Diabetic ketoacidosis is one of the most heavily examined acute presentations in UK medical exams, because it tests fluid management, electrolyte handling and a clear, protocolised emergency in one scenario. This guide covers the high-yield essentials as examiners frame them — diagnosis, investigations, management to the current Joint British Diabetes Societies (JBDS) standard, and the traps that separate a correct answer from a near miss. Always follow your local protocol and current guidance in practice; figures here reflect JBDS guidance as of mid-2026.
What DKA is
DKA is an acute hyperglycaemic emergency, classically of type 1 diabetes, driven by absolute or relative insulin deficiency. Without insulin, cells cannot use glucose, so the body breaks down fat into ketones, producing a high-anion-gap metabolic acidosis, while the high glucose drives an osmotic diuresis and profound dehydration. The three defining features — hyperglycaemia, ketonaemia and acidosis — are what you diagnose and what you reverse. It is worth distinguishing DKA from the hyperosmolar hyperglycaemic state (HHS), the other major hyperglycaemic emergency: HHS occurs more often in type 2 diabetes, develops over days, and is characterised by very high glucose and osmolality with little or no ketosis or acidosis, and it is managed differently — a comparison examiners frequently draw.
Diagnosis: the triad
UK practice diagnoses DKA on three criteria together: capillary or blood ketones of 3 mmol/L or above (or significant ketonuria, 2+ or more on dipstick); blood glucose above 11 mmol/L (or known diabetes); and a venous pH below 7.3 and/or bicarbonate below 15 mmol/L. All three are needed — and recognising that the glucose can be only modestly raised is a common exam point.
Investigations
Beyond the diagnostic triad, examiners expect a venous blood gas (pH, bicarbonate), urea and electrolytes (especially potassium), glucose and ketones, and a search for the precipitant — an infection screen (cultures, chest X-ray, urinalysis), an ECG, and a careful drug and adherence history. Capillary ketone meters allow bedside monitoring of the response to treatment. The most common precipitants are infection, non-adherence to insulin, and a previously undiagnosed first presentation of diabetes. Assessing severity matters because it determines the level of care. Features that mark severe DKA, and should prompt consideration of critical-care input, include a blood pH below 7.0, ketones above 6 mmol/L, bicarbonate below 5 mmol/L, a potassium below 3.5 mmol/L on admission, a reduced conscious level, oxygen saturations below 92%, a systolic blood pressure below 90 mmHg, or a heart rate above 100 or below 60 beats per minute.
Management to the JBDS standard
The pillars are fluids, insulin and potassium, with close monitoring.
Fluids come first: restore circulating volume with intravenous 0.9% sodium chloride. A shocked patient needs a rapid bolus; otherwise replacement is steady, with caution in young adults and those at risk of cerebral oedema. Children and adolescents are managed under separate paediatric protocols because of their higher cerebral-oedema risk.
Fixed-rate intravenous insulin: start a fixed-rate insulin infusion at 0.1 units/kg/hour. The JBDS update allows reducing this to 0.05 units/kg/hour once blood glucose falls below 14 mmol/L, to reduce the risk of hypoglycaemia and hypokalaemia. Crucially, continue the patient's usual long-acting (basal) insulin throughout — stopping it is a classic error.
Glucose: once blood glucose falls below 14 mmol/L, add intravenous 10% glucose alongside the saline so that insulin can continue clearing ketones without causing hypoglycaemia.
Potassium: this is where marks are won and lost. Serum potassium is often normal or high at presentation despite total-body depletion, and it falls rapidly once insulin drives it into cells — so potassium is added to the fluids once it is within or below the normal range and urine output is adequate, with frequent monitoring.
Monitoring and resolution: check ketones, glucose and potassium regularly. DKA is resolved when ketones are below 0.6 mmol/L and venous pH is above 7.3; the patient is then converted to subcutaneous insulin, ideally with the meal-time dose given before the infusion stops. Add venous thromboembolism prophylaxis and involve seniors or critical care for severe cases.
High-yield exam points and traps
A handful of points recur:
- Euglycaemic DKA: patients on SGLT2 inhibitors (the "-gliflozins") can develop DKA with near-normal glucose. Diagnose on ketones and acidosis, not glucose — a favourite trap. It can also be precipitated by reduced carbohydrate intake, illness or surgery in someone taking these agents.
- Do not stop the long-acting insulin: basal insulin continues alongside the infusion.
- Potassium falls with treatment: replace early and monitor; a normal presenting potassium is not reassuring.
- It is the acidosis and ketonaemia that define resolution, not the glucose — glucose often normalises first.
- Cerebral oedema is the feared complication, particularly in children and young adults; avoid overly rapid fluid shifts.
- Bicarbonate is not given routinely, even with marked acidosis. Insulin, not bicarbonate, corrects the acidosis by switching off ketogenesis.
A few common questions
What are the diagnostic criteria for DKA? Ketones of 3 mmol/L or above (or 2+ ketonuria), glucose above 11 mmol/L or known diabetes, and venous pH below 7.3 and/or bicarbonate below 15 mmol/L — all three together.
What is the insulin regimen in DKA? A fixed-rate intravenous infusion at 0.1 units/kg/hour, reduced to 0.05 units/kg/hour once glucose is below 14 mmol/L, with the usual basal insulin continued.
Why is potassium so important in DKA? Insulin drives potassium into cells, so a normal or high presenting level falls quickly; potassium is replaced in the fluids once it is within or below the normal range, with close monitoring.
Can you have DKA with a normal glucose? Yes — euglycaemic DKA, classically with SGLT2 inhibitors; diagnose on ketones and acidosis.
How does DKA differ from HHS? HHS is typically a type 2 diabetes emergency developing over days, with very high glucose and osmolality but minimal ketosis or acidosis; DKA is defined by ketonaemia and acidosis and is more often a complication of type 1 diabetes.
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