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N522: Primary Care III COPD

By

J. Patterson Johnson, Ed.D, FNP Primary Source: Global Initiative for COPD, WWW.GOLDCOPD.COM (2009 expert panels recommendations)

OVERVIEW
COPD (chr. Obstr.pulmonary disease) 4th leading cause of death & morbidity in the U.S. Mortality s with age, men > women Symptoms manifest after significant lung tissue damage

DEFINITION

American Thoracic Society: Air flow obstruction caused by chronic bronchitis or emphysema; the airflow obstruction is generally progressive,may be accompanied by airway hyperactivity,and may be partially reversible

DEFINITIONS [CONT]
Emphysema - Abnormal permanent stretching of the alveoli with destruction of their walls which results in air trapping. Chronic bronchitis - excessive sputum production/recurrent cough on most days for more that 3 mons. /yr.for at least 2 consecutive yrs.

DEFINITION [CONT.]

THE GOLD report defines COPD as A disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases

CAUSES OF AIRFLOW LIMITATION


IRREVERSIBLE CAUSES: fibrosis & narrowing of the airways Loss of elastic recoil due to alveolar destruction Destruction of alveolar support that maintains patency of small airways.

CAUSES OF AIRFLOW LIMITATION [CONT.]


Reversible: Accumulation of inflammatory cells, mucus, and plasma exudate in bronchi Smooth muscle contraction in peripheral and central airways Dynamic hyperinflation during exercise

RISK FACTORS
Cigarette smoking (primary cause) 1 -antitrypsin deficiency -- an inherited disorder Occupational dusts & chemical Infections Socioeconomic status

CLINICAL MANIFESTATIONS
Chronic cough, chronic sputum production, dyspnea, and history of exposure to risk factors. As a rule cough is the earliest symptom of COPD chronic sputum production suggest COPD regardless of the pattern

CLINICAL MANIFESTATION [cont.]


Dyspnea that is persistent, worsens over time, and worsens with resp. infections or exercise is also characteristic of COPD. Even patients without dyspnea, but with a chronic cough, sputum production and risk factors should be screened with pulmonary function tests

PHYSICAL FINDINGS Advanced Disease


Emphysema - thin, muscle wasting, increased use of accessory resp. muscles. Reduced diaphragramatic excursion, barrel chest diminished breath sounds, no clubbing no cyanosis. Chronic bronchitis - overweight, cyanosis, copious sputum, wheezes, crackles at the bases

DIFFERENTIAL DIAGNOSIS

Asthma, TB, congestive heart failure, bronchiectasis, obliterative bronchiolitis


Studies show that COPD is most often misdiagnosed for asthma

DIFFERENTIAL DIAGNOSIS Features


COPD: Onset in mid-life Symptoms slowly progressive Long smoking history Dyspnea during exercise largely irreversible airflow limitation

DIFFERENTIAL DIAGNOSIS Features


ASTHMA: Onset early in life Symptoms vary from day to day Symptoms at night & early morning Allergy, rhinitis, & or eczema also present Family history of asthma largely reversible air flow

DIFFERENTIAL DIAGNOSIS Features


CHF: fine basilar crackles on auscultation CXR shows dilated heart, pulmonary edema PFTs indicate volume restriction not airflow limitation

DIFFERENTIAL DIAGNOSIS Features


BRONCHIECTASIS: Large volumes of purulent sputum commonly associated with bacterial infection Coarse crackles on auscultation CXR/CT shows bronchial wall thickening

DIFFERENTIAL DIAGNOSIS Features


TUBERCULOSIS: Onset all ages CXR shows lung infiltrate or nodular lesions Microbial confirmation High local prevalence of TB

DIFFERENTIAL DIAGNOSIS Features


OBLITERATIVE BRONCHIOLITIS: Onset in younger age, nonsmokers May have history of rheumatoid arthritis or fume exposure CT scan on expiration shows hypodense areas

LABORATORY STUDIES
Pulmonary function tests - spirometry, static lung volumes, and single breath maximal diffusion capacity of carbon monoxide (DlCOSB) Spirometry - FEV1, FVC, FEV1/ FVC Static lung volume - TLC, FRC, RV

LAB. STUDIES [cont.]


DLCOSB -measures the rate at which co is taken up by hemoglobin in the pulmonary capillaries CXR -excludes other diagnoses and helps diagnosis if bullous disease ABGS Alpha-1 antitrypsin deficiency screening

CLASSIFICATION
Post-Bronchodilator

Stage I: Mild -FEV1/FVC < 0.70; FEV1 80% predicted Stage II: Moderate FEV1/FVC <0.70; 50% FEV1 < 80% predicted Stage III: Severe - FEV1/FVC < 0.70; 30% FEV1 <50% predicted Stage IV: Very severe FEV1/FVC < 0.70; FEV1 < 30% predicted or FEV1 <50% predicted, plus chronic resp. failure

DISEASE MANAGEMENT
Treatment modalities - Education, pharmacotherapy, rehabilitation,and oxygen administration. Education - smoking cessation, reduction of risk factors, use of medication, recognition of exacerbation, and reduction of dyspnea

DISEASE MANAGEMENT

Education in the last stage of COPD should include instruction on: disease complication, oxygen therapy, and end of life decisions (advanced directives)

KEY POINTS: STRATEGIES TO HELP PT. QUIT


systematically identify all tobacco users at every visit strongly urge all tobacco users to quit determine willingness to make quit attempt Aid the patient in quitting Schedule follow-up contact

DISEASE MANAGEMENT [cont]


Pharmacotherapy Note: Studies show that none of the existing meds for COPD serve to modify the long term decline in lung function that is the hallmark of the disease. Pharmacotherapy is used to decrease symptoms and or/complications

DISEASE MANAGEMENT [cont.]


Medications - Bronchodilators are central to the symptomatic management of COPD. They are given on an as needed basis or on a regular basis to prevent or reduce symptoms. Principal bronchodilator treatments are beta2 -agonists, anticholinergics, theophylline, and combo of these drugs

DISEASE MANAGEMENT [cont.]


Inhalation is the preferred route of bronchodilators To improve delivery, breath-activated devices or spacers should be used Routine use of nebulizers for medication administration is discouraged because of the added cost.

DISEASE MANAGEMENT [cont.]


The long-acting beta2-agonist salmeterol significantly improves health status and is more convenient than the short-acting eg. Albuterol the anticholinergic ipratropium (atrovent) also improves health status but requires frequent dosing

DISEASE MANAGEMENT [cont.]


Combination therapy using a fixed ratio of short-acting beta2-agonist and ipratropium have been shown to have enhanced effects. Theophylline although effective is no longer considered a first-line drug. This is due the higher rate of adverse reaction and toxicity.

DISEASE MANAGEMENT [cont.]


Steroid use is controversial. Glococorticosteroids may be helpful during exacerbation but less effective for routine management. Glucocorticosteroid Reversibility Testing glucocorticosteroid be added to bronchodilator for a 6-12 week trial

DISEASE MANAGEMENT [cont.]


Determine benefit of steroid by comparing FEV1 at end of trial with baseline. Positive response = FEV1 increase of 200ml and 15% above bronchodilator baseline

DISEASE MANAGEMENT [cont.]


Other Meds - antibiotics (prophylactic antibiotics use is not supported in Lit.), vaccines, alpha1- antitrypsin augmentation. Rehabilitation; recommended for all stages. Components - exercise training, counseling, and education.

DISEASE MANAGEMENT [cont.]


Oxygen therapy has been found to improve survival as well as mental and physical status. Should be reserved for patients with severe COPD. Indication is by waking PaO2 or desaturation during activity.

DISEASE MANAGEMENT [cont.]


Indication for O2 PaO2 < 55 mm Hg or SaO2 < 88% at rest; PaO2 < 55 mm Hg or SaO2 <89% with exercise or during sleep; PaO2 bet.55- 60 mm Hg or SaO2 < 89% with evidence of pulmonary hypertension or cor pulmonale

DISEASE MANAGEMENT [cont.]


Surgical Intervention: Lung volume reduction surgery. A large US trial (the national Emphysema Treatment) started in 1996 and scheduled to end in 2003 is in progress. Lung transplantation may provide opportunity for survival.

DISEASE MANAGEMENT [cont.]


Exacerbation - Common causes include resp. infection and air pollution Signs of exacerbation - accessory muscle use, worsening or new onset of central cyanosis, dev. Of peripheral edama, hemodynamic instability, right heart failure, decreased level of alertness

DISEASE MANAGEMENT [cont.]


Managing Exacerbation Increase bronchodilators, initiate antibiotics if indicated (increased sputum amount and purulence). Pt. Should be assessed hours after initial treatment adaptation. If not adequately improved add oral corticosteroid. If no improvement or worsening, hospitalize

COMPLICATIONS OF COPD
Hypoxemia Hypercapnia Pulmonary hypertension Cor Pulmonale