Euglycemic Diabetic Ketoacidosis: A Diagnostic Challenge in Clinical Practice

Euglycemic diabetic ketoacidosis: A diagnostic challenge in clinical practice

Merline Grace. S^1*, S. Princy², Rabakka³, Dr. Bharath Kumar⁴

¹Diabetic Nurse, Kauvery Hospital, Radial Road, Chennai, Tamil Nadu

²Staff Nurse, Kauvery Hospital, Radial Road, Chennai, Tamil Nadu

³Staff Nurse, Kauvery Hospital, Radial Road, Chennai, Tamil Nadu

⁴Senior Consultant, Cardiology, Kauvery Hospital, Radial Road, Chennai, Tamil Nadu

*Correspondence

Introduction

Euglycemic diabetic ketoacidosis (Eu-DKA or EDKA) represents a rare yet perilous metabolic crisis, defined by ketoacidosis and high anion gap metabolic acidosis occurring with blood glucose levels below 250 mg/dL. Unlike traditional diabetic ketoacidosis (DKA) which hinges on the classic triad of hyperglycaemia, acidosis, and ketosis EDKA evades detection due to near-normal glucose, often delaying critical intervention and risking severe dehydration, cerebral edema, shock, or coma.

Pathophysiology

Carbohydrate shortage cuts insulin, boosts glucagon/cortisol/catecholamines driving lipolysis, ketone production (acetoacetate, β-hydroxybutyrate, acetone), acidosis sans hyperglycaemia. SGLT2 inhibitors (SGLT2i) deplete glycogen, increase urinary glucose loss.

What are Triggers?

SGLT2i, fasting, pregnancy, alcohol, infection/sepsis, surgery, drugs.

Incidence: 2.6–3.2% DKA euglycemic; SGLT2i: 0.1%, Risk in T2DM.

Case Presentation

An 88-year-old woman with type 2 diabetes, hypertension, and coronary artery disease arrived with poor oral intake, profound weakness, oliguria, and sudden dyspnoea. Diagnostics confirmed EDKA: Anion gap 25 mmol/L, PH 7.10, bicarbonate 4.7 mmol/L, glucose 252 mg/dL, positive ketones compounded by acute kidney injury (AKI) and rapid atrial fibrillation. Her regimen included metformin, sitagliptin, telmisartan, bisoprolol, aspirin, calcium, and zinc; surgical past: L3-L5 laminectomy, hysterectomy, bilateral cataracts.

Clinical Findings

S.No	Book picture	Patient picture
1	General Symptoms • Nausea and persistent vomiting • Abdominal pain • Generalized weakness and fatigue • Anorexia or poor oral intake • Weight loss (acute or subacute)	• History of decreased oral intake for one week. • Progressive generalized weakness and fatigue for one week.
2	Respiratory Features • Kussmaul respiration (deep, rapid breathing) • Shortness of breath • Compensatory hyperventilation due to metabolic acidosis	• Kussmaul respiration noted for one day prior to presentation. • Acute onset shortness of breath for one day.
3	Neurological Features • Headache • Altered sensorium (restlessness, confusion) • Drowsiness or lethargy • In severe cases: reduced level of consciousness or coma.	• Drowsiness and lethargy for one day prior to presentation.
4	Signs of Dehydration • Dry mucous membranes • Reduced skin turgor • Tachycardia • Hypotension (especially in advanced cases) • Reduced urine output	• Dry mucous membranes on arrival. • Reduced skin turgor on admission. • Tachycardia with a heart rate of 121 Bpm • Hypotension with blood pressure of 90/60 mmHg. • Reduced urine output for one day prior to presentation.

Diagnostic Assessment

Laboratory Features
• Normal or mildly elevated blood glucose (<250 mg/dL) • High anion gap metabolic acidosis • Positive serum or urine ketones • Low serum bicarbonate • Low arterial or venous pH • Possible electrolyte disturbances (hyponatremia, hypokalemia)	• Capillary blood glucose: 252 mg/dL • Anion gap: 25 mmol/L (Arterial blood gas analysis) • Serum ketones: 0.45 mmol/L • Serum bicarbonate: 4.7 mmol/L • Arterial pH: 7.10 • Serum sodium: 129 mmol/L (hyponatremia) • Serum potassium: 5.5 mmol/L (hyperkalemia)

ECG: Atrial fibrillation with rapid ventricular response.

Echo: Mild LV systolic dysfunction (EF ~43%), severe tricuspid regurgitation, severe pulmonary hypertension, dilated non-collapsing IVC.

Diagnosis: Eu-DKA with high anion gap acidosis, complicated by AKI and rapid AF.

Management

S.no	Book picture	Patient picture
1	Initial Assessment • Assess airway, breathing, circulation (ABCs) • Monitor vital signs • Establish two large-bore IV lines • Cardiac monitoring • Strict input–output charting	• Airway, breathing, and circulation (ABCs) were assessed on arrival. • Oxygen saturation was 90% on room air in the emergency department. • Supplemental oxygen was initiated at 2 L/min via nasal prongs, followed by non-invasive ventilation due to persistent respiratory distress. • Continuous vital sign monitoring was established. • The patient was placed on cardiac monitoring. • Strict intake and output charting was maintained.
2	Fluid Resuscitation First-line therapy • Start with 0.9% Normal Saline 15–20 mL/kg (≈1–1.5 L) in the first hour • Continue isotonic fluids based on hemodynamic status and corrected sodium - Fluid therapy corrects dehydration, improves renal perfusion, and reduces counter-regulatory hormones.	• 1.5 L bolus of 0.9% normal saline was administered. • Maintenance intravenous fluids (Kabilyte) were initiated at 100 mL/hour. • Noradrenaline infusion was commenced at 5 mL/hour for hemodynamic support. • Amiodarone infusion was initiated with a loading dose of 600 mg, followed by maintenance at 60 mg/hour for rate control of atrial fibrillation. • Intravenous fluids were subsequently continued at 50 mL/hour based on hemodynamic status.
3	Insulin Therapy Even though glucose is normal, insulin is essential to stop ketogenesis. • Start IV regular insulin infusion units/kg/hour (Bolus may or may not be given depending on protocol) • Do not delay insulin because glucose is normal.	• Intravenous regular insulin (Actrapid) 12 units was administered as a stat dose, followed by a continuous infusion at 4 units/hour. • The patient subsequently developed severe hypoglycemia following initiation of insulin therapy.
4	Early Dextrose Administration (Key Difference in EDKA) Since glucose is <250 mg/dL • Start 5% dextrose with 0.45% saline (D5/½NS) when glucose <250 mg/dL • Increase to 10% dextrose (D10) if needed to maintain glucose 140–200 mg/dL • This allows continuation of insulin infusion to clear ketones while preventing hypoglycaemia.	• Capillary blood glucose was 258 mg/dL at the time of initiating 5% dextrose infusion at 50 mL/hour started prophylactically • But subsequently, there is a drop in blood glucose to 55 mg/dL, indicating severe hypoglycaemia. • A bolus of 25% dextrose was administered for correction of hypoglycaemia. • The insulin infusion was temporarily discontinued, and 25% dextrose infusion was started at 20 mL/hour.
5	Potassium Management Before insulin initiation • If K⁺ <3.3 mEq/L → Correct potassium first (hold insulin) • If K⁺ 3.3–5.3 → Add 20–30 mEq K⁺ per liter of IV fluid • If K⁺ >5.3 → Monitor closely (no immediate supplementation) Insulin drives potassium intracellularly and may cause hypokalaemia.	• Prior to initiation of insulin infusion, hyperkalemia was addressed. • Arterial blood gas potassium was 5.5 mmol/L, and serum potassium was 5.8 mmol/L. • Hyperkalemia was managed with nebulized salbutamol (Asthalin) 5 mg and intravenous regular insulin 10 units administered with 25% dextrose (100 mL).
6	Bicarbonate Therapy Not routinely recommended. Consider only if pH <6.9	In view of severe metabolic acidosis, intravenous sodium bicarbonate (50 mEq) was initiated at an infusion rate of 50 mL/hour, with close monitoring of arterial blood gases and electrolyte levels.
7	Monitoring • Capillary blood glucose: hourly • Serum electrolytes as per doctor’s order • Anion gap as per doctor’s order • Serum ketones as per doctor’s order • ABG/VBG as per doctor’s order • Urine output-Hourly	• Capillary blood glucose was monitored hourly until normalization of the anion gap. • Serum electrolytes were assessed every 12 hours. • Anion gap was evaluated every 12 hours. • Serum ketone levels were monitored as per physician orders. • Arterial or venous blood gas analysis was performed as clinically indicated. • Urine output was monitored hourly.
8	Identify & Treat Precipitating Causes • Infection → antibiotics • Starvation → nutritional support • Insulin omission → education • Medication-related cause → discontinue offending drug.	• In view of suspected septic shock, empirical broad-spectrum antimicrobial therapy was initiated. • Intravenous meropenem 2 g was administered as a stat dose, followed by 1 g twice daily. • Intravenous teicoplanin 800 mg was given as a loading dose, followed by 400 mg every 12 hours for two additional doses.

Treatment and Progress

Care involved halting triggers, 1-1.5L saline boluses, IV insulin infusion (0.1 units/kg/h) paired with dextrose to avert hypoglycaemia, electrolyte tweaks, vasopressors, antibiotics for sepsis, and continuous renal replacement therapy (CRRT). Monitoring encompassed hourly glucose/ketones, anion gap, and outputs. In CCU, acidosis resolved, anion gap normalized, potassium stabilized, renal function rebounded post – CRRT, hemodynamic steadied, and oxygen needs dropped. By day 3, inflammation/lactate improved; vasopressors tapered. Discharge: afebrile, stable, semi-ambulatory, tolerating intake, off support prescribed diabetic/low salt/fat diet (<1.5L fluids/day), light activity, cardiology/nephrology follow-up.

Insights and Role of Nursing

This elderly case underscores diagnostic pitfalls from mild hyperglycaemia (~250 mg/dL), with contributors like starvation, sepsis, AKI, and cardiac issues. Hypoglycemia post-insulin highlighted dextrose necessity; CRRT addressed clearance woes. Multidisciplinary input (critical care, nephrology, ID, cardiology) optimized results, balancing insulin, electrolytes, and cardiorenal dynamics. Nurses excelled via hemodynamic/glucose surveillance, I/O charting, hypoglycaemias response, arrhythmia watches (e.g., amiodarone), NIV/CRRT/vasopressor oversight, and discharge teaching averting neuro harm and tracking recovery.

Key Learnings

EDKA demands suspicion for unexplained acidosis, prompt ABG/ketone checks regardless of glucose, precise insulin-dextrose dosing, hemodynamic aggression, and team/nursing vigilance. Early action fosters recovery in high-risk elders.

Reference

Kitabchi, A. E., Umpierrez, G. E., Miles, J. M., & Fisher, J. N. (2009). Hyperglycemic crises in adult patients with diabetes. Diabetes Care, 32(7), 1335–1343. https://doi.org/10.2337/dc09-9032.
Munro, J. F., Campbell, I. W., McCuish, A. C., & Duncan, L. J. P. (1973). Euglycaemic diabetic ketoacidosis. The American Journal of Medicine, 54(5), 573–577.
Barski, L., Eshkoli, T., Brandstaetter, E., & Jotkowitz, A. (2019). Euglycemic diabetic ketoacidosis. Clinical Endocrinology, 90(1), 1–9. https://doi.org/10.1111/cen.13851 .
Umpierrez, G. E., & Korytkowski, M. (2016). Diabetic emergencies—ketosis, ketoacidosis and hyperosmolar state. New England Journal of Medicine, 375(18), 1785–1786.
Peters, A. L., Buschur, E. O., Buse, J. B., Cohan, P., Diner, J. C., & Hirsch, I. B. (2015). Euglycemic diabetic ketoacidosis: A potential complication of treatment with sodium–glucose cotransporter 2 inhibition. Diabetes Spectrum, 28(3), 190–193. https://doi.org/10.2337/diaspect. 28.3.190.

Euglycemic Diabetic Ketoacidosis: A Diagnostic Challenge in Clinical Practice

Euglycemic diabetic ketoacidosis: A diagnostic challenge in clinical practice

Merline Grace. S1*, S. Princy2, Rabakka3, Dr. Bharath Kumar4

Nightingale Journals

Merline Grace. S^1*, S. Princy², Rabakka³, Dr. Bharath Kumar⁴