Ep 122 Sepsis and Septic Shock From Emergency Medicine Cases

This is another great podcast from Emergency Medicine Cases:

 Helman, A. Gray, S., Morgenstern, J., Spiegel R., Kovacs, G., Simard, R. Sepsis and Septic Shock – What Matters. Emergency Medicine Cases. March, 2019. https://emergencymedicinecases.com/sepsis-septic-shockAccessed April 1, 2019.

Here is the lead in summary from the podcast:

In this podcast Dr. Sara Gray, intensivist and emergency physician, co-author of The CAEP Sepsis Guidelines, answers questions such as: How does one best recognize occult septic shock? How does SIRS, qSOFA and NEWS compare in predicting poor outcomes in septic patients? Which fluid and how much fluid is best for resuscitation of the septic shock patients? What are the indications for norepinephrine, and when in the resuscitation should it be given in light of the CENSER trial? What are the goals of resuscitation in the patient with sepsis or septic shock? When should antibiotics administered, given that the latest Surviving Sepsis Campaign Guidelines recommend that antibiotics be administered within one hour of arrival for all patients suspected of sepsis or septic shock? What are the indications for a second vasopressor after norepinephrine? Given the conflicting evidence for steroids in sepsis, what are the indications for steroids? Should we be considering steroids with Vitamin C and thiamine for patients in septic shock? What are the pitfalls of lactate interpretation, and how do serial lactates compare to capillary refill in predicting poor outcomes in light of the ANDROMEDA trial? Is procalcitonin a valuable prognostic indicator in septic patients? and many more…With interludes by Rory Spiegel on the ANDROMEDA-SHOCK RCT, Justin Morgenstern on the CENSER trial, and Rob Simard on the value of IVC girth and collapsibility for guiding fluid management in septic shock as well as George Kovacs on airway considerations in the septic shock patient.

[Note to myself: The show notes are simply outstanding so there is no point in publishing excerpts but I did anyway. I couldn’t help it.]

And here is the direct link to the podcast.

Here are some excerpts:

And at 59:33 Dr. Kovacs, one of Canada’s leading airway experts, weighs in with some incredibly important advice:

Dr. Kovacs says:

This patient [with septic shock] represents a triple threat. You know our septic patients it is not uncommon that they are potentially hemodynamically unstable. It is not uncommon that there is a respiratory source so they are hypoxemic. And that they are acidotic.

So they don’t represent a traditional difficult airway from an anatomic or pathologic point of view. But they are a difficult airway. They have difficult physiology.

If you look at [the] presentation of this patient, based on the initial vitals  [he] had a Shock Index* of 0.9.

*Shock Index – MDCalc

We know if we intubate that patient, with that shock index, there is a high incidence of bad things happening including cardiac arrest afterward.

So we’ve all heard about resuscitate your patient first. These patients don’t get better from a tube in their trachea.

In fact, often they will get worse because we’re doing positive pressure ventilation. Positive pressure ventilation decreases venous return. We’re increasing their afterload.

They’ve lost their sympathetic drive [because you had to sedate them when you intubated them, I believe, is what he is getting at here.]

So what Dr. Kovacs is talking about are what Dr. Weingart terms the HOP killers: hypoxia, hypotension, and Ph problems [meaning failure to hyperventilate a patient who needs respiratory compensation for their metabolic acidosis].

And here are links to Dr. Weingart’s posts on the HOP killers:

The Components

HOp Killers

Here is the wee on the HOp Killers: Hemodynamic Kills, Oxygenation Kills, and pH Kills

RSI or Awake? · DSI? · RSA? · ICP/Vascular?

Resuming excerpts from Ep 122 Sepsis and Septic Shock

The latest definitions of sepsis and septic shock

As per the Third International Consensus Definitions for Sepsis and Septic Shock [1]:

Sepsis is “life-threatening organ dysfunction caused by a dysregulated host response to infection” with a SOFA score* ≥2.

*Sequential Organ Failure Assessment (SOFA) Score – MDCalc

Septic shock is “a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone”, identified clinically by a vasopressor requirement to maintain a MAP ≥ 65 and serum lactate ≥ 2 mmol/L in the absence of hypovolemia.

Severe sepsis is no longer part of the definitions.

Starting norepinephrine in sepsis and septic shock: Is earlier better?

Probably. The Surviving Sepsis Campaign 2018 Update suggests starting norepinephrine if the patient is hypotensive during or after fluid resuscitation to maintain a MAP ≥ 65. There is no need to wait for 2-3L of crystalloid to go in. A more recent study, CENSER, is the first ever prospective randomized trial looking at vasopressors in sepsis. Patients in Thailand presumed to be septic with a MAP <65 were randomized to receive norepinephrine 0.05 micrograms/kg/min without titration for 24hrs or placebo [18]. The primary outcome was shock control by 6 hours. This was defined as sustained MAP>65 (>15 minutes) plus 2 consecutive hours of urine output >0.5ml/kg/hr or decrease in serum lactate >10% from the initial lactate level. 76.% in the early norepinephrine group vs 48% of the control group achieved shock resolution at 6 hours. Mortality was lower in the early norepinephrine group (16% vs 22%) but not statistically significant. This study is consistent with previous data that suggests that early initiation of norepinephrine is septic shock is preferable, although large RCTs are pending. Currently, the CLOVERS trial [19] is underway comparing early vasopressors to IV fluid resuscitation.

We know that we can give norepinephrine through a peripheral line safely and quickly if done carefully through a large proximal IV with hourly extremity checks. A central line is not a priority in the early resuscitation phase.

Dosing norepinephrine in septic shock

Start at 5 mcg/kg and titrate immediately after each q5minute BP check. This will likely require you to stay at the bedside. Note that a radial arterial line may underestimate MAP compared to a femoral arterial line by as much as 5mmHg in early septic shock and >5 in advanced shock, leading to higher doses of norepinephrine than are necessary. [20]

Vasopressin is the second line vasopressor in septic shock

Vasopressin reduces the need for norepinephrine but does not reduce mortality

The VANISH study suggested that while early vasopressin does maintain blood pressure and reduce the requirement for norepinephrine and renal replacement therapy, it does not reduce the number of renal replacement free days or mortality rate [21]. The VASST study did not show a mortality benefit from adding vasopressin if the MAP was adequately maintained with norepinephrine [22].

Vasopressin dosing 0.03-0.04 units/min

When should vasopressin be initiated in septic shock?

There is no clear evidence for the indications for staring vasopressin in patients with septic shock. Our expert recommends starting vasopressin when moderate doses of norepinephrine (as in 0.5 mcg/kg/min or 35 mcg/min) have been reached.

What are the indications for steroids in septic shock?

Bottom line: Although the evidence is mixed as to whether or not steroids are beneficial in septic shock, our expert recommends administering steroids for:

  1. Vasopressor refractory shock (i.e. patient remains in shock despite norepinephrine 0.5mcg/kg/min)
  2. Patients who are taking steroid medications at baseline
  3. Patients with concomitant adrenal suppression

Take home points on sepsis and septic shock

Calculate NEWS* to detect subtle cases of occult septic shock.

*From MDCalc

Less saline, more Ringer’s, even if acute heart failure, especially in renal failure and severe acidosis.

Norepinephrine whenever MAP <65 – earlier rather than later.

Early antibiotics (within 1hr of the diagnosis rather than 1 hour of arrival at ED), given over 5 minutes (except vancomycin over 30 minutes), chosen wisely according to local antibiograms.

Use a combination of MAP, GCS, urine output, initial lactate, capillary refill time, POCUS IVC to guide initial fluid resuscitation, individualized to each patient.

If the lactate is rising despite resuscitative efforts call your intensivist. Early to ICU is preferable, but remember that capillary refill time may be as good, or even better than lactate at guiding resuscitation.

Consider vasopressin and hydrocortisone if a MAP of 65 cannot be maintained with 35mcg/min norepinephrine and ongoing fluid resuscitation.

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