eMedicine Specialties > Radiology > Gastrointestinal

Portal Hypertension: Multimedia

Author: Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP, Chairman of Medical Imaging, Professor of Radiology, NGHA, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia
Coauthor(s): Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute; Murad Ali, MBBS, PhD, DTCD, Consulting Radiologist, Department of Radiology, Postgraduate Medical Institute, Lady Reading Hospital, Pakistan; David Sherlock, MBBS, FRCS, Consulting Staff, Department of Surgery, North Manchester General Hospital, Christie Hospital
Contributor Information and Disclosures

Updated: Feb 5, 2009

Multimedia

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Media file 1: Barium swallow in the left lateral decubitus position shows multiple mucosal nodules in the mid to lower esophagus. In a patient with cirrhosis, these are suggestive of esophageal varices.

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Barium swallow in the left lateral decubitus position shows multiple mucosal nodules in the mid to lower esophagus. In a patient with cirrhosis, these are suggestive of esophageal varices.

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Media file 2: Barium swallow in a 56-year-old man with known cirrhosis who had a recent episode of hematemesis shows thickened mucosal folds and multiple polypoid filling defects at the lower end of the esophagus. These are suggestive of varices.

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Barium swallow in a 56-year-old man with known cirrhosis who had a recent episode of hematemesis shows thickened mucosal folds and multiple polypoid filling defects at the lower end of the esophagus. These are suggestive of varices.

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Media file 3: Endoscopic findings in a 47-year-old man with a history of polycythemia rubra vera who had a recent episode of hematemesis. Endoscopy showed a normal esophagus, but multiple polypoid submucosal lesions were seen in the fundus and body of the stomach (same patient as in Images 4-6 in Multimedia). The final diagnosis was left-sided portal hypertension secondary to splenic vein thrombosis.

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Endoscopic findings in a 47-year-old man with a history of polycythemia rubra vera who had a recent episode of hematemesis. Endoscopy showed a normal esophagus, but multiple polypoid submucosal lesions were seen in the fundus and body of the stomach (same patient as in Images 4-6 in Multimedia). The final diagnosis was left-sided portal hypertension secondary to splenic vein thrombosis.

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Media file 4: Part of an upper gastrointestinal tract barium series (same patient as in Images 3-6 in Multimedia) shows multiple polypoid filling defects within the fundus of the stomach. The final diagnosis was a left-sided portal hypertension secondary to splenic vein thrombosis.

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Part of an upper gastrointestinal tract barium series (same patient as in Images 3-6 in Multimedia) shows multiple polypoid filling defects within the fundus of the stomach. The final diagnosis was a left-sided portal hypertension secondary to splenic vein thrombosis.

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Media file 5: Venous phase of a digital subtraction celiac-axis angiogram (same patient as in Images 3-6 in Multimedia) shows no splenic vein, but multiple collateral venous pathways are seen through the stomach wall (straight arrows), which feed a normal portal vein (curved arrows). Several varices are noted within the body of the stomach. The final diagnosis was left-sided portal hypertension secondary to splenic vein thrombosis.

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Venous phase of a digital subtraction celiac-axis angiogram (same patient as in Images 3-6 in Multimedia) shows no splenic vein, but multiple collateral venous pathways are seen through the stomach wall (straight arrows), which feed a normal portal vein (curved arrows). Several varices are noted within the body of the stomach. The final diagnosis was left-sided portal hypertension secondary to splenic vein thrombosis.

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Media file 6: Venous phase of a digital subtraction superior mesenteric angiogram (same patient as in Images 3-5) shows a normal portal vein (PV) with no streaming effect from splenic venous flow (arrow), suggestive of splenic vein thrombosis. The final diagnosis was left-sided portal hypertension secondary to splenic vein thrombosis.

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Venous phase of a digital subtraction superior mesenteric angiogram (same patient as in Images 3-5) shows a normal portal vein (PV) with no streaming effect from splenic venous flow (arrow), suggestive of splenic vein thrombosis. The final diagnosis was left-sided portal hypertension secondary to splenic vein thrombosis.

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Media file 7: Splenoportogram in a patient with known alcoholic cirrhosis and two episodes of variceal bleeding in the past. The procedure was performed as a prelude to surgical portosystemic shunt placement. The splenoportogram shows a dilated coronary vein (CV) feeding the lower esophageal and gastric varices (arrows). Retrograde filling of the inferior mesenteric vein (I) is present, but the main portal vein flow is hepatopetal in direction.

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Splenoportogram in a patient with known alcoholic cirrhosis and two episodes of variceal bleeding in the past. The procedure was performed as a prelude to surgical portosystemic shunt placement. The splenoportogram shows a dilated coronary vein (CV) feeding the lower esophageal and gastric varices (arrows). Retrograde filling of the inferior mesenteric vein (I) is present, but the main portal vein flow is hepatopetal in direction.

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Media file 8: Digital subtraction splenoportogram in a patient with portal hypertension shows a subcapsular contrast leak (arrows), which is a known complication of splenoportography.

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Digital subtraction splenoportogram in a patient with portal hypertension shows a subcapsular contrast leak (arrows), which is a known complication of splenoportography.

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Media file 9: Splenoportogram in a 3-year-old child with a history of serious febrile illness in infancy and recent hematemesis. Splenoportogram shows a thrombosed distal portal vein and a cavernous malformation at the porta hepatis (C). The arrow marks gastric and esophageal varices. The inferior mesenteric vein is outlined because of reverse flow (I).

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Splenoportogram in a 3-year-old child with a history of serious febrile illness in infancy and recent hematemesis. Splenoportogram shows a thrombosed distal portal vein and a cavernous malformation at the porta hepatis (C). The arrow marks gastric and esophageal varices. The inferior mesenteric vein is outlined because of reverse flow (I).

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Media file 10: CT scan through the spleen of a 43-year-old man with a known history of intravenous drug abuse and hepatitis C cirrhosis. The patient presented to the emergency department with a sudden onset of a hypotensive episode and clinical features of hepatic encephalopathy. The scan shows splenomegaly with a dilated tortuous splenic vein/varices at the splenic hilum and free peritoneal fluid (same patient as in Images 11-16). The final diagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), and arterioportal shunting (which had developed inside the ruptured tumor, giving rise to severe portal hypertension).

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CT scan through the spleen of a 43-year-old man with a known history of intravenous drug abuse and hepatitis C cirrhosis. The patient presented to the emergency department with a sudden onset of a hypotensive episode and clinical features of hepatic encephalopathy. The scan shows splenomegaly with a dilated tortuous splenic vein/varices at the splenic hilum and free peritoneal fluid (same patient as in Images 11-16). The final diagnosis was hepatitis C cirrhosis, hepatocellular carcinoma of the left hepatic lobe (which had ruptured into the peritoneum), and arterioportal shunting (which had developed inside the ruptured tumor, giving rise to severe portal hypertension).

CT scan through the liver (same patient as in <a ...

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Media file 11: CT scan through the liver (same patient as in Images 10-16) was not of optimal quality because of patient movement, but the attenuation in the left lobe of the liver was patchy, suggestive of a mass lesion. 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).

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CT scan through the liver (same patient as in Images 10-16) was not of optimal quality because of patient movement, but the attenuation in the left lobe of the liver was patchy, suggestive of a mass lesion. 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).

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Media file 12: Power Doppler sonogram through the spleen (same patient as in Images 10-16) 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).

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Power Doppler sonogram through the spleen (same patient as in Images 10-16) 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).

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Media file 13: Duplex spectral Doppler sonogram of the portal vein (same patient as in Images 10-16) 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).

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Duplex spectral Doppler sonogram of the portal vein (same patient as in Images 10-16) 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).

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Media file 14: Digital subtraction selective common hepatic artery angiogram (same patient as in Images 10-16) 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).

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Digital subtraction selective common hepatic artery angiogram (same patient as in Images 10-16) 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).

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Media file 15: Delayed venous phase of a selective common hepatic angiogram (same patient as in Images 10-16) shows the portal vein (P), with filling of the coronary 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).

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Delayed venous phase of a selective common hepatic angiogram (same patient as in Images 10-16) shows the portal vein (P), with filling of the coronary 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).

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Media file 16: Digital subtraction venous phase of a superior mesenteric artery angiogram (same patient as in Images 10-15) shows retrograde flow into the coronary 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).

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Digital subtraction venous phase of a superior mesenteric artery angiogram (same patient as in Images 10-15) shows retrograde flow into the coronary 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).

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Media file 17: Conventional angiogram of the superior mesenteric artery shows a replaced hepatic artery in the right lobe of the liver in a patient with a previous history of abdominal tuberculosis and a recent history of hematemesis. Note the multiple calcific foci in the splenic region as a result of old healed tuberculous granulomas. Two previous liver biopsies had not revealed the changes of cirrhosis (same patient as in Images 18-20). The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causing portal vein stenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.

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Conventional angiogram of the superior mesenteric artery shows a replaced hepatic artery in the right lobe of the liver in a patient with a previous history of abdominal tuberculosis and a recent history of hematemesis. Note the multiple calcific foci in the splenic region as a result of old healed tuberculous granulomas. Two previous liver biopsies had not revealed the changes of cirrhosis (same patient as in Images 18-20). The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causing portal vein stenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.

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Media file 18: Venous phase of a superior mesenteric angiogram shows a stenosis of the portal vein near the porta hepatis with poststenotic aneurysmal dilatation of the portal vein. Filling of the gastric varices and the splenic vein are seen as a result of retrograde flow (same patient as in Images 17-20). The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causing portal vein stenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.

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Venous phase of a superior mesenteric angiogram shows a stenosis of the portal vein near the porta hepatis with poststenotic aneurysmal dilatation of the portal vein. Filling of the gastric varices and the splenic vein are seen as a result of retrograde flow (same patient as in Images 17-20). The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causing portal vein stenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.

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Media file 19: Intraoperative portogram shows portal vein stenosis and a portal vein aneurysm. The splenic vein is outlined because of retrograde flow (same patient as in Images 17-20). The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causing portal vein stenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.

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Intraoperative portogram shows portal vein stenosis and a portal vein aneurysm. The splenic vein is outlined because of retrograde flow (same patient as in Images 17-20). The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causing portal vein stenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.

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Media file 20: Line diagram of findings on portal venous phase angiogram (same patient as in Images 17-19). The superior mesenteric vein has been added for anatomic clarity. The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causing portal vein stenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.

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Line diagram of findings on portal venous phase angiogram (same patient as in Images 17-19). The superior mesenteric vein has been added for anatomic clarity. The final diagnosis was tuberculous calcified lymph nodes at the porta hepatis causing portal vein stenosis by extrinsic pressure, portal hypertension, and esophageal and gastric varices.

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Media file 21: A 52-year-old man with known hepatitis B cirrhosis was found to have a hypoechoic mass in the region of the liver hilum. CT was performed for further characterization. Nonenhanced CT scan shows multiple polypoid masses at the splenic hilum (arrow), suggestive of a dilated tortuous splenic vein or varices (same patient as in Images 22-26). The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

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A 52-year-old man with known hepatitis B cirrhosis was found to have a hypoechoic mass in the region of the liver hilum. CT was performed for further characterization. Nonenhanced CT scan shows multiple polypoid masses at the splenic hilum (arrow), suggestive of a dilated tortuous splenic vein or varices (same patient as in Images 22-26). The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

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Media file 22: A 52-year-old man with known hepatitis B cirrhosis was found to have a hypoechoic mass in the region of the liver hilum (same patient as in Images 21-26). CT was performed for further characterization. Nonenhanced CT scan shows multiple polypoid masses at the splenic hilum (solid arrow), suggestive of a dilated tortuous splenic vein or varices, and the origin of a large splenic vein (open arrow). The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

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A 52-year-old man with known hepatitis B cirrhosis was found to have a hypoechoic mass in the region of the liver hilum (same patient as in Images 21-26). CT was performed for further characterization. Nonenhanced CT scan shows multiple polypoid masses at the splenic hilum (solid arrow), suggestive of a dilated tortuous splenic vein or varices, and the origin of a large splenic vein (open arrow). The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

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Media file 23: Contrast-enhanced axial CT (same patient as in Images 21-26) shows a cavernous transformation at the porta hepatis (arrows) caused by portal vein thrombosis. The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

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Contrast-enhanced axial CT (same patient as in Images 21-26) shows a cavernous transformation at the porta hepatis (arrows) caused by portal vein thrombosis. The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

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Media file 24: Contrast-enhanced axial CT scan shows a dilated left renal vein (arrow; same patient as in Images 21-26). The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

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Contrast-enhanced axial CT scan shows a dilated left renal vein (arrow; same patient as in Images 21-26). The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

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Media file 25: Venous phase of digital subtraction superior mesenteric angiogram shows the portal vein to be reduced to a threadlike structure (arrow). Retrograde flow into the splenic vein (S) is seen (same patient as in Images 21-26). The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

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Venous phase of digital subtraction superior mesenteric angiogram shows the portal vein to be reduced to a threadlike structure (arrow). Retrograde flow into the splenic vein (S) is seen (same patient as in Images 21-26). The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

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Media file 26: Venous phase of a digital subtraction superior mesenteric angiogram shows a shunt between the splenic vein (S) and the left renal vein (R), and the IVC (V) is outlined with contrast material. Arrows mark the tiny threadlike portal vein (same patient as in Images 21-25). The final diagnosis was hepatocellular carcinoma (not shown), cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

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Venous phase of a digital subtraction superior mesenteric angiogram shows a shunt between the splenic vein (S) and the left renal vein (R), and the IVC (V) is outlined with contrast material. Arrows mark the tiny threadlike portal vein (same patient as in Images 21-25). The final diagnosis was hepatocellular carcinoma (not shown), cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

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Media file 27: Transverse sonogram of the liver in a patient with hepatitis B cirrhosis shows a coarse echo structure of the liver.

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Transverse sonogram of the liver in a patient with hepatitis B cirrhosis shows a coarse echo structure of the liver.

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Media file 28: Sagittal oblique sonogram of the liver shows a small liver with an irregular surface, moderate ascites, and a dilated portal vein. Note the thick gallbladder wall.

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Sagittal oblique sonogram of the liver shows a small liver with an irregular surface, moderate ascites, and a dilated portal vein. Note the thick gallbladder wall.

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Media file 29: Sagittal oblique sonogram of the liver shows a dilated portal vein (22 mm in transverse diameter) in a patient with portal hypertension.

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Sagittal oblique sonogram of the liver shows a dilated portal vein (22 mm in transverse diameter) in a patient with portal hypertension.

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Media file 30: End-stage liver cirrhosis showing a small liver, gross ascites, and a dilated portal vein

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End-stage liver cirrhosis showing a small liver, gross ascites, and a dilated portal vein

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Media file 31: Doppler sample volume in portal vein reveals continuous venous flow without evidence of respiratory variation, consistent with a hypertensive portal venous system. Note the coarse liver echo structure and ascites.

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Doppler sample volume in portal vein reveals continuous venous flow without evidence of respiratory variation, consistent with a hypertensive portal venous system. Note the coarse liver echo structure and ascites.

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Media file 32: Doppler sample volume in portal vein reveals bidirectional flow in the portal vein associated with portal hypertension.

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Doppler sample volume in portal vein reveals bidirectional flow in the portal vein associated with portal hypertension.

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Media file 33: Sagittal oblique sonogram of the liver shows several tubular structures at the porta hepatis resulting from cavernous transformation secondary to portal vein thrombosis.

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Sagittal oblique sonogram of the liver shows several tubular structures at the porta hepatis resulting from cavernous transformation secondary to portal vein thrombosis.

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Media file 34: Duplex power Doppler sonogram shows an enlarged spleen; varices are apparent at the splenic hilum.

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Duplex power Doppler sonogram shows an enlarged spleen; varices are apparent at the splenic hilum.

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Media file 35: Doppler sonogram at the splenic hilum reveals hepatofugal venous flow in a patient with portal hypertension.

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Doppler sonogram at the splenic hilum reveals hepatofugal venous flow in a patient with portal hypertension.

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Media file 36: Spleen in portal hypertension, with a positive splenic interface sign.

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Spleen in portal hypertension, with a positive splenic interface sign.

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Media file 37: Color Dopper ultrasound showing pericholecystic varices.

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Color Dopper ultrasound showing pericholecystic varices.

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Media file 38: Color Dopper ultrasound showing pericholecystic varices.

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Color Dopper ultrasound showing pericholecystic varices.

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Media file 39: Peripancreatic varices as shown on power Doppler.

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Peripancreatic varices as shown on power Doppler.

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Media file 40: Peripancreatic varices as shown on power Doppler.

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Peripancreatic varices as shown on power Doppler.

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Media file 41: Peripancreatic and perihilar varices as shown on real-time scanner.

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Peripancreatic and perihilar varices as shown on real-time scanner.

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Media file 42: Periportal varices on power Doppler

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Periportal varices on power Doppler

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Media file 43: Periportal varices on conventional Doppler and power Doppler

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Periportal varices on conventional Doppler and power Doppler

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Media file 44: Periportal varices conventional Doppler and power Doppler.

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Periportal varices conventional Doppler and power Doppler.

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Media file 45: Dilatation of umbilical vein as shown on color Doppler.

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Dilatation of umbilical vein as shown on color Doppler.

More on Portal Hypertension

Overview: Portal Hypertension

Imaging: Portal Hypertension

Follow-up: Portal Hypertension

Multimedia: Portal Hypertension

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Schraufnagel DE, Kay JM. Structural and pathologic changes in the lung vasculature in chronic liver disease. Clin Chest Med. Mar 1996;17(1):1-15. [Medline].

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Keywords

portal hypertension, PH, portal HTN, portal venous pressure, hepatic venous pressure, portal venous flow, hematemesis, bleeding esophageal varices, portosystemic collateral vessels, portosystemic collaterals, cirrhosis, splenoportography

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Contributor Information and Disclosures

Author

Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP, Chairman of Medical Imaging, Professor of Radiology, NGHA, King Fahad National Guard Hospital, King Abdulaziz Medical City, Riyadh, Saudi Arabia
Ali Nawaz Khan, MBBS, FRCS, FRCP, FRCR, LRCP is a member of the following medical societies: American Institute of Ultrasound in Medicine, Radiological Society of North America, Royal College of Physicians, Royal College of Physicians and Surgeons of the United States, Royal College of Radiologists, and Royal College of Surgeons of England
Disclosure: Nothing to disclose.

Coauthor(s)

Sumaira MacDonald, MBChB, PhD, MRCP, FRCR, Lecturer, Sheffield University Medical School; Endovascular Fellow, Sheffield Vascular Institute
Sumaira MacDonald, MBChB, PhD, MRCP, FRCR is a member of the following medical societies: British Medical Association, Royal College of Physicians, and Royal College of Radiologists
Disclosure: Nothing to disclose.

Murad Ali, MBBS, PhD, DTCD, Consulting Radiologist, Department of Radiology, Postgraduate Medical Institute, Lady Reading Hospital, Pakistan
Disclosure: Nothing to disclose.

David Sherlock, MBBS, FRCS, Consulting Staff, Department of Surgery, North Manchester General Hospital, Christie Hospital
Disclosure: Nothing to disclose.

Medical Editor

Eric P Weinberg, MD, Associate Professor, Department of Radiology, University of Rochester Medical Center, Strong Memorial Hospital
Eric P Weinberg, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

George Hartnell, MB, Professor of Radiology, Tufts University School of Medicine, Director of Cardiovascular and Interventional Radiology, Department of Radiology, Baystate Medical Center
George Hartnell, MB is a member of the following medical societies: American College of Cardiology, American College of Radiology, American Heart Association, Association of University Radiologists, British Institute of Radiology, British Medical Association, Massachusetts Medical Society, Radiological Society of North America, Royal College of Physicians, Royal College of Radiologists, and Society of Cardiovascular and Interventional Radiology
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Kyung J Cho, MD, FACR, William Martel Professor of Radiology, Interventional Radiology Fellowship Director, University of Michigan Health System
Kyung J Cho, MD, FACR is a member of the following medical societies: American College of Radiology, American Heart Association, American Medical Association, American Roentgen Ray Society, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

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eMedicine Specialties > Radiology > Gastrointestinal

Portal Hypertension: Multimedia

Multimedia

Barium swallow in the left lateral decubitus position shows multiple mucosal nodules in the mid to lower esophagus. In a patient with cirrhosis, these are suggestive of esophageal varices.

Barium swallow in a 56-year-old man with known cirrhosis who had a recent episode of hematemesis shows thickened mucosal folds and multiple polypoid filling defects at the lower end of the esophagus. These are suggestive of varices.

Part of an upper gastrointestinal tract barium series (same patient as in Images 3-6 in Multimedia) shows multiple polypoid filling defects within the fundus of the stomach. The final diagnosis was a left-sided portal hypertension secondary to splenic vein thrombosis.

Digital subtraction splenoportogram in a patient with portal hypertension shows a subcapsular contrast leak (arrows), which is a known complication of splenoportography.

Contrast-enhanced axial CT scan shows a dilated left renal vein (arrow; same patient as in Images 21-26). The final diagnosis was hepatocellular carcinoma, cirrhosis, and portal vein thrombosis/portal hypertension complicated by a spontaneous splenorenal shunt.

Transverse sonogram of the liver in a patient with hepatitis B cirrhosis shows a coarse echo structure of the liver.

Sagittal oblique sonogram of the liver shows a small liver with an irregular surface, moderate ascites, and a dilated portal vein. Note the thick gallbladder wall.

Sagittal oblique sonogram of the liver shows a dilated portal vein (22 mm in transverse diameter) in a patient with portal hypertension.

End-stage liver cirrhosis showing a small liver, gross ascites, and a dilated portal vein

Doppler sample volume in portal vein reveals continuous venous flow without evidence of respiratory variation, consistent with a hypertensive portal venous system. Note the coarse liver echo structure and ascites.

Doppler sample volume in portal vein reveals bidirectional flow in the portal vein associated with portal hypertension.

Sagittal oblique sonogram of the liver shows several tubular structures at the porta hepatis resulting from cavernous transformation secondary to portal vein thrombosis.

Duplex power Doppler sonogram shows an enlarged spleen; varices are apparent at the splenic hilum.

Doppler sonogram at the splenic hilum reveals hepatofugal venous flow in a patient with portal hypertension.

Spleen in portal hypertension, with a positive splenic interface sign.

Color Dopper ultrasound showing pericholecystic varices.

Color Dopper ultrasound showing pericholecystic varices.

Peripancreatic varices as shown on power Doppler.

Peripancreatic varices as shown on power Doppler.

Peripancreatic and perihilar varices as shown on real-time scanner.

Periportal varices on power Doppler

Periportal varices on conventional Doppler and power Doppler

Periportal varices conventional Doppler and power Doppler.

Dilatation of umbilical vein as shown on color Doppler.

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