Pancreatitis. By: Casey Allred, Kerri Bell, Chelsey Evans, Jillayne Gee and Bonnie Ross. March 8, 2010 NDFS 356

Transcription

1 Pancreatitis By: Casey Allred, Kerri Bell, Chelsey Evans, Jillayne Gee and Bonnie Ross March 8, 2010 NDFS 356 1

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 2

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). 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 4

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 5

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 6

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 7

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). 8

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). 9

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). 10

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 11

12 (85-100%) is similar to amylase. Another similarity to amylase is the influence of nonpancreatitis 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 12

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. 13

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 14

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 15

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 16

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 17

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 18

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 19

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 20

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. 21

22 References 1) Nutrition Care Manual. Pancreatitis. Available at: Accessed February 24, ) Uliyargoli A. Lecture Slides. Pancreas: Anatomy & Physiology, Sinai Hospital, October 30, ) University of Cincinnati Pancreatic Disease Center. Pancreatitis Accessed February 25, ) MedlinePlus. Acute pancreatitis. Available at: Accessed February 19, ) Mayo Clinic. Pancreas transplant. Available at: Accessed February 28, ) Children s Hospital Boston. Pancreatitis. Available at: Accessed February 19, ) 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: ) Feldman M, Friedman LS, Sleisenger MH. Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management. 7th ed. Philadelphia, PA: Saunders; 2002;1: ) Andrén-Sandberg Å. Pancreatic pseudocysts and aneurysms. North Am J Med Sci 2010;2: ) Petzel M. Nutrition support of the patient with pancreatic cancer. Supp Line. 2005; 26(3): ) American Dietetic Association. What is considered one serving of alcohol? Available at: Accessed February 25, ) American Dietetic Association. Food nutrient data for choose your foods: Exchange lists for diabetes, Available at: Accessed March 7, ) Apte MV, Pirola RC, Wilson JS. Mechanisms of alcoholic pancreatitis. J Gastroenterol Hepatol. 2010;25(12):

23 14) Love BL, Kehr H, Olin JL. Hypertriglyceridemia-induced acute pancreatitis due to patient noncompliance. J Clin Pharm Ther. 2009;34: ) Pagana, K.D., Pagana, T.J.: Mosby s Manual of Diagnostic and laboratory Tests. 3 rd ed. St. Louis, Missouri ) 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: ) Forsmark CE. Treatment of severe acute pancreatitis. In: Pancreatitis and Its Complications. Totowa, NJ: Humana Press; 2005: ) Munsell MA, Buscaglia JM. Acute pancreatitis. J Hosp Med. 2010;5: ) Voelzke BB, McAninch JW. The current management of renal injuries. Am Surg. 2008;74(8): ) Bowden RA, Ljungman P, Snydman DR. Transplant Infections. Philadelphia: Lippincott Williams & Wilkins; ) ADA Evidence Library. What is the effect of enteral nutrition versus parenteral nutrition on infectious complications in critically ill patients? Available at: itis&home=1. Accessed February 26,

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

25 Normal Functioning Pancreas A gland posterior to the stomach, near the duodenum It performs endocrine and exocrine function

26 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

27 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

28

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

30 Etiology

31 More causes of Pancreatitis Unknown Post op infection Endoscopic Retrograde Cholangiopancreatography (ERCP) Tumor

32 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

33 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.

34 Age groups and Prevalence Children-rare Cystic Fibrosis Pregnancy Gallstones High School and College students Alcohol 5-80 new cases per 100, die each year from complications of AP

35 Genetics, Lifestyle and Risk factors Same as etiology Alcohol addictions Cystic Fibrosis Trauma Drugs Infections Obesity *Genetic Pancreatitis

36 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

37 Diagnosis

38 Diagnostic Tools for Acute Tools: Physical examination Laboratory tests

39 Physical Examination Mild Pancreatitis Patients with mild pancreatitis may not look ill or feel pain Severe Pancreatitis Patients will look very ill and feel pain, and have abdominal distention Upper abdominal pain is often tender, doctors use percussion to determine this

40 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

41 Laboratory Tests for Acute Lipase Lipase is only produced by the pancreas Lipase and amylase combined=acute pancreatitis >3 times higher than normal

42 Diagnosing Chronic Pancreatitis Diagnoses: Gold standard: histology (pancreas tissue biopsy) Laboratory data CT scan

43 Laboratory Tests for Chronic Trypsinogen Trypsinogen levels decrease in chronic pancreatitis Levels <20 ng/ml specific indication of CP Lipase and amylase Normal in chronic pancreatitis

44 CT Scan for Chronic Big-duct Small-duct CT scans view of CT scans view=absence of pancreas= extensive big-duct view abnormalities of the pancreatic duct or gland, calcified ducts, or atrophy of the pancreas

45 Triglyceride and Pancreatitis Glucose 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 Triglycerides 1-4% of pancreatitis is caused by high levels of triglycerides Often seen in alcoholics or patients with uncontrolled diabetes Pathology unclear

46 Differentiating Between Gallstone or Alcoholic Pancreatitis Diagnostic Tools Age& gender: Male, 40=alcoholic pancreatitis Female, >40=gallstone pancreatitis Laboratory data & ultrasound

47 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

48 Forecasting Severity of Pancreatitis Ranson Criteria APACHE 2 and 3 CT severity index

49 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.

50

51 Pathophysiology

52 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

53 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

54

55 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 o Release of inflammatory cytokines Leads to the secretion of a pancreatic juice rich in protein

56 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

57 Complications

58 Several complications: osirs opseudocysts obleeding opseudoaneurysms ocancer

59 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

60 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 Pancreatic Pseudocyst

61 Pancreatic Pseudocyst Cont 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

62 Treatment: Percutaneous drainage Endoscopic guided ultrasound drainage Surgery Pancreatic Pseudocyst Cont

63 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

64 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

65 Chronic Complications Bile duct obstruction, Duodenal Obstruction o Gallbladder often removed Diabetes o o Extensive damage to the pancreas 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

66 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

67 Pancreatic Cancer Caused by CP Cigarette smoking Age Race Gender Genetics Diet Obesity 4 th leading cause of cancer death in men, 5 th in women Only one in four diagnosed survive past one year of diagnoses 5-year survival rate is 4%

68 Whipple Procedure AKA: pancreaticoduodenectomy Most common treatment for cancer patients Removes the head of the pancreas and surrounding areas month survival rate after surgery Severe nutritional implications

69 Whipple Procedure

70 Alcohol

71 Recommendations Men: 2 drinks/day Women:1 drink/day Recommendations based on body sizes

72 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.

73 Ethanol Content 12 oz. beer-14 g 12 oz. light beer-11g 5 oz. wine-15g 1.5 oz. distilled spirit-14g

74 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.

75 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

76 Alcohol Metabolism

77 Alcohol Metabolism cont'd Acinar cells o Changes in enzyme production o Produce toxins o o Lead to injury or disruption of the pancreatic cells Digestive enzymes are leaked out and activated within the pancreatic tissue Stellate cells o Increased secretion of building proteins Fibrosis

78 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

79 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.

80 Treatment

81 Treatment for Mild AP Fasting Until nausea, vomiting and pain subside Fluid infusion Keep patient hydrated

82 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

83 Treatment for Severe AP Monitoring Fasting Fluid Resuscitation Antibiotics Analgesia

84 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

85 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

86

87 Respiratory Monitoring Increased risk for ARDS Keep arterial oxygen saturation at 90%

88 Decrease Pancreatic Secretions H2 receptor antagonists Proton pump inhibitors Antacids Anticholinergic drugs Gabexate Mesilate: protease inhibitor

89 Antibiotic Treatment Antibiotics given for fever, leukocytosis, and sepsis Imipenem: broad spectrum antibiotic for intramuscular administration Meropenem: broad spectrum antibiotic given intravenously

90 Antibiotic Treatment Combination of a Quinolone and Metronidazole: anti bacterial and protozoal agents Cefuroxime: broad spectrum antibiotic

91 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

92 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

93 Infected Necrosis Debridement of necrotic tissue Surgical through abdomen Significantly increases patient s stay in hospital. Percutaneously Through use of catheters

94 Mortality Rate 5-10% in hospitalized patients 10-35% with sepsis

95 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

96 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

97 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

98 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

99 Enzyme Therapy Cont. Nonenteric-coated (tablet) enzymes shown to reduce pain more than entericcoated More likely to benefit small-duct CP or idiopathic CP rather than big-duct CP

100 Big-duct Pain Relief Drainage to remove obstructions by endoscopic therapy Stent Therapy Pancreatic duct sphincterotomy For stone removal For stent replacement

101

102 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

103 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

104 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

105 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

106 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.

107 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

108 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.

109 Medical Nutrition Therapy

110 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

111 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.

112 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.

113 Acute Pancreatitis-Severe cont'd Start parenteral nutrition ONLY: o o If patient is unable to tolerate enteral nutrition. 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.

114 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

115 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

116 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

117 Case Study Cont... ALT(AlanineTransaminase): HIGH ASP(Alanine Asparatate Transaminase) Cholesterol, Triglycerides: 225, HIGH HDL: 40 WBC: 14.5, HIGH

118 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

119 Case Study Cont... Dietary: NPO 5-7 days REE: 1,894 kcal x 1.3 Stress Factor= 2,462 kcal

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

121 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

122

123 Monitor and Evaluation Follow up in 30 days on weight gain, compliance to diet, and alcohol cessation

124 One Day Sample Diet for Pancreatitis Meal Calories Fat (g) Sugar (g) Breakfast: 1/2 Cup Egg Substitute Buttermilk Pancakes ¼ Cup Sugar Free Syrup Banana Cup Coffee Cup Skim Milk TOTAL: Morning Snack: 8 oz Non Fat Yogurt Cup Strawberries ½ Cup Granola TOTAL: Lunch: Chicken Pita 3 oz grilled chicken Medium Pita ½ Cup Lettuce ¼ Cup Sprouts ¼ Cup Diced Tomato ¼ Cup Diced Cucumber Tbs Hummus oz Feta Cheese Green Salad 2 Cups Romaine Lettuce ½ Cup Shredded Carrots Tbs Light Balsamic Vinaigrette Diet Coke Medium Pear TOTAL:

125 Dinner: Halibut Italiano 6 oz Halibut (Baked) /3 Cup Spaghetti Sauce ¼ Cup Sliced Mushrooms Tbs Sliced Olives /8 C Reduced Fat Mozzarella Cheese Lemon and Parsley (garnish) oz Cup Pasta Whole Wheat Roll tsp margarine ½ Cup Fat Free Ice Cream TOTAL: Evening Snack: 1 Bag Decaf Tea Whole Wheat Toast tsp Margarine Cup Red Grapes TOTAL: Day Total: 2464 kcal 42 g fat 152 g sugar

126 Diet Management for Acute and Chronic Pancreatitis 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. Pancreatitis 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. Pancreatitis For more information... PMH / DS PMH / and Regaining Your Normal Life

127 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. Acute Pancreatitis Often in acute pancreatitis, the pancreatic enzymes will start breaking down pancreatic 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 abdomen Chronic Upper abdominal pain Indigestion Losing weight without trying Oily, smelly stools (steatorrhea) 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 alcohol and eating a low fat diet