Macaulay Amechi Chukwukadibia Onuigbo
1,2,3*, Nneoma Agbasi
4, Emeka Joseph Amadi
3, Uchenna Chigozie Okeke
2, Abdul Khan
21 Mayo Clinic College of Medicine, Rochester, MN, USA
2 Department of Nephrology, Mayo Clinic Health System, Eau Claire, WI, USA
3 Department of Hospital Medicine, Mayo Clinic Health System, Eau Claire, WI, USA
4 North East London NHS Foundation Trust, United Kingdom
Abstract
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.
Implication for health policy/practice/research/medical education:
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.