From the abstract:
Sepsis should be defined as life-threatening organ dysfunction caused by a dysregulated host response to infection.
That's the definition in concept. The notion of a dysregulated host response is new and means that the response is inappropriate in some way. That is why inflammation, specifically SIRS, which represents an appropriate (and beneficial to the host) response, is de-emphasized. That is not to say inflammation is not important, but it is not the entire picture and is not enough to produce sepsis. This is in recognition of increasing evidence of injurious non-inflammatory pathways that are activated, and of studies like this one showing that SIRS criteria will miss a considerable number of infected patients in need of critical care.
The move beyond SIRS criteria is not really new. Remember that the 2012 Surviving Sepsis guidelines had already broadened the definition by replacing SIRS criteria with the mere requirement that there be “some” of a long list of signs and symptoms including but not limited to SIRS.
Again, from the abstract, moving on to the specific criteria:
For clinical operationalization, organ dysfunction can be represented by an increase in the Sequential [Sepsis-related] Organ Failure Assessment (SOFA) score of 2 points or more, which is associated with an in-hospital mortality greater than 10%. Septic shock should be defined as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone. Patients with septic shock can be clinically identified by a vasopressor requirement to maintain a mean arterial pressure of 65 mm Hg or greater and serum lactate level greater than 2 mmol/L (greater than 18 mg/dL) in the absence of hypovolemia.
There's a lot to unpack here. What is meant by the absence of hypovolemia? That's not clear at all for multiple reasons. First, is this term relative to what would be considered euvolemia for the patient's size, or is it relative to whether the patient might be volume responsive, which might be something very different in a septic patient. Worse, there is ongoing debate on how this can even be assessed. Most clinicians, for practical purposes, will assume this means persistent hypotension requiring pressors after the initial fluid resuscitation.
Note that post fluid resuscitation the shock criteria in terms of BP and lactate are now both/and (low MAP and lactate elevation) rather than either/or as was the case in the old definition, although the lactate cutoff has been lowered from 4 to 2.
It is not made clear in the new definition whether infection need merely be suspected (as in the old definition) or must be confirmed. Given the rapidity with which sepsis needs to be recognized and treated, “suspected” would be appropriate at the bedside. Whether that is enough for reporting purposes is not made clear.
Although the qSOFA score, a rapid bedside determination based on clinical criteria, is suggested as an assessment tool, the full SOFA score appears to be necessary to satisfy the definition. That means you have to get an ABG, a full set of labs and do a GCS (not that you wouldn't do those things anyway).
Note that the category “severe sepsis” has been eliminated. Now there is just “plain Jane sepsis” and septic shock. This may pose a problem for the “clinical documentation” coders who want you to code “severe sepsis.” It is just another example of the fact that coding terminology is generally years, sometimes decades, behind current clinical definitions. That is nothing new, and is something we will continue to have to navigate around.
It would appear that the new definitions have sacrificed clarity and simplicity of use for a scheme that better reflects the current understanding of the pathophysiology of sepsis.