That’s not a gap, its the Grand Canyon!

When I talk about toxic alcohols causing anion gap metabolic acidosis I emphasize that these patients have large anion gaps. When you see an anion gap of 16 or 20 think uremia and lactic acid, not methanol. The cases I have seen have almost all had gaps greater than 25 and typically they run in the 30s.

But I have never heard of or seen a gap as big the one that came into the ICU this week-end:

To summarize the data from above. A patient was admitted with an anion gap of 65 that went up to 70 in the next 6.5 hours. I can visualize the ER doc reading the first chemistries, freaking out and re-ordering them, assuming that if the anion gap is greater than the chloride it must be a lab error, hence the repeat labs at 150 minutes after the first set.

Think about that, the anion gap was larger than the chloride concentration.

What kind of alien infestation causes numbers like that?

So when working up a large anion gap one tries to explain the anion gap. The lactic acid was only 34.5 mmol/L. So this patient has the highest lactic acid ever, yet it only covers half the gap. She also had serum ketones that remained positive at a 1:8 dilution and a creatinine of 14.

So is that it? Lactic acidosis, ketosis and uremia for an anion gap of 70? I sent off a D-lactic acid and a 5-oxoproline level, cause what the hell, when’s the next time I’m going to see an anion gap of 70. A toxic alcohol screen was sent.

To compete the picture the ABG was: 6.95/13.4/187 with a measured bicarb of 3. With numbers this crazy a trip to the Henderson-Hasselbalch formula is probably not a bad idea:

MedCalc has a sweet HH calculator

So 6.97 is pretty close to the 6.95 measured, so no lab error at least in the ABG. Running Winter’s formula (1.5 x HCO3) + 8 ±2 gives a predicted pCO2 of 13, so no respiratory component to the metabolic acidosis.

The next step is to look for toxic alcohols while waiting for the assay to come back from toxicology lab at Children’s Hospital of Michigan. The osmolal gap calculation should be greater than 10 in the presence of methanol, isopropyl alcohol or ethylene glycol. The measured osmolality was 327.

MedCalc also has a sweet osmolar gap calculator

So no significant osmolal gap rules out a toxic alcohol. This was confirmed by the toxicology screens that eventually came back. Given the anuric renal failure, profound intractable acidosis and unknown anions still unaccounted for we initiated CVVHD. You can see the effect that had on her bicarbonate and creatinine.

The patient has since recovered and we have learned that she was on metformin so we are toying with metformin induced lactic acidosis as the etiology. Any other thoughts?

The cost of blogging

Michael Hyatt has an a good read about the costs of blogging and advises against getting bogged down in details about design, custom software and hosting. Find a way to cut through that BS inorder to start writing.

He recommends, premium version for $12-17 a year. He doesn’t say why he would choose that over Blogger (the host of PBFluids).

Today I received my bill for blogging for the next year here at PBFluids:

Blogging. Total bargain.

$10. That’s all.

Here is Dr. Ves on Medical Blogging. He is actually quoting Seth Godin and Tom Peters. This best sums up my feelings on blogging:

It doesn’t matter if anyone reads it. What matters is the humility that comes from writing it. What matters is the metacognition of thinking about what you’re going to say.

No single thing in the last 15 years professionally has been more important to my life than blogging. It has changed my life, it has changed my perspective, it has changed my intellectual outlook, it’s changed my emotional outlook.

And it’s free.

And the baby with the baboon heart. Or It’s an iPad world

I was giving my cardiorenal syndrome lecture on Friday and during the question and answer session one of the residents asked why furosemide drips were more effective than boluses. I explained about the results from this Cochrane review and this recent RCT. Unfortunately I had not read the table of contents from this weeks NEJM:
So of course one of the interns mentions the article and asked if I had read it. I copped to the truth but what happened next was incredible. Across the lecture room I could see dozens of iPads flick to life as nearly everyone started pulling up to check out the latest.

Medicine is magical and magical is art
The Boy in the Bubble
And the baby with the baboon heart

Cardiorenal syndrome

Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact or the authorOn the first Friday of every month I give a lecture to the residents at St. John Hospital and Medical Center. I like to do an electrolyte lecture but for March the chief resident asked me to talk about cardiorenal syndrome. In researching the lecture I came across this article by Claudio Ronco.

The article defines cardiorenal syndrome as any condition with simultaneous kidney and heart failure. He then goes on to subdivide cardiorenal syndrome into 5 types:

  1. Acute heart failure causing acute renal failure
  2. Chronic heart failure causing chronic kidney disease
  3. Acute kidney injury causing any type of acute cardiac dysfunction (including arrhythmia)
  4. Chronic kidney disease causing any chronic cardiac disease
  5. Any systemic condition that causes renal and cardiac dysfuction (e.g. sepsis)
This is terrible. Cardiorenal syndrome used to signify the unique cause of acute kidney injury where the decrease in function is due to apparent volume depletion in a patient that obviously overloaded. It named the only scenario where acute kidney injury responded to diuresis. It was unique and specific. Ronco comes along and says, yes I like your version of cardiorenal syndrome so I will make it type 1 in my new all purpose definition of cardiorenal syndrome. Now whenever there is cardiac dysfunction and simultaneous kidney dysfunction we can just call it cardiorenal syndrome.

It doesn’t have to be this way look at the example of hepatorenal syndrome. The syndrome does not refere to just any situation with simultaneous renal and liver dysfunction. It is a very specific diagnosis that only occurs with chronic liver disease and ascites. The patients must be oliguric, there is no non-oliguric HRS. Patients must be sodium avid and unresponsive to fluids and albumin. Additionally the patients cannot have laboratory or imaging evidence for an alternative cause of renal failure. Because of this definition hepatorenal syndrome identifies a very specific disorder, with a specific pathophysiology and unique prognosis and treatment options.

Ronco takes the beautiful and evocative name cardiorenal syndrome, strips it of all specificity and then tries to restore it by tacking on five different types. The fifth type 5 is the one that makes my brain explode. Sepsis, really? Acute kidney injury from sepsis that happens in the same patient who also suffers from sepsis induced cardiomyopathy should now be considered to have cardiorenal syndrome? Ronco is a man who has spent his life studying sepsis and acute renal failure, I can’t believe he is actually referring to that condition as CRS type 5.

I’m not buying what Ronco’s selling. Cardiorenal syndrome begins and ends with type 1 for me.

FYI: Here is the lecture (Keynote, PDF). It still needs some work. I’d like to add a section on ultrafiltration and I need to include the NEJM article on furosemide that was published yesterday.

Go green: recycle your organs

On of my patients, whose daughter had a kidney transplant, came into clinic wearing this T-shirt. Love it.
It says. “My child contains recycled parts. Be a hero, be a donor.”