Severe Symptomatic Hyponatremia Due to Syndrome of Inappropriate Antidiuretic Hormone From Mild Closed Head Trauma and Concussion

Abstract

We report the first published case of severe, symptomatic hyponatremia resulting from syndrome of inappropriate antidiuretic hormone (SIADH) incurred as the result of a blow to the head inducing a concussion without any additional signs of head injury. A 38-year-old male in excellent health suffered a fall from a tree causing a right leg fracture and blunt trauma to the head with concussion but no other signs of head injury. The patient was discharged several days after surgery for repair of his leg fracture and subsequently became severely ill with nausea, vomiting, headache, and seizures. He was readmitted with a serum sodium of 114 mEq/L (mmol/L) with a presumed diagnosis of dehydration. After several days of saline administration he was discharged, but within 24 hours he again experienced severe, symptomatic hyponatremia and was admitted for the third time with a serum sodium of 110 mEq/L (mmol/L). A diagnosis of SIADH was made, and the patient was successfully treated with fluid restriction, intravenous saline, and demeclocycline resulting in a full recovery without further incident. This case emphasizes the need to consider SIADH as a possible cause of severe hyponatremia in patients sustaining relatively minor closed head trauma.

The possible role of hydration in concussions and long-term symptoms of concussion for athletes. A review of the evidence

“…As with any fluid movement, the production of CSF will be impacted and governed by Starling's law for fluid movements along with hormone regulation of the permeability at the choroid plexus. 24,36,[49][50][51]53,58,59 Thereby, one can assume that the volume of CSF being produced is regulated by hormonal osmolarity regulation (i.e. antidiuretic hormone, aldosterone, angiotensin II), cation concentration (i.e.…”

“…In which increases in ANP induces additional fluid lost, that in turn triggers additional reductions in CSF that then triggers additional fluid loss and with reduced CSF an increased likelihood for amyloid accretion and accumulation. 24,36,51,58 The unfortunate effect of this limited recovery may be one of the possible culprits for the high incidence rates reported for neurodegenerative disease among athletes that have an extensive history of participation in contact sports. 17,19,21,[66][67][68]70,73 Additionally, there are aspects of fitness that not only impact the likelihood for suffering concussive injuries but also impact the acute recovery allowing for return to play.…”