Question regarding fluids and hemodynamics/case

[CavGas]

Hello to the respected forum of anesthesia..

Had a case recently and I was thinking about it. Pt was 80 y.o. Male with preexisting HTN on ACE-I, mild dementia, overweight ( 100kg at around 1,80) and pertinent surgical Hx of repaired ing hernia 2 years prior. Had no bowel movement over 3 days and was posted for exlap for possible mechanical SBO. Labs were wnl, except Hb which was 9, Cr of 4.0, BUN of 100 ( prerenal AKI? )
On presentation he was in apparent distress, looking septic HR 110 in Afib, BP 170/90, Spo2 95% on Venturi 50%, tachypneic with a hugeee abdomen. Anyways we put an aline, induce, CVC and surgery proceeds. I started some fluids and give around 3L for presumed deficit then I continued at 1-2ml/kg/hr. Oxygenation remained acceptable at an FiO2 55%, PEEP of 8, Peaks around 30-35 which subsided to 23-25 after abdomen was opened. Urine output was at ~500cc for the first hr Patient was stable with HR in 80's ( Afib so no PPV, SPV guidance), normal MAP's around 90. Surgery went on because apparently pt had a tumor in right colon that had caused a hole in the colon with spillage of bowel content so they had to resect it and they did an anastomosis( no colostomy?). Anyway I was alone in the first hour, then my attending came back and told me why was I withholding the fluids, that the patient was profoundly hypovolemic due to ileus so we started giving more LR+NS . At around the 6L mark patient started to look worse with norepi requirement and a little worsening oxygenation. I think we gave 2 more liters after that, and the surgery was coming to a close. Patient now had a 2.5-3ug/kg/min norepi req + bumps of epi to sustain MAP>65. Oxygenation was PaO2 of 90 at 70% FiO2 with the same PEEP.

Of course we didn't extubate and my attending considered the pt terminal due to the huge pressor requirement. Anyways I shifted the pt to ICU and called it a night since it was 6am.
48 hrs later I went to check on the pt and to my big surprise he is extubated on a venturi 40% with minimal norepi req. I asked the fellow about mgmt, echo?. He said they gave some more fluids but also put the pt on CVVHD for worsening hyperkalemia and reduced urine output and of course gave broad spectrum Abx. No echo done yet ( pt only got a single dose of ciprofloxacin in the ED ). Then I lost the pt since I was rotating at a different hospital.




I am having a thought and so far none of the answers of my attendings satisfied my curiosity. So, we all know that fluid management should be a thoughtful process and overload can have deleterious effects on ileus, LOS, wound healing etc, but what I wanted to know is : Is it possible to cause iatrogenic cardiogenic shock with fluid administration in a patient like this with possible untreated diastolic heart failure, but also in a patient without any hint of heart failure? Or was the deterioration due to sepsis that was improved with proper Abx? Actual hypovolemia that needed more fluids?

Thanks in advance for reading the post. Any wisdom is really appreciated!

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[Hork Bajir]

Very hard to know what happened here, any answers you get will be pure conjecture (despite the confidence with which some ppl will state them). This would have been a good case for a rescue echo in the OR.

To answer your question, it is relatively easy to cause R heart failure with acute volume overload. Acute LV systolic dysfunction as a result of volume loading would be less common. You can certainly get an elevated wedge pressure, pulmonary edema, etc ... But it’s not like your LVEF drops substantially. However the RV commonly can dilate and fail with acute dramatic increases in venous return. Add on top of that some component of abdominal compartment syndrome with ischemia/reperfusion of the viscera, probably some vasodilator shock from abdominal sepsis, PPV, anesthesia, and all bets are off.

With all that being said, do you have any evidence to suggest heart failure as the cause of the hemodynamic instability? Was the patient cold and clammy, or were the legs warm? Unless there’s some other aspect to the story, or pre-existing RV dysfunction, my money is on the belly as the cause for the hypotension. Lots of transient endotoxins released when the ischemic gut is reperfused and the peritoneal space is contaminated, leading to profound vasoplegia. A day or two of abx, source control, and correction of the acidosis w/ CVVH will do wonders for that, and patients can really turn around quickly.

 

[GassYous]

I don't give more than 2 liters usually because why waste time changing the bag? Also it's hard to give that much fluid when the case is less than 2 hours long. I've heard of patients getting significantly fluid overloaded with just 2 L rum quickly in trendelenburg position.

 

[JiPo]

Does your institution place an Aline and a central line on a routine basis for cases like this? You presented a case as a typical SBO undergoing exlap.

Unless you were suspecting bowel perf, this seems overkill to me, and your initial description of the case didnt mention any perf until surgeons reported their findings.

But the colon CA did cause perf, so it was the right call in hindsight.

As for the likely cause of hypotension, I would guess it is vasoplegia from washing out the perforated colon.

Also, look at the CXR that ICU got immediately after receiving the patient. They shouldve gotten one to confirm the tube position.

 

[JiPo]

2 L rum quickly in trendelenburg position.

That is a lot of rum for anyone to handle.

 

[GassYous]

Does your institution place an Aline and a central line on a routine basis for cases like this? You presented a case as a typical SBO undergoing exlap.

Unless you were suspecting bowel perf, this seems overkill to me, and your initial description of the case didnt mention any perf until surgeons reported their findings.

But the colon CA did cause perf, so it was the right call in hindsight.

As for the likely cause of hypotension, I would guess it is vasoplegia from washing out the perforated colon.

For me it depends on the patient and the surgeon. Patient looks like crap or surgeon is bad buys an a line. Helps with the ppv too although there was an article recently in anesthesiology that showed that flotrac didn't really help in ortho patients. If i have good access I skip the cvl unless the patient looks like crap or is a cardiac cripple.

 

[deleted171991]

Hello to the respected forum of anesthesia..

Had a case recently and I was thinking about it. Pt was 80 y.o. Male with preexisting HTN on ACE-I, mild dementia, overweight ( 100kg at around 1,80) and pertinent surgical Hx of repaired ing hernia 2 years prior. Had no bowel movement over 3 days and was posted for exlap for possible mechanical SBO. Labs were wnl, except Hb which was 9, Cr of 4.0, BUN of 100 ( prerenal AKI? )
On presentation he was in apparent distress, looking septic HR 110 in Afib, BP 170/90, Spo2 95% on Venturi 50%, tachypneic with a hugeee abdomen. Anyways we put an aline, induce, CVC and surgery proceeds. I started some fluids and give around 3L for presumed deficit then I continued at 1-2ml/kg/hr. Oxygenation remained acceptable at an FiO2 55%, PEEP of 8, Peaks around 30-35 which subsided to 23-25 after abdomen was opened. Urine output was at ~500cc for the first hr Patient was stable with HR in 80's ( Afib so no PPV, SPV guidance), normal MAP's around 90. Surgery went on because apparently pt had a tumor in right colon that had caused a hole in the colon with spillage of bowel content so they had to resect it and they did an anastomosis( no colostomy?). Anyway I was alone in the first hour, then my attending came back and told me why was I withholding the fluids, that the patient was profoundly hypovolemic due to ileus so we started giving more LR+NS . At around the 6L mark patient started to look worse with norepi requirement and a little worsening oxygenation. I think we gave 2 more liters after that, and the surgery was coming to a close. Patient now had a 2.5-3ug/kg/min norepi req + bumps of epi to sustain MAP>65. Oxygenation was PaO2 of 90 at 70% FiO2 with the same PEEP.

Of course we didn't extubate and my attending considered the pt terminal due to the huge pressor requirement. Anyways I shifted the pt to ICU and called it a night since it was 6am.
48 hrs later I went to check on the pt and to my big surprise he is extubated on a venturi 40% with minimal norepi req. I asked the fellow about mgmt, echo?. He said they gave some more fluids but also put the pt on CVVHD for worsening hyperkalemia and reduced urine output and of course gave broad spectrum Abx. No echo done yet ( pt only got a single dose of ciprofloxacin in the ED ). Then I lost the pt since I was rotating at a different hospital.




I am having a thought and so far none of the answers of my attendings satisfied my curiosity. So, we all know that fluid management should be a thoughtful process and overload can have deleterious effects on ileus, LOS, wound healing etc, but what I wanted to know is : Is it possible to cause iatrogenic cardiogenic shock with fluid administration in a patient like this with possible untreated diastolic heart failure, but also in a patient without any hint of heart failure? Or was the deterioration due to sepsis that was improved with proper Abx? Actual hypovolemia that needed more fluids?

Thanks in advance for reading the post. Any wisdom is really appreciated!

Your attending got lucky. World class mismanagement, very likely.

A patient with a urine output of 500 cc/hr and high BP is unlikely to be hypovolemic, not with a Hgb of 9 (unless his baseline Hgb was much lower). He probably had preop AKI from abdominal hypertension (as evidenced by the excellent urine output after opening the belly). Intraop hypotension from bacteremia should have been expected, and treated mostly with pressors.

One doesn't need CHF to have the heart fail after a ton of fluids from bad doctors, but the patient's chronic HTN almost guaranteed a diastolic CHF. The persistent hypoxemia should have been a hint for fluid overload.

Kudos to you for asking yourself these questions.

 

[Radetzky]

In my opinion fluids should always be titrated to some end point rather than given “empirically for a presumed deficit”.

Yes fluid overload can cause right heart distension and LV compression but it also worsens vasodilatory shock. There are some interesting animal studies showing that animals with hyper dynamic sepsis end up on more pressor when given aggressive fluids- probably a mechanism of endothelial injury.

Hypovolemia should be banned from the lexicon. Terminology that means whatever the physician wants it to mean, usually as a justification for mindless fluid therapy.

 

[Hork Bajir]

To the point above- I don’t have the paper easily accessible at the moment, but I’ve seen pretty convincing literature demonstrating that once you get beyond 5-6L of crystalloid, the compliance of the interstitial space changes and the time constant for leakage of IV crystalloids out of the intravascular compartment decreases (they stay intravascular for even less time than usual before redistributing into TBW). The proposed mechanism was changes in the endothelial glycocalyx: as it gets “pulled apart”, the attraction between neighboring protein/sugar elements decreases and pulling them apart further (thus increasing capillary leak) becomes easier. This is one of the only “evidence based” uses if albumin, AFAIK (administration to compensate for changes in the time constant of crystalloids once you get beyond 5-6L)

 

[Airway]

Simply (imo not there just read your posts not a psychic god etc etc) too much fluid, for anyone. Remember renal perfusion may decrease as cvp increases.
This is an excellent paper just to show you the insanity of so many text book assumptions

A Rational Approach to Perioperative Fluid Management

Replacement of assumed preoperative deficits, in addition to generous substitution of an unsubstantiated increased insensible perspiration and third space loss, plays an important role in current perioperative fluid regimens. The consequence is a positive fluid balance and weight gain of up to...

pubs.asahq.org

 

[WholeLottaGame7]

What made your attending think the patient was "profoundly" hypovolemic in the absence of hypotension? ABGs? Did you have a big metabolic acidosis? Sounds like some real 1980s **** to just randomly give 6L of crystalloid "just because" with no supporting data. Did he have you running 12ml/kg tidal volumes, too?

 

[nimbus]

What made your attending think the patient was "profoundly" hypovolemic in the absence of hypotension? ABGs? Did you have a big metabolic acidosis? Sounds like some real 1980s **** to just randomly give 6L of crystalloid "just because" with no supporting data. Did he have you running 12ml/kg tidal volumes, too?

Yep. I wonder how old this attending is. “Unguided” massive crystalloid resuscitation is so 1980s. Although most patients survived this during the 1980s too. The attending sounds like an old dinosaur that has not kept up to date. At the very least, he is out of style.

 

[deleted697127]

Pt was 80 y.o. Male with preexisting HTN on ACE-I, mild dementia, overweight ( 100kg at around 1,80) and pertinent surgical Hx of repaired ing hernia 2 years prior. Had no bowel movement over 3 days and was posted for exlap for possible mechanical SBO. Labs were wnl, except Hb which was 9, Cr of 4.0, BUN of 100 ( prerenal AKI? )
On presentation he was in apparent distress, looking septic HR 110 in Afib, BP 170/90, Spo2 95% on Venturi 50%, tachypneic with a hugeee abdomen.

Sorry, you clearly care or wouldn’t be following up and asking. I don’t know how to say this without being a dick but try to be more concise. I suspect some details may have escaped you with this case (and possibly your attending). An ICU doc sat me down once after rounds and gave me this harsh and not so concise talk:

You need to tell a story people can follow before you lose their attention. Presentations need to have some semblance of traditional form. Emphasize the details that matter.

“Pre-existing HTN on ACE-i” is too much for run of the mill HTN. Just say HTN unless he’s on a gazillion meds has bad LVH or there is a specific reason to give it more attention than it deserves. This guy has a mass and perforation and everything that goes with waiting 3 days to fix it.

Mild dementia? Is he coming from home? Still a practicing vascular surgeon or politician? Was he ignored in a nursing home for a week until his abdomen exploded? Loaded word without relevant qualifiers.

I still don’t know what he actually presented with? Just 3 days with no bowel movement? No pain. Wasn’t concerned with his distended abdomen? N/v? Appetite? Don’t learn the hard way why these details matter for inducing an SBO.

inguinal hernia repair history? Sure maybe related to why he has a SBO....but then it’s not. He has a mass and perforation. Wouldn’t change my management one way or another.

you said he looks septic... he goes on to have fecal matter in his belly for god knows how long. What were his temp, white count, and lactate? Partial SBO, complete SBO, perforation are on a spectrum based on clinical stability with different management strategies.

Did he have imaging? Free air? Dilated bowel? Mass? Fluid levels and fluid in his stomach?

So let’s try this again:

81YO 100kg male with HTN, mild dementia who is still highly functional and able to live on his own came in to the ED with worsening abdominal pain, distension, and 3 days without a bowel movement. He is alert and oriented, appears septic, febrile, tachycardic, hypertensive, visibly tachypneic but able to maintain sat 95 on face mask and provide adequate history in full sentences. He has a massively distended and tender abdomen. Found to be in new onset A Fib. Labs significant for WBC 22, BUN/Cr 100/4 with normal electrolytes. Hgb 9. Lactate 6 pH 7.2 Distended bowel without free air on imaging. Booked for emergent ex lap. He is NPO for 3 days due to nausea/loss of appetite and does not yet have an NGT.

———-

When exactly did the pressor requirement start? It’s certainly possible this is sepsis rather than just fluid overload. Like yea RV talk sounds fancy but the guys belly is filled with ^*#%. I don’t like giving 6L to stiff old Hearts and believe in washing out the glycocalyx leading to capillary permeability/pulm edema but I’m skeptical that this is why he developed a pressor requirement.

————
Yes, it’s true SBO causes hypovolemia which would make the starting HgB of 9 suspicious for being heme concentrated and would make me more likely to give blood preferentially early rather than crystalloid but 6L is a lot. His total blood volume is 6L. You should rarely give more than a liter at a time without reassessing the strategy to see what it may be helping and hurting.

NGT prior to induction should definitely be considered. NGT output may effect fluid replacement strategy.

You said the ED only gave Cipro. I’m guessing he was started on broad spectrum antibiotics in the OR but definitely make sure he’s on the correct antibiotics once the diagnosis changes from possible obstruction to there’s fecal matter in the belly with a new pressor requirement. If broad spectrum antibiotics did not happen until the ICU, well then, there’s your answer.

Frequent ABGs and labs are necessary. Is there a lactate. PF ratios. What are the trends. Is it getting harder to ventilate as i give fluids. How dilute are his Hgb, platelets, and Coags.

The first hour of urine is not helpful to me. He’s 81 and demented. Is that 500mL old urinary retention? So much is going on in the first hour after the foley goes in like central line, prepping, the nurse who placed the foley going home without sign out, etc. What’s the trend? Is he now oligo/anuric? Is K increasing?

Talk to your surgeons during the case. Low urine output, creatinine of 4, worsening oxygenation, and increasing pressor requirement in an 81YO might need to go to the unit with an open belly and colostomy for renal replacement therapy and stabilization prior to anastomosis. Don’t assume they know everything you do if major changes are happening and you don’t tell them.

 

[LineAndBerry]

That is a lot of rum for anyone to handle.

Agree, all my bowel cases get rum, but never that much. I think this was a case of acute RV alcohol intoxication.

 

[CavGas]

First of all, thanks for everybody taking the time to answer! This is a very interesting discussion for a trainee like me.

I 'll try to answer to all of you

@Hork Bajir

I wish we could have done a TEE. Unfortunately only ~10% of the attendings in my program are facile with it and still very reluctant to use it outside the heart rooms.
Extremities of the patient were cold but he was also on a massive norepinephrine dose by the time I checked so that may be confusing things? I was thinking about acute heart failure because of the volume infused, progressive oliguria and increasing oxygen requirement. Simple sepsis also sounds very probable in hindsight.
However I didn't know if it was actually possible to get such a degree of cardiogenic shock from fluid infusion, hence the question here. Usually it's only pulmonary edema. You are mentioning acute R heart failure. Is it possible to treat an acutely volume overloaded RV with diuresis, nitrates or it is simply pressors and hope for the best?

@JiPo

A-line and CVC is ''mandatory'' for all emergency exlap cases at my institution, even if pt has good access. I think it also has to do with surgeon preference/habit for post-op management.

@FFP

It seemed to me at the time that this was too much fluid but I'm also not a specialist. Hopefully I can recognize my mistakes in retrospect and not repeat them in the future!

@Airway

I will give it a read!

@WholeLottaGame7 @nimbus

Attending is young but apparently with an old mindset. I 'd say half of my attendings love fluids. Relative hypovolemia was inferred from ABG with a -6 HCO deficit. Tidal volumes are modern at 6-8ml/kg IBW

@SnapperRocks

I think your criticism has good intentions so it is most welcome. I 'll try to keep the relevant details. Your presentation sounds much better than mine tbh .
I will confess to focusing on the minute to minute case management (no anesthesia nurse available) and leaving the Hx/Imaging/Labs review/management decisions to my attending. In retrospect I should have been more involved so I can appreciate the pathophysiology. I managed to administer proper Abx but with a considerable delay due to logistics.
We talked to the surgeons regarding post-op ventilation, pressor requirement, switching op plan to no anastamosis and shorter operation, ICU transfer etc but they were adamant about doing the anastomosis with a total operation time of 3.5hrs

 

[deleted171991]

Isolated RV failure does not produce (interstitial) pulmonary edema (i.e. hypoxemia). 8L of fluids do. And isolated RV failure is much rarer than biventricular failure (most PHTN is due to left heart disease). This patient had no PMH suggestive for isolated RV failure.

8L of IV fluids would bother even a young healthy patient. I would take 8 bags of LR, hang them on the attending, and make him walk around with a sign: "I WILL NOT GIVE 8L OF FLUID TO ANY EX-LAP!".

 

[deleted697535]

very unusual for an 80 perf acute abdomen to be so sick on 3 norepi to bounce back that quickly and be extubated in 2 days but maybe with good source control...
was your aline reading correctly? did they resite another on diff arm? what was the lactate and ph trend?
we dont know any labs for this guy

he did well, 99% of other 80yr olds wouldnt

imno surgeon but doing a primary anastamosis in an abdomen full of poop might not be the best idea

 

[deleted171991]

Simply (imo not there just read your posts not a psychic god etc etc) too much fluid, for anyone. Remember renal perfusion may decrease as cvp increases.
This is an excellent paper just to show you the insanity of so many text book assumptions

A Rational Approach to Perioperative Fluid Management

Replacement of assumed preoperative deficits, in addition to generous substitution of an unsubstantiated increased insensible perspiration and third space loss, plays an important role in current perioperative fluid regimens. The consequence is a positive fluid balance and weight gain of up to...

pubs.asahq.org

Here is an excellent explanation why humans need just enough fluid to maintain mean systemic pressure (i.e. normal venous return, not MAP) at normal SVR. If the SVR decreases, the solution is (mostly) not IV fluids.




The pathophysiology of edema in the body is seriously dependent on lymphatic flow (forget the Starling equilibrium at the venous end, that was last century). It's the lymph that returns the excess fluid from the interstitium, not the venules.

At one end of the lymphatic system it's the interstitium. At the other end it's the SVC system. Hence the importance of a high CVP, such as in hypervolemia, or biventricular failure. This is true even for the pleura and peritoneum. The lymph drainage from the peritoneal space is low, about 1.2L/day. much slower than from the extremities, or even the pleural space.

Because of this, one should be extremely careful when there is an abdominal process that may sequester fluids in the belly. Despite classical teaching, not even in pancreatitis should one give uncontrolled amount of fluids. One should not aim for hemodilution, just avoiding hemoconcentration. Give as much as needed to maintain normovolemia at normal SVR; that's what the body is used to. And, since we're talking about pancreatitis (and similar "third-spacing" abdominal processes), if one sees hypoxemia in such a patient, one should assume it's fluid overload (not ARDS) until proven otherwise.

Also, IV fluids # oral fluids. IV fluids are proven to be pro-inflammatory, hence the damage to the glycocalyx. IV fluids are drugs. Give PO fluids whenever possible (in the ICU).

Don't forget all the "benefits" of fluid overload:

 

[Hoya11]

Hello to the respected forum of anesthesia..

Had a case recently and I was thinking about it. Pt was 80 y.o. Male with preexisting HTN on ACE-I, mild dementia, overweight ( 100kg at around 1,80) and pertinent surgical Hx of repaired ing hernia 2 years prior. Had no bowel movement over 3 days and was posted for exlap for possible mechanical SBO. Labs were wnl, except Hb which was 9, Cr of 4.0, BUN of 100 ( prerenal AKI? )
On presentation he was in apparent distress, looking septic HR 110 in Afib, BP 170/90, Spo2 95% on Venturi 50%, tachypneic with a hugeee abdomen. Anyways we put an aline, induce, CVC and surgery proceeds. I started some fluids and give around 3L for presumed deficit then I continued at 1-2ml/kg/hr. Oxygenation remained acceptable at an FiO2 55%, PEEP of 8, Peaks around 30-35 which subsided to 23-25 after abdomen was opened. Urine output was at ~500cc for the first hr Patient was stable with HR in 80's ( Afib so no PPV, SPV guidance), normal MAP's around 90. Surgery went on because apparently pt had a tumor in right colon that had caused a hole in the colon with spillage of bowel content so they had to resect it and they did an anastomosis( no colostomy?). Anyway I was alone in the first hour, then my attending came back and told me why was I withholding the fluids, that the patient was profoundly hypovolemic due to ileus so we started giving more LR+NS . At around the 6L mark patient started to look worse with norepi requirement and a little worsening oxygenation. I think we gave 2 more liters after that, and the surgery was coming to a close. Patient now had a 2.5-3ug/kg/min norepi req + bumps of epi to sustain MAP>65. Oxygenation was PaO2 of 90 at 70% FiO2 with the same PEEP.

Of course we didn't extubate and my attending considered the pt terminal due to the huge pressor requirement. Anyways I shifted the pt to ICU and called it a night since it was 6am.
48 hrs later I went to check on the pt and to my big surprise he is extubated on a venturi 40% with minimal norepi req. I asked the fellow about mgmt, echo?. He said they gave some more fluids but also put the pt on CVVHD for worsening hyperkalemia and reduced urine output and of course gave broad spectrum Abx. No echo done yet ( pt only got a single dose of ciprofloxacin in the ED ). Then I lost the pt since I was rotating at a different hospital.




I am having a thought and so far none of the answers of my attendings satisfied my curiosity. So, we all know that fluid management should be a thoughtful process and overload can have deleterious effects on ileus, LOS, wound healing etc, but what I wanted to know is : Is it possible to cause iatrogenic cardiogenic shock with fluid administration in a patient like this with possible untreated diastolic heart failure, but also in a patient without any hint of heart failure? Or was the deterioration due to sepsis that was improved with proper Abx? Actual hypovolemia that needed more fluids?

Thanks in advance for reading the post. Any wisdom is really appreciated!

I don't think the fluid was so obviously mismanaged.

What guides were possible to use?

The guy is in AF so no PPV.

Renal failure so no Urine output.

CVP we all know is not very accurate.

He's hypotensive and in severe renal failure with a SBO.

I would also assume he is septic from bowel perf and dehydrated - both causing renal failure.

What evidence was there that the 8L of fluid was too much?

The urine output was likely retained urine after foley placement or decompressing abdomen as others have mentioned.

He didn't just go from making 500 in the first hour to requiring dialysis post op. Some urine at least was old urine.

Its a tough situation. A hypotensive septic shock guy who needs hydration but with no way to release the fluid as the renal failure was severe.

Similar to a ESRD HD patient undergoing a big bloody operation.

In this situation I would give what I thought to be a reasonable amount of fluid and cover the rest of the hypotension with pressors.

Leave intubated as you did.

Good for him that he was extubated after HD. Nothing you did wrong that he became so critically ill during surgery IMO.

 

[drmwvr]

CVP we all know is not very accurate.

Not taken on it's own, but CVP (RAP) probably would have been pretty useful here insofar as it's relationship to the MAP over the course of the case. Rising CVP from a failing heart as a reflection of an impediment to venous return is pretty easily discerned. The Guyton diagram is a little more useful than a bike pump cartoony thingy to describe this.

 

[deleted171991]

Not taken on it's own, but CVP (RAP) probably would have been pretty useful here insofar as it's relationship to the MAP over the course of the case. Rising CVP from a failing heart as a reflection of an impediment to venous return is pretty easily discerned. The Guyton diagram is a little more useful than a bike pump cartoony thingy to describe this.

CVP does not correlate with fluid status and should not be used for that purpose (or basically any purpose). It also doesn't correlate with heart function. Heck, even PCWP does not correlate well with LV function.

The bike pump is about MS(F)P. Good luck explaining that concept, and its importance, even to attendings. That video is a gem, especially for trainees, and non-anesthesiologists/non-intensivists. People who understand it stop resuscitating shock with a ton of fluids.

 

[Hork Bajir]

CVP does not correlate with fluid status and should not be used for that purpose (or basically any purpose). It also doesn't correlate with heart function. Heck, even PCWP does not correlate well with LV function.

The bike pump is about MS(F)P. Good luck explaining that concept, and its importance, even to attendings. That video is a gem, especially for trainees, and non-anesthesiologists/non-intensivists.

If you want to explain mean systemic filling pressure to someone, have them watch a DHCA case. Pump flow on, pump flow off, giving pressors during a period of circulatory standstill increases stressed volume vs unstressed volume, etc.

Admittedly I used to be in the same camp as you, that CVP was a useless garbage number. However after spending enough time in the cardiac OR, I now feel differently- while it may be the most widely misused number in medicine, CVP without a doubt adds valuable diagnostic information to the assessment of the failing circulation. CVP represents the point where the venous return curve and the cardiac output curve intersect - nothing more, nothing less. When integrated in the context of a comprehensive assessment, it can help to understand where those curves lie.

If you take it as a number which is a proxy for a preload, you’re doing it way wrong. If you ignore it altogether (like I used to), then there is probably an opportunity to add some sophistication to your hemodynamic assessment

 

[drmwvr]

CVP does not correlate with fluid status and should not be used for that purpose (or basically any purpose). It also doesn't correlate with heart function. Heck, even PCWP does not correlate well with LV function.

The bike pump is about MS(F)P. Good luck explaining that concept, and its importance, even to attendings. That video is a gem, especially for trainees, and non-anesthesiologists/non-intensivists. People who understand it stop resuscitating shock with a ton of fluids.

They stop resuscitating with a ton of fluids because they understand the relationship between MSFP, RAP and cardiac function. And if a sophisticated understanding of those elements is what is desired, the VR/CO curves would seem to speak to those issues more than a cartoon.

And while were on the topic of PAC's, a stable or falling CVP (RAP) in the setting of elevated PAP is absolutely a reassuring surrogate for RV function.

 

[deleted171991]

@Hoya11, I will dissect your post a bit, for the trainees, so I will begin with a disclaimer: based on many previous posts, I consider you a very good anesthesiologist. This is not about/against you. We are all Monday morning quarterbacks here.

I also apologize to everybody for being judgmental; it's in my nature.

I don't think the fluid was so obviously mismanaged.

Whenever a 100 kg person gets 8L of IV fluid in 4 hours, it's most likely wrong. Heck, it's most likely wrong even in 24.

In this case, we started with a septic looking, hypertensive and tachycardic patient in AFib, hypoxemia, AKI and SBO. So one should ask oneself, preop: WHY? Why each and all of these? That's not the mark of a "flea"; that's the mark of a good doctor.

Why is this patient in AFib? Is it baseline, is it pain, is it bacteremia, is it fever, or is it increased RA pressure from PREOP fluid overload or other sympathetic stimulus, for example bladder distention? This is where a GOOD HISTORY and PHYSICAL EXAM help a lot. Talk to the patient. Examine him, especially things that are pertinent in shock, such as skin temperature, capillary refill and his extremities (e.g. knee mottling).

One thing is clear: fluid overload on top of AFib would be no bueno.

What guides were possible to use?

The guy is in AF so no PPV.

Renal failure so no Urine output.

CVP we all know is not very accurate.

He's hypotensive and in severe renal failure with a SBO.

I would also assume he is septic from bowel perf and dehydrated - both causing renal failure.

OK, here we go with more PREOP questions. What was the cause of this patient's renal failure? Was it prerenal/intrarenal/postrenal? Why? Again the H&P would help. Did he come in with an AKI, or did that happen later? How did the creatinine change during his admission? What's his baseline?

This is where the question of that first hour of urine output comes up. 500 cc of urine is a lot. Most old men won't sit around with 500 for many hours (if he's barely making urine), unless obstructed. Which makes me think he was either making good urine preop, or he started making it intraop, once the belly was opened. The OP did not say that there was a lot of urine when they put in the Foley. The OP said "Urine output was at ~500cc for the first hr". Maybe he did not pay attention to how much urine there had been initially in the bladder, but most likely the patient did make good urine in that hour.

If I walk in on a patient, and see 500 cc of urine in his bag, how do I figure out how the kidney is doing? I look at the color of the urine in the bag and tubing. Male doctors should be experts in associating urine color with probable hydration levels. A creatinine of 4 is some serious AKI, but, not necessarily intrarenal injury, especially with IAH.

What evidence was there that the 8L of fluid was too much?

The urine output was likely retained urine after foley placement or decompressing abdomen as others have mentioned.

He didn't just go from making 500 in the first hour to requiring dialysis post op. Some urine at least was old urine.

In my mind/experience, intra-abdominal hypertension seriously decreases urine production. So I somehow doubt that he had 500 cc of urine just sitting in his renal pelvis. It was either in the bladder, or he started making urine as soon as the IAP and renal venous pressure dropped. That would have been a very good sign intraop.

Btw, if that urine was old and he was actually almost anuric the whole surgery, giving 8L of fluids in a case without major fluid loss is even worse.

Its a tough situation. A hypotensive septic shock guy who needs hydration but with no way to release the fluid as the renal failure was severe.

Similar to a ESRD HD patient undergoing a big bloody operation.

In this situation I would give what I thought to be a reasonable amount of fluid and cover the rest of the hypotension with pressors.

Was it a big bloody operation? It didn't sound so. I would have loved to be able to examine this guy preop, because a BP of 170/90 (even with pain) doesn't jive with sepsis, dehydration (Hgb of 9!), prerenal AKI, not even with inserting a CVC post-induction.

And that HYPOXEMIA... Why was this patient so hypoxemic PREOP? Was he hypoventilating/splinting from pain/abdominal distension? Was the 95% O2 sat due to peripheral vasoconstriction (e.g. cold hands)? Again, was this baseline, was this much worse than baseline (I assume so)? 100 kg in a 1.80 person is a BMI of 30.9, unimpressive as obesity goes. What was his baseline exercise tolerance? And again, what was his cardiorespiratory history and physical exam? Oxygenation doesn't improve septic shock, but it improves heart failure, so why did this patient need 50% FiO2? Was he already in hypervolemia from his preop AKI, or from having gotten preop IV fluids ("for SBO")?

See where I am going? The last thing this guy needed was 8L of fluids, especially when he became hypotensive intraop WITHOUT MAJOR FLUID LOSSES. What were they replacing? Fluid losses due to open belly are seriously overestimated in the classical literature. If it was "third-spacing" from peritonitis, still, 8 liters in 4 hours??? The intestinal edema from all that fluid can be much worse than some pressors. Third spacing tends to respond to fluids initially; the effect just doesn't last long, so, after a few boluses, it's pretty clear that the patient needs pressors, not more fluid in his organs and spaces.

So how to manage this guy? My role is to maintain/restore homeostasis; I am no god, no genius, but the human body usually is. I try to stay out of its way. FIRST DO NO HARM.

I don't chase urine output in abdominal surgeries (and most ICU patients). But if it's there, very reassuring.

I keep looking at that capillary refill even intraop. I want my patient to be warm, with warm and well-perfused extremities. At least with a strong pulse ox signal, if possible, even if cold extremities. I try to keep the patient as close to what I think his normal baseline is as possible.

I personally don't care about PPV/SPV and similar. The fact that the patient is fluid responsive # the patient needs fluids. And most patients don't qualify anyway. Plus they may be different than most people in a particular study.

Fluid-wise, I tend to replace the lost fluids that I can SEE and approximate well (e.g. suction, 4x4s, pools of blood, Foley etc.), maybe an empirical extra 1-2L, depending on preop fluid status. And then I give pressors. That's why I watch intraop fluid losses like a HAWK. I walk around the OR every 30-60 minutes, more frequently in a bloody surgery. I watch the surgeon. I generally do NOT trust surgeons' estimates of fluid losses. This way, I have a pretty good idea of I/O's at all times, so I know whether the patient needs more fluids or more pressors, at least to bring him to preop levels. Because the least an anesthesiologist should do is return the patient in the same shape as preop (if not much better, from a LONG TERM outcome standpoint).

Leave intubated as you did.

Good for him that he was extubated after HD. Nothing you did wrong that he became so critically ill during surgery IMO.

I think this patient was very lucky to be in pretty good shape at his age. I've seen people start circling the drain from this amount/speed of fluid overload, especially in sepsis, especially w/ AKI. My guess is that they removed a lot of that fluid with CVVH, and that he was not as sick as the OP thought.

It's also pretty unclear how much norepi he was on intraop. Definitely not 2.5-3 mcg/kg/min, as OP wrote. If it was just 3 mcg/min, and only after 6L IVF had been given, that again makes this whole case very interesting. Also the fact that the patient got worse (including oxygenation) after 6L of fluids.

In the end, what matters is that the patient did well. Still, it's the PROCESS that makes a good doctor, not the OUTCOME. One can have occasional good outcomes with bad doctors/processes, and the other way round. This one almost sounded like a surgeon-directed resus, obsessive about avoiding pressors.

Sorry for the long post.

 

[deleted171991]

Btw, like peritonitis, acute pancreatitis is among the worst third-spacing systemic inflammatory syndromes one can have in a belly (except we encounter many more cases of the latter). This is the modern approach (and it works):

"traditional dogma: large volume fluid resuscitation

• Traditionally patients have been treated with massive fluid resuscitation (e.g. 250-500 ml/hr, resulting in ~8-14 liters fluid administration over the first day). This is insanity.
• There is no evidence to support massive volume administration. Available prospective studies show that more aggressive fluid administration increases rates of infection, abdominal compartment syndrome, ARDS, and death.10 11

reasonable approach?​

• Nobody knows the best approach, there is little high-quality prospective data to guide this.
• A reasonable approach to resuscitation is probably similar to a septic shock resuscitation:
  • Give fluid based on hemodynamic assessment (e.g. with ultrasonography). Most patients may benefit from a moderate amount of fluid initially (e.g. 2-4 liters total over the first day).
  • Don't give much fluid after the initial resuscitation (e.g. beyond 12-24 hours). Following stabilization, it's generally wise to target an even fluid balance (inputs = outputs).
  • Use vasopressors (e.g. norepinephrine) early, as needed to maintain an adequate MAP. This may reduce the amount of fluid given, thereby reducing the risk of abdominal compartment syndrome (more on this below).
• Be careful about the use of fluid-responsiveness in these patients. Even if the patient is fluid-responsive, administered fluid will rapidly leak out of the vascular space. Pancreatitis patients will often be fluid-responsive regardless of how much fluid they are given.
• Patients will often develop renal failure due to acute tubular necrosis. This doesn't respond to additional fluid administration."

Acute Pancreatitis (including hypertriglyceridemic pancreatitis)

CONTENTS Rapid Reference 🚀 Diagnosis Clinical findings Laboratory studies (lipase) Radiology Diagnostic criteria Evaluating the cause of pancreatitis Risk stratification – who needs ICU? Treatment General principle: pancreatoseptic equivalence Treatment of causative factors ERCP? Resuscitation...

emcrit.org

 

[vector2]

Hello to the respected forum of anesthesia..

Had a case recently and I was thinking about it. Pt was 80 y.o. Male with preexisting HTN on ACE-I, mild dementia, overweight ( 100kg at around 1,80) and pertinent surgical Hx of repaired ing hernia 2 years prior. Had no bowel movement over 3 days and was posted for exlap for possible mechanical SBO. Labs were wnl, except Hb which was 9, Cr of 4.0, BUN of 100 ( prerenal AKI? )
On presentation he was in apparent distress, looking septic HR 110 in Afib, BP 170/90, Spo2 95% on Venturi 50%, tachypneic with a hugeee abdomen. Anyways we put an aline, induce, CVC and surgery proceeds. I started some fluids and give around 3L for presumed deficit then I continued at 1-2ml/kg/hr. Oxygenation remained acceptable at an FiO2 55%, PEEP of 8, Peaks around 30-35 which subsided to 23-25 after abdomen was opened. Urine output was at ~500cc for the first hr Patient was stable with HR in 80's ( Afib so no PPV, SPV guidance), normal MAP's around 90. Surgery went on because apparently pt had a tumor in right colon that had caused a hole in the colon with spillage of bowel content so they had to resect it and they did an anastomosis( no colostomy?). Anyway I was alone in the first hour, then my attending came back and told me why was I withholding the fluids, that the patient was profoundly hypovolemic due to ileus so we started giving more LR+NS . At around the 6L mark patient started to look worse with norepi requirement and a little worsening oxygenation. I think we gave 2 more liters after that, and the surgery was coming to a close. Patient now had a 2.5-3ug/kg/min norepi req + bumps of epi to sustain MAP>65. Oxygenation was PaO2 of 90 at 70% FiO2 with the same PEEP.

Of course we didn't extubate and my attending considered the pt terminal due to the huge pressor requirement. Anyways I shifted the pt to ICU and called it a night since it was 6am.
48 hrs later I went to check on the pt and to my big surprise he is extubated on a venturi 40% with minimal norepi req. I asked the fellow about mgmt, echo?. He said they gave some more fluids but also put the pt on CVVHD for worsening hyperkalemia and reduced urine output and of course gave broad spectrum Abx. No echo done yet ( pt only got a single dose of ciprofloxacin in the ED ). Then I lost the pt since I was rotating at a different hospital.




I am having a thought and so far none of the answers of my attendings satisfied my curiosity. So, we all know that fluid management should be a thoughtful process and overload can have deleterious effects on ileus, LOS, wound healing etc, but what I wanted to know is : Is it possible to cause iatrogenic cardiogenic shock with fluid administration in a patient like this with possible untreated diastolic heart failure, but also in a patient without any hint of heart failure? Or was the deterioration due to sepsis that was improved with proper Abx? Actual hypovolemia that needed more fluids?

Thanks in advance for reading the post. Any wisdom is really appreciated!

What was the patient's heart rate as their norepi requirement skyrocketed and you started giving bumps of epi? Sick pts with afib do not tolerate RVR, especially if they have any degree of LVH (i.e. diastolic dysfunction), MR, or a transiently reduced EF. I'm sure he had some degree of sepsis mediated vasodilatation from the nastiness in his belly, but keep in mind that cardiac output also drops to atrociously low levels when afib is not rate controlled.

 

[drmwvr]

Much has been made of the patient's oxygenation...he started with a Hgb of 9 and then got 8 L of crystalloid....extravasation/lung injury aside...would not be scratching my head....

 

[Hoya11]

@Hoya11, I will dissect your post a bit, for the trainees, so I will begin with a disclaimer: based on many previous posts, I consider you a very good anesthesiologist. This is not about/against you. We are all Monday morning quarterbacks here.

I also apologize to everybody for being judgmental; it's in my nature.


Whenever a 100 kg person gets 8L of IV fluid in 4 hours, it's most likely wrong. Heck, it's most likely wrong even in 24.

In this case, we started with a septic looking, hypertensive and tachycardic patient in AFib, hypoxemia, AKI and SBO. So one should ask oneself, preop: WHY? Why each and all of these? That's not the mark of a "flea"; that's the mark of a good doctor.

Why is this patient in AFib? Is it baseline, is it pain, is it bacteremia, is it fever, or is it increased RA pressure from PREOP fluid overload or other sympathetic stimulus, for example bladder distention? This is where a GOOD HISTORY and PHYSICAL EXAM help a lot. Talk to the patient. Examine him, especially things that are pertinent in shock, such as skin temperature, capillary refill and his extremities (e.g. knee mottling).

One thing is clear: fluid overload on top of AFib would be no bueno.


OK, here we go with more PREOP questions. What was the cause of this patient's renal failure? Was it prerenal/intrarenal/postrenal? Why? Again the H&P would help. Did he come in with an AKI, or did that happen later? How did the creatinine change during his admission? What's his baseline?

This is where the question of that first hour of urine output comes up. 500 cc of urine is a lot. Most old men won't sit around with 500 for many hours (if he's barely making urine), unless obstructed. Which makes me think he was either making good urine preop, or he started making it intraop, once the belly was opened. The OP did not say that there was a lot of urine when they put in the Foley. The OP said "Urine output was at ~500cc for the first hr". Maybe he did not pay attention to how much urine there had been initially in the bladder, but most likely the patient did make good urine in that hour.

If I walk in on a patient, and see 500 cc of urine in his bag, how do I figure out how the kidney is doing? I look at the color of the urine in the bag and tubing. Male doctors should be experts in associating urine color with probable hydration levels. A creatinine of 4 is some serious AKI, but, not necessarily intrarenal injury, especially with IAH.


In my mind/experience, intra-abdominal hypertension seriously decreases urine production. So I somehow doubt that he had 500 cc of urine just sitting in his renal pelvis. It was either in the bladder, or he started making urine as soon as the IAP and renal venous pressure dropped. That would have been a very good sign intraop.

Btw, if that urine was old and he was actually almost anuric the whole surgery, giving 8L of fluids in a case without major fluid loss is even worse.


Was it a big bloody operation? It didn't sound so. I would have loved to be able to examine this guy preop, because a BP of 170/90 (even with pain) doesn't jive with sepsis, dehydration (Hgb of 9!), prerenal AKI, not even with inserting a CVC post-induction.

And that HYPOXEMIA... Why was this patient so hypoxemic PREOP? Was he hypoventilating/splinting from pain/abdominal distension? Was the 95% O2 sat due to peripheral vasoconstriction (e.g. cold hands)? Again, was this baseline, was this much worse than baseline (I assume so)? 100 kg in a 1.80 person is a BMI of 30.9, unimpressive as obesity goes. What was his baseline exercise tolerance? And again, what was his cardiorespiratory history and physical exam? Oxygenation doesn't improve septic shock, but it improves heart failure, so why did this patient need 50% FiO2? Was he already in hypervolemia from his preop AKI, or from having gotten preop IV fluids ("for SBO")?

See where I am going? The last thing this guy needed was 8L of fluids, especially when he became hypotensive intraop WITHOUT MAJOR FLUID LOSSES. What were they replacing? Fluid losses due to open belly are seriously overestimated in the classical literature. If it was "third-spacing" from peritonitis, still, 8 liters in 4 hours??? The intestinal edema from all that fluid can be much worse than some pressors. Third spacing tends to respond to fluids initially; the effect just doesn't last long, so, after a few boluses, it's pretty clear that the patient needs pressors, not more fluid in his organs and spaces.

So how to manage this guy? My role is to maintain/restore homeostasis; I am no god, no genius, but the human body usually is. I try to stay out of its way. FIRST DO NO HARM.

I don't chase urine output in abdominal surgeries (and most ICU patients). But if it's there, very reassuring.

I keep looking at that capillary refill even intraop. I want my patient to be warm, with warm and well-perfused extremities. At least with a strong pulse ox signal, if possible, even if cold extremities. I try to keep the patient as close to what I think his normal baseline is as possible.

I personally don't care about PPV/SPV and similar. The fact that the patient is fluid responsive # the patient needs fluids. And most patients don't qualify anyway. Plus they may be different than most people in a particular study.

Fluid-wise, I tend to replace the lost fluids that I can SEE and approximate well (e.g. suction, 4x4s, pools of blood, Foley etc.), maybe an empirical extra 1-2L, depending on preop fluid status. And then I give pressors. That's why I watch intraop fluid losses like a HAWK. I walk around the OR every 30-60 minutes, more frequently in a bloody surgery. I watch the surgeon. I generally do NOT trust surgeons' estimates of fluid losses. This way, I have a pretty good idea of I/O's at all times, so I know whether the patient needs more fluids or more pressors, at least to bring him to preop levels. Because the least an anesthesiologist should do is return the patient in the same shape as preop (if not much better, from a LONG TERM outcome standpoint).


I think this patient was very lucky to be in pretty good shape at his age. I've seen people start circling the drain from this amount/speed of fluid overload, especially in sepsis, especially w/ AKI. My guess is that they removed a lot of that fluid with CVVH, and that he was not as sick as the OP thought.

It's also pretty unclear how much norepi he was on intraop. Definitely not 2.5-3 mcg/kg/min, as OP wrote. If it was just 3 mcg/min, and only after 6L IVF had been given, that again makes this whole case very interesting. Also the fact that the patient got worse (including oxygenation) after 6L of fluids.

In the end, what matters is that the patient did well. Still, it's the PROCESS that makes a good doctor, not the OUTCOME. One can have occasional good outcomes with bad doctors/processes, and the other way round. This one almost sounded like a surgeon-directed resus, obsessive about avoiding pressors.

Sorry for the long post.

Nice post. Appreciate the discussion - no offense taken!

I agree the devil is in the details and not enough other history/info was provided to form a definitive opinion.

From a birds eye view, you've got a guy whos got an SBO. Therefore he hasn't been eating and is dehydrated. Likely severely dehydrated from decreased PO intake and vomiting alone. Then he's got sepsis from the SBO bacteremia on top of that. This severe hypovolemia has been ongoing and is causing him to have AKI. This AKI has been worsening and is causing decreased urine output. I just dont buy that he made 500ml the first hour and then due to fluid overload, failed to make anymore urine. I think that is a red herring here and it was old urine or miscalculated somehow. I think he was hypoxic in pre-op due to septicimia and pulmonary capillary vasodilation - while being hypovolemic systemically. Hes hypoxic and dry and septic and acidotic. thats what im picturing..

I picture this surgery as an open ex lap that is 3-4hrs long. I see this guy as down 2-3L at least from the get-go. I see evaporative losses/EBL from the open surgery for 3-4hrs requiring another 2-3L. So I don't think the 8L is THAT far off. Personally, it would be hard for me to make a case for or against fluid resuscitation based on cap refill and just observing the field..

I agree it would be very frustrating to be told to avoid pressors.

More frequently than overloading by physicians, I have seen severe dehydration and inappopriate inaction by the surgical team/floor nurses. I can absolutely count on my patient who is septic and having AKI having a 22g IV going at 100ml/hr and everyone wondering why hes not improving.. To me, this seemed like that kind of situation. A mismanaged floor patient now in big trouble ...

 

[deleted171991]

Nice post. Appreciate the discussion - no offense taken!

I agree the devil is in the details and not enough other history/info was provided to form a definitive opinion.

From a birds eye view, you've got a guy whos got an SBO. Therefore he hasn't been eating and is dehydrated. Likely severely dehydrated from decreased PO intake and vomiting alone. Then he's got sepsis from the SBO bacteremia on top of that. This severe hypovolemia has been ongoing and is causing him to have AKI. This AKI has been worsening and is causing decreased urine output. I just dont buy that he made 500ml the first hour and then due to fluid overload, failed to make anymore urine. I think that is a red herring here and it was old urine or miscalculated somehow. I think he was hypoxic in pre-op due to septicimia and pulmonary capillary vasodilation - while being hypovolemic systemically. Hes hypoxic and dry and septic and acidotic. thats what im picturing..

I picture this surgery as an open ex lap that is 3-4hrs long. I see this guy as down 2-3L at least from the get-go. I see evaporative losses/EBL from the open surgery for 3-4hrs requiring another 2-3L. So I don't think the 8L is THAT far off. Personally, it would be hard for me to make a case for or against fluid resuscitation based on cap refill and just observing the field..

I agree it would be very frustrating to be told to avoid pressors.

More frequently than overloading by physicians, I have seen severe dehydration and inappopriate inaction by the surgical team/floor nurses. I can absolutely count on my patient who is septic and having AKI having a 22g IV going at 100ml/hr and everyone wondering why hes not improving.. To me, this seemed like that kind of situation. A mismanaged floor patient now in big trouble ...

This guy had ileus from peritonitis (from a perforated right colon tumor), not the usual mechanical SBO. Given his normal labs (except for the creatinine, and the Hgb - which was probably low from chronic bleeding), my guess is that the ileus/peritonitis was pretty acute. Three days without a BM suggest something like a day of ileus, which may have caused the AKI (but with a normal BP, hmm). They didn't even have time to decompress his belly with an NGT in the hospital.

That BP of 170/90 (even if pain contributed) is also weird, especially with a normal CBC. This guy was not in septic shock, just septic. I don't think he was very dry preop, at least not much drier than the usual hypertensive. And I still don't think he needed all those fluids. Evaporative losses are more in the range of 200-300 ml/hr, even with an open belly (the OR is cold), and see my post about pancreatitis regarding third-spacing and fluids.

And yes, the surgical floors under-resuscitate patients all the time. And anesthesiologists over-resuscitate them all the time. Only ICU geniuses like me, who inherit the iatrogenic problems, tend to do the right thing. </sarcasm> </cynicism>

Thanks for playing.

 

[Beeftenderloin]

Lots of great thoughts on here. Only thing I would add is when you getting to around 0.1-0.2 mcg/kg/min (10mcg/min) of levo, time to add something else, vaso in presumed sepsis seems like the most clever move give the available data. If you’re thinking myocardial dysfunction would probably add epi next. If no myocardial dysfunction and purely distributive picture would add ang II if you’ve got it.

 

[deleted171991]

Lots of great thoughts on here. Only thing I would add is when you getting to around 0.1-0.2 mcg/kg/min (10mcg/min) of levo, time to add something else, vaso in presumed sepsis seems like the most clever move give the available data. If you’re thinking myocardial dysfunction would probably add epi next. If no myocardial dysfunction and purely distributive picture would add ang II if you’ve got it.

ADH deficiency in septic shock seems to be another of those overhyped things, like insensitive losses during surgery. I would rather give a dose of steroid if I suspect stress hormone insufficiency. The norepi+vaso combo can be pretty vasoconstrictive, and may depress CO in patients with bad hearts.

And there is no proven limit for norepinephrine. It differs from patient to patient (as with every vasoconstrictor, watch the peripheral perfusion, e.g. capillary refill).

I tend to stay away from protocolized prescriptions and algorithms. While norepi is best for non-anesthesiologists/non-intensivists, every patient should be on individualized pressors, like you mentioned, depending on HR/BP/contractility/access etc. The best pressor/combo is the one that brings the patient and the organs closest to their baseline physiology.

If my patients are not intubated, I ask them about the last time they were feeling well, or at their baseline. Sometimes that allows me to pinpoint the beginning of iatrogenic interventions that I can reverse (e.g. diuresis after fluids).

 

[GassYous]

FFP it is like I am reading my own thoughts

 

[deleted875186]

Good posts above.

should have anticipated hypotension in this case, unclear how much norepi this guy was on, would have added a second pressor of some kind. After 4 liters you need to really stop and think, ABG trend and monitors need to be correlated. In these cases I would send ABGs every hour on the dot, set a timer to remind yourself, I think it’s the best way to trend the patient.

would have thought about a rescue echo, or placing a PAC if you in undifferentiated shock.

Someone mentioned above dampening art line and inaccuracy in sepsis, good point, a brachial/axillary or femoral might have had different MAPs.

 

[abolt18]

Here is an excellent explanation why humans need just enough fluid to maintain mean systemic pressure (i.e. normal venous return, not MAP) at normal SVR. If the SVR decreases, the solution is (mostly) not IV fluids.




The pathophysiology of edema in the body is seriously dependent on lymphatic flow (forget the Starling equilibrium at the venous end, that was last century). It's the lymph that returns the excess fluid from the interstitium, not the venules.

At one end of the lymphatic system it's the interstitium. At the other end it's the SVC system. Hence the importance of a high CVP, such as in hypervolemia, or biventricular failure. This is true even for the pleura and peritoneum. The lymph drainage from the peritoneal space is low, about 1.2L/day. much slower than from the extremities, or even the pleural space.

Because of this, one should be extremely careful when there is an abdominal process that may sequester fluids in the belly. Despite classical teaching, not even in pancreatitis should one give uncontrolled amount of fluids. One should not aim for hemodilution, just avoiding hemoconcentration. Give as much as needed to maintain normovolemia at normal SVR; that's what the body is used to. And, since we're talking about pancreatitis (and similar "third-spacing" abdominal processes), if one sees hypoxemia in such a patient, one should assume it's fluid overload (not ARDS) until proven otherwise.

Also, IV fluids # oral fluids. IV fluids are proven to be pro-inflammatory, hence the damage to the glycocalyx. IV fluids are drugs. Give PO fluids whenever possible (in the ICU).

Don't forget all the "benefits" of fluid overload:

The Vimeo link you shared doesn't seem to work for me.

 

[nimbus]

Good posts above.

should have anticipated hypotension in this case, unclear how much norepi this guy was on, would have added a second pressor of some kind. After 4 liters you need to really stop and think, ABG trend and monitors need to be correlated. In these cases I would send ABGs every hour on the dot, set a timer to remind yourself, I think it’s the best way to trend the patient.

would have thought about a rescue echo, or placing a PAC if you in undifferentiated shock.

Someone mentioned above dampening art line and inaccuracy in sepsis, good point, a brachial/axillary or femoral might have had different MAPs.

Echo is extremely useful for cases like this. Takes much of the guesswork out of it.

 

[Hork Bajir]

Echo is extremely useful for cases like this. Takes much of the guesswork out of it.

Agree 100%. However OP stated that the attending for this case wasn’t facile with echo, and honestly I have to commend them for NOT trying to echo... As has been discussed elsewhere on this forum, rescue echo is one of those things that everyone thinks is easy to do but actually takes a fair amount of sophistication to do correctly. I know some ppl who are not facile with echo who would have tried anyway, and then confidently acted on bad information (prime example being misinterpretation of a hyperdynamic ventricle with end systolic collapse as “being empty”, leading to resuscitation with a stupid volume of fluids...)

 

[deleted875186]

Agree 100%. However OP stated that the attending for this case wasn’t facile with echo, and honestly I have to commend them for NOT trying to echo... As has been discussed elsewhere on this forum, rescue echo is one of those things that everyone thinks is easy to do but actually takes a fair amount of sophistication to do correctly. I know some ppl who are not facile with echo who would have tried anyway, and then confidently acted on bad information (prime example being misinterpretation of a hyperdynamic ventricle with end systolic collapse as “being empty”, leading to resuscitation with a stupid volume of fluids...)

If not good with echo why not a PAC. The hemodynamics numbers can be very helpful.

 

[Radetzky]

Agree 100%. However OP stated that the attending for this case wasn’t facile with echo, and honestly I have to commend them for NOT trying to echo... As has been discussed elsewhere on this forum, rescue echo is one of those things that everyone thinks is easy to do but actually takes a fair amount of sophistication to do correctly. I know some ppl who are not facile with echo who would have tried anyway, and then confidently acted on bad information (prime example being misinterpretation of a hyperdynamic ventricle with end systolic collapse as “being empty”, leading to resuscitation with a stupid volume of fluids...)

Agree, badly done echo is worse than no echo. The amount of times people say the heart looks “empty” or there are signs of “hypovolemia”...🙄

Even worse is an “underfilled LV” when the cause of LV underfilling is a massive RV and septal shift.

 

[Planktonmd]

Hello to the respected forum of anesthesia..

Had a case recently and I was thinking about it. Pt was 80 y.o. Male with preexisting HTN on ACE-I, mild dementia, overweight ( 100kg at around 1,80) and pertinent surgical Hx of repaired ing hernia 2 years prior. Had no bowel movement over 3 days and was posted for exlap for possible mechanical SBO. Labs were wnl, except Hb which was 9, Cr of 4.0, BUN of 100 ( prerenal AKI? )
On presentation he was in apparent distress, looking septic HR 110 in Afib, BP 170/90, Spo2 95% on Venturi 50%, tachypneic with a hugeee abdomen. Anyways we put an aline, induce, CVC and surgery proceeds. I started some fluids and give around 3L for presumed deficit then I continued at 1-2ml/kg/hr. Oxygenation remained acceptable at an FiO2 55%, PEEP of 8, Peaks around 30-35 which subsided to 23-25 after abdomen was opened. Urine output was at ~500cc for the first hr Patient was stable with HR in 80's ( Afib so no PPV, SPV guidance), normal MAP's around 90. Surgery went on because apparently pt had a tumor in right colon that had caused a hole in the colon with spillage of bowel content so they had to resect it and they did an anastomosis( no colostomy?). Anyway I was alone in the first hour, then my attending came back and told me why was I withholding the fluids, that the patient was profoundly hypovolemic due to ileus so we started giving more LR+NS . At around the 6L mark patient started to look worse with norepi requirement and a little worsening oxygenation. I think we gave 2 more liters after that, and the surgery was coming to a close. Patient now had a 2.5-3ug/kg/min norepi req + bumps of epi to sustain MAP>65. Oxygenation was PaO2 of 90 at 70% FiO2 with the same PEEP.

Of course we didn't extubate and my attending considered the pt terminal due to the huge pressor requirement. Anyways I shifted the pt to ICU and called it a night since it was 6am.
48 hrs later I went to check on the pt and to my big surprise he is extubated on a venturi 40% with minimal norepi req. I asked the fellow about mgmt, echo?. He said they gave some more fluids but also put the pt on CVVHD for worsening hyperkalemia and reduced urine output and of course gave broad spectrum Abx. No echo done yet ( pt only got a single dose of ciprofloxacin in the ED ). Then I lost the pt since I was rotating at a different hospital.




I am having a thought and so far none of the answers of my attendings satisfied my curiosity. So, we all know that fluid management should be a thoughtful process and overload can have deleterious effects on ileus, LOS, wound healing etc, but what I wanted to know is : Is it possible to cause iatrogenic cardiogenic shock with fluid administration in a patient like this with possible untreated diastolic heart failure, but also in a patient without any hint of heart failure? Or was the deterioration due to sepsis that was improved with proper Abx? Actual hypovolemia that needed more fluids?

Thanks in advance for reading the post. Any wisdom is really appreciated!

Your answer is already in your presentation: You said the patient had 500 ml of urine output during the first hour of surgery! Do you think a hypovolemic patient can do that?
You also did not mention the patient's baseline renal function? does he have CKD? What are the previous creatinine values?
My guess is that you were too aggressive with the fluids and too late with the pressors. Very simple case.

 

[Beeftenderloin]

And there is no proven limit for norepinephrine. It differs from patient to patient (as with every vasoconstrictor, watch the peripheral perfusion, e.g. capillary refill).

Although you’re technically right about this, a lot of people use it as an excuse to be lazy and practice bad medicine.

I think about it like outpatient management of antihypertensives. No one gets maxed on their ACE inhibitor before starting a second agent. And when they start that second agent, it doesn’t make sense for it to be an ARB, you use something with a different mechanism of action.

Pressers should be treated the same way. No sense flogging them with more and more alpha agonism when moderate to high doses aren’t getting the job done and escalating further could lead to complications. Time to start thinking about the underlying issue a little more thoughtfully and maybe target a different mechanism.

 

[chessknt]

Although you’re technically right about this, a lot of people use it as an excuse to be lazy and practice bad medicine.

I think about it like outpatient management of antihypertensives. No one gets maxed on their ACE inhibitor before starting a second agent. And when they start that second agent, it doesn’t make sense for it to be an ARB, you use something with a different mechanism of action.

Pressers should be treated the same way. No sense flogging them with more and more alpha agonism when moderate to high doses aren’t getting the job done and escalating further could lead to complications. Time to start thinking about the underlying issue a little more thoughtfully and maybe target a different mechanism.

That is actually false--most people will max out each agent in sequence because we know that the more meds people have to take the less likely they are to actually take them consistently.

 

[IlDestriero]

hour of urine is not helpful to me. He’s 81 and demented. Is that 500mL old urinary retention? So much is going on in the first hour after the foley goes in like central line, prepping, the nurse who placed the foley going home without sign out, etc. What’s the trend? Is he now oligo/anuric

Agree.
Interesting discussion.
His acuteish decompensation was probably due to sepsis and the release of the evil humors.
I don’t think I would have managed him the same way, but in the end it was a win. It could have easily ended with tachycardia, hypotension, MI, withdraw support.
The take home is don’t pound with fluid unless there’s a reason to. For all we know if you ran him dry, you may have had to tank him up anyway because of hypotension unresponsive to pressors. Just like analgesia is multimodal, so is pressure management.
I’m pretty sure our surgeons wouldn’t charge for hours on hooking this guy back up when he’s going septic and actively trying to die either.
Laparotomy, some profanity, damage control, ostomy, wash out, GTFO.
Live to fight another day.

 

[Arch Guillotti]

Echo is extremely useful for cases like this. Takes much of the guesswork out of it.

Sure but many of us are not even credentialed for it.

 

[Arch Guillotti]

If not good with echo why not a PAC. The hemodynamics numbers can be very helpful.

No way I am going to float a PAC if I haven’t done one in a long time.

 

[Beeftenderloin]

That is actually false--most people will max out each agent in sequence because we know that the more meds people have to take the less likely they are to actually take them consistently.

Your right about that in certain patient populations, but structuring medication dosing to optimize compliance is a different argument than structuring dosing to optimize patient benefit. Higher dose = more side effects.

 

[chessknt]

Your right about that in certain patient populations, but structuring medication dosing to optimize compliance is a different argument than structuring dosing to optimize patient benefit. Higher dose = more side effects.

From an acei? Do you practice outpatient medicine because I do and I have next to no concern about acei side effects 20 vs 40 lisinopril vs someone remembering to take 2 meds instead of 1 (or more commonly 4-5 instead of 3-4). It is infuriating to see people come in on 4 meds at half doses all treating the same thing.

 

[Beeftenderloin]

From an acei? Do you practice outpatient medicine because I do and I have next to no concern about acei side effects 20 vs 40 lisinopril vs someone remembering to take 2 meds instead of 1 (or more commonly 4-5 instead of 3-4). It is infuriating to see people come in on 4 meds at half doses all treating the same thing.

No, I don’t (thank god) just drawing a corollary between the way I think about presser management and the way I was taught to manage outpatient antihypertensives just a few short years ago by people who do that for a living.

I’ll happily defer to someone who has more expertise managing outpatient HTN than I do, but I stand by my original point as it applies to vasopressors.

 

[chessknt]

No, I don’t (thank god) just drawing a corollary between the way I think about presser management and the way I was taught to manage outpatient antihypertensives just a few short years ago by people who do that for a living.

I’ll happily defer to someone who has more expertise managing outpatient HTN than I do, but I stand by my original point as it applies to vasopressors.

Absolutely I agree that maxing norepinephrine before adding another agent is usually suboptimal care. In my experience people needing 3 or more agents without something acute and immediately fixable however generally do very poorly no matter what kind of care they get.

 

[WheezyBaby]

Curious how well the patient was followed outpatient. My guess is he has relatively poorly controlled hypertension and resulting ckd 4ish. Anemia likely mixed anemia of ckd and aocd related to malignancy. I think his BP is at or near baseline. I think his AKI occurred over a day or so and is primarily related to poor PO and IAH + ARB predisposing. I suspect part of his brisk UOP if truly present was related to the combination of initial intravascular volume correction and IAH relief with lap. Intraop hypotension related to "release of humors" and sepsis response as above with vasodilation in setting of diastolic heart failure with acutely impaired filling with afib, and poor UOP initially related to this + having a MAP below the patients autoregulatory curve (probably considerably higher than 65) and subsequently related to impaired renal perfusion pressure with volume overload. Sepsis response resolved and fluid status improved status post CRRT. Surprised patient didn't full blown ARDS though. There is my crystal ball anyway

 

[anbuitachi]

no one should be getting 8 liters of crystalloids that fast