PORTAL HYPERTENSIONPORTAL HYPERTENSION

BY P.VENUMADHAV

6a group5th course

BY P.VENUMADHAV

6a group5th course

Introduction Introduction

The portal vein is formed by the confluence of the splenic vein with the superior mesenteric vein and its formation mostly occurs behind the pancreas in the retroperitoneum. It transports the blood mainly from the gastro-intestinal tract and the spleen to the liver.

Seventy percent of the total blood supply to the liver is contributed by the portal vein while the hepatic artery contributes to the remaining thirty percent.

The portal vein is formed by the confluence of the splenic vein with the superior mesenteric vein and its formation mostly occurs behind the pancreas in the retroperitoneum. It transports the blood mainly from the gastro-intestinal tract and the spleen to the liver.

Seventy percent of the total blood supply to the liver is contributed by the portal vein while the hepatic artery contributes to the remaining thirty percent.

The portal venous system is the only venous system in our body, which begins with capillaries and ends with capillaries. The intrahepatic branches of the portal vein terminate in small vessels that supply the hepatic sinusoids.

Embryologically, the systemic veins of our body develop from the intra-embryonic anterior and posterior cardinal veins while the portal system develops from the extra-embryonic vitelline and umbilical veins, which drain from the yolk sac and the placenta

The portal venous system is the only venous system in our body, which begins with capillaries and ends with capillaries. The intrahepatic branches of the portal vein terminate in small vessels that supply the hepatic sinusoids.

Embryologically, the systemic veins of our body develop from the intra-embryonic anterior and posterior cardinal veins while the portal system develops from the extra-embryonic vitelline and umbilical veins, which drain from the yolk sac and the placenta

Portal Hypertension (PH)Portal Hypertension (PH)

Portal vein pressure above the normal range of 5 to 8 mm Hg

Portal vein - Hepatic vein pressure gradient greater than 5 mm Hg (>12 clinically significant)

Represents an increase of the hydrostatic pressure within the portal vein or its tributaries

Portal vein pressure above the normal range of 5 to 8 mm Hg

Portal vein - Hepatic vein pressure gradient greater than 5 mm Hg (>12 clinically significant)

Represents an increase of the hydrostatic pressure within the portal vein or its tributaries

A rise in the portal pressure leads to splenomegaly and the development of natural porto-systemic shunts at the following sites:

• Lower end of the oeophagus and cardia through th e gastro-oesophageal veins

• The anal canal via the haemorrhoidal veins

• In the falciform ligament via the umbilical veins

• In the abdominal wall and retroperitoneum The diagnosis of portal hypertension should be suspected in a

child after the occurrence of any large gastro-intestinal bleed. In this age group, oesophageal varices are the most likely cause for such an event. Variceal bleeding is associated with a mortality rate of 5 – 9 percent in children with portal vein obstruction but there is a higher risk of death of those with cirrhosis

A rise in the portal pressure leads to splenomegaly and the development of natural porto-systemic shunts at the following sites:

• Lower end of the oeophagus and cardia through th e gastro-oesophageal veins

• The anal canal via the haemorrhoidal veins

• In the falciform ligament via the umbilical veins

• In the abdominal wall and retroperitoneum The diagnosis of portal hypertension should be suspected in a

child after the occurrence of any large gastro-intestinal bleed. In this age group, oesophageal varices are the most likely cause for such an event. Variceal bleeding is associated with a mortality rate of 5 – 9 percent in children with portal vein obstruction but there is a higher risk of death of those with cirrhosis

pathologypathology

1. LIVER The liver is congested and

enlarged in suprahepatic causes.

The liver in cirrhosis is shrunken with sharp edge .

The liver is normal in intrahepatic causes.

1. LIVER The liver is congested and

enlarged in suprahepatic causes.

The liver in cirrhosis is shrunken with sharp edge .

The liver is normal in intrahepatic causes.

2. SPLEEN Splenomegaly due to:-

Hyperplasia pf the RES. Congestive effect of Portal Hypertension. Splenic vein thrombosis.

The most important diagnostic sign of portal hyp. Its size is related to the level of portal pressure but

its size is affected also by:- Age of the patient (larger in young due to fibrosis). Degree of collaterals. Type of cirrhosis ( larger in macronodular cirrh).

Effects of splenomegaly:- Compression on the surroundings Secondary hypersplenism.

2. SPLEEN Splenomegaly due to:-

Hyperplasia pf the RES. Congestive effect of Portal Hypertension. Splenic vein thrombosis.

The most important diagnostic sign of portal hyp. Its size is related to the level of portal pressure but

its size is affected also by:- Age of the patient (larger in young due to fibrosis). Degree of collaterals. Type of cirrhosis ( larger in macronodular cirrh).

Effects of splenomegaly:- Compression on the surroundings Secondary hypersplenism.

3. COLLATERAL CIRCULATION

[1] INFRAHEPATIC OBSTRUCTION:- The collaterals attempt to bypass the obstruction and

return blood towards the healthy liver ( hepatopetal). The intrahepatic vasculature is normal.

Ascending vein of Sappy in hepatogastric ligament Deep cystic vein Veins of the omentum Hepato-colic veins. Hepatorenal veins. Diaphragmatic veins.

[2] INTRAHEPATIC OBSTRUCTION:- The venous blood flow from the hepatic veins is

reduced in cirrhosis and the remainder enters the collateral circulation to systemic circulation (Hepatofugal)

3. COLLATERAL CIRCULATION

[1] INFRAHEPATIC OBSTRUCTION:- The collaterals attempt to bypass the obstruction and

return blood towards the healthy liver ( hepatopetal). The intrahepatic vasculature is normal.

Ascending vein of Sappy in hepatogastric ligament Deep cystic vein Veins of the omentum Hepato-colic veins. Hepatorenal veins. Diaphragmatic veins.

[2] INTRAHEPATIC OBSTRUCTION:- The venous blood flow from the hepatic veins is

reduced in cirrhosis and the remainder enters the collateral circulation to systemic circulation (Hepatofugal)

Portosystemic collaterals are classified into 4 groups:

Four main groups of collaterals varices:

1.Lower end of the esophagus and fundus of the stomach and rectum

2.Umbilical veins 3.Spleno-renal 4.Retroperitoneal Blood from gastro-esophageal and other collaterals

ultimately reaches the superior vena cava via the azygos system

Portosystemic collaterals are classified into 4 groups:

Four main groups of collaterals varices:

1.Lower end of the esophagus and fundus of the stomach and rectum

2.Umbilical veins 3.Spleno-renal 4.Retroperitoneal Blood from gastro-esophageal and other collaterals

ultimately reaches the superior vena cava via the azygos system

Portal Vein CollateralsPortal Vein Collaterals

Coronary vein and short gastric veins -> veins of the lesser curve of the stomach and the esophagus, leading to the formation of varices

Inferior mesenteric vein -> rectal branches which, when distended, form hemorrhoids

Umbilical vein ->epigastric venous system around the umbilicus (caput medusae)

Retroperitoneal collaterals ->gastrointestinal veins through the bare areas of the liver

Coronary vein and short gastric veins -> veins of the lesser curve of the stomach and the esophagus, leading to the formation of varices

Inferior mesenteric vein -> rectal branches which, when distended, form hemorrhoids

Umbilical vein ->epigastric venous system around the umbilicus (caput medusae)

Retroperitoneal collaterals ->gastrointestinal veins through the bare areas of the liver

Pathophysiology of PHPathophysiology of PH

As pressure increases, blood flow decreases and the pressure in the portal system is transmitted to its branches

Results in dilation of venous tributariesIncreased blood flow through collaterals and

subsequently increased venous return cause an increase in cardiac output and total blood volume and a decrease in systemic vascular resistance

With progression of disease, blood pressure usually falls

As pressure increases, blood flow decreases and the pressure in the portal system is transmitted to its branches

Results in dilation of venous tributariesIncreased blood flow through collaterals and

subsequently increased venous return cause an increase in cardiac output and total blood volume and a decrease in systemic vascular resistance

With progression of disease, blood pressure usually falls

Pathophysiology of PHPathophysiology of PH

Cirrhosis results in scarring (perisinusoidal deposition of collagen)

Scarring narrows and compresses hepatic sinusoids (fibrosis)

Progressive increase in resistance to portal venous blood flow results in PH

Portal vein thrombosis, or hepatic venous obstruction also cause PH by increasing the resistance to portal blood flow

Cirrhosis results in scarring (perisinusoidal deposition of collagen)

Scarring narrows and compresses hepatic sinusoids (fibrosis)

Progressive increase in resistance to portal venous blood flow results in PH

Portal vein thrombosis, or hepatic venous obstruction also cause PH by increasing the resistance to portal blood flow

PORTAL HYPERTENSIONPORTAL HYPERTENSION

INCREASED HEPATIC INCREASED HEPATIC VASCULAR RESISTANCEVASCULAR RESISTANCE

INCREASED PORTAL VENOUS INCREASED PORTAL VENOUS INFLOWINFLOW

STRUCTURALSTRUCTURAL VASCULAR TONEVASCULAR TONE

FIBROSISFIBROSIS

REGENERATION REGENERATION

THROMBOSISTHROMBOSIS

ENDOTHELIALENDOTHELIAL

RELAXATION FACTORSRELAXATION FACTORS

NO and othersNO and others

NA/HCONA/HCO22

ENHANCEMENT OF ENHANCEMENT OF ENDOGENOUS ENDOGENOUS

VASOCONTSRICTIONVASOCONTSRICTION

SPLANCHNIC AND SPLANCHNIC AND SYSTEMIC SYSTEMIC VASODILITATIONVASODILITATION

( NO AND OTHERS)( NO AND OTHERS)

EtiologyEtiologyThe aetiology of portal hypertension in children is classified as

1.Cirrhotic - e.g. biliary atresia, cystic fibrosis

2. Non- cirrhotic : (a)Pre-hepatic - e.g. portal vein thrombosis (b) Intra-hepatic :– • Presinusoidal – e.g. congenital hepatic fibrosis. • Parasinusoidal – e.g. fatty liver, nodular

hyperplasia . • Postsinusoidal – e.g. veno-occlusive disease of

liver . (c) Supra-hepatic – e.g. Budd-Chiari syndrome

The aetiology of portal hypertension in children is classified as

1.Cirrhotic - e.g. biliary atresia, cystic fibrosis

2. Non- cirrhotic : (a)Pre-hepatic - e.g. portal vein thrombosis (b) Intra-hepatic :– • Presinusoidal – e.g. congenital hepatic fibrosis. • Parasinusoidal – e.g. fatty liver, nodular

hyperplasia . • Postsinusoidal – e.g. veno-occlusive disease of

liver . (c) Supra-hepatic – e.g. Budd-Chiari syndrome

Pre-hepatic PHPre-hepatic PH

Caused by obstruction to blood flow at the level of portal vein

Examples: congenital atresia, extrinsic compression, schistosomiasis, portal, superior mesenteric, or splenic vein thrombosis

Caused by obstruction to blood flow at the level of portal vein

Examples: congenital atresia, extrinsic compression, schistosomiasis, portal, superior mesenteric, or splenic vein thrombosis

Supra-hepaticSupra-hepatic

Caused by obstruction to blood flow at the level of hepatic vein

Examples: Budd-Chiari syndrome, chronic heart failure, constrictive pericarditis, vena cava webs

Caused by obstruction to blood flow at the level of hepatic vein

Examples: Budd-Chiari syndrome, chronic heart failure, constrictive pericarditis, vena cava webs

Budd-Chiari SyndromeBudd-Chiari Syndrome

Caused by hepatic venous obstructionAt the level of the inferior vena cava,

the hepatic veins, or the central veins within the liver itself

result of congenital webs (in Africa and Asia), acute or chronic thrombosis (in the West), and malignancy

Caused by hepatic venous obstructionAt the level of the inferior vena cava,

the hepatic veins, or the central veins within the liver itself

result of congenital webs (in Africa and Asia), acute or chronic thrombosis (in the West), and malignancy

Budd-Chiari SyndromeBudd-Chiari Syndrome

Acute symptoms include hepatomegaly, RUQ abdominal pain, nausea, vomiting, ascites

Chronic form present with the sequelae of cirrhosis and portal hypertension, including variceal bleeding, ascites, spontaneous bacterial peritonitis, fatigue, and encephalopathy

Diagnosis is most often made by US evaluation of the liver and its vasculature

Cross-sectional imaging using contrast-enhanced CT or MRI

Acute symptoms include hepatomegaly, RUQ abdominal pain, nausea, vomiting, ascites

Chronic form present with the sequelae of cirrhosis and portal hypertension, including variceal bleeding, ascites, spontaneous bacterial peritonitis, fatigue, and encephalopathy

Diagnosis is most often made by US evaluation of the liver and its vasculature

Cross-sectional imaging using contrast-enhanced CT or MRI

Budd-Chiari SyndromeBudd-Chiari Syndrome

Gold standard for the diagnosis has been angiography

Management has traditionally been surgical intervention (surgical decompression with a side-to-side portosystemic shunt)

Minimally invasive treatment using TIPS may be first-line therapy now

Response rates to medical therapy are poor

Gold standard for the diagnosis has been angiography

Management has traditionally been surgical intervention (surgical decompression with a side-to-side portosystemic shunt)

Minimally invasive treatment using TIPS may be first-line therapy now

Response rates to medical therapy are poor

Portal Vein ThrombosisPortal Vein Thrombosis

Most common cause in children (fewer than 10% of adult pts.)

Normal liver function and not as susceptible to the development of complications, such as encephalopathy

Diagnosis by sonography, CT and MRIOften, the initial manifestation of portal

vein thrombosis is variceal bleeding in a noncirrhotic patient with normal liver function

Most common cause in children (fewer than 10% of adult pts.)

Normal liver function and not as susceptible to the development of complications, such as encephalopathy

Diagnosis by sonography, CT and MRIOften, the initial manifestation of portal

vein thrombosis is variceal bleeding in a noncirrhotic patient with normal liver function

Portal Vein Thrombosis - Causes

Portal Vein Thrombosis - Causes

Umbilical vein infection (the most common cause in children)

Coagulopathies (protein C and antithrombin III deficiency),

Hepatic malignancy, myeloproliferative disorders

Inflammatory bowel diseasepancreatitistraumaMost cases in adults are idiopathic

Umbilical vein infection (the most common cause in children)

Coagulopathies (protein C and antithrombin III deficiency),

Hepatic malignancy, myeloproliferative disorders

Inflammatory bowel diseasepancreatitistraumaMost cases in adults are idiopathic

Portal Vein ThrombosisPortal Vein Thrombosis

Therapeutic options are esophageal variceal ligation and sclerotherapy

Distal splenorenal shunt Rex shunt in patients whose

intrahepatic portal vein is patent (most commonly children)

Therapeutic options are esophageal variceal ligation and sclerotherapy

Distal splenorenal shunt Rex shunt in patients whose

intrahepatic portal vein is patent (most commonly children)

Splenic Vein ThrombosisSplenic Vein Thrombosis

Most often caused by disorders of the pancreas (acute and chronic pancreatitis, trauma, pancreatic malignancy, and pseudocysts)

Related to the location of the splenic vein Gastric varices are present in 80% of patientsOccurs in the setting of normal liver functionReadily cured with splenectomy (variceal

hemorrhage), although observation for asymptomatic patients is acceptable.

Most often caused by disorders of the pancreas (acute and chronic pancreatitis, trauma, pancreatic malignancy, and pseudocysts)

Related to the location of the splenic vein Gastric varices are present in 80% of patientsOccurs in the setting of normal liver functionReadily cured with splenectomy (variceal

hemorrhage), although observation for asymptomatic patients is acceptable.

Complications of PHComplications of PH Bleeding:- From esophageal varices due to:-

Rupture due to increase portal pressure. Erosion as in reflux esophagitis hematemesis &/or

melena. Hypovolemic shock.

Anemia:- Iron deficiency anemia, due to chronic blood loss. Hemorrhagic anemia. Decrease intake of vitamins.

Hypersplenism. Encephalopathy: Due to ammonia intoxication and

hypokalemia. Liver Cell Failure. Electrolyte Disturbance:-

Hypokalemia due to increase aldosterone. Hyponatremia due to restriction of sodium intake.

Bleeding:- From esophageal varices due to:- Rupture due to increase portal pressure. Erosion as in reflux esophagitis hematemesis &/or

melena. Hypovolemic shock.

Anemia:- Iron deficiency anemia, due to chronic blood loss. Hemorrhagic anemia. Decrease intake of vitamins.

Hypersplenism. Encephalopathy: Due to ammonia intoxication and

hypokalemia. Liver Cell Failure. Electrolyte Disturbance:-

Hypokalemia due to increase aldosterone. Hyponatremia due to restriction of sodium intake.

Common Clinical Symptoms - Portal

Hypertension

Common Clinical Symptoms - Portal

HypertensionPortal Hypertension

↓Esophageal Varices

↓Splenomegaly

↓Thrombocytopenia

↓Ascites

Portal Hypertension↓

Esophageal Varices↓

Splenomegaly↓

Thrombocytopenia↓

Ascites

Criteria diagnos

is

Criteria diagnos

is

Signs of Liver DiseaseSigns of Liver Disease

AscitesJaundicePalmar erythemaAsterixisTesticular atrophy, gynecomastiaMuscle wasting, Dupuytren

contractureSplenomegaly

AscitesJaundicePalmar erythemaAsterixisTesticular atrophy, gynecomastiaMuscle wasting, Dupuytren

contractureSplenomegaly

(A) Lab Studies(A) Lab Studies

LFTsPT/PTTAlbuminHepatitis serologyPlateletsANA, Antimitochondrial antibodiesAlpha 1-antitrypsin deficiency

LFTsPT/PTTAlbuminHepatitis serologyPlateletsANA, Antimitochondrial antibodiesAlpha 1-antitrypsin deficiency

Imaging StudiesImaging Studies1 .X-RAY

Plain radiographic findings .Barium study findings of esophageal varices

2. CT SCAN

3 .MRI

4 .ULTRASOUND

5 .ANGIOGRAPHY

MRI of the portal venous system demonstrates extensive esophageal varices (arrows) in conjunction with splenic and gastric varices.

ENDOSCOPIC INVESTIGATIONS

ENDOSCOPIC INVESTIGATIONS

Esophagogastodudenoscopy: Colonoscopy Proctoscopy

Esophagogastodudenoscopy: Colonoscopy Proctoscopy

The size of the varix must be graded:

G 1: the varices can be depressed by the endoscope

G 2: the varices cannot be depressedG 3: the varices are confluent around

the circumference of the esophagus

A large varix and a red color sign predict variceal bleeding

The size of the varix must be graded:

G 1: the varices can be depressed by the endoscope

G 2: the varices cannot be depressedG 3: the varices are confluent around

the circumference of the esophagus

A large varix and a red color sign predict variceal bleeding

EndoscopyEndoscopy

ESOPH VARICES

VaricesVarices

Most life threatening complication is bleeding from esophageal varices

Distal 5 cm of esophagusUsually the portal vein-hepatic vein

pressure gradient >12 mm HgBleeding occurs in 25-35% of pts.

With varices and risk is highest in 1st yr.

Most life threatening complication is bleeding from esophageal varices

Distal 5 cm of esophagusUsually the portal vein-hepatic vein

pressure gradient >12 mm HgBleeding occurs in 25-35% of pts.

With varices and risk is highest in 1st yr.

Prevention of VaricesPrevention of Varices

Primary prophylaxis: prevent 1st episode of bleeding

Secondary prophylaxis: prevent recurrent episodes of bleeding

Include control of underlying cause of cirrhosis and pharmacological, surgical interventions to lower portal pressure

Primary prophylaxis: prevent 1st episode of bleeding

Secondary prophylaxis: prevent recurrent episodes of bleeding

Include control of underlying cause of cirrhosis and pharmacological, surgical interventions to lower portal pressure

Prevention of VaricesPrevention of Varices

Beta blockade: Beta blockade (Nadolol, Propranolol)

Nitrates:Organic nitratesSurgery: No longer performed*

Endoscopy: Sclerotherapy (no longer used*) and variceal ligation

* Refers to primary prophylaxis

Beta blockade: Beta blockade (Nadolol, Propranolol)

Nitrates:Organic nitratesSurgery: No longer performed*

Endoscopy: Sclerotherapy (no longer used*) and variceal ligation

* Refers to primary prophylaxis

Treatment of VaricesTreatment of Varices

Initial Management:1. Airway control2. Hemodynamic monitoring3. Placement of large bore IV lines4. Full lab investigation (Hct, Coags,

LFTs,)5. Administration of blood products6. ICU monitoring

Initial Management:1. Airway control2. Hemodynamic monitoring3. Placement of large bore IV lines4. Full lab investigation (Hct, Coags,

LFTs,)5. Administration of blood products6. ICU monitoring

Pharmacologic Treatment of Varices

Pharmacologic Treatment of Varices

Decreases the rate of bleedingEnhances the endoscopic ability to

visualize the site of bleedingVasopressin - potent splanchnic

vasoconstrictor; decreases portal venous blood flow and pressure

Somatostatin: decrease splanchnic blood flow indirectly; fewer side effects

Octreotide: Initial drug of choice for acute variceal bleeding

Decreases the rate of bleedingEnhances the endoscopic ability to

visualize the site of bleedingVasopressin - potent splanchnic

vasoconstrictor; decreases portal venous blood flow and pressure

Somatostatin: decrease splanchnic blood flow indirectly; fewer side effects

Octreotide: Initial drug of choice for acute variceal bleeding

Endoscopic Therapy for Varices

Endoscopic Therapy for Varices

Endoscopic Sclerotherapy: complications occur in 10-30% and include fever, retrosternal chest pain, dysphagia, perforation

Endoscopic variceal ligation: becoming the initial intervention of choice; success rates range from 80-100%

Endoscopic Sclerotherapy: complications occur in 10-30% and include fever, retrosternal chest pain, dysphagia, perforation

Endoscopic variceal ligation: becoming the initial intervention of choice; success rates range from 80-100%

Balloon TamponadeBalloon Tamponade

Sengstaken-Blakemore tubeMinnesota tubeAlternative therapy for pts. who fail

pharmacologic or endoscopic therapy

Complications: aspiration, perforation, necrosis

Limited to 24 hrs; works in 70-80%

Sengstaken-Blakemore tubeMinnesota tubeAlternative therapy for pts. who fail

pharmacologic or endoscopic therapy

Complications: aspiration, perforation, necrosis

Limited to 24 hrs; works in 70-80%

TIPSTIPS

Transjugular inrahepatic portasystemic shunt

1st line treatment for bleeding esophageal varices when earlier-mentioned methods fail

Performed in IRSuccess rates 90-100%Significant complication is hepatic

encephalopathy

Transjugular inrahepatic portasystemic shunt

1st line treatment for bleeding esophageal varices when earlier-mentioned methods fail

Performed in IRSuccess rates 90-100%Significant complication is hepatic

encephalopathy

Surgical InterventionSurgical Intervention

Liver transplantation: only definitive procedure for PH caused by cirrhosis

ShuntsTotally diverting (end-side portacaval)Partially diverting (side-side portacaval)Selective (distal splenorenal shunt)

Devascularization

Liver transplantation: only definitive procedure for PH caused by cirrhosis

ShuntsTotally diverting (end-side portacaval)Partially diverting (side-side portacaval)Selective (distal splenorenal shunt)

Devascularization

1945 Whipple and Blakemore in Columbia performed 1st shunt1945 Whipple and Blakemore in Columbia performed 1st shunt

REDUCTION FUNCTION SHUNT OPERATIVE MORTALITY

A 30 % 0-5%

B 50%10-15%

C 90% >15%

REDUCTION FUNCTION SHUNT OPERATIVE MORTALITY

A 30 % 0-5%

B 50%10-15%

C 90% >15%

Child-Pugh ClassificationChild-Pugh Classification

SURGERY-SHUNTSURGERY-SHUNTSURGERY-SHUNTSURGERY-SHUNT

1- TOTAL DIVERTING SHUNTS1- TOTAL DIVERTING SHUNTS• END-SIDE PORTACAVAL SHUNTEND-SIDE PORTACAVAL SHUNT

• >10MM SIDE-TO-SIDE PORTOCAVAL SHUNT>10MM SIDE-TO-SIDE PORTOCAVAL SHUNT

• MESOCAVAL MESOCAVAL

• CENTRAL SPLENORENAL SHUNTCENTRAL SPLENORENAL SHUNT

COMPLICATIONS

1- WORSEN LIVER FUNCTION

2- ENCEPHALOPATHY

3- PORTA HEPATIS DISSECTED MAKES VERY DIFFUCLT FOR OLT

Total ShuntsTotal ShuntsTotal ShuntsTotal Shunts

End to Side Portocaval Side to Side Portocaval

Interposition Shunts Central Splenorenal

End-to-side portacaval shunt Side-to-side portacaval shunt,

Interposition shunt (portacaval [1], mesocaval [2], and mesorenal [3]),

Conventional (proximal) splenorenal shunt.

SURGERY-SHUNTSURGERY-SHUNTSURGERY-SHUNTSURGERY-SHUNT

2- PARTIAL DIVERTING2- PARTIAL DIVERTING

A- DECOMPRESSED WHILE MAINTAINS A- DECOMPRESSED WHILE MAINTAINS HEPATOPETAL FLOW REDUCE TO 12MMHG AND HEPATOPETAL FLOW REDUCE TO 12MMHG AND MAINTAIN 80-90% OF PATIENTS MAINTAIN 80-90% OF PATIENTS

*-INTERPOSITION MESOCAVAL SHUNTS (8 MM *-INTERPOSITION MESOCAVAL SHUNTS (8 MM SIDE TO SIDE )SIDE TO SIDE )

*- PORTACAVAL SHUNT ( SARFEH)*- PORTACAVAL SHUNT ( SARFEH)

1- COMPONENT IS LEFT GASRTIC V. 1- COMPONENT IS LEFT GASRTIC V. LIGATION AS WELL AS GASTROEPIPLOIC AND OTHER LIGATION AS WELL AS GASTROEPIPLOIC AND OTHER COLLATERALSCOLLATERALS

Splenorenal ShuntSplenorenal Shunt

Distal Splenorenal ShuntDistal Splenorenal ShuntDistal Splenorenal ShuntDistal Splenorenal Shunt

Distal splenorenal shunt

SURGERY-SHUNTSURGERY-SHUNTSURGERY-SHUNTSURGERY-SHUNT3- 3- SELECTIVE DIVERTING SHUNTSSELECTIVE DIVERTING SHUNTS

•Two separate drainage systems with in portal venous Two separate drainage systems with in portal venous system system

•high pressure in portcaval systemhigh pressure in portcaval system

•low pressure in esophagogastric systemlow pressure in esophagogastric system3- SELECTIVE DIVERTING SHUNTS 3- SELECTIVE DIVERTING SHUNTS ADVANATGESADVANATGES

•90% stop bleeding 90% stop bleeding

•no porta hepatis dissectionno porta hepatis dissection

•hepatopetal flow maintainedhepatopetal flow maintained

•encephalopathy 5-24%encephalopathy 5-24%

•liver failure is lowerliver failure is lower

•distal splenorenal contradindicated in ascitesdistal splenorenal contradindicated in ascites

DevascularizationDevascularizationDevascularizationDevascularization

Sugiura procedureSugiura procedure

mortality is 10-35%mortality is 10-35%

5% recurrence rate of rebleeding5% recurrence rate of rebleeding

thoraco & abdominal incisionthoraco & abdominal incision

splenectomy, devasc. Stomach, splenectomy, devasc. Stomach, esopsophagus, transect the esoph with esopsophagus, transect the esoph with reanastamosis, ligate all collateralsreanastamosis, ligate all collaterals

Sugiura procedureSugiura procedure

mortality is 10-35%mortality is 10-35%

5% recurrence rate of rebleeding5% recurrence rate of rebleeding

thoraco & abdominal incisionthoraco & abdominal incision

splenectomy, devasc. Stomach, splenectomy, devasc. Stomach, esopsophagus, transect the esoph with esopsophagus, transect the esoph with reanastamosis, ligate all collateralsreanastamosis, ligate all collaterals

TIPSTIPSTTransjugular ransjugular IIntrahepatic ntrahepatic PPortocaval ortocaval

SShunthunt

TIPSTIPSTTransjugular ransjugular IIntrahepatic ntrahepatic PPortocaval ortocaval

SShunthunt

Technically feasible

Complications 9 - 50%

Infection Intraperitoneal Bleeding

Congestive Failure Subcapsular Hematoma

Acute Renal Failure Hemobilia

Mortality (30 day) 3 - 13%

Technically feasible

Complications 9 - 50%

Infection Intraperitoneal Bleeding

Congestive Failure Subcapsular Hematoma

Acute Renal Failure Hemobilia

Mortality (30 day) 3 - 13%

TIPSTIPSTIPSTIPS

For continued bleeding despite medical and endoscopic treatment in patients with Child C disease and selected Child B disease.

It is only useful in portal hypertension of hepatic origin.

Internal jugular to hepatic vein thru hepatic parenchyma to portal vein. Tract dilated and stented.

For continued bleeding despite medical and endoscopic treatment in patients with Child C disease and selected Child B disease.

It is only useful in portal hypertension of hepatic origin.

Internal jugular to hepatic vein thru hepatic parenchyma to portal vein. Tract dilated and stented.

TipsTips

TIPSTIPS

Active bleeding despite endoscopic or pharmacologic treatment

Recurrent variceal bleeding despite adequate endoscopic treatment.

Potential indications include bleeding gastric fundic varices, refractory ascites

Active bleeding despite endoscopic or pharmacologic treatment

Recurrent variceal bleeding despite adequate endoscopic treatment.

Potential indications include bleeding gastric fundic varices, refractory ascites

Accepted IndicationsAccepted Indications

Hematoma, cardiac arrythmias, bacteremia

Perihepatic hematoma, rupture of liver capsule

Extrahepatic punture of portal veinArterioportal fistula, portobiliary

fistulaEncephalopathy (30%)Liver failure

Hematoma, cardiac arrythmias, bacteremia

Perihepatic hematoma, rupture of liver capsule

Extrahepatic punture of portal veinArterioportal fistula, portobiliary

fistulaEncephalopathy (30%)Liver failure

Complications of TIPSComplications of TIPS