Wernicke's Encephalopathy Flashcards

1
Q

Define Wernicke’s encephalopathy

A

Triad of mental change, ophthalmoplegia and gait dysfunction caused by thiamine deficiency
May progress to Korsakoff’s psychosis if left untreated – irreversible, profound memory
impairment and confabulation

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2
Q

What are the causes/risk factors of Wernicke’s encephalopathy?

A
  • Alcohol dependence
  • AIDS
  • Cancer and chemotherapy
  • Malnutrition
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3
Q

What are the symptoms of Wernicke’s encephalopathy?

A
  • Mental slowing
  • Impaired concentration
  • Apathy
  • Frank confusion
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4
Q

What are the signs of Wernicke’s encephalopathy?

A

• Ophthalmoplegia – gaze palsy, CN
VI palsy
• Ataxia

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5
Q

What investigations are carried out for Wernicke’s encephalopathy?

A

• Thiamine Treatment Trial - clinical response to parenteral thiamine, which can be seen in a few hours or days.
• FBC - macrocytosis is common in alcoholics
• Blood Thiamine - while the blood thiamine levels are usually low, the critical blood concentrations of thiamine for treating the condition have not been determined
• Magnesium - magnesium deficiency is common in persons who misuse alcohol on a chronic basis. Magnesium deficiency may impair the therapeutic benefit of thiamine, because magnesium serves as a co-factor in enzymes that need thiamine pyrophosphate.
• MRI Brain - shows brain lesions consistent with Wernicke’s Encephalopathy.
- Degeneration mammillary bodies, the dorsomedial nucleus of the thalami, periaqueductal grey matter, the floor of the fourth ventricle, and cerebellar vermis.
• CT Scan - not very good for showing Wernicke’s encephalopathy lesions.
• U&Es - to eliminate electrolyte imbalance as a cause of confusion.
• Finger-Prick Glucose - usually normal unless there are co-existent conditions e.g. alcoholic liver disease.
• Serum Ammonia: - typically normal, unless there is hepatic encephalitis

*You need to give thiamine first then glucose else the glucose will be converted to to lactic acid leading to metabolic acidosis

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