Chronic Obstructive Pulmonary Disease and Emphysema in Emergency Medicine Follow-up

  • Author: Paul Kleinschmidt, MD; Chief Editor: Barry E Brenner, MD, PhD, FACEP   more...
 
Updated: Jan 4, 2011
 

Further Inpatient Care

  • In patients with chronic obstructive pulmonary disease (COPD) who are in extremis, CPAP or BiPAP may be attempted prior to intubation. This can be started in the ED and continued for several hours in the hospital. Usual recommended settings are an inspiratory positive airway pressure (IPAP) of 10 cm H2 O and an expiratory positive airway pressure (EPAP) of 2 cm H2 O, with further adjustments based on the individual. This is contingent on the patient's ability to withstand the mask. This treatment is not a substitute for intubation; rather, it is a means of trying to avoid intubation.
  • Heliox is an additional strategy that can be attempted prior to intubation. Whether Heliox or CPAP is used will depend on the individual patient and local hospital availability. Again, like several other therapies mentioned in this article, study results both for and against Heliox have been published. The current summation of that literature indicates that Heliox may actually decrease the work of breathing while the patient is breathing the mixture, but its effects are not long lasting once it is removed. The proper mixture of the gases and the ability to deliver enough oxygen to the patient are also issues.
  • Inhaled nitric oxide has been suggested, but at this point does not seem to have a role in acute treatment.
  • Lung volume reduction surgery has also been touted as effective, but most recent studies demonstrate varying levels of success.
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Further Outpatient Care

  • Disposition from the ED depends on the clinical picture for each patient more than any single laboratory value or test. In general, the longer the exacerbation, the more airway edema and debris are present, making resolution in the ED increasingly more difficult. Patients who state that they "feel back to normal" and have no overt reason for admission can reasonably be discharged home with follow-up arrangements. The corollary to this is that patients who state they "do not feel comfortable," regardless of the numbers, are the best predictors of outcome and probably should be admitted. Data on risk factors for relapse and need for admission are limited at present.
  • For patients who are sent home, nearly all should receive a short steroid burst and an increase in the frequency of inhaler therapy. Close follow-up should be arranged with the patient's regular care provider. Other therapies should be considered on a case-by-case basis.
  • Patients with severe or unstable disease should be seen monthly.
  • When their condition is stable, patients may be seen biannually.
  • Check theophylline level with each dose adjustment, then every 6-12 months.
  • For patients on home oxygen, check ABGs yearly or with any change in condition. Monitor oxygen saturation more frequently than ABGs.
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Inpatient & Outpatient Medications

  • Bronchodilators
    • Beta2-adrenoceptor agonists
      • See the Medication. Again, these agents are first-line therapy for COPD, both for acute exacerbations and for acute treatment.[6] Bronchodilators are given on an as-needed basis or on a regular basis to prevent or reduce symptoms. Short-acting agents are usually used for immediate relief of symptoms, whereas long-acting inhaled agents are better for day-to-day mitigation of the disease.
      • Epinephrine or terbutaline can be administered subcutaneously when intravenous access is not possible or the patient is moving so little air that nebulizer therapy is ineffective. Terbutaline is thought to be safer in older patients, and it has shown to be more efficacious than epinephrine.
    • Methylxanthines: Theophylline increases collateral ventilation, respiratory muscle function, mucociliary clearance, and central respiratory drive. Despite this, many questions exist as to its true efficacy. In general, if the patient is already on theophylline and has a subtherapeutic level, a mini-loading dose is appropriate. If the patient is not on theophylline, the delay before benefit of the oral form makes it not worth using. Intravenous aminophylline has a propensity to cause arrhythmias, especially in a population that already has cholinergic excess coupled with coronary disease.
    • Anticholinergics: These are as effective as beta-agonists in acute attacks, and they have synergistic properties with the beta-agonists. They act by antagonizing the vagal innervation of the tracheobronchial tree. Vagal tone can be increased by as much as 50% in patients with COPD.
  • Corticosteroids: These also have bronchodilatory properties, although they primarily act by decreasing inflammation in the tracheobronchial tree. Although 8-12 hours are required for full effect, corticosteroids should be administered in the ED, as some mild improvements may be noted much earlier.
  • Antibiotics
    • Antibiotics effectively reduce treatment failure and mortality rates in patients with severe COPD exacerbations.[2] However, with mild or moderate exacerbations, antibiotics may or may not be indicated.
    • In cases of severe acute exacerbations of chronic bronchitis (AECB), recent guidelines suggest using fluoroquinolone antibiotics as first-line therapy.[11, 12] This suggestion is based on level I evidence from several trials that show clinical and microbial superiority of these agents.
    • Use of fluoroquinolones has also been shown to shorten hospital stay, reduce recurrences, and lower costs.
    • Fortunately, resistance to these agents is still very low, and reserving them for use in populations at risk should preserve their effectiveness for some time.
  • Magnesium
    • Although controversial, administration of magnesium is thought to produce bronchodilation through the counteraction of calcium-mediated smooth muscle constriction.
    • Magnesium depletion is known to occur in periods of adrenergic excess (eg, asthma exacerbations, diuretic use).
  • CPAP and BiPAP
    • These devices help to decrease the work of breathing and maintain positive end-expiratory pressure (PEEP).
    • Patients must be alert with no excess secretions.
  • Heliox
    • Heliox usually is a 60:40 mixture of helium and oxygen.
    • Helium is a smaller particle than oxygen and in small airways promotes laminar flow and facilitates both oxygen transport and carbon dioxide diffusion.
    • Many patients who seem to breathe better on Heliox return to a worsened respiratory state when removed from Heliox.
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Deterrence/Prevention

  • For the vast majority of patients, cessation of smoking is the only true means of prevention.
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Complications

  • Some complications that must be anticipated in COPD treatment include the following:
    • Incidence of pneumothorax due to bleb formation is relatively high; consider pneumothorax in all patients with COPD who have increased shortness of breath.
    • In patients who require long-term steroid use, the possibility of adrenal crisis is very real; at a minimum, patients with steroid-dependent COPD should receive stress dosing in the event of an exacerbation or any other stressor.
    • Infection (common)
    • Cor pulmonale
    • Secondary polycythemia
    • Bullous lung disease
    • Acute or chronic respiratory failure
    • Pulmonary hypertension
    • Malnutrition
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Prognosis

  • Patient's age and postbronchodilator FEV1 are the most important predictors of prognosis. Young age and FEV1 greater than 50% of predicted are associated with a good prognosis. Older patients and those with more severe lung disease do worse.
  • Supplemental oxygen (when indicated) has been shown to increase survival rates.
  • Smoking cessation improves the prognosis.
  • Cor pulmonale, hypercapnia, tachycardia, and malnutrition indicate a poor prognosis.
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Patient Education

  • The best education comes in 2 forms.
    • Educate patients to the dangers of smoking and the improvement in quality of life attainable with smoking cessation.
    • Instruct patients with COPD to present early during an exacerbation and to not wait until they are in distress.
  • This author's observation is that many people with respiratory disease do not know the basic ways to monitor their own disease fluctuations. In addition, they are frequently not taking/using their inhalers as prescribed. Spending the 5 minutes it takes to make sure they have an aero chamber, are using the right dosages, the right medicines, and know when to seek help can go a long way in preventing a respiratory disaster.
  • Printed material is available from the National Jewish Hospital in Denver, Colorado, as well as the American Lung Association.
  • Instruct patients about appropriate pulmonary toilet.
  • For excellent patient education resources, visit eMedicine's Lung and Airway Center. Also, see eMedicine's patient education articles Chronic Obstructive Pulmonary Disease (COPD), Cigarette Smoking, Asthma, and Emphysema.
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Contributor Information and Disclosures
Author

Paul Kleinschmidt, MD  Consulting Staff, Department of Emergency Medicine, Womack Army Medical Center

Paul Kleinschmidt, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: ScrubCast, INC Ownership interest Other

Specialty Editor Board

David FM Brown, MD  Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Paul Blackburn, DO, FACOEP, FACEP  Program Director, Department of Emergency Medicine, Maricopa Medical Center; Assistant Professor, Department of Surgery, University of Arizona

Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical Association, and Arizona Medical Association

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP  Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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Chronic obstructive pulmonary disease (COPD). Histopathology of chronic bronchitis showing hyperplasia of mucous glands and infiltration of the airway wall with inflammatory cells.
Chronic obstructive pulmonary disease (COPD). Histopathology of chronic bronchitis showing hyperplasia of mucous glands and infiltration of the airway wall with inflammatory cells (high-powered view).
Posteroanterior (PA) and lateral chest radiograph in a patient with severe chronic obstructive pulmonary disease (COPD). Hyperinflation, depressed diaphragms, increased retrosternal space, and hypovascularity of lung parenchyma is demonstrated.
Chronic obstructive pulmonary disease (COPD). A lung with emphysema shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on lateral chest radiograph.
Chronic obstructive pulmonary disease (COPD). A lung with emphysema shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on posteroanterior chest radiograph.
Subcutaneous emphysema and pneumothorax.
 
 
 
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