Cirrhosis hepatic encephalopathy

The cirrhosis patient is in a vicious circle regarding protein metabolism cirrhosis hepatic encephalopathy protein restriction malnutrition catabolism Thus, prolonged protein restriction and catabolism may considerably worsen the prognosis of cirrhosis. In this hazardous situation, the dietary and therapeutic use of branched-chain amino acids (BCAA), i.e. valine, leucine and isoleucine, is a logical therapeutic intervention. 

O Portal hypertension is the precipitating factor for the complications of cirrhotic liver disease—ascites, spontaneous bacterial peritonitis (SBP), variceal bleeding, and hepatic encephalopathy. Lowering portal pressure can reduce the complications of cirrhosis and decrease morbidity and mortality. 

Cirrhosis is the progressive replacement of normal hepatic cells by fibrous scar tissue. This scarring is accompanied by the loss of viable hepatocytes, which are the functional cells of the liver. Progressive cirrhosis is irreversible and leads to portal hypertension that is in turn responsible for many of the complications of advanced liver disease. These consequences include (but are not limited to) spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, and variceal bleeding.1... 

Drug therapy for portal hypertension and cirrhosis can alleviate symptoms and prevent complications but it cannot reverse cirrhosis. Drug therapy is available to treat the complications of ascites, varices, spontaneous bacterial peritonitis, hepatic encephalopathy, and coagulation abnormalities. 

Blei AT, Cordoba J, and the Practice Parameters Committee of the American College of Gastroenterology. Hepatic encephalopathy practice guidelines. Am J Gastroenterol 2001 96 1968-1976. Gines P, Cardena A, Arroyo V, Rodes J. Management of cirrhosis and ascites. N Engl J Med 2004 350 1646-1654. 

Chronic hepatitis (disease lasting longer than 6 months) is usually associated with hepatitis B, C, and D. Chronic viral hepatitis may lead to the development of cirrhosis, which may induce end-stage liver disease (ESLD). Complications of ESLD include ascites, edema, jaundice, hepatic encephalopathy, infections, and bleeding esophageal varices. Therefore, prevention and treatment of viral hepatitis may prevent ESLD. 

Liu Q, Duan ZP, Ha DK, Bengmark S, Kurto-vic J, Riordan SM Symbiotic modulation of gut flora Effect on minimal hepatic encephalopathy in patients with cirrhosis. Hepatololy 2004 39 1441-1449. 

FIGURE 34-3 Positron emission tomography using 13NH3 showing increased brain ammonia uptake in a patient with liver cirrhosis and mild hepatic encephalopathy. CMRA, cerebral metabolic ratio for ammonia HE, hepatic encephalopathy PS, permeability/surface area product. (With permission from reference [9].)... 

Hepatic cirrhosis and ascites In these patients, sudden alterations of electrolyte balance may precipitate hepatic encephalopathy and coma. Do not institute therapy until the basic condition is improved. 

Carbonic anhydrase inhibitor-induced alkalinization of the urine decreases urinary excretion of NH4+ (by converting it to rapidly reabsorbed NH3) and may contribute to the development of hyperammonemia and hepatic encephalopathy in patients with cirrhosis. 

Portal hypertension most commonly occurs as a consequence of chronic liver disease. Portal hypertension Is caused by Increased blood flow within the portal venous system and increased resistance to portal flow within the liver. Splanchnic blood flow is increased in patients with cirrhosis due to low arteriolar resistance that is mediated by increased circulating vasodilators and decreased vascular sensitivity to vasoconstrictors. Intrahepatic vascular resistance is increased in cirrhosis due to fixed fibrosis within the spaces of Disse and hepatic veins as well as reversible vasoconstriction of hepatic sinusoids and venules. Among the consequences of portal hypertension are ascites, hepatic encephalopathy, and the development of portosystemic collaterals—especially gastric or esophageal varices. Varices can rupture, leading to massive upper gastrointestinal bleeding. 

A 70-year-old woman with a 2-year history of primary biliary cirrhosis confirmed by histological and immunological criteria took colestyramine sachets twice daily for 2 months and developed lethargy, confusion, and drowsiness (3). She had signs of chronic liver disease, portal hypertension, and hepatic encephalopathy. Laboratory investigations confirmed a metabolic acidosis (pH 7.15) and hyperchloremia. Multiple cultures failed to reveal sepsis, and a urinary pH of 4.85 together with tests of renal acidification excluded renal tubular acidosis. No other cause was found and she responded to 600 mmol of sodium bicarbonate intravenously over 36 hours. 

Cirrhosis is often asymptomatic until complications of liver disease are present. Mrs MW may present with itching, jaundice, dark urine, pale fatty stools, abdominal pain, nausea, fatigue, bleeding - such as nose bleeds, hepatic encephalopathy, hepatomegaly, ascites, distended abdominal veins, spider angiomata, palmar erythema and asterixis. She may also present with the signs and symptoms of alcohol withdrawal, which include irritability, anxiety, tachycardia, tremor, sweating, confusion and hallucinations. 

Case study level 1 - Alcoholic cirrhosis alcohol withdrawal 338 Case study level 2 - Alcoholic cirrhosis management of bleeding risk and treatment for the maintenance of alcohol abstinence 339 Case study level 3 - Hepatic encephalopathy and ascites 341 Case study level Ma - Pulmonary tuberculosis 342 Case study level Mb - Liver failure 344... 

Mehndiratta, M.M., Sood, G.K., Sarin, S.K., Gupta, M. Comparative evaluation of visual, somatosensory, and auditory evoked potentials in the detection of subclinical hepatic encephalopathy in patients with nonalcoholic cirrhosis. Amer. J. Gastroenterol. 1990 85 799-803... 

Saxena, N., Bhatia, M., Joshi, Y.K., Garg, P.K., Tandon, R.K. Auditory P 300 event-related potentials and number connection test for subclinical hepatic encephalopathy in patients with cirrhosis of the liver a follow-up study. J. Gastroenterol. Hepatol. 2001 16 322—327... 

Shiota, T. Quantitative psychometric testing and subclinical hepatic encephalopathy-comparative study between encephalopathic and non-en-cephalopathic patients with liver cirrhosis. Acta Med. Okayama 1984 38 193-205... 

While hepatic encephalopathy is nearly always found in acute liver failure, it can only be expected in some 25-40% of patients with a portosystemic shunt. When these two preconditions coincide, as in the case of liver cirrhosis, manifest hepatic encephalopathy is witnessed in 30-50% of patients and a subclinical course of disease in 50-70%. In other words, the frequency, the degree of severity and the course taken by HE depend on the underlying conditions. 

Bustamante, J., Rimola, A., Ventura, P.J., Navasa, M., Cirera, I., Rega-ardo, V., Rodes, J. Prognostic significance of hepatic encephalopathy in patients with cirrhosis. X. Hepatol. 1999 30 890-895... 

Cabre, E., Periago, J.L., Gonzalez, J., Gonzalez-Huix, F., Abad-Lacruz, A., Gil, A., Sancbez-Medina, F., Esteve- Comas, M., Fernandez-Ban-ares, F., Planas, R., Gassull, M.A. Plasma polyunsaturated fatty acids in liver cirrhosis with or without chronic hepatic encephalopathy a preliminary study. X. Parenter. Enter. Nutr. 1992 16 359-363... 

Gitlin, N., Lewis, D.C., Hinkley, L. The diagnosis and prevalence of subclinical hepatic encephalopathy in apparently healthy, ambulant, non-shunted patients with cirrhosis. J. Hepatol. 1986 3 75-82... 

Hnber, M., Rossle, M., Siegerstetter, V., Ochs, A., Haag, K., Kist, M., Blnm, H.E. Helicobacter pylori infection does not correlate with plasma ammonia concentration and hepatic encephalopathy in patients with cirrhosis. Hepato-Gastroenterol. 2001 48 541 -544... 

Silva, G., Segovia, R., Ponce, R., Backhouse, C., Palma, M., Roblero, J.R, Abadal, J., Quijada, C, Troncoso, M., Iturri a, H. Effects of 5-isosorbide mononitrate and propranol on subclinical hepatic encephalopathy and renal functions in patients with liver cirrhosis. Hepato-Gastroenterol. 2002 49 1357-1362... 

Strauss, E., Ferreira da Costa, M. The importance of bacterial infections as precipitating factors of chronic hepatic encephalopathy in cirrhosis. Hepato-Gastroenterol. 1998 45 900—904... 

Tarter, R.E., Hegedus, AJM., van Thiel, D.H., Schade, R.R., Gavaler, J.S., Starzl, T.E. Nonalcoholic cirrhosis associated with neuropsychological dysfunction in the absence of overt evidence of hepatic encephalopathy. Gastroenterology 1984 86 1421-1427... 

Kircheis, G., Nilius, R., Held, C., Berndt, H., Buchner, M., Gortelmeyer, R., Hendridis, R., Kruger, B., Kuklinski, B., Meister, H., Otto, H.-J., Rink, C., Rosch, W., Stanch, S. Therapeutic efficacy of L-ornithine-L-aspartate infusions in patients with cirrhosis and hepatic encephalopathy results of a placebo-controlled, double-blind study. Hepatology 1997 25 1351-1360... 

Loguercio, C., Abbiati, R., Rinaldi, M., Romano, A., Dei VeccMo Bianco, C., Coitori, M. Long-term effects of Enterococcus faecium SF 68 versus lactulose in the treatment of patients with cirrhosis and grade 1-2 hepatic encephalopathy. X Hepatol. 1995 23 39-46... 

Disorders of cerebral functions on the one hand and of the water and electrolyte balance on the other hand are the earliest and most reliable hints of the onset of decompensation in severe liver disease, especially cirrhosis. In clinical terms, they can be easily diagnosed as latent hepatic encephalopathy (by carrying out psychometric tests) and/or latent oedema (by recording the increase in body weight). For this reason, these examination methods are also of fundamental importance in the follow-up of chronic liver disease, (s. fig. 15.3)... 

Fig. 16.13 Enonnous refractory ascites in alcoholic cirrhosis. Bilateral inguinal hernia with scrotal oedema. Muscular atrophy. Hepatic encephalopathy (II—III) (same patient as in fig. 16.14)...

In liver cirrhosis, hepatorenal syndrome is nearly always (> 80%) accompanied by ascites. HRS is most common in alcoholic cirrhosis. In some 75% of cases, hepatic encephalopathy is witnessed at the same time, and jaundice is evident in about 40% of cases. HRS occurred in 18% of all cirrhotic patients with ascites within one year and in 32% within 5 years. (21)... 

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