NUTRITION IN LIVER DISEASE
21 likes9,989 views
The document discusses liver disease and nutrition. It begins by reviewing the functions of the liver and various liver diseases. It then discusses nutritional features of end-stage liver disease and nutritional assessment and management guidelines. Specific topics covered include neurological symptoms associated with liver disease, nutritional assessment tools for patients with end-stage liver disease, daily energy expenditure calculation methods, progression of liver disease, and ESPEN guidelines on enteral and parenteral nutrition for various liver diseases.
NUTRITION IN LIVER DISEASE
- 2. • Review the functions of the liver • Review diseases of the liver • Understanding neuro-psychological symptoms associated with liver disease • Nutritional features of end stage liver disease • Nutritional assement of end stage liver disease • Nutritional management –ESPEN GUIDELINES IN LIVER DISEASE
- 3. Functions of the Liver: • Largest organ in body, integral to most metabolic functions of body, • Only 10-20% of functioning liver is required to sustain life • Removal of liver will result in death within 24 hours
- 4. • Main functions include: – Metabolism of CARBOHYDRATE, protein, fat – Storage/activation vitamins and minerals – Formation/excretion of bile – Steroid metabolism, detoxifier of drugs/alcohol – Action as (bacteria) filter and fluid chamber – Conversion of ammonia to urea • Gastrointestinal tract significant source of ammonia • Generated from ingested protein substances that are deaminated by colonic bacteria • Ammonia enters circulation via portal vein • Converted to urea by liver for excretion
- 5. (L)UREA CYCLE—TRANSAMINASE IN LIVER
- 6. REVIEW OF DISEASE OF LIVER CLASSIFICATION. • Duration – Acute vs Chronic • Pathophysiology – Hepatocellular vs Cholestasic • Etiology – Viral – Alcohol – Toxin – Autoimmune • Stage/Severity – ESLD – Cirrhosis
- 7. Viral hepatitis A, B, C, D, E (and G) Fulminant hepatitis Alcoholic liver disease Non-alcoholic liver disease Cholestatic liver disease Hepatocellular carcinoma Inherited disorders
- 8. PROGRESSION OF LIVER DISEASE
- 9. Understanding neuro-psychological symptoms associated with liver disease All neurological and psychological symptoms in patients with liver disease that cannot be explained by presence of other pathologies • Brain and nervous system damage secondary to severe liver dysfunction (most often chronic disease) resulting from failure of liver to remove toxins • Multifactorial pathogenesis with exact cause unknown • Symptoms vary from nearly undetectable, to coma with decerebration – Characterized by various neurologic symptoms • Cognitive impairment • Neuromuscular disturbance • Altered consciousness • Reversible syndrome
- 10. Pathogenesis Theories • Endogenous Neurotoxins – Ammonia – Mercaptans – Phenols • Increased Permeability of Blood-Brain Barrier • Change in Neurotransmitters and Receptors – GABA – Altered BCAA/AAA ratio • Other – Zinc defficiency
- 11. Neurotoxic Action of Ammonia • Readily crosses blood-brain barrier • Increased NH3 = increased glutamate – α-ketoglutarate+NH3+NADH→glutamate+NAD – glutamate+NH3+ATP→glutamine+ADP+Pi • As a-ketoglutarate is depleted TCA cycle activity halted • Increased glutamine formation depletes glutamate stores which are needed by neural tissue – Irrepairable cell damage and neural cell death ensue. – In liver disease, conversion of ammonia to urea and glutamine can be reduced up to 80%
- 12. False Neurotransmitter Hypothesis • Liver cirrhosis characterized by altered amino acid metabolism • Increased Aromatic Amino Acids in plasma and influx in brain • Decrease in plasma Branched Chain Amino Acids • Share a common carrier at blood-brain barrier • DECREASE BCAAs in blood may result in INCREASE AAA transport to brain
- 13. • AAA are precursors to neurotransmitters and elevated levels result in shunting to secondary pathways
- 14. Change In Neurotransmitters and Receptors • BRANCH CHAIN AMINOACID. • Fischer and colleagues, published their ‘‘unifiedhypothesis on the pathogenesis of HE’’ based on the observation that during hepatic failure, plasma levels of BCAA decreased and the AAA increased, DUE TO increased BCAA catabolism in muscle and decreased AAA breakdown in the failing liver.
- 15. • A reduction in the insulin/glucagon ratio was hypothesized to play a key role in disturbing the balance between anabolism and catabolism. • Give rise to a decrease in the BCAA/AAA ratio, which was called the Fischer-ratio (BCAA/AAA ratio).
- 16. The increase in plasma AAA incombination with an increased blood brain barrier permeability for neutral amino acids has been suggested to contribute to an increased influx of AAA in the brain, because they compete for the same transporter (large neutral amino acid transporter). This, inturn, would lead to imbalances in neurotransmitter synthesis and accumulation of falsneurotransmitters, such as octopamine in thebrain, which may contribute to HE
- 17. • hyperammonemia during liverfailure, ammonia is detoxified by alternative pathways, the most important of which, although essentially temporary, is the formation of glutamine from ammonia and glutamate maInly in muscle & brain. • In muscle BCAA transaminate with a- ketoglutarate in the BCAA transferasereactions , yielding glutamate, explaining why hyperammonemia may contribute to low plasma BCAA
- 18. • coupling of ammonia to glutamate in the glutaminsynthetase reaction as an alternative ammonia detoxification route, • glutamine is exported from muscle and brain.The increased cerebral release of glutamine in this hypothesis was thought to facilitate the rapid exchange of glutamine for neutral amino acids, notably the AAA, by the large neutral amino acid carrier- This increased influx of AAA in the brain would raise the availability of precursors for neutrotransmitters.
- 19. • BCAA levels are crucially determined by nutritional factors, whereas AAA levels appear to depend much more upon intact hepatic metabolism.
- 20. Increase Permeability of Blood- Brain Barrier • Astrocyte (glial cell) volume is controlled by intracellular organic osmolyte • Organic osmolyte is glutamine. • glutamine levels in the brain result in volume of fluid within astrocytes resulting in cerebral edema (enlarged glial cells) • Neurological impairment – N=Normal Astrocytes – A=Alzheimer type II astrocytes – Pale, enlarged nuclei – characterisic of HE
- 21. Nutritional Assessment of patients with ESLD Weight? Weight history? Protein markers of nutritional status? Descriptive history of wasting? Skinfolds? Intake? Appetite?
- 22. Assement… SGA for patients with liver disease .. Anthropometry Food history Nausea Anorexia Taste changes Diarrhoea Early satiety Functional capacity Grip strength
- 23. Daily energy expenditure 1) predictive equation;-harris benedict equation( based on sex,ideal body wt, height). • Men: BMR = 66 + ( 13.7 x wt,kg ) + ( 5 x ht inch ) - ( 6.7 x age in year ) • Women: BMR = 655 + ( 9.6 x wt,kg ) + ( 1.8 x ht inch ) - ( 4.7 x age in years )
- 24. • BEE(KCAL/DAY)- 25 x WT IN KG • To allow the thermal effect of food intake the BEE multiplied by 1.2 to derive the resting energy expenditure-is in resting tate but not on fasted state. • In hypermetabolic condition – • Mild stress-BEEx1.2 • Mod stress-BEEx1.4 • Severe stress –BEEx1.6
- 25. • 2) indirect calorimetry. It is impossibel to mesure metabolic heat production in clinical practise, the metabolic energy expenditure is mesured indirectly by mesuring whole body vo2 and vco2,technique called indirect calorimetry.
- 26. • ESPEN Guidelines on Enteral Nutrition: Liver disease
- 27. ;NUTRION IN ALCOHOLIC HEPATITIS subject recommendation grade general Use simple bedside methods such as the SubjectiveGlobal Assessment (SGA) or anthropometry to identify patients at risk of undernutrition. Recommended energy intake: 35–40 kcal/kg BW/d Recommended protein intake: 1.2–1.5 g/kgBW/d C c c application Use supplementary enteral nutrition when patients cannot meet their caloric requirements through normal food. In general, oral nutritional supplements are recommended. A
- 28. subject recommendation gerad route Use tube feeding if patients are not able to maintain adequate oral intake (even when oesophageal varices are present) PEG placement is associated with a higher risk of complications and is not recommended A C Type of formula Whole protein formulae are generally Recommended. Consider using more concentrated high-energy formulae in patients with ascites. Use BCAA-enriched formulae in patients with hepatic encephalopathy arising during enteral nutrition. C C A
- 29. nutrition in liver cirrhosis subject recommendation grade General Use simple bedside methods such as the Subjective Global Assessment (SGA) or anthropometry to identify patients at risk of undernutrition. Recommended energy intake: 35–40 kcal/kgBW/d Recommended protein intake: 1.2–1.5 g/kgBW/d C C C application Use supplementary enteral nutrition when patients cannot meet their caloric requirements through normal food. In general, oral nutritional supplements are recommended. A A
- 30. route Use tube feeding if patients are not able to maintain adequate oral intake (even when oesophageal varices are present) PEG placement is associated with a higher risk of complications and is not recommended A c Type of formula Whole protein formulae are generally recommended. Consider using more concentrated high-energy formulae in patients with ascites. Use BCAA-enriched formulae in patients with hepatic encephalopathy arising during enteral nutrition. The use of oral BCAA supplementation can improve clinical outcome in advanced cirrhosis C C A B
- 31. Nutrition in transplantation AND SURGERY .surgerySUBJ RECOMME.. GRADE preoperative Follow recommendations for cirrhosis. B postoperative Initiate normal food/enteral nutrition within 12–24 h postoperatively. Initiate early normal food or enteral nutrition after other surgical procedures B route preop Follow recommendations for cirrhosis. postop Use nasogastric tubes or catheter jejunostomy for early enteral nutrition. b FORMULA- PREOP Follow recommendations for cirrhosis. POSTOP Whole protein formulae are generally recommended. In patients with ascites prefer concentrated high energy formulae for reasons of fluid balance. Use BCAA-enriched formulae in patients with hepatic encephalopathy arising during enteral nutrition. C C A
- 32. OUTCOME- PREOP An improvement of perioperative mortality or complication rate by preoperative tube feeding or oral nutritional supplements has not yet been showN. OUTCOME- POSTOP Early normal food or enteral nutrition is recommended for transplant and surgery patients with LC in order to minimise perioperative—in particular infectious—complications.
- 33. ESPEN GUIDELINES ON PARENTRAL NUTRITION
- 34. NUTRTION IN ALCOHOLIC STETOHEPATITIS SUBJECT RECOMMEN.. GRADE GENERAL Use simple bedside methods such as the Subjective Global Assessment (SGA) or anthropometry to identify patients at risk of undernutrition. Start PN immediately in moderately or severely malnourished ASH patients, who cannot be fed sufficiently either orally or enterally. Give i.v. glucose (2–3 g kg1 d1) when patients have to abstain from food for more than 12 h. Give PN when the fasting period lasts longer than 72 h. C A C C ENERGY Provide energy to cover 1.3REE . Give glucose to cover 50–60 % of non-protein energy requirements. Use lipid emulsions with a content of n-6 unsaturated fatty acids .. C C C
- 35. AMINOACID S Provide amino acids at 1.2–1.5 g kg1 d C MICRONUTR IENT Give water soluble vitamins and trace elements daily from the first day of PN. Administer vitamin B1 prior to starting glucose infusion to reduce the risk of Wernicke’s encephalopathy C C MONITORIN G Employ repeat blood sugar determinations in order to detect hypoglycemia and to avoid PN related hyperglycemia. Monitor phosphate, potassium and magnesium levels when refeeding malnourished patients. C C
- 36. IN LIVER CIRRHOSIS SUBJECT RECOMMEN.. GRAD E GENERAL Start PN immediately in moderately or severely malnourished cirrhotic patients, who cannot be fed sufficiently eitherorally or enterally. Give i.v. glucose (2–3 g kg1 d1) when patients have to abstain from food for more than 12 h. Give PN when the fasting period lasts longer than 72 h. Consider PN in patients with unprotected airways and encephalopathy when cough and swallow reflexes are compromised. Use early postoperative PN if patients cannot be nourished sufficiently by either oral or enteral route. After liver transplantation, use early postoperative nutrition; PN is second choice to EN. C A C C C A
- 37. ENERGY Provide energy to cover 1.3 x REE Give glucose to cover 50 % - 60 % of non-protein energy requirements. Reduce glucose infusion rate to 2–3 g kg1 d1 in case of hyperglycemia and use consider the use of i.v. insulin. Use lipid emulsions with a content of n-6 unsaturated fatty acids lower than in traditional pure soybean oil emulsions C C C AMINOACID S Provide amino acids at 1.2–1.5 g kg In encephalopathy III or IV, consider the use of solutions rich in BCAA and low in AAA, methionine and tryptophane C A
- 38. MICRONUTR IENT Give water soluble vitamins and trace elements daily from the first day of PN. In alcoholic liver disease, administer vitamin B1 prior to starting glucose infusion to reduce the risk of Wernicke’sencephalopathy C C MONITORIN G Employ repeat blood sugar determinations in order to avoid PN related hyperglycemia. Monitor phosphate, potassium and magnesium levels when refeeding malnourished patients A C
- 39. IN ACUTE LIVER FAILURE GENERAL Commence artificial nutrition when patient is unlikely to resume normal oral nutrition within the next 5–7 days. Use PN when patients cannot be fed adequately by EN. C C ENERGY Provide energy to cover 1.3 REE. Consider using indirect calorimetry to measure individual energy expenditure. Give i.v. glucose (2–3 g kg1 d1) for prophylaxis or treatment of hypoglycaemia. In case of hyperglycaemia, reduce glucose infusion rate to 2–3 g kg1 d1 and consider the use of i.v. insulin. Consider using lipid (0.8 – 1.2 g kg1 d1) together with glucose to cover energy needs in the presence of insulin resistance C C C C C
- 40. IN ACUTE LIVER FAILURE SUBJ RECOMMEN GRAD E AMINOACID In acute or subacute liver failure, provide amino acids at 0.8–1.2 g kg1 d1. C MONITORIN G Employ repeat blood sugar determinations in order to detect hypoglycaemia and to avoid PN related hyperglycaemia. Employ repeat blood ammonia determinations in order to adjust amino acid provision. C C
- 41. References • Cornelis H. C. Dejong,4* Marcel C. G. van de Poll,4 Peter B. Soeters,4 Rajiv Jalan,5and Steven W. M. Olde Damink4, Aromatic Amino Acid Metabolism duringLiver Failure1–3. • ESPEN Guidelines on Parenteral Nutrition: Hepatology,Mathias Plauth a, Eduard Cabre´ b, Bernard Campillo c, Jens Kondrup d, Giulio Marchesini e,Tatjana Schu¨ tz f, Alan Shenkin g, Julia Wendon h. • Current Theories on the Pathogenesis ofHepatic Encephalopathy (43770)DARRELDL. MOUSSEAUA ND ROGERF . BUTTERWORT…
- 42. • Branched-chain amino acids increase arterial blood ammonia in spite ofenhanced intrinsic muscle ammonia metabolism in patients with cirrhosisand healthy subjects,Gitte Dam,1 Susanne Keiding,1,2 Ole Lajord Munk… • ESPEN Guidelines on Parenteral Nutrition: Intensive care,Pierre Singer a, Mette M…. • ESPEN Guidelines on Enteral Nutrition: Liver disease$M. Plautha,, E. Cabre´b, O. Riggioc, M. Assis- Camilod,
- 43. • NEUROTRANSMITTERS IN HEPATIC ENCEPHALOPATHY,W. Agnieszka FOGEL, Wojciech ANDRZEJEWSKIand Czeslaw MASLITSSKI.. Thank you.