Page created on February 19, 2019. Last updated on May 16, 2020 at 20:48
The portal vein drains most of the GI tract, from the lower parts of the oesophagus to the middle part of the rectum. The portal vein drains into the liver, where nutrient-rich blood is filtered through the hepatic sinusoids before draining into the inferior vena cava.
There are multiple points in the body where veins that drain into the portal system and veins that drain into the vena caval system anastomose. They are called porto-caval anastomoses, and can be found in:
- The oesophagus
- The rectum
- The paraumbilical region
When the pressure increases inside the portal circulation for any reason is there portal hypertension. This occurs most frequently due to an increase in the resistance of the portal circulation. This increased resistance can come from prehepatic, intrahepatic or posthepatic causes.
- Prehepatic – reduced flow in portal circulation
- Portal vein thrombosis
- Splenic vein thrombosis
- Compression due to tumor
- Intrahepatic – reduced portal flow through the liver
- Posthepatic – reduced flow after the liver
- Inferior vena cava thrombosis
- Right-sided heart failure
- Budd-Chiari syndrome
The most common cause is cirrhosis, and it’s probably the only intrahepatic cause you need to know.
No matter the cause are the consequences the same:
- Splanchnic congestion
- Mesenterial thrombosis
- Decreased effective circulating arterial blood volume -> hepatorenal syndrome
- See topic 18
- Portal blood is shunted through porto-caval anastomoses
- Oesophageal varices
- Rectal varices
- Caput medusae
- Toxins and stuff from the gut directly enter the systemic circulation
As the pressure increases inside the portal circulation will there be congestion of the splanchnic circulation. This causes splenomegaly (hemolysis and pancytopaenia), malabsorption, disorder of gut motility and increased tendency for mesenterial thrombosis due to the slower circulation.
In portal hypertension will there be more vasodilation in the splanchnic circulation due to increased production of vasodilators like NO. This “steals” perfusion from other organs to the abdominal organs, which causes a relative increase of blood in the splanchnic circulation and a relative decrease of blood in the non-splanchnic circulation. This causes a reduction of effective circulating arterial blood volume, which mimics hypovolaemia. Especially the renal perfusion is decreased, which is the beginning of hepatorenal syndrome.
Portal hypertension forces the portal blood through the porto-caval anastomoses. They are then called varices and are fragile and have a large probability of breaking and bleeding. As cirrhosis often involves a coagulopathy and thrombocytopaenia is often also present can ruptures oesophageal varices cause life-threatening bleeding. As portal blood is shunted through the paraumbilical veins will caput medusae be visible.
The liver usually sifts through the nutrient-rich portal blood and filters or metabolizes everything that would be harmful to the body. As more blood bypasses the liver by going through anastomoses will more harmful substances absorbed from the GI tract enter the systemic circulation directly. These substances include ammonia, short-chain fatty acids, biogenic amines and GABA. This contributes to portal encephalopathy, a component of hepatic encephalopathy. Symptoms like confusion are especially prominent after protein-rich meal, as digested proteins are partly converted to ammonia.
Treatment: Transjugular intrahepatic portosystemic shunt (TIPS) is a procedure where an artificial channel is created inside the liver that communicates between the portal vein and the hepatic vein. This relieves the portal hypertension. It’s performed in patients who have uncontrolled variceal bleeding.
One thought on “17. Portal hypertension”
I just wanted to point out a cool (after my opinion) paradox!
You mention the effect of the NO produced in the splanchnic circulation, and how that steals the blood from the rest of the organs and worsening the p.hypertension.
As the liver damage progress, it’s ability to synthesize NO is diminishing, and it will eventuality stop. This is quite sad, as NO locally in the liver would help with vasodilation and lower the p.hypertension!
So after all of this, NO would be a both helpful, if locally, and harmful, if systemically.
It’s at least a cool paradox to tell the examiners, while you figure at what they actually want to hear 💡