Patients with cirrhosis may lose nutrients either because of malabsorption^^^ or because of im paired utilization^^^. Excess loss may also occur in relation to the complications of the disease such as gastrointestinal bleeding^^ or else as a result of treatm ent, for example the loss of protein which occurs following repeated paracentesis for ascites^^^.
4.4.1 Malabsorption
While m alabsorption is considered under the section of nutrient loss, it is acknowledged that it may also be regarded as a failure of nutrient intake. M alabsorption of fat is common in patients with chronic liver disease; faecal fat excretion is increased in 50-60% of adults with cirrhosis^^^’^^^’"^^. O ne of the major causes of fat malabsorption is a reduction in the intralum inal concentration of bile salts resulting from the im pairm ent of bile acid uptake, synthesis and secretion^^^.
However, m alabsorption may also arise from the direct effect of alcohol on the intestinal mucosa resulting in the depletion of brush border enzymes and im pairm ent of sodium, water, glucose and amino acid absorption^^^.
The presence of liver disease does not affect the absorptive capacity of the small bowel per se^^^. However, patients with liver disease may develop gastrointestinal disorders which themselves cause malabsorption, for example prim ary biliary cirrhosis and coeliac disease^®^.
Chapter 4 Factors contributing to malnutrition 126
The consequence of malabsorption is to increase intestinal losses of nutrients. The relationship betw een m alabsorption and nutritional status has not yet b een studied in patients with chronic liver disease.
4.4.2 Impairment of protein metabolism
T he liver plays an im portant role in the metabolism of protein by processing dietary and endogenous amino acids, regulating their supply to the rest of the body and converting am m onia into urea for excretion. In cirrhosis, liver glycogen stores are depleted^^^’^^^ and this is associated with reduced fasting splanchnic blood glucose concentrations'^^^. In order to m aintain the level of circulating glucose, the rate of hepatic gluconeogenesis is increased^^ which results in additional losses of am ino acids with potential depletion of protein stores.
T he studies on whole body protein synthesis and breakdow n in cirrhotic patients have produced conflicting results, mainly because of the confounding effects of variables such as the patient’s nutritional status and recent protein intake, and the fact that tracers used may perform differently in patients with liver disease than in healthy volunteers. Consequently, whole body protein synthesis rates have been reported as increased^^^’^^^’^^^, unchanged^^®’^^^’"^^ or reduced^^^ '^^^
T here is some evidence that nitrogen loss in breath and faeces may be increased in patients w ith chronic liver disease. Fasting expiratory am m onia concentrations are generally higher in patients with cirrhosis than healthy volunteers, particularly in those with encephalopathy who also have higher blood am m onia concentrations^^®. The concentration of am m onia in the breath of patients with cirrhosis appears relatively low at 7-16 ptg/1^^®. However, if the tidal volum e is 500 ml and respiratory rate 13 breaths per minute"^^, approximately 0.05-0.12 g of m etabolized nitrogen could be lost in breath daily or the equivalent of 9-23 g protein p er month.
Faecal nitrogen concentrations are generally not increased in patients with cirrhosis. However, faecal nitrogen losses are increased in those taking lactulose
and other non-absorbable disaccharides for the treatm ent of hepatic encephalopathy as these drugs stimulate the incorporation of nitrogen into bacterial protein within the intestinal lumen^^^’^^^. While treatm ent with non-absorbable disaccharides increases faecal nitrogen, it reduces urinary nitrogen excretion by reducing blood am m onia and may also reduce expiratory losses^^^. Thus the overall effect of non-absorbable disaccharides on nitrogen balance may not b e significant.
4.4.3 Paracentesis
C urrent treatm ent of ascites includes bed rest, sodium restriction, diuretics and therapeutic paracentesis^^. The removal of large volumes of ascitic fluid m ust be accom panied by intravenous replacem ent of protein with salt-poor album in to prevent haemodynamic disturbances and renal failure^^^’"^^^. The protein content of ascitic fluid varies between 5-60 g/1 and although only patients with malignant or infected ascites have concentrations approaching 60 g /1, up to 30% of patients
with uncomplicated ascites have protein concentrations in excess of 30 g/1^^. A typical treatm ent regimen involves the replacem ent of 40 g albumin for every 4-6 1 of ascites removed^^^ and patients may, therefore, have a net p rotein loss of up to 50 g protein per litre of ascites removed. Some patients undergo repeated large volume paracentesis and if the protein losses are not adequately replaced, protein stores may diminish.
B ertrân and colleagues^^ investigated the nutritional effects of paracentesis in 17 patients with cirrhosis by measuring TSF and MAMC before and 2 days after a single paracentesis. They concluded that the procedure had no long-term effects on nutritional status because they observed no changes in the m easurem ents over this time period. However, it is extremely unlikely that changes in anthropom etric variables would be detected over such a short time period^^^. Thus while relieving ascites by repeated paracentesis is clearly beneficial to the patient and allows them to increase their food intake, a gradual depletion of protein stores may also occur unless adequate replacem ent is given.
Chapter 4 Factors contributing to malnutrition 128
4.4.4 Gastrointestinal bleeding
G astrointestinal bleeding, another complication of chronic liver disease, is associated with decreased hepatic function and an increase in m ortality of betw een 3% and 36% in the first two days following a bleeding episode^^’^^^. Bleeding usually occurs from oesophageal or gastric varices which develop as a consequence of portal hypertension. Acute variceal haem orrhage is a medical em ergency and priority is given to correcting hypovolaemic shock by replacing blood volum e with whole blood, plasm a proteins and colloid expanders^^; once the p atien t has been resuscitated attem pts are made to stop the bleeding with drugs which alter portal haemodynamics and by local approaches on the varices themselves. In general, patients are undertransfused as increasing the circulating volume excessively might result in further variceal haemorrhage^^^’"^^. As each litre of blood contains 205 g of protein^^^ repeated haem orrhage and undertransfusion might have nutritional consequences.
N utrient losses are increased in patients with cirrhosis and, as with reductions in nutrient intake, these losses are more evident in individuals with decom pensated liver disease. The mechanisms by which these losses occur are not, in all cases, fully understood nor is the extent to which they affect nutritional status known. Consequently there is a need for further studies.