Wednesday, July 29, 2009

What is the electrolyte book for me?

I received this e-mail question today:

I am a second year nephrology fellow. I always find acid base and electrolytes interesting but have always looked for a good book which would help me get a better perspective on this topic. Are there any books that you would recommend.

There is only one answer to this question. If you are nephrology fellow who wants to own electrolytes get Burton Rose's masterpeice: Clinical Physiology of Acid-Base and Electrolyte Disorders.

You can find this and other recommended nephrology books at PBFluids' Amazon Store of Knowledge.

Disclosure: I do receive a kickback if anybody every buys a book through these amazon links (still looking to lose my amazon affiliate cherry)

July 24 Lecture to medical students: Acid-Base

I did my standard Acid-Base work shop with the medical students and Providence Hospital last week. Here is the handout. Corrected an embarrassing error on page 9 and changed a few of the problems a little bit.

And the pages document if you want to modify it:

Saturday, July 25, 2009

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.

Wednesday, July 22, 2009

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.

Tuesday, July 21, 2009

Highest creatinine in chronic renal failure

Mr. S., a 38 y.o. African American male, came to the hospital with nausea, vomiting and fatigue. Initial creatinine was 36.2 mg/dl. After hydration overnight it came back at 38 mg/dl.
Update: one of the comments asked about the patients body habitus, rhabdo and BUN.
  • Mr S. is muscular but no body builder
  • He was not in rhabdo. I would not include an elevated creatinine due to muscle breakdown under the crazy numbers tag as it essentially represents a lab error, in that the creatinine is no longer a measure of severity of the renal failure or the chronicity but rather a measure of the aggregate muscle damage.
  • His BUN was 139 mg/dL
This patient had a remote diagnosis of hypertension but had been out of any medications for months. The computer showed a 2 year old creatinine of 2 but the patient denied any memory of being told he had CKD.

One of my co-fellows, Rajiv Poduval, used to call this acute ESRD. Chronic kidney disease that goes unrecognized until the patient rolls into the ED in need of dialysis.


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:

Lecture to medical students July 17th

Lecture on IV Fluids and sodium

I had eight 3rd year medical students. I did a quick pole and 6 of the 8 had or were planning on getting an iPhone/iPod touch. One student had an Android G1. No Blackberries, no Windows Mobile.

Is it too early to declare a winner in the medical smart phone arena?

Friday, July 17, 2009

Great article in the New Yorker summarizing books on obesity


Elizabeth Kolbert reviews the current crop of what she calls obesity books
Though weight-loss books will doubtless always be more popular, what might be called weight-gain books, which attempt to account for our corpulence, are an expanding genre.

It is very good. Nothing on uric acid or fructose or an infectious etiology but a lot of interesting thoughts on our expanding wastlines.

Friday, July 10, 2009

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.

Tuesday, July 7, 2009

Acute renal failure links from the NEJM

Abuelo. Normotensive ischemic acute renal failure. N Engl J Med (2007) vol. 357 (8) pp. 797-805 (Pubmed)

Schrier and Wang. Acute renal failure and sepsis. N Engl J Med (2004) vol. 351 (2) pp. 159-69 (Pubmed)

Wednesday, July 1, 2009

Happy July 1st, and don't worry about the July phenomenon. All myth.

According to this article in Newsweek from last July:

the July medical-training period is associated with between 1,500 and 2,750 accelerated deaths every year. In a study of the July phenomenon from which initial findings were released in 2005 by the National Bureau of Economic Research, Harvard Business School health-care economists Robert Huckman and Jason Barro compared mortality rates in teaching and non-teaching hospitals around the country. They found that there are 4 percent more incidences of accelerated death in average-sized teaching hospitals in July and August.
They also found length of stay increased 2%. It is not clear from the above paragraph but the 1,500 to 2,750 deaths is also part of the same study by Huckman and Barro. A good review of the paper is found on this blog, A New Start. Here is a link to the abstract, full article costs $5.

A study done on hospitals in Ohio found no increase in mortality in ICU patients admitted in July through September. It looks like a massive study with rigorous methodology and it is more recent by nearly a decade.
In analyses of over 48,000 patients admitted to ICUs in 5 major teaching hospitals, using a validated method of adjusting for admission severity of illness, several important findings emerge. First, in-hospital mortality and LOS were similar in patients admitted to intensive care units from July through September and during later months of the academic year. Moreover, results were consistent when July, August, and September were analyzed separately, and there was no discernible pattern of variation when examining outcomes for individual months over the entire year. Furthermore, we were unable to detect differences when individual academic years, surgical and nonsurgical patients, and individual hospitals and ICUs were examined separately. These results were all similar in analyses of roughly 108,000 patients admitted to minor teaching and nonteaching hospitals.

With its unremarkable findings and disruption of the common wisdom is it any wonder that it is given short shift in the Newsweek article.

Cool article on Hippocratics Aphorisms

The authors describe aphorisms as:

...terse and trenchant, facilitating maximum comprehension in minimum expression. The Hippocratic aphorisms are just that: concise, often pithy, and memorable statements of literal truths and frequently obvious wisdoms.

Sounds like Hippocrates would have had a ton of followers on Twitter.

This aphorism is probably the first description of casts associated with ATN.

Here is the article
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