Episode 104: Sepsis with Pam Lipsett

Anesthesia and Critical Care Reviews and Commentary (ACCRAC) Podcast
Anesthesia and Critical Care Reviews and Commentary (ACCRAC) Podcast
Episode 104: Sepsis with Pam Lipsett

In this 104th episode I welcome Dr. Pam Lipsett to the show to discuss the diagnosis and treatment of sepsis.

CME: https://earnc.me/DtOhNH


Sepsis-3 guidelines from JAMA: https://jamanetwork.com/journals/jama/fullarticle/2492881

Marik Sepsis cocktail: Marik PE et al. Hydrocortisone, Vitamin C, and Thiamine for the Treatment of Severe Sepsis and Septic Shock. 2017: 151(6);1229–1238.

ADRENAL trial: https://www.nejm.org/doi/full/10.1056/NEJMoa1705835

APROCCHSS Trial: https://www.nejm.org/doi/10.1056/NEJMoa1705716

SEPSISPAM Trial: https://www.nejm.org/doi/full/10.1056/NEJMoa1312173

8 thoughts on “Episode 104: Sepsis with Pam Lipsett”

  1. Great talk. I completely agree with Dr. Lipsett’s emphasis on incorporating patient’s history to make an accurate diagnosis. By the sepsis 3 definition, any patient in the ICU with significant worsening of organ function (increasing SOFA >= 2) with suspected infection has sepsis by definition. It is especially important now to investigate further patient’s history and hemodynamic profile to verify whether the cause of the shock state is infection or something else. The worst thing that can happen is treating a patient in cardiogenic shock for sepsis, which may very well be an established diagnosis based on sepsis 3, but delay the appropriate diagnostic workup and treatment. PA catheter might not make a difference as a continuous monitoring device for most patients but it is still an extremely important diagnostic tool. It’s important to differentiate the purposes of monitoring from diagnosis.

  2. From the perspective of a trainee this was an awesome discussion of sepsis. If for no other reason it gives a framework to think about the overarching themes of sepsis, a topic we don’t get much exposure to except for maybe in critical care units.
    As a med student we all saw that table with the arrows pointing up and down indicating the changes in hemodynamic parameters in vasodilatory, hypovolemic, and cardiogenic shock. While prepping for the ITE there were a few points I found surprising, and maybe even counterintuitive that I wanted to share.

    -Ejection fraction (EF) is decreased in septic shock: One of the hemodynamic derangements I remembered from med school was the heart is hyperdynamic. Before looking into it I didn’t realize what was driving this, and I would have thought EF was the same or maybe increased considering how much fluid we give these patients…but that doesn’t make too much sense, why would sepsis improve the pumping function of the heart? As it turns out, hyperdynamic only means there is an increased volume of circulation with decreased systemic vascular resistance (SVR), usually with an increased heart rate (HR) and cardiac index (CI) to compensate. Between the systemic inflammatory state, and large fluid resuscitation (a lot of fluid is presumed to have been administered because the patient has survived so far) the end diastolic volume of the ventricle is increased quite a bit, so the denominator for EF has increased without the numerator changing, giving a decreased EF. There is a really great diagram explaining this in ref [1] figure 2, you may be able to see it here https://www.nejm.org/na101/home/literatum/publisher/mms/journals/content/nejm/1993/nejm_1993.328.issue-20/nejm199305203282008/production/images/img_medium/nejm199305203282008_f2.jpeg
    But this brings me to my next point

    -Stroke volume (SV) is typically preserved in septic shock. This is the numerator that remains constant that I referenced in the point above. The pumping function of the heart is decreased, but the heart maintains output by the frank starling mechanism by increasing the left ventricular end diastolic volume (LVEDV). If you weren’t given any other variables you could use this to differentiate septic from cardiogenic shock. Both have an increased LVEDV, but cardiogenic shock would have a decreased SV, whereas SV would be the same in septic shock.

    -pumping function is decreased in septic shock – this was one of the points I struggled with…if we know the heart is hyperdynamic, HR, is increased, and SV is maintained that sounds like pretty good pumping function to me? But why would a heart be performing better if a patient is profoundly sick?? This point wasn’t clear to me until I saw ref[2] figure 1…you may be able to see a similar one here https://heart.bmj.com/content/87/6/507
    End systolic pressure volume relationship (ESPVR – the diagonal line) best reflects the contractility of the heart. It is unaffected by pre- and afterload conditions, and is therefore superior to EF. In septic patients it is decreased as evidenced by the decreased slope in that figure.

    -Leif Ericksen
    CA-2, Stony Brook University

    1. Parrillo, J.E., et al., Septic shock in humans. Advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy. Ann Intern Med, 1990. 113(3): p. 227-42.
    2. Gamkrelidze, M., et al., Myocardial dysfunction during septic shock (review). Georgian Med News, 2014(237): p. 40-6.

  3. My point is more of a practical one. We are defining sepsis mostly by organ dysfunction, which could be caused by many acute disorders, and less by hard evidence (only a suspected infection is necessary). It is potentially life saving that we would give antibiotics and fluid early for the diagnosis of sepsis but the investigative process sometimes needs to continue. Cardiac pathophysiology due to sepsis aside, if the primary disorder is cardiogenic shock but due to a suspicion of infection (let’s say the urine or BAL bacterial culture is also positive) sepsis gets diagnosed and the opportunity to reverse the underlying cause is missed.

    Out of curiosity, where do people think SIRS stands in the era of sepsis 3? I’m sure it still influences our decision making.

    1. Good point, and definitely very important never to exclude other possible diagnoses because you think you have identified one likely diagnosis. We are not infrequently wrong in our initial diagnosis! I am definitely interested to hear what others think about SIRS. I think it does what its name says, which is to help identify inflammation (not necessarily from an infectious cause). It can still be used for that, and of course we do use the components of SIRS whether formally or informally. For examplke, we ask ourselves “why is this patient’s white count elevated” even if we’re not plugging it into a SIRS algorithm.

  4. Great sepsis overview! I was hoping for some more discussion on the Surviving Sepsis guidelines, as I recently learned that they have been very controversial. EMCrit has a petition to retire them, with a thorough criticism of them here: http://emcrit.org/pulmcrit/ssc-petition/. Interestingly, the Infectious Disease Society of American has refused to endorse them as well.

    1. Hi Mike,

      Yes, the SSC guidelines are definitely controversial and I think the petition brings up some good points. One of the main ones, with which I agree, is that we should not be punishing doctors for not following guidelines that aren’t based on very solid evidence.

  5. This article along with others helps integrating old and new definitions of sepsis.

    A Comparison of the Quick-SOFA and Systemic Inflammatory Response Syndrome Criteria for the Diagnosis of Sepsis and Prediction of Mortality

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