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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- DKA triad: hyperglycaemia (glucose >11 mmol/L), ketonaemia (blood ketones >3 mmol/L), acidosis (pH <7.3 or bicarb <15)
- Treatment: aggressive IV fluid resuscitation (0.9% NaCl) + fixed-rate IV insulin infusion (0.1 units/kg/h)
- Monitor potassium closely — insulin drives K⁺ intracellularly. Replace K⁺ when <5.5 mmol/L. NEVER give insulin if K⁺ <3.5 before replacement
- DO NOT stop long-acting background insulin (e.g. Lantus) during DKA treatment
- Cerebral oedema: most feared complication — especially in children and young adults. Avoid overly rapid fluid correction
- Commonest precipitants: infection, missed insulin doses, new diagnosis of T1DM
Overview
Diabetic ketoacidosis is an acute, life-threatening metabolic emergency resulting from absolute or relative insulin deficiency. Without insulin, cells cannot utilise glucose, leading to unrestrained lipolysis and hepatic ketogenesis. The resulting ketonaemia (beta-hydroxybutyrate, acetoacetate) causes a metabolic acidosis. Osmotic diuresis from hyperglycaemia causes profound dehydration and electrolyte derangement. DKA is most commonly associated with type 1 diabetes (first presentation or missed insulin) but can occur in type 2 with significant insulin deficiency, or with SGLT2 inhibitors (euglycaemic DKA).
Epidemiology
DKA is the leading cause of death in young people with type 1 diabetes. UK incidence is approximately 4–8 episodes per 1,000 patient-years in T1DM. ~25% of T1DM presents with DKA as the first manifestation. Mortality is approximately 1% overall but higher in elderly. Precipitants: infection (most common ~40%), missed insulin doses, newly diagnosed diabetes, intercurrent illness, myocardial infarction, and drugs (steroids, SGLT2 inhibitors). Euglycaemic DKA (glucose <11 mmol/L but ketonaemia + acidosis) is an emerging entity associated with SGLT2 inhibitor use.
Clinical Features
Symptoms
Polyuria, polydipsia, dehydration
Nausea and vomiting
Abdominal pain (can mimic acute abdomen — especially in children)
Fatigue, weakness
Confusion, drowsiness, reduced consciousness
Weight loss (if new presentation of T1DM)
Signs
Dehydration: dry mucous membranes, reduced skin turgor, tachycardia, hypotension
Kussmaul breathing: deep, sighing hyperventilation (respiratory compensation for metabolic acidosis)
Acetone (pear-drops/nail varnish) smell on breath
Tachycardia
Hypothermia (even in the presence of infection)
Reduced GCS, coma (severe DKA)
Investigations
First-line
Blood glucoseTypically >11 mmol/L (may be >30). Note: can be near-normal in euglycaemic DKA (SGLT2i)
Blood ketones≥3.0 mmol/L confirms significant ketonaemia. Point-of-care testing — essential for monitoring response
Venous blood gaspH <7.3 and/or bicarbonate <15 mmol/L. Severity: mild pH 7.25–7.3; moderate 7.0–7.24; severe <7.0
U&EsPotassium critical — may be high on admission (acidosis shifts K⁺ out of cells) but total body K⁺ is depleted
Second-line
FBC, CRPInfection screen — WCC may be raised from DKA itself (stress response), so CRP is more reliable
Blood cultures, urine dip, CXRSearch for precipitating infection
ECGHyperkalaemia/hypokalaemia changes; exclude MI as precipitant
Urinary ketonesLess reliable than blood ketones (lag behind). Blood ketones preferred for monitoring
Specialist
Serum osmolalityIf concern about HHS overlap or mixed picture
CT headIf reduced consciousness does not improve with treatment — exclude cerebral oedema (especially in children)
1
Fluid resuscitation
- 0.9% NaCl IV: 1 L over first hour, then 1 L over next 2 h, then 1 L over 2 h, then 1 L over 4 h, then 1 L over 4 h (total ~6 L in 12–14 h — adjust for weight/comorbidities)
- Add glucose (10% dextrose) when blood glucose falls below 14 mmol/L — this allows continued insulin infusion to clear ketones
- Slower replacement in young adults/children — risk of cerebral oedema
2
Fixed-rate IV insulin infusion (FRIII)
- 0.1 units/kg/hour (e.g. 50 units Actrapid in 50 mL NaCl at rate = weight in kg ÷ 10 mL/h)
- DO NOT stop long-acting background insulin (Lantus/Levemir) — continue at usual dose
- Target: blood ketones falling by ≥0.5 mmol/L/h, glucose falling by ≥3 mmol/L/h, bicarb rising by ≥3 mmol/L/h
- If targets not met: increase FRIII rate by 1 unit/h
3
Potassium replacement
- K⁺ >5.5: no replacement (but recheck in 1–2 h)
- K⁺ 3.5–5.5: add 40 mmol KCl per litre of fluid
- K⁺ <3.5: replace potassium BEFORE starting insulin — risk of cardiac arrhythmia
- Monitor K⁺ every 1–2 hours initially
4
Monitoring and resolution
- Hourly blood glucose and blood ketones for first 6 h
- VBG at 2 h, 4 h, 8 h, 12 h
- DKA resolved when: pH >7.3, bicarb >15, ketones <0.6 mmol/L
- Once resolved and eating: switch to SC insulin (give SC insulin 30 min before stopping FRIII)
- Senior review if not improving by 6 h
Complications
- Cerebral oedema: Most dangerous complication — particularly in children/young adults. Presents with headache, reduced GCS, bradycardia, hypertension. Treat with IV mannitol 20% or hypertonic saline. Risk increased by overly rapid fluid/glucose correction
- Hypokalaemia: Insulin drives K⁺ into cells — can cause fatal cardiac arrhythmias if not replaced
- Hypoglycaemia: From insulin infusion — add dextrose when glucose <14 mmol/L
- VTE: Dehydration and immobility — consider prophylactic LMWH
- Aspiration pneumonia: Reduced consciousness + vomiting
- ARDS: Rare but recognised complication of severe DKA
UKMLA Exam Tips
- 1DKA triad: glucose >11, ketones >3, pH <7.3 (or bicarb <15). Know these numbers
- 2FRIII rate = 0.1 units/kg/h. Do NOT bolus insulin. Do NOT stop background insulin
- 3Potassium <3.5 = replace BEFORE starting insulin. This is a life-saving step
- 4Add 10% dextrose when glucose <14 — this lets you keep running insulin to clear ketones
- 5Euglycaemic DKA: SGLT2 inhibitor patient with normal glucose but ketonaemia + acidosis — tricky exam scenario
- 6Cerebral oedema: headache + falling GCS during DKA treatment = give IV mannitol immediately
- 7DKA resolution criteria: pH >7.3, bicarb >15, ketones <0.6, patient eating. Switch to SC insulin 30 min before stopping IV
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