A 67-year-old female presents with encephalopathy, ataxia, and this finding on physical exam 👇
What is the diagnosis and what is the pathophysiology of this condition?
A thread 🧵🧵🧵(1/11)
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Wernicke encephalopathy (WE) is a known complication of thiamine deficiency first described by Carl Wernicke in 1881 characterized by the classic triad of:
1⃣Acute encephalopathy
2⃣Oculomotor dysfunction
3⃣Gait ataxia
(2/11)
Thiamine (Vitamin B1) is an important cofactor for several enzymes involved in metabolism ➡️ It is more important in areas with high metabolic requirements such as the brain. (3/11)
Defects in cellular energy utilization and also the formation of reactive oxygen species (ROS) ultimately leads to neurotoxicity. (4/11)
Although WE is most commonly seen in those with chronic alcoholism, it should be noted that it could be seen in any condition with ⬆️ metabolic demand or ⬆️ loss of thiamine. (5/11)
Patients w/ cancer, even without a history of alcohol misuse, are at risk for thiamine deficiency and WE. (6/11)
WE can also be seen in association with hemodialysis or peritoneal dialysis (⬆️loss of water soluble vitamins). (7/11)
Apart from the classic clinical triad of WE, other subtle clinical clues such as hypothermia are commonly reported among the unsuspected cases in autopsy series. Notably, lesions in postero-lateral hypothalamus (thermoregulatory center) are mostly seen in these patients.
(8/11)
Treatment w/ thiamin has been shown to lead to significant improvement in these thermoregulatory deficits. (9/11)
Clinical findings, laboratory and imaging studies can confirm the diagnosis of WE. HOWEVER, given the serious consequences of the progression of WE (i.e., coma, death), diagnostic testing should not delay treatment. Intravenous thiamine is safe, inexpensive, and effective.(10/11)
❗️The classic triad is not seen in many of the patients with WE.
❗️WE can also be seen in those w/o chronic alcohol consumption.
❗️Do not delay treatment when you suspect WE.
(11/11)
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