Allergic Rhinitis Mono

AAFP VIDEO CME PROGRAM

Allergic Rhinitis and Asthma: A Clinical Practice Update

In Cooperation with

American Academy of Family Physicians in cooperation with

National Heart, Lung, and Blood Institute, American Lung Association National Institute of Allergy and Infectious Diseases, American Thoracic Society

Presents:

Allergic Rhinitis and Asthma: A Clinical Practice Update as part of the Annual Clinical Focus: AFC 2001: Asthma, Allergy, and Respiratory Infections, bringing state-of-the-art clinical information on asthma, allergy, and respiratory infections to family physicians. This program was supported by educational grants from: Bristol-Myers Squibb Company Schering Laboratories/Key Pharmaceuticals Aventis Pharma Glaxo Wellcome, Inc Roche Laboratories Pharmacia Corporation, Diagnostics Division Alcon Laboratories, Inc

Presenters: Barbara P. Yawn, MD, MSc Director of Research Olmsted Medical Center Associate Clinical Professor Family and Community Medicine University of Minnesota Rochester, Minnesota

Greg Lee Ledgerwood, MD Associate Clinical Professor Department of Family Practice University of Washington School of Medicine Omak, Washington

AAFP Video CME Medical Editor:

AAFP Special Projects Manager:

REBECCA A. RUBLE, MD Clinical Assistant Professor Department of Family Medicine The University of Kansas Medical Center Kansas City, Kansas

LEIGH McKINNEY American Academy of Family Physicians Leawood, Kansas

This monograph is designed to be used in conjunction with the corresponding AAFP CME videotape. For more information contact: American Academy of Family Physicians 11400 Tomahawk Creek Parkway Leawood, Kansas 66211-2672 1-800-274-2237

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INTRODUCTION Allergic rhinitis and asthma are both common, chronic, and costly conditions. Despite advances in managing the inflammatory processes driving the progression of these conditions, the prevalence of both continues to increase. By being vigilant in diagnosing these diseases and aggressively and continuously treating them, family physicians can enhance patients’ quality of life, slow disease progression, and reduce the severe and possibly life-threatening, complications of asthma.

LEARNING OBJECTIVES Upon completion of this program, physicians should be able to: • Discuss the relationship between allergic rhinitis and asthma. • Identify the early signs and symptoms of allergic rhinitis and asthma. • Review techniques to manage symptoms in patients with allergic rhinitis. • Describe therapies to manage asthma with an emphasis on maintaining long-term control of symptoms and on preventing exacerbations and the need for emergency treatment.

CME ACCREDITATION INFORMATION CME Program Approval

AAFP Members

This activity has been reviewed and is acceptable for up to one (1) Prescribed credit hour by the American Academy of Family Physicians. Term of approval is for one year from beginning distribution date of 1/01, with option for yearly renewal.

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CME Credit For More Than One Viewer NOTE: CME credit for this program can be received only for viewing the videotape and completing the corresponding Post-Test. A Post-Test is provided with each videotape purchased. For more information contact: American Academy of Family Physicians CME Production Department 11400 Tomahawk Creek Parkway Leawood, Kansas 66211-2672

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One monograph Post-Test is included with each Video CME program. If you have colleagues who would like to receive CME credit for viewing the videotape and reading the monograph you purchased, additional copies of the Post-Test may be purchased for $10.00 each.

TABLE OF CONTENTS OVERVIEW . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 IMPACT OF ALLERGIC RHINITIS AND ASTHMA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 LINK BETWEEN ALLERGIC RHINITIS AND ASTHMA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 ALLERGIC RHINITIS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 Establishing the Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 Treatment Options . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 ASTHMA. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 Role of Inflammation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 Establishing a Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 Goals of Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 Pharmacotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 Immunotherapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Stepped Approach to Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Follow-Up . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Patient-Physician Partnership . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 SUMMARY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 PATIENT HANDOUTS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13-16 BIBLIOGRAPHY

Disclosure Policy: The AAFP has selected and provides funding for all faculty appearing in this program. According to AAFP policy, all relationships between speakers and manufacturers of any commercial products discussed in the educational presentation will be disclosed. Dr. Ledgerwood has returned a disclosure form indicating that he is on the Speakers Bureau for Glaxo Wellcome Inc, and is a consultant/scientific advisor for Schering Corporation. Dr. Yawn has returned a disclosure form indicating that she has received grant/research support from American College of Asthma, Allergy, and Immunology and is a consultant/scientific advisor for Key Pharmaceuticals. Drs. Ledgerwood and Yawn have returned forms declaring that the content of their presentation(s) in this AAFP-sponsored CME event will not include discussion of unapproved or investigational uses of products or devices. The views and opinions expressed herein are those of the faculty and not necessarily those of the American Academy of Family Physicians, the National Heart, Lung and Blood Institute, the American Lung Association, the National Institute of Allergy and Infectious Diseases, American Thoracic Society, Bristol-Myers Squibb Company, Schering Laboratories/Key Pharmaceuticals, Aventis Pharma, Glaxo Wellcome Inc, Roche Laboratories, Pharmacia Corporation, Diagnostics Division, Alcon Laboratories Inc, or the producers. Mention of particular therapeutic entities in this program does not imply an endorsement, claim, or representation by the American Academy of Family Physicians.

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Table 1: Possible Factors Contributing to Increased Prevalence of Allergic Rhinitis/Asthma ■ ■ ■ ■ ■

Dietary (ie, maternal and/or infant diet) The “hygiene hypothesis” Increased exposure to indoor allergens Environmental pollution More sedentary lifestyle

OVERVIEW Physicians and patients may not always take allergic rhinitis seriously. Physicians may consider allergic rhinitis more of a nuisance than an illness. Both patients and their physicians may overlook the fact that there is more to allergic rhinitis than a runny nose or itchy, watery eyes. Allergic rhinitis can cause nonnasal symptoms, such as cough and sore throat; psychosocial and cognitive problems; and may lead to sleep disturbances, including sleep apnea. In children, allergic rhinitis can also lead to dental malocclusions and facial deformities. Consequently, it can impair performance at work, learning at school, and reduce overall quality of life. Untreated, allergic rhinitis can develop into a chronic state of inflammation and nasal obstruction that may lead to serious airway diseases that are difficult and costly to treat. Allergic rhinitis is a risk factor for sinusitis, otitis media with effusion, and nasal polyps. It is also closely linked with asthma, which is a potentially lifethreatening condition. Despite the advances in treating asthma and allergic rhinitis, both conditions are increasing in the United States and worldwide. Family physicians play a key role in diagnosing and managing these diseases, and in preventing disease progression and development of comorbid conditions, such as sinusitis and otitis media.

IMPACT OF ALLERGIC RHINITIS AND ASTHMA The prevalence of allergic rhinitis and asthma is increasing worldwide. Factors that account for this increase include possible dietary or food reactions and the “hygiene hypothesis” (Table 1). The hygiene hypothesis suggests that newborn children in modern societies are no longer exposed to childhood infections due to immunizations. Early infection has been found to be negatively associated with atopy. Therefore, this reduction in childhood infections may be shifting the immune system towards a tendency to develop allergy and asthma. Additional reasons for this increase are not completely clear, but may include increased exposure to house dust mites and other indoor allergens, exposure to cigarette smoke at an early age, higher concentrations of environmental pollutants, and a trend toward a more sedentary lifestyle.

Table 2: Impact of Allergic Diseases Allergic Rhinitis

Asthma

■ Affects 1 in 5 adults and children in US ■ Prevalence may be as high as 40% ■ Direct and indirect annual costs: $2.4 billion

■ Americans with asthma: 15 million ■ Children with asthma: 4.8 million ■ Missed school days: >10 million/year ■ $6.2 billion/year (1990) ■ $11 billion/year (1996) ■ 1.8 million ER visits ■ Hospitalizations: 0.5 million/year ■ Asthma deaths: >5,000/year

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Allergic rhinitis affects approximately 1 in 5 adults and children in the United States. Estimates of the prevalence of allergic rhinitis range from as low as 4% to as high as 40%. The direct medical costs of treating allergic rhinitis, together with the indirect costs of lost productivity and absences from work, were conservatively estimated to be $2.4 billion a year in 1990 (Table 2). When the costs of treating associated airway diseases such as asthma are added, the economic impact of allergic rhinitis might be well over $10 billion per year. Asthma has been estimated to affect about 15 million Americans, including 4.8 million children under 18 years of age. The overall prevalence of asthma in children has increased steadily for more than 35 years, and asthma is now the most common chronic childhood disease. Approximately 10 million school days a year are missed by children with asthma. In 1990, the annual cost of asthma to the US economy was estimated to be $6.2 billion, with the majority of the expense attributed to medical care. By 1996 the estimated cost of asthma was over $11 billion per year. Asthma accounts for approximately 1.8 million emergency room visits and 500,000 hospitalizations annually. In addition, more than 5,000 people die of asthma each year. Morbidity and mortality rates are higher for women than men, and are markedly higher for blacks compared with whites. Blacks have a fourfold higher rate of hospitalization, a fivefold higher rate of emergency room visits, and a threefold higher mortality rate when compared with whites.

LINK BETWEEN ALLERGIC RHINITIS AND ASTHMA Allergic rhinitis and allergic asthma are both atopic, that is, an inherited tendency to develop IgE immune responses. Allergic rhinitis is commonly triggered by seasonal outdoor allergens such as ragweed and other weed pollens, grass pollens, and tree pollens. Asthma (and some rhinitis) is often triggered by dust mites, cats and dogs, and cockroaches (Table 3). Cross-sectional epidemiologic studies have shown that asthma and allergic rhinitis frequently coexist. Rhinitis is diagnosed in up to 78% of patients with asthma, and asthma is diagnosed in up to 58% of patients with rhinitis. In the general population of patients with both diseases, rhinitis precedes asthma in up to 64% of cases. This suggests that allergic rhinitis may be a significant risk factor for asthma. In a 23-year follow-up study, allergic rhinitis patients had a threefold increase in the incidence of asthma compared with those without rhinitis.

Table 3: Links Between Allergic Rhinitis and Asthma ■ Atopic conditions ■ Allergic triggers ■ Common asthma triggers - dust mites - cats, dogs - cockroaches ■ Asthma and allergic rhinitis frequently coexist ■ Rhinitis precedes asthma in ~64% of cases ■ Hyperreactive airways in patients with allergic rhinitis ■ Antihistamines and intranasal corticosteroids beneficial for asthma symptoms and lung function

Patients with seasonal and perennial allergic rhinitis and no asthma symptoms frequently have hyperreactive airways. This change in lung function also seems to suggest that rhinitis is a risk factor for asthma or that these patients may actually have mild asthma. Antihistamines and intranasal corticosteroids, which are commonly used to treat patients with allergic rhinitis, have been noted to improve asthma symptoms and lung function. However, these medications alone are not sufficient to treat asthma effectively.

ALLERGIC RHINITIS Allergic rhinitis is an inflammation of the nasal mucosa caused by IgE-mediated hypersensitivity reactions to specific inhaled allergens. The condition may occur seasonally, usually in response to pollens from trees, grasses, and weeds. It may also be perennial, a response to constant exposure to animal dander, dust mites, molds, cockroaches, or chemicals in the workplace. There is very often a genetic predisposition to developing allergic rhinitis. Adults with a family history of asthma or rhinitis have a twofold to sixfold risk of developing rhinitis compared with adults without such a family history. The onset of allergic rhinitis is common in children and adolescents, and symptoms often continue into adulthood. However, in 10% to 20% of children, the condition resolves within 10 years.

Establishing the Diagnosis It is important to keep in mind that allergic rhinitis is one possible diagnosis in patients with chronic runny and stuffy noses. Rhinitis can be allergic, nonallergic, or both. Allergic rhinitis can be seasonal or perennial. Symptoms of nonallergic rhinitis are similar to allergic rhinitis, but there is no pruritus and no evidence of allergic disease. Nonallergic rhinitis can be divided into infectious and noninfectious rhinitis (Table 4). Infectious rhinosinusitis is an infection that causes an inflammation of the paranasal sinuses. Acute rhinosinusitis is usually viral and occasionally bacterial, whereas chronic rhinosinusitis can be due to viral, bacterial, or fungal etiologies. Noninfectious rhinitis includes vasomotor rhinitis, nonallergic rhinitis with eosinophilia, rhinitis medicamentosa (caused by the use of cocaine or over-the-counter nasal decongestants), and occupational rhinitis (due to exposure to airborne irritants or allergens in the workplace). It may also result from granulomatous diseases (such as rhinoscleroma, sarcoidosis, and tuberculosis) and structural problems (such as septal deviation or tumors). Making a correct diagnosis requires a thorough history and

Table 4: Differential Diagnosis for Allergic Rhinitis ■ Infectious Rhinosinusitis - viral - bacterial - fungal ■ Non-infectious Rhinitis - idiopathic or vasomotor - nonallergic rhinitis with eosinophilia - rhinitis medicamentosa - occupational exposure - granulomatous diseases - structural problems

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Table 5: Findings in History and Exam in Patients With Allergic Rhinitis ■ Physical Symptoms - headache - postnasal drip - recurrent head colds - “stuffy” head - chronic “sinusitis” - chronic cough - plugged or itchy ears - diminished smell and taste - sleep disturbances and sleep apnea ■ Psychological Symptoms - depression - anxiety - fatigue

physical examination. Differentiating allergic and nonallergic rhinitis may require screening tests of allergens. A thorough evaluation, including a personal and medical history, family history, physical examination, and selected tests, should be conducted in all patients.

History Patients usually describe nose, eye, or throat symptoms, but they should also be questioned about other relevant symptoms (Table 5). Rhinitis symptoms may include headache, postnasal drip, recurrent head colds, “stuffy” head, chronic “sinusitis,” chronic cough, plugged or itchy ears, diminished smell and taste, and sleep disturbances, including sleep apnea. Psychological symptoms may include depression, anxiety, and fatigue. It is important to determine symptom severity, whether symptoms occur seasonally or are constant, and if they occur in response to specific triggers, such as common allergens and irritants. Information about potential common allergens in home, work, and school environments is essential in diagnosing allergic diseases. When taking the patient history, it is important to have a complete list of the patient’s current medications, including over-the-counter medications. Clinical response (or nonresponse) to previous medications must also be considered.

Physical Examination The physical examination should focus on the nose, eyes, and throat. The nose may be inspected with a short, wide speculum mounted on a handheld otoscope. Signs of allergic rhinitis include a pale, swollen, “boggy” mucosa, turbinate distension, and clear, watery secretions. Physicians can also observe patients for mouth breathing and “allergic shiners,” a darkening of the infraorbital skin. Polyps and structural abnormalities may be the cause of chronic rhinitis or may complicate allergic rhinitis. In addition, the ears, sinuses, and lungs should be examined to rule out related airway disorders. Signs or symptoms of eustachian tube blockage and hearing loss may suggest otitis media with effusion. Sinus tenderness, which may be associated with thickened mucosa, suggests sinusitis. Persistent coughing and wheezing on the chest exam suggest asthma. Spirometry is appropriate in all patients with long-standing and severe allergic rhinitis and in patients who commonly cough following exercise, laughing, or exposure to cold air or who often develop a chronic cough after a viral respiratory tract infection.

Table 6: Patient Education About Allergic Rhinitis ■ Pathophysiology of allergic rhinitis ■ Comorbidities (asthma, sinusitis) ■ Effects on mood, functioning, quality of life ■ Allergen and irritant avoidance and environmental control ■ Types of medications, how they work, and side effects ■ Importance of self-management skills

Treatment Options Patients differ in the amount of information they want about their disease and treatment. However, patients who understand their allergic rhinitis and how to control it are better able to cooperate in managing their disease. Optimally, physicians should provide information about disease pathophysiology; complications and comorbidities; disease and treatment effects on personality, mood, functioning, and quality of life; allergen and irritant avoidance and environmental control; types of medications, how they work, and side effects; and self-management skills to maintain adherence (Table 6). In the limited time that is usually available, it is essential that the physician address at least the topics of disease pathophysiology, complications, and self-management skills. Patient education can be reinforced and expanded on by other healthcare providers in the office.

Allergen Avoidance Avoiding exposure to allergens should be thoroughly investigated in patients with seasonal or perennial allergic rhinitis. Providing patients with specific instructions on allergen avoidance and environmental control in a written handout or video is essential. Limiting exposure to pollen, dusts, and molds in the home; chemical or biologic agents in the workplace; or contact with pets may not be easy, but any reduction in exposure will contribute to better control of symptoms.

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Families with a history of atopic conditions can undertake a number of measures that may help prevent sensitization in newborns and the development of allergic diseases. These include breastfeeding; delaying the introduction of solid food until after 4 months of age; avoiding exposure to indoor allergens, such as dust mites and cat and dog dander; and avoiding irritants, particularly tobacco smoke. However, the effectiveness of these measures is currently unproven.

Table 7: Allergic Rhinitis Pharmacotherapy Antihistamines

■ Block H1 receptors ■ Relieve sneezing, itching, rhinorrhea ■ First-line therapy ■ May be used in combination with topical corticosteroids or nasal cromolyn ■ First-generation can cause sedation ■ Second-generation usually nonsedating

Oral Decongestants

Two types of antihistamines are available: first-generation antihistamines, which may cause sedation and other central nervous system effects such as dizziness, disturbed coordination, tremor, or convulsions; and second-generation, usually nonsedating antihistamines. Low doses or nighttime dosing of sedating antihistamines may be appropriate for controlling symptoms in some patients. Even these doses of sedating antihistamines can reduce performance. In general, sedating antihistamines should not be prescribed for children or for people who drive or work with heavy equipment.

■ Sympathomimetic agents ■ Relieve symptoms of nasal congestion ■ May cause systemic side effects ■ Use with caution in patients with heart disease, hypertension, thyroid disease, diabetes, difficulty in urination

Topical Decongestants

Oral decongestants are sympathomimetic drugs that relieve symptoms of nasal congestion or blockage by constricting the capacitance vessels in the turbinates. These agents may cause systemic side effects such as hypertension, insomnia, and urinary retention. Oral decongestants should be used with caution in patients with heart disease, high blood pressure, thyroid disease, diabetes, or difficulty in urination.

■ Act rapidly and effectively ■ Relieve nasal congestion ■ Few systemic side effects but can cause rebound effect ■ Limit course of therapy to 3 to 5 days to avoid rebound

Intranasal Corticosteroids

■ Prophylactic use can reduce congestion, sneezing, rhinorrhea, palatal pruritus, cough ■ Systemic side effects are minimal ■ Must be used regularly, even in absence of symptoms

Oral Corticosteroids

■ Potent antiinflammatory agents ■ Effective in relieving severe symptoms and reducing polyps ■ 3- to 7-day course of therapy may achieve symptom control ■ Avoid use of intramuscular corticosteroids, especially in growing children

Intranasal Cromolyn Sodium

■ Topical nonsteroidal antiinflammatory agent ■ Relieves sneezing, rhinorrhea, nasal congestion, nasal pruritus ■ Few side effects ■ Administered 2 to 4 times daily

Pharmacotherapy There are a number of effective oral and topical medications that can be used to reduce inflammation and control the symptoms of allergic rhinitis (Table 7). Antihistamines are the mainstay of pharmacotherapy for allergic rhinitis. They block H1 receptors and relieve histamine-induced symptoms, including sneezing, itching, and rhinorrhea. Antihistamines are first-line treatment for allergic rhinitis and may be combined with topical corticosteroids for optimal control of moderate and severe allergic rhinitis. Nasal cromolyn may also be used in place of topical corticosteroids.

Topical (intranasal) decongestants act more rapidly and effectively than oral decongestants to relieve nasal congestion, and have fewer systemic side effects. However, a major side effect of topical decongestants is rhinitis medicamentosa, a rebound phenomenon that occurs after repeated applications. The use of topical decongestants should be limited to a maximum of 3 to 5 days to avoid this side effect. Decongestants are not specific therapy for allergic rhinitis. Corticosteroids treat the inflammatory component of the disease. Intranasal corticosteroids are the first-line of therapy when obstruction is a major component of the patient’s rhinitis. Steroids can reduce congestion, sneezing, rhinorrhea, palatal pruritus, and cough. Intranasal corticosteroids have minimal systemic side effects. However, local side effects include stinging, burning, dryness, and epistaxis. To maintain effectiveness these agents must be used regularly, even in the absence of symptoms. Oral corticosteroids are potent antiinflammatory agents that are extremely effective in relieving severe symptoms of allergic rhinitis and reducing polyps. A short course (3 to 7 days) of therapy may be necessary to achieve symptom control. Use of intramuscular steroids should be avoided because of the potential for severe systemic side effects, especially in growing children. Mast cell stabilizer is a term referring to cromolyn and similar agents. Intranasal cromolyn sodium is a topical over-the-counter nonsteroidal antiinflammatory agent that relieves sneezing, rhinorrhea, nasal congestion, and nasal pruritus. It has an excellent safety profile with few side effects but must be administered 2 to 4 times per day. Table 8 (page 8) from The Allergy Report conveniently summarizes the symptom management profile of the various classes of pharmacologic agents and is based on the consensus opinions of a group of allergists.

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Immunotherapy

Table 8: General Pharmacologic Management of Allergic Rhinitis Agent Oral Antihistimines Nasal Antihistimines Intranasal Corticosteroids Oral Decongestants Intranasal Decongestants Intranasal Mast Cell Stabilizers

Congestion Rhinorrhea

Eye Symptoms

Sneezing

Itching

++

++

+/-

++

++

+

+

+/-

+

-

++

++

++

++

+

-

-

+

-

-

-

-

++

-

-

+

+

+

+

-

- = provides no benefit +/- = provides little or minimal benefit + = provides modest benefit ++ = provides substantial benefit Adapted and modified from Diseases of the Atopic Diathesis, The Allergy Report, Vol. 2, American Academy of Allergy, Asthma and Immunology, Milwaukee, WI 2000.

When the history and physical examination indicate perennial allergic rhinitis, screening tests such as prick/puncture tests for common allergens may be advisable. Skin prick/puncture tests demonstrate IgE-mediated reactions to specific allergens and are necessary if immunotherapy is considered and quite useful if allergen avoidance measures will be instituted. Positive allergy test results can be used to reinforce to patients the importance of environmental control measures and can help justify the expense and effort needed to implement them. Immunotherapy involves injecting a patient with increasing doses of the specific allergen that is causing the allergic reactions; this is done with regular subcutaneous injections over an extended period. Specific immunotherapy may be indicated if severe symptoms occur all year or during a major portion of the year; if avoidance and pharmacotherapy do not adequately control symptoms; if pharmacotherapy causes adverse effects; or if a patient’s history and allergy testing indicate a clear relationship between symptoms and exposure to an unavoidable allergen. Immunotherapy may result in reduced symptoms and the ability to reduce doses of medications. Immunotherapy may also result in long-term beneficial effects, even after injections are stopped. This therapy is usually prescribed by an allergist and may be administered in the office of the family physician.

ASTHMA Until recently asthma was thought to be characterized by episodic airway hyperresponsiveness, reversible airflow obstruction, and airway inflammation, with the main etiologic emphasis on contraction of airway smooth muscle. Inflammation was thought to be characteristic of severe asthma. Scientific advances have led to the current recognition that regardless of its severity, asthma is a chronic inflammatory disorder.

Role of Inflammation Recent studies indicate that inflammation is present in all stages of asthma, is a key element in the pathogenesis of asthma, and is the driving force in hyperresponsiveness and airflow limitations of various kinds. Airway inflammation causes an increase in existing bronchial hyperresponsiveness to a variety of stimuli such as allergens, cold air, irritants, exercise, and viral infections. Inflammation is directly linked to acute bronchoconstriction, airway edema, and mucous plug formation, all of which limit airflow and cause acute and chronic symptoms. Chronic inflammation also injures the ciliated epithelium of the lower airways and may result in structural changes or remodeling. Remodeling of airway tissue is characterized by shedding of epithelial cells, proliferation of epithelial cells and myofibroblasts beneath the epithelium, and deposition of interstitial collagens in the basement membrane, which causes it to thicken. Remodeling may be the reason why obstruction persists in some patients with asthma and may be only partially reversible even with aggressive treatment with antiinflammatory and bronchodilator drugs. Atopy is now considered the strongest predisposing factor for asthma. Asthma is the result of a complex interaction between a variety of environmental factors and the genetic predisposition to develop allergic diseases. An adult with a family history of asthma or rhinitis has a threefold to fourfold higher risk of developing asthma than an adult without a family history.

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Establishing a Diagnosis A number of indicators in the medical history that suggest further examination are necessary to determine if asthma is present (Table 9). In the history, relevant findings include recurrent episodes of coughing or wheezing; chest tightness or shortness of breath; symptoms worsening with exposure to allergens, irritants, or exercise; symptoms occurring or worsening at night, awakening the patient; patient with allergic rhinitis or atopic dermatitis; or close relatives have asthma, allergy, sinusitis, or rhinitis. In examining the upper respiratory tract, chest, and skin, relevant findings may include sounds of wheezing during normal breathing or a prolonged phase of forced exhalation; increased nasal secretions or mucosal swelling; sinusitis, rhinitis, or nasal polyps; and atopic dermatitis or eczema. It is important to keep in mind that patients who are between exacerbations may present without symptoms. Patients with a severe exacerbation may have diminished breath sounds without wheezing. A diagnosis of asthma is established by a combination of the following characteristics: the patient has past or current episodic symptoms of airflow obstruction, such as wheezing, shortness of breath, tightness in the chest, or cough, and the airflow obstruction is at least partially reversible. Spirometry, before and after inhalation of a 2-agonist, should be used to establish airflow obstruction and its reversibility, defined as forced expiratory volume at one second (FEV1) of less than 80% of the anticipated volume and FEV1/FVC (forced vital capacity) ratio <65% or below the lower limit of normal. In adults and children older than 5 years of age, reversibility is established if FEV1 increases more than 12% and at least 200 mL after using a short-acting inhaled 2-agonist. In addition, there should be no signs or symptoms that indicate alternative diagnoses, such as vocal cord dysfunction, foreign bodies, or other pulmonary diseases (Table 10). Complete pulmonary function tests including arterial blood gases may be necessary when coexisting conditions such as chronic obstructive pulmonary disease are suspected. Directed allergy testing may be undertaken, but only to assess sensitivity in patients with persistent asthma. Relevant allergens are typically perennial, not seasonal. In infants and children younger than 5 years of age, the same diagnostic criteria apply except that spirometry usually cannot be done. Upper respiratory tract viral infection is the most common cause of wheezing in this age group. A diagnosis of asthma is not needed to begin treatment. A trial of asthma medications may aid in the eventual diagnosis.

Table 9: Findings That May Suggest Asthma Medical History ■ Episodic wheeze, chest tightness, shortness of breath, coughing ■ Symptoms worsen with exposure to allergens and irritants or with exercise ■ Symptoms occur or worsen at night ■ Patient has allergic rhinitis or atopic dermatitis ■ Close relatives have asthma, allergy, sinusitis, rhinitis

Physical Examination ■ Sounds of wheezing during normal breathing or a prolonged phase of forced exhalation ■ Increased nasal secretions, mucosal swelling ■ Sinusitis, rhinitis, nasal polyps ■ Atopic dermatitis/ eczema or other signs of allergic skin problems

Table 10: Diagnostic Criteria for Asthma ■ History or presence of episodic symptoms of airflow obstruction ■ Airflow obstruction and reversibility is diagnosed by spirometry ■ Obstruction: FEV1 < 80%; FEV1/FVC < 65% ■ Reversible: FEV1 improvement of >12% and 200 mL after 2-agonists ■ Alternative diagnoses are excluded

Table 11: Severity Classifications of Asthma (NIH 1997) Symptoms

Nighttime Symptoms

Lung Function

Severe Persistent

■ Continual symptoms ■ Limited physical activity ■ Frequent exacerbations

Frequent

FEV1 or PEF ≤60% predicted PEF variability >30%

Moderate Persistent

■ Daily symptoms ■ Daily use of rescue medications ■ Exacerbations affect activity ■ Exacerbations ≥2/week

>1/week

FEV1 or PEF >60-<80% predicted

Mild Persistent

■ Symptoms >2/week but <1/day ■ Exacerbations may affect activity

>2/month

FEV1 or PEF ≤80% predicted PEF variability 20% to 30%

Mild Intermittent

■ Symptoms ≤ 2/week ■ Asymptomatic and normal PEF between exacerbations ■ Exacerbations brief

≤2/month

FEV1 or PEF ≥80% predicted PEF variability ≤20%

Determining Disease Severity The clinician should determine each patient’s level of disease severity in order to recommend the appropriate therapy. The National Heart, Lung, and Blood Institute has established criteria for classifying severity based on symptoms and lung function (Table 11). Levels of severity are mild intermittent, mild persistent, moderate persistent, and severe persistent.

Consultation The decision to seek collaborative care with an asthma specialist will vary from patient to patient and among physicians. Specialists’ offices may have teams of educators who can provide important but time intensive information. Referrals or collaboration will depend on available resources, the severity of the patient’s asthma, and the physician’s comfort with asthma management. Collaboration with an asthma specialist should be considered if standard therapy fails or proves inadequate; if well-controlled asthma suddenly worsens; if testing is required; or to manage unexpected complications of disease or side effects of medication.

PEF variability >30%

FEV1 = forced expiratory volume in one second PEF = peak expiratory flow Adapted from Guidelines for the Diagnosis and Management of Asthma: Expert Panel Report 2. Bethesda, MD: National Heart, Lung, and Blood Institute, 1997. NIH publication no. 97-4051.

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Table 12: Asthma Therapy

Goals of Therapy

Goals ■ Prevent asthma symptoms and exacerbations ■ Maintain normal activity levels ■ Normal or near-normal lung function ■ No or minimal side effects to medications Components ■ Objective measures of lung function ■ Environmental control ■ Comprehensive pharmacologic therapy ■ Patient education that fosters a partnership between patient, family, and physician

The goals of asthma therapy are to prevent chronic asthma symptoms and asthma exacerbations during the day and night, maintain normal activity levels, have normal or near-normal lung function, and have no or minimal side effects to medications. Patients and their family must participate in care decisions and be comfortable and satisfied with their care. The four components necessary to achieve these goals are as follows: objective measures of lung function to assess disease severity and monitor therapy; environmental control measures to avoid or eliminate factors that precipitate symptoms or exacerbations; comprehensive pharmacologic therapy for long-term management of inflammation and prevention of acute exacerbations; and patient education to foster partnership among the patient, his or her family, and the family physician to enhance patient adherence to medical and educational advice (Table 12).

Controlling Factors Contributing to Severity Controlling the factors that provoke inflammation and contribute to asthma severity is important in achieving long-term control and in reducing symptoms and the need for rescue medications. Allergy triggers for asthma are almost always inhaled allergens (Table 13). Other asthma triggers include pollution and certain medications.

Table 13: Factors Contributing to Asthma Severity (NIH1997) Allergy ■ House dust mite ■ Cockroach allergen ■ Animal dander ■ Indoor molds ■ Pollen Irritants ■ Tobacco smoke ■ Indoor/outdoor pollution

Coexisting Conditions ■ Rhinitis/sinusitis ■ Gastroesophageal reflux disease ■ Viral respiratory infection Medications ■ Aspirin, other NSAIDs ■ ACE inhibitors

NSAIDs = nonsteroidal antiinflammatory drugs ACE = angiotensin converting enzyme Adapted from Guidelines for the Diagnosis and Management of Asthma: Expert Panel Report 2. Bethesda, MD: National Heart, Lung, and Blood Institute, 1997. NIH publication no. 97-4051.

To help the patient limit exposure to allergens that trigger his or her asthma, identify allergens to which the patient is exposed; determine and confirm sensitivity to specific allergens with medical history or allergy testing; obtain patient’s cooperation in initiating one or two simple control measures; provide a patient handout with specific instructions on allergen avoidance; add additional control measures after the first ones are implemented; and follow up with the patient to measure progress.

Pharmacotherapy Treating persistent asthma, regardless of its severity, requires both daily long-term therapy to achieve and maintain control of inflammation and symptoms, and appropriate rescue medications to manage acute exacerbations (Table 14). Recent studies have shown that using antiinflammatory agents early in the course of the asthma (such as in patients with mild persistent asthma) may prevent or reverse the development of airway remodeling and irreversible airway obstruction.

Long-Term Control Medications Inhaled corticosteroids are first-line therapy for gaining long-term control of asthma. A short course of 7 to 10 days of systemic corticosteroids may be needed to gain prompt control of the disease when initiating long-term therapy. Early, aggressive treatment and inhaled corticosteroids are first-line therapy for mildpersistent and moderate-persistent asthma. Cromolyn sodium and nedocromil are mild antiinflammatory agents that may be initial choices for children and pregnant women. These agents can also be used as preventive therapy before exercise or allergen exposure. The clinical response to cromolyn and nedocromil is less predictable than the response to inhaled corticosteroids. In patients with severe asthma that is not adequately controlled with low to moderate doses of inhaled corticosteroids, a long-acting bronchodilator may be added to the daily regimen to spare patients from increasing the dosage of inhaled corticosteroids or adding oral corticosteroids. Patients accustomed to the quick onset of action of short-acting 2-agonists should be instructed about the slower onset of action of the long-acting bronchodilator so that they do not take additional doses when they do not get the fast response that they expect. Having the patient place a distinctive mark on the long-term 2-agonist inhaler may prevent its accidental use as a rescue medication. It is important to remember, however, that long-acting 2-agonists should not be used as monotherapy. Sustained-release theophylline is a mild to moderate bronchodilator that may help control nighttime symptoms as an adjunct to inhaled corticosteroids.

10

Leukotriene modifiers may be added to corticosteroids, especially in patients with milder asthma, instead of increasing corticosteroids. The position of leukotriene modifiers as monotherapy in asthma is not fully established. Physicians and patients are sometimes concerned about the safety of inhaled corticosteroids. These agents are generally well tolerated at recommended dosages. To reduce the potential for possible adverse effects such as osteoporosis, cataracts, and growth suppression, the lowest possible dosage to maintain control should be prescribed. Although inhaled corticosteroids may induce some adverse effects, the potential risks are outweighed by the benefits. Patients should be instructed to use a spacer or holding-chamber device with a metered-dose inhaler to deliver inhaled steroids. Spacers hold the aerosol medication so the patient can inhale it easily. Spacers eliminate the problem of coordinating actuation of the metered-dose inhaler with the inhalation, improve the flow of medication into the lungs, and prevent oral candidiasis. Patients also should be told to rinse their mouths and spit following inhalation.

Rescue Medications Quick-relief or rescue medications are used to provide prompt treatment of acute airflow obstruction and its accompanying symptoms such as coughing, chest tightness, shortness of breath, and wheezing. These medications include short acting inhaled 2-agonists and anticholinergics, which may be used in special circumstances.

Immunotherapy The role of immunotherapy in the treatment of asthma is controversial. The best data for beneficial effects are based on immunotherapy for a single allergen. However, for managing patients allergic to multiple allergens, the benefit of immunotherapy is lower. Preliminary data with a recombinant humanized monoclonal antibody (anti-IgE) are encouraging as a treatment for patients with moderate or severe allergic asthma.

Stepped Approach to Management The NAEPP/NHLBI guidelines recommend an aggressive step-up/step-down approach to pharmacotherapy based on each patient’s level of disease severity. At initial diagnosis, pharmacologic therapy with corticosteroids is “stepped up” to a higher level than symptoms might indicate in order to establish prompt control. For example, a mild-persistent asthmatic experiencing symptoms may be started on a short course of oral steroids. When symptoms are under control, therapy is then “stepped down” to lower daily doses of inhaled steroids until evaluation determines the minimum dosage needed for adequate control. Therapy may need to be stepped up again if signs of poor control appear. These include wakening at night with symptoms, an urgent care visit, or more frequent use of rescue medications.

Table 14: Asthma Pharmacotherapy Daily Long-Term Control Medications ■ Inhaled Corticosteroids - first-line treatment ■ Systemic Corticosteroids - often used to gain prompt control when initiating long-term inhaled corticosteroids ■ Cromolyn Sodium and Nedocromil - may be initial choice in children - can also be used as preventive therapy before exercise or allergen exposure ■ Long-Acting ß2-Agonists (salmeterol) - used concomitantly with antiinflammatory medications - steroid sparing - not for acute symptoms or exacerbations ■ Methylxanthines (sustained-release theophylline) - mild to moderate bronchodilator - adjunct to inhaled corticosteroids for nocturnal symptoms ■ Leukotriene Modifiers - position not fully established Rescue Medicatons ■ Short-acting Inhaled ß2-Agonists - first choice for acute symptoms and prevention of exercise-induced bronchospasm - should be prescribed for all patients ■ Anticholinergics (ipratropium bromide) - some additive benefit to inhaled ß2-agonists in severe exacerbations - alternative bronchodilator for patients intolerant of inhaled ß2-agonists

Follow-Up Each patient’s asthma will change over time, depending on environmental exposures, the patient’s activities, and disease management. Consequently, even when patients have their asthma under control, regular monitoring and daily treatment are necessary to maintain control. Asthma is a chronic disease requiring long-term management. Regular periodic clinical assessments are essential for optimal asthma care: Asthma severity can wax and wane; patients’ exposure to asthma triggers may change; and patients need to have proper self-management practices reinforced. The frequency of patient follow-up visits depends primarily on the severity of the asthma and the patient’s ability to control and monitor symptoms. However, the first follow-up visit after a new diagnosis or exacerbation should be within one month. Physicians should review symptom history, lung function, responses to

11

Table 15: Periodic Clinical Assessments ■ Review - symptom history - lung function - responses to medications and side effects - use of rescue medications - emergency or hospital care - missed work or school - changes in activity levels - nocturnal awakenings - satisfaction with care ■ Perform a physical examination ■ Have patient demonstrate techniques with peak flow meter and metered-dose inhaler

medications and side effects, use of rescue medications, emergency or hospital care visits, missed work or school, changes in activity levels, nocturnal awakenings, and satisfaction with care. A physical examination should also be performed during each visit (Table 15). It is especially important at each visit to check the proper use of peak flow meters and metered-dose inhalers, including initializing, reactualizing, and replacement when empty or outdated. Patients should be asked to demonstrate how they use their inhaler(s) and peak flow meter if they have one. Spirometry tests should be performed at least every 1 to 2 years when asthma is stable, more often when it is unstable. Daily peak flow monitoring is recommended for patients with moderate or severe persistent asthma, and for patients with a history of severe exacerbations. Monitoring peak flow can tell patients if their condition is under control, if it is worsening, or if they need emergency treatment. A written guide to care, including guidelines for seeking emergency care, can help patients monitor their asthma.

Patient-Physician Partnership Long-term control of asthma requires that patients and their families be proactively involved in managing their disease. They need to work together with physicians and their medical staff in monitoring their condition, taking their medications regularly and properly, and avoiding triggers that cause exacerbations. To do these things patients and their family need to understand the causes of asthma. They need to know what their specific triggers are and how to avoid them. They should be informed about how their medications work, possible side effects, and how to comply with treatment. They need to be instructed in the use of metered-dose inhalers and spacers, peak flow meters, and have a personalized action plan. Asthma education messages can be reinforced by participation in programs like the American Lung Association’s “Open Airways for Schools” and “A is for Asthma.” Physicians can facilitate such programs in their community schools. Preparing patients to manage exacerbations is essential. The family physician has the opportunity to keep patients out of the emergency department by making a proper diagnosis, prescribing appropriate treatment, and educating the patient about self-management. The family physician should work with patients and their families to develop an emergency action plan. Patients should also receive clear instructions on how to follow the plan. The plan should include information on how to recognize signs of worsening asthma that indicate the need to call the doctor or seek emergency care; on the prompt use of short-acting ß2-agonists for mild exacerbations and oral corticosteroids for moderate-to-severe exacerbations; and on monitoring their response to these medications.

SUMMARY At this time, it may not be possible to prevent or cure allergic rhinitis or asthma. But patients do not need to suffer through allergy seasons, adults do not have to miss work, children do not have to miss school or avoid physical activities, and patients do not have to fear rushing to the emergency room at night because they cannot breathe. Family physicians and patients working together can gain and maintain control of these chronic diseases with a comprehensive management approach that includes patient education, objective monitoring of lung function, allergen avoidance and environmental control, and pharmacologic therapy.

12

Patient Handout 1

CONTROLLING THINGS THAT MAKE YOUR ALLERGIES WORSE If you have an allergic condition, like asthma or nasal allergies, your immune system reacts to harmless substances in the air, like pollen or pet dander, as if they were harmful bacteria. This overreaction causes symptoms like a runny nose and sneezing in people with allergies, or an asthma attack in people with asthma. Not everyone is allergic to the same things. You may know some of the things that trigger this reaction or make your condition worse. Your physician can help you identify others. One of the most important things you can do to control your asthma or nasal allergy symptoms is to limit your contact with these triggers. Some of the most common triggers are listed below, along with suggestions on how to avoid them.

Dust Mites

Indoor Mold

You can’t see dust mites but they live in cloth or carpet. Many people are allergic to them.

Molds thrive on moisture and their spores are common triggers.

• • • • • • •

Cover your mattress and pillows with special dust-proof covers.* Wash sheets and blankets each week in hot water (over 130˚ F). If possible, remove wall-to-wall carpets in the bedroom. Keep household humidity to less than 50%. Use dehumidifiers or central air conditioners, not ceiling fans. Vacuum carpets and rugs once or twice a week. If the person with asthma must vacuum, use a dust mask, a double-layered or micro filter vacuum cleaner bag, or a vacuum cleaner with a HEPA filter.*

Animal Dander Flakes of skin or dried saliva from animals with fur or feathers trigger allergies. • • •

Keep furry or feathered pets out of the bedroom at all times and outdoors if possible. Use a HEPA filter in the bedroom or cover air vents with a heavy material.* Bathe pets and wash pet bedding weekly.

Cockroaches Many people are allergic to the dried droppings and remains of cockroaches. • •

Always keep food and garbage in closed containers. Have a professional exterminate your house or use commercial products, like poison baits.

• • • •

Fix leaky faucets, pipes, or other sources of water. Try not to use humidifiers or, if necessary, wash them often with bleach. Check basements, attics, and crawl spaces for mold and moisture. Do not keep plants in the bedroom.

Pollen and Outdoor Mold Find out when pollen and mold levels are high during allergy season and do the following. • • •

Stay indoors with windows closed and the air conditioner running when pollen and mold counts are highest. Avoid mowing the lawn and raking leaves. Clean furnace and air conditioner filters often.

Smoke, Strong Odors, and Sprays There are substances in the air that can irritate your nose or lungs and make your condition worse, such as tobacco smoke. You should try to avoid these. • • • • •

If you smoke, ask your doctor for ways to help you quit. Do not allow smoking in your home or around you. Do not use a wood-burning stove, kerosene heater, or fireplace. Try to stay away from strong odors and sprays, such as perfume, talcum powder, hair spray, and paints. Ask co-workers not to use heavy perfumes.

* Contact these organizations for information on the products mentioned above. Asthma and Allergy Foundation of America (800-727-8462) Allergy and Asthma Network/Mothers of Asthmatics, Inc (800-878-4403) American Academy of Allergy, Asthma, and Immunology (800-822-2762)

13

Patient Handout 2

TAKE CONTROL OF YOUR ASTHMA Asthma is a condition that you will have all your life, but it can be treated so that you do not have symptoms all or most of the time and you can lead a normal life. You have an important role to play in taking control of your asthma. With your doctor’s help, you need to do the following things.

Understand Your Disease Asthma causes the airways in your lungs to be inflamed, which means they are swollen and sensitive. The swelling is there all or most of the time, even when you feel fine and have no symptoms like wheezing or difficulty breathing. This swelling can be controlled with medicine and by avoiding the things that inflame or irritate your airways. Because asthma can’t be cured, you and your doctor need to watch for any changes in your condition or in how your medicines are working.

doctor can help you learn what these triggers are and how to stay away from them, as much as possible. Anything you can do to lessen your contact with these triggers can help avoid attacks.

Take the Medicines Recommended by Your Doctor •

•

Avoid the Things That Cause Attacks Many things in your home, school, workplace, or outdoors can cause asthma attacks. An asthma attack occurs when your airways narrow, making it harder to breathe. Asthma attacks are sometimes called flareups, exacerbations, or episodes. Things in the air that you are allergic to (like house dust mite) can cause an asthma attack. So can things that irritate your airways like tobacco smoke. These are called triggers. Your

• •

Know what your medications are and how they work. You may be given a daily medication to control inflammation and help prevent attacks and another one to use only when you have an attack. Learn how to use metered-dose inhalers and spacers (see illustrations). Check whether your medicine is controlling your symptoms. Your doctor may recommend that you use a peak flow meter. Your asthma doesn’t go away when your symptoms go away. So you need to continue taking your regular medications until your doctor tells you otherwise.

Steps for Using Your Inhaler Examples of Spacer/Holding Chamber Devices

Getting ready

1. Take off the cap and shake the inhaler. 2. Breathe out all the way. 3. Hold your inhaler the way your doctor said (A, B, or C below).

Breathe in slowly

4. As you start breathing in slowly through your mouth, press down on the inhaler one time. (If you use a holding chamber, first press down on the inhaler. Within 5 seconds, begin to breathe in slowly.) 5. Keep breathing in slowly, as deeply as you can. 6. Hold your breath as you count to 10 slowly, if you can. 7. For inhaled quick-relief medicine (ß2-agonists), wait about 1 minute between puffs. There is no need to wait between puffs for other medicines.

Hold your breath

A. Hold inhaler 1 to 2 inches in front of your mouth (about the width of two fingers).

B. Use a spacer/holding chamber. These come in many shapes and can be useful to any patient.

C. Put the inhaler in your mouth. Do not use for corticosteroids.

Adapted from Practical Guide for the Diagnosis and Management of Asthma. Bethseda, MD: National Heart, Lung, and Blood Institute; 1997. NIH publication 97-4053.

Watch for Signs That Your Asthma Is Getting Worse The following are signs that your asthma is worsening. • • • • • •

14

Symptoms, such as coughing, wheezing, shortness of breath, or tightness in the chest Awakening at night because of symptoms Needing to use your quick-relief medicine more frequently Asthma symptoms keep you from going to work or school or from exercising Having to go to the emergency department or hospital Peak flow meter reading falls below 80% of your personal best (into the yellow or red zone.)

Your physician can write an action plan for you. It will tell you what medicines to take if your asthma symptoms get worse or if you need to contact the doctor or go to the emergency department.

Keep in Touch With Your Doctor Over time, your asthma may change. It could get worse and you may need additional medicine to prevent symptoms. That’s why you need to keep in touch with your doctor. See your doctor at least once every 6 months.

Patient Handout 3

TAKE CONTROL OF YOUR NASAL ALLERGIES Nasal allergies, called allergic rhinitis, are one of the most common chronic diseases in both children and adults. While allergic rhinitis can’t be cured, together you and your doctor can get rid of your symptoms or at least keep them under control. You have an important role to play in taking control of your nasal allergies. You need to do the following things.

Talk With Your Doctor Allergic rhinitis causes obvious symptoms like stuffy, congested, or runny nose, sneezing, and itchy, watery eyes. These may be annoying but you may not think they require your doctor’s attention. However, allergic rhinitis can also cause other symptoms like headache, sore throat, postnasal drip, recurrent head colds, chronic cough, plugged or itchy ears, difficulty smelling and tasting, mouth breathing, and snoring. It can make you feel tired, irritable, and restless. It can make it harder for you to concentrate and sleep well and interfere with your work at school or on the job. If it is not treated, allergic rhinitis can sometimes lead to complications like sinusitis, ear blockage, infections, and asthma. Allergic rhinitis can be treated, so talk to your doctor about your symptoms.

Understand Your Disease Allergic rhinitis simply means “inflammation of the nose due to an allergy.” Not everyone develops allergies and the reason why some people do is not known. Allergies tend to run in families, so if one or both of your parents have allergic rhinitis, you probably will too. Different things (called allergens) trigger allergic reactions in different people. The pollens released by trees, grasses, and weeds in the spring and fall cause seasonal allergic rhinitis, also called hay fever. In areas of the county where the growing season lasts year-round, hay fever symptoms may be constant. Indoor allergens, such as dust mites, molds, and animal dander, cause perennial allergic rhinitis, with symptoms that last year-round.

Avoid Things That Cause Symptoms Limiting your contact with your allergen triggers is one of the most important ways to control symptoms. Your doctor can help you find out what you are allergic to and recommend ways to avoid them. Your physician may suggest allergy testing to confirm the things that trigger your allergies, especially if he or she thinks you may benefit from allergy shots. Allergy shots, called immunotherapy, may reduce your sensitivity to allergens. This procedure involves a series of injections of increasing doses of allergens, given over an extended period of time.

Take the Medicines Recommended by Your Doctor Since it is usually not possible to eliminate all contact with allergens, your physician may prescribe one or more types of medications to control inflammation and allergy symptoms. These include: • Oral antihistamine relieves sneezing, runny nose, and itchy nose and eyes. Antihistamines generally work best when started before allergy season begins and continued until it is over, even if you have no symptoms. If your rhinitis is perennial, you may need to take them on a regular daily basis. • Oral decongestant decreases stuffiness, but do not control other symptoms. You can take an antihistamine and decongestant combined in one pill. • Corticosteroid nasal spray relieves inflammation as well as symptoms. It may be prescribed alone for mild hay fever or together with an antihistamine to treat perennial allergic rhinitis. • Cromolyn sodium nasal spray also relieves allergic symptoms by reducing inflammation.

15

16

Very short of breath, or Quick-relief medicines have not helped, or Cannot do usual activities, or Symptoms are same or get worse after 24 hours in Yellow Zone

➧ ❑ 2 or ❑ 4 puffs

How much to take

➧ 5 to 60 minutes before exercise

When to take it

2 or 4 puffs, every 20 minutes for up to 1 hour Nebulizer, once

❑

❑ Call the doctor

❑ before

❑

➧

(oral steroid)

___________________________________________ mg

❑

6 puffs or

■ Take ❑ 4 or ❑ 6 puffs of your quick-relief medicine AND ■ Go to the hospital or call for an ambulance (_____________________) NOW!

■ You are still in the red zone after 15 minutes AND ■ You have not reached your doctor.

Then call your doctor NOW. Go to the hospital or call for an ambulance if:

❑

(short-acting beta2-agonist)

4 or

❑

Nebulizer

within _______________ hours after taking the oral steroid.

(oral steroid)

Add: ____________________________________________mg per day For _______(3-10) days

(short-acting ß2-agonist)

If your symptoms (and peak flow, if used) return to GREEN ZONE after 1 hour of above treatment: Take the quick-relief medicine every 4 hours for 1 to 2 days. Double the dose of your inhaled steroid for ____________(7-10) days. -OrIf your symptoms (and peak flow, if used) do not return to GREEN ZONE after 1 hour of above treatment: ❑ Take: ___________________________________________ ❑ 2 or ❑ 4 puffs or ❑ Nebulizer

❑

Take this medicine: ❑ ___________________________________________ ❑

Second

➧ ❑❑

First

your GREEN ZONE medicine ➧ Add: Quick-Relief Medicine — and keep taking ❑ ❑

❑ ______________________________

Medicine

Take These Long-Term Control Medicines Each Day (include an anti-inflammatory)

Reprinted from National Asthma Education and Prevention Program: National Heart, Lung, and Blood Institute: NIH Publication No. 87-4053.

■ Trouble walking and talking due to shortness of breath ■ Lips or fingernails are blue

DANGER SIGNS

Peak flow: less than _________ (50% of my best peak flow)

-Or-

■ ■ ■ ■

RED ZONE: Medical Alert!

Peak flow: _________ to _________ (50% - 80% of my best peak flow)

-Or-

■ Cough, wheeze, chest tightness, or shortness of breath, or ■ Waking at night due to asthma, or ■ Can do some, but not all, usual activities

YELLOW ZONE: Asthma Is Getting Worse

Before exercise

My best peak flow is:__________________

(80% or more of my best peak flow)

And, if a peak flow meter is used, Peak flow: more than ______________

■ No cough, wheeze, chest tightness, or shortness of breath during the day or night ■ Can do usual activities

GREEN ZONE: Doing Well

Doctor’s Phone Number_____________________________________________________________Hospital/Emergency Room Phone Number________________________________________

Asthma Action Plan For_______________________________________________________Doctor’s Name__________________________________________Date ________________

Patient Handout 4

ASTHMA ACTION PLAN

BIBLIOGRAPHY Action Against Asthma. A strategic plan for the Department of Health and Human Services. Available at: http://aspe.hhs.gov/splasthma/. Accessed June 5, 2000.

Milgrom H, Fich RB Jr, So JQ, et al. Treatment of allergic asthma with monoclonal anti-IgE antibody. N Engl J Med. 1999;341:2006-2008.

American Academy of Allergy, Asthma, and Immunology. Diseases of the Atopic Diathesis. Milwaukee, WI: The American Academy of Allergy, Asthma, and Immunology, Inc; 2000. The Allergy Report; vol. 2.

(NIAID) National Institute of Allergy and Infectious Diseases. Asthma: A concern for minority populations. January, 1997.

Barnes PJ. Anti-IgE antibody therapy for asthma [Editorial]. N Engl J Med. 1999;341:2006-2008. Beasley R, Crane J, Lai CKW, Pearce N. Prevalence and etiology of asthma. J Allergy Clin Immunol. 2000;105:S466-S472. Burrows B, Martinez FD, Halonen M, Barbee RA, Cline MG. Association of asthma with serum IgE levels and skin reactivity to allergens. N Engl J Med. 1989;320:271-277. Busse WW. Inflammation in asthma: the cornerstone of the disease and target of therapy. J Allergy Clin Immunol. 1998;102:S17-S22. (DHHS) Department of Health and Human Services. HHS Targets Efforts on Asthma. May 21, 1998. Djukanovic R. Asthma: disease of inflammation and repair. J Allergy Clin Immunol. 2000;105:S522-S526. Grant JA, Nicodemus CF, Findlay SR, et al. Cetirizine in patients with seasonal allergic rhinitis and concomitant asthma: prospective randomized, placebo-controlled trial. J Allergy Clin Immunol. 1995;95:923-932. Howarth PH. Is allergy increasing? – Early life influences. Clin Exp Allergy. 1998;6(suppl):2-7. Laitinen LA, Laitinen A, Hantela T. A comparative study of the effects of the inhaled corticosteroid budesonide and the ß-agonist terbutaline on airway inflammation in a newly diagnosed asthma: a randomized, double-blind, parallel-group controlled trial. J Allergy Clin Immunol. 1992;90:32-42. Laitinen LA, Altraja AA, Karjalainen E-M, Laitinen A. Early intervention in asthma with inhaled corticosteroids. J Allergy Clin Immunol. 2000;105:S582-S585. Lasley MV. Allergic disease prevention and risk factor identification. Immunol Allergy Clin North Am. 1999;19:149-159.

National Institutes of Health. Expert Panel Report 2. Guidelines for the Diagnosis and Management of Asthma. Bethesda, Md: National Institutes of Health, 1997; Publication #97- 4051. National Institutes of Health. Practical Guide for the Diagnosis and Management of Asthma. Bethesda, Md: National Institutes of Health, 1997; Publication #97-4053. Monthly Vital Statistics Report, August 14, 1997;46(1):table 6. (MMWR) Surveillance for asthma - United States 1960-1995. Morbidity and Mortality Weekly Report, April 24, 1998;47(SS-l). Open Airways for Schools. American Lung Association website. Available at: http://www.lungusa.org/school/oas.html. Accessed June 5, 2000. Platts-Mill TA. How environment affects patients with allergic disease: indoor allergens and asthma. Ann Allergy. 1994;72:381-384. Platts-Mill TA, Rakes G, Heymann PW. The relevance of allergen exposure to the development of asthma in childhood. J Allergy Clin Immunol. 2000;105:S503-S508. Rachelefsky GS. National guidelines needed to manage rhinitis and prevent complications. Ann Allergy Asthma Immunol. 1999;82:296-305. Schoenwetter WF. Allergic rhinitis: epidemiology and natural history. Allergy Asthma Proc. 2000;21:1-6. Settipane RJ, Hagy GW, Settipane GA. Long-term risk factors for developing asthma and allergic rhinitis: a 23-year follow-up study of college students. Allergy Asthma Proc. 1994;15:21-25. Sly RM, O'Donnell RO. Stabilization of asthma mortality. Ann Allergy Asthma Immunol. 1997;78:347-354. Strannegard IL, Larsson LO, Wennergren G, Strannegard O. Prevalence of allergy in children in relation to prior BCG vaccination and infection with atypical mycobacteria. Allergy. 1998;53(3):249-254.

Lundback B. Epidemiology of rhinitis and asthma. Clin Exp Allergy. 1998;28(suppl 2):3-10.

Verdiani P, DiCarlo S, Baronti A. Different prevalence and degree of nonspecific bronchial hyperreactivity between seasonal and perennial rhinitis. J Allergy Clin Immunol. 1990;86:576-582.

McMenamin P. Costs of hay fever in the United States in 1990. Ann Allergy. 1994;73:35-39.

Vital and Health Statistics, December 1995;10(193):table 62.

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