How are selective shunts used in the treatment of portal hypertension?

Answer

Selective shunts provide selective decompression of gastroesophageal varices to control bleeding while at the same time maintaining portal hypertension to maintain portal flow to the liver. One example is the distal splenorenal shunt, which is the most commonly used decompressive operation for refractory variceal bleeding; it is used primarily in patients who present with refractory bleeding and continue to have good liver function. The distal splenorenal shunt decompresses the gastroesophageal varices through the short gastric veins, the spleen, and the splenic vein to the left renal vein.

Portal hypertension is maintained in the splanchnic and portal venous system, and the shunt maintains portal flow to the liver. This type of shunt provides the best long-term maintenance of some portal flow and liver function, with a lower incidence of encephalopathy (10-15%) compared with total shunts. The operation produces ascites because the retroperitoneal lymphatics are diverted.

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Media Gallery

Large esophageal varices with red wale signs seen on endoscopy. Courtesy of Wikimedia Commons.
Uphill esophageal varices. Barium swallow demonstrates multiple serpiginous filling defects primarily involving the lower one third of the esophagus with striking prominence around the gastroesophageal junction. The patient had cirrhosis secondary to alcohol abuse.
Barium swallow demonstrating esophageal varices involving the entire length of the esophagus. This appearance may be seen in advanced uphill varices or downhill varices secondary to superior vena cava obstruction at or below the level of the azygous vein.
Computed tomography scan showing esophageal varices. Note the extensive collateralization within the abdomen adjacent to the spleen as a result of severe portal hypertension.
Normal venous flow through the portal and systemic circulation. IMC = inferior mesenteric vein; IVC = inferior vena cava; SVC = superior vena cava.
Redirection of flow through the left gastric vein secondary to portal hypertension or portal venous occlusion. Uphill varices develop in the distal one third of the esophagus. IMC = inferior mesenteric vein; IVC = inferior vena cava; SVC = superior vena cava.
Portal vein and associated anatomy.
Power Doppler sonogram through the spleen shows varices at the hilum of an enlarged spleen. The final diagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), and portoarterial fistula (which had developed inside the ruptured tumor, giving rise to severe portal hypertension).
Duplex spectral Doppler sonogram of the portal vein (same patient as in the previous image) shows a bidirectional flow within the vein. The final diagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), and portoarterial fistula (which had developed inside the ruptured tumor, giving rise to severe portal hypertension).
Digital subtraction selective common hepatic artery angiogram shows immediate filling of the portal venous radicles in the left lobe of the liver (straight arrow) and early filling of portal vein (curved arrow), suggestive of hepatic arterial-portal vein fistula. The final diagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), and portoarterial fistula (which had developed inside the ruptured tumor, giving rise to severe portal hypertension).
Delayed venous phase of a selective common hepatic angiogram (same patient as in the previous image) shows the portal vein (P), with filling of the left gastric vein caused by retrograde flow feeding gastric and lower esophageal varices (arrows). Retrograde flow in enlarged umbilical veins also is seen. The final diagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), and portoarterial fistula (which had developed inside the ruptured tumor, giving rise to severe portal hypertension).
Digital subtraction venous phase of a superior mesenteric artery angiogram (same patient as in the previous 2 images) shows retrograde flow into the left gastric vein (curved arrow) and the inferior mesenteric vein (straight arrow). Note the flow defect of the distal portal vein caused by retrograde flow (open arrowhead). The final diagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), and portoarterial fistula (which had developed inside the ruptured tumor, giving rise to severe portal hypertension).
This video, captured via esophagoscopy, shows band ligation of esophageal varices. Video courtesy of Dan C Cohen, MD, and Dawn Sears, MD, Division of Gastroenterology, Scott & White Healthcare.

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Author

Jesus Carale, MD Consulting Gastroenterologist, Arkansas Valley Regional Medical Center, La Junta, Colorado

Jesus Carale, MD is a member of the following medical societies: American Gastroenterological Association

Disclosure: Nothing to disclose.

Coauthor(s)

Samy A Azer, MD, PhD, MPH Professor of Medical Education, Chair of Medical Education Research and Development Unit, Faculty of Medicine, Universiti Teknologi MARA, Malaysia; Visiting Professor of Medical Education, Faculty of Medicine, University of Toyama, Japan; Former Senior Lecturer in Medical Education, Faculty Education Unit, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne and University of Sydney, Australia

Samy A Azer, MD, PhD, MPH is a member of the following medical societies: American College of Gastroenterology, Association for Psychological Science, Gastroenterological Society of Australia, New York Academy of Sciences, Royal Society of Medicine, Sigma Xi

Disclosure: Nothing to disclose.

Parit Mekaroonkamol, MD Assistant Professor of Medicine, Department of Internal Medicine, Division of Digestive Diseases, Emory University School of Medicine; Advanced Endoscopist/Gastroenterologist, Emory University Hospital

Parit Mekaroonkamol, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, Medical Council of Thailand

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

Samy A Azer, MD, PhD, MPH Professor of Medical Education and Head of Curriculum Development Unit, King Saud University, Riyadh, Saudi Arabia; Visiting Professor of Medical Education, Faculty of Medicine, University of Toyama, Japan; former Professor of Medical Education, Chair of Medical Education Research and Development Unit, Faculty of Medicine, Universiti Teknologi MARA, Malaysia; former Consultant to the Victorian Postgraduate Medical Foundation, Melbourne, Australia; former Senior Lecturer in Medical Education, Faculty Education Unit, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne and University of Sydney, Australia

Samy A Azer, MD, PhD, MPH is a member of the following medical societies: American College of Gastroenterology, Association for Psychological Science, Gastroenterological Society of Australia, New York Academy of Sciences, Royal Society of Medicine, and Sigma Xi