Cirrhosis of the Liver Community
Portal Hypertension Tests
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Portal Hypertension Tests

What tests are used to diagnose portal hypertension...abdominal ulrasound?  MRI?   CT?

I have heard there are stages of portal hypertension.  My egd did see some grade 2 non bleeding varices on my last scope in 2012   He did not give me any meds for them...my bp usually runs on the lower side.  I've had low bp since I was young.



Thanks in advance...
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446474_tn?1404424777
The preferred, albeit indirect, method for assessing portal pressure is the wedged hepatic venous pressure (WHVP) measurement, which is obtained by placing a catheter in the hepatic vein and wedging it into a small
branch or, better still, by inflating a balloon and occluding a larger branch of the hepatic vein.
This is rarely done as the exact pressure is not needed and what is important is to stop the resulting complications such as life-threatening variceal bleeds. Also . Limitations of HVPG measurement are the lack of local expertise and poor adherence to guidelines that will ensure reliable and reproducible measurements, as well as its invasive nature.

The normal HVPG is 3-5 mmHg. Patients with cirrhosis and gastroesophageal varices have an HVPG of at least 10-12 mm Hg.

Gastroesophageal varices are present in approximately 50% of patients with cirrhosis. Their presence correlates with the severity of liver disease while only 40% of Child A patients have varices, they are present in 85% of Child C patients.


An ultrasound can detect portal flow issues and is cheap and non-invasive. It can also see the enlarged spleen which is a complication of portal hypertension.

Portal hypertension is a result of complete cirrhosis and limited blood flow through the liver due to scarring. Only if the liver disease is reserved early can the portal hypertension be reversed. SO we focus many on the affects of portal hypertension. Ascites, HE, collateral blood flow.

The portal vein supplies the majority of blood to the liver. That blood comes from the GI tract and the spleen.
When scar tissue in the liver interferes with that blood flow--- pressure can build in the portal vein ("portal hypertension"). Portal Hypertension can cause the spleen to enlarge and varices to form in the GI tract.
---> As the spleen enlarges-- platelets are trapped in the spleen. (The platelet count in the bloodstream falls.) (Platelets help our blood to clot. So as the platelet count falls... bleeding time is increased.)
---> Varices are dangerous because there's a risk that they can burst and bleed (hemorrhage).

Sometimes people ask why cirrhosis can progress, even when the cause of the liver disease is removed such as curing HCV. The reason is that sometimes cirrhosis itself (scar tissue) can interfere so much with blood flow through the liver-- it causes more cells to die even thought the scarring is not increasing.

Grade 2 varices are enlarged, twisted varices occupying less than one third of the lumen.
Grade 3 and red wheals are in danger of bleeding and intervention should be performed before the first bleed.

'In patients with medium/large varices that have not bled and are not at the highest risk of hemorrhage (Child A patients and no red signs), nonselective -blockers (propranolol, nadolol) are preferred and EVL (banding) should be considered in patients with contraindications or intolerance or non-compliance to-blockers (Class I, Level A).'

Your doctor is not treating you according to the standard guidelines.
Is this a hepatologist at a transplant center?
You should ask them why you have not been prescribed a beta-blocker unless you have other health issues that prevent treatment such as your low blood pressure? If that is the case you will need more surveillance with endoscopy and possible banding to prevent bleeding.

You want to take preventative action now. Once you have the first bleed there is no going back.
'Patients who survive an episode of acute variceal hemorrhage have a very high risk of rebleeding and death. The median rebleeding rate in untreated individuals is around 60% within 1-2 years of the index hemorrhage, with a
mortality of 33%.'

Talk to your hepatologist soon. Do not strain yourself by lifting large weights, doing situps and bench pressing weights as it can cause a bleed.

Good luck!
Hector
3 Comments Post a Comment
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446474_tn?1404424777
The preferred, albeit indirect, method for assessing portal pressure is the wedged hepatic venous pressure (WHVP) measurement, which is obtained by placing a catheter in the hepatic vein and wedging it into a small
branch or, better still, by inflating a balloon and occluding a larger branch of the hepatic vein.
This is rarely done as the exact pressure is not needed and what is important is to stop the resulting complications such as life-threatening variceal bleeds. Also . Limitations of HVPG measurement are the lack of local expertise and poor adherence to guidelines that will ensure reliable and reproducible measurements, as well as its invasive nature.

The normal HVPG is 3-5 mmHg. Patients with cirrhosis and gastroesophageal varices have an HVPG of at least 10-12 mm Hg.

Gastroesophageal varices are present in approximately 50% of patients with cirrhosis. Their presence correlates with the severity of liver disease while only 40% of Child A patients have varices, they are present in 85% of Child C patients.


An ultrasound can detect portal flow issues and is cheap and non-invasive. It can also see the enlarged spleen which is a complication of portal hypertension.

Portal hypertension is a result of complete cirrhosis and limited blood flow through the liver due to scarring. Only if the liver disease is reserved early can the portal hypertension be reversed. SO we focus many on the affects of portal hypertension. Ascites, HE, collateral blood flow.

The portal vein supplies the majority of blood to the liver. That blood comes from the GI tract and the spleen.
When scar tissue in the liver interferes with that blood flow--- pressure can build in the portal vein ("portal hypertension"). Portal Hypertension can cause the spleen to enlarge and varices to form in the GI tract.
---> As the spleen enlarges-- platelets are trapped in the spleen. (The platelet count in the bloodstream falls.) (Platelets help our blood to clot. So as the platelet count falls... bleeding time is increased.)
---> Varices are dangerous because there's a risk that they can burst and bleed (hemorrhage).

Sometimes people ask why cirrhosis can progress, even when the cause of the liver disease is removed such as curing HCV. The reason is that sometimes cirrhosis itself (scar tissue) can interfere so much with blood flow through the liver-- it causes more cells to die even thought the scarring is not increasing.

Grade 2 varices are enlarged, twisted varices occupying less than one third of the lumen.
Grade 3 and red wheals are in danger of bleeding and intervention should be performed before the first bleed.

'In patients with medium/large varices that have not bled and are not at the highest risk of hemorrhage (Child A patients and no red signs), nonselective -blockers (propranolol, nadolol) are preferred and EVL (banding) should be considered in patients with contraindications or intolerance or non-compliance to-blockers (Class I, Level A).'

Your doctor is not treating you according to the standard guidelines.
Is this a hepatologist at a transplant center?
You should ask them why you have not been prescribed a beta-blocker unless you have other health issues that prevent treatment such as your low blood pressure? If that is the case you will need more surveillance with endoscopy and possible banding to prevent bleeding.

You want to take preventative action now. Once you have the first bleed there is no going back.
'Patients who survive an episode of acute variceal hemorrhage have a very high risk of rebleeding and death. The median rebleeding rate in untreated individuals is around 60% within 1-2 years of the index hemorrhage, with a
mortality of 33%.'

Talk to your hepatologist soon. Do not strain yourself by lifting large weights, doing situps and bench pressing weights as it can cause a bleed.

Good luck!
Hector
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89592_tn?1391278022
I had an Abd US and they did not mention anything about the portal hypertension. It stated that the spleen was normal...everything was normal sized except for the mild hetergeneous echocencity of the liver which was non specific for heptocellular disease but........my labs are mildly abnormal in all those that point towards liver disease.

My gastro performed the EGD and when I rcvd my results 15 days later (online...no call from the dr)  the egd report said Normal..no mention of varices though he had sent me to the hosp for the ABD US.  I called their office and asked about the varices.  "Monica" said that the gastro does not do anything with the varices if they're not bleeding or look like they will bleed.  Thats when I decided to see another gastro and switch.  I will see the new gastro on Feb 5th and ask about seeing a hep.  

There is a Hepatolgy clinic here.  I am close (45 mins) to the Cleveland Clinic/University Hospitals.

My Meld score is 7 or 8.  

I will know more of what's going on in Feb...I'm sure thats when I'll be referred to a hepatologist.

Long history of rheum arthritis, etc etc etc

Thank you Hector...  How are you doing?  I'm going to order the book you mentioned in a previous post.  
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Thank you so much for the detailed explanation. I was wondering how it was detected.

PaulaAnn, thank you for asking the question. I have been wondering how they find out, was hesitant to ask
Dee
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