Portal Hypertension

portal venous pressure > 5 mmHg

collaterals > 10 mmHg

bleeding > 12 mmHg

Portal Hypertension

intrahepatic - sinusoidal / post-sinusoidal (cirrhosis) pre-sinusoidal (schistosomiasis)

posthepatic - Budd-Chiari syndrome Veno-occlusive disease

prehepatic - portal vein thrombosis cavernous transformation of the portal vein

isolated splenic vein thrombosis left sided portal hypertension (inflammation – tumor)

Cirrhosis

alcoholviral hepatitis B & Ccholestatic primary biliary cirrhosis

secondary biliary cirrhosis primary sclerosing cholangitis

autoimmune lupoidmetabolic hemochromatosis

Wilson’s alpha 1 – antitrypsin deficiency

cryptogenic

Cirrhosis

hepatocellular necrosis - fibrosis & nodular regeneration

two major phenomena:

loss of cell mass - hepatocellular failure

increased hepatic vascular resistance -

portal hypertension

Portal Hypertension

splenomegaly

porto-systemic collaterals - coronary & short gastric veins to azygos vein–

esophageal varices

- recanalized umbilical vein–

caput medusae

- retroperitoneal

- hemorrhoidal venous plexus

Bleeding

esophageal varices 80%

gastric varices 20%

portal hypertensive gastropathy

Bleeding

patients with varices – bleeding in 33 - 50%

acute variceal bleeding – mortality 25 - 30%

rebleeding - 70%

Bleeding

chronic liver disease spider angiomas palmar erythema testicular atrophy

gynecomastia jaundice

ascites splenomegaly

caput medusae asterixis (liver flap)

Immediate Management

hemodynamic stabilization -PT

- platelets - electrolytes -creatinine

endoscopy - diagnostic - therapeutic

Pharmacotherapy

splanchnic vasoconstrictors

vasopressin )hypertension, bradycardia, decreased cardiac output,

coronary vasoconstriction (Tx combined with nitroglycerin

glypressin – terlipressin

somatostatin - octreotide

Endoscopic Treatment

variceal sclerosis – sclerotherapy

variceal ligation – banding

control of bleeding – 85%

Balloon Tamponade

Sengstaken – Blakemore tube

Encephalopathy

neomycin–

suppresses urease containing bacteria

lactulose–

acidifies colonic contents

cathartic effect

Further Treatment

rebleeding – 70% options:

pharmacotherapy – propranolol repeat endoscopic therapy

TIPS porto-systemic shunt operations

devascularization procedures liver transplantation

Hepatic Functional Reserve

Child’s classification

A B C

albumin (g/dl) > 3.5 3 – 3.5 < 3 bilirubin (mg/dl) < 2 2 – 3 > 3

ascites none mild moderate encephalopathy none minimal markednutritional state excellent good poor

Hepatic Functional Reserve

Child – Pugh classification

points 1 2 3

albumin (g/dl) > 3.5 2.8 – 3.5 < 2.8

bilirubin (mg/dl) < 2 2 – 3 > 3

PT (sec prolonged) 1 – 4 4 – 6 > 6

ascites none mild moderate

encephalopathy none minimal marked

Hepatic Functional Reserve

Pugh score 5 – 6 = Child’s A

good hepatic reserve

good operative candidate < 5 % mortality

Pugh score 7 – 9 = Child’s B moderate hepatic reserve

modest operative candidate 10 – 15 % mortality

Pugh score 10 – 15 = Child’s C low hepatic reserve

poor operative candidate > 25 % mortality

Portosystemic Shunts

effective decompression of portal system

- effective in preventing recurrent bleeding

diversion of portal blood

- accelerated hepatic failure

- encephalopathy

Portal Blood

cerebral toxins - ammonia

bypass of the liver prevents inactivation

hepatotrophic elements – insulin

diversion causes atrophy

Surgical Shunts

nonselective (total) end-to-side portocaval shunt (Eck’s fistula)

other nonselective shunts side-to-side meso-caval spleno-renal

selective shunts distal spleno-renal (Warren shunt)

TIPS

Transjugular Intrahepatic Portosystemic Shunt

major advantage – nonoperative

disadvantage -

nonselective shunt – encephalopathy 30%

shunt stenosis or occlusion at 1 year 50%

Devascularization Procedures

transection & reanastomosis

- of esophagus = Sugiura procedure

- of stomach = Tanner procedure