Vomiting, drowsiness and a glucose of 812 mg/dL in a non-adherent type 2 diabetic
A 46-year-old man with type 2 diabetes on metformin and glargine has not taken his medication for two weeks. He is brought in after three days of vomiting and diffuse abdominal pain. He is drowsy but rousable. HR 118, BP 104/66, RR 28 and deep, T 37.9 °C, weight 82 kg. The capillary glucose meter reads HI; laboratory glucose is 812 mg/dL (45 mmol/L). Sodium 129, potassium 4.9, chloride 96, bicarbonate 9 mmol/L, urea 68 mg/dL, creatinine 1.9 mg/dL (baseline 0.8). Arterial pH 7.14, pCO2 20 mmHg, serum beta-hydroxybutyrate 6.8 mmol/L, measured osmolality 330 mOsm/kg. Urine output is 20 mL/h and urine ketones are 3+. Two large-bore lines are in place, but no fluid and no insulin have been given yet. The night resident writes "hyperosmolar hyperglycaemic state" in the notes and plans a 10-unit insulin bolus followed by a sliding-scale regimen.
1. Characterise the metabolic disorder using the numbers, and explain why the label the resident chose changes management.
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Acid–base first.
- Anion gap = 129 − (96 + 9) = 24 (high-anion-gap metabolic acidosis).
- Delta ratio = (24 − 12)/(24 − 9) = 0.8 → a single high-AG acidosis, with no important concurrent metabolic alkalosis or normal-AG acidosis.
- Winter formula: expected pCO2 = 1.5 × 9 + 8 = 21.5 ± 2; measured 20 → respiratory compensation is appropriate, so there is no additional respiratory disorder.
- Beta-hydroxybutyrate 6.8 mmol/L with pH 7.14 and bicarbonate 9 defines diabetic ketoacidosis.
Now the sodium trap. Measured Na 129 looks like hyponatraemia, but glucose drags water out of cells. Corrected Na = 129 + 1.6 × (812 − 100)/100 = 129 + 11.4 ≈ 140 mmol/L. The true sodium is normal; treating the 129 as real hyponatraemia would lead to fluid restriction and worsens the picture.
Osmolality. Calculated total osmolality = 2 × 129 + 812/18 + 68/2.8 ≈ 258 + 45 + 24 = 327 mOsm/kg, against a measured 330 → osmolar gap only ~3, so no toxic alcohol or other osmole is involved.
Conclusion. This is ketoacidosis-predominant diabetic ketoacidosis with hyperosmolar features (effective osmolality >320 with corrected sodium). It is managed on the DKA pathway, not with a bolus-and-sliding-scale regimen: an unopposed insulin bolus before volume repletion drops the blood pressure and drives potassium intracellularly, and sliding scale does not clear ketones.
2. Write the first six hours of management with explicit numbers, and state two findings that would make you withhold or delay the insulin infusion.
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Fluids. 0.9% sodium chloride 1–1.5 L (15–20 mL/kg) in the first hour, then reassess blood pressure, urine output and sodium. Estimated deficit is 6–9 L; replace over 24–48 h, with the rate falling as the glucose falls. Switch to a dextrose-containing solution when glucose is under 250 mg/dL.
Potassium. K is 4.9 but total-body potassium is always depleted. Start 20–40 mmol/L of potassium in the fluid once K is below 5.2 and urine output is established, and keep K between 4 and 5 mmol/L with 2-hourly checks.
Insulin. 0.1 units/kg/h = 8 units/h by infusion pump; a bolus is optional if volume resuscitation has been adequate. Target a glucose fall of 50–75 mg/dL/h. When glucose falls below 250 mg/dL, add 5–10% dextrose and continue insulin at 0.05–0.1 units/kg/h until the anion gap closes (≤12) and ketones clear - stopping insulin at that point causes rebound ketosis.
What must not be done. No bicarbonate at pH 7.14: it worsens hypokalaemia, causes paradoxical CSF acidosis, and shifts the oxygen dissociation curve. Reserve it for pH <6.9.
Hold or delay insulin if:
- Potassium <3.3 mmol/L - replace first, because insulin will precipitate arrhythmia and respiratory muscle weakness.
- Systolic BP <90 mmHg after fluid resuscitation - give more volume first; insulin-mediated vasodilation will deepen the shock.
Monitoring. Hourly glucose, 2-hourly potassium and electrolytes, VBG until the gap closes, hourly urine output, cardiac monitoring, catheter, neurological checks for cerebral oedema, and a search for the precipitant (infection, myocardial infarction, missed insulin).
3. At hour eight the glucose is 320 mg/dL, and the patient is now more confused, with headache, pulse 52 and BP 160/95. How do you interpret this and what do you do?
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Interpretation. In a young adult treated for hyperglycaemic crisis, the triad of falling conscious level, headache, bradycardia and hypertension is cerebral oedema until proven otherwise. It reflects a fall in effective osmolality that is too rapid (a rise in brain cell water) - check what the corrected sodium and calculated osmolality have done over the last eight hours. A corrected sodium that is falling while the glucose falls means free water is being given faster than the sodium is being replaced.
Immediate actions.
- Stop or slow the hypotonic/dextrose fluid; keep the osmolality change under about 3 mOsm/kg/h.
- Give 3% hypertonic saline 100–150 mL IV over 10–20 minutes, or mannitol 0.5–1 g/kg, and repeat if there is no response.
- Elevate the head of the bed, protect the airway, secure ICU-level monitoring, and arrange urgent CT head to exclude other causes (haemorrhage, thrombosis, stroke).
- Target a modest rise in serum sodium, keep glucose falling no faster than 50–75 mg/dL/h, and avoid over-correction.
Teaching point. The risk is highest in young patients and in those whose corrected sodium falls during treatment; the sodium trend, not the glucose trend alone, is the early warning signal.