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6 Cards in this Set

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What is the role of protein restriction in hepatic encephalopathy?
Pts with cirrhosis are often malnourished and protein restrictions are associated with increased mortality, so pts with hepatic encephalopathy should generally NOT have their protein intake restricted.

In pts whose symptoms worsen with protein intake, substitution of proteins from fish, milk or meat with vegetable proteins may improve nitrogen balance and mental status. As a general rule, only pts who have a TIPS or surgical shunt have hepatic encephalopathy severe enough to warrant use of vegetable protein or protein restriction with branched chain amino acids.
What are precipitating causes of hepatic encephalopathy?
GI bleeding
Infection (including SBP and UTIs)
Hypokalemia (increases renal ammonia production) and/or metabolic alkalosis
Renal failure
Hypovolaemia - dehydration (vomiting, diarrhea, diuretics, large volume paracentesis)
Hypoxia
Drugs - alcohol, narcotics, benzodiazepines
Hypoglycemia
Constipation
Rarely -HCC and/or vascular occlusion (hepatic vein or portal vein thrombosis)
What are the two steps involved in the ACUTE management of hepatic encephalopathy?
i) identification and correction of precipitating causes
ii) measures to lower the blood ammonia concentration
How can blood ammonia concentrations be lowered?
Lactulose 30ml PO 2-4 times per day titrated to achieve two to three soft stools per day.

Enemas can be given if the pt cannot tolerate PO lactulose

For pts who have not improved within 48 hours or who cannot take lactulose -> Rifaximin 400mg TDS or 550mg bd
How are patients with recurrent encephalopathy managed?
Lactulose 30ml PO 2-4 times per day titrated to achieve two to three soft stools per day.

If needed, Rifaximin can be added to the regimen
What is the mechanism of action of lactulose?
In the colon, lactulose is catabolised by the bacterial flora to short chain fatty acids (e.g. lactic acid and acetic acid), which lower the colonic pH to about 5.0. The reduction in pH favors the formation of nonabsorbable NH4+ from NH3, trapping NH4+ in the colon and thus reducing plasma ammonia concentrations