Intraop Oliguria

[MoMoGesiologist]

Hey everyone,

So what do you guys think about intraop oliguria/anuria? Does it matter? How do you manage it?

Had a spine case on an obese gentleman, prone position. He stopped making urine during the case, down to 5cc an hour for a couple hours. Tried fluid boluses to no avail. His BPs and lactate were stable the whole time. Flipped him supine at the end of the case and he started making urine again. Was I just treating a number with the fluid boluses?

From what I've read, intubation, positive pressure ventilation, surgery all cause increased release of ADH and urine output drops and doesn't correlate with intraop or postop renal function. What do you think? Do you guys try to trouble shoot oliguria? And with what: crystalloid, albumin, Lasix, mannitol? Does it differ whether you're doing an ex lap or big vascular case or spine or cardiac bypass case?

I feel like if BP is adequate and lactate stable and the patient is euvolemic, and it's not a mechanical issue with the foley, I shouldn't chase urine output, but wanted to get the opinion of the hive mind!

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[deleted171991]

Does it matter? No. To me, it has about the same value as the CVPee.

As long as the MAP is well-maintained (above 70-75 mmHg of MAP - for normal intra-abdominal pressure, don't forget to correct for laparoscopy or prone position or other causes of IAH), blood loss is accurately replaced (preferably with blood), and there is no urine retention, urine output is just a matter of feel-good CYA "medicine". Why 70-75? The kidney actually likes higher pressures than the rest of the body. Adjust for hypertensives and fat people; think about their usual physiology and BP/IAP values.

Same goes for SIRS-y patients; inflammation increases fluid retention and more fluids only cause more inflammation in the affected organ(s), hence more fluid leak, hence more interstitial water, hence more interstitial pressure, hence poor perfusion. All surgical patients will have inflammation due to surgery, the bigger the insult the more inflamed the organ. That's where all those extra fluids will go in a patient who has decided not to make urine, just to piss you off.

I would forget the continuous maintenance LR infusion model (for hugely overblown ongoing evaporative surgical losses in the OR, or for last century resus in the ICU), the NPO fluid replacement model (for hugely overblown overnight fluid deficits - which are also far from 20+weight/hr) and any other crap that's not evidence-based. I use KVO + boluses to replace the losses I see, and I overshoot 30 ml/kg max (only for piss of mind - it's tough to watch olig-/anuria for hours and not to CYA).

 

[2Fast2Des]

Does this idea still apply to the post operative patient in the ICU? Common pages on call from nurses is about oliguria that we just keep on fluid'ing up. I feel a bit at a loss when they are significantly net positive, especially if they have been around for a while that people continue making positive. And then we play the diurese game with lasix

 

[Noyac]

Prone spine cases IMO are the most likely cases in which we see this. I don’t worry too much about it. Maybe I will give a little extra fluid just to be on the safe side but they always pee when you flip them over and wake them up. But if the case has been going on long and I want to it wrap up soon then I use it to my advantage at times. “Yo surgery dude, my pt isn’t peeing, can you hurry it up?"

 

[deleted171991]

Does this idea still apply to the post operative patient in the ICU? Common pages on call from nurses is about oliguria that we just keep on fluid'ing up. I feel a bit at a loss when they are significantly net positive, especially if they have been around for a while that people continue making positive. And then we play the diurese game with lasix

I don't chase urine output in the ICU, unless the patient needs to be diuresed for some reason. That's like ICU nurses bullying me as an intern to put patients on dopamine infusion, back when we already knew (even as interns) that we shouldn't do that.

The fact that you have to diurese after having given fluids suggests that you shouldn't have done the latter in the first place. Most periop patients do better if euvolemic; less edema and thus better perfusion at the surgical site. Plus earlier and safer extubation.

I give fluids if the patient is fluid-responsive, as measured by CO increase or evidence-based surrogates. I may give one liter to prove to the nurses that I am right, but that's where we stop.

In my experience, surgeon-directed fluid resuscitation (and intensive care) is a decade behind current science. I try not to go to war over minor stuff that won't change outcome.

 

[leaverus]

exactly. I don't worry about it too much but surgeons worry about it like crazy and they want us to do SOMETHING about it.

 

[fakin' the funk]

In my opinion and experience, intraop oliguria, despite adequate volume status, perfusion pressures, etc etc etc, is really common. The ADH/stress response/positive pressure ventilation explanation is the most reasonable, even though we can't prove it. It's one reason to not go crazy with IVF boluses unless you have some predictor of fluid responsiveness.

If it's a case where you do care about I/O balance (typically longer cases like thoracic, big abdominal case going to ICU, free flaps, head and neck, etc.) go ahead and give a little lasix. I've given as little as 2.5mg before, but 5 or 10 might just spring the leak you want to keep the pt from being 40ml/kg positive after a several-hours case. If you need a inopressor AND some diuresis, then dopamine certainly ticks both boxes. The more pee you get, the more you need to care about the K+.

 

[fakin' the funk]

Prone spine cases IMO are the most likely cases in which we see this. I don’t worry too much about it. Maybe I will give a little extra fluid just to be on the safe side but they always pee when you flip them over and wake them up.

Agreed. I wonder if somehow the neurohormonal state and/or renal perfusion is actually different in the prone position. (Not to mention a possible positional issue with the Foley draining properly while prone). When I have had longer cases with this euvolemic mystery oliguria and an immediate postop creatinine, there's no bump. My anecdotal experience.

 

[fakin' the funk]

Does this idea still apply to the post operative patient in the ICU? Common pages on call from nurses is about oliguria that we just keep on fluid'ing up. I feel a bit at a loss when they are significantly net positive, especially if they have been around for a while that people continue making positive. And then we play the diurese game with lasix

Early postop patients tend to be spongy and need volume.

POD2-3 patients tend to autodiurese, or if they don't, tend to need help to diurese.

This is a thing.

 

[vector2]

Does this idea still apply to the post operative patient in the ICU? Common pages on call from nurses is about oliguria that we just keep on fluid'ing up. I feel a bit at a loss when they are significantly net positive, especially if they have been around for a while that people continue making positive. And then we play the diurese game with lasix

Ffp is mostly right, but you have to take into account that your post-surgical ICU patient has likely undergone some major cardiac, thoracic, or abdominal procedure. The more extensive the surgery, the bigger the inflammation/basement membrane/capillary leak will be. In the first 24h I would not hesitate to give more fluid as long as surrogate markers of perfusion (CO, flotrac, lactate clearance, Echo VTI, cap refill, extremity warmth) are still responsive. If you've resuscitated to the point where there is no further response to fluid challenges, don't chase a borderline low UOP just because the nurse is bugging you. Most of these patients will lose the fluid on their own, but some will require lasix even after the inflammation has started to subside and body water partitioning has started to normalize. This does not make the strategy of early fluid, late lasix inappropriate for everyone.

 

[Laryngophed]

In my opinion and experience, intraop oliguria, despite adequate volume status, perfusion pressures, etc etc etc, is really common. The ADH/stress response/positive pressure ventilation explanation is the most reasonable, even though we can't prove it. It's one reason to not go crazy with IVF boluses unless you have some predictor of fluid responsiveness.

If it's a case where you do care about I/O balance (typically longer cases like thoracic, big abdominal case going to ICU, free flaps, head and neck, etc.) go ahead and give a little lasix. I've given as little as 2.5mg before, but 5 or 10 might just spring the leak you want to keep the pt from being 40ml/kg positive after a several-hours case. If you need a inopressor AND some diuresis, then dopamine certainly ticks both boxes. The more pee you get, the more you need to care about the K+.

I'm glad you guys are mentioning this. I take a fair bit of heat from surgeons (particularly our trauma/SICU guys) when they ask about UOP and I tell them it is low but no, I won't give another bolus. If the patient is euvolemic and has adequate MAPs, I trust that their internal regulation is smarter than I am. Or at least, that if I try to outsmart it, I won't be helping the patient. I think UOP is such a poor marker of resuscitation in most patients, it isn't really worth it to make decisions on in most cases. (Not all, but most.) And I feel like I see oliguria in prone cases all of the time. SO much that I'm more surprised when they aren't oliguric than when they are.

As the big cases, when I have one like that, I will hook up an EV-1000 (which certainly has its flaws) to get some numbers to help assess my interventions/lack of interventions.

 

[BigRedBeta]

The fact that you have to diurese after having given fluids suggests that you shouldn't have done the latter in the first place.

I don't know think that should be the take away necessarily. There are plenty of times that you have to rob Peter to pay Paul in moment and then play catch up on down the line. I'd much rather deal with a patient who has been overresuscitated rolling into the my PICU from the floor, the ED or the OR than the opposite.

I think UOP is such a poor marker of resuscitation in most patients

This is definitely true and strikes at the heart of the matter. If they're peeing great, all is well, but anything that takes an hour or two to get a proper sense of, is less than helpful. Nevermind the fact that depending on your co-morbidities, you might be further down the RIFLE scale than you realize pre-admission.

 

[deleted171991]

I don't know think that should be the take away necessarily. There are plenty of times that you have to rob Peter to pay Paul in moment and then play catch up on down the line. I'd much rather deal with a patient who has been overresuscitated rolling into the my PICU from the floor, the ED or the OR than the opposite.

Respectfully, that's because you don't deal with sick adults with cardiovascular, respiratory and renal comorbidities. Your repair cars that are still relatively new, where most things still work, while we deal with wrecks. You fix one thing, something else breaks.

Children behave differently than adults, respond differently to pressors and fluids, and are generally just a different animal, even in critical care.

Fluid overload is not good for the adult critical care patient. One should aim for a zero or negative balance by day 3, which means not overdoing IV fluids (too much) in the first two days.

 

[nimbus]

Respectfully, that's because you don't deal with sick adults with cardiovascular, respiratory and renal comorbidities. Your repair cars that are still relatively new, where most things still work, while we deal with wrecks. You fix one thing, something else breaks.

Children behave differently than adults, respond differently to pressors and fluids, and are generally just a different animal, even in critical care.

We've all learned over the years that a lot depends on what you're using for resuscitation. Blood and plasma=good. Crystalloid=bad.

I trained in the days when we were taught to replace x blood loss with 3x crystalloid until the hemacrit dropped to some ridiculous arbitrary number. Then start blood. The patients often ended up looking like s***. We caused a lot of harm. When we transitioned to an early transfusion strategy a few years ago I couldn't believe how much better the patients did. Say what you will about military medicine but kudos to them for innovating on this front.

 

[deleted171991]

We've all learned over the years that a lot depends on what your using for resuscitation. Blood and plasma=good. Crystalloid=bad.

Then we learned that colloid is as bad as crystalloid. Or crystalloid as good as colloid. And that we shouldn't give blood except to replace blood loss.

Btw, crystalloids are pro-inflammatory, and albumin does not improve outcomes. And all leak about the same.

This is about sepsis, mostly, but applies very well to every shock where there is a component of SIRS and vascular leak (e.g. postop): https://emcrit.org/wp-content/uploads/2015/07/Marik-Deresus.pdf

 

[deleted171991]

We've all learned over the years that a lot depends on what you're using for resuscitation. Blood and plasma=good. Crystalloid=bad.

I trained in the days when we were taught to replace x blood loss with 3x crystalloid until the hemacrit dropped to some ridiculous arbitrary number. Then start blood. The patients often ended up looking like s***. We caused a lot of harm. When we transitioned to an early transfusion strategy a few years ago I couldn't believe how much better the patients did.

I agree that it's ridiculous not to replace acute and/or ongoing blood loss with blood, unless the blood loss is small or the patient is tolerating it well (risks vs benefits).

I cringe when I see a patient who got 5-6L of crystalloids in the OR, and no PRBCs.

 

[nimbus]

@FFP

Would love your opinion on the following scenario.

80yo pt w PMH cad/DM/Htn/CRI who is septic/hypotensive/Hypovolemic/anemic (hct 28) patient coming to the OR for expl lap for presumed perf'd viscous without significant expected or ongoing blood loss. Crystalloid, colloid or PRBC and plasma? I get the feeling that they would do better with cells/plasma but I'm not up on the data.

 

[deleted171991]

@FFP

Would love your opinion on the following scenario.

80yo pt w PMH cad/DM/Htn/CRI who is septic/hypotensive/Hypovolemic/anemic (hct 28) patient coming to the OR for expl lap for presumed perf'd viscous without significant expected or ongoing blood loss. Crystalloid/colloid or blood?

That's an interesting scenario. It also depends on how bad the CAD and CRI are (i.e. can the patient tolerate fluid overload, can he be diuresed if needed?).

If you go by knee-jerk bureaucratic rules, you don't give blood. Assuming he looks hypovolemic and hypoperfused, I would look at his baseline Hgb. If it was 14 when he came to the hospital, he may get 1-2 units of PRBCs, depending how well he tolerates them (easier to do in the OR, no pushback from the blood bankers). I would also look at the fluid balance to make sure it's indeed hypovolemia, not fluid overload (and dilutional anemia) and CHF. A focused cardiopulmonary echo is a must in this type of patient.

Assuming he doesn't need blood, the question is crystalloid, colloid or pressor? The answer is most likely pressor (and/or possibly inotrope) after some crystalloid challenge (till I am satisfied he is not fluid-responsive). A colloid will give better SVR and BP numbers short-term, but it too will leak. I may try a bottle of 5% albumin, to see the response, if any (most likely nil, long-term). I don't like invasive monitors in everybody, but this is the guy that needs a monitor that can give me a good estimate of the cardiac output and SVR, especially if I don't have an echo.

P.S. I almost forgot. He also needs the Marik sepsis protocol, after informed consent. Huge upside, minimal downside.

 

[Psai]

I agree that it's ridiculous not to replace acute and/or ongoing blood loss with blood, unless the blood loss is small or the patient is tolerating it well (risks vs benefits).

I cringe when I see a patient who got 5-6L of crystalloids in the OR, and no PRBCs.

Had a patient getting tahbso who lost over 1.5 L. Ended up giving 5 Ls of LR. I was following hgb, started at 13 and ended up around 9-10. I had a bottle of albumin about to start and 2 units in the fridge but patient was rock solid so I decided to hold off. Do you think she should have gotten albumin or blood earlier? She ended up doing okay.

 

[deleted171991]

Had a patient getting tahbso who lost over 1.5 L. Ended up giving 5 Ls of LR. I was following hgb, started at 13 and ended up around 9-10. I had a bottle of albumin about to start and 2 units in the fridge but patient was rock solid so I decided to hold off. Do you think she should have gotten albumin or blood earlier? She ended up doing okay.

I too go by risks vs benefits. ASA 2 tolerating well the blood loos -> why risk transfusions? Still, even in those patients, when I get above 1 L (i.e. 25% blood loss), I become antsy.

I don't give albumin for blood loss. If crystalloids are not enough, it's blood they need.

 

[nimbus]

That's an interesting scenario. It also depends on how bad the CAD and CRI are (i.e. can the patient tolerate fluid overload, can he be diuresed if needed?).

If you go by knee-jerk bureaucratic rules, you don't give blood. Assuming he looks hypovolemic and hypoperfused, I would look at his baseline Hgb. If it was 14 when he came to the hospital, he may get 1-2 units of PRBCs, depending how well he tolerates them (easier to do in the OR, no pushback from the blood bankers). I would also look at the fluid balance to make sure it's indeed hypovolemia, not fluid overload (and dilutional anemia) and CHF. A focused cardiopulmonary echo is a must in this type of patient.

Assuming he doesn't need blood, the question is crystalloid, colloid or pressor? The answer is most likely pressor (and/or possibly inotrope) after some crystalloid challenge (till I am satisfied he is not fluid-responsive). A colloid will give better SVR and BP numbers short-term, but it will also leak. I may try a bottle of 5% albumin, to see the response if any. I don't like invasive monitors in everybody, but this is the guy that needs a monitor that can give me a good estimate of the cardiac output and SVR, especially if I don't have an echo.

Thanks for reply. It's a pretty common scenario. Assume he's chronically anemic. We often get these from icu on levophed titrated to MAP>70. Agree echo would be useful. If it reveals a small poorly filled ventricle and low SV what is the best thing to hang? It's really a practical and rhetorical question for everyone.

 

[nimbus]

Had a patient getting tahbso who lost over 1.5 L. Ended up giving 5 Ls of LR. I was following hgb, started at 13 and ended up around 9-10. I had a bottle of albumin about to start and 2 units in the fridge but patient was rock solid so I decided to hold off. Do you think she should have gotten albumin or blood earlier? She ended up doing okay.

You can get away with this in most patients but I think the same management strategy could lead to complications in old frail patients. Even young healthy patients look better immediately postop when they are resuscitated with blood instead of crystalloid. I probably would have given some blood and less crystalloid for a 1.5l blood loss.

 

[deleted171991]

Thanks for reply. It's a pretty common scenario. Assume he's chronically anemic. We often get these from icu on levophed titrated to MAP>70. Agree echo would be useful. If it reveals a small poorly filled ventricle and low SV what is the best thing to hang? It's really a practical and rhetorical question for everyone.

The answer depends on fluid responsiveness. If the patient is not fluid-responsive (i.e. the CO does not increase with preload), there is no sense in giving (much) more fluids (especially if already edematous). They will end up in the lung and belly and tissues, and worsen lung and kidney function, and the outcome. I may try some 5% albumin, because there is an entire (unproven) theory that it may help the glycocalyx in sepsis. But what that patient needs most is decreased vascular permeability (vitamin C and steroids?) and probably pressors.

It's tough. Many of these fluid-unresponsive people don't do well, unless they are started on pressors early and get lucky.

Blood is also a possibility, especially in the OR. I tend to give whatever I see an undeniable response to. I just don't keep doing something that obviously is not working, and try not to chase numbers (except for MAP and O2).

 

[DoctwoB]

What about the large body of evidence of poor outcomes independently associated with blood transfusion, from post op infection, thromboembolic events, to even things like development of metastatic disease after surgery of localized malignancy. IMO a blood transfusion is a lot riskier then most think. Obviously some patients need it, but in the above scenario where you have a stable patient that is compensating well for surgical blood loss, why take that risk?

 

[MoMoGesiologist]

What do you say to surgeons who want IV fluids titrated to urine output? Often vascular surgery and ENT flap cases is where I encounter this. They think pressors are bad for perfusion and insist on giving more mIVF and IVF boluses to goal UO 0.5mg/kg. In the ICU it kinda annoys me some surgical services are adamant about avoiding pressors and demand more fluids for low urine output, even when patients have gotten multiple liter boluses and UO and BP aren't responding and the patient looks like water balloons.

 

[nimbus]

What about the large body of evidence of poor outcomes independently associated with blood transfusion, from post op infection, thromboembolic events, to even things like development of metastatic disease after surgery of localized malignancy. IMO a blood transfusion is a lot riskier then most think. Obviously some patients need it, but in the above scenario where you have a stable patient that is compensating well for surgical blood loss, why take that risk?

The problem is that all fluids are associated with increasing complications. And longer and more complicated procedures with larger blood loss require more fluids. Association is not causation. And you have to replace with something. Pick your poison. And as FFP states, maybe the right answer in many instances is less fluid and more pressors.

As an example, I never transfuse during total hip replacement with certain surgeons who complete the operation in 60-70 min. I do occasionally transfuse with another surgeon who sometimes takes 2-3hrs for the same operation. It's not surprising to me that the latter surgeon has a higher infection rate. Blood transfusion may contribute to it. But it may also be because the joint is open for a much longer time and the instruments are also laying around for a much longer time with a greater risk of contamination.

 

[deleted171991]

What about the large body of evidence of poor outcomes independently associated with blood transfusion, from post op infection, thromboembolic events, to even things like development of metastatic disease after surgery of localized malignancy. IMO a blood transfusion is a lot riskier then most think. Obviously some patients need it, but in the above scenario where you have a stable patient that is compensating well for surgical blood loss, why take that risk?

I think we all agree that the patient compensating well for blood loss doesn't need blood.

 

[deleted171991]

What do you say to surgeons who want IV fluids titrated to urine output? Often vascular surgery and ENT flap cases is where I encounter this. They think pressors are bad for perfusion and insist on giving more mIVF and IVF boluses to goal UO 0.5mg/kg. In the ICU it kinda annoys me some surgical services are adamant about avoiding pressors and demand more fluids for low urine output, even when patients have gotten multiple liter boluses and UO and BP aren't responding and the patient looks like water balloons.

If they have a flap or they are vascular patients, they have a Doppler, so there's the answer (especially if my pulse ox has beautiful signal). As long as the flow is good, why chase the urine? And it's not like we never sneak in pressors without the surgeon's knowledge. I think the key is to promptly replace larger blood losses in these cases. I also try to be careful with my anesthetic level, which can also be a source of hypotension.

But, again, it's not worth going to war over 1-2L of fluid. I just don't make an ASA 4 patient a water balloon, at least not without significant resistance.

Of course, if things go wrong, the surgeon will blame anybody but himself. That comes with the job, so one must have a good answer for that (maintaining a good BP without pressors and a good peripheral perfusion in a warm patient definitely help).

 

[deleted171991]

tl;dr:

I try to look at the big picture, risks vs benefits, long-term outcome etc., for the particular patient. I don't have the CRNA mentality ("I want them to look good on paper while they are in the OR, and I don't care what happens after" - to paraphrase one). Uop is not sensitive or specific for bad outcomes, it's just one part of the picture, and a pretty unreliable one. Yes, having a good urine output is reassuring (while the opposite may bring up the spectrum of AKI) but, even in AKI, fluids beyond normovolemic and normotensive levels don't help.

Or, to paraphrase my PD, during my residency: if the drop in BP is due to decreased SVR, you don't treat it with fluids, you treat it with pressors.

 

[BigRedBeta]

Respectfully, that's because you don't deal with sick adults with cardiovascular, respiratory and renal comorbidities. Your repair cars that are still relatively new, where most things still work, while we deal with wrecks. You fix one thing, something else breaks.

Children behave differently than adults, respond differently to pressors and fluids, and are generally just a different animal, even in critical care.

Fluid overload is not good for the adult critical care patient. One should aim for a zero or negative balance by day 3, which means not overdoing IV fluids (too much) in the first two days.

No I totally agree, but as you pointed out in subsequent posts, there's a lot more nuance to management for patients of any age. I just disagreed with the sentiment that needing to diurese automatically meant that something had been done improperly days earlier.

And my post-op cardiac babies are easily comparable to the sickest adults, so it's not like I haven't seen some ****ty patients in my time.

 

[Noyac]

@FFP

Would love your opinion on the following scenario.

80yo pt w PMH cad/DM/Htn/CRI who is septic/hypotensive/Hypovolemic/anemic (hct 28) patient coming to the OR for expl lap for presumed perf'd viscous without significant expected or ongoing blood loss. Crystalloid, colloid or PRBC and plasma? I get the feeling that they would do better with cells/plasma but I'm not up on the data.

I would start with some blood on this pt. Then add some pressor as needed. Pt is 80yo. He will need some help.

 

[Noyac]

What about the large body of evidence of poor outcomes independently associated with blood transfusion, from post op infection, thromboembolic events, to even things like development of metastatic disease after surgery of localized malignancy. IMO a blood transfusion is a lot riskier then most think. Obviously some patients need it, but in the above scenario where you have a stable patient that is compensating well for surgical blood loss, why take that risk?

The pt is 80.

 

[Noyac]

Had a patient getting tahbso who lost over 1.5 L. Ended up giving 5 Ls of LR. I was following hgb, started at 13 and ended up around 9-10. I had a bottle of albumin about to start and 2 units in the fridge but patient was rock solid so I decided to hold off. Do you think she should have gotten albumin or blood earlier? She ended up doing okay.

No need for blood but I betcha she got some POD #1or 2. Especially, if she was a slug and not ambulatory much, complaining of fatigue, etc.

 

[Laryngophed]

tl;dr:

I try to look at the big picture, risks vs benefits, long-term outcome etc., for the particular patient. I don't have the CRNA mentality ("I want them to look good on paper while they are in the OR, and I don't care what happens after" - to paraphrase one). Uop is not sensitive or specific for bad outcomes, it's just one part of the picture, and a pretty unreliable one. Yes, having a good urine output is reassuring (while the opposite may bring up the spectrum of AKI) but, even in AKI, fluids beyond normovolemic and normotensive levels don't help.

Or, to paraphrase my PD, during my residency: if the drop in BP is due to decreased SVR, you don't treat it with fluids, you treat it with pressors.

I think you allude to the most important part of this. Do your damnedest to prevent damage, rather than trying to bandaid it with IVF. You can't protect every bean from AKI, or every branched striated myocyte from ischemia, but you do your best to minimize patient exposure to the things that cause them. I think use of semi-invasive monitors (like the EV-1000/Flo-Trac/flavor of the month for pulse wave analysis) and/or the TEE are helpful in patients undergoing long complex procedures or those that are critically ill. Sure, we can guess that hypovolemia is the problem, or decreased vascular tone, or whatever, or we can gather more info and make a more guided (maybe less blindly guided?) decision to intervene.

It isn't worth the argument over a liter of fluid in most people, especially when there is a component of hypovolemia, but a subtle reminder that while we are a team, *resuscitation in the operating room is driven by anesthesiologists in conjunction with surgical goals and not the other way around*, in the same way that I work to not change the surgical plan unless the patient's condition demands it.

*this really only works and is acceptable when you are choosing your resuscitation based on what is best for the patient overall, not the "make 'em look good on paper in the OR" because that stuff had better be going the way of the dodo bird.

 

[deleted171991]

No I totally agree, but as you pointed out in subsequent posts, there's a lot more nuance to management for patients of any age. I just disagreed with the sentiment that needing to diurese automatically meant that something had been done improperly days earlier.

And my post-op cardiac babies are easily comparable to the sickest adults, so it's not like I haven't seen some ****ty patients in my time.

Sorry if it came across as if I was underestimating the sickness level of some of your patients.

Regarding the need for diuresis on adult floors and SICUs: in 90% of the cases I see, it's due to fluid overload and accompanied by dyspnea, tachypnea, hypoxemia, "pulmonary (interstitial) edema" on CXR. A lot of people don't know where to stop, because they've been taught to treat hypotension and/or low urine output with fluids. Plus they run 100 ml/hr of "maintenance" fluids (without taking another look at the patient for 24 hours). That's just a sign of a lazy physician (especially if in the ICU).

If anything, I would forbid long-term fluid infusions beyond KVO; people drink in boluses, so that's how they should get their maintenance fluids, too (as 500 ml boluses infused as tolerated). Marik was a genius when he did something similar in his ICU (if I remember correctly).

 

[vector2]

P.S. I almost forgot. He also needs the Marik sepsis protocol, after informed consent. Huge upside, minimal downside.

Have you been doing this anecdotally on your patients? Was discussing this with an ICU pharmacist a few months ago and it does seem pretty low risk especially if the steroids are used judiciously.

 

[deleted171991]

Have you been doing this anecdotally on your patients? Was discussing this with an ICU pharmacist a few months ago and it does seem pretty low risk especially if the steroids are used judiciously.

I haven't had the chance yet (haven't been in the ICU since he came out with it). I find very little downside. Plus I am one of those guys who swears that high dose vitamin C decreases inflammation big time every time he has a cold.

He basically uses vitamin C to fix the endothelium, thiamine to decrease the chances that the vitamin C is degraded into oxalate (and possibly precipitate as stones), and stress dose-level hydrocortisone (also to decrease inflammation). Beyond the risk of stones (really minimal - the treatment takes a few days only), I think there are some people who get allergic reactions from thiamine.

 

[zzsleepytinizz]

Does it matter? Well, it depends. It depends on the situation; the surgical case, whether or not contrast is being used, positioning of the patient, whether or not PPV is being utilized, preoperative fluid status, renal function.

I think it is just important to understand that UOP is not a reliable marker of intraoperative fluid status. As stated earlier, surgical stress results in increase ADH levels, laparoscopy may result in decrease urine output secondary to vascular compression, same with PPV. It can go the opposite way as well such as with cold diuresis or DI. Its important to monitor UOP, but look at the whole picture by taking into account multiple markers for fluid status. I just don't think its good to say it doesn't matter at all.

 

[vector2]

Ran across this excellent presentation on dynamic vs static fluid status management including some of the techniques / devices out there and the validation of each. The bullet points are at the bottom.

Allison: Volume responsiveness in the ICU, the Lebowski way! | University of Maryland