Endocrine Abstracts

Disorders of salt and water homeostasis are common following traumatic brain injury. Diabetes insipidus is a well-recognized complication of TBI. Polyuria occurs immediately after significant brain injury in up to 22% of cases, nearly always occurring within the first 2–3 days. The great majority of cases resolve spontaneously, and cross-sectional studies of long-term survivors of TBI report low rates of chronic diabetes insipidus. It is likely that in the absence of formal diagnostic assessment of AVP secretion, many patients with “subclinical” diabetes insipidus remain undiagnosed and maintain normal plasma osmolality through increased water intake.

Approximately 15% of patients recovering from TBI develop hyponatremia in the acute recovery phase. In over 80% of these cases, hyponatremia is due to SIADH. The natural history is for resolution of hyponatremia after recovery from the neurological acute insult. Although ACTH deficiency may occur in the acute recovery phase of TBI, hyponatremia is only rarely due to glucocorticoid deficiency in this context, but cases do occur and a high index of suspicion is required.

This talk will discuss the clinical management of neurohypophseal disorders following traumatic brain injury.