Lyceum Bullets: DKA

Featured on #FOAMED REVIEW 2ND EDITION – Thank you to Michael Macias from emCurious for the shout out!

By Adaira Landry, MD and Manpreet Singh, MD
emDocs Editorial Staff

Edited by Alex Koyfman, MD

Adapted, with permission, from EM Lyceum.

1. When you are suspicious for DKA do you obtain a VBG or an ABG? How good is a VBG for determining acid/base status?

Five Findings of DKA

  • Acidosis (pH <7.30)
  • Serum Bicarbonate
  • Anion gap >10 mEq/L
  • Presence of ketonuria / ketonemia
  • Glucose > 250mg/dL

ABG VS. VBG in Acidosis Measurement

  • ABG
    • Time-consuming, and not pain-free (may require multiple sticks).
    • Complications can result, such as radial artery aneurysm, radial nerve injury, and compromised blood flow due to PVD or inadequate ulnar circulation (negative Allen’s test).
  • VBG
    • Less painful and time-consuming (can be obtained on initial IV placement).
  • Mean difference in pH compared to ABG can be between 0.03-0.06
    • Not clinically significant enough to alter treatment decisions.

Bottom Bullet

VBG is adequate enough to determine a patient’s pH and HCO3- level.

2. Do you use serum or urine ketones to guide your diagnosis and treatment of DKA?

Urine Testing

  • More rapid and used frequently, but misleading.
    • Via nitroprusside assay, checks ONLY for acetoacetate (minor ketone produced in DKA), which is converted into β-hydroxybutyrate as DKA is treated.
      • Patients with DKA may have urine with more β-hydroxybutyrate than acetoacetate.
        • Can give false reassurance if initially negative.
      • As you treat patient for DKA, the urine will have more ketones, this can make the UA more positive for ketones.
        • Can give false impression that patient worsening.

Serum Testing

  • Detects β-Hydroxybutyrate (predominant ketone), but unavailable test in many hospital systems.
    • Not proven to be superior in clinical evaluation nor during treatment evaluation.

Bottom Bullet

Obtain UA and if (+) urine ketones, serum testing not needed. If (-) urine ketones and diagnosis unclear, consider serum testing.

3. Do you use IV bicarbonate administration for the treatment of severe acidosis in DKA? If so, when?


  • Not shown to decrease time to resolution of acidosis, time to discharge, glucose concentrations, or ketone levels.
  • No existing studies included patients with a pH < 6.9, making it hard to know what to do with the sickest patients


  • Associated with delayed improvement in ketosis, worsening hypokalemia, worsening intracellular/CNS acidosis, or cerebral edema (in pediatric patients).

Bottom Bullet

IV Bicarbonate still recommended by the American Diabetes Association (ADA), but there is emerging evidence against its use.

4. When do you start an insulin infusion in patients with hypokalemia? Do you give a bolus followed by a drip?


  • Reverses the mobilization of free fatty acids, and production of ketoacids and glucose.
  • Can worsen hypokalemia by driving potassium from serum into cells.
    • Start insulin after K+ > 3.3mEq/L.
    • Add 20-30mEq KCL to fluids if level < 5.5mEq/L.


  • Initial Thoughts:
    • Bolus initially believed to rapidly activate insulin receptors to resolve hyperglycemia, ketosis, and acidosis.
  • Recent Thoughts:
    • Can pose greater risk of hypoglycemic events.
    • No clear benefit.

Bottom Bullet

Check your potassium before giving insulin to DKA patients. No clear role for insulin bolus as it can lead to hypoglycemia.

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