DKA and HHS

Question 1

What are the three key features in the definition of DKA?

Answer 1

Diabetic ➔ hyperglycemia
Ketonemia ➔ high levels of ketones
Acidosis ➔ low pH

Question 1

What are the 2 main features of HHS?

Answer 1

Hyperglycemia and hyperosmolarity

• high blood sugar
• severe ECFV depletion and hyperosmolarity (increased osmolality from dehydration and increased concentration of blood)

Question 2

Is HHS acute or chronic?

Answer 2

HHS is more chronic

Question 3

Is DKA more acute or chronic?

Answer 3

DKA is more acute

Question 4

which type of DM is more common in DKA and HHS?

Answer 4

DKA: T1DM and severe T2DM
HHS: T2DM

Question 5

What are the 6 Is for triggers of DKA and HHS?

Answer 5

I - infection
I - ischemia/infarction
I - inflammation - pancreatitis
I - insulin - deficiency or first presentation
I - intoxication
I - Iatrogenic

Question 6

What is euglycemic DKA?

Answer 6

it is DKA was near-normal plasma glucose or a midler degree of hyperglycemia

Question 7

in what pt population do we typically see euglycemic DKA in?

Answer 7

pregnant pts or pts taking SGLT2i

Question 8

What other things (2) can trigger DKA and HHS that are not apart of the 6 I’s?

Answer 8

surgery
medications - thiazide diuretics, atypical antipsychotics, glucocorticoids

Question 9

Explain the electrolytes pathophysiology in DKA

Answer 9

Normal electrolytes: with glucose/ATP in the cell
- Na pumped OUT of cell
- K pumped INTO the cell

Pathogenic: NO glucose/ATP in the cell
- Na accumulates in the cell
- K accumulates outside of the cell

Question 10

What would the electrolyte lab values look like in DKA and HHS?

Na and K

Answer 10

DKA: sodium may be normal or low; K may be normal or higher
- K may look normal or low, bc there is an overall net deficit in K because of polyuria (however in the extracellular volume, there is more K in it)

HHS: similar electrolytes but more profound/extreme values because dehydration is more severe and has been building over time

Question 11

Explain the pathophys of DKA

Answer 11

physiologic stress ➔ decreased insulin (either absolute or there is not enough to meet metabolic demand)
- without insulin, there is no suppression of glycogenolysis and gluconeogenesis and ketogenesis
- in the liver, glucose is produced/released ➔ contributes to hyperglycemia
- fatty acids are released from adipose tissue ➔ to the liver ➔ ketones are produced
- ketones are acidic and consume bicarbonate ➔ results in a metabolic acidosis and creates an anion gap

• w/o insulin there is hyperglycemia ➔ increased urination bc increased osmolarity in the plasma being filtered by the kidney so water passively diffuses (osmosis) into the urine, increasing the amount (osmotic diuresis) ➔ dehydration

Question 12

Why is there no ketogenesis in HHS?

Answer 12

Because there is still insulin in the body, which suppresses ketogenesis

Question 13

Explain the pathophys of HHS

Answer 13

relative decrease in insulin ➔ hyperglycemia ➔ increased urination bc increased osmolarity in the plasma being filtered by the kidney so water passively diffuses (osmosis) into the urine, increasing the amount (osmotic diuresis) ➔ dehydration

Question 14

What are the D.K.A s/s of DKA?

Answer 14

D-dehydration s/s
- decreased skin turgur
- dry mucus membranes
- no tears
- dark urine
- polydipsia
- fatigue/weakness

K-kussmaul respirations

A-acetone breath/acidosis s/s
- nausea/vomitting
- abdo pain
- altered mental status

+ hyperglycemia s/s

Question 15

What s/s do we expect in HHS?

Answer 15

Dehydration s/s
- more commonly have neurological s/s because severe cerebral dehydration ➔ focal neurological deficit, visual changes, delirium, coma
- increased risk of cardiovascular collapse

hyperglycemia s/s

Question 16

How would w/u a potential DKA/HHS pt ix wise?

Answer 16

1. electrolytes ➔ gives us anion gap + potassium levels
2. VBG ➔ gives us bicarb
3. serum/urine ketone ➔ absence/presence of ketones
4. random plasma glucose ➔ gives idea of hyperglycemia
5. serum osmolality ➔ high in HHS, lower in DKA
6. serum creatinine ➔ eGFR
7. urine analysis ➔ albumin to creatinine ratio

Question 17

How would you treat DKA/HHS?

Answer 17

Mnemonic: D - dehydration, K - replace potassium, A - address acidosis

**we’re monitoring bloodwork (electrolytes and VBG every hour…)
1. aggressive fluid resuscitation
2. replace potassium if normo- or hypokalemic ➔ potassium is required for glucose to enter the cells, so need to be replaced before initiating insulin
3. once potassium is corrected, begin giving IV short-acting insulin (could also consider replacing bicarb but mixed evidence)
4. if pts ends up hypoglycemic because of the insulin; KEEP ON INSULIN because correcting the acidosis is more important, give IV dextrose
5. once anion gap closes (<12), IV insulin can be transitioned to sq insulin

**also find and treat underlying etiology once pt is stablized