Yesterday the great @MohitHarshMD tagged me in a post about euglycemic DKA.
Then I got an email from the knowledge-hungry master clinician (AKA @DxRxEdu) about the same topic.
This is something!
Starting from scratch: Demystifying DKA. Let's untangle its complexity.๐งต
1/13
Then I got an email from the knowledge-hungry master clinician (AKA @DxRxEdu) about the same topic.
This is something!
Starting from scratch: Demystifying DKA. Let's untangle its complexity.๐งต
1/13
Let's go back to hormone physiology in simple terms!
Counter-regulators are important in hormone balance, but there's almost always a key player calling the shots.
For instance:
Ca: PTH
K: aldosterone
Na: ADH
Glucose: insulin
2/13
Counter-regulators are important in hormone balance, but there's almost always a key player calling the shots.
For instance:
Ca: PTH
K: aldosterone
Na: ADH
Glucose: insulin
2/13
Let's break down some basic physiology.
In simple terms, how does insulin act?
You eat, your blood sugar takes a little hike, and insulin levels rise.
Onto fat tissue: insulin turns on lipoprotein lipase (lipogenesis) and hits pause on hormone-sensitive lipase (lipolysis).
3/13
In simple terms, how does insulin act?
You eat, your blood sugar takes a little hike, and insulin levels rise.
Onto fat tissue: insulin turns on lipoprotein lipase (lipogenesis) and hits pause on hormone-sensitive lipase (lipolysis).
3/13
Let's be very simple:
- After eating: insulin goes up, telling us we've got energy to spare, so let's store it.
- Fasting: insulin takes a dip, signaling that it's time to tap into stored energy. Breaking down triglycerides (beta oxidation) gives us ATP and ketone acids!
4/13
- After eating: insulin goes up, telling us we've got energy to spare, so let's store it.
- Fasting: insulin takes a dip, signaling that it's time to tap into stored energy. Breaking down triglycerides (beta oxidation) gives us ATP and ketone acids!
4/13
Ketone acids are part of our daily routine.
Why don't we have DKA all the time?
It's all about insulin!
We can didactically divide insulin secretion in basal and prandial (~50% for each). Even in a long fasting, the body still has enough insulin to prevent ketoacidosis.
5/13
Why don't we have DKA all the time?
It's all about insulin!
We can didactically divide insulin secretion in basal and prandial (~50% for each). Even in a long fasting, the body still has enough insulin to prevent ketoacidosis.
5/13
In the situation above, ketones are produced, but they are also excreted and do not cause significant acid-base impairment.
Now, let's say you do not have insulin.
What happens? Hyperglycemia and if you really don't have insulin, DKA!
6/13
Now, let's say you do not have insulin.
What happens? Hyperglycemia and if you really don't have insulin, DKA!
6/13
DKA= very very low insulin
When insulin is in super short supply, the body thinks, "No glucose? Time to bust open those triglycerides for energy!"
If ketone bodies are produced in such a high amount in a short period of time: DKA!
7/13
When insulin is in super short supply, the body thinks, "No glucose? Time to bust open those triglycerides for energy!"
If ketone bodies are produced in such a high amount in a short period of time: DKA!
7/13
Can someone get DKA while on usual dose of insulin? Yes!
Just like you can have HF with a healthy heart ( high-output HF), it's possible for the insulin demand to spike (like during an infection). This can plummet the usual insulin levels to rock-bottom, leading to DKA.
8/13
Just like you can have HF with a healthy heart ( high-output HF), it's possible for the insulin demand to spike (like during an infection). This can plummet the usual insulin levels to rock-bottom, leading to DKA.
8/13
Now let's change scenario.
You have insulin in amount to prevent DKA, but still, its levels are super low.
With insulinopenia, glucose can go up to the 1000s mg/dL. Severe dehydration develops and welcome to HHS.
You can only have HHS if you have insulin to prevent DKA!
9/13
You have insulin in amount to prevent DKA, but still, its levels are super low.
With insulinopenia, glucose can go up to the 1000s mg/dL. Severe dehydration develops and welcome to HHS.
You can only have HHS if you have insulin to prevent DKA!
9/13
Back to DKA
DKA = very very low insulin.
With insulin tanking, where does glucose go? Up!
Now the curveball: it is possible to have DKA with normal blood glucose. This is euglycemic DKA!
10/13
DKA = very very low insulin.
With insulin tanking, where does glucose go? Up!
Now the curveball: it is possible to have DKA with normal blood glucose. This is euglycemic DKA!
10/13
Euglycemic DKA due to SGLT2i.
Who? SGLT2i + severe insulinopenia
How?
-Individuals may decrease their insulin due to glucosuria. Very very low insulin=DKA
-SGLT2i increases glucagon, which can accelerate ketogenesis
Why euglycemic?
Glucose slips away in urine!
11/13
Who? SGLT2i + severe insulinopenia
How?
-Individuals may decrease their insulin due to glucosuria. Very very low insulin=DKA
-SGLT2i increases glucagon, which can accelerate ketogenesis
Why euglycemic?
Glucose slips away in urine!
11/13
Euglycemic DKA due to starvation
Who: cachexia + starvation in critically ill pts with T1DM/ advanced T2DM
How?
- Blood glucose may be normal as these individuals are consumed and have low reserve: low glycogen = no glucose spike!
- But if they don't have insulin...DKA!
12/13
Who: cachexia + starvation in critically ill pts with T1DM/ advanced T2DM
How?
- Blood glucose may be normal as these individuals are consumed and have low reserve: low glycogen = no glucose spike!
- But if they don't have insulin...DKA!
12/13
This is intended to facilitate understanding of DKA and not meant to be a comprehensive review!
Feel free to add whatever you want to add!
Thank you @MohitHarshMD and @DxRxEdu for making my day better by making me think about hormones!
13/13
Feel free to add whatever you want to add!
Thank you @MohitHarshMD and @DxRxEdu for making my day better by making me think about hormones!
13/13
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