Portal vein anatomy. Portal vein: functions, structure of the portal circulatory system, diseases and diagnosis The portal vein is formed from the fusion


The portal vein (liver) (v. portae hepatis) occupies a special place among the veins that collect blood from the internal organs. This is not only the largest visceral vein (its length is 5-6 cm, diameter 11-18 mm), but also the afferent venous link of the so-called portal system of the liver. The portal vein of the liver is located in the thickness of the hepatoduodenal ligament behind the hepatic artery and common bile duct along with nerves, lymph nodes and vessels. It is formed from the veins of unpaired abdominal organs: stomach, small and large intestines, spleen, pancreas. From these organs, venous blood flows through the portal vein to the liver, and from it through the hepatic veins into the inferior vena cava. The main tributaries of the portal vein are the superior mesenteric and splenic veins, as well as the inferior mesenteric vein, which merge with each other behind the head of the pancreas. Having entered the portal of the liver, the portal vein divides into a larger one right branch(r. dexter) and left branch(r. sinister). Each of the branches of the portal vein, in turn, breaks up first into segmental branches, and then into branches of ever smaller diameter, which pass into the interlobular veins. Inside the lobules, these veins give off wide capillaries - the so-called sinusoidal vessels, flowing into the central vein. The sublobular veins emerging from each lobule merge to form three to four hepatic veins. Thus, the blood flowing into the inferior vena cava through the hepatic veins passes through two capillary networks on its way. One capillary network is located in the walls of the digestive tract, where the tributaries of the portal vein originate. Another capillary network is formed in the liver parenchyma from the capillaries of its lobules.

Before entering the portal of the liver (in the thickness of the hepatoduodenal ligament), the gall bladder vein (v. cystica) from the gallbladder, the right and left gastric veins (vv. gastricae dextra et sinistra) and the prepyloric vein (v. prepylorica) flow into the portal vein, delivering blood from the corresponding parts of the stomach. The left gastric vein anastomoses with the esophageal veins - tributaries of the azygos vein from the superior vena cava system. In the thickness of the round ligament of the liver, the paraumbilical veins (vv. paraumbilicales) follow to the liver. They begin in the anterior abdominal wall, in the umbilical region, where they anastomose with the superior epigastric veins - tributaries of the internal thoracic veins (from the superior vena cava system) and with the superficial and inferior epigastric veins - tributaries of the femoral and external iliac veins from the inferior vena cava system.

Portal vein tributaries

  1. The superior mesenteric vein (v. mesentenca superior) runs at the root of the mesentery of the small intestine to the right of the artery of the same name. Its tributaries are veins of the jejunum and ileum(vv. jejunales et ileales), pancreatic veins (w. pancreaticael, pancreaticoduodenal veins(vv. panсreaticoduodenales), ileocolic vein(v. ileocolica), right gastroepiploic vein(v. gastroomenialis dextra), right and middle colic veins(vv. colicae media et dextra), appendix vein(v. appendicuiaris). To the superior mesenteric vein, the veins listed above bring blood from the walls of the jejunum and ileum and the appendix, the ascending colon and transverse colon, from the stomach, duodenum and pancreas, and the greater omentum.
  2. The splenic vein (v. splenica) is located along the upper edge of the pancreas below the splenic artery. This vein runs from left to right, crossing the aorta in front. Posterior to the head of the pancreas, it merges with the superior mesenteric vein. The tributaries of the splenic vein are pancreatic veins(vv. pancieaticae), short gastric veins(vv. gastricae breves) and left gastroepiploic vein(v. gastroomentalis sinistra). The latter anastomoses along the greater curvature of the stomach with the right vein of the same name. The splenic vein collects blood from the spleen, part of the stomach, pancreas and greater omentum.
  3. The inferior mesenteric vein (v. mesenterica inferior) is formed as a result of the fusion superior rectal vein(v. rectalis superior), left colic vein(v. colica sinistra) and sigmoid veins(vv. sigmoideae). Located next to the left colic artery, the inferior mesenteric vein heads upward, passes behind the pancreas and flows into the splenic vein (sometimes into the superior mesenteric vein). The inferior mesenteric vein collects blood from the walls of the upper rectum, sigmoid colon, and descending colon.

In men blood flow through the portal vein is about 1000-1200 ml/min.

Oxygen content in portal blood

After eating, the absorption of oxygen by the intestines increases and the difference between arterial and portal blood in oxygen content increases.

Blood flow in the portal vein

The distribution of portal blood flow in the liver is not constant: blood flow to the left or right lobe of the liver may predominate. In humans, it is possible for blood to flow from the system of one lobar branch to the system of another. Portal blood flow appears to be laminar rather than turbulent.

Portal vein pressure in humans the normal level is about 7 mm Hg.

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Collateral circulation

When outflow through the portal vein is impaired, regardless of whether it is caused by intra- or extrahepatic obstruction, portal blood flows into the central veins through venous collaterals, which significantly expand.

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Intrahepatic obstruction (cirrhosis)

Normally, all portal blood can flow through the hepatic veins; with cirrhosis of the liver, only 13% leaks. The rest of the blood passes through collaterals, which can be combined into 4 main groups.

  • Igroup: collaterals passing in the area of ​​​​transition of the protective epithelium into the absorbent one
    • A. In the cardiac part of the stomach there are anastomoses between the left, posterior and short veins of the stomach, which belong to the portal vein system, and the intercostal, diaphragmatic-esophageal and hemizygos veins, which belong to the inferior vena cava system. Redistribution of flowing blood into these veins leads to varicose veins of the submucosal layer of the lower esophagus and the fundus of the stomach.
    • B. In the anal area, there are anastomoses between the superior hemorrhoidal vein, which belongs to the portal vein system, and the middle and inferior hemorrhoidal veins, which belong to the inferior vena cava system. Redistribution of venous blood into these veins leads to varicose veins of the rectum.
  • Group II: veins running in the falciform ligament and associated with the peri-umbilical veins, which are a rudiment of the umbilical circulatory system of the fetus.
  • III group: collaterals passing in the ligaments or folds of the peritoneum, formed during its transition from the abdominal organs to the abdominal wall or retroperitoneal tissue. These collaterals run from the liver to the diaphragm, in the splenorenal ligament and in the omentum. These also include lumbar veins, veins that developed in scars that formed after previous operations, as well as collaterals that form around entero- or colostomy.
  • IV group: veins that redistribute portal venous blood into the left renal vein. Blood flow through these collaterals is carried out both directly from the splenic vein to the renal vein, and through the phrenic, pancreatic, gastric veins or the vein of the left adrenal gland.

As a result, blood from the gastroesophageal and other collaterals through the azygos or semi-gypsy vein enters the superior vena cava. A small amount of blood enters the inferior vena cava; blood may flow into it from the right lobar branch of the portal vein after the formation of an intrahepatic shunt. The development of collaterals to the pulmonary veins has been described.

Extrahepatic obstruction

With extrahepatic portal vein obstruction, additional collaterals are formed, along which blood bypasses the obstruction site in order to enter the liver. They drain into the portal vein at the porta hepatis distal to the site of obstruction. These collaterals include the portal veins of the liver; veins accompanying the portal vein and hepatic arteries; veins running in the ligaments supporting the liver; phrenic and omental veins. Collaterals associated with the lumbar veins can reach very large sizes.

The hepatic portal vein (PV, portal vein) is a large trunk that receives blood from the spleen, intestines and stomach. It then moves to the liver. The organ ensures the purification of the blood, and it again enters the general channel.

The anatomical structure of the portal vein is complex. The trunk has many branches into venules and other blood vessels of different diameters. The portal system is another circle of blood flow, the purpose of which is to cleanse the blood plasma of decay products and toxic components.

A number of diseases affect changes in blood flow through the portal vein system

The changed dimensions of the portal vein make it possible to diagnose certain pathologies. Its normal length is 6–8 cm, and its diameter is no more than 1.5 cm.

Possible pathologies

The most common pathologies of the portal vein are:

  • thrombosis;
  • portal hypertension;
  • cavernous transformation;
  • pylephlebitis.

IV thrombosis

Thrombosis of the portal vein is a severe pathology in which blood clots form in its lumen, preventing its outflow after cleansing. In the absence of treatment, an increase in vascular pressure is diagnosed. As a result, portal hypertension develops.

The main reasons for the formation of pathology are generally considered to be:

  • cirrhosis of the liver;
  • malignant neoplasms of the gastrointestinal tract;
  • inflammation of the umbilical vein during the placement of catheters in infants;
  • inflammation of the digestive system;
  • injuries and surgery of the spleen, liver, gall bladder;
  • blood clotting disorder;
  • infections.

Rare causes of thrombosis include: gestation period, prolonged use of oral contraceptives. Symptoms of the disease include: severe pain, attacks of nausea ending with vomiting, dyspeptic disorders, increased body temperature, hemorrhoidal bleeding (sometimes).

For a progressive chronic form of thrombosis - provided that the patency of the portal vein is partially preserved - the following symptoms are typical: fluid accumulation in the abdominal cavity, an increase in the size of the spleen, pain/heaviness in the left hypochondrium, dilation of the esophageal veins, which increases the risk of bleeding.


Echogram is one of the research methods used

The main way to diagnose thrombosis is an ultrasound examination. On the monitor, a thrombus is defined as a hyperechoic (dense) formation that fills both the venous lumen and branches. Small blood clots are detected during endoscopic ultrasound. CT and MRI techniques allow us to identify the exact causes of pathology and identify concomitant pathologies.

Important! Doppler measurements show a complete absence of blood flow in the area of ​​thrombus formation.

Cavernous transformation

The pathology develops against the background of congenital malformations of veins - narrowing, complete/partial absence. In this case, a cavernoma is detected in the area of ​​the portal vein trunk. It consists of many small vessels, to a certain extent compensating for poor circulation of the portal system.

Cavernous transformation, detected in childhood, is a sign of a congenital disorder of the structure of the vascular system of the liver. In adults, cavernous formation indicates the development of portal hypertension provoked by hepatitis or cirrhosis.

Portal hypertension syndrome

Portal hypertension is a pathological condition characterized by increased pressure in the portal system. Causes the formation of blood clots. The physiological norm of pressure in the portal vein is no higher than 10 mm Hg. Art. An increase in this indicator by 2 or more units becomes a reason for diagnosing portal hypertension.

Factors provoking pathology are:

  • cirrhosis of the liver;
  • hepatic vein thrombosis;
  • hepatitis of various origins;
  • severe heart pathologies;
  • metabolic disorders;
  • thrombi of the splenic veins and portal vein.

The clinical picture of portal hypertension is as follows: dyspeptic symptoms; heaviness in the left hypochondrium, jaundice, weight loss, general weakness.

A characteristic sign of the syndrome is an increase in the volume of the spleen. The cause is venous stagnation. Blood cannot leave the organ due to blockage of the spleen veins. In addition to splenomegaly, there is an accumulation of fluid in the abdominal cavity, as well as varicose veins in the lower part of the esophagus.


Ultrasound diagnostics allows to differentiate pathology

An ultrasound examination reveals an enlarged liver and spleen and fluid accumulation. The size of the portal vein and blood flow are assessed using Doppler ultrasound. Portal hypertension is characterized by an increase in its diameter, as well as expansion of the superior mesenteric and splenic veins.

Pylephlebitis

Among inflammatory processes, the leading place is occupied by purulent inflammation of the portal vein - pylephlebitis. The provoking factor is most often acute appendicitis. In the absence of treatment, necrotization of liver tissue occurs, resulting in the death of a person.

The disease has no characteristic symptoms. The clinical picture looks like this:

  • high fever; chills;
  • signs of poisoning appear;
  • severe abdominal pain;
  • internal hemorrhage in the veins of the esophagus and/or stomach;
  • jaundice caused by damage to the liver parenchyma.

Laboratory studies show an increase in the concentration of leukocytes, an increase in the erythrocyte sedimentation rate. Such a shift in indicators indicates acute purulent inflammation. The diagnosis can only be confirmed using ultrasound, MRI and CT.

Symptoms of portal vein pathologies and possible complications

The disease occurs in acute and chronic forms, which is reflected in the current symptoms. The following symptoms are typical for the acute form: the development of severe abdominal pain, an increase in body temperature to significant levels, fever, an increase in the volume of the spleen, the development of nausea, vomiting, diarrhea.

Symptoms develop simultaneously, which leads to a strong deterioration in the general condition. The chronic course of the disease is dangerous due to the complete absence of any symptoms. The disease is diagnosed completely accidentally during a routine ultrasound examination.


In the absence of adequate therapy, the development of intestinal ischemia is possible, which is expressed in the death of its tissues as a result of blockage of mesenteric vessels

The absence of pathological symptoms causes the launch of compensatory mechanisms. To protect itself from pain, nausea and other manifestations, the body starts the process of vasodilation - an increase in the diameter of the hepatic artery and the formation of a cavernoma.

As the patient’s condition worsens, certain symptoms nevertheless develop: weakness, appetite disturbances. Portal hypertension poses a particular danger to humans. It is characterized by the development of ascites, enlargement of the saphenous veins located on the anterior abdominal wall, as well as varicose veins of the esophagus.

The chronic stage of thrombosis is characterized by inflammation of the portal vein. Signs of the condition may include:

  • dull, incessant pain in the abdomen;
  • long-lasting low-grade fever;
  • enlarged liver and spleen.

Important! Varicose veins of the esophagus can cause internal bleeding.

Diagnostic measures

The main diagnostic technique for detecting changes in the portal vein remains ultrasound. The study can be prescribed to pregnant women, children and elderly patients. Doppler ultrasound, used in conjunction with ultrasound, helps assess the speed and direction of blood flow. Normally, it should be directed towards the organ.

With the development of thrombosis, a hyperechoic (dense) heterogeneous formation is detected in the lumen of the vessel. It can fill the entire lumen of the vessel, or cover it only partially. In the first case, blood movement stops completely.


One of the most common liver vascular pathologies

With the development of portal hypertension syndrome, dilation of the vascular lumen is detected. In addition, the doctor detects an enlarged liver and fluid accumulation. Doppler ultrasound will show a decrease in blood flow velocity.

Cavernoma becomes a possible sign of portal hypertension. The patient is required to undergo an FGDS to assess the condition of the esophageal anastomoses. Additionally, esophagoscopy and radiology of the esophagus and stomach may be recommended.

In addition to ultrasound examination, computed tomography with a contrast agent can be used. The advantage of using CT is the visualization of the liver parenchyma, lymph nodes and other formations located in close proximity.

Angiography is the most accurate method for diagnosing portal vein thrombosis. Instrumental studies are complemented by blood testing. Of clinical interest are indicators of leukocytes, liver enzymes, and bilirubin.

Treatment of pathology

Treatment of the disease involves an integrated approach and includes taking medications and surgery. Drug therapy includes the following medications:

  • drugs from the group of anticoagulants - prevents the formation of blood clots and improves vascular patency;
  • thrombolytics - dissolve existing blood clots, freeing the lumen of the portal vein.


Medicines are prescribed by the attending physician based on current symptoms

If there is no therapeutic result from the selected drug therapy, the person is prescribed surgical treatment. Transhepatic angioplasty or thrombolysis may be performed.

The main complication of surgical treatment is bleeding of the esophageal veins and the development of intestinal ischemia. Any pathology of the portal vein of the liver is a serious condition that requires the appointment of therapy adequate to the condition.

collects blood from all unpaired organs of the abdominal cavity, with the exception of the liver: from the entire gastrointestinal tract, where absorption of nutrients occurs, which enter the portal vein into the liver for neutralization and deposition of glycogen; from the pancreas, where insulin comes from, regulating sugar metabolism; from the spleen, where the breakdown products of blood elements come from, used in the liver to produce bile. The constructive connection of the portal vein with the gastrointestinal tract and its large glands (liver and pancreas) is determined, in addition to the functional connection, by the commonality of their development (genetic connection).

V. portae, the portal vein, is a thick venous trunk located in the lig. hepatoduodenale together with the hepatic artery and ductus choledochus. Added up v. portae behind the head of the pancreas from the splenic vein and two mesenteric veins - superior and inferior. Heading to the gate of the liver in the mentioned ligament of peritoneum, it receives vv along the way. gastricae sinistra et dextra and v. prepylorica and at the porta hepatis divides into two branches that extend into the liver parenchyma. In the liver parenchyma, these branches break up into many small branches that entwine the liver lobules (vv. inter lobulares); Numerous capillaries penetrate into the lobules and ultimately form vv. centrales, which collect in the hepatic veins, flowing into the inferior vena cava.

Thus, the portal vein system, unlike other veins, is inserted between two networks of capillaries: the first network of capillaries gives rise to the venous trunks that make up the portal vein, and the second is located in the substance of the liver, where the division of the portal vein into its final branches occurs. V. lienalis, the splenic vein, carries blood from the spleen, stomach (through v. gastroepiploica sinistra and vv. gastricae breves) and from the pancreas, along the upper edge of which behind and below the artery of the same name it goes to v. lienalis. portae.

Vv. mesentericae superior et inferior, the superior and inferior mesenteric veins, correspond to the arteries of the same name. V. mesenterica superior on its way receives venous branches from the small intestine (vv. intestinales), cecum, ascending colon and transverse colon (v. colica dextra and v. colica media), and, passing behind the head of the pancreas, connects to the inferior mesenteric vein. V. mesenterica inferior begins from the venous plexus of the rectum, plexus venosus rectalis. Heading upward from here, along the way it receives inflows from the sigmoid colon (vv. sigmoideae), from the descending colon (v. colica sinistra) and from the left half of the transverse colon. Behind the head of the pancreas, it, having previously connected with the splenic vein or independently, merges with the superior mesenteric vein.

The portal vein (PV, portal vein) is one of the largest vascular trunks in the human body. Without it, normal functioning of the digestive system and adequate blood detoxification are impossible. The pathology of this vessel does not go unnoticed, causing serious consequences.

The hepatic portal vein system collects blood coming from the abdominal organs. The vessel is formed by connecting the superior and inferior mesenteric and splenic veins. In some people, the inferior mesenteric vein drains into the splenic vein, and then the junction of the superior mesenteric and splenic veins forms the trunk of the PV.

Anatomical features of blood circulation in the portal vein system

The anatomy of the portal vein system (portal system) is complex. This is a kind of additional circle of venous circulation, necessary to cleanse the plasma of toxins and unnecessary metabolites, without which they would immediately fall into the inferior hollow, then into the heart and further into the pulmonary circle and the arterial part of the large one.

The latter phenomenon is observed when the liver parenchyma is damaged, for example, in patients with cirrhosis. It is the absence of an additional “filter” on the way of venous blood from the digestive system that creates the preconditions for severe intoxication with metabolic products.

Having studied the basics of anatomy at school, many remember that most organs of our body include an artery that carries blood rich in oxygen and nutritional components, and a vein emerges that carries “waste” blood to the right half of the heart and lungs.

The portal vein system is structured somewhat differently; its peculiarity can be considered the fact that in addition to the artery, the liver enters a venous vessel, the blood from which again enters the hepatic veins, passing through the parenchyma of the organ. It is as if additional blood flow is created, the work of which determines the condition of the entire organism.

The formation of the portal system occurs due to large venous trunks merging with each other near the liver. The mesenteric veins transport blood from the intestinal loops, the splenic vein leaves the spleen and receives blood from the veins of the stomach and pancreas. Behind the head of the pancreas, the venous “highways” connect, giving rise to the portal system.

Between the layers of the pancreaticoduodenal ligament, the gastric, periumbilical and prepyloric veins flow into the PV. In this area, the PV is located behind the hepatic artery and the common bile duct, together with which it follows to the porta hepatis.

At the gates of the liver, or not reaching them one to one and a half centimeters, division occurs into the right and left branches of the portal vein, which enter both hepatic lobes and there break up into smaller venous vessels. Reaching the hepatic lobule, venules entwine it from the outside, enter inside, and after the blood is neutralized upon contact with hepatocytes, it enters the central veins emerging from the center of each lobule. The central veins gather into larger ones and form hepatic veins, which carry blood from the liver and flow into.

A change in the size of the vein is of great diagnostic importance and can indicate various pathologies - cirrhosis, venous thrombosis, pathology of the spleen and pancreas, etc. The length of the portal vein of the liver is normally approximately 6-8 cm, and the diameter of the lumen is up to one and a half centimeters.

The portal vein system does not exist in isolation from other vascular systems. Nature provides the possibility of dumping “excess” blood into other veins if a hemodynamic disturbance occurs in this section. It is clear that the possibilities of such a discharge are limited and cannot last indefinitely, but they make it possible to at least partially compensate for the patient’s condition in case of severe diseases of the liver parenchyma or thrombosis of the vein itself, although sometimes they themselves become the cause of dangerous conditions (bleeding).

The connection between the portal vein and other venous collectors of the body is carried out thanks to anastomoses, the localization of which is well known to surgeons, who quite often encounter acute bleeding from anastomotic areas.

Anastomoses of the portal and vena cava are not pronounced in a healthy body, since they do not bear any load. In pathology, when the flow of blood into the liver becomes difficult, the portal vein expands, the pressure in it increases, and the blood is forced to look for other outflow routes, which become anastomoses.

These anastomoses are called portocaval, that is, the blood that should have gone to the IV goes into the vena cava through other vessels that unite both blood flow basins.

The most significant anastomoses of the portal vein include:

  • Connection of gastric and esophageal veins;
  • Anastomoses between the veins of the rectum;
  • The junction of the veins of the anterior wall of the abdomen;
  • Anastomoses between the veins of the digestive organs with the veins of the retroperitoneal space.

In the clinic, the anastomosis between the gastric and esophageal vessels is of greatest importance. If the movement of blood through the veins is disrupted, it is dilated, portal hypertension increases, then the blood rushes into the flowing vessels - the gastric veins. The latter have a system of collaterals with the esophageal, where venous blood that does not go to the liver is redirected.

Since the ability to discharge blood into the vena cava through the esophageal veins is limited, overloading them with excess volume leads to varicose veins with the likelihood of bleeding, often fatal. The longitudinally located veins of the lower and middle thirds of the esophagus do not have the ability to collapse, but are at risk of injury when eating, gag reflex, and reflux from the stomach. Bleeding from varicose veins of the esophagus and the initial part of the stomach is not uncommon in liver cirrhosis.

From the rectum, venous outflow occurs both into the venous system (upper third) and directly into the lower cavity, bypassing the liver. With an increase in pressure in the portal system, stagnation inevitably develops in the veins of the upper part of the organ, from where it is discharged through collaterals into the middle vein of the rectum. Clinically, this is expressed in varicose hemorrhoids - hemorrhoids develop.

The third junction of the two venous pools is the abdominal wall, where the veins of the peri-umbilical region take on “excess” blood and expand towards the periphery. Figuratively, this phenomenon is called the “head of Medusa” because of some external resemblance to the head of the mythical Gorgon Medusa, who had writhing snakes on her head instead of hair.

The anastomoses between the veins of the retroperitoneal space and the PV are not as pronounced as those described above, it is impossible to trace them by external signs, and they are not prone to bleeding.

Video: lecture on veins of the systemic circulation

Pathology of the portal system

Among the pathological conditions in which the IV system is involved are:

  1. Thrombosis (extra- and intrahepatic);
  2. Portal hypertension syndrome (PHS) associated with liver pathology;
  3. Cavernous transformation;
  4. Purulent inflammatory process.

Portal vein thrombosis

Portal vein thrombosis (PVT) is a dangerous condition in which blood clots appear in the PV, preventing its movement towards the liver. This pathology is accompanied by an increase in pressure in the vessels - portal hypertension.

4 stages of portal vein thrombosis

According to statistics, among residents of developing regions, LPG is accompanied by thrombus formation in the veins in a third of cases. In more than half of patients who die from cirrhosis, thrombotic clots can be detected postmortem.

The causes of thrombosis are considered:

  • Cirrhosis of the liver;
  • Malignant intestinal tumors;
  • Inflammation of the umbilical vein during catheterization in infants;
  • Inflammatory processes in the digestive organs - cholecystitis, pancreatitis, intestinal ulcers, colitis, etc.;
  • Injuries; surgical interventions (bypass surgery, removal of the spleen, gallbladder, liver transplant);
  • Blood clotting disorders, including certain neoplasias (polycythemia, pancreatic cancer);
  • Some infections (tuberculosis of portal lymph nodes, cytomegalovirus inflammation).

Among the very rare causes of PVT include pregnancy and long-term use of oral contraceptives, especially if the woman has crossed the age of 35-40.

Symptoms of PVT consists of severe abdominal pain, nausea, dyspeptic disorders, vomiting. Possible increase in body temperature, bleeding from hemorrhoids.

Chronic progressive thrombosis, when blood circulation through the vessel is partially preserved, will be accompanied by an increase in the typical pattern of LPG - fluid will accumulate in the abdomen, the spleen will enlarge, giving characteristic heaviness or pain in the left hypochondrium, and the veins of the esophagus will dilate with a high risk of dangerous bleeding.

The main way to diagnose PVT is ultrasound, and a thrombus in the portal vein looks like a dense (hyperechoic) formation that fills both the lumen of the vein itself and its branches. If ultrasound is supplemented with Doppler ultrasound, then there will be no blood flow in the affected area. Cavernous degeneration of blood vessels due to dilation of small-caliber veins is also considered characteristic.

Small thrombi of the portal system can be detected by endoscopic ultrasound, and CT and MRI make it possible to determine the exact causes and look for possible complications of thrombus formation.

Video: incomplete portal vein thrombosis on ultrasound

Portal hypertension syndrome

Currently answering questions: A. Olesya Valerievna, candidate of medical sciences, teacher at a medical university

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How does blood flow in the liver work?

The portal vein (v. portae) begins with a capillary network of unpaired organs located in the abdominal cavity of mammals:

  • intestine (more precisely, the mesentery, from which two branches of the mesenteric veins depart - lower and upper);
  • spleen;
  • stomach;
  • gallbladder.

The allocation of a separate venous system for these organs is due to the absorption processes occurring in them. Substances entering the gastrointestinal tract are broken down into their components (for example, proteins into amino acids). But there are substances that are poorly transformed in the gastrointestinal tract. These are, for example, simple carbohydrates and inorganic chemical compounds. And when proteins are digested, waste products arise - nitrogenous bases. All this is absorbed in the capillary network of the intestines and stomach.

Regarding the spleen, its second name is the red blood cell cemetery. Worn-out red blood cells are broken down in the spleen, releasing toxic bilirubin.

During the experiment on removing the liver from animals, all this led to their rapid death. Dangerous blood must be delivered to the liver bypassing other organs. Therefore, nature has endowed this function with a special venous bed that delivers blood with toxins for neutralization - the portal vein of the liver.

Actually, the portal vein is formed by joining the splenic vein of two rather large mesenteric veins. The superior and inferior mesenteric veins, which collect blood from the intestine and accompany the arteries of the same name, supply the portal vein with blood from the intestine (with the exception of the distal parts of the rectum).

The site of formation of venae portae is most often located between the posterior surface of the head of the pancreas and the parietal layer of the peritoneum. The result is a vessel 2-8 cm long and 1.5-2 cm in diameter. Then it passes through the thickness of the hepatoduodenal ligament until it enters the organ in the same bundle with the hepatic artery.

How does blood circulation work in the liver?

All afferent vessels and nerves approach the liver in one place, the transverse groove. There are the so-called gates of the liver (porta hepatis). The portal vein also fits there. And then we observe what makes this vein unique - it branches again to the capillaries, however, already hepatic. This vein is the only one that organizes blood flow to the parenchymal organ!

Further, according to the number of liver lobes, the portal vein is dichotomously divided into two branches (right and left). Subsequently, each gives rise to segmental parts of the organ. The next link is interlobular and septal. The last section of the portal vein is the capillaries of the liver lobules, which, due to their structure, are called sinusoids. Venules formed from the capillaries of the liver lobules belong to the inferior vena cava system.

This is a natural mechanism that cleanses the blood of harmful substances absorbed in the intestines. The location of the portal vein allows it to serve as a direct highway between harmful “production” and the “plant” for waste treatment.

There are some more interesting facts about the portal vein:

  1. The ligament in which it, together with the hepatic artery, approaches the gate of the liver is in some way not a ligament, but a fold of the omentum. The surgeon can apply pressure with his finger to stop liver bleeding. For a while, of course;
  2. The portal vein has connections (anastomoses) with almost all veins of the abdominal cavity. Normally, this hepatic portal vein system does not manifest itself in any way. It becomes noticeable in diseases of the organ and conditions leading to portal hypertension. Since the liver cannot hurt, manifestations of increased pressure in the portal vein system may be the first symptoms of a serious pathology (cirrhosis of the liver, thrombosis of the abdominal veins);
  3. Such a large blood sampling area makes the portal vein the largest vein in the abdominal cavity;
  4. The portal vein system, together with the liver, is the largest blood depot in the body. Minute blood flow at rest is 1500 ml;
  5. If we remember where the portal vein is formed, it becomes clear why a tumor of the head of the pancreas manifests itself as portal hypertension.

Manifestations of portal hypertension can be very different - spider veins on the anterior wall of the abdomen, varicose veins of the esophagus, often discovered by chance. Even hemorrhoids can (rarely) be a manifestation of a local increase in pressure in the portal vein system.

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