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Asthma

Michael Jay Katz, MD, PhD

Wild Iris Medical Education is an approved provider (#PA-54) of continuing nursing education by the Washington State Nurses Association, an accredited approver by the American Nurses Credentialing Center's Commission on Accreditation. Our courses fulfill continuing nursing education requirements in all 50 states.
Wild Iris Medical Education (CBRN Provider #12300) is approved as a provider of continuing education for RNs, LVNs, and respiratory therapists by the California Board of Registered Nursing.
Nurse practitioners may apply these contact hours to pharmacy continuing education and prescriptive authorization.

This course includes straightforward answers to basic questions about Asthma for nurses and other health professionals who advise patients over the telephone (see Part 3: Telephone Counseling).

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. 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 smoke, dust, cold air, exercise, and emotional stress. An attack of asthma gives a person chest tightness and leaves them breathless, wheezing, and coughing. Most asthma attacks can be reversed by inhaling a bronchodilator medication (ALA, 2007c).

The clinical definitions of asthma stress four features of the condition:

• The patient has recurrent episodes of airway obstruction
• Symptoms of these episodes can be reversed by medication
• The patient's airways are chronically inflamed
• The patient's airways are sensitive to a variety of stimuli to which a normal lung would not react

Inflammation is the central problem in asthma, and the long-term management of the disease has two separate components:

• "Cleaning" the patient's environment, ie, reducing the patient's exposure to triggers of airway inflammation
• Giving the patient anti-inflammatory medicine, ie, reducing their body's inflammatory response to those triggers

PREVALENCE

Asthma is a common condition, and the prevalence of asthma is similar throughout the industrialized world, with populations in countries such as Canada, England, and Germany having asthma rates of 3% to 10% (ALA, 2007a). Overall, about 1 in 20 people has asthma, which makes asthma almost twice as common as diabetes.

In the United States, more than 22 million people have asthma. The prevalence varies from region to region across the country, from a low in Louisiana, where less than 6% of the population has asthma, to a high in Rhode Island, where 10.5% of the population has the disease (Morris, 2007).

Morbidity and Mortality Rates

Asthma is a costly disease for society. Each year, asthma leads to 1.8 million emergency department visits and a half million hospitalizations in the United States. Fortunately, deaths from asthma are uncommon. In the United States, approximately 3900 people die directly from asthma each year—about the same number of deaths as are caused by accidental drowning.

Gender

More adult women than men have asthma. In the United States, 8.9% of women aged 18 and older have asthma, while 5.6% of men have the disease. In childhood, however, the distribution of the disease is reversed: 11% of boys (ages 0–17 years) have asthma, while 7.5% of girls under 18 years old have the disease (ALA, 2007c).

Two factors lead to this disparity between the prevalence in children and the prevalence in adults.

• In adults, new asthma cases show up more often in women than in men.
• Asthma symptoms are more likely to fade or to disappear in young men than in young women.

Race and Ethnicity

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.

Some of the differences in the effect of asthma between different subgroups of Americans are caused by differences in the medical treatment that is received by these groups (NHLBI, 2007).

The latest CDC data (2005) for current asthma prevalence estimated 7.7% of people (22.2 million) currently had asthma. Rates decreased with age: 8.9% of children (6.5 million) had asthma compared to 7.2% of adults (15.7 million). When race/ethnicity is considered, Puerto Ricans had a current asthma prevalence rate 125% higher than non-Hispanic white people and 80% higher than non-Hispanic black people. When only race is considered, Native Americans, Alaska Natives, and African Americans had a 25% higher prevalence than whites.

Age of Diagnosis

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, with the most diagnoses made at age 3 years. In approximately half of the children diagnosed with asthma, the disease symptoms fade or disappear by the time they become adults.

Childhood Asthma

In the United States, asthma is the most common chronic illness of childhood, and it is the third most common cause of hospitalization for children. 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, such as atopic dermatitis (ie, eczema) and food allergies (Barnes, 2008; Kolski, 2008).

During their 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).

DEFINING ASTHMA

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, eczema, and skin allergies.

Pathophysiology

The two main physiologic processes that operate in asthma are:

• Chronic inflammation of the airways of the lung
• Reversible episodes (attacks) of bronchoconstriction

Adding to these problems, 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 the symptoms of asthma. During the first few years of life, a child's immune system is immature, and allergic responses in all young children are more common than in older children and adults. Also, a young child's lungs are more easily obstructed, because their lungs are small and have relatively weak support from their still-soft rib cage (Bacharier et al., 2007).

CHRONIC AIRWAY INFLAMMATION

Fundamentally, asthma is an inflammatory disease of the airways. Asthmatic inflammation is distributed throughout the respiratory airways trachea, bronchi, bronchioles) but the bronchioles are 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.

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).

Inflammatory Cells

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 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.

Local Structural Cells

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 Molecules

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.

In asthma:

• Mast cells secrete histamine, prostaglandins, and cysteinyl-leukotrienes (aka leukotrienes). These inflammatory molecules cause smooth muscle contraction, make capillaries more leaky, increase the amount of mucus secreted into the airways, and attract more inflammatory cells to the vicinity.
• Lymphocytes secrete other inflammatory molecules, such as cytokines, which keep eosinophils active, facilitate the formation of IgE antibodies, and promote many of the phases of allergic reactions.
• Injured epithelial cells in the airways secrete chemokines, which attract inflammatory cells into the region.

The Chain of Cellular Events

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).

INTERMITTENT AIRFLOW OBSTRUCTION

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. Contraction of the smooth muscle in airways (ie, 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.

Bronchoconstriction

The major cause of the airflow limitation in asthma is bronchoconstriction, contraction of the smooth muscle in the walls of the airways of the lungs. 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.

Edema

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.

Mucus

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 things: muscles in the airway walls contract, the airway walls become edematous and swollen, and excess mucus fills the airways (NIH, n.d.a).

LONG-TERM STRUCTURAL CHANGES

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:

• The epithelium lining the airways is fragmented, and many epithelial cells have been dislodged.
• The mucus cells in the epithelial layer are more numerous and enlarged, and they produce excess mucus.
• The smooth muscle cells are more numerous and enlarged.
• Extra blood vessels have grown in the airway walls, and all the local blood vessels tend to be dilated.
• The airway walls are filled with a variety of immune cells. This infiltrate includes lymphocytes, neutrophils, eosinophils, and mast cells.
• These histologic changes are patchy. In a single lung, some regions have more pronounced changes than other regions. Throughout the lung, however, the changes are found mainly in the airway walls and not elsewhere.

Asthma symptoms vary from person to person, but the structural airway changes are similar in all variants of the disease (Chestnutt et al., 2008).

Causes of Asthma

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).

GENETIC CONTRIBUTIONS

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 (ie, 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. Currently, more than one hundred 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).

NONGENETIC AND ENVIRONMENTAL CONTRIBUTIONS

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.

Infections, Th1/Th2 Balance, and the Hygiene Hypothesis

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—eg, respiratory syncytial virus (RSV) and rhinovirus—appear to increase rather than reduce a child's risk of developing asthma (Moore, 2008).)

Inhaled Substances

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 (ALA, 2007c).

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 forestry, metalworking, painting, waitressing, cleaning, laboratory work, and dental technicians (ALA, 2007c).

Ingested Substances

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).

Triggers and Aggravators

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:

• Respiratory infections
• Inhaled substances
• Ingested substances
• Physical factors
• Hormonal factors
• Stresses

VIRAL RESPIRATORY INFECTIONS

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 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).

Note: 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.

INHALED SUBSTANCES

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.

Biologic Allergens

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).

Smoke and Air Pollutants

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 than 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 Vapors

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.

INGESTED SUBSTANCES

Airway constriction is less often set off indirectly, ie, 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 (eg, ibuprofen) worsen their asthma (Bacharier et al., 2007).

PHYSICAL FACTORS, WEATHER, AND EXERCISE

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).

HORMONAL FACTORS

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 ((NHLBI, 2007).

PSYCHOLOGICAL STRESSES

Psychological stresses and strains worsen asthma in many patients. 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).

IDENTIFYING ASTHMA

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 staying 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.

Assessment

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).

HISTORY

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 these sections:

MEDICAL HISTORY OF AN ASTHMA PATIENT

• Symptoms
• Typical pattern of occurrence of symptoms
• Triggers and aggravating factors
• Chronological history of the patient's asthma
• Family history of related medical problems
• Patient's social history
• Current living environments
• Current lifestyle and habits
• Impact of asthma on patient and family
• Perception of the disease by patient and family

Symptoms

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 (Chestnutt 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 their upper back between the shoulder blades, or a feeling of dread or impeding 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 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% to 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, and 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 risk factors, modified from Bacharier and colleagues (2007).

Dyspnea

Dyspnea is the feeling of breathlessness, and it comes from a mix of three sensations, all of which contribute to the dypsnea of asthma:

• The urge to breathe. This urge is triggered by exercise or by the metabolic results of exercise: hypoxemia, hypercapnia, and metabolic acidosis.
• Difficulty breathing. This feeling is produced by excess amounts of chest movement and by unusual amounts of effort of the muscles of respiration during breathing.
• Anxiety. This sensation can be caused by a fear of suffocating or by a memory of past uncomfortable experiences with breathlessness. Anxiety can also come from other sources of stress.

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 lung disease (COPD), as it can be in other obstructive and inflammatory lung conditions (eg, 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 > 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. Although 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).

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.

Typical Patterns

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:

• Whether the symptoms occur in separate episodes or continuously
• How often the symptoms occur each week or each month
• Whether the symptoms occur with a daily or seasonal pattern
• Whether the symptoms occur more often during a certain part of the day or night
• For women, whether the symptoms occur during a particular part of their menstrual cycle

One way to collect this information is via standardized questionnaires such as the one that follows.

Triggers and Aggravating Factors

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 checklist below). Patients should also be asked whether asthma symptoms ever arise for no apparent reason.

Chronology of the Patient's Asthma

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. For example:

• Born 1950
• 1952–1955, some wheezing with colds
• 1958, mild hay fever began yearly
• 1964, started smoking (infrequently)
• 1968, smoking regularly with occasional coughing spells
• 1972, choking/coughing episode, possible asthma diagnosed in ED
• 1972, given inhaler for asthma attacks, stopped smoking
• 1973–1979, used inhaler occasionally
• 1979, divorced, moved to new city, began smoking again
• 1980, two visits to ED for asthma attacks
• 1981–1985, physician changed prn bronchodilator to Isoprel. Slowly stopped smoking completely.
• 2007, current regimen is Proventil prn, which is effective at reversing the 4 to 5 asthma episodes each year, most often in the early summer (hay fever season), and, on occasion in cold wintery weather. Weight is back down to pre-1995 levels. No ED visits in more than 10 years.

Family 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).

Social History

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 their 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 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.

PHYSICAL EXAMINATION

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.

During an Asthma 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 Asthma Attacks

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. The person may have dark rings under their eyes ("allergic shiners"), or their conjunctivae 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 (ie, a full, forced expiration) can be more than twice as long as the normal time of approximately 2 seconds (Barnes, 2008).

STUDIES AND TESTS

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 Data

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 (Chestnutt 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.

Nitrogen Oxide

The amount of nitric oxide exhaled by a patient is a measure of airway inflammation. This, too, may one day be used to monitor how well a patient's asthma is controlled (Morris, 2007).

Imaging Studies

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, or pneumothorax. 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 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).

Lung Function Tests

The best objective measures of asthma are lung function tests, which can quantify the degree of a patient's airflow obstruction.

Tools

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 small, handheld spirometry device can be used for quick office or clinic tests (NIH, n.d.b).

A full-function laboratory spirometry apparatus gives detailed reports on a range of characteristics of a patient's lung ventilation (NIH, n.d.c).

For asthma, spirometry is used to calculate two basic lung characteristics: FVC, the total amount of air that can be forced from the lungs after a complete inhalation, and FEV1, the amount of air that can be forced from the lungs in 1 second after a complete inhalation.

LUNG FUNCTION ABBREVIATIONS

• FVC, forced vital capacity, ie, total forced expiratory volume of air
• FEV1, 1-second forced expiratory volume of air
• 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, and body structure, but the improvement (ie, increase) in FEV1/FVC in any particular asthma patient is an objective measure of the level of control that their therapy has achieved. 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.

The ratio FEV1 to FVC decreases in obstructive airway diseases. If someone were able to exhale their entire vital capacity in 1 second, their 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 their vital capacity in the first second. This ratio, FEV1/FVC (the percent of the vital capacity that can be exhaled in 1 second), declines as a person ages, but even older adults will have FEV1/FVC >0.70 if their lungs are normal.

In obstructive airway diseases, such as 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).

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 their lungs.

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:

• Asthma triggers
• Gradual worsening of asthma, indicating that a medical visit is needed
• Early signs of an asthma attack so that rescue medicines can be taken quickly
• Situations when emergency care is needed

Managing asthma using a peak expiratory flow (PEF) meter. Source: CDC, n.d.a.

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 (Chestnutt et al., 2008).

Uses

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:

• The appearance of reversibility needs objective verification.
• Other medical problems can produce a similar medical history.
• The amount of airway obstruction, the degree to which symptoms are currently controlled, and the responsiveness of the symptoms to medication must be measured in a way that can be objectively repeated to follow the progress of long-term treatments.

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 (ie, exercise-induced asthma), spirometry can measure the increase in airway obstruction. In these tests, baseline spirometric values are measured, and patients then exercises 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%. The finding of only a minimal reduction can exclude the diagnosis of asthma with 95% confidence (Morris, 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 min 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.

Allergy Testing

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.

Asthma by Age Groups

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 (Chestnutt 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.

CHILDREN

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). As for general trends, clinicians often discuss asthma in three age ranges: infants, preschoolers, and school age children.

Infants: Years 0 through 2

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 intermittentwheezing are more likely to have or to develop asthma if:

• They wheeze when they have no respiratory illness
• They develop wheezing with allergies or after inhaling common triggers, such as dust or smoke
• They are prone to developing nasal, conjunctival, or skin signs of allergy, food allergies, or eczema
• A parent has a history of asthma
• Blood tests of the infant show eosinophilia (ie, higher than usual concentrations of eosinophils) (Spahn & Covar, 2008)

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).

Preschoolers: Years 3 through 5

In the preschool years, asthma phenotypes become distinct, and children with wheezing often fall into one of three categories:

• Asthma symptoms that come episodically with colds and other respiratory infections
• Asthma symptoms that are brought on by exercise
• Asthma symptoms that persist throughout the year

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 time they are 21 years old.

School-Age Children: Years 6 through 12

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).

Adolescents

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).

ADULTS

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 gives 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 patient with excess mucus production. The most significant declines in lung function are seen in those asthma patients with severe asthma, frequent asthma attacks, asthma that began in early childhood, or asthma that is poorly controlled (NHLBI, 2007).

Differential Diagnosis

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.

ADULTS

The basic list of other medical problems that bring on asthma-like symptoms includes:

• COPD (ie, chronic bronchitis or emphysema)
• Congestive heart failure
• Mechanical obstruction of the airways (eg, tumors)
• Pulmonary infiltration with eosinophilia
• Cough secondary to drugs (eg, angiotensin-converting enzyme [ACE] inhibitors)
• Vocal cord dysfunction
• Pulmonary embolism

COPD

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.)

Congestive Heart Failure (CHF)

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 come 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.

CHILDREN

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:

• Upper airway diseases (eg, colds, allergic rhinitis, sinusitis)
• Lower airway diseases (eg, viral bronchitis, bronchiolitis, pneumonia)
• Other lung diseases (eg, cystic fibrosis)
• Congenital problems (eg, congenitally narrow airways)
• Foreign body aspiration
• Recurrent fluid or food aspiration (eg, swallowing problems, gastroesophageal reflux) (Bacharier et al., 2007)

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.

TREATING ASTHMA ATTACKS

Asthma therapy has two modes:

• Short-term treatment of asthma attacks
• Long-term treatment of the disease to minimize attacks and to moderate symptoms

Asthma attacks are episodes of progressive breathing difficulty. In an asthma attack, patients get increasingly short of breath, with coughing, wheezing, or chest tightness. During an attack, the patient cannot push air out of their lungs as rapidly as before, and this can be objectively measured using simple lung function tests.

Severity of Attacks

Attacks can range from minor to life threatening. The severity of an asthma attack is classified as mild, moderate, severe, or extremely severe, and the classification of severity is used to determine the initial treatment (Arnold et al., 2008).

In a mild attack, a patient has breathing difficulty (dyspnea) only when pushing themselves 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 will recommend that a short course of oral corticosteroids be taken to prevent a relapse.

In a moderate attack, the patient's dyspnea interferes with their normal activities. Moderate attacks reduce the patient's peak expiratory flow to between 40% and 70% of their 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 their ability to complete a sentence. Severe attacks reduce the patient's peak expiratory flow to <40% of their 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 >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 <25% of their 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 bronchodilator, 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 (Chestnutt et al., 2008).

Treatment Principles

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).

CORRECTING HYPOXEMIA

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 (ie, 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.

REVERSING AIRFLOW OBSTRUCTION

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.

ASSESSING TREATMENT PROGRESS

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, the patient should be evaluated clinically, their blood oxygen saturation (measured with 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, so 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 ED physicians decide which children should be moved from the emergency department to the hospital (NHLBI, 2007).

REDUCING CHANCE OF RECURRENCE

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 with a follow-up visit.

PRE-EXISTING PLAN OF ACTION

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, they or their family should be given a written plan that explains how to deal with an asthma attack.

The asthma action plan should list:

• Early indicators of an attack, such as worsening PEF values
• symptoms of an attack
• A specific rule for deciding when to use rescue medications
• Exact instructions for how much medicine to take
• Instructions for when and how to notify their doctor
• Instructions for when to report to a doctor or clinic in person
• Instructions for when to call 911
• A brief history of the patient's asthma and current medications
• Phone numbers for the patient's asthma physician, other sources of medical advice, and friends or family members who can help

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" below.)

Home Management of an Attack

Asthma patients should have a rescue inhaler that they can carry with them. At home, patients with moderate or severe asthma should have additional medications (eg, 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 specific patient.

The outline of an emergency plan sets out four steps for treating attacks:

• Triage severity of symptoms
• Take rescue medications
• Get medical advice
• Follow the after-the attack instructions

The content of the plan is, essentially:

• Take rescue medicines when symptoms (wheezing, choking cough, difficulty breathing) occur or when your PEF values drop below 80% of your personal-best level
• Take rescue medicines and get immediate medical help when your PEF values drop below 50% of your personal-best level

Following are details of a typical plan for asthma attacks.

FIRST, TRIAGE BY ASSESSING SEVERITY

Begin by deciding the severity of the attack.

Mild

• You develop wheezing, coughing, or difficulty breathing
• You become breathless doing exercise
• You have no problem speaking
• Your PEF = 70% to 80% of your best value

Moderate

• You develop wheezing, coughing, or difficulty breathing
• You become breathless doing normal activities
• You can finish a sentence
• Your PEF = 40% to 70% of your best value

Severe

• You develop wheezing, coughing, or difficulty breathing
• You are breathless just sitting
• You cannot finish a sentence
• Your PEF < 40% of your best value

Extremely Severe

• You develop wheezing, coughing, or difficulty breathing
• You can't catch your breath when sitting
• You are choking, wheezing, or coughing continuously
• You cannot speak a full sentence
• You are sweaty and perhaps confused or sleepy
• Your PEF< 25% of your best value

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."

SECOND, TAKE RESCUE MEDICINES ACCORDING TO SEVERITY

Home treatments always begin with the inhalation of a short-acting bronchodilator, such as albuterol. Although each home management plan must be individualized, here are some common protocols.

Mild

Begin with 2 to 6 puffs of your rescue bronchodilator, Repeat the same dose in 20 minutes. A complete response includes significantly decreased symptoms and a PEF ≥80% of your 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, so consult your doctor.

Moderate

Begin with 2 to 6 puffs of your rescue bronchodilator. Repeat the same dose in 20 minutes. A complete response includes significantly decreased symptoms and a PEF ≥80% of your 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 and you should consult your asthma doctor.

Severe

Begin with 2 to 6 puffs of your rescue bronchodilator. Repeat the same dose in 20 minutes. A complete response includes significantly decreased symptoms and a PEF ≥80% of your 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 your doctor within the day.

If the response is incomplete (persistent wheezing, difficulty breathing, or a PEF of 50% to 80%), begin taking corticosteroids and contact your 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 your physician, and proceed to the emergency department. Call 911 rather than driving yourself.

Extremely Severe

Immediately take 2 to 6 puffs of your rescue bronchodilator and call 911. Then take oral corticosteroids. For increasing symptoms, inject yourself with epinephrine (Epipen), if this is in your asthma attack plan.

THIRD, GET APPROPRIATE MEDICAL ADVICE

Severe or Extremely Severe Initial Symptoms

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 them to call 911 immediately while taking their rescue medicine.

Poor Response to Rescue Medicines

If your symptoms are worsening, or if after 30 minutes you still have marked wheezing and difficulty breathing, or if your PEF <50% of your best value, then follow the above medication regimen (Step 2), contact your physician immediately, and proceed to an emergency department. Call 911 rather than driving yourself, and if you are drowsy, confused, sweating, or turning blue, call 911 immediately.

Incomplete Response to Rescue Medicines

If after 30 minutes you still have wheezing or difficulty breathing or if your PEF is between 50% and 80% of your personal-best value, then follow the above medication regimen (Step 2), and contact your physician within the day for further instructions.

Complete Response to Rescue Medicines

If after 30 minutes you no longer have wheezing or difficulty breathing and your PEF ≥80% of your personal-best value, then follow the above medication regimen (Step 2), and contact your physician later for follow-up instructions.

FOURTH, FOLLOW AFTER-THE-ATTACK INSTRUCTIONS

After an asthma attack, you 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 your improvement can be gradual. The underlying disease flare-up will last for 2 to 3 weeks. Always contact your doctor within a day of the attack for specific after-the attack instructions.

EMS Management of an Attack

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).

Emergency Department Management of an Asthma Attack

FIRST, TRIAGE BY ASSESSING SEVERITY

The ED team makes a judgment of the severity of the attack by assessing:

• Intensity of symptoms, including both the interviewer's and the patient's report of the extent of wheezing, coughing, and dyspnea
• Signs, including heart rate, respiratory rate, use of accessory muscles, sounds heard on chest auscultation, cyanosis, and state of consciousness
• Peak flow or FEV1 values, unless the patient is too dyspneic to perform them, or the symptoms are becoming life threatening
• Blood oxygen saturation by pulse oximetry

SECOND, TREAT ACCORDING TO SEVERITY

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%.

BASIC TREATMENT PROTOCOLS

For mild to moderate symptoms with a PEF > 40% of the predicted value

• Initially give:
• O₂, with a minimum goal of SaO₂ >90%
• inhaled short-acting bronchodilator (nebulizer or MDI) 4 to 8 puffs, repeatable every 20 minutes during the first hour. (Short-acting bronchodilators begin to have an effect in less than 5 minutes.)
• If no improvement within 5 to 10 minutes:
• oral corticosteroids (prednisone 40–80 mg)

For severe symptoms or a PEF < 40% of the predicted value

• Initially give:
• O₂, with a minimum goal of SaO₂ >90%
• inhaled high-dose short-acting bronchodilator (eg, albuterol 5 mg) plus ipratropium (0.5 mg) via nebulizer either every 20 minutes or continuously for 1 hour
• oral or IV corticosteroids (prednisone or methylprednisolone 80 mg)

THIRD, TAKE HISTORY AND DO PHYSICAL EXAM

The history should include:

• Time of onset of current attack
• Possible causes
• Severity of symptoms compared to previous attacks
• Medications taken before ED admission and any change in symptoms as a result
• All current medications and times of last doses
• Approximate number of attacks during the past year
• Any previous attacks that were serious enough to cause loss of consciousness, intubation and mechanical ventilation, or ICU admission
• Other concurrent illnesses, including lung diseases (eg, COPD), heart diseases (eg, heart failure), endocrine diseases, bleeding problems (eg, gastrointestinal ulcers), hypertension, kidney diseases, or psychotic illnesses
• Recent surgeries, prolonged inactivity, or propensity for deep venous thromboses

The physical exam should note especially:

• Severity of the asthma signs and symptoms
• Patient's state of alertness
• Patient's degree of hydration
• Lung complications, such as respiratory infections, chest trauma, chest deformity, or, uncommonly, possible pneumothorax
• Rule out upper airway obstruction, eg, note absence of stridor, absence of dysphonia, absence of localized wheezing, absence of normal PaO₂, no visible pharyngeal obstruction, absence of neck or throat injury
• Signs of heart failure

FOURTH, ASSESS RESPONSE TO INITIAL TREATMENT

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:

• If on reassessment the symptoms are minimal and the PEF >70% of predicted value, the patient is watched for another hour. A continued remission after 60 minutes means the patient can be discharged. In two-thirds of ED asthma patients, the initial 3 doses of bronchodilator will be sufficient to reverse their symptoms and allow them to be discharged. The patient should be sent home with brief counseling, oral corticosteroids (40–60 mg for 5–10 days), and a scheduled outpatient follow-up visit.
• If the patient is not improving after an hour, consider additional therapy (eg, IV magnesium sulfate or heliox).
• If at any time the patient is worsening or if the SaO₂ is dropping, an arterial blood gas should be checked for indications of impending respiratory failure. At that point, intubation, mechanical ventilation, and hospitalization must be considered. (Stapczynski, 2004)

FOR INFANTS AND YOUNG CHILDREN

Special Considerations

The severity of airway obstruction is harder to determine in young children, but an increasing respiratory rate (ie, 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 is 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 (eg, RSV), foreign body obstruction, aspiration (eg, swallowing problems or GERD), chest malformations, congenital airway problems, and cystic fibrosis (NHLBI, 2007).

Rescue Medications

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 aged 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).

WHEN TO HOSPITALIZE

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, then 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 experience 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 breath or in a coma should be intubated immediately.

Adjunct treatments, such as IV magnesium sulfate or helium-oxygen (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.

DISCHARGE FROM THE EMERGENCY DEPARTMENT

Before being discharged, asthma patients need to have their:

• Symptoms largely alleviated
• Lung function values (PEF or FEV1) returned to >70% of the predicted or personal best levels

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).

MANAGING ASTHMA LONG-TERM

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).

Write a Plan with the Patient

The most effective way to ensure that patients understand how to manage their asthma is by giving them a written plan.

GOALS

The goals for asthma treatment are that each patient should 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.

THE PATIENT AS DISEASE MANAGER

Success with these goals requires the continued attentions of a disease manager, and the patient should take that role. With their physicians, asthma patients design a plan that is realistic, and the patients must then ensure that the plan is carried out.

DESIGNING AN ASTHMA ACTION PLAN

To help their patients write an asthma treatment plan, physicians gather the medical data they have collected and then summarize four characteristics of the specific patient:

• The disease's severity and the patient's baseline FEV1 and PEF values
• The patient's triggers
• The patient's related co-existing medical problems (co-morbidities)
• The patient's knowledge of the disease and expectations for its control (NHLBI, 2007)

Individualize the Details

The physician then 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, and schedules a follow-up visit (Schatz, 2008).

Pharmacologic Step Therapy

The NHLBI guidelines (NHLBI, 2007) recommend that physicians plan a patient's medications using a step paradigm, with asthma treatments divided into six successively increasing steps, according to the medications needed to control the asthma symptoms (see table below) (Schatz, 2008).

With this plan, the physician prescribes medications at the minimum necessary step to maintain control of the patient's symptoms.

Using the Step Protocol

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 three consecutive months of good control, the physician attempts to lower the medication level by one step. If this is a success 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 their asthma control is currently adequate (Schatz, 2008).

Determining the Initial Medical Regimen

To choose where on the pharmacologic step chart to start an asthma patient, physicians need to classify the severity of the patient's disease (Krouse & Krouse, 2008). For asthma patients, "severity" means the intensity of the disease when it is not being controlled by medicines.

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).

Monitor Effectiveness of Control

To monitor the degree of asthma control, physicians should couple symptomatic assessments with lung function assessments.

SYMPTOMATIC EVALUATION

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 (see box). The ACT test can be freely downloaded from the internet (see "Resources" below).

OBJECTIVE EVALUATION (PEAK-FLOW MONITORING)

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 (Morris, 2007). Then patients are given these rules:

• PEF >80% of the personal-best value indicates well-controlled asthma
• PEF = 60–80% of the personal-best value indicates not well-controlled asthma
• PEF = 50–60% of the personal-best value indicates poorly-controlled asthma
• PEF <50% of the personal-best value needs medical advice or attention soon

Make Step Changes when Appropriate

The effectiveness of a long-term asthma management program is called the "degree of control," and "well controlled"' means both:

• The absence of impairments, ie, the absence of:
  • Asthma symptoms
  • Need for rescue medicines
  • Sleep disruption
  • Limitations of normal and extra activities
• A low level of risks of asthma attacks

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.

TOOLS FOR MANAGING ASTHMA

Medications

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.

Asthma medications fall into two major classes:

• Daily controllers
• Quick-relievers (rescue medications)

The daily controllers are anti-inflammatory drugs, aimed at damping the ongoing inflammation that underlies the disease. Controller medications include inhaled corticosteroids (often used along with long-acting bronchodilators), leukotriene modifiers, mast cell stabilizers, theophylline, omalizumab, and systemic corticosteroids. Persistent asthma is controlled most effectively by daily long-term-control medications.

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