Clinical Guidelines

Evidence-based health information

Diabetic Ketoacidosis (DKA)

Life-threatening complication of diabetes — emergency management

Diabetic Ketoacidosis (DKA)

Diabetic ketoacidosis (DKA) is a life-threatening metabolic emergency most commonly affecting people with type 1 diabetes. It occurs when severe insulin deficiency leads to uncontrolled ketone production and acidosis. DKA requires immediate hospital treatment and carries significant mortality if not managed promptly.


What is DKA?

DKA is defined by the triad of: blood glucose >11 mmol/L (or known diabetes), blood ketones >3 mmol/L (or urine ketones ≥2+), and metabolic acidosis (pH <7.3 or bicarbonate <15 mmol/L). Without insulin, cells cannot use glucose and the body breaks down fat for energy, producing ketone bodies as a by-product. Ketones are acidic, and their accumulation leads to a life-threatening metabolic acidosis.

Triggers and causes

The most common triggers are infection (the most frequent cause — always look for an underlying infection), missed or insufficient insulin doses, and new-onset type 1 diabetes. Other triggers include myocardial infarction, pancreatitis, trauma, and certain medications (e.g. SGLT-2 inhibitors in some circumstances — euglycaemic DKA). DKA can occasionally occur in type 2 diabetes, particularly in Afro-Caribbean individuals (ketosis-prone T2DM).

Symptoms and diagnosis

Symptoms develop over hours to days and include nausea, vomiting, abdominal pain, excessive thirst, frequent urination, and progressive drowsiness. The characteristic 'fruity' or pear-drop breath results from exhaled acetone. Kussmaul breathing (deep, sighing respirations) is a compensatory response to acidosis. Diagnosis is confirmed by blood glucose, blood ketone meter, venous blood gas (VBG), and urinalysis. Full blood count, U&Es, and blood cultures should be taken. An ECG is essential to assess potassium-related cardiac effects.

Hospital management (JBDS protocol)

The four pillars of DKA management are: IV fluids (0.9% sodium chloride — 1L over 1 hour, then 1L over 2 hours, then titrated); fixed-rate intravenous insulin infusion (FRIII) at 0.1 units/kg/hour; potassium replacement (add KCl to bags once K+ <5.5 mmol/L — DKA causes total body potassium depletion even when initial serum K+ appears high); and identification/treatment of the precipitant. Target resolution criteria: blood ketones <0.6 mmol/L, pH >7.3, bicarbonate >15 mmol/L, and blood glucose >6 mmol/L. Do not stop FRIII until patient is eating and drinking and has received subcutaneous insulin. Following recovery, evaluation of insulin management, injection technique, and sick day rules should be conducted to prevent recurrence.

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