Introduction

The burdens associated with asthma in the United States—and worldwide—are enormous. Although the precise annual numbers are not known, asthma is clearly linked to a multitude of lost school days, countless missed work days, numerous doctor visits, frequent hospital outpatient visits, and recurrent emergency department visits and hospitalizations. According to the Department of Health and Human Services’ Centers for Disease Control and Prevention, within the United States in 2005 more than 22 million people were diagnosed with asthma, more than 12 million people had experienced an asthma episode in the previous year, and nearly 4000 Americans died of asthma.* The World Health Organization (WHO) estimates that about 180,000 people worldwide die because of asthma each year. Clearly, asthma’s impact on health, quality of life, and the economy is substantial.

A relatively new role of the respiratory care practitioner is that of asthma educator. In this function, the practitioner’s goal is to be sure that the patient and the family are cognizant of their role and functions in the care of this usually chronic and often serious condition. The asthma educator must serve as a “change agent,” and his or her effect as a convincing, empathetic communicator will be tested. Toward this end, we have greatly expanded this chapter from previous editions.

Fortunately, over the past two decades several new and important gains have been made by expert panels in the development of evidence-based clinical guidelines directed toward the education, prevention, diagnosis, and management of asthma. These guidelines are based on an extensive scientific foundation that has provided our current understanding of the pathophysiologic mechanisms, clinical manifestations, and treatment recommendations used to control asthma. Updated clinical guidelines are developed and disseminated on a regular basis by the National Asthma Education and Prevention Program (NAEPP) and the Global Initiative for Asthma (GINA).

National Asthma Education and Prevention Program

The first evidence-based asthma guidelines were published in 1991 by NAEPP, under the coordination of the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH). These guidelines were updated in 1997, 2002, and 2007.^† Today the guidelines are structured around the following four components of care: (1) assessment and monitoring of asthma, (2) patient education, (3) control of factors contributing to asthma severity, and (4) the pharmacologic treatments. The NAEPP “stepwise asthma management charts” have been widely used and now specify optimal treatment for specific age groups 0 to 4 years, 5 to 11 years, and 12 years and older.

Global Initiative for Asthma

GINA^* was launched in 1993 in collaboration with the National Heart, Lung, and Blood Institute of NIH and WHO. GINA works with a network of asthma experts and researchers, health-care professionals, professional organizations, and public health-care officials from around the world. GINA gathers and disseminates asthma-related information while also ensuring that a system is in place to incorporate the results of scientific investigations into asthma care. GINA’s specific goals are the following:

Collectively, by using the evidence-based guidelines provided by NAEPP, along with the extensive information gathered worldwide from asthma experts and researchers, GINA now provides an outstanding—and user-friendly—evidence-based guideline program for the management of asthma. As of this writing, the GINA programs, which are freely available on the internet (www.ginasthma.org), include the following publications:

In this chapter, GINA’s five components of asthma care are presented under the general management of asthma section.

Anatomic Alterations of the Lungs

Asthma is described as a lung disorder characterized by (1) reversible bronchial airway smooth muscle constriction, (2) airway inflammation, and (3) increased airway responsiveness to an assortment of stimuli. During an asthma attack, the smooth muscles surrounding the small airways constrict. Over time the smooth muscle layers hypertrophy and can increase to three times their normal thickness. The airway mucosa becomes infiltrated with eosinophils and other inflammatory cells, which in turn causes airway inflammation and mucosal edema. The goblet cells proliferate, and the bronchial mucous glands enlarge. The airways become filled with thick, whitish, tenacious mucus. Extensive mucous plugging and atelectasis may develop. The cilia are damaged, and the basement membrane of the mucosa is thicker than normal. As a result of smooth muscle constriction, bronchial mucosal edema, and excessive bronchial secretions, air trapping and alveolar hyperinflation develop. If chronic inflammation develops over time, these anatomic alterations become irreversible, resulting in loss of airway caliber. A remarkable feature of bronchial asthma, however, is that many of the pathologic anatomic alterations of the lungs that occur during an asthmatic attack are completely absent between asthmatic episodes (Figure 12-1).

The major pathologic or structural changes observed during an asthmatic episode are as follows:

Etiology and Epidemiology

Asthma was first recognized by Hippocrates more than 2000 years ago. It remains one of the most common diseases encountered in clinical medicine. In fact, over the past decade the incidence of asthma has increased dramatically. Today, it is estimated that more than 25 million Americans have asthma. About 500,000 Americans are hospitalized annually for severe asthma, and about 4000 die as a result of asthma annually. According to WHO, about 180,000 people worldwide die because of asthma each year. In the United States, asthma is found in 3% to 5% of adults and 7% to 10% of children. Approximately 50% of people with asthma develop it before age 10. Asthma is the most common chronic illness of childhood. Among young children, asthma is about two times more prevalent in boys than in girls. After puberty, however, asthma is more common in girls.

Risk Factors

Many asthma experts divide asthma into two major types according to its precipitating risk factors: extrinsic asthma, or asthma caused by external or environmental agents, and intrinsic asthma, or asthma that occurs in the absence of (or without clear evidence of) an antigen-antibody reaction. Although some authorities believe that the distinction between these terms is of minimal clinical value, the terms are nevertheless widely used.

According to GINA, the risk factors for asthma can be divided into (1) the risk factors with which one is born that cause the development of asthma (e.g., genetic factors or sex), and (2) the risk factors that trigger asthma symptoms (e.g., domestic mites, furred animals, cockroach allergen, fungi, molds, infections, tobacco smoke). The risk factors for asthma with which the individual is born are primarily genetic in nature; the risk factors that trigger asthma symptoms are usually environmental factors. Regardless of the fact that the various asthma authorities are not in full agreement as to how asthma should be categorized, they are—for the most part—in agreement regarding the following causes, or risk factors, of asthma.

Extrinsic Asthma (Allergic or Atopic Asthma)

When an asthmatic episode can clearly be linked to exposure to a specific allergen (antigen), the patient is said to have extrinsic asthma (also called allergic or atopic asthma). Common indoor allergens include house dust, mites, furred animal dander (e.g., dogs, cats, and mice), cockroach allergen, fungi, molds, and yeast. Outdoor allergens include pollens, fungi, molds, and yeast. In addition, there are a number of occupational substances associated with asthma (see next section).

Extrinsic asthma is an immediate (Type I) anaphylactic hypersensitivity reaction. It occurs in individuals who have atopy, a hypersensitivity condition associated with genetic predisposition and an excessive amount of immunoglobulin E (IgE) antibody production in response to a variety of antigens. From 10% to 20% of the general population are atopic and therefore have a tendency to develop an IgE-mediated allergic reaction such as asthma, hay fever, allergic rhinitis, and eczema. Such individuals develop a wheal-and-flare reaction to a variety of skin test allergens, called a positive skin test result. Extrinsic asthma is family-related and usually appears in children and in adults younger than 30 years old. It often disappears after puberty.

Because extrinsic asthma is associated with an antigen-antibody–induced bronchospasm, an immunologic mechanism plays an important role. As with other organs, the lungs are protected against injury by certain immunologic mechanisms. Under normal circumstances these mechanisms function without any apparent clinical evidence of their activity. In patients susceptible to extrinsic or allergic asthma, however, the hypersensitive immune response actually creates the disease by causing acute and chronic inflammation.

Immunologic mechanism

1. When a susceptible individual is exposed to a certain antigen, lymphoid tissue cells form specific IgE (reaginic) antibodies. The IgE antibodies attach themselves to the surface of mast cells in the bronchial walls (Figure 12-2, A).

2. Reexposure or continued exposure to the same antigen creates an antigen-antibody reaction on the surface of the mast cell, which in turn causes the mast cell to degranulate and release chemical mediators such as histamine, eosinophil chemotactic factor of anaphylaxis (ECF-A), neutrophil chemotactic factors (NCFs), leukotrienes (formerly known as slow-reacting substances of anaphylaxis [SRS-A]), prostaglandins, and platelet-activating factor ([PAP]; Figure 12-2, B).

3. The release of these chemical mediators stimulates parasympathetic nerve endings in the bronchial airways, leading to reflex bronchoconstriction and mucous hypersecretion. Moreover, these chemical mediators increase the permeability of capillaries, which results in the dilation of blood vessels and tissue edema (Figure 12-2, C).

The patient with extrinsic asthma may demonstrate an early asthmatic (allergic) response, a late asthmatic response, or a biphasic asthmatic response. The early asthmatic response begins within minutes of exposure to an inhaled antigen and resolves in approximately 1 hour. A late asthmatic response begins several hours after exposure to an inhaled antigen but lasts much longer. The late asthmatic response may or may not follow an early asthmatic response. An early asthmatic response followed by a late asthmatic response is called a biphasic response.

Occupational sensitizers (occupational asthma)

Occupational asthma is defined as asthma caused by exposure to an agent encountered in the work environment. More than 300 different substances have been associated with occupational asthma. Occupational asthma is seen predominantly in adults. It is estimated that occupational sensitizers cause about 1 in 10 cases of asthma among adults of working age. High-risk work environments for occupational asthma include farming and agricultural work, painting (including spray painting), cleaning work, and plastic manufacturing. Most occupational asthma is immunologically mediated and has a latency period of months to years after the onset of exposure. Although the cause is not fully understood, it is known that an IgE-mediated allergic reaction and cell-mediated allergic reactions are often involved. Box 12-1 shows additional agents known to cause occupational asthma.

Box 12-1   Agents Associated with Occupational Asthma

Animal and Plant Proteins

• Flour, amylase

• Storage mites

• Bacillus subtilis enzymes (detergent manufacturing)

• Colophony, such as pine resin (electrical soldering)

• Soybean dust

• Midges, parasites (fish food manufacturing)

• Coffee bean dust, meat tenderizer, tea, shellfish, amylase, egg proteins, pancreatic enzymes, papain

• Storage mites, Aspergillus, indoor ragweed, grass (granary workers)

• Psyllium, latex (hospital workers)

• Ispaghula, psyllium (laxative manufacturing)

• Poultry droppings, mites, feathers

• Locusts, dander, urine proteins

• Wood dust, such as western red cedar, oak, mahogany, zebrawood, redwood, Lebanon cedar, African maple, eastern white cedar

• Grain dust, molds, insects, grain

• Silk worm moths and larvae

Inorganic Chemicals

• Persulfate (beauticians)

• Nickel salts

• Platinum salts, vanadium

Organic Chemicals

• Ethanolamine diisocyanate (automobile painting)

• Disinfectants, such as sulfathiazole, chloramines, formaldehyde, and glutaraldehyde; latex (hospital workers)

• Antibiotics, piperazine, methyldopa, salbutamol, cimetidine (manufacturing)

• Ethylene diamine, phthalic anhydride

• Toluene diisocyanate, dephenylene, tetramines, trimellitic anhydride, hexamethyl tetramine, acrylates (plastics industry)

Intrinsic Asthma (Nonallergic or Nonatopic Asthma)

When an asthmatic episode cannot be directly linked to a specific antigen or extrinsic inciting factor, it is referred to as intrinsic asthma (also called nonallergic or nonatopic asthma) (Figure 12-3). The etiologic factors responsible for intrinsic asthma are elusive. Individuals with intrinsic asthma are not hypersensitive or atopic to environmental antigens and have a normal serum IgE level. The onset of intrinsic asthma usually occurs after the age of 40 years, and typically there is no strong family history of allergy.

In spite of the general distinctions between extrinsic and intrinsic asthma, a significant overlap exists. Distinguishing between the two is often impossible in a clinical setting. Precipitating factors known to cause intrinsic asthma are referred to as nonspecific stimuli. Some of the more common nonspecific stimuli associated with intrinsic asthma are discussed in the following paragraphs.

Other Risk Factors

Obesity

Obesity has been shown to be a risk factor for asthma. It is thought that certain mediators, such as leptins, may have an effect on airway function that can lead to the development of asthma.

Sex

Male sex is a risk factor for asthma in children. Up to 14 years of age, the prevalence of asthma is nearly twice as great in boys as in girls. The difference in prevalence of asthma in males and in females progressively narrows through the teenage years. By adulthood, the prevalence of asthma is greater in women than in men. The reason for this sex difference in asthma is unclear. It is suggested that the lung size is smaller in males than in females at birth, but larger in adulthood.

Infections

Although bacterial infections may cause asthma, viral upper airway infections are more likely to contribute to asthma. For example, intrinsic asthma is commonly seen in children after respiratory syncytial virus (RSV), parainfluenza virus, or rhinovirus infection. These conditions often produce a pattern of symptoms that parallel many features of childhood asthma. For example, it is estimated that about 40% of children with RSV infection will continue to wheeze or have asthma into later childhood.

Exercise-induced asthma

Asthma is sometimes associated with vigorous exercise. The asthmatic episode typically occurs 3 to 10 minutes after the exercise. The asthmatic episode usually resolves in about 1 hour. Although the precise mechanism is not understood, it is believed that the heat loss, water loss, and increased osmolarity of the lower airways causes the release of certain mediators from the basophils and tissue mast cells. The release of the mediators, in turn, causes bronchospasm. Exercise in cold, dry air (e.g., jogging, ice skating, cross-country skiing) also may provoke an asthmatic response in susceptible individuals.

Outdoor and indoor air pollution

Outbreaks of asthma exacerbations have been reported in areas of increased levels of air pollution. The role of outdoor air pollution in causing asthma remains controversial. Similar associations have been reported in relation to indoor pollutants, such as smoke and fumes from gas and biomass fuels used for heating and cooling, molds, and cockroach infestation. These conditions are not IgE mediated.

Drugs, food additives, and food preservatives

Asthma is associated with the ingestion of aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs). As much as 20% of the asthmatic population may be sensitive to aspirin and NSAIDs. Various beta-adrenergic blocking agents used to treat hypertension and some cardiac disorders (e.g., propranolol, metoprolol) also may provoke an asthmatic episode. The yellow food-coloring agent tartrazine may provoke an asthmatic episode. The ingestion of tartrazine especially is contraindicated in patients sensitive to aspirin. Bisulfites and metabisulfites, commonly used as preservatives and antioxidants in restaurant food (e.g., salad bars, certain wines, beers, dried fruits), are known to provoke bronchoconstriction. About 5% of the asthmatic population is sensitive to foods and drinks that contain sulfites.

Gastroesophageal reflux

Gastroesophageal reflux disease (GERD), or regurgitation, appears to contribute significantly to bronchoconstriction in some patients. The precise mechanism of this relationship is not known. The patient may complain of burning, substernal pain, belching, and a bitter, acid taste, particularly when lying down.

Sleep (nocturnal asthma)

Patients with asthma often have more difficulty late at night or in the early morning. Precipitating factors associated with nocturnal asthma include gastroesophageal reflux, retained airway secretions (caused by a suppressed cough reflex during sleep), exposure to irritants or allergens in the bedroom, and prolonged time between medication doses. Eradication of nocturnal asthma is one measure of good asthma control.

Emotional stress

In some patients the exacerbation of asthma appears to correlate with emotional stress and other psychologic factors.

Perimenstrual asthma (catamenial asthma)

The clinical manifestations associated with asthma often worsen in women during the premenstrual and menstrual periods. The peak of worsening symptoms generally occurs 2 to 3 days before menstruation begins. Perimenstrual asthma correlates with the late luteal phase of ovarian activity, the phase during which circulating progesterone and estrogen levels are at their lowest.

Diagnosis of Asthma

The diagnosis of asthma can often be challenging. For example, the diagnosis of asthma in early childhood is based primarily on the assessment of the child’s symptoms and physical findings—and good clinical judgment. In the older child and the adult, a complete history and physical examination—along with the demonstration of reversible and variable airflow obstruction—will in most cases confirm the diagnosis of asthma. In the elderly patient, asthma is often undiagnosed because of the presence of comorbid diseases that complicate the diagnosis.

Furthermore, the diagnosis of asthma is often missed in the patient who acquires asthma in the workplace. This form of asthma is called occupational asthma (see Box 12-1). Because occupational asthma usually has a slow and insidious onset, the patient’s asthma is often misdiagnosed as chronic bronchitis or COPD. As a result, the asthma is either not treated at all or treated inappropriately. Finally, even though asthma can usually be distinguished from COPD, in some patients—those who have chronic respiratory clinical manifestations and fixed airflow limitations—it is often very difficult to differentiate between the two disorders—that is, asthma or COPD.

GINA provides a general guideline to help in the clinical diagnosis of asthma, which is based on the patient’s symptoms and medical history. There are many signs and symptoms that should increase the suspicion of asthma. This includes wheezing and a history of any of the following:

Other indicators are if the symptoms occur or worsen at night or in a seasonal pattern. The presence of eczema, hay fever or a family history of asthma or atopic disease may also be an indicator. Another sign is if an individual has colds that “go to the chest” or that take more than 10 days to clear up. There are also situations in which asthma related symptoms may worsen, such as exposure to:

These symptoms often respond to appropriate antiasthma therapy.