Portal andor Splenic Vein Thrombosis


The presence of thrombus in the portal vein causes obstruction of the venous drainage of much of the GI system. Risk factors include cirrhosis, abdominal sepsis, pan-

TABLE 118-4. Causes of Portal Vein Thrombosis


Tumor invasion of portal vein Hepatocellular carcinoma Cholangiocarcinoma Abdominal sepsis Oral contraceptive pill Pancreatitis Prothromotic disorders Trauma

Neonatal omphalitis creatitis, hepatic malignancies, trauma/surgery, decreased portal venous flow, and hypercoagulable states, although idiopathic portal vein thrombosis (PVT) is a rare cause of presinusoidal portal hypertension in the Western world. Occasionally, thrombosis is localized to the splenic or superior mesenteric vein (SMV), which causes findings specific to the affected portion of the GI system.


PVT can be an incidental finding on ultrasound or contrast enhanced MRI and CT studies. Cavernous transformation of the thrombosed vein (the appearance of many string-like veins that provide partial venous flow into the liver) can also be seen. Other imaging findings include enlarged sMV and splenic vein, spontaneous portosystemic shunts, splenomegaly, and edematous bowel wall with associated ascites. New symptoms and signs, such as abdominal pain, splenomegaly, and increased abdominal girth, in a patient with known hepatic disease should prompt a search for PVT. In adults, hemoptysis from esophageal varices is not an uncommon initial presentation of PVT. Causes of PVT are shown in Table 118-4.


The diagnosis of PVT is relatively straightforward once it is suspected. MRI and CT, as well as ultrasound, are usually diagnostic and can provide information regarding the extent of disease as well as its cause. All of these modalities can confirm the presence of varices, splenomegaly, and ascites, as well as cirrhosis. A celiac or mesenteric arterio-gram can be extended to show the venous drainage into the portal vein and diagnose PVT. If required, direct trans-hepatic portal vein percutaneous access can be obtained and a porto-venogram performed. It is important to note that in the absence of liver disease, wedged hepatic pressures are normal, whereas preobstructive pressures (intrasplenic, SMV) are elevated. Laboratory values are usually normal with nonspecific findings, such as hypoal-buminemia and hepatocellular dysfunction, occurring late in the disease and more frequently in children.


Idiopathic (no predisposing risk factors identified) PVT has a much more favorable prognosis than PVT which is caused by an underlying disease. Ten-year survival of idiopathic PVT is > 75%. In addition, variceal bleeding is more rare and easily controlled than when associated with cirrhosis because there is no underlying coagulation defect. Bleeding can be treated endoscopically with sclerotherapy or banding with excellent results (> 90% success). Because of the relatively favorable prognosis, thromboly-sis of portal vein is rarely required if the disease is idio-pathic. In the presence of underlying risk factors, portal vein thrombolysis should be undertaken only if the risk factor is addressed at the same time, otherwise rethrom-bosis is expected. Therefore, portal vein thrombolysis is rarely indicated. Exceptions include recurrent variceal bleeding despite treatment in case of idiopathic disease or when recanalization is needed for liver transplantation. Percutaneous thrombolysis performed by interventional radiologists is usually the easiest and safest method. First, access is achieved into the right, left, or both main portal veins using a transhepatic approach under ultrasound guidance. Multi-sideholed infusion catheters are placed along the length of the clot, which is then laced with throm-bolytics. The duration of thrombolysis and amount of drugs used are specified and limited to reduce the rate of complications. Porto-venograms can be performed every 12 to 18 hours to monitor for progress.

In isolated SVT, symptoms are limited to splenomegaly and associated abdominal pain and possible gastro-esophageal varices. Children may also show anemia and thrombocytopenia. If refractory to conservative treatment, such cases may require spleenectomy or preferably transar-terial partial splenic embolization. This alleviates throm-bocytopenia and anemia and decreases splenic blood flow, thus diminishing splenic vein pressure and possibly diminishing varices as well. Partial splenic embolization has the added advantage of preserving splenic immune function.

Constipation Prescription

Constipation Prescription

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