In patients with acute cerebral injury, polyuric states can potentially trigger, maintain and aggravate the primary neurological damage, due to hypovolemia, arterial hypotension and alterations of osmolarity. The true incidence of the condition in this population is unknown. A widely validated definition of polyuric state is lacking and its etiology is multifactorial. There are two principal classes of polyuria: (a) aqueous polyuria with diabetes insipidus as the main cause; and (b) osmotic polyuria in which sodium, glucose or ureaplay the main role. Polyuric states are in close association with disorders of water and sodium metabolism and with alterations in acid-base balance. A detailed analysis of the history, clinical picture and simple laboratory determinations in blood and urine, are required for an adequate assessment of these polyuric states. The problem must be faced with pathophysiological reasoning and a systematic and sequential approach, because each disorder needs a specific therapy.
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