appunti del dott. Claudio Italiano
In the portal hypertension, in the cirrhotic patient, a series of structural
subversions occur in the hepatic lobule for which the nornal architecture is
lost. A compensation mechanism that acts in the opposite direction, that is to
say an effective reduction of the blood flow through the liver, is what is
established through the neoformation of connective-vascular septa that unite the
portal spaces to the centrolobular veins. These abnormal intrahepatic venous
short-circuits - internal Heck fistulae - cause the blood from the portal vein
and the hepatic artery to reach the central veins without passing through the
sinusoids. It does not seem, however, that such shunts significantly reduce
portal hypertension since the subcoula veins, to which said anastomoses occur,
are compressed or obliterated by the regenerative nodules.
Moreover, they create disadvantageous circulatory conditions for the hepatic parenchyma, which, receiving less blood than normally, (also due to the simultaneous formation of extrahepatic porto-systemic collateral circulation and the "capillarization" of sinusoids) can undergo acute hypoxia phenomena , especially when the circulation is further compromised, e.g. from a digestive hemorrhage. Consequences of portal hypertension. They are mainly represented by the formation of collateral venous circles, by ascites, and by spleno-megalia.
Apart from the aforementioned intrahepatic port-caval short circuits, it is mainly through the extrahepatic anastomoses already existing between the portal system and the general venous system that the collateral circulation circle of portal hypertension established by the cirrhotic process is established. On the contrary, these small anastomoses, which are not of functional importance under normal conditions, assume considerable importance in cirrhosis of the liver (and in general in portal hypertension) turning into voluminous collateral vessels that convey a large part of the portal blood directly into the general venous system. normally intended for the liver.
For a better understanding of this collateral circulation it is worth remembering that the portal vein results from the confluence of the superior mesenteric vein (which collects the waste blood from the small intestine, except one part of the duodenum, from the right half of the colon, pancreas and stomach , by means of v., ileal, of the right colic veins, of the pancreatic-duodenal v. and of the right gastroepiplo v.) with the inferior mesenteric vein (which collects the waste blood from the left half of the colon and the rectum, through the left vein colic, sigmoid veins and upper hemorrhoidal v.), and with the splenic vein (which receives 5-6 splenic branches, the short gastric veins, the left gastroepiploic v. and pancreatic and duodenal branches), to which they aggregate, as side affluents, v. right gastroepiploic, the left gastric vein or stomacic coronary, the pyloric vein, the superior pancreatic-duodenal vein and the cystic veins. The main anastomoses between the portal venous system and the general venous system occur at the cardiac, rectum and parietal peritoneum level, to which are added the anastomoses through the accessory port veins.
In the lower third of the esophagus there is anastomosis between the left gastric vein (portal vein affluent) and the lower esophageal veins, through the submucous and periesophageal venous plexuses (which enter into intercostal veins or into the adrenal glands, and are tributaries of the vein upper quarry). It is therefore possible, in the event of a portal obstruction, that the blood coming from the stomach, instead of pouring out as usual in the portal vein, reaches v. upper cavity through the lower esophageal veins (upper hollow circle, blood flow direction: left gastric vein - v. esophageal - veins azygos or emiazygos - superior vena cava). In the formation of this important collateral circulation the cardio-esophageal veins and the upper stomach veins that take on a varicose aspect are dilated.
EGDS: esophageal varices F3, red marks
Cardio-oesophageal varices, almost constant in the cirrhotic, are often so conspicuous that they can be easily highlighted in life with radiological examination. The rupture of one of these varices can cause profuse haemorrhages (hematemesis and melena, sometimes only melena), often fatal. The submucosal site of varicose veins, which leads to a progressive atrophy, until the almost complete disappearance, of the overlying mucosa, the traumatic action of food and the digestive action of gastric juice, explain why esophageal varices thus frequently encounter erosion. Not infrequently, however, at the anatomical table, the breaking point can be identified with difficulty (the intravascular injection of a colored liquid may be useful), given its smallness and postmortal sagging of the varices themselves.
Anastomosis at the rectal level In the lower part of the rectum the veins form a rich venous plexus, known as the hemorrhoidal plexus, from which the upper hemorrhoidal veins (which lead into the inferior mesenteric vein, a tributary of the v. Porta), the middle haemorrhoidal veins (tributaries of the hypogastric vein) ) and the lower hemorrhoidal veins that flow into the internal pudendal vein and then into v. hypogastric and in v. lower quarry). When there is a portal obstruction, blood from the upper hemorrhoidal veins may therefore discharge, rather than in v. door, in v. inferior cava, through the lower hemorrhoidal veins (average hemorrhoidal veins are of little importance): (inferior portal-cava circle, blood flow direction: upper hemorrhoidal vv - lower hemorrhoidal vv - v. internal pudenda - v. hypogastric - v lower ava). It follows the frequent formation of haemorrhoids, external or internal, which can in turn be the cause of hemorrhages (usually less ravi of those with oesophageal varices).
They are found on the very walls of those portions of intestine that make up the back wall of the abdomen (duomo, colon), where the small roots of the mesenteric veins communicate with the small roots of venous truncates that refer to v. lower cavity or one of its tributaries (renal veins, lumbar veins, sacral media, etc.). Through this anastomosis complex, which takes the name of the Retzius system, in the portal hypertension a not indifferent quantity of blood can be deviated from v. leads in v. lower cavity (the opposite occurs in the obstruction of the inferior vault).
The veins carry ancillaries are numerous small veins divided into six groups (epiploic veins, cystic veins, veins of the hilar or nutritious veins, diaphragmatic veins, veins of the suspensory ligament and paraombelical veins), which, mostly running in the thickness of the peritoneal ligaments , bring blood to the liver, regardless of v. door. In the event of an intrahepatic obstacle, blood flow may reverse, by entering the general venous circulation. Particularly important are the paraombelical veins of Sappey, formed by a series of anastomosed venules, which arise from the anterior wall of the abdomen at the level of the navel. From here they are taken to the liver following the suspensory ligament (some branches follow the round ligament - residual of the umbilical vein which exceptionally can persist after birth - by pouring into the left branch of the vault). Their importance derives from the fact that, originally, these veins are widely anastomosed on one side with the roots of the internal mammary veins (tributaries of the v. Superior cavity) and on the other with the inferior epigastric veins and the tegumental veins of the abdomen, tributaries of v. lower quarry.
Extensive anastomoses are thus obtained which make v. door with both hollow veins. Through
these anastomoses, which in cirrhosis of the liver can increase significantly in
size, by inversion of the blood flow that normally has a centripetal course, a
portal blood discharge is possible in the cavity veins (blood direction: v port
- paraombelical veins - mammary veins internal - v. superior cavity, or:
paraombelical veins - inferior or superficial epigastric veins - v. lower cavity).
In such cases the appearance on the surface of the abdomen of a median venous
reticule is manifested almost always more evident in the umbilical area which,
sometimes, due to the conspicuous development of the branches arranged radially
around the navel, takes on the characteristic appearance of the Medusae
".
The latter becomes particularly evident when the umbilical vein remains in
place, which in truth rarely occurs, but creates the danger of umbilical
hemorrhages, even deadly ones. Cruveilhier-Baumgarten syndrome is discussed in
these cases, agreeing to reserve the term Cruveilhier-Baumgarten disease, with
the simple patency of the umbilical vein in cases of congenital hypoplasia of
the portal vein system, without mandatory cirrhosis.
To develop the theme of portal hypertension and esophageal varices (italian
language):
>>Studio della ipertensione portale
>> Emorragie gastrointestinali
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