Portal Hypertension Abdominal Ultrasound Portal hypertension is a pathologic condition characterized by an excessive increase in the pressure within the portal vein or one of its branches. Typical portal vein pressure is 5 to 10 millimeters of mercury (abbreviated mmHg). When the pressure exceeds 5 mmHg above inferior vena cava pressure, it is characterized as portal hypertension. The portal vein carries nutrient rich blood from the digestive system to the liver. Normally, the veins come from the stomach, intestine, spleen, and pancreas.
They merge into the portal vein, which then branches into smaller vessels and travels through the liver. If the vessels in the liver are blocked, it is hard for the blood to flow causing high pressure in the portal system. When the pressure becomes too high, the blood backs up and finds other ways to flow back to the heart, which causes large varices (swollen or knotted bodily vessels, usually veins) to develop across the esophagus and stomach to bypass the blockage. Because of this bypass, substances (such as toxins) that are normally removed from the blood by the liver can pass into the general circulation.
The varices become fragile and can bleed easily, sometimes seriously and occasionally with fatal results. Portal hypertension often causes the spleen to enlarge (splenomegaly) because the pressure interferes with blood flow from the spleen into the portal blood vessels. Pressure in the portal blood vessels may cause fluid from the surface of the liver and intestine to leak into the abdominal cavity producing a condition called ascites (an accumulation of serous fluid in the peritoneal cavity, causing abdominal swelling).
Sonographically speaking, portal hypertension can be separated into presinusoidal and interhepatic. Presinusoidal venous hypertension often occurs in a patient with normal liver function when the portal vein and its branches are compressed before they enter the liver. Presinusoidal portal hypertension can be further divided into extrahepatic and intrahepatic forms. Extrahepatic presinusoidal portal hypertension can be caused by either thrombosis (formation of blood clots) of the portal veins or of the splenic veins. The causes of portal vein thrombosis in adults include rauma, sepsis (blood or tissue infection), hepatocellular carcinoma (cancer of the liver cells), pancreatic carcinoma (cancer of the pancreas), pancreatitis (inflammation of the pancreas), portacaval shunts (shunt between the portal vein and inferior vena cava), splenectomy (removal of the spleen), and hypercoagulable states (excessive blood clotting). This form of portal hypertension should be suspected in any patient that has a normal liver biopsy and any of the clinical signs of portal hypertension (ascites, splenomegaly, and varices).
The intrahepatic presinusoidal portal hypertension is caused by primary biliary cirrhosis, congenital hepatic fibrosis, toxic substances, and schistosomiasis, all of which are diseases (or results of diseases), affecting the portal zones of the liver. The other type of portal hypertension, interhepatic, is almost always caused by cirrhosis, accounting for more than 90% of all cases of portal hypertension in the Western Hemisphere. Cirrhosis results from the healing of a liver injury caused by hepatitis, alcohol abuse, or other causes of liver damage.
Cirrhosis is a chronic progressive liver disease characterized by the replacement of healthy cells with scar tissue. The scar tissue blocks the flow of blood through the liver and slows its processing functions because it is dense enough that it increases the resistance to portal venous blood flow and obstructs hepatic venous outflow, causing portal hypertension. Another liver disease that produces portal hypertension in the same fashion is diffuse metastatic liver disease. Altogether, the most common cause of portal hypertension is cirrhosis.
Thrombosis is another main cause of portal hypertension but other causes of portal hypertension include blockages of the veins that carry the blood from the liver to the heart, parasitic infection called schistosomiasis, and sometimes the cause is unknown. There are many other things that can lead to portal hypertension including thrombotic diseases of the inferior vena cava and hepatic veins, constrictive pericarditis, and any other cause of right-sided heart failure. The onset of portal hypertension may not always be associated with specific symptoms that identify what is happening to the liver.
If there is liver disease that leads to cirrhosis, the chances of developing portal hypertension is high. The main symptoms and complications of portal hypertension include gastrointestinal bleeding (black, tarry stools or blood in the stools; vomiting of blood), ascites, encephalopathy (confusion and forgetfulness), and reduced levels of platelets or decreased white blood cell count. Usually doctors make the diagnosis of portal hypertension based on the presence of ascites or of dilated veins or varices as seen on physical exam of the abdomen or the anus.
Portal hypertension can also be diagnosed by endoscopic examination, X-ray studies, ultrasonography, and lab tests. Further treatment is usually necessary to prevent recurrent bleeding. Among the many sonographic findings of portal hypertension (including the ones previously mentioned) are consequential signs of the development of portosystemic venous collaterals, enlargement of the portal vein, decreased portal vein velocity, increased congestion index, and reversal of portal vein flow.
Portosystemic venous collaterals form when the resistance to blood flow in the portal vessels exceeds the resistance to flow in the small communicating channels between the portal and systemic circulations. The most important portal systemic collaterals to focus on with Doppler ultrasound are the coronary vein and the umbilical vein, although there are five other major sites including the gastroesophageal junction, splenorenal and gastrorenal, intestinal, and hemorrhodial regions. The effects of portal hypertension can be managed through diet, medications, endoscopic therapy, surgery, or radiology.
Once the bleeding is under control, treatment options are prescribed based on the severity of the symptoms and on how well the liver is functioning. Unfortunately, most causes of portal hypertension cannot be treated. Instead, treatment focuses on preventing or managing the complications, especially the bleeding from the varices. When first diagnosed with variceal bleeding, endoscopic therapy or medications are usually prescribed. Diet and lifestyle changes are highly recommended and are very important. Endoscopic therapy consists of either sclerotherapy or banding.
Sclerotherapy is a procedure that is performed by a gastroenterologist in which a solution is injected into the bleeding varices to stop or control the risk of bleeding. Banding is a procedure in which a gastroenterologist uses rubber bands to block the blood supply to each varix. Medications such as beta blockers or nitrates may be prescribed alone or in combination with endoscopic therapy to reduce the pressure in the varices and further reduce the risk of recurrent bleeding. Medications such as propranolol and isosorbide may be prescribed to lower the pressure in the portal vein and reduce the risk of recurrent bleeding.
The drug lactulose can help treat confusion and other mental changes associated with encephalopathy. Maintaining good nutrition and keeping a healthy lifestyle will help the liver to function properly. Some of the things that can be done to improve the function of the liver is not using alcohol or street drugs, not taking over-the-counter or prescription drugs unless cleared by a physician or nurse, and following the dietary guidelines that are given by the physician or nurse. If the variceal bleeding is not controlled, one of the following procedures may be required to reduce the pressure in the portal veins.
Transjugular intrahepatic portosystemic shunt (TIPS) is a radiological procedure in which a stent is placed in the middle of the liver. Distal splenorenal shunt (DSRS) is a surgical procedure that connects the splenic vein to the left renal vein in order to reduce the pressure in the varices and control bleeding. Before either of these procedures takes place, there are several tests that are required to determine the extent and severity of the portal hypertension. These test include (but are not limited to) physical examination, blood tests, angiogram, ultrasound, and endoscopy.
Other tests that may be completed are an electrocardiogram (EKG), chest X-ray, and additional blood tests. The TIPS procedure reroutes blood flow in the liver and reduces pressure in all abdominal veins. This is done by making a tunnel through the liver with a needle, connecting the portal vein to one of the hepatic veins, and inserting a metal stint in the tunnel to keep it open. This procedure controls bleeding in over 90% of patients but in about 30% of those patients, the shunt may narrow causing varices to bleed again at a later time.
The DSRS is a surgical procedure in which the splenic vein is detached from the portal vein and attached to the left renal vein. This surgery selectively reduces the pressure in the varices and controls the bleeding. DSRS controls bleeding in over 90 % of patients and the highest risk of any recurrent bleeding is in the first month. However, the DSRS procedure provides good long-term control of bleeding but a potential complication of the DSRS surgery is ascites, or an accumulation of fluid in the abdomen. This can be treated with diuretics and restricted sodium intake.
Other treatment procedures include liver transplant (which is done in cases of end-stage liver disease) and devascularization (which is a surgical procedure that removes the bleeding varices. ) Devascularization is done when a TIPS or a surgical shunt is not possible or is unsuccessful in controlling the bleeding. Portal hypertension is high pressure in the portal venous system that can wreak havoc on the body. It is broken down into presinusoidal and interhepatic portal hypertension. Presinusoidal portal hypertension can also be further divided into extrahepatic and intrahepatic forms.
The most common cause of all types of portal hypertension is cirrhosis but there are many other causes including thrombosis, venous blockages, parasitic infection, metastatic liver disease, congenital hepatic fibrosis, and toxic substances. Some of the symptoms of portal hypertension include gastrointestinal bleeding, ascites, encephalopathy, and varices. Portosystemic venous collaterals, splenomegaly, enlargement of the portal vein, decreased portal vein velocity, increased congestion index, and reversal of portal vein flow are a few of the sonographic findings associated with portal hypertension.
The effects of portal hypertension can be controlled through diet, medications, endoscopic therapy, surgery, or radiology. Because portal hypertension cannot be treated, treatment focuses on preventing or managing the complications, especially the bleeding from the varices. These treatments include endoscopic therapy, TIPS, DSRS, liver transplant, and devascularization. Using all of these clues, it is possible to diagnose portal hypertension with a high degree of sensitivity and specificity in most patients.