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 Table of Contents  
CASE REPORT
Year : 2017  |  Volume : 9  |  Issue : 6  |  Page : 175-177

Crossing-Duct sign and recurrent pancreatitis: A case report with review of pancreatic embryology


Department of Radiodiagnosis, Sher-i-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India

Date of Web Publication8-Nov-2017

Correspondence Address:
Mohd Ilyas
Department of Radiodiagnosis, Sher-i-Kashmir Institute of Medical Sciences, Soura, Srinagar - 190 011, Jammu and Kashmir
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijmbs.ijmbs_58_17

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  Abstract 


Pancreatic divisum is a congenital anomaly of the pancreatic ductal system wherein the dorsal duct system fails to fuse with ventral ductal system and results in the major pancreatic drainage through the minor duodenal papilla and minor drainage through the major duodenal papilla. It is a rare cause of recurrent pancreatitis.

Keywords: Crossing-duct sign, pancreatic divisum, recurrent pancreatitis


How to cite this article:
Ilyas M, Shafi F, Shabir S, Gojwari T. Crossing-Duct sign and recurrent pancreatitis: A case report with review of pancreatic embryology. Ibnosina J Med Biomed Sci 2017;9:175-7

How to cite this URL:
Ilyas M, Shafi F, Shabir S, Gojwari T. Crossing-Duct sign and recurrent pancreatitis: A case report with review of pancreatic embryology. Ibnosina J Med Biomed Sci [serial online] 2017 [cited 2020 May 30];9:175-7. Available from: http://www.ijmbs.org/text.asp?2017/9/6/175/217871




  Introduction Top


Congenital anomalies of the pancreas are a rare cause of recurrent pancreatitis. Most of these anomalies are asymptomatic but some may produce symptoms of recurrent pancreatitis, and recognition of these anomalies is important so that appropriate surgical or endoscopic management is done at the earliest. The magnetic resonance cholangiopancreatography (MRCP) has become the noninvasive modality of choice for the diagnosis of pancreatic ductal anomalies.[1]


  Case Report Top


A 60-year-old nonalcoholic, male patient presented to the emergency section with history of recurrent epigastric pain for 5 months. The pain was dull-aching type. There was no history of fever. The past history was significant for two attacks of mild pancreatitis 2 years back. The clinical examination was positive for mild epigastric tenderness. The pulse was 73 beats/minute and blood pressure was 120/80 mmHg with normal breathing. Family history was insignificant.

Biochemical tests revealed mildly raised serum amylase (300 IU/l) and lipase (180 IU/l). The hematological profile was within normal limits. The ultrasonography revealed transonic gallbladder with no evidence of obstructive biliopathy; however, pancreas was not assessed due to its obscuration by the gut gases. The MRCP was performed which revealed features of mild pancreatitis. Heavy-weighted thick slab T2 images revealed the predominant pancreatic drainage through dorsal duct into the minor papilla crossing the common bile duct and ventral duct draining into the major papilla along with common bile duct [Figure 1].
Figure 1: Nonannotated thick slab heavy-weighted T2 magnetic resonance image showing the classic picture of pancreaticobiliary drainage in a case of type 1 (classic) pancreatic divisum

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The MR appearance was classical for the type-1 (classic) pancreatic divisum. The “crossing-duct” sign is most specific for diagnosis of type-1 pancreatic divisum wherein dorsal pancreatic duct is seen crossing the common bile duct to empty into the minor papilla of duodenum [Figure 1] and [Figure 2]. Thus, the etiology of recurrent pancreatitis in this patient was attributed to pancreatic divisum.
Figure 2: Annotated thick slab heavy.weighted T2 magnetic resonance image showing the classic picture of pancreaticobiliary drainage in a case of type 1 (classic) pancreatic divisum. (a) Left hepatic duct; (b) Right hepatic duct; (c) Common hepatic duct; (d) Cystic duct; (e) Common bile duct; (f) Dorsal pancreatic duct; (g) Ventral pancreatic duct; (h) Gallbladder

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In the present case, ERCP-guided sphincterotomy of minor papilla was done. The patient was followed monthly for 6 months. The symptoms reduced gradually, and as of now, the patient is symptom free.


  Discussion Top


The pancreas develops as two outpouchings (buds), called the dorsal (cranial) pancreatic anlage and ventral (caudal) pancreatic anlage which develop from the opposite sides of the junction of the primitive foregut and midgut. They rotate to be in proximity and the cranial anlage becomes the body and tail while the ventral anlage becomes head and uncinated process. The ventral bud is also the embryologic origin of the gallbladder, bile duct, and liver. The common origin of the bile duct and pancreatic head explains the common fused opening of pancreatic and bile duct into the duodenum through major papilla.[2]

Majority of the population has single, main pancreatic duct which attributes its origin to the fusion of two ducts from each pancreatic anlage (dorsal duct and ventral duct). Ventral duct is also known as accessory duct and drains through minor papilla. The main pancreatic duct empties into the major papilla usually after the merger with common bile duct. In 20% of cases, only the bile duct enter through the major papilla while the main pancreatic duct enters separately usually near the bile duct through minor papilla.[3] In 10% of the cases, the drainage is through the accessory duct through the minor papilla not through the major papilla. Another exception is pancreatic divisum (the present case), in which the ventral and dorsal pancreatic ducts fail to fuse. The main pancreatic duct is sometimes called as duct of Wirsung and the accessory duct as duct of Santorini.

The other anomalies which can result to abnormal rotation of the pancreatic anlages include annular pancreas and pancreatic agenesis (partial, dorsal, or complete). Most of the pancreatic anomalies are asymptomatic except for pancreatic divisum which can cause recurrent pancreatitis in 5% of cases.[4]

Transabdominal ultrasonography plays a little role in the diagnosis of anatomic variants of the pancreas. The other investigations used for diagnosis of pancreatic divisum include computed tomography, endoscopic retrograde cholangiopancreatography, and MRCP. Of all these investigations, MRCP is one investigation with minimal side effects, which is noninvasive and has better patient compliance with excellent results for diagnosing pancreatic ductal anomalies. Recently introduced endoscopic ultrasound has also been found useful in diagnosing pancreatic divisum in cases of unexplained pancreatitis but that too is an invasive procedure.[5]

The pancreatic divisum is classified into three types:[1]

  1. Type 1 (classic): No communication of dorsal and ventral pancreatic duct with dorsal (major) duct draining into the minor papilla and ventral (minor) duct draining into the major papilla along with common bile duct [Figure 1]
  2. Type 2 (absent ventral duct): Whole of pancreas is drained through minor papilla and major papilla drains only common bile duct
  3. Type 3 (functional): There is only a fibrous connection between dorsal and ventral ducts.


Pancreatic divisum is a rare congenital anomaly which results due to nonfusion of embryonic dorsal and ventral pancreatic drainage system. It is one of the rarest causes of pancreatitis. The pancreatitis in these cases is due to reflux of pancreatic juice from the minor papilla which is not suitable for major drainage.

The crossing-duct sign refers to the appearance of the dorsal duct running across the intrapancreatic common bile duct on coronal MRCP images. This is a specific sign for pancreatic divisum.[6]

The treatment options for the symptomatic pancreatic divisum are sphincterotomy, papillary dilatation, or stent placement of the minor duodenal papilla which results in decongestion of the dorsal pancreatic duct.[7]


  Conclusion Top


MRCP is one of the most sensitive noninvasive modality of investigation for the diagnosis of classic type of pancreatic divisum. The “crossing-duct sign” is easily appreciable on thick slice heavily T2-weighted images. Ductal anomalies should be considered in the differential diagnosis of unexplained recurrent pancreatitis and thoroughly investigated.

Authors' contributions

All the authors had the access to the data and role in the writing of the manuscript.

Financial support and sponsorship

Nil.

Conflicts of interest

None.

Compliance with ethical principles

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given his consent for his images and other clinical information to be reported in the journal anonymously.



 
  References Top

1.
Türkvatan A, Erden A, Türkoǧlu MA, Yener Ö. Congenital variants and anomalies of the pancreas and pancreatic duct: Imaging by magnetic resonance cholangiopancreaticography and multidetector computed tomography. Korean J Radiol 2013;14:905-13.  Back to cited text no. 1
    
2.
Yu J, Turner MA, Fulcher AS, Halvorsen RA. Congenital anomalies and normal variants of the pancreaticobiliary tract and the pancreas in adults: Part 2, pancreatic duct and pancreas. AJR Am J Roentgenol 2006;187:1544-53.  Back to cited text no. 2
[PUBMED]    
3.
Misra SP, Dwivedi M. Pancreaticobiliary ductal union. Gut 1990;31:1144-9.  Back to cited text no. 3
[PUBMED]    
4.
Dawson W, Langman J. An anatomical-radiological study on the pancreatic duct pattern in man. Anat Rec 1961;139:59-68.  Back to cited text no. 4
[PUBMED]    
5.
Borghei P, Sokhandon F, Shirkhoda A, Morgan DE. Anomalies, anatomic variants, and sources of diagnostic pitfalls in pancreatic imaging. Radiology 2013;266:28-36.  Back to cited text no. 5
[PUBMED]    
6.
Li YL, Yu ML, Lee KH. The crossing duct sign. Abdom Radiol 2017. https://doi.org/10.1007/s00261-017-1312-3.  Back to cited text no. 6
    
7.
Ng WK, Tarabain O. Pancreas divisum: A cause of idiopathic acute pancreatitis. CMAJ 2009;180:949-51.  Back to cited text no. 7
[PUBMED]    


    Figures

  [Figure 1], [Figure 2]



 

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