Journal Logo

Letter to the Editor

Letter to the Editor

Same Sepsis Hill, Different Perspectives

doi: 10.1097/01.EEM.0000651044.66335.ce

    Letters to the Editor

    Emergency Medicine News welcomes letters to the editor about any subject related to emergency medicine. Please limit your letter to 250 words, and include your full name, credentials, and city and state of residence or practice.

    Letters may be edited for content, length, and grammar. Submission of a letter constitutes the author's permission to publish on all media, including print, online, and social media, but does not guarantee publication. Letters express the views of the authors and do not necessarily reflect those of Emergency Medicine News and Wolters Kluwer.

    Letters to the editor may be sent to [email protected].


    The recent commentary “Sepsis Is the Hill to Die on” by Mark Mosley, MD, makes an excellent point. (EMN. 2019;41[11]:3; Sepsis has been frustrating to researchers, hospitals, and government health programs because the pathogenesis is something we have never encountered before, making sepsis impervious to traditional methods of research, treatment, and scientific analysis. Because the exact mechanism of sepsis is unknown, we must be open to the possibility that we may not recognize the cause when it appears or even dismiss it as inconsequential when we see it.

    I proposed a novel evidence-based theory of sepsis in 2014, that a generalized hypermetabolic response leads to the production of excess cellular hydrogen peroxide (H2O2) that accumulates to toxic levels in the blood. This causes multiple organ failure, microangiopathic dysfunction, hypotension, shock, and a host of metabolic and physiologic abnormalities such as lactic acidosis, immunosuppression, and disseminated intravascular coagulation, all of which occur in sepsis. (World J Crit Care Med. 2014;3[2]:45;

    Other studies have also shown that blood H2O2 is significantly elevated in sepsis, up to 558 uM, which is more than 100 times the normal upper limit of 5 uM and more than 10 times the 50 uM upper limit, at which H2O2 becomes cytotoxic. (Crit Care Med. 1995;23[1]:A169;; Arch Biochem Biophys. 2016;603:48.) The ability of H2O2 toxicity to mirror the clinical and laboratory findings in sepsis signifies that the elevated levels of blood H2O2 reported in sepsis patients might have a causal role in the pathogenesis of this condition. This is consistent with the multiple organ failure and fatal sepsis reported in a previously healthy young man after he received intravenous hydrogen peroxide. (Arch Dermatol. 2006;142[12]:1658;

    Our current understanding of sepsis is at a standstill, and it's time to consider a novel perspective. We are trying to understand the unknown, so the best we can do is follow the evidence until we can formulate a falsifiable hypothesis. A causal role for H2O2 in the pathogenesis of sepsis is supported by evidence, and can be easily tested by measuring blood H2O2 in sepsis patients. This is a simple procedure that might answer the difficult questions about the origin and etiology of sepsis and go on to save millions of people worldwide who succumb to sepsis every year.

    Jay Pravda, MD, MPH

    Palm Beach Gardens, FL

    Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.