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Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus, primarily affecting individuals with type 1 diabetes but also occurring in those with other types.

DKA is characterised by the rapid onset of symptoms such as vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness. A specific "fruity" smell on a person's breath may also be detected.

Dehydration may be severe in diabetic ketoacidosis, and intravenous fluids are usually needed as part of its treatment.
Dehydration may be severe in diabetic ketoacidosis, and intravenous fluids are usually needed as part of its treatment.

Signs and Symptoms

The symptoms of DKA typically evolve over about 24 hours and include nausea, vomiting, pronounced thirst, excessive urine production, and severe abdominal pain. In severe cases, breathing becomes rapid and deep (Kussmaul breathing), and there may be confusion or a marked decrease in alertness, including coma. Physical examination often reveals dehydration, a dry mouth, decreased skin turgor, rapid heart rate, and low blood pressure. A "ketotic" odour, described as fruity or like pear drops, is often present due to the presence of acetone.

Children with DKA are particularly prone to cerebral oedema, which may cause headache, coma, loss of the pupillary light reflex, and can progress to death.


DKA usually occurs in individuals with type 1 diabetes but can also be the first presentation in those previously undiagnosed. Common triggers include infection, inadequate insulin administration, myocardial infarction, stroke, and certain medications like steroids. SGLT2 inhibitors, used in type 2 diabetes, have been associated with "euglycaemic DKA" where blood sugars may not be significantly elevated.

β-hydroxybutyrate (the conjugate base of β-hydroxybutyric acid, drawn above) despite chemically containing a carboxylate group instead of a ketone, is the principal 'ketone body' in diabetic ketoacidosis.
β-hydroxybutyrate (the conjugate base of β-hydroxybutyric acid, drawn above) despite chemically containing a carboxylate group instead of a ketone, is the principal "ketone body" in diabetic ketoacidosis.


DKA arises from a lack of insulin, leading to increased glucose release by the liver and osmotic diuresis. This results in dehydration, polyuria, and polydipsia. Concurrently, free fatty acids are converted into ketone bodies, leading to metabolic acidosis. Compensatory mechanisms include hyperventilation to lower blood carbon dioxide levels. The condition is further exacerbated by increased levels of counterregulatory hormones and cytokines.


DKA is diagnosed by demonstrating hyperglycaemia, ketones in blood or urine, and acidosis. A pH measurement is performed to detect acidosis, and ketones can be measured in the urine (acetoacetate) and blood (β-hydroxybutyrate). Additional tests include measuring urea, creatinine, electrolytes, markers of infection, and acute pancreatitis. In suspected cerebral oedema, computed tomography may be performed.


Fluid Replacement

Fluid replacement depends on the degree of dehydration. Severe dehydration or shock requires rapid saline infusion, while moderate dehydration allows for calculated rehydration. Mild cases may be treated with oral rehydration and subcutaneous insulin.


Insulin is administered to reduce blood sugars and suppress ketone production. Guidelines differ on the initial bolus dose and the subsequent insulin infusion rates based on blood glucose levels.


Potassium levels need continuous monitoring due to fluctuations during treatment. Potassium is added to intravenous fluids once levels fall below 5.3 mmol/L. If levels drop below 3.3 mmol/L, insulin administration may be paused.

Sodium Bicarbonate

The use of sodium bicarbonate is controversial and generally discouraged unless the pH is extremely low (<6.9). It may worsen intracellular acidosis and increase complications.

Cerebral Oedema

Cerebral oedema requires intensive care, potentially including artificial ventilation and medications like mannitol or hypertonic saline to reduce swelling.


DKA can be prevented by adherence to "sick day rules," which include taking extra insulin when sugar levels are uncontrolled, maintaining a diet rich in salt and carbohydrates, treating infections, and seeking medical help when necessary. Monitoring ketone levels when unwell is also recommended.


The main aim in the treatment of DKA is to replace lost fluids and electrolytes while suppressing high blood sugars and ketone production with insulin. Admission to an ICU may be necessary for close observation.

Self-assessment MCQs (single best answer)

Which type of diabetes is most commonly associated with Diabetic Ketoacidosis (DKA)?

What is a distinct characteristic smell on the breath of someone with DKA?

What is the primary cause of DKA?

Which of the following is NOT a common symptom of DKA?

What is the principal "ketone body" in diabetic ketoacidosis?

What type of breathing is often observed in severe cases of DKA?

Which of the following is a common trigger for DKA?

What immediate treatment is often required for severe dehydration in DKA?

Why is potassium monitoring essential during the treatment of DKA?

What is a controversial treatment option for DKA that is generally discouraged unless pH is extremely low?


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