Diabetic ketoacidosis

Introduction

Diabetic ketoacidosis (DKA) occurs primarily in type 1 diabetes and is characterised by hyperglycaemia, polyuria, polydipsia, hyperventilation and dehydration. Stresses such as infection, inappropriate withdrawal of insulin, acute myocardial infarction or trauma are the commonest precipitants of DKA. In adolescents, omission of insulin is a common cause.

DKA is a medical emergency requiring specialist care. Management should generally be undertaken in hospital, however, it is important that treatment should be commenced as early as possible. Initial treatment includes rehydration using normal saline, and insulin replacement.

Fluids

The fluid deficit in adults is generally at least 3.5 to 7 litres. Sodium chloride 0.9% is usually the intravenous fluid of choice and over the first 2 hours should be given at a rate of 15 to 30 mL/kg per hour. The fluid infusion rate should be reduced to 7.5 mL/kg over the third and fourth hours and thereafter should be given according to further clinical assessment.

In children, rapid rehydration increases the risk of precipitating acute cerebral oedema, which has a high mortality rate. Replacement fluid is calculated according to body size and degree of dehydration, therefore urgent consultation with an expert in paediatric diabetes is essential. Refer to Diabetic ketoacidosis (DKA) in the chapter Paediatric implications.

Insulin

Only short-acting insulin should be used to treat DKA. The intravenous route is preferred if methods are available to regulate the infusion rate. Intravenous insulin therapy is commenced with an infusion at a rate of 2 to 6 units per hour. Close monitoring is required and a mechanical pump, syringe driver or at least a burette to deliver the infusion is recommended. The intramuscular route can be equally successful with 8 to 10 units given every hour. Note that intramuscular injection is not possible using an insulin syringe due to the short needle length.

Potassium

Total body potassium is depleted in DKA despite a normal or even elevated serum potassium level initially. Commencement of potassium therapy should be delayed until the initial serum level is known and adequacy of renal output has been established. Initial therapy should commence with potassium 20 mmol per hour at about the second hour. The infusion rate should thereafter be adjusted according to the serum potassium level, as follows:

if under 3 mmol/L, give 40 mmol/hour

if 3 to 4 mmol/L, give 30 mmol/hour

if 4 to 5 mmol/L, give 10 mmol/hour

if above 5 mmol/L, cease potassium infusion.

In the acute setting, non-standard potassium formulations may be required. Oral potassium replacement is not usually required after the DKA resolves.

Bicarbonate

Treatment with bicarbonate should be reserved for those patients with severe ketoacidosis and considered only if the pH is below 7 and creating an immediate cardiovascular risk. Sodium bicarbonate should be given as an infusion of 1 to 2 mmol/kg with strict attention to potassium levels, which may fall precipitately. The aim of this treatment is to reduce the immediate risks of extremely low pH, not to normalise pH. Use

Monitoring

Blood glucose determinations should be performed every hour. When the blood glucose level approaches 12 to 15 mmol/L, the rate of insulin infusion should be halved and insulin changed to the subcutaneous route if the intramuscular route has been used. Infusion fluid should be changed to glucose 5%. Blood glucose monitoring can usually be reduced to 4 hourly. Venous glucose and potassium status must be monitored at 2- to 4-hourly intervals initially.

Treatment of DKA also includes the thorough search for, and treatment of, any underlying infection or other precipitating factors.

Revised September 2004. ©Therapeutic Guidelines Limited (etg25demo, July 2008).