1. 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)
Essential for life, though survival is possible with 10-20% function
Plays major role in macronutrient and micronutrient digestion, metabolism, and storage
Metabolizes steroids, detoxifies drugs, alcohol, ammonia

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

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

6. Acute Viral Hepatitis
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, 2nd edition, 2005

7. Acute Viral Hepatitis 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
Chronic hemodialysis
Blood transfusion or transplantation prior to 1992 (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
Asian ancestry (HBV)
Unvaccinated health care workers
Birth to mother with chronic HBV or HCV

10. Possible Risk Factors Body piercing or tattooing
Multiple sexual partners or sexually transmitted diseases
Health care workers (HCV)
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
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

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

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

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

15. Alcoholic Liver Disease
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

16. Toxic Effects of Excess Alcohol Use

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

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

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

20. Non-Alcoholic Steatohepatitis (NASH)
Histologically resembles alcoholic hepatitis
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

21. Non-Alcoholic Steatohepatitis (NASH)
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

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
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
May be an immune disorder
50-75% of patients also have inflammatory bowel disease
60-70% are men

24. Cholestatic Liver Diseases
Sclerosing Cholangitis
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
Treated with immunosuppressants

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

26. Inherited Disorders: Wilson’s Disease
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

27. Inherited Disorders: α1-antitrypsin deficiency
Causes cholestasis or cirrhosis and can cause liver and lung cancer
No treatment but liver transplant

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

29. Normal Liver vs. Damaged Liver

30. 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. Clinical Manifestations of Cirrhosis

32. Interpretation of Lab Data In Liver Disease

33. Liver Test Panel Aspartate transaminase (AST)
Alanine aminotransferase (ALT)
Alkaline phosphatase (ALP)
Total bilirubin
Direct bilirubin
PT/PTT
Ceruloplasmin
Total protein
Albumin
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
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
Transaminases relate more to cause of liver injury than prognosis

35. ALP (alkaline phosphatase)
Usually normal in acute and chronic liver disease
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
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

37. Two Forms of Bilirubin
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: mg/dL, or 5-17 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
Cirrhosis
Infectious mononucleosis
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.
Causes high conjugated bilirubin levels due to bile regurgitation

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

42. Ceruloplasmin Normal value: 25-63 mg/dL (250-630 mg/L)
Copper bound to ceruloplasmin constitutes the largest amount of Cu2+ in circulation
In Wilson’s disease Cu2+ mobilization from the liver is drastically reduced because of low production of ceruloplasmin
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

43. Screening for Liver Disease
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 (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
Albumin: serum albumin <2.5 g/dL indicates high risk of death

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

46. Causes of Elevated ALT and/or AST
Key Feature
Screening test
Confirming test
Non-alcoholic steato-hepatitis (NASH)
Most common cause other than viral, alcoholic
None
biopsy
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
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
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
Anthropometric measurements
Creatinine-height index
Nitrogen balance studies
Visceral protein levels
Immune function tests

50. SGA Parameters for Nutritional Evaluation of Liver Transplant Candidates
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
Muscle wasting
Fat stores
Ascites or edema
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)
Well nourished
Moderately malnourished
Severely malnourished

53. Malnutrition and Ascites in End Stage Liver Disease

54. Clinical Manifestations of Cirrhosis

55. Esophageal Varices

56. Causes of Malnutrition in Liver Disease
Anorexia
Early satiety or dysgeusia
Nausea and vomiting
Maldigestion or malabsorption
Restricted diets
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 D
Vitamin E
Vitamin K
Vitamin B6
Vitamin B12
Folate
Niacin
Thiamin
Zinc
Magnesium
Iron
Potassium
Phosphorus
* May be related to fat malabsorption, medications, alcoholism (p. 752 Krause)

60. 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

61. 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

62. End-Stage Liver Disease Hepatic Encephalopathy—cont’d
2. Treat underlying cause.
3. Treat with medications.
• Lactulose
• 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
Use indirect calorimetry where available
Energy: 25 to 30 kcal/kg dry weight
Ascites increases REE by 10%
Hasse et al. ASPEN Nutrition Support Practice Manual, 2nd Edition, 2005, p. 238

64. End-Stage Liver Disease
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

65. End-Stage Liver Disease—cont’d
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 ( mg/day)
Fluid: restrict fluid if hyponatremia is present mL
Hasse. ASPEN Nutrition Support Practice Manual, 2nd edition, 2500, p. 239

66. Amino Acids Commonly Altered in Liver Disease *=essential)
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
—Methionine*
—Glutamine
Asparagine
Histidine*

67. Esophageal Varices

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

69. MNT for Ascites
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

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
Fluid intake restricted to 1 to 1.5 liter per day (as low as urinary loss)
Moderate sodium intake

71. Hepatic Encephalopathy
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, 2nd edition, p. 236

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

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

74. Hepatic Encephalopathy: MNT
Role of protein in encephalopathy controversial
Encephalopathy may be caused by imbalance of aromatic and branched chain amino acids
Protein restriction not proven to improve mental state
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
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)
Occurs because of insulin resistance in peripheral tissues
Hyperinsulinemia, possibly because insulin production increased, hepatic clearance decreased
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)
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
Immediate posttransplantation
Long-term posttransplantation
Calories
Protein
Fat
Carbohydrate
Sodium
Fluid
Calcium
Vitamins

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

80. Liver Transplantation—Diet
Nutrition support: pre- and post-transplant
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
Scientific evidence is mixed

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

83. Summary
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
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)
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

86. Diseases of the Gallbladder: Cholelithiasis
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

87. Choledocholithiasis

88. Choledocholithiasis
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

89. Choledocholithiasis Medical Mgt
Surgical removal of the gallbladder via open lap or laparoscopic procedure
Chemical dissolution or shock wave lithotripsy may be tried
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)
Cholecystitis: low fat diet to prevent gallbladder contractions
After cholecystectomy, diet can be advanced to regular diet as tolerated
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)
Chronic: long term low fat diet (25-30% of calories
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
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
Gastric phase: caused by gastric distention with food; enzyme secretion
Intestinal phase: most potent effect, mediated by the release of cholecystokinin

94. Pancreatitis 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

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

96. Pancreatitis: Diagnosis
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
White blood count >16,000 m3
Blood glucose level >200 mg/dl
Lactic dehydrogenase >350 IU/L
Aspartate transaminase >240 U/L

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

99. Pancreatitis

100. Acute Hemorrhagic Pancreatitis

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

102. Energy Needs in Acute Pancreatitis
Metabolic stress state: Resting energy expenditure as high as 139% of Harris-Benedict
Sepsis may increase energy needs an additional 15%
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
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
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
Give IV fluids
Administer H2-receptor antagonists, somatostatin
Chronic
Manage intestinal pH with antacids, H2 receptor antagonists, proton pump inhibitors
Administer insulin for glucose intolerance

106. Pancreatitis: MNT Acute Withhold oral feeding Support with IV fluids
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
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

108. Pancreatitis: Enteral Recommendations
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

109. Pancreatitis: Enteral Nutrition
Stimulation of the GI tract at lower levels may be beneficial
EN maintains gut integrity and stimulates blood flow to the gut
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 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
HB BEE X activity factor X stress factor of 30-50%
Protein needs: g/kg body weight
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
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
TF can be used when oral diet is inadequate
Supplement pancreatic enzymes
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
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

115. Whipple Procedure
Pancreaticoduodenectomy: often done for pancreatic carcinoma
Cholecystectomy, vagotomy, or partial gastrectomy may also be done
Pancreatic duct renanastamosed to the jejunum
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=263

117. MNT in Liver/Biliary Disease
Disease of the liver/biliary tract has a profound effect on digestion and absorption
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