Portal+hypertension prof GOUDA ELLABBAN

Portal Hypertension

ByDr. GOUDA ELLABBAN

Prof. of General and hepatobiliary surgeryfaculty of medcine

Suez canal university - Egypt

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 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 anatomy

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

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).


B) Intra-hepatic:

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

2- bilharzial periportal fibrosis obstruction is pre-sinusoidal.


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.


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.


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

1- Porto-systemic collaterals:

In normal conditinos collapsed.

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


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)


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)

Portal vein collaterals


2- SplenomegalyThe 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.


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

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.

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.

Detection of oesophageal varices

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.

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 classificationPoints

1 2 3

Bilirubin (mg/dL) < 2 2 – 3 > 3

Albumin (g/dL) > 3.5 2.8 – 3.5 < 2.8

Prothrombin time (seconds) 1 – 3 4 – 6 > 6

Ascites None Slight Moderate

Encephalopathy None Minimal Advanced

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

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.

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.

Treatment

SclerotherapyIntra- 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

Intra-variceal Para-variceal

Complications of Sclerotherapy

LOCAL

Ulceration.

Stricture.

Perforation.

Retrosternal discomfort

for few days.

SYSTEMIC

Fever

Pneumonitis

CNS

Treatment

Endoscopic Banding

Occludes venous channels

Sessions < sclerotherapy

Same results as sclerotherapy

↓ complications vs sclerotherapy

Endoscopic treatment of choice

Endoscopic Banding

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).

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

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.

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.

Balloon tamponade

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.

Treatment

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

Treatment

Indications for TIPSS:Refractory bleedingPrior to transplantChild CRefractory ascites

Main early complication:Perforation of liver capsule massive haemorrhage.

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.

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

1- Porta-caval operation

End to side Side to side

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 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

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)

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

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.

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

Indicated for liver failure

Not for variceal bleeding.

24% in USA die on waiting list

Control of Ascites

Sodium / Water Restriction.

Spironolactone.

Loop Diuretic.

Large Volume Paracentesis.

Peritoneal-Venous Shunt .

TIPSS

THANK YOU

TIPS on

Portal Hypertension for Surgeons

ByPROF/ GOUDA ELLABBAN

VARICEAL BLEEDING

Resuscitation

Treat hemorrhagic shockCrystalloid (Limited)

Platelets (Rarely)

Red Cells + FFP

Goal: Tissue Perfusion

Monitor: Urine Output

Caveat: Do NOT overload

VARICEAL BLEEDING

Initial Treatment

Continue Tx hemorrhagic shock

IV therapy

Sandostatin®

INITIATE WHEN Dx SUSPECTED!!!

VARICEAL BLEEDING Diagnosis

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

Continue I.V. Sandostatin®

Endoscopic Therapy

Sengstaaken-Blakemore tube

TIPS

Emergency operation

VARICEAL BLEEDING

Supportive Therapy

Correct coagulopathyFFP, vitamin K, +/- platelets

Pulmonary

Other infection

Encephalopathy

Nutrition

VARICEAL BLEEDING

Evaluation

Child class

History

Hepatitis profile

Angiography

Transplant evaluation

Child-Pugh Classification

Points

1 2 3

Bilirubin (mg/dL) < 2 2 – 3 > 3

Albumin (g/dL) > 3.5 2.8 – 3.5 < 2.8

Prothrombin time (seconds ↑) 1 – 3 4 – 6 > 6

Ascites None Slight Moderate

EncephalopathyNone Minimal

Advanced

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

VARICEAL BLEEDING

Definitive Therapy

Rationale: 67% rebleed

Most rebleed < 6 weeks

Definitive Tx during initial stay

VARICEAL BLEEDING

Definitive Therapy

Medical

Endoscopic

Surgical

Radiological

VARICEAL BLEEDING

Medical Therapy

Beta blockade

↓ bleeding by ↓ cardiac output

Goal: 25% ↓ in heart rate

Reduces # bleeding episodes

Does not reduce mortality

Use as adjunct

Endoscopic Banding


Multiple sessions + surveillance

>60% rebleed

1/3 fail treatment

↓ complications vs scleroTx

= / ↑ efficacy vs scleroTx

ENDOSCOPIC Tx OF CHOICE

Endoscopic Banding

VARICEAL BLEEDING

SURGICAL OPTIONS

Total Shunt

Selective Shunt

Partial Shunt

Non-Shunt

Total ShuntsEnd to Side Portocaval Side to Side Portocaval

Interposition Shunts Central Splenorenal

Total Shunt Results

Prevent rebleed > 90%

Thrombosis with graft

Encephalopathy rate 40%

Selective Shunts

Goals:

Prevent variceal bleeding and encephalopathy

Mechanism:

Decompress Varices

Maintain Portal Perfusion

Maintain Portal Hypertension

Key:

Decompress only gastrosplenic compartment

Distal Splenorenal Shunt

DSRS vs Total Shunts

Six randomized trials in N.A.

Mean follow-up 39 mos (1-8 yrs)

Partial Shunts

Ease of portocaval

Limited portal diversion

Maintain some liver perfusion

Short, straight PTFE graft

Partial Shunts

Sarfeh Ann Surg 200:706,1986

Partial ShuntsRandomized trial in ETOH cirrhotics

Follow-up @ 20 +/- 11 mos

Non-Shunt Operations

Options

Esophageal transection

Variceal ligation

Devascularize +/-

splenectomy

Very limited role

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

TIPSTransjugular Intrahepatic Portocaval Shunt

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

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

Refractory bleeding

Bridge to transplant

Child C

(all or only “D→Z” ?)

??? refractory ascites

Relative contraindication: Poor f/u

Special Cases of Portal Hypertension

Splenic Vein Thrombosis

Etiology: Pancreatitis - Acute or Chronic

Pancreatic Carcinoma

Hallmark:

Isolated Gastric Varices

Treatment:

Splenectomy (if bleeding)

Portal Vein Thrombosis

Etiology:

Congenital - “Cavernous Transformation”

Hallmark:

Normal Liver Function W/ Varices

Treatment:

Endo Tx OR DSRS

Budd-Chiari SyndromeEtiologyHypercoagulable: Estrogens, XRT, Myeloprolif, PNH

IVC Occlusion: RA Myxoma, Pericarditis, Membrane

Liver Mass

High Dose ChemoTx

Presentation: Classic TriadAbdominal Pain

Ascites

Hepatomegaly

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

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 Points

Selective shunt: ↓ encephalopathy

SV Thrombosis: Presentation & Tx

Budd-Chiari: Classic triad

Transplant for liver failure

Portal Hypertension

Etiology

PRE-HEPATIC

Portal Vein or Splenic Vein Thrombosis

INTRA-HEPATIC

Cirrhosis (ETOH, Hepatitis, Other Toxins)

POST-HEPATIC

Budd-Chiari

Complications of Portal Hypertension

Ascites

Encephalopathy

Variceal bleeding– Initial management– Evaluation– Definitive therapy– Special cases

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

AscitesOrigin:Sinusoidal pressure > colloid oncotic pressure

Induced by:Physiologic Stress

IV Fluids

Complications:Spontaneous Bacterial Peritonitis

“Hepatorenal Syndrome”

Control of Ascites

Sodium / Water Restriction

Spironolactone

Loop Diuretic

Large Volume Paracentesis

Peritoneal-Venous Shunt

(?) TIPS

VARICEAL BLEEDING General Approach

Resuscitation

Initial treatment

Support

Evaluation

Definitive therapy

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®

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 Anatomy

Portal Vein Collaterals

Five Principle Routes

Veins of Retzius

Umbilical Vein

Hemorrhoids

Adhesions

Esophageal Varices

VARICEAL BLEEDING

Sclerotherapy

Intra- or Para- Variceal


Multiple sessions + surveillance

>60% rebleed

1/3 fail treatment

30% complication rate

Endoscopic Sclerotherapy

Intravariceal Paravariceal

Complications of ScleroTx

LOCAL

Ulceration

Stricture

Perforation

SYSTEMIC

Fever

Pneumonitis

CNS

Total Shunts

Divert most (all?) portal flow

Options

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

Interposition Shunt

Central Splenorenal Shunt

Child’s Classification

A B C

Bilirubin < 2 2 – 3 > 3

Albumin > 3.5 2.8 – 3.5 < 2.8

Ascites None Controlled Uncontrolled

Enceph None Minimal Advanced

Nutrition Excellent Good Poor

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

Portal+hypertension prof GOUDA ELLABBAN

Education

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