DKA in anuric ESRD

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StevenRF

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Just had a patient admitted for her 8th DKA episode. From what I read for ESRD, minimize fluid resuscitation since the hyperglycemia cant cause diuresis, dont replete the K until DKA fixed, and if acidosis is too bad you're stuck with dialysis.

My question is on recs for starting fluids given concern for volume overload. We went with D5NS@50/hr with the insulin drip, and despite this, her Na went down.

For something like this, would it be better to go with like a higher dextrose percent at a slower rate or what? Where is the extra fluid coming from to dilute the serum?

The physio is a little confusing since there is no output.

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Just had a patient admitted for her 8th DKA episode. From what I read for ESRD, minimize fluid resuscitation since the hyperglycemia cant cause diuresis, dont replete the K until DKA fixed, and if acidosis is too bad you're stuck with dialysis.

My question is on recs for starting fluids given concern for volume overload. We went with D5NS@50/hr with the insulin drip, and despite this, her Na went down.

For something like this, would it be better to go with like a higher dextrose percent at a slower rate or what? Where is the extra fluid coming from to dilute the serum?

The physio is a little confusing since there is no output.

I assume that is a corrected sodium?
 
Just had a patient admitted for her 8th DKA episode. From what I read for ESRD, minimize fluid resuscitation since the hyperglycemia cant cause diuresis, dont replete the K until DKA fixed, and if acidosis is too bad you're stuck with dialysis.

My question is on recs for starting fluids given concern for volume overload. We went with D5NS@50/hr with the insulin drip, and despite this, her Na went down.

For something like this, would it be better to go with like a higher dextrose percent at a slower rate or what? Where is the extra fluid coming from to dilute the serum?

The physio is a little confusing since there is no output.


Diabetic patients tend to suffer from ketoacidosis less frequently after starting chronic dialysis than prior to it.The prolonged half life of insulin in advanced renal failure and frequent follow up of patients on chronic dilayis have been identified as reasons for the decreased frequency of ketoacidois in the dialysis population. The usual course leading to ketoacidosis is omission of one or more insulin doses, often due to an intercurrent illness. This is of prime importance as an underlying cause should always be looked for at presentation. The common ones being access related infections and myocardial ischemia.

The absence of osmotic diuresis distinguishes dialysis associated hyperglycemia from hyperglycemia observed in patients with normal renal function.The rise in plasma osmolality that is seen in diabetic ketoacidosis and non ketotic hyperosmolar coma is only in part due to the rise in serum glucose. The marked hyperosmolality is primarily due to the glucose osmotic diuresis that causes water loss in excess of sodium and potassium. The importance of effective plasma osmolality in the development of neurological symptoms are illustrated by observations in diabetic patients with end stage renal disease. These patients can develop severe hyperglycemia, with serum glucose concentrations that exceed 1000 to 1500 mg/dl . However because there is little or no osmotic diuresis, the rise in plasma osmolality is limited , hyponatremia is present, and there are few or no neurological symptoms.

Mainly because of the absence of the osmotic diuresis a dialysis patient in DKA may be less likley to be volume depleted and in most cases the extracellular volume is expanded from its baseline, and only if it is deemed clinically necessary should small aliquots of fluid be administered with continuous evaluation
Total body concentrations of potassium is unchanged, and they frequently have a high serum potassium level. Hyperglycemia has muliple effects on serum potassium: lack of insulin causes translocation of intracellular potassium to the extracellular compartment, a second hyperkalemic effect of hyperglycemia is the consequence of associated hypertonicity, which also leads to egress of potassium from the cells to the extracellular compartment

Insulin infusion is the only treatment required in majority of the patients. Emergency hemodialyis may be considered in severe pulmonary edema, profound metabolic acidosis and severe hyperkalemia with EKG mainfestations
 
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Diabetic patients tend to suffer from ketoacidosis less frequently after starting chronic dialysis than prior to it.The prolonged half life of insulin in advanced renal failure and frequent follow up of patients on chronic dilayis have been identified as reasons for the decreased frequency of ketoacidois in the dialysis population. The usual course leading to ketoacidosis is omission of one or more insulin doses, often due to an intercurrent illness. This is of prime importance as an underlying cause should always be looked for at presentation. The common ones being access related infections and myocardial ischemia.

The absence of osmotic diuresis distinguishes dialysis associated hyperglycemia from hyperglycemia observed in patients with normal renal function.The rise in plasma osmolality that is seen in diabetic ketoacidosis and non ketotic hyperosmolar coma is only in part due to the rise in serum glucose. The marked hyperosmolality is primarily due to the glucose osmotic diuresis that causes water loss in excess of sodium and potassium. The importance of effective plasma osmolality in the development of neurological symptoms are illustrated by observations in diabetic patients with end stage renal disease. These patients can develop severe hyperglycemia, with serum glucose concentrations that exceed 1000 to 1500 mg/dl . However because there is little or no osmotic diuresis, the rise in plasma osmolality is limited , hyponatremia is present, and there are few or no neurological symptoms.

Mainly because of the absence of the osmotic diuresis a dialysis patient in DKA may be less likley to be volume depleted and in most cases the extracellular volume is expanded from its baseline, and only if it is deemed clinically necessary should small aliquots of fluid be administered with continuous evaluation
Total body concentrations of potassium is unchanged, and they frequently have a high serum potassium level. Hyperglycemia has muliple effects on serum potassium: lack of insulin causes translocation of intracellular potassium to the extracellular compartment, a second hyperkalemic effect of hyperglycemia is the consequence of associated hypertonicity, which also leads to egress of potassium from the cells to the extracellular compartment

Insulin infusion is the only treatment required in majority of the patients. Emergency hemodialyis may be considered in severe pulmonary edema, profound metabolic acidosis and severe hyperkalemia with EKG mainfestations

That was an educational post. Thank you.

No sarcasm, really...I don't think I could have written such a clear post.

HH
 
My question is on recs for starting fluids given concern for volume overload. We went with D5NS@50/hr with the insulin drip, and despite this, her Na went down.

For something like this, would it be better to go with like a higher dextrose percent at a slower rate or what? Where is the extra fluid coming from to dilute the serum?

The Rec's remain the same, examine your patient. While the beautiful post above is true most of the time, it is still not that uncommon to have a hypovolunemic ESRD pt in DKA. would you not give NS to a ESRD pt in sepsis? If they need fluid, give fluid, if they're hypovolunemic give NS until they're euvolumenic. Just last night I had an ESRD pt in HHK who's serum osmolality was 345 with a BS of 1200 And an uncorrected sodium of 112. They got 2L NS before changing to d5. I once had an old endocrinologist tell me that the body isn't capable of making a blood sugar greater than 500 without a dehydration concentration, I've never found a citation for that claim, but anecdotally, I've found that these pts blood sugars do drop quickly to the 4-500 range with fluid alone.

If ESRD is their only issue, then a little fluid overload isn't going to hurt them anyways, you can always fix with dialysis. I have very few qualms about pushing NS in an ESRD pt if they need it. just be aware of their underlying cardiac function, they're oxygen requirements and always look for MI in these pts.

frankly, Most people are far too timid about giving fluid to this group of pts.
 
Mainly because of the absence of the osmotic diuresis a dialysis patient in DKA may be less likley to be volume depleted and in most cases the extracellular volume is expanded from its baseline, and only if it is deemed clinically necessary should small aliquots of fluid be administered with continuous evaluation

As I stated above, you can use IV fluids in ESRD DKA patients. Just be careful! For the reasons mentioned above, these patients tend not to be as volume contracted as other DKA patients with normal renal function.

And of course, any septic patient required IV fluids and intravascular volume expansion -- and that includes ESRD patients. But again, Septic Dialysis tend to require less volume. Typically, fluids in Dialysis ESRD patients should be given in small 250 - 500 cc boluses depending on their body size with close and continuous observation. Basically, their hemodynamics and blood pressures should guide fluid management. I encourage avoiding standing IV Fluid drips in anuric dialysis patients, but you can give fluids if and when clinically indicated.

I hope this helps!
 
As I stated above, you can use IV fluids in ESRD DKA patients. Just be careful! For the reasons mentioned above, these patients tend not to be as volume contracted as other DKA patients with normal renal function.

And of course, any septic patient required IV fluids and intravascular volume expansion -- and that includes ESRD patients. But again, Septic Dialysis tend to require less volume. Typically, fluids in Dialysis ESRD patients should be given in small 250 - 500 cc boluses depending on their body size with close and continuous observation. Basically, their hemodynamics and blood pressures should guide fluid management. I encourage avoiding standing IV Fluid drips in anuric dialysis patients, but you can give fluids if and when clinically indicated.

I hope this helps!

I disagree with this approach from a critical care stand point. a 250 mL bolus is about worthless for intravascular expansion, a 500mL isn't much better, for dka/hhnk yeah they take less fluid than their non-renal counterparts but they still need fluid, typically in the liters range (not the 8-12 a hhnk may need, but easily 2-6L). but keep in mind dka pts also have huge insensible losses from their increased respiratory drive from the acidosis, and even more so if it is infection induced. honestly what's the worst risk associated with inducing a little fluid overload in these pts? pulm edema? hypercloremic acidosis?

the septic pts I have no qualms about giving them 20-40ml/kg fluid and do so frequently and have yet to push them into so far I had issues oxygenating them. since we're in the critical forum this goes with the assumption you're in a critical care floor, it goes without saying theyre being monitored closely. being CC trained I'm kinda a **** of get off the pot kinda guy, the only time I give less than a liter bolus is in the ESRD who also has significant cardiomyopathy, but if they're hypotensive, most likely they'll still get bolused a liter at a time, and anecdotally, we don't have issues with respiratory status using an agressive approach. now we could argue the risks of a hypercloremic acidosis, but that's of little concern to me when they're hypotensive.

ultimately we're on the same page I think, reevaluate the pt frequently.
 
I disagree with this approach from a critical care stand point. a 250 mL bolus is about worthless for intravascular expansion, a 500mL isn't much better, for dka/hhnk yeah they take less fluid than their non-renal counterparts but they still need fluid, typically in the liters range (not the 8-12 a hhnk may need, but easily 2-6L). but keep in mind dka pts also have huge insensible losses from their increased respiratory drive from the acidosis, and even more so if it is infection induced. honestly what's the worst risk associated with inducing a little fluid overload in these pts? pulm edema? hypercloremic acidosis?

the septic pts I have no qualms about giving them 20-40ml/kg fluid and do so frequently and have yet to push them into so far I had issues oxygenating them. since we're in the critical forum this goes with the assumption you're in a critical care floor, it goes without saying theyre being monitored closely. being CC trained I'm kinda a **** of get off the pot kinda guy, the only time I give less than a liter bolus is in the ESRD who also has significant cardiomyopathy, but if they're hypotensive, most likely they'll still get bolused a liter at a time, and anecdotally, we don't have issues with respiratory status using an agressive approach. now we could argue the risks of a hypercloremic acidosis, but that's of little concern to me when they're hypotensive.

ultimately we're on the same page I think, reevaluate the pt frequently.


I think we are on the same page.

But, Last night, I consulted on an ESRD patient in DKA. He presented with N/V for one day.
Here are his initial labs:
Na 138, K 5.1, Cl 79, CO2 39, BUN 65, Creat 8.5, Glucose 617, Positive serum ketones.
ABG 7.45/53/83/ 94%
His initial BP was 95/60 (which is very low for this Dialysis patient). He normally run blood pressures of 150-170's/80-90's.
So from the labs, he has a huge metabolic Anion gap of 30 and also a concurrent metabolic alkalosis, plus a small Respiratory acidosis.

Guess how much fluid he required?? Three boluses of saline 500 cc ( or just 1.5 liters). By the way, he weighs about 80 kgs. His Blood pressure came up nicely with this to 130/80.

His gap quickly closed with this small amount of fluids and the insulin drip. I dialyzed him this morning, and he weighed in above his dry weight and was hypertensive before the treatment. Basically, if he would have gotten more fluids, it would have been fine, but more for us to ultra filtrate later during dialysis. I try to aim for the smallest, yet most effective volume.

But yes, I think we are on the same page. You can give fluids to dialysis patients!! :):D;)
 
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