Resident Version
Acute and Chronic Pancreatitis Module
Created by Dr. Teodora Konstantinova
Objectives:
1. List two differences in the diagnosis of acute and chronic pancreatitis.
2. Name 4 risk factors for developing pancreatitis
3. List two differences between treatment approaches to acute and chronic
pancreatitis
4. Use Ranson criteria to predict severity of acute pancreatitis.
References:
1. Whitcomb D. C., Acute pancreatitis, N Engl J Med 2006, 354:2142-2150
2. Steinberg W, Tenner S, Medical Progress: Acute pancreatitis, NEnglJMed 1994,
330:1198-1210
3. Michael L. Steer, MD, Irving Waxman, MD and Steve Freedman, MD, Medical
progress: Chronic Pancreatitis, N Engl J Med 1995, 332:1482-1490
4. Ranson JH, Diagnostic Standards for Acute Pancreatitis World J Surg 1997,
21:136-42
CASE:
HPI: A 60 yo female presents to the ER with severe mid-epigastric pain with radiation to
the back, nausea and vomiting that started after lunch the previous day. Vomiting did not
relieve the pain. The patient also reports coughing with yellow sputum for about a day.
She doesn’t report fever, but states she has “chills” post emesis.
PMH:
HTN, depression, GERD, and menopausal symptoms requiring hormone replacement
therapy (HRT). The patient also recently completed a course of nitrofurantoin for
cystitis.
PSH: cholecystectomy 6 months ago.
Social hx: Patient has no history of alcohol abuse.
Medications: Lisinopril, Paxil, cimetidine, estrogen and completed course of
nitrofurantoin 2 days ago.
Physical exam: VS: 100/60, P- 110, R-16, T-37.0 C, P02 - 87 % on RA.
The exam is significant for left lower lung field rales and egophany. The patient also had
moderate mid-epigastric and RUQ tenderness without rebound or guarding. The rest of
the exam is unremarkable.
Labs:
wbc: 16.5, H/H: 12/45
electrolytes are WNL
SGOT/SGPT: 500/400 U/l, alkaline phosphatase 400 U/l , total Bi 2.0 mg/dL
LDH: 860 IU per liter, serum lipase-5000, serum amylase- 2000, TG- 300
UA which is neg for LCE, nitrites, bacteria, WBCs or RBCs.
1. At this point in your evaluation, what should you initially be concerned about?
2. What could be the etiologies of this patient’s pancreatitis?
3. What radiologic studies should you consider obtaining?
4. Are you able to calculate your patient’s Ranson’s score?
Discussion Outline:
I. Differences between acute and chronic pancreatitis:
Acute and chronic pancreatitis are distinguished from each other on the basis of structural
and functional criteria.
1. Acute pancreatitis is an inflammatory condition of the pancreas. Acute disease is
characterized by a normal pancreas that becomes inflamed prior to the attack and once
the attack resolves the pancreas returns to normal.
2. Chronic pancreatitis is a progressive disorder of the pancreas that causes destruction
of the pancreas. It involves long-term inflammation and scarring of the pancreas that is
irreversible.
II. Pathogenesis:
Acute pancreatitis:
1. It relates to inappropriate activation of trypsinogen to trypsin (the key enzyme in the
activation of pancreatic zymogens and a lack of prompt elimination of active trypsin
inside the pancreas.
2. Activation of digestive enzymes causes pancreatic injury and results in an
inflammatory response that is out of proportion to the response of other organs to a
similar insult.
3. The acute inflammatory response itself causes substantial tissue damage and may
progress beyond the pancreas to a systemic inflammatory response syndrome, multiorgan
failure and death.
Chronic pancreatitis:
1. The hypersecretion of protein from acinar cells in the absence of increased fluid or
bicarbonate secretion from duct cells is characteristic of chronic pancreatitis.
2. Plugs formed by the precipitation of protein within the interlobular and intralobular
ducts are an early finding.
3. The plugs contain multiple proteins (digestive enzymes, glycoproteins, and acidic
mucopolysaccharides).
4. The precipitation of calcium carbonate in the plugs results in the formation of
intraductal stones (this is more common in patients with alcohol-induced or tropical
pancreatitis).
5. Patients with idiopathic chronic pancreatitis frequently have an elevated pressure in the
pancreatic duct.
III. Causes of pancreatitis:
1. Gallstones (45 % of cases)
2. Alcohol (35 % of cases)
3. Drugs: Azathioprine, Mercaptopurine, Valproic acid, Estrogen, Tetracyclines,
Metronidazole, Nitrofurantion, Pentamidine, Lasix, Sulfonamides, Methyldopa,
Cimetidine, Ranitidine, Salicylates, Erythromycin
4. Metabolic abnormalities: Hypercalcemia, Hypertriglyceridemia
5. Trauma: accidental or iatrogenic (ERCP, postoperative, endoscopic sphincterotomy)
6. Infections:
Parasitic (ascariasis, clonorchiasis)
Viral (mumps, rubella, Hepatitis A, B, non-A, non-B, coxsackievirus B, Echo virus,
adenovirus, varicella, Epstein-Barr virus, HIV virus)
Bacterial: (mycoplasma, Campylobacter jejuni, Mycobacterium tuberculosis, Legionella,
Leptospirosis)
7. Miscellaneous causes: penetrating PUD, Crohn’s disease, Reye’s syndrome, cystic
fibrosis)
8. Idiopathic (10% of cases)
IV. Diagnosis
Diagnosis of acute pancreatitis:
1. Characteristic abdominal pain (begins in the upper abdomen and spreads through the
back)
2. Nausea and vomiting (usually the vomiting doesn’t relief the pain)
3. Elevated serum levels of pancreatic enzymes (amylase and lipase)
4. Both enzymes remain elevated with ongoing pancreatic inflammation, with amylase
level typically returning to normal shortly before lipase levels in the resolution phase.
5. Imaging:
- Ultrasound of the abdomen remains the most sensitive method of evaluating the
biliary tract in acute pancreatitis. It has a sensitivity of 67% in the urgent diagnosis, and a
specificity of 100%.
- CT scan is the imaging method of choice in delineating the pancreas, as well as
in determining the severity and complications.
- ERCP plays a part in diagnosis in patients in whom no definite cause is found.
Abnormalities revealed by this study include small pancreatic tumors, pancreatic ductal
strictures, gallstones, pancreas divisum, sphincter of Oddi dysfunction.
Diagnosis of chronic pancreatitis:
1. In developed countries, most patients with chronic pancreatitis have a history of
prolonged and heavy alcohol use. They typically have recurrent attacks of upper
abdominal pain, which may radiate to the mid-back, nausea and vomiting.
2. 10-20 % of patients have “painless” pancreatitis. They may present with DM,
jaundice, malabsorption, steatorrhea with weight loss.
3. Malabsorption resulting from exocrine insufficiency may cause fecal fat excretion to
be elevated. Undigested fat is qualitatively detected by Sudan staining of feces.
4. Routine blood studies (such as amylase, lipase) do not necessary show elevations.
5. Plain film of the abdomen: The finding of pancreatic calcification is virtually
diagnostic of chronic pancreatitis, but often this is not found.
6. There are several other tests: US, CT scan of the pancreas, ERCP, EUS, MRCP, MRI
7. ERCP is the gold-standard imaging procedure for the diagnosis of chronic pancreatitis
and planning treatment.
V. Treatment:
Acute pancreatitis:
1. Supportive therapy, vigorous IVF hydration, possible use of NG (especially with ileus
and severe vomiting), correction of electrolytes.
2. Immediate endoscopic removal of impacted stones in patients with severe disease
appears to reduce mortality.
3. Use of antibiotics: A potential role for prophylactic use of antibiotics in severe acute
pancreatitis was initially given support by a randomized trial demonstrating that
imipenem reduces infection complications.
Recent randomized trial failed to demonstrate differences in outcome among patients
treated with Cipro and Flagyl, as compared with placebo, leading some experts to
recommend against routine use of prophylactic antibiotics.
4. Nutritional support: ensuring adequate nutrition is important in patients with severe or
complicated pancreatitis. Recent meta-analysis of 6 randomized trials involving a total of
263 patients demonstrated improved outcomes with enteral nutrition, including decreased
rate of infections and surgical interventions, reduce length of hospital stay, reduced costs.
5. Decision on the appropriateness of surgical management of sterile necrotic tissue
should be made on a case-by-case basis, however, infected necrotic tissue and infected
collections of fluid are best treated by surgical debridement.
Chronic pancreatitis:
1. Pain: abstinence from alcohol, administration of analgesic medications, and nerve
blocks. Exocrine insufficiency may lead to increased cholecystokinin-mediated
stimulation of the pancreas. This process theoretically could be interrupted by
administration of digestive enzymes (trypsin, cholecystokinin receptor antagonists, or
somatostatin).
2. When the pain persists in spite of aggressive noninvasive therapy, patient should
undergo ERCP to define the caliber and morphologic characteristic of the pancreatic
ducts.
3. Malabsorption: when > 90 % of exocrine pancreatic function is lost, clinically overt
malabsorption occurs. Treatment consists of low-fat diet. Medium chain triglycerides
may be useful because their absorption depends on minimal amounts of pancreatic
enzymes and does not require bile salts.
For persistent symptoms pancreatic-enzyme replacement should be given orally just
before meals. Neutralization of gastric acid with orally administration bicarbonate,
inhibition of acid secretion, or enteric coating of enzyme preparation may prevent
degradation of these enzymes as they traverse the stomach.
4. Pseudocysts: develop in 10 % of patients. Most resolve spontaneously but
hemorrhage into a pseudocyst, rupture or infection can occur.
Treatment is indicated for those who persist for 6 weeks or are either enlarging or cause
symptoms. Treatment is resection, external or internal drainage.
5. Pancreatic ascites or pleural fistulas. Diagnosis is made if paracentesis or thoracentesis
yields fluid high in protein and amylase. Currently the treatment is surgery.
VI. Predicting severity of acute pancreatitis:
Many models exist although none are ideal and most of them take about 48 hrs to
complete assessment. They also do not have high sensitivity or specificity, although
relying on routine clinical assessment identifies only 30-40% of patient with severe acute
pancreatitis. These models are usually based on:
1. Presence or absence of organ failure, and local complications.
2. Systems that assess inflammation or organ failure (Ranson criteria)
3. Findings on imaging studies
Ranson criteria to predict severity of acute pancreatitis
At 0 Hours
Age > 55 yo
Wbc> 16 k
Glucose> 200 mg/dL
LDH> 350
SGOT (AST) > 250
At 48hours
Hct fall by > 10%
BUN increase > 5 mg/dl despite fluids
Ca < 8 mg/dL
PO2 < 60 mm/Hg
Base deficit > 4mEq/L
Fluid sequestration > 6L
Mortality per positive criteria:
0-2 <5% mortality
3-4 20% mortality
5-6 40% mortality
7-8 100 % mortalit
11 total criterias in Ranson scoring. The presence of 1 to 3 criteria represents mild
pancreatitis; as the number of criteria increase, the severity of pancreatitis increase and so
does the mortality associated with it.
Review Questions:
1. A 27 yo patient is admitted with acute pancreatitis. Four days after admission patient
develops high fever with worsening abdominal pain. The examination reveals a T of
102F and marked upper abdominal tenderness without rebound. A CT scan of the
abdomen with contrast shows a solid mass and gram stain of the aspirate is positive for
gram-negative organism.
Based upon the above information you will now recommend:
A) IV broad spectrum antibiotics.
B) IV antibiotics plus insert a CT –guided percutaneous drainage tube.
C) IV antibiotics plus surgical debridement.
2.. A 60 yo man with known chronic pancreatitis caused by alcohol reports a 25 lbs
weight loss in the past several months and frequent, greasy, and malodorous stools. A 72hour fecal fat collection confirms steatorrhea. The patient no longer consumes alcohol
and reports no abdominal pain.
Which of the following is the most appropriate first-line treatment for this patient?
A) Administration of enteric-coated pancreatic enzyme replacement tablets with meals
and snacks and concurrent use of a calcium containing antacids.
B) Administration of non-enteric-coated pancreatic enzyme replacement tablets with
meals and snacks with concurrent dosing with a histamine2 blockers.
C) Endoscopic placement of a pancreatic dust stent.
D) Institution of a low-fat diet (less than 20 g fat/day).
E) Subcutaneous administration of octreotide daily.
Post Module Evaluation
Please place completed evaluation in an interdepartmental mail envelope and address to
Dr. Wendy Gerstein, Department of Medicine, VAMC (111).
1) Topic of module:__________________________
2) On a scale of 1-5, how effective was this module for learning this topic? _________
(1= not effective at all, 5 = extremely effective)
3) Were there any obvious errors, confusing data, or omissions? Please list/comment
below:
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
4) Was the attending involved in the teaching of this module? Yes/no (please circle).
5) Please provide any further comments/feedback about this module, or the inpatient
curriculum in general:
6) Please circle one:
Attending
Resident (R2/R3)
Intern
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