Endocrine Abstracts

We present a case of a 70-year-old female patient without comorbidities who was admitted to our institution following head trauma leading to subsequent subarachnoid hemorrhage and vertigo. Conservative management was implemented successfully. Throughout the hospitalization, lab monitoring revealed the emergence of hyponatremia which was corrected by fluid restriction and hypertonic solution administration. The patient was discharged without residual vertiginous complications. Shortly post-discharge, the patient presented to the emergency department manifesting severe hyponatremia (116 mmol/l). Diagnostic investigations revealed reduced plasma osmolality alongside normal urine osmolality and normal sodium urine levels with normal TSH and cortisol values. Notably the absence of chronic therapy and urine sodium concentration >50 mmol/l further underscored the diagnosis of Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) due to head injury. Because of prolonged duration of SIADH, which was more than a month since the head injury and without improvement with time which would be expected, we also did thorough work up to exclude other causes of SIADH, including neoplastic process. Patient continued check-ups and despite corrective measures (dietary intervention with increase solute intake and increase of oral sodium chloride) repeatedly had decrease in serum sodium concentration and was repeatedly hospitalized, with the latest admission to the Nephrology Department. Dietary interventions coupled with fluid restriction and parenteral administration of hypertonic solution were implemented in successfully correcting severe symptomatic euvolemic hyponatremia. The follow-ups were then continued via the Nephrology outpatient clinic. Despite adhering to dietary recommendations and fluid intake restrictions, the patient persisted in experiencing hyponatremic episodes with moderate to severe vertiginous symptoms. Consequently a decision was made to introduce a selective Oral Vasopressin V2-Receptor Antagonist into the therapeutic regimen, specifically tolvaptan at 15 mg once daily. The initiation of tolvaptan was conducted with the approval from the Hospital Committee for Medicinal Products. Following the commencement of this targeted therapy normonatremia was consistently maintained, with transient occurrences of mild hypernatremia leading to brief interruptions in tolvaptan administration which then led to hyponatremic relapses. Since the initiation of tolvaptan, the patient has remained free from hospitalization. Regular checkups including electrolyte levels, liver function parameters, renal function and body weight are conducted via Nephrology clinic. To date, the patient has exhibited no noteworth, adverse effects associated with tolvaptan treatment. Despite existing controvers, in using vasopressin receptor antagonists in treatment of chronic hyponatremia we wanted to present case in which prolonged posttraumatic SIADH was successfully managed using tolvaptan.