Diabetes insipidus (DI) is a clinical syndrome characterised by inappropriate hypotonic polyuria. Urine flow rates in excess of 40 mL/kg per 24 h in adults, or more than 100 mL/kg per 24 h in infants are suggestive of diabetes insipidus. Correct diagnosis often requires the use of the water deprivation test. DI may be central or nephrogenic, and results in inappropriate renal water loss. The majority of patients with DI are able to maintain a normal plasma sodium even in the absence of treatment, as their intact thirst mechanism allows them to maintain a sufficient fluid intake to compensate for excessive urinary losses. However, if their thirst sensation is impaired, for example through the presence of a comorbid condition such as a head injury, hypernatraemia will rapidly develop. In the rare condition of adipsic DI, the patient has both a vasopressin secretory defect and an impaired thirst mechanism, commonly resulting in hypernatraemia. Hypernatraemia has multiple adverse physiological effects, predominantly due to the movement of water from cells to the extracellular space, leading to cell shrinkage. If central DI is present then ddAVP (synthetic, long acting vasopressin) treatment needs to be immediately instigated, as well as correction of the patients volume depletion. Acute central diabetes insipidus is frequently seen in neurosurgical patients. The majority of cases are transient and so a single parenteral (subcutaneous or intramuscular) dose of ddAVP, which is active for six to twelve hours, may be sufficient to provoke antidiuresis and eliminate polyuria. Management of adipsic DI is challenging and requires patients to comply with a strict fluid intake regime. Nephrogenic DI is often medication related and responds to withdrawal of the offending agent. In this session we will examine management challenges relating to diabetes insipidus and potential pitfalls for the clinician to avoid.