Sepsis-3

I’m sure you guys have heard about the new sepsis definitions unveiled at the SCCM conference last week which were originally published in JAMA (2016;315(8):801-810); if not you’re in luck because I’ve outlined them for you below.  Keep in mind the sepsis definition has not been updated since most of you were still in high school- or middle school- I’m showing my age, in 2001, with Sepsis-2.

Sepsis-3:

New Terms and Definitions

  • Sepsis: Life-threatening organ dysfunction caused by a dysregulated host response to infection
  • Organ dysfunction: Acute change in total SOFA score ≥2 points consequent to the infection
  • Identification of patients likely to have poor outcomes:
    • ICU Patients: SOFA score ≥2: Overall mortality risk of approximately 10% in a general hospital population with suspected infection
    • ED patients: qSOFA score >2 (SBP < 100 mm Hg, RR > 22, or altered mental status)
      • These patients are likely to have a prolonged ICU stay or to die in the hospital
    • Septic shock: Sepsis with persisting hypotension requiring vasopressors to maintain MAP ≥65 and a serum lactate level >2 mmol/L despite adequate volume resuscitation
      • Hospital mortality is in excess of 40%
    • The term “severe sepsis” has been abandoned

2015 ACLS GUIDELINES

The new 2015 ACLS guidelines were published this month!  I love new guidelines!  I’ve highlighted the important drug stuff (you guys are on your own for the rest).

Vasopressin: REMOVED FROM ALGORITHM: This was no surprise to me as vasopressin has never been shown to offer any advantage over epinephrine in studies to date.

“Vasopressin offers no advantage as a substitute for epinephrine in cardiac arrest (Class IIb, LOE B-R)”

“Vasopressin in combination with epinephrine offers no advantage as a substitute for standard-dose epinephrine in cardiac arrest (Class IIb, LOE B-R)”

Steroids: I’ve been skeptical of the use of steroids in cardiac arrest since 2009 inhospital cardiac arrest trial (steroids were combined with a vasopressor bundle or cocktail of epi and vasopressin).  Will need much more convincing data before I’ll recommend routine use- and that is exactly what our guidelines endorse as well.  Because: no one in the ICU dies before receiving a course of steroids.  The pre-hospital use of steroids is pretty clear: no benefit.

“In IHCA, the combination of intra-arrest vasopressin, epinephrine, and methylprednisolone and post-arrest hydrocortisone as described by Mentzelopoulos et al may be considered; however, further studies are needed before recommending the routine use of this therapeutic strategy (Class IIb, LOE C-LD)”

“For patients with OHCA, use of steroids during CPR is of uncertain benefit (Class IIb, LOE C-LD)”

Epinephrine: Nothing groundbreaking here.  A few trials did demonstrate ROSC advantage with high-dose epi over standard dose; however, no improvement in survival to discharge (emphasis on good neurologic recover) over standard dose.  There is much concern with adverse effects of higher dose epi in the post-arrest period which may negate potential advantages during intra-arrest period.

“Standard-dose epinephrine (1 mg every 3 to 5 minutes) may be reasonable for patients in cardiac arrest (Class IIb, LOE B-R)”

“High-dose epinephrine is not recommended for routine use in cardiac arrest (Class III: No Benefit, LOE B-R)”

Antiarrhythmics: Really no changes.  Emphasized use of amiodarone over lidocaine (which is not new).

“Amiodarone may be considered for VF/pVT that is unresponsive to CPR, defibrillation, and a vasopressor therapy (Class IIb, LOE B-R)”

“Lidocaine may be considered as an alternative to amiodarone for VF/pVT that is unresponsive to CPR, defibrillation, and vasopressor therapy (Class IIb, LOE C-LD)”

“The routine use of magnesium for VF/pVT is not recommended in adult patients (Class III: No Benefit, LOE B-R)”

Circulation 2015:132:S444-64