Write a short note on diabetic ketoacidosis.

Definition

Diabetic ketoacidosis (DKA) is an acute metabolic emergency defined by the triad:

1. Hyperglycaemia (usually > 250 mg/dL — but see euglycaemic DKA below)

2. Ketosis — raised blood or urine ketones

3. Metabolic acidosis — pH < 7.3 and/or bicarbonate < 15–18 mEq/L, with a high anion gap

It occurs predominantly in type 1 diabetes but is well recognised in type 2, particularly under severe stress.

Pathophysiology

Absolute or relative insulin deficiency combined with excess counter-regulatory hormones (glucagon, catecholamines, cortisol, growth hormone) produces:

• Unrestrained hepatic gluconeogenesis and glycogenolysis with reduced peripheral glucose uptake → hyperglycaemia → osmotic diuresis → profound dehydration and electrolyte loss.
• Unrestrained lipolysis → free fatty acids → hepatic beta-oxidation to ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) → high anion gap metabolic acidosis.
• Total body potassium is severely depleted through osmotic diuresis and vomiting, yet the serum potassium is often normal or high on presentation because acidosis and insulin deficiency shift potassium out of cells. Insulin therapy then causes it to fall precipitously.

PRECIPITANTS — the "5 I's"

Infection (the commonest — urinary, respiratory, skin, and in India tuberculosis), Infarction (myocardial, cerebral), Insulin omission or inadequate dose (very common, including deliberate omission in adolescents), Intercurrent illness/surgery/trauma, and Initial presentation of type 1 diabetes. Drugs — corticosteroids, SGLT2 inhibitors, antipsychotics — also precipitate it.

Clinical Features

• Symptoms: polyuria, polydipsia, weight loss; nausea, vomiting and abdominal pain (which may mimic an acute abdomen); weakness.
• Signs: dehydration with dry mucosae, reduced skin turgor, tachycardia and hypotension; Kussmaul breathing (deep sighing respiration); acetone (fruity) odour on the breath; altered sensorium, from drowsiness to coma.
• Hypothermia or normothermia is usual — fever suggests infection, and its absence does not exclude it.

Investigations

• Capillary and laboratory glucose; blood ketones (beta-hydroxybutyrate) — preferred over urine ketones, which measure acetoacetate and may lag or mislead.
• Arterial or venous blood gas — high anion gap metabolic acidosis; venous pH is adequate for monitoring.
• Electrolytes including potassium (repeatedly), sodium, chloride, bicarbonate, urea, creatinine; corrected sodium (add 1.6 mEq/L per 100 mg/dL glucose above normal).
• CBC (leucocytosis occurs from stress alone and does not prove infection), septic screen — urine, chest X-ray, blood cultures.
• ECG — for hyperkalaemic changes and silent myocardial infarction; HbA1c to assess prior control; serum amylase/lipase may be raised without pancreatitis.

Management — Fluids, Insulin, Potassium

1. Fluids — the first and most important intervention

Restore circulating volume with isotonic saline, rapidly at first and then at a maintenance rate guided by clinical status. Switch to dextrose-containing fluid once glucose falls to around 200–250 mg/dL, continuing insulin to clear ketones. Beware fluid overload in the elderly, in renal impairment and in cardiac disease; beware cerebral oedema in children and young adults, in whom fluids must be more cautious.

2. Insulin

Fixed-rate intravenous infusion of short-acting insulin, continued until the ketosis and acidosis resolve — not merely until glucose normalises. Continue any long-acting basal insulin the patient normally takes throughout. Do not stop the infusion until the patient is eating and subcutaneous insulin has been given and has taken effect, with an overlap.

3. Potassium — the commonest lethal error

Check potassium before starting insulin. If it is low, correct it before or alongside insulin; insulin drives potassium into cells and can precipitate fatal arrhythmia. Add potassium to the fluids once the level is in or below the normal range and urine output is adequate, and monitor hourly to two-hourly.

4. Other measures

• Treat the precipitant — antibiotics for infection, management of myocardial infarction.
• Bicarbonate is not recommended except in extreme acidaemia with haemodynamic compromise; it worsens hypokalaemia and may cause paradoxical CSF acidosis.
• Nasogastric tube if there is vomiting with reduced consciousness; thromboprophylaxis; catheterisation only if needed for accurate output.
• Monitor hourly: glucose, ketones, and clinical status; electrolytes 2–4 hourly.

Resolution criteria: ketones cleared, venous pH > 7.3 and bicarbonate > 18, and the patient eating and drinking.

Complications

Hypokalaemia (of treatment), hypoglycaemia, cerebral oedema (mainly children — headache, deteriorating consciousness during treatment; a leading cause of death in paediatric DKA), pulmonary oedema, ARDS, acute kidney injury, thromboembolism, aspiration pneumonia, and hyperchloraemic acidosis from large-volume saline.