Medical Care: The goal of management is to improve daily living and the quality of life by preventing symptoms and the recurrence of exacerbations by preserving optimal lung function. Once the diagnosis of COPD is established, educate the patient about the disease. Encourage the patient to participate actively in therapy.
Smoking cessation continues to be the most important therapeutic intervention. Many patients with COPD have a history of smoking and continue to smoke. A smoking cessation plan is an essential part of a comprehensive management plan. The success rates are low because of the addictive potential of nicotine, the conditioned response to smoking-associated stimuli, and psychological problems, including depression, poor education, and forceful promotional campaigns by the tobacco industry. The process of smoking cessation must involve multiple interventions.
Oral and inhaled medications are used for patients with stable disease to reduce dyspnea and improve exercise tolerance. Most of the medications employed are directed at 4 potentially reversible causes of airflow limitation in a disease state that has largely fixed obstruction. The following factors may be present: (1) bronchial smooth muscle contraction, (2) bronchial mucosal congestion and edema, (3) airway inflammation, and (4) increased airway secretion.
Smoking cessation, physical intervention
The transition from smoking to not smoking occurs in 5 stages: precontemplation, contemplation, preparation, action, and maintenance. Smoking intervention strategies include self-help, group, physician-delivered, workplace, and community programs.
Establishing a quit date may be helpful. Physicians and other healthcare providers should participate in setting the target date and follow up regarding maintenance.
Successful cessation programs usually employ the following resources and tools: patient education, a quit date, follow-up support, relapse prevention, advice for healthy lifestyle changes, social support systems, and adjuncts to treatment (eg, pharmacological agents).
Smoking cessation, pharmacologic intervention
Supervised use of pharmacologic agents is an important adjunct to self-help and group smoking cessation programs.
Nicotine is the ingredient in cigarettes primarily responsible for the addiction. Withdrawal from nicotine may cause unpleasant adverse effects, including anxiety, irritability, difficulty concentrating, anger, fatigue, drowsiness, depression, and sleep disruption. These effects usually occur during the first several weeks.
Nicotine replacement therapies after smoking cessation reduce withdrawal symptoms. If a person who smokes requires his or her first cigarette within 30 minutes of waking up, they are most likely highly addicted and would benefit from nicotine replacement therapy.
Several nicotine replacement therapies are available. Nicotine polacrilex is a chewing gum and has better quit rates than counseling alone. Transdermal nicotine patches are readily available for replacement therapy. Long-term success rates are 22-42%, compared to 2-25% with a placebo. These agents are well tolerated, and the adverse effects are limited to localized skin reaction.
Nicotine replacement therapy patches are sold under the following trade names: Nicoderm, Nicotrol, and Habitrol. The usual drug-dosing schedule is the same for all 3 brands. Individuals who smoke more than 1 pack per day initially need a 21-mg patch, followed by 14-mg and 7-mg patches.
Nicotine replacement therapy chewing pieces are marketed in 2 strengths (ie, 2 mg, 4 mg). An individual who smokes 1 pack per day should use 4-mg pieces. The 2-mg pieces are to be used by individuals who smoke less than 1 pack per day. Instruct the patient to chew hourly and also to chew when needed to ease the initial cravings for 2 weeks. Gradually reduce the amount chewed over the next 3 months.
The use of an antidepressant medication (eg, Zyban) also is effective for smoking cessation. Another antidepressant, bupropion, is a nonnicotine aid to smoking cessation that enhances central nervous nonadrenergic function. A recent study demonstrated that 23% of patients sustained cessation at 1 year, compared to 12% who sustained cessation with the placebo. Bupropion also is effective in patients who have not been able to quit smoking with nicotine replacement therapy.
The most recent drug to receive approval for smoking cessation is varenicline (Chantix). It is a partial agonist selective for alpha4, beta2 nicotinic acetylcholine receptors. Action is thought to result from activity at a nicotinic receptor subtype, where its binding produces agonist activity while simultaneously preventing nicotine binding. Agonistic activity is significantly lower than nicotine.
Anti-inflammatory agents, inhaled steroids
A minority of patients who respond to oral corticosteroids can be maintained on long-term inhaled steroids.
Despite a lack of conclusive evidence to support the role of inhaled corticosteroids in the management of COPD, the use of these agents is widespread. Researchers completed 3 large placebo-controlled trials investigating the use of these agents in severe, mild, and very mild disease. Based on the rate of decline in FEV1, results from these 3 trials suggest that inhaled corticosteroids did not slow the decline in lung function but decreased frequency of exacerbations and improved disease-specific and health-related quality of life.
Inhaled corticosteroids have fewer adverse effects than oral agents do. Although effective, these agents improve expiratory flows less effectively than oral preparations, even at high doses. These agents may be beneficial in slowing the rate of progression in a subset of patients with COPD who have rapid decline.
Inhaled beta2-agonist bronchodilators activate specific B2-adrenergic receptors on the surface of smooth muscle cells, which increases intracellular cyclic adenosine monophosphate (AMP) and smooth muscle relaxation. Patients, even those who have no measurable increase in expiratory flow, benefit from treatment using beta2 agonists.
Methylxanthines have decreased in popularity over the last decade because of the narrow therapeutic range and frequent toxicity. The mechanism of action may involve increased intracellular calcium transport, adenosine antagonism, and prostaglandin E2 inhibition. Additionally, methylxanthines may improve diaphragm muscle contractility.
In COPD, beta2 agonists produce less bronchodilatation compared to asthma. Furthermore, spirometric changes may be insignificant despite symptomatic benefits. Patients primarily use beta2 agonists for relief of symptoms of COPD. Inhaled beta2 agonists are the initial treatment of choice for acute exacerbations of COPD.
In stable patients, beta2 agonists have an additive effect when used with an anticholinergic agent (eg, ipratropium bromide). Although oral preparations of beta2 agonists are available, the preferred route of administration is inhalation. Use a spacer, if indicated, to improve aerosol delivery and reduce adverse effects.
Two long-acting beta2 agonists (ie, formoterol, salmeterol) are available. They improve symptoms and morning peak flows and may be useful when bronchodilators are used frequently. More studies should establish the best role for these agents.
Anticholinergic agents
Treatment with aerosolized anticholinergic agents (eg, ipratropium bromide) may be more effective than a beta2 agonist in patients with COPD. Ipratropium bromide has bronchodilatory activity with minimum adverse effects and is administered by a metered-dose inhaler.
Studies in patients with stable COPD have shown that ipratropium bromide has equivalent or superior activity when compared with a beta2 agonist. In combination with a beta2 agonist, an additional 20-40% bronchodilation is achieved. This medication has slower onset and a longer duration than a beta2 agonist and is less suitable for use as needed.
Inhaled anticholinergic bronchodilators do not influence the long-term decline of FEV1. Initiate regular therapy with ipratropium at 2-4 puffs 4 times a day and add a beta2 agonist as needed.
Anticholinergic drugs compete with acetylcholine for postganglionic muscarinic receptors, thereby inhibiting cholinergically mediated bronchomotor tone, resulting in bronchodilatation. They block vagally mediated reflex arcs that cause bronchoconstriction. The onset of action is slower (eg, 30-60 min)
Long-acting bronchodilators
In addition to its anti-inflammatory effects, theophylline improves respiratory muscle function, stimulates the respiratory center, and promotes bronchodilation. Adding theophylline to the combination of bronchodilators can result in further benefit in stable COPD. The response to theophylline therapy also may vary among patients with severe COPD. Patients metabolize theophylline primarily by the hepatic enzyme system, a process affected by age, the heart, and liver abnormalities. Monitor serum levels of theophylline during therapy because of the drug's potential for toxicity. Adverse effects include anxiety, tremors, insomnia, nausea, cardiac arrhythmia, and seizures.
Oral steroids
The use of corticosteroids requires a careful evaluation for individual patients on adequate bronchodilator therapy who do not improve sufficiently or who develop an exacerbation. Most studies suggest that 20-30% of patients with COPD improve if administered long-term oral steroid therapy. Carefully document the effectiveness of such therapy (>20% improvement in FEV1) before administering prolonged daily or alternate day treatment.
Researchers found a positive correlation between bronchial eosinophilia and bronchodilator response in patients who had mild-to-moderate airflow obstruction. Outpatients have used oral steroids to treat acute exacerbations with success. However, after stabilization, gradually wean patients off oral corticosteroids because of their potential adverse effects.
In a recent meta-analysis of 16 controlled trials in individuals with stable COPD, researchers found that approximately 10% respond to these drugs. Carefully identify recipients. An increase in FEV1 by more than 20% has been used as a surrogate marker for steroid response. In acute exacerbation of COPD, use steroids routinely to improve symptoms and lung function.
Phosphodiesterase IV inhibitors
Cilomilast and roflumilast are systemically available, second-generation, selective phosphodiesterase-4 inhibitors. They cause a reduction of the inflammatory process (macrophages and CD8+ lymphocytes) in patients with COPD. Cilomilast is completely absorbed following oral administration and its elimination half-life is approximately 6.5 hours. A dose of 15 mg twice daily has been found to be clinically effective. Nausea, presumably of central origin, is the principal adverse reaction. The preliminary clinical studies suggest a favorable clinical effect in COPD.
Antibiotics
In patients with COPD, chronic infection or colonization of the lower airways is common from S pneumoniae, H influenzae, and Moraxella catarrhalis.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. The goal of antibiotic therapy in COPD is not to eliminate organisms but to treat acute exacerbations. Exacerbations are indicated by increased sputum purulence and volume and the development of dyspnea along with other features, including fever, leukocytosis, or infiltrate on a chest radiograph.
The first-line treatment choices include amoxicillin and trimethoprim/sulfamethoxazole. Second-line antibiotic regimens are the more expensive antibiotics, including azithromycin and fluoroquinolones.
The use of antibiotics in patients with COPD is supported by the results of a meta-analysis showing that patients who received oral antibiotic therapy had a small, but clinically significant, improvement in peak expiratory flow rate and a rapid resolution of symptoms. Patients who benefitted most were those whose exacerbations were characterized by at least 2 of the following: increases in dyspnea, sputum production, and sputum purulence (ie, Winnipeg criteria).
Mucolytic agents
These agents reduce sputum viscosity and improve secretion clearance. Viscous lung secretions in patients with COPD consist of mucous-derived glycoproteins and leukocyte-derived DNA. The oral agent N-acetylcysteine has antioxidant and mucokinetic properties and is used to treat patients with COPD.
Oxygen therapy
COPD commonly is associated with progressive hypoxemia. Oxygen administration reduces mortality rates in patients with advanced COPD because of the favorable effects on pulmonary hemodynamics.
Two landmark trials, the British Medical Research Counsel (MRC study) and the National Heart, Lung, Blood Institutes Nocturnal Oxygen Therapy Trial (NOTT), showed that long-term oxygen therapy improves survival 2-fold or more in hypoxemic patients with COPD. Hypoxemia is defined as PaO2 of less than 55 mm Hg or oxygen saturation of less than 90%. Oxygen was used for 15-19 hours per day.
Specialists recommend long-term oxygen therapy, therefore, for patients with PaO2 of less than 55 mm Hg, a PaO2 of less than 59 mm Hg with evidence of polycythemia, or cor pulmonale. Reevaluate these patients 1-3 months after initiating therapy because some patients may not require long-term oxygen.
Many patients with COPD who are not hypoxemic at rest worsen during exertion. Even though the studies designed to determine the long-term benefit of oxygen solely for exercise have not yet been conducted, home supplemental oxygen commonly is prescribed for these patients. Oxygen supplementation during exercise can prevent increases in pulmonary artery pressure, reduce dyspnea, and improve exercise tolerance.
Oxygen therapy generally is safe. Oxygen toxicity from high-inspired concentrations (ie, >60%) is well recognized. Little is known about the long-term effects of low-flow oxygen. The increased survival and quality of life benefits of long-term oxygen therapy outweigh the possible risks. PaCO2 retention from depression of hypoxic drive has been overemphasized. PaCO2 retention is more likely a consequence of ventilation/perfusion mismatching rather than respiratory center depression. While this complication is not common, it is best avoided by titration of oxygen delivery to maintain PaO2 at 60-65 mm Hg.
The major physical hazards of oxygen therapy are fires or explosions. Patients, family, and other caregivers must be warned not to smoke. Overall, major accidents are rare and can be avoided by good patient and family training.
" Oxygen systems
o The continuous flow nasal cannula is the standard means of oxygen delivery for the stable hypoxemic patient. It is simple, reliable, and generally well tolerated. Each liter of oxygen flow adds 3-4% to the fraction of inspired oxygen (FiO2). Nasal oxygen delivery also is beneficial for most mouth-breathing patients.
o Oxygen-conserving devices function by delivering all of the oxygen during early inhalation. These devices improve the portability of oxygen therapy and reduce overall costs. Three distinct oxygen-conserving devices exist-reservoir cannulas, demand pulse delivery devices, and transtracheal oxygen delivery.
o Pharmacologic treatment of COPD is targeted to symptom reduction. With the exception of smoking cessation and continuous long-term oxygen treatment, drug therapy does not modify the natural history of COPD. Recent long-term pharmacologic studies in COPD have evaluated prevention of exacerbations and/or hospitalization as the primary outcome. Tiotropium, a long-acting anticholinergic agent, reduces the frequency of exacerbations and the use of health care resources in patients with moderate-to-severe COPD. Inhaled steroids may also reduce the frequency and severity of exacerbations in patients with severe COPD. Whether the combination of inhaled steroids and long-acting bronchodilators has additive effects on lung function and/or exacerbations is still unclear.
Surgical Care: Over the past 50-75 years, researchers described a variety of surgical approaches to improve symptoms and restore function in patients who have emphysema. Only giant bullectomy and, possibly, the lung volume reduction surgery are useful.
Diet: Inadequate nutritional status associated with low body weight in patients with COPD is associated with impaired pulmonary status, reduced diaphragmatic mass, lower exercise capacity, and higher mortality rates. Nutritional support is an important part of their comprehensive care.
DRUG TREATMENT :
1. ANTIBIOTICS
2. ANTITUSSIVES / EXPECTORANTS
3. BRONCHODILATORS
4. ANTIVIRALS LIKE RIMANTADINE, AMANTADINE
5. ANALGESIC / ANTIPYRETICS
6. INHALED BETA AGONISTS
- ALBUTEROL
- ALUPENT
- FORMOTEROL
- SALMETEROL
7. INHALED CORTICOSTEROIDS
- BUDESONIDE
- FLUTICASONE
8. ANTICHOLINERGICS
- TIOTROPIUM
- IPRATROPIUM
9. METHYL XANTHINES
- THEOPHYLLINE
10. ORAL CORTICOSTEROIDS
- PREDNISONE