Central diabetes insipidus (DI) is a disorder of disrupted water homeostasis characterized by the excretion of large quantities of dilute urine. It is caused by an underlying impairment in total body water balance regulation due to decreased secretion of antidiuretic hormone (ADH) as a result of dysfunction in the hypothalamus and pituitary gland.

Patients will most commonly present with polyuria and polydipsia. Other symptoms include waking at night to urinate and bed-wetting. Patients without free access to water will develop symptomatic hypernatremia. Infants may present with inconsolable crying, irritability, growth retardation, hyperthermia, and weight loss. Children may present with fatigue, anorexia, enuresis, and growth defects.

In adults, the most common cause of central DI is as a complication of neurosurgical intervention with subsequent damage to the hypothalamic-neurohypophyseal pathway. This injury is usually transient and resolves within several days. In addition to neurosurgical intervention and secondary injury, traumatic brain injury, cerebral hemorrhage, or autoimmune, vascular, and infiltrative diseases involving the brain can result in central DI.

In pediatric patients, central DI is typically attributed to an inheritable etiology.

Three other forms of DI include nephrogenic DI, gestational DI, and primary polydipsia (dipsogenic DI). Both gestational DI and dipsogenic DI are caused by vasopressin deficiencies, not by a defect in the neurohypophysis or kidneys. Gestational DI occurs in pregnancy when a placental enzyme terminates ADH in the mother. Dipsogenic DI is caused by excessive intake of fluids. This may result from damage to the hypothalamus or mental illness.

Related topic: Diabetes insipidus