R.E.B.E.L. EM – Acute Pancreatitis

Originally published at R.E.B.E.L. EM on October 17, 2017. Reposted with permission.

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Acute Pancreatitis Background:

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

Epidimiology (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%)

Etiology:

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

Pathophysiology:

• Phase 1: Local inflammation
  • 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
• Phase 2
  • Enzyme digestion leads to necrosis of the pancreas
  • Erosion into vascular structures can occur as well leading to hemorrhage
• Phase 3
  • Release of systemic inflammatory mediators
  • systemic immune response syndrome and multisystem organ dysfunction (i.e. acute renal failure, cardiac dysfunction, ARDS, disseminated intravascular coagulation)

Cullen’s Sign

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 may radiate to the back
  • Nausea and vomiting
  • Patients often have a history of prior similar episodes
• 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:

• Abdominal Pathology
  • Perforated viscus
  • Peptic ulcer
  • Biliary colic
  • Cholecystitis
  • Cholangitis
  • Bowel obstruction
  • Abdominal aortic aneurysm
  • Ectopic pregnancy
• Cardiopulmonary Pathology
  • Acute myocardial infarction
  • ARDS
  • Pericarditis

Ranson’s Criteria (Rosen’s)

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
• 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)
  • 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 (Wu 2008, Papachristou 2010)
  • Clinical score used to predict mortality from pancreatitis
  • Requires less tests than Ranson’s criteria but performs equally well
• 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 chalngiopancreatography (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
        • Hemodynamic instability
        • Organ failure (Hypotension, ARDS, GI bleed, AKI)
        • Ranson score > 3, BISAP > 3 or APACHE > 8
        • Presence of severe pancreatitis
      • 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 the 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 fasciculations, 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
  • 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 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

Clinical 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 with mild pancreatitis who are tolerating oral intake and can reliably follow up, can be discharged home

For More on This Topic Checkout:

• 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:

1. Matsull WR et al. Biochemical markers of acute pancreatitis. J Clin Pathol 2006; 59:340. PMID: 16567468
2. 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
3. Reitz S et al. Biliary, pancreatic, and hepatic imaging for the general surgeon. Surg Clin North Am 2011; 91(1): 59-92. PMID: 21184901
4. Tenner S et al. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol 2013; 108(9): 1400-15. PMID: 23896955
5. Wu BU et al. The early prediction of mortality in acute pancreatitis: a large population-based study. Gut 2008; 57: 1698-1703. PMID:18519429
6. 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:
7. 19861954Kahl S et al. Acute pancreatitis: Treatment strategies. Dig Dis 2003; 21:30. PMID:
8. 12837998Isenmann 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:
9. 15057739Dellinger EP et al. Early antibiotic treatment for severe acute necrotizing pancreatitis. Ann Surg 2007; 245(5): 674-683. PMID: 17457158

Post Peer Reviewed By: Salim R. Rezaie (Twitter: @srrezaie)