Ultrasound signs of portal hypertension

Portal hypertension develops as a result of blood flow disturbance in any part of the portal channel. One of the main reasons for the development of portal hypertension is the presence of an obstacle to the current of portal blood in the liver or in the vessels of the portal vein system, respectively, which distinguish: extrahepatic form of portal hypertension (hepatic and perechochenic), intrahepatic form and mixed. In addition, based on the pressure gradient between the hepatic veins and the portal vein, distinguish: the presynusoidal block, the sinusoidal block and the postsinusoidal block.

Extrahepatic portal hypertension is formed when the permeability of the veins of the portal circulatory system is impaired. The most common causes of thrombosis. Sprouting or extravasal compression of the veins are liver tumors, pancreatic diseases. In chronic pancreatitis, the portal vein is affected only in 5.6% of cases, changes in the splenic vein are more frequent. Isolated lesion of the splenic vein causes left-sided portal hypertension. Of great importance in its development are pancreatic cancer (18%), pancreatitis (65%), pseudocysts and pancreatectomy. Among the causes of extrahepatic portal hypertension, trauma, hypercoagulability, long-term oral contraceptives, infections, congenital anomalies are noted. According to studies, in malignant tumors of the liver, impaired permeability of the veins of the portal system due to thrombosis or extravasal compression was noted in 52% of cases. A similar pattern in 6% of cases was due to the presence of hemangiomas and in 21% of cases - liver cysts. In patients with pancreatic tumors, similar changes were recorded in 30% of cases, and those resulting from the progression of chronic pancreatitis - in 35%.

Methodically, ultrasound portal hypertension includes studies: abdominal organs by standard methods; the main veins of the portal vein (VV) system: the superior mesenteric, splenic and portal veins; the main veins of the inferior vena cava system (LIP): hepatic veins, LIP; celiac trunk and its branches; collateral vessels.

With a hemodynamically significant obstruction in the portal vein system and intact hepatic veins in V-mode studies, the size, echogenicity, structure and contours of the liver (provided there are no concomitant diseases) remain within normal limits; in the presence of focal lesions of the liver, we obtain information about the size, form, location and nature of education. Splenomegaly and ascites are often noted. In acute portal vein thrombosis, ascites appears early and may disappear as the collateral circulation develops.

The main ultrasound sign of extrahepatic portal hypertension is the detection of an obstruction to the blood flow in the portal vein system with the definition of its nature, degree of lesion and localization. Occlusive thrombosis is characterized by the presence of echogenic masses and the absence of blood flow in the lumen of the vessel. UZ-signs of parietal thrombosis or partial germination of the lumen of the vessel with a tumor 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 coded flow in the CDC regime at the lesion site;
• registration of turbulent or propulsive nature of blood flow in triplex mode.

US-signs of extravasal hemodynamically significant compression of the vessel are:

• decrease of the lumen of the vessel;
• increase in the intensity of the coded flow in the DCS mode at the narrowing section;
• recording the turbulent or propulsive nature of the blood stream during scanning in triplex mode.

In this situation, it is often enough to detect widened and up to 3-5 mm in diameter inflows of portal and vertex mesenteric veins, which are normal for ultrasound imaging. In most cases, the main vein proximal to the obstruction is enlarged.

The presence of an obstruction to blood flow in the main veins of the portal system promotes the development of collateral vessels. The functioning of port-caval collateral paths is aimed at reducing the pressure in the portal system, port-portal - to restore blood supply to the liver bypass. Detection of collateral vessels in CDS confirms the presence of PG. Ultrasound examination provides information on the presence of collateral vessels with the definition of their localization and anatomical course. For the diagnosis of port-portal collaterals, the region of the gallbladder, the region of the BB trunk and its lobar branches, and the left lobe of the liver are examined. For the identification of porto-caval collaterals, a splenorenal region, a subdiaphragmatic region to the left, a region of the circular ligament of the liver corresponding to the anatomical location of the umbilical vein, as well as the gastroesophageal region, is being studied. When examining a small omentum when additional vessels are detected, it is advisable to use the method of filling the stomach with liquid to decide whether these vessels belong to the stomach wall and / or a small omentum. The diameter of the collateral vessels is 2-4 mm, the LCS is 10-30 cm / s.

Of particular interest is also the question of the effect of a hemodynamically significant obstruction in the portal vein system on the functional state of the venous and arterial blood circulation and the distribution of blood flow in this complex anatomical system. So, SI. Zhestovskaya at the examination of children with vein thrombosis of the portal vein system noted an increase in the average linear velocity of compensatory blood flow in the common hepatic artery, varicose deformity and an increase in the diameter of the splenic vein, increased blood flow through the hepatic veins due to an increase in the negative phase, which is a mechanism for ensuring the perfusion of the liver by retrograde blood flow in violation of the patency of the portal vein. In addition, the author diagnosed a different state of hemodynamics in the distal sections of the portal vein. So, with cavernous transformation, an increase was recorded, and with thrombosis - a decrease in the blood flow velocity in comparison with the parameters of the control group.

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

Varicose veins of the stomach are especially pronounced with extrahepatic portal hypertension. Varicose veins of the esophagus are almost always accompanied by an expansion 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 is formed when:

• schistosomiasis in 5-10% of observations due to the defeat of small branches of the portal vein. According to ultrasound, depending on the spread of the inflammatory process in periportal tissues, 3 degrees of disease are distinguished. At I degree, hyperechoic areas of periportal tissue are localized in the region of the portal vein and cervical bifurcation; at II degree the process extends along the branches of the portal vein; The third degree includes the changes inherent in the I and II degrees of injury. In addition, in all observations, splenomegaly is detected, in 81-92% of cases - an increase in the size of the gallbladder. There may be an increase in the diameter of the portal, splenic veins, the presence of port-system collaterals;
• congenital liver fibrosis, probably due to an insufficient number of terminal branches of the portal vein;
• myeloproliferative diseases, when a definite role belongs to the thrombosis of the large and small branches of the portal vein, partially portal hypertension is associated with the infiltration of portal zones by hematopoietic cells;
• primary biliary cirrhosis of the portal portal hypertension may be the first manifestation of the disease before the development of nodal regeneration, it seems that portal lesions play a role in the development of portal hypertension and the narrowing of sinuses;
• the effects of toxic substances, for example, arsenic, copper;
• hepatic-portal sclerosis, which is characterized by splenomegaly and portal hypertension without occlusion of the portal and splenic veins. In this case, with portal venography, narrowing of the small branches of the portal vein and a decrease in their number are revealed. Contrast study of hepatic veins confirms vessel changes, veinovenous anastomoses are detected.

The presence of signs of diffuse liver damage with cirrhosis, given by ultrasound, is revealed in 57-89,3% of cases. Since false-positive cases are noted with fatty liver disease, and false-negative cases in the initial stage of the disease, it is possible to reliably distinguish liver cirrhosis from other non-cirrhotic chronic diseases only by revealing the signs of portal hypertension characteristic of cirrhosis of the liver.

To date, considerable experience has been accumulated in studying the diagnosis of portal hypertension in patients with cirrhosis of the liver according to color Doppler scan data. Traditionally, the analysis of parameters of diameter, cross-sectional area, values of linear and volume velocities of blood flow with the 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, evaluation of blood flow in the hepatic and splenic arteries . Despite the heterogeneity in the quantitative evaluation of the studied indicators, most authors agree that the parameters of the portal vein system under investigation depend on the presence and level of the collateral outflow pathways and the stage of the disease. The consequences of impaired patency of the arteries of the liver depend not only on their caliber, the state of the influx of portal blood, but also on the possibility of outflows through the hepatic veins. The consequence of the outflow of blood is not only portal hypertension, but also atrophy of the liver parenchyma. In the presence of a small cirrhotic liver, it is impossible to exclude veno-occlusive changes in the hepatic veins.

Despite the fact that there is no direct correlation between these CSD and the risk of developing gastrointestinal bleeding in patients with portal hypertension, some authors note the informative nature of individual ultrasound criteria, the presence of which may indicate an increase or decrease in the risk of bleeding. Thus, with cirrhosis of the liver, the registration of the hepatofugal direction of the blood flow in the portal shows that there is a reduced 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, there is a tendency to increase the size of varicose veins and increase the risk of bleeding. At high values of the index of congestion (congestion, congesion index), there is a high probability of early development of bleeding from varicose veins. The stagnation index is the ratio of the cross-sectional area to the average linear velocity of blood flow in the portal vein. Normally, the value of the index is in the range 0.03-0.07. With cirrhosis of the liver, the index significantly increases to values of 0.171 + 0.075. Correlation of stagnation index with pressure value in portal vein, degree of hepatic insufficiency and severity of collaterals, index of peripheral resistance in hepatic artery was revealed. The high risk of another complication of portal hypertension - hepatic encephalopathy is associated with the presence of a hepatofugal direction of the blood flow in the portal vein, often observed in patients with a reverse direction of blood flow in the splenic vein and the presence of port-system collaterals.

To reduce the risk of developing hepatic encephalopathy, a port-system shunting is performed to reduce pressure in the portal vein and maintain a common hepatic blood flow. According to SI data. Zhestova, in the study of vascular anastomoses, created surgically. It is advisable to adhere to the following methodological points.

1. Visualization of splenolenal anastomosis "end-to-side" is performed from the side of the patient's back along the left mid-line line with sagittal scanning along the length of the left kidney. Anastomosis is defined as a single additional vessel that extends at different angles from the lateral wall of the left renal vein closer to the upper pole of the kidney.
2. Visualization of spleno-renal anastomosis "side-by-side" is distinguished by the presence of two additional vessels that depart symmetrically from the renal vein in one plane. Vessel adjacent to the upper pole of the kidney. Is visualized to the spleen gates; besides, in addition to examining the patient in the position on the back, an examination is made in the patient's position on the right side in the region of the left hypochondrium along the anterior and middle axillary lines, oblique scanning. The ultrasound image of spleno-renal anastomosis must be differentiated from the testicular vein. The anastomosis is located closer to the upper pole of the kidney, represented as an even tubular structure. Easier to visualize from the back of the patient. The testicle is located closer to the lower pole of the kidney, can have a convoluted course, is easier to visualize with oblique scanning from the left hypochondrium.
3. Visualization of the ileo-mesenteric anastomosis is carried out to the right of the midline of the abdomen from the mesogastric region to the wing of the ilium. The inferior vena cava is examined. Further, the sensor is located in the peri-oophoric region with the slope of the ultrasound ray toward the midline of the abdomen. When the sensor moves from the beginning of the LEL, obliquely to the epigastric region, a vascular anastomosis is visualized, corresponding to the junction of the iliac vein and the superior mesenteric vein.

Direct ultrasound signs confirming the patency of the portosystemic shunt are the staining of the lumen of the shunt in the regime of the central canal or EHD and the recording of the indices of venous blood flow. Indirect signs include data on the decrease in the diameter of the portal vein and the expansion of the recipient vein.

To portal hypertension may result in non-cirrhotic diseases, accompanied by the formation of nodes in the liver. Nodal regenerative hyperplasia, partial nodal transformation is referred to as rare benign liver diseases. In the liver, nodules from cells similar to portal hepatocytes are determined, 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. The ultrasound image of the nodules has no specific signs, and the diagnosis is based on identifying signs of portal hypertension, which are noted in 50% of cases.

At the heart of the Budda-Chiari syndrome lies obstruction of the hepatic veins at any level - from the lobule-borne vein to the site of the inferior vena cava into the right atrium. The causes leading to the development of this syndrome are extremely diverse: primary and metastatic liver tumors, kidney and adrenal gland tumors, hypercoagulable diseases, trauma, pregnancy, use of oral contraceptives, connective tissue diseases, vascular membranes, stenosis or thrombosis of the inferior vena cava. In about 70% of patients, the cause of this condition remains unclear. With ultrasound in the B-mode, there may be hypertrophy of the caudate lobe, a change in the structure of the liver, ascites. Depending on the stage of the disease, the echogenicity of the liver changes: from hypoechoic in the period of acute vein thrombosis to hyperechoic in the long-term period of the disease.

With triplex scanning, depending on the degree of damage to the hepatic or inferior vena cava, a lack of blood flow can be detected; continuous (pseudo-portal) low-amplitude blood flow; turbulent; a blood flow of a return direction.

Double staining of the hepatic veins in the CDC regimen is a pathognomonic sign in the Budd Chiari syndrome. In addition, the central can detect intrahepatic venous bypass, register para-umbilical veins. The detection of intrahepatic collateral vessels plays an important role in the differential diagnosis of the Budda-Chiari syndrome and liver cirrhosis.

The results of the studies indicate the presence of Badd-Chiari syndrome in patients with focal liver formations that resulted from germination or extravasal compression of one or more hepatic veins in hepatocellular carcinoma - in 54% of cases, with liver metastases - 27%, with cystic liver formations - in 30%, in individuals with cavernous hemangiomas of the liver - in 26% of cases.

Veno-occlusive disease (VOB) is characterized by the development of endotheliitis obliterating hepatic venules. Hepatic venules are sensitive to toxic effects, which develops due to prolonged use of azathioprine after kidney or liver transplantation, treatment with cytostatic drugs, liver irradiation (the total dose of irradiation reaches or exceeds 35 grams). Clinically, VOB is manifested by jaundice, the presence of pain in the right hypochondrium, an increase in the liver, and the presence of ascites. Diagnosis of this disease is quite complicated, because the hepatic veins remain passable.