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Portal Hypertension Differential Diagnoses

  • Author: Jesus Carale, MD; Chief Editor: BS Anand, MD  more...
 
Updated: Nov 07, 2015
 
 

Diagnostic Considerations

When evaluating a patient with portal hypertension, also consider the following conditions:

  • Cirrhosis of any etiology (viral hepatitis, autoimmune cirrhosis, alcohol-related cirrhosis, primary biliary cirrhosis, etc)
  • Hepatic infiltrative diseases (eg, Wilson disease, hemochromatosis, sarcoidosis)
  • Hepatoportal arteriovenous fistula
  • Portal vein obstruction
  • Portal vein occlusion (eg, portal vein thrombosis)
  • Primary sclerosing cholangitis
  • Severe congestive heart failure (cardiac cirrhosis)
  • Splenic vein thrombosis
  • Veno-occlusive disease
  • Budd-Chiari syndrome
  • Schistosomiasis
  • Chronic pancreatitis

Patients who present with upper gastrointestinal (GI) bleeding can be approached as whether the bleeding is variceal or nonvariceal. Not all upper GI bleeding in cirrhotic patients are from variceal hemorrhage. It should also be noted that peptic ulcer disease is present more frequently in cirrhotic patients than noncirrhotic patients.[12] The differential diagnosis of variceal hemorrhage includes the following:

  • Acute gastric erosions
  • Duodenal ulcers
  • Gastric cancer
  • Gastric ulcers
  • Mallory-Weiss tear
  • Nasogastric tube trauma
  • Portal hypertensive gastropathy - It is a relatively uncommon cause of significant bleeding

Gastric varices are the source of bleeding in 5-10% of patients with variceal hemorrhage. Higher rates are reported in patients with left-sided portal hypertension due to thrombosis of the splenic vein.

Differential Diagnoses

 
 
Contributor Information and Disclosures
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: New York Academy of Sciences, Sigma Xi, Association for Psychological Science, Gastroenterological Society of Australia, American College of Gastroenterology, Royal Society of Medicine

Disclosure: Nothing to disclose.

Parit Mekaroonkamol, MD Resident Physician, Department of Internal Medicine, Albert Einstein Medical Center

Parit Mekaroonkamol, MD is a member of the following medical societies: American College of Physicians, American Gastroenterological Association, Pennsylvania Medical Society

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

Disclosure: Nothing to disclose.

Simmy Bank, MD Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.

Sandeep Mukherjee, MB, BCh, MPH, FRCPC Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership

Ann Ouyang, MBBS Professor, Department of Internal Medicine, Pennsylvania State University College of Medicine; Attending Physician, Division of Gastroenterology and Hepatology, Milton S Hershey Medical Center

Disclosure: Nothing to disclose.

Waqar A Qureshi, MD Associate Professor of Medicine, Chief of Endoscopy, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine and Veterans Affairs Medical Center

Waqar A Qureshi, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

Noel Williams, MD Professor Emeritus, Department of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; Professor, Department of Internal Medicine, Division of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada

Noel Williams, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

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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 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).
Digital subtraction venous phase of a superior mesenteric artery angiogram (same patient as in the previous 2 images) 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).
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.
Table 1. Interpretation of Surrogate Portal Venous Pressure Measurements in the Differential Diagnosis of Portal Hypertension
Etiology of Portal Hypertension WHVP FHVP HVPG
Prehepatic Normal Normal Normal
Intrahepatic Presinusoidal Normal Normal Normal
Sinusoidal Increased Increased Increased
Postsinusoidal Increased Normal Increased
Posthepatic Budd-Chiari syndrome N/A Hepatic vein cannot be cannulated N/A
Other posthepatic causes Increased Increased Normal
FHVP = free hepatic venous pressure; HVPG = hepatic venous pressure gradient; N/A = not applicable; WHVP = wedged hepatic venous pressure.
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