5th April 2024

Management

Acute hypernatraemia with onset over hours can be corrected rapidly using dextrose 5% and normal saline. The usual rate is 3-6ml/kg/hour with regular monitoring of serum sodium concentrations. Once serum sodium is below 145 mmol/L the infusion rate should be reduced to 1ml/kg/hour to restore sodium concentrations around 140 mmol/L. 

In chronic hypernatraemia, present longer than 48 hours, 5% dextrose fluids are used with the aim to lower sodium concentrations by 10 mmol/L over a 24-hour period.

Diabetes insipidus

Diabetes insipidus (DI) is characterised by hypernatraemia, polydipsia, polyuria and inappropriately dilute urine. Cranial DI is due to a lack of production of arginine vasopressin (AVP), also known as antidiuretic hormone (ADH). Nephrogenic DI occurs from a lack of response to AVP. The hormone is secreted from the posterior pituitary and acts at the distal convoluted tubule and collecting ducts of the nephron to increase water reabsorption.  

Causes of cranial DI include:

• Pituitary surgery
• Craniopharyngioma
• Traumatic brain injury
• Subarachnoid haemorrhage 
• Wolfram syndrome 

Risk factors for nephrogenic DI include:

• Lithium therapy
• Chronic kidney disease
• Chronic hypercalcaemia or hypokalemia

Initial investigations include serum and urine sodium testing, water deprivation test and MRI brain where cranial DI is suspected.

Water deprivation test

This is also called the desmopressin stimulation test (see table below) and can distinguish between psychogenic polydipsia, cranial and nephrogenic DI. Patients are advised to avoid fluids up to eight hours before the test, following which urine osmolality is measured. 

In primary polydipsia, water deprivation alone causes urine osmolality to be high and desmopressin need not be given as the high urine osmolality rules out diabetes insipidus. Administration of desmopressin in primary polydipsia has little effect on urine osmolality. 

Where the urine osmolality is low, synthetic desmopressin (DDAVP) is administered either 20 mcg intranasally or 2 ug intramuscularly and urine osmolality remeasured. 

In cranial DI, where the patient lacks AVP, administration of desmopressin causes water reabsorption by the kidneys and an increase in urine osmolality. In nephrogenic DI, the urine osmolality will remain low before and after desmopressin administration as the kidneys are unable to respond to desmopressin. 

The water deprivation test

Management for cranial DI includes administration of desmopressin. Nephrogenic DI is treated with dietary salt restriction, diuretics and adequate fluid intake.