wernicke's encephalopathy Flashcards
define wernicke’s encephalopathy
nystagmus, ophthalmoplaegia and ataxia, together with apathy, disorientation and disturbed memory.
thiamine (B12) deficiency with a classical triad of: condusion, ataxia, opthalmoplegia (nystagmus, lateral rectus, or conjugate gaze palsies)
pathology of wernicke’s encephalopathy
inadequate dietary intake
EtOH = reduced GI absorption
chronic liver disease = impaired utilisation and storage of thiamine
all = focal areas of brain damage including peraqueductal punctate haemorrhages
thiamine important for Kreb’s cycle - water soluble vitamin stored in the liver, stores last 18days
deficiency = decreased activity of thiamine dependant enzymes - metabolic events = energy compromise - neuronal death in neuronal populations with high metabolic requirments and high thiamine turn over - medial dorsal thalamic nucleus, mamillary bodies, periaqueductal grey matter, floor of 4th ventricle including ocular motor and vestibular nuclei, and cerebellar vermis
Lesions may also involve the fornices, the hippocampus, the area round the third ventricle, the quadrigeminal bodies, and the cortex.
The predilection to affect memory circuits is responsible for the most important sequela of Wernicke’s encephalopathy - Korsakoff’s psychosis.
if rapidly given glucose = permenant damage
aetiology of wernicke’s encephalopathy
acute or subacute deficiency of thiamine in a suseptible person
chronic alcoholism
eating disorders
malnutrition
prolongued vomiting eg with chemo, GI malignancy or hyperemesis gravidarum
signs and sx of wernicke’s encephalopathy
classic traid - confusion, ataxia (broad based gait, clumsy, past pointing), opthalmoplegia (nystagmus, lateral rectus or conjugate gaze palsies, diplopia)
memory disturbance - cant register new info
hypotension
hypothermia
reduced consciousness
mental slowing, impaired concentration, apathy
present rapidly after admission
Ix for wernicke’s encephalopathy
Dx clinical
red cell transketolase activity is decreased - rarely done
therapeutic trial of parenteral thiamine
serum electrolytes may be abnormal if not treated or in late presenting disease
FBC and glucose - normal unless other problem
LFT - elevated
renal func - may be abnormal if not treated or in late presenting disease
urinary and serum drug screen - normal
serum ammonia - normal unless there is decompensation of co-existent alcoholic liver disease in persons who misuse alcohol
blood alcohol level
blood thiamine and metabolites - low but no cut off for treatment
serum mg - may be low (common in alcohol abuse)
epidemiology for wernicke’s encephalopathy
prevalence varies from 0.8-2.8%
higher prevalence in patients with a history of alcohol dependence (12.5%), AIDS (10%), and bone marrow transplantation (6%).
male - increased alcoholism
non-alcohol related is more common in women
Exclusively breastfed infants in developing countries are at a higher risk of developing Wernicke encephalopathy
RF for wernicke’s encephalopathy
chronic alcoholism
AIDs
bone marrow transplant
malnutrition
malignancy
gastric bypass surgery
haemodialysis
hyperemesis gravidarum
history of GI surgery
problem with low mg in wernicke’s encephalopathy
may impair the therapeutic benefit of thiamine,
because magnesium serves as a co-factor in enzymes that need thiamine pyrophosphate.
korsakoff dementia
anterograde dementia - inability to register new info
progression from Wernicke’s encephalopathy
MMSE
episodic memory testing in wernicke/Korsakoff
what did you do today/how did you get here
recent news
where were you on X date
significant personal events
might make stuff up
can remember personal info
mx of wernike’s encephalopathy
urgent administration of parenteral thiamine for 5 days - followed by oral
thiamine before glucose - glucose metabolism needs thiamine
px of wernicke
if give rapid thiamine can recover fully in a few weeks
if no rx - mortality is 20% -> wernike-korsakoff
