Portal hypertension

Portal hypertension.

Description, Causes and Risk Factors:

Abbreviation: PH.

ICD-10: K76.6.

Portal hypertension is high blood pressure of the portal vein. The portal vein, a major vein in the abdomen, collects nutrient- rich blood from the intestines and delivers it to the liver to nourish it, where it is purified for our body to use.

Like other organs, the liver needs oxygen and nutrients to function, which it receives from the portal vein. After the oxygen-rich and nutrient-rich blood passes through the liver, it flows into the hepatic veins and on into the inferior vena cava, which takes it back to the heart. Blocked or reduced blood flow at any point of this process will result in increased pressure inside the portal vein. The search for an alternate route can make the blood travel through the esophagus, the skin of the abdomen and even the veins of the rectum. This unusual transmission can cause any of the following complications:

    Ascites - an accumulation of serous fluid in peritoneal cavity.

  • Hepatic encephalopathy - enlargement of the spleen.

  • Esophageal varices - a condition of extremely dilated sub-mucosal veins in the esophagus.

The hallmark of portal hypertension is a pathologic increase in the pressure gradient between the portal vein and the inferior vena cava, which is measured by the hepatic venous pressure gradient (HVPG). Brie?y, the wedged hepatic vein pressure (WHVP), a marker of sinusoidal pressure, and the free hepatic vein pressure (FHVP) are measured with radiologic assistance. HVPG is calculated by the following formula:


The most common cause of portal hypertension is cirrhosis, which refers to the “hardening” of the liver because of scar tissue. The other primary cause of portal hypertension is due to clots which narrow or block blood flow through the veins to and from the liver. Portal hypertension is fairly uncommon, but when it occurs, it most often happens in older adults and may result in death, if untreated.

Hepatic Causes: Cirrhosis is the most common cause of portal hypertension (PH), and chronic viral hepatitis C is the most common cause of cirrhosis in the United States. Alcohol-induced liver disease and cholestatic liver diseases are other common causes of cirrhosis. Less common causes include hemochromatosis, alpha 1-antitrypsin deficiency, drug-induced liver disease, and (in Eastern countries) hepatitis B. Portal hypertension is considered an advanced complication of cirrhosis. Once it has developed, the term "decompensated cirrhosis" is used (Figure 5).

Infrahepatic Causes: Alterations of portal venous blood flow can also lead to portal hypertension. Arteriovenous malformation of the splenic vasculature, splenomegaly and portal vein thrombosis are examples of infrahepatic causes of portal hypertension. Overall, these are not common conditions.

Suprahepatic Causes: Suprahepatic abnormalities leading to portal hypertension include cardiac disease, hepatic vein etiology, and inferior vena cava thrombosis or webs. Hepatic vein thrombosis, or Budd-Chiari syndrome, has multiple etiologies but is generally related to a hypercoagulable state and often treatable with anticoagulation. Liver fibrosis can result from suprahepatic disease, and cirrhosis can also develop late in the disease course.

Cytokines: The mechanism of portal hypertension has been the subject of extensive research. The pathophysiology is thought to involve vasodilators produced by the body. Namely, cytokines such as tumor necrosis factor-alpha (TNF-alpha) and others may play a role in stimulating endothelial vasodilators such as nitric oxide and prostacyclin as well as non-endothelial vasodilators like glucagon. These molecules may affect pressure and flow in the splanchnic vasculature, leading to portal hypertension.


Symptoms may include:

    Ascites (fluid build-up in the abdomen).

  • Weight loss.

  • Enlarged liver.

  • Internal hemorrhoids—with possible bleeding.

  • Dark stool.

  • Abdominal swelling.

  • Enlarged spleen.

  • Pancytopenia.

  • Gastrointestinal bleeding.

  • Varicose veins of the esophagus (varices)—with possible bleeding.

  • Jaundice (yellowing of the skin).


Portal hypertension can be diagnosed in several ways. Clinical diagnosis can be made in the setting of end-stage liver disease and in the presence of ascites and/or varices. Subclinical portal hypertension is much more difficult to diagnose, but low platelet levels, a large portal vein, and splenic enlargement on imaging studies are suggestive. Direct or indirect measurements of the portal vein may be accomplished using wedged hepatic vein pressure or splenic pulp pressure, but these methods are relatively invasive.

Imaging studies of patients with portal hypertension are helpful to make a diagnosis and to define portal venous anatomy. Duplex Doppler ultrasonography is a noninvasive, low-cost method of diagnosis that provides sophisticated information. It is often the initial procedure performed and provides specifics regarding the direction and velocity of portal flow. Findings of increased hepatic echogenicity, splenomegaly, portal vein dilation, thrombotic occlusion, collaterals, and gallbladder wall thickening are indicative of portal hypertension. MRI and CT scans are not particularly useful in making a diagnosis, but are capable of providing some of the same information.

Portal Pressure Measurement:

Most approaches to portal pressure measurement are relatively invasive, with the exception of newer endoscopic techniques. The most commonly used and preferred method for measuring the portal pressure is by indirectly calculating this pressure after occlusion of the hepatic vein. This is an invasive procedure, typically performed by interventional radiologists.

Endoscopic diagnosis:

Endoscopy is the standard diagnostic approach in patients with acute gastrointestinal hemorrhage after initial resuscitation. In most patients with cirrhosis (60-80%) bleeding is related to esophageal varices. In addition to making a definitive diagnosis, endoscopic therapy may be indicated for bleeding. Endoscopic examination may require endotracheal intubation in patients who have significant alteration in mental status as a result of severe hepatic decompensation.

Gastrointestinal endoscopy allows the physician to visualize and biopsy the mucosa of the upper gastrointestinal tract including the esophagus, stomach, and duodenum. The enteroscope allows visualization of at least 50% of the small intestine, including most of the jejunum and different degrees of the ileum. During endoscopic procedures, a pharyngeal topical anesthetic may be administered to help prevent gagging. Pain medication and a sedative may also be given prior to the procedure.


The treatment for portal hypertension depends mostly on the cause and the severity of the condition. Mostly medication, semi-surgical and surgical procedures are used depending upon the efficiency levels of the liver.

Medical treatment of portal hypertension includes beta-blockers. This class of drugs helps to decrease blood flow into the portal-vein system and to decrease the pressure. Beta-blockers also reduce the risk of bleeding from varices.

Minimally invasive procedures such as endoscopic variceal sclerotherapy (EVS), which involves the injection of solution to seal the bleeding, and endoscopic variceal banding (EVB), which is the placement of a band from inside the esophagus to seal the bleeding are used to stop bleeding from varices.

Another solution for portal hypertension is a procedure known as transjugular intrahepatic portosystemic shunt (TIPSS). This procedure involves a stent between the hepatic vein and a branch of the portal vein. Distal splenorenal shunt (DSRS) is another procedure that connects the vein from the left kidney to the vein from the spleen.

The only way to fully cure portal hypertension is with a liver transplant, which is expensive and afterward the patient needs life- long medical attention. Liver transplantation is indicated only when portal hypertension is accompanied by disorders of the liver and in situations where the liver is unable to produce proteins.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.


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