Portal Hypertension

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Portal hypertension is frequently a systemic complication of liver cirrhosis, however different pathologies such as obstruction at the post-sinusoidal (e.g. hepatic vein), sinusoidal (e.g. cirrhosis) or pre-sinusoidal (e.g. portal vein) level may also cause portal hypertension [27].

The most common cause of portal hypertension is liver cirrhosis. Associated complications include variceal bleeding, ascites and splenomegaly. A primary consequence of the increased pressure in the portal tract is dilatation of vessels. Later, as a result of the development of porto-systemic shunting, the blood flow to the liver diminishes and the size of the portal vessels is again reduced. Increased porto-systemic shunting results in less effective metabolism of absorbed nutrients and accumulation of toxic metabolites such as ammonia in the blood. This may lead to the clinical manifestations of hepatic encephalopathy. As decreased portal flow correlates with the presence of liver atrophy, porto-systemic shunting or portal hypertension contributes to the further regression of liver parenchyma in patients suffering from cirrhosis [35].

An important consequence of portal hypertension is the development of esophageal varices, the rupture of which, either spontaneously or as a result of vomiting, may lead to life-threatening hemorrhage. Esophageal varices are the result of porto-systemic shunting through the lienal vein to the left gastric (coronary) veins, which secondarily drain to thoracic veins such as the vena azygos or hemiazygos [79].

Concomitant varices in the spleno-renal venous system and the paraumbilical venous net, as well as the presence of anorectal shunts, may reduce the risk of rupture of the esophageal varices, but at the increased risk of hepatic encephalopathy [43].

Therapy of esophageal varices consists of scle-rotherapy or surgical intervention to create alternative porto-systemic shunts. Esophageal varices are usually well depicted on T1-weighted or flow sensitive gradient echo images; these are localized

Siderotic Nodules Liver Mri

Fig. 8. Gamna-Gandy bodies of the spleen in a patient with portal hypertension due to liver cirrhosis. The T1-weighted image shows diffuse low signal intensity lesions in the spleen, representing siderotic nodules arising due to portal hypertension. Additionally, typical signs of liver cirrhosis including ascites, hypertrophy of the left liver lobe and liver segment I, and concomitant hypotrophy of the right liver lobe can be seen

Fig. 8. Gamna-Gandy bodies of the spleen in a patient with portal hypertension due to liver cirrhosis. The T1-weighted image shows diffuse low signal intensity lesions in the spleen, representing siderotic nodules arising due to portal hypertension. Additionally, typical signs of liver cirrhosis including ascites, hypertrophy of the left liver lobe and liver segment I, and concomitant hypotrophy of the right liver lobe can be seen anterior to the aorta at the level of the diaphragmatic hiatus [7].

Flow sensitive MRI can give results comparable to those of digital subtraction angiography and endoscopy. As the neighboring aorta and heart may induce pulsatile artifacts, low flip angles or electrocardiogram (ECG) gating should be used for gradient echo sequences. However, if esophageal varices are not seen, then dilated left gastric veins in the gastro-hepatic ligament may indicate the diagnosis.

Whereas spleno-renal shunts, retroperitoneal shunts and puborectal shunts are difficult to demonstrate on ultrasonography, they are well visualized using MR angiography techniques. Moreover, reversed flow in the central portion of the splenic vein can be considered diagnostic [50].

Paraumbilical shunting may be best diagnosed by following the left portal vein to the superficial veins at the umbilicus through the ligamentum teres hepatis. Dilated veins adjacent to the abdominal wall have a characteristic spider-web appearance, called caput medusae.

In patients with large gastroepiploical veins along the greater curvature of the stomach, esophageal varices induced by a single splenic vein occlusion (e.g. caused by pancreatitis), should be taken into account as a differential diagnosis.

Enlargement of the gastroepiploic veins can be considered a specific sign of splenic vein occlusion since they are not present in patients with portal hypertension in whom splenic veins are patent. In contrast, occlusion of the splenic vein can be excluded as a primary cause of portal hypertension in patients with paraumbilical varices. However, gastroesophageal and retroperitoneal collaterals may be seen in both conditions [36].

Portal vein velocity and flow volume may be ascertained on MRI using two-dimensional phase contrast techniques. With this imaging modality, increased portal flow is frequently seen in patients with cirrhosis in cases of recompensation. On the other hand, decreased or even reversed flow within the portal tract has been demonstrated in patients suffering from severe cirrhosis [63].

A thickened gallbladder wall is frequently found in patients with cirrhosis, independent of the primary diseases of the gallbladder.

Further clinical manifestations of portal hypertension are ascites and splenomegaly. So-called Gamna-Gandy bodies, representing siderotic nodules within the spleen, can arise in patients with portal hypertension and may be detected on T2-weighted or contrast-enhanced Tl-weighted MRI [54] (Fig. 8).

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