Diabetic ketoacidosis is a life threatening, medical emergency. It is the most common way that children with a new diagnosis of type 1 diabetes present.
Ketogenesis normally occurs when there is an insufficient supply of glucose and glycogens stores are exhausted. This may happen during prolonged fasting or very low carbohydrate diets. The liver takes fatty acids and converts them to ketones. Ketones are water soluble fatty acids that can be used as fuel. They can cross the blood brain barrier and be used by the brain. Producing ketones is normal and not harmful in healthy patients when under fasting conditions or on a very low carbohydrate, high fat diet. Ketone levels can be measured in the urine using a urine dipstick and in the blood using a ketone meter. People in ketosis have a characteristic acetone smell to their breath.
Ketone acids (ketones) are buffered in normal patients so the blood does not become acidotic. When underlying pathology (i.e. type 1 diabetes) causes extreme hyperglycaemic ketosis, this results in a metabolic acidosis that is life threatening. This is called diabetic ketoacidosis.
Pathophysiology of Diabetic Ketoacidosis (DKA)
Diabetic ketoacidosis occurs in type 1 diabetes, where the person is not producing adequate insulin themselves and is not injecting adequate insulin to compensate for this. It occurs when they body does not have enough insulin to use and process glucose. The main problems are ketoacidosis, dehydration and potassium imbalance.
When the cells in the body have no fuel and think they are starving, they initiate the process of ketogenesis so they have a usable fuel. Over time the glucose and ketone levels get higher and higher. Initially the kidneys produce bicarbonate to buffer the ketone acids in the blood and maintain a normal pH. Over time the ketone acids use up the bicarbonate and the blood starts to become acidic. This is called ketoacidosis.
Hyperglycaemia overwhelms the kidneys and glucose starts being filtered into the urine. The glucose in the urine draws water out with it in a process called osmotic diuresis. This causes the patient to urinate a lot (polyuria). This results in severe dehydration. The dehydration stimulates the thirst centre to tell the patient to drink lots of water. This excessive thirst is called polydipsia.
Insulin normally drives potassium into cells. Without insulin, potassium is not added to and stored in cells. Serum potassium can be high or normal in diabetic ketoacidosis, as the kidneys continue to balance blood potassium with the potassium excreted in the urine, however total body potassium is low because no potassium is stored in the cells. When treatment with insulin starts, patients can develop severe hypokalaemia (low serum potassium) very quickly, and this can lead to fatal arrhythmias.
The most dangerous aspects of DKA are dehydration, potassium imbalance and acidosis. These are what will kill the patient. Therefore the priority is fluid resuscitation to correct the dehydration, electrolyte disturbance and acidosis. This is followed by an insulin infusion to allow the cells to start taking up and using glucose and stop producing ketones.
Children with DKA are at high risk of developing cerebral oedema. Dehydration and high blood sugar concentration cause water to move from the intracellular space in the brain to the extracellular space. This causes the brain cells to shrink and become dehydrated. Rapid correction of dehydration and hyperglycaemia (with fluids and insulin) causes a rapid shift in water from the extracellular space to the intracellular space in the brain cells. This causes the brain to swell and become oedematous, which can lead to brain cell destruction and death.
Neurological observations (i.e. GCS) should be monitored very closely (e.g. hourly) to look for signs of cerebral oedema. Be concerned when patients being treated for diabetic ketoacidosis develop headaches, altered behaviour, bradycardia or changes to consciousness.
Management options for cerebral oedema are slowing IV fluids, IV mannitol and IV hypertonic saline. These should be guided by an experienced paediatrician.
Presentation of DKA
The patient will present with symptoms of the underlying hyperglycaemia, dehydration and acidosis:
- Nausea and vomiting
- Weight loss
- Acetone smell to their breath
- Dehydration and subsequent hypotension
- Altered consciousness
- Symptoms of an underlying trigger (i.e. sepsis)
Check the local DKA diagnostic criteria for your hospital. To diagnose DKA you require:
- Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
- Ketosis (i.e. blood ketones > 3 mmol/l)
- Acidosis (i.e. pH < 7.3)
Principles of DKA Management in Children
Follow local treatment protocols and involve senior paediatricians. The two pillars of correcting DKA are:
- Correct dehydration evenly over 48 hours. This will correct the dehydration and dilute the hyperglycaemia and the ketones. Correcting it faster increases the risk of cerebral oedema.
- Give a fixed rate insulin infusion. This allows cells to start using glucose again. This in turn switches off the production of ketones.
Other important principles:
- Avoid fluid boluses to minimise the risk of cerebral oedema, unless required for resuscitation.
- Treat underlying triggers, for example with antibiotics for septic patients.
- Prevent hypoglycaemia with IV dextrose once blood glucose falls below 14mmol/l.
- Add potassium to IV fluids and monitor serum potassium closely.
- Monitor for signs of cerebral oedema.
- Monitor glucose, ketones and pH to assess their progress and determine when to switch to subcutaneous insulin.
Last updated August 2019