Portal Hypertension Pathophysiology

Portal hypertension is a condition that occurs when there is abnormally high pressure in the portal venous system, which is a network of vessels that drain blood from the abdomen into the liver.

As a quick review, the portal vein is formed by the splenic vein merging with the superior and inferior mesenteric veins.

So it receives blood from the spleen, stomach, pancreas and small and large intestines. This blood contains all the nutrients absorbed in the gi tract as well as ingested medications and potential toxins.

The slow low pressure flow of blood provides adequate time for the liver to extract nutrients, metabolize medications and remove toxins before they reach systemic circulation.

Once the liver processes, the blood it receives, it flows through the hepatic veins to the inferior vena cava and to the right atrium of the heart, the blood then flows through the heart and lungs and oxygenated blood is pumped out to the rest of the body.

Now, portal hypertension is caused by any condition that obstructs blood flow in the portal venous system and can be prehepatic intrahepatic or post hepatic prehepatic causes are those that result in obstruction of blood flow before reaching the liver such as splenic vein, thrombosis or a clot within the splenic vein.

Intrahepatic causes are those which result in an obstruction within the liver. One of the most common causes is cirrhosis, a condition where healthy liver tissue is replaced by scar tissue resulting in increased resistance to blood flow through the liver.

Other causes include certain infections like hepatitis or schistosomiasis. A parasitic infection that can affect multiple organs including the liver.

Lastly, post hepatic causes result in obstruction of blood flow from the liver, like right-sided heart failure where the right ventricle is not pumping, effectively causing blood to back up into the liver.

Ok. So when an obstruction to blood flow develops, pressure builds and blood backs up into the portal system, including the splenic and mesenteric circulation, dilating the venous channels before the obstruction.

In response to the increased pressure. Portosystemic shunting occurs, meaning new pathways for the blood flow are formed called collateral vessels that divert blood flow around the portal venous system.

These collateral vessels involve the dilation and enlargement of existing veins along with some newly formed veins and occur at three points where the systemic venous system and the hepatic portal system are connected first in the esophagus, esophageal varices or fragile enlarged esophageal veins form.

Then in the round ligament of the liver, which used to be part of the umbilical vein. During fetal life opens allowing blood to flow into the systemic veins of the abdomen.

The round ligament collapses after birth, but these veins can dilate and appear to radiate out from the belly button called kit medusae.

Finally, in the rectum and anal canal hemorrhoids form portal hypertension can also cause blood to back up into the spleen causing splenomegaly or an enlarged spleen.

This causes hypersplenism, meaning the spleen traps blood elements like red blood cells, white blood cells and platelets.

Another consequence of portal hypertension is ascites or an abnormal accumulation of fluid in the peritoneal cavity. This happens because the damaged liver produces less albumin decrease in capillary oncotic pressure, which can't overcome the increased hydrostatic pressure in the venous system.

So, fluid in blood vessels is pushed into the peritoneal cavity where it remains. In addition, endothelial cells lining the blood vessels release more nitric oxide.

This makes peripheral arteries dilate. So, BP drops which stimulates the release of aldosterone via the renin angiotensin aldosterone system to try to bring BP back up by telling the kidneys to retain more sodium and water.

This makes the portal hypertension and ascites even worse. And if that wasn't enough translocation of bacteria into the peritoneal cavity can occur, causing bacterial peritonitis.

Finally bypassing the liver means the blood that's usually filtered through the liver isn't detoxified and toxins like ammonia can build up in the blood ammonia and other toxins can pass through the blood brain barrier and cause hepatic encephalopathy.

Clinical manifestations occur as a result of venous congestion in the gi tract and build up of toxins. A common manifestation is bleeding from esophageal varices and when the bleeding is slow and chronic, it can cause melena or black tarry stools and anemia.

However, varices can easily rupture and result in hematemesis or vomiting blood and life threatening blood loss on the abdomen.

Kit medusae will often be noted. Ascites will present as an enlarged rounded abdomen accompanied by rapid weight gain and dyspnea due to a displaced diaphragm, pushing up against the lungs.

If the ascites is accompanied by bacterial peritonitis. Abdominal pain fever and chills will be noted.

And lastly, splenomegaly may result in anemia, leukopenia or thrombocytopenia. Finally, hepatic encephalopathy typically presents with neurologic symptoms like lethargy, subtle personality changes, memory loss, irritability and confusion.

All right, as a quick recap portal hypertension is a condition that occurs when there is an abnormally high pressure in the portal venous system.

This leads to vascular congestion, development of collateral venous structures and toxin accumulation. Clinical manifestations related to these changes can include oesophageal varices, ascites and hepatic encephalopathy.