Note to readers: Everything you need to review Dr Farkas podcast and post is contained in the links in the next paragraph.
I excerpt from the chapter because doing so helps me fix the information in mind [spaced repetition] and when I post on a resource it is easy for me to review the information in the blog using the blog’s Search box or Categories List that are on every page.
In addition to Dr Farkas chapter on thiamine deficiency, for more information on the topic, please see the following posts:
- Wernicke-Korsakoff Syndrome (Thiamine Deficiency) Can Occur In Non-alcoholics As Well As In Alcoholics
Posted on February 15, 2020 by Tom Wade MD
In this post I link to and excerpt from Dr Josh Farkas’ outstanding chapter in the Internet Book Of Critical Care [Link to the Table Of Contents], Wernicke encephalopathy [Link to The Podcast] [Link To The Show Notes]. October 14, 2020.
Dr Farkas writes in the introduction to the podcast:
Wernicke encephalopathy is important because it’s surprisingly common, potentially debilitating, and fully treatable. Some patients may present to the hospital due to Wernicke encephalopathy, while many others may develop this while in the ICU as an iatrogenic complication of critical care.
And here are direct links to each part of the Wernicke Encephalopathy chapter. These are all from Dr Farkas post:
And here are excerpts from Dr. Farkas’ chapter:
- Failure to consider Wernicke encephalopathy in patients with atypical risk factors (e.g., ICU patients, hyperemesis gravidarum, chronic diuretic use for heart failure).
- Inadequate dose and duration of thiamine used for patients with Wernicke encephalopathy. One or two days of IV thiamine isn’t sufficient!
- Incorrectly excluding the diagnosis of Wernicke encephalopathy because patients lack the classic triad of symptoms (confusion, ataxia, ophthalmoplegia). In fact, very rarely will patients with Wernicke encephalopathy display all of these components.
- Inadequate use of thiamine prophylaxis against Wernicke encephalopathy among at-risk critically ill patients. Oral thiamine is probably adequate for this purpose, making the expense of prophylaxis negligible.
- Don’t Wernicke’s, B(1) Happy (Tox & Hound, by Meghan Spyres)
- Wernicke Encephalopathy (RebelEM, by Anand Swaminathan) and also a podcast.
- Wernicke encephalopathy (Radiopaedia, by Craig Hacking and Frank Gaillard)
The above excerpts are actually from the end of Dr Farkas post. I like to start with that part of post.
All that follows are excerpts [I will place any of my comments, if I make any, in brackets]:
Place fig1 here.
- Thiamine is a co-factor in numerous enzymatic reactions involved in energy metabolism, as shown below. Thiamine deficiency has consequences including the following:
- (1) Accumulation of lactate
- (2) Excess production of glutamate, which may lead to excessive excitatory neurotransmission in the brain
- This can cause vasogenic and cytotoxic edema*
- *Pathogenesis of Brain Edema and Investigation into Anti-Edema Drugs. Int J Mol Sci. 2015 May; 16(5): 9949–9975.
Place fig 2 here
pharmacology of thiamine
- The daily requirement of thiamine is ~1-2 mg. Thiamine is absorbed in the jejunum and stored in the liver. Absorption is relatively inefficient; for example, one study of healthy volunteers found that only 5% of a 50-mg oral dose was absorbed.(30146080) However, a recent study suggests that this might be overcome with the use of very high doses of oral thiamine, as shown in the figure below.(22305197)
- Total body stores of thiamine are ~30 mg (but potentially lower in liver disease).
- Inadequate thiamine intake can cause a previously healthy person to become deficient within ~2-4 weeks. (32551830) In the context of acute or chronic illness, deficiency can occur more rapidly.
Place fig3 here.
signs & symptoms
Signs and symptoms are generally unreliable in the diagnosis. The classic triad of encephalopathy, ophthalmoplegia, and ataxia is present in only ~15% of cases. Among non-alcoholic patients with Wernicke encephalopathy, the triad is even less common.(31171116)
#1 = encephalopathy
- Delirium is the most consistent clinical characteristic.
- This may progress to coma.
- Isolated encephalopathy without ocular or cerebellar signs may be more common in nonalcoholic Wernicke encephalopathy.(32390125)
Start here– Insert the two YouTube videos.