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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

By

Dr. GOUDA ELLABBAN

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.


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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.


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Portal vein anatomy


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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

B)Intra-hepatic:

  • 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)

e)Retroperitoneum

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

Posterior abdominal & subdiaphragmatic veins (systemic)


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Portal vein collaterals


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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.


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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 testis the most sensitive liver function.


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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.


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Detection of oesophageal varices


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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.


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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.


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Child Pugh classification

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


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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.


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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.


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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.


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Endoscopic Sclerotherapy

Intra-variceal

Para-variceal


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LOCAL

Ulceration.

Stricture.

Perforation.

Retrosternal discomfort for few days.

SYSTEMIC

Fever

Pneumonitis

CNS

Complications of Sclerotherapy


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Treatment

Endoscopic Banding

  • Occludes venous channels

  • Sessions < sclerotherapy

  • Same results as sclerotherapy

  •  complications vs sclerotherapy

  • Endoscopic treatment of choice


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Endoscopic Banding


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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).


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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


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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.


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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.


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Balloon tamponade


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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.


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Treatment

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


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Treatment

Indications for TIPSS:

  • Refractory bleeding

  • Prior to transplant

  • Child C

  • Refractory ascites

    Main early complication:

  • Perforation of liver capsule  massive haemorrhage.


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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.


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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


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Total shunt operations

1-Porta-caval operation

End to side Side to side


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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.


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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


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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.


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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.


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  • 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.


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Liver Transplant

  • Indicated for liver failure

    Not for variceal bleeding.

  • 24% in USA die on waiting list


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Control of Ascites

  • Sodium / Water Restriction.

  • Spironolactone.

  • Loop Diuretic.

  • Large Volume  Paracentesis.

  • Peritoneal-Venous Shunt .

  • TIPSS


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THANK YOU


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TIPS on Portal Hypertension for Surgeons

By

PROF/ GOUDA ELLABBAN


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VARICEAL BLEEDINGResuscitation

  • Treat hemorrhagic shock

    Crystalloid (Limited)

    Platelets (Rarely)

    Red Cells + FFP

  • Goal: Tissue Perfusion

  • Monitor: Urine Output

  • Caveat: Do NOT overload


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VARICEAL BLEEDINGInitial Treatment

  • Continue Tx hemorrhagic shock

  • IV therapy

    Sandostatin®

    INITIATE WHEN Dx SUSPECTED!!!


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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 l.jpg

VARICEAL BLEEDINGInitial Therapy

  • Continue I.V. Sandostatin®

  • Endoscopic Therapy

  • Sengstaaken-Blakemore tube

  • TIPS

  • Emergency operation


Variceal bleeding supportive therapy l.jpg

VARICEAL BLEEDINGSupportive Therapy

  • Correct coagulopathy

    FFP, vitamin K, +/- platelets

  • Pulmonary

  • Other infection

  • Encephalopathy

  • Nutrition


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VARICEAL BLEEDINGEvaluation

  • Child class

  • History

  • Hepatitis profile

  • Angiography

  • Transplant evaluation


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Child-Pugh Classification

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


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VARICEAL BLEEDINGDefinitive Therapy

  • Rationale: 67% rebleed

  • Most rebleed < 6 weeks

  • Definitive Tx during initial stay


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VARICEAL BLEEDINGDefinitive Therapy

  • Medical

  • Endoscopic

  • Surgical

  • Radiological


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VARICEAL BLEEDINGMedical Therapy

  • Beta blockade

     bleeding by  cardiac output

    Goal: 25%  in heart rate

    Reduces # bleeding episodes

    Does not reduce mortality

    Use as adjunct


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Endoscopic Banding

  • Occludes venous channels

  • Multiple sessions + surveillance

  • >60% rebleed

  • 1/3 fail treatment

  •  complications vs scleroTx

  • = /  efficacy vs scleroTx

  • ENDOSCOPIC Tx OF CHOICE


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Endoscopic Banding


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VARICEAL BLEEDINGSURGICAL OPTIONS

  • Total Shunt

  • Selective Shunt

  • Partial Shunt

  • Non-Shunt


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Total Shunts

End to Side Portocaval

Side to Side Portocaval

Interposition Shunts

Central Splenorenal


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Total Shunt Results

  • Prevent rebleed > 90%

  • Thrombosis with graft

  • Encephalopathy rate 40%


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Selective Shunts

  • Goals:

    Prevent variceal bleeding and encephalopathy

  • Mechanism:

    Decompress Varices

    Maintain Portal Perfusion

    Maintain Portal Hypertension

  • Key:

    Decompress onlygastrosplenic compartment


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Distal Splenorenal Shunt


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DSRS vs Total Shunts

  • Six randomized trials in N.A.

  • Mean follow-up 39 mos (1-8 yrs)


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Partial Shunts

  • Ease of portocaval

  • Limited portal diversion

  • Maintain some liver perfusion

  • Short, straight PTFE graft


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Partial Shunts

Sarfeh

Ann Surg

200:706,1986


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Partial Shunts

Randomized trial in ETOH cirrhotics

Follow-up @ 20 +/- 11 mos


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Non-Shunt Operations

  • Options

    Esophageal transection

    Variceal ligation

    Devascularize +/- splenectomy

  • Very limited role


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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


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TIPSTransjugular Intrahepatic Portocaval Shunt


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TIPS


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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.


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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.


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The Role ForTips

  • Refractory bleeding

  • Bridge to transplant

  • Child C

    (all or only “DZ” ?)

  • ??? refractory ascites

  • Relative contraindication: Poor f/u


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Special Cases of Portal Hypertension


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Splenic Vein Thrombosis

  • Etiology:

    Pancreatitis - Acute or Chronic

    Pancreatic Carcinoma

  • Hallmark:

    Isolated Gastric Varices

  • Treatment:

    Splenectomy (if bleeding)


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Portal Vein Thrombosis

Etiology:

Congenital - “Cavernous Transformation”

Hallmark:

Normal Liver Function W/ Varices

Treatment:

Endo Tx OR DSRS


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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


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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


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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


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Some Take Home Points

Selective shunt:  encephalopathy

SV Thrombosis: Presentation & Tx

Budd-Chiari: Classic triad

Transplant for liver failure


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Portal HypertensionEtiology

  • PRE-HEPATIC

    Portal Vein or Splenic Vein Thrombosis

  • INTRA-HEPATIC

    Cirrhosis (ETOH, Hepatitis, Other Toxins)

  • POST-HEPATIC

    Budd-Chiari


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Complications of Portal Hypertension

  • Ascites

  • Encephalopathy

  • Variceal bleeding

    • Initial management

    • Evaluation

    • Definitivetherapy

    • Special cases


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Encephalopathy

  • Etiology: ? Nitrogen compounds

  • Induced by:

    InfectionDehydration

    ConstipationBlood in gut

  • No test is diagnostic

  • Therapy:

    HydrateCleanse gut

    ↓ proteinFind and treat cause


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Ascites

  • Origin:

    Sinusoidal pressure > colloid oncotic pressure

  • Induced by:

    Physiologic Stress

    IV Fluids

  • Complications:

    Spontaneous Bacterial Peritonitis

    “Hepatorenal Syndrome”


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Control of Ascites

  • Sodium / Water Restriction

  • Spironolactone

  • Loop Diuretic

  • Large Volume Paracentesis

  • Peritoneal-Venous Shunt

  • (?) TIPS


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VARICEAL BLEEDINGGeneral Approach

  • Resuscitation

  • Initial treatment

  • Support

  • Evaluation

  • Definitive therapy


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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


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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


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Portal Vein Anatomy


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Portal Vein Collaterals

Five Principle Routes

Veins of Retzius

Umbilical Vein

Hemorrhoids

Adhesions

EsophagealVarices


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VARICEAL BLEEDINGSclerotherapy

  • 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

Intravariceal

Paravariceal


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LOCAL

Ulceration

Stricture

Perforation

SYSTEMIC

Fever

Pneumonitis

CNS

Complications of ScleroTx


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Total Shunts

  • Divert most (all?) portal flow

  • Options

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

    Interposition Shunt

    Central Splenorenal Shunt


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TIPS


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Child’s Classification


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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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