Portal hypertension

Portal hypertension is a pathological condition characterized by increased pressure in the pool portal vein because of barriers to the flow of blood in it. In severe cases are characterized by splenomegaly (see Spleen), ascites (see), the signs of collateral circulation: expansion of subcutaneous veins in the abdomen and side surface of the chest, varicose veins of the esophagus, stomach and intestines (hemorrhoidal veins). The most common cause of intrahepatic portal hypertension is cirrhosis of the liver, rarely anomaly intrahepatic vessels or tumors in the liver. Portal hypertension extrahepatic origin is connected with the change of the lumen of the portal vein and its branches, and also with thrombosis of the hepatic veins.
The pathogenesis of portal hypertension and liver cirrhosis is associated with difficulty in the portal circulation system in the result of the compression of blood vessels nodes compacted liver. Obstruction of the outflow of blood from the abdomen and the pressure increase in the pool of the portal vein lead to the stagnation of blood in the spleen (an organ giperplaziei and increases, there splenomegaly), as well as to the development of collateral circulation and pathological changes of normal portal circulation (varicose veins of the stomach, esophagus, intestines, giving often fatal bleeding). In the formation of ascites play the role of mechanical factors hindering the normal circulation, increasing the permeability of capillaries and hypoalbuminemia. Important role in the development otern-astiticeski syndrome in diseases of the liver plays aldosteronism (see), contributing to the delay sodium in the tissues and an output of potassium.
Treatment of the main disease; on the testimony of surgical imposition of vascular anastomoses, reduce congestion in the system of portal vein.

Portal hypertension is a pathological condition characterized by a persistent increase in blood pressure in the portal vein, and is usually manifested by enlarged spleen, ascites, extension Porto kafelnyh anastomoses. The immediate cause of portal hypertension in all cases, a violation of the outflow of blood from the portal bed, developing or as a result of obliteration part of hepatic vessels and liver cirrhosis (liver form of portal hypertension), or as a result of thrombosis or sdavljenia portal vein (extrahepatic form of portal hypertension).
Liver cirrhosis growth and subsequent scarring connective tissue at the place of the dead liver cells results in narrowing or complete obliteration part of hepatic sinusoids and intrahepatic vessels. As a result, the blood flow through the liver is difficult, portal the pressure increases. The situation is similar in animals in experimental liver cirrhosis caused by carbon tetrachloride. The main factor causing the development of portal hypertension cirrhosis,reducing the bandwidth hepatic vessels. Hemodynamics in portal hypertension is characterized by decreasing the amount of blood in an unmodified vessels, increased pressure in the portal vein, some decrease of pressure in the inferior Vena cava and the right ventricle.
The most common clinical expression of portal hypertension - classical triad: ascites, splenomegaly and expansion of hemorrhoidal veins, veins of the anterior abdominal wall and esophagus. However it is not necessary to consider each of these shifts-symptoms as a result only one of portal hypertension. In most cases, despite the high portal pressure, there has only been one or two elements of the triad.
In the development of varicose veins of the esophagus, in addition to the high level of portal pressure, significant features of the location Porto kafelnyh anastomoses. Surgical removal of portal hypertension in people by imposing achowskiego Porto kabelnogo anastomosis in most cases does not lead to rapid disappearance of ascites. At that, blood flowing from the portal vein, bypassing the cirrhotic liver, directly into the inferior Vena cava in the portal pressure decreases, however, ascites persists for a long time, and sometimes even appears after the operation. These data justify the idea that in the development of ascites (see), in addition to portal hypertension, an important role is played by other factors, including the delay in the body of sodium, metabolic disorders of the liver, reducing colloid-osmotic pressure of blood plasma, increased capillary permeability portal channel, flowing sluggishly peritonitis and other (F., Angles, A. N. Bakulev and S. A. Galushko). It is shown that the colloid-osmotic pressure of blood plasma and liver cirrhosis are not significantly altered, when diuresis is normal, but as soon as urine output is decreased and there is a water retention, colloid-osmotic pressure of plasma decreases.
The reason for the delay of water while - impaired excretion from the body of hydrophilic sodium ion. Restriction of sodium chloride in the diet slows down the development of ascites and adding it stimulates the development of cirrhosis with portal hypertension. Sodium excretion by the kidneys is consistent with the clinical status of patients: with improved clinical condition the amount of sodium in the urine increases, with the deterioration decreases. Delay sodium in the body with portal hypertension occurs much earlier than the development of significant violations of the portal circulation, long before they appear ascites or swelling. When more significant violations of the portal circulation and the development of ascites sodium retention expressed very sharply.


The deficit excretion renal sodium partly due to the strengthening of reabsorption of sodium in the convoluted tubules. Sharply reduced sodium and all other excretory organs: the content significantly decreases in the sputum, saliva and feces. It is established that in the plasma of blood and urine of patients with ascites contains a factor that can cause a delay of sodium and water in laboratory animals. The nature of this factor was largely clarified Bongiovanni and Eisenmenger (A. M. Bongiovanni, W. S. Eisenmenger), who found that in the formation of ascites in terms of portal hypertension in the urine of patients increases the amount of hormones produced by the adrenal cortex (see). Data on the role of adrenal cortex in the development of ascites was confirmed in experiments Davis (J. O. Davis) and TCS. Calling in dogs ascites by narrowing of the inferior Vena cava, they were removed later in experimental animals the adrenal cortex. After removing the bark has been an increase in urine output, and ascites disappeared within 24-48 hours. Introduction penetrationanal dogs hypertension again led to the development of ascites. It is now established that the greatest potential to cause a delay sodium in the body has the hormone aldosterone, allocated from amorphous faction of the extract of a bark of adrenal glands. Stand out in a larger number of aldosterone is a factor that activates the process of reabsorption of sodium in convoluted renal tubule, blocking all other ways of allocation of sodium from the body and stimulates the development of ascites. Davis and TCS. showed that after narrowing of the inferior Vena cava in dogs, contributing to the development of experimental liver, the concentration of aldosterone in the blood, flowing from the adrenal glands, increases in 2-4 times. Along with hypersecretion of aldosterone in patients with ascites occurs hypersecretion neurohypophysis of antidiuretic hormone (ADH), which content in the blood and urine of such patients have significantly increased. Hyperfunction of the adrenal cortex and neurohypophysis, accompanied by the delay sodium and water, occurs not only with cirrhosis of the liver (see) and related violations portal circulation (see), but under different hemodynamic changes, accompanied by a decrease blood arterial bed. With reduced blood flow in arterial system occurs reflex with so called volume receptors through the hypothalamus (see) on the adrenal cortex and neurolepis, reflex included hypersecretion of aldosterone and ADH that caused a delay of sodium and water, increasing the amount of fluid in the body.
The view on the participation of neuroendocrine mechanism makes it possible to understand some of the phenomena observed in portal hypertension. For example, it is known that a significant portion of patients with portal hypertension caused by cirrhosis or extrahepatic sdavlennoy portal vein, ascites is not present. However, observations [Post and Patek (J. Post, A. J. Patek); Path (O. D. Ratnoff) with al., and others] show that each time after the bloody vomiting associated with more or less blood loss, such patients at some time you receive ascites. T. O. Koryakina (1957) in 22 patients admitted to hospital on the occasion of bleeding from esophageal varices, in all cases observed occurrence of ascites, which until bleeding was absent, despite of portal hypertension. These clinical observations can be explained by the fact that before the bleeding in patients with cirrhosis or extrahepatic sdavlennoy portal vein had some hemodynamic is a certain lack of blood in the arterial system. However, this deficit did not reach the threshold values and not trigger neuroendocrine the mechanism of delay of sodium and water. After blood loss bigger deficit blood, affecting the pituitary and adrenal glands, causing considerable delay sodium and water, which led to the emergence of ascites.
The development of ascites or swelling depends not only on the degree of hemodynamic, but also on the functional state of the nervous system, in particular the centers of the hypothalamus, which regulate the activity of neurohypophysis and adrenal glands, and from the functional state of the pituitary gland (see) and adrenal glands. This explains the emergence of some patients with ascites and swelling at relatively low hemodynamic and the lack of these same phenomena other, despite the expressed cirrhosis, portal hypertension, or severe heart failure, accompanied by severe disturbances of hemodynamics.
Surgical treatment of portal hypertension - see Ascites.