DKA & HHS Flashcards
What 3 factors contribute to the pathophysiology of DKA & HHS? What could cause #1? Give examples of #2 and the three major reasons of increase. Why does #3 occur? What are consequences of #3?
1 - Absolute or relative insulin deficiency. 2 - Increase in counter-regulatory hormones. 3 - Volume depletion. Insulin deficiency: noncompliance, expired insulin, insulin pump failure. Counter-regulatory hormones: Glucagon, Cortisol, GH, Epinephrine – Infection, Insulin (expired, failure, etc.), Infarct (three ‘I’s). Volume depletion: Hyperglycemia-induced osmotic diuresis – consequences: dehydration, polyuria, polydipsia, increased thirst, electrolyte losses (sodium & potassium), tissue hypoperfusion w/ lactic acidosis.
What is the diagnostic criteria for DKA? HHS? What is considered resolution?
DKA: 1 - Hyperglycemia, Metabolic Acidosis, Ketone Production. HHS - Hyperglycemia, Hyperosmolality, Dehydration – * ABSENCE of significant ketoacidosis, usually a much greater blood glucose. Resolution – DKA: Glucose < 200 + 2 of the following: Bicarb > 15 mEq/L, Venous pH > 7.3, AG <13. HHS: Normal osmolality and normal mental status.
What is the best “treatment” for DKA?
AVOID ONSET! – During times of stress, follow “sick day rules” – Take insulin even when not eating, increase frequency of testing & titrate insulin appropriately, drink fluids, monitor urine ketone levels, if continuously high glucose or vomiting: call MD!
What are the three most important variables to treat in DKA? How are fluids replaced if the patient is in cardiogenic shock or severely hypovolemic? What if there is only mild dehydration? What are two important things to remember? Why is a switch made in fluids at a given glucose level? What is the preferred route of insulin replacement? Glucose should decrease by how much, and what if it is not falling by this rate?
1 - Fluid. 2 - Insulin. 3 - Potassium. Fluids: If cardiogeneic shock, severe hypovolemia - IV NS 1-2L or until pt not orthostatic. If mild dehydration - evaluate corrected serum Na, hemodynamics & urine output – IV NS or 1/2NS (if Na normal or high) until serum glucose reaches 200 mg/dL, at which point witch to 1/2NS w/ D5W. Remember: 1 - DONT correct hyperosmolality too quickly (
What is potassium doing in DKA & HHS and why? How is this treated, and should this be treated before or after insulin is given? Besides monitoring blood levels, how can this be monitored?
Potassium is usually HIGH – Insulinopenia, Acidemia. If needed, TREAT BEFORE INSULIN. If low ( 3.3 mEq/L), HOLD INSULIN and give 20-30 mEq/L until K+ > 3.3 mEq/L. If high (>5.2 mEq/L), do not give K+ but check every 2 hrs. Also: monitor EKG for height of T wave – directly proportional to K+ level. If normal K+ (3.3 - 5.2), give 20-30 mEq/hr to keep K+ between 4-5 w/ each liter of IV fluid.
Should bicarbonate be replaced? Giving too much bicarb can cause…? Is phosphate usually replaced/added?
Controversial – Replace only if severe acidosis (pH < 6.9) or severe hyperkalemia (K+ > 6.5 or EKG changes. Too much bicarb: excacerbate hypokalemia, decreased tissue oxygen uptake, cerebral edema, paradoxical CNS acidosis. Phophate is usually not altered.
How is serum osmolality calculated? How is serum sodium corrected for hyperglycemia? How is free water deficit calculated?
Osmolality = 2(Na) + (Glu/18) + (BUN/2.8)…Serum Sodium Correction = measured Na+ + 0.016(Glu - 100)…Free water deficit = [Observed Na+ - Normal Na+] / [Normal Na+ x 0.6kg]
Normal ratio of acetoacetic acid to B-HBA is? Why does this change in DKA? How should ketones be monitored? Why? Should we directly measure them?
Acetoacetic acid:B-HBA should be 1:1 - 1:3. Increase 1:10 as redox state changes in DKA – BHBA is the prominent ketone in DKA. Directly measuring ketones is not helpful because ketones decrease SLOWER than glucose – SO, as redox potential changes with decreasing glucose levels, BHBA is converted into acetoacetate, and direct measurement using the Ames Acid Test (which only measures acetoacetic acid) will reveal a paradoxical ketonuria. Can measure BHBA if AGMA has other causes, but the best way to monitor ketones is FOLLOW GLUCOSE AND THE ANION GAP.
What are the major complications in correcting for DKA and HHS? Which is most severe? How is this treated?
Hypoglycemia, Hypokalemia, Hyperchloremic nonAGMA (self-limited), Cerebral Edema (Most severe – usually fatal with serious neurological consequences). This really cannot be treated (possibly: 1-2 g mannitol, dexamethasone, intubation with hyperventilation)
Evaluate an acid-base disorder.
1 - Acidosis or Alkalosis? 2 - Metabolic or Respiratory? (Remember, if bicarb and pH are changing in the same direction, it’s metabolic!) 3 - Calculate AG = Na+ - (Bicarb + Cl). 4 - Calculate compensation using Winter’s PCO2 should be = 1.5(HCO3-) + 8 +/- 2. 5 - If metabolic acidosis, calculate “delta delta” to determine if there is an AG and a nonAG metabolic acidosis. change in AG = change HCO3. If change in HCO3- is greater than change in AG, then a concomitant nonAGMA must exist. If change in HCO3- is less than change in AG, then a concomitant metabolic alkalosis must exist. (normal AG = 12, normal HCO3- = 24)
