Diabetic ketoacidosis

Overview

DKA is a life-threatening emergency caused by severe insulin deficiency, most commonly in type 1 diabetes. All three criteria must be present:

•Blood glucose >11 mmol/L (or known diabetes mellitus)

•Blood ketones >3 mmol/L (or urinary ketones 2+ or more on dipstick)

•pH <7.3 and/or bicarbonate <15 mmol/L

Presentation

•Polyuria and polydipsia - osmotic diuresis from glycosuria

•Nausea, vomiting, abdominal pain - can mimic a surgical abdomen

•Kussmaul respiration - deep, laboured, sighing hyperventilation; respiratory compensation for metabolic acidosis

•Fruity/acetone breath - exhaled volatile ketones

•Dehydration - dry mucous membranes, prolonged capillary refill, tachycardia, hypotension; fluid deficit 5-8 litres

•Altered consciousness - GCS <12 requires urgent senior review

Investigations

•Capillary blood glucose - >11 mmol/L (note: euglycaemic DKA can occur with SGLT-2 inhibitors)

•Blood ketones - >3 mmol/L confirms ketonaemia

•Venous blood gas - confirms pH <7.3 and/or bicarbonate <15 mmol/L

•U&Es - potassium critical (guides replacement); AKI common

•ECG - hypokalaemia (flattened T-waves, U-waves) or precipitating MI

Differential diagnosis

DKA vs HHS vs Alcoholic ketoacidosis
FeatureDKAHHSAlcoholic ketoacidosis
Glucose>11 mmol/LMarkedly elevated (often >30)Low or normal
Ketones>3 mmol/LAbsent or minimalElevated
pH / acidosispH <7.3, raised anion gapNo acidosisAcidosis present
Typical patientType 1 DMType 2 DMAlcohol excess, starvation

Feature	DKA	HHS	Alcoholic ketoacidosis
Glucose	>11 mmol/L	Markedly elevated (often >30)	Low or normal
Ketones	>3 mmol/L	Absent or minimal	Elevated
pH / acidosis	pH <7.3, raised anion gap	No acidosis	Acidosis present
Typical patient	Type 1 DM	Type 2 DM	Alcohol excess, starvation

Management

•Fluids first - 0.9% saline to correct 5-8 L deficit; fluids must always precede insulin

•Fixed-rate insulin infusion (FRIII) - 0.1 units/kg/hour; target fall in blood ketones ≥0.5 mmol/L per hour

•Potassium replacement - add 40 mmol/L KCl to bags after the first; replace proactively before starting insulin

•Add dextrose when glucose falls below 14 mmol/L to allow continued insulin infusion

•Treat precipitant - infection (e.g. co-amoxiclav for CAP), missed insulin, etc.

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A patient in DKA may have a serum K+ of 5.0 mmol/L on arrival yet be profoundly total-body potassium-depleted. Insulin drives K+ back into cells - starting insulin without potassium replacement can precipitate fatal hypokalaemia and ventricular arrhythmias.

Complications

•Hypokalaemia - most immediately dangerous once insulin started; prevented by proactive potassium replacement

•Hypoglycaemia - from FRIII; prevented by adding dextrose when glucose <14 mmol/L

•Cerebral oedema - rare but life-threatening; more common in children/young adults; caused by rapid osmolality shifts

•Acute kidney injury - from prolonged dehydration and hypoperfusion