Time for some clinical discussion

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Noyac

Noyac

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We may have discussed this before but my aging mind can't remember for sure.

The case:

60 yo M with HTN, DM II, and high cholesterol. Meds are metformin, Losartan/HCTZ, amlodipine, insulin, tradjenta and Crestor. He is in for a long spine case front and back. There is nothing else pertentent in the PMH.
Case starts with induction and BP goes from 130/70 to 70/40. A couple doses of neo get the BP back up to 90/60 and the case proceeds. During the course of the 6 hr surgery anesthesia in maintained with TIVA propofol and fentanyl. Low dose DES added in order to decrease propofol dose. BP is maintained with a neo infusion 50-90mcg/ min with low dose vasopressin adjunct. IVF were 6000, EBL 250, UOP 350.

Pt emerges fine and is following commands without deficits. Taken to PACU were BP begins to fall to 70/50 again. No neo being infused.

What's going on?

What to do?
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Atypical propofol infusion syndrome? Autonomic dysfunction related to DM?
 
Possibly hypotension related to losartan which would usually respond well to vasopressin specifically
 
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Preload, pump, afterload. What is his HR and other vitals? Is he mentating appropriately still in PACU? Chest pain?

Preload: was EBL more than you thought it was? Does he have drains? How much blood is in them? Still making urine? What is his HR? If HR is high and UOP continues to be low I would open up his fluids and check a Hct given the risk of unrecognized bleeding.

Pump: He obviously has risk factors for CAD (DM, HLD, HTN). Is he symptomatic? Diabetics are not always symptomatic. I would check a 12 lead and compare to his baseline. Any ST changes--> check enzymes and manage appropriately. What is his rhythm? He could potentially have a symptomatic arrhythmia (ie AF with RVR/flutter, complete block).

Afterload: I suppose it could be related to his ARB. My experience is the vasoplegia related to ARBs resolves with cessation of the anesthetic. The point about autonomic dysfxn 2/2 DM is an interesting one, although I would expect that to manifest more in orthostatic hypotension or something like that.
 
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There is nothing typical in this case. This guy became symptomatic post-induction (which might have induced an MI), and then needed a ****load of pressors during the case, but he survived it well, which is again atypical for MI (imagine what 6 hours of surgery do to an ischemic heart).

I don't get why he got so much fluids, with such a low EBL. The amount he got seems excessive. Was it titrated to PPV on the A-line intraop? Did they decompensate a CHF/CAD with all those fluids? But then he would be more SOB. Is this a PE?

Of course, losartan is a very possible explanation, but it doesn't really explain the postop problem.
 
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While prone, I would expect fluid responsive-looking PPV owing to higher mean airway pressures and peripheral fluid sequestration associated with positioning...almost regardless of amount of fluid given. PPV was validated in study groups receiving standardized tidal volumes 6-7mL/kg while supine.

ABG w/ lactate, stat EKG to rule out acute pathology and assess for electrolyte aberrations while CMP (w/ Ca/Mag/Phos) is pending. Resume vasopressin infusion and grab an ultrasound to do a quick parasternal eval. of the dude's function.

A lot of possibilities here, but tops on my list are Losartan-related hypotension, dilutional electrolyte abnormalities, and rhabdomyolysis related to positioning for a long case. It would be helpful to know patient's body habitus and what type of hardware was placed (and where).
 
Do a quick TTE and in < 1 min can r/o hypovolemia vs R/L heart failure. Support the BP, send a gas, hopefully sent one or two of these during the case. The fact that a neo and vaso gtt were needed throughout the case to maintain the BP in a pt who is otherwise adequately fluid resuscitated should have raised a red flag
 
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Br J Anaesth. 2010 Apr;104(4):407-13. doi: 10.1093/bja/aeq031. Epub 2010 Feb 26.
Abilities of pulse pressure variations and stroke volume variations to predict fluid responsiveness in prone position during scoliosis surgery.
Biais M1, Bernard O, Ha JC, Degryse C, Sztark F.
Author information
Abstract
BACKGROUND:
Pulse pressure variation (PPV) and stroke volume variation (SVV) are robust indicators of fluid responsiveness in mechanically ventilated supine patients. The aim of the study was to evaluate the ability of PPV and SVV to predict fluid responsiveness in mechanically ventilated patients in the prone position (PP) during scoliosis surgery.

METHODS:
Thirty subjects were studied after the induction of anaesthesia in the supine position [before and after volume expansion (VE) with 500 ml of hetastarch 6%] and in PP (immediately after PP and before and after VE). PPV, SVV, cardiac output (CO), and static compliance of the respiratory system were recorded at each interval. Subjects were defined as responders (Rs) to VE if CO increased > or =15%.

RESULTS:
Three subjects were excluded. In the supine position, 16 subjects were Rs. PPV and SVV before VE were correlated with VE-induced changes in CO (r(2)=0.64, P<0.0001 and r(2)=0.56, P<0.0001, respectively). Fluid responsiveness was predicted by PPV >11% (sensitivity=88%, specificity=82%) and by SVV >9% (sensitivity=88%, specificity=91%). PP induced an increase in PPV and SVV (P<0.0001) and a decrease in the static compliance of the respiratory system (P<0.0001). In PP, 17 patients were Rs. PPV and SVV before VE were correlated with VE-induced changes in CO (r(2)=0.59, P<0.0001 and r(2)=0.55, P<0.0005, respectively). Fluid responsiveness was predicted in PP by PPV >15% (sensitivity=100%, specificity=80%) and by SVV >14% (sensitivity=94%, specificity=80%).

CONCLUSIONS:
PP induces a significant increase in PPV and SVV but does not alter their abilities to predict fluid responsiveness.
 
Br J Anaesth. 2013 May;110(5):713-20. doi: 10.1093/bja/aes475. Epub 2012 Dec 28.
Validation of pulse pressure variation and corrected flow time as predictors of fluid responsiveness in patients in the prone position.
Yang SY1, Shim JK, Song Y, Seo SJ, Kwak YL.
Author information
Abstract
BACKGROUND:
The aim of this prospective trial was to investigate the ability of pulse pressure variation (PPV) and corrected flow time (FTc) to predict fluid responsiveness in the prone position.

METHODS:
Forty-four patients undergoing lumbar spine surgery in the prone position on a Wilson frame were prospectively studied. PPV and FTc were measured before and after a colloid bolus (6 ml kg(-1)) both in the supine and in the prone positions. Fluid responsiveness was defined as an increase in the stroke volume index of ≥ 10% as measured by oesophageal Doppler.

RESULTS:
In the supine position, 26 patients were responders and the areas under the curve (AUC) of the receiver-operator characteristic (ROC) curves of PPV and FTc were 0.935 [95% confidence interval (CI): 0.870-0.999, P<0.001] and 0.822 (95% CI: 0.682-0.961, P<0.001), respectively. The optimal cut-off PPV and FTc values were 15% (sensitivity 73%, specificity 94%) and 358 ms (sensitivity 88%, specificity 78%), respectively. In the prone position, 34 patients were responders and the AUCs of PPV and FTc were 0.969 (95% CI: 0.912-1.000, P<0.001) and 0.846 (95% CI: 0.706-0.985, P=0.001), respectively. The optimal cut-off PPV and FTc values were 14% (sensitivity 97%, specificity 90%) and 331 ms (sensitivity 77%, specificity 90%), respectively.

CONCLUSIONS:
While the predictability of PPV was significantly higher than that of FTc in the prone position, both variables showed high predictability and remained as useful indices for guiding fluid therapy in prone patients with minimal alterations in their optimal cut-off values to predict fluid responsiveness. Clinical trial registration URL: http://www.clinicaltrials.gov/ct2/show/NCT01646359?term=NCT01646359&rank=1 and unique identification number NCT01646359.
 
okayplayer said:
Preload, pump, afterload. What is his HR and other vitals? Is he mentating appropriately still in PACU? Chest pain?

Preload: was EBL more than you thought it was? Does he have drains? How much blood is in them? Still making urine? What is his HR? If HR is high and UOP continues to be low I would open up his fluids and check a Hct given the risk of unrecognized bleeding.

Pump: He obviously has risk factors for CAD (DM, HLD, HTN). Is he symptomatic? Diabetics are not always symptomatic. I would check a 12 lead and compare to his baseline. Any ST changes--> check enzymes and manage appropriately. What is his rhythm? He could potentially have a symptomatic arrhythmia (ie AF with RVR/flutter, complete block).

Afterload: I suppose it could be related to his ARB. My experience is the vasoplegia related to ARBs resolves with cessation of the anesthetic. The point about autonomic dysfxn 2/2 DM is an interesting one, although I would expect that to manifest more in orthostatic hypotension or something like that.
Click to expand...

For med studs and residents... this is the way to think of intraoperative cardiac/bp issues. :thumbup:
 
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Major vascular injury during ant. spinal fusion is in the differential.

Excellent responses.
 
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okayplayer said:
Preload, pump, afterload. What is his HR and other vitals? Is he mentating appropriately still in PACU? Chest pain?

Preload: was EBL more than you thought it was? Does he have drains? How much blood is in them? Still making urine? What is his HR? If HR is high and UOP continues to be low I would open up his fluids and check a Hct given the risk of unrecognized bleeding.

Pump: He obviously has risk factors for CAD (DM, HLD, HTN). Is he symptomatic? Diabetics are not always symptomatic. I would check a 12 lead and compare to his baseline. Any ST changes--> check enzymes and manage appropriately. What is his rhythm? He could potentially have a symptomatic arrhythmia (ie AF with RVR/flutter, complete block).

Afterload: I suppose it could be related to his ARB. My experience is the vasoplegia related to ARBs resolves with cessation of the anesthetic. The point about autonomic dysfxn 2/2 DM is an interesting one, although I would expect that to manifest more in orthostatic hypotension or something like that.
Click to expand...
Preload:
EBP was 250. I looked for other signs of bleeding but found none. Because this started at the very beginning of the case I didn't think it was attributable to EBL. Plus it didn't respond to fluid bolus.
Pump:
12 lead normal with poor R wave progression in lateral leads unchanged from preop. No CP and mentoring normally.
Afterload:
Many possibilities here.

As far as unrecognized vascular injury goes, yes it should be on the top of your differential. Here's what I saw. Very little blood loss in the field. No tachycardia with hypotension. And consistent response to larger than normal doses of neo/vasoppressin remained consistent from start to finish. Hct went from 42 preop to 38 postop after 6L IVF. I'm not suspecting bleeding is the cause.
 
ABG intra-op was
7.35/45/195/-1/25/100% Na140 K 3.1 iCa1.35 Hct 41
ABG END OF CASE:
7.31/ 48/ 191/ -3/ 100%. Na 138 K 3.3 iCa 1. 18 Hct 38
 
Noyac said:
i had a major vascular insult in a case many years ago from the posterior. It was a wild ride for sure.
Click to expand...

I have never had this happen fortunately. I would guess that the mortality rate is very high, even with prompt recognition and treatment. It doesn't sound like bleeding is the case here though.
 
Noyac said:
BP is maintained with a neo infusion 50-90mcg/ min with low dose vasopressin adjunct. IVF were 6000, EBL 250, UOP 350.

Pt emerges fine and is following commands without deficits. Taken to PACU were BP begins to fall to 70/50 again. No neo being infused.

What's going on?

What to do?
Click to expand...

Noyac said:
ABG intra-op was
7.35/45/195/-1/25/100% Na140 K 3.1 iCa1.35 Hct 41
ABG END OF CASE:
7.31/ 48/ 191/ -3/ 100%. Na 138 K 3.3 iCa 1. 18 Hct 38
Click to expand...

Noyac said:
Just to move this case along Arch is right, bleeding was not the issue here.
Click to expand...

That's a lot of fluid for that type of case/bleeding. How come the hct dropped so little with that much fluid and that little urine out put? I give a liter to my pts and the hct drops by 5.

I presume the blood gas is on 100% O2> PaO2 is not great. Pneumothorax will give you hypotension and hypoxemia. Do you have a central line? Is it infiltrated and all fluid is going into the pleura? Regardless, get an x ray in pacu.

Where is the a line? Did you check a cuff pressure in the other arm? Could he have an aberrant subclavian with the hx of right aortic arch? Maybe.

Needs an ekg in pacu also. Just in case ischemia is causing hypotension.

Needs to be on pressors until bp normalizes, not sure why it was stopped at the end of the case. Could just be the losartan/amlodipine.
 
urge said:
That's a lot of fluid for that type of case/bleeding. How come the hct dropped so little with that much fluid and that little urine out put? I give a liter to my pts and the hct drops by 5.

I presume the blood gas is on 100% O2> PaO2 is not great. Pneumothorax will give you hypotension and hypoxemia. Do you have a central line? Is it infiltrated and all fluid is going into the pleura? Regardless, get an x ray in pacu.

Where is the a line? Did you check a cuff pressure in the other arm? Could he have an aberrant subclavian with the hx of right aortic arch? Maybe.

Needs an ekg in pacu also. Just in case ischemia is causing hypotension.

Needs to be on pressors until bp normalizes, not sure why it was stopped at the end of the case. Could just be the losartan/amlodipine.
Click to expand...
Ok great.
I agree the fluids were sort of a lot and the UOP wasn't impressive by any stretch. But drop of 5 with a liter is a bit much.
ABG was on 50% FiO2. Sat's were never an issue as they remained 100%.
A line and cuff pressure always matched and they were on opposite arms. But I like the aortic arch comments.
I think I mentioned it but the ECG in PACU was essentially Except for poor R wave progression in the lateral leads which was unchanged from previously.
I've had a case like this before and all resolved with emergence and removal of anesthetics. I had every hope that this would also be the case. After 10 min in PACU BP was 90/50 which was acceptable. So of course I removed the A line. Shortly after removal the BP was back to 70/30.
Why losartan/amlodipine?
 
There is at least one case report about postop hypotension for 8 hours with amlodipine (I was shocked, too), and losartan is a well-known problem if taken on the day of surgery.

My gut tells me that the lactate was normal, wasn't it? And the patient was feeling OK even at 70/30, right?
 
Noyac said:
Why losartan/amlodipine?
Click to expand...
Risk factors for vasoplegia.

Seems like we cannot find anything wrong with the patient. We are going to have to sit this one out on pressors until the next day most likely.

I have been there before. Patient had profound hypotension with no apparent explanation. Went to icu over night on a lot of pressors. By the next day was fine and got discharged home without any good explanation.
 
FFP said:
There is at least one case report about postop hypotension for 8 hours with amlodipine (I was shocked, too), and losartan is a well-known problem if taken on the day of surgery.

My gut tells me that the lactate was normal, wasn't it? And the patient was feeling OK even at 70/30, right?
Click to expand...
You are right on all counts.
 
urge said:
Risk factors for vasoplegia.

Seems like we cannot find anything wrong with the patient. We are going to have to sit this one out on pressors until the next day most likely.

I have been there before. Patient had profound hypotension with no apparent explanation. Went to icu over night on a lot of pressors. By the next day was fine and got discharged home without any good explanation.
Click to expand...
Ding ding ding ding.
The bell tolls.
Nice job.
This is a classic case of vasoplegia. Caused by high dose ARB in combination with Ca Channel blocker. Also this pts may have had some autonomic dysfunction secondary to poorly controlled diabetes.

Treatment is continued vasopressors. But which ones?
Any other options for treatment?

Yes he did great. Actually didn't need any more pressor after the pacu but was watched over night in ICU. Moved to floor in the am and no e the following day.
 
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Southpaw said:
for anti-hypertensive induced vasoplegia i've used vasopressin with success
Click to expand...
Agreed! but it isn't impressive. It gives just enough to get through the procedure. I was putting 4 units into a 20cc syringe of neo at 100mcg/ cc and running it at 90mcg/min. I was changing out the syringe every 30 minutes or less. I've never seen anyone go thru that much neo. I think the vasopressin gave just enough kick to make it all work.

But there is another treatment. Which I have never used btw.
 
Noyac said:
Agreed! but it isn't impressive. It gives just enough to get through the procedure. I was putting 4 units into a 20cc syringe of neo at 100mcg/ cc and running it at 90mcg/min. I was changing out the syringe every 30 minutes or less. I've never seen anyone go thru that much neo. I think the vasopressin gave just enough kick to make it all work.

But there is another treatment. Which I have never used btw.
Click to expand...

Methylene blue? I've seen it work for pretty severe vasoplegia...
 
Noyac said:
Why

Why would I have a lactate pre whatever?
Click to expand...

By pre/post I just meant for the first gas and the post op gas. And why would you have it -- I'm used to one getting reported as part of a standard ABG. Just curious, trying to understand the large crystalloid volume given... I usually try and avoid giving that much in prone spine cases unless there's lots of blood loss.
 
Ding ding ding

Methylene blue.

Unfortunately it's on backorder and it sounds like the manufacturers may stop making it all together.

Ok one last question, did anyone consider adrenal suppression? Would you have given this guy steroids?
 
Noyac said:
Ok one last question, did anyone consider adrenal suppression? Would you have given this guy steroids?
Click to expand...
Why would we, unless he has a history of recent steroid use? Most of my GA patients get decadron anyway; I am not sure I would have given hydrocortisone on top of it, especially in a DM patient. If desperate enough, I guess...
 
FFP said:
Why would we, unless he has a history of recent steroid use? Most of my GA patients get decadron anyway; I am not sure I would have given hydrocortisone on top of it, especially in a DM patient. If desperate enough, I guess...
Click to expand...

Since decadron has minimal mineralocortacoid effects its not a good choice for stress dose in a hypotensive patient if suspecting adrenal suppression. That being said, I agree here that there is no indication that this patient has adrenal insufficiency.
 
FFP, you are right. Or at least that was my line of thinking. I didn't give decadron either because this pts DM was so poorly controlled preop. But I thought about it. The reason I ask if anyone else thought about this was because the surgeon thought that was the cause. Until I explained what I thought was the case. I guess it wouldn't have hurt much to give it but I was convinced it wouldn't help and would only make things more difficult later.

Here's a decent newsletter article on it.
http://www.apsf.org/newsletters/html/2012/spring/12vasoplegic.htm

Btw this guy would have required 11-22 vials of methylene blue. Whoa!
 
twoliter said:
So 8 units/hour of vasopressin is low dose?
Click to expand...
It was more like 2.5 u/hr. The first batch had 4 u in it then I decreased it as time went on. Total was 20u in 8 hrs.
The half life it 15-20 min. But still that's a lot of vasopressin. And 2 mg of neo were given. Not huge I guess but big enough. All this would get his BP to 90-110/50-60.
 
risnwb said:
Since decadron has minimal mineralocortacoid effects its not a good choice for stress dose in a hypotensive patient if suspecting adrenal suppression. That being said, I agree here that there is no indication that this patient has adrenal insufficiency.
Click to expand...
I was saying something about giving hydrocortisone even after my usual decadron, I am just too old to remember why... :p
 
Has anyone ever seen Clinical hypotension in the O.R. due to adrenal cortical suppression caused by NOT giving stress dose steroids? In all my years we have NEVER Had a single case in the O.R. or PACU.

https://www.uam.es/departamentos/medicina/anesnet/journals/ija/vol1n1/articles/steroid.htm

The review article above seems to think we may be overdoing the stress steroid Rx a bit. Of course, I still give a "stress dose" but perhaps 50 mg is MORE than adequate and even unnecessary.
 
FFP,

I wasn't suggesting that SPV wasn't predictive of fluid-responsiveness in the prone position--it totally can be for the astute clinicians who are watching changes during these prone cases. An obese patient may well have parameters consistent with fluid-responsiveness while prone at the start of the case, merely as a consequence of positioning. They didn't exclude patient's with a BMI >30 in that second study for no reason--the authors recognized it as a confounding factor, as such.

It's not hard to imagine someone checking the SPV 4hrs into the case wondering why persistent pressor requirement exists and seeing a significant variation, giving more fluid...all the while volume isn't the problem.

Noyac, I am in no way here suggesting that you are not astute...just imagining how this particular parameter can be misused.
 
Nice case Noy and nice pick up Urge. I always think of vasoplegia as a CT room phenomena and have not seen it outside of that OR.... unless refractory hypotension secondary to ACE inhibitors/ARBs is the same thing.
 
sevoflurane said:
Nice case Noy and nice pick up Urge. I always think of vasoplegia as a CT room phenomena and have not seen it outside of that OR.... unless refractory hypotension secondary to ACE inhibitors/ARBs is the same thing.
Click to expand...
Yes it is the same thing.
 
risnwb said:
Since decadron has minimal mineralocortacoid effects its not a good choice for stress dose in a hypotensive patient if suspecting adrenal suppression. That being said, I agree here that there is no indication that this patient has adrenal insufficiency.
Click to expand...

Wait.

I don't think this is right. Someone educate me if I'm wrong, but -

Hypotension caused by secondary adrenal insufficiency isn't a mineralocorticoid issue. The renin-angiotensin system isn't involved in or affected by chronic steroid therapy.

The adrenal suppression we often talk about but rarely actually see in the OR, manifesting as refractory hypotension, is almost always caused by chronic glucocorticoid therapy (mostly weeks or more of PO prednisone but also methylprednisolone and dexamethasone). These patients who miss a dose or two and/or have a surgical stress may then exhibit symptomatic adrenal insufficiency (hypotension), the mechanism of which IIRC is inhibition of vascular prostacyclin production.

So from our perspective in anesthesia, given the above etiology and mechanism, dexamethasone (selective glucocorticoid) ought to be sufficient treatment, and we shouldn't need to worry about the mineralocorticoid effects (or lack thereof) of our stress dose steroid choice.

In fact, we probably don't WANT much if any mineralocorticoid effect. Low doses of hydrocortisone (ie not the 100s and 100s of mg given for "stress dose" in years past) don't have much mineralocorticoid effect and are fine. Extra mineralocorticoid levels carry different baggage, fluid retention and Na/K disturbances.

So dexamethasone is perfect.

At least that's what I remember, but some of this endocrine stuff is hard. :)


Thanks for posting the case Noyac :thumbup:
 
I think you are right pgg. Both prednisone and Dexamethasone are glucocorticoid steroids. Therefore if this were an adisonian crisis Dexamethasone should work fine.

Anyone know how I knew this wasn't an adisonian crisis? This is important to know because both conditions, vasoplegia and adisonian crisis manifest similarly in the OR, but are treated differently.
 
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