Sepsis 2.0 vs 3.0

    NextPrevious

    Sepsis 2.0 vs 3.0

    A 65 yo M is bibems tachycardic and hypotensive with one week of worsening cough and sob.  Large LLL infiltrate is present on XRay.  You begin treating your patient for severe sepsis and begin to wonder what has been happening in the world of sepsis recently.

    October 1st, 2015:

    CMS published a new sepsis bundle that we are now following at both hospitals.  The bundle recreated the definitions for severe sepsis and septic shock and outlined treatment goals and timelines to achieve the same.  This is listed below.  They are being monitored and hospital compliance may be linked to funding in the future.  These new definitions are controversial, many claiming there is no supporting evidence for portions of the bundle. Furthermore, treatment guidelines removed physician discretion which is concerning, as CHF and ESRD patients should not be receiving 30 ml/kg boluses.

    Severe Sepsis:

    1. Suspected source of infection
    2. > 2 SIRS criteria
    3. Evidence of Organ dysfunction (regardless of pt’s baseline)
      • SBP < 90 or MAP < 70 or SBP decrease of > 40 from baseline
      • Cr > 2 or UOP < 0.5 ml/kg/hr for 2 hours
      • Bili > 2
      • Platelet count < 100
      • INR > 1.5 or PTT > 60
      • Lactate > 2

    Septic Shock:

    • Tissue hypoperfusion (defined below) persisting in the hour after IVF administration
      • SBP < 90
      • MAP < 65
      • Decrease in SBP by > 40
      • Lactate > 4

    Treatment Guidelines:

    • Initial 3 hours
      • Resuscitate to below parameters by giving 30 ml/kg bolus (regardless of pt co-morbidities)
        • CVP 8-12
        • MAP > 65
        • UOP > 0.5 ml/kg/hr
        • ScvO2 70% or SvO2 65%
        • If elevated lactate, attempt to normalize
      • Draw cultures
      • Administer Antibiotics (w/in 1st hour)
    • Initial 6 hours
      • Apply vasopressors (for hypotension not responsive to IVF resucitation) to maintain MAP > 65
      • If septic shock -> measure CVP and ScvO2
      • Remeasure lactate if initial elevated

    February 2016:

    The Society of Critical Care Medicine (SCCM) published a JAMA article reformatting the definitions of sepsis.  The authors attempted to update the definitions based off new understanding of the biological and clinical pathophysiology associated with sepsis.  The main changes included in this paper are the removal of the term “severe sepsis”.  The other major change is the use of SOFA (Sequential Organ Failure Assessment) and qSOFA (mortality predictors) as tools to replace SIRS.  These guidelines are NOT endorsed by any Emergency Medicine Society and are also creating a lot of controversy.  There is no discussion of sepsis treatment in this update.

    Sepsis = Life-threatening organ dysfunction caused by a dysregulated host response to infection.

    Septic Shock = A subset of sepsis in which underlying circulatory and cellular metabolism abnormalities are profound enough to increase mortality.

    • Sepsis plus the following despite adequate fluid resuscitation:
      • vasopressor required to maintain MAP > 65 AND
      • Serum lactate > 2

    Diagnostic tools to screen sepsis:

    A patient has sepsis if an infection is suspected and rules in by one of the following criteria

    > 2 of qSOFA:

    • Respiratory rate > 22/min
    • Altered mentation (GCS < 15)
    • Systolic blood pressure < 100 mm Hg

    Score of > 2 of SOFA:

    SOFA score

     

    Other resources on this topic:

    Surviving Sepsis Bundle

    SCCM JAMA article

    Jeremy Faust discussing on Foamcast

    PulmCrit

    EmCrit Smaccback

    • Welcome! This is the website for the Mount Sinai Emergency Ultrasound Division. It serves as an information resource for residents, fellows, medical students and others seeking information about point-of-care ultrasound. There is a lot ofRead more

    • renal handling of water

      If you were on a tea & toast diet, how much water would you need to drink before you develop hyponatremia? I haven’t seen anyone work out the numbers before so here are my calculations. AndRead more

    • acute acidemia physiology

      As alluded to in the first post, don’t be fooled by a “normal” potassium in the setting of DKA because osmotic diuresis and H+/K+ exchange means that total body potassium is actually LOW. You all knowRead more

    • renal handling of potassium

      the first symptom of hyperkalemia is death Earlier post covered temporizing measures to counter hyperkalemia — namely, intracellular shift, increasing cardiac myocyte threshold potential. Give furosemide if the patient still urinates and consider dialysis, but then askRead more

    • bicarbonate revisited

      Previous post reviewed the safety of balanced crystalloids in hyper K. But what was up with serum bicarbonate decreasing with saline administration? This post introduces a new way of looking at the anion gap to possiblyRead more

    • hyperkalemia and balanced crystalloids

      Is it safe to give LR or plasmalyte to a hyperkalemic patient (these balanced crystalloids have 4-5 mEq/L K as opposed to 0 mEq/L K in normal saline)? Postponing the discussion of renal handling of potassium toRead more

    • hyperkalemia physiology

      You’ll likely encounter hyperkalemia on your next Resus / Cardiac shift, and you’ll instinctively treat it. But take a moment to review the fascinating physiology behind the “cocktail”! First, consider how K+ is buffered byRead more

    • Slow down your tachycardia (but not really)

      You’re sitting in resus bemoaning the departure of your most beloved attending when suddenly a patient wheels in without warning. The patient looks relatively stable but the triage RN tells you her heart rate wasRead more

    • Otitis externa: use the ear wick!

      Acute otitis externa (AOE) is a common complaint seen in pediatric as well as adult emergency departments. AOE is typically not accompanied by acute otitis media, although concurrent cases are possible. Also called “swimmer’s ear”Read more

    NextPrevious