Transcript No Slide Title

Medical Nutrition Therapy
for Liver, Biliary System,
and Exocrine Pancreas
Disorders
© 2004, 2002 Elsevier Inc. All rights reserved.
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)
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
Diseases of the Liver





Acute viral hepatitis
Fulminant hepatitis
Chronic hepatitis
Alcoholic liver disease, alcoholic
hepatitis, and cirrhosis
Non-alcoholic hepatic steatosis (NASH)
Diseases of the Liver



Cholestatic liver diseases
—Primary biliary cirrhosis
—Sclerosing cholangitis
Inherited disorders
Other liver diseases
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
Acute Viral Hepatitis

Four phases of symptoms:
1. Prodromal phase
2. Preicteric phase
3. Icteric phase
4. Convalescent phase
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
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
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
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
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
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.
Stages of Alcoholic Liver
Disease



Hepatic steatosis
Alcoholic hepatitis
Alcoholic (Leannec’s) cirrhosis
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
Toxic Effects of Excess Alcohol Use
© 2004, 2002 Elsevier Inc. All rights reserved.
Alcoholic Liver Disease
Metabolic Changes





Steatorrhea
Wernicke-Korsakoff syndrome
Peripheral neuropathy
Pellagrous psychosis
Folate deficiency
End-Stage Alcoholic Liver Disease
Possible Characteristics






Malnutrition
Portal hypertension with varices
Ascites
Hyponatremia
Hepatic encephalopathy
Glucose alterations
End-Stage Alcoholic Liver Disease
Possible Characteristics



Fat malabsorption
Osteopenia
Thrombocytopenia with anemia
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
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
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
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
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
Inherited Disorders:
Hemochromatosis
Inherited disease of iron
overload
 Store 20-40 g of iron in the liver
compared with .3 to .8 g in
normal persons
 Causes hepatomegaly,
esophageal varices, glucose
intolerance
 Treated by phlebotomy

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, KayserFleischer rings, low serum ceruloplasmin,
psychiatric symptoms
Always presents before age 40
Treated with copper-chelating agents, zinc
supplementation, low copper diet
Inherited Disorders:
α1-antitrypsin deficiency
Causes cholestasis or cirrhosis and
can cause liver and lung cancer
 No treatment but liver transplant

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
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
menPathology.
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

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
Aspartate transaminase (AST)
Alanine aminotransferase (ALT)
Alkaline phosphatase (ALP)
Total bilirubin
Direct bilirubin
PT/PTT
Ceruloplasmin
Total protein
Albumin
Viral serologies
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 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 (alkaline phosphatase)


Usually normal in acute and chronic
liver disease
High levels are usually indicative of
obstruction of biliary drainage
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
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: 0.3-1.0 mg/dL, or 5-17
micromoles/L
Conjugated: 0.0-0.2 mg/dL 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
 Viral hepatitis
 Cirrhosis
 Infectious mononucleosis
 Reactions of certain drugs such as
chlorpromazine
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
Hemolytic Jaundice
 unconjugated bilirubin
Overproduction of bilirubin resulting
from hemolytic processes
 After blood transfusions
 Pernicious anemia
 Sickle cell anemia
 Transfusion reactions
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
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
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
Lab Tests in Acute Liver
Disease
Disease
Peak ALT
(x URL)*
AST/Alt
Ratio
Peak Bili
(mg/dL)
Viral
hepatitis
10-40
<1
<15
PTT
Prolongati
on (s)
<3
Alcoholic
hepatitis
Toxic
injury
2-8
>2
<15
1-3
>40
>1 early
<5
>5
transient
Ischemic
injury
>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
C282Y
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
young women
anti-HCV
common
Confirming
test
Genetic
analysis, low
serum
copper, high
urine copper
Biopsy
Causes of Elevated ALT
and/or AST
Cause
Key Feature
Primary
biliary
cirrhosis
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
neutrophil
cytoplasmic
antibodies;
ASMA, ANA
may be +
Bile duct
imaging
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
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)
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
SGA Parameters for
Nutritional Evaluation of
Liver Transplant Candidates

Nutritional rating (based on results
of above parameters)
– Well nourished
– Moderately malnourished
– Severely malnourished
Malnutrition and Ascites in
End Stage Liver Disease
Clinical Manifestations of
Cirrhosis
© 2004, 2002 Elsevier Inc. All rights reserved.
Esophageal Varices
Causes of Malnutrition in
Liver Disease

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



Anorexia
Early satiety or dysgeusia
Nausea and vomiting
Maldigestion or malabsorption
Restricted diets
Altered metabolism
Malnutrition in Liver
Disease—
Pathophysiology
Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000. Updated by Jeanette M. Hasse and
Laura E. Matarese, 2002.
Malnutrition in Liver Disease—
Medical and Nutritional
Management
Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000. Updated by Jeanette M. Hasse and
Laura E. Matarese, 2002.
Vitamin/Mineral Deficits*
in Severe Hepatic Failure


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

Vitamin
Vitamin
Vitamin
Vitamin
Vitamin
Vitamin
Folate
A
D
E
K
B6
B12







Niacin
Thiamin
Zinc
Magnesium
Iron
Potassium
Phosphorus
* May be related to fat malabsorption, medications, alcoholism
(p. 752 Krause)
Four Stages of Hepatic
Encephalopathy
Stage
I
II
Symptom
Mild confusion, agitation,
irritability, sleep disturbance,
decreased attention
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
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
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
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 (1500-2000 mg/day)
Fluid: restrict fluid if hyponatremia is
present 1000-1500 mL
Hasse. ASPEN Nutrition Support Practice Manual, 2nd edition, 2500, p. 239
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
—Asparagine
—Methionine*
—Histidine*
—Glutamine
Esophageal Varices
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
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
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 500-750 + urinary
loss)
Moderate sodium intake
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
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
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
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
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
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
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
Nutrition Care Guidelines
for Liver Transplantation



Pretransplantation
Immediate
posttransplantation
Long-term
posttransplantation








Calories
Protein
Fat
Carbohydrate
Sodium
Fluid
Calcium
Vitamins
Medications* Commonly
Used after Liver Tx






Azathioprine
Antithymocyte
globulin
Basiliximab
Cyclosporine
Daclizumab
Glucocorticoids





Muromonab-CD3
Mycophenolate
mofetil
Sirolimus
Tacrolimus
15deoxysperagualin
*Most have drug-nutrition interactions. See p. 756 Krause
Liver Transplantation—
Diet


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
Scientific evidence is mixed
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.
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
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





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



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



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
Chemical dissolution or shock wave
lithotripsy may be tried
Stones in bile ducts may be removed
via endoscopic retrograde
cholangiopancreatography
techniques (ERCP)
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
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)
Chronic: long term low fat diet (2530% of calories
May need water-soluble forms of fatsoluble vitamins if malabsorption is
suspected
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
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
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
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
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
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
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
Pancreatitis
http://www.pennhealth.com/health_info/Surgery/pancreatitis_2.html
Acute Hemorrhagic
Pancreatitis
http://www.pathguy.com/~lulo/lulo0028.htm
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
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
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
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
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
Pancreatitis: MNT
Acute
 Withhold oral feeding
 Support with IV fluids
 If oral nutrition cannot be initiated in 57 days, start nutrition support
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
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
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
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
Pancreatitis MNT
Acute
 Energy needs: AP patients are
hypermetabolic and catabolic
 HB BEE X activity factor X stress factor
of 30-50%
 Protein needs: 1.4-2 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. 434-425. Philadelphia: Saunders, 2003.
Pancreatitis: MNT
Acute (cont)
 Once oral diet is started, provide
– Easily digested foods
– Low fat diet
– 6 small meals
– Adequate protein intake
– Increased calories
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
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
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
Whipple Procedure
Source: Johns Hopkins http://www.hopkins-gi.org/pages/latin/templates/
index.cfm?pg=disease3&organ=4&disease =24&lang_id=1&pagetype=12&pagenum=263
MNT in Liver/Biliary
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