Is there any substantial harm to thiamine repletion? I've always seen it given as a matter of course (in fact, as part of pre-printed order sets) for alcohol intoxication or withdrawal, and is started in emerge. This strikes me as a bad miss, both from the point of view of the doctors involved, and the system (assuming thiamine isn't part of PPOs).
Not much risk of harm that I'm aware of. Quick lit review didn't turn up anything significant, there was this one case report from the 1940s that I'd take with a big grain of salt (https://jamanetwork.com/journals/jama/article-abstract/248627). I think the risks would primarily be related to IV administration (infiltration causing compartment syndrome, accidentally gave the wrong med, etc...)
The B vitamins are water soluble, so any extra would be eliminated through urine or sweat. We used to take B vitamins when hiking because they were supposed to keep the bugs away because our sweat would reek of B vitamins, which was offensive to mosquitoes. I'm pretty sure that's been debunked, though.
No risk at all. It’s basically reflexive practice to put any patient with alcohol abuse on thiamine and folate. If they’re intoxicated and have evidence of other malnutrition, high-dose IV thiamine should be given prior to any glucose containing foods as reintroduction of sugar causes depletion of what little thiamine is left.
I read this through the lens of all the banana bags I've given over 35 years in EM. How on earth could this have happened? About the only possible scenario that I can think of is that this woman must have been well-known to the inpatient team (as a staff nurse, or more likely some sort of nurse-admin) and that the denial of the underlying disease and the unwillingness to discuss it may have contributed to their mistake. A very sad case.
Thiamine deficiency is much more abundant than we’ve previously thought. There is zero harm in giving thiamine. It’s also not only in alcoholics. It’s present in many patients with chronic inflammation such as malignancies, sepsis, diabetes, COPD, and even CHF patients. Hyperemesis gravidarum patients also! Look at the latest literature, in any ICU approximately 30-40% of patients are significantly thiamine deficient. Why aren’t we treating more often? Because the test for thiamine deficiency is a send out lab and takes 3 days to come back. Also, we still think it’s only associated with alcoholics. So we are missing it a great deal in the hospital. A great indirect test for it is Prealbumin; if below 12 there is an 80% chance the patient is thiamine deficient. I am convinced that many patients would heal and recover better with more recognition of thiamine deficiency. Again, don’t take my word for it; look at the latest literature. Google “thiamine deficiency, hiding in plain site” for an amazing peer reviewed study…it will change your practice.
Interesting article (here for anyone else who wants to read it: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8533683/). Good evidence that thiamine deficiency is fairly common, but I'm not convinced that these mild deficiencies are actually clinically significant, or that fixing them will offer any clinical improvements. Its somewhat reminiscent of the entire body of vitamin D research.
I’m not sure that these deficiencies are “mild”. I think that WE is the end result of continuous depletion and we only see the triad of WE in maybe 12-15% of those with significant deficiencies. The initial symptoms of clinically significant vitamin deficiency appear to be 1) Anorexia, or a new GI complaint 2) more frequent falls 3) any new Neuro cognitive deficit (as in new “confusion”). We see this in the ER constantly in the older, decompensated patient population. See this article as well in non alcoholic veterans https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8037750/ validating these observations.
And although I see the analogy of the Vitamin D deficiency craze, I would argue that thiamine (along with magnesium) is a much more fundamental vitamin in the most important metabolic pathways. So it’s difficult for me to think that replenishing thiamine doesn’t have sub clinical benefits in restorative physiology that are difficult to objectively measure.
“The body’s supply of thiamine depends entirely on dietary intake, there is no endogenous synthesis (unlike vitamin D). Thiamine diphosphate is an essential cofactor for the metabolism of carbohydrates and amino acids. TD can develop quickly, within 18 days on a thiamine deficient diet or within 72 h in critically ill patients (3 days?!!). Any disease that adversely affects intake or absorption, accentuates loss of nutrients, or causes acute inflammatory stress can lead to development of TD in a matter of days.”
Again, we don’t make thiamine at all, so when it’s depleted, it’s gone.
“There have been many published accounts of TD in acutely and chronically ill patients with conditions such as end stage renal disease, cancer, heart failure, dementia, acute psychiatric illness, stroke, diabetic ketoacidosis, critical illness, and medically complicated obesity. Acute Illnesses which increase metabolic demands can lead to TD more quickly including severe sepsis. Elderly patients admitted to hospital seem particularly vulnerable. Despite a preponderance of evidence that TD is not rare in these populations, it is still under-diagnosed and under-treated.”
Sincerely, keep looking into it, anecdotally I have been ordering pre albumins on many more patients and identifying shockingly low levels in many patients I would have never previously considered to be thiamine deficient. If more clinicians considered it, I believe outcomes would improve and there would even be diminished hospital days. Call me over convinced but the more I learn the more convinced I become. Thank you for the opportunity for the discourse and highlighting the problem.
Yeah I'm really confused as to why they chose that number. One possibility is that they had an economic expert estimate the cost of nursing home and medical care for the rest of her life and arrived at that number, that the plaintiffs attorney just copy/pasted into the settlement offer.
I might be wrong, but when I saw that precise number it made me think of one of the books I read where there are studies showing that if you use a precise number while negotiating this makes it more likely you get a number close to your offer . The theory is because it looks like you put a lot of work coming up with that number and there must be a good reason behind it. Here is a link discussing the theory https://qz.com/90370/when-it-comes-to-salary-negotiations-ask-for-a-precise-number
Was no radiologist expert required given no radiologist was named? That combo leads me to believe the rads findings are clearly not deviating from standard of care.
That being said, it feels to me like the hospital gives out thiamine like candy given the risk/benefit ratio of over treating vs missing WE so in this case it feels like it would be pretty easy to argue deviation from standard of care for that alone.
Correct, no radiologist was named as a defendant so the plaintiff didn't need a radiologist opinion. As far as I can tell the radiology findings are suggestive but not pathognomonic for WE. Totally agree that the risk/benefit of thiamine and the fact that we give it out like candy makes it hard to argue for the defendants in this case. I'm sure just an honest slip of the mind that perpetuated across multiple handoffs.
Sometimes inpatient psychiatric units can’t do IV lines. I wonder if there is medicolegal risk in doing PO thiamine in these cases. It doesn’t seem like it is in the patient’s best interest to sit on a medical floor if they would benefit from a psychiatric bed. I have advocated for IM thiamine in these cases but have heard it is expensive.
Most sources I read suggest 500mg thiamine IV TID for the first few days if the patient truly has WE. Seems like it would be hard to convince patients to do TID IM injections. If a patient just needs prophylaxis on the psych floor (no active WE) I think PO would be fine. Seems that PO is poorly absorbed at 100mg doses, but there's some toxicology/pharm literature that the absorption might be a lot better at big doses (500+mg/day PO).
I think if someone is having severe enough mentation changes for us to be concerned for Wernicke's then they may need a full medical workup for their encephalopathic state... It would be a hard diagnosis to make upfront in the ED and I would expect them to come to me as hospital medicine.
I give it to every intox I admit, but otherwise no. is everyone putting IVs in their alcoholics who they plan on discharging?
Is there any substantial harm to thiamine repletion? I've always seen it given as a matter of course (in fact, as part of pre-printed order sets) for alcohol intoxication or withdrawal, and is started in emerge. This strikes me as a bad miss, both from the point of view of the doctors involved, and the system (assuming thiamine isn't part of PPOs).
Not much risk of harm that I'm aware of. Quick lit review didn't turn up anything significant, there was this one case report from the 1940s that I'd take with a big grain of salt (https://jamanetwork.com/journals/jama/article-abstract/248627). I think the risks would primarily be related to IV administration (infiltration causing compartment syndrome, accidentally gave the wrong med, etc...)
The B vitamins are water soluble, so any extra would be eliminated through urine or sweat. We used to take B vitamins when hiking because they were supposed to keep the bugs away because our sweat would reek of B vitamins, which was offensive to mosquitoes. I'm pretty sure that's been debunked, though.
No risk at all. It’s basically reflexive practice to put any patient with alcohol abuse on thiamine and folate. If they’re intoxicated and have evidence of other malnutrition, high-dose IV thiamine should be given prior to any glucose containing foods as reintroduction of sugar causes depletion of what little thiamine is left.
I read this through the lens of all the banana bags I've given over 35 years in EM. How on earth could this have happened? About the only possible scenario that I can think of is that this woman must have been well-known to the inpatient team (as a staff nurse, or more likely some sort of nurse-admin) and that the denial of the underlying disease and the unwillingness to discuss it may have contributed to their mistake. A very sad case.
Banana bag has insufficient amount of thiamine to meet the standard of care for treatment of WE! But yes, I agree.
Thiamine deficiency is much more abundant than we’ve previously thought. There is zero harm in giving thiamine. It’s also not only in alcoholics. It’s present in many patients with chronic inflammation such as malignancies, sepsis, diabetes, COPD, and even CHF patients. Hyperemesis gravidarum patients also! Look at the latest literature, in any ICU approximately 30-40% of patients are significantly thiamine deficient. Why aren’t we treating more often? Because the test for thiamine deficiency is a send out lab and takes 3 days to come back. Also, we still think it’s only associated with alcoholics. So we are missing it a great deal in the hospital. A great indirect test for it is Prealbumin; if below 12 there is an 80% chance the patient is thiamine deficient. I am convinced that many patients would heal and recover better with more recognition of thiamine deficiency. Again, don’t take my word for it; look at the latest literature. Google “thiamine deficiency, hiding in plain site” for an amazing peer reviewed study…it will change your practice.
Interesting article (here for anyone else who wants to read it: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8533683/). Good evidence that thiamine deficiency is fairly common, but I'm not convinced that these mild deficiencies are actually clinically significant, or that fixing them will offer any clinical improvements. Its somewhat reminiscent of the entire body of vitamin D research.
I’m not sure that these deficiencies are “mild”. I think that WE is the end result of continuous depletion and we only see the triad of WE in maybe 12-15% of those with significant deficiencies. The initial symptoms of clinically significant vitamin deficiency appear to be 1) Anorexia, or a new GI complaint 2) more frequent falls 3) any new Neuro cognitive deficit (as in new “confusion”). We see this in the ER constantly in the older, decompensated patient population. See this article as well in non alcoholic veterans https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8037750/ validating these observations.
And although I see the analogy of the Vitamin D deficiency craze, I would argue that thiamine (along with magnesium) is a much more fundamental vitamin in the most important metabolic pathways. So it’s difficult for me to think that replenishing thiamine doesn’t have sub clinical benefits in restorative physiology that are difficult to objectively measure.
From the VA study linked above:
“The body’s supply of thiamine depends entirely on dietary intake, there is no endogenous synthesis (unlike vitamin D). Thiamine diphosphate is an essential cofactor for the metabolism of carbohydrates and amino acids. TD can develop quickly, within 18 days on a thiamine deficient diet or within 72 h in critically ill patients (3 days?!!). Any disease that adversely affects intake or absorption, accentuates loss of nutrients, or causes acute inflammatory stress can lead to development of TD in a matter of days.”
Again, we don’t make thiamine at all, so when it’s depleted, it’s gone.
“There have been many published accounts of TD in acutely and chronically ill patients with conditions such as end stage renal disease, cancer, heart failure, dementia, acute psychiatric illness, stroke, diabetic ketoacidosis, critical illness, and medically complicated obesity. Acute Illnesses which increase metabolic demands can lead to TD more quickly including severe sepsis. Elderly patients admitted to hospital seem particularly vulnerable. Despite a preponderance of evidence that TD is not rare in these populations, it is still under-diagnosed and under-treated.”
Sincerely, keep looking into it, anecdotally I have been ordering pre albumins on many more patients and identifying shockingly low levels in many patients I would have never previously considered to be thiamine deficient. If more clinicians considered it, I believe outcomes would improve and there would even be diminished hospital days. Call me over convinced but the more I learn the more convinced I become. Thank you for the opportunity for the discourse and highlighting the problem.
“The initial symptoms of Clinically significant THIAMINE* deficiency, not vitamin deficiency”. Sorry for the typo...
That's the most specific number I've ever seen for a settlement. Also, 12 days??
Yeah I'm really confused as to why they chose that number. One possibility is that they had an economic expert estimate the cost of nursing home and medical care for the rest of her life and arrived at that number, that the plaintiffs attorney just copy/pasted into the settlement offer.
I might be wrong, but when I saw that precise number it made me think of one of the books I read where there are studies showing that if you use a precise number while negotiating this makes it more likely you get a number close to your offer . The theory is because it looks like you put a lot of work coming up with that number and there must be a good reason behind it. Here is a link discussing the theory https://qz.com/90370/when-it-comes-to-salary-negotiations-ask-for-a-precise-number
Was no radiologist expert required given no radiologist was named? That combo leads me to believe the rads findings are clearly not deviating from standard of care.
That being said, it feels to me like the hospital gives out thiamine like candy given the risk/benefit ratio of over treating vs missing WE so in this case it feels like it would be pretty easy to argue deviation from standard of care for that alone.
Correct, no radiologist was named as a defendant so the plaintiff didn't need a radiologist opinion. As far as I can tell the radiology findings are suggestive but not pathognomonic for WE. Totally agree that the risk/benefit of thiamine and the fact that we give it out like candy makes it hard to argue for the defendants in this case. I'm sure just an honest slip of the mind that perpetuated across multiple handoffs.
Sometimes inpatient psychiatric units can’t do IV lines. I wonder if there is medicolegal risk in doing PO thiamine in these cases. It doesn’t seem like it is in the patient’s best interest to sit on a medical floor if they would benefit from a psychiatric bed. I have advocated for IM thiamine in these cases but have heard it is expensive.
Most sources I read suggest 500mg thiamine IV TID for the first few days if the patient truly has WE. Seems like it would be hard to convince patients to do TID IM injections. If a patient just needs prophylaxis on the psych floor (no active WE) I think PO would be fine. Seems that PO is poorly absorbed at 100mg doses, but there's some toxicology/pharm literature that the absorption might be a lot better at big doses (500+mg/day PO).
I think if someone is having severe enough mentation changes for us to be concerned for Wernicke's then they may need a full medical workup for their encephalopathic state... It would be a hard diagnosis to make upfront in the ED and I would expect them to come to me as hospital medicine.