Master the management of hyperglycemia, DKA, and learn to avoid common pitfalls. This episode is packed with clinical pearls from repeat guest, Endocrinologist, Dr. Jeffrey Colburn.
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- Type 1 diabetes (DM1) occurs by autoimmune destruction of beta cells
- occurs at any age
- Typically lean body type and normal lipid profiles
- Type 2 diabetes (DM2)
- Typically obese and insulin resistant
- Eventually fat deposition in pancreas destroys insulin production 15-20 years after onset of DM2 leading to absolute insulin deficiency
- Triad of DKA = hyperglycemia, ketonemia, acidemia
- DKA occurs w/total lack of insulin leads to inability to utilize glucose (hyperglycemia)
- Simulated starvation occurs
- Counter regulatory hormones kick in
- Free fatty acids are broken down for fuel
- Keto acids are made as a by product (ketonemia)
- Acidemia occurs
- DKA can occur in DM2 if overwhelming infection, or infarction (MI or CVA)
- Even just a little bit of insulin can keep patient out of DKA!
- Dehydration is a cardinal issue in DKA from osmotic diuresis
- Often 6-8 liters depleted!
- Sick day rules for Type 1 diabetes
- Early contact with healthcare team
- Reduce, but do not discontinue insulin during the illness (see #9)
- Check frequent fingersticks
- Use antipyretics to manage fever
- Push the fluids
- Educate family members about signs/symptoms of DKA
- If sick, then drop basal insulin by 20% whether SQ or basal rate on insulin pump
- Keep mealtime insulin dose the same, but skip if not eating
- Beta hydroxybutyrate is the predominant ketone in DKA
- Urine ketones measure acetoacetate (strongly) and acetone (weakly) NOT beta hydroxybutyrate
- Serum ketones measure acetoacetate and acetone NOT beta hydroxybutyrate
- Thus, check a direct blood beta hydroxybutyrate level if available
- Follow an algorithm when treating DKA!
- IVF fluids first line therapy in DKA, hyperglycemia
- Make sure to replete potassium above at least 3.3 before giving insulin!
- Insulin drip – insulin out of system in minutes when drip stopped
- Subcutaneous insulin – lasts 4 hours and can “stack” if repeat doses given
- SGLT2 inhibitors can lower blood glucose in the absence of insulin leading to possible “euglycemic DKA”
Goal: Listeners will be able to confidently evaluate, and manage the patient with severe hyperglycemia and/or DKA.
By the end of this podcast listeners will:
- Differentiate between type 1 and type 2 diabetes
- Review the pathophysiology of DKA
- Utilize basic laboratory data to diagnose DKA and differentiate it from other common conditions
- Initiate management of hyperglycemia and/or DKA in the acute setting
- Formulate a plan for sick day management in type 1 diabetes
- Describe the mechanism of DKA in setting of SGLT2 inhibitor use
Dr. Colburn is a member of AACE and helped develop the AACE Algorithm for Type 2 Diabetes.
02:06 Rapid fire questions
07:30 Definitions and classification of diabetes
10:12 DKA in type 2 diabetes?
11:16 Pathophysiology of DKA
13:00 Severe hyperglycemia mislabeled as DKA
14:22 Which type 2 diabetics get DKA?
15:40 The cardinal issue is dehydration
17:11 Starvation ketosis vs DKA vs other
18:33 How to handle severe hyperglycemia in outpatients
22:18 Sick day management in type 1 diabetes
27:48 Initial testing for diagnosis of DKA
31:00 Subcutaneous or IV insulin for DKA
33:35 Initial evaluation and management in ER
36:50 Fluids and electrolyte management
40:12 SGLT2 inhibitors and euglycemic DKA
Links from the show:
- Walden by Henry David Thoreau
- AACE Type 2 Diabetes Management Algorithm on iTunes.
- Hyperglycemic Crises in Adult Patients With Diabetes. Diabetes Care 2009 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2699725/