1

Pancreatitis

By:

Casey Allred, Kerri Bell, Chelsey Evans, Jillayne Gee and Bonnie Ross

March 8, 2010

NDFS 356

2

INTRODUCTION

Pancreatitis is a condition that requires special medical and nutritional attention. This

paper discusses the normal physiology of the pancreas as well as etiology, prevalence,

pathophysiology, diagnosis, treatment, and medical nutrition therapy of acute pancreatitis (AP)

and chronic pancreatitis (CP).

OVERVIEW

The pancreas is a gland that is posterior to the stomach near the duodenum. It performs

both endocrine and exocrine functions. The pancreas’s endocrine function centers on the release

of insulin and glucagon into the blood to help maintain normal blood glucose levels as well as

the release of somatostatin which is a peptide hormone. Insulin, glucagon, and somatostatin are

released from nests of cells called islets of Langerhans. Exocrine functions include the secretion

of digestive enzymes from acinar cells, bicarbonate to neutralize gastric acid and regulate the pH

of the small intestine, and electrolytes to maintain normal concentrations in the gut. All of these

secretions play an important role in the digestion of food. Normally, isozymes such as

trypsinogen are synthesized in the acinar cells, packaged into zymogen granules and released

into the small intestine. Here, trypsinogen is activated into trypsin which goes on to initiate other

enzymes into their active forms to break down protein, carbohydrate, and fat. This mechanism is

performed to protect the pancreas from being digested by the enzymes it releases (1-2).

ETIOLOGY

Pancreatitis is a disease which occurs when the pancreas is inflamed. The extent of the

damage can be categorized into two main categories; acute and chronic. AP can be separated into

mild and severe. Mild pancreatitis is defined as having little or no organ dysfunction and having

an uneventful recovery. Severe pancreatitis has obvious organ failure and/or complications. CP is

3

described by having permanent damage, which ultimately damages the exocrine and endocrine

tissue (3).

Inflammation is caused by many different factors. Chronic alcoholism is the leading cause

of both AP and CP. In the United States 35% of AP is initiated by gallstones. Other factors

include biliary tract disease, hypertriglyceridemia (triglyceride concentration above 1000

mg/dL), hypercalcemia, cystic fibrosis, trauma, either blunt or penetrating, various drugs

including diuretics and antibiotics, and viral infections such as hepatitis or mumps (3).

SIGNS AND SYMPTOMS

The most common symptom of AP is severe abdominal pain, usually in the upper

abdomen and radiating through the back. The pain is usually not constant, but has periods of

intensity. The pain can often be relieved by sitting or leaning forward and is intensified by

moving around and eating. Other symptoms include abdominal distention, nausea, vomiting, and

diarrhea. Diabetes can occur because of impaired enzyme production as well as steatorrhea,

which is a result of the malabsorption of fat due to the lack of digestive enzymes. Clammy skin

and mild jaundice are other symptoms that can be found in AP (4).

Similar to AP, upper abdominal pain, back pain, nausea and vomiting are the most

common symptoms for CP. As the disease progresses, malnutrition, weight loss, and diabetes

can be seen. The pain is dull and constant unless food or alcohol is consumed, which increases

the pain and is considered an attack. Attacks get worse as the disease progresses and can last up

to several weeks in advanced cases. Food is usually poorly digested and as a result the patient

has frequent bowel movements and steatorrhea. If the hormone insulin is impaired the patient

develops diabetes and as a result can have increased thirst, appetite, urination, weight loss, and

fatigue (3).

4

INCIDENCE AND PREVALENCE

Looking at England, Denmark and the United States, the incidence of pancreatitis varies

from 4.8 to 24.2 per 100,000 patients. This range may be incorrect due to misdiagnoses, as well

as taking into account that 10% of individuals with severe cases of pancreatitis die before they

are diagnosed. Pancreatitis occurs almost equally in men and women and is most prevalent

between the ages of 50 to 60 years. AP caused by gallstones is increased in Caucasian women as

they age (5).

AGE GROUPS

In adults the two most common causes of pancreatitis are gallstones and alcoholism. As

age increases so does the risk of developing pancreatitis. Traumatic injury to the abdomen is the

number one cause of childhood pancreatitis. Other causes of childhood pancreatitis are

prescription drugs, hyperlipidemia, which can be inherited, and in rare cases can be caused by

mumps or mononucleosis. AP in pregnancy is rare but still possible, occurring in about one out

of every 10,000 pregnancies. The most common cause of pancreatitis is gallstones, which block

the duct and prevent the pancreas from releasing enzymes into the small intestine. Gallstones can

be caused by the weight gain and hormone change that occurs during pregnancy (6).

GENETIC AND LIFE STYLE LINKS

Cystic fibrosis is the most common genetic cause of pancreatitis. Other genetic factors

include hyperlipidemia and alcoholism. It is important to note that hereditary pancreatitis is a

separate form of pancreatitis. Although there are few genetic links to AP and CP, there are

preventable lifestyle factors. As mentioned previously alcohol intake is one of the leading causes

of pancreatitis. Limiting alcohol intake and drinking within the recommended range will

decrease risk for pancreatitis. Even though it is less common, trauma is another cause of

5

pancreatitis. The risk can be decreased if proper protection is used such as sports gear, seat belts,

and avoiding extreme sports (5).

RISK FACTORS

The following are risk factors that increase the possibility of developing gallstones,

which could lead to AP: age, gender, obesity, weight loss, TPN, pregnancy, drugs, genetic

predisposition, and diseases of the terminal ileum. These are risk factors because they cause an

increased secretion of bile and reduced bile acid synthesis. Another major risk factor is

alcoholism. The more one drinks, the bigger the risk for developing pancreatitis. Other risk

factors include having a history of hypertriglyceridemia, hypercalcemia, drugs, and trauma.

Recurring attacks of AP while under the age of 30 usually develop into CP (5).

PATHOPHYSIOLOGY

Acute Pancreatitis

AP occurs when there is injury to the acinar cells or duct obstruction in the pancreas. This

can cause an inappropriate activation of trypsinogen to trypsin in the pancreas instead of in the

small intestine causing autodigestion of the pancreas. This results in inflammation, swelling,

hemorrhage, and damage to the blood vessels of the pancreas (6). The disease is typically mild,

and patients can recover with minimal to no organ damage. In severe cases of AP, systemic

inflammatory response, organ failure and other complications may occur. Exact pathogenesis is

unknown but alcoholism and biliary tract obstructions from gallstones are the most commonly

associated. In excessive alcohol intake, acinar cells in the pancreas metabolize the ethanol and

produce toxins that lead to injury or disruption of the pancreatic cells. Due to this injury,

digestive enzymes are leaked out and activated within the pancreatic tissue. Trypsinogen is a

zymogen that is released and activated prematurely to the proteolase trypsin (7). The early

6

release and activation of pancreatic proteolases and lipases cause injury to the pancreas due to

autodigestion of the organ and surrounding tissues. This can result in hemorrhage, necrosis, and

fibrosis as well as an acute inflammatory response that can progress beyond the pancreas to

cause a systemic inflammatory response and may lead to CP, organ failure, or death (8). Except

in severe cases of AP the pancreatic function can return to normal (1).

Chronic Pancreatitis

CP is a more serious condition than AP and can result in permanent tissue damage and

insufficiency (1). The main cause of CP is alcohol abuse. Alcohol and several other contributing

factors lead to the secretion of trypsinogen in greater amounts than trypsin inhibitor, production

of toxic metabolites, and the release of inflammatory cytokines (6,7). These insults to the

pancreas cause destruction of the acinar cells and islets of Langerhans through the same pathway

as AP. This can lead to fibrosis, strictures, calcification, duct obstruction, and cysts in pancreatic

tissue (7). Additionally, chronic alcohol ingestion leads to the secretion of a pancreatic juice rich

in protein. Protein precipitates form and have been noted to be present at the beginning of the

progression of alcoholic CP. The proposed pathway is that the protein precipitates obstruct small

ductules resulting in damage to the duct and tissues that are upstream to the obstruction as the

pancreatic enzymes build up and cannot be released. The proteins may also calcify forming

stones that lead to further obstruction and damage in the pancreatic ducts. This calcification is

caused by the inhibition of lithostathine, a protein normally secreted into the pancreatic duct that

inhibits calcium carbonate precipitation, during the pathogenesis of CP. Another pathway that

leads to the progression of CP is repeated episodes of AP, particularly with cellular necrosis

causing lesions on the pancreas. Individuals who experience frequent acute attacks of

7

pancreatitis develop fibrosis as necrotic tissue is replaced with scar tissue during the healing

process (8).

COMPLICATIONS

Pseudocysts

Pancreatic pseudocysts are collections of fluid around the pancreas that have leaked out

of a damaged pancreatic duct. They are one of the most common complications of both AP and

CP. Pseudocysts are often asymptomatic, and no treatment is required as they normally resolve

on their own. If abdominal pain, nausea, vomiting, jaundice, or bleeding is present then the

presence of pseudocysts should be confirmed with diagnostic mechanisms such as a CT scan or

MRI. If a pseudocyst is found it is commonly treated with percutaneous drainage, endoscopic

guided ultrasound drainage, or surgery (9). If a pseudocyst is not treated, enzymes and toxins can

enter the bloodstream and affect the heart, lungs, kidneys, or other organs and lead to a systemic

inflammatory response (8).

Bleeding

Bleeding is another complication that may occur with pancreatitis and often originates

from a pseudocyst, directly from the pancreas, or a pseudoaneurysm. Pseudoaneurysms are seen

in CP and are caused by enzymatic or pressure digestion of the muscular wall of an artery by a

pseudocyst. Rupture of the pseudoaneurysm can occur and cause bleeding, which raises

mortality rates to 40-60%. As soon as a pseudocyst is discovered, diagnostic checks for a

pseudoaneurysm should be performed and treated if found. AP has several other accompanying

complications such as abscesses (localized collection of pus surrounded by inflamed tissue),

central nervous system problems, fat necrosis, gastrointestinal bleeding, and splenic

complications. CP complications range from bile duct and duodenal obstruction to fistulas and

8

cancer. Fistulas can be internal or external and are commonly caused by therapy for pancreatitis

and therapy for rupturing of a pseudocyst. They can be treated with NPO, parenteral nutrition,

and endoscopic techniques such as placing a stent, or surgery (8).

Systemic Complications

Often toxic enzymes, infiltration of macrophages and leukocytes with release of

inflammatory mediators such as TNF, IL-6, IL-8, IL-10 into the bloodstream cause injury to the

kidneys, heart, and lungs. Also, the breakdown of the barrier in the small intestine from lack of

use allows bacterial translocation and can ultimately lead to sepsis, multiple organ failure, and

acute respiratory distress syndrome. These systemic complications require intensive care in the

hospital and have high mortality rates (7).

Pancreatic Cancer

Pancreatic cancer is the fourth leading cause of cancer death in men and the fifth leading

cause of cancer death in women in the United States. It is a complication that can occur in CP,

particularly hereditary pancreatitis but also is common in individuals that have never had AP or

CP. Ductal adenocarcinomas are the most common form of pancreatic cancer, and prognosis is

very poor as only one in four people survive for one year after diagnosis. It is often difficult to

differentiate between CP alone and CP that is complicated by cancer as symptoms such as

abdominal pain, weight loss, and jaundice are present in both. If no metastases are present in the

cancer, diagnostic techniques cannot differentiate between CP and pancreatic cancer. Tumor

markers such as CA 19-9 are elevated in 70-80% of cancer patients and can be a useful tool in

distinguishing between the two diseases. In other cases a laparotomy, a large incision in the

abdominal wall, is required to determine if pancreatic cancer is coexisting with CP (8,10).

9

Whipple Procedure

Aggressive resection of the pancreas is the only hope for curing pancreatic cancer. The

most common surgical resection is the Whipple Procedure, also known as a

pancreaticoduodenectomy. The surgery removes the head of the pancreas, where the tumors are

commonly located, and parts of the surrounding organs (duodenum, stomach, common bile duct,

and gallbladder). The extra organs must be removed because the head of the pancreas shares a

common blood supply with these organs (8). The median survival rate after a

pancreaticoduodenectomy is 12 to 15 months, and only five percent of patients survive for more

than five years as metastasis typically occurs before the surgery is performed. Extensive

nutritional support is also required, as this procedure can cause complications such as diabetes

mellitus, dumping syndrome, lactose intolerance, pancreatic exocrine insufficiency, and

malabsorption (10).

ALCOHOL

In the U.S., the recommendations for alcohol intake are one drink a day for women and

two drinks a day for men. A standard drink depends on the type of alcoholic beverage. The

American Dietetic Association describes a standard drink as 12 oz. of beer or wine cooler, 8 oz.

of malt liquor, 5 oz. of table wine, and 1.5 oz. of 80-proof distilled spirits such as gin, vodka,

whiskey, etc. (11).

The development of CP is typically seen in patients consuming 150 g per day of alcohol

for 5 years or more (8). The grams of alcohol in a standard drink vary from beverage to

beverage. Twelve ounces of beer contain 14 g of alcohol, while 12 oz. of light beer contains 11

g. Five ounces of wine contains 15 g and 1.5 oz. of 80-proof distilled spirits contains 14 g of

alcohol (12).

10

Alcohol is responsible for up to 90% of all CP cases (8). When alcohol is metabolized in

the pancreas it goes through two pathways. The first pathway is oxidative and yields reactive

oxygen species (ROS), which damage proteins, DNA, and membranes inside the pancreas. This

pathway also causes a depletion of proteins responsible for removing ROS, causing a toxic

imbalance. The second pathway is non-oxidative and results in fatty acid ethyl esters (FAEE),

which accumulate in the pancreas after alcohol intake (13).

These metabolites can lead to changes in the enzyme production of acinar cells, which

increase the probability that digestive enzymes will be activated while still inside the pancreas.

In stellate cells these metabolites can cause the development of pancreatic fibrosis by stimulating

these cells to secrete unneeded building proteins (8).

Why do some chronic alcohol abusers develop pancreatitis while others do not? Many

hypotheses have been tested to determine other risk factors, which include smoking and a diet

high in fat and protein. Recent studies have looked at the factor of obesity contributing to the

development of CP. One study reported that alcoholic CP was five times more common among

obese patients when compared with a healthy control. However, obesity had no effect on the

progression of the disease (13). Another factor could be bacterial endotoxins released from the

intestines after an alcoholic binge. The binge increases the permeability of the intestines allowing

translocation of bacteria to the pancreas. Typically, bacteria indicate the severity of AP, but its

part in alcohol induced CP is recently attracting attention (13).

Alcohol causes as many as 30% of the AP cases in the U.S. It is commonly thought that

alcoholics who acquire AP have underlying chronic conditions. This is true in most cases, but in

some cases of AP the patient does not continue to develop CP. However, with continued alcohol

abuse these patients can develop CP (8,13).

11

DIAGNOSIS

Physical examination

Physical findings differ according to the severity of acute pancreatitis. For example,

patients with mild pancreatitis may show little or no signs of pain or may not appear ill. On the

other hand, severe pancreatitis patients will have pain, abdominal distention, and appear very ill.

Despite the differences, nearly all patients will be tender in the upper abdominal region, which is

determined by percussion. Physical findings are useful because they can actually point to a

specific cause of AP (8).

Laboratory Diagnosis

Laboratory data are collected to diagnose pancreatitis mainly by serum levels. Common

serum tests used to diagnosis AP are amylase and lipase. More amylase is produced by the

pancreas during pancreatitis. However, distinguishing between amylase made by the pancreas

and amylase produced by the salivary glands or fallopian tubes requires a specific test. This test

measures pancreatic isoamylase or P-isoamylase. As the name implies, only the pancreas

generates this type of amylase. The P-isoamylase test is 90% accurate for diagnosing AP, thus

making it the best laboratory diagnosis (8). Amylase rises within 12 hours and lowers within

three to five days (7). Nonetheless, a total amylase test is taken because it is quick and

inexpensive. Unfortunately, this leaves room for misdiagnosis. For instance, some diseases can

also cause elevated total amylase levels. Some of these diseases include ovarian cysts, carcinoma

of the lungs and ovaries, mumps and renal failure. Normally, the amylase levels for these

diseases are less than amylase levels in AP (8).

Another serum test used to diagnose AP is lipase. Lipase is sometimes considered superior

to amylase because it is only produced by the pancreas. However, sensitivity for lipase serum

12

(85-100%) is similar to amylase. Another similarity to amylase is the influence of non-

pancreatitis conditions on lipase levels. Lipase can increase with renal insufficiency and with

intra-abdominal conditions. Nevertheless, lipase levels remain normal when amylase levels

increase because of non-pancreatitis conditions. Therefore, lipase and amylase serum data

combined may be a sound indication of acute pancreatitis (8).

Different tests are used to diagnose CP. The gold standard for CP is histology. Histology

requires removal of cells from the pancreas, which can irritate the pancreas and may cause severe

acute pancreatitis. Instead of using invasive procedures, medical professionals use diagnostic

procedures to assess the structure and function of the pancreas. The structure of the pancreas is

viewed by CT scans and can be classified as “big-duct” pancreatitis or “small-duct” pancreatitis.

“Big-duct” pancreatitis is marked by extensive abnormalities of the pancreatic duct or gland,

calcified ducts, or atrophy of the pancreas. “Small-duct” pancreatitis has an absence of these

visuals. The function of a CP pancreas is measured by laboratory data. Contrary to AP, CP has

normal amylase and lipase levels. So instead, serum trypsinogen, a precursor to trypsin, is

measured. Trypsinogen levels decrease in chronic pancreatitis. However, low levels (20 ng/mL)

are specific indicators of advanced stages of CP, but normal levels of trypsin can be seen in less

advanced stages of CP. In addition, low trypsin levels are occasionally seen in pancreatic

adenocarcinoma, which can make diagnosing of CP difficult (8).

Additional laboratory data include glucose and triglyceride levels. High triglycerides may

be the cause of up to 4% of all pancreatitis cases. These cases are frequently observed in chronic

alcoholics or patients with uncontrolled diabetes. Triglycerides generally need to be higher than

1000 mg/dL to cause pancreatitis. It is unclear what the pathology is for hightriglyceridemic

13

pancreatitis (14). Blood glucose serum levels are high in patients with AP. This may be

associated with high serum levels of glucagon (8).

Radiologic Diagnosis

Radiography is also used to diagnose pancreatitis. Abdominal ultrasonography is used to

search for gallstones. Computed tomography (CP) is beneficial in distinguishing AP from other

conditions (8).

Forecasting Severity of Pancreatitis

Physical findings, laboratory, radiologic data, and additional physiological data are all

utilized in scoring systems. These scoring systems are used to access the severity of acute

pancreatitis. This is important because the level of severity enables patients to receive suitable

treatments. Popular scoring systems include: the Ranson Criteria, APACHE 2 and 3, and CT

severity index. The purpose of each prognostic tool differs in what it measures as well as its

disadvantages and advantages. This paper will only touch on the Ranson Criteria (8).

The purpose of the Ranson Criteria is to identify the outcome of hospitalization within the first

48 hours of admittance. The criteria are broken into two parts: criteria taken at admission and

criteria taken during the initial 48 hours. The first part involves these signs: age (>55), white

blood cell count (>16,000), blood glucose level (>200), lactic dehydrogenase (350), aspartate

transaminase (>350). The second part involves these signs: hematocrit decrease (>10), blood

urea nitrogen increase (>5), base deficit (>4), fluid sequestration (>6000), and serum calcium

level (<8). Each sign is labeled as negative or positive. Negative means more severe pancreatitis,

and positive means less severe pancreatitis. Every negative sign equals one point. Mean scores

of 1.6 indicate mild pancreatitis, 2.4 indicate severe, and 5.6 indicate lethal pancreatitis (8).

Therefore, the more negative signs a patient has the more severe their outcome.

14

Differentiating Between Gallstones and Alcohol Pancreatitis

Gallstones and alcohol are common causes of pancreatitis. To differentiate between the

two, doctors view laboratory data and ultrasounds, factoring in age and gender. The laboratory

test most often used to diagnose alcohol pancreatitis measures serum alanine aminotransaminase

(ALT). ALT, a hepatocellular enzyme, is mainly found in the liver. When diseases affect the

liver (e.g., cirrhosis), ALT will break down and be released into the bloodstream. Therefore,

serum ALT is elevated in chronic alcoholics (15). In addition to ALT, a serum lipase and

amylase ratio greater than 2:0 is indicative of alcohol pancreatitis. To diagnose gallstone

pancreatitis, ultrasounds are used. Ultrasounds allow gallstones to be viewed. However,

gallstones can pass after the first acute pancreatitis attack causing doctors to miss viewing them

(8). In addition, age and gender are determining factors for gallstones and alcoholic pancreatitis.

Patients with gallstones are frequently females over 40 years of age. Patients with alcoholic

pancreatitis are often males about 40 years of age. Laboratory data, ultrasound, age, and gender

help differentiate between gallstones and alcohol pancreatitis (8).

TREATMENT

Mild Acute Pancreatitis

Treatment of mild AP mainly consists of fasting, fluid infusion, and lessening pain

without the use of opiates. Demerol or Dilaudid can be used to reduce abdominal pain. Mild AP

is self-limiting and is curable within one week (16).

Severe Acute Pancreatitis

Severe AP is more complex to treat because of the necrosis, fever, leukocytosis, and

sepsis that can occur with it. Medical management of severe AP includes monitoring, fasting,

fluid/electrolytic support, antibiotic treatment, and analgesia. Monitoring of the patient’s vitals

15

includes heart rate, blood pressure, urine production, and arterial oxygen saturation. It is not

uncommon for patients to be put into the ICU because of risk of complications. A Swan-Ganz

catheter is recommended to measure heart output and left ventricular filling in order to monitor

fluid levels. It is also imperative to monitor for potential collection of several liters of fluid in the

third retroperitoneal space. This fluid, often caused by a paralytic ileus, has been described as a

“chemical burn.” The accumulation of this fluid causes hypovolemia and subsequent

hypotension, acute renal failure, and pancreatic hypoperfusion. Tracking hypovolemia helps

decrease risks of myocardial infarction, cardiac arrhythmia, and cardiogenic shock (8). To

combat these potential occurrences, fluid infusion is vital and also helps manage the

hypochloremia, hypernatremia, hypomagnesemia, and hypocalcemia caused by the buildup of

fluids. Fluid infusion can also help correct the renal failure. However, if the renal system does

not improve, dialysis may be needed. Acute respiratory distress syndrome (ARDS) can occur, so

arterial oxygen saturation must be monitored and kept above 90%. Normal function returns when

ARDS is corrected (17).

H2 receptor antagonists, proton pump inhibitors, antacids, and anticholinergic drugs are

used to decrease gastric secretions, which in turn decreases the volume of pancreatic secretions.

Gabexate mesilate has been shown to reduce pancreatic secretions and is the most studied

chemical intervention (16). Although giving prophylactic antibiotics has no effect in the

treatment of mild AP, it has been shown to improve severe AP, but research has shown

conflicting results with increased mortality rate and fungal infections, so it is not currently

recommended by the American College of Gastroenterology (8,17). Imipenem, meropenem, and

a combination of a quinolone and metronidazole are recommended antibiotics to combat fever,

leukocytosis, and sepsis. Also, Cefuroxime was shown to decrease mortality rate by 20% and

16

reduce the risk of infectious complications (8). To prevent organ failure and infection, treatment

includes starting enteral feeding to prevent translocation of bacteria, giving antibiotic

prophylaxis to prevent microbial growth in necrotic pancreatic tissue, and if infection occurs,

drainage of the infected area surgically or percutaneously (8,17,18).

Patients with severe AP are at risk for pancreatic necrosis which occurs in 20% of

patients. If organ failure remains for seven to ten days, a CT scan is used to show where to

aspirate the necrosis and then a gram stain is performed to detect infection. Klebsiella, E. coli, or

Staphylococcus aureus are the usual contaminants of necrosis. If infection occurs, debridement

by dissecting the necrotic tissue through the abdomen must be quickly performed. This surgery

significantly increases the patient’s stay in the hospital because debridement must be performed

every two to three days. Percutaneous debridement of necrotic tissue through use of catheters has

also been shown to be successful in many patients and is less invasive. Debridement usually

increases quality of life for the patient. If necrosis is sterile, patients are usually put on antibiotics

for four to six weeks to prevent infection (18).

Because of potential complications with sepsis, the quality of life in severe AP is less

optimistic than mild AP because there is a 10-35% associated mortality rate (18).

Chronic Pancreatitis

Abdominal pain is the most frequent symptom in patients suffering from CP, so CT scans

(accurate in identifying fluid collections in the retroperitoneal cavity), upper gastrointestinal

barium radiography, or endoscopic retrograde cholangiopancreatography (ERCP) are procedures

used to pinpoint the specific source of pain whether it be due to pseudocysts, compression of the

duodenum or bile duct, carcinomas, or possibly gastroparesis. Most patients will need analgesia.

Aspirin or acetaminophen will be given before narcotics or opioids because of the approximate

17

25% addiction rate of patients treated. However, if pain persists, mild opioids such as Tramadol,

which blocks the reuptake of norepinephrine and serotonin, will be given despite possibility of

addiction. Reducing pain is the highest priority (8).

There are conflicting studies as to whether or not abstaining from alcohol decreases

abdominal pain. However, alcohol intake and smoking increases mortality rate and decreases the

function of the pancreas, which is why patients should be urged to stop drinking (8).

Theory exists that pain in CP can be caused by free radicals and unfortunately many CP

patients are deficient in antioxidants from overconsumption of alcohol. More research on

antioxidant therapy is yet to be completed (8).

Another method for treatment of pain consists of decreasing pancreas pressure by

inhibiting pancreatic secretions. Studies show that pancreatic proteases in the duodenum can

repress pancreatic enzyme secretion because it acts as a negative feedback mechanism to stop

CCK and pancreatic enzyme release. Theoretically during fasting, CCK-releasing peptide is

broken down by pancreatic proteases, so little CCK is released. When a meal is being digested,

those proteases digest the proteins from the meal leaving the CCK-releasing peptide to stimulate

CCK release, which then causes pancreatic secretion. Once dietary proteins have been digested,

the proteases will break down the CCK-releasing peptide. Thus pancreatic enzyme secretion is

stimulated during digestion and inhibited afterwards. The presence of more CCK-releasing

peptide in the small bowel is a potential cause of pain especially if there is pancreatic

obstruction. Orally ingesting pancreatic proteases could potentially lessen pain, as it targets the

CCK-releasing peptide, which then inhibits pancreatic secretion. Although studies are small, they

have shown that nonenteric-coated (tablet) enzymes given to patients helped decrease pain

whereas subjects receiving enteric-coated microsphere enzymes did not. Enzyme therapy is

18

recommended for pain reduction but is more likely to benefit “small-duct” CP or idiopathic CP

rather than “big-duct” or advanced alcoholic CP. Octreotide, synthetic somatostatin, has been

shown in studies to decrease pancreatic secretions by reducing CCK release. However, studies

were small and few, and further research is needed (8).

If obstruction of a pancreatic duct is the cause of pain, drainage by endoscopic therapy is

one method of treatment only if the obstruction is caused by “big-duct” CP that has evidence of

strictures, stones, or dilation of the pancreatic duct. Stent therapy is used to evade strictures and

obstructions in order to decrease pressure. This therapy is rather successful in reducing pain, but

complications with stents including clogged stents, attacks of AP, and sepsis can occur.

Removal of stones can be quite complicated, and the stones are not always the source of pain.

Pancreatic duct sphincterotomy is used to replace stents and remove stones (8).

When pain cannot be obliterated by other means or there are complications with other

organs, surgical treatment is required. Pain surgeries include drainage of ducts and resection.

Ductal drainage is thought to relieve pain by decreasing pressure and removing obstructions and

is only performed for “big-duct” CP. Resection focuses more on the head of the pancreas by

either scraping out the anterior portion of the head and leaving the outer portion, or cleanly

taking out the head without disturbing the duodenum (8). One successful method is total

pancreatectomy with autologous islet transplantation (TPAIT). One study showed that patients

who underwent this surgery experienced decreased symptoms and less pain. Many subjects were

also able to become insulin independent or use sliding scale insulin to control postoperative

diabetes. Although symptoms lessened, most of the subjects experienced malnutrition (19).

Blocking neural transmission from nociceptive stimuli is another form of treatment intended to

lessen pain. However, effectiveness still remains to be determined. Other treatments include

19

30,000 units of lipase before and after a meal to help eliminate steatorrhea, and insulin therapy is

most often needed for ensuing Type 1 diabetes mellitus. In deciding which treatment is best, the

diagnosis must be accurate and complications identified. All patient treatments include a low fat

diet, analgesics, and alcohol suppression (8).

Pancreatic transplants as an option for pancreatitis have not been implemented as a viable

curative method. Pancreatitis is more often a side effect of pancreas transplants and other types

of organ transplants including heart, lung, kidney, and liver (20). Diabetes mellitus is the primary

cause for pancreas transplants and only in cases so severe that it cannot be helped by insulin

therapy (5). When medical management of CP pain has failed, surgical means are taken to

alleviate pain in hopes of improving quality of life.

The quality of life for people with CP depends on the patient’s individual circumstance

and if there are complications involved. There is little research done for quality of life in CP.

Continued alcohol intake and pain are two factors that significantly reduce quality of life. One

study found that the mortality rate of CP patients is 3.6 times higher compared to their normal

age group. This higher mortality rate can be attributed to alcoholism. Statistics show a 70% 10-

year survival rate and a 45% 20-year survival rate. Patient death is usually caused by

complications instead of the AP (8).

MEDICAL NUTRITION THERAPY

In planning a nutrition intervention for AP, it is essential to know how long the patient

has gone without adequate oral intake. AP typically causes pain when food is consumed. As a

result patients may have been abstaining from eating an adequate amount of food in order to

prevent pain. The first recommendation for patients with mild to moderate pancreatitis is nothing

by mouth (NPO) which allows the pancreas to rest. During this time the patient receives IV

20

hydration to stabilize fluid and electrolyte imbalances. Patients can gradually adopt an oral diet

as their symptoms subside. When adopting this oral diet, clear liquids are a good starting point,

and patients can slowly progress to a low-fat, solid diet. During this time it is essential to watch

and listen to the patient for complaints of abdominal pain and steatorrhea because these are

indicative of intolerances in the diet (1).

Patients with severe AP may need enteral nutrition support because their pain may be too

severe to tolerate oral feedings, even after five to seven days of NPO (1). According to the

American Dietetic Association Evidence Library, patients in critical condition benefit more from

enteral nutrition compared to parenteral nutrition. Enteral nutrition can help reduce the number

of infections these patients experience while hospitalized (21). Enteral nutrition can also

decrease length of stay, and it is less expensive than parenteral nutrition. Placing a feeding tube

within 48 hours of admission has been shown to reduce the severity of symptoms and improve

tolerance. A feeding tube in the jejunum, as opposed to the stomach or duodenum, causes the

least amount of pancreatic secretions and may be the best option. The type of formula does not

seem to affect tolerance or complications (1).

Parenteral nutrition should only be used on patients with severe pancreatitis who are NPO

for more than five to seven days. It could also be used if enteral nutrition is not sufficient to

provide nutrition needs, if enteral nutrition is not tolerated, or if access for enteral nutrition is

unavailable. Parenteral nutrition is given to meet patient requirements for fluids, electrolytes, and

nutrients. Lipids are only given if patients have triglyceride levels below 400mg/dL. If lipids are

given, it is important that triglyceride levels are strictly monitored (1).

CP patients need to be counseled to consume a low-fat diet. Patients need to find a

balance between fat intake and steatorrhea. If fat intake is too high, steatorrhea, pain, and

21

malabsorption may develop. Alcohol should be completely cut out of the diet. Patients may need

to have supplemental vitamins and minerals if their intake is inadequate to provide their needed

requirements. Pancreatic enzymes may also be needed at every meal to provide adequate

absorption of fat if the patient is experiencing steatorrhea. A combination of a low fat and

nonalcoholic diet will enable the patient to improve quality of life (1).

Conclusion

AP and CP are serious conditions caused by inflammation of the pancreas. With

chemical, surgical, and medical nutrition therapy, AP can be cured, and symptoms of CP can be

managed to improve mortality rates and quality of life.

22

References

1) Nutrition Care Manual. Pancreatitis. Available at:

http://nutritioncaremanual.org/topic.cfm?ncm_heading=Nutrition%20Care&ncm_toc_id=19869.

Accessed February 24, 2011.

2) Uliyargoli A. Lecture Slides. Pancreas: Anatomy & Physiology, Sinai Hospital, October 30,

2007.

3) University of Cincinnati Pancreatic Disease Center. Pancreatitis

http://www.ucpancreas.org/pancreatitis.htm. Accessed February 25, 2011.

4) MedlinePlus. Acute pancreatitis. Available at:

http://www.nlm.nih.gov/medlineplus/ency/article/000287.htm. Accessed February 19, 2011.

5) Mayo Clinic. Pancreas transplant. Available at: http://www.mayoclinic.com/health/pancreas-

transplant/MY00762/METHOD=print. Accessed February 28, 2011.

6) Children’s Hospital Boston. Pancreatitis. Available at:

http://www.childrenshospital.org/az/Site1414/mainpageS1414P0.html. Accessed February 19,

2011.

7) McCance KL, Heuther SE, Brashers VL, Rote NS. Pathophysiology: The Biologic Basis for

Disease for Adults and Children. 6th ed. Maryland Heights, MO: Mosby Elsevier; 2010:1495-

1496.

8) Feldman M, Friedman LS, Sleisenger MH. Gastrointestinal and Liver Disease: Pathophysiology,

Diagnosis, Management. 7th ed. Philadelphia, PA: Saunders; 2002;1:913-966.

9) Andrén-Sandberg Å. Pancreatic pseudocysts and aneurysms. North Am J Med Sci 2010;2:552-

555.

10) Petzel M. Nutrition support of the patient with pancreatic cancer. Supp Line. 2005; 26(3):11-18.

11) American Dietetic Association. What is considered one serving of alcohol? Available at:

http://www.eatright.org/Public/content.aspx?id=6442451420&terms=alcohol. Accessed

February 25, 2011.

12) American Dietetic Association. Food nutrient data for choose your foods: Exchange lists for

diabetes, 2007. Available at: http://www.eatright.org/search.aspx?search=alcohol. Accessed

March 7, 2011.

13) Apte MV, Pirola RC, Wilson JS. Mechanisms of alcoholic pancreatitis. J Gastroenterol Hepatol.

2010;25(12):1816-1826.

23

14) Love BL, Kehr H, Olin JL. Hypertriglyceridemia-induced acute pancreatitis due to patient non-

compliance. J Clin Pharm Ther. 2009;34:363-367.

15) Pagana, K.D., Pagana, T.J.: Mosby’s Manual of Diagnostic and laboratory Tests. 3rd

ed. St.

Louis, Missouri. 2006.

16) Forsmark CE. Treatment of mild acute pancreatitis and prevention of post-endoscopic retrograde

cholangiopancreatograohy pancreatitis. In: Pancreatitis and Its Complications. Totowa, NJ:

Humana Press; 2005:63-79.

17) Forsmark CE. Treatment of severe acute pancreatitis. In: Pancreatitis and Its Complications.

Totowa, NJ: Humana Press; 2005:81-89.

18) Munsell MA, Buscaglia JM. Acute pancreatitis. J Hosp Med. 2010;5:241-250.

19) Voelzke BB, McAninch JW. The current management of renal injuries. Am Surg.

2008;74(8):667-678.

20) Bowden RA, Ljungman P, Snydman DR. Transplant Infections. Philadelphia: Lippincott

Williams & Wilkins; 2010.

21) ADA Evidence Library. What is the effect of enteral nutrition versus parenteral nutrition on

infectious complications in critically ill patients? Available at:

http://www.adaevidencelibrary.com/evidence.cfm?evidence_summary_id=6&highlight=pancreat

itis&home=1. Accessed February 26, 2011.

Pancreatitis

Casey Allred, Kerri Bell, Chelsey Evans, Jillayne Gee, Bonnie Ross

Normal Functioning Pancreas

• A gland posterior to the stomach, near the duodenum • It performs endocrine and exocrine function

• Endocrine: Iselts of Langerhans:

• Alpha cells: release glucagon to

increase blood glucose levels • Beta cells: release insulin to

lower blood glucose levels • Delta Cells: release

somatostatin; inhibits release of •growth hormone •pancreatic hormones •CCK •Secretions

Exocrine:

• Function: release of digestive enzymes, bicarbonate, fluids from the acinar cells

• Digestive enzymes are produced as isozymes in the

acinar cells in the pancreas • lipases, amylases, proteases • function best at pH of 7

• Release into the small intestine activated by CCK,

enzymes are activated in the lumen of the duodenum

Pancreatitis inflammation of the pancreas Categorized as: Acute Pancreatitis • Mild: 80% • Severe: 20% Chronic Pancreatitis

Etiology

More causes of Pancreatitis

Unknown

Post op infection

Endoscopic Retrograde Cholangiopancreatography (ERCP)

Tumor

Signs and Symptoms of AP Often people dismiss pain which

results in a more severe case The most common:

• Epigastric pain

• N/V/D

• Anorexia

• Fever chills

• Hemodynamic instability-SAP

Signs and Symptoms of CP

•Upper abdominal pain-sometimes no pain

•Wt loss

•N/V/D •Oily stools

*Answer to question: Cause of wt loss.

Age groups and Prevalence Children-rare

• Cystic Fibrosis

Pregnancy • Gallstones

High School and College students • Alcohol

• 5-80 new cases

per 100,000

• 2000 die each

year from

complications of

AP

Genetics, Lifestyle and Risk factors

Same as etiology

•Alcohol addictions

•Cystic Fibrosis

•Trauma

•Drugs

•Infections

•Obesity

*Genetic Pancreatitis

Risk factors continued Hypertriglyceridemia • Exercise • Avoid alcohol • Healthy diet

Gallstones • Healthy wt • Avoid rapid wt loss • Exercise regularly • Healthy diet

• Fiber, whole grains • Fat • Avoid foods high saturated and cholesterol

Diagnosis

Diagnostic Tools for Acute Tools:

Physical examination

Laboratory tests

Physical Examination

Mild

Pancreatitis Severe

Pancreatitis Patients with mild

pancreatitis may not

look ill or feel pain

Patients will look very ill

and feel pain, and have

abdominal distention

Upper abdominal pain is

often tender, doctors

use percussion to

determine this

Laboratory Tests for Acute

Amylase

P-isomylase: produced

only by the pancreas

Total amylase: includes

all amylase producing

organs

◦ Amylase will be three

times higher in acute

pancreatitis than other

causes

Laboratory Tests for Acute

Lipase

Lipase is only

produced by the

pancreas

Lipase and amylase

combined=acute

pancreatitis

◦ >3 times higher than

normal

Diagnosing Chronic Pancreatitis

Diagnoses:

Gold standard: histology

(pancreas tissue biopsy)

Laboratory data

CT scan

Laboratory Tests for Chronic

Trypsinogen Lipase and amylase

Trypsinogen levels

decrease in chronic

pancreatitis

◦ Levels <20 ng/mL

specific indication of

CP

Normal in chronic

pancreatitis

CT Scan for Chronic

“Big-duct”

“Small-duct”

CT scans’ view of

pancreas= extensive

abnormalities of the

pancreatic duct or gland,

calcified ducts, or

atrophy of the pancreas

CT scans’ view=absence of

“big-duct” view

Triglyceride and Pancreatitis

Glucose

Triglycerides

Blood glucose levels are

high in pancreatitis

patients

◦ This could be

associated: with high

serum levels of

glucagon, state of

stress, or cells

blocking glucose

entrance

1-4% of pancreatitis is

caused by high levels of

triglycerides

Often seen in alcoholics

or patients with

uncontrolled diabetes

Pathology unclear

Differentiating Between Gallstone

or Alcoholic Pancreatitis

Diagnostic Tools

Age& gender:

◦ Male, 40=alcoholic

pancreatitis

◦ Female, >40=gallstone

pancreatitis

Laboratory data & ultrasound

Gallstone vs. Alcohol Laboratory

Data and Ultrasound

Gallstones-ultrasound

Alcohol-lab data

Alanine

aminotransaminase

(ALT) or asparate

transaminase (AST)

Lipase/amylase ratio

◦ >2:0 ratio indicates

alcoholic pancreatitis

Forecasting Severity of

Pancreatitis

Ranson Criteria

APACHE 2 and 3

CT severity index

Ranson Criteria

Tests the severity of

pancreatitis and attempts to

forecast hospital outcome

Different severities have

different treatments

Divided into two parts:

(1) criteria taken at admission;

(2) Criteria taken during the

first 48 hours.

Pathophysiology

Acute Pancreatitis

• Overall the cause is unknown and there are several different pathways

• Occurs when there is injury to the

acinar cells or duct obstruction in the pancreas

• Trypsingonen is a zymogen that is released and activated prematurely to the proteolase trypsin

• Causes autodigestion of the organ and surrounding

tissues

Results In: • Hemorrhage • Necrosis • Fibrosis • Acute inflammatory response

Severe: • Systemic inflammatory response • Chronic pancreatitis • Organ failure • Death

Chronic Pancreatitis

• Main cause of chronic pancreatitis is alcohol abuse

o Leads to the secretion of trypsinogen in greater amounts than trypsin inhibitor

o Production of toxic metabolites o Release of inflammatory cytokines o Leads to the secretion of a pancreatic juice rich in

protein

Another pathway in the progression of chronic pancreatitis is repeated episodes of acute pancreatitis -Particularly with cellular necrosis causing lesions on the pancreas. -Fibrosis developing as necrotic tissues are replaced with scar tissues during the healing process

Complications

Several complications:

oSIRS oPseudocysts oBleeding oPseudoaneurysms oCancer

SIRS

• Severe AP and CP • Toxic enzymes • Infiltration of macrophages and leukocytes with release

of inflammatory mediators into bloodstream o TNF, IL-6, IL-8, IL-10

• Cause injury to blood vessels and other organs o Lungs, heart, kidneys

• Translocation of bacteria from gut o Local or systemic infection

Pancreatic Pseudocyst

• Most common complication of both AP and CP

• Collections of fluid

around the pancreas that have leaked out of a damaged pancreatic duct

• Mild are asymptomatic, no treatment is required, normally resolve on their own

• Symptoms: o Abdominal pain o Nausea o Vomiting o Jaundice o Bleeding

• Presence of pseudocysts should be confirmed with diagnostic mechanisms o CT scan o MRI

Pancreatic Pseudocyst Cont…

Treatment:

Percutaneous drainage Endoscopic guided ultrasound drainage Surgery

Pancreatic Pseudocyst Cont…

Pancreatic

Pseudocyst

Cont…

Bleeding and Pseudoaneurysms • Bleeding

• AP or CP • Originates from a pseudocyst, directly from the pancreas,

or rupture of a pseudoaneurysm • Bleeding from the rupture of a pseudoaneurysm raises

mortality rates to 40-60%.

• Pseudoaneurysms seen in chronic pancreatitis

• Caused by: o Enzymatic or pressure digestion of the muscular wall of an

artery by a pseudocyst

Other AP Complications

• Abcesses o Localized collection of pus surrounded by inflamed

tissue • Fat necrosis

o Cellular dissolution from lipases, free fatty acids combine with Ca, Mg, Na ions Saponification

• Gastrointestinal bleeding • Splenic complications

o Thrombosis o Pseudoaneurysm

Chronic Complications • Bile duct obstruction, Duodenal Obstruction

o Gallbladder often removed

• Diabetes o Extensive damage to the pancreas o Cannot secrete insulin, TX similar to diabetes mellitus

• Fistulas

o Treated with NPO, parenteral nutrition, placing stents, surgery

• Cancer o Pancreatic adenocarcinoma o Difficult to differentiate

Symptoms of Chronic Pancreatitis and Cancer

• Present in both chronic pancreatitis and cancer: o Abdominal pain o Weight loss o Jaundice

• Unless metastases is present in the cancer,

diagnostic techniques cannot differentiate

Pancreatic Cancer

Caused by ◦ CP

◦ Cigarette smoking

◦ Age

◦ Race

◦ Gender

◦ Genetics

◦ Diet

◦ Obesity

4th leading cause of cancer death in men, 5th in women

Only one in four diagnosed survive past one year of diagnoses

5-year survival rate is 4%

Whipple Procedure

AKA: pancreaticoduodenectomy

Most common treatment for cancer patients

Removes the head of the pancreas and

surrounding areas

12-15 month survival rate after surgery

Severe nutritional implications

Whipple Procedure

Alcohol

Recommendations

• Men: 2 drinks/day • Women:1 drink/day

• Recommendations based on body sizes

Standard Drink-ADA

• 12 oz. beer or wine cooler • 8 oz. malt liquor • 5 oz. table wine • 1.5 oz. distilled spirits, such as gin, whiskey, vodka, etc.

Ethanol Content

• 12 oz. beer-14 g • 12 oz. light beer-11g • 5 oz. wine-15g • 1.5 oz. distilled spirit-14g

Alcohol and Chronic Pancreatitis

• An ethanol intake of 150g/day for a period of 5 years or more is associated with the development of chronic pancreatitis. o 10 beers or 10 shots or 10 glasses of wine

• Up to 90% of chronic pancreatitis cases are caused by alcohol abuse.

Alcohol Metabolism

• In the pancreas the ethanol is broken down via two pathways o Oxidative

Increased reactive oxidative series (ROS) Decreased proteins

• responsible for removing ROS Causes a toxic imbalance

• Non-oxidative o Fatty acid ethyl esters

accumulate in the pancreas

Alcohol Metabolism

Alcohol Metabolism cont'd

• Acinar cells o Changes in enzyme production o Produce toxins o Lead to injury or disruption of the pancreatic cells o Digestive enzymes are leaked out and activated

within the pancreatic tissue

• Stellate cells o Increased secretion of building proteins

Fibrosis

Why do only a fraction of alcoholics develop pancreatitis?

• Smoking • Diet high in fat and protein • Obesity • Bacterial endotoxins due to translocation from intestines

to pancreas caused by excess alcohol • Not exactly sure why some alcoholics develop

pancreatitis and some do not

Alcohol and Acute Pancreatitis

• Alcohol accounts for as many as 30% of acute pancreatitis cases.

• With continued alcohol abuse acute can develop into chronic pancreatitis.

Treatment

Treatment for Mild AP

Fasting ◦ Until nausea, vomiting and pain subside

Fluid infusion ◦ Keep patient hydrated

Treatment for Mild AP Cont.

Pain reduction ◦ Preferably without narcotics Aspirin or Acetaminophen

◦ Demerol: similar to Morphine and effects the CNS and smooth muscle to provide pain relief and sedation

◦ Dilaudid: believed to effect the opiate receptors in the CNS

Treatment for Severe AP

Monitoring

Fasting

Fluid Resuscitation

Antibiotics

Analgesia

Severe AP: Monitoring Fluids

Common for patients to be put into the ICU

Vital signs ◦ Heart rate

◦ Blood Pressure

◦ Urine production

Swan-Ganz Catheter ◦ Used to track cardiac output and left ventricular filling

Severe AP: Monitoring Fluids Cont.

Fluid accumulation in third retroperitoneal space ◦ Can be several liters of accumulated fluid ◦ Described as a “Chemical burn” ◦ Monitoring

Consequences includes hypovolemia, hypotension, acute renal failure and pancreatic hypoperfusion

Monitoring blood volume levels reduce risk of myocardial infarction, cardiac arrhythmia, and cardiogenic shock

Respiratory Monitoring

Increased risk for ARDS ◦ Keep arterial oxygen saturation at 90%

Decrease Pancreatic Secretions

H2 receptor antagonists

Proton pump inhibitors

Antacids

Anticholinergic drugs

Gabexate Mesilate: protease inhibitor

Antibiotic Treatment

Antibiotics given for fever, leukocytosis, and sepsis

Imipenem: broad spectrum antibiotic for intramuscular administration

Meropenem: broad spectrum antibiotic given intravenously

Antibiotic Treatment

Combination of a Quinolone and Metronidazole: anti bacterial and protozoal agents

Cefuroxime: broad spectrum antibiotic

Prevent Organ Failure and Infection

Start enteral feeding to prevent translocation of bacteria

Give antibiotic prophylaxis to prevent microbial growth in necrotic pancreatic tissue

If infection occurs, drainage of infected area surgically or percutaneously

Risk for Pancreatic Necrosis

20% of patients

If organ failure remains for 7 to 10 days, a CT scan is done to locate necrotic tissue

Drained and tested for infection ◦ If necrosis is sterile, patient is put on antibtiotics for four to six weeks

◦ Klebsiella, E. coli, or Staphylococcus Aureus

Infected Necrosis

Debridement of necrotic tissue ◦ Surgical through abdomen Significantly increases patient’s stay in hospital.

◦ Percutaneously Through use of catheters

Mortality Rate

5-10% in hospitalized patients

10-35% with sepsis

Treatment for Chronic Pancreatitis

Abdominal pain is the most common symptom and needs to be high priority of treatment ◦ CT scans, Upper gastrointestinal barium radiography, ERCP

◦ Pinpoint location of pseudocysts, compression of duodenum or bile duct, carcinomas, or possibly gastroparesis

Pain Relief

Analgesia: pain relief without loss of consciousness ◦ Aspirin or Acetaminophen will be given first before narcotics or opiods because of the approximate 25% addiction rate

◦ If pain persists, treatment will start with mild opioids such as Tramadol which blocks the reuptake of norepinephrine and serotonin

Pain Relief in Theory

Alcohol Cessation ◦ Indicates decreased mortality

Pain can be caused by free radicals ◦ Many are deficient in antioxidants from overconsumption of alcohol

◦ Theory of antioxidant therapy

Pancreatic Enzyme Therapy

Decrease pain by decreasing pancreatic pressure

Pancreatic proteases in duodenum can repress pancreatic enzyme secretion by acting as a negative feedback mechanism to stop CCK and pancreatic enzyme release

Enzyme Therapy Cont.

Nonenteric-coated (tablet) enzymes shown to reduce pain more than enteric-coated

More likely to benefit small-duct CP or idiopathic CP rather than big-duct CP

Big-duct Pain Relief

Drainage to remove obstructions by endoscopic therapy

Stent Therapy

Pancreatic duct sphincterotomy ◦ For stone removal

◦ For stent replacement

Surgery When pain is not obliterated and other

organs are being effected, surgery is most likely necessary. ◦ Ductal Drainage

◦ Resection • Scrape out pancreas head and leave the shell

• Cleanly remove entire head

Surgery Cont.

• Total pancreatectomy with autologous islet transplantation (TPAIT)

• Small study showed subjects became insulin independent or used sliding scale insulin

• Malabsorption in all subjects

Other Treatments

30,000 units of lipase before and after a meal to help eliminate steatorrhea

Insulin for Type 1 diabetes mellitus

Blocking neural transmission from nociceptive stimuli

Deciding on Treatment

Diagnosis is critical!

Enzyme therapy better for small duct

All patients need to be on low fat diet, analgesics, and alcohol suppression

Transplant for Pancreatitis

No evidence

Pancreatitis is actually caused by transplants including heart, lung, kidney, and liver

Diabetes Mellitus is primary cause for pancreas transplants in severe cases unaffected by insulin therapy.

Quality of Life

Continued alcohol intake significantly reduces quality of life.

◦ Mortality rate: 3.6 times higher compared to normal age groups

Also greatly effected by pain

◦ Medical or surgical alleviation

Little data on CP patients and quality of life

Quality of Life Cont. Depends on patient’s individual

circumstance and if there is complication 70%: 10-year survival rate 45%: 20-year survival rate Death caused by complications from

pancreatitis not the pancreatitis itself.

Medical Nutrition Therapy

Acute Pancreatitis-mild

• First we must assess how long the patient has gone with inadequate oral intake o Pancreatitis causes severe pain with intake of food

o Negative connections with food • NPO for 5 to 7

o Allows pancreas to rest • IV hydration

o Fix fluid and electrolyte imbalances

Acute Pancreatitis-mild cont'd

• As symptoms subside, ease onto an oral diet o Start with clear liquids o Slowly progress to low-fat, solid diet o Important to monitor patient for recurrence of

symptoms and steatorrhea.

Acute Pancreatitis-Severe

• If patient is unable to begin oral feeding after 5 to 7 days of NPO, enteral feeding should be started. o Gastric or duodenal vs jejunal feeding don’t seem to

affect complications or length of hospital stay o Jejunal feedings cause less pain because less

pancreatic activity is needed

• Placing a feeding tube within 48 hrs of admission has been shown to decrease complications.

Acute Pancreatitis-Severe cont'd

• Start parenteral nutrition ONLY: o If patient is unable to tolerate enteral nutrition. o If nutrient needs are not being met by enteral intake alone.

• Formula is based on needs for: o Nutrients o Electrolytes o Fluids

• Lipids should only be given if the patient's triglycerides are below 400 mg/dL. o If lipids are given, blood levels should be monitored to

prevent hypertriglyceridemia.

Chronic Pancreatitis

• Patient needs to be counseled on a normal low-fat diet o Find a balance between fat intake and steatorrhea.

• Enzyme capsules will need to be taken with every meal and snack.

• Multivitamin should be taken if oral intake is unable to

meet nutrient needs o Vitamin B12

• COMPLETE CESSATION OF ALCOHOL!!!! o Very difficult

Case Study

Anthropometrics: • 30 y.o. female • 5'8" • Previous Weight: 140# • Current Weight: 112# • 25% Weight Loss Over One Year

• Severe • IBW: 80% • BMI:17

• Underweight

Case Study Cont...

• Biochemical: • Transferrin: LOW • Glucose: HIGH

o Increased glucagon-->breakdown of glycogen-->high blood glucose levels

o Possible damage to islets of langerhan • Billirubin: HIGH

o Stricturing of common bile duct o Accumulation of bilirubin in the bloodstream and

subsequent deposition in the skin causes jaundice

Case Study Cont...

• ALT(AlanineTransaminase): HIGH

• ASP(Alanine Asparatate Transaminase) • Cholesterol, Triglycerides: 225, HIGH • HDL: 40 • WBC: 14.5, HIGH

Case Study Cont...

Clinical: • Chief Complaint: Epigastric pain radiating to back that

lasts for hours to days. • Pt reports steatorrhea, anorexia, nausea • Medications:

o Ortho Tri-cyclen

Case Study Cont...

• Dietary: • NPO 5-7 days • REE: 1,894 kcal x 1.3 Stress Factor= 2,462 kcal

Diagnosis

• PES: Poor oral intake related to epigastric pain and complications of pancreatitis as evidenced by recent unintentional 10# weight loss.

Intervention:

• Educate patient about alcohol intake and its role in pancreatitis. Encourage support group with complete cessation of alcohol intake

• Inform patient about malabsorption, adequate calorie

intake, and proper fat intake • Discuss low fat diet, low added sugar diet o Give sample one day diet

Pt will be able to verbalize low fat, low sugar foods to incorporate into diet

Monitor and Evaluation

• Follow up in 30 days on weight gain, compliance to diet, and alcohol cessation

One Day Sample Diet for Pancreatitis

Meal Calories Fat (g) Sugar (g) Breakfast: 1/2 Cup Egg Substitute 60 0 2

2 Buttermilk Pancakes 120 1.5 0 ¼ Cup Sugar Free Syrup 23 0 0 1 Banana 105 .5 14 1 Cup Coffee 4 0 0 1 Cup Skim Milk 90 0 12 TOTAL: 402 2 28 Morning Snack: 8 oz Non Fat Yogurt 120 0 15

1 Cup Strawberries 53 .5 8 ½ Cup Granola 140 5 6 TOTAL: 313 5.5 29

Lunch: Chicken Pita

3 oz grilled chicken 100 2 0 Medium Pita 170 1.5 .5 ½ Cup Lettuce 4 0 0 ¼ Cup Sprouts 8 0 1 ¼ Cup Diced Tomato 15 0 2 ¼ Cup Diced Cucumber 4 0 .5 2 Tbs Hummus 52 0 3 1 oz Feta Cheese 75 0 6 Green Salad 2 Cups Romaine Lettuce 15 0 2 ½ Cup Shredded Carrots 23 0 3 2 Tbs Light Balsamic Vinaigrette 45 3.5 2 1 Diet Coke 0 0 0 1 Medium Pear 103 0 17 TOTAL: 614 7 37

Dinner: Halibut Italiano

6 oz Halibut (Baked) 189 3 0 2/3 Cup Spaghetti Sauce 79 1 10 ¼ Cup Sliced Mushrooms 20 0 2 2 Tbs Sliced Olives 20 2 0 1/8 C Reduced Fat Mozzarella

Cheese 25 2 0

Lemon and Parsley (garnish) - - - 3 oz Cup Pasta 309 1 3.5 1 Whole Wheat Roll 75 1 2 1 tsp margarine 25 3 0 ½ Cup Fat Free Ice Cream 110 0 15 TOTAL: 970 13 32.5 Evening Snack: 1 Bag Decaf Tea 0 0 0

Whole Wheat Toast 80 1 3 1 tsp Margarine 25 3 0 1 Cup Red Grapes 60 1 15 TOTAL: 165 5 18

Day Total: 2464 kcal 42 g fat 152 g sugar

Acute Pancreatitis

No eating for 5 to 7 days to rest

the pancreas.

Start on a liquid diet and ease into

a low-fat solid diet.

Tube feeding may be initiated

after 5 to 7 days if eating causes

too much pain.

Chronic Pancreatitis

Eliminate all alcohol intake.

A normal low-fat diet is the best

option.

Enzyme replacement should be

taken at every meal and snack.

Take multivitamins, as needed.

Diet Management for Acute

and Chronic Pancreatitis

http://www.ncbi.nlm.nih.gov/pubmedhealth/

PMH0002129/

http://www.mayoclinic.com/health/pancreatitis/

DS00371

http://www.ncbi.nlm.nih.gov/pubmedhealth/

PMH0002129/

Pancreatitis

For more information...

Pancreatitis

and Regaining Your Normal Life

Acute Pancreatitis ———————

Often in acute pancreatitis, the pancreatic

enzymes will start breaking down pancre-

atic tissue, which causes inflammation.

These are some of the causes why the

pancreas’s enzymes spontaneously begin

to cause damage to the pancreas: Alcohol

Trauma to the pancreas

Surgery

Infection

Drugs

Chronic Pancreatitis —————— Commonly, the result of long-term

alcohol abuse. The pancreas incurs

irreversible damage.

Symptoms ———————

Acute

Upper abdominal pain

Abdominal pain that radiates to the

back

Abdominal pain that feels worse after

eating

Nausea/Vomiting

Tenderness when touching the abdo-

men

Chronic

Upper abdominal pain

Indigestion

Losing weight without trying

Oily, smelly stools (steatorrhea)

What is the pancreas? —————————

The pancreas is a gland that sits behind the

stomach and is important in digesting food.

Enzymes, which are pancreatic juices that

help digest your food, are released into the

small intestine.

It produces insulin and glucagon, which

control your body’s ability to use sugar for

energy.

What is pancreatitis? —————–———

An inflammation of the pancreas.

This disease affects 80,000 Americans

every year.

It happens when digestive enzymes

start breaking down the pancreas.

Pancreatitis can be categorized as acute

or chronic.

Treatment

—————————

To cure attacks of acute

pancreatitis treatments include:

Fasting

Fluid infusion

Pain killers

Possibly antibiotics to combat

or prevent infection

With treating chronic pancreatitis

it is important to reduce pain as

much as possible. Different

methods include:

Pain medications

Pancreatic enzymes as a

negative feedback mechanism

Surgery to remove sites

causing pain

Above all, abstaining from al-

cohol and eating a low fat diet