DKA

Diabetes AND significantly elevated serum beta-hydroxybutyrate level (>3 mM/L) and/or anion gap is >>12 mEq/L AND positive urinary ketones

• Can have a normal glucose = euglycemic DKA

  • Think about euglycemic DKA (and order serum ketones and/or β-hydroxybutyrate) in the following patients who present with nausea, vomiting, shortness of breath and/or metabolic acidosis:

    • T1/T2DM Patients taking SGLT-2 inhibitors (the “zins”) 

    • Pregnant patients – due to transplacental glucose transport, will have relative euglycemia (more common in second or third trimester) 

    • Chronic pancreatitis 

    • Bariatric surgery patients – due to absorption issues 

  • Management: Start fluids with dextrose sooner in the treatment process.

• Can have a normal pH and a normal bicarbonate = ketoacidosis and metabolic alkalosis from vomiting

1. Identify the trigger (noncompliance, infection, pancreatitis, pregnancy, trauma, surgery, alcohol/substance abuse, meds)

2. Fluids 

• Usually profoundly volume depleted (e.g. due to vomiting, reduced PO intake, and osmotic diuresis) 

• Most patients will require ~2-4 liters of crystalloid up front (u/s guided resus) 

  • Balanced crystalloid is preferred here (e.g. LR or plasmalyte)

  • NS induces a hyperchloremic acidosis which drops bicarbonate levels in the initial phase of DKA resuscitation, and is probably not the ideal fluid to use

• After bolus > maintenance fluids

  • If the patient's glucose is >300 mg/dL (>16.6 mM), LR at ~200 ml/hr

• After glucose < 300, need to add glucose to fluids

  • One way to do this: 100 ml/hr LR plus 100 ml/hr D10W = D5 1/2 LR

  • If you want to give additional dextrose you can up-tirate the D10W infusion (without giving the patient more sodium and causing volume overload)

• CHF and HD pts: Avoid aggressive volume administration 

3. Potassium 

• IV Calcium and an immediate 10 unit IV insulin bolus for critical hyperkalemia

• Hypokalemia = Hypomagnesemia, cannot replete intracellular potassium without magnesium

  • Serum magnesium level may not correlate with total body stores

• HD pts: Avoid aggressive potassium administration

4. IV Insulin

• Insulin bolus (10 units IV) not in the setting of critical hyperkalemia

  • Unnecessary and potentially harmful 

  • No difference in change in serum glucose, closure of anion gap 

  • Associated with increased hospital length of stay and hypoglycemic episodes

• 0.1 U/kg/hour (up to a max of 15 units/hour in morbid obesity)

• For patients with severe acidosis (e.g. bicarbonate <5 mEq/L) or marked insulin resistance (with high chronic insulin requirements), higher doses will often be needed (e.g. 0.2-0.3 U/kg/hr)

• Glucose checks q1hr, electrolyte checks q2-4

• Once the glucose falls to ~250 mg/dL (14 mM) the insulin infusion rate is typically reduced

• Stop drip when anion gap < 10-12 mEq/L and bicarbonate > 18-20 mEq/L. Then start ~0.08 U/kg rapid-acting insulin per meal. 

  • Note: The anion gap will never normalize in HD pts. DKA resolution in HD pts may correlate with a beta-hydroxybutyrate level which is below ~1 mM

5. SQ Insulin

• Early initiation of long-acting insulin facilitates transitioning off the insulin infusion, reduces the incidence of hyperglycemia, and might decrease hospital length of stay

• Give a full daily/home dose of long-acting insulin immediately upon admission to the hospital. For a patient naive to insulin, a starting dose of 0.25 units/kg daily of glargine (Lantus) may be given.

  • No longer need to extend the infusion in order to overlap with the subcutaneous insulin

  • Reduces rebound hyperglycemia when the insulin infusion is stopped.

• Isotonic Bicarb?

  • Avoid (unless treating hyperchloremic, non-anion-gap acidosis towards the end of resus)

  • Treat acidosis by c/w insulin, consider starting at 0.2 U/kg/hr for the severely acidotic

• Intubation?

  • AVOID b/c their hyperpnea to correct their underlying metabolic acidosis means the ventilator must equally match their large tidal volume and respiratory rate >> this puts the patient at risk for ventilator induced lung injury and subsequent development of ARDS

  • At risk of circulatory collapse peri-intubation as periods of apnea during intubation will cause their pCO2 levels to rise rapidly, worsening the acidosis

  • BiPAP should also be avoided, because DKA patients often have gastroparesis causing emesis into the mask.

  • HFNC to support the patient's breathing and/or for severe acidosis (bicarb <5)

    • FiO2 titrated to achieve a saturation >92% 

    • Increase the flow rate as high as the patient can tolerate (e.g. 60 liters/minute) to reduce dead space and help pt blow off CO2.