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J Am Dent Assoc, Vol 132, No 9, 1229-1239.
© 2001 American Dental Association
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DENTISTRY & MEDICINE

COVER STORY

The dental patient with asthma

An update and oral health considerations



DEREK M. STEINBACHER, D.M.D. and MICHAEL GLICK, D.M.D.


   ABSTRACT
TOP
 ABSTRACT
PATHOPHYSIOLOGY
 DIAGNOSIS AND CLASSIFICATION
 MANAGEMENT AND PHARMACOTHERAPY
 ORAL HEALTH CHANGES IN...
 MANAGEMENT IN DENTAL CARE
 CONCLUSION
 REFERENCES
 
Overview. Asthma is a serious global health problem that has steadily increased in prevalence during the past two decades. New classification and treatment guidelines have been published, and dental providers need to be aware of these changes.

Literature Reviewed. The authors searched textbooks and MEDLINE, looking for the most updated medical information on asthma, as well as for previous publications on treatment of asthmatic patients in a dental setting.

Results. More than 9,000 articles on asthma were published in English between 1997 and 2000. From 1960 until 2000, approximately 40 articles specifically addressed asthma and dental care. The authors reviewed more than 300 articles from the medical literature and all articles after 1980 that directly focused on oral health issues for importance and relevance.

Conclusions. Recent information regarding the etiology, pathogenesis and treatment of asthma had not been adequately addressed in the dental literature. Dental care of asthmatic patients may necessitate considerations beyond what has previously been published in the dental literature.

Clinical Implications. In the treatment of asthma, as with treatment of most medical conditions, oral health care providers play a role that is important in terms of both the patient’s overall health and the systemic condition’s effect on oral health. This article provides dentists with a timely update on asthma and the relationship between asthma and oral health, and it offers suggestions for safe and appropriate dental care.

Asthma is a serious global health problem, affecting more than 100 million people worldwide. The prevalence of asthma in the United States has increased steadily for the past two decades with no end in sight.1 It is estimated that more than 17 million Americans are affected, with a projected increase to as many as 22 million cases by 2010 and 29 million cases by 2020. Although asthma is viewed by many as a fairly benign disorder, the mortality rate for this disease has almost tripled in the past 20 years, reaching a peak of more than 5,000 annual deaths.2 This somber number is projected to double within the next two decades.

In the treatment of asthma, oral health care providers play a role that is important in terms of both the patient’s overall health and the systemic condition’s effect on oral health.

Children, young adults and racial and ethnic minorities living in urban areas compose the group of people at highest risk. This is not surprising, as health disparities play a significant role in putting people at risk of developing this disease. However, other, less understood factors also contribute to the noted increased prevalence.3–6 Poverty-stricken inhabitants of the inner city have a greater chance of developing the disease, and their disease often has a more severe progression. Many different factors have been put forth as explanations of this phenomenon—crowded living conditions with poor ventilation, lack of access to quality health care, reduced long-term adherence to and maintenance of therapeutic regimens, family dysfunction, weak social supports and paucity of education.7–9

Asthma care represents a significant economic and social burden, accounting for numerous hospitalization stays and missed days of school and work.

With increasing numbers of affected patients, oral health care workers need to be adept at recognizing the signs and symptoms of asthma. Modifications to dental treatment may be indicated, and practitioners need to be capable of handling acute exacerbations. To that end, this article provides a review of asthma pathogenesis, diagnosis and classification, treatment and pertinent oral health considerations.


   PATHOPHYSIOLOGY
TOP
 ABSTRACT
 PATHOPHYSIOLOGY
DIAGNOSIS AND CLASSIFICATION
 MANAGEMENT AND PHARMACOTHERAPY
 ORAL HEALTH CHANGES IN...
 MANAGEMENT IN DENTAL CARE
 CONCLUSION
 REFERENCES
 
The definition of a disease needs to be all-encompassing and yet specific enough to single out afflicted people. This is important not only for epidemiologic purposes, but also for the development of efficient and appropriate treatment strategies. When the pathogenesis is poorly understood, management many times will consist mainly of symptomatic therapy. At present, it is not clear if asthma is one of numerous different diseases and conditions that have similar signs and symptoms, but different causes.

Asthma is described as a chronic inflammatory disorder involving many cell types, manifesting with episodes of chest tightness, coughing, labored breathing and wheezing, all of which are related to bronchiole inflammation. Symptoms can last for a few moments or for as long as days. The acceptance of inflammation and subsequent fibrosis as the underlying causes of disease progression was the basis for a 1997 report on asthma diagnosis and management by a National Heart, Lung and Blood Institute, or NHLBI, expert panel.10 The airway obstruction in asthma is initiated by inflammation and muscle spasm but is mostly reversible (boxGo, "Factors That Produce Airway Obstruction in Asthma"). It generally is believed that both genetic and environmental factors, as well as allergens, are important in the initiation and continuation of the airway inflammation.


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  		FACTORS THAT PRODUCE AIRWAY OBSTRUCTION IN ASTHMA.*

 
Airway inflammation in asthma has been characterized as acute, subacute or chronic. The acute state of inflammation is caused by the release of chemical mediators from activated resident cells, such as local airway mast cells undergoing histamine degranulation. Subacute inflammation is marked by early cellular infiltrates, especially eosinophils that release mediators with direct toxic effects on the respiratory epithelium. The airway inflammation is described as chronic when lymphocytes and eosinophils mediate a persistent, ongoing inflammation, thus resulting in a continuous cycle of damage and repair. Longstanding chronic inflammation can lead to irreversible airway obstruction in a subset of patients with asthma.

Bronchial smooth muscle contraction contributes markedly to the airway obstruction seen in asthma, while vasodilation, diapedesis and vascular permeability account for the edematous changes.11 These changes are attributed to cell-derived mediators. Mucus hypersecretion is also observed and can result in the development of mucus plugs and associated dyspnea.

The strongest identified risk factor for the development of asthma is atopy, an inherited propensity to exhibit allergic reactions, and people with a family history of allergy have an increased predilection for developing asthma. Common precipitating allergens underlying asthma pathogenesis include tobacco smoke, dust mites, animal fur, cockroaches, pollens, molds and other airborne irritants (including acrylic and other aerosolized dental materials).8,12 Viral respiratory infections, small birth size and diet also may contribute to the development of asthma.8 The above-listed factors contributing to asthma development also are involved in the provocation of asthmatic attacks. Additional triggers leading to asthma exacerbations include wood smoke, physical activity, emotional upset, cold air, food additives and aspirin.8 People with asthma vary widely in their response to triggering factors.


   DIAGNOSIS AND CLASSIFICATION
TOP
 ABSTRACT
 PATHOPHYSIOLOGY
 DIAGNOSIS AND CLASSIFICATION
MANAGEMENT AND PHARMACOTHERAPY
 ORAL HEALTH CHANGES IN...
 MANAGEMENT IN DENTAL CARE
 CONCLUSION
 REFERENCES
 
Airway inflammation and hyperreactivity characterize asthma but do not have to be elicited for a diagnosis to be made. Demonstration of reversible airway obstruction is the clinical criterion for asthma. In addition to the clinical manifestations of cough, shortness of breath, chest tightness and wheezing, it is not uncommon to see tachypnea, tachycardia, use of accessory respiratory muscles and pulsus paradoxus.13

Classically, reversible airway obstruction is demonstrated by alleviation of the symptoms of obstructed pulmonary functions with a bronchodilator. Pulmonary function tests are not always necessary to diagnose asthma.13 A review of symptoms, such as cough or dyspnea occurring after exercise and relieved by bronchodilator, often suffices.13 Also, if during a clinical examination the clinician observes wheezing and tachypnea, which are accompanied by a respiratory infection that can be reversed with administration of a ß2 agonist, he or she also can suspect a positive asthma diagnosis. During acute exacerbations, patients may show signs of respiratory distress, with tachypnea, intercostal muscle retractions, nasal flaring and cyanosis. However, clinical features can be misleading, and spirometry and peak expiratory flow rate meters are useful diagnostic and monitoring adjuncts.

Chest radiography may be useful, especially as a means of excluding other diseases.

Although recurrent episodes of coughing, breathlessness and wheezing almost always are due to asthma, a clinician should be cognizant that several other causes of airway obstruction manifest themselves in a similar manner. For instance, a localized obstruction of the airways can be due to lower respiratory tract infection such as bronchiolitis, croup, viral infections, acute and chronic bronchitis and bronchiectasis. Several less common conditions are included in the asthma differential diagnosis (boxGo, "Differential Diagnosis of Asthma"[page 1230]). It should be assumed, until proven otherwise, that a patient with wheezing and related symptoms has asthma.


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  		DIFFERENTIAL DIAGNOSIS OF ASTHMA.*

 
The course of the disease can change over time in affected people. For instance, symptoms can be moderate in childhood and mild in adulthood, becoming severe only during certain seasons.8 Asthma exacerbations can be mild, moderate or severe (TableGo). Asthma classifications based on etiology also exist, but these do not give an indication of disease severity (boxGo, "Classification of Asthma by Etiology"). It is important to realize that patients at any level of disease severity may experience acute exacerbations.


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  		TABLE CLASSIFICATION OF ASTHMA BY SEVERITY.*{dagger}

 

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  		CLASSIFICATION OF ASTHMA BY ETIOLOGY.*

 

   MANAGEMENT AND PHARMACOTHERAPY
TOP
 ABSTRACT
 PATHOPHYSIOLOGY
 DIAGNOSIS AND CLASSIFICATION
 MANAGEMENT AND PHARMACOTHERAPY
ORAL HEALTH CHANGES IN...
 MANAGEMENT IN DENTAL CARE
 CONCLUSION
 REFERENCES
 
Treatment of asthma begins with patient education, particularly about avoidance of precipitating factors (such as animal dander). The goal of asthma therapy is to control the symptoms with the least amount of medication necessary (boxGo, "Treatment Goal: Control of Asthma"). This commonly is referred to as a stepwise approach, because with intensifying asthma severity, the number, potency and frequency of pharmacologic agents are increased.8 For patients with mild, intermittent asthma, the occasional use of an inhaled short-acting ß2 agonist is indicated. By contrast, a regular regimen of asthma medication is required for people with persistent moderate asthma. Additionally, pre-emptive measures can be used to prevent exacerbations and severe airway obstruction.


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  		TREATMENT GOAL: CONTROL OF ASTHMA.*

 
The rationale behind antiasthma treatment involves an understanding of the underlying pathophysiologic condition. Appropriate pharmacotherapy is designed with the salient features of asthma pathogenesis in mind and is tailored to the disease’s level of severity. The characteristic airway inflammation and hyperresponsiveness are combated with the use of anti-inflammatory drugs. Controlling inflammation leads to decreased bronchial hyperreactivity and an overall reduction of asthma symptomology. Conversely, inflammation left unchecked can lead to fibrosis and irreversible airway obstruction. To address bronchospasm, asthmatic patients can use an aerosolized bronchodilator (that is, a ß2 agonist or theophylline).

Bronchodilators. Initial asthma therapy involves the use of a ß2 agonist metered-dose inhaler, or MDI, for symptomatic relief. Self-dosage is performed at the onset of an asthmatic episode or before exposure to aggravating stimuli, such as exercise or allergens. The achieved sympathomimetic effects include marked bronchodilation and a reduction in bronchial irritability. The MDI means of formulation and administration is preferable to systemic delivery, because it demonstrates similar efficacy with fewer adverse effects. However, it has been shown that up to one-half of patients using inhalers use them improperly, which results in less than optimal effectiveness.14 Also, use of the parenteral route occasionally may be necessary in people who have severe airway obstruction, owing to the resultant reduction in tidal volume.15 Another option for the person with mild asthma is the inhalation of cromolyn, either alone or in combination with a ß2 agonist inhaler.

Inhaled corticosteroids. When symptoms are more persistent and a short-acting ß2 agonist alone does not provide relief, the next tier of treatment should include inhaled corticosteroids. Generally, the person with moderate asthma requires medication daily. Inhaled corticosteroids are used at a low dose—400 to 800 micrograms per day, or µg/day, of beclamethasone (up to a maximum of 2,600 µg/day).10,16 With inhaled corticosteroids, rare systemic adverse effects are observed. Local untoward manifestations include oral candidiasis, dysphonia and cough.17 If symptomatic relief still is not achieved with a modest dose of aerosolized corticosteroids, the inhalation concentration usually is increased to 2,000 µg of beclamethasone per day (or equivalent), or a long-acting ß2 agonist (such as salmeterol) is added. When these two alternatives are directly compared, the results with salmeterol are favored, but they vary greatly among individual patients.18,19

Cromolyn and nedocromil. If the patient cannot tolerate inhaled corticosteroids, the conventional substitute for prophylactic therapy is either cromolyn sodium or nedocromil sodium. cromolyn is a mast cell stabilizer with virtually no adverse effects and can be used instead of or in addition to aerosolized corticosteroids. Nedocromil sodium is an anti-inflammatory agent that inhibits mediator release and reduces airway hyperreactivity.17 Both cromolyn and nedocromil are used for maintenance therapy, rather than for treatment of acute attack, and both lack the potency of nebulized corticosteroids.

Leukotriene antagonists. Recently, leukotriene antagonists have gained considerable attention as a more progressive treatment modality. Antileukotriene drugs, like zafirlukast, directly inhibit bronchoconstriction and have been shown to exhibit anti-inflammatory effects as well.20 The 1997 NHLBI Expert Panel Report listed antileukotriene drugs as possible alternatives to preferred therapy with inhaled corticosteroids for the treatment of adult patients with mild persistent asthma.10 Although their efficacy has not been wholly established, antileukotriene drugs offer an attractive option for additive therapy in patients who are treated with low to moderate doses of inhaled corticosteroids yet still are symptomatic.

Theophylline. The bronchodilator theophylline also can be used in addition to, or in lieu of, a ß2 agonist.17 However, theophylline has fallen out of favor as of late owing to its narrow therapeutic window and potentially severe adverse effects. Erythromycin should be avoided in patients who are taking theophylline, as concomitant use may result in elevated theophylline blood levels.

Anticholinergics. The role of anticholinergics, such as ipratropium bromide, in the treatment of asthma is not clear. Some patients respond well while others do not. It is known that anticholinergics have a slow peak onset of bronchodilation (up to 90 minutes). No long-standing xerostomic effects are noted when it is administered at therapeutic doses, but a bad taste in the mouth has been reported.21

Systemic corticosteroids. If the pathognomonic pulmonary symptoms of asthma are refractory to aerosolized bronchodilators, anti-inflammatory agents and combinations thereof, the last level of pharmacotherapy involves oral systemic corticosteroids. These usually are reserved for patients who continue to show poor control.

The adverse effects of short-term high doses of steroids include increased appetite, fluid retention, insomnia and mood alteration, while long-term systemic steroid therapy can result in osteoporosis, hypertension, cataracts, diabetes, proximal myopathy and pituitary-adrenal axis suppression.22 With respect to maintenance steroid therapy, it is imperative to use the lowest possible dose in attempts to minimize these negative effects. Patients receiving long-term oral corticosteroid therapy, or who recently have completed such a regimen, may require a larger dose before undergoing dental treatment or in the presence of an odontogenic infection.22

Epinephrine. For treatment of acute exacerbations refractory to nebulized bronchodilator, an epinephrine solution of 1:1,000 weight per volume, or wt/vol, remains the standard of therapy.23,24 For most adults, a dose of three-tenths of a milliliter of a 1:1,000 wt/vol solution is adequate and can be repeated every 15 minutes for up to three doses.23 If signs of severe asthma still are exhibited after the second dose, the patient should be sent to the emergency department.

New therapies. New immunomodulatory treatments are being investigated for asthma management.25–27 These therapies focus on selective antagonism of specific T-lymphocyte function and response, blocking the effect of cytokines such as interleukin-5, as well as blocking the effect of asthma-triggering immunoglobulin E.28 Although specific immunotherapy in the treatment of asthma has shown promise as an additional therapeutic intervention, more research is necessary to substantiate it as a standard of care.


   ORAL HEALTH CHANGES IN PATIENTS WITH ASTHMA
TOP
 ABSTRACT
 PATHOPHYSIOLOGY
 DIAGNOSIS AND CLASSIFICATION
 MANAGEMENT AND PHARMACOTHERAPY
 ORAL HEALTH CHANGES IN...
MANAGEMENT IN DENTAL CARE
 CONCLUSION
 REFERENCES
 
The literature has described several oral health conditions associated with asthma: an increased rate of caries development and reduced salivary flow, an increased prevalence of oral mucosal changes, increased levels of gingivitis and orofacial abnormalities.29–33

Increased rate of caries development and reduced salivary flow. Several studies have suggested that people with asthma have a greater rate of caries development than do their nonasthmatic counterparts.34 This phenomenon has been attributed to prolonged use of ß2 agonists, which is associated with diminished salivary production and secretion.35 The effect of reduced salivary flow has been elucidated in both human and animal studies.34–37 One study demonstrated a reduction of whole and parotid saliva by 26 percent and 36 percent, respectively.38 As reduced salivary flow is accompanied by concomitant increases in lacto-bacilli and Streptococcus mutans in the oral cavity, it is not unlikely that this particular change among asthmatic people may be one of the major contributing factors in the noted increased caries rate.35,39 In addition to reduced salivary concentrations and increases in cariogenic micro-biota, higher rates of caries have been observed in people with asthma, possibly due to antiasthma medications containing fermentable carbohydrate and sugar.40–42 It is evident that oral prophylactic strategies should be used to address the heightened caries risk in asthmatic people. This includes increased frequency of dental maintenance visits, fluoride interventions and adherence to caries-prevention measures.

Oral mucosal changes. The use of nebulized corticosteroids can result in throat irritation, dysphonia and dryness of mouth, oropharyngeal candidiasis and, rarely, tongue enlargement.24,43 These side effects may be attributed to the topical effects of these medications on the oral mucosa, as only 10 percent to 20 percent of the dose from an inhaler actually reaches the lungs; the rest remains in the oropharynx.44 Using a spacer and rinsing the mouth with water after steroid inhalation can minimize the potential for candida growth.45

Gingivitis. Use of inhaled steroids has been linked to increased levels of gingivitis.46,47 However, the common practice of mouth-breathing in asthmatic people, as well as various immunological factors, also may contribute to the observed increase in gingival inflammation. It also has been suggested that asthmatic children exhibit more calculus than do healthy children.47 This possibly is caused by increased levels of calcium and phosphorus found in submaxillary and parotid saliva in children with asthma.48,49

Orofacial abnormalities. The association between asthma and dentofacial morphology has been assessed, evaluated and discussed for many years. The basis for this discourse is the description of impaired nasorespiratory function in asthmatic people, which has been coupled with the presence of specific dentofacial abnormalities.50,51 Studies have described increased upper anterior and total anterior facial height, higher palatal vaults, greater overjets and higher prevalence of posterior crossbites in children with chronic rhinitis and a tendency toward mouth-breathing.52,53 Although a long and tapered facial form, increased lower facial height and narrow maxillary arch have been observed in patients with nasal respiratory obstruction and accompanying mouth breathing, a developmental causative relationship has never been substantiated with unequivocal answers.54,55


   MANAGEMENT IN DENTAL CARE
TOP
 ABSTRACT
 PATHOPHYSIOLOGY
 DIAGNOSIS AND CLASSIFICATION
 MANAGEMENT AND PHARMACOTHERAPY
 ORAL HEALTH CHANGES IN...
 MANAGEMENT IN DENTAL CARE
CONCLUSION
 REFERENCES
 
The administration of safe dental treatment for an asthmatic patient depends on his or her pulmonary function, propensity for developing an acute asthmatic episode at the time of treatment, immune function and adrenal status. Preventing a sudden episode of airway obstruction is essential when treating an asthmatic patient. The frequency of asthmatic attacks, precipitating agents, the types of pharmacotherapy used and the length of time since an emergency visit owing to acute asthma all should be taken into account when identifying the risk of an acute exacerbation.24 As a general rule, elective dentistry should be performed only on asthmatic patients who are asymptomatic or whose symptoms are well-controlled. The symptomatic person should not be treated, and the presence of asthmatic symptoms such as coughing and wheezing necessitate reappointment. However, the clinician also should realize that a patient could have significant airway obstruction and yet be asymptomatic during dental treatment.56

Oral health care providers need to be aware of the potential for dental materials and products to exacerbate asthma. These items include dentifrices, fissure sealants, tooth enamel dust and methyl methacrylate.57–61 Fluoride trays and cotton rolls also have been implicated in promoting asthmatic events.62

Patients’ immune status depends on the level of immunosuppressive medications they are taking. Only the most severely affected asthmatic patients who are taking large doses of systemic corticosteroids fall into this category. The same category of patients also may be at risk of adrenal suppression. The clinician should consider the need for prophylactic administration of antibiotics to prevent postoperative complications and for corticosteroid replacement therapy to prevent acute adrenal crisis.

Before treatment. When an asthmatic dental patient seeks care, the clinician must assess his or her risk level by taking an oral history of the illness: ascertaining the frequency and severity of acute episodes, reviewing the patient’s medications thoroughly (as they provide an indication of disease severity) and determining the patient’s specific triggering agents.

It should be recognized that dental treatment can invoke a significant decrease in pulmonary function among asthmatic patients. Mathew and colleagues56 demonstrated a reduction of lung function in 15 percent of asthmatic patients studied while receiving dental care. However, they did not wholly elucidate the specific causative aspects of dental treatment responsible for this reduction. During dental treatment, the most likely times for an acute exacerbation are during and immediately after local anesthetic administration and with stimulating procedures such as extraction, surgery, pulp extirpation, and induction of or recovery from sedation or general anesthesia. The major concern in the management of asthmatic patients undergoing routine dental care is preventing an acute exacerbation. For most patients, this may consist simply of confirming that they have taken their most recent scheduled dose of medication. The patient’s own metered-dose inhaler bronchodilator should be on hand at each visit. Ideally, to minimize the risk of an attack, the patient’s appointment should be in the late morning or the late afternoon.63 If the asthmatic patient does not use a bronchodilator, he or she should be given one from the emergency kit. Both a bronchodilator and oxygen should be available during treatment.39,64

Inhaled corticosteroids are used for maintenance therapy and do not ameliorate an acute attack. It has been suggested that a prophylactic dose of ß2 agonist bronchodilator could prevent diminished lung function during dental treatment.56 The H1-blocking antihistamines, too, have been shown to be useful in blunting the bronchoconstrictor response with a pretreatment dose. Promethazine and diphenhydramine have the benefit of being antiemetic and sedative as well as antihistaminic.

Anxiety is a known asthma trigger, and the dental environment is a common site for an acute asthmatic attack.65 Therefore, it should be ascertained that the patient has taken his or her most recent scheduled dose of antiasthma medication before treatment. Additionally, substantive stress-management techniques should be used. The anxiolytic protocol can include nitrous oxide, or N2O. According to Malamed,66 the use of N2O in patients with mild-to-moderate asthma can prevent acute symptoms. However, because of its potential for causing airway irritation, N2O is contraindicated for use in patients with severe asthma.66,67 It is advisable to obtain a medical consultation before administering N2O to such patients.

Hydroxyzine and benzodiazepines usually are used when a clinician performs conscious sedation in asthmatic patients. Narcotics and barbiturates should be avoided owing to their histamine-releasing properties, which can lead to bronchospasm and a potentiated allergic response. Clinicians should use extreme caution when using intravenous sedation in patients with asthma because of the limited control of their airways. Ketamine has been used safely in asthmatic patients, but its exuberant adrenergic activity is a concern for patients with a history of cardiovascular or hypertensive heart disease.68,69 It is suggested that dental patients who have more than mild asthma should undergo procedures only where standard monitors and intubation equipment are available. A pulse oximeter is an especially useful monitoring device. An oxygen saturation of 97 percent to 100 percent should be achieved on room air. An oxygen saturation below 91 percent is an indication for hospitalization. Consequently, patients with severe persistent asthma and those who are prone to severe abrupt episodes of airway obstruction are best given dental treatment in the hospital.

The oral health care provider should be aware of the possibly skewed clinical presentation of a patient receiving anti-inflammatory treatment. Long-term use of these medications can complicate diagnoses by masking infection and inflammation. Furthermore, patients who are receiving or who recently finished receiving chronic corticosteroid therapy may need steroid replacement therapy before undergoing dental treatment.70 These same patients also may exhibit an increased susceptibility to bacterial infections, which would indicate the need for antibiotic prophylaxis before receiving treatment.

During treatment. The practitioner should be cognizant of several factors that can accentuate asthma during dental care. Mungo and colleagues62 found that improper positioning of suction tips, fluoride trays or cotton rolls could trigger a hyperreactive airway response in sensitive subjects. Rubber dams should be used judiciously to avoid possible respiratory compromise or aggravation. Prolonged supine positioning, bacteria-laden aerosols from plaque or carious lesions and ultrasonically nebulized water also can be asthma triggers in the dental setting.56 Additionally, aeroallergens such as tooth-enamel dust and methyl methacrylate have been reported to trigger acute episodes in a dental setting.60,61,71 Obviously, potential asthma precipitants should be eliminated or minimized where possible.

In the event of an acute asthmatic attack during dental treatment, the clinician should stop the procedure, remove all intraoral implements and rule out foreign body aspiration, and initiate the emergency protocol for managing acute asthmatic exacerbation (boxGo, "Emergency Protocol for Managing Asthmatic Exacerbation in a Dental Setting").


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  		EMERGENCY PROTOCOL FOR MANAGING ASTHMATIC EXACERBATION IN A DENTAL SETTING.

 
Many articles and books put forth the recommendation of avoiding dental local anesthetics with vasoconstrictors in asthmatic patients, as many vasoconstrictors contain sodium metabisulfite, a preservative that is highly allergenic.72,73 However, vasoconstrictor-containing local anesthetics have been used safely with these patients.74 An additional concern with vasoconstrictors is their interaction with specific medications commonly used by asthmatic patients. Vasoconstrictors may add to the effects of ß2 agonists, causing excessive adrenergic activity that results in palpations, increased blood pressure and dysrhythmias.75 On the other hand, it also has been suggested that stress-induced release of a patient’s own epinephrine may act as a bronchodilator.76 Perusse and colleagues77 recommended a contraindication to vasoconstrictor-containing anesthetics in corticosteroid-dependent asthmatic patients. The premise for this recommendation is the authors’ assumption that corticosteroid-dependent asthmatic people are more severely affected by their asthma and therefore have a higher predilection for having an adverse reaction to sulfites. It is not clear if this is the case.

After treatment. Owing to allergy, as much as 20 percent of patients with asthma may experience severe exacerbations of bronchoconstriction after ingesting aspirin and other nonsteroidal anti-inflammatory drugs, or NSAIDs.78–80 Aspirin-induced asthma is most common in the third or fourth decades of life and, as with other NSAIDs, is thought to be related to the inhibition of the enzyme cyclo-oxygenase as well as to allergy. Examples of offending NSAIDs include ketorolac, ibuprofen and naproxen sodium. As a result, the analgesic of choice for these patients is acetaminophen. However, recent studies (as cited in Shaheen and colleagues81) have suggested that long-term daily or weekly acetaminophen use is associated with a more severe asthma.81 Although there is reason for caution, acetaminophen still is the preferred analgesic for asthmatic patients.

The increased potential for developing toxic levels of theophylline with concomitant use of erythromycin has been addressed in the dental literature.67 There is a theoretical risk of this type of interaction, though there are very few actual documented cases. Yet it is preferable to avoid using macrolide antibiotics when appropriate antibiotic substitutes are available. One viable alternative is azithromycin. Phenobarbitals have the ability to potentiate the breakdown of theophylline via liver enzyme induction, and concomitant use may reduce the efficacy of theophylline owing to an increase in the rate of bio-transformation.


   CONCLUSION
TOP
 ABSTRACT
 PATHOPHYSIOLOGY
 DIAGNOSIS AND CLASSIFICATION
 MANAGEMENT AND PHARMACOTHERAPY
 ORAL HEALTH CHANGES IN...
 MANAGEMENT IN DENTAL CARE
 CONCLUSION
REFERENCES
 
Oral health care providers play an important role in monitoring patients with asthma82 (boxGo, "Dental Care for Asthmatic Patients"). As such, they need to understand the pathogenesis of the condition and what causes exacerbations and relief; recognize the significance and side effects of antiasthmatic medications; and provide safe and appropriate dental care for patients with this disease.


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  		DENTAL CARE FOR ASTHMATIC PATIENTS.

 



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  		Dr. Glick is a professor of oral medicine and the director, Programs for Medically Complex Patients, University of Pennsylvania School of Dental Medicine, 4001 Spruce Street, Philadelphia, Pa. 19104, e-mail "glick{at}biochem.dental.upenn.edu". Address reprint requests to Dr. Glick.

 


   FOOTNOTES
 

Dr. Steinbacher is an intern, Department of Oral & Maxillofacial Surgery, Massachusetts General Hospital, Boston.


   REFERENCES
TOP
 ABSTRACT
 PATHOPHYSIOLOGY
 DIAGNOSIS AND CLASSIFICATION
 MANAGEMENT AND PHARMACOTHERAPY
 ORAL HEALTH CHANGES IN...
 MANAGEMENT IN DENTAL CARE
 CONCLUSION
 REFERENCES
 

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  2. Martin JA, Smith BL, Mathews TS, Ventura SJ. Births and deaths: preliminary data for 1998. Natl Vital Statistics Rep 1999;47(25).

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  9. Weiss K, Gergen PJ, Crain E. Inner-city asthma: the epidemiology of an emerging U.S. public health concern. Chest 1992;101(6 supplement):362S–367S.[Free Full Text]

  10. National Heart, Lung, and Blood Institute. Expert panel report 2. Guidelines for the diagnosis and management of asthma. Baltimore: U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, National Heart, Lung, and Blood Institute; 1997. NIH publication 4051.

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