Wernicke's encephalopathy Flashcards

1
Q

What is WE?

A

Acute/ reversible stage of the manifestation of Vitamin B1/ Thiamine deficiency

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2
Q

What is the role of thiamine in the body?

A

Thiamine needs to be phosphorylated to become thiamine pyrophosphate (it’s metabolically active form) [ATP  AMP]. Thiamine pyrophosphate:

  • Assists other enzymes needed for glucose metabolism
  • In the brain, metabolises lipids and carbohydrates and maintains normal amino acids and neurotransmitter levels.
  • Helps with propagation of neural impulses too
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3
Q

Where is thiamine stored/ absorbed

A

Liver/ duodenum

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4
Q

Therefore, what will a deficiency in thiamine lead to?

A

will reduce glucose metabolism and impact cellular energy.

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5
Q

What are the causes of WE?

A
  1. Alcohol abuse- interferes with the activation (phosphorylation) of thiamine. Excess alcohol also leads to fatty liver/ liver cirrhosis which interferes with thiamine storage. Alcohol is also thought to decrease the gene expression of thiamine 1 transporter in the duodenum.
  2. Inadequate intake- anorexia/ malnutrition can lead to thiamine deficiency.
  3. GI malabsorption of thiamine in the duodenum- due to stomach cancer or IBS
  4. Prolonged vomiting- e.g. with chemotherapy, GI malignancy
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6
Q

what are the symptoms of WE?

A
  1. Confusion/ apathy
  2. Ataxia- unsteady gait
  3. vision changes
  4. Also memory disturbance
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7
Q

Signs of WE:

A
  • Ophthalmoplegia; weakness/ paralysis of eye muscles
  • Nystagmus
  • Altered GCS
  • Hypotension
  • Hypothermia
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8
Q

What are the different areas of the brain WE can affect and what symptoms may occur as a result?

A
  1. Cerebellum affected first causing altered movement and balance
  2. Brainstem- impact cranial nerve function. If medulla affected, HR and breathing will change
  3. Mamillary bodies- haemorrhage, necrosis and complete destruction of the mamillary bodies which are a part of the limbic system (memory, emotion and behaviour)
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9
Q

What investigations would you do for WE?

A
  1. Take a good history
  2. Bloods- FBC, measure thiamine, U&Es, LFTs, glucose, ABG (for hypercapnia)
  3. Red cell transketolase activity will be reduced.
  4. CT/ MRI may show degeneration of the mamillary bodies
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10
Q

What is the treatment for WE?

A
  • Replacement of the thiamine- infusion (IV) over a few days and continue oral supplements until patient is no longer at risk.
  • Infusion also given with glucose (but only when thiamine level are stabilised otherwise it would be pointless).
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11
Q

What are the complications of WE?

A

If left untreated, death occurs in 20% and 85% result in Korsakoff’s syndrome.

This is irreversible/ chronic stage of thiamine deficiency. This is characterised by:

  • Anterograde and retrograde amnesia
  • Confabulation- when person makes up stories and believes they are true due to the lack of memories
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12
Q

Which sort of populations is WE seen in?

A

Areas with socio-economic depression

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