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14 Cards in this Set

  • Front
  • Back
1. Pathophys of ketoacidosis?
a. Insulin deficiency leads to lipid oxidation and metabolism rather than glucose metabolism.
b. The insulin absence results in FFA released from adipose tissue and in unregulated hepatic FFA oxidation and ketogenesis.
2. How do children in DKA usually present?
a. With s/s of severe dehydration and acidosis.
b. The hx is often positive for:
i. Polyuria
ii. N/V
iii. Abdominal complaints
c. Hypothermia
d. Hypotension
e. Kussmaul respiration
f. Acetone on breath
3. Lab data for DKA?
a. Elevated glucose (often 400-800).
b. Metabolic acidosis (with Anion gap i.e. excess endogenous anion production such as from lactic acid)
c. Hyperketonemia
d. Electrolytes usually show hyponatremia and normal or elevated potassium.
e. Often have Elevated BUN and creatinine, reflecting dehydration.
f. WBCs are often elevated, esp if a bacterial infection is exacerbating the condition.
4. Tx of DKA?!?!?!?!
1. First: Vascular volume expansion (Often with Normal saline)!!!!!!!!
2. Then: Correction of hyperglycemia and hyperketonemia.
b. IV fluid boluses sufficient to stabilize the HR and BP are often required, and then a slower IV rate (usually a saline solution w/ or w/o glucose)
c. Potassium is added to IV fluids after Urine output is established!!!!
d. A continuous insulin infusion at a rate of 0.1 U/kg/h is also started ( a bolus of 0.1 U/kg is often given initially). IV rate adjusted based on results of hourly glucose measurements.
5. When is glucose added to IV fluids in tx of DKA?
a. When the serum glucose level drops to 250-300.
b. Additional insulin rate adjustments are made based on serum glucose levels.
6. Why is potassium added in tx of DKA?
a. To counteract the pt’s total body potassium depletion.
b. Insulin will drive it intracellularly. Hypokalemia is an avoidable complication.
7. When can you expect the low plasma pH and ↑ serum ketone level to correct in DKA?!?!?
a. These will correct significantly with treatment in the first 8-10 hours.
8. For how long will Serum bicarb will remain low after starting treatment for DKA?
a. ~24 hours or more
9. What is improvement in DKA characterized by?
a. A decrease in IV insulin rates and resolution of the ketonuria.
b. Then, the pt can take oral feedings, and insulin is converted from the IV to subq route.
10. Is bicarb indicated in tx of DKA?
a. It is avoided except in extreme situations….
11. Why is bicarb usually avoided in tx of DKA?
a. Because It may:
1. Precipitate hypokalemia
2. Shift the oxygen dissociation curve to the left, worsening organ oxygen delivery!
3. Overcorrect acidosis.
4. Result in worsening cerebral acidosis while the plasma pH is being corrected (transfer into the cerebrum of CO2 formed when the bicarb is infused in an acid serum.
i. Cerebral oedema sometimes occurs.
12. How does Cerebral oedema manifest?
a. HA
b. Personality changes
c. Vomiting
d. ↓’d reflexes.
13. Treatment of Cerebral Oedema?
a. Reduction in IV fluids
b. Administration of IV mannitol!
c. Hyperventilation
14. What can episodes of DKA be precipitated by (especially in the known diabetic)?
a. Bacterial infections!!!
b. An evaluation for infection sources w/institution of abx (if appropriate) is required.