Pharmacologic Management of Delirium: Remember Humility

My wife alerted me to an interesting article about a man arrested for driving while intoxicated who reported that he had auto-brewery syndrome. The most recent article I could find in PubMed which had any credibility cast doubt on the authenticity of the condition and I have to admit I don’t have any confidence in the very limited medical literature [1].

There is almost the same lack of confidence in the medical literature about Pharmacologic Approaches to Managing Delirium. OK, almost but not quite. The link takes you to the beginnings of a discussion on the American Delirium Society website about the issue and while I’m waiting for my contribution to be reviewed, I’ll copy it below:

“I’m so glad to see this basic information, although it seems inordinately difficult to do more than simply disseminate it to my colleagues in medicine and surgery. Time and time again I’m consulted to help manage delirium and the expectation is that there is some drug (usually an antipsychotic) that will stop or shorten the course or weaken the intensity of the patient’s delirium.

This can happen when the patient has hypoactive delirium, often found late because the behavioral agitation is missing and the patient doesn’t draw attention to herself. We just recently had a case presentation and short literature review on our consultation service from one of our pharmacy trainees about whether or not there is any compelling evidence that pharmacologic treatment of hypoactive delirium makes any difference in the course of the syndrome. The bottom line is there is none, essentially; at least none that would change my practice,

None of this means that I’m not open to changing my mind in the face of any compelling new evidence if it should appear–and that includes the topic of auto-brewery syndrome.

The remarks of Dr. Karin Neufeld, MD, MPH and Dr. Babar Khan, MD, MS are well taken and Dr. Neufeld’s summary might be something I would consider adding to my usual consultation recommendations:

  • “There is no evidence for the use of medication to prevent or shorten an episode of delirium.
  • We need more research in larger groups of patients with the same kinds of conditions and outcomes to see if there are very specific situations where particular medications may be useful (for example: antipsychotics like risperidone in subsyndromal delirium immediately after surgery, melatonin agonists such as Ramelteon in older hospitalized adults, antipsychotics in relation to the patient’s experience of delirium).
  • Benzodiazepines should not be the first line treatment of fearfulness or anxiety in patients with delirium and should be avoided if possible except in particular situations where indicated (such as in alcohol and or benzodiazepine withdrawal). – See more at:”

And this is a good time to remind you that the American Delirium Society annual meeting is coming up June 1-3, 2016 in Nashville. Here’s the registration link.

My suggestions to consultees and my talks with families revolve around the safest way to help make the patients with delirium as comfortable as possible while facilitating the search for and treatment of the causative medical conditions. It’s usually best to adopt a humble approach and to find a chair and sit down while listening carefully and saying frankly “I don’t know” when that’s called for.

By the way, one way our consultation service has found to promote the development of humility is to take our mascot for a walk about once a week. You have no idea how humbling it can be to walk all the way across the hospital from our office to the gift shop to get Hal recharged with helium. I call it getting small, or cultivating a habit of being more mindful about who we really are and what we can really do for our patients and our colleagues.

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  1. Logan, B. K. and A. W. Jones (2000). “Endogenous Ethanol ‘Auto-Brewery Syndrome’ as a Drunk-Driving Defence Challenge.” Medicine, Science and the Law 40(3): 206-215.
    The concentration of ethanol in blood, breath or urine constitutes important evidence for prosecuting drunk drivers. For various reasons, the reliability of the results of forensic alcohol analysis are often challenged by the defence. One such argument for acquittal concerns the notion that alcohol could be produced naturally in the body, hence the term ‘auto-brewery’ syndrome. Although yeasts such as Candida albicans readily produce ethanol in-vitro, whether this happens to any measurable extent in healthy ambulatory subjects is an open question. Over the years, many determinations of endogenous ethanol have been made, and in a few rare instances (Japanese subjects with very serious yeast infections) an abnormally high ethanol concentration (<80 mg/dl) has been reported. In these atypical individuals, endogenous ethanol appeared to have been produced after they had eaten carbohydrate-rich foods. A particular genetic polymorphism resulting in reduced activity of enzymes involved in hepatic metabolism of ethanol and a negligible first-pass metabolism might explain ethnic differences in rates of endogenous ethanol production and clearance. Other reports of finding abnormally high concentrations of ethanol in body fluids from ostensibly healthy subjects suffer from deficiencies in study design and lack suitable control experiments or used non-specific analytical methods. With reliable gas chromatographic methods of analysis, the concentrations of endogenous ethanol in peripheral venous blood of healthy individuals, as well as those suffering from various metabolic disorders (diabetes, hepatitis, cirrhosis) ranged from 0–0.08 mg/dl. These concentrations are far too low to have any forensic or medical significance. The notion that a motorist’s state of intoxication was caused by endogenously produced ethanol lacks merit.