5/8/24, 11:39 Acute Pancreatitis - Lecturio

Acute Pancreatitis
Acute pancreatitis is an inflammatory disease of the pancreas due to autodigestion. Common etiologies
include gallstones and excessive alcohol use. Patients typically present with epigastric pain radiating to the
back. Diagnosis requires 2 of 3 criteria, including: characteristic abdominal pain, serum amylase and lipase 3
times the upper limit of normal, or characteristic radiology findings. Ranson’s criteria is commonly used to
assess the severity. Management includes aggressive intravenous (IV) hydration, analgesia, nutritional
support, and treatment of the underlying cause.

Last updated: May 17, 2024

CONTENTS

Epidemiology and Etiology

Pathophysiology
Clinical Presentation
Diagnosis
Management
Complications
Differential Diagnosis
References

Epidemiology and Etiology

Epidemiology
Incidence:
United States: 40–50 cases per 100,000 adults
Worldwide: 5–80 per 100,000 adults
Men > women
Men: likely due to alcohol
Women: related to biliary tract disease
Mortality is approximately 5%, overall:
Necrotizing pancreatitis: 17%
Interstitial pancreatitis: 3%

Etiology

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Biliary tract disease:
Approximately 40% of cases
Caused by biliary obstruction due to a stone
Alcohol use:
Approximately 30% of cases
Often an exacerbation of chronic pancreatitis
Usually seen with habitual consumption over 5–15 years, but may be seen after a binge
Endoscopic retrograde cholangiopancreatography (ERCP):
Can cause accidental lodging of stone into the sphincter of Oddi
Increased risk in sphincter of Oddi dysfunction
Abdominal trauma:
More often in penetrating injuries
Blunt trauma may lead to ductal injury
Drugs:
Azathioprine
Sulfonamides
Tetracycline
Valproic acid
Estrogens
Thiazide and loop diuretics
Corticosteroids
Octreotide
Pentamidine
Idiopathic:
Approximately 10%–30% of cases
Occult microlithiasis may be responsible.
Less common causes:
Infections:
Mumps
Hepatitis
Cytomegalovirus
Coxsackievirus
Salmonella
Parasites
Genetic predispositions (e.g., CFTR mutation, as in cystic fibrosis)
Hypercalcemia
Hypertriglyceridemia
Tumors
Toxins:
Organophosphates
Scorpion bite
Vascular or ischemic
Autoimmune pancreatitis (IgG4)
Developmental:
Pancreatic ductus divisum: failure of the dorsal and ventral pancreatic ducts to fuse
Annular pancreas: a band of pancreatic tissue surrounds the 2nd part of the duodenum
Sphincter of Oddi dysfunction

Pathophysiology
Normal pancreatic function

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The pancreas has endocrine (insulin) and exocrine (digestive enzymes) functions.
Digestive enzymes made in acinar cells → stored as zymogens (inactive form) → released in the
pancreatic duct and small intestine → activation by trypsin
Protective mechanisms against organ injury (autodigestion) include:
Negative feedback mechanism (↑ trypsin in duodenum → ↓ cholecystokinin (CCK) and secretin → ↓
pancreatic secretion)
Zymogens are controlled with protease inhibitors.
↓ Acinar cell pH and calcium concentrations → prevent premature activation of trypsin
Anything that disrupts the homeostasis of normal pancreatic function can cause acute pancreatitis.

Acute pancreatitis pathogenesis

1. Initiated through acinar cell injury from:
Biliary obstruction → increased pancreatic duct pressure → acinar cell injury
Direct injury (e.g., toxins, alcohol)
2. Changes in acinar cell pH and calcium concentrations → allows intrapancreatic activation of trypsin →
activation of zymogens → autodigestion
3. Inhibited secretion on zymogens into the pancreatic ducts → exocytosis into the interstitium → not fully
understood, but believed to lead to attraction of inflammatory cells
4. Inflammatory cells arrive → cytokine release → pancreatic inflammation
5. Cytokine release and vascular injury from enzymes → vasodilation and vascular permeability → fluid
shifting to the interstitial space (3rd spacing) → decreased perfusion and hypotension → can result in:
Shock
Acute renal failure
Pancreatic necrosis

Acute pancreatitis

Image by Lecturio.

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Clinical Presentation
Symptoms
Acute abdominal pain:
Epigastric
Dull and steady
Sudden onset, increasing in severity
Radiation to the back (approximately 50% of patients)
Nausea and vomiting
Anorexia
Diarrhea
Low-grade fever

Physical examination

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General:
Tachycardia
Abdominal tenderness
Abdominal distention
Diminished bowel sounds → ileus
Evidence of severe disease:
Fever
Hypotension
Tachypnea and crackles
Pale and diaphoretic
Signs of an underlying cause:
Hepatomegaly → alcoholic pancreatitis
Scleral icterus or jaundice → choledocholithiasis
Muscle spasms → hypocalcemia
Xanthomas → hypertriglyceridemia
Warning signs of retroperitoneal bleeding in severe, necrotizing pancreatitis:
Cullen’s sign: bluish discoloration around the umbilicus due to blood in the peritoneum
Grey-Turner’s sign: reddish-brown discoloration on the flanks due to blood in the retroperitoneum or
pancreatic exudates

Diagnosis
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Diagnostic criteria
The diagnosis of acute pancreatitis requires at least 2 of the following:
Acute onset of epigastric abdominal pain
Serum amylase or lipase > 3 times the upper limit of normal
Characteristic findings on imaging

Laboratory evaluation
↑ Serum amylase
↑ Serum lipase: more specific for pancreatitis
Hepatic function tests:
Alanine transaminase (ALT) > 150 U/L and ↑ bilirubin → pancreatitis secondary to gallstones
Maybe be ↑ with heavy alcohol use
Basic metabolic panel:
Calcium:
↑ Calcium → may be a potential cause of pancreatitis
↓ Calcium → frequently seen, and should be corrected
Electrolyte imbalances can occur due to 3rd spacing of fluids
↑ Blood urea nitrogen (BUN) → severe disease
Lactate dehydrogenase (LDH): ↑ in severe disease
Complete blood count:
↑ Hematocrit → severe disease
↑ WBCs → inflammation
C-reactive protein (CRP): > 150 mg/L at 48 hours → risk of severe pancreatitis and organ failure
Triglycerides: ↑ in hypertriglyceridemia
Immunoglobulin G4 (IgG4): may be checked if autoimmune pancreatitis is suspected
Arterial blood gas:
Should be done if the patient is tachypneic
Can evaluate oxygenation and acid-base status

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Milky plasma seen in a patient with hypertriglyceridemia: If seen, milky plasma should be considered as a potential cause of
acute pancreatitis.

Image (https://openi.nlm.nih.gov/detailedresult?img=PMC3520695_1752-1947-6-412-
1&query=blood%20triglycerides&it=xg&lic=by&req=4&npos=25): “Milky plasma” by the Department of Emergency and Critical Care Medicine,
Ohta Nishinouchi Hospital, 2-5-20 Nishinouchi, Koriyama, Fukushima, 963-8558, Japan. License: CC BY 2.0.
(http://creativecommons.org/licenses/by/2.0)

Imaging
Imaging may not be required if the 1st 2 diagnostic criteria are met, but can be used for evaluating the
underlying cause and complications:

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Computed tomography (CT):
Normal in 30% of cases
Potential findings:
Inflammatory changes of the pancreas
Necrosis, fluid collections, or pseudocysts can be seen later in the course.
Abdominal ultrasound (US):
Can be done if gallstone pancreatitis is suspected
Potential findings:
Gallstones
Common bile duct (CBD) dilation
Pancreatic edema
Peripancreatic fluid
Magnetic resonance cholangiopancreatogram (MRCP):
Can evaluate the biliary system
Findings:
Choledocholithiasis
Biliary dilation
Pancreatic edema
Pancreatic necrosis or pseudocysts
Chest radiograph:
For patients with pulmonary symptoms (dyspnea, tachypnea, hypoxia)
Potential findings:
Pleural effusions
Basal atelectasis
Diffuse, patchy infiltrates indicating acute respiratory distress syndrome (ARDS)
Abdominal radiograph:
Limited role
“Sentinel loop” finding (short segment of ileus near the pancreatic inflammation)

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Prognosis evaluation
Identifying the severity of acute pancreatitis is helpful in order to ensure the patient is treated
appropriately:
Ranson’s criteria (see table):
Widely used
The biggest disadvantage is that it takes 48 hours to complete the assessment.
Bedside index of severity in acute pancreatitis (BISAP) score (see table):
Simple
Calculated during the 1st 24 hours
Acute physiology and chronic health evaluation (APACHE) II score:
Evaluates age, temperature, mean arterial pressure, heart rate, respiratory rate, blood gas results,
WBC count, electrolytes, creatinine, Glasgow coma score (GCS), and other health conditions
Very cumbersome and complex

Table: Ranson's criteria (1 point each)

Present on admission At 48 hours after admission

Age > 55 years Decrease in hematocrit > 10%

WBC > 16,000/μL Increase in BUN by ≥ 5 mg/dL

Blood glucose > 200 mg/dL Serum Ca < 8 mg/dL

Serum LDH > 350 IU/L PaO2 < 60 mm Hg

Aspartate transaminase (AST) > 250 IU/L Base deficit > 4 mEq/L

Estimated fluid sequestration > 6 L

0‒2: Minimal mortality

3‒5: 10%‒20% mortality rate, must be admitted to ICU
> 5: Increased risk of systemic complications and mortality

Definitions:
PaO2 is the partial pressure of oxygen in arterial blood.
Base deficit indicates excess acid in the blood.

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Table: BISAP score (1 point each)

BUN > 25 mg/dL

Impaired mental status GCS < 15

Systemic inflammatory response syndrome (SIRS) Evidence of SIRS

Age > 60 years

Pleural effusion Positive finding on imaging

0‒2 points: lower mortality (< 2%)

3‒5 points: higher mortality (> 15%)

Management
Acute management
Basic treatment:
Aggressive intravenous fluid (IVF) resuscitation
Fluid intake and output monitoring
Close vital sign monitoring
Address electrolyte imbalances
Medications:
Analgesics (typically opioids)
Antiemetics
Initial bowel rest
Early nutritional support:
Can be started as early as 24 hours, if pain is decreasing
Is associated with ↓ morbidity compared to delayed or no nutrition
Mild acute pancreatitis:
Can be treated on a general medical ward
May begin low-residue, low-fat diet as soon as tolerated
Severe acute pancreatitis:
Intensive care setting is preferred.
May require enteral nutrition if the patient cannot tolerate oral intake: Start within 72 hours.

Treating the etiology

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Gallstones
ERCP:
Can perform sphincterotomy and stone extraction
Indicated for choledocholithiasis or evidence of cholangitis
Cholecystectomy:
Surgical removal of the gallbladder
Performed after recovery from pancreatitis
Hypertriglyceridemia:
Goal triglyceride level is < 500 mg/dL.
Intravenous (IV) insulin:
Requires close glucose monitoring
May need a concurrent dextrose infusion to prevent hypoglycemia
Apheresis:
Should be considered in patients with SIRS, hypocalcemia, and multi-organ dysfunction
May not be available at all hospitals
Alcohol:
Patient education
Abstinence

Complications
Infected pancreatic necrosis or abscess
Consider if patients continue to have a fever or increasing leukocytosis
⅓ of patients with pancreatic necrosis will develop infection.
Causative organisms:
E. coli
Pseudomonas
Klebsiella
Enterococcus
Treatment:
Antibiotics:
Carbapenems
Fluoroquinolones with metronidazole
Cefepime or ceftazidime with metronidazole
Image-guided aspiration and drainage
Surgical necrosectomy (debridement of pancreatic necrosis) if less-invasive measures are not
successful

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Pseudocyst
An encapsulated collection of fluid with a well-defined inflammatory wall
Occurs several weeks after the onset of pancreatitis
Most are asymptomatic, but some may have abdominal pain, early satiety, or jaundice.
Diagnosis is made with US, CT, or magnetic resonance imaging (MRI)
Treatment:
Observation:
For those with minimal or no symptoms
Most will reduce in size or resolve
Drainage:
For those who are symptomatic or develop infection
Requires the wall of the pseudocyst to mature, which may take weeks

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Abdominal compartment syndrome

Sustained intra-abdominal pressure with organ failure
Due to significant tissue edema and fluid resuscitation
Presentation:
Tense, distended, painful abdomen
Progressive oliguria
Hemodynamic instability
Pulmonary decompensation
Diagnosis is made by measuring the intra-abdominal pressure.
Treatment:
Hemodynamic support
Pain control
Surgical decompression

Pseudoaneurysm
Results from the erosion of the gastroduodenal or splenic artery into a pseudocyst
Rare, but life threatening
Presents with unexplained gastrointestinal bleeding and anemia
Angiography for diagnosis and embolization

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Splanchnic venous thrombosis

Thrombosis of the splenic, portal, or superior mesenteric veins
Splanchnic venous thrombosis is, many times, found incidentally on imaging.
Treatment:
Treat the underlying pancreatitis.
Anticoagulation if compromising hepatic function or bowel perfusion

Acute respiratory distress syndrome (ARDS)

Respiratory failure with widespread alveolar damage and inflammation of the lungs:
Mediated by cytokines and inflammatory cells
Caused by systemic inflammation from acute pancreatitis
Mortality rate of 30%–40%
Chest radiograph will show diffuse, bilateral opacities.
Treatment:
Oxygen supplementation:
High-flow nasal cannula
Mechanical ventilation
Conservative fluid management

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Differential Diagnosis
Acute cholecystitis: inflammation of the gallbladder resulting from sustained gallstone impaction of the
cystic duct. Patients present with colicky, upper abdominal pain, nausea, and vomiting. Inflammation of the
gallbladder and gallstones are seen on US or CT. Amylase and lipase are usually not elevated, which
differentiates acute cholecystitis from acute pancreatitis. Treatment includes IVF, antibiotics, and
cholecystectomy.
Perforated peptic ulcer disease: complete erosion of an ulcer through the wall of the stomach or
duodenum. Patients present with severe epigastric pain, tachycardia, and abdominal rigidity. Lipase and
amylase may be elevated, but not to the degree seen in acute pancreatitis. Diagnosis relies on imaging,
which will show extraluminal gas. Patients require antibiotics and emergency surgery for repair.
Acute mesenteric ischemia: tissue injury caused when perfusion fails to meet the demands of the
intestines, usually due to an embolism or thrombosis. Patients have periumbilical pain out of proportion to
the exam. Computed tomography with angiography is used to detect vessel stenosis or occlusion. Lipase
can be elevated, but not to the degree seen in acute pancreatitis. Acute ischemia requires
revascularization and resection of the infarcted bowel.
Pancreatic cancer: a neoplasm of the pancreas. Symptom onset is more insidious, and patients may have
unrelenting epigastric pain, weight loss, and jaundice. The diagnosis is confirmed with imaging. The
history, exam, and imaging will differentiate pancreatic cancer from acute pancreatitis. Treatment is usually
aggressive because tumors are usually found late, and includes chemotherapy, radiation, and surgery.
Prognosis for survival is generally poor.

References
1. Tang, J.C.F., & Markus, J.T. (2019). Acute pancreatitis. In Anand, B.S. (Ed.), Medscape. Retrieved November 8, 2020, from
https://emedicine.medscape.com/article/181364-overview ( https://emedicine.medscape.com/article/181364-overview)

2. Vege, S.S. (2019). Clinical manifestations and diagnosis of acute pancreatitis. In Grover, S. (Ed.), UpToDate. Retrieved November
8, 2020, from https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-acute-pancreatitis
(https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-acute-pancreatitis)

3. Vege, S.S. (2019). Etiology of acute pancreatitis. In Grover, S. (Ed.), Uptodate. Retrieved November 9, 2020, from
https://www.uptodate.com/contents/etiology-of-acute-pancreatitis (https://www.uptodate.com/contents/etiology-of-acute-
pancreatitis)
4. Vege, S.S. (2019). Management of acute pancreatitis. In Grover, S. (Ed.), Uptodate. Retrieved November 9, 2020, from
https://www.uptodate.com/contents/management-of-acute-pancreatitis (https://www.uptodate.com/contents/management-of-
acute-pancreatitis)
5. Vege, S.S. (2019). Pathogenesis of acute pancreatitis. In Grover, S. (Ed.), Uptodate. Retrieved November 9, 2020, from
https://www.uptodate.com/contents/pathogenesis-of-acute-pancreatitis (https://www.uptodate.com/contents/pathogenesis-of-
acute-pancreatitis)
6. Bartel, M. (2020). Acute pancreatitis. [online] MD Professional Version.
https://www.msdmanuals.com/professional/gastrointestinal-disorders/pancreatitis/acute-pancreatitis
(https://www.msdmanuals.com/professional/gastrointestinal-disorders/pancreatitis/acute-pancreatitis)

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