Medical Nutrition Therapy for Liver Biliary System and

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.

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

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

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

Acute Viral Hepatitis n 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

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

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

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

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

Fulminant Hepatitis n n n 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) Complications include cerebral edema, coagulopathy, bleeding, cardiovascular complications, renal failure, pancreatitis

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

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

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

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

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

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

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

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

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

Non-Alcoholic Steatohepatitis (NASH) n n Patients with NASH often have abnormal lipid profiles 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 Biopsy is the only diagnostic procedure with adequate specificity

Cholestatic Liver Diseases Primary biliary cirrhosis (PBC) n 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 n 90% of patients are women

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

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

Inherited Disorders: Hemochromatosis n Inherited disease of iron overload n Store 20 -40 g of iron in the liver compared with. 3 to. 8 g in normal persons n Causes hepatomegaly, esophageal varices, glucose intolerance n Treated by phlebotomy

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

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

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

Normal Liver vs. Damaged Liver

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 (From Kanel by weight G, Korula among J. Atlas 750, 000 of Liver men. Pathology. and women. W. B. J Clin Saunders, Epidemiol 1992. ) 32: 563, 1979. ) © 2004, 2002 Elsevier Inc. All rights reserved.

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

Interpretation of Lab Data In Liver Disease

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

AST and ALT n n 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 nonspecific symptoms of acute illness 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

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

Bilirubin n n 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 In viral hepatitis, total bilirubin >257 micromoles/L indicates severe liver injury In alcoholic hepatitis, bilirubin >428 micromoles/L predicts high likelihood of death

Two Forms of. Bilirubin n n 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 Dx: first, measure total bilirubin; if that is high, measure direct and indirect Reference values: Total: 0. 3 -1. 0 mg/d. L, or 5 -17 micromoles/L Conjugated: 0. 0 -0. 2 mg/d. L or 0. 0 -3. 4 micromoles/L

Bilirubin. Circulation

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

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

Hemolytic Jaundice unconjugatedbilirubin Overproduction of bilirubin resulting from hemolytic processes n After blood transfusions n Pernicious anemia n Sickle cell anemia n Transfusion reactions

Ceruloplasmin n n Normal value: 25 -63 mg/d. L (250 -630 mg/L) 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 Values <14 mg/d. L may be expected However, low ceruloplasmin is not the primary defect in Wilson’s disease; some patients with Wilson’s are not low

Screening for Liver Disease n n 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 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 (HBs. Ag, anti-HCV, Ig. M anti-HAV, anti-HBS, HCV-RNA) in addition to ALT

Predictors of Prognosis Prothrombin time: the most important predictor of prognosis; prolonged PTT indicative of poor prognosis n Albumin: serum albumin <2. 5 g/d. L indicates high risk of death n

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

Causes of Elevated ALT and/or AST Cause Key Feature Screening test Confirming test Non-alcoholic steatohepatitis (NASH) Most common cause other than viral, alcoholic None biopsy Hemochromatosis Autosomal recessive trait 1: 200 among northern European ancestry Transferrin saturation >45% HFE gene analysis for C 282 Y mutation Source: NACB Laboratory guidelines for screening, diagnosis, and monitoring of hepatic injury. Dufour, Lou, Nolic, Gretch, Koff, Seeff

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

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

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

SGA Parameters for Nutritional Evaluation of Liver Transplant Candidates n 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)

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

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

Malnutrition and Ascitesin End Stage Liver Disease

Esophageal. Varices

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

Malnutrition in Liver Disease—Pathophysiology Algorithm content developed by John Anderson, Ph. D, and Sanford C. Garner, Ph. D, 2000. Updated by Jeanette M. Hasse and Laura E. Matarese, 2002.

Malnutrition in Liver Disease—Medical and Nutritional Management Algorithm content developed by John Anderson, Ph. D, and Sanford C. Garner, Ph. D, 2000. Updated by Jeanette M. Hasse and Laura E. Matarese, 2002.

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

Four Stages of Hepatic Encephalopathy Stage Symptom I Mild confusion, agitation, irritability, sleep disturbance, decreased attention II Lethargy, disorientation, inappropriate behavior, drowsiness III Somnolence but arousable, incomprehensible speech, confusion, aggression when awake IV Coma

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

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

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

End-Stage Liver Disease n n 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

End-Stage Liver Disease— cont’d n n n May try BCAA formulas for >grade 2 encephalopathy CHO: high intake of both complex and simple carbohydrates Vitamin and mineral supplements Electrolytes: restrict sodium with edema or ascites (1500 -2000 mg/day) Fluid: restrict fluid if hyponatremia is present 1000 -1500 m. L Hasse. ASPEN Nutrition Support Practice Manual, 2 nd edition, 2500, p. 239

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

Esophageal. Varices

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

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

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 n Fluid intake restricted to 1. 5 liter per day (as low as 500 -750 + urinary loss) n Moderate sodium intake n

Hepatic Encephalopathy n n 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 Caused by protein in only 5% 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

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

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

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

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 proteincalorie malnutrition n Provide adequate calories to prevent catabolism of endogenous protein stores n

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

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

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

Medications* Commonly Used after Liver. Tx n n n Azathioprine Antithymocyte globulin Basiliximab Cyclosporine Daclizumab Glucocorticoids n n n Muromonab-CD 3 Mycophenolate mofetil Sirolimus Tacrolimus 15 deoxysperagualin *Most have drug-nutrition interactions. See p. 756 Krause

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

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

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

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

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.

Functions of the Gallbladder n n n Primary function is to concentrate, store, excrete bile (produced by the liver) 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 Gallbladder and pancreas use common duct to release digestive juices into duodenum Diseases of liver, pancreas, and gallbladder interrelated

Diseases of the Gallbladder: Cholelithiasis n n n Calculi form in the gallbladder 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

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

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

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

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

Cholecystitis. MNT Acute: NPO initially. Use PN if prolonged. Then initiate low fat diet (hydrolyzed lowfat enteral feeding or oral diet with 30 -45 g fat/day) n Chronic: long term low fat diet (2530% of calories n May need water-soluble forms of fatsoluble vitamins if malabsorption is suspected n

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

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 n Gastric phase: caused by gastric distention with food; enzyme secretion n Intestinal phase: most potent effect, mediated by the release of cholecystokinin n

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

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

Pancreatitis : Diagnosis n 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

Ranson’s. Criteria At admission or diagnosis n Age >55 years n White blood count >16, 000 m 3 n Blood glucose level >200 mg/dl n Lactic dehydrogenase >350 IU/L n Aspartate transaminase >240 U/L

Ranson’s. Criteria During first 48 hours n Hematocrit decrease of >10 mg/d. L n Blood urea nitrogen increase of >5 mg/dl n Arterial PO 2 <60 mm. Hg n Base deficit >4 m. Eq/L n Fluid sequestration >6000 ml n Serum calcium level <8 mg/d. L

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

Acute Hemorrhagic Pancreatitis http: //www. pathguy. com/~lulo/lulo 0028. htm

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

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

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

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

Pancreatic Disorders: Medical Mgt Acute n Withhold oral feeding n Give IV fluids n Administer H 2 -receptor antagonists, somatostatin Chronic n Manage intestinal p. H with antacids, H 2 receptor antagonists, proton pump inhibitors n Administer insulin for glucose intolerance

Pancreatitis : MNT Acute n Withhold oral feeding n Support with IV fluids n If oral nutrition cannot be initiated in 57 days, start nutrition support

Pancreatitis : Enteral Nutrition n n Enteral nutrition can be used while resting the pancreas Early enteral feeding may exacerbate symptoms (21% of patients in one case series) Feeding below the ligament of Treitz invokes fewer stimulatory factors 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

Pancreatitis : Enteral Recommendations n n n Place nasoenteric tube below the ligament of Treitz 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 Monitor patient for intolerance (N/V, abdominal pain, fever, ↑ amylase/lipase PN may be initiated if patient does not tolerate EN

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

Pancreatitis : PN Acute (cont) n 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

Pancreatitis. MNT Acute n Energy needs: AP patients are hypermetabolic and catabolic n HB BEE X activity factor X stress factor of 30 -50% n Protein needs: 1. 4 -2 g/kg body weight n Fat 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.

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

Pancreatitis : MNT Chronic n Provide oral diet as in acute phase n TF can be used when oral diet is inadequate n Supplement pancreatic enzymes n Supplement fat-soluble vitamins and vitamin B 12

MNT for Chronic. Pancreatitis : Pancreatic Enzymes n n n When pancreatic function diminished by about 90%, malabsorption of protein and fat becomes a problem Avoid large high fat meals and alcohol 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 May substitute some fat with MCT

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

Whipple Procedure Source: Johns Hopkins http: //www. hopkins-gi. org/pages/latin/templates/ index. cfm? pg=disease 3&organ=4&disease =24&lang_id=1&pagetype=12&pagenum=263

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