Wernicke's encephalopathy Flashcards
Define Wernicke’s encephalopathy
A neurological emergency resulting from thiamine deficiency, typically involving mental status changes and gait and oculomotor dysfunction
What is the aetiology of Wernicke’s encephalopathy
Acute or sub-acute deficiency of thiamine in a susceptible person is the usual precipitant
May be due to decreased intake (oral or parenteral), relative deficiency due to increased demand, or malabsorption from the GI tract
(Thiamine deficiency → decreased activity of thiamine-dependant enzymes → metabolic events → energy compromise → neuronal death in neuronal populations with high metabolic requirements and high thiamine turnover. Areas commonly affected: dorsal thalamic nucleus, mammillary bodies, periaqueductal grey matter and 4th ventricle floor.)
What are the risk factors for Wernicke’s encephalopathy
Alcohol dependence
AIDS
Cancer treatment with chemotherapeutic agents
Malnutrition
Malignancy
Gastric bypass surgery
Haemodialysis
Hyperemesis gravidarum
Genetics, bone marrow transplantation, infants who have been fed formula milk deficient in thiamine, male
What is the epidemiology of Wernicke’s encephalopathy
Prevalence higher in males (1.7:1) - attributed to higher alcoholism frequency in men
Non-alcohol-related encephalopathy may be more common in women
What are the symptoms of Wernicke’s encephalopathy
Typical patient = alcoholic patient in hospital who has been NBM or has reduced intake
Mental slowing, impaired concentration, and apathy
Frank confusion
Mild irritability
Coma
Hearing loss, seizures, spastic paraparesis
What is the Wernicke’s encephalopathy triad
(only present in 10% of these patients):
- Confusion / mental status change
- Ataxia (Gait disturbance)
- Ophthalmoplegia /nystagmus
What are the signs of Wernicke’s encephalopathy
Confusion
Ataxia
Oculomotor findings: gaze palsies, sixth nerve palsies, impaired vestibulo-ocular reflexes
Coma
Miosis, Anisocoria, Light-near dissociation
Papilloedema, retinal haemorrhages
Tachycardia or hypotension
Hypothermia or hyperthermia
Hearing loss, seizures, and spastic paraparesis
What is Korsakoff’s psychosis
- Confusion / mental status change
- Ataxia (Gait disturbance)
- Ophthalmoplegia /nystagmus
- Confabulation & anterograde amnesia (unable to remember new information)
What are the differentials for Wernicke’s encephalopathy
Alcohol intoxication
Withdrawal of substance
Viral encephalitis
Miller-Fisher syndrome
CNS malignancy
What investigations should be done for Wernicke’s encephalopathy
A-E assessment
Bedside: CBG, ECG, urine toxicology
Bloods: FBC, U&Es, renal function, LFTs, blood alcohol level, thiamine, serum magnesium, serum ammonia
Other:
Therapeutic trial of parenteral feeding (Thiamine) → clinical response
CT/MRI
± LP for meningitis/encephalitis
What is the management for Wernicke’s encephalopathy
- A-E assessment and stabilise
- Thiamine 250-500mg IV (switch to PO when suitable, at least 5 days)
- Magnesium sulfate 2-4g/day
- Supplement with other water-soluble vitamins (such as nicotinamide and pyridoxine), because persons at risk for thiamine deficiency are commonly at risk.
± folic acid: 400-1000 micrograms/day IV
For those with Wernicke-Korsakoff syndrome offer:
- Supported independent living for those with mild cognitive impairment
- Supported 24-hour care for those with moderate-severe cognitive impairment
What are the complications of Wernicke’s encephalopathy
Ataxia and varying degrees of ophthalmospasms
Korsakoff’s psychosis
Hearing loss
Seizures
Spastic paraparesis
What is the prognosis for Wernicke’s encephalopathy
If the condition is not recognised and treated early, patients can have permanent brain injury, manifested by impairment of recent and remote memory, apathy, and confabulation, along with persistent manifestations of Wernicke’s encephalopathy, including ataxia and varying degrees of ophthalmoparesis.
