Definition: Acute inflammatory process of the pancreas; a retroperitoneal organ with endocrine and exocrine function.

Epidemiology (Rosen’s 2018)

  • US Incidence: 5 – 40/100,000
  • Mortality: 4-7%
  • Progression to severe disease: 10-15% of cases (mortality in this subset 20-50%)

Pancreas Anatomy (Rosen’s)

Etiology

  • Alcohol (~ 35% of cases)
  • Gallstones (~ 45% of cases)
  • Medications/toxins
  • Hypertriglyceridemia
  • Non-gallstone Obstruction (i.e. strictures, masses)
  • Trauma
  • Infectious (Mumps, HIV, Salmonella)

Pathophysiology

  • Mild Pancreatitis
    • Results from obstruction of the pancreatic or bile ducts or direct toxicity to pancreatic cells
    • Inflammation results in pancreatic enzyme activation within the pancreas and ducts
    • Premature enzyme activation leads to pancreatic autodigestion
  • Moderate Pancreatitis
    • Enzyme digestion leads to necrosis of the pancreas
    • Erosion into vascular structures can occur as well leading to hemorrhage
  • Severe Pancreatitis
    • Release of systemic inflammatory mediators
    • systemic immune response syndrome and multisystem organ dysfunction (i.e. acute renal failure, cardiac dysfunction, ARDS, disseminated intravascular coagulation)

Presentation

  • History + Symptoms
    • Abdominal pain
      • Typically epigastric but may be RUQ or LUQ
      • Will become more diffuse as inflammation progresses
      • Rapid onset of pain over a few hours
      • Pain is constant, often severe and often radiates to the back (>50%)
    • Nausea and vomiting (90%) (Banks 2006)
    • Patients often have a history of prior similar episodes
    • Dyspnea: Severe pancreatitis can present with dyspnea from diaphragmatic irritation or ARDS

  • Cullen’s Sign

    Signs

    • Vital sign abnormalities dependent on stage of disease
      • Early on may be normal or with slight tachycardia in response to pain
      • Later in disease, hypotension, tachycardia and frank shock may develop
    • Low grade fever common
    • Epigastric tenderness with or without peritoneal signs
    • Jaundice: indicates obstruction of common bile duct as etiology
    • Hemorrhagic pancreatitis
      • Rare complication
      • Ecchymosis/discoloration around the umbilicus (Cullen’s sign)
      • Ecchymosis/discoloration of the flank(s) (Grey Turner’s sign)

Differential Diagnosis

Diagnostics

  • Basic Diagnostic Criteria (must have at least 2 out of 3)
    • Signs/symptoms consistent with pancreatitis
    • Lipase elevation: > 3X normal reference range (value depends on lab)
    • Imaging (CT scan) consistent with pancreatitis

  • Ranson’s Criteria for Pancreatitis-Associated Mortality (Rosen’s)

    Diagnostic Laboratory Tests

    • Amylase
      • Enzyme produced by pancreas, salivary glands, muscle, intestines and other organs
      • Nonspecific marker of pancreatitis as can be elevated as result of various disease processes (Matsull 2006)
      • May not be elevated in alcohol pancreatitis (>20%)
      • May not be elevated if late presentation (>24h) of pancreatitis (amylase levels return to normal quickly)
    • Lipase
      • Enzyme more specific to pancreas than amylase
      • Specificity: 80-99% depending on where cutoff set (Matsull 2006)
      • False negatives may occur early in disease (levels increase in 4-8 hours of onset of inflammation)
      • Degree of elevation is not a marker of disease severity
    • Triglyceride Level
      • Should be obtained in the absence of gallstone or alcohol as the likely etiology
      • A level > 1000 mg/dl is suggestive that hypertriglyceridemia may be the cause (Tenner 2013)
  • Ranson’s Criteria
    • Aids in determining risk of mortality from pancreatitis
    • Higher score = greater risk of mortality
    • Labs required: CBC, BMP, Hepatic Panel, LDH

  • BISAP Score

    BISAP Score (Wu 2008, Papachristou 2010)

    • Clinical score used to predict mortality from pancreatitis
    • Requires less tests than Ranson’s criteria but performs equally well
  • Additional Laboratory Tests
    • Basic Metabolic Panel (BMP)
    • Hepatic Panel
    • Lactate Dehydrogenase (LDH)
    • Complete Blood Count (CBC)
  • Imaging
    • Plain Radiographs
      • Numerous non-specific findings
      • CXR may show pleural effusions, atelectasis or ARDS
      • AXR may show an ileus, gallstones, calcified areas of pancreas
    • Ultrasound
      • Suboptimal imaging modality to diagnose pancreatitis but useful in establishing the presence or absence of a biliary cause
      • US superior to CT for finding gallstones and common bile duct dilation (Harvey 1999, Reitz 2011)
      • Obtain US as soon as possible
        • One study found that US changed management in 55% (6/11) cases (Harvey 1999)
        • Converts a medically managed disease to a surgically/interventionally managed one
      • High suspicion for biliary disease with negative US should prompt Magnetic resonance cholangiopancreatography (MRCP) or endoscopic retrograde cholangio-pancreatography (ERCP)
    • Computed Tomography
      • Should not be obtained in all patients with pancreatitis during ED evaluation
      • Useful in evaluation of other causes of abdominal pain and for the presence of complications (pseudocyst, abscess, hemorrhagic pancreatitis)
      • Which ED pancreatitis patients should get an immediate CT
        • Diagnosis of pancreatitis is uncertain
        • Presence of severe pancreatitis
          • Hemodynamic instability
          • Organ failure (Hypotension, ARDS, GI bleed, AKI)
          • Ranson score > 3, BISAP > 3 or APACHE > 8
        • Concern for early complications

Management

  • Supportive Care
    • Intravenous fluids
      • Pancreatitis causes 3rd spacing of fluid from the vasculature mainly via increased capillary permeability
      • Traditional recommendations for large volume crystalloids (250-500 cc/hr X 12-24 hours) appears flawed (Farkas 2014)
      • More conservative resuscitation approaches recommend 2 – 4L of balanced solution over 24 hours
        • Give IV fluid boluses as needed for hypotension and volume depletion
        • Consider early administration of vasoactive substances if necessary to support blood pressure
    • Antiemetics
    • Analgesia
      • Pain often refractory to traditional analgesics and patients are likely to require opiates
      • If patient tolerating oral intake, oral administration of analgesia is appropriate
  • Oral Intake
    • Traditional approach discouraged any oral intake and recommended nasogastric tube (NGT) placement
    • Recent evidence supports early enteral nutrition (Kahl 2003)
    • Recommendations
      • If patient tolerates oral intake, start immediately
      • If patient does not tolerate oral intake and has continuous emesis, NGT may be useful along with parenteral nutrition
  • Antibiotics
    • There is no evidence for the use of prophylactic antibiotics in pancreatitis (Tenner 2013)
    • Necrotizing pancreatitis without signs of infection does not benefit from antibiotics (Isenmann 2004, Dellinger 2007)
    • Antibiotics should be administered to patients with infectious complications from pancreatitis or infectious cause of their pancreatitis (i.e. cholangitis from gallstones)
  • Evaluation for Complications
    • Pancreatitis is a common cause of alcohol withdrawal. Carefully evaluate patient for signs of withdrawal if they have a history of alcohol use (tongue , tachycardia, hypertension, anxiety etc)
    • Cholangitis
      • Broad spectrum antibiotics
      • Surgical and interventional radiology consultation for drainage
    • ARDS
  • Gallstone Pancreatitis
    • All patients with pancreatitis should have an assessment for biliary pathology
    • Presence of gallstones should be treated as gallstone pancreatitis until proven otherwise
    • Look for concomitant cholangitis (fever, SIRS, lab abnormalities)
    • Consultation
      • Consult surgery for possible surgical intervention
      • Consult gastroenterology for possible ERCP if biliary obstruction suspected (elevated bilirubin > 5.0 mg/dl) (Tenner 2013)
  • Hypertriglyceridemic pancreatitis
    • Addition of gemfibrozil 600 mg (lipid lowering medication)
    • Plasmapheresis (plasma exchange)
      • Allows for removal of triglycerides from circulation
      • Requires hemodialysis catheter placement
    • Insulin therapy
      • Reduces triglyceride levels by reducing synthesis and accelerating metabolism
      • Dose: 0.25 units/kg/hr (along with a dextrose infusion)
    • Plasmapheresis vs. Insulin therapy
      • Studies comparing plasmapheresis to insulin therapy are limited (Farkas 2017)
      • Plasmapheresis is invasive, more expensive, requires anticoagulation, and requires hematology thus making performance more difficult
      • Consider insulin therapy in conjunction with your ICU team

Disposition

  • Admission to Hospital
    • Any patient with signs or symptoms of severe pancreatitis should be placed in a high-monitored area (ICU) as decompensation is common
    • Patients with inability to tolerate oral intake
    • Patients with pain refractory to oral medications
    • Patients without reliable follow up (i.e. those without insurance, homeless patients, chronic alcoholics etc)
    • Patients with gallstone pancreatitis
  • Patients who are stable, tolerating oral intake, have their pain controlled with oral medications and are able to follow up or return to the ED may be discharged home on a low fat diet

Take Home Points

  • Pancreatitis is diagnosed by a combination of clinical features (epigastric pain with radiation to back, nausea/vomiting etc) and diagnostic tests (lipase 3x normal, CT scan)
  • A RUQ US should be performed looking for gallstones as this finding significantly alters management
  • The focus of management is on supportive care. IV fluids, while central to therapy, should be given judiciously and titrated to end organ perfusion
  • Patients will mild pancreatitis who are tolerating oral intake and can reliably follow up, can be discharged home

Read More

Hemphill RR, Santen SA: Disorders of the Pancreas; in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2010, (Ch) 91: p 1205-1226

PulmCrit: The Myth of Large-Volume Resuscitation in Acute Pancreatitis

PulmCrit: Hypertriglyceridemic Pancreatitis: Can We Defuse the Bomb?

References

Banks PA, Freeman ML. Practice Parameters Committee of the American College of Gastroenterology Am J Gastroenterol. 2006;101(10): 2379-400. PMID: 17032204

Matsull WR et al. Biochemical markers of acute pancreatitis. J Clin Pathol 2006; 59:340. PMID: 16567468

Harvey RT, Niller WT. Acute biliary disease: Initial CT and follow-up US vs. initial US and follow-up CT. Radiology 1999; 213(3): 831-6. PMID: 10580962

Reitz S et al. Biliary, pancreatic, and hepatic imaging for the general surgeon. Surg Clin North Am 2011; 91(1): 59-92. PMID: 21184901

Tenner S et al. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol 2013; 108(9): 1400-15. PMID: 23896955

Wu BU et al. The early prediction of mortality in acute pancreatitis: a large population-based study. Gut 2008; 57: 1698-1703. PMID: 18519429

Papachristou GI et al. Comparison of BISAP, Ranson’s, APACHE-II, and CTSI scores in predicting organ failure, complications and mortality in acute pancreatitis. Am J Gastroenterol 2010; 105: 435-51. PMID: 19861954

Kahl S et al. Acute pancreatitis: Treatment strategies. Dig Dis 2003; 21:30. PMID: 12837998

Isenmann R et al. Prophylactic antibiotic treatment in patients with predicted severe acute pancreatitis: A placebo-controlled, double-blind trial. Gastroenterology 2004; 126(4): 997-1004. PMID: 15057739

Dellinger EP et al. Early antibiotic treatment for severe acute necrotizing pancreatitis. Ann Surg 2007; 245(5): 674-683. PMID: 17457158