Chronic obstructive pulmonary disease (COPD), which includes bronchitis and emphysema, and chronic lower respiratory disease (COPD and asthma), are common pulmonary diseases that cause obstruction in airflow. They are discussed in this chapter along with tuberculosis (TB), the most prevalent contagious disease in the world. Dental practitioners should be aware that pulmonary diseases pose several dental management considerations including risk for acute and chronic airway and breathing issues, as well as risk of disease (i.e., TB) spread.
Chronic Obstructive Pulmonary Disease
Chronic obstructive pulmonary disease is a general term for pulmonary disorders characterized by chronic airflow limitation from the lungs that is not fully reversible. COPD encompasses two main diseases: chronic bronchitis and emphysema. Chronic bronchitis is defined as a condition associated with chronic inflammation of the bronchi that produces excessive tracheobronchial mucus production (at the bronchial level) and a persistent cough with sputum for at least 3 months in at least 2 consecutive years in a patient in whom other causes of productive chronic cough have been excluded. Emphysema is defined as a permanent enlargement of the air spaces in the lung (e.g., distal to the terminal bronchioles) that is accompanied by destruction of the air space (alveolar) walls without obvious fibrosis. These conditions are related, often represent the progression of disease, and may have overlapping symptoms, making differentiation difficult. Accordingly, experts have recommended use of the designation COPD over the traditional terms chronic bronchitis and emphysema. COPD currently is diagnosed on the basis of the presence of cough, sputum production, and dyspnea together with an abnormal measurement of lung function.
Chronic obstructive pulmonary disease is the third leading cause of death in the United States and is estimated to affect more than 24 million people. COPD affects approximately 5% of adults and about 10% of persons older than 45 years in the United States. About 70% of cases occur in people older than age 45 years. The disease is more common in women; however, the death rate is 1.3 times greater in men than women (48.6 vs 36.6 per 100,000). COPD is disabling, second only to arthritis as the leading cause of long-term disability and functional impairment. Prevalence, incidence, and hospitalization rates increase with age. The disease is underdiagnosed in most populations. On the basis of current figures, the average dental practice of 2000 patients is estimated to have about 100 patients who experience features of COPD.
Worldwide, the most important cause of COPD is tobacco smoking. Approximately 12.5% of current smokers, 9% of former smokers, and 8% of those exposed to passive smoke have COPD. 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. 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. Despite the increased risk, only about one in five chronic smokers develops 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 α 1 -antitrypsin are factors that contribute to COPD. The enzyme α 1 -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 surfactant ( Fig. 7.1 ). Obstruction is present on both inspiration and expiration.
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 ( Fig. 7.2 ). Obstruction is caused by the collapse of these unsupported and enlarged air spaces and is evident on expiration, not inspiration.
Chronic obstructive pulmonary disease usually is progressive, and the course is one of deterioration and periodic exacerbations unless intervention is provided early in its onset. 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). 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. Also, coexisting hypertension, ischemic heart disease and risk of arrhythmia, heart failure, and myocardial infarction (MI) as well as muscle wasting and osteoporosis occur in persons with COPD.
Signs and Symptoms
The onset phase of COPD takes many years in most patients and usually begins after age 40 years. 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, and 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.
Traditionally, patients with chronic bronchitis have been described as sedentary, overweight, cyanotic, edematous, and breathless; accordingly, they have been known as “blue bloaters.” Patients diagnosed with emphysema were traditionally known as “pink puffers” because they demonstrated enlarged chest walls (i.e., “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 ).
History: Exposure to risk factors, reduced exercise capacity
Clinical: Cough, sputum production, exertional dyspnea
Laboratory: Spirometry revealing airflow limitation, blood gas abnormalities
Imaging: Chest radiography or computed tomography scan revealing prominent bronchovascular markings or evidence of hyperinflation
Features of chronic bronchitis: onset at the age of approximately 50 years, overweight, chronic productive cough, copious mucopurulent sputum, mild dyspnea, frequent respiratory infections, elevated PCO 2 , decreased PO 2 (hypoxia), cor pulmonale, chest radiograph showing prominent blood vessels and large heart
Features of emphysema: onset at the age of approximately 60 years, thin physique, barrel chested, seldom coughing, scanty sputum, severe dyspnea, few respiratory infections, normal PCO 2 , decreased PO 2 , chest radiograph showing hyperinflation and small heart
Laboratory and Diagnostic 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 smoke. A 6-minute walk distance test can help screen for compromised respiratory function and reduced oxygen uptake; however, the key diagnostic procedures for COPD involve measures of expiratory airflow. Forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV 1 ) are determined by spirometry, a simple objective test that measures the amount of air a person can breathe out ( Fig. 7.3 ). A diagnosis of COPD is assigned when patients have pulmonary symptoms and FEV 1 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 .
Stage I—mild COPD: defined by an FEV 1 /FVC ratio of <70% and an FEV 1 of ≥80% of that predicted and sometimes chronic cough and sputum production
Stage II—moderate COPD: worsening airflow limitation and FEV 1 /FVC <70% and FEV 1 of 50% to <80% predicted, with shortness of breath typically developing on exertion
Stage III—severe COPD: FEV 1 /FVC <70% and FEV 1 of 30% to <50% predicted, with further worsening of airflow limitation and exacerbations that impact a patient’s quality of life
Stage IV—very severe COPD: FEV 1 /FVC <70%; FEV 1 <30% predicted, with chronic respiratory failure and exacerbations that may be life threatening
COPD, Chronic obstructive pulmonary disease; FEV 1 , forced expiratory volume in 1 second; FVC, forced vital capacity.
Arterial blood gas measurement and chest radiographs aid in the diagnosis. Patients with chronic bronchitis have an elevated partial pressure of carbon dioxide (PCO 2 ) and decreased partial pressure of oxygen (PO 2 ) (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 PCO 2 and a decreased PO 2 , 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 ( Fig. 7.4 ). In emphysema, radiographic images demonstrate persistent and marked overdistention of the lungs, flattening of the diaphragm, and emphysematous bullae.
Although COPD is an irreversible process for which no cure exists, treatment can control symptoms and slow disease progression. Management strategies include smoking cessation, avoidance of pulmonary irritants, influenza and pneumococcal vaccinations, and use of short- and long-acting bronchodilators. Other recommended measures include improving exercise tolerance, good nutrition, and adequate hydration. Of note, smoking cessation is the most effective and cost-effective intervention that can reduce risk of COPD and its progression.
Inhaled bronchodilators serve as the cornerstone of pharmacologic management and are recommended in a stepwise manner, as shown in Fig. 7.5 . The primary inhaled agents are short- and long-acting anticholinergics (e.g., ipratropium, tiotropium) that reduce glandular mucus and relax smooth muscle by blocking acetylcholine at the muscarinic receptors and short- and long-acting β 2 -adrenergic bronchodilators that relax smooth muscle by increasing cyclic adenosine monophosphate levels. Combining bronchodilators can lead to pronounced benefits, because they work by different mechanisms ( Table 7.1 ). Inhaled corticosteroids are added to the regimen for symptomatic patients at stage III or above who have repeated exacerbations. Phosphodiesterase inhibitors are alternative agents used. Theophylline, a methylxanthine nonselective phosphodiesterase inhibitor, relaxes bronchial smooth muscle cells but has a limited role in COPD management because of its narrow therapeutic range and likelihood of adverse effects (especially in older adults). When used, theophylline is administered as a slow-release formulation. More recently, phosphodiesterase-4–selective inhibitors (e.g., roflumilast, cilomilast) are being used to reduce exacerbations in patients with more advanced COPD.
|Drug||Trade Name||Dental Considerations|
|Beclomethasone dipropionate||Vanceril, Beclovent||Not intended for acute asthma attacks; may contribute to the development of oral candidiasis if used improperly or excessively|
|Corticosteroids Combination With Long-Acting β 2 -Selective Agonist Inhalers|
|Formoterol–budesonide||Symbicort||Not intended for acute asthma attacks; may contribute to the development of oral candidiasis if used improperly or excessively|
|Salmeterol–fluticasone||Advair HFA inhaler|
|Prednisone||Deltasone or generic||Not intended for acute asthma attacks; possible adrenal suppression, cushingoid features, and osteoporosis with long-term use|
|5-Lipoxygenase inhibitor||Not intended for acute asthma attacks|
|Leukotriene Receptor Antagonists|
|Cromolyn sodium||Intal inhaler||Not intended for acute asthma attacks|
|Fast-Acting Nonselective β–Agonist Inhalers|
|Epinephrine *||Primatene Mist, Bronkaid (available in parenteral form also)||For use during acute asthma attacks|
|Ephedrine †||Eted II|
|Intermediate-Acting Nonselective β-Agonist Inhalers (3–6 hours)|
|Isoproterenol ‡||Isuprel||Not best choice for use during acute asthma attacks|
|Metaproterenol §||Alupent, Metaprel, others|
|β 2 -Selective Agonist Inhalers (4–6 hours)|
|Albuterol ‡||Proventil, Ventolin||For use during acute asthma attacks|
|Terbutaline ‡||Brethaire, Bricanyl|
|Long-Acting β 2 -Selective Agonist Inhalers (>12 hours)|
|Indacaterol||Arcapta Neohaler||For COPD; not indicated for asthma|
|Salmeterol (slow onset, long duration)||Serevent||Not intended for acute asthma attacks|
|Formoterol (rapid onset, long duration)||Foradil|
|Combination β 2 -Selective Agonist Inhalers Plus Anticholinergic in One Inhaler|
|Fenoterol–ipratropium||Duovent||Paradoxical bronchospasm, dry mouth, throat irritation|
|Albuterol (Salbutamol)–ipratropium||Combivent||Headache, dizziness, dry mouth|
|ANTICHOLINERGIC BRONCHODILATORS (QUATERNARY AMMONIUM DERIVATIVES OF ATROPINE)|
|Aclidinium bromide||Tudorza Pressair||Not intended for acute asthma attacks; generally used in combination with other antiasthma drugs or for COPD; can cause headache|
Tiotropium (long acting)
|PHOSPHODIESTERASE (PD) INHIBITORS|
|Theophylline (nonselective)||Theo-Dur||Adverse drug interaction with erythromycin and azithromycin; serum drug levels should be monitored for toxicity|
|Roflumilast (selective PD-4)||Daxas, Daliresp||Adverse effects of headache, coughing may affect diagnostic workup and treatment|
|Cilomilast (selective PD-4)||Ariflo|
|Omalizumab||Xolair||Dizziness, muscle aches|
Antibiotics are used for pulmonary infections, and low-flow supplemental O 2 (2 L/min) is recommended when the patient’s PO 2 is 88% or less. Other important treatment options include pulmonary rehabilitation, screening for comorbid conditions, and continual monitoring for disease progression.
Prevention of Potential Problems
Most patients with COPD have a history of smoking tobacco and may present with a cough, exertional dyspnea, or a change in skin color. Recognition of these features should stimulate the dentist to refer these patients to a physician for care. Also, prevention of disease progression can be influenced by dental health care providers who encourage smokers to quit. By providing information on the diseases associated with smoking and its effect on healthy living, dental health providers can 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 patients implement the method with which they feel most comfortable (see Chapter 8 ).
Before initiating dental care, clinicians should assess the severity of the patient’s respiratory disease and the degree to which it is controlled. A patient coming to the office for routine dental care who displays shortness of breath at rest, a productive cough, upper respiratory infection (URI), or an oxygen saturation (O 2 sat) level less than 91% (as determined by pulse oximetry) is unstable.
Airway and Breathing.
If the patient is stable (O 2 sat >95%) and breathing is adequate (no dyspnea), efforts should be directed toward the avoidance of anything that could further depress respiration ( Box 7.3 ). Pulse oximetry monitoring is advised. Humidified low-flow O 2 —generally at a rate of 2 to 3 L/min—may be provided and should be considered for use when the oxygen saturation level is less than 95%. If the O 2 sat is less than 91% or there is dyspnea or an URI present, then the patient is considered unstable, and the appointment should be rescheduled and an appropriate medical referral made.
Patient Evaluation and Risk Assessment (see Box 1.1 )
Evaluate and determine whether COPD is present.
Obtain medical consultation if the condition is poorly controlled (as manifested by dyspnea, coughing, or frequent upper respiratory infections) or undiagnosed or if the diagnosis is uncertain. Review history and clinical findings for concurrent heart disease.
Encourage current smokers to stop smoking.
Potential Issues and Factors of Concern
|Antibiotics||Avoid erythromycin, macrolide antibiotics, and ciprofloxacin in patients taking theophylline. In patients who have received courses of antibiotics for upper respiratory infections, oral and lung flora may include antibiotic-resistant bacteria.|
|Anesthesia||Local anesthesia can be used without change in technique. Avoid outpatient general anesthesia.|
|Anxiety||Avoid nitrous oxide–oxygen inhalation sedation in patients with severe (stage 3 or worse) COPD. Consider low-dose oral diazepam or another benzodiazepine, although these agents may cause oral dryness.|
|Blood pressure||Patients with COPD can have cardiovascular comorbidity. Assess blood pressure.|
|Chair position||Semisupine or upright chair position may be better for treatment in these patients.|
|Devices||Avoid use of rubber dam in patients with severe disease. Use pulse oximetry to monitor oxygen saturation. Spirometry readings are helpful in determining level of control.|
|Drugs||Avoid use of barbiturates and narcotics, which can depress respiration. Avoid use of antihistamines and anticholinergic drugs because they can further dry mucosal secretions. Supplemental steroids are unlikely to be needed to perform routine dental care; the usual morning corticosteroid dose should be taken on the day of surgical procedures.|
|Equipment||Monitor oxygen saturation with pulse oximeter during sedation and invasive procedures. Use low-flow (2–3 L/min) supplemental O 2 when oxygen saturation drops below 95%; it may become necessary when oxygen saturation drops below 91%.|
|Follow-up||At each follow-up appointment, encourage the patient to quit smoking and examine the oral cavity for lesions that may be related to smoking. Avoid treatment if upper respiratory infection is present.|
Capacity to Tolerate Care.
Dental care can be provided to patients with stages I to III COPD but should be avoided in patients who have stage IV (very severe) COPD. Of note, patients with COPD often have coexisting hypertension and coronary heart disease, a shortened life span, and a higher risk of heart failure, arrhythmia, and MI. If coexisting cardiovascular disease is present, stress reduction measures should be implemented, and vital sign monitoring is advised (see Chapters 3 and 4 ). Supplemental oxygen should be provided as described earlier.
Patients who have moderate to severe disease should be placed in a semisupine or upright chair position for treatment, rather than in the supine position. The more upright chair position helps to prevent orthopnea and a feeling of respiratory discomfort.
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 O 2 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 stage III or IV COPD because the nitrous oxide may accumulate in air spaces of the diseased lung. If this sedation modality is used in a patient with chronic bronchitis, flow rates should be reduced to no greater than 3 L/min, and the clinician should anticipate induction and recovery times with nitrous oxide approximately twice as long as those in healthy patients. 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 because 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 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 reduce the metabolism of theophylline, resulting in theophylline toxicity. 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.
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. Poor oral hygiene, oral bacteria, and periodontitis can contribute to acute respiratory exacerbations and aspiration pneumonia in frail older adults who have COPD. Anticholinergics are associated with dry mouth. In rare instances, theophylline has been associated with the development of Stevens-Johnson syndrome.
Asthma is a chronic inflammatory disease of the airways characterized by reversible episodes of increased airway hyperresponsiveness, which results in recurrent episodes of dyspnea, coughing, and wheezing. The bronchiolar lung tissue of patients with asthma is particularly sensitive to a variety of stimuli. Overt attacks (flare-ups) may be provoked by allergens, URI, exercise, cold air, certain medications (salicylates, nonsteroidal antiinflammatory drugs (NSAIDs), cholinergic drugs, and β-adrenergic blocking drugs), chemicals, smoke, and highly emotional states such as anxiety and stress.
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 8% (affecting 25 million people). Asthma is a disease primarily of children, with 10% of children (6.6 million) affected. 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. The disease has a higher prevalence in families whose income is below the poverty level and affects 6% of older adults. It occurs in all races, with a higher prevalence among African Americans and multirace individuals than among whites and Asians. Patients with asthma in the United States make more than 2 million visits to emergency departments (EDs) annually, and more than 3500 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.
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. 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 H 2) cells, which secrete interleukins and stimulate B cells to produce IgE ( Fig. 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. Histamine and leukotrienes cause smooth muscle contraction (bronchoconstriction) and increased vascular permeability, and they attract eosinophils into the airway. 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.
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.
Ingestion of certain drugs (e.g., aspirin, NSAIDs, 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. 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”). 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.
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. Sulfur dioxide is produced in the absence of sulfite oxidase. The buildup of sulfur dioxide in the bronchial tree precipitates an acute asthma attack.
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 Trichophyton spp., and Mycoplasma organisms) can exacerbate asthma. Treatment of the respiratory infection generally improves control of bronchospasm and constriction.
Pathophysiology and Complications
In asthma, obstruction of airflow occurs as the result of bronchial smooth muscle spasm, inflammation of bronchial mucosa, mucus hypersecretion, and sputum plugging. The most striking macroscopic finding in the asthmatic lung is occlusion of the bronchi and bronchioles by thick, tenacious mucous plugs ( Fig. 7.7 ). Histologic findings are those of inflammation and airway remodeling, including (1) thickening of the basement membrane (from collagen deposition) of the bronchial epithelium, (2) edema, (3) mucous gland hypertrophy and goblet cell hyperplasia, (4) hypertrophy of the bronchial wall muscle, (5) accumulation of mast cell and inflammatory cell infiltrate, (6) epithelial cell damage and detachment, and (7) blood vessel proliferation and dilation. These changes contribute to decreased diameter of the airway, increased airway resistance, and difficulty in expiration.
Asthma is relatively benign in terms of morbidity. Most patients can expect a reasonably good prognosis, especially those in whom the disease develops during childhood. In many young children, the condition resolves spontaneously after puberty. In one reported series, however, two thirds of children with asthma still had symptoms at age 21 years. In a small percentage of patients, both young and old, the condition can progress to COPD, and respiratory failure, or status asthmaticus, the most serious manifestation of asthma, may occur.
Status asthmaticus is a particularly severe and prolonged asthmatic attack (one lasting longer than 24 hours) that is refractory to usual therapy. Signs include increased and progressive dyspnea, jugular venous pulsation, cyanosis, and pulsus paradoxus (a fall in systolic pressure with inspiration). Status asthmaticus often is associated with a respiratory infection and can lead to exhaustion, severe dehydration, peripheral vascular collapse, and death. Although death directly attributable to asthma is relatively uncommon, the disease causes about 3500 deaths per year in the United States. Asthma deaths occur more often in persons older than 45 years of age, are largely preventable, and often are related to delays in delivery of appropriate medical care.
Signs and Symptoms
Asthma is a disease of episodic attacks of airway hyperresponsiveness. For reasons that are unclear, flare-ups often occur at night or on waking, but they 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 wheezing, reversible episodes of breathlessness (dyspnea), cough, chest tightness, and flushing. The onset usually is sudden, with peak symptoms occurring within 10 to 15 minutes. Inadequate treatment results in ED visits for about 25% of patients. 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.
Laboratory and Diagnostic 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. Commonly ordered tests include 6-minute walk test, spirometry before and after administration of a short-acting bronchodilator, chest radiographs (to detect hyperinflation), skin testing (for specific allergens), bronchial provocation (by histamine or methacholine chloride challenge) testing, sputum smear examination and cell counts (to detect neutrophilia or eosinophilia), arterial blood gas determination, and antibody-based enzyme-linked immunosorbent assay (ELISA) for measurement of environmental allergen exposure. Spirometry is widely applied in diagnosing asthma because by definition, the associated airflow obstruction must be episodic and at least partially reversible. Reversibility is demonstrated by an increase in pulmonary function (i.e., FEV 1 ) of 12% or greater from baseline after therapy or after inhalation of a short-acting bronchodilator. Also, a recent drop in FEV 1 can be interpreted as a predictive of an asthma attack (see Fig. 7.3 ), and a drop of more than 10% during exercise fulfills the diagnosis of exercise-induced asthma. Fractional exhaled nitric oxide determination is an additional noninvasive test used to aid in the diagnosis and management of asthma.
Patients with chronic asthma are clinically classified as having intermittent or persistent disease (mild, moderate, or severe asthma). Severity is based on age, frequency of symptoms, impairment of lung function, and risk of attacks ( Box 7.4 ). Persons older than 12 years of age are classified as mild persistent asthma when they have symptoms more than twice per week but not daily and an FEV 1 greater than 85%. Symptoms generally last less than 1 hour. Patients with moderate asthma have FEV 1 greater than 60% but less than 80% and daily symptoms that affect sleep and activity level and, on occasion, require occasional emergency care. Asthma is classified as severe when patients have less than 60% FEV 1 , which results in symptoms throughout the day that limit normal activity. Attacks are frequent or continuous, occur at night, and result in emergency hospitalization.
|Symptoms ≤2 per week; brief exacerbations; asymptomatic between exacerbations; nocturnal symptoms <2 per month; FEV 1 >80% of predicted; FEV 1 /FVC ratio >85% (normal)||Short-acting β 2 -agonist as needed|
|Symptoms >2 per week but not daily; nocturnal symptoms 3–4 per month (limited exercise tolerance; rare ED visits); FEV 1 >80% of predicted; FEV 1 /FVC >85% (normal 8–19 years), 80% (20–39 years), 75% (40–59 years), 70% (60–80 years)||Low-dose inhaled corticosteroids or other antiinflammatory drug as needed; short-acting β 2 -agonist as needed|
|Daily symptoms; daily use of inhaled short-acting β-agonist; exacerbations that may affect activity and sleep; nocturnal symptoms >1 time per week but not nightly (occasional ED visits); FEV 1 60%–80% of predicted; FEV1/FVC reduced 5%||Low- or medium-dose inhaled corticosteroids + long-acting bronchodilator as needed; short-acting β 2 -agonist as needed|
|Symptoms throughout the day; frequent (often 7 times a week) exacerbations and nocturnal asthma symptoms; exercise intolerance; FEV 1 <60%; FEV 1 /FVC reduced >5% (often resulting in hospitalization)||High-dose inhaled corticosteroids + long-acting bronchodilator or montelukast + oral corticosteroid as needed; short-acting β 2 -agonist as needed|
ED, Emergency department; FEV 1 , forced expiratory volume in 1 second; FVC, forced vital capacity.
The goals of asthma therapy are to limit exposure to triggering agents, allow normal activities, restore and maintain normal pulmonary function, minimize the frequency and severity of attacks, control symptoms, and avoid adverse effects of medications. Experts agree that these goals are best accomplished by educating patients and involving them in the prevention or elimination of precipitating factors (e.g., smoking cessation) and comorbid conditions (rhinosinusitis, obesity) that confound management, establishment of a plan for regular self-monitoring, and provision of regular follow-up care. Specifically, it is recommended that a written education and action plan be given to each patient, with appropriate support and instructions for its use. Inexpensive peak expiratory flow meters should be used regularly at home and levels recorded daily in diaries. For patients with known allergies, the importance of avoidance of allergens to prevent attacks should be underscored. This can be conveyed by monitoring of allergen levels (tobacco smoke and pollutants) in the patient’s home, provision of desensitization intradermal injections, and monitoring of the pulmonary function zone on the basis of daily peak flow meter results (spirometry). Unfortunately, poor control of asthma often is related to low socioeconomic status (e.g., the patient cannot afford medication), increased anxiety, poor compliance, and unfavorable home environment.
Antiasthmatic drug selection is based on the type and severity of asthma and whether the drug is to be used for long-term control or quick relief. Current guidelines recommend a “stepwise” approach with the use of inhaled antiinflammatory agents as first-line drugs (the preferred inhalational agent is a corticosteroid preparation, with a leukotriene inhibitor as an alternative) for the long-term management and prophylaxis of persistent asthma ( Fig. 7.8 ). β-adrenergic agonists are recommended for intermittent asthma and are secondary agents that should be added (i.e., not to be used alone) for persistent asthma when antiinflammatory drugs are inadequate alone. Alternative drugs include mast cell stabilizers (cromolyn and nedocromil), immunomodulators, anticholinergics (tiotropium), and theophylline. Combination therapy with these medications often is used to improve lung function.
Inhaled corticosteroids are the most effective antiinflammatory medications currently available for the treatment of persistent asthma. They act by reducing the inflammatory response and preventing the formation of cytokines, adhesion molecules, and inflammatory enzymes. Aerosol dosage is two (for mild to moderate disease) to four times daily (severe asthma). Onset of action usually is after 2 hours, and peak effects occur 6 hours later. Long-term use of steroid inhalers rarely is associated with systemic adverse effects, provided the maximum recommended dose of 1.5 mg/day of inhaled beclomethasone dipropionate (Vanceril) or equivalent is not exceeded. Use of systemic steroids is reserved for asthma unresponsive to inhaled corticosteroids and bronchodilators and for use during the recovery phase of a severe acute attack. Inhaled steroids often are used in combination with long-acting β 2 -adrenergic bronchodilators (salmeterol or formoterol); the trade names for these drugs are Advair, Symbicort, and Dulera. Agents such as omalizumab (Xolair) that block IgE (monoclonal antibody against human IgE) are used for additive therapy in patients with severe persistent asthma who have allergy triggers; however, cost and the injectable-only formulation are major considerations with this drug.
For relief of acute asthma attacks, inhaled short-acting β 2 -adrenergic agonists are the drugs of choice because of their fast and notable bronchodilatory and smooth muscle relaxation properties (see Table 7.1 ). Short-acting β 2 -adrenergic agonists produce bronchodilation by activating β 2 receptors on airway smooth muscle cells, generally in 5 minutes or less. Inhalation corticosteroids, inhaled cromolyn sodium, and oral anticholinergics are not used for this purpose because of their slow onset of action.
β 2 -adrenergic agonists (administered by a metered-dose inhaler [MDI]) and cromolyn sodium (Intal) and nedocromil may be used in preventing exercise-induced bronchospasm. They are taken about 30 minutes before initiation of physical activity. Cromolyn and nedocromil decrease airway hyperresponsiveness by stabilizing the membrane of mast cells and interfering with chloride channel function so that mediators are not released when challenged by exercise or cold air. Theophylline is a mild to moderate bronchodilator to be used as an alternative. Monitoring of its serum concentration is essential.
Identification and Prevention.
The primary goal in dental management of patients with asthma is to prevent an acute asthma attack ( Box 7.5 ). The first step in achieving this goal is to identify patients with asthma by history followed by assessment to elucidate the surrounding details of the problem, along with prevention of precipitating factors.
Patient Evaluation and Risk Assessment (see Box 1.1 )
Evaluate and identify asthma as a medically confirmed or likely diagnosis along with its severity and type if present.
Obtain medical consultation if asthma is poorly controlled (as indicated by wheezing or coughing or a recent hospitalization) or is undiagnosed or if the diagnosis is uncertain. Encourage current smokers to stop smoking.
Potential Issues and Factors of Concern
|Antibiotics||Avoid erythromycin, macrolide antibiotics, and ciprofloxacin in patients taking theophylline.|
|Anesthesia||Clinicians may elect to avoid solutions containing epinephrine or levonordefrin because of sulfite preservative.|
|Anxiety||Provide a stress-free environment through establishment of rapport and openness to reduce risk of anxiety-induced asthma attack. If sedation is required, use of nitrous oxide–oxygen inhalation sedation or small doses of oral diazepam (or both) is recommended.|
|Allergy||Asthmatics with nasal polyps are increased risk for allergy to aspirin. Avoid aspirin use.|
|Blood pressure||Monitor blood pressure during asthma attacks to observe for the development of status asthmaticus.|
|Chair position||Semisupine or upright chair position for treatment may be better tolerated.|
|Devices||Instruct patients to bring their current medication inhalers to every appointment; use prophylactically in moderate to severe disease. Obtain spirometry reading to determine level of control. Use pulse oximetry to monitor oxygen saturation during dental procedure.|
|Drugs||Avoid precipitating odorants and drugs (aspirin). Avoid use of barbiturates and narcotics, which can depress respiration and release histamine, respectively. Supplemental steroids are unlikely to be needed in routine dental care; provide usual morning corticosteroid dose the morning of surgical procedures.|
|Equipment||Use low-flow (2–3 L/min) supplemental O 2 when oxygen saturation drops below 95%; supplemental O 2 also may become necessary when oxygen saturation drops below 91%.|
|Emergencies||Recognize the signs and symptoms of a severe or worsening asthma attack, including inability to finish sentences with one breath, ineffectiveness of bronchodilators to relieve dyspnea, recent drop in FEV 1 as determined by spirometry, tachypnea with respiratory rate of 25 ≥breaths/min, tachycardia with heart rate of ≥110 beats/min, diaphoresis, accessory muscle usage, and paradoxical pulse. Administer fast-acting bronchodilator (note: corticosteroids have delayed onset of action), oxygen, and, if needed, subcutaneous epinephrine (1 : 1000) in a dose of 0.3 to 0.5 mL. Activate EMS; repeat administration of fast-acting bronchodilator every 20 minutes until EMS personnel arrive.|
|Follow-up||Ensure that patient is receiving adequate medical follow-up care on a routine basis.|