Ultrasound signs of portal hypertension

Portal hypertension develops as a result of blood flow disturbance in any part of the portal bed. One of the main reasons for the development of portal hypertension is the presence of an obstruction to the flow of portal blood in the liver or in the vessels of the portal vein system, accordingly, a distinction is made between: extrahepatic portal hypertension (subhepatic and suprahepatic), intrahepatic and mixed. In addition, based on the pressure gradient between the hepatic veins and the portal vein, a distinction is made between: presinusoidal block, sinusoidal block and postsinusoidal block.

Extrahepatic portal hypertension develops when the patency of the veins of the portal circulatory system is impaired. The most common causes of thrombosis, germination or extravasal compression of the veins are liver tumors and pancreatic diseases. In chronic pancreatitis, the portal vein is affected only in 5.6% of cases; changes in the splenic vein are more common. Isolated damage to the splenic vein causes left-sided portal hypertension. Pancreatic cancer (18%), pancreatitis (65%), pseudocysts and pancreatectomy are of great importance in its development. Among the causes of extrahepatic portal hypertension are injuries, a state of hypercoagulation, long-term use of oral contraceptives, infections, and congenital anomalies. According to research, in malignant liver tumors, obstruction of the veins of the portal system due to thrombosis or extravasal compression was noted in 52% of cases. A similar picture in 6% of cases was caused by the presence of hemangiomas and in 21% of cases - liver cysts. In patients with pancreatic tumors, similar changes were registered in 30% of cases, and those resulting from the progression of chronic pancreatitis - in 35%.

Methodologically, ultrasound examination of portal hypertension includes examination of: abdominal organs using standard methods; main veins of the portal vein (PV) system: superior mesenteric, splenic and portal veins; main veins of the inferior vena cava (IVC) system: hepatic veins, IVC; celiac trunk and its branches; collateral vessels.

In case of hemodynamically significant obstruction in the portal vein system and intact hepatic veins, the size, echogenicity, structure and contours of the liver (provided there are no concomitant diseases) remain within the normal range during B-mode examination; in case of focal liver lesion, we obtain information about the size, shape, localization and nature of the formation. Splenomegaly and ascites are often observed. In acute portal vein thrombosis, ascites appears early and may disappear as collateral circulation develops.

The main ultrasound sign of extrahepatic portal hypertension is the detection of an obstruction to blood flow in the portal vein system with determination of its nature, degree of damage and localization. Occlusive thrombosis is characterized by the presence of echogenic masses and the absence of blood flow in the lumen of the vessel. Ultrasound signs of parietal thrombosis or partial tumor growth into the lumen of the vessel are:

• the presence of parietal echogenic masses partially filling the lumen of the vessel;
• incomplete staining of the lumen and an increase in the intensity of the encoded flow in the color Doppler imaging mode at the site of the lesion;
• registration of turbulent or propulsive nature of blood flow in triplex mode.

Ultrasound signs of extravasal hemodynamically significant vessel compression are:

• narrowing of the vessel lumen;
• increasing the intensity of the encoded flow in the CDC mode at the narrowing section;
• registration of turbulent or propulsive nature of blood flow when scanning in triplex mode.

In such a situation, tributaries of the portal and superior mesenteric veins, dilated to 3-5 mm in diameter, are quite often detected, which are not normally visualized by ultrasound. In most cases, the main vein proximal to the obstruction is dilated.

The presence of an obstruction to blood flow in the main veins of the portal system contributes to the development of collateral vessels. The functioning of the portocaval collateral pathways is aimed at reducing pressure in the portal system, while the portoportal ones are aimed at restoring blood supply to the liver bypassing it. Detection of collateral vessels during CDS confirms the presence of PG. Ultrasound examination provides information on the presence of collateral vessels with determination of their localization and anatomical course. To diagnose portoportal collaterals, the gallbladder region, the region of the PV trunk and its lobar branches, and the left lobe of the liver are examined. To detect portocaval collaterals, the splenorenal region, the left subdiaphragmatic region, the region of the round ligament of the liver corresponding to the anatomical location of the umbilical vein, and the gastroesophageal region are examined. When examining the lesser omentum, if additional vessels are detected, it is advisable to use the technique of filling the stomach with liquid to decide whether these vessels belong to the stomach wall and/or the lesser omentum. The diameter of the collateral vessels is 2-4 mm, the LSC is 10-30 cm/s.

Of particular interest is also the issue of the influence of a hemodynamically significant obstacle in the portal vein system on the functional state of venous and arterial circulation and the distribution of blood flow in this complex anatomical system. Thus, S. I. Zhestovskaya, when examining children with thrombosis of the veins of the portal vein system, noted an increase in the average linear velocity of compensatory blood flow in the common hepatic artery, varicose deformation and an increase in the diameter of the splenic vein, an increase in blood flow in the hepatic veins due to an increase in the negative phase, which is a mechanism for ensuring liver perfusion by retrograde blood flow in case of impaired patency of the portal vein. In addition, the author diagnosed different hemodynamic states in the distal sections of the portal vein. Thus, with cavernous transformation, an increase was recorded, and with thrombosis, a decrease in the blood flow velocity compared to the indicators of the control group.

In the context of this problem, it is worth studying the functional state of portal blood flow in patients who are candidates for hemihepatectomy. The state of portal circulation is directly related to liver function. Thus, in patients after extended hemihepatectomy, pancreatoduodenal resection, a comparative analysis of the blood flow velocity in the portal vein and the peripheral resistance index in the hepatic artery with the level of total bilirubin in the blood showed that with high bilirubin values, a decrease in blood flow in the portal vein and an increase in the IPR over 0.75 in the hepatic artery are recorded. With a normal range of bilirubin values, no significant changes in hemodynamic parameters were noted.

Varicose veins of the stomach are especially pronounced in extrahepatic portal hypertension. Varicose veins of the esophagus are almost always accompanied by dilation of the veins of the stomach. The most common complications of portal hypertension are gastrointestinal bleeding and hepatic encephalopathy, which develops quite often, usually after bleeding, infection, etc.

Intrahepatic portal hypertension develops when:

• schistosomiasis in 5-10% of cases due to damage to small branches of the portal vein. According to ultrasound data, depending on the spread of the inflammatory process in the periportal tissues, 3 degrees of the disease are distinguished. At degree I, hyperechoic areas of the periportal tissue are localized in the bifurcation area of the portal vein and the neck of the gallbladder; at degree II, the process spreads along the branches of the portal vein; degree III includes changes characteristic of degrees I and II of damage. In addition, splenomegaly is detected in all cases, and an increase in the size of the gallbladder is found in 81-92% of cases. An increase in the diameter of the portal and splenic veins, and the presence of portosystemic collaterals may be noted;
• congenital liver fibrosis, probably due to an insufficient number of terminal branches of the portal vein;
• myeloproliferative diseases, when a certain role is played by thrombosis of large and small branches of the portal vein, portal hypertension is partially associated with infiltration of portal zones by hematopoietic cells;
• In primary biliary cirrhosis of the liver, portal hypertension may be the first manifestation of the disease before the development of nodular regeneration; apparently, damage to the portal zones and narrowing of the sinuses play a role in the development of portal hypertension;
• the action of toxic substances, such as arsenic, copper;
• hepatic portal sclerosis, which is characterized by splenomegaly and portal hypertension without occlusion of the portal and splenic veins. In this case, portal venography reveals a narrowing of the small branches of the portal vein and a decrease in their number. Contrast examination of the hepatic veins confirms vascular changes, and venovenous anastomoses are detected.

The presence of signs of diffuse liver damage in cirrhosis, as determined by ultrasound, is detected in 57-89.3% of cases. Since false-positive cases are noted in fatty liver dystrophy, and false-negative cases are noted in the initial stage of the disease, it is possible to reliably distinguish liver cirrhosis from other non-cirrhotic chronic diseases only by identifying signs of portal hypertension, characteristic of liver cirrhosis.

To date, considerable experience has been accumulated in studying the issues of diagnosing portal hypertension in patients with liver cirrhosis using color Doppler scanning data. Traditionally, portal hypertension is diagnosed by analyzing the diameter, cross-sectional area, linear and volumetric blood flow rates with subsequent calculation of indices, as well as recording the direction of blood flow in the portal vein, less often in the splenic and superior mesenteric veins, and assessing blood flow in the hepatic and splenic arteries. Despite the heterogeneity in the quantitative assessment of the studied parameters, most authors are unanimous in the opinion that the studied parameters of the portal vein system depend on the presence and level of collateral outflow tracts and the stage of the disease. The consequences of impaired patency of the liver arteries depend not only on their caliber, the state of portal blood inflow, but also on the possibility of outflow through the hepatic veins. The consequence of the blood outflow disorder is not only portal hypertension, but also atrophy of the liver parenchyma. In the presence of a small cirrhotic liver, veno-occlusive changes in the hepatic veins cannot be excluded.

Despite the fact that there is no direct correlation between the CDS data and the risk of gastrointestinal bleeding in patients with portal hypertension, some authors note the informativeness of individual ultrasound criteria, the presence of which may indicate an increase or decrease in the risk of bleeding. Thus, in liver cirrhosis, registration of the hepatofugal direction of blood flow in the portal vein indicates a decrease in the risk of bleeding, the hepatopetal direction in the coronary vein is associated with a low risk of this complication. With varicose veins and the presence of blood flow in the splenic vein, the value of which exceeds the blood flow in the portal vein, a tendency to an increase in the size of varicose veins and an increase in the risk of bleeding is noted. With high values of the congestion index (hyperemia, congesion index), the probability of early bleeding from varicose veins is high. The congestion index is the ratio of the cross-sectional area to the average linear velocity of blood flow in the portal vein. Normally, the index value is in the range of 0.03-0.07. In liver cirrhosis, the index reliably increases to values of 0.171 + 0.075. A correlation was found between the congestion index and the pressure value in the portal vein, the degree of liver failure and the severity of collaterals, and the index of peripheral resistance in the hepatic artery. A high risk of another complication of portal hypertension - hepatic encephalopathy is associated with the presence of hepatofugal blood flow in the portal vein, often observed in patients with reverse blood flow in the splenic vein and the presence of portosystemic collaterals.

To reduce the risk of developing hepatic encephalopathy, portosystemic shunting is performed to reduce pressure in the portal vein and maintain overall hepatic blood flow. According to S. I. Zhestovskaya, when examining vascular anastomoses created surgically, it is advisable to adhere to the following methodological points.

1. Visualization of the end-to-side splenorenal anastomosis is performed from the patient's back along the left mid-scapular line with sagittal scanning along the length of the left kidney. The anastomosis is defined as a single additional vessel extending at different angles from the lateral wall of the left renal vein closer to the upper pole of the kidney.
2. The side-to-side visualization of the spleno-renal anastomosis is distinguished by the presence of two additional vessels extending symmetrically from the renal vein in one plane. The vessel adjacent closer to the upper pole of the kidney is visualized up to the splenic hilum, while, in addition to examining the patient in the supine position, an examination is performed with the patient in the right lateral position in the left hypochondrium along the anterior and middle axillary lines, using oblique scanning. The ultrasound image of the spleno-renal anastomosis must be differentiated from the testicular vein. The anastomosis is located closer to the upper pole of the kidney, is presented as a smooth tubular structure, and is easier to visualize from the patient's back. The testicular vein is located closer to the lower pole of the kidney, may have a tortuous course, and is easier to visualize with oblique scanning from the left hypochondrium.
3. Visualization of the ileomesenteric anastomosis is performed to the right of the abdominal midline from the mesogastric region to the iliac wing. The inferior vena cava is examined. Next, the sensor is placed in the periumbilical region with the ultrasound beam inclined to the abdominal midline. When advancing the sensor from the beginning of the IVC, obliquely to the epigastric region, the vascular anastomosis corresponding to the junction of the iliac vein and the superior mesenteric vein is visualized.

Direct ultrasound signs confirming the patency of the portosystemic shunt are the coloring of the shunt lumen in the color Doppler or EDC mode and the recording of venous blood flow parameters. Indirect signs include data on the decrease in the diameter of the portal vein and the expansion of the recipient vein.

Non-cirrhotic diseases accompanied by the formation of nodules in the liver can lead to portal hypertension. Nodular regenerative hyperplasia, partial nodular transformation are rare benign liver diseases. Nodules of cells similar to portal hepatocytes are determined in the liver, which are formed as a result of obliteration of small branches of the portal vein at the level of the acini. The development of these changes is associated with the presence of systemic diseases, myeloproliferative disorders. Ultrasound imaging of nodules has no specific signs, and the diagnosis is based on the detection of signs of portal hypertension, which are noted in 50% of cases.

The basis of Budd-Chiari syndrome is obstruction of the hepatic veins at any level - from the efferent lobular vein to the place where the inferior vena cava enters the right atrium. The causes leading to the development of this syndrome are extremely diverse: primary and metastatic liver tumors, kidney and adrenal tumors, diseases accompanied by hypercoagulation, trauma, pregnancy, use of oral contraceptives, connective tissue diseases, vascular membranes, stenosis or thrombosis of the inferior vena cava. In approximately 70% of patients, the cause of this condition remains unclear. B-mode ultrasound may reveal hypertrophy of the caudate lobe, changes in liver structure, ascites. Depending on the stage of the disease, the echogenicity of the liver changes: from hypoechoic during acute venous thrombosis to hyperechoic in the late period of the disease.

Triplex scanning, depending on the degree of damage to the hepatic or inferior vena cava, may reveal: absence of blood flow; continuous (pseudoportal) low-amplitude blood flow; turbulent; reverse blood flow.

Double staining of the hepatic veins in the color Doppler imaging mode is a pathognomonic sign of Budd-Chiari syndrome. In addition, color Doppler imaging allows detecting intrahepatic venous shunting and registering para-umbilical veins. Detection of intrahepatic collateral vessels plays an important role in the differential diagnosis of Budd-Chiari syndrome and liver cirrhosis.

The results of the studies indicate the presence of Budd-Chiari syndrome in patients with focal liver lesions that arose as a result of invasion or extravasal compression of one or more hepatic veins in hepatocellular cancer - in 54% of cases, with metastases to the liver - in 27%, with cystic liver lesions - in 30%, in individuals with cavernous hemangiomas of the liver - in 26% of observations.

Veno-occlusive disease (VOD) is characterized by the development of obliterating endophlebitis of the hepatic venules. Hepatic venules are sensitive to toxic effects that develop as a result of long-term use of azathioprine after kidney or liver transplantation, treatment with cytostatic drugs, and liver irradiation (the total radiation dose reaches or exceeds 35 g). Clinically, VOD is manifested by jaundice, pain in the right hypochondrium, liver enlargement, and ascites. Diagnosis of this disease is quite difficult, since the hepatic veins remain patent.