portal hypertension and esophageal varices

1. TROPICAL MEDICINETROPICAL MEDICINE
DEPARTEMENTDEPARTEMENT
Medical Education ProgramsMedical Education Programs
‫الرحيم‬ ‫الرحمن‬ ‫ال‬ ‫بسم‬

3. By
Mahmoud Saad Desoky

4. To a very large extent, the health and well-being of
an individual is dependent on the proper functioning
of this important detoxifying organ. …

5. Portal hypertension
common clinical syndrome, which is
hemodynamically defined as pathological increase
of the portal pressure gradient(the pressure
difference between the portal vein and the inferior
vena cava)
And by the formation of portal–systemic
collaterals that shunt part of the portal blood flow to
the systemic circulation by passing the liver,
Normal values of the portal pressure gradient are of
1–5 mm Hg.

6. Portal hypertension is a frequent complication of
cirrhosis, and plays a crucial role in the transition
from the pre clinical to the clinical phase of the
disease.
Portal hypertension is a contributing factor for the
development of ascites and hepatic encephalopathy and a
direct cause of variceal haemorrhage and of bleeding-
related death, Bleeding from ruptured oesophago-gastric
varices is the most severe complication of cirrhosis, and is
the cause of death in about one third of cirrhotic patients.

7. The yearly rate of development of ‘‘new”
varices is about 5–10% per year in patients
with cirrhosis, and the progression from
small to large varices occur in 10% to 20% of
cases after 1 year.
In the 2 years following the first detection of
EV, the risk of variceal bleeding ranges
between 20% to 30% and results in 25% to
50% mortality within a week of the first
bleeding episode

9. The current recommendations states
that all cirrhotic patients should be
screened for the presence of varices at
the time of initial diagnosis of cirrhosis.
Follow-up endoscopy should be
performed at 2-3 years intervals in
compensated patients with no varices,
and at 1-2 years intervals in
compensated patients with small varices

10. Clinically significant portal hypertension
(CSPH) is diagnosed when clinical
manifestations of the disease appear or when
portal pressure gradient (in case of cirrhosis)
determined by its equivalent, the hepatic
venous pressure gradient (HVPG)) exceeds a
threshold value of 10 mm Hg. Values of
portal pressure gradient between 5 and 9
mm Hg correspond to preclinical portal
hypertension

13. Portal vein
is
not a true vein

14. The intrahepatic circulation has some
unique features. One is the dual blood
supply from portal vein and hepatic
artery. Thirty percent of the flow and
30% to 60% of the oxygen consumed
by the liver comes from the hepatic
artery while the rest comes from the
portal vein

15. 2 The dual hepatic blood supply makes the
normal liver resistant to anoxia. Ligation of
the portal vein, for example, will not
cause hepatocellular necrosis. Similarly,
accidental ligation of the hepatic artery or its
major branches does not necessarily lead to
hepatic failure, except in the transplant
setting, where the organ is much more
dependent on hepatic arterial blood flow.
There is also a unique interrelationship
between hepatic artery and portal vein

16. In both animals and humans, a decrease in portal
venous flow or sinusoidal pressure causes a reflex
increase in hepatic arterial flow. Conversely, an
increase in sinusoidal flow or pressure causes
a reflex decrease in hepatic arterial flow. This
buffer response may be mediated by adenosine,
and the response maintains a constant hepatic
blood flow despite changes in portal venous flow
that occur during digestion.

17. 20 %
80 %

19. Prehepatic
Hepatic
Posthepatic

20. Prehapatic
(portal vein obstruction)
• Thrombosis of portal vein
• Congenital atresia / stenosis
• Extrinsic compression

21. Hepatic
• Cirrhosis
• Schistosomiasis

22. Posthepatic
• Budd-Chiari syndrome
• Cardiac disease

24. Hemodynamic principles and causes of
portal hypertension
Portal hypertension is a pathologic increase in
the portal venous pressure gradient
between the portal vein and the inferior
vena cava. It results from changes in portal
resistance together with changes in portal
inflow, as defined by Ohm’s law:

47. • Group I: where protective epithelium adjoins absorptive epithelium:
• (a) At the cardia of the stomach, where the left gastric vein,
posterior gastric and short gastric veins of the portal system
anastomose with the intercostal, diaphragmo - oesophageal and
azygos minor veins of the caval system. Deviation of blood into these
channels leads to varicosities in the submucous layer of the lower
end of the oesophagus and fundus of the stomach (Kimura K,1999).
• (b) At the anus, the superior haemorrhoidal vein of the portal
system anastomoses with the middle and inferior haemorrhoidal
veins of the caval system. Deviation of blood into these channels may
lead to rectal varices.

48. • Group II:
in the falciform ligament through the paraumbilical
veins, relics of the umbilical circulation of the fetus
• Group III:
where the abdominal organs are in contact with
retroperitoneal tissues or adherent to the abdominal
wall. These collaterals run from the liver to diaphragm
and in the splenorenal ligament and omentum. They
include lumbar veins and veins developing in scars of
previous operations or in small or large bowel stomas.

49. • Group IV:
portal venous blood is carried to the left renal vein. This
may be through blood entering directly from the splenic
vein or via diaphragmatic, pancreatic, left adrenal or gastric
veins. Blood from gastro - oesophageal and other collaterals
ultimately reaches the superior vena cava via the azygos or
hemiazygos systems. A small volume enters the inferior
vena cava. An intrahepatic shunt may run from the right
branch of the portal vein to the inferior vena cava
Collaterals to the pulmonary veins have also been described

55. Hippocrates said that:
some patients get well only by the
goodness of their physicians.