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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 Mortality per positive criteria:
0-2 <5% mortality
3-4 20% mortality
At 48hours 5-6
40% mortality
Hct fall by > 10% 7-8
100 % mortalit
BUN increase > 5 mg/dl despite fluids
Ca < 8 mg/dL
PO2 < 60 mm/Hg
Base deficit > 4mEq/L
Fluid sequestration > 6L
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 72- hour
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 Medical
student
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