Portal hypertension

(Surgical complications)
Portal hypertension
 A persist pressure elevation of > 12mmHg
in the portal vein circulation or an increase
in the portal pressure gradient of > 7mmHg
(difference between the pressure of the
portal vein and that of the inferior vena
cava ) is termed portal hypertension.
 At pressure values of more than 20 mmHg,
collaterals generally develop.
The extra hepatic portal venous circulation

 The portal vein is

formed from the
confluence of the
superior mesenteric
and splenic veins
behind the neck of the
pancreas and is 6 to 8
cm in length and about
1cm in diameter.
Causes of portal hypertension
 An increased resistance in the
portohepatic circulation.

 An increase in the splanchnic vein

blood supply.
portosystemic collateralization
 Portosystemic
collateral pathways
develop where the
portal venous and
systemic venous
systems are in close
apposition.
Portosystemic anastomoses

 The submucosal veins of the proximal

stomach and distal esophagus, which can
receive blood from the coronary and short
gastric veins to drain into the azygous veins
( high blood flow through this pathway
produces gastric varices, esophageal varices
or both ).
Classification and causes of portal
hypertension
 Prehepatic portal hypertension.

 Posthepatic portal hypertension.

 Intrahepatic portal hypertension.

( pre; sinosoidal block; post )
Deposition of collagen in Disse’s space (
and sinosoidal space )
Posthepatic portal hypertension

 Budd-Chiari syndrome

 Veno-occlusive disease (VOD)

 Constrictive pericarditis and heart failure

Intrahepatic portal hypertension

 Pre-sinusoidal block.
(schistosomiasis)

 Sinusoidal block and Post-sinusoidal block.

(alcoholic cirrhosis; HBV; HCV )
Prehepatic portal hypertension

 Portal vein thrombosis

 Cavernous transformation
 Cruveihier-Von Baumgarten disease.
 Arterioportal fistulas.
 Segmental portal hypertension.
( left-sided portal hypertension )
Diagnosis of portal hypertension Ⅰ
 Spider naevus and Palmar erythema ;Atrophic
liver cirrhosis or hepatomegaly; splenomegaly
(hypersplenism); ascites and edema;
esophagogastric varices and variceal hemorrhage.

 Blood RT (anemia, leukopenia, and

thrombocytopenia), hepatitic serologic test
(HBV,HCV), liver function test etc.

 Liver biopsy.
Diagnosis of portal hypertension Ⅱ

 CT angiography.

 Doppler ultrasonography.

 MRI.
Spider naevus and Palmar erythema
Esophagogastric varices
 This barium swallow
demonstrates tortuous
lower oesophageal and
gastric varices in a
patient with portal
hypertension.
Esophageal varices

 This angiogram
demonstrates the portal
and splenic venous
blood flowing into the
esophageal collaterals.
CT angiography
 A three-
dimensional
reconstruction of a
CT angiogram.
Bleeding esophageal varix

 Venous blood is seen

here spurting from the
bleeding varix at 3
o’clock on this
endoscopic view.
Variceal hemorrhage
 Bleeding from esophagogastric varices is
the single most life-threatening
complication of portal hypertension,
responsible for about one third of all deaths
in patients with cirrhosis.
Treatment of the acute bleeding episode

 Resuscitation and diagnosis

 Pharmacotherapy
 Balloon tamponade
 Endoscopic treatment
 Emergency surgery
 Transjugular intrahepatic portosystemic shunt
(TIPS)
Resuscitation and diagnosis
 Rapid initial assessment (airway, breathing,
circulation ).

 Large-bore intravenous access fluid

resuscitation commenced.

 Estimation of blood lost.

Pharmacotherapy for variceal
hemorrhage
 Vasopressin (usually administered
intravenously as a bolus dose of 20 units
over 20 minutes and then as a continuous
infusion of 0.2 to 0.4 unit/minute;
Nitroglycerin should be simultaneously
infused at an initial rate of 40 ug/minute.

 Somatostatin and Octreotide.

Balloon tamponade

 Sengstaken-
Blakemore tube
 This tube is used to
control oesophagastric
variceal haemorrhage
by means of balloon
tamponade.
Endoscopic treatment
 Variceal sclerosis or ligation is the
most commonly used therapy for both
management of the acute bleeding
episode and prevention of recurrent
hemorrhage.
Techniques of endoscopic sclerotherapy
 Endoscopic ligation of esophageal varices

 A , The varix is drawn

into the ligator by
suction.
 B, An O ring is
applied.
Emergency surgery

 Focus on hemorrhage.

 Selection of operation guided by the

experience of the surgeon.

 Hepatic functional reserve.

Transjugular intrahepatic portosystemic
shunt (TIPS)
 A needle is advanced from
an internal jugular vein
through a hepatic vein to a
major portal vein branch
and a guide wire is placed.
 A hepatic parenchymal
tract is created by ballon
dilation, and an
expandable metal stent is
placed, thereby creating
the shunt.
 Measurement of hepatic functional reserve
 In most clinical series,
operative mortality rates
for Child-Pugh classes A,
B, and C patients are in
the range of 0 to 5%, 10%
to 15%, and greater than
25%, respectively.
 An interval of medical
management to improve
the patient from class C to
class A or B is worthwhile
before surgical
intervention if indicated.
Portosystemic shunts

 Nonselective shunts

 Selective shunts

 Partial shunts
Nonselective shunts Ⅰ
Nonselective shunts Ⅱ
 Selective shunts Ⅰ

 Warren---distal
splenorenal shunt.
Selective shunts Ⅱ

 A small-diameter (8
to 10 mm )
interposition
portacaval shunt.
Nonshunt operations

 The Sugiura
procedure
Hepatic transplantation

 A treatment for end-stage hepatic failure,

for majority of patients,variceal bleeding is
associated with end-stage hepatic failure, so
hepatic transplantation is an option for
variceal hemorrhage sometimes.
Complication of operation for portal
hypertension
 Recurrent hemorrhage.

 Encephalopathy.

 Spontaneous bacterial peritonitis.

Recurrent hemorrhage
 Portal hypertensive
gastropathy (PHG).
 Endoscopic view:
snakeskin.
 Vascular ectasia by
raised portal
pressures and may
itself be a source of
bleeding.
Encephalopathy

 Especially portosystemic encephalopathy is

a psychoneurologic syndrome that may
have a variety of manifestations, including
alterations in the level of consciousness,
intellectual deterioration, personality
changes, and neurologic findings such as
the flapping tremor, asterixis.
Spontaneous bacterial peritonitis (SBP )

 Bacterially infected ascitic fluid in liver

cirrhosis, where the exact source of
infection or path of infection is not known.
 I t displays a high number of
polymorphonuclear neutrophils ( >
250/mm3 ), a protein content which is
usually < 1.0 g/dl and a positive bacterial
culture ( >90%).
Budd-chiari syndrome
 B-CS is obstruction of
venous outflow from
the liver due to
endophlebitis
obliterans and
occlusion of the
hepatic veins or
suprahepatic inferior
vena cava from
thrombosis or
obstructing webs.
Doppler US and IVC venography
of B-CS
Hepatic venography of B-CS
 Long segment of
obstruction of IVC.
Operation for B-CS
Ascites
 Ascites is usually an indicator of advanced
cirrhosis and is associated with a 1-year
survival rate of approximately 50%
compared to a 1-year survival rate of
greater than 90% for patients with cirrhosis
but without ascites.
 The chance of surgical treatment for ascites
based on its etiology.
Intractable ascites
Tapping ascitic fluid
Peritoneovenous shunt
 Diagram of the
positioning of a
peritoneovenous
shunt (with
Denver valve)
Pharmacotherapy for portal hypertension

 Propranolol---brings about an
approximate 50% reduction in portal
venous pressure in some two thirds of
patients; Dosage is established in line with
the slowing-down of the heart rate ( to
about 25% less than that of the initial value,
but not below 55/min ).
 Spironolactone (upwards of 50mg/day).
Over !