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© 2004, 2002 Elsevier Inc. All rights reserved. Medical Nutrition Therapy for Liver, Biliary System, and Exocrine Pancreas Disorders.

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Presentation on theme: "© 2004, 2002 Elsevier Inc. All rights reserved. Medical Nutrition Therapy for Liver, Biliary System, and Exocrine Pancreas Disorders."— Presentation transcript:

1 © 2004, 2002 Elsevier Inc. All rights reserved. Medical Nutrition Therapy for Liver, Biliary System, and Exocrine Pancreas Disorders

2 Relationship of Organs of the Upper Abdomen 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.

3 The Liver Largest gland in the body (about 1500 g) Largest gland in the body (about 1500 g) Essential for life, though survival is possible with 10-20% function Essential for life, though survival is possible with 10-20% function Plays major role in macronutrient and micronutrient digestion, metabolism, and storage Plays major role in macronutrient and micronutrient digestion, metabolism, and storage Metabolizes steroids, detoxifies drugs, alcohol, ammonia Metabolizes steroids, detoxifies drugs, alcohol, ammonia

4 Diseases of the Liver Acute viral hepatitis Acute viral hepatitis Fulminant hepatitis Fulminant hepatitis Chronic hepatitis Chronic hepatitis Alcoholic liver disease, alcoholic hepatitis, and cirrhosis Alcoholic liver disease, alcoholic hepatitis, and cirrhosis Non-alcoholic hepatic steatosis (NASH) Non-alcoholic hepatic steatosis (NASH)

5 Diseases of the Liver Cholestatic liver diseases Cholestatic liver diseases —Primary biliary cirrhosis —Sclerosing cholangitis Inherited disorders Inherited disorders Other liver diseases Other liver diseases

6 Acute Viral Hepatitis Widespread inflammation of the liver that is caused by hepatitis viruses A, B, C, D and E Widespread inflammation of the liver that is caused by hepatitis viruses A, B, C, D and E –Hep A: oral-fecal route –Hep B and C: body fluids –Hep D: occurs only in pts with Hep B –Hep E: oral-fecal route; seen more often in Asia, Africa, Mexico Hasse JM et al. ASPEN Nutrition Support Practice Manual, 2 nd edition, 2005

7 Acute Viral Hepatitis Four phases of symptoms: Four phases of symptoms: 1. Prodromal phase 2. Preicteric phase 3. Icteric phase 4. Convalescent phase

8 Risk Factors for Chronic Viral Hepatitis Injection drug use Injection drug use Chronic hemodialysis Chronic hemodialysis Blood transfusion or transplantation prior to 1992 (HCV) Blood transfusion or transplantation prior to 1992 (HCV) Receipt of blood (including needlestick) from a donor subsequently testing positive for HCV Receipt of blood (including needlestick) from a donor subsequently testing positive for HCV

9 Risk Factors for Chronic Viral Hepatitis Receipt of clotting factor concentrates produced before 1987 Receipt of clotting factor concentrates produced before 1987 Asian ancestry (HBV) Asian ancestry (HBV) Unvaccinated health care workers Unvaccinated health care workers Birth to mother with chronic HBV or HCV Birth to mother with chronic HBV or HCV

10 Possible Risk Factors Body piercing or tattooing Body piercing or tattooing Multiple sexual partners or sexually transmitted diseases Multiple sexual partners or sexually transmitted diseases Health care workers (HCV) Health care workers (HCV) Contacts of HCV positive persons Contacts of HCV positive persons Source: NACB Laboratory Guidelines for Screening, Diagnosis, and Monitoring of Hepatic Injury. Dufour, Lott, Nolte, Gretch, Koff, Seeff

11 Fulminant Hepatitis Syndrome in which severe liver dysfunction is accompanied by hepatic encephalopathy within 8 weeks Syndrome in which severe liver dysfunction is accompanied by hepatic encephalopathy within 8 weeks Causes include viral hepatitis (75%), chemical toxicity (acetaminophen, drug reactions, poisonous mushrooms, other poisons) Causes include viral hepatitis (75%), chemical toxicity (acetaminophen, drug reactions, poisonous mushrooms, other poisons) Complications include cerebral edema, coagulopathy, bleeding, cardiovascular complications, renal failure, pancreatitis Complications include cerebral edema, coagulopathy, bleeding, cardiovascular complications, renal failure, pancreatitis

12 Chronic Hepatitis At least 6-month course of hepatitis or biochemical and clinical evidence of liver disease with confirmatory biopsy findings of unresolving hepatic inflammation At least 6-month course of hepatitis or biochemical and clinical evidence of liver disease with confirmatory biopsy findings of unresolving hepatic inflammation Can be caused by autoimmune, viral, metabolic, or toxic etiologies Can be caused by autoimmune, viral, metabolic, or toxic etiologies

13 Alcoholic Liver Disease: Most Common Liver Disease Alcohol excess and abuse Alcohol excess and abuse Most common cause of liver disease in the U.S. Most common cause of liver disease in the U.S. Fourth leading cause of death among middle-aged Americans Fourth leading cause of death among middle-aged Americans Alcohol problems are highest among young adults, ages 18 to 29. Alcohol problems are highest among young adults, ages 18 to 29.

14 Stages of Alcoholic Liver Disease Hepatic steatosis Hepatic steatosis Alcoholic hepatitis Alcoholic hepatitis Alcoholic (Leannec’s) cirrhosis Alcoholic (Leannec’s) cirrhosis

15 Alcoholic Liver Disease Disease resulting from excessive alcohol ingestion characterized by fatty liver (hepatic steatosis), hepatitis, or cirrhosis Disease resulting from excessive alcohol ingestion characterized by fatty liver (hepatic steatosis), hepatitis, or cirrhosis Most common liver disease in the U.S., except perhaps fatty liver secondary to obesity Most common liver disease in the U.S., except perhaps fatty liver secondary to obesity

16 © 2004, 2002 Elsevier Inc. All rights reserved. Toxic Effects of Excess Alcohol Use

17 Alcoholic Liver Disease Metabolic Changes Steatorrhea Steatorrhea Wernicke-Korsakoff syndrome Wernicke-Korsakoff syndrome Peripheral neuropathy Peripheral neuropathy Pellagrous psychosis Pellagrous psychosis Folate deficiency Folate deficiency

18 End-Stage Alcoholic Liver Disease Possible Characteristics Malnutrition Malnutrition Portal hypertension with varices Portal hypertension with varices Ascites Ascites Hyponatremia Hyponatremia Hepatic encephalopathy Hepatic encephalopathy Glucose alterations Glucose alterations

19 End-Stage Alcoholic Liver Disease Possible Characteristics Fat malabsorption Fat malabsorption Osteopenia Osteopenia Thrombocytopenia with anemia Thrombocytopenia with anemia

20 Non-Alcoholic Steatohepatitis (NASH) Histologically resembles alcoholic hepatitis Histologically resembles alcoholic hepatitis Most common cause of chronic hepatic injury other than viruses and alcohol; most common cause of cryptogenic cirrhosis Most common cause of chronic hepatic injury other than viruses and alcohol; most common cause of cryptogenic cirrhosis Commonly in middle-aged women with obesity and/or diabetes but appears in persons without these risk factors Commonly in middle-aged women with obesity and/or diabetes but appears in persons without these risk factors

21 Non-Alcoholic Steatohepatitis (NASH) Patients with NASH often have abnormal lipid profiles Patients with NASH often have abnormal lipid profiles Differs from alcoholic hepatitis in that ALT is higher than AST except in cirrhosis Differs from alcoholic hepatitis in that ALT is higher than AST except in cirrhosis Weight loss may cause significant improvement in enzyme results; in one study a 1% reduction in weight caused an average fall of 8.1% in ALT Weight loss may cause significant improvement in enzyme results; in one study a 1% reduction in weight caused an average fall of 8.1% in ALT Biopsy is the only diagnostic procedure with adequate specificity Biopsy is the only diagnostic procedure with adequate specificity

22 Cholestatic Liver Diseases Primary biliary cirrhosis (PBC) An immune-mediated chronic cirrhosis of the liver due to obstruction or infection of the small and intermediate-sized intrahepatic bile ducts, whereas the extrahepatic biliary tree and larger intrahepatic ducts are normal An immune-mediated chronic cirrhosis of the liver due to obstruction or infection of the small and intermediate-sized intrahepatic bile ducts, whereas the extrahepatic biliary tree and larger intrahepatic ducts are normal 90% of patients are women 90% of patients are women

23 Cholestatic Liver Diseases Sclerosing cholangitis Fibrosing inflammation of segments of extrahepatic bile ducts, with or without involvement of intrahepatic ducts Fibrosing inflammation of segments of extrahepatic bile ducts, with or without involvement of intrahepatic ducts May be an immune disorder May be an immune disorder 50-75% of patients also have inflammatory bowel disease 50-75% of patients also have inflammatory bowel disease 60-70% are men 60-70% are men

24 Cholestatic Liver Diseases Sclerosing Cholangitis Increased risk of fat soluble vitamin deficiencies due to steatorrhea Increased risk of fat soluble vitamin deficiencies due to steatorrhea Hepatic osteodystrophy due to vitamin D and calcium malabsorption resulting in secondary hyperparathyroidism and osteomalacia or rickets Hepatic osteodystrophy due to vitamin D and calcium malabsorption resulting in secondary hyperparathyroidism and osteomalacia or rickets Treated with immunosuppressants Treated with immunosuppressants

25 Inherited Disorders: Hemochromatosis Inherited disease of iron overload Inherited disease of iron overload Store g of iron in the liver compared with.3 to.8 g in normal persons Store g of iron in the liver compared with.3 to.8 g in normal persons Causes hepatomegaly, esophageal varices, glucose intolerance Causes hepatomegaly, esophageal varices, glucose intolerance Treated by phlebotomy Treated by phlebotomy

26 Inherited Disorders: Wilson’s Disease Autosomal recessive disorder associated with impaired biliary copper excretion Autosomal recessive disorder associated with impaired biliary copper excretion Copper accumulates in liver, brain, cornea, and kidneys Copper accumulates in liver, brain, cornea, and kidneys May present with neurological signs, Kayser- Fleischer rings, low serum ceruloplasmin, psychiatric symptoms May present with neurological signs, Kayser- Fleischer rings, low serum ceruloplasmin, psychiatric symptoms Always presents before age 40 Always presents before age 40 Treated with copper-chelating agents, zinc supplementation, low copper diet Treated with copper-chelating agents, zinc supplementation, low copper diet

27 Inherited Disorders: α 1 -antitrypsin deficiency Causes cholestasis or cirrhosis and can cause liver and lung cancer Causes cholestasis or cirrhosis and can cause liver and lung cancer No treatment but liver transplant No treatment but liver transplant

28 Other Liver Diseases Liver tumors Liver tumors Systemic diseases (rheumatoid arthritis, systemic sclerosis) Systemic diseases (rheumatoid arthritis, systemic sclerosis) Nonalcoholic steatohepatitis** Nonalcoholic steatohepatitis** Acute ischemic and chronic congestive hepatopathy Acute ischemic and chronic congestive hepatopathy Parasitic, bacterial, fungal, and granulomatous liver diseases Parasitic, bacterial, fungal, and granulomatous liver diseases

29 Normal Liver vs. Damaged Liver

30 © 2004, 2002 Elsevier Inc. All rights reserved. Microscopic Image of (A) Normal 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.)

31 © 2004, 2002 Elsevier Inc. All rights reserved. Clinical Manifestations of Cirrhosis

32 Interpretation of Lab Data In Liver Disease

33 Liver Test Panel Aspartate transaminase (AST) Aspartate transaminase (AST) Alanine aminotransferase (ALT) Alanine aminotransferase (ALT) Alkaline phosphatase (ALP) Alkaline phosphatase (ALP) Total bilirubin Total bilirubin Direct bilirubin Direct bilirubin PT/PTT PT/PTT Ceruloplasmin Ceruloplasmin Total protein Total protein Albumin Albumin Viral serologies Viral serologies

34 AST and ALT Enzymes released into circulation following injury or death of cells in heart, liver, lungs, and other parts of the body Enzymes released into circulation following injury or death of cells in heart, liver, lungs, and other parts of the body High AST (200 U/L) and ALT (300 U/L) are indicative of liver disease in presence of jaundice or non- specific symptoms of acute illness High AST (200 U/L) and ALT (300 U/L) are indicative of liver disease in presence of jaundice or non- specific symptoms of acute illness Levels are higher in acute hepatic injury; lower in uncomplicated hepatitis and chronic liver disease Levels are higher in acute hepatic injury; lower in uncomplicated hepatitis and chronic liver disease Transaminases relate more to cause of liver injury than prognosis Transaminases relate more to cause of liver injury than prognosis

35 ALP (alkaline phosphatase) Usually normal in acute and chronic liver disease Usually normal in acute and chronic liver disease High levels are usually indicative of obstruction of biliary drainage High levels are usually indicative of obstruction of biliary drainage

36 Bilirubin Results from the breakdown of hemoglobin in the red blood cells and removal from the body by the liver, which excretes it in bile Results from the breakdown of hemoglobin in the red blood cells and removal from the body by the liver, which excretes it in bile Rises when the liver is unable to excrete bilirubin or when there is excessive destruction of red blood cells Rises when the liver is unable to excrete bilirubin or when there is excessive destruction of red blood cells In viral hepatitis, total bilirubin >257 micromoles/L indicates severe liver injury In viral hepatitis, total bilirubin >257 micromoles/L indicates severe liver injury In alcoholic hepatitis, bilirubin >428 micromoles/L predicts high likelihood of death In alcoholic hepatitis, bilirubin >428 micromoles/L predicts high likelihood of death

37 Two Forms of Bilirubin Indirect or unconjugated bilirubin: is protein bound;  with increased destruction of red blood cells Indirect or unconjugated bilirubin: is protein bound;  with increased destruction of red blood cells Direct or conjugated bilirubin: not protein bound; circulates until it reaches the liver, where it is conjugated;  in dysfunction or blockage of the liver Direct or conjugated bilirubin: not protein bound; circulates until it reaches the liver, where it is conjugated;  in dysfunction or blockage of the liver Dx: first, measure total bilirubin; if that is high, measure direct and indirect Dx: first, measure total bilirubin; if that is high, measure direct and indirect Reference values: Total: mg/dL, or 5-17 micromoles/L Reference values: Total: mg/dL, or 5-17 micromoles/L Conjugated: mg/dL or micromoles/L Conjugated: mg/dL or micromoles/L

38 Bilirubin Circulation

39 Hepatocellular Jaundice  direct (conj) bilirubin Injury or disease of the parenchymal cells of the liver caused by Viral hepatitis Viral hepatitis Cirrhosis Cirrhosis Infectious mononucleosis Infectious mononucleosis Reactions of certain drugs such as chlorpromazine Reactions of certain drugs such as chlorpromazine

40 Obstructive Jaundice  Direct bilirubin Obstruction of the common bile or hepatic ducts due to stones or neoplasms. Obstruction of the common bile or hepatic ducts due to stones or neoplasms. Causes high conjugated bilirubin levels due to bile regurgitation Causes high conjugated bilirubin levels due to bile regurgitation

41 Hemolytic Jaundice  unconjugated bilirubin Overproduction of bilirubin resulting from hemolytic processes After blood transfusions After blood transfusions Pernicious anemia Pernicious anemia Sickle cell anemia Sickle cell anemia Transfusion reactions Transfusion reactions

42 Ceruloplasmin Normal value: mg/dL ( mg/L) Normal value: mg/dL ( mg/L) Copper bound to ceruloplasmin constitutes the largest amount of Cu 2+ in circulation Copper bound to ceruloplasmin constitutes the largest amount of Cu 2+ in circulation In Wilson’s disease Cu 2+ mobilization from the liver is drastically reduced because of low production of ceruloplasmin In Wilson’s disease Cu 2+ mobilization from the liver is drastically reduced because of low production of ceruloplasmin Values <14 mg/dL may be expected Values <14 mg/dL may be expected However, low ceruloplasmin is not the primary defect in Wilson’s disease; some patients with Wilson’s are not low However, low ceruloplasmin is not the primary defect in Wilson’s disease; some patients with Wilson’s are not low

43 Screening for Liver Disease Asymptomatic high risk individuals should be screened for chronic hepatitis Asymptomatic high risk individuals should be screened for chronic hepatitis ALT is the most cost-effective screening test for metabolic or drug-induced liver injury ALT is the most cost-effective screening test for metabolic or drug-induced liver injury AST should also be measured with hx of alcohol abuse (in alcoholic hepatitis AST is > ALT) AST should also be measured with hx of alcohol abuse (in alcoholic hepatitis AST is > ALT) Individuals at high risk for viral hepatitis should be screened using specific viral serologies (HBsAg, anti-HCV, IgM anti-HAV, anti-HBS, HCV-RNA) in addition to ALT Individuals at high risk for viral hepatitis should be screened using specific viral serologies (HBsAg, anti-HCV, IgM anti-HAV, anti-HBS, HCV-RNA) in addition to ALT

44 Predictors of Prognosis Prothrombin time: the most important predictor of prognosis; prolonged PTT indicative of poor prognosis Prothrombin time: the most important predictor of prognosis; prolonged PTT indicative of poor prognosis Albumin: serum albumin <2.5 g/dL indicates high risk of death Albumin: serum albumin <2.5 g/dL indicates high risk of death

45 Lab Tests in Acute Liver Disease Disease Peak ALT (x URL)* AST/Alt Ratio Peak Bili (mg/dL) PTT Prolongati on (s) Viral hepatitis 10-40<1<15<3 Alcoholic hepatitis 2-8>2<151-3 Toxic injury >40 >1 early <5 >5 transient Ischemic injury >40 >1 early <5 >5 transient Source: NACB Laboratory guidelines for screening, diagnosis, and monitoring of hepatic injury. Dufour, Lou, Nolic, Gretch, Koff, Seeff *upper reference limit

46 Causes of Elevated ALT and/or AST Cause Key Feature Screening test Confirming test Non-alcoholic steato- hepatitis (NASH) Most common cause other than viral, alcoholic Nonebiopsy Hemo- chromatosis Autosomal recessive trait 1:200 among northern European ancestry Transferrin saturation >45% HFE gene analysis for C282Y mutation Source: NACB Laboratory guidelines for screening, diagnosis, and monitoring of hepatic injury. Dufour, Lou, Nolic, Gretch, Koff, Seeff

47 Causes of Elevated ALT and/or AST Cause Key Feature Screening test Confirming test Wilson’s Disease Autosomal recessive trait. 1:30,000 individuals; hemolytic anemia, renal injury Low cerulo- plasmin in 65-95% homozy- gous; 20% heterozy- gotes Genetic analysis, low serum copper, high urine copper Auto- immune hepatitis Up to 18% of non-viral hepatitis; mainly young women ANA and ASMA; false positive anti-HCV common Biopsy

48 Causes of Elevated ALT and/or AST Cause Key Feature Screening test Confirming test Primary biliary cirrhosis Middle aged women; mainly  ALP; often associated with Sjogren’s Syndrome Anti-mito- chondrial antibody Biopsy Schlerosing cholangitis Young to middle aged men; mainly  ALP; often with IBD Anti neutrophil cytoplasmic antibodies; ASMA, ANA may be + Bile duct imaging

49 Interpretation of Nutrition Assessment Tests in Patients with End-Stage Liver Disease Body weight Body weight Anthropometric measurements Anthropometric measurements Creatinine-height index Creatinine-height index Nitrogen balance studies Nitrogen balance studies Visceral protein levels Visceral protein levels Immune function tests Immune function tests

50 SGA Parameters for Nutritional Evaluation of Liver Transplant Candidates History History –Weight change (fluid changes) –Appetite –Taste changes and early satiety –Dietary recall (calories, protein, sodium) –Persistent gastrointestinal problems (nausea, vomiting, diarrhea, constipation, difficulty chewing or swallowing)

51 SGA Parameters for Nutritional Evaluation of Liver Transplant Candidates Physical Physical –Muscle wasting –Fat stores –Ascites or edema Existing conditions Existing conditions –Disease state and other problems that could influence nutritional stores such as hepatic encephalopathy, GI bleeding, renal insufficiency, infection

52 SGA Parameters for Nutritional Evaluation of Liver Transplant Candidates Nutritional rating (based on results of above parameters) Nutritional rating (based on results of above parameters) –Well nourished –Moderately malnourished –Severely malnourished

53 Malnutrition and Ascites in End Stage Liver Disease

54 © 2004, 2002 Elsevier Inc. All rights reserved. Clinical Manifestations of Cirrhosis

55 Esophageal Varices

56 Causes of Malnutrition in Liver Disease Anorexia Anorexia Early satiety or dysgeusia Early satiety or dysgeusia Nausea and vomiting Nausea and vomiting Maldigestion or malabsorption Maldigestion or malabsorption Restricted diets Restricted diets Altered metabolism Altered metabolism

57 Malnutrition in Liver Disease— Pathophysiology Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, Updated by Jeanette M. Hasse and Laura E. Matarese, 2002.

58 Malnutrition in Liver Disease— Medical and Nutritional Management Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, Updated by Jeanette M. Hasse and Laura E. Matarese, 2002.

59 Vitamin/Mineral Deficits* in Severe Hepatic Failure Vitamin A Vitamin A Vitamin D Vitamin D Vitamin E Vitamin E Vitamin K Vitamin K Vitamin B 6 Vitamin B 6 Vitamin B 12 Vitamin B 12 Folate Folate Niacin Niacin Thiamin Thiamin Zinc Zinc Magnesium Magnesium Iron Iron Potassium Potassium Phosphorus Phosphorus * May be related to fat malabsorption, medications, alcoholism (p. 752 Krause)

60 Four Stages of Hepatic Encephalopathy StageSymptom IMild confusion, agitation, irritability, sleep disturbance, decreased attention IMild confusion, agitation, irritability, sleep disturbance, decreased attention IILethargy, disorientation, inappropriate behavior, drowsiness IILethargy, disorientation, inappropriate behavior, drowsiness IIISomnolence but arousable, incomprehensible speech, confusion, aggression when awake IVComa IVComa

61 End-Stage Liver Disease Hepatic Encephalopathy 1. Consider major causes of encephalopathy GI bleeding GI bleeding Fluid and electrolyte abnormalities Fluid and electrolyte abnormalities Uremia Uremia Use of sedatives Use of sedatives Hypo- or hyperglycemia Hypo- or hyperglycemia Alcohol withdrawal Alcohol withdrawal Constipation Constipation Acidosis Acidosis 1. Consider major causes of encephalopathy GI bleeding GI bleeding Fluid and electrolyte abnormalities Fluid and electrolyte abnormalities Uremia Uremia Use of sedatives Use of sedatives Hypo- or hyperglycemia Hypo- or hyperglycemia Alcohol withdrawal Alcohol withdrawal Constipation Constipation Acidosis Acidosis

62 End-Stage Liver Disease Hepatic Encephalopathy—cont’d 2. Treat underlying cause. 3. Treat with medications. Lactulose Lactulose Neomycin Neomycin 4. Ensure adequate diet is consumed. 2. Treat underlying cause. 3. Treat with medications. Lactulose Lactulose Neomycin Neomycin 4. Ensure adequate diet is consumed.

63 MNT in End-Stage Liver Disease Energy needs are highly variable; 30% of pts are hypometabolic and 20% hypermetabolic Energy needs are highly variable; 30% of pts are hypometabolic and 20% hypermetabolic Use indirect calorimetry where available Use indirect calorimetry where available Energy: 25 to 30 kcal/kg dry weight Energy: 25 to 30 kcal/kg dry weight Ascites increases REE by 10% Ascites increases REE by 10% Hasse et al. ASPEN Nutrition Support Practice Manual, 2 nd Edition, 2005, p. 238

64 End-Stage Liver Disease Fat: 25% to 40% of kcal Fat: 25% to 40% of kcal May try MCT if steatorrhea is present; with severe case, try fat restriction and discontinue if diarrhea does not improve Protein: 1 to 1.5 g/kg dry wt depending on degree of malnutrition, malabsorption, metabolic stress Protein: 1 to 1.5 g/kg dry wt depending on degree of malnutrition, malabsorption, metabolic stress Fat: 25% to 40% of kcal Fat: 25% to 40% of kcal May try MCT if steatorrhea is present; with severe case, try fat restriction and discontinue if diarrhea does not improve Protein: 1 to 1.5 g/kg dry wt depending on degree of malnutrition, malabsorption, metabolic stress Protein: 1 to 1.5 g/kg dry wt depending on degree of malnutrition, malabsorption, metabolic stress

65 End-Stage Liver Disease— cont’d May try BCAA formulas for >grade 2 encephalopathy May try BCAA formulas for >grade 2 encephalopathy CHO: high intake of both complex and simple carbohydrates CHO: high intake of both complex and simple carbohydrates Vitamin and mineral supplements Vitamin and mineral supplements Electrolytes: restrict sodium with edema or ascites ( mg/day) Electrolytes: restrict sodium with edema or ascites ( mg/day) Fluid: restrict fluid if hyponatremia is present mL Fluid: restrict fluid if hyponatremia is present mL Hasse. ASPEN Nutrition Support Practice Manual, 2 nd edition, 2500, p. 239

66 Amino Acids Commonly Altered in Liver Disease *=essential) Aromatic amino acids—serum levels increased Aromatic amino acids—serum levels increased—Tyrosine—Phenylalanine* —Free tryptophan* Branched-chain amino acids—serum levels decreased Branched-chain amino acids—serum levels decreased—Valine*—Leucine*—Isoleucine* Other amino acids—serum levels increased Other amino acids—serum levels increased—Methionine*—Glutamine Aromatic amino acids—serum levels increased Aromatic amino acids—serum levels increased—Tyrosine—Phenylalanine* —Free tryptophan* Branched-chain amino acids—serum levels decreased Branched-chain amino acids—serum levels decreased—Valine*—Leucine*—Isoleucine* Other amino acids—serum levels increased Other amino acids—serum levels increased—Methionine*—Glutamine —Asparagine —Histidine* —Asparagine —Histidine*

67 Esophageal Varices

68 MNT for Esophageal Varices Endoscopic tube used to tamponade bleeding vessels Endoscopic tube used to tamponade bleeding vessels Repeated therapy may cause esophageal strictures, dysphagia Repeated therapy may cause esophageal strictures, dysphagia Cannot feed enterally during acute bleeding episodes Cannot feed enterally during acute bleeding episodes May require PN if patient unable to eat May require PN if patient unable to eat

69 MNT for Ascites Ascites is accumulation of fluid in the abdominal cavity Ascites is accumulation of fluid in the abdominal cavity Caused by portal hypertension, hypoalbuminemia, lymphatic obstruction, renal retention of sodium and fluid Caused by portal hypertension, hypoalbuminemia, lymphatic obstruction, renal retention of sodium and fluid Medical treatment: paracentesis, diuretics Medical treatment: paracentesis, diuretics MNT: restrict sodium to 2 grams or less MNT: restrict sodium to 2 grams or less More severe restrictions may be unpalatable More severe restrictions may be unpalatable MNT: supplement protein if frequent paracentesis MNT: supplement protein if frequent paracentesis

70 MNT for Hyponatremia Occurs because of decreased ability to excrete water because of persistent release of antidiuretic hormone, sodium loss via paracentesis, excessive diuretic use, sodium restriction Occurs because of decreased ability to excrete water because of persistent release of antidiuretic hormone, sodium loss via paracentesis, excessive diuretic use, sodium restriction Fluid intake restricted to 1 to 1.5 liter per day (as low as urinary loss) Fluid intake restricted to 1 to 1.5 liter per day (as low as urinary loss) Moderate sodium intake Moderate sodium intake

71 Hepatic Encephalopathy Can be caused by GI bleeding, fluid/electrolyte abnormalities, uremia, infection, blood glucose derangements, alcohol withdrawal Can be caused by GI bleeding, fluid/electrolyte abnormalities, uremia, infection, blood glucose derangements, alcohol withdrawal Occurs in 50-70% of pts with chronic hepatic failure Occurs in 50-70% of pts with chronic hepatic failure Caused by protein in only 5% Caused by protein in only 5% 95% of persons with cirrhosis tolerate mixed protein diets of up to 1.5 g/kg 95% of persons with cirrhosis tolerate mixed protein diets of up to 1.5 g/kg Hasse ASPEN Nutrition Support Practice Manual, 2 nd edition, p. 236

72 Hepatic Encephalopathy: Medical Treatment Neomycin or lactulose Lactulose: nonabsorbable disaccharide. Acidifies colonic contents, acts as laxative to excrete ammonia Lactulose: nonabsorbable disaccharide. Acidifies colonic contents, acts as laxative to excrete ammonia Neomycin is nonabsorbable antibiotic that decreases colonic ammonia production Neomycin is nonabsorbable antibiotic that decreases colonic ammonia production

73 Hepatic Encephalopathy: Medical Treatment Identify and treat acute causes, e.g. Variceal bleed Variceal bleed Infection Infection Electrolyte imbalance Electrolyte imbalance Sedatives Sedatives Constipation Constipation Hasse JM et al. ASPEN Nutrition Support Practice Manual, 2 nd Edition, 2005

74 Hepatic Encephalopathy: MNT Role of protein in encephalopathy controversial Role of protein in encephalopathy controversial Encephalopathy may be caused by imbalance of aromatic and branched chain amino acids Encephalopathy may be caused by imbalance of aromatic and branched chain amino acids Protein restriction not proven to improve mental state Protein restriction not proven to improve mental state Supplements enriched in BCAA, low in AAA may help Supplements enriched in BCAA, low in AAA may help

75 Hepatic Encephalopathy: MNT If patient is protein sensitive, start with.5 to.7 g protein/kg and increase level to tolerance, up to 1.5 g/kg in protein-calorie malnutrition If patient is protein sensitive, start with.5 to.7 g protein/kg and increase level to tolerance, up to 1.5 g/kg in protein-calorie malnutrition Provide adequate calories to prevent catabolism of endogenous protein stores Provide adequate calories to prevent catabolism of endogenous protein stores

76 Glucose Derangements Glucose intolerance in nearly 2/3 of patients with cirrhosis (10-37% develop diabetes) Glucose intolerance in nearly 2/3 of patients with cirrhosis (10-37% develop diabetes) Occurs because of insulin resistance in peripheral tissues Occurs because of insulin resistance in peripheral tissues Hyperinsulinemia, possibly because insulin production increased, hepatic clearance decreased Hyperinsulinemia, possibly because insulin production increased, hepatic clearance decreased Fasting hypoglycemia d/t decreased glycogen stores; pts may need small, frequent meals Fasting hypoglycemia d/t decreased glycogen stores; pts may need small, frequent meals

77 Steatorrhea Replace LCT with MCT oils (in some nutrition supplements or as oil) Replace LCT with MCT oils (in some nutrition supplements or as oil) May trial low fat diet, but do not restrict unnecessarily; if steatorrhea doesn’t improve, discontinue restriction May trial low fat diet, but do not restrict unnecessarily; if steatorrhea doesn’t improve, discontinue restriction

78 Nutrition Care Guidelines for Liver Transplantation Pretransplantation Pretransplantation Immediate posttransplantation Immediate posttransplantation Long-term posttransplantation Long-term posttransplantation Calories Calories Protein Protein Fat Fat Carbohydrate Carbohydrate Sodium Sodium Fluid Fluid Calcium Calcium Vitamins Vitamins

79 Medications* Commonly Used after Liver Tx Azathioprine Azathioprine Antithymocyte globulin Antithymocyte globulin Basiliximab Basiliximab Cyclosporine Cyclosporine Daclizumab Daclizumab Glucocorticoids Glucocorticoids Muromonab-CD3 Muromonab-CD3 Mycophenolate mofetil Mycophenolate mofetil Sirolimus Sirolimus Tacrolimus Tacrolimus 15- deoxysperagualin 15- deoxysperagualin *Most have drug-nutrition interactions. See p. 756 Krause

80 Liver Transplantation— Diet Nutrition support: pre- and post- transplant Nutrition support: pre- and post- transplant Long-term preventive nutrition to optimize health and to avoid or minimize Long-term preventive nutrition to optimize health and to avoid or minimize —Excessive weight gain —Hyperlipidemia —Hyperglycemia —Hypertension —Osteopenia Nutrition support: pre- and post- transplant Nutrition support: pre- and post- transplant Long-term preventive nutrition to optimize health and to avoid or minimize Long-term preventive nutrition to optimize health and to avoid or minimize —Excessive weight gain —Hyperlipidemia —Hyperglycemia —Hypertension —Osteopenia

81 CAM in Liver Disease Milk Thistle (silymarin) – purported anti-hepatotoxic and anti-inflammatory activity Milk Thistle (silymarin) – purported anti-hepatotoxic and anti-inflammatory activity Scientific evidence is mixed Scientific evidence is mixed

82 CAM in Liver Dx: Potentially Hepatotoxic Products Borage Borage Chaparral Chaparral Coltsfoot Coltsfoot Comfrey Comfrey DHEA DHEA Germander Germander Jin bu huan Jin bu huan Kava kava Kava kava Liferoot Liferoot Pennyroyal Pennyroyal Periwinkle Periwinkle Poke root Poke root Skullcap (American) Skullcap (American) Shark cartilage Shark cartilage Hasse JM. ASPEN Nutrition Support Practice Manual, 2 nd Edition, 2005.

83 Summary Liver disorders—role of liver is so crucial to overall health, its destruction is quite serious Liver disorders—role of liver is so crucial to overall health, its destruction is quite serious Goals—support maintenance of as much normal liver function as possible Goals—support maintenance of as much normal liver function as possible Transplantation, if needed Transplantation, if needed

84 Relationship of Organs of the Upper Abdomen 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.

85 Functions of the Gallbladder Primary function is to concentrate, store, excrete bile (produced by the liver) Primary function is to concentrate, store, excrete bile (produced by the liver) Bile: primary constituents are cholesterol, bilirubin (from hemoglobin) and bile salts Bile: primary constituents are cholesterol, bilirubin (from hemoglobin) and bile salts Bile salts are essential for digestion and absorption of fats, fat soluble vitamins, some minerals Bile salts are essential for digestion and absorption of fats, fat soluble vitamins, some minerals Gallbladder and pancreas use common duct to release digestive juices into duodenum Gallbladder and pancreas use common duct to release digestive juices into duodenum Diseases of liver, pancreas, and gallbladder interrelated Diseases of liver, pancreas, and gallbladder interrelated

86 Diseases of the Gallbladder: Cholelithiasis Calculi form in the gallbladder Calculi form in the gallbladder Choledocholithiasis: stones slip into bile ducts, obstruction, pain, cramps Choledocholithiasis: stones slip into bile ducts, obstruction, pain, cramps Blockage can cause cholecystitis, impaired lipid absorption, light colored stools; secondary biliary cirrhosis; obstruction of the distal common bile duct can lead to pancreatitis if pancreatic duct is blocked Blockage can cause cholecystitis, impaired lipid absorption, light colored stools; secondary biliary cirrhosis; obstruction of the distal common bile duct can lead to pancreatitis if pancreatic duct is blocked

87 Choledocholithiasis

88 Choledocholithiasis Affects millions of Americans each year; many asymptomatic Affects millions of Americans each year; many asymptomatic Risk factors are female gender, pregnancy, older age, family history, obesity, truncal body fat distribution, diabetes, certain drugs (lipid lowering meds, oral contraceptives, estrogens) Risk factors are female gender, pregnancy, older age, family history, obesity, truncal body fat distribution, diabetes, certain drugs (lipid lowering meds, oral contraceptives, estrogens) Rapid weight loss (gastric bypass, fasting, VLC diets) associated with biliary sludge and gallstones Rapid weight loss (gastric bypass, fasting, VLC diets) associated with biliary sludge and gallstones

89 Choledocholithiasis Medical Mgt Surgical removal of the gallbladder via open lap or laparoscopic procedure Surgical removal of the gallbladder via open lap or laparoscopic procedure Chemical dissolution or shock wave lithotripsy may be tried Chemical dissolution or shock wave lithotripsy may be tried Stones in bile ducts may be removed via endoscopic retrograde cholangiopancreatography techniques (ERCP) Stones in bile ducts may be removed via endoscopic retrograde cholangiopancreatography techniques (ERCP)

90 Cholelithiasis MNT Correct risk factors if possible (obesity and VLC diets) Correct risk factors if possible (obesity and VLC diets) Cholecystitis: low fat diet to prevent gallbladder contractions Cholecystitis: low fat diet to prevent gallbladder contractions After cholecystectomy, diet can be advanced to regular diet as tolerated After cholecystectomy, diet can be advanced to regular diet as tolerated Liver secretes bile directly into small intestine; intestine adapts Liver secretes bile directly into small intestine; intestine adapts

91 Cholecystitis MNT Acute: NPO initially. Use PN if prolonged. Then initiate low fat diet (hydrolyzed lowfat enteral feeding or oral diet with g fat/day) Acute: NPO initially. Use PN if prolonged. Then initiate low fat diet (hydrolyzed lowfat enteral feeding or oral diet with g fat/day) Chronic: long term low fat diet (25- 30% of calories Chronic: long term low fat diet (25- 30% of calories May need water-soluble forms of fat- soluble vitamins if malabsorption is suspected May need water-soluble forms of fat- soluble vitamins if malabsorption is suspected

92 Functions of the Pancreas Endocrine Functions: secretes glucagon, insulin, somatostatin into bloodstream for regulation of glucose Endocrine Functions: secretes glucagon, insulin, somatostatin into bloodstream for regulation of glucose Exocrine Functions: secretes enzymes directly into GI tract to digest protein, fat, carbohydrate Exocrine Functions: secretes enzymes directly into GI tract to digest protein, fat, carbohydrate

93 Factors that Govern Pancreatic Secretions Cephalic phase: mediated through the vagus nerve, initiated by the sight, smell, taste and anticipation of food: bicarbonate and pancreatic enzymes Cephalic phase: mediated through the vagus nerve, initiated by the sight, smell, taste and anticipation of food: bicarbonate and pancreatic enzymes Gastric phase: caused by gastric distention with food; enzyme secretion Gastric phase: caused by gastric distention with food; enzyme secretion Intestinal phase: most potent effect, mediated by the release of cholecystokinin Intestinal phase: most potent effect, mediated by the release of cholecystokinin

94 Pancreatitis Inflammation of the pancreas, mild or severe Inflammation of the pancreas, mild or severe Significant morbidity/mortality Significant morbidity/mortality Symptoms: continuous or intermittent pain of varying intensity to severe upper abdominal pain, radiating to back Symptoms: continuous or intermittent pain of varying intensity to severe upper abdominal pain, radiating to back Symptoms may worsen with ingestion of food Symptoms may worsen with ingestion of food Nausea, vomiting, abdominal distention, steatorrhea Nausea, vomiting, abdominal distention, steatorrhea Elevated serum amylase or lipase; however amylase is nonspecific for pancreatitits Elevated serum amylase or lipase; however amylase is nonspecific for pancreatitits

95 Pancreatitis: Causes Chronic alcoholism (most common cause of acute and chronic pancreatitis) Chronic alcoholism (most common cause of acute and chronic pancreatitis) Gallstones (a common cause of acute pancreatitis) Gallstones (a common cause of acute pancreatitis) Trauma, certain drugs Trauma, certain drugs Hypertriglyceridemia Hypertriglyceridemia Hypercalcemia Hypercalcemia Some viral infections Some viral infections

96 Pancreatitis: Diagnosis Tests of pancreatic function Tests of pancreatic function –Secretin stimulation test: measures pancreatic secretion of bicarbonate in response to secretin –Glucose tolerance test: measures endocrine function –72-hour stool fat test: measures fat absorption that reflects pancreatic lipase secretion

97 Ranson’s Criteria At admission or diagnosis Age >55 years Age >55 years White blood count >16,000 m3 White blood count >16,000 m3 Blood glucose level >200 mg/dl Blood glucose level >200 mg/dl Lactic dehydrogenase >350 IU/L Lactic dehydrogenase >350 IU/L Aspartate transaminase >240 U/L Aspartate transaminase >240 U/L

98 Ranson’s Criteria During first 48 hours Hematocrit decrease of >10 mg/dL Hematocrit decrease of >10 mg/dL Blood urea nitrogen increase of >5 mg/dl Blood urea nitrogen increase of >5 mg/dl Arterial PO2 <60 mmHg Arterial PO2 <60 mmHg Base deficit >4 mEq/L Base deficit >4 mEq/L Fluid sequestration >6000 ml Fluid sequestration >6000 ml Serum calcium level <8 mg/dL Serum calcium level <8 mg/dL

99 Pancreatitis

100 Acute Hemorrhagic Pancreatitis

101 Acute Pancreatitis 75% alcohol related 75% alcohol related 15% related to gallstones 15% related to gallstones 10% trauma, hyperlipidemia, hypercalcemia, medications, etc. 10% trauma, hyperlipidemia, hypercalcemia, medications, etc. Mascarenhas et al. ASPEN Nutrition Support Practice Manual, 2 nd edition, 2005, p. 211

102 Energy Needs in Acute Pancreatitis Metabolic stress state: Resting energy expenditure as high as 139% of Harris-Benedict Metabolic stress state: Resting energy expenditure as high as 139% of Harris-Benedict Sepsis may increase energy needs an additional 15% Sepsis may increase energy needs an additional 15% Acute patients more hypermetabolic than chronic patients Acute patients more hypermetabolic than chronic patients Mascarenhas et al. ASPEN Nutrition Support Practice Manual, 2nd edition, 2005, p. 211

103 Nutritional Alterations in Acute Pancreatitis Glucose intolerance in 40 to 90% of patients, caused by stress response, impaired Beta-cell function, and insulin resistance Glucose intolerance in 40 to 90% of patients, caused by stress response, impaired Beta-cell function, and insulin resistance Changes in fat metabolism in 12-15% of patients, primarily steatorrhea and hypertriglyceridemia Changes in fat metabolism in 12-15% of patients, primarily steatorrhea and hypertriglyceridemia

104 Nutritional Alterations in Acute Pancreatitis Hypocalcemia in 25% of patients due to ↓ parathyroid hormone secretion, increased calcitonin, hypomagnesemia, hypoalbuminemia, saponification of calcium Hypocalcemia in 25% of patients due to ↓ parathyroid hormone secretion, increased calcitonin, hypomagnesemia, hypoalbuminemia, saponification of calcium Ethanol abuse → hypomagnesemia, decreased zinc, thiamine and folate deficiencies Ethanol abuse → hypomagnesemia, decreased zinc, thiamine and folate deficiencies Mascarenhas et al ASPEN Nutrition Support Practice Manual, 2005, p. 211

105 Pancreatic Disorders: Medical Mgt Acute Withhold oral feeding Withhold oral feeding Give IV fluids Give IV fluids Administer H2-receptor antagonists, somatostatin Administer H2-receptor antagonists, somatostatinChronic Manage intestinal pH with antacids, H2 receptor antagonists, proton pump inhibitors Manage intestinal pH with antacids, H2 receptor antagonists, proton pump inhibitors Administer insulin for glucose intolerance Administer insulin for glucose intolerance

106 Pancreatitis: MNT Acute Withhold oral feeding Withhold oral feeding Support with IV fluids Support with IV fluids If oral nutrition cannot be initiated in 5- 7 days, start nutrition support If oral nutrition cannot be initiated in 5- 7 days, start nutrition support

107 Pancreatitis: Enteral Nutrition Enteral nutrition can be used while resting the pancreas Enteral nutrition can be used while resting the pancreas Early enteral feeding may exacerbate symptoms (21% of patients in one case series) Early enteral feeding may exacerbate symptoms (21% of patients in one case series) Feeding below the ligament of Treitz invokes fewer stimulatory factors Feeding below the ligament of Treitz invokes fewer stimulatory factors Use of elemental low fat formulas is less stimulating than polymeric, higher fat formulas Use of elemental low fat formulas is less stimulating than polymeric, higher fat formulas Mascarenhas et al ASPEN Nutrition Support Practice Manual, 2005, p. 211

108 Pancreatitis: Enteral Recommendations Place nasoenteric tube below the ligament of Treitz Place nasoenteric tube below the ligament of Treitz Begin infusion with a standard enteral formula Begin infusion with a standard enteral formula If there is concern about a particular patient, a low-fat elemental or peptide formula should be used If there is concern about a particular patient, a low-fat elemental or peptide formula should be used Monitor patient for intolerance (N/V, abdominal pain, fever, ↑ amylase/lipase Monitor patient for intolerance (N/V, abdominal pain, fever, ↑ amylase/lipase PN may be initiated if patient does not tolerate EN PN may be initiated if patient does not tolerate EN

109 Pancreatitis: Enteral Nutrition Stimulation of the GI tract at lower levels may be beneficial Stimulation of the GI tract at lower levels may be beneficial EN maintains gut integrity and stimulates blood flow to the gut EN maintains gut integrity and stimulates blood flow to the gut May preserve immune function and reduce inflammatory response May preserve immune function and reduce inflammatory response Mascarenhas et al ASPEN Nutrition Support Practice Manual, 2005, p. 211

110 Pancreatitis: PN Acute (cont) If enteral feedings are not tolerated, PN should be initiated If enteral feedings are not tolerated, PN should be initiated –If TGs are <400 mg/dl use 3-in-1 solution and monitor TG levels –If TGs are elevated (>400 mg/dl) use a dextrose-based solution, monitor serum glucose frequently, and treat as needed with insulin Mascarenhas et al ASPEN Nutrition Support Practice Manual, 2005, p. 211

111 Pancreatitis MNT Acute Energy needs: AP patients are hypermetabolic and catabolic Energy needs: AP patients are hypermetabolic and catabolic HB BEE X activity factor X stress factor of 30-50% HB BEE X activity factor X stress factor of 30-50% Protein needs: g/kg body weight Protein needs: g/kg body weight Fat up to 2 g/kg/BW/day; monitor TG Fat up to 2 g/kg/BW/day; monitor TG Wall-Alonso, Sullivan, Byrne. In Gottslich and Matarese. Contemporary Nutrition Support Practice, p Philadelphia: Saunders, 2003.

112 Pancreatitis: MNT Acute (cont) Once oral diet is started, provide Once oral diet is started, provide –Easily digested foods –Low fat diet –6 small meals –Adequate protein intake –Increased calories

113 Pancreatitis: MNT Chronic Provide oral diet as in acute phase Provide oral diet as in acute phase TF can be used when oral diet is inadequate TF can be used when oral diet is inadequate Supplement pancreatic enzymes Supplement pancreatic enzymes Supplement fat-soluble vitamins and vitamin B12 Supplement fat-soluble vitamins and vitamin B12

114 MNT for Chronic Pancreatitis: Pancreatic Enzymes When pancreatic function diminished by about 90%, malabsorption of protein and fat becomes a problem When pancreatic function diminished by about 90%, malabsorption of protein and fat becomes a problem Avoid large high fat meals and alcohol Avoid large high fat meals and alcohol Pancreatic enzyme replacements given orally with meals (at least 30,000 IU lipase with each meal) Pancreatic enzyme replacements given orally with meals (at least 30,000 IU lipase with each meal) Level of fat in the diet should be the most pt can tolerate without steatorrhea or pain Level of fat in the diet should be the most pt can tolerate without steatorrhea or pain May substitute some fat with MCT May substitute some fat with MCT

115 Whipple Procedure Pancreaticoduodenectomy: often done for pancreatic carcinoma Pancreaticoduodenectomy: often done for pancreatic carcinoma Cholecystectomy, vagotomy, or partial gastrectomy may also be done Cholecystectomy, vagotomy, or partial gastrectomy may also be done Pancreatic duct renanastamosed to the jejunum Pancreatic duct renanastamosed to the jejunum MNT: similar to chronic pancreatitis MNT: similar to chronic pancreatitis

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

117 MNT in Liver/Biliary Disease Disease of the liver/biliary tract has a profound effect on digestion and absorption Disease of the liver/biliary tract has a profound effect on digestion and absorption Often leads to malnutrition; malnutrition exacerbates effect of disease Often leads to malnutrition; malnutrition exacerbates effect of disease Appropriate nutrition care is key in reducing associated morbidity and mortality and improving quality of life Appropriate nutrition care is key in reducing associated morbidity and mortality and improving quality of life


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