Portal hypertension syndrome symptoms treatment features

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The following forms of portal hypertension are distinguished depending on the location of the obstruction that disrupts the blood flow:

  • Prehepatic form – blood flow is disturbed until the portal vein enters the liver.
  • Intrahepatic portal hypertension – an obstruction of blood flow is localized in that part of the portal vein that is located ins >

Portal hypertension can be mixed. In this case, obstacles to normal blood flow are formed in several places at once.

Signs and clinical manifestations

Most often, patients encounter the following signs of pathology:

  • splenomegaly (in some cases with PG, the first symptom is considered to be an increase in the size of the spleen);
  • varicose veins of the esophagus, stomach, abdomen (jellyfish head) and anus (hemorrhoids);
  • ascites – a pathological accumulation of fluid in the abdominal cavity, which can be combined with hydrothorax;
  • pain in the abdomen and right hypochondrium;
  • lack of appetite, bloating;
  • dyspepsia;
  • symptoms of intoxication;
  • general weakness;
  • weight loss
  • swelling of the ankles;
  • erosion on the mucous system of the digestive system.

If the cause of portal hypertension is blood stasis against a blockage of the hepatic ducts, the patient’s skin turns yellow. Hypersplenism is sometimes diagnosed – a decrease in the number of red blood cells, white blood cells, blood platelets due to increased spleen function.

Signs of GHG in children deserve special attention. They are only extrahepatic, manifested by enlarged spleen, varicose veins of the esophagus, hemorrhages. In this case, bleeding is extremely rare.

Causes of GHG Syndrome

Changes in the parenchyma (tissue) of the liver

Group of reasonsdisease
Hepatitis, tumors of various etiologies, parasitic infestations (schistosomiasis), cirrhosis, infections of various origins, alcoholism
Primary or secondary biliary cirrhosis, tumor growth in the common or bile duct, pancreatic cancer, injuries of the bile ducts, including operating rooms (adhesions, dressings, injuries), cholelithiasis (cholelithiasis)
Toxic lesionsIntoxication with poisons, chemicals, ethanol, nicotine, poisonous mushrooms, drugs
Heart diseases (restrictive cardiomyopathy, constrictive pericarditis), blood vessels, injuries, burns
Sepsis, purulent infections, DIC – disseminated intravascular coagulation or thrombohemorrhagic syndrome, bleeding
Narrowing of the lumen of blood vesselsCongenital atresia, tumor, thrombosis, stenosis

The causes of intrahepatic or perhepatic bleeding are distinguished as a separate group due to the severity of possible complications. If the vessels of the biliary system of the liver are blocked, then the blood flow rate decreases, and the pressure on the walls increases. Portocaval anastomoses, the capillary system between the portal portal and vena cava, begin to work. This can lead to large blood loss, death. In addition to this bleeding provoke:

  • an increase in venous vessels of the stomach, esophagus with a violation of their integrity;
  • vascular bleeding between the vena cava and the umbilical vein;
  • bleeding between the inferior vena cava and part of the rectum (hemorrhoids);
  • splenomegaly (more than half a liter of blood accumulates in the spleen, while the norm is only 50 ml);
  • any vascular pathology in the portal system.

There are a number of factors that exacerbate the course of the pathology, these are:

  • infections of different genesis;
  • active treatment with diuretics;
  • alcoholism;
  • complicated surgical interventions;
  • one-sided protein nutrition (meat diet).

Bleeding with ascites, cachexia, cirrhosis is the destiny of all patients who abuse alcohol for a long time.

In children, portal hypertension is provoked by:

  • abnormal structure of the portal vein;
  • umbilical vein thrombosis in the neonatal period due to incorrect umbilical cord dressing;
  • viral or fetal (congenital) hepatitis of newborns;
  • cholangiopathy (the inability of the bile duct system to prov >

Inflammation of the biliary tract of a child may be the result of non-compliance by the mother with a diet during pregnancy, lactation, taking medications, a latent infection.

Etiological factors are diverse, they can be combined into several groups:

  • Liver diseases with damage to its parenchyma acute hepatitis, chronic hepatitis, liver tumors, parasitic liver lesions.
  • Diseases that occur with intra- and extrahepatic cholestasis: primary biliary cirrhosis, tumors of the hepatic and common bile duct, gallstone disease, pancreatic head tumor, damage and ligation of the bile duct during surgery.
  • Toxic liver damage: poisoning with hepatotropic poisons, including mushrooms, some medications.
  • Diseases of the heart and blood vessels, extensive injuries and burns.
  • Critical conditions in injuries, operations, sepsis, DIC.

In addition to etiological, resolving factors are distinguished that give impetus to the deployment of the clinical picture of portal hypertension syndrome. These include esophageal and gastrointestinal bleeding, infections, sedatives and tranquilizers, massive diuretic therapy, alcohol intake, excessive consumption of animal proteins, surgical procedures Causal factors of portal hypertension can be grouped into three blocks: subhepatic, intrahepatic and posthepatic. In turn, the intrahepatic block can be presinusoidal, when an obstruction of blood flow inside the liver occurs in front of the hepatic hemocapillaries-sinusoids; sinusoidal – as a result of obstruction of blood flow inside the liver during the hepatic sinusoid – and postsinusoidal when an obstacle occurs after the passage of blood through sinusoids.

  • Factors of the prehepatic block: compression or thrombosis of the portal or splenic veins, portal pylephlebitis, aneurysms of the splenic and hepatic arteries, splenomegaly in myeloproliferative diseases, Crewellier-Baumgarten syndrome. The latter occurs in 3-4% of cases among all diseases accompanied by portal hypertension.
  • Factors of intrahepatic presinusoidal portal hypertension: sarcoidosis, alveococcosis, schistosomiasis, cirrhosis, Gaucher disease, polycystic tumors, tumors, nodular transformation of the liver. Intrahepatic hepatitis makes up 85-90% of all cases of GHG.
  • Causes of intrahepatic sinusoidal portal hypertension: chronic hepatitis, tumors, cirrhosis.
  • Causes of postsinusoidal portal hypertension: central lobular liver fibrosis of alcoholic etiology, cirrhosis, veno-occlusive liver disease.
  • Causes of the posthepatic block: Budd-Chiari disease and syndrome, constrictive pericarditis, thrombosis, or compression of the inferior vena cava. The frequency of the posthepatic block is 10-12%.

Portal hypertension: symptoms

Clinical manifestations. Various hemodynamic profiles of portal hypertension determine the diversity of clinical manifestations. The initial and late symptoms of portal hypertension, as well as its stages, are distinguished.

The initial signs of hypertension are characterized by dyspeptic manifestations, flatulence, unstable stools, pain in the epigastrium, left and right hypochondria, in the iliac regions, a feeling of fullness of the stomach after eating. Late manifestations include splenomegaly, hypersplenism, ascites, varicose veins of the esophagus and cardiac section of the stomach, hemorrhagic syndrome.

Often the first symptom of portal hypertension is splenomegaly, which is detected during examination or during instrumental research methods. The severity of splenomegaly, as a rule, is proportional to the level of pressure in the portal vein. The size of the spleen can decrease after bleeding from the varicose veins of the esophagus, stomach, umbilical (caputmedusae) and anorectal regions, lowering the pressure in the vessels of the portal vein system.

With an increase in the size of the spleen, a manifestation of hypersplenism is often observed: a decrease in the level of platelets, leukocytes, red blood cells. Severe polycytopenia indicates a far advanced stage of the process and is a poor prognostic sign.

Sometimes the first sign is bleeding from varicose veins of the esophagus or heavy hemorrhoidal bleeding. Factors contributing to the occurrence of bleeding from these vessels (esophagus and stomach) are a violation of the integrity of their mucous membranes, increased permeability of the vascular wall, an increase in intra-abdominal pressure, disturbances in the blood coagulation system, etc. Bleeding usually begins suddenly, is prone to relapse, develops rapidly acute posthemorrhagic anemia. In a number of patients, ascites is the leading initial syndrome. The presence of ascites usually does not cause difficulties in diagnosis and can be determined with a high degree of probability during anamnesis and an objective examination. Most patients note a recent relatively rapid increase in abdominal volume and the appearance of ankle edema. Due to the concomitant loss of muscle mass, ascites is not always accompanied by an increase in the total weight of patients. Stretching the flanks and shifting the blunting zone in them is a fairly reliable physical method for detecting ascites.

In ascites caused by liver diseases, a low concentration of sodium in the urine is determined in patients. When examining such patients, the dilated veins of the anterior abdominal wall are visible, sometimes the enlarged venous trunks seem to extend from the navel (“jellyfish head”). Patients are concerned about severe flatulence, ascites soon appears and grows. It should be noted some features of the clinical course of the prehepatic block of portal hypertension, which often appear at a young age. History often has intermittent fever, inflammatory diseases of the abdominal cavity, abdominal trauma, malaria, and tuberculosis. Objectively, portal hypertension is most often manifested by splenomegaly, hypersplenism and dilated veins of the esophagus. The liver is not enlarged. Echographic data largely depends on the cause of the prehepatic block.

With thrombosis of the portal or splenic vein, structures of different densities are visible in their lumen, and sometimes a cavernous transformation of the portal vein is determined. Subhepatic GHG usually develops slowly, sometimes with multiple esophageal-gastric bleeding. In cases where the block is caused by compression of the portal vein from the outside, it is possible to determine the volume formation compressing the vein, a tumor of the head of the pancreas or liver; narrowing of the lumen of the vein is observed in a small area.

Patients with an intrahepatic block have a history of past liver diseases, chronic intoxication. The early “symptoms” of hypertension are persistent dyspeptic syndrome, flatulence, unstable stool, and weight loss. Varicose veins with possible bleeding and ascites are late symptoms of PG. In contrast to the subhepatic form, hypertension with intrahepatic block is often the first bleeding from the dilated veins is fatal, since it leads to a deterioration in liver function. The liver is often enlarged, but can be reduced in size.

Splenomegaly is almost always noted. Echographically for the intrahepatic block, in addition to the general signs of portal hypertension (dilatation of the portal system veins), amputation of peripheral intrahepatic branches of the portal vein is also characteristic; recanalization of umbilical and paraumbilical veins, increase in the diameter of the hepatic and splenic arteries. Clogged hepatic venous pressure (HPS) is elevated, while free portal pressure (SPD) and intracranial pressure (VSP) are normal.

The clinical picture of the (sup-) posthepatic block largely depends on the underlying disease. Severe hepatomegaly, moderate splenomegaly are observed. The suprahepatic form of hypertension is manifested by the early development of ascites, which is not amenable to diuretic therapy, accompanied by pain in the liver. Echographic block criteria – a significant increase in the lumen of the hepatic veins, a moderate increase in the diameter of the portal and splenic veins. Often, occlusion of the inferior vena cava above the confluence of the hepatic veins is detected. SPD and VVD are increasing, while HPVD remains normal.

Bleeding from varicose veins of the esophagus and stomach is one of the most serious complications of portal hypertension in cirrhosis.

The following risk factors for bleeding from varicose veins of the esophagus and gastric mucosa are noted:

  • III degree of expansion of the veins of the esophagus and stomach, leading to a concentric narrowing of the lumen of the esophagus.
  • The presence of erosion and red or cherry spots (petechiae) on the surface of varicose veins and gastric mucosa.
  • Violation of the functional state of the liver, determined by Child-Pugh.

Bleeding of portal genesis due to increased portal pressure. The source can be anatomically clearly localized and associated with rupture of the venous vessel, which is the most common variant of hemorrhage. In accordance with the anatomical localization of the sources of bleeding, esophageal and gastric hemorrhages, as well as bleeding from “exotic varices”, are distinguished.

Esophageal varicose veins are the most common cause of bleeding due to the anatomical features of the lower third of the esophagus (increased vascular resistance, the presence of several venous levels connected by communicants, the surface location of veins). 50% of patients with varicose veins of the esophagus develop esophageal bleeding.

Varicose veins of the stomach occur in 2-70% of patients. Due to the deeper location of varicose veins of the stomach, their endoscopic diagnosis is difficult. Gastric bleeding from BPH is potentially more dangerous, so a clear clinical distinction is needed between esophageal and gastric bleeding.

Bleeding from ectopic varicose veins is a rather rare phenomenon and causes certain difficulties in diagnosis. “Ectopic varices” are more characteristic of the extrahepatic form of PG. In addition, they can be a consequence of endoscopic obliteration of the veins of the esophagus. The indicated type of HRV can be a source of bleeding in 5% of cases with intrahepatic and in 40% with extrahepatic form of PG.

The development of a syndrome such as portal gastropathy is caused by portohypertensive changes – ectasia of the capillaries and venules of the mucous membrane and submucosal layer, edema and hyperplasia of the mucous membrane. In patients with manifestations of GH, up to 25% of bleeding may be due to these changes. T. McCormack distinguishes two degrees of severity of mucosal changes in portal gastropathy:

  • Light with pinkish-red spots on the mucous membrane, superficial redness and / or mosaic-like swelling of the mucous membrane.
  • Severe is characterized by the presence of diffuse dark red spots or hemorrhage.

T. Mc Cormack proposed a 4-point scale for assessing the severity of portal gastropathy:

  • lack of gastropathy;
  • mild degree;
  • severe degree;
  • portal gastropathy complicated by bleeding.

Portal gastropathy occurs more often with cirrhosis of the liver than with hypertension of a different genesis.

Clinical manifestations. Various hemodynamic profiles of portal hypertension determine the diversity of clinical manifestations. The initial and late symptoms of portal hypertension, as well as its stages, are distinguished.

The initial signs of hypertension are characterized by dyspeptic manifestations, flatulence, unstable stools, pain in the epigastrium, left and right hypochondria, in the iliac regions, a feeling of fullness of the stomach after eating. Late manifestations include splenomegaly, hypersplenism, ascites, varicose veins of the esophagus and cardiac section of the stomach, hemorrhagic syndrome.

Often the first symptom of portal hypertension is splenomegaly, which is detected during examination or during instrumental research methods. The severity of splenomegaly, as a rule, is proportional to the level of pressure in the portal vein. The size of the spleen can decrease after bleeding from the varicose veins of the esophagus, stomach, umbilical (caputmedusae) and anorectal regions, lowering the pressure in the vessels of the portal vein system.

With an increase in the size of the spleen, a manifestation of hypersplenism is often observed: a decrease in the level of platelets, leukocytes, red blood cells. Severe polycytopenia indicates a far advanced stage of the process and is a poor prognostic sign.

Sometimes the first sign is bleeding from varicose veins of the esophagus or heavy hemorrhoidal bleeding. Factors contributing to the occurrence of bleeding from these vessels (esophagus and stomach) are a violation of the integrity of their mucous membranes, increased permeability of the vascular wall, increased intra-abdominal pressure, disturbances in the blood coagulation system, etc.

Bleeding usually begins suddenly, is prone to relapse, and acute posthemorrhagic anemia develops rapidly. In a number of patients, ascites is the leading initial syndrome. The presence of ascites usually does not cause difficulties in diagnosis and can be determined with a high degree of probability during anamnesis and an objective examination.

Most patients note a recent relatively rapid increase in abdominal volume and the appearance of ankle edema. Due to the concomitant loss of muscle mass, ascites is not always accompanied by an increase in the total weight of patients. Stretching the flanks and shifting the blunting zone in them is a fairly reliable physical method for detecting ascites.

Classification

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According to the form

Given the scale of high pressure coverage of different zones, two forms of GHG are distinguished:

  • total – high pressure throughout the portal portal vein pool;
  • segmental – at the level of blood flow of the splenic vein (mesenteric vessels, portal vein pressure is normal).

Obviously, the first option can lead to more serious negative consequences.

By sight

GHGs are also classified according to the localization of the venous block:

  1. intrahepatic view (up to 90% of all cases of GHG) is divided into:
  • sinusoidal – an obstacle to blood flow inside the sinuses of the liver (hepatitis, cirrhosis, tumors, cysts);
  • presinusoidal – a block in front of the capillaries (schistosomiasis, sarcoidosis, polycystic);
  • postsinusoidal – a block outside the capillaries (liver fibrosis, cirrhosis, alcoholic disease).
  1. The prehepatic view (about 4% of the pathology) occurs due to stenosis or thrombosis of the portal, splenic vein vessels (infections, inflammation, adhesions).
  2. Posthepatic (about 10%) is the result of a thrombus or stenosis of the inferior vena cava (constrictive pericarditis, Budd-Chiari syndrome).
  3. Mixed – extrahepatic and intrahepatic PG due to obstruction of the portal vein blood flow, which is combined with cirrhosis, for example.

All types of GHGs imply a mandatory violation of the rheological (hydrodynamic) properties of blood.

There are four stages of pathology:

  • functional (debut or initial) – dyspepsia, flatulence, heaviness in the right hypochondrium;
  • compensated (with moderate manifestations) – splenomegaly, varicose veins of the esophagus – all mild;
  • decompensated (expressed) – all symptoms are maximal, ascites joins;
  • complicated – with bleeding from venous vessels of different localization, ascites, liver failure, spontaneous peritonitis.

Staging determines the main symptoms of pathology.

Diagnostic process

Diagnosis of portal hypertension is a long process, because it is important not only to identify blood flow disorders, but also to determine the cause of its occurrence.

  • To begin with, the doctor studies the anamnesis, collects information about the symptoms that concern the patient. During a general examination, the specialist notes whether there is yellowing of the sclera, whether there is pain in the right hypochondrium during palpation.
  • A complete blood count helps to detect a decrease in the number of platelets, red and white blood cells.
  • A coagulogram is also mandatory, which helps to identify blood clotting disorders, in particular, a decrease in the rate of blood clot formation.
  • Blood is also examined for the presence of markers of various types of viral hepatitis.
  • A general urinalysis is performed, which helps to determine the presence of certain violations in the work of the kidneys and urinary tract.
  • Fibroesophagogastroduodenoscopy is also informative. During the procedure, the doctor with the help of an endoscope carefully examines the inner surfaces of the esophagus, stomach, and upper parts of the small intestine. The study helps to determine the presence of ulcers, erosion, dilated veins.
  • During an ultrasound examination of the abdominal organs, a specialist can accurately determine the size of the spleen and liver, examine their structure, and check for the presence of neoplasms. In the same way, free fluid in the abdominal cavity can be detected.
  • Dopplerography helps to evaluate the functioning of the portal and hepatic veins, as well as the volume of blood in the vessels, to see the places of their narrowing and expansion.
  • Sometimes X-ray contrast scanning is also performed. A special substance is introduced into the test vessel, and then, with the help of appropriate equipment, the movement of contrast is monitored. This procedure allows you to carefully study the nature of blood flow.
  • The results of computer and magnetic resonance imaging are informative. The doctor can study three-dimensional images of the necessary organs, evaluate their structure, see the vessels and places of their injuries.
  • Blood pressure in the portal system is measured (normally it can vary from 5 to 10 mmHg).
  • If there is a suspicion of damage to the heart and pericardium, then the patient is sent for echocardiography.
  • Elastography allows you to determine the presence of fibrotic changes in the tissues of the liver.
  • A final biopsy of the liver will help to make a final diagnosis with further laboratory examination of the samples taken.
  • If there are neurological symptoms, the patient is sent for a consultation with a psychiatrist. Memory impairment, increased irritability, drowsiness – all this may indicate the development of hepatic encephalopathy.

Diagnostics

Patients with suspected portal hypertension syndrome should undergo an ultrasound scan. Using ultrasound, you can detect hepatomegaly, splenomegaly, the presence of ascites, and clarify the size of the portal, splenic and superior mesenteric veins. An increase in the diameter of the splenic vein over 7-10 mm, portal – more than 15 mm reliably indicates the presence of portal hypertension. A more informative method for assessing this syndrome is ultrasound dopplerography. A necessary condition for successful diagnosis is fibrogastroduodenoscopy (FGDS), during which it is possible to detect the presence of varicose veins (HRV) of the esophagus and cardiac section of the stomach and gastropathy, which cause gastrointestinal bleeding.

The Japanese scientific society for the study of GHG has proposed rules for the description and registration of endoscopic signs of HRV of the esophagus and stomach, including 6 main criteria:

1. Localization (the prevalence of HRV along the esophagus, with VRV of the stomach – location relative to the cardia);

  • the lower third of the esophagus is Li;
  • middle third – Lm;
  • upper third – Ls;
  • VRV of the stomach – Lg:
  • located in the cardia – Lg-c;
  • remote from the cardia – Lg-f;

2. Shape (type and size):

  • lack of veins – F0;
  • short, small caliber – F1;
  • moderately dilated, convoluted VRV – F2;
  • significantly expanded, knobby VRV – F3.

3. Color (estimated wall thickness: blue – significant thinning):

4. “Red markers” of the wall:

  • red cherry spots – CRS;
  • hematocystic spots – HCS;
  • telangiectasias – TE.

The spots of “red cherry” during endoscopy look slightly protruding areas of red color, located on the tops of the SRV of the submucosal layer. They can be multiple, with a diameter of up to 2 mm (observed in 50% of patients with esophageal hypertrophy of the esophagus, most often seen with pronounced expansion of the veins). Hematocystic spots are dilated, located intraepithelially in the projection of the communicative varicose vein venous nodes. Endoscopically, they look like red bubbles, more often single, with a diameter of up to 4 mm. The esophagus in this area is covered with a thin layer of epithelium. Hematocyst spots are the weakest areas of the varicose wall, dangerous in terms of the development of bleeding. Teleangiectasia is a network of small convoluted vessels of the microvasculature located subepithelially, mainly in the lower third of the esophagus.

  • during bleeding:
  • after hemostasis:
    • red blood clot;
    • white blood clot.

Changes in the mucous membrane of the esophagus (as a manifestation of gastroesophageal reflux disease or a consequence of therapeutic endoscopic exposure):

With esophageal-gastric hemorrhage, including portal genesis, endoscopic examination is indicated. The purpose of the latter in acute bleeding is not only the detection of a rupture of the SRV, but also the elimination of a source of bleeding of a different genesis, the planning of subsequent treatment tactics. The crucial point in the diagnostic phase of endoscopy is the distinction between gastric and esophageal bleeding. A factor complicating the search for a bleeding zone is the abundant hemorrhagic contents in the stomach and esophagus, due to ongoing bleeding, as well as with constant regurgitation of the contents of the stomach into the esophagus. To exclude the negative effect of the contents, a patient is examined with a raised head end, and fibroscopes with a large diameter of the suction rope are also used.

In the process of endoscopy, it is necessary to evaluate the size, shape and color of the BPH, the severity of portal gastropathy, bleeding from the BPH of the esophagus and stomach, hemorrhages due to portal gastropathy, bleeding from ulcers induced by sclerotherapy or ligation are distinguished among portal bleeding.

According to the classification of N. Sochendro, K. Binmoeller distinguish the following degrees of BPV of the esophagus and stomach.

I Art. – the diameter of the veins, which are located only in the lower third of the esophagus, does not exceed 5 mm. II Art. – vein diameter from 5 to 10 mm, convoluted veins, spread in the middle third of the esophagus; III art. – the diameter of the veins is more than 10 mm, the veins are strained, with a thin wall, are located close to each other, on their surface there are “red markers”.

I Art. – the diameter of the veins is not more than 5 mm, the veins are barely visible under the mucous membrane of the stomach; II Art. – veins with a diameter of 5-10 mm, solitary-polypoid nature; III art. – veins with a diameter of more than 10 mm, represent an extensive conglomerate of thin-walled, polypoid nature of the nodes.

The larger the veins, the higher the chance of bleeding. VRV are usually white and opaque. Red color indicates increased blood flow. Enlarged subepithelial veins may have the appearance of cherry-red spots rising above the surface of the esophagus. Red color usually indicates HRV of larger veins and indicates a high probability of blood loss from HRV. Damage to the stomach with PG is mainly detected in the bottom, but can spread to the entire stomach.

At a conciliatory symposium in Baverno, rpymfa experts concluded that all patients suffering from chronic liver diseases should have an endoscopic examination of the upper gastrointestinal tract in the absence of an extracorporeal hypertension once every 1–2 years, and in the case of a slight increase in hypertrophy, 3 time per year . A more informative study is endosonography, which allows you to assess the condition of the vascular wall and determine the possible risk of bleeding from varicose nodes. Promising in assessing hepatic hemodynamics are methods based on integral indicators. One of these methods is polyhepatography (PGH), a method for assessing liver hemodynamics based on a joint analysis of several rheograms (blood supply curves) of the portohepatic region and synchronous central pulse curves.

In liver disease, depending on the nature of the violations of hepatic hemodynamics, the blood supply curve can change, acquiring the features of an arterial, venous, arterial, plateau, filiform pulse. In patients with signs of GHG, they measure VVD, SPD and VVPV. VVD is determined by puncture of the spleen and reflects presinusoidal pressure. Patients should undergo hepatic vein catheterization to evaluate LAP and HAP. The measurement of the HVAC and the SVD makes it possible to evaluate the sinusoidal portal pressure. Through the ulnar vein, a cardiac catheter is passed into the superior vena cava, then into one of the hepatic veins before jamming. The pressure measured in this way is equal to sinusoidal. When there is an increase in local resistance in the presinusoidal zone (the initial stage of primary 6-liar cirrhosis of the liver, idiopathic portal hypertension, chronic viral hepatitis B and C), this pressure corresponds to the pressure in the portal vein, measured by the direct method. Free hepatic venous pressure remains unchanged with sinusoidal and presinusoidal hypertension.

Normal VVD and SPD are equal to 16-25 cm of water of the station, and ZVVD – about 5,5 cm of water. Art. Angiographic research methods have not lost their significance: splenoportography, in which a contrast agent is injected into the spleen, portography – contrast is injected directly into the main portal vein trunk, transumbilical portohepatography, when contrast is introduced into the lumen of the umbilical vein. The complexity of direct measurement of portal pressure led to the search for indirect methods that determine the state of hepatic blood flow by the clearance of colloidal drugs labeled with nuclides. For these purposes, an albumin macroaggregate is used, which is “captured” by the liver by 90-95%, and colloidal gold preparations. Liver radioisotope scintigraphy of the liver, which allows indirectly determining the state of hepatic blood flow and the degree of portal hypertension by the clearance of colloidal preparations labeled with nucleides, has also not lost its significance.

The severity of GHG is estimated by the level of isotope accumulation in the spleen, which normally is not more than 10-20%. In addition to these methods, sigmoidoscopy, radiography of the abdominal organs, CT and MRI are used in the diagnosis of GHG. According to our data, echoCG methods with Doppler research and rhythmocardiography are informative for early diagnosis of GHG. At the last stage, it is necessary to establish a nosological diagnosis of the disease, which led to portal hypertension syndrome. It is advisable to conduct a morphological study of the liver. The data obtained are crucial in the implementation of therapeutic correction.

The first symptoms of GHG are a reason to consult a hepatologist or gastroenterologist. You can not hesitate, because the diagnosis of pathology in the early stages guarantees the selection of an adequate tactics for treating a patient, prevents complications, prolongs life. The algorithm is as follows:

  • medical history, physical examination;
  • OAK, OAM – general health screening, diagnosis of hypersplenism;
  • coagulogram – identification of disorders of the blood coagulation system;
  • X-ray of the digestive tract (esophagus, stomach), cardiac region of the ventricle – 18% accurate diagnosis (using cavography, portography, angiography of the mesenteric vessels, splenoportography, celiacography, which allows you to establish the level of formation of blocks);
  • scintigraphy – assessment of hepatic blood flow;
  • biochemical markers (antibodies to hepatitis viruses, bacterial infections, viruses, serum immunoglobulins);
  • FGDS – a condition of the mucosa;
  • Ultrasound, Doppler – the structure, size of blood vessels;
  • CT, MSCT, MRI – exact localization of the pathology;
  • liver puncture – if a tumor is suspected;
  • laparoscopy – examination of the abdominal organs with an endoscope;
  • percutaneous splenomanometry is done to register pressure in the portal vein system;
  • sigmoidoscopy – will detect altered venous capillaries in the rectum of the patient.

If necessary, the doctor may prescribe additional research methods.

Conservative treatment

Drug treatment of portal hypertension directly depends on the cause of the development of the disease.

  • Hormone therapy (taking Somatostatin analogues) helps to narrow the abdominal arterioles and reduce the pressure in the portal vein.
  • Nitrates help dilate blood vessels. As a result of this effect, blood accumulates in the small arterioles and veins, which reduces blood flow to the liver.
  • Beta-blockers are also used, which reduce the strength and frequency of heart contractions.
  • Diuretics are also included in the treatment regimen. These drugs relieve swelling, remove excess fluid from the body.
  • Lactulose preparations provide the excretion of dangerous substances from the intestines, which are formed in the body against the background of liver dysfunction.
  • If hypertension is associated with infectious diseases, then broad-spectrum antibiotics are used.
  • If there was bleeding, then after surgery, the patient is injected with plasma and erythromass.
  • In hypersplenism, patients are prescribed drugs (for example, synthetic analogues of hormones secreted by the adrenal glands) that stimulate the production of blood cells.

The Right Diet

Treatment of portal hypertension necessarily includes a correction of the diet.

  • It is important to limit the amount of salt consumed. Its daily dose should not exceed 3 g. This will help get rid of edema and prevent the accumulation of fluid in the body, reduce blood pressure.
  • It is recommended to reduce the daily amount of protein to 30 g in order to avoid the development of hepatic encephalopathy.
  • It is necessary to abandon alcohol, as their use creates an additional burden on the liver.
  • It is better to include vegetables and fruits in the diet. Dishes are recommended to steam, boil or bake in the oven.
  • Spices, spices from the menu are better to exclude.

Prevention, prognosis

FGDS is regularly performed on the patient, varicose veins are treated, a course of lactulose preparations is prescribed, protein intake is limited.

The prognosis of the intrahepatic form of GHG is unfavorable, since there is a risk of bleeding, cirrhosis of the liver with functional liver failure develops.

The extrahepatic form has a favorable course, especially with the formation of portal anastomoses in case of blood flow disturbance.

Higher medical education. 30 years of working experience in practical medicine.

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Last Updated: August 26, 2019

Surgical treatment of portal hypertension

Unfortunately, in some cases, surgical intervention is indispensable.

Operations with portal hypertension are performed if the following diseases are observed in a sick person:

  • Varicose veins of the stomach and esophagus (the walls of the vessels become thinner, which increases the likelihood of rupture and extensive bleeding).
  • A significant increase in the size of the spleen, the destruction in its tissues of too many blood cells.
  • Accumulation of fluid in the abdominal cavity.
  • With rupture of blood vessels, bleeding, peritonitis, emergency surgical intervention is required.

The choice of treatment methods depends on the degree of vascular damage, the presence of certain complications.

  • Sometimes the so-called portosystemic shunting is performed. In this case, the surgeon creates an additional blood flow path, connecting the cavities of the portal and inferior vena cava. In this case, blood partially passes the liver, which ensures a decrease in pressure.
  • Splenorenal bypass involves the creation of an additional path between the renal and splenic veins.
  • Ligation of some veins and arteries of the stomach and esophagus is effective. This procedure helps prevent bleeding.
  • Hepatic failure requires transplantation. This is a rather complicated procedure, which is not often done, as finding a suitable donor is not easy.
  • If vein rupture has already happened, then they are sutured surgically.
  • Sclerotherapy is sometimes effective. This is an endoscopic operation, during which the doctor, using special equipment, injects a sclerosant inside a bleeding vessel. This substance provides gluing of the walls of the vein.
  • In some cases, surgical removal of the spleen is indicated – so you can restore the normal number of blood cells.

Possible complications

This is a dangerous disease that cannot be ignored. In the absence of timely treatment, the patient’s condition will constantly worsen. The consequences of the disease can be fatal.

  • Hypertension affects the state of the spleen – in its tissues blood cells begin to actively decompose, which leads to anemia, thrombocytopenia, leukopenia. Due to a sharp decrease in the level of leukocytes, the body becomes more susceptible to various kinds of infections.
  • There are other complications that accompany portal hypertension. Bleeding from the veins of the esophagus, stomach, rectum, if untreated, can lead to massive blood loss and even death of the patient.
  • Hidden bleeding within the digestive system is also possible. They often occur without the manifestation of any symptoms, but lead to the development of anemia and other complications.
  • Hepatic encephalopathy is considered extremely dangerous. The fact is that the affected liver at some point ceases to cope with its functions. Nitrogen exchange products appear in the blood, which negatively affect the brain. Encephalopathy is accompanied by drowsiness, weakness, depression, increased anxiety, memory problems, concentration and orientation. Often the disease ends in a coma.
  • The formation of hernias is possible.
  • The list of complications also includes severe forms of ascites, which are practically not treatable, infectious peritonitis, various systemic infections, renal and liver failure.

Predictions for such a disease directly depend on timely diagnosis and adequate treatment.

Detonic – a unique medicine that helps fight hypertension at all stages of its development.

Detonic for pressure normalization

The complex effect of plant components of the drug Detonic on the walls of blood vessels and the autonomic nervous system contribute to a rapid decrease in blood pressure. In addition, this drug prevents the development of atherosclerosis, thanks to the unique components that are involved in the synthesis of lecithin, an amino acid that regulates cholesterol metabolism and prevents the formation of atherosclerotic plaques.

Detonic not addictive and withdrawal syndrome, since all components of the product are natural.

Detailed information about Detonic is located on the manufacturer’s page www.detonicnd.com.

Svetlana Borszavich

General practitioner, cardiologist, with active work in therapy, gastroenterology, cardiology, rheumatology, immunology with allergology.
Fluent in general clinical methods for the diagnosis and treatment of heart disease, as well as electrocardiography, echocardiography, monitoring of cholera on an ECG and daily monitoring of blood pressure.
The treatment complex developed by the author significantly helps with cerebrovascular injuries and metabolic disorders in the brain and vascular diseases: hypertension and complications caused by diabetes.
The author is a member of the European Society of Therapists, a regular participant in scientific conferences and congresses in the field of cardiology and general medicine. She has repeatedly participated in a research program at a private university in Japan in the field of reconstructive medicine.

Detonic