Pancreas divisum (PD) is not an uncommon congenital anatomic variant that results from failure of the ventral and dorsal ductal systems to fuse during the 6
th to 8
th week of embryological development. The main portion of the pancreas is drained by the dorsal pancreatic duct through the accessory papilla and only the posterior-inferior part and the uncinate process of pancreatic head are drained by a small and short ventral duct that joins the common bile duct in the ampulla of Vater [
2]. Drainage of most of the pancreatic secretions through the accessory papilla, that is less wide than the main one, may result in high intraductal pressure in the duct of Santorini. This "functional" obstruction of the dorsal duct orifice has been assumed as a cause of acute pancreatitis [
1,
8,
6]. The prevalence of PD has been reported from 0,8% to 7,5% on ERCP series [
1] and it is found in 5–10% of autopsies [
2]. The diagnosis of PD is based on ERCP findings, when a short isolated ventral duct is depicted, as in our case, or when two separate pancreatic ducts, that do not communicate to each other, are identified [
1]. MRCP is considered an excellent technique in the diagnosis of PD by demonstrating the crossing of the distal common bile duct with the dorsal pancreatic duct and by revealing separate drains for the main pancreatic and common bile ducts [
4,
7]. PD has been associated with episodes of acute recurrent pancreatitis and relapsing abdominal pain [
2,
13,
16]. The relationship of PD with chronic pancreatitis has not been fully illuminated yet, although some reports- based mostly on clinical, laboratory and ERCP data- suggested that this congenital variant, may have a role in the pathogenesis of chronic pancreatitis [
1,
13‐
15]. Pancreatitis due to blunt abdominal trauma in patients with PD has been previously described on ERCP in only three cases, to the best of our knowledge [
16,
17]. Blunt abdominal trauma is considered to be the cause of one fifth of all cases of traumatic pancreatitis and it may result in contusion, parenchymal fracture, or ductal disruption [
17]. Pancreatic trauma may lead to pseudocyst formation, abscess or pancreatic fistula formation [
18]. Pancreatic pseudocyst may also be developed after an acute exacerbation of chronic pancreatitis [
19]. It is unclear if the cyst is related to such an exacerbation of chronic pancreatitis in our patient. But we consider that the cystic lesion might be secondary to the blunt trauma, as a CT scan that was performed by that time, showed a peripancreatic hematoma at the pancreatic head.
Ductal injury is usually followed by a more severe clinical course in the posttraumatic period than in our case. As opposed to the duct of Santorini which was injured, the duct of Wirsung was intact in our patient; this may account for the absence of atrophic changes in the pancreatic head and the relatively mild clinical course. MRCP showed morphological alterations in the dorsal pancreas, consistent with chronic pancreatitis and the cross-sectional T1 and T2-weighted images demonstrated atrophy of the pancreatic body and tail. ERCP failed to depict the dorsal duct probably because its stenotic orifice.
The association of PD with chronic pancreatitis limited to the dorsal duct has been previously described in 16 patients on ERCP [
1] and in 2 patients on MRCP [
3,
5]; in all cases there was no evidence of traumatic injury of the duct. In our case, internal drainage of the pancreatic pseudocyst was beneficial and resulted in symptoms' remission.