Diabetic ketoacidosis with cerebral oedema risk — FFICM MCQ

Instant feedback + full explanation. One question, done properly.

HardRenal and MetabolicDiabetic ketoacidosis with cerebral oedema riskFFICM

A 23-year-old woman with DKA is admitted to ICU. After 6 hours of fixed-rate insulin, glucose has fallen from 32 to 9 mmol/L, ketones remain 3.8 mmol/L and bicarbonate is 12 mmol/L. She becomes increasingly confused with headache and vomiting. Sodium has fallen from 136 to 130 mmol/L corrected for glucose. What is the most appropriate management?

Educational content. Not a substitute for clinical judgement or local policy.

Reveal the answer and explanation

Correct answer: B — Treat suspected cerebral oedema and slow further osmotic change

The correct answer is B, treat suspected cerebral oedema and slow further osmotic change. New headache, vomiting and confusion during DKA treatment, with a falling corrected sodium and rapid glucose reduction from 32 to 9 mmol/L over six hours, are classic warning signs of cerebral oedema from an excessive osmotic shift. Ketones and bicarbonate remain deranged (ketones 3.8 mmol/L, bicarbonate 12 mmol/L), confirming DKA is biochemically unresolved despite the falling glucose, so the neurological picture cannot be attributed to simple recovery. Guidance requires that any neurological deterioration during DKA treatment triggers immediate senior review, consideration of hyperosmolar therapy (mannitol or hypertonic saline) and measures to slow the rate of osmotic change, such as reducing insulin rate and adding dextrose while maintaining ketone clearance. This is a medical emergency that takes priority over routine biochemical targets. Why the other options are wrong: B, stop insulin because glucose is below 10 mmol/L: ketones and bicarbonate show ongoing ketoacidosis, so insulin must continue (with dextrose added) to clear ketones; stopping it would worsen the acidosis. C, give rapid hypotonic fluid to correct dehydration: hypotonic fluid would accelerate the fall in osmolality and sodium, worsening cerebral oedema; fluids should be cautious and isotonic. D, administer bicarbonate to normalise pH: bicarbonate is not recommended in DKA management as it can paradoxically worsen intracellular acidosis and precipitate cerebral oedema. E, discharge because glucose has improved: glucose normalisation does not equal DKA resolution, and the patient is now acutely deteriorating neurologically, making discharge dangerous and inappropriate. Key point: New neurological symptoms during DKA treatment, especially with falling sodium and rapid osmotic change, mandate immediate suspicion and treatment of cerebral oedema regardless of improving glucose.

Reference: Joint British Diabetes Societies for Inpatient Care, The Management of Diabetic Ketoacidosis in Adults, revised June 2021, section on cerebral oedema and controversial areas; https://diabetestimes.co.uk/wp-content/uploads/2021/06/JBDS-02-DKA-Guideline-amended-v2.pdf