Professional Documents
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Acute Pancreatitis
Acute Pancreatitis
Pancreatitis
Resident Conference
October 5, 2004
Rachel Dunagin, MD
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
Pathophysiology
Etiology
• Gallstone (35%) • Vascular Abnormalities
• Microlithiasis • Post-operative
• Alcoholism (30%) • Neoplasm
• Medication • Pancreas Divisum
• Trauma/Sphincter of Oddi • Autoimmune
Dysfunction • Hereditary
• Infection • Idiopathic (30%)
• Duodenal Diverticula • Hypertriglyceridemia
• Hypercalcemia • Cystic Fibrosis
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
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
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
Etiology: Medications
• Uncommon cause
• Azathioprine, 6-mercaptopurine and ddI
have 5-10% risk of acute pancreatitis
• >100 meds implicated
Definitely Cause Pancreatitis
• Azathioprine • 6-mercaptopurine
• Asacol • Metronidazole
• Cytosine arabinoside • Pentamidine
• Estrogens • Tetracycline
• Norethindrone/mestr- • Trimethoprim/sulfame
anol thoxazole (TMP/SMX)
• Isoniazid • Valproic Acid
Implicated Agents
• Industrial chemicals (Parathion)
• Scorpion venom
Viral Infections
• Mumps – most common in adults
• Coxsackie-B
• Epstein-Barr
• Rubella
• Influenza A
• Varicella
• Hepatitis A, B, C, E
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
Rare Etiologies
• SLE
• Polyarteritis Nodosum
• Autoimmune pancreatitis
• Fungal infections
• Bacterial infections: Legionella, Brucellosis
• Ampullary tumors
• Metastatic tumors (breast, lung)
• Pancreas Divisum
Pancreatic Divisum
• Debatable cause
• Represents 5-7% of population per
autopsy and ERCP studies
• Normal Pancreatic Development:
– Dorsal and ventral pancreatic buds fuse
during 8th week gestation to form main
pancreatic duct; drains through major papilla.
– Small duct often persists between the main
pancreatic duct and the minor papilla
Pancreatic Divisum
• Embryonic dorsal and ventral ducts fail to migrate and
fuse abnormally.
• Two noncommunicating duct systems:
– Inferior portion of head of pancreas drained by rudimentary
ventral duct through the major papilla.
– Remainder of pancreas drained by dorsal duct through the minor
papilla.
Pancreatic Divisum:
Hypothesis of pancreatitis etiology
• First proposed in 1977
• Increased resistance to flow through a small minor
papilla.
• If so, would reason that recurrent pancreatitis would stop
after endoscopic minor papilla sphincterotomy, or
insertion of endoscopic stent across the minor papilla.
• Some disagree on basis that incidence of pancreas
divisum is the same in patient with or without pancreatitis
and 95% with pancreatic divisum do not develop
pancreatitis
• Other arguments against: pancreatitis develops in
adulthood, not childhood in those with pancreatic divisum
• Still remains controversial.
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
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
Cullen’s Sign
Grey-Turner’s Sign
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
Nonspecific Lab Findings
• Leukocytosis
• Hyperglycemia
• Hypocalcemia
• LFTs: AST, ALT, AlkPhos, Bilirubin
• Hypertriglyceridemia
• Hypoxemia
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)
Laboratory Tests
• Caution!! -- Other causes of elevated amylase
level
– Can be of pancreatic or salivary origin
– Any inflammatory process of abdomen:
• Perforated peptic ulcer
• Intestinal obstruction
• Cholecystitis
• Generalized peritonitis
• Mesenteric ischemia
• Ruptured AAA/ectopic pregnancy
– Renal failure
– Macroamylasemia: due to benign change in peptide processing
in Golgi (amylase is bound to immunoglobulin or abnormal
serum protein), forms a large complex which is difficult to clear
through the kidneys
Laboratory Testing
• Serum Lipase
– More sensitive and specific than amylase
– Greater than 2-3x upper limit of normal
– Does not correlate with severity of disease
Other Lab Tests
• Pancreatitis associated protein (PAP),
heat shock protein
• Trypsinogen activation peptide (TAP), 5-
amino acid peptide cleaved from
trypsinogen to produce active trypsin
• Non-specific Markers: CRP, neutrophil
elastase, complement, TNF, IL6
• Methemalbumin level
Radiology
• Sonography
• Computer Tomography (CT)
• Magnetic resonance imaging (MRI)
Ultrasound
• Fails to completely to completely image the
pancreas 2/2 overlying bowel gas
• Superior to CT in visualizing gallbladder and
biliary tree for gallstones
• Negative US does not rule out gallstone as
etiology because:
1. Not sensitive for common bile duct stones.
2. Only 50% of those with microlithiasis have + US.
3. View may be obstructed by ileus and underlying
structures obscured by bowel gas.
A B
Ranson Criteria