What went wrong in the management of a patient with type 2 diabetes, postural orthostatic tachycardia syndrome (POTS), chronic fatigue syndrome, depression, fibromyalgia, irritable bowel syndrome (IBS), migraine, and gastroesophageal reflux disease (GERD), who developed diabetic ketoacidosis (DKA) after being treated for acute appendicitis and kept nil per os (NPO) for an extended period?

Critical Management Failures Leading to Euglycemic Diabetic Ketoacidosis (EDKA)

The primary failure was withholding the patient's diabetes medication (likely an SGLT2 inhibitor based on the EDKA presentation) combined with prolonged NPO status (~20 hours) without adequate dextrose-containing IV fluids and continuous insulin therapy, which allowed progressive ketoacidosis to develop despite relatively normal glucose levels. 1

Key Management Errors

1. Medication Withholding Without Appropriate Substitution

• The patient's diabetes medication was withheld on two consecutive days before surgery, which likely included an SGLT2 inhibitor (given the EDKA presentation with relatively preserved glucose levels but severe ketoacidosis). 1
• SGLT2 inhibitors must be discontinued 3-4 days before any planned surgery to prevent euglycemic DKA, not just 1-2 days before. 1
• No basal insulin was initiated when the oral diabetes medication was stopped, leaving the patient without any glucose-lowering or anti-ketogenic therapy during a period of physiologic stress (infection, surgery, NPO status). 2, 3

2. Prolonged NPO Status Without Proper Metabolic Support

• The patient was kept NPO for approximately 20 hours without dextrose-containing IV fluids or insulin therapy, despite having diabetes and developing progressive metabolic acidosis. 3
• The American Diabetes Association guidelines clearly state that patients with diabetes who remain NPO should continue intravenous insulin infusion and add dextrose-containing fluids when glucose falls to prevent both hypoglycemia and ongoing ketogenesis. 3
• The initial 1000 mL NS bolus was insufficient, and there was no transition to dextrose-containing fluids (5% dextrose with 0.45-0.75% saline) to provide substrate while preventing ketosis. 1

3. Failure to Recognize and Treat Early DKA

• Progressive metabolic acidosis was evident but ignored: bicarbonate dropped from 17 → 13 → 6 → 4, with rising anion gap from 15 → 15 → 21 → 23. 1
• The patient met criteria for DKA well before discharge (bicarbonate 6, AG 21, potassium 5.5), yet was discharged without treatment. 1
• No insulin therapy was initiated despite clear evidence of ketoacidosis, which is the cornerstone of DKA treatment. 2

4. Premature Discharge Despite Severe Metabolic Derangement

• Discharging a patient with bicarbonate of 6 and anion gap of 21 represents a catastrophic failure in recognizing life-threatening DKA. 1
• DKA resolution requires: glucose <200 mg/dL, serum bicarbonate ≥18 mEq/L, venous pH >7.3, and anion gap ≤12 mEq/L—none of which were met. 1, 4
• The patient was breathless with high pulse (Kussmaul respirations and compensatory tachycardia), which are classic signs of severe metabolic acidosis. 5

What Should Have Been Done

Preoperative Management

• SGLT2 inhibitors should have been discontinued 3-4 days before surgery, not 1-2 days. 1
• Basal insulin should have been started when oral diabetes medications were withheld, with dosing based on body weight (typically 0.3-0.4 units/kg/day for basal component). 2
• Blood glucose should have been monitored every 2-4 hours during the NPO period. 4

During NPO Period

• Continuous IV insulin infusion at 0.1 units/kg/hour should have been initiated once acidosis was detected (bicarbonate 13, AG 15). 2, 1
• Dextrose-containing fluids (5% dextrose with 0.45-0.75% saline) should have been started to provide glucose substrate while insulin prevents ketogenesis. 1, 3
• Target glucose should have been maintained between 150-200 mg/dL until metabolic parameters normalized. 3, 4

Electrolyte Management

• Potassium monitoring and replacement was critical, especially as the patient developed hyperkalemia (5.5) from acidosis, which would shift to severe hypokalemia with insulin therapy. 1
• Potassium should be added to IV fluids (20-30 mEq/L as 2/3 KCl and 1/3 KPO₄) once adequate urine output confirmed and levels <5.5 mEq/L. 1

Recognition of DKA

• Laboratory monitoring every 2-4 hours should have been performed to track bicarbonate, anion gap, pH, and ketones. 1, 4
• β-hydroxybutyrate measurement (6.51-6.77 mmol/L at readmission) is the preferred method for monitoring ketosis and should have been checked earlier. 1

Critical Pitfalls That Occurred

• Premature termination of metabolic support before resolution of ketosis is a common cause of DKA recurrence and was the fundamental error here. 6
• Failure to add dextrose when continuing NPO status allowed ongoing ketogenesis despite the surgical stress and infection. 1, 3
• Inadequate monitoring and replacement of electrolytes, particularly potassium, which is universally depleted in DKA despite initial normal or elevated levels. 1
• Stopping diabetes medications without insulin substitution during a period of physiologic stress (infection, surgery) guaranteed metabolic decompensation. 2

The EDKA Presentation

• SGLT2 inhibitors cause euglycemic DKA by promoting urinary glucose excretion while simultaneously increasing ketone production through enhanced lipolysis and reduced insulin secretion. 1
• The relatively preserved glucose levels (glucose 6.5 mmol/L = 117 mg/dL) with severe ketoacidosis (β-hydroxybutyrate 6.51-6.77 mmol/L, pH 6.99) is pathognomonic for SGLT2 inhibitor-associated EDKA. 1
• The combination of SGLT2 inhibitor use, surgical stress, infection, and prolonged fasting created a perfect storm for EDKA development. 1

Additional Contributing Factors

• The patient's POTS and chronic fatigue syndrome may have masked early symptoms of metabolic decompensation (tachycardia attributed to POTS rather than DKA). 2
• Infection (appendicitis) is the most common precipitating cause of DKA, occurring in 30-50% of cases, and should have prompted more aggressive metabolic monitoring. 7
• The elevated CRP (30.6) and clinical presentation confirmed significant infection, which increases insulin resistance and ketone production. 1