This document discusses portal hypertension, defined as a portal pressure higher than 5mm hg. Portal hypertension occurs due to increased portal venous resistance and can be prehepatic, intrahepatic, or posthepatic. The most common causes are portal vein thrombosis prehepatically and schistosomiasis or cirrhosis intrahepatically. Investigations include liver function tests, ultrasound, and the Child-Pugh score. Management includes treating varices with beta blockers, endotherapy, balloon tamponade, TIPSS, or shunt surgery. Transplant is the last option if other treatments fail.

1. PORTAL HYPERTENSION

2. DEFINITION
 Portal hypertension is defined by a portal
pressure higher than 5mm hg.
 However higher pressure (>8 mm hg) are
typically required to begin stimulating the
developing of porto systemic
collateralization

3. PATHOPHYSIOLOGY
 Portal hypertension usually occurs because of increased portal venous
resistance that is prehepatic ,intra hepatic or post hepatic in location.
 The most common cause of prehepatic portal hypertension is portal
vein thrombosis . This accounts for approximately 50% of cases of
portal hypertension in children .
 When portal vein is thrombosed in the absence of liver disease
,hepatopetal (to the liver) portal collateral vessels develop to restore
portal perfusion. This combination is termed as cavernomatous
transformation of portal vein.

4.  Most common cause of intrahepatic presinusoidal hypertension is
schistosomiasis.
 Non alcoholic cirrhosis result in presinusoidal portal hypertension
 Alcoholic cirrhosis usually increases resistance to portal flow at the
sinusoidal (secondary to deposition of collagen in the space of
disse)and post sinusoidal (secondary to regeneration nodules
distorting small hepatic veins)

7. INVESTIGATIONS
 Liver function test
 Ultrasound
 Alfafeto protein
 MELD-model for end stage liver disease ,is assessed by specific equation using
creatinine and bilirubin
 Child pugh score system
 Serological assessment –afp, iron sulphide ,antitrypsin ,autoantibodies,
investigations for hepatitis
 Doppler imaging to see vascular pattern ,direction of blood flow, size of vein

8. CHILD PUGH SCORE

10.  Ct/mri –non invasive method to study extrahepatic portal system mainly to
confirm extrahepatic portal vein thrombosis
 Hepatic venous pressure gradient (HVPG) done using balloon catheter.
difference between free hepatic vein pressure and wedged hepatic vein
pressure is HVPG( normal-8mm hg).
 Others- splenoportorrhaphy
liver biopsy
endosonography

11. MANAGEMENT
 General measures
anaemia correction
nutritional supplementation
inj. Vit k
 TREATMENT OF OESOPHAGEAL VARICES
can be asymptomatic
hematemesis- inj propranolol (reduces the portal pressure by 20% with pulse
rate below 55/min
-endotherapy

12. ENDOTHERAPY
 Endoscopic variceal banding
 Endoscopic variceal sclerotherapy
 Endoscopic gluing using tissue adhesive
 Endoscopic thrombin/dilute adrenaline injection into
varices

13. Balloon temponade
 Sengstaken Blakemore tube / 4 lumen Minnesota tube etc
are used for the procedure
 Initially gastric balloon is inflated with 300-400 ml of
air,later the oesophageal balloon is inflated for short
period so as to prevent necrosos of esophagus .
 Xray will confirm its position

14. TIPSS
 Transjugular intrahepatic portosystemic shunt/ stenting
 Done only if earlier methods fail
 Contrls the uncontrolled acute bleeding and prevents
further bleed and acts as a bridge for future transplant

15. SHUNT SURGERY
 INDICATION- childs grade A and B ,surgery contraindicated in child C
 Surgery is divided into – non selective and selective
 NON SELECTIVE- . porto caval shunt(end-side, side to side)
. Mesentericocaval shunt with or without graft
. Proximal splenorenal shunt- lintons shunt
. Mesenterico renal shunt
 SELECTIVE- . Distal splenorenal shunt- warren shunt
. Inokuchi shunt
Lastly if all fails we go for liver transplant.

16. THANK YOU