Sepsis protocols causing a future superbug??

Nurses General Nursing

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I am sure we all work at a hospital where code sepsis's are now a huge deal as evidence has shown that preventing septic shock helps increase the chances of survival. **insert shocked face** (like we all didn't know that.)

Anyways, we all know that is true and people with the potential of becoming septic should be treated with antibiotics and fluids STAT. Although this protocol is probably saving lives all over the U.S., I also think it may be the beginning of a superbug.

Many people that walk through the ER are going to flag for sepsis, but does that truly make them septic?

What is your guys' hospital protocol when it comes to treating sepsis??

I am afraid that if we continue to treat everyone as a code sepsis and load them with tons of antibiotics, we are running the risk of future superbugs which won't respond to these antibiotics.

Any opinions out there?? How can we effectively treat sepsis and distinguish septic from non septic patients to help prevent a future superbug?

Let me know your opinions, or maybe what your guys' hospital protocols are when it comes to a code sepsis.

Specializes in ER.

I'm wondering if any of you have a Sepsis Protocol that is working well for you? Does your computerized charting system gather results already documented into a sepsis document, or do you manually tabulate results on a separate paper flow sheet sending you on ongoing research missions to see what else came in out of range? Do your doctors and PAs take the lead, or does it fall to nursing to "make sure your providers get it right."

Our protocol has arbitrary cutoff levels that can set the healthiest guy in the department onto the sepsis pathway, bolus the wrong people with too much fluid, and, yes, everybody gets antibiotics. A guy who just worked out will hit several triggers, including increased lactic acid, but it's all predicable given his history. But the patient's history and all common sense fly out the window when a couple markers hit and artificial intelligence takes over.

Isn't it more important to deescalate antibiotics appropriately than avoid starting them altogether? I mean, I would be more afraid of a truly sick person with a high bacterial load, thus the greater potential for acquiring resistance, than of the person with no such infection brewing. I get that no antibiotics are safe, but it seems like it would be a shame to not rescue a person that really needs it to avoid an outcome that could be avoided by implementing better deescalation programs and monitoring.

Our protocol has arbitrary cutoff levels that can set the healthiest guy in the department onto the sepsis pathway, bolus the wrong people with too much fluid, and, yes, everybody gets antibiotics. A guy who just worked out will hit several triggers, including increased lactic acid, but it's all predicable given his history. But the patient's history and all common sense fly out the window when a couple markers hit and artificial intelligence takes over.

That appears to be a frequent mistake - I don't see evidence that this understanding of any sepsis protocol is correct.

Sepsis protocols were not meant to be used blindly on patients whose history and presentation offer much more feasible explanations for abnormalities picked up by clinical alert systems built into EMRs. All the accepted protocols are for patients with sepsis. They aren't for "any patient who has X and Y" or "any patient for whom an alert is generated." This always did (and still does) involve clinical correlation and expert judgment - starting at step 1, which is a determination that that there is indeed a suspicion of infection.

This is step 1 of the Surviving Sepsis guidelines, tool.

As this tool demonstrates, the patient does not meet criteria for a protocol to begin with if #1 is not met.

This is the medical version of "common sense."

I am not sure what seems to take things so off-track in some places, but I suspect it is a combination of 1) "Data trackers" who are not experts in these matters and 2) Exhaustion with #1.

ETA: ACEP comment

Specializes in Ambulatory Care-Family Medicine.

Our protocol fires itself based on data in the EHR. If 2 or more parameters are met we get a pop up on the chart and have to acknowledge or decline it and give a reason. Typically it is 2 or more vital signs have had a change since the last recording (temp goes from 97 to 101 and BP or pulse change more than a certain number of points). We can decline the protocol if it is an expected clinical finding (usually only applies to the ICU patients) or we have to acknowledge it. By acknowledging it a set of STAT labs is order and nursing gets an order to obtain IV access (if there is not already one) and call the physician. The physician can still cancel the protocol at his/her discretion, although most won't since it is ultimately just labs and IV access.

Our protocol does not call for starting antibiotics or fluids as those are medications and need to be individualized for the patient. Nursing is responsible for notifying the physician once lab results are in to determine treatment coorifice if any.

Specializes in Critical care.
My biggest issue is not with treating sepsis or suspected sepsis. I have a problem with "throwing" ABX at a patient with no chance of any meaningful recovery, and just turning those persons into a petri dish in their remaining days/weeks of life.

Example...I had a pt in his 80s, severe dementia. Non verbal, non ambulatory. He was being treated, again, for aspiration pneumonia. He was already on isolation precautions for MRSA and VRE, and we continued to give ABX. His sister was POA. I don't know how the doctor phrased the end of life conversation with her, but she refused to accept that he was dying and she refused to have ABX discontinued. Of course, PO vanc was also added to his regimen because he developed C diff. With people (nurses, techs, radiology, IV team, PT, family etc., etc.) constantly in/out of his room, my guess is not everyone was 100% compliant with precautions. (Despite education, his sister would walk into the hall with her gown/gloves on). I know end of life, especially when to withdraw care, is a delicate issue, but this is not the only time in my career that I have given ABX as part of an obviously futile effort. I find this scenario, where ABX are of very little long term help, just as likely to create superbugs than having a sepsis protocol (that could be quite meaningful in save lives). Of course, there is no easy solution for the (near) end-of-life cases.

We have a similar situation with a patient frequently on my unit. I also voiced those very concerns- we are throwing all these antibiotics at a patient with recurrent pneumonia and several MDROs already that has a terminal illness and no chance at recovery. We are just increasing the risk of creating another superbug. It's an incredibly hard and difficult situation, but there comes a time where we have to think of our future and the general good.

Specializes in Hematology-oncology.
I'm wondering if any of you have a Sepsis Protocol that is working well for you? Does your computerized charting system gather results already documented into a sepsis document, or do you manually tabulate results on a separate paper flow sheet sending you on ongoing research missions to see what else came in out of range? Do your doctors and PAs take the lead, or does it fall to nursing to "make sure your providers get it right."

Our protocol has arbitrary cutoff levels that can set the healthiest guy in the department onto the sepsis pathway, bolus the wrong people with too much fluid, and, yes, everybody gets antibiotics. A guy who just worked out will hit several triggers, including increased lactic acid, but it's all predicable given his history. But the patient's history and all common sense fly out the window when a couple markers hit and artificial intelligence takes over.

Our Sepsis Protocol is completely run by our STAT nurses. Bedside nurses don't see the popups, or interact with the warnings in our EHR. If the STAT nurses are concerned about potential sepsis they contact the bedside nurse, charge RN, and/or service...then escalate to an ERT if necessary. I've only seen the process in action a few times on my floor but it seems to work quite well.

It does, and providers are well aware of it. It leads to much more negative sequela than just creation of "superbugs"

NEJM - Error

As a matter of fact, wide application of ANY screening authomatically leads to increase of false positives (i.e. overdiagnosis) of the given condition. That's just how laws of statistics work.

Unfortunately, the system just seems to be made for current CYA/KTA (""cover your a**/kiss their a**) way of practicing medicine and also gives a nice nudge to pharm research. So, things are not going to change in the near future.

P.S. link says "error" but it works

Newly licensed, not yet employed RN here. I have been doing some self-directed CE on sepsis since I graduated so I thank you for the article linked above. I do have a question though. At end of the article, it states "..only about 50% of patients with severe sepsis have bacteremia." My understanding from school and the research I've done subsequently is that bacteremia is a more recent term for sepsis. Is the article using the word "sepsis" to refer to "septic shock?" i.e. using "sepsis" to refer not simply to the presence of bacteria in the blood, but to the immune response that ultimately leads to impaired tissue perfusion and organ failure? Also, wondering if septic shock occurs in response to other pathogens (fungi, viruses) or just bacteria? I've asked this question both in class on the floor and never really gotten a clear answer.

Specializes in Critical Care.

The Sepsis guidelines have never actually recommended initiating basing antibiotic treatment on the screening tools in use, the screening tools are only meant to trigger further assessment to determine if the patient actually requires antibiotics. The most recent guidelines (Sepsis-3) not only reinforce that basic screening tools shouldn't initiate treatment, but that they really shouldn't be used at all since they are too broad.

Specializes in ICU, LTACH, Internal Medicine.
Newly licensed, not yet employed RN here. I have been doing some self-directed CE on sepsis since I graduated so I thank you for the article linked above. I do have a question though. At end of the article, it states "..only about 50% of patients with severe sepsis have bacteremia." My understanding from school and the research I've done subsequently is that bacteremia is a more recent term for sepsis. Is the article using the word "sepsis" to refer to "septic shock?" i.e. using "sepsis" to refer not simply to the presence of bacteria in the blood, but to the immune response that ultimately leads to impaired tissue perfusion and organ failure? Also, wondering if septic shock occurs in response to other pathogens (fungi, viruses) or just bacteria? I've asked this question both in class on the floor and never really gotten a clear answer.

Good questions :)

Sepsis should be defined as life-threatening organ dysfunction caused by a dysregulated host response to infection.

Septic shock should be defined as 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. Patients with septic shock can be clinically identified by a vasopressor requirement to maintain a mean arterial pressure of 65 mm Hg or greater and serum lactate level greater than 2 mmol/L (>18 mg/dL) in the absence of hypovolemia. Neither definition includes bacteriemia, viremia or any other microbiologic ctiteria.

The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)

Sepsis is, by definition, induced by infection - any infection. It can be a bacteria, mycoplasm, fungus or virus - it doesn't matter. What does is how much one's body reacts on it. And, thanks God, SIRS can now R.I.P.

The problem is, every single tool developed for prompt recognition of sepsis and septic shock WILL cover some, probably quite significant number of patients who have no sepsis, no septic shock, and in fact no infection whatsoever. The newest QSOFA-3 bedside scale (different from SOFA -3, which requires more than just bedside assessment) looks like this :

any two or more of the following: altered mentation, respiratory rate ≥22 breaths/min, and systolic blood pressure ≤100 mm Hg means "sepsis suspected"

This would successfully cover patients with afib/RVR, anaphylaxis, ruptured tubal pregnancy and GI bleed. And although authors caution and state that this assessment should not be used as substitute for SOFA (and also critical thinking), there will invariably be those who hang 4 liters of NS and 3 antibiotics first and think second, the latter providing they are capable of any kind of intellectual activity.

1 Votes
Good questions :)

Sepsis should be defined as life-threatening organ dysfunction caused by a dysregulated host response to infection.

Septic shock should be defined as 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. Patients with septic shock can be clinically identified by a vasopressor requirement to maintain a mean arterial pressure of 65 mm Hg or greater and serum lactate level greater than 2 mmol/L (>18 mg/dL) in the absence of hypovolemia. Neither definition includes bacteriemia, viremia or any other microbiologic ctiteria.

The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)

Sepsis is, by definition, induced by infection - any infection. It can be a bacteria, mycoplasm, fungus or virus - it doesn't matter. What does is how much one's body reacts on it. And, thanks God, SIRS can now R.I.P.

The problem is, every single tool developed for prompt recognition of sepsis and septic shock WILL cover some, probably quite significant number of patients who have no sepsis, no septic shock, and in fact no infection whatsoever. The newest QSOFA-3 bedside scale (different from SOFA -3, which requires more than just bedside assessment) looks like this :

any two or more of the following: altered mentation, respiratory rate ≥22 breaths/min, and systolic blood pressure ≤100 mm Hg means "sepsis suspected"

This would successfully cover patients with afib/RVR, anaphylaxis, ruptured tubal pregnancy and GI bleed. And although authors caution and state that this assessment should not be used as substitute for SOFA (and also critical thinking), there will invariably be those who hang 4 liters of NS and 3 antibiotics first and think second, the latter providing they are capable of any kind of intellectual activity.

Wow! Thank you so much! Wealth of information here. I did a little digging after my above post and found the following definition: "Sepsis is the systemic response to infection and is defined as the presence of SIRS in addition to a documented or presumed infection." (Medline.) So this differs from your definition in that SIRS precedes organ dysfunction (if I'm understanding correctly.) I would consider SIRS to be basically a system-wide inflammatory response. The parameters you list above look more like SIRS than MODS (again, if I'm understanding correctly) which I would imagine is your point. So, 4L of NS and 3 antibiotics. My next question is have you seen a big increase in fluid volume overload and C. diff since this protocol was implemented? Again, thank you so much. I'm trying to solidify my understanding of the basics. Of course, nothing would help to solidify understanding like actual employment....

Specializes in ICU, LTACH, Internal Medicine.
Wow! Thank you so much! Wealth of information here. I did a little digging after my above post and found the following definition: "Sepsis is the systemic response to infection and is defined as the presence of SIRS in addition to a documented or presumed infection." (Medline.) So this differs from your definition in that SIRS precedes organ dysfunction (if I'm understanding correctly.) I would consider SIRS to be basically a system-wide inflammatory response. The parameters you list above look more like SIRS than MODS (again, if I'm understanding correctly) which I would imagine is your point. So, 4L of NS and 3 antibiotics. My next question is have you seen a big increase in fluid volume overload and C. diff since this protocol was implemented? Again, thank you so much. I'm trying to solidify my understanding of the basics. Of course, nothing would help to solidify understanding like actual employment....

According to my source above, SIRS is dead and not existing anymore.

Re. fluid overload - oh, yes, man. At least third of my hospital census since January consists of people with classic set of CHF, COPD, HTN, CRF III+ who came in ER with whatever and got 3 to 4 boluses, a liter each, for "dehydration" and "suspected sepsis", then a tankload of Lasix for "elevated BNP" and then good load of vancomycin for continuing "suspucion of sepsis". They got it all within a couple of hours, then dumped on me to fight fluid shifts, lytes derangement, ets. in the setting of their kidneys going to give up and whatever else with what they actually got there.

I tried to at least tell ER PAs not to dump vanco as tap water and got long lecture at 2 AM about WBCs being 12.200 "so important" because their criteria state 12 as cutoff. Lab norm cutoff 12.5.

:banghead:

Good questions :)

The problem is, every single tool developed for prompt recognition of sepsis and septic shock WILL cover some, probably quite significant number of patients who have no sepsis, no septic shock, and in fact no infection whatsoever. The newest QSOFA-3 bedside scale (different from SOFA -3, which requires more than just bedside assessment) looks like this :

any two or more of the following: altered mentation, respiratory rate ≥22 breaths/min, and systolic blood pressure ≤100 mm Hg means "sepsis suspected"

This would successfully cover patients with afib/RVR, anaphylaxis, ruptured tubal pregnancy and GI bleed. And although authors caution and state that this assessment should not be used as substitute for SOFA (and also critical thinking), there will invariably be those who hang 4 liters of NS and 3 antibiotics first and think second, the latter providing they are capable of any kind of intellectual activity.

Hi, Katie -

Isn't the QSOFA score meant to be used for patients with possible/suspected infection, though?

Copied from definition box found at the link (emphasis added):

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection.

Organ dysfunction can be identified as an acute change in total SOFA score ≥2 points consequent to the infection.

The baseline SOFA score can be assumed to be zero in patients not known to have preexisting organ dysfunction.

ASOFA score ≥2 reflects an overall mortality risk of approximately 10% in a general hospital population with suspected infection. Even patients presenting with modest dysfunction can deteriorate further, emphasizing the seriousness of this condition and the need for prompt and appropriate intervention, if not already being instituted.

In lay terms, sepsis is a life-threatening condition that arises when the body's response to an infection injures its own tissues and organs.

Patients with suspected infection who are likely to have a prolonged ICU stay or to die in the hospital can be promptly identified at the bedside with qSOFA, ie, alteration in mental status, systolic blood pressure ≥100 mm Hg, or respiratory rate ≥22/min

One can hope, anyway....?

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