Etiology

Worldwide, the most important cause of COPD is tobacco smoking. Approximately 12.5% of current smokers and 9% of former smokers have COPD.⁴ Smoking also accounts for 85% to 90% of COPD-related deaths in both men and women. The risk for development of COPD is dose-related and increases with the number of cigarettes smoked per day and duration of smoking.^5,6 The risk of death from COPD is 13 times higher in female smokers and 12 times higher in male smokers than in nonsmokers of the same gender.⁵ Despite the increased risk, only about one in five chronic smokers develop COPD. This observation suggests that genetic susceptibility to the production of inflammatory mediators (i.e., cytokines) in response to smoke exposure plays an important role. In addition to cigarette smoking, long-term exposure to occupational and environmental pollutants and the absence or deficiency of α₁-antitrypsin are other factors that contribute to COPD. α₁-antitrypsin is made in the liver and neutralizes neutrophil elastase.

Pathophysiology and Complications

Chronic exposure to cigarette smoke induces pathophysiologic responses of the airways and lung tissue. Chronic bronchitis involves the large and small airways. In the large airways, tobacco smoke and irritants induce thickened bronchial walls with inflammatory cell infiltrate, increased size of the mucous glands, and goblet cell hyperplasia. Obstruction is exacerbated in the small airways by narrowing, scarring, increased sputum production, mucous plugging, and collapse of peripheral airways resulting from the loss of surfactant⁷ (Figure 7-1). Obstruction is present on both inspiration and expiration.

FIGURE 7-1 Gross pathologic specimen shows lung changes (thickened bronchial walls, narrowing of small airways) due to chronic bronchitis.

(Courtesy McLay RN, et al: Tulane gross pathology tutorial, Tulane University School of Medicine, New Orleans, Louisiana, 1997.)

Emphysematous changes occur as chronic smoke inhalation injures lung parenchyma. The alveolar epithelium is damaged, causing a release of inflammatory mediators that attract activated macrophages and neutrophils. These inflammatory cells release enzymes (elastase) that destroy the alveolar walls, resulting in enlarged air spaces distal to the terminal bronchioles and loss of elastic recoil of the lungs (Figure 7-2). Obstruction is caused by the collapse of these unsupported and enlarged air spaces and is evident on expiration—not inspiration.⁷

FIGURE 7-2 A, Pathogenesis of emphysema involving imbalance in proteases-antiproteases that results in tissue damage and collapse of alveoli. B, Gross pathologic specimen of an emphysemic lung.

(A, From Kumar V, Abbas A, Fausto N, editors: Robbins & Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders. B, Courtesy McLay RN, et al: Tulane gross pathology tutorial, Tulane University School of Medicine, New Orleans, Louisiana, 1997.)

COPD usually is progressive, and the course is one of deterioration and periodic exacerbations, unless intervention is provided early in its onset.⁶ The types of complications that develop vary depending on the site of damage. With continued exposure to primary etiologic factors (cigarette smoking, environmental pollutants), COPD usually results in progressive dyspnea and hypercapnia to the point of severe debilitation (clinically significant disability will develop in 15% to 20% of the patients).⁸ Recurrent pulmonary infections with Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae are especially common with bronchitis. These acute exacerbations are managed with antibiotics. Pulmonary hypertension can develop and, in the absence of supplemental oxygen therapy, lead to cor pulmonale (right-sided heart failure). Patients with emphysema more frequently are found to have enlarged air spaces, with a higher incidence of thoracic bullae and pneumothorax. Poor quality of sleep secondary to nocturnal hypoxemia is common with COPD. Although COPD is an irreversible process for which no cure exists, avoidance of pulmonary irritants can be of significant benefit in decreasing the morbidity and mortality rates for both diseases.

Signs and Symptoms

The onset phase of COPD takes many years in most patients and usually begins after age 40. Symptoms develop slowly, and many patients are unaware of the emerging condition. Key indicators are a chronic cough with sputum production that may be intermittent, unproductive or productive, scanty or copious, and dyspnea that is persistent and progressive or worsens with exercise. As the disease progresses, weight loss and decreased exercise capacity also are seen. Comorbid conditions include cardiovascular disease, respiratory infections, osteoporosis, and fractures.⁹

Traditional teaching presented patients who had chronic bronchitis as sedentary, overweight, cyanotic, edematous, and breathless; accordingly, they were known as “blue bloaters.” Patients diagnosed with emphysema were traditionally known as “pink puffers” because they demonstrated enlarged chest walls for a “barrel-chested” appearance, weight loss with disease progression, severe exertional dyspnea with a mild nonproductive cough, lack of cyanosis, and pursing of the lips with efforts to forcibly exhale air from the lungs. Currently, it is recognized that most patients with COPD may exhibit features of both diseases (Box 7-1).

Laboratory Findings

Diagnosing COPD in its early stages can be difficult, but the possibility of this clinical entity should be considered in any patient who experiences dyspnea with previously tolerated activities and demonstrates chronic cough with or without sputum production, as well as exposure to risk factors, especially cigarette smoking. Measures of expiratory airflow are the key diagnostic procedures performed. Forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV₁) are determined by spirometry—a simple objective test that measures the amount of air a person can breathe out (Figure 7-3). A diagnosis of COPD is assigned when patients have pulmonary symptoms and FEV₁ less than 70% of predicted volume (FVC) in the absence of any other pulmonary disease. The four stages of COPD are shown in Box 7-2.²

FIGURE 7-3 A, Measure of forced expiratory volume by spirometry. B, Discussion of daily spirometry results with physician.

Arterial blood gas measurement and chest radiographs aid in the diagnosis. Patients with chronic bronchitis have an elevated partial pressure of carbon dioxide (Pco₂) and decreased partial pressure of oxygen (Po₂) (as measured by arterial blood gases), leading to secondary erythrocytosis, an elevated hematocrit value, and compensated respiratory acidosis. Patients with emphysema have a relatively normal (Pco₂) and a decreased (Po₂), which maintain normal hemoglobin saturation, thus avoiding erythrocytosis. Total lung capacity and residual volume are markedly increased. The ventilatory drive of hypoxia also is reduced in both types of COPD.

Chest radiographs and computed tomography scans assist in classifying COPD and identifying comorbid conditions. In chronic bronchitis, typical radiographic abnormalities consist of increased bronchovascular markings at the base of the lungs (Figure 7-4). In emphysema, films demonstrate persistent and marked overdistention of the lungs, flattening of the diaphragm, and emphysematous bullae.

FIGURE 7-4 Chest radiograph of a patient with chronic obstructive pulmonary disease showing prominent vascular markings (consistent with chronic bronchitis).

Prevention of Potential Problems

Most patients with COPD have a history of smoking tobacco. Dental health care providers can make an important contribution to the management of patients with COPD by encouraging those who smoke to quit. By providing information on the diseases associated with smoking, dental health providers may help patients to start thinking seriously about giving up the habit. Many interventional approaches (e.g., nicotine replacement, bupropion therapy) are available, and providers should help the patient implement the method with which they feel most comfortable (see Chapter 8).^13,14

Before initiating dental care, clinicians should assess the severity of the patient’s respiratory disease and the degree to which it has been controlled. A patient coming to the office for routine dental care who displays shortness of breath at rest, a productive cough, upper respiratory infection, or an oxygen saturation level less than 91% (as determined by pulse oximetry) is unstable. Accordingly, the appointment should be rescheduled and an appropriate referral for medical attention should be made. If the patient is stable and the breathing is adequate, efforts should be directed toward the avoidance of anything that could further depress respiration (Box 7-3). Patients should be placed in a semisupine or upright chair position for treatment, rather than in the supine position, to prevent orthopnea and a feeling of respiratory discomfort. Pulse oximetry monitoring is advised. Humidified low-flow O₂—generally at a rate of 2 to 3 L/minute—may be provided and should be considered for use when the oxygen saturation level is less than 95%.

No contraindication to the use of local anesthetic has been identified. However, the use of bilateral mandibular blocks or bilateral palatal blocks can cause an unpleasant airway constriction sensation in some patients. This concern may be more important in the management of a patient with severe COPD with a rubber dam, or when medications are administered that dry mucous secretions. Humidified low-flow O₂ can be provided to alleviate the unpleasant airway feeling produced by nerve blocks, use of a rubber dam, and/or medications.

If sedative medication is required, low-dose oral diazepam (Valium) may be used. Nitrous oxide–oxygen inhalation sedation should be used with caution in patients with mild to moderate chronic bronchitis. It should not be used in patients with severe COPD and emphysema, because the gas may accumulate in air spaces of the diseased lung. If this sedation modality is used in the patient with chronic bronchitis, flow rates should be reduced to no greater than 3 L/minute, and the clinician should anticipate induction and recovery times with nitrous oxide approximately twice as long as those in healthy patients.¹⁵ Narcotics and barbiturates should not be used, because of their respiratory depressant properties. Anticholinergics and antihistamines generally should be used with caution in patients with COPD, on account of their drying properties and the resultant increase in mucus tenacity; because patients with chronic bronchitis may already be taking these types of medications, concurrent administration could result in additive effects.

Patients with COPD often have comorbid conditions such as hypertension and coronary heart disease that require dental management considerations (see Chapters 3 and 4). Patients taking systemic corticosteroids may require supplementation for major surgical procedures because of adrenal suppression (see Chapter 15). Macrolide antibiotics (e.g., erythromycin, azithromycin) and ciprofloxacin hydrochloride should be avoided in patients taking theophylline because these antibiotics can retard the metabolism of theophylline, resulting in theophylline toxicity.¹⁶ The dentist should be aware of the manifestations of theophylline toxicity. Signs and symptoms include anorexia, nausea, nervousness, insomnia, agitation, thirst, vomiting, headache, cardiac arrhythmias, and convulsions. Outpatient general anesthesia is contraindicated for most patients with COPD.

Treatment Planning Modifications

No technical treatment planning modifications are required in patients with COPD.

Oral Complications and Manifestations

Patients with COPD who are chronic smokers have an increased likelihood of developing halitosis, extrinsic tooth stains, nicotine stomatitis, periodontal disease, premalignant mucosal lesions, and oral cancer. Anticholinergics are associated with dry mouth. In rare instances, theophylline has been associated with the development of Stevens-Johnson syndrome.

Incidence and Prevalence

Asthma affects 300 million persons worldwide and accounts for 1 of every 250 deaths worldwide. In the United States, its prevalence has more than doubled since the 1960s, from about 2% to 7% or greater (affecting 23 million people).¹⁸ Asthma is a disease primarily of children, with 10% of children (6 million) affected.¹⁷ Females have higher rates of asthma than males, although the prevalence is higher during childhood in boys. Higher body mass index (BMI) increases the risk for asthma in women.¹⁹ The disease affects 6% of older adults.²⁰ It occurs in all races, with a slightly higher prevalence among African Americans and a lower prevalence among Hispanics than among other races or ethnic groups.²¹ Patients with asthma in the United States make over 1.8 million visits to emergency departments annually, and more than 4000 asthma-related deaths occur annually. On the basis of current figures, the average dental practice is estimated to include at least 100 patients who have asthma.

Etiology

Asthma is a multifactorial and heterogeneous disease whose exact cause is not completely understood. Its development requires interaction between the environment and genetic susceptibility, with clinical manifestations resulting from dysfunction of the airway epithelium, smooth muscle, immune cells, and neuronal elements. Many triggers of asthma are recognized; these factors traditionally have been grouped into one of four categories based on pathophysiology: extrinsic (allergic or atopic), intrinsic (idiosyncratic, nonallergic, or nonatopic), drug-induced, and exercise-induced. Today, from a management perspective, the type of trigger is more important than the category.

Allergic or extrinsic asthma is the most common form and accounts for approximately 35% of all adult cases. It is an exaggerated inflammatory response that is triggered by inhaled seasonal allergens such as pollens, dust, house mites, and animal danders. Allergic asthma usually is seen in children and young adults.²² In these patients, a dose-response relationship exists between allergen exposure and immunoglobulin E (IgE)–mediated sensitization, positive skin testing to various allergens, and associated family history of allergic disease. Inflammatory responses are mediated primarily by type 2 helper T (T_H2) cells, which secrete interleukins and stimulate B cells to produce IgE (Figure 7-6). During an attack, allergens interact with IgE antibodies affixed to mast cells, basophils, and eosinophils along the tracheobronchial tree. The complex of antigen with antibody causes leukocytes to degranulate and secrete vasoactive autocoids and cytokines such as bradykinins, histamine, leukotrienes, and prostaglandins.²³ Histamine and leukotrienes cause smooth muscle contraction (bronchoconstriction) and increased vascular permeability, and they attract eosinophils into the airway.²⁴ The release of platelet-activating factor sustains bronchial hyperresponsiveness. Release of E-selectin and endothelial cell adhesion molecules, neutrophil chemotactic factor, and eosinophilic chemotactic factor of anaphylaxis is responsible for recruitment of leukocytes (neutrophils and eosinophils) to the airway wall, which increases tissue edema and mucus secretion. T lymphocytes prolong the inflammatory response (late-phase response), and imbalances in matrix metalloproteinases and tissue inhibitor metalloproteinases may contribute to fibrotic changes.

FIGURE 7-6 Processes involved in allergic (extrinsic) asthma.

(From Kumar V, Abbas A, Fausto N, editors: Robbins & Cotran pathologic basis of disease, ed 8, Philadelphia, 2010, Saunders.)

Intrinsic asthma accounts for about 30% of asthma cases and seldom is associated with a family history of allergy or with a known cause. Patients usually are nonresponsive to skin testing and demonstrate normal IgE levels. This form of asthma generally is seen in middle-aged adults, and its onset is associated with endogenous factors such as emotional stress (implicated in at least 50% of affected persons), gastroesophageal acid reflux, or vagally mediated responses.²⁴

Ingestion of drugs (e.g., aspirin, nonsteroidal antiinflammatory drugs, beta blockers, angiotensin-converting [ACE] enzyme inhibitors) and some food substances (e.g., nuts, shellfish, strawberries, milk, tartrazine food dye yellow color no. 5) can trigger asthma.²⁵ Aspirin causes bronchoconstriction in about 10% of patients with asthma, and sensitivity to aspirin occurs in 30% to 40% of people with asthma who have pansinusitis and nasal polyps (the so-called “triad asthmaticus”).²⁵ The ability of aspirin to block the cyclooxygenase pathway appears causative. The buildup of arachidonic acid and leukotrienes mediated by the lipoxygenase pathway results in bronchial spasm.^25,26

Metabisulfite preservatives of foods and drugs (specifically in local anesthetics containing epinephrine) may cause wheezing when metabolic levels of the enzyme sulfite oxidase are low.²⁷ Sulfur dioxide is produced in the absence of sulfite oxidase. The buildup of sulfur dioxide in the bronchial tree precipitates an acute asthma attack.²⁵

Exercise-induced asthma is stimulated by exertional activity. Although the pathogenesis of this form of asthma is unknown, thermal changes during inhalation of cold air provoke mucosal irritation and airway hyperactivity. Children and young adults are more severely affected because of their high level of physical activity.

Infectious asthma is a term previously used to describe persons who developed asthma because of the inflammatory response to bronchial infection. Now it is recognized that several respiratory viral infections during infancy and childhood can result in the development of asthma. Also, causative agents of respiratory infections (bacteria, dermatologic fungi I Trichophyton), and Mycoplasma organisms) can exacerbate asthma. Treatment of the respiratory infection generally improves control of bronchospasm and constriction.

Signs and Symptoms

Asthma is a disease of episodic attacks of airway hyperresponsiveness. For reasons that are unclear, attacks often occur at night but also may follow or accompany exposure to an allergen, exercise, respiratory infection, or emotional upset and excitement. Typical symptoms and signs of asthma consist of reversible episodes of breathlessness (dyspnea), wheezing, cough that is worse at night, chest tightness, and flushing. Onset usually is sudden, with peak symptoms occurring within 10 to 15 minutes. Inadequate treatment results in emergency department visits for about 25% of patients.²⁹ Respirations become difficult and are accompanied by expiratory wheezing. Tachypnea and prolonged expiration are characteristic. Termination of an attack commonly is accompanied by a productive cough with thick, stringy mucus. Episodes usually are self-limiting, although severe attacks may necessitate medical assistance.³⁰

Laboratory Findings

Diagnostic testing by a physician is important in the differentiation of asthma from other airway diseases. Experienced clinical judgment and recognition of the signs and symptoms are essential, because laboratory tests for asthma are relatively nonspecific and no single test is diagnostic. Commonl/>