Twin Cities Toxicology
I apologize for the gap between my last post and now.  I’m in the middle of exploring some other potential blog formats/hosts.  Speaking of gaps…
A recent emergency department consult brought up an interesting and controversial topic within the realm of medical toxicology.  The case, in brief, was a middle aged patient with metabolic acidosis, elevated anion gap, and elevated serum osm gap.  He presented to the ED with suicidal thoughts, admitting to heavy recent EtOH use and consistently denied even the chance of ingesting any other liquid or alcohol.  The primary history takers in the ED thought his history was consistent and believable.  The emergency providers were admitting the patient with diagnoses of alcoholic ketoacidosis, lactic acidosis, agitation, hypertension, tachycardia, and dehydration.  The patient had a history of heavy alcohol abuse, a present-but-low serum EtOH concentration and normal renal function,  The question that came up during the discussion between the admitting physician and the ED was about whether or not a “toxic alcohol” screen (I put this in quotes because it always annoys me that according to that test name apparently ethylene glycol and methanol are toxic but ethanol isn’t) should be done in this context of metabolic acidosis, elevated anion gap, and osm gap.  The list of core questions that need to be answered here are (and this list is not all-inclusive):
1) Why is there a lactic acidosis?
2) Is the anion gap explained by the lactate and AKA?
3) Is the osm gap explained by the lactate and AKA?
4) Is an osm gap reasonable and accurate enough to use to make decisions?
5) Finally, in the case of a middle-aged patient with AKA, lactic acidosis, elevated anion gap, elevated osm gap, do you need to rule out ethylene glycol and methanol as causes, and do you need to order a “toxic alcohol” screen in order to do that?
The following is a short (and again not by any means all inclusive) list of articles that I’ve collected and used to help answer questions in this setting in the past.  Check them out, or just keep them somewhere for yourself, and I’ll come back to give my version of how to approach this issue in the next post.
http://www.ncbi.nlm.nih.gov/pubmed/2400167
http://www.ncbi.nlm.nih.gov/pubmed/17389437.1







http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1950181/?tool=pubmed

http://www.cmaj.ca/content/177/5/489.2.fullhttp://www.ncbi.nlm.nih.gov/pubmed/8215742http://www.ncbi.nlm.nih.gov/pubmed/9247780



 http://www.ncbi.nlm.nih.gov/pubmed/21255564

http://www.ncbi.nlm.nih.gov/pubmed/15862086
http://www.ncbi.nlm.nih.gov/pubmed?term=osmolar%20gap%2C%20hoffman
http://www.clinchem.org/content/56/8/1353.long


http://www.ncbi.nlm.nih.gov/pubmed/17395001
http://www.ncbi.nlm.nih.gov/pubmed/21755818


http://www.ncbi.nlm.nih.gov/pubmed/16455871

http://www.ncbi.nlm.nih.gov/pubmed/15885229

-Sam

I apologize for the gap between my last post and now.  I’m in the middle of exploring some other potential blog formats/hosts.  Speaking of gaps…

A recent emergency department consult brought up an interesting and controversial topic within the realm of medical toxicology.  The case, in brief, was a middle aged patient with metabolic acidosis, elevated anion gap, and elevated serum osm gap.  He presented to the ED with suicidal thoughts, admitting to heavy recent EtOH use and consistently denied even the chance of ingesting any other liquid or alcohol.  The primary history takers in the ED thought his history was consistent and believable.  The emergency providers were admitting the patient with diagnoses of alcoholic ketoacidosis, lactic acidosis, agitation, hypertension, tachycardia, and dehydration.  The patient had a history of heavy alcohol abuse, a present-but-low serum EtOH concentration and normal renal function,  The question that came up during the discussion between the admitting physician and the ED was about whether or not a “toxic alcohol” screen (I put this in quotes because it always annoys me that according to that test name apparently ethylene glycol and methanol are toxic but ethanol isn’t) should be done in this context of metabolic acidosis, elevated anion gap, and osm gap.  The list of core questions that need to be answered here are (and this list is not all-inclusive):

1) Why is there a lactic acidosis?

2) Is the anion gap explained by the lactate and AKA?

3) Is the osm gap explained by the lactate and AKA?

4) Is an osm gap reasonable and accurate enough to use to make decisions?

5) Finally, in the case of a middle-aged patient with AKA, lactic acidosis, elevated anion gap, elevated osm gap, do you need to rule out ethylene glycol and methanol as causes, and do you need to order a “toxic alcohol” screen in order to do that?

The following is a short (and again not by any means all inclusive) list of articles that I’ve collected and used to help answer questions in this setting in the past.  Check them out, or just keep them somewhere for yourself, and I’ll come back to give my version of how to approach this issue in the next post.

http://www.ncbi.nlm.nih.gov/pubmed/2400167

http://www.ncbi.nlm.nih.gov/pubmed/17389437.1

http://www.ncbi.nlm.nih.gov/pubmed/16455871

http://www.ncbi.nlm.nih.gov/pubmed/15885229

-Sam

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