Sequential cerebral salt wasting complicating SIADH in a patient following head trauma

Abstract

We report a 67-year-old female who presented with progressively symptomatic hyponatremia due to the SIADH secretion complicating TBI and neurosurgical intervention. She responded initially to fluid restriction, 3% NaCl infusion and oral NaCl tablets. Nevertheless, by hospital day 8, she had quickly developed polyuria, dumping over 3 liters of urine in the first 4-6 hours of that morning with rapid recurrence of hyponatremia, again. She was, this time, diagnosed with CSW and was managed differently with 0.9% NaCl volume expansion. To our knowledge, this is the first case of the sequential development of symptomatic hyponatremia from SIADH followed by the development of hyponatremia from CSW in the same patient during the same admission. Furthermore, our case further highlighted the contrarian observation that with a high index of suspicion for CSW and its early diagnosis, volume depletion and hypovolemia from polyuria may not be a distinguishing presenting factor, when contrasted with SIADH.Please cite this paper as: Onuigbo MAC, Agbasi N, Amadi EJ, Okeke UC, Khan A. Sequential cerebral salt wasting complicating SIADH in a patient following head trauma. J Renal Inj Prev. 2018;7(1):49-52. DOI: 10.15171/jrip.2018.12. Hyponatremia is the most commonly encountered dyselectrolytemia following head trauma. The two main mechanisms responsible for non-iatrogenic hyponatremia are cerebral salt wasting (CSW) syndrome and the syndrome of inappropriate antidiuretic hormone secretion (SIADH). SIADH is the commonest dyselectrolytemia cause of hyponatremia following traumatic brain injury (TBI) whereas CSW is the most elusive and challenging diagnosis of the causes of hyponatremia from intracranial causes. The need to distinguish between CSW and SIADH is critical because the management of CSW is volume restitution and sodium restoration whereas for SIADH, the management is exact opposite -water restriction. Our recent experience with a 67-year old Caucasian female post-TBI illustrated very interesting observations. To our knowledge, this is the first case of the sequential development of symptomatic hyponatremia from SIADH followed by the development of hyponatremia from CSW in the same patient during the same admission. Furthermore, our case further highlighted the contrarian observation that with a high index of suspicion for CSW and its early diagnosis, volume depletion and hypovolemia from polyuria may not be a distinguishing presenting factor, when contrasted with SIADH.