dietary management of cirrhosis of liver

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

15. CLINICAL MANIFESTATIONS
15

16. 16

17. DIAGNOSIS OF CIRRHOSIS
 clinical+laboratory+radiologic+liver biopsy
17

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

24. DIETARY
MANAGEMENT

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

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)

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.
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