3. INTRODUCTION
• The normal portal venous pressure is about 5-10 mmhg.
• Portal hypertension is define as an elevation of portal pressure >10-
12 mmhg or hepatic venous pressure gradiant >4 mmhg.
• Portosystemic collaterals starts developing with porto venous
pressure of 10 mmhg.
• Variceal bleeding occur when porto venous pressure >12 mmhg.
4. ANATOMY
• The portal system includes all vein
that carry blood from the
abdoiminal part of the alimentary
tract, spleen, pancreas and gall
bladder.
• The portal vein is form by
confluence of the splenic and
superior mesentric vein posterior
to head of pancreas.
• Inferior mesenteric vein drain into
splenic vein anywhere along its
length.
5. COLLATERAL CIRCUALTION
• It develops to carry the portal blood into the systemic vein when the
portal circulation is obstructed whether it be within or outside the
liver.
• There are four main groups of collaterals form during intrahepatic
obstruction.
• GROUP 1
• (A) at cardia of stomach:
Left gastric vein Intercostal vien
Posterior gastric vein Diaphragmo-oesophagel vein
Short gastric vein Azygos minor veins
6. • (B) at anus :
superior haemorrhoidal vein inferior and middle haemorrhoidal
vein
• GROUP 2
paraumbilical veins form collaterals with abdominal wall veins.
• GROUP 3
Where the abdominal organs are in contact with retroperitoneal
tissue or adherent to the abdominal wall.
• GROUP 4
splenic vein forms collaterals with left renal vein via diaphragmatic,
pancreatic, left adrenals or gastric veins.
12. CLINICAL MANIFESTATION
• Gastrointestinal bleeding is most common presentation of portal
hypertension.
• Bleeding most commonly occurs from varices in the disatl
oesophagus and gastric cardia, Rectal bleeding is less common.
• Varicel haemorrhage may take the fom of hematemesis,
hematochezia, melena or chronic anemia.
• Splenomegaly is second most common finding in children with portal
hypertension.
• Hypersplenism occurs particularly in children with extrahepatic portal
vein thrombosis.
13. • Encephalopathy: it occurs in children with advanced liver disease
with jaundice and low level of liver dependent coagulation factors or
low albumin level.
• Learning disability ,behavioral abnormalities are manifestations of
encephalopathy in children.
• Children may also have accompanying hyperammonemia.
• Bleeding from nongut site due to severe thrombocytopenia in the
form of hematuria ,menorrhagia,epistaxis,hematochazia.
• ASCITIS is the presenting sign of portal hypertension in 7-21 % of
children. It can develop at any time with cirrhosis .
15. DIAGNOSIS
• Hemogram for hypersplenism
• Liver function test
• Doppler- ultrasound
• UGI endoscopy for varieces
• Specific investigation for underlying etiology
• Viral markers
• Coagulation profile
• CECT
• MRI
• Venography
• Liver biopsy
16. PORTAL PRESSURE MEASUREMENT
• Hepatic venous pressure gradient = wedged hepatic venous pressure
– free hepatic venous pressure
• The normal HVPG is 5-6 mmHg and >10 mmHg represent clinically
significant portal hypertension.
• HVPG is related to survival and also to prognosis in patient with
bleding oesophageal varices
• It may use to monitor thrapy for instance the effect of beta blockers
such as propranolol.
17. Management of acute variceal bleeding
• MEDICAL MANAGEMENT:
• Fluid resuscitation initially in the form of crystalloid infusion followed
by replacement of red blood cells.
• Care should be taken to overtransfusing children as it increase portal
pressure.
• coagulopathy correction by vitamin k or platelet or FFP .
• Nasogastric tube should be placed to document presence of blood
within the stomach and monitor for ongoing bleeding.
• H2 blocker or PPI i.v.
• i.v. antibiotic as there is higher chances of infection.
18. • Pharmacological therapy :
• VASOPRESSIN AND TERLIPRESSIN : Acts by increasing splancnic
vascular tone and thus decrease portal blood flow.
• S/E: it causes vasoconstriction which can impair cardiac function and
perfusion of heart,bowel and kidney.
• SOMATOSTATIN ANALOG OCTREOTIDE : it decreases splancnic blood
flow with fewer side effect.
19. • SURGICAL MANAGEMENT:
• After failure of medical management endoscopy with variceal band
ligation or variceal sclerotherapy is preffered.
• Sclerotherapy treatment may be associated with
bleeding,bacteremia,esophageal ulceration, stricture formation.
• If patient continue to bleed despite of these treatment ,SENGSTAKEN-
BLAKEMORE TUBE may be placed to decrease hemorrhage by
mechanically compressing esophageal and gastric varices.
20. • PORTOCAVAL SHUNT : it diverts nearly all of the portal blood flow into
the subhepatic inferior right vena cava.
