Wernicke's encephalopathy

Wernicke's encephalopathy is a condition associated with alcohol abuse and other causes of thiamine deficiency. (1,2,3)

It is characterised by acute capillary haemorrhages, astrocytosis and neuronal death in the upper brainstem and diencephalon that leads to:

an acute confusional state

ophthalmoplegia:

• nystagmus
• bilateral lateral rectus palsies
• conjugate gaze palsies
• fixed pupils
• rarely papilloedema
  
  

• ataxia:
  • broad based gait
  • cerebellar signs in the limbs
  • vestibular paralysis

Peripheral neuropathy, usually confined to the legs, occurs in the majority of cases. Most untreated patients proceed to develop a Korsakoff psychosis with loss of recent memory, disordered time appreciation, and confabulation.

Investigations reveal raised plasma pyruvate and reduced red cell transketolase.

Thiamine should be offered to people at high risk of developing, or with suspected, Wernicke's encephalopathy.

Parenteral thiamine should be offered to people with suspected Wernicke's encephalopathy.

• maintain a high level of suspicion for the possibility of Wernicke's encephalopathy, especially if the person is intoxicated
• parenteral treatment should be given for a minimum of 5 days, unless Wernicke's encephalopathy is excluded
• oral thiamine treatment should follow parenteral therapy

Reference:

1. Galvin R, Brathen G, Ivashynka A, et al; EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. Eur J Neurol. 2010 Jul 19.
2. Habas E, Farfar K, Errayes N, et al; Wernicke Encephalopathy: An Updated Narrative Review. Saudi J Med Med Sci. 2023 Jul-Sep;11(3):193-200.
3. NICE. Alcohol-use disorders: diagnosis and management of physical complications. Clinical guideline CG100. Published June 2010, last updated April 2017