PANCREATITIS


I. Acute pancreatitis

  1. Begins and ends with a normal pancreas in 90% of cases; other 10% are "Severe Acute" pancreatitis; can cause rapid death
  2. Causes and risk factors:
    1. Excessive alcohol intake
    2. Trauma including endoscopic retrograde cholangiopancreaticography (ERCP)
      1. MRCP is an alternative but less sensitive as of 2003 (Ann. Int. Med. 139:547, 2003--JW)
      2. Preventing post-ERCP pancreatitis
        1. Pancreatic duct stenting
          1. In a meta-analysis of 5 controlled trials involving 481 undergoing ERCP at high risk for post-ERCP pancreatitis (suspected sphincter of Oddi dysfunction, difficult cannulation, or need for precut sphincterotomy or balloon dilation of the biliary orifice), incidence of post-ERCP pancreatitis was sig. lower in stented pts (5.8% vs. 15.5%) (Gastrointest. Endosc. 60:544, 2004--JW)
        2. Gabexate (a protease inhibitor)-reduces incidence but must be infused continuously for up to 13h
        3. Ulinastatin (a trypsin inhibitor)
          1. Can be administered as a bolus injection
          2. In a study in 406 pts randomized to ulinastatin vs. placebo, incidence of  pancreatitis was sig. lower in ulinastatin group (2.9% vs. 7.4%) (Clin. Gastroent. Hepatol. 3:376, 2005--JW)
        4. Allopurinol
          1. IN a study in 243 pts randomized to allopurinol 600mg 15h prior and 3h prior to ERCP vs. placebo, allopurinol recipients had sig. lower incidence of post-procedure pancreatitis (3.2% vs. 17.8%) (Gastroint. Endoscop. 61:407, 2005--JW)
        5. Somatostatin
        6. Octreotide
          1. Octreotide inhibits pancreatic secretion.
          2. In a study in 202 pts undergoing ERCP randomized to octreotide 500ug SQ vs. placebo at 24, 16, 8, and 1h prior to and 8h after ERCP, incidence of post-ERCP pancreatitis was sig. lower in octreotide group (2% vs.9%) (Gastroint. Endosc. 64:726, 2006--JW)
    1. Infection
      1. Viral: measles, mumps, rubella, coxsackie B
      2. Mycoplasma
      3. Septic shock
    2. Metabolic conditions
      1. Hypertriglyceridemia (at  levels > 1,000
      2. Diabetes mellitus
      3. Uremia
      4. Hypercalcemia
    3. Systemic disease:
      1. Inflammatory: systemic lupus erythematosus, periarteritis nodosa, Henoch-Schoenlein purpura
      2. Cystic fibrosis
      3. Reye syndrome
      4. Inflammatory bowel disease
      5. Certain mutations in the cystic fibrosis conductance regulator gene (CFTR) may predispose to chronic pancreatitis (NEJM 339:645, 1998--JW and NEJM 339:653, 1998--JW)
    4. Drugs: Thiazides, furosemide, azathioprine, sulfon-amides, tetracyclines, steroids, l-asparaginase
    5. Obstruction 
      1. Congenital (atresia/stenoses)
      2. Choledochal cysts
      3. Trauma
      4. Gallstones
        1. Most dislodge spontaneously within about 48h of presentation
        2. If not, can be removed by Endoscopic Retrograde Cholangiopancreatography (ERCP)
        3. In a series of 132 pts with gallstone pancreatitis, those with more severe disease (clinician's impression), persence of bile in gastric aspirate, or high serum bilirubin levels were less likely to have spontaneous passage of the stone (J. Gastroent. 95:122, 2000--JW)
        4. Can be diagnosed by ERCP or (with slightly less sensitivity--see Am. J. Gastroent. 100;1051, 2005--JW) with magnetic resonance cholangiopancreatography (MRCP)
        5. In a study in 103 pts with acute gallstone pancreatitis and evidence of CBD obstruction (distal CBD > 7mm on u/s and total bilirubin > 1.1 mg/dL) but no evidence of cholangitis randomized to early ERCP (within 72h of symptom onset) or conservative management (usually ending in cholecystectomy with intraoperative cholangiography), there were no differences in mortality or various measures of mobidity between the groups (Ann. Ssurg. 245:10, 2007--JW)
  1. Tumors
  2. Pseudocysts
  3. Intraductal infection
  4. Ascaris lumbricoides
  1. Other
    1. Post-operative state
    2. Graft-versus-host (GVH) disease
    3. Penetrating peptic ulcer
    4. Scorpion bites
  1. Clinical features:
    1. Rapid-onset abdominal pain, usually epigastric, in some cases radiating to back, flank, or lower abdomen
    2. Typically have abdominal tenderness without rigidity
    3. Serum lipase is highly sensitive and specific
    4. Elevated C-reactive protein > 48h after symptom onset is associated with pancreatic necrosis and elevated risk of complications
    5. Differential diagnosis: perforated duod. ulcer, cholecystitis, bowel obstr., thrombosed mesenteric vein
    6. Early Complications:
      1. Renal failure
      2. Alkalosis
      3. Massive fluid sequestration
      4. ARDS
    7. Other complications:
      1. Pancreatic necrosis
        1. Associated with HCT > 44% and elevated serum Cr (causality, or lack of it, is unclear)
      2. Phlegmon (big and hard, progress fluid accumulation and necrosis)--reversible, recognizable on CT, must be cultured and debrided, may progress to pancreatic abscess
      3. Pancreatic abcess (after 3 wks)--inf. comes from lymph.drainage of colon, which is shared by pancreas
      4. Pseudocyst--results from leakage from duct into interstitium; can burst, causing pancreatic ascites. Takes about 6 wks to mature, then walls are strong enough to suture, so if no complications, wait and then operate. But can rupture, bleed, get infected, or obstuct neighboring structures; may require fistulization to another hollow viscus, e.g. Roux en Y
      5. Hemorrhage and thrombosis; can infarct other organs
  2. "Ransom's Criteria" for grading severity: poor prog. with
    1. Age > 55
    2. WBC >16k
    3. Glu > 200
    4. LDH > 350
    5. OT > 250
    6. HCT > 10%
    7. BUN > 5
    8. pO2 < 60
    9. Ca < 8
    10. Fluid requirement > 6 liters
  3. Management
    1. Analgesics, usually opiates
    2. Diet
      1. Patients are generally kept NPO until stable
      2. Enteral nutrition may be associated with better outcomes than parenteral nutrition
        1. In a meta-analysis of 6 randomized trials of enteral nutrition (usually w/a jejunal tube) vs. parenteral nutrition in pts with acute pancreatitis, enteral nutrition was ass'd with RR 0.45 (sig.) for infection and RR 0.48 (sig.) for surgical inteventions (BMJ 328:1407, 2004--JW)
    3. Monitor ABGs in case of ARDS
    4. Oral pancreatic enzymes may provide pancreatic "rest"
    5. Consider ICU care and abdominal CT with contrast (to look for pancreatic necrosis) if APACHE II score > 8 or show signs of organ failure
    6. Antibiotics
      1. Generally used when pancreatic necrosis is present (often detected on CT) to prevent peritonitis, though results are mixed
        1. In a study in 114 pts with acute pancreatitis and serum C-reactive protein > 150mg/L and/or necrosis on CT randomized to (ciprofloxacin 400mg and metronidazole 500mg BID) vs. placebo; there were no sig. diffs. in mortality or systemic complications (Gastroent. 126:997, 2004--abst)
        2. In a study in 100 pts with acute pancreatitis and > 30% pancreatitis on CT randomized to meropenem vs. placebo within 5d of sx onset, over 6wks, there were no sig. diffs. in incidence of infection, need for surgical intervension, or mortality (Ann. Surg. 245:674, 2007--JW)
      2. Administration to all patients with pancreatitis may improve outcomes
        1. In a study in 215 pts with acute pancreatitis randomized to meropenem 500mg TID vs. waiting 48h, checking CT, and giving meropenem if evidence of pancreatic necrosis was present (all pts had CT done; early-tx group had antibiotics d/c'd if CT showed no evidence of pancreatic necrosis), there was no sig. diff. between the groups in incidence of multi-organ failure or death, though late-treatment group had sig. higher incidence of extrapancreatic infection (45% vs. 17%) and surgery (38% vs. 12%); also sig. longer mean hospital stay (30d vs. 18d) (Am. J. Gastroenterol. 101:1348, 2006--JW)
II. Chronic pancreatitis
  1. Very different from acute
  2. Begin and end with abnormal pancreas; continuous deteriorating course
  3. Smoking is a risk factor for chronic pancreatitis
  4. Pain can respond to pancreatic duct stenting if pancreatic duct is dilated (Gastroint. Endoscp. 61:576, 2005--JW)
  5. Diagnosis can be challenging, at least early on
    1. Pancreatic CT abnormalities can be absent
    2. Cholecystokinin pancreatic function tests (administer CCK and collect duodenal fluid and measure lipase content)-More sensitive, but less specific, than ERCP in one prospective study (Clin. Gastroent. Hepatol. 6:1432, 2008-JW)
    3. ERCP
    4. Endoscopic ultrasound
  6. Anti-oxidants to reduce pain associated with chronic pancreatitis
    1. In a study in 127 pts with chronic pancreatitis and abdominal pain severe enough to require analgesics or hospitalization in prior 3mos, all on pancreatic enzyme replacement therapy, randomized to daily anti-oxidant supplementation (selenium, ascorbic acid, beta carotene, alpha-tocopherol, and methionine) vs. placebo x 6mos, the anti-oxidant group had sig. greater reduction in # of painful days per month (7.4 vs. 3.2d) and sig. greater reductions in use of oral analgesics.  (Gastroenterology 136:149, 2009-JW)
(Sources include Core Content Review of Family Medicine, 2012)