portal hypertension UG class by Prof. Ajay Khanna, IMS, BHU, Varanasi, India

Ajay Khanna
PORTAL HYPERTENSION
x

DEFINITION
 Normal Portal Pressure : 5-10 mm
 Pressure of > 12 mm : Portal Hypertension
 Portal Hypertension is characterized by gradient of >5
mm Hg between portal venous and central venous
pressure.
 At gradient of 8-10 mm Hg – Varices develops
 If gradient >12 mm Hg – Bleeding from varices

ANATOMY
• Hepatic blood flow
• 2/3rd – Portal vein
• 1/3rd – Hepatic artery
• Portal vein length – 6-8 Cm
• Diameter - 13-16 mm
1/3
2/3

Portosystemic Collateral Formation
Lower end of esophagus
Azygos vein Lt gastric V
Umblicus
Ant abd. veins Paraumblical
Lower end Rectum
Middle and Inf Superior Haem.
Haemmorrhoidal V
Retroperitoneum
Bare area of liver

Porta Systemic Collaterals
esophageal and gastric
veins
inferior rectal-anal veins
anterior abdominal wall
veins
retroperitoneal venous
plexus

PATHOPHYSIOLOGY
 Portal pressure = resistant X flow
Resistance to portal flow
Rise in portal pressure
Development of portasystem collaterals
Hyperdynamic circulation

ETIOLOGY
Extrahepatic (Prehepatic/ EHPVO)
 Portal cavernoma
 Portal vein thrombosis (most common cause)
 Splenic vein thrombosis
 Compression from outside
Intrahepatic
 Presinusoidal
 Schistosomiasis (most common cause)
 Primary biliary cirrhosis
 Sinusoidal
 Alcoholic cirrhosis (most common cause)
 Postsinusoidal
 Alcoholic cirrhosis (most common cause)
 Veno-occlusive disease
 Non Cirrhotic Portal Fibrosis

ETIOLOGY (Contd)
 Posthepatic
 Budd-Chiari syndrome (most common cause)
 Right sided heart failure
 Constrictive pericarditis
 High-flow portal hypertension
 Hepatic artery-portal vein fistula
 Splenic arteriovenous fistula
 Massive splenomegaly
 Left Sided Portal Hypertension (Sinistral)

Clinical features
 Bleeding (Upper GI)
 Splenomegaly
 Jaundice
 Encephalopathy
 Ascites
 Growth Retardation
 Coagulopathy
 Recurrent Infection

Examination
 Jaundice
 Hepatomegaly
 Splenomegaly
 Ascites
 Veins on abdominal wall
 Oedema
 Encepahlopathy
 Hernia

INVESTIGATIONS
• Hematological: CBC, Platelet,
• Biochemical: LFT, PT
• Radiological: Triple Phase Portography, MRI, CT
• Ultrasonography/Doppler
• Endoscopy
• Pressure studies
• Liver Biopsy

Barium swallow
multiple irregular filling defects as
“string of beads” or “earthworm”

ESOPHAGOGASTRO DUODENOSCOPY
Grading as per Endoscopy
 Paqet Grading
 Grade I: Small varices without luminal prolapse
 Grade II: Mod. Size varices showing luminal
prolapse along with minimal obscuring of
gastro esophageal junction.
 Grade III: Large varices showing luminal prolapse
substantially obscuring the gastro
esophageal junction.
 Grade IV: Very large varices completely obscuring
gastroesophageal junction.

USG/Doppler USG:
 Portal vein diameter, thrombus, collaterals , splenomegaly &
ascites.
 Portal flow direction and velocity – Hepatopetal/Fugal
 Portosytemic surgical shunt follow up
 To evaluate patency of shunt
 To evaluate direction of flow

Portography:
 Splenoportovenography
 Transhepatic/transjugular
 Umblical portography
 Triple Phase Portography (CT)
 MRI Portograophy

Portal Pressure Measurement
 Wedged hepatic venous pressure
 Occluded Pressure (SOPP/HOPP)
 Splenic pulp pressure
 Catheterization of umbilical vein
Liver Biospy
Laparoscopy

Child’s grade
(Pugh Modification)
Point 1 Point 2 Point 3
Bilirubin mgm/dl <2 2-3 >3
Albumin (gm/dl) >3.5 3-3.5 <3
Ascites None Controlled Uncontrolled
Encephalopathy None Mild Mod-severe
Prothrombin Time* <3 Sec prolonged 3-6 Sec prolonged >6 Sec prolonged
Total : 5-15
Child A < 6 Child B 7-9 Child C 10-15
* In Original Child score it was nutritional status

TREATMENT
Portal hypertension treatment involves three
level of management
 Reduction of portal pressure
 Treatment of complications arising from
portal hypertension
 Variceal bleeding
 Hypersplenism
 Treatment of underlying liver disease and its
complications

TREATMENT OF VARICEAL BLEEDING
 Primary Prophylaxis : No prior H/O bleed
 Propranolol
 EST
 Secondary Prophylaxis
 Propranolol
 EST
 Surgery

Emergency Treatment of Bleed
 Resuscitation
 Pharmacological therapy
 Endoscopic therapy
 Balloon Temponade
 Transjugular intrahepatic portosystemic
shunt (TIPS)
 Surgical treatment

PHARMACOLOGICAL THERAPY
 Beta blockers
 Vasopressin with or without
nitroglycerine
 Glypressin
 Somatostatin / octreotide
 Metoclopramide
 Long acting nitrates

Beta blockers
  bleeding by  cardiac output.
 Dose 20-60 mg bid  25%  in HR.
 Reduces 40% of bleeding episodes

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 pain, & 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).

ENDOSCOPIC THERAPY
 Injection sclerotherapy
 Variceal band ligation
 Gastric variceal injection
 Thrombin injections

EST
Techniques:
 Intravariceal injection
 Paravariceal injection
 Combination of both
intravariceal +
paravariceal injection

Sclerosants :
 5% Ethanolamine oleate
 0.5% sodium polidocanol
 5% sodium morrhuate
 1% to 3% sodium tetradecyl sulphate
 High concentration of alcohol
 3% phenol

ENDOSCOPIC VARICEAL LIGATION (EVL)
 Occludes venous channels
Sessions < sclerotherapy
Same results as sclerotherapy
 complications vs sclerotherapy
Endoscopic treatment of choice

BALLOON TEMPONADE
 Temporary measure
 Hazardous in infants and small children
 Success rate is 80-90%
 Complications : Aspiration pneumonia,
pressure necrosis , obstruction of
pharynx, ulceration of esophagus,
rupture of balloon, re-bleeding after
deflation (60%).

TYPES OF BALLOON TEMPONADE TUBE:
 Sengstaken Black’s more tube
 Linton-Nicholos tube for gastric variceal haemorrhage
 Minnesota tube – 4 lumen tube

TIPS(Transjugular Intrahepatic Porta systemic shunt)
• Shunt between portal vein
and hepatic vein
• Can be used as short term
bridge to liver
transplantation
• Goal – To reduce
portosystemic gradient
< 12 mm Hg

SURGICAL TREATMENT
SHUNT SURGERY
 Prophylactic
 Emergency shunt surgery
 Reduced with advent of other non surgical procedure
 End to side porto-caval shunt preferred
 Elective shunt surgery

Types of Shunt Surgery
 Non Selective
 Portacaval (end to side/ side to side)
 Mesocaval (With or without graft)
 Proximal Leino Renal Shunt
 Spleen preserving Side to side Splenorenal
shunt (Mitra)
 Selective Shunt
 Distal Leino Renal Shunt (Warren)
 Coronary Caval (Inokuchi)
 Porta Caval (SARFEH SHUNT) 8 mm graft

Warren
Distal Leino Renal Shunt

Types of Operation
 Non Shunt Surgery:
 Stapler transection, (Johnston)
 Boerema,
 Milnes Walker
 Suigura and Futagawa,
 Tanner,
 Hassab,
 Liver Transplantation

Non Selective 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
splenectomy 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
anastomosis 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.
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.
encephalopathy is low, and
the liver functions remain
normal.

Non Shunt Surgery
 Stapler Transection (Johnston)
 Boerema Crile
 Milnes Walker
 Suigura Futagawa
 Tanner
 Hassab

 Sugiura and Futagawa procedure
(1973)  Transthoracic
paraesophageal devascularization
and esophageal transaction
combined with an abdominal
component consisting of
splenectomy, devascularization of
upper stomach, vagotomy and
pyeloroplasty
Modified Sugiura procedure  (Ginsberg 1982) –
Abdominal approach. Splenectomy, paraesophageal and
gastric devascularization, vagotomy, stapler esophageal
transaction via gastrostomy and pyeloroplasty.

HYPERSPLENISM
SELECTIVE SPLENIC EMBOLIZATION :
 Splenic immune function is conserved, size of spleen is
reduced and portal flow is maintained.
 Aim of procedure is to infarct 70-80% of splenic tissue.
 Pneumococcal vaccination is given with this therapy and
sometimes long term antibiotics prophylaxis is needed.
SPLENECTOMY:
 Usually not advocated
 Indicated in isolated portal vein thrombosis with recurrent or
life threatening haemorrhage and a massive spleen.
Shunt Procedures

Ascites
 Disordered albumin synthesis and decreased plasma
colloid osmotic pressure caused by hepatocellular
function damage
 Increased capillary filter pressure due to increased portal
hypertension
 Lymph liquid leakage into abdominal cavity from surface
of the liver because of lymph back-flow obstruction
 Salt and water retention by aldosterone and antidiuretic
hormones deactivation disturbance

 Complications of ascites
 Respiratory embarrasement
 Spontaneous bacterial peritonitis
 Hernia
 Investgations:
 SAAG > 1.1 (Serum Ascitic Albumin Gradient)
 Treatment :
 Salt Restriction
 Diuretics
 Paracentesis
 Shunt - Le Veen Shunt, Denver Shunt
 TIPS
 Liver Transplant

Encephalopathy
 Lactulose
 Stop bleeding
 Neomycin
 Enemas

Budd Chiari syndrome
 Syndrome due to obstruction of hepatic
veins
 Causes :
 Spontaneous thrombosis
 Myeloproliferative disorders
 Web
 Neoplasms
 Polycyathemia
 Contraceptive pills

Presentation of
Budd Chiari Syndrome
 Acute :
 Nausea, vomiting, severe pain in Rt hypochondrium,
rapid enlargement of liver, hypotension, death
 Sudden onset
 Rapid development of Ascites, hepatic insufficiency,
oedema, coma
 Chronic
 Cirrhosis, Ascites, Varices, infection, hepatic failure
Classic Triad
Abdominal Pain
Ascites
Hepatomegaly

Treatment of
Budd Chiari Syndrome
 Anticoagulation
 Membrane IVC : Tranatrial Meatotomy
 Meso atrial Shunt : Shunt between Rt. Atrium
and Sup Mesenteric vein

portal hypertension UG class by Prof. Ajay Khanna, IMS, BHU, Varanasi, India

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portal hypertension UG class by Prof. Ajay Khanna, IMS, BHU, Varanasi, India