DKA

• Diabetic ketoacidosis (DKA) occurs as a consequence of inadequate insulin. The most common scenarios for diabetic ketoacidosis to occur are:

  • The initial presentation of type 1 diabetes
  • An existing type 1 diabetic who is unwell for another reason, often with an infection
  • An existing type 1 diabetic who is not adhering to their insulin regime
• The three key features are: 

  • Ketoacidosis
  • Dehydration 
  • Potassium imbalance
• Without insulin, the body’s cells cannot recognise glucose, even when there is plenty in the blood, so the liver starts producing ketones to use as fuel.
• High blood glucose levels (hyperglycaemia) overwhelm the kidneys, and glucose leaks into the urine. The glucose in the urine draws water out by osmotic diuresis. This causes increased urine production (polyuria) and results in severe dehydration. Dehydration results in excessive thirst (polydipsia).
• Insulin normally drives potassium into cells. Without insulin, potassium is not added to and stored in cells. The serum potassium can be high or normal as the kidneys 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, leading to fatal arrhythmias.
• DKA leads to metabolic acidosis with a low bicarbonate
• Presentation of DKA:

  • Polyuria
  • Polydipsia
  • Nausea and vomiting
  • Acetone smell to their breath
  • Dehydration 
  • Weight loss
  • Hypotension (low blood pressure)
  • Altered consciousness
  • Abdominal pain
• A diagnosis requires all three of:

  • Hyperglycaemia (blood glucose above 11 mmol/L)
  • Ketosis (blood ketones above 3 mmol/L or urinary ketones ++ or above)
  • Acidosis (pH below 7.3 or bicarbonate < 15)
• Patients in DKA can present with an acetone (pear drop) smell to their breath
• Management of DKA:

  • Fluids - IV fluid resuscitation with normal saline - most important intervention
  • Insulin - fixed rate insulin infusion - patients should continue their normal regime
  • Glucose - closely monitor and add a glucose infusion when less than 14 mmol/L
  • Potassium - add to IV fluids and monitor closely - insulin will cause low serum potassium
  • Treat underlying cause such as infection
  • Chart fluid balance
  • Monitor ketones
• The key complications during the treatment are:

  • Hypoglycaemia (low blood sugar)
  • Hypokalaemia (low potassium)
  • Cerebral oedema, particularly in children
  • Pulmonary oedema secondary to fluid overload or acute respiratory distress syndrome
• Clinical signs:

  • Tachycardia
  • Hypotension
  • Dehydration - sunken eyes, prolonged CRT, reduced skin turgor
  • Reduced urine output
  • Reduced GCS
  • Kussmaul breathing - deep sighing respiration
• Ketogenesis:

  • Normally occurs when there is an insufficient supply of glucose and glycogen stores are exhausted
  • Liver converts fatty acids to ketones
  • Ketones are water soluble fatty acids that can be used as fuel
  • Over time the glucose and ketone levels get higher - kidneys produce bicarbonate to buffer the ketone acids
  • Over time ketone acids use up the bicarbonate and the blood becomes acidic = ketoacidosis
• Cerebral oedema:

  • Children with DKA are high risk of developing
  • Dehydration and hyperglycaemia cause water to move from the intracellular space to the extracellular space - brain cells become dehydrated
  • Rapid correction of dehydration and hyperglycaemia causes a rapid shift in water into the intracellular space - brain becomes oedematous
  • Monitor GCS for signs - headaches, altered behaviours, bradycardia or changes to consciousness are concerning
• The main precipitants of DKA:

  • Infection: 30-40%
  • Non-compliance: 25%
  • Inappropriate dose alteration: 13%
  • New diagnosis of diabetes: 10-20%
  • Myocardial infarction: 1%
• Signs

  • Abdominal tenderness
  • Dehydration
  • Hypotension
  • Kussmaul breathing - deep rapid breathing to compensate for metabolic acidosis
  • Ketotic breath
  • Reduced consciousness
  • Coma
• One or more of the following parameters would warrant referral to a high-dependency unit

  • Blood ketone > 6 mmol/L
  • Bicarbonate level < 5 mmol/L
  • pH < 7.0
  • GCS ≤ 12
  • Systolic BP < 90 mmHg
  • Hypokalaemia on admission < 3.5 mmol/L
• Euglycaemic DKA:

  • Near-normal or normal blood glucose levels
  • Associated with higher mortality
  • May occur in the presence of exhausted glycogen stores e.g. protracted vomiting, alcohol use, malnutrition
  • Associated with SGLT-2 inhibitor use
• Fluid replacement:

  • Initial fluid choice is 0.9% normal saline
  • Should be given immediately
  • Typical fluid regimen =
  • 1L normal saline over 1 hour
  • 2L over 2 hours
  • 2L over 4 hours
  • At all times potassium replacement should be considered
• Insulin therapy:

  • Immediately start on a fixed rate IN insulin infusion
  • 0.1 units/kg/hr - infusion set up by mixing 50 units of short-acting insulin with 50ml of normal saline
  • When blood glucose levels fall < 14 - IV 10% dextrose over 8 hours
  • Continue patients long acting insulin
  • Fixed rate insulin should be continued until the ketones are less than 0.6, venous pH over 7.3 and/or bicarbonate over 18
• Potassium should be added to fluids if levels fall below 5.5
• Insulin infusion should not exceed 15ml/hr regardless of weight