Hi, my name is Michael Matthews, and I'm the presenting author for Urea as Effective Treatment for Hyponatremia and Severe Traumatic Brain Injury. I am presenting this case along with Dr. Juan K. Rubin and Dr. Diane Mortimer from the University of Minnesota Department of Physical Medicine and Rehabilitation and Minneapolis VA Health Care System, respectively. This case involves a 71-year-old male with a significant past medical history consisting of diabetes mellitus type 2, hypertension, COPD, PTSD, and depression. This gentleman sustained a ground-level fall after slipping on ice in a parking lot. Witnesses of this fall found him seizing on the scene. Upon presentation to the emergency department, his CT imaging, which is shown below, demonstrated multiple subdural hemorrhages as well as a traumatic subarachnoid hemorrhage. He required an emergent left frontal temporal craniotomy. Postoperatively, he was found to be hyponatremic and was served on salt tablets. He presented to the acute rehab unit on post-injury day 11 and was receiving 2 grams of salt tablets three times per day. His serum sodium level upon presentation to the acute rehab unit was 134 milliequivalents per liter. His rehab course was extensive and complicated by several episodes of severe hyponatremia, which required a formal consultation from the nephrology team. With their expertise, this gentleman was started on therapeutic urea. Moving down the poster, we have provided the table, which reviews some common causes of hyponatremia within the traumatic brain injury population. We know that there is some controversy surrounding the diagnosis of cerebral salt wasting syndrome but feel it is necessary to compare and contrast this diagnosis with syndrome of inappropriate secretion of antidiuretic hormone, otherwise known as SIDH. More specifically, these two entities can be distinguished utilizing diagnostic data from urine osmolality, serum osmolality, and urine sodium concentrations. Moving to the middle column of the poster, we can see figure 1, which demonstrates serum sodium concentration on the y-axis along with time in days on the x-axis. Each plot represents an episode of hyponatremia that presented within the same patient during his inpatient rehab stay. Though these episodes were distinctly separate, each episode presented similarly in terms of diagnostic data and all pointed towards the diagnosis of SIDH. Each episode was also successfully treated with urea along with fluid restriction. During a stay, we were able to identify factors that could be contributing to this hyponatremia. Most notably, the patient suffered from an episode of diarrhea prior to and during the first episode of hyponatremia. The patient was also on an SSRI due to his history of PTSD and depression. It appears this patient may have been suffering from SIDH prior to his presenting injury and had never been diagnosed. Of course, this information was not available to us in real time. Along with salt tablets and fluid restriction, oral urea treatment allowed the patient to remain in the rehab unit without transfers for acute care. Certainly, this enhanced and expedited his recovery. A review of the literature will show that the prevalence of hyponatremia within the traumatic brain injury population varies. Rajagopal and his colleagues retrospectively looked at 1,500 patients suffering from TBI and found the prevalence of hyponatremia to be about 14%. A practical diagnostic approach requires urine sodium, serum sodium, serum osmolality, and urine osmolality values to make a proper diagnosis. Urea acts as an ineffective osmol and can lead to osmotic diuresis by pulling water from the intracellular space into the intravascular space. Typically, you will see urea used as a powdered form that can be mixed with water and taken orally. Its doses typically range from 15 grams once a day to 15 grams four times per day. An advantage of using urea to treat hyponatremia is that it will only increase serum sodium concentrations at three milliequivalents per liter within a 24-hour period. Thus, it reduces the risk of central pontine myelinolysis. Further studies elucidating the optimal duration and dosing for efficacy and safety is needed to further guide recommendations on the use of urea for the treatment of hyponatremia. It was my pleasure to be able to share this case with you. I would like to thank the University of Minnesota for sponsoring my rotation with the PM&R department, as well as my co-authors for their hard work and collaboration. Lastly, thank you so much for listening.

traumatic brain injury

hyponatremia

SIDH

urea treatment

optimal dosing