ICD9 = ICD9|577.0-ICD9|577.1
OMIM = 167800
MedlinePlus =
eMedicineSubj = emerg
eMedicineTopic = 354
MeshID = D010195

Pancreatitis is the inflammation of the pancreas. See also acute pancreatitis and chronic pancreatitis for more details.


There are different forms of pancreatitis, which are different in causes and symptoms, and require different treatment:

Acute pancreatitis

Acute pancreatitis is an acute episode of pancreatitis.

Chronic pancreatitis

Chronic pancreatitis is the "inflammation of the pancreas that is characterized by recurring or persistent abdominal pain with or without steatorrhea or diabetes mellitus" [cite web |url= |title=Pancreatitis, Chronic |accessdate=2007-08-30 |format= |work=|author=National Library of Medicine]


The most common cause of acute pancreatitis is gallstones. Excessive alcohol use is often cited as the second most common cause of acute pancreatitis. Less common causes include hypertriglyceridemia (but not hypercholesterolemia) and only when triglyceride values exceed 1500 mg/dl (16 mmol/L), hypercalcemia, viral infection (e.g. mumps), trauma (to the abdomen or elsewhere in the body) including post-ERCP (i.e. Endoscopic Retrograde Cholangiopancreatography), vasculitis (i.e. inflammation of the small blood vessels within the pancreas), and autoimmune pancreatitis. Pregnancy can also cause pancreatitis, but in some cases the development of pancreatitis is probably just a reflection of the hypertriglyceridemia which often occurs in pregnant women. Pancreas divisum, a common congenital malformation of the pancreas may underlie some cases of recurrent pancreatitis.

The more mundane, but far more common causes of pancreatitis, as mentioned above, must always be considered first. However, the known porphyrinogenicity of many drugs, hormones, alcohol, chemicals and the association of porphyrias with autoimmune disorders and gallstones do not exclude the diagnosis of heme disorders when these explanations are used. A primary medical disorder, including an underlying undetected inborn error in metabolism, supersedes a secondary medical complication or explanation.

Autoimmune disorders, lipid disorders, gallstones, drug reactions and pancreatitis itself are not primary medical disorders.

It is worth noting that pancreatic cancer is seldom the cause of pancreatitis.Fact|date=August 2007

People with diabetes should promptly seek medical care if they experience unexplained severe abdominal pain with or without nausea and vomiting. []

A useful mnemonic for remembering the causes of acute pancreatitis is; 'GET SMASHED', that is:
*Autoimmune causes
*Scorpion venom
*Drugs (Such as Azathioprine)


Acute hepatic porphyrias, including acute intermittent porphyria, hereditary coproporphyria and variegate porphyria, are genetic disorders that can be linked to both acute and chronic pancreatitis. Acute pancreatitis has also occurred with erythropoietic protoporphyria.

Conditions that can lead to gut dysmotility predispose patients to pancreatitis. This includes the inherited neurovisceral porphyrias and related metabolic disorders. Alcohol, hormones and many drugs including statins are known porphyrinogenic agents. Physicians should be on alert concerning underlying porphyrias in patients presenting with pancreatitis and should investigate and eliminate any drugs that may be activating the disorders.

Still, notwithstanding their potential role in pancreatitis, the porphyrias (as a group or individually) are considered to be rare disorders. However, since there are no systematic studies to determine the actual incidence of latent dominantly-inherited porphyrias in the world population, there is DNA or enzyme evidence of high rates of latency of classic textbook symptoms in families where porphyrias have been detected and the technology is not developed to detect all latent porphyrias, the diagnosis of underlying inborn errors of metabolism impacting heme should not be routinely eliminated in pancreatitis.


Many medications have been reported to cause pancreatitis. Some of the more common ones include the AIDS drugs DDI and pentamidine, diuretics such as furosemide and hydrochlorothiazide, the chemotherapeutic agents L-asparaginase and azathioprine, and estrogen. Just as is the case with pregnancy-associated pancreatitis, estrogen may lead to the disorder because of its effect of raising blood triglyceride levels.


Hereditary pancreatitis may be due to a genetic abnormality that renders trypsinogen active within the pancreas, which in turn leads to digestion of the pancreas from the inside.

Pancreatic diseases are notoriously complex disorders resulting from the interaction of multiple genetic, environmental and metabolic factors.

Three candidates for genetic testing are currently under investigation:
* Trypsinogen mutations (Trypsin 1)
* Cystic Fibrosis Transmembrane Conductance Regulator Gene ("CFTR") mutations
* "SPINK1" which codes for PSTI - a specific trypsin inhibitor. [ cite web | author=D. Whitcomb|year=2006 | title=Genetic Testing for Pancreatitis|url=]

ymptoms and signs

Severe upper abdominal pain, with radiation through to the back, is the hallmark of pancreatitis. Nausea and vomiting (emesis) are prominent symptoms. Findings on the physical exam will vary according to the severity of the pancreatitis, and whether or not it is associated with significant internal bleeding. The blood pressure may be high (when pain is prominent) or low (if internal bleeding or dehydration has occurred). Typically, both the heart and respiratory rates are elevated. Abdominal tenderness is usually found but may be less severe than expected given the patient's degree of abdominal pain. Bowel sounds may be reduced as a reflection of the reflex bowel paralysis (i.e. ileus) that may accompany any abdominal catastrophe.


The diagnostic criteria for pancreatitis are "two of the following three features: 1) abdominal pain characteristic of acute pancreatitis, 2) serum amylase and/or lipase ≥3 times the upper limit of normal, and 3) characteristic findings of acute pancreatitis on CT scan."cite journal |author=Banks P, Freeman M |title=Practice guidelines in acute pancreatitis |journal=Am J Gastroenterol |volume=101 |issue=10 |pages=2379–400 |year=2006 |pmid=17032204 | doi=10.1111/j.1572-0241.2006.00856.x]

Laboratory tests

Most frequently, measurement is made of amylase and/or lipase, and often one, or both, are elevated in cases of pancreatitis. Two practice guidelines state:

Most,cite journal |author=Smith RC, Southwell-Keely J, Chesher D |title=Should serum pancreatic lipase replace serum amylase as a biomarker of acute pancreatitis? |journal=ANZ J Surg |volume=75 |issue=6 |pages=399–404 |year=2005 |month=June |pmid=15943725 |doi=10.1111/j.1445-2197.2005.03391.x |url=] cite journal |author=Treacy J, Williams A, Bais R, "et al" |title=Evaluation of amylase and lipase in the diagnosis of acute pancreatitis |journal=ANZ J Surg |volume=71 |issue=10 |pages=577–82 |year=2001 |month=October |pmid=11552931 |doi= 10.1046/j.1445-2197.2001.02220.x|url=] cite journal |author=Steinberg WM, Goldstein SS, Davis ND, Shamma'a J, Anderson K |title=Diagnostic assays in acute pancreatitis. A study of sensitivity and specificity |journal=Ann. Intern. Med. |volume=102 |issue=5 |pages=576–80 |year=1985 |month=May |pmid=2580467 |doi= |url=] cite journal |author=Lin XZ, Wang SS, Tsai YT, "et al" |title=Serum amylase, isoamylase, and lipase in the acute abdomen. Their diagnostic value for acute pancreatitis |journal=J. Clin. Gastroenterol. |volume=11 |issue=1 |pages=47–52 |year=1989 |month=February |pmid=2466075 |doi= |url=] cite journal |author=Keim V, Teich N, Fiedler F, Hartig W, Thiele G, Mössner J |title=A comparison of lipase and amylase in the diagnosis of acute pancreatitis in patients with abdominal pain |journal=Pancreas |volume=16 |issue=1 |pages=45–9 |year=1998 |month=January |pmid=9436862 |doi= 10.1097/00006676-199801000-00008|url=] but not allcite journal |author=Ignjatović S, Majkić-Singh N, Mitrović M, Gvozdenović M |title=Biochemical evaluation of patients with acute pancreatitis |journal=Clin. Chem. Lab. Med. |volume=38 |issue=11 |pages=1141–4 |year=2000 |month=November |pmid=11156345 |doi= 10.1515/CCLM.2000.173|url=] cite journal |author=Sternby B, O'Brien JF, Zinsmeister AR, DiMagno EP |title=What is the best biochemical test to diagnose acute pancreatitis? A prospective clinical study |journal=Mayo Clin. Proc. |volume=71 |issue=12 |pages=1138–44 |year=1996 |month=December |pmid=8945483 |doi= |url=] individual studies support the superiority of the lipase. In one large study, there were no patients with pancreatitis who had an elevated amylase with a normal lipase.cite journal |author=Smith R, Southwell-Keely J, Chesher D |title=Should serum pancreatic lipase replace serum amylase as a biomarker of acute pancreatitis? |journal=ANZ J Surg |volume=75 |issue=6 |pages=399–404 |year=2005 |pmid=15943725 | doi=10.1111/j.1445-2197.2005.03391.x] Another study found that the amylase could add diagnostic value to the lipase, but only if the results of the two tests were combined with a discriminant function equation.cite journal |author=Corsetti J, Cox C, Schulz T, Arvan D |title=Combined serum amylase and lipase determinations for diagnosis of suspected acute pancreatitis |journal=Clin Chem |volume=39 |issue=12 |pages=2495–9 |year=1993 |pmid=7504593]

Conditions other than pancreatitis may lead to rises in these enzymes and, further, that those conditions may also cause pain that resembles that of pancreatitis (e.g. cholecystitis, perforated ulcer, bowel infarction (i.e. dead bowel as a result of poor blood supply), and even diabetic ketoacidosis.


Although ultrasound imaging and CT scanning of the abdomen can be used to confirm the diagnosis of pancreatitis, neither is usually necessary as a primary diagnostic modalitycite journal |author=Fleszler F, Friedenberg F, Krevsky B, Friedel D, Braitman L |title=Abdominal computed tomography prolongs length of stay and is frequently unnecessary in the evaluation of acute pancreatitis |journal=Am J Med Sci |volume=325 |issue=5 |pages=251–5 |year=2003 |pmid=12792243 | doi = 10.1097/00000441-200305000-00001] . In addition, CT contrast may exacerbate pancreatitis,cite journal |author=McMenamin D, Gates L |title=A retrospective analysis of the effect of contrast-enhanced CT on the outcome of acute pancreatitis |journal=Am J Gastroenterol |volume=91 |issue=7 |pages=1384–7 |year=1996 |pmid=8678000] although this is disputed.cite journal |author=Hwang T, Chang K, Ho Y |title=Contrast-enhanced dynamic computed tomography does not aggravate the clinical severity of patients with severe acute pancreatitis: reevaluation of the effect of intravenous contrast medium on the severity of acute pancreatitis |journal=Arch Surg |volume=135 |issue=3 |pages=287–90 |year=2000 |pmid=10722029 |doi=10.1001/archsurg.135.3.287] See acute pancreatitis.


There are several scoring systems used to help predict the severity of an attack of pancreatitis. The Apache II has the advantage of being available at the time of admission as opposed to 48 hours later for the Glasgow criteria and Ranson criteria. However, the Glasgow criteria and Ranson criteria are easier to use.


Ranson criteria

At admission:

# age in years > 55 years
# white blood cell count > 16000 /mcL
# blood glucose > 11 mmol/L (>200 mg/dL)
# serum AST > 250 IU/L
# serum LDH > 350 IU/L

After 48 hours:

# Haematocrit fall > 11.3444%
# increase in BUN by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration
# hypocalcemia (serum calcium < 2.0 mmol/L (<8.0 mg/dL))
# hypoxemia (PO2 < 60 mmHg)
# Base deficit > 4 Meq/L
# Estimated fluid sequestration > 6 L

The criteria for point assignment is that a certain breakpoint be met at anytime during that 48 hour period, so that in some situations it can be calculated shortly after admission. It is applicable to both biliary and alcoholic pancreatitis.


* If the score ≥ 3, severe pancreatitis likely.
* If the score < 3, severe pancreatitis is unlikely


* Score 0 to 2: 2% mortality
* Score 3 to 4: 15% mortality
* Score 5 to 6: 40% mortality
* Score 7 to 8: 100% mortality

Glasgow criteria

Glasgow's criteriacite journal |author=Corfield AP, Cooper MJ, Williamson RC, "et al" |title=Prediction of severity in acute pancreatitis: prospective comparison of three prognostic indices |journal=Lancet |volume=2 |issue=8452 |pages=403–7 |year=1985 |pmid=2863441 |doi=10.1016/S0140-6736(85)92733-3] : The original system used 9 data elements. This was subsequently modified to 8 data elements, with removal of assessment for transaminase levels (either AST (SGOT) or ALT (SGPT) greater than 100 U/L).

On Admission
# Age > 55 yr
# WBC Count > 15 10 exp 9 /Lit
# Blood Glucose > 10 mmol/L (No Diabetic History)
# Serum Urea > 16 mmol/Lit ( No response to IV fluids)
# Arterial Oxygen Saturation < 60

Within 48 hours
# Serum Calcium < 2 mmol/L
# Serum Albumin <32 gm/L
# LDH > 600 units/L
# AST/ALT >200 Units/L

=Complications=Acute (early) complications of pancreatitis include
* shock,
* hypocalcemia (low blood calcium),
* high blood glucose,
* dehydration, and kidney failure (resulting from inadequate blood volume which, in turn, may result from a combination of fluid loss from vomiting, internal bleeding, or oozing of fluid from the circulation into the abdominal cavity in response to the pancreas inflammation, a phenomenon known as Third Spacing).
* Respiratory complications are frequent and are major contributors to the mortality of pancreatitis. Some degree of pleural effusion is almost ubiquitous in pancreatitis. Some or all of the lungs may collapse (atelectasis) as a result of the shallow breathing which occurs because of the abdominal pain. Pneumonitis may occur as a result of pancreatic enzymes directly damaging the lung, or simply as a final common pathway response to any major insult to the body (i.e. ARDS or Acute Respiratory Distress Syndrome).
* Likewise, SIRS (Systemic inflammatory response syndrome) may ensue.

* Infection of the inflamed pancreatic bed can occur at any time during the course of the disease. In fact, in cases of severe hemorrhagic pancreatitis, antibiotics should be given prophylactically.

Late complications

Late complications include recurrent pancreatitis and the development of pancreatic pseudocysts. A pancreatic pseudocyst is essentially a collection of pancreatic secretions which has been walled off by scar and inflammatory tissue. Pseudocysts may cause pain, may become infected, may rupture and hemorrhage, may press on and block structures such as the bile duct, thereby leading to jaundice, and may even migrate around the abdomen.

=Treatment=The treatment of pancreatitis will, of course, depend on the severity of the pancreatitis itself. Still, general principles apply and include:

# Provision of pain relief. In the past this was done preferentially with meperidine (Demerol), but it is now not thought to be superior to any narcotic analgesic. Indeed, given meperidine's generally poor analgesic charactersitics and its high potential for toxicity, it should not be used for the treatment of the pain of pancreatitis. The preferred analgesic is morphine for acute pancreatitis.
# Provision of adequate replacement fluids and salts (intravenously).
# Limitation of oral intake (with dietary fat restriction the most important point). NG tube feeding is the preferred method to avoid pancreatic stimulation and possible infection complications caused by bowel flora.
# Monitoring and assessment for, and treatment of, the various complications listed above.

When necrotizing pancreatitis ensues and the patient shows signs of infection, it is imperative to start antibiotics such as Imipenem due to the high penetration of the drug in the pancreas. Floroquinolone + metronidazole is another treatment option.


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