INTRODUCTION COPD is a preventable and treatable disease characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and is associated with an enhanced abnormal response of the lungs to noxious particles or gases
COMPONENTS OF COPD: Emphysema: Emphysema is pathologically defined as an abnormal permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by the destruction of alveolar walls and without obvious fibrosis Chronic bronchitis: a clinically defined condition with chronic cough and sputum production on most days for 3 months of 2 successive years ; and small airways disease, a condition in which small bronchioles are narrowed.
Aetiology : Cigarette Smoking 95% of cases are smoking-related, typically >20 pack years. Respiratory Infections Occupational Exposures; coal mining, gold mining, and cotton textile dust. Biomass use Low birth weight α 1 Antitrypsin Deficiency
PATHOPHYSIOLOGY: COPD results from the combined processes of peripheral airway inflammation and narrowing of the airways. This leads to airflow limitation and the destruction and loss of alveoli, terminal bronchioles and surrounding capillary vessels and tissues, which adds to airflow limitation and leads to decreased gas transfer capacity . The extent of airflow limitation is determined by the severity of inflammation, development of fibrosis within the airway and presence of secretions or exudates . Reduced airflow on exhalation leads to air trapping, resulting in reduced inspiratory capacity, which may cause breathlessness (also known as dyspnoea ) on exertion and reduced exercise capacity.
DEFINITION OF ACUTE EXACERBATION OF COPD: an acute event characterized by a worsening of the patient’s respiratory symptoms that is beyond normal day-to-day variations and leads to a change in medication
Precipitating factors: Respiratory tract infections: Exposure to air pollutants Pneumonia heart failure noncompliance with medication use.
Organisms Implicated: Mild to moderate exacerbations Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalis Chlamydia pneumoniae Mycoplasma pneumoniae Viruses Severe exacerbations Pseudomonas species Other gram-negative enteric bacilli
•Negatively affect a patient’s quality of life Have effects on symptoms and lung function that take several weeks to recover Accelerate the rate of decline of lung function . Are associated with significant mortality, particularly in those requiring hospitalization Have high socioeconomic costs
Because no curative therapy is available, management of severe exacerbations of COPD should be directed at relieving symptoms and restoring functional capacity Patients with COPD often have poor baseline functional status with few respiratory reserves. Infections can worsen their condition and lead to a quick decline in pulmonary function.
Goals of treatment: • Minimize the impact of the current exacerbation Prevent subsequent exacerbations
Examination findings: Respiratory distress Tripod posture Pursed lips breathing Neck – marked dilated neck vein , accessory muscles in use Chest – increase antero -posterior diameter , deep suprasternal notch , paradoxical motion of abdomen , scattered expiratory wheezing, prolonged expiratory phase . •
Signs of severity are: Use of accessory respiratory muscles Paradoxical chest wall movements Worsening or new onset central cyanosis Development of peripheral edema Hemodynamic instability Deteriorated mental status
OXYGEN THERAPY: Initial therapy should focus on maintaining oxygen saturation at 90 percent or higher. Oxygen supplementation by nasal cannula or face mask is frequently required. With more severe exacerbations, intubation or a positive-pressure mask ventilation method (e.g., continuous positive airway pressure [CPAP]) is often necessary to provide adequate oxygenation. Such interventions are more likely to be needed when hypercapnia is present, exacerbations are frequent or altered mental status is evident. 12
BRONCHODILATORS: Inhaled beta 2 agonists should be administered as soon as possible during an acute exacerbation of COPD. Use of a nebulizer to provide albuterol (Ventolin) or a similar agent with saline and oxygen enhances delivery of the medication to the airways. Beta 2 agonists can be delivered effectively by metered-dose inhaler if patients are able to use proper technique, which may be difficult during an exacerbation
. Salmeterol ( Serevent ), a long-acting beta 2 agonist, has been shown to relieve symptoms in patients with COPD. 29 Twice-daily dosing is an added benefit and may be convenient for many patients. Orally administered beta 2 agonists have more side effects than inhaled forms. Hence, oral agents generally are not used to treat exacerbations of COPD.
ANTICHOLINERGICS: In inhaled forms, anticholinergics have few adverse effects because of minimal systemic absorption. Use of a combination product such as ipratropium-albuterol ( Combivent ) may simplify the medication regimen, thereby improving compliance.
ANTIBIOTICS: , antibiotic administration should be considered at the beginning of treatment for exacerbations of COPD. Therapy for moderate acute exacerbations of chronic bronchitis and emphysema should be directed at S. pneumoniae , H. influenzae and M. catarrhalis , which are the most common pathogens, with C. pneumoniae and Mycoplasma pneumoniae occurring less often.
Antibiotic resistance poses an increasing problem, especially in infections caused by S. pneumoniae , beta-lactamase-producing H. influenzae and M. catarrhalis . Consequently, physicians often are forced to use broader spectrum antibiotics for empiric therapy. Cultures of respiratory samples are useful for guiding antibiotic therapy in patients .
CORTICOSTEROIDS: Short courses of systemic corticosteroids may provide important benefits in patients with exacerbations of COPD