Why DKA Is a Core OSCE Topic
Diabetic ketoacidosis is a life-threatening metabolic emergency predominantly affecting people with type 1 diabetes. It carries a mortality of 1-5% and is increasing in incidence. OSCEs examine it in acute management stations, prescribing stations (write the fluid and insulin prescription), and clinical reasoning (this type 1 diabetic is unwell — what is happening?).
⚠️ Red Flag
DKA can occur at normal or near-normal blood glucose levels — "euglycaemic DKA" occurs with SGLT-2 inhibitors (empagliflozin, dapagliflozin, canagliflozin). Never exclude DKA on the basis of a "normal" glucose alone if the clinical picture fits.
Diagnostic Criteria (JBDS UK Guidelines)
DKA requires all three of the following:
| Criterion | Threshold |
|---|---|
| Ketonaemia | Blood ketones 3.0 mmol/L or above (or urine ketones 2+ or above) |
| Hyperglycaemia | Blood glucose above 11.0 mmol/L (or known diabetes) |
| Acidosis | Bicarbonate below 15.0 mmol/L, or venous pH below 7.3, or both |
Severity Classification
| Severity | pH | Bicarbonate | Ketones | GCS |
|---|---|---|---|---|
| Mild | 7.25-7.30 | 15-18 | 3.0-5.9 | 15 |
| Moderate | 7.00-7.24 | 5-14 | 6.0-9.9 | 12-14 |
| Severe | Below 7.00 | Below 5 | 10.0 or above | Below 12 |
Severe DKA requires HDU/ITU admission.
Finding the Precipitant — THE 6 Is
🧠 Mnemonic
THE 6 Is — DKA precipitants:
- I nfection (most common — 30-40%)
- I nsulin omission or non-compliance
- I nfarction (MI, mesenteric ischaemia)
- I ntercurrent illness (any acute stress)
- I atrogenic (steroids, SGLT-2 inhibitors, antipsychotics)
- I nitial presentation (new diagnosis type 1 diabetes)
Initial Management — The First Hour
1. Airway, Breathing, Circulation
- Assess airway — GCS below 12 requires anaesthetic review
- High-flow oxygen if SpO2 below 94%
- IV access x2 large bore
- Attach monitoring: ECG (hypokalaemia), SpO2, hourly observations
2. IV Fluid Resuscitation
Key principle: fluids before insulin (insulin shifts potassium intracellularly — causes dangerous hypokalaemia if given when potassium is already low and patient is volume-depleted).
| Potassium on admission | First action |
|---|---|
| Below 3.5 mmol/L | Do NOT start insulin — correct potassium first with IV KCl; seek senior help |
| 3.5-5.5 mmol/L | Start fluids and insulin together |
| Above 5.5 mmol/L | Start fluids; do not add potassium; recheck in 1 hour |
Fluid protocol (0.9% sodium chloride):
| Time | Volume | Rate |
|---|---|---|
| 0-60 min | 1000 mL | Stat |
| 1-2 hours | 1000 mL | Over 1 hour |
| 2-4 hours | 1000 mL | Over 2 hours |
| 4-6 hours | 1000 mL | Over 2 hours |
| 6-12 hours | 1000 mL | Over 6 hours |
Switch to 10% glucose 125 mL/hour when blood glucose falls to 14 mmol/L (to maintain glucose while continuing insulin to clear ketones).
3. Fixed-Rate Intravenous Insulin Infusion (FRIII)
- 0.1 units/kg/hour of human soluble insulin (Actrapid)
- Weight in kg x 0.1 = mL/hour of 1 unit/mL solution
- Example: 70 kg patient = 7 units/hour = 7 mL/hour
- Continue until DKA resolved (ketones below 0.6 mmol/L, pH above 7.3, bicarbonate above 18 mmol/L)
- Continue long-acting subcutaneous insulin throughout DKA if already on it — do not stop
⚠️ Red Flag
Do not use a variable rate (sliding scale) — fixed-rate insulin is mandated by JBDS guidelines in DKA as it provides consistent ketone clearance. Sliding scale rates that reduce insulin when glucose drops will slow ketone clearance.
4. Potassium Replacement
| Serum potassium | KCl supplementation per litre |
|---|---|
| Above 5.5 mmol/L | Nil |
| 3.5-5.5 mmol/L | 40 mmol/L |
| Below 3.5 mmol/L | Senior review — higher dose replacement, hold insulin |
Monitoring Targets
| Parameter | Target rate of change | Method |
|---|---|---|
| Ketones | Fall by 0.5 mmol/L/hour | Bedside ketone meter hourly |
| Bicarbonate | Rise by 3 mmol/L/hour | VBG hourly |
| Blood glucose | Fall by 3 mmol/L/hour | Bedside glucose meter hourly |
| Potassium | Maintain 4.0-5.5 mmol/L | VBG/bloods every 2 hours |
If not meeting targets at 1 hour, increase FRIII rate by 1 unit/hour increments.
Resolution Criteria and Transition to Subcutaneous Insulin
DKA resolved when all three are met:
- Blood ketones below 0.6 mmol/L
- Venous pH above 7.3
- Bicarbonate above 18 mmol/L
Transition process:
- 1Give subcutaneous insulin with a meal
- 2Wait 30-60 minutes before stopping IV insulin (prevents rebound ketosis)
- 3Refer to diabetes specialist nurse or team for education if precipitated by insulin omission
DKA vs HHS
| Feature | DKA | HHS (Hyperosmolar Hyperglycaemic State) |
|---|---|---|
| Diabetes type | Usually T1DM | Usually T2DM |
| Glucose | Usually 11-25 mmol/L | Usually above 30 mmol/L |
| Ketones | Elevated (3+ mmol/L) | Absent or trace |
| pH | Below 7.3 | Normal |
| Osmolality | Normal or mildly raised | Markedly raised (above 320 mosmol/kg) |
| Onset | Hours | Days to weeks |
| Fluid deficit | 3-5 litres | 8-10 litres |
💎 Clinical Pearl
HHS carries higher mortality than DKA (15-20% vs 1-5%) because patients are often elderly, profoundly dehydrated, and have severe hyperosmolality causing thrombotic complications. Fluid replacement is slower (over 48 hours) and insulin is not given until glucose stops falling with fluids alone.
Frequently Asked Questions
"Why is potassium so important in DKA management?"
DKA causes total body potassium depletion through osmotic diuresis, vomiting, and intracellular shift. However, the acidosis and insulin deficiency push potassium out of cells, so the admission serum potassium may appear normal or even elevated despite total body depletion. Starting insulin corrects the acidosis and potassium shifts back into cells, causing rapid and potentially fatal hypokalaemia. This is why potassium must be checked before starting insulin and replaced throughout treatment.
"What is the difference between DKA and a hyperosmolar state?"
DKA results from absolute insulin deficiency (type 1 DM or severe type 2) — without insulin, lipolysis and ketogenesis are unchecked, producing the ketone-driven acidosis. HHS results from relative insulin deficiency — enough insulin to suppress ketogenesis but not enough to prevent hyperglycaemia. HHS presents with extreme hyperglycaemia (often above 50 mmol/L), severe dehydration, and hyperosmolality but no significant acidosis or ketosis.
"What is euglycaemic DKA and who is at risk?"
Euglycaemic DKA presents with blood glucose below 11 mmol/L but still meets criteria for ketosis and acidosis. It occurs in patients taking SGLT-2 inhibitors (empagliflozin, dapagliflozin, canagliflozin) — these drugs increase renal glucose excretion, masking hyperglycaemia while ketogenesis continues. Precipitants include reduced carbohydrate intake, fasting, alcohol, surgery, or intercurrent illness. All patients on SGLT-2 inhibitors admitted to hospital unwell should have ketones checked.
"When do you stop the FRIII and switch to subcutaneous insulin?"
When all three resolution criteria are met: ketones below 0.6 mmol/L, pH above 7.3, bicarbonate above 18 mmol/L. Give the patient a meal and their usual subcutaneous insulin dose simultaneously. Wait at least 30-60 minutes before stopping the IV insulin infusion to avoid rebound ketosis from the gap between subcutaneous absorption and IV cessation.
"What cerebral oedema risk exists in DKA and who is most at risk?"
Cerebral oedema is a rare but potentially fatal complication of DKA, predominantly in children and young adults. It is associated with overly rapid fluid resuscitation, excessive sodium correction, or insulin given before adequate fluid resuscitation. Signs: headache, declining GCS, bradycardia, hypertension, papilloedema. Treatment: IV mannitol 0.5-1 g/kg, head-up 30 degrees, urgent CT, neurosurgical review. Adult DKA guidelines have moved to more cautious fluid replacement for this reason.
Related Posts
- Diabetes History OSCE — taking a systematic diabetes history including type, complications, and control
- Blood Results Interpretation OSCE — interpreting VBG, ketones, and electrolytes in metabolic emergencies
- Acute Kidney Injury OSCE — AKI as a complication of DKA and HHS