The Most Complex Part of the Human Venous System: The Hepatic Portal Venous System
In the systemic circulation, arterial blood is pumped out by the left ventricle and carried through arteries of all orders to the organs of the whole body; after metabolism, the venous blood is collected by veins, converges into the superior and inferior vena cava systems, and finally flows into the right atrium. This is the blood-circulation process of ordinary organs and tissues. But one organ is the exception, and that organ is our liver.
Our liver has two sets of blood-vessel systems entering it. One is the hepatic arterial system, which includes the common hepatic artery, the proper hepatic artery, and their branches; the hepatic arterial system delivers arterial blood to the liver. The other is the hepatic portal vein. The hepatic portal vein and the hepatic vein differ by only one character, yet they are entirely different. The hepatic portal vein injects blood into the liver, whereas the hepatic vein carries the venous blood produced within the liver out of it and into the inferior vena cava. The hepatic portal vein collects venous blood from the major digestive organs in the abdomen other than the liver; after collecting this venous blood, the hepatic portal vein injects it into the liver.
The liver also has a system of vessels leaving it, namely the hepatic veins, which output the venous blood produced by the liver.
Why is the liver's blood-circulation system so special? It is determined by the liver's special physiological functions.
The liver is a digestive gland with important digestive functions: it absorbs nutrients from the venous blood flowing out of other digestive organs and carries out a series of biochemical reactions within the liver, turning them into various endogenous nutrients our body needs, such as certain essential amino acids.
At the same time, the liver is a detoxifying organ. Toxic components in the food or drugs absorbed by our digestive system must be detoxified in the liver before being injected into the inferior vena cava, and then through the inferior vena cava into the right atrium, so that they are harmless to the body. Therefore, once liver function is damaged, our body cannot detoxify normally, which is very dangerous.
The hepatic portal vein has many tributaries that collect various venous blood from the digestive system; the venous system composed of the hepatic portal vein and its tributaries is called the hepatic portal venous system. Its main tributaries include the superior mesenteric vein, splenic vein, inferior mesenteric vein, right gastric vein, cystic vein, and paraumbilical veins; these veins mostly accompany the arteries of the same name.
Although the blood flowing into the liver through the hepatic portal vein is venous blood, it also contains a relatively large amount of oxygen. Portal venous blood accounts for about three-quarters of the total blood entering the liver, and its oxygen content is about half of that entering the liver. Thus, when liver surgery requires temporarily embolizing the hepatic artery, the liver can still receive oxygen from the portal vein and will not fail from hypoxia.
The venous blood flowing in through the portal vein is rich in nutrients. After being processed in the liver, these nutrients become the various endogenous nutrients the body needs. This blood then leaves the liver through the hepatic veins into the inferior vena cava and finally into the right atrium. It passes from the right atrium to the right ventricle, is pumped from the right ventricle into the pulmonary trunk, and then distributed through the left and right pulmonary arteries to the arterial systems of the lungs. Finally, within the capillaries of the alveoli it completes oxygen binding, ultimately becoming arterial blood rich in oxygen and nutrients that supplies and nourishes the tissues at all levels throughout the body.
The hepatic portal system does not communicate only with the portal vein; it also has communication channels with the superior and inferior vena cava systems. But under healthy conditions, the amount of portal-systemic blood directly entering the superior and inferior vena cava systems is very small. The adult hepatic portal vein is about 8 cm long and about 1.5 cm in diameter—a very large vessel. Most of the venous blood collected by the portal system passes through the portal vein into the hepatic sinusoids; after a series of complex biochemical reactions are completed in the liver, it leaves the liver.
However, when a problem arises in the hepatic portal vein, abdominal venous blood enters the superior and inferior vena cava systems through collateral channels other than the portal vein, accompanied by a series of pathological phenomena.
There are mainly four communication pathways between the hepatic portal system and the superior and inferior vena cava systems: 1. Through the esophageal venous plexus in the submucosa of the abdominal segment of the esophagus, forming a communication between the left gastric vein of the portal system and the azygos and hemiazygos veins of the superior vena cava system; 2. Through the rectal venous plexus, forming a communication between the superior rectal vein of the portal system and the inferior rectal veins and anal veins; 3. Through the paraumbilical venous network, forming a communication between the paraumbilical veins of the portal system and the thoracoepigastric and superior epigastric veins of the superior vena cava system, or the anterior and inferior epigastric veins of the inferior vena cava system; 4. Through the internal and external vertebral venous plexuses, forming a communication between small veins of the portal system on the anterior abdominal wall and the posterior intercostal and lumbar veins of the superior and inferior vena cava systems.
In addition, small veins of the portal system in the bare area of the liver, pancreas, duodenum, and ascending and descending colon also communicate with the inferior phrenic, intercostal, renal, and lumbar veins of the superior and inferior vena cava systems.
One can imagine that if the hepatic portal vein becomes diseased and return flow is obstructed, the venous blood stagnating in the portal system will flow out through the above collateral channels. These collateral channels are normally relatively small vessels and cannot bear the huge blood volume produced by the portal system. The result is that each collateral vessel becomes enlarged and tortuous, forming varices. It is just as when a high-traffic artery fails: the small side roads become jammed with traffic and eventually clog up to the point of traffic paralysis.
Once these collateral circulations (communication pathways) develop varices, a series of symptoms result. If the esophageal venous plexus ruptures, hematemesis and melena appear; varices of the paraumbilical venous plexus produce dilated superficial veins on the abdominal wall around the navel, clinically called "caput medusae," which TCM refers to as "blood distention" (xue gu) among the "distention" (gu zhang) syndromes; varices of the rectal venous plexus can cause fresh bloody stool. Portal hypertension can cause congestion of organs within the drainage area, leading to splenomegaly and ascites. Because this blood bypasses hepatic metabolism and decomposition and directly enters the vena cava systems, excessively high blood ammonia levels can also cause hepatic encephalopathy.
What we commonly call portal hypertension is hepatic portal hypertension, a comprehensive pathological phenomenon caused by excessive pressure in the hepatic blood-supply system, most often seen in patients with cirrhosis. But cirrhosis is not the only cause. According to the location of the obstruction, the causes of portal hypertension fall into three major categories:
The first is prehepatic (obstruction at the portal-system inlet); common situations include portal vein thrombosis blocking the vessel, splenic vein thrombosis obstructing venous return, and compression of the vessels by a massively enlarged spleen.
The second is intrahepatic (microcirculatory disturbance within the liver), which is the most common. It is further divided into three types: 1. Presinusoidal portal hypertension caused by schistosome eggs blocking the tiny vessels in the liver; 2. Sinusoidal portal hypertension caused by destruction of hepatocyte structure in cirrhosis and alcoholic liver disease; 3. Postsinusoidal portal hypertension caused by obstruction of intrahepatic venous return in certain special types of liver disease.
The third is posthepatic. This kind of portal hypertension is caused by obstruction of hepatic venous outflow or of the inferior vena cava, leading to elevated portal pressure. Common causes include Budd-Chiari syndrome, constrictive pericarditis, and right-sided heart failure; the main manifestations are ascites, splenomegaly, and esophagogastric varices.
Western medicine diagnoses portal hypertension relying on imaging examinations (such as ultrasound and CT); treatment requires relieving the obstruction, controlling complications (such as bleeding and ascites), and treating the primary disease.
Different types of portal hypertension require different TCM treatment principles. Portal hypertension belongs to gu zhang (distention) or gu zheng in TCM, and there are many TCM formulas for treating gu zhang.
For example, Jin Kui Shen Qi Wan, Ling Gui Zhu Gan Tang, and Gui Pi Tang, used by pattern differentiation as spleen-kidney yang deficiency, mostly have a cardiotonic effect and are somewhat effective for portal hypertension caused by heart failure. Da Zhe Chong Wan, Xia Yu Xue Tang, Tao Hong Si Wu Tang, and Gui Zhi Fu Ling Jiaonang, used by pattern differentiation as blood distention, mostly activate blood and resolve stasis and are somewhat effective for portal hypertension caused by venous thrombosis. Renshen Biejia Jian Wan and Biejia Ruangan Pian, used by pattern differentiation as "malarial mass" (nüe mu) or abdominal masses (zheng jia), usually have some effect on cirrhosis and liver cancer. But gu zhang is one of the four incurable diseases of TCM internal medicine, with a poor prognosis; although TCM treatment can have some effect, the overall effective rate is not high, and the cure rate is very limited.
If we can combine the modern medical understanding of portal hypertension, we can more precisely select TCM formulas for treating gu zhang and raise the clinical effective rate. From this we can also see that those who study TCM genuinely need to learn modern medicine if they wish to further improve their clinical level; the richer a doctor's knowledge system, the higher the clinical level.