COPD Mimics: What are we missing?

Authors: Tobin Dennis, MD (EM Resident Physician, Virginia Tech Carilion) and Tim Fortuna, MD (EM Attending Physician, Virginia Tech Carilion) // Edited by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)


A 49-year-old male with a history of COPD presents to the ED with “my usual COPD exacerbation”. He has a heart rate of 122, BP of 165/92, RR of 31, and pulse ox of 86% on 2L NC. He has decreased air movement and wheezing bilaterally on exam. He is given nebulized albuterol/ipratropium, IV steroids, and started on NIPPV. He continues to be dyspneic on NIPPV with nebulizers.  


Chronic lower respiratory disease was the third leading cause of death in the United States in 2014.1 Over 15 million people have been diagnosed with COPD, and a large portion of people likely have COPD without a dianosis.1 COPD is a chronic, usually progressive disease most often caused by respiratory irritants such as chronic tobacco use. It should be considered in patients with chronic dyspnea, emphysematous changes, and/or chronic bronchitis and is definitively diagnosed by spirometry. Emergency physicians frequently evaluate and manage patients with COPD exacerbations.

A COPD exacerbation is defined as worsening dyspnea, new cough, or increased sputum production. Exacerbations are usually caused by a trigger, the most common being an upper respiratory infection.2 Patients often present to the ED with wheezing, difficulty speaking, change in sputum, and tachycardia/tachypnea. Since exacerbations are often preceded by a URI, patients may also complain of constitutional symptoms.

Patients who present with dyspnea, wheezing, and a history of COPD are often presumed to have a COPD exacerbation. Given the lack of a specific test for a COPD exacerbation, emergency physicians should keep their differential diagnoses broad when presented with a COPD patient.


Asthma: Asthma and COPD share many clinical features. They both involve dyspnea and wheezing and are chronic reactive airway diseases. They share similar treatment paths including beta agonists, anticholinergics, and steroids. Asthma is often thought of as a disease developing in childhood; however, there is also adult onset asthma. Distinction between the two is difficult in an acute exacerbation due to the similarity of symptoms, patient presentation, and risk factors.3

Congestive Heart Failure: CHF can present with symptoms of dyspnea and wheezing from increased fluid in the lungs. Differentiation between COPD and CHF involves physical exam, imaging, and laboratory testing. Patients with CHF show signs of volume overload and vascular congestion manifesting with PE findings of elevated JVD, S3 heart sound, and peripheral edema. Chest X-rays often show cardiomegaly, pleural effusions, and vascular congestion.4 The use of BNP can be helpful in ruling out congestive heart failure. Levels <100 ng/dL have a high negative predictive value.4 Another form of imaging which can useful in differentiating COPD from COPD and CHF is US.  Several US findings can increase or decrease the likelihood of CHF.5

US has been used to predict the likelihood of a patient having a CHF exacerbation. One method is to break the chest into 8 zones and assess each zone.6 Each view will have findings of either A-lines or B-lines. A-lines are hyper echoic horizontal lines. B-lines long vertical line between rib spaces and are artifact that show interstitial edema. For a zone to be positive it must have 3 or more B-lines. Having 2 positive zones was considered positive making CHF exacerbation likely. More recently a 2-zone approach has shown to perform similarly to the 8-zone approach.5


Pneumonia: Pneumonia is an infection of the lung tissue. It is most commonly caused by the bacteria Streptococcus pneumoniae, Haemophilus influenzae, and Klebsiella pneumoniae. Patients may complain of cough, sputum production, fever, altered mental status, and dyspnea. Patients may present from all ages, and diagnosis requires a combination of history, PE, laboratory evidence, and chest ray. Physical exam findings may include rales, rhonchi, dullness to percussion, tactile fremitus or egophony.7 X-ray is the initial imaging of choice to look for evidence that infiltrates or lobar consolidations.7 Treatment includes antibiotics tailored to illness severity and whether pneumonia is hospital vs community acquired.8 Disposition for patient is determined by clinical judgement combined with the scores such as the CURB-65 score.8

Pulmonary Embolism: The most common complaint for patients with a PE is dyspnea followed by chest pain, cough, and finally evidence of DVT.9 These patients can be difficult to pick out from the myriad of other conditions causing dyspnea. Diagnosis is usually done with the assistance of clinical scoring rules in properly selected patients. Patient can undergo risk stratification with clinical scores (Wells criteria) and PERC. Definitive diagnosis requires advanced imaging including CTA or V/Q Scan.9 PE can mimic COPD exacerbations or can cause COPD exacerbations. A recent meta-analysis looking at 7 studies on PE in COPD which included 880 patients looking specifically at COPD exacerbation showed “that PE is common in unexplained acute exacerbation-COPD, with an estimated prevalence of 16%. Moreover, two-thirds of these emboli are located in the main pulmonary arteries, lobar arteries, or interlobar arteries, suggesting that the majority of these embolisms have important clinical consequences”.10 Patients in the study were more likely to have PE if they experienced pleuritic chest pain with the exacerbation and had no URI-like symptoms preceding the exacerbation.10 It is therefore important to consider PE in COPD patients as both a mimic and cause for a COPD exacerbation.

Pneumothorax: Pneumothorax is the presence of air in the pleural space. Presenting symptoms include dyspnea and chest pain. Diagnosis is usually made with physical exam and imaging. Chest X-ray is the primary imaging for diagnosis, but CT can be used for difficulty to interpret CXR.11 An important imaging study in the ED for pneumothorax can also be ultrasound, which may demonstrate higher sensitivity.12 Pneumothorax can be defined as primary (no precipitating event or lung disease), or secondary (underlying lung disease).  Pneumothorax should always be considered in patients with shortness of breath and a history of COPD since COPD is the most common risk factor for pneumothorax.12

Identifying pneumothorax with ultrasound: Ultrasound has been found to be more sensitive and about as specific as chest X-ray in multiple studies. Using ultrasound can be helpful as a quick imaging modality readily available in most EDs. When using an ultrasound to assess for pneumothorax, physicians need to look for both lung sliding and a comet tail sign. Lung sliding is shown as movement at the pleura line while comet tails show artifact coming down from the pleura line. A good instructional video on looking at pneumothorax can be found at and Ultrasound is best used as a rule out test. When a patient exhibits both lung sliding and comet tailing, pneumothorax can be ruled out. Patient’s with COPD are at high risk for false positives given their chances of having anatomic features like blebs, and so a positive US for pneumothorax should be followed with more advanced imaging.13

Vocal Cord Dysfunction (VCD): VCD is a paradoxical motion of the vocal cords in which they adduct during inhalation, resulting in stridor. It is often confused for asthma but may also mimic COPD exacerbation given the similarity of the two diseases including symptoms of respiratory distress, anxiety, and dyspnea.14 Patients can present in what appears to be significant respiratory distress with stridor. Given the appearance of respiratory distress, patients with VCD may be intubated or undergo cricothyrotomy. Information that will help to differentiate VCD and other pathology include a history of similar symptoms, lack of efficacy of asthma and COPD medications and symptoms localizing to the throat. Definitive diagnosis is made by laryngoscopy. Treatment includes breathing exercises, NIPPV, and a multidisciplinary approach to limit recurrence.

Central Airway Obstruction (CAO): CAO can be caused by many sources including malignancy, post-intubation strictures, or tracheobronchomalacia. The condition is defined as occlusion of > 50% of the large airways from the trachea to the lobar bronchus.15 Patients will often present with prolonged, slowly worsening dyspnea. History may also include symptoms of weight loss or prior intubation. Diagnosis includes imaging and will often require fiberoptic scoping for definitive diagnosis.

Foreign Body Aspiration: Aspiration of a foreign body can mimic COPD with respiratory distress and wheezing. Patients at risk for COPD are usually able to give you the diagnosis with history; however, at-risk populations including those with severe dementia may not be able to provide this information. Different materials can cause varying symptoms, and organic material often causes the worst symptoms due to the inflammatory response.16 Patients may require basic life support and bronchoscopy depending on what is aspirated and symptoms.


Patients who present with severe dyspnea require emergent resuscitation and therapy. For patients with concern for COPD exacerbation, management includes NIPPV, nebulized beta agonist/ipratropium, and glucocorticoids. Severe exacerbation warrants antibiotics.

Multiple studies demonstrate the utility of NIPPV. NIPPV has been shown to work 80-85% of the time and to decrease mortality, rates of intubation, and hospital length of stay with the use of NIPPV for COPD exacerbations.2,17 However, patients may require intubation. The decision to intubate is often based on patients who fail other treatments (including NIPPV) or those not appropriate for NIPPV.

The decision to use antibiotics is controversial, though antibiotics are warranted in severe exacerbations. According to the 2017 GOLD Executive survey, “antibiotics should be given to patients with acute exacerbations who have three cardinal symptoms: increase in dyspnea, sputum volume, and sputum purulence; have two of the cardinal symptoms, if increased purulence of sputum is one of the two symptoms; or require mechanical ventilation”.2 A patient with acute, severe exacerbation should be given antibiotics, while considering mimics. Empiric antibiotics for a COPD exacerbation include a 5-7 day course of a macrolide (azithromycin), fluoroquinolone (levofloxacin), tetracycline (doxycycline), or amoxicillin with clavulanic acid.2

After emergent stabilization, a more thorough history and physical exam should be performed. Providers need to keep a broad differential and concern for mimics when dealing with acute dyspnea in a COPD patient. This is especially true when symptoms are not responding as expected to normal COPD management. A broad differential including the mimics discussed is essential, as well as consideration for risk factors for the mimics of COPD.

Patients with COPD exacerbations may require admission to the hospital. Indications for admission include therapeutic failure, relapse after treatment, multiple comorbidities, arrhythmias, altered mental status, worsening hypoxia, or poor social support/inability to follow-up.18

Case Resolution:

The patient was discovered to have unilateral leg swelling, and CTA showed a lobar PE. He is started on heparin drip and admitted to the hospital for a pulmonary embolism.


Key Points:

– Patients with COPD often have multiple comorbidities and are at risk for multiple disease processes.

NIPPV improves rates of intubation, hospital admissions, and length of stay in COPD exacerbations.

– Use the GOLD criteria for antibiotic use in COPD exacerbations.

– Keep a wide differential in patients with COPD and suspected exacerbations.

– Pulmonary Embolism can both mimic and cause a COPD exacerbation

– Mimics include pulmonary embolism, CHF, pneumonia, asthma, and foreign body aspiration


Referenced/Further Reading:

  1. Chronic Obstructive Pulmonary Disease (COPD). (2016, September 16). Retrieved July 31, 2017, from
  2. Vogelmeier, C. F., Criner, G. J., Martinez, F. J., Anzueto, A., Barnes, P. J., Bourbeau, J., . . . Agustí, A. (2017). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease 2017 Report. GOLD Executive Summary. American Journal of Respiratory and Critical Care Medicine, 195(5), 557-582. doi:10.1164/rccm.201701-0218pp
  3. Abramson MJ, Perret JL, Dharmage SC, McDonald VM, McDonald CF. Distinguishing adult-onset asthma from COPD: a review and a new approach. International Journal of Chronic Obstructive Pulmonary Disease. 2014;9:945-962. doi:10.2147/COPD.S46761.
  4. Hedayati T, Afifi N. Congestive Heart Failure. In: Sherman SC, Weber JM, Schindlbeck MA, Rahul G. P. eds. Clinical Emergency Medicine, 1e New York, NY: McGraw-Hill; 2014. Accessed August 01, 2017.
  5. Liteplo, A. S., Marill, K. A., Villen, T., Miller, R. M., Murray, A. F., Croft, P. E., Capp, R. and Noble, V. E. (2009), Emergency Thoracic Ultrasound in the Differentiation of the Etiology of Shortness of Breath (ETUDES): Sonographic B-lines and N-terminal Pro-brain-type Natriuretic Peptide in Diagnosing Congestive Heart Failure. Academic Emergency Medicine, 16: 201–210. doi:10.1111/j.1553-2712.2008.00347.x
  6. Volpicelli G, Mussa A, Garofalo G, et al. Bedside lung ultrasound in the assessment of alveolar-interstitial syndrome. Am J Emerg Med. 2006; 24:689–96
  7. Tudor BC. Pneumonia. In: Sherman SC, Weber JM, Schindlbeck MA, Rahul G. P. eds. Clinical Emergency Medicine, 1e New York, NY: McGraw-Hill; 2014. Accessed August 01, 2017.
  8. NICE. National Institute for Health and Care Excellence. Pneumonia (including community acquired pneumonia). 2014.
  9. Taylor Thompson, MD, Christopher Kabrhel, MD, MPH. Overview of acute pulmonary embolism in adults. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on August 2nd, 2017.)
  10. Floor E. Aleva, Lucas W.L.M. Voets, Sami O. Simons, Quirijn de Mast, André J.A.M. van der en, Yvonne F. Heijdra, Prevalence and Localization of Pulmonary Embolism in Unexplained Acute Exacerbations of COPD, Chest, Volume 151, Issue 3, 2017, Pages 544-554, ISSN 0012-3692,
  11. Pneumothorax. In DynaMed Plus[database online]. EBSCO Information Services. Updated May 02, 2017. Accessed October 9, 2017.
  12. GUO, Y., XIE, C., RODRIGUEZ, R. M. and LIGHT, R. W. (2005), Factors related to recurrence of spontaneous pneumothorax. Respirology, 10: 378–384. doi: 10.1111/j.1440-1843.2005.00715.x
  13. Ding, Wu et al. Diagnosis of Pneumothorax by Radiography and Ultrasonography. CHEST, Volume 140, Issue 4, 859-866.
  14. Dunn NM, Katial RK, Hoyte FCL. Vocal cord dysfunction: a review. Asthma research and practice. 2015;1:9. doi:10.1186/s40733-015-0009-z.
  15. Murgu, S. D., MD FAACP, & Egressy, K., MD, … Hogarth, K., MD FAACP, Central Airway Obstruction: Benign Strictures, Tracheobronchomalacia, and Malignancy-related Obstruction. Retrieved August 07, 2017, from
  16. Cavagnaro CS. Upper Respiratory Emergencies—Stridor and Drooling. In: Cydulka RK, Fitch MT, Joing SA, Wang VJ, Cline DM, Ma O. eds. Tintinalli’s Emergency Medicine Manual, 8e New York, NY: McGraw-Hill;. Accessed August 07, 2017.
  17. McCurdy B. Noninvasive Positive Pressure Ventilation for Acute Respiratory Failure Patients With Chronic Obstructive Pulmonary Disease (COPD): An Evidence-Based Analysis. Ontario Health Technology Assessment Series. 2012;12(8):1-102.
  18. Poznanski SL. Asthma and Chronic Obstructive Pulmonary Disease. In: Cydulka RK, Fitch MT, Joing SA, Wang VJ, Cline DM, Ma O. eds. Tintinalli’s Emergency Medicine Manual, 8e New York, NY: McGraw-Hill; . Accessed August 07, 2017.

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