Acute Pancreatitis

Acute pancreatitis is a common condition, with lethal potential. Incidence varies widely, due to differences in geographic and aetiological factors; additionally affected by the precision with which the diagnosis is made, but it can be as high as 79.8 per 100,000 per year [1]. The incidence of acute pancreatitis in the UK appears to be rising. This is certainly true in Scotland [2] and appears also to be the case in the South of England [3-4]. Incidence ranges in the UK from 150 to 420 cases per million population [2, 4].
Gallstones and alcohol are commonly reported as the main causative agents, increasing use of the latter being implicated in the recent rise in incidence of acute pancreatitis in Scotland [2]. Approximately 20% of cases of acute pancreatitis are severe; although the overall mortality of all cases of acute pancreatitis is 4-6%, this increases to 17-39% in the severe subgroup [5-8]. This mortality is biphasic, with deaths in the first two weeks or so being attributed to systemic inflammatory response syndrome, whereas those in the later phase, being related to infection. Pancreatic necrosis begins to develop within days of symptom onset, but does not often become infected before the third week [9]. Overall at least a third of cases of severe pancreatitis complicated by pancreatic necrosis will become infected [10]. In those cases where infected necrosis is detected, surgery has a vital role to play in survival as cases left untreated have almost 100% mortality [11].
Acute pancreatitis initially comprises of series of complex cascading events, all of which, start in the pancreatic acinar cells. The critical initiating event is the intracellular activation of pancreatic zymogens, which result in autodigestion of pancreas. Trypsinogen, a serine protease, is now thought to be the first enzyme to be activated [12-15]. Subsequently, other digestive proenzymes are cleaved and activated. The pancreas has a variety of mechanisms to prevent intracellular...