Portal vein thrombosis
From Medical-Wiki
The increased use of ultrasound has revealed that portal vein thrombosis (PVT) is more common than once thought. This is also true for transient PVT.
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Etiologies of portal vein thrombosis
The splenic vein and the superior mesenteric vein join to form the portal vein posterior to the pancreatic head. With intrahepatic processes such as cirrhosis and tumor, thrombosis begins within the liver and spreads to the extrahepatic portal vein. In the majority of other etiologies, thrombosis begins at the origin of the portal vein. It is also possible for thrombosis of the splenic vein to propagate to the portal vein. This may occur when there is an adjacent inflammatory process such as chronic pancreatitis.
Coagulopathies and stasis can also lead to PVT. Cirrhosis is the most common cause of stasis. The extrahepatic portal vein may be obstructed by the growth of adjacent tumors. Finally, inflammation and infection are also associated with an increased incidence of PVT.
Clinical course of portal vein thrombosis
The reason that PVT does not influence liver function per se is because there is a rapid compensatory increase in flow through the hepatic artery. In addition, on a more chronic basis, collaterals are formed—perhaps as early as 12 days after acute thrombis formation. [1][2]
PVT has a 10 year survival rate of between 38% and 60%. Of these deaths, most are secondary to the primary pathology. This fact is also true for portal vein hypertension. In children, 10 year survival rate is greater than 70%. This is probably due to the low accompanying comorbidities of malignancy and cirrhosis.
Diagnosing portal vein thrombosis
Clinical presentation
The clinical presentation of acute PVT is often unimpressive. When there are symptoms, they are primarily right upper quadrant pain and/or fever. Other presentations include increasing ascites, intestinal ischemia and its associated symptoms, and worsening symptoms of portal hypertension. There are also cases of acute esophageal bleeding.
Following an acute episode, there are certainly cases of complete and partial resolution. This adds to the belief that a significant number of acute episodes go unnoticed.
Those patients who have chronic PVT usually have symptoms related to portal hypertension. In 90% of cases, the presenting complaint is an esophageal bleed. Chronologically, this may occur as long as 4 years later and there have been reports of a delay as long as 12 years.
If malignancy is the etiology of PVT, there is a lower incidence of bleeding. the harsh reality is that they do not survive long enough to develop the sequelae of portal hypertension.
On rare occasions, patients with PVT will present with a fever of unknown origin. [3]
Findings on physical exam
On physical examination, more than three quarters of patients have splenomegaly. Ascites is uncommon. Most symptoms are contingent upon the degree of underlying liver disease. A unique physical finding is the so called caput medusae. This nest of dilated veins forms because following posthepatic or intrahepatic hypertension, there is recanalization of the umbilical vein. This vein connects with the left hepatic branch of the portal vein, and its recanalization will not be observed in isolated extrahepatic portal vein obstruction because the obstruction is below the origin of the umbilical vein. [4]
Treating portal vein thrombosis
If detected early, portal vein thrombosis can be treated with anticoagulation—heparin followed by coumadin. This does not statistically increase the possibility of bleeding, reduces the chances of mesenteric infarction, and is often accompanied by early recanalization. Transhepatic angioplasty, thrombolysis and/or portosystemic shunt, and distal splenorenal shunts are also sometimes used.
In the face of significant hepatic dysfunction, shunts may increase the incidence of encephalopathy. [5]
![[2]](http://www.med-ars.it/gastroenterology/caput_medusae.JPG){kind=link}