GASTROINTESTINAL Last edited: 3/4/2024

13. PANCREATITIS
I. PATHOPHYSIOLOGY III. CLASSIC FINDINGS OF IV. COMPLICATIONS OF V. DIAGNOSTIC APPROACH TO VI. TREATMENT OF
A. ACUTE PANCREATITIS PANCREATIC DISORDERS PANCREATIC DISORDERS PANCREATIC DISORDERS PANCREATIC DISORDERS
B. CHRONIC PANCREATITIS A. EPIGASTRIC ABDOMINAL PAIN A. ACUTE PANCREATITIS A. ACUTE PANCREATITIS A. ACUTE PANCREATITIS
II. CAUSES B. CHRONIC PANCREATITIS B. CHRONIC PANCREATITIS B. CHRONIC PANCREATITIS
A. ACUTE PANCREATITIS C. CHRONIC PANCREATITIS
B. CHRONIC PANCREATITIS

00:50
I. Pathophysiology
00:50 B. Chronic Pancreatitis 06:18
A. Acute Pancreatitis
o Pancreatic Duct or Acinar Cell Injury → o Repeated Pancreatic Duct or Acinar Cell Injury →
Inadvertent activation of pancreatic enzymes → Autodigestion Repeated inadvertent activation of pancreatic enzymes →
of pancreas → Acute pancreatic inflammation, pancreatic Repeated autodigestion of pancreas →
edema, pancreatic necrosis, and possibly pancreatic Repeated pancreatic inflammation occurs →
hemorrhage develops Results in Fibrosis and Calcification of the pancreatic tissue

Acinar Cell Injury Ductal Cell Injury

+ Autodigestion of pancreas +

Acinar cell

+ +
+ Proteases
+ Lipases
+ Amylases
+ +

Ductal cells
Inflammation

Acute pancreatitis
Epigastric pain
+ Edema
+ Necrosis
TNF-α
IL-1 Repeated + Hemorrhage
SIRS IL-6 bouts of
Effect + inflammation Local complications

Chronic pancreatitis
II
II

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 II. Causes
A. Pancreatic Duct Injury
Ductal cell injury
1. Acute Pancreatitis
Acute causes o Gallstone near the hepatopancreatic ampulla → blocks flow of
pancreatic enzymes → Inadvertent activation of pancreatic
Gallstone (*) enzymes
ERCP  One of the most common causes
o Endoscopic Retrograde Cholangiopancreatography (ERCP) →
Pancreatic duct injury when maneuvering throughout the
biliary and pancreatic ductal tree → Inadvertent activation of
pancreatic enzymes

Chronic causes 2. Chronic Pancreatitis

Cystic fibrosis o Cystic Fibrosis → Repeated mucus plugging of pancreatic ducts
→ Repeatedly blocks flow of pancreatic enzymes → Inadvertent
activation of pancreatic enzymes

B. Pancreatic Acinar Cell Injury

1. Acute Pancreatitis
o Alcohol Abuse → Acinar cell injury →
Inadvertent activation of pancreatic enzymes
 One of the most common causes
o Hypertriglyceridemia (> 1000) → Acinar cell injury →
Inadvertent activation of pancreatic enzymes
o Hypercalcemia → Inadvertent activation of pancreatic
enzymes
o Drugs (e.g. Steroids and Antiretrovirals) → Acinar cell injury →
Inadvertent activation of pancreatic enzymes

2. Chronic Pancreatitis
o Chronic Alcohol Abuse → Repeated acinar cell injury →
Inadvertent activation of pancreatic enzymes

00:56
III. Classic Findings of Pancreatic Disorders
A. Epigastric Abdominal Pain
Inflammation of the pancreas causes pain to localize to the
anatomical location of the pancreas →
Epigastric region, but can also radiate to the back
(interscapular region)
o Positional Pain
 Worse with lying flat
 Better with leaning forward

FIGURE 1. ↑PAIN LYING SUPINE FIGURE 2. ↓PAIN LEANING FORWARD

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IV. Complications of Pancreatic Disorders
A. Acute Pancreatitis
Pancreatitis
+ +

IL-1
TNF-α
Blood

Lipases

Permeability 3rd spacing

1. Hypovolemia 2. Acute Respiratory Distress Syndrome (ARDS)

Pathophysiology: Pathophysiology: 3rd spacing
o Pancreatic inflammation attracts macrophages and neutrophils o Pancreatic inflammation
→ ↑Release of IL-1 and TNF-alpha → ↑Systemic vasodilation attracts macrophages and neutrophils →
and ↑Capillary permeability → Leakage of fluid into interstitial ↑Release of IL-1 and TNF-alpha →
spaces → ↓Intravascular blood volume → Hypovolemia ↑Diffuse pulmonary capillary permeability →
Presentation: Leakage of fluid into alveolar and
Shunting
o Hypotension and Tachycardia interstitial spaces →
 Hypovolemia → ↓SV → ↓BP → Compensatory Tachycardia Diffuse alveolar filling →
o AKI Pulmonary shunt arises →
 Hypovolemia → ↓SV → ↓BP → Poor renal perfusion Severe impairment in gas
 ↑Creatinine and ↓Urine output support AKI exchange
o ↑Risk of Infected Pseudocyst and Walled-Off Necrosis: Presentation: Diffuse alveolar
 Hypovolemia → Poor bowel and pancreatic perfusion → o Refractory Hypoxemia filling
Bowel and pancreatic necrosis → Bowel integrity lost →  ↓SPO2 despite oxygen administration O2
ARDS RR
Bacterial translocation → Bacteria invade pseudocyst or o Bilateral infiltrates on CXR
WOB
necrotic tissue  There is potential for a large pleural effusion
3rd spacing o Respiratory distress (↑WOB, ↑RR)

3. Disseminated Intravascular Coagulation (DIC)

+
Hypovolemia Pathophysiology:
HR o Pancreatic inflammation attracts macrophages and neutrophils →
↑Release of Il-1 and TNF-alpha →
+ Tissue factor
↑Tissue factor production →
↑Activation of procoagulants →
↑Formation of diffuse clotting → Consumption
+ of platelets, RBCs, and clotting factors →
Renal Clotting
↑Risk of bleeding
BP perfusion (diffuse)
Presentation:
UOP o Bleeding
Shock AKI
Cr/BUN  Mucocutaneous bleeding
(Hypovolemic  GI bleeding Consumption
shock) Necrosis/infections  Bleeding from IV sites
o ↓Platelets and ↓RBCs PLTS PT/INR
 Secondary to consumption RBC’s PTT
D-Dimer
o ↑PT/INR and ↑PTT
 Secondary to consumption of clotting factors
Risk of
leading to prolonged bleeding time or time to
bleeding
clot (DIC)
o ↑D-dimer
 Secondary to ↑Clot formation

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 29:29
4. Acute Pancreatic Fluid Collection (APFC)
Pathophysiology:
o Pancreatic inflammation attracts macrophages and neutrophils
→ ↑Release of IL-1 and TNF-alpha → ↑Pancreatic vessel
vasodilation and ↑Capillary permeability → Leakage of fluid
into pancreatic tissue spaces
Presentation:
o Typically, asymptomatic and found incidentally on CT scan < 4
weeks after diagnosis of pancreatitis

5. Pancreatic Pseudocyst
Pathophysiology:
o Pancreatic inflammation attracts macrophages and neutrophils
→ ↑Release of IL-1 and TNF-alpha → ↑Pancreatic vessel
vasodilation and ↑Capillary permeability → Leakage of fluid
into pancreatic tissue spaces → Walling-Off of Pancreatic Fluid
Collection
Presentation:
o Typically, asymptomatic → However, may develop some
symptoms/complications:
 ↑Epigastric Abdominal Pain:
• ↑Size of pancreatic pseudocyst → ↑Epigastric pain
 ↑Risk of SBO:
• ↑Size of pancreatic pseudocyst → ↑Compression of small
bowel
 ↑Risk of Pseudocyst Rupture:
• Rupture of pseudocyst into peritoneal cavity →
inflammation of the peritoneum → peritonitis
 ↑Risk of Infected Pseudocyst:
• Hypovolemia → Poor bowel and pancreatic perfusion →
Bowel and pancreatic necrosis → Bowel integrity lost →
Bacterial translocation → Bacteria invades pseudocyst or
necrotic tissue
o CT scan finding > 4 weeks after diagnosis of pancreatitis

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 IL-1
TNF-

+ Necrosis (~15%)
+ Hemorrhage
Pancreatic vessels

Autodigestion + Tissue necrosis

BV

6. Acute Pancreatic Necrosis

Pathophysiology: Acute pancreatic
o Pancreatic inflammation attracts macrophages and neutrophils
necrosis
(<4 wks)
→ ↑Release of IL-1 and TNF-alpha → ↑Pancreatic vessel
(>4 wks)
vasodilation, ↑Capillary permeability, and ↑Lipase enzymes
lead to pancreatic edema and necrosis (Hypovolemia can
worsen this)
Presentation:
o ↑Epigastric pain, ↑WBC and ↑Fever
o CT scan finding < 4 weeks after diagnosis of pancreatitis Walled off
necrosis

7. Walled-Off Necrosis BV
Pathophysiology:
Infected
o Pancreatic inflammation attracts macrophages and neutrophils
→ ↑Release of IL-1 and TNF-alpha → ↑Pancreatic vessel necrosis
vasodilation, ↑Capillary permeability, and ↑Lipase enzymes WBC
lead to pancreatic edema and necrosis (Hypovolemia can Fever
worsen this) → The necrotic tissue can also be walled
off/encapsulated
Presentation:
o ↑Epigastric pain, ↑WBC and ↑Fever
o CT scan finding > 4 weeks after diagnosis of pancreatitis

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8. Retroperitoneal Hemorrhage
Pathophysiology:
+ Tissue necrosis
o Pancreatic inflammation attracts macrophages and neutrophils
→ ↑Release of IL-1 and TNF-alpha → ↑Pancreatic vessel
vasodilation, ↑Capillary permeability, and ↑Lipase enzymes
lead to pancreatic edema, necrosis and erosion into nearby Erodes into vessel
arteries → Blood can leak into the retroperitoneum (<4 wks)
Presentation: Acute pancreatic
necrosis
o Cullen's Sign:
 Hematoma near umbilicus
o Gray-Turner Syndrome:
 Hematoma along the flank Retroperitoneal
bleeding

Gray turner Cullen’s

syndrome sign

9. Abdominal Compartment Syndrome

Ascites IVF IABP

3rd spacing
Abdominal
compartment
syndrome

Pathophysiology: Presentation:
o Pancreatic inflammation attracts macrophages and neutrophils o Respiratory Distress:
→ ↑Release of IL-1 and TNF-alpha → ↑Pancreatic vessel  ↑IABP → Elevation of the diaphragm → ↓Ability to inflate
vasodilation and ↑Capillary permeability → Leakage of fluid the lungs fully → Requires a ↑WOB
into pancreatic tissue spaces and retroperitoneum → Pressure o Hypotension:
in the retroperitoneum builds up resulting in an increase in  ↑IABP → Compression of the IVC → Reduced venous return
intra-abdominal pressure (IABP) to the heart → ↓CO → ↓BP
 This can be exacerbated by over aggressive fluid o AKI:
resuscitation  ↑IABP → Compression of the renal artery → Reduced renal
perfusion
o IABP > 20mmHg:
 Measured via a bladder pressure from a foley catheter

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 B. Chronic Pancreatitis 45:26

1. Global Malabsorption 2. Diabetes Mellitus

Pathophysiology: Pathophysiology:
o Chronic Pancreatitis →
Malabsor ption Diabetes
o Chronic Pancreatitis →
syndrome mellitus
Exocrine pancreatic Insufficiency → Endocrine pancreatic Insufficiency →
Loss of function in the exocrine Loss of function in the endocrine
portion of the pancreas → portion of the pancreas →
↓Pancreatic proteases, lipases, and ↓Insulin production → Hyperglycemia
amylases are released into the Presentation:
Exocrine
intestinal lumen → function o Polyphagia -

Leads to the inability to digest o Polydipsia G G G G

proteins, fats, and carbohydrates in o Polyuria
Glucose
the stool
Presentation:
o Weight Loss
3. ↑Risk of Pancreatic Cancer
 This is due to ↓protein absorption → Leads to muscle Pathophysiology:
wasting o Chronic Pancreatitis → Pancreatic
o Chronic Diarrhea Chronic pancreatic inflammation → cancer
 This is due to ↓carbohydrate absorption → Leads to water ↑Risk of dysplasia
being pulled into the bowel lumen → Larger volumes of Presentation:
liquid stool pass through the intestines o Epigastric Pain
• This is often associated with Abdominal pain from bowel o Courvoisier’s Sign: Dysplasia
distention from increased fluid in the intestinal lumen  Nontender distended gallbladder and
• This is often associated with Flatulence from increased gas Jaundice
production as a byproduct of carbohydrate breakdown by o Trousseau's Syndrome: Pancreatic
bacteria in the intestinal lumen  Hypercoagulable state → adenocarcinoma
o Steatorrhea: Superficial thrombophlebitis
 Due to ↓fat absorption → Leads to greasy and foul-smelling
stools
o Vitamin A, D, E, K Deficiency:
 Due to ↓Fat absorption → Leads to the inability to assist in
the co-absorption of fat-soluble vitamins across the small
intestines
• Vitamin A Deficiency:
o May present with night blindness
• Vitamin D Deficiency:
o May present with hypocalcemia, rickets, or
Osteomalacia
• Vitamin E Deficiency:
o May present with hemolytic anemia or neuropathy
• Vitamin K Deficiency:
o May present with bleeding
o Anemia:
 This is due to ↓B12, Folate, and Iron absorption →
Leads to the inability of the bone marrow to mature and
produce RBCs → ↓RBCs enter the circulation
• B12 and Folate deficiency → Macrocytic Anemia
• Iron deficiency → Microcytic Anemia

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V. Diagnostic Approach to Pancreatic Disorders

A. Acute Pancreatitis
1. Assess for Evidence of Acute Pancreatitis

a) Obtain Lipase
Indications:
o High degree of suspicion for Acute Pancreatitis
Abnormal Findings:
o ↑Lipase (3x upper limit of normal)
 This is specific for the diagnosis of pancreatitis
 The presence of epigastric pain and ↑Lipase → Supports the
diagnosis of acute pancreatitis

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2. Assess for Local Pancreatic Complications

Obtain CT Abdomen
Indications: iii) Pancreatic Pseudocyst
o Epigastric pain is present, but lipase level is inconclusive →  Well-defined margins containing a large fluid collection
A CT would assist in the diagnosis of pancreatitis centered around the pancreas
o Assess for complications of pancreatitis if presenting with:  This is present in > 4 weeks after diagnosis of pancreatitis
↑Fevers, ↑WBC, Hypotension, and worsening abdominal pain

Abnormal Findings:

i) Acute Peripancreatic Fluid Collection

 Fat stranding and pancreatic fluid collections around the
pancreas that do not have clear margins
 This is present in < 4 weeks after diagnosis of pancreatitis

ii) Acute Pancreatic Necrosis

 Areas of poorly defined margins of pancreatic necrosis and
areas of edema along with fat stranding
 This is present < 4 weeks after diagnosis of pancreatitis

FIGURE 5. CT INDICATING PANCREATIC PSEUDOCYST

iv) Walled-Off Necrosis

 Well-defined margins containing a large amount of
pancreatic necrosis and areas of edema along with fat
stranding
FIGURE 3. CT INDICATING ACUTE PANCREATIC NECROSIS  This is present > 4 weeks after diagnosis of pancreatitis
• This necrotic tissue is susceptible to becoming infected
and requires fine needle aspiration (FNA) to definitively
diagnose the presence of infected necrosis

FIGURE 4. CT INDICATING PANCREATIC EDEMA AND FAT STRANDING

FIGURE 6. CT INDICATING WALLED-OFF NECROSIS

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3. Assess for Gallstone-Related Pancreatitis
Obtain RUQ U/S
Indications:
o Diagnosis of pancreatitis
o Presence of Jaundice
o Presence of ↑AST, ALT, ALP and
Bilirubin
Abnormal Findings:
o Stone present in the common bile
duct
o Dilation of the common bile duct
FIGURE 7. RUQ U/S INDICATING GALLSTONE FIGURE 8. RUQ U/S INDICATING DUCTAL DILATION

B. Chronic Pancreatitis 1

1. Assess for Loss of 2. Assess for Evidence of Pancreatic Fibrosis and

Pancreatic Function Calcifications

Obtain Fecal Elastase Obtain CT Abdomen

Indications: Indications:
o Epigastric pain with normal lipase levels, but the presence of o Epigastric pain with normal lipase levels, but ↓Fecal elastase
Malabsorption and Diabetes Mellitus with concern for Chronic levels supporting Chronic Pancreatitis
Pancreatitis Abnormal Findings:
Abnormal Findings: o Pancreatic ductal dilation related to strictures from fibrosis
o ↓Fecal elastase highly supports Chronic Pancreatitis mixed with calcification
 This reveals a “Chain of Lakes” appearance

FIGURE 9. STOOL SAMPLE FOR FECAL ELASTASE LEVELS FIGURE 10. CT ABDOMEN INDICATING PANCREATIC CALCIFICATION & FIBROSIS

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 56:12
VI. Treatment of Pancreatic Disorders
A. Acute pancreatitis
1. Management of Abdominal Pain and Nausea/Vomiting
Treatment:
o NPO TABLE 1. ACUTE PANCREATITIS OVERVIEW
o NGT decompression if severe
Purpose:
o NPO
 By preventing the further intake of food and fluids, the
buildup of substances before the swollen pancreas, which is
compressing the small intestine, is reduced. This leads to
decreased vomiting and bowel dilation, thereby reducing
distention and pain. It also allows time for the inflammation
in the pancreas to subside
o NGT
 Initiating decompression alleviates the accumulation of fluid
and contents ahead of the swollen pancreas, which is
pressing on the small bowel. This action reduces vomiting,
lessens bowel dilation, minimizes distention, and decreases
pain, thereby providing time for the inflammation in the
pancreas to subside
 This may also prevent aspiration of gastric contents,
especially in a patient with a decreased level of
consciousness, which increases the risk for aspiration PNA
Monitoring:
o Improvement/Resolution of abdominal pain, nausea and
vomiting

2. Management of Gallstone Pancreatitis

Treatment:
o ERCP
Indications:
o RUQ U/S with the diagnosis of Gallstone in Hepatopancreatic
Ampulla
Purpose:
o Decompress the pressure proximal to the hepatopancreatic
ampulla obstruction
Monitoring:
o Improvement/Resolution in abdominal pain, LFTs, and jaundice

Endoscopic Retrograde
Cholangiopancreatography
(ERCP)

Procedure that is used to

remove Gallstones from the Bile Duct

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3. Management of Complications

a) Hypovolemia c) Infected Pancreatic Necrosis

Treatment: Treatment:
o Intravenous Fluids o Antibiotics and/or Debridement
Indications: Indications:
o Diagnosis of Acute Pancreatitis with the presence of o Diagnosis of Infected Necrosis
Hypotension and AKI  Presence of ↑fever, ↑WBC, hypotension, CT evidence of
Purpose: suspected infected necrosis, fine needle aspiration (FNA)
o Prevent or reduce the progression of Hypotension, AKI, and with evidence of infection
pancreatic necrosis, and prevent the risk of infected necrosis Purpose:
Monitoring: o Eradicate infection (via antibiotics and debridement) and
o Improvement in BP and HR removal of necrotic tissue (via debridement)
o Improvement in AKI (↓Creatinine and ↑Urine output) Monitoring:
o Improvement in abdominal pain, fever, WBC count
o Monitor CT for improvement in pancreatic necrosis and
b) Symptomatic Pseudocyst infection
Treatment:
o Endoscopic Drainage
Indications: d) Abdominal Compartment Syndrome
o ↑Epigastric abdominal pain: Treatment:
 ↑Size of pancreatic pseudocyst → ↑Epigastric pain o Surgical Decompression
o ↑Risk of SBO: Indications:
 ↑Size of pancreatic pseudocyst → ↑Compression of small o Diagnosis of Abdominal Compartment Syndrome based on
bowel IABP > 20mmHg and presence of complications (e.g. AKI,
Purpose: Hypotension, Impaired ventilation)
o To alleviate the nearby compression of the enlarging Purpose:
pseudocyst o To reduce IABP quickly
Monitoring: Monitoring:
o Improvement in abdominal pain and SBO symptoms o Improvement in IABP via bladder pressure measurements
o Improvement in AKI, BP, Ventilation

FIGURE 11. ENDOSCOPIC DRAINAGE OF PSEUDOCYST

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4. Utilization of Ranson's Criteria

a) Purpose:
o Helps in determining the severity of pancreatitis and guide therapy

b) Parameters:
On admission (Remember mnemonic GA LAW): At 48 hrs (Remember mnemonic C- HOBB):
o Glucose > 200 mg/dL: Hyperglycemia can result from the o Calcium Level < 8 mg/dL: This can occur due to calcium
stress response and is indicative of metabolic derangements binding to fatty acids released during fat necrosis in the
o Age (> 55 years): Older age is associated with a higher risk of pancreas
severe pancreatitis. The mechanism behind this criterion is o Hct Drop of > 10%: Suggests bleeding from retroperitoneal
likely related to the decreased physiological reserve and hemorrhage, which can be a complication of severe
potential for more complications in elderly patients pancreatitis
o Lactate Dehydrogenase (LDH) level > 350 IU/L: Released from o Oxygen (PaO2) < 60 mmHg: Suggests respiratory
damaged tissues and cells, reflecting tissue injury and dysfunction such as ARDs, which may necessitate oxygen
inflammation therapy or mechanical ventilation in severe cases
o AST > 250 IU/L: Indicates more severe pancreatitis. AST is an o BUN Increase > 5 mg/dL after 48 hours: Indicates renal
enzyme found in the liver and other tissues, and elevated levels dysfunction secondary to hypovolemia, which can be a sign
can be a sign of tissue damage and inflammation of severe pancreatitis
o WBC Count >16,000/mm3: Indicates systemic inflammation o Base Deficit (Arterial pH < 7.35 or Base Deficit > 4 mEq/L):
and suggests a more severe form of acute pancreatitis Metabolic acidosis related to lactic acidosis, as indicated by a
low arterial pH or elevated base deficit within the first 48
hours, is a marker of severe pancreatitis. It reflects impaired
tissue perfusion and oxygenation

c) Interpretation:
Mild Acute Pancreatitis Moderate Acute Pancreatitis Severe Acute Pancreatitis
(0-2 Ranson's Criteria): (3-4 Ranson's Criteria): (≥ 5 Ranson's Criteria):
o Patients with mild acute pancreatitis o Patients with moderate acute o Patients with severe acute
typically have a lower risk of pancreatitis are at a higher risk of pancreatitis are at high risk of
complications. complications. developing complications such as
o Treatment primarily involves supportive o They may require more aggressive fluid pancreatic necrosis, organ failure,
care, including fasting from oral intake, resuscitation and close monitoring for and infection.
intravenous fluids for hydration, and signs of organ dysfunction, infection, or o They often require admission to an
pain management. pancreatic necrosis. Enteral nutritional intensive care unit (ICU) for
o Monitoring for signs of improvement or support may be considered. aggressive management.
deterioration is essential. o Treatment may involve intensive fluid
resuscitation, nutritional support
(possibly through enteral or
parenteral routes), antibiotics if
infection is suspected, and
consideration of interventional
procedures or surgery for
complications like infected necrosis.

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 B. Chronic pancreatitis
1. Management of Abdominal pain
Treatment:
o Treatment of underlying cause (e.g. alcohol abstinence)
 In the interim manage pain via the following escalation in
therapy:
• Opiates
• Nerve blocks
• Surgical resection
Monitoring:
o Improvement in abdominal pain

2. Management of Malabsorption
Treatment:
o Pancreatic Enzyme Replacement
Indications:
o Diagnosis of chronic pancreatitis that is causing EPI
Purpose:
o Provide exogenous pancreatic enzymes to ensure any nutrients
being ingested are properly digested and subsequently
absorbed
Monitoring:
o Improvement in steatorrhea, weight gain, and resolution of
complications (e.g., anemia, vitamin deficiency, etc.) ensures
the efficacy of therapy

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