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Diabetic Ketoacidosis: MCCQE Notes

Fluid first, then insulin, and never start insulin before you know the potassium.

MCCQEEndocrinology5 min read

The diagnostic triad

  • Hyperglycaemia — usually > 14 mmol/L, but euglycaemic DKA occurs with SGLT2 inhibitors, in pregnancy, and with starvation
  • Metabolic acidosis — pH < 7.3, bicarbonate < 18, raised anion gap
  • Ketosis — beta-hydroxybutyrate is the test to ask for; urine ketones measure acetoacetate and can lag or mislead

Sequence of management

Order matters, and the exam tests the order.

  1. Fluid. Isotonic saline, typically 1–1.5 L in the first hour, then adjusted. Volume depletion is the immediate threat and fluid alone lowers glucose substantially
  2. Potassium. Check it before insulin. Total body potassium is always depleted even when the serum level is high, because acidosis shifts it out of cells
    • K < 3.3 → replace potassium before starting insulin
    • K 3.3–5.0 → add potassium to fluids and start insulin
    • K > 5.0 → start insulin, recheck in 2 hours
  3. Insulin. Regular insulin infusion at roughly 0.1 units/kg/h. A bolus is optional and often omitted
  4. Dextrose added once glucose falls below about 14 mmol/L, so the insulin can continue clearing ketones without causing hypoglycaemia
  5. Bicarbonate is not routine — reserve it for pH < 6.9

Monitoring and endpoint

Track the anion gap and beta-hydroxybutyrate, not the glucose. Glucose normalises long before ketosis resolves, and stopping insulin at that point is the classic error.

Resolution: anion gap closed, bicarbonate ≥ 18, pH > 7.3. Only then overlap subcutaneous insulin with the infusion for 1–2 hours before stopping it — stopping the infusion without overlap causes rebound.

Find the precipitant

Every case has one:

  • Infection — the commonest
  • Insulin omission, deliberate or from pump failure
  • Ischaemia — myocardial infarction, which may be silent
  • New-onset type 1 diabetes
  • Drugs: steroids, SGLT2 inhibitors, antipsychotics
  • Pregnancy, pancreatitis, alcohol

Complications to anticipate

  • Cerebral oedema — mainly in children; correcting glucose and osmolality too fast is the risk. Presents with headache and declining consciousness during treatment
  • Hypokalaemia from insulin driving potassium intracellularly
  • Hypoglycaemia from failing to add dextrose
  • Hyperchloraemic metabolic acidosis from large-volume saline — expected, self-limiting, and not a sign of treatment failure

DKA versus HHS

HHS is the type 2 counterpart: glucose often above 33 mmol/L, osmolality above 320, minimal ketosis and no significant acidosis, with a longer prodrome and more profound dehydration and neurological signs. Fluid replacement is the mainstay and is given more cautiously; mortality is higher.

dkaendocrinologyemergencymccqe

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