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  1. 1. ALCOHOLIC LIVER DISEASE Aetiology ; Pathophysiology & Nutritional management MANSI M.SHAH M.Sc CLINICAL NUTRITION
  2. 2. INTRODUCTION Largest gland - 1500g
  3. 3. FUNCTIONS Ability to regenerate itself ; 10- 20% of functioning liver CHO , lipid
  4. 4. INDIAN JOURNAL OF PUBLIC HEALTH , 2014 Trends of chronic liver disease in a tertiary care referral hospital in Eastern India Background: There is scarce Indian data on time trends of hepatitis, an impediment to formulate an effective public health policy on the matter. Objective: The aim was to study secular trends and burden of hepatitis in a railway population. Materials and Methods: Outdoor, indoor, endoscopy unit and mortality records of patients attending this hospital from January 2003 to December 2011 were searched manually and relevant parameters of hepatitis patients were noted, especially etiology, clinical features, treatment, and mortality. Cochran-Armitage trend test was used to test significance of any trend in these parameters. Binary logistic regression analysis of various factors was carried out to study their effect on the liver related mortality of hepatitis B and C cases and Kaplan-Meyer survival curves were generated for significant factors. Two-sided P < 0.05 was considered to be significant. Result: Chronic liver disease (CLD) due to alcohol showed a significant rising trend with early age (mean 48.4 years) and high percentage of decompensated disease (75%) at presentation and high early mortality (63%). No trend was observed for hepatitis B and C, but significant reduction in mortality was observed when definitive therapy was given. Cryptogenic CLD showed a decreasing trend though overall it still remained the most important etiology and survival was better compared with alcohol even with conservative therapy. Only 4% patients had hepatocellular carcinoma. Conclusion: A menace of alcohol related liver disease affecting young productive work force in this part of India is foreseen, which might impact the country's economy and mandates immediate containment policy.
  5. 5. METABOLISM OF ALCOHOL First pass metabolism - stomach mucosa • ADH - alcohol dehydrogenase pathway • MEOS - microsomal ethanol oxidizing system Change In Redox Potential In Liver • Suppression Of Krebs Cycle (Increased Transformation From Pyruvate To Lactate) • Impaired Gluconeogenesis , Hypoglycemia • Increased Fatty Acid Synthesis • Hyperuricemia
  6. 6. Pathogenesis There are a number of hypotheses regarding the pathogenesis of alcoholic liver injury. Ethanol metabolism usually takes place in the mitochondria. Ethanol is oxidised to acetaldehyde by alcohol dehydrogenase, which in turn is oxidised to acetate by acetaldehyde dehydrogenase. These oxidation reactions are associated with the formation of NADH and NAD alter the redox state of the cell. This has harmful effects on lipid and carbohydrate metabolism—for example, steatosis. In habitual drinkers, a microsomal mixed function oxidase, the microsomal ethanol oxidising system, is increased by enzyme induction and is also responsible for production of acetaldehyde.
  7. 7. The quantity of alcohol consumed is the most important risk factor for ALD. ALD - Alcohol consumption of >40g/day Cirrhosis - Alcohol consumption of >60-80g/day Women - twice sensitive to hepatotoxicity Several variables predispose some people to alcoholic liver disease. These include • genetic polymorphisms of alcohol • gender (women more than men), • simultaneous exposure to other drugs, • infections with hepato- tropic viruses, • immunologic factors, • obesity, and poor nutrition status. RISK FACTORS
  8. 8. CLINICAL PRESENTATION • Alcohol can cause significant liver damage without producing any symptoms or signs of liver disease. Many people are diagnosed when they have routine liver function tests as part of a medical check-up. • Patients may present with non-specific features such as nausea, vomiting, abdominal discomfort, or diarrhoea. • Patients with fatty liver usually look well and often have only mild hepatomegaly with no other stigmata of chronic liver disease. • Patients with advanced liver disease may present with jaundice, ascites, encephalopathy, or upper gastrointestinal bleeding.
  9. 9. • obtaining a reliable history of prolonged alcohol abuse • Increased γ-Glutamyltransferase • Increased mean corpuscular volume • Carbohydrate deficient transferrin - follow up patients • Bilirubin (markedly raised in acute alcoholic hepatitis) • Serum transaminases • Prothrombin time • Hypoalbuminemia • Electrolyte abnormalities - hyponatraemia and hypokalaemia and less commonly hypocalcaemia and hypomagnesaemia • Serum fibrosis markers: procollagen III propeptide, laminin, type IV collagen • Liver ultrasound: detect splenomegaly and ascites • Liver biopsy BIOCHEMICAL MARKERS
  10. 10. MALNUTRITION IN THE ALCOHOLIC • Primary: displacing other nutrients in diet;high energy content • Secondary: maldigestion / malabsorption NUTRITIONAL EFFECTS OF ALCOHOLISM • Imbalanced diet or anorexia • Intestinal maldigestion & malabsorption • Increased catabolism of visceral proteins & skeletal muscle • Increased excretion of vitamins
  11. 11. The pathogenesis of alcoholic liver disease progresses in three stages: Hepatic steatosis (Fatty liver) - 80% Alcoholic hepatitis - 10 - 35 % Cirrhosis - 10% SPECTRUM OF LIVER DISEASE
  12. 12. HEPATIC STEATOSIS • 90% chronic alcohol abuser ; asymptomatic • Clinical sign - hepatomegaly • Elevated SGOT & SGPT levels • Benign & Reversible condition (abstinence from alcohol) • Accumulation of lipid exceeds 5% of liver weight • fatty liver - steatosis • fatty liver with inflammation - steatohepatitis • CAUSES: Increased availability of fatty acids in the liver • From Adipose tissue • Lipids synthesised by liver • Dietary lipids • Increased synthesis & decreased degradation
  13. 13. • The most common and difficult to handle myth about liver disease is that there should be almost complete restriction of dietary fat and protein intake in diet, which is in contrast to the actual scientific dietary advices for such patients. • Protein should be 1.5 g/kg/day and restricted only in the presence of encephalopathy. Protein should be from vegetable source and inclusion of Medium chain triglycerides in the diet should be done as they are easily digested in the absence of bile. • Supplementation of vitamins and minerals should be taken. • Always take consultation of registered Dietitian which provides a right diet for right treatment.
  14. 14. ALCOHOLIC HEPATITIS • Toxic liver injury - inflammation of liver • Chronic ethanol consumption • Increased susceptibility to infection ( pneumonia ; septicaemia) • Antibiotics & Corticosteroids - complexity of nutritional management • Symptoms: fatigue; anorexia; weakness; fever, hepatomegaly. • High mortality rates are seen (30%–60%).
  15. 15. MNT • Spare liver & provide nutrients needed for regeneration 1. Abstention from alcohol 2. Small frequent meals 3. Energy: 30-35kcal /kg (conc. liquid formulas) severe vomiting or diarrhoea- 5-10% glucose 4. CHO - 60 - 65% of calories 5. Protein : 1 - 1.2 g/kg 6. Fat : 20 - 30% of calories bile obstruction- reduce fat 7. Vitamin -K supplementation (less prothrombin time) 8. Na & K (vomiting or diarrhoea) 9. Correction of nutritional deficiencies: multivitamin(B12;folate ;thiamine ;pyridoxine ;vit-a ;vit-d) mineral supplement (Zn; Mg; Ca;Ph)
  16. 16. CIRRHOSIS • Chronic liver disease - healthy tissue replaced by scar tissue, blocking the flow of blood through the organ - loss of liver function • Causes- chronic alcohol consumption; HCV; alcohol toxicity, genetic predisposition & malnutrition • Therapeutic interventions & Nutritional treatment - prevent complications • Laennec’s cirrhosis - scar tissue fat accumulation portal hypertension esophageal varices • Clinical manifestations - hepatomegaly; necrosis of liver cells; serum protein is low; SGOT is elevated; decreased Hb levels. Jaundice; ascites ; edema ; fever ; anorexia; diarrhoea; delirium
  17. 17. MANAGEMENT • Abstinence: support groups, alcohol withdrawal syndrome. 1. Small frequent meals 2. Energy: 40 - 50 kcal /kg dry body weight (minimise endogenous protein catabolism) 3. CHO - 300 - 400g to spare protein 4. Protein : 1 - 1.5 g/kg dry weight 5. Fat : 30 - 40% of non protein calories restrict fat in case of jaundice • Vitamins & minerals - thiamine, folic acid, and other B vitamins carotenoids, selenium, vitamin E, folate and zinc. • Nutrition supplements: nasogastric feeding in malnourished
  18. 18. Journal of nutrition and food science , 2013 Effect of a Late Evening Snack of Amazake in Patients with Liver Cirrhosis: A Pilot Study Yumiko Nagao1 and Michio Sata Background: Liver Cirrhosis (LC) is a state of accelerated starvation. A late evening snack improves protein energy malnutrition, caused by overnight starvation and the catabolic state of patients with LC. This study was designed to evaluate the effects of amazake, a traditional sweet Japanese beverage, as a late evening snack for cirrhotic patients. Methods: Serum biochemical parameters and the visual analogue scale (VAS) were examined at 0, 4, 8, and 12 weeks. Each patient drank 200 kcal of amazake at bedtime every night for 12 weeks. Results: Four patients (mean age 67.3 ± 5.7 years) with viral LC were recruited and their VAS score determined, along with a biochemical examination of the blood. White blood cell counts (WBC), especially neutrophil counts, were elevated following a period of amazake intake. Each VAS score was reduced following amazake intake. Amazake intake improved the Quality of Life (QOL) in all terms of sense of abdomen distension, edema, fatigue, muscle cramps, loss of appetite, taste disorder, constipation, diarrhea, vomiting, and sleep disorder. Any sense of abdominal distension, constipation and vomiting had disappeared after 8 weeks of amazake intake and taste disorder and sleep disorder had disappeared after 12 weeks of amazake intake. No major clinical events or virological rebounds occurred in the subjects. Conclusions: Amazake, which is rich in vitamins and amino acids, could be effective in reducing the subjective symptoms and improving the QOL of patients with LC.
  19. 19. Probiotics for patients with compensated liver cirrhosis: a double-blind placebo-controlled study. Pereg D1, Kotliroff A, Gadoth N, Hadary R, Lishner M, Kitay-Cohen Y., February , 2011 BACKGROUND: Gut flora is related to the major complications of liver cirrhosis including hepatic encephalopathy, spontaneous bacterial peritonitis, and variceal bleeding. Prior studies have reported a beneficial effect of gut flora modification with probiotic bacteria in patients with minimal hepatic encephalopathy. We aimed to study the effect of probiotics on clinical and laboratory parameters of patients with compensated cirrhosis. METHODS: A double-blind placebo-controlled study that included patients with liver cirrhosis and at least one major complication of cirrhosis in the past, clinical evidence of portal hypertension, or decreased hepatic synthetic function. Participants were randomly assigned to receive probiotic capsules containing Lactobacillus acidophilus, Lactobacillus bulgaricus, Bifidobacterium lactis, and Streptococcus thermophiles or placebo for a period of 6 months. RESULTS: A total of 36 patients were available for final analysis (distributed equally between the probiotic and placebo groups). The administration of probiotics was not associated with significant differences in either clinical or laboratory parameters between the two groups. Because the lack of a beneficial effect may be related to the compensated liver disease of patients, we conducted a subanalysis of patients with baseline ammonia levels > 50 mmol/L. In this subgroup, the administration of probiotics appeared to significantly reduce the ammonia levels starting after 1 month of treatment. However, this effect diminished and lost its significance following comparison to the placebo group.
  20. 20. The effect of a late-evening protein-containing snack on nitrogen balance in cirrhotic patients , 2014 tanta medical journal Purpose The aim of the study was to evaluate the effect of a late-evening protein-containing snack on nitrogen balance in cirrhotic patients. Patients and methods Thirty cirrhotic patients were divided into the following groups: group I, comprising 15 patients who received a late-evening 300-cal, 15-g protein-containing snack daily for 15 days; and group II, comprising 15 patients who received a late-evening supplement of amino acids (branched and essential) containing 22-g protein daily for 15 days. All patients were subjected to full history taking, clinical examination, and pelvic abdominal ultrasound. Liver function tests, complete blood picture analysis, and estimation of blood urea and serum creatinine, urinary nitrogen loss, urea concentration in both serum and urine, and nitrogen balance were performed for all patients. Results There was a significant increase in the mean level of serum albumin and red blood cell counts. The mean nitrogen balance significantly increased in both groups but more in patients who received branched chain amino acid (BCAA) supplementation. The mean serum ammonia significantly decreased in group II patients who received a late-evening BCAA supplementation, but not in patients of group I who received a late-evening protein-containing snack. There was no statistically significant difference in the levels of serum bilirubin or fasting blood glucose in either group.
  22. 22. MNT • High protein to replenish serum albumin & raise oncotic pressure • salt restriction - 2g / day • fluid restriction- 1500ml/day if Na is below 120 mEq/l • Acute bleeding episodes - PN • Adequate energy • Diuretic therapy • Paracentesis • TIPS (Transjugular intrahepatic portosystemic shunt )
  23. 23. HEPATIC ENCEPHALOPATHY • Syndrome of impaired mental status & abnormal neuromuscular function resulting in failure of liver function • Contributing factors: • degree of hepatocellular failure • portosystemic shunting • exogeneous( sepsis& variceal bleeding) • Clinical manifestations: • changes in mental status & personality • neuromuscular changes • Asterixis
  24. 24. Child - Pugh score
  25. 25. Nitrogen metabolism plays a major role in the development of hepatic encephalopathy (HE) in patients with cirrhosis. 1. Energy and nitrogen requirements in patients with HE are unlikely to differ substantially from those recommended in patients with cirrhosis per se viz. 35-45 kcal/g and 1.2-1.5g/kg protein daily. 2. Small meals evenly distributed throughout the day and a late-night snack will help minimize protein utilization. 3. Diets rich in vegetables and dairy protein may be beneficial and are therefore recommended. 4. Branched chain amino acid (BCAA)supplements ; Increasing dietary fiber & probiotics may be of value. 5. Short-term multivitamin & mineral supplementation should be considered in patients admitted with decompensated cirrhosis. 6. Hyponatremia may worsen HE; it should be prevented as far as possible and should always be corrected slowly. 7. Effective management of these patients requires an integrated multidimensional approach. American association for the study of liver disease AASLD , 2013
  26. 26. Probiotic VSL#3 Reduces Liver Disease Severity and Hospitalization in Patients With Cirrhosis: A Randomized, Controlled Trial , 2014 Background & Aims Little is known about whether probiotics can affect outcomes of patients with cirrhosis and hepatic encephalopathy (HE). We assessed the efficacy of a probiotic preparation in preventing the recurrence of HE (primary outcome) and reducing the number of hospitalizations and severity of liver disease in patients with cirrhosis. Methods We performed a double-blind trial at a tertiary care hospital in India. Patients with cirrhosis who had recovered from an episode of HE during the previous month were assigned randomly (using computer-generated allocation) to groups given a probiotic preparation (VSL#3, 9 × 1011 bacteria; CD Pharma India Private Limited, New Delhi, India) (n = 66) or placebo (n = 64) daily for 6 months. Results There was a trend toward a reduction in the development of breakthrough HE among patients receiving the probiotic (34.8% in the probiotic group vs 51.6% in the placebo group; hazard ratio [HR], 0.65; 95% confidence interval [CI], 0.38–1.11; P = .12). Fewer patients in the probiotic group were hospitalized for HE (19.7% vs 42.2%, respectively; HR, 0.45; 95% CI, 0.23–0.87; P = .02) or for complications of cirrhosis (24.2%) than in the placebo group (45.3%) (HR, 0.52; 95% CI, 0.28–0.95; P = .034). Child–Turcotte–Pugh and model for end-stage liver disease scores improved significantly from baseline to 6 months in the probiotic group, but not in the placebo group. There were no adverse events related to VSL#3. Conclusions Over a 6-month period, daily intake of VSL#3 significantly reduced the risk of hospitalization for HE, as well as Child–Turcotte–Pugh and model for end-stage liver disease scores, in patients with cirrhosis.
  27. 27. LIVER TRANSPLANT • Atleast 6 months of alcohol abstinence • Psychosocial & nutritional status MNT - individualised • Goal - lessen the effects of malnutrition & complications (ascites) • Before transplant: 35 - 45 kcal/kg; • 1.0 - 1.5g protein/kg • After transplant: 30 - 35kcal/kg; • 1.0 - 1.2g protein/kg • Immunosuppressant drugs- hyperglycaemia.
  28. 28. Bacterial sepsis after living donor liver transplantation: the impact of early enteral nutrition. , 2012 Ikegami T1Shirabe K, Yoshiya S, Yoshizumi T, Ninomiya M, Uchiyama H, Soejima Y, Maehara Y. BACKGROUND: Bacterial sepsis is a significant problem that must be addressed after living donor liver transplantation (LDLT). STUDY DESIGN: A retrospective analysis of 346 adult-to-adult LDLT patients was performed. RESULTS: Forty-six patients (13.3%) experienced bacterial sepsis, with primary and secondary origins in 23.9% and 76.1%, respectively. Gram-negative bacteria accounted for 71.7% of the bacteria isolated. The 2-year cumulative graft survival rate in patients with bacterial sepsis was 45.7%. Patients with bacterial sepsis secondary to pneumonia (n = 12) had poorer 2-year graft survival rates (16.7%) than did those with primary or other types of secondary sepsis (p = 0.004). Multivariate analysis showed that intraoperative massive blood loss >10L (p < 0.001) and no enteral feeding started within 48 hours after transplantation (p = 0.005) were significant risk factors for bacterial sepsis. Among patients who received enteral nutrition, the incidences of bacterial sepsis in patients who received enteral nutrition within 48 hours (n = 135) or later than 48 hours (n = 57) were 5.9% and 21.0%, respectively (p = 0.002). The incidence of early graft loss was 8-fold higher in recipients with massive intraoperative blood loss without early enteral nutrition (p < 0.001). CONCLUSIONS: Early enteral nutrition was associated with significantly reduced risk of developing bacterial sepsis after LDLT.
  29. 29. Parenteral Nutrition improves nutritional state and liver function in malnourished patients . PN is safe and improves mental state in patients with cirrhosis and severe HE. In acute liver failure PN reduces the rate of complications & is a safe second-line option to adequately feed patients in whom enteral nutrition is insufficient or impossible.
  30. 30. POMR: A 40yr old male came with c/o right upper quadrant pain ; anorexia; nausea ; dysgeusia & frequent loose stools. PMH: N/K/C/O - DM;HTN;BA;TB PSH: Nil significant SH: alcohol abuse x 15yrs Diagnosis: alcoholic hepatitis; on biopsy - steatosis and fibrosis A/D Height : 177cm Weight : 67kg IBW : 77kg UBW : 82kg (5 yrs ago ) 73kg( 6 months ago ) B/P Serum albumin : 2.5 g/dl Ammonia : 55mmol/l Transferrin: 150mg/dl Elevated liver enzymes & total bilirubin Megaloblastic anemia profile. CASE STUDY
  31. 31. C/E : mild peripheral edema with jaundice muscle wasting ; stomatitis PLAN : (Dry weight = 66kg) Energy: 1980kcal/day @ 30kcal/kg/DW Protein: 79.2g/day @ 1.2g/kg/DW CHO : 321g/day @ 65% of T.calories Fat : 41g/day @ 19% of T.calories Fluid : 1900ml ~ 2L/day Fibre : 25g/day Salt : 5g/day • Abstention from alcohol • Small frequent meals with late evening snacks • Vegetable protein to be included ; MCT to be given • Multivitamin supplementation
  32. 32. THANK YOU !!
  33. 33. REFERENCES Krause’s Food Nutrition & Diet Therapy - 11Th Edition - Kathleen Mayan Saliva ; Escort Stump (Pg 743 - 755) Nutrition Therapy & Pathophysiology -Marcia Nelms (Pg 510 - 532) Present Knowledge In Nutrition - 10Th Edition -John W. Edam (Pg 912-930) Krause - Food & Nutrition Care Process - 13Th Edition Kathleen Mayan Saliva ; Escort Stump (Pg 651 - 653) Modern Nutrition In Health & Disease -Catharine (Pg 1115-11124) Modern Nutrition In Health & Disease - 10Th Edition -Maurice Shills (Pg1246-1256) Contemporary Nutrition Support Practice - A Clinical Guide -Laura E Matures ; Michele M Gottschlich (Pg 455)