Furthermore, the elephant in everyone’s room is the troubling prevalence of false-positive imaging for PE, particularly when the pretest likelihood is low.⁴ In this cohort, 24 of 72 patients undergoing CTPA had found PE in segmental or subsegmental locations. Between one-quarter and one-half of PEs in these distal branches were found to be false-positives on subsequent subspecialty radiologist review.⁵ Another 24 patients received diagnosis of PE based on ventilation-perfusion scanning, and half of those found perfusion defects in between 1 and 25 percent of the area of both lungs. Again, as the size of the defect decreases, the likelihood of false-positives increases.

Lastly, we enter into the complicated question of whether these PEs are acutely related to the syncopal episode or whether they represent chronic or incidental findings. In the syncope patient without any clinical symptoms relating to PE, it is reasonable to hypothesize some of these radiographic findings are unrelated and of uncertain clinical significance. Attributing temporary global cerebral hypoperfusion to PE requires a complicated cascade of vascular obstruction, vasoconstriction, and right ventricular afterload. In the instance that these are incidental or represent overdiagnosis, it is reasonable to be concerned about the bleeding risks of long-term anticoagulation in this mostly elderly cohort. PE is not a zero-miss diagnosis for this precise reasoning. The risks of treatment outweigh the benefits for some patients diagnosed with PE.

At the end of the day, the important takeaway is this: These data don’t generalize to our typical emergency department, which pursues a reasonable explanation for vital sign abnormalities and clinical signs suspicious for DVT. It is important to consider the diagnosis of PE in patients with syncope, but most of the patients with clinically important or true-positive PE will have obvious signs pointing to a need for objective testing. There is no indication this study reflects an otherwise unexpected population of PE in syncope following admission to the hospital. I fear this study will lead to an increase in harmful low-value overtesting.

References

1. Prandoni P, Lensing AW, Prins MH, et al. Prevalence of pulmonary embolism among patients hospitalized for syncope. N Engl J Med. 2016;375:1524-1531.
2. Cook OG, Mukarram MA, Rahman OM, et al. Reasons for hospitalization among emergency department patients with syncope. Acad Emerg Med. July 18, 2016; [ePub ahead of print]
3. Blanc JJ, L‘her C, Touiza A, et al. Prospective evaluation and outcome of patients admitted for syncope over a 1 year period. Eur Heart J. 2002;23(10):815-820.
4. Stein PD, Fowler SE, Goodman LR, et al. Multidetector computed tomography for acute pulmonary embolism. N Engl J Med. 2006;354(22):2317-2327.
5. Hutchinson BD, Navin P, Marom EM, et al. Overdiagnosis of pulmonary embolism by pulmonary CT angiography. AJR Am J Roentgenol. 2015;205:271-277.