Urine Output Control in Central Diabetes Insipidus with Severe Hypernatremia After Traumatic Brain Injury: A Case Report

Introduction: Central diabetes insipidus (CDI) is a secondary injury complication of traumatic brain injury (TBI). Neurohypophysis injury causes posterior pituitary insufficiency to secrete arginine vasopressin (AVP) in hyperosmolality condition, lead to hypovolemic hypernatremia thus increasing mortality and morbidity. Prevalence of hypernatremia in TBI patient is more than 35% with possible causes of dehydration and hypovolemia and mortality rate 86.8%. Case Presentation: We reported a case of a 20-year-old man with CDI and severe hypernatremia post TBI. He underwent ventriculoperitoneal shunt surgery and admitted to intensive care unit post operative. Patient showed polyuria with urine output 3.2 ml/kg/hour with a sodium level of 190 mmol/L. Hypernatremia correction with KA-EN 3B intravenously and oral fluid intake was given to replace free water deficit. Oral desmopressin was given to compensate AVP deficiency to reducing ongoing fluid loss. A good response was achieved on the second day of treatment, indicated by a decrease in urine output to 1.4 mL/kg/hour and decrease in sodium levels with target 10-12 mEq/L/day. No side effects of desmopressin found in this patient. Our case shows that close monitoring and appropriate therapy result in good outcomes in CDI patients with severe hypernatremia post TBI. Conclusion: Patients with CDI and severe hypernatremia after TBI responded well after receiving desmopressin therapy to treat AVP deficiency, as well as fluid replacement with KA-EN 3B and oral intake according to free water deficit. Keywords: traumatic brain injury, central diabetes insipidus, severe hypernatremia, polyuria