Regardless of whether the initiating event is alcohol, gallstones or some o
ther less common cause, acute pancreatitis progresses in a predictable mann
er eventually leading to failure of multiple unrelated organs. Very quickly
following the inciting event, a local inflammatory process is initiated wh
ich results in the local production of inflammatory mediators. Virtually al
l patients with acute pancreatitis will experience some symptoms related to
this local inflammation, with some resolving completely at this point. Mos
t patients will go on to develop a systemic hyperinflammatory state express
ed as the development of fever, tachycardia, tachypnea, and mild acid-base
disturbances. Although this systemic hyperinflammatory state is usually mil
d, occasionally it may be very severe resulting in overt distant organ fail
ure. With a more thorough understanding of the inflammatory mediators respo
nsible for this hyperinflammatory state, many new therapeutic approaches ar
e on the horizon.