Pancreatitis

1. Core 1 (Pre-Clerkship)
   • Integrative Systems
     • Gastroenterology
       • Physiology of the pancreas and bile salts
       • Neoplastic states of the pancreas and gallbladder
2. Core 2 (Clerkship)
3. Core 3 (Post Clerkship) Electives that may further knowledge - Peds GI

Acute Pancreatitis 

• Requires at least 2 of the following for diagnosis:
  • Abdominal pain compatible with acute pancreatitis (ie. epigastric location, classically with radiation to the back)
  • Serum amylase and/or lipase ≥ 3x upper limit of normal
    • Lipase is generally preferred as it is more sensitive/specific for pancreatitis (amylase can also be produced in other organ systems or be elevated with kidney disease) and because it has a longer half-life (peaks at 48 hours and can remain elevated for a week, amylase may normalize by 24 hours so may be falsely normal)
  • Findings on imaging consistent with acute pancreatitis
    • Abdominal US is first line imaging and can be helpful if elevated lipase with non-specific symptoms (children often cannot describe “classic” pancreatitis symptoms and this only occurs in 2-6% of pediatric patients).
    • We also routinely get abdominal ultrasound in all patients with diagnosis of pancreatitis to evaluate for peri-pancreatic fluids, signs of necrosis, or biliary tree dilation/obstruction that could affect management. 

Acute Recurrent Pancreatitis

• Requires 2 distinct episodes of acute pancreatitis with 1 of the following:
  • Complete resolution of pain between episodes for ≥ 1 month
  • Complete normalization of serum pancreatic enzyme concentrations WITH resolution of pain symptoms irrespective of time interval 

Chronic Pancreatitis 

• Requires 1 of the following:
  • Abdominal pain consistent with pancreatic origin and imaging findings suggestive of chronic pancreatic damage
  • Evidence of pancreatic insufficiency and suggestive imaging findings
  • Surgical or pancreatic biopsy demonstrating histologic features of chronic pancreatitis.  

Source: Adapted from UpToDate 

Acute Pancreatitis Management

CHOP Acute Pancreatitis Pathway 

Mainstay of treatment of acute pancreatitis regardless of etiology: 

• Hyperhydration – 1.5x maintenance rate of IV fluids (LR preferred)
  • Most important in the first 24-48 hours to improve outcomes by maintaining intra-vascular volume/organ perfusion in the setting of SIRS reaction/leaky vasculature and to preserve pancreatic microcirculation to prevent pancreatic necrosis.
  • There is no evidence for continued hyperhydration after 48h, consider weaning based on hydration status
  • Close monitoring of fluid status: clinical exams, daily weights, urine output, daily Can consider use of specific gravity as an objective marker of hydration status.
  • Calculating maintenance fluid rate:
    • 4 mL/kg/hour for the first 10kg of body weight + 2mL/kg/hour for the next 10kg of body weight + 1mL/kg/hour for each additional kg above 20kg
      • Ex: 15kg child = 50mL/hr for 1x maintenance
    • If >20kg, you can just add 40 to the weight to get the total mL/kg/hour
      • Ex: 25kg child = 65mL/hr for 1x maintenance
• Pain management 
  • Consider scheduling alternating IV acetaminophen and IV ketorolac around the clock
    • PRN opioids for breakthrough pain.
• Early enteral nutrition within at least 48-72 hours
  • Evidence in adults that early introduction of enteral nutrition helps to decrease length of hospital stay
    • Advance diet as tolerated as soon as able (usually within 24-48h)
    • There is NO evidence for use of low fat or restricted diet after acute pancreatitis
  • Consider NG/NJ feeds if PO intake is not progressing well by 48-72h
    • NJ feeds theoretically can cause less stimulation of the exocrine pancreas and can improve tolerance
  • In severe cases, can consider central line placement/TPN if prolonged intolerance of any enteral nutrition especially by day 5
• If mild pain with good PO intake, pancreatitis can be managed at home
• Repeating lipase is NOT routinely recommended as it is not correlated with clinical course/severity and does not affect management

Complications from Acute Pancreatitis 

• Fluid overload/shock
  • In severe cases, SIRS response can progress to shock and cause multi-organ dysfunction.
  • Inflammation from acute pancreatitis can cause a SIRS response which can cause vasodilation and leaky capillaries. This in combination with hyperhydration puts patients at risk for edema and fluid overload.
• Pancreatic Necrosis
  • May take 48-72 hours to develop necrosis, thus, CT may be more sensitive for necrosis after 72 hours.
  • Significantly increased risk of infection with necrotizing pancreatitis, although utility of empiric antibiotics is debated. This usually happens later in the clinical course (>10 days of treatment).
• Pancreatic pseudocyst/Walled off Necrosis
  • Takes >4 weeks after acute pancreatitis episode for this to develop
  • These fluid collections may become superinfected or can cause pain/obstructive symptoms depending on size/location
    • If asymptomatic, can monitor with serial imaging and may self-resolve
    • If symptomatic, can consider drainage after 4-6 weeks
      • Prior to 4-6 weeks, the walls of the pseudocyst/walled off necrosis are not mature enough to be safely drained

• Diagnosis requires 2 of the following: typical abdominal pain, elevated lipase or amylase ≥ 3x upper limit of normal, or consistent imaging findings 

• Mainstay of treatment is early hyperhydration, pain control, and early introduction of enteral nutrition 

• Most common cause of pancreatitis in children is idiopathic 

Answers 

Q1. Acute pancreatitis is diagnosed when at least two of the following are met:

• Abdominal pain (typically epigastric, radiating to the back)

• Elevated lipase or amylase ≥ 3 times the upper limit of normal

• Imaging findings consistent with acute pancreatitis

Q2. Lipase is preferred. It is more sensitive and specific than amylase, has a longer half-life, and remains elevated longer (up to 7 days). Amylase may normalize within 24 hours and can be produced by other organs, leading to false negatives.

Q3. The main treatment components are:

• Early hyperhydration (e.g., 1.5× maintenance D5LR for 24–48 hours)

• Pain control, typically with scheduled Tylenol and Toradol, and PRN opioids

• Early enteral nutrition, started within 48–72 hours and advanced as tolerated

Q4. Most common cause is idiopathic (~25%). Other causes include trauma, genetic mutations (e.g., CFTR), medications, and infections.

Q5. Diagnosis of chronic pancreatitis requires one of the following:

• Chronic pancreatic-type abdominal pain + imaging findings suggestive of chronic damage

• Evidence of pancreatic insufficiency + supportive imaging

• Histologic evidence on biopsy or surgical specimen

Q6. Workup for underlying etiology is generally pursued after the second episode of pancreatitis, unless there’s a clear known risk factor (e.g., trauma, medication).

Q7. Hyperhydration is most critical during the first 24–48 hours. There’s no evidence supporting continued aggressive hydration beyond that. After 48 hours, monitor closely for fluid overload.

Q8. Lipase should not be routinely repeated—its level does not correlate with disease severity or clinical course and does not impact management.

Q9. Pancreatic necrosis typically takes 48–72 hours to develop. CT scans are more sensitive for detecting necrosis after 72 hours.

Q10. Pancreatic pseudocyst or walled-off necrosis takes >4 weeks to develop. Asymptomatic cases can be monitored; symptomatic cases may require drainage, but it’s generally not safe to drain before 4–6 weeks when the walls are mature.

• CHOP Pathway for Management of Acute Pancreatitis 

• NAPSGHAN Summary of Evidence for Management of Acute Pancreatitis