Chapter 2.

Managing the Patient with

Severe Respiratory Problems




by Mitchell B. Day, DDS


Abstract: The dental management of patients with severe respiratory problems continues to be a significant challenge to the dental health care practitioners. Chronic obstructive pulmonary diseases, such as chronic bronchitis and emphysema, are the fourth leading cause of death in the United States. Asthma has increased in prevalence during the past 20 years, and the rate of death from this chronic inflammatory disease of the airways has also risen despite recent advances in medical treatments. This article will review the pathophysiology and medical treatment modalities for these chronic pulmonary diseases, as well as discuss the recognition and management of dental patients with these diseases and provide an understanding on how to avoid precipitating factors that could initiate an acute episode in the dental care setting.


The dentist in practice today must be prepared to provide care for patients with complex medical conditions. As people live longer, and with advances in medical care, dentists will be treating more medically compromised individuals. Consequently, dentists now find themselves increasingly committed to understanding dental patients’ overall medical diagnosis and therapy. Because dentists operate at the origin of the upper airway, and many dental procedures are deemed stressful, patients with chronic respiratory diseases are at special risk. Routine dental care can be provided in the dental office when the dentist is knowledgeable about pulmonary diseases and pays specific attention to risk assessment and those precautions that are necessary to prevent acute exacerbations of a respiratory disease state. The entire dental team should be familiar with the signs, symptoms, and management of an emergent episode associated with asthma or chronic obstructive pulmonary diseases.








Asthma is a chronic inflammatory disease of the airways characterized by nonspecific hypersensitivity to a variety of stimuli that can precipitate acute episodes of bronchospasm and mucous secretion that result in airway obstruction. 1 It is estimated that more than 14 million people in the United States have asthma, with as many as 4.8 million children being affected. 2,3 The prevalence of asthma has increased in the United States since 1960, and the mortality rate has risen significantly throughout the 1980s and 1990s. 4-6 In California from 1983 to 1996, there was a 30 percent increase in the number of hospital admissions for patients with a diagnosis of asthma.

Individuals with asthma experience acute episodes of tracheobronchial irritation that present with coughing, wheezing, and dyspnea, the classic clinical triad of the disease. Although asthma was once thought to be isolated acute exacerbations of bronchospasm, medical research has now clearly defined the role of inflammation in its pathophysiology. 7 Contemporary medical management now emphasizes patient education and compliance in the use of long-term control medications that have anti-inflammatory effects on the airways, such as corticosteroids, Nedocromil, Cromolyn sodium, and the leukotriene inhibiting agents. During acute exacerbations or "attacks," fast-acting or "quick-relief" medications, inhaled beta 2 agonists, and anticholinergics are used to reverse the airway obstruction resulting from bronchial smooth muscle contraction, epithelial edema, and mucous secretion.



The etiology of asthma is not clearly defined. Given the varied expression of the disease, it appears to be multifactorial in origin. The traditional classification of asthma describes two basic types: extrinsic and intrinsic.

Extrinsic or allergic asthma is associated with an allergic stimulus that results in the activation of airway epithelial mast cells. The immunoglobin E (IgE)-dependent process is initiated when the individual is exposed to an environmental allergen such as dust, pollen, tobacco, wood smoke, molds, house mites, or animal dander. The mast cells release the inflammatory mediators (i.e., histamine), which promote an immediate bronchospasm often referred to as the "early phase" reaction. With the continued action of these mediators, eosinophils and neutropils migrate into the airways and a "late phase" reaction results in tissue injury leading to airway obstruction through bronchial smooth muscle contraction, epithelial cell shedding, mucous secretion, plasma extravasation, and airway edema. 8,9

The extrinsic asthmatic patient presents with a known allergic history that has its onset in childhood or early teens. Skin tests to allergies are positive, and blood tests often reveal elevated IgE levels. Extrinsic asthmatic attacks tend to be intermittent and exhibit seasonal variation.

In contrast, intrinsic or nonallergic asthma is different in that no allergic stimulus is identified. Skin testing is negative and elevated IgE levels are not seen in this form. The onset of intrinsic asthma is usually seen in adults, and the acute exacerbations tend to be continuous. Endogenous factors, including emotional stress, or other idiopathic stimuli are thought to initiate the attacks. 10

It should he noted that very few patients who are diagnosed with asthma exhibit the features of a purely extrinsic or intrinsic form and most will have complex or varied presentation. Furthermore, other forms of asthma have been described, and include drug-induced asthma associated with the intake of aspirin, NSAIDs, angiotension- coverting enzyme inhibitor, and metabisulfite preservatives. 11 Exercise-induced asthma is another form that is seen in adolescents and young adults and attributed to vigorous physical activity.

The National Asthma Education and Prevention Program has developed a revised classification for asthma. 2 Individuals with chronic asthma are classified based on the severity of their symptoms, when the symptoms occur, and how often they occur. In addition, the assessment of lung function is vital to the classification. Patients are assigned as mild intermittent, mild persistent, moderate persistent, or severe persistent. This newer classification has resulted in a stepped approach to diagnosis and medical management that addresses the causal inflammatory processes with the goal of preventing or limiting the acute symptoms of the disease.



At initial presentation, patients with asthma give a history of recurrent coughing, wheezing, difficulty breathing, and chest tightness. Based on the severity and frequency of these symptoms, pulmonary function testing further delineates the degree of airway obstruction. Spirometry is used to quantify the degree of disease with forced expiratory volume in one second (FEV 1 ). In addition, peak expiratory flow (PEF) can be followed daily by patient-administered spirometry in a moderate to severe diagnosis as a method of monitoring the disease and evaluating the response to medication therapies.

Individuals with mild intermittent asthma (experience symptoms twice a week or less) exhibit relatively normal PEF values between attacks and have nocturnal symptoms less than two times per month. These patients rarely require daily medications for long-term control. Behavior modification to avoid factors that stimulate acute exacerbations and use of fast-acting beta-adrenergic brochodilators define the first step approach in these patients.

If symptoms occur more than two times per week, nocturnal episodes occur more than twice a month, and pulmonary function values show a decreased ratio of FEV 1 to forced vital capacity (FVC) with variability in PEF of 20 percent to 30 percent, then these patients are classified as having mild persistent asthma. Initial therapy and additional stepwise therapies may be more complex for these individuals. Long-acting anti-inflammatory drugs are used daily and may include low-dose inhaled corticosteroids, the mast cell stabilizers Cromolyn sodium or Nedocromil, and the newer leukotriene antagonist drugs such as Zafirlukast and Zileuton. 12-14

Patients with a diagnosis of moderate persistent asthma exhibit symptoms daily, use fast-acting beta-adrenergic brnchodilators daily, and experience nocturnal symptoms more than once a week. These patients have FEV 1 to FVC ratios that are less than 80 percent and the variability in PEF can be greater than 30 percent. Treatment with multiple therapeutic agents may be required to establish long-term control of their symptoms. In addition, medium- to high-dose inhaled corticosteroids are often indicated. Many of these patients may be placed on the long-acting beta-selective agonist bronchodilator, Salmeterol, for prolonged maintenance. 15-16 In addition, albuterol’s beta agonist properties can be used as a long-acting agent when given orally as an extended release tablet and are useful in long-term control of nocturnal symptoms. The diagnosis of moderate persistent asthma requires that the patient also take an active role in the treatment and monitoring of his or her disease state. Long-term control of this disease can be greatly enhanced by educating the patient on the complex medication regimens, the value of self-monitoring with spirometry, and the proper technique in using inhalers and nebulizers, as well as avoiding exposure to potential stimulating factors. 2, 17

Patients with severe persistent asthma can experience daily symptoms and acute exacerbations, which can, in turn, limit their physical activities. Nocturnal symptoms are common. Lung function is highly variable with the FEV 1 to FVC ratio at 60 percent or lower and variability in PEF at more than 30 percent. The multiple medication regimens used to treat moderate persistent asthma may prove to be inadequate. A step-up in therapy is now indicated for severe persistent asthma with higher dose inhaled corticosteroids and long-acting beta agonists serving as the preferred pharmacotherapy.When severe asthma exacerbations continue, systemic corticosteroids are used as a short-term therapy to help alleviate the severity of the exacerbations despite the potential significant systemic side effects of oral administration. 12,18 In addition, sustained-release theophylline is considered in the management of the severe persistent asthmatic not responding to the other drug modalities. Once a mainstay in asthma therapy, theophylline is now a secondary or tertiary agent mainly used to treat the nocturnal symptoms because of concerns for the drug’s narrow therapeutic range requiring frequent serum level monitoring, potential drug interactions and adverse effects on multiple organ systems. 19, 20

Given the varied expression of asthma, long-term successful management of the disease is achieved through very individualized stepwise drug therapy and an emphasis on patient education and compliance. All patients with asthma can experience mild, moderate, or severe exacerbations, which can evolve to a life-threatening episode. The stepwise approach to diagnosis and therapy has greatly decreased the severity and frequency of asthma symptoms in many patients. While quick-relief, fast-acting inhaled bronchodilator drugs treat the severe symptoms of bronchial airway obstruction in the acute asthmatic attack, long-term control medications offer the greatest potential to alleviate asthma symptoms, improve pulmonary function, and diminish the disease’s overall morbidity. Table 1 provides both a classification and treatment protocol for the medical management of asthma. This format can assist the dentist in the development of a patient’s risk assessment prior to initiating dental treatment.



The primary objective for the dentist in the management of a patient with a medical condition is to prevent any complications related to that condition as a result of dental treatment. The asthmatic patient can be treated for his or her dental needs when the dental health practitioner has developed a risk assessment that is individualized for that patient. This assessment begins with an appropriate understanding of the patient’s medical history. The health history questionnaire and a comprehensive interview by the dentist is the foundation of the risk assessment process.

For the asthmatic patient, the dentist should determine the following aspects of that patient’s disease history:

n Classification or type of asthma;

n Current medication regimens;

n Patient’s understanding and compliance with medical treatment;

n Factors that precipitate acute exacerbations;

n Frequency and timing of episodes;

n How often the fast-acting or quick-relief bronchodilators are used; and

n History of emergency room visits or hospitalizations.

This information is then used to determine the stability and severity of the disease, provide an indication for a medical consultation prior to dental treatment, and guide the practitioner in the development of an appropriate management protocol. The patient’s understanding of his or her disease and compliance with the prescribed medical therapies is of vital importance. 20 The asthmatic patients who are most likely to experience frequent acute exacerbations and present a higher risk of having a complication associated with dental treatment are those who are not compliant with their complex drug regimens and have a poor perception of the diagnosis of asthma. These patients and patients with a diagnosis of severe asthma should have a medical consultation prior to any extensive or stressful dental treatments.



Given the complex expression of asthma, management protocols for asthmatic patients should be tailored to their individual needs based on the dentist’s risk assessment. With stress being a primary precipitating factor for the stimulation of an acute asthmatic attack, a stress-free environment is essential in treating all asthmatic dental patients. The anxious patient may require sedation for dental procedures. The use of nitrous oxide- oxygen inhalation sedation should be considered and can be combined with short-acting oral benzodiazepines. Nitrous oxide is not irritating to the airway, does not cause a depression of respiration, and may have an analgesic effect to supplement the use of local anesthesia for pain control. The time of day and the length of dental treatment visits should be adjusted to prevent a stress-inducing situation. For those patients with moderate to severe persistent asthma, it is appropriate to have them prophylactically administer their own fast-acting bronchodilator medication preoperatively to their treatment appointment and ensure they have used their inhaled corticosteroid medications as scheduled.

The preoperative management of the asthmatic patient centers on avoiding factors that can stimulate an exacerbation of acute symptoms leading to bronchospasm. In dental treatment, the potential of drug interactions is of primary consideration. Aspirin and nonsteroidal antiinflammatory drugs should be avoided in the management for postoperative pain, as they are known to stimulate asthmatic attacks. Relative contradictions for both narcotics and barbiturates have been identified for asthmatic patients. Drugs from both groups can increase the risk of bronchospasm and should not be used.

Furthermore, the use of certain antibiotics to treat orofacial infection is contraindicated in moderate to severe asthmatics who are taking theophylline. Ciprofloxacin and the macrolides (i.e., erythromycin, clarithromycin and azithromycin) alter the metabolism of theophylline, which can result in toxic serum levels of this drug.

The selection of a local anesthetic is important when treating asthmatics. Many local anesthetic solutions contain sulfites as a preservative. Sulfites are known to precipitate acute asthmatic attacks and allergic reactions. 22,23 These compounds are found in local anesthetic preparations containing epinephrine and levonordefin, and these preparations should not be used in patients known to be sensitive to sulfites.



1) Mild Intermittent Asthma

Fast-acting bronchodilators –for quick-relief acute episodes

A. Non-selective beta agonist

• Epinephrine (Primatene Mist)

• Ephedrine (Eted II)

B. Selective beta 2 agonist

• Albuterol (Ventolin, Proventil)

• Terbutaline (Brethaire)

• Tirbuterol (Maxair)

• Bitolterol (Tornalate)

2) Mild Persistent Asthma

Fast-acting bronchodilators –for quick-relief acute episodes

Long-term control medication anti-inflammatory

Usually one medication daily

A. Low-dose inhaled corticosteroids

• Triamcinolone (Azmacort)

• Fluticasone (Flonase)

• Flunisolide (Aerobid)

• Budesonide (Plumicort)

• Beclomethasone (Beclovent)

B. Inhaled nonsteroidal anti-inflammatory

• Cromolyn sodium (Intal)

• Nedocromil (Tilade)

C. Leukotriene-inhibiting drugs

• Zafirlukast (Accolate)

• Zileuton (Zyflo)


3) Moderate Persistent Asthma

Fast-acting bronchodilator –for quick-relief acute episodes

Long-term control medication anti-inflammatory


One to two medications daily

A. Meduim-dose inhaled corticosteroids

B. Inhaled nonsteroidal anti-inflammatory

C. Leukotriene-inhibiting drugs

D. Long-acting bronchodilators

• Isoproterenol (Isuprel)

• Metaproterenol (Alupent)

• Salmeterol (Serevent)

• Albuterol (Oral Tablets)

4) Severe Persistent Asthma

Fast-acting bronchodilator –for quick relief acute episodes

Long-term control medications anti-inflammatory

Multiple medications daily

A. High-dose inhaled corticosteriods

B. Long-acting bronchodilator

C. Methylxanthines

• Sustained-release theophylline

D. Oral Corticosteriods

• Prednisone (Deltasone)

• Prenisolone (Delta-Cortef)

• Methylprednisolone (Soll-Medrol)




The onset of symptoms associated with an acute asthmatic attack can vary considerably in asthmatic patients. With stress being a major factor in stimulating asthmatic bronchospasm, the practitioner should be alert to increasing anxiety or apprehension in patients. Most asthmatic episodes are accompanied with the onset of a cough, the patient complaining of a feeling of chest tightness, dyspnea, and wheezing. Once an acute episode is diagnosed, the following maneuvers are indicated to reverse the underlying bronchospasm:


n Discontinue dental treatment;

n Place the patient in an upright sitting position;

n Assist the patient in the administration of fast-acting bronchodilator, or administer albuterol (Ventolin/ Proventil) from an emergency kit metered-dose inhaler;

n Administer oxygen using a nasal cannula, nasal hood or full-face mask at 2-3 L/ minute; and

n Reassure the patient and act calmly.

If the episode resolves, consider the need for a medical consultation and reevaluate the office stress-reduction protocol, the length and time of the dental appointments, and the need for sedation with further appointments.

If the attack continues after initial maneuvers, a serious medical emergency is indicated:

n Call 911 or contact the community emergency medical response number;

n Administer epinephrine by injection sublingual, intramuscular, or subcutaneous. A 1:1000 concentration is used, give 0.3 to 0.5 ml; repeat doses can be given at 20 minute intervals.

n Assist airway, breathing, and circulation as needed;

n Continue oxygen; and

n Monitor vital signs.

The patient will require transfer to a medical facility by trained emergency medical personnel for treatment with intravenous corticosteroids, airway management, and evaluation of the medical treatment for the asthma.










The American Thoracic Society has defined chronic obstructive pulmonary disease as a disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema; the airflow obstruction is generally progressive, may be accompanied by airway hyperactivity, and may be partially reversible. 24 It is estimated that 12 to 14 million people in the United States suffer from chronic obstructive pulmonary disease, and the disease is currently the fourth leading cause of death. 25 While deaths due to cardiovascular disease are on the decline, death from chronic obstructive pulmonary disease has increased by more than 40 percent since the early 1980s. 26, 27

Two very different conditions are included in the definition of chronic obstructive pulmonary disease: chronic bronchitis and emphysema. These two conditions have their own distinctive set of symptoms and underlying pathophysiology. Chronic bronchitis is described in clinical terms as the presence of a cough with the production of sputum for at least three months for a minimum of two years in succession. Emphysema is defined in pathological terms as the abnormal, nonreversible enlargement of the air spaces distal to the terminal bronchioles associated with alveolar wall destruction. It should be noted, however, that very few patients with chronic obstructive pulmonary disease exhibit symptoms exclusive of chronic bronchitis or emphysema. In fact, many patients share symptoms attributed to both conditions. 24



Both conditions share a common etiology, with exposure to tobacco smoke being the primary cause of chronic obstructive pulmonary disease. However, for reasons that are unclear, only about 15 percent of cigarette smokers actually develop clinically significant chronic obstructive pulmonary disease, while tobacco smoking is known to account for 80 percent of the risk of acquiring the disease. 28,29 The incidence of chronic bronchitis in cigarette smokers increases with age and the amount of cigarettes consumed, indicating that the risk is dose- and duration-dependent. Passive smoking or "second-hand smoking" may also contribute to the development of the disease. Children of smokers are known to have a higher incidence of respiratory symptoms, and respiratory function is decreased when measured through pulmonary function testing. 24

Other identifiable risk factors include environmental pollutants such as ambient air pollution, indoor irritants, and occupational airborne hazards. Based on epidemiological evidence, a nonspecific hyperresponsive airway condition has been identified as another possible risk factor leading to chronic obstructive airflow disease; but the specific causes of this condition have not been well-defined.

A genetic disorder of a l -antitrypsin deficiency is known to cause chronic obstructive pulmonary disease and accounts for less than 1 percent of those individuals diagnosed with chronic obstructive pulmonary disease.

a 1 - antitrypsin is produced in the liver and acts in the lungs to inhibit the action of neutrophil elastase, which leads to the enzymatic breakdown of the lungs’ elastin connective tissue. 31 Multiple autosomal co-dominant alleles at a single locus contribute to the inheritance of a 1 - antitrypsin, which in turn results in a varied expression of this genetic abnormality. When a severe deficiency of a 1 - antitrypsin is present, nonsmokers can develop bronchiectasis, chronic bronchitis, and basilar emphysema. The onset of airflow obstruction can develop before the age 50, and individuals with this condition are at extreme risk of acquiring clinically significant chronic obstructive pulmonary disease.



The anatomical and physiological changes that result in the clinically significant chronic airflow obstruction condition occur over a long period of time with exposure to the predisposing causative agent. Expiratory flow values are used to diagnose and establish the severity of the disease. Cigarette smokers with obstructive disease will show a progressive decline in the FEV l at a rate two to three times faster than nonsmokers. With smoking cessation in individuals with mild to moderate airflow obstruction, the rate of deterioration can return to that seen in nonsmokers, and their symptoms may decrease. 33

In patients with chronic bronchitis, the airflow obstruction is the result of sustained inflammation that proceeds with mucus cell metaplasia and increased mucus production, loss of respiratory epithelium, mucous, and fibrosis of the associated bronchiolar and alveolar walls. Early on in the disease process, there is a marked increase in the airflow resistance in the peripheral airways. Over time with progressive deterioration, the obstruction extends to the bronchiolar walls. Acute exacerbations of this condition have been associated with respiratory tract infections. Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis have been isolated in the lower bronchi of patients with chronic bronchitis. The exact role of infection in the long-term progression of the disease process is poorly understood . 34

Emphysema develops when there is an irreversible enlargement of the bronchioles and the alveoli. Distal to the terminal bronchiole, there is a concomitant breakdown in the alveolar ducts and the alveolar sacs, which will extend to the collapse of the terminal bronchiole. This leads to an airflow obstruction that hinders expiration. The breakdown of the distal air spaces occurs as a result of a protease-antiprotease imbalance, which leads to a degradation in the elastin in the alveolar walls. It is proposed that cigarette smoke can activate macrophages in the lungs to release factors that directly stimulate neutrophils to secrete elastases and combine with oxidants and free radicals, which in turn oxidize a l -antitrypsin. 35 The combined effect on the lung parenchyma is a destructive process that is characterized by the degradation of elastin and an inhibition of new elastin synthesis. 35

Several different types of emphysema have been described based on the anatomical areas within the lung that are affected. Centriacinar (centrilobular) emphysema is most often seen in the chronic cigarette smoker and is associated with the respiratory bronchioles, first with airway enlargement and destruction and then advancing distally. Panacinar (panlobular) emphysema is a uniform enlargement and breakdown of the air spaces throughout the acinus and is observed in patients with severe a l antitrypsin deficiency.

The airflow obstruction in both chronic bronchitis and emphysema develops over a long period with exposure to cigarette smoke. The anatomical changes are irreversible once a moderate amount of disease progression is established.



Individuals with chronic obstructive pulmonary disease usually present after the fifth decade of life with increasing complaints of chronic cough with sputum production or acute chest illness, which includes dyspnea, or shortness of breath on exercise. The individual with advanced chronic bronchitis is often described as a "blue bloater," presenting with a chronic productive cough. The patient's lung sounds are wet, characterized by rates and rhonchi. The patient reports a history of frequent chest infections. Findings of wheezing and dyspnea in this patient could be erroneously diagnosed as asthma. A chest radiograph appears normal. Arterial blood gas studies reveal a marked reduction in PaO 2 (hypoxia) and increase PaCO 2 (cyanosis). The patient also shows signs of peripheral edema associated with right heart failure, (cor pulmonale) and may have marked pulmonary hypertension.

The patient with emphysema is described as a "pink puffer," presenting with dyspnea and minimal or no cough. Typically, the patient is thin with a "barrel chest" appearance and quiet chest sounds on auscultation. Hyperinflated lung fields and an increase in the anterior to posterior dimensions of the patient's chest are noted. The chest radiograph shows hyperinflation, a "small" heart and a flattened diaphragm. Arterial blood gas studies reveal normal to slightly reduced PaO 2 and PaCO 2 .

Both chronic bronchitis and emphysema show marked decrease in the FEV 1 /FVC ratio. When lung volumes are measured, there is an increase in the residual volume (RV), and a normal or increased functional residual capacity (FRC) is observed. Pulmonary function tests are essential in determining the severity of the disease state, with FEV 1 serving to quantify the degree of airflow impairment. When correlated with factors such as age and the assessment of the levels of hypoxia and hypercapnia through arterial blood gas analysis, this information is used to individualize the diagnosis, prognosis, and treatment regimen appropriate for the patient with chronic obstructive pulmonary disease.

Because chronic obstructive pulmonary disease cannot be cured, medical treatment is directed at reducing the degenerative effects of the disease and managing the acute and chronic symptoms of chronic bronchitis or emphysema. Smoking cessation is the single most important therapy for patients with obstructive airway disease and proves to be the greatest challenge for the patient and the physician in managing the disease. 36

The reasons that people smoke cigarettes are multifactorial and include issues of nicotine addiction, education, income, conditioned psychological responses, and mental health. Clinician intervention, community support, and pharmacological treatments combined offer the best hope in achieving smoking abstinence in patients, and even still long-term success rates are often less than one-third of the patients that enroll in multifaceted programs. 37 Exposure to other potential inhaled irritants such as air pollution, home and personal care aerosolized products, and industrial or workplace irritants can cause acute exacerbations in patients and should be avoided.

Treatment of chronic bronchitis is directed at reversing or preventing airflow obstructions caused by inflammation, infection, and mucus secretion. Immunization with pneumococcal and influenza vaccines is an important component in the long-term management of the disease. The use of antibiotics is reserved for acute exacerbations and directed at known pathogens that can cause a superimposed acute bacterial tracheobronchitis. As with the treatment of asthma, the pharmacological treatment of chronic bronchitis and emphysema is managed in an individualized stepwise manner correlated to the severity of the disease. To ensure the patient’s participation in successful long-term management of the disease, it is essential to educate the patient about the diagnosis, disease severity, and indications for the medications used in treating the disease.

Bronchodilators are used in the treatment of both chronic bronchitis and emphysema. The beta 2 agonists can contribute to the relief of symptoms but do not contribute the same type of sustained bronchodilation with improved pulmonary function that can be seen in asthmatics.

In older chronic obstructive pulmonary disease patients, these drugs may also have sympathomimetic side effects that complicate concomitant cardiovascular diseases. Anticholinergic inhaled agents offer a slower onset, longer action, and fewer side effects. The atropine derivative, ipratropium bromide, is available as a metered-dose aerosol and has shown to be effective in relieving symptoms resulting from chronic airway obstruction.

When the symptoms associated with chronic obstructive pulmonary disease are continuous or more severe and their management with the bronchodilators is suboptimal, the use of sustained-release theophylline is considered. Theophylline has been shown to improve respiratory muscle function, stimulate the respiratory center, and improve mucociliary clearance. 38 Patients with co-existing cardiac disease, cor pulmonale, and pulmonary hypertension may benefit from the improved cardiac output, reduced pulmonary vascular resistance, and improved myocardium perfusion that theophylline can produce. 39

The use of corticosteroids has limited applications in the treatment of chronic obstructive pulmonary disease given that the disease process is primarily one of tissue degeneration and destruction with little or no reversible component.

For patients with chronic bronchitis, the inhaled corticosteroids may have an application in treating airway inflammation. 40 Because of the potential long-term effects of high-dose oral corticosteroids, their use is limited to selected patients that show improvement on treatment of acute exacerbations that respond to short-course therapy.























I. Mild to Moderate Disease

A. Smoking cessation–physician intervention

• Behavior modification program

• Nicotine replacement therapy

• Transdermal patch and oral medications

• Support groups

B. Eliminate environmental exposure/causes

• Air pollution

• Industrial or workplace irritants

• Household sources

C. Physical conditioning (improving functional capacity)

• Exercise training to improve respiratory function and exercise tolerance

• Nutrition and hydration

D. Immunizations: influenza and pneumococcal

E. Antibiotic therapy for acute infections/ exacerbations of chronic bronchitis at- tributed to known pulmonary pathogens

F. Treat symptoms of bronchospasm

• Anticholinergic aerosol agents–ipratropium bromide (Atrovent)

• Sympathomimetic agents–beta 2 agonist meter-dosed inhalers

II. Moderate Disease

A through F

When symptoms continue and improved pulmonary function is suboptimal

G. Sustained-release theophylline

H. Systemic or inhaled corticosteroids

• High-dose prednisone short course

• Lowest dose prednisone in long-term management

• Prolonged systemic steroid therapy is avoided

III. Severe Disease

A through H

With evidence of progressive hypoxia and hypercarbia

I. Supplemental oxygen therapy, minimum 18 hours daily with PaO 2 £ 55mm Hg or SaO 2 £ 89%

J. Note therapy for congestive heart failure, cor pulmonale and polycythemia


Patients with co-existing heart disease such as cor pulmonale and right heart failure will often be placed on diuretics or arterial vasodilators to treat pulmonary hypertension that develops with severe chronic obstructive disease. Their overall medical management is complex, and these patients will require constant observation by the treating physician. As the effects of the disease become more severe, monitoring and treating progressive hypoxemia and pulmonary hypertension will require long-term supplemental oxygen administration. The use of oxygen therapy has been shown to enhance survival rates and greatly improve the quality of life for individuals with severe chronic obstructive pulmonary disease. The supplemental administration of oxygen for a minimum of 18 hours/day at a rate of 2L/minute via nasal cannula maintains oxygen saturation levels of greater than 90 percent. When patients present with a PaO 2 of less than or equal to 55 mm Hg or a SaO 2 of less than 88 percent, this is considered an absolute indication for oxygen therapy. 41 Long-term oxygen administration can improve cardiac function, reverse polycythemia, and reduce the symptoms associated with cor pulmonale.

Pulmonary rehabilitation is a multifaceted effort directed at educating the patient, improving physical conditioning and nutrition, and supporting the psychological needs of patients with chronic obstructive pulmonary disease. Table 2 summarizes the stepwise treatment protocol for the medical management of chronic obstructive pulmonary disease patients.



Patients with moderate to severe chronic obstructive pulmonary disease seeking dental care require a risk assessment that identifies the type of disease, establishes the severity of the condition, and documents the success or compliance of the patient's medical treatment. In addition, other medical conditions, which may affect the chronic airway obstructive disease, should be identified and evaluated. While the majority of patients with significant symptoms of productive cough or shortness of breath will have sought medical evaluation and treatment, the dental health practitioner must be alert to patients with untreated or undiagnosed symptoms of chronic bronchitis or emphysema. The health history questionnaire and the dentist-patient dialogue can alert the practitioner to possible concerns for respiratory disease. The physical exam, through observation and auscultation of the patient, can reveal signs of chronic obstructive pulmonary disease.

When a concern for a patient’s respiratory status is noted and an understanding of the functional airway reserve is desired, a simple "breath holding" test can be performed. For example, with the patient sitting upright, have him or her take as deep an inspiratory breath as possible while holding the nostrils closed. Ask him or her to hold his breath as long as possible. Note the length of time before he or she must exhale and desire another breath. People that can only hold their breath for 10 to 20 seconds may have a moderate degree of pulmonary compromise, while those that cannot go longer than 10 seconds may have severe obstructive airway disease. Patients with moderate to severe airflow obstruction should have a medical consultation prior to any extensive or stressful dental treatment.



The reduction of stress and avoidance of any procedures that may depress a patient’s respiratory function are essential in the management of patients with moderate to severe chronic obstructive pulmonary disease.

Patients should be offered a professional and reassuring environment with short, focused dental treatments early in the day. If appropriate, sedation can be considered, but potent sedatives, barbiturates, or narcotics should be avoided as they can depress the respiratory drive. Nitrous oxide and high flow rates of oxygen are contraindicated because their use can result in respiratory depression in patients with severe disease exhibiting CO 2 retention. Placing a patient in a reclined position or the use of a rubber dam can contribute to a sense of respiratory compromise. Low-flow supplemental oxygen administration via nasal cannula at rates of 2 to 4 L/minute is appropriate even in patients with severe disease.

The use of certain drugs in the dental-related treatment of chronic obstructive pulmonary disease patients should be avoided. Anticholinergic or antihistamines can alter tracheobronchial secretion, which may promote an acute respiratory infection or stimulate inflammation or irritation to the airways leading to further airflow disturbance. When antibiotic therapy is indicated for an odontogenic infection or prophylaxis, patients taking theophylline should not be given macrolides, ciprofloxin, or clindamycin, which can lead to methylxanthine toxicity.


A primary concern for patients with moderate to severe chronic obstructive airway disease is avoiding situations in dental treatment that will promote an acute episode of respiratory distress. When concomitant cardiovascular disease is present, these patients will also have a risk of myocardial infarct, heart failure, morbid arrhythmias, and acute pulmonary edema precipitated by respiratory depression. The early recognition and treatment by the dental team of a patient with chronic obstructive pulmonary disease developing respiratory failure is paramount. Shortness of breath, wet airway sounds, expiratory wheezing, elevated blood pressure and heart rate, and increasing apprehension or agitation may all accompany a patient in respiratory distress. Once an acute episode is diagnosed and treatment has stopped, the following maneuvers are indicated:

n Place patient in an upright sitting position;

n Administer oxygen at a low-flow rate of 2-4 L/minute via nasal cannula or hood;

n Assess and assist airway, breathing and circulation;

n Monitor vital signs; and

n Summon emergency medical assistance.

The severity of the disease and the patient's medical management must be reassessed and warrants the transfer of the patient to a medical facility for further evaluation.



Dental care for patients with respiratory diseases continues to be an important aspect of the practice of contemporary dentistry. Routine dental care can be provided for patients with severe respiratory problems when the dentist is knowledgeable about pulmonary diseases and is familiar with the signs, symptoms, and management of an emergent episode associated with asthma or chronic obstructive pulmonary disease. Patients with severe respiratory problems can receive safe and appropriate care when the dental team has conducted a proper risk assessment and tailored the necessary dental treatment to each individual patient's needs and tolerance. Preparation is vital to the prevention of a medical emergency arising from dental treatment in patients that are compromised by serious health conditions.


Author / Mitchell B. Day, DDS, maintains a private practice in oral and maxillofacial surgery in San Jose, Calif., and serves as a clinical associate professor in the Departments of Anatomy and Orthodontics at the University of the Pacific School of Dentistry.




1. Beasley R, Burgess C, et al, Pathology of asthma and its clinical complications. J Allergy Clin Immunol

92:148-54, 1993.


2. National Asthma Education and Prevention Program, Guidelines for the diagnosis and management of asthma. Expert Panel Report 2. National Institutes of Health, Bethesda, MD, 1997.


3. Current Estimates From the National Health Interview Survey, 1994. National Center for Health Statistics, Hyattsville, MD,1995; DHHS publication no (PHS) 95-1521.


4. Mannino DM, Homa D, et al, Surveillance for asthma - United States, 1960-1995. Mor Mortal Wkly Rep CDC Surveill Summ 47(1):1-27, 1998.


5. Sly RM, Changing asthma mortality. Ann Allergy 73: 259-68, 1994.


6. Sears MR, Worldwide trends in asthma mortality. Bull Int Union Tuberc Lung Dis 66:79-83, 1997.


7. Horwitz RJ, Busse WW, Inflammation and asthma. Clin Chest Med 16:583-620, 1995


8. Hogg JC, Pathology of asthma. J Allergy Clin Immunol 92:1-5, 1993.


9. Barnes PJ, Molecular mechanisms of antiasthma therapy. Ann Med 27:531-5, 1995.


10. Rumbak MJ, Self TH, A diagnostic approach to "difficult" asthma. Postgrad Med 92:8090, 1992.


11. Mathison DA, Stevenson DD, Simon RA, Precipitating factors in asthma: aspirin, sulfites and other drugs and chemicals. Chest 87:50-4, 1985.


12. Kemp JP, Comprehensive asthma management: guidelines for clinicians. J Asthma 35:601-20, 1998.


13. Baldinger SL, Shore ET, Focus on zafirlukast: leukotriene receptor antagonist for the prophylaxis and chronic treatment of asthma. Formulary 31:1029-1052, 1996.


14. Owens CA, Grundy GW, Focus on zileuton: first FDA approved agent of a new class of drugs, 5-lipoxygenase inhibitors, for the management of asthma. Formulary 32:455-71, 1997.


15. D’Alopnzo GE, Nathan RA et al, Salmeterol xinafoate as maintenance therapy compared with albuterol in patients with asthma. JAMA 271:1412-16, 1994.


16. Greening AP, Ind PW, et al, Added salmeterol versus higher dose corticosteroids in asthma patients with symptoms on existing inhaled corticosteroids. Lancet 344:219-24, 1994.


17. Stoloff SW, Janson S, Providing asthma education in primary care practice. Am Fain Phys 56:117-26, 1995.


18. Bone RC Goals of asthma management: step-care approach. Chest 109:1056-65, 1996.


19. Kidney J, Dominquez M, et al, Immunodulation by theophylline in asthma. Am J Respir Crit Care Med 151:1907-14, 1995.


20. Finnerty JP, Lee C, et al, Effects of theophylline on inflammatory cells and cytokines in asthmatic subjects. EUR Respir:J9:672-7, 1996.

21. Bremner P, Asthma management in adults. Australian Fain Physician 28:475-8 1999.

22. US Department of Health and Human Services, Waring on prescription drugs containing sulfites. FDA Drug Bull 17:2-3 1987.

23. Cuestaa-Herranz J, et al, Allergic reactions caused by local anesthetic agents belonging to amide group. J Allergy Clin Immunology 99:427-8, 1997.

24. American Thoracic Society, Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 152:S77-121, 1995.

25. National Center for Health Statistics: Birth and Deaths, United States, 1996. Monthly Vital Statistics Report 46:5, 1997.

26. Feinlieb M, Rosenberg H, et al, Trends in COPD morbidity and mortality in the United States. Am Rev Respir Dis 140:59-518, 1989.

27. Speizer FE, The rise in chronic obstructive pulmonary disease mortality: overview and summary. Am Rev Respir Dis 140:5106-7, 1989.

28. Sherril DL, Lebowitz M, Burrows B, Epidemiology of chronic obstructive pulmonary disease. Clin Chest Med 11:375-88, 1990.

29. Davis RM, Novotny TE, The epidemiology of cigarette smoking and its impact on chronic obstructive pulmonary disease. Am Rev Respir Dis 140:582-4 1990.

30. Burrows B, Epidemiological evidence for different types of chronic airflow obstruction Am Rev Respir Dis 143:1452-5, 1992.

31. Brandy M, Nukiwa T, Crystal R, Molecular basis of al - antitrypsin deficiency Am J Med 84: 13-31 1998.

32. Stoller JK, Clinical features and natural history of severe a 1 -antitrypsin deficiency. Chest 111:5123-8, 1997.

33. Brown CA, Crombie IK, Smith WCS, The impact of quitting smoking on symptoms of chronic bronchitis: result of the Scottish heart health study. Thorax 46:112-4, 1991.

34. Murphy TF, Sethi S, Bacterial infection in chronic obstructive pulmonary disease. Am Rev Respir Dis 146:1067-83, 1992.

35. Gapek JE, Pacht ER, Pathogenesis of hereditary emphysema and replacement therapy for a, antitrypsin deficiency: insight into the more common forms of emphysema. Chest 110: 2485, 1996.

36. Fiore MC, Bailey WC, et al, Smoking Cessation. Clinical Practice Guideline, No 18. USDHHS Public Health Service, Agency for Health Care Policy and Research (Publication No. 960692). Rockville, Maryland, April, 1996.

37. Edmunds M, Conner H, et al, Evaluation of a multicomponent group smoking cessation program. Prev Med 20: 404-13, 1996.

38. Zimet I Pharmacological therapy of obstructive airway disease. Clin Chest Med 11:461-86, 1990.

39. McKay SE, Howie ALL et al, Value of theophylline in patients handicapped by chronic obstructive pulmonary disease. Thorax 48:227-32, 1993.

40. Keating VM, Jatakanon A, et al, Effects of inhaled and oral glucocorticoids on inflammatory indices in asthma and COPD. Am J Repir Crit Care Med 155:542-8, 1997.

41. Ferguson GT, Cherniack RM, Management of chronic obstructive pulmonary disease. N Engl Med 328: 7 017-22, 7 993.



CDA Journal. Vol. 28, No. 8, Aug. 2000.

Reprinted with permission.