Correspondence  |   August 2016
Fallacy…. Really?
Author Notes
  • University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania (R.G.E.). roderic.eckenhoff@uphs.upenn.edu.
  • (Accepted for publication April 20, 2016.)
    (Accepted for publication April 20, 2016.)×
Article Information
Correspondence
Correspondence   |   August 2016
Fallacy…. Really?
Anesthesiology 8 2016, Vol.125, 426-428. doi:10.1097/ALN.0000000000001180
Anesthesiology 8 2016, Vol.125, 426-428. doi:10.1097/ALN.0000000000001180
The word “fallacy” stands out in the title of the recent editorial by Avidan and Evers.1  It is a word rarely encountered in the biomedical lexicon, because it implies a nontruth, or in this case, that the null hypothesis has been proven. Since the null hypothesis can only be disproven, the choice of the noun, “fallacy,” appears unduly well settled to us, particularly when used to characterize data presented in the authors’ evidentiary pyramid. It is instructive to recall that level I evidence is only achieved from a systematic review of level II evidence (randomized controlled trials [RCTs]). The systematic reviews referred to by Avidan and Evers are of level III and IV evidence. Thus, their “highest quality of evidence” is actually far from level I evidence. Moreover, many of the studies on the “not supporting an effect” edge of the pyramid report, on closer examination, reported clinically significant effect sizes of 20 to 50% in favor of persistent cognitive decline after surgery but were underpowered.2–4  In our view, studies that cannot rule out clinically important effects cannot be used to bolster either side of the argument. Moreover, the positive study by Liu et al.5  was a prospective randomized trial, and Williams-Russo et al.’s6  randomized trial addressed a completely different question (regional vs. general anesthesia). Of note, the investigation being advocated as the nail-in-the-coffin was itself statistically positive, although the effect size was considered by its authors to be negligible.7  Which edge of the pyramid does this go on? Would the effect size have been larger if those lost to follow-up (1.3 times more likely to have had surgery) were included? Within the discordant twin pairs wherein previous surgery was associated with persistent cognitive decline (about half), was there an unrevealed risk factor leading to a larger effect size? Recent work by Sprung et al.8  is similar in that surgery was associated with persistent cognitive decline only when the additional risk factor of age was included. A study just released from Oregon Health and Science University9  went a step further. In a longitudinal prospective cohort, surgery was associated with persistent cognitive decline in the entire group, an effect that became stronger when focusing on subgroups, women, and ApoEε4 carriers. It has been argued that these “vulnerability” factors are simply comorbid surrogates for an accelerated downward cognitive trajectory as compared to others, hence the association with postoperative cognitive decline. However, there is sound clinical evidence for a superimposed inflammatory event accelerating such a trajectory,10  so the possibility cannot be discounted with a one-model-fits-all notion. Subgroup analyses are essential.
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