Key Facts

DKA is a medical emergency requiring prompt treatment. The UK JBDS-IP (Joint British Diabetes Societies) guidelines standardise management. The key priorities are fluid resuscitation, insulin administration, and potassium monitoring. Resolution is defined by ketone clearance, not glucose normalisation.

Epidemiology

Incidence: ~4-8 per 1,000 person-years in T1DM. DKA is the presenting feature in ~25% of new T1DM (higher in children). Mortality ~1% in UK (higher in elderly and those with comorbidities). Recurrent DKA: associated with psychosocial factors, eating disorders, insulin omission.

Aetiology

Precipitants (the 5 I's):

• Infection (commonest precipitant — UTI, pneumonia, skin)
• Insulin omission/insufficient insulin (commonest cause in known T1DM)
• Infarction (MI, stroke)
• Intercurrent illness (surgery, trauma)
• Intoxication/drugs (steroids, SGLT2 inhibitors, cocaine)

Pathophysiology

Insulin deficiency + counter-regulatory hormone excess (glucagon, cortisol, catecholamines, GH) → unrestrained lipolysis → free fatty acids → hepatic ketogenesis (acetoacetate, β-hydroxybutyrate, acetone) → metabolic acidosis. Simultaneously: hepatic gluconeogenesis + reduced peripheral glucose uptake → hyperglycaemia → osmotic diuresis → dehydration + electrolyte loss (Na⁺, K⁺, Cl⁻, PO₄³⁻). Total body potassium is DEPLETED (renal losses) even if serum K⁺ is normal/high at presentation (acidosis shifts K⁺ out of cells). Insulin drives K⁺ back into cells → serum K⁺ falls rapidly with treatment → hypokalaemia risk.

Symptoms

• Polyuria, polydipsia (hyperglycaemia)
• Nausea, vomiting, abdominal pain (ketosis — may mimic acute abdomen)
• Weakness, fatigue, malaise
• Confusion, drowsiness → coma (severe)

Signs

• Kussmaul breathing: deep, rapid respiration (respiratory compensation for metabolic acidosis)
• Ketotic breath: fruity/pear-drops smell (acetone)
• Dehydration: dry mucous membranes, reduced skin turgor, tachycardia, hypotension
• Tachycardia: dehydration + sympathetic drive
• Hypothermia: may occur (infection may not cause fever in DKA)

Severity (JBDS-IP)

• Mild: pH 7.25-7.3, bicarb 15-18
• Moderate: pH 7.0-7.24, bicarb 10-14
• Severe: pH <7.0, bicarb <10, GCS <12, SpO₂ <92%, SBP <90, HR >100 or <60, anion gap >16

Red Flags

• GCS <12 → severe DKA; consider HDU/ITU
• K⁺ <3.5 → do NOT start insulin until K⁺ corrected (risk of cardiac arrest)
• pH <7.0 → severe; consider bicarbonate (rarely needed)
• Persistent acidosis despite treatment → search for precipitant (sepsis, MI)

Immediate

• Capillary blood glucose: elevated (usually >14 mmol/L; may be near-normal in euglycaemic DKA)
• Blood ketones: ≥3.0 mmol/L (β-hydroxybutyrate); urine ketones ≥2+ if blood ketones not available
• VBG (venous blood gas): pH, bicarbonate, potassium, lactate
• U&Es: potassium (critical — guide replacement), sodium (corrected Na⁺), renal function
• FBC: WCC may be raised (stress response — does not necessarily indicate infection)
• CRP: infection screen
• Blood cultures, urine MC&S, CXR: identify precipitant
• ECG: hyperkalaemia/hypokalaemia changes; MI screen
• Serum osmolality: if HHS suspected (>320 mOsm/kg = HHS)

Monitoring (JBDS-IP)

• Hourly: capillary glucose, blood ketones (target fall ≥0.5 mmol/L/hr)
• 2-hourly: VBG (pH, bicarb, K⁺)
• K⁺: every 1-2 hours initially (falls rapidly with insulin)
• Fluid balance: strict input/output; consider urinary catheter if oliguric
• GCS: regular neurological observations (especially children — cerebral oedema)

IV Fluids (JBDS-IP Protocol)

• 0.9% NaCl: 1L over 1 hour → 1L over 2 hours → 1L over 2 hours → 1L over 4 hours → 1L over 4 hours → 1L over 6 hours (total ~6L in 24 hours; adjust for clinical status)
• When glucose <14 mmol/L: add 10% glucose infusion (alongside 0.9% NaCl) to prevent hypoglycaemia while continuing insulin to clear ketones
• Caution in young patients (<25), elderly, HF, renal impairment — risk of fluid overload

Fixed-Rate Insulin Infusion (FRII)

• 0.1 units/kg/hour IV (e.g., 50 units Actrapid in 50mL 0.9% NaCl via syringe pump)
• Target: blood ketones fall ≥0.5 mmol/L/hr, glucose fall 3 mmol/L/hr
• Continue long-acting basal insulin (if already prescribed) — do NOT stop
• If blood ketones not falling adequately: increase FRII rate by 1 unit/hr

Potassium Replacement (Critical)

• K⁺ <3.5 mmol/L: add 40 mmol KCl per litre; DO NOT start insulin until K⁺ >3.5 (risk of cardiac arrest)
• K⁺ 3.5-5.5 mmol/L: add 40 mmol KCl per litre of fluid
• K⁺ >5.5 mmol/L: no potassium replacement; recheck in 1-2 hours
• Maximum rate: 20 mmol/hr via peripheral line; cardiac monitoring if giving >10 mmol/hr

Other

• VTE prophylaxis: LMWH (enoxaparin 40mg SC OD) — DKA is prothrombotic
• Treat precipitant: antibiotics if infection, MI pathway if infarction
• Bicarbonate: NOT routinely recommended; consider only if pH <6.9 (seek senior advice)
• Phosphate: routine replacement not recommended unless severely low

Resolution and Transition

• Resolution criteria: pH >7.3, bicarb >15 mmol/L, blood ketones <0.6 mmol/L, patient eating/drinking
• Transition to SC insulin: give SC rapid-acting insulin with a meal; continue FRII for 30-60 minutes AFTER SC dose before stopping
• If new diagnosis T1DM: initiate basal-bolus regimen; specialist diabetes team review

Cerebral Oedema (Mainly Children)

• Rare (<1% of paediatric DKA) but ~25% mortality
• Risk factors: young age, new diagnosis, excessive fluid, rapid glucose correction, failure of Na⁺ to rise
• Symptoms: headache, confusion, GCS decline, Cushing response
• Treatment: hypertonic saline 3% (2.5-5 mL/kg IV over 10-15 min) or mannitol 20% 0.5-1 g/kg IV; reduce fluids; intubation if needed

Referral Criteria

• All DKA: acute medical team (may need HDU/ITU for severe)
• Specialist diabetes team: before discharge
• Recurrent DKA: psychology, specialist nursing (assess adherence, psychosocial factors)

UK mortality ~1% overall; higher in elderly and those with significant comorbidities. Recurrent DKA is associated with insulin omission (psychosocial factors, eating disorders) and is a marker of poor long-term prognosis. With modern protocol-driven management, outcomes are excellent. Cerebral oedema mortality ~25% (children). Long-term: each DKA episode may accelerate cognitive decline and residual beta cell loss.

DKA vs HHS

JBDS-IP DKA Monitoring Summary