© 2004, 2002 elsevier inc. all rights reserved. medical nutrition therapy for liver, biliary...

© 2004, 2002 Elsevier Inc. All rights reserved.

Medical Nutrition Medical Nutrition Therapy for Liver, Therapy for Liver, Biliary System, and Biliary System, and Exocrine Pancreas Exocrine Pancreas DisordersDisorders

Relationship of Relationship of Organs of the Upper Organs of the Upper AbdomenAbdomen

A, Liver (retracted upward); B, gallbladder; C, esophageal opening of the stomach; D, stomach (shown in dotted outline); E, common bile duct; F, duodenum; G, pancreas and pancreatic duct; H, spleen; I, kidneys.

Courtesy The Cleveland Clinic Foundation, Cleveland, Ohio, 2002.

The LiverThe Liver

Largest gland in the body (about Largest gland in the body (about 1500 g)1500 g)

Essential for life, though survival Essential for life, though survival is possible with 10-20% functionis possible with 10-20% function

Plays major role in macronutrient Plays major role in macronutrient and micronutrient digestion, and micronutrient digestion, metabolism, and storagemetabolism, and storage

Metabolizes steroids, detoxifies Metabolizes steroids, detoxifies drugs, alcohol, ammoniadrugs, alcohol, ammonia

Diseases of the LiverDiseases of the Liver

Acute viral hepatitisAcute viral hepatitis Fulminant hepatitisFulminant hepatitis Chronic hepatitisChronic hepatitis Alcoholic liver disease, alcoholic Alcoholic liver disease, alcoholic

hepatitis, and cirrhosishepatitis, and cirrhosis Non-alcoholic hepatic steatosis Non-alcoholic hepatic steatosis

(NASH)(NASH)

Diseases of the LiverDiseases of the Liver

Cholestatic liver diseasesCholestatic liver diseases

——Primary biliary cirrhosisPrimary biliary cirrhosis

——Sclerosing cholangitisSclerosing cholangitis Inherited disordersInherited disorders Other liver diseasesOther liver diseases

Acute Viral HepatitisAcute Viral Hepatitis Widespread inflammation of the Widespread inflammation of the

liver that is caused by hepatitis liver that is caused by hepatitis viruses A, B, C, D and Eviruses A, B, C, D and E– Hep A: oral-fecal routeHep A: oral-fecal route– Hep B and C: body fluidsHep B and C: body fluids– Hep D: occurs only in pts with Hep Hep D: occurs only in pts with Hep

BB– Hep E: oral-fecal route; seen more Hep E: oral-fecal route; seen more

often in Asia, Africa, Mexico often in Asia, Africa, Mexico Hasse JM et al. ASPEN Nutrition Support Practice Manual, 2nd edition, 2005

Acute Viral HepatitisAcute Viral Hepatitis

Four phases of symptoms:Four phases of symptoms:

1. Prodromal phase1. Prodromal phase

2. Preicteric phase2. Preicteric phase

3. Icteric phase3. Icteric phase

4. Convalescent phase4. Convalescent phase

Risk Factors for Risk Factors for Chronic Viral HepatitisChronic Viral Hepatitis Injection drug useInjection drug use Chronic hemodialysisChronic hemodialysis Blood transfusion or transplantation Blood transfusion or transplantation

prior to 1992 (HCV)prior to 1992 (HCV) Receipt of blood (including Receipt of blood (including

needlestick) from a donor needlestick) from a donor subsequently testing positive for subsequently testing positive for HCVHCV

Risk Factors for Risk Factors for Chronic Viral HepatitisChronic Viral Hepatitis Receipt of clotting factor Receipt of clotting factor

concentrates produced before concentrates produced before 19871987

Asian ancestry (HBV)Asian ancestry (HBV) Unvaccinated health care workersUnvaccinated health care workers Birth to mother with chronic HBV Birth to mother with chronic HBV

or HCVor HCV

Possible Risk FactorsPossible Risk Factors

Body piercing or tattooingBody piercing or tattooing Multiple sexual partners or Multiple sexual partners or

sexually transmitted diseases sexually transmitted diseases Health care workers (HCV)Health care workers (HCV) Contacts of HCV positive personsContacts of HCV positive persons

Source: NACB Laboratory Guidelines for Screening, Diagnosis, and Monitoring of Hepatic Injury. Dufour, Lott, Nolte, Gretch, Koff, Seeff

Fulminant HepatitisFulminant Hepatitis Syndrome in which severe liver Syndrome in which severe liver

dysfunction is accompanied by hepatic dysfunction is accompanied by hepatic encephalopathy within 8 weeksencephalopathy within 8 weeks

Causes include viral hepatitis (75%), Causes include viral hepatitis (75%), chemical toxicity (acetaminophen, drug chemical toxicity (acetaminophen, drug reactions, poisonous mushrooms, other reactions, poisonous mushrooms, other poisons)poisons)

Complications include cerebral edema, Complications include cerebral edema, coagulopathy, bleeding, cardiovascular coagulopathy, bleeding, cardiovascular complications, renal failure, pancreatitiscomplications, renal failure, pancreatitis

Chronic HepatitisChronic Hepatitis

At least 6-month course of hepatitis At least 6-month course of hepatitis or biochemical and clinical or biochemical and clinical evidence of liver disease with evidence of liver disease with confirmatory biopsy findings of confirmatory biopsy findings of unresolving hepatic inflammationunresolving hepatic inflammation

Can be caused by autoimmune, Can be caused by autoimmune, viral, metabolic, or toxic etiologiesviral, metabolic, or toxic etiologies

Alcoholic Liver Disease: Alcoholic Liver Disease: Most Common Liver Most Common Liver DiseaseDisease Alcohol excess and abuseAlcohol excess and abuse Most common cause of liver Most common cause of liver

disease in the U.S.disease in the U.S. Fourth leading cause of death Fourth leading cause of death

among middle-aged Americansamong middle-aged Americans Alcohol problems are highest Alcohol problems are highest

among young adults, ages 18 to among young adults, ages 18 to 29.29.

Stages of Alcoholic Stages of Alcoholic Liver DiseaseLiver Disease Hepatic steatosisHepatic steatosis Alcoholic hepatitisAlcoholic hepatitis Alcoholic (Leannec’s) cirrhosisAlcoholic (Leannec’s) cirrhosis

Alcoholic Liver DiseaseAlcoholic Liver Disease

Disease resulting from excessive Disease resulting from excessive alcohol ingestion characterized by alcohol ingestion characterized by fatty liver (hepatic steatosis), fatty liver (hepatic steatosis), hepatitis, or cirrhosishepatitis, or cirrhosis

Most common liver disease in the Most common liver disease in the U.S., except perhaps fatty liver U.S., except perhaps fatty liver secondary to obesitysecondary to obesity


Toxic Effects of Excess Alcohol Toxic Effects of Excess Alcohol UseUse

Alcoholic Liver DiseaseAlcoholic Liver DiseaseMetabolic ChangesMetabolic Changes

SteatorrheaSteatorrhea Wernicke-Korsakoff syndromeWernicke-Korsakoff syndrome Peripheral neuropathyPeripheral neuropathy Pellagrous psychosisPellagrous psychosis Folate deficiencyFolate deficiency

End-Stage Alcoholic Liver End-Stage Alcoholic Liver DiseaseDiseasePossible CharacteristicsPossible Characteristics

MalnutritionMalnutrition Portal hypertension with varicesPortal hypertension with varices AscitesAscites HyponatremiaHyponatremia Hepatic encephalopathyHepatic encephalopathy Glucose alterationsGlucose alterations

End-Stage Alcoholic Liver End-Stage Alcoholic Liver DiseaseDiseasePossible CharacteristicsPossible Characteristics Fat malabsorptionFat malabsorption OsteopeniaOsteopenia Thrombocytopenia with anemiaThrombocytopenia with anemia

Non-Alcoholic Non-Alcoholic Steatohepatitis (NASH)Steatohepatitis (NASH) Histologically resembles alcoholic Histologically resembles alcoholic

hepatitishepatitis Most common cause of chronic Most common cause of chronic

hepatic injury other than viruses and hepatic injury other than viruses and alcohol; most common cause of alcohol; most common cause of cryptogenic cirrhosiscryptogenic cirrhosis

Commonly in middle-aged women Commonly in middle-aged women with obesity and/or diabetes but with obesity and/or diabetes but appears in persons without these risk appears in persons without these risk factorsfactors

Non-Alcoholic Non-Alcoholic Steatohepatitis (NASH)Steatohepatitis (NASH) Patients with NASH often have abnormal Patients with NASH often have abnormal

lipid profileslipid profiles Differs from alcoholic hepatitis in that Differs from alcoholic hepatitis in that

ALT is higher than AST except in cirrhosisALT is higher than AST except in cirrhosis Weight loss may cause significant Weight loss may cause significant

improvement in enzyme results; in one improvement in enzyme results; in one study a 1% reduction in weight caused study a 1% reduction in weight caused an average fall of 8.1% in ALTan average fall of 8.1% in ALT

Biopsy is the only diagnostic procedure Biopsy is the only diagnostic procedure with adequate specificitywith adequate specificity

Cholestatic Liver Cholestatic Liver DiseasesDiseases

Primary biliary cirrhosis (PBC)Primary biliary cirrhosis (PBC) An immune-mediated chronic An immune-mediated chronic

cirrhosis of the liver due to cirrhosis of the liver due to obstruction or infection obstruction or infection of the small and intermediate-sized of the small and intermediate-sized intrahepatic bile ducts, whereas the intrahepatic bile ducts, whereas the extrahepatic biliary tree and larger extrahepatic biliary tree and larger intrahepatic ducts are normalintrahepatic ducts are normal

90% of patients are women90% of patients are women

Cholestatic Liver Cholestatic Liver DiseasesDiseases

Sclerosing cholangitisSclerosing cholangitis Fibrosing inflammation of Fibrosing inflammation of

segments of extrahepatic bile segments of extrahepatic bile ducts, with or without ducts, with or without involvement of intrahepatic involvement of intrahepatic ductsducts

May be an immune disorderMay be an immune disorder 50-75% of patients also have 50-75% of patients also have

inflammatory bowel diseaseinflammatory bowel disease 60-70% are men60-70% are men

Cholestatic Liver Cholestatic Liver DiseasesDiseasesSclerosing CholangitisSclerosing Cholangitis Increased risk of fat soluble vitamin Increased risk of fat soluble vitamin

deficiencies due to steatorrheadeficiencies due to steatorrhea Hepatic osteodystrophy due to Hepatic osteodystrophy due to

vitamin D and calcium vitamin D and calcium malabsorption resulting in malabsorption resulting in secondary hyperparathyroidism secondary hyperparathyroidism and osteomalacia or ricketsand osteomalacia or rickets

Treated with immunosuppressantsTreated with immunosuppressants

Inherited Disorders: Inherited Disorders: HemochromatosisHemochromatosis

Inherited disease of iron Inherited disease of iron overloadoverload

Store 20-40 g of iron in the Store 20-40 g of iron in the liver compared with .3 to .8 g liver compared with .3 to .8 g in normal personsin normal persons

Causes hepatomegaly, Causes hepatomegaly, esophageal varices, glucose esophageal varices, glucose intoleranceintolerance

Treated by phlebotomyTreated by phlebotomy

Inherited Disorders: Inherited Disorders: Wilson’s DiseaseWilson’s Disease Autosomal recessive disorder associated Autosomal recessive disorder associated

with impaired biliary copper excretionwith impaired biliary copper excretion Copper accumulates in liver, brain, Copper accumulates in liver, brain,

cornea, and kidneyscornea, and kidneys May present with neurological signs, May present with neurological signs,

Kayser-Fleischer rings, low serum Kayser-Fleischer rings, low serum ceruloplasmin, psychiatric symptoms ceruloplasmin, psychiatric symptoms

Always presents before age 40Always presents before age 40 Treated with copper-chelating agents, Treated with copper-chelating agents,

zinc supplementation, low copper dietzinc supplementation, low copper diet

Inherited Disorders: Inherited Disorders: αα11-antitrypsin deficiency-antitrypsin deficiency

Causes cholestasis or cirrhosis Causes cholestasis or cirrhosis and can cause liver and lung and can cause liver and lung cancercancer

No treatment but liver No treatment but liver transplanttransplant

Other Liver DiseasesOther Liver Diseases

Liver tumorsLiver tumors Systemic diseases (rheumatoid Systemic diseases (rheumatoid

arthritis, systemic arthritis, systemic sclerosis)sclerosis)

Nonalcoholic steatohepatitis**Nonalcoholic steatohepatitis** Acute ischemic and chronic Acute ischemic and chronic

congestive hepatopathycongestive hepatopathy Parasitic, bacterial, fungal, and Parasitic, bacterial, fungal, and

granulomatous liver diseasesgranulomatous liver diseases

Normal Liver vs. Normal Liver vs. Damaged LiverDamaged Liver


Microscopic Image of (A) Normal Microscopic Image of (A) Normal Liver; (B) cirrhotic liver)Liver; (B) cirrhotic liver)

(Adapted from Bray GA. Gray DS, Obesity, part 1: Pathogenisis. West J Med 149:429, 1988; and Lew EA, Garfinkle L; Variations in mortality by weight among 750,000 men and women. J Clin Epidemiol 32:563, 1979.)(From Kanel G, Korula J. Atlas of Liver Pathology. W.B. Saunders, 1992.)


Clinical Manifestations Clinical Manifestations of Cirrhosisof Cirrhosis

Interpretation of Lab Interpretation of Lab Data Data In Liver DiseaseIn Liver Disease

Liver Test PanelLiver Test Panel Aspartate transaminase (AST)Aspartate transaminase (AST) Alanine aminotransferase (ALT)Alanine aminotransferase (ALT) Alkaline phosphatase (ALP)Alkaline phosphatase (ALP) Total bilirubinTotal bilirubin Direct bilirubinDirect bilirubin PT/PTTPT/PTT CeruloplasminCeruloplasmin Total proteinTotal protein AlbuminAlbumin Viral serologiesViral serologies

AST and ALTAST and ALT

Enzymes released into circulation following Enzymes released into circulation following injury or death of cells in heart, liver, lungs, injury or death of cells in heart, liver, lungs, and other parts of the bodyand other parts of the body

High AST (200 U/L) and ALT (300 U/L) are High AST (200 U/L) and ALT (300 U/L) are indicative of liver disease in presence of indicative of liver disease in presence of jaundice or non-specific symptoms of acute jaundice or non-specific symptoms of acute illnessillness

Levels are higher in acute hepatic injury; lower Levels are higher in acute hepatic injury; lower in uncomplicated hepatitis and chronic liver in uncomplicated hepatitis and chronic liver diseasedisease

Transaminases relate more to cause of liver Transaminases relate more to cause of liver injury than prognosisinjury than prognosis

ALP (alkaline ALP (alkaline phosphatase)phosphatase)

Usually normal in acute and Usually normal in acute and chronic liver diseasechronic liver disease

High levels are usually indicative High levels are usually indicative of obstruction of biliary drainageof obstruction of biliary drainage

BilirubinBilirubin Results from the breakdown of hemoglobin in Results from the breakdown of hemoglobin in

the red blood cells and removal from the the red blood cells and removal from the body by the liver, which excretes it in bilebody by the liver, which excretes it in bile

Rises when the liver is unable to excrete Rises when the liver is unable to excrete bilirubin or when there is excessive bilirubin or when there is excessive destruction of red blood cellsdestruction of red blood cells

In viral hepatitis, total bilirubin >257 In viral hepatitis, total bilirubin >257 micromoles/L indicates severe liver injurymicromoles/L indicates severe liver injury

In alcoholic hepatitis, bilirubin >428 In alcoholic hepatitis, bilirubin >428 micromoles/L predicts high likelihood of deathmicromoles/L predicts high likelihood of death

Two Forms of BilirubinTwo Forms of Bilirubin

Indirect or unconjugated bilirubin: is protein bound; Indirect or unconjugated bilirubin: is protein bound; with increased destruction of red blood cells with increased destruction of red blood cells

Direct or conjugated bilirubin: not protein bound; Direct or conjugated bilirubin: not protein bound; circulates until it reaches the liver, where it is circulates until it reaches the liver, where it is conjugated; conjugated; in dysfunction or blockage of the in dysfunction or blockage of the liverliver

Dx: first, measure total bilirubin; if that is high, Dx: first, measure total bilirubin; if that is high, measure direct and indirectmeasure direct and indirect

Reference values: Total: 0.3-1.0 mg/dL, or 5-17 Reference values: Total: 0.3-1.0 mg/dL, or 5-17 micromoles/Lmicromoles/L

Conjugated: 0.0-0.2 mg/dL or 0.0-3.4 micromoles/LConjugated: 0.0-0.2 mg/dL or 0.0-3.4 micromoles/L

Bilirubin Circulation Bilirubin Circulation

Hepatocellular Hepatocellular Jaundice Jaundice direct (conj) bilirubin direct (conj) bilirubinInjury or disease of the parenchymal Injury or disease of the parenchymal

cells of the liver caused bycells of the liver caused by Viral hepatitisViral hepatitis CirrhosisCirrhosis Infectious mononucleosisInfectious mononucleosis Reactions of certain drugs such as Reactions of certain drugs such as

chlorpromazinechlorpromazine

Obstructive JaundiceObstructive Jaundice Direct bilirubin Direct bilirubin Obstruction of the common bile or Obstruction of the common bile or

hepatic ducts due to stones or hepatic ducts due to stones or neoplasms. neoplasms.

Causes high conjugated bilirubin Causes high conjugated bilirubin levels due to bile regurgitationlevels due to bile regurgitation

Hemolytic JaundiceHemolytic Jaundice unconjugated bilirubin unconjugated bilirubin

Overproduction of bilirubin Overproduction of bilirubin resulting from hemolytic resulting from hemolytic processes processes

After blood transfusionsAfter blood transfusions Pernicious anemiaPernicious anemia Sickle cell anemiaSickle cell anemia Transfusion reactionsTransfusion reactions

CeruloplasminCeruloplasmin Normal value: 25-63 mg/dL (250-630 Normal value: 25-63 mg/dL (250-630

mg/L)mg/L) Copper bound to ceruloplasmin constitutes Copper bound to ceruloplasmin constitutes

the largest amount of Cuthe largest amount of Cu2+2+ in circulation in circulation In Wilson’s disease CuIn Wilson’s disease Cu2+2+ mobilization from mobilization from

the liver is drastically reduced because of the liver is drastically reduced because of low production of ceruloplasminlow production of ceruloplasmin

Values <14 mg/dL may be expectedValues <14 mg/dL may be expected However, low ceruloplasmin is not the However, low ceruloplasmin is not the

primary defect in Wilson’s disease; some primary defect in Wilson’s disease; some patients with Wilson’s are not lowpatients with Wilson’s are not low

Screening for Liver Screening for Liver DiseaseDisease Asymptomatic high risk individuals should Asymptomatic high risk individuals should

be screened for chronic hepatitisbe screened for chronic hepatitis ALT is the most cost-effective screening ALT is the most cost-effective screening

test for metabolic or drug-induced liver test for metabolic or drug-induced liver injuryinjury

AST should also be measured with hx of AST should also be measured with hx of alcohol abuse (in alcoholic hepatitis AST is alcohol abuse (in alcoholic hepatitis AST is > ALT)> ALT)

Individuals at high risk for viral hepatitis Individuals at high risk for viral hepatitis should be screened using specific viral should be screened using specific viral serologies (HBsAg, anti-HCV, IgM anti-HAV, serologies (HBsAg, anti-HCV, IgM anti-HAV, anti-HBS, HCV-RNA) in addition to ALTanti-HBS, HCV-RNA) in addition to ALT

Predictors of Predictors of PrognosisPrognosis Prothrombin time: the most Prothrombin time: the most

important predictor of prognosis; important predictor of prognosis; prolonged PTT indicative of poor prolonged PTT indicative of poor prognosisprognosis

Albumin: serum albumin <2.5 Albumin: serum albumin <2.5 g/dL indicates high risk of deathg/dL indicates high risk of death

Lab Tests in Acute Lab Tests in Acute Liver DiseaseLiver Disease

DiseaseDisease Peak ALT Peak ALT (x URL)*(x URL)*

AST/Alt AST/Alt RatioRatio

Peak Bili Peak Bili (mg/dL)(mg/dL)

PTT PTT ProlongaProlongation (s)tion (s)

Viral Viral hepatitishepatitis

10-4010-40 <1<1 <15<15 <3<3

Alcoholic Alcoholic hepatitishepatitis

2-82-8 >2>2 <15<15 1-31-3

Toxic Toxic injuryinjury

>40>40 >1 early>1 early <5<5 >5 >5 transienttransient

Ischemic Ischemic injuryinjury

>40>40 >1 early>1 early <5<5 >5 >5 transienttransient

Source: NACB Laboratory guidelines for screening, diagnosis, and monitoring of hepatic injury. Dufour, Lou, Nolic, Gretch, Koff, Seeff

*upper reference limit

Causes of Elevated ALT Causes of Elevated ALT and/or ASTand/or AST

CauseCause Key FeatureKey Feature Screening Screening testtest

Confirming Confirming testtest

Non-Non-alcoholic alcoholic steato-steato-hepatitis hepatitis (NASH)(NASH)

Most Most common common cause other cause other than viral, than viral, alcoholicalcoholic

NoneNone biopsybiopsy

Hemo-Hemo-chromatosischromatosis

Autosomal Autosomal recessive recessive traittrait

1:200 among 1:200 among northern northern European European ancestryancestry

Transferrin Transferrin saturation saturation >45%>45%

HFE gene HFE gene analysis for analysis for C282Y C282Y mutationmutation

Source: NACB Laboratory guidelines for screening, diagnosis, and monitoring of hepatic injury. Dufour, Lou, Nolic, Gretch, Koff, Seeff




Wilson’s Wilson’s DiseaseDisease

Autosomal Autosomal recessive trait. recessive trait. 1:30,000 1:30,000 individuals; individuals; hemolytic hemolytic anemia, renal anemia, renal injuryinjury

Low Low cerulo-cerulo-plasmin in plasmin in 65-95% 65-95% homozy-homozy-gous; 20% gous; 20% heterozy-heterozy-gotesgotes

Genetic Genetic analysis, analysis, low serum low serum copper, copper, high urine high urine coppercopper

Auto-Auto-immune immune hepatitishepatitis

Up to 18% of Up to 18% of non-viral non-viral hepatitis; hepatitis; mainly young mainly young womenwomen

ANA and ANA and ASMA; ASMA; false false positive positive anti-HCV anti-HCV commoncommon

BiopsyBiopsy




Primary Primary biliary biliary cirrhosiscirrhosis

Middle aged Middle aged women; women; mainly mainly ALP; ALP; often often associated associated with Sjogren’s with Sjogren’s SyndromeSyndrome

Anti-mito-Anti-mito-chondrial chondrial antibodyantibody

BiopsyBiopsy

SchlerosinSchlerosing g cholangiticholangitiss

Young to Young to middle aged middle aged men; mainly men; mainly ALP; often with ALP; often with IBDIBD

Anti Anti neutrophil neutrophil cytoplasmicytoplasmic c antibodies; antibodies; ASMA, ANA ASMA, ANA may be +may be +

Bile duct Bile duct imagingimaging

Interpretation of Nutrition Interpretation of Nutrition Assessment Tests in Patients Assessment Tests in Patients with End-Stage Liver Diseasewith End-Stage Liver Disease

Body weightBody weight Anthropometric Anthropometric

measurementsmeasurements Creatinine-Creatinine-

height indexheight index Nitrogen Nitrogen

balance studiesbalance studies

Visceral protein Visceral protein levelslevels

Immune function Immune function teststests

SGA Parameters for SGA Parameters for Nutritional Evaluation of Nutritional Evaluation of Liver Transplant Liver Transplant CandidatesCandidates HistoryHistory

– Weight change (fluid changes)Weight change (fluid changes)– AppetiteAppetite– Taste changes and early satietyTaste changes and early satiety– Dietary recall (calories, protein, Dietary recall (calories, protein,

sodium)sodium)– Persistent gastrointestinal problems Persistent gastrointestinal problems

(nausea, vomiting, diarrhea, (nausea, vomiting, diarrhea, constipation, difficulty chewing or constipation, difficulty chewing or swallowing)swallowing)

SGA Parameters for SGA Parameters for Nutritional Evaluation of Nutritional Evaluation of Liver Transplant Liver Transplant CandidatesCandidates PhysicalPhysical

– Muscle wastingMuscle wasting– Fat storesFat stores– Ascites or edemaAscites or edema

Existing conditionsExisting conditions– Disease state and other problems Disease state and other problems

that could influence nutritional that could influence nutritional stores such as hepatic stores such as hepatic encephalopathy, GI bleeding, renal encephalopathy, GI bleeding, renal insufficiency, infectioninsufficiency, infection

SGA Parameters for SGA Parameters for Nutritional Evaluation of Nutritional Evaluation of Liver Transplant Liver Transplant CandidatesCandidates Nutritional rating (based on Nutritional rating (based on

results of above parameters)results of above parameters)– Well nourishedWell nourished– Moderately malnourishedModerately malnourished– Severely malnourishedSeverely malnourished

Malnutrition and Ascites Malnutrition and Ascites in End Stage Liver in End Stage Liver Disease Disease


Clinical Manifestations Clinical Manifestations of Cirrhosisof Cirrhosis

Esophageal VaricesEsophageal Varices

Causes of Malnutrition Causes of Malnutrition in Liver Diseasein Liver Disease AnorexiaAnorexia Early satiety or dysgeusiaEarly satiety or dysgeusia Nausea and vomitingNausea and vomiting Maldigestion or malabsorptionMaldigestion or malabsorption Restricted dietsRestricted diets Altered metabolismAltered metabolism

Malnutrition in Liver Malnutrition in Liver Disease—Disease—PathophysiologyPathophysiology

Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000. Updated by Jeanette M. Hasse and Laura E. Matarese, 2002.

Malnutrition in Liver Disease—Malnutrition in Liver Disease—Medical and Nutritional Medical and Nutritional ManagementManagement

Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000. Updated by Jeanette M. Hasse and Laura E. Matarese, 2002.

Vitamin/Mineral Vitamin/Mineral Deficits* in Severe Deficits* in Severe Hepatic Failure Hepatic Failure Vitamin AVitamin A Vitamin DVitamin D Vitamin EVitamin E Vitamin KVitamin K Vitamin BVitamin B66

Vitamin BVitamin B1212

FolateFolate

NiacinNiacin ThiaminThiamin ZincZinc MagnesiumMagnesium IronIron PotassiumPotassium PhosphorusPhosphorus

* May be related to fat malabsorption, medications, alcoholism (p. 752 Krause)

Four Stages of Hepatic Four Stages of Hepatic EncephalopathyEncephalopathyStageStage SymptomSymptom

II Mild confusion, agitation, Mild confusion, agitation, irritability, sleep disturbance, irritability, sleep disturbance, decreased attention decreased attention

IIII Lethargy, disorientation, Lethargy, disorientation, inappropriate behavior, inappropriate behavior,

drowsinessdrowsinessIIIIIISomnolence but arousable, Somnolence but arousable,

incomprehensible speech, confusion, incomprehensible speech, confusion, aggression when awakeaggression when awake

IVIV ComaComa

End-Stage Liver End-Stage Liver DiseaseDiseaseHepatic EncephalopathyHepatic Encephalopathy

End-Stage Liver End-Stage Liver DiseaseDiseaseHepatic EncephalopathyHepatic Encephalopathy1. Consider major causes of encephalopathy 1. Consider major causes of encephalopathy

• • GI bleedingGI bleeding

• • Fluid and electrolyte abnormalitiesFluid and electrolyte abnormalities

• • Uremia Uremia

• • Use of sedativesUse of sedatives

• • Hypo- or hyperglycemia Hypo- or hyperglycemia

• • Alcohol withdrawalAlcohol withdrawal

• • ConstipationConstipation

• • AcidosisAcidosis

1. Consider major causes of encephalopathy 1. Consider major causes of encephalopathy

• • GI bleedingGI bleeding

• • Fluid and electrolyte abnormalitiesFluid and electrolyte abnormalities

• • Uremia Uremia

• • Use of sedativesUse of sedatives

• • Hypo- or hyperglycemia Hypo- or hyperglycemia

• • Alcohol withdrawalAlcohol withdrawal

• • ConstipationConstipation

• • AcidosisAcidosis

End-Stage Liver End-Stage Liver DiseaseDiseaseHepatic Encephalopathy—Hepatic Encephalopathy—cont’dcont’d

End-Stage Liver End-Stage Liver DiseaseDiseaseHepatic Encephalopathy—Hepatic Encephalopathy—cont’dcont’d2. Treat underlying cause.2. Treat underlying cause.

3. Treat with medications. 3. Treat with medications. • • LactuloseLactulose • • NeomycinNeomycin4. Ensure adequate diet is 4. Ensure adequate diet is consumed.consumed.

2. Treat underlying cause.2. Treat underlying cause.3. Treat with medications. 3. Treat with medications.

• • LactuloseLactulose • • NeomycinNeomycin4. Ensure adequate diet is 4. Ensure adequate diet is consumed.consumed.

MNT in End-Stage MNT in End-Stage Liver DiseaseLiver Disease Energy needs are highly variable; Energy needs are highly variable;

30% of pts are hypometabolic and 30% of pts are hypometabolic and 20% hypermetabolic20% hypermetabolic

Use indirect calorimetry where Use indirect calorimetry where availableavailable

Energy: 25 to 30 kcal/kg dry Energy: 25 to 30 kcal/kg dry weightweight

Ascites increases REE by 10%Ascites increases REE by 10%Hasse et al. ASPEN Nutrition Support Practice Manual, 2nd Edition, 2005, p. 238

End-Stage Liver End-Stage Liver Disease Disease End-Stage Liver End-Stage Liver Disease Disease

Fat:Fat: 25% to 40% of kcal 25% to 40% of kcal

May try MCT if steatorrhea is present; with May try MCT if steatorrhea is present; with severe case, try fat restriction and severe case, try fat restriction and discontinue if diarrhea does not improvediscontinue if diarrhea does not improve

Protein:Protein: 1 to 1.5 g/kg dry wt depending on 1 to 1.5 g/kg dry wt depending on degree of malnutrition, malabsorption, degree of malnutrition, malabsorption, metabolic stressmetabolic stress

Fat:Fat: 25% to 40% of kcal 25% to 40% of kcal

May try MCT if steatorrhea is present; with May try MCT if steatorrhea is present; with severe case, try fat restriction and severe case, try fat restriction and discontinue if diarrhea does not improvediscontinue if diarrhea does not improve

Protein:Protein: 1 to 1.5 g/kg dry wt depending on 1 to 1.5 g/kg dry wt depending on degree of malnutrition, malabsorption, degree of malnutrition, malabsorption, metabolic stressmetabolic stress

End-Stage Liver End-Stage Liver Disease—cont’dDisease—cont’d May try BCAA formulas for >grade 2 May try BCAA formulas for >grade 2

encephalopathyencephalopathy CHO: high intake of both complex and CHO: high intake of both complex and

simple carbohydratessimple carbohydrates Vitamin and mineral supplementsVitamin and mineral supplements Electrolytes: restrict sodium with Electrolytes: restrict sodium with

edema or edema or ascites (1500-2000 mg/day)ascites (1500-2000 mg/day) Fluid: restrict fluid if hyponatremia is Fluid: restrict fluid if hyponatremia is

present 1000-1500 mLpresent 1000-1500 mL

Hasse. ASPEN Nutrition Support Practice Manual, 2nd edition, 2500, p. 239

Amino Acids Amino Acids Commonly Altered in Commonly Altered in Liver Disease Liver Disease *=essential)*=essential) Aromatic amino acids—serum levels increasedAromatic amino acids—serum levels increased

——TyrosineTyrosine

——Phenylalanine*Phenylalanine*

——Free tryptophan*Free tryptophan* Branched-chain amino acids—serum levels decreasedBranched-chain amino acids—serum levels decreased

——Valine*Valine*

——Leucine*Leucine*

——Isoleucine*Isoleucine* Other amino acids—serum levels increasedOther amino acids—serum levels increased

——Methionine*Methionine*

——GlutamineGlutamine

Aromatic amino acids—serum levels increasedAromatic amino acids—serum levels increased

——TyrosineTyrosine

——Phenylalanine*Phenylalanine*

——Free tryptophan*Free tryptophan* Branched-chain amino acids—serum levels decreasedBranched-chain amino acids—serum levels decreased

——Valine*Valine*

——Leucine*Leucine*

——Isoleucine*Isoleucine* Other amino acids—serum levels increasedOther amino acids—serum levels increased

——Methionine*Methionine*

——GlutamineGlutamine —Asparagine—Histidine*

—Asparagine—Histidine*

Esophageal VaricesEsophageal Varices

MNT for Esophageal MNT for Esophageal VaricesVarices Endoscopic tube used to Endoscopic tube used to

tamponade bleeding vesselstamponade bleeding vessels Repeated therapy may cause Repeated therapy may cause

esophageal strictures, esophageal strictures, dysphagiadysphagia

Cannot feed enterally during Cannot feed enterally during acute bleeding episodesacute bleeding episodes

May require PN if patient unable May require PN if patient unable to eatto eat

MNT for AscitesMNT for Ascites Ascites is accumulation of fluid in the Ascites is accumulation of fluid in the

abdominal cavityabdominal cavity Caused by portal hypertension, Caused by portal hypertension,

hypoalbuminemia, lymphatic obstruction, hypoalbuminemia, lymphatic obstruction, renal retention of sodium and fluidrenal retention of sodium and fluid

Medical treatment: paracentesis, diureticsMedical treatment: paracentesis, diuretics MNT: restrict sodium to 2 grams or lessMNT: restrict sodium to 2 grams or less More severe restrictions may be More severe restrictions may be

unpalatableunpalatable MNT: supplement protein if frequent MNT: supplement protein if frequent

paracentesisparacentesis

MNT for HyponatremiaMNT for Hyponatremia Occurs because of decreased ability to Occurs because of decreased ability to

excrete water because of persistent excrete water because of persistent release of antidiuretic hormone, sodium release of antidiuretic hormone, sodium loss via paracentesis, excessive diuretic loss via paracentesis, excessive diuretic use, sodium restrictionuse, sodium restriction

Fluid intake restricted to 1 to 1.5 liter per Fluid intake restricted to 1 to 1.5 liter per day (as low as 500-750 + urinary loss)day (as low as 500-750 + urinary loss)

Moderate sodium intakeModerate sodium intake

Hepatic Hepatic EncephalopathyEncephalopathy Can be caused by GI bleeding, Can be caused by GI bleeding,

fluid/electrolyte abnormalities, uremia, fluid/electrolyte abnormalities, uremia, infection, blood glucose derangements, infection, blood glucose derangements, alcohol withdrawalalcohol withdrawal

Occurs in 50-70% of pts with chronic Occurs in 50-70% of pts with chronic hepatic failurehepatic failure

Caused by protein in only 5%Caused by protein in only 5% 95% of persons with cirrhosis tolerate 95% of persons with cirrhosis tolerate

mixed protein diets of up to 1.5 g/kgmixed protein diets of up to 1.5 g/kg

Hasse ASPEN Nutrition Support Practice Manual, 2nd edition, p. 236

Hepatic Hepatic Encephalopathy: Encephalopathy: Medical TreatmentMedical TreatmentNeomycin or lactuloseNeomycin or lactulose Lactulose: nonabsorbable Lactulose: nonabsorbable

disaccharide. Acidifies colonic disaccharide. Acidifies colonic contents, acts as laxative to excrete contents, acts as laxative to excrete ammoniaammonia

Neomycin is nonabsorbable Neomycin is nonabsorbable antibiotic that decreases colonic antibiotic that decreases colonic ammonia productionammonia production

Hepatic Hepatic Encephalopathy: Encephalopathy: Medical TreatmentMedical TreatmentIdentify and treat acute causes, Identify and treat acute causes,

e.g.e.g. Variceal bleedVariceal bleed InfectionInfection Electrolyte imbalanceElectrolyte imbalance SedativesSedatives ConstipationConstipationHasse JM et al. ASPEN Nutrition Support Practice Manual, 2nd Edition, 2005

Hepatic Encephalopathy: Hepatic Encephalopathy: MNTMNT

Role of protein in Role of protein in encephalopathy controversialencephalopathy controversial

Encephalopathy may be caused Encephalopathy may be caused by imbalance of aromatic and by imbalance of aromatic and branched chain amino acidsbranched chain amino acids

Protein restriction not proven to Protein restriction not proven to improve mental stateimprove mental state

Supplements enriched in BCAA, Supplements enriched in BCAA, low in AAA may helplow in AAA may help

Hepatic Hepatic Encephalopathy: MNTEncephalopathy: MNT If patient is protein sensitive, start If patient is protein sensitive, start

with .5 to .7 g protein/kg and with .5 to .7 g protein/kg and increase level to tolerance, up to increase level to tolerance, up to 1.5 g/kg in protein-calorie 1.5 g/kg in protein-calorie malnutritionmalnutrition

Provide adequate calories to Provide adequate calories to prevent catabolism of prevent catabolism of endogenous protein storesendogenous protein stores

Glucose DerangementsGlucose Derangements Glucose intolerance in nearly Glucose intolerance in nearly

2/3 of patients with cirrhosis 2/3 of patients with cirrhosis (10-37% develop diabetes)(10-37% develop diabetes)

Occurs because of insulin Occurs because of insulin resistance in peripheral tissuesresistance in peripheral tissues

Hyperinsulinemia, possibly Hyperinsulinemia, possibly because insulin production because insulin production increased, hepatic clearance increased, hepatic clearance decreaseddecreased

Fasting hypoglycemia d/t Fasting hypoglycemia d/t decreased glycogen stores; pts decreased glycogen stores; pts may need small, frequent mealsmay need small, frequent meals

SteatorrheaSteatorrhea Replace LCT with MCT oils (in Replace LCT with MCT oils (in

some nutrition supplements or as some nutrition supplements or as oil)oil)

May trial low fat diet, but do not May trial low fat diet, but do not restrict unnecessarily; if restrict unnecessarily; if steatorrhea doesn’t improve, steatorrhea doesn’t improve, discontinue restrictiondiscontinue restriction

Nutrition Care Nutrition Care Guidelines for Liver Guidelines for Liver TransplantationTransplantation PretransplantationPretransplantation Immediate Immediate

posttransplantation posttransplantation Long-term Long-term

posttransplantationposttransplantation

CaloriesCalories ProteinProtein FatFat CarbohydrateCarbohydrate SodiumSodium Fluid Fluid Calcium Calcium VitaminsVitamins

Medications* Medications* Commonly Used after Commonly Used after Liver Tx Liver Tx AzathioprineAzathioprine Antithymocyte Antithymocyte

globulinglobulin BasiliximabBasiliximab CyclosporineCyclosporine DaclizumabDaclizumab GlucocorticoidsGlucocorticoids

Muromonab-CD3Muromonab-CD3 Mycophenolate Mycophenolate

mofetilmofetil SirolimusSirolimus TacrolimusTacrolimus 15-15-

deoxysperagualindeoxysperagualin

*Most have drug-nutrition interactions. See p. 756 Krause

Liver TransplantationLiver Transplantation—Diet—DietLiver TransplantationLiver Transplantation—Diet—Diet

Nutrition support: pre- and post-Nutrition support: pre- and post-transplanttransplant

Long-term preventive nutrition to Long-term preventive nutrition to optimize health and to avoid or optimize health and to avoid or minimizeminimize—Excessive weight gainExcessive weight gain—Hyperlipidemia Hyperlipidemia —HyperglycemiaHyperglycemia—HypertensionHypertension—OsteopeniaOsteopenia

Nutrition support: pre- and post-Nutrition support: pre- and post-transplanttransplant

Long-term preventive nutrition to Long-term preventive nutrition to optimize health and to avoid or optimize health and to avoid or minimizeminimize—Excessive weight gainExcessive weight gain—Hyperlipidemia Hyperlipidemia —HyperglycemiaHyperglycemia—HypertensionHypertension—OsteopeniaOsteopenia

CAM in Liver DiseaseCAM in Liver Disease

Milk Thistle (silymarin) – Milk Thistle (silymarin) – purported anti-hepatotoxic and purported anti-hepatotoxic and anti-inflammatory activityanti-inflammatory activity

Scientific evidence is mixedScientific evidence is mixed

CAM in Liver Dx: CAM in Liver Dx: Potentially Hepatotoxic Potentially Hepatotoxic ProductsProducts BorageBorage ChaparralChaparral ColtsfootColtsfoot ComfreyComfrey DHEADHEA GermanderGermander Jin bu huanJin bu huan

Kava kavaKava kava LiferootLiferoot PennyroyalPennyroyal PeriwinklePeriwinkle Poke rootPoke root Skullcap Skullcap

(American)(American) Shark cartilageShark cartilage

Hasse JM. ASPEN Nutrition Support Practice Manual, 2nd Edition, 2005.

SummarySummary

Liver disorders—role of liver is so Liver disorders—role of liver is so crucial to overall health, its crucial to overall health, its destruction is quite seriousdestruction is quite serious

Goals—support maintenance of as Goals—support maintenance of as much normal liver function as much normal liver function as possiblepossible

Transplantation, if neededTransplantation, if needed

Relationship of Relationship of Organs of the Upper Organs of the Upper AbdomenAbdomen

A, Liver (retracted upward); B, gallbladder; C, esophageal opening of the stomach; D, stomach (shown in dotted outline); E, common bile duct; F, duodenum; G, pancreas and pancreatic duct; H, spleen; I, kidneys.

Courtesy The Cleveland Clinic Foundation, Cleveland, Ohio, 2002.

Functions of the Functions of the GallbladderGallbladder Primary function is to concentrate, Primary function is to concentrate,

store, excrete bile (produced by the store, excrete bile (produced by the liver)liver)

Bile: primary constituents are Bile: primary constituents are cholesterol, bilirubin (from hemoglobin) cholesterol, bilirubin (from hemoglobin) and bile saltsand bile salts

Bile salts are essential for digestion Bile salts are essential for digestion and absorption of fats, fat soluble and absorption of fats, fat soluble vitamins, some mineralsvitamins, some minerals

Gallbladder and pancreas use common Gallbladder and pancreas use common duct to release digestive juices into duct to release digestive juices into duodenumduodenum

Diseases of liver, pancreas, and Diseases of liver, pancreas, and gallbladder interrelatedgallbladder interrelated

Diseases of the Diseases of the Gallbladder: Gallbladder: CholelithiasisCholelithiasis Calculi form in the gallbladderCalculi form in the gallbladder Choledocholithiasis: stones slip into Choledocholithiasis: stones slip into

bile ducts, obstruction, pain, crampsbile ducts, obstruction, pain, cramps Blockage can cause cholecystitis, Blockage can cause cholecystitis,

impaired lipid absorption, light impaired lipid absorption, light colored stools; secondary biliary colored stools; secondary biliary cirrhosis; obstruction of the distal cirrhosis; obstruction of the distal common bile duct can lead to common bile duct can lead to pancreatitis if pancreatic duct is pancreatitis if pancreatic duct is blockedblocked

CholedocholithiasisCholedocholithiasis

http://www.nlm.nih.gov/medlineplus/ency/images/ency/fullsize/17038.jpg

CholedocholithiasisCholedocholithiasis Affects millions of Americans each Affects millions of Americans each

year; many asymptomaticyear; many asymptomatic Risk factors are female gender, Risk factors are female gender,

pregnancy, older age, family history, pregnancy, older age, family history, obesity, truncal body fat distribution, obesity, truncal body fat distribution, diabetes, certain drugs (lipid diabetes, certain drugs (lipid lowering meds, oral contraceptives, lowering meds, oral contraceptives, estrogens)estrogens)

Rapid weight loss (gastric bypass, Rapid weight loss (gastric bypass, fasting, VLC diets) associated with fasting, VLC diets) associated with biliary sludge and gallstonesbiliary sludge and gallstones

Choledocholithiasis Choledocholithiasis Medical MgtMedical Mgt Surgical removal of the Surgical removal of the

gallbladder via open lap or gallbladder via open lap or laparoscopic procedurelaparoscopic procedure

Chemical dissolution or shock Chemical dissolution or shock wave lithotripsy may be triedwave lithotripsy may be tried

Stones in bile ducts may be Stones in bile ducts may be removed via endoscopic removed via endoscopic retrograde retrograde cholangiopancreatography cholangiopancreatography techniques (ERCP) techniques (ERCP)

Cholelithiasis MNTCholelithiasis MNT Correct risk factors if possible Correct risk factors if possible

(obesity and VLC diets)(obesity and VLC diets) Cholecystitis: low fat diet to Cholecystitis: low fat diet to

prevent gallbladder contractionsprevent gallbladder contractions After cholecystectomy, diet can be After cholecystectomy, diet can be

advanced to regular diet as advanced to regular diet as toleratedtolerated

Liver secretes bile directly into Liver secretes bile directly into small intestine; intestine adaptssmall intestine; intestine adapts

Cholecystitis MNTCholecystitis MNT Acute: NPO initially. Use PN if Acute: NPO initially. Use PN if

prolonged. Then initiate low fat diet prolonged. Then initiate low fat diet (hydrolyzed lowfat enteral feeding (hydrolyzed lowfat enteral feeding or oral diet with 30-45 g fat/day)or oral diet with 30-45 g fat/day)

Chronic: long term low fat diet (25-Chronic: long term low fat diet (25-30% of calories30% of calories

May need water-soluble forms of May need water-soluble forms of fat-soluble vitamins if malabsorption fat-soluble vitamins if malabsorption is suspectedis suspected

Functions of the Functions of the PancreasPancreas Endocrine Functions: secretes Endocrine Functions: secretes

glucagon, insulin, somatostatin glucagon, insulin, somatostatin into bloodstream for regulation of into bloodstream for regulation of glucose glucose

Exocrine Functions: secretes Exocrine Functions: secretes enzymes directly into GI tract to enzymes directly into GI tract to digest protein, fat, carbohydratedigest protein, fat, carbohydrate

Factors that Govern Factors that Govern Pancreatic SecretionsPancreatic Secretions Cephalic phase: mediated through the Cephalic phase: mediated through the

vagus nerve, initiated by the sight, vagus nerve, initiated by the sight, smell, taste and anticipation of food: smell, taste and anticipation of food: bicarbonate and pancreatic enzymesbicarbonate and pancreatic enzymes

Gastric phase: caused by gastric Gastric phase: caused by gastric distention with food; enzyme secretiondistention with food; enzyme secretion

Intestinal phase: most potent effect, Intestinal phase: most potent effect, mediated by the release of mediated by the release of cholecystokinincholecystokinin

PancreatitisPancreatitis Inflammation of the pancreas, mild or Inflammation of the pancreas, mild or

severesevere Significant morbidity/mortalitySignificant morbidity/mortality Symptoms: continuous or intermittent Symptoms: continuous or intermittent

pain of varying intensity to severe upper pain of varying intensity to severe upper abdominal pain, radiating to backabdominal pain, radiating to back

Symptoms may worsen with ingestion of Symptoms may worsen with ingestion of foodfood

Nausea, vomiting, abdominal distention, Nausea, vomiting, abdominal distention, steatorrheasteatorrhea

Elevated serum amylase or lipase; Elevated serum amylase or lipase; however amylase is nonspecific for however amylase is nonspecific for pancreatititspancreatitits

Pancreatitis: CausesPancreatitis: Causes Chronic alcoholism (most common Chronic alcoholism (most common

cause of acute and chronic cause of acute and chronic pancreatitis)pancreatitis)

Gallstones (a common cause of Gallstones (a common cause of acute pancreatitis)acute pancreatitis)

Trauma, certain drugsTrauma, certain drugs HypertriglyceridemiaHypertriglyceridemia HypercalcemiaHypercalcemia Some viral infectionsSome viral infections

Pancreatitis: DiagnosisPancreatitis: Diagnosis Tests of pancreatic functionTests of pancreatic function

– Secretin stimulation test: measures Secretin stimulation test: measures pancreatic secretion of bicarbonate in pancreatic secretion of bicarbonate in response to secretinresponse to secretin

– Glucose tolerance test: measures Glucose tolerance test: measures endocrine functionendocrine function

– 72-hour stool fat test: measures fat 72-hour stool fat test: measures fat absorption that reflects pancreatic absorption that reflects pancreatic lipase secretionlipase secretion

Ranson’s CriteriaRanson’s Criteria

At admission or diagnosisAt admission or diagnosis Age >55 yearsAge >55 years White blood count >16,000 m3White blood count >16,000 m3 Blood glucose level >200 mg/dlBlood glucose level >200 mg/dl Lactic dehydrogenase >350 IU/LLactic dehydrogenase >350 IU/L Aspartate transaminase >240 U/LAspartate transaminase >240 U/L

Ranson’s CriteriaRanson’s Criteria

During first 48 hoursDuring first 48 hours Hematocrit decrease of >10 mg/dLHematocrit decrease of >10 mg/dL Blood urea nitrogen increase of >5 Blood urea nitrogen increase of >5

mg/dlmg/dl Arterial PO2 <60 mmHgArterial PO2 <60 mmHg Base deficit >4 mEq/LBase deficit >4 mEq/L Fluid sequestration >6000 mlFluid sequestration >6000 ml Serum calcium level <8 mg/dLSerum calcium level <8 mg/dL

PancreatitisPancreatitis

http://www.pennhealth.com/health_info/Surgery/pancreatitis_2.html

Acute Hemorrhagic Acute Hemorrhagic PancreatitisPancreatitis

http://www.pathguy.com/~lulo/lulo0028.htm

Acute PancreatitisAcute Pancreatitis

75% alcohol related75% alcohol related 15% related to gallstones15% related to gallstones 10% trauma, hyperlipidemia, 10% trauma, hyperlipidemia,

hypercalcemia, medications, etc.hypercalcemia, medications, etc.

Mascarenhas et al. ASPEN Nutrition Support Practice Manual, 2nd edition, 2005, p. 211

Energy Needs in Acute Energy Needs in Acute PancreatitisPancreatitis Metabolic stress state: Resting Metabolic stress state: Resting

energy expenditure as high as energy expenditure as high as 139% of Harris-Benedict139% of Harris-Benedict

Sepsis may increase energy Sepsis may increase energy needs an additional 15%needs an additional 15%

Acute patients more Acute patients more hypermetabolic than chronic hypermetabolic than chronic patientspatients

Mascarenhas et al. ASPEN Nutrition Support Practice Manual, 2nd edition, 2005, p. 211

Nutritional Alterations Nutritional Alterations in Acute Pancreatitisin Acute Pancreatitis Glucose intolerance in 40 to 90% Glucose intolerance in 40 to 90%

of patients, caused by stress of patients, caused by stress response, impaired Beta-cell response, impaired Beta-cell function, and insulin resistancefunction, and insulin resistance

Changes in fat metabolism in 12-Changes in fat metabolism in 12-15% of patients, primarily 15% of patients, primarily steatorrhea and steatorrhea and hypertriglyceridemiahypertriglyceridemia

Nutritional Alterations Nutritional Alterations in Acute Pancreatitisin Acute Pancreatitis Hypocalcemia in 25% of patients Hypocalcemia in 25% of patients

due to due to ↓ parathyroid hormone ↓ parathyroid hormone secretion, increased calcitonin, secretion, increased calcitonin, hypomagnesemia, hypomagnesemia, hypoalbuminemia, saponification of hypoalbuminemia, saponification of calciumcalcium

Ethanol abuse → hypomagnesemia, Ethanol abuse → hypomagnesemia, decreased zinc, thiamine and folate decreased zinc, thiamine and folate deficienciesdeficiencies

Mascarenhas et al ASPEN Nutrition Support Practice Manual, 2005, p. 211

Pancreatic Disorders: Pancreatic Disorders: Medical MgtMedical MgtAcuteAcute Withhold oral feedingWithhold oral feeding Give IV fluidsGive IV fluids Administer H2-receptor antagonists, Administer H2-receptor antagonists,

somatostatinsomatostatin

ChronicChronic Manage intestinal pH with antacids, H2 Manage intestinal pH with antacids, H2

receptor antagonists, proton pump receptor antagonists, proton pump inhibitorsinhibitors

Administer insulin for glucose intoleranceAdminister insulin for glucose intolerance

Pancreatitis: MNTPancreatitis: MNT

AcuteAcute Withhold oral feedingWithhold oral feeding Support with IV fluidsSupport with IV fluids If oral nutrition cannot be initiated If oral nutrition cannot be initiated

in 5-7 days, start nutrition supportin 5-7 days, start nutrition support

Pancreatitis: Enteral Pancreatitis: Enteral Nutrition Nutrition Enteral nutrition can be used while Enteral nutrition can be used while

resting the pancreasresting the pancreas Early enteral feeding may exacerbate Early enteral feeding may exacerbate

symptoms (21% of patients in one symptoms (21% of patients in one case series)case series)

Feeding below the ligament of Treitz Feeding below the ligament of Treitz invokes fewer stimulatory factorsinvokes fewer stimulatory factors

Use of elemental low fat formulas is Use of elemental low fat formulas is less stimulating than polymeric, higher less stimulating than polymeric, higher fat formulasfat formulas


Pancreatitis: Enteral Pancreatitis: Enteral RecommendationsRecommendations Place nasoenteric tube below the Place nasoenteric tube below the

ligament of Treitzligament of Treitz Begin infusion with a standard enteral Begin infusion with a standard enteral

formulaformula If there is concern about a particular If there is concern about a particular

patient, a low-fat elemental or peptide patient, a low-fat elemental or peptide formula should be usedformula should be used

Monitor patient for intolerance (N/V, Monitor patient for intolerance (N/V, abdominal pain, fever, abdominal pain, fever, ↑ amylase/lipase↑ amylase/lipase

PN may be initiated if patient does not PN may be initiated if patient does not tolerate ENtolerate EN

Pancreatitis: Enteral Pancreatitis: Enteral NutritionNutrition Stimulation of the GI tract at Stimulation of the GI tract at

lower levels may be beneficiallower levels may be beneficial EN maintains gut integrity and EN maintains gut integrity and

stimulates blood flow to the gutstimulates blood flow to the gut May preserve immune function May preserve immune function

and reduce inflammatory and reduce inflammatory responseresponseMascarenhas et al ASPEN Nutrition Support Practice Manual, 2005, p. 211

Pancreatitis: PNPancreatitis: PNAcute (cont)Acute (cont) If enteral feedings are not If enteral feedings are not

tolerated, PN should be initiatedtolerated, PN should be initiated– If TGs are <400 mg/dl use 3-in-1 If TGs are <400 mg/dl use 3-in-1

solution and monitor TG levelssolution and monitor TG levels– If TGs are elevated (>400 mg/dl) use If TGs are elevated (>400 mg/dl) use

a dextrose-based solution, monitor a dextrose-based solution, monitor serum glucose frequently, and treat serum glucose frequently, and treat as needed with insulinas needed with insulin


Pancreatitis MNTPancreatitis MNT

AcuteAcute Energy needs: AP patients are Energy needs: AP patients are

hypermetabolic and catabolichypermetabolic and catabolic HB BEE X activity factor X stress HB BEE X activity factor X stress

factor of 30-50%factor of 30-50% Protein needs: 1.4-2 g/kg body weightProtein needs: 1.4-2 g/kg body weight Fat up to 2 g/kg/BW/day; monitor TGFat up to 2 g/kg/BW/day; monitor TG

Wall-Alonso, Sullivan, Byrne. In Gottslich and Matarese. Contemporary Nutrition Support Practice, p. 434-425. Philadelphia: Saunders, 2003.


Acute (cont)Acute (cont) Once oral diet is started, provideOnce oral diet is started, provide

– Easily digested foodsEasily digested foods– Low fat dietLow fat diet– 6 small meals6 small meals– Adequate protein intakeAdequate protein intake– Increased caloriesIncreased calories


ChronicChronic Provide oral diet as in acute Provide oral diet as in acute

phasephase TF can be used when oral diet is TF can be used when oral diet is

inadequateinadequate Supplement pancreatic enzymesSupplement pancreatic enzymes Supplement fat-soluble vitamins Supplement fat-soluble vitamins

and vitamin B12and vitamin B12

MNT for Chronic Pancreatitis: MNT for Chronic Pancreatitis: Pancreatic EnzymesPancreatic Enzymes

When pancreatic function diminished When pancreatic function diminished by about 90%, malabsorption of by about 90%, malabsorption of protein and fat becomes a problemprotein and fat becomes a problem

Avoid large high fat meals and Avoid large high fat meals and alcoholalcohol

Pancreatic enzyme replacements Pancreatic enzyme replacements given orally with meals (at least given orally with meals (at least 30,000 IU lipase with each meal)30,000 IU lipase with each meal)

Level of fat in the diet should be the Level of fat in the diet should be the most pt can tolerate without most pt can tolerate without steatorrhea or painsteatorrhea or pain

May substitute some fat with MCTMay substitute some fat with MCT

Whipple ProcedureWhipple Procedure Pancreaticoduodenectomy: often Pancreaticoduodenectomy: often

done for pancreatic carcinomadone for pancreatic carcinoma Cholecystectomy, vagotomy, or Cholecystectomy, vagotomy, or

partial gastrectomy may also be partial gastrectomy may also be donedone

Pancreatic duct renanastamosed to Pancreatic duct renanastamosed to the jejunumthe jejunum

MNT: similar to chronic pancreatitisMNT: similar to chronic pancreatitis

Whipple ProcedureWhipple Procedure

Source: Johns Hopkins http://www.hopkins-gi.org/pages/latin/templates/ index.cfm?pg=disease3&organ=4&disease =24&lang_id=1&pagetype=12&pagenum=263

MNT in Liver/Biliary MNT in Liver/Biliary DiseaseDisease Disease of the liver/biliary tract has a Disease of the liver/biliary tract has a

profound effect on digestion and profound effect on digestion and absorptionabsorption

Often leads to malnutrition; Often leads to malnutrition; malnutrition exacerbates effect of malnutrition exacerbates effect of diseasedisease

Appropriate nutrition care is key in Appropriate nutrition care is key in reducing associated morbidity and reducing associated morbidity and mortality and improving quality of lifemortality and improving quality of life

© 2004, 2002 elsevier inc. all rights reserved. medical nutrition therapy for liver, biliary...

Documents