Yosemite hyponatremia case
Hi Tami and Marty, I just spoke with Clark Coler, the internist whose father became profoundly hyponatremic and quite symptomatic while hiking recently in Yosemite. He has reviewed some of your articles in the literature and is anxious to learn more about this disorder. Dr. Coler and his father would be happy to discuss the details of their experience with you guys and has given permission for a case study report if appropriate. Dr. Coler states that his dad did not drink that much free water while hiking and suspects that SIADH was involved in the precipitous drop in serum sodium levels. Clark also noted that his father was getting significant volumes of normal saline in the ICU and was developing signs of CHF until Lasix was administered and he agrees that hypertonic saline would almost certainly have been a better choice, especially in an older patient. Dr. Coler's cell phone is (206) 499-3773. His email address is clark.coler@swedish.org. He will be happy to communicate with you two either by phone or email and can get you in touch with his dad as well. Gary

Thanks for your call and interest Gary. We would be pleased to contribute in any way we can and most interested to understand the aberrant physiology here. I've hiked all over with my sturdy old dad for years, though this trip had some "perfect storm" elements that may have contributed to his abrupt delirium.

He has mild diastolic dysfunction with a normal EF, but modest pulmonary HTN around 40mm. I had asked him to stop his low dose of cozaar/HCTZ and his low dose beta blocker (for HTN) during our most strenuous hiking days as I was concerned that his cardiac output is relatively fixed at age 86 with a paced rhythm and didn't want meds compromising his exercise tolerance further. We got caught unprepared in a summer rain storm and very hypothermic the night before as we arrived in Vogelzang. Coming down the mountain from 9-6PM he felt relatively well and maintained a steady slow pace all day. He drank three quarts of water at most over 9 hours. We moved too slowly to sweat and he had no other solute losses to my knowledge.

When he told me he felt unusually sleepy around 6PM, I proposed we rest a couple hours on the trail before finishing the last 2 miles. I left him for less than 5 minutes to get material to pad the trail and returned to find him quite confused, mumbling incoherently, and unable to follow any directions or respond purposefully. Thinking he was hypoglycemic, or simply exhausted, I built a fire and tucked him into the sleeping bag. When he showed no sign of improving over several hours I summoned help from the valley. I see a great deal of hyponatremic confusion states as a Hospitalist, but have never encountered such a brisk threshold between normal mentation and such profound impairment.

When he airlifted to Modesto 9 hours after the onset of the delirium he was not improved. He arrived there with a sodium 120. This was communicated to me in the Rangers office and was great news, as you can imagine, being reversible. When I arrived in Modesto at 1AM he had been inadvertently volume overloaded with saline, and quickly improved with a small lasix dose. His mentation at that time was clearly much improved at a sodium 123. As he recovered over the next week he developed a bad viral URI and is still far from his old self.

We thought a combination of total body salt depletion from HCTZ, extraordinary physical stresses of hypothermia and high altitude hiking, combined with a viral illness, all contributed together to a posterior pituitary that was vigorously favoring volume at the expense of osmolality. The normal mechanism in someone whose solutes are not being depleted would be to drop ADH production and pee off that free water as it is taken on.

We're very curious to understand what it is about these events that might promote an SIADH, since the AHD production here seemed clearly inappropriate. He is not other meds like SSRIs or opiates that would stimulate ADH, and has no edema forming states, endocrinopathy or neuroendocrine tumors (etc.) though I bet his BNP is high given the pulmonary HTN at baseline and this might promote some natiuresis.

Happy to contribute in any way we can.

Warm regards,

Clark