Rajvilas Anil Narkhede1* and Snehal Ashok Naphade2
1Department of Surgical Gastroenterology, Global hospital, Lakdi Ka Pul, Hyderabad, India 2M V P Medical College, Nasik, Maharashtra, India
Received: 20 June, 2016; Accepted: 02 July, 2016; Published: 04 July, 2016
Dr. Rajvilas Anil Narkhede, Pushpanjali, Shemba, Nandura, Buldana, Maharashtra, 440103, India, Tel: +918897389898; E-mail:
Narkhede RA, Naphade SA (2016) Pancreatic Siphon: A Major Determinant of Selective Shunts. Is it a Historical Entity now?. J Surg Surgical Res 2(1): 039-042.10.17352/2455-2968.000029
© 2016 Narkhede RA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Pancreatic siphon; Distal spleno-renal shunt; Intra-pancreatic collaterals; Spleno-pancreatic disconnection; Selective shunt
Surgical management of portal hypertension has changed according to time, evolving from just complete shunts to selective shunts and to liver transplantation. The outcomes also greatly improved owing to better understanding of portal hemodynamics and disease nature. Introduction of selective shunts showed promising results just to be challenged by poor outcome with development of “pancreatic siphon” which then studies in detail. This intra-pancreatic and peri-pancreatic collateral veins which connected portal and splenic veins formed basis of systemic loss of portal flow and thus ending up in failure of selectivity. Pancreatic siphon was found to be associated with increased rates of hepatic encephalopathy post selective shunting along with increased rates of hepatic failure. In addition to this pancreatic siphon led to metabolic sequel like new onset of diabetes, ischemic or compressive pancreatic ductopathy and intrapancreaic cholangiopathy. Although the shunting procedures are not that commonly done, pancreatic siphon has moved out of the limelight. It was just an attempt of recapping the existence of an unfamiliar entity forming delicate balance in the portal circulation.
Treatment of portal hypertension has evolved greatly over last few decades. Of these Distal splenorenal shunt (DSRS) was found to provide long lasting solution to the problem. DSRS was based on the idea that esophageal and gastric varices will be decompressed into renal vein via short gastric vessels and spleen after disconnecting coronary vein at the same time maintaining hepatopetal flow in mesentericoportal circulation and supply of hepatotropic factors to liver . But over time the shunt showed loss of this selectivity and showed increased rates of hepatic failure secondary to loss of portal flow from portal circulation to systemic circulation through peri-pancreatic and intra-pancreatic surgery. The ‘pancreatic siphon’ term gained its existence only after the popularisation of distal splenorenal shunt. It was found to be the communication between mesenerico-portal and the disconnected gastrosplenic compartments. This pancreatic and peripancreatic venous collaterals decompressing portal circulation into splenic vein after DSRS is said to be “pancreatic siphon”.
What is exactly “Pancreatic siphon”?
Large collaterals leave the portal vein into the head of the pancreas, drain through the body and tail of the pancreas via intrapancreatic branches that communicate directly with the shunt distal splenic vein . In 65.79 % anatomical pieces studied by Piras C et al., showed that the veins of the pancreatic tail flowed in segmentary branches of the splenic vein. These branches could be responsible for the loss of distal splenorenal shunt selectivity . Since the portal system is valve less; retrograde flow through this siphon is possible; away from portal system to the shunt (Figure 1).
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