Wernicke's encephalopathy Flashcards

1
Q

what is the general presentation of Wernicke’s encephalopathy?

A

Acute presentation of confusion, opthalmoplegia (e.g. nystagmus), and ataxia –> korsakoff: alert (no longer confused), cerebellar signs remain but now have amnesia and confabulation

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2
Q

what are the differences between hepatic ecephalopathy and wernicke’s encephalopathy?

A

hepatic encephalopathy is due to liver disease and/ or shunting of blood around liver-> results in altered metabolism of nitrogenous substances

wernicke’s encephalopathy is due to thiamine deficiency

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3
Q

Define Wernicke’s encephalopathy?

A

presence of neurological symptoms caused by biochemical lesions of the central nervous system following exhaustion of vitamin B (particularly thiamine/B1) reserves

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4
Q

what is the main cause of Wernicke’s encephalopathy?

A

CHRONIC ALCOHOL CONSUMPTION-> results in THIAMINE DEFICIENCY by causing

  • inadequate nutritional thiamine intake
  • low content of vitamins in alcohol
  • low storage capacity in liver
  • decreased intestinal absorption
  • impaired conversion of thiamine to its active form ( thiamine pyrophosphate)
  • increased demand to metabolise carbohydrates in alcohol
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5
Q

what are the other causes of thiamine deficiency?

A

malnutrition + eating disorders

history of GI surgery

prolonged vomiting eg with chemotherapy

GI malignancy

chronic subdural haematoma

AIDS

Hyperemesis gravidarum

Thyrotoxicosis

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6
Q

what are the effects of thiamine deficiency?

A

thiamine needed to produce a cofactor in the Krebs cycle -> leads to neuronal death in neuronal populations with high metabolic requirements and high thiamine turnover

-> leads to abnormal cellular function in CEREBRAL CORTEX, HYPOTHALAMUS, CEREBELLUM

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7
Q

Outline the epidemiology of Wernicke’s encephalopathy?

A
  • 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
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8
Q

what are the presenting symptoms of Wernicke’s encephalopathy?

A
  • Vision changes: diplopia, eye movement abnormalities, ptosis
  • Loss of muscle coordination: unsteady gait
  • Loss of memory
  • Mental slowing and impaired concentration
  • Inability to form new memories
  • Hallucinations
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9
Q

what are the signs of Wernicke’s enephalopathy on physical examination?

A
  • Wernicke’s triad of signs
  • patient is usually mentally alert with vocabulary, comprehension, motor skills, social habits and naming ability maintained
  • Some show signs suggestive of polyneuropathy
  • 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
  • Korsakoff’s psychosis
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10
Q

what is wernicke’s triad of signs?

A
  • Confusion
  • Ophthalmoplegia (nystagmus, lateral rectus or conjugate gaze palsies)
  • Ataxia (wide based gait)
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11
Q

what is korsakoff’s physchosis?

A

occurs when condition deteriorates further leading to additional symptoms

  • amnesia
  • Confabulation- memory error defined as the production of fabricated, distorted, or misinterpreted memories about oneself or the world, without the conscious intention to deceive.
  • IRREVERSIBLE?
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12
Q

what are the appopriate investigations for Wernicke’s encepahlopathy?

A
  • FBC (high MCV is a common feature amongst alcoholics; an infection may trigger acute decomp of thiamine deficiency and elevated WBC)
  • U&Es (exclude metabolic imbalances as a cause of confusion; magnesium deficiency is also common in people who misuse alcohol)
  • LFTs (chronic alcohol use => elevated LFTs)
  • Blood alcohol level
  • Glucose
  • ABG (hypercapnia and hypoxia can cause confusion)
  • Serum ammonia - A metabolic encephalopathy due to hyperammonaemia can easily mimic or be confused with Wernicke’s encephalopathy.
  • Serum thiamine
  • Red cell transketolase activity is decreased – rarely done
  • Therapeutic trial of PE thiamine-> see If there is clinical response to treatment
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