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Pancreatitis
Classification and external resources
ICD-10 K85., K86.0-K86.1
ICD-9 577.0-577.1
OMIM 167800
DiseasesDB 24092
eMedicine emerg/354
MeSH D010195

Pancreatitis is inflammation of the pancreas that can occur in two very different forms. Acute pancreatitis is sudden while chronic pancreatitis "is characterized by recurring or persistent abdominal pain with or without steatorrhea or diabetes mellitus."[1]

Contents

Causes

Excessive alcohol use is often cited as the most common cause of acute pancreatitis, yet gallstones are actually the most common cause. 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. Pancreatitis is less common in pediatric population.

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. As mentioned above, pancreatitis is less common in children but if seen, abuse or abdominal trauma should be suspected.

Rarely, calculi can form or become lodged in the pancreas or its ducts. Treatment varies but is of course aimed are removal of the offending stone. This can be accomplished endoscopically, surgically, or even by the use of ESWL. [2]

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.

Type 2 diabetes subjects have 2.8 fold higher risk for pancreatitis compared to non diabetic subjects. [3] People with diabetes should promptly seek medical care if they experience unexplained severe abdominal pain with or without nausea and vomiting. [4]

Some of the causes of acute pancreatitis can be remembered by the acronym GET SMASHED [5]

Gallstones; Ethanol; Trauma;

Steroids; Mumps; Autoimmune; Scorpion sting; Hypercalcaemia, hypertriglyceridaemia, hypothermia; ERCP; Drugs e.g., azathioprine, diuretics;

Porphyrias

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.

Medications

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 anticonvulsants divalproex sodium and valproic acid, 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. Pancreatitis due to statins first started appearing in the medical literature as early as 1990. All statins currently in use reportedly can cause pancreatitis, a not surprising observation when one considers that all statins are reductase inhibitors and can be expected to have similar side effect profiles.

Genetics

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:

Virus infection

Viruses can cause profound inflammation in, and destruction of, the pancreas. This is true of several viruses in the coxsackievirus group.

Symptoms 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.

Diagnosis

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."[7]

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

It is usually not necessary to measure both serum amylase and lipase. Serum lipase may be preferable because it remains normal in some nonpancreatic conditions that increase serum amylase including macroamylasemia, parotitis, and some carcinomas. In general, serum lipase is thought to be more sensitive and specific than serum amylase in the diagnosis of acute pancreatitis".[7]
Although amylase is widely available and provides acceptable accuracy of diagnosis, where lipase is available it is preferred for the diagnosis of acute pancreatitis (recommendation grade A)".[8]

Most,[9][10][11][12][13] but not all[14][15] 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.[9] 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.[16]

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.

Imaging

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 modality[17] . In addition, CT contrast may exacerbate pancreatitis,[18] although this is disputed.[19] See acute pancreatitis.

Prognosis

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.

APACHE II

Ranson criteria

At admission:

  1. age in years > 55 years
  2. white blood cell count > 16000 /mcL
  3. blood glucose > 11 mmol/L (>200 mg/dL)
  4. serum AST > 250 IU/L
  5. serum LDH > 350 IU/L

After 48 hours:

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

Interpretation

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

Or

  • 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 criteria[20]: 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

  1. Age >55 yrs
  2. WBC Count >15 x109/L
  3. Blood Glucose >200 mg/dL (No Diabetic History)
  4. Serum Urea >16 mmol/L ( No response to IV fluids)
  5. Arterial Oxygen Saturation <76 mmHg

Within 48 hours

  1. Serum Calcium <2 mmol/L
  2. Serum Albumin <34 g/L
  3. LDH >219 units/L
  4. AST/ALT >96 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:

  1. 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.
  2. Provision of adequate replacement fluids and salts (intravenously).
  3. 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.
  4. Monitoring and assessment for, and treatment of, the various complications listed above.
  5. ERCP if gallstone pancreatitis

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.

References

  1. ^ National Library of Medicine. "Pancreatitis, Chronic". http://www.nlm.nih.gov/cgi/mesh/2007/MB_cgi?mode=&term=CHRONIC+PANCREATITIS. Retrieved 2007-08-30.  
  2. ^ Macaluso JN: Editorial Comment: re ESWL for obstructing pancreatic calculi. Journal of Urology, Vol 158, #2, 522-525, August 1997
  3. ^ http://care.diabetesjournals.org/content/32/5/834.abstract
  4. ^ http://www.fda.gov/CDER/Drug/InfoSheets/HCP/exenatide2008HCP.htm
  5. ^ Page 584, Oxford Handbook of Clinical Medicine, 7th Edition, ISBN 978 0 19 856837 7
  6. ^ D. Whitcomb (2006). "Genetic Testing for Pancreatitis". http://www.touchalimentarydisease.com/articles.cfm?article_id=6374&level=2.  
  7. ^ a b Banks P, Freeman M (2006). "Practice guidelines in acute pancreatitis". Am J Gastroenterol 101. doi:10.1111/j.1572-0241.2006.00856.x. PMID 17032204.  
  8. ^ UK Working Party on Acute Pancreatitis (2005). "UK guidelines for the management of acute pancreatitis". Gut 54 Suppl 3: iii1. doi:10.1136/gut.2004.057026. PMID 15831893. http://gut.bmj.com/cgi/content/full/54/suppl_3/iii1.  
  9. ^ a b Smith RC, Southwell-Keely J, Chesher D (June 2005). "Should serum pancreatic lipase replace serum amylase as a biomarker of acute pancreatitis?". ANZ J Surg 75 (6): 399–404. doi:10.1111/j.1445-2197.2005.03391.x. PMID 15943725. http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=1445-1433&date=2005&volume=75&issue=6&spage=399.  
  10. ^ Treacy J, Williams A, Bais R, et al. (October 2001). "Evaluation of amylase and lipase in the diagnosis of acute pancreatitis". ANZ J Surg 71 (10): 577–82. doi:10.1046/j.1445-2197.2001.02220.x. PMID 11552931. http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=1445-1433&date=2001&volume=71&issue=10&spage=577.  
  11. ^ Steinberg WM, Goldstein SS, Davis ND, Shamma'a J, Anderson K (May 1985). "Diagnostic assays in acute pancreatitis. A study of sensitivity and specificity". Ann. Intern. Med. 102 (5): 576–80. PMID 2580467.  
  12. ^ Lin XZ, Wang SS, Tsai YT, et al. (February 1989). "Serum amylase, isoamylase, and lipase in the acute abdomen. Their diagnostic value for acute pancreatitis". J. Clin. Gastroenterol. 11 (1): 47–52. PMID 2466075.  
  13. ^ Keim V, Teich N, Fiedler F, Hartig W, Thiele G, Mössner J (January 1998). "A comparison of lipase and amylase in the diagnosis of acute pancreatitis in patients with abdominal pain". Pancreas 16 (1): 45–9. doi:10.1097/00006676-199801000-00008. PMID 9436862. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0885-3177&volume=16&issue=1&spage=45.  
  14. ^ Ignjatović S, Majkić-Singh N, Mitrović M, Gvozdenović M (November 2000). "Biochemical evaluation of patients with acute pancreatitis". Clin. Chem. Lab. Med. 38 (11): 1141–4. doi:10.1515/CCLM.2000.173. PMID 11156345.  
  15. ^ Sternby B, O'Brien JF, Zinsmeister AR, DiMagno EP (December 1996). "What is the best biochemical test to diagnose acute pancreatitis? A prospective clinical study". Mayo Clin. Proc. 71 (12): 1138–44. doi:10.4065/71.12.1138. PMID 8945483.  
  16. ^ Corsetti J, Cox C, Schulz T, Arvan D (1993). "Combined serum amylase and lipase determinations for diagnosis of suspected acute pancreatitis". Clin Chem 39 (12): 2495–9. PMID 7504593.  
  17. ^ Fleszler F, Friedenberg F, Krevsky B, Friedel D, Braitman L (2003). "Abdominal computed tomography prolongs length of stay and is frequently unnecessary in the evaluation of acute pancreatitis". Am J Med Sci 325 (5): 251–5. doi:10.1097/00000441-200305000-00001. PMID 12792243.  
  18. ^ McMenamin D, Gates L (1996). "A retrospective analysis of the effect of contrast-enhanced CT on the outcome of acute pancreatitis". Am J Gastroenterol 91 (7): 1384–7. PMID 8678000.  
  19. ^ Hwang T, Chang K, Ho Y (2000). "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". Arch Surg 135 (3): 287–90. doi:10.1001/archsurg.135.3.287. PMID 10722029.  
  20. ^ Corfield AP, Cooper MJ, Williamson RC, et al. (1985). "Prediction of severity in acute pancreatitis: prospective comparison of three prognostic indices". Lancet 2 (8452): 403–7. doi:10.1016/S0140-6736(85)92733-3. PMID 2863441.  

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