Continuing on the theme of Toxic Alcohols (osmolal gap, ethylene glycol), this Paucis Verbis card focuses on methanol toxicity. Useful are the American Academy of Clinical Toxicologists recommendations on when to administer an antidote (fomipezole) and when to perform hemodialysis. I redrew the flowchart based on what’s relevant to the ED in the initial stages.

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Following last week’s Paucis Verbis card on calculating the osmolal gap, here is the first installment of the Toxic Alcohols cards. First up — ethylene glycol. There are useful American Academy of Clinical Toxicologists recommendations on when to administer an antidote (fomipezole) and when to perform hemodialysis.

Here’s a quick review of the metabolism of the different toxic alcohols. The parent compounds for ethylene glycol and methanol are innocuous and the metabolites are toxic.

PV Card: Ethylene Glycol Toxicity

Adapted from [1-3]
Go to ALiEM (PV) Cards for more resources.

See Dr. Leon Gussow’s great review on The Poison Review and tips of a recent Annals of EM4 paper on identifying a small subset of patients with ethylene glycol who did well despite NOT receiving hemodialysis.

References

1. Kraut J, Kurtz I. Toxic alcohol ingestions: clinical features, diagnosis, and management. Clin J Am Soc Nephrol. 2008;3(1):208-225. [PubMed]
2. Jammalamadaka D, Raissi S. Ethylene glycol, methanol and isopropyl alcohol intoxication. Am J Med Sci. 2010;339(3):276-281. [PubMed]
3. Marraffa J, Cohen V, Howland M. Antidotes for toxicological emergencies: a practical review. Am J Health Syst Pharm. 2012;69(3):199-212. [PubMed]
4. Levine M, Curry S, Ruha A, et al. Ethylene glycol elimination kinetics and outcomes in patients managed without hemodialysis. Ann Emerg Med. 2012;59(6):527-531. [PubMed]

We often talk about calculating the anion gap in the evaluation of patients. What about the osmolal gap? When do you calculate this? What’s the differential diagnosis for an increased gap?

I recently came upon a nice 2011 review in the American Journal of Kidney Disease called “Approach to the evaluation of a patient with an increased serum osmolal gap and high-anion-gap metabolic acidosis”. It’s always nice to revisit and review this concept. You’ll always learn something new. For instance, I didn’t know that salicylates cause anion gaps as well as osmolal gaps.

So don’t forget to calculate an osmolal gap for patients with an unexplained metabolic acidosis anion gap.

PV Card: Approach to Osmolal Gap

Adapted from [1]
Go to ALiEM Cards for more resources.

Reference

1. Kraut J, Xing S. Approach to the evaluation of a patient with an increased serum osmolal gap and high-anion-gap metabolic acidosis. Am J Kidney Dis. 2011;58(3):480-484. [PubMed]

I have always been envious of the residents who carry around the Continuous Infusions cheat-sheet card, which was created by the UCSF Critical Care Units as part of a campaign for Safe Medication Prescriptions. I want one! So I finally managed to wrangle one away for a few minutes and xerox copy it. Here is the abbreviated card, after paring down the list to just ED-focused medications.

PV Card: Continuous Infusions

Go to ALiEM (PV) Cards for more resources.

Background

Serotonin syndrome is caused by the excess of serotonin and presents classically as:

• Altered mental status
• Autonomic instability
• Neuromuscular hyperactivity

Fortunately, there’s a nice algorithm (Hunter’s decision rule) which helps you decide whether it is serotonin syndrome or not. I also include a table, which I adapted from a New England Journal of Medicine review article, which helps you to differentiate it from its mimickers, such as anticholinergic syndrome, neuroleptic malignant syndrome, and malignant hyperthermia.

PV Card: Serotonin Syndrome

Adapted from [1, 2]
Go to ALiEM (PV) Cards for more resources.

A video to remind you what clonus looks like:

Thanks to Dr. Steve MacDade (Univ of Florida, Jacksonville EM resident) for the idea!

References

1. Boyer E, Shannon M. The serotonin syndrome. N Engl J Med. 2005;352(11):1112-1120. [PubMed]
2. Ables A, Nagubilli R. Prevention, recognition, and management of serotonin syndrome. Am Fam Physician. 2010;81(9):1139-1142. [PubMed]

Did you know that the American Association of Poison Control Centers reports that 10% of poison center calls are related to acetaminophen ingestions? That’s a lot. This Paucis Verbis card reviews the basics of acetaminophen toxicity. I included the Rumack Matthew nomogram to help you plot out the patient’s risk for hepatotoxicity.

In the Emergency Department, we often screen for acetaminophen toxicity for patients who may have ingested substances as a suicide attempt. We check the serum acetaminophen level 4 hours post-ingestion. Occasionally, we are surprised by a toxic level because in the first 24 hours, because symptoms are can be mild and nonspecific (abdominal pain, nausea, lethargy).

Rule of 150

• The toxic ingestion dose of acetaminophen is 150 mg/kg.
• The serum acetaminophen level when N-acetylcysteine treatment should be started is 150 mcg/mL (see Rumack Matthew nomogram)
• The starting IV dose of N-acetylcysteine is 150 mg/kg over 15 minutes.

PV Card: Acetaminophen Toxicity

Adapted from [1]
Go to ALiEM (PV) Cards for more resources.

Reference

1. Larson A. Acetaminophen hepatotoxicity. Clin Liver Dis. 2007;11(3):525-48, vi. [PubMed]