Portal Hypertension

By
Dr. Ahmed Elabd

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 10 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).

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 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 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 hypertension

Increased portal blood flow
A) Arterial-portal venous fistula.
B) Increased splenic flow:
1- Bantis 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.

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 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)

Portal vein collaterals

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 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
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 classification

Points
1

<2

23

>3

Albumin (g/dL)

> 3.5

2.8 3.5

< 2.8

Prothrombin time (seconds)

13

46

>6

Ascites

None

Slight

Moderate

Encephalopathy

None

Minimal

Advanced

Bilirubin (mg/dL)

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
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

Intra-variceal

Para-variceal

Complications of Sclerotherapy
LOCAL

SYSTEMIC

Ulceration.

Fever

Stricture.

Pneumonitis

Perforation.

CNS

Retrosternal discomfort
for few days.

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 bleeding
Prior to transplant
Child C
Refractory 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 3050% 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

TIPS
on
Portal Hypertension
for
Surgeons
By
PROF/ GOUDA ELLABBAN

VARICEAL BLEEDING

Resuscitation
Treat hemorrhagic shock
Crystalloid (Limited)
Platelets (Rarely)
Red Cells + FFP

Goal: Tissue Perfusion

Monitor: Urine Output
Caveat: Do NOT overload

VARICEAL BLEEDING

Initial Treatment
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 Dxd:
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 coagulopathy
FFP, 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

23

>3

Albumin (g/dL)

> 3.5

2.8 3.5

< 2.8

Prothrombin time (seconds )

13

46

>6

Ascites

None

Slight

Moderate

Encephalopathy

None

Minimal

Advanced

Bilirubin (mg/dL)

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
Occludes venous channels
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 Shunts
End to Side Portocaval

Interposition Shunts

Side to Side Portocaval

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 Shunts
Randomized 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

TIPS
Transjugular Intrahepatic Portocaval Shunt

TIPS

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 DZ ?)
??? 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 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 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
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

Ascites
Origin:
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

-s

Mesenteric Flow
Portal Pressure
Stops Bleeding in >80%

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
Occludes venous channels
Multiple sessions + surveillance
>60% rebleed
1/3 fail treatment
30% complication rate

Endoscopic Sclerotherapy

Intravariceal

Paravariceal

Complications of ScleroTx
LOCAL

SYSTEMIC

Ulceration

Fever

Stricture

Pneumonitis

Perforation

CNS

Total Shunts
Divert most (all?) portal flow
Options

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

Interposition Shunt
Central Splenorenal Shunt

TIPS

Childs Classification
A

Bilirubin

<2

23

>3

Albumin

> 3.5

2.8 3.5

< 2.8

Ascites
Enceph

None

None

Minimal

Advanced

Nutrition

Excellent

Good

Poor

Controlled Uncontrolled

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