Wet beriberi, dry beriberi and Wernicke-Korsakoff syndrome
Mnemonic
“COAT” for Wernicke’s encephalopathy, and the treatment it demands:
- C - Confusion
- O - Ophthalmoplegia, classically a sixth nerve palsy, and nystagmus
- A - Ataxia
- T - give Thiamine
The classic triad is present in fewer than a fifth of cases, so any one feature in an at-risk patient warrants treatment.
Korsakoff’s psychosis follows untreated Wernicke’s and adds anterograde and retrograde amnesia with confabulation; it is largely irreversible.
Give thiamine before any glucose load. Glucose consumes the last of the thiamine as a cofactor for pyruvate dehydrogenase and can precipitate Wernicke’s in a susceptible patient.
“Wet beriberi is the heart, dry beriberi is the nerves”: high output cardiac failure versus a symmetrical peripheral neuropathy.
Expansion
Thiamine pyrophosphate is the cofactor for pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase and transketolase. Blocking the first two halts aerobic metabolism, so pyruvate accumulates and lactate rises.
Syndromes
- Wet beriberi: high output cardiac failure with peripheral vasodilatation, oedema and tachycardia
- Dry beriberi: symmetrical peripheral neuropathy with wasting
- Wernicke encephalopathy: the classic triad of confusion, ataxia and ophthalmoplegia, though all three are present in only about 10 per cent. Nystagmus is common
- Korsakoff psychosis: irreversible anterograde and retrograde amnesia with confabulation, following untreated Wernicke
- Lactic acidosis, from blocked pyruvate dehydrogenase
At risk: alcohol dependence, hyperemesis gravidarum, bariatric surgery, prolonged vomiting, malnutrition, refeeding and dialysis.
Wernicke encephalopathy is a clinical diagnosis and a medical emergency: treatment is high-dose parenteral thiamine, given immediately and before or with any glucose, since delay risks permanent Korsakoff amnesia.