Portal
Hyper-
tension
Hepatic veins Coronary (gastric)
Short gastric
Left
gastroepiploic
Splenic
Right
gastroepiploic
Pancreatic
Inferior
mesenteric
Hepatic
Centrilobular vein
vein Hepatic
11--- - - pert al
Bile
- -M vein
duct
c- 1
Hepat
...,,._ ic
artery
(d
Lobule
DD
Bile Hepatic Hepaltc
duct artery portal
vein
-- Interlobular veins
(to hepatic vein) Central vein
Sinusoids
Plates o
hepatoc
Bile duct (receives
bile from bile
canaliculi)
Fenestrated lining
(endothelial
cells) of sinusoids
Bile duct
J-
Portal venule Portal triad
Portal arteriole
le\
Introduction
• Caused by increased resistance to portal
venous blood flow.
• Portal pressure measured by hepatic
venous pressure gradient.
• Normal < 5 mm Hg
• Portal hypertension ≥ 5 mm Hg
• Risk of variceal bleeding if exceeds 12
mm Hg
• Causes classified into:
• Prehepatic
• Intrahepatic
• Posthepatic
• Liver cirrhosis is by far the most common
cause.
Heart
Rise irf° t r ia l 'Post- sinu soid al'
p ressur e, e.g. Venocc lusive d isease
const rict ive Alco ho lic central
pericar dit is hyaline sclerosis
Inferior
vena cava
W ebs, t u mo ur
in vasio n, 'Sinu soidal'
th ro m b osis Cirr hosis
Non -cir rhot ic:
Hepatic veins Acute alcoholic
Large: hepatit is
t hrombosis, Cyt oto xic drugs
web, t um our Vit amin A
inva sio n int oxicat io n
----- -----
Small: ......
\ 'Pre-sinu soid al'
.... I
ve nocclus ive Sch isto sorniasis
___ diseas_e _ _ _ _ _ _ _ _ _ _ _ - - - - - -/ E.1. rly pr irn c1ry
_ /
/ bili,i r y cirr hosis
/
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I
I
I
Chronic ,icliv<'
/
LIVE
I hep,i ti ti s
,,/ I In creased Con c n il ,11 ilep,itic
I
R / I
I blood fibro,;is
/
I I
/ I
/
// I
I
I
flow Sor coi do si
I I To xins: vinyl < h lo r id
/ //
I I Idiopathic
/
/
/
I II
c ar seni c. co ppe r
/ / Portal I Splenic 1 t ro p ica l
/
/ I I
Id i o p a th ic po r t,11
/ vein I vein splenomegaly hypertension Sin uso id s (S)
/ I I
/
/
I \ Art eriovenous ,1nd
Thrombosis 1 T h ro m bo 1 f ist ula
I collaterals (C)
Invasion or I si s Invasio I
/ I I
/ co m pressio n n or I
/ II I
(a / compressio n (b)
/ I I
) / by t um o ur I
I by tumour
Effects
• Collateral pathways develop
• Principal sites of portosystemic shunting:
– Oesophageal veins
– Veins of the anterior abdominal wall
– Rectal plexus
• Hypersplenism
• Ascites
Portal Vein Tributaries: Portacaval
Anastomoses
I ak i1o r111.in cl ro und hl :
.1:1nc11ts Blood irom superior
mesente ric ,•ei n
Blood from splenic, gastrit and
inferior mesenteric ,·eins
Mixture of above lwo
Caval tributa ries
vein
lei1
g.istro
cpiploic
(g J Sl fO•
omcm1.
o,
vein
Po:;<1:ri
o Anter i
or
inferior
J),lrlOC.lt
duodco
veins
l.ei1;;1nd rig
h1
sup l'rio r
veins rcc lJI vein s
A1p>c ndi cu
lar
vein
Porlacaval anasto
moses
t h o p hagcal 2 P.1r,1umbi lica l
3 Rc,ri. l 4 Rclf opcrito1,cal
Clinical features
• Depends on underlying cause.
• Cirrhosis:
– Sx & signs of liver disease.
• May have an enlarged spleen.
• Caput medusae
• May present with complication, such as
upper gastrointestinal haemorrhage
Assessment
• Assess severity of underlying liver
dysfunction, using Child-Pugh score:
Measure 1 point 2 points 3 points
Total Bilirubin,
<34 34-50 >50
μmol/l
Serum Albumin, g/L >35 28-35 28
PT INR <1.7 1.71-2.30 > 2.30
Ascites None Mild Moderate to Severe
Grade I-II (or
Hepatic Grade III-IV (or
None suppressed with
encephalopathy refractory)
medication)
Points Class One year survival Two year survival
5-6 A 100% 85%
7-9 B 81% 57%
10-15 C 45% 35%
Oesophageal varices
• Dilated sub-mucosal veins in the lower
third of the oesophagus.
• Severity and risk of bleeding are related
to severity of underlying liver disease.
• Decompensated liver failure and ongoing
alcohol abuse are risk factors for
progression of varices and bleeding.
• Likelihood of bleeding also related to size
of varices.
• Oesophageal varices categorised into two
groups:
– Small is < 5 mm
– Large is > 5 mm
• Also important to note cherry-red spots
or red wale markings – denote increased
risk of bleeding.
Preprimary prevention Primary prevention Secondary prevention
(EV 5 mm)
Hemostasis
•
l
Cirrhosis start
t
EV development First bleeding
Primary
prevention
• Pt that has not had an acute bleed.
• Rx indicated in large varices or patients
with decompensated liver failure with
small varices.
• Rx of choice = non-selective ß-blocker or
banding or combination of the above.
• Aim = to decrease HVPG < 12 mm Hg or
decrease of > 20% from baseline.
Acute variceal bleeding
Priorities in
Mx
• Active resuscitation
• Assessment of coagulation status
• Urgent endoscopy
• Control of bleeding
• Treatment of
hepatocellular
decompensation
• Treatment/prevention of
portosystemic encephalopathy
• Prevention of further bleeding from
Active resuscitation
• Group and cross-match blood.
• Prior to any diagnostic maneuvers, support of circulating
blood volume with adequate resuscitation is imperative.
• Maintenance of Hb at approximately 7-8 g/dL is
recommended.
• Antibiotic prophylaxis shown to decrease variceal
rebleeding and bacterial infection. 1st cephalosporin is
ideal.
• PPI can also be given; weak evidence that they prevent
rebleed.
• Somatostatin or its analogues should be given as soon
as variceal bleeding is suspected.
• Initial bolus dose of 50 μg IV followed by 50 μg/h for
duration of 72-96 h.
Assessment of coagulation status
• Prothrombin time
• Platelet count
– Can often have thrombocytopenia due
to hypersplenism
Urgent endoscopy – control of bleeding
• Endoscopic banding
• TIPPS procedure
• Tamponade – Sengstaken-blakemore
tube; SEMS
• Pharmacological measures
Endoscopy
• Should be performed at earliest
opportunity.
• If banding fails consider Sengstaken tube
and rescue therapy:
– TIPS
– Devascularization
– Emergency surgical shunt
Gasrtic and - - -,-.-
Esophageal Sengstaken
Suclion Blakemor
e Tube
I
f
0-£'
Gastlf'ic -
<l foGastric
.!:
Balloon Ba.lloon
: el o Eso
; ;:
<11,
phageal
Balloon
Rebleedin
•
g
Risk of recurrent bleeding = 70%
• Mortality = 30%
• Highest risk within 6/52 of index bleed
• There is consensus that all pts who have
previously bled should have secondary therapy to
prevent recurrent bleed.
• Factors that influence risk of rebleeding:
– Severity of liver disease
– Continued EtOH abuse
– Variceal size
– Inability to reduce HVPG to <12 or reduce by 20%
Prevention of further
bleeding
• Pharmacological
• Banding
• Devascularization
• Emergency portosystemic shunting
• Transplant
Pharmacologica
l
• ß-blockers reduce risk of rebleed from
63% - 42% and lowers mortality rate from
27% - 20%.
Devascularization
• Procedure during which a number of
veins are ligated in the distal oesophagus
and proximal half of stomach.
• Described with or without oesophageal
transection and reanastomosis and with or
without splenectomy.
• Rebleeding rate low after procedure
– around 10% in most series
• High mortality rate in the emergency setting
– between 20-40%
Surgical shunt
• A shunt creates an artificial anastomosis
between the portal and systemic circulation
bypassing the liver.
• Divided into selective and non-selective
based on the degree of shunting.
• Mostly indicated in patients with repeated
variceal bleeding that is not due to liver
cirrhosis or in well compensated cirrhotics.
• Can also be used as a bridge to liver
transplant.
TIPS
• Transjugular intrahepatic
portosystemic shunt
• Percutaneously placed shunt between
hepatic vein and portal vein
• Acts as non-selective side-to-side shunt.
• Indicated as rescue therapy in patients
who have had unsuccessful endoscopic
attempts at arresting variceal bleeding.
Right
hepatic
A B
Figure 1 . Schemes for TIPS techni qu e compreh ension. A: Insertionof an appropnate needle for punc
turing the po<tal vein from the right hepatic vein. B: Insertion of guide-wire into the portal system. C:
Dilatation of hepatic parenchyma between the portal vein and the hepatic vein. D: Ste n t pla oem ent in
the newly fo,med course.
Transplan
t
• Is the ultimate treatment in patients with
end-stage liver disease.
• Corrects portal hypertension and
addresses underlying liver disease.
• Uncontrollable or recurrent variceal
bleeding may form part of indication for
liver transplant.
NONALCOHOLIC &
ABSTINENT ALCOHOLIC
CIRRHOTICS
Transplant
candidate
C-P C or C-P A/B with C-P A/B with
symptomatic stable disease symptomatic stable
disease
TIPS if
banding Transplant Ready access Poor access or
does not gastric varices
control
acute
bleeding Progressiv Banding Selective Shunt
e
disease
Failure
Stable disease
NONCIRRHOTIC,ACTIVE ALCOHOLIC,
ELDERLY, SIGNIFICANT
CARDIOPULMONARY DISEASE
Not transplant
candidate
Compliant, ready access Noncompliant, poor access,
gastric varices
Banding Good operative risk Poor operative risk
Failure Surgery TIPS
Poor operative risk
Controllable Intractable Splanchnic
ascites, ascites venous
TIPS compatible thrombosis
anatomy
Selective shunt Nonselective shunt Devascularization
Summary and important points
• Portal hypertension is almost always due
to obstruction to portal flow.
• Liver cirrhosis is the most common cause.
• Portosystemic shunts develop at certain
anatomical sites.
• Varices in the submucosa of the lower
oesophagus is a common cause of upper
GI bleeding.
• Variceal bleeding is a surgical
• Child’s grading based on ascites,
encephalopathy, albumin, bilirubin
and INR.
• Long-term outcome after variceal
bleeding determined by the nature and
severity of underlying liver disease.
