Fluids and sepsis

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cbrons

cbrons

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Why does the EGDT/Surviving Sepsis guidelines say to run crystalloid up to a CVP of 8 mmHg? The normal CVP is like 1 or 2. And increasing CVP lowers venous return, at least that is what I learned in basic cardiovascular physiology.

Was reading and listening to the EMBasic episode on Sepsis and it says, "run in fluids like theres no tomorrow." In the show notes it even says that fluid loading should proceed to the target CVP even if it requires intubation for pulmonary edema.

This seems absolutely idiotic and make no sense to me at all.
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alpinism said:
I'll just add that CVP is useless and should not be used to guide fluid resuscitation.

Any educational resource that mentions using it is out of date (cough cough EM basic).
Click to expand...

I disagree with CVP being completely useless. Like everything else in resuscitation it certainly shouldn't be only piece of information being looked at. People who rely on only one thing (IE surgeons who only use urine output to guide fluid administration) are foolish. I think CVP has value when it comes to low numbers. If CVP is low the patient likely needs more fluid. Now if it is high then it is less useful. Doesn't necessarily mean the patient is completely volume replete because many things can drive up the CVP, but few things keep it low other than volume depletion.

In addition, watching the CVP wave itself and looking for respiratory variation, not even the absolute number, can be useful as well. Same idea as looking at the IVC with ultrasound

Sometimes I have been in situations where one of the few objective pieces of information I can get is CVP. As long as you know the limitations and put it in context with other factors it does have its usefulness
 
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cbrons said:
Why does the EGDT/Surviving Sepsis guidelines say to run crystalloid up to a CVP of 8 mmHg? The normal CVP is like 1 or 2. And increasing CVP lowers venous return, at least that is what I learned in basic cardiovascular physiology.

Was reading and listening to the EMBasic episode on Sepsis and it says, "run in fluids like theres no tomorrow." In the show notes it even says that fluid loading should proceed to the target CVP even if it requires intubation for pulmonary edema.

This seems absolutely idiotic and make no sense to me at all.
Click to expand...

You're making it way more complex than it needs to be. Just think of any type of shock as the pipe (the vessels), the pump (the heart) and the tank (the blood). In septic shock the vessels are dilated and leaky. To fill the vessels you need to load them with fluid. For someone whose hemoglobin is not critically low, chrystalloids work for this function and likely decrease viscosity making flow through the pipes easier.
 
Unfortunately, the CMS rule for core measures does have that 30mL/kg bolus for people with evidence of shock (low MAP, elevated lactate). The problem is, while we all think we know that elevated lactate is super specific for end organ dysfunction, there is evidence that other things also influence lactate, at least in other animal models.
And, the FEAST trial showed that willy nilly loading of fluids impacted mortality in the direction we don't want it to. I'm not fully on board with the glycocalyx model, but there's enough evidence out there that says we probably should be judicious about the fluids. All of us have seen the people weeping from everywhere after a few days in the ICU. Some guys (John Hinds et al) put people on lasix drips to prevent so much third spacing.
Unfortunately, just like with antibiotics in 6 hours for pneumonia, and blood cultures for the same, we have the government telling us to do something based on bad science and heightened emotions.
So yeah, dump fluid in them or something.
http://emcrit.org/blogpost/current-state-of-severe-sepsis-quality-measures/
 
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WildcatS11 said:
Good question good question.

Normal cvp is more like 4-8 , for a normal young healthy human it can be a bit lower.

The terrible, deadly part of early sepsis is due to basically vasoplegia. The infection at some point becomes widespread enough that there is a huge release of inflammatory mediators, cytokines, etc. this causes basically dilation of arteries and large veins. So you have the same amount of fluids in a now larger vessel, giving a lower MAP.

The goal is to restore that circulating volume quickly to avoid loss of blood to critical organs. If the MAP remains low, you're risking injury to kidney, liver, heart, gut, brain. Restoring volume quickly and adequately prevents that.

The point they are trying to make is that in true septic shock, your goal should be to get that CVP up to 8 with fluids no matter what. If you have accurate cvp measurements, you probably won't hit that endpoint of Pulm edema/intubation. But often we don't have that. One of my old critical care attending a used to berate us for starting pressers before a patients O2 requirement jumped. I.e. Don't start pressure until fluids are max'ed and you're pushing into the Pulm edema stage.

Last point - CVP basically is venous return. They're mostly interchangeable for our daily use in dealing with patients.
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The normal CVP is not that high. And CVP is not venous return. VR is mean systemic filling pressure minus CVP divided by RVR (as the review article in the third post states).

Vasoplegic shock would imply that the problem has to do with a lack of resting sympathetic tone (probably from endothelial damage). Therefore what would make the most sense is the use of vasopressors rather than dumping a lake full of saline into them.

I would also think fluid responsiveness should be measured beforehand, since something like 50% of patients with sepsis are non-responders.
 
Dude, as the saying goes, "keep it simple, stupid". Early fluids and antibiotics. If their BP is not responding after what you believe to be an adequate amount of fluids, start that levophed drip and throw in a CVC and call the ICU. Don't worry about BS like CVP and SvO2 or whatever other metric that hasn't been shown to improve outcomes by closely monitoring.
 
What about using colloids when and where you can, rather than just crystalloids? Course, it was nice when we had more openness to hemodynamic indices, as you have after say OHS or other serious surgeries. SVRI can certainly help with fluid guidance, no?
 
engineeredout said:
I disagree with CVP being completely useless. Like everything else in resuscitation it certainly shouldn't be only piece of information being looked at. People who rely on only one thing (IE surgeons who only use urine output to guide fluid administration) are foolish. I think CVP has value when it comes to low numbers. If CVP is low the patient likely needs more fluid. Now if it is high then it is less useful. Doesn't necessarily mean the patient is completely volume replete because many things can drive up the CVP, but few things keep it low other than volume depletion.

Sometimes I have been in situations where one of the few objective pieces of information I can get is CVP. As long as you know the limitations and put it in context with other factors it does have its usefulness
Click to expand...

Based on what data?

http://www.aaemrsa.org/UserFiles/MayJune2013RJR-print.pdf

"Of the five trials that addressed CVP and its relation to the measured blood volume, the pooled correlation coefficient was 0.16. The pooled correlation coefficient between change in CVP and change in cardiac index (CI) following a fluid challenge was 0.11. Based on the findings above, Marik et al. concluded that there was no association between CVP and blood volume, and that CVP did not predict fluid responsiveness."

Personally I'd much rather use dynamic measures to assess volume status rather than static ones.
 
cbrons said:
The normal CVP is not that high. And CVP is not venous return. VR is mean systemic filling pressure minus CVP divided by RVR (as the review article in the third post states).

Vasoplegic shock would imply that the problem has to do with a lack of resting sympathetic tone (probably from endothelial damage). Therefore what would make the most sense is the use of vasopressors rather than dumping a lake full of saline into them.

I would also think fluid responsiveness should be measured beforehand, since something like 50% of patients with sepsis are non-responders.
Click to expand...

You are correct. Flow = pressure/resistance. The problem is that measuring a patient's mean systemic filling pressure is easier said than done. A prospective measure of fluid responsiveness is exactly what we're looking for. However, given that:
a) We currently lack a perfect prognosticating test.
b) Taking all comers, fluids are less harmful than pressors.
It makes sense to start with a fluid challenge, then move on to more invasive measures once it's apparent that fluids won't fix the problem.

Whether that bolus is 250cc or 3000cc is another question. Throwing 3L at everyone with SIRS is madness.
 
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Going off topic

The 30mL/kg thing is driving me nuts...

Had a nice old lady with clear aspiration pneumonia the other day, choking on food 3d prior and developing worsening cough over the next 3d, hx of bad aspiration pneumonia some months prior as well... Also hx of CHF. Low grade fever, with RR 24 on arrival, mildly hypoxic (responded to 4L NC), and her CBC shows 11% bands on a WBC of 8k, and lactate 2.4.

Her HR is 75. Her BP is 145/85.

So she has Sepsis (infection, 2 SIRS [bands, RR... her fever wasn't high enough]).

Not only that, by the SEP-1 measure she has SEVERE SEPSIS (lactate >2 = end organ failure).

So she needs not only a mandatory 30mL/kg bolus (you REALLY want me to hit her with 2.5L NS fast?) and BROAD antibiotics (not CLINDA alone).

Seems silly, eh?

I mean, at the BEST I have to fill my MDM with a bunch of caveats "appears fluid overloaded clinically, normal hemodynamics, 30mL bolus will likely cause pulmonary edema and thus trigger mechanical ventilation, as such will hold fluids and closely monitor instead" and HOPE that whomever is doing the chart abstraction months later accepts this justification and doesn't "fail" me on my protocolized treatment of "severe sepsis".
 
alpinism said:
Based on what data?
http://www.aaemrsa.org/UserFiles/MayJune2013RJR-print.pdf
"Of the five trials that addressed CVP and its relation to the measured blood volume, the pooled correlation coefficient was 0.16. The pooled correlation coefficient between change in CVP and change in cardiac index (CI) following a fluid challenge was 0.11. Based on the findings above, Marik et al. concluded that there was no association between CVP and blood volume, and that CVP did not predict fluid responsiveness."
Click to expand...
2 posts in 2 days of Paul Marik.
I told you, he knows his ****.
 
Dr.McNinja said:
2 posts in 2 days of Paul Marik.
I told you, he knows his ****.
Click to expand...
Well having done some research, I found this little gem from the recent SMACC conference. It was a panel discussion with John Myburgh, Paul Marik, Scott Weingart, and others:



Starting at 45:15, Weingart gets to the topic of fluids and sepsis and Dr. Marik discusses the concept of iatrogenic salt-water drowning, which I think is quite apt and powerful.
 
Janders said:
Going off topic

The 30mL/kg thing is driving me nuts...

Had a nice old lady with clear aspiration pneumonia the other day, choking on food 3d prior and developing worsening cough over the next 3d, hx of bad aspiration pneumonia some months prior as well... Also hx of CHF. Low grade fever, with RR 24 on arrival, mildly hypoxic (responded to 4L NC), and her CBC shows 11% bands on a WBC of 8k, and lactate 2.4.

Her HR is 75. Her BP is 145/85.

So she has Sepsis (infection, 2 SIRS [bands, RR... her fever wasn't high enough]).

Not only that, by the SEP-1 measure she has SEVERE SEPSIS (lactate >2 = end organ failure).

So she needs not only a mandatory 30mL/kg bolus (you REALLY want me to hit her with 2.5L NS fast?) and BROAD antibiotics (not CLINDA alone).

Seems silly, eh?

I mean, at the BEST I have to fill my MDM with a bunch of caveats "appears fluid overloaded clinically, normal hemodynamics, 30mL bolus will likely cause pulmonary edema and thus trigger mechanical ventilation, as such will hold fluids and closely monitor instead" and HOPE that whomever is doing the chart abstraction months later accepts this justification and doesn't "fail" me on my protocolized treatment of "severe sepsis".
Click to expand...


CMS measures you only need the fluid bolus for lactate >4.0 or for septic shock (defined as any one episode of MAP <65). Sounds like your lady had severe sepsis (unless she got hypotensive), which needs abx <90 min after cx's, lactic w/ repeat lactic. Also, standard aspiration pna tx (Rocephin + Clinda for pna) would cover broad-spectrum, but honestly if aspiration, might as well whip out Zosyn.

BTW, you can't caveat your way out of CMS measures (even if DNR, CHF, or whatever)--only way out is to have pt or family refuse. POLST forms will help for this.

These sepsis measures suck, but it's important you make them not suck more by miss-interpreting what you need. Highly recommend you work with your hospital committees to make less terrible, and educate staff. Our admin thought we needed fluids for severe sepsis (which used to be called regular sepsis or SIRS 3 months ago) b/4 we showed them measures.

upload_2016-1-25_6-37-55.jpeg
 
Lol, of course I was looking at the draft memo about the sepsis criteria which had the same error (fluid bolus for severe sepsis, not septic shock). Fixed.

I would still argue in a relatively well lady with community aspiration Clindamycin alone provides adequate coverage. I love zosyn but our stocks are low.

At least I didn't need to do a CVP on her.
 
Janders said:
Lol, of course I was looking at the draft memo about the sepsis criteria which had the same error (fluid bolus for severe sepsis, not septic shock). Fixed.

I would still argue in a relatively well lady with community aspiration Clindamycin alone provides adequate coverage. I love zosyn but our stocks are low.

At least I didn't need to do a CVP on her.
Click to expand...

Maybe I missed something above, as I didn't read the whole thread...but it seems like you are saying clinda only for CAPna. What about GNRs?

---

Also, remember Unasyn. Unless there is Pseudomonas risk.

HH
 
Have never, and will never use CVP, plenty of evidence out there stating it is useless.

That being said, I am judicious with fluids if BP is good. We were told that as long as we documented in the chart why we were deviating from CMS's guidelines we would be ok, so that's what I have been doing.
 
🙂

[Intravenous fluids — In patients with sepsis, intravascular hypovolemia is typical and may be severe, requiring rapid fluid resuscitation.

Volume — The optimal volume of resuscitative fluid is unknown. Several studies of early goal directed therapy reported intravenous fluid infusions targeted to physiologic endpoints and resulted in volumes ranging from 3 to 5 liters [18-20]. The volume of fluid that was administered within the initial six hours of presentation was targeted to set physiologic endpoints (eg, mean arterial pressure). While an early study of early goal-directed therapy (EGDT) reported mean infusion volume in the first six hours of 3 to 5 liters [18], later trials reporting mean infusion volumes of 2 to 3 liters [19,20]. Thus, rapid, large volume infusions of intravenous fluids are indicated as initial therapy for severe sepsis or septic shock, unless there is coexisting clinical or radiographic evidence of heart failure. Suggested targets for fluid resuscitation are discussed separately. (See 'Goals of initial resuscitation' below.) ]

http://www.uptodate.com/contents/ev...t-of-severe-sepsis-and-septic-shock-in-adults

Literature review current through: Dec 2015. |This topic last updated: Jan 08, 2016.
A number of the references listed are close to being within 5 years.
 
jl lin said:
🙂

[Intravenous fluids — In patients with sepsis, intravascular hypovolemia is typical and may be severe, requiring rapid fluid resuscitation.

Volume — The optimal volume of resuscitative fluid is unknown. Several studies of early goal directed therapy reported intravenous fluid infusions targeted to physiologic endpoints and resulted in volumes ranging from 3 to 5 liters [18-20]. The volume of fluid that was administered within the initial six hours of presentation was targeted to set physiologic endpoints (eg, mean arterial pressure). While an early study of early goal-directed therapy (EGDT) reported mean infusion volume in the first six hours of 3 to 5 liters [18], later trials reporting mean infusion volumes of 2 to 3 liters [19,20]. Thus, rapid, large volume infusions of intravenous fluids are indicated as initial therapy for severe sepsis or septic shock, unless there is coexisting clinical or radiographic evidence of heart failure. Suggested targets for fluid resuscitation are discussed separately. (See 'Goals of initial resuscitation' below.) ]

http://www.uptodate.com/contents/ev...t-of-severe-sepsis-and-septic-shock-in-adults

Literature review current through: Dec 2015. |This topic last updated: Jan 08, 2016.
A number of the references listed are close to being within 5 years.
Click to expand...
Yes... it is well known that there is intravascular volume contraction in septic shock. The problem is that most of the infused crystalloid does not remain intravascular.
 
cbrons said:
Yes... it is well known that there is intravascular volume contraction in septic shock. The problem is that most of the infused crystalloid does not remain intravascular.
Click to expand...

Yes. Seen it in many patients over the years. In some places, we would measure, among other things, colloidal osmotic pressure, and based on the particulars of the whole, give some preference to colloidal based fluid replacement. It can work like a charm--depending..., but obviously that will depend upon how far gone the state of sepsis is in the individual, the related vascular and organ function, and how well they are responding to pressors.

BTW, the general problem with crystalloids not remaining intravascularly is an issue for many patients post-operatively and with other states. When possible, anecdotally, I can say that when blood products or other colloids can be carefully given, it can make a difference. It's finding the "right recipe" for the individual patient. Also, although pressors may be needed and helpful, I have also seen them cause a lot of damage as well.
 
jl lin said:
Yes. Seen it in many patients over the years. In some places, we would measure, among other things, colloidal osmotic pressure, and based on the particulars of the whole, give some preference to colloidal based fluid replacement. It can work like a charm--depending..., but obviously that will depend upon how far gone the state of sepsis is in the individual, the related vascular and organ function, and how well they are responding to pressors.

BTW, the general problem with crystalloids not remaining intravascularly is an issue for many patients post-operatively and with other states. When possible, anecdotally, I can say that when blood products or other colloids can be carefully given, it can make a difference. It's finding the "right recipe" for the individual patient. Also, although pressors may be needed and helpful, I have also seen them cause a lot of damage as well.
Click to expand...
Colloids don't help based on studies. No matter how much we want them to, they just don't.
 
Dr.McNinja said:
Colloids don't help based on studies. No matter how much we want them to, they just don't.
Click to expand...

Albumin may be of some benefit very early on in sepsis if you believe John Myburgh, but its efficacy has nothing to do with intravascular colloid osmotic pressure but more likely that it is an essential component for proper function of the endothelial glycocalyx. In fact, the Starling forces most especially intravascular oncotic pressure are probably irrelevant. http://lifeinthefastlane.com/ccc/glycocalyx-in-critical-illness/
 
Dr.McNinja said:
Colloids don't help based on studies. No matter how much we want them to, they just don't.
Click to expand...

OK, but not at all what I have witnessed with the benefit of hemodynamic indices as well as other parameters, such as u.o., etc. Of course, I was not talking about HES or starch-based agents. More favorable results seen with albumin or blood products, when there is some indication for use. Seems like some folks are more open than others to their use.

Are not septic states, in particular, a game of time--as in phase, which affects treatment approach? Add on other issues, and well.

Sounds like this poor fellow was pretty far along into sepsis.
http://www.dailymail.co.uk/news/art...lapsing-just-THIRTY-MILES-finishing-line.html

(Why would anyone attempt to "do Antarctica" alone?) Sad.
 
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Which trial did the 30 ml/kg bolus come from? I can't seem to find it. All I see is the good ol' 2 liters.
 
pianoman511 said:
Surviving sepsis guidelines - http://www.survivingsepsis.org/sitecollectiondocuments/bundle-3-hour-step4-fluids.pdf
Click to expand...

Sorry, I should have been more clear. I wasn't asking for the guidelines. I was asking for the evidence behind it. Because, after looking at the protocols for these studies, there is no mention of any 30ml/kg fluid bolus.

Here's what I can deduce:
  • The ARISE trial set forth a goal of 20ml/kg bolus within their protocol. This number makes historical sense to me, as it seems in line with pediatric care.
  • The PROCESS trial had the 2 liter bolus written into their protocol. However, after a post hoc analysis, it seems most everyone got a 30ml/kg bolus across the boards.
Thus the 30ml/kg IVF bolus was born... I just think it's funny that after multiple RCTs were done, the guidelines are not in line with the trials' protocols, Instead they go by post-hoc analysis. Am I reading this right?

Here's the data: TOP of the table on page 17/21.
http://www.nejm.org/doi/suppl/10.1056/NEJMoa1401602/suppl_file/nejmoa1401602_appendix.pdf
 
You are correct based on my reading as well. Both studies made a point to state the map and lactate clearance goals which just happened to coincide with the endpoint of 30.
 
Goal-Directed Resuscitation for Patients with Early Septic Shock
The ARISE Investigators and the ANZICS Clinical Trials Group

In conclusion, the results of our trial show that EGDT, as compared with usual resuscitation practice, did not decrease mortality among patients presenting to the emergency department with early septic shock. Our findings suggest that the value of incorporating EGDT into international guidelines as a standard of care is questionable.
 
Janders said:
my RNs love it when I order 2047.23mL to hit that 30mL/kg goal
Click to expand...

Just add the volume used to reconstitute your antibiotics and you're there after 2L.*


*I'm not sure that would actually work.
 
Also, there is this re: severe sepsis:

"The results suggested a trend toward reduced 90-day mortality in severe sepsis patients resuscitated with albumin compared with crystalloid and saline. Moreover, the use of albumin for resuscitation significantly decreased the 90-day mortality in septic shock patients.

Crit Care. 2014; 18(6): 702.
Published online 2014 Dec 15. doi: 10.1186/s13054-014-0702-y
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4284920/
 
TooMuchResearch said:
You may find this shocking, but unless it's one of our better nurses, the patient you're describing probably gets 3 L instead of 2 or 2.047.

I know you don't find it shocking.
Click to expand...

I'm shocked, shocked to find that gambling is going on in here!
 
cbrons said:
I highly doubt this, especially if we're talking about Levophed. AKI and ARDS are quite common and likely related to fluid overload in the vast majority of cases.
Click to expand...

The claims that norepinephrine is safer than crystalloid, and that crystalloid commonly causes AKI are both pretty contrary to received wisdom. Now, received wisdom is often proved wrong but it shouldn't be carelessly discarded.

Can you provide some evidence in support?
 
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WilcoWorld said:
The claims that norepinephrine is safer than crystalloid, and that crystalloid commonly causes AKI are both pretty contrary to received wisdom. Now, received wisdom is often proved wrong but it shouldn't be carelessly discarded.

Can you provide some evidence in support?
Click to expand...
Here's one on why, maybe, we really shouldn't be using NS for fluid replacement.

http://www.ncbi.nlm.nih.gov/pubmed/23073953
 
Siggy said:
Here's one on why, maybe, we really shouldn't be using NS for fluid replacement.

http://www.ncbi.nlm.nih.gov/pubmed/23073953
Click to expand...

All the end points that really matter weren't statistically significant. If it didn't lead to long term dialysis, longer length of stay, or increased hospital mortality - there is something more to the story. That study threw some crap at the wall and looked for whatever would stick statistically. It reminds me of all the useless proteomic nonsense being published these day - can't go to a poster hall without half of it being filled with that crap.
 
jdh71 said:
All the end points that really matter weren't statistically significant. If it didn't lead to long term dialysis, longer length of stay, or increased hospital mortality - there is something more to the story. That study threw some crap at the wall and looked for whatever would stick statistically. It reminds me of all the useless proteomic nonsense being published these day - can't go to a poster hall without half of it being filled with that crap.
Click to expand...

Where's this fairy tail location where dialysis (even 1 session) is free of costs and complications?
 
That study is interesting, and I was not previously aware of it, but it is far from showing pressors to be safer than crystalloid. I liked Siggy's post, because it din't overstate the conclusion.

However it's no surprise that when you took more experienced clinicians giving carefully considered fluids, and compared that to trainees reflexively giving everyone saline boluses, that the first group did better. If anything, I'd post that study in the thread on ACEP discussing NP equivalence...except that NP's weren't part of that study. Or post it in a thread on the wisdom of CMS-mandated sepsis bundles.
 
Siggy said:
Where's this fairy tail location where dialysis (even 1 session) is free of costs and complications?
Click to expand...

That place doesn't exist.

But it also doesn't actually matter to my point. There is something odd when making a case for increased risk for renal harm if there is no actual long term end point issues especially when making the claim from an observational study.
 
I wondered in here after a search looking for what I call the "CVP is horse****" study so I can hand it to my residents in the morning.

The problem, as always, is that EBM in the ICU is largely nonsense because of what it always has to restrict in order to make any kind of legitimate case for a real statically difference in a single variable. I'd say based on my experience patients need fluid . . . Until they don't. And too much fluid also kills people per a good amount of the same kind of studies I just made the case were kind of garbage. So. Yeah. Good luck. And try to do no harm. At the end of the day even being "scientific" about it, putting in a swan didn't save anyone anymore than anything else. It's all clinical gestalt. All of it. Be aware. Be aggressive early. Give abx. And for the love of all things good and holy don't check a CVP. I mean you can. But most of us will laugh at you in the doc's lounge.
 
jdh71 said:
All the end points that really matter weren't statistically significant. If it didn't lead to long term dialysis, longer length of stay, or increased hospital mortality - there is something more to the story. That study threw some crap at the wall and looked for whatever would stick statistically. It reminds me of all the useless proteomic nonsense being published these day - can't go to a poster hall without half of it being filled with that crap.
Click to expand...

What is this proteomic nonsense that you speak of?
 
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