[P] Medicine Management & Administration



Chronic obstructive pulmonary disease (COPD) is the fourth-ranked cause of death. Chronic obstructive pulmonary disease is defined as “disease state characterized by airflow limitation that is not fully reversible. Airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases.”PathophysiologyA. Airflow obstruction is the result of both small airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema). The relative contributions of each vary from person to person, and can be accompanied by partially reversible airways hyper-reactivity.B. Chronic bronchitis is defined by the presence of chronic productive cough for three months in each of two successive years.C. Emphysema is the abnormal permanent enlargement of air- spaces distal to the terminal bronchioles, accompanied by destruction of their walls without obvious fibrosis. Emphysema is frequently present in patients with moderate and severe COPD.D. Asthma is defined as an inflammatory disease of the airways characterized by an increased responsiveness of the trachea and bronchi to various stimuli, and manifested by a widespread narrowing of the airways.E. Cigarette smoking is the major cause of COPD. However, only about 15 to 20 percent of smokers develop COPD suggesting that host factors (most likely genetic) also contribute to pathogenesis of the disease.F. Alpha-1 antitrypsin deficiency. The only established genetic abnormality that predisposes to lung disease clinically and pathologically similar to COPD is alpha-1 antitrypsin [AAT] deficiency. Severe AAT deficiency has a frequency of about 1 in 3,000 live births. Persons with known COPD, or asthma with non-remittent airflow obstruction, should be screened for AAT deficiency.Clinical featuresA. History. Patients with COPD have usually been smoking at least 20 cigarettes per day for 20 or more years before symptoms develop. Chronic productive cough, sometimes with wheezing, often begins when patients are in their forties.B. Dyspnoea on effort does not usually begin until the mid sixties or early seventies. Sputum production is insidious, initially occur- ring only in the morning; the daily volume rarely exceeds 60 mL. Sputum is usually mucoid but becomes purulent with an exacerbation.C. Acute chest illnesses occur intermittently, and are characterized by increased cough, purulent sputum, wheezing, dyspnoea, and occasionally fever.D. With disease progression, the intervals between acute exacerbations shorten. Late in the course of the illness, an exacerbation may give rise to hypoxemia with cyanosis. Associated findings also include:1. Weight loss - Approximately 20 percent of patients with moderate and severe disease experience weight loss and loss.2. Hypercapnia with more severe hypoxemia in the setting of end-stage disease.3. Morning headache, which suggests hypercapnia.4. Cor pulmonale with right heart failure and oedema.5. Haemoptysis. Since bronchogenic carcinoma occurs with increased frequency in smokers with COPD, an episode of haemoptysis raises the possibility that carcinoma has developed. However, most episodes of haemoptysis are due to bronchial mucosal erosion.Diagnosis of chronic obstructive pulmonary diseaseHistorySmoking historyAge at initiationAverage amount smoked per dayDate when stopped smoking or a current smokerEnvironmental historyCoughChronic productive cough for at least one quarter of the year for two successive years is the defining characteristic of chronic bronchitis. Sputum, blood or blood streaking in the sputum.WheezingAcute chest illnessesFrequency of episodes of increased cough and sputum with wheezing.DyspnoeaAmount of effort required to induce uncomfortable breathing.Physical examinationChestThe presence of severe emphysema is indicated by: over-distension of the lungs in the stable position; decreased intensity of breath and heart sounds and prolonged expiratory phase.Wheezes during auscultation on slow or forced breathing and prolongation of forced expiratory time.Severe disease is indicated by pursed-lip breathing, use of accessory respiratory muscles, and retraction of lower interspaces.OtherUnusual positions to relieve dyspnoea at rest.Digital clubbing suggests the possibility of lung cancer or bronchiectasis.Mild dependent oedema may be seen in the absence of right heart failure.Differential diagnosis of COPDDiagnosisFeaturesCOPDOnset in mid-lifeSymptoms slowly progressive Long smoking history Dyspnoea during exerciseLargely irreversible airflow limitationAsthmaOnset in childhoodSymptoms vary from day to daySymptoms at night/early morningAllergy, rhinitis, and/or eczema also presentFamily history of asthmaLargely reversible airflow limitationHeart failureFine basilar cracklesChest X-ray shows dilated heart, pulmonary oedemaPulmonary function tests indicate volume restriction, not airflow limitationBronchiectasisLarge volumes of purulent sputumCommonly associated with bacterial infection Coarse crackles/clubbing on auscultation Chest X-ray/CT shows bronchial dilation, bronchial wall thickeningDiagnosisFeaturesTuberculosisOnset all agesChest X-ray shows lung infiltrateMicrobiological confirmationHigh local prevalence of tuberculosisObliterative bronchiolitisOnset in younger age, non-smokersMay have history of rheumatoid arthritis or fume exposureCT on expiration shows hypodense areasDiffuse panbronchiolitisMost patients are male and non-smokers. Almost all have chronic sinusitisChest X-ray and HRCT show diffuse small centrilobular nodular opacities and hyperinflationClassification of Severity of Chronic Obstructive PulmonaryDiseaseStageCharacteristics0: At riskNormal spirometryChronic symptoms (cough, sputum production)I: Mild COPDFEV1/FVC <70 percent EV1 >80 percent predictedWith or without chronic symptoms (cough, sputum production)II: ModerateCOPDFEV1/FVC <70 percent30 percent <FEV1 <80 percent predictedIIA: 50 percent <FEV1 <80 percent predictedIIB: 30 percent <FEV1 <50 percent predictedSevereCOPDFEV1/FVC <70 percentFEV1 30 percent predicted or FEV1 <50 percent predicted plus respiratory failure or clinical signs of right heart failureE. Physical examination1. Early in the disease there is only prolonged expiration and wheezes on forced exhalation. As obstruction progresses, hyperinflation becomes evident, and the anteroposterior diameter of the chest increases. The diaphragm is depressed and limited in its motion. Breath sounds are decreased and heart sounds often become distant. Coarse crackles may be heard at the lung bases. Wheezes are frequently heard.2. If the history and chest radiograph are compatible, a clinical diagnosis of COPD may be made. However, a forced expiratory spirogram before and after bronchodilator is always necessary for confirmation and quantification of the airflow obstruction.3. Patients with end-stage COPD may adopt positions which relieve dyspnoea, such as leaning forward with arms out- stretched and weight supported on the palms. Other signs in a patient with end-stage disease may include:a. The full use of the accessory respiratory muscles of the neck and shoulder girdle.b. Expiration through pursed lips.c. Paradoxical retraction of the lower interspaces during inspiration (Hoover's sign).d. Cyanosis.e. An enlarged, tender liver secondary to right heart failure. Neck vein distension, especially during expirationf. Asterixis due to severe hypercapnia.4. Plain chest radiography is insensitive for diagnosing emphysema; only about half of the instances are detected when the disease is of moderate severity.a. Over-distension of the lungs is indicated by a low, flat diaphragm and a long, narrow heart shadow. Flattening of the diaphragmatic contour and an increased retrosternal air- space are observed on the lateral projection. Rapid tapering of the vascular shadows accompanied by hypertransradiancy of the lungs is a sign of emphysema.b. Bullae, presenting as radiolucent areas larger than one centimeter in diameter and surrounded by arcuate hairline shadows, are proof of the presence of emphysema. How- ever, bullae reflect only locally severe disease and are not necessarily indicative of widespread emphysema.c. Pulmonary hypertension and right ventricular hypertrophy are indicated by prominent hilar vascular shadows and encroachment of the heart shadow on the retrosternal space as the right ventricle enlarges anteriorly.5. Pulmonary function tests are necessary for diagnosing and assessing the severity of airflow obstruction, and are helpful in following its progress. The FEV1 has less variability than other measurements of airways dynamics.a. The FVC is also readily measured, although it is dependent on the expiratory time in severe COPD. In the mildest degree of airflow obstruction, the FEV1/FVC ratio falls below 0.70 and the FEV1 percent predicted is normal. The FEV1 and the FEV1/FVC ratio fall progressively as theSeverity of COPD increases. Up to 30 percent of patients have an increase of 15 percent or more in their FEV1 following inhalation of a beta-agonist aerosol.b. Lung volume measurements reveal an increase in total lung capacity, functional residual capacity, and residual volume, and often a decrease in the vital capacity. The single breath carbon monoxide diffusing capacity is de- creased in proportion to the severity of emphysema.6. Arterial blood gases reveal mild or moderate hypoxemia without hypercapnia in the early stages. As the disease progresses, hypoxemia becomes more severe and hypercapnia supervenes. Hypercapnia is observed with increasing frequency as the FEV1 falls below one litre.7. Erythrocytosis increases as arterial PO2 falls below 55 mmHg.8. Sputum examination. In stable chronic bronchitis, sputum is mucoid and the predominant cell is the macrophage. During an exacerbation, sputum usually becomes purulent with an influx of neutrophils. The Gram stain usually shows a mixture of organisms. The most frequent pathogens cultured from the sputum are Streptococcus pneumoniae and Haemophilus influenzae. Other oropharyngeal flora such as Moraxella catarrhalis have been shown to cause exacerbations.Management of stable chronic obstructive pulmonary diseaseA. Bronchodilators can improve symptoms and reduce airflow limitation in patients with COPD.1. Metered dose inhalers (MDI) result in a bronchodilator response equivalent to that of a nebulizer. However, nebulizer therapy may still be necessary if dyspnoea and severe bronchospasm during exacerbations impair proper MDI technique.2. Beta agonists. The primary pharmacologic therapy of COPD is the sympathomimetic bronchodilator. Among these, short- acting selective beta-2 agonists (e.g., albuterol) are the agents of choice. Beta-2 agonists can cause tremor and reflex tachycardia due to peripheral arterial dilation. Hypokalemia can also occur in extreme cases. There is no advantage of using short-acting beta-2 agonists on a regular basis instead of as- needed.B. Anticholinergics. Inhaled anticholinergic bronchodilators (e.g., ipratropium and tiotropium) are an integral component of COPD treatment. Anticholinergic drugs reduce the frequency of severe exacerbations and respiratory deaths.1. Tiotropium (Spiriva), a long-acting inhaled anticholinergic agent, confers longer bronchodilation than ipratropium (Atrovent) and also appears to lessen the frequency of acute exacerbations.2. The effects of anticholinergics and beta-2 agonists are additive. Combination therapy may be simplified by the use of a single metered dose inhaler that delivers a combination of ipratropium and albuterol.C. Theophylline provides clear benefits to some patients with COPD. Theophylline is associated with decreased dyspnoea, improved arterial blood gases, improved spirometry, and improved respiratory muscle function. Theophylline also has pulmonary vasodilator and cardiac inotropic effects, resulting in improvements in right ventricular performance in cor pulmonale.1. Serum levels should be maintained in the 8 to 12 mcg/mL range. The use of a long-acting preparation at night may reduce the nocturnal decrements in respiratory function and the morning respiratory symptoms.D. Systemic corticosteroids have long been used to treat patients with COPD; however, chronic use can have significant adverse effects. Inhaled corticosteroids have substantially fewer adverse consequences.1. Chronic corticosteroid administration does not benefit most patients with COPD. However, as many as 20 percent of stable patients with COPD demonstrate objective improvement in airflow with oral corticosteroid treatment.2. Chronic steroid therapy should be considered only in patients who have continued symptoms or severe airflow limitation despite maximal therapy with other agents. Only patients with documented improvement in airflow should be considered for long-term therapy. Steroids should be reduced to the lowest dose possible. Alternate day or inhaled steroid usage should be considered.3. Inhaled corticosteroids may benefit patients with COPD with chronic bronchitis and frequent exacerbations.Therapy at each stage of COPDStageCharacteristicsRecommended treatmentsALLAvoidance of risk factor(s) Influenza vaccination0: At riskChronic symptoms (cough, sputum) Exposure to risk factor(s)I: MildCOPDFEV1/FVC<70 percent FEV1 >80 percent predicted with or without symptomsShort-acting bronchodilator when needed StageCharacteristicsRecommended treatmentsII: Moderate COPDIIAFEV1/FVC <70 percent50 percent <FEV1 <80 percentWith or without symptoms Regular treatment with one or more bronchodialtors RehabilitationInhaled glucorticosteroids if significant symptoms and lung function responseIIBFEV1/FVC <70 percent50 percent <FEV1 <50 percent With our without symptoms Regular treatment with one or more bronchodilators RehabilitationInhaled glucorticosteroids if significant symptoms and lung function response or if repeated exacerbationsIII: SevereCOPD FEV1/FVC <70 percent FEV1 <30 percent predicted or presence of respiratory or right heart failureRegular treatment with one or more bronchodilators Inhaled glucorticosteroids if significant symptoms and lung function response or if repeated exacerbations Treatment of complications RehabilitationLong-term oxygen therapy if respiratory failureSurgical treatmentsE. Supplemental therapy1. Oxygen. Assessment of arterial blood gases or pulse oximetry is the only reliable method for detecting hypoxemia. Arterial blood gas analysis is also helpful in assessing the presence and severity of hypercapnia.2. Surgery. Selected patients may benefit from lung volume reduction surgery or lung transplantation. Indications for lung transplantationa. FEV1 is <25 percent of predicted, orb. PaCO2 is >55 mmHg, orc. Cor pulmonale is present.d. Candidates must be under 65 years of age, not have dysfunction of major organs other than the lung, and not have active or recent malignancy or infection with HIV, hepatitis B, or hepatitis C viruses.Management of acute exacerbations of chronic obstructive pulmonary diseaseA. An acute exacerbation of chronic obstructive pulmonary disease (COPD) is characterized by an acute worsening of symptoms accompanied by an impairment of lung function.B. Precipitants. Acute exacerbations of COPD are most commonly precipitated by infection (bacterial or viral), air pollution or temperature.C. Other medical conditions can mimic or cause COPD exacerbation include myocardial ischemia, congestive heart failure, pulmonary embolism, or aspirationD. Criteria for hospitalization:1. High risk co-morbidities including pneumonia, cardiac arrhythmia, congestive heart failure, diabetes mellitus, renal failure, or liver failure2. Inadequate response to outpatient management3. Marked increase in dyspnoea4. Inability to eat or sleep due to symptoms5. Worsening hypoxemia6. Worsening hypercapnia7. Changes in mental status8. Inability to care for oneself9. Uncertain diagnosis10. Acute respiratory academiaE. Pharmacologic treatment1. The major components of managing an acute exacerbation of COPD include inhaled beta adrenergic agonists, anticholinergic bronchodilators, corticosteroids, and antibiotics.2. Inhaled beta-2 adrenergic agonists such as albuterol are the mainstay of therapy for an acute exacerbation of COPD. These medications may be administered via a nebulizer or a metered dose inhaler (MDI) with a spacer device. Nebulized therapy is preferred in this clinical setting.a. Albuterol (Ventolin) dosages are 180 mcg (two puffs) by metered dose inhaler, or 2.5 mg (diluted to a total of 3 mL) by nebulizer, given every one to two hours.b. Subcutaneous injection of beta adrenergic agonists is reserved for situations in which inhaled administration is not possible. Parenteral use may cause arrhythmias or myocardial ischemia.3. Anticholinergic bronchodilators, such as ipratropium bromide and glycopyrrolate, may be used in combination with beta adrenergic agonists to produce greater bronchodilation. a. Ipratropium (Atrovent) may be administered during acuteExacerbations either by nebulizer (500 mcg every two toFour hours) or via MDI (two puffs [36 mcg] every two to four hours with a spacer).4. Corticosteroids. Methylprednisolone (60 to 125 mg intravenously, two to four times daily) is given to inpatients. Prednisone (40 to 60 mg orally, once daily) is given to outpatients.5. Antibiotics are recommended for acute exacerbations of COPD with increased secretions. Outpatients should be prescribed a ten day course of amoxicillin, doxycycline, or trimethoprim-sulfamethoxazole. Beta-lactam antibiotics with a beta-lactamase inhibitor should be administered to hospitalized patients. Hospitalized patients at risk for infection with pseudomonas aeruginosa should receive a fluoroquinolone.Choice of empirical antibiotic therapy for COPD exacerbationFirst-line treatmentDosage*Amoxicillin (Amoxil, Trimox, Wymox)500 mg tidTrimethoprim-sulfamethoxazole(Bactrim, Cotrim, Septra)1 tablet (80/400 mg) bidDoxycycline100 mg bidErythromycin250-500 mg qidSecond-line treatment**Amoxicillin-clavulanate(Augmentin)500-875 mg bidSecond- or third-generation cephalosporin (eg, cefuroxime [Ceftin])250-500 mg bidMacrolidesClarithromycin (Biaxin)250-500 mg bidAzithromycin (Zithromax)500 mg on day 1, then 250 mg qdX 4 daysQuinolonesCiprofloxacin (Cipro)500-750 mg bidLevofloxacin (Levaquin)***500 mg qd*May need adjustment in patients with renal or hepatic insufficiency.**For patients in whom first-line therapy has failed and those with moderate to severe disease or resistant or gram-negative pathogens.***Although the newer quinolones have better activity against Streptococcus pneumoniae, ciprofloxacin may be preferable in patients with gram-negative organisms.6. Methylxanthines. Aminophylline and theophylline are not recommended for the management of acute exacerbations of COPD. Randomized controlled trials of intravenous aminophylline in this setting have failed to show efficacy.F. Oxygen therapy1. Acute hypoxemia during an acute exacerbation of COPD may cause tissue hypoxia. Supplemental oxygen should be given to achieve a target PaO2 of 60 to 65 mmHg, with haemoglobin saturation around 90 percent.2. Venturi masks are the preferred means of oxygen delivery because they permit a precise delivered fraction of inspired oxygen (FiO2). Venturi masks can deliver a FiO2 of 24, 28, 31, 35, or 40 percent.3. During oral feedings, nasal cannulae are also more comfort- able and convenient for the patient. They can provide flow rates up to 6 L/min with FiO2 of approximately 44 percent.4. When higher inspired concentrations of oxygen are needed, simple facemasks can provide an FiO2 up to 55 percent using flow rates of 6 to 10 L/min. Non-rebreather masks with a reservoir, one-way valves, and a tight face seal can deliver an inspired oxygen concentration up to 90 percent.5. Adequate oxygenation must be assured, even if it results in acute hypercapnia due to altered ventilation-perfusion relationships, the Haldane effect of unloading CO2 from oxyhemoglobin, or decreased ventilatory drive. Hypercapnia is generally well tolerated in patients whose PaCO2 is chronically elevated; however, non-invasive positive pressure ventilation or intubation may be required when hypercapnia is associated with depressed mental status, profound acidemia, or cardiac dysrhythmias.G. Non-invasive positive pressure ventilation (NIPPV) is effective and less morbid than intubation for selected patients with acute exacerbations of COPD. Early use of NIPPV is recommended when each of the following is present:a. Respiratory distress with moderate-to-severe dyspnoea.B. pH less than 7.35 or PaCO2 above 45 mm Hg.c. Respiratory rate of 25/minute or greater.2. NIPPV is contraindicated in the presence of cardiovascular instability (e.g., hypotension, serious dysrhythmias, and myocardial ischemia), craniofacial trauma or burns, inability to protect the airway, or when indications for emergent intubation are present. Approximately 26 to 31 percent of patients initiallyTreated with NIPPV ultimately require intubation and mechanical ventilation.H. Surgical management1. Lung volume reduction surgery (LVRS) is recommended in patients with upper lobe predominant disease and low exercise capacity.2. Indications for lung transplantationa. FEV1 is <25 percent of predicted, OR b. PaCO2 is >55 mm Hg (7.3 kPa), OR c. Cor pulmonale is present.d. Candidates must be under 65 years of age, not have dysfunction of major organs other than the lung, and not have active or recent malignancy or infection with HIV, hepatitis B, or hepatitis C viruses. ................
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