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Acute Pancreatitis

  • Acute Pancreatitis refers to acute inflammation of the pancreas due to inappropriate release of pancreatic digestive enzymes within the body of the pancreas.
  • A wide variety of etiologies can cause acute pancreatitis and we mention only the most common below. Given the diversity of etiologies it is likely that there is not a single common pathway to acute pancreatitis, but rather a diversity of mechanisms that funnel into a common pathogenic sequence
  • Cholelithiasis is the most common cause and accounts for the majority (~60%) of cases
  • Alcohol abuse is associated with a significant minority (~20%) of cases
  • Hypertriglyceridemia is associated with roughly 2% of cases
  • Surgical trauma can cause acute pancreatitis especially during Endoscopic Retrograde Cholangiopancreatography (ERCP)
  • Overview
    • How the above etiologies initiate the pathogenic sequence thought to drive acute pancreatitis is not well-understood. In the case of cholelithiasis it is thought that gallstones obstruct the Ampulla of Vater, resulting in obstruction of pancreatic outflow. This in turn increases intra-pancreatic pressure which somehow results in the pathogenic sequence described below. In the cases of alcohol- and triglyceride-initiated acute pancreatitis, the connection between etiology and pathogenesis is even more poorly-understood. Whatever the case, following initiation, the pathogenesis of acute pancreatitis appears to involve the following basic sequence.
  • Intracellular Activation of Pancreatic Enzymes
    • Pancreatic digestive enzymes are normally stored in pancreatic acinar cells as inactive zymogens and their enzymatic activity is suppressed until their secretion into the GI tract. Acute Pancreatitis appears to involve inappropriate activation of pancreatic digestive enzymes within the pancreatic acinar cells resulting in significant local cellular injury and destruction.
  • Pancreatic Inflammation
    • Injured pancreatic acinar cells induce a potent acute inflammatory response through release of inflammatory cytokines. This leads to an influx of neutrophils which may exacerbate damage to the organ.
  • Systemic Effects
    • Liberation of pancreatic enzymes and release of inflammatory cytokines not only have local effects, but also gain access to the systemic circulation, resulting in potent pathological effects on distant organs. Furthermore, during the process of injury and inflammation bradykinins are activated and released systemically which cause systemic vasodilation and increased vascular permeability, thus leading to hypotension that in some cases evolves into shock.
Clinical Consequences
  • Abdominal Pain:
    • Abdominal pain is the characteristic symptom of acute pancreatitis and may be mild to extremely severe. Usually the pain is described as periumbilical or epigastric with radiation to the back or less frequently the chest.
  • Complications
    • Hypotension and shock occur in some patients due to release of bradykinins (See above)
    • Hypocalcemia occasionally occurs due to sequestration of calcium by fatty acids generated during fat necrosis
    • Acute Respiratory Distress Syndrome is a common complication due to systemic release of pancreatic enzymes
    • Hemoperitoneum may surround the ubilicus with a faint blue color
  • Serum Amylase Elevation
    • Elevation of serum amylase is a highly sensitive test for acute pancreatitis during the first 12-48hrs days after initiation. However, levels usually return to normal within 2-3 days after injury; furthermore, a variety of other pancreatic and salivary pathologies can restul in serum amylase elevation although usually not to the high levels seen in acute pancreatitis.
  • Serum Lipase Elevation
    • Serum lipase usually remains elevated for up to two weeks after initiation and is more specific for a pancreatic etiology.
  • Fat Necrosis
    • Fat Necrosis is the pathological hallmark of acute pancreatitis and is described in more detail on its own page. It is caused by the action of liberated pancreatic enzymes, particularly lipases, on adipose tissue surrounding and adjacent to the pancreas.
  • Hemorrhage
    • In more severe cases of pancreatitis, pancreatic digestive enzymes induce necrosis of vasculature within and around the pancreas resulting in significant hemorrhage into the peritoneum (i.e. hemoperitoneum).
  • Acute Inflammation
    • An acute inflammatory infiltrate, typified by neutrophils is present throughout affected areas.
  • Destruction of Pancreatic Architecture
    • Release of enzymes results in a generalized destruction of the pancreas with attendant disfiguring of the normal pancreatic architecture.