Diabetic Ketoacidosis with Hypokalemia and a Surgical Distraction

1. Volume resuscitation. Give 1–1.5 L of isotonic crystalloid (0.9% saline or a balanced solution) in the first hour, then reassess. She is tachycardic and hypotensive with a creatinine double her baseline - this is profound volume depletion from osmotic diuresis plus vomiting. Restoring perfusion lowers glucose and improves insulin sensitivity.

2. Potassium repletion, started immediately in parallel. Her potassium is 3.1 mEq/L despite total-body potassium depletion, and it will fall further the moment insulin drives potassium intracellularly.

Why insulin waits:

• Insulin shifts potassium into cells. Giving insulin at a potassium of 3.1 can precipitate life-threatening hypokalemia - arrhythmia, respiratory muscle weakness, ileus. Standard practice is to hold insulin until potassium is at least 3.3 mEq/L, while giving 20–40 mEq/h of potassium with cardiac monitoring and frequent rechecks.
• This is the single most testable judgment in DKA: the potassium is the gate, not the glucose.

Once potassium is above 3.3, start the insulin infusion and continue repletion. Note her corrected sodium: 132 + 1.6 × ((342−100)/100) ≈ 136 - a value that would fall rather than rise with saline alone, which is a clue that free water loss is substantial.

Pump: disconnect it - a site unchanged for five days in a patient who is vomiting is the likely precipitant (occlusion, absorption failure, or infection). Treat with intravenous insulin.

Infusion:

• Regular insulin 0.1 units/kg/h (≈5.8 units/h) once potassium is above 3.3. A bolus is not required for most patients and is avoided in those already on subcutaneous insulin; it is reasonable in severe dehydration or shock.
• Target a glucose decline of roughly 50–75 mg/dL per hour. If glucose is not falling, first check that the infusion is actually running, then consider doubling the rate.

Dextrose:

• When glucose falls below about 200–250 mg/dL, add 5–10% dextrose and continue insulin. The insulin is needed to close the anion gap, so it must not be stopped when glucose normalizes - this is where DKA protocols go wrong.

Transition criteria (all of these):

• Anion gap ≤12 mEq/L (or closing), pH >7.3, bicarbonate ≥15–18 mEq/L, and the patient able to eat.
• Overlap: give subcutaneous basal insulin 1–2 hours before stopping the infusion, otherwise the patient rebounds. Restart home basal dosing plus correction; do not restart the pump until she is eating and stable.

To the surgeon: her abdominal pain is most likely part of the DKA - ketoacidosis causes gastroparesis, ileus, and mesenteric vasoconstriction, and pain typically resolves as the acidosis and dehydration correct. A leukocytosis is also expected. Taking an acidotic, hypotensive, hypokalemic patient to the operating room is a high-risk plan. Ask for a reassessment after 2–4 hours of fluid and insulin; if she develops localized right lower quadrant peritonitis, focal tenderness, or does not improve as the gap closes, then image (ultrasound or CT) and operate. Order imaging early if there is genuine diagnostic concern, but do not delay DKA treatment.

Pregnancy:

• DKA in pregnancy occurs at lower glucose levels and progresses faster; pregnancy itself is ketogenic. Treat the DKA aggressively - pregnancy is not a reason to under-resuscitate.
• Notify obstetrics, place her in a left lateral tilt position, and arrange fetal monitoring once she is stabilized.
• Exclude other precipitants (urinary tract infection, endometritis, hyperemesis) and check for infection given the low-grade fever.
• Confirm the pregnancy with a quantitative beta-hCG; long-term counseling about glycemic targets in pregnancy follows recovery.

Bicarbonate: do not give it at a pH of 7.14. Bicarbonate is considered only at pH below about 6.9, and even then its benefit is unproven; it risks hypokalemia, paradoxical CSF acidosis, and overshoot alkalosis.