Wernicke's Encephalopathy Flashcards
What is Wernicke’s encephalopathy?
The presence of neurological symptoms caused by biochemical lesions of the central nervous system following exhaustion of vitamin B (particularly thiamine/B1) reserves
(Acute, reversible condition) manifesting in a triad of specific clinical symptoms: ataxia, confusion, and ocular abnormalities.
What causes Wernicke’s encephalopathy?
- Main cause is CHRONIC ALCOHOL CONSUMPTION which results in thiamine deficiency by causing:
- Inadequate nutritional thiamine intake
- Decreased thiamine absorption
- Impaired thiamine utilisation by cells - Other causes of thiamine deficiency:
- Eating disorders
- Malnutrition
- Prolonged vomiting e.g. with chemotherapy
- GI malignancy
- Chronic subdural haematoma
- AIDS
- Hyperemesis gravidarum
- Thyrotoxicosis - Thiamine deficiency results in abnormal cellular function in the cerebral cortex, hypothalamus and cerebellum
Summarise the epidemiology of Wernicke’s encephalopathy
Alcohol-related brain damage accounts for 10-24% of all dementia
Prevalence rates are higher in areas of socio-economic deprivation
Higher prevalence in 50-60 year olds
What are the presenting symptoms of Wernicke’s encephalopathy
- Vision changes: diplopia, eye movement abnormalities, ptosis
- Loss of muscle coordination: unsteady gait
- Loss of memory
- Inability to form new memories
- Hallucinations
What signs of Wernicke’s encephalopathy can be found on physical examination
- Wernicke’s is classically defined by a triad of signs:
- Confusion
- Ophthalmoplegia (nystagmus, lateral rectus or conjugate gaze palsies)
- Ataxia (wide based gait) - The patient is usually mentally alert with vocabulary, comprehension, motor skills, social habits and naming ability maintained
- Some show signs suggestive of polyneuropathy (simultaneous malfunction of many peripheral nerves throughout the body.)
- Reflexes may be decreased
- Abnormal gait and coordination
- Eye abnormalities on movement: nystagmus, bilateral lateral rectus palsy, conjugate gaze palsy
- Low temperature
- Rapid pulse
- Some may be cachectic
- NOTE: Korsakoff’s Psychosis occurs when the condition deteriorates further, leading to the additional symptoms of:
- Amnesia
- Confabulation (patient generates a false memory without the intention of deceit)
What investigations are used to diagnose/ monitor Wernicke’s encephalopathy?
- Usually a clinical diagnosis
- Decreased blood thiamine levels
- MRI → atrophy of mamillary bodies
- Screening tool for alcohol withdrawal = Clinical Institute Withdrawal Assessment for Alcohol (CIWA)
How is Wernicke’s encephalopathy managed?
- Immediate IV Thiamine (Pabrinex) (if patient at risk of Wernicke Encephalopathy, supplement diet with thiamine)
- Delirium Tremens (if hallucinations) → Tx with a benzodiazepine (chlordiazepoxide).
- Abstinence from Alcohol
What complications are associated with Wernicke’s encephalopathy?
- Ataxia
- Hearing loss
- Seizures
- Failure to treat leads to Wernicke-Korsakoff syndrome