Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is chronic airway irritation, mucus production, loss of elasticity in lung parenchyma, and airflow obstruction.11-15 The terms chronic bronchitis and emphysema are no longer included in the formal definition. Chronic bronchitis, a clinical term, describes a productive cough and sputum production for ≥ three months during two successive years. Emphysema, a pathological term, describes destruction of alveolar capillary membrane.

Exposure to tobacco smoke is the most significant risk factor for COPD.11-15 Other risk factors include advanced age; secondhand cigarette smoke; chronic exposure to occupational pollutants such as silica, coal, and concrete dust; chronic exposure to environmental pollutants such as cotton, hemp, and grain dust and welding fumes; alpha1‑antitrypsin deficiency (a genetic anomaly); childhood history of recurrent respiratory infections; and family history of COPD.11-15

On exertion (physical or emotional stress), patients with COPD typically experience coughing, dyspnea (air hunger), and wheezing (a high-pitch whistling sound).11-13 Other signs and symptoms include the use of accessory muscles of respiration, pursed-lip breathing (air is inhaled slowly through the nose and exhaled slowly through pursed lips); pulmonary hyperinflation (widened anteroposterior chest diameter and diminished breath sounds); and, less commonly, cyanosis.11-13

COPD is a systemic disease with important non-pulmonary components such as weight loss, and respiratory and skeletal muscle abnormalities.11-13 Weight loss is related to increased circulating inflammatory mediators and pulmonary cachexia; respiratory muscles are overworked and fatigued; and skeletal muscles are underworked and atrophied. Persistent pulmonary damage can lead to right-sided heart failure, peripheral edema, jugular vein distention, and hepatomegaly.11-13

Treatment delays/reduces the risk of acute exacerbations, i.e., sustained worsening of dyspnea, cough and/or sputum excretion.14 Maintenance therapy may include an inhaled corticosteroid with a long-acting selective beta2‑adremergic receptor agonist such as fluticasone w/salmeterol or an inhaled long-acting muscarinic M3‑receptor antagonist, such as ipratropium.2,3,14 Long-term oxygen therapy, indicated if O2 saturation is ≤88%, corrects hypoxemia.

When a patient with COPD presents in an oral healthcare setting determine residual respiratory and physical impairment and restriction of normal activities.15 Patient with mild disease reports shortness of breath when hurrying on flat ground or climbing a slight hill or a flight of stairs.15 The exacerbation can be controlled with an increase in the dosage of the regular medication, i.e., an inhaled corticosteroid with a long-acting selective beta2‑adremergic receptor agonist.2,3,15

Patients with moderate disease stop to breath after walking 100 meters on flat ground. The exacerbation cannot be controlled with an increase in dosage of regular medication.15 The patient requires medical referral and treatment with systemic corticosteroids and/or antibiotics. The patient with severe disease is short of breath when dressing and, in general, is housebound from breathlessness. Patient requires evaluation in an emergency room and, likely, hospitalization.

Patients with COPD placed in a supine position may experience orthopnea soon after reclining. Treat patients in a semi-reclining position and monitor oxygen saturation with a pulse oximeter. Severe exacerbation of COPD (i.e., fast, labored breathing, hypoxemia, signs of right-sided heart failure such as peripheral edema and cyanosis, arrhythmia, chest pain, altered mental status, and sudden extreme dyspnea) warrants immediate medical referral.