- HHS is defined by hyperglycemia and hyperosmolarity due to volume depletion with resultant altered mental status
- Profound hypokalemia is common as a result of osmotic diuresis. Replete aggressively
- Hypokalemia = hypomagnesemia. Replete both of these electrolytes simultaneously
- Fluid repletion is the key point in management but careful repletion is vital as patients may not tolerate aggressive administration
- All patients should have an exhaustive investigation of the cause of their decompensation. Look for signs of infection, ischemia, trauma etc.
- Guidelines recommend checking an ABG or VBG in all patients with DKA. This practice is not evidence-based and should be abandoned.
- ABG or VBG provides little information about whether or not the patient has DKA (beyond what is already known from the serum chemistries).
- Rather than pH, serum bicarbonate may be used to gauge the severity of acidosis.
- There is no evidence that detecting or reacting to a very low pH is helpful.
- Decisions about the level of ventilatory support that a patient needs can almost always be made on a clinical basis. When in doubt, close attention to the patient with serial examination is often a sound approach. Focus on the patient, not the blood gas.
- VBG might be helpful in cases where it is unclear whether the patient requires intubation, or if there is a significant underlying respiratory disease (e.g. COPD or obesity hypoventilation syndrome).
Myth #1: We should get ABGs instead of VBGs in DKA…Busted: VBG can be used in place of ABGs
Myth #2: After Intravenous Fluids (IVF), Insulin is the Next Step…Busted: After starting IVF, the next step in DKA management is electrolyte replacement, NOT Insulin.
Myth #3: Once pH <7.1, Patients Need Bicarbonate Therapy…Busted: Intravenous bicarbonate therapy may transiently make acidemia better, but there is no improvement of glycemic control, time on insulin, time to hospital discharge, and in kids can worsen cerebral oedema.
Myth #4: We Should Bolus Insulin Before Starting the Infusion…Busted: Insulin boluses increase hypoglycemic events without other clinical benefits in the treatment of DKA.
Sodium bicarbonate therapy in DKA (or any other acidosis for that matter) is associated with risks that outweigh NO BENEFITS…DO NO HARM!!!
- Neither a recent systematic review nor the largest single retrospective cohort of severe DKA support routine use of bicarbonate therapy in DKA
- Bicarbonate is associated with risk of cerebral oedema and prolonged hospitalisation in paediatric DKA
- A VBG is adequate for the diagnosis and ongoing management of patients with DKA. ABGs offer no added benefit and are associated with increased pain and complications.
- Patients with DKA may present with a weak or absent nitroprusside assay reaction on urinalysis for ketones as this test only checks for acetoacetate (the minor ketone body produced in DKA). Serum beta-hydroxybutyrate testing may be helpful in certain cases in making the diagnosis.
- There is no established role for administration of sodium bicarbonate to patients with DKA regardless of their pH. Sodium bicarbonate administration is associated with more complications including hypokalemia and cerebral edema.
- Insulin should not be started in patients with DKA until the serum potassium level is confirmed to be > 3.5 mEq/L. The use of an insulin bolus prior to infusion has not been shown to improve any patient centered outcomes or surrogate markers and is associated with an increased rate of hypoglycemic episodes.