Portal hypertension: treatment

Treatment of portal hypertension is to identify and eliminate the cause of the disease. It can be more serious than portal hypertension. For example, hepatocellular carcinoma, sprouting into the portal vein, is a contraindication for the active treatment of bleeding varicose-dilated esophagus veins. If bleeding from varicose veins develops as a result of portal vein thrombosis in erythremia, before reducing any surgical treatment, reduce the number of platelets by bleeding or the appointment of cytotoxic agents; may require the administration of anticoagulants.

Preventive treatment of varicose veins is not indicated. The rupture of these veins may not be, since collaterals develop over time.

In acute portal vein thrombosis, by the time the treatment starts, the thrombus usually has time to organize, so anticoagulant therapy is not appropriate. With timely diagnosis, the appointment of anticoagulants can prevent continued thrombosis.

With adequate treatment, including blood transfusions, children after bleeding usually survive. It must be ensured that the transfused blood is compatible, and if possible, maintain the peripheral veins. Avoid the appointment of aspirin. Infection of the upper respiratory tract is subject to serious treatment, as it promotes the development of bleeding.

Somatostatin may be required, and sometimes the use of the Sengsteichen-Blakmore probe.

Endoscopic sclerotherapy is the main method of emergency therapy.

With significant or recurrent bleeding, sclerotherapy can also be used as a delayed measure. Unfortunately, it is not applicable for large varicose-dilated veins of the stomach bottom, so congestive gastropathy remains in such patients.

Surgery to reduce pressure in the portal vein is usually not possible, because there are no veins suitable for shunting. Even veins that have a normal appearance on the veins are unsuitable, which is mainly due to their thrombosis. Children have very small veins, they are difficult to anastomose. The operation also makes it difficult to have many small collaterals.

The results of all types of surgical interventions are extremely unsatisfactory. The least successful splenectomy, after which the greatest percentage of complications is observed. The most favorable results are obtained by shunting (portocaval, mesentericocavalous, splenorenal), but usually it can not be performed.

If, in spite of massive blood transfusion, blood loss progresses, it may be necessary to cross the esophagus and then restore it with a stapler. This method does not manage to stop bleeding from the varicose-dilated veins of the stomach. In addition, the frequency of postoperative complications is significant. The TVSH usually fails.

Bleeding from esophageal varices

Forecasting the gap

Within 2 years after the detection of cirrhosis, bleeding from esophageal varices occurs in 35% of patients; at the first episode of bleeding 50% of patients die.

Between visible at the endoscopy the size of varicose-dilated veins and the probability of bleeding there is a distinct correlation. The pressure inside the varicose veins is less important, although it is known that in order to form varicose enlargement and subsequent bleeding, the pressure in the portal vein should be above 12 mm Hg.

An important factor that indicates a greater likelihood of bleeding is the red spots that can be seen with endoscopy.

To assess the function of hepatocytes in cirrhosis, the Child's system of criteria is used , which includes 3 groups-A, B, and C. Depending on the degree of impairment of hepatocyte function, patients are referred to one of the groups. The Child group is the most important indicator for assessing bleeding probability. In addition, this group correlates with the size of varicose veins, the presence of red spots in endoscopy and the effectiveness of treatment.

Three indicators - the sizes of varicose-dilated veins, the presence of red spots and the hepatic-cell function - allow the most reliable prediction of bleeding.

With alcoholic cirrhosis, the risk of bleeding is highest.

The probability of bleeding can be predicted using Doppler ultrasound. At the same time, the velocity of the blood flow through the portal vein, its diameter, the size of the spleen and the presence of collaterals are estimated. At high values of the stagnation index (the ratio of the portal vein area to the blood flow in it), there is a high probability of early development of bleeding.

Prevention of bleeding

It is necessary to strive to improve the function of the liver, for example by abstaining from alcohol. Avoid aspirin and NSAIDs. Dietary restrictions, such as the exclusion of spices, as well as the administration of H2-blockers of prolonged action, do not prevent the development of coma.

Propranolol is a non - selective beta-blocker that reduces pressure in the portal vein by constricting the vessels of the internal organs and, to a lesser extent, reducing the cardiac output. Reduces blood flow to the hepatic artery. The drug is prescribed in a dose that lowers the pulse at rest by 25% 12 hours after admission. The degree of pressure decrease in the portal vein is not the same in different patients. Taking even high doses in 20-50% of cases does not give the expected effect, especially when cirrhosis is far gone. Pressure in the portal vein should be maintained at a level no higher than 12 mm Hg. It is desirable to monitor the pressure of wedging of the hepatic veins and portal pressure, which is determined endoscopically.

Classification of hepatic-cell function in Child's cirrhosis

Index	Child Child Group
	A	AT	FROM
Serum bilirubin level, μmol / l	Below 34.2	34.2-51.3	Above 51.3
The level of albumin in the serum, g%	Above 3.5	3.0-3.5	Below 3.0
Ascites	No	Easily treatable	Poorly treatable
Neurological disorders	No	The minimum	Precoma, coma
Food	Good	Low	Exhaustion
Hospital lethality,%	5	18	68
Annual survival rate,%	70	70	Thirty

Propranolol should not be prescribed for obstructive lung diseases. This may make it difficult to resuscitate if bleeding occurs. In addition, it promotes the development of encephalopathy. In propranolol, the effect of "first passage" is significantly pronounced, therefore, with far-reaching cirrhosis, in which excretion of the drug by the liver is delayed, unpredictable reactions are possible.

In particular, propranolol somewhat suppresses mental activity.

A meta-analysis of six studies suggests a reliable reduction in the frequency of bleeding, but not lethality. A subsequent meta-analysis of 9 randomized trials revealed a significant reduction in the frequency of bleeding in the treatment with propranolol. Select patients who are shown this treatment is not easy, because 70% of patients with varicose veins of the esophagus do not bleed. Propranolol is recommended for significant dimensions of varicose-veins and for the detection of red spots in endoscopy. With a gradient of venous pressure of more than 12 mm Hg, patients should be treated regardless of the degree of expansion of the veins. Similar results were obtained with the appointment of nadolol. Similar indicators of survival and prevention of the first episode of bleeding were obtained in the treatment of isosorbide-5-mononitrate. This drug can worsen the function of the liver, so it should not be used with far-reaching cirrhosis with ascites.

A meta-analysis of studies on prophylactic sclerotherapy has revealed generally unsatisfactory results. No data on the effectiveness of sclerotherapy in preventing the first episode of bleeding or improving survival. Prophylactic sclerotherapy is not recommended.

Diagnosis of bleeding

In the clinical picture of bleeding from varicose-esophageal veins of the esophagus, in addition to the symptoms observed in other sources of gastrointestinal bleeding, symptoms of portal hypertension are noted.

Bleeding can be mild and manifest more melancholy than bloody vomiting. The intestine can be filled with blood before the bleeding, which lasted several days, is recognized.

Bleeding from varicose-dilated veins with cirrhosis adversely affects hepatocytes. The reason for this may be a reduction in oxygen delivery due to anemia or an increase in metabolic needs due to protein breakdown after bleeding. Reducing blood pressure reduces blood flow in the hepatic artery, which supplies blood to the nodes of regeneration, so that necrosis is possible. Increasing the absorption of nitrogen from the intestine often leads to the development of the hepatic coma. Deterioration of hepatocyte function can cause jaundice or ascites.

Often there is also bleeding not associated with varicose veins: from duodenal ulcers, stomach erosions or Mallory-Weiss syndrome.

In all cases, an endoscopic examination should be performed to identify the source of bleeding). Mandatory also ultrasound for determining the lumen of portal and hepatic veins and for the exclusion of volume education, for example hepatocellular carcinoma.

Based on the biochemical analysis of blood it is impossible to differentiate bleeding from varicose-dilated veins from ulcerative.

Forecast

With cirrhosis, the lethality from bleeding from varicose-veins is about 40% for each episode. In 60% of patients, bleeding recurs before discharge from the hospital; the mortality rate for 2 years is 60%.

The prognosis is determined by the severity of liver-cell insufficiency. The triad of unfavorable signs - jaundice, ascites and encephalopathy - is accompanied by an 80% mortality rate. The annual survival rate at low risk (group A and B by Child) is about 70%, and at high risk (group C on Child) - about 30%. The definition of survival is based on the presence of encephalopathy, prothrombin time and the number of doses of blood transfused within the previous 72 hours. The prognosis is worse with alcoholic liver damage, since he has a more pronounced impairment of hepatocyte function. Abstinence from alcohol significantly improves prognosis. If the activity of chronic hepatitis is maintained, the prognosis is also unfavorable. In primary biliary cirrhosis (PBC), bleeding is relatively well tolerated.

Survival is worse with low blood flow velocity in the portal vein, determined by Doppler ultrasound.

The value of hepatocyte function emphasizes the fact that, with its relative safety, for example in schistosomiasis, noncyrrotic portal hypertension in India and Japan and with portal vein thrombosis, the bleeding prognosis is relatively favorable.

General medical care

When hospitalized for bleeding from varicose veins of the esophagus in all patients, the hepatic-cellular function of Child is evaluated. Bleeding can continue, so careful monitoring is necessary. If possible, it should be carried out in the intensive care unit by specially trained personnel with in-depth knowledge of hepatology. The patient from the very beginning should be observed jointly by the therapist and the surgeon, who must coordinate the treatment tactics.

Classification by Child-Pugh and hospital mortality from bleeding

Group	Number of patients	Hospital mortality
A	65	3 (5%)
AT	68	12 (18%)
FROM	53	35 (68%)
Total	186	50 (27%)

It may require massive blood transfusion. On average, during the first 24 hours, 4 doses are poured, and for the entire period of hospitalization - up to 10 doses. It should avoid the introduction of salt solutions. Excessive volume of circulating blood promotes the resumption of bleeding. Studies in animals have shown that this is due to increased pressure in the portal vein, caused by increased resistance in collateral vessels after bleeding.

There is a threat of insufficient coagulation factors, so it is best to transfuse freshly prepared blood, or freshly prepared erythrocyte mass, or freshly frozen plasma. Transfusion of platelet mass may be required. Immediately intramuscularly administered vitamin K.

Assign cimetidine or ranitidine. Although their effectiveness in patients with severe hepatic-cell insufficiency is not proven in controlled studies, they often develop stressful acute ulcers. With gastrointestinal bleeding against cirrhosis, the risk of infection is high, so antibiotics, such as norfloxacin, should be prescribed to suppress the intestinal microflora.

It is necessary to avoid the appointment of sedatives, and if they are necessary, oxazepam (nosepam, tazepam) is recommended. In patients with alcoholism at risk of delirium development, chlordiazepoxide (chlozepid, elenium) or hemineurin (clomethiazole) can be effective. If portal hypertension is caused by the presynusoidal block and liver function is preserved, the probability of hepatic encephalopathy is low and sedatives can be prescribed freely.

To prevent hepatic encephalopathy in cirrhosis, it is necessary to restrict the intake of protein with food, prescribe lactulose, neomycin 4 g / day, aspirate the contents of the stomach and put phosphate enemas.

With tense ascites, careful paracentesis and the administration of spironolactone are acceptable to reduce intra-abdominal pressure.

To treat bleeding from varicose-veins, numerous methods or combinations thereof are used. These include esophageal esophageal sclerotherapy (the "gold standard"), vasoactive drugs, the Sengsteichen-Blakemore probe, TDS, and emergency surgical intervention. In controlled studies, it was not possible to show a significant advantage of any one treatment method, although all of them can stop bleeding from esophageal varices. The results of sclerotherapy of varicose-veins and the use of vasoactive drugs are surprisingly similar.

Vasoactive drugs

Vasoactive drugs are used for acute bleeding from varicose-dilated veins to reduce portal pressure both before sclerotherapy and in addition to it.

Vasopressin. The mechanism of action of vasopressin is to reduce the arterioles of the internal organs, which causes an increase in resistance to the influx of blood into the intestine. This allows you to reduce bleeding from varicose veins by reducing pressure in the portal vein.

Intravenous for 10 minutes, 20 IU of vasopressin are injected into 100 ml of a 5% glucose solution. Pressure in the portal vein is reduced by 45-60 minutes. It is also possible to prescribe vasopressin in the form of prolonged intravenous infusions (0.4 IU / ml) for no more than 2 hours.

Vasopressin causes a decrease in coronary vessels. Before its introduction it is necessary to remove an electrocardiogram. During the infusion, there may appear colicky abdominal pains, accompanied by emptying of the intestine, face pimple.

Temporal decrease in blood flow in the portal vein and blood pressure contributes to the formation of a clot in the damaged vein and stop bleeding. Reduction of the arterial blood supply to the liver with cirrhosis is undesirable.

With repeated use, the effectiveness of the drug is reduced. Vasopressin can stop bleeding, but it should be used only as a preliminary remedy before beginning treatment with other methods. If bleeding is caused by blood clotting disorders, vasopressin is less effective.

Nitroglycerin is a powerful venous and moderately active arterial vasodilator. Its use in combination with vasopressin can reduce the number of blood transfusions and the frequency of tumescent esophagus, but the incidence of side effects and hospital mortality are the same as with vasopressin. When treating bleeding from varicose-esophageal veins of the esophagus, nitroglycerin is administered intravenously (40 mg / min) or transdermally in combination with vasopressin at a dose of 0.4 IU / ml. If necessary, the doses are increased to provide systolic blood pressure at a level of more than 100 mm Hg.

Terlipressin is a more stable and long-acting substance than vasopressin. It is administered intravenously in jet at a dose of 2 mg, and then 1 mg every 4 hours for 24 hours. The pressure in the esophageal varicose veins decreases, which helps to stop the bleeding.

Somatostatin affects the smooth muscles and increases resistance in the arteries of the internal organs, thereby reducing pressure in the portal vein. In addition, it suppresses the action of a number of vasodilating peptides, including glucagon. It causes a small number of serious side effects.

In a controlled study, the frequency of recurrent bleeding was reduced by a factor of 2 compared with that in the placebo-treated control group, the frequency of blood transfusions and the use of esophageal tamponade decreased by half. In patients of group C on Child, the drug was ineffective. In one study, somatostatin was better than vasopressin, stopped bleeding, in another the results were contradictory. In general, treatment with somatostatin is safe and as effective as sclerotherapy.

Intravenous infusion of the drug adversely affects blood circulation in the kidneys and water-salt metabolism in the tubules, therefore, with ascites, it should be administered with caution.

Octreotide is a synthetic analogue of somatostatin, which shares with it identical 4 amino acids. His T1 / 2 is much larger (1-2 hours). It is shown that in the treatment of acute bleeding from esophageal varices, octreotide is as safe and effective as sclerotherapy, but does not reduce the frequency of early recurrence of bleeding.

Scheduled sclerotherapy of the esophagus

Scheduled sclerotherapy of varicose-dilated esophagus veins is less effective than an emergency, undertaken to stop bleeding. Injections are given at an interval of 1 week until all varicose-veins are not thrombosed. The frequency of repeated bleeding decreases.

Between 30% and 40% of varicose veins after sclerotherapy are enlarged annually. Repeated procedures lead to fibrotic esophagitis, in which varicose veins are obliterated, but varicose-dilated veins of the stomach increase and may bleed constantly.

Endoscopic ligation of varicose-dilated veins

The method used does not differ from ligation of hemorrhoidal veins. The veins are bandaged with small elastic rings. In the lower part of the esophagus, a conventional gastroscope with an end view is inserted and an additional probe is conducted under its control. Then the gastroscopy is removed and fixed to its end by a ligating device. After that, the gastroscope is reintroduced into the distal esophagus, a varicose-dilated vein is identified and aspirated into the lumen of the ligation device. Then, by pressing the wire lever attached to it, an elastic ring is put on the vein. The process is repeated until all varicose-dilated veins are ligated. On each of them impose from 1 to 3 rings.

Sclerotherapy of varicose-veins

Prophylactic	Emergency	Scheduled
Efficacy not proven	Need experience Ceases bleeding Impact on survival (?)	Mortality from bleeding decreases Numerous complications The commitment of the patient to treatment is important Survival does not change

The method is simple and gives fewer complications than sclerotherapy, although more sessions are required to ligate varicose veins. The most common complication is transient dysphagia; the development of bacteremia is also described. An additional probe can cause a perforation of the esophagus. In places where the rings are applied, ulcers can subsequently develop. Rings sometimes slip, causing massive bleeding.

Ring ligation allows you to stop acute bleeding from esophageal varices in the esophagus no less effectively than sclerotherapy, but it is more difficult to produce in conditions of continued bleeding. It prevents repeated episodes of bleeding, but does not affect survival. This method can replace generally more accessible endoscopic sclerotherapy only in specialized centers. It can not be combined with sclerotherapy.

Emergency Surgery

With the introduction of sclerotherapy, vasoactive drugs, balloon tamponade and especially TSSH, surgical interventions are used much less often. The indication to them is mainly the ineffectiveness of all the listed methods of treatment. Bleeding can be effectively stopped by an emergency portocaval shunting. Mortality, as well as the incidence of encephalopathy in the postoperative period, are significant among patients in group C. If the bleeding is massive and recurs after 2 sclerotherapy procedures, TSS is the method of choice. Alternative methods of treatment are the emergency formation of mesentericocaval anastomosis, or the imposition of a narrow (8 mm) portocaval shunt, or the intersection of the esophagus.

Emergency intersection of the esophagus with a stapler

Under general anesthesia, anterior gastrosome is performed and the apparatus is inserted into the lower third of the esophagus (Figures 10-59). Immediately above the cardia, a ligature is applied, which draws the esophagus wall between the head and the body of the apparatus. Then stitch and cross the esophagus wall. The apparatus with the excised wall of the esophagus is removed. The wound of the stomach and anterior abdominal wall is sutured. Intersection of the esophagus by means of the device always allows to stop a bleeding. However, one third of patients die during hospitalization from liver failure. Intersection of the esophagus with a stapler has become a recognized method of treating bleeding from esophageal varices. Time of operation is small, mortality is low, complications are few. The operation is not indicated for prophylactic purposes or routinely. Within 2 years after the operation, varicose veins usually recur and are often complicated by bleeding.

Prevention of bleeding recurrence

Repeated bleeding from varicose veins develops within 1 year in 25% of patients in group A, 50% in group B, and 75% in group C. One of the possible methods of preventing recurrence is prescribing propranolol. In the first controlled study, in a group of patients with alcoholic cirrhosis of the liver with large varicose-dilated veins and a satisfactory general condition, a significant decrease in the frequency of relapses was revealed. Data from other studies have been controversial, which is probably related to the type of cirrhosis and the number of alcoholics included in the study. With decompensated cirrhosis, propranolol therapy is ineffective. The later treatment is started, the better the results, since the patients from the highest risk group are already dying by this time. In patients with a low risk, the effectiveness of propranolol does not differ from that of sclerotherapy. The use of propranolol reduces the risk of recurrence of bleeding, but probably has little effect on survival, it is justified in portal gastropathy. The combination of nadolol and isosorbide mononitrate is more effective than sclerotherapy, reduces the risk of recurrence of bleeding.

Planned sclerotherapy of varicose-extended veins of the esophagus is carried out at weekly intervals until all the veins are thrombosed. Usually, from 3 to 5 procedures are required, they can be performed on an outpatient basis. After sclerosing, frequent endoscopic observation and repeated injections of drugs are not indicated, since they do not increase survival. Sclerotherapy should be performed only with relapses of bleeding. Scheduled esophageal sclerotherapy reduces the frequency of bleeding recurrences and the need for blood transfusions, but does not affect survival in the long-term.

If sclerotherapy is ineffective, as a measure of emergency help resort to shunting - the formation of a portocaval or splenorenal shunt or to the TSSH.

Portosystemic shunting

Portosystemic shunting is performed in order to reduce pressure in the portal vein, maintenance of the common hepatic and, in particular, portal blood flow and, most importantly, to reduce the risk of hepatic encephalopathy complicating portal hypertension. None of the current methods of shunting allows you to fully achieve this goal. Survival of patients is determined by the functional reserve of the liver, since after the shunting the hepatic-cellular function worsens.

Portage shunting

In 1877, Eck first performed portocaval shunting on dogs; currently it is the most effective method of reducing portal hypertension.

The vein is connected to the inferior vena cava or the end to the side with a portal vein ligation, or side to side, without disturbing its continuity. The pressure in the portal and liver veins decreases, and the blood flow increases in the hepatic artery.

The end-to-side coupling probably results in a more pronounced pressure decrease in the portal vein, about 10 mmHg. Technically, this operation is easier.

Currently, the portocaval shunt is rarely applied, as it is often complicated by encephalopathy. Decreased hepatic blood flow impairs liver function. This complicates the subsequent transplantation of this organ. The application of the portocaval shunt is still resorted to after a bleeding stop, with a good functional reserve of the liver, in the absence of the opportunity to observe the patient in a specialized center or if there is a risk of bleeding from varicose-dilated veins of the stomach. It is also shown in the initial stages of primary biliary cirrhosis, with congenital liver fibrosis with a preserved function of hepatocytes and obstruction of the portal vein in the region of the liver gates.

After portocaval bypass, the probability of ascites, spontaneous bacterial peritonitis and hepatorenal syndrome decreases.

In assessing the indications for bypass surgery, it is important to have an indication in the history of bleeding from varicose veins of the esophagus, the presence of portal hypertension, the safety of the portal vein, the age younger than 50 years, the absence of episodes of hepatic encephalopathy in the anamnesis, belonging to the A or B group on Child. In patients older than 40 years, survival after surgery is lower and in 2 times the incidence of encephalopathy.

Mesentericovascular shunting

With mesentericocaval shunting, a shunt made of a dacron prosthesis is sutured between the superior mesenteric and inferior vena cava.

The operation technique is simple. The lumen of the portal vein does not close, but the blood flow along it becomes insignificant. Over time, occlusion of the shunt often occurs, after which bleeding recurrences may occur. Mesentericocaval shunt does not complicate liver transplantation in the future.

Selective "distal" splenorenal shunting

With selective splenorenal shunting, varicose-dilated veins pass through the gastroesophageal junction, resulting in blood flowing through the short gastro-spleen veins into the spleen vein anastomosed to the left renal. It was assumed that the circulation in the portal vein will be preserved, but, as it turned out, this does not happen.

The preliminary results of the operation were satisfactory; The mortality rate was 4.1%, the incidence of encephalopathy was 12%, and the 5-year survival rate was 49%. Subsequently, in a larger randomized trial, patients with alcoholic cirrhosis of the liver found that the death rate and frequency of encephalopathy did not differ from those of non-selective splenorenal shunting. In non-alcoholic cirrhosis, more favorable results were obtained, especially in cases where varicose veins of the stomach were the main problem. In addition, the use of this method is justified for bleeding from varicose-dilated veins in schistosomiasis, non-cirrhotic portal hypertension with an enlarged spleen vein. The operation does not interfere with the subsequent transplantation of the liver.

The technique of distal splenorenal shunting is complex, and the surgeons who own it are few.

General results of portosystemic shunting

In the low-risk group, the operational mortality rate is approximately 5%. In the high-risk group, it reaches 50%.

When the operation is performed on the portal vein damaged by the pathological process, the shunt is often closed; this complication often ends in death, the cause of which is often liver failure.

With the normal functioning of the portocaval anastomosis, the end is applied to the side, bleeding from the varicose-dilated esophagus and stomach can be prevented.

After bypass, venous collaterals of the anterior abdominal wall disappear, and the size of the spleen decreases. With endoscopy after 6-12 months, varicose veins do not reveal.

If the shunt is nonselective, both portal pressure and hepatic blood flow decrease. As a result, the liver function worsens.

In the postoperative period, jaundice often develops due to hemolysis and impaired liver function.

Decrease in pressure in the portal vein on the background of maintaining a low level of albumin causes edema of the ankles. The increase in cardiac output, combined with heart failure, can also play a role in its development.

The passage of the shunt is monitored by ultrasound, CT, MRI, Doppler ultrasound or angiography.

Hepatic encephalopathy can be transient. In 20-40% of cases, chronic changes develop and in about a third of cases - personality changes. Their frequency is higher the larger the diameter of the shunt. Most likely their development with the progression of liver disease. Encephalopathy is more common in elderly patients.

In addition, shunting can be complicated by paraplegia due to myelopathy, parkinsonism and symptoms of cerebellar involvement.

Transjugular intrahepatic portosystemic shunting

The first attempts to create intrahepatic portosystemic shunts in dogs and in humans proved to be unsuccessful, as the communication between the hepatic and portal veins created with the help of a balloon quickly closed. The preservation of the shunt patency was possible when using a straightening Palmaz stent, which is installed between the intrahepatic branch of the portal vein and the branch of the hepatic vein.

Usually, TSS is performed to stop bleeding from varicose veins of the esophagus or stomach. However, before resorting to this method of treatment, it is necessary to be convinced of the failure of other methods, in particular sclerotherapy and the introduction of vasoactive drugs. With continued bleeding, the results are unfavorable. The procedure is performed under local anesthesia after premedication with sedatives. Under the supervision of ultrasound, bifurcation of the portal vein is detected. Through the jugular vein, the middle hepatic vein is catheterized, and a needle is passed through this catheter into the branch of the portal vein. A needle is inserted through the needle and a catheter is inserted through it. The needle is removed and the pressure gradient in the portal vein is determined. The puncture channel is dilated with a balloon, followed by angiography. Then insert a metal balloon straightening stent Palmaz or self-expanding metal stent Wallstent, having a diameter of 8-12 mm. The diameter of the stent is selected so that the portal pressure gradient is below 12 mm Hg. If portal hypertension is preserved, parallel to the first one, you can install a second stent. The entire procedure is performed under the supervision of ultrasound. It lasts 1-2 hours. TSSH does not interfere with the subsequent transplantation of the liver.

TVPSH is a technically complex intervention. With sufficient experience of the staff, it can be performed in 95% of cases. However, according to one study, technical difficulties, early recurrence of bleeding, stenosis and thrombosis of the shunt required a re-TBT in the period of one hospitalization of the patient in 30% of cases. In 8% of cases, even after repeated intervention, it was not possible to stop the bleeding.

Mortality in the stent is less than 1%, and lethality for 30 days - from 3% to 13%. Intervention can be complicated by bleeding - intra-abdominal, biliary or under a capsule of the liver. It is possible to move the stent, and the Wallstent stent has to be stretched to its former state with a loop.

An infection often develops, which can lead to death. Antibiotics should be administered prophylactically. If renal dysfunction and after intravenous injection of a large amount of contrast agent, renal failure may develop. The steel mesh of the stent can damage the red blood cells and cause intravascular hemolysis. If the stent is incorrectly inserted into the right hepatic artery, a liver infarction develops. Hyperplenism after shunting remains.

Stenosis and stent occlusion. A low pressure gradient between the portal and the hepatic vein promotes the development of occlusion. The most important reason for closing the stent is low blood flow along it. It is important to control the stent patency in dynamics. This can be done through routine portography or Doppler and duplex ultrasound, which give a semi-quantitative assessment of the functional state of the shunt. Occlusion of the shunt often leads to a relapse of bleeding from varicose-dilated veins.

Early stent occlusion is observed in 12% of cases, usually due to thrombosis and is associated with technical difficulties in its installation. Late occlusions and stenosis are associated with excessive changes in the intima of the hepatic vein site connected to the stent. More often they occur in patients of group C on Child. Stenosis and occlusion of the stent develop in a third of patients for 1 year and two-thirds for 2 years. The frequency of these complications depends on the effectiveness of the diagnosis. When the stent is occluded, its revision is performed under local anesthesia. You can expand the lumen of the stent by percutaneous catheterization or install another stent.

Stop bleeding. TSSH reduces the portal pressure by approximately 50%. If bleeding is caused by portal hypertension, then it stops regardless of whether the bleeding vein is localized in the esophagus, stomach or intestine. This is especially important for bleeding that does not stop after sclerotherapy and occurs against a background of decreased liver function. TVSH more effectively reduces the frequency of bleeding recurrence than sclerotherapy, but its effect on survival is negligible. The frequency of recurrences of bleeding after 6 months is from 5% to 19%, and after 1 year - 18%.

Encephalopathy after TSSH. The imposition of a non-selective portosystemic shunt side by side causes a decrease in portal blood supply to the liver, so the liver function deteriorates after TSSH. It is not surprising that the incidence of encephalopathy after this intervention is almost the same (25-30%), as after surgical portocaval shunting. In 9 out of 30 patients with established stent 24 episodes of hepatic encephalopathy were noted, and in 12% they arose de novo. The risk of developing hepatic encephalopathy depends on the age of the patient, the Child group and the size of the shunt. Encephalopathy is most pronounced during the first month after the operation. With spontaneous closure of the stent, it decreases. It can be reduced by installing another stent of smaller size into the functioning intrahepatic stent. Resistant encephalopathy is an indication for liver transplantation.

Hyperdynamic type of blood circulation, characteristic of cirrhosis, is aggravated after TSSH. The cardiac output and volume of circulating blood increase. Possible stagnation of blood in internal organs. If the patient suffers from concomitant heart disease, heart failure may develop.

Other indications. The intrahepatic stent, which is established with TSSH, constituting a portosystemic shunt, the superimposed end in the side, makes it possible to reduce ascites in patients of Group B by Child. In controlled studies, however, it was no more effective than traditional treatments, and did not increase survival.

With hepatorenal syndrome, TSSH improves the condition of patients and increases their chances of waiting for liver transplantation.

TVSH is effective in ascites and chronic syndrome of Budd Chiari.

Conclusions. TSSH is an effective method of stopping acute bleeding from varicose veins of the esophagus and stomach with ineffective sclerotherapy and vasoactive drugs. Its use in recurrent bleeding from varicose-esophageal veins of the esophagus should probably be limited to cases of hepatic-cell failure in which liver transplantation is planned.

The method is technically complex and requires a certain amount of experience. Persistent therapeutic effect is hampered by complications such as stent occlusion and the development of hepatic encephalopathy. TSSH is a simpler method of treatment and causes fewer complications than surgical imposition of a portosystemic shunt. It can be expected that complications in the long-term after stent placement will be similar to those observed with surgical shunt insertion.

Liver transplantation

With cirrhosis of the liver and bleeding from varicose veins, the cause of death may not be hemorrhage itself, but liver-cell insufficiency. In these cases, the only way out is liver transplantation. Survival after transplantation does not depend on whether sclerotherapy or portosystemic shunting has been performed before. Survival after sclerotherapy with subsequent liver transplantation is higher than only after sclerotherapy. This may be due to the fact that patients with lower risk were sent to the transplant centers. Unstable bleeding from varicose veins and the terminal stage of liver disease are an indication for transplantation of this organ.

The previously imposed portocaval shunt technically hampers transplantation, especially if manipulations were performed at the gates of the liver. Splenorenal and mesentericocaval shunts, as well as TSSH, are not a contraindication to liver transplantation.

After transplantation, most of the hemodynamic and humoral changes caused by cirrhosis are reversed. The blood flow in the unpaired vein is normalized slowly, which indicates a slow closure of the portal collaterals.

Pharmacological effect on the blood flow in the portal vein

The syndrome of portal hypertension is one of the manifestations of the hyperdynamic type of circulation with an increase in cardiac output and a decrease in peripheral resistance. This syndrome significantly changes the activity of the autonomic nervous system. The involvement of a variety of hormonal factors indicates the possibility of pharmacological effects on certain manifestations of portal hypertension. Theoretically, the pressure (and blood flow) in the portal vein can be reduced by reducing cardiac output, reducing blood flow by vasoconstriction of the internal organs, dilatation of the veins of internal organs, reducing intrahepatic vascular resistance, or, finally, surgical portocaval shunting. It should strive to maintain blood supply to the liver and its function, therefore, methods of reducing pressure by decreasing vascular resistance are more preferable than by decreasing blood flow.

Decreased cardiac output

Reductions in cardiac output can be achieved by blocking beta 1 -adrenoceptors of the myocardium. Partially, this effect is given by propranolol. Metoprolol and atenolol - cardioselective blockers - reduce pressure in the portal vein less efficiently than propranolol.

Reduction of blood flow through the portal vein

The use of vasopressin, terlipressin, somatostatin and propranolol, which cause vasoconstriction in the internal organs, has already been discussed.

Portal and intrahepatic vasodilators

Smooth muscles of the portal vein contain beta _1- adrenoreceptors. Probably, the portositem collaterals have already been maximally expanded, the muscular layer in them is poorly developed. They are weaker than large veins, they respond to vasodilating stimuli. A significant reduction in the vessels of the portal system causes serotonin, acting through S2-receptors. The sensitivity of collaterals to serotonin can be increased. The serotonin inhibitor ketanserin causes a decrease in portal pressure with cirrhosis. Its wide use as an antihypertensive drug is prevented by side effects, including encephalopathy.

With cirrhosis of the liver, it is also possible to influence the tone of the muscles of the venous wall. On an isolated perfused liver it was shown that an increase in vascular resistance in the portal vein can be reduced by vasodilators, including prostaglandin E ₁ and isoprenaline. Apparently, their action is directed to contractile myofibroblasts. Decrease in portal pressure is possible when taking nitroglycerin, 5-isosorbide dinitrate or mononitrate and is probably due to systemic vasodilation. In addition, these drugs cause a slight decrease in intrahepatic resistance in the isolated liver and in cirrhosis.

It is shown that verapamil - a blocker of calcium channels - reduces the pressure gradient in the portal vein and intrahepatic resistance. However, this effect could not be proved with the appointment of patients with cirrhosis of the liver. Alcoholic cirrhosis increases the activity of the sympathetic nervous system. Intravenous administration to patients with alcoholic cirrhosis of the clonidine - agonist a-adrenergic receptors of the central action - led to a decrease in postsynusoidal vascular resistance. Reducing systemic blood pressure limits the use of this drug.

Conclusion: Pharmacological control

The relationship between cardiac output, system resistance and blood flow and portal resistance and blood flow is not easy to assess. Between the hepatic arterial blood flow and the portal blood flow there are reciprocal relationships - an increase in one entails a decrease in the other.

In the future, more appropriate drugs for the treatment of portal hypertension can be expected.

[1], [2], [3], [4]