Management of Pediatric DKA

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EvoDevo

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From another thread:

Case from the other day:

12 yoM with known T1DM p/w abdominal pain after mother stated that he had missed "only one dose of insulin." Extremely tachycardic, tachypneic, extremely dry/cracked lips, could barely talk due to amount of dehydration. Exquisite RUQ abdominal pain. Borderline mental status

From memory...

pH: 6.99 (ABG)
Lactate 5.8
K: 6.5
CO2: 4
WBC: 33K
Glucose: 814
Serum Osm: 364

Shipped that kid off in a helo ASAP. Door to helo liftofff under 60 minutes.

Wanted to slap that mother.....

In this case, I simply started a 20 ml/kg fluid bolus, insulin bolus and drip and shipped. However, RF made the point that perhaps we should have a discussion. +/- on sodium bicarb? Other management?

Discuss.

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From the stuff I have read:

Bicarb has no benefit
Insulin bolus doesn't matter, you can just make the drip faster

I am under the impression IVF is more unpredictable with regards to dropping blood glucose and you can cause a precipitous drop if you give too much (>40ml/kg in 4 hours). Insulin on the other hand is a little more predictable, but of course these kids need fluid due to the amount of dehydration from the hyperglycemia.

I'm nervous about giving any of these kids cerebral edema.
 
Copy and pasted from the other thread:

"Paradoxical cerebral acidosis can occur with NaHCO3 administration due to formation and diffusion of CO2 from the systemic circulation into the central nervous system. Rapid administration of NaHCO3 can cause intracellular influx of potassium and induce acute hypokalemia. NaHCO3 therapy has been associated with cerebral edema, the most common cause of mortality for children with DKA. NaHCO3 supplementation should only be considered in the critical instance of severe acidosis (serum pH < 7.0) associated with myocardial depression and circulatory insufficiency."

"Pediatric Diabetic Ketoacidosis: An Outpatient Perspective On Evaluation and Management", EB Medicine, March 2013 Volume 10, Number 3. By William Bonadio, MD

Also, I would gingerly hydrate them with 0.9%NS at 10mL/kg as there have been circumstances where cerebral edema has occurred with too large of a fluid bolus.

---

Morris LR, Murphy MB, Kitabchi AE. Bicarbonate therapy in severe diabetic ketoacidosis. Ann Intern Med. 1986;105(6):836- 840. (Prospective randomized study; 21 patients)

Green SM, Rothrock SG, Ho JD. Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis. Ann Emerg Med. 1998;31(1):41-48. (Retrospec- tive study; 147 cases)

Ohman JL Jr, Marliss EB, Aoki TT, et al. The cerebrospinal fluid in diabetic ketoacidosis. N Engl J Med. 1971;284(6):283- 290.

Soler NG, Bennett MA, Dixon K, et al. Potassium balance during treatment of diabetic ketoacidosis with special reference to the use of bicarbonate. Lancet. 1972;2(7779):665-667. (Prospective study)

Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med. 2001;344(4):264-269.
 
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but we should point out, once again that association and causation are two different things. there is concern about the amount of insulin IV, Bicarb IV and the amount of fluids causing cerebral edema. But I know of no trials for any of these things.

Rather, looking at Glaser et al - it appears that sicker kids are more likely to get more interventions and more likely to have cerebral edema as a complication.
 
No HCO3.
No insulin bolus prior to gtt.
The cerebral edema is probably a myth, but given the lack of refutation for said myth, as long as the resuscitation isn't so slow it's harmful...it's probably not harmful. Kupperman & PECARN are evaluating this prospectively.
 
Copy and pasted from the other thread:

"Paradoxical cerebral acidosis can occur with NaHCO3 administration due to formation and diffusion of CO2 from the systemic circulation into the central nervous system. Rapid administration of NaHCO3 can cause intracellular influx of potassium and induce acute hypokalemia. NaHCO3 therapy has been associated with cerebral edema, the most common cause of mortality for children with DKA. NaHCO3 supplementation should only be considered in the critical instance of severe acidosis (serum pH < 7.0) associated with myocardial depression and circulatory insufficiency."

"Pediatric Diabetic Ketoacidosis: An Outpatient Perspective On Evaluation and Management", EB Medicine, March 2013 Volume 10, Number 3. By William Bonadio, MD

Also, I would gingerly hydrate them with 0.9%NS at 10mL/kg as there have been circumstances where cerebral edema has occurred with too large of a fluid bolus.

---

Morris LR, Murphy MB, Kitabchi AE. Bicarbonate therapy in severe diabetic ketoacidosis. Ann Intern Med. 1986;105(6):836- 840. (Prospective randomized study; 21 patients)

Green SM, Rothrock SG, Ho JD. Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis. Ann Emerg Med. 1998;31(1):41-48. (Retrospec- tive study; 147 cases)

Ohman JL Jr, Marliss EB, Aoki TT, et al. The cerebrospinal fluid in diabetic ketoacidosis. N Engl J Med. 1971;284(6):283- 290.

Soler NG, Bennett MA, Dixon K, et al. Potassium balance during treatment of diabetic ketoacidosis with special reference to the use of bicarbonate. Lancet. 1972;2(7779):665-667. (Prospective study)

Glaser N, Barnett P, McCaslin I, et al. Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics. N Engl J Med. 2001;344(4):264-269.

Being careful with your volumes in little kiddos I can get behind.
10 cc/kg of NS in severe DKA?!? I can't get behind that.
 
As above. Don't go nuts (100mL/kg) with boluses, but at the same time, don't under-resuscitate them.
In the end, the kids who get cerebral edema are likely getting it from something other than just "fluid" by itself.
 
This "replace the bicarbonate" discussion has been going on for decades. There is always this strong temptation to "treat the number" whatever it is. "Make the numbers look better, and the patient will be better" or "Buffing the chart" as in The House of God. It's not always the case. Often times, the opposite is true. In kids with DKA, it almost seems as if most of the ways you run into trouble, is by doing too much, too fast.
 
This is a little off topic, but there was a recent EMCrit Podcast on insulin use and he stated using regular insulin IV versus subcutaneous somehow affects the glucose differently (not just because of onset, peak and duration of action). This seems counterintuitive to me because insulin is insulin and I feel it shouldn't matter how we give it because the body should treat it is same regardless (except of course for pharmacokinetics). Similar to toradol IM, just because it is given IM and not PO doesn't mean it is magically free of GI side effects.

Any clarification would be greatly appreciated.
 
As above. Don't go nuts (100mL/kg) with boluses, but at the same time, don't under-resuscitate them.
In the end, the kids who get cerebral edema are likely getting it from something other than just "fluid" by itself.

I should have been more careful with my wording. I would start with 10mL/kg IVF boluses and keep giving them if necessary to resuscitate but I wouldn't start with 20mL/kg right off the bat.
 
As with adults - no insulin bolus, no bicarb.

Slow and steady wins the race. It took them a long while to go into DKA, bring them out gradually.
 
Slow and steady definitely wins the race....well said doctb

in my opinion, there aren't too many endocrine emergencies that need immediate rapid correction -- terminal hyperkalemia and critical hypoglycemia are really the only ones that come to mind.

I support the no insulin bolus and the 10 cc/kg fluids. you need to initiate the treatment and get them to the ICU, not fix the entire DKA episode (unless boarding is an issue). kids, and adults for that matter shouldn't die from DKA. their M&M typically comes from poor management by the provider.

and mind the potassium. over reliance on "red flag" colors on lab read outs may cause you to miss the relative hypokalemia. a "normal" value is going to become low very fast as insulin is infused.

frequent re-evaluations of clinical status, pH, blood sugar, and K need to be done
 
No peds at my shop, so I get this easy. 10-20cc NS/kg, insulin gtt started, bus off straight to an ICU bed a few miles down the street. I love having a dedicated children's hospital nearby. I was always taught no bicarb, and to leave the more complex double bag system to the ICU as they're the ones who are experienced with the management anyway. All I continually monitor in the single hour+ I have them for is the fingersticks, the EKG, and general gestalt.
 
Agree with what others have stated: slow and steady.
I've had DKAs with pH of 6.8 turn around just fine. 20/kg bolus of NS is perfectly fine, but don't overdo the fluids. No insulin bolus is needed. Instead, get insulin started at 0.1/kg/hr and let it run. Add in between 1.5 and 2 x MIVF (NS +K) for age, then Y in D10NS as the sugars fall (our current protocol adds in D10 when glucose hits 300). Mind the K. Most of us in peds consider bicarb administration to be malpractice (I mean no offense!).

The real question is when do you give 3%? Our ED gives it up front pretty aggressively, but in the unit we are less so.
 
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I don't see kids and thus no nothing about the monsters apart from anecdotal knowledge as a father of 5, but I never give bicarbonate to adults in DKA. Ever. Even a severe one not too long ago at 6.7 unresponsive. She got tubed and had fluids dumped in with insulin. No bicarbonate. Lived to do it again in 3 weeks knowing her. He only indication I can think of is if they actually arrest with severe acidemia. Then I would treat them like any other arrest. But if there heart function is fine, I don't give bicarbonate. In fact I very rarely give bicarbonate for any AGMA unless its effecting vasopressor function in shock or leading to arrythmia. The non-gappers, all the time. But essentially never in DKA. When I discussed this with nephro and endocrine here they agreed. No role in adult DKA.
 
No peds at my shop, so I get this easy. 10-20cc NS/kg, insulin gtt started, bus off straight to an ICU bed a few miles down the street. I love having a dedicated children's hospital nearby. I was always taught no bicarb, and to leave the more complex double bag system to the ICU as they're the ones who are experienced with the management anyway. All I continually monitor in the single hour+ I have them for is the fingersticks, the EKG, and general gestalt.

agreed. we have 2 peds ICU's in our hospital system so i have a peds intensivist on the phone right away and transfer as soon as i can get transport. they do that double bag stuff but i just stick to boluses prn and the drip. i want a repeat fingerstick before they go for sure, but having to redraw anything starts to wear on my nurses since it's a kid so i just want them gone!
 
There was a recent EMCrit Podcast on insulin use and he stated using regular insulin IV versus subcutaneous somehow affects the glucose differently (not just because of onset, peak and duration of action). This seems counterintuitive to me because insulin is insulin and I feel it shouldn't matter how we give it because the body should treat it is same regardless (except of course for pharmacokinetics). Similar to toradol IM, just because it is given IM and not PO doesn't mean it is magically free of GI side effects.

Any clarification would be greatly appreciated.
 
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