Portal hypertension :
pathophysiology,medical and
endoscopic management
ABRAHAM PALACIOS HERNANDEZ
DIGESTIVO TEORICA II
I.C.E.S.T.
Introduction
Often defined as a portal pressure gradient of 10
mmhg.
* Represents the difference in pressure between
portal vein and cava inferior vein
• The PPG result from interaction between
portal blood flow and vascular resistance.
• The relation between these elements can be
explicated with the OHM LAW:
P= Q x R
Acording to the law, the portal pressure can be
increase by a increase of Q or R
Physiophatology
The primary factor The increase in intrahepatic
sinusoidal resistance to portal blood flow.
Bhatal & Grossman described a dynamic
component of the hepatic microcirculation.
* They modified the resistance to blood flow with
vasodilator substances, in livers with cirrhosis
• The results suggested an increase in the
intrahepatic vascular resistance in the
diseased livers (cirrhosis) in response to a
greater amount of blood circulating
vasoconstrictor substances
Like that: norephinephrine
reninangiotensin
vasopressin
Increased portal flow has been
extensively studied
in 1980 showed that in patients with cirrhosis with
elevated levels of glucagon, could help in the
pathogenesis of PH by increasing of portal blood
flow by splanchnic vasodilation*
* Arteriolar vasodilationporta vein = >p.pressure
In Intrahepatic level there is an decrease in the
activity of the eNOs in the liver with cirrhosis.
this due a increased levels of in caveolin 1
This open new possibilities for tratment of the
PH directed to increase intrahepatic levels of
NO and reduction of caveolina 1
• In the increase of the intrahepatic resistance;
besides decrease of NO; there increased levels
of vasoconstrictor substance (norepinephrine,
angiotensin II, vasopressin, endothelin)
• Aggravating the PH syndrome
TREATMENT
PRIMARY PROPHYLAXIS
(Prevention of first bleeding event)
• > 40% of patient with cirrhosis have
esophageal varices at the time of diagnosis.
• 30% of them will have the first episode of
bleeding in the next 20 years; with the
possibility of rebleeding around 60% to 1 year.
With mortality of each episode of 20%
Pharmacological treatment
(B- BLOCKER)
The use of b-blocker allows a reduction of 50%
in the risk of the first variceal bleeding event.
Oral in 2 doses per day, increasing the dose
every 2 days to achieve a reduction of 25% of
heart rate ( get a heart rate of 55 beats per
minute)
• The reduction of the pressure in the portal
territory does not correlate with reduced
heart rate
• * is useful for dispensing the medication
• the way for identify the response to beta
blocker consist in measure porta vein pressure
(by direct puncture)
Measurement of hepatic venous
pressure located
Consits in measure the pressure of
suprahepatics vein and get the “enclave
suprahepatic pressure” ( PSHE) y “free
suprahepatic venous pressure” (PSHL).
The difference between the 2 values is the
“hepatic venous pressure gradient” (GPVH)
GPVH = PSHE - PSHL
• Is considered that there portal hypertension
when the GPVH its more of 5mmhg (1-5
mmhg)
• When the GPVH it`s > 10 mmhg = esophageal
varices
• GPVH >12 mmhg = bleeding and ascites
B-blocker plus isosorbide mononitrate
• This combination can increase the
hemodynamic response in a 30% in patients
who did not respond to b-blocker.
• is not necessary add MNI in patients who
respond a monotherapy
Variceal ligation
• Its indicated in patients who dont respond to
b-blocker treatment.
endoscopic ligation
acts locally at the site of varicose veins
does not alter the physiopathology
is effective but not for long (because the
pressure and portal flow remain unchanged
and the varices recurs in 50% to 2 years
Secondary prophylaxis
(prevention of rebleeding)
Patients who survive the first event of bleeding
have a high risk of rebleeding ( 60%)
Derivation surgery
Has been used for over 50 years.
Consist in derived blood flow from the high pressure site
diverting it of portal territory
DISADVANTAGES: increase the encephalopathy and liver
failure in non-selective derivations
For this, used selective derivations, such as derivation
splenorenal
Transjugular intrahepatic
portosystemic shunt (TIPS)
This derivation does not require surgical
intervention and the morbidity and mortality is
low.
DISADVENTAGES:
50% will have dysfunction due to intimal
proliferation within the prosthesis
Increase of 20 to 30% encephalopathy
B-blocker plus endoscopic ligadure
The combination of variceal ligation more beta
blocker is a good option and is the most
recommended practice today
TIPS and surgery must be used when it has
failed medical and endoscopic treatment
Acute bleeding
by
esophageal varices
Represents an emergency and must start with
volume replacement (to maintain hematocrit
25 to 30%)
Avoid prolonged hypovolemia is important to
prevent infectious complications or renal
failure
Vasoactive therapy should be kept at least 48
hours and 5 days are recommended to
prevent rebleeding
ACUTE BLEEDING by GASTRIC VARICES
Represents 5 to 10% of cases of upper
gastrointestinal bleeding in patients with
cirrhosis
The usual treatment consist in vasoactive drugs
and uses of Sclerotherapy
TIPS and surgery are treatments for rescue in
case of failure to medical and endoscopic
treatment
BIBLIOGRAFÍA
PRINCIPIOS DE GASTROENTEROLOGIA 3 EDICIÓN
