musings of a salt whisperer
Sodium including electrolyte free water (Keynote, Powerpoint PDF)
This is an older version of my hyponatremia lecture. This lecture has gone through various versions and though I like my most current version, others may like older variations better. Additionally the Keynote version (2014) is similar but not identical to the Powerpoint version (2013).
At Lankenau Medical Center in Philadelphia at 8:00 AM, January 12. I will be talking about Spooky Sodium 👻.
Here is the title slide
If you can’t make it, first of all, what’s wrong with you? But second of all don’t worry, you can get the high points from the man who discovered them in this 13 minute TedX Talk from Vanderbilt.
And from this article in the NYT
And a deep dive in this lecture at Indiana University by Jans Titze’s collaboratorDr. Fred Left.
And don’t forget about the excellent NephJC coverage, including an editorial from Rodby.
I will eventually post a slidecast of my presentation.
My work-shop on sodium includes a bit on all the cases of hyponatremia due to fraternity hazing.
I also include the crazy case of Jennifer Strange.
But I had never heard of idiot induced hypernatremia until this case report:
A nineteen year old male drank a quart sized bottle of soy sauce on a bet.
Two hours later he was brought to the ER comatose and seizing. His sodium was 177. They initiated hypotonic fluids and arranged transfer to a tertiary care center. At the tertiary care center the sodium was still higher at 191. The doctors then changed the fluids to D5W at 12,000 mL per hour. They gave 6 liters of D5W in 30 minutes.
After the infusion he opened his eyes and regained spontaneous movement. He was discharged on hospital day four neurologically intact with only some minor abnormalities on the head MRI, all attributed to postictal changes.
How high is a sodium of 191? MedCalc will not even accept it as a possible sodium concentration:
A couple items of note:
Some nerdery about the sodium exposure: He drank a quart of soy sauce. A quart is 946 mL. The article states that soy sauce is 17-18% sodium chloride. Here are some meta calculations, in case you are interested:
Update from Twitter:
@kidney_boy I would guess they used a pressure bag or infuser (e.g. Trauma 1) to get in a L every 5 min
— Seth Trueger (@MDaware) June 10, 2013
@mdaware @kidney_boyA good 14 ga 1.75 inch peripheral IV can do 333 cc/min with a 1 meter pressure head to gravity.
— philroman (@philroman) June 11, 2013
@kidney_boy I’ve seen 216 before. Started at 196, rose more with initial NS administration. Kid with ichthyosis, and bad dehydration.
— Ken Tegtmeyer (@pccm_doc) June 11, 2013
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| A series of sodiums from 176-188 mmol/L |
Those are not glucoses. They are Sodiums. And, except for maybe an infant with congenital adrenal hyperplasia when I was a resident, those are the highest sodiums I have ever seen.
The primary management concern was the speed of correction. The first Na at 188 was drawn at 4:32 pm. Four hours later it was 177, a change of 11 mEq. Too fast. Here is the salient section from UpToDate:
Rate of correction in chronic hypernatremia — There are no definitive clinical trials, but data in children (particularly infants) suggest that the maximum safe rate at which the serum sodium concentration should be lowered in patients with chronic hypernatremia is 12 meq/L per day. To be safe, we suggest a maximum rate of correction of the serum sodium of 10 meq/L per day in patients who have had hypernatremia for at least 24 hours. The following findings provide support for this conclusion:
- A retrospective case control study included 97 children with hypernatremia and dehydration; the mean baseline serum sodium was 165 meq/L. The rate of reduction in serum sodium was significantly faster in the children who developed cerebral edema compared with children who had no complications following correction of the hypernatremia (1.0 versus 0.5 meq/L per hour).
- Similar findings were noted in another report in which the rate of reduction in serum sodium was 1.0 meq/L per hour in the nine infants who developed seizures compared with 0.6 meq/L per hour or less in 31 infants who did not develop seizures.
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Burton Rose
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My patient moves 11 mEq in 4 hours after receiving 500 mL of normal saline. Now what? I was convinced that continuing normal saline would perpetuate the overly rapid correction of the sodium and put the patient at risk of cerebral edema. But since the patient was still in hypovolemic shock, I couldn’t just stop the fluids.
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| docx | pdf |
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| iPhone, a surprisingly effective photocopier. |
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| What book did this great page on maintenance fluids come from? |
Nine of the first 47 patients developed seizures that could not be explained by other etiologies (fever, hypocalcemia, hypoglycemia) and so were ascribed to rapid fluid restoration, Group I. They matched these nine to 22 age-matched children who were treated contemporaneously but did not have a seizure, Group II. The investigators then changed the protocol for treating infants with hypernatremia to 120 mL/kg/day and included data on 9 patients under 5 months who were treated this way, Group III.
Here is the primary data on the three groups:
All three groups had similar sodiums but Group I had significantly higher BUNs than Group II, with I +II vs III and I vs III being non-signifigant.
The net result was a wide spread in the rate of correction of sodium:
Fang looked at 97 children with hypernatremia. Mean sodium was 164.5. Mean age 13 months. He performed a case-control study with the cases being patients who developed cerebral edema. Manifestations included seizures, eyelid edema, papilledema in all the patients and bulging fontanel in 36 and pupillary abnormalities in 9 cases.
The data shows cerebral edema was more common with bolus therapy, especially when the bolus was faster, higher sodiums were associated with cerebral edema but much of that disappeared in multivariate analysis as higher sodiums were also associated with increased rate of correction and ind increased bolus rates. Using ROC the investigators found a rate of fluid administration of 6.8 ml/kg/hr was safest. And the average decrease in serum sodium in the cerebral edema group was 1 mEq/L/hr and 0.5 mEq/L/hr without cerebral edema.
The final reference is Blum’s study of oral rehydration, this is the reference my med student was upset with. As he outlined, this was a study of oral rehydration rather than a study of rates of treatment. The cohort was composed of eighteen infants, 6 months or younger admitted with hypernatremia (Na > 150) and treated with oral fluid resuscitation. They compared the hypernatremia outcomes to a second cohort of 26 infants who received IV rehydration for hypernatremia. Average sodium for both groups was 160.
In both groups the reduction of sodium was slow (0.3 mEq/L/hr) and no patient developed seizures.
In Burton Rose’s Clinical Physiology of Acid-Base and Electrolyte Disorders this observational study with no seizures is the sole reference behind the recommendation for a slow restoration of normal sodium. Weak sauce. Of note Androgue’s review of hypernatremia in the NEJM from 2000 references the same Blum and Khan articles to support its recommendation of slow treatment.
So in the end, the recommendation for slow normalization of sodium is based on a handful of studies in infants with no randomized or even prospective studies. What is unbelievable to me is no one references a study that reviews the functional/neurological outcomes of patients with the highest sodiums admitted to a large hospital based on the speed of correction. Seems like an easy study and in its absence we are left to trust in the physiology of babies.
As has been the tradition since 2008, I had the honor of giving the morning report on July 1st for the St John Hospital and Medical Center Internal Medicine Residency Program. July one, openning day of the academic year. The conference room was crackling with the energy of fresh interns and the equally excited second years ready to run their own teams.
Giving the lecture was a lot of fun. There were a lot of insightful questions, some because the questioner is terrified and others to show how smart she is. Nobody looked sleep deprived, so the ratio of deer-in-the-headlights to asleep-at-their-desk was unnaturally high.
The lecture covered three topics:
The lungs serve to maintain the composition of the extra-cellular fluid with respect to oxygen and carbon dioxide, and with this their duty ends. The responsibility for maintaining the composition of this fluid in respect to other constituents devolves on the kidneys. It is no exaggeration to say that the composition of the body fluids is determined not by what the mouth takes in but what the kidneys keep: they are the master chemists of our internal environment. Which, so to speak, they manufacture in reverse by working it over some fifteen times a day. When among other duties, they excrete the ashes of our body fires, or remove from the blood the infinite variety of foreign substances that are constantly being absorbed from our indiscriminate gastrointestinal tracts, these excretory operations are incidental to the major task of keeping our internal environments in the ideal, balanced state.
Here is the lecture in PDF and Powerpoint
Today I did a noon conference on sodium for the neph fellows. Instead of a comprehensive sodium lecture I focused on a number of different elements and interesting aspects of hyponatremia. Mostly a deeper dive into aspects that you don’t have time to cover in standard sodium lecture.
I opened with 17 quick slides on free water clearance. These slides are old and I think I could do better. Definitely due for an update.
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| Download the slides here. |
Then I used a slide deck which covers:
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| download the slides here |
Yesterday:
Today I went to see Richard Stern talk about Therapeutic Considerations in the Hyponatremic Patient. It was an excellent talk. One of the concepts he introduced, at least to me, was the use of DDAVP in the patient with severe hyponatremia.
His argument was that the biggest threat to to these patients is the overly rapid correction of sodium due to the sudden suppression of endogenous ADH in the middle of therapy. This is exactly what I was worried about when I was treating that severe case of hyponatremia a couple of weeks ago. My solution up to now is to write an order for the nurse to call me if the patient’s urine output rises over 100 mL an hour. Unfortunately this is an unusual call order and nurse compliance with it is questionable.
He proposes using DDAVP to essentially lock, or hold constant urinary losses. Then you use 3% saline and the increases in plasma sodium should be more predictable.
This maneuver has a high degree of difficulty but I think it solves an important problem. I’m going to try this on my next case of extreme hyponatremia.
Has anyone else used this technique?
– Posted using BlogPress from my iPad
I’m not sure if it is really the lowest sodium but it definately was among the lowest.
I received a call regarding a consult for a patient with a sodium of 105.
The patient is a 60 year old caucasian woman who had been started on chlorthalidone 3 days prior to admission. Her physician had been wrestling with hypertension and changed her from 25 mg of hydrochorothiazide to 50 mg of chlorthalidone. (The internist was keeping up with her American Journal of Hypertension. Though 50 mg is a whole lotta chlorthalidone.)
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| Both figures are from Ernst Et al. Hypertension 2006 |
After one or two days of the new diuretic the patient started vomiting and developed diarrhea. The only thing she was able to keep down was water. When she came to the ER she hadn’t eaten anything solid for two days.
This patient was at risk of overcorrection because she had two of the most common clinical settings in which such overcorrection occurs: thiazide use and hypovolemia.
Patients with hypovolemic hyponatremia send conflicting signals to the hypothalamus regarding ADH release. The volume deficiency stimulates ADH (if the body volume deficient, let’s not lose any water via the kidneys) and low osmolality surpresses ADH (the body is too diluted so let’s lose some water to bring the concentration up). In the case of this conflict, volume rules. As I tell my medical students,
Remember the ABC’s, Airway, breathing and circulation. O for osmoregulation is way down in the alphabet.
The problem of rapid correction occurs when you correct the volume deficiency and all of the sudden the hypothalamus asks itself, why am I releasing any ADH with an osmolality of 260?
Then the kidney starts producing urine that you could probably bottle and sell as organically filtered water. Electrolyte free water clearance begins to approach the urine output and the sodium also starts to climb and climb fast.
To protect this patient I told the nurse to decrease the normal saline to 100 mL per hour and to call me if the urine output goes over 200 per hour. We also started checking the sodium every six hours and I ordered urine osmolality, sodium and potassium.
Her sodium started to rise slowly, the urine output increased but never resembled Niagra. After two days her sodium was in the 120s her urine still appeared volume depleted and volume status began to look wet. She developed wheezes and she had a few rales. We had to abandon the normal saline. We started tolvaptan. She received 30 mg once and then 15 mg the next day after she had a brisk response. After that her urine electrolytes resembled SIADH.
Once the sodium crossed 130 I stopped the tolvaptan, restricted her free water, and added a gram of sodium chloride twice a day. Her sodium stabilized around 130.
Around this time I sent a renin aldo ratio. I usually order these before I start a patient on aldactone, because after you start it you need to wash them out for weeks prior to checking for primary hyperaldosteronism. Our patient had difficult to treat hypertension and hypokalemia on admission, so I checked it. I just found out that it came back positive. The high aldosterone was after we had corrected her volume deficiency. I think it is primary, and this may explain why she had persistently low urine sodiums despite successful volume resuscitation.
We looked for a cause of the SIADH, but couldn’t find anything. No narcotics, no pulmonary disease, no malignancy, normal TSH and cortisol, no anti-depressants. She had a normal non-contrast head CT scan on admission. I even ordered a contrasted CT scan of the chest to make sure she didn’t have a cancer in there. Nothing. Idiopathic SIADH hiding behind, at least initially, volume depletion and in the background of primary hyperaldosteronism. Strange case.
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