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Cirrhosis of liver. final pptx

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dietary management of cirrhosis of liver

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Cirrhosis of liver. final pptx

  1. 1. CIRRHOSIS OF LIVER AND DIETARY MANAGEMENT Dev Ram Sunuwar M.Sc.Nutrition and Dietetics1
  2. 2. OBJECTIVE At the end of presentation, participants will be able to: 1. Define liver Cirrhosis 2. Enumerate the different types of liver cirrhosis 3. Enumerate the predisposing/ contributing factors of liver cirrhosis 4. Discuss the pathophysiological changes and clinical manifestations of patients with liver cirrhosis. 5. Nutritional assessment in CLD patient 6. Dietary management 2
  3. 3. OUTLINE  Definition  Causes and predisposing factor in cirrhosis of liver  Pathophysiology  Type of cirrhosis and clinical manifestation  Complication  Nutritional assessment  Dietary management  Conclusion 3
  4. 4. DEFINITION OF CIRRHOSIS Cirrhosis is derived from Greek word kirros=orange or tawny and osis=condition -WHO definition: a diffuse process characterized by liver necrosis and fibrosis and conversion of normal liver architechture into structurally abnormal nodules that lack normal lobular organisation. 4
  5. 5. COMMON CAUSES 1. Chronic alcoholism & NASH 2. Chronic hepatitis B& C 3. Autoimmune diseases: autoimmune hepatitis. 4. Biliary disease 5. Cholestatic liver disease:PBC,PSC 6. Hemochromatosis (Iron overload) 7. Cryptogenic 10% 8. Wilson's disease, 9. Alpha-1 anti-trypsin deficiency. 10. Obesity 11. Inherited diseases 12. Drugs & toxins 5
  6. 6. PREDISPOSING/ PRECIPITATING FACTORS:  malnutrition  effects of alcohol abuse  chronic impairment of bile excretion – biliary obstruction in the liver and common bile duct (gallbladder stones)  necrosis from hepatotoxins or viral hepatitis  Congestive heart failure 6
  7. 7. PATHOPHYSIOLOGY -modularity(regenerating nodules). fibrosis(deposition of dense fibrous septa)-fragmentation of sample. abnormal liver architecture Hepatocyte abnormalities:pleomorphism,dysplasia,hyperplasia Gross pathology: irregular surface ,yellowish colour,small,firm 7
  8. 8. CirrhosisNormal Nodules surrounded by fibrous tissue 8 HISTOLOGICAL IMAGE OF A NORMAL AND A CIRRHOTIC LIVER
  9. 9. 9
  10. 10. 10
  11. 11. 11
  12. 12. 12
  13. 13. CLINICAL MANIFESTATIONS Sign/Symptoms - early:  anorexia, nausea, indigestion  aching or heaviness in right upper quadrant  weakness & fatigue 13 Assessment:
  14. 14. CLINICAL MANIFESTATIONS Late signs:  abnormal liver function tests:  bilirubin (N=0-0.9mg/dl),  AST (N=4.8-19U/L)  ALT (N= 2.4-17U/L)  Serum alkaline phosphatase (N=30-40U/L)  Ammonia (plasma) (N= 15-45umol/L)  AST / ALT ratio > 1  Low albumin (< 3.8 g/dL)  Prolonged prothrombin time (INR > 1.3)  Low platelet count (< 175 x1000/ml)  intermittent jaundice, pruritus  edema, ascites, prominent abdominal wall veins  Ecchymosis, bleeding tendencies  anemia  Infection  Gynecomastia, testicular atrophy  Neurologic changes 14
  15. 15. CLINICAL MANIFESTATIONS 15
  16. 16. 16
  17. 17. DIAGNOSIS OF CIRRHOSIS  clinical+laboratory+radiologic+liver biopsy 17
  18. 18. 20
  19. 19. COMPLICATIONS  The ultimate mechanism of deaths in most cirrhotic patients is  (1) progressive liver failure,  (2) a complication related to portal hypertension, or  (3) the development of hepatocellular carcinoma. 21 Ascites Esophageal variceal bleeding Hepatic encephalopathy Hepatorenal syndrome Spontaneous bacterial peritonitis Portal hypertensive gastropathy Infection Liver failure Hepatocellular carcinoma
  20. 20. Subjective Global Assessment Anthropometric measurements Bioelectric impedance analysis Handgrip strength test 22
  21. 21. 23
  22. 22. DIETARY MANAGEMENT
  23. 23. The measures in dietetic treatment are: • Assuring the adequate intake of protein and of the correct types of proteins • Assuring an adequate supply of energy • Increased dietary intake of fiber • Administration of branched-chain amino acids • Reduced intake of sodium • Restriction of fluid • Increased intake of potassium
  24. 24. A. ENERGY REQUIREMENTS 26 Patients usually need 35-45 kcal/kg/day. They should supply 60-70% of non nitrogen calories. Cirrhosis is a disease of accelerated starvation ,so patients should avoid long time without feeding. Patients often do better on multiple small meals with alate bed-time meal.
  25. 25. B. LIPIDS 27 Around 20- 30% of total calorie intake should be supplied as fat. MCT oil are preferred as they are easily digestible and assimilable A mixed fuel system improves nitrogen balance compared to glucose alone. Even in decompensated cirrhosis, high lipid containing parenteral mixtures were found to be well tolerated and improve encephalopathy.
  26. 26. B. LIPIDS CONT.. 28  Thus lipid restriction has no scientific basisin patients withcirrhosis.  Fat should be provided aspolyunsaturated fatty acids, with less than 50% long chain triglycerides.  Fat helps make food tastier. This is important for people who suffer from a suppressed appetite due to chronic liverdisease.
  27. 27. B. LIPIDS CONT.. 29  fat need in order to properly absorb the four fat-soluble vitamins—A, D,E, and K.  Without some fat, these vitamins may become deficient in the body, even if they are taken in supplemental form.
  28. 28. C. PROTEINS. 30  Proteins should not be restricted in patients with liver disease unless they become protein intolerant due to encephalopathy.  Protein intakeshould be in the rangeof 1-1.5 g/kg/day.  Several studies have shown that a daily protein supply of 1.0-1.2g/kg/day may be sufficient to prevent negative N2 balance in cirrhosis  With mild stress, this has to increase to 1.5 g/kg/day, and with acute exacerbations of hepatitis or decompensation to 2.0g/kg/day
  29. 29. C. PROTEINS. CONT. 31  Special attention should be paid topatients on beta-blockers for prevention of variceal bleeding. Beta-blockers increase protein oxidation (an alternative method of protein metabolism withoutenergy production), and may increase protein requirement. patients on propranolol should be placed on the higherend of the protein intake.
  30. 30. AMINO ACIDS COMMONLY ALTERED IN LIVER DISEASE  Aromatic amino acids—serum levels increased  —Tyrosine  —Phenylalanine*  —Free tryptophan*  Branched-chain amino acids—serum levels decreased  —Valine*  —Leucine*  —Isoleucine*  Other amino acids—serum levels increased 32
  31. 31. Oral BCAAs in cirrhosis with or without chronic encephalopathy  BCCAs supplement can only be recommended in pat. At high risk of encephalopathy.  branched-chain amino acids, at doses of 12 to 14 grams per day  BCAA-enriched formulations can be useful in p’twhoare intolerant to protein and malnourished, which can improve protein synthesis and reduce post injurycatabolism.  Leucine is the most active in promoting protein synthesis and inhibitingprotein breakdown.  Isoleucine and valine increase nitrogen balance and increase tissue concentrationof leucine. 33
  32. 32. DIETARY RECOMMENDATION : Energy and protein : 34 Clinical condition Energy ( kcal/kg/day) Protein (gm/kg/day) Compensated cirrhosis 25 – 35 1.0 – 1.2 Decompensated cirrhosis 35 - 40 1.2 – 1.5 Hepatic encephalopathy Grade 1 -2 25 - 35 1.0 – 1.5 Hepatic encephalopathy Grade 3 -4 25 - 35 1.0 – 1.5 BCAA enriched formula
  33. 33. 25% of cirrhotics have small intestinal bacterial overgrowth Probiotics decrease intestinal pH, inhibiting growth of pathogenic bacteria Probiotics with fructo-oligosaccharides equal to lactulose for hepatic encephalopathy Generally safe and well 36
  34. 34. Fluid intake 30-40mL/kg/day maintains fluid balance Dilutional hyponatremia develops due to decreased renal blood flow and greater free water accumulation Fluid restriction of 1.5L/day only if with ascites and hyponatremia <120mEq/L 37
  35. 35. Vitamins A, D, E, and K, zinc and selenium supplementation for all cirrhotics  If with chronic cholestasis, check serum levels of vitamin A and 25(OH)-D annually  B12 levels falsely elevated due to inactive cobalamin analogues  Alcoholics need folate and thiamine supplements 38
  36. 36. 39 • Strict low sodium diet (1 g of table salt per day) • Low sodium diet (3 g of table salt per day) • Sodium-reduced diet (6 g of table salt per day)
  37. 37. (Prof. Dr. Mathias Plauth and Klinik für Innere Medizin)
  38. 38. CASE STUDY Name: lal bdr. Thapa Age/sex: 58/M Bed number:- 619A gastroenterology ward Weight: 68 kg Height: 5.2” Address: Butwal Occupation: farmer BMI:27 (ascites) Adjusted body weight- 60.5kg Abdominal girth: 95cm
  39. 39. INVESTIGATION REPORT TC- 4800 Hb- 7.7 PCV- 21.7 PT/INR- 1.44 Platelets- 63000 RBS- 9.8 Urea- 16 Creatinine- 612 Total billirubirin- 155 SGPT-15 SGOT-42 Alkaline phosphate- 133 Total protein- 68 LDH-112 Uric acid- 22 Ascitis fluid TC-110 Protein-1.5 Albumin- 5.6 I/O- 950/1000ml
  40. 40. Diagnosis:- ALD/CLD with HTN with ascites Total energy requirement= 2100kcal Serving size:- 26 Nutrient distribution Protein- 91.5gm(18%)- 1.5gm/kg/BW Carbohydrate- 320gm(60%) Fat- 52gm(22%)
  41. 41. Food group List Unit Protein Fat CHO CHO 1 11 22 198 2 2 36 Protein 3 3 27 15 4 3.5 14 17.5 21 5 3.5 21 3.5 45.5 Fat 6 1.5 13.5 Vitamin/mi nerals 7 1.5 7.5 1.5 19.5
  42. 42. SAMPLE MENU बिहानको नास्ता(७:००-८:००) दूध/चिया:-१ चिलास अन्डा:- १ वटा पुरै + ३ वटा सेतो मात्रै पाउरोटी:- २ slice वा ४ पपस बिस्कु ट फलफु ल:१ वटा बिहानको खाना(१०:००-११:००) भात:- ३+१/२ चिलास दाल:- १ चिलास सब्जी:- १ चिलास दही/दूध/मासु/:- १/१ चिलास वा ३-४ पपस हररयो सलाद:- थोरै मध्यान्ह(१:००) फलफु ल:१ वटा अन्डाको सेतो भाि:- २ वटा
  43. 43. दिउँसोको खाजा(३:००-४:००) िेडािुडी:- १ चिलास दही:- १ चिलास पाउरोटी/बिस्कु ट:- १ slice वा ३-४ पपस िेलुकाको खाना(७:००-८:००) रोटी:- ३-४ वटा दाल:- १ चिलास सािसब्जी:- १ चिलास दूध/दही/माछा,मासु:- १/१ चिलास/ ३-४ पपस ग्रीन सलाद:- इच्छाअनुसार
  44. 44. CONCLUSION  Adequate caloric intake (35 kcal per kg body weight daily)  Adequate intake of protein (1.2–1.5 g per kg body weight daily)  Adequate intake of vegetable fiber or roughage  Regular exercise to maintain muscle mass  Timely addition of enteral dietary supplementation  Timely addition of branched-chain amino acids
  45. 45. RFERENCE  https://www.slideshare.net/SNBhattacharya/cirrhosis-of-liver  https://www.slideshare.net/tozki/liver-cirrhosis  Prof. Dr.Plauth M.; Klinik für Innere Medizin and Städtisches Klinikum Dessau “A Guide for Patientswith Liver Diseases including Guidelines for Nutrition”2006  www.slideshare.net/dinujustin/liver-cirrhosis-ppt  Gluud LL, Dam G, Borre M, Les I, Cordoba J et al. Oral BCAAs have a beneficial effect on manifestations of hepatic encephalopathy in a systematic review with meta-analyses of RCTs. J Nutr 2013;143:1263- 1268.  Johnson TM, Overgard EB, Cohen AD, DiBaise JK. Nutrition assessment and management in advanced liver disease. Nutr in Clin Practice 2013; 28: 15- 29.  Koretz RL, Avenell A, Lipman TO. Nutritional support for liver disease. Cochrane Review 2012; issue 5.  Plauth M, Cabre E, Riggio O, Assis-Camilo M, Pirlich M et al. ESPEN guidelines on enteral nutrition: liver disease. Clin. Nutr. 2006; 25: 285-294. 49
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dietary management of cirrhosis of liver

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