Question about anesthesia for peritonitis

[parcus]

I recently did this case of a patient with peritonitis, perforated bowel from a colonoscopy. Pt arrived shocked in ED, they gave him some fluids, he came to us with a bp of 100x60, lethargic. Attending decided to do induction with ketamine-S (people don't like the regular ketamine here)/fent/benzo, maintained with sevo/ intermitent ketamine boluses. It went downhill from there, he became hypotensive, had to give him high doses of norepi/epi. Afterwards, 22 issues at the ICU he stayed in the room and became hypotensive again after a few hours => opened him again, found out he was bleeding. Now, 6 days later he is recovering pretty well. Many more things happened, but I'll not go into details about the mess.

So, I imo doing this with ketamine only could be a better alternative (the extra fent, midaz only served to push his BP lower, or maybe it was just a confounder for something that would happen anyways?). I could not find any reason not to. For maintenance, same thing: why am I battling sevo vasodilation with vasoactive drugs when I could just keep him on a ketamine infusion? Pretty sure all these different things going on (extra boluses of midaz, lowering epi while sevo vasodilation was running out) only delayed us from figuring out he was bleeding. Also, running sevo at low doses make me scarred he might awake. Sure, I'd have to give him a little benzo at the end, but that sounds to me much more controlled.

I looked for it, but couldn't find anything saying: don't do ketamine infusion, or X may happen except maybe in a small subset of patients with certain specific diseases, like heart ischemia, or any report of serious harm from ketamine infusions at all. Am I missing something?

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[Iso4ane]

Why is ketamine so hemodynamically stable (relative to say propofol)? I think the answer to that will give you the answer you need.

 

[Hoya11]

I recently did this case of a patient with peritonitis, perforated bowel from a colonoscopy. Pt arrived shocked in ED, they gave him some fluids, he came to us with a bp of 100x60, lethargic. Attending decided to do induction with ketamine-S (people don't like the regular ketamine here)/fent/benzo, maintained with sevo/ intermitent ketamine boluses. It went downhill from there, he became hypotensive, had to give him high doses of norepi/epi. Afterwards, 22 issues at the ICU he stayed in the room and became hypotensive again after a few hours => opened him again, found out he was bleeding. Now, 6 days later he is recovering pretty well. Many more things happened, but I'll not go into details about the mess.

So, I imo doing this with ketamine only could be a better alternative (the extra fent, midaz only served to push his BP lower, or maybe it was just a confounder for something that would happen anyways?). I could not find any reason not to. For maintenance, same thing: why am I battling sevo vasodilation with vasoactive drugs when I could just keep him on a ketamine infusion? Pretty sure all these different things going on (extra boluses of midaz, lowering epi while sevo vasodilation was running out) only delayed us from figuring out he was bleeding. Also, running sevo at low doses make me scarred he might awake. Sure, I'd have to give him a little benzo at the end, but that sounds to me much more controlled.

I looked for it, but couldn't find anything saying: don't do ketamine infusion, or X may happen except maybe in a small subset of patients with certain specific diseases, like heart ischemia, or any report of serious harm from ketamine infusions at all. Am I missing something?

Ketamine is a powerful psychoactive hypnotic. It is not used for maintenance alone due to the superiority of drugs like sevo (very CV stable in low doses and more pleasant sleep/total anesthetic). Ketamine as a sole maintenance agent is cruel and unusual. Most anesthesiologists agree that when you give ketamine you should also give some midaz to relax and combat any scary hallucinations/dreams occuring(which by the way midaz is very CV stable). Also, ketamine has some analgesic properties but your going to need to give some narcotic if you want to actually be a merciful human here, and so fentanyl is unavoidable and the most HD stable of the opiates. So midaz and fentanyl more than appropriate.

Overall, I think the management of the anesthesiologist was more than appropriate, and the use of ketamine to spare some sevo MAY have helped keep BP up, but probably not a ton. Things like Shock and Hypovolemia (and now being given PPV on the vent) are way more likely to contribue to HD instability than the difference that you are arguing between ketamine and sevo.

When you have someone who is on multiple powerful pressors, has multiple reasons for hypotension (shock, hypovolemia) it can be hard to pick up on an acute surgical bleed as being the immediate cause of worsening hypotension. I wouldnt look at the anesthesia (esp a little sevo vs more ketamine) as a major factor at all.

 

[narcusprince]

I think the anesthetic management was more then adequate. Whats missing here is the information about the rescucitative management. Aline? What was your attendings assessment of volume status and how did he correct it. Looking at the inhaled agent versus ketamine infusion versus blah blah blah. What markers did you use to guide your management. If you had S ketamine you surely had access to serial abgs.

 

[parcus]

I think the anesthetic management was more then adequate. Whats missing here is the information about the rescucitative management. Aline? What was your attendings assessment of volume status and how did he correct it

Yes, Aline. At first we did 5 liters of RL during the first surgery (about 3 hours). His Hb dropped from 12 => 11. After it ended and we turned off the sevo, his MAP started going to 90s. That is when attending decided to reduce the norepi dose by 25%, we did another bolus of midazolam. Then his MAP started tanking to 30s. At that point we ramped the pressors up again and waited a little bit, there was some questions about validity of Aline by another attending (curve looked bigeminal, not sure what that means). Tried correcting his hypocalcemia, did not work. Afterwards the other attending looked at him and said "he looks dry like an orange peel". We don't have fancy ways of monitoring fluid status, most we can do here is measuring CVP changes; we didn't do it here, also, I don't know how useful that is. We did a fluid bolus and he responded. Around that point his hemoglobin went to 6.6. Blood took like an hour to arrive for some reason, so we kept the RL flowing.

Looking at the inhaled agent versus ketamine infusion versus blah blah blah. What markers did you use to guide your management. If you had S ketamine you surely had access to serial abgs.

Urine output and MAP, we did serial ABGs, it has base excess only seemed to go from like -5 to -7, don't remember exactly.

 

[Psai]

Don't follow urine output. Don't follow base excess lol

Instead of sevo you can maybe try iso/nitrous

If you have hypotension, run high levo. Pressor requirement should go down once dead bowel is out.

I'm less concerned about recall during surgery and more concerned about the patient DYING. It's easier to say sorry for the ****ty analgesia than it is to say sorry for killing you.

If you're concerned about opiates, you can try opioid free anesthesia with ketamine, lido, precedex, tylenol, nsaids, etc.

 

[IlDestriero]

His BP problem was certainly because he had a perforated bowel and was in septic shock. It sounds like he was managed ok. You need to hammer the fluids in these newly septic and unstable patients, plus abx and pressors. He probably came in barely resuscitated and then went off the cliff from 3rd spacing, vasodilatation, anesthetics, SIRS, etc.
You didn’t provide many details but I would have paralyzed him and kept him paralyzed, given liters of crystalloid, probably 1L+ pre induction, started epi/norepinephrine immediately and ran him on 1/2 Mac sevo and fent boluses. Ketamine was an OK choice for induction, but if he’s pretty obtunded you don’t need much of anything. Less is more because you know he’s likely to bottom out. One more reason for a 20/kg pre induction LR bolus. One thing I’ve noticed is that if you give 20/kg and nothing happens, you’re probably in trouble. Your ABGs are consistent with that. Did you check lactates?


--
Il Destriero

 

[vector2]

Don't follow urine output. Don't follow base excess lol

Instead of sevo you can maybe try iso/nitrous

If you have hypotension, run high levo. Pressor requirement should go down once dead bowel is out.

I'm less concerned about recall during surgery and more concerned about the patient DYING. It's easier to say sorry for the ****ty analgesia than it is to say sorry for killing you.

If you're concerned about opiates, you can try opioid free anesthesia with ketamine, lido, precedex, tylenol, nsaids, etc.

Yea, I personally would not be running nitrous on a case involving bowel excisions and anastomoses.


But in regard to the case, the post-induction hypotension was probably due to decompensation of distributive, septic and/or hypovolemic shock. Patients in shock have usually already fully ramped up their intrinsic sympathetic nervous system by the time their bp is borderline low and they're in extremis. Vapor and opiates will certainly blunt this compensation, but it's folly to think that running a general anesthetic level ketamine infusion is going to spare this effect and you magically wouldn't need exogenous norepi for a sick bowel perf. The patient's endogenous epi and norepi are already maxed out so you likely won't get much secondary adrenergic release from ketamine, but you certainly will get some cardiac depression if the dose is high enough and the patient is sick enough.

In regard to fluid management during surgery on septic patients, be judicious once you've hit the 30cc/kg mark on crystalloids, especially if you're not seeing an improvement in any surrogate markers of perfusion with further fluid. Once the dead bowel is out, be very judicious. A soggy, swollen, inflamed bowel is exactly the kind that dehisces or bleeds after the anastomosis is complete.

 

[dannyboy1]

The anesthetic management is pretty simple etomidate, sux for induction and maintenance on a whiff of sevo. This patient needs to be resuscitated, give at least 30 cc/kg of crytalloid and start pressers early. MAP needs to go up and lactate needs to go down. Would also not have waited till you saw a hemoglobin of 6 to transfuse. You know this patient will be getting blood, why overload him with crystalliod first?

 

[deleted697535]

Why do think anything was wrong with the anesthetic?
Someone basically stabbed this guy in the guts. That will **** your **** up. Probably kill most older people

This sounds like a fairly standard sick laparotomy. Get used to it. You'll probably see it 3 times a week for the rest of your career...

There are no fancy monitors for this. There is no test better that the good old fashioned leg raise to tell you does he need fluid or not. There is no test to tell you does he need blood or not.
Almost all perf's need norepi. Id prob use vaso as my second line and given blood earlier but thats about it. Everything else the same. Bolus epi when youre screwed. Drop the head of the bed, stop the sevo when hes about to code...
Boluses of fent or sufent for analgesia and get on with it.

i wouldnt dream of doing a laparotomy on ketamine infusion. No-one would i know. sevo or des is perfect. midaz only causes ante grade amnesia. you mentioned using this at the end dont know why.

 

[anbuitachi]

I recently did this case of a patient with peritonitis, perforated bowel from a colonoscopy. Pt arrived shocked in ED, they gave him some fluids, he came to us with a bp of 100x60, lethargic. Attending decided to do induction with ketamine-S (people don't like the regular ketamine here)/fent/benzo, maintained with sevo/ intermitent ketamine boluses. It went downhill from there, he became hypotensive, had to give him high doses of norepi/epi. Afterwards, 22 issues at the ICU he stayed in the room and became hypotensive again after a few hours => opened him again, found out he was bleeding. Now, 6 days later he is recovering pretty well. Many more things happened, but I'll not go into details about the mess.

So, I imo doing this with ketamine only could be a better alternative (the extra fent, midaz only served to push his BP lower, or maybe it was just a confounder for something that would happen anyways?). I could not find any reason not to. For maintenance, same thing: why am I battling sevo vasodilation with vasoactive drugs when I could just keep him on a ketamine infusion? Pretty sure all these different things going on (extra boluses of midaz, lowering epi while sevo vasodilation was running out) only delayed us from figuring out he was bleeding. Also, running sevo at low doses make me scarred he might awake. Sure, I'd have to give him a little benzo at the end, but that sounds to me much more controlled.

I looked for it, but couldn't find anything saying: don't do ketamine infusion, or X may happen except maybe in a small subset of patients with certain specific diseases, like heart ischemia, or any report of serious harm from ketamine infusions at all. Am I missing something?

Looks fine to me. Doesnt really seem like a crazy case anesthetic wise. Also seems like your attending did fine from what you described. Anesthesia isn't just if x happens do y. there's a lot of differentials and diagnosis, and treating it accordingly. I would say hypotension from something like this, the top thing on differential is worsening septic shock, probably from surgeons disrupting the whole abdomen of feces. I wouldn't just immediately tell the surgeon to reopen him up after an episode of hypotension since there are many reasons for patient to be hypotensive. But off course bleeding is on the differential as well.

With regards to the ketamine. The patient's autonomics are most likely maxed oout. It won't really matter if you use ketamine or sevoflurane, you'll still use pressors. And also it wont make it easier to find the bleeder than just using sevo. Just don't use 1 MAC of it.

The anesthetic management is pretty simple etomidate, sux for induction and maintenance on a whiff of sevo. This patient needs to be resuscitated, give at least 30 cc/kg of crytalloid and start pressers early. MAP needs to go up and lactate needs to go down. Would also not have waited till you saw a hemoglobin of 6 to transfuse. You know this patient will be getting blood, why overload him with crystalliod first?

I think he checked a crit and it happened to be 6.6, not he waited from 7 to 6.6 before transfusing . But still, how do you know this patient will be getting blood? Only ended up getting it due to a missed bleeder.

 

[deleted697127]

Don't follow urine output. Don't follow base excess lol

Instead of sevo you can maybe try iso/nitrous

If you have hypotension, run high levo. Pressor requirement should go down once dead bowel is out.

I'm less concerned about recall during surgery and more concerned about the patient DYING. It's easier to say sorry for the ****ty analgesia than it is to say sorry for killing you.

If you're concerned about opiates, you can try opioid free anesthesia with ketamine, lido, precedex, tylenol, nsaids, etc.

You don’t follow urine output or base excess?

 

[Urzuz]

You don’t follow urine output or base excess?

I think most people will follow UOP and BE/BD, but I don't think you should use them as silver bullets to alter treatment and make major treatment decisions. A lot of factors can affect both UOP and BD, and it would be silly to wildly change your care based on these two markers. But, like anything, they help paint an overall picture as to a patient's physiologic state and can serve as small pieces of a much bigger jigsaw puzzle.

 

[dhb]

your going to need to give some narcotic if you want to actually be a merciful human here

I'm a monster

 

[vector2]

UOP is next to worthless for measuring anything but UOP, especially under the stress of surgery/anesthesia which can cause AVP release and lower UOP even when the pt is euvolemic. BD at the minimum has a retrospective correlation in the trauma and burn literature with need for ongoing resuscitation, and in sepsis it appears to have a decent correlation with lactate derangement. Bottom line is, think very carefully about giving 10+ Liters to someone unless it's an open TAAA repair, 80% burn, HIPEC, clamshelled and chevroned polytrauma etc

 

[deleted697535]

I write all those things down (for legal purposes) and then ignore them.

 

[deleted171991]

I think most people will follow UOP and BE/BD, but I don't think you should use them as silver bullets to alter treatment and make major treatment decisions. A lot of factors can affect both UOP and BD, and it would be silly to wildly change your care based on these two markers. But, like anything, they help paint an overall picture as to a patient's physiologic state and can serve as small pieces of a much bigger jigsaw puzzle.

Once and forever, BD is prehistorical BULL****!

Let's use Wikipedia:
"Base excess is defined as the amount of strong acid that must be added to each liter of fully oxygenated blood to return the pH to 7.40 at a temperature of 37°C and a pCO2 of 40 mmHg (5.3 kPa).[2] A base deficit (i.e., a negative base excess) can be correspondingly defined in terms of the amount of strong base that must be added.

A further distinction can be made between actual and standard base excess: actual base excess is that present in the blood, while standard base excess is the value when the hemoglobin is at 5 g/dl. The latter gives a better view of the base excess of the entire extracellular fluid.[3]

The term and concept of base excess were first introduced by Poul Astrup and Ole Siggaard-Andersen in 1958."

"Base excess can be estimated from the serum bicarbonate concentration ([HCO3−]) and pH by the equation:[4]

Base excess = 0.93 x ([HCO3-] - 24.4 +14.8 x (pH-7.4)), with units of mEq/L."

"Base excess beyond the reference range indicates

• metabolic alkalosis if too high (more than +2 mEq/L)
• metabolic acidosis if too low (less than −2 mEq/L)"

Stupid surgical teaching says to give fluids when the patient has a base deficit (i.e. metabolic acidosis). Really? When we know that hypovolemia can also cause "contraction" metabolic alkalosis, i.e. "base excess". So when should one give fluids, when there is a base deficit, or when there is a base excess??? The BD brainfart probably comes from the trauma literature (and it makes me itch to just traumatize those who still use the concept and hurt patients). Healthy trauma patients who are hypovolemic (i.e. have lost blood), will have organ ischemia, ergo metabolic acidosis, ergo base deficit. But BD doesn't mean **** for fluid replacement in any (other) context. Forget that it even exists. Just stop using acid-base status for fluid replacement altogether. Same goes for lactate levels, and other fairy tales.

A patient with peritonitis does NOT need "at least" 30 ml/kg fluids upfront. Like most septic patients, he needs AT MOST 30 ml/kg fluids (unless there is proof of hypovolemia, e.g. low CO despite a normal/high EF and a normal/high SVR). What he does need is pressors, and replacement of objective fluid/blood losses. Please stop drowning critical patients and their internal organs. All that fluid will just extravasate where inflammation and gravity will break the endothelial barrier (at least the surgical site = the abdomen, the lung and the kidneys), will cause local venous congestion with local ischemia and failure of those organs (flow is not dependent just on MAP, but on perfusion pressure, which is calculated similarly to the cerebral perfusion pressure, i.e. MAP minus venous pressure or compartment pressure), and may end up killing those patients (early AKI alone, e,g, from abdominal hypertension/fluids, has a 30% chance of dying within a year). But, hey, one gets beautiful MAP numbers for a few hours, for defending oneself in court from similar "experts". And then the patient is f*cked up for days, because INTERSTITIAL FLUID IS MOSTLY REABSORBED THROUGH LYMPATHICS, which is a slow process; there is little Starling-type reabsorption at the venous end of the capillary in real life, especially with inflammation. Another fairy tale.

We, anesthesiologists, are on the brain side of the blood-brain barrier. So we should think, not just do. Don't just give fluids blindly; prove that the patient needs fluids, based on contemporary science.

I would argue that the one thing a really sick patient actually needs is a PAC or TEE probe for SVR and CO estimation. It's ridiculous to treat a distributive + possibly cardiogenic + possibly hypovolemic shock (that's what septic shock actually is) while just monitoring the MAP, UOP, ABG, lactate, and other unreliable guesstimates of peripheral oxygen delivery. I don't expect people to start watching microscopic nail perfusion (as a proxy for peripheral capillary perfusion) and use both pressors and peripheral vasodilators at the same time, as some smart intensivists do, but don't just "do something". FIRST DO NO HARM. When one treats a septic patient, one should think like a good medical intensivist. Also, one shouldn't use arbitrary numbers, such as the 7 g/dL transfusion threshold, for everybody. Every patient is different, and even the best science (which is not the case here) has exceptions.

And midazolam is not a "CV stable" drug. It's a VASODILATOR. Hence the increased pressor requirement after giving it to a patient whose compensatory mechanisms have been already depleted. Same goes for the idea of ketamine infusion in a profoundly septic patient. When the sympathetic axis is already exhausted, it DEPRESSES myocardial contractility.

Also, sepsis is associated with hypocalcemia. It doesn't mean ****. Do NOT correct it. Same goes for compensatory tachycardia, unless excessive for that particular patient.

This case wasn't even a big deal. Perfed colon after having been prepped for colonoscopy? Yawn...

</rant>

 

[dannyboy1]

I think he checked a crit and it happened to be 6.6, not he waited from 7 to 6.6 before transfusing . But still, how do you know this patient will be getting blood? Only ended up getting it due to a missed bleeder.

This patient got a bunch of fluid in the ED followed by more intraop and no doubt will get more in the ICU. He is going to be mechanically ventilated for at least 24 hours post procedure and likely for longer. He will be getting frequent blood draws around the clock. You know that his hemoglobin will decreasing to at least 8 (it seems to settle around there for most ICU patients) I’m just advocating a balanced fluid approach since he will be more than likely getting transfused during this stay, why not get the benefit from it in the OR.

 

[deleted697535]

Is calcium induced myocardial stunning still/ever a thing? I've seen people tank from a bolus of calcium chloride. Ive always taken lots of care when giving it.

 

[anbuitachi]

This patient got a bunch of fluid in the ED followed by more intraop and no doubt will get more in the ICU. He is going to be mechanically ventilated for at least 24 hours post procedure and likely for longer. He will be getting frequent blood draws around the clock. You know that his hemoglobin will decreasing to at least 8 (it seems to settle around there for most ICU patients) I’m just advocating a balanced fluid approach since he will be more than likely getting transfused during this stay, why not get the benefit from it in the OR.

personally, with all the studies showing negative outcome with transfusion, id rather transfuse when i need to, and not transfuse prophylactic ally unless i know an acute hemorrhage is likely . Id be fine with 8 in the icu.

 

[parcus]

Why is ketamine so hemodynamically stable (relative to say propofol)? I think the answer to that will give you the answer you need.

Increases release of catecholamines, blocks re-uptake, depress myocardium a bit, but this is usually made up for for increased sympathetic/decreased parasympathetic tone to the heart. Apparently the direct myocardial depression effect is more of a theoretical issue than a practical one; overall effect is increase in BP, HR, CO. Sounds like what I want in a patient with severe shock about to enter septic shock.

Ketamine is a powerful psychoactive hypnotic. It is not used for maintenance alone due to the superiority of drugs like sevo (very CV stable in low doses and more pleasant sleep/total anesthetic). Ketamine as a sole maintenance agent is cruel and unusual. Most anesthesiologists agree that when you give ketamine you should also give some midaz to relax and combat any scary hallucinations/dreams occuring(which by the way midaz is very CV stable). Also, ketamine has some analgesic properties but your going to need to give some narcotic if you want to actually be a merciful human here, and so fentanyl is unavoidable and the most HD stable of the opiates. So midaz and fentanyl more than appropriate.

Overall, I think the management of the anesthesiologist was more than appropriate, and the use of ketamine to spare some sevo MAY have helped keep BP up, but probably not a ton. Things like Shock and Hypovolemia (and now being given PPV on the vent) are way more likely to contribue to HD instability than the difference that you are arguing between ketamine and sevo.

The addition of midaz at the beginning of surgery is to blunt the stimulant effects of ketamine on the cv system, which makes sense in a normal patient, not in a septic patient about to enter PPV. I can see that as beneficial to avoid his HR from shooting up, but fent still doesn't have a place in this induction imo. Hallucinations occur at awakening according to Miller's. Though I don't know how frequent exceptions to the rules are when it comes to ketamine, doesn't look like very extensive studies have been done with it as a sole anesthetic/induction agent. In any case, if the patient goes to lala land but survives 22 it, sounds like a worthy tradeoff to me. My patient went from no pressors to 2 mcg/kg/min of norepi and low dose epi, I am somewhat skeptical that this would be mostly about PPV or other factors, especially after so much hydration, but you may be right.

Don't follow urine output. Don't follow base excess lol

I normally look at those for mere curiosity.

Instead of sevo you can maybe try iso/nitrous

Not quite excited about nitrous in bowel case. Iso sounds like an interesting option for the right patient, but I don't think we have it here, will check that.

Your ABGs are consistent with that. Did you check lactates?

Sadly not. Not much of a culture to target lactate levels intraoperatively here. But, in sepsis there is derangement of metabolic pathways 22 inflammation, not something I can target with fluids or pressors, if it was going up, great, if it was going down... shrug? Sounds like something to monitor to see if ATBx are working in the long term to me. Haven't done a very thorough review on this recently, maybe my knowledge isn't current?

The patient's endogenous epi and norepi are already maxed out so you likely won't get much secondary adrenergic release from ketamine, but you certainly will get some cardiac depression if the dose is high enough and the patient is sick enough.

But at the end of the day it also blocks reuptake/decreases parasympathetic tone, which could theoretically always make up for it?

In regard to fluid management during surgery on septic patients, be judicious once you've hit the 30cc/kg mark on crystalloids, especially if you're not seeing an improvement in any surrogate markers of perfusion with further fluid. Once the dead bowel is out, be very judicious. A soggy, swollen, inflamed bowel is exactly the kind that dehisces or bleeds after the anastomosis is complete.

In this specific case the bleeding came from an abdominal wall artery they perforated while putting the drain in. Anyways, his whole bowel was swollen as hell even before all the hydration, I wonder how much harm the extra hydration did here. I suctioned litters of fluid out of his NGT, his inside is opened and loosing water to the environment, maybe with some more fancy method of measuring intravascular volume I could minimize the hydration. The 30cc/kg sounds like come from sepsis guidelines, is it really valid here? I am not very acquainted with the anesthesia literature about this.

There are no fancy monitors for this. There is no test better that the good old fashioned leg raise to tell you does he need fluid or not. There is no test to tell you does he need blood or not.
Almost all perf's need norepi. Id prob use vaso as my second line and given blood earlier but thats about it. Everything else the same. Bolus epi when youre screwed. Drop the head of the bed, stop the sevo when hes about to code...

Didn't think about the leg raise test, sounds like I could try it.

I'm a monster

Me too, isn't there increasing evidence showing that the more opioids we do intraoperatively, the more opioids the patient needs postoperatively (when it really matters)?

Is calcium induced myocardial stunning still/ever a thing? I've seen people tank from a bolus of calcium chloride. Ive always taken lots of care when giving it.

After a ton of hydration Miller's recommend replacing Calcium, didn't check the references though. It also says calcium gluconate is safer because of less extravasation tissue damage and lability in calcium levels.

Stupid surgical teaching says to give fluids when the patient has a base deficit (i.e. metabolic acidosis). Really? When we know that hypovolemia can also cause "contraction" metabolic alkalosis, i.e. "base excess". So when should one give fluids, when there is a base deficit, or when there is a base excess??? The BD brainfart probably comes from the trauma literature (and it makes me itch to just traumatize those who still use the concept and hurt patients). Healthy trauma patients who are hypovolemic (i.e. have lost blood), will have organ ischemia, ergo metabolic acidosis, ergo base deficit. But BD doesn't mean **** for fluid replacement in any (other) context. Forget that it even exists. Just stop using acid-base status for fluid replacement altogether. Same goes for lactate levels, and other fairy tales.

Ok, sounds reasonable.

I would argue that the one thing a really sick patient actually needs is a PAC or TEE probe for SVR and CO estimation. It's ridiculous to treat a distributive + possibly cardiogenic + possibly hypovolemic shock (that's what septic shock actually is) while just monitoring the MAP, UOP, ABG, lactate, and other unreliable guesstimates of peripheral oxygen delivery. I don't expect people to start watching microscopic nail perfusion (as a proxy for peripheral capillary perfusion) and use both pressors and peripheral vasodilators at the same time, as some smart intensivists do, but don't just "do something". FIRST DO NO HARM. When one treats a septic patient, one should think like a good medical intensivist. Also, one shouldn't use arbitrary numbers, such as the 7 g/dL transfusion threshold, for everybody. Every patient is different, and even the best science (which is not the case here) has exceptions.

No anesthesiologists here know how to do TEE, or even simple TTEs for that matter. Even if they did, US, let alone TEE is hard to come by in the OR here. Same goes for CO monitors and PP variation. Limitations of life... shrug.

And midazolam is not a "CV stable" drug. It's a VASODILATOR. Hence the increased pressor requirement after giving it to a patient whose compensatory mechanisms have been already depleted. Same goes for the idea of ketamine infusion in a profoundly septic patient. When the sympathetic axis is already exhausted, it DEPRESSES myocardial contractility.

Again, it doesn't only release more catecholamines, besides, all other maintenance anesthetics depress myocardial contractility/vasodilate to one degree or another. I didn't say anything different about midazolam, hence why I enterntain the possibility of a ketamine only induction and maintenance.

Also, sepsis is associated with hypocalcemia. It doesn't mean ****. Do NOT correct it. Same goes for compensatory tachycardia, unless excessive for that particular patient.

Fair point, but Miller's recommend replacing Calcium below 1.8 mEqs/L to "support inotropy", I'll check the reference later.

This case wasn't even a big deal. Perfed colon after having been prepped for colonoscopy? Yawn...

</rant>

Agreed, pretty common, but I tried to look up what the standard management for these patients are and I could not find any. Trying to find people with experience doing things differently.

 

[OB1🤙]

Just throwing out one quick consideration- one thing I see too often from those ignoramuses who still use "normal" saline to resuscitate, AND use the i-stat cartridges that don't show chloride- many times that "refractory acidosis" is iatrogenic from hyperchloremia. And yet these folks keep chasing the acidosis with saline, thinking they must still be behind on fluid...

This KILLS me when I see it.

 

[deleted697535]

Just throwing out one quick consideration- one thing I see too often from those ignoramuses who still use "normal" saline to resuscitate, AND use the i-stat cartridges that don't show chloride- many times that "refractory acidosis" is iatrogenic from hyperchloremia. And yet these folks keep chasing the acidosis with saline, thinking they must still be behind on fluid...

This KILLS me when I see it.

But has there ever been a trial to show one fluid better than another in hard facts? Like mortality.
Hyperchloremic MA is interesting but I don't think it means anything. I'm thinking of the SPLIT trial 2015

 

[deleted171991]

The SPLIT trial was done on mostly post-elective surgery patients, not the ultrasick true ICU population. Only 4% had septic shock. Also, the median of fluids administered during the ICU stay was only 2L, which makes the study basically irrelevant for real life .

One can give a total of 2L of NS to my ICU patients anytime, as far as I am concerned. I use NS in the OR all the time, since the IV fluid shortage, and couldn't care less. At 2L, the crystalloid choice really doesn't matter.

There is no doubt in my mind that hyperchloremic MA due to a lot of NS is a real entity, and it's the last thing an already acidemic patient needs. One can see the drop in the strong ion difference even without an ABG.

 

[OB1🤙]

Yeah I'm talking about the 4-6+ liter of saline trauma resuscitations, that show up in the ICU afterward with chlorides of 115+.

Agreed that a liter or two of saline won't hurt anyone.

 

[anbuitachi]

The SPLIT trial was done on mostly post-elective surgery patients, not the ultrasick true ICU population. Only 4% had septic shock. Also, the median of fluids administered during the ICU stay was only 2L, which makes the study basically irrelevant for real life .

One can give a total of 2L of NS to my ICU patients anytime, as far as I am concerned. I use NS in the OR all the time, since the IV fluid shortage, and couldn't care less. At 2L, the crystalloid choice really doesn't matter.

There is no doubt in my mind that hyperchloremic MA due to a lot of NS is a real entity, and it's the last thing an already acidemic patient needs. One can see the drop in the strong ion difference even without an ABG.

Yeah I'm talking about the 4-6+ liter of saline trauma resuscitations, that show up in the ICU afterward with chlorides of 115+.

Agreed that a liter or two of saline won't hurt anyone.

I see this in the ICU all the time when get called for intubations. Patients pH is 7.0, and is being resuscitated with NS especially in the MICU, which i dont quiet understand. NS has a pH of 5, tons of chloride, and not much of anything else. Am i missing something?

But has there ever been a trial to show one fluid better than another in hard facts? Like mortality.
Hyperchloremic MA is interesting but I don't think it means anything. I'm thinking of the SPLIT trial 2015

Not that i know of but lack of evidence doesn't mean evidence of no difference. I think when there isn't evidence, why resuscitate someone with a pH of 5, and is hypernatremic, hyperchloremic?? I see no benefit. I think we base a lot of stuff on studies that looks at short term morbidity/mortality. I wonder how the stats will play out if the time range studied is changed?

 

[Iso4ane]

Increases release of catecholamines, blocks re-uptake, depress myocardium a bit, but this is usually made up for for increased sympathetic/decreased parasympathetic tone to the heart. Apparently the direct myocardial depression effect is more of a theoretical issue than a practical one; overall effect is increase in BP, HR, CO. Sounds like what I want in a patient with severe shock about to enter septic shock.

Think about ephedrine. In regard to the hemodyanmic stability, they're similar. One big issue with ephedrine is tachyphylaxis. Now add known myocardial depression on top and you're asking for trouble. As induction agent cool, continuous infusion for sedation (in a septic patient no less) not so cool. Plus, if he's that sick already you're gonna want some 'cleaner' acting medications.

 

[vector2]

But at the end of the day it also blocks reuptake/decreases parasympathetic tone, which could theoretically always make up for it?

In this specific case the bleeding came from an abdominal wall artery they perforated while putting the drain in. Anyways, his whole bowel was swollen as hell even before all the hydration, I wonder how much harm the extra hydration did here. I suctioned litters of fluid out of his NGT, his inside is opened and loosing water to the environment, maybe with some more fancy method of measuring intravascular volume I could minimize the hydration. The 30cc/kg sounds like come from sepsis guidelines, is it really valid here? I am not very acquainted with the anesthesia literature about this.

Everyone knows what the book pharmacology says about ketamine or etomidate, etc, but you're talking to a group of anesthesiologists who have collectively taken care of thousands of critically ill patients. In the real world, regardless of the mechanisms involved, we still use these agents judiciously in sick patients because we've seen post-induction hypotension so often. Just the other day I had to induce a 60kg female for significant bleeding after a possibly septic abortion. She had already received 2u prbc and 2l crystalloid. Presenting vitals as she rolled to OR from ER were hr 115 and and sbp 85-90. Started pressure bagging another 1l LR, administered neo, and pushed 1mg/kg ketamine and 2mg versed. She still dropped her pressure after a so-called gentle induction, likely because she was still hypovolemic and/or in early sepsis and the loss of consciousness blunted her SNS more than the ketamine helped it. The point is that for patients in bona fide shock of all types, you should throw what Miller says about induction drugs out the window and treat the patient in the room.

In regard to fluid, the takeaway point is not that there's some magic number where fluid administration is enough or too little. 'All' exogenous fluid administration carries risk, and unless you can make an argument as you did where there is significant ongoing losses (ngt, largely exposed viscera, active bleeding) PLUS an improvement in perfusion as you're giving more and more fluid, then you need to put the brakes on large volume resuscitation. It's really a shame that you don't have access to TEE, pulse contour analysis, swans etc, because otherwise you're flying blind using only UOP and BD when managing a patient with complex or mixed shock.

 

[deleted162650]

But has there ever been a trial to show one fluid better than another in hard facts?

There's the study comparing NS to LR in renal transplant cases which had to be stopped early due to patient safety concerns in the NS group.

 

[Psai]

There's the study comparing NS to LR in renal transplant cases which had to be stopped early due to patient safety concerns in the NS group.

Yet I still have attendings telling me to use normal saline on renal patients.

 

[Iso4ane]

Yet I still have attendings telling me to use normal saline on renal patients.

I've said this before you give a renal patient 4mEqs over 8 hours people lose their minds. The patient drinks a banana smoothie and no one cares.

 

[deleted162650]

I've said this before you give a renal patient 4mEqs over 8 hours people lose their minds. The patient drinks a banana smoothie and no one cares.

Or the notion that somehow a fluid with 4mEq’s of K per liter when given to a patient with a plasma K of 4.8 will somehow raise the plasma K level. Someone explain to me the chemistry at work there.

 

[anbuitachi]

There's the study comparing NS to LR in renal transplant cases which had to be stopped early due to patient safety concerns in the NS group.

Yet I still have attendings telling me to use normal saline on renal patients.

Yes , i always get annoyed when people tell me to use NS in ESRD patients. The acidity of NS causes a higher intraoperative potassium level than Plasmalyte/LR

 

[deleted171991]

Or the notion that somehow a fluid with 4mEq’s of K per liter when given to a patient with a plasma K of 4.8 will somehow raise the plasma K level. Someone explain to me the chemistry at work there.

Those people forget that intracellular K+ is 145-150 mEq/L, hence acidosis (i.e. NS) does much more damage than LR, especially since the intracellular space is almost triple the size of the intravascular one.

 

[nimbus]

Preaching to the choir but....

Myth-busting: Lactated Ringers is safe in hyperkalemia, and is superior to NS.

 

[repititionition]

Preaching to the choir but....

Myth-busting: Lactated Ringers is safe in hyperkalemia, and is superior to NS.

On surgery as an M3, the senior surgical resident said "We should switch to NS" (in setting of new-onset hyperkalemia). I mentioned this and was subsequently reamed out in front of the entire ICU, thus proving the "not always right but never in doubt" quote.

 

[deleted171991]

On surgery as an M3, the senior surgical resident said "We should switch to NS" (in setting of new-onset hyperkalemia). I mentioned this and was subsequently reamed out in front of the entire ICU, thus proving the "not always right but never in doubt" quote.

I always say that surgeons are 10 years behind internists knowledge-wise. Stop learning internal medicine from surgeons.

 

[anbuitachi]

On surgery as an M3, the senior surgical resident said "We should switch to NS" (in setting of new-onset hyperkalemia). I mentioned this and was subsequently reamed out in front of the entire ICU, thus proving the "not always right but never in doubt" quote.

In situations like this, quoting the study that showed this can help, though obviously this is not easy to do

 

[Psai]

In situations like this, quoting the study that showed this can help, though obviously this is not easy to do

Nah, it's a bad idea to make your senior look like an idiot after they just reamed you out despite the fact that they are clearly wrong.

 

[vector2]

Nah, it's a bad idea to make your senior look like an idiot after they just reamed you out despite the fact that they are clearly wrong.

God only knows how many people we've killed throughout the course of human history cause a person in a junior position was afraid to question someone more senior

 

[Iso4ane]

God only knows how many people we've killed throughout the course of human history cause a person in a junior position was afraid to question someone more senior

At least a few planes have crashed due to this phenomenon.

 

[Psai]

God only knows how many people we've killed throughout the course of human history cause a person in a junior position was afraid to question someone more senior

It generally gets you nowhere as they are ultimately not your patient and feathers get ruffled. I'd like to have a job at the end of this long journey.

 

[IlDestriero]

God only knows how many people we've killed throughout the course of human history cause a person in a junior position was afraid to question someone more senior

Just light them up, though not the attending.
If you’re going to try to burn me down, you better bring more than dogma because I was actually pretty smart back in the day. If necessary print out the article(s) and present it on PM rounds.
(This only works if you’re smarter than your senior resident. Lots of dunces out there.
You have to pick your battles, but dogma disproven a decade or two ago spouted by a dunce trying to belittle me would be a good choice.)
You can do it on the sly by asking several clarifying questions that point out the errors in their decision making as well. That can often lead to them displaying their ignorance for all to see, and they won’t see it coming. After all, you’re just asking some clarifying questions to expand your understanding of the many benefits of NS.


--
Il Destriero

 

[deleted697535]

Senior not having a notion what they're talking about happens all the time.

It's a big north north american problem. Residency's are so short you are taught to sound confident long before competence...

 

[Urzuz]

Once and forever, BD is prehistorical BULL****!

Let's use Wikipedia:
"Base excess is defined as the amount of strong acid that must be added to each liter of fully oxygenated blood to return the pH to 7.40 at a temperature of 37°C and a pCO2 of 40 mmHg (5.3 kPa).[2] A base deficit (i.e., a negative base excess) can be correspondingly defined in terms of the amount of strong base that must be added.

A further distinction can be made between actual and standard base excess: actual base excess is that present in the blood, while standard base excess is the value when the hemoglobin is at 5 g/dl. The latter gives a better view of the base excess of the entire extracellular fluid.[3]

The term and concept of base excess were first introduced by Poul Astrup and Ole Siggaard-Andersen in 1958."

"Base excess can be estimated from the serum bicarbonate concentration ([HCO3−]) and pH by the equation:[4]

Base excess = 0.93 x ([HCO3-] - 24.4 +14.8 x (pH-7.4)), with units of mEq/L."

"Base excess beyond the reference range indicates

• metabolic alkalosis if too high (more than +2 mEq/L)
• metabolic acidosis if too low (less than −2 mEq/L)"

Stupid surgical teaching says to give fluids when the patient has a base deficit (i.e. metabolic acidosis). Really? When we know that hypovolemia can also cause "contraction" metabolic alkalosis, i.e. "base excess". So when should one give fluids, when there is a base deficit, or when there is a base excess??? The BD brainfart probably comes from the trauma literature (and it makes me itch to just traumatize those who still use the concept and hurt patients). Healthy trauma patients who are hypovolemic (i.e. have lost blood), will have organ ischemia, ergo metabolic acidosis, ergo base deficit. But BD doesn't mean **** for fluid replacement in any (other) context. Forget that it even exists. Just stop using acid-base status for fluid replacement altogether. Same goes for lactate levels, and other fairy tales.

A patient with peritonitis does NOT need "at least" 30 ml/kg fluids upfront. Like most septic patients, he needs AT MOST 30 ml/kg fluids (unless there is proof of hypovolemia, e.g. low CO despite a normal/high EF and a normal/high SVR). What he does need is pressors, and replacement of objective fluid/blood losses. Please stop drowning critical patients and their internal organs. All that fluid will just extravasate where inflammation and gravity will break the endothelial barrier (at least the surgical site = the abdomen, the lung and the kidneys), will cause local venous congestion with local ischemia and failure of those organs (flow is not dependent just on MAP, but on perfusion pressure, which is calculated similarly to the cerebral perfusion pressure, i.e. MAP minus venous pressure or compartment pressure), and may end up killing those patients (early AKI alone, e,g, from abdominal hypertension/fluids, has a 30% chance of dying within a year). But, hey, one gets beautiful MAP numbers for a few hours, for defending oneself in court from similar "experts". And then the patient is f*cked up for days, because INTERSTITIAL FLUID IS MOSTLY REABSORBED THROUGH LYMPATHICS, which is a slow process; there is little Starling-type reabsorption at the venous end of the capillary in real life, especially with inflammation. Another fairy tale.

We, anesthesiologists, are on the brain side of the blood-brain barrier. So we should think, not just do. Don't just give fluids blindly; prove that the patient needs fluids, based on contemporary science.

I would argue that the one thing a really sick patient actually needs is a PAC or TEE probe for SVR and CO estimation. It's ridiculous to treat a distributive + possibly cardiogenic + possibly hypovolemic shock (that's what septic shock actually is) while just monitoring the MAP, UOP, ABG, lactate, and other unreliable guesstimates of peripheral oxygen delivery. I don't expect people to start watching microscopic nail perfusion (as a proxy for peripheral capillary perfusion) and use both pressors and peripheral vasodilators at the same time, as some smart intensivists do, but don't just "do something". FIRST DO NO HARM. When one treats a septic patient, one should think like a good medical intensivist. Also, one shouldn't use arbitrary numbers, such as the 7 g/dL transfusion threshold, for everybody. Every patient is different, and even the best science (which is not the case here) has exceptions.

And midazolam is not a "CV stable" drug. It's a VASODILATOR. Hence the increased pressor requirement after giving it to a patient whose compensatory mechanisms have been already depleted. Same goes for the idea of ketamine infusion in a profoundly septic patient. When the sympathetic axis is already exhausted, it DEPRESSES myocardial contractility.

Also, sepsis is associated with hypocalcemia. It doesn't mean ****. Do NOT correct it. Same goes for compensatory tachycardia, unless excessive for that particular patient.

This case wasn't even a big deal. Perfed colon after having been prepped for colonoscopy? Yawn...

</rant>

100% agree with you. But, in case you were trying to refute what I said (which is that BD can be useful to paint an overall picture of a patient's health/state), let me give you a simple example: I can tell you with 99.99999999% certainty that a patient with a BD of -30 is not doing well. IDGAF what else is going on, there is close to no chance that a healthy person with somewhat normal physiology has a BD of -30. Now, does that say anything about what is causing them to have such a screwed up number? No, of course not. Is it telling you that they are "dry" and you need to pump them full of crystalloid? NO. But, it does serve to help you create a "feel" for what kind of a patient you going to encounter. In the same way that the "eyeball" test and trusting your gut can be useful, using data to form an overall picture of a patient's physiologic state is equally important IMO. You shouldn't alter or change your treatment based on these data, but at least you know you won't be kicking back on SDN during the case and your index of suspicion for s#$& hitting the fan will be higher.

 

[repititionition]

Just light them up, though not the attending.
If you’re going to try to burn me down, you better bring more than dogma because I was actually pretty smart back in the day. If necessary print out the article(s) and present it on PM rounds.
(This only works if you’re smarter than your senior resident. Lots of dunces out there.
You have to pick your battles, but dogma disproven a decade or two ago spouted by a dunce trying to belittle me would be a good choice.)
You can do it on the sly by asking several clarifying questions that point out the errors in their decision making as well. That can often lead to them displaying their ignorance for all to see, and they won’t see it coming. After all, you’re just asking some clarifying questions to expand your understanding of the many benefits of NS.
--
Il Destriero

Dude I thought I had fair-sized balls for a medical student but this **** would be next-level. No way was I going to snap back with anything, much less pimping the resident, after the thorough ass-kicking she delivered to me in front of everyone. She was scared, and you don't poke a scared animal.

 

[Psai]

100% agree with you. But, in case you were trying to refute what I said (which is that BD can be useful to paint an overall picture of a patient's health/state), let me give you a simple example: I can tell you with 99.99999999% certainty that a patient with a BD of -30 is not doing well. IDGAF what else is going on, there is close to no chance that a healthy person with somewhat normal physiology has a BD of -30. Now, does that say anything about what is causing them to have such a screwed up number? No, of course not. Is it telling you that they are "dry" and you need to pump them full of crystalloid? NO. But, it does serve to help you create a "feel" for what kind of a patient you going to encounter. In the same way that the "eyeball" test and trusting your gut can be useful, using data to form an overall picture of a patient's physiologic state is equally important IMO. You shouldn't alter or change your treatment based on these data, but at least you know you won't be kicking back on SDN during the case and your index of suspicion for s#$& hitting the fan will be higher.

If you need a base deficit to tell you that someone with a base deficit of 30 is doing ****ty...

 

[Urzuz]

If you need a base deficit to tell you that someone with a base deficit of 30 is doing ****ty...

Whoosh. Way to miss the point of the post.

And thanks for (in a bizarre douchey way) supporting my whole point.

 

[IlDestriero]

Dude I thought I had fair-sized balls for a medical student but this **** would be next-level. No way was I going to snap back with anything, much less pimping the resident, after the thorough ass-kicking she delivered to me in front of everyone. She was scared, and you don't poke a scared animal.

No, you don’t poke it, you euthanize it.
It’s not pimping the resident, it’s asking clarifying questions. She knows why NS is superior after all, so let her explain it. Acidosis and intracellular potassium, acidosis from NS boluses, how a Lower K solution than her current blood K can increase her K. I’d want to know. I want to know now. But I’m not a biochemist, just an old country doctor.


--
Il Destriero