EDITOR’S NOTE: The late Robert S. Gold, MD tackled the issue of sepsis even before the advent of the 1992 SIRS criteria. He made certain that healthcare professionals should be aware that capturing the true clinical picture should be first and foremost on the agenda. This is the second in a series of articles on the subject of sepsis. Dedicated to Dr. Gold’s memory, this series has been written by Cesar M. Limjoco, MD, vice president of clinical services for DCBA, Inc., a consulting firm co-founded by Dr. Gold.                                                       

It may seem that rules come and go, changing with the prevalent estimation of the current thinking. But are we really slaves to the winds of interpretation? For example, consider the first, second, and third definitions of sepsis – did they really change what it truly means? 

“Sepsis should be defined as life-threatening organ dysfunction caused by a dysregulated host response to infection.” This current definition reiterates that sepsis is an abnormal (or toxic) response to infection. Well, what about the four systemic inflammatory response syndrome (SIRS) criteria – are they, by themselves, signs of a toxic response to infection? Folks need to understand the origin of these criteria. They stemmed from clinical studies on patients in the critical care environment. These four criteria are commonalities in the ICU setting and are great screening tools for us to use in order to make an impact on sepsis mortality.

But, taken as is, fever is part and parcel of the regular reaction to infection. So is leukocytosis. Tachypnea and tachycardia can be normal reactions to volume issues. But in the appropriate context, these four horsemen of the apocalypse can portend an ominous process resulting in organ dysfunction(s) and ultimately, death.

There needs to be a line drawn in the sand to delineate what is the “regular” as opposed to an “abnormal” response to infection. There will be regular reactions in infections such as pneumonia, UTI, cellulitis, acute pyelonephritis, etc. When the process takes a serious turn to a toxic reaction leading to organ failure and possible death, this is when sepsis develops. Otherwise, any of the above infections might as well be considered part and parcel of sepsis. The distinction disappears and the significance of true sepsis is obscured. Pneumonia (or insert any other local infection here) can present with or without sepsis. Meeting two of the four criteria does not necessarily mean that the local infection caused mortality risk to rise to that of sepsis.  

The sequential sepsis-related] organ failure assessment (SOFA) score is an intrepid attempt to further elucidate what folks may have taken literally with the two-out-of-four SIRS criteria:

Lactatemia (or lactic acidosis) is another laboratory finding that is supportive of sepsis. But, then again, there are other causes of lactatemia:

An adroit provider will look at all of the patient’s circumstances and laboratory findings, then analyze and discern what is going on, and then come to a conclusion as to the true nature of the patient’s condition. It is something that may require some time (a day or two) in order to fully appreciate what is happening internally. Documentation needs to show what was on the provider’s mind at the time. Initial impressions may change as information trickles in. 

Appropriate documentation should reflect what the definitive diagnosis is, upon discernment.

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