T1DM/DKA
Cards (8)
- Patients with type 1 diabetes are more likely to develop:
- Autoimmune thyroid disease
- Coeliac disease
- Primary adrenal insufficiency (Addison’s disease)
- Vitiligo
- Pernicious anaemia
- About 25 – 50% of new type 1 diabetic children present in diabetic ketoacidosis (DKA).
- Less typical presentations include secondary enuresis (bedwetting in a previously dry child) and recurrent infections.
- The management of DKA in paediatric patients differs to that in adults due to the higher risk of developing cerebral oedema in the rehydration phase of treatment
- Cerebral oedema:
- Dehydration and hyperglycaeia cause water to move from the intracellular space in the brain to the extracellular space - brain cells become dehydrated
- Correction of dehydration and hyperglycaemia causes a fall in the extracellular osmolarity and a shift in the water from the extracellular space to the intracellular space in the brain cells
- Causes the brain to swell and become oedematous - brain cell death
- Neurological observations need to be monitored very closely
- Signs of cerebral oedema:
- Headache
- Irritability
- Bradycardia or other signs of raised ICP
- Reduced GCS
- Falling sodium levels
- General management:
- If patient shocked - 10ml/kg bolus NS stat
- If not shocked - 10ml/kg bolus NS over 30 mins
- Then calculate remainder of fluid deficit and correct over 48 hours (mild/moderate = 5%, severe = 10%)
- Fluid requirements is fluid deficit + maintenance fluids - potassium is added at this point
- Fixed rate insulin infusion (0.05-0.1 units/kg/hr) is started 1-2 hours after starting IV fluids
- Other important principles:
- Treat underlying triggers (e.g., antibiotics for bacterial infections)
- Prevent hypoglycaemia with IV glucose once the blood glucose falls below 14mmol/l
- Include potassium in IV fluids (40 mmol/litre) and monitor serum potassium closely
- Monitor for signs of cerebral oedema
- Monitor glucose, ketones and pH to assess progress and determine when to switch to subcutaneous insulin