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Dr.Roshan Kumar Shah
Phase A Resident
Dept. of Paediatric Surgery
BSMMU
CONTENTS
• ANATOMY
• INTRODUCTION
• CAUSES OF PORTAL HYPERTENSION
• PATHOPHYSIOLOGY
• CLINICAL EVALUATION
• MANAGEMENT
PORTAL VEIN
 Drains the blood from the abdominal part
of alimentary tract, except the lower part of
rectum and anal canal
 Also receives the veins from the spleen,
pancreas, gall bladder.
 These veins unite to form the trunk of
portal vein, finally drains into the inferior
vena cava via hepatic vein.
PORTAL VEIN FORMATION
 Portal vein is formed by
the union of superior
mesenteric vein and
splenic vein behind the
neck of pancreas, in
front of inferior vena
cava, at the level of L2
vertebrae.
CHARACTERISTIC OF PORTAL VEIN:
 It measures about 8cm in length and 2cm
in width(adult).
 The normal portal venous pressure is 5-
15mm of Hg
 Portal vein and its tributaries are devoid of
valves, although developmentally valves
are present.
 It acts as reservoir of blood.
CHARACTERISTIC OF PORTAL
VEIN:
 Two streams of blood
circulate through the trunk of
portal vein:
-Blood from superior
mesenteric vein is conveyed
by the right branch of portal
vein.
-Blood from splenic vein is
conveyed by its left branch.
TRIBUTARIES OF PORTAL VEIN:
PORTAL CIRCULATION:
SITE OF PORTOSYSTEMIC
ANASTOMOSIS
PORTAL HYPERTENSION:
 Portal hypertension is an increase in the blood
pressure with in a system of veins called the
portal venous system.
 Portal hypertension may be defined as pressure
in the portal venous bed that exceeds above 40
mm of Hg
MEASUREMENT:
Measurement of PVP:
1. Direct measurement – by
catheterization of the portal vein or one of
its tributaries and insertion of a manometer
(cm H2O).
2. Indirect measurement - by
catheterization of the splenic pulp & by
angiographic balloon-tipped catheterisation
into the jugular or femoral vein .
CAUSES OF PORTAL
HYPERTENSION
CAUSES OF EXTRA HEPATIC
PORTAL VEIN OCCLUSION:
 Septicaemia
 Thrombophilia
 Pancreatitis
 Splenectomy
 Umbilical sepsis
 Umbilical vein catheterization
 Cholangitis/choledochal cyst
PATHOPHYSIOLOGY OF
PORTAL HYPERTENSION:
Obstructive, stenotic, or constrictive vascular
lesions
Increased resistance to flow in the vessels
Fibrosis/ capillarization of sinusoids,
presence of microthrombi in intrahepatic
vasculature & regenerative nodule
formation
Production of vasoactive substances
-NO, PGE2 (vasodilators)
PATHOPHYSIOLOGY OF
PORTAL HYPERTENSION:
-endothelin-1, angiotensin ||, leukotrienes,
(vasoconstrictors)
Impaired sinusoidal relaxation
Activation of hepatic stellate cells(lipid storing cells)
Increases IHVR
CLINICAL EVALUATION
& MANAGEMENT
DIAGNOSIS:
Diagnosis is made by-
1.Clinical information
2.Laboratory investigations
3.Imaging
HISTORY TAKING
• Acute: hematemesis, hematochezia, melena,
shock.
• Other cases:
• History of Acute bleeding
• Anemia
• Abdominal distension
• Abdominal mass
• Disorientation, Convulsion
• Jaundice
CLINICAL FEATURES:
 Gastrointestinal hemorrhage.
 Portal hypertensive gastropathy.
 Splenomegaly and hypersplenism.
 Ascites.
 Encephalopathy.
 Bleeding from non gut sites.
 Pulmonary disorder.
CLINICAL PRESENTATION:
 Gastrointestinal hemorrhage:
 Most common, dramatic and ominous sign.
 Bleeding most commonly occurs from varices in the
distal esophagus and gastric cardia.
 Variceal hemorrhage may take the form of
hematemesis, hematochezia, melena, or chronic
anemia.
 The bleeding may be sudden and life threatening
and is usually not accompanied by abdominal pain.
CLINICAL PRESENTATION:
 Varices may be present in
the lower GI tract as well.
 Melena or the passage of
gross blood through the
rectum or accompanying a
bowel movement may occur
in the absence of
hematemesis.
INVESTIGATIONS
• Laboratory
• Imaging
LABORATORY
• Complete Blood Count
• Liver Function Test
• Renal Function Test
• RBS
IMAGING:
 Abdominal ultrasonography
 Computed tomography (CT) scan
 Magnetic resonance (MR)angiography
 Trans jugular hepatic venography
 Retrograde trans jugular portal venograms
 Hepatic vein angiography
MANAGEMENT
MANAGEMENT OF PATIENTS WITH
ACTIVELY BLEEDING OESOPHAGEAL
VARICES
 Hospitalisation & Resuscitation
 2 wide bore cannula is inserted
 A blood sample is taken & sent for grouping &
cross matching
 NG tube insertion & catheterization
 Restoration of blood volume should be rapid
 Overexpansion of the circulation should be
avoided
 Correct of coagulopathy – by Vitamin K
PHARMACOLOGICAL
• Octreotide
• Vasopressin
• Terlipressin
ENDOSCOPIC THERAPY
• Sclerosant Injection
• Band Ligation
EMERGENCY SURGERY
TRANS JUGULAR INTRA HEPATIC
PORTO SYSTEMIC SHUNTS
The percutaneous
insertion
of vascular stents to
create
channels between the
portal vein and
hepatic veins with in
the parenchyma of
the liver
The percutaneous
inertion
of vascular stents to
create
channels between the
portal vein and
hepatic veins with in
the parenchyma of
the liver
DEFINITIVE SURGERY
• Main treatment is Liver Transplantation
• Other Definitive Procedure:
SURGERY FOR PORTAL
HYPERTENSION
 Shunt operations:
The aim is to lower
the portal pressure
by shunting the portal
blood away from the
liver,e.g,
1.Porta-caval shunting:
End to side
Side to side
2.Proximal spleno-renal shunt.
3.Meso-caval shunt.
4.Selective shunt
(warren Shunt)
5.MESENTERIC-TO-LEFT
PORTAL VEIN BYPASS
(Rex shunt)
NON SHUNT OPERATIONS
 Sugiura
 Modified Sugiura
 Shafiqul’s procedure
SUGIURA OPERATION
MODIFIED SUGIURA
OPERATION
Gastro intestinal endoscopy:
 Establish the cause of GI bleeding
 Presence of varices in the esophagus and
stomach.
 Variceal diameter greater than 5 mm,may show
‘red signs’ of recent or impending variceal
hemorrhage .
 Portal gastropathy is characterized by mucosal
hyperemia
Portal gastropathy in the gastric antrum
(the pylorus is on the right)
PERCUTANENOUS LIVER
BIOPSY:
If there are no contraindications a
percutaneous biopsy is usually undertaken
to diagnose or exclude underlying liver
diseases.
TIPSS
Indication:
Variceal bleeding failed to control by
endoscopic procedure or medical therapy.
Refractory bleeding.
Refractory ascites.
Hepatic venous outflow obstruction in both
transplant and nontransplant patients
Hepatorenal syndrome
TIPSS
Complication:
 Shunt thrombosis
 Shunt occlusion
 Aggravation of preexisting encephalopathy
 Aggravate of liver failure

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