Fig.17.2A ).Fat necrosis results from enzymatic destruction of fat cells; the releasedfattyacidscombinewithcalciumtoforminsolublesalts thatprecipitateinsitu.
Inmoresevereforms,suchasacute necrotizing pancreatitis,thedamagealsoinvolvesacinarandductalcells,theislets ofLangerhans,andbloodvessels.Macroscopically,thepancreas exhibits red-blackhemorrhagic areasinterspersedwith foci of yellow-white,chalkyfat necrosis(
Fig.17.2B ).Fatnecrosisalso canoccurinextrapancreaticfat,includingtheomentumandbowel mesentery,andevenoutsidetheabdominalcavity(e.g.,insubcutaneousfat).Inmostcases,theperitoneumcontainsaserous, slightlyturbid,brown-tingedfluidwithglobulesoffat(derivedfrom enzymaticallydigestedadiposetissue).Inthemostsevereform, hemorrhagic pancreatitis, extensive parenchymal necrosis isaccompaniedbydiffusehemorrhagewithinthesubstanceof thegland.
Abdominal pain is the cardinal manifestation of acute pancreatitis.Its severity varies from mild and uncomfortable to severe and incapacitating. Acute pancreatitis is diagnosed primarily by the presence of elevated plasma levels of amylase and lipase and the exclusion of other causes of abdominal pain. In 80% of cases, acute pancreatitis is mild and self-limiting; the remaining 20% develop severe disease.
Full-blown acute pancreatitis is a medical emergency of the first order.Affected individuals usually experience the sudden calamitous onset of an “acute abdomen” with pain, guarding, and the ominous absence of bowel sounds. Characteristically, the pain is constant, intense and referred to the upper back; it must be differentiated from pain of other causes such as perforated peptic ulcer, biliary colic, acute cholecystitis with rupture, and occlusion of mesenteric vessels with infarction of the bowel.
The manifestations of severe acute pancreatitis are attributable to systemic release of digestive enzymes and
Fig. 17.2 Acutepancreatitis.(A)Themicroscopicfieldshowsaregionoffatnecrosis(right) andfocalpancreaticparenchymalnecrosis(center). (B)Thepancreashasbeensectionedlongitudinallytorevealdarkareasofhemorrhageinthepancreaticsubstanceandafocalareaofpalefatnecrosisintheperipancreaticfat(upper left).
explosive activation of the inflammatory response. The initial clinical evaluation may reveal leukocytosis, disseminated intravascular coagulation (Chapter 12), acute respiratory distress syndrome (due to diffuse alveolar damage) (Chapter 13), and diffuse fat necrosis. Peripheral vascular collapse (shock) can rapidly ensue as a result of increased microvascular permeability and resultant hypovolemia, compounded by endotoxemia (from breakdown of the barriers between gastrointestinal flora and the bloodstream), and renal failure due to acute tubular necrosis (Chapter 14).
Laboratory findings include markedly elevated serum amylase during the first 24 hours, followed (within 72–96 hours) by rising serum lipase levels. Hypocalcemia can result from precipitation of calcium in areas of fat necrosis; if persistent, it is a poor prognostic sign. The enlarged inflamed pancreas can be visualized by computed tomography (CT) or magnetic resonance imaging (MRI).