This document discusses acute pancreatitis and acute cholangitis. It defines acute pancreatitis as a condition caused by pancreatic duct and acinar injury leading to autodigestion. Common causes include gallstones, alcohol use, genetic factors, medications and infections. Symptoms include abdominal pain, nausea and vomiting. Diagnosis requires characteristic pain plus elevated lipase or amylase levels and imaging. Management involves fluid resuscitation, nutritional support, analgesia and treating any underlying causes or complications which can include pancreatic necrosis, fluid collections and systemic effects.
3. ACUTE PANCREATITIS
PATHOGENESIS:
Pancreatic duct and acinar injury via direct or indirect toxicity
損 impaired secretion and premature activation of digestive enzymes -損 autodigestion and acute
inflammation
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5. ETIOLOGIES:
Gallstones (40%): F> M , usually small stones (<5 mm) or microlithiasis/sludge
Alcohol(30%):M>F ,1st attack after10y heavy use; usually chronic w/acute flares
Anatomic: divisum, annular pancreas, duodenal duplication cysts, Sphincter of Oddi dysfunction.
Autoimmune: can p/w chronic disease,pan mass or pan duct strictures, HIGH lgG4,+ANA
Drugs: 5-ASA, 6-MP/AZA, ACEI, cytosine, didanosine, dapsone, estrogen, furosemide,
Isoniazid, metronidazole, pentamidine, statins, sulfa, thiazides, tetracycline, valproate
Familial: associated with mutations in PRSS1, CFTR, SPINK1; suspect if early onset (age <20 y)
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6. Infections: ascariasis, clonorchiasis, coxsackie, CMV, HIV, mumps, mycoplasma ,T B, t oxo
Ischemia: vasculitis, cholesterol emboli, hypovolemic shock, cardiopulmonary bypass
Metabolic: hypertriglyceridemia (TG >1000; type I and V familial hyperlipemia), hyperCa
Neoplastic: panc/ampullary tumors, mets (RCC most common, breast, lung, melanoma)
Post ERCP (5%): prophylaxis w/ PR indomethacin (NEJM 2012:366:1414), pane duct stent if
high risk
Post trauma: blunt abdominal trauma, pancreatic/biliary surgery
Toxins: organophosphates, scorpion toxin, methanol
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7. CLINICAL MANIFESTATIONS
Epigastric abdominal pain (90%), only 50% p/w classic bandlike pain radiating to back
10% pain-free (due to analgesic/steroid use, immunosuppressed, AMS, ICU, post-op), /
amylase/lipase in Pts w / unexplained shock (AmJ Gastro 1991:86:322).
Nausea and vomiting (90%)
Abdominal tenderness/guarding, increased bowel sounds (ileus), jaundice if biliary
obstruction
Signs of retroperitoneal hemorrhage (Cullen's = periumbilical; Grey Turners = flank) rare
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9. DIFFERENTIAL DIAGNOSIS
acute cholecystitis
perforated viscus
Small Bowel Obstruction
mesenteric ischemia
inferior wall MI
AAA leak
distal aortic dissection
ruptured ectopic pregnancy
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10. DIAGNOSTIC STUDIES
Dx requires 2 of 3:
characteristic abdominal pain
lipase or amylase >3x ULN
+ imaging
Laboratory (AmJGastro2013:108:1400)
levels of both amylase and lipase do not correlate w/ severity of disease.
HIGH amylase: >3x ULN >90% sensitive, >70% specific for acute pancreatitis
/false -ve : acute on chronic (eg, alcoholic); hypertriglyceridemia (decreased
amylase activity).
false +ve: other abd or salivary gland process, acidemia, renal failure,
macroamylasemia .
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11. High lipase: >3x ULN 99% sensitive, 99% specific for acute pancreatitis
false +ve:
renal failure, other abd process, diabetic ketoacidosis, HIV, macrolipasemia longer half-life than
amylase:
useful in Pts w/ delayed presentation after onset of sx lipase >10,000 has 80% PPV for biliary
dx,99% NPV for EtOH (D/gD/sSc/2011:56:3376)
ALT >3x ULN has 95% PPV for gallstone pancreatitis [Am]Gastro 1994;89:1863)
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12. IMAGING STUDIES
Abd U/S: typically not useful to visualize pancreas (obscured by bowel gas) but should be
ordered for all pts with AP to r/o biliary etiology (i.e., gallstones, BD dilatation)
Abd CT: not rec for initial eval unless dx unclear (local complic. not yet visible & concern for
AKI w/ IV contrast). However, if persistent pain and/or clinical deterioration after 48- 72 h,
CT(l+) useful to r/o local complications (necrosis, fluid collections).
MRI/MRCP: Can detect necrosis; also used to assess for stones & ductal disruption
Endoscopic U/S (EUS): limited role; useful for occult biliary disease (microlithiasis)
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13. SEVERITY
Severity defined by presence of organ failure (AKI, resp failure, GIB, shock) & local or
systemic complic. (pane necrosis, fluid collections, gastric outlet obstruction, splenic & PVT).
Mild: 80% of cases. No organ failure or local/systemic complications, low mortality.
Moderate: transient (<48 h) organ failure 賊 local/systemic complications, high morbidity
Severe: persistent (>48 h) organ failure, very high mortality
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15. MANAGEMENT
Fluid resuscitation: early aggressive IVF, titrate to UOP >0.5 mL/kg/h, goal to lower BUN &
Hct over first 12-24 h. LR may be superior to NS (decreases SIRS, CRP at 24 h; avoid if high Ca)
Nutrition
Early enteral feeding encouraged (maintains gut barrier, decrease bacterial translocation)
though new data suggest may not be superior to oral feeding at 72 h (NEJM 2014:317:1983)
Mild: Start feeding once pain-free w/o ileus. Low-fat low-residue diet as safe as liquid diet.
Severe: early (w/in 48-72 h) enteral nutrition indicated and preferred over TPN b/c it decreases
infectious complications, organ failure, surgical interventions, and mortality.
Nasogastric feeding shown to be non-inferior to nasojejunal feeding.
nasojejunal feeding is preferred.
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16. Analgesia: IV opioids (monitor respiratory status, adjust dosing if worsening renal
impairment)
Gallstone pancreatitis: urgent (w/in 24 h) ERCP w/ sphincterotomy if cholangitis, sepsis,
Or Tbili >5. For mild disease, Cholecystectomy during initial hospitalization to decrease risk of
recurrence , defer surgery if necrotizing AP until improvement in inflam., fluid collections.
Hypertriglyceridemia:
No role for prophylactic antibiotics in absence of infectious complications (World;
Gastroenterol 2012:18:279)
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17. COMPLICATIONS
Systemic: ARDS, abdominal compartment syndrome, AKI, GIB (pseudoaneurysm), DIC
Metabolic: hypocalcemia, hyperglycemia, hypertriglyceridemia
Fluid collections:
Acute fluid collection: seen early, not encapsulated, most resolve w/in 1-2 wk w/o Rx
Pseudocyst: -4 wk after initial attack, encapsulated. No need for Rx if asymptomatic
(regardless of size/location). If symptomatic-> endoscopic (Gostro2013:145:583) vs.
perc/surg drainage.
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18. Pancreatic necrosis: Nonviable pancreatic tissue. CT-guided FNA if infection suspected
Sterile necrosis :if asymptomatic, can be managed expectantly, no role for prophylactic
antibiotics
Infected necrosis (5% of all cases, 30% of severe): high mortality.
Rx w/ carbapenem or MDZ+FQ.
"Step-up Rx w/ perc drainage and minimally invasive surg debridement or
endoscopic necrosectomy superior to open necrosectomy (NEJM2010:362:1491)
Pancreatic abscess: circumscribed collection of pus (usually w/o pancreatic tissue),
usually seen >4 wk into course.
Rx with abx + drainage (CT-guided if possible).
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19. REFERENCE:
American journal of gastroenterology
New England journal of medicine
Sanford guide for antimicrobial therapy
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