Diabetic Ketoacidosis
Direct answer
Diabetic ketoacidosis (DKA) is an acute hyperglycaemic emergency caused by absolute or severe relative insulin deficiency, producing uncontrolled lipolysis, ketoacidosis and dehydration. It is defined by the triad of hyperglycaemia (typically above 250 mg/dL), metabolic acidosis (arterial pH below 7.30 or serum bicarbonate below 18 mEq/L) and ketonaemia or ketonuria. Management is intravenous isotonic saline first, then regular insulin infusion at 0.1 units/kg/hour, with potassium replacement and a search for the precipitating cause — infection being the commonest.
What you must remember
- Diagnostic triad: hyperglycaemia, high-anion-gap metabolic acidosis and positive ketones; beta-hydroxybutyrate is the dominant ketone.
- Precipitants: infection is the commonest; missed insulin, new-onset type 1 diabetes, myocardial infarction, pancreatitis and surgery follow. SGLT2 inhibitors can cause euglycaemic DKA.
- Fluids first: isotonic (0.9%) saline, about 15-20 mL/kg over the first hour, then guided by hydration and corrected sodium.
- Insulin: intravenous regular insulin at 0.1 units/kg/hour; ensure serum potassium is above 3.3 mEq/L before starting — insulin drives potassium intracellularly.
- Potassium: add 20-30 mEq/L to fluids once potassium falls below about 5.2 mEq/L and urine output is established; hypokalaemia causes the arrhythmias that kill during treatment.
- Glucose target: target a fall of 50-75 mg/dL/hour; when glucose reaches about 200 mg/dL, add 5% dextrose and continue insulin until the anion gap closes — insulin stops ketogenesis, not just hyperglycaemia.
- Bicarbonate: only if arterial pH is below 6.9. Cerebral oedema, mainly paediatric, is treated with mannitol or hypertonic saline.
Common confusion
DKA is most often contrasted with hyperglycaemic hyperosmolar state (HHS): HHS presents over days to weeks with profound dehydration, marked sensorium change, glucose usually above 600 mg/dL, effective osmolality above 320 mOsm/kg, and crucially no significant ketoacidosis (pH above 7.30, bicarbonate above 18 mEq/L) — residual insulin suppresses lipolysis. DKA evolves over hours to a few days, involves type 1 or advanced type 2 diabetes, and shows prominent ketones. Beware euglycaemic DKA with SGLT2 inhibitors: a near-normal glucose falsely reassures, so check ketones and the anion gap when the picture suggests acidosis.
Exam-focused takeaway
NEET-PG-style questions on DKA test sequence and thresholds more than definitions. Expect a vignette asking the next best step (intravenous isotonic saline), the insulin dose and route, the potassium rule before starting insulin, when to add dextrose (around 200 mg/dL), and when bicarbonate is justified (pH below 6.9). Stems also probe precipitating causes, laboratory interpretation — blood gas with high anion gap, serum ketones, hyponatraemia of hyperglycaemia — and complications such as cerebral oedema. Mechanism questions cover glucagon-driven lipolysis and the dominant ketone (beta-hydroxybutyrate). Learn the protocol as an ordered ladder — option sets are built from its steps.
Practise NEET-PG-style DKA questions — previous-year stems, a structured question bank and exam-format mocks — inside the PrepElephant app, where flagged questions resurface until the protocol is reflexive.
Frequently asked questions
What is the first step in managing DKA?
Intravenous isotonic saline. Fluid resuscitation begins before the insulin infusion, which starts once potassium is known to be safe.
What is the correct insulin regimen in DKA?
A regular insulin infusion at 0.1 units/kg/hour, continued until ketoacidosis resolves (anion gap normalises), with dextrose added at about 200 mg/dL.
Why is potassium checked before insulin?
Insulin shifts potassium into cells; giving it with hypokalaemia (below 3.3 mEq/L) risks fatal arrhythmias, so potassium is replaced first.
When is bicarbonate given in DKA?
Only when arterial pH is below 6.9 — routine bicarbonate does not help and may worsen outcomes.
How do DKA and HHS differ?
DKA: ketoacidosis, pH below 7.30, onset in hours to days. HHS: severe hyperosmolality without significant ketosis, profound dehydration and altered sensorium, over days to weeks.
What is the expected rate of glucose fall in treated DKA?
About 50-75 mg/dL per hour; faster falls risk cerebral oedema, especially in children.
Practise this in the PrepElephant app
Question banks, previous-year questions, mock tests and revision tools — for Diabetic Ketoacidosis and Medicine. Free to start.