Pancreatitis

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Pancreatitis

• Pancreatitis is a potentially serious disorder characterized by inflammation of the pancreas that may cause autodigestion of the organ by its own enzymes. This disease has two manifestations: acute pancreatitis and chronic pancreatitis (patho 912)
  

Acute Pancreatitis

• Acute pancreatitis is the result of an inflammatory process involving the pancreas caused by the release of activated pancreatic enzymes. In addition to the pancreas, this disorder can also affect surrounding organs, as well as cause a systemic reaction. This form of pancreatitis is generally brief in duration, milder in symptom presentation, and reversible. However, while this form of the disease resolves both clinically and histologically, approximately 15% of patients with acute pancreatitis will develop chronic pancreatitis (patho 912, merck 128).
• Acute pancreatitis may present as mild or severe. Milder forms of acute pancreatitis involve only the interstitium of the pancreas, which accounts for 80% of all cases, and has a temperate presentation with fewer complications. However, severe forms involve necrosis of the pancreatic tissue, which occurs in 20% of cases, and results in increased complications and mortality (patho 912, merck 128).

Chronic Pancreatitis

• Chronic pancreatitis develops from chronic inflammation of the pancreas that results in irreversible and progressive histologic changes. This includes fibrosis and ductal strictures, which destroy the pancreas directly, as well as decreased endocrine and exocrine functions, which can negatively affect other body systems. Unlike acute pancreatitis, this form of the disease is characterized by recurrent or persistent symptoms (patho 914 and 912, merck 128).

Prevalence

Acute Pancreatitis

• There are an estimated 50,000 to 80,000 cases in the United States each year, and 210,000 hospitalizations as a result. Of these, 80% are mild in nature, while 20% are necrotizing and severe, and approximately 2,000 patients die each year from associated complications. In addition, men are affected more frequently than women (foundation, cleveland, nddic).

Chronic Pancreatitis

• Worldwide, there are approximately 1.6 to 23 cases per 100,000 each year. In the United States alone chronic pancreatitis results in over 122,000 outpatient visits and 56,000 hospitalizations each year. Chronic pancreatitis also has a higher prevalence in men than women, and often develops between the ages of 30 and 40. This disease is rare in children (nddic, cleveland).

Characteristics/Clinical Presentation

Acute Pancreatitis

Mild Pancreatitis

• The primary symptom of acute pancreatitis is abrupt abdominal pain in the mediepigatsrium, often involving the entire upper abdomen that increases in intensity for several hours and cast last from days to more than a week. In addition, approximately 50% of patients with acute pancreatitis experience radiating pain in the back and, though rare, some patients may first experience pain in the lower abdomen. While characteristically continuous and boring in nature overall, pain may initially present as mild, dull, and nonspecific, but may increase to profound, sharp, and severe pain in conjunction with systemic symptoms, and result in shock, coma, or death. In addition, onset of pain is typically sudden when secondary to gallstones, but progresses over several days when derived from alcohol consumption. Specific movements can also affect pain; sitting upright and leaning forward may reduce pain, while coughing, vigorous activity, walking, lying supine, and deep breathing may intensify it. Furthermore, pain may be triggered or exacerbated by eating fatty foods or consuming alcohol. Along with pain, the disease also tends to cause nausea, anorexia, and vomiting in 90% of people with pancreatitis (patho 913, dd 139).
• Patients also display marked changes in appearance resulting from changes in bodily functions. Generally patients appear acutely ill and sweaty and report feelings of malaise, while about 20% experience upper abdominal distention attributable to gastric distention or displacement of the stomach by a pancreatic inflammatory mass. Grey Turner’s sign and/or Cullen’s sign, or a bluish discoloration to the flanks and umbilicus, may also be noted and are indicative of severe hemorrhagic pancreatitis, while other patients present with jaundice. Vital signs are also affected, with the heart rate increasing to 100-140 beats/min, a shallow and rapid breathing pattern, and an interim high or low blood pressure with significant postural hypotension. Temperature may remain normal initially, but rise to 100° - 101° F, and sensation may also be diminished (merck 129, dd 392).
• Palpation reveals apparent abdominal tenderness, typically in the upper quadrants. While there may be mild tenderness in the lower abdomen, the rectum is not sore and the stool is devoid of blood. Along with tenderness, the upper abdominal muscles may be rigid; however, this is rare in the lower abdominal region. In rare cases, severe peritoneal irritation can lead to a rigid and board-like abdomen. Furthermore, auscultation of bowel sounds may reveal hypoactivity, and general muscle weakness may be noted (merck 129).

Severe Pancreatitis

• In addition to these symptoms, a small percentage of cases develop into severe pancreatitis, which can have serious complications. Severe pancreatitis includes the aforementioned signs and symptoms, as well as a systemic inflammatory process with shock, multiorgan failure, and/or local complications. Symptoms of severe pancreatitis development include tachycardia, hypoxia, tachypnea, and changes in mental status (patho 913, merck 128).
• Complications that may occur with severe forms of this disease include pancreatic fluid-filled collections (57% of cases), pseudocysts, and necrosis. Fluid-filled collections can enlarge and increase pain, and both the fluid-filled collections and necrotic areas can become infected, resulting in pain, leukocytosis, fever, hypotension, and hypovolemia. Ascites and pleural effusions are also possible, but rare, complications (patho 913).

Chronic Pancreatitis

• Like acute pancreatitis, the central problem arising from chronic pancreatitis is abdominal pain, although 10 to 15% of patients have no pain and present with malabsorption. This pain is typically located in the epigastric and left upper quadrant with referral into the upper left lumbar region, and is frequently associated with nausea, vomiting, anorexia, constipation, flatulence, and weight loss. When the head of the pancreas is primarily affected, pain typically manifests in the T5-T9 regions; however, when the tail of the pancreas is involved pain tends to be referred to the left shoulder due to its innervation by C3-5. Pain is made worse with eating, and relieved by bringing the knees to the chest or bending forward. However, the frequency and severity of the pain may vary, with some patients experiencing acute attacks lasting only a few hours that become more chronic in nature lasting as long as two weeks and increasingly frequent over time, while others have continuous pain that gradually becomes more intense in due course. Patients with alcohol-related pancreatitis often experience pain 12 to 48 hours after imbibing large quantities of alcohol, while those with gallstone-associated pancreatitis have pain after consuming a large meal. This severe and chronic pain frequently leads to an abuse of opioids, decreased appetite, weight loss, and decreased quality of life, and is also the main reason surgery is performed in people with this disease (patho 915-916, merck 132, dd 139).
• Along with chronic pain, the destruction of pancreatic tissue and the consequential loss of pancreatic function often result in diarrhea and steatorrhea. Steatorrhea, or bulky, oily, and foul-smelling stools, occurs in late stages of the disease when the majority of the ancinar cells have been destroyed and less than 10% of normal lipase levels is being produced, resulting in fat maldigestion. Poor digestions leads to malnutrition due to the excretion of fat in the stool, and can cause patients to lose weight, despite normal appetites and eating habits. Other complications that may arise include the development of large pseudocysts, bleeding from pseudoaneurysms, splenic vein thrombosis, and fistula formation (patho 915-916. nddic).
• Diabetes mellitus may also develop in later stages of the disease, especially if the pancreas has been surgically removed. Because both beta cells, which produce insulin, and alpha-cells, which produce glucagon, are destroyed, this can result in severe hypoglycemia with the use of insulin for an extended length of time (patho 915).

Associated Co-morbidities

Acute Pancreatitis

• Alcoholism
• 15% of patients with acute pancreatitis develop chronic pancreatitis
• 5-7% mortality rate for milder forms with inflammation confined to the pancreas
• 10-50% for severe forms with necrosis and hemorrhage of the gland and a systemic inflammatory response
• Infection of necrotic pancreatic tissue may occur after 5-7 days 100% mortality for pancreatic infection without extensive surgical debridement or drainage of the infected area
• Patients with peripancreatic inflammation or one area of fluid collection have a 10 to 15% chance of abscess formation
• Patients with two or more areas of fluid collection have a 60% incidence of abscess formation
• Diabetes mellitus (increased risk in alcoholic pancreatitis)
• Recurrent episodes (increased risk in alcoholic pancreatitis) (patho 914, merck 128, 130-131)

Chronic Pancreatitis

• Alcoholism
• Cystic fibrosis
• Diabetes mellitus develops in 20-30% of patients within 10-15 years of onset
• Pancreatic cancer develops in 3% to 4% of patients
• Chronic disability
• 70% 10-year survival rate
• 45% 20-year survival rate
• 60% mortality rate for patients with alcohol-related chronic pancreatitis who do not cease alcohol intake (patho 915-916)

Medications

Acute Pancreatitis

• To alleviate pain, parenteral opiods, such as morphine, are often prescribed. Also, antiemetic drugs, such as prochlorperazine 5-10 mg IV every 6 hours, may be given to patients to minimize vomiting. Parenteral H2 blockers or proton pump inhibitors are given as well. (merck 131).

Severe Pancreatitis

• Evidence has shown no beneficial effects of medications aimed at improving the physiological process of severe pancreatitis, including platelet-activating factor inhibitors, somatostatin, and protease inhibitors. In addition, the use of prophylactic antibiotics for severe pancreatitis is currently controversial and under debate.
• Antibiotic prophylaxis with imipenim (500 mg IV every 8 hours) may be administered to prevent infection of necrotic pancreatic tissue, although its effect on decreasing mortality is unclear (merck 131).

Chronic Pancreatitis

• Non-narcotics analgesia, such as nonsteroidal anti-inflammatory drugs, acetaminophen, and tramadol, are typically used to treat the chronic pain associated with chronic pancreatitis. However, because this disease is progressive, patients may eventually need low doses of mild narcotics, such as codeine 15 to 60 mg/day, or propxyphene 65 to 260 mg/day. Should the pain persist, stronger opiates may be prescribed (Cleveland).
• Pancreatic enzymes may be taken if maldigestion occurs. There are many pancreatic enzyme preparations available, which differ in composition of enzymes, use of microspheres or microtablets, and the presence or absence of a coating. Despite this, lipase is a key ingredient to mixtures due to the fact that a minimum of 30,000 U lipase per meal is need for adequate digestion of fat and protein in the majority of patients; however, as much as 60,000 to 80,000 U lipase per meal may be given since not all of the lipase will necessarily reach the small intestine when active.
• Because uncoated enzyme preparations can be denatured by gastric acid, an H2 blocker or proton pump inhibitor, such as 20 mg of omeprazole once daily, is often prescribed in conjunction with pancreatic enzyme therapy to suppress the acid (Cleveland).

Diagnostic Tests/Lab Tests/Lab Values

Acute Pancreatitis

• The diagnosis of acute pancreatitis is formulated from patient’s clinical presentation, serum markers, and the absence of other causes that would produce similar symptoms. Because of this, a variety of tests are generally obtained, including a CBC, electrolytes, Ca, Mg, glucose, BUN, creatinine, amylase, and lipase. Other tests include an ECG and abdominal series of the chest, flat, and upright abdomen, as well as a urine dipstick for trypsinogen-2 which has >90% sensitivity and specificity for acute pancreatitis (merck 130).

Laboratory Tests

• Because acute pancreatitis results in the release of pancreatic enzymes from injured ancinar cells, an increase in serum enzymatic levels is key to diagnosing this disorder. The two pancreatic enzymes that become elevated in the serum in the first 24 to 72 hours of an acute pancreatic attack are amylase and lipase. While amylase levels typically rise three times greater than normal within the first two hours of symptom onset, the levels quickly decrease in 36 hours, rendering it useful only if a person seeks medical attention very early on. However, lipase levels increase within 4 to 8 hours of symptom onset, peak around 24 hours, and remain elevated for at least 14 days. Levels of 10 to 140 U/L, or 3 times the normal range, are indicative of acute pancreatitis. In addition, it is important to note that previous episodes on pancreatitis can result in the destruction of ancinar cells, therefore decreasing the amount of enzymes released into serum causing amylase and lipase levels to appear normal. Similarly, patients with pancreatitis caused by hypertrygliceridemia often have a circulating inhibitor present in their serum that masks the presence of elevated amylase until the serum is diluted (patho 913 and merck 130).
• While elevated lipase and amylase levels are elevated with all causes of acute pancreatitis, including alcohol abuse, an increase in alanine aminotransferase (ALT) levels from the normal 5 to 35 U/L range is present solely when gallstones are the cause of the pancreatitis (patho 913, 1645).
• Other tests suggestive of acute pancreatitis include hypertriglyceridemia and hypercalcemia, an increase in the white blood cell count to 12,000 – 20,000/ųL, a rise in hematocrit to as high as 50 to 55% due to third space fluid losses, and an increase of bilirubin in 15 to 25% of patients because pancreatic edema compresses the common bile duct (patho 913, merck 130).

Medical Imaging

• CT scans are often used to evaluate the pancreas during the diagnostic process and are able to accurately identify necrotizing pancreatitis, which provides valuable management and prognostic information. They can also identify fluid collections or pseudocysts when administered in conjunction with IV contrast, and is particularly recommended for severe pancreatitis or the development of complications (patho 913, merck 130).
• An MRI may be used for patients with contraindications for CT with contrast, as this test can also identify the presence of necrosis.
• Transabdominal ultrasound is used to examine the gallbladder and cystic duct when the presence of gallstones is suspected, which is a leading cause of this disorder.
• In addition, endoscopic ultrasonography (EUS), magnetic resonance cholangiopancreatography (MRCP), and Endoscopic Retrograde Cholangiopancreatography (ERCP) tests can also be performed to identify gallstones in the common bile duct (patho 913).

Screening for Severity

• The severity of acute pancreatitis can be determined through collecting the Ranson criteria, which requires gathering data both at admission and 48 hours later. At admission, five signs are documented: age > 55 years, WBC > 16,000/ųL, serum LDH > 350 IU/L, AST > 250 IU/L, and serum glucose > 200 mg/dL. Two days later, five other values are reviewed: hematocrit decrease > 10%, BUN increase > 4 mg/dL, serum calcium < 8 mg/dL, PaO2 < 60 mmHg, and fluid sequestration > 6 L. The risk of mortality increases with the number of positive signs. If less than 3 of the above are positive, the mortality rate is < 5%; if 3-4 are positive, the rate increases to 15-20% (merck).
• Also on the second day of admission, the severity of the disease is determined by the Acute Physiology and Chronic Health Evaluation score (APACHE II). This predicts the severity of the disease, complications, and chance of death. In patients with a severe form of the disease, they will have an elevated C-reactive protein level, an increase in hematocrit above 44%, and a body mass index greater than 30 (obesity). Knowing this information will determine aggressiveness of care and level of observation during medical management (patho 914).

Chronic Pancreatitis

• Unlike acute pancreatitis, diagnosing chronic pancreatitis is often difficult, especially in the early stages of the disease when little functional or structural changes are present in the pancreas.

Laboratory Tests

• Because patients with chronic pancreatitis experience significant loss of pancreatic function over time, lipase and amylase are often not elevated in the early stages, rendering these laboratory tests ineffective. Similarly, bilirubin may only be abnormal if there is considerable bile duct compression from a pseudocyst or fibrosis.
• In addition to these tests, more specialized tests have been developed. These tests either directly measure pancreatic enzymes that are produced by the pancreas, indirectly measure a product from the action of a pancreatic enzyme, or identify the presence of a pancreatic enzyme by-product in the serum or stool; however, these tests are neither well-tolerated nor available everywhere.

Medical Imaging

• Unlike laboratory tests, imaging tests are able to identify structural changes within the pancreas. These include strictures, pancreatic stones, lobularity, atrophy, and dilated pancreatic ducts (both large and small). Dilation of large pancreatic ducts, or large duct disease, is generally seen with alcohol use and is associated with functional problems, while dilation of small pancreatic ducts, or small duct disease, is more difficult to diagnose and idiopathic in nature. While several different imaging procedures can accurately illustrate these changes and diagnose this disease, the gold standard is an endoscopic retrograde cholangiopancreatography (ERCP), in which an endoscope and contrast injections are passed into the duodenum while the patient is sedated so that the pancreatic and bile ducts can be visualized on x-ray film. However, there is a 5-10% chance of causing acute pancreatitis just by administering this test (patho 916, foundation)
• Other tests that are used include transabdominal ultrasonography, CT scans, endoscopic ultrasonography (EUS), endoscopic retrograde cholangiopancreatography (ERCP), magnetic resonance cholangiopancreatography (MRCP), or MRI (patho 916).
• In the late stages of pancreatitis, tests of exocrine function become abnormal, such as the 72-hour stool fat test for steatorrhea , secretin pancreatic function testing, and decreased serum trypsinogen and fecal chymotrypsin levels; however, these tests are less sensitive and proactive at diagnosis this disease as the aforementioned methods (merck 132).
• Despite these tests, it is nut uncommon for chronic pancreatitis to go undiagnosed for months or even years (foundation).

Causes

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Systemic Involvement

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Medical Management (current best evidence)

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