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ABOUT THIS COURSE
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Wild Iris Medical Education is an approved provider of continuing education by the American Occupational Therapy Association (AOTA), Provider #3313. Courses are accepted by the NBCOT Certificate Renewal program.
LEARNING LEVEL: Intermediate
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Domain of OT: Client Factors
OT Process: Evaluation
Professional Issues: Outcomes
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COURSE OBJECTIVE: The purpose of this course is to present an up-to-date discussion of asthma, including its prevalence, pathophysiology, medical evaluation, acute treatment and long-term management, medications, and special populations.
Upon completion of this course, you will be able to:
Asthma is one of the obstructive lung diseases—a class of problems, such as emphysema, that cause difficulty with the mechanics of breathing. The symptoms of asthma come in episodes, or attacks, in which patients cannot get enough air. These episodes occur most often at night or early in the morning. Symptoms may be persistent, daily, and unrelenting. Asthma is a common disorder. It runs in families, and people who have asthma often have allergies too, such as hay fever (Kolski, 2008).
Asthma is sometimes called hyper-reactive airway disease because the airways of an asthmatic patient constrict more easily than normal to a wide variety of stimuli. The trigger stimuli vary from person to person, but common triggers include allergens, smoke, strong odors, viral respiratory infections, seasonal changes, exercise, and emotional stress. An attack of asthma gives a person chest tightness and leaves them breathless, wheezing, and coughing (ALA, 2011c; AAAAI, 2011). Most asthma attacks can be reversed by inhaling a bronchodilator medication (ALA, 2011a).
The clinical definitions of asthma stress four features of the condition:
Inflammation is the central problem in asthma, and the long-term management of the disease has two separate components:
Asthma is a common condition, and the prevalence of asthma is similar throughout the industrialized world, with populations in countries such as Canada, England, Australia, Germany, and New Zealand having asthma rates of 2% to 10% (Morris, 2011). In the United States, asthma affects more than 24 million people, or roughly 1 in 12 Americans. The overall prevalence of asthma in this country has increased by 12.3% over the last decade (CDC, 2011b; McCook, 2011; Morris, 2011). The prevalence varies from region to region across the country, from a low in Louisiana, where 6.3% of the population has asthma, to a high in Oregon, where 11% of the population has the disease (ALA, 2011b; CDC, 2010).
Asthma is a costly disease for society. Each year, asthma leads to 1.75 million emergency department (ED) visits, nearly a half million hospitalizations, and 13.9 million visits to private physician offices in the United States. Fortunately, deaths from asthma are uncommon. In the United States, approximately 3,400 people die directly from asthma each year—about the same number of deaths as are caused by accidental drowning (Akinbami et al., 2011; CDC, 2011a).
More adult women than men have asthma. In the United States, 9.7% of women aged 18 and older have asthma, while 5.5% of men have the disease. In childhood, however, the distribution of the disease is reversed: 11.3% of boys (ages 0–17 years) have asthma, while 7.9% of girls under 18 years old have the disease (ALA, 2011b).
Two factors lead to this disparity between the prevalence in children and the prevalence in adults.
All races and ethnicities can develop asthma. In the United States, Puerto Ricans have a higher frequency of asthma than other Hispanic groups and also a higher frequency than whites or African Americans. African Americans have a higher prevalence of asthma than whites, and morbidity and mortality rates are higher among those African Americans who have asthma than among whites with asthma (Akinbami et al., 2011).
The latest CDC data (2009) for current asthma prevalence estimated 8.2% of people (24.6 million) currently had asthma. Rates decreased with age: 9.6% of children (7.1 million) had asthma compared to 7.7% of adults (17.5 million). When race/ethnicity is considered, Puerto Ricans had a current asthma prevalence rate of 16.6%, twice that of non-Hispanic white people (8.2%) and nearly 50% higher than that of non-Hispanic black people (11.1%). When only race is considered, African Americans had a 35% higher prevalence than whites (11.1% vs. 8.2%), while the prevalence among Native Americans/Alaska Natives was only slightly higher (8.8%) than that among whites.
To a certain extent, these racial and ethnic disparities can be attributed to socioeconomic factors. The CDC data document a higher prevalence of asthma in persons with a family income below the federal poverty level as compared to those classified as “near poor” (family income 100% to less than 200% of the federal poverty level) and “not poor” (at or above 200% of the poverty level). The “near poor” also have a higher prevalence than the “not poor.” Additionally, non-Hispanic blacks have relatively low rates of ambulatory healthcare visits compared with their use of urgent care visits, which may indicate underuse or lower access to preventive services (Akinbami, 2011).
Asthma is first diagnosed in people of all ages, although two thirds of asthma cases will have been diagnosed by the time patients are 18 years old (Morris, 2011). In approximately half of the children diagnosed with asthma, the disease symptoms fade or disappear by the time they become adults (Martin et al., 1980).
In the United States, asthma is one of the most common chronic illnesses of childhood, and it is the third most common cause of hospitalization for children (ALA, 2010b). The prevalence of childhood asthma has increased during the last three decades, and this increase was most dramatic among inner-city and African American children. The increasing commonness of asthma correlates with increases in other atopic diseases (i.e., those characterized by a hereditary predisposition toward developing certain hypersensitivity reactions, such as hay fever, atopic dermatitis [i.e., eczema] or chronic urticaria [hives], upon exposure to specific antigens) and food allergies (Barnes, 2008; Kolski, 2008).
During adolescence, many asthmatic children become asymptomatic. However, the disease can return in adulthood, especially in patients whose childhood asthma was severe. In contrast, most adults with asthma remain symptomatic throughout their lives (Barnes, 2008).
Asthma is an obstructive disease. Asthma patients have airway walls that easily become inflamed when exposed to a host of common irritants, and asthma causes breathing difficulty because the inflamed airways become swollen and constricted. In addition, the airways are sometimes plugged with mucus.
Most people with asthma were born with hypersensitive immune systems, with those immune cells that are exposed to the external environment tending to overreact. This hyperreactivity can go beyond asthma, and the same patients who develop asthma often have hay fever, food allergies, and eczema.
The two main physiologic processes that operate in asthma are:
Adding to these problems, in some patients the chronic inflammation gradually produces permanent structural changes in the lung, which worsen the breathing difficulty that occurs during episodes of bronchoconstriction.
In infants, additional factors contribute to the development of wheezing. Viral infections can lead to narrowing of the airways (which in small children are already relatively narrow), producing wheezing. Because about 50% of children who wheeze before the age three years will not wheeze after that, the diagnosis of asthma in young children may be difficult. Also, a young child's lungs are more easily obstructed because the lungs are small and have relatively weak support from a still-soft rib cage (Bacharier et al., 2007).
Fundamentally, asthma is an inflammatory disease of the airways. Asthmatic inflammation is distributed throughout the respiratory airways (i.e., the trachea, bronchi, and bronchioles), with the bronchioles being the most heavily involved. Although asthma causes a variety of clinical syndromes—such as intermittent asthma, persistent asthma, and exercise-induced asthma—all forms of asthma are characterized by similar chronic airway inflammation.
Inflammation is a reactive process that is initiated by the immune system and that often produces collateral damage in normal tissues. The particular inflammatory processes of asthma are an atopic reaction (an immune hypersensitivity to external allergens), and asthma is closely related to allergic diseases such as allergic rhinitis (hay fever), eczema, and food allergies. Allergies trigger asthma attacks in 60%–90% of children and in 50% of adults with asthma (Kelly, 2011).
In asthma, the inflammation is chronic, but it only becomes symptomatic with exposure to certain irritants. The problematic irritants can vary from patient to patient. In other words, the inflammation is always present, but the symptomatic episodes (acute exacerbations or asthmatic attacks) make the disease intermittently visible.
At one time, treatments for asthma focused on relieving the bronchoconstriction of acute attacks. With the realization that asthma is a persistent inflammatory disease, long-term management plans for asthma now emphasize reducing airway inflammation. For this reason, all the physiologic players in the asthmatic inflammatory response are being actively investigated in search of potential targets for new medications.
The body’s inflammatory reactions involve a host of cells. In asthma, these include inflammatory cells (lymphocytes, eosinophils, and mast cells) and airway wall cells (epithelial cells and muscle cells). The cellular interactions are mediated by many inflammatory molecules, including leukotrienes, histamine, prostaglandins, cytokines, chemokines, and immunoglobulin E (IgE).
T lymphocytes are white blood cells that recognize and react to antigens. One subspecies of T lymphocyte, the T helper 2 (Th2) cell, is more numerous in the airway walls of people with asthma than in people without the disease. This form of lymphocyte activates antibody responses to antigens and is a key player in allergic reactions, keeping the nearby populations of eosinophils and mast cells active.
People born with atopy (a genetic predilection for developing allergic reactions) have a higher tendency to develop asthma. Atopy correlates with, and may be caused by, an excess of Th2 cells compared to their cousins, the Th1 cells. This imbalance leads to higher levels of IgE in affected people; a higher sensitivity to allergens, viruses, and mitogens; and a predisposition to develop allergies (Bacharier et al., 2007).
Eosinophils are the white blood cells of allergic reactions, and most people with asthma have increased numbers of eosinophils in the walls of their airways. Inhaled irritants activate eosinophils, and when activated, eosinophils release inflammatory molecules such as leukotrienes and pro-inflammatory cytokines, which encourage continued inflammation.
Mast cells are white blood cells that have taken up residence outside blood vessels in tissues near a surface of the body, such as the skin, the airways of the lung, and the walls of the gastrointestinal tract. Both allergens and changes in the extracellular fluid activate mast cells, which then release inflammatory molecules, including histamine, a muscle constrictor.
The epithelial cells that line the inner surfaces of the airway walls act as a barrier that keeps irritants from penetrating the airway walls and causing inflammation. Some airway epithelial cells also secrete enzymes that reduce local inflammation and a hormone (epithelial-derived relaxant factor) that relaxes the constrictor muscles in the airway walls.
Damage to epithelial cells allows irritant allergens to reach and activate mast cells and Th2 cells inside the airway walls. Moreover, when epithelial cells are injured or inflamed, they themselves secrete inflammatory molecules. In people with asthma, injured epithelial cells heal poorly, contributing to the chronically sensitive and inflamed state of their airways.
A layer of smooth (involuntary) muscle cells inside the airway wall surrounds the epithelial tube. The constriction of this muscle during an asthmatic attack narrows the inner diameter of the airways and is the main cause of airflow obstruction.
In a patient with asthma, the smooth muscle in the airways is normal, and the overactive airway constriction that is the hallmark of the disease is not a muscle problem. Instead, the main problem in asthma is the excessive release of inflammatory molecules that constrict muscle.
Inflammatory cells produce most of their effects by secreting specific molecules that either activate (change the behavior of) other cells or chew up nearby cells, molecules, and debris.
Inflammatory cells and molecules interact in a cascade of reactions. The asthma cascade is triggered when inhaled irritants stimulate both mast cells and Th2 lymphocytes in the walls of the airways. These cells then secrete a variety of inflammatory molecules, such as histamine, leukotrienes, and cytokines. Locally, these molecules cause muscle constriction and edema. At a distance, via the bloodstream, the molecules reach the bone marrow, where eosinophils are recruited. As the eosinophils pass through the lung, they are attracted to the inflamed airways, where they stick and begin secreting additional inflammatory molecules.
Meanwhile, in the airway walls, the Th2 cells are interacting with B-lymphocytes. B-lymphocytes generate IgE antibodies, and this sets off the local allergic reactions.
By now, some inflammatory molecules have injured epithelial cells in the vicinity. More irritants can get through the damaged epithelial barrier, and these intrusive substances foment the inflammation. At the same time, when sufficient histamine, leukotrienes, and prostaglandins have been released, the smooth muscle in the airways contracts. This narrows the air passages and produces the clinical result of wheezing, coughing, and difficulty breathing (Barnes, 2008).
Narrowed airways cause the most serious symptom of asthma and dyspnea (difficulty breathing). Typically, the dyspnea of asthma is not a continuous feature of the disease. Instead, dyspnea arises intermittently in the form of sudden attacks.
Dyspnea is a complex phenomenon. Bronchoconstriction is a large contributor, but the airflow obstruction in asthma involves other factors, including swelling (edema) of the airway walls, mucus clogging the airways, and permanent thickening of the airway walls. Smooth muscle contraction, edema, and excess mucus are usually reversible and account for the intermittent airflow obstruction. On the other hand, the thickening of airway walls in response to chronic inflammation is continual and usually permanent.
The major cause of the airflow limitation in asthma is bronchoconstriction. People with asthma have hyper-responsive airways. This means that strong bronchoconstriction can be induced by a wide variety of normally innocuous stimuli. In an asthma attack, IgE recognition of allergens causes local mast cells to release histamine, leukotrienes, and prostaglandins, and these molecules make airway wall muscles contract. The entire process is rapid, so bronchoconstriction can occur quickly.
Besides causing bronchoconstriction, histamine also makes capillaries leaky, allowing fluid into surrounding tissues and leading to edema. The cascade of inflammatory responses to the IgE recognition of allergens causes additional edema and, unlike bronchoconstriction, which happens rapidly, airway edema peaks slowly, 6 to 24 hours after an asthma attack begins. The airway obstruction from edema is called the late asthmatic response.
Over the years, the chronic inflammation of airways leads to increasing secretion of mucus. The mucus of asthma mixes with extracellular proteins and cellular debris and becomes unusually thick, and it can plug small airways and worsen obstruction.
During an asthma attack, the airways of the lung narrow and the movement of air is obstructed. This narrowing is caused by three processes: muscles in the airway walls contract, the airway walls become edematous and swollen, and excess mucus fills the airways. (Source: NHLBI, 2011.)
The exacerbations that characterize asthma are reversible, and administering a bronchodilator medication will relieve the airway constriction of an asthma attack. At the same time, the relentless underlying inflammation of asthma causes permanent changes in the structure of the airways, and over time these changes make asthma attacks less than completely reversible.
The collection of structural changes seen in longstanding asthma is called airway remodeling. Airway remodeling is the body’s natural response to the tissue injury produced by chronic inflammation. Inside the lung of a person with long-standing asthma, the airways appear narrowed, red, and swollen. A microscopic examination shows:
Asthma symptoms vary from person to person, but the structural airway changes are similar in all variants of the disease (Chesnutt et al., 2008).
As with many human diseases, asthma develops in people with a genetic predisposition to the problem. In asthma, this predisposition needs nongenetic activation or “encouragement,” and early exposure to certain external substances appears to determine the extent to which a susceptible person develops the disease (NHLBI, 2007).
Asthma runs in families, and if one identical twin has asthma, the other twin is likely to have it. Observations such as these demonstrate that the tendency to develop asthma is inherited.
An inherited tendency (i.e., certain features of a person’s genome) determines whether exposure to nongenetic and environmental factors can induce asthma. Classical genetic analysis indicates that the genetic predisposition for asthma is polygenic (i.e., pertaining to two or more genes). Currently, more than 100 genes have been identified as potential contributors to asthma susceptibility, and at least ten of these genes are known to be frequently involved. At the moment, however, the interactions of the culprit genes remain complex and unclear (Warrier & Hershey, 2008).
In a person with asthma, substances in the environment can trigger an episode of bronchoconstriction. In addition, it appears that exposure to some of the same substances can initiate the disease. The following is a brief review of some things that may be involved in the initiation of asthma in genetically susceptible people.
Among the T lymphocytes, two variant helper cells, Th1 cells and Th2 cells, are found in different relative concentrations in different people. In some people the circulating population of Th1 cells is greater than the circulating population of Th2 cells, while in other people the balance is reversed. People with asthma tend to be of the second type, with a predominance of Th2 cells.
All newborns have immune systems with a preponderance of Th2 cells, and one theory proposes that an early exposure to infections, which shifts the balance in favor of Th1 cells, is protective and makes the eventual development of asthma less likely. Support for this idea comes from the observation that children who get a variety of infectious diseases or parasites increase their Th1 cell populations and also have less asthma than children who have lived a life sheltered from microbes (Bacharier et al., 2007). It is possible that exposure to certain pet allergens at an early age may have the same protective effect.
This proposal has been called the “hygiene hypothesis,” because, in simple terms, it suggests that if asthma-susceptible children are raised in an environment that is too clean, then they are more likely to develop asthma. (Complicating this hypothesis is the fact that certain early viral infections—e.g., respiratory syncytial virus [RSV] and rhinovirus—appear to increase rather than reduce a child’s risk of developing asthma (Moore, 2008).)
By inhaling, we bring foreign substances into direct contact with our airway walls, where these irritants can provoke inflammation. Because asthma is caused by the chronic inflammation of airway walls, inhaled substances are high on the list of probable initiating causes of asthma.
Most studies have shown that exposure to biological allergens such as cockroaches, dust mites, pets, or mold spores increases a child’s risk of developing asthma, and these substances may have a role in causing asthma; however, the story is not simple, because very early exposure to at least some of these allergens, as stated earlier, has the opposite effect, seeming to protect infants from developing asthma (Moore, 2008).
Air pollutants are related to the development of asthma. In a pregnant woman who smokes, some of the toxic chemicals in tobacco smoke pass through the placenta to her fetus. This may explain why children of mothers who smoke are twice as likely to develop asthma as are children of nonsmokers. Even when their mothers smoked less than 10 cigarettes a day during their pregnancies, children of smokers had a 23% higher chance of developing asthma by age 7 years than children of nonsmokers (Jaakkola & Gissler, 2007).
On the other hand, postnatal exposure to smoke and other air pollution, while common triggers of asthma attacks, do not seem to trigger asthma initially. For example, there is no clear link between the number of cases of asthma and cities with high levels of air pollution (Moore, 2008).
Later in life, occupational exposure to vapors, dust, or smoke will sometimes instigate adult-onset asthma, presumably in people with a genetic predisposition for the disease. Vapors from various sprays, including home cleaning sprays, chemical solvents, dyes, cooling oils, paints, wood preservatives, pesticides, and the specific chemicals toluene, diisocyanate, and trimellitic anhydrate have been identified as probably causes of asthma.
Similarly, people in certain occupations have a higher than normal risk for developing adult-onset asthma. These occupations include mining, forestry, metalworking, painting, waitressing, cleaning, health-related industries, laboratory work, teaching, and dental technicians. For some of these occupations, the increased risk of asthma can be attributed to exposure to harmful substances such as coal dust (as in the mining industry), sulfur compounds and paper dust (as in the forestry industry), irritative chemicals (as in the cleaning industry), or environmental tobacco smoke (as has been documented among waitresses) (McHugh et al., 2010; Jaakkola et al., 2003).
For healthcare workers, reasons for increased asthma risk may include exposure to detergents, disinfectants, latex, formaldehyde, general cleaning products, and aerosolized medications. Teachers may have a higher risk of asthma due to exposure to indoor air pollutants, cleaning products, solvents and hydrocarbons, dusts, mold, and miscellaneous chemicals (McHugh et al., 2010).
A recent study suggests that climate change may contribute to asthma in children. Using regional and atmospheric models of climate change, researchers linked New York State Department of Health climate and air quality information with data on asthma-related ED visits by children in 14 counties that comprise the New York City metropolitan area. The team then simulated ozone levels for the summer months in five consecutive years in the 2020s and compared them with ozone levels in the 1990s. The model showed an overall 7.3% increase in asthma-related ED visits by children up to age 17, with increases in individual counties ranging from 5.2% to 10.2%. The researchers called for stronger efforts to reduce pollution that contributes to climate change and pollution that forms ozone (Sheffield et al., 2011).
Breastfeeding helps to prevent predisposed infants from developing atopic diseases such as eczema, allergies, and asthma (Greer et al., 2008). No other nutritional factors have been demonstrated to either protect against or cause a person to develop asthma. There is, however, some indication that obesity may make the development of asthma more likely (Moore, 2008).
JONAH, AGE 11
Jonah Bachman is an 11-year-old boy whose identical twin brother, Adam, was diagnosed with asthma at age 8. Jonah is brought to the pediatrician’s office by his mother, Laura, who tells the office nurse that Jonah has been experiencing episodes of wheezing and shortness of breath over the last two weeks, during which time there have been several days of high humidity and poor air quality. When asked about Jonah’s medical history as part of the nursing assessment, Laura cannot recall any early respiratory infections, though she notes that he seems to have become more susceptible to colds in recent years. She also reports that she tries to maintain a spotlessly clean home and has been especially vigilant about doing so after spotting a cockroach in the kitchen about a month ago. When asked about her own history, Laura recalls periodic episodes of wheezing and coughing when she was a young girl, but she was never screened for asthma.
The nurse orders a battery of diagnostic tests for Jonah. These tests, which are part of the routine assessment protocol in the office, confirm a diagnosis of asthma.
Once it is acquired, asthma is a disease of episodic bouts of wheezing, coughing, and difficulty breathing. These attacks occur because the airways of asthma patients are hyper-responsive, and things that would cause little or no reaction in normal airways can trigger a strong bronchoconstrictor response.
Typical generic (nonspecific) triggers include air pollution, allergens, volatile chemicals exercise, upper respiratory tract infections, rhinitis, sinusitis, postnasal drip, aspiration, gastroesophageal reflux, changes in the weather, and stress. Some people are also susceptible to more specific chemical triggers, such as aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and tartrazine dyes.
On the other hand, for some asthma patients, the triggers are hard to identify, and their asthma symptoms seem to appear spontaneously.
To control the symptoms of their asthma, individuals should know their triggers (Schatz, 2008). The basic classes of triggers are:
Upper respiratory viruses are the most common triggers of asthma attacks in children, and their asthma adds wheezing, coughing, and shortness of breath to the usual viral symptoms. The culprit microorganisms are usually rhinoviruses (colds), RSV (bronchiolitis [inflammation of the membranes lining the bronchioles] or viral pneumonia), and parainfluenza virus (croup or bronchitis). Because these viruses also damage the airways and temporarily worsen any underlying chronic inflammation, an asthma sufferer can remain prone to asthmatic attacks even after the viral disease has resolved (NHLBI, 2007).
When infants or toddlers develop wheezing with respiratory infections, it does not necessarily mean that they have asthma. In children, wheezing may be due to the small size of their airways.
Asthma attacks are usually set off by things that directly contact the airway linings. Therefore, most triggers are inhaled. These include biological allergens, smoke, air pollution, or chemical vapors.
When a person has been sensitized to an allergen, further exposure activates mast cells, and in asthmatics this allergic reaction will lead to bronchoconstriction. The common seasonal allergens are grass pollens, ragweed, tree pollens, and fungal spores. These cause rhinitis (hay fever) in susceptible individuals, and they can cause an episode of bronchoconstriction in asthmatics.
Other allergens can be perennial. Perennial allergens include dust mites, cockroaches, pets, and mold. In homes that remain damp or have high humidity, mold and dust mites are common. In inner cities, cockroaches and dust mites are quite common, and they are both hard to control (Kolski, 2008).
Air pollutants, including particulates, sulfur dioxide, ozone, and nitrogen oxide, increase the frequency of asthma symptoms; and local traffic and industry bring with them higher rates of asthma attacks. Indoor air pollution, such as tobacco smoke, is especially harmful to children who have a predisposition for developing asthma. Fortunately, indoor air pollution is a trigger that can be avoided; keeping pediatric asthma patients away from environments with tobacco smoke is an important practical way to prevent asthma attacks and other respiratory problems.
Chemical fumes are common asthma triggers. Chemical triggers range from perfumes and chlorine to cleaning solutions and industrial solvents. Avoidance is the best preventive for these triggers, although good ventilation can overcome some of the dangers; for instance, asthmatic children can usually swim in chlorinated pools when the level of chlorine in the air is kept low by efficient ventilation.
Airway constriction is less often set off indirectly, i.e., by substances that do not directly contact the airways. Foods rarely cause asthma symptoms. On the other hand, a few food additives, notably sulfites (preservatives), can be triggers. Although food allergies appear to initiate asthma symptoms, the effect is usually a different and whole-body reaction (anaphylaxis), which can include wheezing.
In contrast to foods, certain medicines will trigger asthma symptoms. Beta-adrenergic blockers can worsen asthma and may even be fatal, and these drugs should not be used by people with asthma; even topical or selective beta-blockers should be avoided. Some patients also find that aspirin or NSAIDs (e.g., ibuprofen) worsen their asthma (Bacharier et al., 2007).
Sudden changes in the temperature or the water content of the air can trigger asthma symptoms. Cold air, extreme temperatures, weather changes, thunderstorms, and high humidity are all potential triggers. Similarly, hyperventilation can initiate asthma symptoms because it causes sudden changes in the volume of air to which the person’s airways are exposed. In the lungs, the actual trigger is the sudden increase in water evaporation from the lining of the airways, which increases the osmolality of the fluid and activates nearby mast cells to release bronchoconstrictor molecules.
Hyperventilation is a characteristic of exercise, and exercise-induced asthma is common, especially in children. Even laughing and crying spells can result in hyperventilation that leads to an asthma attack. Exercise in cold dry weather increases the loss of airway water, and winter sports are more common asthma triggers than are summer sports. Exercise-induced asthma is not an IgE-mediated phenomenon, and the symptoms usually resolve (within about 30 minutes) with rest and breathing warm, lightly humidified air.
Aerobic exercise contributes to good health. Therefore, asthma should be medically controlled so that patients, especially children, can stay active and exercise regularly (Bacharier et al., 2007).
Excesses or deficiencies in thyroid hormone can increase asthma symptoms. Another endocrine change, the fall in progesterone near the end of a woman’s menstrual cycle, sometimes worsens asthma (Haggerty et al., 2003; Shames et al., 1998).
Psychological stresses and strains worsen asthma in many patients (Wisnivesky et al., 2010). Job pressures, family difficulties, anger, rage, anxiety, and depression can make asthma more difficult to keep under control. In children, asthma symptoms can worsen when their parents are under stress (Wolf et al., 2008).
Asthma is a disease of airway inflammation. Most people who have asthma were born with an immune system that is predisposed to develop allergic reactions, and then, for a variety of reasons, these people’s airway walls became sensitized to certain common irritants, leaving their airways continually reacting and inflamed.
Difficulty breathing is the symptom that brings an asthmatic to the doctor. This problem shows up in flares called “exacerbations” or “attacks” that include a spasm of wheezing, coughing, chest tightness, and increased mucus production. Asthma attacks are often brought on by contact with identifiable triggers, such as smoke, cold air, or chemical fumes. Such attacks can be infrequent or almost continuous, and they can be mild or severe enough to require hospitalization.
When a person presents with intermittent attacks of wheezing, coughing, or difficulty breathing, asthma is high on the list of probable diagnoses. These symptoms can, however, be caused by other lung problems, heart problems, or systemic disorders. In children, wheezing is a common symptom with colds, and the pediatric possibilities of similar breathing symptoms include respiratory infections, foreign body aspiration, congenital malformations, and genetic diseases. Moreover, in any age group, sudden difficulty breathing can be an emergency. Therefore, even with a classic history of asthma-like symptoms, patients need a thorough medical evaluation, including a history, a physical examination, and lung function tests (Gordon, 2008).
The pathologic process in asthma is chronic inflammation of hypersensitive airways. The consequences of the common underlying problem can play out somewhat differently in different people, and the clinical appearance of the disease varies. For instance, some asthma sufferers find that their attacks are so easily triggered that the patient is almost continually ill and must spend an inordinate amount of time in the hospital or emergency department. Other patients will have only rare asthmatic attacks, and the episodes will be quickly and completely reversed by inhalation of a bronchodilator.
Given the wide variation in presentation, a detailed history is needed to understand each individual’s particular asthma variant. In their 2007 Guidelines for the Diagnosis and Management of Asthma, the National Heart Lung and Blood Institute’s Expert Panel (NHLBI, 2007) recommends that the history of a patient with asthma include those elements listed in the box below.
MEDICAL HISTORY OF AN ASTHMA PATIENT
Asthma symptoms vary from patient to patient. The symptoms can also change as the patient ages. Nonetheless, many patients have a typical symptom profile, a set of problems that develop with most of their asthma attacks (Chesnutt et al., 2008). Note that, for some patients, an asthma attack will also include a prodrome, a set of feelings that precede the attack. The prodrome can include itching under the skin, an uncomfortable feeling in the upper back between the shoulder blades, or a feeling of dread or impending doom (Barnes, 2008).
Coughing: Coughing is a sign of airway irritation, and asthma attacks often include coughing. In some asthmatics the cough is dry, while in others the cough can be mucus-filled. Cough may be the only symptom of asthma, and there is a debate as to whether people with cough-variant asthma will go on to develop other asthma symptoms later in life. People with cough-variant asthma tend to maintain better control of their disease by using anti-inflammatory medications than by using bronchodilators.
Asthma should be considered in anyone who has a chronic cough, a seasonal cough, or a cough repeatedly brought on by exposure to chemical vapors, cold air, or exercise. Lung function tests and computed tomography (CT) scans can help distinguish cough-variant asthma from other causes of cough.
Wheezing: Wheezing is produced by air being forced through narrowed airways, and in asthma the affected airways are mainly the small bronchioles of the lung. When wheezing is heard with a stethoscope on a routine exam of an asymptomatic person, the chances are 80%–90% that the individual has asthma. If wheezing is not heard, however, the patient may still have asthma.
During an asthma attack, most people with asthma wheeze, but other problems can also bring on wheezing. For example, congestive heart failure can lead to wheezing, accompanied by difficulty breathing and sometimes a cough. A vocal cord spasm or a foreign body trapped in the airways can cause wheezing, difficulty breathing, and a choking feeling.
Wheezing occurs at some time in more than half of all children younger than 6 years. This wheezing is most often caused by a viral respiratory infection and not by asthma. When wheezing is caused by asthma, it is often accompanied by difficulty breathing or by effects on the child’s sleep or normal daily activities. Nonetheless, persistent or episodic wheezing of a young child must be explored, because early intervention can improve the asthma patient’s physical fitness, general health, and quality of life. In addition, other serious diseases, such as cystic fibrosis, must be ruled out.
Certain clues can indicate that a young child has a greater than usual risk of developing asthma by the teenage years, and recurrent wheezing is the most significant. The following table presents the range of risk factors.
|Increased Risk||Medical History|
|Source: Modified from Bacharier et al., 2007.|
|15.0 x||Recurrent wheezing in years 4 to 6|
|4.7 x||Recurrent wheezing in first 3 years|
|3.9 x||Family history of sinusitis|
|3.3 x||Any wheezing episodes in first 3 years|
|2.2 x||Allergic rhinitis (hay fever–type allergies)|
|2.0 x||Family history of asthma|
|1.9 x||Atopic dermatitis (eczema)|
|1.5 x||>2 episodes of otitis media|
Dyspnea: Dyspnea is the feeling of breathlessness, and it comes from a mix of three sensations, all of which contribute to the dyspnea of asthma:
Normally, we use our diaphragm muscles to pull air into our lungs, but we empty our lungs without muscular effort, relying instead on the elastic recoil of our lungs and our chest wall to push the air out. This changes during an asthma attack.
During an asthma attack, the narrowed airways resist the movement of air, and a patient must use chest muscles to force air out of the lungs. The increased pressure this generates pushes on all parts of the lung tissue and collapses some of the airways, leaving air trapped in the lung. The leftover air then takes up space that cannot be filled during the next breath. The result is that during an asthma attack a patient does considerably more work but gets less air exchange.
During an attack, an asthma patient feels the bronchoconstriction—the chest feels tight. The difficulty of breathing, the chest tightness, and the need for more air make patients feel anxious and panicky, and this heightens their sensation of breathlessness.
Dyspnea is a subjective sensation, and people vary in how severely they rate similar degrees of bronchoconstriction. Some asthma patients are “hypoperceivers,” who do not always recognize the severity of their asthma attacks. Approximately one quarter of the people with chronic obstruction from long-term asthma do not consider that they have significant dyspnea, and the number is higher for asthma patients older than 65 years. These observations suggest that clinicians cannot always judge the severity of an asthma attack by questioning the patient about the degree of breathlessness.
Besides being subjective, dyspnea is not a specific symptom for diagnosing asthma. Other lung and heart problems are also characterized by breathlessness. Dyspnea is the chief complaint of most people with chronic obstructive pulmonary disease (COPD), as it can be in other obstructive and inflammatory lung conditions (e.g., pulmonary fibrosis, sarcoidosis). Pulmonary emboli will produce sudden dyspnea, and congestive heart failure is noted for its dyspnea. In addition, patients with dyspnea can have more than one cause simultaneously; smokers, for example, can have both COPD and asthma, and in as many as one third of cases, it may not be possible to decide whether the person has COPD, asthma, or both.
Asthma Can Be a Cause of Chest Pain in Children
In middle-aged and older adults, heart problems must always be considered as the cause of chest pain. In children, however, chest pain usually arises from a noncardiac problem. When children report chest pain, the problem typically originates in the respiratory system or the chest wall, shoulder, or diaphragm. Between 10% and 20% of pediatric chest pain is respiratory, and asthma, especially exercise-induced asthma, is one of the respiratory causes of pediatric chest pain.
As many as 80% of children with asthma have a characteristic set of symptoms when exercising. Brief (1–2 minutes) running is not a problem. However, running for more than 3 minutes causes bronchoconstriction with coughing, wheezing, dyspnea, and chest tightness or pain. This exercise-induced asthma is worsened by cold temperature, air pollution, respiratory infections, or allergens, and it sometimes leads to the complaint of chest pain (Park, 2008).
Excess Airway Mucus: Patients with severe asthma or with asthma that is not well controlled produce enough extra mucus to worsen the obstruction in their airways. The mucus produced in asthma is thicker and stickier than normal. Asthmatic mucus is more likely to form plugs in the airways, and patients find it more difficult to clear their lungs by coughing.
Sleep Disturbances: More than two thirds of people with asthma have sleep disturbances that lead to excess sleepiness during the day. Even when their asthma is well controlled, as many as 20% of patients may experience sleep disturbances. Although they are a nonspecific symptom, sleep disturbances should be recognized, because when they are not treated they decrease a patient’s quality of life (Mastronarde et al., 2008; Braido et al., 2008).
Additional Symptoms in Children
For children younger than 2 years of age, in addition to difficulty breathing, airway obstruction can produce noisy breathing, vomiting with cough, chest retractions when breathing, difficulty feeding, or changes in the rate of breathing. For children older than 2 years, airway obstruction can cause shortness of breath, easy fatigability, complaints of feeling ill, poor school performance, and avoidance of normal activities such as playing outside or visiting friends.
Although asthma is described as a disease with episodic attacks, the pattern of clinical symptoms varies from person to person. In the medical history, the symptom pattern of the individual should be described, noting these features:
One way to collect this information is via standardized questionnaires such as the one that follows.
SCREENING QUESTIONS FOR POTENTIAL ASTHMA SUFFERERS
The NHLBI Expert Panel report of 2007 offers this set of questions as a screening for people who might have asthma. A “yes” answer to any question suggests that an asthma diagnosis is likely.
In the past 12 months …
In the past 4 weeks, have you had coughing, wheezing, or shortness of breath …
Source: NHLBI, 2007.
Asthma symptoms are often set off by identifiable factors, such as mold, viral infections, or smoke. Avoiding or reducing these triggers is a key to managing a patient’s disease. Triggers vary from patient to patient, and the medical history should list the person’s known and probable triggers. After asking patients for a list, the interviewer should give them a checklist to further jog their memory (see box). Patients should also be asked whether asthma symptoms ever arise for no apparent reason.
POTENTIAL ASTHMA TRIGGERS
Circle known or suspected triggers.
Emotional situations: stress, anger, frustration, laughter, crying
Hormonal changes: premenstrual days, pregnancies
In this section of the asthma history, the major disease events and treatments should be listed, including the first appearance of symptoms, the date of diagnosis, the dates of ED visits and hospitalizations (note any ICU admissions or intubations), the dates of related medical and health problems, and the treatment history.
It is particularly important to note any intubations, because a history of asthma attacks of that severity is the most accurate predictor of fatal asthma attacks. The section should end by describing the treatment routine that is currently in effect.
JAMES, AGE 61
James, age 61, recently moved to another town and paid his first visit to a new primary care physician. As part of his intake assessment, the office nurse took the following asthma history:
The family history section of the medical history should list those close relatives with atopic illnesses such as asthma, allergies, sinusitis, rhinitis, eczema, or nasal polyps (a condition that is associated with asthma).
A key part of asthma management is discovering and avoiding triggers and other aggravating factors. In addition to the usual items, such as a brief biography and a review of social and financial support, the social history section of the medical history should record features of the patient’s environment and lifestyle that have the potential to induce asthma symptoms.
Current Living Environments: The places in which the patient spends most of his or her time should be noted. These include home (age, type of heating and cooling systems, type and age of floor coverings, areas of mold or mildew, and presence of any smokers), school or daycare, workplace (exposure to chemicals, tobacco smoke, air pollutants), vacation places, and locations of other activities.
Asthma symptoms can begin hours after exposure to certain triggers. Therefore, descriptions of the workplace environment can sometimes point to triggers previously unrecognized by the patient.
Current Lifestyle: The features and habits of the patient’s daily life are listed, including smoking, diets and dietary supplements, recreational drugs, exercise routines, pets, and hobbies.
Impact of Asthma on Patient and Family: It is always important to deal with diseases in a way that solves practical problems in patients’ lives. The goal of this section of the medical history is to elicit the practical difficulties that are posed by the patient’s asthma.
The interviewer should list how often and in what ways asthma symptoms disrupt the patient’s normal routine. For example, the number of unplanned health visits (urgent care, ED, or hospitalization) and the number of days missed from school or work are recorded. In addition, the list should enumerate the limitations imposed by asthma, such as activities that cannot be undertaken and frequency of sleep disturbances. This section should also include an estimate of the drain on the family’s finances caused by the disease.
Perception of the Disease by Patient and Family: As with all those who have chronic diseases, asthma patients must be the day-to-day managers of their medical care. In this section, the interviewer should describe the patient’s and the family’s understanding of the disease process and the current management plan. The interviewer should find out whether the patient and the family can realistically carry out their current management plan, whether they can afford the current plan, and whether they believe that the current plan is worth the cost and effort required.
DEBORAH, AGE 24
Deborah Hartley is a 24-year-old teacher’s aide who works in a public elementary school. She has come to her doctor’s office complaining of a chest cold that she has had for two weeks and which does not seem to be getting better. She tells the office nurse she has been having frequent bouts of coughing, which sometimes bring up thick, sticky mucus, and also notes that she has had occasional bouts of wheezing, difficult breathing, and sleep disturbances.
The nurse has Deborah fill out an asthma screening questionnaire. Her responses indicate a family history of asthma, a personal history of allergies, worsening of coughing and wheezing during periods of humid weather and poor air quality, more frequent episodes of sleep disturbances over the past two months, and a cigarette smoking habit (though she indicates that she is trying to quit). When asked about her work situation, Deborah notes that in addition to using a blackboard and chalk during the school day and “magic markers” to grade students’ papers, she is regularly exposed to first- and second-graders who come to school with coughs and colds. She adds that the school is located in an urban neighborhood not far from a factory with smokestacks that spew out thick, black smoke.
The nurse refers Deborah for lung function testing, the results of which confirm a diagnosis of asthma.
During an asthma attack, a patient’s clinical signs differ from those seen between attacks. Here, first, are the signs and symptoms of an attack.
In the course of a typical asthma attack, the patient begins to cough and becomes breathless. If lying down, the patient sits up and leans forward, sometimes over a table or the back of a chair. The patient becomes worried, looks anxious, and may begin to sweat.
Breathing becomes labored and shoulder and neck muscles (accessory muscles of respiration) are used. The chest remains expanded in an inspiratory position. It takes longer and longer for the patient to empty the lungs. Meanwhile, the patient begins to wheeze. Later, after the attack has subsided, the patient often clears the throat of thick sputum.
Examining a patient during an attack, the clinician finds a person who is breathing laboriously, is sweating, and is tachycardic. If respiratory failure is nearing, the patient will be cyanotic, dulled, and less responsive.
On auscultation of the chest, each breath will have a short inspiration and a prolonged expiration. During most attacks, musical wheezing (high-pitched whistling sounds) will be heard throughout the lung fields. In a severe attack, however, the airflow may be so reduced that no wheezes are produced. Instead, the chest will be hyper-resonant with diminished breath sounds everywhere.
Between symptomatic attacks, an asthma patient may have no abnormal lung findings and no signs related to asthma. Sometimes, however, there are clues.
People with asthma frequently have atopy and signs of allergies. Their skin may be dry and have atopic dermatitis (eczema) or other allergic rashes. They may have dark rings under their eyes (“allergic shiners”), or their conjunctivae (the mucous membranes lining the inner surface of the eyelids) may be red and irritated. Their nasal cavities should be examined, because allergic rhinitis and sinusitis produce inflamed and edematous mucosa, and asthma is associated with nasal polyps.
Even when not symptomatic, some asthma patients have a hyper-resonant chest. Wheezes can sometimes be heard on auscultation, and the time needed to expel all the air from the lungs (i.e., a full, forced expiration) can be more than twice as long as the normal time of approximately 2 seconds (Barnes, 2008).
For the diagnosis and management of asthma, lung function tests are recommended. Other classes of tests, such as x-rays and blood chemistries, are used to follow individual problems and to rule out other disease processes.
Laboratory studies are not usually a major part of diagnosing or following asthma, but a few tests can give supportive evidence.
Blood Chemistries: Patients with asthma can have elevated eosinophil counts of >4% (300–400 cells/μl). Eosinophil counts >8% indicate the possibility of other or additional diagnoses, such as allergic bronchopulmonary aspergillosis, Churg-Strauss syndrome, or eosinophilic pneumonia.
Blood Gases: During severe attacks of asthma, arterial blood gas measurements help to predict respiratory failure and the consequent need for mechanical ventilation (Chesnutt et al., 2008).
Sputum: The concentration of eosinophils increases in the sputum of a patient with asthma. Although not yet a standard tool, measurement of sputum eosinophils may one day be used to assess asthma control.
Nitric Oxide: The amount of nitric oxide exhaled by a patient is a measure of airway inflammation. In recent years a number of devices have been developed to measure exhaled nitric oxide as a means to assess asthma-related inflammation and to monitor how well a patient’s asthma is controlled. Such devices can also be used to predict the onset of asthma symptoms or loss of control (Korn et al., 2010; Khalili et al., 2007; Payne et al., 2001).
A routine chest x-ray of a patient with asthma may show hyperinflation, but the film can also be normal. In long-standing asthma, permanent bronchial wall thickening can sometimes be seen in chest films.
For diagnostic purposes, for atypical presentations, and for hospital admissions, chest x-rays should be taken. In asthma, radiographs can show the presence of superimposed infections, atelectasis (collapse of an expanded lung), or pneumothorax (abnormal presence of air in the pleural cavity, leading to collapse of the lung). Chest films may also help to distinguish asthma from allergic bronchopulmonary aspergillosis, sarcoidosis, congestive heart failure, pulmonary emboli, and foreign body aspiration.
Between attacks, high-resolution CT of an asthmatic lung can show widened bronchi with thickened walls, air trapping, and mucus plugs. Scans of the patient’s head can reveal acute and chronic sinus diseases. When considering other causes of asthma-like symptoms, CT scans of the chest should find bronchiectasis (chronic dilatation of the bronchial tubes) in patients with allergic bronchopulmonary aspergillosis, emphysema in patients with COPD, and diffuse infiltrations and fibrosis in patients with hypersensitivity pneumonitis. In cough-variant asthma, high-resolution CT scans can show bronchial wall thickening, which will not be present in certain other causes of cough (Grenier, 2008).
The best objective measures of asthma are lung function tests, which can quantify the degree of a patient’s airflow obstruction.
Spirometry measures airflow rates and volumes by having a patient exhale into a tube connected to a spirometer. Spirometry records the volume of air exhaled in a defined period of time (Miller et al., 2005). Spirometry measurements can be made in most children who are 5 years of age or older.
A patient breathes into a spirometer. (Source: National Heart, Lung, and Blood Institute).
For asthma, spirometry is usually used to calculate two basic lung characteristics: forced vital capacity (FVC), which is the total amount of air that can be forced from the lungs after a complete inhalation, and forced expiratory volume in 1 second (FEV1), which is the amount of air that can be forced from the lungs in one second after a complete inhalation. Spirometry may also be used to measure the flow of air coming from the lungs during the middle portion of a forced expiration; this portion is usually defined as 25% to 75% of the FVC and is commonly abbreviated as FEV 25-75%. (Normal values for FEV1, FVC, and FEV 25-75% are depicted below.)
Source: Stanojevic, 2008.
|FVC||Forced vital capacity, i.e., total forced expiratory volume of air|
|FEV1||1-second forced expiratory volume of air|
|FEV 25–75%||Middle portion of a forced expiration, or 25% to 75% of the FVC|
|FEV6||6-second forced expiratory volume of air (This is often used as a substitute for the FVC in adults.)|
For people with airway obstruction, it takes longer than normal to empty their lungs. Therefore, the fraction of air expelled in 1 second is reduced. This fraction is FEV1/FVC, and the value of FEV1/FVC goes down when a patient’s airways are narrowed.
Normal values of FEV1/FVC vary with age, gender, ethnicity, and body structure. Different spirometric reference values have been set for Caucasians, African Americans, and Mexican Americans. These different reference values are based on the following observations, which may be attributable to differences in body build (Hankinson et al., 1999):
Nevertheless, the improvement (i.e., increase) in FEV1/FVC in any particular asthma patient is an objective measure of the level of control achieved through therapy. On the other side of the coin, the decrease in FEV1/FVC during as asthma attack is an objective measure of the severity of the symptoms.
If someone were able to exhale his or her entire vital capacity in 1 second, the ratio FEV1/FVC would be 1.00. A normal child or young adult has an FEV1/FVC ≥0.85. In other words, a young person with normal lungs can exhale at least 85% of his or her vital capacity in the first second. This ratio declines as a person ages, but even older adults will have FEV1/FVC >0.70 if their lungs are normal.
The ratio FEV1/FVC decreases in obstructive airway diseases. In the case of asthma and COPD, the patient’s FEV1/FVC is <0.70 (Wagner & West, 2005). When assessing the degree of obstruction, the FEV1/FVC value is compared to the predicted normal value for a person of the same age, gender, height, and weight (Swadron & Mandavia, 2006).
Lung function tests can distinguish obstructive airway problems from restrictive lung problems. Restrictive lung problems include chest wall deformities that limit lung expansion and interstitial lung changes due to collagen-vascular diseases, hypersensitivity pneumonitis, or interstitial fibrosis. In restrictive airway diseases, both FEV1 and FVC are decreased. With these diseases, although the patient has breathing problems, the ratio FEV1/FVC can be normal or even high.
Diseases that obstruct airflow will decrease the FEV1 more than the FVC, so that the FEV1 to FVC ratio is low. In restrictive problems, however, the decreases in the FEV1 and FVC are proportionate. Thus, the ratio of FEV1 to FVC is either normal or high.
Clinicians who see asthma patients should have access to spirometric testing, and when they have their own spirometers, the machines should be calibrated and serviced regularly. In addition to properly maintained machines, reproducible results require that the doctor, nurse, or technician test patients using the correct procedures; for example, the patients must be encouraged to put in a maximal effort for the results to be usable. Patients whose spirometry results are very abnormal or are difficult to interpret should be sent to a lung function lab for further evaluation (NHLBI, 2007).
Managing asthma using a peak expiratory flow (PEF) meter. (Source: CDC.)
For home monitoring, peak expiratory flow (PEF) meters are recommended. PEF meters are inexpensive hand-held devices that record the maximum flow of air while a patient is forcefully emptying his or her lungs. Normal PEF values can vary according to a person’s sex, age, and height, as illustrated in the following graph.
Source: Nunn & Gregg, 1989.
Patients with moderate or severe asthma should keep a PEF meter at home and should record their baseline PEF values when they are symptom-free. The maximum of these baseline values is referred to as the patient’s “personal-best value.” PEF values taken at other times can then be compared to their personal-best value to objectively identify:
PEF results vary with the specific machine and are generally less accurate than spirometry. For the diagnosis and clinical monitoring of asthma, it is recommended that physicians and clinics use spirometry (Chesnutt et al., 2008).
When a patient presents with symptoms of intermittent and reversible airway obstruction, asthma is usually at the top of the list of diagnoses. However, quantifiable characterizations are still needed for at least three reasons:
Lung function tests are the recommended way to make objective measurements of a patient with symptoms of airway obstruction. All patients with suspected asthma should receive a baseline evaluation of their lung function (Schatz, 2008).
Among the features of asthma that vary from individual to individual is the innate degree of hypersensitivity of the patient’s airways. In some patients, a small amount of irritation triggers a severe reaction. Other patients, however, are less sensitive and get much less bronchoconstriction with the same amount of irritation. The degree of hyper-reactivity of each person’s airways can be assessed by bronchial provocation testing.
Two classes of trigger are commonly used for provocation tests: chemicals and exercise. In the chemical test, methacholine (a cholinergic agonist and airway constrictor) or histamine (also an airway constrictor) are administered after baseline spirometric measurements have been taken. (There are standard paradigms for carrying out the tests, which include administering the drugs incrementally by trained technicians in an appropriate facility.)
For patients who develop symptoms of asthma after exercise (i.e., exercise-induced asthma), spirometry can measure the increase in airway obstruction. In these tests, baseline spirometric values are measured, and patients then exercise to 85% to 90% of their maximal heart rate. Afterward, spirometric measurements are taken for 15 to 30 minutes. In exercise-induced asthma, exercise will reduce the patient’s FEV1 by ≥15%.
Bronchial provocation testing can also be used to identify asthma in patients when baseline spirometric values are near normal or when the asthma symptoms are not typical. In asthma, chemical constrictors will reduce the patient’s FEV1 by ≥20% (Birnbaum & Barreiro, 2007).
Using a bronchodilator, spirometry can document the reversibility of a patient’s airway obstruction and assess the asthma’s responsiveness to medication. Demonstrating reversibility will sometimes clarify the diagnosis. For example, in older people who have been smokers, asthma and COPD can be difficult to distinguish. However, COPD is largely irreversible, and a demonstration of reversibility will suggest that asthma is present, and this will guide the choice of therapy. The NHLBI Expert Panel report (NHLBI, 2007) recommends that the effect of a short-acting bronchodilator be tested on all potential asthma patients aged 5 years or older.
In bronchodilator tests, spirometric measurements are taken before and after administering a short-acting bronchodilator inhalation drug. One form of the test has the patient inhale 2 to 4 puffs of albuterol (90 mcg/puff), and measurements are taken 15 minutes later. (For asthma, the “before” measurements of both FEV1 and FEV1/FVC are expected to be low for the person’s age, gender, and size.) If the underlying airway obstruction is reversible, the “after” measurements will show that FEV1 increases by ≥12% or ≥200 ml (NHLBI, 2007).
Before-and-after tests can also be used to monitor the effectiveness of various medications on a particular patient. Spirometric measurements before and 2–4 weeks after the patient begins a new drug can document the degree of improvement.
CALVIN, AGE 46
Calvin Thompson is a 46-year-old African-American male who is overweight and smokes a pack of cigarettes daily. He is suspected of having asthma or COPD and is referred to the clinic for spirometry testing. The nurse measures his baseline FEV1/FVC ratio at 0.63. Bronchial provocation testing with histamine lowers his FEV1 value by 25%. Calvin then undergoes before-and-after inhalation therapy with a short-acting bronchodilator; the second test shows a 15% improvement in his FEV1. Together, the findings suggest a diagnosis of asthma.
Many asthmatics have atopy. In these people, allergic reactions from inhaled biologic substances will increase their sensitivity to asthmatic triggers. The best protection from this increased sensitization is for the patient to avoid inhaling the allergens, and to do this, patients need to identify the allergens that cause them trouble.
As a first step in building a list of probable offending allergens, the patient should keep a diary of exposures and symptoms. The second step is allergy testing to verify or reject at least some of the suspected allergens. Ridding a patient’s environment of offending allergens can be time-consuming and expensive, and allergy testing will indicate which specific types of cleaning and avoidance should be worth the effort.
Allergy testing can be done in vivo and in vitro. In vivo tests (skin tests) use skin pricks to introduce a small quantity of a known allergen into the dermis. This challenges the allergic reactivity of the skin to the antigen.
In vitro tests (blood radioallergosorbent tests, or RASTs) use a blood sample from the patient to detect circulating IgE antibodies to specific allergens. RASTs are more complicated, more expensive, less sensitive, and slower than skin tests. Nonetheless, RASTs are sometimes the best option.
People’s responses to allergens can change, so allergy testing of atopic asthma patients should be repeated, usually at intervals measured in years.
The typical pattern of asthma has periods of no symptoms punctuated by sudden attacks of a cluster of symptoms. These attacks are paroxysms of coughing, wheezing, and difficulty breathing, and they are caused by the tightening of airway muscles, the swelling of the airway walls, and an increased secretion of airway mucus. Although asthma patients have few symptoms between attacks, their airways are always inflamed and hyperreactive (Chesnutt et al., 2008).
A wide range of variants of this typical pattern is played out among individuals with asthma. Moreover, asthma symptoms can vary over the lifetime of each person. Nonetheless, there are some generalities and commonalities that characterize the progression of the disease in various age groups.
Asthma in childhood can go in many different directions. Some children with asthma continue to have the disease for their entire lives. Other children find that their symptoms decrease or even disappear during adolescence. Of those patients whose disease is in remission, some will remain symptom-free for the rest of their lives, while others will develop symptomatic asthma again later in life (Spahn & Covar, 2008). In a study of French children receiving treatment for asthma, each year of life from infancy to adolescence was found to reduce the risk of a severe asthma attack by 15% while similarly enhancing children’s ability to control their asthma (Mahut et al., 2011).
As for general trends, clinicians often discuss asthma in three age ranges: infants, preschoolers, and school-age children.
Many infants wheeze with respiratory diseases, and half of them have at least one episode of wheezing before the age of 3 years. However, infants who repeatedly develop wheezing should be evaluated.
Infants with intermittent wheezing are more likely to have or to develop asthma if:
Some infants can have persistent wheezing or cough. When these infants have atopy or a family history of atopic diseases, asthma is likely, although it is important for them to have an open-minded medical evaluation (Bacharier et al., 2007).
Asthma is a progressive disease that gradually diminishes lung function. All people lose lung function as they age, but people with asthma lose lung function faster. In children, there is an additional risk. The lungs of young children are growing, and childhood asthma can interfere with this growth. Children whose asthma symptoms begin before the age of 3 years have the highest risk for developing a substantial lung deficit from interference with lung growth, and this will show up as a permanently reduced FEV1 (Spahn & Covar, 2008).
In the preschool years, asthma phenotypes become distinct, and children with wheezing often fall into one of three categories:
An important caveat for physicians and parents is that episodes of wheezing in early childhood do not necessarily mean that the child will have a lifetime of asthma. Fifty-five percent of all children who have episodes of wheezing before the age of 7 years will be symptom-free by the time they are 21 years old.
In the pre-adolescent school years, allergen-induced asthma is more common than before, and some children’s asthma begins to develop a clear seasonal pattern. Viral-induced asthma remains a prevalent phenotype in school-age children (Bacharier et al., 2007).
Asthma can first appear in a person at any age, and new cases of asthma develop throughout the adolescent years. Asthma symptoms can also become less frequent or even disappear altogether at any age, and overall about 45% of people with asthma symptoms eventually become symptom-free.
However, adolescents have more remissions of symptomatic asthma than any other age group. During their teen years, between a quarter and a half of all children with asthma symptoms go into remission (NHLBI, 2007).
Children with infrequent wheezing or with wheezing only during viral infections are most likely to lose their symptoms in adolescence. Adolescent remissions are most common in boys, and this male/female difference appears to be due to a male growth spurt of the lungs and airways during and after puberty.
Adolescence also brings new difficulties in asthma management. For instance, some teens begin smoking, and many teens resist the restrictions placed on their lifestyles by their asthma management plans (Bacharier et al., 2007).
Asthma can continue into old age, and the disease does not necessarily burn out. New cases of asthma show up throughout adulthood, and the disease returns in some people who went into remission during adolescence. In a person with new or reappearing asthma symptoms, other diagnoses must always be considered. In older adults, for instance, GERD produces respiratory symptoms (from aspiration) more often than it produces heartburn (Hall & Ahmed, 2007).
On average, lung function declines more rapidly in people with asthma and most rapidly in smokers and in asthma patients with excess mucus production. The most significant declines in lung function are seen in patients with severe asthma, frequent asthma attacks, asthma that began in early childhood, or asthma that is poorly controlled (NHLBI, 2007).
The cluster of coughing, wheezing, and dyspnea, often with thick phlegm, suggests a diagnosis of asthma. Allergies and a family history of allergies or asthma make the diagnosis of asthma even more likely. Nonetheless, other diseases present with many similar symptoms, and some of these diseases can be quite serious (Gordon, 2008). It is also important to remember that a person with asthma can develop an additional cause of coughing, wheezing, or dyspnea.
The basic list of other medical problems that bring on asthma-like symptoms includes:
Patients with an exacerbation of either asthma or COPD typically come to the ED with dyspnea and respiratory distress. As with asthma, exacerbations of COPD often produce cough and wheezing, fast respiratory rates, and tachycardia. In both asthma and COPD, patients will use their accessory muscles of respiration, they can develop cyanosis, and their chest x-rays will probably show hyperinflation of the lungs.
History and lung function tests can usually distinguish asthma from COPD. First, patients with asthma or COPD usually know their diagnosis. Second, most COPD patients are middle-aged or older and have a long history of smoking. Third, while both asthma and COPD are obstructive lung diseases and will cause a reduced FEV1/FVC in spirometric tests, asthma symptoms can be quickly reversed by short-term bronchodilators, while COPD symptoms cannot. (It is important to remember that smokers can have both diseases.)
Left-sided heart failure can present with severe dyspnea that is worsened on exertion and with wheezing, fatigue, and, sometimes, cough. Many features will distinguish heart failure from asthma. Heart failure is a disease of older adults: less than 1% of people younger than 60 years have heart failure. Heart failure patients usually present with a history of cardiovascular problems, and on examination, heart failure patients have an enlarged heart, jugular venous distension, dependent edema, and, sometimes, a gallop cardiac rhythm and pulmonary venous congestion with rales (an abnormal crackling or rattling sound heard upon auscultation of the chest).
In children as in adults, repeated episodes of cough and wheezing suggest asthma, but asthma may be underdiagnosed in children because wheezing is often attributed to a respiratory infection such as bronchiolitis.
Respiratory infections are at the top of the differential diagnosis list for children with asthma-like symptoms. This list differs from the differential diagnosis for adults because children are unlikely to have heart failure, COPD, or pulmonary embolus. Instead, the differential diagnosis for children begins with:
Lung function tests cannot be done on infants and young children, so a diagnosis of asthma must rest on other criteria. Atopy in the child or a family history of asthma supports the possibility of asthma. The reduction of symptoms after administration of a bronchodilator is also consistent with asthma.
Asthma therapy has two modes:
Asthma attacks are episodes of progressive breathing difficulty. In an asthma attack, patients get increasingly short of breath while also experiencing coughing, wheezing, or chest tightness. During an attack, the patient cannot push air out of his or her lungs as rapidly as before, and this can be objectively measured using simple lung function tests.
Attacks can range from minor to life-threatening. The severity of an asthma attack is classified as mild, moderate, severe, or extremely severe, and this classification is used to determine the initial treatment (Arnold et al., 2008).
In a mild attack, a patient has breathing difficulty (dyspnea) only when pushing oneself beyond normal activity levels. (In infants, dyspnea sometimes appears as an increased rate of respiration.) Mild attacks still allow a peak expiratory flow of 70% to 80% of the patient’s predicted or personal-best level. A mild attack can often be treated at home with a short-acting bronchodilator inhaler. Sometimes, the physician may recommend a short course of oral corticosteroids to prevent a relapse. When a mild attack occurs at home or at school, the parent or nurse must assess the causes of the attack and provide an environment that reduces the dyspnea.
In a moderate attack, the patient’s dyspnea interferes with his or her normal activities. Moderate attacks reduce the peak expiratory flow to between 50% and 70% of the patient’s predicted or personal-best level. Moderate attacks are best treated by the healthcare system through either an urgent (unscheduled) office visit or a visit to a clinic, urgent care center, or emergency department. Typically, a moderate attack requires repeated doses of a short-acting bronchodilator plus a course of oral corticosteroids. After a moderate attack, some degree of asthma symptoms lasts for 1 to 2 days.
In a severe attack, the patient has trouble breathing even at rest, and the asthma symptoms interfere with his or her ability to complete a sentence. Severe attacks reduce the patient’s peak expiratory flow to less than 50% of one’s predicted or personal-best level. Severe attacks require an immediate trip to an emergency department. A severe attack is not fully relieved by the patient’s inhaler medication. High doses of short-acting bronchodilators and systemic corticosteroids are needed, along with oxygen. After the attack, some of the symptoms will last for more than 3 days.
In an extremely severe attack, the patient has a very difficult time breathing, begins to perspire, and is too dyspneic to say more than a few words. The patient may also become cyanotic. Extremely severe attacks reduce the patient’s peak expiratory flow to less than 25% of one’s predicted or personal-best level. Extremely severe attacks are life-threatening, so the patient, bystanders, or family should call 911 immediately. Patients should take their rescue medicines, but an acute severe attack also requires a high concentration of oxygen (via face mask), high doses of bronchodilators, and systemic corticosteroids, all as soon as possible. Arterial blood gas levels of carbon dioxide should be followed to watch for respiratory failure. When patients do not respond to the initial treatment in the ED, they will probably have to be hospitalized (Chesnutt et al., 2008).
|Level||Typical Symptoms||PEF (as a percentage of patient’s predicted or personal-best level)||Typical Course of Treatment|
|Source: Chestnutt et al., 2008.|
|Mild||Dyspnea when pushing oneself beyond normal activity levels||70–80%||Short-acting bronchodilator|
|Moderate||Dyspnea interfering with normal activities||50–70%||Short-acting bronchodilator plus oral corticosteroids|
|Severe||Dyspnea even at rest, difficulty speaking||<50%||Emergency administration of short-acting bronchodilator, systemic corticosteroids, oxygen|
|Extremely Severe||Extreme dyspnea, extreme difficulty speaking, cyanosis||<25%||Highly concentrated oxygen, high-dose bronchodilator, systemic corticosteroids|
No matter how mild or severe the asthma attack, the two treatment goals are to correct hypoxemia and to reverse the airflow obstruction (Schatz, 2008).
Therapy for an asthma attack begins with correcting any hypoxemia and maintaining sufficient blood oxygenation. Hypoxemia is a blood oxygen concentration—an arterial blood oxygen partial pressure (PaO2)—less than 60 mm Hg. Clinical signs of hypoxemia are restlessness, tachycardia, and cardiac irritability (i.e., a tendency to develop irregularities in rate and rhythm). Prolonged or significant hypoxemia will lead to bradycardia, hypotension, and cardiac arrest.
An attack of asthma will produce hypoxemia, and this must be corrected. In a mild attack, short-acting bronchodilators can usually relieve the bronchoconstriction sufficiently for the patient’s breathing to maintain appropriate blood oxygen levels. In a severe attack, supplemental oxygen is needed.
The hallmark of an asthma attack is a significant increase in the difficulty of moving air through the bronchi and bronchioles of the lungs. For the patient to maintain a healthy level of blood oxygen, the airway obstruction must be reduced, so one goal when treating an asthma attack is to widen the airways and lessen the obstruction. Airflow obstruction is most quickly reversed by inhaling short-acting bronchodilators and then taking systemic corticosteroids.
The extent and the time course of medical treatment for an asthma attack must be tailored to each specific situation, and often the initial treatment is modified as events progress. For moderate and severe attacks, patients should be evaluated clinically, their blood oxygen saturation (measured via pulse oximetry) followed, and their FEV1 measured at regular intervals. Acutely ill patients must be treated immediately; for them, initial lung function tests are distressing and unnecessary.
Hospitalization of Children with Asthma Attacks
In children, lung function measures are hard to obtain during an asthma attack. Consequently, clinical judgment plays a larger role in guiding treatment, and the need for hospitalization is sometimes a decision based on clinical experience.
In general, when a child’s pulse oximetry value (oxygen saturation) remains <92% to 94% after an hour of treatment, the child should probably be hospitalized. Other specific criteria are included in a number of severity assessment scores, which are available to help emergency physicians decide which children should be moved from the ED to the hospital (NHLBI, 2007).
At the end of acute treatment, the final goal is to reduce the likelihood that the patient will have additional attacks. To this end, a course of systemic corticosteroids is often prescribed. Asthma attacks can be a sign that the patient’s disease is not being managed optimally. Therefore, regardless of the severity of the current attack, at the end of their treatment, all patients seen by physicians should be counseled, given any necessary medications, provided with a telephone number for questions, and scheduled for a follow-up visit.
Relief from an asthma attack requires proper treatment, and it is the patient or the patient’s family who have the responsibility for initiating that treatment. For this reason, when a patient is diagnosed with asthma, the patient or the family should be given a written plan that explains how to deal with an asthma attack.
The asthma action plan should list:
A standardized blank outline of an asthma action plan and an asthma patient’s wallet card with blanks for all the important information can be downloaded from the National Heart, Lung, and Blood Institute (NHLBI) website. (See “Resources” at the end of the course.)
Asthma patients should have a rescue inhaler that they can carry with them to school, work, or any place outside the home. At home, patients with moderate or severe asthma should have additional medications (e.g., oral corticosteroids) and a peak flow meter, and children should have a compressor-driven nebulizer.
All asthma patients need a written plan—an instruction manual on how to handle an attack. This plan should be written clearly enough for a family member or friend to follow. The plan should be tailored to the individual patient.
The outline of an emergency plan sets out four steps for treating attacks:
The content of the plan is, essentially:
Following are details of a typical plan for asthma attacks.
Begin by deciding the severity of the attack.
Extremely severe asthma attacks require immediate attention. For patients likely to have an extremely severe attack, Step 1 of their asthma attack plan should be, “Take rescue medications and call 911.”
Pharmacological self-management should always begin with the inhalation of a short-acting bronchodilator, such as albuterol. Although each self-management plan must be individualized, here are some common protocols.
Begin with 2 to 6 puffs of the rescue bronchodilator. Repeat the same dose in 20 minutes. A complete response includes significantly decreased symptoms and a PEF ≥80% of one’s personal-best value within 30 minutes.
If the response is incomplete, the bronchodilator treatment can be repeated once every 3 to 4 hours for 24 to 48 hours. For an incomplete response, a short course of oral corticosteroids should be considered, in which case the patient should consult his or her doctor.
Begin with 2 to 6 puffs of the rescue bronchodilator. Repeat the same dose in 20 minutes. A complete response includes significantly decreased symptoms and a PEF ≥80% of one’s personal-best value within 30 minutes. For a complete response, repeat the bronchodilator treatment once every 3 to 4 hours for 24 to 48 hours.
If the response is incomplete, the bronchodilator treatment should be repeated every 3 to 4 hours for 24 to 48 hours. In addition, a short course of oral corticosteroids should be started, in which case the patient should consult his or her asthma doctor.
Begin with 2 to 6 puffs of the rescue bronchodilator. Repeat the same dose in 20 minutes. A complete response includes significantly decreased symptoms and a PEF ≥80% of one’s personal-best value within 30 minutes. For a complete response, repeat the bronchodilator treatment once every 3 to 4 hours for 24 to 48 hours. Begin taking oral corticosteroids, and contact one’s doctor within 24 hours.
If the response is incomplete (persistent wheezing, difficulty breathing, or a PEF of 50% to 80%), begin taking corticosteroids and contact one’s asthma doctor within the hour.
If the response is poor (marked wheezing or coughing, difficulty breathing at rest, PEF <50%), repeat the bronchodilator treatment immediately, begin taking oral corticosteroids, call one’s physician, and call 911 rather than driving oneself to the emergency department.
Immediately take 2 to 6 puffs of the rescue bronchodilator and call 911. Then take oral corticosteroids. For increasing symptoms, inject oneself with epinephrine (Epipen) if this is a part of one’s asthma attack plan.
Regardless of the usual severity of their asthma, all patients need a list of symptoms—such as extreme breathlessness, insufficient breath to speak more than a few words at a time, or drowsiness—that suggest the onset of an extremely severe attack. These symptoms should prompt patients to call 911 immediately while taking their rescue medicine.
If one’s symptoms are worsening, or if after 30 minutes the patient still has marked wheezing and difficulty breathing, or if the PEF is less than 50% of the patient’s personal-best value, the patient should follow the above medication regimen (Step 2), contact one’s physician immediately, and proceed to an emergency department. Call 911 rather than driving oneself, and if the patient is drowsy, confused, sweating, or turning blue, call 911 immediately.
If after 30 minutes the patient still has wheezing or difficulty breathing or if the PEF is between 50% and 80% of the patient’s personal-best value, the patient should follow the above medication regimen (Step 2), and contact one’s physician within 24 hours for further instructions.
If after 30 minutes the patient no longer has wheezing or difficulty breathing and the PEF is at least 80% of the patient’s personal-best value, the patient should follow the above medication regimen (Step 2), and contact one’s physician later for follow-up instructions.
After an asthma attack, the patient should continue stepped-up treatments for several days. A full recovery will take 1 to 2 days for moderate symptoms and more than 3 days for severe symptoms, and improvement can be gradual. The underlying disease flare-up will last for 2 to 3 weeks. Always contact one’s doctor within a day of the attack for specific after-the-attack instructions.
Techniques Not Recommended
A few home remedies are not recommended for relief from asthma attacks unless specifically approved by one’s physician. These include:
JONAH, AGE 11 (continued)
Jonah Bachman, the 11-year-old identical twin who was brought to the pediatrician’s office by his mother (as described in the case above), meets with the nurse after being diagnosed with asthma. The nurse gives Jonah the rescue inhaler that the pediatrician has prescribed for him and tells him he is to use it when he experiences an asthma attack while at home or at school. The nurse gives Jonah tips to help him assess the severity of an attack, noting that when he starts to wheeze, cough, and have difficulty breathing or talking during normal activities, those symptoms signal a need for rescue medication.
The nurse also shows Jonah (and his mother) how to use the inhaler, beginning with administering 2 to 6 puffs of the rescue bronchodilator. She tells Jonah to repeat the same dose in 20 minutes and then every 3 to 4 hours for the next 24–48 hours. The nurse also has Jonah practice using a PEF meter and tells him and his mother how PEF values can help them assess Jonah’s response to rescue bronchodilator treatment. The nurse helps prepare a written set of instructions for Jonah and a separate, more detailed set of instructions for his mother; the mother’s instructions focus more specifically on when to repeat bronchodilator treatment, call the doctor, or take Jonah to the emergency department based on his response to the rescue bronchodilator (as determined by PEF values and severity/persistence of symptoms). The nurse makes a separate copy of the mother’s instructions for the school nurse, which Jonah’s mother promises to deliver herself.
Quick treatment with oxygen and bronchodilators is the optimal treatment for a severe asthma attack, and EMS transport is the preferred way for a patient with a severe asthma attack to get to an emergency department.
EMS teams should be trained in the recognition of and response to asthma attacks, and they should be trained to recognize imminent respiratory failure and asphyxiation. They should also have written protocols for the pre-hospital treatment of asthma attacks in children and in adults.
The basic protocol should begin with evaluation of the patient while in the transport vehicle. EMS responders should check vital signs and level of consciousness, listen for breath sounds, record oxygen saturation (SaO2), and administer oxygen. It is ideal for EMS technicians to have standing orders to provide albuterol inhalers for patients suffering from asthma symptoms. When this is allowed, the responding team should give a rescue dose (usually 2 to 6 puffs) of albuterol every 20 minutes. After each treatment, a technician should reassess the patient’s symptoms and record vital signs, SaO2, and lung sounds; the response to treatment should begin in less than 5 minutes.
During long transports, technicians could give a maximum of three treatments of albuterol during the first hour and one treatment per hour thereafter. Usually, oral corticosteroids should also be given during long transports. In a severe asthma attack, subcutaneous epinephrine or terbutaline should be given when an inhaler or nebulizer with a short-acting bronchodilator is not available (Stapczynski, 2004).
HOWARD, AGE 54
Howard Wilson is a 54-year-old asthmatic who calls 911 while experiencing a severe attack at his workplace. The EMS team arrives within 10 minutes and immediately administers oxygen and inhaled albuterol treatment as specified in their protocol. After placing Howard on a stretcher, the team loads him into their ambulance to transport him to the emergency department. While en route to the ED, the team checks Howard’s vital signs, which, aside from an elevated heart rate, are normal. Howard remains conscious during the 30-minute trip to the ED, though his breathing is labored and his SaO2 level is only 70%. The team continues to follow their protocol by administering oxygen, along with a repeat dose of inhaled albuterol (20 minutes after the first dose), while also giving Howard subcutaneous epinephrine. By the time he arrives at the ED, Howard is breathing more easily, and his wheezing and coughing are less severe. After Howard is admitted to the ED, one of the EMTs calls the team’s medical director, who confirms that their actions in this case were appropriate.
The ED team makes a judgment of the severity of the attack by assessing:
Give treatment according to the severity level of the attack. Even if the patient has taken rescue medicines, begin treatment immediately for attacks that are of moderate severity or worse or when the patient has dyspnea at rest, a PEF or FEV1 value <70% of predicted, or an oxygen saturation SaO2 <95%.
ED BASIC TREATMENT PROTOCOLS
For mild to moderate symptoms with a PEF >40% of the predicted value:
For severe symptoms or a PEF <40% of the predicted value:
The history should include:
The physical exam should note especially:
Additionally, the physical exam should rule out upper airway obstruction. For example, the ED team should note the absence of symptoms such as stridor, dysphonia, or localized wheezing, as well as absence of normal PaO2, lack of pharyngeal obstruction, or absence of neck or throat injury.
Record pulse oximetry values regularly and reassess the severity of the asthma symptoms after 1 hour. In addition, look for signs of increasing fatigue from the work of breathing. Then triage to discharge, additional therapy, or hospitalization:
The severity of airway obstruction is harder to determine in young children, but an increasing respiratory rate (i.e., tachypnea) can be the equivalent of dyspnea. Close monitoring is critical for young children because infants have less of a safety margin than older children and can descend rapidly into respiratory failure.
Continuous pulse oximetry is an easy way to monitor an infant’s respiratory status. A decreasing SaO2, or a SaO2 <92% on room air 1 hour after the initial treatment, signals that an infant will probably need hospitalization. As in adults, blood gas measurements of carbon dioxide partial pressure (PaCO2) are the best measures of respiratory status, and a child who is in respiratory distress but who has a normal PaCO2 is at high risk for respiratory failure.
The differential diagnosis of an infant is different from that of an adult. The infant’s list includes viral respiratory infections (e.g., RSV), foreign body obstruction, aspiration (e.g., swallowing problems or GERD), chest malformations, congenital airway problems, and cystic fibrosis (NHLBI, 2007).
As in adults, short-acting bronchodilators are the rescue medicines of choice for the initial management of asthma attacks in children. In this class of medicines, albuterol is the most widely used rescue medicine for children ages 2 to 5 years. The optimal dose is adjusted empirically, balancing symptomatic control against side effects such as tachycardia, dizziness, and jitteriness (Bacharier et al., 2007).
Even with good treatment, 10% to 25% of patients seen in the ED for asthma attacks will need to be hospitalized. Patients should be admitted to an ICU if they need continued careful monitoring, if they are candidates for intubation, or if they are already intubated.
When PEF or FEV1 values begin very low (<25% of predicted) and then increase only minimally (<10%) after treatment, the patient is a candidate for admission to an ICU. Widely fluctuating lung function values also suggest that respiratory function is unstable, and the patient may need to be watched in an ICU. In addition, if serial pulse oximetry values remain low or begin to decrease, there is some form of respiratory compromise, and it is probable that the patient will need to be hospitalized.
Intubation is a difficult procedure in patients with asthma, and it should be done by an experienced physician before a crisis develops. In general, increasing levels of carbon dioxide in the blood, patient exhaustion, and a reduced level of alertness suggest that an asthma patient will need intubation, but clinical judgment and experience are called for. On the other hand, asthma patients who come to the ED unable to breathe or in a coma should be intubated immediately.
Adjunct treatments, such as IV magnesium sulfate or heliox-driven albuterol nebulizers, are sometimes used in an attempt to avoid intubating a patient with severe asthma symptoms. However, the success of adjunct treatments has varied.
Before being discharged, asthma patients need to have their:
Even with a rapid improvement, patients should be watched for 30 to 60 minutes to be certain they are stable before being released.
When asthma patients are discharged, they should be given all necessary medications with written instructions on their use. Patients who have been given systemic corticosteroids should continue the drugs for 3 to 10 days. Some patients should also be put on an inhaled corticosteroid regimen at discharge, because adding inhaled corticosteroids to systemic corticosteroids can reduce relapse rates.
Studies have shown that a brief, focused session of asthma education at the time of discharge can reduce recurrence rates. Educational information should include a list of symptoms that signal the need for re-treatment and phone numbers at which advice is available 24 hours a day. Finally, a follow-up visit should be arranged either with the patient’s physician or with an asthma clinic.
An ED visit can be a sign of poor asthma control, and patients should be encouraged to review their asthma management plan with a physician. For patients who do not have a PEF meter at home, the ED should give a meter to the patient with instructions for its use, because some patients need an objective way to recognize worsening airway obstruction (NHLBI, 2007).
HOWARD, AGE 54 (continued)
Upon arrival at the ED, Howard (see case above) is admitted and assessed for the severity of his symptoms. The EMS technicians tell the ED nurse that Howard’s wheezing, coughing, and dyspnea have improved within the last 10 minutes, and his vital signs are normal, except for an elevated heart rate. Following the routine protocol, the ED nurse conducts spirometry testing, which reveals a PEF of 60% of the predicted value, and pulse oximetry, which shows an SaO2 level of 80%. The nurse relays these results to the other members of the ED team, whereupon they initiate the mild-to-moderate asthma emergency protocol, which involves administration of oxygen and a short-acting bronchodilator.
Ten minutes later, not satisfied with Howard’s response to treatment thus far, the team (which includes the emergency physician) initiates a short course of oral prednisone, followed by a repeat bronchodilator dose 10 minutes after that. The nurse also takes Howard’s history, noting the time of onset of his asthma attack; his self-reported severity of symptoms compared to previous attacks; his current medications, including those taken before his ED admission (and the resulting change in symptoms); and Howard’s report of six attacks during the past year, as well as his admission of habitual inactivity.
After conducting a physical exam, the nurse notes that Howard’s asthma symptoms are moderate, though he has remained alert throughout the admission process as well as during the exam, and he appears to be adequately hydrated, with no signs of lung complications, heart failure, or upper airway obstruction, The nurse continues to conduct pulse oximetry and to assess Howard’s asthma symptoms for the next hour, after which the team judges his symptoms to be minimal, while his PEF has reached 70% of the predicted value.
After watching Howard for another hour, during which time his symptoms appear to stabilize, the team discharges him with a prescription for oral prednisone, but not before the nurse briefly counsels him on anticipating and responding to future attacks, as well as scheduling a follow-up appointment with his physician.
Asthma is a chronic illness, and good asthma therapy is built on a long-term plan. Although each patient needs an individualized plan, most cases are clear-cut and can be managed by internists. The central feature of long-term asthma therapy is pharmacologic, emphasizing anti-inflammatory drugs, but the patient’s efforts at maintaining a non-asthmatic lifestyle can be equally important (Barnes, 2008).
Some patients with asthma may have difficulty adhering to an asthma self-management plan because of inconsistent access to primary care, lack of transportation, or other socioeconomic factors. Many patients and families, particularly those of limited means, are reluctant to seek treatment due to the cost of medical care and/or medications (WHO, 2003). Consideration of these concerns is therefore an important part of developing an individualized asthma management plan.
The most effective way to ensure that patients understand how to manage their asthma is by developing a written plan with them.
The goal of asthma treatment is for each patient to live a near-normal life. This means that asthma control should minimize the symptoms that interfere with work, school, sleep, exercise, and leisure activities. Asthma attacks should be prevented or reduced, and ED visits should be rare.
A successful asthma management plan requires the continued attention of a disease manager, and the patient should take that role. With their physicians, asthma patients should design a plan that is realistic, and the patients must then ensure that the plan is carried out.
The better the patient understands the reason for their healthcare provider’s recommendations, the more likely it is that those recommendations will be carried out. Therefore, medical conversation must be two-way. Providers must shape their recommendations to be realistic for and understandable to the particular patient; they should also listen to be certain that they are working on the goals that the patient wants.
To these ends, providers and patients should design the treatment plan together. Along the way, healthcare professionals must educate their patients, clearly explaining the disease, the medicines, and the nonpharmacologic tools (Schatz, 2008). The education process begins with an initial assessment of what the asthma patient understands about the disease and what the patient is imagining that the medical system can do for him or her. When talking with a patient, the healthcare provider can then begin at the patient’s level of understanding when making comments or giving advice.
The NHLBI Guidelines (NHLBI, 2007) emphasize these features of asthma education:
To help their patients write an asthma treatment plan, clinicians gather the medical data they have collected and then summarize four characteristics of the individual patient:
The physician sits down with the patient and suggests a list of actions that are aimed at effective disease control for that particular person. The plan begins with any daily medications, it suggests how to modify the patient’s surroundings or otherwise avoid triggers, and it offers realistic lifestyle modifications.
The plan should include ways to monitor the state or level of the disease and detail when and how the patient responds to an impending asthma attack. The plan contains phone numbers at which the patient can get answers to questions and concerns as well as schedule a follow-up visit (Schatz, 2008).
The NHLBI guidelines (2007) recommend that physicians plan a patient’s medications using a step paradigm, with asthma treatments divided into six successively increasing steps, incorporating the medications needed to control the asthma symptoms (Schatz, 2008).
6-STEP PLAN FOR LONG-TERM ASTHMA CONTROL
For patients 12 years of age and older, step-by-step preferred medications are:
The NHLBI guidelines include alternate recommendations for Steps 2 to 4.
With this plan, the physician prescribes medications at the minimum necessary step to maintain control of the patient’s symptoms.
At the outset, the physician should use the severity level of a patient’s asthma to set a step at which to begin treatment. At 2- to 6-week intervals, the patient is checked and the medications adjusted until the symptoms seem well controlled.
After 3 consecutive months of good control, the physician attempts to lower the medication level by one step. If this approach is successful for 3 months, the physician lowers the medication level by another step. The goal is to find the lowest level of medication required for satisfactory asthma control.
Asthma is a variable disease that can change over time, and each patient’s treatment plan must be revisited, moving up or down a step when needed. Monitoring requires regular visits, at from 1- to 6-month intervals. At these visits, the patient’s interim history and personal assessment should be added to objective lung function tests (FEV1 or PEF) when determining whether his or her asthma control is currently adequate (Schatz, 2008).
To choose where on the pharmacologic step chart to start an asthma patient, physicians need to classify the severity of the patient’s disease. For asthma patients, “severity” means the intensity of the disease when it is not being controlled by medicines (Wechsler, 2009; NHLBI, 2007).
For treatment decisions, asthma is categorized as intermittent, persistent mild, persistent moderate, and persistent severe. Patients with intermittent asthma should begin treatment at Step 1 of the pharmacology chart, mild persistent asthma should begin at Step 2, moderate persistent at Step 3, and severe persistent at Step 4 or Step 5.
The NHLBI guidelines decide on these severity levels by considering both the patient’s level of impairment and the patient’s risk of having an attack (NHLBI, 2007).
To monitor the degree of asthma control, physicians should couple symptomatic assessments with lung function assessments.
With a small number of standardized questions, physicians can judge how well the symptoms of a patient’s asthma are controlled. Various questionnaires have been devised, and two or three are in wide use. The NHLBI’s control assessment charts include an entry for the results of psychometric measures of asthma control. These measures come from short, validated questionnaires that identify patients whose disease is not effectively managed. One common test is the Asthma Control Test (ACT), which has five multiple-choice questions. The ACT test can be freely downloaded from the Internet (see “Resources” at the end of the course).
ASTHMA CONTROL TEST (ACT)
During the past four weeks (1 month) …
Answers to the questions are multiple choice. Each answer is scored from 1 to 5, and a total score is interpreted as follows:
Physicians should follow their patient’s degree of asthma control using regularly scheduled visits. Between visits, the patient must take responsibility for notifying their physician of problems, and physicians should give patients a list of symptoms and signs that should be reported.
Besides symptoms and signs, asthma control should be judged by lung function tests, and for this task peak-flow meters are the best lung function analyzers for patients to use at home. Peak-flow meters are inexpensive, easy-to-use handheld units with which patients can quickly measure the level of their airflow obstruction.
Patients begin by establishing a baseline of their personal-best peak expiratory flow (PEF) value when they are symptom-free. For general monitoring, patients should use their peak-flow meter first thing in the morning before using a bronchodilator, and they should use the same meter for each measurement (Cincinnati Children’s Hospital, 2009; ALA, n.d.b.). Then patients are given these rules:
MAUREEN, AGE 16
Sixteen-year-old Maureen Feeney, recently diagnosed with asthma, is meeting with the office nurse, who is assessing Maureen’s current status so she can report her findings to Maureen’s physician. The nurse judges Maureen’s asthma severity to be moderate and notes her baseline FEV1 and PEF values. She also notes that Maureen’s asthma appears to be triggered by exercise, dust mites, and fragrances, and that her knowledge of the disease appears to be minimal.
The nurse then counsels Maureen on the basics of asthma management, focusing on issues such as carrying an inhaler (particularly during exercise), avoiding asthma triggers, using a peak-flow meter, and anticipating and handling an attack. These matters are incorporated into the written plan, which includes a diary for Maureen to record the following information:
The medication portion of the written plan outlines the 6-step paradigm for asthma management, starting with short-acting beta-agonist inhalers and progressing to corticosteroids (at increasing doses) and other medications as appropriate, as outlined in the NHLBI guidelines. These instructions emphasize the need to administer the minimal amount of medication to control Maureen’s symptoms, as well as the importance of assessing her asthma severity level at each step of the protocol.
Once Maureen has reviewed and accepted the written plan, she schedules a follow-up appointment in two weeks, at which time her degree of asthma control will be assessed and her medications will be adjusted as necessary.
The effectiveness of a long-term asthma management program is called the “degree of control,” and “well controlled” means both:
When considering therapy changes, physicians should use NHLBI charts as general guides and then take into account the patients’ quality of life, ability to function to their own satisfaction, and ability to recognize and evaluate the status of their disease. It is best to talk these issues over with the patient and to involve the patient in therapy decisions because the success of long-term treatment depends on the patient’s ability to make the treatment plan work.
Drugs are the cornerstone of asthma therapy, and patients with asthma typically take at least one medication daily. Most asthma drugs are taken by using inhalers or nebulizers so the medicine can get directly to the inner lining of the airways.
|Type of Drug||Examples|
|Compound Name||Brand Name(s)|
|Sources: ALA, n.d.a.; MedicineNet.com, n.d.|
|Short-acting beta-2 agonists (inhaled or oral)||Albuterol*||Accuneb, ProAir, Proventil, Ventolin, VoSpire|
|Anticholinergics (inhaled)||Ipratropium bromide||Atrovent|
|Combination anticholinergic and short-acting beta-2 agonist||Ipratropium bromide and albuterol||Combivent, Duoneb|
|Budesonide*||Pulmicort Respules, Pulmicort Flexhaler|
|Long-acting beta-2 agonists (inhaled; commonly used with other asthma medications)||Formoterol*||Foradil|
|Combination bronchodilator and steroid (inhaled)||Budesonide and formeterol||Symbicort|
|Fluticasone and salmeterol||Advair|
|Theophylline*||Elixophyllin, Theo-24, Theochron, Uniphyl|
|Mast cell stabilizers (inhaled)||Cromolyn*||Intal|
|Systemic corticosteroids (oral)||Dexamethasone*||Decadron, DexPak|
|Anti-IgE (subcutaneous injection)||Omalizumab||Xolair|
|* Available as generic.|
Asthma medications fall into two major classes:
Although patients with persistent asthma generally require both of the major classes of drugs, persistent asthma is most effectively controlled with daily long-term control medication. The daily controllers are anti-inflammatory drugs aimed at damping the ongoing inflammation that underlies the disease. Controller medications include inhaled corticosteroids (which are generally considered the most potent and consistently effective long-term medications for asthma), long-acting bronchodilators (often used with inhaled corticosteroids), leukotriene modifiers, mast cell stabilizers, methylxanthines, omalizumab, and systemic corticosteroids.
Quick relievers or rescue medications are used to head off asthma attacks, to reduce worsening asthma symptoms, and to relieve an ongoing attack. The rescue medicines for asthma include short-acting beta-2 agonists (e.g., albuterol) and anticholinergics; systemic corticosteroids are also used to treat moderate or severe attacks because they prevent progression of an attack, speed recovery, and prevent relapses. Asthma is considered to be under good control if the inhalation of a rescue medication is needed less than twice per week. Intermittent asthma can usually be managed using rescue medications (quick relievers) only.
One goal of long-term asthma therapy is to reduce the need for rescue medications. The 6-step pharmacologic protocol is an attempt to institute sufficient controller medication to avoid or minimize attacks while keeping drug side effects to a minimum. To this end, the step plan introduces corticosteroids in the order of increasing collateral effects: low-dose inhaled corticosteroids, medium-dose inhaled corticosteroids, high-dose inhaled corticosteroids, oral corticosteroids (NHLBI, 2007).
Bronchodilators are used to reverse the bronchoconstriction of asthma attacks and in this way to relieve the cough, wheezing, dyspnea, and chest tightness. Bronchodilators are also the primary medicine for preventing exercise-induced asthma.
Bronchodilators have their main effects on the smooth muscle in airway walls. Bronchodilators have very little effect on the ongoing inflammation, which is the essential pathology of asthma. Their lack of effect on inflammation makes bronchodilators ineffective at controlling asthma in patients who have persistent symptoms.
Three classes of bronchodilator are used for asthma:
The commonly used short-acting beta-2 agonists are albuterol (Proventil, Ventolin) and levalbuterol (Xopenex). Long-acting beta-2 agonists, such as salmeterol (Serevent), are also bronchodilators, but they are used as part of the step therapy for persistent asthma rather than as rescue medicines. Ipratropium bromide (Atrovent) is the one anticholinergic bronchodilator currently used as a rescue drug. The final class of asthma bronchodilators is the methylxanthines (theophylline and oxytriphylline), which are used as second- or third-line drugs.
The basic side effects of bronchodilators vary with the class of the medicine. Beta-agonist inhalers can cause rapid or irregular heartbeat, insomnia, and nervousness. Anticholinergic inhalers can cause dry mouth or headache. Methylxanthines are usually taken orally, and they can cause tremor, shakiness, nausea, and vomiting, while overdoses will cause serious problems, such as seizures and cardiac arrhythmias (NHLBI, 2007).
The smooth muscle in lung airways is relaxed by beta-2 adrenergic agonist drugs (relatives of epinephrine), which reverse and prevent further contraction of muscle cells. Beta-2 agonists have a wide array of effects throughout the body. To minimize side effects, beta-2 agonists are administered by inhalation directly to the inner lining of the airways.
Albuterol, isoetharine, isoproterenol, levalbuterol, metaproterenol, pirbuterol, and terbutaline are the short-acting beta-2 agonists used for asthma. When inhaled, they produce an effect in less than five minutes, which is as fast as could be achieved by IV or subcutaneous injections. The effect then lasts for 3 to 6 hours.
Short-acting beta-2 agonists are the recommended initial treatment for acute asthma symptoms. For intermittent asthma, short-acting beta-2 agonists are used to control symptoms, and for persistent asthma these drugs are the first step in resolving asthma attacks. Short-acting bronchodilators can also be used before exercise to prevent exercise-induced asthma symptoms.
For mild to moderate symptoms, 1 to 2 inhalations from a metered-dose inhaler (MDI) will usually bring relief. For severe attacks, 6 to 12 puffs from an MDI with an inhalation chamber are usually needed, and this dose can be repeated every 30 to 60 minutes. Equivalent doses can also be delivered by nebulizer.
Short-acting bronchodilators are not recommended for regular daily use (NHLBI, 2007; ALA, n.d.a.).
TYPICAL DOSAGES OF SHORT-ACTING BRONCHODILATORS
MDI = metered-dose inhaler
prn = as needed
Source: NHLBI, 2007.
Salmeterol and formoterol are the long-acting beta-2 agonists used for asthma. When inhaled, they are slower to produce an effect than short-acting beta-2 agonists, but their effect lasts for about 12 hours.
Long-acting beta-2 agonists are used for persistent asthma that is difficult to control, but they are always used along with an anti-inflammatory medication. When taken with inhaled corticosteroids, long-acting beta-2 agonists allow better asthma control at lower corticosteroid doses. In patients older than 12 years, long-acting beta-2 agonists are only advised as part of Step 3 or greater therapy.
Long-acting beta-2 agonists are taken via inhalation. A typical regimen includes two doses per day.
Long-acting bronchodilators should not be used as the initial drug for acute asthma attacks (NHLBI, 2007). For still-unexplained reasons, the use of long-acting beta-2 agonists is associated with a small increased risk of severe or fatal asthma attacks (Chesnutt et al., 2008).
Safety Issues with Long-Acting Beta-2 Agonists
In 2010, the U.S. Food and Drug Administration (FDA) issued a Drug Safety Communication on appropriate use of long-acting beta-2 agonists based on the risk of severe or fatal asthma attacks. These products’ labels include a warning to reflect this advisory (U.S. FDA, 2010a). The Pediatric Advisory Committee of the FDA is still investigating the use of these agents in pediatric patients. In April 2011, the FDA issued a Drug Safety Communication requiring post-market safety trials for long-acting beta-2 agonists (U.S. FDA, 2011b).
The autonomic nervous system, via the vagus nerve, uses the neurotransmitter acetylcholine to contract smooth muscle in the airways of the lung, and muscarinic receptor antagonists (i.e., anticholinergics) will reverse constriction of airways that is initiated by the autonomic nervous system (i.e., bronchospasm). On the other hand, anticholinergic drugs will not affect airway narrowing caused by histamine. Therefore, airway narrowing due to allergic reactions or exercise will not be reversed by anticholinergics. Anticholinergics may reduce the excess mucus secreted during asthma attacks.
Ipratropium bromide is the anticholinergic that is used for asthma. It is not as effective as short-acting beta-2 agonists for intermittent asthma. In the ED, ipratropium bromide is used as an adjunct to short-acting beta-2 agonists for moderate or severe asthma attacks. It is also the recommended reversal agent for bronchospasm caused by beta-blocker medicines (Chesnutt et al., 2008).
Methylxanthines, or phosphodiesterase inhibitors, are a class of molecules that have adrenergic-like effects. Caffeine is the best known of the methylxanthines.
Theophylline is a methylxanthine with a long history as an asthma medicine, but it has more side effects and is less specific than beta-2 agonists. In a sustained-release form, oral theophylline is sometimes taken in addition to inhaled corticosteroids for mild persistent asthma. However, theophylline is not on the list of preferred asthma medications, and when it is used, serum concentrations must be measured to watch for toxicity (NHLBI, 2007).
Another methylxanthine, aminophylline, is also used as a second- or third-line adjunct in asthma therapy regimens. Neither theophylline nor aminophylline are recommended as rescue medicines (NHLBI, 2007).
Corticosteroids are variants of the natural hormone cortisol. Corticosteroids dampen inflammation at the level of cell nuclei, switching off genes for inflammatory molecules such as cytokines, chemokines, and inflammatory enzymes and activating genes that have anti-inflammatory effects.
Corticosteroids are used as the main treatment for a variety of inflammatory conditions, including myositis, systemic vasculitis, rheumatoid arthritis, and systemic lupus erythematosus. Because of their widespread and sometimes powerful effects, it is preferable to use corticosteroids in low doses or in limited regions of the body.
Corticosteroids tone down inflammation and are the best available long-term controllers for persistent asthma. However, chronic use of corticosteroids can cause serious health problems, including susceptibility to infections, high blood pressure, glaucoma, diabetes, and osteoporosis. To avoid these systemic complications, patients with asthma can inhale corticosteroids. Inhalation enables delivery of a high concentration of medicine directly to the inflamed tissue (i.e., the airway linings) with only a small amount leaking into the systemic circulation.
Inhaled corticosteroids are the recommended treatment for reducing the frequency of asthma attacks and are introduced in Step 2 of the pharmacologic step plan. For asthma, the available inhaled corticosteroids are beclomethasone (QVAR), budesonide (Pulmicort Respules, Pulmicort Flexhaler), ciclesonide (Alvesco), flunisolide (Aerobid), fluticasone (Flovent), mometasone (Asmanex), and triamcinolone (Azmacort).
Side effects of inhaled corticosteroids include cough, hoarseness, and mouth or throat candida infections. These side effects can be reduced by using an MDI with some form of inhalation chamber. The newer inhaled corticosteroids, which include ciclesonide (Alvesco), fluticasone (Flovent), and mometasone (Asmanex), have fewer side effects.
The exact dose and treatment regimen varies with the patient and the specific corticosteroid. However, most patients take two inhaler treatments daily. Using MDI inhalers, patients typically take 2 puffs twice a day; using DPI inhalers, patients typically take 1 actuation twice a day. Patients should rinse their mouths of any excess medicine after each treatment.
The effect of inhaled corticosteroids on persistent asthma builds, and even with daily use, it can take a few months for the peak benefit to be reached. By treating asthma with inhaled corticosteroids early in its course, some of the long-term, irreversible airway changes may be delayed or prevented. Inhaled corticosteroids control but do not cure asthma; if the corticosteroid treatment is stopped, the symptoms will slowly return (Breekveldt-Postma et al., 2008).
Taking systemic corticosteroids for an extended period (weeks, months, or years) can cause serious problems. On the other hand, brief treatments of systemic corticosteroids usually have few long-term deleterious effects. In asthma, systemic corticosteroids, whether administered intravenously (IV) or orally, are a key treatment for moderate or severe episodes of asthma. For patients whose asthma attacks do not resolve promptly after inhalation of their rescue medicines, systemic corticosteroids will speed the widening of airways and will make a near-term recurrence less likely.
When systemic corticosteroids are used acutely to relieve an asthma attack, a continued short course of oral corticosteroids is usually prescribed. The typical drug regimen is 15 to 30 mg of prednisone twice a day for 3 to 10 days. In hospitalized patients with severe attacks, a typical drug regimen would be 1 mg/kg of prednisone every 6 to 12 hours until the patient’s PEF returns to 50% of his or her personal-best value. Prednisone is then decreased to 60 to 80 mg/day until the PEF reaches 70% of the personal-best value.
A small number—perhaps 1%—of asthma patients need long-term systemic corticosteroids to control their asthma. The physician works to find the minimum necessary dose and institutes protective measures to reduce side effects; for example, calcium supplements and vitamin D are used to slow mineral loss from bones. In addition, patients on long-term systemic corticosteroid therapy need to be monitored for osteoporosis, diabetes, hypertension, gastric ulcers, myopathies, glaucoma, cataracts, and depression. In children, the long-term use of systemic corticosteroids can suppress growth (Chesnutt et al., 2008).
Inflammatory molecules called cysteinyl-leukotrienes, or simply “leukotrienes,” cause bronchoconstriction, edema, and mast cell activation, and they play a large role in asthma symptoms. Drugs that specifically reduce the effect of leukotrienes are a relatively new addition to the arsenal of asthma medications.
Currently, there are three anti-leukotriene drugs, and they operate in one of two ways:
Each drug is available as an oral tablet. By themselves, anti-leukotrienes are effective at moderating the symptoms of persistent asthma.
Given the collateral health problems associated with long-term use of corticosteroids, it was hoped that anti-leukotrienes would be safer than inhaled corticosteroids and could replace inhaled corticosteroids in long-term asthma therapy. As the only drug in a treatment regimen, anti-leukotrienes work more slowly, although somewhat better, than inhaled corticosteroids. However, the long-term safety of anti-leukotrienes is still not clear enough to make useful comparisons with the safety of inhaled corticosteroids.
For drug regimens using two medications, the combination of an inhaled corticosteroid with a long-acting beta-2 agonist is more effective than the combination of an inhaled corticosteroid with an anti-leukotriene drug.
The current NHLBI Guidelines recommend that anti-leukotrienes should be alternative but not preferred drugs in asthma treatment regimens (Joos et al., 2008).
Safety Issues with Anti-Leukotrienes
In June 2009 the FDA and the manufacturers of Singulair, Accolate, and Zyflo announced an update of these products’ prescribing information to include a precaution about neuropsychiatric events—tremor, depression, behavior/mood changes, suicidal thinking, and behavior and suicide—that have been reported in some patients. While patients should be aware of these potential events and report them to their healthcare provider if they occur, they should not stop taking any of these medications without consulting their provider (U.S. FDA, 2009b).
Two asthma drugs, cromolyn sodium (Intal) and nedocromil (Tilade), target mast cells and make them less likely to release inflammatory molecules. This effect reduces the symptoms that are triggered by activating mast cells.
Mast cell stabilizers are useful for preventing symptoms, and they work only when taken before exercise or unavoidable exposure to allergens. These drugs will not relieve symptoms that are already present. Both cromolyn and nedocromil act for only a short time after administration, so they do not contribute to long-term asthma control. The drugs are safe, and a typical regimen includes at least 4 protective inhalations a day (Barnes, 2008).
Cromolyn sodium and nedocromil are recommended as alternative but not preferred medications for the treatment of mild persistent asthma (NHLBI, 2007).
IgE is the class of immune molecules that recognize allergens and then trigger allergic responses. Omalizumab (Xolair) is a monoclonal antibody that binds to IgE molecules and prevents them from activating mast cells or basophils. This decreases the activation of these immune cells and reduces the release of inflammatory molecules, such as histamine, prostaglandins, and leukotrienes.
Although omalizumab is expensive, it can be useful in patients with severe persistent asthma and allergies and is recommended as an adjunct therapy (added to inhaled corticosteroids) in Steps 5 and 6 of the pharmacologic plan. Omalizumab is given as a subcutaneous injection. It has the potential to induce anaphylaxis, so omalizumab should be administered only in an appropriately prepared office or clinic where the patient can be monitored for at least 30 minutes after the injection (NHLBI, 2007).
Safety Issues with Omalizumab (Xolair)
In July 2007, the FDA issued a box warning for omalizumab (Xolair), indicating a risk of anaphylaxis. Patients should be aware of this information and told that the reaction may occur 24 hours after the dose is administered. Patients should also be warned to initiate emergency self-treatment if necessary (U.S. FDA, 2007). In 2009, the FDA issued an Early Communication about an ongoing safety review of Xolair, referring to an interim study in which increased numbers of cardiovascular and cerebrovascular adverse events were observed. The FDA continues to review those findings (U.S. FDA, 2009a).
Immunotherapy is an attempt to desensitize allergic patients to specific allergens. The therapy consists of subcutaneous injections of increasing concentrations of a known allergen. Injections continue weekly or monthly for 3 to 5 years.
Immunotherapy will improve allergic rhinitis (hay fever) and certain other common allergic reactions. When the therapy works, the clinical remission of symptoms can last long after the treatments are stopped.
Besides being useful for purely allergic reactions, immunotherapy can also reduce asthma symptoms in people whose disease is triggered by allergens, and immunotherapy is one part of the long-term management plan for patients whose persistent asthma is worsened by certain allergens (Chesnutt et al., 2008). The effectiveness of immunotherapy in asthma patients has been demonstrated objectively (i.e., via controlled studies) in relation to grass, cat dander, dust mites, ragweed, and two indoor fungi, Cladosporium and Alternaria.
The caveat for immunotherapy for asthma is that there is a potential for anaphylactic reactions. Allergen injections should be administered only in an appropriately prepared office or clinic (i.e., with trained personnel and basic life support equipment, including oxygen, and intramuscular-injectable epinephrine), in which the patient can be monitored for at least 30 minutes after the injection (NHLBI, 2007). Treatments should not be given when the patient’s asthma is unstable or symptomatic, and on the day of treatment the patient’s FEV1 should be at least 70% of the predicted value (Bacharier et al., 2007).
THE COSTS OF ASTHMA MEDICATIONS
One of the most important factors affecting adherence to an asthma treatment plan is the cost of medications. In a 2005 survey sponsored by the Kaiser Family Foundation, the Harvard School of Public Health, and the newspaper USA Today, 43% of respondents with asthma said that in the past year they lacked the money to pay for their treatment, and 44% indicated that they tried to save money by not taking their medication or skipping doctor’s visits (Griffin, 2005). A 2004 study published in JAMA found a 32% reduction in medication use among people with asthma when their pharmacy co-payments doubled (Goldman, 2004).
More recent data underscore the economic pressures faced by people with asthma: the Agency for Healthcare Research and Quality (AHRQ) calculates that from 1997 to 2008 the average annual prescription drug expenses for a child with asthma more than doubled, from $349 to $838 (AHRQ, 2011). Some of that increase can be attributed to the phase-out of CFC inhalers (see below), as many patients with asthma now must use more expensive inhalers with ozone-friendly propellants or must take multiple medications to replace their discontinued, CFC-based treatments (Lavelle, 2007).
Many asthma drugs are administered by inhaler to send the medication directly to the target tissue, the inner linings of the airways of the lung. Higher concentrations of medicine can be delivered this way with fewer systemic side effects.
A variety of devices are available for delivering drugs directly into the lungs. The common aerosol devices include:
Spacers or valved holding chambers (VHCs) are often used with non-breath-activated MDIs to minimize local side effects. A spacer is a simple tube added to the mouthpiece of an MDI to move the inhaler farther from the patient’s mouth. A VHC is a spacer with a one-way valve that keeps the patient from exhaling into the MDI.
Most asthma patients use MDIs for their rescue medications. It is easiest to learn the proper use of an MDI through an in-person demonstration. However, these are the essential steps:
Administer the medicine
When inhaling your rescue medicine, wait 60 seconds between puffs. For other medicines, you do not have to wait before taking the prescribed number of puffs (Buddiga, 2011; NHLBI, 2007).
Until a few years ago, many asthma inhalers used chlorofluorocarbons (CFCs) as propellants. International agreements were made to ban CFCs because they damage the ozone layer of the atmosphere. In March 2005, as the first step in the phase-out of all asthma medication devices that use CFCs, the FDA announced that it would ban the production and sale of CFC albuterol inhalers by December 31, 2008. More recently, in April 2010, the FDA announced the phase-out of the following CFC inhalers over a 3-year period:
Additionally, in 2011 the FDA announced that Primatene Mist (epinephrine), the only over-the-counter asthma inhaler sold in the United States, would be phased out by December 31, 2011, due to its use of CFCs (U.S. FDA, 2011c).
Many asthma medications are now available in inhalers that do not use CFCs. Several inhalers, including those for albuterol, levalbuterol, flunisolide, fluticasone, and ipratropium bromide, use a safer propellant, hydrofluoroalkane (HFA) (U.S. FDA, 2011a; ALA, n.d.a.). Patients should be warned that spray from the new inhalers tastes and feels different from the CFC inhalers’ spray and that the new inhalers come with different priming and cleaning instructions (U.S. FDA, 2008).
Medicines are key components of the long-term treatment of asthma. Patients can also reduce their asthma symptoms nonpharmacologically, by controlling the triggers in their environment and by maintaining a healthy lifestyle, which includes regular exercise.
A big part of nonpharmacologic management is avoiding, neutralizing, or eliminating triggers. Triggers and aggravators of asthma include respiratory infections, inhaled substances (biological allergens, chemical vapors, smoke, and air pollutants), ingested substances, physical factors (temperature, weather, and exercise), hormonal factors, and stress.
Patient education is a nonpharmacologic tool that healthcare workers should use. Asthma cannot be controlled at a distance, so physicians and other healthcare providers must enable their patients to manage the disease minute-by-minute and day-by-day. Along with a written treatment plan, physicians should give their patients sufficient information so that:
For an established patient, doctors should look into their nonpharmacological tool kits when new problems arise. Changes in the patient’s environment or lifestyle are frequently the cause of worsening asthma. When a patient’s previously well-controlled asthma becomes increasingly symptomatic, the physician should review the patient’s life, surroundings, and lifestyle before moving the patient to a higher step on the pharmacologic step chart.
Patients will usually know many of the things that trigger or worsen their asthma symptoms. As the patient and doctor work to identify all the environmental factors that are asthma aggravators, it is helpful to give the patient a list showing the wide range of common triggers. (See “Potential Asthma Triggers” box above.)
When asthma symptoms seem to come out of the blue, the patient can keep a diary, recording the appearance of asthma symptoms and a brief description of the preceding situation and environment. In addition, allergy testing can help to identify specific allergens if it is hard to separate triggers from non-triggers that occur at the same time. Yet even with a concerted effort, some patients’ triggers cannot be identified, and their asthma symptoms must be considered as spontaneous.
With a list of triggers, aggravators, and potential triggers, the next step is to formulate a plan to reduce the patient’s exposure to these factors. Simply identifying the triggers and aggravators will help the patient to avoid them. However, some triggers take work to avoid because the patient’s surroundings may need special cleaning or the patient’s daily routines may need to be changed. Here, education is important. When they understand how their triggers work, patients are more motivated to invest the time and effort needed to control their environment (Schatz, 2008).
Particles and chemicals that are inhaled are delivered directly to the hyperreactive airways of people with asthma, and for this reason, things that are inhaled make up most of the asthma triggers and aggravators. Likewise, reducing or eliminating exposure to airborne triggers can go a long way toward lessening a patient’s asthma symptoms. Inhaled substances can be divided into biologic allergens, smoke and air pollutants, and chemical vapors.
Animal allergens are shed by warm-blooded animals—dogs, cats, rodents, and horses—that produce biologic antigens in their dander (shed skin cells) and excretions, and these allergens trigger or aggravate asthma in some patients.
Families are often too attached to household pets to remove them from the home, and the best compromise may be to reduce the patient’s contact with the pet’s allergens. Specific suggestions (not all of which have been demonstrated to be effective in controlled trials) include:
Families who choose to give up their pets should be warned that it could take up to six months for the level of household allergens to fall sufficiently to reduce the patient’s asthmatic reactions.
Dust mites are microscopic arachnids that live in piles of shed human skin cells, and they colonize beds, upholstered furniture, and carpets. Most homes in the United States have detectable levels of dust mite allergens. Dust mites are said to be the most common biologic substance that produces allergic symptoms in people with asthma.
Dust mites do not drink. Instead, they depend on absorbing water from the atmosphere. Therefore, dust mites are more numerous in humid environments. By reducing indoor humidity below 50%, asthma patients can significantly decrease the number of dust mites in their homes.
Specific suggestions for reducing contact with dust mites include:
To make an effective dent in a house’s dust mite population, all of these recommendations should be instituted. Chemical pesticides will reduce dust mite populations, but the effect is too short-lived to be effective for asthma patients.
Cockroaches are found everywhere, and cockroach sensitivity is typical of asthma patients who live in crowded cities. Specific suggestions for reducing contact with cockroach allergens include:
The major outdoor biologic allergens are seasonal mold spores and pollens from trees, grasses, and weeds. Specific suggestions for reducing contact with outdoor allergens during the pollen and mold seasons include the following:
Mold (fungi) spores, which are microscopic and smaller than pollen grains, are an asthma allergen. Indoor mold is common in humid climates and in homes that have continual areas of dampness. Indoor mold usually looks black.
Mold on a damp basement ceiling. In the house, mold usually forms black circular patches on surfaces that are continually damp. (Source: HUD, n.d.)
Specific suggestions for reducing contact with indoor mold include:
People with asthma should stop smoking, and indoor smoke should be avoided. Smoking by mothers increases the chance that their children will develop asthma, and all family members who smoke should be asked to stop or to smoke outside the house. However, even when adults attempt to smoke outdoors, children in the household are usually exposed to too much tobacco smoke. In addition, heavy smokers tend to be the least aware of their effects on children. Therefore, health workers should take the time to explain to family members the value of not smoking when their children have asthma (NHLBI, 2007).
All indoor smoke can be a problem for asthma patients. If it is at all possible, wood-burning stoves, incinerators, kerosene heaters, fireplaces, and unvented gas stoves should not be used in places where asthma patients spend time.
When the level of outdoor pollution is high, asthma patients should stay indoors as much as possible, and they should avoid exertion when they are outdoors. Asthma patients should wear dust masks when passing through areas with high levels of dust or other airborne particulates (e.g., construction sites), because particulate matter, sulfur dioxide (SO2), and nitrogen dioxide (NO2) are common triggers of asthma (Bacharier et al., 2007).
Asthma can be triggered by paint fumes, chemical fumes, aerosol products, cleaners, talcum powder, hair spray, new carpet, particle board, air fresheners, and perfumes. It is best for people with asthma to avoid all chemical vapors and particulate clouds.
Newly finished surfaces, such as new linoleum flooring, synthetic carpeting, wall coverings, new furniture, recent painting, and the interiors of new cars, can release formaldehyde and other chemical vapors. Asthma patients should be warned to be watchful, and if they begin to notice any symptoms, they should avoid newly refurbished areas (NHLBI, 2007).
When an asthma patient’s workplace has chemical vapors in the atmosphere, healthcare workers may be able to help the patient transfer to a safer work environment. In so doing, however, the medical community must be careful to protect the confidentiality of the patient’s medical records (Schatz, 2008).
It is important to protect asthma patients from job reprisals. The NHLBI Expert Panel report (NHLBI, 2007) cautions healthcare workers:
Patient confidentiality issues are particularly important in work-related asthma. Because even general inquiries about the potential adverse health effects of work exposures may occasionally result in reprisals against the patient (e.g., job loss), patients who have asthma need to be informed of this possibility and be full partners in the decision to approach management regarding the effects or control of workplace exposures. This situation may require referral to an occupational asthma specialist
INDOOR AIR CLEANERS
Although an indoor air cleaner would be a useful protection for an asthma patient, there is still not enough evidence to recommend most of the available models. Air-cleaning devices using high-efficiency particulate air (HEPA) filters or electrostatic precipitating filters do reduce allergens, but the studies to date have not shown that these products alone will reduce asthma symptoms.
The NHLBI (2007) recommends that people with asthma avoid air cleaners that generate ozone. Humidifiers and evaporative coolers are also not recommended, because the higher humidity increases the growth of mold and dust mites.
For asthma patients, air conditioning may be the most useful indoor air device. Air conditioning allows windows to be closed and outside air pollution to be kept at a distance. Air conditioning also keeps humidity levels low. A dehumidifier is another useful device. Dehumidifiers can be used year-round to keep the indoor humidity between 40% and 50%, a level that discourages dust mites.
Most vacuum cleaners are the inverse of air cleaners and cause problems for asthma patients. Patients who may be sensitive to house dust or other house allergens should not use conventional vacuum cleaners, and they should stay out of rooms being vacuumed because the allergens get blown into the air and spread through the room. If the patient must vacuum, he or she can wear a dust mask or use a vacuum cleaner designed to avoid spreading dust (i.e., a vacuum cleaner fitted with a HEPA filter or a double bag) (NHLBI, 2007).
Respiratory infections are common triggers for asthma patients. Colds and other viruses are hard to avoid. However, immunization is available against the major yearly influenza strains. Flu shots—injections of inactivated influenza—are recommended for asthma patients older than 6 months of age, with the goal of preventing the serious asthma attacks that can develop during an influenza infection. Importantly, intranasal influenza vaccine (e.g., FluMist) should not be given to patients with asthma (CDC, 2011c).
There are very few foods that cause asthma symptoms. On the other hand, some people react to sulfites, which are preservatives used in processed potatoes, shrimp, dried fruits, wine, and beer. Sulfites have triggered severe asthma attacks in some asthma patients. Asthma sufferers who suspect that they react to sulfites should therefore avoid foods and beverages containing this preservative.
People with asthma are likely to have atopy. Allergies to foods, such as peanuts or shellfish, can cause a severe whole-body reaction (anaphylaxis) that includes asthma symptoms. Anaphylaxis can be fatal in anyone, even people who do not have asthma. Anyone with food allergies should avoid the problem foods entirely (NHLBI, 2007).
Patients often suspect that particular foods or food additives worsen their asthma symptoms. Shellfish, nitrites, food coloring, artificial sweeteners, and dairy products are commonly mentioned in this context. Studies of large populations have not found that these items are general asthma triggers. However, most large studies cannot ferret out individual variants in asthma susceptibility, and anecdotal evidence supports the idea that people may have their own idiosyncratic sensitivities.
Patients who suspect that there are problem foods in their diet should be encouraged to try a scientific experiment by removing individual items from their diets and recording the effect on their asthma symptoms. Extreme diets should be discouraged, and when dairy products are removed from their diet, patients should consider adding calcium supplements.
Nonselective beta-blockers can cause bronchoconstriction. These drugs will also make any pre-existing airway constriction difficult to reverse with beta-2 agonist rescue medicines. Therefore, as a rule, asthma patients should avoid taking nonselective beta-blockers, which include:
Patients with asthma can sometimes take cardio-selective beta-blockers (such as atenolol [Tenormin] and metoprolol [Lopressor, Toprol XL]), but any beta-blocker should be used with caution (NHLBI, 2007).
Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) can trigger severe or even fatal attacks in certain asthma patients, most commonly those with nasal polyps and chronic sinusitis. (An estimated 20% of adult asthma patients and 5% of children with asthma have aspirin sensitivity.) Asthma patients who have shown any sensitivity to these drugs should avoid them. Patients who have severe persistent asthma or nasal polyps appear to have a higher risk of developing aspirin or NSAID sensitivity (NHLBI, 2007). Acetaminophen is usually a safe alternative pain reliever for people with asthma.
Although the goal of long-term asthma treatment is to allow patients to continue in a wide range of activities, there are limits, and asthma patients may have to take more precautions than their companions. This can be hard for children and adolescents to accept. A patient’s control medications, however, should be adequate to allow all normal activities.
Aerobic exercise is needed for patients to remain healthy, and studies have shown that regular exercise and physical training will improve a patient’s degree of asthma control (NHLBI, 2007). People with asthma tend to be less physically fit than their peers; however, with regular training the fitness differences between people with asthma and people without asthma are reduced. Regular aerobic exercise of large muscles is recommended for most asthma patients (Juvonen et al., 2008).
During or after exercise asthma patients can develop bronchoconstriction, with coughing, wheezing, shortness of breath, and chest tightness. In some patients, exercise may be the only trigger for their asthma. The asthmatic reaction to exercise appears to be caused by hyperventilation, which temporarily lowers the humidity and the air temperature in the airways, thus making the airway mast cells more likely to release histamine. Activity in cold and windy weather is thus especially likely to bring on asthma symptoms, and in the winter many patients find it safest to do their strenuous exercising indoors.
For short periods of exercise (say, 10 minutes), the bronchoconstriction often comes approximately 5 minutes after the exercise has ended. The airway obstruction then peaks in 10 to 15 minutes, and it slowly resolves spontaneously after 30 to 60 minutes of rest.
Harder or longer exercise will bring on the symptoms earlier, and the episode will resolve more slowly. A pre-exercise warm-up and a facemask or scarf in cold weather can reduce asthma symptoms. In addition, training will reduce the symptoms (Carlsen et al., 2008).
Inhaled beta-2 agonists prevent exercise-induced asthma in more than 80% of susceptible patients. Specifically, short-acting beta-2 agonists taken 10 to 15 minutes before exercise will control the symptoms for 2 to 3 hours for most asthma patients. Pre-treatment with long-acting beta-2 agonists can last for 12 hours but becomes less effective for this purpose when used regularly. (Asthma patients who do not improve with pre-treatment should be evaluated for allergic asthma or additional underlying health problems.) Training will also reduce exercise-related asthma symptoms, and well-trained asthma patients can be successful in competitive sports (Szefler, 2008).
In the long-term treatment plan, exercise-induced asthma is best controlled using inhaled corticosteroids. Recently, anti-leukotriene drugs have been used as alternatives to inhaled corticosteroids. For a short-term effect, the anti-leukotriene drugs can take a few hours to be effective, and the drugs seem to work for about half of asthma patients with exercise-induced asthma (NHLBI, 2007).
Stress, anxiety, and depression make asthma harder to control, and these conditions should be identified and professionally treated. Psychological problems in the family can be as stressful for patients as their own personal problems. This is especially true for children, in whom the frequency of asthma attacks has been correlated with the presence of clinical depression in the parents (Wolf et al., 2008).
Stress- and anxiety-relieving therapies have been beneficial to asthma patients. Psychologists and mental health counselors can teach breathing and relaxation techniques that patients can continue to use at home and at work when needed. Guided imagery and hypnosis therapies are other available tools. Some psychologists have found it helpful for their asthma patients to keep weekly journals in which they record the stressors and the asthma symptoms that occur in their lives (NHLBI, 2007).
Diet is one thing that people can control, and patients are always hopeful that changes in their diet will lessen their asthma. For this reason, the most common alternative therapies for asthma involve dietary changes. NHLBI guidelines (2007) recommend that patients concentrate on eating healthfully, which usually means eating more fruits, vegetables, and whole grains while eating less saturated and trans fats, salt, and added sugar. Staying trim is an additional helpful goal, because overweight people are more likely to develop asthma (Morris, 2011).
There is some evidence that antioxidant vitamins and omega-3 fatty acids may decrease the severity of asthma symptoms, but “no conclusive evidence shows that any dietary factors prevent or exacerbate the disease” (NHLBI, 2007).
CECILIA, AGE 35
Cecilia Montgomery is a 35-year-old woman who has had asthma since she was a teenager, with varying success at controlling her disease. She is meeting with the office nurse, who is counseling her on avoiding her asthma triggers. The nurse gives Celia an asthma management diary, with instructions on recording on a daily basis her symptoms and possible exposure to triggers and aggravators. The nurse also gives Cecilia some educational brochures on devices she can use at home, such as a dehumidifier and an air-cleaning device with a HEPA filter, and recommends that she use these devices in conjunction with air conditioning. The nurse also recommends yearly flu shots and counsels Cecilia on how best to avoid biologic allergens, smoke and air pollutants, and chemical vapors. The nurse warns Cecilia to be careful about consumption of shellfish, peanuts, and sulfite-containing foods, which may trigger an asthmatic reaction. Finally, the nurse counsels Cecilia on ways to reduce the stress in her life, noting how stress can aggravate asthma symptoms.
Internists and family practitioners are able to handle most asthma patients. Asthma specialists are available for consultation when necessary.
Referral to a pulmonologist is suggested for patients with:
Referral to a fellowship-trained allergist or immunologist is suggested for patients with:
Referral to an otolaryngologist is suggested for patients with:
Referral to a mental health professional is suggested for patients with:
Healthcare workers must always add a patient’s asthma into the mix of factors to be balanced in the care of their patients. Healthcare must be individualized, but there are some useful general guidelines for dealing with certain populations of asthma patients. Two groups of asthma patients who deserve special comment are children and pregnant women.
After puberty (approximately 12 years of age), children with asthma are treated much like adults. In younger children, there are some additional cautions and considerations (Szefler, 2008).
Different criteria are needed to categorize the severity of a young child’s asthma symptoms. One well-documented scale for scoring the severity of asthma symptoms in preschool children is the Preschool Respiratory Assessment Measure (PRAM) (Ducharme et al., 2008). This tool rates a child’s asthma on a 4-point severity scale, using simple observations of:
For children 5 years of age and older, inhaled corticosteroids are the drug of choice for long-term management. On the other hand, the use of high-dose inhaled corticosteroids or systemic (oral) corticosteroids can suppress growth or cause eye problems in children. (All children with asthma, regardless of the drugs they are taking, should have their height and weight measured at each office visit.)
For children, long-acting beta-2 agonists should only be used when paired with an inhaled corticosteroid.
In children with persistent asthma, montelukast (Singulair) can be used as an alternative first-line treatment. Montelukast is also recommended as an adjunct to inhaled corticosteroids when needed. For children 2 to 5 years of age, montelukast has been suggested as an initial treatment for viral-induced wheezing.
With children, it is important to find an inhaler that they will use. It is helpful to offer a number of varieties and let the child pick his or her favorite.
Children have a poor rate of adhering to treatment plans, and extra effort is needed to encourage their compliance. For children, the reports from their home use of peak flow meters are not always accurate, so regular office testing (spirometry) should be done at least once a year.
It is important for children to get exercise and to remain part of normal activities. Teachers and coaches should be informed about children who have exercise-induced asthma and should be reassured (when appropriate) that with a pre-exercise inhaler treatment, the child will be safe.
Diagnosis is less clear-cut and treatment recommendations are still in flux for children ages 0 to 2 years. Infants with persistent asthma (mild to severe) have been effectively treated with nebulized budesonide (a corticosteroid). An experienced pediatric asthma specialist is the best resource for this age group.
Asthma spontaneously goes into remission in many children during adolescence. It is still unclear whether any treatment program can change the innate course of a child’s asthma (Spahn & Covar, 2008).
DAVID, AGE 4
Marla Henderson has brought her 4-year-old son David to the pediatrician, as David was recently diagnosed with asthma. The office nurse shares with Marla the results of David’s PRAM assessment, which indicates asthma of moderate severity. The physician has prescribed montelukast to control David’s wheezing, and the nurse spends several minutes with David to show him how to use his new inhaler. She also counsels Marla to be alert to any exercise-induced exacerbations of David’s asthma and urges her to schedule a follow-up visit for repeat spirometry testing within the year.
Asthma is a common and potentially serious complication of pregnancy. Keeping asthma in a well-controlled state is important to avoid low birthweight or premature infants.
During pregnancy, asthma symptoms improve in some women and worsen in others, so the asthma status of pregnant women should be monitored regularly. For pregnant women with moderate or severe persistent asthma, ultrasound examinations and antenatal fetal testing should be considered (Whitty & Dombrowski, 2007).
The same step plan used for long-term medical management of asthma in other adults is recommended for pregnant women. A few caveats include:
For asthma attacks, extra caution is taken to avoid hypoxemia of the fetus. Typical rescue therapy is 2 to 6 puffs of inhaled albuterol or nebulized albuterol at 20-minute intervals. Treatment should be begun as soon as any symptoms arise or when the woman finds a 20% decrease in her PEF. A good response includes reduced symptoms and a PEF >80% of her personal-best value. Regardless of other considerations, if two rescue treatments do not produce a good response or if the fetus becomes less active, the woman should quickly get medical help.
When a pregnant woman is being treated in the ED or hospital for asthma symptoms, the primary goal is to prevent hypoxemia, and the well-being of the fetus should be monitored if it is old enough for an assessment. As a rule, “patients with FEV1 or PEF measurements greater than or equal to 70% sustained for 60 minutes after last treatment, no distress, and reassuring fetal status may be discharged” from the ED (Dombrowski et al., 2008).
During labor, asthma medications should be continued, women should be well hydrated, and adequate analgesia should be given. Certain medications should be avoided, if possible. These include:
All asthma patients should have an asthma assessment and evaluation before surgery. As a rule, a patient with well-controlled asthma can have general anesthesia with intubation, although asthma patients are more likely to develop respiratory complications during and after surgery. Those asthma patients who have been taking systemic or high-dose inhaled corticosteroids may be at risk for adrenal insufficiency from the stress of surgery.
Asthma patients should schedule dental procedures for late morning, when asthma attacks are less likely. They should bring their rescue medicines, and some dentists recommend taking a prophylactic inhalation at the beginning of the appointment. Patients can be asked to bring their peak flow meters so that it can be ascertained that their PEF is greater than 80% of their personal-best value. During dental procedures, pulse oximetry can be used to identify a drop in oxygen saturation that would warrant oxygen supplementation or other intervention.
Outpatient general anesthesia is contraindicated for asthma patients. Oral premedication with small doses of short-acting benzodiazepines can reduce a patient’s anxiety. Drugs to be avoided include barbiturates, narcotics (especially meperidine), drugs with sulfites (notably, local anesthetics that include epinephrine or levonordefrin), aspirin, and NSAIDs. Patients taking theophylline should not be given macrolide antibiotics such as azithromycin or erythromycin. Odorous substances, such as methyl methacrylate, should be removed from the dental treatment room (Little et al., 2007).
Dental offices should be equipped with oximeters, positive-flow oxygen, and epinephrine.
Asthma often worsens during travel. Patients most likely to have problems are those who were using their rescue medicines at least three times a week before traveling or those whose travels involve significant exercise, such a long hikes. Other factors associated with increased asthma symptoms are exposure to smoke or air pollution and travel to very high altitudes.
Asthma patients planning extensive travel should be medically evaluated before leaving. Those patients planning wilderness trips should take a variety of asthma treatment medications, including epinephrine. Good physical conditioning is a valuable preventive (Olson & Nimec, 2007).
Asthma is an obstructive lung disease in which patients have repeated episodes of coughing, wheezing, and difficulty breathing. In an asthma patient, the airways of the lungs are excessively reactive to irritants (called triggers) and respond by narrowing, swelling, and filling with mucus. This disabling response can usually be reversed by inhaling a short-acting bronchodilator medication.
Asthma is a common problem, and approximately 8% of Americans have the disease. Often, asthma first shows up in childhood, although it can appear at any age. Currently, there is no cure, but the symptoms disappear on their own in a significant number of patients, especially during their teenage years.
Asthma varies in its severity, but a common feature of the disease is the lungs’ sensitivity to stimuli that do not produce symptoms in people with normal lungs. The irritants that trigger asthma can include dust, chemical vapors, exercise, sudden changes in the air temperature or humidity, allergens, psychological stress, or certain medicines, such as aspirin.
Between exacerbations, an asthma patient may have no noticeable breathing difficulties, although measurements of lung function will show an increase in the time that it takes the patient to forcefully empty his or her lungs. However, during an exacerbation or attack, the patient develops a marked airflow obstruction that makes breathing difficult and which, in extremely severe cases, can be fatal.
Mild and intermittent asthma attacks can usually be treated with a pocket inhaler of a beta-2 agonist bronchodilator. Severe attacks need medical attention, and they are treated with bronchodilators, oxygen, and oral corticosteroids.
The best prevention of asthma attacks is long-term treatment with inhaled corticosteroids plus careful avoidance of contact with the patient’s triggers. The specific regimen of controller medications (such as inhaled corticosteroids) must be tailored to the severity of the patient’s underlying disease. A 6-step pharmacologic protocol has been developed by the National Heart, Lung, and Blood Institute as a guide for prescribing effective medication at the minimal necessary dose.
At one time, the focus of asthma treatment was on avoiding or quickly treating attacks. Recently, with the realization that asthma is a chronic inflammatory condition, the goal has also been to control and damp down the inflammation so that the daily life of an asthma patient can include as wide a variety of activities as possible.
Health professionals who advise patients over the telephone should know straightforward answers to basic questions. Here are some common questions and suggested answers about asthma (ALA, 2010a and b; ALA, 2011c).
Q:I think I’m having an asthma attack, what should I do?
Q:I have asthma and I use an inhaler once or twice a week for my symptoms. I just started breastfeeding my new baby. Is she going to be hurt by my medicines? Should I stop breastfeeding?
A:No. Only small amounts of inhaled asthma medicines get into breast milk, so your baby should be safe.
Q:We have a pet dog, and my 6-year-old son has asthma. Do we have to get rid of our dog?
A:Not everyone gets asthma symptoms from a pet. If you have seen instances where contact with your dog causes your son to wheeze, cough, or have difficulty breathing, then you should ask your doctor or an allergist for advice. They can test your son to see if dogs are likely to be a problem for him. It is always possible that the dog is not directly the problem but is, instead, getting some asthma-producing substance, such as pollen or mold, on its fur.
Once you are convinced that your dog does trigger asthma symptoms in your son, you and your doctor should decide how seriously these symptoms affect your son’s life. For mild symptoms, you can reduce the contact that your son has with your dog. The animal should be kept out of your son’s bedroom and off upholstered furniture. Bedrooms are the most important areas to keep clean, and you can buy a HEPA cleaner for your son’s bedroom.
If you decide to give the dog away, be patient. It can take up to 6 months for all the dog “dust” (i.e., dander) to be cleaned out of a household.
Q:Should I be taking any special vitamins for my asthma?
A:Some people have found that vitamin C supplements (250–500 mg, 1–2 times/day) reduce asthma symptoms. Vitamin B6 supplements (100–200 mg/day) have also been reported to decrease episodes of wheezing; however, check with your doctor before taking this vitamin because high doses (more than 500 mg/day) or prolonged use of vitamin B6 may cause nerve problems. Recent studies have indicated that vitamin D deficiency may be associated with poor control of asthma (Sutherland et al., 2010; Brehm et al., 2009).
While not a vitamin, omega-3 fatty acids may reduce asthma symptoms. Omega-3 fatty acids are found in cold-water oily fish such as mackerel, sardines, herring, salmon, and cod. They are also found in flaxseed oil, canola oil, and soy oil. You can also buy fish oil capsules, and the usual dose is 500 mg, 2-3 times a day. The positive effects of omega-3 fatty acids can take months to appear (NHLBI, 2007).
Q:Are there any good herbal remedies that I should try for my asthma?
A:There still aren’t many scientifically sound studies on herbal remedies for asthma, so asthma experts do not yet recommend any herbal treatments.
The medical community is always hesitant about recommending herbal products because they are not standardized and they can have a variety of ingredients. Moreover, some components in herbal products can be dangerous or can interact with your regular medicines.
On the other hand, some of the herbal treatments contain chemicals that are available as medicines. If you check with your doctor, you can find whether a purified and exactly measured dose of this medicine might be helpful for you.
Q:What is asthma?
A:Asthma is a disease that causes episodes of difficult breathing. In most people, asthma is not noticeable until something triggers an attack. Then, the person’s airways tighten, the patient begins to wheeze and cough, and the patient finds it hard to get enough air.
People differ in what things trigger theses flares in their asthma. Common triggers include colds and other respiratory infections, cigarette smoke, exercise, cold air, and allergens such as pollen and mold.
Most asthma attacks can be relieved by inhaling a few puffs of a bronchodilator that asthma patients carry as a “rescue medicine.” Some asthma attacks, however, as so severe that the patient must go to an emergency department to get oxygen and additional medicines.
Q:What’s the difference between allergies and asthma?
A:Allergies are over-reactions of the immune system. They occur when susceptible people come in contact with particular things called “allergens,” such as pollen, insect stings, peanuts, or latex. Hay fever, for example, is an allergy to pollens. Allergic reactions vary, ranging from itchy eyes to skin rashes to swelling (hives). The most severe allergic reaction, which is called anaphylaxis, can put a person into life-threatening shock, with low blood pressure, poor blood circulation, and difficulty breathing.
Asthma is also an over-reaction of the immune system, but in asthma, the reaction occurs in the airways of the lungs. Asthma’s symptoms are always breathing problems, such as wheezing, coughing, chest tightness, and difficulty getting enough air. Many people with asthma are especially prone to allergies, and for them, allergens that get into their lungs (pollen, animal dander, mold spores) will trigger lung symptoms. On the other hand, people with asthma may not have allergies and may not have their symptoms set off by allergens. Similarly, people with allergies need not have asthma.
Q:How serious is asthma?
A:For some people, asthma can be a serious and continuing health problem, and without proper medicines, an asthma attack can even be fatal. On the other hand, with the appropriate medical care, people with asthma can live normal, active lives.
Q:What causes an asthma attack?
A:Asthma is a chronic disease. This means that airways in the lungs of a person with asthma are always inflamed and unusually sensitive. Sometimes, however, the disease is triggered and the person’s airways over-react and constrict. At this point, the person gets symptoms, such as wheezing, coughing, chest-tightness, and difficulty breathing. These sudden over-reactions are called “attacks.”
Asthma attacks can happen for no apparent reason, but there are also certain triggers that will usually set off a patient’s disease. The triggers vary from person to person, but some common triggers include pollen, mold, chemical vapors, dust, smoke, sudden cold air, exercise, and stress.
Q:Can older people get asthma?
A:Yes. A person’s asthma can last one’s whole life, and sometimes asthma first shows up when a person is elderly. In the United States, 2.9 million people older than 65 years have asthma (ALA, 2011b).
Middle-aged and older people who have been long-time smokers sometimes develop chronic obstructive pulmonary disease (COPD). Asthma and COPD can have similar symptoms. At times, it can be difficult to distinguish between the two diseases, but both need medical care.
Q:Is asthma contagious?
A:No. However, asthma runs in families, so it wouldn’t be surprising to find that more than one person living in the same house has asthma.
Q:Can asthma be cured?
A:At the moment, there is no way to make asthma symptoms go away permanently, although many children lose their asthma symptoms spontaneously as teenagers, and some of these children never have symptoms again. Today’s asthma treatments don’t cure the disease. Instead, they keep the disease under control so the asthma patient can live a normal life with as few restrictions as possible.
Q:How is asthma treated?
A:Some people’s asthma produces symptoms only occasionally, and these symptoms can be relieved by inhaling a bronchodilator medicine. Other people keep their asthma symptoms under control by taking daily medicines, which are usually inhaled so that the drugs can get directly into the lungs.
People’s asthma symptoms are often triggered by particular things, such as dust, smoke, or sudden cold wind. Therefore, asthma patients learn to avoid the triggers, to remove the triggers from their environment, or to protect themselves with medicine before coming in contact with the triggers.
Q:I’ve heard that people with asthma can’t exercise. Is that true?
A:Regular exercise is important for everyone’s health, even people with asthma. Some asthma patients get symptoms during or after hard exercise. By inhaling a protective bronchodilator before exercising, these people prevent the symptoms from developing. In addition, physical training reduces the asthmatic response to exercise, and well-conditioned asthma patients can become top competitive athletes.
Q:Does acupuncture treatment reduce asthma symptoms?
A:The medical studies that are currently available haven’t found any evidence that acupuncture is helpful for asthma.
Q:Are there any medicines that are bad for asthma?
A:Some medicines may cause problems for people with asthma. If you are taking any of the following medications, check with your doctor to see if they could cause problems in your particular case:
Q:I heard that some kind of insect—dust mites—might be making my asthma symptoms worse. What’s a dust mite?
A:Dust mites are microscopic relatives of spiders. They live in most houses and like warm, damp climates. Dust mites eat bits of leftover skin, which are always falling off our bodies, especially into things that we rub against, such as beds and furniture.
You probably can’t get rid of all your dust mites, but you can keep their numbers down by regular cleaning. Wash your bedding weekly in water hotter than 130° F. Put special allergen-impermeable dust covers on your pillows and mattresses. Don’t lie or sleep on upholstered furniture. Remove the carpets in your bedroom, and take up any carpets in your house that are laid on concrete. Then, dehumidify your house, ideally to below 50% humidity.
Q:Where can I get good information about asthma?
On the Internet:
Allergy and Asthma Network/Mothers of Asthmatics (AANMA)
American Lung Association
Asthma and Allergy Foundation of America
Asthma Control Test (ACT)
Centers for Disease Control and Prevention (CDC) Asthma Information
CDC Asthma Data and Surveillance
CDC’s National Asthma Control Program
National Heart Lung and Blood Institute (NHLBI) Asthma Information
NHLBI: Outline of a typical asthma action plan
NHLBI: Wallet card for asthma patients
Profiler Treatment Option Tool for Asthma: Interactive website for patients
Agency for Healthcare Research and Quality (AHRQ). (2011). Drug expenses for children with asthma more than doubled in 10 years. AHRQ News and Numbers, July 28. Retrieved October 2011 from http://www.ahrq.gov/news/nn/nn072811.htm.
Akinbami LJ, Moorman JE, Liu X. (2011). Asthma prevalence, health care use, and mortality: United States, 2005–2009. National Health Statistics Reports, 32(January 12), 1–15. Retrieved July 2011 from http://www.cdc.gov/nchs/data/nhsr/nhsr032.pdf.
American Academy of Allergy, Asthma & Immunology (AAAAI). (2011). Diseases 101: asthma. Retrieved July 2011 from http://www.aaaai.org/patients/gallery/asthma.asp.
American Lung Association (ALA). (2011a). Asthma medicines. Retrieved July 2011 from http://www.lungusa.org/lung-disease/asthma/living-with-asthma/making-treatment-decisions/asthma-medicines.html.
American Lung Association (ALA). (2011b). Trends in asthma morbidity and mortality. Retrieved July 2011 from http://www.lungusa.org/finding-cures/our-research/trend-reports/asthma-trend-report.pdf.
American Lung Association (ALA). (2011c). Understanding asthma. Retrieved July 2011 from http://www.lungusa.org/lung-disease/asthma/about-asthma/understanding-asthma.html.
American Lung Association (ALA). (2010a). Asthma in adults fact sheet. Retrieved August 2011 from http://www.lungusa.org/lung-disease/asthma/resources/facts-and-figures/asthma-in-adults.html.
American Lung Association (ALA). (2010b). Asthma and children fact sheet. Retrieved July 2011 from http://www.lungusa.org/lung-disease/asthma/resources/facts-and-figures/asthma-children-fact-sheet.html#4.
American Lung Association (ALA). (n.d.a.). Asthma medicines chart. Retrieved August 2011 from http://www.lungusa.org/assets/documents/ASTHMAMEDICINECHART.pdf.
American Lung Association (ALA). (n.d.b.). Measuring your peak flow rate. Retrieved August 2011 from http://www.lungusa.org/lung-disease/asthma/living-with-asthma/take-control-of-your-asthma/measuring-your-peak-flow-rate.html.
Arnold DH, Gebretsadik T, Minton PA, et al. (2008). Assessment of severity measures for acute asthma outcomes: a first step in developing an asthma clinical prediction rule. American Journal of Emergency Medicine, 26, 473–79.
Bacharier LB, Boner A, Carlsen KH, et al. (2007). Diagnosis and treatment of asthma in childhood: a PRACTALL consensus report. Allergy, 63(1), 5–34.
Barnes PJ. (2008). Asthma. In AS Fauci, et al. (Eds.), Harrison's principles of internal medicine (ch. 248) (17th ed.). New York: McGraw-Hill.
Birnbaum S & Barreiro TJ. (2007). Methacholine challenge testing: identifying its diagnostic role, testing, coding, and reimbursement. Chest, 131, 1932–5.
Braido F, Baiardini I, Ghiglione V, et al. (2008). Sleep disturbances and asthma control: a real life study. Asian Pacific Journal of Allergy and Immunology, 26, 27–33.
Breekveldt-Postma NS, Koerselman J, Erkens JA, et al. (2008). Treatment with inhaled corticosteroids in asthma is too often discontinued. Pharmacoepidemiology and Drug Safety, 17, 411–422.
Brehm JM, Celedon JC, Soto-Quiros ME, et al. (2009). Serum vitamin D levels and markers of severity of childhood asthma in Costa Rica. American Journal of Respiratory and Critical Care Medicine, 179(9), 765–71.
Buddiga P. (2011). Use of metered dose inhalers, spacers, and nebulizers. eMedicine. Retrieved August 2011 from http://emedicine.medscape.com/article/1413366-overview#aw2aab6b4aa.
Burr ML, Matthews IP, Arthur RA, et al. (2007). Effects on patients with asthma of eradicating visible indoor mold: a randomized controlled trial. Thorax, 62, 766–771.
Carlsen KH, Anderson S, Bjermer L, et al. (2008). Treatment of exercise-induced asthma, respiratory and allergic disorders in sports and the relationship to doping: Part II of the report from the Joint Task Force of European Respiratory Society (ERS) and European Academy of Allergy and Clinical Immunology (EAACI) in cooperation with GA2LEN. Allergy, 63(5), 492–505.
Centers for Disease Control and Prevention (CDC), National Center for Injury Prevention and Control, Division of Unintentional Injury Prevention. (2011a). Unintentional drowning: fact sheet. Retrieved July 2011 from http://www.cdc.gov/HomeandRecreationalSafety/Water-Safety/waterinjuries-factsheet.html.
Centers for Disease Control and Prevention (CDC). (2011b). Vital signs: asthma prevalence, disease characteristics, and self-management education—United States, 2001–2009. Morbidity and Mortality Weekly Report, 60(17), 547–552.
Centers for Disease Control and Prevention (CDC). (2011c). Seasonal influenza: Flu and people with asthma. Retrieved August 2011 from http://www.cdc.gov/flu/asthma/.
Centers for Disease Control and Prevention (CDC). (2010). National Center for Health Statistics. Behavioral risk factor surveillance survey, 2000–2009. Analysis performed by the American Lung Association Research and Program Services Division.
Centers for Disease Control and Prevention (CDC). (2009). Asthma: A presentation of asthma management and prevention (slide presentation and speaker notes). Retrieved July 2011 from http://www.cdc.gov/asthma/speakit/.
Chesnutt MS, Murray JA, Prendergast TJ. (2008). Pulmonology: asthma. In SJ McPhee, MA Papadakis, and LM Tierney Jr. (Eds.), Current medical diagnosis & treatment 2008 (47th ed.). New York: McGraw-Hill.
Cincinnati Children’s Hospital Medical Center. (2009). Chest/lungs treatments: peak flow meter. Retrieved August 2011 from http://www.cincinnatichildrens.org/health/info/chest/treat/peak.htm.
Dombrowski MP, Schatz M, ACOG Committee on Practice Bulletins-Obstetrics. (2008). ACOG practice bulletin: clinical management guidelines for obstetrician-gynecologists, number 90, February 2008: Asthma in pregnancy. Obstetrics & Gynecology, 111(2 part 1), 457–464.
Ducharme FM, Chalut D, Plotnick L, et al. (2008) The Pediatric Respiratory Assessment Measure: a valid clinical score for assessing acute asthma severity from toddlers to teenagers. Journal of Pediatrics, 152(4), 476–80.
Ferguson BJ. (2008). Environmental controls of allergies. Otolaryngologic Clinics of North America, 41(2), 411–17.
Goldman DP, Joyce GF, Escarce JJ, et al. (2004). Pharmacy benefits and the use of drugs by the chronically ill. JAMA, 291, 2344–50.
Gordon BR. (2008). Asthma history and presentation. Otolaryngologic Clinics of North America, 41(2), 375–85.
Greer FR, Sicherer SH, Burks AW. American Academy of Pediatrics Committee on Nutrition, American Academy of Pediatrics Section on Allergy and Immunology. (2008). Effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, timing of introduction of complementary foods, and hydrolyzed formulas. Pediatrics, 121(1), 183–91.
Grenier P. (2008). Large airway disease and chronic airflow obstruction. In A Adams & AK Dixon (Eds.), Grainger and Allison's diagnostic radiology (ch. 16) (5th ed.). Philadelphia: Churchill Livingstone.
Griffin RM. (2005). Lowering the costs of asthma treatment. WebMD Asthma Health Center. Retrieved October 2011 from http://www.webmd.com/asthma/features/lowering-costs-asthma-treatment.
Haggerty CL, Ness RB, Kelsey S, Waterer GW. (2003). The impact of estrogen and progesterone on asthma. Annals of Allergy, Asthma & Immunology, 90(3), 284–91.
Hall WJ & Ahmed B. (2007). Pulmonary disorders. In EH Duthie Jr., PR Katz, ML Malone (Eds.), Practice of geriatrics (ch. 40)(4th ed.). Philadelphia: Saunders.
Hankinson JL, Odencrantz JR, Fedan KB. (1999). Spirometric reference values from a sample of the general U.S. population. American Journal of Respiratory and Critical Care Medicine, 159, 179–87.
Jaakkola JJ & Gissler M. (2007). Are girls more susceptible to the effects of prenatal exposure to tobacco smoke on asthma? Epidemiology, 18, 573–6.
Jaakkola JJ, Piipari R, Jaakkola MS. (2003). Occupation and asthma: A population-based incident case-control study. American Journal of Epidemiology, 158, 981–7.
Joos S, Miksch A, Szecsenyi J, et al. (2008). Montelukast as add-on therapy to inhaled corticosteroids in the treatment of mild to moderate asthma: a systematic review. Thorax, 63, 453–62.
Juvonen R, Bloigu A, Peitso A, et al. (2008). Training improves physical fitness and decreases CRP also in asthmatic conscripts. Journal of Asthma, 45(3), 237–42.
Kelly WF III. (2011). Allergic and environmental asthma. eMedicine. Retrieved July 2011 from http://emedicine.medscape.com/article/137501-overview.
Khalili B, Boggs PB, Bahna SL. (2007). Reliability of a new hand-held device for the measurement of exhaled nitric oxide. Allergy, 62, 1171–74.
Kolski GB. (2008). Asthma in children. In RE Rakel and ET Bope (Eds.), Conn's current therapy 2008 (ch. 190) (60th ed.). Philadelphia: Saunders.
Korn S, Telke I, Kornmann O, Buhl R. (2010). Measurement of exhaled nitric oxide: comparison of different analysers. Respirology, 15(8), 1203–8.
Lavelle M. (2007). Asthma’s new expense: phaseout of inhaler leaves patients gasping with sticker shock. U.S. News & World Report, August 19. Retrieved October 2011 from http://health.usnews.com/usnews/health/articles/070819/27asthma.htm.
Little JW, Falace DA, Miller CS, Rhodus NL. (2007). Pulmonary disease. Dental management of the medically compromised patient (ch. 7) (7th ed.). Philadelphia: Mosby.
Mahut B, Trinquart L, Delclaux C. (2011). Influence of age on the risk of severe exacerbation and asthma control in childhood. Journal of Asthma, 48(1), 65–8.
Martin AJ, Landau LI, Phelan PD. (1980). Lung function in young adults who had asthma in childhood. American Review of Respiratory Disease, 122(4), 609–16.
Mastronarde JG, Wise RA, Shade DM, et al. (2008). Sleep quality in asthma: results of a large prospective clinical trial. Journal of Asthma, 45(3), 183–89.
McCook A. (2011). Asthma prevalence up 12% in last decade: CDC. Medscape Medical News, May 3. Retrieved July 2011 from http://www.medscape.com/viewarticle/741989.
McHugh MK, Symanski E, Pompeii LA, Declos GL. (2010). Prevalence of asthma by industry and occupation in the U.S. working population. American Journal of Industrial Medicine, 53(5), 463–75.
MedicineNet.com. (n.d.). Asthma medications. Retrieved February 2011 from http://www.medicinenet.com/asthma/focus.htm.
Miller MR, Hankinson J, Brusasco V, et al. (2005). Standardisation of spirometry. European Respiratory Journal, 26, 319–38.
Moore WC. (2008). Update in asthma 2007. American Journal of Respiratory and Critical Care Medicine, 177, 1068–73.
Morris MJ. (2011). Asthma. eMedicine. Retrieved July 2011 from http://emedicine.medscape.com/article/296301-overview.
National Heart Lung and Blood Institute (NHLBI). (2011). What is asthma? Retrieved July 2011from http://www.nhlbi.nih.gov/health/health-topics/topics/asthma/.
National Heart Lung and Blood Institute (NHLBI). (2007). Expert panel report 3 (EPR3): guidelines for the diagnosis and management of asthma. NIH Publication No. 07-4051. Retrieved July 2011 from http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm.
Nunn AJ & Gregg I. (1989). New regression equations for predicting peak expiratory flow in adults. British Journal of Medicine, 298, 1068–70.
Olson SK & Nimec DL. (2007). Persons with special needs and disabilities. In PS Auerbach (Ed.), Wilderness medicine (ch. 90) (5th ed.). Philadelphia: Mosby.
Park MK. (2008). Child with chest pain. Pediatric cardiology for practitioners (ch. 30) (5th ed.). Philadelphia: Mosby.
Payne DN, Adcock IM, Wilson NM, Oates T, Scallan M, Bush A. (2001). Relationship between exhaled nitric oxide and mucosal eosinophilic inflammation in children with difficult asthma, after treatment with oral prednisolone. American Journal of Respiratory Critical Care Medicine, 164, 1376–81.
Schatz M. (2008). Asthma in adolescents and adults. In RE Rakel and ET Bope (Eds.), Conn's Current Therapy 2008 (ch. 189) (60th ed.). Philadelphia: Saunders.
Shames RS, Heilbron DC, Janson SL, Kishiyama JL, Au DS, Adelman DC. (1998). Clinical differences among women with and without self-reported perimenstrual asthma. Annals of Allergy, Asthma & Immunology, 81(1), 65–72.
Sheffield PE, Knowlton K, Carr JL, Kinney PL. (2011). Modeling of regional climate change effects on ground-level ozone and childhood asthma. American Journal of Preventive Medicine, 41(3), 251–7.
Spahn JD & Covar R. (2008). Clinical assessment of asthma progression in children and adults. Journal of Allergy and Clinical Immunology, 121, 548–57.
Stanojevic S, Wade A, Stocks J, et al. (2008.). Reference ranges for spirometry across all ages: a new approach. American Journal of Respiratory Care and Critical Care Medicine, 1774, 253–60.
Stapczynski JS. (2004). Respiratory distress. In JE Tintinalli et al. (Eds.), Emergency medicine: a comprehensive study guide (ch. 62) (6th ed.). New York: McGraw-Hill.
Sutherland ER, Goleva E, Jackson LP, Stevens AD, Leung DY. (2010). Vitamin D levels, lung function, and steroid response in adult asthma. American Journal of Respiratory and Critical Care Medicine, 181(7), 699–704.
Swadron SP & Mandavia DP. (2006). Chronic obstructive pulmonary disease. In JA Marx, et al. (Eds.), Rosen's emergency medicine: concepts and clinical practice (ch. 73) (6th ed.). Philadelphia: Mosby.
Szefler SJ. (2008). Advances in asthma, allergy, and immunology series 2008: advances in pediatric asthma in 2007. Journal of Allergy and Clinical Immunology, 121, 614–19.
U.S. Department of Housing and Urban Development (HUD). (n.d.). Homes and communities. Retrieved August 2011 from http://www.hud.gov/content/images/mold2-lg.jpg.
U.S. Food and Drug Administration (U.S. FDA). (2011a). Drug treatments for asthma and chronic obstructive pulmonary disease that do not use chlorofluorocarbons. Retrieved August 2011 from http://www.fda.gov/Drugs/DrugSafety/InformationbyDrugClass/ucm082370.htm.
U.S. Food and Drug Administration (U.S. FDA). (2011b). FDA drug safety communication: drug labels now contain updated recommendations on the appropriate use of long-acting inhaled asthma medications called long-acting beta-agonists (LABAs). Retrieved September 2011 from http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm213836.htm.
U.S. Food and Drug Administration (U.S. FDA). (2011c). Primatene mist with chlorofluorocarbons no longer available after Dec. 31, 2011. Retrieved August 2011 from http://www.fda.gov/ForConsumers/ConsumerUpdates/ucm247196.htm.
U.S. Food and Drug Administration (U.S. FDA). (2010a). FDA drug safety communication: FDA requires post-market safety trials for long-acting beta-agonists (LABAs). Retrieved September 2011 from http://www.fda.gov/Drugs/DrugSafety/ucm251512.htm.
U.S. Food and Drug Administration (U.S. FDA). (2010b). Seven inhalers that use CFCs being phased out. Retrieved August 2011 from http://www.fda.gov/ForConsumers/ConsumerUpdates/ucm207864.htm.
U.S. Food and Drug Administration (U.S. FDA). (2009a). Early communication about an ongoing safety review of omalizumab (marketed as Zolair). Retrieved September 2011 from http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/DrugSafetyInformationforHeathcareProfessionals/ucm172218.htm.
U.S. Food and Drug Administration (U.S. FDA). (2009b). Updated information on leukotriene inhibitors: montelukast (marketed as Singulair), Zafirlukast (marketed as Accolate), and Zileuton (marketed as Zyflo and Zyflo CR). Retrieved September 2011 from http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/DrugSafetyInformationforHeathcareProfessionals/ucm165489.htm.
U.S. Food and Drug Administration (U.S. FDA). (2008). Public health advisory: national transition from chlorofluorocarbon (CFC) propelled albuterol inhalers to hydrofluoroalkane (HFA) propelled albuterol inhalers. Retrieved August 2011 from http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/DrugSafetyInformationforHeathcareProfessionals/PublicHealthAdvisories/ucm048717.htm.
U.S. Food and Drug Administration (U.S. FDA). (2007). Omalizumab (marketed as Xolair) information. Retrieved September 2011 from http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm103291.htm.
Wagner PD & West JB. (2005). Ventilation, blood flow, and gas exchange. In RJ Mason, JF Murray, VC Broaddus, JA Nadel (Eds.), Murray and Nadel's Textbook of Respiratory Medicine (ch. 4) (4th ed.). Philadelphia: Elsevier Saunders.
Warrier MR & Hershey GKK. (2008). Asthma genetics: personalizing medicine. Journal of Asthma, 45(4), 257–64.
Wechsler ME. (2009). Managing asthma in primary care: putting new guideline recommendations into context. Mayo Clinic Proceedings, 84(8), 707–17.
Whitty JE & Dombrowski MP. (2007). Respiratory diseases in pregnancy. In SG Gabbe, JR Niebyl, JL Simpson (Eds.), Obstetrics: Normal and problem pregnancies (ch. 35) (5th ed.). Philadelphia: Churchill Livingstone.
Wisnivesky JP, Lorenzo J, Feldman JM, Leventhal H, Halm EA. (2010.) The relationship between perceived stress and morbidity among adult inner-city asthmatics. Journal of Asthma, 47(1), 100–4.
Wolf JM, Miller GE, Chen E. (2008). Parent psychological states predict changes in inflammatory markers in children with asthma and healthy children. Brain, Behavior, and Immunity, 22, 433–41.
World Health Organization (WHO). (2003). Asthma. In Adherence to long-term therapies: evidence for action (sec. 3, ch. 7). Geneva, Switzerland: World Health Organization.
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