Alcoholic ketoacidosis: case report and review

3.5 out of 5 stars

A Patient with Alcoholic Ketoacidosis and Profound Lactemia. Gerrity RS et al. J Emerg Med 2016 Oct;51:447-449.


This is a very good short case-based review of alcoholic ketoacidosis (AKA), and well-worth the 5 – 10 minutes reading time.

Some key points:

  • Development of AKA requires increased (binge) alcohol intake along with starvation (decreased food and water intake.)
  • The characteristic high anion gap metabolic acidosis with elevated lactate and β-hydroxybutyrate levels are the result of dehydration, decreased glycogen stores, increased reducing potential (increased NADH) and release of stress hormones (catecholamines, glucagon, cortisol, and growth hormone.)
  • The critical steps in treating AKA include fluid repletion along with administration of dextrose and parenteral thiamine, followed by feeding the patient as soon the clinical condition allows.
  • Although the differential diagnosis includes most conditions on the metabolic acidosis mnemonic, the key alternative diagnosis is usually toxic alcohol poisoning.

There are some parts of the discussion I wish the authors had expanded upon. The AKA patient in the case report remained hypotensive “despite fluid resuscitation,” was started on norepinephrine. The only fluids detailed in the report were 1 liter of D5NS bolus followed by 150 cc per hour. This is almost certainly grossly inadequate. AKA patients can be profoundly volume depleted from multiple factors such as prolonged decreased fluid intake, vomiting, and the diuretic effect of ethanol. This would be an excellent indication for the Toxicologic Ultrasound in Shock and Hypotension (TUSH) exam, using bedside sonography to visualize collapsibility of the inferior vena cava to help guide fluid resuscitation. Since AKA patients as a rule have increased catecholamine release, giving additional exogenous pressors may not be beneficial, especially if the patient’s tank is not full.

An interesting but ultimately unconvincing accompanying editorial by Cynthia Koh, Alicia Minns and Peter Rosen argues that these patients can often be treated without obtaining any lab tests except a bedside fingerstick glucose and urine pH. Again, the authors of the editorial make no mention of bedside ultrasound.

TPR Podcast Episode #12: 25 years of weird and wacky toxicology papers

25th Anniversary The Poison Review Podcast: Wild, Wacky and Weird Toxicology Articles From The Last Quarter-Century

“It is universally well known, that in ingesting our common food, there is created or produced in the bowels of human creatures, a great quantity of wind.”  Benjamin Franklin


Stool osmolar gap = 290 – 2*(stool Na + stool K)   [normal 50-100 mOsm/kg]

If stool osmolar gap < 50, diarrhea is secretory

If stool osmolar gap > 100, diarrhea is osmotic

Osmotic diarrhea will resolve with fasting; secretory diarrhea will not

Here is a link to a stool osmolar gap calculator


To read WebMD’s discussion of cases similar to that of the airline stewardess,

click here.


NOTE: As indicated above, current thinking is that a normal stool osmolar gap is

between 50 and 100 mOsm/kg. Interestingly, by that measure the stool

osmolar gap in this case of the air stewardess with puzzling diarrhea was

actually normal.


Other items discussed on the podcast:


Hennig Brand

Golden Fountain: The Complete Guide to Urine Therapy (book)

Your Own Perfect Medicine (book)


To read my “Toxicology Rounds” column on autourotherapy, click here



Quizzler (Podcast #11): In James Joyce’s novel Ulysses, Leopold Bloom’s father had committed suicide by self-poisoning. The Quizzler: what agent did Rudolph Bloom (né Rudolph Virág) use to kill himself? The answer: aconite. The winner, Dr. Richard Hamilton of Philadelphia, received a TPR t-shirt. Congratulations to Dr. Hamilton!


This episode’s Quizzler is at the end of the podcast. The winner will receive a $10 Amazon gift certificate as well as the TPR t-shirt. Our rules have changed slightly. Rather than awarding the prize to the first correct answer, we will take all correct answers submitted before the deadline and randomly select a winner. The deadline for submission is October 11, 2016, 6 pm (Chicago time.) Send submissions to: Good luck!


Dr. Steve Aks with a Lava light

Dr. Steve Aks with a Lava light


Dr. Tim Erickson threatening to try autourotherapy

Dr. Tim Erickson threatening to try autourotherapy


Drs. Tim Erickson, Steve Aks, and Leon Gussow

Drs. Tim Erickson, Steve Aks, and Leon Gussow


The Poison Review newsletter, 1998

The Poison Review newsletter, 1998




Must-read post: Why dialyze patients with chronic, asymptomatic hyperlithemia?


About a month ago I discussed a new state-of-the-art review of lithium poisoning, which I rated “four skulls” and called a near must-read. Now comes a superb post entitled “Why dialyze patients with chronic, asymptomatic hyperlithemia” from Josh Farkas from and It is essential reading for all clinicians who deal with lithium poisoned patients.

Dr. Farkas makes the following important points:

  • A single lithium level, not correlated with the patient’s clinical condition or history, does not provide much useful information.
  • The serum lithium level does not correlate well with the CNS level, which is the really important parameter.
  • “Using any single lithium level to trigger dialysis is absurd.”
  • There is no evidence to support dialysis for chronic asymptomatic hyperlithemia, no matter what the level.
  • Guidelines that mandate dialysis based solely on lithium levels (we’re looking at YOU, ExTRIP Workgroup) suffer from failing to admit uncertainty and coming to terms with the lack of good evidence on the topic.

The key conclusion: “There is no evidence to support the use of dialysis in stable patients with chronic asymptomatic hyperlithemia . . . A sensible approach to chronic asymptomatic hyperlithemia in a patient with adequate renal function might be rehydration with close monitoring of lithium and clinical status.” Very well put.

Also, don’t miss the comments section of the post, where there is a very interesting back-and-forth between Dr. Farkas and Marc Ghannoum from the ExTRIP group.

Related posts:


State-of-the-art review of lithium poisoning: almost a must-read

Hemodialysis in lithium poisoning: there is no evidence. Full stop.

Hemodialysis in lithium poisoning: what is the evidence?

Lithium-induced nephrotoxicity

Must-read: ayahuasca in America

Ecuadorian ayahuasca shaman (Ammit Jack/

Ecuadorian ayahuasca shaman (Ammit Jack/

In the current (Sept 12) issue of The New Yorker. Ariel Levy writes about the drug-fueled South American shamanistic ritual ayahuasca (or yagé,) and how its plants and practices are being imported to “hip” American areas such as Brooklyn and Silicon Valley. As TPR has explained before:

Pharmacologically, ayahuasca is quite interesting. It is commonly made by macerating and boiling together parts of the plants Banisteriopsis caapi and Psychotria viridis. Neither of these plants, taken alone, has psychedelic properties. P. viridis does contain DMT, a psychedelic tryptamine that acts — as does LSD and mescaline — at the 5-HT2A receptor. However, because of first-pass metabolism, this compound is broken down by the enzyme monoamine oxidase before it ever reaches the systemic circulation. As it happens, B. caapi contains several beta-carbolines — harmine and harmaline — that act as monoamine oxidase inhibitors. These MAOIs prevent the breakdown of DMT.

Levy’s article, cleverly titled “The Drug of Choice for the Age of Kale,” traces the history of Americans’ fascination with ayahuasca back to the Dennis and Terence McKenna, who sought out ayahuasca in 1971 during a trip to Colombia and Peru. She actually could have gone back further, at least to William Burroughs who wrote The Yage Letters in the 1950s and 60s.

The actual ayahuasca “trip” sounds horrendous, and often involves a good deal of projectile vomiting. One friend told Levy that ayahuasca “takes you to the swampland of your soul.” Author Tim Ferriss calls one of his first “trips” “the most painful experience I’ve ever had by a factor of a thousand . . . I felt like I was being torn apart and killed a thousand times a second for two hours . . . I thought I had completely fried my motherboard.”

Finally, Levy goes to Williamsburg in Brooklyn to take part in an ayahuasca ceremony. I’ll leave you to discover how the ceremony played out when you read the article, but will just say that the author ends up covered in emesis. As to whether the experience was in the end positive or negative, the results are ambiguous.

To my mind, this is the most interesting tox writing in the popular press so far this year. A must-read.

Related posts:

Ayahuasca — a pharmacologically fascinating psychedelic brew

Ayahuasca for tourists

Case series: 8 patients exposed to phony alprazolam (Xanax) containing fentanyl and/or etizolam

3 out of 5 stars

Adverse Effects From Counterfeit Alprazolam Tablets. Arens AM et al. Ann Emerg Med 2016 Aug 8 [Epub ahead of print]


In March of this year,there were 9 deaths reported in Pinellas County, Florida (the Tampa/St. Petersburg area) associated with fake alprazolam (Xanax) tablets containing fentanyl. Earlier, similar counterfeit pills had been seen around San Francisco and in Monroe County Southern Illinois.

This letter, from the University of California-San Francisco and the California Poison Control System describes 8 cases — including 1 cardiac arrest — from that region. An additional victim found at the same location as two of the cases was pronounced dead at the scene. All 8 cases occurred during the two-and-a-half month period from october 15 to December 31, 2015.

Seven of the 8 patients had blood and/or urine positive for fentanyl. Four patients had serum positive for etizolam, a benzodiazepine analog that is not FDA-approved for medical use in the United States. Additional drugs identified in these patients included cocaine, levamisole, chlordiazepoxide, diphenhydramine, sertraline, and diazepam.

Cardiac effects seen in this case series included ischemia, biventricular heart failure with pulmonary edema, and reversible cardiac arrest.

Because of the mixture of drugs involved, it’s hard to draw definite conclusions from this case series, except as a reminder that fentanyl is showing up in a variety of phony medications sold on the street, including Norco. There are also suggestions that this phenomenon may have been responsible for the death of the musician Prince.

I did a Google search and could not find any reports of counterfeit alprazolam containing fentanyl after March 2016.

As the following picture from the San Francisco Health Department shows, the phony pills look quite similar to the real thing:

Xanax Counterfeit