Hyperglycaemia and volume depletion in a patient on multiple diabetic agents
A 58-year-old woman with type 2 diabetes (HbA1c 9.8%), hypertension, and stage 3b CKD (eGFR 38 mL/min/1.73 m²) is admitted with 3 days of vomiting, polyuria, and confusion. Medications: metformin 1 g twice daily, gliclazide 80 mg twice daily, empagliflozin 25 mg daily, ramipril 10 mg daily, and furosemide 40 mg daily. On examination she is drowsy but arousable, BP 96/58 mmHg, HR 118/min, temperature 37.8°C, dry mucous membranes, and capillary refill 4 seconds. Labs: glucose 28 mmol/L, sodium 131 mmol/L, potassium 5.6 mmol/L, bicarbonate 9 mmol/L, chloride 98 mmol/L, urea 22 mmol/L, creatinine 210 µmol/L (baseline 140), pH 7.18, pCO2 22 mmHg, anion gap 28 mmol/L, ketones 3+ in serum, lactate 2.1 mmol/L.
1. What is the acid-base and metabolic diagnosis, and which medications must be stopped immediately?
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Diagnosis: High anion gap metabolic acidosis with respiratory compensation - the pH 7.18, pCO2 22, and anion gap 28 are consistent with a primary metabolic acidosis. The differential for a raised anion gap includes ketoacidosis, lactic acidosis, renal failure, and toxins. Here, serum ketones 3+ with glucose 28 mmol/L establish diabetic ketoacidosis (DKA), and the markedly raised urea/creatinine with a low bicarbonate also suggests a component of acute kidney injury on CKD, which contributes to the gap.
I would calculate the corrected sodium (add 2.4 mmol/L per 5.5 mmol/L glucose above 5.5) - the measured 131 is likely pseudo-hyponatraemia from hyperglycaemia; the corrected value is closer to 141, which matters for fluid tonicity decisions.
Medications to stop now:
- Metformin - risk of metformin-associated lactic acidosis with AKI (lactate 2.1 is not dramatically high, but renal function is impaired).
- Empagliflozin - SGLT2 inhibitors can cause euglycaemic DKA and worsen volume depletion; stop immediately.
- Gliclazide - sulfonylurea with renal impairment risks prolonged hypoglycaemia once insulin is started; hold.
- Ramipril - ACE inhibitor worsens AKI and hyperkalaemia in volume depletion; hold.
- Furosemide - she is volume-depleted; stop.
I would not stop insulin (she needs it), and I would treat the precipitant (infection screen - temperature 37.8°C, consider urine, chest, and skin sources).
2. Outline your fluid, electrolyte, and insulin plan for the first 6 hours, and state two monitoring parameters that would prompt escalation.
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Fluids: She is clinically volume-depleted with BP 96/58 and tachycardia. I would give 0.9% sodium chloride 1 L over the first hour (or 10–15 mL/kg/h), reassessing BP, urine output, and JVP after each bolus. Avoid hypotonic fluids initially given the corrected sodium and risk of cerebral oedema; avoid bicarbonate unless pH <6.9.
Potassium: K 5.6 mmol/L with AKI - do not give potassium-containing fluids. Once insulin is started, potassium will fall; recheck hourly and replace when <5.0 mmol/L. If K remains >6.0 or ECG changes appear, treat with calcium gluconate, insulin-dextrose, and salbutamol, and consider dialysis if refractory in the setting of AKI.
Insulin: Start a fixed-rate IV insulin infusion (0.1 units/kg/h) after the first fluid bolus. Do not give a bolus if there is concern about potassium or volume. Target a glucose fall of 3–5 mmol/L/h; when glucose <12–14 mmol/L, add 10% dextrose and continue insulin until ketones clear and the anion gap closes (this is the key endpoint - not glucose normalisation).
Monitoring / escalation triggers:
- Potassium - hourly initially; escalate if >6.5 mmol/L or ECG changes, or if it falls rapidly (<3.5).
- Anion gap / ketones and pH - repeat 2-hourly; failure to close the gap or worsening acidosis after 6 hours suggests inadequate insulin, ongoing sepsis, or need for renal replacement therapy.
- Also watch urine output and creatinine - oliguria with rising creatinine in AKI warrants nephrology input and consideration of dialysis.
I would also look for the precipitant (infection, myocardial infarction, pancreatitis) and involve critical care if she remains hypotensive or becomes acidotic despite treatment.