DKA
  • DKA
  • Sodium
    • variable, but total body sodium deficit is the rule.  Serum sodium may be transiently low as the osmotic activity of glucose draws water into the extracellular space and dilute the sodium.
    • Corrected [Na]= [Na] + 1.6* (glucose – 100)/ 100
  • Ketones and Ketoacids:
    • Acetoacetate and B-hydroxybutyrate are the primary cause of the anion-gap acidosis.
    • Nitroprusside test for ketone detection in serum/urine measures acetone and acetoacetate but not B-hydroxybutyrate.
    • Serum/urine ketones should be used to confirm the diagnosis but not to monitor therapy.  Instead, the anion gap should be followed as it will be equivalently elevated for either ketoacid. Close it, and keep it closed!
  • Bicarbonate:
    • Low due to acidosis
  • BUN/ Cr:
    • Elevation due to dehydration
  • Potassium:
    • Shifts from acidosis, so it may look falsely elevated
    • Overall total body depletion
  •  Treatment
    • Mnemonic: DKA: treat the D-glucose, K replacement, and A lot of Fluids
    • IVF:  The key here is to Bolus, Bolus, Bolus
      • Average fluid loss is 3-6L
      • Change to D5 ½ NS when glucose <250
    • Insulin gtt: Bolus 0.1u/kg then 0.1u/kg/hr or alternative therapy: 0.14u/kg/hr
    • K: replace once <5.3 (K will shift back into cells)
      • Oral or add to IV fluids
      • If adding 40meq to IV fluids do ½ NS
  • Monitoring
    • Glucose: q2-4 hrs
    • BMP: q2-4 hrs
    • ABG: monitor anion gap and HCO3
  • Goals of therapy
    • GAP B gone.
    • Glucose approx 200
    • AG < 12
    • pH>7.3
    • Bicarb > 18
    • Transition to SQ insulin when eating and leave gtt on for an hour after SQ dose given
  • Complications
    • Cerebral edema- estimated to occur in 1% of children  with DKA with a mortality of 60-80%.  Subclinical brain swelling also documented in adults but clinically significant cerebral edema is rare.
    • Thrombosis- caused by increased viscosity and dehydration (reported mesenteric, iliac and cerebral thromboses).