›Increase the dextrose infusion rate, not decrease insulin, as the first response to a falling glucose above the hypoglycemic range
›Reserve insulin-rate reduction (to 0.05 units/kg/hr) for glucose trending toward hypoglycemia despite maximal reasonable peripheral dextrose
›Deceleration and escalation steps
›If glucose <8.3 mmol/l despite D10W at 150 mL/hr, increase the dextrose concentration or add a second dextrose-containing line
›If glucose <3.9 mmol/l, treat as hypoglycemia per usual protocol (dextrose 50% 25 mL IV push) while continuing, not stopping, the insulin infusion
›Reassess the insulin rate immediately after treating hypoglycemia rather than allowing the infusion to run unmonitored
›Bolus-omission caveat
›Do not give an initial insulin bolus in euglycemic DKA
›A bolus in a patient with a normal starting glucose meaningfully raises early hypoglycemia risk
›Start directly with the continuous infusion
›IV regular insulin infusion
›Adults: 0.1 units/kg/hr IV, no bolus, started concurrently with dextrose-containing fluid
›Continue at this rate as tolerated by glucose; do not down-titrate for a normal glucose alone
›Reduce to 0.05 units/kg/hr only if hypoglycemia persists despite maximal dextrose support
›Monitoring cadence during infusion
›Point-of-care glucose every 1 hour
›Venous blood gas and electrolytes every 2 to 4 hours
›Beta-hydroxybutyrate every 2 to 4 hours if available, in preference to relying on the glucose trend
›Subcutaneous insulin for mild, uncomplicated cases
›Rapid-acting insulin lispro or aspart 0.3 units/kg subcutaneous bolus, then 0.1 units/kg subcutaneous every 1 hour
›Appropriate only if tolerating oral intake and mild acidosis (pH 7.25 to 7.30)
›Continue oral or IV dextrose-containing intake alongside dosing given the absence of hyperglycemia to buffer against
›Subcutaneous basal insulin and transition
›Subcutaneous glargine started early in treatment
›Continue the home dose, or initiate 0.3 units/kg/day if insulin-naive, divided per standard basal dosing
›Overlap with IV insulin by 2 to 4 hours before stopping the infusion, to prevent rebound ketoacidosis
›Resumption of the prior insulin regimen
›Reassess whether the pre-admission insulin dose was reduced in anticipation of the SGLT2 inhibitor's glucose-lowering effect
›Restore an adequate basal insulin dose before, or independent of, any decision to resume the SGLT2 inhibitor
›Initial fluid strategy
›Adults: 1 L 0.9% NaCl IV in the first hour if evidence of hypovolemia
›Volume deficit is typically smaller than in hyperglycemic DKA; reassess frequently rather than using a fixed large-volume protocol
›Subsequent rate 250 to 500 mL/hr guided by volume status
›Transition to dextrose-containing fluid
›Move to a dextrose-containing maintenance fluid promptly given the absence of a hyperglycemic buffer
›Switch the component fluid to 0.45% NaCl with dextrose if corrected sodium is normal or high
›Fluid choice rationale
›Large-volume normal saline risk of hyperchloremic non-anion-gap acidosis
›Can mimic non-resolving ketoacidosis on a repeat blood gas
›Balanced crystalloid may reduce this confound where available
›Avoid hypotonic fluid boluses
›Rapid osmolality shifts, particularly relevant in pediatric patients
Potassium and electrolyte replacement
›Potassium protocol
›K+ <3.3 mmol/l
›Hold insulin
›IV KCl 20 to 30 mmol/hr until K+ >3.3 mmol/l
›K+ 3.3 to 5.3 mmol/l
›Add 20 to 30 mmol K+ per litre of IV fluid with insulin
›Monitor every 2 hours
›K+ >5.3 mmol/l
›Hold potassium replacement
›Recheck every 2 hours with ECG monitoring for hyperkalemia features
›Renal impairment or dialysis-dependent patients
›Replace more cautiously and at lower rates given reduced excretory capacity
›Coordinate with nephrology before standard-rate replacement
›Phosphate and magnesium
›Phosphate replacement not routine
›Consider if phosphate <0.32 mmol/l with symptoms (muscle weakness, respiratory depression)
›Potassium phosphate IV preferred when replacement is indicated
›Magnesium replacement if severely depleted
›Magnesium sulfate 2 g IV over 1 hour for symptomatic severe hypomagnesemia
›Generally not recommended
›Does not improve outcomes in DKA of any glucose profile
›May paradoxically worsen intracellular and CSF acidosis
›Consider only for pH <6.9 to 7.0 with hemodynamic compromise, or severe hyperkalemia
›Sodium bicarbonate 50 mmol (as an 8.4% solution, 50 mL) IV over 2 hours
›Recheck pH after the infusion before repeating; do not give a second dose reflexively
Troubleshooting non-resolving ketoacidosis
›"Therapy is not working" checklist
›Confirm actual insulin delivery
›IV line patency, correct pump rate, and that dextrose is not diluting the effective insulin dose through a shared restricted line
›Reassess the precipitant
›Undiagnosed infection or surgical complication continuing to drive counter-regulatory hormone excess
›Ongoing SGLT2 inhibitor pharmacodynamic effect if the last dose was recent
›Reassess the insulin dose itself
›Persistent reflex down-titration for a normal glucose is the most common preventable cause of non-resolution in this syndrome
›Re-confirm the order specifies titration by beta-hydroxybutyrate and anion gap trend, not by glucose alone
›Consider an alternative or additional diagnosis
›Alcoholic ketoacidosis, toxic alcohol ingestion, or lactic acidosis if the anion gap persists despite adequate insulin and dextrose
›Recheck lactate and osmolar gap if the picture does not fit euglycemic DKA alone
›Definition of failure to progress
›Anion gap not trending toward closure after 4 to 6 hours of appropriately dosed, uninterrupted therapy
›Escalate to endocrinology and consider ICU-level monitoring
›Do not simply extend the same regimen unchanged without this reassessment