DOMElement Object ( [schemaTypeInfo] => [tagName] => table [firstElementChild] => (object value omitted) [lastElementChild] => (object value omitted) [childElementCount] => 1 [previousElementSibling] => (object value omitted) [nextElementSibling] => (object value omitted) [nodeName] => table [nodeValue] => Gallbladder Varicosity In this CT scan through the upper abdomen, portal hypertension has also manifest with venous varicosities (maroon) in the splenic hilum, over the gallbladder and with an enlarged gastroepiploic vein The stomach shows signs of a hypertensive gastropathy with thickened wall and hyperemic mucosa, there is a small amount of ascites behind the liver, and the caudate lobe is enlarged.. 82117c.8s liver cirrhosis caudate lobe enlarged gallbladder varicose vein varicosity stomach wall thickened hyperemeic gastroesophageal varices ascites colon thick walled CTscan Courtesy Ashley DAvidoff MD copyright 2008 [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => table [baseURI] => [textContent] => Gallbladder Varicosity In this CT scan through the upper abdomen, portal hypertension has also manifest with venous varicosities (maroon) in the splenic hilum, over the gallbladder and with an enlarged gastroepiploic vein The stomach shows signs of a hypertensive gastropathy with thickened wall and hyperemic mucosa, there is a small amount of ascites behind the liver, and the caudate lobe is enlarged.. 82117c.8s liver cirrhosis caudate lobe enlarged gallbladder varicose vein varicosity stomach wall thickened hyperemeic gastroesophageal varices ascites colon thick walled CTscan Courtesy Ashley DAvidoff MD copyright 2008 )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => (object value omitted) [lastElementChild] => (object value omitted) [childElementCount] => 1 [previousElementSibling] => [nextElementSibling] => [nodeName] => td [nodeValue] => In this CT scan through the upper abdomen, portal hypertension has also manifest with venous varicosities (maroon) in the splenic hilum, over the gallbladder and with an enlarged gastroepiploic vein The stomach shows signs of a hypertensive gastropathy with thickened wall and hyperemic mucosa, there is a small amount of ascites behind the liver, and the caudate lobe is enlarged.. 82117c.8s liver cirrhosis caudate lobe enlarged gallbladder varicose vein varicosity stomach wall thickened hyperemeic gastroesophageal varices ascites colon thick walled CTscan Courtesy Ashley DAvidoff MD copyright 2008 [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => In this CT scan through the upper abdomen, portal hypertension has also manifest with venous varicosities (maroon) in the splenic hilum, over the gallbladder and with an enlarged gastroepiploic vein The stomach shows signs of a hypertensive gastropathy with thickened wall and hyperemic mucosa, there is a small amount of ascites behind the liver, and the caudate lobe is enlarged.. 82117c.8s liver cirrhosis caudate lobe enlarged gallbladder varicose vein varicosity stomach wall thickened hyperemeic gastroesophageal varices ascites colon thick walled CTscan Courtesy Ashley DAvidoff MD copyright 2008 )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => (object value omitted) [lastElementChild] => (object value omitted) [childElementCount] => 1 [previousElementSibling] => [nextElementSibling] => [nodeName] => td [nodeValue] => Gallbladder Varicosity [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => Gallbladder Varicosity )
DOMElement Object ( [schemaTypeInfo] => [tagName] => table [firstElementChild] => (object value omitted) [lastElementChild] => (object value omitted) [childElementCount] => 1 [previousElementSibling] => (object value omitted) [nextElementSibling] => (object value omitted) [nodeName] => table [nodeValue] => Gallbladder Varicosities In the CTscan above the coronal images (a,b,c,d) show thrombus (naroon) in the portal vein causing obstruction and the development of serpiginous collaterals called cavernous transformation of the portal vein. Sometimes these varicocities involve the gallbladder (green) as seen in image e and f in cross section. 82709c01.8s 60M liver HCC hepatocellular carcinoma portal vein thrombosis hepatic vein thrombosis cavernous transformation of the portal vein gallbladder varicosity ascites CTscan Courtesy Ashley Davidoff MD copyright 2008 CTscan [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => table [baseURI] => [textContent] => Gallbladder Varicosities In the CTscan above the coronal images (a,b,c,d) show thrombus (naroon) in the portal vein causing obstruction and the development of serpiginous collaterals called cavernous transformation of the portal vein. Sometimes these varicocities involve the gallbladder (green) as seen in image e and f in cross section. 82709c01.8s 60M liver HCC hepatocellular carcinoma portal vein thrombosis hepatic vein thrombosis cavernous transformation of the portal vein gallbladder varicosity ascites CTscan Courtesy Ashley Davidoff MD copyright 2008 CTscan )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => (object value omitted) [lastElementChild] => (object value omitted) [childElementCount] => 1 [previousElementSibling] => [nextElementSibling] => [nodeName] => td [nodeValue] => In the CTscan above the coronal images (a,b,c,d) show thrombus (naroon) in the portal vein causing obstruction and the development of serpiginous collaterals called cavernous transformation of the portal vein. Sometimes these varicocities involve the gallbladder (green) as seen in image e and f in cross section. 82709c01.8s 60M liver HCC hepatocellular carcinoma portal vein thrombosis hepatic vein thrombosis cavernous transformation of the portal vein gallbladder varicosity ascites CTscan Courtesy Ashley Davidoff MD copyright 2008 CTscan [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => In the CTscan above the coronal images (a,b,c,d) show thrombus (naroon) in the portal vein causing obstruction and the development of serpiginous collaterals called cavernous transformation of the portal vein. Sometimes these varicocities involve the gallbladder (green) as seen in image e and f in cross section. 82709c01.8s 60M liver HCC hepatocellular carcinoma portal vein thrombosis hepatic vein thrombosis cavernous transformation of the portal vein gallbladder varicosity ascites CTscan Courtesy Ashley Davidoff MD copyright 2008 CTscan )
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DOMElement Object ( [schemaTypeInfo] => [tagName] => table [firstElementChild] => (object value omitted) [lastElementChild] => (object value omitted) [childElementCount] => 1 [previousElementSibling] => (object value omitted) [nextElementSibling] => (object value omitted) [nodeName] => table [nodeValue] => Pre-Sinusoidal Sinusoidal Post-Sinusoidal Splenic Vein Thrombosis Cirrhosis Alcoholic terminal hyaline sclerosis Splenomegaly Alcoholic hepatitis Vascular occlusive disease Splenic AV fistula Budd-Chiari Syndrome Schistosomiasis Inferior vena caval web Nodular regenerative hyperplasia Chronic passive venous congestion Congenital hepatic fibrosis Idiopathic portal fibrosis Chronic active hepatitis Myeloproliferative disorders Sarcoid Graft-versus-host disease [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => table [baseURI] => [textContent] => Pre-Sinusoidal Sinusoidal Post-Sinusoidal Splenic Vein Thrombosis Cirrhosis Alcoholic terminal hyaline sclerosis Splenomegaly Alcoholic hepatitis Vascular occlusive disease Splenic AV fistula Budd-Chiari Syndrome Schistosomiasis Inferior vena caval web Nodular regenerative hyperplasia Chronic passive venous congestion Congenital hepatic fibrosis Idiopathic portal fibrosis Chronic active hepatitis Myeloproliferative disorders Sarcoid Graft-versus-host disease )
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DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => Graft-versus-host disease [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => Graft-versus-host disease )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => [nodeName] => td [nodeValue] => [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => )
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DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => Myeloproliferative disorders [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => Myeloproliferative disorders )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => [nodeName] => td [nodeValue] => [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => Chronic active hepatitis [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => Chronic active hepatitis )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => [nodeName] => td [nodeValue] => [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => Idiopathic portal fibrosis [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => Idiopathic portal fibrosis )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => [nodeName] => td [nodeValue] => [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => Congenital hepatic fibrosis [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => Congenital hepatic fibrosis )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => [nodeName] => td [nodeValue] => Chronic passive venous congestion [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => Chronic passive venous congestion )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => Nodular regenerative hyperplasia [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => Nodular regenerative hyperplasia )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => [nodeName] => td [nodeValue] => Inferior vena caval web [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => Inferior vena caval web )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => Schistosomiasis [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => Schistosomiasis )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => [nodeName] => td [nodeValue] => Budd-Chiari Syndrome [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => Budd-Chiari Syndrome )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => (object value omitted) [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => [lastElementChild] => [childElementCount] => 0 [previousElementSibling] => [nextElementSibling] => (object value omitted) [nodeName] => td [nodeValue] => Splenic AV fistula [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => Splenic AV fistula )
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DOMElement Object ( [schemaTypeInfo] => [tagName] => table [firstElementChild] => (object value omitted) [lastElementChild] => (object value omitted) [childElementCount] => 1 [previousElementSibling] => [nextElementSibling] => [nodeName] => table [nodeValue] => Portal Hypertension Imaging Strategies Author Brian Hashim MS4 Under construction Clinical Considerations: When considering the patient with portal hypertension, it is helpful to consider the potential causes in terms of three categories, those being pre-sinusoidal, sinusoidal, and post-sinusoidal. With portal hypertension, both the severity of disease as well as its sequelae are varied. Thus, when considering what tests to order as well as imaging strategies, the physician must first assess the severity of the patient?s condition clinically and determine if it is feasible to await the results of blood or imaging studies. If a patient?s condition is severe (eg. bleeding esophageal varices), such studies should be put on hold until the patient becomes more stable. Imaging Strategies: Given the patient is stable, the physician should first consider what is most suspicious of as the etiology for the patient?s portal hypertension. If one is suspicious of a clot, either MRI or CT with contrast may be considered, although ultrasound would give helpful data as well. Below is a table of the possible radiographic studies that may be used in the evaluation of portal hypertension as well as their strengths and limitations. Table 1. Radiographic studies in evaluation of portal HTN Study Findings in portal HTN Strengths Limitations Duplex-Doppler U/S Splenomegaly, collateral circulation, nodular liver surface suggestive/non-specific Safe, economical, non-invasive, data regarding blood flow Data reproducibility problematic, interobserver/intraobserver variation, limited by body habitus/bowel gas CT scan Collateral circulation, dilatation of IVC Useful when U/S inconclusive, unaffected by body habitus/bowel gas No venous or arterial flow profile, cannot use contrast w/ renal failure or allergy, expensive MRI Similar to CT scan Useful when U/S inconclusive, MRA shows collaterals as well as vascular obstruction Cannot be used in patient?s w/ metal hardware (eg. Pacemaker), expensive What Study? As an initial screening test, it seems Duplex-Doppler ultrasound is the best choice regardless of the considered etiology. This test provides insight into both the anatomy and physiology of the portal vascular system. Why Duplex-Doppler Ultrasound? As mentioned above, this study provides information with respect to both the anatomy and physiology of the portal vascular system. Along with this strength, ultrasound is a safe, cheap, and non-invasive study. If findings from U/S are non-diagnostic or the study is low yield secondary to patient?s body habitus/bowel gas, the physician should consider further investigation with either CT scan w/ contrast or MRI. Background to Disease: Portal hypertension is defined as an increased pressure within the portal vasculature secondary to either increased portal flow or, in most cases, increased resistance to flow. It should be sought in all patients with a suspicion of liver disease. Normal portal pressure is considered to be 5-10mmHg, with values >10mmHg defining portal hypertension. Alone, portal hypertension is asymptomatic. Patients present with signs/symptoms of portal hypertension once complications such as esophageal varices develop. As mentioned above, the etiology of portal hypertension can be divided into three main groups, those being pre-sinusoidal, sinusoidal, and post-sinusoidal. A table of the different causes may be seen below. In industrialized nations, cirrhosis is by far the most common cause. Over time, as the body remains exposed to high portal pressures, blood flow seeks the path of least resistance, forming portal-systemic venous collaterals. The most dangerous complication associated with the development of such collaterals if bleeding esophageal varices. Table 2. Causes of Portal HTN Pre-Sinusoidal Sinusoidal Post-Sinusoidal Splenic Vein Thrombosis Cirrhosis Alcoholic terminal hyaline sclerosis Splenomegaly Alcoholic hepatitis Vascular occlusive disease Splenic AV fistula Budd-Chiari Syndrome Schistosomiasis Inferior vena caval web Nodular regenerative hyperplasia Chronic passive venous congestion Congenital hepatic fibrosis Idiopathic portal fibrosis Chronic active hepatitis Myeloproliferative disorders Sarcoid Graft-versus-host disease When to Order? In a patient whom is hemodynamically stable, one might consider Duplex-Doppler U/S to assess the degree of compromise of blood flow in the portal vasculature whenever there is a suspicion of liver failure. Patients presenting with bleeding esophageal varices by definition have portal hypertension, and given the mortality associated with this complication, should undergo treatment for the bleeding varices rather than have any radiographic studies performed. How to Order? There is no preparation necessary prior to undergoing Duplex-Doppler U/S for the assessment of portal hypertension. At the time of ordering an U/S, one should include any symptoms that the patient may be exhibiting as well as the pertinent history. One should be sure to include the intent of the imaging study, such as ?the evaluation for possible portal hypertension?. If CT scan w/ contrast is to be ordered, the patient?s allergies should be reviewed to ensure no dye allergies are present. The patient?s BUN and Creatinine should also be assessed so as to limit the occurrence of acute renal failure secondary to contrast. If MRI is to be obtained, one should ensure that the patient will be able to remain still for the length of the study and also ensure that the patient has no metallic implanted devices (eg. Pacemaker). Preparing the Patient: For the hemodynamically stable non-hospitalized patient, any of the above mentioned studies may be performed with the patient returning to work or home the same day. Patients should be reminded that all of the studies are non-invasive and provide same day results. So as to limit anxiety for the patient, time should be allotted to answer any and all questions regarding the imaging modality of choice. For patients with a history of claustrophobia who are to undergo MRI, premedication should be considered. Clinical Red Flags: Any patient presenting with bleeding esophageal varices should have the bleeding varices treated. Imaging studies to diagnose portal hypertension are contraindicated in such cases. Gallbladder Varicosities In the CTscan above the coronal images (a,b,c,d) show thrombus (naroon) in the portal vein causing obstruction and the development of serpiginous collaterals called cavernous transformation of the portal vein. Sometimes these varicocities involve the gallbladder (green) as seen in image e and f in cross section. 82709c01.8s 60M liver HCC hepatocellular carcinoma portal vein thrombosis hepatic vein thrombosis cavernous transformation of the portal vein gallbladder varicosity ascites CTscan Courtesy Ashley Davidoff MD copyright 2008 CTscan Gallbladder Varicosity In this CT scan through the upper abdomen, portal hypertension has also manifest with venous varicosities (maroon) in the splenic hilum, over the gallbladder and with an enlarged gastroepiploic vein The stomach shows signs of a hypertensive gastropathy with thickened wall and hyperemic mucosa, there is a small amount of ascites behind the liver, and the caudate lobe is enlarged.. 82117c.8s liver cirrhosis caudate lobe enlarged gallbladder varicose vein varicosity stomach wall thickened hyperemeic gastroesophageal varices ascites colon thick walled CTscan Courtesy Ashley DAvidoff MD copyright 2008 References: Texts: Schwartz?s Principles of Surgery, 8th edition 2005 Merck Manual, 17th edition, 1999, Centennial edition Griffith?s 5-Minute Clinical Consult, 14th edition, 2006 Web: eMedicine-Portal hypertension [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => table [baseURI] => [textContent] => Portal Hypertension Imaging Strategies Author Brian Hashim MS4 Under construction Clinical Considerations: When considering the patient with portal hypertension, it is helpful to consider the potential causes in terms of three categories, those being pre-sinusoidal, sinusoidal, and post-sinusoidal. With portal hypertension, both the severity of disease as well as its sequelae are varied. Thus, when considering what tests to order as well as imaging strategies, the physician must first assess the severity of the patient?s condition clinically and determine if it is feasible to await the results of blood or imaging studies. If a patient?s condition is severe (eg. bleeding esophageal varices), such studies should be put on hold until the patient becomes more stable. Imaging Strategies: Given the patient is stable, the physician should first consider what is most suspicious of as the etiology for the patient?s portal hypertension. If one is suspicious of a clot, either MRI or CT with contrast may be considered, although ultrasound would give helpful data as well. Below is a table of the possible radiographic studies that may be used in the evaluation of portal hypertension as well as their strengths and limitations. Table 1. Radiographic studies in evaluation of portal HTN Study Findings in portal HTN Strengths Limitations Duplex-Doppler U/S Splenomegaly, collateral circulation, nodular liver surface suggestive/non-specific Safe, economical, non-invasive, data regarding blood flow Data reproducibility problematic, interobserver/intraobserver variation, limited by body habitus/bowel gas CT scan Collateral circulation, dilatation of IVC Useful when U/S inconclusive, unaffected by body habitus/bowel gas No venous or arterial flow profile, cannot use contrast w/ renal failure or allergy, expensive MRI Similar to CT scan Useful when U/S inconclusive, MRA shows collaterals as well as vascular obstruction Cannot be used in patient?s w/ metal hardware (eg. Pacemaker), expensive What Study? As an initial screening test, it seems Duplex-Doppler ultrasound is the best choice regardless of the considered etiology. This test provides insight into both the anatomy and physiology of the portal vascular system. Why Duplex-Doppler Ultrasound? As mentioned above, this study provides information with respect to both the anatomy and physiology of the portal vascular system. Along with this strength, ultrasound is a safe, cheap, and non-invasive study. If findings from U/S are non-diagnostic or the study is low yield secondary to patient?s body habitus/bowel gas, the physician should consider further investigation with either CT scan w/ contrast or MRI. Background to Disease: Portal hypertension is defined as an increased pressure within the portal vasculature secondary to either increased portal flow or, in most cases, increased resistance to flow. It should be sought in all patients with a suspicion of liver disease. Normal portal pressure is considered to be 5-10mmHg, with values >10mmHg defining portal hypertension. Alone, portal hypertension is asymptomatic. Patients present with signs/symptoms of portal hypertension once complications such as esophageal varices develop. As mentioned above, the etiology of portal hypertension can be divided into three main groups, those being pre-sinusoidal, sinusoidal, and post-sinusoidal. A table of the different causes may be seen below. In industrialized nations, cirrhosis is by far the most common cause. Over time, as the body remains exposed to high portal pressures, blood flow seeks the path of least resistance, forming portal-systemic venous collaterals. The most dangerous complication associated with the development of such collaterals if bleeding esophageal varices. Table 2. Causes of Portal HTN Pre-Sinusoidal Sinusoidal Post-Sinusoidal Splenic Vein Thrombosis Cirrhosis Alcoholic terminal hyaline sclerosis Splenomegaly Alcoholic hepatitis Vascular occlusive disease Splenic AV fistula Budd-Chiari Syndrome Schistosomiasis Inferior vena caval web Nodular regenerative hyperplasia Chronic passive venous congestion Congenital hepatic fibrosis Idiopathic portal fibrosis Chronic active hepatitis Myeloproliferative disorders Sarcoid Graft-versus-host disease When to Order? In a patient whom is hemodynamically stable, one might consider Duplex-Doppler U/S to assess the degree of compromise of blood flow in the portal vasculature whenever there is a suspicion of liver failure. Patients presenting with bleeding esophageal varices by definition have portal hypertension, and given the mortality associated with this complication, should undergo treatment for the bleeding varices rather than have any radiographic studies performed. How to Order? There is no preparation necessary prior to undergoing Duplex-Doppler U/S for the assessment of portal hypertension. At the time of ordering an U/S, one should include any symptoms that the patient may be exhibiting as well as the pertinent history. One should be sure to include the intent of the imaging study, such as ?the evaluation for possible portal hypertension?. If CT scan w/ contrast is to be ordered, the patient?s allergies should be reviewed to ensure no dye allergies are present. The patient?s BUN and Creatinine should also be assessed so as to limit the occurrence of acute renal failure secondary to contrast. If MRI is to be obtained, one should ensure that the patient will be able to remain still for the length of the study and also ensure that the patient has no metallic implanted devices (eg. Pacemaker). Preparing the Patient: For the hemodynamically stable non-hospitalized patient, any of the above mentioned studies may be performed with the patient returning to work or home the same day. Patients should be reminded that all of the studies are non-invasive and provide same day results. So as to limit anxiety for the patient, time should be allotted to answer any and all questions regarding the imaging modality of choice. For patients with a history of claustrophobia who are to undergo MRI, premedication should be considered. Clinical Red Flags: Any patient presenting with bleeding esophageal varices should have the bleeding varices treated. Imaging studies to diagnose portal hypertension are contraindicated in such cases. Gallbladder Varicosities In the CTscan above the coronal images (a,b,c,d) show thrombus (naroon) in the portal vein causing obstruction and the development of serpiginous collaterals called cavernous transformation of the portal vein. Sometimes these varicocities involve the gallbladder (green) as seen in image e and f in cross section. 82709c01.8s 60M liver HCC hepatocellular carcinoma portal vein thrombosis hepatic vein thrombosis cavernous transformation of the portal vein gallbladder varicosity ascites CTscan Courtesy Ashley Davidoff MD copyright 2008 CTscan Gallbladder Varicosity In this CT scan through the upper abdomen, portal hypertension has also manifest with venous varicosities (maroon) in the splenic hilum, over the gallbladder and with an enlarged gastroepiploic vein The stomach shows signs of a hypertensive gastropathy with thickened wall and hyperemic mucosa, there is a small amount of ascites behind the liver, and the caudate lobe is enlarged.. 82117c.8s liver cirrhosis caudate lobe enlarged gallbladder varicose vein varicosity stomach wall thickened hyperemeic gastroesophageal varices ascites colon thick walled CTscan Courtesy Ashley DAvidoff MD copyright 2008 References: Texts: Schwartz?s Principles of Surgery, 8th edition 2005 Merck Manual, 17th edition, 1999, Centennial edition Griffith?s 5-Minute Clinical Consult, 14th edition, 2006 Web: eMedicine-Portal hypertension )
DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => (object value omitted) [lastElementChild] => (object value omitted) [childElementCount] => 1 [previousElementSibling] => [nextElementSibling] => [nodeName] => td [nodeValue] => In this CT scan through the upper abdomen, portal hypertension has also manifest with venous varicosities (maroon) in the splenic hilum, over the gallbladder and with an enlarged gastroepiploic vein The stomach shows signs of a hypertensive gastropathy with thickened wall and hyperemic mucosa, there is a small amount of ascites behind the liver, and the caudate lobe is enlarged.. 82117c.8s liver cirrhosis caudate lobe enlarged gallbladder varicose vein varicosity stomach wall thickened hyperemeic gastroesophageal varices ascites colon thick walled CTscan Courtesy Ashley DAvidoff MD copyright 2008 [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => In this CT scan through the upper abdomen, portal hypertension has also manifest with venous varicosities (maroon) in the splenic hilum, over the gallbladder and with an enlarged gastroepiploic vein The stomach shows signs of a hypertensive gastropathy with thickened wall and hyperemic mucosa, there is a small amount of ascites behind the liver, and the caudate lobe is enlarged.. 82117c.8s liver cirrhosis caudate lobe enlarged gallbladder varicose vein varicosity stomach wall thickened hyperemeic gastroesophageal varices ascites colon thick walled CTscan Courtesy Ashley DAvidoff MD copyright 2008 )
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DOMElement Object ( [schemaTypeInfo] => [tagName] => td [firstElementChild] => (object value omitted) [lastElementChild] => (object value omitted) [childElementCount] => 60 [previousElementSibling] => [nextElementSibling] => [nodeName] => td [nodeValue] => Portal Hypertension Imaging Strategies Author Brian Hashim MS4 Under construction Clinical Considerations: When considering the patient with portal hypertension, it is helpful to consider the potential causes in terms of three categories, those being pre-sinusoidal, sinusoidal, and post-sinusoidal. With portal hypertension, both the severity of disease as well as its sequelae are varied. Thus, when considering what tests to order as well as imaging strategies, the physician must first assess the severity of the patient?s condition clinically and determine if it is feasible to await the results of blood or imaging studies. If a patient?s condition is severe (eg. bleeding esophageal varices), such studies should be put on hold until the patient becomes more stable. Imaging Strategies: Given the patient is stable, the physician should first consider what is most suspicious of as the etiology for the patient?s portal hypertension. If one is suspicious of a clot, either MRI or CT with contrast may be considered, although ultrasound would give helpful data as well. Below is a table of the possible radiographic studies that may be used in the evaluation of portal hypertension as well as their strengths and limitations. Table 1. Radiographic studies in evaluation of portal HTN Study Findings in portal HTN Strengths Limitations Duplex-Doppler U/S Splenomegaly, collateral circulation, nodular liver surface suggestive/non-specific Safe, economical, non-invasive, data regarding blood flow Data reproducibility problematic, interobserver/intraobserver variation, limited by body habitus/bowel gas CT scan Collateral circulation, dilatation of IVC Useful when U/S inconclusive, unaffected by body habitus/bowel gas No venous or arterial flow profile, cannot use contrast w/ renal failure or allergy, expensive MRI Similar to CT scan Useful when U/S inconclusive, MRA shows collaterals as well as vascular obstruction Cannot be used in patient?s w/ metal hardware (eg. Pacemaker), expensive What Study? As an initial screening test, it seems Duplex-Doppler ultrasound is the best choice regardless of the considered etiology. This test provides insight into both the anatomy and physiology of the portal vascular system. Why Duplex-Doppler Ultrasound? As mentioned above, this study provides information with respect to both the anatomy and physiology of the portal vascular system. Along with this strength, ultrasound is a safe, cheap, and non-invasive study. If findings from U/S are non-diagnostic or the study is low yield secondary to patient?s body habitus/bowel gas, the physician should consider further investigation with either CT scan w/ contrast or MRI. Background to Disease: Portal hypertension is defined as an increased pressure within the portal vasculature secondary to either increased portal flow or, in most cases, increased resistance to flow. It should be sought in all patients with a suspicion of liver disease. Normal portal pressure is considered to be 5-10mmHg, with values >10mmHg defining portal hypertension. Alone, portal hypertension is asymptomatic. Patients present with signs/symptoms of portal hypertension once complications such as esophageal varices develop. As mentioned above, the etiology of portal hypertension can be divided into three main groups, those being pre-sinusoidal, sinusoidal, and post-sinusoidal. A table of the different causes may be seen below. In industrialized nations, cirrhosis is by far the most common cause. Over time, as the body remains exposed to high portal pressures, blood flow seeks the path of least resistance, forming portal-systemic venous collaterals. The most dangerous complication associated with the development of such collaterals if bleeding esophageal varices. Table 2. Causes of Portal HTN Pre-Sinusoidal Sinusoidal Post-Sinusoidal Splenic Vein Thrombosis Cirrhosis Alcoholic terminal hyaline sclerosis Splenomegaly Alcoholic hepatitis Vascular occlusive disease Splenic AV fistula Budd-Chiari Syndrome Schistosomiasis Inferior vena caval web Nodular regenerative hyperplasia Chronic passive venous congestion Congenital hepatic fibrosis Idiopathic portal fibrosis Chronic active hepatitis Myeloproliferative disorders Sarcoid Graft-versus-host disease When to Order? In a patient whom is hemodynamically stable, one might consider Duplex-Doppler U/S to assess the degree of compromise of blood flow in the portal vasculature whenever there is a suspicion of liver failure. Patients presenting with bleeding esophageal varices by definition have portal hypertension, and given the mortality associated with this complication, should undergo treatment for the bleeding varices rather than have any radiographic studies performed. How to Order? There is no preparation necessary prior to undergoing Duplex-Doppler U/S for the assessment of portal hypertension. At the time of ordering an U/S, one should include any symptoms that the patient may be exhibiting as well as the pertinent history. One should be sure to include the intent of the imaging study, such as ?the evaluation for possible portal hypertension?. If CT scan w/ contrast is to be ordered, the patient?s allergies should be reviewed to ensure no dye allergies are present. The patient?s BUN and Creatinine should also be assessed so as to limit the occurrence of acute renal failure secondary to contrast. If MRI is to be obtained, one should ensure that the patient will be able to remain still for the length of the study and also ensure that the patient has no metallic implanted devices (eg. Pacemaker). Preparing the Patient: For the hemodynamically stable non-hospitalized patient, any of the above mentioned studies may be performed with the patient returning to work or home the same day. Patients should be reminded that all of the studies are non-invasive and provide same day results. So as to limit anxiety for the patient, time should be allotted to answer any and all questions regarding the imaging modality of choice. For patients with a history of claustrophobia who are to undergo MRI, premedication should be considered. Clinical Red Flags: Any patient presenting with bleeding esophageal varices should have the bleeding varices treated. Imaging studies to diagnose portal hypertension are contraindicated in such cases. Gallbladder Varicosities In the CTscan above the coronal images (a,b,c,d) show thrombus (naroon) in the portal vein causing obstruction and the development of serpiginous collaterals called cavernous transformation of the portal vein. Sometimes these varicocities involve the gallbladder (green) as seen in image e and f in cross section. 82709c01.8s 60M liver HCC hepatocellular carcinoma portal vein thrombosis hepatic vein thrombosis cavernous transformation of the portal vein gallbladder varicosity ascites CTscan Courtesy Ashley Davidoff MD copyright 2008 CTscan Gallbladder Varicosity In this CT scan through the upper abdomen, portal hypertension has also manifest with venous varicosities (maroon) in the splenic hilum, over the gallbladder and with an enlarged gastroepiploic vein The stomach shows signs of a hypertensive gastropathy with thickened wall and hyperemic mucosa, there is a small amount of ascites behind the liver, and the caudate lobe is enlarged.. 82117c.8s liver cirrhosis caudate lobe enlarged gallbladder varicose vein varicosity stomach wall thickened hyperemeic gastroesophageal varices ascites colon thick walled CTscan Courtesy Ashley DAvidoff MD copyright 2008 References: Texts: Schwartz?s Principles of Surgery, 8th edition 2005 Merck Manual, 17th edition, 1999, Centennial edition Griffith?s 5-Minute Clinical Consult, 14th edition, 2006 Web: eMedicine-Portal hypertension [nodeType] => 1 [parentNode] => (object value omitted) [childNodes] => (object value omitted) [firstChild] => (object value omitted) [lastChild] => (object value omitted) [previousSibling] => (object value omitted) [nextSibling] => (object value omitted) [attributes] => (object value omitted) [ownerDocument] => (object value omitted) [namespaceURI] => [prefix] => [localName] => td [baseURI] => [textContent] => Portal Hypertension Imaging Strategies Author Brian Hashim MS4 Under construction Clinical Considerations: When considering the patient with portal hypertension, it is helpful to consider the potential causes in terms of three categories, those being pre-sinusoidal, sinusoidal, and post-sinusoidal. With portal hypertension, both the severity of disease as well as its sequelae are varied. Thus, when considering what tests to order as well as imaging strategies, the physician must first assess the severity of the patient?s condition clinically and determine if it is feasible to await the results of blood or imaging studies. If a patient?s condition is severe (eg. bleeding esophageal varices), such studies should be put on hold until the patient becomes more stable. Imaging Strategies: Given the patient is stable, the physician should first consider what is most suspicious of as the etiology for the patient?s portal hypertension. If one is suspicious of a clot, either MRI or CT with contrast may be considered, although ultrasound would give helpful data as well. Below is a table of the possible radiographic studies that may be used in the evaluation of portal hypertension as well as their strengths and limitations. Table 1. Radiographic studies in evaluation of portal HTN Study Findings in portal HTN Strengths Limitations Duplex-Doppler U/S Splenomegaly, collateral circulation, nodular liver surface suggestive/non-specific Safe, economical, non-invasive, data regarding blood flow Data reproducibility problematic, interobserver/intraobserver variation, limited by body habitus/bowel gas CT scan Collateral circulation, dilatation of IVC Useful when U/S inconclusive, unaffected by body habitus/bowel gas No venous or arterial flow profile, cannot use contrast w/ renal failure or allergy, expensive MRI Similar to CT scan Useful when U/S inconclusive, MRA shows collaterals as well as vascular obstruction Cannot be used in patient?s w/ metal hardware (eg. Pacemaker), expensive What Study? As an initial screening test, it seems Duplex-Doppler ultrasound is the best choice regardless of the considered etiology. This test provides insight into both the anatomy and physiology of the portal vascular system. Why Duplex-Doppler Ultrasound? As mentioned above, this study provides information with respect to both the anatomy and physiology of the portal vascular system. Along with this strength, ultrasound is a safe, cheap, and non-invasive study. If findings from U/S are non-diagnostic or the study is low yield secondary to patient?s body habitus/bowel gas, the physician should consider further investigation with either CT scan w/ contrast or MRI. Background to Disease: Portal hypertension is defined as an increased pressure within the portal vasculature secondary to either increased portal flow or, in most cases, increased resistance to flow. It should be sought in all patients with a suspicion of liver disease. Normal portal pressure is considered to be 5-10mmHg, with values >10mmHg defining portal hypertension. Alone, portal hypertension is asymptomatic. Patients present with signs/symptoms of portal hypertension once complications such as esophageal varices develop. As mentioned above, the etiology of portal hypertension can be divided into three main groups, those being pre-sinusoidal, sinusoidal, and post-sinusoidal. A table of the different causes may be seen below. In industrialized nations, cirrhosis is by far the most common cause. Over time, as the body remains exposed to high portal pressures, blood flow seeks the path of least resistance, forming portal-systemic venous collaterals. The most dangerous complication associated with the development of such collaterals if bleeding esophageal varices. Table 2. Causes of Portal HTN Pre-Sinusoidal Sinusoidal Post-Sinusoidal Splenic Vein Thrombosis Cirrhosis Alcoholic terminal hyaline sclerosis Splenomegaly Alcoholic hepatitis Vascular occlusive disease Splenic AV fistula Budd-Chiari Syndrome Schistosomiasis Inferior vena caval web Nodular regenerative hyperplasia Chronic passive venous congestion Congenital hepatic fibrosis Idiopathic portal fibrosis Chronic active hepatitis Myeloproliferative disorders Sarcoid Graft-versus-host disease When to Order? In a patient whom is hemodynamically stable, one might consider Duplex-Doppler U/S to assess the degree of compromise of blood flow in the portal vasculature whenever there is a suspicion of liver failure. Patients presenting with bleeding esophageal varices by definition have portal hypertension, and given the mortality associated with this complication, should undergo treatment for the bleeding varices rather than have any radiographic studies performed. How to Order? There is no preparation necessary prior to undergoing Duplex-Doppler U/S for the assessment of portal hypertension. At the time of ordering an U/S, one should include any symptoms that the patient may be exhibiting as well as the pertinent history. One should be sure to include the intent of the imaging study, such as ?the evaluation for possible portal hypertension?. If CT scan w/ contrast is to be ordered, the patient?s allergies should be reviewed to ensure no dye allergies are present. The patient?s BUN and Creatinine should also be assessed so as to limit the occurrence of acute renal failure secondary to contrast. If MRI is to be obtained, one should ensure that the patient will be able to remain still for the length of the study and also ensure that the patient has no metallic implanted devices (eg. Pacemaker). Preparing the Patient: For the hemodynamically stable non-hospitalized patient, any of the above mentioned studies may be performed with the patient returning to work or home the same day. Patients should be reminded that all of the studies are non-invasive and provide same day results. So as to limit anxiety for the patient, time should be allotted to answer any and all questions regarding the imaging modality of choice. For patients with a history of claustrophobia who are to undergo MRI, premedication should be considered. Clinical Red Flags: Any patient presenting with bleeding esophageal varices should have the bleeding varices treated. Imaging studies to diagnose portal hypertension are contraindicated in such cases. Gallbladder Varicosities In the CTscan above the coronal images (a,b,c,d) show thrombus (naroon) in the portal vein causing obstruction and the development of serpiginous collaterals called cavernous transformation of the portal vein. Sometimes these varicocities involve the gallbladder (green) as seen in image e and f in cross section. 82709c01.8s 60M liver HCC hepatocellular carcinoma portal vein thrombosis hepatic vein thrombosis cavernous transformation of the portal vein gallbladder varicosity ascites CTscan Courtesy Ashley Davidoff MD copyright 2008 CTscan Gallbladder Varicosity In this CT scan through the upper abdomen, portal hypertension has also manifest with venous varicosities (maroon) in the splenic hilum, over the gallbladder and with an enlarged gastroepiploic vein The stomach shows signs of a hypertensive gastropathy with thickened wall and hyperemic mucosa, there is a small amount of ascites behind the liver, and the caudate lobe is enlarged.. 82117c.8s liver cirrhosis caudate lobe enlarged gallbladder varicose vein varicosity stomach wall thickened hyperemeic gastroesophageal varices ascites colon thick walled CTscan Courtesy Ashley DAvidoff MD copyright 2008 References: Texts: Schwartz?s Principles of Surgery, 8th edition 2005 Merck Manual, 17th edition, 1999, Centennial edition Griffith?s 5-Minute Clinical Consult, 14th edition, 2006 Web: eMedicine-Portal hypertension )