Diabetes insipidus occurs due to insufficient secretion (neurogenic) of, or insensitivity (nephrogenic) to Antidiuretic Hormone (ADH). ADH is synthesised in the supraoptic and paraventricular nuclei of the hypothalamus. It is then transported to the posterior pituitary gland where it is stored prior to release. The main action of ADH is the regulation of the expression of the Aquaporin 2 (V2) channel in the collecting ducts of the nephron, which controls permeability to water. Therefore, in the absence of ADH, the nephron loses its ability to concentrate urine resulting in a large volume diuresis and subsequent intravascular volume loss, electrolyte imbalance and cardiovascular instability [4].
Neurogenic Diabetes insipidus is most often caused by trauma to the hypothalamus or posterior pituitary either directly during a traumatic brain injury or indirectly from the mass effect of raised ICP. Diagnosis is usually confirmed by the reduction in urine output response to 1-2mcg boluses of Desmopressin. Repeated doses or an infusion of Arginine Vasopressin are often required to maintain cardiovascular and plasma electrolyte/osmolarity stability [4].
