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FBE University 2020 (D)
JUL
10

Euglycemic DKA (Urine and Ureout)

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In the classical FOAMed style, let’s start with a case.
 

You’re dispatched for a sick person. You walk into a ground level walk-up apartment and meet your patient. He is 38 years old, he looks generally ill but not in any acute distress. He reports 4 days of excessive thirst, hunger, and urination. He is a type 2 diabetic. He managed his diabetes with metformin for years but recently added empagliflozin (Jardiance).

 

You obtain the following vital signs on the monitor: 

 

PC: Chris Kroboth with iSimulate (@capno_medic)

 

Now the moment of truth. We all know where this is headed. You watch the glucometer county down as you await the final piece of the puzzle. As you prepare to pat yourself on the back---- 

 



So now we have information that does not fit with the diagnostic picture we painted in our heads. 

 

So you give the patient a monitor and transport, maybe some fluids. If you were thinking atypical ACS that’s a great thought- but the 12 lead is clean. 

 

You come to find out that he was ultimately diagnosed with DKA. 

 

But the sugar was normal?

 

Luckily for you this paragraph is not a detailed review of the pathophysiology of DKA. There are far better explanations on the internet than I can provide here. If you want a really good explanation of DKA FlightBridgeEd did a good nightmare series case on a DKA patient.

 

The big thing to remember about DKA is that the hyperglycemia is a symptom of the underlying pathology. It’s not the problem itself. The glucose accumulates in the blood because of the insulin resistance at the cellular level. Insulin resistance is the primary disorder. 

So now you secretly google the name of that long drug and see it classified as a "Sodium-glucose Contransporter-2 (SGLT-2)... this doesnt help. 

 

In 2013 the FDA approved a new class of medications called Sodium-glucose Contransporter-2 (SGLT-2) inhibitors. The three medications in this class on the market are:

 
  • Canagliflozen sold as Invokana (sounds like the name of a woman in James bond)
 
  • Gapagliflozen sold as Farxiga 
 
  • Empagliflozen sold as Jardiance
 

Note the “gliflozen” suffix.

 

The main action of these drugs is the excretion of glucose through the kidneys. It does this by inhibiting a protein (SGLT) that facilitates reabsorbtion of glucose in the kidney.

This is very different from the other common therapies for diabetes. Other therapies target the cell’s insulin sensitivity and aid with transport into the cell. Think about it:

 

Insulin - directly transports glucose into the cell

 

Metformin - lowers cellular insulin resistance

 

Sulfonylureas - stimulate insulin production in the presence of glucose

 

Under conventional therapy: 

 


 

As the serum glucose goes so goes insulin. With all of the above therapies the serum glucose will decrease because the cells are able to metabolize the glucose. 

 

If the glucose is simply being excreted via the kidneys two things happen that we do not see with the older therapies:

 

1.The pancreas sees less glucose so it releases less insulin

 

2. The cells are not able to metabolize more glucose since insulin resistance is unaffected

With SGLT-2 therapy:

 

So to recap the cells are still breaking down fatty acids generating ketone bodies, driving the pH down. On top of that - the body is able to lose glucose in the urine.

 

The effect is a patient in DKA with normal blood glucose. The literature refers to this as Euglycemic Diabetic Ketoacidosis. The causes of ketoacidosis in these patients are the same as those seen in a hyperglycemic DKA patient.

 

I’ll wrap this up with the “so what” part. What we had with our case is a set of symptoms that points us in one direction but the centerpiece of the diagnosis didn’t match up. When you have the picture we talked about ETCO2 can give you the last piece of the puzzle. If the ETCO2 is greater than 29mmHg, they are most likely not in DKA. Check out this explanation in ACEP.

 

I used to put ETCO2 on my hyperglycemic patients to try and tease out DKA vs HHNS. Then one day it dawned on me - in the 911 setting it really doesn’t matter. The prehospital treatment for DKA and HHNK is the same. The two key treatments are:

 

1. Fluid resuscitation since these patients run very dry- sometimes liters. 

A note on fluid loading- we only have lactated ringers (LR) at my shop but given the choice I would (as usual) steer clear of normal saline. LR is closer to a neutral pH which is where the patient needs to be corrected to eventually. One step better would be one of the “balanced” solutions such as Plasmalyte. PulmCrit gives a great explanation here: https://emcrit.org/pulmcrit/four-dka-pearls/

 

2. Resisting the urge to do something just to do something (Sodium Bicarbonate, intubation, etc…)

For a great podcast on when sodium bicarb is effective, check out this podcast.

https://foamfrat.libsyn.com/podcast-74-bicarb-or-bye-carb

 

As far at the potassium in these fluids remember that it is a physiologic amount of potassium. You are adding potassium and volume so there is no net difference. On top of that they are probably going to get potassium repletion anyway.

 

This one is a bit of a needle in the haystack, but it’s out there. Please let us know if you have seen this in the field. Did you know it at the time or did you come across it after and piece it together? 

 

Thank you all! 

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