Acute pancreatitis is an inflammatory process of the pancreatic parenchyma that results from premature activation of digestive enzymes within the pancreas. This leads to autodigestion of the pancreas and adjacent tissues. The majority of cases are mild and self-limited, while 15-25% are severe with potential multi-system organ failure. Common causes include gallstones, alcohol use, medications, trauma, infections and other metabolic conditions. Diagnosis involves clinical signs and symptoms confirmed by blood tests and imaging. Treatment focuses on pain management, intravenous hydration and nutritional support to prevent progression to systemic complications. Severe acute pancreatitis can lead to pancreatic necrosis, infection, pseudocyst formation and other serious complications.

1. Acute
Pancreatitis
Hemakshi Singh
Group 479

2. Background
• Acute Inflammatory process of pancreatic parenchyma
• A stimulus leads to release of activated digestive
enzymes from acinar cells into interstitium
• Results in autodigestion of pancreas and adjacent tissue
• Activated inflammatory mediators convert a localized
inflammatory response into a systemic inflammatory
process, resulting in increased tissue and vascular
permeability
• End result: hypovolemia, shock, ARDS, multisystem
organ failure
• Majority: mild self-limited course; 15-25% severe,
complicated course; 5% mortality

3. Etiology
• Gallstone (35%)
• Microlithiasis
• Alcoholism (30%)
• Medication
• Trauma/Sphincter of Oddi
Dysfunction
• Infection
• Duodenal Diverticula
• Hypercalcemia
• Vascular Abnormalities
• Post-operative
• Neoplasm
• Pancreas Divisum
• Autoimmune
• Hereditary
• Idiopathic (30%)
• Hypertriglyceridemia
• Cystic Fibrosis

4. Etiology: Gallstones
• ½ of all cases of acute pancreatitis
• 3-8% patients with symptomatic cholelithiasis
develop pancreatitis
• Older women
• 80% patients previously thought to have
idiopathic etiology are due to microlithiasis, tiny
gallstones, and biliary sludge
• Mechanism unclear – pancreatic ductal
obstruction does not full explain pathogenesis

5. Etiology: Alcohol
• Interferes with normal process of
pancreatic secretion
• Excessive deposition of GP-2 (protein
involved in maintaining normal pancreatic
secretion) leads to ductal obstruction
• Daily consumption 80g alcohol over 5-15
years before first attack of alcoholic
pancreatitis occurs
• Acute attacks 1-3 days after drinking

6. Etiology: Hypertriglyceridemia
• >1000mg/dL
• 50% with hyperTG have falsely normal
amylase level due to interference of
lipemic specimen with assay
• Therefore, must dilute serum to get
accurate serum amylase level

7. Etiology: Medications
• Uncommon cause
• Azathioprine, 6-mercaptopurine and ddI
have 5-10% risk of acute pancreatitis
• >100 meds implicated

8. Definitely Cause Pancreatitis
• Azathioprine
• Asacol
• Cytosine arabinoside
• Estrogens
• Norethindrone/mestr-
anol
• Isoniazid
• 6-mercaptopurine
• Metronidazole
• Pentamidine
• Tetracycline
• Trimethoprim/sulfame
thoxazole (TMP/SMX)
• Valproic Acid

9. Viral Infections
• Mumps – most common in adults
• Coxsackie-B
• Epstein-Barr
• Rubella
• Influenza A
• Varicella
• Hepatitis A, B, C, E

10. AIDS and Pancreatitis
• 10% with AIDS develop acute pancreatitis
• Asymptomatic pancreatic lesions in 30-
50% of autopsy cases
• Common infectious etiologies: CMV, MAC,
Crypto, M. TB, Toxoplasma
• Common medication etiologies:
pentamidine, ddI, ddC and TMP/SMX

11. Rare Etiologies
• SLE
• Polyarteritis Nodosum
• Autoimmune pancreatitis
• Fungal infections
• Bacterial infections: Legionella, Brucellosis
• Ampullary tumors
• Metastatic tumors (breast, lung)
• Pancreas Divisum

12. Diagnosis
Clinical signs and symptoms, confirmed with lab/radiologic studies
Symptoms:
• Acute abdominal pain
– Location: entire abdomen or localized in midepigastric, RUQ or left flank
– Intensity: maximized within 10 – 20 min of acute attack
– Quality: steady, moderate to severe, little relief with change of position,
unbearable, refractory to narcotics
– Radiation: band-like to the back
• Anorexia, nausea, emesis
• CNS manifestations: disorientation, hallucinations, agitation, or
coma

13. Diagnosis
Signs:
Mild Pancreatitis – mild abdominal tenderness, no guarding
Severe Pancreatitis - epigastric tenderness and guarding, rebound
tenderness, abdominal distention (due to gastric ileus or
dilatation of transverse colon)
• Decreased or absent bowel sounds
• May be mistaken for acute abdomen
• If severe, extensive peripancreatic fat necrosis with hemorrhagic
fluid within the peritoneum and/or retroperitoneum → Cullen’s sign,
Grey-Turner’s sign
• Palpable epigastric mass = pseudocyst or large inflammatory mass
• Subcutaneous nodular fat necrosis, thrombophlebitis in legs,
polyarthritis

14. Diagnosis
• Due to third-space fluid loss and systemic
toxicity
– Pulse 100-150
– BP hypertensive in beginning, then
hypotensive due to 3rd spacing and
hypovolemia
– Temp: initially normal, then increase to 101-
103 within 1-3d
– Tachypnea and shallow respirations

15. Nonspecific Lab Findings
• Leukocytosis
• Hyperglycemia
• Hypocalcemia
• LFTs:  AST,  ALT,  AlkPhos,  Bilirubin
• Hypertriglyceridemia
• Hypoxemia

16. Laboratory Testing
• Serum Amylase
– Most widely accepted
– 2-3x upper limit of normal
– Does not correlate with severity of disease
– 30% of Alcoholics with acute pancreatitis have normal
amylase levels
– ? of using elevated lipase to amylase level to predict
alcoholic acute pancreatitis
– ALT 3x upper limit of normal + elevated amylase is
highly sensitive for gallstone pancreatitis (95% PPV)

17. Radiology
• Sonography
• Computer Tomography (CT)
• Magnetic resonance imaging (MRI)

18. Severity:
Open Drainage due to Pancreatic Necrosis

19. Atlanta Symposium Criteria
• 40 Internationally renowned experts on
pancreatic disease met to define severity of
pancreatitis
• Defined based on outcome: organ failure and/or
anatomic complications
• Mild acute pancreatitis: minimal or no organ
system dysfunction with complete and
uneventful recovery; interstitial edema of
parenchyma
• Severe acute pancreatitis: evidence of life-
threatening systemic complications or pancreatic
collection.

20. Treatment
• Goals: halt progression of local disease and
prevent remote organ failure
• Nutritional Support:
– Pancreatitis is catabolic state
– Benefit of pancreatic “rest” by limiting oral intake is
unproven, however is widely used
– Evidence that early enteral nutrition is safe
– Nasojejunal feeding limits pancreatic secretion
– Preferable to oral or nasogastric feeding

21. Treatment
• Fluids
– IV hydration, aggressive (300-500ml.hr) especially in the early phase of illness
with goal hemodilution to Hct 30%
– May need NG tube (if persistent nausea and vomiting or ileus), Foley catheter
and central line or Swan-Ganz catheter to monitor hydration status
• Analgesics
– Adequate pain control is essential
– 50-100mg Meperidine (Demerol) IV q3-4hr
– Hydromorphone (Dilaudid) PCA
– Avoid Morphine b/c it increases sphincter of Oddi tone and increases serum
amylase
• ERCP
– If severe acute gallstone pancreatitits or ascending cholangitis is indicated, then
early ERCP with sphincterotomy and stone extraction is indicated.
– Is not to be used in mild acute pancreatitis

22. Pancreatic Infection:
A Word on Antibiotics
• Antibiotics – there is no role for routine use
– Indicated if severe attack with necrosis of pancreas
– Typical organisms: from gut = E coli, Pseudomonas,
Klebsiella, Enterococcus
– Treatment: selective decontamination of gut with oral
nonabsorbable antibiotics, systemic antibiotics, and
enteral feedings to avoid catheter-related infections.
– Imipenem/cilastin penetrate pancreatic parenchyma
and reduces incidence of intra-abdominal infection.
– Unfortunately, there is a tendency for fungal
superinfection to develop later in clinical course.
– Other options: 3rd gen cephalosporin, piperacillin,
mezlocillin, fluoroquinolones and metronidazole

23. Treatment
Intensive monitoring All patients
Aggressive hydration All patients
Adequate analgesics All patients
H2 receptor
antagonist/proton
pump inhibitors
Unproven benefits
Antibiotic prophylaxis Patients with sterile necrosis
ERCP Early in patients with severe biliary pancreatitis/bilary sepsis;
Late in patients with acute gallstone pancreatitis when liver
function test are persistently elevated prior to cholecystectomy
Surgery If pancreatic abscess
If sterile necrosis and deteriorate or fail to improve after 4-6 wks of
medical management
If infected necrosis
Cholecystectomy for acute gallstone pancreatitis and recurrent,
idiopathic pancreatitis
TPN Patients with necrotizing pancreatitis

24. Complications of Acute Pancreatitis
EARLY COMPLICATIONS
• Cardiovascular Collapse
• Respiratory Failure
• Renal Failure
• GI bleeding
• DIC
• Visual Disturbance
• Change in mental status
• Metabolic disturbance
• Acute fluid collections
• Pancreatic Necrosis
LATE COMPLICATIONS
• Pseudocysts
• Pseudoaneurysms
• Perforation
• Obstruction
• Fistulization
• Infection (abscess,
infected necrosis)