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. March, 2019 from Emergency Medicine Cases.

[Note to occasional readers: The show notes are simply outstanding so there is really no point in publishing excerpts. I do it because it helps me remember the post.]

And here is the direct link to the podcast.

Here are some excerpts:

Take home points on sepsis and septic shock

Calculate NEWS (National Early Warning Score)* to detect subtle cases of occult septic shock.

*Link is to the NEWS score on MDCalc.

*See also NEWS2 Is Superior to qSOFA in Detecting Sepsis with Organ Dysfunction in the Emergency Department PMID: 31362432 J Clin Med. 2019 Aug; 8(8): 1128.

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.

The latest definitions of sepsis and septic shock:

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

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.

What is the best clinical tool to aid in the recognition of sepsis and septic shock?

Early recognition of sepsis is essential. In cases that are not obvious, it is recommended to use a clinical tool to help prognosticate and guide management.

A recent retrospective study compared the clinical tools SIRSqSOFA, and NEWS (National Early Warning Score) for the early identification of sepsis in the ED, and found that NEWS was more accurate that both SIRS and qSOFA for the early recognition of septic shock [2].

The beauty of the NEWS* is that it can be calculated rapidly at triage without the need for blood test results and it allows for improved risk stratification.

*Please see Sick Or Not Sick? Resources On The National Early Warning Score (NEWS and NEWS2)
Posted on October 4, 2019 by Tom Wade MD

Lab tests in the early management of sepsis and septic shock

If you are still unsure if your patient is septic or not after calculating the NEWS, obtain a serum lactate early.

Tip: Send a venous gas with your initial labs, and have the lab run the lactate on that so you get it back fast. You might be surprised to get back a very elevated lactate on a patient with an otherwise low pretest probability for sepsis, and this may help guide your management.

We know that lactate is useful to help identify occult septic shock in those patients who don’t present in florid septic shock, but it is very nonspecific and there are many false positives including any type of shock, liver failure, seizures, Type B Lactic Acidosis from many drugs including Ventolin/albuterol.

Procalcitonin as a diagnostic marker for sepsis and septic shock

Other studies suggest that procalcitonin may help risk stratify pneumonia and guide antibiotic de-escalation, but it’s use in sepsis in the ED is probably not very helpful.

Resuscitation fluid of choice in sepsis and septic shock

.   .   .   our expert nonetheless recommends Ringer’s Lactate as the initial resuscitation fluid of choice in sepsis and septic shock because normal saline is thought to be associated with worsening hyperchloremic metabolic acidosis [8] as well as renal vasoconstriction from the chloride load resulting in poor renal function [9], and these recent studies, while flawed, do suggest worse renal function and possibly increased mortality with saline compared to balanced solutions.

Logistics of giving RL. You’ll need one IV line for your antibiotics and a separate one for RL because Ceftriaxone, as well as some formulations of Piperacillin-Tazobactam are incompatible with Ringer’s Lactate.

Endpoint of resuscitation: How much fluid should be given up front in sepsis and septic shock?

There is no cookbook recipe here. The Surviving Sepsis Campaign 2018 Update [10] suggests starting a rapid administration of 30mL/kg crystalloid for patients with hypotension or a lactate ≥ 4, while the Canadian Guidelines from 2008 suggest “an initial bolus of 1–2 L of crystalloid or 500–1000 mL of colloid should be given over 30–60 minutes and repeated as required to correct tissue perfusion and/or blood pressure abnormalities.”[11] The ProCESS [12], ARISE [13] and ProMISe [14] trials bring no clarity as to the optimal amount of fluid for sepsis and septic shock.

Even for patients with a history of heart failure or who have signs of acute heart failure, crystalloid boluses should be given to maintain adequate end-organ perfusion [Dr. Gray states do the foregoing even if it means you have to intubate and provide respiratory support–inadequate resuscitation just means slow death over the next few days]. Fluid should be administered via at least two proximal large bore peripheral IVs, wide open, under pressure.

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.

Antibiotic timing, administration and choice in sepsis and septic shock

We know that with each passing hour that antibiotics are not initiated in septic shock, survival drops – it’s a time bomb. Which may not be the case for sepsis without septic shock [23]. Nonetheless, this prompted the newest Surviving Sepsis Campaign Guidelines to mandate antibiotics within the 1st hour of the patient hitting triage for anyone suspected of sepsis as part of their Sepsis Management Bundle [10]. There has been a huge backlash against this mandate, because we would end up giving expensive antibiotics to many patients who do not need them, possibly get distracted.

How fast should antibiotics be given in sepsis and septic shock? We use push dose pressors – why not push dose antibiotics?

Once the decision to give IV antibiotics has been made they should be given over 5 minutes (rather than the usual 30 minutes) in order to reach peak effect as early as possible. The exception is vancomycin which must be given slowly. Give the most important antibiotic first, and consider administering the second antibiotic orally at the same time as the IV antibiotic if the second antibiotic has excellent bioavailability (e.g. cephalexin, ciprofloxacin, doxycycline etc).

Which antibiotics are best for sepsis without an apparent source?

We also know from a study out of Chest in 2009 that inappropriate antibiotic choice decreases survival in sepsis [24]. So it is important to choose your antibiotics wisely based on local antibiograms. Work with your ID team to develop local guidelines and ideally build them into your EMR.

Chest, urine, abdomen are #1, #2 and #3 of sources of infection that are not immediately obvious on clinical exam. After that don’t forget line sepsis and meningitis because those require removal of the line and early LP.

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 concommitant adrenal suppression.

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?

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