Portal Hypertension

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 threedimensional 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 !