High K+, pre-renal

[epidural man]

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I had something happen in a case the other day that I don't think I have seen in a long time, if ever.

Case -

39 y/o Post-partum s/p C-section- bleeding into abdomen.

Patient had slightly elevated creatinine.

Hgb - ~7.

She had pre-elampsia (I don't know how severe) and was on Mg+.

She gets rushed to the OR. Upon arrival she was mildly tachycardic, very hypertensive, and obtunded but arousable.

On her EKG, I thought it looked like peaked T's but wasn't suspecting elevated K at that time. (I'm sure there is a rule about what exactly is a peaked T - something like 1/3 of the height of Q?)

Anyway, after non-eventful induction and a-line placement, her K+ was 6.5. We treated her with a bunch of calcium and it didn't change the EKG morphology.

Here were my worries. She needed RBC's (still bleeding), but I was worried about the K+. She has severe pre-elampsia, so worried about giving too much volume quickly.

Also, as the case proceeded, she had zero urine output (first 2 or 3 hours).

Using the Belmont rapid infuser, we pushed 4 RBCS, FFP in a 1:1 ration and gave some cryoprecipitate, and some platelets. The Belmont was set at 100ml/min (fast, but not usual Belmont fast), and didn't rush between units. I don't recall if her a-line ever showed systolic pressure variation. I wonder if a pre-elcamptic state effects that parameter/measure.

We treated the K+ with the usual (calcium, beta-agonist, insulin, bicarb, glucose) - but held off on the lasix.

Her peaked T waves resolved (well...wether they were true peaked or not, the morphology changed to rounded and smaller).

But here is the thing I haven't really seen. After all that volume and treating the K+, her kidneys started POURING out urine. It was a crazy amount. I think in a matter of 30 minutes, she put out almost 1.5, maybe 2 L or urine. Her K+ corrected very nicely. It helps to have a working kidney.

Have any of you seen something like that? Is it common to see renal function reverse that quickly? (In the back of my head I transiently thought "Holy crap, did she have a hemorrhagic stoke and now is having DI?" - which has been described by the way.)

A side note for me - it was the first time I had used Cleviprex. The residents have all been using it forever and love it. It worked really well.

 

[vector2]

In this situation, I think the rapid improvement in UOP isn't crazy irregular. Preeclamptics tend to be vasoconstricted, intravascularly depleted, have leaky capillaries, and are run relatively dry pre delivery. In a matter of hours you literally did all the best treatments for preeclamptic AKI, I.e. Delivered the baby, controlled the rampant vasoconstriction with an alpha blocker, corrected electrolytes, and increased circulating volume, CO and oxygen delivery to the kidney via autotransfusion and products.

As for SPV/PPV, I doubt it's ever been validated in pregnancy let alone preeclamptic hypertensive crisis, so I'd take the readings with a grain of salt.

 

[dhb]

You corrected her hypovolemia and intra-abdominal pressure from the bleeding so the urine output is a good indicator that you did something right.

 

[dhb]

What was her pH? K coulda been high because of the lactic acidosis.

 

[Hoya11]

I had something happen in a case the other day that I don't think I have seen in a long time, if ever.

Case -

39 y/o Post-partum s/p C-section- bleeding into abdomen.

Patient had slightly elevated creatinine.

Hgb - ~7.

She had pre-elampsia (I don't know how severe) and was on Mg+.

She gets rushed to the OR. Upon arrival she was mildly tachycardic, very hypertensive, and obtunded but arousable.

On her EKG, I thought it looked like peaked T's but wasn't suspecting elevated K at that time. (I'm sure there is a rule about what exactly is a peaked T - something like 1/3 of the height of Q?)

Anyway, after non-eventful induction and a-line placement, her K+ was 6.5. We treated her with a bunch of calcium and it didn't change the EKG morphology.

Here were my worries. She needed RBC's (still bleeding), but I was worried about the K+. She has severe pre-elampsia, so worried about giving too much volume quickly.

Also, as the case proceeded, she had zero urine output (first 2 or 3 hours).

Using the Belmont rapid infuser, we pushed 4 RBCS, FFP in a 1:1 ration and gave some cryoprecipitate, and some platelets. The Belmont was set at 100ml/min (fast, but not usual Belmont fast), and didn't rush between units. I don't recall if her a-line ever showed systolic pressure variation. I wonder if a pre-elcamptic state effects that parameter/measure.

We treated the K+ with the usual (calcium, beta-agonist, insulin, bicarb, glucose) - but held off on the lasix.

Her peaked T waves resolved (well...wether they were true peaked or not, the morphology changed to rounded and smaller).

But here is the thing I haven't really seen. After all that volume and treating the K+, her kidneys started POURING out urine. It was a crazy amount. I think in a matter of 30 minutes, she put out almost 1.5, maybe 2 L or urine. Her K+ corrected very nicely. It helps to have a working kidney.

Have any of you seen something like that? Is it common to see renal function reverse that quickly? (In the back of my head I transiently thought "Holy crap, did she have a hemorrhagic stoke and now is having DI?" - which has been described by the way.)

A side note for me - it was the first time I had used Cleviprex. The residents have all been using it forever and love it. It worked really well.

I dont think correcting her K and her increased urine output were all that related... you gave her volume and she started peeing, independently, you corrected her K. Its not as if due to your correction of the K, her kidneys kicked back into action. Her real K was probably 5.8 and she was super dry, add all the volume and she starts peeing... maybe there was another cause of 0 urine output and then started suddenly pouring urine, in addition to your resuscitation, which could have been the surgeon somehow compressing it during the action of the case unknowingly (

 

[deleted171991]

I doubt the K increase was from pre-renal AKI. I think the hyperkalemia was from the magnesium infusion (plus/minus some renin-aldosterone imbalance, possibly due to pre-eclampsia). It's been reported even without AKI, see below.

I would believe the SPV/PPV as long as you satisfy the conditions for it: 100% controlled ventilation, VT of 8 ml/kg or higher, sinus rhythm. However, don't forget that even healthy people are volume-responsive and can have PPV.

In your case, it's obvious that she was vasoconstricted (hence dry) as hell, and she started making urine once you fixed her hypovolemia and vasoconstriction (i.e. delivered the baby), Again, probably mediated by the RAA axis (angiotensin II increases secretion of ADH).

"Abstract
We report the case of a woman who first received MgSO(4) for eclampsia prophylaxis and then was treated with MgSO(4) for eclampsia. She developed hyperkalemia without severe renal failure or another explanation. We recommend close monitoring, including serial measurements of electrolytes, when MgSO(4) is administered for eclampsia prophylaxis or treatment."

Postpartum Hyperkalemia Associated with... (PDF Download Available). Available from: https://www.researchgate.net/public...yperkalemia_Associated_with_Magnesium_Sulfate [accessed Apr 07 2018].

 

[Noyac]

I think her elevated K+ was due to absorption of hemorrhage. And exacerbated by her prerenal condition.

Otherwise, nice job.

 

[deleted643396]

She likely had ATN as part of her acute renal failure (did you spin her urine and look for casts? 😉). Excessive diuresis is relatively common after an episode of ATN, but I’m not sure the pathophysiology is well understood. You do have to keep an eye on it though, because it can lead to volume depletion.

 

[Mman]

Aside from other things already mentioned I'm going to assume you gave some succinylcholine as part of your induction which temporarily elevates the serum potassium so you might have been drawing your ABG at the peak of that effect.

 

[drmwvr]

As an aside, if there ever were a hyperkalemia concern with giving packed cells quickly, running them through the cell saver first will mitigate that.

 

[deleted547339]

She likely had ATN as part of her acute renal failure (did you spin her urine and look for casts? 😉). Excessive diuresis is relatively common after an episode of ATN, but I’m not sure the pathophysiology is well understood. You do have to keep an eye on it though, because it can lead to volume depletion.

I’ve never heard of post ATN diuresis occuring 1-2h after an insult....more like several days.

The patient was probably dry and slightly acidemic - her kidneys got the volume they needed and she started peeing out potassium.

 

[vector2]

I would believe the SPV/PPV as long as you satisfy the conditions for it: 100% controlled ventilation, VT of 8 ml/kg or higher, sinus rhythm. However, don't forget that even healthy people are volume-responsive and can have PPV.

The average pregnant pt at baseline has increased CO, arterial compliance, ECF volume, decreased SVR, not to mention some degree of IVC compression while supine, slight lung volume changes, and increased pressure transmitted to the diaphragm and thorax. I find it hard to believe that a PPV of 12-15% means the same thing for them as a non-parturient.

 

[deleted171991]

The average pregnant pt at baseline has increased CO, arterial compliance, ECF volume, decreased SVR, not to mention some degree of IVC compression while supine, slight lung volume changes, and increased pressure transmitted to the diaphragm and thorax. I find it hard to believe that a PPV of 12-15% means the same thing for them as a non-parturient.

PPV has been used in fluid resuscitation for sepsis, which is exactly increased CO, decreased SVR, increased ECF volume from all the idiots giving tons of fluids, IAH etc. IVC compression may decrease preload and increase PPV, but then the patient is supposed to be in LUD. And PPV is used in ventilated patients, even obese ones, so there is increased intra-thoracic pressure. Still, you have a point.

In the (almost) healthy bleeding patient, my resuscitation would not be based on PPV anyway. It's based on MAP (at baseline), peripheral perfusion (warm extremities with good pulse oxymeter signal) and need for pressors (just an occasional bolus or low dose phenylephrine infusion to compensate for anesthesia). This is the patient that I may even over-resuscitate a touch, because she will not hold on to the fluids for long (hence even the old school surgical thinking works). What preeclampsia adds is mostly significant vasoconstriction and hypovolemia, so I'm even more inclined to be less conservative with the fluids/blood products (with an eye on avoiding hypervolemia though). It's not like the septic or major surgical patient, where all that inflammation may just hold on to the fluid and cause complications, and where I err on the side of some hypovolemia. The bigger the surgery, or if the patient is edematous, the more my thinking goes into "septic" mode.

@epidural man, I just love the (almost) 1:1:1 resuscitation. Most people tend to muck that up, and then chase the ensuing coagulopathy. I am not sure she needed all that volume, hence the diuresis. She may have had some AKI/ARF there from the severe pre-eclamptic vasoconstriction (which is probably where the cleviplex helped). Also, even in the absence of postpartum hemorrhage, pre-eclamptic women can have oliguria for hours after delivery. Who knows? Interesting case.

 

[dhb]

What was her pH? K coulda been high because of the lactic acidosis.

What was her pH on the first blood gas?

 

[Noyac]

As an aside, if there ever were a hyperkalemia concern with giving packed cells quickly, running them through the cell saver first will mitigate that.

Doesn’t that defeat the point of “giving them quickly”?😉

 

[epidural man]

pH -I haven’t answered yet because I’m embarrassed I don’t remember. I want to say it was 7.3. However,I think the fact that I don’t remember means I wasn’t too concerned about it.

Regarding FFP point about maybe too much volume. That is likely true. She ended with a Hgb of 9.5.

 

[epidural man]

Oh also regarding sux - yes that likely contributed to the first ABG, but persisted after giving calcium.

Had I suspected elevated k before induction, we would have certainly avoided it.

 

[deleted171991]

Oh also regarding sux - yes that likely contributed to the first ABG, but persisted after giving calcium.

Calcium doesn't decrease potassium, friend. It just stabilizes the cardiac cell membranes.

 

[CodeBlu]

Calcium doesn't decrease potassium, friend. It just stabilizes the cardiac cell membranes.

More calcium the better when the K+ is over 9000 in my opinion, shift later. Avoiding asystole. No one likes asystole.

 

[Mman]

I just love the (almost) 1:1:1 resuscitation

I sure hope you aren't giving 1 bag of platelets for every unit of blood and FFP you are giving. Or are you calling one bag the old "6 pack" and counting it as 6? Personally I find we end up closer to 5 RBCs to 4 FFP to 1 platelet in our 20+ unit transfusion cases.

 

[deleted171991]

I sure hope you aren't giving 1 bag of platelets for every unit of blood and FFP you are giving. Or are you calling one bag the old "6 pack" and counting it as 6? Personally I find we end up closer to 5 RBCs to 4 FFP to 1 platelet in our 20+ unit transfusion cases.

That's what everybody means when they say 1:1:1. One wants to restore about 10,000 platelets per gram of Hgb (and equivalent volume of plasma) transfused.

 

[fakin' the funk]

TXA?

 

[epidural man]

Calcium doesn't decrease potassium, friend. It just stabilizes the cardiac cell membranes.

Yes. I misspoke. Would one expect stabilization to correct T-waves? That is what I expected to happen.

Two doses of TXA given before patient arrived to OR.

 

[fakin' the funk]

The average pregnant pt at baseline has increased CO, arterial compliance, ECF volume, decreased SVR, not to mention some degree of IVC compression while supine, slight lung volume changes, and increased pressure transmitted to the diaphragm and thorax. I find it hard to believe that a PPV of 12-15% means the same thing for them as a non-parturient.

You haven't detailed *how* those circulatory parameters would invalidate the use of PPV to predict fluid responsiveness; you just listed them.

 

[fakin' the funk]

Doesn’t that defeat the point of “giving them quickly”?😉

Or you can have them washed if you anticipate giving a lot of them, quickly or not.

 

[fakin' the funk]

More calcium the better when the K+ is over 9000 in my opinion, shift later. Avoiding asystole. No one likes asystole.

The calcium and the lasix are both in the drug drawer.

 

[fakin' the funk]

I had something happen in a case the other day that I don't think I have seen in a long time, if ever.

Case -

39 y/o Post-partum s/p C-section- bleeding into abdomen.

Patient had slightly elevated creatinine.

Hgb - ~7.

She had pre-elampsia (I don't know how severe) and was on Mg+.

She gets rushed to the OR. Upon arrival she was mildly tachycardic, very hypertensive, and obtunded but arousable.

On her EKG, I thought it looked like peaked T's but wasn't suspecting elevated K at that time. (I'm sure there is a rule about what exactly is a peaked T - something like 1/3 of the height of Q?)

Anyway, after non-eventful induction and a-line placement, her K+ was 6.5. We treated her with a bunch of calcium and it didn't change the EKG morphology.

Here were my worries. She needed RBC's (still bleeding), but I was worried about the K+. She has severe pre-elampsia, so worried about giving too much volume quickly.

Also, as the case proceeded, she had zero urine output (first 2 or 3 hours).

Using the Belmont rapid infuser, we pushed 4 RBCS, FFP in a 1:1 ration and gave some cryoprecipitate, and some platelets. The Belmont was set at 100ml/min (fast, but not usual Belmont fast), and didn't rush between units. I don't recall if her a-line ever showed systolic pressure variation. I wonder if a pre-elcamptic state effects that parameter/measure.

We treated the K+ with the usual (calcium, beta-agonist, insulin, bicarb, glucose) - but held off on the lasix.

Her peaked T waves resolved (well...wether they were true peaked or not, the morphology changed to rounded and smaller).

But here is the thing I haven't really seen. After all that volume and treating the K+, her kidneys started POURING out urine. It was a crazy amount. I think in a matter of 30 minutes, she put out almost 1.5, maybe 2 L or urine. Her K+ corrected very nicely. It helps to have a working kidney.

Have any of you seen something like that? Is it common to see renal function reverse that quickly? (In the back of my head I transiently thought "Holy crap, did she have a hemorrhagic stoke and now is having DI?" - which has been described by the way.)

A side note for me - it was the first time I had used Cleviprex. The residents have all been using it forever and love it. It worked really well.

One way to summarize your case is, patient got sux, had a high K, we did many therapies not including K elimination, and then she peed and everything was good. Much less mysterious this way.

 

[anbuitachi]

It's also possible that the foley was kincked or being compressed somewhere. the surgeon couldve accidently been compressing the foley .

 

[drmwvr]

Doesn’t that defeat the point of “giving them quickly”?😉

You got me Tex... still... if time permits, and it frequently does, washing cells gets a lot of garbage out of PRBC's

 

[WheezyBaby]

Yes. I misspoke. Would one expect stabilization to correct T-waves? That is what I expected to happen.

Two doses of TXA given before patient arrived to OR.

Not sure specifically in regard to T waves, but I've definitely watched Ca shorten the QRS in hyperK