COPD (Chronic Obstructive Pulmonary Disease)

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Definition and Epidemiology:-

Chronic obstructive pulmonary disease (COPD) is a disease state characterized by chronic airflow obstruction; thus, pulmonary function testing is central to its diagnosis. The presence of airflow obstruction is determined by a reduced ratio of the forced expiratory volume in 1 s (FEV1) to the forced vital capacity (FVC). Among individuals with a reduced FEV1/FVC, the severity of airflow obstruction is determined by the level of reduction in FEV1 (Table-1): ≥80% is stage I, 50-80% is stage II, 30-50% is stage III, and <30% is stage IV. Cigarette smoking is the major environmental risk factor for COPD. The risk of COPD increases with cigarette smoking intensity, which is typically quantified as pack -years. (One pack of cigarettes smoked per day for 1 year equals 1 pack-year.) Individuals with airway hyperresponsiveness  and certain occupational exposures (e.g., coal mining, gold mining, and cotton textiles) are likely also at increased risk for COPD. In countries in which biomass combustion with poor ventilation is used for cooking, an increased risk of COPD among women has been repoted. COPD is a progressive disorder; however , the normal individuals, FEV1 reaches a lifetime peak at around age 25 years, enters a plateau phase, and subsequently declines gradually and progressively. Subjects can develop COPD by having reduced maximally attained lung function, shortened plateau phase, or accelerated decline in lung function.

  Symptoms often occur only when COPD is advanced; thus, early detection requires spirometric testing. The Pao2 typically remains near normal until the FEV1 falls to <50% of the predicted value. Hypercarbia and pulmonary hypertension are most common after FEV1 has fallen to <25% of predicted. COPD pts with similar FEV1 values can vary markedly in their respiratory symptoms and functional impairment. COPD often includes periods of increased respiratory symptoms, such as dyspnea, cough, and phlegm production, which are known as exacerbations. Exacerbations are often often triggered by bacterial and/or viral respiratory infections. These exacerbations become more common as COPD severity

TABLE -1 GOLD CRITERIA FOR COPD SEVERITY

Gold stage	Severity	Symptoms	Spirometry
I	Mild	With or without chronic cough or sputum production	FEV1/FVC<0.7 and FEV1≥80% predicted
II	Moderate	With or without chronic cough or sputum production	FEV1/FVC<0.7 and 50%≤FEV1<80%predicted
III	Severe	With or without chronic cough or sputum production	FEV1/FVC<0.7 and 30%≤FEV1<50% predicted
IV	Very Severe	With or without chronic cough or sputum production	FEV1/FVC<0.7 and FEV1<30%predicted  Or FEV1<50% predicted with respiratory failure or signs of right heart failure

 Note: Gold, Global Initiative for Chronic Obstructive Pulmonary Disease (COPD).

Source: From RA Pauwels et al. Am J Respir Crit Care Med 163:1256, 2001; with permission.

increases, but some individuals are much more susceptible to developing exacerbation than others with similar degrees of airflow obstruction.

CLINICAL MANIFESTATIONS

History: Subjects with COPD usually have smoked ≥20 pack-years of cigarettes. Common symptoms include cough and phlegm production; individuals with chronic productive cough for 3 months per year for the preceding 2 years have chronic bronchitis. However, chronic bronchitis without airflow obstruction is not included within COPD.  Dyspnea, especially with exertion, is a common and potentially disabling symptom in COPD subjects. Exercise involving upper-body activity is especially difficult for severe COPD pts. Weight loss and cachexia are common in advanced disease. Hypoxemia and hypercarbia may result in fluid retention, morning headaches, sleep disruption, erythrocytosis, and cyanosis.

            Exacerbations are more frequent as disease progresses and are most often triggered by respiratory infections, often with a bacterial component. Exacerbations may also be precipitated by left ventricular failure, cardiac arrhythmia, pneumothorax, pneumonia, and pulmonary thromboembolism.

Physical Findings: The physical examination may be normal until COPD is fairly advanced. As disease progresses, sign of hyperinflation may become more prominent. Wheezing is occasionally observed, but it does not predict the severity of obstruction or response to therapy. Persistently localized wheezing raises the possibility of lung cancer.

      During COPD exacerbations, signs of respiratory distress may be prominent, including tachycardia, tachypnea, use of accessory muscles of respiration, and cyanosis.

Radiographic Findings: Plain chest x-ray may show hyperinflation, emphysema, and pulmonary hypertension. It is typically performed to exclude other disease processes during routine evaluation, and to exclude pneumonia during exacerbations. Chest CT scanning has much greater sensitivity for detecting emphysema but is typically reserved for the evaluation of advanced disease when surgical options such as lung volume reduction and lung transplantation are being considered.

Pulmonary Function Tests:  Objective documentation of airflow obstruction is essential for diagnosis COPD. Standardized staging of COPD is based on post-bronchodilator spirometry. In COPD, the FEV1/FVC ratio is reduced below 0.7. Despite prolonged expiratory efforts, subjects may not be able to achieve a plateau in their FVC. Increases in total lung capacity and residual volume, as well as reduced diffusing capacity for carbon monoxide, are typically seen in emphysema.

Laboratory Tests:  α1 antitrypsin (α1AT) testing, typically by measurement of the protein level in the bloodstream, is recommended to exclude severe α1AT deficiency. Augmentation therapy (a weekly IV infusion) is available for individuals with severe α1AT deficiency. Pulse oximetry can determine the O2 saturation. However, arterial blood gases remain useful to assess the severity of CO2 retention as well as acid-base disorders. During acute exacerbations, arterial blood gases should be considered in pts with mental status changes, significant respiratory distress, very severe COPD, or a history of hypercarbia. Complete blood counts are useful in advanced disease to assess for erythrocytosis, which can occur secondary to hypoxemia, and anemia, which can worsen dyspnea.

MANAGEMENT OF COPD EXACERBATIONS

COPD exacerbations are a major couse of morbidity and mortality . Critical decisions in management include whether hospitalization is required. Although there are not definitive guidelines to determine which COPD pts require hospitalization for an exacerbation, the development of respiratory acidosis, significant hypercarbia, worsening hypoxemia, pneumonia, or social situations without adequate home support for the treatment required should prompt consideration of hospitalization.

      Key components of exacerbation treatment include bronchodilators, antibiotics, and short courses of systemic glucocorticoids.

ANTIBIOTICS:  Because bacterial infections often trigger COPD exacerbations, antibiotic therapy should be strongly considered, especially with increased sputum volume or change n sputum color. Common pathogens include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Antibiotic choice should depend on the local antibiotic sensitivity patterns, previous sputum culture results for a particular pt, and the severity of disease. Trimethoprim-sulfamethoxazole, doxycycline, and amoxicillin are reasonable choices for subjects with mild to moderate COPD; broader-spectrum antibiotics should be sonsidered for subjects with more severe underlying COPD and/or more severe exacerbations. Outside of the setting of an acute exacerbation, chronic antibiotic therapy is not recommended in COPD.

BRONCHODILATORS:  Bronchodilator therapy is essential during COPD exacerbations. Short-acting β-adrenergic agonists by inhalation (e.g., albuterol q1-2h) are used; addition of anticholinergics is likely of benefit (e.g. ipratropium q4-6h). Administration of bronchodilators by nebulizer is often used initially because it is easier to administration to pts in  respiratory distress. Conversion to metered-dose inhaler administration can be successfully achieved with appropriate training of the pt and staff.

GLUCOCORTICOIDS: Systemic steroids hasten resolution of symptoms and reduce relapses and subsequent exacerbations for up to 6 months. Dosing is not well worked out, but 30-40 mg of prednisone dily (or IV equivalent) is standard, with a total course  of 10-14 days. Hyperglycemia is the most commonly reported complication and should be monitored.

OXIGEN:   Hypoxemia often worsens during COPD exacerbations. Supplemental O2 should be dministered to maintain Sao2≥90%. Delivery systems include nasal prongs at 1-2 L/min or 24% Ventury Mask. Very high O2 delivery can worsen hypercarbia, primarily due to increasing ventilation-perfusion mismatch. However, providing adequate O2 to obtain saturation of ~90% is the key goal. Therefore, supplemental O2 delivery should be focused on providing adequate oxygenation without providing unnecessarily high O2 saturations. Pts may require use of supplemental O2 after hospital discharge until the exacerbation completely resolves.

VENTILATORY SUPPORT:    The diagnosis of acute respiratory failure is made on the basis of a decrease in PaO2 by 10-15 mmHg from baseline or an increase in PaO2 associated with a PH<7.30. Numerous studies suggest that noninvasive mask ventilation [noninvasive positive pressure ventilation (NPPV)] can improve outcomes in acute COPD exacerbatioins with respiratory failure (PaCO2>45 mmHg). Contraindications to NPPV include cardiovascular instability, impaired mental status, inability to cooperate, copious secretions, craniofacial abnormalities or facial trauma, extreme obesity, or significant burns. Progressive hypercarbia, refractory hypoxemia, or alterations in mental status that compromise ability to comply with NPPV therapy may necessitate endotracheal intubation for mechanical ventilation.