Severe symptomatic acute hyponatremia in traumatic brain injury responded very rapidly to a single 15 mg dose of oral tolvaptan; a Mayo Clinic Health System hospital experience – need for caution with tolvaptan in younger patients with preserved renal function

Tolvaptan is now well established as a potent pharmaceutical agent for symptomatic hyponatremia from syndrome of inappropriate antidiuretic hormone secretion (siadh), congestive heart failure and liver cirrhosis. previous studies had recruited older (63-65 years) patients with mild renal impairment (serum creatinine, 1.3-1.4 mg/dl). a 2012 report in the journal of neurology, neurosurgery & psychiatry described tolvaptan as a “lifesaving drug”. a major outcome concern in the treatment of chronic hyponatremia is potentially fatal pontine demyelination from over-rapid correction of serum sodium >0.5 meq/dl/h. the maximum reported correction of serum sodium within 24 hours was 13 meq/l in a case of siadh. we recently experienced the dramatic correction of hyponatremia at 1 meq/dl/h over 18 hours, following 15 mg of oral tolvaptan in a 32-year old male patient with normal kidney function (serum creatinine 0.76 mg/dl), following traumatic brain injury (tbi). tolvaptan is indeed an effective and life-saving drug for post-tbi hyponatremia. however, we strongly recommend the use of lower doses of tolvaptan (≤15 mg/d) in younger patients with more preserved renal function to avoid the development of life-threatening pontine demyelination.