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Portal Hypertension. By Dr. GOUDA ELLABBAN Ass. Prof. of General and hepatobiliary surgery. Portal vein anatomy. The portal vein is formed in front of IVC and behind the neck of the pancreas ( at the level of 2 nd lumber vertebra ) by union of the splenic & SMV.

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Portal hypertension l.jpg

Portal Hypertension



Ass. Prof. of General and hepatobiliary surgery

Portal vein anatomy l.jpg
Portal vein anatomy

  • The portal vein is formed in front of IVC and behind the neck of the pancreas ( at the level of 2nd lumber vertebra ) by union of the splenic & SMV.

  • It is 7-8 cm in length & contains no valves.

  • It courses in the lesser omentum posterior to both the common hepatic artery & common bile duct.

Portal vein anatomy3 l.jpg
Portal vein anatomy

  • It bifurcates into the Lt & Rt trunks in , or just below the hillum of the liver.

    Its main tributaries are :

  • The coronary (Lt gastric) vein.

  • Pyloric vein.

  • Cystic vein.

  • Pancreaticodudenal vein.

  • Ligamentum teres (umbilical vein).

  • Ligamentum venosum.

Portal vein anatomy5 l.jpg
Portal vein anatomy

  • The portal venous branches ramify in an arterial like pattern and end in dilated channels called sinusoids, which are equivalent to systemic capillaries.

  • From here blood drains into the hepatic venous system.

  • The normal portal pressure is 5-7 mmHg (8-12 cm of water).

  • Portal hypertension is present when the portal vein pressure exceeds 12 mmHg

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Causes of portal hypertension

  • Increased resistance to flow

    A)Pre-hepatic (portal vein obstruction):

  • 1- congenital atresia or stenosis.

  • 2- thrombosis of portal vein.

  • 3- thrombosis of splenic vein.

  • 4- Extrinsic compression (e.g , tumor).

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Causes of portal hypertension


  • 1- liver cirrhosis  obstruction is sinusoidal & post-sinusoidal.

  • 2- bilharzial periportal fibrosis  obstruction is pre-sinusoidal.

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Causes of portal hypertension

The causes of portal hypertension in cirrhotic patients are:

  • Diminution of the total vascular bed by obliteration, distortion, & compression of sinusoids.

  • Compression of the tiny radicals of portal & hepatic veins by excessive fibrosis.

  • Development of multiple arteriovenous shunts between the branches of the hepatic artery & portal vein.

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Causes of portal hypertension

C) Post-hepatic:

  • 1- Budd-Chiari syndrome ( hepatic vein thrombosis )  prominent ascites ,hepatomegaly & abdominal pain.

  • 2- Veno-occlusive disease.

  • 3- Cardiac disease:

    a- constrictive pericarditis.

    b- valvuar heart disease.

    c- right heart failure.

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Causes of portal hypertension

  • Increased portal blood flow

    A)Arterial-portal venous fistula.

    B)Increased splenic flow:

    1- Banti’s syndrome

    ( liver disease secondary to splenic disease, result from cirrhosis & other hepatic disorders)

    2- Splenomegaly (e.g tropical splenomegaly ,hematologic diseases).

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Sequelae & Clinical picture

1-Porto-systemic collaterals:

  • In normal conditinos  collapsed.

  • In portal hypertension  engorged  divert blood away from the portal circulation.

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Sequelae & Clinical picture

  • The important sites of these collaterals are:

    a)At the lower end of oesophagus

    Oesophageal tributaries of Lt gastric vein (portal)

    Oesophageal tributaries of hemiazygous vein (systemic).

    b)Around the umbilicus

    Para umbilical vein (portal)

    Superior & inferior epigastric veins (systemic)

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Sequelae & Clinical picture

c)Lower rectum & analcanal

Superior rectal vein (portal)

Middle & Inferior rectal veins (systemic)

d)At the back of the colon

Rt & Lt colic veins (portal)

Rt & Lt renal veins (systemic)


Tributaries of superior & inferior mesentric veins { Retzius } (portal)

Posterior abdominal & subdiaphragmatic veins (systemic)

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Sequelae & Clinical picture

2- Splenomegaly

  • The most constant physical finding.

  • In 80% of patients regardless the cause.

    * In Bilharzial cases :

  • at 1st due to reticuloendothelial hyperplasia due to absorption of bilharsial toxins.

  • With progress of portal hypertension  due to congestion.

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Sequelae & Clinical picture

3-Congestion of the whole GIT

  • Leads to anorexia, dyspepsia, indigestion, and malabsorption.

    4-Bleeding varices.

    5-Ascites (multifactorial)

  • Portal hypertension alone cannot cause ascites.

  • Hypoalbuminaemia  below 3 gm/100 ml.

  • Salt &water retention high level of aldosterone, oestrogens & anti-duretic hormone.

  • Increased lymphatic transudation from liver surface.

Investigations l.jpg

1.Assessment of liver function tests

  • (a)Hypoalbuminaemia.

    The liver is the only site of albumin synthesis.

  • (b)ALT & AST are moderately raised.

  • (c)Prothrombin time and concentration are disturbed.

    This test is the most sensitive liver function.

Investigations18 l.jpg

2.Detection of oesophageal varices by:

(a)Fibreoptic upper endoscopy

(b)Barium swallow can visualize varices in 90% of cases.

They appear as multiple, smooth, rounded filling defects (honey-comb appearance)

(c)Duplex scan can show dilated portal vein and collaterals.

Investigations20 l.jpg

3.Detection of splenic sequestration and hypersplenism.

  • (a) Blood picture anaemia, leucopenia, thrombocytopenia or pancytopenia.

  • (b) Bone marrow examination hypercellularity.

  • (c) Radioactive isotope studies :

    using the patients own RBCs tagged with 51Cr diminished half life of RBCs & increased radioactivity over the spleen.

Investigations21 l.jpg

4.Diagnosis of the aetiology of liver disease is performed by:

  • (a) Immunological tests for hepatitis markers.

  • (b) Liver biopsy after assessment of prothrombin time and concentration.

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Child Pugh classification

Grade A, 5-6 points; Grade B, 7-9 points; Grade C, 10-15 points

Treatment l.jpg

Management of patients with actively bleeding oesophageal varices


The patient should be admitted to hospital.


  • A wide bore cannula is inserted.

  • A blood sample is taken.

  • Restoration of blood volume should be rapid.

  • Overexpansion of the circulation should be avoided .

  • Morphine and Pethidine are contraindicated.

Treatment24 l.jpg

3.Correct coagulopathy.

  • Vitamin K is administered intravenously.

    4.Prevent encephalopathy.

    Blood in the intestine will be fermented to ammonia and other nitrogenous products.

  • Repeated enemas.

  • Oral lactulose.

    This is a disaccharide sugar, fermented by the intestinal flora  lactic acid combines with ammonia.

  • Neomycin 0.5 gm every 4 hours can reduce the bacterial flora.

Treatment25 l.jpg


  • Intra- or Para- Variceal.

  • 1-3 ml sclerosant (ethanolamine oleate).

  • Occludes venous channels.

  • Multiple sessions (2 weekly).

  • Control bleeding in 80-95 %.

  • About 50% rebleed.

  • 30% complication rate.

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Endoscopic Sclerotherapy



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Retrosternal discomfort for few days.





Complications of Sclerotherapy

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Endoscopic Banding

  • Occludes venous channels

  • Sessions < sclerotherapy

  • Same results as sclerotherapy

  •  complications vs sclerotherapy

  • Endoscopic treatment of choice

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Vasopressin vasoconstriction of the splanchnic circulation.

  • Dose 0.2 unit/kg wt, dissolved in 200 ml of 5% dextrose, over 20 minutes.


  • colicky abdominal pains, & diarrhoea .

  • anginal pains, so it is contraindicated in the elderly.

  • Produce temporary control of bleeding in about 80% of cases.

  • To prolong its action it is combined with glycine (Glypressin).

Treatment31 l.jpg


  • lower the intravariceal pressure without significant side effects.

  • Initial bolus 100 microgram continuous infusion of 25 microgram/ h for 24 hs.

Beta blockare

 bleeding by  cardiac output.

Does 20-60 mg bid  25%  in HR.

Reduces 40% of bleeding episodes

Does not reduce mortality

Treatment32 l.jpg

Balloon tamponade by Sengestaken or Linton tube.

  • The gastric balloon is inflated first by 200 ml of air, and pulled upwards to press the gastric fundus.

  • If bleeding continues, the oesophageal balloon is inflated.

  • The pressure in the oesophageal balloon should not exceed 40 mm Hg.

  • This therapy is effective in controlling bleeding in 80-90% of cases.

Treatment33 l.jpg

Disadvantages :

  • Discomfort to the patient.

  • The patient cannot swallow his saliva

  • Liability to cause oesophageal ulceration or stricture.

  • Once the tube is deflated, there is liability to rebleeding in 60-80% of patients.

    Balloon tamponade is only used as a temporary measure before sclerotherapy or surgery.

Treatment35 l.jpg

Emergency surgery.

If all the previous measures fail to stop bleeding, surgery is recommended.

  • If the general condition of the patient is satisfactory  splenectomy, portoazygos disconnection and stapling of the oesophagus.

  • If the patient is not very fit stapling alone can be performed.

Treatment36 l.jpg

  • Trans-juguJar Intra-hepatic Porto-Systemic Shunt ( TIPSS )

Treatment37 l.jpg

Indications for TIPSS:

  • Refractory bleeding

  • Prior to transplant

  • Child C

  • Refractory ascites

    Main early complication:

  • Perforation of liver capsule  massive haemorrhage.

Treatment38 l.jpg

Treatment of patients with history of bleeding oesophageal varices:

  • 1. Repeated sclerotherapy until the varices are obliterated is the first choice.

  • 2. Elective surgery is mainly indicated if sclerotherapy failed to stop recurrent attacks of bleeding provided that they are fit.

Treatment39 l.jpg

Operations for portal hypertension

Shunt operations.

  • The idea of these operations is to lower the portal pressure by shunting the portal blood away from the liver

Total shunt operations l.jpg
Total shunt operations

1-Porta-caval operation

End to side Side to side

Porta caval operation l.jpg
Porta-caval operation

  • very efficient in lowering the portal pressure  no bleeding occurs from the varices.


  • deprives the liver of portal blood flow  accelerates the onset of liver failure.

  • Recurrent hepatic encephalopathy in 30-50% of patients.

Proximal spleno renal shunt l.jpg
Proximal spleno-renal shunt

  • indicated if the portal vein is thrombosed or if splenectormy is indicated due to hypersplenism .

  • The incidence of encephalopathy is less than after porta caval shunt.

  • it is less effective In preventing further bleeding.

  • If the splenic vein is less than 1 cm the anastmosis is liable to thrombosis.

Mesocaval drapanas shunt l.jpg
Mesocaval (Drapanas) shunt

  • insertion of a a synthetic graft as dacron, or autogenic vein between the superior mesenteric vein and inferior vena cava.

  • The incidence of thrombosis is high

Selective shunt warren shunt l.jpg
Selective shunt (Warren shunt)

  • The Rt and Lt gastric vessels are ligated.

  • The proximal end of splenic vein is ligated while the distal end is anastomosed to the left renal vein.

  • The short gastric veins are preserved and will selectively decompress the lower end of the oesophagus.

  • The incidence of encephalopathy is low, and the liver functions remain normal.

Porta azygos disconnection operations l.jpg
Porta azygos disconnection operations

There are many techniques for performing devascularization.

Hassab Khairy operation

  • splenectomy & ligation of the Rt and Lt gastric vessels, the short gastric vessels and the vascular arcade along the greater curvature of the stomach leaving only the right gastroepiploic vessels.

Slide46 l.jpg

Liver transplant l.jpg
Liver Transplant are ligated.

  • Indicated for liver failure

    Not for variceal bleeding.

  • 24% in USA die on waiting list

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Control of Ascites are ligated.

  • Sodium / Water Restriction.

  • Spironolactone.

  • Loop Diuretic.

  • Large Volume  Paracentesis.

  • Peritoneal-Venous Shunt .


Slide49 l.jpg

THANK YOU are ligated.

Tips on portal hypertension for surgeons l.jpg

TIPS are ligated.on Portal Hypertension for Surgeons



Variceal bleeding resuscitation l.jpg
VARICEAL BLEEDING are ligated.Resuscitation

  • Treat hemorrhagic shock

    Crystalloid (Limited)

    Platelets (Rarely)

    Red Cells + FFP

  • Goal: Tissue Perfusion

  • Monitor: Urine Output

  • Caveat: Do NOT overload

Variceal bleeding initial treatment l.jpg
VARICEAL BLEEDING are ligated.Initial Treatment

  • Continue Tx hemorrhagic shock

  • IV therapy



Variceal bleeding diagnosis l.jpg
VARICEAL BLEEDING are ligated.Diagnosis

  • 50% UGI bleeds not variceal

    (MW Tear, Gastritis, Gastric/Duodenal Ulcer)

  • Early endoscopy mandatory

  • Variceal bleeding Dx’d:

    Active bleeding


    Varices and NO other source

Variceal bleeding initial therapy l.jpg
VARICEAL BLEEDING are ligated.Initial Therapy

  • Continue I.V. Sandostatin®

  • Endoscopic Therapy

  • Sengstaaken-Blakemore tube

  • TIPS

  • Emergency operation

Variceal bleeding supportive therapy l.jpg
VARICEAL BLEEDING are ligated.Supportive Therapy

  • Correct coagulopathy

    FFP, vitamin K, +/- platelets

  • Pulmonary

  • Other infection

  • Encephalopathy

  • Nutrition

Variceal bleeding evaluation l.jpg
VARICEAL BLEEDING are ligated.Evaluation

  • Child class

  • History

  • Hepatitis profile

  • Angiography

  • Transplant evaluation

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Child-Pugh Classification are ligated.

Grade A, 5-6 points; Grade B, 7-9 points; Grade C, 10-15 points

Variceal bleeding definitive therapy l.jpg
VARICEAL BLEEDING are ligated.Definitive Therapy

  • Rationale: 67% rebleed

  • Most rebleed < 6 weeks

  • Definitive Tx during initial stay

Variceal bleeding definitive therapy59 l.jpg
VARICEAL BLEEDING are ligated.Definitive Therapy

  • Medical

  • Endoscopic

  • Surgical

  • Radiological

Variceal bleeding medical therapy l.jpg
VARICEAL BLEEDING are ligated.Medical Therapy

  • Beta blockade

     bleeding by  cardiac output

    Goal: 25%  in heart rate

    Reduces # bleeding episodes

    Does not reduce mortality

    Use as adjunct

Endoscopic banding61 l.jpg
Endoscopic Banding are ligated.

  • Occludes venous channels

  • Multiple sessions + surveillance

  • >60% rebleed

  • 1/3 fail treatment

  •  complications vs scleroTx

  • = /  efficacy vs scleroTx


Endoscopic banding62 l.jpg
Endoscopic Banding are ligated.

Variceal bleeding surgical options l.jpg

  • Total Shunt

  • Selective Shunt

  • Partial Shunt

  • Non-Shunt

Total shunts l.jpg
Total Shunts are ligated.

End to Side Portocaval

Side to Side Portocaval

Interposition Shunts

Central Splenorenal

Total shunt results l.jpg
Total Shunt Results are ligated.

  • Prevent rebleed > 90%

  • Thrombosis with graft

  • Encephalopathy rate 40%

Selective shunts l.jpg
Selective Shunts are ligated.

  • Goals:

    Prevent variceal bleeding and encephalopathy

  • Mechanism:

    Decompress Varices

    Maintain Portal Perfusion

    Maintain Portal Hypertension

  • Key:

    Decompress onlygastrosplenic compartment

Dsrs vs total shunts l.jpg
DSRS vs Total Shunts are ligated.

  • Six randomized trials in N.A.

  • Mean follow-up 39 mos (1-8 yrs)

Partial shunts l.jpg
Partial Shunts are ligated.

  • Ease of portocaval

  • Limited portal diversion

  • Maintain some liver perfusion

  • Short, straight PTFE graft

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Partial Shunts are ligated.


Ann Surg


Partial shunts71 l.jpg
Partial Shunts are ligated.

Randomized trial in ETOH cirrhotics

Follow-up @ 20 +/- 11 mos

Non shunt operations l.jpg
Non-Shunt Operations are ligated.

  • Options

    Esophageal transection

    Variceal ligation

    Devascularize +/- splenectomy

  • Very limited role

Liver transplant73 l.jpg
Liver Transplant are ligated.

  • Indicated for liver failure

    Not for variceal bleeding

  • Number  > 3,500/yr in U.S.

  • 20,000 potential recipients in U.S.

  • 5,000 listed for transplant

  • 24% die on waiting list

Tips t ransjugular i ntrahepatic p ortocaval s hunt l.jpg
TIPS are ligated.Transjugular Intrahepatic Portocaval Shunt

Slide75 l.jpg
TIPS are ligated.

Slide76 l.jpg
TIPS are ligated.

  • Technically feasible

  • Complications 9 - 50%

    Infection Intraperitoneal Bleeding

    Congestive Failure Subcapsular Hematoma

    Acute Renal Failure Hemobilia

  • Mortality (30 day) 3 - 13%

  • (1) Rossie NEJM 1994;330:165, (2) Rosch Hepatology 1992;16:884,

  • (3) LaBerge Radiology 1993;187:913.

Problems with tips l.jpg
Problems With TIPS are ligated.

  • Encephalopathy minimum 15%

  • Occlusion 33 - 73% @ one year

  • Rebleeding

    18% @ one year (1)

    19% @ 4.7 months (3)

  • (1) Rossie NEJM 1994;330:165, (2) Rosch Hepatology 1992;16:884, (3) LaBerge Radiology 1993;187:913.

The role for tips l.jpg
The Role For are ligated.Tips

  • Refractory bleeding

  • Bridge to transplant

  • Child C

    (all or only “DZ” ?)

  • ??? refractory ascites

  • Relative contraindication: Poor f/u

Special cases of portal hypertension l.jpg

Special Cases of are ligated.Portal Hypertension

Splenic vein thrombosis l.jpg
Splenic Vein Thrombosis are ligated.

  • Etiology:

    Pancreatitis - Acute or Chronic

    Pancreatic Carcinoma

  • Hallmark:

    Isolated Gastric Varices

  • Treatment:

    Splenectomy (if bleeding)

Portal vein thrombosis l.jpg
Portal Vein Thrombosis are ligated.


Congenital - “Cavernous Transformation”


Normal Liver Function W/ Varices



Budd chiari syndrome l.jpg
Budd-Chiari Syndrome are ligated.

  • Etiology

    Hypercoagulable: Estrogens, XRT, Myeloprolif, PNH

    IVC Occlusion: RA Myxoma, Pericarditis, Membrane

    Liver Mass

    High Dose ChemoTx

  • Presentation: Classic Triad

    Abdominal Pain



Budd chiari syndrome83 l.jpg
Budd-Chiari Syndrome are ligated.

  • Diagnosis

    • U/S, CT, Angio

  • Treatment

    • NOT a static disease

    • If NO necrosis  Symptomatic Tx

    • If necrosis  Shunt (PCS or MAS) or Transplant

Some take home points l.jpg
Some Take Home Points are ligated.

  • Child A better than Child C

  • Start Sandostatin when Dx suspected

  • β blockade  bleeding by  C.O

  • Banding safer than scleroTx

  • TIPS: Encephalopathy & occlusion rate

Some take home points85 l.jpg
Some Take Home Points are ligated.

Selective shunt:  encephalopathy

SV Thrombosis: Presentation & Tx

Budd-Chiari: Classic triad

Transplant for liver failure

Portal hypertension etiology l.jpg
Portal Hypertension are ligated.Etiology


    Portal Vein or Splenic Vein Thrombosis


    Cirrhosis (ETOH, Hepatitis, Other Toxins)



Complications of portal hypertension l.jpg
Complications of Portal Hypertension are ligated.

  • Ascites

  • Encephalopathy

  • Variceal bleeding

    • Initial management

    • Evaluation

    • Definitivetherapy

    • Special cases

Encephalopathy l.jpg
Encephalopathy are ligated.

  • Etiology: ? Nitrogen compounds

  • Induced by:

    Infection Dehydration

    Constipation Blood in gut

  • No test is diagnostic

  • Therapy:

    Hydrate Cleanse gut

    ↓ protein Find and treat cause

Ascites l.jpg
Ascites are ligated.

  • Origin:

    Sinusoidal pressure > colloid oncotic pressure

  • Induced by:

    Physiologic Stress

    IV Fluids

  • Complications:

    Spontaneous Bacterial Peritonitis

    “Hepatorenal Syndrome”

Control of ascites91 l.jpg
Control of Ascites are ligated.

  • Sodium / Water Restriction

  • Spironolactone

  • Loop Diuretic

  • Large Volume Paracentesis

  • Peritoneal-Venous Shunt

  • (?) TIPS

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VARICEAL BLEEDING are ligated.General Approach

  • Resuscitation

  • Initial treatment

  • Support

  • Evaluation

  • Definitive therapy

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Vasopressin are ligated.

  • 8-Arginine Vasopressin (ADH)

  • Intense constriction (all beds)

    +’s  Mesenteric Flow

     Portal Pressure

    Stops Bleeding in >80%

    -’s Peripheral Ischemia

    Myocardial Ischemia

  • NTG ’s adverse effects

Sandostatin l.jpg
Sandostatin® are ligated.

  • Long acting STS analogue

    +’s  Mesenteric Flow

     Portal Pressure

    Stops bleeding in > 85%

    Good as VP but  side effects

    -’s Cost


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Portal Vein Anatomy are ligated.

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Portal Vein Collaterals are ligated.

Five Principle Routes

Veins of Retzius

Umbilical Vein




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VARICEAL BLEEDING are ligated.Sclerotherapy

  • Intra- or Para- Variceal

  • Occludes venous channels

  • Multiple sessions + surveillance

  • >60% rebleed

  • 1/3 fail treatment

  • 30% complication rate

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Endoscopic Sclerotherapy are ligated.



Complications of sclerotx l.jpg

LOCAL are ligated.








Complications of ScleroTx

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Total Shunts are ligated.

  • Divert most (all?) portal flow

  • Options

    Portocaval Shunt (E-S or S-S; +/- Graft)

    Interposition Shunt

    Central Splenorenal Shunt

Slide101 l.jpg
TIPS are ligated.

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SclTx are ligated.vs TIPS

Five Randomized Trials - 360 patients

Mean Follow-up 15 mos (1-36)

* p < 0.05 in all but one study

** p < 0.05 in all studies

*** n.s. in all but one study where survival  w/ SclTx