Abstract
In over 90% of healthy people, the dorsal and ventral endodermal pancreatic buds fuse to form the adult pancreas. However, in about the remaining 10% of the population where the fusion does not occur, pancreatic divisum (PD) results. This indeed is the commonest congenital anomaly of pancreas. The dorsal root usually drains a part of pancreatic head, the body and tail of the pancreas via a minor papilla into the duodenum. The ventral root drains the uncinate process and part of the pancreatic head with the CBD via the major papilla into the duodenum and the two roots are communicated with one another. In classic PD (type1) there is a complete failure of fusion of ducts, and a small ventral duct (Santorini) drains through the larger major papilla, and a larger dorsal duct (Wirsung) drains through the smaller minor papilla. In type 2, there is a complete absence of duct of Wirsung. While in type (incomplete PD), there is a filamentous or tiny caliber communication between the dominant dorsal duct of Wirsung and duct of Santorini. In the western countries, the incomplete PD is uncommon with a reported incidence of 0.13%-0.9%. However recent reports from Japan and Korea show a much higher prevalence of 48% to 52%, of incomplete PD. In patients with a large duct, the majority of the pancreatic secretions pass through the minor papilla (instead of major) resulting in inadequate drainage and pain caused by obstruction. However while these features of PD are relatively well known, there are some aspects of PD, which are not so obvious. These include its true prevalence, its role in development of pancreatitis and carcinoma of pancreas, the genetic abnormalities and its association with pancreatitis in presence of PD and the appropriate management of these patients when symptomatic
Highlights
In a recent comprehensive analysis to determine the prevalence of pancreatic divisum (PD) in idiopathic pancreatitis (IP) compared to general population, data from 23 autopsy studies, 41 Endoscopic retrograde cholangiography (ERCP) studies and 13 magnetic resonance cholangiography (MRCP) studies was analysed and the following observations were made [7,8]
1) An increased incidence (50% or 25.6%) of PD is noted on ERCP, in patients with idiopathic or recurrent acute pancreatitis respectively [6,14]
PD may be an etiological factor in patients who develop idiopathic and recurrent acute pancreatitis in the presence of CFTR gene mutations
Summary
In over 90% of healthy people, the dorsal and ventral endodermal pancreatic buds fuse to form the adult pancreas [1,2]. In classic PD (type1) there is a complete failure of fusion of ducts, and a small ventral duct (Santorini) drains through the larger major papilla, and a larger dorsal duct (Wirsung) drains through the smaller minor papilla [3] (Figure 1). In patients with a large duct, the majority of the pancreatic secretions (up to 2000 ml daily) pass through the minor papilla (instead of major) resulting in inadequate drainage and pain caused by obstruction [2]. While these features of PD are relatively well known, there are some aspects of PD, which are not so obvious. They are less likely to consume alcohol and are more likely to be female and have recurrent acute pancreatitis attack [6]
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