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Asthma 20-1073596 3 Hours Back to Course Index

Asthma

 

Introduction

Asthma is a chronic inflammatory disease that affects your airways.  The airways are the tubes that carry air in and out of your lungs. When an individual has Asthma, the inside walls of their airways are swollen. The inflammation makes the airways very sensitive, and they tend to react strongly to irritation. When the airways react, they get narrower, and less air flows through to your lung tissue. This disease causes recurrent episodes of wheezing, shortness of breath, coughing, and chest tightness.

Asthma cannot be cured, but most people with asthma can control it so that they have few infrequent symptoms and can live active lives.

Prevalence

Although the disease most commonly begins in childhood, asthma affects people of all ages.  Asthma has reached epidemic proportions in the United States, affecting an estimated 20 million people (National Heart, Lung, and Blood Institute, 2006). According to the Centers for Disease Control and Prevention (CDC), in 2004, asthma accounted for:

  • More than 4000 deaths
  • Nearly half a million hospitalizations
  • Nearly 2 million emergency department (ED) visits

Asthma is the most common chronic disease in children and the leading cause of school absenteeism, accounting for more than 12 million lost school days. Some children experience less severe symptoms as they grow older, and, in some cases, the disease may resolve altogether. However, recent research suggests that symptoms may recur in more than one-third of those with a history of childhood asthma (Taylor et al., 2003), perhaps due to a change in environmental exposure.  

Asthma is also the leading cause of work loss for adults, accounting for an estimated 24 million lost workdays each year. Asthma affects proportionately more children than adults, more women than men, and more nonwhites than whites (Mannino et al., 2002). Incidence is highest among African American children living in urban areas.

Asthma can be life-threatening. Despite the development of more effective medications for asthma, the death rate from asthma has increased in recent years. The mortality rate has decreased for children since 1996; however, it is increasing among adults over the age of 75 (American Lung Association, 2006).

Beyond the tremendous cost of suffering, asthma also has a staggering financial effect. According to the American Lung Association, direct healthcare costs for asthma in the United States exceed $11.5 billion, nearly half of which represents the cost of prescription drugs. The cost of lost productivity adds another $4.6 billion for a total of more than $16 billion.

The Cause of Asthma

Asthma is considered a multifactorial disease to which familial, allergenic, socioeconomic, and environmental factors may contribute. The most common predisposing factor in childhood asthma is inherited susceptibility to allergic reactions and atopy. A child whose mother has asthma is almost three times as likely to develop asthma as a child whose mother does not have asthma. However, genetic factors cannot explain the rapid increase in asthma prevalence because it takes many generations for genetic changes to occur. Many people diagnosed with asthma have no family history of atopy or asthma.

 

Factors Contributing to Asthma

Environmental Factors

Several environmental factors have been identified as triggers for asthma attacks, and some of them may even cause asthma.   These triggers include indoor, outdoor, and viral irritants. 

Indoor-air contaminants include animal dander, dust mites, cockroach droppings, wood smoke, oil smoke, and secondhand tobacco smoke.

Research suggests that prenatal exposure to secondhand smoke may cause immune system changes that predispose infants to the early development of asthma and allergies. Maternal exposure to secondhand smoke during pregnancy can affect the respiratory health of the fetus as well as increase the risk of low birth weight and premature delivery (CDC, 2006). Mothers who smoke during pregnancy compromise their infants’ pulmonary function, increasing the risk of persistent wheezing in their children at least until age 6. Breastfeeding appears to mitigate the effects of these exposures since breastfed infants are less likely to develop asthma than those fed infant formula (Kull et al., 2005).

Many studies have proposed that reducing prenatal and early childhood exposure to potential asthma triggers can significantly reduce the prevalence of asthma in childhood. In one large prospective Canadian study, researchers found that prenatal lifestyle modifications before birth and during the first year of life reduced the prevalence of asthma in the intervention group by 56 percent at age 7. The intervention included avoidance of house dust, pets, and environmental tobacco smoke beginning before birth, coupled with breastfeeding and delayed introduction of solid foods during the first 12 months of life (Chan-Yeung et al., 2005).

Moreover, other studies have explored delaying the introduction of solid foods, particularly those linked to the increased risk for allergies such as cow’s milk, for at least the first six months to one year of life to reduce asthma. According to the American College of Asthma and Allergy (ACAAI) consensus document (Fiochi et al., 2006), breastfeeding protects children against allergies.

Chlorinated indoor swimming pools may also increase the risk of asthma. The most recent of several studies implicating the byproducts of chlorination of water as a risk factor for asthma found a relationship between asthma prevalence and the number of indoor chlorinated swimming pools per inhabitant in 21 European countries (Marc & Bernard, 2006). The researchers reported that in the United Kingdom, for example, asthma rates rose by 2.73 percent for every chlorinated pool available to residents. A study in Sweden found that repeated exposure to chlorination byproducts in the air of indoor swimming pools increased the inflammatory response in lung tissue by impairing the anti-inflammatory function of Clara cell protein (CC16) (Lagerkvist et al., 2004). Researchers in Belgium and Australia earlier reported similar findings, linking exposure to chlorinated pools with hyperpermeability of lung tissue and asthma prevalence (Bernard et al., 2003).

Dampness and mold are also linked with asthma and asthma-related symptoms in both children and adults. A study in Finland found a significant increase in new cases of adult-onset asthma related to the presence of visible mold and/or mold odor in the workplace: More than one-third of exposed workers developed asthma; women, the young, and smokers were most vulnerable to the effects of workplace mold (Jaakkola et al., 2002). Many other studies have identified residential dampness and mold as triggers of asthma-related symptoms and asthma attacks.

Contaminants in outdoor air include pollen, herbicides, pesticides, ozone, nitrogen oxides (NOx), particulate matter (PM), and vehicle exhaust, especially diesel exhaust. The earlier in life a child is exposed to these contaminants, the greater the risk of developing asthma.

Obesity

The rise in the number of overweight persons over the past two decades has paralleled the rise in asthma rates. Several recent studies suggest that the association between asthma and obesity may be causal rather than by chance (Gilliland et al., 2003; Guerra et al., 2004; Poulain, 2006). Australian scientists have identified a protein¡ªacid-binding protein aP2¡ªwhich not only causes obesity and Type 2 diabetes but also plays a role in allergic respiratory diseases such as asthma (Shum et al., 2006). Fat tissue also produces several inflammatory mediators such as C-reactive protein, tumor necrosis factor-¦Á, and interleukin-6 in the serum of obese persons, which may contribute to airway inflammation (Weiss, 2005; Bergeron et al., 2005).

According to Reuters Health, obese women without allergies are at greater risk for asthma than obese men without allergies.  According to the investigators, one unit increase in BMI was associated with about a 6-percent increase in asthma risk in women, compared to 3 percent in men. The study also suggests that obesity is more likely to be associated with nonallergic asthma and that nonallergic asthma is more common in women.  (Reuters Limited, 2006)

Pregnancy

Pregnancy also appears to increase a woman’s risk of asthma, and the risk rises with the number of births. The reason for this link is unclear, but researchers suspect it may be related to hormonal changes during pregnancy (Jenkins et al., 2006).

Women who have asthma before becoming pregnant are at high risk of premature birth and having a low birth weight infant, both of which put the child at risk of developing respiratory complications. A recent study indicates that many women on Medicaid stop or reduce their use of asthma medications during pregnancy, even though national guidelines recommend continued use of these drugs (Enriquez et al., 2006).

Researchers in Detroit found that obese women with asthma have a higher incidence of preeclampsia and cesarean deliveries than women without asthma. However, they surmised that the complications are more likely related to obesity rather than to asthma (Hendler, 2006).

Occupational Asthma

Adult-onset asthma may be caused by workplace and/or home exposure, and symptoms can be exacerbated by smoking. Occupational asthma is the most common type of occupational lung disease in the developed world. According to the American Academy of Allergy, Asthma, and Immunology, up to 15 percent of asthma cases in the United States may be related to workplace exposures; therefore, clinicians should consider occupational exposures in all adults known or suspected to have asthma.

Scientists expect the prevalence of occupational asthma to remain high because more than 250 industrial chemicals, referred to as chemical sensitizers, are known to cause the disease, and new chemicals are introduced into the workplace each year. Chemical agents are estimated to cause 40 percent of cases of occupational asthma (Bernstein, 2003).

Chemical sensitizers known to cause asthma and trigger asthma attacks in pre-existing asthma include isocyanates, acid anhydrides, methacrylates, complex amines, metalworking fluids, and several metals. Chronic exposure to latex, certain pesticides, grain dust, wood dust, and bacterial toxins, and high-level exposure to certain chemicals such as corrosive, acid, or alkaline smoke, vapor, or gas, can also cause asthma. The box below shows the major causes of occupational asthma and workers at risk. Workers who smoke are at higher risk of developing asthma-related occupational exposure than nonsmokers.

Clinicians must ask adult patients about work-related exposures that could cause or exacerbate asthma. Patients may need a referral to an allergist/immunologist for evaluation to confirm the diagnosis of asthma, determine whether the asthma is caused or triggered by workplace exposures, and initiate appropriate avoidance therapy.

 

OCCUPATIONAL ASTHMA AND WORKERS AT RISK

 

Source

Agents

Workers at risk

Animals, insects,
and fungi

Animal proteins

Animal handlers, laboratory research workers, poultry workers

Prawns, crabs

Processors of these foods

Egg protein

Egg producers

Fungal amylase

Bakers

Grains, flours, plants

Grain dust

Grain storage workers, farmworkers

Wheat, rye, soy flour

Bakers, millers

Latex

Healthcare workers

Green coffee beans, castor beans

Coffee bean baggers and handlers, coffee roasters, chemists

Drugs and enzymes

Proteases from Bacillus subtilus

Detergent industry workers

Pancreatin, papain, pepsin

Food technologists, laboratory workers

Methyldopa, salbutamol, dichloramine, piperazine, dihydrochloride, spiramycin, penicillins, sulphathiazole, sulphonechloramides, chloramines-T, phosdrin, pancreatic extracts

Pharmaceutical workers

Wood dust

Western red cedar, California redwood, cedar of Lebanon, iroko, ramin, African zebrawood

Sawmill workers, joiners, carpenters, woodworkers

Mahogany, mansonia, oak

Sawmill workers,
pattern makers

Chemicals

Di-isocyanates

Polyurethane, plastics, varnish workers, foam manufacturers printers, laminators, rubber workers, boat builders, office workers, refrigerator manufacturers, toymakers

Acid anhydrides

Epoxy resins, alkyd resins, plastics workers

Complex amines

Photographers, shellac workers, painters

Azodicarbonamide

Plastics workers,
rubber workers

Reactive dyes

Textile workers

Methyl methacrylate

Healthcare workers

Metals

Platinum salts

Platinum-refining workers

Cobalt

Hard-metal grinders

Chromium, nickel

Metal-plating workers

Other

Metalworking fluids

Machinists

Aluminum pot room emissions

Aluminum-refining workers

Colophony in solder flux

Electronics workers

Source: Canadian Centre for Occupational Health and Safety, 2005.

Occupational asthma leads to substantial disability, resulting in loss of income and quality of life. Early diagnosis, elimination of the causative exposure, and early use of inhaled steroids are key to minimizing these effects. However, the prevention of new cases is equally important and requires collaboration between industry and occupational health professionals.


Pathophysiology

Asthma results from complex interactions among inflammatory cells, mediators, and other cells and tissues in the airway. The inflammatory process of asthma is accompanied by bronchial hyperreactivity (hyperresponsiveness). The severity of hyperreactivity depends on the severity of the inflammation.

During an acute asthma episode (an exacerbation), the smooth muscles in the bronchi constrict, narrowing the airways and obstructing airflow. In addition, the acute inflammatory response increases mucus secretion and edema of the airway mucosa, damaging the airway epithelium. Over time, this sequence of events causes the airways to stiffen, contributing to persistent abnormalities in lung function. The graphic below, created by the National Heart, Lung, and Blood Institute, shows the effect.

National Heart, Lung and Blood Institute, May 2006


Key Elements In Diagnosis 

Clinicians may overlook or misdiagnose asthma in adults, attributing their symptoms to cardiac, pulmonary, or bronchial conditions. This is particularly true among older adult patients.

To establish the diagnosis of asthma, the clinician must determine that:

  • Episodic symptoms of airflow obstruction are present.
  • Airflow obstruction is at least partly reversible.
  • Alternative diagnoses are excluded.

This process requires a detailed medical history, the example below; physical examination focusing on the upper respiratory tract, chest, and skin; and spirometry to demonstrate reversibility (NAEPP, 1997).

 

SUGGESTED ITEMS FOR MEDICAL HISTORY*

 

A detailed medical history of the new patient who is known to, or thought to have asthma should address the following items:

1.    Symptoms

o        Coughing

o        Wheezing

o        Shortness of breath

o        Chest tightness

o        Sputum production

2.    Pattern of symptoms

o        Perennial, seasonal, or both

o        Continual, episodic, or both

o        Onset, duration, frequency (number of days or nights per week or month)

o        Diurnal variations, especially nocturnal and on awakening in the early morning

3.    Precipitating and/or aggravating factors

o        Viral respiratory infections

o        Environmental allergens, indoor (e.g., mold, house-dust mite, cockroach, animal dander or secretory products) and outdoor (e.g., pollen)

o        Exercise

o        Occupational chemicals or allergens

o        Environmental change (e.g., moving to a new home; going on vacation; and/or alterations in the workplace, work processes, or materials used)

o        Irritants (e.g., tobacco smoke, strong odors, air pollutants, occupational chemicals, dust and particulates, vapors, gases, and aerosols)

o        Emotional expressions (e.g., fear, anger, frustration, hard crying or laughing)

o        Drugs (e.g., aspirin, beta-blockers, including eye drops, nonsteroidal anti-inflammatory drugs, others)

o        Food, food additives, and preservatives (e.g., sulfites)

o        Changes in the weather, exposure to cold air

o        Endocrine factors (e.g., menses, pregnancy, thyroid disease)

4.    Development of disease and treatment

o        Age of onset and diagnosis

o        History of early-life injury to airways (e.g., bronchopulmonary dysplasia, pneumonia, parental smoking)

o        Progress of disease (better or worse)

o        Present management and response, including plans for managing exacerbations

o        Need for oral corticosteroids and frequency of use

o        Co-morbid conditions

5.    Family history

o        History of asthma, allergy, sinusitis, rhinitis, or nasal polyps in close relatives

6.    Social History

o        Characteristics of home including age, location, cooling, and heating system, wood-burning stove, humidifier, carpeting over concrete, presence of molds or mildew, characteristics of rooms where the patient spends time (e.g., bedroom and living room with attention to bedding, floor covering, stuffed furniture)

o        Smoking (patient and others in home, workplace, or daycare)

o        Daycare, workplace, and school characteristics that may interfere with adherence

o        Social factors that interfere with adherence, such as substance abuse

o        Social support/social networks

o        Level of education completed

o        Employment (if employed, characteristics of work environment)

7.    Profile of typical exacerbation

o        Usual prodromal signs and symptoms

o        Usual patterns and management (what works?)

8.    Impact of asthma on patient and family

o        Episodes of unscheduled care (emergency department, urgent care, hospitalization)

o        Life-threatening exacerbations (e.g., intubation, ICU admission)

o        Number of days missed from school/work

o        Limitation of activity, especially sports and strenuous work

o        History of nocturnal awakening

o        Effect on growth, development, behavior, school or work performance, and lifestyle

o        Impact on family routines, activities, or dynamics

o        Economic impact

9.    Assessment of patient’s and family’s perceptions of disease

o        Patient, parental, and spouse’s or partner’s knowledge of asthma and belief in the chronicity of asthma and the efficacy of treatment

o        Patient perception and beliefs regarding use and long-term effects of medications

o        The ability of the patient and parents, spouse, or partner to cope with the disease

o        Level of family support and patient’s and parent’s, spouse’s, or partner’s capacity to recognize the severity of an exacerbation

o        Economic resources

o        Sociocultural beliefs

* This list does not represent a standardized assessment or diagnostic instrument. The validity and reliability of this list have not been assessed.
Source: NAEPP, 1997.

 

 

SAMPLE QUESTIONS* FOR THE INITIAL ASSESSMENT OF ASTHMA

 

A yes answer to any of the following questions suggests a likely asthma diagnosis.

In the past 12 months¡­

  • Have you had a sudden severe episode or recurrent episodes of coughing, wheezing (high-pitched whistling sounds when breathing out), or shortness of breath?
  • Have you had colds that “go to the chest” or take more than ten days to get over?
  • Have you had coughing, wheezing, or shortness of breath during a particular season or time of the year?
  • Have you had coughing, wheezing, or shortness of breath in certain places or when exposed to certain things (e.g., animals, tobacco smoke, perfumes)?
  • Have you used any medications that help you breathe better? How often?
  • Are your symptoms relieved when the medications are used?

In the past four weeks, have you had coughing, wheezing, or shortness of breath¡­

  • At night that has awakened you?
  • In the early morning?
  • After running, moderate exercise, or other physical activity?

* These questions are examples and do not represent a standardized assessment or diagnostic instrument. The validity and reliability of these questions have not been assessed.
Source: NAEPP, 1997.

The medical history can help:

  • Identify the symptoms likely to be due to asthma.
  • Identify patterns of symptoms and/or family history of asthma or allergies.
  • Assess the severity of asthma based on symptom frequency and severity, exercise tolerance, hospitalizations, and current medications.
  • Identify possible precipitating factors, such as viral respiratory infections and environmental exposures at home, work, daycare, or school.

The physical examination focused on the upper respiratory tract, chest, and skin can reveal findings that increase the probability of asthma, such as:

  • Hyperextension of the thorax, especially in children; use of accessory muscles; hunched shoulders; and chest deformity.
  • Sounds of wheezing during normal breathing or a prolonged phase of forced exhalation. Wheezing during forced exhalation does not necessarily indicate airflow limitation. Wheezing may be absent in mild, intermittent asthma or between exacerbations.
  • Increased nasal secretion, mucosal swelling, and nasal polyps.
  • Atopic dermatitis/eczema or other manifestations of an allergic skin condition.

Asthma is classified according to the severity of symptoms and frequency of acute attacks or exacerbations: mild intermittent, mild persistent, moderate persistent, and severe persistent. Criteria for establishing these classifications are shown in the box below (NAEPP, 1997).

 

CLASSIFICATION OF ASTHMA SEVERITY: CLINICAL FEATURES BEFORE TREATMENT*

 

Level

Symptoms**

Nighttime symptoms

Lung Function

STEP 4
severe persistent

Continual symptoms
Limited physical activity
Frequent exacerbations

Frequent

FEV1 or PEF ¡Ü 60% of predicted function

STEP 3
moderate persistent

Daily symptoms
Daily use of inhaled short-acting beta2-agonist
Exacerbations affect activity
Exacerbations ¡Ý two times a week; may last days

>1 time a week

FEV1 or PEF >60% to <80% of predicted function

STEP 2
mild persistent

Symptoms >2 times a week but <1 time a day
Exacerbations may affect the activity

>2 times a month

FEV1 or PEF ¡Ý 80% or more of predicted
function

STEP 1
mild intermittent

Symptoms ¡Ü two times a week
Asymptomatic and normal PEF between exacerbations
Exacerbations are brief (from a few hours to a few days); intensity may vary

¡Ü two times a month

FEV1 or PEF ¡Ý 80% or more of the predicted function

* The presence of one of the features of severity is sufficient to place a patient in that category. An individual should be assigned to the most severe grade in which any feature occurs. The characteristics noted in this table are general and may overlap because asthma is highly variable. Furthermore, an individual’s classification may change over time.
** Patients at any level of severity can have mild, moderate, or severe exacerbations. Some patients with intermittent asthma experience severe and life-threatening exacerbations separated by long periods of normal lung function and no symptoms.
Source: NAEPP, 2003.


Signs and Symptoms

The onset of asthma symptoms may be sudden or gradual, and symptoms may resolve quickly or persist for hours or even days. Because allergies contribute to most cases of asthma, asthma triggers vary from person to person, depending on their allergies.

Key indicators for considering a diagnosis of asthma are summarized in the box below. These indicators include wheezing, a cough that worsens at night, and/or a history of difficulty breathing or chest tightness. Pulmonary function testing (spirometry) is necessary to determine whether airflow limitations are reversible.

 

KEY INDICATORS FOR A DIAGNOSIS OF ASTHMA*

 

Consider asthma and perform spirometry if any of the following are present. These indicators are not diagnostic by themselves, but multiple key indicators increase the probability of a diagnosis of asthma. Spirometry is needed to establish a diagnosis of asthma.

  • Wheezing-high-pitched whistling sounds when breathing out, especially in children. (Lack of wheezing and a normal chest examination do not exclude asthma.)
  • History of any of the following:
    • A cough, worse at night
    • Recurrent wheeze
    • A recurrent difficulty in breathing
    • Recurrent chest tightness
  • The reversible airflow limitation and diurnal variation as measured by using a peak flow meter, for example:
    • Peak expiratory flow (PEF) varies 20 percent or more from PEF measurement on arising in the morning (before taking an inhaled short-acting beta2-agonist) to PEF measurement in the early afternoon (after taking an inhaled short-acting beta2-agonist).
  • Symptoms occur or worsen in the presence of:
    • Exercise
    • Viral infection
    • Animals with fur or feathers
    • House-dust mites (in mattresses, pillows, upholstered furniture, carpets)
    • Mold
    • Smoke (tobacco, wood)
    • Pollen
    • Changes in weather
    • Strong emotional expression (laughing or crying hard)
    • Airborne chemicals or dust
    • Menses
  • Symptoms occur or worsen at night, awakening the patient.

* Eczema, hay fever, or a family history of asthma or atopic diseases are often associated with asthma, but they are not key indicators.
Source: NAEPP, 1997.


Acute Asthma Episode: EXACERBATIONS

Asthma exacerbations are acute or subacute episodes of progressively worsening shortness of breath, cough, wheezing, chest tightness, or some combination of these symptoms (NAEPP, 1997). Exacerbations are characterized by decreases in expiratory airflow that can be documented and quantified by simply measuring lung function (spirometry or PEF). These objective measures indicate the severity of an exacerbation more reliably than the severity of symptoms.

If not treated promptly and appropriately, exacerbations can be life-threatening. Patients at high risk of asthma-related death (Box 8, above) require intensive education, monitoring, and care. They should be counseled to seek medical care early during an exacerbation and instructed about the availability of ambulance services. The following boxes present risk factors for death from asthma.

 

RISK FACTORS FOR DEATH FROM ASTHMA

 

  • History of sudden severe exacerbations
  • Prior intubation for asthma
  • Prior admission for asthma to an intensive-care unit
  • Two or more hospitalizations for asthma in the past year
  • Three or more emergency-care visits for asthma in the past year
  • Hospitalization or an emergency-care visit for asthma within the past month
  • Use of >2 canisters per month of inhaled short-acting beta2-agonist
  • Current use of systemic corticosteroids or recent withdrawal from systemic corticosteroids
  • Difficulty perceiving airflow obstruction or its severity
  • Comorbidities, such as cardiovascular diseases or chronic obstructive pulmonary disease (COPD)
  • Serious psychiatric or psychosocial problems
  • Low socioeconomic status and urban residence
  • Illicit drug use
  • Sensitivity to Alternaria

Source: NAEPP, 1997.

Infants also require special attention because they are at high risk for respiratory failure (Box 10).

 

INFANT RISK FACTORS FOR ASTHMA DEATH

 

  • Assessment depends on physical examination rather than objective measurements. The use of accessory muscles, paradoxical breathing, cyanosis, and a respiratory rate greater than 60 are key signs of serious distress.
  • Objective measurements, such as less than 91 percent oxygen saturation, also indicate serious distress.
  • Response to beta2-agonist therapy can be variable and may not be a reliable predictor of a satisfactory outcome. However, because infants are at greater risk for respiratory failure, a lack of response noted by either physical examination or objective measurement should be an indication of hospitalization.
  • The use of oral corticosteroids early in the episode is essential but should not substitute for careful assessment by a physician.
  • Most acute wheezing episodes result from viral infections and may be accompanied by fever. Antibiotics are generally not required.

Source: NAEPP, 1997.

Tests

Pulmonary Function (Spirometry)

Spirometry measurements (FEV1, FVC, FEV1/FVC) before and after inhalation of a short-acting bronchodilator such as albuterol help determine the presence of airflow obstruction and whether it is reversible in the short term. Spirometry is generally useful in children ages four and older; However, some children cannot manage the maneuver until after age 7.

Spirometry measures the maximal volume of air forcibly exhaled from the point of maximal inhalation (forced vital capacity, FVC) and the volume of air exhaled during the first second of the FVC (forced expiratory volume in 1 second, FEV1). Airflow obstruction is indicated by reduced FEV1 and FEV1/FVC values relative to a reference or predicted values. Significant reversibility is indicated by an increase of >12 percent and 200 mL in FEV1 after inhaling a short-acting bronchodilator (American Thoracic Society, 2001).

Additional Tests

Depending on the patient, additional tests may be necessary to help rule out other respiratory or cardiac conditions and to identify asthma triggers, assess severity, and investigate potential complications.

Additional pulmonary function studies include lung volumes and inspiratory and expiratory flow-volume loops to confirm or rule out co-existing chronic obstructive pulmonary disease, a restrictive defect, or possible central airway obstruction. A diffusing capacity test can help differentiate between asthma and emphysema in smokers and older patients.

Assessment of diurnal variation in peak expiratory flow (PEF) over 1 to 2 weeks is recommended in patients who have asthma symptoms but normal spirometry. The PEF is usually lowest on the first awakening and highest several hours before the midpoint of the waking day (between noon and 2 p.m.). The PEF should be measured close to those two times before taking an inhaled short-acting beta2-agonist in the morning and after taking one in the afternoon. A 20 percent difference in these two measurements suggests asthma.

A chest x-ray may be needed to rule out other diagnoses, such as tumors. Allergy testing helps to identify asthma triggers. The nose should be evaluated for possible polyps, and the sinuses should be evaluated for infectious or inflammatory disease. It may be necessary to investigate gastroesophageal reflux disease.

Conclusion

Comprehensive guidelines for the diagnosis and management of asthma are available from the National Asthma Education and Prevention Program (NAEPP) and the Global Initiative on Asthma (GINA). Despite these efforts, asthma remains underdiagnosed and inadequately controlled. Challenges include early and accurate diagnosis difficulties, lack of appropriate clinician, patient, and family education, and poor compliance with prescribed therapeutic regimens.

The effective treatment of asthma begins with the correct diagnosis and classification of the disease. Clinical judgment is essential to this process because signs and symptoms vary within and among individuals over time. Some patients experience only mild and infrequent symptoms, while others experience more severe and frequent symptoms.