Possible Sepsis

[Clipper1]

Ah, perhaps we're speaking past each other. I had in mind a BLS field situation as described by the OP. Obviously if you have more resources available (better means of airway management, pharmacotherapy, etc), they'll be more effective than any "stretch and squint" BLS solution. On our humble trucks the question is often how effective you can be with what's available, not what would be optimal if you had it.

Could you clarify what you're referring to by "flow"? I'm afraid I'm not catching your drift.
.

Flow does not necessarily equal FiO2. It seems in EMS a "high flow" device means giving an FiO2 of 1.0. The FiO2 is dependent upon the minute volume or tidal volume demand. A high flow device is designed to meet that demand.

If you actually know the limitations of the oxygen device or how it works you might be more effective at making the most appropriate decision for transporting this patient. Wouldn't teaching the basics of your equipment be more beneficial to the BLS EMT rather than throwing in stuff which will just exhaust the O2 tanks and not provide adequate FiO2 and/or flow to meet demand? Call ALS and/or a helicopter. Don't waste time running your O2 tanks dry on a futile delivery method. The headlines on your Med Directors desk will read "ran out of O2" rather than heroic rigging attempt of an O2 device. Trying to pull a MacGyver should not supersede education. Even MacGyver had a strong foundation academically and experience before rigging up things to blow up.

Of course, re-educating the EMT about the "shock position" and time of its usefulness would also be appropriate for a patient such as this.

 

[Handsome Robb]

I was one of the posters advocating running two lines....

The patient may have rales, but the patient also has near nothing in their vasculature. The wet lungs that you'd hear aren't from the patient being fluid overloaded; they're from a fluid shift caused by an increase in membrane permeability (or pneumonia...). The patient still needs fluid, and a lot of it. Pressors aren't going to do you much good if the patient is significantly fluid depleted.

You beat me to it. No point in "clamping the tank down" if there's nothing for it to clamp down on. The hypotension isn't a result from low cardiac output, it's a result of massive vasodilation and subsequent fluid shift into the interstitial space.

Dobutamine would not be a good option, in my opinion. It is purely an inotrope and this patient needs vasoconstriction. I may be mistaken but I believe dobutamine can also cause mild vasodilation as well but don't quote me. To be honest it isn't even indicated in this scenario. This isn't a cardiogenic shock, it's a distributive shock.

Levophed would be a good option. Wouldn't be surprised to see the hospital use neo-synephrine or vasopressin either.

Dopamine at high doses would be my only option. Start at 10 mcg/kg/min and work up from there.

Hell if you can work it a third line for the pressor would be cool but good luck. This patient is getting a CVC pretty soon after they get to the ER though.

Someone said it, this patient is potentially very far into septic shock and we are very far behind the 8-ball.

 

[Carlos Danger]

You beat me to it. No point in "clamping the tank down" if there's nothing for it to clamp down on. The hypotension isn't a result from low cardiac output, it's a result of massive vasodilation and subsequent fluid shift into the interstitial space.

Dobutamine would not be a good option, in my opinion. It is purely an inotrope and this patient needs vasoconstriction. I may be mistaken but I believe dobutamine can also cause mild vasodilation as well but don't quote me. To be honest it isn't even indicated in this scenario. This isn't a cardiogenic shock, it's a distributive shock.

Levophed would be a good option. Wouldn't be surprised to see the hospital use neo-synephrine or vasopressin either.

Dopamine at high doses would be my only option. Start at 10 mcg/kg/min and work up from there.

Hell if you can work it a third line for the pressor would be cool but good luck. This patient is getting a CVC pretty soon after they get to the ER though.

Someone said it, this patient is potentially very far into septic shock and we are very far behind the 8-ball.

I was one of the posters advocating running two lines....

The patient may have rales, but the patient also has near nothing in their vasculature. The wet lungs that you'd hear aren't from the patient being fluid overloaded; they're from a fluid shift caused by an increase in membrane permeability (or pneumonia...). The patient still needs fluid, and a lot of it. Pressors aren't going to do you much good if the patient is significantly fluid depleted.

There are different trains of thought about when to use pressors, and how much fluid should be given first. The EGDT protocol seems a bit unclear on it, assuming you are having a hard time reaching your CVP goal with fluid alone. (I do need to read the paper though; I'm familiar with the protocol but don't think I've ever read the actual paper). And of course there are all the problems that come along with massive fluid resuscitation - could some of those be avoided with earlier use of pressors? Some say that IVC fluid responsiveness and SVV are good indicators, but I'm not sure how well they've really been validated and SVV, while great technology, requires that the patient be intubated and mechanically ventilated. Obviously those aren't options in the field, anyway.

The way I have been trained, and what makes sense to me, and I think is quite applicable to the field, is to keep in mind that the root of the hemodynamic problem here is vasodilation and increased vascular permeability, and the lack of intravascular volume simply follows that. So in a patient who is severely hypotensive and has evidence of lack of perfusion to vital organs, I'd give a bolus of a couple liters quickly, reassess, and give a second bolus, reassess, and give a third, and keep doing that as long as improvements in perfusion were evident. Where this is a little different from what you often see is that if at any point the fluids don't seem to be improving things, I'd be quick to give a vasopressor, whereas many others want to give really massive fluid volumes before going to pressors. If I've given 4 liters of fluid and have seen no or only a very minimal improvement in pressure, and end-organ dysfunction is still suspected, I'd reach for the pressors for sure.

You are right about dobutamine not being indicated here. Think of dobutamine and milrinone as only being indicated for LV failure; though they work by different mechanisms, both increase inotropy and decreased afterload by arterial vasodilation. I'm don't think the literature shows a clear advantage of any 1 pressor over the others, but I'd rather stick to phenylephrine and avoid the b-stimulation of dopamine or norepi.

 

[Brandon O]

If you actually know the limitations of the oxygen device or how it works you might be more effective at making the most appropriate decision for transporting this patient.

My friend, that is my goal. But let's address the problem by conveying ideas, not just complaining about the problem.

Let me make sure I'm understanding your point... Are you suggesting that, for a sufficiently large minute volume, a device like a non-rebreather may be unable to provide a high FiO2 regardless of the flow rate at the regulator?

This is probably true. But with the maximum rates with typical equipment (40-60LPM with most wall-mounted regs I've seen -- there may be some that limit it lower), the shortfall should be pretty small. A hypothetical minute volume of 60 liters per minute would be quite impressive in any human being, sick or otherwise.

Obviously chasing a high concentration of inspired oxygen is not going to solve a septic patient's problems, any more than sheltering under your desk will protect you from a nuclear blast. But let's give everyone the benefit of the doubt and presume they realize this, since smart folks in this thread have already hit on the other major points such as rapid access to fluid resuscitation, pressors, and so forth. Once all that is in motion, it is very reasonable for a BLS provider to take steps (or at least have options available) to maximize the patient's oxygen tension.

 

[Clipper1]

My friend, that is my goal. But let's address the problem by conveying ideas, not just complaining about the problem.

Let me make sure I'm understanding your point... Are you suggesting that, for a sufficiently large minute volume, a device like a non-rebreather may be unable to provide a high FiO2 regardless of the flow rate at the regulator?

This is probably true. But with the maximum rates with typical equipment (40-60LPM with most wall-mounted regs I've seen -- there may be some that limit it lower), the shortfall should be pretty small. A hypothetical minute volume of 60 liters per minute would be quite impressive in any human being, sick or otherwise.

Obviously chasing a high concentration of inspired oxygen is not going to solve a septic patient's problems, any more than sheltering under your desk will protect you from a nuclear blast. But let's give everyone the benefit of the doubt and presume they realize this, since smart folks in this thread have already hit on the other major points such as rapid access to fluid resuscitation, pressors, and so forth. Once all that is in motion, it is very reasonable for a BLS provider to take steps (or at least have options available) to maximize the patient's oxygen tension.

I have to ask again why you would want an EMT to drain their oxygen tanks blasting a NRB mask at 40 liters. If a hospital has to resort to that by not having the appropriate equipment or KNOWLEDGE then that is a sad place to take any patient. Also with the suspicion this pt is septic and a NRB is all they have why waste time especially since other interventions are needed?

A sick pt on a ventilator can easily do over 30 l of MV and until other interventions happen.

 

[FLdoc2011]

Levophed is the go-to pressor in septic shock. From there you can also add on a fixed dose of vasopressin if still not meeting goals.

There is also a role for dobutamine in specific situations. If you're meeting all other goals (MAP > 65, CVP > 8) but SCVO2 is still low a d assuming not severely anemic, then that's where dobutamine can be added. Sepsis is not always a hyperdynamic/high cardiac output state, you can get myocardial depression in sepsis as well.

It was already brought up, but I encourage you to look up the early goal directed therapy and the surviving sepsis guidelines. There's a decent website with a lot of data including the most recent updates that were published in 2012.

More and more hospitals are implementing sepsis protocols/bundles that are specifically meant to resuscitate these patients in septic shock in the first 6 hours of recognition and frankly treating these patients in a time sensitive manner like they would a STEMI or stroke alert. We've even started calling sepsis alerts in the ED and on the floor to address this and focus attention on quickly intervening.

 

[Handsome Robb]

There are different trains of thought about when to use pressors, and how much fluid should be given first. The EGDT protocol seems a bit unclear on it, assuming you are having a hard time reaching your CVP goal with fluid alone. (I do need to read the paper though; I'm familiar with the protocol but don't think I've ever read the actual paper). And of course there are all the problems that come along with massive fluid resuscitation - could some of those be avoided with earlier use of pressors? Some say that IVC fluid responsiveness and SVV are good indicators, but I'm not sure how well they've really been validated and SVV, while great technology, requires that the patient be intubated and mechanically ventilated. Obviously those aren't options in the field, anyway.

The way I have been trained, and what makes sense to me, and I think is quite applicable to the field, is to keep in mind that the root of the hemodynamic problem here is vasodilation and increased vascular permeability, and the lack of intravascular volume simply follows that. So in a patient who is severely hypotensive and has evidence of lack of perfusion to vital organs, I'd give a bolus of a couple liters quickly, reassess, and give a second bolus, reassess, and give a third, and keep doing that as long as improvements in perfusion were evident. Where this is a little different from what you often see is that if at any point the fluids don't seem to be improving things, I'd be quick to give a vasopressor, whereas many others want to give really massive fluid volumes before going to pressors. If I've given 4 liters of fluid and have seen no or only a very minimal improvement in pressure, and end-organ dysfunction is still suspected, I'd reach for the pressors for sure.

You are right about dobutamine not being indicated here. Think of dobutamine and milrinone as only being indicated for LV failure; though they work by different mechanisms, both increase inotropy and decreased afterload by arterial vasodilation. I'm don't think the literature shows a clear advantage of any 1 pressor over the others, but I'd rather stick to phenylephrine and avoid the b-stimulation of dopamine or norepi.

This is a bad response but per protocol I have to give 2 L of NS before I can jump to dopamine. With that said, I see what you're getting at about basing pressors off of response to IVF boluses, it seems as though we're both still talking in the 2-4L range before starting a pressor. Also, where does the "least invasive way possible" come in to play, especially in the EMS environment when it comes to running pressors through peripheral lines that often are tough to obtain in these patients. If they are responding to fluids hold off on pressors until the hospital can establish a CVC and give it centrally rather than peripherally.

My question is, and this may sound contradictory to my above statement about "clamping down the container" but, as you said, knowing that the problem behind the hypotension is severe vasodilation would it not be better to start pressors sooner rather than later? Maybe in the 1-2L range rather than the 3-4L?

Another question I have is what are people's thoughts about antibiotics in the field? If I'm not mistaken they are part of EGDT, correct? Now I'm again going to contradict myself with this study, http://www.ncbi.nlm.nih.gov/m/pubmed/21883637/ , which shows no difference in mortality despite earlier antibiotic administration. The study looks at door-to-antibiotic time of patients that present to triage vs patients that come in via EMS. Not exactly what I was looking for but similar...

Sorry about all the contradictions. I'm kinda thinking out loud at this point from lots of different angles. I need to go to bed.

 

[RocketMedic]

We are getting levophed.

 

[Carlos Danger]

Levophed is the go-to pressor in septic shock. From there you can also add on a fixed dose of vasopressin if still not meeting goals.

There is also a role for dobutamine in specific situations. If you're meeting all other goals (MAP > 65, CVP > 8) but SCVO2 is still low a d assuming not severely anemic, then that's where dobutamine can be added. Sepsis is not always a hyperdynamic/high cardiac output state, you can get myocardial depression in sepsis as well.

It was already brought up, but I encourage you to look up the early goal directed therapy and the surviving sepsis guidelines. There's a decent website with a lot of data including the most recent updates that were published in 2012.

I am going to review those guidelines and read as much of the supporting literature as I can later today.

Regarding levo as the first line pressor, my understanding is that neo was left out of original recommendations due to concerns for excessive splanchnic vasoconstriction, but that subsequent studies have found no difference in outcome between the two. My protocols have always allowed for either, and it is also what we primarily used in SICU for sepsis, along with vaso. IME, neo seems generally easier to use and of course doesn't cause the significant tachycardia that you sometimes see with levo and dopa.

 

[FLdoc2011]

I am going to review those guidelines and read as much of the supporting literature as I can later today.

Regarding levo as the first line pressor, my understanding is that neo was left out of original recommendations due to concerns for excessive splanchnic vasoconstriction, but that subsequent studies have found no difference in outcome between the two. My protocols have always allowed for either, and it is also what we primarily used in SICU for sepsis, along with vaso. IME, neo seems generally easier to use and of course doesn't cause the significant tachycardia that you sometimes see with levo and dopa.

That's sort of the classic/theoretical concern with Neo though I'm not sure how clinically relevant/important that is.

Ultimately there just haven't been good large studies comparing vasopressors in general. Levo is currently holds a grade 1B rec in septic shock as it has been what was used in studies. I think in 2010 there was a head to head between Levo and dopamine with no outcome difference BUT more adverse effects from dopamine so we tend to not go to dopamine first.

I saw I think it was a small 2008 critical care article comparing levo to Neo with no outcome differences in hemodynamic parameters.

Ultimately I don't think Neo is a bad choice IF you're running into arrhythmias that may preclude the use of something with some beta agonist activity such as levo and dopamine. But ultimately it's not the initial recommended recommended pressor so we tend to stick with standard of care and current guidelines unless other clinical parameters preclude that.

Also, the first line resuscitation treatment is still fluids... THEN pressors if needed. Basically keep giving fluid until they're no longer fluid responsive or if fluid impairs gas exhange (pulm edema) and then if still hypotensive/hypoperfusing THEN add a pressor.

The trick is how do we tell when they ARE or ARE NOT fluid responsive..... Turns out CVP may not be as good as we thought it was but it's still in the guidelines so we use it, but there's also passive leg raise, arterial pulse variation, IVC diameter/variation, and other clinical parameters we're studying. So ultimately we just don't have a great way of monitoring or predicting responsiveness besides using a combination of the above tools.

Ultimately I'd rather over resuscitate someone with fluids and have to intubate/mechanically ventilate them for pulm edema than under resuscitate leave in a state of shock with possible permanent end organ damage. I can always get the fluid back off later once they're out of shock.

 

[Anonymous]

What is this patient's SpO2?

 

[Wes]

With a patient in extremis like this, why does it matter? Would you withhold oxygen if they had a high saturation? Any reason NOT to oxygenate a patient in septic shock?

 

[Carlos Danger]

The trick is how do we tell when they ARE or ARE NOT fluid responsive..... Turns out CVP may not be as good as we thought it was but it's still in the guidelines so we use it, but there's also passive leg raise, arterial pulse variation, IVC diameter/variation, and other clinical parameters we're studying. So ultimately we just don't have a great way of monitoring or predicting responsiveness besides using a combination of the above tools.

Ultimately I'd rather over resuscitate someone with fluids and have to intubate/mechanically ventilate them for pulm edema than under resuscitate leave in a state of shock with possible permanent end organ damage. I can always get the fluid back off later once they're out of shock.

Good point.

 

[Rialaigh]

Really? Most of the ones in this area do.

Yeah, no thermometers on any service I know of anywhere near here except critical care interfacility transport.

There is some evidence for early intubation, just to improve the hemodynamic status, but it only comes after a sequence of other actions in the EGDT algorithm.

I wouldn't consider the patient in the OP's scenario to be in the final stages, actually. First off, we don't know the time course. Second, nothing had been done yet. I wouldn't start getting pessimistic until we had given ≥ 2 liters, dropped a central line, check a CVP, dialed up the pressors, dumped in some broad-spectrum abx, and checked to see if there was any infection that could be cut or sucked out!

OP's scenario is entirely age and history dependant. If this is 75 year old grandma with a cardiac and respiratory history then yes, to make a broad generalization (not an absolute) this is is end stage sepsis, she's not recovering, she's not ever coming off the vent after you put her on, and sooner or later she's not going to make it. I would have to say a VAST minority of patients in this age group with any kind of "normal" american medical history would have any positive outcome.

Now if this is 42 year old female or male with limited medical history and otherwise relatively healthy it's a whole different ball game. Fact is most of the sepsis patients you pick up fall in the first category.

There will always be exceptions but its a very age and history dependant scenario.



I am very interested in solutions or initiatives for early goal directed therapy and what hospital ER's and EMS agencies can do to increase the recognition of sepsis in time to prevent permanent lasting effects (ultimately death).

 

[Handsome Robb]

Yeah, no thermometers on any service I know of anywhere near here except critical care interfacility transport.

Really? We carry temp-a-dots, regular oral thermometers like mom has, a temporal thermometer and the continuous temperature probe for the MRx.

Also have a pediatric fever protocol, it's bet specific, option for PO liquid Tylenol or PR suppositories. We don't treat fevers in adults.

I agree with your assessment about the different demographics of patients and their mortality in this scenario.

 

[DesertMedic66]

Really? We carry temp-a-dots, regular oral thermometers like mom has, a temporal thermometer and the continuous temperature probe for the MRx.

Also have a pediatric fever protocol, it's bet specific, option for PO liquid Tylenol or PR suppositories. We don't treat fevers in adults.

I agree with your assessment about the different demographics of patients and their mortality in this scenario.

We don't carry any kind of thermometers on the ambulance (county doesn't require us to). The fire departments do carry them (county requires it).

 

[Rialaigh]

Really? We carry temp-a-dots, regular oral thermometers like mom has, a temporal thermometer and the continuous temperature probe for the MRx.

Also have a pediatric fever protocol, it's bet specific, option for PO liquid Tylenol or PR suppositories. We don't treat fevers in adults.

I agree with your assessment about the different demographics of patients and their mortality in this scenario.

I wish we carried them, you kinda look like an idiot when you show up at the ER with a unresponsive nursing home patient and say "last seen normal last night, vitals are fine" and the ER gets a rectal temp of like 92 degrees or something.....happens pretty frequently....

Would love to have it for Tylenol admin for pedis as well

 

[Handsome Robb]

We don't carry any kind of thermometers on the ambulance (county doesn't require us to). The fire departments do carry them (county requires it).

That's kinda backasswards.

I wish we carried them, you kinda look like an idiot when you show up at the ER with a unresponsive nursing home patient and say "last seen normal last night, vitals are fine" and the ER gets a rectal temp of like 92 degrees or something.....happens pretty frequently....

Would love to have it for Tylenol admin for pedis as well

The only ones I really trust are the "mom" ones textually ", we use probe covers and cidex the hell out of them afterwards, or the MRx attachment. It actually works pretty well if you have a patient hold it under their tongue if they aren't to the point of putting in esophageally or rectally.

The temp-a-dots confuse my two brain cells and the temporal one always spits out anywhere from 97.8-98.4 99.9% of the time. You'll get a crazy low or high reading then 98.0 three times then a crazy high or low reading again. They just aren't consistent.

I think it's hilarious how much kids like our liquid Tylenol. They always are all about it. It smells nasty though.

 

[Rialaigh]

On the sepsis topic does anyone have any good articles about Levophed vs. Neo, I did a google search and waded through a few articles but I am hoping for something a little more well written and in depth. The hospital in my area uses Neo as first line (from what I have seen) for most ICU hypo tension. The ER generally uses dopamine for everything....

Just curious if there is research out there that you guys have stumbled across about the negative chronotropic effects of Neo and safe HR ranges for sepsis patients? I know thats delving more into ICU micro management of sepsis but I am curious.

 

[Carlos Danger]

On the sepsis topic does anyone have any good articles about Levophed vs. Neo

There is tons of stuff on Pubmed on the topic of pressors in shock, but the only two articles I found that compared the two drugs head to head clinically in humans were these. I think the pdf's for both of these were available for free:

Comparison of phenylephrine and norepinephrine in the management of dopamine-resistant septic shock. Indian J Crit Care Med. 2010 Jan;14(1):29-34

Phenylephrine versus norepinephrine for initial hemodynamic support of patients with septic shock: a randomized, controlled trial. Crit Care. 2008;12(6)

This article provides a good overview / review of the clinical usage of vasopressors & inotropes in septic shock:

Inotrope & Vasopressor Therapy in Septic Shock

I still haven't really gotten to the guidelines; been busy doing family stuff and studying for a pharm exam that is scheduled on my first day back from break.