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PANCREATITIS
INTRODUCTION
Pancreatitis is an inflammatory process of the pancreas; it can be acute or chronic.
Acute pancreatitis develops and resolves quickly, although in some cases it can be
recurrent and/or lead to chronic pancreatitis. Chronic pancreatitis develops slowly
worsens over time, and can cause serious complications. Alcohol abuse is the most
common cause of acute and chronic pancreatitis. The other causes of the disease include:
gallstones, toxic/metabolic issues, genetic, autoimmune, idiopathic, obstruction, and
recurrent pancreatitis itself, and other sources. Most of these – except for gallstones and
idiopathic pancreatitis – are very uncommon.
Treatment for acute pancreatitis is essentially symptomatic and supportive.
Occasionally, surgical and/or endoscopic treatment is needed. Chronic pancreatitis is also
treated with much the same symptomatic/supportive care, but surgical and endoscopic
treatments are also available.
OBJECTIVES
When the student has finished this module, she/he will be able to:
1. Identify the correct definition of pancreatitis.
2. Identify the differences between acute and chronic pancreatitis.
3. Identify four causes of acute pancreatitis.
4. Identify the two most common causes of acute pancreatitis.
5. Identify two relatively uncommon causes of acute pancreatitis.
6. Identify three common signs and symptoms of acute pancreatitis.
7. Identify a laboratory result that is used to confirm the diagnosis of acute pancreatitis.
8. Identify two serious complications of acute pancreatitis.
9. Identify four causes of chronic pancreatitis.
10. Identify the two most common causes of chronic pancreatitis.
11. Identify three signs and symptoms of chronic pancreatitis.
12. Identify two complications of chronic pancreatitis.
13. Identify three critical areas in the treatment of acute pancreatitis.
14. Identify three medical management techniques used to treat chronic pancreatitis.
15. Identify the two basic goals of surgical treatment of chronic pancreatitis.
THE PANCREAS
The pancreas is located partly in the left side of the abdomen and partly in the
epigastric area. The pancreas is both an endocrine gland (releasing its secretions directly
into the bloodstream) and an exocrine gland (releasing its secretions into a duct that leads
to the external environment which in this case is the gut).
Learning Break: Because the pancreas is not encapsulated, inflammation of the pancreas
can easily spread.
The pancreas produces digestive enzymes such as trypsin (which breaks down amino
acids), lipase (which breaks down fats), and amylase (which breaks down carbohydrates
and glycogen). These enzymes move through the pancreatic duct and into the duodenum.
The pancreas also produces insulin, glucagon, and somatostatin. Insulin is produced in
the β cells of the Islets of Langerhan. Insulin has many functions, but perhaps its most
important is to function as a transport molecule that allows for entry of glucose into the
cells. Glucagon, in contrast, causes serum glucose to rise by stimulating the conversion
and release of liver glycogen. Somatostatin is a hormone that regulates the release of
growth hormone and thyroid-stimulating hormone.
Learning Break: Inflammation and damage to the pancreas affects digestive function
and insulin function, causing malabsorption, various gastrointestinal signs/symptoms, and
diabetes mellitus.
EPIDEMIOLOGY
The exact incidence of pancreatitis is not known. Acute pancreatitis has been estimated
to result in approximately 3000,000 hospital admissions and 3200 deaths each year and to
affect 4.8 to 24.2 patients per 100,000.1 The statistics for chronic pancreatitis are less
abundant and less clear. Estimates of its incidence based on hospital discharge data
indicate that approximately 87,000 cases occur each year.2 The disease appears to affect
African-Americans more frequently than Caucasians, and it is almost twice as common
among men.3 Chronic pancreatitis occurs most frequently between ages 40 to 60.4 The
incidence of chronic pancreatitis, worldwide, appears to be growing,5 and some
authorities believe that the cause(s) of chronic pancreatitis are slowly and subtly shifting.6
PATHOPHYSIOLOGY
Both acute pancreatitis and chronic pancreatitis are caused by inflammation. However,
acute pancreatitis is caused by an acute inflammation, the clinical presentation is different
than that of chronic pancreatitis, and the disease most often – for the most part – resolves.
Chronic pancreatitis is caused by a chronic inflammation, this inflammation is
irreversible, and the clinical course and clinical presentation are different than that of
acute pancreatitis.7 There are several theories about the pathogenesis and progression of
the inflammation that causes pancreatitis, but the exact cause is not known.
ACUTE PANCREATITIS: THE CAUSES
Acute pancreatitis is caused by alcohol abuse, gallstones (these account for
approximately 80% of all cases),8 trauma to the pancreas, congenital anatomical
abnormalities, medications, toxins, medical procedures, infections, hypercalcemia, and
hypertriglyceridemia.9

Alcohol abuse: There is a strong relationship between alcohol abuse and acute
pancreatitis. Alcohol abuse is the second-most common cause of acute
pancreatitis, and accounts for approximately 36% of all cases.10 However, only a
small percentage of people (approximately 2%-3%) who are heavy drinkers
develop pancreatitis.11 The mechanism or mechanisms by which alcohol abuse
causes acute pancreatitis are not known. It may be that alcohol sensitizes the
pancreas making it more susceptible to injury.12 It is also possible that alcohol
abuse alone cannot cause acute pancreatitis; co-factors such as genetic
susceptibility, cigarette smoking, a high-lipid diet, and infections may be needed
to initiate the inflammatory process.13 Together, these may cause oxidative stress
that damages the pancreas.14
Learning Break: There is some evidence that acute pancreatitis caused by alcohol abuse
initiates chronic lesions in the pancreas, and patients with this disease are at a relatively
higher risk for developing chronic pancreatitis.

Gallstones: Gallstones are the most common cause of acute pancreatitis.15
Gallstones account for approximately 50% of all cases of acute pancreatitis.
Biliary pancreatitis appears to be related to the size of the gallstones and gender:
men who have gallstones develop acute pancreatitis more often than women who
have gallstones.16 No one is sure why gallstones cause pancreatitis; a likely
suspect is the reflux of infected bile into the pancreas that is caused by duct
obstruction by a gallstone. This would cause inflammation and obstruction of the
pancreatic duct which in turn would cause more inflammation and “autodigestion” of the pancreas by pancreatic enzymes.17

Hypercalcemia: Hypercalcemia caused by primary hyperparathyroidism is a very
rare cause of pancreatitis.18,19 There are other causes of hypercalcemia that have
been associated with acute pancreatitis, e.g., milk-alkali syndrome, but these are
not often seen. It is not clear why an elevated serum calcium level can, at times,
cause acute pancreatitis. It may be that excess calcium is deposited in the
pancreatic duct and creates an obstruction or the excess calcium may stimulate the
release of pancreatic enzymes and cause auto-digestion.20

Hypertriglyceridemia: Hypertriglyceridemia is another rare cause of acute
pancreatitis; it accounts for approximately 1% - 4% of all cases.21 Acute
pancreatitis usually occurs only after the serum triglycerides have reached t least
1000 mg/dL.

Drug-induced pancreatitis: Drug-induced pancreatitis is unusual; the incidence
has been estimated to be 1% - 4% of all cases of the disease.22 There are dozens of
drugs that have been implicated as causative agents for pancreatitis: methyldopa,
sulfonamides, tetracycline, furosemide, corticosteroids, octreotide, and estrogens
have all been mentioned and there are many others.23 However, many of these
cases appear to be anecdotal and idiosyncratic, and the association between drug
and disease not firmly established.24 Valproic acid is a commonly prescribed drug
and it is often mentioned as a possible cause of drug-induced pancreatitis, and
children seem to be especially at risk.25 However, there is still controversy over
whether or valproic acid actually causes pancreatitis and how commonly this
occurs and why it occurs.26

Post-ERCP acute pancreatitis: Endoscopic retrograde cholangiopancreatography
(ECRP) is an endoscopic and fluoroscopic procedure that is used diagnostically
and therapeutically for diseases of the biliary and pancreatic systems.
Approximately 5% of patients who have had ECRP will develop acute
pancreatitis after the procedure.27

Infections: Infections are an unusual cause of acute pancreatitis, accounting for
approximately 1% or less of all cases.28 Epstein-Barr virus, coxsackie virus,
measles, echovirus, and varicella zoster have all been associated with acute
pancreatitis.29

Trauma: Trauma is an infrequent (approximately 5%) cause of acute
pancreatitis.30

Anatomical abnormalities: Pancreas divisum is a common congenital abnormality
of the pancreatic duct. It is a rare cause of acute pancreatitis.31
These are among the most common causes of acute pancreatitis, but there are certainly
more. Cigarette smoking may be a risk factor for developing acute pancreatitis. Tumors
of the pancreas or the pancreatic duct, postoperative pancreatitis, autoimmune
pancreatitis, hereditary pancreatitis, cystic fibrosis, pancreatic cancer, idiopathic cases,
and infestation with ascaris (a parasitic worm that can cause duct obstruction) have also
been identified as possible, albeit relatively rare, causes of acute pancreatitis.32,33
SIGNS AND SYMPTOMS OF ACUTE PANCREATITIS
Acute pancreatitis typically manifests with acute abdominal pain, nausea, vomiting,
fever, and tachycardia.34 The abdominal pain is usually located in the upper abdomen and
occurs suddenly and without warning signs or symptoms. The white blood cell count is
often elevated, the serum calcium is low, and the serum glucose is high. The diagnosis is
confirmed if the serum amylase and/or lipase are elevated threefold or higher.35
CLINICAL COURSE AND PROGNOSIS OF ACUTE PANCREATITIS
For most patients acute pancreatitis is a relatively benign disease. Many patients have
one or two episodes and recover, but approximately 25% of all patients with the disease
have recurrent pancreatitis.36 Acute pancreatitis can also progress to chronic pancreatitis.
People who chronically abuse alcohol or smoke cigarettes and have acute pancreatitis
will often develop the chronic disease.37
However, although most cases of acute pancreatitis are mild, some patients do develop
severe acute pancreatitis (SAP). Approximately 20% of all patients admitted to a hospital
with acute pancreatitis have SAP.38 Mild cases of acute pancreatitis are associated with a
mortality rate of approximately < 5%, but SAP is associated with a mortality rate of up to
25%.39 Severe acute pancreatitis can cause shock, renal failure, bleeding, sepsis, and
multi-system organ failure. Death is usually caused by infected pancreatic necrosis.
Learning Break: Pancreatic necrosis is not one of the more common complications of
the disease, but infection of the necrotic pancreas is common, it is very serious, and
carries a high risk of morbidity and mortality.
It is difficult to predict which patients with mild acute pancreatitis will develop SAP
and none of the predictive criteria that have been developed have been proven to have
good negative predictive power, but suboptimal positive predictive power.40 Some of the
criteria that have been used to predict progression to SAP and mortality have included
patients who: are over the age of 70, who have a body mass index (BMI) >30; develop
any significant organ failure (e.g., renal failure, shock); are hemoconcentrated
(hematocrit > 44%); have elevated serum transaminases, serum glucose, and/or white
blood cell count.41,42
CHRONIC PANCREATITIS: THE CAUSES
There are six major etiologies for chronic pancreatitis: Toxic/metabolic, idiopathic,
genetic, autoimmune, recurrent and severe acute pancreatitis, and obstruction.
Collectively these are called the TIGAR-O classification system.43

Toxic/metabolic: Toxic/metabolic causes of chronic pancreatitis include chronic
alcohol abuse, cigarette smoking, medications, hypercalcemia, and
hyperlipidemia.44 Chronic alcohol abuse is the most common cause of chronic
pancreatitis; it accounts for approximately 70%-80% of all cases.45 Cigarette
smoking is also considered to be a significant cause of and/or contributing factor
to, the development of chronic pancreatitis.46
Learning Break: There is some evidence that obesity might increase the risk of
developing chronic pancreatitis if the patient also chronically abuses alcohol.

Idiopathic: Idiopathic pancreatitis is relatively common. Approximately 25%-30%
of all cases of chronic pancreatitis are considered to be idiopathic in etiology.47,48

Genetic: Genetic factors almost certainly do not act alone to cause chronic
pancreatitis, but they increase the susceptibility of the pancreas to stressors such
as cigarette smoking, drugs, elevated lipids, alcohol, etc.49 For example, these
genetic factors (or some of them) affect the control of the secretion of pancreatic
enzymes precursors such as trypsinogen and increased levels of these can cause
damage to the pancreas.50,51

Autoimmune: This is an uncommon cause of chronic pancreatitis. It accounts for
approximately 1% - 11% or less of all cases.52,53

Recurrent pancreatitis: As mentioned earlier, approximately 25% of all patients
with acute pancreatitis will develop chronic pancreatitis.

Obstruction: Obstruction that causes chronic pancreatitis can caused by a
congenital structural abnormality or blunt force trauma.54
There are other causes of chronic pancreatitis: Groove pancreatitis (an obstructive
form), tropical pancreatitis (associated with malnutrition), pancreatitis associated with
cystic fibrosis, and ectopic pancreatic tissue.55 These are very uncommon.
DIAGNOSING CHRONIC PANCREATITIS
Chronic pancreatitis is diagnosed using the clinical history (e.g., signs and symptoms,
risk factors such as the presence of gallstones or a history of chronic alcohol abuse), and
diagnostic procedures such as CT scan, endoscopic ultrasonography, MRI, or ERCP.
Magnetic resonance cholangiopancreatography is a non-invasive technique for imaging
the pancreas that is as effective as ECRP, but safer.
SIGNS AND SYMPTOMS OF CHRONIC PANCREATITIS
Most patients with chronic pancreatitis have severe abdominal pain. These attacks are
intermittent, unpredictable, and usually last several hours. Diarrhea and weight loss are
also common. Because the pancreatic enzyme secretion is disrupted, steatorrhea,
bloating, indigestion, and dyspepsia are common, as well.56
CLINICAL COURSE OF CHRONIC PANCREATITIS
The inflammation that occurs in chronic pancreatitis is progressive and irreversible,
and fibrosis of the pancreas is inevitable. The patient will suffer some degree, over time,
of exocrine and endocrine dysfunction.57,58 The overall survival rate of patients with
chronic pancreatitis at 10 years after diagnosis is 70% and 45% at 20 years; if the patient
is diagnosed at a relatively older age, smokes, and/or drinks alcohol, the prognosis is
worse.59
There are multiple complications associated with chronic pancreatitis.

Type 2 diabetes is possible; some sources indicate that chronic pancreatitis is a
common cause of type 2 diabetes, but some do not.60,61,62

Pancreatic pseudocyst: A pancreatic pseudocyst is a collection of fluid surrounded
by fibrous tissue. They are located in the body of the pancreas and connect to the
pancreatic duct system. They are a common complication of the disease, and they
occur in approximately 30% - 40% of all patients with chronic pancreatitis.63
Most pancreatic pseudocysts are caused by alcohol-related chronic pancreatitis.
They usually respond to symptomatic/supportive care and the pseudocyst
resolves, but infection, bleeding, fistulas, and obstruction are possible
complications.64

Exocrine dysfunction: The production of the pancreatic enzymes that are needed
for digestion can be significantly decreased without disrupting normal digestion.
However, patients with chronic pancreatitis often suffer from exocrine
dysfunction because of pancreatic insufficiency cause by the inflammation of the
disease. The dysfunction manifests as steatorrhea (excretion of > 6 grams of fat in
the feces each day), weight loss, vitamin A, D, E, and K deficiencies, bloating,
weight loss, and anorexia.65 Fat absorption is particularly affected in chronic
pancreatitis because lipase has a shorter half-life and is more rapidly degraded in
the gut than the other pancreatic enzymes.

Pancreatic cancer: The presence of chronic pancreatitis significantly increases an
individual’s risk of developing pancreatic cancer by as much as 26-fold, and if the
patient has hereditary pancreatitis, this risk is almost 50-fold.66 For most patients,
although the risk of developing pancreatic cancer is much worse than that of the
general population, it is still uncommon.67
Other complications which can be seen but are uncommon include pancreatic-pleural
fistulas, bile duct fistulas, pseudoaneurysm, common bile duct stenosis, and splenic and
portal venous obstruction.68
TREATMENT OF ACUTE PANCREATITIS
Acute pancreatitis is treated with symptomatic and supportive care. A useful acronym
for remembering the therapeutic approach to treating acute pancreatitis is PANCREAS.69

Perfusion: The patient should receive fluid support that maintains urine output of
0.5 – 1.0 ml/kg per hour. Fluid therapy is crucial for ensuring the patient
health and reducing complications. Patients with acute pancreatitis are often
dehydrated and may not be able to tolerate oral intake; hypovolemia reduces
microcirculation and can cause hemoconcentration, hypotension, decreased renal
perfusion, and prerenal azotemia.70,71 The patient should receive supplemental
oxygen, if needed, to ensure oxygen saturation > 95%.

Analgesia: Pain control is a critical area in treating acute pancreatitis. Pain is
managed with parenteral narcotics, e.g., morphine, fentanyl, and hydromorphone.
There is no evidence that one drug is more effective than another.72

Nutrition: Nutrition is critical for ensuring patient health and good outcomes.
The patient has high metabolic needs and is often unable or unwilling to eat.
Good nutrition lowers the risk of mortality.73 Oral, feedings, jejeunal tube
feedings, or total parenteral nutrition may be used.

Clinical: This refers to careful assessment and triage of all cases of acute
pancreatitis. The goal is to identify patients who have a high risk for complication
and/or death.

Radiology: Imaging studies should be used to detect complications such as
necrosis.

ECRP: ECRP should be performed if it is suspected that the patient has
cholangitis or obstruction.

Antibiotics: Prophylactic antibiotics have been used in the past when the patient
with acute pancreatitis had, or was suspected to have, pancreatic necrosis. The
goal was to prevent infection and sepsis. However, this approach is no longer
recommended. Several large studies found that morbidity and mortality rateswere
not improved by the use of prophylactic antibiotics.74,75 unless a needle biopsy
and aspiration confirms the presence of an infection involving 30% or more of the
pancreas.76

Surgery: Surgery is indicated if the patient with acute pancreatitis has not
responded to symptomatic, supportive care and conservative management.77
Surgery is also indicated if the patient suffers from a perforation, hemorrhage, an
infected, necrotic pancreas with sepsis, or biliary pancreatitis.78
Learning Break: Octreotide is a synthetic version of somatostatin. Somatostatin inhibits
pancreatic exocrine secretion. Some physicians have used octreotide to treat patients with
chronic pancreatitis; the rationale has been that inhibition of pancreatic enzyme secretion
allows the inflamed pancreas to rest. Some clinical trials have shown octreotide to be
useful, others have not. Currently there is no conclusive evidence that it provides any
benefit to patients with chronic pancreatitis.79
TREATMENT OF CHRONIC PANCREATITIS
Chronic pancreatitis can be treated with medical management or with surgery.
Medical Treatment
Medical management of chronic pancreatitis starts with lifestyle changes. The patient
should be encouraged to stop drinking alcohol if this is appropriate and to stop smoking.
Special diets – particularly low-fat diets and low-protein – may help decrease pain.
Vitamin D supplements may be helpful to prevent osteopathy. Analgesics should be used
to alleviate pain.
Pancreatic enzyme replacement therapy has long been used to provide symptomatic
relief for patients with chronic pancreatitis who have with exocrine dysfunction and
steaorrhea. It has been proven to improve malabsoprtion and decrease steatorrhea.80
Pancrelipase is a commonly used pancreatic enzymes preparation. These are most often
given as enteric-coated oral capsules.
Learning Break: Pancrelipase (Creon® is a common brand name) is a combination of
amylase, lipase and protease. It is supplied as a capsule (there are varying strengths). The
dosing for adults is individualized and will depend on the patient’s symptoms and the
amount of steatorrhea that is present. The drug is taken several times a day with meals or
food. Bloating, abdominal pain, diarrhea, and constipation are common side effects.
Enzyme replacement therapy has also been used to try and treat the pain caused by
chronic pancreatitis. This therapy has been less successful, and the available data gives
conflicting result as to its effectiveness for treating pain.81,82
Celiac plexus blockade (CPB) is another medical approach for treating chronic
pancreatitis. This technique involves endoscopic, ultrasound-guided administration of a
corticosteroid and a local anesthetic into the celiac plexus. This a group of nerves that
innervates abdominal organs, blood vessels, etc. CPB is used after other medial
management techniques have failed to treat pain experienced by patients with chronic
pancreatitis. The nerve can also be destroyed by injecting an absolute alcohol; this
process is called celiac plexus neurolysis. The techniques are usually done as out-patient
procedures, they do not take long (approximately 30 minutes) and there are few
complications.83 CPB appears to be effective for about 50% of patients with chronic
pancreatitis, and the patients are pain-free for an average of three to six months.84,85
Surgical Treatment
There is a wide a variety of surgical procedures that be used to treat chronic
pancreatitis. These can include endoscopic procedures and traditional surgery. Although
both approaches can be useful, several studies have indicated that traditional surgery is
more effective at relieving pain, provides longer-lasting pain relief, and improves quality
of life to a greater degrees than endoscopic procedures.86,87 Endoscopic treatment,
however, does have its place. For example patients with certain simple pancreatic
strictures that obstruct flow are good candidates for endoscopic dilating and stenting, but
patient s with complex strictures and stones are better treated with surgery.88
Surgical procedures for chronic pancreatitis are designed to decompress the
pancreas by drainage, to resect the pancreas (if there is a tumor, duct anomalies,
significant inflammation), or to do a combination of both.89 An example of drainage
procedures is the lateral pancreaticojejunostomy (basically an anastomosis of the
pancreatic duct and the jejunum); an example of a resection procedure is the partial
pancreatoduodectomy (the head of the pancreas and part of the duodenum are excised);
an example of a combination procedure is the Berger procedure (part of the pancreas is
removed, but the duodenum is preserved and there is reconstruction to allow for
pancreatic drainage).90,91
NURSING CARE OF THE PATIENT WITH PANCREATITIS
Nursing care of the patient with pancreatitis should focus on these areas: evaluation
and assessment for possible complications; pain control; elimination; fluid and electrolyte
status; nutrition; patient education about lifestyle issues.

Evaluation and assessment for possible complications: These would include
infection, sepsis, diabetes, nausea and vomiting, and intractable pain.

Pain control: This is a critical area to focus on. People with pancreatitis are often
in severe pain and require narcotic analgesics. The nurse will need to understand
the patient’s pain pattern, individual expression of pain, tolerance for pain, and
response to analgesics. Serious side effects and dependency are possible, and the
patient with chronic pancreatitis may need to use narcotic analgesics for many
years, and needs education about these issues. This patient would need help, as do
many people with chronic pain, in learning how to integrate the pain experience
and its treatment into daily life.

Elimination: Many patients with pancreatitis suffer from diarrhea and steatorrhea.
Skin integrity and perineal comfort can be concerns as can maintaining adequate
hydration.

Fluid and electrolyte status: It is very important for patients with pancreatitis to be
well hydrated. The RN must be well aware of this, monitor the patient’s fluid
status closely, and educate the patient about the need for adequate fluid intake.

Nutrition: The RN must closely monitor the patient’s nutrition status and educate
the patient about the need for good nutrition.

Lifestyle issues: Alcohol abuse, cigarette smoking, and (quite possibly because of
the association with obesity and gallstones) obesity play a role in initiating,
prolonging, and aggravation the process of pancreatitis. Part of the cure for the
disease is lifestyle modification, and the RN needs to make sure that the patient
for whom these lifestyle issues are contributing factors to the disease is aware of
this. The RN must also be sure that the patient has the resources needed to make
healthy choices and changes.
SUMMARY













Pancreatitis is an inflammation of the pancreas.
Pancreatitis can be acute or chronic.
Most cases of acute pancreatitis resolve.
Acute pancreatitis can cause residual scarring, some people have recurrent acute
pancreatitis, and some develop chronic pancreatitis.
Acute pancreatitis has many causes: by far the most common are alcohol abuse
and gallstones.
Acute pancreatitis can be complicated by necrosis and infection and severe acute
pancreatitis (SAP).
Chronic pancreatitis does not resolve; it gets progressively worse.
The most common causes of chronic pancreatitis are alcohol abuse and idiopathic
chronic pancreatitis.
Chronic pancreatitis can be complicated by exocrine and endocrine dysfunction,
necrosis and infection, and pancreatic cancer.
Acute pancreatitis is treated with fluids, analgesics, and good nutrition.
Acute pancreatitis with complications can be treated with surgery or endoscopic
procedures.
Chronic pancreatitis is treated medically with supportive care, enzyme therapy,
analgesics, and occasionally celiac plexus blockade.
Chronic pancreatitis is treated surgically by procedures for drainage and resection.
REFERENCES
1. Banks PA, Conwell DL, Toskes PP. The management of acute and chronic
pancreatitis. Gastroenterology & Hepatology. 2010;6:1-16.
2. Obideen K, Wehbi M. Pancreatitis, chronic. eMedicine. December 22, 2009.
http://emedicine.medscape.com/article181554.
Accessed September 6, 2010.
3. Obideen K, Wehbi M. Pancreatitis, chronic. eMedicine. December 22, 2009.
http://emedicine.medscape.com/article181554.
Accessed September 6, 2010.
4. Banks PA, Conwell DL, Toskes PP. The management of acute and chronic
pancreatitis. Gastroenterology & Hepatology. 2010;6:1-16.
5. Jupp J, Fine D, Johnson CD. The epidemiology and socioeconomic impact of chronic
pancreatitis. Best Practice & Clinical Research Gastroenterology. 2010;24:219-231.
6. Pezzilli R. Etiology of chronic pancreatitis: has it changed in the last decade? World
Journal of Gastroenterology. 2009;15:4737-4740.
7. Obideen K, Wehbi M. Pancreatitis, chronic. eMedicine. December 22, 2009.
http://emedicine.medscape.com/article181554.
Accessed September 6, 2010.
8. Banks PA, Conwell DL, Toskes PP. The management of acute and chronic
pancreatitis. Gastroenterology & Hepatology. 2010;6:1-16.
9. Banks PA, Conwell DL, Toskes PP. The management of acute and chronic
pancreatitis. Gastroenterology & Hepatology. 2010;6:1-16.
10. Wang GJ, Gao CF, Wei D, Wang C, Ding SQ. Acute pancreatitis: Etiology and
common pathogenesis. World Journal of Gastroenterology. 2009;15:1427-1430.
11. Banks PA, Conwell DL, Toskes PP. The management of acute and chronic
pancreatitis. Gastroenterology & Hepatology. 2010;6:1-16.
11. Banks PA, Conwell DL, Toskes PP. The management of acute and chronic
pancreatitis. Gastroenterology & Hepatology. 2010;6:1-16.
12. Clemens DL. Mahan KJ. Alcoholic pancreatitis: Lessons from the liver. World
Journal of Gastroenterology. 2010;16:1314-1320.
13. Clemens DL. Mahan KJ. Alcoholic pancreatitis: Lessons from the liver. World
Journal of Gastroenterology. 2010;16:1314-1320.
14. Obideen K, Wehbi M. Pancreatitis, chronic. eMedicine. December 22, 2009.
http://emedicine.medscape.com/article181554.
Accessed September 6, 2010.
15. Hazem Z. Acute biliary pancreatitis: Diagnosis and treatment. Saudi Journal of
Gastroenterology. 2009;15:147-155.
16. Hazem Z. Acute biliary pancreatitis: Diagnosis and treatment. Saudi Journal of
Gastroenterology. 2009;15:147-155.
17. Hazem Z. Acute biliary pancreatitis: Diagnosis and treatment. Saudi Journal of
Gastroenterology. 2009;15:147-155.
18. Wang GJ, Gao CF, Wei D, Wang C, Ding SQ. Acute pancreatitis: Etiology and
common pathogenesis. World Journal of Gastroenterology. 2009;15:1427-1430.
19. Lenz JI, Jacobs JM, Op de Beeck B, Huyghe IA, Pelckmans PA, Moreels TG. Acute
necrotizing pancreatitis as first manifestation of primary hyerparathyroidism. World
Journal of Gastroenterology. 2100;16:2959-2962.
20. Lenz JI, Jacobs JM, Op de Beeck B, Huyghe IA, Pelckmans PA, Moreels TG. Acute
necrotizing pancreatitis as first manifestation of primary hyerparathyroidism. World
Journal of Gastroenterology. 2100;16:2959-2962.
21. Hahn SJ, Park JH, Lee JH, Lee JK, Kim KA. Sever hypertriglyceridemia in diabetic
ketoacidosis accompanied by acute pancreatitis: a case report. Korean Journal of Medical
Science. 2010;25:1375-1378.
22. Lankisch PG, Dröge M, Gottesleben F. Drug induced pancreatitis: incidence and
severity. Gut. 1995; 37:565-567.
23. Tonsi AF, Bacchion M, Crippa S, Malleo G, Bassi C. Acute pancreatitis at the
beginning of the 21st century: the state of the art. World Journal of Gastroenterology.
2009;15:2945-2959.
24. Wilmink T, Frick TW. Drug-induced pancreatitis. Drug Safety. 1996.14:406-423.
25. Werlin SL, Fish SL. The spectrum of valproic acid-associated pancreatitis. Pediatrics.
2006;118:1660-1663.
26. Nørgaard M, Jacobsen J, Ratanajamit C, Jepsen P, McLaughlin JK, Pedersen L,
Søresnsen HT. Valproic acid and risk of acute pancreatitis: a population-based casecontrol study. American Journal of Therapeutics. 2006;13:113-117.
27. Freeman ML, Nelson DB, Sherman S, Haber GB, Herman ME, Dorsher PJ, et al.
Complications of endoscopic biliary sphincterectomy. New England Journal of Medicine.
1996;335:909-918.
28. Tonsi AF, Bacchion M, Crippa S, Malleo G, Bassi C. Acute pancreatitis at the
beginning of the 21st century: the state of the art. World Journal of Gastroenterology.
2009;15:2945-2959.
29. Parenti DM, Steinberg W, Kang P. Infectious causes of acute pancreatitis. Pancreas.
1996;13:356-371.
30. Tonsi AF, Bacchion M, Crippa S, Malleo G, Bassi C. Acute pancreatitis at the
beginning of the 21st century: the state of the art. World Journal of Gastroenterology.
2009;15:2945-2959.
31. Tonsi AF, Bacchion M, Crippa S, Malleo G, Bassi C. Acute pancreatitis at the
beginning of the 21st century: the state of the art. World Journal of Gastroenterology.
2009;15:2945-2959.
32. Shanbhogue AKP, Fasih N, Srahabi VR, Doherty GP, Shanbhogue DKP, Sethi SK. A
clinical and radiologic review of uncommon types and causes of pancreatitis.
RadioGraphics. 2009;29:1003-1026.
34. Tonsi AF, Bacchion M, Crippa S, Malleo G, Bassi C. Acute pancreatitis at the
beginning of the 21st century: the state of the art. World Journal of Gastroenterology.
2009;15:2945-2959.
35. Greenberger NJ, Toskes PP. Acute and chronic pancreatitis. In: Fauci AS, Braunwald
E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo J, eds. Harrison’s Principles
of Internal Medicine. 17th ed. New York, New York. McGraw-Hill;2008:2004-2017.
36. Greenberger NJ, Toskes PP. Acute and chronic pancreatitis. In: Fauci AS, Braunwald
E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo J, eds. Harrison’s Principles
of Internal Medicine. 17th ed. New York, New York. McGraw-Hill;2008:2004-2017.
37. Lankisch PG, Breuer N, Bruns A Weber- Dany B, Lowenthal AB, Maisonneuve P.
Natural history of acute pancreatitis: a long-term population-based study. American
Journal of Gasteroenterology. 2009;104:2797-2805.
38. Gravante G, Garcea G, Ong SL, Berry DP, Lloyd DM, Dennison AR. Prediction of
mortality in acute pancreatitis: a systematic review of the published evidence.
Pancreatology. 2009;9:601-614.
39. Gravante G, Garcea G, Ong SL, Berry DP, Lloyd DM, Dennison AR. Prediction of
mortality in acute pancreatitis: a systematic review of the published evidence.
Pancreatology. 2009;9:601-614.
40. Gravante G, Garcea G, Ong SL, Berry DP, Lloyd DM, Dennison AR. Prediction of
mortality in acute pancreatitis: a systematic review of the published evidence.
Pancreatology. 2009;9:601-614.
41. Greenberger NJ, Toskes PP. Acute and chronic pancreatitis. In: Fauci AS, Braunwald
E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo J, eds. Harrison’s Principles
of Internal Medicine. 17th ed. New York, New York. McGraw-Hill;2008:200542. Tonsi AF, Bacchion M, Crippa S, Malleo G, Bassi C. Acute pancreatitis at the
beginning of the 21st century: the state of the art. World Journal of Gastroenterology.
2009;15:2945-2959.
43. Banks PA, Conwell DL, Toskes PP. The management of acute and chronic
pancreatitis. Gastroenterology & Hepatology. 2010;6:1-16.
44. Banks PA, Conwell DL, Toskes PP. The management of acute and chronic
pancreatitis. Gastroenterology & Hepatology. 2010;6:1-16.
45. Spanier BW, Dijkgraaf MG, Bruno MJ. Epidemiology, aetiology and outcome of
acute and chronic pancreatitis: an update. Best Practice & Research Clinical
Gastroenterology. 2008;22:45-63.
46. Tolstrup JS, Kristiansen L, Becker U, Grønbaek M. Smoking and risk of acute and
chronic pancreatitis among women and men: a population-based cohort study. Archives
of Internal Medicine. 2009;169:603-609.
47. Keller J, Layer P. Idiopathic chronic pancreatitis. Best Practice & Research Clinical
Gastroenterology. 2008;22:105-113.
48. Obideen K, Wehbi M. Pancreatitis, chronic. eMedicine. December 22, 2009.
http://emedicine.medscape.com/article181554.
Accessed September 6, 2010.
49. Whitcomb DC. Genetic aspects of pancreatitis. Annual Review of Medicine.
2010;61:413-424.
50. Whitcomb DC. Genetic aspects of pancreatitis. Annual Review of Medicine.
2010;61:413-424.
51.Obideen K, Wehbi M. Pancreatitis, chronic. eMedicine. December 22, 2009.
http://emedicine.medscape.com/article181554.
Accessed September 6, 2010.
52. Shanbhogue AKP, Fasih N, Srahabi VR, Doherty GP, Shanbhogue DKP, Sethi SK. A
clinical and radiologic review of uncommon types and causes of pancreatitis.
RadioGraphics. 2009;29:1003-1026.
53.Obideen K, Wehbi M. Pancreatitis, chronic. eMedicine. December 22, 2009.
http://emedicine.medscape.com/article181554.
Accessed September 6, 2010.
54. Obideen K, Wehbi M. Pancreatitis, chronic. eMedicine. December 22, 2009.
http://emedicine.medscape.com/article181554.
Accessed September 6, 2010.
55. Shanbhogue AKP, Fasih N, Srahabi VR, Doherty GP, Shanbhogue DKP, Sethi SK. A
clinical and radiologic review of uncommon types and causes of pancreatitis.
RadioGraphics. 2009;29:1003-1026.
56. Banks PA, Conwell DL, Toskes PP. The management of acute and chronic
pancreatitis. Gastroenterology & Hepatology. 2010;6:1-16.
57. Bachman K, Mann O, Izbicki JR, Strate T. Chronic pancreatitis – a surgeon’s view.
Medical Science Monitor. 2008;14:RA198-RA205.
58. Büchler MW, Martignoni ME, Friess H, Malfertheiner P. A proposal for a new
clinical classification of Chronic pancreatitis. BMC Gastroenterology. 2009;9:93
59. Obideen K, Wehbi M. Pancreatitis, chronic. eMedicine. December 22, 2009.
http://emedicine.medscape.com/article181554. Accessed September 6, 2010.
60. Angelopoulos N, Dervenis C, Goula A, Rombopoulos G, Livadas S, Klatsas D, et al.
Endocrine pancreatic insufficiency in chronic pancreatitis. Pancreatology. 2005;5:122131.
61. Khan AN, McDonald S, Sheen AJ. Pancreatitis, chronic. eMedicine. March 12, 2009.
http://emedicine.medscape.com/article/371772-overview Accessed September 14, 2010.
62. Büchler MW, Martignoni ME, Friess H, Malfertheiner P. A proposal for a new
clinical classification of chronic pancreatitis. BMC Gastroenterology. 2009;9:93.
http://www.biomedcentral.com/content/pdf/1471-230X-9-93.pdf.
Accessed September 12, 2010.
63. Habashi S, Draganov PV. Pancreatic pseudocyst. World Journal of Gastroenterology.
2009;15:38-47.
64. Habashi S, Draganov PV. Pancreatic pseudocyst. World Journal of Gastroenterology.
2009;15:38-47.
65. Pezzilli R. Chronic pancreatitis: maldigestion, intestinal ecology and intestinal
inflammation. World Journal of Gastroenterology. 2009;15:1673-1676.
66. Erickson RA, Larson CL, Shabahang M. Pancreatic cancer. eMedicine. September 1,
2010. http://emedicine.medscape.com/article/280605-overview. Accessed September 15,
2010.
67. Lowenfels AB, Maisonneuve P, Cavillini G, Amman RW, Lankisch PG, Anderson
JR, et al. Pancreatitis and the risk of pancreatic cancer. International Pancreatitis Study
Group. New England Journal of Medicine. 1993;328:1433-1437.
68. Pezzilli R, Bini L, Fantini L, Baroni E, Campana D, Tomasetti P, et al. Quality of life
in chronic pancreatitis. World Journal of Gastroenterology. 2006;12:6249-6251.
69. Khaliq A, Dutta U, Kochhar R, Singh K. Management of acute pancreatitis:
‘PANCREAS’ contains eight easy steps to remember the treatment. Journal of Pancreas
Online. 2010;11:492-493.
70. Banks PA, Conwell DL, Toskes PP. The management of acute and chronic
pancreatitis. Gastroenterology & Hepatology. 2010;6:1-16.
71. American Gastroenterological Association (AGA) Institute. AGA Institute position
statement on acute pancreatitis. Gastroenterology. 2007;132:2019-2021.
72. Banks PA, Freeman ML. Practice guidelines in acute pancreatitis. American Journal
of Gastroenterology. 2006;101:2379-2400.
73. Al-Omran M, Albalawi ZH, Tashkandi MF, Al-Ansary LA. Enteral versus parenteral
nutrition for acute pancreatitis. Cochrane Database of Systematic Reviews.
2010;1:CD002837.
74. Bai Y, Gao J, Zou DW, Li ZS. Prophylactic antibiotics cannot reduce infected
pancreatic necrosis and mortality in acute necrotizing pancreatitis: evidence from a metaanalysis of randomized controlled trials. American Journal of Gastroenterology.
2008;103:104-110.
75. Villatoro E, Bassi C, Larvin M. Antibiotic therapy for prophylaxis against infection
of pancreatic necrosis in acute pancreatitis. Cochrane Database of Systematic Reviews.
2006;CD002941.
76. Forsmark CE, Baillie J. AGA Institute technical review on acute pancreatitis.
Gastroenterology. 2007;132:2022-2044.
77. Kleespies A, Thasler WE, Schäfer C, Meimarakis G, Eichorn ME, Bruns CJ, et al.
Acute pancreatitis: is there a need for surgery? Z Gastroenterology. 2008;46:790-798.
78. Kleespies A, Thasler WE, Schäfer C, Meimarakis G, Eichorn ME, Bruns CJ, et al.
Acute pancreatitis: is there a need for surgery? Z Gastroenterology. 2008;46:790-798.
79. Banks PA, Conwell DL, Toskes PP. The management of acute and chronic
pancreatitis. Gastroenterology & Hepatology. 2010;6:1-16.
80. Waljee AK, Dimagno MJ, Wu BU, Scoenfeld PS, Conwell DL. Systematic review:
pancreatic enzyme treatment of malabsorption associated with chronic pancreatitis.
Alimentary Pharmacology & Therapeutics. 2009;29:235-246.
81. Ferrone M, Raimondo M, Scolapio JS. Pancreatic enzyme pharmacotherapy.
Pharmacotherapy. 2007;27:910-920.
82. Shafiq N, Rana S, Bhasin D, Pandhi P, Srivastata P. Sehmby SS, et al. Pancreatic
enzymes for chronic pancreatitis. Cochrane Database of Systematic Reviews.
2009;7:CD006302.
83. Yoo BM, Lehman GA. Update on endoscopic treatment of chronic pancreatitis.
Korean Journal of Internal Medicine. 2009;24:169-179.
84. Kaufman M, Singh G, Das S, Concha-Parra R, Erber J, Micames C, et al. Efficacy of
endoscopic ultra-sound-guided celiac plexus block and celiac neurolysis for managing
abdominal pain associated with chronic pancreatitis and pancreatic cancer. Journal of
Clinical Gastroenterology. 2010;44:127-144.
85. Yoo BM, Lehman GA. Update on endoscopic treatment of chronic pancreatitis.
Korean Journal of Internal Medicine. 2009;24:169-179.
86. Cahne DL, Gouma DJ, Nio Y, Rauws EA, Boermeester MA, Busch OR, et al.
Endoscopic versus surgical drainage of the pancreatic duct in chronic pancreatitis. New
England Journal of Medicine. 2007;356:676-684.
87. Dite P, Ruzicka M, ZborilV, Novotny A. A prospective, randomized trial comparing
endoscopic and surgical therapy for chronic pancreatitis. Endoscopy. 2003;35:553-558.
88. Yoo BM, Lehman GA. Update on endoscopic treatment of chronic pancreatitis.
Korean Journal of Internal Medicine. 2009;24:169-179.
89. Bachman K, Mann O, Izbicki JR, Strate T. Chronic pancreatitis – a surgeon’s view.
Medical Science Monitor. 2008;14:RA198-RA205.
90. Bachman K, Mann O, Izbicki JR, Strate T. Chronic pancreatitis – a surgeon’s view.
Medical Science Monitor. 2008;14:RA198-RA205.
91. Banks PA, Conwell DL, Toskes PP. The management of acute and chronic
pancreatitis. Gastroenterology & Hepatology. 2010;6:1-16.