. Usually, such regional hypoxia and hypercarbia trigger compensatory pulmonary vasoconstriction to match regional ventilation and perfusion; however, these compensatory mechanisms fail during an asthma exacerbation due to the vasodilatory effects of prostaglandins that are upregulated during an exacerbation. Most patients can compensate by hyperventilating, but in severe exacerbations, diffuse bronchoconstriction causes severe gas trapping, and the respiratory muscles are put at a marked mechanical disadvantage so that the work of breathing increases. Under these conditions, hypoxemia worsens and PaCO2 rises. Respiratory acidosis Respiratory Acidosis Respiratory acidosis is primary increase in carbon dioxide partial pressure (Pco2) with or without compensatory increase in bicarbonate (HCO3−); pH is usually low but may be near... read more and metabolic acidosis Metabolic Acidosis Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly... read more may result and, if left untreated, cause respiratory and cardiac arrest. Unlike hypertension (eg, in which one parameter [blood pressure] defines the severity of the disorder and the efficacy of treatment), asthma causes a number of clinical and testing abnormalities. Also, unlike most types of hypertension, asthma manifestations typically wax and wane. Thus, monitoring (and studying) asthma requires a consistent terminology and defined benchmarks. The term status asthmaticus describes severe, intense, prolonged bronchospasm that is resistant to treatment. Severity is the intrinsic intensity of the disease process (ie, how bad it is—see table
Classification of Asthma Severity
Classification of Asthma Severity*
It is important to remember that the severity category does not predict how serious an exacerbation a patient may have. For example, a patient who has mild asthma with long periods of no or mild symptoms and normal pulmonary function may have a severe, life-threatening exacerbation.  Control is the degree to which symptoms, impairments, and risks are minimized by treatment. Control is the parameter assessed in patients receiving treatment. The goal is for all patients to have well-controlled asthma regardless of disease severity. Control is classified as
Impairment refers to the frequency and intensity of patients' symptoms and functional limitations (see table
Classification of Asthma Severity
Classification of Asthma Severity*
Risk refers to the likelihood of future exacerbations or decline in lung function and the risk of adverse drug effects. Risk is assessed by long-term trends in spirometry and clinical features such as
Symptoms and Signs of AsthmaPatients with mild asthma are typically asymptomatic between exacerbations. Patients with more severe disease and those with exacerbations experience dyspnea, chest tightness, audible wheezing, and coughing. Coughing may be the only symptom in some patients (cough-variant asthma). Symptoms can follow a circadian rhythm and worsen during sleep, often around 4 AM. Many patients with more severe disease waken during the night (nocturnal asthma). Signs include wheezing,
pulsus paradoxus
Pulsus paradoxus Complete examination of all systems is essential to detect peripheral and systemic effects of cardiac disorders and evidence of noncardiac disorders that might affect the heart. Examination... read more
Symptoms and signs disappear between exacerbations, although soft wheezes may be audible during forced expiration at rest, or after exercise, in some asymptomatic patients. Hyperinflation of the lungs may alter the chest wall in patients with long-standing uncontrolled asthma, causing a barrel-shaped thorax. All symptoms and signs are nonspecific, are reversible with timely treatment, and typically are brought on by exposure to one or more triggers.
Diagnosis is
based on history and physical examination and is confirmed with pulmonary function tests. Diagnosis of causes and the exclusion of other disorders that cause wheezing are important. Asthma and
chronic obstructive pulmonary disease
Chronic Obstructive Pulmonary Disease (COPD) Chronic obstructive pulmonary disease (COPD) is airflow limitation caused by an inflammatory response to inhaled toxins, often cigarette smoke. Alpha-1 antitrypsin deficiency and various occupational... read more
Asthma-COPD overlap (ACO) is being increasingly recognized as a unique entity that presents with persistent airflow obstruction and several features of both asthma and COPD. Key features include fixed airway obstruction not responsive to bronchodilators, significant exposure to tobacco smoking or pollutants, and traditional asthma features, including blood or sputum eosinophilia and reversible airflow obstruction. ACO represents an important subset of patients with asthma (15 to 35%) and COPD (10 to 40%) that might respond to drugs not typically indicated for the disorder corresponding to the patient's main diagnosis (eg, prescribing roflimulast/azithromycin in an patient diagnosed with asthma or T2 biologic therapies in a patient diagnosed with COPD. Asthma that is difficult to control or refractory to commonly used controller therapies should be further evaluated for alternative causes of episodic wheezing, cough, and dyspnea such as
allergic bronchopulmonary aspergillosis
Allergic Bronchopulmonary Aspergillosis (ABPA) Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity reaction to Aspergillus species (generally A. fumigatus) that occurs almost exclusively in patients with asthma... read more
Provocative testing, in which inhaled methacholine (or alternatives, such as inhaled histamine, adenosine, or bradykinin, or exercise testing) is used to provoke bronchoconstriction, is indicated for patients suspected of having asthma who have normal findings on spirometry and flow-volume testing and for patients suspected of having cough-variant asthma, provided there are no contraindications. Contraindications include FEV1 1 L or < 50% predicted, recent myocardial infarction or stroke, and severe hypertension (systolic BP > 200 mm Hg; diastolic BP > 100 mm Hg). A decline in FEV1 of > 20% on a provocative testing protocol is relatively specific for the diagnosis of asthma. However, FEV1 may decline in response to drugs used in provocative testing in other disorders, such as COPD. If FEV1 decreases by < 20% by the end of the testing protocol, asthma is less likely to be present. Other tests may be helpful in some circumstances:
DLCO testing can help distinguish asthma from COPD. Values are normal or elevated in asthma and usually reduced in COPD, particularly in patients with emphysema. Sputum evaluation for eosinophils is not commonly done; finding large numbers of eosinophils is suggestive of asthma but is neither sensitive nor specific. Peak expiratory flow (PEF) measurements with inexpensive handheld flow meters are recommended for home monitoring of disease severity and for guiding therapy. Patients with asthma with an acute exacerbation are evaluated based on clinical criteria but should sometimes also have certain tests:
The decision to treat an exacerbation is based primarily on an assessment of signs and symptoms. PEF measures can help establish the severity of an exacerbation but are most commonly used to monitor response to treatment in outpatients. PEF values are interpreted in light of the patient’s personal best, which may vary widely among patients who are equally well controlled. A 15 to 20% reduction from this baseline indicates a significant exacerbation. When baseline values are not known, the percent predicted PEF based on age, height, and sex may be used, but this is less accurate than a comparison to patient's personal best. Although spirometry (eg, FEV1) more accurately reflects airflow than PEF, it is impractical in most urgent outpatient and emergency department settings. It may be used for office-based monitoring of treatment or when objective measures are required (eg, when an exacerbation appears to be more severe than perceived by the patient or is not recognized).
Asthma resolves in many children, but for as many as 1 in 4, wheezing persists into adulthood or relapse occurs in later years. Female sex, smoking, earlier age of onset, and sensitization to household dust mites, are risk factors for persistence and relapse. Although a significant number of deaths each year are attributable to asthma, most of these deaths are preventable with treatment. Thus, the prognosis is good with adequate access and adherence to treatment. Risk factors for death include increasing requirements for oral corticosteroids before hospitalization, previous hospitalization for acute exacerbations, and lower peak expiratory flow values at presentation. Several studies show that use of inhaled corticosteroids decreases hospital admission and mortality rates. Over time, the airways in some patients with asthma undergo permanent structural changes (remodeling) and develop to baseline airflow obstruction that is not completely reversible. Early aggressive use of anti-inflammatory drugs may help prevent this remodeling.
Treatment objectives are to minimize impairment and risk, including preventing exacerbations and minimizing chronic symptoms, including nocturnal awakenings; to minimize the need for emergency department visits or hospitalizations; to maintain baseline (normal) pulmonary function and activity levels; and to avoid adverse treatment effects. Triggering factors in some patients may be controlled with use of synthetic fiber pillows and impermeable mattress covers and frequent washing of bed sheets, pillowcases, and blankets in hot water. Ideally, upholstered furniture, soft toys, carpets, curtains, and pets should be removed, at least from the bedroom, to reduce dust mites and animal dander. Dehumidifiers should be used in basements and in other poorly aerated, damp rooms to reduce mold. Steam treatment of homes diminishes dust mite allergens. House cleaning and extermination to eliminate cockroach exposure are especially important. Although control of triggering factors is more difficult in urban environments, the importance of these measures is not diminished. High-efficiency particulate air (HEPA) vacuums and filters may relieve symptoms, but no beneficial effects on pulmonary function and on the need for drugs have been observed. Sulfite-sensitive patients should avoid sulfite-containing food (eg, certain wine and salad dressings). Nonallergenic triggers, such as cigarette smoke, strong odors, irritant fumes, cold temperatures, and high humidity should also be avoided or controlled when possible. Limiting exposure to people with viral upper
respiratory infections is also important. However, exercise-induced asthma is not treated with exercise avoidance because exercise is important for health reasons. Instead, a short-acting bronchodilator is given prophylactically before exercise and as needed during or after exercise (rescue inhaler); controller therapy (step 2 and above in Table
Steps of Asthma Management
Steps of Asthma Management* Patients with aspirin-sensitive asthma can use acetaminophen, choline magnesium salicylate, or highly selective NSAIDs like celecoxib when they need a pain reliever. Asthma is a relative contraindication to the use of nonselective beta-blockers (eg, propranolol, timolol, carvedilol, nadolol, sotalol), including topical formulations, but cardioselective drugs (eg, metoprolol, atenolol) probably have no adverse effects. Major drug classes commonly used in the treatment of asthma and asthma exacerbations include Bronchial thermoplasty is a bronchoscopic technique in which heat is applied through a device that transfers localized controlled radiofrequency waves to the airways. The heat decreases the amount of airway smooth muscle remodeling (and thus the smooth muscle mass) that occurs with asthma. In clinical trials in patients with severe asthma not controlled with multiple therapies, there have been modest decreases in exacerbation frequency and improvement in asthma symptom control. However, some patients have experienced an immediate worsening of symptoms, sometimes requiring hospitalization immediately after the procedure. Expert recommendations are to avoid bronchial thermoplasty unless a patient places a low value on the potential for adverse outcomes and a high value on short-term potential benefits. If possible, bronchial thermoplasty should be done in centers where it is done routinely(1 Treatment reference Asthma is a disease of diffuse airway inflammation caused by a variety of triggering stimuli resulting in partially or completely reversible bronchoconstriction. Symptoms and signs include dyspnea... read more ). Criteria for consideration of bronchial thermoplasty include severe asthma not controlled with inhaled corticosteroids and long-acting beta agonists, intermittent or continuous use of oral corticosteroids, FEV1 ≥ 50% of predicted, and no history of life-threatening exacerbations. Patients should understand the risk of post-procedure asthma exacerbation and need for hospitalization before proceeding with the procedure. The long-term efficacy and safety of bronchial thermoplasty is not known. There are no data in patients with > 3 exacerbations per year or an FEV1 < 50% of predicted because these patients were excluded from the clinical trials. Guidelines recommend office use of spirometry (FEV1, FEV1/FVC, FVC) to measure airflow limitation and assess impairment and risk. Spirometry should be repeated at least every 1 to 2 years in patients with asthma to monitor disease progression, and a step-up in therapy might be required if lung function declines or becomes impaired with evidence of increased airflow obstruction (see table
Classification of Asthma Control
Classification of Asthma Control*,† The importance of patient education cannot be overemphasized. Patients do better when they know more about asthma—what triggers an exacerbation, what drug to use when, proper inhaler technique, how to use a spacer with a metered-dose inhaler (MDI), and the importance of early use of corticosteroids in exacerbations. Every patient should have a written action plan for day-to-day management, especially for management of acute exacerbations, that is based on the patient’s best personal peak flow rather than on a predicted normal value. Such a plan leads to much better asthma control, largely attributable to improved adherence to therapies. The goal of asthma exacerbation treatment is to relieve symptoms and return patients to their best lung function. Treatment includes
Current asthma guidelines recommend treatment based on the severity classification. Continuing therapy is based on assessment of control (see
table Classification of Asthma Control
Classification of Asthma Control*,† Exercise-induced asthma can generally be prevented by prophylactic inhalation of a short-acting beta-2 agonist or mast cell stabilizer before starting the exercise. If beta-2 agonists are not effective or if exercise-induced asthma causes symptoms daily or more frequently, the patient requires controller therapy. The primary treatment for aspirin-sensitive asthma is avoidance of aspirin and other NSAIDs. Celecoxib does not appear to be a trigger. Leukotriene modifiers can blunt the response to NSAIDs. Alternatively, desensitization can be done in either the inpatient or outpatient clinic setting depending on the severity of aspirin sensitivity and asthma severity; desensitization has been successful in the majority of patients who are able to continue desensitization treatment for more than one year. Multiple therapies are being developed to target specific components of the inflammatory cascade. Therapies directed at interleukin 6 (IL-6), thymic stromal lymphopoietin, tumor necrosis factor-alpha, other chemokines, and cytokines or their receptors are all under investigation or consideration as therapeutic targets. Children > 5 years and adolescents with asthma can be treated similarly to adults except that long-acting
muscarinic antagonists are not recommended. Also, zileuton should only be used in children ≥ 12 years. Children > 5 years of age and adolescents with asthma should be encouraged to maintain physical activities, exercise, and sports participation. Predicted norms for pulmonary function tests in adolescents are closer to childhood (not adult) standards. Adolescents and mature younger children should participate in developing their own asthma management plans and establishing their
own goals for therapy to improve adherence. The action plan should be understood by teachers and school nurses to ensure reliable and prompt access to rescue drugs. Cromolyn and nedocromil are often tried in this group but are not as beneficial as inhaled corticosteroids. Long-acting drugs prevent the problems (eg, inconvenience, embarrassment) of having to take drugs at school. Asthma drugs have not been
shown to have adverse fetal effects, but safety data are lacking. (See also guidelines from the National Asthma Education and Prevention Program, Managing Asthma During Pregnancy: Recommendations for Pharmacologic Treatment–Update 2004.) In general, uncontrolled asthma is more of a risk to mother and fetus than adverse effects due to asthma drugs. During pregnancy, normal blood PCO2
level is about 32 mm Hg. Therefore, carbon dioxide retention is probably occurring if PCO2 approaches 40 mm Hg.
The following are some English-language resources that may be useful. Please note that THE MANUAL is not responsible for the content of these resources. Click here for Patient Education What tests are used to diagnose asthma?Spirometry. This is the main test doctors generally use to diagnose asthma in people 5 years or older. To help determine how well your lungs are working (pulmonary function), you take a deep breath and forcefully breathe out (exhale) into a tube connected to a spirometer.
What assessments should be performed for a patient with asthma?Assessment of a patient with asthma includes the following:. Assess the patient's respiratory status by monitoring the severity of the symptoms.. Assess for breath sounds.. Assess the patient's peak flow.. Assess the level of oxygen saturation through the pulse oximeter.. Monitor the patient's vital signs.. What is the response of asthma?During an asthma attack, also called an asthma exacerbation, the airways become swollen and inflamed. The muscles around the airways contract and the airways produce extra mucus, causing the breathing (bronchial) tubes to narrow. During an attack, you may cough, wheeze and have trouble breathing.
What labs are important for asthma attacks?They are very important tests to help diagnose asthma and to monitor it.. Spirometry test. ... . Lung volume test. ... . Gas transfer test. ... . Bronchial challenge tests. ... . Asthma control questions. ... . Hyperventilation questionnaire. ... . Depression and anxiety questionnaires. ... . Chest X-ray.. |
Which test result identifies that a patient with asthma is responding to treatment?
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