External liver thrombus and method of treatment. Timely treatment of hepatic vein thrombosis
Thrombosis is dangerous disease, affecting arterial and venous vessels. It is accompanied by a narrowing of the vascular cavity due to its blockage blood clot. Portal vein thrombosis is a dangerous disorder of the functioning of the liver and adjacent organs. Most often, blockage of this vessel is not independent disease, but a complication of pathological processes occurring in the body. Even minor factors can provoke thrombosis. When neglected, it can lead to internal bleeding and fatal outcome.
In this article we will tell you:
Hepatic portal vein thrombosis
Portal vein thrombosis is a disease characterized by blocking of the vascular lumen by a thrombus, up to complete occlusion. In 5% of cases, the disease develops against the background of cirrhosis, in 30% - as a result of hepatocellular carcinoma.
Circulatory disorders are noted not only in abdominal area, but also throughout the body. As a result, the functioning of the digestive tract is disrupted, which is accompanied by a number of unpleasant symptoms.
Reasons for the development of the disease
The causes of hepatic portal vein thrombosis vary. In newborns, the disease occurs as a result of infection through the umbilical cord. In adulthood, the pathological process may develop after acute appendicitis.
The causes of the disease in adults are as follows:
- bacterial damage to the vein or the development of purulent pylephlebitis;
- availability cystic formations on a vein;
- cirrhosis;
- period of bearing a child;
- hereditary predisposition to vascular pathologies;
- increased blood clotting;
- chronic heart failure;
- malignant or benign tumors in the area of the affected vein and nearby organs;
- postoperative period.
Main symptoms
To spend timely diagnosis, you should familiarize yourself with the clinical picture of portal vein thrombosis. Symptoms vary at each stage of the disease. They depend on concomitant diseases and localization of the thrombus.
The most common signs of impaired blood flow include:
- presence free liquid V abdominal cavity;
- presence of blood in the stool;
- pronounced pain in the peritoneum;
- flatulence;
- bleeding from the esophagus into the stomach;
- complete absence of stool;
- dark vomit.
In the presence of thrombosis, the patient may notice the disappearance of physiological hunger. At the same time, the urge to go to the toilet disappears, and constipation is observed.
If the disease occurs in an acute form, the stool becomes liquid. Painful sensations concentrate in epigastric region and periodically give it to right hypochondrium.
Classification and forms
The symptoms and manifestations of the disease largely depend on its type. By severity pathological process distinguish between heavy, medium and light form thrombophlebitis.
They differ in the following characteristics:
- At mild flow disease, the thrombus covers only half of the vein cavity. It is located in the area of the transition of the portal vein to the splenic vein.
- The average form of the disease is characterized by a thrombus affecting the area of the mesenteric vessel.
- In severe cases, thrombosis affects all veins located in the abdominal cavity. Blood flow slows down significantly, which affects the functioning of the digestive organs.
There are also chronic and acute form diseases. In the first case, the course of the disease is long, accompanied by other pathological processes. In acute thrombosis, a rapid increase in the intensity of symptoms is observed. In this case, there is a risk of death.
After successful elimination blood clot, the patient must undergo regular preventive examinations at the phlebologist.
Diagnostic measures
A thrombus in the portal vein of the liver is diagnosed using standard methods. The first priority is to examine and interview the patient.
After collecting an anamnesis, the following procedures are prescribed:
- Dopplerography, which is an addition to ultrasound examination, helps to identify disturbances in blood flow in the abdominal cavity.
- Liver tests are necessary to evaluate liver health and diagnose primary diseases organ.
- Donating blood for coagulation tests gives an idea of the likelihood of a blood clot forming.
- Contrast venography helps to identify the exact location of the formed blood clot.
Treatment of portal vein thrombosis
It is highly recommended not to ignore the symptoms of portal vein thrombosis. Treatment is selected individually, taking into account the severity of the disease. Application drug therapy appropriate for chronic thrombosis.
If bleeding develops, the patient is admitted to the hospital. A probe is inserted into the abdominal cavity to stop the bleeding. Also accepted medicines to stop bleeding.
The goals of conservative therapy are as follows:
- reduction of signs of portal hypertension;
- preventing excessive blood clotting;
- blood thinning.
Medication method
Drug therapy for vascular thrombosis requires an integrated approach. The dosage of drugs is selected by the attending physician on an individual basis. Average duration taking medications is 1 month. After graduation treatment course tests are repeated.
Used the following groups medicines:
- anticoagulants are not direct action(Neodicoumarin and Syncumar);
- thrombolytic medicines(Streptokinase and Fibrinolysin);
- antimicrobial drugs (Tienam, Meronem);
- direct anticoagulants (Fraxiparin, Heparin).
Intravenously administered saline solution or Reopoliglucin in a dosage of 400 or 200 ml. Direct anticoagulants are used in urgently in the first hour after the onset of symptoms of the disease.
They are administered intravenously at a concentration of 40,000 units over 4 hours. Thrombolytic drugs are administered using a dropper at a dosage of 20,000 units.
Operation
Depending on the nature of the disease, a treatment method is selected. Treatment surgically is carried out when medications are insufficiently effective in the first 3 days of hospital stay.
The following types of intervention are used:
- Sclerosing injection therapy. The procedure involves injecting a gluing solution into the vein to narrow the enlarged areas. The operation is performed in conjunction with esophagoscopy.
- Splenorenal anastomosis. This type of intervention is practiced if the patency of the splenic vein remains.
- Application of mesenteric-caval anastomosis. It is carried out if it is necessary to eliminate portal hypertension.
- Prosthetics are performed if the splenic vein is blocked. The prosthesis is placed in the area between the superior mesenteric and inferior vena cava.
At prolonged bleeding resort to surgery using the Tanner method. The stomach area is crossed in the cardiac section. After this, its walls are stitched together. If pylephlebitis develops, its complications are prevented by installing drainage.
Complications and prognosis
Thromboembolism in liver cirrhosis and other diseases of internal organs leads to various complications. If treatment is not started on time, the risk of coma, the development of purulent peritonitis, intestinal infarction, hepatorenal syndrome and extensive bleeding increases.
The prognosis in these cases is unfavorable. If the mesenteric vein is completely blocked, the likelihood of death increases.
Timely therapy can prevent the clot from moving through the portal vein. Following all the doctors’ recommendations, the patient is fully back on his feet in 3-5 weeks. Small blood clots respond well to drug therapy. The earlier treatment is started, the more favorable the outcome will be.
Cardio gymnastics, yoga and physical therapy provide positive impact on the functioning of the vascular system.
How to prevent the disease?
To prevent the development of portal vein thrombosis, it is necessary to lead a healthy lifestyle and be observed by a phlebologist. In persons who have alcohol addiction, the likelihood of developing pathology is much higher.
Ethyl alcohol has a damaging effect on the liver. Disruption of its functioning provokes the development of thrombosis.
The following measures help improve blood circulation and blood composition:
- regular hiking and moderate physical activity;
- timely consultation with a doctor if pathologies of internal organs are detected;
- drinking the required amount of fluid;
- reception vitamin complexes in order to prevent deficiency of nutrients;
- adherence to the principles of proper nutrition.
It must be remembered that even compliance with all preventive measures does not insure 100% against the occurrence of the disease. In some cases, thrombosis develops under the influence of factors beyond a person’s control. In such a situation, the effectiveness of treatment directly depends on the speed of diagnosis.
Thrombosis – serious illness, requiring timely treatment. If you consult a doctor on time, you can avoid dangerous consequences. The patient is required to strictly follow the prescribed recommendations and maintain healthy image life.
The first mention of a disease that develops with obstruction of the hepatic veins was noticed in 1845. It was described by the Englishman G. Budd. In 1899, the Austrian H. Chiari studied more than 10 patients with the same syndrome. The names of the researchers formed the basis for the name of this severe pathology. Budd-Chiari disease is a disease caused by blockage of the hepatic and portal veins. Rare disease(occurs in 1 person out of 100 thousand), leading to a malfunction of the liver due to difficulty draining blood from it and manifested by signs high pressure in the portal vein.
The reasons leading to blockage of blood flow are:
- Endophlebitis of the hepatic veins, directly causing their thrombosis, obliteration and blockage. Develops after an abdominal injury, diseases of the hemocoagulation system, complicated pregnancy or delivery, or surgical interventions.
- Congenital disorders of the structure of the hepatic veins.
A pathology that manifests itself with the same symptoms, but is based on an obstruction of blood flow from the liver of an indirect nature (that is, not caused by damage and thrombosis of the hepatic veins), is considered as Budd-Chiari syndrome. Scientists are still arguing about the practical need to separate the concept of disease from syndrome.
Budd-Chiari syndrome can develop due to the following pathologies:
- inflammation in the abdominal cavity or in the heart sac;
- tumor formations of the abdominal region (liver, kidney, adrenal tumors, Williams tumor);
- congenital decrease in the lumen of the inferior vena cava or its narrowing due to thrombosis;
- membranous fusion of the inferior vena cava (an extremely rare pathology found in the population of Japan and Africa);
- cirrhosis;
- congenital liver defects;
- hemocoagulation disorders (myeloproliferative diseases, polycythemia, vasculitis);
- long-term use of contraceptives;
- postoperative mechanical blocks;
- infectious diseases (tuberculosis, echinococcosis, amebiasis, syphilis).
Often these pathologies are accompanied by varicose dilatation of the esophageal veins, accumulation of transudate in the abdominal cavity, or cirrhosis. In a quarter of patients, it remains unclear why this symptom complex developed. This condition is called idiopathic syndrome. There are cases when the syndrome was provoked in newborns by placing a catheter in the inferior vena cava.
Clinical course of the disease
The disease affects both women and men. The age of most patients is about 45 years.
The developing clinical picture has a number of symptoms characteristic of hypertension of the hepatic and portal veins:
- dull, aching pain in the area right half belly;
- ascites;
- increased volume of the liver and spleen;
- the liver surface is soft and painful to the touch;
- yellowing skin;
- nausea and vomiting;
- disorders of blood coagulation function;
- brain damage.
The severity of symptoms varies depending on the duration of the disease, the degree of blockage of the hepatic and portal veins, the severity of thrombosis, and the level of vasoconstriction.
Budd-Chiari syndrome is divided into 3 types based on the location of the narrowing of the venous vessel:
- Type 1 - blockage of the inferior vena cava and secondary blockage of the hepatic vein;
- Type 2 - blockage of large hepatic veins;
- Type 3 - blockage of small venous vessels of the liver.
The course of the disease is divided into acute (duration less than one month) and chronic:
- The acute form is observed in 5-20% of patients. Reason acute development The disease becomes thromboembolism of the hepatic veins or inferior vena cava. Characterized by significant pain in the area of the liver projection and above the navel, rapid growth liver size, vomiting, yellowing of the skin. Within a few days, fluid accumulation in the abdominal cavity is possible. Often accompanied by portal vein thrombosis and, as a consequence, edema lower limbs, dilatation of the vascular venous network of the abdomen (symptom “head of the jellyfish”). Massive bleeding occurs, fluid accumulates in the slit-like cavity surrounding the lungs. Diuretics quickly become ineffective. Often ends in the death of the patient in less than a week.
- In most people, Budd-Chiari syndrome develops as a chronic pathology. A chronic form develops due to thrombosis and fibrosis of the liver vessels after any inflammatory processes. On initial stages the disease does not manifest itself in any way, except for an increase in the size of the liver. Only with an advanced form do pain in the liver area and a feeling of nausea begin to appear. Vomiting blood often occurs. After presenting complaints, the examination process already reveals hepatomegaly, splenomegaly, cirrhosis of the liver and varicose veins portal vein and venous network of the anterior surface of the body.
The final stage of development of Budd-Chiari syndrome is: irreversible dilatation of the inferior vena cava and portal veins, accompanied by bleeding, liver failure, blockage of the peritoneal vascular bed by blood clots and intestinal thrombosis. Patients with ascites may develop peritonitis. If the cause of the syndrome was membranous fusion of the vessel, then in 30-45% of cases the formation of hepatocellular carcinoma can be expected.
Diagnosis of the disease
To clarify the diagnosis, in addition to the complaints made by patients, and clinical signs it is necessary to conduct a series of studies that will help determine the type and structure of the liver and portal veins, detect blood clots or narrow lumens in the vascular bed of the liver, and determine the degree of disturbance of blood flow.
- Blood test. General analysis And biochemical research in the acute or chronic form of the syndrome will show an increase in the number of leukocytes, a decrease in the content of blood proteins and their imbalance, and an acceleration of ESR. Thrombosis of the hepatic veins is characterized by an increase in protein and serum albumin levels. A coagulogram study will reveal an increase in prothrombin time over 15-20 seconds.
- Ultrasound of the liver, radiography, computed tomography or magnetic resonance tomography will show a change in the size of the organ, circulatory failure. Budd-Chiari syndrome is determined by atrophy of the extreme parts of the liver and enlargement of the central parts. In every second patient, an enlarged caudate lobe is visualized.
- Doppler ultrasonography. Accurately determines the presence of thrombosis and visualizes the location of blood clots in blood vessels.
- Cavography and venohepatography with a contrast agent will show the contours of the venous network, the presence of narrowings or blockages of blood vessels. Often used during operations.
- Percutaneous liver biopsy will reveal dying liver cells, stagnation venous blood and thrombosis in the area of the terminal branches of the veins.
Before making a diagnosis, it is necessary to exclude veno-occlusive disease (develops after transplantation) bone marrow, chemotherapy) and heart failure of the right ventricular type.
Patients must be under the supervision of a gastroenterologist and surgeon.
Treatment and prevention of the disease
Drug treatment is aimed at reducing the severity of symptoms of the disease. The following groups of drugs are used:
- hepatoprotectors;
- stimulating metabolic processes;
- diuretics;
- glucocorticosteroids;
- drugs that affect blood clotting and resolve blood clots.
For varicose dilatation of the esophageal veins, veins of the stomach and intestines, drugs from the group of beta-blockers are prescribed to prevent bleeding from them.
Conservative treatment of Budd-Chiari syndrome is palliative. If not produced surgery, the mortality rate from this disease reaches 90% within two years.
The main treatment of the disease is surgical. The type of surgical intervention depends on what triggered the development of the disease:
- anastomosis on the affected veins;
- transatrial membranetomy;
- vein prosthetics;
- dilatation of narrowed areas of the vessel;
- portal vein bypass;
- liver transplantation.
To eliminate such a dangerous condition as ascites, a laparocentesis technique is used, during which fluid is removed through small incisions in the abdominal wall. Liver transplantation and shunting between the portal and hepatic veins also have a positive and lasting effect.
Prevention of exacerbations requires constant use of anticoagulant drugs and lifelong diet.
Forecast
Acute Budd-Chiari syndrome is usually severe and often results in a hepatic coma with a fatal outcome. The chronic form of the disease with appropriate treatment allows 55% of patients 10 years or more to have a satisfactory quality of life. Liver transplantation increases the survival rate of patients to 70% at 5 years of follow-up. If the course of the disease is unfavorable, death occurs due to the development of liver failure and ascites.
The life prognosis depends on the reasons that caused the development of the syndrome and the timing of treatment. A special formula for calculating the prognostic index has been created. The prognosis is considered favorable if the result is less than 5.4.
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Classification
The dimensions of the portal vein are quite impressive, its length reaches 8 cm and width 1.5 cm. In addition, in the liver it breaks up into many small vessels that distribute the incoming blood to all lobules of the organ, and after cleaning, they discharge it into the inferior vena cava, circulation in which it is directed towards the heart.
Portal vein thrombosis can occur anywhere along the entire length of the vessel.
The blockage can be localized either at the gate of the liver or in the middle of the organ itself. Also, occlusion is often located near other organs from which blood is drawn via vein.
The disease is classified into several types and stages, differing in the course of development, the presence of symptoms, the location of the blockage and the complications that arise.
Based on the time of occurrence, the disease is divided into the following types:
| Acute portal vein occlusion |
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| Chronic thrombosis |
|
According to the stages of development, portal vein thrombosis is classified into:
Reasons
Blockage of the portal vein, like other venous thrombosis, occurs due to certain factors affecting the functioning of the circulatory system.
Causes of portal vein thrombosis:
| Decreased blood flow rate |
|
| Increased clotting | The following factors influence the increase in blood clotting:
Also, thrombus formation against the background of increased coagulability occurs due to purulent pylephlebitis, which often develops with advanced cholangitis, lymphadenitis or ulcerative colitis. Changes in coagulability are also affected long-term use hormonal contraceptives. Therefore, portal vein thrombosis is often diagnosed in women. |
| Trauma to the venous wall | It may occur due to surgery or thrombophlebitis - an inflammatory process in vascular tissues. |
Symptoms
Clinical manifestations depend on the duration of thrombosis and its location. The presence of symptoms is also influenced by the degree of development of the disease and complications.
The most dangerous manifestation Portal vein occlusion is liver infarction or segment death. If thrombosis occurs in conjunction with blockage of the mesenteric veins, then most often the attack ends in death.
The most obvious symptom Portal vein thrombosis is extensive hemorrhage into the esophagus. The syndrome is accompanied by loss of appetite, bloating, lack of stool and other symptoms indicating intestinal dysfunction.
Blockage of the main trunk of the portal vein occurs:
| Spicy |
|
| Chronically |
|
Diagnostics
The easiest way to diagnose acute thrombosis is that it develops rapidly and has obvious symptoms. In differential diagnosis, exclude similar diseases, for example, blockage hepatic artery, possible based on availability clinical picture.
When the portal vein is occluded, the liver does not enlarge; however, liver failure develops quite quickly, characterized by bleeding and dysfunction gastrointestinal tract.
More difficult to determine chronic form portal vein thrombosis. This process is very similar to liver cirrhosis, therefore, for accurate diagnosis it is necessary to resort to laboratory and instrumental research methods.
For diagnostic purposes, the following is carried out:
- Doppler ultrasound;
- liver tests (in laboratory conditions);
- coagulogram;
- Ultrasound of the abdominal cavity.
In severe cases, when standard methods do not provide accurate results, the patient undergoes an MRI or CT scan with contrast. This kind of hardware research helps determine the location of the thrombus, assess the degree of occlusion, the size of the clot, the presence of complications, and identify whether there are other blockages nearby.
Laboratory blood tests for portal vein thrombosis record an increase in fibrinogen content, an increase in PTI and increased coagulability.
It is very important to start thrombosis therapy as early as possible. Treatment is carried out strictly in a hospital setting and lasts about two weeks.
In acute cases of occlusion, thrombolysis is used, especially in hypercoagulable states and blockages that have recently arisen.
The main goal of treatment is to stop the development of the disease, prevent the development of consequences and restore blood flow. Therapy is also aimed at preventing further growth of the clot and removing it.
Treatment of thrombosis consists of surgery and conservative therapy.
Let's look at both methods in more detail:
| Conservative | Drug treatment is carried out with direct-acting anticoagulants, which are given to the patient in the first hours of occlusion. high doses. Usually, for this purpose, Heparin or Fraxiparine is used intravenously for 3–4 hours. Among other things, the patient is prescribed thrombolytic drugs and anticoagulants indirect action:
Reopolyglucin and saline solution, 200–400 ml, are also used intravenously through a dropper. If thrombosis is accompanied purulent complications, or arose against the background of such processes in the body, then the main treatment must be supplemented with antibiotics wide range(Meronem, Tienam). The dosage of all drugs is selected individually for each patient. It depends on the severity of the disease, the degree of damage to the peritoneal organs, concomitant diseases, the age of the patient and individual characteristics body. |
| Operational | TO surgical intervention resort in case of ineffectiveness conservative treatment. To understand that the medications do not help, it should take 1 to 3 days. The operation is performed while maintaining the patency of the splenic vein; otherwise, a mesenteric-caval anastomosis is created using an arterial prosthesis with a diameter of about 18 mm, which is installed between the inferior vena cava and the superior mesenteric vein. For portal vein thrombosis, the following surgical methods are used:
If the disease is accompanied by bleeding from the esophagus, then suturing of the affected veins of the gastric and intestinal tract is performed. In the presence of pylephlebitis, the liver is opened, followed by drainage of abscesses. After surgery, the patient continues to be given drug therapy, after which re-diagnosis is carried out. |
Prevention
The development of portal vein thrombosis can be avoided if preventive measures are followed. This is especially important for people who are at increased risk for this disease.
Effective methods against thrombosis:
- proper nutrition;
- giving up bad habits;
- compliance normal level physical activity;
- using cardio exercises;
- taking medications to strengthen the vascular and cardiac systems;
- If you have increased blood clotting, take medications that help thin it.
To prevent exacerbation or recurrence of occlusion, it is necessary to regularly take medications prescribed by your doctor, and also be diagnosed every six months. People who are registered should immediately contact a specialist if their condition worsens.
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Causes of portal vein thrombosis
The occurrence of portal vein thrombosis, like any thrombotic process, is determined by a number of factors - changes in the surface vascular wall, slowing down blood flow and increasing the thrombus-forming properties of blood. Thus, inflammatory changes in the wall of the portal vein during various infections such as phlebosclerosis, atherosclerosis, syphilis, and finally, specific changes in neoplasms contribute to the formation of a blood clot in the portal vein. Conditions for the occurrence of thrombosis are also created in diseases that occur with portal hypertension, in which there is a slowdown in blood flow in the portal vein system. Especially important role this factor plays a role in liver cirrhosis, in which thrombosis is often observed in this vascular system.
The role of impaired blood clot-forming properties is emphasized by the frequency of portal vein thrombosis in polycythemia and some other diseases associated with thrombocythemia. In these cases, there is a significant increase in coagulants in the blood, which sometimes cannot be compensated by an increase in the anticoagulant and fibrinolytic properties of the blood. Thrombosis in polycythemia is a common complication of this disease, in to a large extent weighing him down. An increase in thromboplastic activity, probably associated with an increase in the content shaped elements blood, including platelets, as well as other procoagulants, and a decrease in anticoagulant capabilities, creates conditions for the occurrence of thrombosis. Of course, the increase in blood viscosity, vascular permeability and slower blood flow, characteristic of polycythemia, are also important.
However, in the mechanisms of thrombus formation in polycythemia, changes in the thrombus-forming properties of blood undoubtedly play a major role. Moreover, the increased tendency to thrombus formation depends not only on the increase in thromboplastic activity of the blood, but also on the release during the breakdown of blood cells, substances that inhibit the action of anticoagulants and fibrinolytic enzymes. Platelets and erythrocytes contain lipids that have not only thromboplastic properties, but also antiheparin and antifibrinolytic activity.
Similar possibilities of increasing the tendency to thrombus formation should be taken into account in other blood diseases, especially those accompanied by either a significant increase in formed elements or their increased decay (Marchiafava disease, some types of anemia, etc.). The series released during the breakdown of red blood cells, erythrocytin and other substances can create conditions for the formation of a blood clot. Thrombosis of various vascular areas is observed in polycythemia.
Some doctors associate vein thrombosis with sensitization vascular endothelium under the influence of previous changes in blood plasma. It's about about the development of thrombosis due to a violation of the relationship between the blood and the vascular wall. It is suggested that an increase in coarse fractions leads to a change in the electrical charge of blood platelets, which contributes to their gluing, disintegration and thrombus formation. The pathogenesis of portal vein thrombosis is complex; the disease depends on a number of factors, and it is often not possible to identify the significance of each of them. There are four forms of portal vein thrombosis depending on the location of the thrombus: in the vessels of the gastrointestinal tract, in the intrahepatic branches and the trunk of the portal vein itself. And finally, he introduced thrombosis of the splenic vein (thrombophlebitic splenomegaly) as a special nosological unit. With all forms of portal vein thrombosis, portal hypertension develops to one degree or another, causing a number of symptoms of this disease - ascites, splenomegaly, etc.
Symptoms and signs of portal vein thrombosis
However, the symptoms of the disease depend on the degree and location of the thrombotic process. With thrombosis of the mesenteric veins, gastrointestinal disorders, in particular the phenomena of enterocolitis, come to the fore, while thrombosis of the splenic vein gives a clearly defined picture of the so-called thrombophlebitic splenomegaly.
Thrombosis of the main trunk of the portal vein can occur acutely or chronically. An acute process is characterized by the sudden appearance sharp pain in the epigastric region and right hypochondrium, often accompanied by bloody vomiting. Ascites develops quickly and the spleen enlarges. There is a tendency to diarrhea. Due to stasis in the vessels of the gastrointestinal tract, numerous infarctions and bleeding can occur. It is interesting to note that the spleen, as noted by some authors, may decrease in volume when bleeding occurs.
The chronic process is characterized by a more sluggish and slow course, the symptoms of the disease appear gradually. In addition to ascites, splenomegaly, and bleeding, in these cases collateral circulation may develop with varicose veins characteristic of portal hypertension. Low-grade fever and sometimes leukocytosis are observed. In both acute and chronic processes, liver failure often develops, which, along with other symptoms, complicates the differential diagnosis between portal vein thrombosis and liver cirrhosis. The same difficulties exist in differentiating from Budd-Chiari syndrome.
Acute portal vein thrombosis is usually asymptomatic unless associated with another disease such as pancreatitis (causing it) or another complication such as thrombosis mesenteric vein. The most common symptoms, splenomegaly and variceal bleeding, appear over time and are secondary to portal hypertension. Ascites is rare (10%) with postsinusoidal portal hypertension. Precipitating factors for ascites include cirrhosis of the liver or a decrease in serum albumin (and, therefore, oncotic pressure) after replacing a large volume of fluid due to severe gastrointestinal bleeding.
Diagnosis of portal vein thrombosis
It is easier to diagnose acute thrombosis when the characteristic acute clinic allows you to more accurately determine the presence of a thrombus in the portal vein. In contrast to hepatic vein thrombosis, portal vein thrombosis does not increase the size of the liver, but the speed of the pathological process with an increase in aspitis, liver failure, and early appearance bleeding and gastrointestinal disorders allows us to differentiate it from liver cirrhosis.
Diagnosis is difficult chronic process, which is difficult to distinguish from cirrhosis of the liver. In addition, portal vein thrombosis often develops against the background of a severe underlying disease ( malignant tumor, liver cirrhosis), being its complication. The picture of thrombosis itself can be leveled out in these cases by the symptoms of the underlying disease. That is why the diagnosis of portal vein thrombosis in a chronic process is rarely made during the patient’s lifetime and is usually a sectional finding.
The thrombus can be localized only in the mesenteric branches of the portal vein, causing circulatory impairment in the intestinal vessels. This process leads to intestinal infarctions of venous origin, in contrast to intestinal damage that develops in connection with thrombosis arterial vessels. Mesenteric vein thrombosis is an extremely rare disease.
In the occurrence of necrosis great value has a fortune collateral circulation. There are cases where the application of a ligature even to the superior mesenteric vein did not cause circulatory disorders. Venous arcades located parallel to the intestine allow blood to flow to the inferior and superior vena cava. Thus, the possibility of hemorrhagic intestinal infarction and the development of necrosis is determined by the localization of the thrombus, its size and the severity of collateral circulation. Pathologically, thrombosis of the mesenteric veins usually reveals hemorrhagic intestinal infarction, congestion(swelling of the intestine, mesentery). There is bloody impregnation in the intestinal wall, multiple focal hemorrhages, and sometimes ulcers form. Naturally, those patients in whom thrombosis of the mesenteric veins was the cause of death, i.e., when the pathological process is severe, are subjected to pathological examination.
Diagnosis of portal vein thrombosis
- Clinical assessment and laboratory liver function tests,
- Doppler ultrasound.
Doppler ultrasonography is a method showing reduced or absent venous blood flow and sometimes thrombus. Complex cases may require MRI or CT with contrast. For bypass surgery, angiography may be required.
Treatment of portal vein thrombosis
- In some acute situations, thrombolysis.
- Long-term anticoagulant therapy.
- Management of portal hypertension and its complications.
In acute cases, thrombolysis can be used successfully, especially if it is performed in cases of recent occlusion, in particular in hypercoagulable states. Anticoagulants do not lyse clots but have some value in the long-term prevention of recurrent thrombosis in hypercoagulable states, despite the risk of variceal bleeding. Correction of portal hypertension and its complications is also necessary; possible intravenous administration of octreotide and endoscopic ligation to control variceal bleeding, as well as the prescription of non-selective beta-blockers to prevent recurrent bleeding. This treatment reduces the need for surgical shunts (eg, mesocaval, splenorenal), which can also be occluded, and the operative mortality rate is 5-50%. With TIPS, monitoring (including frequent angiography) is necessary to assess its patency, which can be blocked, which will interfere with adequate liver decompression.
The diagnosis of mesenteric vein thrombosis is very difficult. Some authors consider it generally impossible, at least clinically, to carry out a differential diagnosis between arterial and venous thrombosis. This probably does not have much practical significance, since the doctor’s tactics for these diseases are the same. During the operation, which until recently was the only effective method of treatment, it is possible to detect some features that make it possible to differentiate arterial and venous thrombosis. Preserved pulsation mesenteric arteries speaks of vein thrombosis; extensive damage to the entire thickness of the intestinal wall is more typical of arterial thrombosis.
Clinically, with thrombosis of the mesenteric veins, the appearance of acute, cramping pain in the abdomen is noted, which is subsequently accompanied by vomiting of “coffee grounds” and melena. On palpation abdominal wall in the first period it is mild, diffuse soreness is noted. Maybe the same as with arterial thrombosis, a testy tumor is detected in the depths of the abdominal cavity. Characteristic feature thrombosis of the mesenteric veins is the testiness of the rectum during digital examination, depending on venous stasis. Necrosis with venous thrombosis develops more slowly, which is why clinical symptoms diseases, unlike arterial thrombosis, are less pronounced. Painting intestinal obstruction, symptoms of peritonitis appear later. From the blood side, high leukocytosis with a shift to the left is noted. It should only be pointed out that with extensive venous thrombosis, the disease can be acute from the very beginning, with rapid development symptoms of intestinal obstruction and peritonitis.
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Features of the disease
According to ICD-10, portal vein thrombosis has code I81, according to which it is also called “portal vein thrombosis.”
- In newborns, portal vein thrombosis usually develops due to infectious processes, affecting the umbilical cord stump, through which it affects the portal vein.
- If the child is older, then the cause of the pathology may be acute appendicitis.
- In adulthood, the cause of the disease is often previous surgery, pregnancy, tumors, cirrhosis or hypercoagulability syndrome. In almost every case, obstruction develops. Below you will find a photo of portal venous thrombosis.
Classification and forms
- The first stage of the disease is characterized by the fact that less than 50% of the vessels remain blocked, and the blood clot is located at the junction of the vein with the splenic vein.
- In the second degree, the thrombus already occupies the area up to the mesenteric vessel.
- The third stage is characterized by the preservation of normal blood flow or only a slight disturbance, but thrombosis already affects all veins in the abdominal cavity. On last stage circulatory disturbance occurs.
The form of blockage of blood vessels can be acute or chronic.
- In the first case, thrombosis can quickly lead to death, since complications develop at lightning speed.
- The chronic form of the course is long-lasting and develops against the background of other problems, which complicates diagnosis. This degree of blockage often has the most different manifestations abdominal diseases.
Read on to learn more about the causes and symptoms of portal vein thrombosis.
You will learn about what portal vein thrombosis looks like in the following video:
Causes of portal vein thrombosis
Thrombosis may occur due to congenital features and defects, including those described above. There are several pathogenic factors that can create a favorable development background for pathology. These include:
- hereditary predisposition,
- the presence of tumors or cysts in the vein,
- purulent pylephlebitis,
- high blood clotting,
- the presence of chronic inflammation,
- surgical interventions.
Symptoms
The narrowing of the lumen of the portal vein is divided into stages, each of which is characterized by the presence of several different signs. However, the disease progresses rapidly, so the clinical picture appears soon after its onset.
The most significant symptom is extensive hemorrhage in the esophagus due to dilated veins. Flatulence, lack of appetite, bloating or lack of stool, as well as others may appear. similar symptoms, indicating intestinal dysfunction.
Yellowing eyeballs can also become a symptom of thrombosis, like other signs that appear in liver failure. As for ascites, it rarely occurs against the background of pathology, so its appearance may indicate other diseases.
Diagnostics
When diagnosing " portal hypertension“Doctors always suspect vein thrombosis. The following research methods are used:
- Ultrasound. The lumen of the portal vein is checked to detect a blood clot and an abscess. When contrast is introduced into the vascular cavity, there may be no signal from the blood flow. Often, ultrasound helps to determine the root causes of the pathology, including liver cirrhosis, hepatocellular carcinoma, metastases, etc.
- Coagulogram, which is used to determine a number of signs characteristic of thrombosis (increased PTI, increased fibrinogen, short blood clotting time).
- MRI reveals abnormal signal on different areas vessels.
- Using CT, the thrombus itself is detected, and the defect in the filling of the portal vein is also determined.
- Angiography is used as the main method for confirming the diagnosis. The vascular cavity may not contrast at all or a filling defect may be detected.
Treatment
The goal of treatment for portal vein thrombosis is to prevent the consequences characteristic of the pathology, restore blood flow and prevent further blockage of blood vessels.
We will start by understanding what drugs are used for venous thrombosis.
Medication method
Antibiotics are used only for the development of pylephlebitis, and with a wide spectrum of action. The main treatment for portal vein thrombosis remains the use of a number of anticoagulants. First, drugs are selected that are administered intravenously. The selection of medications is carried out strictly individually, therefore they are selected in accordance with the results of thromboelastography, blood clotting and tolerance to plasma heparin. Next, indirect-acting medications are used, gradually reducing the dose.
There are also contraindications to the use of anticoagulants:
- previous operations,
- bleeding,
- intolerance,
- pregnancy.
They are selected with caution after strokes, when peptic ulcers. Thromboembolic drugs are used in combination with them.
Operation
Surgical treatment does not necessarily imply intervention, since there are also conservative methods therapy.
- The Sengstaiken-Blakemore tube is placed in the stomach, after which it begins to pump air. This helps press the veins against the wall of the esophagus. The cylinders must be emptied of air for a few minutes after 6 hours, which helps avoid bedsores. Continuous use of the probe is also limited in time and amounts to 48 hours.
- Sclerosing injection therapy. In this case enter special drug(thrombovar), which helps to glue varicose veins. This intervention is performed during esophagoscopy (a method of examining the esophagus).
Surgical treatment is used in cases where neither medication nor conservative technique therapy does not produce results.
- If the splenic vein remains patent, a splenorenal anastomosis can be performed.
- If it is blocked, the vessel is restored using a prosthesis, which is placed between the inferior vena cava and the superior mesenteric vein.
If the bleeding is prolonged and does not stop, stitching is used. So, during the Tanner operation, the stomach in the cardiac section is transversely cut, and the walls themselves are sutured. If the patient has developed pylephlebitis, then further liver abscess must be prevented. To do this, existing areas are opened and drainage is installed.
Disease prevention
The progression of portal vein thrombosis can be avoided if you carefully follow the preventive recommendations and follow them accurately. This is especially true for those patients who are at risk. Most effective methods are:
- maintaining a normal level of physical activity, walking;
- proper nutrition;
- refusal bad habits, including overuse caffeine;
- doing cardio exercises;
- usage various methods strengthening the cardiovascular system.
About how it goes acute pancreatitis, complicated by portal vein thrombosis, read on.
Acute pancreatitis complicated by PVT
Acute pancreatitis is a disease characterized by rapid development. Often it can lead to death. Its likelihood increases if there is a blockage of the veins. Once the attack begins, prompt hospitalization is necessary.
The cause of PVT is often pancreatitis. The clinical picture is complemented by symptoms of both pathologies, which complicates accurate diagnosis. Thrombosis in pancreatitis often affects the portal and splenic veins.
Complications
Subject to absence therapeutic measures purulent peritonitis or another infection develops, which leads to attacks of intoxication. With a complex picture of the course of the disease, a violation occurs temperature regime, the liver changes pathologically, which can be felt even with palpation - it becomes lumpy, dense, enlarged, and pressure is painful.
Prolonged delay in treatment is fraught with massive bleeding, intestinal infarction, and development of various kinds abscesses or the occurrence of purulent peritonitis. All these pathologies greatly worsen the prognosis of the disease.
Read on to learn about the prognosis for portal vein thrombosis.
Forecast
The most severe stages of portal vein blockage have the most unfavorable prognosis, so under no circumstances should you delay treatment. The outcome of such events is almost always fatal.
Even more useful information on the issue of thrombosis contains the following video:
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Everyone knows that blood flows through veins from organs. But in our body there is an exception. We are talking about the portal vein. It is formed by 2 mesenteric and one splenic vein. Collects blood from the gastrointestinal tract, then enters the liver.
Portal vein thrombosis is dangerous condition when a blood clot forms in the lumen of a vessel. Accordingly, blood flow is disrupted.
Reasons
The disease can develop not only in adults. Even babies are subject to certain risks. A complication of infection of the umbilical cord stump is portal vein thrombosis. Acute appendicitis can also provoke the development of serious consequences.
Let's look at the main causes of portal vein thrombosis. The German scientist Rudolf Virchow discovered that in order to implement of this disease 3 conditions are required.
- Violation of the integrity of the vascular wall. Namely the endothelium. If the surface does not have pathological changes, the formed clots move with the blood flow. Well, in case of injury or inflammatory processes, the structure of the endothelium changes. The formed clots settle in these places, gradually accumulating. As a result, vessel obstruction occurs.
- Surgical interventions.
- Phlebitis.
- Arteritis.
- Increased blood clotting. The disease can be either genetically determined or acquired.
Etiological factors:
- Congenital pathologies (protein S deficiency, antithrombin deficiency, protein C deficiency, antiphospholipid syndrome, hyperhomocysteinemia).
- Oncological diseases.
- Taking oral contraceptives.
- Antitumor drugs.
Increased coagulability is also observed in pregnant women. The postpartum period is also at risk for developing hypercoagulability. This is explained by physiologically based processes: the level of procoagulant factors increases and anticoagulant activity decreases.
- Reduced blood flow speed.
- Heart failure.
- Pre- and postoperative long-term immobilization.
- Sedentary lifestyle.
- Long flights.
Main manifestations
The severity of the clinical picture, based on which a doctor can diagnose portal vein thrombosis, depends on the course of the disease (acute or chronic), the location of the thrombus and the length of the pathological focus.
- If the course is acute, compensatory mechanisms They don’t manage to work on time. In the case of combined portal and mesenteric vein thrombosis, the outcome can be fatal.
- In a chronic course, changes increase gradually. Collateral blood flow takes over the functions of the lost area. The prognosis is more favorable.
Signs
- Portal hypertension.
- Enlarged spleen.
- Bleeding from dilated veins of the esophagus. At the same time, patients complain about severe pain, black chair. Possible vomiting of “coffee grounds”.
- Pain in the intestines, flatulence, symptoms of intoxication. The reason for this is paralytic ileus of the intestine as a result of lack of blood flow through the mesenteric veins.
- Liver enlargement, pain, chills. Occurs as a result of purulent pylephlebitis.
- Yellowness of the face, sclera.
- Encephalopathy may develop as a result of liver failure.
It should be noted that a heart attack does not only develop in the heart muscle. Occlusion of the lumen of the mesenteric vein leads to serious complication- intestinal infarction. And this, in turn, causes peritonitis.
Examination of the patient
For diagnostic purposes, both laboratory and instrumental methods research. Let's look at them in more detail.
- In first place, of course, is ultrasound. The doctor checks not only the lumen of the portal vein (after administration of a contrast agent), but also the condition of the liver and all organs of the digestive system. There are cases when it is necessary to conduct a comprehensive inspection to identify the root cause. Sometimes during the examination it is possible to detect liver diseases (cirrhosis, malignancy– hepatocellular carcinoma).
- When performing a coagulogram, the following signs indicate thrombosis:
- Elevated fibrinogen levels.
- Increased PTI (prothrombin index).
- Reduced blood clotting time.
- Angiography. Basics instrumental study, which confirms not only the diagnosis of “portal vein thrombosis”, but also allows one to identify the exact localization of the thrombus, the extent and even the speed of blood flow both through the portal vein and through the hepatic and portacaval vessels. This is being carried out as follows. Injected into the portal vein contrast agent. The X-ray monitor examines the uniformity of blood flow.
- With the help of CT and MRI, it is possible to detect not only a blood clot, but also to record accompanying pathological signs. Namely: varicose dilation of portocaval anastomoses, ascites (accumulation of fluid in the abdominal cavity), enlarged spleen.
Treatment
First of all, drug therapy is prescribed. The treatment regimen for patients diagnosed with portal vein thrombosis includes:
- Thrombolytic agents. Fibrinolysin is administered intravenously (using droppers).
- Anticoagulants of indirect action. Neodicoumarin, Syncumar.
- Reopolyglucin to replenish the required volume of circulating fluid.
- Antibiotics are prescribed for the development of purulent complications.
First aid for thrombosis is Heparin (Fraxiparin). This drug belongs to the group of direct-acting anticoagulants. Apply in the first hour of development of signs of the disease.
If no positive dynamics are observed during conservative treatment, surgical intervention is resorted to. The task of the latter is to recreate collaterals to restore blood flow. As a rule, a splenorenal anastomosis is performed.
Portal vein thrombosis can cause intestinal infarction, peritonitis, massive bleeding, renal and liver failure. Therefore, when you identify the first signs, you should consult a doctor. This way you can avoid dangerous complications without resorting to surgery.
Hepatic vein thrombosis, or Budd-Chiari syndrome, is a disorder of blood flow resulting from the formation of clots in the liver and blood vessels. This causes liver thrombosis and leads to disorder normal operation cardiovascular system.
Reasons
The syndrome develops due to the following reasons:
- abdominal trauma;
- oncological diseases (neoplasms in the pancreas, kidneys and adrenal glands);
- lupus erythematosus;
- use of drugs that increase blood clotting;
- infectious diseases (syphilis, tuberculosis, etc.);
- pregnancy;
- long-term use of oral contraceptives;
- heredity.
Symptoms
Thrombosis of the hepatic vessels occurs individually in each person, but there are some common symptoms:
- Enlarged spleen and liver. This can be judged by the enlargement of the abdomen, and the person often feels heaviness and bloating.
- Painful sensations. Despite the different pain threshold, many patients report severe pain that deprives them of sleep.
- An enlarged abdomen due to the accumulation of fluid in the abdomen - ascites.
- Hepatic encephalopathy.
- Jaundice.
- Bleeding from dilated veins of the esophagus and stomach.
If at least one of these signs appears, you should immediately contact a specialist.
Diagnostic measures
Since it is extremely difficult to determine thrombosis without studies and tests, they use using the following methods identifying it:
- Doppler ultrasound helps detect the syndrome - the presence of blood clots in the veins of the liver. In this case, it is possible to determine whether they are attached to the walls of the vein or not, and also to find out the age of the connective tissue.
- Angiography. When using this method a catheter is inserted into the hepatic veins with special solution, which makes it possible to do several x-rays. Sometimes in combination with with a special drug Substances that detect and destroy a blood clot are injected.
Radionuclide testing, additional tests and MRI of the abdominal cavity are also carried out, allowing a more accurate diagnosis of the disease and prescribing effective treatment.
How to treat the phenomenon
The treatment of hepatic vascular thrombosis should be approached comprehensively. For this purpose, medications, physical therapy, and in more severe cases, surgery are used.
During drug therapy, diuretics, antibiotics, anticoagulants, thrombolytics and other drugs are prescribed that help resolve the blood clot and normalize liver function. The dosage is determined by the doctor depending on the severity of the disease, complications in the form of other diseases, the patient’s age, as well as his tolerability of the medicinal components. If similar treatment doesn't give positive results within a few days, then other measures must be taken.
Such measures include surgical intervention. It can be carried out in 3 ways depending on the stage of the disease:
- Angioplasty. A prepared substance is injected into the hepatic veins to destroy the blood clot. With such an operation, there is a risk that the clot will break off (if it is connected to the venous wall) and begin to move along the vein. In this case, a complication in the form of thromboembolism is possible.
- Bypass surgery of the hepatic vessels. This operation involves the application of artificial vessels that provide normal movement blood.
- Liver transplantation is indicated in severe cases of acute disease. Applicable on late stages with severe complications.
Treatment of hepatic vascular thrombosis is complex and quite expensive. As a preventative measure (especially if there is hereditary predisposition syndrome), you should limit your alcohol consumption, monitor your diet, exercise, and be examined by a doctor at least once a year.
