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 < 90), or elevated lactate, and (3) Septic Shock, if they meet criteria for Severe Sepsis and continue to be hypotensive despite fluid resuscitation.
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 . 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”. 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:
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”
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:
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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 < 90), or elevated lactate, and (3) Septic Shock, if they meet criteria for Severe Sepsis and continue to be hypotensive despite fluid resuscitation.
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 . 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”. 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”
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:
-
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