1. 1
    Current Diagnosis

    • Acute pancreatitis is usually caused by gallstones, and chronic pancreatitis is usually caused by alcohol abuse.

    • Other less-common causes of acute and chronic pancreatitis are considered only when gallstones and alcohol are definitively ruled out.

    • Pancreatic cancer and chronic pancreatitis can sometimes be difficult to distinguish.

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  2. 2
    Current Therapy

    • There has been a recent trend toward conservative medical therapy for acute and chronic pancreatitis, reserving surgery as a last resort.

    • In acute pancreatitis, try to avoid necrosectomy except in the setting of infected necrosis with organ failure.

    •   Asymptomatic pseudocysts can generally be observed.

    • Persistent symptomatic pseudocysts can often be addressed endoscopically.

    • Medical therapy for chronic pancreatitis includes pain management, nutrition, diabetes control, and cessation of drinking alcohol and smoking.

    • Surgical treatment for chronic pancreatitis currently favors strict patient selection and parenchyma-preserving techniques.

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  3. 3
    Acute Pancreatitis

    Acute pancreatitis is an inflammatory disease of the pancreas that is associated with little or no fibrosis of the gland. It can be initiated by several factors including gallstones, alcohol, trauma, and infections, and in some cases it is hereditary (Box 1). Very often, patients with acute pancreatitis develop additional complications such as sepsis, shock, and respiratory and renal failure, resulting in considerable morbidity and mortality.

    Box 1
    Common Causes of Acute  Pancreatitis




    Trauma (including iatrogenic: ERCP or surgery)

    Drugs: azathioprine, furosemide, mercaptopurine, opiates, pentamidine, steroids, sulfasalazine, sulindac, tetracycline, trimethoprim-sulfamethoxazole, valproic acid


    Infection (parasitic and viral)


    Abbreviation: ERCP = endoscopic retrograde cholangiopancreatography.


    The annual incidence of acute pancreatitis is probably about 50 cases per 100,000 population in the United States. Roughly 3000 of these cases are severe enough to lead to death.

    Risk Factors

    Biliary tract stone disease accounts for 70% to 80% of the cases of acute pancreatitis. Alcoholism accounts for another 10%, and the remaining 10% to 20% is accounted for either by idiopathic disease or by a variety of iatrogenic and miscellaneous causes including trauma, endoscopy, surgery, drugs, heredity, infection, and toxins.


    Pancreatitis begins with the activation of digestive zymogens inside acinar cells, which cause acinar cell injury. Digestive zymogens are colocalized with lysosomal hydrolase, and cathepsin-B catalyzed trypsinogen activation occurs, resulting in acinar cell injury and necrosis. This triggers acinar cell inflammatory events with the secretion of inflammatory mediators. Studies suggest that the ultimate severity of the resulting pancreatitis may be determined by the events that occur subsequent to acinar cell injury. These include inflammatory cell recruitment and activation, as well as generation and release of cytokines, reactive oxygen species, and other chemical mediators of inflammation, ultimately leading to ischemia and necrosis. Early mortality in severe acute pancreatitis is caused by a systemic inflammatory response syndrome with multiorgan failure. If the patient survives this critical early period, a septic complication caused by translocated bacteria, mostly Gram-negative microbes from the intestine, leads to infected pancreatic necrosis. Late deaths are caused by infected necrosis, leading to septic shock and multiorgan failure.


    Gallstones are present in about 15% to 20% of patients older than 60 years, but only a fraction become symptomatic. Although gallstone pancreatitis can rarely be the first symptom of gallstones, most patients have symptoms of cholecystitis before developing pancreatitis. Thus it is important to make early and prompt referral of patients with symptomatic cholelithiasis for laparoscopic cholecystectomy to prevent life-threatening complications such as acute pancreatitis.

    Clinical Manifestations

    All episodes of acute pancreatitis begin with severe pain, generally following a substantial meal. The pain is usually epigastric, but it can occur anywhere in the abdomen or lower chest. It has been described as penetrating through to the back, and it may be relieved by the patient’s leaning forward. It precedes the onset of nausea and vomiting, with retching often continuing after the stomach has emptied. Vomiting does not relieve the pain, which is more intense in necrotizing than in edematous pancreatitis.

    On examination the patient may show tachycardia, tachypnea, hypotension, and hyperthermia. The temperature is usually only mildly elevated in uncomplicated pancreatitis. Voluntary and involuntary guarding can be seen over the epigastric region. The bowel sounds are decreased or absent. There are usually no palpable masses. The abdomen may be distended with intraperitoneal fluid.

    There may be pleural effusion, particularly on the left side. With increasing severity of disease, the intravascular fluid loss may become life-threatening as a result of sequestration of edematous fluid in the retroperitoneum. Hemoconcentration then results in an elevated hematocrit. However, there also may be bleeding into the retroperitoneum or the peritoneal cavity. In some patients (about 1%), the blood from necrotizing pancreatitis can dissect through the soft tissues and manifest as a bluish discoloration around the umbilicus (Cullen’s sign) or in the flanks (Grey Turner sign). The severe fluid loss can lead to prerenal azotemia, with elevated blood urea nitrogen and creatinine levels. There also may be hyperglycemia, hypoalbuminemia, and hypocalcemia sufficient in some cases to produce tetany.


    Although serum amylase is often elevated in acute pancreatitis, there is no significant correlation between the magnitude of serum amylase elevation and severity of pancreatitis. Other pancreatic enzymes also have been evaluated to improve the diagnostic accuracy of serum measurements. Specificity of these markers ranges from 77% to 96%, the highest being for lipase. Measurements of many digestive enzymes have methodologic limitations and cannot be easily adapted for quantitation in emergency laboratory studies. Because serum levels of lipase remain elevated for a longer time than total or pancreatic amylase, it is the serum indicator of highest probability of the disease.

    Abdominal ultrasound examination is the best way to confirm the presence of gallstones in suspected biliary pancreatitis. It also can detect extrapancreatic ductal dilations and reveal pancreatic edema, swelling, and peripancreatic fluid collections. However, in about 20% of patients, the ultrasound examination does not provide satisfactory results because of the presence of bowel gas, which can obscure sonographic imaging of the pancreas.

    A computed tomographic (CT) scan of the pancreas is more commonly used to diagnose pancreatitis. CT scanning is used to distinguish milder (nonnecrotic) forms of the disease from more severe necrotizing or infected pancreatitis, in patients whose clinical presentation raises the suspicion of advanced disease (Figures 1 and 2). Pancreatic protocol computed tomography (CT) scan of the abdomen and pelvis is recommended when not limited by renal insufficiency. A tri-phasic thin, multislice CT scan with an arterial, venous, and delayed phase in conjunction with sagital and coronal views. No oral contrast, instead drink 1000 cc water to opacify the stomach. The scan assesses the degree of pancreatic necrosis, peripancreatic fluid collections, and the surrounding vascular structures.

    FIGURE 1    Computed tomographic scan confirming acute  edematous pancreatitis.

    FIGURE 2    Computed tomographic scan confirming acute  necrotizing, emphysematous pancreatitis.

    Magnetic Resonance Cholangiopancreatography (MRCP) is also of value to assess the pancreatic duct and biliary tree. This can often reveal pancreatic ductal disruption.

    Differential Diagnosis

    The clinical diagnosis of pancreatitis is one of exclusion. Hyperamylasemia can also occur as a result of conditions not involving pancreatitis. The other upper abdominal conditions that can be confused with acute pancreatitis include perforated peptic ulcer and acute colecystitis, and occasionally a gangrenous small bowel obstruction. Because these conditions often have a fatal outcome without surgery, urgent intervention is indicated in the small number of cases in which doubt persists. A tumor should be considered in a nonalcoholic patient with acute pancreatitis who has no demonstrable biliary tract disease. Approximately 1% to 2% of patients with acute pancreatitis have pancreatic carcinoma, and an episode of acute pancreatitis can be the first clinical manifestation of a periampullary tumor.


    The severity of acute pancreatitis covers a broad spectrum of illness, ranging from the mild and self-limiting to the life-threatening necrotizing variety. Some cases are so mild they can be treated in an outpatient setting. However, most cases require hospitalization for observation and diagnostic study. A conservative approach has been advocated in the treatment of acute pancreatitis (Box 2). Severity is assessed with imaging results and clinical parameters and is quantitated with scores such as Ranson’s criteria (Box 3), the Atlanta classification, and the APACHE II (Acute Physiology And Chronic Health Evaluation) score. Severe acute pancreatitis is defined by associated organ dysfunction. The Atlanta classification is based on an international consensus conference held in Atlanta in 1992 and has been updated. APACHE II was designed to measure the severity of disease for adult patients admitted to intensive care units. Though not specific to pancreatitis, APACHE II can be used in an effort to differentiate patients with mild and severe acute pancreatitis.

    APACHE II scores of 8 points or more correlate with a mortality rate of 11% to 18%.

    Box 2
    Treatment of Acute Pancreatitis
    Assessment of severity

    Fluid resuscitation and oxygenation

    Early nasojejunal feeding

    Avoid prophylactic antibiotics (reserve antibiotic therapy for specific infections)

    Avoid or postpone necrosectomy if possible Options for necrosectomy

    •   Open anterior approach with closed lavage

    •   Open anterior approach with packing and reoperation

    •   Open retroperitoneal approach

    •   Laparoscopic anterior approach with closed lavage

    •   Video-assisted retroperitoneal débridement (VARD)

    Box 3

    Ranson’s Criteria
    There are 11 Ranson signs. Five of the signs are evaluated when the patient is admitted to the hospital, and the remaining six are evaluated 48 hours after admission. The signs are added to reach a score:

    •   If the score <3, severe pancreatitis is unlikely.

    •   If the score ≥3, severe pancreatitis likely.


    •   Score 0-2: 2% mortality

    •   Score 3-4: 15% mortality

    •   Score 5-6: 40% mortality

    •   Score 7-8: 100% mortality

    At Admission

    Age in years >55 years

    White blood cell count >16,000 cells/mm3 Blood glucose >11 mmol/L (>200 mg/dL) Serum AST >250 IU/L

    Serum LDH >350 IU/L

    At 48 Hours

    Calcium (serum calcium) <2.0 mmol/L (<8.0 mg/dL) Hematocrit fall >10%

    Oxygen (hypoxemia Po2  <60 mm Hg)

    BUN increased by ≥1.8 mmol/L (≥5 mg/dL) after IV fluid hydration Base deficit (negative base excess) >4 mEq/L

    Sequestration of fluids >6 L

    Abbreviations: AST = aspartate aminotransferase; BUN = blood urea nitrogen.

    Upon confirmation of the diagnosis, patients with severe disease should be transferred to the intensive care unit for observation and maximum support. Adequate fluid resuscitation optimizing organ perfusion and oxygenation is essential. The use of prophylactic intravenous antibiotics in the initial stages of severe acute pancreatitis is not proved to be useful. Two randomized, controlled studies failed to show any benefit from antibiotics. Prophylactic antibiotics did not decrease the incidence of infected pancreatic necrosis or lower mortality. Data from these well-designed trials refutes prior data from less-rigorous studies suggesting prophylactic antibiotics were useful. Additional studies are required, but there is increasing concern that the prolonged use of potent antibiotics might result in an increased prevalence of fungal infections and possibly increased mortality.

    Currently, antibiotic therapy should be reserved for treatment of specific infections such as positive blood, sputum, and urine cultures or percutaneous or operative cultures of necrotic tissue.

    Randomized clinical trials have also shown a benefit from early nasojejunal feeding compared to total parenteral nutrition. Gastric decompression with a nasogastric tube is selectively used in patients with severe ileus and vomiting but is not necessary in a majority of cases.

    In biliary pancreatitis, the gallbladder must eventually be removed or recurrent acute pancreatitis will occur in 30% to 60% of cases. The timing of the cholecystectomy depends on the severity of the pancreatitis. Usually laparoscopic cholecystectomy is performed during the index admission as soon as the attack of acute pancreatitis has resolved. In more-severe cases, the cholecystectomy is delayed and often combined with interventions for late complications of acute pancreatitis. In cases with severe comorbidity, endoscopic sphincterotomy has been considered as an alternative to cholecystectomy. However, if the patient has a postinflammatory fluid collection, bacteria can be introduced during endoscopic retrograde cholangiopancreatography (ERCP), and sphincterotomy should be delayed.

    Currently, there is no role for routine early laparotomy and necrosectomy or resection in the setting of acute necrotizing pancreatitis. If the necrotic pancreas becomes infected and the patient fails to respond to conservative treatment, then necrosectomy may be warranted. Patients with infected necrosis are rarely managed conservatively without eventual surgical intervention. However, even in the setting of infected necrosis, there has been consideration for antibiotic therapy until the acute inflammatory response has subsided, if possible, with the view that surgery that is deferred for several weeks is more easily accomplished with one intervention. Patients who suffer from infected necrosis without having clinical signs of sepsis or other systemic complications might not need immediate surgical necrosectomy.

    A nonsurgical alternative for the treatment of infected necrosis is percutaneous catheter drainage. This is considered a temporary measure to allow stabilization of the patient so that a safer surgical necrosectomy can be done at a later time. Multiple large drains are required, and patients frequently undergo repeat CT and revision of the drains. Current recommendations are to postpone surgery for as long as possible, usually beyond the second or third week of the disease or later, when necrotic tissue can be easily distinguished from viable pancreas and débridement without major blood loss can be performed. When surgery is performed, tissue-preserving digital necrosectomy is the usual technique rather than a classic surgical resection of the pancreas (Figure 3).

    FIGURE 3    Necrotic material débrided from the retroperitoneum in  a case of acute necrotizing pancreatitis.

    Necrosectomy can be performed by an open anterior approach with closed lavage or with leaving the abdomen open and packing. The packing is replaced at intervals of 24 to 72 hours. Sometimes a left lateral retroperitoneal approach is helpful. Newer approaches are the video-assisted retroperitoneal débridement (VARD). This procedure is a combination of percutaneous drainage and the open lateral retroperitoneal approach. An anterior laparoscopic approach has also been described and mimics the open anterior approach using laparoscopic ports. Surgical necrosectomy is indicated in patients with sepsis caused by infected necrosis and in selected patients with extended sterile necrosis causing severe systemic organ dysfunction and sepsis without a septic focus.

    In some cases, the acute inflammatory process can lead to erosion into retroperitoneal vessels, and acute hemorrhage occurs. This acute emergent complication is best managed with immediate angiography to determine the exact site of bleeding and can often be treated with embolization rather than surgery (Figure 4).

    FIGURE 4    Acute necrotizing pancreatitis. A, Erosion into the  splenic artery as seen on computed tomography. B, Erosion into the splenic artery as seen on angiogram. C, This complication of acute pancreatitis is best treated with angiographic  embolization.

    Although previously frowned upon, there has been a move toward enteric drainage of all necrotic collections (even when infected) when technically feasible.


    Despite a conservative operative approach, endocrine and exocrine insufficiency develop in as many as half of the patients and are determined by the extent of pancreatic necrosis. Therefore, patients must be monitored with blood glucose measurements, stabilization of body weight, and proper nutrition.


    The most common complication after successful management of acute pancreatitis is a pseudocyst. The term ‘‘pseudocyst’’ is currently used to broadly categorize most pancreatic and peripancreatic fluid collections (including walled-off pancreatic necrosis [WOPN] and acute peripancreatic fluid collection). The Acute Pancreatitis Classification Working Group recently proposed a revised Atlanta classification refers to collections within 4 weeks of symptom onset as either acute peripancreatic fluid collections (APFC) or postnecrotic pancreatic fluid collections (PNPFC) depending upon the absence or presence of pancreatic/peripancreatic necrosis, respectively. After 4 weeks of the onset of symptoms, persistent collections with discrete walls are referred to as pseudocyst or WOPN, again depending upon the absence or presence of necrosis, respectively. In addition, these collections are further classified as sterile or infected and the term ‘‘pancreatic abscess’’ has been abolished.

    The management of pseudo- cysts has followed a minimally invasive trend. Most pseudo- cysts resolve spontaneously, even beyond 6 weeks, so asymptomatic pseudocysts are usually observed. (70% of pseudocysts will resolve without intervention) Endoscopic cystogastrostomy is the approach of choice for symptomatic fluid- predominant pseudocysts when there is minimal necrosis. If there is significant necrotic debris or a solid-predominant pseudocyst, surgical drainage with laparoscopic cystogastrostomy is preferred (Figure 5).

    This can also be performed with the traditional open technique. Cystjejunostomy (laparoscopic or open) is used in cases in which the site of the pseudocyst precludes drain- age into the posterior aspect of the stomach.

    FIGURE 5    Computed tomographic scan showing  fluid-predominant

    (A) and solid-predominant (B) pseudocysts. The former can be treated with endoscopic cystogastrostomy, and the latter is best treated  with laparoscopic cystogastrostomy.


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  4. 4
    Chronic Pancreatitis

    Chronic pancreatitis is a chronic inflammatory disease of the pancreas characterized by irreversible morphologic changes that typically are associated with pain or permanent loss of function, or both.


    Population studies suggest a prevalence of chronic pancreatitis that ranges from 5 to 27 persons per 100,000 population, with considerable geographic variation. Autopsy data are difficult to interpret because a number of changes associated with chronic pancreatitis, such as fibrosis, duct ectasia, and acinar atrophy, are also present in asymptomatic elderly patients. Differences in diagnostic criteria, regional nutrition, alcohol consumption, and medical access account for variations in the frequency of the diagnosis, but the overall incidence of the disease has risen progressively since the 1960s.

    Chronic pancreatitis in the United States currently results in more than 120,000 outpatient visits and more than 50,000 hospitalizations per year.

    Risk factors

    Alcohol consumption and alcohol abuse are associated with chronic pancreatitis in up to 70% of cases. Other major causes include tropical (nutritional) and idiopathic disease, as well as hereditary causes.

    There is a linear relationship between exposure to alcohol and the development of chronic pancreatitis. The incidence is highest in heavy drinkers (15 drinks/day or 150 g/day). However, chronic pancreatitis can occur in patients who drink very little, and it occurs in less than 15% of documented alcoholics. The duration of alcohol consumption is definitely associated with the development of pancreatic disease. The onset of disease typically occurs between ages 35 and 40 years, after 16 to 20 years of heavy alcohol consumption. Recurrent episodes of acute pancreatitis are typically followed by chronic symptoms after 4 or 5 years.


    Multiple episodes (or a prolonged course) of pancreatic injury ultimately leading to chronic disease is widely accepted as the pathophysiologic sequence. Most investigators believe that alcohol metabolites such as acetaldehyde, combined with oxidant injury, result in local parenchymal injury that is preferentially targeted to the pancreas in predisposed persons. Repeated or severe episodes of toxin-induced injury activate a cascade of cytokines, which in turn induces pancreatic stellate cells to produce collagen and cause fibrosis.

    The pain caused by chronic pancreatitis is thought to be due to increased pressure in the pancreatic ducts and tissue. Neural and perineural inflammation is also thought to be important in pathogenesis of pain in chronic pancreatitis. Neuropeptides released from enteric and afferent neurons and their functional interactions with inflammatory cells might play a key role.


    Because alcohol is the cause of most cases of chronic pancreatitis, cessation of alcohol consumption is recommended to prevent progression to chronic pancreatitis. Unfortunately, the majority of patients are not able to recover from alcoholism, and relapse is common.

    Clinical Manifestations

    Symptoms of chronic pancreatitis may be identical to those of acute pancreatitis, typically midepigastric pain penetrating through to the back. Patients with chronic pancreatic pain typically flex their abdomen and either sit or lie with their hips flexed, or lie on their side in a fetal position. Unlike ureteral stone pain or biliary colic, the pain causes the patient to be still. Nausea or vomiting can accompany the pain, but anorexia is the most common associated symptom. Patients with continuous pain can have a complication of chronic pancreatitis, such as an inflammatory mass, a cyst, or even pancreatic cancer. Other patients have intermittent attacks of pain with symptoms similar to those of mild to moderate acute pancreatitis. The pain sometimes is severe and lasts for many hours or several days.

    As chronic pancreatitis progresses, endocrine and exocrine insufficiency begin to appear. Patients describe a bulky, foul-smelling, loose (but not watery) stool that may be pale and float on the surface of toilet water. Patients often describe a greasy or oily appearance to the stool or describe an “oil slick” on the water’s surface. In severe steatorrhea, an orange, oily stool is often reported. As exocrine deficiency increases, symptoms of steatorrhea are often accompanied by weight loss. Patients might describe a good appetite despite weight loss, or they might have diminished food intake due to abdominal pain. The combination of decreased food intake and malabsorption of nutrients usually results in chronic weight loss. As a result, many patients with severe chronic pancreatitis are below ideal body weight. Usually islet cells are spared early in the disease process despite being surrounded by fibrosis, but eventually the insulin-secreting beta cells are also destroyed, gradually leading to diabetes.


    The diagnosis of chronic pancreatitis depends on the clinical presentation, a limited number of indirect measurements that correlate with pancreatic function, and selected imaging studies. Diagnosis is usually simple in the late stages of the disease because of the presence of structural and functional alterations of the pancreas.

    Early in the disease, the diagnosis is more difficult. Various classification systems have been developed. The Cambridge classification uses imaging tests such as ERCP, CT, and ultrasound to grade severity. The Mayo Clinic system is based on functional as well as imaging results. Tests of pancreatic function include the secretin- cerulein test, Lundh test, fecal excretion of pancreatic enzymes, and quantitation of fecal fat.

    Chronic pancreatitis can be classified as calcifying (lithogenic), obstructive, inflammatory, autoimmune, tropical (nutritional), hereditary, or idiopathic. Autoimmune and hereditary pancreatitis have recently been better understood and diagnosed more than before. Autoimmune pancreatitis is associated with fibrosis, a mononuclear cell (lymphocyte, plasma cell, or eosinophil) infiltrate, and an increased titer of one or more autoantibodies. It is usually associated with autoimmune diseases such as Sjögren’s syndrome. Increased levels of serum β-globulin or immunoglobulin (Ig)G4 are often present. This disease can be mistaken for chronic pancreatitis, with an inflammatory mass in the head of the pancreas suspicious for pancreatic cancer (Figure 6). Diagnosis is important because steroid therapy is uniformly successful in ameliorating the disease, including any associated bile duct compression.

    FIGURE 6    Computed tomographic scan of a patient with  autoimmune pancreatitis and an inflammatory mass in the head of the pancreas. Preoperative diagnosis is not always possible, but surgery should  be avoided because this disease often responds to steroid  therapy.

    Hereditary pancreatitis first occurs in adolescence with abdominal pain; patients develop progressive pancreatic dysfunction, and the risk of cancer is greatly increased. The disease follows an autosomal dominant pattern of inheritance with 80% penetrance and variable expression. Recent mutational analysis has revealed a missense mutation resulting in an Arg to His substitution at position 117 of the cationic trypsinogen gene, or PRSS1, one of the primary sites for proteolysis of trypsin. This mutation prevents trypsin from being inactivated by itself or other proteases, and it results in persistent and uncontrolled proteolytic activity and autodestruction within the pancreas. Similarly, PSTI, also known as SPINK1, has been found to have a role in hereditary pancreatitis and some cases of sporadic chronic pancreatitis. SPINK1 specifically inhibits trypsin action by competitively blocking the active site of the enzyme.

    It is likely that many of the “idiopathic” forms of chronic pancreatitis, as well as some patients with the more common forms of the disease, will be found to have a genetic linkage or predisposition.

    Differential Diagnosis

    There are several clinical conditions from which chronic pancreatitis needs to be distinguished. Other causes of upper abdominal pain, such as peptic ulcer disease, biliary tract disease, mesenteric vascular disease, or malignancy must be excluded. The major difficulty in the differential diagnosis of chronic pancreatitis is distinguishing it from pancreatic ductal adenocarcinoma. Chronic pancreatitis can closely mimic pancreatic cancer, both clinically and morphologically. In addition, chronic pancreatitis is a risk factor for the development of pancreatic cancer. Although in pancreatic resection specimens this problem may be finally resolved, distinguishing these two diseases preoperatively in small (needle) biopsy specimens is a formidable challenge for the pathologist. Therefore, especially in the setting of an inflammatory mass in the head of the pancreas, consideration of pancreatic cancer and surgical referral is important. Work up of these patients should include a pancreatic protocol CT scan, a MRCP, and an endoscopic ultrasound to evaluate the parenchyma and the ducts of the pancreas.

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  5. 5

    Therapy for chronic pancreatitis is aimed at managing associated digestive dysfunction and relieving pain (Box 4). It is important to first address malabsorption, weight loss, and diabetes. When pancreatic exocrine capacity falls below 10% of normal, diarrhea and steatorrhea develop. Lipase deficiency tends to manifest itself before trypsin deficiency, so the presence of steatorrhea may be the first functional sign of pancreatic insufficiency. As pancreatic exocrine function deteriorates further, the secretion of bicarbonate into the duodenum is reduced, which causes duodenal acidification and further impairs nutrient absorption. Frank diabetes is seen initially in about 20% of patients with chronic pancreatitis, and impaired glucose metabolism can be detected in up to 70% of patients.

    Box 4
    Treatment of Chronic Pancreatitis
    Pancreatic enzyme replacement

    Proper nutrition and vitamin supplementation Blood sugar control

    Long-acting narcotic analgesics at lowest effective doses Cessation of alcohol and tobacco

    Endotherapy (pancreatic duct stenting and removal of stones)

    Parenchymal preserving surgery (Frey, Beger) in carefully selected patients

    The medical treatment of chronic or recurrent pain in chronic pancreatitis requires the use of analgesics, a cessation of alcohol use, oral enzyme therapy, and endoscopic stent thearpy. Administration of pancreatic enzyme (e.g., Pancrease MT, Pancrelipase, Creon) serves to reverse the effects of pancreatic exocrine insufficiency and might also reduce or alleviate the pain1 experienced by patients. Interventional procedures to block visceral afferent nerve conduction or to treat obstructions of the main pancreatic duct are also an adjunct to medical treatment. It has been taught that the pain of chronic pancreatitis decreases with increasing duration of the disease, the so called burn- out phase, where endocrine and exocrine insufficiency occurs and the pain decreases. However, recent studies have called this concept into question, demonstrating continued pain in patients with chronic pancreatitis despite long-standing disease and pancreatic insufficiency. Cessation of alcohol abuse, if possible, causes the pain to stop in about half of the patients.

    Pain relief usually requires the use of narcotics, but these should be titrated to achieve pain relief with the lowest effective dose. Opioid addiction is common, and the use of long-acting analgesics by transdermal patch together with oral agents for pain exacerbations slightly reduces the sedative effects of high-dose oral narcotics. Celiac plexus neurolysis has been an effective form of analgesic treatment in patients with pancreatic carcinoma. However, its use in chronic pancreatitis has been disappointing, with about half of the patients deriving a benefit that lasts 6 months or less.

    Pancreatic duct stenting is used for treatment of proximal pancreatic duct stenosis, decompression of a pancreatic duct leak, and drainage of pancreatic pseudocysts that can be catheterized through the main pancreatic duct. Pancreatic duct stones can also be removed endoscopically. Stent therapy in chronic pancreatitis definitely plays a role and can help select patients for successful operative therapy.

    However, the duration of success with stent therapy for chronic pancreatitis is probably less than with surgical therapy.

    Major pancreatic resections for chronic pancreatitis have a high complication rate, both early and late. Patients with large duct disease who can have nutrition restored, are working, are not drinking alcohol, and have a supportive family structure fare better. Failure to carefully select patients leads to disappointing results. The surgical management of pancreatic duct stones and stenoses has been shown to be superior to endoscopic treatment in randomized clinical trials.

    Beger introduced the duodenum-preserving pancreatic head resection (DPPHR) in the early 1980s. Later in the decade, Frey and Smith described the local resection of the pancreatic head with longitudinal pancreaticojejunostomy, which included excavation of the pancreatic head including the ductal structures in continuity with a long ductotomy of the dorsal duct. This operation is basically a hybrid of the Beger and Puestow (Partington-Rochelle modification) procedures and is more popular in the United States (Figures 7 and 8).

    FIGURE 7    Computed tomographic scan of a patient with  chronic calcific pancreatitis and a massively dilated pancreatic  duct.

    FIGURE 8    A, The pancreatic duct is opened to reveal  a preoperatively placed pancreatic duct stent. B, The residual stones removed from the pancreatic duct. C, In the Frey procedure, the head of the pancreas is cored out in addition to a longitudinal pancreatic ductotomy. The pancreas is drained with a Roux-en-Y limb of  jejunum.

    Recent randomized prospective studies have compared the Whipple, Beger, and Frey procedures for chronic pancreatitis. Patients who had a Beger procedure had a shorter hospital stay, greater weight gain, less postoperative diabetes, and less exocrine dysfunction than standard Whipple patients over a 3- to 5-year follow-up. Pain control was similar between the two procedures. In a study comparing the pylorus-preserving Whipple to the Frey procedure, there was a lower postoperative complication rate associated with the Frey procedure (19%) compared to the pylorus-preserving Whipple group (53%), and the global quality-of-life scores were better (71% versus 43%, respectively). Both operations were equally effective in controlling pain over a 2-year follow-up. Operation times, intraoperative blood loss, and transfusion requirements have been shown to be decreased with the Frey and Beger procedures compared to the Whipple procedure. In long-term (>8 years) follow-up, there was no difference between the Beger and Frey procedures in pain relief, pancreatic insufficiency, quality of life, and late mortality. Compared to the Whipple procedure, the Beger and Frey procedures seem to produce a lower incidence of immediate complications and diabetes but no significant differences in pain relief. Although these limited pancreatic procedures have a lower initial rate of endocrine dysfunction, the long-term risk of diabetes is more related to the progression of the underlying disease than to the effects of operation.

    Recent refinements in the methods of harvesting and preserving pancreatic islets, and standardization of the methods by which islets are infused into the portal venous circuit for intrahepatic engraftment, have improved the success and rekindled interest in islet autotransplantation for chronic pancreatitis. The ability to recover a sufficient quantity of islets from a sclerotic gland depends on the degree of disease present, so the selection of patients as candidates for autologous islet transplantation is important. As success with autotransplantation increases, patients with nonobstructive, sclerotic pancreatitis may be considered for resection and islet autotransplantation earlier in their course, because end-stage fibrosis bodes poorly for transplant success. As the necessary expertise with islet transplantation becomes more widespread, this therapy could become routine in the treatment of chronic pancreatitis.


    Chronic pancreatitis is of course a chronic disease, so continued monitoring and maintenance therapy is essential after an acute exacerbation of chronic pancreatitis. Pain control, proper nutrition, and alcohol and smoking cessation must be maintained as an outpatient. The clinician must also be looking for the development of common complications.


    Pseudocysts in the setting of chronic pancreatitis are less likely to resolve without intervention. Often, the pancreatic duct and bile duct are compressed, and the compression might need to be addressed at the same time as the pseudocyst. A trend toward minimally invasive management remains appropriate, with endoscopic drainage preferred over laparoscopic cystogastrostomy unless additional procedures are required. Resection of a pseudocyst is sometimes indicated for cysts located in the pancreatic tail, or when a midpancreatic duct disruption has resulted in a distally located pseudocyst. Distal pancreatectomy for removal of a pseudocyst, with or without splenectomy, can be a challenging procedure in the setting of prior pancreatitis. An internal drainage procedure of the communicating duct, or of the pseudocyst itself, should be considered when distal resection is being contemplated.

    Pancreatic ascites results from a disrupted pancreatic duct with extravasation of pancreatic fluid that does not become sequestered as a pseudocyst but drains freely into the peritoneal cavity. Occasionally, the pancreatic fluid tracks superiorly into the thorax, causing a pancreatic pleural effusion. Both complications are seen more often in patients with chronic pancreatitis, rather than after acute pancreatitis. Paracentesis or thoracentesis reveals noninfected fluid with a protein level greater than 25 g/L and a markedly elevated amylase level.

    Paracentesis is critical to differentiate pancreatic from hepatic ascites.

    ERCP is most helpful to delineate the location of the pancreatic duct leak and to elucidate the underlying pancreatic ductal anatomy.

    Pancreatic duct stenting may be considered at the time of ERCP. Paracentesis and antisecretory therapy with the somatostatin analogue octreotide acetate, together with bowel rest and parenteral nutrition, is successful in more than half of patients. Reapposition of serosal surfaces to facilitate closure of the leak is considered a part of therapy, and this is accomplished by complete paracentesis. For pleural effusions, a period of chest tube drainage can facilitate closure of the internal fistula. Surgical therapy is reserved for those who fail to respond to medical treatment.

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  6. 6

    Acute Pancreatitis Classification Working Group. Revision of the Atlanta Classification of Acute Pancreatitis. 2010. Available at: [accessed 25.08.14].

    Beger H.G., Matsuno S., Cameron J.L. Diseases of the pancreas: Current surgical therapy. Berlin: Springer-Verlag; 2008.

    Beger H.G., Warshaw A.L., Buchler M.W., et al., eds. The pancreas: An integrated textbook of basic science, medicine, and surgery. ed 2nd Malden, MA: Blackwell Publishing; 2008.

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    Dellinger E.P., Tellado J.M., Soto N.E., et al. Early antibiotic treatment for severe acute necrotizing pancreatitis: A randomized, double-blind, placebo-controlled study. Ann Surg. 2007;245:674–683.

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    1  Not FDA approved for this  indication.

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Genomic Medicine UK is the home of comprehensive genomic testing in London. Our consultant medical doctors work tirelessly to provide the highest standards of medical laboratory testing for personalised medical treatments, genomic risk assessments for common diseases and genomic risk assessment for cancers at an affordable cost for everybody. We use state-of-the-art modern technologies of next-generation sequencing and DNA chip microarray to provide all of our patients and partner doctors with a reliable, evidence-based, thorough and valuable medical service.