Investigation and Management of Diabetic Ketoacidosis

DKA is an acute metabolic emergency defined by the triad of hyperglycaemia, ketosis and metabolic acidosis, caused by absolute or relative insulin deficiency with excess counter-regulatory hormones.

In older people DKA is less common than HHS (hyperosmolar hyperglycaemic state), but many elderly patients present with a “mixed” picture — glucose 270–450 mg/dL, pH 7.2–7.3, without marked dehydration or coma.

Older subjects with hyperglycaemic comas have higher mortality, longer hospital stay, more previously undiagnosed diabetes, more renal impairment, and need larger insulin doses than the young.

Commonest precipitants are infection (chest, urine, foot), myocardial infarction, stroke, inadequate or omitted insulin, and inappropriate drug treatment.

Thiazide diuretics and corticosteroids raise blood glucose and can precipitate DKA; thiazides and furosemide particularly precipitate HHS.

Care-home residence, dementia, thirst impairment and dependence on carers are important risk factors; COVID-19 and other acute illness can cause rapid decompensation.

Classical polyuria, polydipsia and weight loss may be absent or blunted; presentation is often non-specific — confusion, falls, drowsiness, incontinence, poor oral intake.

Look for Kussmaul breathing, ketotic breath, dehydration, hypotension, tachycardia and abdominal pain; hypothermia and absent fever may mask underlying sepsis.

Capillary and venous blood glucose; venous (not arterial) blood gas for pH and bicarbonate.

Bedside quantitative beta-hydroxybutyrate (β-OHB) is the preferred ketone test; urine ketones (nitroprusside) detect only acetoacetate and are less reliable.

Serum electrolytes — sodium (corrected for glucose), potassium, chloride, bicarbonate; anion gap; blood urea and creatinine.

Effective serum osmolality = 2 × Na (mEq/L) + glucose (mg/dL)/18 — to identify overlap with HHS.

Search for precipitant: full blood count, CRP, blood and urine cultures, chest X-ray, ECG and troponin (silent infarction is common), foot examination.

Diagnostic criteria (current international consensus): glucose ≥200 mg/dL or known diabetes; β-OHB ≥3.0 mmol/L or urine ketones ≥2+; pH <7.3 and/or bicarbonate <18 mEq/L. Severity is graded by pH, bicarbonate and mental state.

Euglycaemic DKA (glucose <200 mg/dL) must be actively excluded in patients on SGLT2 inhibitors, in starvation, and in chronic liver disease.

Fluids first — 0.9% saline or balanced crystalloid, typically 1 litre over the first hour, then titrated. In the elderly with heart failure or CKD, give slower and monitor closely for pulmonary oedema.

Fixed-rate intravenous insulin infusion 0.1 units/kg/hour, without a bolus in most patients; aim to fall β-OHB by 0.5 mmol/L/hour and glucose by 50–75 mg/dL/hour.

Potassium: withhold insulin if K <3.3 mEq/L until replaced; add 20–40 mEq/L to fluids when K is 3.3–5.2 mEq/L; withhold if K >5.2 mEq/L.

Add 5–10% dextrose when glucose falls to about 250 mg/dL, continuing insulin until ketosis clears. Bicarbonate only if pH <7.0; phosphate only if <1.0 mg/dL with cardiac or respiratory weakness.

Resolution: β-OHB <0.6 mmol/L with pH >7.3 or bicarbonate ≥18 mEq/L; then overlap intravenous insulin with subcutaneous basal insulin by 1–2 hours before stopping the infusion.

Complications to prevent: hypoglycaemia, hypokalaemia, fluid overload, aspiration, venous thromboembolism, and (rarely in old age) cerebral oedema.

Prevention: sick-day rules, ketone meters at home, structured education of patients and care-home staff, avoidance of insulin omission, and review of diabetogenic drugs.