Posted by Hanne (Denmark)

In Reply to: posted by menth

Hello Jamie - here are some more information on Portal hypertension (My
husband suffers from this and has had it for more than 3 years).

Alan (Firebird) wrote >>Your abdomen swells up.<<
Oh well - not nescessarily the only sign... and not always connected to a
variceal bleeding ( I know from my husbands two major variceal bleedings)
- the swolen abdomen is called ascites - and that is not the only sign of
portal hypertension - it might be one of the signs.

Acute portal hypertension may cause mild to moderate enlargement of the
spleen, but marked enlargement requires sustained portal hypertension over a
long period of time. Sustained elevations in pressure occur when cirrhosis
is present. The blood volume is expanded in patients with chronic liver
disease.

If you might want to know more - please contact me on this e-mail:
hepatitis@hepatitis.dk
Hanne (Denmark)

Also our website www.hepatitis.dk with a lot of information in English might
be some help.

Here are some extracts:

Portal hypertension is a complication of cirrhosis and fibrosis.

Portal hypertension is a manifestation of cirrhosis, however numerous other
causes of portal hypertension can produce many of these same clinical
manifestations, such as ascites (fluid within the abdominal cavity) and
variceal bleeding (bleeding from veins in the neck, stomach, and elsewhere).

Portal hypertension is the build-up of pressure in the portal vein (the vein
connecting the intestines and the liver). Normally, the pressure is low
compared with the arterial pressure, but slightly above the pressure in the
other veins in our body system. The most common cause of portal hypertension
and its clinical consequences is liver disease.

Usually, portal hypertension is secondary to liver disease.

It is primarily related to progressive hepatic fibrosis. However, the cause
of chronic liver disease is also important because it may produce specific
symptoms early in the course of disease, such as itching with mechanical
biliary obstruction or severe fatigue with autoimmune chronic active
hepatitis (CAH).

Severity of chronic liver disease is related to deposits of collagen,
leading to fibrosis (scar tissue) in the liver. Therefore, we can define
serious chronic liver disease as any hepatic process stimulating the
progressive deposition of fibrous tissue. The deposition of collagen
(fibrous tissue) causes intrahepatic shunting, disruption in the hepatic
architecture, resulting in portal hypertension, and, eventually, formation
of a fibrous encasement around the liver, which limits regeneration.

Background
The liver has a dual blood supply from the hepatic artery and portal vein.
Blood flow to the intestines, spleen and pancreas eventually drains into the
portal vein and, from there, to the liver. All substances that enter the
body orally are filtered by the liver after absorption by the intestines.

Less than 3% of the liver by weight is normally made up of collagenous
(fibrous) material. As fibrosis increases, a point is reached at which blood
flow in hindered by distortion of the usual flow of blood and the portal
pressure must increase to preserve flow. The hepatic flow of blood comes
from both the hepatic artery (20%) and the portal vein (80%). As hepatic
resistance increases from progressive hepatic fibrosis, portal hepatic flow
must decrease and/or portal pressure must increase. Inevitably, both occur.

Intrahepatic portal hypertension contributes to fluid accumulation in the
abdominal cavity (ascites) by forcing more fluid across the liver capsule
into the abdominal cavity than the body is capable of draining.

What happens in the body?
Visceral congestion causes a larger percent of blood to be pooled in the
portal system. It is analogous to water build-up behind a dammed-up stream.
This occurs slowly as liver disease develops, allowing the body to
compensate by formation of more blood. Thus, the total amount of blood in
the body (intravascular blood volume) increases by 10% to 30%. When a stream
is dammed up, water accumulates until the dam overflows or streams develop
around the dam. The rate at which this occurs depends on the speed with
which the water builds up. The portal pressure builds up in response to
fibrosis. As the portal pressure increases, more blood flows into the liver,
but some tries to find another route to the lower-pressure vena cava system.

Portal hypertension allows some forward portal flow into the liver, but at
the expense of a pressure gradient that produces collaterals (side
branches/secondary blood vessels).

Collaterals form in areas where capillaries and venous systems are
contiguous, and often, had been joined during the embryonic stage. They also
form by reopening fetal connections between vascular systems that closed at
the time of birth. Connections from the portal system to the inferior vena
cava (IVC) system induced by portal hypertension include the hemorrhoidal
veins, splenorenal collaterals, and some abdominal wall and retroperitoneal
collaterals. Connections to the superior vena cava (SVC) system include
collaterals via esophageal and gastric varices, the reopened umbilical vein
through abdominal wall collaterals to the internal mammary system, and
retroperitoneal collaterals.

The primary clinical importance of collaterals is their tendency to bleed
and the diversion of blood away from the liver, thus avoiding the usual
first-pass filtering of toxins and bacteria entering the portal system from
the intestines. Esophageal varices, gastric varices, and hemorrhoids account
for more than 85% of bleeding in patients with cirrhosis. The majority of
life-threatening episodes of bleeding are from esophageal varices.

Metabolic Effects of Portal Hypertension
The liver is a major filter for the removal of substances in the blood.
Substances that enter the body from the intestines must pass through the
liver prior to entering the systemic circulation. This includes orally
ingested foods and drugs, and products secreted into the intestine by the
liver that are reabsorbed by the intestines, such as bile acids. The impact
of liver disease on the blood levels of these substances can be profound. A
decreased first-pass filtering & removal of hormones, toxins, and bacteria
increases the amount of these substances reaching the systemic circulation.

Liver disease also decreases hepatic clearance of substances from the
systemic circulation. Another effect of liver disease is to increase or
decrease the portal input of portal substances such as ammonia with
gastro-intestinal (GI) bleeding or bile acids by decreasing hepatic
synthesis. Substances that are highly extracted by the liver may enter
systemic circulation without the benefit of the first-pass filtering due to
progressive liver disease. If the substance is a drug or toxin that bypasses
the liver, serious side effects may ensue.

Diagnosis
The presence of significant portal hypertension is implied by ascites,
collaterals, or encephalopathy that occurs in the presence of known chronic
liver disease or peripheral clinical evidence of chronic liver disease (firm
liver, enlarged spleen, spider angiomas, clubbing of fingers, palmar
erythema).

An ultrasound test can assess the presence of collaterals (gastric varices
or umbilical vein dilatation), the width of the portal vein, and portal
blood flow with deep Doppler. Improvement in certain ultrasound techniques,
including the FM ultrasound, may allow assessment of the degree of hepatic
fibrosis. The CT scan can be used to assess the presence but not the degree
of portal hypertension.

The demonstration of esophageal varices by endoscopy or barium swallow
implies portal hypertension, as do significant intraabdominal collaterals at
any site.

If you might want to know more - please contact me on this e-mail:
hepatitis@hepatitis.dk
Hanne (Denmark)

Also our website www.hepatitis.dk with a lot of information in English might
be some help.

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