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Pancreatitis
The most terrible of all calamities that occur in connection with the abdominal viscera. The suddenness of its
onset, the illimitable agony which accompanies it, and the mortality attendant upon it render it the most
formidable of catastrophes.
--B. Moynaham, Annals of Surgery, 1925.

Key Points:
1. Alcohol and gallstones are the most common causes of pancreatitis, but a careful consideration of other causes
should be considered for the minority.
2. Lipase is more specific for pancreatitis than amylase, but is not a good marker of disease regression due to its
longer half-life.
3. Antibiotics may be helpful in case of severe pancreatitis.
4. There is not good data as to when patients can eat, but in general, control of pain and an appetite are good
indicators to proceed.
What are some of the less common causes of pancreatitis?
Gallstones and alcohol account for over 75% of the causes of acute pancreatitis in the US.
Drugs: ddI, pentamidine, MTZ, lasix, thiazides, tetracycline, several of the IBD drugs, VPA, sulindac,
salicylates, calcium, estrogen
Infections:
Viruses: mumps, coxsackie, HBV,CMV, VZV, HSV.
Bacteria: mycloplasma, legionella, leptospira, salmonella
Fungi: aspergillosis
Parasites: toxoplasma, crypto, ascaris
Metabolic: hypercalcemia, hypertriglyceridemia
Vascular: ischemia, emboli, vasculitis
Other: pregnancy, post ERCP, renal transplant, trauma
What about those patients who dont have an obvious cause?
! In 30% of pts with their first episode of pancreatitis, you wont find an etiology with the usual
investigations of history, physical, basic labs including calcium and triglycerides, and ultrasound. In one
retrospective study, only 1/31 pts with unexplained pancreatitis went on to suffer another episode in the
next 3 years.
! One prospective study of 126 pts with >1 episode of pancreatitis underwent ERCP, sphincter of Oddi
manometry, and bile analysis. A presumed cause was found in 79% (papillary stenosis 21%, pancreas
divisum 7%, choledocholithiasis 5%, Oddi sphincter dysfunction 21% of those with gallbladder and 47%
of those without. 75% of cases were considered endoscopically treatable, and pancreatitis-free rates
ranged from 67-100% in over 2 years of follow-up.
! The next step is debatable. Most will get a CT, but ERCP or ultrasound are other options to evaluate for
anatomic or functional problems.
Should I order an amylase or a lipase?
* Lipase is produced primarily in the pancreas, with a small amount in the liver, intestine, tongue, and
stomach. Amylase is derived primarily from the pancreas and salivary glands; it is also present in the ovaries,
small and large intestine, and skeletal muscle.
* Serum amylase is most commonly used lab test. Serum lipase is believed to be more specific and will stay
elevated for a longer period of time, as hyperlipasemia persists for 7 days and amylase should normalize within
4 days.
* Cost of each test is currently $49 at SFGH. At many institutions, amylase may be cheaper.
Should I follow the lipase?
No. Given the time that lipase remains elevated, there is no benefit in following lipase as a marker of
resolution. Symptoms will be a better indicator.
What other entities could cause an elevated amylase or lipase?
Disease can occur in other organs that produce amylase/lipase.

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Transmural absorption in intestinal infarction and transperitoneal absorption with a perforated viscus and
peritonitis probably explain the hyperamylasemia/hyperlipasemia in these conditions.
There is decreased renal clearance in patients with renal failure. Macroamylasemia is a condition in which
amylase is bound to a larger protein moiety that prevents renal excretion. Thus, serum amylase is elevated
in absence of pancreatitis. Macroamylasemia is diagnosed by detecting a low renal amylase clearance.
Increased amylase and lipase in cholecystitis is probably due to subclinical or undiagnosed coexistent
pancreatitis.

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**NOTE: The sensitivity of lipase and amylase is poor for chronic pancreatitis or pancreatic cancer.
What is the evidence and recommendations behind antibiotics?
The pancreas can become secondarily infected with bowel flora leading to more extensive necrosis (Ecoli,
Pseudomonas, Enterococcus- Most are monomicrobial).
Infection is usually a late manifestation
Prevention modalities include: early enteral feeding to avoid central line infections, selective gut
decontamination with nonabsorbable antibiotics (One RCT not placebo controlled, found a mortality
benefit by using norfloxacin, colistin, and amphotercin all PO), prophylactic systemic antibiotics
1. Saino et al, Early Antibiotic Treatment in Acute Necrotizing Pancreatitis, Lancet 1995 Sep 9;346:
663-7
Randomized placebo controlled study 60 patients with alcohol induced NP. Cefuroxime vs. Placebo. Defined
NP as C reactive protein of >120mg/dl and CT low enhancement. Outcomes: mortality 23% vs. 3.3% P=.04
in the non-antibiotic treated group. Most common causes of sepsis was Staph Epi. Most common organism in
pancreas at autopsy was Staph Epi.
2. Pederzoli, A randomized multicenter clinical trial of antibiotic prophylaxis of septic complications
in acute necrotizing pancreatitis with Imipenem. Surg Gynec Obstet1993
Randomized, not placebo controlled study of 74 patients who met CT criteria 72 hours after admission . All
patients had CT guided needle biopsies. Outcome: pancreatic infection. 12.2 vs. 30.3 % P=.01.
3. Luiten, Ann Surg 1995: 22: 57-65.
This randomized, multicenter trial of 102 patients with severe pancreatitis based on CT criteria received either
standard therapy or norfloxacin, colistin, and amphotericin. Decrease in mortality of antibiotic group 22% vs
35% (mostly seen as beneficial for late mortality over 2 weeks out).
Bottom line: Antibiotics may have an impact on mortality and probably should be initiated in patients with
very severe pancreatitis. (Consider fungal coverage as well)
When should I allow the patient to eat?
In reviewing the literature, there is not definitive data on when to allow patients to eat. In general, control of
pain and a desire to eat are indicators that oral intake is acceptable, realizing that pain medicines may mask
ongoing discomfort which would normally discourage a patient from eating.
1. Levy et al. Frequency and risk factors of recurrent pain during refeeding in patients with acute
pancreatitis: a multivariate multicentre prospective study of 116 patients.
Gut. 1997 Feb;40(2):262-6.
This study looked at predictors for relapse of pain after refeeding patients with pancreatitis based on
clinicians decision to do so. 21% experienced a relapse of pain. Statistically significant risk factors for
recurrent pain included necrotizing pancreatitis, lipase >3x normal value, longer periods of pain prior to
refeeding.
2. Lobo, et al. Evolution of nutritional support in acute pancreatitis. Br J Surg. 2000 Jun;87(6):695-707.
This article reviewed the literature over the last 25 years regarding nutritional support in pancreatitis. It
concluded that there is no evidence to show that nutritional support affects disease process but it does
prevent undernutrition and starvation.
Other references in addition to those in text:
NEJM. Acute pancreatitis review. 1994.
UpToDate 10.2
Ballinger, et al. Is intervention necessary after a first episode of acute idiopathic pancreatitis? Gut 1996.