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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

Portal Hypertension

By

Dr. GOUDA ELLABBAN

Ass. Prof. of General and hepatobiliary surgery

portal vein anatomy
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
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
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
causes of portal hypertension
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).
causes of portal hypertension7
Causes of portal hypertension

B)Intra-hepatic:

  • 1- liver cirrhosis  obstruction is sinusoidal & post-sinusoidal.
  • 2- bilharzial periportal fibrosis  obstruction is pre-sinusoidal.
causes of portal hypertension8
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.
causes of portal hypertension9
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.

causes of portal hypertension10
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).

sequelae clinical picture
Sequelae & Clinical picture

1-Porto-systemic collaterals:

  • In normal conditinos  collapsed.
  • In portal hypertension  engorged  divert blood away from the portal circulation.
sequelae clinical picture12
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)

sequelae clinical picture13
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)

e)Retroperitoneum

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

Posterior abdominal & subdiaphragmatic veins (systemic)

sequelae clinical picture15
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.
sequelae clinical picture16
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
Investigations

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
Investigations

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
Investigations

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
Investigations

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.
child pugh classification
Child Pugh classification

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

treatment
Treatment

Management of patients with actively bleeding oesophageal varices

1.Admission.

The patient should be admitted to hospital.

2.Resuscitation.

  • 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
Treatment

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
Treatment

Sclerotherapy

  • 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.
endoscopic sclerotherapy
Endoscopic Sclerotherapy

Intra-variceal

Para-variceal

complications of sclerotherapy
LOCAL

Ulceration.

Stricture.

Perforation.

Retrosternal discomfort for few days.

SYSTEMIC

Fever

Pneumonitis

CNS

Complications of Sclerotherapy
treatment28
Treatment

Endoscopic Banding

  • Occludes venous channels
  • Sessions < sclerotherapy
  • Same results as sclerotherapy
  •  complications vs sclerotherapy
  • Endoscopic treatment of choice
treatment30
Treatment

Drugs

Vasopressin vasoconstriction of the splanchnic circulation.

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

Disadvantages

  • 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
Treatment

Somatostatin

  • 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
Treatment

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
Treatment

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
Treatment

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
Treatment
  • Trans-juguJar Intra-hepatic Porto-Systemic Shunt ( TIPSS )
treatment37
Treatment

Indications for TIPSS:

  • Refractory bleeding
  • Prior to transplant
  • Child C
  • Refractory ascites

Main early complication:

  • Perforation of liver capsule  massive haemorrhage.
treatment38
Treatment

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
Treatment

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
Total shunt operations

1-Porta-caval operation

End to side Side to side

porta caval operation
Porta-caval operation
  • very efficient in lowering the portal pressure  no bleeding occurs from the varices.

disadvantages:

  • 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
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
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
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
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
All vessels surrounding the lower 5-10 cm of the oesophagus are ligated.
  • There is no encephalopathy following this operation and the portal blood flow is intact.
  • There is a low incidence of rebleeding following the operation, but it can usually be controlled by sclerotherapy.
liver transplant
Liver Transplant
  • Indicated for liver failure

Not for variceal bleeding.

  • 24% in USA die on waiting list
control of ascites
Control of Ascites
  • Sodium / Water Restriction.
  • Spironolactone.
  • Loop Diuretic.
  • Large Volume  Paracentesis.
  • Peritoneal-Venous Shunt .
  • TIPSS
variceal bleeding resuscitation
VARICEAL BLEEDINGResuscitation
  • Treat hemorrhagic shock

Crystalloid (Limited)

Platelets (Rarely)

Red Cells + FFP

  • Goal: Tissue Perfusion
  • Monitor: Urine Output
  • Caveat: Do NOT overload
variceal bleeding initial treatment
VARICEAL BLEEDINGInitial Treatment
  • Continue Tx hemorrhagic shock
  • IV therapy

Sandostatin®

INITIATE WHEN Dx SUSPECTED!!!

variceal bleeding diagnosis
VARICEAL BLEEDINGDiagnosis
  • 50% UGI bleeds not variceal

(MW Tear, Gastritis, Gastric/Duodenal Ulcer)

  • Early endoscopy mandatory
  • Variceal bleeding Dx’d:

Active bleeding

Stigmata

Varices and NO other source

variceal bleeding initial therapy
VARICEAL BLEEDINGInitial Therapy
  • Continue I.V. Sandostatin®
  • Endoscopic Therapy
  • Sengstaaken-Blakemore tube
  • TIPS
  • Emergency operation
variceal bleeding supportive therapy
VARICEAL BLEEDINGSupportive Therapy
  • Correct coagulopathy

FFP, vitamin K, +/- platelets

  • Pulmonary
  • Other infection
  • Encephalopathy
  • Nutrition
variceal bleeding evaluation
VARICEAL BLEEDINGEvaluation
  • Child class
  • History
  • Hepatitis profile
  • Angiography
  • Transplant evaluation
child pugh classification57
Child-Pugh Classification

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

variceal bleeding definitive therapy
VARICEAL BLEEDINGDefinitive Therapy
  • Rationale: 67% rebleed
  • Most rebleed < 6 weeks
  • Definitive Tx during initial stay
variceal bleeding definitive therapy59
VARICEAL BLEEDINGDefinitive Therapy
  • Medical
  • Endoscopic
  • Surgical
  • Radiological
variceal bleeding medical therapy
VARICEAL BLEEDINGMedical Therapy
  • Beta blockade

 bleeding by  cardiac output

Goal: 25%  in heart rate

Reduces # bleeding episodes

Does not reduce mortality

Use as adjunct

endoscopic banding61
Endoscopic Banding
  • Occludes venous channels
  • Multiple sessions + surveillance
  • >60% rebleed
  • 1/3 fail treatment
  •  complications vs scleroTx
  • = /  efficacy vs scleroTx
  • ENDOSCOPIC Tx OF CHOICE
variceal bleeding surgical options
VARICEAL BLEEDINGSURGICAL OPTIONS
  • Total Shunt
  • Selective Shunt
  • Partial Shunt
  • Non-Shunt
total shunts
Total Shunts

End to Side Portocaval

Side to Side Portocaval

Interposition Shunts

Central Splenorenal

total shunt results
Total Shunt Results
  • Prevent rebleed > 90%
  • Thrombosis with graft
  • Encephalopathy rate 40%
selective shunts
Selective Shunts
  • Goals:

Prevent variceal bleeding and encephalopathy

  • Mechanism:

Decompress Varices

Maintain Portal Perfusion

Maintain Portal Hypertension

  • Key:

Decompress onlygastrosplenic compartment

dsrs vs total shunts
DSRS vs Total Shunts
  • Six randomized trials in N.A.
  • Mean follow-up 39 mos (1-8 yrs)
partial shunts
Partial Shunts
  • Ease of portocaval
  • Limited portal diversion
  • Maintain some liver perfusion
  • Short, straight PTFE graft
partial shunts70
Partial Shunts

Sarfeh

Ann Surg

200:706,1986

partial shunts71
Partial Shunts

Randomized trial in ETOH cirrhotics

Follow-up @ 20 +/- 11 mos

non shunt operations
Non-Shunt Operations
  • Options

Esophageal transection

Variceal ligation

Devascularize +/- splenectomy

  • Very limited role
liver transplant73
Liver Transplant
  • 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
slide76
TIPS
  • 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
Problems With TIPS
  • 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
The Role ForTips
  • Refractory bleeding
  • Bridge to transplant
  • Child C

(all or only “DZ” ?)

  • ??? refractory ascites
  • Relative contraindication: Poor f/u
splenic vein thrombosis
Splenic Vein Thrombosis
  • Etiology:

Pancreatitis - Acute or Chronic

Pancreatic Carcinoma

  • Hallmark:

Isolated Gastric Varices

  • Treatment:

Splenectomy (if bleeding)

portal vein thrombosis
Portal Vein Thrombosis

Etiology:

Congenital - “Cavernous Transformation”

Hallmark:

Normal Liver Function W/ Varices

Treatment:

Endo Tx OR DSRS

budd chiari syndrome
Budd-Chiari Syndrome
  • Etiology

Hypercoagulable: Estrogens, XRT, Myeloprolif, PNH

IVC Occlusion: RA Myxoma, Pericarditis, Membrane

Liver Mass

High Dose ChemoTx

  • Presentation: Classic Triad

Abdominal Pain

Ascites

Hepatomegaly

budd chiari syndrome83
Budd-Chiari Syndrome
  • 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
Some Take Home Points
  • 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
Some Take Home Points

Selective shunt:  encephalopathy

SV Thrombosis: Presentation & Tx

Budd-Chiari: Classic triad

Transplant for liver failure

portal hypertension etiology
Portal HypertensionEtiology
  • PRE-HEPATIC

Portal Vein or Splenic Vein Thrombosis

  • INTRA-HEPATIC

Cirrhosis (ETOH, Hepatitis, Other Toxins)

  • POST-HEPATIC

Budd-Chiari

complications of portal hypertension
Complications of Portal Hypertension
  • Ascites
  • Encephalopathy
  • Variceal bleeding
    • Initial management
    • Evaluation
    • Definitivetherapy
    • Special cases
encephalopathy
Encephalopathy
  • 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
Ascites
  • Origin:

Sinusoidal pressure > colloid oncotic pressure

  • Induced by:

Physiologic Stress

IV Fluids

  • Complications:

Spontaneous Bacterial Peritonitis

“Hepatorenal Syndrome”

control of ascites91
Control of Ascites
  • Sodium / Water Restriction
  • Spironolactone
  • Loop Diuretic
  • Large Volume Paracentesis
  • Peritoneal-Venous Shunt
  • (?) TIPS
variceal bleeding general approach
VARICEAL BLEEDINGGeneral Approach
  • Resuscitation
  • Initial treatment
  • Support
  • Evaluation
  • Definitive therapy
vasopressin
Vasopressin
  • 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
Sandostatin®
  • Long acting STS analogue

+’s  Mesenteric Flow

 Portal Pressure

Stops bleeding in > 85%

Good as VP but  side effects

-’s Cost

  • DRUG OF CHOICE
portal vein collaterals96
Portal Vein Collaterals

Five Principle Routes

Veins of Retzius

Umbilical Vein

Hemorrhoids

Adhesions

EsophagealVarices

variceal bleeding sclerotherapy
VARICEAL BLEEDINGSclerotherapy
  • Intra- or Para- Variceal
  • Occludes venous channels
  • Multiple sessions + surveillance
  • >60% rebleed
  • 1/3 fail treatment
  • 30% complication rate
endoscopic sclerotherapy98
Endoscopic Sclerotherapy

Intravariceal

Paravariceal

complications of sclerotx
LOCAL

Ulceration

Stricture

Perforation

SYSTEMIC

Fever

Pneumonitis

CNS

Complications of ScleroTx
total shunts100
Total Shunts
  • Divert most (all?) portal flow
  • Options

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

Interposition Shunt

Central Splenorenal Shunt

scltx vs tips
SclTx 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

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