Tolvaptan, an oral antagonist of the vasopressin V2 receptor, has been found to improve hyponatremia in patients with SIAD. We report the case of a 65-years-old male, who developed recurrent episodes of hyponatremia after severe traumatic brain injury, TBI, with polytrauma (CGS=8, decompressive craniectomy, spontaneous breathing by percutaneous tracheotomy). During hospitalization in intensive care unit he resumed alertness and received i.v. hypertonic saline infusion and oral fludrocortisone therapy for hyponatremia. At admission to the intensive rehabilitation unit (1 month after TBI) he was on fludrocortisone therapy and i.v. sodium supplementation, and presented an extremely severe disability (Functional Independence Measure, FIM=18/126; Disability Rating Scale, DRS=21/30; Levels of Cognitive Functioning, LCF=3/8), needing enteral nutrition. After discontinuing sodium supplementation, hyponatremia recurred (125 mEq/l); at the same time the patient underwent ventriculo-peritoneal shunt for hydrocephalus and presented seizures requiring antiepileptic drug (levetiracetam). Serum sodium continued to fluctuate for 2 months, despite fludrocortisone therapy, prolonged sodium supplementation (i.v. or enteral) and/or water restriction. Hypoadrenalism and hypothyroidism were excluded and SIAD was diagnosed, after endocrinologist consultation. Sodium returned to normal values and remained stable for 3 months. A sudden drop in sodium levels again required hypertonic saline infusion. Diagnosis of SIAD was confirmed and therapy with oral tolvaptan was started (SAMSCA 15 mg/die for one month, then 7.5 mg/die). Serum sodium rose to >135 mEq/l in three days and remained stable throughout treatment for five months until now. No side effects were observed, seizures disappeared, antihypertensive drugs were discontinued due to normal blood pressure levels. At discharge from inpatient rehabilitation, cognitive and motor functioning scales improved (FIM=35, DRS=16, LCF=4), but the patient still presented severe disability. This case demonstrates that tolvaptan is safe and effective in the treatment of hyponatremia due to SIAD after severe TBI.

Efficacy of tolvaptan treatment in a patient with syndrome of inappropriate antidiuresis (SIAD) after severe traumatic brain injury

BONDANELLI, Marta;MALASPINA, Alessandra;AMBROSIO, Maria Rosaria;LAVEZZI, Susanna;BASAGLIA, Nino;ZATELLI, Maria Chiara;DEGLI UBERTI, Ettore
2012

Abstract

Tolvaptan, an oral antagonist of the vasopressin V2 receptor, has been found to improve hyponatremia in patients with SIAD. We report the case of a 65-years-old male, who developed recurrent episodes of hyponatremia after severe traumatic brain injury, TBI, with polytrauma (CGS=8, decompressive craniectomy, spontaneous breathing by percutaneous tracheotomy). During hospitalization in intensive care unit he resumed alertness and received i.v. hypertonic saline infusion and oral fludrocortisone therapy for hyponatremia. At admission to the intensive rehabilitation unit (1 month after TBI) he was on fludrocortisone therapy and i.v. sodium supplementation, and presented an extremely severe disability (Functional Independence Measure, FIM=18/126; Disability Rating Scale, DRS=21/30; Levels of Cognitive Functioning, LCF=3/8), needing enteral nutrition. After discontinuing sodium supplementation, hyponatremia recurred (125 mEq/l); at the same time the patient underwent ventriculo-peritoneal shunt for hydrocephalus and presented seizures requiring antiepileptic drug (levetiracetam). Serum sodium continued to fluctuate for 2 months, despite fludrocortisone therapy, prolonged sodium supplementation (i.v. or enteral) and/or water restriction. Hypoadrenalism and hypothyroidism were excluded and SIAD was diagnosed, after endocrinologist consultation. Sodium returned to normal values and remained stable for 3 months. A sudden drop in sodium levels again required hypertonic saline infusion. Diagnosis of SIAD was confirmed and therapy with oral tolvaptan was started (SAMSCA 15 mg/die for one month, then 7.5 mg/die). Serum sodium rose to >135 mEq/l in three days and remained stable throughout treatment for five months until now. No side effects were observed, seizures disappeared, antihypertensive drugs were discontinued due to normal blood pressure levels. At discharge from inpatient rehabilitation, cognitive and motor functioning scales improved (FIM=35, DRS=16, LCF=4), but the patient still presented severe disability. This case demonstrates that tolvaptan is safe and effective in the treatment of hyponatremia due to SIAD after severe TBI.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/1685292
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