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  Respiratory infections are responsible for most acute exacerbations of chronic obstructive pulmonary disease (COPD).

  
  
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  Beta-adrenergic agonists and anticholinergic drugs remain the primary bronchodilators and are most effective when used together.

  
  
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  Steroids should be given to nearly all patients presenting to the emergency department (ED) with COPD exacerbations, and ongoing therapy should be prescribed for those patients who are discharged.

  
  
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  Antibiotics are an important adjunct to therapy, although their use should be guided by the patient’s signs and symptoms.

  
  
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  Noninvasive ventilation is a critical component of therapy that is best used early in the ED course to avoid the need for intubation.

Chronic obstructive pulmonary disease (COPD) is defined as an illness characterized by irreversible, progressive airway obstruction that is associated with inflammatory pulmonary changes. It is extraordinarily common, and patients with exacerbations of COPD will continue to inundate emergency departments (EDs) in search of respiratory relief. In the United States, COPD is the fourth most common cause of death.

The use of the term COPD encompasses patients with chronic bronchitis and emphysema, as well as those patients with asthma who have a component of irreversible airflow obstruction. Airflow obstruction is the end result of a process that begins with particulate air pollution exposure (usually from tobacco smoke). Particulate exposure initiates a cascade of events, including airway inflammation and narrowing of the small airways, as well as airway destruction and remodeling in the setting of diminished repair mechanisms and fibrosis, resulting in fixed airflow obstruction and air trapping. Although there are clearly pathophysiologic differences between these groups, their evaluation and treatment is largely the same.

A COPD exacerbation is an event characterized by a worsening of the patient’s respiratory symptoms beyond the normal day-to-day variation. Typically, this involves one or all of the following: worsening dyspnea, increased sputum as well as a change in the character of sputum, and an increase in the frequency and severity of cough.

History

The critical aspects of the history in evaluating patients with dyspnea due to a presumed COPD exacerbation are to establish the patient’s baseline function, assess the severity of the exacerbation, determine a cause, and rule out disorders that may mimic a COPD exacerbation. Most patients experiencing a COPD exacerbation present with complaints of increased dyspnea in the setting of a recent onset respiratory infection (ie, upper respiratory infection). As a result, they may complain of a productive or sometimes a nonproductive cough that differs from their baseline cough, rhinorrhea and nasal congestion, and fevers and chills, as well as the constitutional symptoms that frequently accompany systemic illness. Most such patients are chronically ill and often quite frail, so the key to determining the severity of the exacerbation is establishing their baseline health. To do this, it helps to ascertain their oxygen use, their current treatment regimen, their level of function and ability to perform activities of daily living, the frequency of hospitalizations and the timing of their most recent hospitalization, their history of mechanical ventilation, and any comorbid illnesses (eg, ischemic heart disease and congestive heart failure [CHF]).

Patients who present with symptoms that seem to develop over a long period of time may actually have underlying CHF, whereas patients with abrupt onset symptoms may have a pneumothorax (from a ruptured bleb) or a pulmonary embolus (PE). Although acute coronary syndrome should also be considered among patients presenting with dyspnea, chest tightness is a common complaint among patients with relatively uncomplicated COPD or asthma exacerbations. One helpful historical detail is to discern whether chest tightness is a common feature of past COPD exacerbations.

Physical Examination

Patients with COPD exacerbations frequently present with tachypnea, tachycardia, and hypoxia. Because the majority of patients have an underlying respiratory infection, they may also have a fever. Most of what the clinician needs to make a quick assessment can be gathered from vital signs and a quick glance at the patient on entering the room. Patients with severe exacerbations may be sitting upright or leaning forward in the “tripod” position with both of their hands planted on their knees. Such patients may be confused and diaphoretic, unable to converse comfortably, and use accessory muscles in the neck and chest wall to help them breathe. Cyanosis is an ominous, but uncommon finding. Patients with less severe exacerbations speak in complete sentences, and the chest exam reveals diffusely diminished breath sounds with wheezing or a prolonged expiratory phase. Patients with emphysema pathology are often thin and frail appearing with a barrel chest. Some patients with prolonged COPD will have evidence of right heart failure including jugular venous distension and lower extremity edema. Finally, although bedside spirometry in the form of a peak expiratory flow rate (PEFR) assessment is more useful in asthma, it can be a helpful adjunct to the physical exam of COPD patients because several patients with COPD have a reversible component to their disease. In patients with a known baseline, an easy comparison can be made to determine the severity of airflow obstruction. Most patients do not recall past PEFR values, but a PEFR <200 L/min suggests a significant component of airflow obstruction.