Adult Critical Care Update: New Definitions of Sepsis and Septic Shock

The proceeding article discusses new changes to the current definition of sepsis and septic shock and new tools for assessing patients are at risk from a recent publication by an international task force on sepsis.

Adult Critical Care Update: New Definitions of Sepsis and Septic Shock

If you haven't already read or heard about it, the Society of Critical Care Medicine and the European Society of Intensive Care Medicine have released a new document called Sepsis-3 otherwise known as the Third International Consensus Definitions for Sepsis and Septic Shock in late February 2016. As members of the healthcare team, we all strive to improve the prompt identification and treatment of sepsis as it continues to be a leading cause of mortality and ICU admission. Those on the financial end of healthcare are just as involved because sepsis accounts for a large cost of in-hospital care.

Because there is no single diagnostic test that identifies a patient as septic, previous definitions of sepsis relied heavily on the systemic inflammatory response that patients with sepsis exhibit. The Systemic Inflammatory Response (SIRS) Criteria were widely used as a screening tool to identify those patients who may have sepsis. Under the definitions we have been using, patients who meet 2 or more findings in the SIRS Criteria were further stratified into a tiered classification system based on severity that starts with (1) Sepsis, if they also have a suspected source of infection, (2) Severe Sepsis, if they met the criteria for Sepsis and have either signs of end organ damage, hypotension (SBP Levy et al, 2003)

Many of us in Critical Care and those who work in Rapid Response Teams are familiar with this language. I'm very certain that nurses have filled out countless sepsis screening forms and triggered hospital-wide sepsis activation pages using these tools.

Recent research, have revealed that the criteria we've been using lacks the validity in predicting in-hospital mortality for sepsis (Seymour et al, 2016). I think those of us in clinical practice realize this even before the research findings were released. How many times have you triggered a sepsis alert on a patient meeting the SIRS Criteria, ongoing infection, and elevated lactate yet had other reasonable etiologies for such findings that do not necessarily go along with sepsis?

Sepsis-3 now defines sepsis as a "life-threatening organ dysfunction caused by a dysregulated host response to infection" (Singer et al, 2016)). A new tool to quantify organ dysfunction being proposed is the Sequential Organ Failure Assessment (SOFA).

Organ dysfunction is deemed present if there is an acute change in the total SOFA score ≥2 points consequent to the infection with the understanding that baseline SOFA score is zero in patients without known preexisting organ dysfunction. A quick SOFA (qSOFA) can be used as a quick tool for identifying those with a risk of mortality or requiring an ICU admission since SOFA relies on parameters not immediately available in some situations (i.e., non ICU patients). See below:

qSOFA (Quick SOFA) Criteria

Respiratory rate ≥22/min
Altered mentation
Systolic blood pressure ≤100 mm Hg

Finally, septic shock is now defined as a "subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality. Patients with septic shock can be identified with a clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP ≥65 mm Hg and having a serum lactate level >2 mmol/L (18 mg/dL) despite adequate volume resuscitation" (Singer et al, 2016)).

With these new definitions and tools, we are likely to see an overhaul of our previous system of sepsis monitoring in our respective healthcare institutions. It may mean new forms that reflect these new definitions to fill out for sepsis screening. Feel free to express your thoughts.

References:

- Assessment of Clinical Criteria for Sepsis

- 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference

- The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)

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Corey Narry

About Corey Narry, MSN, RN, NP

Advanced Practice Columnist / Guide

Juan De La Cruz, MSN, RN, ACNP, CCRN-CSC is a Nurse Practitioner with over 10 years of experience in the field of Critical Care.

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Specializes in Nursing.

This is a huge topic of discussion in my organization right now. Thank you for clarifying. I had heard that the new definition removes severe sepsis shock and eliminates SIRS. Is there a comparison tool available between the old and the new definitions?

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Specializes in Med-Tele; ED; ICU.

Appreciate the read. I was just reading the SIRS/sepsis articles on UpToDate last night and was interested to see the PaO2/FiO2 ratio prominently featured as well as the creatinine levels.

My organization is rolling out non-invasive cardiac output monitoring at the bedside in the ED to guide fluid resuscitation because they're finding patients who are ending up fluid-overloaded as the result of aggressive resuscitation.

Parenthetically and tangentially, I've been hearing from our burn unit that they're getting a lot of overloaded patients due to blind adherence to the Parkland formula.

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Much appreciated. As an Acute Dialysis RN, I deal frequently with AKI in the context of sepsis. This is a helpful read.

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Appreciate the read. I was just reading the SIRS/sepsis articles on UpToDate last night and was interested to see the PaO2/FiO2 ratio prominently featured as well as the creatinine levels.

My organization is rolling out non-invasive cardiac output monitoring at the bedside in the ED to guide fluid resuscitation because they're finding patients who are ending up fluid-overloaded as the result of aggressive resuscitation.

Parenthetically and tangentially, I've been hearing from our burn unit that they're getting a lot of overloaded patients due to blind adherence to the Parkland formula.

If they're worried about aggressive fluid caused failure, measuring cardiac output isn't the way to avoid it. It's also interesting that dopamine is still widely used (enough to fall into identification criteria for sepsis).

There is a lot that ICU's are missing if dopamine and cardiac output are mainstays of treatment of shock in sepsis.

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Specializes in Med-Tele; ED; ICU.
If they're worried about aggressive fluid caused failure, measuring cardiac output isn't the way to avoid it.
I likely misspoke. They're not using CO, they're using the change in CO in response to a fluid challenge.

We'll see how it plays out in clinical practice but the theory is sound... use the Starling curve to guide resuscitation.

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Specializes in ACNP-BC, Adult Critical Care, Cardiology.

@ann_marie_oregon:

Yes, the new Sepsis-3 document removed the emphasis on SIRS. Previously, sepsis was defined as SIRS + infection with sepsis being classified based on severity from sepsis to septic shock. The new definitions place emphasis on organ dysfunction which is measured by the SOFA Score. Now, we only have sepsis and septic shock defined. I don't know yet how hospitals will roll out a new system of monitoring in light of the change. However, a proposed algorithm is actually in the article itself:

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To all others:

Sepsis-3 as a document, only defines how we are to identify sepsis and septic shock. The management would still be the same as before and resources are available on the Surviving Sepsis campaign website.

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Specializes in CVICU/ICU.

As we progress on identifying different conditions like sepsis we are improving other aspect of healthcare. For instance, the lactic acid lab that we use as one of the identifiers of sepsis is great. The problem that this helped me to identify was that nurses generally are not trained in how to properly collect labs in general. We aren't rarely if ever trained what the standards are or how to comply with them. The lactic acid is a good example. Most facilities have protocols procedures that say it needs to be collected "On Ice". Actually the specimen is suppose to be chilled not frozen. Here is a link to one of the vacuum tube manufactures and their recommendations: Click Here

That is just the tip of the iceberg. There are Venipuncture Standards produced by the CLSI(Clinical & Laboratory Scientific Institute). There are some very important steps in the preanalytical process that we are not doing correctly like the "Order of Draw" how many times we invert each specific vacuum tube etc. I am working on bringing hospitals up to standards and then improving upon them to include standards for drawing blood off of devices like alines, PICC lines etc. I also would like to see the styandards go from consensus based to evidence based.

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Specializes in ER.

Thanks for the interesting read on! I have vast interest in sepsis because we see so much of this in the ED frequently, and understanding pathophysiology is a lot better than just doing the protocols. Thanks!

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I likely misspoke. They're not using CO, they're using the change in CO in response to a fluid challenge.

We'll see how it plays out in clinical practice but the theory is sound... use the Starling curve to guide resuscitation.

It will help, but CO can absolutely rise in the presence of relative volume overload. Lots of work being done with MSFP determination, which is where the conversation is moving in certain centers (Rivers, Pinsky et al). Pulse pressure variation guided volume combined with RAP/CVP response is as good as CO imho

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So is anyone trying to incorporate the new recommendations and definitions into their current sepsis protocols? If so, how are you reconciling the CME core measure reporting requirements that are based on the outdated info?

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I likely misspoke. They're not using CO, they're using the change in CO in response to a fluid challenge.

We'll see how it plays out in clinical practice but the theory is sound... use the Starling curve to guide resuscitation.

Re-quoting you here, not to put too fine a point on this.... the non invasive CO monitors, Flo Trac etc. have their issues, but they have been seen as an alternative to the gold standard PA catheter. My point is that reliable determination of fluid responsiveness is very much possible without a PA catheter or a potentially problematic "non invasive" CO monitor.

Your point is taken.

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