Enlarged Lumen Diameter

Portal hypertension is defined as a pressure of more than 10 mmHg in the portal vein. The pressure depends on the resistance of the runoff bed within the liver, the blood volume in the splanchnic vessels, and the pressure in the inferior vena cava. The etiology of its various types and causes is classified according to the location of the flow impediment. Accordingly, portal hypertension may be subdivided into prehepatic, intrahepatic, and posthepatic types, with the intrahepatic type being subdivided into postsinusoidal, sinusoidal, and presinusoidal forms (Table 1.2).

Table 1.2 Formation of possible collaterals in portal hypertension (after Seitz et al24)

Cephalad-draining collaterals

●Right gastric vein

●Short gastric veins

●Periumbilical veins

●Portogastric collaterals

●Portorenal collaterals

●Hepatic, phrenic, and splenic capsule veins

Caudad-draining veins

●Paraumbilical veins

●Gastrosplenic shunts

●Splenorenal shunts

●Splenolumbar shunts

●Hemorrhoidal plexus via the mesenteric veins

The pathophysiology of portal hypertension is characterized by a drop in flow velocity, enlarged vein diameter, sclerosis, opening up of collaterals, and flow reversal in the portal vein or its tributaries. The collaterals are differentiated by the direction of their drainage, i. e., they are subdivided into cephaladand caudaddraining shunts (Table 1.3).

Sonographic studies in portal hypertension will yield presumed and rather firm findings. Images similar to 1.7 should raise the suspicion of portal hypertension:

Table 1.3 Etiology of portal vein thrombosis (after Seitz et al24)

●Idiopathic

●Cirrhosis of the liver

●Malignancies

●Diseases of the pancreas

●Parainfectious

●Posttraumatic

●Collagen disorders

●Thrombophilia

●Myeloproliferative disorders

●Enlarged vena cava and hepatic veins (

1.7a,b)

●Demonstration of ascites ( 1.7c,d)

●Demonstration of liver cirrhosis ( 1.7a–d)

●No respiratory variation in the diameter of the portal vessels ( 1.7e,f)

●Thickening of the gallbladder wall, thickening of the gastric/intestinal wall ( 1.7 g–i)

●Fibrosis of the liver, splenomegaly, flow alterations in portal vein and hepatic artery ( 1.7j–l)

Fibrosis of the liver, splenomegaly, altered flow in the portal vein and hepatic artery

g–i Congested walls in portal hypertension.

g Thickening of the gallbladder wall (arrows) in liver cirrhosis (L) with ascites (A).

j Completely cirrhotic liver (L) with markedly coarse hepatic parenchyma.

h Stomach, with marked thickening of the gastric wall in cirrhosis of the liver and portal hypertension. A = ascites, MA = gastric wall; LE = liver.

k Portal hypertension with pronounced splenomegaly (M).

i Pronounced intestinal wall in portal hypertension.

l Posthepatic cirrhosis of the liver with decreased portal blood flow and increased flow in the hepatic artery (AH). VP = portal vein.

With ~80% of cases, intrahepatic block is by far the most common cause of portal hypertension. The most important factors are hepatic disorders, in particular cirrhosis of the liver.

Cirrhotic vascular changes. The sonographic criteria for transformation of the hepatic parenchyma should be noted since the cirrhotic vascular changes will point the way toward the diagnosis of portal hypertension:

●Enlarged diameter of the portal vein and sudden diameter changes in the branches

of the portal vein (Fig.1.93)

● Pronounced periportal encasement (Fig.1.94)

● Rarified peripheral vascular tree in the liver

Collaterals. Demonstration of any collaterals is of particular interest, the following collateral systems being of primary importance:

●Enlarged left gastric vein with flow reversal ( 1.8a,b)

Splenic hilum varices and collaterals (short gastric vessels)

m Numerous collateral veins running from the splenic hilum to the gastric wall (Magen) in cirrhosis of the liver.

Splenorenal shunts

p Splenorenal collaterals. Inflow from splenic hilum varices into the renal vein. N = kidney, Mi = spleen.22

Shunts: Intrahepatic portocaval shunts or intrasplenic varices, draining cranially

s–u Intrasplenic venous “watershed”. The hilar splenic veins exhibit normal drainage into the hilum, whereas the cortical splenic veins drain toward the surface of the spleen (flow reversal).

s CDS The color-coded (red/blue) vessel with arrows showing the flow direction.

n and o Massive splenic varices in portal hypertension.

n B-mode.

q Suspiciously dilated renal vein (NV). AO = aorta.

t CDS with spectral analysis of the cortical splenic veins draining toward the surface of the spleen (flow reversal).

o CDS.

r Hilar splenic varices (V) draining into the renal vein (NV), resulting in a splenorenal shunt.

u CDS with spectral analysis of the hilar splenic veins with normal drainage into the hilum.

Posthepatic Block

Posthepatic block is quite rare and occurs in around 1% of all patients with portal hypertension. Budd–Chiari syndrome is really a thrombosis with occlusion of the major hepatic veins. The most important etiological factors are systemic hematological disease, disorders

in hemostasis, and hepatic metastasis. In venous occlusive disease the major hepatic veins are patent while the small veins at the microscopic level are thrombosed. The primary etiological factor is graft rejection after allogeneic bone marrow transplant. Chronic constrictive

pericarditis (armored heart) is a rare cause of posthepatic block, and another rare causative entity is primary tumor of the vena cava (Figs. 1.95, 1.96, 1.97).

Fig. 1.95 A 23-year-old patient with acute lymphocytic leukemia (ALL) after allogeneic bone marrow transplantation.

a Clinical diagnosis of hepatic veno-occlusive disease (VOD) with flow reversal in the portal vein (VP).

b Post-therapy demonstration of normal direction of flow in the portal vein.