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Hepatic encephalopathy: dietary therapy 375Jurnalul de Chirurgie (Iaşi), 2012, Vol. 8, Nr. 425-30% cereals and 45-50% milk and milkproducts. The feeding pattern was designedto provide 4 meals during the day and a latenightsnack rich in carbohydrates at 10 p.m.They were asked to choose from a menuwith several alternatives by individualpreference and tolerance. The tolerance ofthe cirrhotic patients to dietaryrecommendation was excellent; no onewithdrew from this study because of lack ofcompliance.The protocol conformed to theDeclaration of Helsinki and Guidelines forGood Clinical Practice in Clinical Trials andwas approved by the Elias EmergencyHospital Committee. All patients signed aninformed consent.A descriptive study of the quantitativevalues was undertaken by using mean andstandard deviation values, and qualitativevalues were expressed as frequencies.RESULTSA series of 68 hospitalized patientswith cirrhosis, 43 male (63%) and 25 female(37%), was included, the median age was 54(range 30-68).The etiology of liver disease wasalcoholic in 26 patients (38%), viral-related:B, C, B+D, B+C in 24 (35%), mixed:alcohol + viral in 13 patients (19%) andother etiologies (autoimmune, primarybiliary cirrhosis, cryptogenic) in 5 patients(8%).The degree of liver disease wasassessed using the Child Pugh classification.Liver function was relatively well preserved(Child A) in 19 patients (28%), moderatelycompromised (Child B) in 46 patients (67%)and severely compromised (Child C) in 3patients (5%).Clinical examination included theevaluation of the presence of ascites andedema. 53 patients (77%) had ascites, asfollowed: 33 patients with slight ascites(63%) and 20 with moderate ascites (37%),and 15 patients (23%) didn’t have. Only 9patients had edema (13%).From all that patients (28) only 10patients had abnormal NCT (36%),corresponding to minimal hepaticencephalopathy (MHE).A significant decrease in the bloodammonia levels was observed after a monthof HPHC diet, when all patients included inthe study were considered. The decrease inblood ammonia level was observed in allpatients as it is revealed in Table I.Table I The ammonia level and NCT scores beforeand after HPHC dietBeforediet(mean)Afterdiet(mean)P valueBlood ammonia * 58.3 35.2
376 Teiuşanu A. et al.Jurnalul de Chirurgie (Iaşi), 2012, Vol. 8, Nr. 4when the initial scores were compared withthe scores obtained after a month of HPHCdiet.Taking into account the severity ofliver disease, 63% of patients (29 patients) inChild B stage had an improvement in thegrade of HE, compared with only one patient(33%) with Child C cirrhosis.Table III Global repartition of different West Havenstages, before and after the dietNo of patients Stage 0 Stage I Stage IIBefore diet 28 22 18After diet 56 38 4The improvement of HE after the dietwas not as good in patients with alcoholiccirrhosis as in patients with viral or mixedetiology. 35% of alcoholic patients improvedtheir mental status after HPHC diet,compared with 43% of patients with viraletiology and with 46% of patients withmixed etiology, but this difference didn’treach statistical significance (P=0.06).Body weight was slightly butsignificantly increased after a month of diet.Mean value before diet was 68.3 kg andafter the HPHC diet reached up to 69.2 kg(P =0.008). Mid-arm muscle circumference(MAMC) increased from 28.6 cm to 29.3 cmafter one month diet, but not statisticallysignificant.DISCUSSIONHepatic encephalopathy (HE) is aneuropsychiatric condition of impairedmental status and abnormal neuromuscularfunction that may occur in patients withadvanced liver disease and has a potentialfor full reversibility [8].Minimal hepatic encephalopathy(MHE) has no recognizable clinicalsymptoms. It is present in 30-84% ofpatients with liver cirrhosis. It is diagnosedby neuropsychological tests.Hepatocellular failure, portosystemicshunting, sepsis, variceal bleeding, excessdietary intake or electrolyte imbalance arethe most common precipitating factors thatcontribute to develop of HE [8].European Society for ClinicalNutrition and Metabolism (ESPEN)recommends that patients with liver cirrhosisshould receive 35-40 kcal/kg per day [11].Protein requirements are increased incirrhotic patients and high protein diets aregenerally well tolerated in the majority ofpatients.The inclusion of adequate protein inthe diets of malnourished patients is oftenassociated with a sustained improvement intheir mental status. Protein helps preservelean body mass; skeletal muscle makes asignificant contribution to ammoniaremoval. Protein restriction must be avoidedand the recommendation is to maintain 1.2-1.5 g proteins/kg/day [12].In severely protein-intolerant patientsit is recommended branched-chain aminoacids (BCAA) supplementation. Theseamino acids (leucine, isoleucine and valine)cannot be synthetized de novo.Chronic liver disease is characterizedby a decrease in the serum level of BCAA,whereas hyperammonemia increases theirutilization [13].The Fischer ratio, the balance betweenbranched-chain amino acids (BCAA) andaromatic amino acids (AAA), is 3:1 inhealthy population. It becomes inverted incirrhotic patients. BCAA are essential forprotein production and prevent thecatabolism. AAA are precursors for “false”neurotransmitters such as octopamine andphenylethylamine, contributing toneurologic dysfunction [13].A meta-analysis of BCAAsupplementation revealed the improved rateof recovery from episodic HE, but did notdemonstrate a survival advantage [14].Long-term oral supplementation withBCAA mixture is better than ordinary foodto improve the serum albumin level and theenergy metabolism in cirrhotic patients [15].In the same study body weight was slightlybut significant increase in the BCAA group.A significant correlation wasestablished with midarm muscle
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