Tag: Dysnatremias

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What causes hyponatremia in marathon runners

Me, running the NYC Marathon

One of the first blog posts ever on PBFluids was a review of Almond Et al’s study of hyponatremia. With this year’s Boston Marathon now complete I have re-reviewed the subject.

The Almond study was high profile and did a good job of demonstrating the risk factors for marathon induced hyponatremia. (See this post for a review) However some of the findings were self evident: increased weight gain was associated with hyponatremia. What is not answered is, why those who developed hyponatremia gained 3 liters of water. Why didn’t these patients just urinate the excess water? Normally, a falling sodium, shuts down ADH like a bordello on Easter. The retention of water is indirect evidence of ADH. Could it be that marathon running and ultra-endurance events could be added to the list of causes of the Syndrome of Anti Diuretic Hormone (SIADH).

It would have been nice to see a U/A or urine osmolality in Almond’s data to confirm this.

Siegel et al. (PDF) has done the most detailed study I am aware of on exercise induced hyponatremia. They did detailed biochemical assessments on 39 runners in the 2001 Boston Marathon. They drew pre-race (day before) and post-race (within 2 hous of finishing) samples for:

  • CPK
  • IL-6
  • ADH (vasopressin)
  • cortisol
  • prolactin
  • CRP

They also looked at 308 runners who collapsed during the 2004 Boston Marathon and measured:

  • IL-6
  • ADH (vasopressin)

Additionally they did some blood tests on 2 runners who had died of cerebral edema from exercise induced hyponatremia. One from the 2002 Marine marathon and the other from the 2002 Boston Marathon.

The normal patients had spikes in their CPK from 150 to 2,323. They also had a doubling of cortisol and prolactin but no change in ADH levels. The rise in CPK was matched by increases in IL-6 followed by an increase in CRP.

Of the 308 collapsed runners only 16 had hyponatremia. All of the hyponatremic runners reported a lack of urination during the race. 7 of the 16 had inappropriately high ADH levels in the blood. The authors concluded that lack of urination (though only driven by ADH in half the patients) rather than fluid loading was the predominant cause of hyponatremia.

The article then describes the laboratory and clinical scenario surrounding the two deaths in 2002. The data is summarized in the following table:

Importantly, both patients were initially treated with 150 mL/hr of normal saline without improvement. Two years later, two patients presented with similar symptoms and responded well to 3% saline:
The primary conclusions from this study, which admittedly is a bit schizophrenic with numerous anecdotal reports from various populations, is that exercise induced hyponatremia is not due to sodium loss but rather from fluid retention. Some of this fluid retention is driven by ADH and hence introduces exercise induced hyponatremia as a novel cause of SIADH. The diagnosis of SIADH is backed up by elevated urine sodium, elevated urine osmolality and normal (or high in the case of cortisol) cortsiol and TSH levels.

The elevated urinary sodium levels (consistent with SIADH) are a critical fact in the etiology of hyponatremia. If we were dealing with hypovolemia (commonly, but erroneously, referred to as dehydration), a cause of hyponatremia, one would expect a low urine sodium (usually less than 10 but always less than 20). The high urine sodium means that these patients were not volume depleted, It was not loss of sodium through the sweat which lead to the low sodium. This means that changing the sodium content of sport drinks is unlikely to prevent the complication.

The authors point out NSAIDs (ibuprofen, Motrin, Advil, naproxen) enhance renal response to ADH and should be avoided in the 24-hours prior to a race.

The authors recommend treating acute symptomatic hyponatremia from a marathon with 3% saline 1 mL/kg/hr to raise serum sodium 4-6 mEq/L and then to slow the rate to target 12 mEq/L in the first 24 hours of therapy. Just as is in all cases of SIADH 0.9% saline may not improve the serum Na.

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William Schwartz, the co-discoverer of SIADH has died

William Schwartz has died.

Every Monday at noon during fellowship we had the fluid and electrolyte conference with Dr. Fred Coe. Dr. Coe has extra-sensory powers for electrolytes. When you presented, you would give just the electrolytes and he would re-create the entire case from the metabolic panel. During the lecture he would ask you to explain a certain pathophysiology and then excoriate you if your thoughts were lazy and poorly organized.

If you ever blamed a poorly characterized hyponatremia on SIADH, Dr. Coe would look at you and ask “If Bartter and Schwartz were here, at this table, right now, and were looking at the same data that you have provided, would they agree that this is SIADH? Would they?”

JASN re-printed the original 1957 article describing SIADH in 2001.

Goodbye Dr. Schwartz, yours are the shoulders we stand-on in the daily grind of clinical nephrology.

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Lecture at Providence Hospital on Electrolytes

I am trying to do a monthly lecture for the Providence internal medicine residents on electrolytes. I gave my second one last Friday. It was an interesting case we had of hypernatremia on the consult service last summer.

I did this lecture in Keynote and I am blown away by how good it presents through SlideShare. Really impressive.

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iPhone Medical Applications

I have four medical applications on my iPhone, of which I use two. Here is a quick review.

To show how the iPhone equipped physician approaches clinical problems I will use the DB’s Medical Rants most recent acid-base problem. He presents a case with the following information:

49-year-old man, previously in good health, presents after a few weeks of progressive weakness and dizziness. He admits to polyuria. Your job is to extensively discuss his lab tests.

The first step in my mind is to fully interpret the ABG. To do this we will use the application ABG.

ABG

This simply named program is an ABG calculator that runs through the standard algorithms for detecting multiple primary acid-base abnormalities. Can’t remember Winter’s Formula. As long as you don’t have boards coming up you can just plug’n chug and turn DB’s ABG into the following:

This does two of the calculations that DB describes at length:

  1. Winter’s formula (16 * 1.5 + 8 ±2) shows that the predicted pCO2 is 30-34. The patient’s CO2 is 33 so the patient has isolated and appropriately compensated pCO2 of 33. ABG displays this information in the second line when it describes the acid-base disorder as “Compensated metabolic acidosis.” It does not describe a second primary condition such as respiratory acidosis or alkalosis.
  2. Gap-Gap or delat-delta. The patient has a dramatically elevated anion gap at 27 (15 over the upper limit of normal of 12) but his bicarb of 16 is only 8 below normal. The difference between the delta gap and the delta anion gap is 7 (15-8) when this is added to the normal bicarbonate you get 31; so the patient had a pre-existing metabolic alkalosis with a bicarbonate of 31. ABG displays this information as the corrected bicarbonate.

The next step is adjusting his sodium for the hyperglycemia. To do this we will use Mediquations though Medical  Calc works just as well.

Mediquations
DB, in his discussion, states that he has unpublished data proving that no formula is effective at adjusting the serum sodium for the hyperglycemia. For those of us without his unpublished data should adjust the sodium using Katz’s traditional conversion (pdf of a letter to JAMA discussing adjusting sodium for hyperglycemia in DKA. Katz’s original conversion was discussed in a letter to the NEJM) of a drop in Na of 1.6 for every 100 the glucose is over 100 mg/dL. Nephrology fellows should additionally be aware of Hillier’s data showing the sodium falling 2.4 for every 100 of glucose. Both Mediquations and Medical calculator adjust the sodium using Katz’s conversion.

Of coarse you wouldn’t know it was Katz’s conversion because even if you tap on “More Info,” Mediquation does not provide the reference. Likewise you will not get the reference with Medical Calc.

Though DB did not explore free water defecits in his discussion of the case this is a clinically relevent point. You can use Mediquation to calculate the water deficit.


I feel that using ABG and Mediquations will make you a more effective physician without forcing you to memorize equations used only periodically.
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Teaching Medical Students


Last Friday I started teaching third year medical students. This is the first time I have taught medical students (in isolation, there are always medical students at my lectures for the residents) since 2003, when I ran a teaching section for renal physiology for first year medical students at Pritzker School of Medicine, University of Chicago with John Asplin.

I am now teaching the medical students two lectures every rotation, the first on sodium and the second on potassium and calcium. I hope to expand this to ABGs and another electrolyte lecture so I can isolate potassium and spend an entire hour on it.

I modified my Don’t Panic handout for the students. During the lecture I realized that the SIADH section was weak and too complex for the students. I will probably change it to focus on the fact that ADH reduces water excretion and that this can be adaptive (early CHF, volume depletion, hyperosmolar) or maladaptive (SIADH). I will change the section on the dilution of urine to a background box as I think it is important but only interesting to nephrologists and similar wierdos.

I will add a focus on a few clinical scenarios with increased ADH.

I still need to expand the hypernatremia section.

Handout
iPhone version

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Sodium and Potassium for ER residents


Yesterday I lectured the St John ER residency program. The ER residency has an impressive commitment to education. They set aside a half day every wednesday for their resident to get dedicated didactic time. They have great attendance with a good number of attendings showing up.

I have been asked to give three lectures and yesterday was the first. I gave a double lecture (running time about 90 minutes) on sodium and potassium. The fact that I could run over the standard 50 minute alotment normally given for medicial education is due to the fact that they have blocked an entire afternoon rather than try to shoehorn a lecture into lunch or before rounds.

The sodium lecture was the first time I used the Sodium handout I created for the St John IM residents. I gave the lectuer Seder-Style with the residents reading different sections, answering questions and me adding commentary. The ER residents are smart and empowered to ask questions. I felt that there was great two-way interactivity.

Dont Panic Sodium

Sodium iPhone format
Sodium booklet format

The potassium lectuer is an abrdged potassium lecture which is stripped to the bare bones of differential and treatment. It is a traditional powerpoint lecture. Immediately when I started this lectuer I saw about half a dozen exhausted interns fall asleep. My next project is to create a potassium haggadah.

Potassium powerpoint

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The Acid-Base lecture for the residents of St John Hospital


Today I gave my second lecture of the year for the St John Residency.

I used my Acid-Base workshop handout and added a slide show to facilitate the large group.

I still called on individual residents to answer questions to keep them involved.

I started the lecture with some audience participation. My previous lecture on IV Fluids, diuretics and dysnatremias began with me stating how ubiquitous these subjects were.

I had everyone stand then I asked people to sit down if, in the last three weeks they had not:

  • Used any diuretics: no one sat down
  • Used any IV diuretics: about half a dozen people sat down
  • Used a thiazide diuretic to counter the effect of loop diuretic resistance: lost a lot of people there but still had about a dozen left
  • Used a lasix drip to counter loop diuretic resistance from heart failure: everybody sat down but about 3 residents and the amazing Dr. Dhungel, my first year fellow on the consult service.
  • Used torsemide instead of furosemide for better pharmacokinetics: only Dr Dhungel remained standing.

I then tried to repeat the excercise for IV fluids and dysnatremias but it didn’t work very well. Should have quit after the first one.

When I gave that IV Fluids, diuretics and dysnatremias lecture I didn’t have a hand out. In the last three weeks I have worked up a handout:

iPhone version
Booklet form