Noninvasive Cross-Sectional and Vascular Imaging of Portal Hypertension

Chapter 3: Noninvasive Cross-Sectional and Vascular Imaging of Portal Hypertension

Celia P. Corona-Villalobos, Luciana G. Matteoni-Athayde, Neda Rastegar, and Ihab R. Kamel


Patients with chronic liver disease, especially those with cirrhosis, are at a higher risk of developing portal hypertension (PHT).1 PHT is a compromise of the portal venous system as the result of a variety of benign and malignant conditions that cause increase in pressure in the portal venous inflow because of an increase in vascular resistance.2 It is a major complication in cirrhosis caused by sinusoidal fibrosis and vasoconstriction, which increases intrahepatic resistance, leading to collateral veins and portosystemic shunts.

Portal hypertension has been classified based on the site of increased resistance to portal blood flow. Suprahepatic or prehepatic causes are most commonly caused by thrombosis of the portal or the splenic vein (SV); intrahepatic causes are subdivided into presinusoidal, sinusoidal, and postsinusoidal; and extra-hepatic causes (Budd-Chiari syndrome, neoplastic infiltration through the hepatic veins, chronic right ventricular failure, and constrictive pericarditis, among others) overlap often with intrahepatic diseases such as Budd-Chiari syndrome.3

Normal portal pressure is between 5 and 10 mm Hg. Portal pressure above 10 mm Hg will diagnose PHT, and if portal pressure exceeds 12 mm Hg (images Fig. 3.1), the threshold for variceal rupture is elevated.4 Hepatic venous pressure gradient (HVPG) and free portal pressure are available methods for accurate evaluation of portal vein (PV) pressure. However, because of their invasiveness, they are not routinely performed. Therefore, there is a need to develop noninvasive and reliable imaging techniques for accurate diagnosis of PHT.

This chapter discusses the anatomy and imaging features of PHT by noninvasive cross-sectional imaging techniques. It also discusses novel cross-sectional techniques that could potentially be applicable to cases of PHT.

Venous Pathways in Portal Hypertension

There are several pathways of collateral circulation that return portal flow to the systemic venous circulation without passing through the liver. Most of the portosystemic collateral veins are preexistent (images Fig. 3.2) and simply enlarge in PHT. Despite the formation of collateral circulation, portal pressure usually remains elevated. These facts suggest that other mechanisms besides occlusion are involved in PHT.5 Noninvasive imaging techniques are used to accurately assess the main PV, diagnose PHT, and detect portosystemic collateral veins. Increased blood flow through collaterals transmitted from portal venous branches results in dilatation of the venous tributaries (images Table 3.1). The main pathways for collateral circulation include the following (images Fig. 3.3):

1. Esophageal and paraesophageal varices

Esophageal varices are tortuous veins along the distal esophageal wall. These are commonly known as cardiac varices along the submucosa in the lower third of the esophagus (images Fig. 3.4). Paraesophageal varices are collaterals in the posterior mediastinum beyond the esophageal wall. They connect with the left gastric vein, azygos, hemiazygos, and vertebral plexus (images Fig. 3.5). These varices do not communicate with the esophageal submucosa, which differentiates them from periesophageal veins.6 Esophageal and paraesophageal varices are the most common causes of upper gastrointestinal bleeding in PHT.6

2. Gastric varices

Retrogastric varices are supplied by the left gastric vein (coronary vein), and they drain to the esophageal or paraesophageal vein and then to the azygos system. These veins could present reverse flow direction to form submucosal esophageal and periesophageal varices.

Gastric veins are primarily supplied by the short gastric vein that connects the gastric fundus and the left side of the greater curvature of the stomach to the SV.68 In most cases, they drain into the superior vena cava (SVC) via the esophageal varices (images Fig. 3.6) and remain connected to the inferior vena cava (IVC) via the left renal vein (splenorenal shunt).7,9,10

3. Paraumbilical varices and abdominal wall varices

Paraumbilical veins usually are collapsed, forming the falciform ligament. In patients with PHT, they tend to enlarge, arising from the left PV and coursing along the falciform ligament.9,11 Recanalization of the paraumbilical vein is seen in 43% of the patients with PHT.12 The majority of paraumbilical veins drain into the SVC through the inferior epigastric veins9 (images Fig. 3.7).

Table 3.1 Portosystemic Collateral Circulation in Portal Hypertension

Collaterals draining to the superior vena cava

Esophageal varices

Paraesophageal varices

Left gastric vein

Short gastric vein

Posterior gastric vein

Gastric varices

Gastrorenal shunt

Splenorenal shunt

Collaterals draining to the inferior vena cava

Paraumbilical vein

Abdominal wall vein

Retroperitoneal shunt

Mesenteric varices

Omental collateral vessels

Rectal varices

Abdominal varices are commonly described as caput medusa because of their radiating pattern, emerging from the umbilicus and draining into the epigastric veins. Abdominal veins are located in the subcutaneous fat and may extent to the pelvis, connecting to the iliac veins (images Fig. 3.8).

4. Perisplenic varices

Perisplenic varices usually transverse the splenocolic ligament and are seen as dilated veins in the anterior and posterior aspect of the spleen. Varices at the splenic hilum communicate with retrogastric varices or inferior phrenic veins (images Fig. 3.9).

5. Retroperitoneal varices

Retroperitoneal varices may arise from the colic branches, the SV, or the left gastric vein. These veins can form spontaneous shunts that are associated with an increased incidence of encephalopathy (images Fig. 3.10).

6. Rectal varices

The rectal plexus drains through the superior hemorrhoidal vein to the inferior mesenteric vein. Reverse flow from the inferior rectal vein forms the rectal and pararectal varices, which drain into the deep pelvic inferior epigastric veins.

7. Shunts

Spontaneous splenorenal shunt in the portosystemic circulation can develop with or without the presence of collateral circulation. Shunts are seen as large, tortuous veins in the region of the splenic and left renal hilum that drain to the left renal vein9 (images Fig. 3.11). Other shunts include gastrorenal shunts, which develop between retrogastric varices and the left renal vein.11 Formation of a splenorenal or gastrorenal shunt increases the incidence of hepatic encephalopathy.11

Noninvasive Imaging Diagnosis

Ultrasonography (US), computed tomography (CT), and magnetic resonance imaging (MRI) are commonly used to evaluate patients with PHT. The choice of imaging modality is probably not as important as strict attention to the imaging features such as detection of collateral circulation and identification of associated abnormalities such as chronic liver disease or cirrhosis, splenomegaly, ascites, thrombosis, or liver neoplasms.


Ultrasonography is widely used as the first imaging modality to evaluate patients with PHT. It is well known that US is operator and equipment dependent. However, it is a widely available and fast imaging method with low cost and without the added risk of radiation. These advantages should be valued because patients with PHT are imaged not only for diagnosis but also periodically for therapeutic monitoring. US protocols routinely used include gray-scale imaging and color and spectral Doppler (images Table 3.2).

Gray-scale images are of great importance in evaluating the splenoportal anatomy. The main PV is present in the hepatoduodenal ligament and is identified by following the SV to the right until its junction with the superior mesenteric vein (SMV).13 At the crossing point of the PV with the IVC, the PV diameter should be assessed. The PV diameter varies widely according to the site of measurement, fasting state of the patient, and respiratory cycle.14 Normal diameter of the main PV is considered to be up to 12 mm when measured from the inner anterior to the inner posterior wall and acquired with the patient in a supine position, fasting, and breathing quietly.15 The SV and SMV should also be measured in the assessment of PHT (images Fig. 3.12).

The upper limit diameter of normality for these two vessels is considered 9 mm.16 An increase in caliber of any of the three vessels that comprise the portal venous system is associated with PHT. A PV caliber over 13 mm acquired with the protocol previously described is indicative of PHT with a specificity of 100% and a sensitivity of 45% to 50%.17 Patients with known PHT who present with small PV diameters (<8 mm) should be evaluated carefully (images Fig. 3.13). Usually in these cases, periportal collaterals are identified in addition to chronic thromboses of the PV, suggesting cavernous transformation.

Patency of the splenoportal venous system is evaluated by gray-scale and Doppler images (images Fig. 3.14). The presence of echogenic material within these vessels is highly suspicious for thrombosis (images Fig. 3.15). In some cases, however, acute thrombus has low echogenicity or is even anechoic and therefore is difficult to be identified on B-mode imaging. When thrombosis is suspected, Doppler images must be performed. The absence of color and spectral Doppler signal confirms the presence of the suspected thrombus. However, in some situations, flow can be identified, suggesting that the vessel is partially thrombosed. Acute thrombus usually enlarges the caliber of the affected vascular segment, and chronic thrombosis tends to decrease it. Cavernous transformation (images Fig. 3.16) is observed in the later phases of chronic thrombosis of the PV when periportal collaterals are identified at the porta hepatis and the main PV is usually no longer visualized. Another tool that can be used while evaluating the patency of a vein by US exam is the manual compression of the vessel with the US probe. In PV thrombosis, the vessel shows reduced or absent compressibility.18

Table 3.2 List of Features Evaluated by Ultrasonography in Portal Hypertension

Gray-scale imaging

Liver morphology, edge, surface, and parenchymal texture

Spleen size and texture

Splenoportal anatomy

Portal vein diameter

Portal systemic collaterals

Doppler imaging

Portal vein flow and velocity

Portal vein congestion index

Suprahepatic vein flow

Hepatic artery flow and velocity

Hepatic artery resistance index

Portosystemic collaterals

The velocity of blood flow in the PV ranges from 15 to 18 cm/s when acquired with the patient breathing quietly.17 These values can vary greatly if the patient is not fasting or has recently exercised.19 For an accurate measurement of the PV velocity, the angle between the long axis of the vessel and the Doppler beam should be less than 60 degrees (images Fig. 3.17). In the setting of PHT, the PV velocity decreases, and flow direction alters. Normally, the PV flow is toward the liver (hepatopetal) and varies with respiration and heart rate. As PHT increases, flow may become biphasic. Worsening the degree of PH causes reversal of flow, which may even be monophasic and hepatofugal (images Fig. 3.18). When the patient’s condition improves or the collateral circulation is set (images Fig. 3.19), hepatopetal flow can recover because of decompression of the portal circulation.17

Oct 29, 2018 | Posted by in CARDIOLOGY | Comments Off on Noninvasive Cross-Sectional and Vascular Imaging of Portal Hypertension

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