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Dietary management of hepatic encephalopathy Too many myths persist
Myths are difficult to dispel and may delay good evidence based clinical practice. This is illustrated well by a paper in this week's issue on the dietary management of hepatic encephalopathy in patients with cirrhosis (p 1391).1 Protein restriction in symptomatic patients with hepatic encephalopathy has been the cornerstone of treatment since the 1950s,2 yet there is no evidence that it has any clinical benefit. Hepatic encephalopathy is a syndrome of impaired mental status and abnormal
neuromuscular function which results from major failure of liver
function. Important factors contributing to it are the degree of
hepatocellular failure, portosystemic shunting, and exogenous factors
such as sepsis and variceal bleeding.3
The pathogenesis of the syndrome is still uncertain, although
current hypotheses include impaired hepatic detoxification of ammonia
absorbed from the gut4
and an increase in aromatic amines, which are precursors for false
transmitters in the brain Protein restriction as a treatment conveniently began with 20 g protein/day and, with clinical recovery, 10 g increments were introduced every 3-5 days, as tolerated by the patient, to a limit of 0.8-1.0 g/kg body weight3; this was considered sufficient to achieve a positive nitrogen balance. This practice continues despite evidence showing that patients with stable cirrhosis have a higher protein requirement than normal, around 1.2 g/kg dry body weight to remain in positive balance.7 Protein energy malnutrition, defined by anthropometric criteria, may occur in 20-60% of patients with cirrhosis depending on the severity of the liver disease.8 It is a common finding, with causative factors which include anorexia, nausea, malabsorption, and a hypermetabolic state. Intake may be further reduced by use of unpalatable low protein diets, already restricted in sodium and fluid. In 1997 the European Society for Parenteral and Enteral Nutrition published consensus guidelines recommending that the daily protein intake in patients with liver disease should, if possible, be around 1.0- 1.5 g/kg depending on the degree of hepatic decompensation.7 The guidelines also recommended that in patients who were intolerant of dietary protein 0.5 g protein/kg should be used transiently and that the remainder of their requirements should be achieved by giving branched chain amino acids.9 However, not all studies agree on the use of branched chain amino acids.10 Furthermore, aggressive enteral nutritional support of patients with alcoholic liver disease accelerates improvement without exacerbating hepatic encephalopathy.11 Taking smaller meals more often and eating a late evening meal also improve nitrogen balance without exacerbating hepatic encephalopathy.12 This may also be achieved with vegetable protein as opposed to animal proteins.13 The dilemma for the clinician arises in patients with acute
hepatic encephalopathy, where increasing protein intake may worsen
the condition in 35% of patients.4
Use of branched chain amino acids may improve nitrogen balance but
without producing any clinical improvement in the encephalopathy.9
However, there is no consensus about the rate at which dietary
protein should be reintroduced and at what clinical stage this is
appropriate Soulsby and Morgan provide recent evidence of perpetuation of the myth
of protein restriction in patients with encephalopathy and, perhaps
more alarmingly, that this therapy is used in patients with cirrhosis
who have no neuropsychiatric impairment.1
We agree with them on the importance of following evidence based
guidelines in the dietary and medical management of cirrhotic
patients and on the need for a combined approach from hepatologists
and specialist dietitians to achieve nitrogen balance without
exacerbating neurological symptoms. Furthermore, we need clinical
trials to determine markers for assessing when patients should
restrict their protein intake and when and at what rate they should
return to a more normal diet and maintain nitrogen balance without
exacerbating neurological symptoms. At the current state of knowledge
it seems sensible to give as much protein (up to 1.5 g/day) to
maintain a good nutritional state St George's Hospital Medical School, London SW17 0RE
© BMJ 1999
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for
example, octopamine
-aminobutyric acid-benzodiazepine
inhibitory neurotransmitter system may be implicated in the
development of hepatic encephalopathy.