Edited By: Scott Sherman
John H. Stroger Hospital, Chicago, Illinois
- Discuss the significance of chronic obstructive pulmonary disease (COPD) in the Emergency Department (ED)
- Describe the typical patient presentation of a COPD exacerbation
- Understand the routine treatment of a patient with a COPD exacerbation
- Discuss adjunct therapy for a COPD exacerbation, including non-invasive positive pressure ventilation
- Review the indications for intubation of a COPD patient and basic ventilator therapy
Chronic obstructive pulmonary disease (COPD) is a common disease that affects up to 15% of adults. On average, exacerbations of COPD result in 600,000 ED visits per year. It is the fourth leading cause of death in adults. There is a broad spectrum of disease from patients with mild symptoms and occasional flares to the patient who is oxygen dependent and frequently hospitalized. Worldwide, important secondary causes of COPD include air pollution, use of indoor cooking fires, and alpha-1 antitrypsin deficiency. However, far and away, smoking tobacco is the leading cause of COPD.
The classic presentation of a patient with a COPD exacerbation includes wheezing, productive cough, dyspnea on exertion, hypoxia, and tachycardia. The patient may relate increased use of inhalers, sputum change, or a new requirement of an upright sleeping position (eg, chair). However, these symptoms have a significant overlap with other causes of dyspnea and a wide differential diagnosis should be entertained initially.Typical Symptoms of COPD
- Chest congestion
- Sputum change in color or quantity
The spectrum of symptoms can range from mild to severe. The mildly affected patient may note mild dyspnea on exertion. More symptomatic patients may complain of mild to severe dyspnea at rest. Some may only be able to speak one sentence due to breathlessness: "I can't breathe." The most severely affected will not be able to speak at all.
Astute ED clinicians will also ask their patient and themselves: Why today? COPD is a chronic illness with ups and downs. However, asking the patient a few focused questions will help confirm the correct diagnosis as well as the areas to focus your treatment efforts. "Are you currently smoking?" "Are you taking your medications as prescribed?" "Are you able to afford your medications?" "What has caused you to come to the ED in the past with your COPD?" Frequently, the answers will help you with the next steps in your diagnostic reasoning and treatment.Causes of an Acute Decompensation of a COPD Patient
- Superimposed infection
- Continued smoking
- Lack of usual medications or oxygen therapy
- Spontaneous pneumothorax
The physical examination should initially focus on the patient's overall work of breathing. Look for use of accessory muscles. Look for retractions and respiratory rate. Look for pursed lip breathing and cyanosis. Severely affected patients may have finger clubbing. The lung exam may reveal wheezing, rhonchi, or even rales. The lung sounds may be diminished throughout or even seem absent bilaterally in those with severe bronchospasm. Patients may appear confused with delirium or have a depressed Glasgow Coma Scale due to hypoxia or elevated carbon dioxide. In addition to typical findings, those patients affected with cor pulmonale (ie, pulmonary hypertension) will present with symptoms one may associate as only being present in congestive heart failure: jugular venous distention, leg edema, and hepatomegaly.Typical Signs of a Patient with a COPD Exacerbation
- Pursed lip breathing
- Use of accessory muscles
- Intercostal retractions
- Barrel chest
- Hyper-resonant chest
- Prolonged expiratory phase
Initial Action and Primary Survey
Begin by assessing airway, breathing, and circulation.
Obtain vital signs including the pulse oximetry reading.
Oxygen. Apply controlled oxygen to all hypoxic patients who present with suspected COPD. In general, use a delivery system such as a Venturi mask or nasal cannula. Avoid routine use of a non-rebreather mask with 15 L/min of oxygen, unless the patient is not responding to lower flow rates. In some patients with chronic carbon dioxide retention, high flow oxygen may cause respiratory depression with the rapid rise in oxygen depressing the central ventilatory drive.
Place the ill patient on the monitor, attach continuous pulse oximetry, and insert an intravenous line. Observe the patient?s work of breathing and mental status, looking for signs of respiratory distress and fatigue. COPD patients may require immediate intubation or non-invasive ventilatory support.
Quick and decisive therapy based on the initial clinical assessment will yield the best outcome for these very ill patients. Diagnosis should focus on a consistent clinical history with typical signs and symptoms supplemented with focused supportive and exclusionary testing. Classic confirmatory testing is done by spirometry (ie, pulmonary function testing) showing decreased FEV-1 and reduced vital capacity, but this is not possible in the ED setting.
Since COPD patients are typically older with a history of smoking and multiple co-morbidities they require a broad differential diagnosis highlighting some of emergency medicine?s most common serious diseases. Avoiding anchoring bias will help capture the chronic COPD patient who presents with breathlessness from another etiology. Entities such as CHF, acute coronary syndrome, pulmonary embolus, pneumothorax, pericardial effusion, and pneumonia can all masquerade as an acute COPD exacerbation. In the ED, obtaining a chest x-ray, electrocardiogram, BNP (brain naturetic peptide), ABG (arterial blood gas), and cardiac markers may be necessary.
So how do I make the diagnosis?
Like a migraine headache patient, a sufferer of COPD may relate to the ED physician the current episode is exactly like a prior episode which improved with standard treatment of oxygen, bronchodilators, steroids, and antibiotics. Little is absolutely pathognomonic about the presentation, except significant clinical improvement with bronchodilator therapy and supplemental oxygen.
A chest radiograph is the most common study necessary in evaluating the COPD patient. Click the pictures to the left to enlarge them.
A typical chest x-ray will show increased AP diameter, flattening of the diaphragm, decreased lung markings and the absence of another acute abnormality, such as pneumothorax, pulmonary edema or infiltrate. Significant abnormalities such as pneumonia, pulmonary edema or pneumothorax will require a change in therapy.
The EKG is rarely specific in COPD, but frequently necessary in the evaluation of elderly patients with multiple co-morbidities to help exclude other disease processes. The EKG may diagnose a significant arrythymia, STEMI, or show acute ischemic changes suggestive of an acute coronary syndrome. A rare, but specific finding in COPD patients is multifocal atrial tachycardia (Figure 2)Common EKG Features of COPD
- Low voltage, right axis deviation and rightward axis deviation
- P pulmonale- peaked P waves in II, III, aVF
- Right atrial hypertrophy
- Multifocal atrial tachycardia (rare, but specific to COPD)
Consider obtaining and assessing an arterial blood gas (ABG) if the patient is critically ill and not responding to standard treatment. Evaluate for degree of hypoxia, acidosis, and CO2 retention. Serial arterial blood gases may be needed to assess trends in the ill patient.
While no laboratory test is diagnostic of COPD, several studies may be indicated to exclude other diagnoses. A d-dimer (with subsequent chest CT angiography if positive) in patients felt to be at risk for PE or in non-responders to standard treatment. Cardiac enzymes may be indicated in patients who you suspect are at risk for an acute coronary syndrome. Obtaining a newly elevated BNP may suggest a component of congestive heart failure since the typical x-ray findings may be delayed in those with acute onset pulmonary edema.
Consider obtaining a bedside ultrasound evaluating for pericardial effusion or evidence for pneumothorax. In pericardial effusion, the parasternal or sub-xiphoid views will demonstrate a hypoechoic collection surrounding the heart. Loss of comet-tail artifact, loss of lung sliding and the bar-code sign in M-mode are all suggestive of pneumothorax.
In general, treatment revolves around use of bronchodilators, corticosteroids, and antibiotics to treat superimposed infection.
After oxygen, the use of bronchodilators to treat acute decompensation is the initial treatment. Inhaled albuterol, the preferred beta-agonist, provides the most rapid response in most patients. Even after multiple doses a clinical response may occur. The only limiting factor to ongoing use is tachycardia and other cardiovascular side effects such as ischemia. There is no role for long acting beta-agonists such as salmeterol in treatment of the acute exacerbation.
Use of anti-cholinergic bronchodilators such as ipatropium bromide, is also first line therapy. Ipatropium is typically given every 4 hours, not in stacked or repeated doses like albuterol. Systematic review has not shown combination therapy with beta-agonists to be superior, but it is frequently used.
Steroids are also helpful in most acute decompensations of COPD. An IV steroid such as methlyprednisolone or prednisone orally should be started in the ED to help treat the inflammatory component. The optimum regimen is not established, but typical regimens are 10-14 days with tapering doses in contrast to the 5 day pulse therapy employed with asthma. Many end stage COPD patients are steroid dependent. Corticosteroids have been shown to reduce treatment failure, hospital stay, and the need for additional medical therapy. Complications of steroid use are worsening hypertension, elevated blood sugars, gastritis, and even steroid psychosis.
Empiric antibiotics are used if signs of infection are present and in patients with moderate to severe exacerbations. Exam and historical features that suggest infection are fever, color change of sputum, and increased volume of sputum. Multiple appropriate antibiotic options are available. Common options include macrolides, fluoroquinolones, tetracyclines and cephalosporins. Complications of antibiotics include: allergic reaction, gastritis, and C dificile colitis.
Adjunctive Therapy for Decompensated Patients
Continuing respiratory decompensation with worsening carbon dioxide retention and hypoxia despite standard treatment are indications for adjuctive therapy with non-invasive positive pressure ventilation (NPPV) or endotracheal intubation.
The decision to initiate one of these adjunctive therapies can be a purely clinical one, based on overall assessment of work of breathing, or via direct measurement of arterial blood gases. There is no absolute guideline for level of carbon dioxide and it is not uncommon for severely affected patients to be awake and relatively stable with a PC02 over 60. However, worsening acidosis and unresponsive hypoxia are good markers for the need for adjunctive therapy.
Non-invasive positive pressure ventilation is a mode of mechanical ventilation given by facemask that aids oxygen delivery and decreases work of breathing). It is the next logical step in therapy for the patient not responding to standard treatment. However, it should be started early before acute neurologic deterioration or respiratory depression occurs. An experienced respiratory therapist is invaluable in managing these patients and will help guide the clinician in determining the optimal oxygen flow and pressure settings.
Rapid sequence intubation (RSI ) may be necessary for airway control, correction of hypoxia, and correction of carbon dioxide retention (Figure 5). After intubation and sedation, the ventilator is set with a tidal volume of 4-5 ml per kg of ideal body weight (best calculated by length measurement of the patient). The initial oxygen flow is typically 50-100% depending on pulse oximetry and blood gas measurement. The initial mode of ventilation is typically assist control with a fixed number of ventilations being delivered even if the patient is paralyzed or taking insufficient breaths per minute
General ventilator guidelines include: correcting acidosis, correcting hypoxia, avoiding high peak and plateau airway pressures by ongoing use of bronchodilators and aggressive suctioning of secretions. In the COPD patient, peak pressures may also become increased due to a stacking phenomenon. The elevated pressure is relieved by disconnecting the endotracheal tube and then starting with a more prolonged expiratory phase or decreasing the minute ventilation.
Ultimate disposition is a clinical decision based on assessment of work of breathing, pulse oximetry, and social supports. One simple test is a structured walk around the ED with continuous pulse oximetry. Patients who de-saturate significantly or become too dyspneic to complete ambulation cannot be discharged home. Those with moderate exacerbations are admitted to the medical wards for oxygen, steroid, and bronchodilator therapy. Those who require non-invasive ventilation or intubation are admitted to the ICU.
Further explanation of how disposition decisions are reached in patients with COPD exacerbations is provided in the clinical vignettes below the outline patients with mild, moderate, and severe disease.
A 45 year old smoker presents to the ED with cough, yellow sputum, and a low grade fever. He had no chest pain. For the past 5 days he used albuterol at home and has now run out. He has never been intubated or admitted. On arrival the room air oxygen saturation is 94% and the respiratory rate is 20/min. There is moderate wheezing on exam. The chest x-ray is negative. In the ED, prednisone, albuterol nebulizer x2 and ipatropium nebulizer are given with good effect. The patient is discharged on a macrolide, prednisone, and albuterol inhaler. Patient is to follow-up with his primary care physician. Smoking cessation counseling discussed.
A 65 year old smoker with a history of hypertension presents to the ED with SOB, cough, yellow sputum and ?chest tightness.? The patient slept only about 6 hours in a chair last night. At home the patient used a nebulizer every 4 hours during the night. In the last 5 years, she has been admitted twice with COPD exacerbations. On arrival, the O2 sat is 91% on room air, the patient is tachypneic to 30/min and there is severe wheezing. A chest x-ray, EKG, CPK, and troponin are obtained with no acute changes. In the ED, albuterol nebs x 4, nebulized ipatropium, prednisone, and azithomycin are given with good effect. After 4 hours in the ED the patient felt much better and tried to ambulate with pulse oximetry monitoring. However, within 1 minute, she desaturated to 86% on room air and became very short of breath. The patient is admitted to the medical floor.
EMS arrives at 4AM to the ED with a 65 year old smoker who was up all night using a nebulizer every 2-3 hrs. The patient is only able to speak in short sentences. On arrival, the oxygen saturation was 84% on room air and the respiratory rate was 35/min. In route, the patient had received albuterol and ipatropium nebulized. In the ED, the patient is using accessory muscles, intercostal retractions, and has pursed lip breathing and cyanotic lips. Additional nebulizer treatments and intravenous steroids are given with minimal improvement. The patient receives broad spectrum antibiotics. Portable chest-ray and EKG show no acute changes. After 30 minutes, NPPV is applied. Initially, the patient improves with a decreased work of breathing. However, after 1 hour the patient becomes more somnolent with a decreased respiratory rate. An ABG is obtained with a pH= 7.25, a pCO2= 60, a PO2 =59, with an oxygen sat of 89%. A decision is made to intubate with RSI and the patient is admitted to the ICU.
Pearls and Pitfalls
- Assess what patient factors may have caused the exacerbation
- Always consider alternate diagnoses such as PE, ACS, pneumonia, and CHF in the COPD patient
- Give oxygen early and give enough
- Use a combination of bronchodilators, steroids, and consider antibiotics in moderate and severe exacerbations
- Start NIPPV early in patients who have persistent increased work of breathing
- AHRQ Evidence Report on Management of Acute Exacerbations of Chronic Obstructive Pulmonary Disease. Summary Evidence Report/Technology Assessment: Number 19 AHRQ publication No. 00-E020, September 2000. Agency for Healthcare and Quality, Rockville, MD.
- American Thoracic Society Guidelines for the management of COPD
- McCrory, Douglas C; Brown, Cynthia D Anticholinergic bronchodilators versus beta2-sympathomimetic agents for acute exacerbations of chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews. 4, 2009.
- Qoun BS, Gan WQ, Sin DD. Contemporary Management of Acute Exacerbations of COPD systematic review and metaanlysis Chest 2008 Mar; 133(3): 756-66. 4, 2009.