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DITOR’S NOTE: This is the first in a two-part series on the enigma of sepsis.

The term “sepsis” was coined by Hippocrates around 400 B.C., derived from the Greek word “sipsi,” which translates as “make rotten,” and it referred to the decomposition of organic matter. In the 19th century, Ignaz Semmelweis deduced that medical personnel were instigating childbed fever (O85, puerperal sepsis) by not washing their hands after pathology lessons and between patients.

Louis Pasteur (1822-1895) discovered the etiologic agent of infection, microbes, and the fact that heating could sterilize a fluid by killing those bacteria. Joseph Lister (1827-1912) connected the dots and originated the practice of antisepsis.

In 1914, Hugo Schottmüller (1867-1936) posited that “sepsis is present if a focus has developed from which pathogenic bacteria … invade the bloodstream in such a way that this causes subjective and objective symptoms,” and he theorized that “a therapy should not be directed against bacteria in the blood but against the released bacterial toxins.”

Fast forward to today, and Merriam-Webster defines sepsis as “a toxic condition resulting from the multiplication of pathogenic bacteria and their products in a region of infection and their absorption into the bloodstream.” In the early 1990s, the American College of Chest Physicians and Society of Critical and Medicine convened a “consensus conference” to get a handle on how to define, recognize, and treat sepsis, which was felt to be a systemic inflammatory response to infection that led to a progressive injurious process with a high mortality rate. The intent was that “early diagnosis and treatment may lead to improved survival in these critically ill patients.” Since then, there have been multiple revisions of the Surviving Sepsis Campaign – which, in 2012, settled on sepsis being “a systemic, deleterious host response to infection, leading to severe sepsis and septic shock.”

Let’s consider the 2012 guidelines. The diagnostic criteria were “infection, documented or suspected, and some of the following,” wherein “the following” was subdivided into general variables (vital sign criteria, altered mental status, edema, hyperglycemia); inflammatory variables (abnormal white blood cell count, plasma CRP, or plasma procalcitonin); hemodynamic variables (blood pressure criteria); organ dysfunction variables (hypoxemia, oliguria, increase in creatinine, coagulopathy, ileus, thrombocytopenia, hyperbilirubinemia); or tissue perfusion variables (elevated lactic acid, abnormal capillary refill). This is important to remember, because many people simplified this down to mandating 2/4 systemic inflammatory response, or SIRS, criteria (hyperthermia/hypothermia, HR > 90 bpm, tachypnea > 20, and leukocytosis/leukopenia/bandemia) to diagnose sepsis, dismissing all of the other variables that could constitute criteria for sepsis. The basic dilemma is that sepsis has no reliable gold-standard diagnostic test.

The incidence of sepsis appears to be increasing. It is postulated that it may be due to an expanding aging population with more comorbidities (true increase), greater recognition (constant prevalence, just better detection), or, possibly, in some countries (i.e., the U.S.), reimbursement-favorable coding (spurious increase). This latter situation gave impetus to looking for a different way to recognize and diagnose truly septic patients in order to find efficacious treatment for sepsis.

My hypothesis is that somewhere along the line, folks forgot that the goal was to identify critically ill patients in order to intervene and prevent death from sepsis/severe sepsis/septic shock. They misapplied SIRS criteria, which are pretty easy to meet (anyone with a significant enough fever could mount an appropriate corresponding tachycardia), and their wide net, even with compliant coding, made MS-DRGs 871/870 skyrocket, causing auditors’ Spidey sense to tingle. If we were to adhere to my personal sepsis criteria, “the patient needs to be SICK (all-caps and bolded), meet some sepsis diagnostic variables, and have a presumed or confirmed infection.”

If we only diagnosed sepsis/severe sepsis/septic shock when truly appropriate, we wouldn’t be in this predicament. 


Erica E. Remer, MD, CCDS

Erica Remer, MD, FACEP, CCDS, has a unique perspective as a practicing emergency physician for 25 years, with extensive coding, CDI, and ICD-10 expertise. As physician advisor for University Hospitals Health System in Cleveland, Ohio for four years, she trained 2,700 providers in ICD-10, closed hundreds of queries, fought numerous DRG clinical determination and medical necessity denials, and educated CDI specialists and healthcare providers with engaging, case-based presentations. She transitioned to independent consulting in July 2016. Dr. Remer is a member of the ICD10monitor editorial board and is the co-host on the popular Talk Ten Tuesdays weekly, live Internet radio broadcasts.

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