Tag: sodium

Posted on

week-end call and a pair of crazy numbers: Glucose and Calcium

Glucose
I saw the highest glucose I can remember in a patient without ESRD. I have seen the glucose go over 2,700 in a patient with the misfurtune to have both DKA and anuric ESRD. Without the osmotic diuresis to lower the glucose the glucose can shoot the moon. This patient had HyperOsmolar Non-Ketotic Coma (or HONK as my fellow calls it, love that) and baseline Cr of 0.83 and a peak glucose of 1,600 mg/dL.
I love the twin graphs showing the falling glucose and the simultaneous resolution of the pseudohyponatremia. The patient had enough pre-existing osmotic diuresis to cause hypernatremia which was masked by the hyperglycemia. As the glucose comes down the sodium goes up from 136 to 162.

Calcium
The other crazy number was the most severe hypercalcemia I have ever seen. The calcium was 18 mg/dL with an albumin of 3.7 g/dL. The patient is a kidney transplant recipient who was recently seen in the outpatient clinic with hypocalcemia. His calcium was 6.5 and his calcitriol was increased from 0.5 mcg to 1 mcg twice daily. He was also continued on his calcium carbonate.

Admission labs:

The other pertinent calcium labs:

  • PTH: 3.2 pg/mL
  • Vit D 1,25 dihydroxy: 36 pg/mL
  • SPEP/UPEP: unremarkable
  • PTHrp: pending
I think this is milk-alkali syndrome from the calcium carbonate exacerbated by the calcitriol. One supporting string of evidence supporting this is the fact that his calcium came down and has not reoccurred. If it was hypercalcemia of malignancy I would have expected his calcium to be resistant to conservative therapy.  
Posted on

Fellow talk on sodium

I was scheduled to give a talk on disorders of sodium and water to the fellows yesterday. We have a particularly clever cohort of fellows this year and I really couldn’t give them a warmed over version of my resident and student sodium lecture so I put together this talk which looks five different issues with hyponatremia and some data regarding them:

  1. mannitol induced pseudohyponatremia
  2. TURP syndrome
  3. uremia and propensity for myelinolysis
  4. exercise induced hyponatemia
  5. differentiation of salt delpetion from SIADH with FENa, FEUrea and FE Uric acid with a couple of slides on treating SIADH with saline

Remember, downloading the native Keynote file will give you animations and a better  looking experience.

Posted on

Articles that changed the way I practice: Sodium intake, hypertension and mortality

I have long been skeptical towards the party line that salt intake is a driver of high blood pressure, as I wrote here and here. Though hypertension is nearly unheard of in primitive cultures with sodium intake below 50 mmol/day (1.6 g day), increasing sodium intake has modest effects on blood pressure. Three mm of systolic per 100 mmol of sodium (2.3 grams) according to the Intersalt Study (PDF). This 3 mm of systolic agrees with the change in blood pressure in the DASH-Sodium trial. Similar effect size has been documented in meta-analysis:
  • A 2002 meta-analysis by Lee Hooper of 11 trials of at least 6 months duration found a 1.1/0.6 mmHg reduction from a 35 mmol (810 mg) reduction in sodium intake.
  • A broader meta-analysis published in JAMA in 1998 looked at 114 trials and found a reduction of 3.9/1.9 in hypertensive patients and 1.2/0.3 in normotensive participants.
Despite these seemingly modest results all of the clinical practice guidelines on hypertension have adopted sodium restriction as a key part of blood pressure control:
My position when talking with patients about dietary modifications for high blood pressure had been to mention sodium restriction and weight loss but focus on the DASH diet (PDF) and exercise. But this strategy has recently evolved as I became aware of a pair of studies, one by Cook et al which strengthened the sodium argument and one by Larry Appel which weakened his own DASH research.
The Rise of Sodium
The article by Nancy Cook is a follow-up on the Trial of Hypertension Prevention I and II. These were randomized controlled trials of patients with high normal blood pressure which tried to determine which lifestyle modifications were effective. Patients randomized to sodium reduction were given individual and group counseling sessions on how to reduce sodium in the diet. After 18 months the patients in the TOHP I reduced sodium intake by 44 mmol/day (1 g sodium) and blood pressure fell 1.7/0.8 mmHg. In TOHP II, after 36 months, sodium intake was reduced by 33 mmol/day (750 mg of sodium) and blood pressure fell 1.2/0.7. The decreases in blood pressure in both studies are unimpressive.
Cook went back to these studies, 10 years after TOHP I and 5 years after the completion of TOHP II, and looked at the rate of cardiovascular events (primary outcome: MI , CVA, CABG, PTCA, CV Death). They found a 25% reduction in events in patients in the low sodium group (p=0.04) that increased to 30% reduction when the study was adjusted for baseline sodium excretion and weight. These results are incredible to me, modest reductions in sodium intake that were achieved through patient education had negligible effects on blood pressure but dramatic benefits on morbidity.

The strengths of this evidence comes from two lines of reasoning:
  1. It is a randomised trial. Even though the current data comes from an observational extension of the original RCT, this does not change the fact that we are looking at two groups that were orignially randomized.
  2. This is a study which looks cardiovascular events rather than blood pressure or other intermediate outcomes.
The fall of the DASH
The DASH Trial (Appel 1997) used a diet rich in fruits and vegetables to provide increased fiber and potassium along with other trace minerals. Low-fat dairy products provide increased calcium while keeping the diet low in saturated and total fat. Participants randomized to the DASH diet were served meals with 4-5 servings of fruit, 4-5 servings of vegetables, 2-3 servings of of low fat dairy and <25%>

The results were dramatic:
  • Decreased blood pressure of 5.5/3.0 mmHg
  • Decreased in hypertensives 11.4/5.5 mmHg
  • Maximal blood pressure response occurred after only 2 weeks

The primary weakness in the DASH trials is that I’m not going to provide my patients with all of their food. It is not a clincally relevent intervention. As physicians, all we can do is educate and cousel on diet. Appel did a follow-up study where he did just that and the DASH was no longer so impressive.
The PREMIER Trial randomized patients to three groups:
  1. Control group with no interventions
  2. Standard advice: 18 face-to-face meetings to go over weight loss, and strategies to reduce sodium and alcohol consumption
  3. Standard + DASH: 18 face-to-face meetings with the same contant as the standard group with additional counseling on adopting the DASH diet
Counseling resulted in significant weight loss of 5 kg in both experimental groups versus loss of 1 kg in the control group. There was no difference in physical activity, but physical fitness did improve from baseline all three groups. They didn’t find a reduction in alcohol or sodium intake however there was good separation in the potassium intake with the greatest increase in potassium in the DASH group as would be expected. Both of the experimental groups had greater reductions in blood pressure than the control group. 40% of the patients randomized to the Standard advice and 48% of the patients in the Standard + DASH were able to lower their blood pressure below 120/80. This difference was not statistically significant.

There was no improvement in blood pressure control with the addition of the DASH diet over counseling patients on established risk factors.
Posted on

Things have been coming in pairs: electrolyte free water and hypernatremia

First we had the highest creatinine followed by the lowest creatinine.

Then we had a case of hyponatremia/SIADH that we evaluated with the concept electrolyte free water and now we have a case of hypernatremia that we also evaluated with electrolyte free water.

I have a special fondness for dysnatremia formulas that work with either hyper- or hyponatremia because there is an elegance in using a model that works at both extremes.
Both the change of sodium formula and electrolyte free water calculation work as well with hypernatremia as they do with hyponatremia.
The case: 56 year old African American nursing home resident with a history of bipolar disease. She presents with altered mental status and initial labs reveal acute kidney injury and hypernatremia.
Body weight 70 kg
Na 177
Cr 4.18
On exam the patient had obvious hypovolemia and the elevated sodium reveals dehydration. The primary team appropriately uses half normal saline to correct both of these deficiencies.
The sodium came down to 167 the following day and after that they have been unable to further correct it. The patient remained in the ICU for 4 days prior to us being consulted for persistant hypernatremia. The creatinine rapidly corrected over four days to 1.6.
Additional data:
Admission urine sp grav 1.011
Admission urine Na 10
Admission urine osmolality 330
On the fourth day of the admission the urine output was 1,500 over the prior 8 hours
The primary team had been using the water deficit formula to estimate the amount of fluid to give the patient to correct the sodium over 2 days:
The water deficit equation asks how much water will be needed to dilute all the solutes to some ideal. In many books and programs the ideal sodium is fixed at 140 mmol/L. I usually use 145 mmol/L, which is the least amount of change in sodium to get a normal sodium. I do this because the downside of correcting sodium is all on the side over correction and inducing cerebral edema.
The equations often wont let you determine the % body water and fill in 60%. This is a large source of error because in the United States we’re all fat and fat people are relatively anhydrous. Also, since typical internal medicine patient is about 100, and old people are likewise anhydrous 60% is a over estimation of total body water. My fellow estimated the total body water to be 35 liters.
The calculated free water water deficit is 7.7 liters. I usually administer half of that in the first 24 hours unless the sodium is very high, as in this case, and then I would have given about a third of the volume in the first day and correct the sodium over three days. I shoot for a change of about 12 mmol/l per day.
The equation worked well initially with the sodium going from 177 to the mid 160’s but after that they stalled. The reason the sodium stopped improving was that they cured the patient of her renal failure and the urine output increased. Neither the team nor the water deficit formula accounted for this.
We can account for the urine output by replacing the electrolyte free water clearance:
So one would have to add 2.8 liters of electrolyte free water to the free water deficit calculation to account for urinary loss of electrolyte free water. If one were to recalculate the water formula using the partially corrected sodium of 167 you get:
If you plan to give half that in the first day that is 2.65 liters. Compare that to the electrolyte free water loss of 2.8 liters and it immediately becomes obvious why the sodium remained stable for days.
Teaser: An elevated electrolyte free water clearance in the presence of hypernatremia is presumptive evidence of diabetes insipidis. I will save that discussion for my next post.
Posted on

Crazy numbers: lowest creatinine

The consult team is now taking care of a patient with what I think is the lowest creatinine I have ever seen: 0.29 mg/dL. I’m not a bench nephrologist but I think that is a pretty typical mouse creatinine.

Update: some commenters asked about the BUN: 6 mg/dL. FYI today the Cr is down to 0.28 and the BUN fell to 3!

The patient has SIADH and low creatinines are a usual finding. She also has a crazy low uric acid of 1.4. Not quite Uricase low but getting close. Her admission sodium was 108, her urine sodium today was a whopping 156 with a urine potassium of 34. So if you calculate her electrolyte free water clearance (the amount of her urine which is electrolyte free water):

You get a negative 826 mL. A negative electrolyte free water is not unusual in SIADH and distinguishes it from the hyponatremia seen with heart failure (or other conditions of decreased effective circulating volume).
In this case the negative clearance means that for every liter of urine this patient makes it is as if she drank 826 mL of fluid. The very act of urinating lowers the sodium further by diluting the plasma sodium.
This throws a wrench in the standard plan of adding the urinary output to the insensible losses and setting the fluid restriction to be 200-500 mL below that. This works in conditions like heart failure where the electrolyte free water is positive but with a negative free water clearance you need to account for the negative free water clearance by adding it to the water intake, not the renal losses.
See this presentation on electrolyte free water clearance for further details.
Posted on

Consult service: electrolyte free water

Yesterday I started on the consult service mid-month. We are experimenting with having the atendings rotate from the dialysis floor to the consult service every two weeks. I am skeptical because of the lack of continuity but in the spirit of 80-hour weeks we are trying it out.

Yesterday I lectured on electrolyte free water clearance and tea and toast syndrome.

Here is the lecture on Electrolyte free water:

The online version doesn’t look great. Download the file and then try it.

The lecture on tea and toast syndrome is below:

Posted on

My first two lectures to the IM Intern Class of 2012

On July first I gave a lecture on IV fluids, total body water and hyponatremia. This handout is similar to the lecture I give to the medical students titled sodium and water. It adds a half baked section on potassium but this handout really needs to have th sodium section tightened up and shortened, the potassium section finished and short sections on the treatment of phos, magnesium and calcium disorders.

  • Here is the PDF
  • Here is the native Pages documentin case you use Pages and are interested in finishing this work in progress.

On July 9th I gave a lecture on acute renal failure. The handout is 28 5.5 x 8.5 pages. The book is designed as a workshop with questions and points for discussion throughout.

  • Here is the PDF of the 28 page handout. It is very readable and one of the best handouts I have put together.
  • Here is the native Pages document in case you use Pages and are interested in editing my masterpiece.