The document discusses portal hypertension, which occurs when portal venous blood pressure is greater than 12 mmHg. It can be caused by conditions that affect blood flow pre-hepatically, hepatically, or post-hepatically. Complications include esophageal and gastric variceal bleeding. Management involves treating the underlying cause, reducing portal pressure with medications, banding or sclerotherapy of varices, and shunt procedures or transplant for severe cases.

1. Dr. Ashok Jaisingani

2.  The hepatic portal circulation carries blood from
GI tract (i.e. from the distil esophagus to anorectal
junction) to the liver.
 Porto – systemic anastomosis occurs in junctional
areas of venous drainage.
 Portal venous blood drain into liver venous
sinusoids and hence in to the hepatic veins.

3.  Portal hypertension develop when there is
elevation of portal pressure is greater than 12
mmHg, while normal portal pressure is 5 –
10mmHg.
 As portal hypertension produce no symptoms it is
usually diagnosed following presentation with
decompensated chronic liver disease
encephalopathy, ascites or variceal bleeding.

4.  Pre – Hepatic:
1- Congenital portal atresia
2- Portal vein thrombosis (Neonatal sepsis)
3- Phlebitis of portal vein (abdominal infection)
4- Trauma or thrombosed porto – caval shunt.
 Hepatic:
1- Cirrhosis (alcoholic most frequently)
2- Chronic Active hepatitis
3- Parasitic diseases (Schiatosomiasis)
 Post – Hepatic:
1- Budd – Chiari syndrome (Hepatic venous thrombosis)
2- Constrictive pericarditis
3- Tricuspid valve incompetence

5.  Decrease or reverse portal blood flow to the liver promote
the development of the portosystemic anastomosis
between the portal system and systemic circulation.
1- Left gastric vein into the esophageal veins at gastro-
esophageal junction – esophageal and gastric varices.
2- Superior rectal vein into inferior rectal vein at lower
rectum rectal varices.
3- Obliterated umbilical vein into epigastric vein – capute
medusae.
 Esophageal and gastric varices may bleed torrentially
 Liver cell dysfunction/liver failure occurs in hepatic and
post – hepatic causes
 Splenomegaly (hypersplenism may be result)
 The child – pug classification use to asses the severity.

6. Conditions Point – 1 Point – 2 Point - 3
Bilirubin (µmol/L) <34 34 – 51 >51
Albumin (g/L) >35 28 – 35 <28
PT (sec) <3 3 – 10 >10
Ascites None Moderate Moderate – severe
Encephalopathy None Moderate Moderate – severe

7.  Many investigations may be used at different time
in portal hypertension such as
 1- FBC, Urea & electrolytes and clotting
 2- Screening tests for the causes of the cirrhosis
 3- CT & ultrasound scan to assess liver
morphology, diagnose Portal hypertension and
assess cause.
 4- Transabdominal Doppler ultrasound to assess
blood flow in the portal vein and hepatic artery.
 Gastroscopy in acute variceal bleeding

8.  General resuscitation
 Anti – coagulation for Budd – Chiari syndrome
 Treatment of hepatic cause
 Treatment Of Chronic Complication such as Esophageal gastric
varices:
1- Beta – blocker (propranolol or nadolol), reduce portal venous
pressure.
2- Repeated injection sclerotherapy or variceal ligation
3- Elective porto – systemic shunt (spleno – renal anastomosis)
4- Liver transplant may be considered for treatment if associated with
severe liver diseases.
 Rectal Varices: Injection sclerotherapy
 Symptomatic splenomegaly: laparoscopic or open splenectomy.
 Ascites: Oral spironolactone, in cases of ascites, paracentesis may be
required with IV albumin replacement.

9.  Hemorrhage from the varices is acute
complication of the portal hypertension.
 Mortality rate of first variceal bleed established
portal hypertension is 30%.
Causes & Features:
 Typical variceal bleeding is rapid in onset, copious
dark blood with little mixing with food.
 Feature of established portal hypertension e.g.
capute medusae
 Feature of developing hepatic encephalopathy
(ingested blood provide an extremely rich meal)

10.  Established large caliber IV access, give crystalloid fluid up
to 1000 mL, if tachycardic or hypotensive.
 Only use O - ve blood if the patient is in extremis,
otherwise wait for cross – match blood.
 Catheterize and place on fluid balance chart if hypotensive.
 Send blood for FBC, HB conc. WCC, U&E, Na, K, LFT,
albumin and clotting.
 Always consider HDU, variceal bleeding can deteriorate
extremely rapidly.
 Monitor pulse rate, BP and urinary output.
 Insertion Of sangstaken Blackmore gastro-esophageal tube
may be a life saving resuscitation manure, usually only
inserted without prior gastroscopy if the patient known to
have varices and has life – threatening bleeding.

11.  Blood transfusion
 Correct coagulopathy
 Esophageal balloon tamponade (sangstaken
Blackmore tube)
 Drug therapy (vasopressin or octreotide)
 Endoscopic sclerotherapy or banding
 Assess portal vein patency (Doppler ultrasound or CT)
 Transjuglar intrahepatic portosystemic stent shunt
Surgery:
 Portosystemic shunts
 Esophageal transection
 Splenectomy and gastric devescularization.