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CIRRHOSIS OF LIVER
AND
DIETARY MANAGEMENT
Dev Ram Sunuwar
M.Sc.Nutrition and Dietetics1
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
OUTLINE
 Definition
 Causes and predisposing factor in cirrhosis
of liver
 Pathophysiology
 Type of cirrhosis and clinical manifestation
 Complication
 Nutritional assessment
 Dietary management
 Conclusion
3
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
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
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
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
CirrhosisNormal
Nodules surrounded
by fibrous tissue 8
HISTOLOGICAL IMAGE OF A NORMAL AND A CIRRHOTIC LIVER
9
10
11
12
CLINICAL MANIFESTATIONS
Sign/Symptoms - early:
 anorexia, nausea, indigestion
 aching or heaviness in right upper quadrant
 weakness & fatigue
13
Assessment:
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
CLINICAL MANIFESTATIONS
15
16
DIAGNOSIS OF CIRRHOSIS
 clinical+laboratory+radiologic+liver biopsy
17
20
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
Subjective Global Assessment
Anthropometric measurements
Bioelectric impedance analysis
Handgrip strength test
22
23
DIETARY
MANAGEMENT
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
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.
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.
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.
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.
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
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.
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
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
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
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
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
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
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)
(Prof. Dr. Mathias Plauth
and Klinik für Innere
Medizin)
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
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
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%)
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
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
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
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
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
50

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Cirrhosis of liver. final pptx

  • 1. CIRRHOSIS OF LIVER AND DIETARY MANAGEMENT Dev Ram Sunuwar M.Sc.Nutrition and Dietetics1
  • 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. 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. 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. 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. 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. 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. CirrhosisNormal Nodules surrounded by fibrous tissue 8 HISTOLOGICAL IMAGE OF A NORMAL AND A CIRRHOTIC LIVER
  • 9. 9
  • 10. 10
  • 11. 11
  • 12. 12
  • 13. CLINICAL MANIFESTATIONS Sign/Symptoms - early:  anorexia, nausea, indigestion  aching or heaviness in right upper quadrant  weakness & fatigue 13 Assessment:
  • 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
  • 16. 16
  • 17. DIAGNOSIS OF CIRRHOSIS  clinical+laboratory+radiologic+liver biopsy 17
  • 18.
  • 19.
  • 20. 20
  • 21. 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
  • 22. Subjective Global Assessment Anthropometric measurements Bioelectric impedance analysis Handgrip strength test 22
  • 23. 23
  • 25. 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
  • 26. 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.
  • 27. 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.
  • 28. 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.
  • 29. 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.
  • 30. 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
  • 31. 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.
  • 32. 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
  • 33. 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
  • 34. 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
  • 35.
  • 36. 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
  • 37. 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
  • 38. 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
  • 39. 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)
  • 40.
  • 41. (Prof. Dr. Mathias Plauth and Klinik für Innere Medizin)
  • 42. 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
  • 43. 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
  • 44. 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%)
  • 45. 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
  • 46. 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
  • 47. 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
  • 48. 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
  • 49. 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
  • 50. 50