In this episode, I will discuss how I would treat Wernicke’s Encephalopathy if I were completely out of IV thiamine.
Wernicke’s encephalopathy is an acute disorder that has significant mortality and neurologic morbidity associated with it. Usual treatment for Wernicke’s involves high doses IV thiamine.
At the time of this recording, there is an ongoing shortage of IV thiamine products in the US, although some manufacturers do seem to have product available.
When not contained by a drug shortage, IV thiamine is liberally recommended for the prophylaxis of Wernicke’s Encephalopathy at a dose of 250 mg per day, while the treatment dose has been recommended to be as much as 1500 mg IV thiamine daily.
These high dose recommendations were constructed under the premise that IV thiamine is cheap, safe, and widely available so it is better to risk giving too much if the alternative when giving too little thiamine is permanent neurological damage.
During a time of shortage, I prefer to conserve IV thiamine for those patients most likely to have Wernicke’s, and use alternative sources of IV thiamine if possible for other patients.
However, it is likely that clinicians may be faced with the dilemma of having a patient with suspected Wernicke’s Encephalopathy and no IV thiamine available to provide treatment.
In this scenario, the only alternative source of thiamine would be enteral thiamine tablets.
Oral thiamine has not been recommended to treat Wernicke’s because it is widely believed that it has poor bioavailability due to a saturable active absorption process.
However, a study published in 2012 in BMC Clinical Pharmacology challenges that concept and seems to show that at very high doses there must be some form of passive, non-saturable absorption of thiamine.
Healthy subjects were given oral thiamine at doses of 100 mg, 500 mg, and 1500 mg.
The 500 mg dose achieved plasma thiamine levels approximately equivalent to those achieved by 100 to 200 mg IV doses. The peak concentration for the oral 500 mg dose of thiamine occurred at 3 hours.
The 1500 mg dose achieved plasma levels 3.5 times that of the 500 mg dose. The peak concentration for the oral 1500 mg dose of thiamine occurred at 4 hours.
The results of the study suggest that there is both an active and passive mechanism of thiamine absorption. In the study, high blood levels comparable with some doses of IV thiamine were achieved rapidly, in 4 hours or less.
It should be noted that the study was performed in healthy patients, not critically ill patients with suspected Wernicke’s Encephalopathy.
However, this study appears to be the only information available on the pharmacokinetics of high doses of oral thiamine. If I were faced with a situation of treating Wernicke’s without any IV thiamine I would use the evidence in this study to guide my thiamine dose decision-making.
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