Other complications of alcohol use disorder

Wernicke- Korsakoffs syndrome

Werncike- Korsakoffs syndrome is a neurological complication of chronic alcohol misuse caused by nutritional thiamine deficiency. Wernickes presents with confusion, ataxia, nystagmus and ophthalmoplegia. If untreated this can progress to Korsakoffs which is characterised by cerebellar ataxia, peripheral neuropathy and memory loss6. Patients with Korsakoffs are classically described as exhibiting confabulation where they fabricate stories to fill in the gaps in their memory. 

NICE recommend that patients who attend with malnourishment or decompensated liver disease and who have presented either to the emergency department or with an acute illness should be offered parenteral thiamine replacement9. 

Refeeding syndrome 

Patients who drink heavily are at risk of refeeding syndrome. Poor nutritional intake leads to changes in energy metabolism with the body sacrificing muscle stores of glycogen to maintain glucose levels. This causes depletion of potassium, magnesium and phosphate. When the patient is fed again (such as occurs on admission to hospital) these adaptations are rapidly reversed primarily by an increase in insulin levels. 

This causes a large shift of extracellular potassium, magnesium and phosphate into cells. This shift gives rise to the clinical condition known as refeeding charachterised by27:

  • arrhythmia 
  • acute heart failure 
  • neurological disturbance- seizure, paraesthesia, muscle weakness and confusion
  • respiratory failure
  • renal failure secondary to ATN

NICE recommends that all patients at risk of refeeding should have electrolyte levels (U+Es/bone profile/Mg) regularly checked and be referred for review by a dietician. Electrolyte abnormalities should be corrected promptly28. 

Hepatic Encephalopathy 

Hepatic encephalopathy can occur in both chronic and acute liver failure. It is caused by the inability of the damaged liver to clear digested proteins (particularly ammonia) which are absorbed by the gut.

Increased serum ammonia causes direct inhibitory effects on neurones via its action on GABA and also causes brain oedema. This causes a syndrome of initial drowsiness with associated flapping tremor progressing to altered consciousness and then coma. Patients with severe encephalopathy can develop focal neurology such as pupillary signs and extensor posturing. 

Diagnosis Is based on the clinical picture, imaging (CT/MRI can reveal evidence of brain oedema) and EEG. Serum ammonia can be measured but is not diagnostic alone for HE. 

First line treatment is lactulose for HE secondary to both acute and chronic liver disease. In patients with chronic liver disease and recurrent HE the antibiotic rifaxamin can be added. Both of these work to alter the gut microbiome to reduce the amount of ammonia producing bacteria present. Underlying precipitants such as GI bleed and infection should be identified and corrected29. 

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