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Steven Q. Simpson, MD, FCCP
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FINANCIAL/NONFINANCIAL DISCLOSURES: See earlier cited article for author conflicts of interest.

Division of Pulmonary and Critical Care Medicine, University of Kansas, Kansas City, KS

CORRESPONDENCE TO: Steven Q. Simpson, MD, FCCP, Division of Pulmonary and Critical Care Medicine, University of Kansas, 3901 Rainbow Blvd, Mailstop #3007, Kansas City, KS 66160


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2017;151(2):519-520. doi:10.1016/j.chest.2016.11.050
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Bermejo-Martin and colleagues make a point about my recent editorial in CHEST with which I wholeheartedly agree: that we must ultimately move from diagnosing sepsis by using syndrome to diagnosing sepsis by using pathophysiology. Much as acute coronary syndrome is confirmed to be acute myocardial infarction by an increased level of circulating troponin I or by localized ST-segment elevation, we need confirmatory studies that are indicative of infection-induced organ dysfunction or severe sepsis. The authors propose several candidate immunologic studies that could ultimately be used to define sepsis. I agree with them that large-scale prospective testing and defining are necessary before any of these candidates can be accepted individually or collectively as the diagnostic features of severe sepsis.

Even when we do determine the laboratory test(s) that correctly and definitively diagnosis sepsis, physicians will need to recognize which patients warrant testing by recognizing some combination of history and physical findings (eg, a syndrome). There will come a day when the electronic medical record is intelligent enough to correctly point us to at-risk patients, but for now, sepsis recognition remains a strictly human enterprise in which our interaction with a patient is the key diagnostic tool. Patients will always need us to identify them via the syndrome with the most sensitivity. Both prudent patient care and economics dictate that we identify sepsis early and intervene while effective treatment comprises the relatively simple antibiotics and fluid boluses.

If, as Bermejo-Martin and colleagues note, most physicians use “sepsis,” rather than “severe sepsis,” to describe infection that requires ICU care, it results from an abject failure of those of us who deal daily with severe sepsis to teach them the meaning of the definitions from the first and second international consensus conferences. The definitions convey that infection does not leap in a single bound from being a simple infection to being life-threatening but evolves through phases with increasing risk of death. Patients progress from having an infection that is at first undetectable, to infection causing signs of physiological distress, to infection causing organ dysfunction, and finally to infection causing shock and death. Without timely intervention, only good fortune prevents a patient from steady downward progression.

I emphasize what I stated in the original editorial: our history of steady advances in severe sepsis diagnosis and associated reduction in mortality rate demands that any diagnostic change (whether guided by biomarkers, immune studies, or a re-defined syndrome) must be preceded by prospective evaluations that show even more substantial mortality reduction.

References

Simpson S.Q. . New sepsis criteria: a change we should not make. Chest. 2016;149:1117-1118 [PubMed]journal. [CrossRef] [PubMed]
 

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References

Simpson S.Q. . New sepsis criteria: a change we should not make. Chest. 2016;149:1117-1118 [PubMed]journal. [CrossRef] [PubMed]
 
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